This international open‐label study evaluated the tolerability and efficacy of zolmitriptan (Zomig®, 311C90), a selective 5‐HT1B/1D receptor agonist in the long‐term treatment of multiple migraine attacks. Patients who had previously participated in placebo‐controlled zolmitriptan studies were recruited. A total of 2058 patients treated 31 579 migraine attacks (average 15 per patient), for up to 1 year. Twenty‐six percent of attacks treated with a single zolmitriptan 5‐mg dose were associated with at least one adverse event (24% treated with two doses). The most frequent adverse events induded asthenia (14% of patients), nausea (12%), somnolence (10%), dizziness (11%), and paresthesia (11%). The rank order of the most common adverse events was not influenced by sex, age, or number of zolmitriptan doses taken and was similar between attacks 1 and 45. The majority of adverse events (59%) occurred within 2 hours of dosing, were of either mild (59%) or moderate (35%) intensity, of 4 hours' duration or less (67%), and required no further action (94%).Following an initial 5‐mg dose of zolmitriptan, the 2‐hour headache response rate (reduction in headache pain from moderate or severe before treatment to mild or no pain at 2 hours posttreatment) was 81% in patients treating moderate and severe attacks (19 639 of 24 161). Patients were pain‐free at 2 hours in 55% of all attacks (16 510 of 29 808). The efficacy of zolmitriptan was not influenced by age, sex, weight, use of prophylactic antimigraine medication, or association of attacks with menstruation. Analysis of the overall population and a subgroup who treated 30 or more migraine attacks showed that zolmitriptan was consistently effective across attacks. Overall, 67% of patients who treated five or more attacks reported zolmitriptan to be effective in 80% to 100% of attacks. Zolmitriptan produced meaningful migraine relief and improvement in normal activity impairment in 73% and 78% of moderate and severe attacks, respectively. Patients treated recurrence of moderate or severe headache with a second zolmitriptan dose in 32% of attacks which responded to the first dose within 2 hours. Where required, a second zolmitriptan 5‐mg dose for treatment of recurrence produced a headache response rate of 90% at 2 hours postdose. Thus, zolmitriptan 5 mg (plus an optional second 5‐mg dose for treatment of recurrence) is well tolerated and effective in the acute treatment of multiple migraine attacks over periods up to 1 year.

Platelet aggregability and fibrinolytic activity were studied repeatedly in 83 patients with reversible cerebral ischemic attacks over a median follow-up period of 26 months. Platelet hyperaggregability, defined as in vitro secondary aggregation obtained by adenosine diphosphate concentration less than or equal to 1 mumol/l, was demonstrated in 36.1% or the patients examined 5-8 days after the attack, but only in 6% of age- and sex-matched blood donors (p less than 0.001). Fibrinolytic activity was reduced in 57.8% of the patients, as compared with 20.5% of the controls. At the time of follow-up only 8% of the survivors showed platelet hyperaggregability, whereas the fibrinolytic activity was still reduced in 44.4%. Over the observation period 21.7% of the patients had a stroke or died. No significant correlation was found between abnormalities of platelet aggregability or of fibrinolytic activity, when observed 5-8 days after the ischemic episode, and the subsequent risk of stroke or death. It is concluded that in patients with recent cerebral ischemic attacks the demonstration of platelet hyperaggregability or reduced fibrinolytic activity appears to be without prognostic significance.

Two hundred and three patients, 148 males and 55 females, who during the last month before admission had experienced at least one reversible cerebral ischemic attack of less than 72 hours duration, were randomly assigned to treatment with either acetylsalicylic acid (ASA) 1000 mg daily (101 patients) or placebo (102 patients). The average follow-up period was 25 months. The two treatment groups were comparable with respect to age, sex, associated diseases, risk factors, number and duration of cerebral ischemic attacks. No statistically significant differences were found between the treatment groups as to the primary end point: stroke or death (ASA group 20.8%, placebo group 16.7%). Occurrence of transient ischemic attacks during the treatment period was not reduced by ASA treatment, whereas there was a trend suggesting fewer myocardial infarctions in the ASA group (5.9%) than in the placebo group (13.7%). The difference, however, was not statistically significant (p = 0.10). We were thus unable to demonstrate any favorable influence of ASA 1000 mg daily in patients with reversible ischemic attacks. This study does not, of course, prove that ASA treatment is ineffective in stroke prevention.

