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PubMed1980

Tardive dyskinesia: summary of a Task Force Report of the American Psychiatric Association. By the Task Force on Late Neurological Effects of Antipsychotic Drugs.

Abnormal movements associated with the prolonged use of antipsychotic drugs (tardive dyskinesia) occur in at least 10%-20% of the patients at risk; prevalence is higher among the elderly. The casue is unknown, but increased sensitivity to dopamine in the basal ganglia may contribute to the pathophysiology. Many treatments have been evaluated; none is satisfactory. While the problem is serious, an alarmist view is unwarranted, especially since many cases are detected early and improve spontaneously. The best approach currently is to use antipsychotic drugs thoughtfully for clear indications, the best supported of which, scientifically, is chronic schizophrenia. There is a search for new agents with much less adverse neurologic effect but with adequate antipsychotic efficacy. This article summarizes an APA Task Force Report.

Adult↗
PubMed1975

The neurologic effects of noxious marine creatures.

The concept of the sea as a source of noxious agents is perhaps not a familiar one to clinical neurologists, judging by the lack of reference to these agents in standard textbooks. Chemical, physiologic, and pharmacologic laboratories are increasingly investigating the properties of marine toxins, finding in them compounds with interesting and novel structures or unusual physiologic effects. Such substances are seen as possible agents for biologic and, more particularly, physiologic research, and as possible sources of new pharmaceuticals. These include hormone-like substances and antiviral or antitumor agents. Despite these specialized developments, which are in large measure a consequence of the technological advances of the present century, the clinician is at times directly concerned with the effects of marine toxic substances. For example, in Japan, puffer fish or tetrodotoxic poisoning is one of the major causes of deaths from food poisoning. Another marine toxin that has caused many explosive outbreaks of food poisoning. with many deaths in various parts of the world, comes from clams or mussels. This toxin, saxitoxin, is produced by species of marine protozoa including Gonyaulax, and is concentrated in filter-feeding molluscs. These two examples were of significant interest in medicine long before the technologic developments of the twentieth century. In the last few decades, entirely new problems of marine intoxication have arisen as a result of marine pollution from the disposal of industrial wastes in the sea. The most striking example of a man-made marine intoxication has been the outbreak of Minamata disease. In Minamata, Japan, the disposal of mercury-contaminated industrial wastes from a plastics factory into an enclosed bay, followed by human consumption of the contaminated fishes, crabs, or shellfish, led to many instances of acute cerebral degeneration. With the increasing exploration of the sea for both pleasure and economic exploitation, which is a feature of the second half of the twentieth century, it may be expected that the frequency and variety of human intoxications by marine creatures will be increased. This chapter reviews the neurologic effects of noxious substances of marine biologic origin. The subject is now developing so rapidly that overall surveys, such as this, of the general animal life of theocens will soon be beyond the scope of a single review. Nevertheless, it is hoped that the references given will enable the interested reader to pursue particular aspects further.

Adult↗
PubMed1987

The neurologic effects of thiopental therapy after cardiac arrest.

We studied the effect of thiopental loading during resuscitation of 53 patients following cardiopulmonary arrest and compared the outcome with that found in 54 patients treated conventionally in the 30 previous months. Thiopental therapy (10 mg/kg i.v.) was begun within 30 min of the arrest once hemodynamic stability had been established. Thiopental infusion (20 mg/kg over 6 h) was followed by phenobarbital sodium (125 mg every 12 h), tolerance to the initial dose having been assessed. The in-hospital mortality rate for both groups was similar. In patients with ischemic heart disease, the mortality rate within the first 6 h was significantly higher in the thiopental group (p less than 0.05), although for the remaining patients there were more survivors among the thiopental treated patients (p less than 0.05). Excluding the patients who died within the first 6 h, 61% of the patients in the thiopental group survived cardiac arrest with normal cerebral performance, whereas only 37% in the standard treatment group showed normal functional outcome (p less than 0.03). These results suggest a favorable neurologic effect of thiopental loading during resuscitation of patients without ischemic heart disease. In patients with ischemic heart disease, an initial hemodynamic deterioration may contribute to minimising the beneficial effect of barbiturate therapy.

Adult↗
PubMed2003

[Neurological effects of chemical and biological weapons].

