Equipotency of lacosamide to levetiracetam in new onset focal epilepsy: A randomized controlled trial.

Objectives: Levetiracetam (LEV) is a well-established broad spectrum antiseizure medication (ASM) effective in focal, generalized, and myoclonic seizures whereas lacosamide (LCM) is a comparatively newer ASM currently approved only as an add-on agent in focal seizures. The aim of the study was to assess the efficacy and the tolerability of oral LCM as monotherapy in adult people with epilepsy (PWE) with new onset focal onset epilepsy compared with those receiving LEV. Materials and Methods: In this open-label single-center non-inferiority trial, PWE aged between 16 and 65 years suffering from new onset focal seizures, with or without secondary generalization were put on LCM monotherapy or LEV monotherapy. Data regarding demographic characteristics, seizure type and etiology, LCM and LEV daily dose, seizure frequency at baseline and at 6 months of follow-up, and seizure freedom rates were recorded. Results: Thirty-five PWE on LCM (24 males), their mean age: 38.20 ± 16.62 years and 35 PWE on LEV (25 males, mean age: 38.91 ± 17.13 years) were enrolled. The most common type of seizure observed was focal to bilateral tonic-clonic seizure >70% followed by focal impaired awareness seizure and focal awareness seizure. Structural epilepsy was found in 21 among LCM group and 22 of LEV group. In the LCM group, the seizure frequency decreased from 3.33 ± 1.88 to 0.85 ± 1.09 (P = 0.001) at 6 months and from 3.61 ± 3.12 to 0.94 ± 1.24 (P = 0.001) in LEV group, intergroup difference (P = 0.74). At 6-month follow-up period, 78.9% in LCM arm and 87.9% in the LEV arm had experienced a 50% of reduction in seizure frequency while seizure freedom was attained in 43.3% of PWE in both the arms (P = 1). The most common treatment emergent adverse effects in the LCM group were fatiguability, dyspepsia, headache, and dizziness, while in the LEV group; somnolence and behavioral abnormality. Conclusion: Treatment with LCM met the non-inferiority criteria when compared with LEV. Therefore, it might be useful as first-line monotherapy for adults with newly diagnosed focal epilepsy.

A Study of Organophosphorus Induced Delayed Myelopathy: Uncommon Sequelae of a Common Poisoning.

Introduction: Organophosphorus (OP) compounds, with their lipophilicity, are responsible for a spectrum comprising of acute cholinergic symptoms, intermediate syndrome, as well as delayed neurological sequelae in the form of OP-induced delayed neuropathy and subsequently, myeloneuropathy with predominantly thoracic cord affection, manifested on partial recovery of the neuropathy. The pathogenesis of this myeloneuropathy in humans is still not well perceived. Aim of Study: To determine the onset and course of development of delayed myeloneuropathy in patients of OP poisoning. Materials and Methods: Twelve patients of OP ingestion presenting with delayed myeloneuropathy were evaluated with prior history, examination, MR imaging, nerve conduction and electromyography studies, and various evoked potentials to elicit the pattern of disease manifestation and progression. Results: Among the included patients, a majority had consumed chlorpyrifos and permethrin composition, a majority had undergone gastric lavage. Five (41.7%) had experienced acute worsening and 8 (66.7%) patients had developed intermediate syndrome. OPIDN had appeared after a median of 4 (1-8) weeks after the poisoning. All patients had lower limb hypertonia with wasting and distal more than proximal weakness with pure motor or sensorimotor involvement. MRI showed thoracic cord atrophy in 3 (25%) patients. Motor-evoked potential with reduced amplitude was noted in lower limbs on lumbar stimulation but absent on cortical stimulation. Conclusion: Various animal models have shown similar patterns of neurotoxicity in OP poisoning with predominant thoracic cord pathology. Further research in humans may be undertaken to elicit the pathogenesis, thereby improving the treatment modality.

Isolated intracranial hypertension without cerebral venous sinus thrombosis in APLA syndrome: an unique association.

BACKGROUND: Antiphospholipid antibody (APLA) syndrome is an autoimmune disorder predisposing to thrombotic complications affecting CNS either by arterial vaso occlusion or venous thrombosis. Cerebral venous sinus thrombosis (CVST) secondarily produces raised intracranial pressure (ICP). However intracranial hypertension without evidence of CVST is rare entity. CASE PRESENTATION: We present two cases of elevated ICP with absence of identifiable CVST. Case 1, a 28-year-old female presented with a 2 months history of headache followed by bilateral vision loss. Cerebrospinal fluid (CSF) opening pressure and fundoscopy along with Contrast Magnetic resonance imaging (MRI) was suggestive of Idiopathic intracranial hypertension (IIH) and patient improved with acetazolamide. 5 months later she presented with acute onset right sided hemiparesis. MRI showed acute left Middle cerebral artery (MCA) territory infarct with normal contrast Magnetic resonance venography (MRV). Anti-cardiolipin and Beta 2 glycoprotein (both IgG and IgM) titres were elevated. Case 2, a 23-year-old female presented with headache and diplopia of 2 months duration. Based on CSF, fundoscopy and contrast MRI brain was diagnosed as IIH and she too responded to diuretics. 2 years later she presented with recurrence of headache and APLA profile showed elevated beta 2 glycoprotein IgG and IgA. CONCLUSION: This is an important non thrombotic complication of APLA syndrome and requires further large-scale study for insight into the pathogenesis and early recognition to avoid future complications.

A Study of Diffusion Tensor Imaging in Central Post-Stroke Pain: Traveling Beyond the Pain Pathways.

Introduction: Central post-stroke pain (CPSP), seen in the aftermath of a stroke, is an underdiagnosed entity but quite a disabling complication. All the postulated theories regarding the pathogenesis of CPSP point to its origin in the central pain pathways. However, this study attempts to demonstrate the role of other contributing areas in the generation of CPSP. Materials and Methods: In this single-center tertiary care hospital-based study, 24 patients with both ischemic and hemorrhagic strokes of variable durations were recruited, and Magnetic Resonance Imaging (MRI) imaging with diffusion tensor imaging (DTI) acquisition was done. Fractional anisotropy (FA) and apparent diffusion coefficient (ADC) values of the spinothalamic tract (STT), corticospinal tract (CST), superior thalamic radiation (STR), basal ganglia (BG), and primary somatosensory cortex (SSC) were compared between normal and abnormal sides and also in extrathalamic lesions separately. Results: Significant differences with lower FA were noted in STT, CST, STR, and SSC and higher ADC values in BG, STR, CST, and SSC on comparison between the normal and lesion sides. On individual sub-analysis, ischemic stroke had significant changes in the FA value of CST and the ADC value of STR and CST, while hemorrhagic stroke had significant changes in the FA and ADC values of STR and SSC, as well as the FA value of STT. In the analysis of the extrathalamic strokes, significance persisted in all the studied parameters except the BG. The CST abnormalities were evident even in patients with clinical motor improvement. On multivariate analysis, visual analogue scale score severity was correlated with thalamic lesions. Conclusion: Contrary to the belief that STT is solely responsible for CPSP, the role of CST, STR, BG, and SSC as contributing areas is evident from this study and may be more well established if studied in a larger population.