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A 52‐year‐old gentleman presented with fearfulness, insomnia, decreased speech output, and mild slowness of gait, of 1 month duration. On further questioning, he said that he had developed transient nausea and blurred vision following rapid ascent of 20,000 feet (6096 m) in the mountains 1 month ago. On examination, speech was hypophonic with decreased spontaneity of speech, minimal bradykinesia, no rigidity, and normal gait. Magnetic resonance imaging (MRI) brain showed bilateral globus pallidus (GP) hyperintensities in fluid attenuated inversion recovery/T2 sequences (Fig. 1A) with normal T1 and susceptibility weighted imaging sequences. Nine months later, he developed low motivation and lack of interest in routine activities. Repeat MRI brain showed cystic changes of bilateral GP (Fig. 1B–D) in addition to microbleeds in GP (Fig. 1E,F) and corpus callosum. Prominent behavioral changes with mild parkinsonism have been reported after mountaineering. 1 , 2 Secondary vasoconstriction after rapid ascent may cause hypoxia because of sudden decline in oxygen pressure, resulting in basal ganglia (BG) damage. 1 Transient BG hypometabolism may explain reversible parkinsonism and normal imaging after ascent. Bilateral GP necrosis was reported in brain anoxia, and disulfiram, cyanide toxicity, and carbon monoxide poisoning. 2 To prevent acute mountain sickness, ascent up to 3000 m on the first day followed by 2 to 3 nights' stay at that altitude and subsequent slow ascent, is recommended.