THE NEUROLOGICAL EXAM:

1) get proper history (acute vs slow onset; acute always imply vascular, slow can be mass
lesion, demyelination)

2) Do cognitive score, but remember it says nothing about insight and judgement. Ask if
someone is forgetful, can they still calculate, do they struggle to read, do they get lost? 3) Ask separately about all the cranial nerves 4) Ask about mood and sleep 5) Ask about power Myasthenia gets worse with exertion (fatigability) Lower limb: can you get up out of chair? Walk up the stairs? Upper limb: can you brush your hair and your teeth? Open taps or bottles? Do you drop things? On examination the most important thing with motor is to decide UMN or LMN (with UMN no wasting, brisk reflexes, Babinski en Hoffmans, spasticity, no fasciculation, muscles affected in groups, ie flexor group)

6) Ask about sensation: increased or loss of sensation? Increase in sensation includes

paresthesias, hyperesthesia, hyperalgesia (Increased or heightened sensitivity to pain) and allodynia (feeling of pain with non-painful stimuli). Only places where dermatomes are of importance are with radiculopathy and myelopathy If sensory doesnt fit, discard too subjective

7) Ask about neuro problems with intermittent signs such as headache, epilepsy, TIA, MS,
episodic ataxia, episodic paralysis. 8) Ask about autonomic problems such as bowel and bladder incontinence, frequency, urgency, nocturia Ask about cerebellar are you ever clumsy, dizzy, suffer from vertigo? VANISH DDT Vertigo (hallucination of movement) Ataxia: broad based gait, reeling, heel-toe walk (tandem) clumsy Nystagmus: horizontal nystagmus, and gaze evoked will not see in primary position; pt may also have broken saccades (non-smooth eyemovements), saccadic intrusion Intention tremor (draw circle on hand, pick up a pen) Speech: staccato and monotone, may have bursts of irregular speech (cerebellar dysarthria) Hypotonia and rebound: push down arms will jerk up, oscillation, (hypotonia and reflexes with lag) Dysdiadokineses: remember patient must not brace arm elbow must be away from body Dysmetria: toe to finger, nose to finger will have past-pointing, also ocular dysmetria eyes overshoot when looking at something (remember to lift shoulders and elbows pt must not brace his arm)

Page 1 of 61

Titubation: (vermis pathology) Before you comment on cerebellar signs, think about weakness, spasticity or rigidity it can all look like cerebellar problems Causes of cerebellar problems: alcohol, drugs, infections such as VZV (gives diffuse inflammation, called cerebellitis), space occupying lesions (hemi-ataxia), paraneoplastic syndromes, stroke in posterior circulation, MS. spino-cerebellar ataxia Cerebellum and CN VIII very sensitive to hypoxic or toxic damage perinatal hypoxia and childhood infections with meningo-encephalitis often give deafness and cerebellar signs as sequelae Friedrichs ataxia gives a combination of posterior column fallout due to cord atrophy and well as cerebellar signs due to cerebellar atrophy. GAIT: Aided or not? Look at feet, are they wide-based or not? Do they lift or drag? Arm movement Are the knees bent or straight? Straight line? How does he turn? Waddle weak girdle muscles myopathy Scissor (spasticity) UMN Toe walking (S1), on heels (L5) When you present: 1. Cognition do cognitive score

2. Cranial nerves: if not involved at all the problem is not in the brain. II, V, VII
does not have bilateral supply look especially for defects with them if you have a stroke patient. If checkerboard means brainstem look especially for logical defects in CN (III alone, VI with VII, IX with X)

3. Motor system: this is combination of power, tone and reflexes, present them
as one. a) Start with power in UL and LL, say what patient is able to do: the patient is not able to sit up, to walk; dont mention power individually say the power in the UL is overall 2/5 and the LL 3/5 (arm more affected MCA), or the UL is overall 3/5 and the LL is 1/5 (leg more affected ACA). Mention whether the power is equal proximally and distally, or worse distally (neuropathy) or worse proximally

Page 2 of 61

(myopathy) look for Beevor sign in non-ambulant patient pt must try to sit up in bed, if the umbilicus goes up the lesion is at T10 if no Beevor sign the lesion must be above T8) Quick check for power: UL proximal, lift arms above head, distal grip fingers; LL proximal squat, distal walk on heels and toes b) Tone: UL and LL: Low tone usually implies LMN, or UMN in the acute phase before spasticity sets in; with low tone due to LMN youll get long history, not acute, recent onset. Increased tone is either spasticity, or rigidity, or paratonia Spasticity implies UMN lesion a cortico-spinal problem where you get claspknife phenomena with a catch and release sign. This is velocity dependant wont elicit it is you move too slowly. Start slowly and increase your speed. It will be more noticeable in the flexors of the UL and extensors of the lower limbs (this is natures way of keeping you upright when tone has to compensate for weakness, the arm is flexed and adducted close to body, and the leg is extended with knee locked to be able to stand increase tone can keep someone walking dont decrease tone too much with Baclofen) Test for tone in the biceps, pronator and supinator, flex and extension of wrist (and rotation of wrist for rigidity) Spasticity is a hard UMN sign if you pick it up in a dementia patient you know there is diffuse degeneration (such as in multi-infarct dementia and multi-system atrophy, not in AD) Rigidity: implies increased tone of extra-pyramidal origin, it is not velocity dependant, and involves the flexors and extensors equally. You get lead-pipe rigidity where there is increased tone throughout the range of movement, and cogwheel rigidity that youll feel on wrist rotation this is a combination of rigidity and a tremor. If you say rigidity you imply parkinsons with bradikinesia en tremor

If rigidity is the main problem the patient will c/o falling (usually backwards due to axial rigidity) think of PD. With parkinsons plus youll often get minimal tremor and cogwheel rigidity. A patient with cognitive decline whose complaint is falling think of MSA

Page 3 of 61

Paratonia: most dementia patients will have this. It feels as if the patient is resisting youre movement although the patient may appear relaxed and co-operative. There will also be other signs of cognitive decline. Even NPH can get paratonia eventually. In general, SAY something and then discount it, such as this myelopathy could be due to Vit B12 deficiency, but the intact dorsal columns are against this. Remember, if the face is not involved the lesion cannot be cortical If all four limbs are weak, but NO FACE involvement, the lesion must be not higher than medulla Beevor's sign is the movement of the navel towards the head on flexing the neck. It is caused by weakness of the lower abdominal muscles, and is characteristic of spinal cord injury between T6 and T10 levels. The upper abdominal rectus abdominus muscle are intact at the top of the abdomen but weak at the lower portion. Thus when the patient is asked to do a sit up only the upper muscles contract pulling the umbilicus toward the head. So if Beevor sign is positive localise lesion at T10, if it is negative the lesion can be anything between T8 and T1 the next place where you can localise is at the hand (C8, T1) Sensation is about 2 things: 1) quality (sharp vs blunt) and 2) intensity (how strong do you feel it) Reflexes: see end of notes dr Kakaza tutorial; Babinski under foot; Shadock next to foot; Oppenheim stroke down tibia; Bing tick on nailbed of big toe; (remember triceps and crossed adductors) End off with cerebellar signs and mention if there are EPS. DERMATOMES: This is the area of skin supplied by a single spinal root C2 post half of skull C3 poloneck C4 level of T-shirt C6 thumb, C7 middle finger, C8 pinky T4 nipples

Page 4 of 61

T10 umbilicus T12 pubic bone L1 inguinal ligament L3 to the knee L4 to the floor L5 top of foot S 1 bottom and side of foot S2-4 - perineum MYOTOMES AND REFLEXES Shoulder deltoid - abduction C5 Latissimus dorsi adduction C6,7 Elbow - Biceps flexion C5, 6 (and biceps and brachioradialis reflex therefor also C5, 6) Triceps extension C6, 7 Pro-and supinations also C 6,7 Wrist extension C6, 7 Flexion C6, 7, 8, T1 Fingers extension - C6, 7 Fingers flexions, abduction or adduction C8, T1 Hip: flexion L1, 2, adduction L2, 3 Hip abduction L4, 5, extension L5, 6 Knee extension: L 3, 4 (knee reflex (L3) Knee flexion: L5, S1 (also ankle eversion)

Page 5 of 61

Ankle dorsiflexion and inversion L4, 5 Plantar flexion S1, 2 Ankle Reflex S1 NEUROLOGY SYSTEMS: Neurology is a system consisting of muscle, NM junction, nerve, spinal cord, brain stem, brain. First ask yourself which system is involved? 1) Muscle: Myopathy and myasitis (dermatomyositis, polymyasitis, inclusion body myositis) The patient will complain of proximal weakness (difficulty climbing stairs, getting up out of chair, brushing hair) There will be no sensory complaints. Reflexes will be normal until late (if muscle is severely wasted may decrease reflexes) The onset of myopathy is usually subacute (2-3 weeks), it is proximal, symmetrical, with no bladder problems. If it is very severe the patient may have bulbar symptoms (such as difficulty swallowing) Myopathy: conduction studies normal, treat with prednisone 2) Neuromuscular junction (MG and Lambert Eaton) Always put MG on any differential diagnoses, otherwise youll miss it. The key-word here is FATIGABILITY. No sensory complaints Visual complaints are common especially ptosis or diplopia towards end of day At the end of the meal the patient may experience difficulty swallowing or chewing the start avoiding foods that needs lot of chewing rather mince than steak. The voice may also change at the end of the day, get a more nasal quality. 3) Peripheral nerve = neuropathy This is the first time that sensory complaints come in. The patient has distal weakness (long axons first to suffer and die (far from protective cell body) Distribution is glove and stocking Distal reflexes will be diminished Skin may be discoloured, thin, hairless

Page 6 of 61

There are two major types of neuropathy: a) demyelinating (GBS and CIDP) and b) axonal (diabetes, HIV, alcohol, trigliserides, Vit B12 deficiency, drugs (3TC, stavudine, INH reversed by pyridoxine) Normal EMG exludes many of the neuropathys but not all (small fibres not picked up) Causes of diminished ankle reflex (S1) usually peripheral neuropathy or old age 4) Radiculopathy: Will have weakness and absent reflexes in the myotomes, sensory problems will depend on where the root catches

5) Spinal cord myelopathy see dr Kakazas tutorial at the end

Sensory level Bilateral motor weakness Bladder and bowel involvement May have autonomic level (dry skin abnormal, feel with back of hand) Motor and sensory level will hardly ever be the same 6) Brain stem Checkerboard involvement is the key CN will be affected on the one side (side of pathology), body other side 7) Cortical: Hemi, face will be involved, all on one side 8) Basal ganglia: Will give extra-pyramidal symptoms With stroke there will always be spasticity (not initially) Clinical case: patient with subacute progressive weakness and urinary retention: on examination he had signs of 3-in-1 (myelopathy, radiculopathy, peripheral neuropathy) myeloradiculoneuropathy: Vit B 12 HIV Copper deficiency In the end the patient had CMV myeloradiculopathy with necrosis of the myelin of the cord and roots, with underlying HIV neuropathy treated with ganciclovir and ARVs (CMV causes encephalitis in patients with HIV with CD4 < 100) CAUDA EQUINA SYNDROME:

Page 7 of 61

Urinary complaints, severe pain, may be assymetrical Arachnoiditis may also present like this SYRINX: Always LMN signs

Page 8 of 61

EPILEPSY: A seizure is a paroxysm (an attack) of synchronised electrical discharges (with summation of discharges due to imbalance between excitation and inhibition) from the brain that cannot be predicted. It is usually random and unprovoked. These summated electrical discharges increase the metabolism of the neurons tremendously, and neurons can be permanently damaged by the demand made on them (glutamate cytotoxicity). Pathophysiology: processing of the impulse at the axon is dependent on the ion channels mutations in the Na channels cause epilepsy, may be mild (febrile convulsions) or severe that is why people with epilepsy have good and bad spells channels function about 6/12 before new ones are made the channels wont always be abnormal, when normal channels are formed the epilepsy reduce for a while Catamenial epilepsy: Increase in seizures in the week before menstruation When patient presents with first onset seizures do CT brain to exclude tumor, abscess, bleed, TBI, and do base line bloods and LP this will give answer in about 17% of cases Therapy is not always indicated after first seizure (only 1/3 will have another seizure), but treat if EEG is clearly abnormal (EEG: can predict the risk of recurrence of seizure) Patient should be advised to keep seizure calendar and to stop alcohol intake If you treat start with single agent, increase dose until seizures are under control or patient has symptoms of toxicity. Most patients control on monotherapy If it does not control start with other drug, and taper first one when second one has reached therapeutic concentrations. Third drug can be tried, either as mono-therapy or in combination. For partial and secondary generalised seizures Tegretol, Epilim and Lamotrigine can be used For primary generalised seizures Epilim and Lamotrigine are drugs of choice Lamotrigine can be given to women in childbearing years, but is less effective than Epilim Tegretol induces the metabolism of oral contraceptives must increase dose Epilim has no interaction with oral contraceptive but should be avoided during pregnancy. STATUS EPILEPTICUS: Status: Seizures > 30min, or recurrent seizures without waking up but in reality any convulsion that lasts longer than 2 minutes is considered to be impending status. Management of status:

Airway: Position patient on his side with a pillow under his head so that vomit or mucus will run out of mouth (risk of aspiration). Give O2 with mask (rebreath) and

Page 9 of 61

set O2 at 15 liters of flow (need high flow because you want O2 in bag, not CO2). If O2 sats less than 90% - pt in trouble. Any irregular or obstructive breathing needs airway protection or intubation. Look for signs of cyanosis. NEVER put in airway it paralysis the tongue and prevent patient from swallowing higher risk of aspiration. Breathing Circulation (pulse, BP): pulse rate >120bpm pt probably hypoxic and in need of intubation. Put up drip immediately but do not give glucose because the convulsing brain is in anaerobic metabolism and the glucose will be converted to lactic acid, which will make seizures more resistant to treatment. Only give NaCl. Drugs: A. Stop convulsion: Lorazepam 4mg ivi stat beware of respiratory depression and hypotension (10mg diazepam has same effect) - If BP drops give fluids. ** you can give valium 10mg ivi over 2 minutes, and also give lorazepam imi but it will take 30min before action too long for status. Can mix the valium in a 20ml syringe and give slowly. B. Load: You will load anyway, even if patient stops fitting with the lorazepam. Phenytoin 20mg/kg (1.2 gram) in 200ml saline over 30min or even better, put 4 ampoules in a 20ml syringe and get someone to inject it slowly 1ml per minute should be in after 20min. (One ampoule of phenytoin has 250mg/ml 70 kg person will need 5,5 ampoules) Beware of arrythymia patient should have ECG monitor if you give phenytoin too quickly can go in to cardiac arrest. The preservative in phenytoin can also lead to drop in BP Phenytoin precipitates in anything, best is to give it in saline. If there is any glucose in the line the phenytoin will form lumps. Phenytoin is a life saver in status, but Epilim is easier can give faster and has less side effects. Better to load with valproic acid 30mg/kg (2.4 gram ) Acute side effects of epilim: can increase ammonia level dramatically, and makes platelets dysfunctional they dont stick, even if the number of platelets is normal. Can give 2nd dose of lorazepam if still fitting after loading, and another 10mg per kg of Epilim or phenytoin if still fitting after second dose of lorazepam if pt still fits needs intubation and anathesia (dormicum at high high high doses) Focal status: patient is awake and talking to you dont need to act very aggressively. Find cause of status as soon as initial emergency management is completed:

Page 10 of 61

Do FBC, U&E, CRP, s-osmol, LFT, levels, tox screen (paracetamol), CMP, syphilis, HIV if you can (HIV is epileptogenic in itself, as well as secondary illnesses associated with HIV), CT scan may be indicated, CXR later if aspiration pneumonia is suspected, EEG, urine and LP (30% of patients with status have meningitis) SIDE EFFECTS OF ANTI-EPILEPTIC DRUGS: - USUALLY DOSE-DEPENDANT EPANUTIN: Epanutin is enzyme inducing other drugs, and itself, metabolised faster S/E: gum hypertrophy, coarsening of face EPILIM: Valproate is an enzyme inhibitor, thus it reduces the metabolism of drugs such as Tegretol and lamotrigine can lead to toxic levels of other drugs Common: GIT (nausea, vomiting, constipation, diarree), sedation. Is considered to be a major teratogen all females in reproductive years should be on folate. Uncommon: tremor, interference with platelet function, hepatotoxicity, pancreatitis, rash (especially in combination with lamotrigine), hair loss, increase in weight Toxicity: cerebellar symptoms (symptoms of co-ordination) CARBAMAZEPINE: Common: Sedation, ataxia, dizziness, GIT, dry mouth common Uncommon: skin rash (Steven Johnsons), SIADH with low sodium and water retention, bonemarrow suppression with agranulocytosis, thrombocytopenia, aplastic anemia, osteoporosis due to reduced Ca absorption Toxicity: nystagmus, ataxia, confused, blurred vision, speech disturbance, drowsy, hallucinations, abnormal movements Because serum levels of drugs do not correlate with concentration in CSF it is not recommended to do levels for therapeutic reasons. Indications for levels would be 1)suspected non-compliance 2) suspected toxicity 3) to determine baseline level of effective concentration CRANIOPHARYNGIOMA: Slow growing, calcified, cystic tumor Occupies suprasellar region Arises from remnants of the craniopharyngeal duct Has benign histology but malignant behaviour (invades tissue and recur after surgery) Usually in kids and older adults (60y+) Accounts for 1-3% of intracranial tumors

Page 11 of 61

Excellent survival in young patients, not so good in older patients Symptoms only when tumor is 3cm plus usually then had tumor for 1-2 years Symptoms: Headache: dull, continuous, positional Endocrine problems: 40% have hypothyroidism with weight gain, fatigue, cold intolerance, constipation 25% have adrenal failure with low BP, low glucose, high potassium, lethargy, vomiting 20% have diabetes insipidus with poliuria and polydipsia 90% have Erectile dysfunction or amenorree depending on gender Visual problems: often; if tumor is pre-chiasmal optic atrophy with reduced acuity and fields If post chiasmal: hydrocephalus with increased ICP and papil edema with double vision. CNS LYMPHOMA: 3% of all brain tumors Very common in HIV when CD4 drops below 50 Males predominate, usually 50+, but younger in HIV patients CNS lymphoma is an AIDS defining illness and ARV reduces the risk Etiology: Unknown, possibly chronic stimulation of lymphocyte clones by EBV >50% of the tumors have Human Herpes 8 in them - ? significance HHV8 also associated with Kaposi sarcoma Pathology: Mostly B-cells, arise in, and is confined to the CNS 25-50% of patients will have multiple lesions that may look like mets Tumor often grows around small vessels, and ocular involvement common Clinical: Frontal lobe mostly involved neurocognitive presentation with dementia and lethargy. Convulsions are not common because it is rather the deep structures that are affected, and not the seizure-prone cerebral cortex Blurred vision common symptoms Focal deposits on cranial and spinal nerve roots may lead to neuropathy and radiculopathy Diagnoses: FBC, HIV, T. gondii serology (looks like toxoplasmosis on MRI with smooth, round dense lesions with ring enhancement) (toxo and lymphoma often co-exist in AIDS) Rx with radio- and chemotherapy, not surgery has poor prognosis, dead after 3/12 Clinical case: 23 year old on TBRx, c/o pain in feet past 3/7 with weakness in both legs/ Think: Peripheral neuropathy GBS

Page 12 of 61

Myelopathy ADEM Devic (optic neuritis with cervical spine fallout) is common with TB

Can differentiate GBS from other causes of neuropathy with EMG. If both eyes are affected, think gaze palsy first, not cranial nerves Gaze palsy: if stroke is in the frontal lobe, pt will look toward the lesion Horisontal gaze FEF and pons; FEF supplied by ACA Vertical gaze midbrain Motor strip supplied by MCA Tongue has bilateral supply in most people, and will only deviate with brain stem lesions.

Page 13 of 61

STROKE Stroke: acute onset of neurological deficit with focal signs, presumed to be of vascular origin (infarction, embolus, bleed) Drugs can cause stroke (diet meds, cocaine) also pregnancy and hypertension DW: white is pathology ADC superimposed on this now pathology is black 85% of strokes occur in the anterior circulation, 15% in posterior circulation Strokes can be classified according to vascular supply (ant vs post) or large vessel, small vessel, embolic stroke and other, or according to time (hyperacute, acute, subacute and old) If no corneal reflex hard sign of cranial nerve V lesion would expect a dense sensory deficit VII palsy: upper bit of face gets bilateral supply stroke in one part of brain forehead will still be okay due to bilateral supply from other cortex UMN only lower half of face affected Brainstem: VII and VI next to one another in brain stem stroke often VII and ipsilateral VI (lateral gaze affected) 80% of patients with stroke will have an acute hypertensive crisis within 24 hours - it is possibly due to the autonomic system. BP should not be dropped too low no perfusion of brain, because auto-regulation does not work and the perfusion depends on the MAP. The area around the stroke is called the penumbra no electrical activity post-stroke in this area, but the cells are still viable do not drop BP too low, otherwise youll lose this area Dont treat HT unless the systolic is >180 and the diastolic is >110mmgHg. Brain stem stroke often a lot worse on post mortem than on MRI. Bleed vs thrombus: bleed will give more patchy sensory loss, because blood often just push fibres away, do not affect all the fibres adversely, whereas thrombus often leads to occlusion with area of necrosis and more fibres affected. If you want to detect facial sensation in an unconscious stroke patient can do corneal reflex (not completely absent, but reduced), or tickle in the nose with cotton wool. TIA is a neurological deficit that will completely resolve within 24 hours, usually within 20 minutes to one hour TIA score: a patient who presents with TIA is at high risk to develop a stroke, and should be worked out within 2/52. Risk factors that TIA will progress to stroke includes: atrial fibrillation, >60 years of age, hypertension, diabetes

Page 14 of 61

TIAs give NEGATIVE PHENOMENA (epilepsy gives positive phenomena) such as Blind (instead of lights) Weakness (instead of jerking) Numbness (instead of tingling) Investigations of stroke patient: CXR: aspiration LFT: if deranged can increase risk of bleeding Cholesterol: if too low can increase risk of bleeding (cell wall integrity involved), if too high atherosclerosis Glucose: to exclude DM FBC: infection, polycythemia, thrombocytosis (any increase in cells will cause increase in viscosity with risk of thrombosis) ESR: inflammation and infection, Ca, auto-immune disease (often cause of young stroke), severe anemia Anti-nuclear antibodies U&E: end organ damage secondary to hypertension, electrolyte disturbance Thyroid functions: hyperthyroidism may give arrhythmia - stroke RPR, TPHA Treatment of stroke: Dispirin is an anti-platelet prevents clots Simvastatin (Zocor) functions to stabilize the plaque (dont give if cholesterol is <2.3) Lipitor is given for secondary prevention and Zocor for primary prevention (in state only use Zocor) Anti-hypertensive treatment, even if not hypertensive (indapamide), Coversyl promotes vascular re-modeling Modify risk factors (Stop oral contraceptives etc) Steroids or not: vasogenic edema responds well to steroids, cytotoxic edema does not with stroke you get cytotoxic edema, but we sometimes give steroids anyway

When you present a stroke patient, show the examiner that you are thinking of the lobes involved it will usually be either parietal lobe (look for 2 point discrimination, astereognosis, speech problems/Gerstman/depression if left parietal lobe, and agnosia/apraxia if right parietal lobe) or frontal lobe (motor problems, FEF, gait, rarely personality change need bilateral damage for frontal lobe syndromes) If sensory loss is EXACTLY in the midline be wary probably supra-tentorial, fibres always overlap, never exactly in middle

Page 15 of 61

Strokes are divided into hyper-acute (<6h), acute (6-24h), subacute (24h-2/52), old >2/52 MRI will pick up 50-80% of acute strokes CT will pick up 45% within the first 6 hours and 60% at 24 hours DWI much more sensitive in the acute stroke, but normalises in 2/52 How does HIV contribute to risk for stroke?

1. HIV causes vasculitis which may lead to occlusion of the vessel 2. Cardiomyopathy with mural thrombus and then embolus 3. HIV itself may give sterile endocarditis with valvular lesions 4. HIV causes hypercoaguble state (it lowers protein C and S), but prot C
and S is low in all HIV patients, and not all get stroke

5. stroke may be due to bleed secondary to micro-aneurysms secondary to

vasculitis, or bleed due to low or dysfunctional platelets (remember epilim gives dysfunctional platelets with or without drop in total number, tegretol and phenytoin also thrombocytopenia, also dysfunctional platelets in kidney failure) How does alcohol cause stroke? 1. Due to complications get rebound thrombocytosis if they stop drinking 2. Bleeding disorders 3. Cardiomyopathy Pontine stroke: Pinpoint pupils Skew deviation Ocular bobbing Top of the basilar syndrome: The basilar artery is the most important artery of the posterior circulation, formed by the confluence of the two vertebral arteries. 1/3 of strokes occur in the posterior circulation. Black and Asian patients have a high incidence of stenosis of the intracranial arteries. Risk factors for this include HT, DM, CHD, smoking and high cholesterol Sclerosis occludes the middle segment, whilst embolus usually get stuck in the distal 1/3. There is often a history of TIAs. The typical syndrome is Locked In Syndrome, where only the tegmentum of the pons is spared the patient can breath and open eyes, and thats it. Top of Basilar syndrome refers to visual disturbances (blindness) and CNIII palsy. Remember in stroke dont reduce BP within the first at least 24 hours

Page 16 of 61

And dont give heparin in the first 24hours (with a thrombus, start on day 3) How to differentiate Bells palsy from a stroke: VII paralysis, hyperaccusis on affected side (stapedius inhibits sound, now not working) Change in taste: tongue must be out of mouth when you test taste, rub wooden stick with salt on lateral side of tongue, and sugar on the tip pt must nod when they can taste Vesicles in ears (then Ramsy Hunt) Trick: if you have power of 5 in big toe no long tract involvement

