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)

Cortical spreading depression (SD) was induced by applying 25% KCl to the frontal cerebral cortex in female rats under continuous ether anesthesia. Three weeks previously the animals had been subjected to sham operation, bilateral surgical "deefferentation" of the amygdala or transection of the dorsal columns of the fornix. During the week prior to experiment the rats were made "pseudopregnant" by treatment with PMS and hCG. Plasma prolactin was measured by radioimmunoassay in blood samples obtained from the peripheral circulation at 20 min intervals. After two control samples had been taken, KCl was applied to the cortex and sampling continued for another 100 min; In the sham-operated group prolactin levels increased with time following the application of KCl. Fornix-cut animals showed a similar, although briefer, increase with values significantly lower than those found in sham-operated animals at 80 min. The increase in plasma prolactin observed in sham-operated and fornix groups was completely abolished in amygdala-cut animals. These results indicate that limbic structures play a significant role in the mechanisms by which cortical SD elevates plasma prolactin levels under the present experimental conditions.
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PMID:Limbic system involvement in the increase in plasma prolactin following cortical spreading depression in gonadotropin-treated female rats. 109 5

Female rats rendered "pseudopregnant" by treatment with PMS and hCG and ovariectomized rats injected with estradiol and progesterone (OVX-E2-P) were subjected to cortical spreading depression (SD). Within 7-10 min under ether anesthesia in a stereotaxic instrument a frontal craniotomy was performed and a cotton ball saturated with physiological saline (control) or 25% KCl was applied to the exposed dura, covered with dental cement and skin sutured. The animals were then placed in separate containers in an isolated room and decapitated for collection of trunk blood at 0, 15, 30, or 60 min after surgery. In PMS-hCH saline-treated control animals, prolactin levels had dropped by 15 and 30 min when compared with the zero-time values but by 60 min had increased significantly above the 30-min level. At that time (60 min), prolactin values in the KCl group were significantly lower than in the controls. Corticosterone levels were high at both 15 and 60 min in control and KCl groups. In OVX-E2-P control animals, plasma prolactin levels also rose at 60 min compared with 15- and 30-min samples and at 60 min were significantly higher than in the KCl group. In control animals, LH levels were lower at 15 and 60 min than at zero time, but they remained unchanged in the KCl group. The dato are interpreted as indicating that cortical SD suppresses the stress responses observed in saline-treated control animals.
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PMID:Effects of spreading depression on stress-induced changes in plasma prolactin and LH. 118 96

The diagnosis of PMS depends on the identification of a core symptom complex, including behavioral symptoms of either irritability, accompanied by an internal state of anxiety or depression, and fatigue. (Fatigue is the most common symptom of PMS.) At least one core physical symptoms, bloating of the abdomen or extremities, breast tenderness, and headache also is required to establish the diagnosis. Although these core symptoms are required, none is pathognomonic for the disorder and the timing of the symptoms with respect to the menstrual cycle also must be established. This can only be done accurately using valid and reliable prospective recording instruments, such as COPE. Personality factors, the degree of psychosocial stress faced by the woman, and biochemical markers have little utility in establishing the diagnosis. The literature with respect to the prevalence of PMS in the population, effective treatments for the disorder, and the diagnosis of the disease must be interpreted by recognizing the inclusion in these studies of women with comorbid psychiatric disease, invalid and unreliable symptom inventories, and inadequate characterization of menstrual cycle phases. There are sociologic reasons why the true prevalence and treatment response to interventions may not be seen by the clinician. Nonetheless, the availability of effective treatment for the disorder necessitates accurate diagnosis of the syndrome based on the strict criteria presented. Additional research founded on the development of psychoneuroendocrine models is likely to provide insight into both the pathophysiology and treatment alternatives for PMS.
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PMID:Issues in the diagnosis and research of premenstrual syndrome. 152 87

