Professional Documents
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OF THE BRAIN
SAFUAN AWANG
WHY NOT CT/MRI
Radiopharmaceuti
Clinical problem Imaging technique cal Biological behaviour
Head
Cerebrovascular accident Cerebral perfusion 99m Tc HMPAO Uptake proportional to
SPECT blood flow
Hydrocephalus
CSF rhinorrhoea Cerebrospinal fluid In DTPA
111 Marker of CSF flow.
(CSF) study (intrathecal)
Encephalitis Blood–brain barrier 99m Tc HMPAO Passage across
(BBB) study disrupted BBB
Dementia Cerebral perfusion 99m Tc HMPAO Uptake proportional to
SPECT blood flow
18F
Cerebral Marker of glucose
metabolism PET fluorodeoxyglucose metabolism
Epilepsy (presurgical localization) Ictal SPECT 99mTc HMPAO Uptake proportional to
blood flow
18F
Interictal PET Marker of glucose
fluorodeoxyglucose metabolism
Two high-powered imaging
instruments in nuclear
medicine
use the tomographic
approach
and range in the same
general size ,category and
PET AND cost,
GLUCOSE METABOLISM
for measurements of metabolic rate + mapping of functional activity
C-11 glucose:
rapid uptake, metabolization, and excretion by brain
F-18 fluorodeoxyglucose (FDG):
diffuses across blood-brain barrier --the brain is normally a r rapid user of
glucose, since brain pathologies greatly decrease brain metabolism of glucose
The consumption of FDG--- indicates the extent of brain activity.
By indicating the consumption of FDG, PET imaging gives---------a key to
the working of a patient's brain
TECHNIQUE(FDG PET IMAGING)
Preparation:
fasting for 4-18 hours (FDG tumor uptake is diminished by an
elevated serum glucose level)
Dose: 10 mCi (370 MBq)
Physical half-life: 110 minutes
Imaging time:
50-60-70 minutes after administration (trade-off between
decreasing background activity and declining counting
statistics)
BRAIN PET IN
ONCOLOGY
- Definition
1----REFRACTORY SEIZURES/EPILEPSY
2----FRONTO-TEMPORAL LOBE DEMENTIA AND ALZHEIMER’S DISEASE
AIM’s CRITERIA TO DETERMINE
IF FDG-PET DEMENTIA EVALUATION IS INDICATED
The use of FDG-PET scan in the diagnosis of Alzheimer’s disease (AD) and Fronto-Temporal Lobe
Dementia(FTD) is Approved provided
The patient’s clinical symptoms meet the diagnostic criteria for (AD), (FTD)
a comprehensive clinical evaluation which has included:comprehensive medical history,physical and
mental status exam
neuropsychological testing, laboratory testing, and structural imaging ---MRI or CT----to aid in identifying
structural, metabolic, and chemical abnormalities as a cause for cognitive impairment.
Alzheimer's dementia(Case 1)
severely reduced FDG activity ---in the bilateral parietal, temporal lobe and
frontal lobe. The primary sensorimotor cortex, visual cortex, basal ganglia,
thalamus and cerebellum are normal and spared
Alzheimer's
dementia (Case 2)
an area of
FDG uptake in
the rest
of the cerebral
cortex, subcortical gray
matter, cerebellum is
within normal range.
DEMENTIAS--------------
There is mild-moderate
hypometabolism
involving both frontal
and contiguous temporal
lobes.
The brain otherwise has
normal symmetric
metabolism without
focal abnormality.
FRONTO TEMPORAL
LOBE DEMENTIA.
PARKINSONS DISEASE
abnormally high activation of the left part of the brain of a patient during an
epileptic seizure
PET------- IN
EPILEPSY
EPILEPSY - LESIONAL
MESIAL TEMPORAL SCLEROSIS
(MTS)
MRI:
Atrophy, enlarged temporal horn.
Increased T2 signal.
Bilateral changes in 10%.
PET:
Hyp
omet
aboli
sm
Path
Mesial Temporal Sclerosis (MTS)
SPECT