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National Health Service Hospitals are under pressure to reduce waiting lists within the constraints of a limited infrastructure. We implemented two systems to reduce waiting times for elective non-complex spinal surgery. The first of these was the introduction of managed generic waiting lists for both initial outpatient appointments and subsequent surgery. Thereafter, the MRI booking system was integrated with outpatient review appointments. Times from referral to first outpatient appointment and from scan to outpatient review and time on waiting list for surgery were analysed before and after implementation of these changes. Despite constant unit capacity there was a global decrease in waiting times. Before introduction of the generic waiting list, 37% of listed patients waited for more than 9 months; this figure fell to zero. Time from scan to outpatient review was 185 days before integration, 30 days after. Changes of this sort demand a quorum of consultants who will accept each others’ recommendations. The generic waiting list will have impact only when there are large disparities in waiting times for different consultants. Targets are met at the expense of continuity of care.

We present the use of a zig-zag bicoronal scalp incision for cranial-facial cases in paediatric neurosurgery.The authors believe that this technique leads to improved cosmesis, especially when the hair is wet.

Review of epilepsy out‐patients is often inadequate. Time constraints encourage a largely reactive approach to ‘follow‐ups’, with little questioning of existing diagnoses or exploration of the patient's agenda, and undue emphasis on counting seizures, adjusting medication, and restating lifestyle and driving restrictions. Compared to new cases, follow‐ups in secondary care are more likely to be delegated to less experienced team members: seeing a different doctor at each visit is dispiriting to both parties. Yet patients with epilepsy certainly require detailed and long‐term follow up, not least because the diagnosis is too often incorrect, particularly in non‐specialist hands.1 Epilepsy is diagnosed predominantly on clinical grounds, and where there is doubt, it may be necessary to retake the history (with witness accounts) over several visits. Review appointments also provide an opportunity to check patients' knowledge, understanding, expectations and beliefs about epilepsy and its lifestyle implications. Further, epilepsy generally requires long‐term medication, and this also requires long‐term supervision. The choice of treatment, and the need for medication at all, deserves repeated reconsideration. The lessons from felbamate (aplastic anaemia), vigabatrin (visual field constriction), and anti‐epileptic teratogenicity, demonstrate the dangers of complacency about the long‐term side‐effects of anti‐epileptic medication. Existing primary care guidelines recommend annual review of all patients with epilepsy, with re‐referral to specialist services when appropriate.2 However, it appears increasingly necessary to make regular specialist review available to all patients with epilepsy, even those not actively seeking medical attention. Such specialist review would have …

Background Epilepsy is a common neurological condition, affecting 0.5 to 1% of the population. Nearly 30 per cent of people with epilepsy have seizures that are refractory to currently available drugs. In response to this problem, potential new drugs are being developed. Remacemide is one of these. Objectives To evaluate the effects of add-on treatment with remacemide upon seizures, adverse effects, cognition and quality of life for people with drug-resistant localization related epilepsy. Search strategy We searched the Cochrane Epilepsy Group trials register (4 July 2002), the Cochrane Controlled Trials Register (The Cochrane Library Issue 2, 2002) and MEDLINE (28 May 2002). In addition, we contacted AstraZeneca (makers of remacemide) and colleagues in the field to see if they were aware of any trials that we had missed. Selection criteria Randomized placebo controlled add-on trials of people of any age with localization related seizures, in which an adequate method of concealment of randomization was used. The studies could be blinded or unblinded and be of parallel or crossover design. They had to have a minimum treatment period of eight weeks. Data collection and analysis Two reviewers independently selected trials for inclusion and extracted data. Any disagreements were resolved by discussion. Outcomes investigated included 50 per cent or greater reduction in seizure frequency, treatment withdrawal, adverse effects, effects on cognition and quality of life. The primary analyses were by intention-to-treat. Dose response was evaluated in regression models. Main results Two parallel group trials were included representing 514 individuals. Daily doses of 300, 600, 800 and 1200mg of remacemide were tested. The overall relative risk (RR) for remacemide versus placebo with 95% confidence intervals(CI) for a 50 per cent or greater reduction in seizure frequency was 1.59(95% CI 0.91 to 2.79). Due to differences in response rates among trials, regression models were unable to provide reliable estimates of responses to individual doses. Regression models did however suggest a significant effect for 800-1200mg remacemide per day. Remacemide was more likely to be withdrawn than placebo, the RR for treatment withdrawal was 1.90(95% CI 1.00 to 3.60). The RR for dizziness indicates that it is significantly associated with remacemide 3.08(99% CI 1.37 to 6.95). Effects on cognition and quality of life were not reported. Reviewer's conclusions Given the modest effect on seizure frequency and significant withdrawal rate it is unlikely that remacemide will be further developed as an antiepileptic drug.

