THE SENSORIMOTOR SYSTEM (CHAP 8)
Web Links:
Motor Neuron Nuclei: Spinal Cord & Brainstem:
Descending pathways: Corticospinal and Corticobulbar Tracts:
Descending pathways originating in Brainstem:
This one also has other systems:
http://www.physpharm.fmd.uwo.ca/undergrad/medsweb
Three principles of Sensorimotor Function
1. The Sensorimotor System is Hierachically organizanized (Fig. 8.1).
From general goals (cortical level) to specific details of action (lower levels).
Information flow is down, while in the Sensory system informtion flows through the hierarchy.
2. Motor Output is Guided by Sensory Input.
Sensory feedback plays an important role in the control of movement (exception: ballistic movements).
3. Learning Changes the Nature and Locus of Sensorimotor.
From conscious control (cortical level) to "Automatic Pilot" (lower levels).
Sensorimotor Association Cortex.
Sensory information is integrated in Association cortex. Two Major areas:
Posterior Parietal Associationn Cortex
Dorsolateral Prefrontal Association Cortex
1. Posterior Parietal Association Cortex (Fig. 8.2)
This cortex receives input from
The somatosensory system,
The visual system and
The auditory system.
This information specifies the initial conditions for the programming of action:
The original position of the body parts to be moved.
The position of external objects
Damage to the posterior parietal cortex causes Apraxia and Contralateral neglect.
Apraxia: difficulty in executing a movement when ordered to do so, but able to do it when not thinking about it. Lesion is often on the left side.
Contralateral Neglect: Patient does not respond to sensory stimulation from the side opposite to the lesion of the parietal cortex (usually on the right side).
The output of the Posterior Parietal Association Cortex goes to the Dorsolateral Prefrontal Association Cortex, and to the Frontal Eye Field (Fig. 8.2).
2. Dorsolateral Prefrontal Association Cortex. Plays a role in the evaluation of external stimuli and the initiation of voluntary reaction to them. Some neurons fire before the response and continue to fire until response is complete.
Sends projections to (Fig. 8.4):
Secondary Motor Cortex
Primary Motor Cortex
Frontal Eye Field
Secondary Motor Cortex.
Involved in the programming of specific patterns of movement. It receives input from association cortex and send input to Primary Motor Cortex (Fig.8.5)
Secondary motor cortex consists of seven areas in the frontal lobe (FIG. 8.5):
-Two supplementary motor area: elicits complex movements of the body.
-Two premotor areas. Neurons respond just before a reaching movement is initiated, suggesting a programming function.
-Three small cingulate motor areas.
Primary Motor Cortex.
Information from secondary motor cortex is passed to Primary Motor Cortex: (Fig. 8.5)
Located in the precentral gyrus of the frontal lobe.
It is somatotopically organized (motor homunculus) (Fig. 8.6.)
Damage to the primary motor cortex
-does not produce paralysis because many fibers bypass the primary motor cortex, and other subcortical structures can initiate motor programs.
-produces astereognosia: deficit in stereognosis, capacity of identifying objects by touch. Damage reduces force, accuracy and speed of movements.
Descending Motor Pathways
The primary motor cortex sends commands to muscles by means of two descending motor pathways:
The Pyramidal System and the Extrapyramidal System (terms not in book) .
1. The Pyramidal System:
Originates in large motor neurons in motor cortex, called Betz cells.
Axons of these neurons synapse with neurons in the ventral horn of the spinal cord.
Descending axons follow two major pathways:
A. Dorsolateral (or lateral) corticospinal tract.
B. Ventromedial (or anterior) corticospinal tract.
Web Figure: Dorsolateral (lateral) and Ventromedial (anterior) corticospinal tracts; pyramidal decussation
A. Dorsolateral Corticospinal Tract (FIG. 8.7): Web Figure : Dorsolateral corticospinal tract
Axons from Betz cells in motor cortex and red nucleus in mesencephalon end up in lateral parts of the spinal cord.
80% of these axons cross to the opposite side of the spinal cord (pyramidal decussation) at the level of the medulla in a region called the medullary pyramids.
Lesions above the decussation produce contralateral paralysis, whereas lesions below the decussation produce ipsilateral paralysis.
Innervates small, distal muscles (finger, toes) involved in fine and independent movement of digits. Stereognosis: identifying objects by touch, skin provides feedback.
B. Ventromedial Corticospinal Tract (FIG. 8.8):
Axons from Betz cells end up in ventral parts of the spinal cord.
Only 20% of the axons cross the midline. Therefore, lesions produce motor deficits that are mostly ipsilateral.(same side paralysis).
Innervates large, proximal muscles (neck, shoulder, trunck, pelvis) involved in walking, climbing and control of posture (bilateral movements).
2. The Extrapyramidal System: (not explicitly covered in book, but some of its componenets are described).
Regulates and modulates movement, but does not initiate movement.
