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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Neuropsychiatric Systemic Lupus Erythematosus. 1109 72

Pain is prevalent and undertreated in nursing home residents, despite the existing wide array of effective pharmacological and nonpharmacological treatment modalities. In order to improve the quality of life of these vulnerable individuals, practitioners require education about the correct approach to assessment and management. Assessment should be comprehensive, taking into account the basic underlying pathology (e.g. osteoarthritis, osteoporosis, peripheral neuropathy, fibromyalgia, cancer) as well as other contributory pathology (e.g. muscle spasm, myofascial pain) and modifying comorbidities (e.g. depression, anxiety, fear, sleep disturbance). Pharmacological management should be guided by a stepped-care approach, modelled after that recommended by the World Health Organization for treatment of cancer pain. Nonopioid and opioid analgesics are the cornerstone of pharmacological pain management. Tricyclic antidepressants and anticonvulsants can be very effective for the treatment of certain types of neuropathic pain. In addition to treating the pain per se, attention should be given to prevention of disease progression and exacerbation, as maintaining function is of prime importance. Nursing home residents with severe dementia challenge the practitioner's pain assessment skills; an empirical approach to treatment may sometimes be warranted. The success of treatment should be measured by improvement in pain intensity as well as physical, psychosocial and cognitive function. Effective pain management may impact any or all of these functional domains and, therefore, substantially improve the nursing home resident's quality of life.
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PMID:Pain in nursing home residents: management strategies. 1123 36

It is reported a case of quadriplegia occurring in a 67-year-old women after she commits suicide with flunitrazepam. The patient stayed during around twenty hours unconscious, in the sitting position, with an extreme flexion of the neck on the left side. After injection of flumazenil the patient's consciousness was restored. Nevertheless a complete sensitive and motor deficit at the C4 and C5 level was then observed. Several diagnosis such as peripheral neuropathy, infectious disease, or arterial occlusion were eliminated and we finally postulated that the regulation of the spinal blood flow had likely been disturbed by the prolonged flexion of the neck, the hypotension and the putative respiratory depression. The fact that the patient suffered from cervicarthrosis would have already impaired the spinal blood flow regulation and consequently had probably damaged the spinal cord. No clinical improvement of the quadriplegia was noticed and the patient died in the intensive care unit thirteen days after admission. Such an exceptional complication after a toxic coma remind us the necessity to avoid long lasting vicious position of the cervical spine in anaesthesia and emergency practice.
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PMID:[Tetraplegia in the course of coma from drug intoxication]. 1169 94

To investigate the influence of the succinic acid treatment on geriatric patients with type 2 diabetes. Succinic Acid has some positive biological properties. One of its is a neglecting of an aerobic glycolysis. In this study we evaluated the efficacy of the combination of the succinic acid ("MITOMIN") on treating of diabetic neuropathy of geriatric patients with type 2 diabetes. The analysis was carried out using 26 patients (aged 60-76 years). The duration of diabetes was 9.15 +/- 1.43 years. Biomedical parameters were measured by standard methods; microalbuminuria was measured by "Micral-Test". Quality of life (psychosocial disorders) was estimated with the help of "SANDOZ"-scale for geriatric assessment. The therapy was assigned 1.5 g of mitomin per day during a month. All patients were examined on having late diabetic complications: 7.69%--had diabetic retinopathy; 11.54%--diabetic nephropathy; 73.08%--diabetic neuropathy; 46.15%--chronic failure of brain vessels; 11.5%--macroangiopathy of lower extremities and 100%--had ischeamic heart disease of different levels. Mitomin therapy improved basal and postprandial glycemic control (NS), variance of pallesthesia (p < 0.001), parameters of quality of life, i.e. depression (p < 0.001), anxiety (p < 0.01), short memory (p < 0.05) and emotionality (p < 0.001). Mitomin therapy plays a positive role in management of elderly patients with type 2 diabetes. It improves glycemic control, pallestesia and quality of life. Combination of succinic acid renders central and peripheral neuropathy protective efficacy.
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PMID:[Diabetes mellitus in the elderly: succinic acid compounds in treating diabetic neuropathies]. 1209 44

