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2018| January-March | Volume 21 | Issue 1
Online since
March 29, 2018
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ORIGINAL ARTICLES
Mercury toxicity following unauthorized siddha medicine intake – A mimicker of acquired neuromyotonia - Report of 32 cases
G Gnanashanmugam, R Balakrishnan, SP Somasundaram, N Parimalam, P Rajmohan, MB Pranesh
January-March 2018, 21(1):49-56
DOI
:10.4103/aian.AIAN_274_17
PMID
:29720798
Context:
Mercury is used extensively in the preparation of Siddha medicines, after purification. In this study, we present 32 patients of mercury toxicity following unauthorized Siddha medicine intake who mimicked neuromyotonia clinically. We analyzed the clinical features of these patients, the role of autoimmunity in etiopathology, and compared it with acquired neuromyotonia.
Subjects and Methods:
This is a retrospective study to analyze inpatients in a tertiary care center, admitted with mercury toxicity following Siddha medicine intake from August 2012 to October 2016. We analyzed the clinical features, laboratory data including mercury, arsenic and lead levels in blood, and serum voltage-gated potassium channels (VGKC)-CASPR2 Ab in selected patients.
Results:
Thirty-two patients who had high blood mercury levels following Siddha medicine intake were included in the study. All patients (100%) had severe intractable neuropathic pain predominantly involving lower limbs. Twenty-six (81.25%) patients had fasciculations and myokymia. Fifteen patients (46.86%) had autonomic dysfunction (postural hypotension and resting tachycardia). Nine (28.12%) patients had encephalopathic features such as dullness, apathy, drowsiness, or delirium. Anti-VGKC Ab was positive in 12 patients with myokymia. All the patients in the study consumed Siddha medicines obtained from unauthorized dealers.
Conclusions:
Mercury toxicity following Siddha medicine intake closely mimics acquired neuromyotonia; severe intolerable neuropathic pain is the hallmark feature; Positive VGKC-CASPR2 antibody in some patients must be due to triggered autoimmunity secondary to mercury toxicity due to Siddha medicine intake. The government should establish licensing system to prevent distribution of unauthorized Siddha medicines.
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REVIEW ARTICLES
Recent advances in antisense oligonucleotide therapy in genetic neuromuscular diseases
Ashok Verma
January-March 2018, 21(1):3-8
DOI
:10.4103/aian.AIAN_298_17
PMID
:29720791
Genetic neuromuscular diseases are caused by defective expression of nuclear or mitochondrial genes. Mutant genes may reduce expression of wild-type proteins, and strategies to activate expression of the wild-type proteins might provide therapeutic benefits. Also, a toxic mutant protein may cause cell death, and strategies that reduce mutant gene expression may provide therapeutic benefit. Synthetic antisense oligonucleotide (ASO) can recognize cellular RNA and control gene expression. In recent years, advances in ASO chemistry, creation of designer ASO molecules to enhance their safety and target delivery, and scientific controlled clinical trials to ascertain their therapeutic safety and efficacy have led to an era of plausible application of ASO technology to treat currently incurable neuromuscular diseases. Over the past 1 year, for the first time, the United States Food and Drug Administration has approved two ASO therapies in genetic neuromuscular diseases. This overview summarizes the recent advances in ASO technology, evolution and use of synthetic ASOs as a therapeutic platform, and the mechanism of ASO action by exon-skipping in Duchenne muscular dystrophy and exon-inclusion in spinal muscular atrophy, with comments on their advantages and limitations.
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ORIGINAL ARTICLES
Evaluation of various movement disorders in patients of genetically proven spinocerebellar ataxia: A study from a Tertiary Care Center in Northern India
Divya M Radhakrishnan, Vinay Goyal, Achal Kumar Srivastava, Garima Shukla, Madhuri Behari
January-March 2018, 21(1):24-28
DOI
:10.4103/aian.AIAN_266_17
PMID
:29720794
Background:
Movement disorders are one of the prominent nonataxic symptoms in patients of spinocerebellar ataxia (SCA). The type of movement disorder may provide clinical clue to the type of SCA.
