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Spinal Cord Motor Organization And Locomotion

Spinal Cord Motor Organization And Locomotion
Spinal cord motor organization
In addition to containing the α- and γ-motor neurones (MNs), the spinal cord also contains a large number of interneurones (INs).
These INs can form networks that are intrinsically active and whose output governs the activity of MNs, central pattern generators (CPGs). These CPGs, which may underlie locomotion, are modulated by both central and peripheral inputs (see Chapters 36 and 38). Such CPGs are not unique to locomotion as they can be seen in other parts of the central nervous system (CNS) controlling rhythmical motor activities, e.g. respiration and the brainstem respiratory network.

Descending motor pathways (see Table 37.1) The descending motor pathways can be classified according to:
 their site of origin, namely pyramidal or extrapyramidal tracts (although clinically extrapyramidal disorders refer to diseases of he basal ganglia; see Chapter 42);
       their location within the cord and the muscles they ultimately innervate.
Thus, the pyramidal (corticospinal) and rubrospinal tracts are associated with a lateral MN pool that innervates the distal musculature, while the vestibulo, reticulo and tectospinal tracts are more associated with a ventromedial MN pool that innervates the axial and proximal musculature.
These latter MNs are linked by long propriospinal neurones, while the converse is true for the lateral MN pool. Thus, the lateral motor system is more involved in the control of fine distal movements, while the ventromedial system is more concerned with balance and posture.
The MNs of the anterior horn are further organized such that the most ventral MNs innervate the extensor muscles, while the more dorsally located MNs innervate the flexor musculature.

The control of locomotion is complex, as it requires the coordinated movement of all four limbs in most mammals. Each cycle in locomotion is termed a step and involves a stance and a swing phase the latter being that part of the cycle when the foot is not in contact with the ground.
     Each cycle requires the correct sequential activation of flexors and extensors. The simplest way to achieve this is to have two CPGs (half centres) which activate flexors and extensors, respectively, and which mutually inhibit each other.
      This mutual inhibition can perhaps best be modelled using the
inhibitory Ia IN and Renshaw cells.
     Renshaw cells are INs that, when activated by MNs, inhibit those same MNs (see Chapter 17). Thus, the activation of a MN pool by a CPG leads to its own inhibition and the removal of an inhibitory input to the antagonistic CPG, thus switching the muscle groups activated.
This half centre model for locomotion can be modulated by a range of descending and peripheral inputs. The Golgi tendon organ can switch the CPGs, while a range of cutaneous inputs can cause the cycle to be modified when an obstacle is encountered. These afferents, termed flexor reflex afferents, cause the limb to be flexed so stepping over or withdrawing from the noxious or obstructive object.
       CPGs within the spinal cord communicate with each other through propriospinal neurones.
     In contrast, supraspinal communication of information from and about the CPGs is relayed indirectly in the form of muscle spindle Ia afferent activity via the dorsal spinocerebellar tract (DSCT) and dorsal columns and spinal cord interneuronal activity via the ventral spinocerebellar tract (VSCT).

Clinical disorders of spinal cord motor control and locomotion
Although experimental animals can locomote in the absence of any significant supraspinal inputs (fictive locomotion), this is not the case in humans. However, clinical disorders of gait are relatively common and may occur for a number of reasons.
   Disorders of spinal cord INs such as in stiff person syndrome are rare and present with increased tone or rigidity in the axial muscles with or without spasms caused by the continuous firing of the MNs as a result of the loss of an inhibitory interneuronal input primarily to the ventromedial MNs. This condition is associated with anti-bodies against the synthetic enzyme for γ-aminobutyric acid (GABA), glutamic acid decarboxylase (GAD).
  Damage to the descending pathways can produce a range of deficiencies. The most devastating is that seen with extensive brain- stem damage when the patient adopts a characteristic decerebrate posture with arching of the neck and back and rigid extension of all four limbs. In contrast, a more rostrally placed lesion in one of the cerebral hemispheres produces weakness down the contralateral side (hemiplegia or hemiparesis) with increased tone (hypertonia) and increased tendon reflexes (hyperreflexia) which may produce spontaneous or stretch–induced rhythmic involuntary muscular contractions (clonus) (an upper motor neurone lesion). This situation is also seen with interruption of the descending motor pathways in the spinal cord (see Chapters 9, 35 and 55). The pattern of weakness in such lesions characteristically involves the extensors more than the flexors in the upper limb and the converse in the lower limb. This is misleadingly termed a pyramidal distribution of weakness, as damage confined to the pyramidal tract in monkeys leads only to a deficiency in fine finger movements with a degree of hypotonia and hypo or areflexia.