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Biomedical subjects

M D Ferrari

Publications and source records attributed to M D Ferrari.

At least 145 records · Page 8Linked to original sources
PubMed1995

Is familial hemiplegic migraine a hereditary form of basilar migraine?

We studied aura symptoms in 83 patients from 6 unrelated families suffering from familial hemiplegic migraine. Fifty-five of the patients reported symptoms that allowed us to categorize them as basilar migraine (BM) patients, in accordance with the International Headache Society (IHS) criteria. In a control group of 33 patients suffering from migraine with aura and 33 patients suffering from migraine without aura, 9 patients complained of vertigo, and only one patient of diplopia during one of her attacks. None of these control patients fulfilled the IHS criteria for BM. We suggest that familial hemiplegic migraine and BM may share certain pathophysiologic mechanisms, which may consist of a (genetically determined) disturbance of basilar artery blood flow.

Adolescent↗
PubMed1995

Acute treatment of migraine attacks.

Migraine is a chronic neurological disorder, characterized by attacks of severe, usually unilateral and throbbing headache accompanied by nausea, vomiting, and photophobia and photophobia. Sometimes transient neurological (aura) symptoms may precede or accompany the headaches. Acute drug therapy comprises nonspecific drugs, including simple analgesics and non-steroidal anti-inflammatory drugs, often in combination with antiemetics, and specific antimigraine drugs, such as ergotamine, dihydroergotamine and sumatriptan. Sumatriptan is a potent and selective serotonin1D receptor agonist, which can be administered orally and via the subcutaneous or intranasal route. The drug is well tolerated and is consistently highly effective in most patients. Significant limitations, however, include the occurrence of chest symptoms, suggestive of cardiac ischaemia; recurrence of the headache within 24 h after initial successful treatment; and in a minority of patients, abuse of sumatriptan with daily 'sumatriptan-dependent headaches'. Administration during the aura phase does not affect the aura itself, but is not recommended because the subsequent headache will not be prevented in that case. Preliminary data of new serotonin1D receptor agonists, such as 311C90 and MK-462 are promising in terms of increased efficacy after oral administration, but side-effect profile and incidence of headache recurrence are similar to those observed after the use of sumatriptan. Intranasal administration of dihydroergotamine may also be effective, but data are very limited.

Adolescent↗
PubMed1995

Oral sumatriptan in preventing headache recurrence after treatment of migraine attacks with subcutaneous sumatriptan.

Headache recurrence (HR) may occur within 24 hours in approximately 40% of migraine attacks initially treated successfully with 6 mg subcutaneous (SC) sumatriptan. This may be due to the short plasma half-life of sumatriptan. We studied whether an additional dose of 100 mg oral sumatriptan 4 hours after treatment of a migraine attack with 6 mg SC sumatriptan could prevent HR. Patients (n = 667) treated up to three migraine attacks in a randomized, double-blind, placebo-controlled, parallel-group, multicenter clinical trial. For each attack, they initially took open-label 6 mg SC sumatriptan by autoinjector. Four hours later all patients took either 100 mg oral sumatriptan or matched placebo. Patients could take an additional optional oral dose of 100 mg sumatriptan to treat HR. The primary efficacy end point was the number of successfully treated patients without HR within 24 hours after the initial SC injection for the first study attack. Two hundred twenty-five patients were not assessable for HR, mainly because of protocol violations. Of 442 assessable patients, 82/212 in the sumatriptan-treated group (39%) and 89/230 in the placebo-treated group (39%) reported HR in attack 1. Median times to recurrence were 15.6 hours after sumatriptan and 10.3 hours after placebo (p = 0.006). One hundred mg oral sumatriptan taken 4 hours after 6 mg SC sumatriptan does not prevent HR but significantly delays time to recurrence.

Administration, Oral↗
PubMed1994

Genetic heterogeneity of familial hemiplegic migraine.

