Dementia is the loss of mental functionssuch as thinking, memory, and reasoningthat is severe enough to interfere with a persons daily functioning. Dementia is not a disease itself, but rather a group of symptoms that might accompany certain diseases or conditions. Symptoms also might include changes in personality, mood, and behavior. Dementia is irreversible when caused by disease or injury, but might be reversible when caused by drugs, alcohol, hormone or vitamin imbalances, or depression. Dementia develops when the parts of the brain that are involved with learning, memory, decision-making, and language are affected by any of various infections or diseases. The most common cause of dementia is Alzheimers disease, but there are numerous other known causes. Most of these causes are very rare. http://www.clevelandclinic.org/health/health-info/docs/2300/2340.asp Dementia can cause changes in the behaviour of a person. Such changes are very common, but they can place enormous stress on families and carers. It can be upsetting when someone who has previously been gentle and loving behaves in a strange or aggressive way. Causes of behaviour change
Dementia affects people in different ways. Understanding why someone is behaving in a particular way may help families and carers to cope.
There are many reasons why a persons behaviour may change. Dementia is a result of changes that take place in the brain which affect the persons memory, mood and behaviour. Sometimes behaviour may be related to these changes taking place in the brain. In other instances, the behaviour may be triggered by changes in the persons environment, health or medication.
Where to begin talk to your doctor
Always discuss concerns about behaviour changes with the family doctor, who will be able to check whether there is a physical illness or discomfort present and can provide some advice. The doctor will also be able to advise if there is an underlying psychiatric illness.
Changed behaviours are not deliberate
Coping with changed behaviours can be very difficult and is often a matter of trial and error. Always remember that the behaviour is not deliberate.
Anger and aggression are often directed against family members and carers because they are closest. The behaviour is out of the persons control and they may be quite frightened by it. They need reassurance, even though it may often not appear that way.
Ways to cope with changed behaviours
Suggestions for coping with changed behaviours include: Provide a calm, unstressed environment in which the person with dementia follows a familiar routine this can help to avoid some difficult behaviours. Try to keep the environment familiar. People with dementia can become upset if they find themselves in a strange situation or among a group of unfamiliar people where they feel confused and unable to cope. If behaviour becomes difficult, do not attempt any form of physical contact such as restraining the person, leading them away or approaching them from behind. Leave them alone until they have recovered or call a friend or neighbour for support. Dont take changed behaviour personally. Try not to raise your voice. Speak slowly in a calm and reassuring voice. Avoid punishment. The person may not remember the event and is therefore not able to learn from it. Try to remain detached; do not become provoked or drawn into an argument.
http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/Dementia_changed_behaviours Facts About Dementia The term "dementia" is used to describe patients with impaired intellectual capacity. Dementia patients may also be labeled as having "presenile" or "senile" dementia, "chronic" or "organic brain syndrome," "arterio-sclerosis," or "cerebral atrophy." Dementia is not a normal part of the aging process. Dementia can be caused by abnormal disease processes and can affect younger as well as older persons. Symptoms of Dementia Short-term memory loss Inability to think problems through Inability to complete complex tasks Confusion Difficulty concentrating and paranoid, inappropriate or bizarre behavior Possible Causes of Dementia Deteriorating intellectual capacity may be caused by a variety of diseases and disorders. The National Institute on Aging states that some 100 conditions which mimic serious disorders are actually reversible. These are sometimes called "pseudodementias," and are often treatable. Examples of conditions causing reversible symptoms of dementia are: Reactions to medications: Older persons taking prescription drugs may suffer adverse reactions, including confusion. Sedatives, hypnotics, neuroleptics, antihypertensives and antiarthritic medications are among the most common. All medications, including over-the-counter drugs and herbal remedies, should be monitored by a physician to reduce the possibility of side effects. Emotional distress: Depression or major life changes such as retirement, divorce or loss of a loved one can effect one's physical and mental health. A physician should be informed about major stressful events. Severe delusional states should also be diagnosed by psychiatrists. Metabolic disturbances: Problems including renal failure, liver failure, electrolyte imbalances, hypoglycemia, hyperglycemia, hepatic disease or pancreatic disorders can provoke a confusional state, changes in sleep, appetite or emotions. Vision and hearing: Undetected problems of vision or hearing may result in inappropriate responses. This could be misinterpreted as dementia because an individual is unable to perceive surroundings or understand conversations. Hearing and eye examinations should be performed. Nutritional deficiencies: Deficiencies of B vitamins (folate, niacin, riboflavin and thiamine) can produce cognitive impairment. Special attention should be given to patients who have difficulty in chewing, swallowing, or digesting food. Loss of taste and smell, loss of appetite, poorly fitting dentures or even difficulty shopping or preparing food may lead to nutritional deficiencies. Endocrine Abnormalities: Hypothryroidism, hyperthyroidism, parathyroid disturbances or adrenal abnormalities can cause confusion which mimics dementia. Infections: Older persons can develop infections which produce a sudden onset of a confusional states. They should be brought to the attention of a physician. Confusion caused by an infection is often treatable. Subdural Hematoma (blood clot on the surface of the brain): Clots can form which create collections of fluid that exerts pressure on the brain. These clots can be treated by draining the fluid before it has caused permanent damage. Normal Pressure Hydrocephalus: The flow and absorption of spinal fluid, which is manufactured inside the brain, is interrupted. When the fluid is not absorbed properly, it builds up inside the reigning creates pressure. Surgery can be performed to drain the spinal fluid into the bloodstream to relieve the pressure. Brain tumors: Tumors in the brain can cause mental deterioration. Benign tumors can be surgically removed. For other tumors, a combination of surgery and radiation/chemotherapy can help patients. Atherosclerosis (hardening of the arteries): Intellectual impairment can result when a series of small strokes occur (multi-infarct dementia). Although damage from small strokes is typically a irreversible, built up atherosclerotic placques can be surgically removed or medically treated in order to prevent future strokes from occurring. If action is taken early enough the person can be helped. Irreversible Cognitive Impairment Conditions Traumatic brain injury: Traumatic brain injury can occur at any age. Trauma from a fall or an accident can precipitate personality, cognitive or behavior changes. If brain injury is mild, previous functioning may be restored over time. In cases of moderate to severe head trauma, brain impairment may be lasting. Careful attention should be paid to any blows to the head. Head injuries should be examined by an neurologist or rehabilitation specialist. Cerebral degenerative diseases: If dementia is caused by a degenerative disease, a progressive cognitive deterioration cannot be reversed. The most common irreversible dementia is Alzheimer's disease. Other degenerated diseases which can also cause dementia include dimension with Lewy's bodies, Parkinson's disease, Huntington's chorea and Picks disease. Other causes of intellectual impairment include stroke, loss of oxygen to the brain, Creutzfeld-Jakob's disease, Binswanger disease, AIDS and multiple sclerosis http://www.blhc.org/dementia.aspx There are several situations that could cause dementia: Diseases that cause degeneration or loss of nerve cells in the brain such as Alzheimer's, Parkinson's and Huntington's. Diseases that affect blood vessels, such asstroke, which can cause a disorder known as multi-infarct dementia. Toxic reactions, like excessive alcohol or drug use. Nutritional deficiencies, like vitamin B12 and folate deficiency. Infections that affect the brain and spinal cord, such as AIDS dementia complex and Creutzfeldt-Jakob disease. Certain types of hydrocephalus, an accumulation of fluid in the brain that can result from developmental abnormalities, infections, injury, or brain tumors. Head injury -- either a single severe head injury or chronic smaller injuries that often occur from boxing. Illnesses other than in the brain, such as kidney, liver, and lung diseases, can all lead to dementia. Alzheimer's disease causes 50% to 60% of all dementias. But researchers have found that two nervous diseases, which were originally incorrectly diagnosed as Alzheimer's, are emerging as major causes of dementia: Lewy body disease andPick's disease.
How dementia impacts behaviour In the initial stages, patients appear so normal that people around them forget that they are suffering from a disease that has affected their brain. While theoretically people know that the patients have a disease, they do not correlate the apparently inconsistent or inconsiderate behaviour of the patients with the disease. Caregivers may assume that the patient is being uncooperative or stubborn or just not trying hard enough, and therefore get irritated or sad or angry. Patients sense this emotion and this, too, affects their behavior. The intention of this page is to give caregivers some idea on how behavior is impacted by problems that dementua patients faceains. It is by no means an exhaustive list; it only aims to help caregivers orient themselves to dementia behavior so that they set realistic expectations and can think of ways to handle behaviors that could harm the patient and others around them. The brain gets damaged in dementia How dementia affects the ability to do things How dementia affects the emotional state of the patient What caregivers can remember about dementia behaviour The brain gets damaged in dementia In order to see how dementia affects behaviour, we need to understand that the diseases that cause dementia affect the brain, and that the patients problems occur because of these organic changes to the brain.
The brain is a very complex organ, with billions of cells (neurons) that communicate with each other so that we can do things. Different parts of the brain perform different tasks. Dementing diseases affect the brain. The parts of the brain affected, and how the damage increases over time, depends on the disease causing the dementia. Image courtesy for image on left: National Institute on Aging/National Institutes of Health The damage to the brain increases as dementia progresses. The damage may become more severe, and more areas of the brain may also get damaged. To illustrate the increasing damage to the brain, the image panel below uses images of brains of patients with Alzheimers Disease, the leading cause of dementia. Image courtesy for images below: National Institute on Aging/National Institutes of Health
Images showing Pre-clinical Alzheimers Disease, Mild Alzheimers Disease and Severe Alzheimers Disease
How dementia affects the ability to do things
Explanation Impact on behaviour
Image courtesy: National Institute on Aging/National Institutes of Health Different patients have damage in different parts of the brain When the disease progresses, it may affect different parts in different people Different patients will face different types of problems. For example, some may have more problems walking, while others may have more problems while speaking. Over time, the patients ability to do things will get worse.
Image courtesy: National Institute on Aging/National Institutes of Health As dementia progresses, the damage to the brain increases. More areas of the brain may get impacted. Visible symptoms increase depending on the areas of the brain affected, and the severity of the damage. As more and more parts of the brain are impacted, the patients ability to perform activities of daily living keeps decreasing. Communication is often impacted. Memory loss is common in many types of dementia. Major personality changes are seen in some types of dementia. There is an overall deterioration. In the final stages, the patient is fully dependent and often unable to communicate
Every task we do has multiple steps. Inability to do any step results in inability to complete a task If the dementing disease has affected the patients ability to do part of a task, the patient will not be able to do that task independently and will need assistance
Every task requires coordination of various parts of our body and the ability to pay attention. Multiple parts of the brain have to function properly to perform this. For example, to light the gas stove, we need to position the lighter near the burner and click its button at the exact moment that we turn the corresponding knob of the gas stove. As dementia progresses, at least some parts of the brain required for this coordination and focus are likely to be damaged Patients will no longer be able to do complex tasks that require precision and coordination. Attempts to do such tasks are likely to lead to frustration or accidents
All of us have some fluctuation in our abilities over days, depending on our mood and health and energy. In dementia patients, we often find fluctuations in the abilities to do a specific task or remember something. Fluctuations in cognitive ability are particularly common in Lewy Body Dementia To persons interacting with dementia patients, it seems strange to see the person able to remember something on one day, and not be able to remember it later. When they see the patient do something on one day and not be able to do it the very next day, people begin thinking the person is not trying hard enough. It is helpful to know that such fluctuations may be characteristic of their dementia.
Often, patients get disoriented because of problems like loss of memories, visio-spatial problems, discomfort with too much stimulus or noise, inability to understand objects around them, etc. This leads to multiple problems, such as The patient may wander and forget the way back home The patient may consider himself/ herself as younger and expect a different home, and may not recognize the children and grandchildren, or mistake the daughter for the wife The patient may keep insisting he/ she wants to go home The patient may be anxious about not knowing where the toilet is
Patients often cannot communicate what they want. They may have problems remembering the right word, or may not know the meaning of words others use. They may not be able to frame sentences. Patients may also have problems knowing what they are feeling; they may not realize they are hungry or thirsty or hot or cold, or even that they are unwell or in pain. They may not be able to tell caregivers what they want. They may not be able to indicate that they are unwell or are in pain. So their needs remain unfulfilled. This may also frustrate, distress, or anger them, even if they dont know how to express it. If they are ill, their illness will affect their ability to do things, but caregivers may not understand why the patient is acting differently today. Also, the caregiver may not realize that the patient needs rest/ treatment.
In many types of dementia, recent memories are lost, and patients often revert to older memories, or (unconsciously) try to fill gaps in their memories using their imagination Patients cannot recognize people or places, and may not even recognize their home and family
Often, patients are unable to create new memories. They may also have problems understanding complex instructions or concepts. This affects their ability to learn new things, use new devices, and adjust to new places. They may also get stressed when they meet new persons or see new things, and start avoiding such situations
In many types of dementia, the part of the brain that tells people how to interact socially is not damaged initially. This social interaction ability deteriorates at a slower pace in most patients Patients may cover up for memory loss and other problems by giving evasive answers, thus masking the problem in the presence of guests
In some types of dementia, people become disinhibited or are unable to behave in socially correct ways because the part of the brain that regulates behavior is damaged. The patients personality changes. Emotions may also get flattened and the patient may show apathy. Such problems are typical in behavior-variant fronto- temporal dementia. Often, this leads to embarrassing situations where people may assume the patient has bad character or is inconsiderate and insensitive. For example, the patient may made rude remarks (even sexual comments), yell or abuse. Or the patient may laugh when others are crying. Or the patient may lose interest in everything and not show any reaction to emotions of persons nearby.
In some forms of dementia, notably Lewy Body Dementia, patients may suffer from hallucinations. Delusions and paranoia are also present in some forms of dementia Patients who hallucinate may sometimes realize they are hallucinating, but at other times, they may be confused or frightened because they believe what they are seeing or hearing. Hallucinations may make familiar tasks difficult when they cannot distinguish between reality and hallucination (for example, if they see a road split into four, they cannot drive). People near them may not realize that the patient is hallucinating and hence confused/ frightened. Delusions and paranoia also affect how the patient interacts with others. They may accuse people of stealing their possessions or even of trying to kill them. It is difficult to make the patient understand what is real and what is delusion, or to calm down a paranoid patient.
Repetitive behavior and compulsive behavior are common in many forms of dementia. (this is also called perseveration). Such behavior may occur for many reasons, such as forgetting having said or done the thing earlier, boredom, anxiety, agitation, etc. Common examples are the patient may say the same thing repeatedly, ask the same question, make the same gesture, do the same action, etcetera. Often, such repetitive behavior is harmless, but at times it may be problematic (like the patient insisting on eating breakfast multiple times) or even harmful (taking medication mutliple times) or exhausting (such as packing/ unpacking a suitcase or pacing). It can also be annoying or distressing for caregivers if they dont understand it is happening because of dementia and dont know how to cope with it.
In many instances, dementia patients show changed behavior in the evenings/ night, called sundowning. While causes for such behavior are not fully understood, they are expected to be related to day time activities, exhaustion, body clock, food cycles, intake of liquid foods near dinner time, and so on. Patients start acting agitated as evening approaches. They may be restless and start pacing. They may seem more agitated and anxious. Sleeplessness is another problem. They may walk up and down all night, mumbling or even shouting at times. All this can be very tiring for the patients and their caregivers
2. What are the correlation between the age with the patien problems? Risk factors that can't be changed Age. The risk of Alzheimer's disease, vascular dementia and several other dementias increases significantly with age. However, dementia isn't a normal part of aging. Family history. People with a family history of dementia are at greater risk of developing it. However, many people with a family history never develop symptoms, and many people without a family history do. If you have specific genetic mutations, you're at significantly greater risk of developing certain types of dementia. Tests to determine whether you have such genetic mutations are available, but only for the disorders in which the specific mutation is known, for example, Huntington's disease. Down syndrome. By the time they reach middle age, most people with Down syndrome develop the plaques and tangles characteristic of Alzheimer's disease, according to studies. Many, but not all, also develop dementia.
Risk factors you can change To reduce your risk of dementia, you can take steps to control the following factors. Alcohol use. Consuming large amounts of alcohol appears to increase the risk of dementia. Although studies have shown that moderate amounts of alcohol one drink a day for women and two for men especially red wine, have a protective effect, abuse of alcohol puts you at increased risk of developing dementia. Atherosclerosis. This buildup of fats and other substances in and on your artery walls (plaques) is a significant risk factor for vascular dementia because it interferes with blood flow to your brain. This can lead to stroke. Studies have also shown a possible link between atherosclerosis and Alzheimer's disease. Blood pressure. Blood pressure that's too high, and also possibly too low, can put you at risk of developing Alzheimer's disease and vascular dementia. Cholesterol. High levels of low-density lipoprotein (LDL) cholesterol, the "bad" cholesterol, can significantly increase your risk of developing vascular dementia. Some research has also linked it to an increased risk of developing Alzheimer's disease. Depression. Although not yet well understood, late-life depression, especially in men, may be an indication for the development of Alzheimer's-related dementia. Diabetes. If you have type 2 diabetes, you're at increased risk of developing both Alzheimer's disease and vascular dementia. High estrogen levels. High levels of total estrogen in women have been associated with greater risk of developing dementia. This can be determined through a blood test. Homocysteine blood levels. Elevated blood levels of homocysteine a type of amino acid produced by your body may increase your risk of developing Alzheimer's disease and vascular dementia. When working properly, your body breaks down homocysteine using vitamins B-6, B-12 and folic acid. If this isn't happening properly, it may be because you don't metabolize these vitamins well, or you don't have enough of them in your diet. Blood tests can determine whether you have elevated homocysteine levels. Smoking. Smoking likely increases the risk of developing dementia because it puts you at a higher risk of atherosclerosis and other types of vascular disease. http://www.mayoclinic.com/health/dementia/DS01131/DSECTION=risk-factors Age The greatest known risk factor for Alzheimers is advancing age. Most individuals with the disease are age 65 or older. The likelihood of developing Alzheimers doubles about every five years after age 65. After age 85, the risk reaches nearly 50 percent. One of the greatest mysteries of Alzheimer's disease is why risk rises so dramatically as we grow older. Aging is the main risk factor for all types of dementia. Some diseases that cause dementia (such as early-onset Alzheimer's disease and some frontotemporal dementias) may run in families. You have a greater chance of developing vascular dementia if you: Are male. Have high blood pressure. Have had a heart attack. Have atherosclerosis, a buildup of fat andcalcium in the arteries, which can lead tocoronary artery disease. Have diabetes. Have high cholesterol. Have had a stroke or transient ischemic attack (TIA). http://www.webmd.com/alzheimers/tc/dementia-what-increases-your-risk 3. Why doctor give haloperidol and rivastigmine? HALOPERIDOL Type of medicine Antipsychotic Used for Schizophrenia and other mental health problems affecting thoughts, feelings and behaviours Motor tics (involuntary body movements or twitches) Gilles de la Tourette's syndrome (a condition with involuntary body twitches and the urge to say obscene words or make noises) Persistent hiccups Short-term treatment of anxiety Feeling or being sick Also called Dozic, Haldol, Serenace Available as Tablets Capsules Oral liquid Injection
Haloperidol is used to treat mental health problems which affect the way you think, feel or behave. These problems may make you hear, see or sense things that are not there, or believe things that are not true, or feel unusually suspicious.
Mental health problems like schizophrenia, are thought to be caused by over-activity of certain areas of the brain. Haloperidol works by blocking receptors in the brain to alter the activity in these areas. It helps to improve disturbed thoughts and behaviour and produces a calming effect where there is aggression and agitation.
