The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)
The resection or removal of the innervation of a muscle or muscle tissue.
The removal or interruption of some part of the autonomic nervous system for therapeutic or research purposes.
The removal or interruption of some part of the sympathetic nervous system for therapeutic or research purposes.
The removal or interruption of some part of the parasympathetic nervous system for therapeutic or research purposes.
The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.
Sympathectomy using chemicals (e.g., 6-hydroxydopamine or guanethidine) which selectively and reversibly destroy adrenergic nerve endings while leaving cholinergic nerve endings intact.
Derangement in size and number of muscle fibers occurring with aging, reduction in blood supply, or following immobilization, prolonged weightlessness, malnutrition, and particularly in denervation.
Removal of an autonomic or sensory ganglion by any means.
Contractile tissue that produces movement in animals.
Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls.
The synapse between a neuron and a muscle.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
The interruption or removal of any part of the vagus (10th cranial) nerve. Vagotomy may be performed for research or for therapeutic purposes.
Renewal or physiological repair of damaged nerve tissue.
The dilated portion of the common carotid artery at its bifurcation into external and internal carotids. It contains baroreceptors which, when stimulated, cause slowing of the heart, vasodilatation, and a fall in blood pressure.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
The 10th cranial nerve. The vagus is a mixed nerve which contains somatic afferents (from skin in back of the ear and the external auditory meatus), visceral afferents (from the pharynx, larynx, thorax, and abdomen), parasympathetic efferents (to the thorax and abdomen), and efferents to striated muscle (of the larynx and pharynx).
Disorders of one or more of the twelve cranial nerves. With the exception of the optic and olfactory nerves, this includes disorders of the brain stem nuclei from which the cranial nerves originate or terminate.
Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.
A guanidine analog with specific affinity for tissues of the sympathetic nervous system and related tumors. The radiolabeled forms are used as antineoplastic agents and radioactive imaging agents. (Merck Index, 12th ed) MIBG serves as a neuron-blocking agent which has a strong affinity for, and retention in, the adrenal medulla and also inhibits ADP-ribosyltransferase.
A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.
Diseases of the parasympathetic or sympathetic divisions of the AUTONOMIC NERVOUS SYSTEM; which has components located in the CENTRAL NERVOUS SYSTEM and PERIPHERAL NERVOUS SYSTEM. Autonomic dysfunction may be associated with HYPOTHALAMIC DISEASES; BRAIN STEM disorders; SPINAL CORD DISEASES; and PERIPHERAL NERVOUS SYSTEM DISEASES. Manifestations include impairments of vegetative functions including the maintenance of BLOOD PRESSURE; HEART RATE; pupil function; SWEATING; REPRODUCTIVE AND URINARY PHYSIOLOGY; and DIGESTION.
The craniosacral division of the autonomic nervous system. The cell bodies of the parasympathetic preganglionic fibers are in brain stem nuclei and in the sacral spinal cord. They synapse in cranial autonomic ganglia or in terminal ganglia near target organs. The parasympathetic nervous system generally acts to conserve resources and restore homeostasis, often with effects reciprocal to the sympathetic nervous system.
A small cluster of chemoreceptive and supporting cells located near the bifurcation of the internal carotid artery. The carotid body, which is richly supplied with fenestrated capillaries, senses the pH, carbon dioxide, and oxygen concentrations in the blood and plays a crucial role in their homeostatic control.
An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord.
The musculofibrous partition that separates the THORACIC CAVITY from the ABDOMINAL CAVITY. Contraction of the diaphragm increases the volume of the thoracic cavity aiding INHALATION.
Neurons which send impulses peripherally to activate muscles or secretory cells.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Elements of limited time intervals, contributing to particular results or situations.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The 9th cranial nerve. The glossopharyngeal nerve is a mixed motor and sensory nerve; it conveys somatic and autonomic efferents as well as general, special, and visceral afferents. Among the connections are motor fibers to the stylopharyngeus muscle, parasympathetic fibers to the parotid glands, general and taste afferents from the posterior third of the tongue, the nasopharynx, and the palate, and afferents from baroreceptors and CHEMORECEPTOR CELLS of the carotid sinus.
Nerve fibers liberating catecholamines at a synapse after an impulse.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Neurons which activate MUSCLE CELLS.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
Use of electric potential or currents to elicit biological responses.
Dopamines with a hydroxy group substituted in one or more positions.
The hollow, muscular organ that maintains the circulation of the blood.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
Recording of the changes in electric potential of muscle by means of surface or needle electrodes.
Cells specialized to detect chemical substances and relay that information centrally in the nervous system. Chemoreceptor cells may monitor external stimuli, as in TASTE and OLFACTION, or internal stimuli, such as the concentrations of OXYGEN and CARBON DIOXIDE in the blood.
The specialized postsynaptic region of a muscle cell. The motor endplate is immediately across the synaptic cleft from the presynaptic axon terminal. Among its anatomical specializations are junctional folds which harbor a high density of cholinergic receptors.
The protein constituents of muscle, the major ones being ACTINS and MYOSINS. More than a dozen accessory proteins exist including TROPONIN; TROPOMYOSIN; and DYSTROPHIN.
A response by the BARORECEPTORS to increased BLOOD PRESSURE. Increased pressure stretches BLOOD VESSELS which activates the baroreceptors in the vessel walls. The net response of the CENTRAL NERVOUS SYSTEM is a reduction of central sympathetic outflow. This reduces blood pressure both by decreasing peripheral VASCULAR RESISTANCE and by lowering CARDIAC OUTPUT. Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure.
Sodium excretion by URINATION.
A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles.
Large, multinucleate single cells, either cylindrical or prismatic in shape, that form the basic unit of SKELETAL MUSCLE. They consist of MYOFIBRILS enclosed within and attached to the SARCOLEMMA. They are derived from the fusion of skeletal myoblasts (MYOBLASTS, SKELETAL) into a syncytium, followed by differentiation.
Skeletal muscle fibers characterized by their expression of the Type II MYOSIN HEAVY CHAIN isoforms which have high ATPase activity and effect several other functional properties - shortening velocity, power output, rate of tension redevelopment. Several fast types have been identified.
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
A progressive neurodegenerative condition of the central and autonomic nervous systems characterized by atrophy of the preganglionic lateral horn neurons of the thoracic spinal cord. This disease is generally considered a clinical variant of MULTIPLE SYSTEM ATROPHY. Affected individuals present in the fifth or sixth decade with ORTHOSTASIS and bladder dysfunction; and later develop FECAL INCONTINENCE; anhidrosis; ATAXIA; IMPOTENCE; and alterations of tone suggestive of basal ganglia dysfunction. (From Adams et al., Principles of Neurology, 6th ed, p536)
The 5th and largest cranial nerve. The trigeminal nerve is a mixed motor and sensory nerve. The larger sensory part forms the ophthalmic, mandibular, and maxillary nerves which carry afferents sensitive to external or internal stimuli from the skin, muscles, and joints of the face and mouth and from the teeth. Most of these fibers originate from cells of the TRIGEMINAL GANGLION and project to the TRIGEMINAL NUCLEUS of the brain stem. The smaller motor part arises from the brain stem trigeminal motor nucleus and innervates the muscles of mastication.
An increase in the excretion of URINE. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Excessive sweating. In the localized type, the most frequent sites are the palms, soles, axillae, inguinal folds, and the perineal area. Its chief cause is thought to be emotional. Generalized hyperhidrosis may be induced by a hot, humid environment, by fever, or by vigorous exercise.
Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
An alkylamide found in CAPSICUM that acts at TRPV CATION CHANNELS.
A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.
A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.
The dilatation of the aortic wall behind each of the cusps of the aortic valve.
The 12th cranial nerve. The hypoglossal nerve originates in the hypoglossal nucleus of the medulla and supplies motor innervation to all of the muscles of the tongue except the palatoglossus (which is supplied by the vagus). This nerve also contains proprioceptive afferents from the tongue muscles.
A highly poisonous compound that is an inhibitor of many metabolic processes and is used as a test reagent for the function of chemoreceptors. It is also used in many industrial processes.
NERVE FIBERS which project from the central nervous system to AUTONOMIC GANGLIA. In the sympathetic division most preganglionic fibers originate with neurons in the intermediolateral column of the SPINAL CORD, exit via ventral roots from upper thoracic through lower lumbar segments, and project to the paravertebral ganglia; there they either terminate in SYNAPSES or continue through the SPLANCHNIC NERVES to the prevertebral ganglia. In the parasympathetic division the fibers originate in neurons of the BRAIN STEM and sacral spinal cord. In both divisions the principal transmitter is ACETYLCHOLINE but peptide cotransmitters may also be released.
Nerve fibers which project from cell bodies of AUTONOMIC GANGLIA to SYNAPSES on target organs.
A paravertebral sympathetic ganglion formed by the fusion of the inferior cervical and first thoracic ganglia.
Disorders of the AUTONOMIC NERVOUS SYSTEM occurring as a primary condition. Manifestations can involve any or all body systems but commonly affect the BLOOD PRESSURE and HEART RATE.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
A degenerative disease of the AUTONOMIC NERVOUS SYSTEM that is characterized by idiopathic ORTHOSTATIC HYPOTENSION and a greatly reduced level of CATECHOLAMINES. No other neurological deficits are present.
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.
A myogenic regulatory factor that controls myogenesis. Myogenin is induced during differentiation of every skeletal muscle cell line that has been investigated, in contrast to the other myogenic regulatory factors that only appear in certain cell types.
Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.
Ganglia of the sympathetic nervous system including the paravertebral and the prevertebral ganglia. Among these are the sympathetic chain ganglia, the superior, middle, and inferior cervical ganglia, and the aorticorenal, celiac, and stellate ganglia.
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.
A muscular organ in the mouth that is covered with pink tissue called mucosa, tiny bumps called papillae, and thousands of taste buds. The tongue is anchored to the mouth and is vital for chewing, swallowing, and for speech.
