Brain Imaging

1. The BBB: Excludes Substances From Entering The

Extracellular Spaces.

2. Old Brain Imaging Studies:

A. Showed Structural Pathology

B. Brains Shows As A Cold Area: A Normal Study.

C. Indications For Old Brain Imaging:

Indications: Indicates Pathologies The Imaging
Procedures Will Indicate & Visualize.
1. Vascular Diseases:
A. CVA
1. Ischemic Infarct
2. Hemorrhagic Infarct
2. Tumors:
1. Benign
2. Carcinomas: Primary Tumors
Metastatic Tumors
3. Infections
1. Abscesses
2. Herpes Encephalitis
4. Trauma:
1. Intracranial Hemorrhage
2. Cerebral Contusions
5. Brain Death

D. Brain Death:
1. Used
A. Tc99m DTPA Or
B. HMPAO
2. Dynamic Imaging Was Done For Brain Death
A. Assess Displacement Of Vascular Structures
B. Alterations In Disturbances Of Blood Flow: Obstruction
C. PIV Time: Immediate
1. Why? You Are Giving An IV Injection.
Imaging No Longer Performed Today:

3. Static Imaging: Assesses Alterations In The Blood Brain Barrier

At Site Of Pathology
PIV Time = 1 Hour
A. Mechanisms Of Localization Of The Radiopharmaceutical:
1. Simple Diffusion Of The Radiopharmaceutical Into The Site
Of Pathology
B. Radiopharmaceuticals Used In The Past:
1. Tc99m DTPA
2. Tc99m Pertechnetate
The Radiopharmaceuticals Were Normally Excluded From The
BBB & Extracellular Spaces.

The Radiopharmaceutical Would Remain In The Blood Stream.

The Target/ Non-Target Ratio On Normal Studies:

1. Cool Spots For The Brain
2. Hot Spot For Other Tissues & The Face

4. When Pathology Occurred Such As:

1. Tumors
2. Infections: Abscess
3. Infarcts
4. Infarcts
The BBB Broke Down & The Radiopharmaceutical
Entered The ECF.
Therefore: The Pathology Was A Hot Spot.

F. Imaging Of The Brain With DTPA Disappeared.

Why? Development of CT & MRI With Better Resolution
Developed.
3. New Brain Imaging:
A. PET & SPECT
1. Functional Pathology
B. The Radiopharmaceutical Crosses The BBB.
C. Normal Images Appear As Hot Spot
D. Examples Of New Radiopharmaceuticals:
1. 18 FDG: Crosses The BBB
2. Tc99m HMPAO: Lipid Soluble: Crosses The BBB
E. Gives Functional Pathology/ Metabolic Information
About The Brain.
F. However: PET & SPECT :
1. Functional Imaging Of The Brain
Can Also Be Used For Structural Pathologies
G. Functional Pathologies Assessed By PET & SPECT:
1. Neurologic Disorders: Examples
A. Epilepsy
B. Seizures
C. Parkinson’s Disease
D. Huntington’s Disease
E. Suspected Brain Death
F. Acute Stroke
G. TIA
H. Differentiation Of Recurrent Tumor From
Radiation Necrosis
2. Psychiatric Disorders: Examples
A. Alzheimer’s Dementia
B. Various Other Forms Of Dementia
C. Schizophrenia ( In Research)
H. Pathology On PET & SPECT Shows Up
Such As:
A. Cold Areas Or
B. Hotter Spots Than Normal
4. Fusion Imaging:

A. PET/CT & SPECT /CT

B. Structural Pathology & Functional Pathology Seen

C. Helps MD Make More Precise Diagnoses of Pathology.

D. Helps MD Pinpoint Exact Location Of Pathology:

Example: Tumor Location.

Summary:

1. Old Brain Imaging: DTPA & Pertechnetate

2. Functional Pathology: 18F- FDG & Tc99m HMPAO

3. Fusion Pathology:
A. Shows Structural & Functional Pathology

B. Functional Pathology If:

1. PET Scan: Hot
2. CT Scan: Normal Scan

C. Structural Pathology If:

1. PET Scan : Hot Spots
2. CT Scan: Hot Spots Or Pathologic
Images Are Seen On CT.
Questions in Brain Imaging

1. What Is Meant By Structural Pathologies:

A. Structural Pathology ?
1. Anatomical Structural Changes.
2. Changes In Structural Anatomy

2. What Is Meant By Functional Pathology ?

A. Has To Due With Neurologic Activity.

3. What Does The BBB Mean ?

A. Excludes Certain Substances From the ECF
& The Neurons Of The Brain.
B. It Keeps Substances In The Bloodstream.

4. How Do Radiopharmaceuticals: DTPA, HMPAO &

18 FDG Cross The BBB ?
And If They Do Cross The BBB How Do They Localize
In Brain Tissue ?

A. DTPA:
1. Cannot Cross The BBB.
2. Does Not Localize In Normal Brain Areas.
3. Brain In Old Imaging Was Viewed As A Cold-Cool
Spot.

B. 18 FDG & HMPAO

1. Cross The BBB
2. Pathology Shows Up As:
A. Cold Spots Or
B. Hotter Spots Than Normal
5. The Patient Needs To Be Evaluated For
A Structural Brain Pathology.
What Diagnostic Imaging Procedures Would Be The Most
Sensitive For Evaluation Of This Pathology?

A. CT & MRI:
1. Have Excellent Resolution
2. Most Sensitive For Structural Pathology.

6. Do Radiopharmaceuticals Such As HMPAO & 18 FDG

Localize In Normal Brain Areas With New SPECT/ PET
Functional Brain Imaging?
Why Do They Localize In This Way?

A. Yes: FDG & SPECT : Used For Functional Pathology.

B. 18 FDG & HMPAO:

1. Cross The BBB.
2. Are Lipid Soluble.

C. Localize In Normal Brain Areas As:

Hot To Warm To Cold Images

7. How Do HMPAO & 18 FDG Localize In the Brain?

A. Via Regional Cerebral Blood Flow (rCBF)
Directly Related To Neuronal and Brain Function.
B. When There Is Increased Blood Flow: There Is
High Amounts Of Glucose Metabolism
(The Brain Uses Glucose For Energy)
Therefore Neurons Are Active Metabolically.
C. Neurons With Decreased rCBF Leads To
Less Active Neurons Or Fewer Neurons.
D. Normal Brain:
Images Will Be Warm To Cold.
HMPAO:
A. Crosses The BBB & Attaches To Neurons
B. High Amounts; Hot Spots
C. Intermediate: Medium Spots
D. Low Amounts: Cool Spots
E. Mechanism Of Localization In Brain Tissue:
1. Not Completely Understood But Involves Crossing
The Blood Brain Barrier According To The Degreee
Of Regional Cerebral Blood Flow (rCBF) Which Is
Directly Related To The Amount Of Brain Metabolism
It Concentrates From Hot To Warm To Cool Due To The
Degree Of rCBF & Brain Metabolism/ Neuron Acitivity

F. HMPAO=Hexamethylpropyleneamineoxide

18F-FDG: 18-Fluorodeoxyglucose:
A. Most Important Part Of 18FDG=Glucose.
B. Why? Glucose Analog
C. Localization In Brain Tissue :
1. Not Completely Understood But It Involves It
Crossing The BBB According To The Degree Of
Regional Cerebral Blood Flow (rCBF), Which Is
Directly Related To Neuronal Activity & Enters A Neuron But
Does Not Get Metabolized Like Glucose.& Remains In The
Neuron. It ConcentratesFrom Hot To Warm To Cool Due To The
Degree Of rCBF And Brain Metabolism/ NeuronActivity.
8. How Do Functional Pathologies Visualize When Performing
PET Or SPECT Functional Brain Imaging ?
As A Hot Or Warm Or Cold Spot ? Why Do They Visualize This Way?

Allows You To See Normal Areas Of The Brain:

1. High Amounts= Hot
2. Intermediate =Medium
3. Low Amounts= Cool Areas
They Visualize This Way Because:
1. Relation Of Radiopharmaceutical Localization
2. Overamounts of Blood Flow Or Over Active Neuron
Metabolism = Hotter Spots.=Hotter Spots
3. Underamounts Or Lower Amounts Of Metabolism
& Lesser Amounts of RP= Cold Spots

9. For Which Pathology Did Patient Need a CT Department?

Structural Pathologies: Radiology Department
A. Shows Up On CT
B. Functional Pathology:
1. Send Them To Nuclear Medicine Department
1. SPECT With HMPAO
2. 18-FDG PET
C. Functional Pathology: Nuclear Medicine Department
1. Examples: Alzheimer’s Dementia
2. Does Not Show Up On CT Or MRI
3. Shows Up On 18 F-FDG-PET & SPECT With HMPAO

10. PET/CT &SPECT/CT

A. Look For Anatomic Structural Pathology On CT Imaging.
B. Look For Functional Pathology On PET Imaging
C. Benefits Of Fusion Imaging:
1. Pinpoints Structural Pathologic Changes & Their Location.
2. Helps MD Make Exact Localization Of Pathology
3. For The Patient: Benefits Patient With More
Helpful Treatment Regimes
11. What Are The Anatomical Landmarks Seen On Normal
Anterior Dynamic Blood Flow Studies Of The Brain:
A. Past: Always Used The Anterior View
B. Blood Vessels Seen:
1. Common Carotid Artery
2. Internal Carotid Artery
3. Vertebral Artery
4. Anterior Cerebral Artery
5. Right & Left Middle Cerebral Artery
Passes Into:
6. Superior Sagittal Sinuses:
A. Drains Blood From The Brain
To the Jugular Foramen
C. Look For Pitchfork & Middle Cerebral Arteries

12. Older Brain Imaging Uses?

A. Used Dynamic Blood Flow Studies
1. Brain Death Studies
A. Radiopharmaceuticals:
1. DTPA
2. HMPAO
B. No Activity Seen In Brain Equated
With Brain Death
C. The Only Study Of Dynamic Blood Flow
Study Used Today Is For Brain Death Studies
D. Brain Death = No Brain Activity
A. Absence Of Perfusion On Angiographic
Phase & Lack Of Cerebral Activity On
Subsequent Static Planar & SPECT
Images Confirm Brain Death
B. Advantages Over Conventional
Tc99m Pertechenetate & Tc99m DTPA
Imaging Are Conferred By Static Planar
Or SPECT Imaging
1. Renders The Examination Less Dependent
On The Radionuclide Angiographic Phase
A. Including Bolus Adequacy
B. Problems Associated With Interfering
Superficial Scalp Blood Flow & Sagittal Sinus
Activity
C. 99m TcHMPAO With SPECT Imaging Was
Was Found To Be 95.7% Sensitive For
Confirmation Of Brain Death &100% Specific
 NUCLEAR MEDICINE QUIZ

1. A) Why Does The Blood Brain Barrier Exist ?

To Prevent Passage Of Selective Toxic Substances To The Brain.

A Selective Barrier.

B) The Blood Brain Barrier Functions Because Of:

High Selective Permeability Of The Capillary Walls Of The

Brain.

2. What Does The Term Indications Refer To In Regards To An Organ

System That Is Being Imaged?

It Refers To The Pathologies In Regard To An Organ System That

One Is Imaging.

3. What Is Meant By Structural Pathologies Of The Brain?

Structural Pathologies Of The Brain Deals With Anatomic

Structural Changes Involving Abnormal Pathologies Such As A
Tumor. Imaging Of Structural Pathology Is Also Performed By
CT & MRI.

4. Name 2 Structural Pathologies Of The Brain We Can Image.

1. Vascular Diseases:
A. CVA:
1. Hemorrhagic Infarct
2. Ischemic Infarct
2. Tumors:
A. Benign
B. Malignant: Carcinomas
5. What Is Meant By Functional Pathologies Of The Brain?

Functional Pathology Involves Physiologic Functional Abnormalites

Of The Brain. On PET & SPECT Functional Pathologies Show Up
As Areas Of Hypometabolism.