Haloperidol also acts on receptors in the brain that control feelings of sickness and it is sometimes used to provide relief from nausea and vomiting. It can also be used for hiccups that do not go away Before taking haloperidol Before taking haloperidol make sure your doctor or pharmacist knows: If you are pregnant, trying for a baby or breast-feeding. If you have liver or kidney problems. If you have any heart or circulation problems. If you have breathing problems. If you suffer from Parkinson's disease. If you have epilepsy, depression, myasthenia gravis (a muscle weakening disease), prostate problems or glaucoma. If you have ever had jaundice (yellowing of the skin and whites of the eyes) or a problem with your blood. If you have phaeochromocytoma (a growth affecting the adrenal glands). If you know you have low amounts of calcium, potassium or magnesium in your blood. If you have ever had a subarachnoid haemorrhage(bleeding in the brain). If you are taking other medicines, including those available to buy without a prescription, herbal or complementary medicines
http://www.patient.co.uk/medicine/Haloperidol.htm
Indications Haloperidol is indicated for the treatment of schizophrenic patients who require prolonged parenteral antipsychotic therapy also used in Tourette's syndrome and Severe hyperactivity. Haloperidol is indicated to treat psychotic disorders and symptoms such as hallucinations, delusions, and hostility and to control muscular tics of the face, neck, hands, and shoulders. It is also used to treat severe behavioral problems in children and in hyperactive children (short-term use).
A phenyl-piperidinyl-butyrophenone that is used primarily to treat schizophrenia and other psychoses. It is also used in schizoaffective disorder, delusional disorders, ballism, and tourette syndrome (a drug of choice) and occasionally as adjunctive therapy in mental retardation and the chorea of huntington disease. It is a potent antiemetic and is used in the treatment of intractable hiccups. (From AMA Drug Evaluations Annual, 1994, p279)
Contraindications Since the pharmacologic and clinical actions of Haloperidol Decanoate 50 and Haloperidol Decanoate 100 are attributed to Haloperidol (haloperidol) as the active prescription, Contraindications, Warnings, and additional information are those of Haloperidol, modified only to reflect the prolonged action. Haloperidol is contraindicated in severe toxic central nervous system depression or comatose states from any cause and in individuals who are hypersensitive to Haloperidol or have Parkinsonis disease. Side Effects Haloperidol side effects that you should report to your health care professional or doctor as soon as possible: - confusion; - constipation; - difficulty breathing or fast breathing; - difficulty urinating or loss of bladder control; - drowsiness; - dry mouth; - eye pain or discoloration; - fast, irregular, or pounding heartbeat; - fever; - fine worm-like tongue movements; - headache; - restlessness; - restlessness or pacing; - seizures or convulsions; - severe muscle stiffness; - shuffling walk; - skin rash; - slow, jerky movements; - tremor; - unusual bleeding or bruising; - unusual face, mouth, or jaw movements; - unusual tiredness or weakness; - weight gain; - yellowing of the skin or eyes; http://www.genrxinfo.net/drugs/Haloperidol.htm Drug Interactions Haloperidol has been reported to interfere with the anticoagulant properties of phenindione in an isolated case, and the possibility should be kept in mind of a similar effect occurring when haloperidol is used with other anticoagulants.
Haloperidol may antagonize the action of epinephrine and other sympathomimetic agents and reverse the blood-pressure-lowering effects of adrenergic-blocking agents such as guanethidine. Enhanced CNS effects have been reported when haloperidol is used in combination with methyldopa.
As with all antipsychotic agents, haloperidol should not be used alone where depression is predominant. It may be combined with antidepressants to treat those conditions in which depression and psychosis coexist.
If concomitant antiparkinson medication is required, it may have to be continued after stopping haloperidol if its excretion is faster than that of haloperidol in order to avoid the development or aggravation of extrapyramidal symptoms.
Haloperidol inhibits the metabolization of tricyclic antidepressants, thereby increasing plasma levels of these drugs.
In pharmacokinetic studies, mild to moderately increased haloperidol levels have been reported when haloperidol was given concomitantly with the following drugs: quinidine, busipirone, fluoxetine. It may be necessary to reduce the haloperidol dosage.
When prolonged treatment with enzyme-inducing drugs such as carbamazepine, phenobarbital, rifampin is added to haloperidol therapy, this results in a significant reduction of haloperidol plasma levels. Therefore, during combination treatment, the haloperidol dose should be adjusted, when necessary. After stopping such drugs, it will be necessary to reduce the dosage of haloperidol.
Haloperidol may impair the antiparkinson effects of levodopa. If an antiparkinson agent is used concomitantly with haloperidol, both drugs should not be discontinued simultaneously, since extrapyramidal symptoms, previously controlled by antiparkinson agents, may occur due to the slower excretion rate of haloperidol.
The physician should keep in mind the possibility of an increase in intraocular pressure when anticholinergic drugs, including antiparkinson agents, are administered concomitantly with haloperidol.
When haloperidol is used to control mania in cyclic disorders, there may be a rapid mood swing to depression.
The antiemetic action of haloperidol may obscure signs of toxicity due to overdosage of other drugs or mask the symptoms of some organic diseases, such as brain tumor or intestinal obstructions.
Severe neurotoxicity (rigidity, inability to walk or talk) may occur in patients with thyrotoxicosis who are also receiving antipsychotic medication, including haloperidol.
Carcinogenicity studies in mice (18 months) and rats (24 months) showed a significant increase in mammary gland neoplasia and total tumor incidence in female mice at 1.25 and 5 mg/kg/day and in pituitary gland neoplasia in female mice at 5 mg/kg. A significant dose- related increase in pituitary gland hyperplasia was observed in female rats at 1.25 and 5 mg/kg/day. The potential significance of these findings in man is not known. Neuroleptic drugs elevate prolactin levels; the elevation persists during chronic administration. Tissue culture experiments indicate that approximately one-third of human breast cancers are prolactin dependent in vitro, a factor of potential importance if the prescription of these drugs is contemplated in a patient with a previously detected breast cancer. Although disturbances such as galactorrhea, amenorrhea, gynecomastia, and impotence have been reported, which are presumed to be linked to elevated prolactin levels, the clinical significance of elevated serum prolactin levels is unknown for most patients. An increase in mammary neoplasms has been found in rodents after chronic administration of neuroleptic drugs. Neither clinical studies nor epidemiologic studies conducted to date, however, have shown an association between chronic administration of these drugs and mammary tumorigenesis. The available evidence is considered too limited to be conclusive at this time.
Occupational Hazards: Effects on driving ability and use of machinery: Some degree of sedation or impairment of alertness may occur, particularly with higher doses and at the start of treatment and may be potentiated by alcohol. Patients should be advised not to drive or operate machinery during treatment, until their susceptibility is known. www.news-medical.net/health/Haloperidol-Pharmacokinetics.aspx
Pharmacodynamics Haloperidol is a psychotropic agent indicated for the treatment of schizophrenia. It also exerts sedative and antiemetic activity. Haloperidol principal pharmacological effects are similar to those of piperazine-derivative phenothiazines. The drug has action at all levels of the central nervous system-primarily at subcortical levels-as well as on multiple organ systems. Haloperidol has strong antiadrenergic and weaker peripheral anticholinergic activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic and antiserotonin activity. Pharmacokinetics
Haloperidol blocks postsynaptic dopamine D1 and D2 receptors in the mesolimbic system and decreases the release of hypothalamic and hypophyseal hormones. It produces calmness and reduces aggressiveness with disappearance of hallucinations and delusions.
Absorption Readily absorbed from the GI tract (oral).
Distribution Crosses the blood-brain barrier; enters breast milk. Protein-binding: 92%.
Metabolism Hepatic via oxidative N-dealkylation and reduction of the ketone group; undergoes enterohepatic recycling.
Excretion Urine and faeces; 12-38 hr (elimination half-life).
http://www.drugsupdate.com/generic/view/59
RIVASTIGMINE Pharmacodynamics. Rivastigmine is an acetylcholinesterase inhibitor that facilitates cholinergic neurotransmission by slowing the degradation of acetylcholine released by functionally intact cholinergic neurons. Thus, rivastigmine may have an ameliorative effect on cholinergic-mediated cognitive deficits associated with Alzheimer disease. Rivastigmine is a carbamate derivative that binds to the steric site of the acetylcholinesterase and dissociates slowly; thus, it provides a longer duration of action than tacrine and donepezil, which are short-acting agents, because binding to acetylcholinesterase is hydrolyzed within minutes. In addition to acetylcholinesterase, rivastigmine inhibits butylcholinesterase, and as a result of this dual inhibition, it can optimize cholinergic function. Rivastigmine markedly inhibits cerebrospinal fluid acetylcholinesterase after a single oral dose of 3 mg; it also has central nervous system selectivity over the peripheral inhibition of acetylcholinesterase. An oral 3 mg dose decreases acetylcholinesterase activity in cerebrospinal fluid by approximately 40% within the first 1.5 hours after administration. Activity of the enzyme returns to baseline levels about 9 hours after the maximum inhibitory effect has been achieved. In patients with Alzheimer disease, inhibition of acetylcholinesterase in cerebrospinal fluid by rivastigmine was found to be dose-dependent up to 6 mg given twice a day (the highest dose tested). Alterations in the clinical and cognitive status of patients receiving rivastigmine are paralleled by changes in regional cerebral blood flow as measured by SPECT. These values are enhanced in responders and reduced in nonresponders. Various studies indicate that rivastigmine improves cognition and activities of daily living in patients with dementia associated with Parkinson disease, resulting in a clinically meaningful benefit (Moretti et al 2007). Pharmacokinetics. Important points pertaining to pharmacokinetics include the following: Rivastigmine is rapidly and completely absorbed. Peak plasma concentrations are reached in approximately 1 hour. As a consequence of the drugs interaction with its target enzyme, the increase in bioavailability is about 1.5-fold greater than that expected from the increase in dose. Rivastigmine is weakly bound to plasma proteins (approximately 40%). It readily crosses the blood-brain barrier. Rivastigmine is rapidly and extensively metabolized (half-life in plasma approximately 1 hour) primarily through cholinesterase-mediated hydrolysis to the decarbamoylated metabolite. Total plasma clearance of rivastigmine was approximately 130 L/h after a 0.2 mg intravenous dose, and it decreased to 70 L/h after a 2.7 mg intravenous dose. Unchanged rivastigmine is not found in the urine; renal excretion of the metabolites is the major route of elimination. Following administration of 14-C-rivastigmine, renal elimination was rapid and essentially complete (greater than 90%) within 24 hours. Less than 1% of the administered dose is excreted in the feces. No accumulation of rivastigmine or the decarbamoylated metabolite is present in patients with Alzheimer disease. Transdermal rivastigmine maintains steady drug levels in the bloodstream as compared to fluctuations with the capsule form of the drug (Mercier et al 2007). Transdermal rivastigmine enables maintenance of a lower peak of drug concentration, fewer gastrointestinal side effects, and an efficacy similar to the oral capsules of rivastigmine (Salmon 2008). Despite the advantages of transdermal rivastigmine, the effects of environmental factors such as fever or skin abrasions or tears on drug pharmacokinetics are unknown, and the need for titration to the target dose is not eliminated (Guay 2008). http://www.medmerits.com/index.php/article/rivastigmine/P1 Indications Indications include the symptomatic treatment of mild to moderately severe Alzheimer dementia and mild to moderate dementia related to Parkinson disease. Ongoing studies are examining the effect of rivastigmine in patients with severe Alzheimer disease. Contraindications Rivastigmine is contraindicated in patients with known hypersensitivity to rivastigmine, other carbamate derivatives, or to any excipients used in the formulation. Another contraindication is severe liver impairment. Side effect
Rivastigmine may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away: nausea vomiting loss of appetite heartburn or indigestion stomach pain weight loss diarrhea constipation gas weakness dizziness headache extreme tiredness lack of energy tremor or worsening of tremor increased sweating difficulty falling asleep or staying asleep confusion Some side effects can be serious. The following symptoms are uncommon, but if you experience any of them, call your doctor immediately: fainting black and tarry stools red blood in stools bloody vomit vomiting material that looks like coffee grounds difficulty urinating painful urination seizures depression anxiety aggressive behavior hearing voices or seeing things that do not exist) uncontrollable movements and muscle contractions http://www.nlm.nih.gov/medlineplus/druginfo/meds/a602009.html
Haloperidol is a neuroleptic and a butyrophenone. Due to its strong central antidopaminergic action, it is classified as a highly potent neuroleptic. It is approximately 50 times more potent than chlorpromazine (sold under the brand name Thorazine, among others) on a weight basis (50 mg chlorpromazine is equivalent to 1 mg haloperidol). Haloperidol possesses a strong activity against delusions and hallucinations, most likely due to an effective dopaminergic receptor blockage in the mesocortex and the limbic system of the brain. It blocks the dopaminergic action in the nigrostriatal pathways, which is the probable reason for the high frequency of extrapyramidal-motoric side-effects (dystonias, akathisia, pseudoparkinsonism). It has minor antihistaminic and anticholinergic properties, therefore cardiovascular and anticholinergic side-effects such as hypotension, dry mouth, constipation, etc., are seen quite infrequently, compared with less potent neuroleptics such as chlorpromazine. Haloperidol also has sedative properties and displays a strong action against psychomotor agitation due to a specific action in the limbic system. However, in some cases Haloperidol may worsen psychomotor agitation via its potent Dopamine receptor antagonism. Dopamine receptor antagonism, notably of the D2 receptor subtype, can cause akathisia, psychomotor agitation, anxiety, and restlessness, which may worsen the condition of some patients. The peripheral antidopaminergic effects of haloperidol account for its strong antiemetic activity. There, it acts at the chemoreceptor trigger zone (CTZ). Haloperidol is useful to treat severe forms of nausea/emesis such as those resulting from chemotherapy. The peripheral effects lead also to a relaxation of the gastric sphincter muscle and an increased release of the hormone prolactin, with the possible emergence of breast enlargement and secretion of milk (galactorrhea) in both sexes. Haloperidol adalah antipsychotic khas. Dalam kelas butyrophenone obat-obatan yang antipsychotic dan memiliki farmakologi efek yang mirip dengan phenothiazines. Haloperidol adalah antipsychotic tua yang digunakan dalam pengobatan skizofrenia, lebih akut, perawatan akut psikotik Serikat dan igauan. Ester decanoate berkelanjutan digunakan sebagai panjang bertindak injeksi yang diberikan setiap 4 minggu untuk orang-orang dengan skizofrenia atau penyakit terkait yang telah miskin sesuai dengan obat dan menderita kambuh lebih sering penyakit, atau untuk mengatasi kekurangan yang melekat dengan rekan diberikan secara lisan yang meledak dosis meningkatkan risiko atau intensitas efek samping. Di beberapa negara, ini bisa menjadi disengaja di bawah perintah perawatan masyarakat. Haloperidol dijual di bawah nama dagang Aloperidin, Bioperidolo, Brotopon, Dozic, Duraperidol (Jerman), Einalon S, Eukystol, Haldol, Halosten, Keselan, Linton, Peluces, Serenace, Serenase, dan Sigaperidol. Dalam medis slang, haloperidol kadang-kadang disebut vitamin H. Haloperidol ditemukan oleh Paul Janssen. Dikembangkan pada tahun 1958 oleh perusahaan Belgia Janssen Pharmaceutica dan diserahkan kepada uji klinis pertama di Belgia pada tahun yang sama. Setelah ditolak oleh perusahaan AS Searle karena untuk efek samping, itu kemudian dipasarkan di AS oleh McNeil laboratorium. Disetujui oleh US Food and Drug Administration pada tanggal 12 April 1967. Komprehensif meninjau haloperidol telah menemukan untuk menjadi agen yang efektif dalam perawatan gejala yang berkaitan dengan skizofrenia. Haloperidol juga digunakan dalam pengendalian gejala: Psikosis akut, seperti obat psikosis (LSD, psilocybin, amfetamin, ketamine dan phencyclidine), psikosis terkait dengan demam tinggi atau penyakit metabolik Akut fase manik sampai obat-obatan lini pertama yang secara bersamaan tertentu seperti litium atau valproate efektif Hiperaktif, agresi. Akut delirium Sebaliknya tak terkendali parah perilaku gangguan di anak-anak dan remaja Agitasi dan kebingungan yang terkait dengan otak sclerosis Ajuvan perawatan alkohol dan opioid penarikan Pengobatan gangguan neurologis seperti tic gangguan, sindrom Tourette, dan chorea Pengobatan parah mual/emesis (pasca-operasi, efek samping dari radiasi dan kanker kemoterapi) Ajuvan pengobatan sakit kronis parah, selalu bersama-sama dengan analgesik Terapeutik percobaan dengan gangguan kepribadian seperti gangguan kepribadian batas Juga digunakan dalam pengobatan terselesaikan cegukan Beberapa minggu atau bahkan berbulan-bulan perawatan mungkin diperlukan sebelum pengampunan skizofrenia jelas. Di beberapa klinik penggunaan atipikal neuroleptics (misalnya clozapine, risperidone, olanzapine, ziprasidone) umumnya pilihan atas haloperidol, karena obat ini memiliki insiden lumayan rendah extrapyramidal efek samping. Masing-masing obat-obatan ini, namun, memiliki spektrum sendiri berpotensi serius-efek samping (misalnya, agranulocytosis dengan clozapine, berat badan dengan peningkatan risiko diabetes dan stroke). Neuroleptics atipikal juga jauh lebih mahal dan baru-baru ini telah menjadi subyek meningkatkan kontroversi mengenai keampuhan mereka dibandingkan dengan produk-produk yang lebih tua dan efek samping. Haloperidol dianggap sangat diperlukan untuk mengobati psikiatri situasi darurat, meskipun obat-obatan atipikal baru telah mendapatkan peran yang lebih besar dalam beberapa situasi seperti diuraikan dalam serangkaian ulasan konsensus yang diterbitkan antara tahun 2001 dan 2005. Mendaftarkan diri di dunia kesehatan organisasi daftar dari penting obat. Seperti biasa dengan neuroleptics yang khas, haloperidol jauh lebih aktif terhadap "positif" gejala psikotik (delusi, halusinasi dll) daripada terhadap "negatif" Gejala (sosial penarikan, autism dll). Dengan pengecualian dari clozapine sangat efektif, efektivitas haloperidol melawan gejala positif telah tidak telah mengungguli oleh Anti-kejang obat baru. UK multi-tahun studi oleh Alzheimer penelitian Trust menyarankan bahwa ini dan obat-obatan anti-psychotic lain neuroleptic umumnya diberikan Alzheimer pasien dengan masalah-masalah kelakuan yang ringan sering membuat kondisi mereka yang lebih buruk. Studi menyimpulkan bahwa Kontroversial non-medis menggunakan Ada beberapa laporan dari pembangkang Soviet, termasuk staf medis, penggunaan haloperidol di Uni Soviet untuk tujuan hukuman atau hanya untuk istirahat para tahanan akan. Pembangkang terkenal yang diberikan haloperidol sebagai bagian dari Pengadilan memerintahkan perawatan adalah Sergei Kovalev dan Leonid Plyushch. Account Plyushch di barat, setelah ia diizinkan meninggalkan Uni Soviet pada tahun 1976, yang berperan dalam pengutukan Barat memicu Soviet praktek di dunia Psychiatric Association's 1977 pertemuan. Penggunaan haloperidol di Uni Soviet sistem jiwa adalah lazim karena itu salah satu obat-obatan psikotropika beberapa diproduksi dalam kuantitas di Uni SOVIET. Haloperidol telah digunakan untuk efek menenangkan selama deportasi Alien Amerika Serikat imigrasi dan Penegakan Bea Cukai (ICE). Selama 2002-2008, federal imigrasi personil dulu haloperidol tenang 356 deportees. Tahun 2008, diikuti pengadilan tantangan atas praktek, haloperidol diberikan kepada tahanan hanya 3. Setelah tuntutan hukum, para pejabat AS berubah prosedur sehingga melakukannya hanya dengan rekomendasi dari personel medis dan di bawah perintah pengadilan. Haloperidol is a typical antipsychotic. It is in the butyrophenone class of antipsychotic medications and has pharmacological effects similar to the phenothiazines. Haloperidol is an older antipsychotic used in the treatment of schizophrenia and in the treatment of acute psychotic states and delirium. A long-acting decanoate ester is used as an injection given every 4 weeks to people with schizophrenia or related illnesses who have a poor compliance with medication and suffer frequent relapses of illness, or to overcome the drawbacks inherent to its orally administered counterpart that burst dosage increases risk or intensity of side effects. In some countries, injections of antipsychotics such as haloperidol can be ordered by a court at the request of a psychiatrist. Haloperidol is sold under the tradenames Aloperidin, Bioperidolo, Brotopon, Dozic, Duraperidol (Germany), Einalon S, Eukystol, Haldol, Halosten, Keselan, Linton, Peluces, Serenace, Serenase, and Sigaperidol
RIVASTIGMINE Rivastigmine (sold under the trade name Exelon) is a parasympathomimetic or cholinergic agent for the treatment of mild to moderate dementia of the Alzheimers type and dementia due to Parkinson's disease. The drug can be administered orally or via a transdermal patch; the latter form reduces the prevalence of side effects, [1] which typically include nausea and vomiting. [2]
The drug is eliminated through the urine, and appears to have relatively few drug-drug interactions. [2]
Administration Rivastigmine tartrate is a white to off-white fine crystalline powder that is both lipophilic (soluble in fats) and hydrophilic (soluble in water). Like other cholinesterase inhibitors, it requires doses to be increased gradually over several weeks; this is usually referred to as the titration phase. [2] Oral doses of rivastigmine should be titrated with a 3 mg per day increment every 2 to 4 weeks. Rivastigmine is classified as Pregnancy category B, with insufficient data on risks associated with breastfeeding. In cases of overdose, atropine is used to reverse bradycardia. Dialysis is ineffective due to the drug's half-life. [edit] Pharmacodynamics Rivastigmine is a cholinesterase inhibitor that inhibits both butyrylcholinesterase and acetylcholinesterase (unlike donepezil, which selectively inhibits acetylcholinesterase). It is thought that rivastigmine works by inhibiting these cholinesterase enzymes, which would otherwise break down the brain chemical acetylcholine. [6]
[edit] Indication The U.S. Food and Drug Administration has approved rivastigmine capsules and the rivastigmine patch for the treatment of mild to moderate dementia of the Alzheimers type and for mild to moderate dementia related to Parkinson's disease. It has been used in more than 6 million patients worldwide. [citation needed]
Rivastigmine has demonstrated significant treatment effects on the cognitive (thinking and memory), functional (activities of daily living) and behavioural problems that are commonly associated with Alzheimers [7][8][9][10] and Parkinson's disease dementias. [11]
[edit] Efficacy In patients with either type of dementia, rivastigmine has been shown to provide meaningful symptomatic effects that may allow patients to remain independent and be themselves for longer. In particular, rivastigmine appears to show marked treatment effects in patients showing a more aggressive course of disease, such as those with a younger age of onset, a poor nutritional status, or those experiencing symptoms such as delusions or hallucinations. [12] For example, the presence of hallucinations appears to be a predictor of especially strong responses to rivastigmine, both in Alzheimers and Parkinson's disease patients. [13][14] It has been proposed that these effects might reflect the additional inhibition of butyrylcholinesterase, which is implicated in symptom progression and might provide added benefits over acetylcholinesterase- selective drugs in some patients. [12][15] Multi-infarct dementiamay be slight improvement in executive functions and behaviour. There are no firm evidences supporting usage in schizophrenia patients. Its efficacy is similar to donepezil and tacrine. Doses below 6 mg/d may be ineffective. The effects of this kind of drugs in different kinds of dementia (including Alzheimer's dementia) are modest, and it is still unclear which AcCh(ButCh) esterase inhibitor is better in Parkinson's dementia, though rivastigmine is well-studied. [edit] Side effects Side effects may include nausea and vomiting. [2]
It has been postulated that the strong potency of rivastigmine, provided by its dual inhibitory mechanism, leads to more nausea and vomiting during the titration phase of oral rivastigmine treatment. [2] This enforces the importance of taking oral forms of these drugs as prescribed with food. [4] However, rates of nausea and vomiting are markedly reduced with the once-daily rivastigmine patch (which can be applied at any time of the day, with or without food). In a large clinical trial of the rivastigmine patch in 1,195 patients with Alzheimers disease, the target dose of 9.5 mg/24 hour patch provided similar clinical effects (e.g. memory and thinking, activities of daily living, concentration) as the highest doses of rivastigmine capsules, but with three times fewer reports of nausea and vomiting. [1] . [edit] Pharmacokinetics When given orally, rivastigmine is well absorbed with a bioavailability of about 40% in the 3 mg dose. Pharmacokinetics are linear up to 3 mg BID but non-linear at higher doses. Elimination is through the urine. Peak plasma concentrations are seen in about one hour, with peak CSF concentrations at 1.43.8 hours. When given by once-daily transdermal patch, the pharmacokinetic profile of rivastigmine is much smoother, compared with capsules, with lower peak plasma concentrations and reduced fluctuations. [16] The 9.5 mg/24 h rivastigmine patch provides comparable exposure to 12 mg/day capsules (the highest recommended oral dose). [16]
The compound does cross the blood-brain barrier. Plasma protein binding is 40%. [17] The major route of metabolism for rivastigmine is by its target enzymes via cholinesterase-mediated hydrolysis. Elimination bypasses the hepatic system so hepatic cytochrome P450 (CYP) isoenzymes are not involved. [18] It has been suggested that this means there is a low potential for drug-drug interactions (which could lead to adverse effects) between rivastigmine and the many common drugs that use the cytochrome P450 metabolic pathway. [2]
