Self-limiting symptomatic peri-ictal bradyarryhthmia due to junctional AV rhythm
A 66-year-old gentleman had generalized tonic-clonic seizures (GTCS) since the age of 14 years, which was well controlled for nearly two to three decades with antiepileptic drug (AED) viz., phenytoin – 300 mg/day and phenobarbitone – 120 mg/day. Cranial CT scan was reported to be normal. For the last 10 months, there was recurrence of seizures. The seizure frequency was 1-2 episodes per month in spite of polypharmacy with valproate (900 mg/day), carbamazepine (800 mg/day) and phenobarbitone (120 mg/day). He did not have any comorbid illnesses such as ischemic heart disease, diabetes mellitus or hypertension.\nHe was presented to us 3 days following an episode of GTCS with a confusional state. Initial examination revealed a disoriented patient with gait ataxia, fine tremor of outstretched hands, pes cavus and hammer toes and diminished ankle jerks. There were no other neurological or systemic deficits. Routine investigations including hemogram were within normal limits. Routine ECG on admission was normal. Scalp EEG at admission showed generalized slowing in theta range and there was no epileptiform activity. Routine serum biochemical parameters including liver and renal function tests and electrolytes were normal. Plasma ammonia was slightly raised (76.8 μmol/L; range: 11-35 μmol/L). MR imaging of brain carried out showed mild generalized atrophy with a cystic lesion secondary to gliosis of the left anterior temporal region []. The serum levels of phenobarbitone was elevated [53.35 μg/ml; reference range: 15-40 μg/ml], while that of carbamazepine was 7.11 μg/ml [range: 4-12 μg/ml] and valproate was 33.58 μg/ml [range: 50-100 μg/ml] were within therapeutic limits. A possibility of chronic uncontrolled symptomatic localization related secondary generalized epilepsy due to gliosis in the left temporal region with phenobarbitone toxicity was considered after evaluation. Tablet phenobarbitone was tapered and levetiracetam was initiated (1000 mg/day).\nOn the third day of hospitalization, the patient had a generalized seizure. During the immediate postictal period, he was drowsy and diaphoretic, with shallow respiration, bradycardia [pulse rate: 52/min, feeble radial pulse] and hypotension [systolic blood pressure: 60 mmHg]. There was no cyanosis. An electrocardiogram obtained at this time showed a heart rate of 43/min, with p-wave coming after QRS complex suggestive of junctional AV rhythm []. He was given supportive treatment with nasal oxygen (3 L/min), intravenous fluids and dopamine (10 μg/kg/min). About 40 minutes later, the heart rate normalized to 72 per minute and blood pressure rose to 100/80 mmHg. The 2-D echocardiogram showed only a mild left ventricular hypertrophy. The serum creatine kinase-MB [21 U/l; normal 9-25 U/l) and Troponin-I done after 4 hours was 0.6 ng/ml (ref: Up to 0.1). Repeat Troponin-I was 0.6 ng/ml. A repeat ECG carried out 2 hour later was normal []. He recovered completely and at the time of discharge 11 days later, he did not have any neurological deficits.\nThis event led to a possibility of self-remitting in-hospital symptomatic ictal bradyarrythmia (junctional AV rhythm) and hypotension during a generalized seizure. After 6 months of follow-up, he was asymptomatic and seizure free on levetiracetam and valproate.