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| LETTER TO EDITOR |
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| Year : 2011 | Volume
: 59
| Issue : 4 | Page : 631-632 |
Reversible cerebellar ataxia: A rare presentation of depletional hyponatremia
Premkumar Asokumar, Yashpal Vikas Gogate, Prathosh Gangadhar, Anil Bhansali
Department of Endocrinology, PGIMER, Chandigarh, India
| Date of Submission | 15-May-2011 |
| Date of Decision | 15-May-2011 |
| Date of Acceptance | 21-May-2011 |
| Date of Web Publication | 30-Aug-2011 |
Correspondence Address:
Anil Bhansali
Department of Endocrinology, PGIMER, Chandigarh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0028-3886.84356
How to cite this article:
Asokumar P, Gogate YV, Gangadhar P, Bhansali A. Reversible cerebellar ataxia: A rare presentation of depletional hyponatremia. Neurol India 2011;59:631-2 |
Sir,
Hyponatremia is a common medical emergency presenting with neurological manifestations. Cerebellar ataxia as the presenting feature of hyponatremia is extremely uncommon [1],[2] and we present one such case.
A 66-year-old man, a known case of type 2 diabetes, hypertension, and coronary artery disease, presented with vertigo, easy fatigability, and decreased appetite of 7 days duration. Further enquiry revealed imbalance while walking, tendency to fall, and slurred speech. He was on torsemide, spironolactone, telmisartan, and carvedilol for congestive cardiac failure. Neurological examination revealed staccato speech, dysmetria, dysdiadokinesia, limb and gait ataxia, and no nystagmus. He had no other neurological deficits. Investigations revealed serum sodium, 106 meq/l (135-145 mEq/l); potassium, 3.5 mEq/l (3.5-5.5 mEq/l); urea, 61 mg/dl (20-40 mg/dl); creatinine, 0.8 mg/dl (0.7-1.2 mg/dl); urine osmolality, 370 mosm/kg H 2 O (500-800 mosm/ kg H 2 O); serum osmolality, 254 mosm/kg H 2 O (280-290 mosm/kg H 2 O); fT 4 was 1.44 ng/dl (0.7-2.0 ng/dl); Thyroid stimulating hormone(TSH), 0.104 μIU/ml (0.27-4.2 μIU/ml); and 0800hr serum cortisol, 620 nmol/l (171-536 nmol/l). 2D echocardiogram showed severe left ventricular dysfunction with ejection fraction of 20%. Brain magnetic resonance imaging (MRI) done at baseline showed cerebral and cerebellar atrophy with no evidence of central pontine myelinosis (CPM). Dose of diuretic was decreased and he was started on 0.9% normal saline and oral salt supplementation. His serum sodium was normalized over the next 7 days to 143 mEq/l and his cerebellar symptoms improved parallel to correction of hyponatremia. At four weeks of follow up, his neurological examination showed no cerebellar signs. An MRI done at 4 weeks did not show any pontine or extrapontine myelinosis [Figure 1] and [Figure 2].
Our patient had hypovolemic hypotonic hyponatremia, more likely drug induced and he was receiving torsemide, angiotensin receptor blocker, and carvedilol. Cerebellar ataxia as the presenting manifestation of hyponatremia with complete resolution of ataxia with correction of hyponatremia has rarely been described. Misra et al.[1] reported two such patients with resolution of ataxia with correction of hyponatremia in 3 days and both of them had volume depletion as cause of hyponatremia. Kelsey et al.[2] had reported two patients with reversible cerebellar ataxia which improved over 7 days with correction of hyponatremia and in both of them, volume depletion was the cause for hyponatremia. However, in both these case reports, MRI brain was not available but ataxia improved within a period of 3 to 7 days which is unlikely with CPM. Other differential diagnosis for reversible ataxia include alcoholism, Wernicke's encephalopathy, acute intermittent porphyria, carbamazepine toxicity, enteric fever, acute demyelinating encephalomyelitis, and CPM. [3],[4],[5] All these causes were excluded in our patient. Cerebellar ataxia has been reported as a consequence of rapid correction of hyponatremia leading to CPM due to involvement of pontocerebellar fibers and sometimes with extrapontine myelinosis. Usually, in patients with CPM, the neurological signs take a longer duration to recover (3 to 6 months) or the recovery may be partial. [6],[7] In our patient, the cerebellar ataxia is most likely due to hyponatremia and it is possible that the cerebellar atrophy present premorbidly might have contributed to the clinical presentation.
| » References | |  |
| 1. | Misra A, Kumar S, Venkatchalan U, Mukhopadhyay DK, Bhatla B. Cerebellar ataxia due to hyponatremia. Postgrad Med J 1992;68:230-1. 
[PUBMED] [FULLTEXT] |
| 2. | Kelsey SM, Williams AC, Corbin D. Hyponatraemia as a cause of reversible ataxia. Br Med J (Clin Res Ed) 1986;293:1346.
[PUBMED] [FULLTEXT] |
| 3. | Ashton MG, Ball SG, Thomas TH, Lee MR. Water intoxication associated with carbamazepine treatment. Br Med J 1977;1:1134-5.
[PUBMED] [FULLTEXT] |
| 4. | Lipshutz DE, Reiter JM. Acute intermittent porphyria assocociated with inappropriately elevated ADH secretion. JAMA 1974;230:716-7.
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| 5. | Sawney IM, Prabhakar S, Dhand UK, Chopra JS. Acute cerebellar ataxia in enteric fever. Trans R Soc Trop Med Hyg 1986;80:85-6.
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| 6. | Steller U, Koschorek F, Strenge H. Cerebellar ataxia with recovery related to central pontine myelinolysis. J Neurol 1987;235:379-81.
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| 7. | Somarajan A, Paul MB, Kabeer KA, Krishnapriyam SK. Ataxic form of central pontine myelinolysis. Ann Indian Acad Neurol 2007;10:112-4.
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[Figure 1], [Figure 2]
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