Slender processes of NEURONS, including the AXONS and their glial envelopes (MYELIN SHEATH). Nerve fibers conduct nerve impulses to and from the CENTRAL NERVOUS SYSTEM.
Developmental events leading to the formation of adult muscular system, which includes differentiation of the various types of muscle cell precursors, migration of myoblasts, activation of myogenesis and development of muscle anchorage.
The propagation of the NERVE IMPULSE along the nerve away from the site of an excitation stimulus.
Toxic proteins produced from the species CLOSTRIDIUM BOTULINUM. The toxins are synthesized as a single peptide chain which is processed into a mature protein consisting of a heavy chain and light chain joined via a disulfide bond. The botulinum toxin light chain is a zinc-dependent protease which is released from the heavy chain upon ENDOCYTOSIS into PRESYNAPTIC NERVE ENDINGS. Once inside the cell the botulinum toxin light chain cleaves specific SNARE proteins which are essential for secretion of ACETYLCHOLINE by SYNAPTIC VESICLES. This inhibition of acetylcholine release results in muscular PARALYSIS.
An enzyme that catalyzes the hydrolysis of ACETYLCHOLINE to CHOLINE and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC
The medial terminal branch of the sciatic nerve. The tibial nerve fibers originate in lumbar and sacral spinal segments (L4 to S2). They supply motor and sensory innervation to parts of the calf and foot.
The small mass of modified cardiac muscle fibers located at the junction of the superior vena cava (VENA CAVA, SUPERIOR) and right atrium. Contraction impulses probably start in this node, spread over the atrium (HEART ATRIUM) and are then transmitted by the atrioventricular bundle (BUNDLE OF HIS) to the ventricle (HEART VENTRICLE).
Treatment of muscles and nerves under pressure as a result of crush injuries.
Branch-like terminations of NERVE FIBERS, sensory or motor NEURONS. Endings of sensory neurons are the beginnings of afferent pathway to the CENTRAL NERVOUS SYSTEM. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called PRESYNAPTIC TERMINALS.
Removal of tissue with electrical current delivered via electrodes positioned at the distal end of a catheter. Energy sources are commonly direct current (DC-shock) or alternating current at radiofrequencies (usually 750 kHz). The technique is used most often to ablate the AV junction and/or accessory pathways in order to interrupt AV conduction and produce AV block in the treatment of various tachyarrhythmias.
Nerve structures through which impulses are conducted from a peripheral part toward a nerve center.
Characteristic properties and processes of the NERVOUS SYSTEM as a whole or with reference to the peripheral or the CENTRAL NERVOUS SYSTEM.
An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order TETRAODONTIFORMES, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction.
A fold of the mucous membrane of the CONJUNCTIVA in many animals. At rest, it is hidden in the medial canthus. It can extend to cover part or all of the cornea to help clean the CORNEA.
The ENTERIC NERVOUS SYSTEM; PARASYMPATHETIC NERVOUS SYSTEM; and SYMPATHETIC NERVOUS SYSTEM taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the CENTRAL NERVOUS SYSTEM, especially the HYPOTHALAMUS and the SOLITARY NUCLEUS, which receive information relayed from VISCERAL AFFERENTS.
Skeletal muscle fibers characterized by their expression of the Type I MYOSIN HEAVY CHAIN isoforms which have low ATPase activity and effect several other functional properties - shortening velocity, power output, rate of tension redevelopment.
Ganglia of the parasympathetic nervous system, including the ciliary, pterygopalatine, submandibular, and otic ganglia in the cranial region and intrinsic (terminal) ganglia associated with target organs in the thorax and abdomen.
Disorders characterized by an abnormal reduction in muscle volume due to a decrease in the size or number of muscle fibers. Atrophy may result from diseases intrinsic to muscle tissue (e.g., MUSCULAR DYSTROPHY) or secondary to PERIPHERAL NERVOUS SYSTEM DISEASES that impair innervation to muscle tissue (e.g., MUSCULAR ATROPHY, SPINAL).
A general term most often used to describe severe or complete loss of muscle strength due to motor system disease from the level of the cerebral cortex to the muscle fiber. This term may also occasionally refer to a loss of sensory function. (From Adams et al., Principles of Neurology, 6th ed, p45)
Neurotoxic proteins from the venom of the banded or Formosan krait (Bungarus multicinctus, an elapid snake). alpha-Bungarotoxin blocks nicotinic acetylcholine receptors and has been used to isolate and study them; beta- and gamma-bungarotoxins act presynaptically causing acetylcholine release and depletion. Both alpha and beta forms have been characterized, the alpha being similar to the large, long or Type II neurotoxins from other elapid venoms.
Muscles arising in the zygomatic arch that close the jaw. Their nerve supply is masseteric from the mandibular division of the trigeminal nerve. (From Stedman, 25th ed)
Clusters of neurons and their processes in the autonomic nervous system. In the autonomic ganglia, the preganglionic fibers from the central nervous system synapse onto the neurons whose axons are the postganglionic fibers innervating target organs. The ganglia also contain intrinsic neurons and supporting cells and preganglionic fibers passing through to other ganglia.
An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.
A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
A sensory branch of the trigeminal (5th cranial) nerve. The ophthalmic nerve carries general afferents from the superficial division of the face including the eyeball, conjunctiva, upper eyelid, upper nose, nasal mucosa, and scalp.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Disease or damage involving the SCIATIC NERVE, which divides into the PERONEAL NERVE and TIBIAL NERVE (see also PERONEAL NEUROPATHIES and TIBIAL NEUROPATHY). Clinical manifestations may include SCIATICA or pain localized to the hip, PARESIS or PARALYSIS of posterior thigh muscles and muscles innervated by the peroneal and tibial nerves, and sensory loss involving the lateral and posterior thigh, posterior and lateral leg, and sole of the foot. The sciatic nerve may be affected by trauma; ISCHEMIA; COLLAGEN DISEASES; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, p1363)
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
Nerve structures through which impulses are conducted from a nerve center toward a peripheral site. Such impulses are conducted via efferent neurons (NEURONS, EFFERENT), such as MOTOR NEURONS, autonomic neurons, and hypophyseal neurons.
Peripheral, autonomic, and cranial nerve disorders that are associated with DIABETES MELLITUS. These conditions usually result from diabetic microvascular injury involving small blood vessels that supply nerves (VASA NERVORUM). Relatively common conditions which may be associated with diabetic neuropathy include third nerve palsy (see OCULOMOTOR NERVE DISEASES); MONONEUROPATHY; mononeuropathy multiplex; diabetic amyotrophy; a painful POLYNEUROPATHY; autonomic neuropathy; and thoracoabdominal neuropathy. (From Adams et al., Principles of Neurology, 6th ed, p1325)
A branch of the trigeminal (5th cranial) nerve. The mandibular nerve carries motor fibers to the muscles of mastication and sensory fibers to the teeth and gingivae, the face in the region of the mandible, and parts of the dura.
The most anterior portion of the uveal layer, separating the anterior chamber from the posterior. It consists of two layers - the stroma and the pigmented epithelium. Color of the iris depends on the amount of melanin in the stroma on reflection from the pigmented epithelium.
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.
The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and SALIVARY GLANDS, and convey afferent information for TASTE from the anterior two-thirds of the TONGUE and for TOUCH from the EXTERNAL EAR.
An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.
The act of breathing with the LUNGS, consisting of INHALATION, or the taking into the lungs of the ambient air, and of EXHALATION, or the expelling of the modified air which contains more CARBON DIOXIDE than the air taken in (Blakiston's Gould Medical Dictionary, 4th ed.). This does not include tissue respiration (= OXYGEN CONSUMPTION) or cell respiration (= CELL RESPIRATION).
Refers to animals in the period of time just after birth.
Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.
The vessels carrying blood away from the heart.
A sporadic neurodegenerative disease with onset in middle-age characterized clinically by Parkinsonian features (e.g., MUSCLE RIGIDITY; HYPOKINESIA; stooped posture) and HYPOTENSION. This condition is considered a clinical variant of MULTIPLE SYSTEM ATROPHY. Pathologic features include a prominent loss of neurons in the zona compacta of the SUBSTANTIA NIGRA and PUTAMEN. (From Adams et al., Principles of Neurology, 6th ed, p1075-6)
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
The circulation of the BLOOD through the vessels of the KIDNEY.
Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
Calcitonin gene-related peptide. A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in neural tissue of the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator.
Paired bundles of NERVE FIBERS entering and leaving the SPINAL CORD at each segment. The dorsal and ventral nerve roots join to form the mixed segmental spinal nerves. The dorsal roots are generally afferent, formed by the central projections of the spinal (dorsal root) ganglia sensory cells, and the ventral roots are efferent, comprising the axons of spinal motor and PREGANGLIONIC AUTONOMIC FIBERS.
Forced expiratory effort against a closed GLOTTIS.
An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC
Compounds containing the hexamethylenebis(trimethylammonium) cation. Members of this group frequently act as antihypertensive agents and selective ganglionic blocking agents.
One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.
A branch of the facial (7th cranial) nerve which passes through the middle ear and continues through the petrotympanic fissure. The chorda tympani nerve carries taste sensation from the anterior two-thirds of the tongue and conveys parasympathetic efferents to the salivary glands.
An antiseptic and disinfectant aromatic alcohol.
The lateral of the two terminal branches of the sciatic nerve. The peroneal (or fibular) nerve provides motor and sensory innervation to parts of the leg and foot.
The larger subunits of MYOSINS. The heavy chains have a molecular weight of about 230 kDa and each heavy chain is usually associated with a dissimilar pair of MYOSIN LIGHT CHAINS. The heavy chains possess actin-binding and ATPase activity.
A partial adrenergic agonist with functional beta 1-receptor specificity and inotropic effect. It is effective in the treatment of acute CARDIAC FAILURE, postmyocardial infarction low-output syndrome, SHOCK, and reducing ORTHOSTATIC HYPOTENSION in the SHY-RAGER SYNDROME.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A 9,10alpha-dihydro derivative of ERGOTAMINE. It is used as a vasoconstrictor, specifically for the therapy of MIGRAINE DISORDERS.
A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.
Sweat-producing structures that are embedded in the DERMIS. Each gland consists of a single tube, a coiled body, and a superficial duct.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
Injuries to the PERIPHERAL NERVES.
The largest of the three pairs of SALIVARY GLANDS. They lie on the sides of the FACE immediately below and in front of the EAR.

