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)

The purpose of this study was to determine whether the PRBS-VEP-determined temporal frequency characteristics (TFCs) of the visual pathways are useful for evaluating the properties of the visual system of glaucomatous patients. The VEPs elicited by pseudorandom stimulation (PRBS) with red LEDs were recorded from 26 eyes with primary open angle glaucoma and 11 age-matched normal eyes. The glaucomatous patients were divided into 3 groups according to the size and shape of their visual field defect; early (9), moderate (9), and severe (8). The cross-spectrum between the PRBS and PRBS-VEPs was used as the TFCs. The TFC of each glaucomatous group were compared to those of the normal controls. A depression of the TFC was found for the middle and high frequencies (18-28 Hz) in the moderate group, and the depression spread to lower frequencies (4-16 Hz) in the severe groups. The TFC values at 14-20 Hz were depressed in the moderate group and most frequencies were depressed significantly with the progression of glaucoma (p < 0.05). The sensitivity of the TFC at 18-20 Hz was 56%, 89% and 100% in the early, moderate and severe glaucoma groups, respectively, and the specificity was 82%. We conclude that the PRBS-determined TFC is altered in glaucomatous eyes, and the frequencies depressed were related to the degree of glaucoma. These findings indicate that the PRBS-determined TFC can be useful for evaluating visual function of glaucomatous eyes.
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PMID:PRBS-determined temporal frequency characteristics of VEP in glaucoma. 1510 65

SSRIs are the most commonly prescribed antidepressant drugs, in part because of their favourable safety profile compared with older antidepressants. However, the widespread use of SSRIs leads to an increased occurrence of rare adverse effects. This review, based on data from published experimental research, clinical studies and case reports, describes the role of serotonin in the control of intraocular pressure (IOP) and the evidence for IOP modifications in patients receiving SSRIs. In a small percentage of patients with depression, the cause of SSRI withdrawal has been the occurrence of ill-defined visual disturbances. It can be speculated that in some of these patients, the iatrogenic ocular alterations could have been due to changes in IOP. There have also been a limited number of case reports of acute attacks of glaucoma occurring during treatment with SSRIs. Although causality is not exactly specified, the relationship between SSRIs and this ocular adverse event is strongly implied. Nevertheless, in a small clinical study assessing the effect of a single dose of fluoxetine on IOP, the drug was shown to increase this parameter, although the effect was asymptomatic. The clinical signs of unexpected adverse drug effects are often disregarded, with the exception of those characterised by serious symptoms (such as acute angle-closure glaucoma in the case of IOP modifications). Also, the distribution of iridocorneal angle configurations in the general population implies that an adverse effect on IOP will be pauci- or asymptomatic in most patients (intermittent, sub-acute or progressive angle-closure glaucoma). As a result, it is likely that the incidence of SSRI-related IOP modifications is underestimated. Until the involvement of SSRIs in IOP modifications is better understood, ophthalmological consultations should be considered before starting and during treatment with any SSRI in patients with glaucomatous risk factors, especially those who are elderly.
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PMID:SSRIs and intraocular pressure modifications: evidence, therapeutic implications and possible mechanisms. 1659 50

