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1.  Major outcomes of patients with tuberculous meningitis on directly observed thrice a week regime 
Revised National Tuberculosis Control Programme (RNTCP) of Government of India provides intermittent thrice-a-week directly observed treatment short course (RNTCP regimen).
Assessments of all-cause mortality and nine-month morbidity outcomes of patients with tuberculous meningitis (TBM) on RNTCP regimen.
Materials and Methods:
We prospectively followed up patients registered with RNTCP center, with a diagnosis of TBM from January 1st, 2010 to December 31st, 2011. Morbidity was assessed using modified Rankin Scale (mRS).
We had 43 patients with median duration for follow-up of 396 days and that of survivors of 425 days. Two patients defaulted. Fourteen patients (32.5%) had mRS score of 4 to 6 and 29 had mRS of 0 to 3 after 9-month treatment. Severe disability was not related to any factor on logistic regression. Severe disability was seen in one patient (6.66%) among the 15 patients with stage 1, nine (37.5%) out of 24 patients with stage 2 and three (75%) out of 4 patients with stage 3 disease. Eight patients died (18.6%) of whom 4 died during the intensive phase and 4 during the continuation phase of RNTCP regimen. Mortality was independently related to treatment failure with adjusted Hazard ratio of 8.29 (CI: 1.38-49.78) (P = 0.02). One patient (6.66%) died out of the 15 patients with stage 1 disease, 5 (20.8%) out of 24 patients with stage 2 disease and 2 (50%) out of the 4 with stage 3 disease.
Discussion and Conclusion:
RNTCP regimen was associated with good compliance, comparable mortality and morbidity.
PMCID: PMC4162013  PMID: 25221396
Meningeal Tuberculosis; morbidity; mortality; prognosis; treatment
2.  Clinical profile of patients with nascent alcohol related seizures 
The aim of this study is to characterize the clinical profile of patients with alcohol related seizures (ARS) and to identify the prevalence of idiopathic generalized epilepsy (IGE) in the same.
Materials and Methods:
100 consecutive male patients presenting to a tertiary care center in South India with new onset ARS were analyzed with alcohol use disorders identification test (AUDIT) score. All underwent 19 channel digital scalp electroencephalography (EEG) and at least computed tomography (CT) scan.
A total of 27 patients (27%) who had cortical atrophy on CT had a mean duration of alcohol intake of 23.62 years compared with 14.55 years in patients with no cortical atrophy (P < 0.001). Twenty-two patients (22%) had clustering in the current episode of whom 18 had cortical atrophy. Nearly, 88% patients had generalized tonic clonic seizures while 12% who had partial seizures underwent magnetic resonance imaging (MRI), which identified frontal focal cortical dysplasia in one. Mean lifetime duration of alcohol intake in patients presenting with seizures within 6 hours (6H-gp) of intake of alcohol was significantly lower (P = 0.029). One patient in the 6H-gp with no withdrawal symptoms had EEG evidence for IGE and had a lower AUDIT score compared with the rest.
CT evidence of cortical atrophy is related to the duration of alcohol intake and portends an increased risk for clustering. Partial seizures can be a presenting feature of ARS and those patients may benefit from MRI to identify underlying symptomatic localization related epilepsy (8.3% of partial seizures). IGE is more likely in patients presenting with ARS within first 6 hours especially if they do not have alcohol withdrawal symptoms and scalp EEG is helpful to identify this small subgroup (~1%) who may require long-term anti-epileptic medication.
PMCID: PMC3841594  PMID: 24339573
Alcohol use disorders identification test; anti-epileptic drugs; convulsions; electroencephalography; ethanol; magnetic resonance imaging
4.  Electrophysiological study in neuromuscular junction disorders 
This review is on ultrastructure and subcellular physiology at normal and abnormal neuromuscular junctions. The clinical and electrophysiological findings in myasthenia gravis, Lambert-Eaton myasthenic syndrome (LEMS), congenital myasthenic syndromes, and botulinum intoxication are discussed. Single fiber electromyography (SFEMG) helps to explain the basis of testing neuromuscular junction function by repetitive nerve stimulation (RNS). SFEMG requires skill and patience and its availability is limited to a few centers. For RNS supramaximal stimulation is essential and so is display of the whole waveform of each muscle response at maximum amplitude. The amplitudes of the negative phase of the first and fourth responses are measured from baseline to negative peak, and the percent change of the fourth response compared with the first represents the decrement or increment. A decrement greater than 10% is accepted as abnormal and smooth progression of response amplitude train and reproducibility form the crux. In suspected LEMS the effect of fast rates of stimulation should be determined after RNS response to slow rates of stimulation. Caution is required to avoid misinterpretation of potentiation and pseudofacilitation.
