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Biomedical subjects

L A Weisberg

Publications and source records attributed to L A Weisberg.

At least 19 recordsLinked to original sources

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.

AIDS-Related Opportunistic Infections↗

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.

Acute Disease↗

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.

Humans↗

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.

Humans↗

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.

Aged↗

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.

Cerebral Angiography↗

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.

Adult↗

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.

Brain Diseases↗

Nontraumatic temporal subcortical hemorrhage. Clinical-computed tomographic analysis.

Thirty patients with temporal hematomas were analyzed. Four with frontal extension survived. Of 6 with ganglionic extension, three had residual deficit. Of 8 with parietal extension, 4 had delayed deterioration and died, two patients recovered, and two with peritumoral hemorrhage due to glioblastoma multiforme died. Five patients with posterior temporal hematomas recovered. In 7 patients with basal-inferior temporal hematomas, angiography showed aneurysms in 3 cases, angiomas in 2 cases and no vascular lesion in 2 cases. Of 23 cases with negative angiography and no systemic cause for temporal hematoma, 12 patients were hypertensive and 11 were normotensive. Ten hypertensive patients without evidence of chronic vascular disease had the largest hematomas, extending into the parietal or ganglionic regions. Seven of these patients died; 3 had residual deficit. Eleven normotensive and two hypertensive patients with evidence of chronic vascular change had smaller hematomas. They survived with good functional recovery.

Adult↗

Putaminal hemorrhage: clinical-computed tomographic correlations.

Ninety-two percent of 100 patients with putaminal hemorrhage were hypertensive. Of the eight normotensive patients, seven were substance abusers or had bilateral putaminal hemorrhages. The one other normotensive patient was less than 40 years old. The 100 hemorrhages had the following locations: 1. medial putaminal (17 cases; six were normotensive and less than 40 years old and five were substance abusers); 2. lateral putaminal extending through the external capsule (eleven cases); 3. putaminal-capsular and subcortical white matter (32 cases); 4. putaminal cerebral hemispheric (19 cases); 5. putaminal-thalamic (19 cases); 6. bilateral (two cases). A disproportionate number of black patients suffered hematoma extension to the cerebral hemispheres or thalamus (46%) compared to Caucasians (23%). Overall mortality was 20% (17 blacks and three Caucasians) and occurred in patients with hematoma extension to the thalamus or cerebral hemispheres. Contrast-enhanced CT was performed in all 100 patients and provided no additional diagnostic yield. This indicates limited use for enhanced CT in hypertensive patients with putaminal hemorrhage who have a characteristic appearance of the acute hemorrhage on the nonenhanced CT.

Adult↗

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.

Brain↗

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.

Cerebral Hemorrhage↗

AIDS dementia complex. Characteristics of a unique aspect of HIV infection.

A common complication of acquired immunodeficiency syndrome (AIDS) is being increasingly recognized. Known as AIDS dementia complex, the disorder is characterized by global impairment of intellectual and cognitive functions, personality and behavioral disturbances, and motor dysfunction manifested by impaired speech, gait, and coordination. AIDS dementia complex progresses rapidly and inexorably from psychomotor slowing to dementia, then to an akinetic mute state in which the patient becomes immobile and incapable of speaking, and finally to coma. Differentiation of AIDS dementia complex from a potentially treatable condition, such as reactive depression, is important. Zidovudine (Retrovir), the drug currently used to treat AIDS, has shown promise in the treatment of AIDS dementia complex. Clinical trials are now under way to determine its efficacy in this application.

Acquired Immunodeficiency Syndrome↗

Neurologically asymptomatic patients with a single cerebral lacuna.

Sixteen patients with CT evidence of a single cerebral lacuna had no clinical findings to indicate stroke syndromes. All patients had systemic arterial hypertension; 12 (75%) had cardiographic evidence of left ventricular hypertrophy, ten (63%) had radiologic evidence of cardiomegaly, and ten (63%) had clinical signs of hypertensive retinopathy. All lacunas were located in the supratentorial region (seven in the anterior capsular limb, three in the caudate, two in the external capsule, two in the putamen, one in the corona radiata, and one in the thalamus). During the three-year follow-up period, seven had clinical lacunar stroke syndrome, three had cortical stroke, two had myocardial infarction, and one died suddenly of unknown cause.

Aged↗

Nontraumatic frontal lobe hemorrhages: clinical-computed tomographic correlations.

Correlation of lesion location and appearance with clinical sequelae in 25 patients with CT-proven frontal lobe hematomas reveals 10 of 25 hematomas were located above the frontal horns of the lateral ventricles. Nine of the 10 patients were normotensive. All presented with contralateral motor and sensory deficits. Four of 25 hematomas were situated inferior to the frontal horns. All these patients were hypertensive, rapidly became comatose and exhibited hemiplegia, hemianesthesia and gaze preference contralateral to the hemiplegia. Five patients had frontal hematomas which extended inward from the interhemispheric fissure or caval-septal region. All were normotensive. All had anterior cerebral-anterior communicating artery aneurysms on angiography. Four patients had hematomas involving both the frontal and temporal region. All were normotensive with no known cause for hemorrhage. Two patients had bifrontal hematomas; one had butterfly appearance extending across the interhemispheric fissure and the other was midline but had no interhemispheric blood. Both were normotensive. One had an anterior cerebral-anterior communicating artery aneurysm.

Adult↗