Letters to Editor
2.
Yiğit A, Bingöl A, Mutluer N, Taşçilar N. The one‑and‑a‑half syndrome in systemic lupus erythematosus. J Neuroophthalmol 1996;16:274‑6. 3. Cogen MS, Kline LB, Duvall ER. Bilateral internuclear ophthalmoplegia in systemic lupus erythematosus. J Clin Neuroophthalmol 1987;7:69‑73. 4. Dutta I, Gohar S, Balakrishnan C, Mangat G, Mittal G, Bhaba SK, et al. Unilateral inter‑nuclear ophthalmoplegia in systemic lupus erythematosus. J Assoc Physicians India 2000;48:1210‑1. 5. Galindo M, Pablos JL, Gomez‑Reino JJ. Internuclear ophthalmoplegia in systemic lupus erythematosus. Semin Arthritis Rheum 1998;28:179‑86. 6. Jackson G, Miller M, Littlejohn G, Helme R, King R. Bilateral internuclear ophthalmoplegia in systemic lupus erythematosus. J Rheumatol 1986;13:1161‑2. 7. Keane JR. Eye movement abnormalities in systemic lupus erythematosus. Arch Neurol 1995;52:1145‑9. 8. Efthimiou P, Blanco M. Pathogenesis of neuropsychiatric systemic lupus erythematosus and potential biomarkers. Mod Rheumatol 2009;19:457‑68. Figure 2: Axial brain MRI at the time of presentation. No pathologic signal changes are evident
feature was OHS, which is a rare presentation of SLE. Literature review revealed two cases of OHS in known patients of SLE.[1,2] Yigit et al.,[2] reported a case of SLE presenting with diplopia and dysarthria with pontine infarction on MR imaging. Kunavarapu et al.,[1] reported OHS in a patient with SLE with infarction zone in lower midbrain on MRI. In contrast to these patients, no pathologic signal changes in related regions of gaze control were seen on MRI in the present patients. The OHA is a subtype of INO, an uncommon condition in patients with SLE as well.[3‑6] In the two patients of SLE with OHA, the cause was ischemic infarct.[7] Other possible mechanisms have also been proposed for central nervous system involvement in lupus and they include vasculopathy, autoantibodies, and cytokines.[8] In their review, Cogen et al., argue that unilateral INO is more frequent than the bilateral form in SLE and the probable cause could be selective localization of the blood supply to the medial longitudinal fasciculi in contrast to plaques of multiple sclerosis which are nonselective and bilateral INO is more frequent in multiple sclerosis. Immune complex deposition and microvascular injury might probably be the basis of the clinical presentation in this patient. This possible mechanism was further supported by low complement levels and multiple positive autoantibodies observed in this patient.
Payam Sasannejad, Nahid Olfati, Mohsen Soltani Sabi, Ali Ghabeli Juibary Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran E‑mail: [email protected]
References 1.
Kunavarapu C, Kesavan RB, Pevil‑Ulysee M, Mohan SS. Systemic lupus erythematosus presenting as “one‑and‑a‑half syndrome”. J Rheumatol 2001;28:874‑5.
