[Apropos of 2 cases of extensive carotid thromboses. The limits of surgical possibilities].
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Fine-needle aspiration (FNA) of the liver is a procedure considered virtually risk-free. We report here a patient with carcinoma of the pancreas, who suffered a fatal hemoperitoneum (HP) subsequent to FNA of the liver under the guidance of ultrasound. The patient had presented with migratory deep vein thrombosis (DVT), and recurrent cerebral embolism. The prothrombin time (PT) and partial thromboplastin time (PTT) had been normal, and FNA demonstrated adenocarcinoma cells. Autopsy findings demonstrated carcinoma in the tail of the pancreas with liver and adrenal metastases, massive HP, and findings of chronic disseminated intravascular clotting (DIC). Since chronic DIC with enhanced fibrinolysis might have participated in the fatal bleeding, we recommend that FNA should be contraindicated in patients suspected of having malignancy with migratory DVT and recurrent arterial embolism, despite normal PT and PTT tests, unless the appropriate laboratory tests succeed in excluding DIC.
We investigated the anticardiolipin antibody (ACA) in a series of patients with cerebral infarction without systemic lupus erythematosus (SLA). Clinical and laboratory data were assessed from a series of 250 non-SLE patients with cerebral infarction who visited our clinic from 1988 to 1990. The concentration of anticardiolipin IgG antibody was measured by an enzyme-linked immunosorbent assay technique. An elevated ACA level was defined as one which was greater than 3 standard deviations above the mean level for normal controls. We examined the CT findings and risk factors for stroke such as hypertension, diabetes mellitus, hyperlipidemia and cardiac disease. Laboratory data such as the platelet count, the presence of lupus anticoagulant and a biologic false-positive test for syphilis were also investigated. Among the 250 patients with infarction, IgG ACA was detected in 22 (8.8%). There was no significant difference in incidence of ACA between the patients with cerebral thrombosis and those with cerebral embolism. On CT scan, multiple cerebral infarcts were noted in 18 of the 22 patients. As regards the location of the infarct, the cerebral cortex together with the basal ganglia was more common than isolated lesions of the cortex or basal ganglia. Concerning the risk factors for stroke, hypertension was noted in 12, diabetes mellitus in 2, hyperlipidemia in 2 and cardiac disease in 2. Lupus anticoagulant and thrombocytopenia were not detected in any of the cases. A biologic false-positive test for syphilis was observed in one case. Dementia was present in 12 of the 22 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The authors report the case of an active 32 year old man who developed right leg DVT. Before heparinisation, he was discovered to have a low antithrombin III level (biological activity (B) 60%, immunological level (I) 50) and a further inquiry showed the same abnormality in 4 members of the family, leading to a diagnosis of a congenital deficit: a 35 year old sister with a bilateral post-DVT changes had antithrombin III levels of 70% (B) and 45% (I); two nephews, sons of the affected sister: the one aged 5 years was asymptomatic despite antithrombin III levels of 50% (I) and 70% (B); the other had experience DVT at the age of 2 and, on oral anti-vitamin K drugs, had antithrombin III levels of 55% (I) and 67% (B) at the age of 15 years; the patient's brother died at the age of 29 of cerebral vein thrombosis after pulmonary embolism. The recurrence of local signs of DVT after 12 day's heparin therapy with AT III levels (B) of 40%, led to a change in management with infusion of purified AT III concentrate at a dose of 40 U per kg (2 500 U per hour). This induced a rise in AT III activity to over 100% and enabled early introduction of anti-vitamin K therapy. The patient remains asymptomatic after 6 months follow-up. This case illustrates the value of determining AT III activity in all patients who developed DVT without obvious reason.(ABSTRACT TRUNCATED AT 250 WORDS)
Anticardiolipin antibody (aCL) is considered to be one of the contributory factors in the development of cerebral infarction. We compared the recurrence and prognosis of 20 ischemic stroke patients with positive IgG aCL who had no collagen vascular diseases with those in 120 patients with negative IgG aCL. The aCL-positive patients comprised 18 females and 2 males aged 43-79 (mean 64) years and the mean follow-up period was 5.6 years. The aCL-negative patients comprised 82 males and 38 females aged 40-84 (mean 64.2) years and the mean follow-up period was 5.8 years. There was no significant difference in age and mean follow-up period between the two groups. We examined the recurrence rate and the intervals from the onset to the recurrence in both groups. We investigated the relationship between the recurrence of stroke and chronological changes in titer of aCL in patients with positive aCL. We also evaluated the effectiveness of antiplatelet agents for the prevention of recurrent stroke in both groups. A positive aCL level was defined as one which was > 3 standard deviations (S.D.) above the mean level for normal controls. A high titer of aCL was defined as being > 7 S.D. above the normal mean value. Among the 20 patients with positive aCL, recurrence of ischemic stroke occurred in 10 (50%) (cerebral thrombosis in 8 and cerebral embolism in 2) and myocardial infarction developed in 2 patients. As regards the number of ischemic episodes of stroke, recurrence occurred twice in 4 and once in 6 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
