Neuro Pathology

The so-called Duret hemorrhages seen here in the pons are secondary to downward compression that leads to stretching and ischemia of perforating arterioles. The compression can result from a variety of lesions--hemorrhages, edema, mass lesions of any type.

The microscopic appearance of this acute cerebral infarction reveals marked edema (the pale areas).

The neurons are the most sensitive cells to anoxic injury. Seen here are red neurons which are dying as a result of hypoxia.

Subacute infarct This cerebral infarction demonstrates the presence of many macrophages at the right which are cleaning up the lipid debris from the liquefactive necrosis.

remote infarct Resolution of the liquefactive necrosis in a cerebral infarction leads to the formation of a cystic space.

Bacterial meningitis Microscopically, a neutrophilic exudate is seen involving the meninges at the left, with prominent dilated vessels. There is edema and focal inflammation (extending down via the Virchow-Robin space) in the cortex to the right. This acute meningitis is typical for bacterial infection. This edema can lead to herniation and death. Resolution of infection may be followed by adhesive arachnoiditis with obliteration of subarachnoid space leading to obstructive hydrocephalus.

The characteristic microscopic findings of Alzheimer's disease include "senile plaques" which are collections of degenerative presynaptic endings along with astrocytes and microglia. These plaques are best seen with a silver stain, as seen here in a case with many plaques of varying size. senile plaques made of amyloid bielchowski silver stain

The plaques of Alzheimer's disease are seen here with a silver stain. Such plaques are most numerous in the cerebral cortex and hippocampus. This dementia is marked mainly by progressive memory loss. senile plaques of amyloid bielchowski silver stain

A number of neuritic plaques with Alzheimer's disease are seen here. They have an amyloid core as seen here with Congo red stain. Small peripheral cerebral arteries may also be involved. There appears to be a problem with beta amyloid precursor protein, but the exact pathogenesis is unknown. It is interesting that the gene coding for cerebral amyloid is on chromosome 21--and persons with trisomy 21 living to age 40 invariably develop Alzheimer's disease.

Senile plaques of amyloid bielchowski silver stain Here is another Alzheimer's plaque. The major biochemical defect in Alzheimer's disease is a loss of choline acetyltransferase and acetylcholine in the cerebral cortex.

H&e tau tangle This is a neurofibrillary "tangle" of Alzheimer's disease. The tangle appears as long pink filaments in the cytoplasm. They are composed of cytoskeletal intermediate filaments.

Neurofibrillary tangles of Alzheimer's disease are also seen best with a silver stain, as shown here.

Pick's FT atrophy superior temporal gyrus spared

Microscopically, the caudate nucleus in Huntington's disease demonstrates loss of neurons along with gliosis. The onset of this disease occurs in middle age. This disease results from an abnormal gene on chromosome 4 which codes for a protein containing increased trinucleotide repeat sequences. The greater the number of repeats, the earlier the onset of the disease. Spontanenous new mutations are uncommon.

The loss of pigmentation in the substantia nigra of the midbrain at the left in a patient with Parkinson's disease is contrasted with a normal midbrain at the right. Parkinson's disease is marked clinically by a "pill-rolling" tremor at rest, mask-like facies, and cogwheel rigidity of limbs, among other findings.