Biomedical subjects
Publications and source records attributed to L M Weinberger.
We report a patient with delayed postanoxic demyelination who had pseudodeficiency of arylsulfatase A, reducing his enzyme activity to 10 to 30% of normal. This may have implications regarding the pathogenesis of postanoxic demyelination.
We describe an atypical neurologic presentation of Wegener's granulomatosis (WG) with striking meningeal and cerebral involvement, responding to immunosuppressive therapy. WG may cause treatable intracranial complications in the absence of nasal or renal disease and without cerebral angiographic abnormalities, CSF pleocytosis, or a positive assay for antineutrophil cytoplasmic antibodies.
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The proposal was made in 1949 that occipital neuritis/neuralgia was frequently of traumatic origin. The hypothesis was advanced that the C2 sensory root lay unprotected between the lateral masses of the atlas and axis and was vulnerable to squeezing on extreme extension or rotation of the head. This conjecture converted a hitherto banal neurologic affliction into the sequela of a banal trauma. Hence, it has been exploited in the diagnosis and treatment of whiplash injuries as well as for headaches of unknown origin. Evidence is presented that the original anatomic proposition was erroneous and that the C2 root is not exposed and is not vulnerable. Indeed, a survey of the "worst" traumatic and pathologic disruptions of the craniospinal junction shows that although they would be expected to injure the C2 root, in fact, they do not. The theory as well as the operations based upon it, particularly intradural section of the C2 root, should be abandoned.
Traumatic fibromyositis is not an inflammation; there is no fever, leukocytosis or increased sedimentation rate; electrical characteristics and serum enzyme levels are within normal limits, and there are no observable pathologic alterations, although they have been carefully searched for. Recent attempts to express the effects of muscular sprain or strain as a biochemical disturbance expressed in an unusual pattern of lactate dehydrogenase isoenzymes appear not only to be technically flawed but inconsistent with results of conventional enzyme studies on other muscle and interstitial inflammations. In the author's view, "traumatic" fibromyositis is no more than a verbal construct arrived at by adding an adjectival modifier to the old terms for idiopathic rheumatic disorders. An examination of the evolution of the concept of traumatic fibromyositis shows that it lacks validity as a clinical diagnosis and ought to be abandoned.
Neurophysiology does not provide a satisfactory theory which explains the phenomenon of muscular "spasm" which is said to be present in the neck following soft-tissue injury. Lacking knowledge as to whether long continued intermittent traction--ranging from 10 pounds to total body weight pull--is therapeutic or traumatic, such treatments nevertheless are prescribed in physiotherapy departments and at home for months. They are believed to be non-physiological and irrational and, in the author's opinon, represent the persistence of several medical myths associated with the "rear-end" collision. The question is moot whether the intractable complaints following such injuries are not caused, in large part, by the repeated traumas to muscles, disks, and joints produced by strong intermittent distraction. Experimental anatomical studies also argue against the hopes expressed in favor of such treatment, namely: to relieve spasm and/or traumatic fibro-myositis (?), to enlarge the neural foramina and relieve "radiculitis," and to hasten recovery by means of a conjectured internal massage.