Weigand, Stephen D.

OBJECTIVE—The prevalence of autonomic symptoms and deficits in certain systems is known, but a comprehensive autonomic symptom profile in diabetes is not available. We aimed to estimate this using a laboratory evaluation of autonomic function and a validated self-report measure of autonomic symptoms in patients and matched control subjects from the population-based Rochester Diabetic Neuropathy Study. RESEARCH DESIGN AND METHODS—Participants included 231 patients with diabetes (type 1, n = 83; type 2, n = 148) and 245 healthy age-matched control subjects. We assessed symptoms using a validated self-report instrument (Autonomic Symptom Profile) and evaluated the severity and distribution of autonomic deficits (cardiovagal, sudomotor, adrenergic) with the objective, laboratory-based Composite Autonomic Severity Score (CASS). RESULTS—Autonomic symptoms were present more commonly in type 1 than in type 2 diabetes, with symptoms of orthostatic intolerance, secretomotor, urinary control, diarrhea, and sleep disturbance and pupillomotor, vasomotor, and erectile dysfunction significantly increased over healthy control subjects in type 2 diabetic patients. The prevalence of autonomic impairment was 54% in type 1 and 73% in type 2 diabetic patients. Severity of autonomic failure was mild overall (mean CASS 2.3; maximum 10), with orthostatic hypotension occurring in 8.4 and 7.4% of type 1 and 2 diabetic patients, respectively. Fourteen percent of patients had a CASS ≥5, indicating moderate to severe generalized autonomic failure. The correlation of symptoms with autonomic deficits (CASS) was better in type 1 than type 2 diabetic subjects and was weak overall. CONCLUSIONS—These findings indicate that autonomic symptoms and deficits are common in diabetes, but mild in severity, and that the correlation between symptom scores and deficits is overall weak in mild diabetic neuropathy, emphasizing the need to separately evaluate autonomic symptoms.

Background and Purpose— The aim of this study was to analyze the distribution patterns of delayed cerebral ischemia after subarachnoid hemorrhage (SAH) and the factors that determine their occurrence. Methods— We analyzed clinical and radiological data of 143 consecutive patients with aneurysmal SAH. Computed tomography scan revision was blinded to clinical information. Superficial infarctions were defined as territorial lesions with cortical involvement. Perioperative infarctions were excluded. Results— Fifty-six patients (39%) had cerebral infarctions. They were unilateral in 34 patients (61%) and involved a single territory in 29 (52%). Location was cortical in 34 patients (61%), deep in 10 (18%), and combined cortical and deep in 12 (21%). Single infarctions were cortical in 23 of 28 cases (79%). Deep territory ischemia was more common with multiple lesions (16/28, 57% versus 6/29 with single lesions, 21%; P <0.01). Single infarctions occurred frequently in the territory of the ruptured aneurysm (22/28 patients; 79%), whereas multiple infarctions were often distant to the site of rupture (21/28 cases, 75%). History of diabetes ( P =0.05), early hydrocephalus ( P =0.05), and requirement of external ventricular drainage ( P =0.02) were associated with the occurrence of multiple infarctions on univariate analysis. On multivariable analysis, this association only remained significant for the requirement of external ventricular drainage. Conclusion— The 2 most common patterns of delayed cerebral ischemia after aneurysmal SAH are single cortical infarction, typically near the ruptured aneurysm, and multiple widespread lesions including subcortical locations and often unrelated to the site of aneurysm rupture. These 2 patterns may represent different pathophysiological mechanisms or different degrees of severity of the same vascular process.