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This study explores the relationship between the frequency of psychogenic nonepileptic seizures (PNES) and health-related quality of life (HRQoL), as well as the effect of psychological distress and other physical symptoms on this relationship. Data were collected on 96 patients with PNES. Correlations of seizure frequency with HRQoL, psychological distress, and physical symptoms were computed. Partial correlations of seizure frequency with HRQoL while controlling for psychological distress and physical symptoms were also computed. Seizure frequency was found to be significantly related to subjective HRQoL, although the relationship with HRQoL was rendered nonsignificant when the effects of psychological distress and the number of other physical symptoms were taken into account. The results of this study suggest that summary scores of HRQoL are not independently related to frequency of PNES and that there is a close association between PNES frequency, levels of psychological distress, and number of other physical symptoms experienced.

This chapter explains how psychogenic nonepileptic seizures (PNES) can be used as an expression of “neurologic” pathology. Individual “neurologic,” “physical,” or “organic” factors explain PNES. PNES have been characterized as “episodes of altered movement, emotion, sensation, or experience, similar to those seen in epilepsy, but which have purely emotional causes.” The large number of studies describing neuropsychological performance deficits in patients with PNES supports the idea of PNES as a neurologic disorder. The chapter also explains brain abnormalities; many patients with PNES have neuroimaging or electroencephalographic abnormalities. Constitutional and developmental factors, neurologic factors, and psychogenic factors are briefly explained.

Psychogenic nonepileptic seizures (PNES) superficially resemble epileptic seizures, but are not associated with ictal electrical discharges in the brain. PNES constitute one of the most important differential diagnoses of epilepsy. However, despite the fact they have been recognized as a distinctive clinical phenomenon for centuries and that access to video/EEG monitoring has allowed clinicians to make near-certain diagnoses for several decades, our understanding of the etiology, underlying mental processes, and, subsequently, subdifferentiation, nosology, and treatment remains seriously deficient. Emphasizing the clinical picture throughout, the first part of this article is intended to "look and look again" at what we know about the epidemiology, semiology, clinical context, treatment, and prognosis of PNES. The second part is dedicated to the questions that remain to be answered. It argues that the most important reason our understanding of PNES remains limited is the focus on the visible manifestations of PNES or the seizures themselves. In contrast, subjective seizure manifestations and the biographic or clinical context in which they occur have been relatively neglected.

Summary Objectives: To explore the relationship of epilepsy and criminal behavior. Methods: Case series based on all criminal cases found “not guilty by reason of insanity” (NGRI) because of epilepsy in England and Wales between 1975 and 2001. Data were extracted from medico-legal reports held by the Mental Health Unit at the Home Office and the Department for Constitutional Affairs in London, UK. Results: Thirteen cases were identified, accounting for 7.3% of all verdicts of NGRI. Charges included murder (1), attempted murder (1) assault (7), arson (2), abduction/kidnapping (3), and burglary (1). Of the defendants, 92.3% were male, 76.9% had neuropsychological impairments, 84.6%% had psychiatric comorbidity, 92.3% were unemployed at the time of the offence, and 69.2% had been convicted of criminal offences previously. Eight of 10 defendants treated with antiepileptic drugs were complying poorly with medication. A total of 61.5% offenses were committed in a state of alcohol intoxication. Psychotic symptoms may have been present when the offense was committed in 52.8% of cases. Over two-thirds of offenses probably occurred during the postictal period. Conclusions: This case series suggests that it is exceptional for epileptic seizures to cause criminal acts or omissions. The relatively low standard of proof required means that some of cases found NGRI on account of epilepsy were not actually related to seizures. There were no definite examples of ictal criminal behavior. Most offenses related to seizures are likely to have occurred in the postictal phase.

This naturalistic study describes potential etiological factors in outpatients with functional neurological symptoms recorded during a screening interview with a single psychotherapist in 59 consecutive patients. The most commonly identified predisposing/precipitating factors were trauma (78.0%), family dysfunction (62.7%), and bereavement (62.7%). Family dysfunction (54.2%) and affective disorder (42%) were the commonest perpetuating factors. Trauma was more common in non-epileptic seizures; health anxiety, in men; family problems, in women. This study demonstrates the heterogeneity of this patient population. Further research is indicated to explore differences in predisposing, precipitating, and perpetuating factors in different patient groups with functional symptoms.

Background: The diagnosis of nonconvulsive status epilepticus (NCSE) is particularly challenging in elderly patients. Confusion, personality change, dysphasia, subtle motor activity and nystagmus may be the only presenting signs. Objective: To review current knowledge about NCSE with special focus on older people. Methods: Systematic review of the current literature via Medline search. Conclusion: Although prospective studies are still lacking, NCSE may be one of the most frequently missed diagnoses in patients presenting with altered mental status. Elderly patients are at particular risk of diagnostic errors because of the broad range of presentations of NCSE, significant comorbidities (especially cerebrovascular disease), limited awareness of this particular seizure emergency or difficulties with access to electroencephalography. Although diagnostic criteria and treatment remain controversial, the diagnosis of NCSE is important because it is potentially reversible.

AimRecent public policy documents have emphasised the need for healthcare practitioners to give patients choice. As part of a larger qualitative project investigating how neurologists give patients choices, we explored whether evidence of patient choice is associated with higher patient satisfaction.MethodFourteen neurologists and 223 patients were recruited in neurology outpatient clinics in Glasgow and Sheffield. All participants completed post-appointment questionnaires assessing whether choice was offered or perceived. Clinicians also rated the extent to which symptoms were medically explained. Patients completed the Medical Interview Satisfaction Scale-21 (MISS-21).ResultsTwo dominant factors contributed to the total MISS-21 scale, ‘rapport’ and ‘distress-relief’. Regression analysis showed that the extent to which symptoms were medically explained predicted most of the variance on both subscales and the total MISS-21 score. Spearman's rho correlations showed greater patient satisfaction if symptoms were medically explained and if no choice had been offered or perceived.ConclusionThere was no evidence that giving patients choices in interaction increased patient satisfaction with clinical encounters. Our findings suggest that patient satisfaction is most strongly influenced by the extent to which neurologists perceive symptoms as medically explained.

