Tight hamstring syndrome and extra- or intraspinal diseases in childhood: a multicenter study.
(17/79)
Tight hamstrings syndrome (THS) has been attributed to a number of disorders. Most authors argue that tight hamstring syndrome is determined in the majority of cases by a protruding or slipped vertebral disc. The term "disc related tight hamstring syndrome" is usually used to describe the condition. However, tight hamstring syndrome in childhood can also be an initial symptom of a usually severe disease. We reviewed retrospectively 102 children who had presented to our clinics with tight hamstring syndrome in the past 22 years (between 1980 and 2001). To our knowledge, this study includes the largest number of patients with tight hamstring syndrome analysed so far. Seventy four children (73%) suffered from severe underlying diseases. In more than one-third of all THS cases (38 of 102 cases; 37%), we observed intra- or extraspinal tumorous alterations. In 15% of the cases (15 of 102), osteomyelitis or spondylodiscitis was diagnosed. Only in 27% of the cases (28 of 102), disc protrusion, one of the commonly known underlying diagnoses (14 cases), or higher-grade spondylolisthesis/spondyloptosis (14 cases) were the inciters. Our results suggest that tight hamstring syndrome in childhood can be an initial symptom of an associated, usually severe disease. We conclude that therefore further diagnostic evaluation is required when tight hamstring syndrome is observed. A rapid initiation of an adequate primary therapy could be indicated. (+info)
Long-term effect of shock wave therapy on upper limb hypertonia in patients affected by stroke.
(18/79)
BACKGROUND AND PURPOSE: Spasticity is a disabling complication of stroke and different noninvasive treatments are used to reduce muscle hypertonia. Shock waves are defined as a sequence of single sonic pulses largely used in the treatment of diseases involving bone and tendon as well as muscular contractures. The effect and duration of extracorporeal shock wave therapy (ESWT) was investigated on muscle hypertonia of the hand and wrist. METHODS: A total of 20 patients affected by stroke associated with severe hypertonia in upper limbs were evaluated. Placebo stimulation was performed 1 week before active stimulation in each patient. Evaluation was performed using the National Institutes of Health and Ashworth scales and video monitoring with a digital goniometer before and immediately after placebo or active stimulation. Motor nerve conduction velocity from abductor digiti minimi were recorded. Patients were monitored at 1, 4, and 12 weeks after active treatment. RESULTS: After active ESWT, patients showed greater improvement in flexor tone of wrist and fingers compared with placebo stimulation. At the 1- and 4-week follow-up visits, a significant decrease of passive muscle tonicity was noted on muscles in all patients receiving active treatment. At 12 weeks after therapy, 10 of the 20 patients showed persistent reduction in muscle tone. There were no adverse events associated with ESWT. CONCLUSIONS: ESWT reduces hypertonia of the wrist and finger muscles for > or =12 weeks after treatment. The possible mechanisms of action of ESWT are discussed. (+info)
Electromyographic analysis of the orbicularis oris muscle in oralized deaf individuals.
(19/79)
Electromyography has been used to evaluate the performance of the peribuccal musculature in mastication, swallowing and speech, and is an important tool for analysis of physiopathological changes affecting this musculature. Many investigations have been conducted in patients with auditory and speech deficiencies, but none has evaluated the musculature responsible for the speech. This study compared the electromyographic measurements of the superior and inferior fascicles of the orbicularis oris muscle in patients with profound bilateral neurosensorial hearing deficiency (deafness) and healthy volunteers. Electromyographic analysis was performed on recordings from 20 volunteers (mean age of 18.5 years) matched for gender and age. Subjects were assigned to two groups, as follows: a group formed by 10 individuals with profound bilateral neurosensorial hearing deficiency (deaf individuals) and a second group formed by 10 healthy individuals (hearers). Five clinical conditions were evaluated: suction, blowing, lip projection and compression, and production of the syllable "Pa". It was found that the deaf patients presented muscle hyperactivity in all clinical conditions, and that the inferior fascicle of the orbicularis oris muscle showed higher electromyographic activity rates, suggesting the need for a hearing-speech treatment with emphasis on oral motricity. (+info)
Safety and efficacy of tramadol in the treatment of idiopathic detrusor overactivity: a double-blind, placebo-controlled, randomized study.
(20/79)
AIM: To evaluate the efficacy and safety of tramadol in patients with idiopathic detrusor overactivity (IDO). METHODS: A total of 76 patients 18 years or older with IDO were randomly assigned to receive 100 mg tramadol sustained release (group 1, n = 38) or placebo (group 2, n = 38) every 12 h for 12 weeks. Clinical evaluation was performed at baseline and every 2 weeks during treatment. All patients underwent urodynamics and ice water test at baseline and 12-week treatment. Main outcome measures were number of voids per 24 h, urine volume per void and episodes of urge incontinence per 24 h on a frequency volume chart and detailed recording of adverse effect. RESULTS: After 12 weeks of treatment mean number of voids per 24 h +/- SD decreased from 9.3 +/- 3.2 to 5.1 +/- 2.1 (P < 0.001 vs. placebo) [95% confidence interval (CI) -5.1--0.4]. At that time mean urine volume per void increased from 158 +/- 32 to 198 +/- 76 ml (P < 0.001 vs. placebo) (95% CI 8-22), while mean number of incontinence episodes per 24 h decreased from 3.2 +/- 3.3 to 1.6 +/- 2.8 (P < 0.001 vs. placebo) (95% CI -2-0.3). Tramadol induced significant improvements in urodynamic parameters. More adverse effects were associated with tramadol treatment than with placebo (P < 0.05). The main adverse event with tramadol was nausea. CONCLUSIONS: In patients with non-neurogenic IDO tramadol provided beneficial clinical and urodynamic results. Further studies are required to draw final conclusions on the efficacy of this drug in IDO. (+info)
Muscarinic regulation of neonatal rat bladder spontaneous contractions.
