Neuroimaging in dementia

Abstract

Although dementia is a clinical diagnosis, neuroimaging often is crucial for proper assessment. Magnetic resonance imaging (MRI) and computed tomography (CT) may identify nondegenerative and potentially treatable causes of dementia. Recent neuroimaging advances, such as the Pittsburgh Compound-B (PIB) ligand for positron emission tomography imaging in Alzheimer's disease, will improve our ability to differentiate among the neurodegenerative dementias. High-resolution volumetric MRI has increased the capacity to identify the various forms of the frontotemporal lobar degeneration spectrum and some forms of parkinsonism or cerebellar neurodegenerative disorders, such as corticobasal degeneration, progressive supranuclear palsy, multiple system atrophy, and spinocerebellar ataxias. In many cases, the specific pattern of cortical and subcortical abnormalities on MRI has diagnostic utility. Finally, among the new MRI methods, diffusion-weighted MRI can help in the early diagnosis of Creutzfeldt-Jakob disease. Although only clinical assessment can lead to a diagnosis of dementia, neuroimaging is clearly an invaluable tool for the clinician in the differential diagnosis.

Figure 1

T1-weighted MRI scans in patients with pathologically-proven AD. (A) Coronal image showing bilateral hippocampal atrophy (arrows) in an 83-year-old woman (MMSE score 21). (B) Axial image showing biparietal and posterior cingulate atrophy (arrows) in a 62-year-old woman with early age of onset AD (MMSE 22). (C) Sagittal image showing thinning of the posterior body of the corpus callosum (arrow), associated with significant parietal and posterior frontal atrophy in a 59-year-old woman with early onset AD (MMSE 21). AD, Alzheimer’s disease, MMSE, Mini Mental Status Exam.

Figure 2

Molecular and functional PET in (A,C) a patient with AD and (B,D) a healthy control. PET neuroimaging with the Aβ amyloid ligand Pittsburgh Compound-B in (A) a 67-year-old man with moderate AD and (B) a 73-year-old cognitively normal woman. Axial DVR images referenced to the cerebellum are shown in neurologic orientation. (A) The patient with AD has increased tracer binding in the frontal, posterior cingulate, parietal and temporal cortices, and the striatum (not shown). (B) In contrast, the cognitively normal control does not demonstrate tracer uptake in the cortex. (C,D) Fluorodeoxyglucose PET in the same subjects. Axial images normalized to mean activity in the pons (Norm) are presented in neurologic orientation. (C) The patient with AD demonstrates prominent hypometabolism, particularly in parietal cortex (arrows), while (D) the normal control shows normal glucose metabolism. (Images courtesy of Gil Rabinovici, University of California, San Francisco, and William Jagust, University of California, Berkeley.) PET, positron emission tomography; AD, Alzheimer’s disease; DVR, distribution volume ratio.

Figure 3

Brain coronal T1-weighted MRI from patients with different clinical presentations of frontotemporal lobar degeneration. (A) BvFTD in a 62-year-old man, MMSE score 24. (B) SD in a 66-year-old man, MMSE 26. (C) PNFA in a 66-year-old woman, MMSE 28. Note the bilateral gray matter loss in the inferior frontal gyrus (arrow), superior frontal gyrus (dashed arrow), the insula (dotted arrow), and the anterior cingulate (arrowhead) in (A) the patient with bvFTD; the atrophy of the left temporal lobe (arrow) in (B) the patient with SD; and the prominent atrophy in the left perisylvian region (arrow) in (C) the patient with PNFA. MRI, magnetic resonance imaging; bvFTD, behavioral variant frontotemporal dementia; MMSE, Mini Mental Status Exam; SD, semantic dementia; PNFA, progressive nonfluent aphasia.

Figure 4

Axial T2 images in four patients with different types of VaD. (A) An 84-year-old woman with cognitive deficits (MMSE 26, which 2 years later declined to 15). T2-weighted MRI shows chronic right temporal pole infarction and only mild left hippocampal atrophy. (B) A 79-year-old man with behavioral, frontal-executive, and memory problems (MMSE 19). T2-weighted MRI shows chronic left thalamic lacunar stroke, bilateral caudate and frontal white matter small vessel disease, as well as bifrontal atrophy. (C) A 72-year-old woman with memory impairment (MMSE 24) diagnosed with mixed AD-VaD. T2-weighted MRI shows bilateral hippocampal atrophy and multiple microhemorrhages (focal hypointensities, arrows) suggestive of amyloid angiopathy. (D–F) A 49-year-old man with CADASIL and progressive behavioral and memory disturbances (MMSE 27). Axial T2-weighted MRI shows diffuse bilateral leukoencephalopathy involving (D) the centrum semiovale, (D,E) anterior and posterior deep white matter, (E) internal and external capsules (arrow), (F) subcortical white matter of temporal poles (arrows), and the pons, and (E) a lacunar stroke in the right thalamus and microhemorrhages primarily in the left thalamus. This MRI pattern, with the bilateral anterior temporal lobe white matter hyperintensity, is highly suggestive of CADASIL. VaD, vascular dementia; MMSE, Mini Mental Status Exam; MRI, magnetic resonance imaging; AD, Alzheimer’s disease; CADASIL, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

