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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and preclinical studies provide convincing evidence for persistent neurological/psychiatric impairments and possible neuronal degeneration associated with chronic cocaine/stimulant abuse. These impairments include multifocal and global cerebral ischemia, cerebral hemorrhages, infarctions, optic neuropathy, cerebral atrophy, cognitive impairments, and mood and movement disorders. These findings may encourage the placement of stimulant addiction into the category of organic brain disorders. Functional and microanatomical anomalies in the frontal and temporal cortex as well as other brain regions may be responsible for certain aspects of phenomenology and neuropsychopathology that are characteristic of stimulant polydrug addictions. These may include broad spectrum of deficits in cognition, motivation, and insight; behavioral disinhibition; attention deficits; emotional instability; impulsiveness; aggressiveness; depression; anhedonia; and persistent movement disorders. Although it is still debated whether the hypofrontality and other brain anomalies observed in stimulant abusers are a consequence or an antecedent of drug abuse, this debate seems purely academic and irrelevant with respect to the importance of compensating for these deficits in the development of treatment strategies. The neuropsychiatric impairments accompanying stimulant abuse may contribute to the very high rate of relapse in addicts that can take place after long periods (years) of abstinence. It is possible that the neurological deficits present in stimulant addicts, whether they are primary or secondary to stimulant abuse, are responsible for perpetual drug abuse which may be a form of self-medication (Weiss et al. 1991, 1992). In this context, addiction to stimulants, once fully developed, may represent a true biological dependency on drugs that temporarily compensate for existing neurological deficits. The concept of self-medication by drug addicts is supported by major theories of biological psychiatry. While a majority of drug addicts are polydrug users, there seems to be a preference for a particular type of drug among different populations of addicts. Addicts who experience distress, anxious dysphoria, and turbulent anger prefer the calming actions of opiates, whereas addicts with preceding attention deficit disorder, depression, or bipolar disorder often prefer stimulants (Khantzian 1985). Figure 1 presents conceptual relationships between brain damage and cocaine/stimulant abuse. More clinical studies are needed to establish unequivocally the epidemiological relationships between preexisting neurological deficits-resulting either from genetic, developmental, traumatic, or neurotoxic factors- and vulnerability to drug addictions. Nonetheless, deducing from the results of preclinical studies, it is conceivable that individuals with neurological deficits associated with attention deficit disorder, developmental neuroanatomical abnormalities, lead poisoning, alcoholism, posttraumatic brain lesions, and PTSD may be more vulnerable to stimulant addiction. This notion has significant empirical support as preclinical studies have shown that animals with lesioned prefrontal cortex became supersensitive to cocaine (Schenk et al. 1991) and animals with lesions at the amygdala, VTA, or raphe nuclei manifest more rapid acquisition of amphetamine self-administration than control rats (Deminiere et al. 1989). The above arguments, postulating neuropathology as an intrinsic component of stimulant addiction, should be taken into consideration with the caveat that the clinical manifestations of the disease are heterogenous and addicts may express varying stages and degrees of the disease as determined by environmental and genetic factors. Therefore, it is likely that stimulant addicts who have less advanced neuropathology may recover spontaneously after detoxification with proper nutritional and psychotherapeutic support if they can sustain abstinence. (ABSTR
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PMID:Cocaine addiction as a neurological disorder: implications for treatment. 880 51

A large Swedish family with members affected by progressive external ophthalmoplegia with hypogonadism were followed-up and reviewed. Hypogonadism included delayed sexual maturation, primary amenorrhea, early menopause, and testicular atrophy. Cataracts, cerebellar ataxia, neuropathy, hypoacusia, pes cavus, tremor, parkinsonism, depression, and mental retardation were other features observed in this family. Muscle biopsy samples of advanced cases showed ragged-red fibers, focal cytochrome c oxidase deficiency, and multiple mtDNA deletions by Southern blot analysis. An autosomal dominant mode of inheritance was evident with anticipation in successive generations. Linkage analysis excluded the chromosome 10q23.3-q24.3 region reported as being linked to the disease in a Finnish family with autosomal dominant progressive external ophthalmoplegia. We report for the first time clinical evidence for anticipation in a family with autosomal dominant progressive external ophthalmoplegia. We hypothesize that the nuclear gene causing this enigmatic disorder may be directly influenced by an expansion of an unstable DNA sequence and that the resulting phenotype is caused by a concerted action with multiple deletions of mtDNA.
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PMID:Anticipation of autosomal dominant progressive external ophthalmoplegia with hypogonadism. 894 Dec 70