Objective We describe the roll-out of a brief psycho-education intervention for individuals with non-Epileptic Attack Disorder (NEAD), which has been developed for healthcare professionals with limited experience in delivering psychological treatments. Method The psycho-education package is comprised of four one-to-one sessions. The first session provides an explanation of the NEAD diagnosis and introduces the patient to idea that mind and body are linked. The second session teaches behavioural strategies for controlling seizures, including sensory grounding, relaxation and imagery. The third session focuses on identifying and reducing avoidance behaviours that may have been adopted due to seizure symptoms. The final session focuses on values and going forward. Eighteen nurses and therapists attended a training to deliver this package. The two day training intervention included lectures and interactive workshops with actors. The initial roll out stage involved fourteen NHS trusts across the country. Ten months following training, therapists were asked to complete a survey to assess the extent they used this intervention and that they found it to be relevant, comprehensive, and sufficient. Patients with NEAD who attended for psycho-education were also asked to complete pre and post questionnaires including the following measures; Work and Social Adjustment scale (WSAS), Brief Illness Perception Questionnaire (Brief IPQ), Clinical outcomes in routine evaluation (CORE) and the EuroQoL-5D3L and NewQOL quality of life measures. Results Since the training, the package has been delivered in four centres. Recruitment and data collection are ongoing. Preliminary analysis of the pre and post participant data shows that following intervention, participants viewed their seizures as significantly less threatening (IPQ, p=0.002), and reported significantly less distress (CORE, p=0.01) The collection of therapist feedback about the use of the intervention is ongoing. Conclusion It is feasible for healthcare professionals with minimal training in psychological intervention to deliver a brief psycho-education package for individuals with NEAD. Further analysis is needed to understand the full effectiveness of this intervention but preliminary results show that this intervention may have positive effects on the way individuals view their seizures and on their overall wellbeing.

Objective The illness perceptions of the relatives of patients with functional neurological symptom disorders (FNSD) and the relation to patients9 illness perceptions have been little studied. We aimed to compare illness perceptions of relatives of patients with FNSD to those held by patients themselves. We used control pairs with neurological diseases (ND) to examine the specificity of the findings to FNSD. Method Patients with FNSD (functional limb weakness and psychogenic non-epileptic seizures) and patients with ND causing limb weakness and epilepsy, and their relatives, completed adapted versions of the Illness Perception Questionnaire Revised (IPQ-R). Results We included 112 pairs of patients with FNSD and their relatives and 60 ND patient and relative pairs. Relatives of patients with FNSD were more likely to endorse psychological explanations and, in particular stress as a causal factor than patients with FNSD (p Conclusion The main difference in illness perceptions between relatives and patients with FNSD was a tendency for relatives to see psychological factors as more relevant than patients. Some other differences were observed between FNSD relatives and patients but the same differences were also seen in ND pairs. These other differences were therefore not specific to FNSD. Discussion about possibly relevant psychological factors with patients suffering from FNSD may be helped by including relatives.

Objective Our overall aim is to evaluate the clinical and cost effectiveness of specifically adapted Cognitive Behavioural Therapy (CBT) (plus Standardised Medical Care – SMC) in comparison to SMC alone for outpatients with dissociative seizures (DS), within a pragmatic, multi-centre UK-based RCT. This will redress the limited evidence base for psychotherapy in this patient group. Method Adults with DS but without currently active epilepsy will receive their diagnosis and information from a neurologist/epilepsy specialist and their seizure occurrence will be monitored. Three months post diagnosis they will be reviewed by a psychiatrist with interest and expertise in DS who will represent the diagnosis and deliver an information leaflet. Those continuing to experience DS in the previous 8 weeks and meeting other inclusion criteria will, if willing, be consented, undergo baseline assessments and be randomised to receive either 12 sessions of CBT (plus a booster session) as well as SMC or SMC alone. We aim to randomise 298 patients (149 to each arm). DS frequency will be monitored fortnightly and follow-ups will occur at 6 and 12 months post randomisation. An intention to treat analysis will evaluate effectiveness in outcomes relating to seizure frequency severity and freedom, mood and psychological state, quality of life and health service use. A qualitative study will investigate participants’ experiences of the interventions and barriers to participation that might affect subsequent implementation in the NHS. Results Multiple sites in England, Wales and Scotland have been enlisted. Recruitment in neurology clinics has commenced. Training for service user advisors, research workers and CBT therapists has been delivered. Conclusion The design and progress will be described. This is the largest planned trial for patients with DS to date. See ISRCTN05681227 for further details. FUNDING: NIHR HTA reference 12/26/01.

Objective To examine cognitive responses to stress-related stimuli in patients with seizures and to explore whether the response patterns differ in patients with epilepsy, patients with psychogenic non-epileptic seizures (PNES) and healthy individuals. We also aimed to investigate self-perceived and physiological stress responses in patients with epilepsy and those with PNES, compared to healthy individuals, and to examine the relationships between the cognitive, self-perceived and physiological stress responses in patients with seizures. Method A group of 54 patients with refractory seizures admitted for diagnostic video-telemetry assessment (epilepsy n=21, PNES n=26) and 21 healthy volunteers completed self-report questionnaires and performed an emotional Stroop test. Cognitive responses were investigated by exploring attentional biases in responses to neutral versus threatening stimuli comprising generally and socially threatening as well as somatic and seizure-related words. Heart rate variability (HRV) parameters were extracted from resting electrocardiogram recordings taken prior to the Stroop test and used as physiological stress markers. Results Patients with seizures, particularly those with epilepsy, showed greater attentional biases towards threatening information than healthy individuals across all word categories (ps Conclusion Many patients perceive stress as the commonest trigger of their seizures; however, the relationship between psychological and physiological processes relating stress and seizures has been poorly understood. Our findings show that patients with seizures are characterised by a pattern of abnormal attentional vigilance to threatening stimuli, high self-perceived stress and an altered autonomic nervous system responses. The relationships between attentional biases and HRV in patients with epilepsy suggest there may be a reciprocally causative relationship between cognitive responses, PNS tone and seizures. The long-term experience of stress and seizures could lead to a diminished PNS tone, which could exacerbate patients9 attentional responses to stressors. In turn, the biased attentional responses could trigger more frequent physiological stress responses, causing further alterations of the autonomic nervous system and further increasing patients9 vulnerability to stress and seizures.

