Dural sinus thrombosis mimicking "capsular warning syndrome".
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Publications and source records attributed to T P Melo.
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BACKGROUND AND PURPOSE: The first medical contact of an acute stroke victim is often a nonneurologist. Validation of stroke diagnosis made by these medical doctors is poorly known. The present study seeks to validate the stroke diagnoses made by general practitioners (GPs) and hospital emergency service physicians (ESPs). METHODS: Validation through direct interview and examination by a neurologist was performed for diagnoses of stroke made by GPs in patients under their care and doctors working at the emergency departments of 3 hospitals. RESULTS: Validation of the GP diagnosis was confirmed in 44 cases (85%); 3 patients (6%) had transient ischemic attacks and 5 (9%) suffered from noncerebrovascular disorders. Validation of the ESP diagnosis was confirmed in 169 patients (91%); 16 (9%) had a noncerebrovascular diagnosis. Overall, the most frequent conditions misdiagnosed as stroke were neurological in nature (cerebral tumor, 3; subdural hematoma, 1; seizure, 1; benign paroxysmal postural vertigo, 1; peripheral facial palsy, 2; psychiatric condition, 6; and other medical disorders, 7). CONCLUSIONS: In the majority of cases, nonneurologists (either GPs or ESPs) can make a correct diagnosis of acute stroke. Treatment of acute stroke with drugs that do not cause serious side effects can be started before evaluation by a neurologist and CT scan.
Few data exist on headache in survivors of acute cerebrovascular disease. During the second year of follow-up of a cohort of intracerebral hemorrhages (ICH), the lifetime history of headache before stroke and 2 years after stroke was characterized through a neurologic interview and a headache questionnaire. Headaches were classified following the International Headache Society classification categories. Disability (Rankin scale) and depression (CERAD depression scale) were also evaluated. Ninety survivors were interviewed. Comparing the distribution of pre- and post-ICH headaches, 24 subjects (27%) never had headaches, 39 subjects (43%) had ongoing headaches, 10 subjects (11%) complained of headaches only after ICH, and 17 subjects' (19%) headaches remitted after ICH. There was usually a delay of weeks or months between ICH and the first headache episode. Poststroke headaches were in general less severe and frequent than prestroke headaches. New-onset headaches after ICH were mainly of the tension type and were significantly associated with depression but not with new intracranial lesions. Headaches in remission after ICH were related to acute alcohol consumption and migraines. Chronic post-ICH headaches are usually tension type and occur in association with depression. Remission of headaches after ICH is related to removal of headache precipitants (alcohol) and possibly to structural or functional changes of the trigeminovascular system secondary to intracranial bleeding.
BACKGROUND AND PURPOSE: Interobserver reliability of the diagnosis of transient ischemic attack (TIA) is low, and diagnosis of TIA made by nonneurologists is often erroneous. We sought to validate the diagnosis of TIA made by general practitioners (GPs) and by hospital emergency service physicians (emergency MDs). METHODS: A list of 20 neurological symptoms was distributed to 20 GPs and 22 neurologists who graded the compatibility of each symptom with the TIA diagnosis. At least two neurologists validated TIA diagnoses made by GPs for patients under their care or by emergency MDs. RESULTS: Compared with neurologists, GPs considered "confusion" and "unexplained fall" more often compatible with TIA and "lower facial palsy" and "monocular blindness" less often compatible with TIA. Validation of diagnosis by GP was confirmed in 10 patients (19%); 26 patients had strokes, and 16 (31%) had a noncerebrovascular disorder. Validation of diagnosis by emergency MD was confirmed in 4 patients (13%); 10 patients had strokes, and 17 (55%) had noncerebrovascular disorders. The most frequent conditions misdiagnosed as TIAs were transient disturbances of consciousness, mental status, and balance. CONCLUSIONS: The TIA concept is understood differently by neurologists and nonneurologists. GPs and emergency MDs often label minor strokes and several nonvascular transient neurological disturbances as TIAs. Until this misconception of TIA is changed, the term TIA should probably be avoided in the communication between referring physicians and neurologists. If not referred to a neurologist, one third to one half of patients labeled with a diagnosis of TIA will be inappropriately managed.