Neurological manifestations of chemical and biological weapons are reviewed. Nerve agents in current use, storage, or production include tabun, sarin, soman and VX. The initial effects of exposure to a nerve agent depend on the dose and on the route of exposure. Sarin, the agent studied most thoroughly in man in Matumoto and Tokyo attacked by Aum shinrikyo will cause miosis, rhinorrehea and shortness of breath are initial complaints immediately after inhalation exposure of the vapor. The severe cases showed loss of consciousness and convulsions. Respiratory arrest may occur. The most toxic of the nerve agents is VX. It is thought to be 100 times as toxic as sarin for humans by the percutaneous rout. The similar findings to sarin exposure are also observed in cases exposured to VX. Atropin and PAM will be effective in the early stage. BZ (benzilate) is a delayed onset incapacitation agent. It causes severe hallucination. The cyanide compounds are among the most rapidly acting of war gases, resulting in death. Anthrax has been the most attractive biological weapon for a long time. Anthrax is an acute bacterial infection of the skin and lungs in man and animals. Meningoencephalitis has been reported in the terminal stage in anthrax infection. In autopsy, it is really confirmed in the characteristic findings of the meningeal abnormality. The potential weaponization of variola virus continues to pose a military threat because the aerosol infectivity of the virus and the development of susceptible populations. A high rate of lethality, a staunch resistance to treatments and a rapid onset of severe generalised muscle weakness make botulinum toxin a suitable agent for biological warfare particularly by oral administration.

Animals↗
PubMed1974

Development of behavioral tests for the assessment of neurologic effects of lead in sheep.

Reports of neurologic impairment of children following recovery from acute lead encephalopathy have raised questions concerning the effects of chronic low-level lead exposure on the central nervous system. Behavioral toxicologic techniques have been employed to assess the effects of lead on the central nervous system in sheep. Mature sheep receiving daily doses of 100 mg lead/kg showed a significant decrease in performance on an auditory signal detection task. Daily oral doses of 120 and 230 mg lead/sheep for 27 weeks did not alter the performance of mature sheep on a fixed-interval schedule of reinforcement behavioral task. Prenatal exposure to maternal blood lead levels of 16 or 34 mug/100 ml during gestation and postnatal daily ingestion of 16, 8, 4, or 2 mg lead/kg did not alter performance of lambs on a closed-field maze task. Slowed learning was demonstrated in lambs prenatally exposed to maternal blood lead levels of 34 mug/100 ml during gestation when tested on nonspatial, two-choice visual discrimination problems at 10-15 months of age.

Administration, Oral↗
PubMedDate not supplied

A review of biomechanics of the central nervous system--Part III: spinal cord stresses from postural loads and their neurologic effects.

OBJECTIVE: To review literature pertaining to neurologic disorders stemming from abnormal postures of the spine. DATA COLLECTION: A hand search of available reference texts and a computer search of literature from Index Medicus sources was performed, with special emphasis placed on spinal cord stresses and strains caused by various postural rotations and translations of the skull, thorax, and pelvis. RESULTS: Spinal postures will often deform the neural elements within the spinal canal. Spinal postures can be broken down into four types of loading: axial, pure bending, torsion, and transverse, which cause normal and shear stresses and strains in the neural tissues and blood vessels. Prolonged stresses and strains in the neural elements cause a multitude of disease processes. CONCLUSION: Four types of postural loads create a variety of stresses and strains in the neural tissue, depending on the exact magnitude and direction of the forces. Transverse loading is the most complex load. The stresses and strains in the neural elements and vascular supply are directly related to the function of the sensory, motor, and autonomic nervous systems. The literature indicates that prolonged loading of the neural tissue may lead to a wide variety of degenerative disorders or symptoms. The most offensive postural loading of the central nervous system and related structures occurs in any procedure or position requiring spinal flexion. Thus flexion traction, rehabilitation positions, exercises, spinal manipulation, and surgical fusions in any position other than lordosis for the cervical and lumbar spines should be questioned.

Biomechanical Phenomena↗
PubMed1995

Long term exposure to manganese in rural well water has no neurological effects.