Familial hemiplegic migraine (FHM) is a distinctive form of migraine with an autosomal dominant mode of inheritance. The migraine-like attacks are associated with transient hemiparesis. A locus for FHM has recently been assigned to chromosome 19 by linkage mapping. In the present study, five unrelated pedigrees with multiple members suffering from hemiplegic migraine were investigated. In two of the pedigrees additional symptoms, cerebellar ataxia and benign neonatal convulsions, respectively, were observed in affected members. Three pedigrees showed linkage to loci D19S391, D19S221, and D19S226 at chromosome 19p13. Haplotyping suggested a location of a FHM gene between D19S391 and D19S221. In the two remaining families, evidence against linkage was found. These results confirm the localization of a gene for familial hemiplegic migraine to the short arm of chromosome 19, but locus heterogeneity not corresponding to the observed clinical heterogeneity is likely to exist.

Chromosome Mapping↗
PubMed1994

Phenytoin parahydroxylation is not impaired in patients with young-onset Parkinson's disease.

Impaired hepatic detoxification capacity by cytochrome P450 subsystems has been implicated in the pathogenesis of Parkinson's disease. We have demonstrated that hepatic parahydroxylation of phenytoin (PHT) is impaired in patients with late-onset Parkinson's disease. In the present study, we have investigated the hypothesis that PHT parahydroxylation is even more impaired in patients with young-onset Parkinson's disease (age at onset before 40 years). We determined PHT parahydroxylation capacity in 21 patients with young-onset Parkinson's disease and 15 healthy age-matched controls. PHT parahydroxylation capacity was assessed by measuring the ratio of PHT to its major metabolite p-hydroxyphenyl-phenylhydantoin in serum 6 h after an oral test dose of 300 mg PHT. PHT parahydroxylation did not differ significantly between patients and controls. These results argue against the hypothesis that impaired activity of the cytochrome P450 isoenzyme responsible for PHT parahydroxylation is involved in the etiology of Parkinson's disease.

Administration, Oral↗
PubMed1994

Intracellular and plasma magnesium in familial hemiplegic migraine and migraine with and without aura.

Familial hemiplegic migraine (FHM) is an autosomal dominant type of migraine and probably represents the most extreme end of migraine with aura. Reduced magnesium facilitates the development of spreading depression and possibly aura. Cellular magnesium levels are under genetic control. We hypothesized that FHM patients would have significantly reduced intracellular magnesium levels. We determined intracellular and plasma magnesium levels in blood of 38 afflicted and 11 non-afflicted members of three families with FHM and in 32 migraine patients (9 with and 23 without aura) and 32 age and sex matched healthy controls. We found no significant differences between the magnesium levels in the five study groups. We conclude that reduced blood magnesium is unlikely to be related to migraine pathophysiology.

Adolescent↗
PubMed1994

Oral sumatriptan: effect of a second dose, and incidence and treatment of headache recurrences.

Oral sumatriptan in a dose of 100 mg aborts about 60% of migraine attacks within 2 h, but the headache may recur within 24 h. We investigated: (i) the incidence of headache recurrence after oral sumatriptan (ii) whether a second tablet of sumatriptan at 2 h increases initial efficacy and/or (iii) prevents headache recurrence and (iv) whether a further tablet of sumatriptan treats headache recurrence. In a randomized parallel-group clinical trial, 1246 patients treated one to three migraine attacks (with or without aura), with 100 mg oral sumatriptan. Two hours later they all took a double-blind randomized second table of sumatriptan (group I) or placebo (group II). Patients who initially improved, but then experienced headache recurrence took a further double-blind randomized tablet of sumatriptan or placebo. Proportions of patients who improved from moderate/severe headache to mild/none were similar in groups I and III at 2 h (55 vs 56%) and 4 h (80 vs 77%). Incidences of headache recurrence (moderate/severe-any grade of headache) and median times to headache recurrence were also similar: 22-32% at 16 h in group I and 25-33% at 16.5 h in group II. Sumatriptan was superior to placebo in treating headache recurrence: 74 vs 49% (p = 0.017) in group I and 70 vs 30% (p = 0.0001) in group II. Thus, one-fourth of patients experience headache recurrence at about 16 h after successful treatment of a migraine attack with 100 mg oral sumatriptan. A second tablet of sumatriptan at 2 h does not increase initial efficacy and neither prevents nor delays headache recurrence.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1994

Migraine. Identifying and removing barriers to care.