Possible role of serotonin in Merkel-like basal cells of the taste buds of the frog, Rana nigromaculata. (1/1756)

Merkel-like basal cells in the taste buds of the frog were examined by fluorescence histochemistry, immunohistochemistry and electron microscopy. There were about 16-20 basal cells arranged in a radial fashion at the base of each taste bud. These cells were strongly immunopositive for serotonin antiserum. They were characterised by the presence of numerous dense-cored granules in the cytoplasm ranging from 80 to 120 nm in diameter, and of microvilli protruding from the cell surface. For 4 mo after sensory denervation by cutting the gustatory nerves, all cell types of the taste bud were well preserved and maintained their fine structure. Even at 4 mo after denervation, the basal cells exhibited a strong immunoreaction with serotonin antiserum. To investigate the function of serotonin in the basal cells in taste bud function, serotonin deficiency was induced by administration of p-chlorophenylalanine (PCPA), an inhibitor of tryptophan hydroxylase, and of p-chloroamphetamine (PCA), a depletor of serotonin. After administration of these agents to normal and denervated frogs for 2 wk, a marked decrease, or complete absence, of immunoreactivity for serotonin was observed in the basal cells. Ultrastructurally, degenerative changes were observed in both types of frog; numerous lysosome-like myelin bodies were found in all cell types of the taste buds. The number of dense-cored granules in the basal cells also was greatly decreased by treatment with these drugs. Serotonin in Merkel-like basal cells appears to have a trophic role in maintenance of the morphological integrity of frog taste bud cells.  (+info)

Expression of Mash1 in basal cells of rat circumvallate taste buds is dependent upon gustatory innervation. (2/1756)

Mash1, a mammalian homologue of the Drosophila achaete-scute proneural gene complex, plays an essential role in differentiation of subsets of peripheral neurons. In this study, using RT-PCR and in situ RT-PCR, we investigated if Mash1 gene expression occurs in rat taste buds. Further, we examined dynamics of Mash1 expression in the process of degeneration and regeneration in denervated rat taste buds. In rat tongue epithelium, Mash1 gene expression is confined to circumvallate, foliate, and fungiform papilla epithelia that include taste buds. In taste buds, Mash1-expressing cells are round cells in the basal compartment. In contrast, the mature taste bud cells do not express the Mash1 gene. Denervation and regeneration experiments show that the expression of Mash1 requires gustatory innervation. We conclude that Mash1 is expressed in cells of the taste bud lineage, and that the expression of Mash1 in rat taste buds is dependent upon gustatory innervation.  (+info)

Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats. (3/1756)

Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of intracisternal CRF on carbon tetrachloride (CCl4)-induced acute liver injury was examined in rats. Intracisternal injection of CRF dose dependently enhanced elevation of the serum alanine aminotransferase (ALT) level induced by CCl4. Elevations of serum aspartate aminotransferase, alkaline phosphatase, and total bilirubin levels by CCl4 were also enhanced by intracisternal CRF injection. Intracisternal injection of CRF also aggravated CCl4-induced hepatic histological changes. Intracisternal CRF injection alone did not modify the serum ALT level. Intravenous administration of CRF did not influence CCl4-induced acute liver injury. The aggravating effect of central CRF on CCl4-induced acute liver injury was abolished by denervation of hepatic plexus with phenol and by denervation of noradrenergic fibers with 6-hydroxydopamine treatment but not by hepatic branch vagotomy or atropine treatment. These results suggest that CRF acts in the brain to exacerbate acute liver injury through the sympathetic-noradrenergic pathways.  (+info)

Nitric oxide mediates sympathetic vasoconstriction at supraspinal, spinal, and synaptic levels. (4/1756)

The purposes of this study were to investigate the level of the sympathetic nervous system in which nitric oxide (NO) mediates regional sympathetic vasoconstriction and to determine whether neural mechanisms are involved in vasoconstriction after NO inhibition. Ganglionic blockade (hexamethonium), alpha1-receptor blockade (prazosin), and spinal section at T1 were used to study sympathetic involvement. NO was blocked with Nomega-nitro-L-arginine methyl ester (L-NAME). Regional blood flow in the mesenteric and renal arteries and terminal aorta was monitored by electromagnetic flowmetry in conscious rats. L-NAME (3-5 mg/kg iv) increased arterial pressure and peripheral resistance. Ganglionic blockade (25 mg/kg iv) significantly reduced the increase in resistance in the mesentery and kidney in intact and spinal-sectioned rats. Ganglionic blockade significantly decreased hindquarter resistance in intact rats but not in spinal-sectioned rats. Prazosin (200 micrograms/kg iv) significantly reduced the increased hindquarter resistance. We concluded that NO suppresses sympathetic vasoconstriction in the mesentery and kidney at the spinal level, whereas hindquarter tone is mediated at supraspinal and synaptic levels.  (+info)

Erythromycin enhances early postoperative contractility of the denervated whole stomach as an esophageal substitute. (5/1756)

OBJECTIVE: To determine whether early postoperative administration of erythromycin accelerates the spontaneous motor recovery process after elevation of the denervated whole stomach up to the neck. SUMMARY BACKGROUND DATA: Spontaneous motor recovery after gastric denervation is a slow process that progressively takes place over years. METHODS: Erythromycin was administered as follows: continuous intravenous (i.v.) perfusion until postoperative day 10 in ten whole stomach (WS) patients at a dose of either 1 g (n = 5) or 2 g (n = 5) per day; oral intake at a dose of 1 g/day during 1.5 to 8 months after surgery in 11 WS patients, followed in 7 of them by discontinuation of the drug during 2 to 4 weeks. Gastric motility was assessed with intraluminal perfused catheters in these 21 patients, in 23 WS patients not receiving erythromycin, and in 11 healthy volunteers. A motility index was established by dividing the sum of the areas under the curves of >9 mmHg contractions by the time of recording. RESULTS: The motility index after IV or oral administration of erythromycin at and after surgery was significantly higher than that without erythromycin (i.v., 1 g: p = 0.0090; i.v., 2 g: p = 0.0090; oral, 1 g: p = 0.0017). It was similar to that in healthy volunteers (i.v., 1 g: p = 0.2818; oral, 1 g: p = 0.7179) and to that in WS patients with >3 years of follow-up who never received erythromycin (i.v., 1 g: p = 0.2206; oral, 1 g: p = 0.8326). The motility index after discontinuation of the drug was similar or superior to that recorded under medication in four patients who did not experience any modification of their alimentary comfort, whereas it dropped dramatically parallel to deterioration of the alimentary comfort in three patients. CONCLUSIONS: Early postoperative contractility of the denervated whole stomach pulled up to the neck under either i.v. or oral erythromycin is similar to that recovered spontaneously beyond 3 years of follow-up. In some patients, this booster effect persists after discontinuation of the drug.  (+info)

Heterogeneous cardiac sympathetic denervation and decreased myocardial nerve growth factor in streptozotocin-induced diabetic rats: implications for cardiac sympathetic dysinnervation complicating diabetes. (6/1756)

Heterogeneous myocardial sympathetic denervation complicating diabetes has been invoked as a factor contributing to sudden unexplained cardiac death. In subjects with diabetic autonomic neuropathy (DAN), distal left ventricular (LV) denervation contrasts with preservation of islands of proximal innervation, which exhibit impaired vascular responsiveness. The aims of this study were to determine whether this heterogeneous pattern of myocardial sympathetic denervation occurs in a rat model of diabetes and to explore a potential association with regional fluctuations in myocardial nerve growth factor (NGF) protein. Myocardial sympathetic denervation was characterized scintigraphically using the sympathetic neurotransmitter analog C-11 hydroxyephedrine ([11C]HED) and compared with regional changes in myocardial NGF protein abundance and norepinephrine content after 6 and 9 months in nondiabetic (ND) and streptozotocin-induced diabetic (STZ-D) rats. In ND rats, no difference in [11C]HED retention or norepinephrine content was detected in the proximal versus distal myocardium. After 6 months, compared with ND rats, myocardial [11C]HED retention had declined in the proximal segments of STZ-D rats by only 9% (NS) compared with a 33% decrease in the distal myocardium (P < 0.05). Myocardial norepinephrine content was similar in both ND and STZ-D rats. At 6 months, LV myocardial NGF protein content in STZ-D rats decreased by 52% in the proximal myocardial segments (P < 0.01 vs. ND rats) and by 82% distally (P < 0.01 vs. ND rats, P < 0.05 vs. proximal segments). By 9 months, [11C]HED retention had declined in both the proximal and distal myocardial segments of the STZ-D rats by 42% (P < 0.01 vs. ND rats), and LV norepinephrine content and NGF protein were decreased in parallel. Therefore, 6 months of STZ-induced diabetes results in heterogeneous cardiac sympathetic denervation in the rat, with maximal denervation occurring distally, and is associated with a proximal-to-distal gradient of LV NGF protein depletion. It is tempting to speculate that regional fluctuations of NGF protein in the diabetic myocardium contribute to heterogeneous cardiac sympathetic denervation complicating diabetes.  (+info)

Hypoxia inhibits baroreflex vagal bradycardia via a central action in anaesthetized rats. (7/1756)

It is known that arterial baroreflexes are suppressed in stressful conditions. The present study was designed to determine whether and how hypoxia affects arterial baroreflexes, especially the heart rate component, baroreflex vagal bradycardia. In chloralose-urethane-anaesthetized rats, baroreflex vagal bradycardia was evoked by electrical stimulation of the aortic depressor nerve, and the effect of 15 s inhalation of hypoxic gas (4% O2) was studied. Inhalation of hypoxic gas was found to inhibit baroreflex vagal bradycardia. The inhibition persisted after bilateral transection of the carotid sinus nerve. Cervical vagus nerves were cut bilaterally and their peripheral cut ends were stimulated to provoke vagal bradycardia of peripheral origin so as to determine whether hypoxia could inhibit vagal bradycardia by acting on a peripheral site. In contrast to baroreflex vagal bradycardia, the vagus-induced bradycardia was not affected by hypoxic gas inhalation. It is concluded that baroreflex vagal bradycardia is inhibited by hypoxia and the inhibition is largely mediated by its direct central action.  (+info)

A substituted dextran enhances muscle fiber survival and regeneration in ischemic and denervated rat EDL muscle. (8/1756)

