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(8th Edition - Robbins and Cotran, p. 1291 | 7th Edition -Robbins and Cotran, p. 1361)

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Global ischemia

A 44-year-old alcoholic had acute hemorrhagic pancreatic necrosis, circulatory collapse, renal failure, respiratory distress, then cardiac arrest with resuscitation after about 10 minutes. He was on a respirator for about 4 days. He was declared dead with 25 minutes of electroencephalographic tracings showed no electrical activity and other signs of brain death had developed.

At autopsy there was widespread red mottling of the cerebral cortex grossly, the discoloration being like that often seen in recent cerebral infarcts. Microscopically, there is widespread necrosis of cortex with minimal polymorphonuclear leukocytic infiltration; this same process is also seen in the basal ganglia, and hippocampus, and throughout the rest of the brain. Histologically, dead neurons are reduced in size with eosinophilic cytoplasm and disintegrating nuclei. Vessels are congested; they have leaked blood and fibrin. Events that would require several days to develop are absent, such as proliferation of vascular endothelial and adventitial cells, formation of phagocytes, more advanced dissolution of cell bodies and neuropil, and disappearance of polymorphonuclear leukocytes. Thus the pathologic changes are about 24 hours old. If some patchy necrosis of neurons and other elements had developed during the first day after the arrest, they would be obscured by this more widespread delayed process, probably resulting from progressive impairment of the cerebral circulation while the rest of his body was being kept alive.

  1. Central nervous system cells are variably susceptible to global cerebral ischemia. Which cells are most susceptible to ischemia?

  2. The changes of ischemia involved all portions of the brain. Would one expect such widespread changes to be accounted for by the obstruction of a single blood vessel?


(8th Edition - Robbins and Cotran, p. 1310 - 1312)

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Multiple sclerosis
(Luxol and silver stain)

A 34-year-old man had multiple sclerosis for about 8 years, beginning with blurred vision in one eye and followed about 4 years later by diplopia and unsteady gait. Motor difficulties progressed intermittently until severe intention tremors of both upper extremities made it impossible for him to care for himself. A right cryothalamotomy was performed which relieved this considerably for about 10 days, when he lost his voice, motor control of his jaw and lower face, and his gag reflex. He could not swallow. His pupils became dilated and fixed. He died about 36 hours after these cranial nerve signs developed.

At autopsy, the brain showed many demyelinated regions – “plaques” – including the characteristic ones around the lateral ventricles. Of interest was the relationship of the lesions in the brain stem to the clinical signs late in the patient’s disease. There was extensive demyelination of the dorsal part of the midbrain involving the oculomotor complex, portions of the pons, and the caudal region of the floor of the 4th ventricle (including 12th nerve). These regions had been demyelinated for a long time: there was no longer any breakdown of myelin with phagocytosis and there was established gliosis. Eye movements and tongue functions were at least serviceable up until the last 36 hours.

The section here is of pons. It is stained with Cajal’s pyridine silver nitrate, cresyl violet, and Luxol fast blue. Within affected areas (“plaques”), the axis cylinders are devoid of myelin. Axis cylinders are black or gray, myelin blue, and cell bodies and nuclei take both the silver and violet stain.

  1. What is the gross appearance of the plaques or areas of demyelination?

  2. What is the histopathologic appearance of an active plaque?

  3. Which CSF abnormalities may be present in multiple sclerosis patients?

(8th Edition - Robbins and Cotran, p. 1306 | 7th Edition - Robbins and Cotran, p. 1377)

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Subacute sclerosing panencephalitis

A five-year-old boy was thought to have this form of encephalitis 2 years before his death. His central nervous system function deteriorated gradually until he was little more than a vegetative organism; he died of pneumonia.

There was atrophy of the cortex at autopsy, and microscopically there is evidence of varying degrees of old destruction of the cortex and white matter. Nerve cells in the better preserved, more recently affected parts of the cortex, and oligodendroglia in the white matter, show intranuclear inclusions (Cowdry Type A). They are presumed to represent a virus. The inclusions are round eosinophilic bodies filling the nucleus. In some nerve cells there is a red center, then a clear rim, and, outside this, a blue rim of nuclear material – sort of like a red, white, and blue target. These latter affected nuclei look superficially like those in chickenpox and some other diseases.

  1. What infectious disorder is usually associated with subacute sclerosing panencephalitis?

  2. In addition to the intranuclear inclusions, what other histopathologic features are present?

(8th Edition - Robbins and Cotran, p. 1299 | 7th Edition - Robbins and Cotran, p. 1369)

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Acute meningitis

A 19-year-old student complains of chills, headache, nausea, and vomiting. Over the next day, the patient became confused and semicomatose. Physical examination revealed neck rigidity and a petechial skin rash. Although a diagnosis was promptly made, the patient succumbed to his illness.

Microscopically, there are a large number of inflammatory cells (predominantly neutrophils) in the leptomeninges. The brain itself is relatively spared by the inflammation. There is a mild degree of edema and a few of the blood vessels near the leptomeninges show minimal inflammation.

  1. A variety of infectious organisms can cause acute pyogenic meningitis. Which organisms commonly cause meningitis in neonates? What is the most common pathogen among adolescents and young adults? Which organisms commonly cause meningitis in the elderly?

  2. Which CSF abnormalities are usually found in patients with pyogenic meningitis?

  3. What late complications may arise from pyogenic meningitis?

(8th Edition - Robbins and Cotran, p. 1300 | 7th Edition - Robbins and Cotran, p. 1361)

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Cerebral abscess
(Trichrome stain)

A 52-year-old man had been a heavy drinker (alcohol) for years, and, after a head injury some years before death, he had intermittent rhinorrhea thereafter. About 6 weeks before his death, he had “flu” and bronchopneumonia, and 4 weeks before he was admitted to the hospital for confusion; he had a high fever. Spinal fluid showed numerous leukocytes and he was treated for meningitis with antibiotics. Further examination indicated an adrenal mass interpreted as a tumor. He developed hemiparesis and had a convulsion. A brain scan, arteriogram, and EEG supported the diagnosis of brain abscesses in the right frontal and temporal regions. A craniotomy was done, but attempts to drain the abscesses with a cannula failed. An old fracture of the cribriform plate, the cause of his rhinorrhea of cerebrospinal fluid, was recognized and the dural defect overlying it was repaired. Two weeks later he died.

At autopsy, there were about 100 cc of blood under the dura over the left hemisphere, hemorrhagic necrosis of the ventral parts of the frontal poles related to the attempts to drain the abscesses, and multiple abscesses throughout the forebrain. The largest abscess, shown here, was in the right mid-temporal region. There were also multiple abscesses of the adrenal; there was no neoplasm.

Microscopically, the abscess shows a collagenous connective tissue wall with vigorous astrocytic response around it. Islands of reactive astrocytes have become incorporated in the outer part of the connective tissue wall. The center of the abscess, composed of polymorphonuclear leukocytes, cellular debris, and some phagocytes, has largely fallen out during sectioning, but some of it is retained. Some of the phagocytes are multinucleate, appearing as “foreign body giant cells.”

From your knowledge of the time sequences in histologic processes in brain disease, can you say how long, at least, this abscess was present? The hypertrophied astrocytes indicate the passage of at least three weeks. That some of them seem to have been caught in an advancing “wall” of the abscess suggests an even older process. Note that brain damage represented by hypertrophied astrocytes extends far beyond the “wall.” Thus brain abscesses are not truly walled off.

  1. How might a brain abscess arise?

  2. Which CSF abnormalities may be found in patients with a brain abscess?

  3. What complications may arise if the abscess were to rupture?


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