6. Name 2 Functional Pathologies Of The Brain That We Can Image.

A. Neurologic:
1. Epilepsy
2. Parkinsons Disease

B. Psychiatric Disorders
1. Alzheimer’s Dementia
2. Other Forms of Dementia
C. Schizophrenia

7. A. Dynamic Blood Flow Studies Of The Brain Almost Always

Are Taken Of The Anterior View of The Patient Of The
Anterior View Of The Patient.

B. What Is The Only Pathology That Planar Dynamic Blood Flow

Imaging Is Performed Today?
1. Brain Death Studies

8. Define What PET/CT & SPECT/CT Fusion Imaging Means?

Combines The Image Of PET & CT & Superimposes The Image To

Obtain A More Precise Localization Of The Pathologic
Abnormality. The Same Applies SPECT/CT .
9. Give 3 Benefits Of SPECT/CT & SPECT/CT Fusion Imaging?

A. Gives MD Exact Pinpoint Location Of Pathology.

B. Allows Better Treatment Regimens For The Patient To Be
Performed.
C. More Accurate Diagnosis.

10. Explain The Specific Steps How Tc99m HMPAO Localizes In

Brain Tissue.

Not Completely Understood But Involves It Crossing The Blood

Brain Barrier According To The Degree Of Regional Cerebral Blood
Flow (rCBF), Which Is Directly Related To The Amount Of Brain
Metabolism/Neuron Activity & Attaches Onto A Neuron. It
Concentrates From Hot To Warm To Cool Due To The Degree Of
rCBF & Brain Metabolism / Neuronal Activity.

10. Explain The Specific Steps Of How F-18 FDG Localizes In The
Brain.

Not Completely Understood But It Involves Crossing The Blood

Brain Barrier According To The Degree Of rCBF, Which Is Directly
Related To The Amount Of Neuronal Activity & Enters A Neuron.
Following Transport From The Vascular Space Into the Brain
Parenchyma Phosphorylation Of FDG By Hexokinase Is The Rate
Limiting Step To FDG-6-PO4. & 18F-FDG-6-PO4 Remains In The
Neuron. It Concentrates From Hot To Warm To Cool Due To The
Degree Of rCBF & Neuronal Activity.
Brain Scintigraphy:

1. Nuclear Scans Begun In 1970s

2. Early Period Used: Blood Serum Albumin I 131

3. Agents Which Do Not Cross The Blood Brain Barrier:

Under Normal Conditions:
1. I 131 Albumin
2. Tc 99m Pertechnetate
3. Tc 99m Albumin
4. Tc 99m DTPA
5. Glucoheptonate
6. Tc 99m HMPAO

These Agents Under Normal Conditions Show No

Activity In Gray Or White Matter

4. Note That Pertechnetate Shows Activity

In:
1. Choriod Plexus
2. Salivary Glands
3. Thyroid Gland
4. The Mucosal Membranes
5. The Gastric Mucosa

5. Normal Cerebral Blood Flow In An Adult?

A. Approximately 50 Ml/Min/100Gr

Normal Cerebral Blood Flow In A 3-10 Year OldChild?

A. Approximately 100Ml/Min/100Gr
6. Agents That Cross The Blood Brain Barrier Under
Normal Conditions:
1. Xenon 133 Gas:
A. Used For Quantitative Measures
Of Regional Cerebral Blood Flow
2. 123 I: IMP: Iodoamphetamine:
A. Was The First Approved Cerebral
Perfusion Agent
B. Nearly Ideally Perfusion Agent
C. Presumed Mechanism: Crosses The BBB
By Passive Diffusion Due To Several Factors:
1. pH Gradients
2. Lipophilicity
3. Interaction With Non-Specific Binding Sites
D. Can Differentiate Between Cerebral Infarct
& Cerebral Ischemia
E. Maximum Brain Activity Seen in 20-30 Minutes
Post Injection
F. 70% Trapped In The Blood
G. Also Trapped in Lungs & Liver
H. Partly Excreted In The Urine
I. Localization In Cerebral Structures Stable
Up To One Hour
J. Later There is some Redistribution
Mostly Due To Movement From The
Lungs & Liver
K. Metabolism By MAO & Mixed Function Oxidases
L. The Critical Organ For 123 I-IMP Is The Lung
& Its Radiation Dose Is 0.84 Rad (8.4mGy)/6mCi
(222MBq)
 L. Phases:
1. Early Phase:
1. First 20 Minutes Of Study
2. Look For Defect
2. Late Phase:
A. 3-4 Hours Later
B. If Defect Stays = Cold = Infarct
C. If Defect Fills = Hot = Ischemia
M. Gray Matter/ White Matter Ratio: 4/1
N. Other Organs That Take Up IMP
1. Lung
2. Liver
3. Kidneys
O. Only Brain Radiopharmaceutical To
Redistribute In The Brain
. P. Widely Used In Japan
Q. No Longer Commercially Available In The USA

3. Tc99m ECD: (Neurolite Or Bicisate)

A. Ethylene L-Cystineate Dimer
B. Developed At Dupont
C. ECD Metabolism Linked To Esterase Levels
D. Advantage Of Bicisate
1. Very Stable Compound
2. Rapidly Localized In Brain Tissue
In Proportion To rCBF With Slow Clearance
3. Retained In Brain Tissue By Rapid Re-Esterification
To A Polar Metabolite That Does Not Cross the BBB
4. Therefore Maintains Residence Within The Brain Tissue
5. No Intracerebral Redistribution
6. High Ratio Of Gray/White Matter Over Time
7. Intracerebral Activity Peaks Several Minutes
After Administration: About 6% Of Dose Localizing
Within The Brain.
8. More Rapid Clearance From Blood Pool Thus
Reducing Background Activity And Increasing
Target To Background Activity

9. Better Chemical Stability With Longer Post

Preparation Shelf Half Life Of 6 Hours
 10. Better Target/Non-Target Ratio Than HMPAO
11. More Rapid Washout Than HMPAO
12. Faster Clearance From Non Target Tissues
13. Allows Earlier Injection Imaging
14. Improved Image Quality
15. Rapid Fixation In The Cerebrum Allows
For Evaluation Of Perfusion/Metabolic Status
Of Cerebrum During A Brief Interval
1-3 Minutes After Injection
16. More Stable Than Ceretec 99mTcHMPAO
17. Can Be Injected At A Later Time Period
E. Disadvantages:
1. $ 800.00 For Four Injections
2. Very Costly

Advantages of ECD Over HMPAO For SPECT Imaging

1. Better Target/Non-Target Ratio
2. More Rapid Clearance From The Bloodstream
3. Can Be Injected Up To 6 Hours After Preparation

4. 99m Tc Exametazine: Tc99m:HMPAO: Ceretec

A. Will Cross An Intact BBB
B. Methylene Blue Is Added Is Added
As A Stabilizer.
C. Believed To Metabolized By
Glutathione & Influenced By
Oxidation-Reduction State
D. How To Inject: Rapid Bolus Injection
E. Behaves Like Chemical Microspheres
F. High Extraction Ratio
1. Long Residence Time in The Brain
Without Redistribution
F. Only 40% Goes Directly To The Brain
But It Fixes In The Brain & You Are Able
To Image Up To 3-4 Hours
G. Cheaper, More Available
H. Lipophilic Agent
 I. 4-6% Of HMPAO Actually Localizes In The Brain.
J. Rapid First Pass Uptake
K. Activity Is Highest In The Gray Matter
And Is Proportional To Regional Cerebral Blood Flow (rCBF)
L. Excretion Through The GI Tract (50%)
& Kidneys (40%)
M. Should Be Injected Within 30 Minutes After
Its Preparation
N. A Stabilized Form Is Available That Can
Be Used Up To 4 Hours After Preparation.
O. The Critical Organ Is The Lacrimal Gland
With a Radiation Dose With 5.2 Rad (52 mGy/20mCi)
(740 MBQ)
These Agents Cross The Blood Brain Barrier
Enter The Cortex, Thalamus, Basal Ganglia
Cerebellum Etc But Gray Matter Takes Up These
More Than White Matter

5. 111 In DTPA:
A. Physiological Governed By CSF Flow
B. T1/2= 2.8 Days
C. Energies= 173 Kev, 247 Kev
D. Low Patient Radiation Dose
E. Low Chemical Toxicity
F. Very High Purity
G. Administration:
1. Intrathecal : L3-L4
2. 500 uCi
3. Samples: Routine Tests &Chemical Tests Of CSF
4. Keep Patient Horizontal For 2 Hours After Injection
A. Avoid Headaches
B. Avoid Changes in CSF Pressure

6. 99Tc DTPA:
A. The Common Dose Of Injection
For A Radionuclide Angiogram: 10 mCi
B. Planar Images Of The Brain
Are Obtained 1 Hour After Injection
 6. 123 HIPDM
A. Earlier Peak Activity Compared To IMP
B. Peaks At 10-15 Minutes
C. 90% Extraction Rate
D. More Stable
E. Slower Redistribution
7 Cyclic Amines:
A. 99m Tc Proplylene Amine Oxime
1. High Extraction Efficiency
2. Side Effects: Short Residence Time In
The Brain
8. Tl 201 DDC:
A. Fast Uptake
B. No Redistribution Over Many Hours
C. Disadvantage: T1/2=78 Hours
1. Give Tracer In Acute Period
D. Image Quality Not As Good As I123 Or TC99m
9. 99m Tc Pertechnetate:
A. A Patient Is Given An Injection Of Potassium
Perchlorate Before 20mCi Of 99mTcPertechnetate
The Choroid Plexus May Be Seen 1 Hour After Injection
For Static Brain Imaging.
B. If 99mTc Pertechenetate Is To Be Used In Brain Flow
Scintigraphy, The Patient Should Be Given Potassium
Perchlorate To Block the Choroid Plexus.
C. Choroid Plexus Papilloma Is A Neoplasm That Accumulates
Excessive Amounts Of Pertechenetate.

7. Metabolic Agents In Brain Imaging:

1. Tl201 Chloride
2. I123 Ligands
3. In 111 Octreotide

8. PET Agents In Brain Imaging:

1. 18F-FDG 18F: T1/2=110 Minutes
2. (15O) H20 15O: T1/2=2 Minutes
3. 13N Amino Acids 13N: T1/2= 10 Minutes
4. 11C 11C: T1/2= 20 Minutes
5. 13N Methionine
9. 99m Pertechnetate Studies:
A. Flow Phase Of Study
1. Every 1-2 Seconds It Enters TheCarotid
Arteries Then The Cerebral Arteries
Then Enters The Circle OF Willis
A. In Brain Death Tc99m Pertechnetate
Travels Up The Internal Carotid Artery
But No Further.
B. The Static Study:
1. No Activity In The Cortex In Brain Death
C. If There Is Brain Death This Agent Will Only
Cover the Rim Of The Cranial Bones And Outer
Muscle

10. Gray Matter/ White Matter Ratios:

Ceretec 2.5/1

IMP 4/1

Bicisate >5/1

11. Summary Dosages:

Ceretec 99mTcHMPAO 10-20 mCi

IMP 3-6 mCi

Bicisate 99m Tc ECD 10-30 mCi

What Dose Could Be Used 99m Tc ECD Or

99mTc HMPAO For SPECT Imaging ?
Answer: 20 mCi
12. Pharmacologic Agents That Measure Regional
Cerebrovascular Reserve:
A. Acetazolamide:
1. Clinically Accepted For Cerebral Vasodilation
In Cerebral Perfusion Imaging
B. Adenosine
C. Dipyramidole
D. Carbon Dioxide Inhalation
1. CO2 Also Leads To Moderate Increased
Cerebral Perfusion

13. Uses Of Pharmacologic Cerebrovascular Stress:

A. To Assess Cerebrovascular Reserve
Similar To Adenosine Use In Its Evalaution
Of Coronary Vascular Reserve In Myocardial
Perfusion
B. Potential Uses of Acetazolamide: Carbonic Anhydrase Inhibitor
1. Pre-Operative Evaluation Of Need For
Selective Carotid Shunting During
Carotid Endarterectomy
7. Evaluation Of TIAs
8. Hemodynamic Significance Of
Carotid Occlusive Disease