Hormones are partial determinants of certain sexually dimorphic behaviors and interact with psychosocial, environmental, and other physiologic factors. The part played by sex hormones in the direct control of overt human behavior is, compared with that found in lower animals, slight and less readily definable. In humans, these hormones, although necessary for maintenance of libido and sexual behavior, seem to control the intensity of such behavior rather than its direction. In most women of reproductive age, the different phases of the menstrual cycle are not associated with major physical or psychologic discomfort. Some women actually report positive changes during the premenstrual period. Only 5-10% of women in this age group have changes in mood, sleep, eating habits, level of energy, and physical symptoms that appear to be linked temporally to the late-luteal phase of the cycle. It is plausible to assume that women with LLPDD are vulnerable to the menstrual cycle as a Zeitgeber. In these women, a cascade of events triggered originally along the HPG axis brings about the shift from an existing vulnerability to the actual manifestations of LLPDD and other forms of female-specific mood disorders. The degree of vulnerability becomes apparent at puberty when girls are exposed to increasing estrogenic influences. Particularly vulnerable times are the periods that mark shifts in the reproductive stages (menarche, the premenstruum, puerperium, and menopause), periods associated with major hormonal turmoil and psychosocial stresses. A conditioning-sensitization model has been described to explain the longitudinal course of affective disorders, and it also has been proposed for PMS. According to this model, even low levels of psychosocial stress are capable of triggering episodes of dysphoria in vulnerable previously sensitized subjects. LLPDD is associated strongly with a lifetime diagnosis of major depression, and the concurrent comorbidity in these women is also high. Future epidemiologic studies on depression should consider the effects of female-specific Zeitgeber on mood disorders in the populations studied.
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PMID:Female-specific mood disorders. 152 88

In a study of 144 women, mainly self-designated PMS sufferers, the premenstrual depression experienced was, apart from its shorter duration, quantitatively and qualitatively similar to major depressive disorder for a substantial proportion of subjects. The associations with previous history of depression were complex: the severity of premenstrual depression was related to previous history of postnatal depression, whereas its duration (i.e., whether it persisted through longer) was related to a history of treatment with antidepressants. Two independent dimensions are proposed. (i) A menstrual cycle-related factor which in vulnerable women can results in severe and disabling premenstrual dysphoria, and which may be aetiologically related to a subgroup of postnatal depression. (ii) In a minority of women a more general propensity for depressive illness evidence as a tendency for any premenstrual depression to be prolonged.
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PMID:The relationship between perimenstrual depressive mood and depressive illness. 177 24

The NIMH Diagnostic Interview Schedule (n = 43), and the Hopkins Symptom Checklist and Weissman Social Adjustment Scale (n = 35) was administered to assess the prevalence of psychiatric disorders and psychosocial maladjustment present in women seeking treatment in a multidisciplinary Premenstrual Syndrome Clinic. We found a 67 percent lifetime prevalence of DIS/DSM-III psychiatric disorders: 50 percent Major Affective Disorder (primarily Depression), 53 percent Anxiety Disorder (primarily Phobias or Generalized Anxiety Disorder), and 40 percent Psychosexual Dysfunction (notably Inhibited Sexual Desire or Excitement). Our group had significantly greater Major Depression, Dysthymia, and any one psychiatric disorder compared with female general population samples. Two-thirds of women with premenstrual symptoms had true Premenstrual Syndrome. In our sample, social maladjustment as well as psychiatric symptomatology was significantly greater than in normals and closer to that in psychiatric out-patient norms, and was independent of cycle phase. Presence or absence of PMS, social maladjustment and sexual dysfunction was each not significantly different in women with or without psychiatric disorder.
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PMID:Sexual dysfunction, social maladjustment, and psychiatric disorders in women seeking treatment in a premenstrual syndrome clinic. 189 58

Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most likely to respond. Treating seizures is a major part of a neurologic practice. Our current therapeutic agents are only partially successful and limited by multiple side effects. One problem is that patients often have to take these agents for an entire lifetime, further raising the risk of toxicity. If pyridoxine supplementation can improve the efficacy of currently used medications, it will be gladly accepted into our therapeutic arsenal. Headache, chronic pain, and depression all appear to run together in many of our patients. The observations that serotonin deficiency is a common thread between them and that pyridoxine can raise serotonin levels open a wide range of therapeutic options. Small studies have been carried out with mixed success. Comparison with amitriptyline in the treatment of headache appears to show about equal efficacy, although side effects would be expected to be more of a problem with the amitriptyline. Behavioral disorders are relatively common and continue to be a major problem, disrupting the lives of the patients and their families. Current treatments are not acceptable to most people because of the risk of side effects with long-term usage. If, as Dr. Feingold suggests, many of these problems are caused by "toxic" exposures to chemicals that are pyridoxine antagonists, supplementation at early ages may reduce the incidence of hyperactivity and aggressive behavior. This raises the question of safety. Is pyridoxine safe for long-term use in large segments of the population, including children? The studies on children with Down's syndrome and autism, utilizing much higher doses than are used for other therapeutic purposes, seem to indicate relative safety if carefully monitored. Studies involving large population groups with carpal tunnel syndrome, all adults, using 100-150 mg/day have shown minimal or no toxicity in five- to 10-year studies. Women self-medicating for PMS taking 500 to 5000 mg/day have shown peripheral neuropathy within one to three years. It would appear from this retrospective analysis that pyridoxine is safe at doses of 100 mg/day or less in adults. In children there is not enough data to make any sort of suggestion. Because the major neurologic complication is a peripheral neuropathy and the causes of this condition are myriad, pyridoxine may cause neuropathy only in patients with a pre-existing susceptibility to this condition.
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PMID:Vitamin B6 in clinical neurology. 216 44

PMS is a constellation of symptoms, both somatic (breast tenderness, bloating, headache) and psychologic-behavioral (irritability, hostility, depression) that recur prior to the menses in about 5% to 20% of all menstruating women. Such women should be evaluated with a thorough history and physical examination, and if the diagnosis is firmly established by observing a temporal relationship of the symptoms with the premenstruum, therapy should be initiated. When treating PMS, reassurance should always be offered to the patient along with counseling regarding life-style and dietary changes. Symptomatic relief may be provided with any number of medications, including diuretics, NSAIDs, and possibly progesterone. Oral contraceptive therapy may also be helpful. Although patience is certainly required in order to deal with this often frustrating problem, it should be remembered that patient satisfaction is commonly within reach.
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PMID:Premenstrual syndrome. 404

Previous work has indicated a genetic contribution to premenstrual symptom reporting, regularity and menarche but no genetic contribution to cycle length, and no consistent genetic contribution to premenstrual symptom reporting. This paper reports the results (n = 634) of multivariate genetic analysis in which premenstrual symptom reporting is included in a general personality factor along with extroversion (E), neuroticism (N) and depression (D). The results showed that N, E, D and PMS all fitted on a common personality factor. There was no evidence for a specific genetic contribution of depression or premenstrual symptom reporting over and above those shown in the common personality factor. There were, however, unique/specific environmental contributions for PMS. For E and N, in contrast, both unique genetic and environmental contributions were apparent.
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PMID:Genetic and environmental factors in premenstrual symptom reporting and its relationship to depression and a general neuroticism trait. 756 77

Movements that are performed with maximal velocity and acceleration can be considered ballistic actions. Ballistic actions are characterized by high firing rates, brief contraction times, and high rates of force development. A characteristic triphasic agonist/antagonist/agonist electromyographic (EMG) burst pattern occurs during ballistic movement, wherein the amount and intensity of antagonist coactivation is variable. In conditions of low-grade tonic muscular activity, a premovement EMG depression (PMD; or silent period, PMS) can occur in agonist muscles prior to ballistic contraction. The agonist PMD period may serve to potentiate the force and velocity of the following contraction. A selective activation of fast twitch motor units may occur in ballistic contractions under certain movement conditions. Finally, high-velocity ballistic training induces specific neuromuscular adaptations that occur as a function of the underlying neurophysiological mechanisms that subserve ballistic movement.
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PMID:Ballistic movement: muscle activation and neuromuscular adaptation. 784 54


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