Neurology India | May-Jun 2014 | Vol 62 | Issue 3
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.136983
Received: 08‑04‑2014 Review completed: 12‑04‑2014 Accepted: 29‑05‑2014
Cerebral venous sinus thrombosis presentation in severe scrub typhus infection: A rare entity Sir, Scrub typhus is a common re‑emerging infection in the Indian subcontinent.[1] The severity of infection can range from mild symptoms and signs to multi organ failure. Severe scrub infection can have varied presentation: Pulmonary edema, interstitial pneumonia, congestive heart failure, circulatory collapse, glomerulonephritis, and central nervous system (CNS) dysfunction, including confusion, delirium, and seizures. This report describes a case of scrub typhus with cerebral sinus thrombosis (CST), an unreported complication of scrub typhus. A 48‑year‑old man presented with fever headache and vomiting of five days duration followed by right side focal seizures and altered sensorium for 2 days. One week before admission, he had symptoms of an upper respiratory tract infection with productive cough and sore throat. At admission, neurological examination revealed Glasgow Coma Scale (GCS) score of 11/15 (E3V3M5), 301
Letters to Editor
bilateral papilloedema, paucity of right side movement with hypoesthesia, and an extensor plantar response on right side. He had a high grade persistent fever (~39°C) and no rash or eschar. Laboratory findings revealed thrombocytopenia (55,000/mm3); hematuria, elevated creatinine (2.73 mg/dl); urea (62 mg/dl); elevated aspartate aminotransferase (183 IU/L) and alanine aminotransferase (79 IU/L); and serum Creatine phosphokinase and Lactate dehydrogenase were 20,842 U/L and 1906 U/L respectively. Fever work‑up profile was non‑contributory. Work‑up for disseminated intravascular coagulation (DIC) was within normal limits: Prothrombin time (11.9 seconds), activated partial thromboplastin time (25.7 seconds), and fibrinogen level (372.7 mg/dl). IgM and IgG serology for dengue was negative. Diagnosis of scrub typhus was confirmed by serum IgM ELISA. Chest X‑ray showed bilateral pulmonary infiltrates suggestive of interstitial pneumonitis. Magnetic resonance imaging (MRI) of brain showed thrombosis of the anterior portion of superior saggitial sinus with hemorrhagic venous infarct in left frontal lobe and a midline shift of 4 mm to right side [Figure 1]. A comprehensive thrombotic work‑up was normal. Ham’s test and sucrose lysis test were negative. Genetic markers for thrombosis like factor V Leiden mutation, methylene tetra hydro folate reductase, and prothrombin gene polymorphism were negative. He was treated with doxycycline, azithromycin, unfractionated heparin and anti‑edema measures. On day-3 of admission, his sensorium worsened to a GCS score of 7/15 with radiologically detoriation as well, and emergency left front otemporoparietal decompressive hemicraniectomy was done. Intra‑operatively, the brain was tense, and multiple thrombosed cortical veins were
seen. Post‑operatively, he was weaned off ventilator. He developed acute kidney injury and hypotension which were managed successfully. After comprehensive rehabilitative and medical therapy at 6‑months follow‑up, he had improved to a modified Rankin scale of 2. Repeat brain MRI showed marked improvement with complete recanalization of the superior sagittal sinus and reduction in size of the left high frontal hematoma [Figure 2]. The spectrum of neurological complications in scrub typhus include: Aseptic meningitis, meningoencephalitis, cerebellitis[2], myelitis[3], cerebral hemorrhage[4], and cerebral infarction. [5] Autopsy study has revealed punctate focal brain hemorrhages.[3]
Figure 1: (Day-1): Magnetic resonance imaging/magnetic resonance venography (MRI/MRV) of the brain - T2, T1W images reveals acute hemorrhagic venous infarct and swelling in the left high frontal region; midline shift to the right with mild subfalcine herniation, MRV demonstrates thrombosis in anterior part of the superior sagittal sinus extending into the cortical vein on the left
Figure 2: (6 months later): Reducing extension and degree of enhancement of previous subacute venous infarction involving left frontal lobe, suggestive of improvement. Complete recanalization of the superior sagittal sinus
302
Neurology India | May-Jun 2014 | Vol 62 | Issue 3
Letters to Editor
The cytokines released by acutely inflamed vascular endothelial cells secondary to invasion by Orientia tsutsugamushi damage endothelial integrity causing fluid leakage. There is localized platelet aggregation, polymorphs, and monocyte proliferation, leading to focal occlusive and angiitis causing micro infarcts in various tissues. This localized process can also cause venous thrombosis and peripheral gangrene. [6] The brain pathology reveals a diffuse or focal mononuclear cell exudate in the leptomeninges and typhus nodules (clusters of microglial cells) in the parenchyma.
4. 5. 6. 7.
8.
