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Objective: Poor documentation following lumbar puncture (LP) had always been a matter of concern. This study aimed to investigate the documentation pattern of neurology house officers, registrars (Regs), and specialist Regs following LP in a major teaching hospital. Materials and Methods: Total hundred patient records were examined in the light of a carefully designed proforma containing 15 important indicators of good-quality LP documentation. Result: Mean number of indicators overall documented by doctors was found to be 6.24 ± 3.0037. The mean number of indicators recorded by house officers was 5.11 ± 3.01 and Regs was 7.56 ± 3.28. A total of 33% LPs were performed without a documented consent. Only 36% performers documented the type and size of needle they used during the procedure. Only 46% documents revealed the strength and name of the local anesthetic used. Statistically significant difference between senior house officers and Regs in terms of numbers of indicators documented was noted. Conclusion : The documentation standard among neurology junior doctors remained poor.

Introduction: Our present observational study attempted to evaluate the clinical profiles, diagnosis, treatment and follow-up results of 51 pediatric neurocysticercosis patients over a mean duration of five years (from January 2006 to December 2010). Materials and Methods: Diagnosis was mainly based on clinical features, computed tomography (CT)/magnetic resonance imaging scan and exclusion of other causes. Patients with active, transitional cysts and seizure were treated with albendazole for 28 days, steroids and anticonvulsants. Results: A total of 38 patients completed this study. Mean age of the presentation was 8.47 ± 3.19 years 52.6% of the patients were female. Overall patients presented with generalized seizure in 55.3%, focal in 31.6%, headache ± vomiting in 63.2%, focal neurodeficit in 10.5% and combination of symptoms in 60.5% cases. Contrast CT brain showed a solitary lesion in 27 (71.1%) and multiple in the rest. At presentation lesions were transitional in 58.2%, inactive in 20% and mixed in 14.6%. After a mean of 2 years, seizure persisted in 9 (23.7%) and headache in 8 (21.1%) of whom six had normal electroencephalography (EEG) while one each showed focal slowing, generalized slowing and epileptiform discharges. During the follow-up, CT scan brain 44.7% lesions calcified, 31.6% disappeared, 10.5% regressed and the rest persisted. Conclusion: Solitary ring enhancing lesions (transitional stage) involving the parietal lobe was the commonest CT picture at presentation. Generalized tonic-clonic seizure was the most common type of seizure. Number of lesions, persistence of lesion, number of seizures, EEG abnormality at presentation were not found to be prognostically significant (P > 0.05).

This sign is observed in atypical parkinsonism mainly in Progressive Supranuclear Palsy. The exact mechanism of this sign is not clear but the contraction of the Corrugator Supercilii muscle is the most important factor for the generation of vertical forehead creases. Though the wrinkling of forehead is a complex phenomenon involving multiple muscles but the 'Corrugator sign' would be a better term to describe this phenomenon. Despite the controversies regarding the mechanism and nomenclature, the 'Procerus sign' remains an important clinical clue for early Progressive Supranuclear palsy.

A 48 year old female presented with headache and an illusory sensation of spinning of head in respect to environment for last 8 weeks. Her head spinning or vertigo had no particular direction or not precipitated by any specific head posture. Headache is non- specific in nature and intensified in last few days.Her neurological examination revealed a central positional vertigo with horizontal gaze evoked nystagmus and ataxia. Her MRI scan brain showed the presence of a large solitary ring enhancing lesion in the left cerebellar hemisphere. The lesion was surgically excised and was examined histopathologicaliy that revealed a chronic inflammatory granuloma with caseation necrosis and multinucleated giant cells suggestive of tuberculosis

Objective: To present a case of Charcot Marie Tooth Disease. Backgrounds: A 22 years old boy presented with very slowly progressive symmetrical weakness of both lower limbs with distal muscular atrophy. He has a family member with similar problem. Methods: The patient was clinically examined and investigations done accordingly like Nerve Conduction Velocity studies (NCV). Results: The patient was diagnosed to be a case of Charcot Marie Tooth disease type 1 with classical features like” inverted Champagne bottle” like legs. Conclusion: Charcot Marie Tooth disease is rare and often undiagnosed yet it is the commonest hereditary neuropathy worldwide and India is not an exception

A 12-year-old boy presented with three episodes of partial seizures with secondary generalization. On investigation, he was diagnosed as a case of neurocysticercosis of the left parietal lobe. He was treated with albendazole and phenytoin and was followed for the next eight years. Computerized tomography scan showed signs of resolution with no further seizure activity.