BACKGROUND: There is debate on the neurological impact of chronic exposure to Manganese (MN). METHODS: MN burden from rural well water was studied cross-sectionally in two proband cohorts from rural dwellings located in northern Germany. Both cohorts had exposure times for up to 40 years and were separated on the basis of well water MN content. Group A (41 subjects; mean age 57.5 years) was exposed to MN water contents of at least 0.300 mg/l (range 0.300 to 2.160), while group B (74 subjects; mean age 56.9 years) was exposed to concentrations of less than 0.050 mg/l. Both proband groups were homogenous with regard to age, sex, nutritional habits, and drug intake. Neurological assessments by clinical investigators blinded for proband's exposure status was done using structured questionnaires, standardized neurological examination with assessment of possible Parkinsonian signs by the Columbia University Rating Scale, and instrumental tests of fine motor coordination. RESULTS: No significant difference in any neurological measure was found between groups. Results were not confounded by demographic and dietary features. CONCLUSION: Exposure to high body burden of MN does not result in detectable neurological impairment. Exposure to MN in drinking water does not seem to be a risk factor for idiopathic Parkinson's disease.

Adult↗
PubMed2005

Toward a more efficient and effective neurologic examination for the 21st century.

Practice pressures and quality improvement require greater efficiency and effectiveness in the neurologic examination. I hypothesized that certain 'marginal' elements of the examination rarely add value and that 'core' elements, exemplified by the plantar response (Babinski), are too often poorly performed or interpreted. I analyzed 100 published, neurologic clinicopathologic conferences (CPCs) and 180 ambulatory neurologic consultations regarding 13 hypothetically 'marginal' examination components (including 'frontal' reflexes, olfaction, jaw strength, corneal reflex, etc.); also, 120 exams on medical inpatients with neurologic problems, recording definitive errors. I surveyed the recalled practices of 24 non-neurologists and reviewed the literature for relevant data or guidance. In the CPCs the 'marginal' elements of the examination were rarely provided, requested, or used diagnostically, nor did they contribute in the 180 ambulatory consultations. In the chart review errors and omissions dominated testing of plantar responses, with missed Babinski signs in 14% of all cases and 77% of patients with Babinski signs. House officers harbored unrealistic expectations for performance of 'marginal' examination elements. Most textbooks omit detailed guidance (and none cite evidence) on achieving greater efficiency. Exams should be streamlined, while improving 'core' skills. Neurologists should apply evidence to update the exam taught to students and non-neurologists.

Humans↗
PubMed1983

A depot neuroleptic withdrawal study neurological effects.

A double-blind withdrawal trial in 41 chronic schizophrenic outpatients was carried out over 6 months. Depot neuroleptics (fluphenazine decanoate or flupenthixol decanoate) were compared with placebo to evaluate neurological side effects during continued therapy and during withdrawal. The drugs were significantly more effective than placebo in preventing relapse and rehospitalization. In the placebo group 62% relapsed compared to 27% in the drug group. A difference was observed in the occurrence of extrapyramidal symptoms (EPS) between the neuroleptics in the study. Akathasia was observed in 9/38 (23.7%) cases, significantly more frequent in the fluphenazine decanoate group. Tardive dyskinesia (TD) was observed in six cases (15.8%); four cases existed at the start of the study and two others were observed after 3-6 weeks of withdrawal. There was no relation between TD symptoms and relapse. There was a significant decrease in the EPS scores during the placebo treatment and also a significant weight decrease.

Adult↗
PubMedDate not supplied

[Quantitative analysis of neurological effects after cranio-caudal gamma-irradiation of rats].

A study was made of the frequency and duration of neurological disorders after cranio-caudal irradiation of rats with doses of 7.5-500 Gy delivered to the head. As the mean effective dose increased the neurological disorders occurred in the following order: tremor, rotatory movements hyperkinesia, opisthotonos, and convulsions. The neurophysiological disorders observed were subjected to a pathophysiological analysis.

Animals↗
PubMed1982

The neurologic effects of thiopental therapy following experimental cardiac arrest in cats.

