·         Descending Motor Pathways

·         Pathways from brain carrying motor commands down to “lower motor neurons”

 

·         “Lower Motor Neurons” (LMNs)

·         Neurons whose axons synapse on skeletal muscle fibers (to stimulate contraction)

·         aka “alpha motor neurons”

·         aka “final common path”

·         majority are in ventral horns of cord

·         some are in the brainstem (cranial nerve motor neurons)

 

·         Motor Units

·         Motor unit = a single LMN + the extrafusal muscle fibers it synapses on

·         Some motor units are small (axon synapses on just a few fibers); some motor units are large (axon synapses on ~1000 fibers).

·         All fibers of a motor unit would be stimulated by neurotransmitter (ACh) release at the same time.

·         All movements depend on LMNs.

 

 

·         Spinal Anatomy and Physiology
Spinal Nerves

·         Myotomes

·         Muscle and tissue of the body innervated by spinal nerve roots

·         Key myotomes

·         Arm extension:  C-5

·         Elbow extension:  C-7

·         Small finger abduction:  T-1

·         Knee extension:  L-3

·         Ankle flexion:  S-1

·         “Upper Motor Neurons”(UMNs):

·         The brain cells that send motor commands down to the LMNs.

·         UMNs are the source of the “descending motor pathways”

·         Damage to UMNs affects motor  function/control because there is a loss of commands to the LMNs

 

·         The Corticospinal or Pyramidal Pathway

·         Most direct route for UMNs to influence LMNs (Cortex to LMN)

·         Evolutionarily recent, largest in man

·         Most important for fine, precise, rapid, skilled voluntary movements of small motor units (e.g. hands, facial muscles)

·         Big body muscles receive more input from other “extrapyramidal” motor pathways

 

 

·         Spinal Reflexes

·         Spinal cord is not just a cable between brain and body. Segments of cord also have “local” functions relatively independent of the brain.

·         Monosynaptic stretch reflex

·         Multisynaptic withdrawal or flexor reflex

·         Multisynaptic withdrawal plus crossed extensor reflex

 

·         Stretch Reflex

 

 

 

 

 

 

·         Muscle Fibers Depend on Their Innervation

·         Muscle fibers that lose their LMN show:

·         no reflexive contraction (so no muscle tone)

·         no voluntary contraction

·         This is called “flaccid paralysis”

·         atrophy of the muscle fibers over time

·         These are “symptoms of LMN damage”

 

·         Poliomyelitis

·         Viral infection causing a summer cold/flu –like illness in most, but which, in some, infects LMNs – most often those controlling the lower limbs.

·         If those neurons die, the muscle fibers in their motor units will be paralyzed, show no reflexes and will atrophy.

·         Example of LMN Damage:
Polio Induced Paresis(weakness)
& Paralysis

·         Muscle Atrophy

·         Cause by loss of LMNs due to polio

 

·         Other Descending Tracts:
Extrapyramidal Motor Pathways

·         Rubrospinal pathway to regulate tone of flexors in limbs for locomotion & to organize repetitive movements that involve the flexors (e.g. walking, running, crawling)

·         Vestibulospinal pathway to stimulate extensors (antigravity) for standing, posture

·         Tectospinal pathway for reflexive motor reactions to visual stimuli

·         Reticulospinal pathway to regulate muscle tone by modulating the stretch reflex

·         Corticospinal path modulates activity of these tracts as well as spinal reflexes

 

·         Babies Are Born With Pre-Programmed Reflexes

 

·         Upper Motor Neurons Modulate Muscle Tone Via Gamma Motor Neurons

·         “Gamma motor neurons” (the “other” motor neurons) do not go to the extrafusal fibers that move us.

·         They synapse on “intrafusal muscle fibers” inside stretch receptors/muscle spindle receptors.

·         Tensing these little fibers makes stretch receptors more sensitive.

·         UMN also can inhibit stretch reflex to allow movement, so we are not stiff statues.

 

 

·         Symptoms of UMN Damage

·         Reflexes and muscle tone still present and, in fact, intensifiedàhyperreflexia

·         Voluntary control impaired

·         “Spastic paralysis” (excess muscle tone & loss of voluntary control of movement)

·         No denervation induced atrophy (LMNs are okay)

·         Reflex Changes After UMN Damage

·         hyperactive stretch reflex, particularly in anti-gravity muscles

·         too much muscle tone (hypertonia or spasticity)

·         clonus (rapid repetitive response to stretch)

·         altered Babinski & cremasteric reflexes after corticospinal damage

·         Normal vs. Positive Babinski

 

·         Clonus

·         Without descending modulation from brain, stretch reflex leads to repetitive contractions

 

·         UMN Syndromes

·         UMN damage above red nucleus à ”decorticate posture” with arms flexed, hands fisted (upper picture)

·         UMN damage between red nucelus and vestibulospinal & reticulospinal tractsàdecerebrate posture”

 

·         Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig’s Disease

·         Fatal progessive loss of LMNs as well as corticospinal pathway (UMNs). Several genes involved.

·         Onset most often in late 50’s-early 60’s; more men affected

·         70% will die within 5 years      (eventually cannot swallow,         breathe)

 

·         ALS – Symptoms

·         First symptoms usually muscle cramping & twitching, with feelings of fatigue & weakness in a limb

·         Loss of LMNs causes weakness, paralysis, loss of reflexes & atrophy in affected muscles. Loss of UMNs causes spasticity (muscle stiffness, cramping from too much tonus).

·         Combination of UMN + LMN symptoms at multiple levels is fairly diagnostic

·         New treatments : riluzole (Rilutek) slows progression a little but research on gene therapy or stem cell implants probably critical

·         Spinal Cross section

·         Cross-Sections

·         Notice 1) the difference in the amount of white matter in the upper vs lower cord

·         2) Size of ventral horns (which reflects # of LMNs at each level

·         You should be able to recognize the level of these sections

 

·         Spinal Cord Injuries (SCI)

·         ~10,000/yr in US; 50% disabled

·         Today about 10% die  (used to be 90%)

·         Estimated 500,000 survivors, 200,000 in wheelchairs

·         About 2/3 are under 30; 82% are males

·         Causes of SCIs

·         Similar pattern to head injury data:

·         ~45% in motor vehicle accidents

·         ~22% in falls

·         ~16% due to violence

·         ~13% in sports

·         Must assume those with head injuries have spinal injury too until we know otherwise.

 

·         What Damages Cord?

·         Can have SC concussion or contusion

·         Overstretching or twisting of cord (like a CHI)

·         Fracture or dislocation of vertebrae causing laceration or compression of cord

·         Penetrating injury (e.g. bullet)

·         Vascular problem causing infarct

·         SCIWORA - spinal cord injury without radiographic abnormality

 

·         Location of Damage

·         Cervical vertebrae most fragile & likely to fracture

·         Most mobile parts of spine (C5-C6, T12-L1, C1-C2) most likely to dislocate or overstretch

·         Cervical injuries - quadriplegia

·         Lumbar injuries - paraplegia

·         Can also have incomplete injuries

 

·         Consider the anatomy and function of the pathways we have discussed and where each crosses the midline:

·         Dorsal column pathway

·         Spinothalamic pathway

·         Corticospinal pathway

 

 

·         Use That Info to Predict the Impairments In This Case (10 pt)

·         John has suffered a bullet wound to the right half of the spinal cord at the thoracic level. Draw out the various pathways to decide what will and won’t John be able to feel with each of his 4 limbs. What will and won’t he be able to move normally? Will any muscles show denervation atrophy? Will any muscles show hyperreflexia & spasticity? Explain your answer.