DESCENDING CONTROL OF SPINAL MOTOR SYSTEMS [Return to Lecture Schedule]
Reflex circuits and pattern generators in the spinal cord ensure that activities such as reciprocity, force maintenance, protective responses are carried out automatically as prescribed by quite complex and flexible local networks. For the proper maintenance of posture, balance and tone, however, and for the continuous regulation of these activities during the genesis of purposive action, the spinal, and the corresponding bulbar systems, have to be subtended to the "descending" control from "higher" centres in the brain. Neurones located in these centres, which project axons onto the lower motoneurones or the local interneurones associated with them, are termed Upper Motoneurones.
As noted before, these descending systems can be divided into a dorsolateral system and a ventromedial system. A third, aminergic system with generalised, modulatory effects, includes the descending serotonergic (5-HT) raphespinal pathway, and catecholaminergic (NE) coerulospinal pathway. A dopaminergic (DA) system, descending from the ventral tegmentum to the cord also modulates the sensitivity of the stretch reflexes and locomotory systems.
The ventromedial system includes:
(1) the vestibulospinal pathway (left) which via vestibular and cerebellar inputs to the vestibular nuclei, regulates posture and balance, and facilitates mainly Aa motoneurones of the postural, anti-gravity (extensor) muscles;
(2) the reticulospinal pathway which has two major divisions: (i) a medullary reticulospinal tract, which descends in the anterolateral column, to inhibit extensor and facilitate flexor motoneurones - targeting the Ag more than the Aa motoneurones; and (ii) a pontine reticulospinal tract, which descends medially to facilitate extensor Ag, and to a lesser extent Aa, motoneurones of the limbs, and inhibit flexors. Both areas receive strong sensory (afferent) and descending cortical input, but the excitatory cortical input predominates in the medullary nuclei;
(3) the tectospinal pathway which originates in the superior colliculus, is crossed, is confined to the cervical segments of the cord, and controls head and eye movements. The interstitiospinal tract originates from the interstitial nucleus of Cajal and pretectal area and runs to lower levels of the cord.
The major role of the medial pathways is to regulate posture and balance, by acting mainly on the more proximal and axial antigravity musculature.
The dorsolateral system includes:
(1) the rubrospinal tract, a crossed tract descending in the lateral white column, which is virtually vestigial in man, and confined to the cervical segments, but which may play a significant part in decorticate rigidity (below);
(2) the corticospinal tract in more advanced primates, expands, occupying more ventral areas in the lateral column, as the rubrospinal tract shrinks. It carries fibres from the premotor/ supplementary motor cortex (roughly a), motor cortex (roughly a) and post-central gyrus/parietal association area (roughly a). 80% of the pyramidal fibres cross and descend as the lateral corticospinal tract, while 20% descend ipsilaterally as the medial corticospinal tract, which projects to the axial musculature. Descending inputs to motoneurone pools directly or indirectly target both Aa and Ag motoneurones of flexor muscles, and inhibitory interneurones to antagonist muscles.
The major function of the lateral system is to over-ride the postural set (inhibit anti-gravity muscles) in order to promote the integrated, but independent and finely controlled, dexterous use of the muscles of the distal appendages, to carry out a highly variable repertoire of movements. [See Ascending & Descending Tracts] [See Summary - Lateral & Medial Systems]
The enormous, time-varying inflow of excitatory and inhibitory inputs to the lower motor centres have, on the balance, a facilitatory effect on spinal and bulbar neurones. Transection of the spinal cord removes these descending inputs, so that the spinal neurones below the lesion become hyperpolarised and unresponsive to segmental stimuli, as well as to descending activity. All reflexes - somatic as well as visceral including vasomotor - are lost, leading to a flaccid paralysis, with retention of urine and faeces, plus loss of sensation, below the level of the lesion. This areflexic syndrome, known as spinal shock, lasts for a period of weeks to months, after which time, some reflexes (but not sensation) gradually return. Loss of the aminergic modulatory pathways may play a significant role in producing spinal shock. The causes for recovery are unknown, and may include (1) development of hypersensitivity in the denervated neurones below the lesion, (2) sprouting of intact nerve terminals below the lesion to make new functional contacts. Ultimately reflexes not only return, but may also become hyperactive or altered in character, as a result of (a) loss of descending modulatory control or (b) newly formed synaptic contacts, and (c) denervation hypersensitivity. These changes could explain why stretch reflexes become enhanced, leading to spasticity (muscle hypertonia - resistance to passive manipulation - due to hyperactive stretch reflexes), while withdrawal and crossed extension reflexes also may be hyperactive. They could also explain the appearance of the abnormal clasp knife reflex and the mass reflex. Loss of corticospinal control will lead to: (a) return of infantile reflexes suppressed by corticospinal tract development: e.g. a Babinski sign (extensor plantar reflex - sign of corticospinal tract lesion) and traction grasp reflex; (b) loss of reflexes dependent on an intact corticospinal tract (e.g. superficial abdominal and cremasteric reflexes); and (c) the appearance of abnormal, novel reflexes (e.g. mass reflex; clasp knife reflex).
