[Consequences of a fortuitous finding: the asymptomatic carotid bruit].
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Biomedical subjects
Publications and source records attributed to J Lodder.
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Two patients are described: one with an aneurysm of the infrarenal aorta and common iliac artery that ruptured posteriorly into the iliac vein, the other with an aneurysm of the distal abdominal aorta that ruptured posteriorly into the iliopsoas muscle. Both patients had symptoms compatible with a radicular compression syndrome. Ruptured aneurysm of one of the major abdominal arteries should be considered in the differential diagnosis of affections of the lumbosacral neural outflow, because immediate operation can be life-saving.
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In a retrospective study 2015 CT scans were studied for the presence of basal ganglia calcifications. These were discovered in 33 cases. No abnormalities in serum calcium or phosphate levels or any other specific clinical symptoms related to these calcifications were found. It is concluded that basal ganglia calcifications casually detected by CT generally have no clinical significance.
A patient is presented suffering a hemiparesis. Megadolicho-vascular malformation of the intracranial part of the internal carotid arteries and some of its branches and of the basilar artery was suggested by CT and confirmed by angiography. The value of CT compared with angiography in relation to intracranial megadolicho vascular malformations is discussed.
Bilateral ballism developed gradually in a 75-year-old woman after head trauma. Computerized tomography revealed bilateral hemorrhagic infarction in the head of the caudate nucleus and the putamen. Haloperidol abolished the symptoms completely within 2 days. After 18 days, haloperidol was gradually withdrawal over 16 days. The patient remained without ballistic movements thereafter.
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The role of the pelvic nerves in the postmating abbreviation of behavioral estrus in domestic female rats was investigated. Mating during a period of 40 min at the beginning of hormonally induced estrus in spayed female rats resulted in a rapid decrease in receptivity as measured hourly by the lordosis response. Moreover, the length of the receptive period was significantly shortened by mating at the start of the period. Bilateral pelvic nerve transection completely abolished these effects of mating. Continuous exposure to sexually active males throughout the period of receptivity resulted in a more pronounced decline in receptivity but again was without effect in pelvectomized females. Apparently genital stimuli mediated by the pelvic nerves are responsible for the postcopulatory decrease in receptive behavior in the female rat.
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The type of small-vessel disease in small deep (lacunar) infarcts (SDIs) remains contentious as opposed to that in primary intracerebral haemorrhage (PICH), which is lipohyalinosis in most cases. Therefore, we compared risk factor profiles as indicators of underlying vessel pathology, between patients with SDI and patients with PICH, and those with a non-cardio-embolic infarct involving the cortex (CORTI). Multivariate regression analysis showed the diabetes mellitus [odds ratio (OR) 0.56; 95% confidence interval (CI) 0.34-0.90] and hypercholesterolaemia (OR 0.63; 95% CI 0.40-0.99) were more strongly associated with CORTI than with SDI. Carotid stenosis was associated with SDI in comparison with PICH (OR 7.5; 95% CI 1.02-54.94). Compared with PICH, CORTI was more strongly associated with diabetes mellitus (OR 3.27; 95% CI 1.38-7.76), carotid stenosis (OR 24.42; 95% CI 4.99-119.45), and hypercholesterolaemia (OR 3.12; 95% CI 1.47-6.65), whereas hypertension was associated with PICH (OR 0.37; 95% CI 0.18-0.79). These data support the hypothesis that small-vessel atheromatosis rather than small-vessel lipohyalinosis underlies lacunar infarcts in most cases.
In preparation of a trial on the neuroprotective effect of GABAergic activation by a benzodiazepine, we performed a feasibility study in 104 patients with acute (less than 24 h) stroke. 5 mg diazepam twice daily for 5 days (n = 44) was well tolerated, feasible, and appeared to be safe. Testing a dose of 10 mg twice daily for 5 days (n = 17) was stopped early because of drowsiness around day 5, interfering with regular patient care. A dose of 10 mg twice daily for 3 days was well tolerated, despite reported drowsiness in 12 of 43 patients. First-dose application by rectiole was feasible in 97% of the 104 patients. No blood pressure drop or respiratory arrest or insufficiency were detected, whereas the 2-week case fatality rate was similar to that of controls matched for age, sex, and stroke severity. We conclude that testing the GABAergic activity during the acute phase of stroke by 10 mg diazepam twice daily for 3 days is well tolerated and practically feasible, and it does not subject patients to an increased risk of potential serious adverse effects. Preparations for a large randomized trial are in a final stage.
We evaluated immediate anticoagulation of embolic stroke. Of 39 patients suffering a focal cerebral ischemia caused by a cardiac embolus, 38 were submitted to CT within 24 hours after onset. Twenty-one patients received direct full anticoagulation and, in 10 patients, treatment was delayed because of hemorrhagic infarction on initial CT (3 cases), cardiac cause 24 hours or more after stroke onset, or treatment delay without specific reason (6 cases). Eight patients with severe deficit were not anticoagulated because of hemorrhagic signs on initial CT, impaired consciousness, or general contra-indications to such treatment. Twenty-one follow-up CT-scans were performed under full anti-coagulation, and in only 2 cases hemorrhagic infarction was noticed without clinical deterioration. No clinical worsening attributable to anticoagulant treatment was observed during the three week observation period. It is concluded that direct anticoagulation therapy does neither induce hemorrhagic infarction nor cerebral hemorrhage in patients with embolic stroke nor does it cause clinical deterioration.
In 48 patients dying within 15 days following a supra-tentorial cerebral infarct, the presence of hemorrhagic infarction at autopsy was related to a cardiac embolic cause of the infarct, and to the cause of death. Hemorrhagic infarcts were more common among patients dying from brain herniation than among those dying from a non-cerebral cause. Cardiac embolic strokes were more often hemorrhagic at autopsy than strokes without such cause; this could be explained by a significant higher rate of brain herniation and death after embolic stroke. On the other hand infarcts with extended hemorrhages more often tended to have a cardiac than a non-cardiac cause. These data, together with earlier clinical findings suggest that autopsy studies are biased in relating hemorrhagic infarction almost exclusively to a cardiac embolic cause of stroke, although cardiac emboli may produce more extended hemorrhages.
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