PMCID: PMC3644779  PMID: 23661960
Acetylcholine; congenital myasthenic syndromes; Lambert–Eaton myasthenic syndrome; myasthenia gravis; repetitive nerve stimulation; single-fiber electromyography
5.  Ode to Epileptologists! 
PMCID: PMC3108087  PMID: 21654931
6.  An elusive diagnosis: Scedosporium apiospermum infection after near-drowning 
A 51-year-old male was admitted in our institute following an episode of near-drowning. He later developed ventriculitis and cerebral ring-enhancing lesions. He died following a subarachnoid hemorrhage due to rupture of a mycotic aneurysm involving the right fetal posterior cerebral artery. Scedosporium apiospermum was isolated from the cerebrospinal fluid. Central nervous system invasion by S apiospermum may present insidiously in near-drowning patients and, therefore, requires a high index of suspicion. In cases with the characteristic cerebral ring-enhancing lesions and concomitant ventriculitis, treatment should be instituted while awaiting fungal culture. With this article we intend to alert neurologists, intensivists, and physicians to this near fatal infection, as early identification and prompt treatment with voriconazole may be life saving.
PMCID: PMC2981763  PMID: 21085536
Fungal meningitis; near-drowning; Pseudallescheria boydii; Scedosporium apiospermum
7.  Alpha coma evolving into spindle coma in a case of acute fulminant hepatic failure: What does it signify? 
A 44-year-old male developed acute fulminant hepatic failure of unknown etiology and expired within four days. His serial electroencephalograms (EEGs) showed diffuse background slowing on day one, which evolved into “alpha coma” and later into “spindle coma” over the ensuing two days. Such EEG transition is hitherto undescribed in patients with hepatic encephalopathy and gives fresh insight into the etiopathogenesis of specific EEG patterns in diffuse encephalopathy.
PMCID: PMC2859594  PMID: 20436753
Alpha coma; electroencephalogram; hepatic failure; metabolic encephalopathy; spindle coma
8.  Status epilepticus 
Status epilepticus (SE) is a medical emergency associated with significant morbidity and mortality. SE is defined as a continuous seizure lasting more than 30 min, or two or more seizures without full recovery of consciousness between any of them. Based on recent understanding of the pathophysiology, it is now considered that any seizure that lasts more than 5 min probably needs to be treated as SE. GABAergic mechanisms play a crucial role in terminating seizures. When the seizure persists, GABA-mediated mechanisms become ineffective and several other putative mechanisms of seizure suppression have been recognized. Early treatment of SE with benzodiazepines, followed if necessary by fosphenytoin administration, is the most widely followed strategy. About a third of patients with SE may have persistent seizures refractory to the first-line medications. They require aggressive management with second-line medications such as barbiturates, propofol, or other agents. In developing countries where facilities for assisted ventilation are not readily available, it may be helpful to use nonsedating antiepileptic drugs (such as sodium valproate, levetiracetam, or topiramate) at this stage. It is important to recognize SE and institute treatment as early as possible in order to avoid a refractory state. It is equally important to attend to the general condition of the patient and to ensure that the patient is hemodynamically stable. This article reviews current knowledge regarding the management of convulsive SE in adults.
PMCID: PMC2824929  PMID: 20174493
Anticonvulsants; barbiturates; lorazepam; midazolam; phenytoin; propofol; refractory status epilepticus; status epilepticus
9.  Muscle channelopathies and electrophysiological approach 
Myotonic syndromes and periodic paralyses are rare disorders of skeletal muscle characterized mainly by muscle stiffness or episodic attacks of weakness. Familial forms are caused by mutation in genes coding for skeletal muscle voltage ionic channels. Familial periodic paralysis and nondystrophic myotonias are disorders of skeletal muscle excitability caused by mutations in genes coding for voltage-gated ion channels. These diseases are characterized by episodic failure of motor activity due to muscle weakness (paralysis) or stiffness (myotonia). Clinical studies have identified two forms of periodic paralyses: hypokalemic periodic paralysis (hypoKPP) and hyperkalemic periodic paralysis (hyperKPP), based on changes in serum potassium levels during the attacks, and three distinct forms of myotonias: paramyotonia congenita (PC), potassium-aggravated myotonia (PAM), and myotonia congenita (MC). PC and PAM have been linked to missense mutations in the SCN4A gene, which encodes α subunit of the voltage-gated sodium channel, whereas MC is caused by mutations in the chloride channel gene (CLCN1). Exercise is known to trigger, aggravate, or relieve symptoms. Therefore, exercise can be used as a functional test in electromyography to improve the diagnosis of these muscle disorders. Abnormal changes in the compound muscle action potential can be disclosed using different exercise tests. Five electromyographic (EMG) patterns (I-V) that may be used in clinical practice as guides for molecular diagnosis are discussed.
PMCID: PMC2781140  PMID: 19966974
Channelopathy; electromyographic; ion channel; myotonia; periodic paralysis

Results 1-9 (9)