Diabetic neuropathy is a most-convoluted complication. Diabetic gastropathy, ulcers, diarrhea, and bladder dysfunction are the major peripheral neuropathies. Peripheral neuropathies have been the primary neuroscience focus of diabetes research. In contrast to the periphery, the brain is not usually thought to be a target of chronic diabetic complications. However, the impact of diabetes mellitus on the central nervous system has recently gained attention. It is well known that diabetes or hyperglycemia influences the sensitivity of laboratory animals to various pharmacological agents. An increased sensitivity of hyperglycemic or diabetic animals to barbiturates and a decreased sensitivity of D-amphetamine, p-chloroamphetamine, and carbon tetrachloride have been demonstrated. Furthermore, it was reported that mice and rats with streptozotocin-induced diabetes and spontaneously diabetic mice are significantly less sensitive than non-diabetic mice to the antinociceptive effect of morphine. However, little information is available regarding the mechanism responsible for these changes. It is well established that anxiety and depression are common in patients with diabetes. Moreover, diabetic animals showed significantly more anxiogenic activity than non-diabetic animals did. However, the mechanisms through which diabetes may contribute to the development of, or be a risk factor for, psychiatric disorders are not clear. We provide an overview of our current understanding of the effects of streptozotocin-induced diabetes on the opioid receptor and the benzodiazepine receptor.
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PMID:[Modifications of several pharmacological actions by diabetes: effects on the opioid receptor agonist and benzodiazepines]. 1237 65

Human exposure to n-hexane (a hexacarbon solvent) is relatively frequent as it is used in many industries as a solvent, a thinner, and a cleaning agent. This report examines a case of peak n-hexane exposure, involving known exposure to high levels over a relatively brief period of time. Peak exposure is a risk factor for persisting neuropsychological impairment. However, cognitive deficits and depression have not been measured in studies of n-hexane, and only peripheral neuropathy, often reversible, is thought to be the neurological risk. This case demonstrates the longitudinal patterns of neuropsychological functions and emotion, and represents the early and late developing effects of n-hexane exposure that parallel the longitudinal change reported in groups of workers with solvent exposure.
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PMID:Longitudinal neuropsychological effects of n-hexane exposure: neurotoxic effects versus depression. 1458 47

Thalidomide, an antiemetic administered in 60th of the 20th century to pregnant women, has become notorious for a range of adverse effects which led to its taking off market. In recent years, its antimyeloma effect was discovered. The aim of the work was to evaluate the incidence of adverse reactions to thalidomide. Its therapeutic effect has not been assessed because of a short period of monitoring and diversity of a sample. The assessed sample consisted of 17 patients with diagnosis of multiple myeloma (10 men and 7 women). An average age of patients was 62.9 +/- 9.4. An average time elapsed from making the diagnosis to starting the treatment with thalidomide was 51.0 +/- 23.7 months. An average length of therapy was 20.1 +/- 9.6 weeks. An average daily maximum therapeutic dose was 138.3 +/- 83.2 mg. Data were collected from outpatient physicians reports, regular laboratory tests, and direct interviews with patients. To classify severity of adverse drug effects (grades 0-4) we used WHO criteria, Cancer and Leukemia Group B criteria, and in cases where certain adverse effects were not included in the above mentioned criteria, we defined our own criteria. The most frequent adverse effects included: leucopenia or neutropenia in 12 (70.6%) patients, altered state of consciousness in 11 (64.7%) patients, obstipation in 10 (58.8%) patients, skin alterations in 9 (52.9%) patients, dizziness in 8 (47.1%) patients, peripheral neuropathy in 7 (41.2%) patients, spasms and spasmodic convulsions in 7 (41.2%) patients, and altered liver tests in 6 (35.3%) patients. From the perspective of necessity to interrupt treatment or reduce the dose the most severe disorders included: peripheral neuropathy in 2 patients (inability to control lower extremities), altered consciousness in 1 patient (protracted somnolence during a day), skin alteration in 1 patient (generalized toxoalergic reaction), leucopenia or neutropenia in 1 patient (1.0 resp < 0.5 x 10(9)/l), altered vision in 1 patient (blurred vision), hypothyroidism in 1 patient, and altered mood in 1 patient (subjective feeling of depression). This work proved thalidomide to be beneficial for the patients with multiple myeloma but it also shoved necessity to intensively monitor its adverse effects and to adjust its doses.
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PMID:[Desirable and undesirable effects of thalidomide in patients with multiple myeloma]. 1468 82