Alzheimer's disease (AD) is the most common form of dementia, as least in western countries. It has been estimated that the cost to society for caring for AD patients will consume the entire gross national product of the U.S.A. by the middle of this century if left unabated. Until recently, the only available drugs for this condition were cholinergic treatments, which symptomatically enhance cognitive state to some degree, but they were not neuroprotective. In fact, many potential neuroprotective drugs tested in clinical trials failed because they were poorly tolerated. However, after our discovery of its clinically-tolerated mechanism of action, one neuroprotective drug, memantine, was recently approved by the European Union and the U.S. Food and Drug Administration (FDA) for the treatment of Alzheimer's disease. Recent phase 3 clinical trials have shown that memantine is effective in the treatment of moderate-to-severe Alzheimer's disease and possibly vascular dementia (multi-infarct dementia). Here we review the molecular mechanism of memantine's action and also the basis for the drug's use in these neurological diseases, which are mediated at least in part by excitotoxicity. Excitotoxicity is defined as excessive exposure to the neurotransmitter glutamate or overstimulation of its membrane receptors, leading to neuronal injury or death. Excitotoxic neuronal cell death is mediated in part by overactivation of N-methyl-d-aspartate (NMDA)-type glutamate receptors, which results in excessive Ca(2+) influx through the receptor's associated ion channel. Physiological NMDA receptor activity, however, is also essential for normal neuronal function. This means that potential neuroprotective agents that block virtually all NMDA receptor activity will very likely have unacceptable clinical side effects. For this reason many previous NMDA receptor antagonists have disappointingly failed advanced clinical trials for a number of neurodegenerative disorders. In contrast, studies in our laboratory have shown that the adamantane derivative, memantine, preferentially blocks excessive NMDA receptor activity without disrupting normal activity. Memantine does this through its action as an uncompetitive, low-affinity, open-channel blocker; it enters the receptor-associated ion channel preferentially when it is excessively open, and, most importantly, its off-rate is relatively fast so that it does not substantially accumulate in the channel to interfere with normal synaptic transmission. Clinical use has corroborated the prediction that memantine is thus well tolerated. Besides Alzheimer's disease, memantine is currently in trials for additional neurological disorders, including other forms of dementia, depression, glaucoma, and severe neuropathic pain. A series of second-generation memantine derivatives are currently in development and may prove to have even greater neuroprotective properties than memantine. These second-generation drugs take advantage of the fact that the NMDA receptor has other modulatory sites in addition to its ion channel that potentially could also be used for safe but effective clinical intervention.
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PMID:Paradigm shift in NMDA receptor antagonist drug development: molecular mechanism of uncompetitive inhibition by memantine in the treatment of Alzheimer's disease and other neurologic disorders. 1566 16

The tragic life of Vincent van Gogh is summarized, emphasizing his early departure from formal education, failure as a successful salesman in the art world, attempt at religious studies, difficulty with female and family relationships, return to the art world, and tendencies toward extremes of poor nutrition or near self-starvation and excessive drinking and smoking. In Paris he joined the Impressionists, but drank very heavily both absinthe and cognac. Southward he went to Arles and was joined by Paul Gauguin, with whom he had major personality problems, causing van Gogh to cut off part of his left ear. He experienced paranoid ideation and confinement in mental institutions in Arles, and then returned to Paris and onto Auvers-sur-Oise, where he committed suicide at age 37. Possible physical diagnoses include glaucoma, Meniere's disease, acute intermittent porphyria, and chronic lead poisoning, but these diagnoses seem unlikely. Possible psychiatric diagnoses include borderline personality disorder, anxiety-depressive disorder with episodes of depression and hypomania, and also paranoid schizophrenia. Van Gogh did not have spontaneous seizures and, therefore, did not have epilepsy. Before he began to drink heavily, when he was near starvation, he had "fainting fits," and after drinking, especially absinthe, a convulsant drug, he continued to have similar attacks. His episodes of unconsciousness can be well explained by chronic malnutrition and alcohol abuse, only possibly exacerbated by drinking large quantities of absinthe. Although van Gogh is an excellent example of the Geschwind syndrome, at times associated with temporal lobe epilepsy, this fact does not establish such an epilepsy. Thus, the syndrome is an orphan without the parent condition.
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PMID:A reappraisal of the possible seizures of Vincent van Gogh. 1590 45

