Cerebellar Syndrome Following Heat Stroke

Freeman, Walter; Dumoff, Edith

doi:10.1001/archneurpsyc.1944.02290250073005

Cited by 28 publications

(4 citation statements)

References 3 publications

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“…This also agrees with the lack of marked astrocytic response.8,4·22 If one can be permitted to comment on illustrations or text published by other investigators, the rarefication or loosened structure of the granular layer following heat stroke24·21 probably refers to edema of the granular layer. The illustration by Freeman and Dumoff 8 of the same condition clearly shows a marked edema of granular cells and of Berg¬ mann glia; it is indistinguishable from our human material as well as experimental "metabolic" changes in rat cerebellar cortex.…”

Section: Commentsupporting

confidence: 54%

Cerebellar Edema

Friede¹

1963

Arch Neurol

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The neuropathological description of cell loss, atrophy, gliosis, etc., is usually based on the subjective impression of changes of cell density one gets from a microscopic study. This impression can be quite misleading, as has been shown for the so-called gliosis in atrophic fiber tracts, which, in fact, results from tissue shrinkage.15 Collection of quantitative data on tissue volume, regional density of cells, and the regional composition of the cell population furthers the approach toward quantitative, objective neuropathology. Methods are easily found and adjusted to the problem in question, once the need for quantitation is recognized.7This work represents an effort to utilize quantitative methods and histochemical data for the analysis of cerebellar edema. The clear-cut arrangement of its cellular elements renders the cerebellar cortex an ideal region for quantitative studies. Material and MethodsSince a variety of studies was reported, certain methodological details have been included in the results to help the interpretation. Planimetric Technique.\p=m-\Ten-micronparaffin sec¬ tions of formalin-fixed tissue, which was blocked exactly perpendicular to the axis of the gyri and sulci, were projected on paper, and the outline of the individual layers were drawn. In each of these drawings, several continuous cortical convolutions were selected for planimetry ; these portions were delineated from the rest of the cortex either at a flat part of the cortex or at the bottom of a sulcus where it was possible to draw a dividing line cutting each layer at 90°. The area of molecular and granular layer was measured planimetrically in these drawings, and the ratio of the layers was cal¬ culated. In human postmortem material, it was found necessary to select deep portions of the cortex for measurement, since exposure of the brain sur¬ face to air during autopsy produced shrinkage of the molecular layer. Selective sampling was not necessary in experimental material in which ex¬ posure to air was minimized.The ratio of the layers could be used as an indi¬ cator of volume changes of the granular layer, pro¬ vided that the thickness of the molecular layer was

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Section: Commentsupporting

confidence: 54%

Cerebellar Edema

Friede¹

1963

Arch Neurol

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“…Protected this case the skull distortion from compression might have led to some squeezing effect of the brain towards the tentorial opening, with resulting midbrain damage. It might be thought that hyperpyrexia (Freeman and Dumoff 1944) might lead to damage causative of these striking signs, and in Case 1 there was high fever. In hyperpyrexia, however, the motor dysfunction is symmetrical and purely cerebellar.…”

Section: Mid-brain Syndrome After Head Injurymentioning

confidence: 98%

A Mid-Brain Syndrome Following Head Injury

Kremer¹,

Wr²,

Ge³

1947

Journal of Neurology, Neurosurgery & Psychiatry

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“…A cerebellar syndrome is the most common persistent abnormality.' [5][6][7] Residual pyramidal signs and mental status changes commonly have been reported.5 Dysarthria, dysphagia, hemiplegia and lower motor neuron findings may also persist after heat stroke. ' 3 8 Patients with heat stroke are generally hypotensive, tachypnoeic and tachycardic on presentation.…”

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confidence: 99%

Cerebellar syndrome following neuroleptic induced heat stroke.

Lefkowitz¹,

Ford²,

Rich³

et al. 1983

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY We report a patient in whom extreme hyperthermia, rhabdomyolysis, acute renal failure and a residual pancerebellar syndrome occurred while taking a combination of perphenazine and amitriptyline. We postulate that impaired thermoregulation due to psychotropic drugs was responsible for the development of heat stroke and that the cerebellar syndrome resulted directly from the elevated temperature.Residual neurological deficits after recovery from hyperthermia, particularly heat stroke, are well known' and probably result directly from elevated body temperature.2 Impaired thermoregulation in patients taking neuroleptic drugs may lead to hyperthermia. We present a case in which hyperthermia with rhabdomyolysis, renal failure, and a persistent cerebellar syndrome developed during therapy with perphenazine and amitriptyline.Case report A 50-year-old woman was found in her home one hour after having collapsed. When discovered, she was alert, sweating, and unable to walk without assistance. She repeatedly became sweaty and subsequently collapsed again without losing consciousness, but was confused and was admitted to hospital. She had been taking a perphenazine and amitriptyline combination 4-25 and diazepam 10 mg each four times a day for seven years. On physical examination rectal temperature was 42-5C and *Present address:

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Cerebellar Syndrome Following Heat Stroke

Cited by 28 publications

References 3 publications

Cerebellar Edema

Cerebellar Edema

A Mid-Brain Syndrome Following Head Injury

Cerebellar syndrome following neuroleptic induced heat stroke.

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