Autolysis of the granular layer of the cerebellar cortex in brain death

Abstract

In a study of duration of brain death, granular layer autolysis (GLA) of the cerebellar cortex was analyzed in 45 patients who died of acute cerebrovascular diseases (CVDs). Twelve patients who died of causes other than intracranial disease served as controls. Tonsillar herniation occurred in all who died of acute CVDs. More advanced GLA was seen in the central folia adjacent to the central white medullary body of the cerebellum as compared with the peripheral folia. Widespread GLA involving the most of the peripheral folia was found solely in patients in whom brain death had been present over 18 h. Of the 12 control patients, 4 showed GLA only in the central folia. Although GLA of the central folia might develop during immersion fixation of the brain, the alteration of the peripheral folia is assumed to develop in the period of brain death. Widespread GLA extending to the peripheral folia could be a pathological finding characteristic of brain death, where intracranial blood flow could be absent or significantly reduced. Brain death for little less than 1 day would be necessary for GLA to develop.

Temporal Sequence of Autolysis in the Cerebellar Cortex of the Mouse

“…An autolytic pathogenesis for this cerebellar change is supported by the fact that granule cell depletion is usually symmetrical in both hemispheres, is not related to the pattern of vascular supply, no reactive glial or vascular changes are found, and there is no inflammatory infiltrate (Albrechtsen, 1977a,b;Ogata et al, 1986). Similar histological changes were also found in vitro when human cerebellar material was incubated in ventricular fluid or isotonic sodium chloride at an optimal temperature (37e45 C) for 24e48 h, with maximal, near complete, granular layer destruction evident at 48 h (Ikuta et al, 1963).…”

An Australian Brain Bank: a critical investment with a high return!

“…The granular cell layer of the cerebellum is assessed microscopically to determine the degree of autolytic degradation by an experienced neuropathologist. Degradation is graded as nil, mild, moderate or severe as previously described by Albrechtsen and Ogata et al (Albrechtsen 1977;Ogata et al 1986). They defined mild (slight) as a definite decrease in the number of the nuclei stained by hematoxylin, moderate when there is a diffuse decrease in the number of nuclei and severe as complete loss of nuclei.…”

Primary brainstem death: a clinico-pathological study.

“…In classical brain death absence of blood flow during a period lasting a little more than a day is known to induce autolysis of the granular layer of the cerebellar cortex. 5 The cerebrum was not macerated. The lesions of the supra-and infratentorial structures showed active tissue responses and the blood vessels contained fresh red blood corpuscles.…”

“…Sensory evoked potentials on median nerve stimulation were absent on day 4. A monopolar electroencephalogram (EEG) obtained on day 7 showed disorganised irregular [5][6] Hz, 10-30 pV theta activity. No response was noted to voice or painful stimuli.…”