Ischemia and denervation of EDL muscle of adult rat induce a large central zone of degeneration surrounded by a thin zone of peripheral surviving muscle fibers. Muscle regeneration is a complex phenomenon in which many agents interact, such as growth factors and heparan sulfate components of the extracellular matrix. We have shown that synthetic polymers, called RGTA (as regenerating agents), which imitate the heparan sulfates, are able to stimulate tissue repair when applied at the site of injury. In crushed muscles, RGTA were found to accelerate both regeneration and reinnervation. In vitro, RGTA act as protectors and potentiators of various heparin binding growth factors (HBGF). It was postulated that in vivo their tissue repair properties were due in part to an increase of bioavailability of endogenously released HBGF. In the present work, we show that ischemic and denervated EDL muscle treated by a unique injection of RGTA differs from the control after 1 wk in several aspects: 1) the epimysial postinflammatory reaction is inhibited and the area of fibrotic tissue among fibers is reduced; 2) the peripheral zone, as measured by the number of intact muscle fibers, was increased by more than twofold; and 3) In the central zone, RGTA enhances the regeneration of the muscle fibers as well as muscle revascularization. These results suggest that RGTA both protects muscle fibers from degeneration and preserves the differentiated state of the surviving fibers. For the first time it is demonstrated that a functionalized polymeric compound can prevent some of the damage resulting from muscle ischemia. RGTA may therefore open a new therapeutic approach for muscle fibrosis and other postischemic muscle pathologies.  (+info)

There are several types of muscular atrophy, including:

1. Disuse atrophy: This type of atrophy occurs when a muscle is not used for a long period, leading to its degeneration.
2. Neurogenic atrophy: This type of atrophy occurs due to damage to the nerves that control muscles.
3. Dystrophic atrophy: This type of atrophy occurs due to inherited genetic disorders that affect muscle fibers.
4. Atrophy due to aging: As people age, their muscles can degenerate and lose mass and strength.
5. Atrophy due to disease: Certain diseases such as cancer, HIV/AIDS, and muscular dystrophy can cause muscular atrophy.
6. Atrophy due to infection: Infections such as polio and tetanus can cause muscular atrophy.
7. Atrophy due to trauma: Traumatic injuries can cause muscular atrophy, especially if the injury is severe and leads to prolonged immobilization.

Muscular atrophy can lead to a range of symptoms depending on the type and severity of the condition. Some common symptoms include muscle weakness, loss of motor function, muscle wasting, and difficulty performing everyday activities. Treatment for muscular atrophy depends on the underlying cause and may include physical therapy, medication, and lifestyle changes such as exercise and dietary modifications. In severe cases, surgery may be necessary to restore muscle function.

Some common examples of cranial nerve diseases include:

1. Bell's palsy: A condition that affects the facial nerve, causing weakness or paralysis of one side of the face.
2. Multiple sclerosis: An autoimmune disease that damages the protective covering of nerve fibers, leading to communication problems between the brain and the rest of the body.
3. Trigeminal neuralgia: A condition that affects the trigeminal nerve, causing facial pain and numbness.
4. Meningitis: An inflammation of the meninges, the protective covering of the brain and spinal cord, which can damage the cranial nerves.
5. Acoustic neuroma: A type of non-cancerous tumor that grows on the nerve that connects the inner ear to the brain.
6. Cranial polyneuropathy: A condition where multiple cranial nerves are damaged, leading to a range of symptoms including muscle weakness, numbness, and pain.
7. Tumors: Both benign and malignant tumors can affect the cranial nerves, causing a variety of symptoms depending on their location and size.
8. Trauma: Head injuries or trauma can damage the cranial nerves, leading to a range of symptoms.
9. Infections: Bacterial or viral infections such as meningitis or encephalitis can damage the cranial nerves, leading to a range of symptoms.
10. Genetic disorders: Certain genetic disorders such as Charcot-Marie-Tooth disease can affect the cranial nerves, leading to a range of symptoms.

It's important to note that this is not an exhaustive list and there may be other causes of cranial nerve damage. If you are experiencing any symptoms that you think may be related to cranial nerve damage, it's important to seek medical attention as soon as possible for proper diagnosis and treatment.

There are many different types of ANS diseases, including:

1. Dysautonomia: a general term that refers to dysfunction of the autonomic nervous system.
2. Postural orthostatic tachycardia syndrome (POTS): a condition characterized by rapid heart rate and other symptoms that occur upon standing.
3. Neurocardiogenic syncope: a form of fainting caused by a sudden drop in blood pressure.
4. Multiple system atrophy (MSA): a progressive neurodegenerative disorder that affects the autonomic nervous system and other parts of the brain.
5. Parkinson's disease: a neurodegenerative disorder that can cause autonomic dysfunction, including constipation, urinary incontinence, and erectile dysfunction.
6. Dopamine deficiency: a condition characterized by low levels of the neurotransmitter dopamine, which can affect the ANS and other body systems.
7. Autonomic nervous system disorders associated with autoimmune diseases, such as Guillain-Barré syndrome and lupus.
8. Trauma: physical or emotional trauma can sometimes cause dysfunction of the autonomic nervous system.
9. Infections: certain infections, such as Lyme disease, can affect the autonomic nervous system.
10. Genetic mutations: some genetic mutations can affect the functioning of the autonomic nervous system.

Treatment for ANS diseases depends on the specific condition and its underlying cause. In some cases, medication may be prescribed to regulate heart rate, blood pressure, or other bodily functions. Lifestyle changes, such as regular exercise and stress management techniques, can also be helpful in managing symptoms. In severe cases, surgery may be necessary to correct anatomical abnormalities or repair damaged nerves.

The symptoms of Shy-Drager Syndrome can vary widely among individuals and may include:

* Cognitive decline
* Memory loss
* Difficulty with speech and language
* Loss of coordination and balance
* Dysphagia (difficulty swallowing)
* Weakness or paralysis of the limbs
* Bladder and bowel dysfunction
* Sleep disturbances

The exact cause of Shy-Drager Syndrome is not yet fully understood, but it is believed to be related to an autoimmune response, in which the body's immune system mistakenly attacks healthy cells in the brain. Genetic factors may also play a role in the development of the disorder.

There is no cure for Shy-Drager Syndrome, but various medications and therapies can help manage its symptoms. These may include:

* Cholinesterase inhibitors to improve cognitive function and slow the progression of dementia
* Anticholinergic drugs to reduce muscle rigidity and tremors
* Physical therapy to maintain mobility and strength
* Speech and language therapy to improve communication skills
* Occupational therapy to support daily living activities

The prognosis for Shy-Drager Syndrome is generally poor, with a median survival time of around 10-15 years after onset of symptoms. However, the rate of progression can vary widely among individuals, and some may experience a more gradual decline over several decades.

Overall, Shy-Drager Syndrome is a rare and complex disorder that requires careful management by a multidisciplinary team of healthcare professionals. While there is no cure for the condition, various therapies can help manage its symptoms and improve the quality of life for affected individuals.

There are two main types of hyperhidrosis: primary and secondary. Primary hyperhidrosis is idiopathic and has no identifiable cause, while secondary hyperhidrosis is caused by another medical condition or medication. Some common triggers for secondary hyperhidrosis include anxiety, stress, fever, infection, and certain medications such as antidepressants and beta blockers.

Symptoms of hyperhidrosis can vary in severity and can include:

* Excessive sweating on the palms, soles, face, or underarms
* Sweating that is not related to heat or physical activity
* Sweating that worsens at night or in cold temperatures
* Sweating that interferes with daily activities
* Skin irritation and infections due to excessive sweating

Hyperhidrosis can be diagnosed through a combination of medical history, physical examination, and laboratory tests. Treatment options for hyperhidrosis depend on the severity of symptoms and the underlying cause, but may include:

* Antiperspirants or deodorants that contain aluminum chloride or other active ingredients to reduce sweating
* Prescription medications such as beta blockers, anticholinergics, or botulinum toxin injections to reduce sweating
* Surgical procedures such as sympathectomy (nerve surgery) to destroy the nerves that regulate sweating
* Lifestyle modifications such as avoiding triggers and wearing loose, breathable clothing to manage symptoms.

It's important to note that hyperhidrosis can have a significant impact on quality of life, and seeking medical attention is recommended if symptoms are severe or persistent.

1. Difficulty regulating body temperature, leading to episodes of hyperthermia (elevated body temperature) or hypothermia (low body temperature).
2. Abnormal heart rate and rhythm, including bradycardia (slow heart rate) or tachycardia (fast heart rate).
3. Poor digestion and gastrointestinal problems such as constipation, diarrhea, nausea, and vomiting.
4. Difficulty swallowing, which can lead to respiratory problems.
5. Orthostatic intolerance, which can cause dizziness, lightheadedness, or fainting when standing up.
6. Seizures and other neurological symptoms such as tremors, muscle weakness, and loss of coordination.
7. Cognitive impairment, including developmental delays, intellectual disability, and learning disabilities.
8. Sleep disturbances, including insomnia and sleep apnea.
9. Emotional difficulties such as anxiety, depression, and mood swings.
10. Vision problems, including blurred vision, double vision, and light sensitivity.

Primary dysautonomias are caused by genetic mutations that affect the development or function of the autonomic nervous system. There are several subtypes of primary dysautonomias, each with distinct symptoms and characteristics. These conditions are rare and can be difficult to diagnose, as they often resemble other more common conditions such as anxiety disorders or attention deficit hyperactivity disorder (ADHD). Treatment for primary dysautonomias typically involves a combination of medication and lifestyle modifications, such as reducing stress, increasing fluid intake, and avoiding overexertion. In some cases, surgery may be necessary to correct anatomical abnormalities or to implant medical devices that help regulate the autonomic nervous system.

There are two types of hypertension:

1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.

Some common causes of secondary hypertension include:

* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use

There are also several risk factors for hypertension, including:

* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress

Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:

* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease

Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.

There are many different types of nerve degeneration that can occur in various parts of the body, including:

1. Alzheimer's disease: A progressive neurological disorder that affects memory and cognitive function, leading to degeneration of brain cells.
2. Parkinson's disease: A neurodegenerative disorder that affects movement and balance, caused by the loss of dopamine-producing neurons in the brain.
3. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
4. Multiple sclerosis: An autoimmune disease that affects the central nervous system, causing inflammation and damage to nerve fibers.
5. Diabetic neuropathy: A complication of diabetes that can cause damage to nerves in the hands and feet, leading to pain, numbness, and weakness.
6. Guillain-Barré syndrome: An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and paralysis.
7. Chronic inflammatory demyelinating polyneuropathy (CIDP): An autoimmune disorder that can cause inflammation and damage to nerve fibers, leading to muscle weakness and numbness.