The characteristic eschar seen in scrub typhus infection, indicative of the vector bite, is present in less than 50% of patients reported from India.[7] Papilledema as seen in the present patient was reported in the earlier studies.[8] Thrombocytopenia and DIC may aggravate the extent of the cerebral hemorrhage. Abnormal chest radiographs have been reported in about 70% of patients. Hepatocellular dysfunction in scrub typhus is transient and usually normalises within 2 weeks.[9] We used an Enzyme-linked immunosorbent assay (Scrub Typhus Group ELISA Kit InBios, Seattle, WA, USA) test to detect IgM antibodies to Orientia tsutsugamushi. This kit uses a 56‑kDa recombinant cocktail of antigens (Karp, Gilliam, Kato and TA763) and has diagnostic specificity and sensitivity of ~90% and provides positive results within 3-4 days after the onset of illness. Ig M ELISA test has 86.5% sensitivity and 97.5% specificity.[10] Various systemic or CNS infections are possibly risk factors for CST. In this patient, risk factors for thrombosis, such as drugs or hereditary hypercoagulable state or local and systemic infections other than scrub typhus were not present. We postulate that the disseminated endothelial damage causing cerebral vasculopathy and perivasculitis of the capillaries and venous stasis due to increased intracranial pressure as the most likely mechanisms of sinus thrombosis.
Subhransu S. Jena1, Alexander Mathew1, Aaron Sanjith1, Sivadasan Ajith1, Bijesh R. Nair1,2, John A. J. Prakash3 1
Departments of Neurological Sciences and 3Clinical Microbiology, 2 Section of Neurosurgery, Christian Medical College, Vellore, TamilNadu, India. E‑mail: [email protected]
References 1. Kelly DJ, Fuerst PA, Ching WM, Richards AL. Scrub typhus: The geographic distribution of phenotypic and genotypic variants of Orientia tsutsugamushi. Clin Infect Dis 2009;48 Suppl 3:S203‑30. 2. Silpapojakul K, Ukkachoke C, Krisanapan S, Silpapojakul K. Rickettsial meningitis and encephalitis. Arch Intern Med 1991;151:1753‑7. 3. Kim DE, Lee SH, Park KI, Chang KH, Roh JK. Scrub typhus Neurology India | May-Jun 2014 | Vol 62 | Issue 3
9. 10.
encephalomyelitis with prominent focal neurologic signs. Arch Neurol 2000;57:1770‑2. Shih‑Hsien Y, Lih‑Shinn W, Chung‑Chao L, Yu‑Huai H. Scrub typhus complicated by intracranial hemorrhage‑ A case report. Tzu Chi Med J 2005;17:111‑4. Kim JH, Lee SA, Ahn TB, Yoon SS, Park KC, Chang DI, et al. Polyneuropathy and cerebral infarction complicating scrub typhus. J Clin Neurol 2008;4:36‑9. Cowan G. Rickettsial diseases: The typhus group of fevers: A review. Postgrad Med J 2000;76:269‑72. Chrispal A, Boorugu H, Gopinath KG, Prakash JA, Chandy S, Abraham OC, et al. Scrub typhus: an unrecognized threat in South India ‑ clinical profile and predictors of mortality. Trop Doct 2010;40:129‑33. Varghese GM, Mathew A, Kumar S, Abraham OC, Trowbridge P, Mathai E. Differential diagnosis of scrub typhus meningitis from bacterial meningitis using clinical and laboratory features. Neurol India 2013;61:17‑20. Yang CH, Hsu GJ,Peng MY, Young TG. Hepatic dysfunction in scrub typhus. J Formos Med Assoc 1995;94:101‑5. Prakash JA, Abraham OC, Mathai E. Evaluation of tests for serological diagnosis of scrub typhus. Trop Doct 2006;36:212‑3. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.136991
Received: 11‑06‑2014 Review completed: 30‑06‑2014 Accepted: 15‑06‑2014
Vertebral artery thrombosis in a case of traumatic atlantoaxial dislocation with delayed presentation: Emphasis on preoperative evaluation and operative steps to prevent a catastrophe Sir, Vertebral artery (VA) thrombosis and dissection has been documented in cervical spine injuries.[1,2] These vascular injuries are often asymptomatic and their pick up rates have increased with the advent of magnetic resonance imaging (MRI) and MR-angiogram.[2] VA thrombosis following traumatic atlanto‑axial dislocation (TAAD) has rarely been reported. Few case reports have described early reduction and management of injured VA. The intraoperative steps to prevent a catastrophe while handling an injured VA have not been described.[3,4] 303
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
2.
