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Objective The goal of this article was to describe the clinical characteristics and outcomes of patients diagnosed with psychogenic nonepileptic seizures (PNES). Methods We conducted a retrospective review of patients diagnosed with PNES in a 5-year period. Results Fifty patients with PNES were identified, giving an estimated incidence of 0.91/100,000 per annum. Thirty-eight were included for review, 15 of whom were male (39%). Eighteen patients had been diagnosed with epilepsy as well as PNES (47%). We demonstrated a gender difference in our patients, with males having higher seizure frequencies, more antiepileptic drug use, and a longer interval before diagnosis of PNES. Females were diagnosed with other conversion disorders more often than males. Impaired social function was observed in PNES, as was resistance to psychological interventions with a subsequent poor response to treatments. Conclusions PNES remains a difficult condition to treat, and may affect males in proportions higher than those described in previous studies.

Depression is a significant risk factor for and consequence of both cardiovascular disease and stroke. The pathophysiological processes underlying this association are poorly understood. This study utilised a technique for measurement of whole blood platelet surface glycoproteins involved in early adhesion and aggregation in sample populations of patients with depression and stroke, and healthy controls. We analysed the platelet surface glycoproteins GPIb and GPIIbIIIa using flow cytometry in eight depressed subjects (Hamilton depression score >17), 14 post-stroke subjects (seven depressed and seven non-depressed), and in eight healthy control subjects. The number of GPIb receptors was significantly increased in subjects with depression and in post-stroke subjects compared to control subjects. The number of GPIb receptors from post-stroke subjects was not significantly different from that of depressed subjects. There were no differences between any groups in measures of GPIIbIIIa receptor numbers. No additive effect of co-morbid depression on the surface expression level of either marker could be detected in the post-stroke subjects. Platelet dysfunction may be involved in the pathophysiological process underlying the association between depression and cerebrovascular disease.

We have investigated the effect of a number of group I, II and III metabotropic glutamate (mGlu) receptor agonists and antagonists on paired pulse depression in the medial perforant path of the rat dentate gyrus in vitro. A triphasic pattern of a large depression at short intervals (10-50 ms), a reduction of this depression at intermediate intervals (50-200 ms) and again a large depression at late intervals (200 ms) was observed. The group I mGlu receptor agonist, (S)-3,5-dihydroxy phenylglycine ((S)-DHPG; 20 microM) had no significant effect on paired pulse depression at any interstimulus intervals. The mGlu receptor group II and III agonists, L-CCG-1 ((2S,3S,4S)-alpha-(carboxy-cyclopropyl)-glycine), DCG-IV ((2S,1'R,2'R,3'R)-2-2',3'-dicarboxy cyclopropylglycine), 1S,3R-ACPD (1S,3R-1-aminocyclopentate-1,3-dicarboxylic acid) and L-AP4 (L-2-amino-4-phosphono butyric acid) reduced paired pulse depression at interstimulus intervals of 200 ms or less. Application of the non specific mGlu receptor antagonist, MCPG (alpha-methyl carboxy-phenylglycine; 200 microM) completely inhibited the 1S,3R ACPD-induced reduction in paired pulse depression but was without effect on the L-AP4 response. The relatively specific group II antagonist MCCG ((2S,3S,4S)-2-methyl-2-carboxy cycloproprylglycine) at 200 microM and 500 microM, attenuated but did not completely inhibit the DCG-IV induced reduction of paired pulse depression. The putative group III pre-synaptic mGlu receptor antagonist alpha-methyl-L-AP4 and MSOP ((RS)-alpha-methylserine-O-phosphate) both at 200 microM inhibited the L-AP4-induced reduction in paired pulse depression at intermediate phase interstimulus intervals but not at early interstimulus intervals. These results specifically demonstrate the involvement of group III and III mGlu receptor ligands in the modulation of paired pulse depression in the medial perforant pathway.

Introduction: Irritable bowel syndrome (IBS) is a functional disorder which has been linked with abnormal serotonin functioning. It has a high psychiatric co-morbidity with depressive and anxiety disorders, conditions which result from a central serotonergic deficit. Tryptophan (TRP) forms the substrate for serotonin biosynthesis, but alternatively TRP can also be catabolised to kynurenine (KYN). Tryptophan catabolism along the kynurenine pathway is regulated by the enzyme indoleamine 2,3-dioxygenase (IDO), and therefore the ratio of kynurenine to tryptophan provides a measurement of IDO activity. The main inducer of IDO is the pro-inflammatory cytokine, interferon-gamma (IFN-γ). Aims: The primary aim of this study was to investigate tryptophan catabolism in IBS, and to relate such catabolism to immune activation and psychiatric co-morbidity. We hypothesised that there would be increased IFN-γ levels in IBS, and consequently, increased shunting of tryptophan along the kynurenine pathway at the expense of serotonin biosynthesis. Method: 42 female IBS subjects and 22 female healthy controls had plasma kynurenine and tryptophan concentrations measured using an HPLC method. Interferon-γ was assayed using an electro-chemiluminescence multiplex system imager. Co-morbid depressive and anxiety disorders were identified using a valid and reliable self-report tool, the Patient Health Questionnaire (PHQ), and the severity of IBS was assessed using a summary score of 4-point ordinal scales in accordance with a previously published method. Results: Of the 42 IBS subjects, 17 had severe IBS, 16 reported moderate symptoms and 9 reported mild IBS symptomatology. There was a significant positive correlation between IBS severity and Kyn/Trp ratio(r = 0.47, p=0.002). Those with severe IBS symptoms demonstrated increased tryptophan catabolism along the kynurenine pathway (i.e. increased Kyn/Trp ratio)compared to those with mildto-moderate IBS and healthy controls(p = 0.004); and those with severe IBS were over twice as likely to have depression or anxiety compared to those with less severe symptoms (RR = 2.2;95% C.I 1.2-3.9). No difference in IFN-γ levels was observed between the IBS patients and controls; however IFN-γ was positively correlated with Kyn:Trp ratio in the IBS group (r = 0.58, p = 0.005) and this was not seen in the controls (r = 0.05, p = 0.8). Conclusion: Our results indicate an increased sensitivity to IFN-γ in the regulation of tryptophan catabolism in IBS. This may predispose to the increased rate of Kyn production observed in severe IBS cases and to the high co-morbidity with depressive and anxiety disorders in this group.