The causes of nerve degeneration are not always known or fully understood, but some possible causes include:

1. Genetics: Some types of nerve degeneration may be inherited from one's parents.
2. Aging: As we age, our nerve cells can become damaged or degenerate, leading to a decline in cognitive and physical function.
3. Injury or trauma: Physical injury or trauma to the nervous system can cause nerve damage and degeneration.
4. Infections: Certain infections, such as viral or bacterial infections, can cause nerve damage and degeneration.
5. Autoimmune disorders: Conditions such as Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy (CIDP) are caused by the immune system attacking and damaging nerve cells.
6. Toxins: Exposure to certain toxins, such as heavy metals or pesticides, can damage and degenerate nerve cells.
7. Poor nutrition: A diet that is deficient in essential nutrients, such as vitamin B12 or other B vitamins, can lead to nerve damage and degeneration.
8. Alcoholism: Long-term alcohol abuse can cause nerve damage and degeneration due to the toxic effects of alcohol on nerve cells.
9. Drug use: Certain drugs, such as chemotherapy drugs and antiviral medications, can damage and degenerate nerve cells.
10. Aging: As we age, our nerve cells can deteriorate and become less functional, leading to a range of cognitive and motor symptoms.

It's important to note that in some cases, nerve damage and degeneration may be irreversible, but there are often strategies that can help manage symptoms and improve quality of life. If you suspect you have nerve damage or degeneration, it's important to seek medical attention as soon as possible to receive an accurate diagnosis and appropriate treatment.

In other words, pure autonomic failure refers to a situation where an individual experiences a decline in their autonomic nervous system's ability to regulate involuntary functions, such as heart rate, blood pressure, digestion, and body temperature, without any identifiable underlying cause. This can result in a range of symptoms, including fatigue, dizziness, lightheadedness, and difficulty maintaining balance.

Pure autonomic failure is rare and often presents challenges for diagnosis and treatment. It may be associated with other medical conditions, such as autoimmune disorders or neurodegenerative diseases, but in some cases, the cause remains unknown. Treatment options are limited and may include medication, lifestyle modifications, and management of symptoms.

There are several types of atrophy that can occur in different parts of the body. For example:

1. Muscular atrophy: This occurs when muscles weaken and shrink due to disuse or injury.
2. Neuronal atrophy: This occurs when nerve cells degenerate, leading to a loss of cognitive function and memory.
3. Cardiac atrophy: This occurs when the heart muscle weakens and becomes less efficient, leading to decreased cardiac output.
4. Atrophic gastritis: This is a type of stomach inflammation that can lead to the wasting away of the stomach lining.
5. Atrophy of the testes: This occurs when the testes shrink due to a lack of use or disorder, leading to decreased fertility.

Atrophy can be diagnosed through various medical tests and imaging studies, such as MRI or CT scans. Treatment for atrophy depends on the underlying cause and may involve physical therapy, medication, or surgery. In some cases, atrophy can be prevented or reversed with proper treatment and care.

In summary, atrophy is a degenerative process that can occur in various parts of the body due to injury, disease, or disuse. It can lead to a loss of function and decreased quality of life, but with proper diagnosis and treatment, it may be possible to prevent or reverse some forms of atrophy.

Examples of atrophic muscular disorders include:

1. Muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength, leading to muscle wasting and weakness.
2. Myotonia congenita: An autosomal dominant disorder characterized by muscle stiffness and spasms, particularly in the neck, shoulder, and limb muscles.
3. Inclusion body myositis: An inflammatory muscle disease that leads to progressive muscle weakness and wasting, with deposits of abnormal protein called inclusion bodies in the muscle fibers.
4. Limb-girdle muscular dystrophy: A group of inherited disorders that cause progressive loss of muscle mass and strength in the arms and legs, leading to muscle wasting and weakness.
5. Facioscapulohumeral muscular dystrophy: An inherited disorder characterized by progressive weakness of the facial, shoulder, and upper arm muscles, with a loss of motor neurons in the spinal cord.

The symptoms of atrophic muscular disorders can vary depending on the specific disorder and its severity, but may include:

1. Muscle weakness and wasting
2. Muscle cramps and spasms
3. Difficulty walking or standing
4. Fatigue and decreased endurance
5. Loss of motor neurons in the spinal cord
6. Cognitive impairment
7. Developmental delays
8. Vision loss
9. Hearing loss
10. Skeletal deformities

Atrophic muscular disorders can be diagnosed through a combination of clinical evaluation, electromyography (EMG), and muscle biopsy. Treatment is focused on managing the symptoms and slowing the progression of the disease, and may include:

1. Physical therapy to maintain muscle strength and function
2. Medications to manage pain and spasms
3. Assistive devices such as braces and walkers
4. Respiratory support in advanced cases
5. Gene therapy is an area of ongoing research, but it is not yet widely available for the treatment of atrophic muscular disorders.

It is important to note that atrophic muscular disorders are a group of rare and complex conditions, and each type has its own unique set of symptoms and characteristics. If you suspect that you or someone you know may be experiencing symptoms of an atrophic muscular disorder, it is important to consult with a healthcare professional for proper evaluation and diagnosis.

1. Complete paralysis: When there is no movement or sensation in a particular area of the body.
2. Incomplete paralysis: When there is some movement or sensation in a particular area of the body.
3. Localized paralysis: When paralysis affects only a specific part of the body, such as a limb or a facial muscle.
4. Generalized paralysis: When paralysis affects multiple parts of the body.
5. Flaccid paralysis: When there is a loss of muscle tone and the affected limbs feel floppy.
6. Spastic paralysis: When there is an increase in muscle tone and the affected limbs feel stiff and rigid.
7. Paralysis due to nerve damage: This can be caused by injuries, diseases such as multiple sclerosis, or birth defects such as spina bifida.
8. Paralysis due to muscle damage: This can be caused by injuries, such as muscular dystrophy, or diseases such as muscular sarcopenia.
9. Paralysis due to brain damage: This can be caused by head injuries, stroke, or other conditions that affect the brain such as cerebral palsy.
10. Paralysis due to spinal cord injury: This can be caused by trauma, such as a car accident, or diseases such as polio.

Paralysis can have a significant impact on an individual's quality of life, affecting their ability to perform daily activities, work, and participate in social and recreational activities. Treatment options for paralysis depend on the underlying cause and may include physical therapy, medications, surgery, or assistive technologies such as wheelchairs or prosthetic devices.

Parkinson's disease is the second most common neurodegenerative disorder after Alzheimer's disease, affecting approximately 1% of the population over the age of 60. It is more common in men than women and has a higher incidence in Caucasians than in other ethnic groups.

The primary symptoms of Parkinson's disease are:

* Tremors or trembling, typically starting on one side of the body
* Rigidity or stiffness, causing difficulty with movement
* Bradykinesia or slowness of movement, including a decrease in spontaneous movements such as blinking or smiling
* Postural instability, leading to falls or difficulty with balance

As the disease progresses, symptoms can include:

* Difficulty with walking, gait changes, and freezing episodes
* Dry mouth, constipation, and other non-motor symptoms
* Cognitive changes, such as dementia, memory loss, and confusion
* Sleep disturbances, including REM sleep behavior disorder
* Depression, anxiety, and other psychiatric symptoms

The exact cause of Parkinson's disease is not known, but it is believed to involve a combination of genetic and environmental factors. The disease is associated with the degradation of dopamine-producing neurons in the substantia nigra, leading to a deficiency of dopamine in the brain. This deficiency disrupts the normal functioning of the basal ganglia, a group of structures involved in movement control, leading to the characteristic symptoms of the disease.

There is no cure for Parkinson's disease, but various treatments are available to manage its symptoms. These include:

* Medications such as dopaminergic agents (e.g., levodopa) and dopamine agonists to replace lost dopamine and improve motor function
* Deep brain stimulation, a surgical procedure that involves implanting an electrode in the brain to deliver electrical impulses to specific areas of the brain
* Physical therapy to improve mobility and balance
* Speech therapy to improve communication and swallowing difficulties
* Occupational therapy to improve daily functioning

It is important for individuals with Parkinson's disease to work closely with their healthcare team to develop a personalized treatment plan that addresses their specific needs and improves their quality of life. With appropriate treatment and support, many people with Parkinson's disease are able to manage their symptoms and maintain a good level of independence for several years after diagnosis.

1. Muscular dystrophy: A group of genetic disorders that cause progressive muscle weakness and degeneration.
2. Amyotrophic lateral sclerosis (ALS): A progressive neurological disease that affects nerve cells in the brain and spinal cord, leading to muscle weakness, paralysis, and eventually death.
3. Spinal muscular atrophy: A genetic disorder that affects the nerve cells responsible for controlling voluntary muscle movement.
4. Peripheral neuropathy: A condition that causes damage to the peripheral nerves, leading to weakness, numbness, and pain in the hands and feet.
5. Myasthenia gravis: An autoimmune disorder that affects the nerve-muscle connection, causing muscle weakness and fatigue.
6. Neuropathy: A term used to describe damage to the nerves, which can cause a range of symptoms including numbness, tingling, and pain in the hands and feet.
7. Charcot-Marie-Tooth disease: A group of inherited disorders that affect the peripheral nerves, leading to muscle weakness and wasting.
8. Guillain-Barré syndrome: An autoimmune disorder that causes inflammation and damage to the nerves, leading to muscle weakness and paralysis.
9. Botulism: A bacterial infection that can cause muscle weakness and paralysis by blocking the release of the neurotransmitter acetylcholine.
10. Myotonia congenita: A genetic disorder that affects the nerve-muscle connection, causing muscle stiffness and rigidity.

These are just a few examples of neuromuscular diseases, and there are many more conditions that can cause muscle weakness and fatigue. It's important to see a doctor if you experience persistent or severe symptoms to receive an accurate diagnosis and appropriate treatment.

1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.

2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.

3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.

4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.

5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.

6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.

7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.

8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.

9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.

10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.

There are several types of diabetic neuropathies, including:

1. Peripheral neuropathy: This is the most common type of diabetic neuropathy and affects the nerves in the hands and feet. It can cause numbness, tingling, and pain in these areas.
2. Autonomic neuropathy: This type of neuropathy affects the nerves that control involuntary functions, such as digestion, bladder function, and blood pressure. It can cause a range of symptoms, including constipation, diarrhea, urinary incontinence, and sexual dysfunction.
3. Proximal neuropathy: This type of neuropathy affects the nerves in the legs and hips. It can cause weakness, pain, and stiffness in these areas.
4. Focal neuropathy: This type of neuropathy affects a single nerve, often causing sudden and severe pain.

