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Nucs Board Review > Oral Exam - CNS > Flashcards

Oral Exam - CNS Flashcards

1
Q

Dural tear findings

A

In111-DTPA cisternogram:

Extravasation of radiotracer into the extradural space

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2
Q

Cribiform plate leak findings

A

Tc99m -DTPA cisternogram:
Activity extending below the skull base and into the frontal sinus, nose, and nasopharyxn

Activity in stomach suggests rhinorrhea due to swallowing
Activity in bladder or kidney = dose extrav

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3
Q

CSF leak protocol

A

Intrathecal 0.5 mCi In111 or Tc99 DTPA
○ 2, 6,. 12, 24 hours imaging
- Pledgets - Pack counts positive if > 1.5 x blood

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4
Q

CSF Shunt patency study protocol

A

Supine

0.5 mCi In/Tc DTPA 25G needle into reservoir
Expect clearance into abdomen within 15-20 minutes

LEAP with Tc99, Medium energy collimator with In111
Serial ant planar q1 min x 20 min
+/- SPECT CT to help localize

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5
Q

Shunt occlusion locations

A

Children = proximal tubing more common

Adults -= distal

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6
Q

Shunt occlusion finings (distal occlusion)

A

Activity confined to CSF space

Absent activity in peritoneal cavity

Abrupt termination of activity along expected course of shunt tubing

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7
Q

NPH Protocol

A

0.5 mCi In111-DTPA intrathecal

Planar images 4, 24, 48 hrs

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8
Q

Radionuclide cisternography - Normal findings

A

– 1hr: Radiotracer reaches basal cisterns
– 2-6hrs:Radiotracer reaches Sylvian fissures
– 12hrs:Radiotracer reaches cerebral convexities
– 24hrs:Radiotracer reaches superior sagittal sinus and
is absorbed by arachnoid villi

Normally noradiotracer enters ventricles, although transient activity in ventricles at 4 hrs is still considered normal

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9
Q

NPH findings

A

○ NPH
– Radiotracer activity in ventricles at ≥ 24hrs
– Absence of radiotracer activity in cerebral convexities
by 24 hrs
□ Heart configuration: Appearance of radiotracer
activity in lateral ventricles on anterior view
□ Comma (also c-shaped) configuration: Appearance of radiotracer activity in lateral ventricles on lateral
views
□ Butterfly configuration: Appearance of radiotracer
activity in lateral ventricles on posterior view

○ SPECT/CT can help confirm ventricular activity

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10
Q

NPH symptoms

A

Gait disturbance, urinary incontinence, dementia

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11
Q

NPH DDx

A

DDx:
AD - Type II or IIIa flow pattern
Normal aging - Type II pattern
Non-communicating hydrocephalus - normal actiivty in convexities

– Type II: Delayed activity in cerebral convexities at 24
hrs without ventricular activity
□ Cerebral atrophy or aging

– Type IIIa: Radiotracer activity in cerebral convexities at
24 hrs with early transient ventricular activity □ Indeterminate (can be seen with
noncommunicating hydrocephalus, developing or resolving communicating hydrocephalus, or cerebral atrophy)

– TypeIIIb:Noradiotraceractivityincerebralconvexities at 24 hrs with early transient ventricular activity
□ Suggestive of NPH (communicating hydrocephalus)

– TypeIV:Noradiotraceractivityincerebralconvexities at 24 hrs with persistent ventricular activity
□ SuggestiveofNPH(communicatinghydrocephalus)

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12
Q

AD Amyloid PET findings

A

Amyloid PET best for ruling out AD

F18 florbetapir

○ Absence of amyloid plaque rules out AD in patients with
dementia
– View in black-on-white background at high contrast levels
– Cerebellumgray-whitedifferentiationisbaselinefor
discerning normal gray matter from physiologic tracer
retained in white matter

– Signs of amyloid deposition
□ Decreasing cortical gray-white differentiation compared to cerebellar gray-white differentiation
□ Increasing gray matter uptake int emporal,parietal, and frontal cortices
□ Uptake in posteriorcingulategyrus

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13
Q

AD F18-FDG PET OR HPMPAO/ECD SPECT findings

A

Posterior temporal and parietal + posterior cingulate

Sparing of sensorimotor, basal ganglia, thalamus, primary visual cortex

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14
Q

Mild cognitive impairment findings

A

Medial temporal lobe hypometabolism: Most

sensitive marker for predicting MCI

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15
Q

AD FDG protocl

A

□ Patient should fast, stop IV fluids containing dextrose, stop parenteral feeding for 4-6 hrs
□ Bloodsugarshouldbe<150-200mg/dL
□ Patientshouldbeplacedinquiet,dimlylitroom
prior to and after injection for 30 min
– Radiopharmaceutical:F-18FDG
– Dose:5-20mCi
– Dosimetry:Urinarybladderreceiveslargestdose
– Imageacquisition: 30-60minafterinjection

