K. M A Welch

Improved Reliability of the NIH Stroke Scale Using Video Training

Despite the frequent use of clinical rating scales in multicenter therapeutic stroke trials, no generally acceptable method exists to train and certify investigators to use the instrument consistently. We desired to train investigators to use the National Institutes of Health Stroke Scale in a study of acute stroke therapy so that all examiners rated patients comparably. Methods We devised a two-camera videotape method that optimizes the visual presentation of examination findings. We then measured the effectiveness of the training by asking each investigator to evaluate a set of 11 patients, also on videotape. We tabulated the evaluations, devised a scoring system, and calculated measures of interobserver agreement among the participants in this study. Results We trained and certified 162 investigators. We found moderate to excellent agreement on most Stroke Scale items (unweighted K>0.60). TWO items, facial paresis and ataxia, exhibited poor agreement (unweighted K<0.40) and should be revised in future editions of the scale. Performance improved with video training compared with previous studies. Inclusion of the motor rating of the unaffected limbs in the total score did not affect reliability. Conclusions Video training and certification is a practical and effective method to standardize the use of examination scales. Two cameras must be used during the taping of patients to accurately present the clinical findings. This method is easily adapted to any study in which a large number of investigators will be enrolling patients at multiple clinical centers.

Cerebrovascular Complications of the Use of the Crack Form of Alkaloidal Cocaine

BACKGROUND AND METHODSnThe use of cocaine, especially one of its alkaloidal forms (crack), has been increasingly associated with cerebrovascular disease. To clarify the clinical, radiologic, and pathological features of the events associated with cocaine use, we identified 28 patients at four medical centers who had stroke temporally related to the use of alkaloidal cocaine (during or within 72 hours of use).nnnRESULTSnThe 28 patients had the following types of cerebrovascular event: cerebral infarction (n = 18 [2 hemorrhagic; 1 fatal]) in the areas supplied by the middle cerebral artery (n = 10), anterior cerebral artery (n = 3), posterior cerebral artery (n = 1), and vertebrobasilar arteries (n = 4); subarachnoid hemorrhage (n = 5); intraparenchymal hemorrhage (n = 4); and primary intraventricular hemorrhage (n = 1). Eighteen patients (64 percent) had acute neurologic symptoms immediately or within one hour of using cocaine. Fifteen patients (45 percent) with either occlusive or hemorrhagic strokes had sever headache as an early symptom. Vasculitis was not suggested by radiography in any patient, nor was it identified on pathological examination in one patient who died. All the patients were young (mean age, 34 years; range, 23 to 49) and had no other apparent, direct cause of stroke. Other risk factors for stroke among the patients included mild mitral-valve prolapse (n = 4), hypertension (n = 4), cigarette smoking (n = 8), and regular alcohol use (n = 6).nnnCONCLUSIONSnThere is a strong temporal association of the use of alkaloidal cocaine with both ischemic and hemorrhagic cerebrovascular events. Cocaine-related stroke probably has many causes. A thorough history focusing on the use of cocaine and toxicologic screening of urine and serum should be part of the evaluation of any young patient with a stroke.

Transient hyperthermia protects against subsequent forebrain ischemic cell damage in the rat

We heated Wistar rats (n = 10) to 41.5 ± 0.2 °C for 15 minutes, 24 hours before the induction of forebrain cerebral ischemia. We subjected 23 rats to forebrain ischemia without prior heating. Ischemic cell damage in the medial, lateral, and overall CA 1/2 hippocampus, inferior frontal cortex, and dorsal-lateral striatum was significantly (p < 0.05) less severe in heated animals than in nonheated animals.

Cerebrovascular and neurologic disease associated with antiphospholipid antibodies: 48 cases

Lupus anticoagulants and anticardiolipin antibodies are antiphospholipid antibodies (APLAb) with related antigenic specificities and are newly recognized markers for an increased risk of thrombosis. We studied 48 patients who presented with cerebral or visual dysfunction associated with APLAb to help clarify the diagnostic, clinical, laboratory, radiologic, and pathologic features in these patients. Most patients presented with transient cerebral ischemia or cerebral infarction. Recurrent and stereotypic events were frequent. Visual disturbances resulted from amaurosis fugax, retinal arterial or venous occlusion, occipital ischemia, diplopia, and migraine-like disturbances. Three patients presented with severe atypical classic migraine. Recurrent infarcts of brain and eye were significantly associated with the presence of cigarette smoking, hyperlipidemia, and a positive antinuclear antibody. During 44.4 patient-years of prospective follow-up, the combined stroke and systemic thrombotic event rate was 0.27 events per patient-year and was 0.54 events per patient-year if TIA and death were included. Forty (83%) of the patients did not have systemic lupus erythematosus (SLE). Thrombocytopenia was present in 15 (31%) and a false-positive VDRL in 11 (23%) of the patients. Cerebral angiography was normal or revealed large-vessel occlusion or stenosis without changes suggestive of vasculitis. Patients with only transient dysfunction generally had normal radiologic studies, including angiography. Organs and arterial vessels studied pathologically revealed thrombotic occlusive disease without vasculitis. APLAb are strongly associated with an immune-mediated thrombotic tendency, generally in the absence of SLE. Other stroke risk factors may add to the risk of recurrent ischemic events in patients with APLAb.

