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At least 1,801 records · Page 100Linked to original sources
PubMed2006

Vascularised bone grafts for the management of non-union.

Non-union of the long bones may have severe consequences, particularly when combined with other post-traumatic sequelae, such as tendon adhesions, reflex sympathetic dystrophy and infection, among others. In these cases, it is important to treat the delayed union or non-union first or at the same time with the other problems in order to achieve adequate function. Once the normal bony healing process has been slowed or stopped, it is necessary to provide both stability to the fracture site, as well as a biological stimulus for the fibrocartilagenous callus to finish the healing process. Vascularised grafts, such as the free fibula, offer not only structural support, but also promote bone healing. The later is achieved by trabecular bone formation, as well as vascular sprouting from pedicle vessels.

Bone Transplantation↗
PubMed1997

Neurophysiology of gait disorders: present and future applications.

This article will review those electrophysiological investigations which have addressed the neuronal mechanisms underlying impaired gait. The aims of the review are to provide further insights to the underlying pathophysiology of impaired gait and also towards the selection of an appropriate treatment. From the patients' point of view the first indication of a central motor system lesion is an impairment of movement, most notably locomotion. These symptoms are characteristic in cases of spasticity, cerebellar lesion or Parkinson's disease. Clinical examination reveals typical changes in tendon tap reflexes and muscle tone which were believed to account for the movement disorder presented. However, we now know that there is only a weak relationship between the physical symptoms observed during clinical examination under passive motor conditions and the altered neuronal mechanisms underlying the impairment during active motion. By recording and analysing electrophysiological and biomechanical parameters during functional movements such as locomotion, the significance of impaired reflex behaviour or the pathophysiology of muscle tone and its contribution to the movement disorder can be reliably assessed. Consequently, the treatment should not be cosmetic, i.e. the correction of an isolated clinical parameter, but should be based on the pathophysiology and significance of those mechanisms underlying the impairment of the patients' movements. Data from electrophysiological and biomechanical investigations of locomotion of patients with spasticity, cerebellar disorder or Parkinson's disease are discussed in this review. The neuronal mechanisms, which are essentially central programs and afferent input, involved in disorders of gait are evaluated on the basis of their function in healthy subjects. The impact of this analysis in deciding an appropriate treatment are discussed with respect to the pathophysiology underlying the gait disorder (spasticity, cerebellar disorder or Parkinson's disease). At the present time we have only a basic understanding of the essential receptor systems, such as leg extensor load receptors, and their interaction with other systems involved in postural control. In the future, the knowledge gained from gait analysis may help in the selection of the appropriate pharmacological and physical treatment required even though the patient may only be at an early stage of motor impairment.

Ataxia↗
PubMed2000

[Basic principles and therapy of spasticity].

An acute central nervous system lesion is followed by a phase of "shock" with flaccid muscle tone. After some weeks the syndrome of spastic paresis develops which is characterized by increased muscle tone and exaggerated tendon tap reflexes. During the last years it could be shown that the characteristic spastic movement disorder is mainly due to secondary changes of muscle properties which require a specific treatment. Exaggerated reflexes do only little contribute to the movement disorder.

Acute Disease↗
PubMed2005

Effect of a single dose of levodopa on sexual response in men and women.

From animal research, there is ample evidence for a facilitating effect of dopamine on sexual behavior. In humans, little experimental research has been conducted on the inter-relation between dopamine and sexual response, even less so in women than in men. We investigated the effect of levodopa (100 mg) on sexual response in men and women following a double-blind, placebo-controlled crossover design. Genital and subjective sexual responses were measured as well as somatic motor system activity by means of Achilles tendon (T) reflex modulation. Genital and subjective sexual arousal were not affected by levodopa. However, the drug increased T reflex magnitude in response to sexual stimulation in men, but not in women. These results support the view that dopamine is involved in the energetic aspects of appetitive sexual behavior in men. The observed gender difference in the effect of levodopa is discussed in the perspective of possible dopamine-steroid interaction.

Adolescent↗
PubMed2000

Spastic movement disorder.

This review deals with the neuronal mechanisms underlying spastic movement disorder, assessed by electrophysiological means with the aim of first, a better understanding of the underlying pathophysiology and second, the selection of an adequate treatment. For the patient usually one of the first symptoms of a lesion within the central motor system represents the movement disorder, which is most characteristic during locomotion in patients with spasticity. The clinical examination reveals exaggerated tendon tap reflexes and increased muscle tone typical of the spastic movement disorder. However, today we know that there exists only a weak relationship between the physical signs obtained during the clinical examination in a passive motor condition and the impaired neuronal mechanisms being in operation during an active movement. By the recording and analysis of electrophysiological and biomechanical parameters during a functional movement such as locomotion, the significance of, for example, impaired reflex behaviour or pathophysiology of muscle tone and its contribution to the movement disorder can reliably be assessed. Consequently, an adequate treatment should not be restricted to the cosmetic therapy and correction of an isolated clinical parameter but should be based on the pathophysiology and significance of the mechanisms underlying the disorder of functional movement which impairs the patient.

