Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fatigue or piercing feeling of weakness, lack of strength and energy or total exhaustion is a common complaint of patients with neurological disorders. From 40 to over 90 per cent of individuals with multiple sclerosis, Parkinson disease, amyotrophic lateral sclerosis, neuroboreliosis, post polio syndrome or stroke confirm its experience. It is not infrequently numbered among most disabling complaints. A separate entity, with fatigue as a cardinal sign, is a chronic fatigue syndrome, a disorder, though controversial, more and more frequently diagnosed. Fatigue ought to be discriminated from fatigability, paresis, somnolence and, first of all depression which commonly coexists in chronic disorders. The assessment is almost entirely based on self-estimate scales filled in by a patient. Attainable results of neuroimaging, electrophysiological, polisomnographic, vegetative, psychological and biochemical surveys have not allowed yet to define the pathogenesis of fatigue. The treatment basis consists of behavioral therapy, psychotherapy and a proper treatment of the basic disease.
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PMID:[The problem of fatigue in neurological disorders]. 1733 30

The performance of clinical signs as a diagnostic test for the detection of BTV-8 outbreaks during the 2006-epidemic in The Netherlands was evaluated by constructing and analysing receiver operating characteristic (ROC) curves. The area under the ROC curve of the BT-associated clinical signs in cattle was 0.77. An optimal efficient test (maximising both sensitivity and specificity) in cattle herds combined a sensitivity (Se) of 67% with a specificity (Sp) of 72%, comprising the following clinical signs: ulcerations and/or erosions of oral mucosa or erosions of lips/crusts in or around nostrils or oedema of the nose or hyperaemic/purple coloration of tongue, tongue protrusion or coronitis or apathy/tiredness or muscle necrosis, stiffness of limbs or loathing or refusal to move, prostration or torticollis or anoestrus. The area under the ROC curve of the BT-associated clinical signs in sheep was 0.81. The optimal efficient test in sheep flocks combined a Se of 76% with a Sp of 72%, comprising the following clinical signs: ulcerations of oral mucosa or serous nasal discharge or erosions/ulceration of tongue mucosa or hypersensitivity of the skin or muscle necrosis, stiffness of limbs or coronitis or grinding of teeth or salivation or weakness/paresis.
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PMID:Performance of clinical signs to detect bluetongue virus serotype 8 outbreaks in cattle and sheep during the 2006-epidemic in The Netherlands. 1816 48

Propylthiouracil (PTU) is a frequently prescribed drug in the treatment of hyperthyroidism. The use of PTU is, however, accompanied by numerous potentially serious side effects including vasculitis. PTU-related vasculitides can present as haematuria, pulmonary haemorrhage, or cutaneous lesion together with aspecific symptoms such as fever, myalgia, arthralgia, and fatigue. Cerebral involvement is seldom observed. We present a 49-year-old female with Graves' disease and asthma, who developed paresis of the proximal extremities, eosinophilia, pulmonary, and cutaneous lesions following treatment with PTU. A cerebral vasculitis consistent with Churg-Strauss syndrome (CSS) was suspected. Although cerebral involvement is seldom observed with PTU treatment, cerebral vasculitis should be considered in patients developing CNS symptoms.
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PMID:Churg-Strauss Syndrome following PTU Treatment. 2010 67

The term chronic renal failure (CRF) usually means the final stage of chronic kidney disease (CKD) with a decline in glomerular filtration rate (GF) below 0.25 mL/s. CRF is a world-wide serious health and economic issue with an increasing incidence and prevalence. CRF patients are, in comparison to other patients, hospitalized more often and for longer and, despite improvements in care, their quality of life is usually low and morbidity and mortality high. We present an overview of the most important CKD risk factors and the diseases most likely to result in CRF. Diabetic nephropathy, followed by various forms ofischemic renal disease and primary and secondary glomerulopathy, chronic tubulointerstitial nephritis and autosomal dominant polycystic kidney disease are the leading causes of CRF. We provide a brief overview of other disease states that may result in renal failure. Clinical manifestations of CRF are discussed, mainly cardiovascular, gastrointestinal, haematological and neurological symptoms. Breathlessness is a consequence of hypervolaemia, metabolic acidosis and anaemia. The disease often presents with symptoms, such as headache and visual disturbances, resulting from arterial hypertension. Gastrointestinal symptoms and fatigue, usually caused by anaemia, are frequent. Platelet dysfunction is manifested as an increased bleeding time. Paradoxically, apart form tendency to abnormal bleeding, CRF also tends to be associated with thromboembolic complications. Patients may experience itching, bone, joint and muscle aches, are more prone to infections. They may suffer from insomnia, concentration disorders and apathy. The signs of peripheral mixed sensory-motor neuropathy include paraesthesia, paresis and restless leg syndrome. However, renal failure may also be oligosymptomatic or asymptomatic. Cardiovascular complications are the most frequent cause of morbidity and mortality of CRF patients.
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PMID:[Aetiology and a clinical picture of chronic renal failure]. 2187 93

