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In Reply.— We apologize to Dr Khurana for overlooking his previous report of recovery from suspected central pontine myelinolysis (CPM). As he points out, the localization of the lesion in his and our cases was indeed "clinically obvious," as one would hope with such a presumptive diagnosis. However, the localization of the lesion has not been clinically obvious in most of the 100 or more cases of proved CPM reported in the literature; we know of only three of these cases in which the lesion was recognized clinically. 1-3 Several reports have emphasized that the localization of the lesion is not often discernible from the clinical findings, even in retrospect. 4-6 There are several reasons for this: (1) the lesion may remain confined to the functionally silent area in the midline of the basis pontis where it originates, producing no signs or symptoms 7 ; (2) with centrifugal spread of the lesion

Excerpt To the editor: Spontaneous spinal epidural hemorrhage causing acute spinal cord compression is a relatively rare occurrence, with slightly more than 100 cases reported (1). We report here a...

Based on findings from two patients with hereditary brachial neuropathy and their families, an autosomal dominant mode of inheritance with high penetrance is suggested. The first attack usually occurs before age 20. Most patients have several attacks, infrequently more than four. The likelihood of further episodes of neuropathy decreases with age. Longrange prognosis is good except for occasional minor neurological deficits usually involving proximal muscles of the upper extremities. Based on electromyographic and nerve conduction studies, patients with this disorder do not appear to have a generalized neuropathy. The clinical picture of hereditary brachial neuropathy is indistinguishable from nonfamilial brachial plexus neuropathy except for earlier onset, recurrence of attacks, and family history.

Physicians have generally accepted as fact that the (A-New Jersey-76) swine influenza vaccine administered to 45 million persons in the United States between Oct 1 and Dec 16,1976, was causally associated with an increase in Guillain-Barre syndrome (GBS). Yet, the only substantive evidence for that association is a single study based on data collected by health officers during a hectic and highly publicized program that began shortly before the moratorium on the immunizations on Dec 16, 1976, and continued for six weeks until Jan 31, 1977. The foundation for the thousands of claims against the US government for compensation for GBS and other disorders is the report by Schonberger et al that describes the epidemiologic features of 1,100 cases reported to the Centers for Disease Control (CDC) as GBS by the state and territorial health officers. 1 Of the 1,100 cases, all but two were "certified" by the CDC as

• We discuss three patients with clinical findings of central pontine myelinolysis (CPM). Two patients survived with minimal neurological deficits, and one patient died from medical complications while recovering from his neurological deficit. Postmortem examination showed the typical lesion of CPM. Brain stem auditory evoked potential studies in two of our patients indicate that there was impairment of function in auditory pontine pathways that returned to normal as the patients improved clinically. We conclude that CPM can be diagnosed clinically and that patients may recover if intercurrent illnesses are vigorously treated.

All Olmsted County, Minnesota, residents who experienced brain injury from 1935 through 1979 were identified and their medical records reviewed for survival and neurologic outcome. Minimum inclusion criteria included loss of consciousness or post-traumatic amnesia or neurologic evidence of brain injury or skull fracture. Of 4,660 cases identified, skull fractures were observed in 28%. Over half of brain-injured patients who died did so within 24 hours of trauma; among 1-day survivors, subsequent survival was moderately impaired, especially in older individuals. Mortality was lowest in subjects without a skull fracture and increased with fracture severity. Associated neurologic injuries, complications, and deficits were generally more common in patients with skull fracture than those without and were much more frequent with more severe skull fractures. The types of neurologic deficits differed little between those with and without fractures, except that subjects with complicated skull fractures had higher proportions of special sensory deficits and multiple deficits.

Using age-specific rates for multiple sclerosis (MS) based on a national survey, the number of "naturally occurring" new cases of MS among the 45 million swine flu vaccine recipients in the United States is estimated as 1,624 during the year after vaccination, or 31 cases per week. Information from available reports and publications indicates no excess over the expected frequencies. Analyses of admissions for MS before, during, and after the immunization program showed no increase to the US Army hospitals or to the Mayo Clinic. Three independent controlled clinical investigations performed on patients with MS showed no increase in the frequency of exacerbations among those receiving swine flu vaccine as compared with those receiving placebo. Epidemiologic features of MS do not implicate killed virus vaccine as an etiologic factor in onset or exacerbations of the disease. There is no indication from these analyses of any association or cause-and-effect relationship between swine flu vaccine and MS. ( JAMA 1984;251:2672-2675)

Epileptic beagle dogs were studied with surface and depth electrodes. Recording during the resting state showed rare independent spike discharges, usually arising bilaterally from temporal pole, amygdala and hippocampus and, less often, from central and anterior cortical areas. Intravenous administration of pentylenetetrazol, methohexital and thiopental, activated spike discharges primarily in the same areas. During pentylenetetrazol infusion, 300 to 500 Hz activity was observed in tegmental and pontine reticular formation preceding generalized seizure discharges. The findings suggest that in the epileptic beagle a diffuse cerebral irritability exists, manifesting itself primarily in those areas prone to develop epileptiform activity regardless of the underlying etiology. No evidence was found to implicate a primary abnormality in the reticular formation or thalamus.