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16
Q

Frontotemporal - best imaging tools

A

• Bestimagingtool
○ F-18FDGPEThelpstodifferentiatebetweenFTDand
other causes of dementia, e.g., Alzheimer disease (AD)
and Lewy body disease (DLB)
○ PET/SPECTmaybeusedinearlydiagnosis
○ Correlateswithdiseaseprogression

• SPECT
○ 2nd-linestudyifF-18FDGPETisnot
available/reimbursed

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17
Q

FTD - Findings

A

F18-FDG PET
○ Glucose hypometabolism first in frontal lobes with progression to include regions of temporal/parietal lobes
– Anteriorcingulatecortex,frontalinsula,caudate
nuclei, thalamus may also have hypometabolism
bilaterally
– Relative sparing of motor cortex

• Tc-99mHMPAOSPECT
○ Pattern is similar to F-18 FDGPET,with decreased
radiotracer activity in frontal/temporal lobes
– SPECT generally has less sensitivity and quantitative
potential compared to PET
○ More sensitive than structural MR indetecting early
changes

18
Q

Corticobasal Degeneration findings

A
  • Commonlypresentswithsignificantextrapyramidal symptoms, visual/spatial and cognitive impairment
  • Asymmetric cortical atrophy (left>right) infrontal and parietal structures, especially within superior parietal lobe
  • Bilateral atrophy of basal ganglia
19
Q

Progressive Supranuclear Palsy findings

A
  • Characterizedbyimpairmentsingait/balance,supranuclear ophthalmoplegia (impaired downward gaze), behavioral/personality changes, parkinsonism, and dementia
  • Atrophyofstructureswithinmidbrainandbasalganglia
20
Q

FTD Age of onset

A

• Age
○ Mean age of onset: 50-60 years
○ Approximately10%>70years
○ YoungeronsetthanAD,whichisgenerally>65years

21
Q

LBD - DAT findings

A

• Best imaging tool
○ Dopamine transporter (DaT) SPECT with I-123 FP-CIT
(ioflupane)
– DaT magingd ifferentiates between LBD abnormal
DaT) and AD (normal DaT)
– Cannotreliablydistinguishbetweenotherdisorders
with parkinsonism

– LBD and PD both demonstrate low uptake in
putamen ± preservation in caudate head

22
Q

LBD - FDG findings

A

○ F-18FDGPET
– Generalized glucose hypometabolism with significant occipital lobe hypometabolism
□ Occipital lobe involvement may help distinguish
from AD-like pattern of hypometabolism
□ Similar hypometabolic pattern seen in PD and PDD

Predmoninantly tau

23
Q

DATscan imaging protocol

A

□ off all interferingd dopaminergic medications
□ Pretreat with thyroid blocker(oralpotassium
solution, Lugols) 1 hour before tracer injection

– Dose: 3-5mCi(111-185MBq) I123-ioflupane
– Image acquisition: 3-6 hours after injection

Predominantly alpha-synuclein (alpha-syn)

24
Q

Multiinfarct dementia findings

A

• F-18FDGPET/CT
○ Glucose hypometabolism in multifocal
pattern of cortical with subcortical regions
- subcortical areas spared in AD

• AmyloidPET imaging does not demonstrate graymatter
amyloid deposition
• SPECTwithTc-99mHMPAOorTc-99mECDshowssimilar
asymmetrically decreased perfusion

25
Q

Brain abscess/encepahlaitis findings

A

• PET
○ Abscess
– Focal CNSinfection (bacterial,fungal,parasitic etiologies)
□ Usually:Peripheral hypermetabolism with central hypometabolism on F-18 FDG PET/CT

– Toxoplasmagondii
□ Common opportunistic infection in HIV/AIDS
patients
□ Toxoplasmosis is hypometabolic on F-18 FDG
PET/CT
□ Lymphoma is hypermetabolic on F-18 FDG PET/CT

○ Encephalitis
– CNS inflammation; most common etiology is viral (e.g.,
herpes simplex encephalitis)
□ Acute: Hypermetabolism on F-18 FDG PET/CT
□ Subacute: May be isointense to gray matter on F-18
FDG PET/CT
□ Chronic,nonactive:HypometaboliconF-18FDG
PET/CT

26
Q

Herpes Simplex findings

A

Herpes simplex virus type 1 (HSV-1)

○ Medial temporal and inferior frontal lobes; cingulate
gyrus and contralateral temporal lobe highly suggestive

○ Limbic system most typically (temporal lobes, insula,
subfrontal, cingulate gyri)

27
Q

Rasmussen encephalitis

A

Chronic, unilateral brain inflammation; etiology unclear
○
Unilateral cerebral atrophy
– Initiallyfocalinvolvement,thenhemispheric
– Whenhemispheric,worseprecentralandinferior
frontal

28
Q

Limbic encephalitis

A

• Limbic encephalitis
○ Rare paraneoplastic syndrome associated with primary tumor, often lung
○ Imaging may be indistinguishable from herpes simplex encephalitis on MR and F-18 FDG PET/CT
○ Subacute symptom onset (weeks to months) vs. acute in herpes simplex encephalitis

