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PubMed1980

[Report on familial paroxysmal hypokalaemic paralysis in relation to postoperative intensive care (author's transl)].

A case is reported of familial paroxysmal hypokalaemic paralysis, which postoperatively was complicated by a disturbance of carbohydrate metabolism. Paralysis commenced in a state of postoperative hypokalaemia and persisted afterwards in a state of severe hyperkalaemia. The intensive treatment is presented and the problem of episodic paralysis is widely discussed.

Atrial Fibrillation↗

PubMed1995

[Thyrotoxic hypokalemic periodic paralysis: 18 cases with different forms of thyrotoxicosis].

Thyrotoxic periodic paralysis (TPP) is a rare complication of thyrotoxicosis in whites but it is commonly reported in oriental populations. Eighteen males with TPP were studied from 1966 to 1993 (17 years) with a mean age of 32.8 years (range: 22-50 years). Their ancestor, traced back as possible, was hispanic in 15 and autoctonous indigens (mapuche) in three. They had one or more episodes of flaccid paralysis with complete recovery associated with thyrotoxicosis and hypokalemia (in the twelve patients who had their serum potassium determined). Two patients had respiratory compromise. Ten patients had their crisis onset after physical exertion and/or copious ingestion of carbohydrates. Only one of the patients had severe thyrotoxicosis and the diagnosis was made after the periodic paralysis in ten of them. The types of thyrotoxicosis associated with TPP were: Graves-Basedow disease in 13, subacute thyroitidis in three, and overdosage of thyroid hormone in two patients. In summary, TPP can occur in latin american populations, may be fatal, and is not always associated with Graves-Basedow disease.

Adult↗

PubMedDate not supplied

[Anesthesia in a case of hyperkalemic familial periodic paralysis].

Periodic familial hyperpotassemic paralysis is a dominant autosomic disease of brief periods of acute flaccid paralysis with complete posterior recovery. During surgical-anesthesia a number of factors concur which may trigger a paralytic episode. To this effect anesthetic drugs such as barbiturates and muscle relaxants have been involved. The case of a 12 year old patient with familial hyperpotassemic paralysis who received general anesthesia with propofol and atracurium besylate for emergency appendectomy is presented. During surgery the plasma levels of potassium were monitored and prophylaxis of the factors which potentially trigger a paralytic picture was performed. Both, the perioperative and the postoperative period, were without complications.

Anesthesia, General↗

PubMed1977

[A new case of chronic progressive bulbo-pontine paralysis and deafness].

The author reports a new case of chronic progressive bulbo-pontine paralysis with deafness. This case differed from other cases previously published on the basis of the later age of onset of labio-glosso-laryn-geal paralysis, by the absence of any vestibular changes despite bilateral involvement of the acoustic centres and above all by the normality of deep tendon reflexes. The author feels that chronic progressive vulvo-pontine paralysis with deafness is a specific individual condition, worthy of consideration as an autonomic clinical entity.

Age Factors↗

PubMed1995

[Observation of compensatory head posture in superior oblique muscle paralysis].

PURPOSE: Superior oblique muscle paralysis is the most common disease in clinic. We analysed the cause, machanism and regularity of compensatory head posture in superior oblique muscle paralysis. METHODS: All of 27 cases with superior oblique muscle paralysis aere examined regularly, and special muscle, binocular single vision function with synoptophore examined. Bielschowsky test was made. RESULTS: In our cases, the incidence rate of compensatory head posture was 40.7%, which had relations with age when a patient had disease, period and function of binocular single vision. CONCLUSION: The existance of binocular single vision function is the physiological bases leading to compensatory head posture, and the patients whose ages are older than 3 years and the course is less than 10 years may present the compensatory head posture. So we should pay attention to early diagnosis and training to restore the binocular single vision function.

Adolescent↗

PubMed1997

[Mutation analysis of the CACNL1A3 gene in Japanese hypokalemic periodic paralysis families].