Allgrove Syndrome or triple A syndrome is a rare familial multisystem disorder characterized by achalasia, alacrima and adrenal insufficiency. The objective was to describe a case of 4A syndrome where autonomic dysfunction was the presenting feature. A 22-year-old male presented with erectile dysfunction and loss of spontaneous morning erections for six months. He was having nocturnal diarrhea and recurrent postural dizziness for three months. He was found to have hyperpigmentation at pressure points, postural hypotension and other features of autonomic dysfunction. Laboratory investigations and imaging studies revealed hypoadrenalism, achalasia, alacrima and peripheral neuropathy. Autonomic neuropathy-related features persisted even after correction of hypoadrenalism. Based on clinical features and investigation he was diagnosed as a case of 4A syndrome presenting with autonomic dysfunction. Allgrove or 4A syndrome should be considered as a rare differential diagnosis of someone presenting with features of autonomic neuropathy.

Silent thyroiditis is a rare cause of thyrotoxic periodic paralysis. The objective was to present a case of silent thyroiditis presenting as periodic paralysis. A 23-year-old man presented with recurrent acute flaccid predominantly proximal weakness of all four limbs. He had a similar episode 3 weeks back. On examination he was found to have hypokalemia secondary to thyrotoxicosis. Clinically there were no features of thyrotoxicosis or thyroiditis. He was initially treated with intravenous and later oral potassium supplementation and propranolol. At 8 weeks of follow-up his thyroid profile became normal and his propranolol was stopped. He had no further recurrence of paralysis. He was diagnosed as a case silent thyroiditis presenting as thyrotoxic periodic paralysis. In cases of recurrent or acute flaccid muscle paralysis, it is important to suspect thyrotoxicosis, even if asymptomatic. Definitive treatment of thyrotoxicosis prevents recurrence.

We present three cases of thyrotoxic periodic paralysis (TPP) due to painless thyroiditis presenting as acute quadriparesis. All responded to potassium supplementation and propranolol. TPP may be due to thyrotoxicosis of any etiology, commonly Grave′s disease. The absence of clinical signs of thyrotoxicosis can delay diagnosis and treatment. Thyroid function tests should be a routine evaluation in all cases of hypokalemic periodic paralysis.

Clinical History: A 57‐year old woman presented with left hand pain, periodic leg movement during sleep, gradual onset of stiffness, clumsiness, and falls. Neurological examination showed: generalized rigidity and bradykinesia. There was left hand dystonic posturing and ideomotor apraxia, as well as mirror movements of upper limbs and stimulus‐sensitive myoclonus. The patient had a high‐pitched voice and hypophonia (Video S1). Discussion: Experts discuss localization and the syndromic diagnosis and predict the underlying pathology. The pathological diagnosis is then provided and clinical learning points are considered. View Supplementary Video 1 [ABSTRACT FROM AUTHOR]

Keywords: Transcranial sonography; corticobasal degeneration EN Transcranial sonography corticobasal degeneration 581 582 2 07/03/20 20200701 NES 200701 We thank Dr. Daniel Richter and colleagues for their comments on our recently published I Movement Disorders Clinical Practice i ( I MDCP i ) article.[[1]] We welcome any guidance with regard to the diagnosis of atypical parkinsonism given that it can often be difficult especially at the first assessment. The diagnosis is still a clinical diagnosis, and we await validation of various biomarkers to guide accurate diagnosis. Transcranial sonography (TCS) is one of these noninvasive biomarkers, and Richter and colleagues emphasise its role in distinguishing between idiopathic Parkinson's disease (IPD), MSA, PSP, and corticobasal syndrome (CBS). [Extracted from the article]