29
Q

Parkinson’s disease findings

A

○ DopaminetransporterSPECT(I-123FP-CIT)
– dopamine transporters located on presynaptic nigrostriatal axons

in putamen and caudate nucleus
– I-123 FP-CIT confirms loss of dopaminergic neurons
– Sensitivity > 90% for differentiating PD and essential
tremor

Differentiates PD and APS from essential tremor and
drug-induced parkinsonism
– Does not differentiate PD from APS or between APSs

○ F-18FDGPET/CT
– TypicallynormalinPD
□ Preserved F-18FDGPET/CT in basalganglia
differentiates PD from parkinsonian syndromes

30
Q

MSA findings

A

○ Parkinsonism,ataxia,and autonomic
dysfunction
– Cerebellar dominant(MSA-C) and parkinsonian
dominant (MSA-P)

○ F-18FDGPET
– MSA-P shows decreased putamen activity
– MSA-C shows decreased activity in cerebellum

○ Amyloid PET negative
○ I-123FP-CITSPECTpositive

31
Q

PSP findings

A 
○ F-18FDGPET/CT
– Decreased F-18FDG activity in basal ganglia, frontal
lobes, anterior cingulate, midbrain
○ Amyloid PET negative
○ Ioflupane SPECT positive
32
Q

Corticobasal degeneration(CBD)

A 
akinesia,rigidity,dystonia,apraxia,
executive dysfunction, aphasia
○ Patientsdonotrespondtolevodopa
○ F-18FDGPET/CT
– Relative decreased activity in contralateral cortexand basal ganglia
○ AmyloidPETnegative
○ I-123 FP-CIT SPECT positive, typically asymmetric and
decreased contralateral to symptoms
33
Q

Parkinson differential

A
  1. Atypical parkinsonian syndromes
  2. Benign essential tremor
  3. Vascular parkinsonism
  4. Drug induced
34
Q

Brain death findings

A

• Imaging may confirm brain death but does not substitute
for clinical criteria

Brain parenchyma scintigraphy
○ Tc-99mexametazime(HMPAO),Tc-99methylcysteinate
dimer (ECD)
○ Tc-99mHMPAO preferred since it accumulates in brain
parenchyma within 2 min and takes several hrs before
significant redistribution
○ Absentcerebraluptake
– Nouptakeinallportionsofbrain
– Hotnosesign
□ Early increased activity in nasopharyngeal region on anterior view

• Brainnuclearangiogram
○ Flow radiotracers: Tc-99mDTPA or Tc-99m pertechnetate
○ Only allows assessment of anterior brain circulation
○ Requires good bolus technique and adequate cardiac output

35
Q

Brain Angiogram findings (DTPA, pertechnetate)

A

– Angiographic phase
□ Trident sign: Early simultaneous visualization of the paired anterior cerebral arteries (ACAs) and each middle cerebral artery (MCA)
– Blood pool phase
□ Visualization of venous sinuses but not brain

○ Absent cerebral perfusion
– Angiographic phase
□ Absence of trident; empty lightbulb sign; hotnose sign
– Bloodpool phase
□ Delayed images may visualize venous sinuses from
centrally draining scalp perforators
□ Lack of superior sagittal sinus activity helps confirm
lack of cerebral perfusion

36
Q

Brain death protocol

A

○ Dose
– Brain parenchyma: 15-20mCi (555-740MBq) for adults; 0.3 mCi/kg for children
– Brain bloodflow: Up to 30mCi(1.1GBq)

○ Image acquisition
– Gamma camera with field of view large enough to
image entire head and neck

– Flowimages
□ Brainparenchyma:Imageacquisitionstartingat time of radiotracer injection and ending well after venous phase
□ 1-3 sec per frame for at least 60 sec
□ Brainangiogram: Tracer flow should be observed
from level of carotids to skull vertex

– Static planar images
□ Brainparenchyma:Anteriorandlateralplanarviews should be obtained after at least 20 min

– SPECT
□ May be obtained in addition to flow and planar
images with brain parenchyma tracers
□ Allowsbettervisualizationofperfusiontoposterior
fossa and brainstem structures

○ Reporting recommendations
– Cerebral and cerebellar perfusion absent
– Cerebral and cerebellar perfusion present
– Cerebralandcerebellarperfusionpresent,although
abnormal (discuss specific regions of uptake/lack of
uptake)

37
Q

Photopenic defect brain

A 
Infarct
Cyst
Necrotic tumour
Hematoma
Abscess
Previous irradiation
38
Q

Spect increased uptake

A

Ictal seizure focus

Encephalitis

39
Q

PET decreased uptake

A

Atrophy
Infarct
Inter-ictal seizure focus
Low grade tumour

40
Q

Huntington’s

A

Decreased metabolism in BG

41
Q

Dimished flow reserve with diamox

A

Decreased perfusion with acetazolamide to most of the hemisphere

Nucs Board Review (21 decks)

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