Motor Systems and Tracts CH13/14

Cocontraction

agonist and antagonist muscles contract at same time

stabilizes joint

cocontraction when using a new skill looks more (smooth or rigid)

rigid

motor pools

cell bodies with axons to a single muslce

anterior/ventral cell bodies innervate

extensors

posterior/dorsal cell bodies innervate

flexors

motor neurons

convey signals to extrafusal and intrafusal m fibers

2 types of motor neurons

alpha

gamma

motor neuron cell bodies located in what horn

ventral horn

alpha motor neurons

project to extrafusal m

large cell bodies and myelinated

release ACh to contract innervated m

gamma motor neurons

project to intrafusal m

medium sized and myelinated

regulate m tension

alpha-gamma coactivation

maintain stretch and sensitivity of m spindle

extrafusal contracts so intrafusal contracts

spinal cord coordination

through neural communication with spinal cord

SC mechanisms synchronize m contractions through

reciprocal inhibition

muscle synergies

proprioceptive input

stepping pattern generators SPGs

SC proprioceptive inputs from

joint capsule/ligament receptors

m. spindle receptors

golgi tendon organs

golgi tendon organs in proprioception role

register tendon tension

adjust m. contraction

does NOT inhibit voluntary m. contraction

golgi tendon organs direct

direct circuit in spinal cord

activates type Ib afferents

GTO input can

facilitate or inhibit motor neuron firing

SC stepping pattern generators

spinal interneurons that activate motor neurons to flex/extend the hips and knees

SPGs afferent input

adjusts timing, transitions, and muscle activations

spinal reflexes

involuntary motor response to external stimulus

tell us info about PNS and CNS

types of spinal reflexes

phasic stretch reflex

cutaneous reflex

phasic stretch reflex: muscle spindles

muscle contraction in response to quick stretch

quick m stretch activates m spindles to alpha mn

cutaneous reflex

withdrawl reflex

(step on a leggo -> pick your leg up reflex)

a cutaneous stimulation that causes reflex

located in SC

reciprocal inhibition

contract muscle

signal to SC

inhibits antagonist

(so you don't fight opposite m.)

relationship btwn reflexive and voluntary movement

will override reflex to do protective voluntary movement

-arousal levels change this

-modifies/adjusts m. spindle output

contractures

can't fully elongate m. thru full ROM

contracture causes

long periods of not using or moving thru ROM

being in cast

coma

sarcromere changes with contractures

sarcomeres disappear in shortened position

add sarcomeres in lengthened position

involuntary m contractions

muscle cramps

fasciculations- quick, with fatigue

myoclonus - breif

fibrillations- not visible

tremors

muscle cramps

severe, painful m contractions

seconds to minutes

tremors

involuntary contracations

types: resting, action, physiologic

physiologic tremor

normal

low level

from anxiety, stress, meds, withdrawl

resting tremors

in parkinsons dz, affect mainly hands and LE

slight rolling of hands

action tremors

cerebellar tremors

severe during final part of movement

ex. reach for something, hand shaking

lower motor neuron lesions

signs = weakness, atrophy, flaccidity, lack of contraction

to detect = NCS, EMG

polio

impacts motor neuron cell bodies

symptoms = m. weakness, pain, fatigue, trouble breathing

tend to overuse few neurons you have

polio implications

implications for strength, control and fatigue

sensory contribution to movement control

sensation necessary to learn new movement

absent vision -> depend on somatosensation and proprioception

Central motor system

signals from somatosensory neurons and decending motor tracts determine output from MN to m.

cerebellum and motor basal ganglis adjust activity

in all regions of CNS

sensory info adjusts motor activity

medial motor tracts

posture, gross limb movement

occur automatically

ex. turn before you register what something is

lateral motor tracts

selective/ skilled fine motor movements

ventral horn posture/movement

levels of excitation in cord/reflex arcs

medial tracts

reticulospinal tract

medial and lateral vestibulospinal tracts

medial corticospinal tract (axial mvmt)

lateral tracts

rubrospinal tract

lateral corticospinal tract

reticulospinal tract

posture and gross limb mvmt

coordinate trunk during walking

posture adjustments

control m. synergies

neck reflexes

lateral motor tracts selective motor control

activate m. independently (isolated)

lateral corticospinal tract

starts in motor planning of primary motor cortex

most decussates in lower medulla

to spinal cord then specific m.

cortical motor areas

primary motor cortex

-prepare for movement

-premotor area and supplementary motor area

-homunculus

signs of UMN tract lesions

paresis and paralysis

abnl reflexes

myoplasticity

abnl m. tone

atrophy

cant isolate movements

abnl cocontraction

abnl m. synergies

hemiplegia

weakness on one side of body

paraplegia

weakness below arms (lower body)

tetraplegia

weakness of all four limbs

paresis

weakness, abnl motor neurons

paralysis

no movement below complete spinal cord lesion

babinski sign

abnl reflex

The toes flex upward when sole of foot is stimulated

indicating motor nerve damage

clonus

abnl reflex

involuntary beats/ m. contractions

clasp-knife

abnl reflex

resist thru part of PROM, then drips all of a sudden

phasic stretch hyperreflexia

high velocity stretch

1st PROM, then quick stretch

excessive motor neuron response to afferent stretch receptors

myoplasticity

adaptive structural changes in muscle

response to changes in neuro activity

from chronic m disuse, sarcomeres disappear, optimal force in new resting length

ex. contracture

muscle tone

resistance to stretch in resting muscle

PROM to assess

resistance range

flaccid - no resistance

hypotonia- floppy

normal

hypertonia/spacicity- high tone, inc with fast mvmt

rigid

causes of flaccidity and hypotonicity

MN lesions

developmental disorders

intracranial hemorrhage

acute MT lesions/CNS shock

hypertonia

strong resistance/high tone

two types- velocity-dependent and rigid

causes of hypertonia

chronic UMN lesions

basal ganglia disorders

Spasiticity

velocity-dependent hypertonia

more tone with faster movement

from changes in m. tissue and neuro overactivity

decerebrate rigidity

rigid extension of UE

decorticate rigidity

flexed U limbs

extended neck and L limbs

plantarflexion

muscle atrophy

loss of m. bulk

disuse or neurogenic (damage to NS)

frequent neural stimulation

is essential for the health of skeletal m.

abnl co-contraction

compensatory- to compensate for weak m

pathologic- when it interferes with movement

abnormal synergy

exaggerated interlimb neural coupling

ex. pt with CP has arm bent, hand floppy on one side but normal on other side

Amyotrophic Lateral Sclerosis (ALS)

bilateral UMN and LMN degradation

can affect frontal lobe

affects motor, CNs, but not sensations

die from respiratory failure