Letters to the Editor

secreted by small usually benign mesenchymal tumors,[1] which are sometimes difficult to localize. Clinically, patients present with weakness, fatigue, diffuse aches, myopathy and bone pain from osteomalacia.[2] They may also sustain multiple fractures due to poor mineralization of bone and biochemically it is characterized by low serum phosphorus, low urinary phosphorus reabsorption, low or inappropriately normal 1,25(OH)2 vitamin D, high FGF-23 and high PTH. Diagnosis is made by functional imaging[3] (fluorodeoxyglucose PET CT, 68 Ga-dotanoc PET CT and if needed, venous sampling with FGF-23 measurements). Surgery with wide excision of tumor is the treatment of choice and which is curative of disease. In case tumor is not localized, medical therapy with Phosphorus and Calcitriol can be tried until surgery can be performed.

Consultant Endocrinologist2, Care Hospital, Banjara Hills, Hyderabad, Andhra Pradesh, India Department of Pathology3, Krishna Institute of Medical Sciences, Secunderabad. For correspondence: Dr. Hanmayyagari Babulreddy, Flat No. A 904, Sri Sai Ram

Towers, Beside Alwyn Colony, Water Tank, Hafeezpet, Hyderabad - 500 049, Andhra Pradesh, India. E-mail: [email protected]

References 1. 2. 3.

In conclusion, TIO should be included in the differential diagnosis of painful myopathy, as it is rewarding to the physician and gratifying to the patient. This communication in this journal on TIO may provide readers with an opportunity to refresh their knowledge about this rare entity.

Harvey JN, Gray C, Belchetz PE. Oncogenous osteomalacia and malignancy. Clin Endocrinol (Oxf) 1992;37:379-82. Chong WH, Molinolo AA, Chen CC, Collins MT. Tumor-induced osteomalacia. Endocr Relat Cancer 2011;18:R53-77. Khadgawat R, Singh Y, Kansara S, Tandon N, Bal C, Seith A, et al. PET/CT localisation of a scapular haemangiopericytoma with tumour-induced osteomalacia. Singapore Med J 2009;50:e55-7.

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Hanmayyagari Babul Reddy, Guntaka Mounika1, V. Sri Nagesh2, I. Satish Rao3 Consultant Endocrinologist, Krishna Institute of Medical Sciences, Secunderabad, Department of Biochemistry 1 Prime Hospital, K.P.H.B, Kukatpally,

DOI: 10.4103/0972-2327.132657

Alcohol-related seizures: Need for clarity Sir, With regard to the recently published article by Sandeep et al.,[1] we wish to raise a few methodological issues, which can impact the study findings. Most importantly, there is a need for clarity on the criteria for seizures to qualify as alcohol-related seizures (ARS). At the out-set of paper,[1] authors have referred to ARS as ‘adult-onset seizures that occur in the se ing of chronic alcohol dependence’. Contrary to that, the study did not made any a empt to establish a diagnosis of alcohol dependence in patients presenting with seizures. Authors have neither used the standard diagnostic criteria (e.g. WHO ICD-10)[2] nor any diagnostic instrument to establish the same. No criteria were set to operationally define the threshold of amount or duration of alcohol intake at which a patient can be included in the study. The AUDIT, though used in the study, is an instrument meant to detect harmful or hazardous use (at cut-off score of 8) only. The scores over 20 on AUDIT may indicate possible dependence,[3] but it is to be noted that AUDIT was also not employed as a screening tool, rather as an instrument for assessment. Further, it appears from the AUDIT score of sample [21.9 ± 4.86; Table 1] Annals of Indian Academy of Neurology, April-June 2014, Vol 17, Issue 2

that at least a proportion of the patients scored below 20, and comprised of hazardous but non-dependent users. It appears that it was an over-inclusive sample. Coming to question of why it is important to establish dependence in cases of ARS, we wish to emphasize that alcohol-withdrawal seizures can occur only if there is a physical or physiological dependent state. The underlying assumption of the authors that a proportion of alcoholrelated seizures may be induced by alcohol itself remains a hypothesis at best. The methodology of the current study was not geared to prove or disprove this assumption. Rather, there may be a sampling bias. It appears that the patients with new-onset epilepsy presenting to emergency or OPD were included even though the alcohol use may be an incidental or unrelated finding. Nearly 15 of 100 patients in the study did not have any withdrawal symptoms, indicating nondependent alcohol use. Few additional methodological issues are briefly summarized. Authors have mentioned that ‘patients without a prior diagnosis of epilepsy’ were included. Alcohol withdrawal seizures are known to be recurrent, having occurred during the previous abstinent a empts. Whether such patients were