Objective This study was intended to describe the neuropsychological phenomenology of focal nonconvulsive status epilepticus (NCSE). Methods Ictal, postictal, and interictal neuropsychological testing (NPT) was performed on six patients who developed NCSE during video/electroencephalographic monitoring in the context of presurgical evaluation. Results Neuropsychological impairments were marked in four of six and discrete in two of six patients. The majority of patients had selective rather than global neuropsychological deficits. The most important deficits involved consciousness, speech, praxis, cognitive functions, and affect. Impairment of consciousness was characterized by reduced vigilance, reactivity, and orientation. Some patients exhibited combined deficits of several higher cognitive functions (apraxia, acalculia, alexia, and aphasia with or without additional memory disturbance). Several patients had relatively subtle expressive or receptive aphasia. More severe language deficits were associated with reduced vigilance. Speech deficits may have caused poor performance in other areas evaluated with NPT. Conclusion NPT demonstrated that focal NCSE can be associated with pleomorphic but often discrete neuropsychological deficits.

Contains fulltext : 50730.pdf (Publisher’s version ) (Closed access) It is well recognized that the incidence of atypical language lateralization is increased in patients with focal epilepsy. The hypothesis that shifts in language dominance are particularly likely when epileptic lesions are located in close vicinity to the so-called language-eloquent areas rather than in more remote brain regions such as the hippocampus has been challenged by recent studies. This study was undertaken to assess the effect of lesions in different parts of the left hemisphere, lesions present during language acquisition, on language lateralization. We investigated 84 adult patients with drug-resistant focal epilepsy with structural lesions and 45 healthy control subjects with an established functional MRI language paradigm. Out of the 84 patients 43 had left hippocampal sclerosis, 13 a left frontal lobe lesion and 28 a left temporal-lateral lesion. All these lesions were likely to have been present during the first years of life during language acquisition. To assess the lateralization of cerebral language representation globally as well as regionally, we calculated lateralization indices derived from activations in four regions of interest (i.e. global, inferior frontal, temporo-parietal and remaining prefrontal). Patients with left hippocampal sclerosis showed less left lateralized language representations than all other groups of subjects (P < 0.005). This effect was independent of the factor of region, indicating that language lateralization was generally affected by a left hippocampal sclerosis. Patients with left frontal lobe or temporal-lateral lesions displayed the same left lateralization of language-related activations as the control subjects. Thus, the hippocampus seems to play an important role in the establishment of language dominance. Possible underlying mechanisms are discussed.

Summary: Purpose: To examine whether seizure remission is a comprehensive marker of outcome in psychogenic nonepileptic seizures (PNESs). Methods: A postal questionnaire was returned by 147 patients with PNESs a mean of 4.2 years after diagnosis (mean age at follow-up, 38.1 years). The proportion of patients who were “unproductive” (receiving health-related state benefits) at follow-up was determined, with a comparison of markers of ongoing psychopathology (Global Severity Index, anxiety and depression scores of the Symptom Checklist 90, Somatization Index DSM of the SOMS-2) in three outcome groups: group 1, continuing seizures; group 2, seizures stopped but patients “unproductive;” and group 3, seizures stopped, patients “productive.” Results: Of the patients, 71.4% continued to have seizures, and 28.6% had achieved seizure remission; 60.0% of patients with continuing seizures and 42.7% of patients in remission were “unproductive” (difference, NS). Ongoing psychopathology was related to the factor “group membership” with higher values in groups 2 and 3 than in group 1 (GSI, p < 0.001; anxiety, p = 0.01; depression, p = 0.02; Somatization Index DSM, p < 0.001). Across all patients and in the subgroup with PNESs and additional epilepsy, differences were significant only between groups 2 and 3, not between groups 1 and 2. In patients with PNESs alone, differences were significant only between groups 1 and 2. Conclusions: Seizure remission is not a comprehensive measure of good medical or psychosocial outcome in PNESs. Nearly half the patients who become seizure free remain unproductive. Many of these patients continue to report symptoms of psychopathology. Seizure control should not be the only focus of treatment in clinical practice or outcome observation in research studies.

Psychogenic nonepileptic seizures are relatively common, often disabling and costly to patients and society. Most authorities consider psychologic treatment as the therapeutic intervention of choice. This review is intended primarily for psychologists and therapists who treat patients with psychogenic nonepileptic seizures, and for neurologists who make the diagnosis and wish to find out more about psychologic treatment options. The first section describes the nature and etiology of psychogenic nonepileptic seizures. General questions regarding the psychologic treatment of patients with psychogenic nonepileptic seizures are addressed, before discussing specific therapeutic approaches. The final part summarizes the authors’ views on optimal treatment and the direction of future research.