The purpose of the present review is to assess the evidence published in scientific literature that industrial organic solvents as a generic group have the ability to induce long-term nervous system damage in workers that can be detected by techniques other than neuropsychological testing. The main body of evidence considered in this review was 40 studies involving the use of brain imaging, neurophysiological testing, gross autopsy or histopathology in groups of workers with long-term solvent exposure. Case reports involving both solvent abuse and occupational exposure, and experimental animal data have also been reviewed as supporting data. A number of the studies in groups of workers provide evidence of the presence of marginal atrophic abnormalities in the brain or deficits in nerve conduction velocity in solvent-exposed workers. However, there are limitations in the design of many of these studies, the strength of association between exposure and effect is not consistently strong, no dose-response relationship can be detected, the reported changes lack specificity and there is no coherence between the human and experimental animal data. Overall, it is not possible to draw reliable conclusions with respect to the presence or absence of nervous system damage related to the common properties of organic solvents.

To review all patients who had received vigabatrin at the Walton Centre to determine the incidence of visual field defect, seizure outcome if vigabatrin had been stopped, and adherence to guidelines on the use of vigabatrin in clinical practice.Retrospective review of 583 patients prescribed vigabatrin at any time between 1989 and 2001 from a regional and satellite epilepsy clinic. Data were collected on dose and duration of treatment, results of quantitative perimetry, and reasons for, and outcome of, discontinuation.The visual fields were abnormal with no alternative cause in 42 of the 98 tested (43%). There was no clear relation between the cumulative dose of vigabatrin received and the occurrence of a visual field abnormality. Fifty patients continued taking vigabatrin, and a further 84 were lost to follow up while taking vigabatrin. In 75 patients who had stopped vigabatrin due to a visual field abnormality or concern over this potential adverse effect, the seizure control was no different or had improved in 66 (88%), while it had deteriorated in only 7 (9%).This study confirms the previously reported high incidence of asymptomatic visual field defects associated with vigabatrin. Many patients taking vigabatrin may not have been counselled about the risks, and there are significant cost implications in tracing and assessing those patients lost to follow up. Switching over to another antiepileptic drug usually does not result in deterioration in seizure control, but in clinical practice an individual risk to benefit ratio needs to be taken into consideration.

Methods To assess effects of treatment patterns on epilepsy outcome, we obtained clinical details of patients admitted to hospitals in Greater Glasgow with Status Epilepticus (SE) from mid-1990s to present day. This allowed collection of data on aetiology, morbidity, mortality, and treatment. Results 132 cases have been reviewed so far. Of those with prior diagnosis of epilepsy (n=24), 83% recovered without any new neurological deficit. Death occurred in ITU in one patient, and in one further patient in the subsequent 3 years. After De Novo Status Epilepticus (DNSE – those with no previous history of epilepsy–n=62) 61% recovered with no neurological deficit. 41 DNSE patients (66%) had a history of preceding alcohol or drug-related problems. Three deaths (5%) occurred in ITU, but in the year following admission, 8 further deaths brought 1-year mortality of DNSE to 18%. Only 9% (2/22) of patients with super-refractory epilepsy (Admission to ITU>7 days), recovered without neurological deficit. Three patients (14%) died in the year following admission. Conclusion SE has a significant mortality risk beyond discharge from ITU especially as a De Novo presentation. Further work may highlight role of baseline AEDs and demographic factors in influencing mortality and morbidity of SE.

