Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review deals with the common E.E.G. characteristics of dysmetabolic encephalopathies and described the particular features of hepatic, respiratory and renal encephalopathies, as well as those resulting from a disturbance in carbohydrate, water and electrolyte metabolism. These now classical data are compared with the principal electroclinical appearances seen during parenteral alimentation : slow, ample wases, non-reactive, associated with a calm coma; overall depression of basal rhythm, with excessive myogram activity and corresponding to paroxysms of muscular hypertonia seen during the coma.
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PMID:[Electroencephalographic study of functional metabolic encephalopathies and comas during parenteral alimentation]. 2 98

Dantrolen sodium is a muscle relaxant, which is used in the treatment of spasticity. Although it is given chronically, little is known about its pharmacokinetic behaviour. The relationship between the effect of a single oral dose of dantrolene sodium and its plasma concentration in healthy volunteers was studied by measuring the effect on the twitch tension, and in spastic patients on the decrease in muscle hypertonia. On the twitch tension dantrolene gave a depression of 49.1 +/- 9.4% (+/- DS) within 1.15 and 3.45 h after ingestion of 100 mg. The mean maximal plasma concentration was 1.24 +/- 0.32 microgram/ml (+/- SD). The effect and the plasma concentration were correlated. No relationship between the plasma concentration of dantrolene sodium and its effect could be established in patients, although definite activity in 6 out of 7 patients was observed after a single oral dose of 100 mg, and plasma concentration of dantrolene sodium greater than 0.3 microgram/ml were consistenly associated with better results than placebo treatment in 6 out of 7 patients.
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PMID:Relationship between plasma concentration and effect of dantrolene sodium in man. 49 21

Congestive heart failure is a complex clinical syndrome that has its basis in an abnormality of myocardial cell function resulting in impaired ventricular performance, exercise intolerance, and ventricular arrhythmias. The functional defect in myocardial performance may be related to alterations in receptor function, in regulatory proteins, or in biochemical mechanisms. Remodeling of the left ventricle has been observed to play an important role in the natural course of heart failure. The complex interplay between cellular elongation, reactive hypertrophy, and the influence of the change from ellipsoid to spheroidal shape of the left ventricle after acute myocardial infarction are just beginning to be understood. Prevention of this remodeling effect by pharmacologic intervention is being widely explored, although the mechanisms are poorly defined. Impedance to left ventricular ejection is also an important determinant of cardiac performance in heart failure. Constriction of arteriolar resistance vessels and reduction in compliance of arterial conductance vessels is a common manifestation of heart failure and may be under the influence of neural, hormonal, endothelial, and local regulatory factors. Increased tone of venous capacitance vessels contributes to a shift of blood centrally and to an increase in ventricular preload. Vasodilator drugs by relaxing the arterial, arteriolar, and venous vasculature result in a reduction in impedance and left ventricular afterload and a decrease in cardiac filling pressure and preload. Structural changes of hypertrophy and remodeling apparently contribute to the changes in resistance, compliance, and capacitance in the vasculature. Treatment of heart failure is aimed at relieving symptoms and prolonging life. Interventions to improve left ventricular function are critical to symptom relief. Vasodilators have been most effective for this purpose, and new positive inotropic drugs are being tested for efficacy. Long-term benefit may require interference with the myocardial and peripheral vascular remodeling processes that lead to progressive depression of ventricular performance. New insights into the cellular and subcellular mechanisms of this progression are critical to the development of innovative therapeutic strategies.
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PMID:Heart failure: mechanisms of cardiac and vascular dysfunction and the rationale for pharmacologic intervention. 221 Jan 53

Baclofen, the most effective drug for treating spasticity, is a specific agonist of gamma-aminobutyric acid-B receptors, and is very abundant in the superficial layers of the spinal cord. Given orally, baclofen does not easily penetrate the blood-brain barrier, and is distributed equally to the brain and spinal cord. Direct intrathecal administration was given in order to change the distribution of the drug by preferentially perfusing the spinal cord. Eighteen patients presenting a severe spastic syndrome were treated with chronic intrathecal infusion of baclofen in the lumbar cerebrospinal fluid. After clinical preselection, 38 patients were implanted with a lumbar access port allowing long-term trials in order to determine the efficacy of baclofen therapy and the effective 12-hour dose. The 18 patients selected for chronic administration were implanted with a programmable pump. The pathology in these cases was: multiple sclerosis (6 cases), posttrauma spastic syndrome (eight cases), and (one case each) cerebral palsy, ischemic cerebral lesion, spinal ischemia, and transverse myelitis. The mean follow-up period was 18 months (range 4 to 43 months). The clinical results were evaluated according to muscular hypertony on Ashworth's scale (changed for occurrence of painful spasms) and functional improvement. Results were better for spastic syndrome secondary to traumatic medullary lesion than for demyelinating disease. Hypertonia was improved in all cases as confirmed by the registration of the Hoffman (H) reflex. Painful muscular spasms disappeared in 14 of the 16 affected patients. Significant functional improvement was noted in nine patients and was considerable in three. The risk of side effects secondary to overdose (such as excessive hypotonia or central depression) and the absence of a specific baclofen antagonist stresses the necessity for accurate determination of the efficient dose. After an initial titration period and adjustment of the therapeutic dose, the individual doses were from 21 to 500 micrograms/24 hrs (mean 160 micrograms/24 hrs). This new conservative method is very effective, perfectly reversible, and safe when administered in conditions favorable to its use.
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PMID:Chronic intrathecal baclofen administration for control of severe spasticity. 230 74