Persons with advanced human immunodeficiency virus type one (HIV-1) infection seek medical advice for a wide range of neurological disorders including, but not limited to, peripheral neuropathy, toxoplasmosis, cryptococcal meningitis, cytomegalovirus retinitis progressive multifocal leukoencephalopathy, lymphoma and dementia. The diagnosis of HIV-1-associated dementia (HAD) induced as a direct consequence of HIV infection of the brain comes commonly by exclusion. Diagnostic decisions can often be clouded by concomitant depression, motor impairments, and lethargy that follow debilitating immune suppression and weight loss. Indeed, cognitive, motor and behavior abnormalities underlie a variety of neurological dysfunctions associated with advanced HIV-1 infection. Thus, even combinations of clinical, laboratory and neuroimaging tests [for example, magnetic resonance imaging (MRI), computed tomography (CT), single photon emission computed tomography (SPECT) and positron emission tomography (PET)] often fail to provide conclusive diagnostic information. Nonetheless, the recent development of quantitative MR spectroscopic imaging has improved diagnostic possibilities for HAD. We are pleased to discuss these developments as well as taking a forward look into what will soon be made available to improve neuroimaging diagnostic precision. New MR and SPECT testing are being developed in our laboratories and elsewhere both for animal model systems and in humans with HIV-1 disease. Such tests can facilitate dynamic measures of HIV-1 neuropathogenesis providing information for disease events that even 2 years ago were unattainable.
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PMID:Advances in neuroimaging for HIV-1 associated neurological dysfunction: clues to the diagnosis, pathogenesis and therapeutic monitoring. 1505 41

The objective of this paper was to identify predictors of attrition in a study designed to assess whether cognitive behavioural therapy (CBT) was more helpful than supportive therapy (SP) in reducing pain associated with peripheral neuropathy in HIV-positive patients. Sixty-one subjects were randomized into either CBT or SP for six weekly one-hour sessions. Twenty-eight subjects dropped out before week six. Demographic variables such as age, gender, ethnicity, socioeconomic status and level of education were not predictive of attrition. However, higher scores on the Hamilton Depression Inventory (HAM-D, 17-item) (t (59) = - 0.09, p<0.05) were predictive. These findings suggest that while dropouts were not more physically ill (e.g. CD4 counts, viral loads and opportunistic infections were not statistically higher), they reported greater psychological distress.
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PMID:Predictors of attrition in HIV-positive subjects with peripheral neuropathic pain. 1520 32

Chlorophenoxy herbicides are used widely for the control of broad-leaved weeds. They exhibit a variety of mechanisms of toxicity including dose-dependent cell membrane damage, uncoupling of oxidative phosphorylation and disruption of acetylcoenzyme A metabolism. Following ingestion, vomiting, abdominal pain, diarrhoea and, occasionally, gastrointestinal haemorrhage are early effects. Hypotension, which is common, is due predominantly to intravascular volume loss, although vasodilation and direct myocardial toxicity may also contribute. Coma, hypertonia, hyperreflexia, ataxia, nystagmus, miosis, hallucinations, convulsions, fasciculation and paralysis may then ensue. Hypoventilation is commonly secondary to CNS depression, but respiratory muscle weakness is a factor in the development of respiratory failure in some patients. Myopathic symptoms including limb muscle weakness, loss of tendon reflexes, myotonia and increased creatine kinase activity have been observed. Metabolic acidosis, rhabdomyolysis, renal failure, increased aminotransferase activities, pyrexia and hyperventilation have been reported. Substantial dermal exposure to 2,4-dichlorophenoxy acetic acid (2,4-D) has led occasionally to systemic features including mild gastrointestinal irritation and progressive mixed sensorimotor peripheral neuropathy. Mild, transient gastrointestinal and peripheral neuromuscular symptoms have occurred after occupational inhalation exposure. In addition to supportive care, urine alkalinization with high-flow urine output will enhance herbicide elimination and should be considered in all seriously poisoned patients. Haemodialysis produces similar herbicide clearances to urine alkalinization without the need for urine pH manipulation and the administration of substantial amounts of intravenous fluid in an already compromised patient.
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PMID:Poisoning due to chlorophenoxy herbicides. 1557 61


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