Acta Neurologica ScandinavicaVolume 65, Issue S90 p. 176-177 ACETYLSALICYLIC ACID IN THE PREVENTION OF STROKE IN PATIENTS WITH REVERSIBLE ISCHEMIC ATTACKS: P. Soelberg Srarensen, P. Soelberg Srarensen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorH. Pedersen, H. Pedersen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorJ. Marquardsen, J. Marquardsen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorH. Petersson, H. Petersson Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorA. Heltberg, A. Heltberg Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorN. Simonsen, N. Simonsen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorO. Munck, O. Munck Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorL.A. Andersen, L.A. Andersen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this author P. Soelberg Srarensen, P. Soelberg Srarensen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorH. Pedersen, H. Pedersen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorJ. Marquardsen, J. Marquardsen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorH. Petersson, H. Petersson Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorA. Heltberg, A. Heltberg Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorN. Simonsen, N. Simonsen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorO. Munck, O. Munck Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this authorL.A. Andersen, L.A. Andersen Departments of Neurology, Gentofte Hospital, Glostrup Hospital, Frederiksberg Hospital, Bispebjerg Hospital, Copenhagen, and Aalborg Hospital, Aalborg, Coagulation Laboratory, Municipal Hospital Copenhagen.Search for more papers by this author First published: March 1982 https://doi.org/10.1111/j.1600-0404.1982.tb03440.xCitations: 1AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume65, IssueS90March 1982Pages 176-177 RelatedInformation

Three groups of epileptic out-patients (juvenile myoclonic epilepsy, psychomotor epilepsy, and cryptogenic grand mal) were studied. The groups were matched as closely as possible with each other with regard to sex, age, and treatment. Out-patients suffering from Menière's disease served as a control group; these patients were treated with placebo and matched with the epilepsy groups with regard to sex, duration of disease and social level. The Marke-Nyman inventory was used as a quantitative assessment of personality traits. This inventory is an operative definition of Sjöbring's neurophysiological model of personality, including the three dimensions: validity, stability and solidity. Our results showed that epileptic patients irrespective of the type of seizures were substable. Low validity was found in patients with juvenile myoclonic epilepsy and in patients with psychomotor epilepsy with temporal EEG focus. In those latter epilepsy groups a tendency to subsolidity was also observed. In Sjöbring's frame of reference these substable patients of low validity have a psychological vulnerability since they are unable to overcome the small concrete adversities of life. They adhere to problems, and being unable to solve them they tend to react in a mood of discontent or of maladjustment. In the usual psychiatric frame of reference substable patients of low validity are classified as psychoastenic patients with emotional instability.

