SUMMARYPurpose: To assess the relationship between epilepsy and toxocariasis in adult subjects by means of a case-control study in Catania, Italy. Methods: People with epilepsy (PWE) were randomly selected from the database of the center of epilepsy of our department. Epilepsy was diagnosed according to the definition proposed by the International League Against Epilepsy. One healthy control per each case was selected among subjects who went to the central laboratory for a hematological check. Control subjects underwent a complete neurological examination to exclude the presence of neurological disorders. PWE and controls were assessed serologically for antibodies against Toxocara canis (T. canis) by an immunoblotting assay. Results: Two hundred thirty-one PWE (110 men and 121 women) and 201 controls (126 men and 75 women) were enrolled in the study. Of the 231 PWE, 152 presented partial seizures. Antibodies anti-T. canis were found in 38 PWE (16.4%) and in 13 controls (6.6%) giving a crude OR of 2.85 (95% CI 1.47-5.51). Adjusted OR estimated by logistic regression was 3.90 (95% CI 1.91-7.98). This association was mainly due to a significant association between Toxocara antibodies and partial epilepsy (adjusted OR 4.69; 95% CI 2.24-9.80), while a positive, but not significant, association was found with generalized seizures (adjusted OR 1.74; 95% CI 0.60-5.05). Conclusion: We found a significant association between T. canis seropositivity and epilepsy and a stronger association was found with partial epilepsy. Our finding suggests that toxocariasis may increase the risk of epilepsy.

Ethanol stimulating transient receptor potential vanilloid 1 (TRPV1) on primary sensory neurons promotes neurogenic inflammation, including calcitonin gene-related peptide (CGRP)-mediated coronary dilation. Alcoholic beverages trigger migraine attacks and activation of trigeminal neurons plays a role in migraine. We have investigated in guinea pigs whether ethanol by TRPV1 stimulation causes neurogenic inflammation in the trigeminovascular system. Ethanol-evoked release of neuropeptides from slices of dura mater was abolished by Ca(2+) removal, capsaicin pretreatment and the TRPV1 antagonist, capsazepine. Intragastric ethanol increased plasma extravasation in dura mater, an effect abolished by capsazepine and the NK1 receptor antagonist, SR140333, and caused vasodilation around the middle meningeal artery, an effect abolished by capsazepine and the CGRP receptor antagonist, BIBN4096BS. Vasodilation of meningeal vessels by TRPV1 activation and CGRP release may be relevant to the mechanism by which alcohol ingestion triggers migraine attacks.

SAI detected using [(123) I]FP-CIT SPECT can be used to differentiate VP and PD with a good degree of certainty.

The timed up and go test (TUG) is a widely used clinical test for the evaluation of balance and mobility. An instrumented version of TUG (iTUG) has been proposed to provide quantitative information on TUG performances. Here, we hypothesized that L-dopa may differently influence gait parameters recorded by a portable inertial sensor. To test this idea, we evaluated iTUG test in patients with Parkinson's disease (PD), both in L-dopa OFF and ON state. Twenty-eight PD patients performed the iTUG. Subjects were instructed to perform the task both in practical "OFF" and "ON" state. The system differentiated the test in six phases, recording phase durations, three-axial accelerations, average and peak angular speeds during turning. In all patients, sit-to-stand vertical and medio-lateral accelerations together with turning phase duration and angular speeds improved after L-dopa administration, while sit-to-stand and stand-to-sit phases antero-posterior accelerations were less responsive. In PD, L-dopa modulates iTUG in different ways, mostly improving the turning phases and less acting on postural controls during the sit-to-stand and stand-to-sit phases. Our results suggest different involvement of dopaminergic mechanisms on gait as assessed by iTUG. This is important for those aspects which are not improved by pharmacological therapy.