A 57-year-old man presented with first episode of loss of consciousness at work in February 2014. He experienced no symptoms prior to this syncope event. He was witnessed by his colleagues to have tonic rigidity over his upper limbs, with a bite mark evident over the lateral aspect of his tongue. He had experienced a right-sided temporal headache characterised as dull and persistent for 3 weeks prior to this incident without any precipitating factors or aura identified.He enjoyed good past health and had been educated to high school level. He was currently working as an accountant. He did not smoke or drink, had no recent travel history, and was not on any long-term medication or taking herbs. He could not recall any febrile convulsion during childhood or significant family history of neurological diseases.He was fully oriented and remained afebrile on admission. Routine blood tests (electrolytes, glucose, and inflammatory markers), physical examination, and initial computed tomographic (CT) brain were unremarkable. The patient refused lumbar puncture and was discharged against medical advice.Three days after discharge, he was admitted to a private hospital with generalised tonic-clonic convulsion. Electroencephalography was normal and magnetic resonance imaging (MRI)/magnetic resonance angiography brain showed no mass lesion or infarct. He was discharged with a prescription of levetiracetam in view of the second episode of seizure.He was again admitted to us in early March 2014 with breakthrough seizure and post-ictal drowsiness, despite good drug compliance and no identifiable precipitating factors. His seizure was initially controlled with levetiracetam with the addition of phenytoin, but he remained disoriented with confused speech. His Mini-Mental State Examination (MMSE) score was 14/30: his main deficit was delayed recall with failure to perform serial sevens and to copy a polygon. He developed a low-grade fever of 37.8°C with negative septic workup. Lumbar puncture did not reveal any evidence of central nervous system infection (white cell count, <1/mm 3 , protein level not elevated, and negative culture result). Electroencephalography showed right temporal spikes only. He was prescribed empirical Augmentin (Sandoz, Australia) 1.2 g every 8 hours intravenously and his fever settled. One week after admission, he experienced multiple episodes of generalised tonic-clonic seizure without progression to status epilepticus. Doses of both phenytoin and levetiracetam were increased along with the addition of valproic acid. His seizures abated but cognition was not improved. Electroencephalography was repeated and demonstrated left temporal polyspikes over F7/T3/T5 in addition to bitemporal sharp waves (Fig 1). Brain MRI was also repeated and showed no abnormality (Fig 2). Blood tests were unremarkable with normal electrolytes, negative tumour markers (alphafetoprotein/carcinoembryonic antigen/prostatespecific antigen), negative autoimmune markers (antinuclear antibodies/rheumatoid factor), normal thyroid functio...

Obstructive sleep apnoea is usually associated with obesity and is caused by recurrent collapse of the pharyngeal airway during sleep at multiple levels. Vocal cord paralysis is an uncommon cause of obstructive sleep apnoea. We describe a patient with obstructive sleep apnoea caused by idiopathic vocal cord paralysis. He also had features of autonomic failure including orthostatic hypotension and urinary retention.