PubMed · 1119964
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J G Sacks. 1975. Letter: Third nerve palsy.. https://doi.org/10.1001/archneur.1975.00490450088015
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Moyamoya disease is a rare vascular anomaly of the cerebral arteries. The etiology of the disease has not yet been clearly identified. We report the noninvasive diagnosis of Moyamoya disease in a patients with a very early onset of symptoms in infancy. The diagnosis was made by colour coded Doppler sonography and confirmed by angiography at the age of 6 months, following two episodes of cerebral infarction. A bilateral encephalodurosynangiosis was performed at the age of 7 months with subsequent slight improvement of the neurological deficits. Colour Doppler sonography revealed early vascularisation from the fascia temporalis graft into the arachnoid space. At the age of 10 months the patient developed arterial hypertension caused by left renal artery stenosis. Our case suggests, that in infancy Moyamoya disease can be suspected noninvasively by colour Doppler sonography of the cerebral arteries. Patients should be carefully screened for possible extracranial arterial stenoses which may develop in the course of time. Encephalodurosynangiosis seems to be a good therapeutic option for patients with severe neurological symptoms.
1. KC-404 (10(-9)-10(-6) g/ml) produced concentration-dependent relaxations in human middle cerebral arteries contracted with prostaglandin F2 alpha. 2. KC-404 (10(-8) and 10(-7) g/ml) has the ability to significantly potentiate prostaglandin I2-induced relaxations in human middle cerebral arteries. 3. KC-404, at least in low concentrations, may elicit human cerebral vasodilation predominantly by potentiating relaxant responses to prostaglandin I2 produced spontaneously in vascular wall. 4. KC-404 is expected to increase cerebral blood flow at least by dilation of major cerebral arteries, and this agent may be beneficial for the treatment of cerebrovascular disorders.
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.