Post-insult valproate treatment potentially improved functional recovery in patients with acute middle cerebral artery infarction.

Animal stroke models suggest that valproate has multiple neuroprotective mechanisms against ischemic brain damage. This study investigated whether valproate improves functional recovery in patients with acute middle cerebral artery (MCA) infarction. This was an open-label controlled trial. Three to 24 hours after acute MCA infarction, patients were assigned to either the valproate group (n = 17) or the non-valproate group (n = 17). The valproate group received intravenous valproate (400 mg) at enrollment, and then every 12 hours for three days, followed by oral valproate (500 mg) every 12 hours for three months. Neurological function, laboratory data, and brain magnetic resonance imaging were examined at stroke onset, and at two-week and three-month follow-up. No significant differences were observed between the groups with regard to demographics or baseline characteristics. All patients were elderly, had a high pretreatment score on the NIH stroke scale (NIHSS), and slow stroke lesion growth with a final large infarct volume at two-week follow-up. At the three-month follow-up, functional outcome between pre- and post-treatment had improved significantly in the valproate group (NIHSS, p = 0.004; modified Rankin scale (mRS), p = 0.007; Barthel index (BI), p = 0.001). No such improvement was noted in the NIHSS or mRS for the non-valproate group, though mild improvement was seen on the BI (p = 0.022). This open-label trial is the first to demonstrate that valproate treatment markedly improves functional outcome in patients with acute MCA infarction.

Acute bilateral hearing loss as a "worsening sign" in a patient with critical basilar artery stenosis.

We report a patient who presented with an acute-onset transient vertigo and unsteady gait with bilateral hearing loss. Brain MRI revealed a critical basilar artery (BA) stenosis at the lower pons and infarction in various areas on both sides in the territories of the posterior inferior cerebellar arteries (PICA). Further, we could not visualize the right anterior inferior cerebellar artery (AICA). The bilateral hearing loss may be ascribed to stroke due to the critical BA stenosis, causing hypoperfusion injury extending from the PICA to the AICA on both sides. Local intra-arterial thrombolytic therapy with the administration of 1×10(6) IU of urokinase aided partial recanalization of the BA, after which the right AICA reappeared. The neurological function of the patient recovered to normal, and no hemorrhagic complications were observed. Therefore, practitioners should be alert when treating patients with acute bilateral hearing loss, which may be related to an underlying catastrophic stroke.