Overheating – Rapid Recovery is not always the Outcome Raghu Maddela, Pegah Dehghan, Gary Inwald Montefiore Medical Center –Department of PM&R ResultsConclusionDiscussion Introduction Heat stroke results from prolonged exposure to high temperatures combined with dehydration. It can cause death or damage to the brain and other internal organs. The neurologic manifestations is as follows: Deep coma, areflexia, absent brainstem reflexes, automatic complex movements (chewing, swallowing). Recovery is usually uncomplicated but rarely developed pancerebellar syndrome or Gullian Barre syndrome. By the time she was admitted to acute rehab, the power in her extremities was 2 to 3-/5 and she had mild contractures in the distal muscles. She was completely dependent in almost all of her daily activity. She made improvement during the course of rehab and was able to ambulate 8 feet with bilateral dorsiflexion wraps within parallel bars requiring moderate assistance. She was discharged at wheel chair level of independence. Heat stroke can cause neurological sequelae by affecting the cerebellum or by causing Gullian Barre syndrome (GBS) like polyneuropathy. It can destroy the Purkinje cells in the cerebellum leading to cerebellar symptoms. It can activate the immune system by cytokine release and exposing the peripheral nerve antigens leading to GBS like polyneuropathy GBS like neuropathies with heat stroke have been reported in Saudi Arabia, but are uncommon in the United States. But an increase in sports activities during hot weather can put athletes at risk of heat stroke. The neurological sequalae are directly proportional to the duration of hyperthermia. ImagesMethods 17 year old female with no significant medical problems was admitted for heat stroke when she was found unconscious while attempting to cross over the Arizona border on foot. Initially she was confused, with generalized weakness and poor intake. She was stabilized and her mental status improved but was found to have quadriparesis. CT and MRI of the head were negative. She was subsequently transported to New York and admitted to the acute inpatient rehab unit as her weakness did not improve. Repeat CT and MRI of the brain were normal. She underwent NCS which suggested to have chronic diffuse sensorimotor peripheral neuropathy. She was also recommended CSF studies but she refused lumbar puncture. She had a prolonged course of inpatient rehab and was discharged home with services. References 1. Neurophysiological studies in a patient with heat stroke. Kalita J, Misra UKJ Neurol 2001;248:993– Peripheral neuropathy after heatstroke. Bouges F, Vijayan G, JauVerally F. Lancet1987;i: Guillain-Barré syndrome after heat stroke G Pfeiffer and W Steffen J Neurol Neurosurg Psychiatry March; 66(3): MR Imaging of Heat Stroke: External Capsule and Thalamic T1 Shortening and Cerebellar Injury Carol T. McLaughlin, Arthur G. Kane, and Andrew E. Auber AJNR Am J Neuroradiol : Neurologic manifestations of heatstroke at the Mecca pilgrimage Basim A. Yaqub, MRCP (UK) Neurology June 1987 vol. 37 no Top Left Aidife.blogspot.com Top Right Navyadancement.tpub.com MR Imaging of Heat Stroke: External Capsule and Thalamic T1 Shortening and Cerebellar Injury Carol T. McLaughlin, Arthur G. Kane, and Andrew E. Auber AJNR Am J Neuroradiol : Proton density–(A) and T2-weighted (B) axial MRI at the level of the third ventricle show hyperintensity (arrows) in the external capsules and medial thalami and altered signal intensity in the adjacent third ventricle.