Up to 50 or 60% of patients with chronic epilepsy have various mood disorders including depression and anxiety. Whereas the relationship between epilepsy and depression has received much attention, less is known about anxiety disorders. It is now recognized that anxiety can have a profound influence on the quality of life of patients with epilepsy. The relationship between anxiety disorders and epilepsy is complex. It is necessary to distinguish between different manifestations of anxiety disorder: ictal, postictal, and interictal anxiety. Preexisting vulnerability factors, neurobiological factors, iatrogenic influences (antiepileptic drugs, epilepsy surgery), and psychosocial factors are all likely to play a role, but with considerable individual differences. Despite the high prevalence of anxiety disorders in patients with epilepsy, there are no systematic treatment studies or evidence-based guidelines for best treatment practice. Nevertheless, a practical approach based on the temporal relationship between anxiety and epileptic seizures allows clinicians to consider appropriate treatment strategies to reduce the psychiatric comorbidity in patients with epilepsy.

Between 10 and 30% of patients seen by neurologists have symptoms for which there is no current pathophysiological explanation. The objective of this review is to answer questions many neurologists have about disorders characterised by unexplained symptoms (functional disorders) by conducting a multidisciplinary review based on published reports and clinical experience. Current concepts explain functional symptoms as resulting from auto-suggestion, innate coping styles, disorders of volition or attention. Predisposing, precipitating, and perpetuating aetiological factors can be identified and contribute to a therapeutic formulation. The sympathetic communication of the diagnosis by the neurologist is important and all patients should be screened for psychiatric or psychological symptoms because up to two thirds have symptomatic psychiatric comorbidity. Treatment programmes are likely to be most successful if there is close collaboration between neurologists, (liaison) psychiatrists, psychologists, and general practitioners. Long term, symptoms persist in over 50% of patients and many patients remain dependent on financial help from the government. Neurologists can acquire the skills needed to engage patients in psychological treatment but would benefit from closer working relationships with liaison psychiatry or psychology.

The availability of new antiepileptic drugs has broadened the spectrum of medical treatment options in epilepsy. The new agents, together with established drugs, offer substantial choice for doctors treating patients with focal or generalised epilepsy. The newer antiepileptic drugs are not necessarily more effective but usually better tolerated than the traditional agents, mainly because of favourable pharmacokinetic profiles and fewer interactions. Because treatment options have increased, drug therapy can now be tailored to the requirements of individual patients. Nevertheless, significant safety and efficacy issues continue to exist and there is a need for the development of even better agents. This review describes the clinical use of the new antiepileptic drugs, but focuses in particular on monotherapy, the treatment of generalised seizures, teratogenicity, and the cognitive side effect profile of the newer compounds.

Purpose: To examine the course of depression and anxiety in patients with temporal lobe epilepsy (TLE) treated with epilepsy surgery (and anticonvulsant drugs) or medical means alone. Methods: Of 94 TLE patients evaluated for epilepsy surgery, 76 underwent a resective procedure, 18 continued on medical treatment alone. Depression (Beck Depression Inventory (BDI)) and anxiety scores (Self-Rating Anxiety Scale (SRAS)) were examined during presurgical evaluation (T1) and after a mean of 16 months (T2), or 12 months after surgery. Depression and anxiety scores were related to type of intervention, underlying epileptogenic lesion, change of seizure control and anticonvulsant therapy. Results: At T1, depression and anxiety scores were higher in patients with TLE than scores in published normal populations. At T2, depression but not anxiety scores were significantly lower than at T1. Change of depression scores interacted with improvements of seizure control. Conclusions: Evidence of depression and anxiety is commonly found in patients with TLE. Depression improves not because of epilepsy surgery per se , but because of improved seizure control. This is more commonly achieved by surgery than medical treatment. The results are consistent with the hypothesis that depression in TLE is caused by pathological epileptic activity rather than a fixed structural defect.

The licensing of new antiepileptic drugs (AEDs) has led to a marked increase in the pharmaceutical armamentarium available for the treatment of epilepsy since 1990. The new drugs have now secured their place in the pharmacotherapy of epilepsy. The main reason for their success is their good general tolerability (especially with regard to cognitive function), the low rate of drug-drug interaction and the high anticonvulsant potency of some of the compounds. It is fortunate that many of the new AEDs have also proven effective in the treatment of generalised seizures, although they were originally developed for the treatment of focal seizures. However, the wide treatment choice has not solved the problems associated with the medical treatment of epilepsy. In monotherapy, none of the new AEDs have been shown to be superior in their potency to control seizures to older AEDs in comparative studies. Nonetheless, the greater choice of drugs allows treatment to be better tailored to the requirements of individual patients. Now there is a need to study patients whose seizures were not controlled by initial or alternative monotherapy to create an evidence-base for truly rational combination therapy in the future. Additional improvements in the medical treatment of epilepsy may come from AEDs currently in development, many of which use novel or unknown modes of action. So far, however, there is no evidence that any of these compounds will have radically different effects from the drugs currently available, or that they will have antiepileptic rather than purely anticonvulsant potential.

The population incidence of psychogenic nonepileptic seizures (PNES) may be only 4% that of epilepsy, but many patients with PNES have a tendency to seek medical attention, and PNES make up a larger share of the workload of neurologists and emergency and general physicians. Although a great number of publications describe how PNES can be distinguished from epileptic seizures, it usually takes several years to arrive at this diagnosis, and three-quarters of patients (with no additional epilepsy) are treated with anticonvulsants initially. However, the management of PNES as epileptic seizures can lead to significant iatrogenic harm. Moreover, the failure to recognize the psychological cause of the disorder detracts from addressing associated psychopathology and enhances secondary somatization processes. This review provides an overview of studies of the diagnosis, etiology, treatment, and prognosis of PNES. Physicians should always consider PNES in the differential diagnosis of a seizure disorder. If a diagnosis of PNES is possible, or a diagnosis of epilepsy in doubt, a clear diagnostic categorization should be sought. This should involve the assessment of the patient by a physician versed in the diagnosis of seizure disorders and, in many cases, the documentation of a typical seizure by video-EEG. Outcome may be improved if the diagnosis is more actively sought, made earlier, and communicated more convincingly.

