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Larry B Goldstein

Publications and source records attributed to Larry B Goldstein.

At least 37 records · Page 2Linked to original sources
PubMed2005

Is this patient having a stroke?

CONTEXT: Patients suspected of having a stroke or transient ischemic attack require accurate assessment for appropriate acute treatment and use of secondary preventive interventions. OBJECTIVE: To update a 1994 systematic review of the accuracy and reliability of symptoms and findings on neurological examination for the evaluation of patients with suspected stroke or transient ischemic attack. DATA SOURCES: We identified potential articles dated between 1994 and 2005 by multiple search strategies of the MEDLINE database and review of article and textbook bibliographies along with private collections. STUDY SELECTION: Selected articles provided primary data or appropriate summary statistics of the accuracy and/or reliability of the history or physical examination for diagnosis or short-term prognosis of patients with neurological signs prompting a consideration of stroke. Articles addressing accuracy also needed to provide a final diagnosis following neuroimaging and all relevant laboratory tests. DATA EXTRACTION: The authors reviewed and abstracted data for estimating sensitivities, specificities, positive and negative likelihood ratios (LRs). Reliability assessment was based on reported kappa (kappa) statistics or intraclass correlation coefficients as appropriate. DATA SYNTHESIS: The prior probability of a stroke among patients with neurologically relevant symptoms is 10%. Based on studies using modern neuroimaging, the presence of acute facial paresis, arm drift, or abnormal speech increases the likelihood of stroke (LR of > or =1 finding = 5.5; 95% CI, 3.3-9.1), while the absence of all 3 decreases the odds (LR of 0 findings = 0.39; 95% CI, 0.25-0.61). The accurate determination of stroke subtype requires neuroimaging to distinguish ischemic from hemorrhagic stroke. Early mortality increases among those with any combination of impaired consciousness, hemiplegia, and conjugate gaze palsy (LR of > or =1 finding = 1.8; 95% CI, 1.2-2.8 and LR of 0 findings = 0.36; 95% CI, 0.13-1.0). Symptoms associated with high agreement for the diagnosis of stroke or transient ischemic attack vs no vascular event are a sudden change in speech, visual loss, diplopia, numbness or tingling, paralysis or weakness, and non-orthostatic dizziness (kappa = 0.60; 95% CI, 0.52-0.68). The reliabilities of individual neurological findings vary from slight to almost perfect, but can be improved with standardized scoring systems such as the National Institutes of Health Stroke Scale. Based on examination findings, stroke vascular distribution can be determined with moderate to good reliability (kappa = 0.54; 95% CI, 0.39-0.68). CONCLUSIONS: The history and clinical findings provide the basis for evaluating patients with possible stroke and choosing appropriate treatments. Focusing on 3 findings (acute facial paresis, arm drift, or abnormal speech) might improve diagnostic accuracy and reliability.

Emergency Medical Services↗
PubMed2005

Non-atherosclerotic vascular disease in the young.

There are a large variety of non-atherosclerotic causes of ischemic stroke in the young. Arterial dissection, most commonly associated with non-traumatic causes, is among the most common. Both the carotid and vertebrobasilar circulations can be affected. The vasculitidies represent a rare, but potentially treatable series of conditions that can lead to stroke through diverse mechanisms. Moyamoya is a nonatherosclerotic, noninflammatory, nonamyloid vasculopathy characterized by chronic progressive stenosis or occlusion of the distal internal carotid arteries and/or proximal portions of the middle and/or anterior cerebral arteries. Moyamoya can be idiopathic (moyamoya disease) or the result of other conditions. An appreciation of the unusual causes of stroke in the young is important when considering secondary prevention measures.

Adolescent↗
PubMed2004

Risk of ischemic stroke with tamoxifen treatment for breast cancer: a meta-analysis.

