Acute Contralateral Hemibody Hyperhidrosis in Gasperini Syndrome Associated With Intracranial Vertebral Artery Dissection: A Case Report

Gasperini syndrome is a rare crossed brainstem syndrome caused by lesions of the caudal pontine tegmentum, characterised by ipsilateral cranial nerve (CN) V-VIII dysfunction and contralateral hemibody hypoalgesia; fewer than 20 cases have been documented since its original description in 1912.We present a 57-year-old man who developed acute left peripheral facial palsy, left abducens palsy, left facial hypoaesthesia, left (clinically assessed) hypoacusis, and gait instability, with clinically complete ipsilateral CN V-VIII involvement.Contralateral pain and temperature and touch sensation were formally tested and intact.From the initial presentation, he exhibited prominent diaphoresis restricted to the contralateral (right) hemibody, without ipsilateral anhidrosis or Horner syndrome, and remained afebrile throughout admission.Brain MRI demonstrated an acute ischaemic infarct at the medial posterior left pontine tegmentum.Susceptibility-weighted imaging showed an eccentric crescent-shaped intramural haematoma at the left intracranial vertebral artery (V4), confirming vertebral artery dissection; digital subtraction angiography showed a long intracranial stenosis of the left vertebral artery and the right vertebral artery terminating in the posterior inferior cerebellar artery (PICA), a recognised anatomical variant.To our knowledge, contralateral hemibody hyperhidrosis has not previously been reported in Gasperini syndrome.We propose, as an anatomical hypothesis rather than a demonstrated mechanism, that it reflects disruption of crossed sympatho-inhibitory sudomotor fibres in the medial/paramedian pontine tegmentum, with sparing of the dorsolateral excitatory and oculosympathetic pathways, concordant with the medial lesion topography and the absence of Horner syndrome.