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V Dietz - One of the best experts on this subject based on the ideXlab platform.

  • spinal cord lesion effects of and perspectives for treatment
    Neural Plasticity, 2001
    Co-Authors: V Dietz
    Abstract:

    Following central motor lesions, two forms of adaptation can be observed which lead to improved mobility: (1) the development of Spastic muscle tone, and (2) the activation of spinal locomotor centers induced by specific treadmill training. Tension development during Spastic Gait is different from that during normal Gait and appears to be independent of exaggerated monosynaptic stretch reflexes. Exaggerated stretch reflexes are associated with an absence or reduction of functionally essential polysynaptic reflexes. When supraspinal control of spinal reflexes is impaired, the inhibition of monosynaptic reflexes is missing in addition to a reduced facilitation of polysynaptic reflexes. Therefore, overall leg muscle activity becomes reduced and less well modulated in patients with Spasticity. Electrophysiologicai and histological studies have shown that a transformation of motor units takes place following central motor lesions with the consequence that regulation of muscle tone is achieved at a lower level of neuronal organization which in turn enables the patient to walk. Based on observations of the locomotor capacity of the spinal cat, recent studies have indicated that spinal locomotor centers can be activated and trained in patients with complete or incomplete paraplegia when the body is partially unloaded. However, the level of electromyographic activity in the gastrocnemius (the main antigravity muscle during Gait) is considerably lower in the patients compared to healthy subjects. During the course of a daily locomotor training program, the amplitude of gastrocnemius, electromyographic activity increases significantly during the stance phase, while inappropriate tibialis anterior activation decreases. Patients with incomplete paraplegia benefit from such training programs such that their walking ability on a stationary surface improves. The pathophysiology and functional significance of Spastic muscle tone and the effects of treadmill training on the locomotor pattern underlying new attempts to improve the mobility of patients with paraplegia are reviewed.

  • impaired modulation of quadriceps tendon jerk reflex during Spastic Gait differences between spinal and cerebral lesions
    Brain, 1999
    Co-Authors: M Faist, Matthias Ertel, W Berger, V Dietz
    Abstract:

    In healthy subjects, functionally appropriate modulation of short latency leg muscle reflexes occurs during Gait. This modulation has been ascribed, in part, to changes in presynaptic inhibition of Ia afferents. The changes in modulation of quadriceps tendon jerk reflexes during Gait of healthy subjects were compared with those of hemi- or paraparetic Spastic patients. The Spasticity was due to unilateral cerebral infarction or traumatic spinal cord injury, respectively. The modulation of the quadriceps femoris tendon jerk reflex at 16 phases of the step cycle was studied. The reflex responses obtained during treadmill walking were compared with control values obtained during Gait-mimicking standing postures with corresponding levels of voluntary muscle contraction and knee angles. In healthy subjects the size of the reflexes was profoundly modulated and was generally depressed throughout the step cycle. In patients with spinal lesion the reflex depression during Gait was almost removed and was associated with weak or no modulation during the step cycle. In patients with cerebral lesion there was less depression of the reflex size associated with a reduced reflex modulation on the affected side compared with healthy subjects. On the `unaffected' side of these patients reflex modulation was similar to that of healthy subjects, but the reflex size during Gait was not significantly different from standing control values. These observations suggest that the mechanisms responsible for the depression of reflex size and the modulation normally seen during Gait in healthy subjects are impaired to different extents in Spasticity of spinal or cerebral origin, possibly due to the unilateral preservation of fibre tracts in hemiparesis.