Page 17 of 61

HEADACHE MIGRAINE: This is a unilateral, throbbing headache, better when lying down. Most patients will NOT have an aura (i.e. visual disturbances) Migraine is a recurrent headache someone has to have at least 5 episodes before you can say he is a migraine sufferer. Can abort with NSAIDS, panado, triptans or ergotamine Triptans (Maxalt) are serotonin1b/1d agonists it inhibits the release of cytokines and promotes vasoconstriction: dont use in heart disease, hypertension, pregnant Also give anti-emetics metoclopramide, prochlorperazine, chlorpromazine Migraine prophylaxis with 1) beta-blockers (takes 3/12 to work) 2) Ca-channel blockers (tolerance develops quickly) 3) TAD and possibly SSRIs (S/E of TAD: sedation, dry mouth, constipation, blurred vision, urine retention 4) anti-convulsants gabapentin, topiramate TENSION-TYPE HEADACHE: Most prevalent headache, infrequent, episodic, bilateral, non-pulsating, aggravated by climbing stairs. Not always easy to treat. It has nothing to do with stress, although there is an increase of anxiety and depression in patients with TTH. Chronic low grade migraine may present like chronic TTH (transformed headache) Can give prophylaxis in the patient with chronic headache TAD is first line, SNRI, topiramate, exercise and CBT also helpful To determine whether treatment for headache is successful: 1) Can you plan your day? 2) Does it recur regularly 3) Is the side-effects of the meds manageable 4) Does the headache improve within 2-4 hours CLUSTER HEADACHE: Male:female 4:1 Unilateral, throbbing headache, orbital or temporal, lasts 15-180 minutes, occurs with conjunctival injection, ptosis, runny nose. The headache is episodic and may occur many times a day, or during the night. It is often seasonal, and is worse with smoking. This is a form of Trigeminal Autonomic Syndrome. The patient may have Horners syndrome with ptosis, miosis, anhidrosis and enoftalmos due to the sympathetic disturbance. Rx with triptans or oxygen first line, prednisone 60mg po x5/7 decrease then with 10mg /d no nausea, not

Page 18 of 61

TEMPORAL ARTERITIS: Inflammation of the medium and small arteries. Pt may have headache, jaw claudication, with local tenderness and no pulse. Usually older male patient, will have raised ESR, CRP, and may have low Hb and high platelets on FBC with peripheral neuropathy. There is only a few causes of a raised ESR>100 TB, malignancy, temporal arteritis, rheumatoid arthritis and polymyalgia rheumatica SECONDARY HEADACHES: Due to SAH, glaucoma, infective (meningitis or referred pain from sinusitis), post-traumatic gliosis, tumor, drugs (codeine, steroids, ro-accutane, anti-epileptics, anti-hypertensives), low pressure headache after LP. Straining your eyes does NOT give you a headache! Mx of low pressure headache: Lie down for 4-6 hours, take in lots of fluid, strict bedrest, caffeine. The headache may last for days. Can be avoided by the use of thinnest needle, and poke as little as possible Dr Kakaza ward round: Motor Neuron Disease History: progressive difficulty in walking, speaking, swallowing O/E: combination of UMN and LMN, although you also get MND that is predominantly LMN or UMN. About 1% of patients with MND also have cognitive decline. MND is usually a pure motor pathway problem it starts with the pyramidal cells in the cortex, if the die-back is extensive youll get other frontal lobe signs. Look for atrophy and fasciculations (remember snuffbox muscle on hand is called 1 st dorsal interossieus muscle, and on palm the thumb muscle is called thenar muscle.) If you have JUST LMN think CIDP, syrinx (cranial nerves may also be affected), MND, SMA (different forms can present in baby or in adult only affect the anterior motor neuron horn cells) Must exclude hypothyroidism, hypercalcemia, AIDS, Lithium toxicity in any case of LMN weakness can look exactly like MND. What diseases can give you swallowing problems? ADEM Myasthenia Gravis Strokes GBS Myopathy (dystrophia)

Page 19 of 61

MND (progressive bulbar palsy) Botulism (MG and GBS both respond to IVIG)

Diseases that gives multisystem neuro involvement: TB Alcohol Syphilis HIV MS Vit B12 deficiency

Page 20 of 61

DR KAKAZA TUTORIAL NUMBER 1: CRANIAL NERVES Cranial nerve nuclei in the brainstem are regarded as LMN. Remember cortical problems ALL lesions, including CN, will be on contralateral side CRANIAL NERVE I: OLFACTORY Fibres start in nose, through cribiform plate, through orbito-frontal area, to temporal lobe 1) Anosmia: Common problem, but patient will often rather complain of abnormal taste than of anosmia Usually due to smoking or sinusitis Sometimes whip-lash injury (even a mild injury can cause thin fibres to break as they go through cribiform plate) Anosmia may also be due to neuro-degenerative disease such as Parkinsons. (The first thing to go in Parkinsons is the sense of smell may precede other symptoms by years) this is because the small, thin fibres degenerate first. Meningioma in orbito-frontal area also causes anosmia 2) Abnormal smell: Patient may complain about an episodic bad smell usually part of epilepsy DIGRESS TO EPILEPSY: First determine whether it is partial or generalised Classification of epilepsy: Partial seizures: Simple (no loss of consciousness) Complex (consciousness impaired) Evolving to secondary generalised convulsions Generalised seizures: Absence seizure Tonic Tonic-clonic Myoclonic Atonic Epilepsy, migraine and mood disorders often run in families, and may overlap in one patient this is because the pathogenesis of these diseases is almost the same, namely they are all channelopathies. Because channels are not permanent the symptoms may be episodic. New channels are formed every few months (about 6/12) and they dont have the same degree of

Page 21 of 61

abnormality every time (you have each time a chance to make normal channels) it is because of this reason that patients may report bad spells and good spells that may lasts for months. Depending on the dysfunction of the channel the patient may have one, 2 or all 3 of the diseases. The channels involved are mainly Na, Cl, and Ca depending on the gene Epilim works on multiple channels (Na, Cl, GABA) Partial seizures (aka focal seizures aka auras) Partial seizure implies that the seizure originates from a focus partial seizures and focal seizures are interchangeable terms. During a simple partial seizure the patient is totally awake and is able to tell you what is happening Motor SPS: If seizure presents with motor phenomena it means the seizure originates from the motor cortex in the precentral gyrus, frontal lobe. Sensory SPS: Jacksonian march: sensory focal simple partial seizure: pins and needles go up the arm and then down the leg. Special sensory SPS: Simple partial seizures can also be autonomic or special sensory (smell, or hear bells) Simple partial seizures used to be called auras it was incorrectly thought that this happened before the seizure The way a simple partial seizure presents tell you where it originates SPS can repeat, up to 10x per day, and then go into secondary generalised seizure Prodrome to a seizure is not the same as an aura (an aura IS the seizure). The patient may say during the prodrome I feel funny when I feel like this I know Ill get an attack within 2/7 AURA: An aura is a subjective sensation may be accompanied by changes in mood and behaviour Can find in epilepsy, TIA and migraine (must differentiate from panic attack) How to differentiate: the aura of a migraine takes long to develop, lasts long, up to an hour, and it does not recur; whereas the aura of epilepsy is instantaneous, never lasts longer than a minute but may repeat The aura of migraine and epilepsy both have positive phenomena such as seeing lights and tingling sensation. Visual aura in migraine is common (30%), can see shapes with lines. Not always easy to differentiate aura of epilepsy from panic attack epilepsy can also give you anxiety and elation Visual symptoms in epilepsy can be just light, or well formed pictures such as seeing a fire COMPLEX PARTIAL SEIZURES:

Page 22 of 61

Used to be called TLE The patient is awake but is unaware of what he is doing They will look confused (other people will realise something is wrong) They may have automatisms: this is what you can do automatically without thinking, because you do it every day, such as driving a car, packing and unpacking cupboards Automatisms are often used as a defence in court, but you CANNOT PRE-MEDITATE while you are having a seizure. You can reverse over someone while having an automatism if youre driving every day, but you cannot go to cupboard and get knife and stab someone. There are often visual symptoms as part of CPS The term TLE is not used anymore, because extensive EEGs showed that >50% of TLEs originates from temporal lobe, the rest originates from the frontal lobe or parietooccipital junction. Most frontal lobe epilepsy will also present as CPS the patient classically assumes a fencing posture. The CPS is often preceded by a SPS (simple partial seizure/aura) where the patient may feel an egigastric sensation, have a bad taste in the mouth, or smell something bad. After this they will have a blackout according to them, but they dont fall and will now have the CPS. Eyewitnesses will say that the patient was awake, but was behaving strangely, and would do or say inappropriate things (i.e. one lady complaint that her husband would get up from dinner table to get the comb, and then sit combing his hair while they have dinner), or patient may go out of the house to undress on front lawn this may easily be confused with dementia!! If the CPS lasts about a minute, and the patient is post-ictal and confused afterwards, and the patient get several attacks per day, very easy to confuse with dementia. Is called Epilepsy Partialis Continua, and is treated with low dose Tegretol (200mg bd) EEG in CPS will often only show focal slowing in temporal lobe, but no focus. If you do a sleep EEG you may be lucky and see a spike and wave pattern. When they come to from the CPS, they are in a post-ictal state of confusion and wkll have amnesia for the event. You must be able to differentiate an absence seizure from a CPS: Absence seizures are very rare in adults (kids uruadly outgrow them) Absence seizure is very shOrt never longer than 30 seconds whereas SPS will lcst at least a minute or longer. If a patient has an absence seizure whilst valkng he will stop in the middle$of the sentence, look blank for 20(seconds and then resume!the senTence EXACTLY where he left off. Th%re will be no confusion. In CPS the pati%nt will be confused afterwards. Complex partial status is very difficult to diagnose, and can easily be"confused with$psychosis but what the patient does (the automatism) will be cyclical theyll

Page 23 of 61

repeat what theyre doing, maybe with short lukid periods in between, wiereas psychotic behqwiour is usually more disorganised. he activity will also not involve you, they wont fight unless you bother them. *j any rePeated strange behaviur think epilepsy Absence seizures can be!treated with ethosuximide, a finicky drug that ONLY works for partial seizures, whereas Epilim works for all forms of epilepsy (partial and generalised) Tegretol is the drug of choice for partial seizures (whether SPS or CPS) and is considered the gold standard for partial seizures, even though epilim is often used due to the sideeffects of Tegretol (more sedation and dizziness) In adult patients generalised epilepsy is more common that partial seizures, and CPS is more common than SPS (GE>CPS>SPS) (SPS is only aura, CPS aura and automatism) In elderly patients (>60 years) CPS are the most common form of epilepsy (more common than generalised epilepsy) often misdiagnosed as dementia must really always do EEG before you diagnose dementia with strange presentation If you give a confused elderly patient lorazepam and he becomes alert diagnoses of epilepsy made Causes of epilepsy: 18-30 years usually idiopathic 45-60y usually due to stroke, sometimes tumors >60y usually due to neurodegeneration HIV has higher incidence of epilepsy than the general population

GENERALISED SEIZURES: Definition: Either loss of consciousness (will fall down), OR EEG shows generalised firing in the hemispheres. A patient with CPS will NOT fall down, unless they have secondary generalised seizure. Generalised seizure implies that the hemispheres are equally involved from the onset of the seizure. Types of generalised seizures: 1. Absence seizures 2. Generalised tonic clonic seizures (grand mal) 3. Tonic seizures (stiff and fall down) 4. Clonic seizure (immediately jerking with no initial stiffness 5. Atonic seizures just loses tone and fall. Myoclonic seizures: arms may lift once as if the patient had a fright, they do NOT lose consciousness. It usually occurs as part of a seizure syndrome (together with generalised tonic-clonic). Treatment is important myoclonic seizures do not respond to Tegretol or phenytoin, and the generalised tonic clonic seizures may actually worsen if myoclonic

Page 24 of 61

seizures are present you should treat with Epilim. ** a sudden jerk just before falling asleep is called physiological myoclonus. Surgery for epilepsy: It has the side-effect of severe depression in all patients that may last up to two years patient needs psychiatrist before and after surgery Patient who had surgery wont ever be off meds just possible to taper down to one drug Surgery is not a permanent solution: seizures come back after 5 years DR KAKAZA TUTORIAL 2 (18/1/2011) CRANIAL NERVE II: Look for visual fields, visual acuity, light reflex and retina The patients main complaint is usually I cant see The first question you must ask is: is this in the eye, or behind the eye? The pupil reflex answers this question If the pupil is dilated the cause of blindness is in the eye, if the pupil is reactive the cause of blindness must be in the brain Direct light reflex: afferent is from CN II sends info to the EWN in the midbrain, from where info goes out bilaterally to both eyes to give the consensual light respons. If CNII is disrupted there will be an afferent pupillary defect the pupil will be big and wont contract. If the lesion is in occipital lobe (lesion behind the reflex) the direct and consensual reflexes will be intact. You need a bilateral lesion to be blind from occipital pathology (lesion in basilar artery). If there is swelling of the occipital lobes, such as you find in eclampsia and hypertensive encephalopathy with a sudden increase in BP, there may be sudden onset of blindness. Unilateral blindness the problem is not in the occipital lobe, must be in the retina or optic nerve (the pupil will be dilated) MARCUS GUNN PUPIL: Afferent pupillary defect shine light in normal eye both eyes will constrict (consensual light reflex from EWN) then move light over to the abnormal side both pupils will dilate (is dilating because light is moving away from normal eye, normal eye assumes the primary position (as does the abnormal eye due to consensual reflexes) and abnormal eye does not pick up the light shining into). This is due to an optic nerve defect in one eye, with reduced entry of light into the nerve. If the pupil goes a bit smaller, then bit bigger again normal phenomena, much like hippus.