Yiğit A, Bingöl A, Mutluer N, Taşçilar N. The one‑and‑a‑half syndrome in systemic lupus erythematosus. J Neuroophthalmol 1996;16:274‑6. 3. Cogen MS, Kline LB, Duvall ER. Bilateral internuclear ophthalmoplegia in systemic lupus erythematosus. J Clin Neuroophthalmol 1987;7:69‑73. 4. Dutta I, Gohar S, Balakrishnan C, Mangat G, Mittal G, Bhaba SK, et al. Unilateral inter‑nuclear ophthalmoplegia in systemic lupus erythematosus. J Assoc Physicians India 2000;48:1210‑1. 5. Galindo M, Pablos JL, Gomez‑Reino JJ. Internuclear ophthalmoplegia in systemic lupus erythematosus. Semin Arthritis Rheum 1998;28:179‑86. 6. Jackson G, Miller M, Littlejohn G, Helme R, King R. Bilateral internuclear ophthalmoplegia in systemic lupus erythematosus. J Rheumatol 1986;13:1161‑2. 7. Keane JR. Eye movement abnormalities in systemic lupus erythematosus. Arch Neurol 1995;52:1145‑9. 8. Efthimiou P, Blanco M. Pathogenesis of neuropsychiatric systemic lupus erythematosus and potential biomarkers. Mod Rheumatol 2009;19:457‑68. Figure 2: Axial brain MRI at the time of presentation. No pathologic signal changes are evident
feature was OHS, which is a rare presentation of SLE. Literature review revealed two cases of OHS in known patients of SLE.[1,2] Yigit et al.,[2] reported a case of SLE presenting with diplopia and dysarthria with pontine infarction on MR imaging. Kunavarapu et al.,[1] reported OHS in a patient with SLE with infarction zone in lower midbrain on MRI. In contrast to these patients, no pathologic signal changes in related regions of gaze control were seen on MRI in the present patients. The OHA is a subtype of INO, an uncommon condition in patients with SLE as well.[3‑6] In the two patients of SLE with OHA, the cause was ischemic infarct.[7] Other possible mechanisms have also been proposed for central nervous system involvement in lupus and they include vasculopathy, autoantibodies, and cytokines.[8] In their review, Cogen et al., argue that unilateral INO is more frequent than the bilateral form in SLE and the probable cause could be selective localization of the blood supply to the medial longitudinal fasciculi in contrast to plaques of multiple sclerosis which are nonselective and bilateral INO is more frequent in multiple sclerosis. Immune complex deposition and microvascular injury might probably be the basis of the clinical presentation in this patient. This possible mechanism was further supported by low complement levels and multiple positive autoantibodies observed in this patient.
Payam Sasannejad, Nahid Olfati, Mohsen Soltani Sabi, Ali Ghabeli Juibary Department of Neurology, Mashhad University of Medical Sciences, Mashhad, Iran E‑mail: [email protected]
References 1.
Kunavarapu C, Kesavan RB, Pevil‑Ulysee M, Mohan SS. Systemic lupus erythematosus presenting as “one‑and‑a‑half syndrome”. J Rheumatol 2001;28:874‑5.