The exact cause of diabetic neuropathies is not fully understood, but it is thought to be related to high blood sugar levels over time. Other risk factors include poor blood sugar control, obesity, smoking, and alcohol consumption. There is no cure for diabetic neuropathy, but there are several treatments available to manage the symptoms and prevent further nerve damage. These treatments may include medications, physical therapy, and lifestyle changes such as regular exercise and a healthy diet.

Striatonigral degeneration can be caused by various factors such as genetics, exposure to toxins, or certain medical conditions. It is also associated with other neurodegenerative disorders such as Parkinson's disease, Huntington's disease, and multiple system atrophy.

The diagnosis of striatonigral degeneration typically involves a combination of clinical evaluation, imaging studies, and laboratory tests to rule out other conditions that may cause similar symptoms. There is currently no cure for the condition, but various treatments can help manage its symptoms, including medications such as dopaminergic agonists and deep brain stimulation.

Overall, striatonigral degeneration is a rare and complex disorder that affects the brain's ability to regulate movement and cognitive function, leading to significant impairment in quality of life. Further research is needed to understand its underlying causes and develop more effective treatments for this debilitating condition.

Types of Peripheral Nerve Injuries:

1. Traumatic Nerve Injury: This type of injury occurs due to direct trauma to the nerve, such as a blow or a crush injury.
2. Compression Neuropathy: This type of injury occurs when a nerve is compressed or pinched, leading to damage or disruption of the nerve signal.
3. Stretch Injury: This type of injury occurs when a nerve is stretched or overstretched, leading to damage or disruption of the nerve signal.
4. Entrapment Neuropathy: This type of injury occurs when a nerve is compressed or trapped between two structures, leading to damage or disruption of the nerve signal.

Symptoms of Peripheral Nerve Injuries:

1. Weakness or paralysis of specific muscle groups
2. Numbness or tingling in the affected area
3. Pain or burning sensation in the affected area
4. Difficulty with balance and coordination
5. Abnormal reflexes
6. Incontinence or other bladder or bowel problems

Causes of Peripheral Nerve Injuries:

1. Trauma, such as a car accident or fall
2. Sports injuries
3. Repetitive strain injuries, such as those caused by repetitive motions in the workplace or during sports activities
4. Compression or entrapment of nerves, such as carpal tunnel syndrome or tarsal tunnel syndrome
5. Infections, such as Lyme disease or diphtheria
6. Tumors or cysts that compress or damage nerves
7. Vitamin deficiencies, such as vitamin B12 deficiency
8. Autoimmune disorders, such as rheumatoid arthritis or lupus
9. Toxins, such as heavy metals or certain chemicals

Treatment of Peripheral Nerve Injuries:

1. Physical therapy to improve strength and range of motion
2. Medications to manage pain and inflammation
3. Surgery to release compressed nerves or repair damaged nerves
4. Electrical stimulation therapy to promote nerve regeneration
5. Platelet-rich plasma (PRP) therapy to stimulate healing
6. Stem cell therapy to promote nerve regeneration
7. Injection of botulinum toxin to relieve pain and reduce muscle spasticity
8. Orthotics or assistive devices to improve mobility and function

It is important to seek medical attention if you experience any symptoms of a peripheral nerve injury, as early diagnosis and treatment can help prevent long-term damage and improve outcomes.

