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)

Trimethyltin (TMT) is an alkyltin that targets neurons of the limbic system. A gene probe (i.e., mRNA) for myelin basic protein (MBP), a major component of central nervous system myelin, was used to monitor this toxic neuropathy in Sprague-Dawley rats. Animals were administered a single intraperitoneal injection of TMT-hydroxide at a neuropathic (8.0 mg/kg/body wt) or nonneuropathic (0.8 mg/kg/body wt) dose and sampled at 1, 3, or 7 days postexposure to correlate the progression of hippocampal neuropathology with probe (i.e., MBP-mRNA) levels. Microscopic examination of the brain showed only moderate but progressive damage over the 7-day postexposure period in animals treated with the neuropathic dose. Neuronal loss was first observed in the dendate gyrus and CA4 at 1 day postexposure, and progressed to the CA3c sector at 3 and 7 days postexposure. Elsewhere in the brain, minimal involvement of the entorhinal cortex neurons occurred 3 days postexposure and intensified by 7 days. No histological damage was seen at the nonneuropathic (0.8 mg/kg) dose. For gene probe analysis, the brain was divided into anterior and posterior halves. In rats treated with the neuropathic dose of TMT, the anterior brain showed progressive depressions of MBP-mRNA levels over the 1-, 3-, and 7-day postexposure period that correlated with increasing hippocampal neuropathology. The posterior brain showed no significant changes in MBP-mRNA levels with respect to that of controls over the same time period. At the nonneuropathic dose (0.8 mg/kg) a significant depression of MBP-mRNA levels occurred in the anterior brain at 7 days postexposure in the absence of overt histological damage.
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PMID:Myelin basic protein-mRNA used to monitor trimethyltin neurotoxicity in rats. 170 32

Neurologic manifestations of vitamin B12 deficiency are protean, including neuropathy, depression, and dementia. We present evidence to dispel confounding myths about vitamin B12 deficiency. Hematologic indices are normal in up to 30% of patients with vitamin B12 deficiency, and results of the Schilling test may be normal in patients with symptoms of deficiency. Isolated neuropathy or myelopathy may occur independently, but often appear concurrently. The neuropathy is primarily axonal and predominantly sensory. Myelopathy is caused by demyelinated areas in posterior and lateral columns. After therapy, recovery from neuropathy is incomplete or may extend for several years. Vitamin B12 replacement should not be withheld from patients with borderline vitamin B12 levels, since the consequences of allowing myelopathy, neuropathy, dementia, and mental disorders to worsen clearly outweigh any disadvantage of therapy.
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PMID:Myths about vitamin B12 deficiency. 174 82

Studies of sexual dysfunction in diabetic women have been less conclusive than those of sexual dysfunction in diabetic men. We examined the relationship between symptoms of sexual dysfunction, neuropathy, and depression in diabetic women. Diabetic women with neuropathy experienced significantly more symptoms of sexual dysfunction and depression than diabetic women without neuropathy. Furthermore, among women with neuropathy, there was a significant positive correlation between the degree of sexual dysfunction experienced and the degree of depression. These results indicate that depressive symptoms should be examined in studies of sexual dysfunction in diabetic women, and that a biopsychosocial approach is best for assessing sexual dysfunction in diabetic women.
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PMID:Symptoms of sexual dysfunction and depression in diabetic women. 183 Mar 17

Nineteen cases are described, including 12 cases from three different families and 7 nonfamilial cases, in which multisystem neurological disease was associated with acanthocytosis in peripheral blood and normal plasma lipoproteins. Mild acanthocytosis can easily be overlooked, and scanning electron microscopy may be helpful. Some neurologically asymptomatic relatives with significant acanthocytosis were identified during family screening, including some who were clinically affected. The mean age of onset was 32 (range 8-62) yrs and the clinical course was usually progressive but there was marked phenotypic variation. Cognitive impairment, psychiatric features and organic personality change occurred in over half the cases, and more than one-third had seizures. Orofaciolingual involuntary movements and pseudobulbar disturbance commonly caused dysphagia and dysarthria that was sometimes severe, but biting of the lips or tongue was rarely seen. Chorea was seen in almost all symptomatic cases but dystonia, tics, involuntary vocalizations and akinetic-rigid features also occurred. Two cases had no movement disorder at all. Computerized tomography often demonstrated cerebral atrophy. Caudate atrophy was seen less commonly, and nonspecific focal and symmetric signal abnormalities from the caudate or lentiform nuclei were seen by magnetic resonance imaging in 3 out of 4 cases. Depression or absence of tendon reflexes was noted in 13 cases and neurophysiological abnormalities often indicated an axonal neuropathy. Sural nerve biopsies from 3 cases showed evidence of a chronic axonal neuropathy with prominent regenerative activity, predominantly affecting the large diameter myelinated fibres. Serum creatine kinase activity was increased in 11 cases but without clinical evidence of a myopathy. Postmortem neuropathological examination in 1 case revealed extensive neuronal loss and gliosis affecting the corpus striatum, pallidum, and the substantia nigra, especially the pars reticulata. The cerebral cortex appeared spared and the spinal cord showed no evidence of anterior horn cell loss. Two examples of the McLeod phenotype, an X-linked abnormality of expression of Kell blood group antigens, were identified in a single family and included 1 female. The genetics of neuroacanthocytosis are unclear and probably heterogeneous, but the available pedigree data and the association with the McLeod phenotype suggest that there may be a locus for this disorder on the short arm of the X chromosome.
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PMID:Neuroacanthocytosis. A clinical, haematological and pathological study of 19 cases. 199 79

