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

Due to the high incidence of lifelong infections in persons with spinal cord injury (SCI), the authors examined level of injury-related immune characteristics in a cohort of subjects with chronic SCI. Since the sympathetic nervous system and the endocrine system are known to be modulators of immune function, one possible explanation for heightened incidence of infections includes dysregulation of sympathetic outflow tracts in individuals with tetraplegia or high paraplegia. Natural killer cell cytotoxicity (NKCC) and bactericidal function of circulating neutrophils were assayed in a group of 10 individuals with chronic complete cervical SCI, a group of 8 individuals with paraplegia with injuries below the main sympathetic outflow (T-10 and below) and a group of 18 age- and sex-matched controls. In addition, a psychiatric assessment of depression was performed as well as assays of pituitary and adrenal functions. Analyses revealed no significant differences in immune function between all subjects with SCI combined and their matched controls. Further analyses stratifying based on presence or absence of sympathetic dysregulation revealed significantly impaired phagocytic ability and a trend toward reduced NKCC in the group with tetraplegia compared with their controls. Hormonal assays showed that dehydroepiandrosterone (DHEA), and dehydroepiandrosterone sulfate (DS) were higher in individuals with tetraplegia than controls, but no such differences were observed in individuals with paraplegia compared with their controls. The results of this study suggest that individuals sustaining complete cervical SCI experience alterations in immune function, while those with lesions at or below T-10 do not. These findings of level of injury related immune alteration could not be explained by mood differences. This paper is a review of previously published work and the authors' current thinking regarding increased acquisition of infections in this population.
J Spinal Cord Med 2000
PMID:Influence of neurological level on immune function following spinal cord injury: a review. 1091 53

A broad spectrum of neuropathologic changes are encountered in the brains of heroin abusers. The main findings are due to infections, either due to bacterial spread from bacterial endocarditis, mycoses, or from HIV-1 infection. Other complications include hypoxic-ischemic changes with cerebral edema, ischemic neuronal damage and neuronal loss, which are assumed to occur under conditions of prolonged heroin-induced respiratory depression, stroke due to, for example, thromboembolism, vasculitis, septic emboli, hypotension, and positional vascular compression. Myelopathy is believed to be the result of an isolated vascular accident within the spinal cord due to an as yet unknown mechanism. A distinct entity, spongiform leukoencephalopathy, has been described mainly after inhalation of pre-heated heroin. A lipophilic toxin-induced process was considered to be due to contaminants and to be induced or enhanced by cerebral hypoxia, but a definite toxin could not be identified. At the cellular level, abnormalities in signal transduction systems and changes of various receptor densities have been reported. The exact etiology of the different neuropathological alterations associated with heroin abuse is still unclear, but may also be related to additional substances used as adulterants.
 ...
PMID:The neuropathology of heroin abuse. 1097 59

Antiphospholipid antibodies (aPL) have been most strongly associated with a syndrome (APS) characterized by venous and/or arterial thrombosis, thrombocytopenia, recurrent fetal losses and a variety of non-thrombotic and thrombotic neurological disorders. Cerebral ischemia associated with aPL is the most common arterial thrombotic manifestation. Other neurological syndromes, such as cognitive dysfunction, dementia, psychosis, depression, seizures, chorea and transverse myelopathy, have all been associated with antiphospholipid antibodies.
 ...
PMID:Neurological involvement in antiphospholipid antibodies syndrome (APS). 1107 18

