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After a 4-week baseline period during which daily ratings of headache activity were made and all participants took several psychological tests, 91 patients with chronic headache (33 tension, 30 migraine, and 28 combined tension and migraine) were given a 10-session relaxation-training regimen. Patients who did not show substantial reductions in headache activity from the relaxation therapy were given a 12-session regimen of biofeedback (thermal biofeedback for vascular headaches, frontal electromyograph biofeedback for tension headaches). Relaxation therapy alone led to significant improvement for all three headache groups, with a trend for the tension headache group to respond the most favorably. Biofeedback therapy led to further significant reduction in headache activity for all who received it, with a trend for combined migraine and tension headache patients to respond the most favorably. Overall, 73% of tension headache patients and 52% of vascular headache patients were much improved. Multiple regression analyses revealed that approximately 32% of the variance in end-of-treatment headache diary scores could be predicted after relaxation and that 44% of the variance after biofeedback could be predicted using standard psychological tests. Moreover, over 72% of each headache group could be correctly classified as successful or not successful using the same tests in discriminant function analyses.Chronic recurring headache of either the Freundlich, & Meyer, 1975; Holroyd, Antension or vascular variety is a widespread drasik, & Noble, 1980). To date, this literhealth problem in this country afflicting up ature includes approximately 12prospectiveto 40% of the adult population (Ziegler, controlled trials involving tension headache Hassanein, & Couch, 1977). The last 10 and 8 similar trials for migraine headache, years have witnessed an ever-growing liter-The two principal nonpharmacological ature on the nonpharmacological treatment treatments for headache are varieties of bioof headache (Adams, Feuerstein, & Fowler, feedback training and several types of re-1980; Blanchard, Ahles, & Shaw, 1979). laxation training. Numerous controlled, di-This work has included several large-scale, rect comparisons of these two procedures uncontrolled retrospective studies (e.g., Ad-have generally shown them to be equally ler & Adler

Rat retinal ganglion cell layer (GCL) was examined ultrastructurally 1-180 days after intraorbital crushing of one optic nerve. It was confirmed quantitatively that axotomized ganglion cells lost cisternal membranes of the rough endoplasmic reticulum (RER) and showed disintegration of Nissl bodies and ribosomal rosettes 3 days postoperatively. Between 60 and 180 days after neurotomy there was partial reversion of the RER towards normal. At postoperative intervals of 14-60 days, chromatin aggregation became conspicuous and some nuclei were prominently furrowed and contained electron-dense inclusions. Concurrently, profiles of dead ganglion cells were encountered. Mean mitochondrial area increased in axotomized neurons but mitochondrial density declined, while the Golgi apparatus, lamellar specializations of the RER and the size of nuclei did not change significantly. Cytoplasmic atrophy was profound, however. Small nerve cells of the GCL appeared morphologically distinct from ganglion cells and did not undergo appreciable alteration. A decline in neuronal density, approximating 35%, occurred between the third and seventh postoperative day and progressed slowly thereafter. Neuronal density was 32% of normal 180 days postoperatively. A temporary increase in glial density 3-28 days after operation was due to microglial hyperplasia. Müller cell and astrocytic processes hypertrophied, infiltrated nerve fibre bundles, and surrounded and intruded into neuronal somata. Bundles of unmyelinated small axons, invested by astrocytes and basal lamina, were present within the necrotic cavity of the lesioned nerve 28-90 days postoperatively and had cytologic features of regenerative axonal sprouts. We conclude that intraorbital optic nerve crush is followed by a noteworthy degree of regenerative axonal sprouting which occurs and persists against a background of slow but relentless decline in the retinal ganglion cell population. This slow decline follows a rapidly-sustained loss of approximately one-third of the axotomized retinal ganglion cells during the first postoperative week. Intraorbital, as opposed to intracranial, injury of the optic nerve appears, paradoxically, to induce both a greater degree of ganglion cell death and a greater amount of regenerative axonal sprouting. Cytologic changes in axotomized retinal ganglion cells resemble those described for other populations of mammalian intrinsic neurons subjected to like injury.(ABSTRACT TRUNCATED AT 400 WORDS)