Normal intraocular pressure (IOP) glaucoma is a clinical condition characterized by pathologic optic nerve excavation and visual field impairment, defined as optic neuropathy with certain features of a disease known as glaucoma. Glaucomatous optic nerve lesion is characterized by optic disk excavation or depression, however, this feature may greatly vary. The level of IOP is considered only one of the multiple risk factors involved in the disease development. In normal IOP glaucoma, papillary lesions and visual field impairments may differ from those occurring in primary open-angle glaucoma. In modern ophthalmology, the terminology has been modified, so the term low IOP glaucoma has been replaced by the term normal IOP glaucoma. It is now believed that various factors play a role in the development of glaucomatous optic neuropathy in normal IOP glaucoma and show variable interference depending on IOP level. Additional studies are needed to define these interactions and their impact on the mechanism of glaucomatous excavation. This will hopefully pave the way to new therapeutic approaches and help in clinical decisions concerning the prognosis and treatment of individual patients.
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PMID:[Clinical approach to normal intraocular pressure glaucoma]. 1590 86

In western countries, Alzheimer's disease (AD) is the most common form of dementia. In fact, if left uncurbed, the economic cost of caring for AD patients could consume the entire gross national product of the USA by the middle of this century. Until recently, the only available drugs for this condition were cholinergic treatments, which symptomatically enhance cognitive state to some degree, but they were not neuroprotective. In fact, many potential neuroprotective drugs tested in clinical trials failed because they were poorly tolerated. However, after our discovery of its clinically-tolerated mechanism of action, one neuroprotective drug, memantine, was recently approved by the European Union and the U.S. Food and Drug Administration (FDA) for the treatment of Alzheimer's disease. Recent phase 3 clinical trials have shown that memantine is effective in the treatment of both mild and moderate-to-severe Alzheimer's disease and possibly vascular dementia (multi-infarct dementia). Here we review the molecular mechanism of memantine's action and also the basis for the drug's use in these neurological diseases, which are mediated at least in part by excitotoxicity. Excitotoxicity is defined as excessive exposure to the neurotransmitter glutamate or overstimulation of its membrane receptors, leading to neuronal injury or death. Excitotoxic neuronal cell death is mediated in part by overactivation of N-methyl-d-aspartate (NMDA)-type glutamate receptors, which results in excessive Ca2+ influx through the receptor's associated ion channel. Physiological NMDA receptor activity, however, is also essential for normal neuronal function. This means that potential neuroprotective agents that block virtually all NMDA receptor activity will very likely have unacceptable clinical side effects. For this reason many previous NMDA receptor antagonists have disappointingly failed advanced clinical trials for a number of neurodegenerative disorders. In contrast, studies in our laboratory have shown that the adamantane derivative, memantine, preferentially blocks excessive NMDA receptor activity without disrupting normal activity. Memantine does this through its action as an uncompetitive, low-affinity, open-channel blocker; it enters the receptor-associated ion channel preferentially when it is excessively open, and, most importantly, its off-rate is relatively fast so that it does not substantially accumulate in the channel to interfere with normal synaptic transmission. Clinical use has corroborated the prediction that memantine is thus well tolerated. Besides Alzheimer's disease, memantine is currently in trials for additional neurological disorders, including other forms of dementia, depression, glaucoma, and severe neuropathic pain. A series of second-generation memantine derivatives are currently in development and may prove to have even greater neuroprotective properties than memantine. These second-generation drugs take advantage of the fact that the NMDA receptor has other modulatory sites in addition to its ion channel that potentially could also be used for safe but effective clinical intervention.
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PMID:The molecular basis of memantine action in Alzheimer's disease and other neurologic disorders: low-affinity, uncompetitive antagonism. 1597 13