[edit] Synthesis
R. Amstuz, M. Marzi, M. Boelsterli, M. Walsinshaw, Helv. Chim. Acta 73, 739 (1990).
4. What are the correlation between of hypertension and DM which the patien on symptom? Hypertension Hypertension (HT) and dementia are common disorders in the elderly. HT in the elderly is associated with increased occurrence rates of dementia including Alzheimer's disease (AD) and vascular dementia (VaD). In connection to this, some studies have suggested that HT in old age correlates with the pathogenesis of dementia. Since HT is potentially reversible, a number of randomized trials have examined whether antihypertensive treatment may help in preventing dementia occurrence. We review five studies, all using subjects 60 years or older, which investigated different antihypertensive pharmacological treatments. Data from two trials (Syst-Eur, PROGRESS) open the way toward the prevention of dementia (AD or VaD) by antihypertensive treatments. In the Syst-Eur study, with the dihydropyridine calcium antagonists, a reduction in both types of dementia was demonstrated (risk reduction 55%). The PROGRESS study showed that the use of angiotensin-converting enzyme inhibitors (ACEIs), with or without diuretics, resulted in decrease incidence of stroke-related dementia (risk reduction 19%), but dementia without stroke was not reduced. In contrast, the SHEP trial, treatment with a chlorthalidone-based antihypertensive regimen, did not significantly reduced the incidence of dementia. The SCOPE study (candesartan or hydrochlorothiazide versus placebo) and the HYVET-COG study (indapamide or perindopril versus placebo) found no significant difference between the active treatment and placebo group on the incidence of dementia. We found conflicting results regarding treatment benefits in dementia prevention. Recent clinical trials and studies on animal models suggest that blockades of RAS system could have reduced cognitive decline seen in Alzheimer's disease and vascular dementia. Future trials primarily designed to investigate the effects of antihypertensive agents on impaired cognition are needed. In general, the risk of HT, which is defined as a systolic blood pressure (SBP) 140mmHg and/or a diastolic blood pressure (DBP) 90mmHg, increases with advancing age. In fact, the prevalence of HT in individuals 60 years and older is double that of those aged 4959 years. In Framingham study, 90% of all 65-year-old men and women with normal BP later developed HT. This condition carries a very high risk for cerebrovascular disease (CVD) as well as coronary heart disease (CHD). Dementia is one of the most important neurological disorders in the elderly. Many studies have identified HT as marker for the pathogenesis of dementia AD and VaD, while longitudinal studies have suggested that HT is associated with a higher incidence of dementia in old age. It has been observed that long-standing HT may lead to severe atherosclerosis and impaired cerebrovascular autoregulation, which in turn is thought to correlate with dementia. For these reasons, several studies have investigated whether antihypertensive treatment may retard cognitive decline or dementia. Although the importance of lowering BP in HT subjects is well known, the relationship between HT and cognitive function is controversial. To this date, the associations between BP and dementia have been inconclusive. Considering that the incidence of dementia among the elderly population is rising rapidly worldwide and accumulating evidence that HT may contribute to the development of both AD and VaD, there is a reason to believe effective management of HT may translate into major health benefits through the protection of dementia. HT has long been known to cause CV. Midlife HT ranks as an important modifiable risk factor for late-life cognitive decline, mild cognitive impairment (MCI) and VaD. In longitudinal cohort studies, elevated BP is associated with cognitive decline although some cross-sectional studies showed mixed relationships between higher BP and cognition, with many studies showing no correlation or even J- or U-shaped associations. Findings from these prospective cohort studies for DBP and cognitive decline are less consistent; however, many have reported a similar inverse relation. The data on the role of BP and HT in later life are not consistent, leaving open the issue of BP treatment in elderly people. The controversy about the association between HT in the elderly and dementia arises because the longitudinal relationship between BP and cognitive change is sensitive to the effects of age, duration of followup and hypertensive treatment status, comorbidity with CVD and CHD, and possibly subclinical dementia. More recently, a total of 668 community- dwelling Japanese individuals without dementia, aged 65 to 79 years, were followed up for 17 years, and examined the associations of late-life and midlife HT with the risk of AD and VaD. During the followup, 123 developed AD, and 76 subjects experienced VaD, and the age- and sex-adjusted incidence of VaD significantly increased with elevated midlife BP levels regardless of late-life BP levels. There were not a significant association between BP levels and AD. Li et al. followed a total of 837 subjects with MCI for 5 years, 298 subjects converted to AD, while 352 remained MCI at the end of the followup. Subjects with HT increased the risk of dementia conversion. Given their results, treatment of HT was associated with a reduced progression in MCI to AD dementia. R. S. Vasan, A. Beiser, S. Seshadri et al., Residual lifetime risk for developing hypertension in middle-aged women and men: the Framingham Heart Study, Journal of the American Medical Association, vol. 287, no. 8, pp. 10031010, 2002 Diabetes mellitus People with diabetes are at increased risk of having a heart attack or stroke at an early age, but that's not the only worry. Diabetes appears to dramatically increase a person's risk of developing Alzheimer's disease or other types of dementia later in life, according to a new study conducted in Japan. In the study, which included more than 1,000 men and women over age 60, researchers found that people with diabetes were twice as likely as the other study participants to develop Alzheimer's disease within 15 years. They were also 1.75 times more likely to develop dementia of any kind. "It's really important for the [public's] health to understand that diabetes is a significant risk factor for all of these types of dementia," says Rachel Whitmer, Ph.D., an epidemiologist in the research division of Kaiser Permanente Northern California, a nonprofit health-care organization based in Oakland, California.
Whitmer, who studies risk factors for Alzheimer's but wasn't involved in the new research, stresses that many questions remain about the link between diabetes and dementia. The new study was "well done" and provides "really good evidence that people with diabetes are at greater risk," she says, "but we really need to look at other studies to find out why." Diabetes could contribute to dementia in several ways, which researchers are still sorting out. Insulin resistance, which causes high blood sugar and in some cases leads to type 2 diabetes, may interfere with the body's ability to break down a protein (amyloid) that forms brain plaques that have been linked to Alzheimer's. High blood sugar (glucose) also produces certain oxygen- containing molecules that can damage cells, in a process known as oxidative stress. In addition, high blood sugar -- along with high cholesterol -- plays a role in the hardening and narrowing of arteries in the brain. This condition, known as atherosclerosis, can bring about vascular dementia, which occurs when artery blockages (including strokes) kill brain tissue.
"Having high glucose is a stressor to the nervous system and to the blood vessels," says David Geldmacher, M.D., a professor of neurology at the University of Alabama at Birmingham. "The emerging information on Alzheimer's disease and glucose shows us that we do need to remain vigilant on blood sugar levels as we get older." Studies dating back to the late 1990s have suggested that people with diabetes are more likely to develop Alzheimer's disease and other types of dementia, but the research has been marred by inconsistent definitions of both diabetes and dementia. The authors of the new study, led by Yutaka Kiyohara, M.D., an environmental medicine researcher at Kyushu University, in Fukuoka, sought to address this weakness by using the gold standard of diabetes diagnosis, an oral glucose tolerance test. This involves giving a person a sugar-loaded drink after they have fasted for at least 12 hours, and then measuring how much glucose remains in their blood two hours later.
At the beginning of the study, the tests showed that 15% of the participants had full-fledged diabetes, while 23% had prediabetes, also known as impaired glucose tolerance. The participants were all dementia-free when the tests were done, but over the next 15 years 23% received a diagnosis of dementia. Slightly less than half of those cases were deemed to be Alzheimer's disease, with the remainder roughly split between vascular dementia and dementia due to other causes. (The diagnoses were confirmed with brain scans of living patients and brain autopsies in deceased patients.) Both diabetes and prediabetes were associated with an increased risk of dementia diagnosis, although the association was weaker for prediabetes. And the link persisted even after the researchers took into account several factors associated with both diabetes and dementia risk, such as age, sex, blood pressure, and body mass index.
Demensia Tipe Alzheimer Walaupun penyebab demensia tipe Alzheimer masih tidak diketahui, telah terjadi kemajuan dalam mengerti dasar molekular dari deposit amiloid yang merupakan tanda utama neuropatologi gangguan. Faktor genetik dianggap berperan dalam perkembangan gangguan dalam sekurangnya beberapa kasus. Dukungan tambahan tentang peranan genetik adalah bahwa angka persesuaian untuk kembar monozigotik adalah lebih tinggi dari angka untuk kembar dizigotik. Neuropatologi. Observasi makroskopis neuroanatomik klasik pada otak dari seorang pasien degan penyakit Alzheimer adalah atrofi difus dengan pendataran sulkus kortikal dan pembesaran ventrikel serebral. Temuan mikroskopis klasik dan patognomonik adalah bercak-bercak senilis, kekusutan neurofibriler, hilangnya neuronal (kemungkinan sebanyak 50 persen di korteks), dan degenerasi granulovaskular pada neuron. Kekusutan neurofibriler bercampur dengan elemen sitoskeletal, terutama protein tau berfosforilasi, walaupun protein sitoskeletal lainnya juga ditemukan. Kekusutan neurofibriler adalah ti- dak unik pada penyakit Alzheimer, karena keadaan tersebut juga ditemukan pada sindroma Down, demensia pugilistik (punch-drunk syndrome), Kompleks demensia-Parkinson dari Guam, penyakit Hallervorden-Spatz, dan otak orang lanjut usia yang normal. Kekacauan neurofibriler biasanya ditemukan di korteks, hipokampus, substansia nigra, dan lokus sereleus. Plak senilis, juga dikenal sebagai plak amiloid, adalah jauh lebih indikatif untuk penyakit Alzheimer, walaupun keadaan tersebut juga ditemukan pada sindroma Down dan, sampai derajat tertentu, pada penuaan normal. Plak senilis terdiri dari protein tertentu, beta/A4 dan astrosit, prosesus neuronal distrofik, dan mikroglia. Jumlah dan kepadatan plak senilis yang terdapat pada otak orang yang telah meninggal (postmortem) telah dihubungkan dengan beratnya penyakit pada orang yang terkena tersebut. Protein prekursor amiloid. Gen untuk protein prekursor amiloid adalah pada lengan panjang dari kromosom 21. Melalui proses penyambungan diferensial, sesungguhnya terdapat empat bentuk protein prekursor amiloid. Protein beta/A4, yang merupakan kandungan utama dari plak senilis, adalah suatu peptida dengan 42 asam amino yang merupakan produk penghancuran protein prekursor amiloid. Pada sindroma Down (trisomi 21), terdapat tiga cetakan protein prekursor amiloid, dan pada penyakit di mana terjadi mutasi pada kodon 717 dalam gen protein prekursor amiloid, suatu proses patologis menghasilkan deposisi protein beta/A4 yang berlebihan. Pertanyaan apakah proses pada protein prekursor amiloid yang abnormal adalah penyebab utama yang penting pada penyakit Alzheimer masih belum terjawab; tetapi, banyak kelompok peneliti secara aktif mempelajari proses metabolik normal dari protein prekursor amiloid dan prosesnya pada pasien dengan demensia tipe Alzheimer dalam usaha untuk menjawab pertanyaan tersebut. Kelainan neurotransmiter. Neurotransmiter yang paling berperan dalam patofisiologis adalah asetilkolin dan norepinefrin, keduanya dihipotesiskan menjadi hipoaktif pada penyakit Alzheimer. Beberapa penelitian telah melaporkan data yang konsisten dengan hipotesis bahwa suatu degenerasi spesifik pada neuron kolinergik ditemukan pada nukleus basalis Meynerti pada pasien dengan penyakit Alzheimer. Data lain yang mendukung adanya defisit kolinergik pada penyakitAlzheimer adalah penurunan konsentrasi asetilkolin dan kolin asetiltransferase di dalam otak. Kolin asetiltransferase adalah enzim kunci untuk sintesis asetilkolin, dan penurunan konsentrasi kolin asetiltransferase menyatakan penurunan jumlah neuron kolinergik yang ada. Dukungan tambahan untuk hipotesis defisit kolinergik berasal dari observasi bahwa antagonis kolinergik, seperti scopolamine dan atropine, mengganggu kemampuan kognitif, sedangkan agonis kolinergik, seperti physostigmine dan arecholine, telah dilaporkan meningkatkan kemampuan kognitif. Penurunan aktivitas norepinefrin pada penyakit Alzheimer diperkirakan dari penurunan neuron yang mengandung norepinefrin di dalam lokus sereleus yang telah di- temukan pada beberapa pemeriksaan patologis otak dari pasien dengan penyakit Alzheimer. Dua neurotransmiter lain yang berperan dalam patofisiologi penyakit Alzheimer adalah dua peptida neuroaktif, somatostatin dan kortikotropin, keduanya telah dilaporkan menurun pada penyakit Alzheimer. Penyebab potensial lainnya. Teori kausatif lainnya telah diajukan untuk menjelaskan perkembangan penyakit Alzheimer. Satu teori adalah bahwa kelainan dalam pengaturan metabolisme fosfolipid membran menyebabkan membran yang kekurangan cairan-yaitu, lebih kaku-dibandingkan normal. Beberapa peneliti telah menggunakan pencitraan spektroskopik resonansi molekular (molecular resonance spectroscopic; MRS) unt uk memeriksa hipotesis tersebut pada pasien dengan demensia tipe Alzheimer. Toksisitas aluminium juga telah dihipotesiskan sebagai faktor kausatif karena kadar aluminium yang tinggi telah ditemukan dalam otak beberapa pasien dengan penyakit Alzheimer. Suatu gen (E4) telah dihubungkan dalam etiologi penyakit Alzheimer. Orang dengan satu salinan gen menderita penyakit Alzheimer tiga kali lebih sering daripada orang tanpa gen E4. Orang dengan dua gen E4 mempunyai kemungkinan menderita penyakit delapan kali lebih sering dan pada orang tanpa gen E4. Demensia Vaskular Penyebab utama dari demensia vaskular dianggap adalah penyakit vaskular serebral yang multipel, yang menyebabkan suatu pola gejala demensia. Demensia vaskular paling sering pada laki-laki, khususnya pada mereka dengan hipertensi yang telah ada sebelumnya atau faktor risiko kardiovaskular lainnya. Gangguan terutama mengenai pembuluh darah serebral berukuran kecil dan sedang, yang mengalami infark dan menghasilkan lesi parenkim multipel yang menyebar pada daerah otak yang luas. Penyebab infark mungkin termasuk oklusi pembuluh darah oleh plak arteriosklerotik atau tromboemboli dari tempat asal yang jauh (sebagai contohnya, katup jantung). Suatu pemeriksaan pasien dapat menemukan bruit karotis, kelainan unduskopi, atau pembesaran kamar jantung 5. Explain about organic mental GANGGUAN MENTAL ORGANIK DEFINISI Gangguan mental organik adalah gangguan mental yang berkaitan dengan penyakit/gangguan sistemik atau otak yang dapat didiagnosis tersendiri. Termasuk gangguan mental simtomatik, di mana pengaruh terhadap otak merupakan akibat sekunder dari penyakit/gangguan sistemik di luar otak (ekstra cerebral). Yang termasuk dalam gangguan mental organik adalah : 1. Sindrom gangguan psikopatologik (misalnya demensia) 2. gangguan yang mendasari (misalnya penyakit Alzheimer)
apa saja gambaran utama dari gangguan mental organic? a. gangguan fungsi kognitif daya ingat, daya pikir, daya belajar b. gangguan sensorium gangguan kesadaran dan perhatian c. sindrom dengan manifestasi yang menonjol dalam bidang persepsi, isi pikiran, suasana, perasaan,dan emosi d. onset sangat berpengaruh dalam penentuan diagnosis PPDGJ III
F00 F09 GANGGUAN MENTAL ORGANIK` (TERMASUK GANGGUAN MENTAL SIMTOMATIK) F00 DEMENSIA PADA PENYAKIT ALZHEIMER F01 DEMENSIA VASKULAR F02 DEMENSIA PADA PENYAKIT LAIN YDK F03 DEMENSIA YTT F04 SINDROM AMNESIK ORGANIK BUKAN AKIBAT ALKOHOL dan ZAT PSIKOAKTIF LAINNYA F05 DELIRIUM BUKAN AKIBAT ALKOHOL dan ZAT PSIKOAKTIF LAINNYA F06 GANGGUAN MENTAL LAINNYA AKIBAT KERUSAKAN dan DISFUNGSI OTAK dan PENYAKIT FISIK F07 GANGGUAN KEPRIBADIAN dan PERILAKU AKIBAT PENYAKIT,KERUSAKAN DAN DISFUNGSI OTAK F08 GANGGUAN MENTAL ORGANIK ATAU SIMTOMATIK YTT PPDGJ III