The course of depression in patients with comorbid medical illness is poorly understood. We report a 5-year follow-up study of 25 diabetic patients who had participated in an 8-week depression treatment trial. When a patient completed the trial, primary physicians were informed of patient outcomes and advised to monitor for relapse and treat those with ongoing depression. At the 5-year reevaluation depression was assessed using DSM-III-R criteria, and a depression severity scale was formed that reflected the presence, severity, frequency, and duration of depression episodes as well as a global assessment of functioning. Recurrence or persistence of depression occurred in 23 (92%) of the patients with an average of 4.8 depression episodes over the 5-year follow-up period. The duration of the longest episode averaged 16 +/- 4 months. Reversion to major depression occurred frequently and rapidly also in the subset that remitted during the treatment trial: 58.3% were depressed again within the first year. At the time of the follow-up interview, major depression was evident in 16 (64%) of the subjects, and glycemic control was significantly worse in this group compared with those without depression (gHb: 13.3% +/- 2.6% vs 11.1% +/- 1.9%, P = 0.03). Severity of depression over follow-up was related to the presence of neuropathy at entry and to incomplete remission during the initial treatment trial. Nineteen patients (82.6% of those who relapsed) received additional courses of antidepressant therapy, but none was treated continuously for depression prophylaxis. In this diabetic sample, depression was a recurrent condition in the vast majority of cases, and initial treatment response did not confer lasting euthymia. Whether maintenance antidepressant medication would be useful in preventing depression recurrence and promoting better glycemic control in diabetes remains to be studied.
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PMID:The course of major depression in diabetes. 909 68

Functional defects of glaucomatous optic neuropathy are reviewed and summarized. Glaucomatous visual field defects are basically comprised of four major patterns: an isolated scotoma, an arcuate scotoma, a nasal step, and generalized depression. The field loss progresses conforming to the optic nerve head and retinal nerve fiber changes. Interpretation of the visual field and some tips of the interpretation are outlined in addition to describing differential diagnosis. Lastly, blue-on-yellow perimetry and high-pass resolution perimetry, both of which are promising tools for early detection of glaucoma, are introduced.
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PMID:Glaucomatous visual field defects: their characteristics and how to detect them. 929 56

The authors assessed 72 human immunodeficiency virus (HIV)-infected patients with a self-rating slowness scale (SRSS) concerning mental and motor slowness in their activities of daily living. In order to understand the relationship between complaints of slowness and predictor variables, the investigators developed a preliminary model using multiple regression analysis. Reports of slowness on the SRSS were independently associated with self-reported cognitive and neurological symptoms and with peripheral neurological syndromes (e.g., neuropathy, myopathy). Lesser contributions to self-perceived mental and motor slowness were found for neuropsychological measures of information processing speed, severity of the infection, depression, HIV encephalopathy, and sociodemographic factors (e.g., age, education). The relationship among the predictor variables showed that complaints of slowness reflect neurological, psychiatric/psychological, and cognitive symptomatology of the HIV infection.
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PMID:Neurobehavioral correlates of perceived mental and motor slowness in HIV infection and AIDS. 970 43

