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At least 19 recordsLinked to original sources
PubMedDate not supplied

White matter changes: neurobehavioral manifestations of Binswanger's disease and clinical correlates in Alzheimer's disease.

Although white matter lesions (WMLs) are among the most common structural neuroimaging changes found on computed tomography and magnetic resonance imaging of older persons with dementia, their presence should not be misconstrued as proof that vascular disease is causing or contributing to the dementia. We report the results of several studies examining the neurobehavioral manifestations of persons meeting explicit operational criteria for Binswanger's disease (BD) and the clinical correlates of white matter changes in persons with autopsy-proven Alzheimer's disease (AD). The findings suggest that relative to persons with AD of comparable dementia severity, persons with BD have less profound impairments in episodic memory, more depressive symptomatology and a more variable rate of cognitive decline; among persons with AD, some WMLs are associated with incontinence and gait disturbance, but they do not appear to contribute to dementia severity.

Alzheimer Disease↗
PubMed1993

Neurobehavioral manifestations following closed head injury.

This study was designed to examine neurobehavioral sequelae following closed head injuries. It adapted the Neurobehavioral Rating Scale (NRS) which was designed by Harvey S. Levin in 1987. The scale has been proven to be valid and reliable in previous Western studies and was translated by the authors into Mandarin with the consent of its designer. A total of 335 cases of closed head injury in eight major hospitals in Taipei were studied. The main findings obtained from this preliminary study were: 1) the correlation coefficients between raters ranged from 0.749 to 0.956, manifesting satisfactory reliability; 2) seven factors were obtained through factorial analysis of NRS, explaining 65.5% of the variance; and 3) significant differences in neurobehavioral change were found in patients with various degrees of severity and various types of head injuries. The results demonstrate that NRS is applicable to Chinese patients. Possible modification as well as elaboration of this scale is suggested.

Analysis of Variance↗
PubMed1996

Neurobehavioral manifestations of symptomatic HIV-1 disease in children: can nutritional factors play a role?

Central nervous system (CNS) abnormalities are significant and frequent complications of human immunodeficiency virus (HIV-1) infection in infants and children. Although the predominant cause of neurological and neuropsychological abnormalities appears to be related to HIV infection of the CNS, other factors including malnutrition may also play a role. We retrospectively evaluated the association of change in body weight with changes in neurocognitive function, ventricular brain ratio, and cerebrospinal quinolinic acid levels in a small cohort of children (n=15; mean age 6.3 years) with symptomatic HIV-1 disease before and after 6 months of antiretroviral therapy with continuous intravenous infusion of zidovudine (ZVD). Significant increases in weight and neurocognitive function as well as decreases in ventricular brain ratio and cerebrospinal quinolinic acid levels were noted after therapy. Only the relation between increase in weight and decrease in ventricular brain ratio was statistically significant (P< .01); contrary to expectations, an increase in weight seemed to correlate with a decrease in neurocognitive function (NS). Another group of children treated at the same time with oral intermittent ZVD, but otherwise receiving the same care did not show the same magnitude of improvement in neurocognitive function. These results seem to suggest that general supportive and medical care as well as nutritional factors may only play a limited role in the neurocognitive improvements after antiretroviral therapy with continuous infusion ZVD. Our sample size was, however, small and the nutritional measure rather global; thus these findings have to be considered as very preliminary.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Neurobehavioral manifestations in obstructive sleep apnea syndrome before and after treatment with continuous positive airway pressure.

Obstructive sleep apnea syndrome (OSAS) is characterized by recurrent apneas during sleep, resulting in repetitive hypoxemic episodes and a constant interruption of the normal sleep pattern. Vigilance impairment and neuropsychological deficits are among the main symptoms seen in this condition. One of the major questions in this field concerns the reciprocal interactions between nocturnal hypoxemia, sleep disruption, excessive daytime sleepiness and cognitive deficits. Results of this study suggest that vigilance impairment is attributable mostly to nocturnal hypoxemia. However, in cognitive deficits, hypoxemia seems to play a major role in executive and psychomotor tasks, whereas attention and memory functions appear to be related to vigilance impairment. After treatment, hypoxemia-related deficits and some degree of sleepiness persist. These results raise the possibility of an irreversible anoxic central nervous system (CNS) damage in severe OSAS.

Adult↗
PubMed1999

Neurobehavioral manifestations and sequelae of HIV and other infections.

Central nervous system infections in children and adolescents involve a wide spectrum of illnesses, ranging from acute self-limited diseases, such as enteroviral meningitis, to severe diffuse or focal infections (i.e., arboviral encephalitis) resulting in devastating neurologic sequelae. All the clinical manifestations of CNS infections occur to some degree secondary to toxic mediators such as cytokines. These factors are neurotoxic and produce clinical manifestations such as encephalopathy, motor abnormalities, and seizures. Many of these diseases also produce radiculoneuropathies and vasculopathies (stroke). As a result, chronic neurologic conditions may result and are frequently associated with psychiatric disturbances and situational depression.

