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)

The article presents data on the clinico-morphological study of three patients suffering from thyrotoxicosis with attacks of periodic paralysis. The muscles obtained by biopsy in two patients at the moment of attack and in one patient--in the absence of attack were investigated by the electron microscopy method. The data obtained make it possible to assume that in the thyrotoxic periodic paralysis the action of the thyroid hormones causes not only impairment of the mineral metabolism, but brings about changes in the structure of the membranes of the sarcolemma and T-system, which leads to disturbances of conductance of action potential into the fibre. These changes affect the function of the end cisterns and lead to distorsion of the processes of conjugation of excitation-contraction with resulting development of paresis and paralysis of muscles. Moreover, during the attack there take place secondary disturbances of carbohydrate metabolism, which aggravates the pathological process.
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PMID:[Change in the ultrastructure of the muscles in thyrotoxic periodic paralysis]. 102 2

The case of a 42-year-old man is reported, who on four occasions developed a hypokalaemic periodic paralysis after an intramuscular injection of "Ambene". The detailed examination of this patient shows, that it is the primary, autosomal dominant inherited form of hypokalaemic periodic paralysis, and not the secondary form, which is caused by a renal or gastrointestinal loss of potassium. Clinical and electrophysiological, as well as histopathological and electron microscopic findings are presented, showing the typical vacuolar myopathy with submicroscopic tubular structures. In the literature there is evidence for an increased sensitivity of the muscle membrane to insulin with an increased potassium-shift inside the cell in hypokalaemic periodic paralysis. "Ambene" is a combination, which contains amongst other substances dexamethasone and the local anaesthetic drug lidocain. In the present case the paresis was possibly caused by a combined effect of dexamethasone with a consequent hyperglycaemia and lidocain with a change in the excitability of the muscle membrane. The pathophysiological mechanism of hypokalaemic periodic paralysis is discussed in terms of the release by the combination of these two drugs. It has not previously been reported that "Ambene" can provoke a hypokalaemic periodic paralysis. This is a severe side effect because of the resulting cardiac and respiratory problems.
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PMID:[Hypokalemic periodic paralysis provoked by "Ambene"]. 293 67

A case of hypokalemic periodic paralysis, is reported, characterized by a positive family history and by repeated attacks of transient motor weakness since the age of 14 involving one all limbs. An induction test under ECG and EMG monitoring, carried out by infusing glucose and insulin when the patient was symptom-free, provoked motor paresis comparable to the spontaneous attacks and confirmed the diagnosis.
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PMID:Familial hypokalemic paralysis: a case study. 657 50

We report a case of thyrotoxic hypokalemic periodic paralysis occurring in a black man. This previously healthy 41-year-old man had a 3-year history of recurrent paroxysmal episodes of paresis in the upper and lower extremities proximally, often occurring after heavy exercise. The patient had no history of hyperthyroidism, nor family history of periodic paralysis. This case reveals a particularly rare characteristic of this disorder in which periodic paralysis is the presenting symptom of hyperthyroidism. This condition has been reported most commonly among Asians and is extremely rare in black men, only five cases having been described during the past 30 years.
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PMID:Thyrotoxic periodic paralysis in a black man. 868 66

Channelopathy is a term used to describe clinical problems caused by disorders of membrane ion channels. Included in this disease category are certain types of periodic paralyses, ataxia, myotonia, migraine headache, epilepsy, nephrolithiasis, and long QT syndrome. This article briefly summarizes membrane ion channel structure and function and details several relatively common channelopathies. In hyperkalemic periodic paralysis, mutant skeletal muscle sodium channels fail to close completely after an action potential. This evokes two apparently opposite symptoms: myotonia (caused by a small depolarization and repetitive excitation) or paralysis (caused by larger depolarization and inexcitability). In hypokalemic periodic paralysis, mutation affects the closing of skeletal muscle calcium channels, causing transient paresis or paralysis. The task of the advanced practice nurse is to recognize these disorders, institute appropriate prophylactic measures and treatments, monitor symptom progression, and avoid complications. Understanding of channelopathies is advancing rapidly. On the horizon are therapies tailored to counter specific membrane ion channel defects.
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PMID:Channelopathies: potassium-related periodic paralyses and similar disorders. 1123 35