Miller-Fisher syndrome, a variant of an acute inflammatory neuropathy is often associated with serum antibodies to the ganglioside GQ1b, but the pathogenic role of these antibodies and other serum factors is unclear. We here investigated the effect of highly purified immunoglobulin G (IgG) from patients with typical Miller-Fisher syndrome, recording quantal endplate currents by means of a perfused macro-patch-clamp electrode on hemidiaphragms of adult mice. The GQ1b-positive and the GQ1b-negative Miller-Fisher IgG as well as its monovalent Fab-fragments depressed evoked quantal release in a fast and fully reversible, concentration and voltage dependent manner. The time-course of quantal release was changed with the late releases becoming more frequent. The extent of depression of release followed a Michaelis-Menten kinetic and depended on the extracellular calcium concentration. In addition the amplitude of quanta was reduced postsynaptically. IgG and sera from healthy subjects had no effect. Our results indicate that in Miller-Fisher syndrome, IgG antibodies to an undetermined antigen depress the release process, most likely by interfering with the presynaptic Ca2+ inflow or by interacting with proteins of the exocytotic apparatus, and prevent the activation of postsynaptic channels. Antibodies thus seem to be one pathogenic factor for muscle weakness in Miller-Fisher syndrome and our findings may explain why muscle strength recovers rapidly after therapeutical plasmapheresis.
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PMID:Pre- and postsynaptic blockade of neuromuscular transmission by Miller-Fisher syndrome IgG at mouse motor nerve terminals. 975 37

Short and long-term health effects from exposure to organophosphorus (OP) military and insecticidal nerve agents are evaluated based on the abundant scientific literature published over five decades on health effects in humans (from human experimentation and occupational exposures) and in laboratory animals. Four distinct health effects are identified: acute cholinergic toxicity; organophosphate-induced delayed neuropathy (OPIDN); subtle long-term neuropsychological and neurophysiological effects; and a reversible muscular weakness called 'intermediate syndrome'. Some effects are subtle and difficult to differentiate from health effects caused by other diseases or occupational exposures. Each effect has data suggesting threshold exposure levels below which it is unlikely to be clinically detectable. Therefore, meaningful interpretation of human and animal studies requires rigid exposure characterization. Because precise exposure levels are often difficult to reconstruct, a system for characterizing exposure is proposed based upon observed initial acute signs and symptoms, as high-level (definitive cholinergic poisoning); intermediate-level (threshold cholinergic effects including miosis, rhinorrhea or clinically measurable depression of cholinesterase); and low-level (no immediate clinical signs or symptoms) exposure. Threshold exposure levels for known long-term effects from OP nerve agent are at or above intermediate-level exposure. Long-term health effects seen at intermediate-level exposures or in many survivors of high-level exposure are subtle, detectable in exposed populations but not individuals, and not reported in individuals experiencing low-level exposure alone. Co-exposure to other pharmaceutical agents may promote or protect against health effects from OP nerve agents, but qualitatively they are the same effects seen with OP nerve agents alone. Thus, the system for characterizing exposure based on initial acute effects is also useful for evaluating health outcomes from co-exposure to OP nerve and other agents.
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PMID:Review of health consequences from high-, intermediate- and low-level exposure to organophosphorus nerve agents. 984 Jul 47

The behaviour of rats with spinal nerve ligation-induced neuropathic pain was studied using tests developed to measure depression and anxiety. Adult male Sprague-Dawley rats were tested with the open field test, elevated plus maze, two compartment test and forced swimming test. Spontaneous motility was measured in a photocell observation box. Mechanical sensitivity was tested with von Frey hairs and cold sensitivity with the acetone drop test. The L5-6 spinal nerves were ligated or a sham operation was performed and the rats were followed for 2 weeks before the same set of tests were repeated. Most of the neuropathy operated rats had mechanical and cold allodynia. With post-injury there was a significant decrease in the activity in the open field test and motility box tests, when compared with the pre-injury results. In the elevated plus maze test there was a significant reduction in the motility, but there was no change in the time spent in the closed wings. In the two compartment test there were no significant differences between the pre- and post-injury results. There were no differences between the rats with spinal nerve ligation injury and the sham operated rats in any of the tests. The results were also comparable when rats that developed a high degree of neuropathy were compared with the rats with low degree of neuropathy and the sham operated group. In conclusion, spinal nerve ligation injury of the spinal nerves L5-6 induces mechanical and cold allodynia, but it does not seem to produce general suffering or measurable anxiety to the animals. Furthermore, tests for anxiety and depression were not able to predict which animals were vulnerable to express symptoms of neuropathic pain after nerve injury.
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PMID:Behavioural measures of depression and anxiety in rats with spinal nerve ligation-induced neuropathy. 1020 47