SUMMARYA double‐blind study of the antiepileptic effect and side effects of carbamazepine (CARB) and diphenylhydantoin (DPH) was undertaken in 38 patients with psychomotor epilepsy and without grand mal epilepsy except for a single previous seizure. The patients were treated with CARB and DPH only, each in periods of 16 weeks and with a crossover of 4 weeks. The initial dosage of 6 mg/kg DPH or 15 mg/kg CARB was corrected according to the serum values aiming at therapeutic intervals of 8–16 mg/1 DPH and 6–10 mg/1 CARB. The trial had to be discontinued in 12 patients. The effect of the two drugs in preventing psychomotor seizures was the same. Some patients, however, had considerably fewer seizures while on CARB; others had fewer seizures on DPH. It seems advisable, therefore, to try both drugs separately before proceeding to combined medication. During CARB treatment the selected therapeutic interval was more easily reached and maintained than during DPH. During the latter treatment, one‐third of the monthly serum value determinations were below the level in spite of dosage corrections. Side effects were equally mild and occurred as often during DPH as during CARB treatment.RESUMENSe ha realizado un estudio doble ciego para valorar los efectos antiepilépticos y los signos tóxicos de la carbamazepina (CARB) y de la difenilhidantoina (DPH) en 38 enfermos con epilepsía psicomotora y sin epilepsía gran mal con la excepción de una sola convulsión previa.Los enfermos fueron tratados exclusivamente con CARB y DPH durante periodos de 16 semanas cada uno con 4 semanas de tratamiento cruzado.La dosis inicial de 6 mg/Kg de DPH o 15 mg/Kg de CARB fué corregida según los nivelés séricos y tendiendo a alcanzar intervales terapéuticos de 8 a 16 mg/L de DPH y 6 a 10 mg/L de CARB. Este estudio tuvo que ser interrumpido en 12 enfermos.El efecto de ambas medicaciones fué el mismo en lo que se refiere a la prevención de los ataques. Sin embargo algunos enfermos tuvieron muchos menos episodios con la CARB y otros con la DPH. Por esta razón es aconsejable ensayar ambas drogas por separado antes de proceder a la combinación medica‐mentosa.Los intervalos terapeúticos se alcanzaron y se mantuvieron con mas facilidad durante el tratamiento con CARB que con la DPH.Durante el tratamiento con DPH, un tercio de las determinaciones mensuales de los valores séricos resultaron inferiores al valor deseado a pesar de las correcciones de las dosis. Los efectos tóxicos fueron poco intensos e igualmente frecuentes durante los dos tratamientos.ZUSAMMENFASSUNGDoppelblindstudie der antiepileptischen Wirkung und der Nebenwirkungen von Carbamazepin (CARB) und Diphenylhydantoin (DPH) an 38 Pa tien ten mit psychomotorischer Epilepsie aber ohne Grand‐Mal‐Anfäile mit Ausnahme eines einzelnen früheren Anfalls. Die Patienten wurden nur mit CARB und DPH behandelt; jedes Medikament wurde in Perioden von 16 Wochen mit einem cross‐over von 4 Wochen verabfolgt. Die Initialdosis von 6 mg/kg DPH oder 15 mg/kg CARB wurde entsprechend den Serumspiegeln angepasst, um therapeutische Bereiche von 8–16 mg/1 DPH und 6–10 mg/1 CARB zu erzielen. Bei 12 Patienten musste der Versuch abgebrochen werden. Beide Medikamente waren hinsichtlich der Vermeidung psychomotorischer Anfälle gleichermassen wirksam. Einige Patienten hatten jedoch beträchtlich weniger Anfälle unter Carbamazepin, einige unter DPH. Es scheint daher ratsam, jedes Medikament getrennt zu versuchen, ehe eine kombinnerte Behandlung eingeleitet wird. Der therapeutische Dosierungsbereich wurde während CARB Behandlung leichter erreicht und aufrechterhalten als mit DPH. Unter der DPH‐Behandlung lag 1/3 der monatlichen Serumbestimmungen unterhalb des ange‐strebten Spiegels trotz entsprechenden Dosi‐erungskorrekturen. Die Nebenwirkungen waren geringfügig und traten ebenso häufig bei DPH und unter CARB auf.

In a double blind study no difference was found between carbamazepine and diphenylhydantoin with regard to efficacy in preventing temporal lobe seizures, i.e. partial seizures with complex symptomatology, when the drugs were given without other medication for periods of 16 weeks, and when the serum concentrations were within selected therapeutic levels corresponding to usual therapeutic dosage. Some patients, however, had considerably fewer seizures on carbamazepine, some on diphenylhydantoin. It therefore seems advisable to try both drugs separately, before using a combined medication.