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At least 19 recordsLinked to original sources
PubMed2003

The effects of arsenic exposure on the nervous system.

Arsenic (As) is a common environmental contaminant widely distributed around the world. Human exposure to this metalloid comes from well water and contaminated soil, from fish and other sea organisms rich in methylated arsenic species, and from occupational exposure. It has been reported that human arsenic exposure causes several health problems such as cancer, liver damage, dermatosis, and nervous system disturbances such as polyneuropathy, EEG abnormalities and, in extreme cases, hallucinations, disorientation and agitation. Although there is evidence that arsenic exposure has a toxic effect on the nervous system there are few studies that address this issue. The purpose of this review is to describe what is presently known about the effects of arsenic compounds on the nervous system in humans and rodents and to discuss its possible mechanisms of action.

Animals↗
PubMed1996

Detection of scrapie agent in the peripheral nervous system of a diseased sheep.

In an attempt to determine whether scrapie infectivity can be found in the peripheral nervous system of a scrapie-diseased sheep, mice were inoculated intracerebrally or intraperitoneally with 10-fold dilutions of homogenates of Nervus (N.) axillaris, N. ulnaris, N. medianus, N. ischiadicus, N. tibialis, N. fibularis, and N.saphenus. Mice were observed for clinical signs of scrapie for 700 days and their brains were analyzed for accumulation of pathological prion protein by immunoblot. Substantial amounts of infectivity were found in all peripheral nerves tested except N.saphenus. Infectivity at titers of approximately 10(4.5) mouse infectious units (MIU)/g were detected in N. axillaris and N. ischiadicus, of approximately 10(3.0) MIU/g in N. ulnaris, N. medianus, N. tibialis, and N.fibularis, and of 10(6) MIU/g in the cerebellum. Since muscles are traversed by the nerve tracts tested, mutton of scrapie-diseased animals should not be regarded as being free of scrapie agent.

Animals↗
PubMed2004

Evaluation of topiramate as an anti-hyperalgesic and neuroprotective agent in the peripheral nervous system.

Abstract Topiramate (TPM), a novel anti-convulsant currently approved for the treatment of epileptic disorders, has been shown to possess neuroprotective effects in models of cerebral ischemia, status epilepticus, and facial nerve lesion. Furthermore, pilot studies showed an effect of TPM in neuropathic pain models. Here, we studied the anti-hyperalgesic and neuroprotective efficacy of TPM in rat models of peripheral nerve lesions. Rats with a unilateral chronic constrictive injury (CCI) or a crush lesion of the sciatic nerve were treated with a twice-daily dose of 20 mg/kg of TPM. Behavioral and neurophysiological tests were used to measure pain-related behavior, motor, and sensory function. Morphometry was performed to evaluate sciatic nerves. In CCI, treatment with TPM attenuated mechanical hyperalgesia and cold allodynia. In sciatic nerve crush, TPM reduced cold allodynia and attenuated thermal hyperalgesia at the early and late phase of the observation. There was no difference in the numbers of surviving or regenerating nerve fibers between saline- and TPM-treated rats in either model. Electrophysiological studies carried out over a period of 3 months after sciatic nerve crush did not show major differences between TPM- and saline-treated rats. In conclusion, we could show moderate anti-hyperalgesic effects but could not prove a neuroprotective effect of TPM in these two rat nerve injury models using electrophysiological and morphometric methods.

Animals↗
PubMed2006

The preventive treatment of migraine.

BACKGROUND: Migraine is a common, chronic, and disabling disorder. The treatment of migraine includes a combination of nonpharmacologic and pharmacologic techniques. Pharmacologic approaches are subdivided in preventive therapies and acute care. REVIEW SUMMARY: In this review article, we review the current approaches to the preventive treatment of migraine. Preventive treatment should be initiated in those with frequent or disabling headaches. The goals include (1) reducing attack frequency, intensity, and duration; (2) minimizing headache-related disability; (3) improving health-related quality of life; (4) avoiding headache escalation and medication misuse. In this article, we also discuss the principles of migraine prevention, as well as drugs available for this goal. We divide preventive medications on those of common use, nutraceutical compounds, and medications less frequently used. We close by briefly discussing some in-development potential preventive drugs. CONCLUSION: Preventive therapies are well suitable for migraineurs with attack-related disability despite appropriate acute care.

