The 0-10 NRS and responder PP analyses demonstrated that Sativex treatment resulted in a significant reduction in treatment-resistant spasticity, in subjects with advanced MS and severe spasticity. The response observed within the first 4 weeks of treatment appears to be a useful aid to prediction of responder/non-responder status.

The clinical relevance of the interaction of enzymeinducing anticonvulsants (AEDs) with thyroxinereplacement therapy has sometimes been underestimated. We report here a case of severe hypothyroidism precipitated by AEDs in the intensive care setting (ICU).A 72-year-old woman with arterial hypertension and primary hypothyroidism due to Hashimoto thyroiditis and stabilized on 100-µg levothyroxine-replacement therapy was admitted to our neurological ICU for an acute ischemic stroke, complicated by epileptic convulsions. Phenytoin (PHT) was given intravenously for 4 days (250-mg bolus, followed by an infusion of 1,000 mg/24 h on the first day, and then tapered off: 375 mg on day 2, 250 mg on day 3, and gradually discontinued on day 4), and was substituted thereafter with carbamazepine (CBZ), 400 mg orally on day 4 and 800 mg daily there after. On day 3, sodium valproate (VPA) was added and increased gradually from 500 to 1,000 mg daily until day 23, when it was discontinued. Convulsions were rapidly suppressed by the PHT bolus, and did not recur. The patient's level of consciousness, however, worsened progressively (day 1: somnolent but oriented and communicating in short sentences; day 6: single words; day 18: no verbal response, just eye opening to loud voice). Consistent with the computed tomography (CT) scan finding of large ischemic lesions in the right hemisphere, left-sided hemiplegia occurred with left facial nerve palsy. Although circulatory and respiratory parameters were initially stable, the patient died on day 30 of septicemia secondary to a urinary tract infection.On admission, her thyroid function tests were normal: thyrotrophin (TSH), 1.07 mIU/L, total thyroxine (tT 4 ) 104.6 nM, and total triiodothyronine (tT 3 ), 1.39 nM. On day 14, however, despite continuation of 100 µg levothyroxine daily, her TSH increased to 43.5 mIU/L, whereas free thyroxine (fT 4 ) decreased to 6.29 pM, and free triiodothyronine (fT 3 ) decreased to undetectable values (<1.0 pM), suggesting severe primary hypothyroidism.Although on day 18, levothyroxine was increased to 200 µg daily, on day 20, TSH increased to 91.4 mIU/L, fT 4 was 3.73 pM, and fT 3 was undetectable. Clinical signs of hypothyroidism included lethargy, constipation, and eyelid edema and were possibly confounded by the ischemic brain damage, infection, and drugs. No bradyarrhythmias or hypothermia was found. However, during progression of her infectious complication in the last 2 weeks, her heart rate was slower (80 to 90 beats/min), and her temperature did not reach 38.0• C. A decrease in thyroid hormone levels caused by PHT was first described in 1961 (1). Further studies have shown complex interactions between some AEDs, including PHT and/or CBZ, and thyroid hormones at multiple levels (2-4). These interactions may include decreased plasma protein binding (4) and, more important, increased metabolism of thyroid hormones (3,5). Patients with intact pituitary/thyroid axis respond to decreased availability of thyroid hormones by feedback increase in their prod...

A simple topographic method has been developed for the localisation of the venous angle on the lateral cerebral phlebogram. The principle depends on an angular measurement and an estimation of proportions which are statistically independant of each other. The method was tested on 103 phlebograms of adult patients with supratentorial spaceoccupying lesions. It was compared with conventional measurements; a number of advantages were found for using our method and its accuracy is as good as the other, most precise, methods.

BACKGROUND AND PURPOSE: To test the design and feasibility of a very large randomised controlled trial assessing the efficacy and safety of antithrombotic therapy started within 48 hours of symptom onset in patients with suspected acute ischaemic stroke. DESIGN: Randomised controlled multicentre open study, with a 3 x 2 factorial design, allocating patients to: medium dose subcutaneous heparin (12,500 units twice per day), versus low dose subcutaneous heparin (5000 units twice per day) versus no heparin; and aspirin (300 mg daily) versus no aspirin. Treatment was given for two weeks or until discharge from hospital if sooner. RESULTS: 984 patients were randomised. CT was performed in 924 (94%) (before randomisation in 622/984 (63%). Within 14 days: 97 patients had died (10%), 30 (3.0%) had a fatal or non-fatal recurrent ischaemic stroke, nine (0.9%) had fatal or non-fatal recurrent stroke due to intracranial haemorrhage, and eight (0.8%) had a fatal or non-fatal pulmonary embolus. At six months, vital status was known for 975 patients (99%), of whom 210 (22%) were dead, 373 (38%) were alive but dependent, and 225 (23%) were independent but not fully recovered. CONCLUSIONS: The trial procedures proved practicable and a wide variety of patients were recruited. Sample size calculation based on the event rates confirmed that reliable evidence on the balance of risk and benefit of early antithrombotic therapy might require a study with more than 20,000 patients. Recruitment rates in the pilot study indicated that if about 200 hospitals participated, recruitment could be completed by 1997.

One of the less frequent complications of anticoagulant therapy is damage to the femoral and sciatic nerves due to bleeding. This report presents two cases and discusses the pathogenetic mechanism and treatment of this medical problem.