The effects of conditioning stimulation of a mixed nerve in the leg, the common peroneal nerve (CPN), on the ipsilateral soleus H-reflex were compared with the effects of stimulating its cutaneous branch, the superficial peroneal nerve (SPN), in two groups of subjects--normals and patients with spinal spasticity subsequent to a clinically complete transection of the spinal cord. Condition-test delays of 20 msec to 2 sec, measured from the end of the 20 msec train (3 pulses at 100 Hz), were investigated. In normal subjects, CPN stimulation at 1.4 X MT profoundly depressed the soleus H-reflex. There was an initial depression (peak 40-90 msec) followed by a slow recovery which was incomplete at condition-test delays of 2 sec. One-half of the subjects showed a late facilitation, or disinhibition, peaking at 170-190 msec. The inhibitory effects were attributed to activation of low threshold, groups I and II, muscle afferents because stimulation of the SPN, at 1.5 X threshold for a compound action potential recorded from the CPN, had only facilitatory effects on the soleus H-reflex. Facilitation occurred at condition-test delays of 30-190 msec. The cutaneous stimulation was presumed to activate the largest, A beta, cutaneous afferents as it elicited a weak paraesthesia on the dorsum of the foot. The results suggested that cutaneous afferents may have contributed to the late facilitation seen with CPN conditioning stimulation. In spinal cord-lesioned subjects, CPN stimulation depressed the soleus H-reflex but the decrease was less and the recovery was faster and more complete than in normals. The magnitude of the initial depression at 20-100 msec varied with the severity of the spasticity, subjects with mild spasticity showing less of a depression. Weak cutaneous conditioning stimulation either had no effect or produced a slight depression of the soleus H-reflex, providing clear evidence that transmission in the pathways mediating the facilitatory effects of cutaneous afferents onto extensor motoneuronal pools is depressed in spinal spasticity. This may shift the balance of activity toward the flexor motoneurones, thus favouring the development of, for example, flexor spasms and flexor hypertonia. Since inhibitory effects from cutaneous stimulation are associated with activation of higher threshold afferents in normal man, the present results may reflect a decrease in the threshold for flexor withdrawal reflexes commonly associated with spasticity of spinal origin.
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PMID:Inhibitory and facilitatory effects from the peroneal nerve onto the soleus H-reflex in normal and spinal man. 244 16

Extensive investigation of the role of the fusimotor system in the production of hypotonic and hypertonic disorders of posture and tone has been undertaken in humans and experimental animals. The data from human studies have usually been from indirect assessment of the fusimotor system, and results are often contradictory. Results are now available from animal studies utilizing direct recording of muscle spindle afferent discharge in a number of models of human disorder. Conditions resulting in hypotonia, e.g. cerebellar ablations, medullary pyramidotomy, VL nucleus, thalamotomy, acute spinal cord transection, and acute motor cortex ablation uniformly result in a depression of muscle spindle primary afferent discharge. Conditions resulting in hypertonia, e.g. chronic spinal cord transection and chronic motor cortex ablation, fail to show heightened muscle spindle afferent discharge, however. Rather the spindle afferent discharge returns to control levels in the models. Recovery from the hypotonic to the hypertonic state is, however, associated with significant recovery of spindle afferent function.
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PMID:Rehabilitation following brain damage: some neurophysiological mechanisms. Physiological correlates of clinically observed changes in posture and tone following lesions of the central nervous system. 622 98

