Michael Anthony

THE CONTROL OF CRANIAL ARTERIES BY HUMORAL MECHANISMS AND ITS RELATION TO THE MIGRAINE SYNDROME

SEVERAL RECENT PAPERS on the temporary abolition of pain using electrophysiological stimulation deserve comment in this space. This phenomenon is based on the knowledge that activity in the large peripheral sensory nerves, which carry nonpainful impulses, inhibits within the spinal cord subsequent activity of the smallest nerve fibers considered essential to pain conduction. The stimuli used must produce impulses only in the larger diameter fibers but since these have the lowest electrical threshold this can, in fact, be accomplished. Wall and Sweet (Science 155:108, 1967) have reported their results in eight patients with intense chronic cutaneous pain in whom sensory nerves or roots supplying the painful area were stimulated. Square-wave 0.1 milli-second pulses at 100 cycles/second were applied, and the voltage was raised until the patients reported tingling in the area. During the period of stimulation pressure on previously sensitive areas failed to evoke pain. Four patients with chronic disease of their peripheral nerves experienced relief of their pain for more than 30 minutes after stimulation for 2 minutes. Wall and Sweet concluded that this procedure is of interest in an experimental and theoretical study of pain, but that its therapeutic implications are at present only equivocal. Nonetheless, two patients previously seriously incapacitated by chronic pain who were stimulated many times each day reported a decreased intensity of their former pain after several months had passed, without further stimulation.

Controlled trials of cimetidine in migraine and cluster headache.

SYNOPSIS

PLASMA FREE FATTY ACIDS AND PROSTAGLANDIN E1 IN MIGRAINE AND STRESS

SYNOPSIS

THERMOGRAPHIC, HORMONAL AND CLINICAL STUDIES IN MIGRAINE

THE PRESENT CONCEPT of migraine is that of an hereditary vascular instability which renders the individual susceptible to alteration in the level of humoral vasoactive substances, particularly serotonin, which can be in turn affected by a variety of circumstances, such as the ingestion of tyramine-containing foods15 or vasodilator drugs, stress, relaxation following stress, and the hormonal fluctuations responsible for the menstrual cycle.

Relief of facial pain.

Pain in the face has always been a diagnostic and therapeutic challenge to the practising clinician. As a presenting symptom, it immediately sharpens and arouses the interest of the neurologist, in spite of the fact that its definitive diagnosis is not always easy. The majority of patients with facial pain suffer from paroxysmal episodes, and those with prolonged attacks or persistent pain are in the minority. In the former case, the term neuralgia is used, and since the pain is experienced in the distribution of cranial nerves, it is commonly referred to as cranial neuralgia (e.g. trigeminal, postherpetic neuralgia, etc) The remaining syndromes are called some form of headache (e.g. cluster headache), or simply facial pain of a particular variety (e.g. atypical facial pain) [table 1]. It is obvious from the above, that no single common mechanism can be responsible for the production of all forms of facial pain. As a result, little can be gained by a lengthy discussion on the mechanisms involved in the production of facial pain. Instead a brief reference will be made to the underlying pathophysiology of each variety of pain, as each topic is discussed individually. I. Trigeminal Neuralgia

Plasma Serotonin Levels in Migraine

Publisher Summary The chapter presents the study on plasma serotonin levels in 33 migraine attacks. The results were observed as follows: a sudden and marked fall in plasma 5-HT occurred at the onset of the attack in 31 of the 33 headaches studied. Mean plasma 5-HT (μg/l0 9 platelets) was 0.74 in headache-free periods, 0.81 in the 24 hours preceding headache, 0.44 during the migraine attack, and 0.73 in the 24 hours following headache. No comparable drop in 5-HT level was observed after stressful procedures, such as pneumoencephalography. Plasma 5-HT fell after the injection of reserpine, precipitating a migraine attack in 10 out of 11 patients. Incubation of “headache-free platelets” with “migraine plasma” from the same patient, produced a drop in platelet 5-HT to a level comparable with that of “migraine platelets.” These facts indicate that an endogenous 5-HT releasing factor is present in plasma during migraine headache, and suggest that the drop in plasma 5-HT plays a part in the mechanism of migraine.