To define the utility of high-dose barbiturate therapy following an episode of complete global cerebral ischemia, we investigate the effects of 60 mg/kg of thiopental given to cats five minutes after resuscitation from 12, 14, or 16 min of electrically induced ventricular fibrillation (VF). All aspects of the arrest, resuscitation, with post-arrest care were carefully controlled, with the EEG becoming isoelectric 20-25 s after the onset mean resuscitation time of 2.5 +/- 0.2 (SEM) min. For any given duration of VF, there were no differences (control vs thiopental) in any pre- or post-arrest parameters (blood pressure, blood gases, electrolytes, etc.) A total of 68 resuscitated cats were entered into various treatment and control groups, and all but one group received 20-24 h of post-resuscitation paralysis, mechanical ventilation, and ICU support before being extubated. Cats received an additional six days of aggressive nursing care, and daily examinations were performed with the assignment of a neurologic deficit score (NDS) between 0 (normal) and (brain dead). Autopsies were performed to determine the cause of death in animals which died before the end of the seven-day observation period. The early post-arrest period was marked by the occurrence of repetitive, rhythmic bursts of high-frequency electroencephalographic (EEG) activity (? seizures) in 38 per cent of control animals (16/42, all arrest times combined). Ten of these animals died as a result of severe neurologic injuries. By contrast, only 12 per cent of treated cats (3/26) developed similar EEG patterns (P less than 0.05) and there were no neurologic deaths in the thiopental groups. The differences in the incidence of neurologic deaths (control vs. thiopental) was significant (P less than 0.02). The change in overall mortality did not quite reach significance (36 per cent vs. 21 per cent), and treatment had no effect on the incidence of deaths due to cardiovascular causes (e.g., myocardial infarctions). In spite of the effects on mortality, treatment had no effect on the neurologic function of survivors (assessed by NDS). These findings suggest that thiopental improved survival rates by suppressing an unusual post-arrest EEG pattern (? anticonvulsant effect), but had no additional cerebral protective effects.

Animals↗
PubMed1994

Neurologic effects of alcoholism.

Alcoholism, a worldwide disorder, is the cause of a variety of neurologic disorders. In this article we discuss the cellular pathophysiology of ethanol addition and abuse as well as evidence supporting and refuting the role of inheritance in alcoholism. A genetic marker for alcoholism has not been identified, but neurophysiologic studies may be promising. Some neurologic disorders related to longterm alcoholism are due predominantly to inadequate nutrition (the thiamine deficiency that causes Wernicke's encephalopathy), but others appear to involve the neurotoxicity of ethanol on brain (alcohol withdrawal syndrome and dementia) and peripheral nerves (alcoholic neuropathy and myopathy).

Alcoholic Intoxication↗
PubMed2003

[Neurological effects of American trypanosomyiasis: clinical aspects].

Trypanosoma cruzi, causative agent of Chagas disease, affects not only cardiac and intestinal structures but also neurological structures. A high prevalence of T. cruzi infection occurs in Colombia, prompting the present study. First, a qualitative metaanalysis was undertaken using the PubMed database, the electronic internet engine Altavista, Colombian journals indexed by Colciencias, and three relevant textbooks. The following key words were used: Trypanosoma, Chagas disease, nervous system, spinal cord, central nervous system, peripheral nervous system, neuromuscular junction, autonomic nervous system, muscle, muscle disorders, neuromuscular disease, neuromuscular disorders, synapticopathies and dysautonomia. The documents analyzed numbered 116 and included original papers, reviews, case reports, editorials, brief communications, conferences and book chapters. At minimum, each document included data involving ELISA testing, indirect immunofluorescense, or parasitemia levels in the clinical, serological or histopathological studies. Polymerase chain reaction (PCR) studies were not included because of the recent introduction of PCR as a confirmatory technique for Chagas disease in Colombia. Chagas disease affects the central, the peripheral and the autonomic nervous system in humans, although its effects on the antonomic system is most commonly investigated in Colombia. Neurological lesions must be evaluated carefully, because patients may be misdiagnosed and treated as carriers of 'idiopathic' diseases. Neurological pathologies poses a serious threat in Colombia due to the prevalence of Chagas disease.

Central Nervous System Protozoal Infections↗
PubMed2026

Neurological effects of encapsulated dexamethasone sodium phosphate in children aged 6-9 years with ataxia telangiectasia (NEAT): a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial.

