Abdominal epilepsia partialis continua in a patient with astrocytoma treated with Lacosamide - value of repetitive EEG recordings.

OBJECTIVE: Isolated abdominal epilepsia partialis continua (EPC) without the involvement of other body parts is rarely seen. Abdominal EPC usually occurs either as a part of hemibody EPC or as an evolution of refractory EPC after initial treatment. As the isolated abdominal EPC was rarely reported up to date, the data regarding its pathophysiology and management are limited. Herein, we aimed to describe the clinical, neuroimaging, and electroencephalographic findings of a patient with abdominal EPC. PATIENTS AND METHODS: A 48-year-old woman with a history of surgical resection for right posterior frontal astrocytoma was admitted with left abdominal EPC. Magnetic resonance imaging of the brain showed a residual mass lesion and encephalomalacia in the right frontoparietal region. RESULTS: Although the initial electroencephalography (EEG) was normal, independent spikes were detected in the right frontal and parietal derivations in the second EEG. Although her EPC was refractory to levetiracetam, lamotrigine, phenytoin, and gabapentin, oral lacosamide treatment ceased the seizures. CONCLUSIONS: The history of this patient emphasizes the necessity of repetitive recordings in case of a normal initial EEG. The independent spikes in her frontal and parietal regions suggested the presence of a large epileptogenic zone generating independent epileptiform activities in the pre-central motor cortex and the post-central sensory cortex as the pathophysiologic phenomena in persistent abdominal EPC. To the best of our knowledge, this is the first report presenting a patient experiencing an abdominal EPC due to a cerebral mass resolved with lacosamide suggesting this drug is a promising treatment option in resistant EPC.

Nerve conduction studies of the axillary, musculocutaneous and radial nerves in elite ice hockey players.

AIM: The peripheral nerves of the upper extremity are exposed to acute and chronic mechanical injuries in ice hockey players, because of the high repetition of motions, high muscular forces and extreme shoulder positions. This study was performed to evaluate the effect of ice hockey playing on the axillary, musculocutaneous and radial nerves crossing the upper arm region. METHODS: The ice hockey group consisted of 20 first-division male ice hockey players and the control group consisted of 20 non-active males. The neurophysiological study consisted of motor nerve conduction latency of the axillary, musculocutaneous and radial nerves. RESULTS: The values of distal motor latency (DML) of the axillary, radial and musculocutaneous nerves were significantly prolonged in the ice hockey players compared with the controls. Ice hockey can repetitively stress the upper extremity during shooting, because of forceful throwing to move the puck from the stick blade to the opponent's net. The mechanism of prolonged DML in the axillary nerve may both tract and compress as the axillary nerve stretches across the humerus during movement. From this study it emerged that using the biceps and coracobrachialis muscles can create notable muscle compartment pressure on the musculocutaneus nerve. The significant differences detected in the neurophysiologic study of the musculocutaneous nerve between the ice hockey players and controls may reflect the fact that the forces acting on the shoulder and the elbow during ice hockey matches can effectively influence DML. CONCLUSIONS: The authors suggest two plausible causes for prolonged radial nerve DML: direct compression by the hypertrophied triceps muscle and stretching of the arm. The study suggests it is likely that a combination of skeletal muscle hypertrophy and excessive biomechanical demands on neurological structures during ice hockey matches may be a major etiologic factor in compression of the axillary, musculocutaneous and radial nerves.

Does metoprolol inhibit the cortical spreading depression? Acute effects of systematic metropol on CSD in rats.

Cortical spreading depression (CSD) is supposed to be the underlying biological basis of the migraine aura. Metoprolol was proven to be effective in migraine prophylaxis in clinical trials, but its mechanism of action has not been clarified yet. We studied direct effects of metoprolol on a continuous CSD induction model in rats. Six adult Wistar rats were anaesthetized with intraperitoneal thiopental (50 mg/kg). CSD was induced with application of 1 m KCL through a burr hole into the left frontal dura-mater, and recorded by an Ag/AgCl DC electrode on the left parietal dura-mater. After a basal recording of CSD induction during the first 40-min period, metoprolol (5 mg/kg) was infused within 4 min. Then DC recordings were maintained for a further 120 min. Any significant differences in total number and duration of CSDs before and after metoprolol administration were not detected. This study suggests that the mode of action of metoprolol in prophylaxis is not via direct CSD inhibition.