14. Most Common Nuclear Medicine Imaging

Procedures In The Brain:
A. Planar Brain Imaging:
1. Only Performed For Brain Death Studies
B. SPECT Brain Perfusion Imaging:
1. Uses A Lipophilic Agent That Crosses The BBB
2. Localizes In Normal Brain Tissue & Pathologic Processes
In Proportion To Cerebral Blood Flow.
3. Most Commonly Used Radionuclide Brain
C. PET Metabolic Brain Imaging:
1. Uses Functional Positron Emitting Radiopharmaceuticals
2. Examples:
A. 18-FDG (Glucose Analog)
B. Neuroreceptor Agents
15. Planar Radionuclide Brain Imaging : Old Brain Imaging:
Brain Death Most Common Applications:
A. Two Phases:
1. Dynamic Study Or Angiographic Study
Routinely In The Anterior View:
A. Rapid Bolus IV Injection
B. 15-20 mCi Of 99m Tc-Labelled Brain
Imaging Agent:
C. Rapid Sequential 2-3 Second Images
For 30-60 Seconds On The Arrival
Of The Radioactive Bolus In The Cerebral
Hemispheres
D. Imaging Begins When Then RP First
Appears In The Proximal Carotid Arteries
E. Delayed Static Imaging:
1. 500,000 Count View After A Delay
Of 50-60 Minutes.
D. Views Taken:
1. Anterior
2. Posterior
3. Right Lateral
4. Left Lateral
As Needed
To Determine Intracerebral Activity & Redistribution
E. Provides A Record Of The Distribution
Of The RP In The Sagittal Sinus & Cerebral
Regions Including Any Abnormal Concentrations
Or Absences.
16. Normal Planar Brain Scans:
A. Agents Used:
1. Transient Perfusion Agents: Old Brain Imaging:
A. Tc99m DTPA: (Diethylenetriaminepentaacetic Acid)
B. Tc99m Pertechnetate
2. First Pass Perfusion Agents: That Are Extracted By
Brain On First Pass
A. Tc99m HMPAO: (HexamethlypropylamineOxide)
B. Tc99m ECD: (Ethylene L-Cysteinate Dimer)
However, They Will Demonstrate Activity In The Brain
Substance (Primarily If The Gray Matter Is Compromised)
A. Clinical Reasons Include:
1. CVA
2. Tumors
3. Infections :
A. Examples:
1. Cerebral Abscess
2. Herpes Encephalitis
3. Angiographic Images:
A. Prompt Symmetric Perfusion In The Anterior
Projection (Looks Like A Trident)
B. Middle Cerebral Arteries Are Seen On The Left
& Right.
C. Anterior Cerebral Artery: Seen As A Vertical Line
Of Activity
D. Perfusion Should Extend To The Calvarial
Convexities Bilaterally
E. Symmetry Is The Hallmark Of The Arterial-Capillary
Phase.
F. Asymmetry In The Venous Phase Is Common
Due To Variations In Venous Anatomy
4. Static Imaging: Acquire 500K Counts
A. Agents Used:
1. Tc99m DTPA
2. Tc99m Pertechnetate
B. Radioactivity Does Not Lie Within The Brain
Itself.
C. Activity Lies In The Spaces That Outline The
Cerebral Hemisphers Such As:
1. The Soft Tissue
2. Calvarium
3. Subarachnoid Spaces
D. Normal Image Landmarks:
1. Posterior Views: Symmetric Transverse Sinus
2. Both Lateral Views Are Normally Obtained
A. Suprasellar & Sylvian Regions
B. The Venous Sinuses Less Well Defined
C. Activity In Soft Tissues of The Ears
Just Anterior To The Sigmoid Sinus
E. The Sagittal Sinus Is Usually Seen On Both Anterior
& Posterior Views.
F. When Tc99m Pertechnetate Is Used :
1. Choroid Plexus Is Visualized

5. Delayed Static Imaging:

A. Usually Shows Increased Activity In The Area
Of Abnormality
When ?
1. When The Integrity Of The BBB Is Compromised
Such As:
A. CVA
B. Tumors
B. Infections:
1. Cerebral Abscess
2. Herpes Encephalitis
17. SPECT Brain Imaging: Functional Perfusion Brain Imaging:
1. Uses: Lipophilic RP Agents
A. Tc99m HMPAO: (Exametazine)
B. Tc99m ECD: (Bicisate)
2. The RP Crosses The BBB.
& Are Retained By The Brain Tissue In Proportion
To Regional Cerebral Blood Flow (rCBF).
3. Thus The RP Maps The Distribution Of Brain Pefusion
In Both Normal And Pathologic Brain Tissue
4. Normal SPECT Scan Of The Brain:
A. Significantly Greater Activity In Cortical
Gray Matter Consistent With Greater Blood Flow
Than The White Matter.
B. Symmetric Activity & Greater Along The Convexities
Of The Frontal, Parietal, Temporal & Occipital
Brain Regions.
C. High Activity Is Also Seen In:
1. Subcortical Gray Matter:
A. Basal Ganglia
B. Thalamus
D. Primary Purpose Of The Imaging Study
1. Evaluate The rCBF Rather Than Structural Detail.
5. Image Interpretation:
A. Inspect The Cerebral Perfusion Images For
1. Symmetry Of Radiopharmaceutical Distribution
2. Continuity Of Perfusion In The Rim of the Cortical
Gray Matter
B. In General: Local Perfusion Is Measured As;
4. Increased Perfusion Or
5. Similar Perfusion Or
6. Decreased Perfusion
C. Pathologic Processes That Alter Local
Brain Perfusion Areas Of Increased Or Decreased
Activity Depend On Changes In Blood Flow In The Brain
 D. Clinical Applications Of SPECT:
1. Suspected Brain Death
2. Acute Stroke
3. TIA
4. Differentiation Of Recurrent Brain Tumor
From Radiation Necrosis
5. Epilepsy
6. Dementias Especially Alzheimer’s Disease
E. Brain Death Via SPECT
1. Lack Of Cerebral Activity On The Radionuclide
Angiographic Phase:
A. Includes Bolus Injection Adequacy
B. Problems Associated With Interfering
Scalp Blood Flow & Sagittal Activity
2. Brain Flow Scintigraphy Is Unaffected By
For Brain Death Is Unaffected By
Barbiturate Intoxication or Body Temperature
3. Hot Nose Sign:
A. May Be Seen In Brain Death Studies
B. Is Due To Increased Flow In The External
Carotid Circulation
4. Faint Visualization Of The Superior Sagittal Sinus
In The Absence Of Arterial Flow Is Consistent With
Brain Death
(Remember The Lights Should Dimmed During Injection
For SPECT Brain Imaging.)

18. SPECT Imaging Agents That Measure Perfusion:

A. 82 RbCl
B. 15O-H2O
C. 13N-NH3

19. Bismuth Germinate (BGO) Crystals Are Preferred

Over NaI Crystals For PET Imaging Because:
A. They Have Better Energy Resolution.
B. They More Efficient Scintillators.
C. They Are More Sensitive To 511 KeV.
20. Advantages Of PET Imaging Vs SPECT Imaging
A. PET Imaging Agents Generally Have Shorter Half Lives
B. PET Is More Sensitive.
C. PET Has Better Spatial Resolution
D. Attenuation Correction Is Possible With PET.
E. PET Has More Uniform Resolution & Higher
Sensitivity Than SPECT.

21. PET Studies Of The Brain Have Been Used For:

A. In -Vivo Quantification Of Glucose Utilization.
B. In-Vivo Quantification Of Blood Flow.
C. In-Vivo Quantification Of Blood Volume.
D. In -Vivo Quantification Of CSF Production Rates
E. In -Vivo Quantification Of Blood Brain Barrier Integrity
F. In -Vivo Quantification Of Receptor Sites.

22. Cerebral Blood Flow Volume Can Be Measured

Using 11C Or 15O Labelled CO2.

23. The Major Limitation On Determination Of Local

Cerebral Metabolic Rates Of Glucose By PET Studies
Is:
A. Size Of The Area Of Interest

24. The Local Cerebral Metabolic Rates Of Glucose

(Such As The Thalamus, Basal Ganglia And The Lobes
Of The Brain Can Be Determined By PET Studies.

25. 18F- FDG Crosses Freely Across The BBB

Via The Same Carrier Mediated Transport System
As Glucose/

26. With Respect To PET Imaging Of The Brain

The Term CMR glc Refers To:
A. Cerebral Metabolic Rate Of Glucose

27. The Normal Global CMRglc Based On Studies

In Normal Healthy Volunteers Is Appx.
30 umol Glucose.mm/100Grams Of Brain.
Neuroanatomy:

1. Divisions Of The Nervous System

A. Central Nervous System:

1. Brain &Spinal Cord
B. Peripheral Nervous System:
1. All Peripheral Nerves
C. Autonomic Nervous System
1. Parasympathetic Control
2. Sympathetic Control

2. Cells Of The Nervous System

A. Neuron: Basic Cell Of The Nervous System
1. Consists Of Three Components
A. Dendrites
1. Conduct Impulses To The Cell Body
Of The Neuron
B. The Cell Body
C. Axons:
1. Conduct Impulses Away From The Cell Body
To The Next Neuron

3. Classification Of Neurons:
A. Sensory Neurons:
1. Conduct Impulses To The Spinal Cord
Brain
B. Motor Neurons:
1. Send Impulses Away From The Spinal Cord & Brain
To the Muscles And Glands
C. Interneurons
1. Conduct Impulses From Sensory Neurons
To Motor Neurons
4. Other Cells Of The Neuronal System
A. Supporting Cells:
1. Bring The Cells Of The Neuron Tissue
Together Strucutrally & Functionally
B. Glial Cells: Neuroglia
1. Types Of Glial Cells In The CNS:
A. Astrocytes
1. Star Shaped Cells That Anchor Small Blood
Vessels To Neurons
B. Microglia:
1. Small Cells That Move Into Inflammed Brain
Tissue & Engulf By Phagocytosis The Damaged
Brain Tissue
C. Oligodendrocytes:
1. Form The Covering Myelin Sheath Of Axons
Of The Nerves
B. Schwann Cells
1. Form The Myelin Sheath On Axons In The Peripeheral
Nervous System

5. Nerve Impulses:
A. Definition:
A. Self-Propagating Wave Of Electrical Disturbance
That Travels Along The Surface Of The Neuronal
Membrane.
B. Mechanism:
A. The Stimulus Triggers The Opening Of Sodium
Channels In The Plasma Membrane Of TheNeuron
B. Sodium Enters The Neuron Leaving An Excess
Of Negative Ions Outside the Membrane Marking The
Beginning Of The Nerve Impulse. During This Period
There Is A Rise in the Action Potential
C. Calcium Maintains The Plateau Of the Action Potential.
D. Potassium Restores The Action Potential With A Drop
In The Action Potential.
E. The Relative RefractoryPeriod
1. The Period During Which Stimulation Of The Nerve
Membrane Can Activate Another Nerve Impulse
 F. The Absolute Refractory Period:
1. The Period During Which Time No Impulse Can
Be Further Activated Or Propagated.

6. The Synapse:
1.Definition:
A. The Synapse Is The Site Where Chemicals (Neurotransmitters)
Are Released From Axon Terminals Of A Pre-Synaptic Neuron
Into The Neuronal Cleft.
B. Neurotransmitters Bind To Specific Receptors On The Membrane
Of The Post Synaptic Neuron & Open Ion Channels & Thereby
Stimulate Conduction By The Membrane.
C. Neurotransmitters Include
1. Acetylcholine
2. Catecholamines: Norepinephrine, Dopamine, Epinephrine:
3. Serotonin

7. The Reflex Arc:

A. Reflex Arcs
1. Neuron Pathways Which Conduct Nerve Impulses
From Receptors To Effectors That Result In A Reflex
Such As Contraction Of A Muscle Or Secretion By A Gland
2. The Simplest Arc:
A. The 2 Neuron Arc Consisting Of Sensory Neurons
In The Spinal Cord With Motor Neurons
3. Three Neuron Arc:
A. Sensory Neurons Synapsing In The Spinal Cord
With Interneurons That Synapse With Motor Neurons
Eg. The Muscle Cell

8. The Nerve
A. The Nerve:
1. A Bundle Of Peripehral Axons
B. A Tract:
1. Is A Bundle Of Central Axons
C. The White Matter:
1. Tissue Composed Of Myelinated Axons
9. The Major Nerve Tracts:
A. The Corticospinal Tract:
1. Takes Axons & Carries Impulses From A Muscle To The Spinal
Cord White Matter To The Cerbral Cortex For Motor Function
(For Muscle Motor Movement)
B. The Spinothalamic Tract:
1. Uses Axons From The Periphery & Carries Pain & Temperature
Sensation To The Spinal Cord & Then The VPL Nucleus Of The
Thalamus & Then To The Post-Central Gyrus Of The Cerebral
Cortex
C. Dorsal Columns
D. Rubrospinal Ract
E. Tectospinal Tract
F. Spinocerebellar Tract
G. Etc.