Adrenergic beta-Antagonists↗
PubMed1983

Effects of the new beta-adrenoceptor blocking agent, S-596 on the peripheral autonomic nervous system and smooth muscles.

The effects of the new beta-adrenoceptor blocking agent, S-596, on the peripheral autonomic nervous system and smooth muscles were studied in comparison with propranolol. In urethane or alpha-chloralose anesthetized cats S-596 (10 micrograms/kg, i.v.) antagonized the cardiovascular responses induced by isoproterenol. S-596, in doses ranging from 100 to 300 micrograms/kg (i.v.) reduced the contractions of the nictitating membrane induced by electrical stimulation of preganglionic and postganglionic fibers to the superior cervical ganglion. Higher doses of S-596 were required to depress the effects of noradrenaline and tyramine. In spinal cats the tyramine and noradrenaline dose-response curve was shifted to the right by S-596. In isolated rat aortic strips S-596 displaced the noradrenaline dose-response curve to the right in a parallel fashion indicating a competitive antagonism. Its potency was about one tenth of that of phentolamine. These results suggest that S-596 possesses both alpha-and beta-adrenoceptor blocking activities.

Adrenergic beta-Antagonists↗
PubMed2003

Irritable bowel syndrome: a primer on management.

Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by abdominal pain, bloating, and either constipation or diarrhea. Managing this chronic condition requires a coordinated effort between patient and physician. The diagnosis of IBS should be made as early as possible in the evaluation of a patient, so that treatment can be initiated as soon as possible. Treatment usually requires a multifactorial approach, including patient education, reassurance, lifestyle changes, and pharmacotherapy. In this article, medications commonly used to treat the individual symptoms of IBS are reviewed, based on evidence from the literature. In addition, new agents that affect the serotonin system and treat the global symptoms of IBS are described.

Antidepressive Agents, Tricyclic↗
PubMed2006

Availability, stability, and sterility of pralidoxime for mass casualty use.

STUDY OBJECTIVE: Pralidoxime is indicated to treat patients poisoned with nerve agents. It is available in intravenous formulation for more seriously ill hospitalized patients and intramuscular formulation for field treatment and less seriously ill patients. Our study describes a method to convert the intramuscular formulation for intravenous use and determines the stability and sterility of the resulting formulation over time and under various environmental conditions. METHODS: An inventory was taken of all intravenous (Protopam) and intramuscular (Mark I Autoinjector kits) pralidoxime available in Franklin County, Ohio hospitals, and out-of-hospital stockpiles. A method was devised to safely convert the intramuscular pralidoxime to an intravenous formulation, which was then tested for stability and sterility under a variety of environmental temperatures over time. RESULTS: In Franklin County, Ohio (population 1.1 million), the 10 acute care hospitals and out-of-hospital community have 36 g of intravenous pralidoxime and 4,398 g (7,270 Mark I kits) of intramuscular pralidoxime. The reformulated pralidoxime retained greater than 90% stability and remained sterile at all environmental temperatures through day 28. CONCLUSION: Available pralidoxime in Franklin County is predominantly in the intramuscular preparation. Conversion of intramuscular to intravenous pralidoxime results in a stable and sterile solution for up to 28 days under a variety of environmental conditions and should be considered in a mass casualty situation in which additional intravenous supplies are needed.

Antidotes↗
PubMed2006

Neuroprotection in the peripheral nervous system: rationale for more effective therapies.