A series of 4816 patients with cerebrovascular disease have undergone CT and/or MRI examinations over the last 25 years at the Higashi Nagoya National Hospital and the Nagoya National Hospital. Of these, we experienced 5 cases (4 men and 1 woman) of Weber's syndrome: two cases were resulted from cerebral embolism and three from cerebral thrombosis. All of the patients had left hemiparesis and right oculomotor palsy. On full investigation, complete unilateral external and internal oculomotor palsy was seen in two patients, while the remaining three patients showed pupillary sparing. The patients with complete oculomotor palsy presented with left hemiparesis as the initial symptom. In addition to oculomotor palsy and crossed hemiparesis, two patients had paralysis of the face and one patient had tongue muscle on the opposite side of the lesion and disorders of sensation. Positive Babinski's sign was found in four of the five patients. In one patient with unilateral glossoplegia on the side of hemiparesis, CT or MRI revealed a limited low-density or low signal intensity (T1) area in the inner part of the crus cerebri, and in the other patient who also had hemihypesthesia, the low-density or low-signal intensity (T1) area expanded into the dorsal midbrain. We would like concluded that the frequency of Weber's syndrome was very low though this syndrome was well celebrated, and the careful clinical observation of the neurological features of affected patients guided to the obvious site of lesion in the midbrain.
Single photon emission computed tomography (SPECT) using 123I-Iomanzenil (IMZ), a tracer which binds specifically to central-type benzodiazepine receptors, was performed in patients with cerebrovascular diseases (CVD) to determine the clinical signicigance of IMZ SPECT studies in evaluating the pathophysiology of CVD. IMZ SPECT images obtained three hours after administration of the tracer were compared with the images of cerebral blood flow (CBF) studies in 206 cases. In regions with decreased CBF, the uptake of IMZ was relatively preserved in patients with cerebral thrombosis in comparison with cerebral embolism, and in those with perforator branch infarction in comparison with cortical infarction. The uptake of IMZ decreased as a function of both the severity of the decrease in the CBF and the duration of illness in regions with a significantly decreased perfusion reserve. These results suggest that decreased IMZ binding in ischemic stroke reflects the neuronal damage caused by the cerebral ischemia. On the other hand, in patients with intracerebral hemorrhage, the cortical uptake of IMZ was relatively well-preserved in regions with decreased CBF, and the decrease in the uptake of IMZ was more profound as a function of the decrease in the CBF, especially in cases of putaminal hemorrhage. These results also suggest that the decreased cortical CBF is a remote effect caused by a neuronal disconnection, and neuronal damage may occur in regions with severely impaired CBF.
A clinicopathological analysis of myocardial infarction with an onset of stroke-like symptoms was carried out on 30 autopsy cases at the Tokyo Metropolitan Geriatric Hospital. The cases were classified into four groups according to the types of brain lesions, I: embolism (n = 17), II: thrombosis (n = 9), III: bleeding (n = 2), and IV: no remarkable focal lesion (n = 2). Classification was made based on clinical findings, and pathological features. The characteristic clinical findings were conciousness disturbance, no elevation of blood pressure at the onset of stroke, hemiplegia and shock. However, the typical anginal chest pain was found in only 17% of cases. The underlying diseases and complications were hypertension, atrial fibrillation (Af), disseminated intravascular coagulation (DIC), renal failure, malignant neoplasma, and diabetes mellitus. The incidences of Af, DIC, mural thrombus, non-bacterial thrombotic endocarditis (NBTE) were significantly higher in the group with cerebral embolism than in the group with cerebral thrombosis. The coronary stenotic index was also smaller in the group with cerebral embolism. Therefore, the major etiology of cardio-cerebral apoplexy was a simultaneous embolism to the brain and heart due to Af, NBTE or, DIC.
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Of 171 patients evaluated prospectively and consecutively for cerebral ischemia, 26 (15%) developed symptoms while hospitalized. Cerebral ischemia complicated operative procedures in 12 patients, unsuccessful cardioversion in one and coronary angiography in another. Twelve patients had apparent cerebral embolism and 14 patients had cerebral thrombosis as a mechanism of their symptoms. Hospitalized patients who suffered cerebral ischemia had one or more of the following: risk factors for stroke including cardiac source of embolus, previous stroke, diagnostic or therapeutic procedures for vascular disease, or chronic hypertension complicated by acute hypotension.
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