The presence of an inflammatory response in the pathophysiology of acute brain ischemia is relatively well established, but less is known about the anti-inflammatory mechanisms. The aim of the present study was to evaluate part of the immune response in acute stroke patients and to analyze a possible correlation with other hematological parameters, clinical outcome, size of infarct and subtypes of strokes. We prospectively studied 42 stroke patients, without signs of infections or inflammatory diseases, at days 0, 1, 3, 7 and 14, and 39 healthy control subjects. We measured serum levels of the anti-inflammatory cytokine interleukin-10 (IL-10) and the pro-inflammatory cytokine interleukin-6 (IL-6) by ELISA method. We observed a highly inverse correlation between these two molecules in control subjects (r=-0.78, p=0.0000001), and this correlation was lost in stroke patients. Patients had significantly lowered IL-10 serum levels soon after the acute event (p=0.00005), with a slight increase at the seventh day. On the other hand, patients had increased IL-6 serum levels compared with controls after day one until day 14 (p<0.04), with a maximum increase at day 3. Interleukin-6 correlated with clinical outcome whereas interleukin-10 did not. Low levels of interleukin-10 indicate that the antiinflammatory response is down-regulated in acute stroke patients. The pro-inflammatory response begins 24 hours after the onset of acute cerebral ischemia, as indicated by the increased serum levels of interleukin-6. The physiological balance between these two molecules is altered in acute stroke patients.

Platelet levels of glutamic and aspartic acid and glycine were measured in patients with migraine with aura, migraine without aura, tension headache and cluster headache. High levels of these amino acids were found in patients with migraine with aura compared to normal subjects and other headache groups. During headache, glutamate levels further increased in migraine with aura patients. These findings may have relevance to the neurological symptoms of migraine with aura.

Homocysteine increases in the acute phase of ischaemic stroke and from the acute to the convalescent phase, suggesting that hyper-homocysteinaemia may be a consequence rather than a causal factor. Therefore we measured homocysteine plasma levels in stroke patients in order to investigate possible correlations of homocysteine with stroke severity and clinical outcome. Further we looked for eventual differences in stroke subtypes. We prospectively studied plasma homocysteine levels in acute stroke patients admitted to the stroke unit of our department. Seven hundred and seventy-five ischaemic stroke patients, 39 cerebral haemorrhages and 421 healthy control subjects have been enrolled. Stroke severity and clinical outcome were measured with the Scandinavian Stroke Scale, the Rankin Scale and the Barthel Index. Stroke severity by linear stepwise regression analysis was not an independent determinant of plasma homocysteine levels. Homocysteine was not correlated with outcome measured by the Barthel Index. Mean plasma homocysteine of both ischaemic and haemorrhagic stroke was significantly higher than controls (p<0.05). Homocysteine had an adjusted odds ratios (OR) of 4.2 (95% CI 2.77-6.54) for ischaemic stroke and of 3.69 (95% CI 1.90-7.17) for haemorrhagic stroke. Compared with the lowest quartile, the upper quartile was associated with an adjusted OR of ischaemic stroke due to small artery disease of 17.4 (95% CI 6.8-44.3). Homocysteine in the acute phase of stroke was not associated with stroke severity or outcome. Elevated plasma homocysteine in the acute phase of stroke was associated with both ischaemic and haemorrhagic stroke. Higher levels are associated with higher risk of small artery disease subtype of stroke.

Objective: To investigate the prevalence of connective tissue abnormalities in patients with spontaneous cervical artery dissections (sCeAD). Methods:We systematically assessed clinically detectable signs of connective tissue aberration in a series of consecutive patients with sCeAD and of age-and sex-matched patients with ischemic stroke unrelated to CeAD (non-CeAD IS) by a standard examination protocol including 68 items, and performed extensive molecular investigation for hereditary connective tissue disorders in all patients with sCeAD.

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Platelet tyrosine and catecholamine (CA) content was measured in cluster headache sufferers during the different phases of the illness. Compared with controls, cluster headache sufferers had lower platelet levels of norepinephrine (NE) and epinephrine (E) in all phases of the syndrome. Tyrosine levels were increased significantly during the cluster headache attack. We suggest that these results provide biochemical evidence of sympathetic nervous system (SNS) hypofimction in cluster headache. Norepinephrine and epinephrine assay procedure Subjects were resting in a supine position in a quiet room when blood samples were drawn.Platelets were obtained from 20 ml blood as previously described.8 The platelet pellet was sonicated in 1 ml perchloric acid, centrifuged and the supernatant placed in a filtration column (Baker 10-SPE) containing 25 mg acid-washed alumina (INC Biomedicals) and 1 ml of 1'5 M TRIS buffer, pH 8 6. After the column was washed with HPLC grade water the catecholamines were separated from the alumina by passing a 200 pl aliquot of 0G1 M perchloric acid through the column. NE and E were detected by HPLC using coulometric detection. The system consisted of a Rheodyne injector (Model 7125), Waters pump and ESA 51 00A coulochem detector together with an ESA model 5021 conditioning cell and an ESA model 5011 analytical cell. The potentials for detector 1, detector 2 and the conditioning cell were + 0 05,-0 -30 and + 0 40 V respectively. (An ESA HR-80 column was used for the separation). The mobile phase consisted of 0 0575 M monobasic sodium phosphate, 1 25 mM heptanesulphonic acid and 0-215 mM EDTA, adjusted to pH 3-6 with phosphoric acid and combined with 3% HPLC grade methanol. A 50 ,ul sample was injected directly onto the column. The retention times for NE and E were 1 9 and 3-1 minutes respectively. Dihydroxybenzylamine was used as an internal standard.

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