Thirty-one patients with acute cerebral infarction were treated with the thrombolytic agent urokinase for either a single or a double infusion period, each of ten hours. The effects of urokinase therapy administered at dosage rates of 1,200, 1,500 or 1,700 CTA urokinase units per pound of body weight per hour were followed by serial blood coagulation and other biochemical studies. In the dosage used, urokinase produced a prompt sustained increase, 20-fold to 40-fold, of plasma thrombolytic activity with relatively minor disturbance of the blood coagulation system. Nevertheless, hemorrhagic complications occurred in several patients and distinctly favorable therapeutic effects were not observed.
A prospective, controlled, double-blind study was designed to evaluate the effect of steroid treatment on the natural history of Bell's palsy. Fifty-one patients were included in the study between 1972 and 1974. The patients were evaluated and started on treatment within two days of onset of Bell's palsy and followed for six months. Treatment was given in randomized double-blind fashion and consisted of either vitamins or a total of 410 mg of prednisone plus vitamins in descending doses over 10 days. The recovery of facial motor function was determined by three physicians who had no knowledge of the treatment received by the patients. They examined photographs of the patients taken six months after onset of paralysis in eight positions of facial function and categorized them as to complete fair, or poor recovery of facial function. These results of this evaluation were submitted to the biostatistician who broke the treatment code. The results of this study demonstrate no statistically significant beneficial effect of steroid therapy upon recovery from Bell's palsy. Factors considered included the patients' age, sex, the presence of pain, ageusia, hyperacusis, diabetes, hypertension, the progression and degree of palsy, the results of nerve excitability and salivary flow tests, and the time at which recovery was first noted or became complete. Bell's palsy remains without a proven efficacious treatment.
SUMMARY Plasma fibrinogen chromatography is a method for quantification of high molecular weight fibrinogen complexes (HMWFC), native fibrinogen and other fibrinogen derivatives in plasma. Enhanced formation of fibrin, intravascular coagulation, thrombus formation, etc., are reflected by elevation of plasma HMWFC, and the method distinguishes between subjects with normal and pathological rates of fibrin formation.Serial standard blood coagulation assays, including plasma fibrinogen chromatography, and neurological studies were performed on 220 patients admitted to a stroke unit.Findings from patients with cerebral infarction were compared against those of three control groups: (1) normals, (2) a stroke control group and (3) a stroke risk factor group. Plasma HMWFC findings were significantly (p < 0.001) higher in the stroke risk factor group than in the normals. Plasma HMWFC values were significantly higher (p < 0.001) in the cerebral infarction patients than in any of the control groups, and plasma fibrinogen, plasminogen, alpha,-antitrypsin and alpha^macroglobulin also were significantly higher (p < 0.001) in the patients. The greater the degree of initial neurological deficit, the greater were plasma HMWFC values (p < 0.001), and high HMWFC values were associated with poor clinical outcome.Plasma HMWFC values were significantly higher (p < 0.001) in patients with intracerebral hemorrhage, subarachnoid hemorrhage and cerebral embolism.These findings document the fact that a high proportion of stroke patients have coagulopathy, characterized by pathological enhancement of fibrin formation.
Abstract:Brain Scanning in Cerebral Vascular Disease: A Reappraisal• The frequency of abnormal brain scans in patients with cerebral vascular disease admitted to a stroke intensive care unit has been evaluated in relation to diagnosis, time after onset of symptoms, effect of delayed imaging and the degree of clinical neurological recovery. In patients with completed thromboembolic infarction, 33% had abnormal scans including 39% of those with hemispheric lesions and 14% with posterior fossa lesions. Completed hemorrhagic infarction occurred in seven patients, and three (43%) had abnormal brain scans. Of 14 patients with either transient ischemic attacks or reversible ischemic neurological deficit, two (14%) had abnormal scans. Twenty-seven percent of brain scans in patients with completed thromboembolic infarction were abnormal in the first two days after infarction, a higher frequency than previously reported. Delayed images confirmed the initial interpretation that the scan was either normal or abnormal in 71 % of the cases while in 10% of the cases only the delayed views were abnormal. The frequency of abnormal scans was significantly greater in patients who died or had a large neurological deficit at discharge than in patients with lesser residual deficit.
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