Page 25 of 61

Fundoscopy: look at retina for swelling or atrophy of disc with swelling the margins will be blurred and vessels engorged. papiledema and optic neuritis: Papiledema has NORMAL visual acuity loses vision only at late stage when they have optic atrophy. Optic neuritis: patient will have reduced vision, may be blind (sometimes central scotoma, which is blind spot in the middle of the visual field). Optic neuritis is not an uncommon condition with acute onset of vision loss and pain in the eye on movement. It will start in one eye, and often move to the other eye. The commonest cause is demyelinating lesion, such as focal ADEM (called sight restricted ADEM) which is usually bilateral, or MS, where the neuritis will occur in the one eye, then in the other, but NEVER in both eyes at the same time Sight restricted ADEM: Acute demyelinating Monophasic Post infectious Can involve whole brain, or just brainstem or just optic nerve Rx with steroids If the disc is swollen, you must differentiate between

Optic atrophy: the patient will have 1) gradual visual loss, a 2) dilated pupil and a 3) pale disk and 4) less than 7 small vessels entering disc, With primary optic atrophy the margins are crisp but with secondary optic atrophy due to papiledema the margins will be blurred. Sometimes youll see a pale disk with normal visual acuity this may be normal variant of disk. Visual fields: test all the quadrants Commonest problem is bitemporal hemi-anopia (due to pituitary lesion pressing on the optic chiasm) Homoanymous hemi-anopia lesion in optic radiation Quadrantanopia (only of visual fields involved) occurs with lesions in the T, P or O lobe usually Occipital lobe Can also do confrontation test in patient in ICU, blind patient Sensory extinction: with double simultaneous stimulation: patient not aware of the stimlulus on one side. Stimulus may be touch; sound; visual input. If you have a stroke with hemi-anopia means BIG lesion involves parietal lobe DIGRESS TO MULTIPLE SCLEROSIS:

Page 26 of 61

Multiple sclerosis (MS) is an immune-mediated (both cellular and humoral components), inflammatory and demyelinating disease of the CNS neurodegenerative disease of the CNS responsible for a significant amount of disability worldwide. Types: relapsing remitting course most common Secondary progressive (start off as relapsing remitting) Primary progressive bad, poor prognosis History very important if you suspect MS patient must have had diverse neurological complaints over a period of time (lesions disseminated in time and space). For instance may have had an episode of visual problems that had improved, then episode of hemiparesis that had improved. (If ALL the episodes involved the same site, i.e. all episodes R hemiparesis rather think vascular (TIA). The different episodes in time and space had to be at least 6/12 apart to differentiate it from ADEM which may also relapse for a while. On Examination: MS is an UMN condition, often accompanied by clumsiness and eye signs. Look for subtle signs Eye signs: Optic neuritis Diplopia INO (internuclear ophtalmoplegia) MLF lesion Trigeminal neuralgia Often dont see disc swelling in MS the demyelination is retrobulbar and fundoscopy normal INO: If you look to the Right, the Right eye will go out with nystagmus, but the left eye does not go in. The pathology is in the MLF (medial longitudinal fasciculus) (Vertical gaze controlled by dorsal midbrain: in PSP there is destruction of the dorsal midbrain, and the patient will be unable to look up or down (with normal aging the upward look is also impaired, but can always look down) Horisontal gaze is controlled by the FEF (frontal eye fields, ACA) that will send impulse to PPRF (pontine reticular formation on the contralateral side. The FEF pushes the eyes to the opposite direction (Left FEF pushes eye to the right horizontal direction) From the PPRF the connection goes to the VI on that same side, and with the MLF to the III on the side of the FEF (MLF is between VI and III). Plague of MS loves the MLF for some unknown reason. You dont get full III fall out only the little bit that goes to the medial rectus is involved (MLF only involves the medial rectus)

Page 27 of 61

Why does the eye that is looking outwards have nystagmus? This is an attempt of the brain to avoid diplopia INO can be unilateral or bilateral Horisontal gaze palsy if lesion is in frontal lobe the eyes will look towards the lesion (function of the FEF is to PUSH the eyes AWAY), if lesion is in the pons, the eyes will look away from the lesion. Horizontal gaze palsy can be due to lesion in frontal lobe, or due to lesions in the pons such as Ca or tuberculoma of central pons, and central pontine myelinolysis. Initially MS will recover after an episode, but over time residual symptoms will develop. The pathogenesis is that the myelin sheath (made by the oligodendrocytes) is attacked, but not the oligodendrocytes. Initially there is remyelination of the axons, but over time there is a dying back of the oligodendrocytes, and no more remyelination occurs. In the primary progressive type of MS there is death of the oligodendrocytes from the start. Devic syndrome: Black patient, bilateral optic neuritis, signs of myelopathy DIAGNOSES: 1) Primary diagnostic test is MRI, the criteria is called Mc Donald criteria (you need periventricular plagues, also at least one infra-tentorial (cerebellum, brain stem or spinal cord) T1: (CSF dark on this one and can see the anatomy well) old plagues will look like black holes. T2, T2 flair and gadolinium: active plagues MRI often done with galidinium - active lesions will light up. With MRI not really necessary for the clinical criteria of disseminated in time and space because youll pick up old, previously asymptomatic lesions (was in silent area of the brain) even with first symptomatic presentation and can start with treatment early.

2) LP: will have increased protein (more than 1 gram) and no cells called cytoalbumino dissociation. Do oligoclonal bands and IgG index (send blood with the CSF sot that the ratio between the IgG in the blood and CSF can be determined. (It should be the same 1:1, but intra-thecal synthesis of antibodies occur in MS, with production of IgG in the CSF. This is not specific for MS it will also be found in meningitis and in auto-immune diseases. 3) Evoked potentials visual, auditory and somatosensory will pick up subclinical deficits due to previous attacks that the patient was unaware of. There will be slow movement of the impulses will prove dissemination in time and space. TREATMENT OF MS:

Page 28 of 61

1) First episode (or any acute attack) is treated with steroids

Solumedrol 500mg ivi daily x 5/7 (doesnt need Ca and Slow K with short courses, but always give ulsanic to prevent gastritis, patient may also need short term bzp for insomnia caused by steroids. Remember never to treat optic neuritis with oral steroids always ivi was shown that people on oral steroids actually did worse than people who did not receive any medicine. patient TCB 3/12, repeat MRI with gadolinium why? Because active plague remains active for <6/52, if new active plagues after then 3/12 it must be MS (even with the relapsing remitting types you have new plagues the whole time, they just not always symptomatic. Only plagues in the motor strip, cerebellum and brain stem really gives symptoms that patient will notice. In primary progressive type you still give solumedrol but response not great patients often die quickly of pneumonia. The symptomatic treatment for MS and ADEM in the acute setting is the same (steroids), but the disease modifying treatment for MS is interferon patients on interferon has less relapses, but the disability after 5 years is the same, although the QOL within that 5 years is better. Common clinical manifestations of MS involve motor, sensory, brainstem, visual, cerebellar and neuropsychiatric symptoms. Spinal cord lesions are not uncommon. The cervical cord is more commonly affected than the thoracic cord.

How to differentiate between ADEM and MS: ADEM is monophasic, but the patient is sicker, there is more diffuse involvement of the hemispheres and brainstem, and there is usually a suppressed level of consciousness. Can make the diagnoses with the MRI where you can see that lesions of ADEM are of the same age, confluent lesions the whole brain lights up with a gadolinium scan. ADEM is usually post vaccination or post viral treat with solumedrol. Guillian Barre is the same as ADEM except that it is peripheral whereas ADEM is central. Neuromyelitis optica (Divecs disease): cord symptoms (quadriparesis) plus eyes. This also due to demyelination of cord the MRI of the brain will be normal, but the MRI of the cord will show demyelination you get this more in black patients it is not as responsive as MS to solumedrol and INF also does not work.

Page 29 of 61

DR KAKAZA TUTORIAL NUMBER 3; CRANIAL NERVES III, IV, VI CRANIAL NERVE III: Control eye movements (oculomotor nerve) Supplies all the eye muscles, except Lateral rectus and Superior Oblique CN III also supplies the eye lid and pupil, thats why CN III will give you ptosis, dilated pupil, and down and out movement of eyeball. IF YOU HAVE A PATIENT WIH PTOSIS: Always think Horners, CN III problem or MG Pupil size important to differentiate

Horners implies involvement of the sympathetic pathways the problem can be

anywhere, but commonly in brain stem, or where the chain exists the upper thoracic cord, or where it goes over the apex of the lung, or close to carotid artery. Horners is always ipsilateral, but it is not considered to be a localising sign. 1. The patient will have partial ptosis (levator palpebrae superioris gets sympathetic supply) (palpebral fissures not the same)

2. Small pupil, but it can dilate in a dark room (miosis)

3. Anhidrosis (skin smooth and dry on affected side, feel both sides with back of hand) 4. Enoftalmos 5. Eye movements normal Horners is seen in: 1. the setting of a lateral brainstem stroke 2. Collapse of the upper thoracic vertebra 3. Pancoast tumor

4. Carotid artery thrombus ipsilateral Horners, but face, arm and leg contralateral
(Stroke in MCA will never have Horners) Schematic diagram of brain stem: Brain stem is divided into 6 subsets, and EACH of these 6 are supplied by different artery R and L, each divided in lateral and medial SCA AICA PICA III VI, VII IX, X

Page 30 of 61

All Motor nuclei are MEDIAL as well as Cortico-spinal tract also medial (crosses in medulla) All sensory nuclei are LATERAL, spinothalamic tract also lateral Thus, if you have a stroke at CN III nuclei, will have ipsilateral III and contralateral hemi (will also catch CS tract) Cranial nerve fallout is always on the same side of the problem, and CN fallout will be those that are supplied by same artery, in other words, you wont have a III together with a VI and VII, or together with a IX and X A stroke will only affect one of the 6 parts, youll also get EITHER a corticospinal fallout OR a spinothalamic falljuT, thqS in c/rtical stroke the rule is that youll be weak and numb, in brain stm stroke youll be either weak OR numb. If you have CN deficits that do not fit, such as a IYI"together with a VI think patlology outside brainstem (such as malignat meningitis) or that the patient is herniating. (CNIII exists the brainstem and enters the brain between the parahippocampal gyrus and tentori}m is a ominous sign of raised ICP) Ramember You(can get CN involvement with meningitis it is either due to ynflammitimn of the vasa nervorm or due to raised intra-cranial pressure. CN III then goes past the`circle of Willis "posterior cerejral artery aoeurysm may$press on III, with didation of pupil (surgical III) patient may present with a thunderclap headache when it ruptures or leaks (do CT brain to r/o SAH, if it is newative can do LP to confirm blood/bilirubin) Then into cavernous sinus: travels with IV, VI, and V1.MIn the event of a cavernous sinus thrombosis the patient will present with a headac(e, total oftalmoplegia (the eye will not move in any direction), ptosis and numbness of the forehead. CAUSES OF CAVERNOUS SINUS THROMBOSIS: 1. Post partum period and pregnancy due to hypercoaguble state 2. Chronic sinusitis 3. meningioma in cavernous sinus In any thrombosis should differentiate between clot due to hypercoagubility or due to infection if you give klexane when there is an infective process, will disseminate the clot. CAUSES OF CN III FALLOUT:

1. Brainstem infarct (posterior circulation) 2. Meningitis, especially syphilitic and TB due to the exudate that forms between the
optic chiasm, pons and temporal lobe, where III runs. If you have a CN III deficit in a patient with meningitis think 1) possibly herniating 2) strokes due to widespread vasculitis secondary to the meningitis brainstem strokes are common in bacterial meningitis

3. Temporal lobe herniation or any cause of raised intracranial pressure Page 31 of 61

4. Posterior cerebral artery aneurysm 5. Cavernous sinus thrombosis, thrombosis of small vessels in DM or HIV, A/I
diseases 6. Follosa-Hunt syndrome (granulomatous lesion in cavernous sinus, is a autoimmune disorder, treat with predisone Medical III: Pupil often not dilated (parasympathetic fibres in periphery of nerve, and ischemia often spares the periphery (problem starts in the centre) Surgical III: The pupil is dilated, BLOWN pupil, even before motor fallout occurs, because the nerve is compressed from the outside, and thus the parasympathetic fibres are caught first. Mimickers of CN III palsy: 1) MG MG can cause any muscle to be weak. The picture will fluctuate, but almost all patients with MG will have ptosis 2) Mitochondrial myopathy progressive, external ophtalmoplegia, bilateral and symmetrical. The patient does not have diplopia because the weakness is bilateral. NUCLEI IN MIDBRAIN: CRANIAL NERVE IV: Very rare to get an isolated IV deficit can only perceive a problem with IV when you go up or down steps. Sometimes get it in patients who had Graves disease previously Superior oblique manages accommodation makes eye turn down and in. NUCLEI IN PONS CRANIAL NERVE VI: Nucleus is in pons it is a motor nucleus, so its medial in the pons Ennervates lateral rectus abduction of eye, with lateral rectus palsy the eye is adducted, cannot look out If VI is weak the eye will be in the middle, or turn inwards, and the patient will have diplopia (horizontal) CN VI fallout in raised ICP this is a non-specific marker of raised pressure, and it is sensitive to pressure effects due to its long intracranial course the fallout need not be bilateral even with raised pressure, or it may be due to meningitis with vasculitis of the vessels that supply VI Other causes of CN VI, if not a structural lesion: auto-immune, diabetes, HIV, sarcoidosis It also comes out of the brainstem at a 90degree angle, and is therefore more susceptible to traction.