Contains fulltext : 135771.pdf (Publisher’s version ) (Open Access) In rodents, cyclically fluctuating levels of gonadal steroid hormones modulate neural plasticity by altering synaptic transmission and synaptogenesis. Alterations of mood and cognition observed during the menstrual cycle suggest that steroid-related plasticity also occurs in humans. Cycle phase-dependent differences in cognitive performance have almost exclusively been found in tasks probing lateralized neuronal domains, i.e., cognitive domains such as language, which are predominantly executed by one hemisphere. To search for neural correlates of hormonally mediated neural plasticity in humans, we thus conducted a functional magnetic resonance imaging study measuring brain activity related to a semantic decision task in the language domain. This was contrasted with a letter-matching task in the perceptual domain, in which we expected no steroid hormone-mediated effect. We investigated 12 young healthy women in a counterbalanced repeated-measure design during low-steroid menstruation and high-steroid midluteal phase. Steroid serum levels correlated with the volume and lateralization of particular brain activations related to the semantic task but not with brain activity related to the perceptual task. More specifically, bilateral superior temporal recruitment correlated positively with progesterone and medial superior frontal recruitment with both progesterone and estradiol serum levels, whereas activations in inferior and middle frontal cortex were unaffected by steroid levels. In contrast to these specific interactions, testosterone levels correlated nonselectively with overall activation levels by neural and/or vascular factor(s). In conclusion, our data demonstrate steroid hormone responsivity in the adult human brain by revealing neural plasticity in the language domain, which appears hormone, task, and region specific.

To explore the clinical significance of a history of recurrent psychogenic nonepileptic seizure status (PNES-status), this study describes the frequency of PNES-status in 85 consecutive PNES patients and examines whether there are relevant differences between patients with a history of recurrent PNES-status and other PNES-patients. PNES patients were also compared with 64 patients with epilepsy. Data were extracted from hospital records and a postal questionnaire (Dimensional Assessment of Personality Pathology-Basic Questionnaire; Screening for Somatoform Symptoms; Dissociative Experience Scale). Of the PNES-patients, 77.6% reported at least one seizure > 30 minutes (PNES-status), 27 % admission to intensive care with status. 38.8% reported recurrent hospital admissions with status (PNES-status group), the remaining patients served as PNES-controls. The only clinical difference between the two PNES groups was that status patients were younger than PNES-controls (mean age 20.3 vs. 30.3 years, p = 0.001). Our results suggest that PNES status is common and often unrecognised. There were no substantial psychometric differences between patients with recurrent PNES-status and other PNES patients although both PNES-groups had more abnormal somatisation, dissociation and personality scores than patients with epilepsy.

Tiagabine was used as add-on therapy in the treatment of epilepsy with partial and/or secondarily generalised seizures to evaluate tolerability and efficacy. Five hundred and seventy-four patients (299 men and 275 women, mean age 38.1 years), with refractory partial seizures, were enrolled in this prospective, open-label study. Tiagabine was added to one (44.1%) or more (up to nine) antiepileptic drugs. The median daily dose of tiagabine was 30 mg (mean 29.1, SD 12.0). The mean duration of follow-up was 94.9 42.7 days. 12.3% of patients were completely seizure-free at the end of the observation period. Median total seizure frequency decreased from 4.5 to 2.0 seizures/4 weeks. Adverse events occurred in 78 patients (13.6%). Tiagabine proved to be a well-tolerated AED.

Our knowledge of longer term outcome in psychogenic nonepileptic seizures (PNESs) patients is limited; we know less still about factors predicting prognosis. This study was intended to describe outcome in a large cohort and to identify predictive clinical and psychological factors to generate new ideas for treatment. One hundred sixty-four adult patients with PNESs (66.7%) responded to outcome, personality, and psychosymptomatology questionnaires (Dimensional Assessment of Personality Pathology-Basic Questionnaire [DAPP-BQ], Dissociative Experiences Scale, and Screening Test for Somatoform Symptoms) a mean of 11.9 years after manifestation and 4.1 years after diagnosis of PNES. Additional clinical data were retrieved from hospital records. The responses showed that 71.2% of patients continued to have seizures and 56.4% were dependent on social security. Dependence increased with follow-up. Outcome was better in patients with greater educational attainments, younger onset and diagnosis, attacks with less dramatic features, fewer additional somatoform complaints, and lower dissociation scores. Better outcome was associated with lower scores of the higher order personality dimensions "inhibitedness," "emotional dysregulation," and "compulsivity" but not "dissocial behavior" (DAPP-BQ). Outcome in PNESs is poor but variable. Clinical and personality factors can be used to provide an individualized prognosis. By generating a patient-specific profile, they show particular maladaptive traits or tendencies that can identify goals for psychological therapy.

Background: Patients with physical brain abnormalities have an increased risk of developing psychogenic nonepileptic seizures (PNES). Here we describe patients who developed PNES after intracranial neurosurgery for indications other than the control of refractory epileptic seizures and explore whether neurosurgical intervention is at risk factor for PNES. Method: We searched the database of 372 patients diagnosed with PNES at our department over the last 10 years and identified 17 patients (4.6%) in whom PNES first started after intracranial neurosurgery. Surgical procedures included the complete or partial resection of a meningioma, AV malformation, cavernoma, plexus papilloma, neurinoma, astrocytoma, oligodendroglioma, dysontogenetic cyst, the drainage of a brain abscess and removal of a subdural hematoma. PNES were documented by ictal video-EEG, ictal EEG, or ictal observation and examination in all cases. The diagnosis of additional epileptic seizures were confirmed by ictal EEG/video-EEG, or made on the basis of a clinical assessment by an experienced epileptologist. Findings: Five patients had purely psychogenic postoperative seizure disorders, twelve had epileptic and psychogenic attacks. Median age at neurosurgery was 32 years (range 5–54), median latency between surgery and onset of PNES was 1 year (range 0–17 years). Interpretation: PNES may develop after intracranial neurosurgery undertaken for other indications than the control of refractory epileptic seizures. Younger patients with a history of pre-operative psychiatric problems or epileptic seizures and surgical complications may be at higher risk. A diagnosis of PNES should be considered in patients who develop refractory seizures after neurosurgery.

