Letters to Editor

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Figure 1: (a) Computed tomography scan head showing bilateral globus pallidus hypodensities (b) magnetic resonance imaging (MRI) brain (gadolinium enhanced) showing nonenhancing T1 hypointensity in bilateral pallidal regions and subcortical paraventricular white matter (c) MRI brain showing T2 hyperintensities in bilateral pallidal regions and subcortical paraventricular white matter

Table 1: Conditions presenting with bilateral symmetrical globus pallidus lesions Carbon monoxide poisoning Cyanide poisoning Heroin/3.4 methylenedioxy‑N‑ methylamphetamine (MDMA; Ecstasy) Kernicterus Neurodegeneration with brain iron accumulation Pantothenate kinase associated Hepatic encephalopathy degeneration Methylmalonic academia Neurofibromatosis type‑1

of dopamine. Carbon disulfide induces severe microangiopathy and lesions of basal ganglia particularly pallidoputamen.[2] In the acute phase, enhancement of pallidal lesions has been reported. The gadolinium enhancement disappears later due to restoration of blood brain barrier.[1,3] Extensive signal changes in bilateral subcortical white matter observed in our patient have not been typically reported in literature. There are reports of delayed onset disulfiram‑related toxicity with clinical and radiological manifestations developing as late as 30 years after disulfiram treatment.[4] Our patient did not show signal changes in substantia nigra on MRI as reported in some earlier studies.[5] There is resurgence of interest in disulfiram after its’ reported value in treating cocaine and other stimulant dependence.[6] Disulfiram neurotoxicity should be considered in patients presenting with acute encephalopathy and parkinsonism. While symmetrical T2 basal ganglia hyperintensities are observed in other conditions as well [Table 1], pallidoputaminal lesions with greater involvement of globus pallidus on MRI brain indicates disulfiram toxicity in appropriate clinical setting.

Bhupender Kumar Bajaj, Anand Singh Department of Neurology, Post Graduate Institute of Medical Education and Research and Dr. Ram Manohar Lohia Hospital, New Delhi, India E‑mail: [email protected] 540

References 1. Lemoyne S, Raemakers J, Daems J, Heytens L. Delayed and prolonged coma after acute disulfiram overdose. Acta Neurol Belg 2009;109:231‑4. 2. Chuang WL, Huang CC, Chen CJ, Hsieh YC, Kuo HC, Shih TS. Carbon disulfide encephalopathy: Cerebral microangiopathy. Neurotoxicology 2007;28:387‑93. 3. Boukriche Y, Weisser I, Aubert P, Massoon C. MRI findings in a case of late onset disulfiram induced neurotoxicity. J Neurol 2000;247:714‑5. 4. Borrett D, Ashby P, Bilbao J, Carlen P. Reversible late onset disulfiram‑induced neuropathy and encephalopathy. Ann Neurol 1985;17:396‑9. 5. Park JW, Chung SW, Lee SJ, Lee KS, Kim BS. Selective vulnerability of nigrostriatopallidal dopaminergic pathway after disulfiram intoxication: Two cases with clinical and magnetic resonance study. Eur J Radiol Extra 2003;46:1‑5. 6. Kosten TR, Wu G, Huang W, Harding MJ, Hamon SC, Lappalainen J, Nielsen DA. Pharmacogenetic randomized trial for cocaine abuse: Disulfiram and dopamine beta hydroxylase. Biol Psychiatry 2013;73:219‑24. Access this article online Quick Response Code:

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121944

Received: 29‑08‑2013 Review completed: 03‑09‑2013 Accepted: 13‑10‑2013

Facial pain in carcinoma colon Sir, A 26‑year‑male, operated case of adenocarcinoma transverse colon, presented with left facial pain and Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5

Letters to Editor

numbness. Clinical examination was revealed sensory deficit on the left side of face. Brain magnetic resonance imaging(s) revealed abnormal T2/fluid‑attenuated inversion recovery hyperintense oval lesions causing diffuse enlargement of cisternal part of left trigeminal nerve [Figure 1a and b, thick arrow] and both trigeminal ganglia in Meckel’s cave [Figure 1a and b, thin arrows]. Three dimensional‑T2W‑driven equilibrium radiofrequency reset pulse axial and sagittal oblique images excellently demonstrated the spread along trigeminal pathways [Figure 1c-e]. These lesions appear heterogeneously hypointense on pre‑contrast T1‑weighted images [Figure 2a]. Post‑contrast scan shows homogenous enhancement of mass lesions as long cisternal part of left trigeminal nerve and both trigeminal ganglia [Figure 2b‑d].

No extension was seen along the branches of trigeminal nerves. Brainstem revealed no focal lesion at the expected location of trigeminal nuclei. These findings are suggestive of bilateral trigeminal metastasis. This case illustrates the classic imaging findings in metastatic spread along central trigeminal pathways. Patient is being treated with palliative radiotherapy. Malignant trigeminal neuropathy is commonly due to perineural spread along the branches of trigeminal nerve secondary to squamous cell carcinomas and adenoid cystic carcinomas in head and neck region. Trigeminal nerve metastasis is uncommon reported manifestation in breast cancer, melanoma and colon cancer.[1,2] To the best of our knowledge; bilateral trigeminal metastasis with trigeminal ganglion involvement due to metastatic colon carcinoma is not reported.

Prashant S. Naphade, Abhishek R. Keraliya Department of CT/MRI, ESIC Hospital, Mumbai, Maharashtra, India [email protected] a

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1. Mastronardi L, Lunardi P, Osman Farah J, Puzzilli F. Metastatic involvement of the Meckel’s cave and trigeminal nerve. A case report. J Neurooncol 1997;32:87‑90. 2. Hirota N, Fujimoto T, Takahashi M, Fukushima Y. Isolated trigeminal nerve metastases from breast cancer: An unusual cause of trigeminal mononeuropathy. Surg Neurol 1998;49:558‑61.

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Figure 1: Axial T2 (a) and fluid‑attenuated inversion recovery (b) images reveal hyperintense mass lesions causing diffuse enlargement of cisternal part of left trigeminal nerve (thick arrow) and both trigeminal ganglia (thin arrows). Driven equilibrium radiofrequency reset pulse (three dimensional‑T2W‑driven equilibrium radiofrequency reset pulse) axial (c), reformatted right (d) and left (e) sagittal oblique images excellently demonstrates spread along trigeminal pathways

Access this article online Quick Response Code:

Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.121945

Received: 17‑10‑2013 Review completed: 17-10-2013 Accepted: 24‑10‑2013

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Figure 2: Pre‑contrast T1 axial (a) reveals hypointense mass lesions along cisternal part of left trigeminal nerve and both trigeminal ganglia with homogenous enhancement on post‑contrast T1 axial (b), reformatted right (c) and left (d) sagittal oblique images

Neurology India | Sep-Oct 2013 | Vol 61 | Issue 5

Spinal epidural hematoma with myelitis and brainstem hemorrhage: An unusual complication of dengue fever Sir, Dengue fever is the commonest arboviral disease.[1] The common neurologic complications include encephalitis and encephalopathy. Hemorrhagic complications due 541

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