10 Nerve Coverings: Fibrous Connective Tissues:

1. Endoneurium:
A. Surrond Individual Fibers In A Nerve

2. Perineurium:
A. Surounds A Group (Fascicle) Of Nerve Fibers

3. Epineurium:
A. Surrounds The Entire Nerve

11. The Central Nervous System Components:

A. The Cerebral Cortex
B. The Brainstem:
1. The Medulla Oblongata: Cranial Nerve Bodies 9,10,11,12
2. Pons: Cranial Nerve Bodies 5 & 7
3. Midbrain Or Mesencephalon : Cranial Nerve Bodies 3, 4 &6

12. Role Of The Gray Matter:

1. Reflex Center For Control Of Respiration
2. Heart Rate
3. Blood Vessel Diameter
13. White Matter Composition:
A. Sensory Tracts
1. Sensory Tracts In The Brainstem From The Spinal Cord
Conduct Impulses To Higher Parts Of The Brain
A. The Thalamus
B. Cerebral Cortex
B. Motor Tracts:
1. Motor Tracts Conduct Motor Impulses From The Higher Parts
Of the Brain & Spinal Cord & Eventually To Muscles & Glands

14. The Five Lobes Of The Brain

A. Frontal Lobe:
1. Anterior/ Above The Orbits& Nasal Cavities
Lower Border is 1/2” Inch Above Zygomatic Suture
2. Function:
A. Motor Muscle Function
3. Pre-Frontal Area: Conscious Thought
4. Broca’s Area: Motor Aphasia
A, In CVA (Stroke)
1. Can Understand But Garbles One’s Speech
B. Temporal Lobe:
1. Lower Border Corresponds To The
Upper Border Of The Zygoma
2. Hearing Area (Area 41)
C. Occipital Lobe:
1. Runs Above the Zygomatic Arch Down To
External Occipital Protuberance
2. Visual Association cortex And Visual Cortex
D. Parietal Lobe:
1. Lies In The Posterior Cranial Fossa Below
The Level of The Inion
2. Components:
1. Superior Parietal Lobule
2. Inferior Parietal Lobule
A. Supramarginal Gyrus
B. Angular Gyrus
 3. Function:
A. Sensory Function:
1. Receives Pain, Temperature,Propioception
& Soft & Deep Touch & Taste
B. Wernicke’s Area:
1. Sensory Aphasia: In CVA (Stroke)
A. Can Talk But Cannot Understand
E. The Insula:
1. The Fifth Lobe

16. Major Fissures Of The Brain:

A. Longitudinal Fissure:
1. Divides The Cerebrum Into 2 Hemispheres
2. Separation Is Anterior/Posterior
3. Fissure Also Contains The Falx Cerebri.
Which Is An Extension Of The Dura Mater

B. Transverse Fissure:
1. Separates The Cerebrum From The Cerebellum

C. Central Fissure of Rolando

1. Separates Frontal And Parietal Lobes

D. Lateral Sylvian Fissure:

1. Separates The Frontal & Parietal Lobes
Above & Temporal Lobe Below

E. Parietal/ Occipital Fissure:

1. Separates Parietal Lobe & Occipital Lobe
17. Components Of The Brain:

A. Cerebral Cortex
1. Largest & Most Prominent Part Of The Brain
2. Has Two Hemispheres
3. The Layers:
A. Molecular Or Plexiform Layer
B. The External Granular Layer
C. The External Pyramidal Layer
D. The Internal Granular Layer
E. The Internal Pyramidal Layer
F. The Multiform Or Fusiform Layer
4. The Cellular Components:
A. Pyramidal Cells
B. Stellate or Granule Cells
C. Stellate Or Star Pyramidal Cells
D. Fusiform Cells
E. Horizontal Cells Of Cajal
F. Cells Of Martinotti (Cells With Ascending Axons)
5. Functions:
A. Governs All Higher Mental Processes
B. Stimulates Sensation
C. Controls Motor Activities
D. Center of Reason, Intellect, Memory, Language
Consciousness
B. Diencephalom
1. Located Between The Cerebrum
& Mesencephalon
2. Components
A. Epithalamus: Pineal Gland
B. Thalamus
C. Hypothalamus
D. Subthalamus
3. Lies Near The Third Ventricle
4. Hypothalamus:
A. Connects To The Pituitary Gland
B. Sends Releasing Factors & Hormones
To The Pituitary Gland
C. Major Control Center For:
1. The Autonomic Nervous System Viz.
A. Parasympathetic System
1. Relaxation
B. The Sympathetic System:
1. Fight Or Flight Response
D. Contains Centers For:
1. Appetite
2. Wakefulness
3. Pleasure
5. Thalamus:
A. Anatomy:
1. Dumbell Shaped Masses Of Gray Matter Just
Below The Cerebral Cortex
B. Functions:
1. Relays Sensory Impulses From The Spinal Cord
& Brainstem To The Cerebral Cortex
2. Produces Pleasant & Unpleasant Emotions
6. Epithalamus: Pineal Gland
A. Functions:
1. In Control Of Day /Night Wake Cycles
2. Secretes The Hormone Melatonin For Control
Of Day/Night Wake Cycle
C. Limbic System:
A. Components:
Amygdala
Hippocampus
Fornix
Cingulate Gyrus
Parahippocampal Gyrus
B. Function:
1. Emotional Center Of Body

D. Deep Nuclei:
1. The Caudate Nucleus
2. Putamen
3. Globus Pallidus

E. The Midbrain: Mesencephalon:

1. Smallest Aspect Of The Brainstem
2. Extends From the Pons To the Diencephalon
3. Rests On The Sphenoid Bone
4. Function:
A. Hearing & Visual Reflexes
F. Pons
1. Bridge Between The Midbrain
& The Medulla Oblongata
2. Function:
Relays Information Between The Cerebrum
& The Cerebellum
E. The Medulla Oblongata:
1. Most Inferior Portion Of The Brain Stem
2. Continuous With The Spinal Cord
3. Function:
A. Controls Heart Rate, Respiration, Blood Pressure
4. The Cerebellum:
A. The Second Largest Part Of The Brain
B. The Basic Structure:
1. Flocculonodular Lobe
2. Paleocerebellum :
A. The Anterior Lobe
3. Neocerebellum
A. Posterior Lobe
4. The Vermis
C. The Layers Of The Cerebellar Cortex:
1. Molecular Layer
A. Basket Cells
B. Outer Stellate Cells
2. The Purkinje Layer:
A. Purkinje Cells
3. The Granular Layer:
A. Granule Cells
B. Golgi Type II Cells
C. Glomerulus
D. Nuclei:
1. Dentate Nucleus
2. Emboliform Nucleus
3. Globose Nucleus
4. Fastigial Nucleus
E. Disease Of The Midline Zone Of The Cerebellum:
1. Broad Base Stance And Gait
2. Titubation: Rythmic Tremor of The Body Or Head
3. Rotated Or Tilted Posture Of The Head
4. Ocular Motor Disorders: Oscillatory Movements
F. Disease Of The Lateral Zone Of The Cerebellum:
1. Hypotonia
2. Dysarthria
3. Dysmetria
4. Dysadiadokinesia: Decomposition Of Movement
5. Ataxia
6. Tremor
7. Oculomotor Disorders
E. The Peduncles:
1. Superior Cerebellar Peduncle
A. Fastigiobulbar Tracts
B. Afferents From The Ventral Spinocerebellar Tract
2. Middle Cerebellar Peduncle:
A. Major Projections To Pontine Nuclei Via
Pontocerebellar or Transverse Pontine Fibers
3 Inferior & Middle Cerebellar Peduncles
A. Spinocerebellar Tracts
B. Cuneocerebellar Tracts
C. Olivocerebellar Tracts
E. Fibers;
1. Climbing Fibers
2. Mossy Fibers

19. The Gray Matter

A. Groups Of Cell Bodies &Dendrites
B. On The Surface Called : The Cortex
C. Deep in The Brain called: TheNuclei

20. White Matter:

A. Bundles Of Axons & Myelin Sheaths
B. Forms The Conduction Pathways Of Nerve
Tracts Which Propagate Messages From
One Area Of Gray Matter To The Next Gray
Matter
21. The Meninges: Covering Of The Brain
A. Dura Mater
1. Tough Outer Layer Of the Brain
That Lines The Cranial Cavity &
Spinal Cord
B. Arachnoid:
1. Non-Vascular Membrane Passing Over
The Sulci Dipping Into It & Extends
As A Perineural Epithelium Along The
Roots Of The Cranial Nerves.
C. Pia Mater:
1. Forms The Perivascular Space
D. Subarachnod Space:
1. Between The Arachnoid & Pia Mater
A Cobweb Like Trabeculae From Pia
Mater To Arachnoid 2
22. The Ventricles
A. The Choroid Plexus Produces The CSF
In The 3rd Ventricle & Lateral Ventricles.
They Are Projections Of Arterial Capillaries
Into The Ependyma
1. Function Of CSF:
A. Bathes & Protects The Brain & Spinal Cord
B. Provides A Protective Cushion
C. Contains Electrolytes, Water & Proteins
2. Pathophysiology:
A. 400-500 Ml/ Day Of CSF Is Formed In Adults
B. Volumes:
1. Range Of CSF: 120-150 Ml Of
Which 40 Ml Is In The Ventricular System
3. Components Of The CSF:
1. NaCl: Increased In CSF Compared To Plasma
2. Glucose, Ca, PO4, Uric Acid Levels Decreased
In CSF Compared To Plasma
3. Proteins
4. Recumbent CSF Pressure: 60-120 mm H20
Sitting CSF Pressure: 200-300 mm H20
 B. Promotes Ultrafiltration And Secretion of CSF.
C. Fluid Filled Cavities Within The Brain
Where CSF Fluid Flows.
D.CSF Flows From The Lateral Ventricles
To The Third Ventricle Through The
Interventricular Foramen: The Foramen
Of Monro
E. From The Posterior 3rd Ventricle
Through The Acqueduct Of Sylvius
To the 4th Ventricle.
F. From the 4thVentricle Through
The Foramina of Magendie & Luscka
To the Subarachnoid Space.

