Facial palsy: interpretation of neurologic findings.

A review of the otoneurologic findings in 500 patients with facial paralysis revealed their importance for diagnosis, prognosis, and understanding the pathophysiology of Bell's palsy. Diagnosis. The presence of simultaneous bilateral palsy, facial paralysis associated with lateral rectus palsy, slowly progressive facial weakness with or without hyperkinesis, and facial paralysis that showed no recovery after six months excluded Bell's palsy from the diagnosis. Ipsilateral recurrent palsies were another indication to suspect an underlying cause, since a tumor of the facial nerve caused the paralysis in 30% of the patients with this finding. Signs such as intact forehead movement, alterations in facial sensation, and corneal hypesthesia--although often associated with lesions in the cerebral cortex, cerebellopontine angle, or internal auditory canal--were also found in patients with Bell's palsy. Prognosis. A spontaneous complete recovery following Bell's palsy occurs in about 70% of the patients; but in the presence of a dry eye or dysacousis, the prognosis for a complete recovery drops 10 and 25%, respectively. Pathophysiology. It is proposed that the wide range of neurologic findings associated with Bell's palsy is due to a viral polyneuropathy. This is a disorder that primarily involves sensory nerves, and the facial motor deficit results from involvement of the sensory fibers carried with the facial nerve within the fallopian canal.

The use of steroids in Bell's palsy: a prospective controlled study.

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.

Natural history of bell's palsy: the salivary flow test and other prognostic indicators.

Fifty-one patients with Bell's palsy were evaluated within two days of onset and followed for six months without surgical intervention or effective medical treatment in order to observe the natural history of the disease. Sixty-three percent had a complete return while 37 percent had incomplete return. Age, the presence of pain, and taste alterations had no prognostic value. The progression of the palsy, response to maximal stimulation and salivary flow testing were approximately 80 percent accurate in predicting outcome. The salivary flow test was the most useful prognostic indicator since salivary flow became reduced within two days of onset in the patients likely to develop denervation while the other tests did not become altered until 3 to 14 days after onset. In patients with Bell's palsy, the salivation test seems to be the only method capable of predicting denervation before it begins; therefore, it should be ideal for selecting patients for appropriate treatment.

A pilot study of urokinase therapy in cerebral infarction.

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.

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.