Separate discussion of immune-mediated neuropathies from other neuropathies is justified by the serious consequences of the natural course of these diseases, like disability and sometimes even life threatening conditions. On the other hand nowadays effective treatments already exist, and with timely and correct diagnosis an appropriately chosen treatment may result in significant improvement of quality of life, occasionally even complete recovery. These are rare diseases, and the increasing number of different variants makes it more difficult to recognize them. Their diagnosis is based on the precise knowledge of clinical signs and symptoms, and it is verified by the help of neurophysiologic and laboratory, first of all CSF examinations. Description of clinical features of the classic acute immune-mediated neuropathy, characterized by ascending paresis and demyelination is followed by a summary of characteristics of newly recognized axonal, regional and functional variants. Chronic immune-mediated demyelinating polyneuropathies are not diagnosed in due number even today. This paper does not only present the classic form but it also introduces the ever increasing special variants, like distal acquired demyelinating sensory neuropathy, Lewis-Sumner syndrome, multifocal motor neuropathy and paraproteinemic neuropathies. Vasculitic neuropathies can be divided into two groups: systemic and non-systemic ones. The first sign of a vasculitic neuropathy is a progressive, painful mononeuropathy; the classic clinical presentation is the mononeuritis multiplex. It is characterized by general signs like fever, loss of weight, fatigue. In systemic vasculitis organ specific symptoms are also present. From the paraneoplastic diseases the subacute sensory neuropathy and the sensory neuronopathy are members of the immune-mediated neuropathies, being most frequently associated with small cell lung cancer.
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PMID:[Diagnosis of immune-mediated neuropathies]. 2192 Aug 42

The prevalence of factors associated with functional disability was estimated six and twelve months after traumatic brain injury (TBI) in patients initially treated in the emergency unit of reference for the Metropolitan Region of Salvador, Bahia, Brazil. A prospective cohort study was performed, including 307 individuals with TBI between the ages of 15 and 65 years whose diagnosis was confirmed via neuroimaging. Using data from the period of hospitalization, 242 patients were contacted six months after the injury and 222 patients after twelve months. Functional impairment was evaluated with the Disability Rating Scale. The overall prevalence of functional disability (60.3% in the first evaluation and 40.5% in the second) was significantly associated with age, the initial gravity of the TBI and the duration of the patient's hospitalization, as well as with: fatigue; aphasia; memory, attention and concentration disorders; balance disorders; paresis; and lack of medical consultations with specialists. The high frequency of overall functional disability in the six or twelve-month follow-up period, even for patients with mild traumas, shows the relevance of TBI as a cause of disability and impairment, as well as the need for follow-up services.
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PMID:[Factors associated with overall functional disability one year after traumatic brain injury]. 2450 May 47

The patient was a 58-year-old man with 1-year history of cognitive decline, which was diagnosed as Alzheimer's disease in another hospital. He was admitted to our hospital for extreme fatigue, weight loss, and dysphagia, subsequent to the left peripheral facial paresis. Brain magnetic resonance (MR) imaging showed bilateral diffuse white matter lesions and hippocampal atrophy. After admission, he presented with sudden high fever, recurrent exacerbations of consciousness, and increased C-reactive protein level with marked neutrophilia, with the result that he underwent mechanical ventilation. Routine cerebrospinal fluid findings at the exacerbation were normal i.e. 4.7 cells/mm(3), 40 mg/dl of protein, but IL-6 concentration was mildly elevated to 22.2 pg/ml. After confirming the positivity of HLA (human leukocyte antigen) B54 and Cw1, we administered steroid to him and his physical activity and state of consciousness significantly improved. During the course of treatment, dermal lesion characterisitic of Sweet disease was absent. We diagnosed this case was possible neuroSweet disease proposed by Hisanaga in 2005.
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PMID:[A case of possible neuro-Sweet disease with prolonged disturbance of consciousness and no dermal lesion during the course of dementia]. 2458 87

