Magnetic Resonance Imaging Reveals Selective Vulnerability of the Cerebellum and Basal Ganglia in Malignant Hyperthermia

Park, Jeong‐Wook; Choi, Young-Bin; Park, Soung-Kyung; Kim, Yeong-In; Lee, Kwang‐Soo

doi:10.1001/archneur.61.9.1462

Cited by 10 publications

(8 citation statements)

References 4 publications

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“…Identification of RYR1 mutations in such individuals is important, even post mortem, to clarify the cause of death and to advice asymptomatic carrier relatives about their potential MH risk. Interestingly, a similar pattern of CNS injury has previously also been reported in a patient with a genetically unresolved MH episode [13], further supporting a tentative link between the pattern of CNS involvement in our patient, MH and heat-induced brain injury in general.…”

Section: Discussionsupporting

confidence: 90%

RYR1-related malignant hyperthermia with marked cerebellar involvement – A paradigm of heat-induced CNS injury?

Forrest

Foulds

Millar

et al. 2015

Neuromuscular Disorders

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Section: Discussionsupporting

confidence: 90%

RYR1-related malignant hyperthermia with marked cerebellar involvement – A paradigm of heat-induced CNS injury?

Forrest

Foulds

Millar

et al. 2015

Neuromuscular Disorders

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“…9 Malignant hyperthermia, a reaction to anesthetic gases which raises the body temperature, has also been shown to result in selective injury to the cerebellum and basal ganglia. 10 Neuroleptic malignant syndrome, which also leads to extreme hyperthermia, is shown to induce selective death of neurons in the cerebellum. 11 This syndrome is an idiosyncratic, life-threatening complication of treatment with antipsychotic drugs, is characterized by severe muscle rigidity and caused by blockade of dopamine receptors.…”

Section: Discussionmentioning

confidence: 99%

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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“…After WBH, lesions to CNS only occur in the presence of other physiological derangements. In a recent report on malignant hyperthermia, damage has been observed primarily in the cerebellum [56].…”

Section: Discussionmentioning

confidence: 99%

Effects of hyperthermia on the central nervous system: What was learnt from animal studies?

Haveman

Sminia

Wondergem

et al. 2005

International Journal of Hyperthermia

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Animal studies show that nervous tissue is sensitive to heat. Although inter-species variations may play a role, the data indicate that the maximum heat dose without obvious complications after localized hyperthermia in regions of the central nervous system (CNS) lies in the range of 40-60 min at 42-42.5 degrees C or 10-30 min at 43 degrees C. Expression of thermotolerance after a 'conditioning' heat dose was clearly observed in the spinal cord of rodents and the thermotolerance ratio's (ratio between heat doses with and without conditioning required to obtain a certain defined effect) were high, approximately 2. The thermotolerant state of CNS is shown to protect also against other types of injury as well: pre-treatment of rats with hyperthermia protected against spinal cord ischemic injury. During the rather long period required for temperature elevation which is inherent to WBH, some degree of thermotolerance may develop. The correlation between thermotolerance and hsp70 induction in CNS is obvious. Heat, at least if applied shortly after X-rays, enhances the response of nervous tissue to radiation. Data on the combined effects of X-ray irradiation and hyperthermia on rodent spinal cord clearly show that the radiation response can be enhanced with a factor of 1.1-1.3. There are no clear experimental data indicating an increase in adverse effects specific to the CNS after localized or whole body hyperthermia as a result of combined treatment with chemotherapy.

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Magnetic Resonance Imaging Reveals Selective Vulnerability of the Cerebellum and Basal Ganglia in Malignant Hyperthermia

Cited by 10 publications

References 4 publications

RYR1-related malignant hyperthermia with marked cerebellar involvement – A paradigm of heat-induced CNS injury?

RYR1-related malignant hyperthermia with marked cerebellar involvement – A paradigm of heat-induced CNS injury?

Brain pathology in fatal serotonin syndrome: Presentation of two cases

Effects of hyperthermia on the central nervous system: What was learnt from animal studies?

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