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A 46-year-old woman presented with tetraplegia contrasting with a relatively preserved consciousness following aneurysmal subarachnoid hemorrhage (SAH). Multiple ischemic lesions were detected by magnetic resonance imaging (MRI), in the absence of vasospasm or signs of increased intracranial pressure. During the weeks before SAH, the patient had repeatedly used a nasal decongestant containing phenylephrine. After coiling of the aneurysm harboured by the right posterior cerebral artery, symptomatic vasospasm developed in the territory of the right middle cerebral artery and required aggressive therapy by intra-arterial infusion of milrinone followed by continuous intravenous administration. Follow-up MRI did not reveal new ischemic lesions. Echocardiography had demonstrated the presence of a patent foramen ovale. At 3 months follow-up, a major motor deficit persisted with akinetic mutism. The mechanisms of multiple early infarction following aneurysmal SAH are still debated, as vasospasm is usually not seen on the first imaging. Among precipitating factors of microvascular vasospasm, vasoactive substances like phenylephrine, may play a significant role.

A 73-year-old man developed a fulminant form of Guillain-Barrd syndrome with abolition of brainstem reflexes. Antibodies to GQ1b were positive (1:180). The clinical findings mimicked a "brain death" pattern for a period of 12 days. In contrast, the EEG showed remaining cerebral electrical activity. Brainstem auditory evoked potentials, long-latency auditory potentials and flash-evoked visual potentials were normal. However, no peripheral and cortical somatosensory evoked potentials could be elicited. Accordingly, nerve conduction studies were indicative of motor and sensory axonal neuropathy. After 5 months, the patient had no apparent cognitive deficit but was still quadriplegic and dependent from the mechanical ventilation. He died on day 158 from nosocomial infection, without motor recovery. Other published cases with a similar admission pattern were reviewed. The prognosis is usually very poor; as most of the patients died or remained severely disabled.

A 61-year-old man without previous medical history was admitted for Guillain-Barré syndrome (GBS). Carbamazepine was prescribed on day 72 for dysesthesia occurring at the time of recovery. Subsequently, severe cardiac conduction disturbances (asystole, atrioventricular block) were observed and a permanent pacemaker had to be inserted. The possible relationship between carbamazepine therapy and cardiac side effects is discussed in this condition, as GBS itself is often complicated by cardiac arrhythmias.

Severe Guillain-Barré syndrome (GBS) usually results in life-threatening autonomic disturbances requiring a close monitoring of the patient in an Intensive Care Unit. Besides dangerous cardiac manifestations, neuroendocrine changes are also reported and could induce electrolytes and fluid balance impairments. Polyuria has been observed in a severe case of GBS occurring in a 16-year-old boy. Consecutive blood samples were obtained for renin, aldosterone, antidiuretic hormone and atrial natriuretic factor measurements. Polyuria in GBS is multifactorial and would be partly due to a dysregulation of osmoreceptors.

A case of Streptococcus suis meningitis is observed in a 39-year-old and previously healthy meat factory worker. Neurological recovery was incomplete despite adequate and sustained antimicrobial therapy. Early deafness was demonstrated by brainstem auditory evoked potentials. Death due to aspiration pneumonia, cardiac arrest and subsequent cerebral anoxia occurred late in the course of the illness.