23. The Venous Sinuses:

A. Are Channels Between The Layers Of
The Dura Mater
B. Components:
1. Superior Sagittal Sinus
A. Runs From Glabella To Inion
2. Inferior Sagittal Sinus
3. Rectus Sinus
4. The Great Cerebral Vein Of Galen
5. Pterygoid Plexus
6. Petrosal Sinuses: Superior & Inferior
7. Cavernous Sinus
8. The 2 Transverse Sinuses:
A. At Inion It Travels Lateral To &
Posterior: Opposite The Base Of
The Mastoid Process.
5. Sigmoid Sinus
6. Internal Jugular Foramen
24. The Cisterns:
A. Actual Continuations Of The Arachnoid Space.
B. Hold Large Quantities Of CSF
C. Examples Of Cisterns
1. Chiasmaticus
2. Interpenducularis
3. Superior
4. The Superior Magna
5. Cistern Of The Corpus Callosum
6. Cistern Of The Filum Terminale
25. Peripheral Nervous System:
A. Cranial Nerves:

Cranial Nerves Function

1. Olfactory Smell

2. Optic Vision

3. Oculomotor Eye Movements

4. Troclear Eye Movements

(Superior Oblique Muscle)

5. Trigeminal Sensation Of The Face, Scalp & Teeth

Chewing: Mastication Muscles

6. Abducens Eye Movements

(Lateral Rectus Muscle)

7. Facial Muscles Of Facial Expression

Sense Of Taste

8. Vestibulocochlear Hearing
Sense Of Balance

9. Glossopharyngeal Sensory To Throat, Taste

& Deglutition: Swallowing
Secretion Of Saliva

10. Vagus Sensory To the Throat, Larynx, Thoracic &

Abdominal Cavity; Swallowing, Voice Production,
Slows Heart Rate, Acceleration Of Peristalsis

11. Spinal Accessory Shoulder Movements & Movements Of

The Head (Sternocleidomastoid Muscles)

12. Hypoglossal Tongue Movements

B. Spinal Nerves:
8 Cervical Nerves
12 Thoracic Nerves
5 Lumbar Nerves
5 Sacral Nerves
1 Coccygeal Nerve

Functions:
A. Sensory & Motor
B. Sensations Described In Dermatomes

26. Structure Of The Spinal Cord:

A. Outer Part
1. Composed Of Many Tracts of Myelinated Axons
B. Inner Part:
1. Composed Of Cell Bodies & Unmyelinated Fibers

C. General Components Of The Outer Part Of The

Spinal Cord
1. Anterior Compartment:
A. Anterior Corticospinal Tract
B. Anterior Spinothalamic Tract
C. Reticulospinal Tract
D. Tectospinal Tract

2. Lateral Outer Component:

A. Lateral Corticospinal Tract
1. Carries Motor Function From The Brain
To The Muscles
2. The Pathway:
The Motor Pathway Begins From the Motor
Cortex ( The Pre-Central Gyrus. Then->
Travels Down To The Pyramids In The Medulla.
Then Decussates In The Pyramids. Then
Descends ->In The Lateral Corticospinal Tract.
Then Synapses Directly On The Alpha & Gamma
Motor Neurons In Lamina IX.
 3. Corticospinal Tract Lesions:
Rostral To The Pyramidal Decussation:
A. Contralateral Spasticity
B. Muscle Weakness
C. Positive Babinski Sign

B. Lateral Spinothalamic Tract:

1. Carries Pain & Temperature Impulses
2. Pathways:
The Axons Cross Anterior To The Central
Canal In The Ventral White Commissure
& Then Rostrally In The Anerolateral
Funiculus To Ventral Posterior Lateral Nucleus
(VPL) Of The Thalamus Then To The
Somatosensory Cortex(3,1,2) Of The
PostCentral Gyrus Of The Brain Cortex

C. Anterior & Posterior Spinocerebellar Tracts

3. Posterior Outer Component

A. Dorsal Columns:
1. Carry Propioceptive Impulses To The Brain
From The Periphery.
B. The Pathway:
1. The Fibers Start From Muscle Spindles (1A Fibers)
& Golgi Tendon Organs (1B Fibers)
Ascend In The Posterior Funiculus &
Form Fasciculus Gracilis From The Legs
& Fasciculus Cuneatus From The Upper Limbs
& Terminate In Their Respective Nuclei.
Then Cross To the Opposite Side In
The Decussation Of The Medial Lemniscus.
Ascend As The Medial Lemniscus &Terminate In The
VPL Of The Thalamus.
Then Continue To The Post-Central Gyrus
Of The Cerebral (Somatosensory ) Cortex
C. Injury To The Lemniscal Pathways:
1. Inability To Recognize Limb Position
2. Asterognosis:
A. Loss Or Impairment To Recognize
Common Objects Such As Keys, Coins
By Handling Them With Your Eyes Closed
3. Loss Of Two Point Discrimination
4. Loss Of Vibratory Sense
5. Positive Romberg Sign:
A. Stand With Feet Placed Together
B. Compare The Amount Of Sway
With The Eyes Open Compared To
Eyes Closed.
C. A Positive Romberg Sign =
Actual Loss Of Balance With Eyes
Closed Due To Deficiency In Conscious
Recognition of Muscle & Joint Position.
27. The Autonomic Nervous System:
1. Definition:
A. Consists Of Motor Neurons That
1. Conduct Impulses From The CNS
A. Cardiac Muscle
B. Smooth Muscle
C. Glandular Epithelial Tissue
B. Regulation:
1. Body’s Autonomic Or Involuntary Function

2. Structure:
A. Pre-Ganglionic Autonomic Neurons Conduct From
The Spinal Cord Or Brainstem To The Autonomic Ganglion
B. Post-Ganglionic Neurons Conduct From The Autonomic Ganglia To:
1. Cardiac Muscle
2. Smooth Muscle
3. Epithelial Glandular Tissue
C. Autonomic Or Visceral Effectors:
1. The Tissues To Which The Autonomic Neurons
Conduct Impulses:
A. Cardiac Muscle, Smooth Muscle &
B. Epithelial Glandular Tissue

3. Divisions Of The Autonomic Nervous System:

A. Sympathetic Nervous System
B. Parasympathetic Nervous System

4. Conduction Pathways:
A. Sensory Pathways
1. Consist of Two Neuron Relays:
A. Pre-Ganglionic Neurons
1. From The CNS To Autonomic Ganglia
Synapses With Post Ganglionic Neurons
B. The Post Ganglionic Neurons:
1. From The Ganglia To The Visceral Effectors
A. Cardiac Muscle
B. Smooth Muscle
C. Epithelial Glandular Tissue
 B. Motor Pathways:
1. Motor Neurons Conduct From The CNS
To Somatic Effectors Viz:
1. With Intervening Synapses

The Sympathetic Nervous System:

A. Structure:
Dendrites & Cell Bodies Of The Sympathetic
Pre-Ganglionic Neurons Are Located :
A. In The Gray Matter Of The Thoracic & Lumbar
Segments Of The Spinal Cord
B. Axons:
A. Leave The Spinal Cord In The Anterior Roots Of The
Spinal Nerves
B. Extend To The Sympathetic Ganglion Chain &
C. There They Synapse With Post Ganglionic Neurons
Whose Axons Extend To The Spinal Nerves To Terminate
In Visceral Effectors.
C. The Chain Of Sympathetic Ganglions Are:
1. Located Anterolaterally
On The Spinal Column
D. Functions of the Sympathetic Control:
A. Acceleration of the Heart Rate
B. Constriction Of Blood Vessels
C. Dilates Blood Vessels In Skeletal Muscle
D. Decreases Peristalsis
E. Inhibits Defecation
F. Closes The Urinary & Anal Sphincter
G. Dilates The Iris To Cause Pupillary Dilation
H. Inhibits The Ciliary Muscles For Accomodation
Of Far Vision
I. Stimulates The Hair Arrector Pili Muscles Causing
Goose Bump
J. Increases Epinephrine Secretion By The Adrenal Medulla
K. Increases Sweat Secretion By the Sweat Glands
L Decreases Secretion Of Digestive Juices
Summary of Function Of Sympathetic Nervous System:
A. Serves As The Emergency Or Stress System
1. During Strenous Exercise
2. Or Strong Emotions Such As Anger, Fear Or Anxiety
B. Combines The Flight Or Fight Response

The Parasympathetic Nervous System:

1. Structure:
A. Pre-Ganglionic Neurons
1. Have Their Cell Bodies & Dendrites In The Gray
Matter Of The Brainstem &Sacrum Of The Spinal Cord
B. Pre-Ganglionic Neurons Terminate In The Parasympathetic
Ganglia Located In:
1. The Head &
2. Thoracic& Abdominal Cavities
Close To The Visceral Effectors
1. Cardiac Muscle
2. Smooth Muscle
3. Glandular Epithelial Tissue: Example: The Celiac Plexus
C. Each Parasympathetic Neuron Synapses With:
1. Post-Ganglionic Neurons To Only One Effector
D. Functions
1. Reduction In The Heart Rate
2. Increases Peristalsis &Aids In Digestion
3. Contraction Of The Bladder
4. Opens The Sphincters For Defecation & Voiding
5. Causes Iris To Contract
6. Stimulation Of The Ciliary Fibers For Near Vision
7. Increases Secretion of Digestive Juices Such As HCl
Of The Digestive Glands

E. Summary Of Function Of Function Of The Parasympathetic Nervous

System
1. Dominates Control Of Every Day Normal Conditions
Neurologic Topics:

Epilepsy:

A. First Treat With Medication.

B. If Refractory To Medical Treatment
Diagnose The Site Of Epilepsy by Brain Scan
C. Then Remove Epileptic Focus By
Surgery

D. Diagnostic Examinations:
1. Neurologic Examination
2. Physical Examination
3. EEG/ Scalp EEG
4. CT/ MRI
5. Wade Test: Analyzes The Side Of Brain In Memory Or Language

E. Types Of EEGS;
1. Interictal EEGs: To Discern The Side OF Brain’s Epileptic Focus
2. Prolonged Monitoring EEG: To Obtain Information About Ictus Phase
3. Brain Surgical Depth Electrodes:
A. Via Sterotactic Surgery
1. Interictal Or Ictal

F. Diagnostic Tests:
1. PET Scans: 18F-FDG (Metabolic Agents)
A. Choice For Evaluating Metabolism
2. SPECT: Ceretec(HMPAO) Or Bicisate (ECD) (Perfusion Agents)
A. Evaluation Of Perfusion Status
G.PET Scans:
1. FDG Localizes The Source Of Epileptic Focus
Not Visualized Many Times By CT Or MRI
Or Depth Placed Electrodes

H. Dr. Antar MD/PhD Research: At Cleveland Clinic

1. Position Head At Required Tilt
Why? Temporal Lobe Is Not Horizontal

I. Seizure Disorders: Epileptic Foci:

Interictal Period Ictal Phase Post Ictal Phase

Hypoperfusion Hyperperfusion Hyperperfusion

On SPECT On SPECT On SPECT

Decreased Metabolism Increased Metabolism Increased Metabolism

On PET On PET On PET

J. Ictal SPECT Imaging:

1 .Uses: 99m TcHMPAO or ECD

A. Do Not Redistribute
B. Can Be Injected Duriing A Seizure Or Within
30 Seconds After Its Completion
2. Hospitalization Needed With Monitoring EEG
3. The RP Is Injected During The Seizure.
4. Diagnosis:
A. Epileptogenic Focus Appears As
Area Of Increased Activity (Hyperperfusion)
B. May Involve Entire Temporal Lobe Or Small Mesial Focus
5. Sensitivity: 85-90%
K. Interictal SPECT Imaging;
1. Blood Flow Between Seizures To Epileptic Focus
Is Normal Or Reduced
2. Decreased Uptake Of HMPAO ( Hypoperfusion)
3. Several Patterns Recognized:
A. Decreased Temporal Lobe Activity
More Pronounced Laterally Than Mesially.
B. With Mesial Temporal Lobe Epilepsy:
1. Assymetrically Decreased Bilateral Temporal
Perfusion
2. Decreased Temporal Lobe Activity With
Ipsilateral Decreased Frontal Lobe Perfusion
4. Interictal Seizure Focus Causes An Increased
In Regional Cerebral Blood Flow
5. Sensitivty: 70%

L. Conclusions:
Thus : Epileptic Seizure Foci Typically Show
Increased Uptake Of the HMPAO During The
Ictal Phase And Decreased Uptake During
Interictal Phase .

L. PET Imaging:
A. With 15O-Water Or15 Carbon Dioxide Or
133 Xe Imaging With A Multiprobe Detector
Quantify Absolute Regional Cerebral Blood Flow.
B Study
A. Interictal Glucose Hypometabolism
& Hypoperfusion
C. Sensitivity Studies:
1. Ictal Studies More Sensitive Than Interictal
Studies For Temporal Lobe Seizures
A. Sensitivity:
1. Ictal : 85-95%
2. Interictal: 75%
N. Partial Focal Epilepsy:
1. May Benefit Surgical Intervention
2. Most Common Pathology At These Foci:
A. Mesial Temporal Sclerosis
3. 70% Of Patients With Partial Temporal
Lobectomy Experience Amelioration
& Eradication Of Seizures.

