Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004093 (asthenia)
 2,650 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Generalized weakness, intermittent dysphagia, and a 40-pound weight loss developed in an elderly man over a six-month period. Examination revealed weakness, atrophy and fasciculations of extremity musculature, pseudobulbar speech, hyperactive upper extremity reflexes, and extensor toe signs without sensory loss. Results of electrodiagnostic studies were consistent with an axonal polyneuropathy. Endocrinologic results were compatible with hyperthyroidism. Radioiodine therapy resulted in resolution of clinical neurologic symptoms and signs within seven months. This case illustrates a previously undescribed concurrence of hyperthyroid associated polyneuropathy and pyramidal tract dysfunction that led to an initial clinical diagnosis of amyotrophic lateral sclerosis.
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PMID:Pyramidal tract deficits and polyneuropathy in hyperthyroidism, Combination clinically mimicking amyotrophic lateral sclerosis. 299 Feb 4

From among a large group of dogs with acute tetraparesis, we identified 10 dogs with a distinct peripheral nerve disorder. Prior to the onset of signs, all of the dogs had been healthy, and none was known to have been exposed to a neurotoxin or raccoon bite. Weakness, with hypoactive or absent segmental reflexes, became progressively worse for 1 to 21 days. Results of electromyography and nerve conduction studies invariably were compatible with a diagnosis of polyneuropathy that predominantly affected proximal nerve segments. Appearance of nerve biopsy specimens and the short time course for functional recovery suggested a demyelinative component to the disorder. The extent of recovery was variable but often rapid and complete in dogs that did not succumb to complications in the early period. Corticosteroid therapy did not demonstrably influence the outcome. This acute idiopathic polyneuropathy in the dog shares many clinical and pathologic features with idiopathic polyradiculoneuritis (Coonhound paralysis).
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PMID:Acute idiopathic polyneuropathy in the dog. 627 46

The use of activated charcoal haemoperfusion can play a complementary role in the substitutive treatment of chronic uraemia. This study reports the preliminary results of a regular combined haemodialysis-haemoperfusion treatment. The effectiveness of this treatment was observed on the subjective symptomatology (anorexia, nausea, asthenia) and on the polyneuropathy evaluated by electrophysiological assessments. The biocompatability of the system proved satisfactory.
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PMID:Preliminary report on the efficiency of combined haemodialysis-haemoperfusion treatment in chronic uraemia. 652 56

We describe six patients with painful polyneuropathy associated with hyperlipidemia. Each had mild, slowly progressive neuropathy characterized by pain in feet, without proximal extension or involvement of hands. Weakness and autonomic symptoms and signs were absent. Three patients had normal tendon reflexes; three others had decreased ankle reflexes. Serum cholesterol levels were moderately increased; serum triglyceride levels were exceedingly high. In one patient, symptoms resolved with correction of hypertriglyceridemia. No other cause of peripheral neuropathy was found. Marked increases in serum triglycerides may cause painful small-fiber neuropathy.
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PMID:Neuropathy associated with hyperlipidemia. 750 Nov 85

Ten patients with paraparesis due to peripheral neuropathies showed an unusual symptom characterized by an inability to stand still despite the ability to walk. The symptom was transient in the eight cases recovering from profound paraparesis due to acute or subacute polyneuropathies, and has continued for several years in two chronic polyneuropathy cases who have been suffering over ten years. All the patients take a series of to-and-fro steps forward and backward while standing until they initiate locomotion. We call this symptom "astasia without abasia", or the "stilts phenomenon", because the symptom reminds us of children's play with stilts. Weakness of the lower limbs was predominant in the ankle joints and muscle strength about the hip joints was relatively preserved. This pattern of weakness produced abnormal mechanical properties of the body in an upright posture. Postural movements of the patients thus consisted mainly of the movement about the hip joints (hip sway). The movement about the ankle joints (ankle sway) which maintains forward and backward leaning in upright posture was impaired. Although clinical examination revealed no significant sensory disturbances, impairment of the somatosensory system which stabilizes postural sway was proven in four patients by antero-posterior sway components around 1 Hz. Astasia without absia consists of maintaining body mass not on a fixed base but on a moving one. BOth abnormalities of postural movements and defective somatosensory feedback for postural stabilization may be responsible for this symptom.
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PMID:[Astasia without abasia due to peripheral neuropathy]. 817 34

In July 2000, a 62-year-old female, with a ten-year history of chronic hepatitis C virus infection and persistently normal aspartate amino-transferase and alanine aminotransferase levels, presented with asthenia, weight loss, peripheral polyneuropathy and increased levels of aspartate aminotransferase (8 times upper normal limit), alanine aminotransferase (10 times upper normal limit) and gamma glutamyl-transferase (6 times upper normal limit). The ultrasound findings were consistent with massive liver steatosis. The patient had been previously diagnosed elsewhere as having hepatitis C virus-related "hepatitic flare" with neurological involvement related to concomitant mixed type-III cryoglobulinaemia. However intense exposure to trichloroethylene since April 2000 was revealed and liver histology was fully consistent with non-alcoholic steatohepatitis. The pathogenetic role of the solvent was definitely supported by the complete clinical and biochemical remission within six months of trichloroethylene withdrawal.
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PMID:"Hepatitic flare", asthenia, peripheral polyneuropathy and diffuse liver steatosis in a hepatitis C virus asymptomatic chronic carrier. 1143 16

POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy, skin disorders) is a rare multisystemic disease associated with plasma cell dyscrasia. A 68-year-old woman with chronic renal insufficiency and arterial hypertension included in her medical history was admitted to the hospital with confusion, somnolence and asthenia. She presented ascites, hepatosplenomegaly, leg oedema, distal dysesthesias, leuconychia and multiple nodular purple red angiomas on the trunk, upper limbs and fingers. Hypothyroidism was revealed in the laboratory investigations and monoclonal IgG peak in immunoelectrophoresis. Electromyography showed both demyelinisating and axonal degenerative neuropathy. The diagnosis of POEMS syndrome was based on the dermatopathological examination of a cutaneous angioma; histology revealed features of glomeruloid angioma, a specific marker of this syndrome.
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PMID:POEMS syndrome revealed by multiple glomeruloid angiomas. 1207 35

Paclitaxel (TXL) and docetaxel (TXT), especially TXL, cause neurotoxicity manifested as polyneuropathy. In clinical practice, detailed knowledge of the symptoms and effect on quality of life (QOL) of neurotoxicity is crucially important both for diagnosis of neuropathy and for management of patients treated with taxanes. In this review, we summarize the symptoms of neurotoxicity caused by taxanes, and highlight the importance of QOL assessment in breast cancer patients treated with taxanes. The most common feature of taxane neurotoxicity is a predominant sensory distal neuropathy, and the incidence and severity of the neuropathic manifestations appear to be related to dose level and cumulative dose. A mixture of paresthesias and dysesthesias is often prominent, and the complaints include burning dysesthesia, numbness, tingling, and shooting pains, typically in a stocking-glove distribution. In contrast to sensory disturbances, motor neuropathy is not well recognized, and is believed to be much less common than sensory neuropathy. Weakness is usually mild, and distal motor neuropathy caused by taxanes rarely affects patients' activities of daily living. The effect of neurotoxicity on QOL is not fully understood, as no study has specifically assessed QOL in terms of neurotoxicity. There is therefore a clear need to collect more detailed data about QOL using well validated, reliable instruments. This will enable us to provide the information that patients require when treatment decisions are being made, and will help in the pursuit of the ameliorative interventions.
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PMID:Neurotoxicity of taxanes: symptoms and quality of life assessment. 1471

Weakness of the limbs and respiratory muscles has increasingly been found to be a frequent event that complicates the medical history of patients in Intensive Care. The problem normally affects more serious cases and presents as muscular weakness leading to flaccid paralysis and difficulty in weaning patients off mechanical ventilation. This latter sign leads the intensivist to suspect possible involvement of the neuromuscular respiratory system. Unfortunately, in-depth clinical assessment of the neuromuscular respiratory system is difficult with critically ill patients, and electrophysiological studies have been used instead to overcome this problem. Of these latter, electric and electromagnetic stimulation of the phrenic nerve have been successful (along with needle electromyography of the diaphragm) in identifying the causes of neuromuscular respiratory insufficiency, especially in Intensive Care. In this brief chapter, we will be discussing the technique of electric stimulation of the phrenic nerve and neuromuscular respiratory insufficiency within the field of critical illness polyneuropathy.
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PMID:Phrenic nerve stimulation. 1828 40

Imexon [AOP99.0001 (4-imino-1,3-diazobicyclo[3. 1. 0]-hexan-2-one)] belongs to a novel class of promising anticancer agents that induce tumor apoptosis through oxidative stress. Clinical experience since the late 1960s has provided initial evidence for a clinical antitumor activity. Our open-label, multicenter phase I clinical trial was designed to further investigate the adverse event (AEs) profile and pharmacokinetics of AOP99.0001 in pretreated myeloma patients and collect initial data on the potential clinical efficacy in this indication. Thirty-six patients with relapsed or refractory myeloma, who had been pretreated with at least two lines of therapy earlier, were included. Imexon was applied intravenously on 5 consecutive days for 2 weeks (d1-5 and d8-12) for a 3-week cycle. The plasma half-life of AOP99.0001 and its active metabolite AOP99.0002 was found to be approximately 1.2 and 2.6 h, respectively. The mean duration of treatment with Imexon was 6.8 weeks in a dose range between 50 and 1000 mg/m without reaching dose-limiting toxicity. Drug-related AEs occurring with a frequency of greater than 10% were fatigue, nausea, constipation, headache, asthenia, anemia, thrombocytopenia, leukopenia and creatinine increase. A total of nine severe adverse events occurred in three patients. No mortality was encountered when patients were on treatment with Imexon. Preliminary antimyeloma efficacy of AOP99.0001 was observed with 1 minimal response, 12 (36%) stable disease responses, and all other evaluable patients had progressive disease. Remarkably, the patient with minimal response also experienced a complete clinical resolution of myeloma-associated polyneuropathy. Overall, Imexon was safe and well tolerated in the dose range investigated. Imexon showed minor clinical activity as a single agent in heavily pretreated myeloma patients. On account of its unique mechanism of action, favorable toxicity profile, initial clinical evidence for antimyeloma activity, and its known synergistic activity in combination with approved agents for myeloma treatment, AOP99.0001 is recommended for future clinical studies in combination regimens in multiple myeloma.
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PMID:Combined phase I/II study of imexon (AOP99.0001) for treatment of relapsed or refractory multiple myeloma. 2057 55


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