Neurology India | May-Jun 2014 | Vol 62 | Issue 3
Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.136983
Received: 08‑04‑2014 Review completed: 12‑04‑2014 Accepted: 29‑05‑2014
Cerebral venous sinus thrombosis presentation in severe scrub typhus infection: A rare entity Sir, Scrub typhus is a common re‑emerging infection in the Indian subcontinent.[1] The severity of infection can range from mild symptoms and signs to multi organ failure. Severe scrub infection can have varied presentation: Pulmonary edema, interstitial pneumonia, congestive heart failure, circulatory collapse, glomerulonephritis, and central nervous system (CNS) dysfunction, including confusion, delirium, and seizures. This report describes a case of scrub typhus with cerebral sinus thrombosis (CST), an unreported complication of scrub typhus. A 48‑year‑old man presented with fever headache and vomiting of five days duration followed by right side focal seizures and altered sensorium for 2 days. One week before admission, he had symptoms of an upper respiratory tract infection with productive cough and sore throat. At admission, neurological examination revealed Glasgow Coma Scale (GCS) score of 11/15 (E3V3M5), 301
Letters to Editor
bilateral papilloedema, paucity of right side movement with hypoesthesia, and an extensor plantar response on right side. He had a high grade persistent fever (~39°C) and no rash or eschar. Laboratory findings revealed thrombocytopenia (55,000/mm3); hematuria, elevated creatinine (2.73 mg/dl); urea (62 mg/dl); elevated aspartate aminotransferase (183 IU/L) and alanine aminotransferase (79 IU/L); and serum Creatine phosphokinase and Lactate dehydrogenase were 20,842 U/L and 1906 U/L respectively. Fever work‑up profile was non‑contributory. Work‑up for disseminated intravascular coagulation (DIC) was within normal limits: Prothrombin time (11.9 seconds), activated partial thromboplastin time (25.7 seconds), and fibrinogen level (372.7 mg/dl). IgM and IgG serology for dengue was negative. Diagnosis of scrub typhus was confirmed by serum IgM ELISA. Chest X‑ray showed bilateral pulmonary infiltrates suggestive of interstitial pneumonitis. Magnetic resonance imaging (MRI) of brain showed thrombosis of the anterior portion of superior saggitial sinus with hemorrhagic venous infarct in left frontal lobe and a midline shift of 4 mm to right side [Figure 1]. A comprehensive thrombotic work‑up was normal. Ham’s test and sucrose lysis test were negative. Genetic markers for thrombosis like factor V Leiden mutation, methylene tetra hydro folate reductase, and prothrombin gene polymorphism were negative. He was treated with doxycycline, azithromycin, unfractionated heparin and anti‑edema measures. On day-3 of admission, his sensorium worsened to a GCS score of 7/15 with radiologically detoriation as well, and emergency left front otemporoparietal decompressive hemicraniectomy was done. Intra‑operatively, the brain was tense, and multiple thrombosed cortical veins were
seen. Post‑operatively, he was weaned off ventilator. He developed acute kidney injury and hypotension which were managed successfully. After comprehensive rehabilitative and medical therapy at 6‑months follow‑up, he had improved to a modified Rankin scale of 2. Repeat brain MRI showed marked improvement with complete recanalization of the superior sagittal sinus and reduction in size of the left high frontal hematoma [Figure 2]. The spectrum of neurological complications in scrub typhus include: Aseptic meningitis, meningoencephalitis, cerebellitis[2], myelitis[3], cerebral hemorrhage[4], and cerebral infarction. [5] Autopsy study has revealed punctate focal brain hemorrhages.[3]
Figure 1: (Day-1): Magnetic resonance imaging/magnetic resonance venography (MRI/MRV) of the brain - T2, T1W images reveals acute hemorrhagic venous infarct and swelling in the left high frontal region; midline shift to the right with mild subfalcine herniation, MRV demonstrates thrombosis in anterior part of the superior sagittal sinus extending into the cortical vein on the left
Figure 2: (6 months later): Reducing extension and degree of enhancement of previous subacute venous infarction involving left frontal lobe, suggestive of improvement. Complete recanalization of the superior sagittal sinus
302
Neurology India | May-Jun 2014 | Vol 62 | Issue 3
Letters to Editor
The cytokines released by acutely inflamed vascular endothelial cells secondary to invasion by Orientia tsutsugamushi damage endothelial integrity causing fluid leakage. There is localized platelet aggregation, polymorphs, and monocyte proliferation, leading to focal occlusive and angiitis causing micro infarcts in various tissues. This localized process can also cause venous thrombosis and peripheral gangrene. [6] The brain pathology reveals a diffuse or focal mononuclear cell exudate in the leptomeninges and typhus nodules (clusters of microglial cells) in the parenchyma.
4. 5. 6. 7.
8.
