We present epidemiologic, etiologic, and clinical data for 1,000 consecutive patients with a first stroke (cerebral infarction or hemorrhage) admitted to the Centre Hospitalier Universitaire Vaudois since 1982. The patients were evaluated using a standard protocol of tests (computed tomography, Doppler ultrasonography, and electrocardiography in all patients, as well as angiography and specific cardiac investigations in selected patients). Each case was coded prospectively into a computerized registry. We believe that the Lausanne Stroke Registry is the first registry with complete computed tomography and Doppler ultrasonography data on all patients, which allows correlation between clinical findings, presumed etiology, and stroke location. Although the Lausanne Stroke Registry is not population-based, it gives a good estimate of the stroke-related problems in patients admitted to a primary-care center since our hospital is the sole acute-care facility for stroke in the Lausanne area. (Stroke 1988; 19:1083-1092) S troke data banks can provide the best available information for unanswered questions relative to diagnosis and management of patients with cerebrovascular disease.1 One of the best stroke registries recorded 694 patients 2 but lacked uniform computed tomography (CT) and ultrasonography data. In two more recent registries, 3 -5 CT was obtained in 90% of the patients, allowing an accurate diagnosis of hemorrhagic versus ischemic stroke. Data from other stroke registries have been published, 6 -8 but clinical details were often scarce and specific investigations were not performed systematically.We set up our own registry in 1983 using systematic computer coding of data from patients admitted with their first stroke. Although ours was not a population-based registry, we believed that the information given by the registry would be of great value because most acute stroke patients are referred to the Centre Hospitalier Universitaire Vaudois, which is the only public hospital in the Lausanne area and is located in a city of 200,000 people. Moreover, this hospital has the only department of neurology in the entire county. Subjects and MethodsInformation from all patients with a first stroke (cerebral infarction or hemorrhage, neurologic deficit lasting >24 hours) admitted since 1982 have been prospectively coded and entered into a computerized data bank. This article presents the analysis of the first 1,000 patients. Patients with pure subarachnoid hemorrhages and recurrent stroke have been excluded. Systematic investigations performed in every patient included brain CT (one to five examinations) with and without contrast (except in patients with known allergy), Doppler ultrasonography with frequency spectral analysis (common, external, and internal carotid arteries; vertebral arteries at the retromastoid level; subclavian arteries; ophthalmic arteries), twelve-lead electrocardiography (ECG), and standard blood and urine tests including venous hematocrit and fasting blood cholesterol concentration. Cerebral ...

We studied forty patients with CT-proven thalamic infarcts without involvement of the superficial territory of the posterior cerebral artery. The delineation into four arterial thalamic territories (inferolateral, tuberothalamic, posterior choroidal, paramedian) corresponded clinically to four different syndromes. The most common etiologies were lacunar infarction, large artery atherosclerosis with presumed artery-to-artery embolism, cardioembolism, and migrainous stroke. We found no risk factor other than age or oral contraceptive use in six patients. One patient died in the acute phase. During follow-up (45.6 months), the stroke or death rate was 7.4% per year. Delayed pain developed in three patients and abnormal movements in three. Late disability was mainly secondary to persisting neuropsychological dysfunction (thalamic dementia).

No abstract

No abstract

Neuronal growth factors hold promise for providing therapeutic benefits in various neurological disorders. As a means of ensuring adequate central nervous system delivery of growth factors and minimizing significant adverse side effects associated with systemic delivery methods, we have developed an ex vivo gene therapy approach for protein delivery using encapsulated genetically modified xenogeneic cells. Ciliary neurotrophic factor (CNTF) has been shown in various rodent models to reduce the motor neuron cell death similar to that seen in amyotrophic lateral sclerosis (ALS). The initial trials focusing on the systemic administration of CNTF for ALS have been discontinued as a result of major side effects, thus preventing determination of the potential efficacy of the molecule. In order to deliver CNTF directly to the nervous system, we conducted a phase I study in which six ALS patients were implanted with polymer capsules containing genetically engineered baby hamster kidney cells releasing approximately 0.5 microgram of human CNTF per day in vitro. The CNTF-releasing implants were surgically placed within the lumbar intrathecal space. Nanogram levels of CNTF were measured within the patients' cerebrospinal fluid (CSF) for at least 17 weeks post-transplantation, whereas it was undetectable before implantation. Intrathecal delivery of CNTF was not associated with the limiting side effects observed with systemic delivery. These results demonstrate that neurotrophic factors can be continuously delivered within the CSF of humans by an ex vivo gene therapy approach, opening new avenues for the treatment of neurological diseases.