Letters to the Editor

included or not remains unclear from the available description. No objective test (e.g. urinalysis) was employed to rule out concurrent substance abuse, in particular, benzodiazepine use, which has the potential to induce withdrawal seizures similar to alcohol. It has been mentioned that all subjects gave informed wri en consent to participate in the study; however, some patients had delirium as reported in the paper. From an ethical perspective, a mention must be made of the consent from a legal guardian. Table 1 shows mean time interval between alcohol intake to seizure (19.35 ± 35.94 h) where the standard deviation is quite high compared to the mean. Instead, median and range would have conveyed be er information on variance or dispersion from mean. Finally we strongly disagree with one of the inferences in study discussion ‘14 patients in our study had seizures within 6 h of intake of alcohol. When we analyzed this subgroup we found that 8 patients had no significant withdrawal symptoms and the mean lifetime duration of alcohol intake was significantly lower in them compared with the rest…… Hence this group of patients can potentially be considered to have alcohol induced seizures rather than withdrawal seizures’. From the aforementioned pointers, none is conclusively pointing toward a role of alcohol. A person can have seizures even when there is reduction (not necessarily complete cessation) of alcohol use compared to his usual dose. The absence of withdrawal symptoms may also be due to administration of benzodiazepines given for emergency seizure management. There is mixed and contradictory evidence in the literature regarding the role of alcohol in inducing seizures.[4,5] While the issue may be researched further in a separate study, but the above-discussed findings in a small subset of patients should not be taken to assert the link further. From a research perspective, the study ventures into an important area. However, it is important to study it using a rigorous methodology and refining the operational criteria for inclusion in the study.


Raman Deep Pattanayak National Drug Dependence Treatment Centre, Department of Psychiatry, All India Institute of Medical Sciences, New Delhi, India For correspondence: Dr. Raman Deep Pattanayak, Assistant Professor, NDDTC,

Department of Psychiatry, All India Institute of Medical Sciences, Ansari Nagar, New Delhi - 110 029, India. E-mail: [email protected]

References 1.

2. 3.



Sandeep P, Cherian A, Iype T, Chitra P, Suresh MK, Ajitha KC. Clinical profile of patients with nascent alcohol related seizures. Ann Indian Acad Neurol 2013;16:530-3. World Health Organization. The ICD-10 Classification of Mental and Behavioral Disorders. Geneva: WHO; 1992. Babor TF, Higgins-Biddle JC, Saunders JB, Monteiro MG, editors. AUDIT: The Alcohol Use Disorders Identification Test: Guidelines for Use in Primary Care, 2nd ed. Geneva: World Health Organization; 2006. Leone M, Bottacchi E, Beghi E, Morgando E, Mutani R, Amedeo G, et al. Alcohol use is a risk factor for a first generalized tonicclonic seizure. The ALC.E. (Alcohol and Epilepsy) Study Group. Neurology 1997;48:614-20. Leone M, Tonini C, Bogliun G, Monaco F, Mutani R, Bottacchi E, et al. Chronic alcohol use and first symptomatic epileptic seizures. J Neurol Neurosurg Psychiatry 2002;73:495-9. Access this article online Quick Response Code:

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DOI: 10.4103/0972-2327.132660

Seasonal and monthly trends in the occurrence of Guillain-Barre syndrome over a 5-year period: A tertiary care hospital-based study from South India Sir, Seasonal variations have not been adequately studied in Guillain-Barre Syndrome (GBS). During our clinical practice, it was observed that there was clustering in the occurrence of GBS during certain seasons and months of the year. We did a retrospective study in our institute, a tertiary care center in South India from June 2008 to May 2013, in the departments of Neurology, Medicine, and Pediatrics to analyze the monthly and seasonal occurrence of GBS. The outpatient and inpatient records of all patients who had presented to our hospital with symptoms of acute flaccid paralysis were reviewed retrospectively from June 2008 to May 2013 with special

a ention to the time of occurrence with respect to month and season. A diagnosis of GBS was made when the clinical features, electrophysiological findings, and CSF parameters satisfied the Asbury and Cornblath diagnostic criteria.[1] Patients with other causes of acute flaccid quadriparesis like acute transverse myelitis, hypokalemic paralysis, polymyositis, and myasthenia gravis were excluded. The seasons in India were divided as: Summer: March to May; Monsoon: June to September; PostMonsoon: October to November: Winter: December to February according to the seasonal classification of Indian Meteorological Department.[2] Annals of Indian Academy of Neurology, April-June 2014, Vol 17, Issue 2

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