Shivaji Rao

National Institute of Mental Health and Neurosciences

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Arun B. Taly

National Institute of Mental Health and Neurosciences

Sanjib Sinha

National Institute of Mental Health and Neurosciences

A B Taly

National Institute of Mental Health and Neurosciences

ArchanaB Netto

National Institute of Mental Health and Neurosciences

ArunB Taly

National Institute of Mental Health and Neurosciences

Santosh K. Chaturvedi

National Institute of Mental Health and Neurosciences

K P Sivaraman Nair

National Institute of Mental Health and Neurosciences

G.R. Arunodaya

Sultan Qaboos University Hospital

Chaitra T. Ramachandraiah

National Institute of Mental Health and Neurosciences

Girish Baburao Kulkarni

National Institute of Mental Health and Neurosciences

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National Institute of Mental Health and Neurosciences

National Institute of Mental Health

Christie's

Neurology, Inc

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All India Institute of Medical Sciences

National Institutes of Health

University of Sydney

St.John's Medical College Hospital

Manipal Academy of Higher Education

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Cardiac involvement in Wilson's disease--an electrocardiographic observation.

PubMed (2004)

S. Meenakshisundaram Shweta Sinha M RAO Prashanth Lingappa Kukkle G.R. Arunodaya

Wilson's disease is known for its protean manifestations; however electrocardiographic abnormalities have not received much attention.To evaluate the various electrocardiographic (ECG) changes in patients with Wilson's disease.The resting ECGs of 50 patients with Wilson's disease were systematically analyzed independently by three observers after excluding other causes that could induce ECG abnormalities.Fifteen patients had at least one abnormality in the ECG. Sinus tachycardia was seen in eight and sinus bradycardia in six. Other abnormalities included: bifid P wave (1), ST elevation (2), ST depression (2), T inversion (4), ventricular premature contraction - VPC (1) and prominent U waves (1). QRS axis, PR interval, QRS complex, R/S amplitude ratio and QT interval were normal in all. Ventricular premature beats were not recorded in any. None had features of ventricular hypertrophy. There was no statistically significant difference in ECG abnormalities with reference to age, gender, duration of illness or treatment, serum copper or ceruloplasmin, and severity of neurological impairment.ECG abnormalities are not uncommon in Wilson's disease and are presumably related to an underlying cardiomyopathy due to deposition of copper in heart.

T wave

Abnormality

Sinus bradycardia

Wilson's disease

Sinus tachycardia

Left axis deviation

PR interval

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Sleep in Wilson′s disease: Questionnaire based study

Annals of Indian Academy of Neurology (2011)

Sanjib Sinha ArchanaB Netto ArunB Taly Samhita Panda Shivaji Rao

We proposed to detect sleep abnormalities in Wilson's disease, (WD) using sleep questionnaires.Twenty-five patients (M:F = 18:7; age: 24.4 ± 9.2 years) with WD and 24 controls (all males; age: 33.1 ± 9.7 years) were recruited. They underwent phenotypic/magnetic resonance imaging (MRI) evaluation followed by administration of Pittsburg Sleep Quality Index (PSQI) and Epworth Sleepiness Scale (ESS) questionnaires.The mean age at presentation and diagnosis was 24.4 ± 9.2 and 17.6 ± 7.5 years, respectively. The duration of illness at diagnosis was 14 ± 21.9 months. On PSQI, 15 patients with WD had abnormal PSQI scores of >5 as compared to 6 patients among the controls. The mean PSQI score was significantly more (P = 0.03) in patients compared to the controls. The PSQI worst scores were noted only in WD. Evaluation with ESS showed that three patients with WD scored >10/24, while two among the controls qualified for excessive daytime sleepiness. Overall, assessment by sleep questionnaires detected abnormality in 16 patients with WD as compared to 8 controls (P = 0.004). Subgroup analysis revealed that patients whose duration of illness was >8 years and who were on decoppering treatment had significantly lesser excessive daytime somnolence.Sleep disturbances were observed more often in WD than in controls. Better designed studies will provide a better understanding.

Sleep

10.4103/0972-2327.78047

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Citations (23)

Autonomic dysfunction in Wilson's disease - a clinical and electrophysiological study

Clinical Autonomic Research (2002)

Salvadeeswaran Meenakshi‐Sundaram Arun B. Taly Vikram Kamath G.R. Arunodaya Shivaji Rao

Dysautonomia

Subclinical infection

Familial dysautonomia

Valsalva maneuver

10.1007/s10286-002-0038-6

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Citations (62)

Alteration in polysomnographic profile in ‘migraine without aura’ compared to healthy controls

Sleep Medicine (2012)

Naveen Karthik Sanjib Sinha Arun B. Taly Girish Baburao Kulkarni Chaitra T. Ramachandraiah

Epworth Sleepiness Scale

Sleep

Sleep onset latency

10.1016/j.sleep.2012.10.019

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Citations (36)

On the Stochastic Non-sequential Production-planning Problem

Journal of the Operational Research Society (1990)

Shivaji Rao George O. Schneller

Sequence (biology)

Stochastic modelling

10.1038/sj/jors/0410307

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Sympathetic skin response in myelopathies

Clinical Autonomic Research (1998)

K P Sivaraman Nair A B Taly G.R. Arunodaya Shivaji Rao T Murali

Somatosensory evoked potential

Tibial nerve

10.1007/bf02267783

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Citations (8)

Acute idiopathic axonal neuropathy (AIAN): a clinical and electrophysiological observation

Acta Neurologica Scandinavica (2009)

SK Gupta Arun B. Taly Suresh Thontadarya Shivaji Rao D Nagaraja

Twenty patients (M:F 15:5) with electrophysiological evidence of predominant axonal lesion and fulfilling clinical criteria for Guillain Barré Syndrome were observed during a period of 6 years (1985-1990). Their mean age was 27.5 years (range 5-55). Seven patients had antecedent febrile illness. Peak motor deficit was reached at a mean period of 6.5 days (range 2-21 days). All the patients had distal muscle weakness out of proportion to proximal muscle weakness. Facial paresis (13 patients), bulbar palsy (2), respiratory failure (1), sensory deficits (7) and dysautonomia (1) were other salient features. CSF analysis revealed albumino-cytological dissociation in 12 patients. One patient died and in the remaining patients the recovery was delayed and incomplete. Presence of predominant distal muscle wasting and weakness, low amplitude CMAP or inexcitable nerves, absence of conduction block or significant temporal dispersion, normal or only slightly reduced conduction velocity and evidence of poor recovery suggest that the primary pathology in these patients may be axonal degeneration. These cases may represent a distinct entity and need to be differentiated from the more commonly observed acute idiopathic demyelinating neuropathy.

Paresis

Bulbar palsy

10.1111/j.1600-0404.1994.tb01665.x

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Citations (30)

Authors′ reply

Annals of Indian Academy of Neurology (2013)

Sanjib Sinha ArchanaB Netto ArunB Taly Samhita Panda Shivaji Rao

10.4103/0972-2327.116952

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Citations (0)

Altered polysomnographic profile in juvenile myoclonic epilepsy