Case Reports

Indian Pediatrics 2000;37: 203-205

Repeated Unifocal Seizure in Post Neonatal Infants with Hypocalcemia

Kishore S. Agarwal, R.S. Beri and Jacob M. Puliyel

From the Department of Pediatrics and Neonatology, St. Stephen's Hospital, Delhi, India.

Reprint requests: Dr. Kishore S. Agarwal, Department of Pediatrics, St. Stephen's Hospital, Tis Hazari, Delhi 110 054, India. E-mail: puliyel@vsnl.com

Manuscript Received: April 13, 1999;

Initial review completed: May 20, 1999;

Revision Accepted: August 18, 1999

Evidence in literature of repeated unifocal seizures affecting same part of the body and caused by hypocalcemia is rare except in neonates. A medline search yielded only one previous report(1). This case had focal seizure with focal EEG changes due to hypocalcemia.

We report 4 cases of repeated unifocal seizures with hypocalcemia in infants 7 week to 9 month of age.

Case Reports

Case 1: A 3-month-old breastfed male child was admitted to the hospital with a history of repeated clonic seizures of the right upper limb.Each episode lasted from 30 seconds to 1 minute. He had one seizure on the first day and eight on the second day. The parents sought admission on the third day of the illness. He had two seizures in the hospital witnessed by the pediatrician in the ward. He was conscious through the episodes. His serum calcium at admission was 6.2 mg/dl, phosphorous was 5 mg/dl, alkaline phosphatase was 1370 IU, C-reactive protein was negative and the cerebro spinal fluid was clear. CT scan was normal. He was treated with 10% calcium gluconate solution intravenously (2 ml, i.e., 18 mg per kilogram of body weight) followed by oral calcium and vitamin D supplementation and had no further seizures.

Case 2: A 4.4 kg, seven-week-old full term infant was seen with a 6 day history of left sided seizures involving both upper and lower limbs and deviation of the angle of mouth to the left. There was no loss of consciousness. After admission to the hospital four similar fits were witnessed by the resident pediatrician. She was exclusively breastfed. The infant's serum calcium was 6.5 mg/dl. Her blood culture and CSF culture were normal. The C-reactive protein, blood urea nitrogen and serum sodium levels were unremarkable. CT scan done on account of the focal nature of the fits was normal. She had no fits after the administration of intravenous calcium. This was followed by oral administration of calcium and vitamin D.

Case 3: A 5-month-old girl weighing 5.65 kg had a 3 day history of repeated clonic seizures involving the left upper limb. Two of these were documented in the hospital. Her serum calcium was 5.9 mg/dl, serum phsophorus 3.5 mg/dl and alkaline phosphatase was 1714 units. Cranial ultrasound was normal. CSF and blood cultures were sterile. She had no convulsions after the administration of intravenous calcium. This was followed up with oral calcium and vitamin D.

Case 4: A 9-month-old boy weighing 7.5 kg had three focal fits involving the right upper and lower limbs. He was administered intravenous diazepam after the second fit. Three hours later he had the third episode lasting for a few seconds. His serum calcium was 6.5 mg/dl, serum phosphorus was 4.3 mg/dl and alkaline phosphatase was 589 units. Blood and CSF were sterile on culture. He had no fits after intravenous calcium was given. This was followed up with oral calcium and vitamin D supplementation.

The birth histories and blood sugar were normal in all 4 children

All the four cases are being followed up over the last 6-8 months. There have been no subsequent seizures and their milestones and development are normal.

Discussion

Metabolic seizures are usually generalized or multifocal in nature. However unifocal seizures due to hypocalcemia have been known to occur in the neonates(2,3). Incomplete myelination and lack of arborization in the newborn brain prevent the spread of electrical discharges(4_6) and this could result in focal seizures. Focal metabolic seizures are rare beyond the neonatal age. Only one such case has been reported earlier(1) in whom focal EEG changes were documented during hypo-calcemia. Follow up EEG done after 10 days showed no focal discharge.

Each child reported here had repeated seizures affecting the same part of its body. The unifocal seizures affected different areas in each of the four children and it would seem that no regon of the brain is especially susceptible to the adverse effect of hypocalcemia. EEG was not done in our cases but in a given child, the fits recurred in the same part of the body and this suggests that it arose from the same focus in the brain. Neuroimaging study in the form of CT scan done in 2 infants and Ultrasound brain in other two did not shown any focal pathology.

Epileptiform activity which appears to be endogenous, has been recorded in the dentate gyrus before the onset of synchronized seizures and this is termed as cellular bursting. Pan et al. have demonstrated in vivo that local increase in cellular potassium and decrease in calcium results in cellular bursting(6). It is tempting to postulate that cellular bursting may have caused the epileptiform activity in a certain part of the brain in our cases, resulting in repeated unifocal seizures with hypocalcemia. Long term follow-up will be needed to see for how long the deleterious effects last and if such children are prone to focal seizures in the future. It would appear that although not documented widely, focal seizures due to hepocalcemia in post neonatal infants are not uncommon.

References

1. Oki J, Takedatsu M, Itoh J, Yano K, Cho K, Okuno A. Hypocalcemic focal seizures in a one month old infant of a mother with a low circulating level of vitamin D. Brain Dev. 1991; 13: 132-134.

2. Rose AL, Lambroso CT. Neonatal seizure states. A study of clinical, pathological and electroencephalographic features in 137 full term babies with a long term follow-up. Pediatrics. 1970; 45: 404-425.

3. Cockburn F, Brown JK, Belton NR, Forfar JO. Neonatal convulsions associated with primary disturbance of calcium, phosphorous and magnesium metabolism. Arch Dis Child 1973; 48: 99-108.

4. Bernes SM, Kaplon AM. Evolution of neonatal seizure. Pediatr Clin North Am 1994; 41: 1069-1103.

5. Marin-Padilla M. Prenatal and early postnatal ontogenesis of the human motor cortex: A Golgi study 1. The sequential development of the cortical layers. Brain Res 1970; 23: 167-183.

6. Pan E, Stringer JL. Role of potassium and calcium in the generation of cellular bursts in the dentate gyrus. J Neurophysiol 1997; 77: 2293-2299.