[Effect of urea on neurological effects on the heart muscle].
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Health effects classification and its role in the derivation of minimal risk levels: neurological effects.
The agency for Toxic Substances and Disease Registry (ATSDR) uses substance-specific minimal risk levels (MRLs) to assist in evaluating public health risks associated with exposure to hazardous substances. By definition, "MRLs are estimates of daily human exposure to a chemical that are likely to be without an appreciable risk of adverse noncancer health effects over a specified duration of exposure." MRLs serve as screening levels for health assessors to identify contaminants and potential health effects that may be of concern for population living near hazardous waste sites and chemical releases. MRLs for each substance are derived for acute (1-14 days), intermediate (15-364 days), and chronic (365 days and longer) exposure durations, and for the oral and inhalation routes of exposure. The MRLs are derived from data compiled from a current comprehensive literature search and are presented in ATSDR's toxicological profile for that substance. In this paper we outline ATSDR's guidance for evaluating the neurological end point as discussed in the agency's toxicological profiles. Ranking neurological effects into less serious and serious categories and applying this procedure to the derivation of health guidance values or MRLs are also described. Specific examples of ATSDR MRLs based on neurological effects are presented.
Cholinesterase Inhibitors↗
Paraneoplastic syndromes. How to recognize the remote neurologic effects of cancer.
Neurologic paraneoplastic syndromes occur in patients with all forms of malignancy. Their effects on the central and peripheral nervous systems are devastating. A neurologic abnormality may be the first manifestation of malignancy or can occur late in the course of the disease. Early recognition can lead to effective treatment of a paraneoplastic syndrome and a potential cure of the underlying cancer.
Humans↗
Mefloquine induces dose-related neurological effects in a rat model.
Mefloquine is one of the drugs approved by the FDA for malaria chemoprophylaxis. Mefloquine is also approved for the treatment of malaria and is widely used for this purpose in combination with artesunate. However, the clinical utility of the compound has been compromised by reports of adverse neurological effects in some patients. In the present study, the potential neurological effects of mefloquine were investigated with six 7-week-old female rats given a single oral dose of the compound. Potential mefloquine-induced neurological effects were monitored using a standard functional observational battery, automated open field tests, automated spontaneous activity monitoring, a beam traverse task, and histopathology. Plasma mefloquine concentrations were determined 72 h after dosing by using liquid chromatography-mass spectrometry. Mefloquine induced dose-related changes in endpoints associated with spontaneous activity and impairment of motor function and caused degeneration of specific brain stem nuclei (nucleus gracilis). Increased spontaneous motor activity was observed only during the rats' normal sleeping phase, suggesting a correlate to mefloquine-induced sleep disorders. The threshold dose for many of these effects was 187 mg/kg of body weight. This dose yielded plasma mefloquine concentrations after 72 h that are similar to those observed in humans after the treatment dose. Collectively, these data suggest that there may be a biological basis for some of the clinical neurological effects associated with mefloquine.
Animals↗
A comparison of the perioperative neurologic effects of hypothermic circulatory arrest versus low-flow cardiopulmonary bypass in infant heart surgery.
BACKGROUND: Hypothermic circulatory arrest is a widely used support technique during heart surgery in infants, but its effects on neurologic outcome have been controversial. An alternative method, low-flow cardiopulmonary bypass, maintains continuous cerebral circulation but may increase exposure to known pump-related sources of brain injury, such as embolism or inadequate cerebral perfusion. METHODS: We compared the incidence of perioperative brain injury after deep hypothermia and support consisting predominantly of total circulatory arrest with the incidence after deep hypothermia and support consisting predominantly of low-flow cardiopulmonary bypass in a randomized, single-center trial. The criteria for eligibility included a diagnosis of transposition of the great arteries with an intact ventricular septum or a ventricular septal defect and a planned arterial-switch operation before the age of three months. RESULTS: Of 171 patients with D-transposition of the great arteries, 129 (66 of whom were assigned to circulatory arrest and 63 to low-flow bypass) had an intact ventricular septum, and 42 (21 assigned to circulatory arrest and 21 to low-flow bypass) had a ventricular septal defect. After adjustment for diagnosis, assignment to circulatory arrest as compared with low-flow bypass was associated with a higher risk of clinical seizures (odds ratio, 11.4; 95 percent confidence interval, 1.4 to 93.0), a tendency to a higher risk of ictal activity on continuous electroencephalographic (EEG) monitoring during the first 48 hours after surgery (odds ratio, 2.5; 95 percent confidence interval, 1.0 to 6.4), a longer recovery time to the first reappearance of EEG activity (only in the group with an intact ventricular septum, P < 0.001), and greater release of the brain isoenzyme of creatine kinase in the first 6 hours after surgery (P = 0.046). Analyses comparing durations of circulatory arrest produced results similar to those of analyses comparing treatments. CONCLUSIONS: In heart surgery in infants, a strategy consisting predominantly of circulatory arrest is associated with greater central nervous system perturbation in the early postoperative period than a strategy consisting predominantly of low-flow cardiopulmonary bypass. Assessment of the effect of these findings on later outcomes awaits follow-up of this cohort.