Recent genetic research has revealed that hereditary periodic paralysis is an ion channel disorder. Genetic linkage analysis has mapped the autosomal dominant hypokalemic periodic paralysis (HypoPP) locus to chromosome 1q31-32, where the dihydropyridine sensitive calcium channel alpha 1 subunit (CACNL1A3) is located. Subsequently, two predominant missense point mutations were found in the CNCNL1A3 gene. Both mutations substitute arginine to histidine (Arg528His and Arg1239His). The Arg528His mutation is characterized by incomplete penetrance in females, whereas Arg1239His is not. We analyzed Japanese hypokalemic periodic paralysis patients (familial, sporadic and thyrotoxic), and detected the Arg528His mutation in one HypoPP family. This family shows more severe symptoms in successive generations, and the severity of the symptoms is higher in males than in females within the same family.

Asian People↗

PubMed1997

[Oculomotor nerve paralysis with complete ptosis in herpes zoster ophthalmicus: 2 cases].

INTRODUCTION: Only few studies focus on ocular motor paralyses in herpes zoster ophtalmicus. We report 2 cases of complete ptosis resulting from paralysis of the superior lid levator, appearing at day 6 and 7 of an ophtalmic herpes zoster under treatment with acyclovir. CASE REPORTS: Case 1: A 68 year old woman presented an history of ophtalmic herpes zoster with kerato-conjunctivitis and uveitis treated with acyclovir. At the third day of the treatment and 7th day of the ophtalmic zoster, an incomplete paralysis of the oculomotor nerve appeared resulting in a complete ptosis. The treatment was carried on until the 21st day without improvement. Four months later, all symptoms had completely cleared. CASE 2: A 66 year old woman was treated with acyclovir for an ophtalmic herpes zoster without ocular involvement. At the 4th day of the treatment and 6th day of the onset of the ophtalmic zoster, a paralytic ptosis and a acute epithelial keratitis appeared. Acyclovir treatment was continued for 10 days. The ptosis resolved gradually during 2 months. DISCUSSION: The manifestation of a complete ptosis with paralysis of the oculomotor nerve or of one of its branch is rarely seen in ophtalmic herpes zoster. However minor symptoms are often detected when patients were carefully examined with regard to external ocular movements. The physiopathological mechanism are discussed about. The possible action of an early antiviral treatment on the prevention of these complications is not known. In our two cases, a paralytic ptosis broke out suddenly, even under treatment with acyclovir for respectively 3 and 4 days. For future prospective studies about antiviral drugs for ophtalmic herpes zoster, a systematic evaluation of these neurological symptoms would be interesting.

Acyclovir↗

PubMed1998

[Periodic hypokalemic paralysis disclosing thyrotoxicosis].

BACKGROUND: Hypokaliemic periodic paralysis is an uncommon complication of hyperthyroidism occurring sporadically almost exclusively in young Asian men. The clinical presentation is the same as in familial hypokaliemic periodic paralysis. Treatment consists of conventional management for thyrotoxicosis. CASE REPORT: A Laotian man aged 42 years had suffered episodes of pain and fatigue in the lower limbs lasting 2 to 7 days over the last few months. The patient was hospitalized with severe limb pain. Clinical examination found severe motor deficit involving all four limbs. Laboratory findings induced hypokaliemia (1.8 mmol/l) and hyperthyroidism (free thyroxin 36 pmol/l, TSH < 0.005 mlU/l). Thyroid echography revealed multinodular goitre with two heterogeneous nodules. Strong uptake was seen on the scintigram. The motor deficit regressed within 8 hours and the kaliemia was restored with 1.50 g KCl. The patient was discharged with carbimazole (30 mg/d). Three months later he was euthyroid and symptom free. Total thyroidectomy was performed and L-thyroxin prescribed. The patient remains symptom-free at the last follow-up, 5 months after thyroidectomy. DISCUSSION: The pathogenesis of hypokaliemic periodic paralysis involves the ATPase-dependent sodium-potassium pump whose activity is stimulated by thyroid hormones. The reasons for the ethnic and male predominance are poorly elucidated.

Adult↗

PubMed1997

Nerve paralysis after surgery in the submandibular triangle: review of University of Tokyo Hospital experience.

BACKGROUND: We assessed the incidence of neural complications in submandibular surgery in relation to the type of surgery, experience of the surgeon, and other factors. METHODS: We retrospectively reviewed the records of 133 patients who underwent excision of the submandibular triangle components at the University of Tokyo Hospital during the last 19 years. RESULTS: The most frequent complication was mandibular branch paralysis. Excluding 12 patients with malignant tumors, facial weakness was present postoperatively in 29.8% (37) or 124 resections. All palsies subsequently resolved. The paralysis was more frequent when nerve identification was performed than when it was not. CONCLUSIONS: The cardinal factors in minimizing incidence of nerve damage are an understanding of the anatomy of the nerves, low and generous skin incision, awareness of orientation in the surgical planes, avoidance of the use of metal retractors, and avoidance of elaborate identification of the nerve.

