Background and Purpose Internal carotid artery dissection has increasingly been reported as a cause of transient ischemic attack or stroke. However, scarce data exist on the natural history of the arterial lesions and the temporal profile of recanalization.Methods We followed 48 patients with 50 angiographicalry confirmed internal carotid artery dissections by sequential duplex Doppler studies in 2-to 4-day intervals during the first weeks after the onset of symptoms and after 4 weeks in 1-to 2-month intervals for up to 2 years. We assessed sonographic features as well as the frequency and time course of resolution.Results Initial Doppler findings were abnormal in all patients, most of whom (68%) presented with a characteristic bidirectional high-resistance Doppler signal in the internal
Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.
Background and Purpose-Severe motor deficits are the predominant cause of long-term disability in stroke patients. In particular, progressive hemiparesis in the initial stage after stroke onset is frequently devastating. Therefore, we attempted to define the population at risk with respect to the presumed pathogenesis. Methods-Among 941 stroke patients hospitalized during a 3-year period, 92 patients (41 men, 51 women; mean age, 68 years) had a severe motor deficit (Ͻ25 of 42 points on the 7 motor items of the European Stroke Scale) resulting from brain infarcts. Risk factors, neurological examinations, comprehensive diagnostic tests, and therapy were documented. The study population was separated into patients with (group A) and without (group B) progressive motor deficits. Progression was defined as a further decrease of at least 5 points on the initial European Stroke Scale motor score during the first 5 days after stroke onset. Results-Of the 92 patients, 23.9% had significant worsening of motor function with a decrease in the mean European Stroke Scale motor score from 20.3 to 12.9 points (PϽ0.01). Infarcts in group A patients were subcortical in 59.1%, whereas most infarcts were cortical in group B (61.4%, PϽ0.05). Progressive hemiparesis was also significantly associated with lacunar stroke (group A:, 59.1%; group B, 24.3%; PϽ0.01). With regard to risk factors, diagnostic studies, and neuroimaging, small-vessel disease was the predominant presumed cause of stroke in group A (63.6%, PϽ0.01), whereas infarcts in group B patients were frequently caused by embolism from cardiac or undetermined sources (61.4%, PϽ0.01). Prevalence of high-grade carotid stenosis was not significantly different between groups A and B; however, subtotal stenoses and complete internal carotid artery occlusions were found only among patients without progressive motor deficits. Conclusions-Lacunar stroke caused by small-vessel disease is the major cause of progressive motor deficits, probably because of stepwise occlusion of the branches of small penetrating arteries.
Richter's hernia is a deceptive entity whose high death rate can be reduced by accurate diagnosis and early surgery. Considering the increasing incidence at laparoscope insertion sites, awareness of this special type of hernia with its misleading clinical appearance is important and of general interest.
Compared with asymptomatic middle cerebral artery disease, there was a high and continuous recurrence rate of ischemic events in symptomatic patients, which was even higher than in patients with symptomatic extracranial carotid artery disease.
Numerous reports have described a variety of clinical syndromes resulting from posterior cerebral artery (PCA) infarction, whereas only a few pathoanatomical and retrospective clinical studies have investigated the underlying mechanisms. Therefore we attempted to determine the causes of infarction in the superficial posterior cerebral artery (PCA) territory by means of a more comprehensive, modern vascular and cardiac study. During a 4-year period 74 consecutive patients (49 men, 25 women) with acute PCA infarction documented on CT (n = 74) and MRI (n = 41) were included in the study. Patients had a neurological examination, vascular studies [extra- and transcranial Doppler (n = 74), magnetic resonance (n = 31) or intra-arterial (n = 22) angiography], cardiac evaluation [ECG (n = 74), transthoracic (n = 74) and transoesophageal echocardiography (n = 30)], and coagulation tests. A cardiac source of embolism was established in 31%, significant vertebrobasilar artery disease in 22%, and PCA stenosis or occlusion in 8% of the patients. Rare causes, such as hypercoagulopathy or paradoxical embolism via a patent foramen ovale, were present in 15%. However, in spite of the comprehensive diagnostic evaluation, the cause of the stroke remained undetermined in 24% of the cases. Apart from complete infarcts of the posterior branches of the PCA, which occurred more frequently in cardioembolic strokes (18%, P < 0.05), the topographical patterns of infarct extension and the coincidence of infarction in the deep territories of the PCA, the cerebellum and brainstem were not significantly different among the causal subgroups. The frequency of haemorrhagic transformation (18%) was highest among cardioembolic strokes (44%, P < 0.001). This prospective study of PCA infarction demonstrated embolism from cardiac and vascular sources as the predominant cause. In contrast to previous studies, we found no evidence of migraine as a cause of PCA infarction, whereas paradoxical embolism was the presumed cause in a considerable number of cases. Whereas the cause of stroke could not reliably be derived from infarct topography, haemorrhagic transformation indicated there had been cardioembolism in most cases.
Cerebral ischaemia is a common complication of bacterial meningitis. Although cerebrovascular involvement in the acute phase of inflammation may be particularly important for the still unacceptably high morbidity and mortality, only, a few studies have investigated cerebrovascular changes in bacterial meningitis. We prospectively investigated changes of intracranial cerebral blood flow velocities (CBFV) in 22 patients (12 men, 10 women, mean age 48 years, 19 years, SD) with bacterial meningitis, by means of transcranial Doppler sonography (TCD). According to previously published criteria the degree of arterial narrowing was assessed and related to the patients' outcome. Elevated CBFVs in the middle cerebral artery were documented in 18/22 patients with markedly increased systolic peak velocities (CBFV of > 210 cm/s) in 7 patients. Serial examinations performed in 11 patients showed elevated CBFV as early as day 1, reaching peak CBFV between day 3 and day 6 after onset of symptoms in most cases. Furthermore, cerebrovascular involvement was also documented by disturbances of physiological slow spontaneous oscillations of blood flow velocities in 5/10 patients examined with TCD. Low Glasgow Coma Scales (< 7) on admission (29% vs 0%), focal cerebral ischaemic deficits (29% vs 7%) and, seizures (43% vs 7%) were more frequent in patients with CBFV of > 210 cm/s. Finally, a poor clinical outcome was significantly related to severe vascular involvement (P < 0.05). In conclusion, cerebrovascular complications are frequently found in patients with bacterial meningitis. TCD is an easily applicable technique for revealing vascular changes non-invasively, even in severely ill patients. Since our data suggest an unfavourable course of the disease in association with increased CBFV in intracranial arteries, probably indicating vasospasm, TCD could potentially be used to identify high-risk patients who could benefit from adjuvant therapeutic interventions.
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