OBJECTIVES: We sought to describe the frequency and location of headache in intracerebral hematoma (ICH) and to analyze its clinical and CT predictors by means of multivariate analysis. BACKGROUND: Headache is more common in intracerebral hemorrhage than in ischemic stroke, and its frequency varies with hematoma location, but the pathophysiologic mechanisms of headache associated with ICH are not fully known. METHODS: We examined a cohort of 289 patients with ICH during a 14-month period in a university hospital. Clinical, including the presence and location of headache, and CT features were collected by two neurologists. RESULTS: One hundred and sixty-five (57%) patients with ICH had a headache at the onset of their stroke. Headache was more common in cerebellar and lobar hemorrhages than in deep ones (thalamic, caudate, capsuloputaminal, brainstem). Headache was also more common in women, patients younger than 70 years, those who vomited, and those with meningeal signs, a Glasgow Coma Scale score < 10, a hematoma volume > 10 ml or CT evidence of intraventricular or subarachnoid bleeding, moderate to severe hydrocephalus, or transtentorial herniation or midline shift. In multiple logistic regression analysis, only meningeal signs (odds ratio [OR] = 2.3), cerebellar or lobar location (OR = 2.1), transtentorial herniation (OR = 1.8), and female gender (OR = 1.6) were significant predictors of headache at the onset of ICH. CONCLUSIONS: Hematoma location, meningeal signs, and gender are more predictive of headache than hematoma volume, suggesting that headache is more often related to the activation of an anatomically distributed system in susceptible individuals and to subarachnoid bleeding than to intracranial hypertension.
PURPOSE AND SETTING: To describe the prevalence and risk factors for carotid stenosis in TIA/stroke patients with non valvular atrial fibrillation (AF) and to compare clinical and CT characteristics of TIA/stroke in AF patients with and without carotid stenosis. SUBJECTS: 50 TIA/stroke patients with AF who had ultrasound investigation of the extracranial vessels, included in a prospective hospitalar registry. RESULTS: Twenty-two patients had some degree of carotid stenosis, but only 5 had more than 50% stenosis, including one with occlusion. Stenosis was neither more frequent nor more severe on the symptomatic side. Smokers were significantly more frequent in AF patients with > 50% stenosis. Clinical and CT features were quite similar in patients with and without carotid stenosis. CONCLUSION: The association in a TIA/Stroke patient of AF and severe carotid stenosis on the symptomatic side is exceptional. TIA/strokes related to carotid stenosis cannot be identified by their clinical/CT characteristics. Management of these patients must be decided by stratification of risk of recurrence for AF and from carotid stenosis and balance of these risks with that of endarterectomy.
BACKGROUND: van Gijn and co-workers identified "Perimesencephalic haemorrhage" (PM) as distinct, benign, non-aneurysmal subarachnoid haemorrhage. However, there is only one retrospective series of this entity outside the Netherlands. PURPOSE: to confirm (or not) the benign nature of perimesencephalic subarachnoid haemorrhage by evaluating its clinical course and long-term follow-up in a consecutive series of patients admitted to a University Hospital. METHODS: Patients with subarachnoid haemorrhage and negative cerebral angiography admitted between January 1985 and April 1992 were classified according to the distribution of blood on a CT scan performed within 72 hours after onset, in perimesencephalic and non-perimesencephalic haemorrhages. Demographic and clinical data (collected consecutively), complications and long-term follow-up (obtained by chart review and follow-up by mail) were compared in the two groups. RESULTS: Seventy one cases, 36 perimesencephalic and 35 nonperimesencephalic were included. Sex and age distribution were similar in the two groups. A normal examination on admission was the rule in the perimesencephalic group. Only one patient with perimesencephalic haemorrhage had a complication--transient neurological signs during angiography--and there were no deaths or morbidity during follow-up. In the non-perimesencephalic group three patients rebleed, four developed hydrocephalus and two had delayed cerebral ischaemia. Mean duration of follow-up was 27.6 months for the perimesencephalic and 30.8 months for the non-perimesencephalic group. After discharge there was a fatal rebleed in the latter group. Fifteen percent of the subjects (11% of the perimesencephalic group and 20% of the non-perimesencephalic group) retired from work during the follow-up period. Headaches and depression were found in similar percentages (22-25%) in both groups. CONCLUSIONS: This study confirms that perimesencephalic haemorrhage is a distinct entity within the larger group of subarachnoid haemorrhage with negative angiograms, with a good short term and long-term prognosis, and no need for repeated angiographic investigation.
Thirty-four percent of 182 ischemic stroke patients registered during 1 year in a prospective hospital stroke data base complained of headache within a 72-hour interval of stroke onset. Headache was more common in patients under 70 years of age, in nonsmokers, in those with a past history of migraine, and in subjects presenting transient loss of consciousness, nausea/vomiting, or visual field defects. Headache was more frequent in vertebrobasilar (57%) than in carotid (20%) territory strokes, more so in posterior cerebral artery (90%) and cerebellar infarcts (80%), and was infrequent in subcortical infarcts (7%) and lacunes due to single perforator disease (9%). In multiple regression analysis, vertebrobasilar stroke (odds ratio 6.9), lacuanr stroke (odds ratio 0.06), and past history of migraine (odds ratio 6.7) were significant independent predictors of headache, suggesting that ischemic stroke location is the major determinant of stroke-associated headache, most probably related to activation of the trigeminovascular system, whose threshold may be modified by individual susceptibility.