Adolescent↗

PubMed2002

Periodic paralysis: understanding channelopathies.

Familial periodic paralyses are typical channelopathies (i.e., caused by functional disturbances of ion channel proteins). The episodes of flaccid muscle weakness observed in these disorders are due to underexcitability of sarcolemma leading to a silent electromyogram and the lack of action potentials even upon electrical stimulation. Interictally, ion channel malfunction is well compensated, so that special exogenous or endogenous triggers are required to produce symptoms in the patients. An especially obvious trigger is the level of serum potassium (K+), the ion responsible for resting membrane potential and degree of excitability. The clinical symptoms can be caused by mutations in genes coding for ion channels that mediate different functions for maintaining the resting potential or propagating the action potential, the basis of excitability. The phenotype is determined by the type of functional defect brought about by the mutations, rather than the channel effected, because the contrary phenotypes hyperkalemic periodic paralysis (HyperPP) and hypokalemic periodic paralysis (HypoPP) may be caused by point mutations in the same gene. Still, the common mechanism for inexcitability in all known episodic-weakness phenotypes is a long-lasting depolarization that inactivates sodium ion (Na+) channels, initiating the action potential.

Electrophysiology↗

PubMed2004

Vocal cord and diaphragm paralysis, as clinical features of a French family with autosomal recessive Charcot-Marie-Tooth disease, associated with a new mutation in the GDAP1 gene.

Axonal forms of Charot-Marie-Tooth disease, either dominantly or recessively inherited, are clinically and genetically heterogeneous. We describe the clinical and electrophysiological characteristics of an axonal autosomal recessive form of Charot-Marie-Tooth disease in a French family, associated with a new mutation of the ganglioside-induced differentiation-associated protein-1 gene (GDAP1). Two sisters, born to non-consanguineous parents, presented severe proximal and distal sensorimotor deficit, areflexia, pes cavus, scoliosis and vocal cord and diaphragm paralysis. They lost ambulation in the third decade and since then they have been wheelchair bound. Nerve conduction studies were consistent with an axonal neuropathy. Clinical and electrophysiological examination of their parents and their brother was normal. Genetic analysis revealed a homozygous thymidine deletion at nucleotide position 558 resulting in a frameshift at codon 186 and a stop codon at position 205. This axonal form of Charot-Marie-Tooth disease associated with a new GDAP1 mutation is recessively inherited and is characterized by a severe phenotype, since patients become wheelchair bound in the third decade, and present vocal cord and diaphram paralysis, which may be missed as they had no respiratory symptoms until the third decade.

Adult↗

PubMed1994

Hemidiaphragm paralysis: CT diagnosis.

We describe the use of computed tomography (CT) in diagnosing and documenting diaphragmatic paralysis in a patient with right lung cancer that invaded the mediastinum. The patient was unable to breath hold during CT scanning, and the images were degraded by motion artifact. Motion artifact, however, was noted only in the left lung. In patients with suspected phrenic nerve dysfunction who are having chest CT for any reason, we suggest obtaining several dynamic images at the lung bases during forced exhalation. The lack of motion artifact in the lung parenchyma may be useful for diagnosing phrenic nerve injury and hemidiaphragm paralysis.

Artifacts↗

PubMed1977

Acupuncture in two cases of peripheral nerve paralysis.

This is a report on a case of peripheral paralysis of the right side of the larynx. The patient was a 34 year-old male who became completely aphonic following a grippal infection. After 3 weeks of conventional treatment by a well-known specialist, he underwent acupuncture treatment. After 4 months the voice was again normal; however, the laryngoscopy showed a completely normal larynx only 7 months after the illness. The loci used and the reasons for their selection are discussed in detail. The second case was a 62 year-old male with facial paralysis. This patient underwent acupuncture treatment shortly after he was stricken. After 6 days distinct improvement was seen; he was completely healed after 2 months. The loci and the reasons for their selection are discussed. The cases are compared.

Acupuncture Therapy↗

PubMed2002

Force assessment in periodic paralysis after electrical muscle stimulation.

