P. 548

An Urban Experience
Evaluation of postural reactions
General proprioception is concerned with the ability to sense stimuli arising within the body and extremities regarding position, motion, and equilibrium. Such stimuli are registered by sensors located in tendons, muscles and joints, from where signals are transported to the brain through ascending proprioceptive pathways. After being consciously processed, the efferent pathways
originating from Upper Motor Neuron cell bodies situated in the cerebral motor cortex send their axons to descend through the midbrain, brainstem and spinal cord to in uence spinal cord Lower Motor Neurons. From the spinal cord, peripheral nerves (formed from several nerve roots) travel peripherally to connect with- and  nally cause an adequate response from the skeletal effector muscles.
CNS/PNS structures involved
Postural reactions
Evaluate main function by performing the following tests:
-Wheel barrowing -Hopping
-Hemi-standing -Hemi-walking -Proprioceptive positioning
Ascending pathways
Proprioceptive receptors in joints, tendons and muscles - peripheral sensory nerve - sensory root -ascending spinal cord (spinothalamic tract) and brainstem pathways - cerebral cortex somatic sensory area (contralateral)
Descending pathways
Cerebral cortex motor area - descending brainstem and spinal cord UMN pathways - LMN in spinal cord gray matter – motor root - peripheral motor nerve – skeletal muscle
Upper Motor Neuron (UMN) & Lower Motor Neuron (LMN)
Understanding the UMN and LMN system and the clinical signs arising from dysfunction of UMN/LMN respectively, are essential when trying to localise lesions in the spinal cord.
The UMN acts as an inhibitor of LMN activity, initiates movement and sustain extensor tone. The LMN is the efferent neuron of the peripheral nervous system connecting the CNS with an effector organ (muscle).
UMN (cerebral cortical motor neurons/1. neurons) are primarily situated in the cerebral motor cortex pyramidal system, but also in the diencephalon basal nuclei and in the brainstem extrapyramidal system. The UMN axons travel in their descending tracts through the spinal cord, where they synapse with interneurons to communicate with LMN.
LMN (2.neurons) are situated in all segments of the spinal cord (ventral horn grey matter). LMN axons leave the spinal cord in the ventral (motor) root of the spinal nerves. The peripheral nerves are formed by the union of spinal nerves.
Spinal re exes are evaluated with the purpose of evaluating spinal cord LMN functionality. Spinal re exes performed in the front limb evaluate spinal cord segments C6-T2, the brachial plexus (formed by spinal nerves from cervical spinal cord segments C6-T2)
and the associated peripheral nerves. Spinal re exes
performed in the hind limb and perineal region evaluate spinal cord L4-S3, the lumbo-sacral plexus (formed by spinal nerves from cervical spinal cord segments L4-S3) and the associated peripheral nerves.
Evaluation of re ex quality
Dysfunction of the UMN-LMN system interaction is re ected in the quality of the spinal re exes and in muscle tone. With lesions of the UMN pathways the inhibitory effect on the LMN is decreased or lost caudal to the lesion. This is re ected clinically by exaggerated spinal re exes (hyperre exia) and muscle hypertonia
or spasticity. A spastic paresis or paralyses may be present. With lesions of the LMN in the spinal cord, the associated spinal re exes are decreased to absent, muscle tone may be decreased to lost and  accid paresis or paralysis may be present. LMN-signs are associated directly with the dysfunctional segments
of the spinal cord affected by the lesion. Loss of LMN function will cause rapid and pronounced muscle atrophy of the muscles innervated from the damaged spinal cord segments, so-called neurogenic muscle atrophy.
Lesions affecting the above pathways where they are travelling in the thalamus, capsula interna or cortex will result in contra lateral de cits of limb function, whereas lesions situated caudally to the thalamus (where these pathways crosses the midline) and in the spinal cord will result in ipsi-lateral de cits of limb function caudal to the lesion.

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