Sixty (29%) of 205 consecutive patients with transient ischemic attacks registered in a hospital stroke data base had headache within 72 hours of onset. Headache was significantly more common in nonsmokers (odds ratio = 2.8; 95% confidence interval = 6.7 to 1.2). Headache was infrequent in patients with amaurosis fugax, and was not significantly associated with any other particular clinical presentation of transient ischemic attack. Headache was more common in vertebrobasilar (33%) than in carotid distribution (24%) episodes, and was not rare in transient ischemic attacks presenting as lacunar syndromes (29%). Headache was less frequent in patients whose computerized tomograms showed an infarct appropriate to the symptoms (odds ratio = 0.2; 95% confidence interval = 0.02 to 1.4). A diffuse headache was more common in patients with lacunar events than in patients with cortical attacks (odds ratio = 3.0; 95% confidence interval = 13 to 0.07). No other association was found between headache location and the presumed involved vascular territory. Headache in patients with transient ischemic attacks is poorly related/explained by the clinical characteristics of the ischemic event.
To evaluate if short (less than one hour) or recurrent, or both, episodes of transient global amnesia (TGA) have an epileptic origin or carry a subsequent risk of epilepsy a group of patients with these types of TGA attacks was studied. The group was selected from a prospective series of 103 patients with TGA. Sixteen patients had an episode lasting less than one hour, 13 had more than one episode, and five patients had both short and recurrent attacks. For each patient the number of recurrences was small (four or less) and they were separated by months or years. During short attacks of TGA many subjects showed other typical features of TGA including repeated questioning (12 subjects) and performance of purposeful complex acts (eight subjects). Twelve short attacks were closely related to a characteristic precipitating event. During follow up only one patient had a seizure (partial motor). No other association between either short or repeated attacks of TGA and past history of epilepsy or paroxysmal discharges were seen on the EEG. Short or recurrent, or both, attacks of TGA are not epileptic and do not carry a relevant risk of subsequent seizures.
We report a patient with recurrent cardioembolism and hemorrhagic infarcts, who developed a fatal intracerebral hemorrhage 3 days after intravenous anticoagulation. At autopsy, cerebral amyloid angiopathy (CAA) was found. Because CAA and anticoagulation may add up to trigger cerebral hemorrhage, the possibility of underlying CAA should be raised before anticoagulating elderly patients with stroke.
Seventeen patients with hemiataxia as a manifestation of thalamic infarction were studied. Hemiataxia had the main clinical characteristics of a "cerebellar type" of ataxia, though it never occurred in isolation, being associated with ipsilateral sensory disturbance (hemiataxia-hypaesthesia) in 7 patients, with ipsilateral sensory disturbance and hemiparesis (hypaesthetic ataxic hemiparesis) in 8 patients, and with hemiparesis (ataxic hemiparesis) in 2 patients. Recovery was good, and in all patients the sensory and motor disturbances improved or cleared before the hemiataxia. All patients had an infarct involving the lateral part of the thalamus (thalamogeniculate territory in 16, tuberothalamic territory in 1), also affecting the posterior limb of the internal capsule (PLIC) in 7 patients. Hemiataxia seemed linked to involvement of the caudal part of the ventral lateral nucleus of the thalamus or the immediately adjacent medial part of the PLIC. These structures are near the corticospinal pathways and the ventral posterior nucleus of the thalamus, explaining why hemiataxia is associated with hemiparesis or hypaesthesia in this type of infarct.
A case control study of transient global amnesia (TGA), transient ischaemic attacks (TIA) and normal controls is described. Each of the 51 TGA patients, selected between January 1985 and March 1990, was compared with four controls (two TIAs and two normals) for the presence of vascular risk factors (hypertension, diabetes, smoking habits, cholesterol, triglycerides and haematocrit levels, heart disease, previous stroke), previous TGA, migraine, psychiatric illness and recent head trauma. Patients with TGA had less diabetes, hypercholesterolaemia and hypertriglyceridaemia than TIA. TGA subjects had significantly more hypertension (odds ratio = 3.31) and migraine (odds ratio = 8.67) than normal controls. During a mean of 17.4 mths of follow-up (range 1-96 mths), three subjects had recurrent TGA, one sustained a TIA and a minor stroke, but none had seizures. Thrombo-embolism and epilepsy are unlikely to be the cause of this benign disorder. The role is stressed of appropriate precipitants, including haemodynamic changes, and of individual susceptibility (of which migraine is probably a marker) in the genesis of TGA.