Objective: To undertake a systematic review and meta-analysis of placebo controlled add-on trials of levetiracetam, oxcarbazepine, remacemide and zonisamide for patients with drug resistant localization related epilepsy. Methods: We searched Medline, The Cochrane Library and contacted the relevant pharmaceutical companies. Outcomes were 50% or greater reduction in seizure frequency and treatment withdrawal for any reason. Data were synthesised in a meta-analysis. The effect of dose was explored in regression models for levetiracetam and remacemide. Results: We found four trials (1023 patients) of levetiracetam, two (961) of oxcarbazepine, two (388) of remacemide and three (499) of zonisamide. Ignoring dose, the relative risks (95% CI) for a 50% response were 3.78 (2.62–5.44), 2.51 (1.88–3.33), 1.59 (0.91–2.97) and 2.46 (1.61–3.79), respectively. There was evidence for increasing effect with increasing dose for levetiracetam, oxcarbazepine and remacemide. The relative risks for treatment withdrawal were 1.21 (0.88–1.66), 1.72 (1.35–2.18), 1.90 (1.00–3.60) and 1.64 (1.02–2.62), respectively. Conclusions: These data suggest a useful effect for levetiracetam, oxcarbazepine and zonisamide. Levetiracetam has the more favourable ‘responder-withdrawal ratio’ followed by zonisamide and oxcarbazepine.

As the century ends, the proliferation in medical literature has made it increasingly easy to become lazy about the quality and source of any data with which we are presented. This struck home as I was browsing through a CD Rom textbook ( Neurobase , Arbor Inc, 1999). While skimming through theories on the aetiology of multiple sclerosis, my mind's wandering was interrupted by a feeling of unease. I returned to the end of the preceding paragraph: “Humans injected with multiple sclerosis brain extracts are not at an increased risk of multiple sclerosis.” > We all have a duty to avoid recognising any work that is less than ethically rigorous This was an arresting sentence: injection with diseased brain extract? Who could have carried out such a study? Could anyone have given informed consent? The study author was named as Dr Schaltenbrand, and my suspicions about the nature of the work increased when the German title of the book, published in Leipzig in 1943, was translated …

Gabapentin (GBP) is a recently licensed antiepileptic, drug whose mode of action remains to be fully elucidated. The following studies were designed to investigate the effects of GBP on several gamma-aminobutyric acid (GABA) related neurochemical parameters in mouse brain. GBP (0-75 mg/kg) was administered by intraperitoneal injection either as a single dose or twice daily for 8 days. Animals were sacrificed 4 h after the final administration and their brains removed and analysed for concentrations of GABA, glutamate and glutamine and the activities of GABA-transaminase (GABA-T) and glutamic acid decarboxylase (GAD). Single dose GBP increased brain GABA-T activity and glutamine concentration but was without effect on GAD activity or the concentrations of GABA and glutamate. Following repeated treatment with GBP, brain GABA-T activity was consistently decreased and there was also a decrease in brain glutamate concentration. Repeated drug treatment was without effect on the activity of GAD or on the concentrations of GABA and glutamine. These results suggest that GBP has effects on the GABAergic system which may contribute to its antiepileptic and/or neuroprotective actions.

A randomized, double-blind, placebo-controlled cross-over study of adjuvant treatment with remacemide hydrochloride was carried out in 17 patients taking sodium valproate (VPA) as monotherapy. Plasma concentration profiles of VPA, remacemide, and its active desglycinyl metabolite (ARL12495XX) were determined following single (300 mg) and multiple dosing (150 or 300 mg twice daily) of remacemide hydrochloride for 14 days with a 300-mg final dose. Central nervous system side-effects were more common at the higher dose, which prompted dosage reduction to 150 mg twice daily for subsequent patients partway through the study. The mean area under the concentration-time curve, peak concentration and pre-dose concentration of VPA were unchanged by remacemide hydrochloride in three patients on the higher and in 10 patients on the lower dose of remacemide. The pharmacokinetic parameters of remacemide and its active metabolite in the VPA-treated patients were similar to those described previously in healthy volunteers. Thus, remacemide hydrochloride does not interfere with the pharmacokinetics of VPA and vice versa.

