Brain injury following neuroleptic malignant syndrome: Case report and review of the literature

Labuda, Anna; Cullen, Nora

doi:10.1080/02699050600663022

Cited by 10 publications

(9 citation statements)

References 18 publications

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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: 93%

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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Section: Discussionmentioning

confidence: 93%

Brain pathology in fatal serotonin syndrome: Presentation of two cases

et al. 2010

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“…Majority of the cases reported were in burn, traumatic brain injury or perioperative setting 5 – 10. All neuroleptics have been implicated in the genesis of NMS, although, high-potency agents like haloperidol is reported most often with NMS 11 12.…”

Section: Discussionmentioning

confidence: 99%

Neuroleptic malignant syndrome associated with haloperidol use in critical care setting: should haloperidol still be considered the drug of choice for the management of delirium in the critical care setting?

2013

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A 48-year-old man was brought to the emergency department because of intoxication. The patient was in respiratory distress, subsequently intubated for airway protection. On hospital day 5, he was diagnosed with delirium. Haloperidol was initiated at 5 mg intravenous every 6 h and titrated up to a dose of 60 mg /day over 5 days. On hospital day 18, his temperature peaked to 107.1°F. Other symptoms included mental status change, muscular rigidity and autonomic dysfunction. Neuroleptic malignant syndrome (NMS) associated with haloperidol was suspected. No other causes for these symptoms were present. Concurrent medications were reviewed and ruled out for possible drug-induced fever. Haloperidol was discontinued and dantrolene and bromocriptine was initiated. The temperature decreased to 102.2°F within 3 h and other symptoms resolved overtime. The temporal relationship between the patient's fever decline with the discontinuation of haloperidol, and improvement with dantrolene and bromocriptine, the diagnosis was believed to be haloperidol-induced NMS.

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“…These may be mild, or severe, up to and including severe global dementia. They have been reported after CHS [ 18 ], EHS [ 19 ], and drug-induced hyperthermia [ 20 , 21 ].…”

Section: Clinical Patternsmentioning

confidence: 99%

The neurological and cognitive consequences of hyperthermia

2016

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An elevated temperature has many aetiologies, both infective and non-infective, and while the fever of sepsis probably confers benefit, there is increasing evidence that the central nervous system is particularly vulnerable to damage from hyperthermia. A single episode of hyperthermia may cause short-term neurological and cognitive dysfunction, which may be prolonged or become permanent. The cerebellum is particularly intolerant to the effects of heat. Hyperthermia in the presence of acute brain injury worsens outcome. The thermotoxicity involved occurs via cellular, local, and systemic mechanisms. This article reviews both the cognitive and neurological consequences and examines the mechanisms of cerebral damage caused by high temperature.

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Brain injury following neuroleptic malignant syndrome: Case report and review of the literature

Cited by 10 publications

References 18 publications

Brain pathology in fatal serotonin syndrome: Presentation of two cases

Brain pathology in fatal serotonin syndrome: Presentation of two cases

Neuroleptic malignant syndrome associated with haloperidol use in critical care setting: should haloperidol still be considered the drug of choice for the management of delirium in the critical care setting?

The neurological and cognitive consequences of hyperthermia

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