Item does not contain fulltext PURPOSE: To examine interictal EEG abnormalities in patients with psychogenic nonepileptic seizures (PNESs). METHODS: (a) Retrospective study of EEG reports of 187 consecutive patients with PNES seen at the Department of Epileptology, Bonn, Germany; (b) Blinded, multirater comparison of EEGs of all PNES patients with no other clinically recognizable cause of EEG disturbance (n = 50) and healthy controls (n = 50). RESULTS: Of 187 consecutive patients with PNESs, 57 patients had PNESs and epilepsy (PNES+E), and 130 patients, PNESs alone. The diagnosis of additional epilepsy was based on ictal (video-) EEG or on the critical assessment of all clinical data by an experienced epileptologist. Retrospective review of all available EEG reports showed that 92.9% of patients in the PNES+E and 53.8% in the PNES-only group had one or more abnormal EEGs (median number of EEGs per patient, three; range, one to 42). In the PNES-only group, EEG changes were nonspecific in 42.3% of patients. Only 50 of 130 patients with PNESs alone had no other clinically recognizable cause of EEG disturbance and entered the controlled study. In this study, 18% of patients and 10% of controls had abnormal EEGs. The frequency of epileptiform EEG changes was similar to that in previous population studies in both groups (2.0%). CONCLUSIONS: PNESs often occur in patients with organic brain disease. Even in patients with PNESs alone and no clinically recognizable cause of EEG disturbance, nonspecific abnormalities are found 1.8 times as often as in healthy controls. Interictal EEG changes are common in patients with PNESs and, in isolation, should not be interpreted as evidence of epilepsy.

Epilepsy is commonly associated with reproductive endocrine disorders. These include polycystic ovary syndrome (PCOS), isolated components of this syndrome such as polycystic ovaries, hyperandrogenaemia, hypothalamic amenorrhoea, and functional hyperprolactinaemia.To summarise the currently known relations between epilepsy and reproductive endocrine disorders.A review of clinical experience and published reports.The most likely explanations for endocrine disorders related to epilepsy or antiepileptic drugs are: (1) a direct influence of the epileptogenic lesion, epilepsy, or antiepileptic drugs on the endocrine control centres in the brain; (2) the effects of antiepileptic drugs on peripheral endocrine glands; (3) the effects of antiepileptic drugs on the metabolism of hormones and binding proteins; and (4) secondary endocrine complications of antiepileptic drug related weight changes or changes of insulin sensitivity. Regular monitoring of reproductive function at visits is recommended, including questioning about menstrual disorders, fertility, weight, hirsutism, and galactorrhoea. Particular attention should be paid to patients on valproate and obese patients or those experiencing significant weight gain. Single abnormal laboratory or imaging findings without symptoms may not constitute a clinically relevant endocrine disorder. However, patients with these kinds of abnormalities should be monitored to detect the possible development of a symptomatic disorder associated with, for example, menstrual disorders or fertility problems.If a reproductive endocrine disorder is found, antiepileptic drug treatment should be reviewed to ensure that it is correct for the particular seizure type and that it is not contributing to the endocrine problem. The possible benefits of a change in treatment must be balanced against seizure control and the cumulative side effect of alternative agents.

While the diagnostic features of psychogenic non-epileptic seizures have been better characterized in recent years, comparatively little is written about management. This review provides guidance to clinicians involved in the treatment of patients with psychogenic non-epileptic seizures and generates ideas for future research. It summarizes the recent literature specifically dealing with the treatment of such seizures and draws on the wider psychiatric literature on effective treatments for patients with other medically unexplained symptoms.

Item does not contain fulltext OBJECTIVE: To assess whether surgery to reduce or control epileptic seizures is safe and effective in patients known to have additional psychogenic seizures. DESIGN: We reviewed our computerized database of 1342 patients examined for epilepsy surgery and identified 13 patients with both epileptic and psychogenic seizures on whom postoperative outcome data were available. Data were gathered from the patients' records. Mean postoperative follow-up was 56 months. RESULTS: Epilepsy surgery led to clinically relevant improvements in 11 of 13 patients. Seven patients became free of epileptic and psychogenic seizures, 2 patients became free of epileptic seizures but continued to have infrequent psychogenic seizures, 1 patient reported more than an 80% improvement in epileptic seizure frequency and an abolishment of psychogenic attacks, and in 1 patient nondisabling epileptic seizures persisted at lower frequency but psychogenic seizures stopped. In 2 of 13 patients, epilepsy surgery failed to produce notable improvements. Although 1 patient became free of epileptic attacks and the other had fewer than 3 epileptic seizures per year, the severity or frequency of psychogenic seizures and pseudo-status epilepticus increased postoperatively. One of these patients had a preoperative diagnosis of somatization disorder; in the other, pathological illness behavior had been noted. CONCLUSION: A diagnosis of additional psychogenic seizures should not be considered an absolute contraindication to epilepsy surgery, although patients should undergo careful preoperative psychiatric evaluation.