Page 32 of 61

A VI due to raised pressure is not as ominous as a III due to raised pressure (implies imminent transtentorial herniation) CN VI and VII is close to one another in the brainstem, and VII circles around VI, so you mostly get VI and VII together if the lesion is in, or just outside the brainstem (with a contralateral hemiplegia) If there is vertical malalignment it points to a lesion anywhere in the brainstem. MG can mimic vertical diplopia (If both eyes are involved, think of gaze palsy.)

CN VII: Look for Bells sign when a patient closes his eyes, the eyes will roll automatically to the back if the eyes do not roll back it is either due to poor effort from the patient, or due to ophtalmoplegia. Gaze palsy: will be towards lesion if problem is in frontal lobe (FEF), away from lesion if problem is in pons HOW TO DIFFERENTIATE PARKINSONS DISEASE AND PARKINSONISM: PD is due to destruction of the nigro-striatal pathway with decreased production of dopamine. Normally the basal ganglia are balanced by Ach and Dopamine If the dopamine decreased there is a relative (not absolute) increase of Ach this will produce the resting tremor (this is called the pill- rolling tremor, it is a slow tremor and will temporarily disappear if you give patient something to hold in hand. The tremor is usually in one hand, then in leg, then other hand, then other leg. This is a slowly progressive condition after a decade the patient will be stiff, with affected gait, then stooped posture and festinating gait (start slowly, then faster and faster). Also blunt affect with poverty of movement. Cognitive impairment is late manifestation (15-20 years after onset of disease). The same degeneration that started in the nigrostriatal pathway later affects all lobes. Because the initial tremor is due to increased Ach, you can dampen the tremor with anticholinergics, but it ONLY works on the tremor, does nothing for the rigidity or bradikinesia. There is some controversy about how soon Sinemet should be started it is possibly neuroprotective and should be started immediately. Sinemet is effective for both tremor and rigidity. Dopamine agonists work, not as good as Sinemet not used on their own, but in combination with Sinemet Parkinson Plus (such as Parkinsons disease

PSP) /Parkinsonism

Page 33 of 61

Causes

PSP, MSA (includes Shy-drager syndrome with postural hypotension months Rapid deterioration, months after diagnosis Early Present Very rigid, falls

PD

History duration Deterioration tempo Cognitive impairment Eye signs Limbs

falling

Years Slowly progressive Late None Tremor

easily, but

is

the

most

tremor not noticeable

significant problem, the pt does not fall easily, but is also rigid (not as) None

UMN

on

examination,

has

dystonias, Respons Sinemet Response to AP to

corticobasal Responds well Not so very sensitive to APs.

degeneration and Lewy bodies Does not respond well Very sensitive, causes

hallucinations DR KAKAZA TUTORIAL 24/1/2011: EYES CONTINUE COMMON CONJUGATE MOVEMENTS:

1) Downward deviation of eyes bilateral in unconscious patient usually due to

thalamic stroke (vertical gaze centrum in the midbrain is suppressed) also gets this in kids with hydrocephalus due to pressure of huge 3 rd ventricle on midbrain setting sun sign

2) Bobbing: both eyes go fast down and slow up pontine lesion. Patient will also have
small pupils and skew deviation 3) Roving eye movements sinusoidal movements the eyes go in a figure 8 the whole time - it tells you the patient is in a coma, and its probably a metabolic cause

4) OPSOCLONUS: pt is awake but eyes go in all directions in a haphazard way seen

in neuroleptics and cerebellitis (HIV, paraneoplastic syndromes). The patient is usually not bothered by it. It disappear in sleep. The cerebellum is very sensitive to hypoxia or toxins 5) If a patient cannot look down the PSP (looking up can become a problem with age) Nystagmus is usually gaze directed CRANIAL NERVE V: two components motor and sensory Motor: muscles of mastication (temporalis, masseter, pterygoid) Sensation: face

Page 34 of 61

Jaw and corneal reflex Motor nucleus of V: medially in pons Sensory nucleus is long, through whole of brainstem and synapses at C2. Lies laterally. Back of head sensation supplied by C2. The motor part of V has bilateral supply, whereas the sensory part only unilateral supply it is therefore very unusual to have motor fall out with V after a stroke. If the lesion is in the brainstem wont get fallout of BOTH sensory and motor usually only sensory fallout especially as part of lateral medullary stroke (in which case the fallout may be bilateral) If you have malignant meningitis just outside the brainstem - will give you both motor and sensory. Bulbar weakness V, VII, IX, X, XII involved see later If you have LMN involvement of MULTIPLE cranial nerves, but NO limbs involvement the lesion must be outside the brainstem, such as with malignant meningitis (any tumour, usually lymphoma) Weakness of the jaw: feel masseter, temporalis (both close mouth) and pterygoid (opens mouth). With LMN lesion: atrophy of masseter and temporalis the only way to differentiate between a LMN and UMN is with the jawjerk normally absent or minimal, also absent in LMN and brisk in UMN think pseudobulbar palsy then. Trigeminal nerve involvement: If problem is in central pons (TB granuloma) There will be weakness of the jaw and bulbar palsy Trigeminal neuralgia: It involves the nerve just after it exists the brainstem. Vessels loops and kinks around V. Neuralgic pain will follow nerve distribution (V1, 2) Has sharp, shooting character, lasts a few seconds and repeats There will be no sensory fallout, but touching the face may provoke the pain Normal power and reflexes and normal MRI, there is not even always a vascular loop present. Rx with carbamazepine, amitriptillene, lyrica it does not completely take pain away, but it helps. Trigeminal neuropathy: Patient will have atrophy and weakness, there is a higher chance of having a vascular loop, usually surgery to lift the vessel. V can also be damaged as it goes through the cavernous sinus.

Page 35 of 61

V involvement is usually bad sign with stroke, because it implies bilateral damage or pons damage. CORNEAL REFLEX A PROTECTIVE REFLEX Afferent is V Efferent is VII When you stimulate one side both eyes will close. Often not complete loss of reflex with a stroke, but one side may be weaker. Sensation in comatose patient: corneal reflex (look for asymmetry, not complete absence) and tickle in nose (V2) Absence bilateral is bad sign implies brain stem death DR KAKAZA TUTORIAL 1/2/2011 CRANIAL NERVE XI: May see deficit in patient with dystrophia. If you turn the neck left, you turn the right SCM CRANIAL NERVE XII: Its action is to elongate the tongue UMN: tongue will deviate away from lesion LMN: will go towards lesion Whether UMN or LMN the strong side will always push weak side away (in) but with UMN the problem is contralateral to weak side, thats why away from lesion. Will unilateral weakness the tongue will deviate to weak side (strong side pushes it over), but the tongue has bilateral nerve supply, so many patients with unilateral lesions of XII will be asymptomatic due to this bilateral supply. Unilateral lesion of XII implies LMN (because of bilateral supply if the lesion is in the cortex) If lesion is in the brainstem bilateral fall-out With bilateral weakness the patient will not be able to stick tongue out, and wont be able to do fast alternating movements with tongue clinically such a patient will have dysarthria (may also be the first thing the patient complains about I talk funny) as well as dysphagia. Pseudo XII: you get this with CN VII palsy the tongue has to push past the weak orbicularis oculi it looks then as if the tongue is deviating because it comes out skew from the mouth When you evaluate tongue problem, first decide whether it is UMN or LMN. If UMN: - PSEUDOBULBAR PALSY the tongue will have normal bulk and will be spastic (patient will have difficulty with fast alternating movements)

Page 36 of 61

Pseudobulbar palsy implies bilateral involvement of the hemispheres not found in ordinary stroke Corticobulbar fibres of V, VII, IX, X, XII affected UMN; this patient will also have UMN in the limbs CN V: weak, but jaw jerk CN VII: bilateral weak with snout, glabellar tap (>3 abnormal), pe-pe-pe soft CN IX, X: weak soft palate but brisk gag CN XII: spastic tongue, no atrophy, no fast alternating movements, la-la-la is monotonous with merging syllables. Look for UMN in limbs as well as LABILE EMOTIONS Nasal voice due to weak soft palate CAUSES OF PSEUDOBULBAR PALSY: (MAM) Multi-infarct dementia (multiple, bilateral strokes) MND (ALS) MS Butterfly glioma INVESTIGATIONS FOR PSEUDOBULBAR PALSY: MRI BULBAR WEAKNESS: this is LMN involving cranial nuclei in the medulla and pons. Corticospinal tracts often also involved (UMN). Cranial nerves V, VII, IX, X, XII involved. Therefore if face is LMN, and limbs are UMN think brainstem! If LMN: BULBAR palsy the tongue is atrophic early on, with fasciculations ( the patient must keep the tongue in the mouth when you look for this shine your light inside the mouth and look at resting tongue) (Fasciculations main cause is disruption of anterior horn cell multiple fasciculations in polio. Bilateral CN V: weak, no jaw jerk Bilateral CN VII: weak, no snout Bilateral IX, X: weak soft palate, no gag Bilateral XII: atrophy and fasciculations CAUSES OF BULBAR PALSY: MND or brainstem tumour, such as pontine glioma, also TB granuloma most common causes, also ADEM and listeria ** If you talk about bulbar palsy you just say the soft palate is weak the cause can be anything does not have to involve the brainstem bulb.

Page 37 of 61

** careful with forehead in CN VII: cannot use if there is bilateral involvement of VII. With bilateral VII can only differentiate between UMN and LMN with the snout and glabellar taps. ** A mute patient may have severe dysarthria (even seen in Parkinsons) , or severe aphasia (global or Brocas) or hysteria. CN X mainly supplies the vocal cords DYSARTHRIA: 1) Dysarthria due to Cerebellar causes: Voice is monotone (aprosody no melodic intonation) and staccato, pt says pe.te.ke instead of peteke 2) Dysarthria due to Bulbar palsy: The patient will have slurring speech, with words merging into one. Speech will also have nasal quality (air escapes through the nose due to weak soft palate) is called Donald Duck speech. 3) Dysarthria due to Parkinsons disease: Soft, monotone voice called dysphonia 4) Dysarthria due to Pseudobulbar palsy: Weak palate with slow la-la-la Spastic tongue talks as if hot potato in the mouth If you ever make diagnoses of multi-infarct dementia look for subtle signs of UMN lesions and stepwise deterioration If you have a patient with cognitive decline and UMN signs think multi-infarct dementia or MSA. CRANIAL VII: Nucleus of VII in medial pons. Motor division supplies all muscles of facial expression Sensory : small patch behind ear Special sensory: anterior 2/3 of tongue for taste (V is sensation of anterior tongue) Stroke in brainstem will have LMN VII and contralateral corticospinal involvement Cortical stroke: Will have UMN VII and ipsilateral corticospinal involvement of body DR KAKAZA 25/01/2011 VII CONTINUES: VII can be affected in the brain stem, then in ear. Bells palsy is inflammation of the nerve as it goes through the bony canal no space for swelling and nerve is compressed. Bells Palsy implies the cause of the paralysis is idiopathic. If it is secondary to sarcoidosis, HIV, TB or herpes youll say CNVII fallout due to x.

