Within a 10-y period, fatal strokes occurred during parenteral administration of amphotericin B and surgical debridement of paranasal sinuses in 6 pathologically verified cases of rhino-orbito-cerebral mucormycosis (ROCM). All patients had unnoticed type-2 diabetes mellitus without ketoacidosis. They presented with unilateral orbital cellulitis and cavernous sinus syndrome. Fatal malignant cerebral infarctions occurred in the carotid system in 5 patients, and in the basilar artery or its major branches in 2 patients. Accelerated thrombotic occlusion of the cavernous portion of the carotid artery or the basilar artery was likely to be due to mucormycosis associated-vasculopathy and diabetic vasculopathy. One patient died of massive subarachnoid hemorrhage following rupture of the mycotic aneurysm. Despite parenteral administration of amphotericin B, fatal outcome of ROCM in patients with unnoticed diabetes mellitus occurs due to mucormycosis-associated malignant strokes. To improve outcome, a combination of early radical debridement, ocular exenteration, parenteral and local administration of amphotericin B, and decompression craniotomy should be considered.
AbstractTo determine one-year clinical outcome of patients with first-ever acute ischemic stroke involving the territory of paramedian mesencephalic arteries (PMAS), we conducted a prospective study evaluating the cognitive functions of 28 patients with PMAS. Neuropsychological tests were performed during the first month of stroke onset and at the 12th month of follow-up. There were 12 women and 16 men. Mean age of onset for women and men was 70 years and 65 years, respectively. Progressing strokes occurred in 62% of patients and 96% developed a full-blown picture of the clinical triad of akinetic mutism, hypersomnolence, and bilateral blepharoptosis and ophthalmoparesis. Involuntary movements occurred in 6, and focal myoclonus in 4 patients. The top four associated risk factors were hypertension (68%), hyperlipidemia (57%), diabetes mellitus (46%), and atrial fibrillation (36%). Unilateral midbrain infarctions occurred in 12 patients and bilateral lesions in 16. Thalamic infarctions were unilateral in 10 and bilateral in 13 cases. Three of the 28 (11%) patients died of recurrent cerebral infarctions within 1 year of the onset of PMAS. The recurrent infarctions involved the basilar artery territory in two cases and the carotid system in another. One patient died of acute myocardial infarction. Of the 24 patients who had survived the stroke by 1 year, 20 (71%) developed dementia. We conclude that first-ever ischemic stroke with PMAS is not a benign syndrome. Most patients developed dementia by 1 year after the stroke.
We report on silent brain infarction (SBI) and leuko- araiosis (LA) of 23 patients with clinically diagnosed “first-ever” acute ischemic lacunar stroke. The lacunar syndromes were pure motor hemiparesis (10), pure sensory syndrome (2), ataxic hemiparesis (3), dysarthria clumsy hand syndrome (3), and sensory- motor deficit (5). Nineteen out of the 23 patients presented with completed strokes on arrival to the hospital, and 4 (17%) developed evolving-stroke within 24 hours of stroke onset. A lacune corresponded to the acute stroke could be found in all patients on brain magnetic resonance imaging (MRI), and in 18 (78%) on brain computed tomography (CT). MRI showed additional subclinical or asymptomatic “silent brain infarctions or lacunes” (SBI) in 19 (83%) of 23 patients, and leuko-araiosis (LA) of moderate to severe degree (> grade 2) was present in 61% of patients although dementia was absent. Hypertension is the risk factor in 78% of cases followed by diabetes mellitus, smoking, and elevated plasma cholesterol level. Independence of the types of lacunar syndromes, patients with hypertension and diabetes mellitus are associated with high grade LA. None with normal blood pressure and plasma glucose had grade 3 or grade 4 LA (p < 0.05). In conclusion, evolving-stroke occurs in one- fifth of patients with “first-ever” lacunar infarct within the first 24 hours of stroke onset. SBI was found in 83% of cases. Hypertension and diabetes mellitus are associated with additional SBI and high grade LA. The severity of leuko-araiosis per se dictates the cerebrovascular risks
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