6. Demensia (definition,etiologi,classification, risk factor,criteria diagnostic, management terapy, DD) Definisi : Demensia merupakan sindroma yang ditandai oleh berbagai gangguan fungsi kognitif tanpa gangguan kesadaran. Fungsi kognitif yang dapat dipengaruhi pada demensia adalah inteligensia umum, belajar dan ingatan, bahasa, memecahkan masalah, orientasi, persepsi, perhatian, dan konsentrasi, pertimbangan, dan kemampuan sosial. Kepribadian pasien juga terpengaruhi. SINOPSIS PSIKIATRI , KAPLAN DAN SADOCK Etiology : There are many causes of dementia, including neurological disorders such as Alzheimer's disease, blood flow-related (vascular) disorders such as multi-infarct cognitive impairment, inherited disorders such as Huntington's disease, and infections such as HIV. The most common causes of dementia include:
Degenerative neurological diseases, such as Alzheimer's, frontotemporal lobar degenerations, dementia with Lewy bodies, Parkinson's, and Huntington's Vascular disorders, such as multi-infarct dementia, which is caused by multiple strokes in the brain Infections that affect the central nervous system, such as HIV dementia complex and Creutzfeldt-Jakob disease Chronic drug use Depression Certain types of hydrocephalus, an accumulation of fluid within the brain that can result from developmental abnormalities, infections, injury, or brain tumors Alzheimer's disease accounts for 50 percent to 70 percent of all dementia. However, many patients with Alzheimers disease also have evidence of co-existing cerebrovascular disease, usually consisting of multiple small areas of ischemic changes (often call "mini-strokes") on MRI and on post-mortem examination of the brain. Thus, many of these patients can be considered to have a "mixed" dementia. Frontotemporal lobar degenerations, of which several types are known, account for a substantial number of dementias, especially among those in their 50s and 60s. Dementia with Lewy bodies has also been diagnosed with increasing frequency in recent years. These patients have clinical signs of parkinsonism as well as dementia; its relationship to the dementia of Parkinsons disease is still incompletely understood. http://www.clevelandclinic.org/health/health-info/docs/2300/2340.asp
DEMENSIA DEFINISI Demensia merupakan sindroma yang ditandai oleh berbagai gangguan fungsi kognitif tanpa gangguan kesadaran. Fungsi kognitif yang dapat dipengaruhi pada demensia adalah inteligensia umum, belajar dan ingatan, bahasa, memecahkan masalah, orientasi, persepsi, perhatian, dan konsentrasi, pertimbangan, dan kemampuan sosial. Kepribadian pasien juga terpengaruhi. SINOPSIS PSIKIATRI , KAPLAN DAN SADOCK Demensia adalah keadaan dimana seseorang mengalami penurunan kemampuan daya ingat dan daya pikir, dan penurunan kemampuan tersebut menimbulkan gangguan terhadap fungsi kehidupan sehari-hari. Bentuk gangguan yang sangat menyolok adalah penurunan perilaku yang secara lengkap disebut perilaku sosial (social skill) dan perilaku ini dapat dirinci lebih lanjut menjadi: ADL (Activity of Daily Living yaitu kemampuan seseorang untuk mengurus dirinya sendiri) dimulai dari bangun tidur, mandi, berpakaian dan seterusnya sampai pergi tidur kembali, pokoknya segala kegiatan orang untuk mengurus kebutuhannya sendiri. Perilaku Okupasional yaitu perilaku yang dilaksanakan seseorang untuk menjalankan kehidupannya untuk bekerja dan mencari nafkah, yaitu sekolah, bekerja, berorganisasi, menjalankan ibadah, mengisi waktu luang. Partisipasi sosial yaitu perilaku seseorang untuk hidup bermasyarakat seperti mematuhi kewajiban sebagai warga masyarakat, misalnya mengurus KTP, SIM, Kerja Bakti, berorganisasi sosial, menghadiri undangan dan sebagainya. (Kecerdasan pada usia lanjut dan demensia,FKUI,Prof.Dr.dr.SM.Lumbantobing)
ETIOLOGI Demensia mempunyai banyak penyebab tetapi demensia tipe Alzheimer dann demensia vaskular secara bersama-sama berjumlah sebanyak 75 persen dari semua kasus. Penyebab demensia lainnya yang disebutkan dalam DSM-IV adalah penyakit Pick, penyakit Creutz-Feldt-Jakob, penyakit Huntington, penyakit kinson, human immunodeficiency virus (HIV) dan trauma kepala.
Dari segi etiologi dibedakan antara demensia reversibel dan irreversibel. Untuk demensia reversible penyebabnya adalah : 1
1. Drugs Antidepresi, antiansietas, sedatif, antiaritmia, antihipertensi, antikonvulsan, obat-obat jantung termasuk digitalis, obat-obat antikolmergik. 2. Emosi/depresi Depresi, shizofrenta, mania, psikosis. 3. Metabolik / endokrin Penyakit tiroid, hipoglikemi, hipernatremi dan hiponatremi, hiperklasemi, gagal ginjal, gagal hati, penyakit Cushing, penyakit wilson. 4. Eye/ear nutrisi Difensiasi tiamin, difensiasi vitamin B12 (anemia pernisiosa), Difensiasi asam fosfat, difensiasi vitamin B6 (pellagra). 5. Trauma Trauma kranioserebal, hematon subdural akut dan kronis. 6. Tumor Glioma, meningioma, tumor metastatis. 7. Infeksi Meningitis dan ensefalitis bakterialis, meningitis dan ensefalitis Akibat jamur, meningitis akibat kriptokokus, meningitis dan Ensefalitis viral, abses otak, neurosifilis, AIDS. 8. Autoimun Lupus eritematosus diseminata, multiple sklerosis. Dan di samping itu ada juga arterioseklerosis dan alkohol. Untuk dementia yang irreversibel penyebabnya adalah: 1 1. Penyakit degeneratif Penyakit Alzaimer, dementia Frontotemporal, penyakit Huntington, penyakit Parkinson, penyakit Lewy bodies, atrofi olivopontoserebelar, amiotropik lateral sklerosis/ dementia parkinsonism kompleks. 2. Penyakit vaskular Infrak multipel, emboli serebral, arteritis, anoksia skunder akibat henti jantung, gagal jantung atau keracunan karbon monoksida. 3. Trauma Trauma kranioserebral berat 4. Infeksi Sub akut spongiform ensefalopati (creutzfeldt-jacob disease), post ensefalitis, Leukoensefalopati multifokal progresif.
FAKTOR RESIKO Tipe Alzheimer - Usia 65 thn - Wanita - Sanak saudara tingkat pertama - Punya riwayat cedera kepala - Sindroma down Tipe Vaskular - paling sering ditemukan pada usia antara 60 dan 70 thn - lebih sering pada laki-laki dr pd wanita
Kaplan.H.I, Sadock. B.J, Sinopsis Psikiatri : Ilmu Pengetahuan Perilaku Psikiatri Klinis, edisi ketujuh, jilid satu. Binarupa Aksara, Jakarta 1997. hal 502-540.
KLASIFIKASI a. Demensia tipe alzheimer SINOPSIS PSIKIATRI PPDGJ-III Perkembangan defisit kognitif yang dimanifestasikan oleh baik : 1) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi baru dan untuk mengingat informasi yang telah dipelajari sebelumnya ) 2) Satu ( atau lebih ) gangguan kognitif berikut : a) Afasia ( gangguan bahasa ) b) Apraksia ( gangguan kemampuan untuk aktivitas motorik walaupun fungsi motorik adalah utuh ) c) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun fungsi sensorik adalah utuh ) d) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, Terdapatnya gejala demensia Onset bertahap ( insidious onset ) dengan deteriorasi lambat. Onset biasanya sulit ditentukan waktunya yang persis, tiba orang lain sudah menyadari adanya kelainan tersebut. Dalam perjalanan penyakitnya dapat terjadi suatu taraf yang stabil ( plateau ) secara nyata Tidak adanya bukti klinis, atau temuan dari pemeriksaan khusus, yang menyatakan bahwa kondisi mental itu dapat disebabkan oleh penyakit otak atau sistemik lain yang dapat menimbulkan demensia ( misalnya hipotiroidisme, hiperkalsemia, defisiensi vitamin B12, defisiensi mengorganisasi, mengurutkan dan abstrak ) Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan bermakna dari tingkat fungsi sebelumnya Perjalanan penyakit ditandai oleh onset yang bertahap dan penurunan kognitif yang terus-menerus Defisit kognitif dalam kriteria A1 dan A2 bukan salah satu dari berikut : 1) Kondisi sistem saraf pusat lain yang menyebabkan defisit progresif dalam daya ingat dan kognisi ( misalnya, penyakit serebrovaskular, penyakit Parkinson, penyakit Huntington, hematoma subdural, hidrosefalus tekanan normal, tumor otak ) 2) Kondisi sistemik yang diketahui menyebabkan demensia ( misalnya, hipotiroidisme, defisiensi vitamin B 12
atau asam folat, defisiensi niasin, hiperkalsemia, neurosifilis, infeksi HIV ) 3) Kondisi akibat zat Defisit tidak terjadi semata-mata selama perjalanan suatu delirium Gangguan tidak lebih baik diterangkan oleh gangguan aksis I lainnya ( misalnya, gangguan depresif berat, skizofrenia ) niasin, neurosifilis, hidrosefalus bertekanan normal, atau hematoma subdural Tidak adanya serangan apoplektik mendadak, atau gejala neurologik kerusakan otak fokal seperti hemiparesis, hilangnya daya sensorik, defek lapangan pandang mata, dan inkoordinasi yang terjadi dalam masa dini dari gangguan itu ( walaupun fenomena ini dikemudian hari dapat bertumpang tindih )
b. Demensia vaskular SINOPSIS PSIKIATRI PPDGJ-III Perkembangan defisit kognitif yang dimanifestasikan oleh baik : 1) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi baru dan untuk mengingat informasi yang telah dipelajari sebelumnya ) 2) Satu ( atau lebih ) gangguan kognitif berikut : a) Afasia ( gangguan bahasa ) b) Apraksia ( gangguan kemampuan Terdapatnya gejala demensia Hendaya fungsi kognitif biasanya tidak merata ( mungkin terdapat hilangnya daya ingat, gangguan daya pikir, gejala neurologis fokal ). Daya tilik dari ( insight ) dan daya nilai (judgment) secara relatif tetap baik Suatu onset yang mendadak atau deteriorasi yang bertahap, disertai adanya gejala neurologis fokal, untuk aktivitas motorik walaupun fungsi motorik adalah utuh ) c) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun fungsi sensorik adalah utuh ) d) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, mengorganisasi, mengurutkan dan abstrak ) Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan bermakna dari tingkat fungsi sebelumnya Tanda dan gejala neurologis fokal ( misalnya, peninggian refleks tendon dalam, respon ekstensor plantar, palsi pseudobulbar, kelainan gaya berjalan, kelamahan pada satu ekstremitas ) atau tanda laboratorium adalah indikatif untuk penyakit serebrovaskular ( misalnya, infark multipel yang mengenai korteks dan substansia putih di bawahnya )yang dianggap berhubungan secara etiologi dengan gangguan Defisit tidak terjadi semata selama perjalanan delirium meningkatkan kemungkinan diagnosis demensia vaskuler. Pada beberapa kasus, penetapan hanya dapat dilakukan dengan pemeriksaan CT-Scan atau pemeriksaan neuropatologis
c. Demensia karena kondisi medis umum lain SINOPSIS PSIKIATRI Perkembangan defisit kognitif yang dimanifestasikan oleh baik : 1) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi baru dan untuk mengingat informasi yang telah dipelajari sebelumnya ) 2) Satu ( atau lebih ) gangguan kognitif berikut : a) Afasia ( gangguan bahasa ) b) Apraksia ( gangguan kemampuan untuk aktivitas motorik walaupun fungsi motorik adalah utuh ) c) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun fungsi sensorik adalah utuh ) d) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, mengorganisasi, mengurutkan dan abstrak ) Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan bermakna dari tingkat fungsi sebelumnya Terdapat bukti dari riwayat penyakit, pemeriksaan fisik, atau temuan laboratorium bahwa gangguan adalah akibat fisiologis langsung dari salah satu kondisi medis yang tertulis di bawah ini Defisit tidak terjadi semata selama perjalanan delirium
d. Demensia menetap akibat zat SINOPSIS PSIKIATRI Perkembangan defisit kognitif yang dimanifestasikan oleh baik : 1) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi baru dan untuk mengingat informasi yang telah dipelajari sebelumnya ) 2) Satu ( atau lebih ) gangguan kognitif berikut : a) Afasia ( gangguan bahasa ) b) Apraksia ( gangguan kemampuan untuk aktivitas motorik walaupun fungsi motorik adalah utuh ) c) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun fungsi sensorik adalah utuh ) d) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, mengorganisasi, mengurutkan dan abstrak ) Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan bermakna dari tingkat fungsi sebelumnya Defisit tidak terjadi semata hanya selama perjalanan suatu delirium dan menetap melebihi lama yang lazim dari intoksikasi atau putus zat Terdapat bukti dari riwayat penyakit, pemeriksaan fisik, atau temuan laboratorium bahwa defisit secara etiologis berhubungan dengan efek menetap dari pemakaian zat ( misalnya, suatu obat yang disalahgunakan, medikasi )
e. Demensia karena penyebab multipel SINOPSIS PSIKIATRI Perkembangan defisit kognitif yang dimanifestasikan oleh baik : 3) Gangguan daya ingat ( gangguan kemampuan dalam mempelajari informasi baru dan untuk mengingat informasi yang telah dipelajari sebelumnya ) 4) Satu ( atau lebih ) gangguan kognitif berikut : e) Afasia ( gangguan bahasa ) f) Apraksia ( gangguan kemampuan untuk aktivitas motorik walaupun fungsi motorik adalah utuh ) g) Agnosia ( kegagalan untuk mengenali atau mengidentifikasi benda walaupun fungsi sensorik adalah utuh ) h) Gangguan dalam fungsi eksekutif ( yaitu merencanakan, mengorganisasi, mengurutkan dan abstrak ) Defisit kognitif dalam kriteria A1 dan A2 masing menyebabkan gangguan yang bermakna dalam fungsi sosial atau pekerjaan dan menunjukkan suatu penurunan bermakna dari tingkat fungsi sebelumnya Terdapat bukti dari riwayat penyakit, pemeriksaan fisik, atau temuan laboratorium bahwa gangguan memiliki lebih dari satu penyebab ( misalnya, trauma kepala ditambah penggunaan alkohol kronis, demensia tipe Alzheimer dengan perkembagan demensia vaskular selanjutnya ) Defisit tidak terjadi semata selama perjalanan delirium
f. Demensia yang tidak ditentukan SINOPSIS PSIKIATRI Kategori ini digunakan untuk mendiagnosis demensia yang tidak memenuhi kriteria tipe spesifik yang dijelaskan dalam bagian ini. Contohnya adalah gambaran klinis demensia yang tidak terdapat bukti cukup untuk menegakkan etiologi spesifik
1) Dari segi gambaran klinik : Demensia global Global : menyeluruh. Kemunduran fungsi diseluruh bidang Demensia afasik Afasia : tidak bisa berbahasa. Kemunduran terutama di bidang bahasa. Demensia visuoperseptif. Kemunduran terutama di bidang visual, memahami rangsang visual (penglihatan ) 2) Dari segi anatomi dibedakan antara ; Demensia kortikal Demensia yang terjadi karena kerusakan di daerah korteks otak Demensia subkortikal Demensia yang terjadi karena kerusakan di daerah subkorteks, misalnya di daerah ganglia basal. 3) Dari segi etiologi dan perjalanan penyakit Demensia yang reversibel Demensia irreversibel Neurogeriatri, FKUI, Prof. Dr. dr. S.M. Lumbantobing, SpS(K), SpKJ FOO DEMENSIA PADA PENYAKIT ALZHEIMER F00.0 Demensia pada penyakit Alzheimer dengan onset dini F00.1 Demensia pada penyakit Alzheimer dengan onset lambat F00.2 Demensia pada penyakit Alzheimer, tipe tak kh atau tipe campuran F00.9 Demensia pada penyakit Alzheimer YTT FOI DEMENSIA VASKULAR F01.0 Demensia vaskular onset akut F01.1 Demensia multi-infark F01.2 Demensia vaskular subkortikal F01.3 Demensia vaskular campuran kortikal dan subkortik F01.8 Demensia vaskular lainnya F01.9 Demensia vaskular YTT F02 DEMENSIA PADA PENYAKIT LAIN YDK F02.0 Demensia pada penyakit Pick F02.1 Demensia pada penyakit Creutzfeldt-Jakob F02.2 Demensia padapenyakit Huntington F02.3 Demensia pada penyakit Parkinson F02.4 Demensia pada penyakit human immunodeficiency virus (HIV) F02.8 Demensia pada penyakit lain YDT YDK F03 DEMENSIA YTT Karakter kelima dapat digunakan untuk menentukan demensia pada FOO - F03 sebagai berikut : .x0 Tanpa gejala tambahan .xl Gejala lain, terutama waham .x2 Gejala lain, terutama halusinasi .x3 Gejala lain, terutama depresi .x4 Gejala campuran lain PPDGJ III MENURUT SINOPSIS PSIKIATRI KAPLAN DEMENSIA TIPE ALZHEIMER (DAT) Alzheimer adalah penurunan konsentrasi asetilkolin dan kolin asetiltransferase di dalam otak Demensia alzheimer adalah demensia progresif dimana semua kausa reversibel yang diketahui telah disingkirkan. Dua tipe, senilis dengan kemunculan umur 65 tahun atau lebih dan presenilis dengan usia kemunculan setelah 65 tahun. Perbedaan antara keduanya tidak bersifat konvensional yang tidak didasari ats perbedaan riil apapun selain usia kemunculan EPIDEMIOLOGI DAN FAKTOR RESIKO DAT lebih sering terjadi pad wanita. Angka DAT itu sendiri itu lebih rendah pada negara non industri, tapi ini mungkin suatu artefak akibat rendahnya perawatan media dan oleh karena itu kurangnya kepekaan dalam membuat diagnosis tersebut. Usia pun mempengaruhi terjadinya DAT. DEMENSIA MULTI INFARK (MID) Biasanya demensia ini berjalan progresif secara bertahap dengan infark rekuren. Pasien akan menemukan suatu secra spesifik dmn fungsi merekak menjadi lebih buruk dan akan membaik seddikit beberapa hari berikutnya sa,pai terjadi infark berikutnya. Seringkali terdapat tanda neurologik. Gangguan kognisi dapat bersifat bercak dengan area tertentu intak. Demensia ini lebih jarang daripada tipe DAT, lebih sering pada pria daripada wanita. Kemunculan pada umur lebioh muda. Faktor resiko termasuk hipertensi, penyakit jantung, dan faktor resiko lain untuk sttroke. PENYAKIT PICK Secara klinis mirip benar dengan DAT. Tapi klobus kanan jelas terkena, dan tanda frrontal dari perilaku disinhibisi dapat muncul dini. Gliosis reaktif terjadi di lobus frontal dan temporal. PENYAKIT CREUZFELDT-JAKOB Disebabkan oleh virus lambat menular. Kemunculannya biasa terjadi di usia 40 atau 50an. Tanda pertama berupa keluhan somatik samar ataubrasa cemas tak jelas. Termasuk atasia, tanda ekstrapiramidal, koreoatetosis, dan disatria. PENYAKIT HUNTINGTON Penyakit dominan autosom dengan penetrasi lengkap (kromosom 4) ditandai oleh gerak koreoatetoid dan demensia. Seseorang dengan orang tua yang memiliki huntington memiliki peluang 50% menderita p[enyakit ini. PENYAKIT PARKINSON Gangguan gerak idiopatik dengan kemunculan biasanya pada usia lanjut, ditandai oleh bradikinensia, tremor istirahat, tremor menggulung-pil, fasies mirip topeng, rigiditas, cara berjalan perlahan-lahan. Gangguan intelektual ini sering terjadi dan 40-80% menjadi demensia.