Objective:
The objective of this study is to evaluate various movement disorders in patients of genetically proven SCAs and to establish a probable clinico-genetic correlation.
Methods:
Ninety-Five patients of genetically proven SCAs were assessed for the presence of various movement disorders.
Results:
Patients with SCA (75.8% males) with at least one movement disorder contributed 43.16%. Age for onset of movement disorder was 43.39 ± 13.43 years. SCA-12 (38.95%) was the most common subtype. Among the patients with at least one movement disorder, action tremor of hands contributed majority (90.2%). Dystonia and parkinsonism were present in 17.07% and 12.2% of patients (with movement disorder), respectively. Action tremor of hands was present in 34 patients with SCA-12 (91.89%), and 20 patients (54.05%) had onset of hand tremor preceding the onset of ataxia. Majority of patients with SCA-12 (81%) were of the same ethnic origin belonging to Agrawal community. Patients with movement disorder had a later onset (45 ± 13.88 years) of ataxic symptoms compared to those without a movement disorder (32.8 ± 11.92) (
P
= <0.0005). There was no significant association between severity of ataxia and presence of movement disorder.
Conclusion:
Movement disorders are present in about 43% of patients with SCA and can precede or succeed the onset of ataxia. Tremor onset SCA predicted SCA-12, especially in Agrawal community.
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REVIEW ARTICLES
Preventing “neurophobia”: Remodeling neurology education for 21
st
-century medical students through effective pedagogical strategies for “neurophilia”
Bhaskara P Shelley, Thomas V Chacko, Balakrishnan R Nair
January-March 2018, 21(1):9-18
DOI
:10.4103/aian.AIAN_371_17
PMID
:29720792
Neurology has a reputation, particularly as a complex “head-to-toe” discipline for undergraduate medical students. Neurophobia syndrome, a global phenomenon, fundamentally stems from pedagogical deficiencies during the undergraduate curriculum, the lack of vertical integration between basic neurosciences and clinical bedside neurology, the lack of clinical reasoning exercises, cognitive heuristics, and clinical problem-solving, errors in diagnostic competence, and hyposkilia. This ultimately results in poor clinical competence and proficiency in clinical neurology and causes attrition in nurturing a passion for learning the neurology discipline. This article explores plausible factors that contribute to the genesis of neurophobia and multifaceted strategies to nurture interest in neurosciences and provide possible solutions to demystify neurology education, especially the need for evidence-based educational interventions. Remodeling neurology education through effective pedagogical strategies and remedial measures, and using the Miller's pyramid, would provide a framework for assessing clinical competence in clinical bedside neurology. Technology-enhanced education and digital classrooms would undoubtedly stamp out neurophobia in medical students of the 21
st
century. It will not frighten off another generation of nonneurologist physicians to empower them to hone expertise in order to tackle the increasing burden of neurological disorders in India. Furthermore, promoting neurophilia would facilitate the next generation of medical students in pursuing career options in neurology which would be quintessential not only in closing India's looming neurologist workforce gap but also in fostering interest in research imperatives in the next generation of medical students.
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ORIGINAL ARTICLES
Value of motor nerve conduction studies in the diagnosis of idiopathic tarsal tunnel syndrome: A single-center prospective observational study from India
Ajoy Sodani, Mukesh Dube, Rahul Jain
January-March 2018, 21(1):35-41
DOI
:10.4103/aian.AIAN_320_17
PMID
:29720796
Background:
Nerve conduction studies are considered to be the gold standard for diagnosing secondary tarsal tunnel syndrome (
s
TTS), but their utility in the diagnosis of idiopathic tarsal tunnel syndrome (
i
TTS) is largely unknown.
Objective:
We sought to investigate the value of motor nerve conductions studies (MNCS) in the diagnosis of clinically suspected
i
TTS.
Materials and Methods:
Twenty-six (52 limbs) adult patients of clinically suspected
i
TTS were subjected to motor nerve conductions of posterior tibial nerve, and its branches and motor conduction parameters were compared with those of 45 healthy controls.