OBJECTIVE: To assess the overall risk of stroke, specifically ischemic stroke, associated with tamoxifen use by performing a meta-analysis of data reported in breast cancer trials. BACKGROUND: Tamoxifen increases the risk of venous thromboembolism in women with breast cancer, but its relationship to stroke risk is uncertain. METHODS: A systematic review of randomized controlled trials of tamoxifen for breast cancer management and prevention published since 1980 was performed using MEDLINE. The summary odds ratio (OR) and 95% CI were calculated using the Mantel-Haenszel method, followed by a statistical test for heterogeneity. RESULTS: Nine trials met the inclusion criteria, and six trials specified ischemic stroke outcomes. The Mantel-Haenszel summary OR was 1.82 (95% CI, 1.41 to 2.36) for ischemic stroke and 1.40 (1.14 to 1.72) for any stroke. The chi2 heterogeneity test was 6.0 (p > 0.1) for ischemic stroke and 16.1 (p < 0.05) for any stroke. The random-effects summary OR of Der Simonian and Laird for any stroke was 1.29 (0.92 to 1.81). During a mean follow-up period of 4.9 years, the frequency of ischemic stroke was 0.71% with tamoxifen vs 0.39% for controls (absolute increased risk, 0.32%; number needed to harm [NNH], 313). CONCLUSIONS: Women with breast cancer who were treated with tamoxifen had an 82% increased risk of ischemic stroke and a 29% increased risk of any stroke, but the absolute risk is small. Further studies assessing prespecified cerebrovascular outcomes are ongoing and will further clarify the risk of stroke associated with tamoxifen use.

Antineoplastic Agents, Hormonal↗
PubMed2004

Charlson Index comorbidity adjustment for ischemic stroke outcome studies.

BACKGROUND AND PURPOSE: The Charlson Index is commonly used in outcome studies to adjust for patient comorbid conditions, but has not been specifically validated for use in studies of ischemic stroke. The purpose of the present study was to determine whether outcomes of ischemic stroke patients varied on the basis of the Charlson Index. METHODS: The Department of Veterans Affairs (VA) Stroke Study prospectively identified stroke patients admitted to 9 VA hospitals between April 1995 and March 1997. The Charlson Index was scored on the basis of discharge International Classification of Diseases, 9th Revision, Clinical Modification coding and dichotomized (low comorbidity 0 or 1 versus high > or =2) for analysis. Validity was assessed on the basis of modified Rankin score at hospital discharge (good outcome 0 or 1 versus poor > or =2 or dead) and 1-year mortality, adjusting for initial stroke severity. RESULTS: Of the 960 enrolled ischemic stroke patients, 23% had a Charlson Index of 0, 34% 1, 22% 2, 12% 3, and 8% > or =4. Forty-eight percent of those with a low Charlson Index had a good outcome at discharge versus 37% of those with a high Charlson Index (P<0.001). For 1-year mortality, the proportions were 16% versus 26%, respectively (P<0.001). Logistic regression adjusting for initial stroke severity showed that those with a high Charlson Index had 36% increased odds of having a poor outcome at discharge (P=0.038) and 72% greater odds of death at 1 year (P=0.001). Every 1-point increase in Charlson Index was independently associated with a 15% increase in the odds of a poor outcome at discharge (P<0.005) and a 29% increase in the odds of death by 1 year (P<0.001). CONCLUSIONS: These data support the validity of the Charlson Index as a measure of comorbidity for use in ischemic stroke outcome studies.

Aged↗
PubMed2004

Seizures and epilepsy after ischemic stroke.

BACKGROUND: Although a long-recognized clinical phenomenon, there remain many questions regarding the epidemiology of seizures and epilepsy after ischemic stroke, their effect on outcome, and their treatment. SUMMARY OF REVIEW: Interpretation of the various studies that have been conducted of postischemic stroke seizures and epilepsy are complicated by their heterogeneous designs, inconsistent uses of terminology, small sample sizes, different periods of follow-up, and ambiguities in seizure identification and classification. Estimates of the rate of early postischemic stroke seizures range from 2% to 33%. The rates of late seizures vary from 3% to 67%. The rate of postischemic stroke epilepsy is approximately 2% to 4% and is higher in those who have a late seizure. Data reflecting seizure subtypes are limited. Aside from cortical location and, possibly, stroke severity, no other risk factors for postischemic stroke seizures have been consistently demonstrated. CONCLUSIONS: Much additional work is needed to better understand the epidemiology and social impact of postischemic stroke seizures and epilepsy, their prevention, and optimal management.

