The F-18 FDG Brain PET-CT images show mild age appropriate atrophy with
mildy decreased metabolism in the bilateral posterior temporo-parietal lobes
and severely decreased metabolism in the bilateral occipital lobes. Normal
metabolic activity is present within the frontal lobes, cerebellum, and the
subcortical nuclei. These findings are highly suggestive of Lewy body
disease (1). After Alzheimer's disease, Lewy body disease is the second most
common cause of senile degenerative dementia. Common symptoms include
progressive cognitive dysfunction, psychotic symptoms (mainly visual
hallucinations), parkinsonian motor signs (especially rigidity), and rapid
cognitive fluctuations(2).
mildy decreased metabolism in the bilateral posterior temporo-parietal lobes
and severely decreased metabolism in the bilateral occipital lobes. Normal
metabolic activity is present within the frontal lobes, cerebellum, and the
subcortical nuclei. These findings are highly suggestive of Lewy body
disease (1). After Alzheimer's disease, Lewy body disease is the second most
common cause of senile degenerative dementia. Common symptoms include
progressive cognitive dysfunction, psychotic symptoms (mainly visual
hallucinations), parkinsonian motor signs (especially rigidity), and rapid
cognitive fluctuations(2).
An 84 year old African American male with long history of memory difficulty
and visual hallucinations, as well as, legal blindness presented to clinic for
follow up. He has REM sleep behavior with occasional confusion and
agitation during his sleep. His memory seemed to be stable for quite some
time per his family. However, upon starting Aricept his visual hallucinations
worsened. Aricept was subsequently discontinued. A head CT showed mild
subcortical chronic ischemic in the subinsular region bilaterally. Dystrophic
calcifications were noted in the right globe and along the right retina. Left
scleral band was noted. A PET CT of the brain was ordered suspecting lewy
body disease (LBD).
and visual hallucinations, as well as, legal blindness presented to clinic for
follow up. He has REM sleep behavior with occasional confusion and
agitation during his sleep. His memory seemed to be stable for quite some
time per his family. However, upon starting Aricept his visual hallucinations
worsened. Aricept was subsequently discontinued. A head CT showed mild
subcortical chronic ischemic in the subinsular region bilaterally. Dystrophic
calcifications were noted in the right globe and along the right retina. Left
scleral band was noted. A PET CT of the brain was ordered suspecting lewy
body disease (LBD).
Clinical criteria Lewy body dementia has been delineated to allow clinical
diagnosis (3). The clinical criteria provide excellent specificity (90–97%), but
are lacking in sensitivity (only 22–75%) (4). Progressive debilitating mental
impairment progressing to dementia is characteristic, however, this is
common in many dementias. Impairments in attention, problem solving and
visuospatial difficulties are early manifestations. Features which are helpful
in differentiating Lewy body disease from Alzheimer’s disease include:
fluctuations in cognitive function, spontaneous motor features of
parkinsonism, and marked visual hallucinations (4). Previously autopsy was
relied upon for the definitive diagnosis.
In this patient the diminished occipital uptake is likely due to Lewy body
disease and not due to orbital pathology. A prior study performed on eight
patients with congenital homonymous hemianopsia (seven with damage to
optic radiations and one with optic tract abnormality; all with largely intact
occipital cortex), showed minimal abnormalities in the resting visual cortex
glucose metabolism of the “pathologic” visual cortex (5).
1. Mettler F., Guiberteau M. Essentials of Nuclear Medicine Imaging. 2006.
p391
2. Mirzaei S, et al. Assessment of diffuse Lewy body disease by 2-[18F]
fluoro-2-deoxy-D-glucose positron emission tomography (FDG PET). BMC
Nucl Med. 2003 Feb 20. doi: 10.1186/1471-2385-3-1.
3. McKeith IG, et al. Consensus guidelines for the clinical and pathologic
diagnosis of dementia with Lewy bodies (DLB): report of the consortium on
DLB international workshop. Neurology. 1996;47:1113–1124.
4. Ransmayr G, et al. Demenz mit Lewy-Körperchen. Nervenarzt. 2000;71:
929–935. doi: 10.1007/s001150050689.
5. Bosely TM, et al. Neuro-imaging and positron emission tomography of
congenital homonymous hemianopsia. Am J Opthalmol. 1991 Apr 15; 111(3):
413-8.
This case was compiled by Bradley J. Potsic M.D, BCM
diagnosis (3). The clinical criteria provide excellent specificity (90–97%), but
are lacking in sensitivity (only 22–75%) (4). Progressive debilitating mental
impairment progressing to dementia is characteristic, however, this is
common in many dementias. Impairments in attention, problem solving and
visuospatial difficulties are early manifestations. Features which are helpful
in differentiating Lewy body disease from Alzheimer’s disease include:
fluctuations in cognitive function, spontaneous motor features of
parkinsonism, and marked visual hallucinations (4). Previously autopsy was
relied upon for the definitive diagnosis.
In this patient the diminished occipital uptake is likely due to Lewy body
disease and not due to orbital pathology. A prior study performed on eight
patients with congenital homonymous hemianopsia (seven with damage to
optic radiations and one with optic tract abnormality; all with largely intact
occipital cortex), showed minimal abnormalities in the resting visual cortex
glucose metabolism of the “pathologic” visual cortex (5).
1. Mettler F., Guiberteau M. Essentials of Nuclear Medicine Imaging. 2006.
p391
2. Mirzaei S, et al. Assessment of diffuse Lewy body disease by 2-[18F]
fluoro-2-deoxy-D-glucose positron emission tomography (FDG PET). BMC
Nucl Med. 2003 Feb 20. doi: 10.1186/1471-2385-3-1.
3. McKeith IG, et al. Consensus guidelines for the clinical and pathologic
diagnosis of dementia with Lewy bodies (DLB): report of the consortium on
DLB international workshop. Neurology. 1996;47:1113–1124.
4. Ransmayr G, et al. Demenz mit Lewy-Körperchen. Nervenarzt. 2000;71:
929–935. doi: 10.1007/s001150050689.
5. Bosely TM, et al. Neuro-imaging and positron emission tomography of
congenital homonymous hemianopsia. Am J Opthalmol. 1991 Apr 15; 111(3):
413-8.
This case was compiled by Bradley J. Potsic M.D, BCM
PET-CT case of the month (03/10): Lewy Body Disease
