No abstract

Allodynia is not specific to migraine but is frequent in all headache patients: acute allodynia was reported in half those interviewed and in over a third of patients in each headache category; interictal allodynia was reported by nearly 25%.

Antiretroviral toxic neuropathy causes morbidity in human immunodeficiency virus (HIV) patients under dideoxynucleoside therapy, benefits only partially from medical therapy, and often leads to drug discontinuation. Proposed pathogeneses include a disorder of mitochondrial oxidative metabolism, eventually related to a reduction of mitochondrial DNA content, and interference with nerve growth factor activity. Carnitine is a substrate of energy production reactions in mitochondria and is involved in many anabolic reactions. Acetyl carnitine treatment promotes peripheral nerve regeneration and has neuroprotective properties and a direct analgesic role related to glutamatergic and cholinergic modulation. The aim of this study was to evaluate acetyl-l-carnitine in the treatment of painful antiretroviral toxic neuropathy in HIV patients. Twenty subjects affected by painful antiretroviral toxic neuropathy were treated with oral acetyl-l-carnitine at a dose of 2,000 mg/day for a 4-week period. Efficacy was evaluated by means of the modified Short Form McGill Pain Questionnaire with each item rated on an 11-point intensity scale at weekly intervals and by electromyography at baseline and final visit. Mean pain intensity score was significantly reduced during the study, changing from 7.35 +/- 1.98 (mean +/- SD) at baseline to 5.80 +/- 2.63 at week 4 (p = 0.0001). Electrophysiological parameters did not significantly change between baseline and week 4. In this study, acetyl-l-carnitine was effective and well tolerated in symptomatic treatment of painful neuropathy associated with antiretroviral toxicity. On the contrary, no effect was noted on neurophysiological parameters.

About 60% of patients complain of cutaneous allodynia during migraine episodes, often in the periorbitary region of the pain side. Pre-clinical studies have shown that the underlying mechanism is sensitisation of primary nociceptors and central trigeminovascular neurons and that patients have a lower pain threshold for mechanical stimulation compared to controls. The objective of this study was to determine the prevalence of allodynia during headache attacks in different forms of migraine. The subjects were 221 outpatients consecutively evaluated in the Headache Center of the L. Sacco Hospital in Milan: 114 had only attacks of migraine without aura (MO), 63 had also attacks with aura (MA) and 44 patients with chronic migraine with and without drug overuse (CM). Presence of head allodynia was investigated by a semistructured interview. Statistical analysis was performed by chi square test with Bonferroni correction for multiple comparisons. Forty-seven out of 114 MO patients (41.2%) complained of allodynia during headache episodes, 41 out of 63 MA patients (65.0%), and 29 out of 44 CM patients (65.9%). A higher frequency of allodynia in MA and CM with respect to MO patients was observed (p<0.01 at chi square test). Allodynia was a common complaint in migraineurs, being present in more than 40% patients of each group. A higher frequency was observed in MA and in CM patients. This observation may suggest that both frequency of attacks and presence of aura episodes may contribute to induce changes in neuronal activation threshold thought to sustain allodynia.