BACKGROUND: Ataxia telangiectasia is a rare, multisystem disorder with progressive cerebellar neurodegeneration and no approved treatments. The efficacy of corticosteroids, including erythrocyte encapsulated dexamethasone sodium phosphate (eDSP), which have been studied for two decades in this disease, has not yet been proven in randomised trials. We aimed to investigate the safety and efficacy of eDSP in children aged 6-9 years with ataxia telangiectasia. METHODS: NEAT was a multicentre, randomised, double-blind, placebo-controlled phase 3 study, conducted at 20 sites across nine countries (Denmark, Germany, Italy, Norway, Poland, Spain, Switzerland, UK, and USA). Eligible participants were children aged 6 years or older weighing at least 15 kg, with a genetic diagnosis of ataxia telangiectasia and presence of neurological symptoms. Participants were randomly assigned (1:1) to the eDSP or placebo group via an independent interactive web response system and were stratified by age (6-9 years or ≥10 years), sex, and region (USA vs other countries). All participants, investigators, sponsors, and raters were masked to treatment assignments. eDSP was given intravenously every 21-30 days for six doses. All randomly assigned participants were included in the intention-to-treat (ITT) and safety populations; the primary and secondary efficacy analyses were conducted in participants aged 6-9 years in the ITT population. The primary efficacy endpoint was the change in Rescored Modified International Cooperative Ataxia Rating Scale (RmICARS) score between baseline and month 6, and a mixed-model-repeated-measures analysis was used. The trial was registered at ClinicalTrials.gov, NCT06193200, and is completed. FINDINGS: Between June 24, 2024, and Dec 17, 2025, we screened 125 participants for eligibility, of whom 105 (84%) were randomly assigned to the eDSP group (n=51 [49%]) or the placebo group (n=54 [51%]) and received at least one dose of treatment. The mean age was 8·5 years (SD 1·9) in the eDSP group and 8·6 years (2·3) in the placebo group (overall age range 6-17 years). In the eDSP group, 24 (47%) of 51 participants were girls and 27 (53%) were boys and, in the placebo group, 26 (48%) of 54 were girls and 28 (52%) were boys. Of ITT participants aged 6-9 years, 38 (95%) of 40 in the eDSP group and 41 (95%) of 43 in the placebo group completed the study. Compared with the placebo group, no significant differences were identified in change in RmICARS score from baseline to 6 months in participants aged 6-9 years: least squares mean difference -1·30 (95% CI -2·77 to 0·18; p=0·085). Adverse events were reported in 47 (92%) of 51 participants in the eDSP group and in 50 (93%) of 54 participants in the placebo group. The most common treatment-emergent adverse events were vomiting, pyrexia, pruritus, nasopharyngitis, cough, headache, and fatigue. There were no reports of treatment-related serious adverse events or deaths. Safety laboratory parameters did not identify adverse effects on growth, metabolism, bone mineral density, or endocrine function in any of the treatment groups. INTERPRETATION: The primary efficacy endpoint was not achieved, because the effect of eDSP on neurological symptoms did not reach statistical significance. The favourable safety profile of eDSP, previously described in a large study of children with ataxia telangiectasia, was confirmed in this trial. The eDSP programme, comprising two randomised studies and treating the largest cohort of patients with ataxia telangiectasia to date, underscores the need for rigorously designed trials of sufficient duration to detect sustained clinical benefit. FUNDING: Quince Therapeutics.

Humans↗
PubMed1992

Evaluation of the utility of a standard history questionnaire in assessing the neurological effects of solvents.

Using a standard battery of medical surveillance questions, a study was undertaken to determine if an increase in reported neurologic symptoms was resulting from solvent exposure at a pharmaceutical research, development, and manufacturing site. The prevalence of positive responses to 13 interval history questions pertaining to neurological symptoms was compared between those enrolled in exposed surveillance programs (n = 840) and those enrolled in other, non-solvent exposed surveillance programs (n = 1,042). The ratio of positive responders between the exposed and unexposed groups was used to generate a relative prevalence ratio (RPR). No significantly elevated RPRs were seen when the analysis was adjusted for the confounding factors of age, sex, smoking, alcohol use, noise exposure, and number of interval histories. These results suggest that workplace solvent exposures in the employees studied did not appear to result in obvious neurologic symptoms. However, low-level neurotoxic exposures can cause asymptomatic or sub-clinical disorders. Therefore, more sensitive neurotoxic surveillance systems need to be developed.

Adult↗
PubMed1982

Adverse neurologic effects of metoclopramide.

Metoclopramide hydrochloride is now commonly prescribed for a variety of gastrointestinal disorders. Over a 2-year period 18 patients with neurologic disorders induced by metoclopramide were assessed at the Parkinson's disease clinic of the Ottawa Civic Hospital. During metoclopramide therapy acute transient dystonic reactions were seen in 4 patients, and parkinsonism, which was frequently misdiagnosed and treated as classic Parkinson's disease, was seen in 12 patients. After treatment with metoclopramide was stopped, tardive dyskinesia appeared in seven patients and has persisted for up to 15 months in three patients. Parkinsonism and tardive dyskinesia occurred in older patients undergoing long-term therapy with metoclopramide. This experience, therefore, suggests that such treatment, especially in older patients, should be avoided.

Aged↗