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Background: Registries of cerebral vascular disease (CVD) are useful in the study of the natural history of acute cerebrovascular disease (ACBD). Nonetheless there are few series which analyze the different stroke subtypes (SS) of CVD., Methods: A descriptive and comparative clinical analysis was performed of the different SS of CVD from the registry of CVD of the La Alianza-Central Hospital of Barcelona (Spain). A prospective study of 1,000 consecutive patients with ACVD admitted in the Neurology Department from 1986-1991 was carried out. The registry recommended by the Study Group of Cerebrovascular Diseases of the Sociedad Española de Neurología (SEN) were used and the stroke subtypes classified in agreement with the Glossary of Neurology of the SEN., Results: The mean age of the series was of 71 +/- 13 years with 537 patients being males. The frequency of the stroke subtypes in focal cerebral ischemia (FCI) was: thrombotic infarction 26%, lacunar infarction 16.9%, essential infarction 14.8%, cardioembolic infarction 12.4%, transient ischemic attacks 9% and infarction of unusual cause 3.5%. The frequency of the SS in cerebral hemorrhage (CH) was: intraparenchymatous hemorrhage 14.1%, subarachnoid hemorrhage 2.0%, subdural hematoma 1.2% and epidural hematoma 0.1%. Mortality of the series was 16.7% predominating in CH (28%) versus FCI (14%) (p < 0.00001). This was found to be greatest in cases of intraparenchymatous hemorrhage (31%) and in the cardioembolic infarction (28%) and lowest in the lacunar infarctions (0.6%)., Conclusions: The most common stroke subtypes were those of thrombotic infarctions, lacunar infarctions and intraparenchymal hemorrhages. Essential infarctions constitute 14.8% of acute cerebral vascular disease. The classification of cerebral vascular disease in its different subtypes is recommendable since this has prognostic and therapeutic implications.

We discuss in this paper the cases of two patients with pure motor hemiparesis which were secondary to chronic subdural hematoma who evolved satisfactorily only with medical treatment. Of 1,000 consecutive patients with cerebro-vascular pathology admitted in our Neurology Department in the last 5 years, said two patients were the only ones (0.2%) in whom the lacunar syndrome "pure motor hemiparesis" was secondary to a chronic subdural hematoma. Such cases show that a subdural hematoma can manifest itself as a lacunar syndrome and that in selected cases the medical treatment of chronic subdural hematoma can yield goods results.

Background: Headache is a little known aspect in the study of acute ischemic cerebrovascular disease (AICVD)., Methods: To contribute to the knowledge of the clinical characteristics of headache in the different nosologic entities of AICVD a prospective study was performed in 195 patients consecutively studied by CT scan and/or cerebral MRI., Results: There was headache in 32% of the total and in 41% of the thrombotic infarctions, 39% of the cardioembolisms, 26% of the transient ischemic attacks (TIA) and 23% of the lacunar infarcts. The mean duration was 25 +/- 28 hours. Headache was focal in 74% of the cases and of slight or moderate intensity in 74%. Headache was significantly more common in thrombotic infarctions than in lacunar ones (p < 0.05). It was more frequent when the topography is vertebrobasilar (57.5%), in comparison with carotid (21%) or undetermined (17.5%) (p < 0.0001). Headache was more common when topography was cortical (56.5%) in comparison with subcortical (26.5%) (p < 0.005). Eight per cent of the patients presented sentinel headache: 22% of the cardioembolic infarctions, 7% of the lacunars, 6.5% of the TIA and 5.5% of the thrombotic., Conclusions: Headache in acute ischemic cerebrovascular disease is not uncommon predominating in thrombotic infarctions and cardioembolisms of cortical topography and of vertebrobasilar vascular territory.