GEJALA KLINIS Pada stadium awal demensia, pasien menunjukkan kesulitan untuk mempertahankan kinerja mental, fatigue, dan kecenderungan untuk gagal jika suatu tugas adalah baru atau kompleks atau memerlukan penggeseran strategi pemecahan maslah. Ketidakmampuan melakukan tugas menjadi makin berat dan menyebar ke tugas-tugas harian, seperti berbelanja, saat demensia berkembang. Akhirnya, pasien demensia mungkin memerlukan pengawasan dan bantuan yang terus menerus untuk melakukan bahkan tugas yang paling dasar dalam kehidupan sehari-hari. Defek utama dalam demensia melibatkan orientasi, ingatan, persepsi, fungsi intelektual, dan pemikiran, dan semua fungsi tersebut menjadi secara progresif terkena saat proses penyakit berlanjut. Perubahan afektif dan perilaku, seperti kontrol impuls yang defektif dan labilitas emosional, sering ditemukan, seperti juga penonjolan dan perubahan sifat kepribadian premorbid. Gangguan Daya Ingat Gangguan ingatan biasanya merupakan ciri yang awal dan menonjol pada demensia, khususnya pada demensia yang mengenai korteks, seperti demensia tipe Alzheimer. Pada awal perjalanan de- mensia, gangguan daya ingat adalah ringan dan biasanya paling jelas untuk peristiwa yang baru terjadi, seperti melupakan nomor telepon, percakapan, dan peristiwa hari tersebut. Saat perjalanan dimensia berkembang, gangguan emosional menjadi parah, dan hanya informasi yang dipelajari paling baik (sebagai contohnya, tempat kelahiran) dipertahankan. Orientasi Karena daya ingat adalah penting untuk orientasi terhadap orang, tempat, dan waktu, orientasi dapat terganggu secara progresif selama perjalanan penyakit demensia. Sebagai contohnya, pasien dengan demensia mungkin lupa bagaimana kembali ke ruangannya setelah pergi ke kamar mandi. Tetapi, tidak masalah bagaimana beratnya disorientasi, pasien tidak menunjukkan gangguan pada tingkat kesadaran. Gangguan Bahasa Proses demensia yang mengenai korteks, terutama demensia tipe Alzheimer dan demensia vaskular, dapat mempengaruhi kemampuan berbahasa pasien. Pada kenyataannya, DSM-IV me- masukkan afasia sebagai salah satu kriteria diagnostik. Kesulitan berbahasa mungkin ditandai oleh cara berkata yang samar-samar, stereotipik, tidak tepat, atau berputar-putar. Pasien mungkin juga memiliki kesulitan dalam menyebutkan nama suatu benda. Perubahan Kepribadian Perubahan kepribadian pasien demensia merupakan gambaran yang paling mengganggu bagi keluarga pasien yang terkena. Sifat kepribadian sebelumnya mungkin diperkuat selama perkem- bangan demensia. Pasien dengan demensia juga mungkin menjadi introvert dan tampaknya kurang memperhatikan tentang efek perilaku mereka terhadap orang lain. Pasien demensia yang mempunyai waham paranoid biasanya bersikap bermusuhan terhadap anggota keluarga dan pengasuhnya. Pasien dengan gangguan frontal dan temporal kemungkinan mengalami perubahan kepribadian yang jelas dan mungkin mudah marah dan meledak-ledak. Psikosis Diperkirakan 20 sampai 30 persen pasien demensia, terutama pasien dengan demensia tipe Alzheimer, memiliki halusinasi, dan 30 sampai 40 persen pasien memiliki waham, terutama dengan sifat paranoid atau persekutorik dan tidak sistematik, walaupun waham yang kompleks, menetap, tersistematik dengan baik juga dilaporkan pada pasien demensia. Agresi fisik dan bentuk kekerasan lainnya adalah sering pada pasien demensia yang juga mempunyai gejala psikotik. Gangguan Lain Psikiatrik. Di samping psikosis dan perubahan kepribadian, depresi dan kecernasan adalah gejala utama pada kira-kira 40 sarnpai 50 persen pasien demensia, walaupun sindroma gangguan depresif yang sepenuhnya mungkin hanya ditemukan pada 10 sampai 20 persen pasien demensia. Pasien dengan demensia juga menunjukkan tertawa atau menangis yang patologis-yaitu, emosi yang ekstrim tanpa provokasi yang terlihat. Neurologis. Di samping afasia pada pasien demensia, apraksia dan agnosia adalah sering, dan keberadaannya dimasukkan sebagai kriteria diagnostik potensial dalam DSM-IV. Tanda neurologis lain yang dapat berhubungan dengan demensia adalah kejang, yang terlihat pada kira- kira 10 persen pasien dengan demensia tipe Alzheimer dan 20 persen pasien dengan demensia vaskular, dan presentasi neurologis yang atipikal, seperti sindroma lobus parietalis nondominan. Refleks primitif-seperti refleks menggenggam, moncong, mengisap, kaki-tonik, dan palmomental mungkin ditemukan pada pemeriksaan neurologis, dan jerks mioklonik ditemukan pada 5 sampai 10 persen pasien. Pasien dengan demensia vaskular mungkin mempunyai gejala neurologis tambahan-seperti nyeri kepala, pusing, pingsan, kelemahan, tanda neurologis fokal, dan gangguan tidur-mungkin menunjukkan lokasi penyakit serebrovaskular. Palsi serebrobulbar, disartria, dan disfagia juga le- bih sering pada demensia vaskular dibandingkan demensia lain. Reaksi katastropik. Pasien demensia juga menunjukkan penurunan kemampuan untuk menerapkan apa yang disebut oleh Kurt Goldstein sebagai perilaku abstrak. Pasien mempunyai kesulitan dalam generalisasi dari suatu contoh tunggal dalam membentuk konsep, dan dalam mengambil perbedaan dan persamaan di antara konsep-konsep. Selanjutnya, kemampuan untuk memecahkan masalah, untuk memberikan alasan secara logis dan untuk membuat pertimbangan yang sehat adalah terganggu. Goldstein juga menggambarkan suatu reaksi katastropik, yang ditandai oleh agitasi sekunder karena kesadaran subjektif tentang defisit intelektualnya di bawah keadaan yang me- negangkan. Pasien biasanya berusaha untuk mengkompensasi defek tersebut dengan menggunakan strategi untuk menghindari terlihatnya kegagalan dalam daya intelektual, seperti mengubah subyek, membuat lelucon, atau mengalihkan pewawancara dengan cara lain. Tidak adanya pertimbangan kontrol impuls yang buruk sering ditemukan khususnya pada demensia yang terutama mempengaruhi lobus frontalis. Contoh dari gangguan tersebut adalah bahasa yang kasar, humor yang tidak sesuai, pengabaian penampilan dan higine pribadi, dan mengabaikan aturan konvensional tingkah laku sosial. Sindroma "sundowner." Sindroma downer ditandai oleh mengantuk, konfusi, ataksia dan terjatuh secara tidak disengaja. Keadaan ini terjadi pada pasien lanjut usia yang mengalami sedasi berat dan pada pasien demensia yang bereaksi secara menyimpang bahkan terhadap dosis kecil obat psikoaktif. Sindroma juga terjadi pada pasien demensia jika stimuli eksternal, seperti cahaya dan isyarat yang menyatakan interpersonal adalah menghilang. Onset yang perlahan-lahan dengan perjalanan yang memburuk secara progresif, tidak adanya tanda neurologis, tidak adanya riwayat trauma atau penyakit serebrovaskular, hasil tes darah yang normal, dan bukti atrofi kortikal pada CT scan berarti diagnosis demensia tipe Alzheimer. Karena tidak terdapat ciri psikotik atau gangguan mood, diagnosis dicatat tanpa komplikasi. Beratnya demensia dinyatakan sebagai moderat karena pasien memerlukan suatu pengawasan.
DIAGNOSIS adanya penurunan daya ingat dan daya pikir, yang sampai mengganggu kegiatan harian seseorang seperti mandi, berpakaian, makan, kebersihan diri, BAK, dan BAB. Tidak ada gangguan keasadaran Gejala dan disabilitas sudah nyata untuk paling sedikit 6 bulan (PPDGJ III)
Diagnosis
Diagnosis difokuskan pada 3 hal: Pembedaan antara delirium dan demensia Bagian otak yang terkena Penyebab yang potensial reversibel Perlu pembedaan dan depresi (ini bisa diobati relatif mudah) Pemeriksaan untuk mengingat 3 benda yg disebut Mengelompokkan benda, hewan dan alat dengan susah payah Pemeriksaan laboratonium, pemeriksaan EEC Pencitraan otak amat penting CT atau MRI
F00 DEMENSIA PENYAKIT AZLZHEIMER o Terdapat gejala demensia o Onset bertahap (insidious onset) dengan deteriorasi lambat.. inset biasanya sulit ditentukan waktunya yang persis, tiba2 orang lain sudah menyadari adanya kelainan tersebut. Dalam perjalanan penyakitnya dapat terjadi suatu taraf yang stabil (plateau) secara nyata o Tidak adanya bukti klinis, atau temuan dari pemeriksaan khusus, yang menyatakan bahwa kondisi mental itu dapat disebabkan oleh penyakit otak/ sistemik lain yang dapat meneimbulkan demensia. o Tidak adanya serangan apoplektik mendadak, atau gejala neurologik kerusakan otak fokal seperti hemiparesis, hilangnya daya sensorik, defek lapangan pandang mata, dan inkordinasi yang terjadi dalam masa dini dari dari gangguan itu. F00.0 DEMENSIA PADA PENYAKIT ALZHEIMER DENGAN ONSET DINI Onsetnya sebelum usia 65 tahun Perkembangan gejalanya cepat dan progresif Adanya riwayat keluarga yang mengalami demensia alzheimer merupakan faktor penyokong diagnosis tetapi tidak harus dipenuhi F00.1 DEMENSIA PADA PENYAKIT ALZHEIMER DENGAN ONSET LAMBAT o Sama tersebut diatas, hanya onsetnya sesudah berusia 65 tahun dan perjalanan penyakitnya lamban dan biasanya dengan gangguan daya ingat sebagai gangguan utamanya o F00.2 TIPE TAK KHAS ATU TIPE CAMPURAN Yang tidak cocok dengan pedoman untuk F00.0 atau F00.1, tipe campuran adalah demensia alzheimer + vaskuler o FOO.3 DEMENSIA PADA PENYAKIT ALZHEIMER YTT F01 DMENSIA VASKULER Terdapat gejala demensia Hendaya fungsi kognitif biasanya tidak merata (mungkin terdapat hilangnya day ingatan, gangguan daya pikir, gejala neurologis fokal). Daya tilik diri(insight) dan daya nilai (judgment) secara relatif tetap baik. Suatu onset yan mendadak atau deteriorasi yang bertahap, disertai adanya gejala neurologis fokal, meningkatkan kemungkinan diagnosis demensia vaskuler. Pada beberapa kasus, penetapan hanya dapat dilakukan dengan px CT-Scan atau pemeriksaan neuropatologis F01.0 DEMENSIA VASKULER ONSET AKUT o Biasanya terjadi secara cepat sesudah serangkain stroke akibat trombosis serebrovaskuler, embolisme, atau perdarahan. Pada kasus-kasus yang jarang, suatu infark yang besra dapat sebagai penyebabnya F01.1 DEMENSIA MULTI INFARK o Onsetnya lebih lambt, biasanya setelah serangkaina episode iskemnik minor yang menimbulkan akumulasi dariu infark pada parenkim otak. F01.2 DEMENSIA VASKULER SUBKORTIKAL o Fokus kerusakan akibat iskemik pada substansia alba di hemisferi serebral, yang dapat diduga secara klinis dan dibuktikan dengan CT_Scan. Korteks serebri biasanya tetap baik, walaupun demikian gambaran klinisnya masih mirip dengan dmensia pada penyakit alzheimer. F01.3 DEMENSIA VASKULAR CAMPURAN KORTIKAL DANM SUBKORTIKAL Komponen campuran kortikal dan subkortikal dapat diduga dari gambaran klinis, hasil pemeriksaan, atau keduanya. F01.8 DEMENSIA VASKULAR LAINNYA F01.9 DEMENSIA VASKULAR YTT F02 DEMENSIA PADA PENYAKIT LAIN YDK F02.0 DEMENSIA PADA PENYAKIT PICK o Gejala yang progresif o Gambaran neuropatologis o Manifestasi gangguan perilaku pada umumnya mendahului gangguan daya ingat F02.1 DEMENSIA PADA PENYAKIT CREUTZFELDT-JAKOB o Trias yang sangat mengarah pada penyakit ini: o Progresif merusak o Penyakit piramidal dan ekstrapiramidal dengan mioklonus o Elektroensefalogram yang khas (trifasik) F02.2 DEMENSIA PADA PENYAKIT HUNTINGTON Ada kaitan antara gangguan gerakan koreiform, demensia, dan RPK dengan peny huntington Gerakan koreiform yang involunter, terutama pada wajah, tangan, dan bahu, atau cara berjalan yang khas merupakan manbifestasi dini dari gejala ini. Biasanya mendahului gejala demensia. Gangguan fungsi lobus frontalis pada tahap dini, dengan daya ingat relatif masih terpelihara, sampai pada saat selanjutnya. F02.3 DEMENSIA PADA PENYAKIT PARKINSON Berkembang pada seseorang dengan penyakit parkinson yang sudah parah, tidak ada gambaran klinis khusus yang di tampilkan.... F02.4 DEMENSIA PADA PENYAKIT HIV o Demensia yang berkembang pada seseorang dengan penyakit HIV. F02.8 DEMENSIA PADA PENYAKIT LAIN YDT YDK Terjadi sebagai manifestasi atau konsekuensi beberapa macam kondisi somatik dan serebral lainnya F03 DEMENSIA YTT o Digunakan bila kriteria umum untuk diagnosis dmensia terpenuhi, tetapi tidak mungkin di identifikasikan pada salah satu tipe tertentu (F00.9-F02.9)
TERAPI Terapi
Pertama perlu diperhatikan keselamatan pasien, lingkungan dibuat senyaman mungkin, dan bantuan pengasuh perlu. Koridor tempat jalan, tangga, meja kursi tempat barang keperkuannya Tidak diperbolehkan memindahkan mobil dsb. Diberi keperluan yang mudah dilihat, penerangan lampu terang, jam dinding besar, tanggalan yang angkanya besar Obat: Nootropika: o Pyritinol (Encephabol) 1 x 100 - 3 x 200 mg o Piracetam (Nootropil) 1 x 400 - 3 x 1200 mg o Sabeluzole (Reminyl) o Ca-antagonist: o Nimodipine(Nimotop 1- 3 x 30 mg) o Citicholine (Nicholin) 1 - 2 x 100 - 300 mg i.v./i.m. o Cinnanzine (Stugeron) 1 - 3 x 25 mg o Pentoxifylline (Trental) 2 - 3 x 400 mg (oral), 200 - 300 mg infuse o Pantoyl-GABA Acetylcholinesterase inhibitors o Tacnne 10 mg dinaikkan lambatlaun hingga 80 mg. Hepatotoxik o Donepezil (Aricept) centrally active reversible cholinesterase inhibitor, 5 mg 1x /hari o Galantamine (Riminil) 1 - 3 x 5 mg o Rivastigmin (Exelon) 1,5, 3, 4, 5, 6 mg o Memantine 2 x 5 mg 10 mg
Membantu penderita demensia dan keluarganya: 1. Mempertahankan lingkungan yang familiar akan membantu penderita tetap memiliki orientasi. Kalender yang besar, cahaya yang terang, jam dinding dengan angka-angka yang besar atau radio juga bisa membantu penderita tetap memiliki orientasi. 2. Menyembunyikan kunci mobil dan memasang detektor pada pintu bisa membantu mencegah terjadinya kecelekaan pada penderita yang senang berjalan-jalan. 3. Menjalani kegiatan mandi, makan, tidur dan aktivitas lainnya secara rutin, bisa memberikan rasa keteraturan kepada penderita. 4. Memarahi atau menghukum penderita tidak akan membantu, bahkan akan memperburuk keadaan. 5. Meminta bantuan organisasi yang memberikan pelayanan sosial dan perawatan, akan sangat membantu. Obat Untuk Dementia a. Cholinergic-enhancing agents Untuk terapi dementia jenis Alzheimer, telah banyak dilakukan penelitian. Pemberian cholinergic-enhancing agents menunjukkan hasil yang cukup memuaskan pada beberapa penderita, namun demikian secara keseluruhan tidak menunjukkan keberhasilan sama sekali. Hal ini disebabkan oleh kenyataan, bahwa dementia Alzheimer tidak semata-mata disebabkan oleh defisiensi kolinergik. Dementia ini disebabkan juga oleh defisiensi neurotransmitter lainnya. Sementara itu, kombinasi kolinergik dan noradregenik ternyata bersifat kompleks, pemberian obat kombinasi ini harus hati-hati karena dapat terjadi interaksi yang mengganggu system kardiovaskuler b. Choline dan lecithin Defisit asetilkolin di korteks dan hipokampus pada dementia Alzheimer dan hipotesis tentang sebab hubungannya dengan memori mendorong para peneliti untuk mengarahkan perhatiannya pada neurotransmitter. Pemberian precursor, choline dan lecithin merupakan salah satu pilihan dan memberi hasil cukup memuaskan, namun demikian tidak memperlihatkan hal yang istimewa. Dengan choline ada sedikit perbaikan terutama dalam fungsi verbal dan visual. Dengan lecithin hasilnya cenderung negative, walaupun dengan dosis yang berlebih sehingga kadar dalam serum mencapai 120% dan dalam cairan serebrospinal naik sampai 58%. c. Neuropeptida, Vasopresin, dan ACTH Pemberian neuropeptida, vasopresin, dan ACTH perlu memperoleh perhatian. Neuropeptida dapat memperbaiki daya ingat semantic yang berkaitan dengan informasi dan kata-kata. Pada lansia tanpa gangguan psiko-organik, pemberian ACTH dapat memperbaiki daya konsentrasi dan memperbaiki keadaan umum. d. Nootropic Agents Dari golongan nootropic substances, ada dua jenis obat yang sering dipergunakan dalam terapi dementia, ialah nicerogoline dan co-dergocrine mesylate. Co- dergocrine mesylate memperbaiki perfusi serebral dengan cara mengurangi tahanan vascular dan meningkatkan konsumsi oksigen otak. Obat ini memperbaiki perilaku, aktivitas, dan mengurangi bingung, serta memperbaiki kognisi. Dalam suatu penelitian multisenter, diperoleh suatu kesimpulan, bahwa antara nicergoline dan co-dercogrine mesylate, apabila diberikan kepada penderita dementia, akan mempunyai khasiat yang mirip, terutama terhadap perbaikan fungsi kognitifnya. Di sisi lain, nicergoline tampak bermanfaat untuk memperbaiki perasaan hati dan perilaku. e. Dihydropyrdine Pada lansia dengan perubahan mikrovaskuler dan neuronal, L-type calcium channels menunjukkan pengaruh yang kuat. Lipophilic dihydropyridine bermanfaat untuk mengatasi kerusakan susunan saraf pusat pada lansia. Nimodipin bermanfaat untuk mengembalikan fungsi kognitif yang menurun pada lansia dan dementia jenis Alzheimer. Nimodipin memelihara sel-sel endothelial atau kondisi mikrovaskuler tanpa dampak hipotensif, dengan demikian sangat dianjurkan sebagai terapi alternatif untuk lansia terutama yang mengidap hipertensi esensial DELIRIUM Definisi Delirium adalah keadaan yang yang bersifat sementara dan biasanya terjadi secara mendadak, dimana penderita mengalami penurunan kemampuan dalam memusatkan perhatiannya dan menjadi linglung, mengalami disorientasi dan tidak mampu berfikir secara jernih. http://www.medicastore.com Merupakan suatu sindroma bukan penyakit yang ditandai oleh suatu gangguan kesadaran yang biasanya terlihat bersamaan dengan gangguan kognitif secara global. Dan biasanya merupakan tanda prognostic yang buruk. (KAPLAN)
Etiologi Penyebab delirium: Alkohol, obat-obatan dan bahan beracun Efek toksik dari pengobatan Kadar elektrolit, garam dan mineral (misalnya kalsium, natrium atau magnesium) yang tidak normal akibat pengobatan, dehidrasi atau penyakit tertentu Infeksi akut disertai demam Hidrosefalus bertekanan normal, yaitu suatu keadaan dimana cairan yang membantali otak tidak diserap sebagaimana mestinya dan menekan otak Hematoma subdural, yaitu pengumpulan darah di bawah tengkorak yang dapat menekan otak. Meningitis, ensefalitis, sifilis (penyakit infeksi yang menyerang otak) Kekurangan tiamin dan vitamin B12 Hipotiroidisme maupun hipertiroidisme Tumor otak (beberapa diantaranya kadang menyebabkan linglung dan gangguan ingatan) Patah tulang panggul dan tulang-tulang panjang Fungsi jantung atau paru-paru yang buruk dan menyebabkan rendahnya kadar oksigen atau tingginya kadar karbon dioksida di dalam darah Stroke.
