Heat stroke induced acute cerebellar syndrome

Dear Sir, A 47-year-old male patient presented with a history of prolonged exposure to extreme heat after traveling during the summer season. The patient, who had no previous comorbidities or psychiatric history, was initially admitted to an external facility with high-grade fever (106°F) and generalized weakness. On the following day, the patient experienced a seizure, which was followed by a loss of consciousness, necessitating intubation. Upon extubation two days later, the patient remained confused and agitated. Subsequently, he was transferred to our center for further evaluation and treatment. Upon admission, the patient was drowsy, irritable, and unable to cooperate with comprehensive neurological assessment. His axillary temperature was 103°F, with a pulse rate of 120 beats per min and blood pressure of 130/80 mmHg. Initial investigations failed to identify the precise etiology of his altered sensorium. Over the next 3 to 4 days, the patient’s sensorium showed slight improvement, although he remained confused. Following the resolution of his fever, the patient remained mute for an additional 5 to 7 days, though he was unable to follow some commands. On regaining full consciousness, the patient exhibited classic signs of cerebellar dysfunction, including dysarthria, limb ataxia, and titubation. Significant incoordination was observed in both the upper and lower limbs. The fundus examination and ocular movements were within normal limits, with no evidence of nystagmus [Video 1]. {"href":"Single Video Player","role":"media-player-id","content-type":"play-in-place","position":"float","orientation":"portrait","label":"Video 1","caption":"","object-id":[{"pub-id-type":"doi","id":""},{"pub-id-type":"other","content-type":"media-stream-id","id":"1_4vq33tbg"},{"pub-id-type":"other","content-type":"media-source","id":"Kaltura"}]} Routine laboratory tests, including complete blood counts (CBC), liver function tests (LFTs), renal function tests (RFTs), and coagulation parameters, were all within normal limits. Cerebrospinal fluid (CSF) analysis was also unremarkable. Given the subacute onset of seizures followed by cerebellar dysfunction, differential diagnoses of herpes simplex virus (HSV) encephalitis and autoimmune encephalitis were considered. However, both CSF HSV-PCR and the autoimmune encephalitis panel yielded negative results. Brain MRI imaging revealed mild cerebellar and cerebral atrophy, while CT venography ruled out the presence of venous thrombosis [Figure 1].Figure 1: MRI Brain of 43 year old male demonstrating mild cerebellar atrophy in the following sequences. (a) T1, (b) T2, (c) T2 FLAIR, (d) DWI, (e) ADC, (f) SWI. (g) T2 sagittal section, (h and i) show rest of the cortexThe patient was managed conservatively with external cooling, intravenous fluids, antibiotics, and antiepileptic medications. Over time, his sensorium gradually improved; however, cerebellar signs, including titubation, incoordination, and limb weakness, persisted. Upon reexamination, his reflexes were found to be brisk, and plantar responses were mute, suggesting involvement of the pyramidal tract. Despite gradual improvement, the patient was discharged in a bedridden state. At a one-month follow-up, he remained wheelchair-bound and could walk only with significant assistance, with contributed limb incoordination and weakness. Hyperpyrexia, characterized by an exceptionally elevated body temperature, can have devastating effects on multiple organ systems, particularly the central nervous system (CNS). Neurological complications often result from damage to the cerebellum, basal ganglia, anterior horn cells, and peripheral nerves. Damage to the cerebellum, in particular, has been linked to generalized atrophy and degeneration of Purkinje cells. Heat stroke, a severe form of hyperthermia, frequently results in symmetrical cerebellar damage, leading to profound neurological impairment.[1] Neurological manifestations of heat-induced hyperpyrexia may include ataxia, dysarthria, hemiparesis, quadriparesis, seizures, and myelopathy. The cerebellum is particularly vulnerable, with damage typically affecting both the vermis and cerebellar hemispheres, while the cerebral hemispheres are relatively spared.[2] The severity of cerebellar damage is typically correlated with the degree and duration of hyperthermia, with Purkinje cells being affected within the first 24 hours of elevated temperatures.[3] Several case reports have highlighted how hyperpyrexia can lead to cerebellar dysfunction and neurological damage, particularly in Parkinsonism-Hyperpyrexia Syndrome (PHS). PHS is a rare but potentially fatal condition, often caused by the sudden withdrawal of dopaminergic medications in patients with Parkinson’s disease patients. Symptoms of PHS include hyperpyrexia, muscular rigidity, and altered mental status. This syndrome shares similarities with the cerebellar damage induced by heat stroke in hyperpyrexia-related cases.[4] Neuroleptic malignant syndrome (NMS) also involves hyperpyrexia and shares clinical features akin to cerebellar syndrome in hyperpyrexia.[5] In the present case, prolonged exposure to high ambient temperatures likely led to heat stroke and subsequent cerebellar damage. Hyperpyrexia can result from external factors, such as environmental heat, and internal causes, including infections, excessive exertion, or metabolic disturbances (e.g., neuroleptic malignant syndrome). The rapid progression of neurological symptoms in this patient suggests that hyperpyrexia-induced cerebellar syndrome was the key underlying mechanism. Hyperpyrexia constitutes a medical emergency that requires prompt treatment to prevent serious CNS damage, particularly to the cerebellum. Early recognition and intervention in cases of elevated body temperature are essential for minimizing long-term neurological deficits. Patients with heat-induced cerebellar damage, as observed in this case, may experience a prolonged recovery period, with significant residual symptoms despite early treatment. Acknowledgement Nil.