We studied 36 patients with MRI-proven isolated acute pontine infarct. Corresponding to the constant territories of intrinsic pontine vessels, infarcts followed a predictable distribution, enabling us to delineate three main syndromes. Twenty-one patients had a ventral pontine infarct. Motor involvement varied from mild hemiparesis (ventrolateral pontine syndrome) to severe hemiparesis with bilateral ataxia and dysarthria (ventromedial pontine syndrome). In addition, three-fourths of the patients had clinical evidence for usually mild tegmental dysfunction. Eleven patients had a tegmental pontine infarct, presenting tegmental signs (eye movement disorders, cranial nerve palsies, sensory disturbances), and mostly mild motor deficits (tegmental pontine syndrome). Only four patients had alternating deficits, and these never corresponded to any of the so-called classic pontine syndromes. Infarcts in the medial and the extreme lateral tegmental territory were never observed in isolation, being always associated with cerebellar or larger (and multiple) infarctions in the posterior circulation. Four patients with a bilateral ventrotegmental pontine infarct presented with acute pseudobulbar palsy, bilateral motor deficits, and tegmental signs. The results of etiologic work-up emphasize the concept of basilar artery branch disease, which was the most common presumed cause of stroke (16/36, 44%). Basilar artery branch disease was particularly associated with large ventral infarcts, severe clinical symptomatology, progressive or fluctuating course, and local recurrence. Presumed small-artery disease (9/36, 25%) was usually associated with small ventral or tegmental infarcts and rapidly improving lacunar syndromes. Large-artery stenosis (8/36, 22%) and cardioembolism (1/36, 3%) were less common than in series of posterior circulation infarcts that include simultaneous pontine and extrapontine lesions. Recovery was good in two-thirds of the patients, the worse outcome being associated with large ventral infarcts.

We studied 51 patients with symptomatic unilateral watershed (WS) cerebral infarct on CT. In 22 patients, the infarct was between the superficial territory of the anterior and middle cerebral arteries, 20 had an infarct between the superficial territory of the middle and posterior cerebral arteries, and 9 had an infarct between the superficial and deep territory of the middle cerebral arteries. Each type had a characteristic neurologic picture. Syncope at onset (37%) and focal limb shaking (12%) were frequent. Thirty-eight patients (75%) had internal carotid artery occlusion or tight stenosis associated with a hemodynamically significant cardiopathy, increased hematocrit, or acute hypotension. Embolic infarction was probable in only two patients (4%) who had only atrial fibrillation.

In a prospective study of 70 patients with infarcts in the posterior circulation admitted consecutively to a population-based primary-care center, we assessed infarct location and etiology using magnetic resonance imaging, three-dimensional time-of-flight magnetic resonance angiography, and noninvasive cardiac tests. The brainstem (mainly the paramedian pons) was the most commonly infarcted site (41/70, 59%), followed by the cerebellum (33/70, 47%). Combined supra- and infratentorial multiple vertebrobasilar infarcts occurred in 11 patients (16%). Overall, 27 patients (39%) had > or = 50% stenosis or occlusion of the basilar artery. There were other large-artery lesions in 19 patients (27%), including vertebral (V2-V4) stenosis or occlusion (in seven) and dolichoectatic vertebral/basilar arteries (in 12). Fifteen of the 70 patients had a potential cardiac source of embolism, which coexisted with large-artery disease in more than one-third of the cases. Cerebellar infarct without concomitant brainstem or occipital infarct was associated with cardioembolism (67%), while isolated paramedian pontine or midbrain infarct was associated with basilar artery stenosis (71%), suggesting in situ occlusion of the mouth of the perforators off the stenosed basilar artery. After exclusion of other potential causes of stroke, presumed small-artery disease associated with chronic hypertension remained the likely etiology in only 11 patients (16%), but these infarcts were not associated with any of the classical lacunar syndromes. Our findings emphasize the high frequency of severe intracranial large-artery disease in posterior circulation infarcts.