Careful management of victims of spinal trauma through the period of spinal shock is essential. Lesions in the thoraco-lumbar cord produce paraplegia; in the cervical cord, quadriplegia.
Decerebration by lesions at the mid-brain level will produce a very strongly spastic paralysis, with the extensor muscles in both upper and lower limbs being hypertonic (D, Fig to left), and with no prolonged period of "shock". The loss of descending control over the vestibulo-spinal, aminergic, and reticulospinal pathways is probably involved. Loss of excitatory cortical input to the medullary reticular nuclei (extensor inhibitory) is probably involved in producing excessive g-motoneurone activity in the extensor muscles and subsequent spasticity, due to unbalanced excitatory input from the pontine nuclei (extensor facilitatory). Note that the spasticity here is of a different character, strength and origin to that seen in spinal transection. Developing a clear understanding of the underlying bases for the different forms of spasticity, may be important in the formulation of effective treatment strategies.
[See Decerebrate/Decorticate Rigidity].
Destruction of the cerebral cortex (decortication) leaving the red nucleus and basal ganglia intact, is similar to decerebration except that the hypertonia in the upper limb is in the flexors, and the degree of tone is influenced by the position of the head (A-C above). The rubrospinal (flexor facilitatory) and tectospinal systems may play an important role in modifying the pattern of paralysis in the upper limbs. The tonic neck and labyrinthine reflexes are superimposed on the hypertonicity.
Unilateral lesion of the motor and pre-motor cortex or their outflow through the internal capsule may destroy cortico-bulbar and cortico-spinal fibres, projecting to the contralateral side, and so produce spastic paralysis of the contralateral half of the body - viz. hemiplegia or hemiparesis. The muscles of the upper face, which have extensive bilateral innervation, may be spared. Selective damage to the motor cortical strip is similar in effect to pure lateral pyramidal tract lesion: hypotonic paralysis affecting mainly the distal muscles.
Lesions of the Upper Motoneurones (UMN) therefore have very different characteristics to those of the Lower Motoneurones (LMN). In the former condition, there will be weakness and wasting due to voluntary paralysis and disuse, but no extensive atrophy. Nor are there the fasciculations associated with chronic LMN disease, or fibrillations associated with denervated muscle. Stretch reflexes tend to be enhanced rather than weakened, but the causative factors may be different with spinal transection than with decerebration or decortication.
Read Physiology (Berne & Levy) Chapter 15
Neurophysiology - The Essentials (Somjen) Chapter 18.1 and 18.4
Review of Medical Physiology (Ganong) Chapter 12.
[Return to Lecture Schedule]
A clasp knife is simply a pen-knife. Note that in opening a pen-knife, it is at first difficult, as the protruding back of the blade has to be lifted against a spring. Once the initial resistance is overcome, however, opening the blade the rest of the way becomes easy. In decorticate rigidity, the hypertonicity is usually unidirectional, predominantly in the anti-gravity muscles. Thus, in the upper limbs, extension is resisted, and in the lower limbs, flexion is resisted. Attempting to extend the arm, for example, will be met by resistance, and efforts to move the arm faster or to a greater extent will be resisted increasingly strongly. At a critical length of the muscle (biceps) however, the resistance will disappear, and the arm will extend the rest of the way quite easily. Hence, by analogy, the name clasp-knife reflex. If the arm is then flexed so that the muscle length falls below the critical level, the hypertonia will once more resume. [Return]
In the mass reflex which may occur after spinal transection, a mild noxious stimulus may trigger not just withdrawal and crossed extension reflexes, but also micturition, defaecation, sweating, etc. Vasomotor problems are more critical with higher level lesions, because of the increased compromise of sympathetic nervous system control. Note that the influence of baroreceptor and other higher level reflexes will be lost below the level of the lesion. Reports are that the mass reflex can in fact be sometimes invoked to advantage, to elicit voiding on demand, by paraplegics who no longer have direct voluntary control of micturition and defaecation. It has also been suggested that the hyperactive withdrawal and crossed-extension reflexes might be advantageously used by paraplegics, in putting on trousers. It should be clear however, that wide-spread, unconfined reflex responses such as the mass reflex can no doubt be very disconcerting. [Return]
Lateral & Medial descending pathways are shown on the left. Ascending pathways are shown on the right. Propriospinal fibres run in the shaded area around the grey matter of the cord. [Return]
Summary - Lateral & Medial Systems
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