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Case Report/Case Series |

Does a Positive Pittsburgh Compound B Scan in a Patient With Dementia Equal Alzheimer Disease?

Simon Ducharme, MD, MSc1,2; Marie-Christine Guiot, MD, FRCPC3; James Nikelski, PhD4; Howard Chertkow, MD, FRCPC3,4
[+] Author Affiliations
1Department of Neurology, Massachusetts General Hospital and McLean Hospital, Harvard University, Boston
2Department of Psychiatry, McGill University, Montreal, Quebec, Canada
3Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec, Canada
4Lady Davis Institute for Medical Research, Jewish General Hospital, McGill University, Montreal, Quebec, Canada
JAMA Neurol. 2013;70(7):912-914. doi:10.1001/jamaneurol.2013.420.
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Importance  The clinical role of amyloid brain positron emission tomographic imaging in the diagnosis of Alzheimer disease is currently being formulated. The specificity of a positive amyloid scan is a matter of contention.

Observations  An 83-year-old Canadian man presented with a 5-year history of predominantly short-term memory loss and functional impairment. Clinical evaluation revealed significant, gradually progressive short-term memory loss in the absence of any history of strokes or other neuropsychiatric symptoms. The patient met clinical criteria for probable Alzheimer disease but had a higher than expected burden of white matter disease on magnetic resonance imaging. A positron emission tomographic Pittsburgh Compound B scan was highly positive in typical Alzheimer disease distribution. The patient died of an intracerebral hemorrhage 6 months after the assessment. Autopsy revealed cerebral amyloid angiopathy in the complete absence of amyloid plaques or neurofibrillary tangles.

Conclusions and Relevance  This patient demonstrates that a positive Pittsburgh Compound B scan in a patient with clinical dementia meeting criteria for probable Alzheimer disease is not proof of an Alzheimer disease pathophysiological process. A positive Pittsburgh Compound B scan in typical Alzheimer disease distribution in a patient with dementia can be secondary to cerebral amyloid angiopathy alone.

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Figure 1.
Magnetic Resonance Image and Positron Emission Tomographic Scan

A, Axial T2-weighted magnetic resonance imaging showing prominent periventricular white matter changes. B, Positive carbon 11–labeled Pittsburgh Compound B positron emission tomographic scan showing β-amyloid (light color) in typical Alzheimer disease distribution, superimposed on a 3-dimensional rendering of the patient’s structural magnetic resonance image (dark color).

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Figure 2.
Postmortem Immunohistochemistry for β-Amyloid in the Occipital Lobe

Absence of positive amyloid plaques and presence of numerous intraparenchymal cortical and subarachnoid vessels demonstrated strong positivity for β-amyloid (clone 6F/3D [Dako Corp], original magnification ×20).

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