Page 38 of 61

Must look in the ear and soft palate for vesicles give acyclovir in addition to steroids only if vesicles are present (Ramsy Hunt syndrome) Rx of Bells: Steroids must give in first week. Prednisone 60mg daily, taper by 5mg daily Bells palsy patient has problem with eye closure due to weakness of orbicularis oculi give Tearsnaturel and eyepatch to protect against ulceration. When the patient closes eye a bit of white may be visible Bells sign. If it is a UMN VII the eye may be partially affected Bells recover in 6/52- 3/12 EMG only indicated if patient not better after 3/12 Because Bells palsy is probably from viral origin VII is not the only nerve affected - may affect V and palate, but symptoms and signs more obvious with VII due to compression of nerve. UMN VII Forehead spared (may be a bit weak, but can at least close eyes and frommel voorkop, even IF NOT AS good as other side. Cant smile on command, but can smile at joke (smile muscles also innervated from limbic system) LMN VII: Taste is affected (taste fibres join nerve late) Cant smile at all Hyperaccusis branch to Stapedius muscle affected whole face involved, Bells sign BILATERAL FACIAL WEAKNESS: As yourself BULBAR or PSEUDOBULBAR (LMN or UMN) Will decide this with snout reflex it is a frontal release sign And glabellar (both positive in UMN lesion) Will probably find brisk Jaw jerk as well CRANIAL NERVE IX and X Supply the soft palate Both have motor and sensory components But IX more sensory than motor and X more motor than sensory If problems with IX or X the patient will complain of a soft voice, nasal voice and dysphagia that is worse for liquids than for solids. Fluid will come out of nose. When you look into mouth, look at the pillars and uvula to see if it is in the centre (assymetrical uvula usually due to past tonsillectomy). Ask the patient to say AHHH

Page 39 of 61

Soft palate must contract and lift up, but the uvula must remain central - if is pulls to the side, knows it is pulling towards strong normal side. Unilateral weakness of the palate is usually LMN (may be problem in brainstem), because if it is due to stroke bilateral supply will take over weakness not noticeable BILATERAL WEAKNESS OF PALATE: May be bulbar or pseudobulbar. With AHHH it will go up nothing or very little only way to differentiate between UMN and LMN is with gagreflex it will jump up with UMN, and not move with LMN. glabellar, gag, jaw) LATERAL MEDULLARY STROKE: (WALLENBURG syndrome) This patient is not weak the main problem is vertigo This is the MOST COMMON BRAIN STEM STROKE V: sensory - ipsilateral numbness Spinothalamic contralateral numbness of arm and leg Sympathetic fibres: Horners ipsilateral IX, X: dysphagia and dysphonia ipsilateral soft palate weak Cerebellar peduncles off balance will fall towards lesion Diplopia due to skew deviation VIII nausea and vomiting Vertigo is the sensation of movement, patient will say im dizzy True dizziness is for the cardiologist Vertigo is for the ENT or neurologist (dus, in pseudobulbar, will find all the UMN reflexes, namely snout,

Glossopharyngeal neuralgia IX, X involvement Excruciating pain on swallowing also due to vascular loop, Rx with Tegretol, triptilline, lyrica, MRI may help with diagnoses (may visualise loop) Marchiafava Bignami necrosis of CC DR KAKAZA TUTORIAL 4/2/2011 Summary of patient with a stroke in the cerebral hemispheres: In the history ask about onset, function, localisation and high risk factors

1) ONSET: The history will be that of acute onset the patient may develop the
deficit out of the blue, or wake up with the deficit.

Page 40 of 61

Acute onset always think vascular cause, although a stroke may also have a STUTTERING course, in which case the patient was having emboli, or had progressive thrombosis, but the deficit will still usually occur over 24 hour period. If the history is that of progressive weakness, rather think tumor or granuloma (of which toxoplasmosis and TB are the most common causes)

2) MAXIMUM WEAKNESS: Ask the patient about the period of maximum weakness
what could he not do then? Is it staying the same or getting better now? (function)

3) DISTRIBUTION OF WEAKNESS: get the distribution of weakness from the patient

(drooling saliva, numbness, couldnt move) you can make diagnosis of stroke, as well as localise it, on history alone.

4) HIGH RISK FACTORS TO ASK ABOUT:

Hypertension Diabetes mellitus Smoking and alcohol (vessel hardening and atherosclerosis) HIV and ARVs HIV causes stroke by means of a) vasculitis b) endocarditis c) hypercoagubility, d) cardiomyopathy e) thrombocytopenia with bleeding. ARVs cause accelerated atherosclerosis Heart disease: young black patient from rural area think rheumatic fever; older people think atrial fibrillation which is often intermitted and can therefore be missed on clinical exam History of previous stroke, especially if theyre young Familial vasculopathy (relatives with heart problems, strokes) The young stroke = stroke in patient less than 45 years:

1) Could be due to contraceptives: estrogen may cause idiosyncratic reaction

during the first 3/12 of use where it lowers prot C and S and therefore causes hypercoagubility

2) Pregnancy is a hypercoaguble state with increased risk of thrombo-embolism

(Remember in pregnancy as well the lower albumin accelerates drug clearance often need higher doses in pregnancy)

3) Coagulopathy: the most common one is anti-phospholipid syndrome

(clotting disorder, auto-immune based) this can be an inherited trait that occurs in isolation, or it may be associated with other diseases such as SLE. This is the only syndrome proven to cause BOTH arterial and venous occlusion, therefore youll often get history of previous DVT (remember a DVT will cause PE, not stroke, unless person has a right to left shunt). There may also be a history of abortions (the venous blood in the placenta clots)

Page 41 of 61

If you dont find the cause for a stroke in a young patient it is actually good news they have less chance of having another stroke, whereas if you do find a cause in a young patient has a high risk of having another stroke in future. Coagulation profile: prot C and S, anti-phospholipid Ab, homocysteine, factor V Leyden, beta-2 glycoprotein these are specialised tests, not first line 4) low Hb may indirectly lead to stroke body will try to keep viscosity normal in severe anemia easiest bloodcell to make is platelet thats why anemic patient sometimes has thrombocytosis, which is risk factor for stroke (any increase in viscosity is risk factor, also polycythemia vera, leucocytosis)

5) hyperthyroidism may lead to intermittend atrial fibrillation (not necessarily

detectable on physical exam) ON EXAMINATION OF THE STROKE PATIENT: 1) ALWAYS do a cognitive score. A strategically placed stroke can cause dementia with one stroke, i.e. if medial temporal lobe is affected (MCA) Bilateral frontal strokes happen in patients who have only one stem of the ACA if thrombus lodges in this stem bilateral supply cut off this may cause Kluver Bucy syndrome (hypersexuality, hyperorality and placidity can have conversation with the person, seems okay, then they turn around and eat something from the floor) Pontine stroke, even small one, may cause auditory hallucinations (peduncular hallucinosis) Make sure the patient is not delirious, does not have APHASIA, and went to school before you comment on the cognitive score. 2) Bloods to do in stroke patient: FBC: for increase decrease in cells U&E: kidney failure due to HT, or as cause of dysfunctional platelets with bleed Thyroidfunction: s-glucose: DM risk for stroke RPR and TPHA: endarteritis obliterans and vasculitis Auto-immune screen: ANA, ESR, anti-DNS Ab second line test Lipogram: risk for atherosclerosis APHASIA: Due to lesion in the left hemisphere Brocas dictums says even if someone is lefthanded, the speech area is still probably in the left hemisphere. When you hear first: Ear (hears sounds, not words) sounds to association area for primary interpretation Wernickes (further interpretation) arcuate fasciculus Broca motor area for speech. (From Broca fibres also go to lexicon to get words if

Page 42 of 61

you want to respond, if you just listen and do not respond it stays in Wernicke, if you just write it goes to parieto-occipital lobe) When you speak first: it starts in Broca, not in Wernickes this you evaluate with spontaneous speech (pt tells you the history) If it is non fluent: why? If the patient struggles to find a word the problem is Brocas conduit to lexicon is broken 1. Brocas /Expressive /Motor aphasia: Pure Broca is very rare most strokes will involve both Broca and the arcuate fasciculus, often with Wernickes involved as well. With a Brocas aphasia the patient is often very depressed, because he is aware of the deficit he is trying to make himself understood but cannot express himself. The reason for this is that the retrieval of words from the internal lexicon in the parietal lobe is affected (Broca is the conduit between the lexicon (dictionary) and the motor speech area) The patient will speak in a non-fluent way with short sentences, often just verb and noun, often has to describe something rather than naming it (thing u write instead of pen), he may use neologisms, paraphasing (substituting a sound or a letter within a word youll still recognize the word, although it is not exactly correct)) and circumlocutions. Despite the problem the patient has to find a word youll understand what theyre trying to say. The difficulty the patient has expressing himself will also manifest in his writing. A patient with a stroke in Broca will have a right hemiparesis dont diagnose aphasia without this. Broca also difficulty repeating. 2. Wernickes /receptive aphasia: The patient CANNOT COMPREHEND and cannot PRODUCE MEANINGFUL language. The patient is initially not depressed it takes him a while to realise that no one understands him, and that he does not understand other people. Spontaneous speech will be fluent but will not make any sense, will be unrelated to the topic. The patient will keep to common courtesy of dialogue will make eye contact, wait for you to finish speaking before he starts again. The patient cannot read or write or tell you what the matter is make very sure the patient is not confused due to delirium before you diagnose this. Will have difficulty with repeating because he doesnt understand 3. Global (combination) aphasia:

Page 43 of 61

They are marked by a severe impairment of both understanding and expression of language. The symptoms of global aphasia are those of severe Broca's aphasia and Wernicke's aphasia combined. It is usually associated with a large lesion in the perisylvian area. It involves a "left side blowout" which includes Broca's area, Wernicke's area and the Arcuate fasciculus. There is an almost total reduction of all aspects of spoken and written language, in expression as well as comprehension. Improvement may occur in one or both areas (expressive and receptive) over time with rehabilitation. When injury initially occurs to all of these areas, the progression starts out with Global aphasia in the first 12 days due to brain swelling (cerebral edema). From there, it evolves into Brocas or Wernicke's aphasia for 13 months (usually Broca's), then it resolves into a residual anomic aphasia. Studies show that spontaneous improvement, if it happens, occurs within six months, but complete recovery is rare. Persons with global aphasia are usually mute or use repetitive vocalization. The person frequently uses simple words such as expletives. 4. Disconnection syndrome: This is due to a small lacunar infarct in the arcuate fasciculus the main problem with the disconnection syndrome is repetition. This syndrome is very rare! 5. Transcortical aphasia: Opposite to disconnection syndrome, this patient can ONLY repeat what you say. Has difficulty expressing himself either verbally or in writing. This is due to an infarct in the watershed area (usually due to sudden hypotension) between Broca and the association area. It is usually more sensory or more motor (more towards Wernicke or more towards Broca) The transcortical sensory wont understand what youre trying to say, but will be able to repeat words, whereas transcortical motor can understand bit. 6. Aphumia: The patient cannot talk, but CAN write this can easily be confused with hysteria this is when there is a small lacunar infarct just beyond Brocas (between Broca and speech area) the writing area not affected dus can get words, but cannot get them out but can write them.

Page 44 of 61

Must differentiate between aphasia (speech problems of central origin) and dysarthria (difficulty in pronunciation due to local problems) EVALUATION OF APHASIA:

1. Listen to spontaneous speech (Brocas non-fluent, circumlocution, short

sentences, neologisms, paraphrasing, Wernicke fluent but nonsense content)

2. Check comprehension start with 1 step command, increase up to 4 stepcommand, such as close your eyes, close eyes and lift left hand, close eyes, lift left hand and touch nose, close eyes, lift left hand, touch nose, lift right hand. The more complex, and the more peripheral the more difficult to do. Broca will be able to do 3 step command (comprehension intact) Wernickes cannot do at all Global aphasia can do one step

3. Naming objects to confirm diagnosis: what is this? What do we use it for? main
problem with Broca is to find the word they dont know what you call a pen or a cup, but they know what you use it for they may make a new word, or paraphrase, or describe, or just demonstrate Wernicke will not understand the instruction to name the object

4. Repeat a sentence: this test the arcuate fasciculus

Must be relatively difficult long sentence i.e. the fat cat catches the thin mouse if the arcuate fasciculus is involved the sentence will be short such as cat catches mouse (still a bit right) in Wernickes wont be able to repeat at all. Broca will also have difficulty repeating, because the arcuate is usually involved very seldom pure Broca.

5. Reading and writing: will be affected in the same way that spontaneous speech
is affected in Brocas there will be neologisms and short sentences, wrong spelling, with Wernickes it will be meaningless. How to differentiate Wernickes from wordsalad due to psychotic process the patient with Wernickes aphasia keeps to etiquette hell wait for you to finish, then hell speak, then wait for you again. DR KAKAZA TUTORIAL ABOUT HEMISPHERES 8/2/2011 Functions of lobes: 3) Parietal lobe If affected on any side, will get problems with 2-point discrimination and stereognosis, and depending on the side youll either have speech problems and Gerstman syndrome (Left hemisphere) or agnosia and apraxia (right hemisphere) Two-point discrimination is the ability to feel two stimuli at the same time. Patients with parietal lobe lesions can only feel one stimuli at a time, i.e. if they have L hemiparesis, and you touch them one the left hand side, they may be able to detect one stimulus on that

Page 45 of 61

side, but not two. If you then touch right hand side simultaneously as Left, they will not be able to feel the left hand sided stimulus anymore. Stereognosis is the ability to identify something by touch, without visual help. Lesion in either parietal lobe will give astereognosis. THE LEFT HEMISPHERE Parietal lobe Think SPEECH problems, GERSTMAN syndrome and DEPRESSION When the Left hemisphere is affected the patients get VERY DEPRESSED The left hemisphere does all the language, calculations and finger naming (reading, writing, rythmatic) If left parietal lobe is affected, you get Gertsman syndrome Gertsman syndrome:

1. Finger agnosia: the patient is disconnected from his fingers he cant

name them when he folds hands together (church without steeple hands) wont be able to tell where his pinky is, or any of the other fingers. Remember the typist who got to work and realised she couldnt type anymore without actually looking at her fingers when she didnt look, her fingers were not there.

