Abstract: BACKGROUND: Migraine is a complex biochemical dysfunction attributed to a disorder of the trigeminal and hypothalamic pathways. Impairment of glucose metabolism has been reported in migraine, but data are scanty and inconsistent. OBJECTIVE: The main aim was to verify whether migraineurs have abnormalities of the glucose and insulin metabolism.We also studied correlations between blood glucose and insulin and between insulin levels and migraine severity. PATIENTS AND METHODS: Patients with migraine or headache other than migraine, and healthy volunteers were included. All had general blood tests and a standard oral glucose tolerance test after a 12-hour fast, and glucose and insulin were measured. RESULTS: Over a 6-month period, we recruited 84 migraineurs (73 women, 11 men), 25 patients with nonmigraine headache (20 women, 5 men), and 26 healthy controls (24 women, 2 men). Multivariate analysis confirmed a significant difference between groups for glucose levels (P < .0001), but no significant time interaction. The differences were mostly between migraine and healthy controls (P < .0001) and to a lesser extent between other headaches and healthy controls (P < .05). A significant difference between groups was also found for insulin (P < .0001), with a significant time interaction. The difference was confirmed for migraine compared to other headaches (P < .0001) and healthy controls (P < .0001). CONCLUSIONS: Blood glucose levels may be high in headache patients, but do not seem to be specific to migraineurs. Insulin levels were higher in migraineurs, and seemed specific to this group. These findings are in keeping with recent reports on the effects of insulin on brain functions and lend support to the possibility that insulin is involved in the pathogenesis of migraine.

Abstract: Many factors should be considered when an episodic migraine worsens and becomes chronic. Prolactin (PRL) was linked to the origin of pain in patients with microprolactinomas who developed different types of headaches. Our team carried out studies on 27 patients with a background of episodic headaches that became chronic. The patients were evaluated by means of a general examination, a neurological examination and a hormonal profile. Of the 27 patients, 7 of them had an increased level of prolactinaemia. All the patients were women, ranging from 17 to 57 years of age. Four of them had a pure form of migraine without aura, whereas 3 patients had both migraines without aura and tension-type headaches. They suffered from headache for a period ranging from 3 to 32 years and their headache became chronic 4-12 months prior to the visit. Their headache did not change in type, but only in severity and frequency. Two patients had no symptoms referable to high PRL levels; 4 patients had irregular menses or amenorrhoea. One of these patients also suffered galactorrhoea and two of these patients had a microprolactinoma at MRI; one patient was using estroprogestinic drugs, so her menstrual alteration could not be considered. The patients were followed-up for a period of 6-16 months. Six patients responded favourably after being treated with cabergoline, although some had already tried other drugs, which, however, had no effect on their headache. One patient improved after ceasing to take estroprogestinic, in spite of increased levels of PRL. Therefore, on this basis, PRL levels should always be considered when headache worsens. It is an adjunctive worsening factor, which can be easily eliminated.

Abstract: We determined the incidence, risk factors, and short-term mortality of stroke in a well-defined area of southern Italy, i. e. the city of Vittoria, Sicily (58 833 inhabitants). The medical recores of the local hospitals and the outpatient files of the local neurologist referring to the calendar year 1991 were retrospectively investigated. Stroke was defined according to standard criteria and classified as first-ever (FE) and recurrent (R). Risk factors for stroke were diagnosed from medical history, laboratory and instrumental findings, and in the presence of specific treatments. Short-term mortality was assessed as 30-day case-fatality rate. The sample included 120 cases (61 men) aged 34-94 years, 89 of whom (48 men) had a FE stroke. The overall annual crude incidence rate of FE stroke was 165.3 per 100 000 (men, 178.4; women 152.2); for FE and R stroke together it was 222.9 (men, 226.8; women 219.1). The standardized rates were 245.3 (FE stroke) and 321.9 (FE and R stroke). The age-specific rates for FE stroke were 9.4 (<55 years), 262.2 (55-64 years), 645.2 (65-74 years), 2019.7 (75-84 years), and 3246.8 (> or =85 years). The corresponding values for FE and R stroke were 11.7, 412.0, 887.1, 2565.5, and 4220.8. In patients with FE stroke, cerebral infarction was the main type. Hypertension, diabetes and cardiac disorders were the commonest risk factors, with similar distribution among FE and R stroke. The 30-day case-fatality rate was 28% for FE and R stroke and 38% for FE stroke. Compared to other reports, the incidence of stroke in Vittoria was lower in the youngest but higher in the oldest age groups. Although the small sample size and possibility of misdiagnoses may partly explain our findings, the roles of different dietary, social, and genetic factors in the local population warrant investigation.

Abstract: OBJECTIVE: To establish whether chronic alcoholism and alcohol consumption are risk factors for developing a first symptomatic epileptic seizure. METHODS: Multicentre case-control study of 293 patients (160 men, 133 women) with a first seizure symptomatic (either acute or remote) of head trauma, stroke, or brain tumour, matched to 444 hospital controls for centre, sex, age (+/-5 years), and underlying pathology. RESULTS: The risk of first seizure in alcoholics was no higher than in non-alcoholics for men (odds ratio 1.2, 95% confidence interval 0.4 to 3.2) or women (1.5, 0.1 to 54.4). The odds ratio (both sexes) was 1.2 (0.8 to 1.7) for an average intake of absolute alcohol of 1-25 g/day, 0.9 (0.5 to 1.5) for 26-50 g/day, 1.6 (0.8 to 3.0) for 51-100 g/day, and 1.4 (0.5 to 3.5) for >100 g/day. CONCLUSIONS: We found no evidence of an association between alcohol use or alcoholism and a first symptomatic seizure.

Abstract: Nineteen patients with mild or moderate chronic respiratory insufficiency, mean age, 63.3 y., have been investigated with pulmonary function tests, clinical examination and somatosensory (SEPs), visual (VEPs) and brainstem auditory (BAEPs) evoked potentials. Nineteen age and sex matched subjects acted as controls. None of the subjects had conditions known to affect the central nervous system (CNS). SEP N20 latency was significantly prolonged in 7 out of 19 patients and its mean value in the patients' group was significantly higher (21.02 vs 19.49 msec p < 0.001). VEP P100 latency was prolonged in the patients' group in 16/38 and 15/38 eyes with spatial frequencies of 30' and 15' of arc respectively. The P100 mean value was also significantly prolonged in the patients' group for both eyes and spatial frequencies (108.08 vs 101.87 msec p < 0.001 and 115.82 vs 107.63 msec p < 0.001 for spatial frequencies of 30' and 15' respectively). No significant difference was evident with BAEPs The data seem to support the hypothesis of a subclinical involvement of CNS in these cases, with preferential damage to the newer phylogenetic structures.

Abstract: A delta and C fibre function has been investigated in 18 patients affected by neuropathies associated with monoclonal gammopathies. Warm, cold and heat pain thresholds have been determined by means of a Somedic Thermotest, operating on the Peltier principle, in a room at constant temperature. Our results indicate that: 1) there is an involvement of A delta and C fibres in these neuropathies that might be difficult to quantitate only on clinical grounds 2) in IgG and IgA patients, all affected by a subclinical or mild axonal neuropathy, small fibres of both types are always involved 3) in IgM anti-MAG positive severe cases, A delta fibre involvement, suggestive of demyelination is evident, while in one anti-MAG negative patient only C fibres are damaged, probably reflecting a different pathogenetic mechanism.