AIDS Dementia Complex↗
PubMed2003

[Cerebral angiitis and Goodpasture's syndrome].

Goodpasture's syndrome is a form of rapidly progressive glomerulonephritis with pulmonary hemorrhage in the presence of antiglomerular basement membrane antibodies. Concomittant central nervous system manifestations are exceptionally reported. We report such a case of an 55-year-old woman who developed fluctuant neurobehavioral manifestations over a 9 months period. Angiography showed cerebral arterial distal lesions compatible with the diagnosis of angiitis. The antiglomerular basement membrane antibody titer was elevated. Search for anti-neutrophil cytoplasmic antibody was negative. After the reintroduction of cyclophosphamide agent, clinical evolution was favourable. Clinical cerebral manifestations in our case are probably du to a angiitis. Few cases are reported in the literature. The role of antiglomerular basement membrane antibody in the development of the cerebral angiitis is possible.

Anti-Glomerular Basement Membrane Disease↗
PubMed1998

A psychodynamic model of behavior after acute central nervous system damage.

This article describes a conceptual psychodynamic model for understanding the neurobehavioral manifestations of acute central nervous system damage (ACNSD) displayed by patients during the rehabilitation process. According to the proposed model, patientsO behavioral responses are viewed as their only means of emotional expression and therefore may not be considered entirely abnormal when viewed from the perspective of patientsO interpersonal contexts. An improved understanding of the dynamic processes through which recovering patients with ACNSD journey may lead to better interaction between the patient and the therapeutic environment, the interdisciplinary team, and family members. Combining this proposed psychodynamic model with an emerging understanding of the neurobehavioral foundations of aggression and depression may also lead to a more rational approach to intervention with various psychopharmacologic agents. During the rehabilitation process, understanding patients' cognitive deficits, motivational drives, and emotional needs and proper implementation of medical and environmental treatment can ultimately lead to a better psychosocial outcome.

Behavior↗
PubMed2001

Acquired crossed aphasia in dextral children revisited.

In contrast to the estimated low incidence of crossed aphasia in dextral adults (among 1%), crossed aphasia in children has been considered a common finding for almost a century. However, reviewing the literature on crossed aphasia in dextrals (CAD) and its related topics from 1975 onward, we encountered only 5 children in a corpus of 180 cases (2.7%). Critical analysis rendered three of the reported cases ambiguous and hence not suitable to draw potentially relevant conclusions. In this review, the neurobehavioral manifestations of the two representative childhood CAD cases are analyzed and compared with adult CAD and acquired childhood aphasia (ACA). In the light of our findings, which support the position of innate cerebral specialization for language, the long-standing controversy as to whether lateralized hemispheric specialization for language is innate or develops progressively during maturation is briefly discussed.

Aphasia↗
PubMed2000

Methylmercury exposure affects motor performance of a riverine population of the Tapajós river, Brazilian Amazon.

Gold mining and deforestation in the Brazilian Amazon are increasing mercury pollution of the extensive water system, exposing riverine populations to organic mercury through fish-eating. The aim of the present study was to evaluate the effect of such exposure on motor performance. This cross-sectional study was carried out in May 1996, in a village located on the banks of the Tapajós river in the Amazonian Basin, Brazil. Information concerning sociodemographics, health, smoking habits, alcohol drinking, dietary habits and work history were collected using an interview-administered questionnaire. Mercury concentrations were measured by cold vapor atomic absorption in blood and hair of each participant, of whom those aged between 15 and 79 years were assessed for motor performance (n = 84). Psychomotor performance was evaluated using the Santa Ana manual dexterity test, the Grooved Pegboard Fine motor test and the fingertapping motor speed test. Motor strength was measured by dynamometry for grip and pinch strength. Following the exclusion of 16 persons for previous head injury, working with mercury in the goldmining sites, or for diabetes, the relationship between performance and bioindicators of mercury was examined using multivariate statistical analyses, taking into account covariables. All participants in the study reported eating fish, which comprised 61.8% of the total meals eaten during the preceding week. The median hair total mercury concentration was 9 microg/g. Organic mercury accounted for 94.4 = 1.9% of the total mercury levels. Multivariate analysis of variance indicated that hair mercury was inversely associated with overall performance on the psychomotor tests, while a tendency was observed with blood mercury. Semipartial regression analyses showed that hair total mercury accounted for 8% to 16% of the variance of psychomotor performance. Neither hair nor blood total mercury was associated with the results of the strength tests in women and men. Although dose-effect relationships were observed in this cross-sectional study, they may reflect higher exposure levels in the past. The findings of this study demonstrated neurobehavioral manifestations of subtle neurotoxic effects on motor functions, associated with low-level methylmercury exposure.

