Pulse pressure obtained from alternatively calibrated tonometer-derived pressure waves and echo-tracking-derived distension waves demonstrates good accuracy. Accuracy of pulse pressure from internally calibrated applanation tonometer readings at the carotid artery is poor.
These findings suggest that inhibitory systems are activated to a lesser extent by TMS pulses in patients. This observation is in agreement with the hypothesized deficiency of intracortical inhibition of the visual cortex, at least in migraineurs with aura.
An EMG and nerve-conduction-study protocol has been developed and used in all patients with brachial plexus lesions since 1985. The findings of EMG and nerve-conduction studies in obstetric brachial palsy (OBP) mostly suggest a falsely optimistic prognosis. To analyse this, all subjects were selected with complete avulsion of both roots C5 and C6 and/or complete rupture of the upper trunk verified during operation from a group of 162 infants with OBP (aged 4 to 14 months) and a group of 184 child and adult patients (aged 6 to 74 years) with a traumatic brachial plexus lesion. Fourteen infants, approximately 4 months old, with OBP, and 19 adults (aged 16 to 30 years) met the selection criteria. The infants from the group with OBP had at 4 months a nearly normal recruitment pattern of motor units in the biceps brachii and deltoid muscles, with little or no denervation. However, in the older group with traumatic brachial palsy, the same lesion caused complete denervation of both muscles. From the group with OBP, a third group (N=3) with the same lesion plus an additional lesion of C7 or a rupture of the middle trunk was selected. This additional lesion resulted in nearly complete denervation of both muscles. This means that C7 largely contributes to the innervation of both muscles at the time of birth, but this innervation is lost during later life in normally developing individuals (apoptosis). A central mechanism might be responsible for the clinical palsy and later spontaneous improvement which is always found in the infants with OBP.
We examined the effect of standard migraine prophylaxis with sodium valproate on repeated measures of occipital excitability using transcranial magnetic stimulation (TMS). We predicted that, comparing pre- and post-treatment assessments, a reduction in clinical migraine parameters would be paralleled by a decrease in excitability measurements.A total of 31 migraine patients enrolled in the study, for assessment prior to and 1 month after commencement of sodium valproate prophylaxis. At each assessment, we used a standardized protocol to stimulate the occipital cortex with a 90-mm circular (coil A) and 70 mm figure-of-eight (coil B) coil. We recorded the threshold stimulation intensity at which subjects just perceived phosphenes. Subjects kept detailed records of headache parameters 1 month before and also during the study period. Valproate therapy significantly improved headache indexes, as expected. In MA subjects assessed with coil B, phosphene thresholds were significantly higher post-treatment than pre-treatment, but those for MO did not change. Modest correlations were observed in MA patients between increase in phosphene threshold and decrease in headache index. Although preliminary, the findings with coil B lend some support to the notion that effective migraine prophylaxis may be achieved through lowering cortical excitability by gamma-aminobutyric acid (GABA)-ergic intervention. Further investigation of the effect of sodium valproate or other similarly acting substances on cortical excitability in migraine is warranted.
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