Most peripheral neuropathies are length dependent and result in distal axonal degeneration rather than loss of neuronal cell bodies. Available therapies for axonal peripheral neuropathies are designed to control painful symptoms and not to treat the underlying axonal degeneration. Many neuroprotective therapies are being developed, primarily for central nervous system disorders such as stroke or multiple sclerosis. However, strategies with the purpose of promoting survival of injured neurons (ie, preventing cell death) may not be applicable in many peripheral nervous system illnesses when the primary pathologic disorder that leads to symptoms is distal axonal degeneration. Neuronal cell death, if it occurs, is often a late event and may be untreatable in the near future. In contrast, distal axonal degeneration is an early event that may be amenable to treatment. Mechanistic studies that examine the axon-glia interaction and axonal biology are likely to yield novel therapeutic targets for peripheral neuropathies.

Animals↗
PubMed2004

Recent advances in understanding pain mechanisms provide future directions for pain management.

PURPOSE/OBJECTIVES: To review current knowledge of neurobiologic mechanisms that generate and maintain chronic pain and to explain how they might be applied in targeting treatment of chronic, inflammatory, and neuropathic pain syndromes. DATA SOURCES: Published research, literature review articles, and abstracts as well as national statistics. DATA SYNTHESIS: Treatment for chronic pain associated with cancer and other syndromes remains suboptimal and falls significantly short of clinical needs. Data highlight the role that multiple neurobiologic mechanisms play in modulating and maintaining pain at various levels of the central and peripheral nervous systems. Novel agents have been developed that use a more targeted approach to treating chronic pain. CONCLUSIONS: A growing body of evidence highlights the critical role that neurobiologic mechanisms play in the initiation and maintenance of chronic pain. A thorough understanding of these mechanisms ultimately may result in targeted treatment approaches that focus on the central and peripheral mechanisms involved in mediation of chronic, inflammatory, and neuropathic pain syndromes. IMPLICATIONS FOR NURSING: A majority of patients undergoing active treatment for cancer experiences unrelieved pain. By gaining a better understanding of the mechanisms that generate and maintain chronic pain, oncology nurses can promote targeted pain management strategies that incorporate novel therapeutic agents.

Acute Disease↗
PubMed2003

PACAP in avians: origin, occurrence, and receptors--pharmacological and functional considerations.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is a novel member of the secretin/glucagon/vasoactive intestinal peptide (VIP) superfamily. In vertebrates, including avians, it occurs in two forms: PACAP(38) and PACAP(27). PACAP structure is well conserved during evolution, being identical in mammals, and showing one amino acid dfifference in avians (chick, turkey). PACAP is widely distributed in the central nervous system and peripheral tissues and displays a pleiotropic activity, including functions as a hypophysiotropic hormone, neuromodulator, and neurotrophic factor. PACAP exerts its biological actions through three types of receptors designated PAC(1), VPAC(1) and VPAC(1). This review (1) presents the current knowledge on PACAP origin, distribution and function, (2) compares the avian findings with those found in mammals, and (3) describes receptor-linked mechanisms in avians, including recent data on receptor-related signal transduction pathways, with a special emphasis on receptor pharmacology and function.

Amino Acid Sequence↗
PubMed2006

Historical review: ATP as a neurotransmitter.

Purinergic signalling is now recognized to be involved in a wide range of activities of the nervous system, including neuroprotection, central control of autonomic functions, neural-glial interactions, control of vessel tone and angiogenesis, pain and mechanosensory transduction and the physiology of the special senses. In this article, I give a personal retrospective of the discovery of purinergic neurotransmission in the early 1970s, the struggle for its acceptance for approximately 20 years, the expansion into purinergic cotransmission and its eventual acceptance when receptor subtypes for ATP were cloned and characterized and when purinergic synaptic transmission between neurons in the brain and peripheral ganglia was described in the early 1990s. I also discuss the current status of the field, including recent interest in the pathophysiology of purinergic signalling and its therapeutic potential.

