1 - Motor Systems and Movement

Lower motor neurons (LMN)

• Synapse directly into skeletal mms

• Peripheral nerve enters the belly of the skeletal mm at a motor point

Neuromuscular junction

The synapse between a LMN and a mm belly

Neuromuscular junction

Where each axon terminal releases the neurotransmitter acetylcholine

Acetylcholine

Neurotransmitter that binds to receptors on the motor end plate and NA ions flow into the mm cell, which causes the mm cell to depolarize

When a mm depolarizes, what happens?

• Ca+2 ions are released from sarcoplasmic reticulum and enter the mm cell cytoplasm

• Ca+2 ion trigger mm contraction

• After contraction, Ca+2 ions are pumped back into sarcoplasmic reticulum where they are stored until the next contraction of the mm fiber

Motor unit

A single LMN and all the mm fibers it innervates

How is mm force controlled?

By recruited individual motor units until the desired amount of force is achieved

Myasthenia Gravis

A chronic autoimmune NM disease that causes weakness in the skeletal mms (which are responsible for breathing and moving parts of the body)

• Antibodies (immune proteins) block, alter or destroy the receptors for acetylcholine (ACh) at the NM junction - this prevents mm contraction

• Drugs that inhibit acetylcholinesterase can be used to improve mm function

Upper motor neurons (UMN)

• Connect the brain with the LMNs

• Location of cell bodies:

  • Primary motor cortex

  • Premotor cortex

  • Supplementary motor area

  • Primary somatosensory cortex

• Brainstem

Corticobulbar Tracts

• Axons that connect the cortex to the LMN in the cranial nerves

• Most are bilateral and control mms on both sides

Where do the extrapyramidal tracts originate from?

In the 4 brainstem nuclei (reticular formation, vestibular nuclei, superior colliculus, red nucleus)

Reticular formation

2 spinal tracts that control mms involved in gt and posture

Vestibular nuclei

Innervate neck, trunk, and proximal limb extensor mms for maintaining balance

Superior Colliculus

Tectospinal tract controls mms responsible for reflex movements of the trunk

Red nucleus

Rubrospinal tract functions in upper limb control (flexion -decorticate posture)

Muscle tone

• Can be modified by environment or emotions

• Gamma loop reflex is responsible for adjusting this

What does damage to the LMNs result in?

• Prevention of gamma loop from functioning correctly (hypotonicity)

• Paralysis with voluntary mvmt

• Deep tendon reflexes are lost

What does damage to the UMNs result in?

• Overactivity of gamma motor neurons (hypertonicity)

• Paralysis with voluntary mvmt

• Deep tendon reflexes are exaggerated

Polio

• A virus that infect LMN cell bodies

• Remaining LMNs may produce collateral sprouts and re-innervate skeletal mms (causes paralysis and flaccidity)

Amyotrophic Lateral Sclerosis (ALS)

• Progressive disease that affects UMNs and LMNs and paralyzes respiratory mms

• S/S:

  • Mixture of flaccid and spastic paralysis

  • No changed in emotional, cognitive, or sensory function

Parkinson’s Disease

• Disease caused by loss of substantia nigra neurons

• Characterized by:

  • Slow, shuffling gt

  • Little or no facial expression

  • Cog-wheel rigidity

  • Flexes/stooped posture

  • Resting tremor that is rhythmic and most obvious in the hands

  • Depression and slowness of thinking

Huntington Disease

Genetic autosomal dominant disorder that is progressive and fatal

• Appears in middle age

• Abnormal form of a protein damages basal ganglia neurons and causes overstimulation of the motor cortex

• Dementia and emotional disturbances occur

• Involuntary mvmts:

  • Chorea (rapid, jerky, arrhythmic mvmts)

  • Hemiballism (flailing, ballistic mvmt)

  • Athetosis (writhing mvmts of the fingers, hands, and feet)

Tourette Syndrome

Genetic disorder characterized by hypertensive dopamine receptors

• Pts exhibit brief, uncontrolled tics (can be physical, verbal or vocal)

• Report a compulsion or urgency to move that is difficult to repress

Ataxia

Uncoordinated mvmt ipsilateral to the injury; often caused by lesion to the cerebellum

Disequilibrium

Difficulty maintaining and correcting balance

Asynergia

A lack of cooperation between muscles that usually work togethrer

Dysdiadochokinesia

Difficulty doing rapid, alternating mvmts such as pronation and supination

Dyskinesia

Unwanted and unnecessary mvmts

Bradykinesia

Slowness of mvmt

Apraxia

Motor planning deficit; often caused by a lesion to the supplementary motor area