Penyakit intrakranial Epilepsi atau keadaan pasca kejang Trauma otak (terutama gegar otak) Infeksi (meningitis.ensetalitis). Neoplasma. Gangguan vaskular Penyebab ekstrakranial Obat-obatan (di telan atau putus), Obat antikolinergik, Antikonvulsan, Obat antihipertensi, Obat antiparkinson. Obat antipsikotik, Cimetidine, Klonidine. Disulfiram, Insulin, Opiat, Fensiklidine, Fenitoin, Ranitidin, Sedatif(termasuk alkohol) dan hipnotik, Steroid. Racun Karbon monoksida, Logam berat dan racun industri lain. Disfungsi endokrin (hipofungsi atau hiperfungsi) Hipofisis, Pankreas, Adrenal, Paratiroid, tiroid Penyakit organ nonendokrin. Hati (ensefalopati hepatik), Ginjal dan saluran kemih (ensefalopati uremik), Paru-paru (narkosis karbon dioksida, hipoksia), Sistem kardiovaskular (gagal jantung, aritmia, hipotensi). Penyakit defisiensi (defisiensi tiamin, asam nikotinik, B12 atau asain folat) Infeksi sistemik dengan demam dan sepsis. Ketidakseimbangan elektrolit dengan penvebab apapun Keadaan pasca operatif Trauma (kepala atau seluruh tubuh) Karbohidrat: hipoglikemi. (KAPLAN) EPIDEMIOLOGI Merupakan suatu gangguan yang umum. 10-15% pasien di bangsal bedah umum dan 15-25% pasien di bangsal medis umum mengalami delirium di RS selama di rawat. 30% pasien ICU dan rawat jalan intensif dan 40-50% pasien yg dalam pemulihan setelah pembedahan fraktur mengalami delirium. 20% pasien luka bakar berat dan 30% pasien AIDS mengalami delirium saat di rawat di RS. Penyebb delirium pasca operasi : stres pembedahan, jalur pasca operasi, insomnia, medikasi nyeri,dll. Faktor resiko utama delirium : USIA LANJUT. 30-40% pasien uasia lanjut yang di rawat di RS delirium . faktor presdisposisi lain : usia muda (anak-anak), cedera otak yang telah ada sebelumnya(demensia,vaskuler, tumor), riwayat delirium, ketergantungan alkohol, diabetes, dll. Adanya delirium menandakan PROGNOSIS BURUK. Angka mortalitas tiga bulan pada pasien yang mengalami delirium : 50%.
FAKTOR RESIKO Usia lanjut, usia 30-40 tahun. Riwayat cedera otak, seperti demensia, penyakit kardiovaskuler, tumor. Ketergantungan alcohol. Riwayat kondisi medis umum, seperti diabetes, kanker, gangguan sensoris (kebutaan), malnutrisi. (KAPLAN)
KLASIFIKASI Menurut PPDGJ III F05 Delirium bukan akibat alkohol dan psikoaktif lain nya F05.0 Delirium, tak bertumpang tindih dengan demensia F05.1 Delirium, bertumpang tindih dengan demensia F05.8 Delirium lainya. F05.9 DeliriumYTT.
GEJALA KLINIS Kesadaran (Arousal) Dua pola umum kelainan kesadaran telah ditemukan pada pasien dengan delirium, satu pola ditandai oleh hiperaktivitas yang berhubungan dengan peningkatan kesiagaan. Pola lain ditandai oleh penurunan kesiagaan. Pasien dengan delirium yang berhubungan dengan putus zat seringkali mempunyai delirium hiperaktif, yang juga dapat disertai dengan tanda otonomik, seperti kemerahan kulit, pucat, berkeringat, takikardia, pupil berdilatasi, mual, muntah, dan hipertermia. Pasien dengan gejala hipoaktif kadang-kadang diklasifikasikan sebagai depresi, katatonik atau mengalami demensia. 1
Orientasi Orientasi terhadap waktu, tempat dan orang harus diuji pada seorang pasien dengan delirium. Orientasi terhadap waktu seringkali hilang bahkan pada kasus delirium yang ringan. Orientasi terhadap tempat dan kemampuan untuk mengenali orang lain (sebagai contohnya, dokter, anggota keluarga) mungkin juga terganggu pada kasus yang berat Pasien delirium jarang kehilangan orientasi terhadap dirinya sendiri. Bahasa dan Kognisi Pasien dengan delirium seringkali mempunyai kelainan dalam bahasa. Kelainan dapat berupa bicara yang melantur, tidak relevan, atau membingungkan (inkoheren) dan gangguan kemampuan untuk mengerti pembicaraan Fungsi kognitif lainnya yang mungkin terganggu pada pasien delirium adalah fungsi ingatan dan kognitif umum Kemampuan untuk menyusun, mempertahankan dan mengingat kenangan mungkin terganggu, walaupun ingatan kenangan yang jauh mungkin dipertahankan. Disarnping penurunan perhatian, pasien mungkin mempunyai penurunan kognitif yang dramatis sebagai suatu gejala hipoaktif delirium yang karakteristik. Pasien delirium juga mempunyai gangguan kemampuan memecahkan masalah dan mungkin mempunyai waham yang tidak sistematik, kadang kadang paranoid. Persepsi Pasien dengan delirium seringkali mempunyai ketidak mampuan umum untuk membedakan stimuli sensorik dan untuk mengintegrasikan persepsi sekarang dengan pengalaman masa lalu mereka. Halusinasi relatif sering pada pasien delirium. Halusinasi paling sering adalah visual atau auditoris walaupun halusinasi dapat taktil atau olfaktoris. Ilusi visual dan auditoris adalah sering pada delirium. Suasana Perasaan Pasien dengan delirium mempunyai kelainan dalam pengaturan suasana Gejala yang paling sering adalah kemarahan, kegusaran, dan rasa takut yang tidak beralasan. Kelainan suasana perasaan lain adalah apati, depresi, dan euforia. Gejala Penyerta : Gangguan tidur-bangun Tidur pada pasien delirium secara karakteristik adalah tergangga Paling sedikit mengantuk selama siang hari dan dapat ditemukan tidur sekejap di tempat tidurnya atau di ruang keluarga. Seringkali keseluruhan siklus tidur-bangun pasien dengan delirium semata mata terbalik. Pasien seringkali mengalami eksaserbasi gejala delirium tepat sebelum tidur, situasi klinis yang dikenal luas sebagai sundowning. 1
Gejala neurologis Gejala neurologis yang menyertai, termasuk disfagia, tremor, asteriksis, inkoordinasi, dan inkontinensia urin.
Gambaran Delirium Demensia Riwayat Penyakit akut Penyakit kronik Awal Cepat Lambat laun Sebab Terdapat penyakit lain (infeksi, dehidrasi, guna/putus obat Biasanya penyakit otak kronik (spt Alzheimer, demensia vaskular) Lamanya Ber-hari/-minggu Ber-bulan/-tahun Perjalanan sakit Naik turun Kronik progresif Taraf kesadaran Naik turun Normal Orientasi Terganggu, periodik Intak pada awalnya Afek Cemas dan iritabel Labil tapi tak cemas Alam pikiran Sering terganggu Turun jumlahnya Bahasa Lamban, inkoheren, inadekuat Sulit menemukan istilah tepat Daya ingat Jangka pendek terganggu nyata Jangka pendek & panjang terganggu Persepsi Halusinasi (visual) Halusinasi jarang kecuali sundowning(eksaserbasi gejala delirium sebelum tidur) Psikomotor Retardasi, agitasi, campuran Normal Tidur Terganggu siklusnya Sedikit terganggu siklus tidurnya Atensi & kesadaran Amat terganggu Sedikit terganggu Reversibilitas Sering reversibel Umumnya tak reversibel Penanganan Segera Perlu tapi tak segera
Catatan: pasien dengan demensia amat rentan terhadap delirium, dan delirium yang bertumpang tindih dengan demensia adalah umum
DELIRIUM VS DEMENSIA Pada kasus delirium akan terjadi gangguan pada proses pikir, sedangkan pada demensia akan mengalami respon kognitif yang maladaptip Karakteristik Delirium dan demensia
Delirium
Demensia
Onset
- Biasanya tiba-tiba
- Biasanya perlahan
Lama
- Biasanya singkat/ < 1 bulan
-biasanya lama dan progressif - Paling banyak dijumpai pada usia > 65 th
- Fluktuasi tingkat kesadaran - Disorientasi - Gelisah - Agitasi - Ilusi - Hilang daya ingat - Kerusakan penilaian - Perhatian menurun - Perilaku sosial tidak sesuai
- Halusinasi - Pikiran tidak teratur -Gangguan penilaian dan pengambilan keputusan
- Afek labil
- Afek labil - Gelisah - Agitasi
Membedakan Delirium Dengan Demensia Delirium Demensia Terjadi secara tiba-tiba Terjadi secara perlahan Berlangsung selama beberapa minggu Bisa menetap Berhubungan dengan pemakaian obat atau gejala putus obat, penyakit berat, kelainan metabolisme Bisa tanpa penyakit Hampir selalu memburuk di malam hari Sering bertambah buruk di malam hari Tidak mampu memusatkan perhatian Perhatiannya 'mengembara' Kesiagaan berfluktuasi dari letargi menjadi agitasi(cemas) Kesiagaan seringkali berkurang Orientasi terhadap lingkungan bervariasi Orientasi terhadap lingkungan terganggu Bahasanya lambat, seringkali tidak dapat dimengerti & tidak tepat Kadang mengalami kesulitan dalam menemukan kata-kata yg tepat Ingatannya bercampur baur, linglung Ingatannya hilang, terutama untuk peristiwa yang baru saja terjadi
DIAGNOSIS 1. Onset gejala yang tiba-tiba. 2. Pemeriksaan gangguan kognitif dengan MMSE (Mini Mental State Examination). 3. Adanya penyakit fisik yang diketahui, riwayat trauma kepala, ketergantungan alcohol atau zat lain dapat meningkatkan diagnosis. 4. Lab: EEG (Elektro Ensefalo Gram) menunjukkan perlambatan umum aktivitas. (KAPLAN) Menurut PPDGJ III F05 DELIRIUM, BUKAN AKIBAT ALKOHOLK dan ZAT PSIKOAKTIF LAINNYA Pedoman diagnostik Gangguan kesadaran dan perhatian: o Dari taraf kesadaran berkabut sampai dengan koma o Menurunnya kemampuan untuk mengarahkan, memusatkan, mempertahankan, dan mengalihkan perhatian. o Gangguan kognitif secara umum: o Distorsi persepsi, ilusi dan halusinasi seringkali visual o Hendaya daya pikir dan pikiran abstrak, dengan atau tanpa waham yang bersifat sementara, tetapi sangat khas terdapat inkoherensi yang ringan o Hendaya daya ingat segera dan jangka pendek, namun daya ingat jangka panjang relatigf masih utuh o Disorientasi waktu. Pada kasus yang berat terdapat juga disorientasi tempant dan orang o Gangguan psikomotor Hipo/ hiper aktivitas & pengalihan aktivitas yang tidak terduga dari satu ke yang lain. Waktu bereaksi yang lebih panjang Arus pembicaraan yang bertambah atau berkurang Reaksi terperanjat meningkat gangguan siklus tidur bangun o insomnia/ pd kasus yg berat tidak bisa tidur sama sekalui / terbaliknya siklus tidur bangun; mengantuk pada siang hari o gejala yang memburuk pada malam hari o mimpi yang menggangu/ mimpi buruk, yang dapat berlanjut menjadi halusinasi setelah bangun tidur o gangguan emosional: mis depresi, anxietas atau takut, lekas marah, euforia, apatis, atau rasa kehilangan akal. o Omset biasanya cepat, perjalanan penyakitnya hilang timbul sepanjang hari, dan keadaan itu berlangsung kurang dari 6 bulan.
F05.0 DELIRIUM, TAK BERTUMPANG TINDIH DENGAN DEMENSIA Delirium yang tidak bertumpang tindih dengan demensia yang sudah ada sebelumnya F05.1 DELIRIUM, BERTUMPANG TINDIH DENGAN DEMENSIA Kondisi yang memenuhi kriteria di atas tetapi terjadi pada saat sudah ada demensia F05.8 DELIRIUM LAINNYA F05.9 DELIRIUM YTT
pedoman diagnostic gangguan kesadaran dengan penurunan kemampuan untuk memusatkan, mempertahankan, atau mengalihkan perhatian perubahan kognisi atau perkembangan gangguan persepsi yang tidak lebih baik diterangkan demensia yang telah ada sebelumnya, yang telah ditegakkan, atau yang sedang timbul. Gangguan timbul setelah suatu periode waktu yang singkat (biasanya beberapa jam sampai hari) dan cenderung berfluktuasi selama perjalanan hari Teradpat bukti-bukti dari riwayat penyakit, PF, atau temuan laboratorium bahwa gangguan adalah disebabkan oleh akibat fisiologis langsung dari kondisi medis umum. PF : denyut jantung, temperature, tekanan darah, pernafasan, pembuluh darah karotis, kulit kepala& wajah, leher,mata, mulut, tiroid, jantung, paru-paru, pernafasan, hati, system saraf Pemeriksaan laboratorium : pemeriksaan standar (kimia darah),hitung darah lengkap dengan diferensial sel darah putih, tes fungsi tiroid, tes serologis untuk sifilis, tes antibody HIV, urinalisis,EKG,EEG,sinar-x dada,skrining obat dalam darah dan urin. kaplan DD Delirium harus dibedakan dengan kelainan kognitif global. Tabel 1. Kriteria DSM-IV untuk delirium Gangguan kesadaran Penurunan derajat kewaspadaan Tidak bisa memusatkan perhatian Tidak bisa menggeser perhatian Gangguan kognitif Defisit memori Disorientasi Gangguan bahasa Berkembang dalam waktu pendek Jam dan hari Fluktuatif, sundowning Hal-hal tersebut di atas berubah berdasar kondisi medik, intoksikasi, dan atau pengobatan a. Demensia Demensia berbeda karena onsetnya adalah gradual (biasanya tahun), dan persisten. Demensia tidak menyebabkan penurunan kewaspadaan sampai late stages (dapat diketahui dari anamnesa). Pasien dengan dengan demensia mudah menjadi delirium, walaupun demikian, kondisi akut pada pasien demensia bisa delirium atau kondisi akut lainnya. Demensia lewy bodies bisa disertai dengan halusinasi dan psikosis. b. Depresi Depresi bisa terjadi mimic hypoactive deliriumdengan penolakan yang jelas, retardasi psikomotor, melambatnya pembicaraan, apatis, dan pseudodemensia. Depresi tidak mempengaruhi derajat kesadaran. c. Psikosis Psikosis bisa terjadi mimic hyperactive delirium. Psikosis fungsoinal berbeda karena halusinasi suara. Lebih banyak khayalan, dan lebih sedikit fluktuatif. d. CVA CVA jarang disertai dengan delitium, atau salah dianggap sebagai delirium. Contohnya, aphasia mungkin salah dianggap sebagai kebingungan. Juga kelainan difus pada atensi karena stroke pada daerah temporooccipital, parietal, prefrontal, atau region sub kortikal pada hemisfer kanan. Keadaan akut mungkin memperburuk tanda neurologis fokal karena CVA lama. http://medical-free.blogspot.com/2008/06/delirium.html terapi Terapi diawali dengan memperbaiki kondisi penyakitnya dan menghilangkan faktor yang memberatkan seperti: Menghentikan penggunaan obat Obati infeksi Suport pada pasien dan keluanga Mengurangi dan menghentikan agitasi untuk pengamanan pasien Cukupi cairan dan nutrisi Vitamin yang dibutuhkan Segala alat pengekang boleh digunakan tapi harus segera dilepas bila sudah membaik, alat infuse sesederhana mungkin, lingkungan diatur agar nyaman. Obat: o Haloperidoi dosis rendah dulu 0,5 1 mg per os, IV atau IV o Risperidone0,5 3mg perostiap l2jam o Olanzapine 2,5 15 mg per os 1 x sehari o Lorazepam 0,5 1mg per Os atau parenteral (tak tersedia di Indonesia), Perlu diingat obat benzodiazepine mi bisa memperburuk delirium karena efek sedasinya. http://www.idijakbar.com/prosiding/delirium.htm
Organic Mental Disorders
An organic mental disorder is a permanent or temporary dysfunction in the brain that is caused by physiological problems with the brain. The causes range from heredity to an injury of the brain to a disease that affects brain tissue or changes the chemical or hormonal levels of the brain. The symptoms of organic mental disorders vary depending on the underlying issue of what caused the imbalance or malfunction of the brain, but they can be difficult to deal with.