Adolescent↗
PubMed2005

Impairment of syntax and lexical semantics in a patient with bilateral paramedian thalamic infarction.

Bilateral vascular thalamic lesions are rare. Although a variety of neurobehavioral manifestations have been described, the literature is less documented with regard to accompanying linguistic disturbances. This article presents an in-depth neurolinguistic analysis of the language symptoms of a patient who incurred bilateral paramedian ischemic damage of the thalamus. In the post-acute phase of the stroke, a unique combination of transcortical sensory aphasia with syntactic impairment was found. Because of this atypical semiological association, additional analyses of spontaneous speech were performed. In spite of the typological affinity with the grammatic characteristic of marked simplification of syntax observed in Broca's aphasia, only a wordclass specific, lexical-semantic deficit for verbs was objectified. The hypothesis that lexical-semantic disturbances in our patient might result from a functional deafferentiation of both thalami with the frontal lobe is supported by: (1) associated neuropsychological deficits of frontal origin and (2) frontal-like behavioral disturbances.

Aged↗
PubMed1998

Exploratory and displacement behavior in transgenic mice expressing high levels of brain TNF-alpha.

Studies reported recently have shown that tumor necrosis factor-alpha (TNF-alpha) a cytokine released by macrophages and monocytes plays a key role in inflammatory processes and immune and neuro-endocrine regulation. TNF-alpha is also produced in the central nervous system (CNS). However, the role of this cytokine in the CNS is largely unknown, although evidence indicates that it is involved in various neurobehavioral manifestations. Using transgenic mice expressing high amounts of murine TNF-alpha transgene in the neurons of the CNS, we investigated the stereotyped, exploratory, and displacement activities in the hole-board and black/white box. Transgenic mice and their normal control littermates were hybrids of the CBA x C57BL/6 genetic backgrounds and were obtained by backcrossing the CBA x C57BL/6 founder female and her progeny with F1 hybrid mates. Transgenic mice did not show changes in the stereotyped behavior on the hole-board, but they displayed several alterations in the exploratory activities both in the hole-board and black/white box. Transgenic mice also exhibited an increase in grooming when exposed to a highly unfamiliar environmental stimuli in the black/white box. The study suggests that supranormal endogenous TNF-alpha in the brain affects the behavioral responses to stressful conditions.

Animals↗
PubMed2001

CNS synaptogenesis promoted by glia-derived cholesterol.

The molecular mechanisms controlling synaptogenesis in the central nervous system (CNS) are poorly understood. Previous reports showed that a glia-derived factor strongly promotes synapse development in cultures of purified CNS neurons. Here, we identify this factor as cholesterol complexed to apolipoprotein E-containing lipoproteins. CNS neurons produce enough cholesterol to survive and grow, but the formation of numerous mature synapses demands additional amounts that must be provided by glia. Thus, the availability of cholesterol appears to limit synapse development. This may explain the delayed onset of CNS synaptogenesis after glia differentiation and neurobehavioral manifestations of defects in cholesterol or lipoprotein homeostasis.

Animals↗
PubMed2001

Ethanol inhibition of glycine-activated responses in neurons of ventral tegmental area of neonatal rats.

The brain is particularly sensitive to alcohol during the period of its rapid growth. To better understand the mechanism(s) involved, we studied ethanol effects on glycine-activated responses of ventral tegmental area (VTA) neurons isolated from the newborn rat, using whole cell and gramicidin perforated patch-clamp techniques. Previously we reported that 0.1-40 mM ethanol enhances glycine-induced responses of 35% of VTA neurons. We now direct our attention to the inhibitory effects of ethanol observed in 45% (312 of 694) of neonatal VTA neurons. Under current-clamp conditions, 1 mM ethanol had no effect on the membrane potential of these cells, but it decreased glycine-induced membrane depolarization and the frequency of spontaneous action potentials. Under voltage-clamp conditions, 0.1-10 mM ethanol did not elicit a current but depressed the glycine-induced currents. The ethanol-induced inhibition of glycine current was independent of membrane potential (between -60 and +60 mV). Likewise, ethanol did not alter the reversal potential of the glycine-activated currents. Ethanol-mediated inhibition of glycine current depended on the glycine concentration. While ethanol strongly depressed currents activated by 30 microM glycine, it had no appreciable effect on maximal currents activated by 1 mM glycine. In the presence of ethanol (1 mM), the EC(50) for glycine increased from 32 +/- 5 to 60 +/- 3 microM. Thus ethanol may decrease the agonist affinity of glycine receptors. A kinetic analysis indicated that ethanol shortens the time constant of glycine current deactivation but has no effect on activation. In conclusion, by altering VTA neuronal function, ethanol-induced changes in glycine receptors may contribute to neurobehavioral manifestations of the fetal alcohol syndrome.