Diabetes mellitus is very common in older persons. Changes in exercise habits, body habitus, leptin, amylin, tumor necrosis factor alpha, and nitric oxide all play a role in the pathogenesis of age-related insulin resistance. In older persons elevated glucose levels not only produce retinopathy, neuropathy, and nephropathy but also decrease quality of life, pain tolerance, cognition, and functional status and increase injurious falls, nocturia, incontinence, pressure ulcers, and orthostatic hypotension. The availability of multiple new therapies has enhanced the ability of physicians to improve glycemic control in older persons without unacceptable levels of hypoglycemia. Caregivers play an important role in the management of older diabetics. Depression increases mortality rate and hospital admissions in older diabetics. In many nursing homes the quality of diabetic care is marginal. A new causative theory of the metabolic syndrome involving cytokines and nitric oxide-the NO cytokine theory-is proposed.
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PMID:An overview of diabetes mellitus in older persons. 1033 29

Lentinan is a beta 1-->3 glucan isolated from Lentinus edodes (Shiitake mushroom) which has immune modulating properties. We have conducted two phase I/II placebo-controlled trials on a total of 98 patients. In one study at the San Francisco General Hospital (SFGH), ten patients each were administered 2, 5, or 10 mg of lentinan or placebo i.v. once a week for eight weeks. In the second study at the Community Research Initiative in New York (CRI), two groups of 20 patients each were administered 1 or 5 mg of lentinan i.v. twice a week for 12 weeks, and ten patients were administered placebo (vehicle containing mannitol plus dextran 40) i.v. twice a week. Entry criteria were an HIV positive test, CD4 levels of 200-500 cells, age 18-60 years, and without current opportunistic infections. This study confirms, in Caucasian subjects also, the good tolerability of lentinan observed in Japanese cancer patients. Side effects were mainly mild, especially when infusion was carried out over a 30-minute period. In the SFGH study, where administration was over a ten minute period, there were nine side effects severe enough to be reported to the FDA (one case each of anaphylactoid reaction, back pain, leg pain, depression, rigor, fever, chills, granulocytopenia and elevated liver enzymes) and there were four patients who discontinued therapy because of side effects. In the CRI study, where infusion was over a 30-minute period, there were no side effects reportable to the FDA and there were four dropouts due to side effects or personal preference. Most side effects resolved promptly after the discontinuation of medication, and all of them were relieved within 24 hours. Patients in the study have shown a trend toward increases in CD4 cells and in some patients neutrophil activity. Because of the small numbers, these values do not have statistical significance. Inasmuch as no side effects such as anemia, leukopenia, pancreatitis or neuropathy were seen, and in view of the positive effects of lentinan on certain surrogate markers (recognizing that these were small studies), we recommended a long-term clinical trial of lentinan in combination with didanosine (ddI) or zidovudine in HIV positive patients. Most patients in these trials did not have measurable p24 levels. In the CRI trials of ten patients with elevated p24 levels, eight on lentinan and two on placebo had decreased p24 levels. Of these decreases, those with lentinan and one with placebo were marked. These results were provocative and needed confirmation. Subsequent to this study, a trial of lentinan in combination with didanosine (ddI) showed a mean increase of 142 CD4 cells/mm3 over a twelve month period, in contrast to a decrease in CD4 cells in patients on ddI alone (Gordon et al. 1995).
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PMID:A placebo-controlled trial of the immune modulator, lentinan, in HIV-positive patients: a phase I/II trial. 1050 66


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