OBJECTIVE: To obtain an objective measure of muscle force in periodic paralysis, we studied ankle dorsiflexion torque during induced paralytic attacks in hyperkalemic and hypokalemic patients. SUBJECTS, PATIENTS, AND METHODS: Dorsiflexor torque after peroneal nerve stimulation was recorded during provocative tests on 5 patients with hypokalemic or hyperkalemic disorders and on 2 control subjects (1995-2001). Manual strength assessment was simultaneously performed in a blinded fashion. Standardized provocation procedures were used. RESULTS: The loss of torque in hyperkalemic patients roughly paralleled the loss of clinically detectable strength, whereas in the hypokalemic patients, pronounced torque loss occurred well before observed clinical effects. No dramatic changes occurred in the control subjects. Torque amplitude decreased more than 70% in all patients during the provocation tests; such decreases were associated with alterations induced in serum potassium concentrations. CONCLUSIONS: Stimulated torque measurement offers several advantages in characterizing muscle dysfunction in periodic paralysis: (1) it is independent of patient effort; (2) it can show a definitely abnormal response early during provocative maneuvers; and (3) characteristics of muscle contraction can be measured that are unobservable during voluntary contraction. Stimulated torque measurements can characterize phenotypic muscle function in neuromuscular diseases.

Adolescent↗

PubMedDate not supplied

Schmidt syndrome due to idiopathic accessory nerve paralysis.

A patient with Schmidt syndrome due to idiopathic accessory neuropathy has had paralysis of soft palate and larynx as well as trapezius and sternocleidomastoid muscles, reflecting involvement of cranial and spinal roots, respectively. In addition to vocal cord paralysis on the laryngoscopy, videofluoroscopy confirmed diminished mobility of the soft palate. Electrodiagnosis showed accessory neuropathy at the proximal segment. Furthermore, the accessory nerve innervated not only upper but also middle and lower portions of the trapezius muscles.

Accessory Nerve↗

PubMed1977

[Nineteen years experience with surgical correction of disorders of swallowing and voice following vagus nerve paralysis (author's transl)].

An operation for the correction of swallowing and voice following paralysis of the vagus nerve is described. The operation is divided into four parts which are performed either in one or two stages. These include: 1. extramucosal myotomy of the pars fundiformis of the cricopharyngeus muscle; 2. correction of vocal cord paralysis by the rotation of the arytenoid cartilage and cartilage implant into the paralyzed vocal cord; 3. resection of the paralyzed wall of the pharynx; 4. fixation of the paralyzed soft palate to the posterior wall of the pharynx. Nineteen years experience with the four different parts of the operation are discussed.

Deglutition Disorders↗

PubMed1980

Progressive bulbar paralysis associated with neural deafness. A nosological entity.

A complete autopsy verification of progressive bulbar palsy associated with neural deafness was performed. Hearing loss and speech difficulties developed in a five-year-old girl. When she was 24 years old, clinical examination demonstrated deafness and bulbopontine paralysis together with retinitis pigmentosa, peripheral amyotrophies, pyramidal signs, and ataxia. The patients died at 27 years and the autopsy disclosed degenerative changes characterized by simple atrophy and loss of neurons accompanied by gliosis and loss of myelinated fibers. The structures principally affected were the anterior horns and the motor nuclei of the brain stem together with the eighth cranial nerve nuclei. Loss of myelinated fibers was found in the spinocerebellar and pyramidal tracts and in the fasciculus gracilis. Our study suggests that progressive bulbar paralysis with neural deafness should be considered as a nosological entity.

Adolescent↗

PubMed1983

Intravenous treatment of hypokalemic periodic paralysis.

Acute attacks of weakness in patients with hypokalemic periodic paralysis can usually be treated with oral potassium preparations. Occasional patients, however, require intravenous (IV) potassium administration. We studied a patient with hypokalemic periodic paralysis to determine the effect of using 5% glucose as a diluent for potassium administration during acute attacks of weakness. Administration of IV potassium chloride in 5% glucose (50 mEq/L) was associated with a worsening of strength and no rise in potassium level. Intravenous potassium in 5% mannitol was associated with a rise in potassium and improvement in strength. This study confirms the hazard of using glucose-containing solutions for correction of hypokalemia.

Adult↗