Aging↗
PubMed2000

Loss of psychic self-activation after paramedian bithalamic infarction.

BACKGROUND AND PURPOSE: Loss of psychic self-activation has been described after bilateral lesions to the globus pallidus, striatum, and white matter of the frontal lobes, but it is a very rare sign of bithalamic lesions. The exact functional-anatomic mechanism underlying loss of psychic self-activation following bithalamic lesions remains to be elucidated. CASE DESCRIPTION: We present clinical, neuropsychological, structural, and functional neuroimaging data of an 18-month follow-up period of a man with prominent loss of psychic self-activation after coronary arteriography. Except for memory decline, accompanying symptoms remained restricted to the acute phase. The neurobehavioral syndrome consisted mainly of apathy, indifference, poor motivation, and flattened affect, and this remained unchanged during the entire follow-up period. MRI showed a bithalamic infarction involving the nucleus medialis thalami bilaterally. Single-photon emission CT revealed a severe relative hypoperfusion of both thalami, a relative hypoperfusion of both nuclei caudati, and a relative hypoperfusion mesiofrontally. CONCLUSIONS: Single-photon emission CT data support the hypothesis that the neurobehavioral manifestations after bithalamic paramedian infarction are caused by disruption of the striatal-ventral pallidal-thalamic-frontomesial limbic loop. Probably, bilateral disruption at different levels of the striatal-ventral pallidal-thalamic-frontomesial loop may lead to a similar clinical picture consisting of loss of psychic self-activation.

Affect↗
PubMed1988

Transient global amnesia and thalamic infarction.

We describe the clinical and neuroradiologic features of a patient with two episodes of transient amnesia who later developed persistent amnesia and an acute infarction in the left thalamus. The neurobehavioral manifestations were strikingly similar in all three episodes. Cranial computed tomography was normal following the first two episodes. Thalamic ischemia could explain some cases of transient global amnesia.

Aged↗
PubMed2000

Methylphenidate treatment of neuropsychiatric symptoms of central and extrapontine myelinolysis.

OBJECTIVE: Previous reports describe the presentation and course of the neurobehavioral manifestations of central and extrapontine myelinolysis; as of yet, however, there are no specific recommendations for treatment of these problems. We offer the first report of successful treatment. METHOD: We describe a 55-year-old man with chronic alcoholism who developed central and extrapontine myelinolysis following an episode of heavy drinking and rapid correction of hyponatremia. The patient acutely developed motor, cognitive, emotional and behavioral problems best accounted for by central pontine and bilateral striatal myelinolysis. These neuropsychiatric symptoms were treated with methylphenidate over the course of 1 month in an off-on-off-on fashion. The Neuropsychiatric Inventory and other tests were used to assess treatment response. RESULTS: Marked improvements in the patient's neuropsychiatric status were noted only during treatment with methylphenidate. CONCLUSIONS: Methylphenidate effectively reversed the neuropsychiatric symptoms associated with the patient's demyelinating lesions. We discuss possible underlying mechanisms of both symptom formation and treatment effect.

Alcoholism↗
PubMed1976

Behavioral effects of organophosphate in man.

Increasingly widespread application of organophosphate pesticies has underscored the importance of studying their effects on human behavior. Clinical reports and laboratory investigations have generally supported the assumption that neurobehavioral manifestations of organophosphate toxicity are attributable to accumulation of acetylcholine at central and peripheral synapses as a result of cholinesterase inhibition. Despite methodologic shortcomings in many of the published studies, investigators generally agree on the presence of several behavioral sequelae of organophosphate poisoning: (a) impaired vigilance and reduced concentration, (b) slowing of information processing and psychomotor speed, (c) memory deficit, (d) linguistic disturbance, (e) depression, and (f) anxiety and irritability. The few studies of asymptomatic workers at risk for repeated exposure to organophosphate pesticides have produced only equivocal findings concerning the presence of less severe or latent forms of these behavioral abnormalities.

Anxiety↗
PubMedDate not supplied

Pharmacotherapy of multiple sclerosis: current status.

Pharmacotherapy plays an important part in the overall management of patients with multiple sclerosis. Most therapies directed at altering the natural history of the underlying disease process are only partially effective or are controversial or experimental. However, many effective symptomatic therapies are available to the clinician. The action and uses of corticosteroids in multiple sclerosis are discussed, and approaches to the treatment of spasticity, paroxysmal disorders, bladder dysfunction, cerebellar ataxia, neurobehavioral manifestations, fatigue, and acute and chronic pain in patients with multiple sclerosis are examined.

Acute Disease↗