Biomedical subjects
Publications and source records attributed to Bjørn Karlsen.
The review defines status epilepticus and discusses treatment options for convulsive and nonconvulsive status epilepticus. The drug of choice in Norway is diazepam intravenously (0.25 mg/kg), followed by phosphenytoin or sodium valproate intravenously and barbiturate narcosis. Other treatment options are discussed. Underlying causes must be addressed for therapeutic intervention. Given early treatment, the prognosis is generally good.
OBJECTIVE: To examine patients with previous nonparalytic poliomyelitis in search of muscle atrophy, weakness, and other late symptoms of poliomyelitis. DESIGN: A mailed questionnaire followed up with neurologic and neurophysiologic examinations of respondents who reported symptoms possibly related to the late sequelae of polio. SETTING: Neurology department at a university hospital. PARTICIPANTS: Thirty-nine of 47 patients diagnosed with nonparalytic poliomyelitis and hospitalized at a Norwegian hospital between 1950 and 1954, during the Norwegian polio epidemic. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Electromyography to determine function of the anterior tibialis, vastus lateralis, and biceps brachii muscles; nerve conduction studies of the sural, peroneal, and tibial nerves; motor and sensory nerve conduction velocity, and compound muscle and sensory nerve action potentials, and distal latencies. RESULTS: Twenty-five of 47 patients (53.2%) reported symptoms possibly related to the late sequelae of poliomyelitis. Eight of 20 examined symptomatic patients had normal neurologic and neurophysiologic findings, whereas 9 others had other medical conditions that could explain the symptoms. Three patients (6.7%) had neurologic and neurophysiologic findings and development of symptoms consistent with motoneuron damage. CONCLUSION: Some nonparalytic patients may have subclinical acute motoneuron damage with subsequent development and manifestation of motor weakness and neuromuscular symptoms many years later. These symptoms should be considered a differential diagnosis in patients who have a history of nonparalytic poliomyelitis.