1. 1. The effects of repeated administration of the anticonvulsant compounds, vigabatrin (VGB) and tiagabine (TGB), on γ-aminobutyric acid (GABA) concentration and the activities of GABA-transaminase (GABA-T) and glutamic acid decarboxylase (GAD) were investigated in mouse cortex. 2. 2. VGB alone increased GABA levels and decreased GABA-T and GAD activities. 3. 3. TGB alone was essentially without effect. 4. 4. Low doses of VGB and TGB in combination increased GABA levels when neither drug had such an effect alone. 5. 5. Despite this observation, this study failed to establish any conclusive evidence for an interaction between VGB and TGB that might help to explain their reported clinical synergism.

OBJECTIVE: To assess the effect of different doses of gabapentin (GBP) on cognitive function in treated epileptic patients. METHODS: Twenty seven patients with refractory partial seizures commenced a double blind, dose ranging, placebo controlled, crossover study of adjuvant GBP. Each treatment phase lasted three months, during which the dose of GBP or matched placebo was increased stepwise at intervals of four weeks (1200 mg/day, 1800 mg/day, and 2400 mg/day in three daily doses). Psychomotor and memory testing was carried out at the end of each four week period, at which time the patient also completed subjective measures of cognition, fatigue, worry, temper, and dysphoria. A visual analogue scale was used to assess drowsiness and a questionnaire was employed to gauge the severity of side effects. RESULTS: In the 21 patients completing the study, GBP produced a significant reduction in median monthly seizure frequency from 7 to 4.3 (P = 0.02), the decrease being most pronounced for secondarily generalised seizures (from 1.0 to 0.3, P = 0.01). Forty three per cent of patients reported a reduction in seizure frequency of at least 50% throughout all GBP doses. Mean (SD) plasma concentrations of GBP at 1200, 1800, and 2400 mg/day were 4.7 (2.6), 6.8 (3.8), and 8.6 (3.3) mg/l respectively. The drug had no effect on composite psychomotor and memory scores; nor was there alteration in any self assessment subscore. The mean drowsiness (P = 0.03) score was higher during treatment with 2400 mg GBP daily compared with matched placebo. Composite psychomotor (r = -0.47, P < 0.01), tiredness (r = 0.42, P < 0.01), and side effect (r = 0.61, P < 0.001) scores correlated significantly with seizure frequency but not with GBP dose. CONCLUSION: GBP is a well tolerated and effective antiepileptic drug which had no measurable effect on cognition but did produce sedation at the highest dose. This study also supports the suggestion that seizures can cause cognitive impairment.

Introduction Lectures are an efficient and commonly used way of teaching large groups of students. Unfortunately such large groups may not lend themselves to much interaction, limiting and reducing the impact of the teaching material. In particular, anecdotal experience suggests that students are reluctant to ask questions pertaining to lectures when large numbers of other students are present. We implemented a novel method of taking questions during the ‘Neurology Week’ for students in their third year of the undergraduate medical degree course at the University of Glasgow; live text messaging. Methods In the introduction to half of the week9s didactic lectures, students were given a mobile phone number and encouraged to submit ‘live’ text questions to the speakers. A chairperson (EN or KD) would read texts as they arrived and either immediately ask the question to the speaker via a roving microphone or postpone the question until the end of the talk/section. The number and nature of the questions were compared in those sessions with and without the live text facility. Students and speakers took part in a survey to evaluate their experience of the ‘live text’ experiment. Results In 4 hours of lectures with text facility, 86 texts were received; these comprised 56 requesting factual clarification or expansion, 28 jokes, and 1 practical point about the lecture hall. Additionally, 2 oral questions were posed after the lectures. After 4 hours of lectures without text facility, there were 9 questions posed to the individual speakers, all requesting factual clarification. These oral questions and their answers were not shared with the rest of the group. After exclusion of jokes, the number of questions posed to lecturers where live texting was offered was found to be significantly greater than the number posed where no live texting was available (p=0.03, Mann Whitney U test). Students9 and speakers9 survey responses confirmed that they found the text–questioning to be enjoyable and worthwhile. Conclusions Considered use of cheap and readily available technology allows interactive teaching to take place even during large group lectures. Students ask more questions, and this ‘extra’ education is shared with the entire group. We believe that such methods should be utilised more widely and would be equally valuable during postgraduate teaching.

