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G Reinshagen

Publications and source records attributed to G Reinshagen.

7 recordsLinked to original sources
PubMed2001

Aversive learning in patients with unilateral lesions of the amygdala and hippocampus.

The present study applied a visual half field paradigm with emotional facial expressions in patients with selective unilateral amygdalo-hippocampectomy (AHE) to elucidate the contributions of the left and right medial temporal lobe and amygdala to emotional learning. Electrodermal indicators of aversive learning were studied in 14 left AHE and 12 right AHE patients, as well as 13 controls matched in sex and age. In a differential conditioning paradigm with negative (CS+) and positive (CS-) facial expressions, CS+ were associated with an aversive vocalization (US, 95 dB, 3 s). During extinction, stimuli were presented laterally and preattentively using backward masking. Appropriate CS durations yielding preattentive presentation were individually determined prior to conditioning. In contrast to controls, both left and right AHE patients failed to show an autonomic conditioning effect following left visual field presentations of masked negative CS+ during extinction. AHE patients also showed no clear differential acquisition. Moreover, right AHE patients poorly recognised that negative valence was an affiliating dimension of the CS-US compound.

Adult↗
PubMed1999

Characteristics of a unique visual field defect attributed to vigabatrin.

PURPOSE: Vigabatrin (VGB) therapy is associated with a loss of peripheral vision. The characteristics and prevalence of VGB-attributed visual field loss (V-AVFL) and associated risk factors were evaluated in patients with epilepsy. METHODS: The material comprised the visual fields and case notes of 88 patients with suspected V-AVFL (25 spontaneous reports and 63 cases from an open-label extension trial) and of 42 patients receiving alternative antiepileptic drugs (AEDs) from a cross-sectional study. RESULTS: Forty-two reliable cases of visual field loss could not be assigned to an alternative known cause and were therefore attributed to VGB (13 spontaneous reports and 29 from the open-label study). All cases except one were asymptomatic. Seven cases of field loss were present in the reference cohort of 42 patients; all cases could be attributed to a known aetiology. Thirty-six of the 42 confirmed cases of V-AVFL exhibited a bilateral defect that was most profound nasally, and three, a concentric constriction. The prevalence of V-AVFL was 29% (95% confidence interval, 21-39%). Male gender was associated with a 2.1-fold increased relative risk of V-AVFL (95% confidence interval, 1.20-4.6%). Age, body weight, duration of epilepsy, and daily dose of VGB, and concomitant AEDs did not predict the occurrence of V-AVFL. CONCLUSIONS: The unique visual field defect attributed to VGB is profound in terms of the frequency of occurrence and the location and severity of loss. The asymptomatic nature of the field loss indicates that V-AVFL can be elicited only by visual field examination.

Adult↗
PubMed1994

[Allergic vasculitis caused by Vigabatrin].

A patient with focal epilepsy that was resistant to medical treatment received add-on therapy with vigabatrin. Six months after commencement of vigabatrin therapy, allergic vasculitis caused by vigabatrin was diagnosed. The patient displayed unilateral anterior ischaemic optic neuropathy with impairment of vision and concentric loss of visual field. The diagnosis was based on the lymphocyte transformation test and the clinical course. The allergic vasculitis was healed by cortisone therapy.

Adult↗