Neurologic abnormalities in human immunodeficiency virus infection.

Neurologic abnormalities involving the central and peripheral nervous system are common in patients infected with the human immunodeficiency virus (HIV). Evidence of central nervous system infection (cerebrospinal fluid abnormalities) occurs early; however, evidence of central and peripheral nervous system dysfunction usually occurs at later stages. Neurologic manifestations may be due to chronic immunosuppression, direct neurotropic effect of HIV, or medication effects. It is important to recognize that brain and spine imaging studies are highly sensitive in detecting abnormal pathologic processes, but these studies have low specificity for establishing a specific pathologic diagnosis.

Aspiration in patients with acute stroke.

OBJECTIVES: To determine the frequency and clinical predictors of aspiration within 5 days of acute stroke. DESIGN: Case series. SETTING: Tertiary care center. PATIENTS: Consecutive stroke patients (n = 55) with new neurologic deficit evaluated within 5 days of acute stroke. MAIN OUTCOME MEASURES: Comparison of features identified on clinical swallowing and oromotor examinations and occurrence of aspiration (silent or overt) evident on videofluoroscopic swallow study (VSS). RESULTS: Aspiration occurred in 21 of 55 patients (38%). Whereas 7 of 21 patients (33%) aspirated overtly, 14 (67%) aspirated silently on VSS. Chi-square analyses revealed that dysphonia, dysarthria, abnormal gag reflex, abnormal volitional cough, cough after swallow, and voice change after swallow were significantly related to aspiration and were predictors of the subset of patients with silent aspiration. Logistic regression revealed that abnormal volitional cough and cough with swallow, in conjunction, predicted aspiration with 78% accuracy. CONCLUSIONS: Silent aspiration appears to be a significant problem in acute stroke patients because silent aspiration occurred in two thirds of the patients who aspirated. The prediction of patients at risk for aspiration was significantly improved by the presence of concurrent findings of abnormal volitional cough and cough with swallow on clinical examination.

Cerebrovascular disease in the Afro-American population.

The types of stroke which are unique to Afro-American patients are reviewed. The major risk factors which contribute to the higher incidence of stroke in this population are analyzed.

Racial differences in stroke recurrence rate following initial lacunar infarct.

One-hundred fourteen black patients and 50 white patients who had suffered an initial lacunar infarct were retrospectively analyzed to determine the incidence of clinical stroke recurrence within 12 months of the initial stroke. Of the 114 black patients, 35 had recurrent stroke (31%). Of the recurrent stroke, 27 were lacunar infarcts and eight were nonlacunar. Utilization of aspirin at a maximal dose of 325 mg/d did not reduce stroke recurrence. Of the 50 white patients, four had recurrent strokes (8%). Of these, only one represented lacunar infarct and three were nonlacunar. All the black (35) and white (four) lacunar stroke patients who suffered stroke recurrence were hypertensive and had been hypertensive for more than 8 years; they also had evidence of end-organ damage consisting of hypertensive retinopathy and left ventricular hypertrophy or had episodes of congestive heart failure.

Physician attitudes toward treatment options for cerebrovascular disease.

One-hundred physicians older than 50 and 100 physicians younger than 50 were surveyed concerning treatment preferences for patients with transient ischemic attacks (TIAs) or completed stroke. These attitudes were compared to cardiovascular disease prevention strategies for patients with angina pectoris and myocardial infarction. Physicians younger than 50 were therapeutically aggressive for cerebrovascular and cardiovascular disease; physicians older than 50 were aggressive for cardiovascular disease but therapeutically nihilistic for cerebrovascular disease. Physicians younger than 50 were more likely to be aggressive for TIA than for completed stroke patients, and these physicians were more likely to utilize ticlopidine and oral anticoagulants for both TIA and completed stroke patients.

Retrospective analysis of aspirin and ticlopidine in preventing recurrent stroke following an initial lacunar infarct.

Of 73 patients with initial lacunar stroke subsequently treated with aspirin, 13 (18%) developed recurrent stroke (11 lacunar infarcts and 2 nonlacunar infarcts), and 4 (5%) died within 1 year. Of the aspirin-treated lacunar infarct patients, 58 received 325 mg or lower-dose aspirin, and 15 received 600-1,300 mg of aspirin. Thirteen aspirin-treated patients who developed recurrent ischemic stroke received 80 mg or 325 mg of aspirin, whereas recurrent stroke did not occur in 15 patients treated with 600-1,300 mg of aspirin daily. Of 25 patients with lacunar stroke who were subsequently treated with 250 mg of ticlopidine twice daily, 1 patient (4%) developed recurrent lacunar infarct, and none died within 1 year. Of 10 patients who had an initial lacunar stroke and subsequently received no antiplatelet medication, 4 (40%) developed recurrent lacunar stroke, and 1 (10%) died within 1 year.

Management of the TIA patient.