Introduction Clinical experience suggests that patients admitted to general medical wards will rarely undergo a neurological examination if the presenting complaint is perceived to be primarily non–neurological. With evolution of the presentation, any later formal neurological assessment not benefit from a record of the temporal evolution of the neurological signs. We present a rapid neurological screen which may ultimately be used in patients presenting without neurological symptoms and may improve recording of the neurological examination. In this study we performed initial validation for subjects with neurological symptoms presenting to our neurology unit. Methods Two protocols were devised to accommodate both ambulant and non–ambulant patients (Figure 1). A third year medical student (FR) performed the screening examination blind to the formal examination. These results were compared to results from the formal neurological examination performed in either our acute neurology ward, day investigation unit, or the outpatient clinic. Results from formal examination by a neurology registrar or consultant were determined from retrospective review of case notes. For inpatients only, we stipulated that the inter–examination interval should be Results Twelve non–ambulant and eighteen ambulant patients were identified. For non–ambulant patients, the screening examination detected any abnormality with sensitivity and specificity of 100%. Agreement was excellent (Scott9s Pi=1; CI=0.42 to 1). Results for the subgroups of the exam were as follows: Eyes; sensitivity=100%, specificity=87.5%: face; sensitivity=50%, specificity=93%: arms; sensitivity=67%, specificity=100%: legs; sensitivity=83%, specificity=83%. For ambulant patients the screening examination detected any abnormality with a sensitivity of 69% and a specificity of 60%. Agreement was fair (Scott9s Pi=0.25; CI=–0.17 to 0.63). Results for the subgroups of the exam were as follows; Eyes–sensitivity=75%, specificity=78%; face–sensitivity=100%, specificity=100%; arms–sensitivity=100%, specificity=100%; legs–sensitivity=100%, specificity=77%. Conclusion A screening examination by a medical student showed excellent agreement with formal examination in those with significant neurological impairment (non–ambulant patients). In ambulant patients it performed less well, but with a sensitivity of 69 still represents and advance on ‘examination not done’. We argue that further studies to improve sensitivity of this proposed screening examination are indicated to promote adoption in a general medical setting for patients without neurological symptoms.

Summary: Purpose: We wished to determine mutual interaction of two drugs with active metabolism: remacemide, hydrochloride and carbamazepine (CBZ). Methods: A randomized, double-blind, placebo-controlled cross-over study of add-on remacemide hydrochloride was performed in 10 of 14 recruited patients being treated with CBZ monotherapy. Forty-eight-hour concentration profiles of CBZ, its active epoxide metabolite (CBZ-E), remacemide, and its desglycinyl metabolite (ARL12495XX) were assayed after single and multiple dosing. Results: After patients were treated with 300 mg remacemide hydrochloride twice daily for 14 days, the mean area under the concentration-time curve (AUC) of CBZ was increased by 22% (p = 0.12), Cmax was increased by 27% (p = 0.07), and Cmin was increased by 22% (p = 0.29). Trough concentrations of CBZ were higher (p = 0.0037) during active treatment as compared with placebo treatment. CBZ-E levels were unaffected. No symptoms of CBZ toxicity were reported. There was no evidence of autoinduction of remacemide metabolism. However, in CBZ-treated patients, the AUC of remacemide and its active metabolite was 60 and 30%, respectively, of values observed in healthy volunteers treated previously with the same dose. Conclusions: Remacemide hydrochloride inhibits CBZ metabolism, which itself induces that of remacemide hydrochloride and its active metabolite. This mutual interaction between remacemide hydrochloride and CBZ is predictable and modest and should not present a barrier to their clinical use in combination.