O. Intraictal Findings In Focal Seizure

Disorders On A Functional Brain Scan
May Include A Localized Area Of Increased
Uptake

Cerebrovascular Accident (CVA)

1. Causes Of CVAs:
A. Thrombotic Infarct
B. Embolic Infarct
C. Ischemic Infarct
D. Complete Infarct

2. Site Of A CVA Correlates With Specific

Blood Vessel Supply.
A. Anterior Cerebral Artery
1. Close To Midline On Anterior, Posterior,
&Vertex Views
B. Middle Cerebral Artery: More Common Site
C. Posterior Cerebral Artery
1. Least Common Site
2. Branches:
A. Temporal Branches
1. More Lateral Than Occipital Branches
B. Occipital Branches
1. Triangular With Base Next To
Posterior Peripheral Skull On Lateral Views

3. Types Of Infarcts:
A. Laminar Cortical Necrosis
B. Watershed Infarction
1. Area Between Main Arterial Branches
4. Flip-Flop Perfusion Is First Seen On Blood
Brain Imaging In The First Few Days
.
Flip-Flop Phenomenon:
Arterial Phase : Early Phase: Decreased Activity
Venous Phase: later Phase: Increased Activity
Static Image: Increased Activity
5. Luxury Perfusion:
A. Increased Blood Flow To An Infarct
Due To Uncoupling Of Metabolism
Seen Typicaly 5 Days After An Infarct
6. Diagnostic Procedures In CVA
A. Flow Study
1. Anterior or Posterior Views
2. Anterior View Best For Head & Neck Region
B. Immediate Post Injection BP Study:
1. Good For Arterio-Venous Malformation
C. Delayed Views:
1. Wait At Least 30 Minutes For Up To 2-3 Hours
2. Take All Four Views: Anterior, Posterior, R Lateral,
L Lateral Views & SPECT
3. Look At The Major Territory of Blood Supply
Of Brain
4. Also Take A Dome Or Vertex View
7. Diagnosis Via Nuclear Scans:
A. Acute Phase Of CVA
1. First Hours To 2-3 Days After Stroke
2. Requires A Break In The BBB
3. A Reduction In The Blood Flow To Affected Areas
4. A Cold Spot Or Cold Area: Most Sensitive Sign
B. Subacute Phase Of CVA:
1. 1-3 Weeks After Onset
2. Brain Spect Perfusion Complicated By
Increased Or “ Luxury” Perfusion Viz
The Blood Supply Is Greater Than Metabolically
Required Because The Cells Are already Dead Or
Dying
(Luxury Perfusion: A Phenomenon Of High Blood
Flow In Areas Of The Brain Involved In Non-Acute Infarction)
 C. Chronic Phase Of CVA:
1. One Month After Symptom Onset
2. Luxury Perfusion Has Generally Subsided
3. Perfusion Deficits Seen On SPECT Imaging Stabilize
4. SPECT Is Limited Us In The Chronic Phase OF Stroke
3. Intense Rim
4. Good Prognostic Sign

CVA Due To Cerebral Hemorrhage:

1. Causes: Rupture Of Arterial Vessel
2. Less Common Cause OF CVA.
3. More Extensive Damage
4. More Damage To Brain
5. Invades Distribution of Involved Artery
But Also Adjacent Areas Involved
A. Due To Penetration Of Blood Into
Brain Substance With An Irregular Pattern

Crossed Cerebellar Diaschisis:

1. Seen Primarily In Cortical Stroke
2. A Common Phenomenon During
The Acute & Subacute Phases Of Stroke.
3. Should Not Be Confused With
Primary Cerebellar Ischemia Or Other
Pathology

Extradural Hematoma:
1. Definition:
A. Rupture Of The Middle Meningeal Veins
2. Scans:
A. Flow Pattern;
1. Unilateral Flattening of the Flow Pattern
On One Side
2. Contracoup Lesions From Trauma
Subdural Hematoma
1. Shows Bilaterally Reduced Flow On Dynamic Images
With Increased Uptake On Delayed Images
2. Glucoheptonate Which Usually Does Not Cross
the BBB; Crosses The BBB & Fills In A Subdural Hematoma.
3. Shows A Peripheral Crescent Shaped Area Of
Increased Tc-DTPA Uptake Best
Venous Sinus Thrombosis:
1. Often Occurs After:
A. Otitis Media
B. Mastoiditis
C. Sinusiitis
D. Trauma
2. Presents As A Large Cold Area.

Transient Ischemic Attack:

1. In The Setting Of A Normal CT Scan, SPECT & PET
Imaging May Be The Only Technique That Demonstrates
An Abnormality.
2. SPECT Imaging:
A. Any Focal Hypoperfusion Defect Is Consistent
With Clinical Symptoms OF TIA
B. The Sensitivity Is Time Sensitive:
1. 60% Of These Perfusion Defects Are
Detected In the First 24 Hours
2. Less Than 40% of These Perfusion Defects
Are Detected 1 Week After The insult.
C. When Decreased Blood Flow To The Brain
Is Caused By Carotid Stenosis, O2 Supply
To The Brain Is Maintained By Autoregulatory
Compensatiory Vasodilatation Distal To The Site
Of the Stenosis.
D. Autoregulatory Mechanisms
1. May Play A Role In Vasodilatation Distal
To The Site Of Carotid Stenosis
E. Danger Of Ischemia & Stroke Increase With:
1. Increased Vasodilatation Operative
With Little Reserve
 F. The Diamox (Acetazolamide) Test:
With SPECT Brain Perfusion Imaging Is Used/
1. Normal Patient:
1. Increased CBF 3-4 Times With Diamox
2. Areas Of The Brain Where Regional Perfusion
Reserves Are Decreased: Decreased Perfusion
1. Regional Perfusion Defect On SPECT
With Diamox
Why? Autoregulatory Vasodilation Mechanism
Already Maximal.
3. In The Diamox Challenge Study Vascular Disease
Will Appear As Decreased Perfusion After The Use Of
Diamox.
G. Conclusion:
1. 60% Of Patients With TIA Progress To Complete
Stroke.
2. Information May Be Used To Identify High Risk
Patients For:
A. Medical Intervention Or
B. Surgical Intervention
3. A Normal SPECT Perfusion Imaging Study:
A. Valuable Indicator of Low Risk For Stroke

Subarachnoid Hemorrhage:
1. Neurologic Deficits Within Several Weeks Of SAH
Usually The Result Of:
A. Vasospasm Induced Cerebral Ischemia
2. SPECT Imaging:
A. Defines Ischemic Areas
B. Allows For Proper Treatment Of
1. Vasospasm
2. Accompanying Ischemia
Arteriovenous Malformation:
A. Network Of Distended Dilated Vessels
B. Most Common Sites:
1. Circle OF Willis
2. The Convexity
C. Asymptomatic Or Symptomatic
D. Early Flow Images:
1. Cold Area Due To Tortuosity
2. As Time Goes On: Activity Develops There
3. Intense Activity In A Small Space Is Noted
E. Using 99m Tc-RBCs:
1. Intense Uptake On Delayed Images
E. Definitive Dx: CT/MRI

Brain Tumors:
1. 201 Tl: SPECT Brain Perfusion Imaging:
A. Localized Defects That Correspond
To The Mass Lesions
2. Used In Conjunction With Thallium 201
May Distinquish Radiation Necrosis
From Brain Tumors
A. In Malignant Gliomas Treated With
Radiotherapy.
B. May Also Be Used To Localize Recurrences
For Biopsy.
3. Tc99m HMPAO SPECT:
A. Images Show A Focal Defect
In The Region Containing Necrotic
Tissue, Recurrent Tumor Or Both
B. Grades of Activity:
1. Low Grade: Less Than Scalp Activity
2. Moderate Grade: Equal Or Up To
Twice Scalp Activity
3. High Grade: Greater Than Scalp Activity
C. Increased Thallium Activity In The Region
Of HMPAO Defect:
1. Indicative of Tumor Recurrence
D. Low Degree Of Increased Thallium Activity
1. Consistent With Radiation Necrosis
4. 18 F-FDG PET Scans & Brain Tumors:
A. Permits Differentiation Of Recurrent
Hypermetabolic Brain Neoplasia From
Hypometabolic Radiation Necrosis
B. In Patients With Astrocytomas FDG-PET
Studies Have Shown A Linear Correlation
Between Glucose Metabolic Rate & Histologic
Grade.
C. Glucocorticoids May Affect Testing:
Why? Steroid Affect Glucose Metabolism

Crossed Cerebellar Diaschisis

A. A Common Benign Physiologic Condition
Seen on PET Or SPECT Imaging In
1. Supratentorial Lesions:
A. Tumors
B. Stroke
C. Trauma
B. Mechanism:
1. Increased Activity In The Cerebellar
Hemisphere Contralateral To The Supratentorial
Abnormality Due To Increased Blood Flow To The
Cerebellum After A Loss Of Suppressive Neural
Activity From The Contralateral Cortex
C. Do Not Mistake It For A Cerebellar Lesion

Activities With Various Radiopharmaceuticals:

Ceretec Gallium Thallium DTPA

AIDS Decreased Increased Increased Increased

Activity Activity Activity Activity

Lymphoma Decreased Increased Increased Increased

Activity Activity Activity Activity

Vs

Infections Increased Increased Decreased Increased

Toxoplasmosis Activity Activity Activity
Dementia
1. Clinical Findings:
A. Language Difficulties
B. Memory Problems
C. Visual/ Spatial Defects
D. Personality Changes
E. Abstraction/Cognitive Defects
F. Mathematical Defects
G. Poor Comprehension
H. Inappropriate Behaviors
I. Agitation
J. Confusion

2. General Management Of Dementias:

A. Assistance From The Family
& Encourage Caregivers To Participate
In Educational Programs
B. Reassurance Of The Patient
C. Light Restraints If Necessary
D. Mild Sedation For Sleep
Example: Choral Hydrate
Examples: Benzodiazepines
E. Medical Treatment:
1. Aricept: Donepezil
2. Exelom: Rivastigmine
3. Reminyl: Galantamine
4. Namenda: Memantine
5. Vitamin E PO BID: Delays
Progression In Patients With
Moderate Disease
6. Alzhemed: Drug In Development
F. Behavioral & Neuropsychiatric Treament:
1. Atypical Antipsychotics:
A. Olanzapine (Zyprexa)
B. Quietapine ( Seroquel)
2. Antidepressants:
A. Sertraline (Zoloft) C. Cymbalta
B. Citalopram (Celexa)
3. Buspar: For Agitation
3. Alzheimer’s Dementia
A. Pathology:
1. Intracerebral Senile Plaques &
Neurofibrillary Tangles
2. Related Amyloid & Tau Proteins
3. Plaques Destroy Neurons By Cell
Membranes Lysis
4. Neurofibrillary Tangles Fill The Axon
& Dendrite Cytoplasm

B. SPECT: Brain Perfusion Imaging

1. Uses: 99m HMPAO Or 99m ECD
2. Symmetric Bilateral Posterior
Temporal & Parietal Perfusion Defects
(Posterior Association Cortex)
3. 30% Have Asymmetrically Decreased
Cortical Activity.
4. Other Findings:
A. Unilateral Temporal Parietal Hypoperfusion
B. Frontal Hypoperfusion

C. PET Studies: 18F-FDG

1. Bilateral Posterior Temporal Parietal Glucose
Metabolism & Hypoperfusion
A. Due To Decreased Glucose Metabolism
Secondary To:
1. Decreased Glucose Transport
2. Neuronal Loss
2. Highly Predictive
3. Not Pathognomonic

D. Sensitivity Studies
1. Parkinson’s Dementia: 90%
2. Alzheimer Dementia 70%
 E. PET Scanning Used For Alzheimer’s Disease
In Conjunction With:
1. MRI Hemodynamic Imaging
2. MRI Spectroscopy
3. Senstive Volumetric Techniques

F. New Investigational PET Agents For Dementia

1. (18 F-FDDNP) Fluoro-Ethyl,Methyl Amino-2 Napthyl
Ethylidene Malonitrile
A. Crosses the BBB
B. Binds To Senile Plaques & NeurofibrillaryTangles
2. 11C-Nicotine
A. Show Nicotinic (Cholinergic) Receptor Loss
In Alzheimer’s Disease
3. 15O-H2O
A. Can Also Show Reduced Blood Flow In Areas
Of Hypometabolism

