Cerebellar syndrome following neuroleptic induced heat stroke.

Lefkowitz, David; Ford, C S; Rich, Courtney; Biller, José; McHenry, Lawrence C.

doi:10.1136/jnnp.46.2.183

Cited by 31 publications

(10 citation statements)

References 22 publications

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“…In the present case, the cerebellum had lesions similar to those described by Malamud et al,s consistent with the fact that a cerebellar syndrome is the most frequent permanent neurological sequela of the heat stroke. 9 The absence of lesions in the cerebrum in this case does not support the hypothesis of a greater sensitivity of cortical neurons to hyperthermia.…”

Section: Discussioncontrasting

confidence: 63%

Spinal cord lesions in heat stroke.

Delgado¹,

Tuñón²,

Gállego³

et al. 1985

Journal of Neurology, Neurosurgery & Psychiatry

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SUMMARY A clinical and pathological report of a patient who died 15 days after suffering a classic heat stroke is presented. The clinical picture was of a flaccid quadriplegia with anhidrosis and sphincter disturbance. The most severe pathological lesions were to be seen in the anterior and intermedio-lateral horns of the spinal cord. Hyperthermia was the only physiopathological mechanism demonstrated in the patient. It is suggested that the motor neurons and vegetative neurons of the spinal cord are specially sensitive to hyperthermia.There is a considerable literature, as listed in recent reviews, on the epidemiology, pathogenesis, physiopathology and clinical features of heat stroke.' 4 There are few neuropathological studies, in spite of the fact that there are always characteristic signs and symptoms of neurological involvement. The basic neuropathology reference work is still that by Malamud et al in 1946, who studied 125 fatal cases of heat stroke induced by physical exercises and described characteristic lesions in the cerebrum, cerebellum and skeletal muscles. This paper presents a clinical and pathological study of a case of classic heat stroke, with no damage to the cerebrum but with severe neuronal lesions in the spinal cord. Cae reportA 66-year-old man was referred to the Hospital of Navarra; for the previous 3 hours he had remittent rightsided somatomotor partial seizures with secondary generalisation. The patient, who suffered from manic depressive psychosis, was a long term in-patient of a psychiatric hospital which had no air-conditioning. He had been receiving continuous medication with amitryptiline (30 mg/day), imipramine (75 mg/day) and pherphenazine (6 mg/day). For the previous few days, the region had a heat wave with maximum temperatures of 38°C. examination. Neurological examination was normal except for a moderate drowsiness and mental confusion. Routine biological tests, including electrolytes, pH and clotting were normal except for a leucocytosis of 10.000 cells/mm3. CT scan and CSF were normal. The EEG recording was diffusely slowed (5 Hz). The rectal temperature was reduced to 38°C by physical means of cooling over the following 10 hours. Twelve hours after admission, the patient developed an acute respiratory insufficiency owing to weakness of the respiratory muscles and required endotracheal intubation and mechanical ventilation. At the same time he was found to be quadriplegic, with muscular hypotonia, absence of muscle stretch and skin reflexes, retention of urine and faecal incontinence. The cranial nerves, sensation and the level of consciousness were preserved. This neurological situation continued without change for 14 days, after which the patient suddenly died. During all this time, no sweating was seen, continuous physical cooling methods being required to maintain a normal body temperature. During the first 72 hours of the course of this illness, there was a rise in the skeletal isoenzyme of serum creatine kinase to 9-950 U/ml, which gradually became normal over the next...

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Section: Discussioncontrasting

confidence: 63%

Spinal cord lesions in heat stroke.

