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form of primary spinal cysticercosis misdiagnosed as an arachnoid cyst. J Korean Neurosurg Soc 2014;55:226‑9. 4. Qazi Z, Ojha BK, Chandra A, Singh SK, Srivastava C, Patil TB. Isolated intramedullary spinal cord cysticercosis. J Neurosci Rural Pract 2014;5:S66‑8.
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DOI: Figure 2: Magnetic resonance imaging (MRI) dorso-lumbar (DL) spine, T2- 10.4103/0028-3886.152686 weighted images, axial cuts PMID: xxxxx
Reversible onychomadesis following exposure to carbamazepine
Sir, A 10‑year‑old boy presented with a history of recurrent partial seizures with secondary generalization for 2 months. His developmental milestones were normal. His past, as well as family history, were non‑contributory. He had no
Figure 3: (a and b) Histopathological images neurocutaneous markers, and the neurological examination was unremarkable. The electroencephalogram showed left anterior temporal focal epileptiform discharges. He was Patients presenting with acute or progressive neurological started on carbamazepine, the dose of which was slowly deterioration due to compressive symptoms. When the increased over 4 weeks to 400 mg (16 mg/kg). He was also diagnosis is not apparent or in the presence of mass effect, administered folic acid 5mg daily. Three months later, his father [4] the cyst may be surgically excised. The long term usage noticed changes in the nail color. All his nails also became of cysticidal drugs like albendazole and praziquantel are loose [Figure 1]. Examination revealed yellowish discoloration also effective in its management. Corticosteroids are used of all finger and toe nails with onychomadesis [Figure 2]. His as adjuncts to the cysticidal therapy to alleviate symptoms blood counts and serum biochemistry were within normal due to the inflammatory reaction caused by the death of limits. The KOH preparation and culture for fungus were [2] larvae. negative. Possibility of carbamazepine induced nail dystrophy was considered, and he was shifted to levetiracetam 250 mg twice a day. Over the next 4 months, his normal nails slowly Shonali A. Valsangkar, regrew. Hrushikesh Umakant Kharosekar, Deepak A. Palande, Vernon Velho Department of Neurosurgery, Sir Jamsetjee Jeejebhoy Group Nail changes have been associated with various systemic [1,2] of Hospitals and Grant Medical College, Mumbai, Maharashtra, disorders, systemic drug exposures, and infections. The India E‑mail: [email protected] various nail changes reported are; color changes, lateral References or distal detachment of nails (onycholysis), transverse ridging (Beau’s lines), and shedding of nails (onychomadesis). 1. Agrawal R, Chauhan SP, Misra V, Singh PA, Gopal NN. Focal spinal Nail changes secondary to systemic disorders or drug intramedullary cysticercosis. Acta Biomed 2008;79:39‑41. exposures are considered when majority of nails are affected 2. Sinha S, Sharma BS. Neurocysticercosis: A review of current status and management. J Clin Neurosci 2009;16:867‑76. simultaneously. The various drugs causing nail changes are 3. Yoo M, Lee CH, Kim KJ, Kim HJ. A case of intradural‑extramedullary chemotherapeutic agents, psoralens, phenothiazines, lithium,
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oral contraceptives, β‑blockers, heavy metals, anticoagulants, The exact etiopathogenesis of AED‑induced onychomadesis diuretics, oral retinoids, and anticonvulsants.[1] An extensive is not known. AEDs or their metabolites could be inhibiting literature review shows that there are only 10 case reports nail matrix growth in susceptible individuals. Exposure to of nail dystrophy in adults and children secondary to an anticonvulsants such as diphenylhydantoin, trimethadone, antiepileptic drug (AED) exposure.[3‑12] The AEDs reported valproic acid, and carbamazepine during pregnancy is are carbamazepine and valproate. These nail changes are not associated with fingernail and toe-nail hypoplasia in the dose‑related and may be seen at any time during the course newborn.