While there may or may not be a cure for the disorder depending on the exact physiological cause, therapy and counseling may be options that can be helpful for dealing with the symptoms that accompany organic mental disorders. From hallucinations to delusions to personality problems, there is a wide range of problems that may develop because of a physical problem with the brain.
Definition of Organic Mental Disorders
Organic mental disorders affect the brain's chemistry and hormonal balance in a negative way, causing mild to serious problems for those afflicted. From social problems to internal emotional problems, the effects of organic mental disorders can be difficult to overcome. Getting help with any of the many organic mental disorders is possible, with therapy being a popular way for people to deal with the root cause of the problem.
Causes Disorders associated with OBS include: Brain injury caused by trauma Bleeding into the brain (intracerebral hemorrhage) Bleeding into the space around the brain (subarachnoid hemorrhage) Blood clot inside the skull causing pressure on brain (subdural hematoma) Concussion
Breathing conditions Low oxygen in the body (hypoxia) High carbon dioxide levels in the body (hypercapnia)
Cardiovascular disorders Abnormal heart rhythm (arrhythmias) Brain injury due to high blood pressure (hypertensive brain injury) Dementia due to many strokes (multi-infarct dementia) Heart infections (endocarditis, myocarditis) Stroke Transient ischemic attack (TIA)
Degenerative disorders Alzheimer's disease (also called senile dementia, Alzheimer's type) Creutzfeldt-Jacob disease Diffuse Lewy Body disease Huntington's disease Multiple sclerosis Normal pressure hydrocephalus Parkinson's disease Pick's disease
Dementia due to metabolic causes Drug and alcohol-related conditions Alcohol withdrawal state Intoxication from drug or alcohol use Wernicke-Korsakoff syndrome (a long-term effect of excessive alcohol consumption or malnutrition) Withdrawal from drugs (especially sedative-hypnotics and corticosteroids)
Infections Any sudden onset (acute) or long-term (chronic) infection Blood poisoning (septicemia) Brain infection (encephalitis) Meningitis (infection of the lining of the brain and spinal cord) Prion infections such as mad cow disease Late-stage syphilis
Other medical disorders Cancer Kidney disease Liver disease Thyroid disease (high or low) Vitamin deficiency (B1, B12, or folate) Other conditions that may mimic organic brain syndrome include: Depression Neurosis Psychosis
Symptoms of / Reasons for Organic Mental Disorders Hallucinations Inability to perform in social situations Depression Confusion Changes in personality
Types of Organic Mental Disorders
Organic Hallucinosis - People suffering from this may experience many different types of hallucinations that can hamper their ability to lead a normal life. Organic Catatonic Disorder - These are characterized by problems dealing with motor skills or malfunctioning muscles. Organic Delusional Disorder - Someone who insists that something is true even when it's not may be suffering from organic delusional disorder. Organic Mood Disorder - Deep emotional problems may be caused by organic mood disorder, which can cause depression or mania. Organic Anxiety Disorder - Those who have problems with anxiety in public places. Organic Dissociative Disorder - This is characterized by problems with awareness, identity, memory, perception, or a combination thereof. Organic Emotionally Labile Disorder - Those who suffer from wild mood swings in both directions. Organic Personality Disorder - Organic personality disorders deal with problems that cause people to not fit in well with the majority of society in an extreme fashion. Postencephalitic Syndrome - This is brought on during the late stages of Parkinson's Disease as the nerves break down. Postconcussional Syndrome - These are problems that may occur after a concussion due to a blow to the head. Unspecified Organic Disorder - Those organic disorders that are not mentioned above may be classified as unspecified, but they are just as serious.
Treatment for Organic Mental Disorders
The treatment methods are going to vary depending on what type of mental disorder you are dealing with, but for the most part, a professionally guided therapy program and counseling are recommended for long term success with treating organic mental disorders even though there may be no cure.
For many, pursuing online therapy allows them to get the help they need while still being able to function in their day to day life. The therapy can be just as intense online - and just as helpful. The trained therapists here at GoMentor.com can assist you with any of the organic mental disorders that may have developed because of a disease.
Exams and Tests Tests depend on the disorder, but may include: Blood tests Electroencephalogram (EEG) Head CT scan Head MRI
Dementia is a syndrome (a group of related symptoms) associated with an ongoing decline of the brain and its abilities. This includes problems with: memory loss thinking speed mental agility language understanding judgement
People with dementia can become apathetic or uninterested in their usual activities, and have problems controlling their emotions. They may also find social situations challenging, lose interest in socialising, and aspects of their personality may change. A person with dementia may lose empathy (understanding and compassion), they may see or hear things that other people do not (hallucinations), or they may make false claims or statements. As dementia affects a person's mental abilities, they may find planning and organising difficult.Maintaining their independence may also become a problem. A person with dementia will therefore usually need help from friends or relatives, including help with decision making. Your GP will discuss the possible causes of memory loss with you, including dementia. Other symptoms can include: increasing difficulties with tasks and activities that require concentration and planning depression changes in personality and mood periods of mental confusion difficulty saying the right words Most types of dementia can't be cured, but if it's detected early there are ways you can slow it down and maintain mental function. Read more about about the symptoms of dementia.
causes dementia and its symptoms
In a healthy brain, mass and speed may decline in adulthood, but this miraculous machine continues to form vital connections throughout life. However, when connections are lost through inflammation, disease, or injury, neurons eventually die and dementia may result. The prospect of literally losing one's self can be traumatic, but early intervention can dramatically alter the outcome. Understanding causes is the first step. In the past twenty years, scientists have greatly demystified the origins of dementia. Genetics may increase your risks, but scientists believe a combination of hereditary, environmental, and lifestyle factors are most likely at work. Dementia can be caused by: Medical conditions that progressively attack brain cells and connections, most commonly seen in Alzheimer's disease, Parkinson's disease, or Huntington's disease. Medical conditions such as strokes that disrupt oxygen flow and rob the brain of vital nutrients.Additional strokes may be prevented by reducing high blood pressure, treating heart disease, and quitting smoking. Poor nutrition, dehydration, and certain substances, including drugs and alcohol. Treating conditions such as insulin resistance, metabolic disorders, and vitamin deficiencies may reduce or eliminate symptoms of dementia. Single trauma or repeated injuries to the brain. Depending on the location of the brain injury, cognitive skills and memory may be impaired. Infection or illness that affects the central nervous system, including Creutzfeldt- Jakob disease and HIV. Some conditions are treatable, including liver or kidney disease, depression-induced pseudodementia, and operable brain tumors.
Causes
Dementia is caused by damage to brain cells. This damage interferes with the ability of brain cells to communicate with each other. When brain cells cannot communicate normally, thinking, behavior and feelings can be affected. The brain has many distinct regions, each of which is responsible for different functions (for example, memory, judgment and movement). When cells in a particular region are damaged, that region cannot carry out its functions normally.
Take our interactive Brain Tour. Different types of dementia are associated with particular types of brain cell damage in particular regions of the brain. For example, in Alzheimer's disease, high levels of certain proteins inside and outside brain cells make it hard for brain cells to stay healthy and to communicate with each other. The brain region called the hippocampus is the center of learning and memory in the brain, and the brain cells in this region are often the first to be damaged. That's why memory loss is often one of the earliest symptoms of Alzheimer's. While most changes in the brain that cause dementia are permanent and worsen over time, thinking and memory problems caused by the following conditions may improve when the condition is treated or addressed: Depression Medication side effects Excess use of alcohol Thyroid problems Vitamin deficiencies
Dementia risk and prevention Some risk factors for dementia, such as age and genetics, cannot be changed. But researchers continue to explore the impact of other risk factors on brain health and prevention of dementia. Some of the most active areas of research in risk reduction and prevention include cardiovascular factors, physical fitness, and diet. Cardiovascular risk factors: Your brain is nourished by one of your body's richest networks of blood vessels. Anything that damages blood vessels anywhere in your body can damage blood vessels in your brain, depriving brain cells of vital food and oxygen. Blood vessel changes in the brain are linked to vascular dementia. They often are present along with changes caused by other types of dementia, including Alzheimer's disease and dementia with Lewy bodies. These changes may interact to cause faster decline or make impairments more severe. You can help protect your brain with some of the same strategies that protect your heart don't smoke; take steps to keep your blood pressure, cholesterol and blood sugar within recommended limits; and maintain a healthy weight. Physical exercise: Regular physical exercise may help lower the risk of some types of dementia. Evidence suggests exercise may directly benefit brain cells by increasing blood and oxygen flow to the brain. Diet: What you eat may have its greatest impact on brain health through its effect on heart health. The best current evidence suggests that heart-healthy eating patterns, such as the Mediterranean diet, also may help protect the brain. A Mediterranean diet includes relatively little red meat and emphasizes whole grains, fruits and vegetables, fish and shellfish, and nuts, olive oil and other healthy fats.
Types of Dementia
Dementia is a general term for loss of memory and other mental abilities severe enough to interfere with daily life. It is caused by physical changes in the brain.
Type of Dementia
Characteristics Alzheimer's disease Most common type of dementia; accounts for an estimated 60 to 80 percent of cases. Symptoms: Difficulty remembering names and recent events is often an early clinical symptom; apathy and depression are also often early symptoms. Later symptoms include impaired judgment, disorientation, confusion, behavior changes and difficulty speaking, swallowing and walking. New criteria and guidelines for diagnosing Alzheimer's were published in 2011 recommending that Alzheimer's disease be considered a disease with three stages, beginning well before the development of symptoms. Brain changes: Hallmark abnormalities are deposits of the protein fragment beta-amyloid (plaques) and twisted strands of the protein tau (tangles) as well as evidence of nerve cell damage and death in the brain. Learn more about Alzheimer's disease. Vascular dementia Previously known as multi-infarct or post-stroke dementia, vascular dementia is the second most common cause of dementia after Alzheimer's disease. Symptoms: Impaired judgment or ability to plan steps needed to complete a task is more likely to be the initial symptom, as opposed to the memory loss often associated with the initial symptoms of Alzheimer's. Occurs because of brain injuries such as microscopic bleeding and blood vessel blockage. The location of the brain injury determines how the individual's thinking and physical functioning are affected. Brain changes: Brain imaging can often detect blood vessel problems implicated in vascular dementia. In the past, evidence for vascular dementia was used to exclude a diagnosis of Alzheimer's disease (and vice versa). That practice is no longer considered consistent with pathologic evidence, which shows that the brain changes of several types of dementia can be present simultaneously. When any two or more types of dementia are present at the same time, the individual is considered to have "mixed dementia" (see entry below). Learn more about vascular dementia. Dementia with Lewy bodies (DLB) Symptoms: People with dementia with Lewy bodies often have memory loss and thinking problems common in Alzheimer's, but are more likely than people with Alzheimer's to have initial or early symptoms such as sleep disturbances, well-formed visual hallucinations, and muscle rigidity or other parkinsonian movement features. Brain changes: Lewy bodies are abnormal aggregations (or clumps) of the protein alpha-synuclein. When they develop in a part of the brain called the cortex, dementia can result. Alpha- synuclein also aggregates in the brains of people with Parkinson's disease, but the aggregates may appear in a pattern that is different from dementia with Lewy bodies. The brain changes of dementia with Lewy bodies alone can cause dementia, or they can be present at the same time as the brain changes of Alzheimer's disease and/or vascular dementia, with each abnormality contributing to the development of dementia. When this happens, the individual is said to have "mixed dementia." Learn more about dementia with Lewy bodies. Mixed dementia In mixed dementia abnormalities linked to more than one type of dementia occur simultaneously in the brain. Recent studies suggest that mixed dementia is more common than previously thought. Brain changes: Characterized by the hallmark abnormalities of more than one type of dementia most commonly, Alzheimer's and vascular dementia, but also other types, such as dementia with Lewy bodies. Learn more about mixed dementia. Parkinson's disease As Parkinson's disease progresses, it often results in a progressive dementia similar to dementia with Lewy bodies or Alzheimer's. Symptoms: Problems with movement are a common symptom early in the disease. If dementia develops, symptoms are often similar to dementia with Lewy bodies. Brain changes: Alpha-synuclein clumps are likely to begin in an area deep in the brain called the substantia nigra. These clumps are thought to cause degeneration of the nerve cells that produce dopamine. Learn more about Parkinson's disease. Frontotemporal dementia Includes dementias such as behavioral variant FTD (bvFTD), primary progressive aphasia, Pick's disease and progressive supranuclear palsy. Symptoms: Typical symptoms include changes in personality and behavior and difficulty with language. Nerve cells in the front and side regions of the brain are especially affected. Brain changes: No distinguishing microscopic abnormality is linked to all cases. People with FTD generally develop symptoms at a younger age (at about age 60) and survive for fewer years than those with Alzheimer's. Learn more about frontotemporal dementia. Creutzfeldt-Jakob disease CJD is the most common human form of a group of rare, fatal brain disorders affecting people and certain other mammals. Variant CJD (mad cow disease) occurs in cattle, and has been transmitted to people under certain circumstances. Symptoms: Rapidly fatal disorder that impairs memory and coordination and causes behavior changes. Brain changes: Results from misfolded prion protein that causes a "domino effect" in which prion protein throughout the brain misfolds and thus malfunctions. Learn more about Creutzfeldt-Jakob disease. Normal pressure hydrocephalus Symptoms: Symptoms include difficulty walking, memory loss and inability to control urination. Brain changes: Caused by the buildup of fluid in the brain. Can sometimes be corrected with surgical installation of a shunt in the brain to drain excess fluid. Learn more about normal pressure hydrocephalus. Huntington's Disease Huntingtons disease is a progressive brain disorder caused by a single defective gene on chromosome 4. Symptoms: Include abnormal involuntary movements, a severe decline in thinking and reasoning skills, and irritability, depression and other mood changes. Brain changes: The gene defect causes abnormalities in a brain protein that, over time, lead to worsening symptoms. Learn more about Huntingtons disease. Wernicke- Korsakoff Syndrome Korsakoff syndrome is a chronic memory disorder caused by severe deficiency of thiamine (vitamin B-1). The most common cause is alcohol misuse. Symptoms: Memory problems may be strikingly severe while other thinking and social skills seem relatively unaffected. Brain changes: Thiamine helps brain cells produce energy from sugar. When thiamine levels fall too low, brain cells cannot generate enough energy to function properly. Learn more about Wernicke-Korsakoff syndrome.
Dementia treatment and care
"I thought my life was over. I knew about dementia but I never thought it could happen to me." This sentiment reflects the denial, disbelief, and dismay common after a dementia diagnosis. While dealing with dementia is a challenge, the following strategies can ease your journey: Take care of yourself emotionally. As you deal with the symptoms of dementia, make sure you get the emotional support you need. Turn to close family members and friends, join a dementia support group, or talk to a therapist, counselor, or clergyman. Make important decisions early. Avoid future medical, financial, and legal confusion by communicating your wishes and creating a plan. Designate a Power of Attorney for money and legal matters. Discuss and document treatment and end-of-life preferences with your doctors and family members. Create a Living Will and appoint someone you trust to make decisions for you in case you can no longer make them for yourself. Although these conversations may be difficult, making your wishes known is empowering. Watch for treatable changes. Depression, sleep disturbances, and medication interactions can make the symptoms of dementia worse and limit independence. Treating them may require some experimentation with lifestyle changes and medication, but can be well worth the effort. Create a dementia-friendly environment. Think happiness, independence, safety, and accessibility. Preserve your health and autonomy for as long as possible by taking simple actions: encourage memories with pictures and familiar objects; remove tripping hazards; increase lighting; and organize a caregiving network. Planning and flexibility can keep you one step ahead of changing needs. Emphasize joy. When you sense the mind is half-gone, try to see it as half-present. With appropriate support and understanding, people with dementia are capable of experiencing and providing enjoyment and connection - even through the final stages of the disease.
Demensia Alzheimer
Definition Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, or neurons, resulting in loss of memory, thinking and language skills, and behavioral changes. These neurons, which produce the brain chemical, or neurotransmitter, acetylcholine, break connections with other nerve cells and ultimately die. For example, short-term memory fails when Alzheimer's disease first destroys nerve cells in the hippocampus, and language skills and judgment decline when neurons die in the cerebral cortex. Two types of abnormal lesions clog the brains of individuals with Alzheimer's disease: Beta-amyloid plaquessticky clumps of protein fragments and cellular material that form outside and around neurons; and neurofibrillary tanglesinsoluble twisted fibers composed largely of the protein tau that build up inside nerve cells. Although these structures are hallmarks of the disease, scientists are unclear whether they cause it or a byproduct of it. Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older. Alzheimer's disease is not a normal part of aging. Origin of the term Alzheimer's disease dates back to 1906 when Dr. Alois Alzheimer, a German physician, presented a case history before a medical meeting of a 51-year-old woman who suffered from a rare brain disorder. A brain autopsy identified the plaques and tangles that today characterize Alzheimer's disease.
What is Alzheimer's disease?
