Letters to the Editor

vasculopathy involving posterior circulation. Jayakumar, et al.,[4] in their series reported that posterior circulation is frequently involved in MMD as evident by angiography; ischemic events of the posterior circulation are not frequent, as the posterior circulation acts as collateral pathway for the diseased anterior circulation till the later stage. Mugikura, et al., [5] reported high prevalence of clinical strokes and infarctions in patients diagnosed before 4 years of age, associated with advanced steno‑occlusive lesions of the posterior cerebral artery (PCA). To conclude, this is the first report of sporadic exaggerated startle syndrome  (sporadic hyperekplexia) in association with MMD. This case suggests that moyamoya syndrome should be considered in differential diagnosis of exaggerated startle response especially on the background of strokes in childhood.

Rajendra Singh Jain, Rahul Jain, Tarun Mathur, B.S Raghavendra

Rajasthan, India. E‑mail: [email protected]

References 1. Gonzalez‑Alegre P, Ammache Z, Davis PH, Rodnitzky RL. Moyamoya induced paroxysmal dyskinesia. Mov Disord 2003;18:1051‑6. 2. Baik JS, Lee MS. Movement disorders associated with moyamoya disease: A report of 4 new cases and review of literatures. Mov Disord 2010;25:1482‑6. 3. Fahn S, Jankovik J, editors. Principles and Practice of Movement Disorders. Philadelphia: Churchill Livingstone; 2007. p. 527‑8. 4. Jayakumar PN, Vasudev MK, Srikanth SG. Posterior circulation abnormalities in moyamoya disease: A radiological study. Neurol India 1999;47:112‑7. 5. Mugikura S, Higano S, Shirane R, Fujimura M, Shimanuki Y, Takahashi S. Posterior circulation and high prevalence of ischemic stroke among young pediatric patients with moyamoya disease: Evidence of angiography‑based differences by age at diagnosis. AJNR Am J Neuroradiol 2011;32:192‑8. Access this article online Quick Response Code:

Department of Neurology, Sawai ManSingh Medical College, Jaipur, Rajasthan, India

Website: www.annalsofian.org

DOI: 10.4103/0972-2327.120439

For correspondence:

Dr. Rajendra Singh Jain, Department of Neurology, Sawai Man Singh Medical College, Jaipur ‑ 302 004,

A rare presentation of methanol toxicity Dear Sir, We read with great interest the article entitled “A rare presentation of methanol toxicity” by Gupta et al.,[1] Indeed the presentation of methanol toxicity can be variable, with high anion gap metabolic acidosis, visual abnormalities, obtundation, and neurological deficit often associated with death. We also came across a case recently, which was associated with acute onset blindness with encephalopathy after consumption of methanol wherein MRI findings showed bilateral putaminal hemorrhagic necrosis. Patient, however, showed remarkable recovery on follow‑up visits. The reported patient here had sudden onset vision loss after consumption of country liquor. Curiously, fundus findings suggestive of presence of any optic atrophy have not been mentioned. Also the possible explanation of sluggishly reacting pupils in the above patient is not clear. It would have been extremely helpful if the value of P100 latencies on visual evoked response had been mentioned. Also the prolonged latencies were due to demyelination or falsely positive due to cortical blindness the patient was having, has not been clearly ascertained. The patient had infarcts in areas supplied by various vessels and the mechanism given by

authors is cerebral vasospasm but specifically which vessel is involved has not been mentioned, also the lacunae was that, it had not been confirmed by either CT angiography/MR angiography or Digital subtraction angiography. The reported patient is of 51 years of age, so possibility of other vascular risk factors cannot be denied but the authors did not consider either echocardiography or Carotid Doppler in their patient; therefore, looking into the possibility of infarcts involving multiple territory a cardio‑embolic source rather than concomitant country liquor consumption is highly likely. Hence, whether the infarcts were due to methanol intoxication or just an incidental finding is still not clear. The characteristic neuroimaging findings of bilateral hemorrhagic necrosis, cerebral and intra‑ventricular hemorrhage, cerebellar necrosis, and diffuse cerebral edema have been described as sequelae to severe methanol intoxication. Putaminal hemorrhagic necrosis results from direct toxic effect of methanol metabolites and metabolic acidosis. It often has poor prognosis, i.e.,  either death or vegetative state.[2‑4] In a country like ours where easy availability of spurious liquor has been a concern, this article highlighted about the variable presentation of methanol poisoning and that timely institution of treatment can be indeed life‑saving.