Tiagabine (TGB) and vigabatrin (VGB) are two novel anticonvulsant compounds reported to exert their pharmacological effects via an action on the gamma-aminobutyric acid (GABA) system. We have investigated the effects of acute exposure of these drugs on the uptake of GABA into rat cortical astrocytes in primary culture. Astrocytes were prepared from the cerebral cortices of one day-old rat pups by a mechanical dissociation technique and were assayed for GABA uptake activity after 21 days in culture. Tiagabine (100-300 nM) and VGB (100 microM) reduced GABA uptake when compared to control at four hours post-exposure. GABA uptake was also reduced following eight and 24 hour exposures to 200 nM TGB. A combination of TGB (200 nM) and VGB (100 microM) treatments reduced GABA uptake when compared to both control and VGB treated cultures. These results support the efficacy of TGB as a GABA uptake inhibitor and suggest that VGB may also exert an effect by this mechanism.

A rapid and simple method for determination of the novel antiepileptic compound gabapentin [1-(aminomethyl)cyclohexaneacetic acid] in plasma is described. Blank human plasma was spiked with gabapentin (1.0-10.0 micrograms/ml) and internal standard [1-(aminomethyl)-cycloheptaneacetic acid; 5.0 micrograms/ml]. Individual samples were treated with 2 M perchloric acid, centrifuged and then derivatised with o-phthalaldehyde-3-mercaptopropionic acid. Separation was achieved on a Beckman Ultrasphere 5 microns reversed-phase column with mobile phase consisting of 0.33 M acetate buffer (pH 3.7; containing 100 mg/l EDTA)-methanol-acetonitrile (40:30:30, v/v). Eluents were monitored by fluorescence spectroscopy with excitation and emission wavelengths of 330 and 440 nm, respectively. The calibration curve for gabapentin in plasma was linear (r = 0.9997) over the concentration range 1.0-10.0 micrograms/ml. Recovery was seen to be > or = 90%. The inter- and intra-assay variations for three different gabapentin concentrations were < or = 10% throughout. The lower limit of quantitation was found to be 0.5 microgram/ml. Chromatography was unaffected by a range of commonly employed antiepileptic drugs or selected amino acids.

We present a case of fatal pulmonary embolus after knee arthroscopy to raise awareness of the frequency of this complication and the need for consideration of thromboembolic prophylaxis before knee arthroscopy.

Tiagabine is a novel antiepileptic drug which acts by decreasing gamma aminobutyric acid uptake in astrocytes and neurones. Here the first case of deliberate overdose with this compound in a patient on concomitant phenytoin is reported. On admission to hospital his conscious level deteriorated to grade III coma. No changes in the electrocardiogram were noted. Recovery from the initial effects was rapid, and there were no sequelae. Plasma levels of tiagabine (3.1 micrograms/ml) 4 hours after ingestion were 30 times higher than at typical steady state during therapeutic dosing. The effects of poisoning with current first-line antiepileptic drugs are reviewed. The newer agents, particularly those with greater biochemical specificity, may be safer in overdose than the more established anticonvulsants.

In non-insulin-dependent diabetes mellitus (NIDDM) patients, microalbuminuria predicts early mortality, predominantly from cardiovascular disease. Increased free radical activity and abnormalities in hemostasis have been implicated in the development of vascular disease. Therefore, we measured markers of free radical activity (nonperoxide-conjugated diene isomer of linoleic acid [PL-9,11-LA′] and lipid peroxides expressed as malondialdehyde [MDA]) along with the hemostatic variables: fibrinogen, von Willebrand factor (vWf), plasminogen activator inhibitor (PAI-1), tissue plasminogen activator (t-PA), and plasmin activity (Bβ15–42) in 24 NIDDM patients (12 patients with microalbuminuria and 12 without microalbuminuria) and in 12 age-matched control subjects. There were no differences in linoleic acid (PL-9,12-LA) concentrations between the three groups. PL-9,11-LA′ was elevated in the microalbuminuric patients compared with control subjects (P < 0.05), but there was no difference between the two diabetic groups. MDA was elevated in the microalbuminuric diabetic patients compared with those patients without microalbuminuria (P < 0.05) and control subjects (P < 0.001). MDA was also increased in the patients without microalbuminuria compared with control subjects (P < 0.01). Except for Bβ15–42, all the hemostatic variables were increased (P < 0.05) in the diabetic patients compared with control subjects. The microalbuminuric diabetic patients had further increases in vWf (P < 0.03) and t-PA (P < 0.03) compared with patients with microalbuminuria. Our study suggests that there is an increase in free radical activity and abnormalities in hemostatic variables favoring a hypercoagulable state in NIDDM, especially in those with microalbuminuria. These changes may contribute to vascular disease, which is particularly prevalent in NIDDM patients with microalbuminuria.