Animals↗
PubMed2004

Neurological deficits induced by malathion, DEET, and permethrin, alone or in combination in adult rats.

Malathion (O,O-dimethyl-S-[1,2-carbethoxyethyl]phosphorodithionate), DEET (N,N-diethyl-m-toluamide), and permethrin [(+/-)-cis/trans-3-(2,2-dichloroethenyl)-2,2-dimethylcyclopropane carboxylic acid (3-phenoxyphenyl) methyl ester] are commonly used pesticides. To determine the effects of the dermal application of these chemicals, alone or in combination, the sensorimotor behavior, central cholinergic system, and histopathological alterations were studied in adult male Sprague-Dawley rats following a daily dermal dose of 44.4 mg/kg malathion, 40 mg/kg DEET, and 0.13 mg/kg permethrin, alone and in combination for 30 d. Neurobehavioral evaluations of sensorimotor functions included beam-walking score, beam walk time, inclined plane, and grip response assessments. Twenty-four hours after the last treatment with each chemical alone or in combination all behavioral measures were impaired. The combination of DEET and permethrin, malathion and permethrin, or the three chemicals together resulted in greater impairments in inclined performance than permethrin alone. Only animals treated with a combination of DEET and malathion or with DEET and permethrin exhibited significant increases in plasma butyrlcholinesterase (BChE) activity. Treatment with DEET or permethrin alone, malathion and permethrin, or DEET and permethrin produced significant increases in cortical acetylcholinesterase (AChE) activity. Combinations of malathion and permethrin or of DEET and permethrin produced significant decreases in midbrain AChE activity. Animals treated with DEET alone exhibited a significant increase in cortical m2 muscarinic ACh receptor binding. Quantification of neuron density in the dentate gyrus, CA1 and CA3 subfields of the hippocampus, midbrain, brainstem, and cerebellum revealed significant reductions in the density of surviving neurons with various treatments. These results suggest that exposure to real-life doses of malathion, DEET, and permethrin, alone or in combination, produce no overt signs of neurotoxicity but induce significant neurobehavioral deficits and neuronal degeneration in brain.

Acetylcholinesterase↗
PubMed2004

Co-exposure to pyridostigmine bromide, DEET, and/or permethrin causes sensorimotor deficit and alterations in brain acetylcholinesterase activity.

Military personnel deployed in the Persian Gulf War (PGW) were exposed to a combination of chemicals, including pyridostigmine bromide (PB), DEET, and permethrin. We investigated the dose-response effects of these chemicals, alone or in combination, on the sensorimotor performance and cholinergic system of male Sprague-Dawley rats. Animals were treated with a daily dermal dose of DEET and/or permethrin for 60 days and/or PB (gavage) during the last 15 days. Neurobehavioral performance was assessed on day 60 following the beginning of the treatment with DEET and permethrin. The rats were sacrificed 24 h after the last treatment for biochemical evaluations. PB alone, or in combination with DEET, or DEET and permethrin resulted in deficits in beam-walk score and longer beam-walk times compared to controls. PB alone, or in combination with DEET, permethrin, or DEET and permethrin caused impairment in incline plane performance and forepaw grip strength. PB alone at all doses slightly inhibited plasma butyrylcholinesterase activity, whereas combination of PB with DEET or permethrin increased its activity. Brainstem acetylcholinesterase (AChE) activity significantly increased following treatment with combinations of either DEET or permethrin at all doses, whereas the cerebellum showed a significant increase in AChE activity following treatment with a combination of PB/DEET/permethrin. Co-exposure to PB, DEET, and permethrin resulted in significant inhibition in AChE in midbrain. PB alone or in combination with DEET and permethrin at all doses increased ligand binding for m2 muscarinic acetylcholine receptor in the cortex. In addition, PB and DEET together or a combination of PB, DEET, and permethrin significantly increased ligand binding for nicotinic acetylcholine receptor. These results suggest that exposure to various doses of PB, alone and in combination with DEET and permethrin, leads to sensorimotor deficits and differential alterations of the cholinergic system in the CNS.

Acetylcholinesterase↗