Results:
Symptoms were bilateral in 70% (
P
= 0.02), with heel pain in 95% of symptomatic limbs. MNCS was abnormal in 32 (80%) of symptomatic limbs and 8 (66.6%) of asymptomatic limbs (
P
= 0.004). Out of electrophysiologically abnormal nerves (
n
= 67), the pathological process could be identified in all the nerves with abnormal MNCS (
P
= 0.02). Probable demyelination was seen in 58.2% of the electrophysiologically abnormal nerves.
Discussion:
The present study shows that
i
TTS are gender and Body Mass Index neutral with bilateral symptoms being common. Tinel's sign was inconsistent. Heel pain did not correlate with abnormal inferior calcaneal nerve conductions. Motor nerve conduction study was abnormal in a significant number of symptomatic limbs. “Probable demyelination” was more frequent in symptomatic limbs.
Conclusion:
MNCS is significantly abnormal in symptomatic limbs of subjects with
i
TTS. Demyelination is slightly more common than axonopathy in
i
TTS. With a sensitivity of 80% and specificity of 33.3%, MNCS seems to be useful as a screening tool in clinically suspected
i
TTS. This study is Level II: Lesser quality randomized controlled trial or prospective comparative study.
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The Spectrum of Autonomic Dysfunction in Myasthenic Crisis
Rohit Ninan Benjamin, Sanjith Aaron, Ajith Sivadasan, Suresh Devasahayam, Amalan Sebastin, Mathew Alexander
January-March 2018, 21(1):42-48
DOI
:10.4103/aian.AIAN_270_17
PMID
:29720797
Background:
Autoimmune autonomic dysfunction is described in Myasthenia Gravis. In myasthenic crisis, the spectrum of autonomic dysfunction is hitherto uncharacterized.
Objective:
The objective of this study is to describe the spectrum of autonomic dysfunction in myasthenic crises using the composite autonomic symptom scale 31 (COMPASS 31) autonomic symptom questionnaire and power spectral analysis of heart rate variability (HRV), which is a simple way of estimating general autonomic dysfunction.
Methods:
Adult patients with myasthenic crisis from January 1, 2014 to March 15, 2015, were prospectively included in this study. The COMPASS 31 questionnaire for symptoms of autonomic dysfunction and power spectral analysis of HRV were assessed. These were compared with the patient's demographic and clinical parameters and with previous literature. IRB approval was obtained.
Results:
Sixteen patients were included (M:F 3:1). 15/16 patents (93%) had autonomic dysfunction on COMPASS 31 questionnaire. The domains of involvement were gastrointestinal (80%), orthostatic (67.7%), pupillomotor (67.7%); sudomotor (33.3%), and vasomotor (13.3%). Parasympathetic dysfunction predominance was suggested by the symptom profile. HRV analysis showed a low frequency (LF) spectral shift suggesting slowed parasympathetic responsiveness (LF normalized unit (nu): high frequency [HF] nu mean 8.35, standard deviation ± 5.4, 95% confidence interval 2.2–12.5), which significantly exceeded the mean LF nu: HF nu ratios of the majority of previously reported noncrises myasthenic populations.
Conclusions:
Myasthenic crisis has autonomic dysfunction involving multiple organ systems. Increased latency of parasympathetic reflexes is suggested. A comprehensive management protocol addressing different autonomic domains is required for holistic patient care.
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IMAGES IN NEUROLOGY
Uncommon anatomical variant – Types artery of percheron infarcts: Clinical-radiological correlations
T Harisuthan, Anirudh Vilas Kulkarni, Gigy Varkey Kuruttukulam
January-March 2018, 21(1):80-81
DOI
:10.4103/aian.AIAN_363_17
PMID
:29720805
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ORIGINAL ARTICLES
Phrenic nerve conduction study in the early stage of guillain–barre syndrome as a predictor of respiratory failure
Barun Kumar Sen, Alak Pandit
January-March 2018, 21(1):57-61
DOI
:10.4103/aian.AIAN_345_17
PMID
:29720799
Background:
Guillain-Barré syndrome (GBS) has unpredictable clinical course with severe complication of respiratory failure.
