Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of physiotherapy, occupational therapy, and speech therapy for patients with stroke was investigated, and the three treatments were compared. Out of 135 patients with stroke surviving at two weeks, 107 received physiotherapy, but only 35 received occupational therapy and 19 speech therapy. Those who received most physiotherapy were the most severely disabled and had the worst prognosis, and, although almost no recovery occurred after six months, 30 patients continued with treatment beyond this time. Stiff and painful shoulders were present in 21 of the patients by two weeks and had developed in a further 37 by one year. Physiotherapy did not prevent this. The objectives of physiotherapy for patients with stroke need careful definition, with emphasis on treatment in the early months. Alternative treatment, possibly carried out by volunteers or more simply trained personnel, merits further consideration.
 ...
PMID:How much physical therapy for patients with stroke? 64 53

The effects of impact timing during the cardiac cycle on the sensitivity of the heart to impact-induced rupture was investigated in an open-chest animal model. Direct mechanical impacts were applied to two adjacent sites on the exposed left ventricular surface at the end of systole or diastole. Impacts at 5 m/s and a contact stroke of 5 cm at the end of systole resulted in no cardiac rupture in seven animals, whereas similar impacts at the end of diastole resulted in six cardiac ruptures. Direct impact at 15 m/s and a contact stroke of 2 cm at the end of either systole or diastole resulted in perforationlike cardiac rupture in all attempts. At low-impact velocity the heart was observed in high-speed movie to bounce away from the impact interface during a systolic impact, but deform around the impactor during a diastolic impact. The heart generally remained motionless during the downward impact stroke at high-impact velocity in either a systolic or diastolic impact. The lower ventricular pressure, reduced muscle stiffness, thinner myocardial wall and larger mass of the filled ventricle probably contributed to a greater sensitivity of the heart to rupture in diastole at low-impact velocity. However, the same factors had no role at high-impact velocity.
 ...
PMID:Effect of timing and velocity of impact on ventricular myocardial rupture. 684 95

Tennis elbow afflicts 40% to 50% of the average, recreational tennis players; most of these players more than 30 years of age. Tennis elbow is thought to be the result of microtrauma, the overuse and inflammation at the origin of the ECRB as a result of repeated large impact forces created when the ball hits the racket in the backhand stroke. Several authors have found that EMG activity in the ECRB, the muscle and tendon complex afflicted in tennis elbow, is high during the acceleration and early follow-through phases of the groundstrokes and during the cocking phase of the serve. Unfortunately, none of the authors gave evidence to support the claim that muscle activity in the ECRB at ball contact is high. In the one-handed backhand, the torques at impact (17-24 nm) will be absorbed by the tendons of the elbow. Giangarra and his colleagues observed that the two-handed backhand "allows the forces at ball impact to be transmitted through the elbow rather than absorbed by the tissues at the elbow." Other authors have reported that players using a two-handed backhand will rarely develop lateral epicondylitis, because the helping arm appears to absorb more energy and changes the mechanics of the swing. As seen by Morris and colleagues, Giangarra and associates, and Leach and colleagues, players who utilize the two-handed backhand have a very low incidence of tennis elbow. These three studies conclude that the two-handed backhand stroke is probably the most effective backhand stroke to prevent lateral tennis elbow. Studies show that wrist extensors are highly involved in all strokes (serve, forehand, and both one- and two-handed backhand strokes). This relatively high involvement (40%-70% MVC) throughout play may result in overload of this muscular group. Thus, tennis elbow may be caused simply by continued use of this muscular system in all strokes, and not just because of the high forces absorbed at impact. Another theory concerning impact states that if the extensor group is already at near maximum contraction, vibrations and twisting movements are transferred directly through the muscle (muscle stiffness at this point would be great) to the tendinous insertion, causing repeated microtrauma. If the muscle is the stiffest element in the system, the force will be transferred to the tendon. It is evident that a need exists for specific study of muscular response during impact. More microanalysis of the impact phase needs to be conducted specifically for the one-handed backhand groundstroke.
 ...
PMID:The biomechanics of tennis elbow. An integrated approach. 771 57