  • locomotion in patients with spinal cord injuries
    Physical Therapy, 1997
    Co-Authors: V Dietz, Markus Wirz, Lars Jensen
    Abstract:

    Following central motor lesions, two forms of reorganization can be observed that lead to improved mobility: (1) the development of increased muscle tone and (2) the activation of spinal locomotor centers induced by specific treadmill training. Tension development is different from normal during Spastic Gait and appears to be independent of exaggerated monosynaptic stretch reflexes. Exaggerated stretch reflexes are associated with an absence or reduction of functionally essential polysynaptic reflexes. Based on observations of the locomotor capacity of the spinal cat, recent studies have indicated that spinal locomotor centers can be activated and trained in patients with complete or incomplete paraplegia when the body is partially unloaded. The level of electromyographic activity in the gastrocnemius muscle, however, is considerably lower in patients with central motor lesions than in persons without neurological impairments. During the course of a daily locomotor training program, the amplitude of gastrocnemius muscle electromyographic activity increases during the stance phase and inappropriate tibialis anterior muscle activity decreases. Such training programs can improve the ability of patients with incomplete paraplegia to walk on stationary surfaces. This article reviews the pathophysiology and functional importance of increased muscle tone and the effects of treadmill training on the locomotor pattern underlying new attempts to improve the mobility of patients with paraplegia.

Neeraj Kumar - One of the best experts on this subject based on the ideXlab platform.

  • copper deficiency myelopathy human swayback
    Mayo Clinic proceedings, 2006
    Co-Authors: Neeraj Kumar
    Abstract:

    The hematologic manifestations of copper deficiency are well known and include anemia and neutropenia. In the past few years, the neurological manifestations of acquired copper deficiency in humans has been recognized, the most common being a myelopathy presenting with a Spastic Gait and prominent sensory ataxia. The known causes of acquired copper deficiency include prior gastric surgery, excessive zinc ingestion, and malabsorption; however, often the cause is unclear. Hyperzincemia may be present even in the absence of exogenous zinc ingestion. The clinical features and neuroimaging findings are similar to the subacute combined degeneration seen in patients with vitamin B12 deficiency. Copper and vitamin B12 deficiency may coexist. The neurological syndrome may be present without the hematologic manifestations. Copper supplementation resolves the anemia and neutropenia promptly and completely and may prevent the neurological deterioration. Improvement, when it occurs, is often subjective and preferentially involves sensory symptoms. This article describes patients with copper deficiency myelopathy seen at the Mayo Clinic in Rochester, Minn, and reviews the literature on neurological manifestations of acquired copper deficiency in humans.

  • Imaging features of copper deficiency myelopathy: a study of 25 cases
    Neuroradiology, 2006
    Co-Authors: Neeraj Kumar, J. Eric Ahlskog, Christopher J. Klein, John D. Port
    Abstract:

    Acquired copper deficiency presents with a Spastic Gait and sensory ataxia. Spinal cord magnetic resonance imaging (MRI) in patients with copper deficiency myelopathy may show increased T2 signal, most commonly in the dorsal midline cervical and thoracic cord. These imaging findings may be reversible with normalization of serum copper. The clinical and imaging picture is very similar to the subacute combined degeneration seen in patients with vitamin B12 deficiency. Neuroradiologists should consider this possibility when a long segment of symmetric dorsal spinal cord T2-hyperintensity is identified.

Jiang Liang - One of the best experts on this subject based on the ideXlab platform.

  • Syringomyelia with irreducible atlantoaxial dislocation, basilar invagination and Chiari I malformation
    european spine journal, 2010
    Co-Authors: Wang Shenglin, Wang Chao, Yan Ming, Zhou Haitao, Jiang Liang
    Abstract:

    A 27-year-old woman presented with bilateral weakness of her all extremities for 5 years. She had a Spastic Gait and was unable to ambulate without assistance. Neurologic examination revealed increased deep tendon reflexes and positive pathologic reflexes. Radiographs showed occipitalization of the atlas, C2-C3 congenital fusion and fixed atlantoaxial dislocation with an atlanto-dental interval of 10 mm. MRI demonstrated cervicomedullary junction (CMJ) compression from the odontoid, a Chiari type I malformation, and syringomyelia extending from the foramen magnum to C5. The patient underwent transoral atlantoaxial release followed by posterior internal fixation from the occiput to the axis, which resulted in a significant improvement in motor function in all extremities. Post-operative images showed anatomical reduction of the atlantoaxial joint. However, an MRI performed 8 days following surgery showed a new retro-odontoid pannus had developed that was compressing the spinal cord at CMJ. A follow-up CT scan performed at 6 months post-operatively demonstrated a solid bony fusion between the occiput and C2, while an MRI at that time showed complete resolution of the retro-odontoid soft tissue mass with correction of the Chiari I malformation, and resolution of the syringomyelia. Final follow-up at 2-years revealed an excellent clinical outcome.Clinical NeurologyOrthopedicsSCI(E)PubMed7ARTICLE3361-3661

Liang Jiang - One of the best experts on this subject based on the ideXlab platform.

  • syringomyelia with irreducible atlantoaxial dislocation basilar invagination and chiari i malformation
    European Spine Journal, 2010
    Co-Authors: Shenglin Wang, Haitao Zhou, Chao Wang, Liang Jiang
    Abstract:

    A 27-year-old woman presented with bilateral weakness of her all extremities for 5 years. She had a Spastic Gait and was unable to ambulate without assistance. Neurologic examination revealed increased deep tendon reflexes and positive pathologic reflexes. Radiographs showed occipitalization of the atlas, C2–C3 congenital fusion and fixed atlantoaxial dislocation with an atlanto-dental interval of 10 mm. MRI demonstrated cervicomedullary junction (CMJ) compression from the odontoid, a Chiari type I malformation, and syringomyelia extending from the foramen magnum to C5. The patient underwent transoral atlantoaxial release followed by posterior internal fixation from the occiput to the axis, which resulted in a significant improvement in motor function in all extremities. Post-operative images showed anatomical reduction of the atlantoaxial joint. However, an MRI performed 8 days following surgery showed a new retro-odontoid pannus had developed that was compressing the spinal cord at CMJ. A follow-up CT scan performed at 6 months post-operatively demonstrated a solid bony fusion between the occiput and C2, while an MRI at that time showed complete resolution of the retro-odontoid soft tissue mass with correction of the Chiari I malformation, and resolution of the syringomyelia. Final follow-up at 2-years revealed an excellent clinical outcome.

Wang Shenglin - One of the best experts on this subject based on the ideXlab platform.

  • Syringomyelia with irreducible atlantoaxial dislocation, basilar invagination and Chiari I malformation
    european spine journal, 2010
    Co-Authors: Wang Shenglin, Wang Chao, Yan Ming, Zhou Haitao, Jiang Liang
    Abstract:

    A 27-year-old woman presented with bilateral weakness of her all extremities for 5 years. She had a Spastic Gait and was unable to ambulate without assistance. Neurologic examination revealed increased deep tendon reflexes and positive pathologic reflexes. Radiographs showed occipitalization of the atlas, C2-C3 congenital fusion and fixed atlantoaxial dislocation with an atlanto-dental interval of 10 mm. MRI demonstrated cervicomedullary junction (CMJ) compression from the odontoid, a Chiari type I malformation, and syringomyelia extending from the foramen magnum to C5. The patient underwent transoral atlantoaxial release followed by posterior internal fixation from the occiput to the axis, which resulted in a significant improvement in motor function in all extremities. Post-operative images showed anatomical reduction of the atlantoaxial joint. However, an MRI performed 8 days following surgery showed a new retro-odontoid pannus had developed that was compressing the spinal cord at CMJ. A follow-up CT scan performed at 6 months post-operatively demonstrated a solid bony fusion between the occiput and C2, while an MRI at that time showed complete resolution of the retro-odontoid soft tissue mass with correction of the Chiari I malformation, and resolution of the syringomyelia. Final follow-up at 2-years revealed an excellent clinical outcome.Clinical NeurologyOrthopedicsSCI(E)PubMed7ARTICLE3361-3661