Alzheimer's disease (AD) is a slowly progressive disease of the brain that is characterized by impairment of memory and eventually by disturbances in reasoning, planning, language, and perception. Many scientists believe that Alzheimer's disease results from an increase in the production or accumulation of a specific protein (beta-amyloid protein) in the brain that leads to nerve cell death. The likelihood of having Alzheimer's disease increases substantially after the age of 70 and may affect around 50% of persons over the age of 85. Nonetheless, Alzheimer's disease is not a normal part of aging and is not something that inevitably happens in later life. For example, many people live to over 100 years of age and never develop Alzheimer's disease. Cause of Alzheimer
The cause(s) of Alzheimer's disease is (are) not known. The "amyloid cascade hypothesis" is the most widely discussed and researched hypothesis about the cause of Alzheimer's disease. The strongest data supporting the amyloid cascade hypothesis comes from the study of early-onset inherited (genetic) Alzheimer's disease. Mutations associated with Alzheimer's disease have been found in about half of the patients with early-onset disease. In all of these patients, the mutation leads to excess production in the brain of a specific form of a small protein fragment called ABeta (A). Many scientists believe that in the majority of sporadic (for example, non-inherited) cases of Alzheimer's disease (these make up the vast majority of all cases of Alzheimer's disease) there is too little removal of this A protein rather than too much production. In any case, much of the research in finding ways to prevent or slow down Alzheimer's disease has focused on ways to decrease the amount of A in the brain Risk factor
Who develops Alzheimer's disease? The main risk factor for Alzheimer's disease is increased age. As a population ages, the frequency of Alzheimer's disease continues to increase. Ten percent of people over 65 years of age and 50% of those over 85 years of age have Alzheimer's disease. Unless new treatments are developed to decrease the likelihood of developing Alzheimer's disease, the number of individuals with Alzheimer's disease in the United States is expected to be 14 million by the year 2050. There are also genetic risk factors for Alzheimer's disease. Most patients develop Alzheimer's disease after age 70. However, 2%-5% of patients develop the disease in the fourth or fifth decade of life (40s or 50s). At least half of these early onset patients have inherited gene mutations associated with their Alzheimer's disease. Moreover, the children of a patient with early onset Alzheimer's disease who has one of these gene mutations has a 50% risk of developing Alzheimer's disease. There is also a genetic risk for late onset cases. A relatively common form of a gene located on chromosome 19 is associated with late onset Alzheimer's disease. In the majority of Alzheimer's disease cases, however, no specific genetic risks have yet been identified. Other risk factors for Alzheimer's disease include high blood pressure (hypertension),coronary artery disease, diabetes, and possibly elevated blood cholesterol. Individuals who have completed less than eight years of education also have an increased risk for Alzheimer's disease. These factors increase the risk of Alzheimer's disease, but by no means do they mean that Alzheimer's disease is inevitable in persons with these factors. All patients with Down syndrome will develop the brain changes of Alzheimer's disease by 40 years of age. This fact was also a clue to the "amyloid hypothesis of Alzheimer's disease" Symptoms of Alzheimer's
The onset of Alzheimer's disease is usually gradual, and it is slowly progressive. Memory problems that family members initially dismiss as "a normal part of aging" are in retrospect noted by the family to be the first stages of Alzheimer's disease. When memory and other problems with thinking start to consistently affect the usual level of functioning; families begin to suspect that something more than "normal aging" is going on. Problems of memory, particularly for recent events (short-term memory) are common early in the course of Alzheimer's disease. For example, the individual may, on repeated occasions, forget to turn off an iron or fail to recall which of the morning's medicines were taken. Mild personality changes, such as less spontaneity, apathy, and a tendency to withdraw from social interactions, may occur early in the illness. As the disease progresses, problems in abstract thinking and in other intellectual functions develop. The person may begin to have trouble with figures when working on bills, with understanding what is being read, or with organizing the day's work. Further disturbances in behavior and appearance may also be seen at this point, such as agitation, irritability, quarrelsomeness, and a diminishing ability to dress appropriately. Later in the course of the disorder, affected individuals may become confused or disoriented about what month or year it is, be unable to describe accurately where they live, or be unable to name a place being visited. Eventually, patients may wander, be unable to engage in conversation, erratic in mood, uncooperative, and lose bladder and bowel control. In late stages of the disease, persons may become totally incapable of caring for themselves. Death can then follow, perhaps from pneumonia or some other problem that occurs in severely deteriorated states of health. Those who develop the disorder later in life more often die from other illnesses (such as heart disease) rather than as a consequence of Alzheimer's disease. Ten warning signs of Alzheimer's disease The Alzheimer's Association has developed the following list of warning signs that include common symptoms of Alzheimer's disease. Individuals who exhibit several of these symptoms should see a physician for a complete evaluation. 1. Memory loss 2. Difficulty performing familiar tasks 3. Problems with language 4. Disorientation to time and place 5. Poor or decreased judgment 6. Problems with abstract thinking 7. Misplacing things 8. Changes in mood or behavior 9. Changes in personality 10. Loss of initiative It is normal for certain kinds of memory, such as the ability to remember lists of words, to decline with normal aging. In fact, normal individuals 50 years of age will recall only about 60% as many items on some kinds of memory tests as individuals 20 years of age. Furthermore, everyone forgets, and every 20 year old is well aware of multiple times he or she couldn't think of an answer on a test that he or she once knew. Almost no 20 year old worries when he/she forgets something, that he/she has the 'early stages of Alzheimer's disease,' whereas an individual 50 or 60 years of age with a few memory lapses may worry that they have the 'early stages of Alzheimer's disease.' Mild cognitive impairment The criteria for dementia are conservative meaning that a patient must have had considerable decline in the ability to think before a diagnosis of dementia is appropriate. The progression of Alzheimer's disease is so insidious and slow that patients go through a period of decline where their memory is clearly worse than its baseline, yet they still do not meet criteria for dementia. This transitional syndrome is called Mild Cognitive Impairment (MCI). Individuals affected with MCI have cognitive impairment that is demonstrated on formal neuropsychological testing but are still able to function well. Formal neuropsychological testing usually means that the patient is administered a battery of standardized tests of memory and thinking. Some of these tests are something like the IQ tests we may have taken in school. When these tests were developed they were administered to hundreds or thousands of people so that statistics are available to say how a person's score compares to a sample of healthy persons of the same age. If a person scores in the top 50%, it means that he or she did better than at least 50% of other normal people who took the test. Persons with lower scores - often in the bottom 7% - are considered to have MCI. There are several forms of MCI. Perhaps the most common is associated with impairment in memory but not in the ability to plan and reason. Persons with this type called "amnestic MCI" (amnestic comes from "amnesia" and means no memory) have a high risk of developing Alzheimer's disease over the next few years. Persons with preserved memory but impaired reasoning or impaired judgment (call non-amnestic MCI) have a lower risk of developing Alzheimer's disease. As treatments are developed that decrease the risk of developing Alzheimer's disease or slow its rate of progression (as of June 2007, no such medication has been approved by the FDA), recognition of amnestic MCI will be increasingly important. It is hoped that medications will be developed that will slow the rate of progression of MCI to Alzheimer's disease or completely prevent the development of Alzheimer's disease. The most common early symptom of Alzheimer's is difficulty remembering newly learned information. Just like the rest of our bodies, our brains change as we age . Most of us eventually notice some slowed thinking and occasional problems with remembering certain things. However, serious memory loss, confusion and other major changes in the way our minds work may be a sign that brain cells are failing. The most common early symptom of Alzheimer's is difficulty remembering newly learned information because Alzheimer's changes typically begin in the part of the brain that affects learning. As Alzheimer's advances through the brain it leads to increasingly severe symptoms, including disorientation, mood and behavior changes; deepening confusion about events, time and place; unfounded suspicions about family, friends and professional caregivers; more serious memory loss and behavior changes; and difficulty speaking, swallowing and walking. People with memory loss or other possible signs of Alzheimers may find it hard to recognize they have a problem. Signs of dementia may be more obvious to family members or friends. Anyone experiencing dementia-like symptoms should see a doctor as soon as possible. If you need assistance finding a doctor with experience evaluating memory problems, your local Alzheimer's Association chapter can help. Early diagnosis and intervention methods are improving dramatically, and treatment options and sources of support can improve quality of life. Two helpful support resources you can tap into are ALZConnected, our messages boards and online social networking community, andAlzheimer's Navigator, a web tool that creates customized action plans, based on answers you provide through short, online surveys. Alzheimer's and the brain Microscopic changes in the brain begin long before the first signs of memory loss. The brain has 100 billion nerve cells (neurons). Each nerve cell connects with many others to form communication networks. Groups of nerve cells have special jobs. Some are involved in thinking, learning and remembering. Others help us see, hear and smell. To do their work, brain cells operate like tiny factories. They receive supplies, generate energy, construct equipment and get rid of waste. Cells also process and store information and communicate with other cells. Keeping everything running requires coordination as well as large amounts of fuel and oxygen. Scientists believe Alzheimer's disease prevents parts of a cell's factory from running well. They are not sure where the trouble starts. But just like a real factory, backups and breakdowns in one system cause problems in other areas. As damage spreads, cells lose their ability to do their jobs and, eventually die, causing irreversible changes in the brain. The role of plaques and tangles
Plaques and tangles tend to spread through the cortex as Alzheimer's progresses.
Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques are deposits of a protein fragment called beta-amyloid (BAY-tuh AM-uh-loyd) that build up in the spaces between nerve cells. Tangles are twisted fibers of another protein called tau (rhymes with wow) that build up inside cells. Though most people develop some plaques and tangles as they age, those with Alzheimer's tend to develop far more. They also tend to develop them in a predictable pattern, beginning in areas important for memory before spreading to other regions. Scientists do not know exactly what role plaques and tangles play in Alzheimer's disease. Most experts believe they somehow play a critical role in blocking communication among nerve cells and disrupting processes that cells need to survive. It's the destruction and death of nerve cells that causes memory failure, personality changes, problems carrying out daily activities and other symptoms of Alzheimer's disease. Treatment
Dementia is a condition of mental decline that causes progressive memory impairment and problems with learning, judgment, communication, and quality of life. Alzheimers disease, a progressive brain disorder, is the most common form of dementia. While there is no cure for Alzheimer's disease and no treatment to reverse or halt its progression, there are medicines available that can help treat symptoms in some people with Alzheimer's disease. If Alzheimers disease is diagnosed earlier, treatment may enable people to carry out their daily activities and independent living for a longer period of time and may prolong the time that patients can be managed at home. Health care providers may also use other medicines to help manage other troubling symptoms of Alzheimer's disease, including depression, sleeplessness, and behavioral problems such as agitation and aggression. Planning and medical/social management can help ease the burden on both patients and family members. Exercise, good nutrition, activities, and social interaction are important. A calm, structured environment also may help the person with Alzheimer's disease to continue functioning as independently as possible. Recommended Related to Alzheimer's Olympia Dukakis: Health Activist You're a health activist. What sparked your interest? My mother suffered from Alzheimer's. And I was diagnosed with osteoporosis in the early 1990s. It's a message to all women that ... it's not an infirmity you have to endure. Something can be done. Did caring for your mother inspire you to do your new film, Away From Her? As insightful as the movie is about Alzheimer's, it's about the love that a man is capable of -- what a husband is able to do in terms of making sure that his... Read the Olympia Dukakis: Health Activist article > > How Is Alzheimer's Disease Treated? Your doctor will determine the best treatment for the Alzheimers patient based on various factors, including: The patients age, overall health, and medical history Extent of the disease The patients tolerance for specific medicines and therapies Expectations for the course of the disease The patient and his or her caregivers opinions or preferences What Drugs Are Used to Treat Alzheimer's Disease? Cholinesterase inhibitors (Aricept, Cognex, Exelon, Razadyne).Cholinesterase inhibitors curb the breakdown of acetylcholine, a chemical in the brain important for memory and learning. These types of medications help increase the levels of acetylcholine in the brain. These drugs may slow the progression of symptoms for about half of people taking them for a limited time, on average 6 to 12 months. Aricept is the only treatment approved by the FDA for all stages of Alzheimers disease: mild, moderate, and severe. It is available as tablets to swallow or tablets to dissolve in the mouth. Cognex was the first of these drugs to be FDA approved, but it is used less commonly than the other medications. Exelon is approved for use in mild to moderate Alzheimers dementia and is available as a skin patch, capsules, and liquid form. Razadyne (formerly Reminyl) is also approved for mild to moderate Alzheimers dementia and is available as an extended-release capsule, immediate-release tablet, and liquid forms. Common side effects are usually mild for these medications and include diarrhea, vomiting, nausea, fatigue, insomnia, loss of appetite, and weight loss. Cognex use may cause liver damage, so your doctor will need to perform tests to monitor liver function. Namenda. Namenda is approved to treat moderate-to-severe Alzheimer's disease. Namenda works by a different mechanism than other Alzheimer's treatments; it is thought to play a protective role in the brain by regulating the activity of a different brain chemical called glutamate. Glutamate also plays a role in learning and memory. Brain cells in people with Alzheimers disease release too much glutamate. Namenda helps regulate glutamate activity. Namenda is the only drug for Alzheimers that works this way. It may improve mental function and performance of daily activities for some people. Namenda may have increased benefit when used with Aricept, Exelon, Razadyne, or Cognex. Side effects of Namenda include tiredness, dizziness, confusion, constipation, and headache.
Demensia Vaskuler
Definition Vascular dementia is the second most common form of dementia, accounting for up to 40 percent of dementia cases in older adults. Vascular dementia is caused by reduced blood flow to the brainusually from a stroke or series of strokes. While the strokes may be unnoticeably small, the damage can add up over time, leading to memory loss, confusion, and other signs of dementia. With these guidelines, however, it may be possible to prevent further blockages and compensate for brain damage that has already occurred. What is vascular dementia? Vascular dementia refers to a subtle, progressive decline in memory and cognitive functioning. It occurs when the blood supply carrying oxygen and nutrients to the brain is interrupted by a blocked or diseased vascular system. If blood supply is blocked for longer than a few seconds, brain cells can die, causing damage to the cortex of the brainthe area associated with learning, memory, and language. Depending on the person, and the severity of the stroke or strokes, vascular dementia may come on gradually or suddenly. Currently, there is no known cure, but the good news is that making certain lifestyle changes and using practical strategies may help prevent strokes, compensate for cognitive loses, and slow its development.
Causes of vascular dementia Stroke, small vessel disease, or a mixture of the two can cause vascular dementia. Most commonly there is a blockage of small blood vessels somewhere in the vast system of arteries that feeds the brain and enters through the base of the skull. Blockages may be caused by plaque build-up on the inside of the artery wall, or by blood clots which have broken loose and clogged a tributary further downstream. Clots can form as a result of abnormal heart rhythms, or other heart abnormalities. Also, a weak patch on an artery wall can balloon outward and form an aneurysm, which can burst and deprive the brain cells of oxygen. It is estimated that about 50 percent of the cases of vascular dementia result from hypertension, or high blood pressure. Less common causes of vascular dementia are associated with autoimmune inflammatory diseases of the arteries such as lupus and temporal arteritis, which are treatable with drugs that suppress the immune system.
Sign and symptoms Vascular dementia affects different people in different ways and the speed of the progression varies from person to person. Some symptoms may be similar to those of other types of dementia and usually reflect increasing difficulty to perform everyday activities like eating, dressing, or shopping. Behavioral and physical symptoms can come on dramatically or very gradually, although it appears that a prolonged period of TIAsthe mini-strokes discussed aboveleads to a gradual decline in memory, whereas a bigger stroke can produce profound symptoms immediately. Regardless of the rate of appearance, vascular dementia typically progresses in a stepwise fashion, where lapses in memory and reasoning abilities are followed by periods of stability, only to give way to further decline. Common mental and emotional signs and symptoms of vascular dementia Slowed thinking Memory problems; general forgetfulness Unusual mood changes (e.g. depression, irritability) Hallucinations and delusions Confusion, which may get worse at night Personality changes and loss of social skills
Common physical signs and symptoms of vascular dementia Dizziness Leg or arm weakness Tremors Moving with rapid, shuffling steps Balance problems Loss of bladder or bowel control
Common behavioral signs and symptoms of vascular dementia Slurred speech Language problems, such as difficulty finding the right words for things Getting lost in familiar surroundings Laughing or crying inappropriately Difficulty planning, organizing, or following instructions Difficulty doing things that used to come easily (e.g. paying bills or playing a favorite card game) Reduced ability to function in daily life
Diagnosis Because vascular cognitive impairment may often go unrecognized, many experts recommend professional screening with brief tests to assess memory, thinking and reasoning for everyone considered to be at high risk for this disorder. Individuals at highest risk include those who have had a stroke or a transient ischemic attack (TIA, also known as a "ministroke"). Additional high- risk groups include those with high blood pressure, high cholesterol, or other risk factors for heart or blood vessel disease. Professional screening for depression is also recommended for high-risk groups. Depression commonly coexists with brain vascular disease and can contribute to cognitive symptoms. If brief screening tests suggest changes in thinking or reasoning, a more detailed assessment is needed. Core elements of a workup for vascular dementia typically include: A thorough medical history, including family history of dementia Evaluation of independent function and daily activities Input from a family member or trusted friend In-office neurological examination assessing function of nerves and reflexes, movement, coordination, balance and senses Laboratory tests including blood tests and brain imaging According to a 2011 scientific statement issued by the American Heart Association (AHA) and the American Stroke Association (ASA), and endorsed by the Alzheimer's Association and the American Academy of Neurology (AAN), the following three criteria suggest the greatest likelihood that mild cognitive impairment (MCI) or dementia is caused by vascular changes: 1. The diagnosis of dementia or mild cognitive impairment is confirmed by neurocognitive testing, which involves several hours of written or computerized tests that provide detailed evaluation of specific thinking skills such as judgment, planning, problem- solving, reasoning and memory 2. There is brain imaging evidence, usually with magnetic resonance imaging (MRI), showing evidence of either: a. A recent stroke, or b. Other brain blood vessel changes whose severity and pattern of affected tissue are consistent with the types of impairment documented in neurocognitive testing 3. There is no evidence that factors other than vascular changes are contributing to cognitive decline. The guidelines also discuss cases where the diagnosis may be less clear-cut, such as the common situation where vascular changes coexist with brain changes associated with other types of dementia. Vascular dementia prevention and treatment There is not yet a known cure for vascular dementia, so prevention is important. The best way to prevent vascular dementia is to lower your risk of stroke. This means getting high blood pressure under control, avoiding cigarettes, and controlling cholesterol levels and diabetes. But even if you or a loved one have already been diagnosed with vascular dementia, its not too late to do anything about it. If you treat the risk factors that led to vascular dementia, you may be able to slow the progression of the disease and possibly reverse some of the symptoms. The most important thing is minimize your risk of having another stroke and making the dementia worse. While there are not yet any approved medications for the treatment of vascular dementia, a number of medications used to treat the cognitive symptoms of Alzheimers disease appear to work for vascular dementia, too. Prevent and treat vascular dementia by reducing your risk for stroke Know your blood pressure. If high, work with your doctor to lower it. Find out from your doctor if you have atrial fibrillation. If you smoke, stop. If you drink alcohol, do so in moderation. Find out if you have high cholesterol. If so, work with your doctor to control it. If you are diabetic, follow your doctor's recommendations carefully to control your diabetes. Include exercise in the activities you enjoy in your daily routine. Enjoy a lower sodium (salt), lower fat diet.
Medical Care
The mainstay of management of vascular dementia is the prevention of new strokes. This includes administering antiplatelet drugs and controlling major vascular risk factors. Aspirin has also been found to slow the progression of vascular dementia. Recent guidelines from the American Psychiatric Association provide both treatment principles and possible specific therapies. Drug treatment is primarily used to prevent further worsening of vascular dementia by treating the underlying disease such as hypertension, hyperlipidemia, and diabetes mellitus. Antiplatelet agents are indicated. Pentoxifylline and, to a more limited extent, ergoloid mesylates (Hydergine), may be useful for increasing cerebral blood flow. In the European Pentoxifylline Multi-Infarct Dementia Study, which is a double-blinded, placebo-controlled, multicenter study, treatment with pentoxifylline was found to be beneficial for patients with multi-infarct dementia. Significant improvement was observed in the scales used for assessing intellectual and cognitive function. Neuroprotective drugs such as nimodipine, propentofylline, and posatirelin are currently under study and may be useful for vascular dementia. Nicardipine is a dihydropyridine calcium channel blocker that was studied on the treatment of cognitive deterioration of vascular origin. Preliminary studies showed decrease in cognitive deterioration in patients with cerebrovascular disease. [21]
Increasing evidence supports the involvement of the cholinergic system in vascular dementia, similar to that seen in Alzheimer dementia. However, no cholinesterase inhibitors have been approved to date for the treatment of vascular dementia, despite positive results in clinical trials with this medication. The general management of dementia includes appropriate referral to community services, judgment and decision-making regarding legal and ethical issues (eg, driving, competency, advance directives), and consideration of caregiver stress. Agitation and psychosis are common in older adults with dementia and are challenging to manage. Relatively few studies have examined the use of antidepressants for the treatment of agitation and psychosis in dementia; however, the selective serotonin reuptake inhibitors (SSRIs) sertraline and citalopram appear to be associated with a reduction in symptoms of agitation when compared with placebo. [22] Both appear to be reasonably well tolerated when compared with placebo, typical antipsychotics, and atypical antipsychotics. However, more studies are needed to determine if SSRIs, trazodone, or other antidepressants are safe and effective treatments for agitation and psychosis in dementia. http://emedicine.medscape.com/article/292105-treatment