Brain Ischemia↗
Neurological effects of microwave exposure related to mobile communication.
Due to the wide and growing use of mobile communication, there is increasing concern about the interactions of electromagnetic radiation with the human organism, and, in particular, with the brain. In the present report, experimental studies on putative electrophysiological, biochemical and morphological effects of continuous or pulsed microwave radiation are briefly reviewed. Such effects have been described in vitro and in vivo using animals and humans. Particularly, effects on neuronal electrical activity, cellular calcium homeostasis, energy metabolism, genomic responses, neurotransmitter balance and blood-brain barrier permeability have been reported. However, some results have either been disputed, since experimental replication led to contradictory findings, or been related to procedural side effects. Since neurological disturbances induced by mobile telephone devices would be of considerable interest for public health, the authors recognize that further experimental studies, involving strict positive and negative control conditions, will be required in the future. At the present state of knowledge there is no positive evidence that pulsed or continuous microwave exposure in the non-thermal range confers elevated risk to the health of the brain.
Animals↗
Research on the neurological effects of nonionizing radiation at the University of Washington.
This paper reviews research on neurological effects of low-level microwave irradiation, which was performed at the University of Washington, during the decade of the 1980s. We studied in the rat the effects of microwave exposure on the actions of various psychoactive drugs, on the activity of cholinergic systems in the brain, and on the neural mechanisms involved. Our results indicate that endogenous opioids play an important mediating role in some of the neurological effects of microwaves, and that parameters of microwave exposure are important determinants of the outcome of the microwave effects.
Animals↗
Psychiatric and neurological effects of chronic solvent abuse.
This study is a review of the psychiatric and neurological effects of solvent inhalation on a group of 22 patients with chronic histories of solvent abuse, primarily toluene-based solvents. The findings suggest that the chronic inhalation of toluene-based adhesives can produce a paranoid psychosis which may persist. Other findings were a high incidence of temporal lobe epilepsy and decrease in IQ. We suggest that the psychiatric and neurological sequelae of chronic solvent abuse are serious and potentially irreversible. Toluene is felt to be a major factor in the morbidity associated with chronic solvent abuse, and attention is drawn to the necessity for educational programs in this area. The burden caused by the resulting psychiatric problems resulting from solvent abuse may have implications for health care budgets.
Adolescent↗
Assessment of the neurologic effects of dietary deficiencies of phenylalanine and tyrosine in cats.
OBJECTIVE: To determine the neurologic effects of reduced intake of phenylalanine and tyrosine in black-haired cats. ANIMALS: 53 specific pathogen-free black domestic shorthair cats. PROCEDURE: Cats were fed purified diets containing various concentrations of phenylalanine and tyrosine for < or = 9 months. Blood samples were obtained every 2 months for evaluation of serum aromatic amino acid concentrations. Cats were monitored for changes in hair color and neurologic or behavioral abnormalities. Three cats with neurologic deficits underwent clinical and electrophysiologic investigation; muscle and nerve biopsy specimens were also obtained from these cats. RESULTS: After 6 months, neurologic and behavioral abnormalities including vocalization and abnormal posture and gait were observed in cats that had received diets containing < 16 g of total aromatic amino acid/kg of diet. Electrophysiologic data and results of microscopic examination of muscle and nerve biopsy specimens from 3 cats with neurologic signs were consistent with sensory neuropathy with primary axonal degeneration. Changes in hair color were detected in cats from all groups receiving < 16 g of phenylalanine plus tyrosine/kg of diet. CONCLUSIONS AND CLINICAL RELEVANCE: Findings suggested that chronic dietary restriction of phenylalanine and tyrosine in cats may result in a predominantly sensory neuropathy. In cats, the long-term nutritional requirement for phenylalanine and tyrosine appears to be greater for normal neurologic function than that required in short-term growth experiments. Official present-day recommendations for dietary phenylalanine and tyrosine in cats may be insufficient to support normal long-term neurologic function.
Amino Acids, Essential↗
Can epidemiological studies discern subtle neurological effects due to perinatal exposure to PCBs?
