PubMed · 660240
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J T McFadden. 1978. Aneurysm clips.. https://doi.org/10.3171/jns.1978.48.6.1054
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Using the duplex Doppler system, blood velocity was measured serially at two sites of the anterior cerebral artery (ACA) and in the middle cerebral artery (MCA) during the first 3 days of life, in eight term, small for gestational age (SGA) infants (birthweight, 2179 +/- 230 g; mean +/- S.D.), and 13 term, appropriate for gestational age (AGA) infants (3376 +/- 441 g). All infants in both groups had normal Apgar scores and none manifested signs of respiratory distress. At 1 h post partum, the average MCA mean velocity in the SGA group (25.8 +/- 6.9 cm/s) was higher than that in the AGA group (19.6 +/- 5.7 cm/s), whereas the average values of the two ACA sites did not differ between the groups. A significantly increased value of the average mean velocity as compared to the value at 4 h post partum was reached earlier in the AGA group at all three vessel sites. The pulsatility index (as defined by Gosling) was lower at all vessel sites up to 72 h in the SGA group. Pulse pressure was significantly lower in the SGA group due to increased diastolic blood pressure. We suggest the results imply a state of cerebral vasodilation in the SGA infants and a poor ability to respond with an increased perfusion in the frontal regions supplied by the ACA. Changes in blood pressure and cerebral haemodynamics appear to exist in SGA infants in the absence of postnatal hypoxia which might explain the vulnerability of the growth-retarded infant to perinatal hypoxia.
The action of sumatriptan, putatively a selective 5-HT1D or 5-HT1-like receptor agonist which is effective in the treatment of migraine, has been studied on fresh human dural (middle meningeal) arteries. In low concentrations (10(-8)-10(-7) M) it was found to be a significantly stronger vasoconstrictor of dural arteries compared to cerebral and temporal arteries. However, its potency was less than that of 5-HT. The sumatriptan-induced vasoconstriction was antagonized by methiothepin (10(-9)-10(-8) M), but not by ketanserin (10(-7) M). The observations suggest that the sumatriptan-induced contraction of the dural artery is mediated via activation of 5-HT1D or 5-HT1-like receptors, whereas it does not appear to activate the 5-HT2 receptors.
Since the pioneering publication by Dejerine and Roussy, the thalamus has been commonly implicated in the pathogenesis of central pain. It is well known that cerebral lesions that spare the thalamus as well as both small and large ones within that structure produce similar pain syndromes, but could such pain develop if the thalamus were completely destroyed? CT scans of our patients suggested that it could. Moreover, exhaustive physiological explorations of the thalamus with macro- and microstimulation and microelectrode recordings in 2 more patients in whom CT scans suggested thalamic preservation despite massive suprathalamic infarcts, for the purpose of carrying out deep brain stimulation (DBS), revealed no evidence of ascending or descending diencephalic function. Their sensory examinations were similar to those of patients with congenital hemiatrophy who had undergone hemispherectomy. In 1 case, microstimulation of periaqueductal grey-periventricular grey (PAG-PVG) on the unaffected side of the brain induced the spectrum of responses correctly associated with these areas and during acute stimulation nearly abolished the patient's allodynia and hyperpathia. These observations suggest that processes occurring at a subdiencephalic level (or possibly ipsilaterally) may be involved in the generation of pain. Stroke-induced central pain remains a therapeutic dilemma for the pain surgeon, and the mechanisms underlying this pain state remain a mystery.(ABSTRACT TRUNCATED AT 250 WORDS)