Abstracts

2 patients without brain lesions developed focal seizures originating from the appropriate area after sustaining soft tissue injury to the hand.
2 case reports
27 year old woman developed focal seizures at age 19 after a cigarette burn to her middle finger. The burn blistered and healed uneventfully. Within 1day, brief recurrent episodes of tingling of the burned finger started that progressed over 5 months to involve all fingers of her left hand and eventually to march up her left arm to her left chest. The character of the sensory abnormality changed to a jabbing knife-like pain. Four years later, she had secondarily generalized seizures that stopped with Carbamazepine. She continued to have about 3-8 nocturnal simple seizures/month. She denied any sensory or motor activated triggers. Her seizures were characterized by waking, screaming with a look of pain followed by dystonic posturing of the left arm, clonic movements of the left face and then hemibody. She was conscious throughout and postictally was oriented and responding normally with no postictal motor or sensory deficits. Interictally, there were no epileptiform abnormalities and during the seizures, the EEG was obscured by artifacts and there was no focal postictal slowing. MRI of her brain was normal and an FDG-PET showed right parietal hypometabolism. Somatosensory evoked potentials (SEPs) and transcranial magnetic stimulation showed no lateralized cortical hyperexcitability.
23 year-old male developed myoclonic jerks of the right hand within 1 day of crushing his hand in a machine, sustaining a soft tissue injury. Three months later he had his first nocturnal generalized seizure. Seizures were characterized by stiffening of the body with elevation of the right arm, slight head and eye deviation to the right with subsequent generalization. The movement stopped on the right side before the left. Postictally, he had no focal deficits. Electrographically, seizure onset was characterized by muscle artifact followed by rhythmic activity over both hemispheres with predominance over the parasagittal region. Only during one seizure were these changes clearly lateralized to the left parasagittal region. Valproic acid and Carbamazepine resulted in seizure control but there was no improvement in the myoclonic jerks. These occurred at rest or during purposeful movement and were inconsistently triggered by startle causing him to fall and injure himself. MRI of his head and SEPs were normal.
These cases are novel because they developed focal epilepsy starting in the hand shortly after sustaining painful peripheral injuries. Presumably, the injuries led to a plastic change in the sensory/motor cortex resulting in increased excitability and ultimately to seizures. There was no evidence in either patient of underlying lesions but the possibility of a pre-existing occult lesion can not be completely excluded. This suggests that epileptogenesis can occur in response to painful peripheral stimuli.