Delgado¹,

Tuñón²,

Gállego³

et al. 1985

Journal of Neurology, Neurosurgery & Psychiatry

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“…23 Neurologic residual symptoms after neuroleptic malignant syndrome with hyperthermia are also known to occur. 24,25 In conclusion, we present two cases of fatal serotonin syndrome that both showed subtotal loss of Purkinje cells in the cerebellum. A similar loss of Purkinje cells is described in other conditions characterized clinically by hyperthermia.…”

Section: Discussionmentioning

confidence: 94%

Brain pathology in fatal serotonin syndrome: Presentation of two cases

et al. 2010

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Serotonin syndrome is a potentially life-threatening reaction that occurs in patients using drugs that elevate the serotonin level in the body. Excess serotonergic activity in the CNS and peripheral serotonin receptors results in neuromuscular hyperactivity, mental changes and autonomic symptoms. Hyperthermia is a characteristic feature of the syndrome. We describe neuropathological findings from two cases of lethal serotonin syndrome, both patients presenting with hyperthermia and neuromuscular symptoms. One of the patients had been taking amitriptylin and mirtazapin and the other had used amitriptylin and citalopram. They died, respectively, 10 days and 2½ months after the onset of serotonin syndrome symptoms. Post-mortem examination of the brains showed subtotal loss of cerebellar Purkinje cells in both cases. In the case with shorter survival time, areas with partial loss of cerebellar granule cells were observed, whereas in the case with longer survival time general and extensive loss of granule cells was found. Cells in other areas of the brain known to be sensitive to hypoxic injury were not affected. Selective loss of Purkinje cells has previously been described in neuroleptic malignant syndrome and heatstroke, conditions that are characterized by hyperthermia. This suggests that hyperthermia may be a causative factor of brain damage in serotonin syndrome. This is the first report describing neuropathological findings in serotonin syndrome.

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“…Hyperthermia can be extremely harmful and potentially fatal because it may result in permanent neurologic sequelae like Cerebellar syndrome if not treated properly [7] [8]. The hyperthermia may eventually lead to life threatening complications, such as disseminated intravascular coagulation (DIC), renal failure, metabolic acidosis, cardiac dysfunction, and coma [7]- [9].…”

Section: Introductionmentioning

confidence: 99%

“…The mainstay of treatment in hyperthermic conditions includes withdrawal of triggers, supportive therapy with cooling techniques and pharmacotherapy aimed at reducing core body temperature [3]- [7]. Among the few pharmacological options available dantrolene a drug used in the treatment of MH may be beneficial in several hyperthermic conditions [10]- [13].…”

Section: Introductionmentioning

confidence: 99%

Dantrolene in the Treatment of Refractory Hyperthermic Conditions in Critical Care: A Multicenter Retrospective Study

Pawar¹,

Rosenberg²,

Adamson³

et al. 2015

OJAnes

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Purpose: To examine the use of intravenous dantrolene in hospitalized patients. Materials and Methods: Medical Records of patients treated with intravenous dantrolene between 2007 and 2012 at 6 teaching hospitals were reviewed. Temperature, muscle rigidity, creatine kinase levels, and mortality were assessed in association with dantrolene use. Results: Twenty-five patients received intravenous dantrolene, 9 patients with neuroleptic malignant syndrome (NMS), 8 with hyperthermia due to sepsis, 4 with NMS and sepsis, 2 for malignant hyperthermia (MH), and 2 with hypermetabolic syndrome associated with juvenile diabetic ketoacidosis. Dantrolene was administered as a bolus of 1 -3 mg/kg. Core temperature decreased after dantrolene administration in all groups but significant only for MH, NMS cases (Pre 102.3 ± 0.9˚F vs. Post 99.5 ± 0.9˚F; p < 0.001), in Sepsis cases (Pre 104.3 ± 1.5˚F vs. Post 100.6 ± 1.0˚F; p < 0.001). Mean rigidity scores decreased in all groups but significant only for NMS cases, and mean CK did not change significantly in any group. Conclusion: Dantrolene was associated with reductions in temperature and rigidity in hyperthermia of diverse origins in patients admitted to Intensive care settings.

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Cerebellar syndrome following neuroleptic induced heat stroke.

Cited by 31 publications

References 22 publications

Spinal cord lesions in heat stroke.

Spinal cord lesions in heat stroke.

Brain pathology in fatal serotonin syndrome: Presentation of two cases

Dantrolene in the Treatment of Refractory Hyperthermic Conditions in Critical Care: A Multicenter Retrospective Study

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