Cerebral Pathology In Chronic Epilepsy

Hypoxic-ischemic lesions often are encountered in the brains of patients who suffer from epilepsy with generalized tonic-clonic seizures and status epilepticus. The lesions result from respiratory and circulatory

FIGURE 3.7

Prolonged coma following cardiac arrest. Chronic cortical pan-necrosis. Three-month survival in a 69-year-old man. A. Transverse section of the cerebral hemispheres shows thinning and sponginess of the cortex, necrosis of the basal ganglia, and focal softening of the white matter. The cerebral cortex shows (B) ischemic necrosis of the entire width of the cortex (LFB-CV) and (C) intense perinecrotic astrocytic reaction (GFAP).

FIGURE 3.7

Prolonged coma following cardiac arrest. Chronic cortical pan-necrosis. Three-month survival in a 69-year-old man. A. Transverse section of the cerebral hemispheres shows thinning and sponginess of the cortex, necrosis of the basal ganglia, and focal softening of the white matter. The cerebral cortex shows (B) ischemic necrosis of the entire width of the cortex (LFB-CV) and (C) intense perinecrotic astrocytic reaction (GFAP).

Coma Cerebral

FIGURE 3.8

Persistent vegetative state following cardiac arrest with 4.5-year survival. Chronic cortical pan-necrosis. At 7 months of age, a previously healthy baby girl suffered a cardiac arrest for 10 minutes during anesthesia for repair of a diaphragmatic hernia. After 40 minutes, the heart rate returned to normal. The child remained in a permanent vegetative state until her death at age 5 years. A. On examination, at 5 years of age, her eyes were open and moved around but she did not react to visual or verbal stimuli and made no spontaneous movements. Her extremities were spastic, atrophic, and deformed. She slept through the night and also for a few hours during the day. B. On transverse section, the cerebral cortex is thin and spongy, the gray structures are atrophic, the hemispheric white matter is reduced, and the ventricles are enlarged. C. The cortex from the frontal to the occipital lobes underwent cystic necrosis (HE). D. It is replaced by a glial mesodermal network (van Gieson), E. which contains lipid-laden macrophages (oil-red O). F. The hemispheric white matter is devoid of myelin (Weil stain). G. Schematic representation of the sites of the surviving neurons: hypothalamus, brainstem, and parts of hippocampus. H. The cerebellar cortex is totally depleted of Purkinje cells, basket fibers and granule cells; it is outlined by a prominent Bergmann astrocytic layer (Bodian stain).

FIGURE 3.8

Persistent vegetative state following cardiac arrest with 4.5-year survival. Chronic cortical pan-necrosis. At 7 months of age, a previously healthy baby girl suffered a cardiac arrest for 10 minutes during anesthesia for repair of a diaphragmatic hernia. After 40 minutes, the heart rate returned to normal. The child remained in a permanent vegetative state until her death at age 5 years. A. On examination, at 5 years of age, her eyes were open and moved around but she did not react to visual or verbal stimuli and made no spontaneous movements. Her extremities were spastic, atrophic, and deformed. She slept through the night and also for a few hours during the day. B. On transverse section, the cerebral cortex is thin and spongy, the gray structures are atrophic, the hemispheric white matter is reduced, and the ventricles are enlarged. C. The cortex from the frontal to the occipital lobes underwent cystic necrosis (HE). D. It is replaced by a glial mesodermal network (van Gieson), E. which contains lipid-laden macrophages (oil-red O). F. The hemispheric white matter is devoid of myelin (Weil stain). G. Schematic representation of the sites of the surviving neurons: hypothalamus, brainstem, and parts of hippocampus. H. The cerebellar cortex is totally depleted of Purkinje cells, basket fibers and granule cells; it is outlined by a prominent Bergmann astrocytic layer (Bodian stain).

FIGURE 3.9

Post-hypoxic dementia. Following resuscitation from ventricular fibrillation and cardiac arrest, a 23-year-old man became severely demented. Thirteen years later, at age 36 years, he died. A. Multifocal thinning of the cerebral cortex, atrophy of the white matter, and enlargement of the anterior horns. B. Loss of neurons in hippocampal gyrus.

FIGURE 3.9

Post-hypoxic dementia. Following resuscitation from ventricular fibrillation and cardiac arrest, a 23-year-old man became severely demented. Thirteen years later, at age 36 years, he died. A. Multifocal thinning of the cerebral cortex, atrophy of the white matter, and enlargement of the anterior horns. B. Loss of neurons in hippocampal gyrus.

TABLE 3.1.

Comparison Between Clinical Presentation of

Prolonged Coma and Persistent Vegetative State

Prolonged

Persistent

Clinical Presentation

Coma

Vegetative State

Consciousness

Lost

Awareness of self and

environment lost,

wakefulness

retained

Motor activity

Lost

Markedly reduced

Speech

Lost

Reduced to sound,

screaming,

moaning, groaning

Sleep-wake cycle

Lost

Retained

Respiration

Altered

Intact

Autonomic functions

Altered

Retained

TABLE 3.2.

Comparison Between Anatomic Sites of Pathology in Prolonged Coma and Persistent Vegetative State

Anatomic Sites

of Pathology

Prolonged Coma

Persistent Vegetative State

Widespread bi-hemispheric cortical and/or white

Widespread bi-hemispheric cortical and/or white

matter

matter

Diencephalon Rostral brainstem

Bi-thalami

FIGURE 3.10

Permanent global ischemia: Brain death. A 72-year-old man suffered a cardiopulmonary arrest and survived 11 days with the assistance of mechanical ventilation. A. Transverse section of the cerebral hemispheres shows break-up of neural tissue in the basal ganglia and white matter and patchy, dusky discoloration of the cortex. B. Ghost neurons in the brainstem and lack of glial and vascular reactions (HE).

FIGURE 3.1 1

Ammon's horn sclerosis in a 28-year-old woman with generalized tonic-clonic seizures. A. The Ammon's horns are atrophic, and the temporal horns are enlarged. B. Thinning of the Sommer's sector from neuronal losses and dense diffuse astrogliosis in another chronic epileptic patient (Holzer stain).

impairments that occur during and after the seizures. Two characteristic lesions are Ammon's horn sclerosis and cerebellar cortical atrophy.

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