[Primary head and facial pain].
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Biomedical subjects
Publications and source records attributed to H Isler.
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We present data regarding the association of psychiatric syndromes and migraine headache from a prospective epidemiologic cohort study of 27- and 28-year-olds in Zurich, Switzerland. The prevalence of migraine of 13.3% approximates estimates from previous epidemiologic studies in other regions of the world. Consistent with previous reports, there was a strong association between migraine and depression. However, this is the first study to demonstrate this association in an unselected epidemiologic sample with standardized assessment of psychiatric diagnoses by direct interview. The association between migraine and the anxiety disorders was even stronger than that for the affective disorders. The combination of anxiety disorder and major depression, but not pure anxiety disorders, nor pure depression, were significantly associated with migraine. Our data suggest that migraine with anxiety and depression may constitute a distinct syndrome comprising anxiety, often manifested in early childhood, followed by the occurrence of migraine headaches, and then by discrete episodes of depressive disorder in adulthood. Because of the prospective longitudinal design of this study, future assessments of this cohort will provide further information on the stability of these findings and the course of this cohort as subjects proceed through adulthood.
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Using light and electron microscopy, we have observed the presence of rays containing medullary tissue extending across the cortex of rat adrenal glands. Within these rays chromaffin cells, as well as collagen and nerve fibers, were present. It is suggested that these endocrine cells may have a paracrine function within the cortex, possibly via their secretory product.
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Headache patients disassociate themselves from their own automatic responses, relying on the traditional separation of body and mind. On the other hand, patients who obtain voluntary control of automatic functions by biofeedback training modify not only vegetative but also voluntary behaviour patterns, losing "neurotic" traits. The basic misconception of the separation of body and mind, Cartesian dualism, is now ingrained in our culture. In the 17th century Descartes asserted that concepts applied to the soul must be entirely different from those used for the body in order to improve comprehension of the immortality of the soul. This dualism also led to "enlightenment" and to many later social and philosophical developments. But his basic neurophysiology was obsolete when he wrote it down. Other models from mainstream natural philosophy were better compatible with observation and experiments. Gassendi assumed a "body soul" consisting of energy as the functional principle of the nervous system, and Willis accommodated a series of anticipations of 19th century discoveries within this model. No comparable progress resulted from Descartes' own medieval model. Cartesian dualism has become untenable in view of recent neuropsychology but it still obstructs our management of functional patients. Instead of reinforcing the delusion of separation of psyche and soma, we ought to encourage patients to understand that their malfunctioning organs are on-line with their emotions, and with their mind.
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In symptomatic headache treatment is directed against the underlying disease. If this is impossible, its pathogenesis may still respond to treatment such as dexamethasone in inoperable brain tumor, simple psychotherapy in reactive emotional disorder due to intractability of the underlying disease, or migraine management where symptomatic headache is succeeded by migraine, as in posttraumatic headache. Primary headache-migraine, cluster headache, and cephalaea vasomotoria ("tension headache") require positive identification of the syndrome but this does not lead directly to proper treatment; assessment of severity and, where feasible, of the psychological situation is needed. The means are available to influence some of the mechanisms apparent in primary headache both by non-drug and by drug treatment, but the choice must allow for the fact that these methods are not specific but only a little more effective than placebo. Drug abuse is the principal danger in headache problems. It can be treated by tracking down the offending drug under cover of interval medication or, failing this, by abrupt withdrawal in a neurology ward followed by a period of several weeks' exile from the usual daily demands. A short description of drugs used in primary headache is given.
Basilar migraine is a well defined condition which is easily identified by a characteristic clinical picture such as headache associated with visual, cerebellar and brainstem symptoms. Occasionally, severe disturbances of consciousness may occur which blur this otherwise unequivocal clinical condition. Hence, diagnosis may be difficult. CT-scan, electroencephalography and lumbar puncture are then necessary in order to rule out more severe disorders. Treatment of this condition corresponds to the therapy of more common types of migraine. There is, however, no rationale for the administration of drugs conventionally used for migraine prophylaxis in patients with severe disturbances of consciousness, though treatment of brain edema with steroids may be helpful or occasionally even necessary.
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46 migraine patients and 4 patients suffering from "nonmigrainous" vascular headache were treated with 250 mg salicylate daily for 2 months. Platelet aggregability before and under treatment was measured in all patients and in 10 controls. The results confirm platelet hyperaggregability in migraine patients and a reduction of aggregability under salicylate out provide no evidence of any significant clinical improvement, thus falsifying the hypothesis of migraine as a platelet aggregation disorder.
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The effects of human myelin basic protein (HMBP) and its individual microheterogeneous components on the electrical activity of the frog spinal cord are compared with those of bovine MBP (BMBP) and glutamate (Glu). HMBP causes a dose-dependent depolarization of the ventral (VR) and dorsal (DR) roots with a reduction of the evoked root potentials. The amplitude of the depolarization induced by 0.01 mM HMBP corresponds to that observed with application of 1 mM Glu. A weaker depolarization persists during blockade of synaptic transmission by MgSO4 or tetrodotoxin, suggesting a direct depolarizing effect on motoneurones and primary afferents. HMBP causes a long-lasting tachyphylaxis. The individual microheterogeneous components of HMBP (peaks 1, 2 and 3), and a mixture of smaller myelin basic proteins elicit similar responses, whereas BMBP and its microheterogeneous components are slightly less active.
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