What conclusions can be drawn concerning the potential neurological effects of perinatal exposure to either PCBs, or PCBs and other fish-borne contaminants? First, by their very nature epidemiological studies are limited in their ability to detect subtle associations--including possible links between exposure to low levels of environmental contaminants and disease. As stated by Dr. Schantz, both Rogan and the Jacobsons report small changes in motor and cognitive behavior--typically less than one-half of a standard deviation--and only in the most highly exposed children. Given these small changes in CNS function, the substantive criticisms of Paneth (including the Jacobsons' choice to employ a random, rather than matched, control sample and the related fact that fish-eating mothers differed from non-fish-eating mothers on several important characteristics) and similar "generic" concerns raised by Taubes, a critical reader must question both the validity of the findings from the Michigan study and the reasons for discrepancies in results between the Jacobson and Rogan studies. Are the differences in neurobehavioral effects reported by the Jacobsons and colleagues, and Rogan and colleagues, due to the presence of confounders, exposure to different neurotoxicants, or subtle differences in methodologies? At present it is not possible to answer these questions. Nevertheless, certain commonalities exist between the Rogan and Jacobson studies, and most recently, the study conducted by Daly and colleagues in New York. All of these studies report alterations in the Brazelton Neonatal Behavioral Assessment Scale, suggesting that exposure to environmental contaminants (including PCBs) may induce subtle, transient alterations in maturation of the human CNS. Secondly, because contaminated fish contain a large number of putative developmental neurotoxicants (e.g., methyl-mercury, p,p'-DDE, PCBs, and pesticides), I am pessimistic that additional studies of human populations exposed to contaminated aquatic and marine fish and mammals will allow investigators to determine which contaminant(s) may be responsible for the observed association between fish consumption and neurobehavioral deficits. For example, although PCB body burdens have been measured in the majority of the epidemiological studies, PCBs may simply reflect exposure to other fish-borne contaminants. In light of the above statements, future epidemiological studies should focus on highly exposed susceptible populations such as occupationally exposed workers or the aged. Results from these studies would provide important information on the risk of perinatal or adult exposure to PCBs in susceptible populations, although generalization of results obtained in these populations to the general population may be fraught with difficulties. Finally, because of the limitations of epidemiological studies, particularly those studying fish-eating populations, future risk assessments should depend more heavily on laboratory derived data, including studies in nonhuman primates exposed to environmentally relevant mixtures and relevant doses of PCB congeners and other known or suspected neurotoxicants.
Adult↗
Male cerebral palsy hospitalization as a potential indicator of neurological effects of methylmercury exposure in Great Lakes communities.
Perinatal exposure to methylmercury is known to result in severe neurological effects on the developing fetus and infant, including cerebral palsy, mental retardation, and seizures. Males are more susceptible than females to neurological damage from perinatal methylmercury exposures. Preliminary analyses of data and statistics for the hospitalization rates of males for cerebral palsy in the 17 Canadian Areas of Concern in the Great Lakes basin indicate a possible geographic association with locations with elevated mercury from natural or industrial sources.
Canada↗
Lindane: serious neurological effects.
(1) Cutaneous application of lindane carries a risk of systemic adverse effects, including serious neurological disorders. Lindane is readily absorbed through the skin, especially damaged skin and in children. (2) In practice, lindane has no place in the treatment of either lice or scabies.
Child↗
Comparative neurologic effects of diazepam and suriclone, a cyclopyrrolone anxiolytic.
Suriclone selectively displaces benzodiazepines from their binding sites but is structurally unrelated to benzodiazepines. Neurologic effects of suriclone were compared to those of diazepam in 54 subjects in a sequential, double-blind, single dose, randomized study (placebo; diazepam 10 mg; suriclone 0.2, 0.4, 0.6, or 0.8 mg). Data were collected on-line by microcomputer. Suriclone 0.2 mg did not differ from placebo. Suriclone 0.4 mg and 0.6 mg did not differ from diazepam 10 mg. Suriclone 0.8 mg caused significantly more decrement than diazepam 10 mg (p less than 0.05) in manual tracking, force platform stability, and Heath rail walking and in total severity of symptoms. Suriclone 0.8 mg caused nausea (p = 0.02), clumsiness (p = 0.02), and loss of balance (p = 0.01) more frequently than diazepam 10 mg. Suriclone 0.8 mg produced symptoms and signs qualitatively and quantitatively different from diazepam 10 mg, such as vomiting, unusual ocular movement effects, and difficulty walking. Possibly the differences in CNS drug binding for anxiolytics are associated with clinical differences in toxicity.
Adult↗
Fate of manganese associated with the inhalation of welding fumes: potential neurological effects.
