Cognitive Neuroscience, the biology of the mind, by M. Gazzaniga (fourth edition) – Summary chapter 8

The final common pathway of all motor output is the ventral horn in the spinal cord. The dorsolateral part of the ventral horn is involved in distal muscles and fine movements. The ventromedial part of the ventral horn is involved in proximal muscles and posture. Muscles make use of alpha neurons. It involves alpha neurons.

There are different reflexes of the human body:

1. Stretch reflex (posture)
   Activation of one muscle leads to the relaxation of the other muscle. The muscle spindle senses stretching, which activates the alpha motor neurons which leads to the muscle contracting.
2. Golgi tendon reflex (protection from overload)
   Excessive weight on a muscle causes the neuron from the Golgi tendon to fire, inhibiting the motor neuron which leads to relaxation of the muscle.
3. Withdrawal reflex (protection from damage)
   Activation of pain receptors on the skin causes the muscle to contract and withdraw.
4. Crossed extensor reflex
   The flexing of one muscle leads to the relaxation of another.

The central pattern generator is the mechanism in the spinal cord that enables patterns (e.g., walking, breathing, swallowing) to be generated and is activated by a higher brain command or by proprioceptive feedback. Reflexes are processed and generated in the spinal cord. Reciprocal inhibition of antagonistic muscles refers to the relaxation of the flexor as the extensor contracts.

Pyramidal tracts are axons that travel directly from the cortex to the spinal cord. The extrapyramidal tracts are axons that travel through another cortical structure to the spinal cord. There are several extrapyramidal tracts:

1. Rubrospinal tract
   From the upper motor neurons in the red nuclei to the spinal cord. It controls muscle tone and distal limb muscles that perform more precise movements.
2. Tectospinal tract
   From the upper motor neurons in the superior- and inferior colliculi to the spinal cord. It receives auditory and visual information and controls the orienting-response.
3. Vestibulospinal tract
   From the vestibulocochlear nerve (inner ear) to the spinal cord. It monitors the position and movement of the head to maintain posture and balance.
4. Reticulospinal tract
   From the reticular formation to the spinal cord. It receives input from many pathways. It controls many reflexes and the state of arousal.

The pyramidal system is involved in voluntary control of skeletal muscles. It begins at the upper motor neurons of the primary motor cortex and other cortical areas to the spinal cord.

1. Corticobulbar tract
   This pyramidal tract moves towards cranial nerve nuclei that move eye, jaw, face, and throat.
2. Corticospinal tract
   This pyramidal tract controls all non-facial somatic muscles.

Damage to the corticospinal tract leads to paralysis, spasticity (pyramidal weakness) or changed reflexes (Babinski sign). Therapy for pyramidal weakness involves forcing the weak parts to work. The cerebellum provides a subcortical-cortical loop and is involved in the fine tuning of movement and the timing of automated motor movements. It is informed by the motor cortex of the intended movement.

1. Spinocerebellum (affected by alcohol)
   This is involved in balance and walking.
2. Neocerebellum (finger to nose test)
   This is involved in the control of fine movement and speech.
3. Vestibulocerebellum
   This is involved in the coordination of eye movements with body movements.

The basal ganglia consist of the striatum, the caudate nucleus, the putamen, the globus pallidum (externa and interna), substantia nigra and subthalamic nucleus. It acts as a gateway of movement.

The direct pathway inhibits GPi/SNr, leading to less inhibition of the thalamus, which leads to more movement. It makes use of D1 dopamine receptors. The indirect pathway inhibits GPe, so that GPi/SNr activity increases, leading to more inhibition of the thalamus, which leads to fewer movements. It makes use of D2 dopamine receptors.

In Huntington’s disease, the GPe is inhibited less, which leads to excessive movement. In Parkinson’s disease, the substantia nigra does not produce dopamine anymore, which leads to increased inhibition of the thalamus, leading to less movement.

The primary motor cortex (M1) is involved in direct motor control. The premotor cortex (PMC) is involved in externally guided actions (e.g., stimulus-driven). The supplementary motor area (SMA) is involved in internally guided actions. The posterior parietal cortex (PPC) is involved in translating movement from eye-centred to body centred reference frames.

Neurons in the primary motor cortex and the premotor cortex encode movement direction. These neurons are tuned to the direction of limbs, but this tuning is not specific. Actual movement is encoded by a vector sum of population of M1 neurons. Neurons in the premotor cortex are also tuned to specific types of movements. Mirror neurons are neurons that encode an action and are activated by seeing or hearing that action being executed and are located in the premotor cortex and the parietal cortex.

The affordance competition hypothesis states that there are many potential movements (affordances) and all potential actions compete with each other. The winner is the selected action. It implies that decision making is embedded in motor control and not in a detached control centre.

Hemiplegia is half-sided paralysis due to lesions of upper motor neurons from the primary motor cortex. Apraxia is the loss of motor skills due to lesions to the SMA, PMC or PPC. In ideomotor apraxia, a person has an idea of an action, but cannot execute the action. It occurs after lesions to the SMA or the PMC. In ideational apraxia, a person does not know what to do and cannot perform the action. It occurs after lesions to the PPC.