A comparative study of the cerebrovascular complications of cocaine: alkaloidal versus hydrochloride--a review.

Cocaine, especially in its alkaloidal or “crack” form, has been increasingly associated with cerebrovascular disease. Before the crack epidemic, cocaine hydrochloride (HCl) was also implicated as a cause of stroke. However, less is known about the differences in stroke subtypes, age at stroke onset, or presence of underlying structural cerebrovascular disease with different forms of cocaine use. We compared 26 patients (previously reported) from our four institutions plus 16 cases reported in the literature of stroke associated with alkaloidal cocaine to 63 (57 reported in the literature and six not previously reported from our four institutions) cases of stroke associated with cocaine HCl. Ischemic and hemorrhagic strokes are equally likely after alkaloidal cocaine use, whereas cocaine HCl is more likely (approximately 80% of the time) to cause hemorrhagic stroke, with approximately half the intracranial hemorrhages occurring from ruptured cerebral saccular aneurysms or vascular malformations. The presence of an underlying cerebral aneurysm was more common among patients with cocaine HCl-associated strokes than alkaloidal cocaine-associated strokes. Cerebral infarction was significantly more common among the alkaloidal cocaine users than in all the cocaine HCl users, and this was also true when alkaloidal cocaine users were compared with parenteral cocaine HCl (intravenous and intramuscular) users. Only hemorrhagic stroke has been reported with intravenous cocaine HCl use. We conclude that the pathogenesis of cocaine-related stroke is heterogeneous, and depends, in part, on the form of cocaine used.

Sneddon's syndrome: An antiphospholipid antibody syndrome?

A 44-year-old woman with livedo reticularis, multiple ischemic strokes, and transient ischemic attacks (Sneddons syndrome) had anti-phospholipid antibodies—the lupus anticoagulant and anticardiolipin antibodies. This patient provides support for the hypothesis that these antibodies are involved in the pathogenesis of this rare but now potentially treatable disorder.

Viewing stroke pathophysiology: an analysis of contemporary methods.

RELIANCE ON CLINICAL AND ANATOMICAL information alone has proven of limited value in the management of ischemic cerebrovascular disease (CVD). Heretofore, progress in understanding the pathophysiology of ischemic stroke in the clinical patient has been slow due to the lack of readily available, sensitive, accurate and above all non-invasive methods of measuring cerebral hemodynamics and metabolism. Methods that meet some of these required criteria have been developed in recent years and their incorporation into routine clinical investigation appears imminent. Thus it is timely to take stock of the relative merits of these techniques prefaced by a brief discourse on the importance of functional measures in the routine evaluation of stroke. Although the causes of acute ischemic stroke are multiple, the common factor is reduction of cerebral blood flow (CBF) to levels that produce neurological deficit. If the extent and degree of reduction is within the limits of resolution of any of the available methods, then CBF measurement may have use in the diagnosis of ischemic stroke because accepted imaging modalities such as CT frequently reveal no abnormality in the acute stages. Perhaps more importantly and essential to the ideal management of acute stroke, is the knowledge of whether the jeopardized brain tissue is reversibly or irreversibly damaged. Backed by an expanding and persuasive volume of experimental literature the measurement of zero flow and the delineation of blood flow thresholds in a focus of ischemia may have value in this regard.1 Metabolic measures are also essential. For example, a pattern of low cerebral metabolic rate for oxygen (CMRO2) combined with either a reduced or increased oxygen extraction fraction (OEF) obtained by positron emission tomography (PET) can respectively differentiate between infarcted tissue or an ischemic area where viable tissue, though of impaired function, metabolizes proportional to the available perfusion. 2 The former condition renders the issue of CBF adequacy irrelevant for tissue viability, whereas CBF becomes a critical issue in the latter case. The experimental literature also underscores the importance of monitoring

Cerebral blood flow asymmetry in the detection of extracranial cerebrovascular disease.

Regional cerebral blood flow was measured by the 133Xe inhalation technique in patients with unilateral carotid occlusion, unilateral carotid occlusion and contralateral carotid stenosis, bilateral carotid occlusion, or normal arteriograms. After adjusting for age, sex, and history of stroke, hemispheric blood flow asymmetry was shown to be a predictor of unilateral carotid occlusion with a sensitivity of 80.6% and a specificity of 80.5%. Asymmetry of regional cerebral blood flow is useful in the assessment of patients with extracranial cerebrovascular disease.