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J R Soc Med. 2004 July; 97(7): 332–333.
PMCID: PMC1079528

Epilepsia partialis continua stopped by insulin

S Kumar, MD DM

When epilepsia partialis continua develops late in life, likely causes are brain tumours, cerebral infarction and encephalitis.1 But a benign and treatable cause should not be forgotten.

CASE HISTORY

A man aged 75 had for five days experienced tonic-clonic seizures involving the right side of the face and right upper and lower limbs at a frequency of 20-30 per day. He was conscious during and between episodes. He had noted mild weakness of the right upper and lower limbs. There was no history of fever, exposure to toxins or drugs, alcohol abuse or head injury and he had never previously had a seizure. On examination he was conscious but exhausted. He had a mild right hemiparesis including a right upper motor neuron facial paresis. Power in the right upper and lower limbs was grade 3/5. Sensory and cerebellar systems were normal, and there were no signs of meningeal irritation.

The routine biochemical tests were normal apart from a serum sodium of 132 mmol/L and a blood sugar of 19.4 mmol/L; serum osmolality was 304 mosm/kg. No ketone bodies were present in the urine. Plain and contrast CT of the brain, and MRI done later, revealed nothing of note and the cerebrospinal fluid was normal. In the emergency room he was given intravenous lorazepam followed by phenytoin sodium but the seizures continued; he was then started on midazolam by infusion. To lower the blood sugar he was given insulin (actrapid), at first in intermittent subcutaneous doses and subsequently by continuous infusion. Seizures that had persisted despite midazolam 3 mg/h ceased when the actrapid infusion brought the blood sugar below 8 mmol/L. Therefore the cause of his seizures was judged to be non-ketotic hyperglycaemia and the antiepileptic drugs were withdrawn. He was discharged on oral hypoglycaemic agents and at follow-up three months later he was symptom-free.

COMMENT

Epilepsia partialis continua (EPC) is spontaneous regular or irregular clonic muscle twitching of cerebral cortical origin, sometimes aggravated by action or sensory stimuli, confined to one part of the body, and continuing for hours, days or weeks.2 The clonic jerks can affect any muscle group, the extent ranging from a single muscle or muscle group to widespread involvement. Agonists and antagonists are affected together and distal muscles are more commonly affected than proximal ones. EPC can have many causes (Box 1), and in the present patient the most likely was a cerebrovascular accident. This and a brain tumour were ruled out by CT, and encephalitis was excluded by the normal cerebrospinal fluid. When non-ketotic hyperglycaemia was discovered, the cause was in little doubt.

Box 1
Various aetiologies of epilepsia partialis continua

This is not the first report of EPC as the presenting symptom of diabetes mellitus. In a previous study, EPC led to a diagnosis of diabetes mellitus in 9 of 21 patients;3 and in a group of patients with diabetes mellitus presenting with seizures, 20% had EPC (average duration eight days, seizure frequency 15 per day).4 Hyperglycaemia increases the metabolism of gamma-aminobutyric acid and thereby lowers seizure threshold.5 Mild hyperosmolality, mild hyponatraemia and absence of ketoacidosis may also contribute.3 These factors were present in our patient.

It is particularly important to remember non-ketotic hyperglycaemia as a cause of persistent focal motor seizures since administration of phenytoin may do harm by worsening glycaemic control.6 These patients do not require long-term antiepileptic drug prophylaxis.7

References

1. Schomer DL. Focal status epilepticus and epilepsia partialis continua in adults and children. Epilepsia 1993;34(suppl 1): S29-36 [PubMed]
2. Obeso JA, Rothwell JC, Marsden CD. The spectrum of cortical myoclonus. From focal reflex jerks to spontaneous motor epilepsy. Brain 1985;108: 193-24 [PubMed]
3. Singh BM, Strobos RJ. Epilepsia partialis continua associated with nonketotic hyperglycemia: clinical and biochemical profile of 21 patients. Ann Neurol 1980;8: 155-60 [PubMed]
4. Sabitha KM, Girija AS, Vargese KS. Seizures in hyperglycemic patients. J Assoc Physicians India 2001;49: 723-6 [PubMed]
5. Placidi F, Floris R, Bozzao A, et al. Ketotic hyperglycemia and epilepsia partialis continua. Neurology 2001;57: 534-7 [PubMed]
6. Carter BL, Small RE, Mandell MD, Starkman MT. Phenytoin-induced hyperglycaemia. Am J Hosp Pharm 1981;38: 1508-12 [PubMed]
7. Ozer F, Mutlu A, Ozkayran T. Reflex epilepsy and non-ketotic hyperglycemia. Epileptic Disord 2003;5: 165-8 [PubMed]

Articles from Journal of the Royal Society of Medicine are provided here courtesy of Royal Society of Medicine Press