Paroxysmal sympathetic hyperactivity: the storm after acute basilar artery occlusion

Excerpt

A 61-year-old male patient with a history of hypertension presented with acute dysarthria and confusion. He was admitted to the emergency department 3 h after onset. A rapid decline occurred in his level of consciousness to coma with bilateral extensor posturing and intermittent limb shaking. The bilateral pupil diameter was 1.0 mm, and the light reflex disappeared. He was febrile (40.0 °C), sweating, tachycardic (124 beats per min), tachypneic (24 beats per min), and hypertensive (180/95 mmHg). These symptoms lasted 20–30 min and occurred twice within 3 h. The clinical features observed were consistent with the diagnosis of probable paroxysmal sympathetic hyperactivity¹ (PSH). The PSH Assessment Measure [1] score is 22. The patient received intravenous injection of 20 mg diazepam but had a poor response. Brain computed tomography (CT) scan revealed no abnormalities. Standard dose of alteplase was given for intravenous thrombolysis. Subsequently, digital subtraction angiography (DSA) showed basilar artery occlusion (Fig. 1A). The basilar artery was recanalized well after thrombectomy (Fig. 1B). The symptoms of paroxysmal sympathetic hyperactivity disappeared after thrombectomy. Brain magnetic resonance imaging (MRI) showed restricted diffusion in the pons, midbrain, cerebellum, occipital lobe, and thalamus (Fig. 1C). The symptoms improved significantly after 14 days of treatment and the patients was discharged. The National Institutes of Health Stroke Scale (NIHSS) score and modified Rankin Scale (mRS) score at 90 days are 4 and 1, separately. During a 3-year follow-up, he had residual left diplopia and mild dysarthria and had no further stroke.

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