Six patients had isolated hemiataxia and ipsilateral sensory loss, as a manifestation of thalamic infarction in the thalamogeniculate territory. Acute hemiataxia-hypesthesia was not found in 1075 other patients from the Lausanne Stroke Registry who were admitted during the same period. Stroke onset was progressive in five patients and immediately complete in one. Five patients had an objective sensory loss. In two patients this affected light touch, pain and temperature sense, and in another three light touch, pain temperature, position and vibration sense. One patient had a purely subjective sensory disturbance. The sensory deficit cleared or was clearing although the ataxia persisted in all patients. On lesion mapping on CT or MRI, all patients had involvement of the lateral part of the thalamus (ventral posterior nucleus and ventral lateral nucleus). The presumed causes of stroke were cardioembolism in one patient, posterior cerebral artery occlusion in one patient and meningovascular syphilis in one patient, hypertensive small vessel disease in two patients, and undetermined in one patient. Hemiataxia-hypesthesia is a new stroke syndrome involving the perforating branches to the lateral thalamus, but in which small vessel disease may not be the leading cause.
We studied the correlations between the pattern of weakness, stroke type, topography, and etiology in 255 patients whose first stroke was manifested by isolated hemiparesis. They represented 14% of consecutively admitted stroke patients. The weakness distributions were as follows: face, upper limb, and lower limb (FUL) (50%); face and upper limb (FU) (29%); upper limb (U) (10%); and upper and lower limb (UL) (9%). Twenty-nine percent of the patients had dysarthria, which was of no localizing value. Less than one half of the patients had a deep infarct, and one third had a potential embolic source from the heart or large arteries. Logistic regression analysis showed that history of hypertension and type of weakness distribution were the main factors accounting for lesion localization: patients with FUL distribution and hypertension had a 90% probability of deep infarct; patients either with FUL distribution but no hypertension or with UL distribution and hypertension each had 70% probability of deep infarct. Pure motor monoparesis was almost never caused by a deep infarct. We suggest that the assumption of a lacunar etiology to a pure motor stroke should be applied only to patients with FUL involvement.
The aim of the present prospective work was to study the etiologic diagnosis and prognosis of the comatose patients for whom a neurologic examination is requested. It included 148 consecutive cases admitted to the emergency room of a general hospital. Coma was caused by supratentorial lesions in 38%, subtentorial lesions in 10%, diffuse or metabolic brain dysfunction in 49%, and psychiatric disorder in 1% of the patients. CT scan was the most valuable ancillary exam, modifying the initial etiologic diagnosis in 42% of the cases on whom it was performed. Seventy percent of the patients died. Coma caused by structural lesions had a worse outcome than coma caused by diffuse or metabolic brain dysfunction (intoxications excluded), and this type of coma had a worse outcome than drug-induced coma. The presence of anisocoria, the number of brainstem reflexes present and the pattern of motor response, as well as the Glasgow Coma Scale score, predicted the outcome.
UNLABELLED: A prospective study was performed in 106 patients with acute stroke. The main purpose was the cardiac evaluation in the different types of cerebrovascular disease: Intracerebral hemorrhage (H), Cortical ischaemic events (C) and Subcortical ischaemic events (SC) and also to evaluate the interest of echocardiography in detecting occult cardiac sources of emboli. The study population included 54 men and 52 women with a mean age of 66.8 +/- 10.3 years. A thorough neurologic and cardiologic study with a computed tomography of the brain (TAC) and an echocardiogram (ECO) were performed in all patients. It was found 24 (23%) of H, 40 (38%) of C and 32 (30%) of SC. In the past history, heart diseases were more prevalent in C (p less than 0.04); previous stroke and systemic hypertension (HTA) were less prevalent in H (p less than 0.008) and in C (p less than 0.004), respectively. Atrial fibrillation (FA) was more frequent in ischaemic stroke (p less than 0.02) and within these in C (p less than 0.005). No more clinical and functional cardiac features or echocardiographic aspects had any difference in their prevalence in different types of stroke. Without clinical heart disease there were 19 (18%) cases but only in 10 were found in their echocardiograms a potentially embolic heart disease (PEHD) but 8 of them had questionable pathologic significance. IN CONCLUSION: C had more heart disease in their past history; FA is more frequent in C; it is difficult to diagnose a cerebral embolism with only a coexistent C and CPE, but if there is FA or a past history of heart disease in a C, the diagnosis of cerebral embolism is more probable; finally, echocardiography is of limited value to diagnose a PEHD in the elderly, however it makes possible to better evaluate most cardiac situations.