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

Letters to the Editor

Trilochan Srivastava, Kadam Nagpal Department of Neurology, Sawai Man Singh Medical College, Jaipur, Rajasthan, India For correspondence: Dr. Trilochan Srivastava, Department of Neurology,

Sawai Man Singh Medical College, Jaipur ‑ 302 004, Rajasthan, India. E‑mail: [email protected]


intoxication. AJNR Am J Neuroradiol 1995;16:1783‑6. 3. Kuteifan K, Oesterlé H, Tajahmady T, Gutbub AM, Laplatte G. Necrosis and haemorrhage of the putamen in methanol poisoning shown on MRI. Neuroradiology 1998;40:158‑60. 4. Blanco M, Casado R, Vázquez F, Pumar JM. CT and MR imaging findings in methanol intoxication. AJNR Am J Neuroradiol 2006;27:452‑4. Access this article online Quick Response Code:

Website: www.annalsofian.org

References 1. 2.

DOI: 10.4103/0972-2327.120440

Gupta N, Sonambekar AA, Daksh SK, Tomar L. A rare presentation of methanol toxicity. Ann Indian Acad neurol 2013;16:249‑51. Gaul HP, Wallace CJ, Auer RN, Fong TC. MR findings in methanol

Authors' reply: A rare presentation of methanol toxicity Dear Sir, In our manuscript, the MRI of the brain had hemorrhagic conversion of infarct in bilateral parasagittal, parieto-occipital region. An acute infarct was seen in the right cerebellum. There were punctate infarcts in bilateral frontal regions.[1] We would like to point out that the information given by Taheri et al.[2] is quite different from that given in our manuscript. Our patient had hemorrhagic conversion of infarct in bilateral parasagittal, parieto-occipital region, which is rare. Hemorrhage in the putamen has been described.[3] Also, infarct in the frontal lobe in case of methanol poisoning has been described by Ashan et al.[4] and Chen et al.,[5] as per the PUBMED search, which is a rare finding and definitely not reported for the first time. Sefidbakht et al.[6] described bilateral necrosis of the basal ganglia along with other brain lesions which include edema, necrosis of subcortical white and gray matter, cerebellar cortical lesions, subarachnoid hemorrhage, bilateral intracerebral hemorrhage, bilateral tegmental necrosis, and diffuse cerebral edema. Again, there is not any mention of the areas and nature of lesions on the MRI found in our case report. The lesions described in the case report were a mixture of the lesions that have been described in different case series and reports. To our knowledge, hemorrhagic conversion in case of infarcts in methanol poisoning has not been described. Lastly, frontal infarcts in methanol poisoning have been described in only two case reports as mentioned above. Moreover, the typical feature in our case was a mixture of lesions that have been described in different case series and reports.

Department of Medicine, UCMS and GTB Hospital, New Delhi, India For correspondence: Dr. Nikhil Gupta, Department of Medicine, GTB Hospital,

Shahdara, New Delhi - 110 095, India. E-mail: [email protected]

References 1. Gupta N, Sonambekar AA, Daksh SK, Tomar LK. A rare presentation of methanol toxicity. Ann Indian Acad Neurol 2013;16:249‑51. 2. Taheri MS, Moghaddam HH, Moharamzad Y, Dadgari S, Nahvi V. The value of brain CT findings in acute methanol toxicity. Eur J Radiol 2010;73:211-4. 3. Pelletier J, Habib MH, Khalil R, Salamon G, Bartoli D, Jean P. Putaminal necrosis after methanol intoxication. J Neurol Neurosurg Psychiatry 1992;55:234-5. 4. Ahsan H, Akbar M, Hameed A. Diffusion weighted image (DWI) findings in methanol intoxication. J Pak Med Assoc 2009;59:321-3. 5. Chen JC, Schneiderman JF, Wortzman G. Methanol poisoning: Bilateral putaminal and cerebellar cortical lesions on CT and MR. J Comput Assist Tomogr 1991;15:522-4. 6. Sefidbakht S, Rasekhi AR, Kamali K, Borhani Haghighi A, Salooti A, Meshksar A, et al. Methanol poisoning: Acute MR and CT findings in nine patients. Neuroradiology 2007;49:427-35. Access this article online Quick Response Code:

Website: www.annalsofian.org

Nikhil Gupta, Ajinkya Ashok Sonambekar, Sunil Kumar Daksh, Laxmikant Tomar

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

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