6.

7.

8. 9. 10. 11. 12. 13. 14.

Letters to the Editor Noachtar S, Andermann E, Meyvisch P, Andermann F, Gough WB, Schiemann-Delgado J, et al. Levetiracetam for the treatment of idiopathic generalized epilepsy with myoclonic seizures. Neurology 2008;70:607-16. Huber B, Bömmel W, Hauser I, Horstmann V, Liem S, May T, et al. Efficacy and tolerability of levetiracetam in patients with therapy-resistant epilepsy and learning disabilities. Seizure 2004;13:168-75. Rösche J, Pohley I, Rantsch K, Walter U, Benecke R. Experience with levetiracetam in the treatment of status epilepticus. Fortschr Neurol Psychiatr 2013;81:21-7. Eggers C, Burghaus L, Fink GR, Dohmen C. Epilepsia partialis continua responsive to intravenous levetiracetam. Seizure 2009;18:716-8. Haase CG, Hopmann B. Epilepsia partialis continua successfully treated with levetiracetam. J Neurol 2009;256:1020-1. Alsaadi TM, Koopmans S, Apperson M, Farias S. Levetiracetam monotherapy for elderly patients with epilepsy. Seizure 2004;13:58-60. Abou-Khalil B. Levetiracetam in the treatment of epilepsy. Neuropsychiatr Dis Treat 2008;4:507-23. Nakken KO, Eriksson AS, Lossius R, Johannessen SI. A paradoxical effect of levetiracetam may be seen in both children and adults with refractory epilepsy. Seizure 2003;12:42-6. Trinka E, Marson AG, Van Paesschen W, Kälviäinen R, Marovac J, Duncan B, et al. KOMET: An unblinded, randomised, two parallelgroup, stratified trial comparing the effectiveness of levetiracetam

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with controlled-release carbamazepine and extended-release sodium valproate as monotherapy in patients with newly diagnosed epilepsy. J Neurol Neurosurg Psychiatry 2012. [Epub ahead of print] 15. Callenbach PM, Arts WF, ten Houten R, Augustijn P, Gunning WB, Peeters EA, et al. Add-on levetiracetam in children and adolescents with refractory epilepsy: Results of an open-label multi-centre study. Eur J Paediatr Neurol 2008;12:321-7. 16. Szucs A, Clemens Z, Jakus R, Rásonyi G, Fabó D, Holló A, et al. The risk of paradoxical levetiracetam effect is increased in mentally retarded patients. Epilepsia 2008;49:1174-9. 17. Cormier J, Chu CJ. Safety and efficacy of levetiracetam for the treatment of partial onset seizures in children from one month of age. Neuropsychiatr Dis Treat 2013;9:295-306.

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DOI: 10.4103/0972-2327.120430

Bilateral facial nerve palsy: A rare association with hepatitis A Sir, A 17-year-old female presented with a history of sudden onset of inability to close eyes, epiphora as well as inability to drink fluids from cup associated with drooling of fluids along the corners of the mouth bilaterally of 2 days duration. There was no associated history of taste disturbances or hearing abnormalities in either of the ears. No other associated cranial nerve disturbances or long tract symptoms were present. No associated fever, cough, headache, vomiting or other relevant systemic symptoms. Examination was unremarkable except for bilateral lower motor neuron type of facial nerve palsies with sparing of taste sensation and without hyperacusis. A clinical diagnosis of bilateral lower motor neuron facial palsy was made with the possible anatomical site distal to the origin of nerve to stapedius muscle. On detailed assessment, she revealed to have been convalescing from an episode of jaundice, which she had acquired 1 month prior to the onset of the present focal deficit. Work-up was carried out to find out the etiology of bilateral facial palsy. Hemogram parameters were within normal limits including erythrocyte sedimentation rate. (hemoglobin –11.9 g/dl [10-12], total leucocyte count –4580 cells/cumm [4000-11,000], differential count [P –62%, L –30%, M –2%, E –6%] platelet count - 1,89,000 [1,50,000-4,00,000]). Liver function parameters had normalized (S. bilirubin - 0.4 mg/dl [0-1.3], conjugated bilirubin - 0.2 mg/dl, serum glutamic axaloacetic transaminas –16 U/L [0-36], serum glutamic pyruvic transaminas –31 U/L [0-52], alkaline phosphatase –59 U/L [38-126], total protein –7.8 g/dl [6.0-8.2], S. albumin –4.5 g/dl

