Neurophysiological studies in a patient with heat stroke

Sirs: Heat stroke results in a wide variety of neurological complications which are due to cerebellar, basal ganglia, anterior horn cell and peripheral nerve involvement. Computed tomography and MRI studies have revealed cerebellar atrophy and white matter involvement in heat stroke [4]. Neurophysiological studies provide insight into the functional alterations on the nervous system although there are only a few reports on neurophysiological changes in patients with heat stroke which include nerve conduction and F response abnormalities [2,7]. Alterations in somatosensory evoked potentials have been reported in experimental animals [6]. In this communication, we report a comprehensive account of neurophysiological and MRI changes in a patient with heat stroke. In the last week of July 1998, a 75 year old lady after a heavy lunch walked 2–3 km at a sunny noontime when the ambient temperature was 42.2 °C. On reaching her destination she was exhausted, developed high fever and became unconscious. Her temperature reached 42.2 °C. She was subjected to cold sponging and antipyretic therapy. Gradually her consciousness improved after 3 days and she became mentally alert. She however was found to have severe truncal and limb ataxia and head nodding. Two months after her illness she was admitted in our hospital. On examination, her BP was 120/80 mm Hg, pulse 72/min regular and systemic examination was normal. Neurological examination revealed staccato speech with pronounced truncal ataxia and titubation. Her mental status was normal and minimental scale score was 28. There was no nystagmus or cranial nerve palsy. The muscle tone was reduced in all 4 limbs with grade IV power in the upper and grade III in the lower limbs. Deep tendon reflexes were absent bilaterally. Sensations of pinprick, joint position and vibration were normal. Blood sugar was 95 mg%, blood urea nitrogen 20 mg% and serum creatinine 1.2 mg%. Radiograph of chest, ECG and ultrasonography of abdomen were normal. Cranial MRI revealed prominent cerebellar sulci and basal cisterns suggesting brainstem and cerebellar atrophy. Nerve conduction study revealed unrecordable peroneal conductions bilaterally. Median and ulnar motor nerve conduction velocities were normal but compound muscle action potentials (CMAPs) were reduced. Concentric needle electromyography of tibialis anterior, gastrocnemius, vastus medialis, first dorsal interosseus and brachioradialis revealed fibrillations in tibialis anterior, gastrocnemius and first dorsal interosseus. Motor unit potentials were of long duration with 20–30 % polyphasia and recruitment pattern was reduced. Median and tibial somatosensory evoked potentials (SEPs) were normal. Central motor conduction time (CMCT) to abductor digiti minimi was normal bilaterally, 5.6 ms on either side (upper limit of normal 8.1 ms); whereas CMCT to tibialis anterior was prolonged being 20.4 ms on the right and 18.8 ms on the left side (upper limit of normal 16.1 ms; Fig 1). Electroencephalography was normal. Two months following her illLETTER TO THE EDITORS