Bremazocine is a kappa-opioid receptor agonist with potent analgesic and diuretic activities. As an analgesic it is three- to four-times more potent than morphine, as determined in both hot plate and tail flick tests. Bremazocine and other benzomorphan analogs were synthesized in an effort to produce opiates with greater kappa-opioid receptor selectivity and with minimal morphine-like side effects. Unlike morphine bremazocine is devoid of physical and psychological dependence liability in animal models and produces little or no respiratory depression. While bremazocine does not produce the characteristic euphoria associated with morphine and its abuse, it has been shown to induce dysphoria, a property that limits its clinical usefulness. Similarly to morphine, repeated administration of bremazocine leads to tolerance to its analgesic effect. It has been demonstrated that the marked diuretic effect of bremazocine is mediated primarily by the central nervous system. Because of its psychotomimetic side effects (disturbance in the perception of space and time, abnormal visual experience, disturbance in body image perception, de-personalization, de-realization and loss of self control) bremazocine has limited potential as a clinical analgesic. However, its possible utility for the therapy of alcohol and drug addiction warrants further consideration because of its ability to decrease ethanol and cocaine self-administration in non-human primates. In addition, the ability of bremazocine-like drugs to lower intraocular pressure and to minimize ischemic damage in animal models suggests their possible use in the therapy of glaucoma and cardiovascular disease.
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PMID:Bremazocine: a kappa-opioid agonist with potent analgesic and other pharmacologic properties. 1600 40

Systemic arterial hypotension, hypertension and altered ocular blood flow are known risk factors in glaucoma. In this study, 24-h ambulatory blood pressure monitoring was performed in patients with normal tension glaucoma (NTG) and controls to evaluate blood pressure variability. In all, 51 patients with NTG and 28 age-matched controls were included in this prospective study. A 24-h ambulatory blood pressure monitoring (SpaceLabs Medical Inc., Redmond, USA) was performed and systolic, diastolic and mean arterial blood pressures were measured every 30 min during daytime (0800-2000) and night time (0000-0600). To evaluate blood pressure variability a variability index was defined as the s.d. of blood pressure measurements. Night-time blood pressure depression ('dip') was calculated (in percent of the daytime blood pressures). Patients with NTG exhibited higher night-time diastolic (P = 0.01) and mean arterial blood pressure values (P = 0.02) compared to controls, whereas systolic blood pressure data were not significantly different. The variability indices of night-time systolic, diastolic and mean arterial blood pressure measurements were significantly increased in patients with NTG compared to controls (P < 0.05). The night-time blood pressure depression of systolic (P = 0.47), diastolic (P = 0.11) and mean arterial blood pressures (P = 0.28) was not significantly different between patients with NTG and controls. In conclusion, patients with NTG showed increased variability of night-time blood pressure measurements compared to controls. Increased fluctuation of blood pressure may lead to ocular perfusion pressure fluctuation and may cause ischaemic episodes at the optic nerve head.
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PMID:24-h blood pressure monitoring in normal tension glaucoma: night-time blood pressure variability. 1623 98

Children and adolescents are particularly susceptible to injuries because of their fearless manner of play and their athletic immaturity due to which irreparable trauma to the eye is very commonly seen. Glaucoma is another common cause for eye loss in children. The loss of an eye causes disfigurement of the face due to which the children become emotionally weak and conscious and avoid taking part in social events, which in turn causes anxiety, stress and depression at an early age in life. Recovery after the loss of an eye requires an adjustment to monocular vision and improvement of the appearance with the use of artificial eyes carefully prepared to match the remaining natural eye. The custom made ocular prostheses are very comfortable and help children improve their appearances, which in turn, encourages them to build up their self-confidence to return back to their social life.
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PMID:Ocular prosthesis in children--clinical report. 1640 51

Optic disc pit (ODP) can be either congenital or acquired. Congenital ODP is typically unilateral, and the visual acuity and visual field are normal unless associated with macular serous detachment, which occurs in about 25-75% of cases. Acquired ODP is known as an important risk factor for progressive visual field loss in glaucoma. The fundus finding of congenital ODP includes oval depression involving the optic disc, with or without macular serous detachment. We used third-generation Stratus optical coherence tomography (Straus OCT) to investigate the possible pathogenesis of ODP associated with maculopathy and to monitor the anatomic changes before and after treatment.
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PMID:Stratus optical coherence tomography for evaluating optic disc pits associated with maculopathy before and after vitrectomy: two case reports. 1679 58


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