Item does not contain fulltext OBJECTIVES: Patients with intractable epilepsy may benefit from epilepsy surgery especially if they have a radiologically demonstrable cerebral lesion. Dedicated magnetic resonance imaging (MRI) protocols as performed at epilepsy surgery centres can detect epileptogenic abnormalities with great sensitivity and specificity. However, many patients with epilepsy are investigated with standard MRI sequences by radiologist outside epilepsy centres ("non-experts"). This study was undertaken to compare standard MRI and epilepsy specific MRI findings in patients with focal epilepsy. METHODS: Comparison of results of standard MRI reported by "non-expert" radiologists, standard MRI evaluated by epilepsy "expert" radiologists, and epilepsy specific MRI read by "expert" radiologists in 123 consecutive patients undergoing epilepsy surgery evaluation between 1996 and 1999. Validation of radiological findings by correlation with postoperative histological examination. RESULTS: Sensitivity of "non-expert" reports of standard MRI reports for focal lesions was 39%, of "expert" reports of standard MRI 50%, and of epilepsy dedicated MRI 91%. Dedicated MRI showed focal lesions in 85% of patients with "non-lesional" standard MRI. The technical quality of standard MRI improved during the study period, but "non-expert" reporting did not. In particular, hippocampal sclerosis was missed in 86% of cases. Neuropathological diagnoses (n=90) were predicted correctly in 22% of "non-expert" standard MRI reports but by 89% of dedicated MRI reports. CONCLUSIONS: Standard MRI failed to detect 57% of focal epileptogenic lesions. Patients without MRI lesion are less likely to be considered candidates for epilepsy surgery. Patients with refractory epilepsy should be referred to an MRI unit with epileptological experience at an early point.

Item does not contain fulltext Delay to diagnosis was studied in 313 consecutive patients with psychogenic nonepileptic seizures (PNES). On average, patients with PNES were diagnosed 7.2 years after manifestation (SD 9.3 years). Younger age, interictal epileptiform potentials in the EEG, and anticonvulsant treatment were associated with longer delays. Other patient factors did not explain the great variability of the time to diagnosis, suggesting that physician factors contributed to delays.

The 2009 Dementia strategy promoted a ‘memory clinic in every town’. We investigated the patient mix seen in a neurology-led memory clinic. Retrospective review (2004, 2006, 2012) attendees to memory clinic. Prospective review memory clinic from October 2012–Dec 2013. Survey to neurologists in Specialist Interest Group in Cognition (ABN). Survey of local GPs. Results Percentage of attendees with benign memory complaints increased from 30% & 32% in 2004 and 2006 to 55% in 2012. Oct 2012–Dec 2013 >50% attendees do not have dementia or MCI. 9 responders: A mean of 27% of attendees of neurology-led memory clinics in the UK have ‘benign memory complaints’. The following terms were used: ▸ Attentional amnestic disorder, ▸ Attentional cognitive complaints, ▸ Worried well, ▸ Subjective memory complaints, ▸ Subjective memory impairment, ▸ Normal cognitive ageing, ▸ Hypocondrial, ▸ ‘Stress related.’ 4. GPs used; ‘worried well’, ‘benign senescent forgetfulness’, ‘Possible dementia’, ‘mild neurocognitive disorder’ and ‘late life forgetfulness’ & treated with antidepressants but also referred to psychology or memory clinic. People attending memory clinic frequently do not have dementia and currently there is no consensus for diagnostic label or treatment.

The clinical and laboratory phenotype of a paraproteinaemic neuropathy syndrome termed chronic sensory ataxic neuropathy with anti-disialosyl IgM antibodies is described in a series of 18 cases. Previous single case reports have outlined some features of this syndrome. All 18 cases were defined by the presence of serum IgM antibodies which react principally with NeuAc (alpha2-8)NeuAc(alpha2-3)Gal-configured disialosyl epitopes common to many gangliosides including GDlb, GD3, GTlb and GQlb. In 17 out of 18 cases, the serum contained benign IgM paraproteins, and in four of these cases at least two IgM paraproteins were present. The IgM antibodies were also cold agglutinins in 50% of cases. The clinical picture comprised a chronic neuropathy with marked sensory ataxia and areflexia, and with relatively preserved motor function in the limbs. In addition, 16 out of 18 cases had motor weakness affecting oculomotor and bulbar muscles as fixed or as relapsing-remitting features. When present in their entirety, these clinical features have been described previously under the acronym CANOMAD: chronic ataxic neuropathy, ophthalmoplegia, IgM paraprotein, cold agglutinins and disialosyl antibodies. This distribution of clinical features is reminiscent of Miller Fisher syndrome, in which acute-phase anti-disialylated ganglioside IgG antibodies are found. Clinical electrophysiology and nerve biopsy show both demyelinating and axonal features. A partial response to intravenous immunoglobulin and other treatments is reported in some cases.

Neurosurgical interventions often require the presurgical determination of language dominance or mapping of language areas. Results obtained by fMRI are closely correlated with invasive procedures such as electrical stimulation mapping or the intracarotid amobarbital test. However, language fMRI is not used routinely, because postprocessing is time-consuming. We utilized a real-time analysis software installed directly on the MR console computer and SPM99 as reference postprocessing software. We assessed the reliability of the immediate determination of language dominance based on individual activation maps by comparing the results of the visual analysis of images derived from conventional postprocessing with those produced by the real-time tool. All images were rated independently by six senior neurologists blinded to other data. We validated the robustness of the real-time method statistically by comparing global and regional lateralization indices derived from real-time and postprocessing analysis. Functional MRI was performed with a standard 1.5-T whole-body scanner. Brain activity was contrasted between an alternating semantic judgment and letter matching task. Twelve right-handed, healthy control subjects and 12 consecutive patients with drug-resistant, localization-related epilepsy were investigated. The semantic condition induced almost invariably left hemispheric activations in Broca's area, the premotor cortex, the dorsolateral prefrontal cortex, and the temporoparietal region. Although real-time analysis reduced noise less effectively than SPM99, visual ratings and lateralization indices produced highly concordant results with both methods. In conclusion, real-time fMRI, as used here, allowed reliable language lateralization and mapping in less than 15 min during routine clinical MRI investigation with no need for postprocessing.