Objective:
To identify clinical profiles and electrophysiological study particularly non-invasive Phrenic nerve conduction study in patients of early GBS to predict respiratory failure.
Methods:
64 adult (age≥18yrs) patients of early GBS (onset ≤ 14 days) during the study period from January 2014 to October 2015 were evaluated by clinical profiles of age, gender, antecedent infection, time to peak disability, single breath counts, cranial nerve involvement, autonomic dysfunction and non-invasive Phrenic nerve conduction study. Patients with predisposition factors of polyneuropathy like diabetes mellitus, hypothyroidism, vitamin deficiency, renal failure were excluded.
Results:
Among 64 patients abnormal phrenic nerve conduction study was seen in 65.62% cases (42/64) and 45.23% (19/42) of them developed respiratory failure. Phrenic nerve sum latency, amplitude, duration and area were abnormal in those who developed respiratory failure and they had sum of phrenic nerve latency >28 msec, sum of CMAP amplitude <300 μV, sum of CMAP duration >50 msec and sum of area < 4 mVmS. None with normal phrenic nerve study developed respiratory failure. It was found that age, gender, preceding infection, autonomic involvement and types of GB syndrome had no influence on development of respiratory failure (p>0.05). Rapid disease progression to peak disability, more severe disease, shorter single breath counts and cranial nerve involvement were seen more often in patients with respiratory failure.
Conclusion:
Abnormal Phrenic nerve conduction study in the early Guillain-Barré syndrome might be of great value independently in predicting impending respiratory failure.
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CASE REPORTS
Cervical myelopathy after high-voltage electrical burn of the head: Report of an unusual case
Shri Ram Sharma, Masaraf Hussain, Hibo Hibong
January-March 2018, 21(1):76-79
DOI
:10.4103/aian.AIAN_376_17
PMID
:29720804
High-voltage electrical injuries are uncommonly reported and may predispose to both immediate and delayed neurologic complications. We present a case of 27-year-old male who experienced a high-voltage electrical burn of the head resulting in quadriparesis. High-voltage electrocution injuries are a serious problem with potential for immediate, delayed, and long-term neurologic sequelae. The existing literature regarding effective treatment of neurologic complications is limited. Multidisciplinary management and long-term follow up are required.
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ORIGINAL ARTICLES
Necrotizing autoimmune myopathy: Clinicopathologic study from a single tertiary care centre
Sobiya Mahnaz Ayesha, AK Meena, Navatha Vangala, Liza Rajasekhar, Subhash Kaul, Rupam Borgahain, Megha S Uppin
January-March 2018, 21(1):62-67
DOI
:10.4103/aian.AIAN_389_17
PMID
:29720800
Background:
Idiopathic inflammatory myopathies (IIMs) are a group of chronic, autoimmune disorders which include a new entity, necrotizing autoimmune myopathy (NAM). NAM lacks inflammation and presents with markedly elevated creatinine phosphokinase (CPK) levels. It is associated with connective tissue diseases (CTDs), statin use, malignancies, and most cases are idiopathic.
Objectives:
The objectives of this study are to describe the clinicopathologic features in muscle biopsy-proven cases of NAM. To emphasize the role of laboratory parameters such as CPK levels and myositis profile in the diagnosis of NAM.
Materials and Methods:
This is a retrospective study including 15 patients of NAM diagnosed on muscle biopsy over a period of 2 years. The slides of the biopsies were reviewed, and clinical data, electromyography findings, and CPK levels were obtained. Myositis profile was done.
Results:
Necrotizing myopathy accounted for 13.63% (15 cases) of total inflammatory myopathies (110 cases) in the study. These were grouped into CTD-associated NAM, statin-associated NAM, paraneoplastic NAM and idiopathic NAM which was the common type. All cases presented with progressive proximal muscle weakness and had markedly elevated CPK levels. Anti-3-hydroxy-3-methyl-glutaryl-coenzyme A reductase and antisignal recognition particle antibodies were seen to be positive in six patients. Muscle biopsies showed predominant fiber necrosis with significant fiber degeneration and regeneration in the absence of inflammation. All patients received immunotherapy with significant improvement was seen in six patients with two mortalities.
