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Primary Motor Cortex


Primary Motor Cortex
The primary motor cortex (MsI) receives afferent information from the cerebellum (via the thalamus) and more anteriorly placed motor cortical areas such as the supplementary motor area (SMA) and a sensory input from the muscle spindle as well as cortical sensory areas. This latter sensory input emphasizes the artificial way in which the central nervous system (CNS) is divided up into motor and sensory systems. In order to acknowledge this, the primary motor cortex is termed the MsI while the primary somatosensory cortex is termed the SmI (see Chapter 31).

Primary Motor Cortex

Investigation of the organization of MsI has shown that the motor innervation of the body is represented in a highly topographical fashion, with the cortical representation of each body part being proportional to the degree of motor innervation so, for example, the hand and orobuccal musculature have a large cortical representation. The resultant distorted image of the body in MsI is known as the motor homunculus, with the head represented laterally and the feet medially. This organization may manifest clinically in patients with epilepsy that originates in the motor cortex. In such cases, the epileptic fit may begin at one site, typically the hand, and then spread so that the jerking marches out from the site of origin (Jacksonian march, named after the neurologist, Hughlings Jackson). This is in contrast to the clinical picture seen with seizures arising from the SMA, in which the patient raises both arms and vocalizes with complex repetitive movements suggesting that this area has a higher role in motor control (see Chapter 38).

These studies on the motor homunculus by Penfield and col- leagues in the 1950s revealed the macroscopic organization of MsI, but subsequent microelectrode studies in animals showed that MsI is composed of cortical columns (see Chapter 10). The inputs to a column consist of afferent fibres from the joint, muscle spindle and skin which are maximally activated by contraction of those muscles innervated by that same area of cortex. So, for example, a group of cortical columns in MsI will receive sensory inputs from a finger when it is flexed that input being provided by the skin receptors on the front of the finger, the muscle spindles in the finger flexors and the joint receptors of the finger joints. That same column will also send a projection to the motor neurones (MNs) in the spinal cord that innervate the finger flexors. Activation of the corticospinal neurone from that column will ultimately activate the receptors that project to that same column, and vice versa.
Thus, each column is said to have input–output coupling and this may be important in the more complex reflex control of movement as, for example, with the long–latency or transcortical reflexes. These reflexes refer to the delayed and smaller electromyographical (EMG) changes that are seen following the sudden stretch of a muscle the first EMG change being the M1 response of the monosynaptic stretch reflex (see Chapter 36). The afferent limb of the transcortical reflex is from the muscle spindle input via the Ia fibre (relayed via the dorsal column medial lemniscal pathway) and the efferent pathway involves the corticospinal tract (CoST). The exact role of this reflex is not known but it may be important in controlling movements precisely, especially when unexpected obstacles are encountered which activate the muscle spindle.
There has been great controversy as to whether MsI controls individual muscles, simple movements or some other aspect of movements. Neurones within MsI fire before any EMG changes and appear to code for the direction and force of a movement, although this activity is dependent on the nature of the task being performed. Therefore, as a whole, the motor cortex controls movement by its innervation of populations of MNs, as individual corticospinal axons innervate many different MNs.
MsI is capable of being remodelled after lesions or changes in sensory feedback, implying that it maintains a flexible relationship with the muscles throughout life. Thus, cells in a region of MsI can shift from the control of one set of muscles to a new set. Within given areas of cortex there is some evidence that synaptic strengths can be altered with long–term potentiation (see Chapter 45), which suggests that the MsI may be capable of learning new movements, a function traditionally ascribed to the cerebellum (see Chapter 40). Damage to MsI in isolation is rare and experimentally tends to produce deficiencies similar to those seen with selective pyramidal tract lesions. However, damage to both MsI and adjacent pre-motor areas, as occurs in most cerebrovascular accidents (CVAs) involving the middle cerebral artery (see Chapter 6), produces a much more significant deficiency, with marked hemiparesis.