The characteristic eschar seen in scrub typhus infection, indicative of the vector bite, is present in less than 50% of patients reported from India.[7] Papilledema as seen in the present patient was reported in the earlier studies.[8] Thrombocytopenia and DIC may aggravate the extent of the cerebral hemorrhage. Abnormal chest radiographs have been reported in about 70% of patients. Hepatocellular dysfunction in scrub typhus is transient and usually normalises within 2 weeks.[9] We used an Enzyme-linked immunosorbent assay (Scrub Typhus Group ELISA Kit InBios, Seattle, WA, USA) test to detect IgM antibodies to Orientia tsutsugamushi. This kit uses a 56‑kDa recombinant cocktail of antigens (Karp, Gilliam, Kato and TA763) and has diagnostic specificity and sensitivity of ~90% and provides positive results within 3-4 days after the onset of illness. Ig M ELISA test has 86.5% sensitivity and 97.5% specificity.[10] Various systemic or CNS infections are possibly risk factors for CST. In this patient, risk factors for thrombosis, such as drugs or hereditary hypercoagulable state or local and systemic infections other than scrub typhus were not present. We postulate that the disseminated endothelial damage causing cerebral vasculopathy and perivasculitis of the capillaries and venous stasis due to increased intracranial pressure as the most likely mechanisms of sinus thrombosis.
Subhransu S. Jena1, Alexander Mathew1, Aaron Sanjith1, Sivadasan Ajith1, Bijesh R. Nair1,2, John A. J. Prakash3 1
Departments of Neurological Sciences and 3Clinical Microbiology, 2 Section of Neurosurgery, Christian Medical College, Vellore, TamilNadu, India. E‑mail: [email protected]
References 1. Kelly DJ, Fuerst PA, Ching WM, Richards AL. Scrub typhus: The geographic distribution of phenotypic and genotypic variants of Orientia tsutsugamushi. Clin Infect Dis 2009;48 Suppl 3:S203‑30. 2. Silpapojakul K, Ukkachoke C, Krisanapan S, Silpapojakul K. Rickettsial meningitis and encephalitis. Arch Intern Med 1991;151:1753‑7. 3. Kim DE, Lee SH, Park KI, Chang KH, Roh JK. Scrub typhus Neurology India | May-Jun 2014 | Vol 62 | Issue 3
9. 10.
encephalomyelitis with prominent focal neurologic signs. Arch Neurol 2000;57:1770‑2. Shih‑Hsien Y, Lih‑Shinn W, Chung‑Chao L, Yu‑Huai H. Scrub typhus complicated by intracranial hemorrhage‑ A case report. Tzu Chi Med J 2005;17:111‑4. Kim JH, Lee SA, Ahn TB, Yoon SS, Park KC, Chang DI, et al. Polyneuropathy and cerebral infarction complicating scrub typhus. J Clin Neurol 2008;4:36‑9. Cowan G. Rickettsial diseases: The typhus group of fevers: A review. Postgrad Med J 2000;76:269‑72. Chrispal A, Boorugu H, Gopinath KG, Prakash JA, Chandy S, Abraham OC, et al. Scrub typhus: an unrecognized threat in South India ‑ clinical profile and predictors of mortality. Trop Doct 2010;40:129‑33. Varghese GM, Mathew A, Kumar S, Abraham OC, Trowbridge P, Mathai E. Differential diagnosis of scrub typhus meningitis from bacterial meningitis using clinical and laboratory features. Neurol India 2013;61:17‑20. Yang CH, Hsu GJ,Peng MY, Young TG. Hepatic dysfunction in scrub typhus. J Formos Med Assoc 1995;94:101‑5. Prakash JA, Abraham OC, Mathai E. Evaluation of tests for serological diagnosis of scrub typhus. Trop Doct 2006;36:212‑3. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.136991
Received: 11‑06‑2014 Review completed: 30‑06‑2014 Accepted: 15‑06‑2014
Vertebral artery thrombosis in a case of traumatic atlantoaxial dislocation with delayed presentation: Emphasis on preoperative evaluation and operative steps to prevent a catastrophe Sir, Vertebral artery (VA) thrombosis and dissection has been documented in cervical spine injuries.[1,2] These vascular injuries are often asymptomatic and their pick up rates have increased with the advent of magnetic resonance imaging (MRI) and MR-angiogram.[2] VA thrombosis following traumatic atlanto‑axial dislocation (TAAD) has rarely been reported. Few case reports have described early reduction and management of injured VA. The intraoperative steps to prevent a catastrophe while handling an injured VA have not been described.[3,4] 303
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
