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At least 1,171 records · Page 65Linked to original sources
PubMed2001

[The bridle procedure in treatment of foot deformity in children with slight cerebral spastic paralysis].

OBJECTIVE: To evaluate the effectiveness of the Bridle procedure in treatment of foot deformity in children with slight cerebral spastic paralysis. METHODS: From February 1993 to April 1999, 32 cases with 57 deformed feet, due to slight cerebral spastic paralysis, which included 20 males and 12 females, ranging from 4 to 14 years old, were reported after 6 to 74 months' follow-up, averaging 38 months. Bilateral feet were involved in 25 cases and unilateral feet involved in 7 cases. The deformities in all feet, including 26 feet of acroceph-foot deformity in 15 cases, 13 equinovarus deformity in 8 cases and 18 scissors gait deformity in 9 cases, were treated by Bridle procedure, followed by temporal external fixation of long-leg plaster splint for 6 to 8 weeks. RESULTS: Clinical observation revealed complete and permanent correction of deformity in 48 out of all 57 feet (84.2%), reoccurrence of deformity in 7 feet (12.3%), and occurrence of valgus deformity in 2 feet (3.5%). No joint stiffness was observed. CONCLUSION: The Bridle procedure is an easily performed operation and effective in the treatment of foot deformity in children with slight cerebral spastic paralysis.

Adolescent↗
PubMed2000

Prolonged paralysis associated with succinylcholine--a case report.

Prolonged paralysis is a rare complication of succinylcholine. We report a case of palmar hyperhidrosis who underwent transthoracic endoscopic sympathetic ganglionectomy under general anesthesia with a facemask developed prolonged paralysis following the operation. The prolonged paralysis supposedly caused by intraoperative use of succinylcholine was recognized and confirmed by laboratory examination which showed low pseudocholinesterase activity. In this report, we describe the course of the event and discuss the causes of delayed awakening associated with anesthesia and its management.

Adolescent↗
PubMed1986

Electroconvulsive Therapy and Severe Osteoporosis: Use of a Nerve Stimulator to Assess Paralysis.

An elderly patient at high risk for fractures due to severe osteoporosis and other spinal pathology was treated with electroconvulsive therapy (ECT). Suppression of twitch response to peripheral nerve stimulation over the ulnar nerve was a more accurate monitor of degree of paralysis than other clinical indices. Complete paralysis was consistently achieved using this method. Successive doses of succinylcholine were not required with multiple treatments per session when the nerve stimulator was used to verify continued paralysis.

Journal Article↗
PubMed1999

Insulin-like growth factor-I promotes nerve regeneration through a nerve graft in an experimental model of facial paralysis.

Among the pathological sequelae of facial paralysis is a paralytic eye. Apart from the psychological and aesthetic deficits, facial paralysis if left untreated can lead to dryness, ulceration and eventual blindness. Although numerous restorative microsurgical approaches have been introduced to address the sequelae of this problem, complete restoration of function to denervated facial muscles remains elusive.Utilizing the rat model of facial paralysis the present research has as an objective to examine a dual treatment approach. Specifically, this study combined the current microsurgical treatment of the cross-facial nerve graft with local administration of insulin-like growth factor I (IGF-I).The efficacy of this combined approach (cross-facial nerve graft + IGF-I) was assessed in the following ways: (a) behavior measurement of the blink response and (b) histomorphometry light and electron microscopy of the entire nerve graft. These data will help provide insight into the restoration of facial muscle function after trauma and assist in the future development of more potent treatment strategies.7he local adnünistration of IGF-I (50 micro g/ml) to the cross-facial nerve graft was found to restore the blink response faster and to strengthen the degree of eye closure. Light microscopy examination revealed that IGF-I significantly enhanced axonal regeneration within a nerve graft (a 22% increase in the mean number of axons), and increased the mean nerve fiber diameter and myelin thickness. Electron microscopy assessment of the nerve grafts demonstrated that the IGF-I treated grafts possessed a greater density of microtubules, which were evenly distributed within the axoplasm.

Journal Article↗
PubMed1977

Effect of concanavalin A on lymphocyte interactions involved in the antibody response to type III pneumococcal polysaccharide I. Comparison of the suppression induced by con A and low dose paralysis.

Concanavalin A (Con A) administered at the time of immunization induces suppression of the in vivo splenic plaque-forming cell (PFC) response to type III pneumococcal polysaccharide (SSS-III). As with low dose paralysis of the PFC response to SSS-III, Con A-induced suppression could not be demonstrated in congenitally athymic (nu/nu) mice and could be eliminated partially by treatment with anti-lymphocyte serum (ALS). The kinetics for Con A-induced suppression paralleled those for low dose paralysis of the antibody response to SSS-III. These findings support the view that Con A-induced suppression is produced in vivo by suppressor T cells and that this form of suppression shares with low dose paralysis a common pathway through which suppression is mediated.

Animals↗
PubMed2004

Thyrotoxic periodic paralysis in a Maori patient.