Figure 5

(A,B) T2-weighted images showing diffuse asymmetric (L > R) bilateral frontoparietal atrophy (arrows) in a 54-year-old woman with progressive nonfluent aphasia and mild parkinsonism (MMSE 29) due to pathology-proven corticobasal degeneration. (C,E) Sagittal and (D) coronal T1-weighted images from a high-resolution volumetric sequence showing (C, compared with the pons) reduced midbrain area and (D) thinned superior cerebellar peduncles (arrows), compared with (E) the middle cerebral peduncles (arrows) in a 61-year-old man with parkinsonism and frontal-executive dysfunction (MMSE 27) and autopsy-proven progressive supranuclear palsy. (F) Axial FLAIR and (G) coronal T2* images showing posterolateral putamen hypointensity with hyperintense rim (arrow and dotted arrow) in a 64-year-old man with multiple system atrophy (MMSE 26). MMSE, Mini Mental Status Examination; FLAIR, fluid attenuation inversion recovery.

Figure 6

MRI findings in CJD. (A,B) A patient with probable variant CJD and three common MRI patterns in sporadic CJD: (C,D) predominantly subcortical, (E,F) both cortical and subcortical, and (G,H) predominantly cortical. Note that in sporadic CJD the abnormalities are always (C,E,G) more evident on DWI than (D,F,H) on FLAIR images. (A,B) A 21-year-old woman with probable variant CJD with MRI showing bilateral thalamic hyperintensity in the mesial pars (mainly dorsomedian nucleus) and posterior pars (pulvinar) of the thalamus, the so-called “double hockey stick sign.” Also note the “pulvinar sign,” with the posterior thalamus (pulvinar) being more hyperintense than the anterior putamen. The three sporadic CJD cases are pathology-proven. (C,D) A 52-year-old woman with MRI showing strong hyperintensity in bilateral striatum (solid arrows, both caudate and putamen) and slight hyperintensity in mesial and posterior thalamus (dotted arrow). (E,F) A 68-year-old man with MRI showing hyperintensity in bilateral striatum (note anteroposterior gradient in the putamen, which is commonly seen in CJD), thalamus, right insula (dotted arrow), anterior and posterior cingulate gyrus (arrow, L > R), and left temporal-parietal-occipital junction (arrow). (G,H) A 76-year-old woman with MRI showing diffuse hyperintense signal mainly in bilateral parietal and occipital cortex, right posterior insula (dashed arrow) and left inferior frontal cortex (arrow), but no significant subcortical abnormalities. CJD, Creutzfeldt-Jakob disease; MRI, magnetic resonance imaging; DWI, diffusion-weighted imaging; FLAIR, fluid-attenuated inversion recovery.

Figure 7

Two cases of non–prion-related rapidly progressive dementia or ataxia syndromes. Note that in these cases, the abnormalities are best seen in FLAIR images. (A,B) A 66-year-old man with intravascular lymphoma. (B) FLAIR multifocal abnormalities involving cerebral and cerebellar gray and white matter in a vascular distribution. These lesions, also involving the right hippocampus, showed patchy enhancement after contrast administration (not shown). (A) DWI shows a right periventricular focal region with diffusion restriction; DWI hyperintensity is common in lymphomas. (C,D) A 65-year-old woman with anti-Yo paraneoplastic cerebellitis. MRI shows mild diffuse hyperintensity of the cerebellar, compared with the cerebral, cortex with slight atrophy of the lateral folia. Note (D) the strong hyperintense FLAIR signal in superior, medial cerebellum (arrows), and (C) no major hyperintensity in the axial DWI scan. (E,F) A 60-year-old woman with paraneoplastic limbic encephalitis and FLAIR MRI showing hyperintensity of bilateral insula, medial (arrows) and inferior temporal cortex, hippocampus, amygdala (F) on FLAIR and only subtle hyperintensity (E) on DWI. FLAIR, fluid-attenuated inversion recovery; DWI, diffusion-weighted imaging; MRI, magnetic resonance imaging.