Introduction Phenytoin is an effective anticonvulsant for focal epilepsy with the advantage of single daily administration. Its popularity however is in decline, partly because of perception of adverse effects that include gum hypertrophy, hirsutism, osteoporosis and cerebellar ataxia. Whilst phenytoin has been shown to be toxic to cerebellar Purkinje cells in vitro, the frequency, clinical and radiological phenotype and the mechanism of cerebellar degeneration in vivo remains unclear. In this study we aim to identify the frequency and characterise the clinical and radiological phenotype of patients with phenytoin–associated ataxia. Methods Patients were recruited from the epilepsy clinics, Royal Hallamshire Hospital, Sheffield, UK. HLA type and tests for other causes of ataxia were undertaken. The severity of the ataxia was rated using the Scale for the Assessment and Rating of Ataxia (SARA). Patients with clinical evidence of ataxia underwent a 3T MRI including spectroscopy of the cerebellum and had serum phenytoin levels estimated. Results Twenty five patients aged between 32–77 years were recruited. Eleven had focal epilepsy, 6 generalised and 8 unclassified. Age at diagnosis ranged from childhood to 74 years with duration 2–67 years. Fifteen patients (60%) continued taking phenytoin from the time of diagnosis. Mean duration of phenytoin treatment was 21 years and mean dose 350mg. Seventeen patients (68%) complained of poor balance and 13/25 (52%) had clinical evidence of ataxia on examination. All 13 had gait ataxia and the majority also had limb ataxia. SARA scores ranged from 3–17 (median 6). Gait, stance and heel–shin slide subgroups of the SARA scale were mostly affected. Eight out of 17 (47%) patients had the HLA DQ2/DQ8 type, strongly associated with autoimmune ataxias. Volumetric 3T MRI imaging and spectroscopy data were available in 6 of the 13 patients with ataxia. Cerebellar atrophy and abnormal spectroscopy of the vermis was found in three patients. Two of these patients had circulating antigliadin antibodies that signify sensitivity to gluten. Two patients with no ataxia but who had taken phenytoin for more than 20 years had no cerebellar atrophy and normal spectroscopy. Mean phenytoin level was 18 mg/L (5–20 mg/L). One patient had a serum phenytoin level of 65.8 mg/L. Conclusion 68% of patients on long–term phenytoin complained of poor balance and 52% had clinical evidence of ataxia. Cerebellar abnormalities on imaging were seen in 3/6 (50%) patients with ataxia. The primarily vermian involvement seen is similar to that of autoimmune ataxias. In those patients with vermian abnormalities an additional potential cause of ataxia was identified in the form of serological evidence of sensitivity to gluten. It is possible that the mechanism of cerebellar damage in patients on long term phenytoin may involve other mechanisms such as immune mediated damage in genetically (HLA DQ2/DQ8) susceptible individuals and/or sensitivity to gluten.

SynopsisThis analysis examines some of the psychological, philosophical and sociological motives behind the development of pauper lunatic asylum architecture in Ireland during the time of the Anglo–Irish union (1801–1922). Ground plans and structural features are used to define five psycho-architectonic generations. While isolation and classification were the prime objectives in the first public asylum in Ireland (1810–1814), a combination of the ideas of a psychological, ‘moral’, management and ‘panoptic’ architecture led to a radial institutional design during the next phase of construction (1817–1835). The asylums of the third generation (1845–1855) lacked ‘panoptic’ features but they were still intended to allow a proper ‘moral’ management of the inmates, and to create a therapeutic family environment. By the time the institutions of the fourth epoch were erected (1862–1869) the ‘moral’ treatment approach had been given up, and asylums were built to allow a psychological management by ‘association’. The last institutions (1894–1922) built before Ireland's acquisition of Dominion status (1922) were intended to foster the development of a curative society.

A 17-year-old boy presented for the first time with frequent seizures. Attacks consisted of nausea followed by flashing purple images, loss of consciousness, collapse, and bilateral shaking. The diagnosis of epilepsy was thought doubtful from the outset, but anticonvulsants were prescribed. Brain MRI showed no abnormalities. Based on inpatient observation on a neurology ward, ictal EEG and video-EEG of spontaneous typical seizures with apparent loss of consciousness, but no epileptiform activity or postictal changes, a firm diagnosis of nonepileptic attack disorder was made within 3 months of the manifestation of seizures. During his time on the ward, the patient was seen to be studying medical textbooks. On one occasion, he stole and altered his medical charts. He failed to engage in psychotherapy but was admitted to at least 11 different hospitals in his home region with 37 episodes of prolonged seizures over 3 months. Following …

In ordinary neurological practice, the diagnosis of psychogenic non-epileptic seizures (PNES) is often made by exclusion, or on the grounds that seizures lack features of epilepsy. With the exception of linguistic and interactional markers in the conversation with the patient about their symptoms,1 few ‘positive’ signs of PNES have been described. Therefore, this effort to improve our knowledge of the clinical semiology of PNES is welcome. Hubsch et al 2 used multiple correspondence analysis and cluster analysis of video-EEG recordings of PNES to identify five clinical subtypes of attack. The authors conclude that their classification of PNES may provide useful criteria for clinical diagnosis, presumably by giving clinicians a series of ‘models’ they can hold in their heads for evaluation of clinical descriptions of …

Abnormalities of smell and taste have been described in some neurodegenerative diseases including Alzheimer's dementia, idiopathic Parkinson's disease, Huntington's chorea, Korsakoff's syndrome, Pick's disease, the parkinsonian dementia complex of Guam, and amyotrophic lateral sclerosis.1 Hyposmia and hypogeusia are a feature of normal aging but they have not been recorded as a prominent early feature in previous reports of variant Creutzfeldt-Jakob disease (vCJD).2-5 We describe a patient with vCJD whose first symptoms included deficits of taste and smell. At the time of his initial neurological assessment, this 54 year old ceramic tiler had a 12 month history of loss of taste and smell, anxiety, low mood, and unusually short temper. He first became aware that something was wrong when he lost the ability to differentiate the taste of tea from that of beer. Loss of taste and personality change progressed gradually. He began to crave vanilla ice cream although he had never liked sweet foods in the past. He became …