To elucidate the prevalence and features of painless myocardial ischemia among diabetic patients, 44 consecutive patients with angiographically-documented coronary artery disease and positive treadmill tests were examined. They were 26 with diabetes and 18 without it. Painless myocardial ischemia was defined as the absence of chest pain with 1 mm or more ST segment depression during the exercise stress tests. The severity of ischemia was determined by the magnitude of the ST segment depression. Painless myocardial ischemia was observed in 18 of the 26 (69%) diabetics, and in three of the 18 (17%) non-diabetics (p less than 0.005). The frequency of painless ischemia in the diabetics was relatively high regardless of the severity of ischemia, while painless ischemia was less frequent in the non-diabetics with severe ischemia. With a level of 2.5 mm ST depression, 11 of 12 (92%) diabetics were free of pain compared to four of 11 (36%) non-diabetics (p less than 0.01). Absence of chest pain during the exercise tests was not concordant with prior angina in diabetics, as opposed to non-diabetics in whom both clinical and exercise-induced angina developed concordantly. The diabetic patients without chest pain had a higher prevalence of three major diabetic complications such as neuropathy, nephropathy and retinopathy compared to those developing chest pain (p less than 0.025). It was concluded that in diabetics, painless myocardial ischemia is frequently observed during exercise stress tests and its prevalence is relatively high regardless of the severity of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Painless myocardial ischemia in diabetic patients with coronary artery disease: evaluations by treadmill exercise tests]. 210 4

The incidence and mechanism of painless myocardial ischaemia on exercise testing in diabetic patients is not clear. Therefore, two studies were performed. Retrospectively, all exercise tests carried out in our hospital during the past 5 years were reviewed for silent ischaemia. Prospectively, diabetic patients with known or suspected coronary artery disease underwent autonomic function testing and a second exercise test. Of 1653 exercise tests reviewed, 247 were positive (ST depression greater than 0.1 mV). Of the 29 diabetic patients with positive tests 20 (69%) had painless ST depression, compared with 77 (35%) of the 218 non-diabetic patients (p less than 0.001). The diabetic patients with painful and painless ST depression were comparable for age, sex, therapy, but the 20 with no pain on exercise testing had a longer duration of diabetes and a higher incidence of microvascular complications than the 9 with pain (70 vs 22%, p less than 0.05). In the prospective study, 12 of 30 diabetic patients with positive exercise tests had pain in association with ST depression and 18 had no pain. Six patients had mild and 12 severe autonomic neuropathy on formal testing. Twelve had no autonomic dysfunction. Eleven (92%) of 12 patients with severe neuropathy had painless ST depression, compared with 7 (39%) of 18 without severe neuropathy (p less than 0.01). Thus, silent myocardial ischaemia on exercise testing is common among patients with diabetes mellitus and is associated with severe autonomic dysfunction.
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PMID:Autonomic dysfunction and silent myocardial ischaemia on exercise testing in diabetes mellitus. 214 63

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

Computerized static perimetry must be regarded as the method of choice for monitoring the course of optic neuropathy in cases of pseudotumor cerebri. A discrete peripheral visual field depression is the first sign of optic nerve damage. If cranial hypertension persists the visual field depression gradually spreads toward the center. Ultimately central visual acuity deteriorates continuously. If the intracranial hypertension is reduced in good time the visual field defects are largely reversible and optic atrophy can be prevented.
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PMID:[Computed perimetry for the follow-up of optic neuropathy in pseudotumor cerebri]. 219 43

Clinical data from 37 adult males with diabetes mellitus (insulin dependent, n = 22; non-insulin dependent, n = 15) who had undergone psychiatric diagnosis and peripheral nerve conduction studies were reviewed to determine whether psychiatric illness was significantly related to complaints of sexual dysfunction. Main-effects testing revealed that impotence was associated with both neuropathy (P less than 0.01) and psychiatric illness (P less than 0.001). Logistic regression analysis was then used to determine the independent relationships of these two variables with impotence. After controlling for the effects of neuropathy, psychiatric illness (generalized anxiety disorder and depression) remained significantly associated with sexual dysfunction (P less than 0.01). These data allow for the hypothesis that psychiatric illness may be an important contributor to impotence in diabetic men, as it is in nondiabetic men, even when neuropathic complications of the disease are present.
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PMID:Relationship of psychiatric illness to impotence in men with diabetes. 220 27

In non-insulin-dependent diabetes mellitus, performance of complex cognitive tasks requiring the storage and retrieval of new information is poorer than in age-matched controls. By contrast, performance of less demanding tasks such as immediate memory and simple reaction time is essentially equivalent for NIDDM patients and controls. This pattern parallels the cognitive change observed with normal aging, in which age differences are minimal on less demanding immediate memory tasks but older adults perform more poorly than young adults on secondary or long-term memory tasks. Age-related changes in cognitive performance have been attributed to a reduction in processing resources or working memory capacity. Although the explanation for NIDDM-related deficits remains to be identified, reduced glucose control and elevated levels of triglycerides appear to play some role in cognitive impairment. Non-insulin-dependent diabetes is associated not only with elevated levels of depression, but with an increased frequency of self-reported memory problems. Moreover, elevated levels of depression are associated with various indicators of neuropathy and with significant reductions in self-regulated control of glucose at the time of medical office visits. Diabetic patients may perceive less control over their lives as a result of the many restrictions associated with the disease. When provided with the opportunity to exercise control, however, performance on many cognitive tasks can be improved in NIDDM as well as in age-matched controls. This suggests that by providing NIDDM patients with opportunities to exercise increased control over their lives it may be possible to enhance motivation and to increase the likelihood of the patient's adopting more effective self-regulatory behaviors.
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PMID:Cognitive and affective disorders in elderly diabetics. 222 44


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