A case of thyrotoxic periodic paralysis (TPP) in a patient of Maori heritage is described. The epidemiology, aetiology and pathogenesis of TPP are discussed. The case demonstrates that neurological examination and biochemical findings may be normal between episodes of paralysis. Given that there is much racial variation in the prevalence of TPP, and the suggestion that non-thyrotoxic periodic paralysis may be more prevalent in Maori, the case highlights the need for more research into the prevalence and pathogenesis of TPP in Maori patients.

Adult↗
PubMed2005

Cognitive paralysis in an emergency: the role of the supervisory attentional system.

Many witnesses attest that victims of a disaster often perish because they 'freeze' in the face of danger. It has been proposed that this cognitive paralysis occurs due to temporal and cognitive constraints on survival response times while leaving open the question of which cognitive component is implicated in this behavior. This paper proposes, firstly, that the temporal constraints which occur during an emergency inhibit the functioning of the supervisory attentional system (SAS), which leads to the victim showing: (1) an appropriate response, if trained; (2) stereotypical or otherwise irrational behavior, if untrained; or (3) cognitive paralysis. Secondly, that the main role of the SAS is to operate as a temporal buffer, enabling a survival response to be prepared prior to facing a life-threatening event and not as a real-time immediate responder. It is argued that the initial cognitive paralysis differs at the cognitive and neurological levels from the more prolonged hypoactive behavior commonly seen in victims rescued from disasters and which is considered to be a form of disassociative reaction.

Cognition↗
PubMed2005

[Acute divergence paralysis in the Miller Fisher syndrome].

We experienced a 53-year-old man diagnosed as Miller Fisher syndrome (MFS) associated with anti-GQ1b and anti-GT1a antibodies. He presented acute divergence paralysis, bulbar palsy, ascending hyperesthesia, areflexia and diminished vibration sense. External ophthalmoplegia and convergence paralysis were not seen, but he noticed double vision when looking at an object from the distance of more than 70 cm away on a day 10 of hospitalization. Hess chart test revealed an esotropic pattern, so the diagnosis of divergence palsy was made. Brain MRI was normal. Neurological deficits were treated with plasma exchange, resulting in favorable outcome. Divergence paralysis could be one of the clinical manifestations for MFS and might be due to nuclear or supranuclear damge of vergence-related neurons.

Acute Disease↗
PubMed2006

[Comment of the criteria for assessment of therapeutic effects of acupuncture and moxibustion on spastic paralysis of apoplexy].

Acupuncture and moxibustion have obvious therapeutic effect on spastic paralysis of apoplexy, but there is no common standard for evaluation of therapeutic effects. Available standards for assessment of therapeutic effect of acupuncture and moxibustion on spastic paralysis of apoplexy are not complete. Acupuncture and moxibustion improve clinical symptoms of the patient of spastic paralysis of apoplexy to a considerable degree, a evaluation system for results of clinical symptoms of the patient can be set up, so as to perfect the criteria for evaluation of therapeutic effects of acupuncture and moxibustion on this disease.

Acupuncture↗
PubMedDate not supplied

Community ambulation by children with myelomeningocele and high-level paralysis.

It has frequently been noted that high-level paralysis precludes community ambulation for children with myelomeningocele. Of the 87 children in our population with high-level paralysis, however, 45 (52%) did achieve community ambulation by 5 years of age, while 42 (48%) did not. There was no significant difference between these two groups by sex, shunt status, scoliosis, or hip surgery prior to 5 years of age. Among the community ambulating group, there were significantly (p less than 0.001) more children who were not retarded, had received physical therapy for walking, and had compliant parents. We concluded, therefore, that community ambulation is a realistic goal for many children with myelomeningocele and high-level paralysis.

Adolescent↗
PubMed1977

[Hypokalemic familial periodic paralysis with basal electrocardiographic changes].

The authors report the case of an 18 year old girl with nocturnal tetraplegia. There was a family history of Westphal periodic paralysis, and a past history of transient paralysis two years previously. The serum potassium was 2.3 mEq/l. The patient was cured by intravenous drip of potassium chloride. There was a reactionary hyperinsulinism. The red cell potassium was lowered. There was a fall in the exchangeable and total potassium pool. The E.C.G. changes; observed during the acute attack of paralysis, persisted afterwards, which is unusual.

Adolescent↗
PubMed1989

[Hypokalemic periodic paralysis in thyrotoxicosis].

For the first time in Bulgaria a case of hypokalemic periodic paralysis in thyrotoxicosis is described. Three periods of paralysis were observed and documented in a hospital. The thyrotoxicosis was well manifested with disturbed carbohydrate tolerance and responded favourably to methizole treatment. It is suggested that the mechanism for the development of the hypokalemic periodic paralysis is the intracellular blockade of potassium by the surplus of thyroid hormones.

Adult↗
PubMed1977

[Acute isolated vestibular paralysis. A clinical and electronystagmographic follow-up study in 28 patients].