Adenosine Triphosphate↗
PubMed1988

General pharmacological studies on N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate. 2nd communication: effect on the peripheral nervous system and peripheral organs.

The pharmacological actions of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a new antiarrhythmic agent, on the peripheral nervous system and peripheral organs were studied in various laboratory animals in comparison with those of disopyramide and mexiletine, and the following results were obtained. 1. Large doses (50 or 100 mg/kg p.o.) of SUN 1165 as well as mexiletine had little effects on the pilocarpine-induced hypersalivation and the pupil size in mice. At higher concentration (10(-5) g/ml), SUN 1165 had no effects on the various spasmogen acetylcholine (ACh)-, histamine- or BaCl2-induced contractions in the isolated guinea pig ileum, tracheal smooth muscle and urinary bladder. Disopyramide caused mydriasis, inhibited the pilocarpine-induced hypersalivation at antiarrhythmic doses (10-30 mg/kg p.o.), and suppressed ACh-induced contractions in the various organs. 2. SUN 1165, like disopyramide and mexiletine, decreased the contractile amplitude and diastolic tone of the isolated rabbit ileum. SUN 1165 as well as disopyramide had no effect on the intestinal propulsion even at a large dose (100 mg/kg p.o.). Mexiletine inhibited it at antiarrhythmic doses (10-30 mg/kg p.o.). SUN 1165 only at a large dose (100 mg/kg i.d. or p.o.) inhibited volume of pepsin output in the gastric juice in pylorus-ligated rats and caused a damage to the gastric mucosa. 3. SUN 1165, like disopyramide and mexiletine, slightly potentiated the norepinephrine-induced contraction of the rat vas deferens in vitro. Moreover, SUN 1165 as well as disopyramide and mexiletine slightly potentiated the serotonin-induced contraction of the rat isolated fundus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Satellite glial cells in sensory ganglia: from form to function.

Current information indicates that glial cells participate in all the normal and pathological processes of the central nervous system. Although much less is known about satellite glial cells (SGCs) in sensory ganglia, it appears that these cells share many characteristics with their central counterparts. This review presents information that has been accumulated recently on the physiology and pharmacology of SGCs. It appears that SGCs carry receptors for numerous neuroactive agents (e.g., ATP, bradykinin) and can therefore receive signals from other cells and respond to changes in their environment. Activation of SGCs might in turn influence neighboring neurons. Thus SGCs are likely to participate in signal processing and transmission in sensory ganglia. Damage to the axons of sensory ganglia is known to contribute to neuropathic pain. Such damage also affects SGCs, and it can be proposed that these cells have a role in pathological changes in the ganglia.

Animals↗
PubMed2001

The WldS protein protects against axonal degeneration: a model of gene therapy for peripheral neuropathy.

The WldS mouse is a spontaneous mutant that is characterized by the phenotype of delayed degeneration of transected nerves (slow Wallerian degeneration). Molecular genetic analysis identified a mutation in this animal that codes for a unique protein expressed in brain tissue of WldS mice. We asked whether the WldS phenotype, in addition to delaying axonal degeneration after axotomy, might provide neuroprotection against toxic neuropathy. In dorsal root ganglia (DRG) cultures, neurites from WldS transiently exposed to vincristine not only resisted axonal degeneration but resumed growth after withdrawal of the toxin. Neurites from wild type mice died rapidly and did not recover. To prove that the identified mutation and its protein product are responsible for the WldS phenotype, we used an adenoviral gene transfer system to deliver the WldS to rat DRG neurons. Rat neurons expressing the WldS protein were resistant to vincristine-induced axonal degeneration, confirming the functional significance of the identified gene mutation. These data provide evidence that the WldS protein can be neuroprotective against vincristine neuropathy, and possibly other disorders characterized by axonal degeneration. In addition, delivery of this gene to wild type cells can transfer the WldS phenotype, providing the possibility of "gene therapy" for peripheral neuropathy.

Adenoviridae↗