Holmes tremor has a characteristic rest, intention, and postural component. The syndrome arises as a consequence of a lesion in the upper brainstem and cerebral peduncles, which, it is postulated, interrupts the cerebello-rubrothalamic pathway. Ataxia, ophthalmoplegia, and bradykinesia are associated features. We present a case of Holmes tremor secondary to a midbrain cavernoma. Modern neuroimaging techniques in this case confirm that a combination of damage to the cerebello-rubrothalamic pathway and the nigrostriatal pathway is required for the full Holmes tremor syndrome to occur.
Copyright 2006 Movement Disorder Society.