A random sample of 302 children, aged between 6 months and 15 years, of a healthy Mediterranean population were studied. Abnormal values of biochemical parameters of iron status were frequently found. In the 0.5-2 year group, erythrocyte protoporphyrin values were abnormal in 13.5% of subjects, serum ferritin in 9.7%, transferrin saturation capacity in 75.3%, mean red cell volume in 4.1% and haemoglobin in 9.7%. Comparing nutritional intake (24 h dietary recall over 3 days) between individuals at low and high values of biochemical iron status some significant differences were found in each age group but in no case with regard to heme iron intake. In the overall age-adjusted study population, the nutritional intake had a low but significant explanatory capacity of the variance of the measured biochemical iron status parameters (between 1.1% for transferrin saturation capacity and 4.5% for serum ferritin) and a non-significant capacity in those children younger than 3 years. In conclusion, although the dietary pattern in our area favours a good iron bioavailability, in our population the nutritional intake was shown to have a limited relationship with the parameters of biochemical iron status parameters. These data suggest that, in healthy children, abnormal biochemical iron status parameters may be related to factors other than nutritional intake.

Protein C together with its plasmatic cofactor protein S and antithrombin III probably represent the most important plasmatic inhibitor in coagulation. Protein C deficiency constitutes a high risk factor for venous thrombosis. Cerebral venous thrombosis is a manifestation which is scarcely referred to in protein C deficiency. The case of a 32 year old patient with protein C deficiency is presented. The patient was admitted for an endocraneal hypertension syndrome. CT and MR demonstrated multiple hemorrhagic cerebral infarctions. Arteriography confirmed vertebral venous thrombosis. Only six cases sufficiently documenting cerebral venous thrombosis due to protein C deficiency were found in the literature. In most cases coadjuvant factors exist predisposing thromboembolic disease. The present clinical case demonstrates the importance of considering protein C deficiency in the diagnosis of cerebral venous thrombosis in young adults.

The clinical observation of a 74 year old male presenting isolated Wernicke's aphasia due to a temporal left infarction of cardiac embolic origin secondary to paroxysmal auricular flutter is described. Transthoracic and transesophageal echocardiography, computerized tomography and magnetic resonance provided characteristic images which permitted the establishment of the diagnosis of lipomatous hypertrophy of the interauricular septum without requiring the use of invasive techniques. Lipomatous hypertrophy of the interauricular septum is a cardiac tumor of unusual presentation constituted of an abnormal accumulation of non-encapsulated fatty tissue which occupies a thickness greater than 15 mm of the interauricular septum. Wernicke's aphasia as a form of presentation of the lipomatous hypertrophy of the interauricular septum has not previously been described in the literature.

We report a 26-year-old male who developed aphasia due to an ischemic cerebral infarction caused by MELAS (myoencephalophatic syndrome with lactic acidosis and cerebral ischemia). The most common causes of cerebral infarction in young patients were ruled out by laboratory investigations. The diagnosis of MELAS was suspected on the basis of past history of epilepsy, migraine and progressive sensory deafness, and increased resting blood lactic acid. Cerebral computed tomography showed bilateral caudate-putamen-pallidal calcification and nuclear magnetic resonance scan disclosed a left ischemic parietal-temporal-occipital infarction. The diagnosis was confirmed by muscular biopsy, which was characteristic of mitochondrial myopathy showing "red disarrayed" fibers in the histologic modified trichromic Gomori stain. Our patient showed that MELAS should be considered in young adults with cerebral infarction. The diagnosis should initially be suspected on a clinical basis, and confirmed by the presence of "red disarrayed" fibers with modified trichromic Gomori stain histologic muscle study.

To shed some light on the potential value of rifampicin in the treatment of tuberculous meningitis (TBM) in adults, a retrospective analysis has been made of 143 medical records from 4 hospitals for the period 1967-80. Treatment of TBM with rifampicin and other antituberculous drugs in combination (Group B) was compared to other regimes which did not include rifampicin (Group A). There were 64 patients in Group B and 79 in Group A. The two groups of patients did not differ significantly in their prognostic characteristics. The total mortality was 14.7%: it was higher among patients not treated with rifampicin (24%; Group A) than amongst those given rifampicin (3.1%; Group B; chi 2 = 10.74; p less than 0.005). The difference was also statistically significant (chi 2 = 6.88; p less than 0.01) if patients who died during the first 48 h after the institution of treatment were excluded. No significant difference in mortality rate was found when patients treated with rifampicin plus isoniazid (INH) 8-10 mg/kg (1 death out of 41 patients) were compared to patients treated with INH 15 mg/kg (2 deaths out of 20 patients). Neurological sequelae recorded during a 6 month follow-up period were more severe among patients not treated with rifampicin.