The treatment of patients with neuropsychiatric systemic lupus erythematosus (NPSLE) can be difficult and complex owing to the variety of nervous system manifestations that can occur, which include peripheral nerve disease, headaches, seizures, cerebrovascular disease, chorea, transverse myelitis, and psychiatric and cognitive disorders. Many of these manifestations can result from metabolic abnormalities or infection or as side effects of medications. Thus, in any patient with suspected NPSLE, it is crucial to exclude secondary causes of the presenting symptoms before assuming that they are due to NPSLE. It is especially important to exclude infection because this is a common cause of both morbidity and mortality in patients with systemic lupus erythematosus (SLE). Symptoms such as anxiety and depression may or may not be related to disease activity. Treatment decisions are based on accurate diagnosis of the specific NPSLE manifestation, which is usually made using tools such as brain imaging, electroencephalography, cerebrospinal fluid analysis, nerve conduction studies, or special serologic tests (eg, determination of antiphospholipid or antiribosomal P antibody levels). It is also important to assess the degree of other SLE- mediated systemic disease activity in a patient with neurologic manifestations to determine if activation of systemic disease activity is also occurring. This is done by measuring complement levels, anti-double-stranded DNA levels, complete blood count, and urinalysis. For some NPSLE manifestations (eg, infrequent seizures, headaches, depression, anxiety, or peripheral neuropathy) that appear without activation of systemic disease, symptomatic treatment is appropriate. For others (eg, psychosis, delirium, or transverse myelopathy without other obvious cause), treatment with high-dose glucocorticoids with or without cyclophosphamide is appropriate whether there is evidence of other systemic disease activity or not. In general, the activity and severity of the leading organ manifestations dictate pharmacologic treatment.
 ...
PMID:Neuropsychiatric Systemic Lupus Erythematosus. 1109 72

We report a 63-year-old man with acute disseminated encephalomyelitis (ADEM), initially showing depression for one and a half months but subsequently meningoencephalitis followed by acute-onset myelopathy. Neuroradiological examinations of the brain demonstrated no focal lesion causative for his depression, while cerebrospinal fluid revealed elevated levels of inflammatory cytokines in parallel with disease activity. Because depression is usually a rare initial symptom for patients with ADEM, an increased production of inflammatory cytokines in the central nervous system as well as age-related alterations of immune response might have played an important role in the development of depression in this elderly patient.
 ...
PMID:Severe depression as an initial symptom in an elderly patient with acute disseminated encephalomyelitis. 1175 74

S-Adenosyl-L-methionine (SAMe), a metabolite present in all living cells, plays a central role in cellular biochemistry as a precursor to methylation, aminopropylation, and transsulfuration pathways. As such, SAMe has been studied extensively since its chemical structure was first described in 1952. Decades of research on the biochemical and molecular roles of SAMe in cellular metabolism have provided an extensive foundation for its use in clinical studies, including those on depression, dementia, vacuolar myelopathy, liver disease, and osteoarthritis. This article provides an overview of the biochemical, molecular, and therapeutic effects of this pleiotrophic molecule.
 ...
PMID:S-Adenosyl-L-methionine (SAMe): from the bench to the bedside--molecular basis of a pleiotrophic molecule. 1241 93

Celiac disease (CD) long has been associated with neurologic and psychiatric disorders including cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology. These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and neuropathy with positive antiganglioside antibodies. The association between most neurologic syndromes described and gluten sensitivity remains to be confirmed by larger epidemiologic studies. It further has been suggested that gluten sensitivity (as evidenced by high antigliadin antibodies) is a common cause of neurologic syndromes (notably cerebellar ataxia) of otherwise unknown cause. Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington's disease. It remains unclear whether gluten sensitivity contributes to the pathogenesis of these disorders or whether it represents an epiphenomenon. Studies of gluten-free diet in patients with gluten sensitivity and neurologic syndromes have shown variable results. Diet trials also have been inconclusive in autism and schizophrenia, 2 diseases in which sensitivity to dietary gluten has been implicated. Further studies clearly are needed to assess the efficacy of gluten-free diet and to address the underlying mechanisms of nervous system pathology in gluten sensitivity.
 ...
PMID:Neurologic presentation of celiac disease. 1582 33

