[Hashimoto's encephalopathy: a rare cause of status epilepticus]. / Encéphalopathie de Hashimoto : une cause rare d'état de mal épileptique.

Hashimoto's Encephalopathy (HE) is a rare condition defined by the association of encephalopathy and autoimmune thyroiditis with increased levels of antithyroid antibodies. Presenting symptoms of HE may be quite variable. Although seizures are rather frequent, status epilepticus seems very rare (10 reported cases to date) and exceptionally revealing. We report the case of a 48-year-old female, who presented with a series of status epilepticus. The only positive result of the initial exploration was an increased level of antithyroid antibodies. The patient's condition improved only after initiation of corticosteroid treatment, which provided a stable remission. HE pathophysiology still remains poorly understood and controversial. Pathological data are sparse and provide variable pictures. Although an autoimmune mechanism looks very likely, the precise role of antithyroid antibodies is still discussed. A direct toxicity has not been demonstrated and antibodies could simply be a marker of impaired immunity. Occurrence of status epilepticus in HE could be related to the presence of active inflammation of cortical or para-cortical tissue, although such a hypothesis remains to be demonstrated. The diagnosis of HE should be systematically considered in patients with unexplained episodes of status epilepticus. Search for abnormal thyroid function and increased levels of antithyroid antibodies allow both early diagnosis and treatment, with a clear benefit for the patients.

Post-embolization perianeurysmal edema revealed by temporal lobe epilepsy in a case of unruptured internal carotid artery aneurysm treated with bare platinum coils.

We report the case of a patient with an unruptured internal carotid artery (ICA) aneurysm treated with bare platinum coils. The patient had seizures 1 month after treatment. Postoperative imaging showed perianeurysmal edema and enhancement of the aneurismal wall. After aneurysm coiling, perianeurysmal edema is an unusual complication that can be asymptomatic or cause symptoms depending on its location. Epilepsy as a clinical presentation of perianeurysmal edema has not previously been reported. Literature about post-embolization perianeurysmal edema is reviewed.

[Drug treatment of epilepsy: update]. / Traitement médicamenteux des épilepsies: actualité.

Medical treatment of epilepsy has evolved during the last ten years. The "Epileptic Syndrome Classification" established in 1989 and new antiepileptic drugs account for these changes. This article recalls the principal rules of medical treatment of epilepsy and reviews new antiepileptic drugs available in Belgium.

Lupus anticoagulant induced by the combination of valproate and lamotrigine.

A 5-year-old boy with generalized absence seizures was treated with valproate (VPA), 30 mg/kg/day. One month after VPA introduction, routine examination showed moderate reduction in fibrinogen and prolonged partial thromboplastin time (PTT). The search for lupus anticoagulant (LAC) was negative. After 10 months of VPA treatment, seizures persisted, and lamotrigine (LTG), 2 mg/kg/day, was progressively given with VPA. Seizures disappeared, but PTT was more prolonged than before LTG introduction. The search for LAC was positive, and enzyme-linked immunosorbent assays (ELISAs) for immunoglobulin G (IgG) anticardiolipid antibodies were positive. Serum autoantibody screen and rheumatoid factor were negative; serum complement was normal. LAC eventually disappeared with VPA discontinuation. We believe that LTG may have exacerbated an initially mild immune response induced by VPA without clinical evidence of systemic disease. We therefore suggest that careful surveillance for LAC and systemic disease should be instituted when VPA is used with LTG.

Somatosensory evoked potentials at rest and during movement in Parkinson's disease: evidence for a specific apomorphine effect on the frontal N30 wave.

Studies attempting to relate the abnormalities of the frontal N30 components of the somatosensory evoked potentials (SEPs) to motor symptoms in Parkinson's disease (PD) have shown contradictory results. We recorded the frontal and parietal SEPs to median nerve stimulation in 2 groups of PD patients: a group of 17 patients presenting the wearing-off phenomenon, and a group of 10 untreated PD patients. The results were compared with a group of 13 healthy volunteers of the same age and with a group of 10 non-parkinsonian patients. All parkinsonian and non-parkinsonian patients were studied before ("off" condition) and after a subcutaneous injection of apomorphine ("on" condition). The gating effects of a voluntary movement (clenching of the hand) on the SEPs were also studied for the wearing-off group of PD patients (in states off and on) in comparison with the healthy subjects. At rest and in the off condition the amplitude of the frontal N30 was significantly reduced in the 2 groups of PD patients. We demonstrate that the movement gating ability of the PD patient is preserved in spite of the reduced amplitude of the frontal N30. This result suggests that the specific change in the frontal N30 in PD is not the consequence of a continuous gating of the sensory inflow by a motor corollary discharge. Clinical motor improvement induced by apomorphine was associated with a significant enhancement of the frontal N30 wave. In contrast, the subcortical P14 and N18 waves and the cortical N20, P22, P27 and N45 were not statistically modified by the drug. Apomorphine infusion did not change the absolute reduced voltage of the N30 reached during the movement gating. While the frontal N30 component of the non-parkinsonian patients was significantly lower in comparison to healthy subjects, this wave did not change after the apomorphine administration. In the wearing-off PD patient group the frontal N30 increment was positively correlated with the number of off hours per day. This specific apomorphine sensitivity of the frontal N30 was interpreted as a physiological index of the dopaminergic modulatory control exerted on the neuronal structures implicated in the generation of the frontal N30.