The authors review the neural pathways mediating nociceptive flexion reflexes, the method for analyzing these reflexes in human beings, and available data on their modulation by supraspinal, opioid as well as serotonergic systems. They present results of studies of the biceps femoris flexion reflex (RIII) in pain syndromes and various types of headache. Nociceptive flexor reflexes appear to be interesting for studying the pathophysiology of head pain mechanisms and possibly for evaluating analgesic treatment.

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Maximum motor conduction velocity of the median, ulnar and peroneal nerves and maximum sensory conduction velocity of the median nerve have been studied in 635 children, below 12 years of age, free from peripheral nervous system disease. The children fell into four age-group: from 0 to 1 year; from 1 to 3 years: from 3 to 6 years; from 6 to 12 years. No normal values were recorded for the sensory conduction velocity of the median nerve under the age of one year. The motor conduction velocity values significantly rise for the median and ulnar nerves up to 1 year, for the peroneal nerve up to 3 years. The sensory conduction velocity values of median nerve increase significantly up to 6 years.

390 patients with severe head injuries were treated with phenobarbital (PB) orally for a period of 12 months in order to determine whether this drug could reduce the incidence of posttraumatic epilepsy (PTE). An intramuscular PB dose of 2.5-3 mg/kg body weight per day was administered within 24 hours after the trauma; after 5 days, or longer if the coma persisted, the drug was administered orally. Maintenance dosage adjustments, when necessary, were based on serial plasma concentrations of the drug, sustained at between 5 and 30 micrograms/ml. 293 patients completed the study. 66% of these presented one risk factor, while 34% presented two or more. 6 patients (2.04%) had at least one seizure during the twelve months. Plasma drug levels at the time of the seizure, with one exception of 15 micrograms/ml, ranged from 20 to 28 micrograms/ml. The results of the study indicate that PB administered during the first twelve months after the trauma, even at relatively low doses, can have a prophylactic effect on PTE.