Oral Exam - CNS Flashcards
Dural tear findings
In111-DTPA cisternogram:
Extravasation of radiotracer into the extradural space
Cribiform plate leak findings
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
CSF leak protocol
Intrathecal 0.5 mCi In111 or Tc99 DTPA
○ 2, 6,. 12, 24 hours imaging
- Pledgets - Pack counts positive if > 1.5 x blood
CSF Shunt patency study protocol
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
Shunt occlusion locations
Children = proximal tubing more common
Adults -= distal
Shunt occlusion finings (distal occlusion)
Activity confined to CSF space
Absent activity in peritoneal cavity
Abrupt termination of activity along expected course of shunt tubing
NPH Protocol
0.5 mCi In111-DTPA intrathecal
Planar images 4, 24, 48 hrs
Radionuclide cisternography - Normal findings
– 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
NPH findings
○ 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
NPH symptoms
Gait disturbance, urinary incontinence, dementia
NPH DDx
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)
AD Amyloid PET findings
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
AD F18-FDG PET OR HPMPAO/ECD SPECT findings
Posterior temporal and parietal + posterior cingulate
Sparing of sensorimotor, basal ganglia, thalamus, primary visual cortex
Mild cognitive impairment findings
Medial temporal lobe hypometabolism: Most
sensitive marker for predicting MCI
AD FDG protocl
□ 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
Frontotemporal - best imaging tools
• 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
FTD - Findings
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
Corticobasal Degeneration findings
- 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
Progressive Supranuclear Palsy findings
- Characterizedbyimpairmentsingait/balance,supranuclear ophthalmoplegia (impaired downward gaze), behavioral/personality changes, parkinsonism, and dementia
- Atrophyofstructureswithinmidbrainandbasalganglia
FTD Age of onset
• Age
○ Mean age of onset: 50-60 years
○ Approximately10%>70years
○ YoungeronsetthanAD,whichisgenerally>65years
LBD - DAT findings
• 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
LBD - FDG findings
○ 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
DATscan imaging protocol
□ 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)
Multiinfarct dementia findings
• 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
Brain abscess/encepahlaitis findings
• 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
Herpes Simplex findings
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)
Rasmussen encephalitis
Chronic, unilateral brain inflammation; etiology unclear
○
Unilateral cerebral atrophy
– Initiallyfocalinvolvement,thenhemispheric
– Whenhemispheric,worseprecentralandinferior
frontal
Limbic encephalitis
• 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
Parkinson’s disease findings
○ 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
MSA findings
○ 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
PSP findings
○ F-18FDGPET/CT – Decreased F-18FDG activity in basal ganglia, frontal lobes, anterior cingulate, midbrain ○ Amyloid PET negative ○ Ioflupane SPECT positive
Corticobasal degeneration(CBD)
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
Parkinson differential
- Atypical parkinsonian syndromes
- Benign essential tremor
- Vascular parkinsonism
- Drug induced
Brain death findings
• 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
Brain Angiogram findings (DTPA, pertechnetate)
– 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
Brain death protocol
○ 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)
Photopenic defect brain
Infarct Cyst Necrotic tumour Hematoma Abscess Previous irradiation
Spect increased uptake
Ictal seizure focus
Encephalitis
PET decreased uptake
Atrophy
Infarct
Inter-ictal seizure focus
Low grade tumour
Huntington’s
Decreased metabolism in BG
Dimished flow reserve with diamox
Decreased perfusion with acetazolamide to most of the hemisphere