Welding fumes are a complex mixture composed of different metals. Most welding fumes contain a small percentage of manganese. There is an emerging concern among occupational health officials about the potential neurological effects associated with the exposure to manganese in welding fumes. Little is known about the fate of manganese that is complexed with other metals in the welding particles after inhalation. Depending on the welding process and the composition of the welding electrode, manganese may be present in different oxidation states and have different solubility properties. These differences may affect the biological responses to manganese after the inhalation of welding fumes. Manganese intoxication and the associated neurological symptoms have been reported in individual cases of welders who have been exposed to high concentrations of manganese-containing welding fumes due to work in poorly ventilated areas. However, the question remains as to whether welders who are exposed to low levels of welding fumes over long periods of time are at risk for the development of neurological diseases. For the most part, questions remain unanswered. There is still paucity of adequate scientific reports on welders who suffered significant neurotoxicity, hence there is a need for well-designed epidemiology studies that combine complete information on the occupational exposure of welders with both behavioral and biochemical endpoints of neurotoxicity.
Animals↗
Neurologic effects of manganese in humans: a review.
Manganese, which enters the body primarily via inhalation, can damage the nervous system and respiratory tract, as well as have other adverse effects. Occupational exposures occur mainly in mining, alloy production, processing, ferro-manganese operations, welding, and work with agrochemicals. Among the neurologic effects is an irreversible parkinsonian-like syndrome. An estimated 500,000 to 1.5 million people in the United States have Parkinson's disease, and physicians need to consider manganese exposure in its differential diagnosis. Since 1837, there have been many reports of cases and case series describing manganese toxicity. More recently, there have been epidemiologic studies of its adverse effects on health. Occupational medicine physicians can play critical roles in preventing the adverse health effects of manganese.
Central Nervous System↗
Neurological effects of radiofrequency radiation.
BACKGROUND: The health effects of radiofrequency radiation (RFR) and the adequacy of the safety standards are a subject of debate. One source of human data is case reports regarding peripheral neurological effects of RFR, mainly noxious sensations or dysaesthesiae. AIM: To investigate health effects, neurophysiological mechanisms and safety levels for RFR. METHODS: We conducted a literature search for case reports and case series associated with mobile phone technology as well as other RFR sources using specific search terms on PubMed. RESULTS: We identified 11 original articles detailing case reports or case series and matching the search criteria. Five of the identified papers were written by at least one of the authors (B.H. or R.W.). CONCLUSIONS: Cases have arisen after exposure to much of the radiofrequency range. In some cases, symptoms are transitory but lasting in others. After very high exposures, nerves may be grossly injured. After lower exposures, which may result in dysaesthesia, ordinary nerve conduction studies find no abnormality but current perception threshold studies have found abnormalities. Only a small proportion of similarly exposed people develop symptoms. The role of modulations needs clarification. Some of these observations are not consistent with the prevailing hypothesis that all health effects of RFR arise from thermal mechanisms.
Cell Phone↗
Possible neurologic effects of aspartame, a widely used food additive.
The artificial sweetener aspartame (L-aspartyl-L-phenylalanyl-methyl ester), is consumed, primarily in beverages, by a very large number of Americans, causing significant elevations in plasma and, probably, brain phenylalanine levels. Anecdotal reports suggest that some people suffer neurologic or behavioral reactions in association with aspartame consumption. Since phenylalanine can be neurotoxic and can affect the synthesis of inhibitory monoamine neurotransmitters, the phenylalanine in aspartame could conceiveably mediate neurologic effects. If mice are given aspartame in doses that elevate plasma phenylalanine levels more than those of tyrosine (which probably occurs after any aspartame dose in humans), the frequency of seizures following the administration of an epileptogenic drug, pentylenetetrazole, is enhanced. This effect is simulated by equimolar phenylalanine and blocked by concurrent administration of valine, which blocks phenylalanine's entry into the brain. Aspartame also potentiates the induction of seizures by inhaled fluorothyl or by electroconvulsive shock. Perhaps regulations concerning the sale of food additives should be modified to require the reporting of adverse reactions and the continuing conduct of mandated safety research.
Animals↗
IL-1beta-dependent neurological effects of the whole cell pertussis vaccine: a role for IL-1-associated signalling components in vaccine reactogenicity.
Immunization with the whole cell pertussis vaccine (Pw), but not the acellular pertussis vaccine (Pa), is associated with a number of neurological side effects. Previously, we have demonstrated a role for interleukin-1beta (IL-1beta) in Pw reactogenicity. Here we report that parenteral Pw administration resulted in a concomitant increase IL-1 type I receptor (IL-1RI) mRNA and a decrease in IL-1 type II receptor (IL-1RII) mRNA expression in the murine hypothalamus. These Pw-induced changes were accompanied by an increase in caspase-1 and interleukin-1beta (IL-1beta), and were associated with increased activity of the stress-activated kinase, p38. In contrast, immunization with Pa failed to activate pro-inflammatory IL-1 responses but resulted in increased IL-1 receptor antagonist (IL-1ra) production. These results suggest that the neurological effects of Pw are associated with central activation of IL-1beta and IL-1-associated signalling components.
Animals↗