In September 1848, in Cavendish, Vermont, an incident occurred which was to change our understanding of the relation between mind and brain. Phineas P Gage, a 25 year old railroad foreman, was excavating rock. In preparation for blasting he was tamping powder into a drill hole when a premature explosion drove the tamping iron —.1.1 m long, 6 mm in diameter, and weighing 6 kg — through his left cheek and out of the vault of his skull with such force that it threw him on his back and fell several rods behind, “smeared with brain.”1 Despite his injuries he remained conscious and only a few minutes later was sitting in an ox cart writing in his work book. He recognised and reassured Dr Harlow, who had been summoned to the scene. The wound continued to bleed for two days; then followed a virulent infection that rendered Gage semiconscious for a month. His condition was so poor that a coffin had been prepared. Nevertheless, Dr Harlow continued treatment, and by the fifth week the infection had resolved and Gage had regained …

Dear Editor: We read with great interest the article “Unusual Penetrating Cranio-Cerebral Injuries in Children from Main Plugs” by Kanagarajan and Sgouros [1] in the October 2007 edition of Child’s Nervous System. They describe two cases of penetrating brain injuries in children caused by a fall onto a mains plug. These cases were similar to the case published previously by Lopez et al. [2] in February 2006 in this journal. We published a case report of an 18-month-old child who fell off a chair onto a set of Christmas fairy lights, and one of the light bulbs penetrated the skull and entered the brain [3]. Incredibly the bulb remained in tact. The only clue to the extent of the injury was a tiny cut to the scalp that could easily have been dismissed as trivial. However, the parents’ history was vital in the fact that they told the attending doctor that one of the bulbs was missing. We, therefore, would like to echo the authors’ words of caution regarding the lack of external evidence, which is often the case in such injuries. These children are usually very well neurologically, again detracting from the potential seriousness of the injury. We would also like to stress the importance of obtaining a full and accurate history from parents, relatives, or witnesses of children who suffer such injuries, as even the seemingly minor details can be of extreme importance.

Generalized convulsive status epilepticus is a life-threatening disorder characterized by repetitive or prolonged seizures that may result in neuronal death and multi-organ failure. Pseudostatus epilepticus refers to repeated or continuous seizures of psychogenic origin that may resemble those of status epilepticus as there may be tongue biting, incontinence, cyanosis, and even upgoing plantar responses [1]. If pseudostatus is misdiagnosed as true status in a pregnant woman, inappropriate treatment with antiepileptic drugs may lead to respiratory depression requiring intensive care and may rarely result in maternal and fetal death [2,3]. A 23-year-old pregnant woman (gravida 4, para 2, in her 27th week of pregnancy) was admitted to a local district general hospital following recurrent convulsive seizures with no evidence of eclampsia. Persistent seizure activity despite intravenous administration of magnesium, phenytoin, diazepam, and eventually thiopental caused respiratory depression requiring intubation. She was transferred to the Walton Centre for Neurology and Neurosurgery, Liverpool, UK, where cerebral magnetic resonance imaging results were normal, a lumbar puncture showed normal cerebrospinal fluid constituents, and an electroencephalogram showed generalized slowing consistent with thiopentone use. All sedation was stopped without seizure recurrence. The patient required intensive care for 5 days before she was returned to the referring hospital. The patient's old medical notes then became available. Frequent daily “fits” had been misdiagnosed as epileptic seizures in the third trimester of a previous pregnancy although the typical postictal features were absent, and these seizures had proved refractory to pharmacotherapy. After she was delivered of a stillborn infant an epileptologist had concluded that the first “fit” was a postsyncopal reflex anoxic seizure, and that the others were subsequent psychogenic attacks. Two weeks after discharge from the referring hospital, the patient presented again with recurrent refractory seizures and an obstetrician planned delivery by emergency cesarean section. However, the nonepileptic nature of the attacks was explained to the obstetrician, along with a recommendation to delay operative intervention if possible. Pseudostatus epilepticus occurs predominantly in women of childbearing age but there are few reports on this condition in the obstetric literature. The clinical features of pseudoseizures include long duration attacks without fixed pupils, hypoxia, or metabolic acidosis, resistance to eye opening, flexor plantar and eye deviation to alternate sides. Investigation results are typically normal and the attacks are resistant to antiepileptic drug treatment. The frequently acute and dramatic clinical presentation of pseudostatus often causes diagnostic difficulties, and treatment for presumed true status is frequently administered before a background history is available. The fetus is at risk for both hypoxia following attempted seizure suppression and prematurity from needlessly early operative delivery. The optimal management of pseudostatus epilepticus during pregnancy requires close collaboration between obstetricians and neurologists, and diagnostic awareness of the condition is the crucial first step.

