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Biomedical subjects

N H Mayer

Publications and source records attributed to N H Mayer.

13 recordsLinked to original sources
PubMed2004

Laboratory analysis and dynamic polyEMG for assessment and treatment of gait and upper limb dysfunction in upper motoneuron syndrome.

Multiple muscle agonists and antagonists acting for all the joint movements in the upper and lower limb exist. This redundancy of motor control is very valuable in normal physiology, but when a central nervous system injury with resulting upper motor neuron syndrome takes place, the source of the functional impairment may be difficult to localize. In this paper we discuss the use of gait and motor control analysis studies as a tool particularly useful in determining the specific muscles that may be producing limb dysfunction. We present the most frequent patterns of upper motor neuron dysfunction that affect the upper and lower limb as a result of upper motor neuron syndrome. A case description of the features, the electromyographic patterns, and their functional implications are used. Our objective is to clarify the understanding of these patterns of dysfunction and their focal cause with the intent to improved care of the patient with upper motor neuron syndrome.

Journal Article↗
PubMed1997

Clinicophysiologic concepts of spasticity and motor dysfunction in adults with an upper motoneuron lesion.

Spasticity is a disorder of the sensorimotor system characterized by a velocity-dependent increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. It is one component of the upper motoneuron syndrome, along with released flexor reflexes, weakness, and loss of dexterity. Spasticity is an important "positive" diagnostic sign of the upper motoneuron syndrome, and when it restricts motion, disability may result. The "negative" signs--weakness and loss of dexterity--invariably alter patient function when they occur. In an upper motoneuron syndrome, the alpha motoneuron pool becomes hyperexcitable at the segmental level. This hyperexcitability is hypothesized to occur through a variety of mechanisms, not all of which have yet been demonstrated in humans. Spasticity caused by spinal cord lesions is often marked by a slow increase in excitation and over-activity of both flexors and extensors with reactions possibly occurring many segments away from the stimulus. Cerebral lesions often cause rapid build-up of excitation with a bias toward involvement of antigravity muscles. Chronic spasticity can lead to changes in the rheologic properties of the involved and neighboring muscles. Stiffness, contracture, atrophy, and fibrosis may interact with pathologic regulatory mechanisms to prevent normal control of limb position and movement. In the clinical exam, it is important to distinguish between the resistance due to spasticity and that due to rheologic changes, because the distinction has therapeutic implications. Diagnostic nerve or motor point blocks and dynamic or multichannel EMG are useful to distinguish the contributions of spasticity and stiffness to the clinical problem.

Adult↗
PubMed1997

Common patterns of clinical motor dysfunction.

An upper motor neuron syndrome often leads to the development of stereotypical patterns of deformity secondary to agonist muscle weakness, antagonist muscle spasticity and changes in the rheologic (stiffness) properties of spastic muscles. Identification of the spastic muscles that contribute to deformity across a joint allows therapeutic denervation to be implemented with the maximum likelihood of success. Identifying responsible muscles can be complex, since many muscles may cross the joint involved, and not all muscles with the potential to cause deformity will be spastic. Strategies including polyelectromyography and diagnostic blocks with local anesthetics can be used to test hypotheses regarding the deformity, providing information for more long-term denervation. In this review, we discuss frequently observed patterns of deformity associated with problematic spasticity, paresis, contracture, and impaired voluntary motor control.

Diagnosis, Differential↗
PubMed1981

Medial frontal cortex infarction and the alien hand sign.

Two right-handed patients with infarction involving the left medial frontal cortex are described. Both patients exhibited a form of transcortical motor aphasia and a psychomotor disturbance involving the right arm characterized by forced grasping, motor perseveration, and the presence of apparently purposeful movements that appeared to be dissociated from conscious volition. The latter feature is noted to be identical to the alien hand sign as described in the left arm of commissurotomized patients and patients with callosal neoplasm or infarction. It is suggested that the observed dissociation of conscious intention from purposeful movement may be related to dysfunction of the medial frontal cortex contralateral to the impaired extremity as much as to hemispheric disconnection.

Aged↗