2. Aculculia: inability to makes sense of numbers, loses even very simple

maths remember the accountant who had MVA and sustained swelling of the left hemisphere he could not even do 1+1

3. Left/Right disorientation: cannot do evun simphe L/R comoands, e6en

when they thin{ about it (touch your R ear with your L hand) If txey have all 3 Together (cant recognise fingers, nqmbers or left/right) it is called Gertsman syndrome. It means Left Parietal Lobe dxsfunction, and it implkes a big46lesion. The patient wi|l also have visual field defect (R hemi-anopia9 (telporal vision of right eye and medial vision of left eye affectEd). RIGHT HEMISRHERE: The vight hemisphere is for a2t and emotion. The hemisphere of the psychiatrisp( apraxia an agnosma is consequelce of p2oblems here neurologists dont really worry about apraxia and agnosia. AprAxia is the inability to perform an action that they knew how To perform before, not attRibutable to any motor `roblem such as weakness can do individual tasks, but cannot put them together. Dressing apraxia is easily picked up give them a shiru they wont know how to put it on, they may try and faml completely, or just havg difficulty buttoning the shirt. One of the

Page 46 of 61

main reasons for the severe disability of dementia patients is due to apraxia need total care. Agnosia: this is when you neglect something, when you cannot recognise something from very abstract such as inability to recognise humor, to concrete, such as inability to recognise familiar objects. Anosagnosia is the common type when the patient has hemi-neglect A patient with a infarct in Right hemisphere will neglect his left side. This will be noticeable in that if you stand on his left hand side he will seemingly be ignoring you, When you walk to the right hand side hell respond. The patient may even look away from the left side, as if it is not there. Because of agnosia they tend NOT to be depressed, because they dont recognise that there is a problem The patient will always have a hemi-anopia always check visual fields. (cant see the left temporal field also agnosia to the left) 2. Prosopagnosia: another common type of agnosia This is the inability to recognise familiar faces, can only recognise a person by voice and other characteristics, but not by face. FRONTAL LOBE: Personality and executive function is in the frontal lobe: Orbito-frontal syndrome disinhibition, environmental dependency, poor short term memory, inability to sustain attention, inappropriate social behaviour, including sexual disinhibition, easily distractible, mood lability, no insight) Dorso-lateral dysfunction especially executive dysfunction, the patient cannot plan, organise, execute substeps with final goal in mind. Anterior cingulate patient is typically apathetic has motor apathy, emotional apathy and cognitive apathy These syndromes are only found when there is bilateral dysfunction - such as with degenerative processes or multi-infarct dementia seldom with one stroke, unless the patient only had one stem of the ACA and the stroke/thrombus is in the stem. Gait apraxia due to frontal lobe problems also when there is extensive damage. The pt will walk tentatively, with small steps, as if on ice, as if the feet is stuck to the floor later complete inability to move, but when you put him in bed, can make walking movements on request. When you see gait apraxia in an elderly patient, think of NPH, parafalx meningioma or butterfly glioma, parkinsonsism due to drugs, or end stage PD. Cranial nerve fall-out in a cortical stroke II, V, VII do not have bilateral supply look for fall-out with them.

Page 47 of 61

Patient will have hemi-anopia (II), reduced sensation of face (V), weak lower half of face (UMN VII) this will all be on the same side as the weak side, and contralateral side to lesion. A small percentage of patients also have unilateral supply for IX, X may have soft palate weakness. If you get stroke too early may especially have more CN deficits (such as IX, X, XII) because bilateral supply takes some time to take over) DR KAKAZA TUTORIAL: 15/2/20100 CONTINUE WITH STROKE PATIENT: Reflexes: deep tendon reflexes are graded from 0-4, remember to augment (actually only distracts the patient..) 0: 1: 2: 3: 4: this is a hard LMN sign, can find it in a GBS that is still walking flicker felt or seen in muscle (remember to expose muscle) muscle contracts and some movement around joint is seen muscle contracts, brisk joint movement that spreads to other joints (biceps reflex hard UMN sign that implies clonus. This is never normal. Must get at least 5 jerks

and fingers flex, or knee reflex and adductor of other leg contracts (not 3). We only elicit it in the foot and patella Almost all normal people have a 2, but 1 and 3 can also be normal depending on the setting (someone with NO neuro sx, weakness or other UMN signs with a 3 is considered to be normal, whereas is MND, where there is severe atrophy a 2 is considered to be UNN. Asymmetry also important if 1 on one side and 2 on other think previous stroke) Babinski is a hard UMN sign (primitive reflex) the mildest form may just be flaring of the toes, the worst form is withdrawal flexor respons. Also do Oppenheim and Shadock to confirm. A mute response usually means the patient is in shock. Hoffman and finger flexion test: not a strong UMN sign but is suggestive. Patients with a normal 3 may have a Hoffman, but it becomes significant when it is associated with weakness, if it is asymmetrical or if there are other UMN signs. Crossed adductor reflex: seen in UMN lesions. Hit on adductor of knee medial and look at other leg often see it in paraplegic patient Abdominal reflex: these are the only reflexes absent in UMN disease. Not relevant if someone was previously pregnant, previous surgery or obesity. SENSATION: Spinothalamic (ST): pain, temperature and crude touch (fine fibres) Dorsal columns (DC): position, vibration and fine touch (thick fibres) Parietal lobe sensation: 2 point discrimination and stereognosia.

Page 48 of 61

You must check all sensory tracts, because ST runs anterior in cord and crosses immediately whereas the DC runs posterior and cross in the medulla. Always look for a pattern in sensory loss: Neuropathy: glove and stocking Myelopathy: level Brain stem: checkerboard Cerebral hemispheres: hemi Dermatome loss with radiculopathy Vit B 12 deficiency and HIV both gives you myelopathy with UMN, but also neuropathy with glove and stocking. Cerebellum: Dont forget the gait! If they can do tandem walking co-ordination normal Toe heel walking strong distally Squat and stand up strong proximally Lift up arms above head strong proximally Hold your fingers strong distally MARSDEN TEST: Tap index finger quickly on proximal joint of thumb. If the tapping is clumsy or slow, think: 1. Weak 2. Spastic 3. Rigid 4. Apraxia (always give leeway for non-dominant hand) Barre test: hold both arms out, patient closes eyes and counts backwards weak arm will drop, pinky will extend and arm will pronate. THE OFF-BALANCE PATIENT: 1) EPISODIC OR CONTINUOUS? If EPISODIC think EAR: The ear consists of the hearing part (cochlear) and balance part (vestibular). The vestibular part consist of semi-circular canals with endolymph, hairy cells and otoliths.

a) Acute viral vestibulitis: a few days of acute vertigo Page 49 of 61

b) Episodic positional vertigo: suddenly he becomes dizzy, but if he keeps the

head then still, the dizziness will go away this is because one of the otoliths move from its normal position and disturb the haircells. When you stand still the endolymph stops moving, and therefor the otolith and haircell stops moving vertigo goes away. Make diagnoses with the Hall Pike manoeuvre: lower the patient down over the bed so that head is lower than the bed, turn the head to the side and see nystagmus. This can also be the treatment (move head several times from side to side whilst head is low) or give symptomatic treatment (cinnarizine; (Stugeron) or beta-histine; (Serc))

c) Menieres disease: this is a degenerative and disabling condition. The patient

has constant vertigo, progressive hearing loss and a constant ringing in the ears. Treatment is to hasten the destruction of the nerve by injecting gentamicin. COCHLEAR COMPONENT OF VIII: Its job is to hear sounds. The sound goes via the nerve to Hershls gyri (receptive area for hearing). If one ear is deaf must be local problem If both ears are deaf probably still local problem This is because if one of the Hershls areas (superior temporal gyrus) is disturbed, it will not amount to hearing loss. If the problem is bilateral (strategic strokes or rarely syphilis) the patient will still hear sound, although cant differentiate words (can still hear animal sounds, something being dropped, telephone, sometimes music) because these sounds are interpreted somewhere else. Hershl decodes the sound into words, so some sounds can still be heard, but patient has an agnosia for words. This is often associated with aphasia because Hershls gyri is close to the language/speech centres. NON-EPISODIC OFF-BALANCE (ALWAYS FALLING) This is either sensory ataxia or cerebellar ataxia or brainstem pathology that catches the cerebellar pathway. SENSORY ATAXIA: This is usually in the setting of a peripheral neuropathy, when the dorsal columns for propioception are destroyed. The propioceptors tell us where our feet are, and make us look down when the ground becomes uneven. This patient may also complain of distal weakness, pain, and the feeling of having a tight shoe on, or that the feet are wrapped in cotton wool. The patient wont be able to walk at night, because they rely on their eyes not to fall.

Page 50 of 61

Sensory ataxia has a broad based gait, with the patient looking down to see where they are walking. The most common causes include B12 deficiency (postero-lateral cord syndrome), HIV and GBS. If the sensory ataxia is very severe the patient may be totally unable to walk, although he has near normal power, and can make walking movements in bed (this is called abulia, and is also seen in the gait apraxia of dementia.) Central vertigo can also be due to MS plague, brainstem problem or cerebellar problem. If in the cerebellum, expect only cerebellar signs, if in the brain stem will have CN fallout and longtract signs. Dws, if ATAXIA PLUS something else - not pure cerebellar problem. Alcohol attacks the vermis and flocculonodular lobe of the cerebellum with gait and truncal ataxia this is due to nutritional causes as well as direct toxic effects of the OH.

DR KAKAZA TUTORIAL 18/2/2011: SPINAL CORD: Symptoms suggestive of spinal cord pathology includes

1) Weakness either both lower limbs, or all 4 limbs (paraparesis or quadriparesis) 2) Sensory level patient may complain of tightness, a tight belt 3) Urinary symptoms may be presenting symptom, in which case it will be urinary
retention (bladder distends and sphincter remains closed), or, if it is a chronic, slow onset lesion the problem may be frequency and urgency more noticeable at night. This is because of bladder spasticity, and reduced capacity does not expand anymore. If the lesion is in the cauda equine it is bad news the urine dribbles the whole time, and patient will need a catheter the whole time (not intermittend catheterization as in the others) Anal sphincter symptoms will present with constipation and distended abdomen.

4) Back pain may also be complaint: if the pathology is due to vertebral collapse the
patient will feel exquisite, and very localised pain (theyll ask you to turn around and point to your back). If the vertebral collapse also involve a root it will cause a radicular pain (neuralgic). The back ache may also be a pure mechanical pain due to their struggling to walk.

Page 51 of 61

With a chronic lesion the patient may complain that their leg often kicks or flex on its own points to UMN pathology Thus, when you hear the pattern of weakness, sensory fallout and bladder problems, think MYELOPATHY ON EXAMINATION: Confirm the motor weakness, usually UMN with spasticity, Babinski and crossed adductors. Get level and remember Beevor sign. But sometimes youll find LMN signs this could be due to: 1) Shock phase in hyper acute lesion

2) Arachnoiditis (inflammation of the roots will mask UMN signs) 3) MND: truly mixed UMN and LMN, for instance wasted leg with increased
reflexes. 4) Cord lesions involving ONLY the anterior horn cells (polio)

5) ADEM: extensive lesions catching the anterior horn cells (ant horn cells serves
same purpose as the CN nuclei LMN) 6) Syrinx 7) Myelopathy with superimposed radiculopathy (CMV) 8) Myelopathy plus neuropathy (HIV, B12 deficiency, HTLV-1) 9) Cervical spondilosis The patient may also have BOTH UMN and LMN signs: LMN at the level of the lesion UMN: below the level of the lesion If you find the LMN signs you can localise the lesion to that level, for instance if biceps reflex is gone, you know level is C5, 6 or if you see atrophy of the interossei, you know level is C8, T1. Sensory examination: The patient will have a level in a myelopathy, or sometimes a suspended sensory level (can feel above and below level) that is due to central cord lesion. You MUST turn over the patient to check the sacrum and perineum check for sacral sparing which youll get with central cord lesion (sacral fibres at the very outside). You can also have sensation loss ONLY over the perineum (saddle anaesthesia) which you get with cauda equine and conus medullaris lesions. Remember to check the anal sphincter tone in the exam can help you localise lesion (S2-4)

Page 52 of 61

Remember to inspect and palpate the back, run hand down back to find gibbus, and hit lightly for any areas of tenderness. Must examine spinothalamic and dorsal columns separately. Spinothalamic: pain, temp and crude touch (finger) Dorsal columns: vibration, propioception, fine touch (cotton wool) The lesion is usually 2 segments higher than the sensory level (T10 level lesion on T8), whereas the motor level will have the same lesion level; but lesions in the cord usually not uniform, and motor and sensory lesions often dont tally take the highest level for localisation. Co-ordination difficult to test due to weakness, but if a patient can walk it will be spastic gait with scissoring (as opposed to the broad based gait you get with cerebellar and sensory ataxia) AFTER YOUVE DIAGNOSED MYELOPATHY:

1) DO MRI: this will differentiate between compressive and non-compressive

lesions. A compressive lesion needs immediate surgery (could be cold abscess due to TB, or pyogenic abscess due to strep, or metastatis or primary tumor). Anyone who still has sphincter function of a deficit with history of less than 48 hours needs immediate surgery (bladder will not recover if left longer than this) 2) If it is not a compressive lesion the causes are considered to be medical, such as

A. Infections: TB number one (gives both compressive and non-compressive)

Bilharzia, think especially of this if the lower lumbar area is affected HIV Toxoplasmosis, cysticercosis, syphilis, HSV, VSV Transverse myelitis: viral or post-viral cause, dx on MRI the whole cord will light up, but ALSO be swollen (no swelling in MS) B. Demyelinating lesions: MS gives localised demyelination Neuromyelitis optica and ADEM longer lesions Dx on MRI C. Vitamin B12 deficiency D. Vasculitis or occlusion of a vessel d/t emboli

E. Neoplasmas: if it is inside the cord they are non-compressive, can be

primary or secondary

F. Paraneoplastic syndrome: an antibody mediated condition where Ab

against the Ca cross reacts with protein in the cord death within few days.

