Sudden unexpected death in epilepsy (SUDEP) has been recognised for centuries. The precise frequency of occurrence is not well defined. Education of medical professionals is needed, so that death certificates and coronial inquests may appropriately, correctly and consistently record SUDEP as the case of death. Correct identification will then allow further investigation of this misunderstood, and often ignored, epilepsy complication. SUDEP incidence may be increasing, either as a result of increased recognition, or possibly due to a real increase in incidence. All currently available antiepileptic drugs (AEDs) have been associated with SUDEP, and current opinion assumes that the relative proportion of patients suffering SUDEP is representative of average AED usage type for a particular time and locality, however, recently analysed data suggest a strong bias towards carbamazepine. A review of Cardiff Epilepsy Unit data shows that carbamazepine was disproportionately represented in patients suffering SUDEP. In this series, 11 of the 14 SUDEP patients were taking carbamazepine at the time of death. This was calculated as 79% of all patients, compared to average carbamazepine usage by all other Cardiff Epilepsy Unit patients of 38%. The data also indicate that one patient was not taking any drug therapy, and died during his first seizure, reducing the number of evaluable 'drug usage' patients to 13, and increasing the proportion taking carbamazepine at the time of death to 85%, (P < 0.01). Possible mechanisms include carbamazepine induced lengthening of the ECG Q-T interval combined with a mild pro-arrhythmic effect of epileptic seizure discharges, and consequent transient cardiac instability leading to arrhythmic death. Or alternatively, excessive post-seizure brainstem inhibition might result in blunting or transient abolition of central hypoxic and hypercarbic respiratory drive, with consequent post-ictal respiratory arrest, subsequent exacerbation of hypoxia, further cardiac destabilisation and death due to hypoxia/failed re-establishment of respiration and terminal cardiac arrhythmia. Current knowledge about SUDEP remains poor. Education is needed so that case ascertainment can be correctly documented. Delineation of the precise mechanisms involved should lead to definitive prevention strategies. Evaluation of carbamazepine as a significant causative factor in SUDEP is also needed.
We report our experience with lamotrigine add-on therapy in the treatment of 11 patients with Lennox-Gastaut syndrome. Lamotrigine is a novel antiepileptic drug, chemically unrelated to the major anticonvulsants in current use. Ten patients experienced a > 50% reduction in seizure frequency, 1 patient experienced no change in seizure frequency. All patients tolerated lamotrigine satisfactorily and no side-effects were reported.
Several studies have shown that the visual system is affected in Parkinson's disease (PD) with reduced contrast sensitivity, low-contrast acuity, and flicker sensitivity, as well as altered electroretinograms (ERGs) and pattern visual evoked potentials (VEPs). Apparently, however, no study has yet specifically determined whether visual acuity to high-contrast stimuli is impaired in PD. Visual acuity was measured in a group of 16 patients with PD, both on and off drugs (for 24 h), and 16 age- and sex-matched normal control subjects. Acuity was impaired in the PD group both on standard Snellen chart and on a screen in a computerized test of visual resolution. The degree of impairment was 24 and 25%, respectively, in the two tests. The PD patients had marginally better acuity on both tests while receiving drugs, but the differences were not significant. The difference between the two groups was consistent with impaired resolution and could not be accounted for by any perceptual dysfunction that may also have been present in the PD group. Conversely, however, impaired acuity may be implicated in studies that have reported mild deficits of visuospatial/visuoperceptual function in PD. Reduced acuity appears to be a subtle sequela of dopaminergic deficiency in the visual system.
Case report. A 47-year-old Tongan male returning to New Zealand after a 2-week holiday in Tonga presented with 3 days of progressive limb weakness, numbness, unsteady gait, and dyspnea. Two days before departing Tonga (6 days before neurologic symptoms), he developed leg swelling with erythematous and pustular lesions, which were treated with flucloxacillin. He had no medical history, was not taking regular medication, and had a 20 pack-year smoking history.Examination findings included the following: afebrile, pulse 80 beats/min, blood pressure 150/90 mm Hg, respiration 20 breaths/min, and oxygen saturation 98% (air). Cardiovascular and abdominal examinations were unremarkable. Cranial nerves and eye movements were normal. Limbs were hypotonic with globally reduced power (4/5), areflexia, and absent plantar responses. Temperature and pain sensation were impaired in hands and feet. Proprioception and vibratory sensation were impaired in the feet. Romberg test was positive.Full blood count, renal function, electrolytes, creatinine kinase, hemoglobin A 1c , C-reactive protein, thyroid function, B 12 , and folate were normal. Liver enzymes were mildly elevated (ALP 122, GGT 251, and ALT 41 IU/L). Antinuclear antibody was 1:160. CSF showed albuminocytologic dissociation: protein 0.69 g/L (reference 0.15-0.45), white blood cells 2/mL, red blood cells 1/mL, and glucose 3.4 mmol/L (serum glucose 6.0). Spine MRI and chest x-ray were unremarkable. Normal cranial MRI excluded concurrent acute disseminated encephalomyelitis. Nerve conduction study on day 2 of admission revealed demyelinating, predominantly motor, polyneuropathy (table).Serum reverse transcription (RT)-PCR on day 3 after illness onset was negative for chikungunya and dengue RNA and positive for Zika RNA (subsequently negative on day 13). Dengue NS1 antigen (Platelia Dengue NS1; Bio-Rad, Hercules, CA) was negative. Immunoglobulin (Ig)M antibodies (low level) and IgG antibodies (high level) against Zika (EUROIMMUN, Luebeck, Germany) and dengue (PanBio, Brisbane, Australia) were detected on day 3. CSF RT-PCR on day 5 was negative for all 3 viruses.
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