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Chapter 4. Neuroanatomy, Neurophysiology, and Neuropathology of Aging

Warren D. Taylor, M.D.; Scott D. Moore, M.D., Ph.D.; Steven S. Chin, M.D., Ph.D.
DOI: 10.1176/appi.books.9781585623754.387407

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Much has been revealed about the human brain in the past few decades. In vivo visualization of the human brain is more accessible to psychiatrists and other clinicians with the emergence of high-resolution magnetic resonance imaging (MRI). Functional neuroimaging research has rapidly expanded, first with positron emission tomography (PET) and single-photon emission computed tomography (SPECT), and more recently with functional MRI (fMRI), a technique that offers improved resolution and wider access.

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FIGURE 4–1. Illustration of cortical (left) and sagittal (right) views of the brain, marked with selected Brodmann areas.

FIGURE 4–2. Normal brain: lateral view (left). Alzheimer's disease brain: lateral view (right).In the Alzheimer's brain, moderate diffuse cortical atrophy is apparent. The gyri are narrowed, and the sulci are widened.

FIGURE 4–3. Normal brain: coronal section through the basal ganglia (left). Alzheimer's disease brain: coronal section through the basal ganglia (right).In the normal brain, the lateral ventricles are small and there is no atrophy. In the Alzheimer's brain, the lateral ventricles are enlarged and dilated from neuronal loss and atrophy of the cortex.

FIGURE 4–4. Alzheimer's disease brain.The neocortex is filled with senile neuritic plaques and neurofibrillary tangles. (King's silver impregnation stain; original magnification x400.)

FIGURE 4–5. Alzheimer's disease brain: hippocampus, neurofibrillary tangle.Note the fibrillary nature of this intraneuronal inclusion. The tangle is shaped like the neuron and fills the cell body. Tangle formation is due to abnormal assembly of phosphorylated microtubule-associated protein into paired helical filaments. (King's silver impregnation stain; original magnification x1,000.)

FIGURE 4–6. Alzheimer's disease brain: hippocampus.This neuron has undergone granulovacuolar degeneration (small arrows). Granulovacuolar degenerations are seen almost exclusively in the hippocampal formation. The frequency of granulovacuolar degeneration increases as neurofibrillary change increases elsewhere in the neocortex. Also seen here is a Hirano body (large arrow). Hirano bodies are eosinophilic aggregates of actin protein. Hirano bodies are usually closely associated with granulovacuolar degeneration. (Hematoxylin-eosin stain; original magnification x1,000.)

FIGURE 4–7. Dementia with Lewy bodies brain: section through the midbrain (left). Normal brain: section through the midbrain (right).Note the loss of the black neuromelanin pigment in the substantia nigra of the patient with dementia with Lewy bodies. This degeneration of the substantia nigra may cause extrapyramidal symptoms such as tremor, rigidity, and bradykinesia.

FIGURE 4–8. Dementia with Lewy bodies brain: pigmented neuron of the substantia nigra with several Lewy bodies (arrows).Lewy bodies are intraneuronal cytoplasmic inclusions with a clear halo. (Hematoxylin-eosin stain; original magnification x1,000.)

FIGURE 4–9. Dementia with Lewy bodies brain: pigmented neuron of the substantia nigra with numerous Lewy bodies.Many more Lewy bodies are apparent with this -synuclein immunostain than are seen in the routine preparation (Figure 4–8). (-Synuclein immunostain; original magnification x1,000.)

FIGURE 4–10. Normal brain: horizontal section through the basal ganglia (left). Vascular dementia, Binswanger's subcortical arteriosclerotic encephalopathy: horizontal section through the basal ganglia at the same level (right).In the vascular dementia brain, the ventricles are dilated and the white matter is pitted and granular.

FIGURE 4–11. Vascular dementia with multiple lacunar infarcts (arrows): coronal section of brain.Multiple lacunar infarcts are seen in the basal ganglia. These may cause strokes. Because the individual lesions may occur at different times, there is a stepwise progression of dementia.

FIGURE 4–12. Pick's disease: lateral view of the brain.Very severe atrophy ("knife blade") is most pronounced in the frontal and temporal lobes.

FIGURE 4–13. Pick's disease: coronal section through the basal ganglia.This disease causes profound atrophy of the cortex. The ventricles are widely dilated. The caudate nucleus is flattened.

FIGURE 4–14. Pick's disease: hippocampal formation, fascia dentata.Pick's bodies are round, densely homogeneous argyrophilic inclusions that fill the cytoplasm of virtually every neuron. Like neurofibrillary tangles, they contain abnormally assembled tau proteins. (Glees silver stain; original magnification x400.)

FIGURE 4–15. Pick's disease: hippocampal formation, Ammon's horn.Pick's bodies are seen here within pyramidal neurons. (Glees silver stain; original magnification x1,000.)

FIGURE 4–16. Frontotemporal lobar degeneration with tau-negative, ubiquitin-positive inclusions: hippocampal formation, fascia dentata.Tau-negative, ubiquitin-positive inclusions (arrows) are small granular cytoplasmic inclusions that are best observed in the small neurons of the fascia dentata of the hippocampus. These inclusions cannot be seen on routine histological preparations. They stain positively only for ubiquitin. They lack tau, -amyloid, -synuclein, and other proteins that are present in the other major neurodegenerative disorders. (Ubiquitin immunostain; original magnification x1,000.)
Table Reference Number
Table 4–1. Brodmann areas of selected brain regions
Table Reference Number
Table 4–2. Hierarchical distribution and location of major cortical types

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