Twenty-eight patients with unilateral acute vestibular paralysis (vestibular neuronitis) were examined after a period of 4-140 months. Seventeen of these patients were examined by electronystagmography with caloric stimuli at 44 degrees, 30 degrees, 17 degrees and 0 degrees C. Most were free of subjective symptoms only one-third had slight unsteadiness after sudden head movement. Subjective symptoms were independent of the presence of permanent canal paralysis or partial recovery of caloric excitability. Spontaneous nystagmus of 3-6,6% intensities was found in 11 of 17 patients. The normal limit for physiological spontaneous nystagmus should therefore be below 3 degrees/s. The most reliable parameter was the maximum velocity of the slow phase, as a mean value of the 4 caloric responses (values corrected for spontaneous nystagmus). The results were: 6 patients with persistent canal paralysis; 4 patients with considerable hypoexcitability; and 7 patients with moderate hypoexcitability. In no patient complete restoration of normal caloric response was found. This is attributed to the described method of caloric testing, which permits exact measurement of small side differences in excitability.

Acute Disease↗
PubMed1988

Thyrotoxic periodic paralysis in a hispanic man.

Thyrotoxic periodic paralysis occurs much more frequently in Orientals than in whites, and has rarely been reported in patients of Hispanic descent. A 28-year-old Mexican man presented with acute onset of bilateral lower extremity weakness after ingestion of a large carbohydrate meal. Laboratory investigation revealed severe hypokalemia, with a serum potassium level of 2.1 mmol/L (2.1 mEq/L), and hyperthyroidism. Administration of potassium chloride resulted in normalization of the serum potassium level and resolution of muscle weakness. Treatment with propranolol, and subsequent restoration of a euthyroid state with iodine 131, was effective in preventing further episodes of paralysis. Thyrotoxic periodic paralysis, although rare, may occur in Hispanic patients, and should be considered in the differential diagnosis of muscle weakness in this population.

Adult↗
PubMed1984

Familial hyperkalemic periodic paralysis and bipolar disorder: a linkage and treatment study.

Familial hyperkalemic periodic paralysis and bipolar disorder are both hereditary disorders, characterized by episodes of illness separated by periods of remission, and possibly related to abnormalities in cellular ion transport. Recently we discovered a patient who suffered from both illnesses, as did his mother and grandmother. However, a detailed investigation of the pedigree suggested that these two disorders are not linked genetically. Furthermore, a placebo-controlled double-blind trial of lithium carbonate in this patient found lithium ineffective in preventing the attacks of paralysis, in contrast to another recent study which found lithium effective in hypermagnesemic periodic paralysis.

Adult↗
PubMed1981

Hypokalemic periodic paralysis in Sjögren's syndrome.

A 30-year-old woman had scleroderma, Sjögren's syndrome, deforming polyarthritis, distal renal tubular acidosis, hypokalemic periodic paralysis, and persistent mild myopathy. During a five-year period the patient's otherwise mild course of disease was complicated by the occurrence of five episodes of severe flaccid muscle paralysis involving both proximal and distal muscle groups. Between the paralytic episodes the patient functioned well without replacement therapy, and had normal potassium levels. The sicca component was mild and went unrecognized for several years. There was no family history of muscle disease. The data presented in this report support the view that the paralytic episodes were due to hypokalemia secondary to renal tubular acidosis associated with Sjögren's syndrome. Hypokalemic periodic paralysis may occur as a rare complication of Sjögren's syndrome and renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed1981

Childhood recurrent idiopathic paralysis of the lateral rectus.

Five case histories are discussed to emphasize the features of childhood recurrent idiopathic paralysis of the lateral rectus (CRIPLR). These features include (1) at least one recurrence of the paralysis, (2) a paralysis that may be so brief as to be overlooked or ignored; (3) lack of serious sequelae similar to lateral rectus dysfunction following viral illness; (4) left-sided involvement; and (5) the idiopathic nature of CRIPLR reflecting our inability to discover a cause.

Abducens Nerve↗
PubMed1980

[Hypokalemic periodic paralysis. Report of two cases (author's transl)].

The familial periodic hypokalemic paralysis is an infrequent disease characterized by paralytic attacks of sudden appearance affecting the muscles of the trunk and limbs. There is a marked hypokalemia during the paralytic episodes of the disease, and a family history in 80 percent of the cases. The differential diagnosis includes hyperthyroidism with periodic paralysis, congenital paramyotony and adynamia episodica hereditaria. Two typical cases of hypokalemic periodic paralysis are presented, with biological, electrophysiological, clinical, and ultrastructural pictures characteristics of the disease. The clinical manifestations of both patients are discussed, stressing the diagnostic importance of the electrophysiological study during the insulin test, and the interest of the histologic and ultrastructural studies. The spectacular response during the acute episodes to the intravenous perfusion of potassium salts, and the usefulness of the acetazolamide administration to prevent the paralytic episodes are emphasized.

Adolescent↗