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)

In the differential diagnosis of intermittent claudication some rare myopathies have to be considered. The most frequent is phosphorylase deficiency (McArdle's disease). Exercise-induced muscular pain, weakness, contractures and occasionally myoglobinuria are the most prominent clinical signs. Serum creatine phosphokinase, aldolase and lactic dehydrogenase may be elevated after exertion. In the ischemic forearm test there is no rise of serum lactic acid. The enzyme deficiency can be demonstrated by histochemical and biochemical examination of a muscle specimen. Further, but more infrequent, enzymatic disturbances of glycolysis are phosphofructokinase deficiency and phosphohexoisomerase inhibitor, which also yield an abnormal ischemic forearm test and must be demonstrated histochemically and biochemically. Apart from muscular signs, myopathy with lactic acidosis is associated with palpitation, dyspnea and exhaustion, and a disproportionate rise in serum lactic acid level after exertion. Histochemically and electronmicroscopically demonstrable fat accumulation in the muscle can be a sign of a disturbance in lipid metabolism. This type of exercise-induced myopathy has been reported only in a few cases with carnitine-pylmityltransferase deficiency, which has to be demonstrated biochemically. Muscular contractures also exercise-induced but painless and reversible within seconds may be due to deficient uptake of sarcoplasmic calcium in the tubular system. Dyskalemic paralysis causes painless paresis within minutes of hours after exertion, which disappears within hours to a few days. Myopathy with tubular aggregates can be differentiated from other exercise-induced myopathies by morphology. Myotonia combined with painful contractures characterizes myopathia myotonica.
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PMID:[Exercise-induced muscular weakness, myalgia and contractures. I. A clinical review]. 13 80

Based on the examination of 45 dead and 5 moribund female mice during a 2-year period, we are able to describe a new disease entity: ileus of the small intestine in lactating mice caused by a paresis of peristalsis. Diarrhoea was not observed and inflammation and infectious agents were not found. Females were affected during the 2nd week of their first lactation. The condition may have a mortality rate as high as 40%. It is assumed that exhaustion (calcium, glucose, etc.) is the cause of this condition. Consequently, the development of a dietary supplement or of a special diet for lactating mice may prove beneficial in preventing this disease. Endogenic (Clostridia) or exogenic toxic components may also play a role.
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PMID:Paresis of peristalsis and ileus lead to death in lactating mice. 375 26

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

Postictal motor deficits may occur in patients following partial and generalized tonic-clonic seizures. Frequency is unclear, epidemiology being hampered by heterogeneous populations and variable methods of detection. Postictal paresis may affect any body part, may be bilateral, and may occur more frequently in seizures involving the sensorimotor cortex. Duration varies depending on the precise mode of testing from a few minutes to 36 hours. Sensory deficits following seizures have been rarely reported but may be missed if not specifically tested for. The lateralizing value of postical paresis is high (>90%), pointing to a seizure origin in the opposite frontal lobe. Postictal paresis often is lesion associated and should encourage MRI, particularly in new-onset epilepsy. Etiology is unclear, neuronal exhaustion and hyperinhibition being the main pathophysiological theories discussed. As disability from seizures may be increased, postictal paresis should more systematically be asked and tested for and should also be included when evaluating the success of anticonvulsive treatment.
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PMID:Weakness and focal sensory deficits in the postictal state. 2070 21

Central nervous system lesions, such as stroke or spinal cord injury (SCI), are followed by both cortical and spinal neuronal reorganization. In a severe chronic SCI a spinal neuronal dysfunction develops which is reflected in an exhaustion of leg muscle electromyographic (EMG) activity during assisted locomotion and a change in the dominance from an early to a late polysynaptic spinal reflex (SR) component. The aim of this study was to investigate the course of spinal neuronal function after a severe stroke, i.e., a unilateral deprivation of supraspinal input. In 30 hemiparetic stroke subjects locomotor and SR behavior were assessed. SR responses in the tibialis anterior muscle were evoked by non-noxious tibial nerve stimulation on both, the affected and the unaffected leg. In nine stroke subjects EMG activity of the leg muscles was recorded during assisted locomotion. In a similar way to SCI subjects, in severely affected chronic (>12 months post-incidence) stroke subjects a late SR component was prominent in the affected leg, while an early one dominated in the unaffected leg. The late SR component correlated with muscle paresis (rho=0.714) and walking ability (rho=0.493). In contrast to SCI subjects, no exhaustion of the EMG activity was observed in the affected leg muscles during prolonged assisted locomotion. It is concluded that spinal neuronal circuits undergo functional changes also after a stroke which have common as well as divergent features compared to SCI subjects. As a consequence, different rehabilitative strategies might be required.
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PMID:Spinal neuronal dysfunction after stroke. 2222 96

COVID-19 is frequently accompanied by a hypercoagulable inflammatory state with microangiopathic pulmonary changes that can precede the diffuse alveolar damage characteristic of typical acute respiratory distress syndrome (ARDS) seen in other severe pathogenic infections. Parallels with systemic inflammatory disorders such as atypical hemolytic uremic syndrome (aHUS) have implicated the complement pathway in the pathogenesis of COVID-19, and particularly the anaphylatoxins C3a and C5a released from cleavage of C3 and C5, respectively. C5a is a potent cell signalling protein that activates a cytokine storm-a hyper-inflammatory phenomenon-within hours of infection and the innate immune response. However, excess C5a can result in a pro-inflammatory environment orchestrated through a plethora of mechanisms that propagate lung injury, lymphocyte exhaustion, and an immune paresis. Furthermore, disruption of the homeostatic interactions between complement and extrinsic and intrinsic coagulation pathways contributes to a net pro-coagulant state in the microvasculature of critical organs. Fatal COVID-19 has been associated with a systemic inflammatory response accompanied by a pro-coagulant state and organ damage, particularly microvascular thrombi in the lungs and kidneys. Pathologic studies report strong evidence of complement activation. C5 blockade reduces inflammatory cytokines and their manifestations in animal studies, and has shown benefits in patients with aHUS, prompting investigation of this approach in the treatment of COVID-19. This review describes the role of the complement pathway and particularly C5a and its aberrations in highly pathogenic virus infections, and therefore its potential as a therapeutic target in COVID-19.
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PMID:COVID-19: A collision of complement, coagulation and inflammatory pathways. 3260 59