Conclusion:
Necrotizing myopathy is a new addition to the spectrum of IIM. Clinicopathologic correlation is important for appropriate diagnosis. It is found to be refractory to corticosteroids monotherapy. The course of illness is not uniform, and in some patients, there can be rapid worsening with mortality.
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EDITORIAL
As I Sign in…
Vinay Goyal
January-March 2018, 21(1):1-1
DOI
:10.4103/0972-2327.228845
PMID
:29720789
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CASE REPORTS
A viral polymyositis masquerade: Life-threatening case of juvenile dermatomyositis complicated by systemic capillary leak syndrome
Bhaskara P Shelley, Shrijeet Chakraborti
January-March 2018, 21(1):70-74
DOI
:10.4103/aian.AIAN_373_17
PMID
:29720802
This is a case report of an 8-year-old boy who developed an atypical, rare subphenotype of autoimmune inflammatory acute juvenile dermatomyositis (JDM), initially masquerading as viral polymyositis (PM)-like presentation, that was complicated by a hitherto unreported fulminant, life-threatening pediatric systemic capillary leak syndrome (SCLS). We highlight the close differential between viral PM and JDM, the baffling clinical syndromic constellation of hypotension with hemoconcentration – a “shock”-like syndrome, hypoalbuminemia without albuminuria, and generalized edema with the atypical JDM presentation, and stress crucial need to implement early aggressive, multipronged immunomodulatory treatment along with intensive fluid resuscitation which saved the life, this patient from a stormy, and turbulent 4-week clinical illness. This is the first published case description in the current literature of the association of an aggressive subphenotype of JDM and life-threatening pediatric SCLS. This report opens the Pandora's Box to explore the genetic and pathomechanisms of both disorders.
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PRESIDENTIAL ORATION IANCON 2017
Brain at risk
Subhash Kaul
January-March 2018, 21(1):2-2
DOI
:10.4103/aian.AIAN_55_18
PMID
:29720790
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HISTORY OF MEDICINE
Edgar adrian and patrick merton: Names blurred with the passage of time
Kalyan B Bhattacharyya
January-March 2018, 21(1):19-23
DOI
:10.4103/aian.AIAN_271_17
PMID
:29720793
Edgar Douglas Adrian and Patrick Anthony Merton are two supreme neurophysiologists from England in the last century whose names are almost forgotten these days. Adrian's work on all-or-none phenomenon in nerve and muscle excitability ushered in a new era and Merton's servo theory of muscular movement and muscle fatigue added a new dimension to the understanding of stretch reflex and deep tendon reflexes. Both of them trained and worked at Trinity College, Cambridge and both were elected as Fellow of the Royal Society and Adrian in addition, was awarded the Nobel Prize in 1932 along with Charles Scott Sherrington.
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2,551
122
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IMAGES IN NEUROLOGY
Pseudo-subarachnoid hemorrhage sign
Ramnath Santosh Ramanathan
January-March 2018, 21(1):83-84
DOI
:10.4103/aian.AIAN_152_17
PMID
:29720807
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CASE REPORTS
Unilateral limb thinning –Thinking out of the box
Chandramouleeswaran Venkatraman, Shubha Subramanian, Daniel Sweetson Abraham, Kannan Vellaichamy
January-March 2018, 21(1):74-76
DOI
:10.4103/aian.AIAN_416_17
PMID
:29720803
We report an unusual presentation in a 9-year-old girl with unilateral circumferential thinning of the entire right upper limb without any other neurological deficit, with normal nerve conduction and electromyography initially thought of as a neurodegenerative disorder based on clinical presentation. Magnetic resonance imaging of the upper limb showed partial lipoatrophy with normal glucose metabolism and lipid profile and negativity for HIV and autoimmune disease (panniculitis) with no family history of similar disorder. Remember to think out of box before labeling neurodegenerative disease.
