Cigarette smoking and risk of cerebral sinus thrombosis in oral contraceptive users: a case-control study.

Idiopathic cerebral sinus thrombosis (CST) can cause death and serious neurological disability. It is unknown whether smoking, a major risk factor for arterial stroke, is a risk factor also for CST. This work explored the association between smoking and CST in a hospital-based, multicentric, case-control study. In order to avoid the confounding effect of the different risk factors for CST, we analysed the homogeneous subgroup of oral contraceptive users. We compared the prevalence of smoking in a group of 43 young women with CST (cases), whose oral contraceptive use was the only known risk factor, with a sample of 255 healthy contraceptive users of similar age (controls). The prevalence of smoking in cases and controls was similar (26% vs. 29%). The age and geographic area-adjusted odds ratio was 0.9; 95% confidence interval, 0.4-1.8; p=0.7. Smoking in oral contraceptive users does not appear to be associated with CST.

Spontaneous low cerebrospinal pressure: a mini review.

Spontaneous intracranial hypotension (SIH) is a syndrome of low cerebrospinal fluid (CSF) pressure characterised by postural headaches in patients without any history of dural puncture or penetrating trauma. Described by Schaltenbrand in 1938, SIH is thought to result from an occult CSF leak resulting in decreased CSF volume and, consequently, in low CSF pressure. Magnetic resonance imaging of the head and spine has improved the diagnosis of the syndrome showing peculiar radiographic abnormalities including diffuse pachymeningeal enhancement, subdural fluid collections and downward displacement of the cerebral structures. Treatment of SIH headache should start with conservative, non-invasive therapies while epidural blood patch has emerged as the treatment of choice for those symptomatic patients who have failed medical noninvasive approaches.

Hyperhomocysteinemia and other thrombophilic risk factors in 26 patients with cerebral venous thrombosis.

Despite the continuous description of new conditions pre-disposing for cerebral venous thrombosis (CVT), no apparent cause is found in about 30% of cases. Hyperhomocysteinemia (hyper-Hcy) is an established risk factor for deep venous thrombosis and stroke but has not been clearly associated with increased risk of CVT. We assessed the prevalence of hyper-Hcy and other thrombophilic risk factors in a population of 26 consecutive patients with non-pyogenic CVT, by review of a prospectively maintained database. The prevalences of hyper-Hcy and prothrombin G20210A, factor V G1691A and methylenetetrahydrofolate reductase (MTHFR) C677T mutations in these patients were compared with those in 100 healthy controls and 100 patients with cerebroarterial disease. The prevalence of hyper-Hcy was greater in patients with CVT (10/26, 38.5%) than healthy controls (13/100; OR 4.18, 95% CI 1.58-11.16) and comparable with that in patients with cerebroarterial disease (42/100). No significant differences were found in the prevalences of prothrombin or MTHFR mutation. No factor V mutation was found. Our findings indicate that hyper-Hcy is associated with an increased risk of CVT. Additional prospective cohort studies on large series of patients are required to clarify the time relationship between hyper-Hcy and the thrombotic event.

Cerebral vein thrombosis and mild hyperhomocysteinemia: three new cases.

Mild hyperhomocysteinemia is an established risk factor for deep vein thrombosis. We report three patients with cerebral vein thrombosis (CVT) in which the only risk factor we were able to identify was increased blood homocysteine levels and the C677T polymorphism in both alleles of the methylene tetrahydrofolate reductase MTHFR gene. We suggest that hyperhomocysteinemia should also be a risk factor for CVT. Since this condition can be effectively and safely corrected by drugs, we suggest that homocysteine levels should be routinely determined in patients with idiopatic CVT, and even mildly increased levels corrected pharmacologically, in the hope of reducing the risks associated with this condition.

Defective fibrinolytic response in atherosclerotic patients--effect of iloprost and its possible mechanism of action.

Plasma fibrinolytic activity and tissue-type plasminogen activator (t-PA) were defective in response to venous stasis in five out of ten patients with peripheral occlusive artery disease. Discontinuous infusions of iloprost, a stable synthetic analogue of prostacyclin, restored a normal fibrinolytic response in all five patients but did not induce a parallel increase of plasma t-PA. These findings suggest that in addition to the possible benefits due to its vasodilatory and antiplatelet activity, iloprost may improve the fibrinolytic activity in patients with atherosclerotic disease, providing them with further antithrombotic protection. The profibrinolytic effect of iloprost seems not to depend on its ability to induce vascular t-PA release. Rather, it might be related to its inhibitory effect on PAI release from platelets, endothelial cells and/or hepatocytes. Venous occlusion test represents an easy diagnostic approach to fibrinolytic defects, even if related to arterial disease, and may help select patients who need therapeutic intervention.

Resumption of gainful employment in aphasics: preliminary findings.

We report preliminary data on aphasic patients who, in spite of their language problems, have succeeded in finding a reasonably satisfactory occupational resettlement. Patients who: (a) still had a moderate to sever aphasia, (b) had resumed a gainful employment requiring interpersonal communication, were recalled for a check-up and assessed with: (1) a comprehensive aphasia test: (2) a semistructured interview including detailed questioning about the type and reaction to aphasia, the type of work before the onset of aphasia, the type of current work with particular emphasis on the patients' compensatory mechanisms and emotional reactions. Results comprise 10 cases up to date. One case is described in detail. Findings indicate that the ability to resume a gainful occupation is often greater than could be expected on the sole basis of formal language examination. Findings are discussed from a neuropsychological, social and rehabilitation point of view.

Low dose aspirin does not prevent fibrinolytic response to venous occlusion.

Interest in the antithrombotic potential of low-dose aspirin is based on its ability to inhibit thromboxane (Tx)A2-related platelet function with concomitant sparing of vascular prostacyclin (PGI2) production. The aim of this study was to investigate the effect of low-dose aspirin (20 mg daily for 7 days) on the increase in fibrinolytic activity in healthy volunteers after venous occlusion. We also tested the effect of high-dose aspirin (650 mg X 2), of salicylate (569 mg X 2) and of indobufen (200 mg X 2), a new cyclo-oxygenase inhibitor unrelated to salicylates. Low-dose aspirin reduced serum TxB2 generation by about 90% and suppressed arachidonate-induced platelet aggregation. In contrast, fibrinolytic activity, measured by the euglobulin lysis area and the euglobulin lysis time, was not significantly affected. Both high-dose aspirin and indobufen significantly inhibited TxB2 generation and the rise in fibrinolytic activity induced by venous occlusion, without affecting the pre-occlusion values. Salicylate did not significantly affect any parameter studied. Besides offering a favorable solution to the "aspirin dilemma" related to the TxA2/PGI2 balance, low-dose aspirin might leave intact the fibrinolytic capacity of the vessel wall.