2. Multi-Infarct Dementia: Vascular Dementia

A. SPECT:
1. Multiple Bilateral Asymmetric Perfusion Defects
Both The Cortical & Deep Structures

B. PET-F18-FDG:
1. Multiple Scatterd Foci Of Hypoperfusion & Hypometabolism
Scattered Throughout Cortex , Subcortical And
Cerebellar Regions

3. Pick’s Dementia:
A. Bilateral Hypoperfusion In Frontal & Frontotemporal
Regions Favoring Pre-Frontal Regions

4. Lewy Body Dementia:

A. Similar To Alzheimer’s Dementia
B. Less Sparing Of The Occipital Cortex

4. Frontal Type Dementia:

A. May Be A Subset of Alzheimer’s Dementia
B. Bilateral Frontal Or Fronto-Temporal Perfusion Defects
5. AIDS Dementia:
A. A Focal, Neurologic Disease, Or Depression Or Psychosis
B. SPECT:
1. Multifocal Or Patchy Cortical And Subcortical Hypoperfusion :
2. Most Frequent Sites:
A. Frontal Lobe
B. Temporal Lobe
C. Parietal Lobe
D. Basal Ganglia
3. These Deficits May Also Be Seen In:
A. Chronic Cocaine Abuse
B. Multidrug Abuse
4. Interpret Test With Caution
6. Bilateral Frontal Abnormalities May Be Seen In:
A. Early Alzheimer’s Disease
B. Schizophrenia
C. Depression
D. Pick’s Disease
E. Supranuclear Palsy

7. Huntington’s Chorea:
A. Chromosome 4 Defect
B. Autosomal Dominant Disorder
C. Decreased Caudate & Putamen Lobe Perfusion

8. Parkinson’s Disease:
A. SPECT & PET Scan Show Increased
Perfusion To The Contralateral Basal Ganglia.
B. Scans Also Show Decreased Basal Ganglia Perfusion
Ipsilateral To The Affected Limb.

9. Wilson’s Disease:
A. Severe Depression Of Lenticular Nuclei
Glucose Metabolism

10. Herpetic Encephalitis :

1. Using Tc99m DTPA
2. Images:
A. Increased Uptake In Temporal Region
Hydrocephalus

Signs Of Hydrocephalus:
1. Ventricular Distension
2. Thinning Of The Cerebral Hemispheres
3. Atrophy
4. Mental Defects
5. Convulsions
6. Sensory Problems Example: Smell Defects
7. Difficulty In Recognition Of People
8. Visual Disturbances
9. Nausea/ Vomiting
10. Headache
11. Problems in Balance
12. Changes in Mood

Non-Obstructive Hydrocephalus
(Normal Pressure Hydrocephalus)
1. Definition:
Disturbance Of Absorption Or Formation
Of CSF Or The Circulatrion Of CSF
In The Subarachnoid Space In The Granulations
Of Pachioni

2. Some Causes:
A. Meningococcal Meninigitis
B. Thrombosis Of The Intracranial Venous Sinuses

3. Clinical Triad:
A. Ataxia
B. Urinary Incontinence
C. Dementia

4. In NPH , The Radiotracer Preferentially Enters

The Lateral Ventricles
4. Procedure:
A. Lumbar Puncture
1. L3: Iliac Crest Level
2. Radionuclide Must Enter The Subarachnoid Space
3. Causes of Blood On A Lumbar Puncture:
A. A Traumatic Tap
B. Reasons For A Lumbar Puncture:
1. Give Radionuclides Such As 111In DTPA
For Cisternography
2. Release Intracranial Pressure By Decreasing
CSF Volume
5. Classical Findings:
A. Normal Flow:
The Radionuclide Travels Up The Spinal Column
To The Convexities Of The Brain
6. Classic Scintigraphic Patterns Of NPH :
A. Early Entry of RP Into The Lateral Ventricles
At 4-6 Hours.
B. Persistence of Lateral Ventricle Activity At 24-48 Hours
& Even 72 Hours
C. Delay In Ascent To the Parasagittal Region With Or
Without Delayed Clearance Of Activity From The Basilar Cisterns
7. Treatment:
A. Ventriclar-Atrial Shunt Improves
Normal Pressure Hydrocephalus
Dramatically While Non-Communicating
Hydrocephalus Does Not Improve

Non-Communicating Hydrocephalus:
(Obstruction In The Ventricles)
1. By Injecting The Radionuclide Directly
Into The Lateral Ventricles, Communication
Between The Ventricles & The Subarachnoid Space
Can Be Discerned.
2. It May Be Of Value In The Investigation Of
Enlarged Ventricles Noted On CT When
Non-Communicating Hydrocephalus Is Suspected
Dr. Antar MD/ PhD :

Classification of Hydrocephalus:

1. Obstructive Form Site of Obstruction

A. Non-Communicating Interventricular Between
Lateral Ventricles & Basal
Cisterns
Example: Tumor

B. Communicating Extraventicular; Affecting Basal

Cisterns, Cerebral Cavities &
Arachnoid Villi
Examples:
1. Subdural Hematoma
2. NPH
3. Leptomeningitis

2. Non-Obstructive Form

A. Generalized Cerebral Atrophy

B. Localized Porencephaly

3. Type Patterns Etiologies

I Basal Cistern 2-4 Hrs Normal

Sylvian Fissure, 6 Hr Intraventricular Hydrocephalus
Other Convexities ,24 Hr
Decreased Activity , 48Hr

II No Ventricular Activity Cerebral Atrophy

Increased Intracerebral Pressure
Advanced Age
Non-Communicating Hydrocephalus
IIIA
Transient Ventricular Activity Cerebral Atrophy
Clearance By Usual Migration Evolving or Resolving
Hydrocephalus

IIIB
Transient Ventricular Activity Communicating Hydrocephalus
Clearance Without Usual Migration With Alternative Pathway of
Resorption (Transependymal)

IV
Persistent Ventricular Activity Communicating Hydrocephalus
Inadequate Clearance
CSF Leaks:

1. From the Nose Or Ears

2. Most Common Sites Of CSF Fistulas;

A. Cribiform Plate Region
B. Ethmoid Sinuses
C. From The Sella Turcica Into the Sphenoid Sinuses
D. From the Sphenoid Ridge Into the Ears.

3. Leaks Are Frequently Intermittent.

4. Radionuclide Evaluation:
A. Image The Site of The Leak
B. Differential Activity In Pledgets Placed
Deep Into Each Nostril As Appropriate
C. Image Within 1-3 Hours
D. Half Hour Intervals After LP May Better
Allow Determination of Optimal Time To Detect
A Leak
E. Pledgets Placed Before LP Injection Of RP
F. Remove Pledgeets 4-24 Hours After Placement
& Counted In A Well Counter.
G. Concurrent Blood Serum Smaples Should Be Counted.
H. Sample Counts Are Counted In
1. Counts/ Gram
A. To Normalize For Differences In Pledget Sizes
&
C. The Amount Of Absorbed Fluid
I. Pleget/ Serum Ratios > 1.5 Indicate CSF Leaks
Dr. Antar MD/ PhD :

Protocol For CSF Leak:

1. Pledgets Placed In The Nose

2. Maintain The Patient Supine
(Trelendenberg Position) Until
The Time Of Imaging To Pool
The Radiotracer In The Basal Region
3. Put The Patient Into A Position That
Contributes TO The CSF Leak
4. Purpose OF Pledget Placement In Suspected
CSF Leaks To Test Them For Contamination
Suggesting The Presence Of Leaking CSF
From The Nose Or Ears.
Radiopharmaceuticals : In111 DTPA, 250uCi

Camera: Large Field Of View Camera

Collimator: Medium Energy

Imaging Procedure For CSF Leak

1. Begin Imaging when Activity Reaches The

Basal Cisterns 1-4 Hours
2. Position The Patient To Maximize The CSF Leak
3. Rhinorrhea: Lean Patient Forward In The Left &
Right Lateral Position
4. Otorrhea: Obtain Posteior Images Instead Of
Lateral Views

Acquisition:
1. Acquire 5 Minute Frame Images For 1 Hour In
The Selected View
2. Remove The Pledgets & Draw A 5 Ml Blood Sample.
3. Count The Pledgets & Count A 0.5 Ml Aliquot Of
Plasma.
4. Repeat Views May Be Indicated At 6 Hours & 24 Hours
Dr Antar MD/PhD:

Cisternography Protocol Summary:

1. Radiopharmaceutical: 500 uCi : 1111In DTPA

2. Instrumentation: Large Field Of Vew Camera

With Medium Energy Collimator
3. Uses: Images Specifically Look For Leaked
Radioactivity :CSF Leaks
4. Procedure:
A. Inject Slowly Into The Lumbar Subarachnoid Space:
Via Intrathecal Injection Of 11In DTPA
B. Patient Should Remain Recumbent For At Least 1 Hour.
After Injection
C. All Images Should Be Obtained For 50K Counts
D. Imaging Times:
1. One Hour: Thoracic-Lumbar Spine For Evaluation
Of Injection Adequacy
2. Four Hours : Base Of The Skull To Visualize The
Basal Cisterns
3. 24 Hr; 48Hr: Evaluate Ventricular Reflux & Arachnoid
Villi Resorption.
4. Obtain Anterior, Posterior, And Both Lateral Views
Of The Head At 4 Hr , 24 Hrs & 48Hrs
E. The Lateral Ventricles Are Not Visible On A Normal
Cisternogram.
F. Why Is 111 In DTPA Preferred Over 99m Tc DTPA
For Cisternography In Adults?
1. 111In DTPA Has A Longer Half Life Than 99mTcDTPA
Allowing Delayed Imaging.
Shunt Patency:
1. Evaluation Of Ventriculoatrial Or
Ventriculoperitoneal Shunts Used To Treat
Obstructive Communicating And Non-
Communicating Hydrocephalus
2. Radionuclides Used In These Studies:
A. 99m Tc DTPA Or
B. 111 In DTPA: The Preferred Radiotracer
For Nuclear Cisternography
3. Procedure:
A. Consists Of RP Injection Into The Shunt
Shunt Reservoir Or Tubing Under
Strict Aseptic Conditions.
B. Serial Gamma Camera Images Demonstrate
Rapid Passage Of The RP Through The
Distal Limb Of The Shunt Is Noted
In The Peritoneal Cavity Or Right Atrium
Within Minutes of Shunt Injection .
C. This Procedure Provides Information Regarding
The Patency Of The Proximal Limb Of The Shunt.
D. Permits Subsequent Evaluation Of The Rate
Of Ventricular Clearance Of The Radiolabelled
CSF From The Ventricular System By Using
Serial Images.
E. Partial Proximal Limb Obstruction:
1. Failure To Obtain Reflux in The Ventricular
System Or
2. Failure of The RP To Clear From The Ventricles
After Several Hours
F. Complete Distal Limb Obstruction:
1. Inferred From Delayed Clearance of The Injected
RP From the Shunt Reservoir
2. With A Region Of Interest Placed Over The
Reservoir & A Time-Activity Curve Is Generated.
G. The Clearance Half-Time From The Reservoir With A Patent
Distal Shunt Limb Is Several Minutes (Usually Less Than
10 Minutes)
H. The Value of Reservoir Clearance Evaluation In Proximal
Obstruction is Less Clear
4. The Study:
A. Injection For CSF Shunt Patency Study
Is Given Into The Shunt Reservoir Or Tubing
B. A Normal Study:
The Activity Reaching The Peritoneal Cavity
Must Be Seen As Diffuse Throughout The
Abdomen.
C. A Abnormal Study:
If The RP Collects Focally In A Closed Pool
At the Tip of The Catheter: Obstruction
Of The Distal Limb By Entrapment In Adhesions
Is Likely

5. Rx:
1. Shunts Which Divert Flow Of CSF Are
Often Used For:
A. Obstructive Communicating Hydrocephalus
B. CSF Leaks

Sensitvity Of Brain Scintgraphy:

Subdural Hematoma
< 10 Days 50%
Chronic 50%

Brain Abscess >90%

Encephalitis 90%

Brain Tumors 85%

AVM 95%
Substance Abuse:
1. Both Acute & Chronic Cocaine Abuse
Result In Alteration In Cerebral Blood Flow.