A twelve-year-old African-American female presented with two week history of progressively worsening headache and fatigue, and vision difficulties for the past week. The physical examination was normal. The neurological evaluation was normal, except for cranial nerves (CN) testing, which showed bilateral restriction of adduction (CN III) and up gaze (CN IV) motions, vertical nystagmus, and left side facial paresis of central origin (CN VII). The bilateral exotropia and ophthalmoplegia are characteristics of WEBINO (Wall-Eyed Bilateral Intranuclear Ophthalmoplegia) syndrome, associated to a brain stem structural lesion. The following causes were evaluated and ruled out: tumor, infection, ischemic stroke, non-infectious inflammation. Pediatric Acquired Demyelinating Syndromes were then considered. Neuromyelitis Optica was ruled out in the absence of neuritis and normal spinal cord MRI. The differential diagnosis between Clinically Isolated Syndrome and Acute Demyelinating Encephalomyelitis, causing an isolated brain stem syndrome, is discussed.
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PMID:A 12-year-old African American girl with subacute bilateral ophthalmoplegia. 2514 58

Post-polio syndrome occurs 30-40 years after polio virus infection. The main symptoms of PPS are slowly progressive muscle limbs paresis with muscle atrophy, joints pain, paresthesia. In 90% of patients the main symptom is fatigue that leads to physical and mental activity deterioration. The cause of disease remains unknown. Probably it is an effect of motoneurons damage during acute virus polio infection, their overloading and degeneration of remaining ones. In this study we described a case of man who developed PPS 36 years after Heine-Medin disease. The main symptom was intensification of right limb paresis and muscle atrophy. In electromyography there were damage features of muscle clinically affected and unaffected. Changes in lifestyle made possible to continue occupational activity.
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PMID:[Post-polio syndrome - a case report]. 2627 76

Controversy exists about residual symptoms after pharmacological treatment of Lyme neuroborreliosis. Reports of disabling long-term sequels lead to concerns in patients and health care providers. We systematically reviewed the available evidence from studies reporting treatment of Lyme neuroborreliosis to assess the prevalence and spectrum of residual symptoms after treatment. A literature search was performed in three databases and three clinical trial registers to find eligible studies reporting on residual symptoms in patients after pharmacological treatment of LNB. Diagnosis must have been performed according to consensus-derived case definitions. No restrictions regarding study design or language were set. Symptom prevalence was pooled using a random-effects model. Forty-four eligible clinical trials and studies were found: 8 RCTs, 17 cohort studies, 2 case-control studies, and 17 case series. The follow-up period in the eligible studies ranged from 7 days to 20 years. The weighted mean proportion of residual symptoms was 28 % (95 % CI 23-34 %, n = 34 studies) for the latest reported time point. Prevalence of residual symptoms was statistically significantly higher in studies using the "possible" case definition (p = 0.0048). Cranial neuropathy, pain, paresis, cognitive disturbances, headache, and fatigue were statistically significantly lower in studies using the "probable/definite" case definition. LNB patients may experience residual symptoms after treatment with a prevalence of approximately 28 %. The prevalence and spectrum of residual symptoms differ according to the applied case definition. Symptoms like fatigue are not reported in studies using the "probable/definite" case definition. As the "possible" case definition is more unspecific, patients with other conditions may be included. Reports of debilitating fatigue and cognitive impairment after LNB, a "post-Lyme syndrome", could therefore be an artifact of unspecific case definitions in single studies.
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PMID:Prevalence and spectrum of residual symptoms in Lyme neuroborreliosis after pharmacological treatment: a systematic review. 2645 93


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