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ORIGINAL ARTICLES
Determinants of remission in medically treated carpal tunnel syndrome: Study from Central India
Ajoy Sodani, Raunak Dani, Mukesh Dube, Dinesh Choukesey, Sunil Athale
January-March 2018, 21(1):29-34
DOI
:10.4103/aian.AIAN_347_17
PMID
:29720795
Background:
The factors associated with the spontaneous remission (SR) of symptoms in carpal tunnel syndrome (CTS) are not well known.
Objectives:
To look for determinants of SR in medically treated, electrophysiologically proven patients of CTS.
Methods:
We revisited the medical records and nerve conduction study data of 130 hands with CTS and divided them into two groups as per the absence or persistence of the symptoms when contacted after a median time lapse of 3 years following the diagnosis.
Results:
SR occurred in 46.1% of the hands. Higher odds of SR were linked with female gender, symptoms restriction to lateral fingers, symptom duration <10 months, mildly delayed median motor and sensory distal latencies, and median sensory amplitude >20 μV. We developed a seven-point scale, on which a score of ≥4 had a strong association (odds ratio 4.31) with SR.
Discussion and Conclusion:
No single risk factor, standalone, can predict SR in patients with CTS, which could lead to an invasive treatment (Surgery or local injection) to them. We propose that patients scoring ≥4 on our 7 point scale should be treated medically for the initial 10 months after the symptom onset.
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CASE REPORTS
Spinocerebellar ataxia-21 in a Turkish child
Faruk Incecik, Ozlem M Herguner, Patrick Willems, Neslihan O Mungan
January-March 2018, 21(1):68-70
DOI
:10.4103/aian.AIAN_415_17
PMID
:29720801
Hereditary cerebellar ataxias are genetically heterogeneous disorders. Autosomal recessive spinocerebellar ataxia-21 (SCAR21) is a neurologic disorder characterized by the onset of cerebellar ataxia, recurrent episodes of liver failure, peripheral neuropathy, and learning disabilities. Herein, we reported a case presented with gait and balance problems, swallowing difficulties, mild delayed motor development, and mild learning disability with SCAR21 that confirmed by mutation analysis in a Turkish child. To the best of our knowledge, this is the first case of SCAR21 from Turkey.
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LETTERS TO THE EDITOR
Chronic lymphocytic leukemia involvement of central nervous system: Clinical diversity, diagnostic algorithm and therapeutic challenges
Biljana Mihaljevic, Mihailo Smiljanic, Darko Antic, Nada Kraguljac Kurtovic, Milena Todorovic Balint
January-March 2018, 21(1):85-87
DOI
:10.4103/aian.AIAN_442_17
PMID
:29720808
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OBITUARY
Dr. Eddie P. Bharucha (December 28, 1916–December 14, 2017)
Pravina Shah, Shashi Seshia
January-March 2018, 21(1):91-92
DOI
:10.4103/aian.AIAN_21_18
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LETTERS TO THE EDITOR
Recovery of visual scotomas by vortioxetine in a patient with symptomatic occipital lobe epilepsy
Halil Onder, Akin Coskun, M Tugba Goksungur
January-March 2018, 21(1):88-90
DOI
:10.4103/aian.AIAN_291_17
PMID
:29720810
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2,252
108
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IMAGES IN NEUROLOGY
Cysts in White Matter: A Novel Neuroimaging Finding in Infantile GM1 Gangliosidosis
Mahesh Kamate
January-March 2018, 21(1):82-83
DOI
:10.4103/aian.AIAN_343_17
PMID
:29720806
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2,005
116
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LETTERS TO THE EDITOR
Spinal intramedullary cysticercosis: A summary of three cases in Thailand
Beuy Joob, Viroj Wiwanitkit
January-March 2018, 21(1):87-88
DOI
:10.4103/aian.AIAN_370_17
PMID
:29720809
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1,705
100
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© 2006 - Annals of Indian Academy of Neurology | Published by Wolters Kluwer -
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Online since 1
st
March, 2006