... is any loss of nerve supply regardless of the cause. If the nerves lost to denervation are part of the neuronal ... Denervation can be caused by injury or be a symptom of a disorder like ALS, post-polio syndrome, or POTS. Additionally, it can ... This process of denervation is however different from post-polio syndrome in that it only involves upper and lower motor neuron ... Denervation can have many harmful side effects such as increased risk of infection and tissue dysfunction. The loss of nerve ...
... /Denervation hypersensitivity is the sharp increase of sensitivity of postsynaptic membranes to a ... S. Thesleff, L.C. Sellin, "Denervation supersensitivity", Trends in Neurosciences, Volume 3, Issue 5, May 1980, Pages 122-126 ... doi:10.1016/0166-2236(80)90046-6 S. Z. Langer, "Denervation Supersensitivity", in: Principles of Receptor Research Volume 2 of ... chemical transmitter after denervation. It is a compensatory change. ...
... (TLD) is a procedure, that is currently being studied, to try to improve chronic obstructive ...
Terumo's Iberis System and Cordis Corporation's RENLANE Renal Denervation System. Currently[when?], no renal denervation device ... A 2014 consensus statement from The Joint UK Societies did not recommend the use of renal denervation for treatment of ... 9 April 2022). "Long-term efficacy and safety of renal denervation in the presence of antihypertensive drugs (SPYRAL HTN-ON MED ... Renal sympathetic denervation (RSDN) is a minimally invasive, endovascular catheter based procedure using radiofrequency ...
4) Denervation supersensitivity. Like any denervated muscle, the iris becomes supersensitive to its normal neurotransmitter (in ...
Ross AT (November 1958). "Progressive selective sudomotor denervation; a case with coexisting Adie's syndrome". Neurology. 8 ( ...
Ramirez C, Donnellan N (August 2017). "Pelvic denervation procedures for dysmenorrhea". Current Opinion in Obstetrics & ...
The onset of denervation supersensitivity. Langer SZ, Trendelenburg U. J Pharmacol Exp Ther. 1966 Jan;151(1):73-86 ... His research was on the mechanisms involving denervation supersensitivity. with Ullrich Trendelenburg with whom he became ... course of the development of supersensitivity to various amines in the nictitating membrane of the pithed cat after denervation ...
Ramirez C, Donnellan N. (2017). "Pelvic denervation procedures for dysmenorrhea". Curr Opin Obstet Gynecol. 29 (4): 225-230. ...
"Autonomic Renal Denervation Ameliorates Experimental Glomerulonephritis". Journal of the American Society of Nephrology. 19 (7 ...
There is a lack of good quality evidence to support the use of radiofrequency denervation for pain relief. KT Tape has been ... Maas ET, Ostelo RW, Niemisto L, Jousimaa J, Hurri H, Malmivaara A, van Tulder MW (October 2015). "Radiofrequency denervation ...
Radiofrequency denervation may provide temporary relief for specific affected areas in the neck. Transcutaneous electrical ... Niemisto L, Kalso E, Malmivaara A, Seitsalo S, Hurri H (2003-01-20). "Radiofrequency denervation for neck and back pain. A ...
Bunch, W H; Deck, J D; Romer, J (1977-01-01). "The effect of denervation on bony overgrowth after below knee amputation in rats ... Klein, L.; Dawson, M. H.; Heiple, K. G. (1977). "Turnover of collagen in the adult rat after denervation". The Journal of Bone ... Obtunded or absent RAP often accompanies sensory denervation. In neuropathic soft tissue lesions, such as those in diabetics ...
Donald DE; Shepherd JT (1963). "Response to Exercise in Dogs with Cardiac Denervation". The American Journal of Physiology. 205 ...
Denervation Neuroregeneration Targeted reinnervation The Williams Dictionary of Biomaterials. Liverpool University Press. 1999 ...
Needle electromyography studies generally reveal no signs of denervation. Megavitamin-B6 syndrome is characterized mainly by ...
Occasionally, biopsy of skin, nerve, or muscle may be performed, which can show signs of denervation and amyloid deposition ... may show evidence of chronic denervation and reinnervation. Autonomic testing, including quantitative sweat testing, can reveal ...
The affected pupil is thus miotic and the pupillary dilator responds to denervation by increasing α1 receptors. Apraclonidine ... Koc F, Kansu T, Kavuncu S, Firat E (2006). "Topical apraclonidine testing discloses pupillary sympathetic denervation in ...
... and multiple denervations. Muscle biopsies performed in the brother detected chronic partial denervation. Through the siblings ...
Chao CC, Sun HY, Chang YC, Hsieh ST (January 2008). "Painful neuropathy with skin denervation after prolonged use of linezolid ...
Thorne Publishing (C) Zealear, David L.; Hamdan, Abdul-Latif; Ratney, Cheryl L. (1994-10-01). "Effects of Denervation on ... Denervation leads to a slow fibrosis that worsens over many months. The cartilages of the larynx. Posterior view. Muscles of ...
Singh, Kaustabh; Hood, David A. (2011). "Effect of denervation-induced muscle disuse on mitochondrial protein import". American ...
Goebel, F.-D.; Füessl, H.S. (1983). "Mönckeberg's sclerosis after sympathetic denervation in diabetic and non-diabetic subjects ... He has documented loss of thermoregulatory function, cardiac denervation, and loss of vasoconstriction. Recurrence of the ... Because of these difficulties, and because of disabling sequelae associated with sympathetic denervation, conventional or "open ... "Partial cardiac sympathetic denervation after bilateral thoracic sympathectomy in humans". Heart Rhythm. 2 (6): 602-9. doi: ...
Other treatments may include denervation, autotransplantation, renal neurectomy, or nephrectomy. Unfortunately symptoms often ... Pruritus management Maintenance therapy between pain exacerbations Implantable drug delivery system Surgical renal denervation ...
It is true that all inflammatory and non-inflammatory heart disease may display forms of parasympathetic denervation; this ... denervation presents in a descriptive fashion in Chagas' disease. It has also been indicated that the loss of parasympathetic ...
Additional electromyography is helpful to reveal any decelerated nerve conduction velocity, and thus denervation of the ... September 2006). ". Ultrasound findings of teres minor denervation in suspected quadrilateral space syndrome". J Clin ...
Therefore, the diabetic heart shows clear denervation as the pathology progresses. This denervation correlates with ... Other causes of denervation are ischemia from microvascular disease and thus appear following the development of ...
... a novel neurite-outgrowth factor secreted by muscle after denervation". NeuroReport. 8 (16): 3649-3654. doi:10.1097/00001756- ...
... is a rotator cuff denervation syndrome in which the axillary nerve is compressed at the ... Differential considerations include similar rotator cuff denervation syndromes such as Parsonage-Turner syndrome, and ... "Ultrasound findings of teres minor denervation in suspected quadrilateral space syndrome". Journal of Clinical Ultrasound. 34 ( ...
Schwartz PJ, De Ferrari GM, Pugliese L (June 2017). "Cardiac sympathetic denervation 100years later: Jonnesco would have never ... or with surgical procedures including sympathetic denervation and implantation of a defibrillator. It is thought to affect as ... region of the sympathetic nervous system can be intentionally damaged in an operation known as cardiac sympathetic denervation ...
... may help identify patients with treatment-resistant hypertension who are most likely to respond to renal denervation, according ...
This Renal Denervation Market Report : forecasts revenue growth at global, regional, and country levels and analysis on the ... Table 58 ASEAN: Renal Denervation Market Size, By End use, 2020-2030 (USD Mn, CAGR%). Table 59 Rest of APAC: Renal Denervation ... Table 78 MEA: Renal Denervation Market Size, By End use, 2020-2030 (USD Mn, CAGR%). Table 79 UAE: Renal Denervation Market Size ... Figure 11 U.S. Renal Denervation Market, 2020-2030 (USD Mn). Figure 12 Canada Renal Denervation Market, 2020-2030 (USD Mn). ...
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Centers RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.. ...
Kidney denervation is the process of transferring energy to overactive nerves to reduce energy A sympathy signal sent between ... The latest research shows that renal denervation may be an effective treatment for resistant hypertension. USA News by Justice ... Since the 1990s, renal denervation has been considered a possible treatment for resistant hypertension, but it is still in the ... But new research There is some hope that renal denervation, which has long been considered an experimental treatment, may ...
Renal artery stenosis after renal sympathetic denervation. / Kaltenbach, Benjamin; Id, Dani; Franke, Jennifer C. et al. In: ... Renal artery stenosis after renal sympathetic denervation. Journal of the American College of Cardiology. 2012 Dec 25;60(25): ... Renal artery stenosis after renal sympathetic denervation. In: Journal of the American College of Cardiology. 2012 ; Vol. 60, ... Renal artery stenosis after renal sympathetic denervation. Benjamin Kaltenbach, Dani Id, Jennifer C. Franke, Horst Sievert, ...
Denervation and immobilization. Denervation and immobilization were performed as previously described24,51. Eight-week-old male ... b, c GC and TA muscles weight in WT and LONP1 mKO mice in basal conditions (Basal) and after 15 days of denervation (Den). n = ... For denervation, in brief, a 5 mm segment of the sciatic nerve was surgically removed from the right hindlimb, and the non- ... 2h), they showed more pronounced myofiber atrophy and muscle loss in GC and TA muscles in response to denervation (Fig. 2b-e). ...
Denervation. The etiology of the denervation dictates the timing of surgical treatment, if any is to be done. In a patient with ... Facial nerve denervation and paralysis imposes significant psychological and functional impairment. [6, 7] Facial paralysis can ... The subjective nature of the measurements and lack of recorded data limit both methods, and they do not reflect denervation at ... A longer period of denervation translates into a lesser degree of recovery after reinnervation. There is a decrease in ...
Histologic samples can be assessed for patterns of innervation or denervation by the intrinsic nervous system of the gut. ... Assessments of autonomic innervation/denervation. Together with Mayos Autonomic Function Laboratory, tests of cardiac and ...
Cordis has announced receiving the CE mark for its Renlane renal denervation system for the treatment of patients with ...
Catheter-based renal artery denervation: facts and expectations. Catheter-based renal artery denervation: facts and ... Catheter-based renal artery denervation (RAD) is entering a new era. After the disappointing results of SYMPLICITY-HTN 3 trial ... Atrial fibrillation; Blood pressure; Heart failure; Hypertension; Renal artery denervation; SHAM procedure ...
Catheter-based renal denervation: recent developments and new frontiers. Speakers: Professor K. Kario, Doctor P. Qian, Doctor P ... Changes in nocturnal blood pressure post-renal denervation: comparison of treatment versus control groups in SYMPLICITY HTN-3. ... Reduction in blood pressure following renal denervation for patients with differing baseline cardiovascular risk ... Women and non-diabetic patients react more strongly to radiofrequency renal sympathetic denervation ...
... and the results of therapeutic renal sympathetic denervation.. ... Renal denervation for hypertension.. Categories: Posted on July ...
Analysis of data of six randomized sham-controlled trials of renal sympathetic denervation, shows that RSD gave greater ... Renal denervation associated with SBP reduction in meta-analysis of sham-controlled trials Sham-Controlled Randomized Trials of ... Renal denervation in treatment-resistant essential hypertension. A randomized, SHAM-controlled, double-blinded 24-h blood ... 2. Fadl Elmula FEM, Feng YM, Jacobs L, et al., for the European Network COordinating research on Renal Denervation (ENCOReD). ...
Terminal Schwann cells overlying the neuromuscular junction sprout elaborate processes upon muscle denervation. We show here ... Terminal Schwann cells overlying the neuromuscular junction sprout elaborate processes upon muscle denervation. We show here ...
Sympathetic Renal Denervation for the Treatment of Hypertension: A Review of Current Progress, Limitations, Techniques, and the ... Sympathetic Renal Denervation is a novel and potentially powerful method of treatment for hypertension for that selected group ... Catheter-based renal denervation for resistant hypertension rationale and design of the SYMPLICITY HTN-3 Trial. Clin Cardiol ... Initially, renal denervation was contraindicated in patients with 2 hypertension, such as primary aldosteronism and eGFR,45/ml/ ...
ReCor Medical receives the CE mark for its second generation ultrasound-based Paradise Renal Denervation System. 25th January ... It is the only CE-marked system for renal denervation that is based on ultrasound, not radiofrequency (RF), energy. ...
The effect of denervation on the heterogeneous material properties of the tibialis anterior tendon. In Proceedings of the 2005 ... The effect of denervation on the heterogeneous material properties of the tibialis anterior tendon. / Calve, Sarah; Baar, Keith ... The effect of denervation on the heterogeneous material properties of the tibialis anterior tendon. Proceedings of the 2005 ... Calve, S., Baar, K., Mundy, K., & Arruda, E. M. (2005). The effect of denervation on the heterogeneous material properties of ...
Renal denervation - Cardiovasc. Revasc. Med.. - Single versus dual antiplatelets in TAVI - Cardiovasc. Revasc. Med. & Open ... Influence of bias in renal denervation trial, a meta-regression - Heart & Circ. Cardiovasc. Qual. Outcomes - Atrial ... Patient-Level Pooled Analysis of Ultrasound Renal Denervation in the Sham-Controlled RADIANCE II, RADIANCE-HTN SOLO, and ...
Renal denervation alters ambulatory blood pressure-derived salt sensitivity index in patients with uncontrolled hypertension. ...
Renal denervation (RDN) can reduce renal and whole-body sympathetic activity. Aim of this study was to determine the effect of ... Renal denervation (RDN) can reduce renal and whole-body sympathetic activity. Aim of this study was to determine the effect of ... Catheter-based renal denervation reduces atrial nerve sprouting and complexity of atrial fibrillation in goats. ... Catheter-based renal denervation reduces atrial nerve sprouting and complexity of atrial fibrillation in goats. ...
The first record of blepharospasm and lower facial spasm was found in the 16th century in a painting titled De Gaper. At that time, and for several ensuing centuries, patients with such spasms were regarded as being mentally unstable and often were institutionalized in insane asylums.
Effect of liver denervation on compensatory changes in food intake - Texas A&M University (TAMU) Scholar profile, educations, ... Hepatic denervation had no effect on basal enzyme levels in ad libitum-fed animals or on elevated enzyme activity induced by ... Effect of liver denervation on compensatory changes in food intake, body composition and hepatic enzyme induction after food ... Body fat content and body fat recovery rate from below "set point" were not altered by hepatic denervation. These observations ...
