2.21 Motor System 3 Flashcards
What may disorders of the motor system cause?
- paresis and paralysis
- muscle atrophy
- involuntary muscle contractions
- abnormal muscle tone
- abnormal reflexes
- disturbances of movement efficiency and speed
- impaired postural control
paresis
partial loss of voluntary contraction
paralysis
complete loss of voluntary contraction
types of muscle atrophy
- disuse atrophy
- neurogenic atrophy
- denervation of skeletal muscle
disuse atrophy is the result of
lack of muscle use
neurogenic atrophy is caused by
damage to nervous system
What produces the most severe atrophy?
denervation of skeletal muscle
What is essential for the health of skeletal muscle?
frequent neural stimulation, even at a level inadequate to produce muscle contraction
spontaneous involuntary contractions include
- muscle spasms
- cramps
- fasciculations
- myoclonus
- tremors
- fibrillations
- abnormal movements generated by dysfunctional basal ganglia
hypotonia
abnormally low resistance to passive stretch
two types of hypotonia
- velocity-dependent
- velocity-independent
velocity-dependent hypotonia
amount of resistance to passive movement depends on velocity of the movement
velocity-independent hypotonia
resistance to passive movement remains constant, regardless of speed of force application
flaccidity
lack of resistance to passive stretch
What can damage LMNs?
- trauma
- infection
- degenerative disorders
- vascular disorders
- tumors
if LMN cell bodies and/or axons are destroyed, then affected muscles can undergo:
- loss of reflexes
- atrophy
- flaccid paralysis
- fibrillations
UMN lesions can produce several changes in movement control, including:
- paresis or paralysis
- loss of fractionation of movement
- abnormal cutaneous reflexes
- velocity dependent hypertonia
paralysis in UMN syndrome
occurs in muscles innervated by LMNs below the level of a complete spinal cord lesion
paresis in UMN syndrome
- occurs in UMN lesions as a consequence of inadequate facilitation of LMNs
- common after stroke, in spastic CP, TBI, and incomplete SCI
UMN syndrome and loss of fractionation
interferes with fine movements, including fastening buttons or picking up coins, because the fingers of the involved hand act as a single unit
UMN syndrome and loss of fractionation: LE
in a lower limb, loss interferes with dorsiflexing the ankle
UMN syndrome: abnormal cutaneous reflexes
muscle spasms
- in people with SCI, muscle spasms may occur in response to cutaneous stimuli
- spasms begin after recovery from spinal shock
3 most common abnormal reflexes in those with chronic SCIs
- muscle stretch hyperreflexia
- clonus
- clasp-knife response
muscle stretch hyperreflexia
- loss of inhibitory corticospinal input combined with LMN and interneuron development of enhanced excitability
What does the loss of inhibitory corticospinal input combined with LMN and interneuron development of enhanced excitability result in?
excessive LMN response to afferent input from stretch receptors
muscle stretch hyperreflexia: excessive muscle contraction occurs when
when spindles are stretched as a result of excessive LMN firing
involuntary, repeating, rhythmic muscle contractions
clonus
unsustained clonus
fades after a few beats, even with maintained muscle stretch
sustained clonus is always
always pathologic in origin
When is sustained clonus produced?
when lack of UMN control allows activation of oscillating neural networks in spinal cord
When does clasp-knife response occur?
when paretic muscle is slowly and passively stretched and resistance drops at a specific point in the ROM
clasp-knife response: the change in resistance similar to opening of a pocket knife
initial strong resistance to opening gives way to easier movement
What afferents elicit the clasp-knife response?
type II
problems with velocity dependent hypertonia
- limits joint ROM
- interferes with function
- may cause deformity
What is velocity dependent hypertonia caused by?
muscular changes (myoplasticity) and/or spasticity
myoplasticity (velocity dependent hypertonia)
adaptive changes within a muscle in response to changes in NM
spasticity (velocity dependent hypertonia)
NM overactivity, 2˚ to UMN lesion