Humans↗
PubMed1975

Vibratory stimulation. Part II. Vibratory stimulation as an evaluation tool.

Phasic neural mechanisms are heavily involved in volitional movements, where as tonic mechanisms support postural adjustments. Yet, the two systems are so intimately related that any disturbance in one will exert profound effects on the other. Whether one system or the other is involved preferentially in different neural disorders is not known; hence, tests are needed to evaluate phasic and tonic functions independently. In this article, the classical applications of the tendon jerk reflex and H-response for assessing phasic mechanisms are first reviewed. Following this review, the tonic stretch reflex and tonic vibration reflex (TVR) are analyzed and compared. The effects of experimentally ablating or stimulating precise brain regions are described as a means of revealing the role of supraspinal mechanisms in the TVR. Finally, the responses to vibratory stimulation in specific motor disorders are examined and discussed as to their usefulness in prognosis and diagnosis.

Cerebellar Diseases↗
PubMedDate not supplied

Treatment of spasticity with botulinum toxin.

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.

Botulinum Toxins↗
PubMed1997

Positive force feedback control of muscles.

This study was prompted by recent evidence for the existence of positive force feedback in feline locomotor control. Our aim was to establish some basic properties of positive force feedback in relation to load compensation, stability, intrinsic muscle properties, and interaction with displacement feedback. In human subjects, muscles acting about the wrist and ankle were activated by feedback-controlled electrical stimulation. The feedback signals were obtained from sensors monitoring force and displacement. The signals were filtered to mimic transduction by mammalian tendon organ and muscle spindle receptors. We found that when muscles under positive force feedback were loaded inertially, they responded in a stable manner with increased active force. The activation attenuated the muscle stretch (yield) that would otherwise occur in the absence of feedback. With enough positive force feedback gain, yield could actually reverse. This behavior, which we termed the affirming reaction, was reminiscent of the mammalian positive supporting reaction, a postural response elicited by contact of the foot with the ground. Muscles under positive force feedback remained stable, even when the loop gain (Gf) was set at levels of 2 or 3. In a linear system, if Gf > 1, instability occurs when the loop is closed. On further investigation, we found that Gf changed with joint angle: it declined as the load-bearing muscle actively shortened. We inferred that in closed-loop operation, the active muscles always shortened until Gf approached unity. In other words, the length-tension curve of active muscle ensures stability even when force-related excitation of motoneurons is very large. Concomitant negative displacement feedback reinforced and stabilized load compensation up to a certain gain, beyond which instability occurred. In further trials we included delays of up to 40 ms in the positive force feedback pathway, to model the delays recently described for tendon organ reflexes in cat locomotion. Contrary to expectations, this did not destabilize the loop. Indeed, when instability was deliberately evoked by setting displacement feedback gain high, delays in the positive force feedback pathway actually stabilized control. The stabilization of positive force feedback by inherent properties of the neuromuscular system increases the functional scope to be expected of feedback from force receptors in biological motor control. Our results provide a rationale for the delayed excitatory action of Ib heteronymous input on extensor motoneurons in cat locomotion.

Adult↗
PubMed2003

[A case of amyotrophic lateral sclerosis with dementia presenting long clinical course].

We describe a patient with amyotrophic lateral sclerosis with dementia (ALS-D) displaying a long clinical course. A 68-year-old Japanese male with no family history of note was admitted complaining of severe dysarthria and dysphagia. At 63 years old, Pick's disease was diagnosed on the basis of abnormal behavior, such as "Denkfaulheit" and moria, and temporal lobe atrophy observed on magnetic resonance imaging (MRI). Five years after onset, dysarthria and dysphagia emerged, and gradually worsened. On admission, muscular weakness of the upper extremities, fasciculation, and exaggerated tendon stretch reflexes were noted. Needle electromyography performed on the left upper and lower extremities revealed neurogenic pattern changes. Based on these findings and clinical course, ALS-D was diagnosed. Due to severe bulbar palsy, verbal communication was impossible. However, neither specific symptoms of dementia nor abnormal behavior was demonstrated, although this latter had been observed 5 years ago, with only short-term memory impairment apparent. MRI disclosed severe knife-edge atrophy of bilateral temporal lobes, most prominently in the anterior regions. SPECT images revealed decreased uptake of tracer in bilateral inferior temporal lobes, predominantly on the left side. The patient died suddenly 4 months after admission, and post-mortem examination was not conducted. Total clinical course was about 8 years. Several cases of ALS-D have displayed similar clinical courses to the presented case. Some of these would also have initially been diagnosed as Pick's disease. We speculate that cases displaying psychiatric symptoms for several years and initially diagnosed as Pick's disease may finally be diagnosed as ALS-D upon the eventual emergence of motor symptoms(bulbar palsy).

Aged↗

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