Experimental studies have shown the role of excitotoxicity in the pathogenesis of ischemic brain lesions, and glutamate levels have been found to be elevated in CSF and plasma from patients, early after stroke. In this study, we investigated whether platelets could be involved in the mechanism of altered plasma glutamate levels after stroke. Forty four patients, from 6 hours to 9 months after ischemic stroke, 15 age-related healthy controls and 15 controls with stroke risk factors or previous transient ischemic attack were enrolled. Glutamate plasma levels, platelet glutamate release after aggregation and platelet glutamate uptake were assessed. Plasma glutamate levels were increased up to 15 days after the ischemic event in stroke patients, and the levels at day 3 were inversely correlated with the neurologic improvement between day 3 and 15. Ex vivo platelet glutamate release was decreased by 70% in stroke patients, suggesting previous in vivo platelet activation. Moreover, platelet glutamate uptake in these patients was decreased by 75% up to 15 days and was still reduced 90 days after stroke. Our data show a prolonged increase of glutamate in plasma after stroke, which might presumably be linked to altered platelet functions, such as excessive release of the amino acid or impaired uptake.

Glutamate may play an important role in the pathogenesis of migraine: glutamate release in the brain may be involved in the development of spreading depression and increased concentrations of this amino acid have been reported in plasma and platelets from migraine patients. Here we assessed platelet glutamate uptake and release in 25 patients affected by migraine with aura (MA) and 25 patients affected by migraine without aura (MoA), comparing the results with a group of 20 healthy matched controls. Both glutamate release from stimulated platelets and plasma concentrations of the amino acid were assessed by high-performance liquid chromatography, and were increased in both types of migraine, although more markedly in MA. Platelet glutamate uptake, assessed as 3H-glutamate intake, was increased in MA, while it was reduced in MoA with respect to the control group. These results support the view that MA might involve different pathophysiological mechanisms from MoA and, specifically, up-regulation of the glutamatergic metabolism. Understanding these dysfunctional pathways could lead to new, possibly more successful therapeutic approaches to the management of migraine.

We describe a case of a 27-year-old woman who came to the Emergency Department presenting severe abdominal pain. She was evaluated by a gynaecologist and submitted to pelvic ecography without finding relevant alterations. In the successive hours, she presented severe headache in occipital region and in the posterior neck, poorly responsive to analgesic drugs. A cerebral CT scan was performed and was normal, and the patient came to our Department of Neurology. The neurological examination on admission was normal. This woman had a 7 years of long-lasting history of headache, diagnosed in another hospital as migraine without aura, and she referred a recent and progressive worsening of both the frequency and the severity of the headache. In the suspect of subarachnoidal haemorrhage, a lumbar puncture was performed, and was negative for bleeding, showing only a mild increase in the number of cells (12 leucocytes). Following the lumbar puncture, the patient presented a dramatic improvement of the headache. In the successive days, she lamented sellar hypoesthesia and, when asked, she referred a recent history of urinary and faecal retention. She was, therefore, submitted to an NMR of the lumbar and sacral medulla with evidence of a voluminous extradural formation in the sacral region suggestive for extradural sacral meningeal cyst. She was finally dispatched to the Department of Neurosurgery for surgical asportation of the cyst.

Migraine is a common disorder and is a major cause of disability and loss of working performance in western countries. Therefore, many tools have been developed to assess migraine related disability. Among these, the Migraine Disability Assessment (MIDAS) questionnaire has been shown to be of particular interest, as it is valid, reliable and useful for therapeutic decisions. In this pilot study, we address the validity of the MIDAS questionnaire in an unselected population of migraine patients in the emergency setting. We found that the MIDAS scores in the emergency room were similar to those collected in a specialised headache centre. This result suggests that the MIDAS questionnaire could be reliably used in the emergency setting, hence avoiding unnecessary delays in the treatment of migraine patients.