2. Chronic Cocaine Abuse Presents As

Multifocal Alterations In Regional
Cerebral Blood Flow (rCBF) Without Underlying
Structural Damage On CT/ MRI.

3. SPECT Imaging: Cocaine Abuse Presents As:

1. Multiple Perfusion Defects In The Cerebral Cortex
(Especially The Frontal Lobe)
2. Diminished Blood Flow To The Basal Ganglia
3. General Reduciton In Cerebral Blood Flow
4. These Findings May Occur In Asymptomatic Patients
&
5. These Results May Be Partially Reversible With:
A. Abstinence
B. Buprenorphine Therapy
4. The SPECT Imaging Pattern Findings Are Non Specific
& Often Indistinquishable From Early AIDS Related
Dementia.
4. PET Imaging:
A. Hypermetabolism In The Orbitofrontal Cortex
& Basal Ganglia
Pychiatric Disorders & Behavioral Dysfunction:

1. Panic Disorder:
A. PET & SPECT Imaging :
1. Dysfunction In
A. The Temporal Cortex
B. Orbitofrotnal Cortex
C. Thalamus
D. Amgydala:
1. Role In Mediating Fear & Anxiety
Behaviors
B. Rx:
1. Acute Rx:
A. Benzodiazepines:
1. Low Dose Alprazolam
B. Selective Serotonin Reuptake Inhibitors : SSRIs
1. Paroxitene
2. Sertraline
3. Citalopram
4. Escitalopram
5. Fluoxetine
2. Chronic Rx:
A. SSRIs
B. Imipramine
C. Venlafaxine
D. Etc/
2. Anxiety Disorders:
A. H2O PET Imaging:
1. Increased rCBF In The Right Parahippocampal Gyrus
In Lactate Vulnerable Patients In A Resting Non-Panic State
2. Decrease In Glucose Metabolism In The Right Occipital &
Frontal Cortex After Benzodiazepine Administration.
B. Rx:
1. Acute Rx:
1. Benzodiazepines
2. Inderal : Propanolol
2. Chronic Rx:
1. Benzodiazepines:
Example: Valium
2. Buspirone
3. Selective Anti-Depressants For
Ameliorating Insomnia
4. Combination Cognitive-Behavioral Therapy
With Pharmacotherapy

3. Obsessive Compulsive Disorders:

A. PET Imaging:
1. Increased Cerebral Metabolism In
The Orbital Region Of the Frontal Cortex
& Caudate Nuclei
2. Also The Cingulate Gyrus Was Found To Be
Involved
3. With SSRI Rx: Improvement In
Glucose Metabolism In The Frontal-Subcortical
Networks & Parietal-Cerebellar Networks
B. Rx:
1. Acute Rx:
A. PRN : Clonazepam
2. Chronic Rx:
A. Antidepressants With SSRIs
B. Combination Cognitive-Behavioral Therapy
With Pharmacotherapy
3. Affective Disorders :
A. Major Depression:
1. Unipolar Depression:
A. Reduced Cortical Volumes
B. Other Sites Reported:
1. Smaller Caudate And Putamen
& Basal Ganglia Volumes
2. Smaller Cerebellar Volumes
2. Bipolar Depression:
A. Increased Rates of Subcortical White Matter
& Periventricular Hyperintensities
B. Enlarged Amygdalas
3. PET & SPECT Imaging:
A. Hypometabolism In The
1. Caudate Lobe
2. Cingulate Gyrus
3. Fronto-temporal Regions
B. Increased Blood Flow & Glucose Metabolism
Ventral Pre-Frontal Cortex
C. Decreased Blood-Flow/ Glucose Metabolism
In The Dorsal Pre-Frontal Cortex In Depression
4. Rx:
A. Antidepressants:
1. SSRI: First : Main Line Therapy
2. Tricyclic Antidepressants Therapy
3. St John’s Wort: Short Term Management
4. Cognitive-Behavioral Therapy
4. Electroconvulsive Therapy:
A. Severe Medication-Resistant Depression
4. ADHD Disorders: Attention Deficit Hyperactivity Disorders
A. Increased Perfusion Of:
1. Motor Cortex
2. Pre-Motor Cortex
3. Anterior Cingulate Cortex
B. With Methylphenidate:
1. Increased Perfusion In
A. The Pre-Frontal Cortex
B. Caudate Nucleus
C. Rx:
1. Methylphenidate: Ritalin/ Concerta
2. Dextroamphetamine/Amphetamine Combination
(Adderall)
3. Atomoxetine (Strattera)
4.Anti-Depressants:
A. Bupropion
B. Imipramine
C. Nortriptyline

5. Bulimia Nervosa:
A. PET Imaging :
1. Global & Regional Absolute Hypometabolism
& Relative Hypometabolism In The Parietal Cortex
D. Rx:
1. Acute Rx:
A. SSRI: Selective Serotonin Reuptake Inhibitors
B. MAO Inhibitors: Monoamine Oxidase Inhibitors
C. Antidepressants: Were Associated
With More Frequent Remisssions
2. Chronic Rx:
A. Psychotherapy
6. Alcoholism;
A. FDG PET Imaging:
1. Both Cortical & Subcortical Reduction
In Metabolism; The Parietal Areas
Disproportionately Affected
B. Acute Ingestion of Alcohol:
1. Hypometabolism In Occipital, Pre-Frontal
& Cerebellar Cortices
C. Chronic Alcoholism & Cerebellar Degeneration
1. Reduced Regional Cerebral Glucose Metabolic Rates
In The Vermis
D. Acute General Treatment
1. Inpatient Treatment:
A. Lorazepam
B. Thiamine 100 Mg IV Or IM
For At Least Five Days
C. Multivitamins Oral Treament
D. Beta Adrenergic Blockers
E. Hydration IV Or Oral
F. Social Rehabilitation Group Therapy
Including Alcohol Anonymous
2. Alcohol Withdrawal:
A. Diazepam : (Valium)
B. Thiamine
C. Correct Electrolyte Imbalances
Thar May Exacerbate Seizures
3. Delerium Tremens: DTs
A. Detoxification Unit
1. Thiamine
2. Lorazepam: Initial Rx
3. Chlordiazepoxide, Lorazepam Or Diazepam:BZPs
4. Midazolam: Also Effective In Managing DTs
5. Treat Alcoholic Seizures
6. Treat Concomitant Medical, Surgical
And Psychiatric Condtions
 4. Chronic Treatment:
A. Naltrexone
B. Acamprosate
C. Antabuse: Disulfiram

7. Nicotine Addiction:
A. Newest Treatments:
1. Varencicline ( Chantix)
2. Nicotine Patch

8. Schizophrenia:
Physical Presentations:
1. Hallucinations (Mostly Auditory)
2. Delusions: Mostly Bizarre
3. Disorganized Speech & Behavior
4. Catatonic Behavior
5. Negative Symptoms
6. Usually Experience Social Or Occupational Dysfunction
7. Physical Exam Often Asymptomatic, May Find
Sacccadic Eye Movements, Hypervigilance

Psychologic Testing:
1. IQ Tests: Lower Scores
2. Neurospychologic Testing
3. Personality Testing

Imaging:
A. CT Scans:
1. Enlarged Lateral & Third Ventricle, Reduced
Cortical Volumes
B. MRI:
1. Increased Cerebral Ventricles
C. Decreased rCBF In The Pre-Frontal Cortex
D. fMRI Imaging:
1. Decreased Frontal Cortical Activation
 E. PET Scans: (Using D2& 5HT2A Neuroreceptors)
1. Increased Perfusion & Metabolism In The Left
Hemispheric Cerebral Cortex Relative To
The Right Cortex
2. Severity Of Symptoms Correlated With
Degree Of Hyperactivation Of The Left
Hemisphere. & Not With The Degree Of
Hypofrontality.
3. Increased Basal Ganglia Hyperactivity Relative To
The Cerebral Cortex.
4. Early et.al Found An Increase In Blood Flow
To The Left Globus Pallidus With 15O2 PET
5. After Neuroleptic Treatment : Post Therapy Scans:
A. General Increase In Glucose Metabolism In
The Temporal Lobe (DeLisi et.al.)
B. Higher Metabolism In The Temporal Cortex
6. Increased Density Of Dopamine D2 Receptor
Occupancy Occuring Especially in The Basal Ganglia
(Farde et.al).
7. The Drug’s D2 Receptor Occupancy Decreased
On Withdrawal Of Treatment.
8. Sedvall et al Also Found D1 Receptor Blockade &
Was Measured With (11C) SCH23390. This Is
A Particularly True For Clozapine.
9. PET Studies & SPECT Studies Have Shown
Decreased rCBF In The Frontal Lobes In Schizophrenia
E. Rx:
1. Acute Rx:
A. Second Generation Anti-Psychotics:
1. Risperidone
2. Olanzapine
3. Quetiapine
4. Ziprasidone
5. Aripiprazole
6. Clozapine: Resistant Cases
 B. Traditional Neuroleptic Treatment
Such As Haloperidol, Perphenazine,
Fluphenazine, Chlorpromazine Use
Has Decreased Due To Propensity To
Parkinsonian Side Effects And
Eventual Tardive Dyskinesia
C. Cognitive- Behavioral Therapy
D. Family Therapy
E. Social Skills Training

8. Post Traumatic Stress Disorders:

A. Trauma Was Associated With Increased
Metabolism In The Orbital-Frontal Cortex &
Temporal Poles. The rCBF(Regional
Cerebral Blood Flow) Decreases In the
In Both Anterior Frontal And Left Inferior
Frontal Regions In PTSD Patients
B. FDG –PET Imaging:
1. Decreased Medial Frontal Activity
C. Increased Amgydala rCBF May Be Related
To Clinical Features Of PTSD.
D. Rx:
1. SSRI: Sertraline, Paroxitene, Fluoxtine
Best Studied
2. Tricycylic Antidepressants And
MAO Inhibitors May Be Helpful
In Reducing Symptoms Associated With
PTSD.
3. Eye Movement Desensitization Reprocessing
4. Beta Adrenergic Antagonists & Clonidine
May Help Treat Aggression And Other
Psychophysiologic Arousal Symptoms
5. Behavioral Therapy
9. Autistic Spectrum Disorders:
A. Treatment Modalities Include:
1. Seroquel: Quetiapine
2. Strattera: Atomoxetine
3. Haloperidol & Other High Potency
Neuroleptics Are Helpful In
Reducing Aggression & Sterotypy
4. Clomipramine:
A. For Obssesive-Compulsive
& Sterotyped Behaviors
5. Risperidone: Atypical Antipsyhotics
A. Also For Serious Behavioral
Disturbances
6. Naltrexone:
A. Especially Helpful In Rett Syndrome
B. Reduces Hyperactivity In Children
With Autism

10. Some Comments On Brain Receptors

A. Radiolabelled Benzamide, Lisuride, & Spiperone
Derivatives Attach To Dopamine D-2 Brain Receptors.

B. Labelled Benzapine Derivatives Attach To

Dopamine D-1 Receptors In Patients With Psychotic
& Movement Disorders

C. 11C-Labelled Carfentanil Is A High Affinity Opiate

Anatgonist That Binds To The mu Receptors In The
Central Nervous System.
References:

1. Professor Lawrence Hough CNMT: Manhattan College Nuclear

Medicine Class Notes: 2008
2. Professor M. Antar MD/PhD & Professor T. D’Alessandro MD
Nuclear Medicine Class Notes: Northport Veterans Affairs Hospital :
1999-2000
3. Mettler & Guiberteau: Essentials Of Nuclear Medicine Imaging: 2006
4. Henkin et al: Nuclear Medicine: 2006
5. Goldfarb et al. Nuclear Medicine Review: 2007
6. Ramer & Alavi: Nuclear Medicine Technology: Review Questions
Answers For The Board Examinations: 2nd Edition: 2005
7. Andre Parent: Carpenter’s Neuroanatomy: 9th Edition
8. Gilman &Winans”s: Manter & Gatz’s: Essentials Of Clinical
Neuroanatomy & Neurophysiology: 6th Edition
9. Ferri’s : Clinical Advisor: Instant Diagnosis & Treatment : 2008