Some patients with fibromyalgia also exhibit the neurological signs of cervical myelopathy. We sought to determine if treatment of cervical myelopathy in patients with fibromyalgia improves the symptoms of fibromyalgia and the patients' quality of life. A non-randomized, prospective, case control study comparing the outcome of surgical (n = 40) versus non-surgical (n = 31) treatment of cervical myelopathy in patients with fibromyalgia was conducted. Outcomes were compared using SF-36, screening test for somatization, HADS, MMPI-2 scale 1 (Hypochondriasis), and self reported severity of symptoms 1 year after treatment. There was no significant difference in initial clinical presentation or demographic characteristics between the patients treated by surgical decompression and those treated by non-surgical means. There was a striking and statistically significant improvement in all symptoms attributed to the fibromyalgia syndrome in the surgical patients but not in the non-surgical patients at 1 year following the treatment of cervical myelopathy (P <or= 0.018-0.001, Chi-square or Fisher's exact test). At the 1 year follow-up, there was a statistically significant improvement in both physical and mental quality of life as measured by the SF-36 score for the surgical group as compared to the non-surgical group (Repeated Measures ANOVA P < 0.01). There was a statistically significant improvement in the scores from Scale 1 of the MMPI-2 and the screening test for somatization disorder, and the anxiety and depression scores exclusively in the surgical patients (Wilcoxon signed rank, P < 0.001). The surgical treatment of cervical myelopathy due to spinal cord or caudal brainstem compression in patients carrying the diagnosis of fibromyalgia can result in a significant improvement in a wide array of symptoms usually attributed to fibromyalgia with attendant measurable improvements in the quality of life. We recommend detailed neurological and neuroradiological evaluation of patients with fibromyalgia in order to exclude compressive cervical myelopathy, a potentially treatable condition.
 ...
PMID:Treatment of cervical myelopathy in patients with the fibromyalgia syndrome: outcomes and implications. 1742 87

Dexmedetomidine (DEX) is a selective alpha-2 adrenergic agonist that has been used clinically for its analgesic and sedative effects. We report a case of awake intubation with DEX. A 38-year-old male patient with 130 kg in weight, 170 cm in height and with a body mass index of 45 presented with thoracic myelopathy and progressive bladder and bowel control difficulties. Posterior decompression for thoracic myelopathy was planned. He was placed on the operating table with application of routine monitors. DEX infusion was commenced at 5 mcg x kg(-1) x hr(-1) over 10 minutes. Additional DEX at 0.1 mcg x kg(-1) was given 3 times because the patient still felt anxious. During DEX administration, topical anesthesia in the oropharynx, hypopharynx and glottis was achieved using lidocaine 8% spray. The patient was intubated without coughing, movement of limbs or respiratory depression. At the start of laryngoscopy, the patient had a Ramsay sedation score of 6. It was found by pharmacokinetic simulation analysis that the plasma concentration of DEX at intubation was 5.6 ng x ml(-1). We concluded that DEX is a reasonable medication during awake intubation, although further investigations with regard to its safety are required.
 ...
PMID:[Dexmedetomidine infusion for sedation during awake intubation]. 1854 3

To assess the efficacy of nonsurgical treatment of cervical radiculopathy, 50 patients with objective signs and symptoms of cervical discogenic radiculopathy (CDR) without myelopathy, treated conservatively on an outpatient basis with a mean follow-up of 9.4 months were retrospectively reviewed. Then an additional 33 patients were entered sequentially onto a prospective study to assess conservative treatment; they were followed for 100 days or longer with a mean follow-up of 24.7 months. All 83 patients (50 + 33) had objective neurologic deficits (sensory, motor, or both).Of the initial 50 patients, 27 achieved full remission (no neurologic deficits and pain free), 17 were markedly improved (minimal residual sensory or motor deficit and mild to minimal pain), and 6 were unchanged at the time of their last examination. Of the 33 patients followed prospectively, 13 were in full remission and 16 were markedly improved requiring no treatment at the 100-day follow-up evaluation (< 0.05 by one tailed t-test). Of the 33 patients with complicating depression or fibromyalgia, 4 demonstrated minimal or no pain improvement, although 3 of the 4 had full remission of sensory/motor findings. Motor vehicle accidents precipitated symptoms of CDR in 14 patients in the retrospective and 5 in the prospective study. CDR of 15 patients was in full remission by 90 days, and 4 had ongoing chronic and/or mild sensory or motor deficits at 300 days. At the final follow-up, all 33 prospectively studied patients had maintained at least the level of improvement achieved at 100 days (p < 0.05 by one tailed f-test). No one in the total group of 83 patients required surgical intervention or hospitalization.Our results suggest that outpatient nonsurgical conservative management with careful patient education and monitoring of a coordinated conservative regimen can be successful for the majority of patients with CDR.
 ...
PMID:Conservative treatment of cervical radiculopathy. 1907 59


<< Previous 1 2 3 4 5 6 7 8 Next >>