Page 53 of 61

MYELOPATHIES can also be discussed according to ANATOMICAL LOCATIONS (CORD SYNDROMES:

1. Transverse myelitis: the whole cord is affected on horizontal level, but still
patchy (motor and sensory may not be the same) Motor: all below lesion will be affected, at the level of the lesion there will be LMN signs, and UMN below lesion Sensory: ST and DC will be affected 2. Anterior spinal artery occlusion: The anterior artery supplies more than half of the cord, and both hemispheres. Occlusion has a sudden onset, ST level, motor level, but DC intact. Atherosclerosis of the aorta is the most common cause, or AI disease in young people (SLE) 3. Syrinx: This is usually at C5. An early lesion may just disrupt DC crossing with a suspended level or neuralgic pain in shoulder. When the lesion expands it catches the anterior horn cells, and there will be atrophy at the level of the lesion (C8, T1) with pain and atrophy in the hand. The progression of a syrinx usually stops here. If the lesion still expands it will start catching tracts, and a proper sensory level will develop, but a strange level, this is because sensory fibres are laminated, with sacral fibres being on the very outside, and cervical on the very inside (med to lateral: Cx, T, L, Sacral) On the differential would be a syrinx, tumor, granuloma and plague. 4. Hemisection of the cord (Brown Sequard) Ipsilateral to the lesion weakness and DC fallout, contra-lateral to lesion will be ST fallout. Causes: anything lateral could be tumor, trauma (gang-knife violence!), VSV that tracts back into cord from the usually radiculopathy. 5. Posterolateral column syndromes: This is usually due to a destructive process, where the DC are affected and the patient has spasticity (CS affected) but no ST level. The patient can usually still walk despite extensive weakness because the spasticity keeps them upright. Vit B12 and HIV the common culprits 6. Lateral cord syndromes:

Page 54 of 61

Mainly destruction of CS with spasticity as main complaint, caused by HTLV-1, or sometimes hereditary spastic paraparesis or Cassava toxicity. HTLV-1 treated with solumedrol THE PATIENT WITH MYELOPATHY AND COGNITIVE DECLINE:

1. Vit B12 deficiency: patient with cognitive decline, paraparesis, spasticity AND
neuropathy and rarely optic neuritis. Check the psych manifestations of Vit B12 deficiency (usually paranoid)

2. HIV: usually late stage, with CD4 less than 200, often less than 50. The patient
will have a paraparesis caused by vacuoles in the postero-lateral columns (called vacuolar myelopathy). At this stage the patient will also have a superimposed, painful neuropathy, due to the virus itself. 3. Leucodystrophia: (Adrenomyeloneuropathy) This is an inherited disease with a sudden loss of the ability to myelinate, PLUS involvement of the peripheral nerves and adrenals (overweight white boy with hypogonadism and myelopathy, cognitive decline and neuropathy.

4. Syphilis: mainly the dorsal columns affected with sensory ataxia and high
steppage gait and cognitive decline. Remember: Cortical stroke: DC, ST affected same side as motor Brainstem stroke: if lateral stroke will have sensory fallout with motor spared, if medial stroke will have motor fallout but no sensory (bleed in brainstem may be much wider) Spinal cord stroke: will get dissociation between ST and DC DR KAKAZA: 21/2/20100 RADIOLOGY Compare the 4th to the lateral ventricles to decide between

communicating or obstructive hydrocephalus. The prepontine cistern should also be open

Page 55 of 61

BITS AND PIECES: Viral causes of meningitis: Any childhood viral illness, such as MMR, enterovirus, ricketsia and enterovirus Immunosuppressed patient HSV, VSV, CMV, PML Contra-indications to LP: Localising signs (may see false localising signs with raised ICP, or cranial nerve palsy due to exudates, or with infarction or thrombosis Seizures (sign of focal pathology) Local sepsis Bleeding tendencies (platelets <40, or kidney failure with dysfunctional platelets) Discolouration of lower limbs: Vascular insufficiency or neuropathy Significance of Hematuria in Neurology: Stroke Warfarin Bilharzia Auto-immune diseases Prostatic Ca with mets in spine EEG: Delta waves 1-3, very slow, Theta waves 4-7 If you see this on EEG think post-ictal, or Wernickes or hypoxic encephelopathy Anemic patient: Stool occult blood Gastroscopy Fe studies Causes of hypokalemia: Insulin therapy, diarrhoea, diuretics, drugs (steroids) Magnesium is usually supplemented with K Carphologia: lint picking in delirium Wernickes without alcohol due to bulimia, hyperemesis gravidarum, chemotherapy Steroids:

Page 56 of 61

Mineralocorticoids act on water and electrolyte metabolism Glucocorticoids have principle actions of anti-inflammatory, immunosuppressant, and metabolic effects Hydrocortisone (cortisol) is the bodys natural glucocorticoid Daily production is about 10mg if unstressed, if ill and stressed up to 300mg Circadian rhythm, lowest during sleep (early morning) Production regulated by CRH (corticotrophin releasing hormone) and ACTH (pituitary adreno-cortico-trophic hormone) under negative feedback Steroids can merge with lipids principally cellular and subcellular membranes Binds to receptors in cytosol and nuclei where it affects the transcription of genes, and ultimately produced steroid regulated proteins Most notable effect of glucocorticoids is their ability to suppress inflammation Osteoporosis, especially in the spine, a significant adverse effect SIDE EFFECTS OF CORTICOSTEROIDS: With high doses: acute onset reactions such as hyperglycemia, neuropsychiatric reactions (euphoria, behavioural and personality changes, depression and psychosis), GIT disturbances, fluid and electrolyte disturbances, hypertension, leucocytosis, susceptibility to infections With long term therapy: adrenal atrophy and inadequate adrenal response to stress. Other endocrine and metabolic complications are osteoporosis, Cushings (moon face, central obesity, stria, acne, hirsutism), dyslipidemia, growth retardation in children. Diabetes aggravated or unmasked. Myopathy, poor wound healing, easy bruising, unmasking of latent epilepsy. Gaze palsy: if stroke is in frontal lobe, will look towards the lesion Prof Baker: 1) Painful neuropathy: clinical diagnosis EMG may be normal Alcohol, diabetes and triglicerides most common causes Cause found in only 50% Rx underlying problem plus Lyrica 2) CIDP: A debilitating and chronic condition, motor more affected than sensory, pain is seldom a major problem, but it can be. GBS <4/52 rx ivig or plasmapheresis, CIDP > 8/52 Rx with prednisone Diagnose on history neurological deficit lasting longer than 4/52 3) MND: Rx with Rilutex NMDA antagonis or even Lithium

Page 57 of 61

Will have increased reflexes plus wasting an fasciculations, also pseudobulbar palsy with no gag, no snout, no jaw reflex Must exclude thyroid problems, cervical spondilosis, lead toxicity may present exactly like MND Mitochondrial disorders: Mitochondria generate ATP via the Krebs cycle (oxidative phosphorylation, electron transport chain) 1x glucose gives 36 ATP, in anaerobic metabolism 1 x glucose gives 2 ATP Mitochondrial DNA is inherited from mom When you get unrelated and confusing multisystem problem think mitochondria and screen with lactate (normal lactate does not exclude mitochondrial pathology) Huntingtons also has a mitochondrial component Patient presenting with pain on the left side of the face, ringing in left ear, no taste left side of tongue think acoustic neuroma (CNVII sensory fallout) It is usually in females > 30 y, unilateral First symptoms is VIII compression (deaf and tinnitus), then V and VII sensory fallout. VII motor fallout happens last because the motor fibres are more resilient than the sensory fibres. If the hearing loss is neurological (as in this case) the Weber test will localise to the unaffected side Radiology: MRI T1 anatomy, fluid dark T2 fluid bright Diffusion weighted MRI diffusion is random molecular motion, designed to detect random movement of H2O. White matter pathology on MRI: White matter hyperdensities divided into 2 groups, namely 1) demyelinating (myelin destroyed) or 2) dysmyelinating (does not form) Hyperintensities can be diffuse, focal or geographic Focal problems must differentiate MS from deep white matter ischemia and normal aging (leukoariosis) PML can make diagnoses on MRI the peripheral white matter is involved. Trauma: shearing occurs at the gray/white matter junction HIV encephalitis: gives diffuse white matter changes Central pontine myelinolysis: geographic white matter lesions, may look like upside down bat on MRI. Wernickes: mammilary bodies affected can see on MRI

Page 58 of 61

HSV: affects the limbic system (internal temporal lobe, hippocampus and cingulated gyrus) bilaterally. Acute hydrocephalus: will get capping of the ventricals. Anti-psychotics give beta-waves NPH presents with gait apraxia, urinary incontinence, and dementia clinical diagnosis, may have mildly dilated ventricles on scan, but if you do an LP the pressure is normal patient clinically improved after LP. IDIOPATHIC INTRA-CRANIAL HYPERTENSION: Diagnosis by exclusion. Blurry vision due to CN VI palsy (when a patient looks to the side you must not be able to see the lateral sclera) Headache, early morning, worse when coughing, patient may vomit (intracranial pressure is highest at about 2am) Pappil edema with disk swelling but normal visual acuity Causes of papiledema with normal scan: Chronic meningitis Demyelinating illness (usually unilateral edema) Papillitis (also usually unilateral) Venous sinus thrombosis Differentiation between papillitis and papiledema: With papillitis the patient is blind, whereas with papiledema vision is initially intact Papillitis is painful, whereas papil edema is asymptomatic. Parasomnias: Patients have bizarre behaviour during sleep, what they would not normally do. It often precedes neurodegenerative illness. Guillian Barre syndrome: Why increased protein in the CSF? Because the spinal roots may also be demyelinated, protein leaks from the axons in to the CSF Neuropathic gabapentin pain: Tegretol not recommended treatment, rather amytriptiline or

Page 59 of 61

Thalamus: a 3x1.5 cm structure between the lateral wall of the 3rd ventricle and the internal capsule. It is not a uniform cellular complex rather a collection of >100 nuclei. You should not see vessels in a pre-contrast CT, but with old age and atherosclerosis you may see it due to calcification How do we test for pituitary function? Prolactin, growth hormone, TSH, LH, FSH, testosterone The most important consequence of pituitary hypofunction is Addisons syndrome Syndrome of inappropriate ADH (SIADH) caused by Meningitis Stroke Convulsions Tegretol and Lithium Absent ankle reflex: may be just old age (>60y) or due to peripheral neuropathy such as DM, alcohol, drugs, HIV Synkinesia: a simultaneous movement that should not be there, such as the mouth lifting when the eye blinks. It is usually due to aberrant innervation, usually after a Bells palsy. Abnormal movements: dystonias, choreo-athetosis, hemi-ballismus, tremors,

myoclonus, tics, mannerisms, focal dystonia, tardive dyskinesia and more! Tics are more somewhat suppressible and will reduce when patient is distracted, whereas TD will worsen on distraction. The movement of the tic reduces tension of the premonitory urge. Nerve conduction: it tests the electrical impulse between 2 points. It ONLY picks up peripheral nerve damage, and not even all of that (will miss small fibre neuropathy) Types of tremors: postural, intentional, and resting Neurocutaneous syndromes: 1. Neurofibromatosis 2. Sturge Weber syndrome 3. Tuberous sclerosis They all have mental retardation, brain tumors and skin manifestations. Paraneoplastic syndromes: this is non-metastatic manifestation of malignancy, immune mediated. MG (thymoma) and dermatomyositis (breast and gyne Ca) Episodic neurological disorder:

Page 60 of 61

Headache and epilepsy the most common, also paroxysmal movement disorders, hallucinations, sleep disorders, anxiety attacks, motor tics Stress and fatigue may precipitate, and diet and drugs may affect it Usually develops in infancy, worsens over the years, and starts to get better in mid-late adult life. Voltage dependant channels (K, Na, Ca) play a role Episodic disorders with abnormal movements: Primary episodic ataxia (6 types) Attacks of imbalance and in-coordination due to gene mutations leading to disruption of K and Ca channels. The cerebellum and motor neurons have highest concentration of these channels, therefore the specific symptoms. Diagnose with EMG Triggered by stress Paroxysmal dyskinesia: Brief attacks of unilateral dystonia and choreo-athetosis without disturbance of consciousness. It may be idiopathic, familial, or due to trauma or MS. Malignant hyperthermia also voltage gated channelopathy Periodic paralysis: usually in association with K, sometimes too much, sometimes too little can present just like conversion disorder!

Page 61 of 61