[14,15] Concomitant zinc deficiency, especially with of illness. It has been reported as early as 3 weeks to as valproic acid, has been reported in two adults with secondary late as 3 years after the AED exposure. It may be associated skin and nail changes.[16] However, a subsequent case report with mucocutaneous lesions, alopecia, or Stevens–Johnson has also demonstrated normal zinc levels with AED associated syndrome, and an isolated onychomadesis is indeed very onychomadesis.[10] In another study, studying serum and hair rare. These nail changes are reversible, and normal nail zinc levels in children on sodium valproate therapy, found growth was seen in all cases after discontinuing the offending normal zinc levels. This study, therefore, refutes the role of medication [Table 1]. zinc in the pathogenesis of AED associated onychomadesis.[17]
Onychomadesis shares the same pathogenesis as Beau’s lines, The association of AED‑induced isolated onychomadesis that is, a temporary arrest of nail matrix mitotic activity. Apart is highlighted in our case. These dystrophic nail changes from drug exposure, there are case reports of onychomadesis can present at anytime during the course of therapy. secondary to systemic infections such as scarlet fever or Discontinuing the AED ensures a normal nail growth over hand‑foot‑mouth disease, Kawasaki’s disease, and Stevens – the next few months. Johnson syndrome. Local fungal infections, eczema, or trauma may also lead to onychomadesis.[2,13]
a b Figure 1: (a) Finger nails showing yellowish discoloration (black arrow head) and (b) the thumb showing linear groove at the nail bed (red arrow) Figure 2: Yellowish discoloration
Table 1: Case reports of antiepileptic drug‑induced nail dystrophy Author Case Anticonvulsant Dose Additional Period of Outcome symptoms exposure Mishra et al., 1989 31/M Carbamzepine 600 mg ‑ 4 months Normal nails in 9.5 months Prabhakara and Krupa 1996 14/M Carbamazepine 400 mg ‑ 6 months Normal nails in 5 months Grech and Vella 1999 2/M Sodium valproate 20 mg/kg ‑ 13 weeks Normal nails in 4 weeks Chopra et al., 2000 20/M Carbamazepine ‑ ‑ 3 months Normal nails over 6 months Yasushi et al., 2005 3/M Carbamzepine ‑ ‑ 10 months Not mentioned You et al., 2006 35/M Carbamazepine 200 mg ‑ 4 months Normal nails in 3 months Czajkowski et al., 2007 54/M Carbamazepine 400 mg SJS 2 months Nail outcome not mentioned Poretti et al., 2009 7/M Sodium valproate 20 mg/kg ‑ 48 months Normal nails Icagasioglu et al., 2011 5/F Sodium valproate 20 mg/kg Rash, alopecia 3 weeks Normal nails in 2 months Jenerowicz et al., 2011 30/F Sodium valproate 600 mg Acrocyanosis, 36 months Not mentioned leukonychia, onycholysis Current case 10/M Carbamzepine 400 mg (16 mg/kg) ‑ 3 months Normal nails in 4 months SJS - Stevens‑Johnson syndrome
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Neeraj N. Baheti, Dinesh Kabra, Nitin H. Chandak, B. D. Mehta1, Rajesh R. Agrawal2 Spinal lipoma with tibial Department of Neurology, Central India Institute of hemimelia—incidental or Medical Sciences, 1Department of Dermatology, NKP Salve Medical College, 2Department of Pediatrics, Colours Hospital, causative? Revisiting the Nagpur, Maharashtra, India E-mail: [email protected] McCredie-McBride hypothesis References Sir, 1. Damel CR 3rd, Scher RK. Nail changes secondary to systemic drugs. J Am Acad Deratol 1984;10:250‑8. A 32-year-old female with congenitally short left lower limb 2. Silverman R, Baran R. Nail and appendageal abnormalities. In: [Figure 1] who was able to independently ambulate with Schachner LA, Hansen RC, editors. Pediatric Dermatology. Edinburgh: a crutch presented to the Department of Orthopedics for Mosby; 2003. p. 561‑87. lower limb prosthesis. Her radiographs revealed a Type-1 3. Mishra D, Singh G, Pandey SS. Possible carbamazepine induced reversible onychomadesis. Int J Dermatol 1989;28:460‑1. left tibial hemimelia and a dysplastic femur with a poorly 4. Prabhakara VG, Krupa DS. Reversible onychomadesis induced by developed femoral head and acetabulum [Figure 2]. Hence, a carbamazepine. Indian J Dermatol Venereol Leprol 1996;62:256‑57. custom-made lower limb prosthesis with a pelvic support was 5. Grech V, Vella C. Generalized onycholysis associated with sodium planned. On examination, it was found that there was a tuft valproate therapy. Eur Neurol 1999;42:64‑5. 