A 20-year-old man with a 6-year history of infrequent nocturnal focal motor seizures with secondary generalization attended an epilepsy clinic. During the seizures, the patient was stiff and rigid, exhibiting left-side convulsive movements. After each episode he had a short-lived left hemiparesis with associated intense vasomotor disturbance. There was no tongue biting or incontinence, but in the morning the patient would complain of being stiff and sore. These seizures had occurred once every 2 to 4 months. He had never had any daytime episodes, although there was a history of occasional daytime jerking of the limbs. Otherwise the patient had been fit and well. Clinical examination was normal, and it was believed that these seizures originated from the right hemisphere. Brain EEG and CT were unremarkable at the time. Three months later, the patient’s condition had deteriorated dramatically. His affect seemed inappropriate, and he had marked ataxia, as well as …

EDITOR–Since Eke et al's report of severe persistent visual field constriction associated with vigabatrin1 there has been growing interest in studying visual fields in patients taking this drug. MacKenzie and Klistorner report visual field defects in two patients and suggest that field defects may be more common in asymptomatic patients. …

Despite the global improvement in telecommunications, the size and number of international medical conferences continue to grow. Demand for such meetings is fuelled by the often exotic locations, which have been made more accessible by the increasing ease of intercontinental travel. As conferences grow, delegates' fees and subsidies from the pharmaceutical industry ensure that they are now rather profitable and more about business than about education or research. Large medical meetings traditionally allow “experts” to lecture large audiences from high podiums. For some reason, probably a hangover from the over-reaching 1980s, it is rather unfashionable to attend a conference merely to learn something. So in an attempt to involve as many people as …

Background Historically neurosurgeons have accepted head injured patients only in the presence of a mass lesion requiring surgical decompression. Underpinning this is an assumption that these patients have a better outcome than patients without a surgical lesion. This has meant that many patients without a surgical lesion have been managed locally in the referring hospital. However, there is now evidence that treatment of all head injured patients in a specialist centre leads to improved outcomes. Therefore, we have asked the question: does the presence of a surgical lesion imply better outcome from severe head injury? Results We prospectively recorded the Glasgow Outcome score (GOS), at 3 months, of all the severely head injured patients treated at our institution over a two and a half year period. Of 116 patients admitted with an initial Glasgow Coma Score (GCS) of 8 or less, 58 had surgical lesions and 58 non-surgical head injuries. The two groups were well matched for presenting GCS and age. Overall our favourable outcome rate (GOS 4 and 5) at 3-months for the patients with a surgical lesion and for the non-surgical group were 47.3% and 46.6% respectively, with no significant difference between the two (P = 0.54). Conclusion The assumption in the past has always been that patients presenting in coma from traumatic diffuse brain injury will do worse than those that have a mass lesion amenable to surgical decompression. Our series would suggest that this is not the case and all severely head injured patients should expect similar outcome when cared for in a neuroscience centre.

Epilepsy is one of the commonest neurological conditions. For historical reasons, this condition is often managed in the UK by non-specialists. Treatment options have increased markedly in the last 15 years, with a resultant increase in the potential for better seizure control and an enhanced quality of life for patients with epilepsy.