It is a multineural pathway, which ultimately synapses with neurons in the ventral horn of spinal cord.
Along the way it synapses with neurons in several nuclei, including:
Cerebellum (Fig. 3.21): Located in the metencephalon.
Only 10% of the brain mass, but contains half the neurons.
Lesions produce tremor, loss of motor control (jerky movements), disturbaces of balance, speech, eye movements.Learning new motor sequences becomes difficult.
Basal ganglia (Fig. 3.29): Located in the telencephalon, consists of:
Striatum (caudate and putamen)
Globus pallidus
Web Link: Basal Ganglia
It participates in a cortical-basal ganglia- thalamus-motor cortex loop, without descending axons to the spinal cord.
Disorders of Movement
The Basal ganglia are involved in several motor diseases, including
Parkinson's Disease, and Huntington's Disease:
1) Parkinson's Disease, or Parkinsonism. PAGE 245 IN CHAPTER 10!
Affects about 0.5% of the population. More prevalent in males (2.5 times) than in females. Rarely before 50 years of age. Low heritability. Cause is not known.
The most common symptoms are:
1) Tremor, most pronounced during inactivity, and supressed during voluntary movement and sleep.
2) Muscular rigidity
3) Involuntary shifts in posture
4) Slowness of movement (bradykinesia)
5) Shuffling gait.
Caused by degeneration (cell death) of the Substantia Nigra, a midbrain (mesencephalon) nucleus whose neurons project to the Striatum of the basal ganglia. See Web Figure
The neurotransmitter of substantia nigra neurons is dopamine.
Symptoms are alleviated by injections of L-DOPA, the chemical from which dopamine is synthesized in dopaminergic neurons. Effect is usually temporary.
A newer drug is deprenyl, a dopamine agonist that increases the levels of dopamine by inhibiting the enzyme monoamine oxidase.
Certain drugs, toxins may cause Parkinson-like diseases, e.g., MPTP (synthetic heroin)
MPTP abuse incident produced symptoms of Parkinsonism in young adults.
There was loss of neurons in the substantia nigra. This led to an animal model which showed that Deprenyl blocks the effect of MPTP in the model.
2) Huntington's Disease or Huntington's chorea (chorus line). PAGE 246 IN CHAPTER 10!
Rapid, complex movements involving entire limbs (complex dances).
It is rare.
Dementia usually develops.
It has a strong genetic basis, passed on by a single dominant gene. If one parent is affected, about half of offprings will develop disease. Abnormal gene produces protein called huntingtin, whose effect is not yet clear.
The symptoms appear at about 40 years of age, and death occurs about 15 years later.
There is gross degeneration of the striatum of the basal ganglia and diffuse thining of the cerebral cortex. See Web Figure.
Sensorymotor Spinal Circuits
Muscles (Fig. 8.9, 8.10)
Both the pyramidal and extrapyramidal systems synapse with motor neurons in the ventral horn of the spinal cord.
The pyramidal system synapses with alpha motoneurons, whose axons innervate skeletal muscles (FIG. 8.9). The transmitter is acetylcholine.
Skeletal muscles are made of muscle fibers, which run the entire length of the muscle. Attach to the bone by tendons.
Each fiber receives only one synapse from alpha motoneurons.
The extrapyramidal sytem synapses with gamma motoneurons, whose axons innervate the intrafusal muscles or muscle spindles, located inside the squeletal muscles.
Intrafusal muscles regulate the length of skeletal muscles (FIG. 8.11- 8.12).
One alpha motoneuron can innervate one or several muscle fibers.
Motor unit: all of the muscle fibers innervated by a single motoneuron.
Small motor units produce fine movements (fingers), large motor units produce gross movements (back).
Motor pool: All of the motor neurons that innervate the fibers of a single muscle.
Flexor muscles: flex or bend a joint. Example: biceps (Fig. 8.10).
Extensor muscles: straighten or extend joints.Example: triceps (Fig. 8.10).
Synergistc muscles produce the same movement
Antagonistic muscles: oppose each other (flexor vs extensor) FIG. 8.10
Isometric contraction: muscle contraction without shortening of muscle
Dynamic contraction: muscle contraction with shoertening of muscle
Muscles have two types of receptors:
1. Golgi tendon organs, located in tendons, detect tension and protect muscles from rupture.
2. Muscle spindles. Located in body of muscle. Regulate length of muscle. Contain intrafusal muscle, activated by gamma motoneurons in spinal cord. (Figs. 8.11; 8.12)
Stretch reflex: maintains position and stability.
Patellar tendon reflex (knee jerk). (Fig. 8.13).
Maintenance of limb position. (Fig. 8.14)
Withdrawal reflex: withdrawal of limb to avoid painful stimulus. Requires reciprocal innervation. (Fig. 8.15)
Reciprocal innervation: contraction of one muscle and relaxation of antagonist.(Fig. 8.15)