Initial management of the TIA patient is dependent upon the underlying vascular lesion. This is defined by brain imaging and neurovascular studies. For patients with greater than 70% extracranial carotid stenosis, carotid endarterectomy is indicated. For patients with established cardiac emboli source, anticoagulation is indicated. In other TIA patients, antiplatelet medication (aspirin, ticlopidine) is indicated. The choice of antiplatelet medication is dependent upon patient characteristics, eg, gender, race, angiographic abnormality. TIA patients are at high risk for developing completed stroke and emergency hospitalization is warranted after initial TIA.

Evaluation of the patient with transient ischemic attacks.

Transient ischemic attacks (TIA) are warning symptoms of stroke in 35% of patients. A TIA is an episode of focal neurological dysfunction which is of sudden onset; the deficit completely resolves within 24 hours but the majority of TIA episodes last only 5 to 30 minutes. Full neuroimaging and neurovascular evaluation are necessary for all TIA patients. The occurrence of a TIA represents a medical emergency and immediate evaluation is necessary to define the occurrence of TIA mechanism and determine appropriate treatment options to avoid the development of a completed stroke.

The efficacy and safety of ticlopidine and aspirin in non-whites: analysis of a patient subgroup from the Ticlopidine Aspirin Stroke Study.

We analyzed the efficacy of ticlopidine and aspirin in the non-white subgroup of patients from the Ticlopidine Aspirin Stroke Study. In this double-blind, randomized, multicenter study, patients received either ticlopidine 250 mg (312 non-white patients) or aspirin 650 mg (291 non-white patients) twice a day. The 1-year cumulative event rate per 100 patients for nonfatal stroke or death from any cause was 5.5 for ticlopidine and 10.6 for aspirin--an apparent 48.1% reduction in risk with ticlopidine relative to aspirin. The 1-year cumulative event rate for fatal or non-fatal stroke was 3.7 for ticlopidine and 9.4 for aspirin--an apparent 60.8% reduction in risk with ticlopidine relative to aspirin. The cumulative event rates for both endpoints also were lower in ticlopidine-treated patients after the 2nd and 3rd years. These reductions were not significantly different between treatment groups, but were of the same order of magnitude as previously found for the total series, which did attain statistical significance (p = 0.048), and the frequency of adverse events was not significantly different between the two treatment groups. Severe neutropenia, the most serious adverse event associated with ticlopidine use, did not occur in non-white patients. These results suggest that ticlopidine is superior to aspirin for stroke prevention in non-whites.

Racial differences for lacunar infarcts documented by computed tomography: A comparison of black and white patients.

Lacunar stroke in 100 black and 30 white patients with lacunar syndrome and computed tomography (CT) positive for lacunar infarct were compared. Of blacks, 88% were hypertensive, 77% had target-organ damage, and 86% were hypertensive for longer than 8 years. Of whites, 60% were hypertensive, 61% had target-organ damage, and 72% were hypertensive for longer than 8 years. Prior clinical stroke occurred in 7% of blacks and 50% of whites. Transient ischemic attacks (TIAs) were found in 33% of blacks and 53% of whites. In blacks, CT showed single lacunes in 57% and multiple lacunes in 43%. In whites, CT showed single lacunes in 64% and multiple lacunes in 36%. Angiography was abnormal in 22% of blacks and 54% of whites. In blacks, lacunar stroke was associated with hypertension in 88%, and lacunar stroke was the initial cerebrovascular manifestation in 80%; CT showed "silent" lacune(s) in 41% of hypertensive blacks. In whites, lacunar stroke was associated with hypertension in 60%, and 6% had "silent" lacunes. Based on CT findings, only hypertensive patients had "silent" lacunes.

Massive putaminal-thalamic nontraumatic hemorrhage.

Fourteen patients developed massive putaminal-thalamic hemorrhage. All patients were young black men. They were hypertensive but without chronic hypertensive vascular changes. They had been treated with antihypertensive medication for less than 3 yr. All patients presented with a prodromal headache beginning 18-30 h before the brain hemorrhage. Initial clinical signs were heralded by a change in the headache pattern and vomiting. All patients became comatose and hemiplegic within 4-12 h. CT showed a hyperdense putaminal-thalamic hemorrhage which was 60 to 86 mm in maximal diameter. There was marked mass effect with secondary intraventricular extension. All patients died within 72 h, despite rapid and adequate blood pressure control and maximal medical treatment of cerebral edema and increased intracranial pressure.

Nontraumatic posterior temporal lobe hemorrhage: clinical computed tomographic correlations.

Ten patients with nontraumatic posterior temporal hematomas were analyzed. These hemorrhages were spontaneous (four cases) or hypertensive (six cases). With right posterior temporal hematomas, headache and confusion of sudden onset were the initial common characteristic clinical signs. The absence of prominent lateralizing neurological deficit simulated a diffuse toxic or metabolic encephalopathy. With left-sided hematomas, Wernicke-type aphasia was the initial feature. The 10 hematomas were 1.8 to 2.8 cm in maximal diameter. In these 10 cases, clinical outcome was good, as all patients survived and the hematoma resolved spontaneously.

Clinical characteristics of transient ischemic attacks in black patients.