The high levels of pain and disability associated with undiagnosed migraine or inadequate treatment of migraine offer a potential target for healthcare intervention. Both the individual patient and society are affected by decisions regarding which migraine sufferers are most in need of medical care. Pain is the most important symptom for the individual patient, but disability may be the most important consequence of migraine for an increasingly cost-conscious society. These two perspectives are the components of a migraine severity or impact measure being developed to define migraine sufferers most in need of care. The criteria for developing screening programs provide a context for evaluating healthcare interventions for migraine. Barriers to effective care occur on at least three levels: many people with migraine do not consult doctors; consulters may not receive the correct diagnosis; and even when the correct diagnosis is made, many migraineurs do not receive effective treatment. Screening and impact measures may help both to improve diagnosis and to determine which migraineurs are most in need of care. Public and physician education, screening, and impact measures might circumvent many of the barriers to effective care for people with migraine.

Health Services Accessibility↗
PubMed1993

Clinical and experimental effects of sumatriptan in humans.

Recent reviews on the mode of action of the anti-migraine drug sumatriptan arrived at contrasting conclusions. Whereas some reviewers concluded that vasoconstriction is the most important action, others suggest that neuronal inhibition is essential. Both views were based predominantly on animal or in vitro experiments. In this comment, Michel Ferrari and Pramod Saxena review the experimental effects of sumatriptan in humans and discuss the clinical validity of both theories. In addition, they examine the initial efficacy of treatment and the mechanism of recurrence of headache within 24 hours, which is the most important drawback of sumatriptan in clinical practice, next to its possible cardiac side effects.

Animals↗
PubMed1993

On serotonin and migraine: a clinical and pharmacological review.

Migraine patients have chronically low systemic 5-HT, predisposing them to develop migrainous headache once an attack has been initiated. Changes in platelet 5-HT content are not causally related, but reflect similar changes at a neuronal level. Stimulation of vascular 5-HT1 receptors, probably located in the vessel wall within the dural vascular bed, may alleviate the headache and associated symptoms, but does not interact with earlier mechanisms within the pathophysiological cascade. These receptors are of an as yet unidentified 5-HT1 subtype, closely resembling, but not identical to 5-HT1D receptors. Activation of these receptors results in vasoconstriction, inhibiting depolarization of sensory perivascular afferents within the trigemino-vascular system and thus stopping the headache. Additional inhibition of the release of vasoactive neuropeptides may be involved, but seems to be of only secondary clinical importance.

Blood Platelets↗
PubMed1993

Dopamine D2-receptor imaging with 123I-iodobenzamide SPECT in migraine patients abusing ergotamine: does ergotamine cross the blood brain barrier?

Two migraine patients were studied by in vivo SPECT using the dopamine D2-receptor specific radioligand 123I-3-iodo-6-methoxybenzamide (123I-IBZM) during ergotamine abuse and after withdrawal. Results were compared with 15 healthy controls. Striatum/cerebellum and striatum/occipital cortex ratios of count rate density were calculated as a semiquantitative measurement for striatal dopamine D2-receptor binding potential. No differences were found in striatal uptake of 123I-IBZM between healthy controls and the patients when on or off ergotamine. Preliminary evidence suggests that ergotamine may not occupy striatal dopamine D2-receptors to a large extent and thus may not cross the blood brain barrier in large quantities.

Benzamides↗