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| Year : 1999 | Volume
: 47
| Issue : 3 | Page : 244-5 |
Idiopathic hypoparathyroidism presenting as epilepsy in a 40 years female.
Garg R, Garg N, Tandon N, Khurana ML, Ammini AC
How to cite this article:
Garg R, Garg N, Tandon N, Khurana M L, Ammini A C. Idiopathic hypoparathyroidism presenting as epilepsy in a 40 years female. Neurol India 1999;47:244 |
Idiopathic hypoparathyroidism presents most commonly in the age group of 5-10 years.[1] The disease may be familial or sporadic. The familial form is commonly associated with other endocrine abnormalities e.g. Addison's disease, Graves disease, premature gonadal failure etc. The patient may come with hypocalcaemic symptoms like carpopedal spasm, perioral paraesthesias and numbness in limbs. However, overt tetany is rare due to the chronic nature of hypocalcaemia.[1] Hypocalcaemia is associated with hyperphosphataemia. The diagnosis is often missed or delayed if the presentation is at an older age. We report a case of late onset epilepsy due to idiopathic hypoparathyroidism (IH) in a 40 years old lady.
The patient was a 40 year old female who complained of generalized tonic clonic seizures for the last 4 years. The seizures used to occur once in every 2-3 months. The patient was treated with phenytoin sodium in a dose of 300 mg per day along with phenobarbitone 60 mg per day, but seizures were not controlled. There was history of seizures responding to intravenous injection of calcium during an acute episode. The patient was operated for bilateral cataract one year before coming to us. On examination, she was found to be in good health except that she had positive Chvostek's and Trousseau's signs. Nervous system examination was normal. Investigations revealed a serum calcium level of 6.4 mg/dl (normal - 8.5-10.5 mg/dl) and serum phosphate level of 6.4 mg/dl (normal - 2.5-4.5 mg/dl). Serum albumin was 4.0 G/dl (normal - 3.8-4.0 G/dl) and renal function tests were normal. Serum alkaline phosphatase level was 8.8 KA units (normal - 3-13 KA units). Serum parathyroid hormone levels were 28 pg/ml (normal - 11-55 pg/ml) which were inappropriately low in the presence of hypocalcaemia. Plasma cortisol, thyroxin and gonadotropins were within normal range. EEG showed generalized spike and wave pattern. CT scan of the head was normal.
A low serum calcium, normal PTH and high phosphate values are all consistent with the diagnosis of idiopathic hypoparathyroidism. History of cataract indicates that hypocalcaemia had been present for quite some time. Epilepsy may be related to IH itself in this case. The neuronal irritability may be increased by hypocalcaemia leading to epilepsy. EEG abnormalities have been described in IH. Nagashima et al[2] reported bilaterally synchronous sharp and slow wave discharges of unusually long duration in IH and called it parathyroid epilepsy. The seizures are often difficult to control in these patients with antiepileptic drugs alone. Treatment of hypocalcaemia controls the seizure disorder much better.[3],[4] In some cases anticonvulsant treatment may no longer be required.
All these neurological disorders show marked improvement or complete reversal on treatment with alpha hydroxylated form of vitamin D. The treatment has to be life long. Calcium levels should be periodically checked and maintained at low normal values to avoid the risk of renal stones in these cases. Serum calcium should be measured in all cases of epilepsy, dementia and cerebellar ataxia. If due to IH these conditions may get reversed with treatment of hypocalcaemia.
| 1. | Fitzpatrick LA, Arnold A : Hypoparathyroidism. In : DeGroot LJ (eds). Endocrinology, W.B. Saunders. Philadelphia 1995; 2 : 1123-1135.  |
| 2. | Nagashima C, Kubota S : Parathyroid epilepsy with continuous EEG abnormality. Clin Electroencephalogr 1981; 12 : 133-138. |
| 3. | Roca B, Minguez C, Saez-Royuela A et al : Dementia, myopathy and idiopathic hypoparathyroidism (letter). Postgrad Med J 1995; 71 : 702. |
| 4. | Smits M, Gabreels F, Froeling P et al : Autosomal dominant idiopathic hypoparathyroidism and nervous system dysfunction : report of three cases and review of literature. J Neurol 1982; 228 : 113-122. |
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