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The last phase of migraine attack consists of profound tiredness together with a tendency to sleep for a length of time. Migraine attacks vary in frequency, and may be worsened in severity or frequency by uncorrected refractive errors or other optometric factors. The causation of migraine is related to a vascular phenomenon, a theory which is supported by the throbbing nature of the headache and the fact that certain foods especially those containing amines ; e.g. nuts, wine, chocolates and cheese, may precipitate attacks. A phase of vasoconstriction is purported to cause the aura, followed by vasodilatation leading to headache. This hypothesis is also supported by the observation that other cranial vascular phenomena, e.g. haemorrhagic stroke or the administration of vasodilatory drugs such as nifedipine or hydralazine, lead to similar headaches. A more recently accepted theory comprises a wave of depolarisation travelling along the cerebral cortex at a rate of 3-5cm per minute; this is called cortical spreading depression CSD ; and was first proposed by Leo in 194412. This wave of depolarisation leads to cerebral ischaemia which, in turn, results in the aura. There is some evidence that the CSD may sometimes originate in the occipital cortex, which fits in nicely with the frequently observed phenomenon of a visual aura. There are associated fluctuations in cation levels in the cortex, particularly levels of potassium ions K + ; . Other theories, which may operate in conjunction with the above, include one connected with 5-hydroxytryptamine 5-HT ; receptors. There are several subtypes of 5-HT receptors, and the action of agonists at these receptors can affect blood vessel calibre. The idea that 5-HT receptors may be involved in migraine pathogenesis stemmed from the fact that some drugs effective against migraine have activity at these receptors. For example, sumatriptan mentioned below ; has some agonist activity at 5-HT1B and 5-HT1D receptors. Drugs used to treat migraine utilise two main modes of therapy, namely treatment of individual attacks and prophylactic treatment. Drugs in the former group include the NSAIDs, e.g. aspirin, paracetamol, diclofenac, etc; ergotamine CAFERGOT sumatriptan; and calcium antagonists, e.g. nifedipine ADALAT ; , nimodipine the latter has a selective action on cerebral vessels and therefore has potentially greater efficacy ; . Prophylactic drugs used in migraine are substances as diverse as -adrenergic antagonists -blockers ; e.g. propranolol INDERAL ; , metoprolol TRASICOR calcium antagonists; pizotifen SANOMIGRAN angiotensin converting enzyme ACE ; inhibitors like captopril CAPOTEN ; , enalapril INNOVACE ; and lisinopril CARACE and imipramine TOFRANIL ; . -blockers have been found to be very efficacious in preventing migraine attacks and have very few side-effects. Sumatriptan has the alarming side-effect of central tight chest pain which almost exactly mimics the pain of myocardial infarction. It is therefore not suitable for prophylactic treatment as this inherently requires continual administration. hypotension ergotamine is a vasoconstrictor acting on adrenoreceptors and therefore tends to maintain blood pressure by increasing total peripheral resistance ; . The patient developed a bilateral ocular vasculopathy consisting of a generalised vasoconstriction and macular oedema as well as a grossly diminished electroretinogram. These effects were probably related to the administration of ergotamine, and in theory could occur in association with its use in migraine. Sumatriptan relaxes porcine ophthalmic artery16; if this effect can be interpolated to humans, it would suggest increase in calibre of, and therefore in, blood flow in the ophthalmic artery. However, this effect is not likely to have any clinical significance. The common peripheral analgesics used in migraine have already been discussed earlier in this article under NSAIDs. In general, although many anti-migraine drugs have been in use for several years, there is fortunately a dearth of reported serious ocular effects associated with their use.

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Phenobarb.D Behavior Seizures Prolixin Prozac Risperidal Ritalin Secretin Intravenous Transderm. Stelazine TegretolD Behavior Seizures Thorazine T0franil Valium ZarontinD Behavior Seizures Zoloft. These documents will be available at no charge on the sec's web site at site private securities litigation reform act of 1995 - a caution concerning forward-looking statements some statements in this news release may be forward-looking statements for purposes of the private securities litigation reform act of 199 abbott and kos pharmaceuticals caution that these forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from those indicated in the forward-looking statements including: the tender offer may not be completed or the merger may not be consummated for reasons including because conditions precedent to the completion of the acquisition may not be satisfied and lamotrigine and tofranil, for instance, brand name. 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