(21/79)
In vitro preparations of whole urinary bladders of neonatal rats exhibit prominent myogenic spontaneous contractions, the amplitude and frequency of which can be increased by muscarinic agonists. The muscarinic receptor subtype responsible for this facilitation was examined in the present experiments. Basal spontaneous contractions in bladders from 1- to 2-wk-old Sprague-Dawley rats were not affected by M2 or M3 receptor antagonists. However, administration of 0.5 microM physostigmine, an anticholinesterase agent that increases the levels of endogenous acetylcholine, or 50-100 nM carbachol, a cholinergic agonist at low concentrations, which did not cause tonic contractions, significantly augmented the frequency and amplitude of spontaneous contractions. Blockade of M2 receptors with 0.1 microM AF-DX 116 or 1 microM methoctramine or blockade of M3 receptors with 50 nM 4-diphenylacetoxy-N-methylpiperidine methiodide or 0.1 microM 4-diphenylacetoxy-N-(2-chloroethyl)piperidine hydrochloride (4-DAMP mustard) reversed the physostigmine and carbachol responses. M2 and M3 receptor blockade did not alter the facilitation of spontaneous contractions induced by 10 nM BAY K 8644, an L-type Ca2+ channel opener, or 0.1 microM iberiotoxin, a large-conductance Ca2+-activated K+ channel blocker. NS-1619 (30 microM), a large-conductance Ca2+-activated K+ channel opener, decreased carbachol-augmented spontaneous contractions. These results suggest that spontaneous contractions in the neonatal rat bladder are enhanced by activation of M2 and M3 receptors by endogenous acetylcholine released in the presence of an anticholinesterase agent or a cholinergic receptor agonist. (+info)
Intracranial hemorrhage as the initial manifestation of a congenital disorder of glycosylation.
(22/79)
Intracranial hemorrhage in a term neonate is a rare event in the absence of an identifiable precipitating factor such as severe thrombocytopenia, mechanical trauma, asphyxia, infections, or congenital vascular malformations. Congenital disorders of glycosylation are a genetically and clinically heterogeneous group of multisystem disorders characterized by the abnormal glycosylation of a number of glycoproteins. Although bleeding caused by abnormal glycosylation of various coagulation factors is a well-known clinical complication of several types of congenital disorders of glycosylation, intracranial hemorrhage has not been reported as an initial manifestation of this entity. Here we report the detailed history of a family with 2 consecutive male infants, both born at term with intracranial hemorrhage diagnosed within the first 24 hours of life. The diagnosis of a congenital disorder of glycosylation was established in the second infant by an abnormal glycosylation of serum transferrin detected by electrospray-ionization mass spectrometry. Both infants showed significant neurologic deterioration during the first month of life, and both died at 5 months of age. Intracranial hemorrhage in a term neonate without a potential precipitating factor represents yet another clinical feature that should raise the suspicion for a congenital disorder of glycosylation. (+info)
Neonatal hyperekplexia: the Stiff-Baby syndrome.
(23/79)
Neonatal hyperekplexia is a rare autosomal dominant startle disorder. Presenting soon after birth, it is often mistakenly diagnosed as spastic quadriparesis, epilepsy etc. While the long-term prognosis is relatively benign, sudden death due to severe spasms have been seen in sporadic cases. We report a case of hyperekplexia with some typical and some unusual findings. (+info)
Creatine as a compatible osmolyte in muscle cells exposed to hypertonic stress.
(24/79)
Exposure of C2C12 muscle cells to hypertonic stress induced an increase in cell content of creatine transporter mRNA and of creatine transport activity, which peaked after about 24 h incubation at 0.45 osmol (kg H(2)O)(-1). This induction of transport activity was prevented by addition of either cycloheximide, to inhibit protein synthesis, or of actinomycin D, to inhibit RNA synthesis. Creatine uptake by these cells is largely Na(+) dependent and kinetic analysis revealed that its increase under hypertonic conditions resulted from an increase in V(max) of the Na(+)-dependent component, with no significant change in the K(m) value of about 75 mumol l(-1). Quantitative real-time PCR revealed a more than threefold increase in the expression of creatine transporter mRNA in cells exposed to hypertonicity. Creatine supplementation significantly enhanced survival of C2C12 cells incubated under hypertonic conditions and its effect was similar to that obtained with the well known compatible osmolytes, betaine, taurine and myo-inositol. This effect seemed not to be linked to the energy status of the C2C12 cells because hypertonic incubation caused a decrease in their ATP content, with or without the addition of creatine at 20 mmol l(-1) to the medium. This induction of creatine transport activity by hypertonicity is not confined to muscle cells: a similar induction was shown in porcine endothelial cells. (+info)