A pronounced age predisposition was noticed in a study of 30 goats with the neurologic form of caprine arthritis-encephalitis. Most affected animals were between 2 and 4 months of age, but ages ranged from 1 month to 20 years. Clinically, mild to moderate fever was recorded for approximately half of the patients. Brain involvement (in 16 of 30 goats) was most commonly identified by depression, head tilt, torticollis, and circling. Signs of spinal cord involvement were most frequently those of white matter damage: hypertonia, hyperreflexia, and para- or tetraparesis. In approximately 90% of patients, there were increases in protein content and WBC numbers in the cerebrospinal fluid. Microscopic lesions were most frequent in the brain and cervical portion of the spinal cord and consisted of a nonsuppurative inflammatory response and demyelination with preservation of axons.
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PMID:Caprine arthritis-encephalitis: review of the neurologic form in 30 cases. 630 53

An account of the microcirculatory unit according to Zweifach is followed by an explanation of the marked differences in capillary and tissue perfusion in children and aged. Prolonged hypertonia of the metarteriolar smooth muscle cells of the precapillary sphincters depresses capillary perfusion, even though the preferential circulation remains, resulting in marked changes in cellular metabolism in the tissues. If the capillary circulation is excluded for a sufficiently long period, less oxygen and substrates will be transported to the tissues concerned, intravasal red cell clumping will exacerbate hypoxia, and drainage of metabolic residues will be reduced. Microcirculatory vasoconstriction may be the result of heat, touch, noise, hormonal factors, medicaments, toxic, nervous, psychic factors, etc. Whit time, continuous damage to the microcirculation leads to involution of the microcirculation in favour of the preferential circulation, creation of an increasingly large number of arteriovenous short-circuits, and hyperstomia of arteriovenous anastomoses. Depressed capillary circulation leads to a reduced flow of liquids through the vessel walls owing to a diminished diffusion surface with consequent progressive lessening of tissue metabolic activity. Involution of the microcirculation is thus one of the main steps in the ageing process. A cell's metabolic pattern is dependent on the environment in which it lives, as well as its stock of enzymes and differentiation stage. This environment is greatly changed by alterations of the microcirculation. The gradual depression of the microcirculation during ageing, coupled with the consequent diminution of perfusion of tissues and interstitial liquids are thus of significance in ageing itself, in the slowing down of tissue change, and increased entropy to the energy levelling coincident with death.
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PMID:[Microcirculatory changes in infancy and old age]. 673 11

In the last decade focal vulvitis has been identified as a distinct syndrome, characterized by unexplained burning vulvar pain and superficial dyspareunia. A 'Woodruff perineoplasty' has been recommended as a treatment method. A research project was conducted, investigating the long-term results of surgical treatment and the etiology of focal vulvitis. Results showed that the great majority of women continued to suffer from focal vulvitis after the operation, which leads to the conclusion that the procedure should be abandoned. Retrospective data revealed several immediate causes of mechanical and chemical irritation of the vulva. All women exhibited 'inadequate sexual behavior': having intercourse without a sufficient amount of lubrication and/or in the presence of hypertonia of the pelvic floor. Psychosexual processes were further characterized by deterioration of sexual and general well-being, resulting in lack of libido and depression, which contributed considerably to the problem. An integrated approach to treatment is recommended, which incorporates protection of the vulvar skin, relaxation of pelvic muscles and sexological treatment of the psychosexual and relational aspects.
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PMID:Focal vulvitis: a psychosexual problem for which surgery is not the answer. 764 Jul 27

Treatments that postpone hypoxic spreading depression (SD)-like depolarization (also called anoxic depolarization) facilitate recovery of function after transient cerebral hypoxia. Hypertonia reduces cerebral excitability, and we tested whether it also offers protection against SD-like depolarization and hypoxia. Oxygen was withdrawn from hippocampal slices bathed in normal artificial cerebrospinal fluid (ACSF) and, simultaneously, from slices cut from the same hippocampus but bathed in strongly hypertonic ACSF. Extracellular osmolarity (pi(o)) was increased by adding 100 mM mannitol or fructose to ACSF. Slices in normal pi(o) underwent SD-like negative extracellular voltage shift (delta Vo). The hypertonic slices usually showed no SD-like delta Vo but only a small, gradual negative voltage shift. Hypertonia also prevented the precipitate drop of interstitial calcium level ([Ca2+]o). When oxygenation and normal osmolarity were restored, synaptic transmission in the previously hypertonic slices recovered completely, but 3 h after reoxygenation orthodromically transmitted population spikes of the control slices recovered only 25.1% of the initial control amplitude. We conclude that hypertonic treatment during hypoxia improves subsequent recovery of synaptic function. The protection is probably due to the prevention of calcium uptake by blocking the SD-like depolarization, with the prevention of hypoxic cell swelling playing a lesser role.
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PMID:Hypertonic environment prevents depolarization and improves functional recovery from hypoxia in hippocampal slices. 862 50


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