The aims of this study were to determine whether changes in the non-reflex component of spastic plantarflexors had developed 2 and 4 months after stroke and to study their relationship with the level of impairment. One group of adults with hemiparesis (HPs) was tested 2 and 4 months after the onset of stroke, and data were compared with a control group (CTLs) tested once. Twenty-two patients (14 males) admitted over a 4-month period in a rehabilitation centre (mean = 62 yrs +/- 14), and 11 (6 males) non-disabled (CTLs) subjects (mean = 57yrs +/- 12.8) agreed to participate in the study. The resistive torque (RT) recorded with a myometer during slow (8-10 degrees/s) passive dorsiflexions imposed manually served as the primary outcome, whereas, the Ashworth score (spasticity), ankle ROM and Fugl-Meyer motor subscore were used as secondary measures to determine the level of impairment. The mean RT values measured at 0 degrees dorsiflexion on the affected and unaffected sides were compared with those in CTLs. As expected, the RT values 2 and 4 months post-stroke on the unaffected side did not differ from corresponding values in CTLs. Significantly higher RT values on the affected side when compared to the unaffected side were found both at 2 months (39%; p < 0.05) and at 4 months (43%; p < 0.01). No significant difference existed on the affected side between the 2nd and 4th months. A high (r = 0.80) and significant (p < 0.0001) correlation coefficient was calculated between the changes in RT values recorded at 2 and 4 months. Low and not significant correlations were computed between these RT changes and factors such as the ROM (r = -0.24), the Ashworth score (r = 0.23) and the Fugl-Meyer lower extremity motor subscore (r = -0.26). Present results indicate that: (1) changes in the non-reflex component are already present 2 months after stroke but do not increase significantly between the 2nd and 4th months; (2) these changes are not related to the level of impairment; and (3) myometry testing at 2 months could be used as a preventive measure to detect patients more at risk of developing severe passive muscle stiffness.
 ...
PMID:Non-reflex mediated changes in plantarflexor muscles early after stroke. 927 Nov 48

Stiff-legged gait, characterized by limited knee flexion during the swing period, is a common consequence of upper motor neuron injury. The purpose of this investigation was to determine whether the rectus femoris and hamstrings muscles (which act at both the hip and knee) contribute to stiff-legged gait if active during the swing period of the gait cycle. Ten subjects with unilateral stiff-legged gait due to stroke were evaluated. Swing period free gait data were obtained. A biomechanical model of the affected limb was developed for each subject. Muscle and tendon lengths were scaled to individual subjects while constant nominal values for maximum muscle forces were used for all subjects. Torque driven forward dynamic simulations were employed to determine the sensitivity of swing period maximum knee flexion angle to changes in hip and knee torques. Combined torque and muscle driven simulations were used to access the action of specific two-joint muscles. Both hip flexion torque and knee extension torque were found to influence knee angle, but knee angle was more sensitive to changes in torque at the knee joint. The actions of the rectus femoris and long hamstrings are most marked at the knee, although their action at the hip opposes their action at the knee. Rectus femoris activity during early swing acts to limit knee flexion and contributes to stiff-legged gait. Long hamstring activity in early swing contributes to knee flexion.
 ...
PMID:Torque action of two-joint muscles in the swing period of stiff-legged gait: a forward dynamic model analysis. 980 84

The mitochondrial mutation A-->G at nucleotide position 3243 is associated with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and other mitochondrial encephalomyopathies. We found this mutation in a 61-year-old patient who developed at the age of 54 a myopathy with painful muscle stiffness as the predominant symptom. Additionally hypacusis, a mild hemisensory syndrome and impaired glucose tolerance were present. Muscle histopathology showed few ragged red fibers. The mutation was detected heteroplasmatically in DNA from muscle and blood. So far painful muscle stiffness has not been a known phenotype of the 3243 mutation.
 ...
PMID:Mitochondrial 3243 A-->G mutation (MELAS mutation) associated with painful muscle stiffness. 1040 50

The proposed model is characterized by the constant r (Eq. 2-1), the induced potential (Fig. 1), two attached states of a myosin head (Fig. 1), the nonlinear elastic property of the crossbridge (Eq. 2-7), and the expression of U* (Eqs. 3-8 and 3-9), which led us to the following conclusions. 1. The following various magnitudes of myosin head motion are compatible with each other: about 2 nm of the quantity called power stroke by Irving (27), which is the mean moving distance of myosin head in the isometric tension in our model, 4-5 nm of the displacement of a single myosin head during one ATP hydrolysis cycle (Molloy et al. (20)) or a few tens of nm when the actin and myosin filaments are set parallel (Tanaka et al. (21) and Kitamura et al. (42)), and more than 200 nm of the myosin head displacement in a multi-myosin head system below 22 degrees C (Harada et al. (19)). 2. There is one-to-one coupling between the ATP hydrolysis cycle and the attachment-detachment cycle of a myosin head in accordance with the generally accepted concept of chemical reactions, since the head is trapped in the spatially shifting wide potential well (Fig. 1) until epsilon ATP is exhausted. Here, an actin filament interacts with a myosin head like a single molecule. 3. The calculated tension dependence of muscle stiffness agrees well with the observations by Ford et al. (12), as shown in Fig. 9. 4. The calculated shortening velocity V of muscle as a function of P/P0 agreed very well with experimental results as shown in Fig. 13. The deviation from the Hill equation (34) observed by Edman (32) is related with U* being effectively infinite for f1 < kappa b yc0 (Fig. 10). 5. Calculated energy liberation rate W + H as a function of P/P0 has characteristics almost the same as the Hill equation (33), and agrees well with the experimental results as shown in Fig. 14. 6. The time course of tension recovery after a quick length change is determined by four parameters: kappa f, kappa b, a, and Z0. Among them, kappa f, kappa b (Eq. 2-22) and a (Eq. 4-21) are readily determined by analysis of the steady filament sliding and p0. Calculations of T1/T0 and T2/T0 with these three parameters are in very good agreement with experimental data (Fig. 21). Calculated tension variations by assigning the value in Eq. 4-23 to Z0 agree with the observation (Fig. 17). 7. The model suggests that large fluctuations exist in relative positions between the actin and myosin filaments even when the load on a muscle is kept constant (Fig. 23). Taking this fluctuation into account, the time course of the isotonic velocity transient shown in Fig. 22 becomes understandable referring to Fig. 24. 8. The experimental data of the delta yhs vs. delta P/P0 relationship (Fig. 25) is explained. The delta yhs value at delta P/P0 = 0 (about 5 nm) supports the two-attached-state model and thus indicates that the incremental unit step of a myosin head motion along an actin filament is close to L (5.46 nm).
 ...
PMID:Induced potential model of muscular contraction mechanism and myosin molecular structure. 1046 74