6. Chopra A, Kaur M, Kular J, Chopra D. Nail changes after carbamazepine. of hair in her lower back [Figure 1] for which a neurosurgical Indian J Dermatol Venereol Leprol 2000;66:103‑4. opinion was sought. On examination, she was continent with 7. Yasushi I, Hirokazu O, Takayoshi T, Kyoko T, Makiko O. no sphincteric dysfunction. The power was normal in the Carbamazepine‑induced reversible onychomadesis: A case report. J Japan Epilepsy Soc 2005;23:14‑7. right lower limb with normal reflexes. The left lower limb 8. You KA, Jeong JA, Nahm SA, Kim EA. A case of carbamazepine induced was flail although some movement was present at all joints. onychomadesis. J Allergy Clin Immunol 2006;117:P227. There was no sensory deficit in the limbs or in the perianal 9. Czajkowski R, Weiss‑Rostkowska V, Wankiewicz A, Drewa T, Placek W, region. There was a varus deformity of the foot [Figure 1]. Biedka M, et al. Stevens‑Johnson syndrome induced by carbamazepine. Acta Pol Pharm 2007;64:89‑92. X-rays of the lumbosacral (LS) spine showed multilevel spina 10. Poretti A, Lips U, Belvedere M, Schmitt B. Onychomadesis: bifida [Figure 2]. Magnetic resonance imaging (MRI) of the A rare side‑effect of valproic acid medication? Pediatr Dermatol LS spine showed an intraspinal lipoma at D11 to L1 levels 2009;26:749‑50. 11. Icagasioglu D, Ayvaz A, Akyol M. Onychomadesis: A new side effect [Figure 3]. This was present more on the left side and the of sodium valproate therapy in children? Arch Neuropsychiatry cord too was thinned out on the left side [Figure 3]. The 2011;48:79‑81. ultrasound abdomen revealed normal kidneys and bladder 12. Jenerowicz D, Szulczynska‑Gabor J, Polanska A, Sadowska‑Przytocka A, with no evidence of residual post-void urine. No surgery was Osmola‑Mankowska A, Czarnecka‑Operacz M. Finger‑nail onycholysis, leukonychia and acrocyanosis in a patient treated with valproic performed but her family was counseled about the possibility acid – Case report. Postepy Dermatol Alergol 2011;28:522‑4. 13. Clementz GC, Mancini AJ. Nail matrix arrest following hand‑foot‑mouth disease: A report of five children. Pediatr Dermatol 2000;17:7‑11. 14. Convey JM, Kriel RL, Birnbaun AK. Antiepileptic drug therapy in children. In: Swaiman KF, Ashwal S, Ferriero DM, editors. Pediatric Neurology Principles and Practice. 4th ed. Philadelphia: Mosby; 2006. p. 1122‑5. 15. Jones KL, Lacro RV, Johnson KA, Adams J. Pattern of malformations in the children of women treated with carbamazepine during pregnancy. a b N Engl J Med 1989;320:1661‑6. Figure 1: Clinical photograph of the patient showing (a) shortened left lower 16. Lewis‑Jones MS, Evans S, Culshaw MA. Cutaneous manifestations of limb with varus deformity of foot and (b) tuft of hair in the lower back on zinc deficiency during treatment with anticonvulsants. Br Med J (Clin the left side Res Ed) 1985;290:603‑4. 17. Altunbasak S, Biatmakoui F, Baytok V, Herguner O, Burgut HR, Kayrin L. Serum and hair zinc levels in epileptic children taking valproic acid. Biol Trace Elem Res 1997;58:117‑25.
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DOI: 10.4103/0028-3886.152687 a b c
PMID: Figure 2: X-rays showing (a) complete agenesis of left tibia with deformed, shortened femur, (b) dysplastic femoral head, and acetabulum with poorly xxxxx formed ilium, and (c) spina bifida in the lumbar spine
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