A 37-year-old right-handed man was admitted for an evaluation of medically refractory epilepsy. He had no known risk factors for abdominal – epilepsy except that he had fallen from a tree and lost consciousness for an unspecified length of time at 4 years of age. That same year, he experienced his first seizure : he initially complained of abdominal pain, ran out of the house, and had a convulsive seizure. The family physician prescribed sedating antihistamine drops but gave the patient no antiepileptic therapy. The EEGs performed at that time showed nonspecific abnormalities in the left occipitoparietotemporal region but no epileptic discharges.
At the age of 20 years, the patient had a generalized tonic-clonic seizure during military service. Subsequently, therapy with carbamazepine was instituted. Because the patient was not fully compliant with the recommended treatment, another tonic-clonic seizure occurred at the age of 23 years. While the patient was taking a regular carbamazepine dosage of 400 mg 2 times a day, no further convulsive seizures occurred.
Besides these seizures, the patient experienced recurrent episodes of abdominal pain since childhood. This pain was localized in the epigastric region, spreading along the costal margins into the retrosternal region. These episodes of abdominal pain occurred up to 10 times a day, although sometimes none occurred throughout a whole month; their duration varied from seconds to hours. After unremarkable upper and lower endoscopic findings, a diagnosis of irritable bowel syndrome was proposed. Over the years, the episodes of abdominal pain were sometimes so severe that the patient contemplated suicide.
Because of a favorable course with no seizures resulting in loss or alteration of consciousness, the carbamazepine dosage was reduced to 100 mg/d by the time the patient was aged 32 years. After being placed on this low-dose therapy, the patient had a complex partial seizure that was preceded by abdominal pain. This painful episode lasted throughout the entire seizure.
The patient consulted a neurologist who recognized the recurrent episodes of abdominal pain as an epileptic phenomenon. The patient was hospitalized at an epilepsy center where several complex partial seizures were recorded. Before each seizure onset, the patient reported epigastric pain. Interictal EEGs showed an epileptogenic focus in the left front otemporal region; ictal EEGs were characterized by “flattening” in this region before clinical seizure onset. Magnetic resonance imaging revealed left-sided mesial temporal sclerosis. Positron emission tomography with fluorodeoxyglucose F 18 showed regional hypometabolism in the left mesiobasal temporal region.
Although the carbamazepine dosage by now had been increased to 400 mg 3 times a day, complex partial seizures preceded by abdominal pain still occurred repeatedly. Epilepsy surgery was considered at this point, and the patient was referred to our center.
Long-term EEG monitoring was performed by inserting electrodes bilaterally through the foramen ovale6 of the skull base. Since an amygdalar seizure onset was suspected, an additional depth electrode was implanted in the left amygdala. The latter showed ictal discharges in the left amygdala at the onset of the patient’s typical seizures with abdominal pain. A selective temporal lobe memory test with catheterization of the left anterior choroideal artery and application of amobarbital into the territory of the planned operation showed no substantial impairment during simultaneous neuropsychological evaluation. A left-sided selective amygdalohippocampectomy was performed without complications when the patient was 38 years of age.7 Histology confirmed a diagnosis of mesial temporal sclerosis.8
Carbamazepine was discontinued about 2 years postoperatively. During 5 years of postoperative follow-up (2 years with and 3 years without medication), the patient remained free of seizures and abdominal pain.
The above information thankfully comes from the Mayo Clinic.com at the following link.