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.
Locomotion
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.