Renal Denervation Attenuates Adverse Remodeling and Intramyocardial Inflammation in Acute Myocardial Infarction With Ischemia- ... Dive into the research topics of Renal Denervation Attenuates Adverse Remodeling and Intramyocardial Inflammation in Acute ...
Renal denervation and the effect of peptide yy on renal blood flow in rats. / Blaze, C. A.; Vigna, S. R.; Mannon, P. J. et al. ... Renal denervation and the effect of peptide yy on renal blood flow in rats. In: FASEB Journal. 1996 ; Vol. 10, No. 3. pp. A547. ... Renal denervation and the effect of peptide yy on renal blood flow in rats. FASEB Journal. 1996 Dec 1;10(3):A547. ... Blaze, C. A., Vigna, S. R., Mannon, P. J., & Benjamin, B. A. (1996). Renal denervation and the effect of peptide yy on renal ...
Início Relevance of Targeting the Distal Renal Artery and Branches with Radiofrequency Renal Denervation Approaches-A Secondary ... Acute effect of renal sympathetic denervation on blood pressure in refractory hypertensive patients with chronic kidney disease ... Relevance of Targeting the Distal Renal Artery and Branches with Radiofrequency Renal Denervation Approaches-A Secondary ... Relevance of Targeting the Distal Renal Artery and Branches with Radiofrequency Renal Denervation Approaches-A Secondary ...
Is the failure of the SYMPLICITY HTN-3 trial to meet its efficacy endpoint the "end of the road" for renal denervation? Will ... Francis told Angioplasty.Org that it would be a "grave error" if the FDA withheld renal denervation from the American people, ... Another Viewpoint on Renal Denervation and SYMPLICITY HTN-3 from Dr. Darrel Francis. ... renal denervation now land on the heap of failed technologies? I dont think so, and Dr. Darrel Francis, the cardiologist who ...
Although muscle denervation and reduced CMAP amplitudes do not distinguish loss of anterior horn cells from loss of motor axons ... Electrodiagnostic studies showed denervation in thoracic and lumbosacral myotomes, with no muscle activation in the right leg ... Scattered denervation was also seen in the other three limbs. SNAPs had borderline amplitudes and conduction velocities ... Electrodiagnostic studies showed absent CMAPs and profound denervation with no voluntary activation in muscles of the right arm ...
  • Background: Although cardiac sympathetic denervation is associated with ventricular arrhythmias, limited data are available on the predictive value of sympathetic nerve imaging with 123-I MIBG on the occurrence of arrhythmias. (
  • Conclusions: Cardiac sympathetic denervation predicts ventricular arrhythmias causing appropriate ICD therapy as well as the composite of appropriate ICD therapy or cardiac death. (
  • The present experiments were undertaken to investigate the electrophysiological responses of the canine saphenous vein evoked by perivascular nerve stimulation, norepinephrine or selective alpha adrenergic agonists before and after chronic sympathetic denervation. (
  • Cardiac sympathetic denervation (CSD) is a surgical antiadrenergic procedure that can reduce sustained ventricular tachyarrhythmia (VT) and implanted cardioverter defibrillation (ICD) shocks. (
  • In SIMPLICITY HTN-3, patients had resistant hypertension (office SBP 180 mm Hg, with no diastolic cutoff), self-reported drug adherence to 5.1 medications prescribed at randomization, and received denervation of the main renal artery only performed by mostly inexperienced operators using a monoelectrode, sequential ablation system, Böhm said. (
  • Catheter-based renal artery denervation: facts and expectations. (
  • Catheter -based renal artery denervation (RAD) is entering a new era. (
  • A total of thirty-two patients underwent RATS cardiac denervation and thirty-three underwent VATS cardiac denervation. (
  • The RATS approach to cardiac denervation has similar one year follow-up outcomes in reducing recurrent VT as the VATS approach, however, patients undergoing RATS denervation experienced better peri-operative outcomes. (
  • Table 1: Pre-, peri-, and post-operative variables of patients undergoing RATS or VATS cardiac denervation. (
  • To determine the clinical factors associated with the success and failure of radiofrequency denervation of the lumbar facet joints. (
  • Clinical data were garnered from 3 academic medical centers on 192 patients with low back pain who underwent radiofrequency denervation after a positive response to diagnostic blocks. (
  • some studies Recommendations can significantly reduce blood pressure.Others, such as a controlled trial in 2014 , Found that there was no significant difference in blood pressure reduction between people who underwent renal denervation and people who underwent mimic surgery. (
  • Patients were stratified into two groups: those who underwent RATS denervation and those who underwent VATS denervation. (
  • Medtronic has obtained approval in the Europe and Australia to market its next-generation components of Symplicity renal denervation system, designed to reduce ablation time and provide ease of deliverability during renal denervation procedures for patients with uncontrolled hypertension. (
  • After chronic denervation the maximum response of the tissue is increased by 30 to 50% to norepinephrine, acetylcimoline and histamine but not to potassium. (
  • Does anterior plus posterior interosseus neurectomy lead to better outcomes than isolated posterior interosseus denervation in the treatment of chronic wrist pain? (
  • Partial denervation for chronic wrist pain is a salvage procedure that leads to an overall success of 78.4% for pain relief, with no substantial complications. (
  • Some of the AChR loss that follows denervation is correlated with failure of portions of the old synaptic site that lack SC coverage to be reinnervated. (
  • In the adult animal, the terminal SCs (tSCs) extend processes away from the old synaptic site upon denervation ( Reynolds and Woolf, 1992 ), and these processes provide a substrate that leads regenerating axons to vacant synaptic sites and leads them to sprout beyond these sites ( Son and Thompson, 1995 ). (
  • Long-term follow up from the SYMPLICITY HTN-3 trial showed that renal denervation is safe, and no late-emerging complications were found," said Deepak L. Bhatt, MD, MPH, Executive Director of Interventional Cardiovascular Programs at Brigham and Women's Hospital Heart & Vascular Center and Professor of Medicine at Harvard Medical School. (
  • However, several devices are in trial, including Medtronic's Symplicity renal denervation system. (
  • According to the company, the multi-electrode system is built upon the clinical success and strong safety profile of single-electrode Symplicity renal denervation system. (
  • The Symplicity renal denervation system is available for investigational use only in the US. (
  • Image: Symplicity Renal Denervation System. (
  • The Spyral HTN Off-Med trial was started to try to eliminate some of the factors that researchers believe confounded the data in the original pivotal trial, Symplicity HTN-3 ( Decision time for renal denervation firms as Symplicity trial yields little comfort , March 31, 2014 ). (
  • Fatty replacement was observed acutely in hypoglossal denervation but did not manifest until the subacute stage in V3 denervation. (
  • Reinnervation compared with denervation. (
  • In contrast, SPYRAL HTN-OFF MED enrolled patients with an office SBP of 150 to less than 180 mm Hg, an office DBP of at least 90 mm Hg, and a mean 24-hour ambulatory SBP of 140 to less than 170 mm Hg and excluded those with isolated systolic hypertension because they've been shown to be hyporesponsive to renal denervation. (
  • Invited discussant Prof Bryan William (University College London, UK) agreed that the data provide proof of concept that renal denervation lowered blood pressure in "about 75% of patients studied" but said by excluding those with isolated systolic hypertension it missed "the most common and most difficult-to-treat hypertension phenotype. (
  • BOSTON - September 18, 2022 - Long-term results from the first and largest randomized, sham-controlled clinical trial of renal denervation (RDN) for uncontrolled hypertension (HTN) show that the procedure could lower blood pressure (BP) in patients with resistant hypertension over three years. (
  • But new research There is some hope that renal denervation, which has long been considered an experimental treatment, may indeed be an effective solution for drug-resistant hypertension. (
  • Since the 1990s, renal denervation has been considered a possible treatment for resistant hypertension, but it is still in the experimental stage due to the mixed results of clinical trials. (
  • Cordis has announced receiving the CE mark for its Renlane renal denervation system for the treatment of patients with resistant hypertension and has completed the first successful cases in Europe. (
  • While denervation lowered blood pressure significantly further than a sham procedure, the effect was not huge, at just 5mmHg - too small to be able to say that these patients had their blood pressure controlled. (
  • Medtronic might have another crack at persuading European cardiologists - Spyral and many other denervation systems are long since CE marked - to pick their catheters back up. (
  • Kidney denervation is the process of transferring energy to overactive nerves to reduce energy A sympathy signal sent between the kidney and the brain. (
  • The research was funded by Recor Medical Inc., a manufacturer of the heavenly kidney denervation system. (
  • Using HPLC measurement of the glutathione redox potential, we quantified oxidative stress in peripheral nerve and muscle at the onset of denervation. (
  • Finally, drug testing of serum and urine confirmed that 94.3% of patients in the renal-denervation group and 92.7% in the sham control group were not on antihypertensive medications. (
  • Indeed, in 10 patients, blood pressure actually increased after denervation. (
  • Based on the reduction in ambulatory SBP from an average of 154 to 148 mm Hg and in office-based SBP from 162 to 152 mm Hg, patients treated with denervation would still need to take medications to achieve currently recommended BP treatment targets, which are only likely to go lower with revision of guidelines around the world, he said. (
  • Medtronic Renal Denervation vice-president and general manager Nina Goodheart said: "We have significantly enhanced our technology with sophisticated features designed to meet specific unmet needs and we believe these improvements, coupled with our strong safety and efficacy profile, will provide unprecedented benefit to both patients and physicians. (
  • The initial promise of denervation was that it could cut blood pressure in drug-resistant patients by something like 30mmHg - this was the kind of figure seen in some early trials with no sham control group. (
  • Discussing the results, Professor Bryan Williams of University College London, put it bluntly: "Renal denervation did not appear to control blood pressure in the patients treated to currently recommended targets. (
  • METHODS: Findings from 11 patients with V3 denervation and from seven patients with hypoglossal denervation resulting from a variety of abnormalities were reviewed retrospectively. (
  • The study was not powered for statistical significance but "provides biologic proof of principle for the efficacy of renal denervation" and will inform the design of a larger pivotal trial, co-primary investigator Dr Michael Böhm (University Hospital of Saarland, Homburg/Saar, Germany) reported here at the European Society of Cardiology (ESC) Congress 2017 . (
  • One week after preganglionie denervation (decentralization), there is a moderate increase in sensitivity to norepinephrine (2.5-fold) as well as supersensitivity to histamine (2-fold). (
  • So we can't become too excited about these data referable to clinical application, but what we can do is accept the fact that these data initiate the conversations again about renal denervation. (
  • Partial wrist denervation can be performed by isolated posterior interosseous nerve (PIN) or combined PIN plus (+) anterior interosseous nerve (AIN) neurectomy procedures. (
  • New AChR clustering is also induced by axon terminals that follow SC processes extended during denervation. (
  • Histologic samples can be assessed for patterns of innervation or denervation by the intrinsic nervous system of the gut. (
  • Recognition of MR imaging patterns of denervation may allow earlier diagnosis of a denervating lesion and may help to distinguish denervation from similar- appearing processes, such as infection or neoplasia. (
  • No conduction changes occurred as PR and QT intervals were not significantly different between pre- and post-op for both VATS and RATS denervation. (
  • These findings indicate that durable blood pressure reductions with radio-frequency renal denervation in combination with maximal medical therapy can be safely achieved. (
  • Facial nerve denervation and paralysis imposes significant psychological and functional impairment. (
  • The motor denervation appearance and functional compromise of the affected musculature are described in terms of the chronicity of the denervation process. (
  • During the period of denervation, SCs at the NMJ extend elaborate processes from the junction, as shown previously, but they also retract some processes from territory they previously occupied within the endplate. (
  • One week after postganglionic denervation of the vas deferens there are marked changes in the response of the smooth muscle to stimulant drugs. (
  • There is also an increase in the duration of the response to all four stimulants after denervation. (
  • Denervation augments selectively the electrical response to alpha-2 adrenergic stimulation. (
  • RESULTS: The appearance of V3 and hypoglossal motor denervation varies with the chronicity of the process. (
  • Long-standing denervation results in extensive fatty replacement and a decrease in the size of the affected musculature. (
  • The isolated PIN neurectomy technique showed a 15.1% pooled failure rate at a median follow-up of 22 months, while the combined AIN+PIN denervation had a pooled failure rate of 23.6% at a follow-up with a median of 29 months. (
  • Renal denervation, presumed dead in 2014, is starting to show signs of life. (
  • The report also includes profiles and for some of the leading companies in the Renal Denervation Market, with a focus on this segment of these companies' operations. (
  • We report preferential denervation of fast-twitch muscles beginning between 1 and 4 months of age, with relative sparing of slow-twitch muscle. (
  • CONCLUSION: V3 and hypoglossal denervation have a variable appearance depending on the chronicity of the process. (
  • Much opportunity remains in this growing Renal Denervation market. (
  • Along with revenue prediction for the overall world market, there are 3 segmentations of the Renal Denervation market, with forecasts for 4 Technologies, 3 Products, 3 End uses, each forecasted at a global and regional level. (
  • Revenue forecasts to 2030 for 5 regional and 18 key national markets - See forecasts for the Renal Denervation market in North America, Latin America, Europe, Asia-Pacific and MEA. (
  • Visiongain study is for everybody needing commercial analyses for the Renal Denervation market and leading companies. (
  • Branched chain aminoacid aminotransferase activity in the denervation atrophy of amphibian skeletal muscle. (