[3.5-5.0]). Metabolic parameters were normal: S. calcium –9.1 mg/dl (8.4-10.2), S. phosphorous –3.5 mg/dl (2.5-4.5) and S. creatinine –0.8 mg/dl (0.7-1.2). Viral markers were assessed: Human immunodeficiency virus - non-reactive by enzymelinked immunosorbent assay (ELISA), herpes simplex 1, 2 immunoglobulin (Ig)M and IgG antibody (ELISA): Negative, hepatitis B surface antigen (ELISA)-negative, anti-hepatitis C virus-negative, anti-hepatitis E virus IgM (ELISA)-negative, anti-hepatitis A virus (HAV) IgM (ELISA)-positive; 2.66 EU/ ml (cut-off value: 0.600 EU/ml). Serum angiotensin converting enzyme levels were 102.0 IU/L (8-65). Nerve conduction studies revealed bilateral facial nerve axonopathy only. Neuroimaging study [gadolinium contrast enhanced magnetic resonance imaging brain with constructive interference in steady state (CISS) sequences] did not reveal any structural pathology. High resolution computerised tomography scan of the chest did not reveal any structural pathology. Mantoux test was borderline positive (8 mm induration at 72 h). Cerebrospinal fluid evaluation was not performed in view of lack of any clue towards meningeal based pathology. As the dedicated work up for etiology of bilateral lower motor neuron type facial palsy was negative, we postulated it to be probably an immune phenomenon as a consequence to the recent HAV infection from, which she was convalescing. With conservative neurorehabilitative measures and facial nerve stimulation procedures our patient had significant improvement in her neurological status over duration of 8 weeks.

Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4

730

Letters to the Editor

Only a handful of reports are present in the world literature stating the association of hepatitis A with Bell’s palsy, with majority of them being unilateral.[1-3] A recent review on the prevalence of serological markers of hepatitis, cytomegalovirus and rubella in patients with Bell’s palsy revealed a serological positivity for hepatitis B in 15 out of 21 patients (71%) as against 32.1% positivity in the control group. No relation was noted in the above study with hepatitis A serological positivity.[4] Neurological complications during the acute and convalescent phase of acute HAV infection have been reported in the form of aseptic meningitis, cranial neuropathies (trigeminal, facial, vestibulocochlear) and visual disturbances. However, bilateral facial nerve palsies associated with recent acute HAV infection has not been reported so far. The purpose of this letter is to make health care professionals more aware of facial palsy complication of hepatitis A infection. Even though a rare association, the common viral tests for facial palsy could include hepatitis viruses especially, if there is past history suggestive of acute hepatitis.

For correspondence: Dr. Sudhir Sharma, Department of Neurology,

Indira Gandhi Medical College, Shimla - 171 001, Himachal Pradesh, India E-mail: [email protected]

References 1.

Swaroop A, Parihar N, Jain S. Bell’s palsy — A rare association with hepatitis A. J Indian Acad Clin Med 2008;9:51-2. 2. Thapa R, Mallick D, Biswas B, Ghosh A. Childhood hepatitis A virus infection complicated by Bell’s palsy. Clin Pediatr (Phila) 2009;48:427-8. 3. Yildiz B, Yakut A, Bor O, Yarar C. Bell’s palsy and hepatitis infection. Pediatr Int 2006;48:493-4. 4. Unlu Z, Aslan A, Ozbakkaloglu B, Tunger O, Surucuoglu S. Serological examinations of hepatitis, cytomegalovirus and rubella in patients with Bell’s palsy. Am J Phys Med Rehabil 2003;82: 28-32. Access this article online Quick Response Code:

Website: www.annalsofian.org

Sudhir Sharma, Praveen Kesav1 DOI: 10.4103/0972-2327.120432

Departments of Neurology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, 1Postgraduate Institute of Medical Education & Research, Chandigarh, India

Racemose neurocysticercosis and reversible dementia Sir, The recent publication on racemose neurocysticercosis (NCC) and reversible dementia is very interesting.[1] Sharma et al. reported that “The outcome of dementia patients with NCC seems favorable in most cases; therefore, a high index of suspicion for NCC should be kept, especially in endemic areas.”[1] Indeed, the neurological symptom is not rate in NCC. Indeed, the existing of dementia and cognitive function impairment in NCC is more common in non-calcified active NCC. [2] Nearly, 40% of all non-calcified active NCC can present with dementia. In the real life, dementia might be lately detected and clinical work-up does usually not include looking for NCC. Focusing on the outcome; although, the present report showed favorable outcome.[1] Some previous reports mentioned for discordant observation after complete treatment.[3]

For correspondence: Mrs. Somsri Wiwanitkit, Wiwanitkit House,

Bangkhae, Bangkok, Thailand. E-mail: [email protected]

References 1.

Sharma S, Modi M, Lal V, Prabhakar S, Bhardwaj A, Sehgal R. Reversible dementia as a presenting manifestation of racemose neurocysticercosis. Ann Indian Acad Neurol 2013;16:88-90. 2. Rodrigues CL, de Andrade DC, Livramento JA, Machado LR, Abraham R, Massaroppe L, et al. Spectrum of cognitive impairment in neurocysticercosis: Differences according to disease phase. Neurology 2012;78:861-6. 3. Ciampi de Andrade D, Rodrigues CL, Abraham R, Castro LH, Livramento JA, Machado LR, et al. Cognitive impairment and dementia in neurocysticercosis: A cross-sectional controlled study. Neurology 2010;74:1288-95. Access this article online

Somsri Wiwanitkit, Viroj Wiwanitkit1,2,3

Quick Response Code:

Wiwanitkit House, Bangkhae, Bangkok, Thailand, 1Hainan Medical University, China, 2 Faculty of Medicine, University of Nis, Serbia, 3 Joseph Ayobabalola University, Nigeria Annals of Indian Academy of Neurology, October-December 2013, Vol 16, Issue 4

Website: www.annalsofian.org

DOI: 10.4103/0972-2327.120434

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