A 25-year-old Caucasian man is admitted to hospital because of severe hyperthyroidism. Soon after his admission, he develops a lower limbs proximal muscles paresis with tendinous hyporeflexia. He has presented similar episodes in the previous months. Serum potassium level is 2.9 meq/l whereas it was 4.1 meq/l a few hours before. The patient receives intravenous potassium and propranolol. He will not develop a similar episode afterwards. Hypokalemic thyrotoxic periodic paralysis associated with Basedow's disease is diagnosed. Hypokalemic thyrotoxic periodic paralysis is a very rare cause of intermittent muscular weakness in the young Caucasian male. The frequency of this entity is at least ten times higher in Asiatic hyperthyroid people. Its physiopathology involves intracellular potassium shifts in which Na/K ATP-ases of cell membranes, the number and the activity of which increase in hyperthyroid people, seem to play a major role. Treatment consists of correction of hyperthyroidism and administration of potassium during the acute episode Propranolol is efficient in preventing recurrent episodes of paralysis. Points of comparison between hypokalemic thyrotoxic periodic paralysis and hypokalemic familial periodic paralysis are discussed.
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PMID:[Hypokalemic thyrotoxic periodic paralysis: a case report]. 1201 51

Hypokalaemic thyrotoxic periodic paralysis is an enigmatic and uncommon condition which occurs exclusively in males of Asian descent. The underlying causes of thyrotoxicosis may be any of the well-recognized etiologies including a toxic multinodular goiter, Graves' disease or iodine excess. Beside thyrotoxicosis, a number of other hormonal factors have been hypothesized to contribute to hypokalaemic thyrotoxic periodic paralysis, particularly postprandial hyperinsulinaemia and testosterone. We hereby present a case of a 48-year-old hepatitis C positive gender-assigned man in whom all of these factors are proposed to interact, lending further support to these hypotheses. The patient presented with interferon-induced thyroiditis causing acute generalized weakness whilst undergoing combination interferon-alpha-2beta and ribavirin therapy. As part of his hepatitis C infection, marked insulin resistance with hyperinsulinaemia was also present, exacerbating the paresis. Initial treatment with beta-blocker failed to normalize his serum potassium concentration, requiring the novel use of spironolactone, despite euthyroidism. This continued to be required until his testosterone supplement dissipated.
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PMID:Hepatitis C infection and thyrotoxic periodic paralysis--a novel use of an old drug. 1909 28

Paramyotonia congenita (PC), first described in 1886 by Eulenberg, is characterized by cold and exercise-induced muscle stiffness and intermittent flaccid paresis not necessarily related to cold or myotonia. Several authors segregated a pure form of PC, which has no periodic paralysis, even after cold exposure. The existence of this phenotype has been debated in the literature. We describe electrophysiological and molecular genetic features of a patient with PC who had no history of periodic paralysis. Immersion in cold water or potassium load could not induce clinical paralysis. However, repetitive nerve stimulation and exercise test demonstrated a drop in compound muscle action potential amplitude. Genetic analysis revealed the substitution of valine for glycine on the human skeletal muscle sodium channel (SCN4A) gene. The G1306V mutation is rare in the classic form of PC, and moreover might be the first in pure paramyotonia.
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PMID:A case of paramyotonia congenita without periodic paralysis: electrophysiological and molecular genetic studies. 2044 32

Thyrotoxic hypokalemic periodic paralysis is characterized by attacks of generalized weakness associated to hypokalemia in patients with hyperthyroidism. We report a 25-year-old man with a history of spontaneously relapsing episodes of muscular weakness, who consulted for a rapidly evolving upper and lower limb paresis. Hypokalemia associated to a primary hyperthyroidism was detected. Treatment with antithyroid Drugs and potassium supplementation reverted symptoms and the episodes of acute muscular weakness did not reappear.
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PMID:[Thyrotoxic hypokalemic periodic paralysis: report of one case]. 2127 57

Mutations of the skeletal muscle voltage-gated sodium channel (NaV1.4) are an established cause of several clinically distinct forms of periodic paralysis and myotonia. Focal paresis has sometimes already been described. We report a case with atypical clinical manifestation comprising paramyotonia and cold-induced persistent and focal paralysis. A 27-year-old woman presented with paramyotonia congenita since her childhood. She experienced during her childhood one brief episode of generalised weakness. At the age of 27, she experienced a focal paresis lasting for several months. The known mutation p.Val1293Ile was found in the muscle sodium channel gene (SCN4A). Channel inactivation is involved in most Na(+) channelopathies. Fast inactivation is known to be responsible for the myotonia phenotype. We hypothesise that the V1293I mutation may also alter the slow inactivation in specific conditions, for example, prolonged cold exposure or prolonged and intensive exercise. This observation broadens the spectrum of clinical manifestations of this sodium channel mutation.
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PMID:Focal and abnormally persistent paralysis associated with congenital paramyotonia. 2493 54


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