We analyzed the clinical, CT, and angiographic findings in 50 black patients with carotid transient ischemic attacks (TIAs). Thirty-two percent had TIAs lasting less than 1 hour, 26% had TIAs lasting 1 to 6 hours, and 42% had TIAs lasting 6 to 24 hours. Fifty-two percent of TIA patients had CT evidence of cerebral infarction despite complete clinical recovery. CT was abnormal in two of 16 (13%) patients with TIAs lasting less than 1 hour; however, CT was abnormal in 24 of 34 (70%) patients with TIAs lasting longer than 1 hour. Angiographic findings of extracranial carotid disease appropriate to TIA symptoms were present in 12 (24%) patients. Two patients in whom the TIA episode lasted less than 1 hour later had clinical cerebral infarction, whereas 20 patients with longer-duration TIAs developed ischemic stroke within 4 months. Of these black TIA patients, 22 (44%) developed clinical cerebral infarction.

Seizures caused by nontraumatic parenchymal brain hemorrhages.

Seizures occurred in 15% of patients with parenchymal brain hemorrhage (early in 12% and delayed in 3%). Seizures were most frequent with lobar hemorrhages and uncommon with deep subcortical hemorrhages. Lobar hemorrhages in the frontal, parietal, or temporal region were more commonly associated with seizures, whereas occipital hemorrhages were not. Seizures were most common if the hemorrhage was due to an aneurysm, angioma, or neoplasm and less common if hypertensive or spontaneous. If the patient had recurrent seizures or developed delayed seizures, CT showed that the hemorrhage evolved to a hypodense appearance; if the seizure did not recur, CT showed that the hemorrhage evolved to an isodense appearance.

Intraventricular hemorrhage in adults: clinical-computed tomographic correlations.

The clinical and computed tomographic (CT) findings in 100 consecutive adult nontraumatic intraventricular hemorrhage (IVH) cases are analyzed. There were 74 parenchymal brain hemorrhages with secondary ventricular extension. The ventricles were filled with blood and asymmetrically enlarged. If the hemorrhage involved putamen, cerebellum, pons, or subcortical cerebral hemispheric white matter, IVH was associated with large parenchymal hematomas; these patients had poor clinical outcome. With thalamic or caudate hematomas, IVH frequently occurred with large hematomas but may occur with small hematomas. The small hematomas were located directly contiguous to the ventricular walls and caused extensive ventricular blood. Patients with small thalamic and caudate hemorrhage with intraventricular blood had good clinical outcome; whereas patients with large hematomas had poor outcome. Primary IVH occurred in 24 cases. In these cases, blood was seen in all ventricular chambers. Aneurysms involving the anterior cerebral-anterior communicating artery region were the most common etiology for primary IVH.

Lacunar infarction in patients with hypertensive intracerebral hemorrhage.

Of 300 patients with computerized tomographic (CT) evidence of acute hypertensive intracerebral hemorrhage, high-resolution CT scans showed cerebral lacunar infarction (lacunes) in only nine cases (3%). The lacunes were seen in putaminal (six cases), thalamic (one case), and occipital (two cases) hematomas. All patients with lacunes and intracerebral hemorrhage had had systemic arterial hypertension for 7 to 14 years, cardiographic evidence of ventricular hypertrophy, chest radiographic evidence of cardiomegaly, and funduscopic evidence of retinopathy. The intracerebral hemorrhages were small, with maximal diameters of the hematomas 9 to 18 mm. All patients had good clinical outcome. In a 3-year follow-up, three patients had symptomatic lacunar infarcts but none had recurrent hemorrhage, whereas six patients had myocardial infarction or congestive heart failure.

Nontraumatic parenchymal brain hemorrhages.

Before the availability of computerized tomography (CT), it was estimated that 25% of parenchymal brain hemorrhages (PBH) was diagnosed as ischemic stroke. Clinical studies were biased toward large hemorrhages with high mortality rates. More recently, the full clinical spectrum of PBH has been appreciated only with studies correlating clinical findings and CT results. In the pre-CT era, hypertension was thought to be the major risk factor for PBH. Chronic hypertensive vascular changes were believed to cause arteriolar wall damage, and rupture of weakened dilated vessels thought to result in PBH. The occurrence of PBH in previously normotensive patients was underrepresented in pre-CT era studies. Current CT findings in PBH patients have shown that normotensive patients and hypertensive patients with chronic vascular changes have smaller hemorrhages resulting in lower mortality than hypertensive patients without chronic vascular changes. Because chronic hypertensive vascular changes are believed to be common in patients with PBH, this finding is unexpected and previously unreported. Chronic vascular changes may therefore offer some unexplained "protection" for brain blood vessels. Alternatively the mechanism of hypertensive PBH may be somewhat different than previously postulated.

How to identify and manage brain hemorrhage.

With the aid of computed tomography, physicians are able to differentiate parenchymal brain hemorrhage from ischemic stroke. The most common sites of hypertensive hemorrhage are the putamen and thalamus. Lobar hemorrhages are not usually due to hypertension. Therapy for parenchymal brain hemorrhage is based on knowledge of the hemorrhage's natural history. Medical treatment is directed toward reducing blood pressure and intracranial pressure. A number of general factors must be considered before undertaking surgery, because indications are usually undefined.