The objective of this study was to investigate muscle and tendon stiffness in the triceps surae muscles in patients who had previously had a stroke. The participants were 12 men showing slight to moderate degrees of muscle tonus in the affected leg. All patients showed minimal or no overt clinical motor symptoms, and all walked without mechanical aid. Muscle strengths in isometric and isokinetic activities were measured, as was passive resistance during plantarflexion in each leg. Walking speed was also measured. Evaluations of physical performance and muscle tone were made. Muscle and tendon stiffness was calculated from measurements whilst passively stretching during electrical stimulation, separately for each leg. Muscle strength was significantly higher in the non-affected than in the affected leg. Muscle stiffness was significantly higher in the affected leg than in the non-affected leg. Tendon stiffness was significantly higher in the non-affected than in the affected leg. The higher muscle stiffness in the affected leg might enhance the possibility for storing elastic energy during preactivation. Lower tendon stiffness in the affected leg might reduce the development of fatigue in movements at low velocities.
 ...
PMID:Muscle and tendon stiffness in patients with upper motor neuron lesion following a stroke. 1095 69

In the mammalian heart the metabolic costs of pressure loading exceed those of volume loading. As evidence suggests that the opposite may be true in fish, we evaluated the metabolic costs of volume and pressure loading in the isolated trout heart and compared the results with the mammalian heart based on the biomechanical properties of cardiac muscle. The highest power output (2.33+/-0.32 mW g(-1), n=5) appeared at the highest preload pressure tested (0.3 kPa) and at an afterload of 5 kPa. At a higher afterload, power did not increase because stroke volume fell. The highest mechanical efficiency (20.7+/-2.0%, n=5) was obtained at a preload of 0.15 kPa and an afterload of 5 kPa. Further increases in preload or afterload did not increase mechanical efficiency, probably because of increases in ventricular wall stress which increased the oxygen consumed disproportionately more than the stroke work. Under pressure unloading (25% decrease in power output), mechanical efficiency was significantly higher in comparison with volume unloading. Given that stiffness of the ventricular tissue is larger in trout than in rat papillary muscles, it is suggested that the increased strain during volume loading is energetically disadvantageous for stiff muscles like those of trout, but it is advantageous when muscle stiffness is lower as it occurs in the rat papillary muscle.
 ...
PMID:Mechanical efficiency of the trout heart during volume and pressure-loading: metabolic implications of the stiffness of the ventricular tissue. 1219 9

Spasticity is an abnormal increase in muscle contraction often caused by damage to central motor pathways that control voluntary movement. During clinical examination, spasticity manifests as an increase in stretch reflexes, producing tendon jerks and resistance appearing as muscle tone. There are many causes of spasticity, including demyelination from multiple sclerosis, congenital damage from diseases such as cerebral palsy, trauma to the brain or spinal cord, hemorrhage or infarction, and other pathologic conditions that interrupt neural pathways. Effects of spasticity range from mild muscle stiffness to severe, painful muscle contractures and repetitive spasms that reduce mobility and substantially impede normal activities of daily living. Botulinum toxin therapy reduces spasticity and pain associated with several disorders. Local treatment with botulinum toxins can be used as adjunctive therapy, along with oral antispasticity medications, or alone to provide localized decrease in symptoms of spasticity and pain. Botulinum toxin therapy may be particularly useful for patients with spasticity due to stroke, whose treatment can be tailored based on recovery of function over time. In addition, botulinum toxin therapy is safe for pediatric patients, including children with cerebral palsy, who may not be able to tolerate the cognitive side effects of oral medications. Results of studies evaluating botulinum toxin for the treatment of spasticity due to various causes are presented here.
 ...
PMID:Treatment of spasticity with botulinum toxin. 1256 67


1 2 3 4 Next >>