motor system, muscle tone, UMN/LMN

basal ganglia

input: cortex, output: cortex, pedunculopontine nucleus, reticular formation
regulate muscle force, sequencing

cerebellum

input: cortex/brainstem, SC, vestibular system
output: cortex, brainstem, vestibular system
coordinates movement and postural control, timing and error correction

postural control

orientation and balance, requires 3 systems of balance
head position: vestibular, cervical proprioception, visual
postural control: medial tracts

reach and grasp

requires vision and somatosensation
phases: fast approach (feedforward, prediction), slow (homing in, visual feedback), contact and fine adjustment (likely feedforward with error corrections)

reach and grasp descending control

med motor system: control prox muscle and move hand toward object
lat motor system: orient and preshape the hand (feedforward)

locomotion centers: cerebrum

motor, limbic, BG, visual pathways
adaptive control of walking - modulates skill, initiate volitional locomotion, if attention required

locomotion centers: MLR

mesencephalic locomotor region
stepping produced by stimulation here, increased stimulation amplitude increases gait speed

locomotion centers: MRF

medullary reticular formation
interlimb coordination

locomotion centers: spinal cord CPG

central pattern generator
basic stepping pattern generator

muscle tone/stiffness

amount of tension in a resting muscle/resistance to stretch
measured with PROM, should have little to no resistance

muscle tone/stiffness mechanism

mechanical: major contributor, viscoelastic properties of muscle, weak cross-bridge binding
neural: min to no contributor at rest, descending motor control and reflexes

hypotonia

abnormally low resistance to passive stretch
disorders: developmental, acute UMN injury (spinal shock), acute cerebellar disorders, LMN lesions or disease
mechanism: loss LMN input to muscle, decreased descending input

flaccidity

no resistance, complete loss of tone, severe loss of LMN to muscle

hypertonia

velocity-dependent increased resistance felt as joint is passively moved through ROM
associated disorders: chronic UMN disorders
mechanism: neuromuscular overactivity, myoplasticity

myoplastic hyperstiffness

changes due to UMN lesions
loss of sarcomeres, increase weak cross-bridging, atrophy (stroke: type II > I, SCI: type I > II)

hypertonia: stroke

primarily myoplastic: increase in weak cross-bridging and contracture, hyperreflexia not significant
cortical strokes: CS tract disruption (loss fractionation), spasticity (reticulospinal tracts more active), but less hyperreflexia

hypertonia: SCI

myoplastic and neural: increase in weak cross-bridging and contracture and hyperreflexia
limits joint ROM, interferes with function, can cause deformity
lose corticospinal and reticulospinal input so increased excitability leads to more resistance and hyperreflexia

medications for spasticity

work to reduce excitability
baclofen: interferes with NT release in spinal cord
botox: interferes with Ach release from alpha MN
dantrolene: interferes with release of Ca from SR
diazepam: facilitates inhibition of SC

abnormal cutaneous reflexes

with SCI muscle spasms may occur in response to cutaneous stimuli after recovery from spinal shock
most common: muscle stretch hyperreflexia, clonus, clasp-knife response

muscle stretch hyperreflexia

loss of inhibitory CS input, LMN and interneuron increased excitability results in excessive LMN response to afferent stretch input
excessive muscle contraction when spindles are stretched from excessive firing LMNs

tonic stretch reflex

only present in people with UMN lesions, continues as long as stretch is maintained
loss of presynaptic inhibition allows slow or sustained stretch of central spindle to elicit continual muscle contraction, feedback loop that maintains neurologic tone

excess reticulospinal tract drive

corticoreticular lesions diminish cortical control of reticulospinal tract, absence of contra CS control so ipsi CS tract increases drive to reticulospinal tract
causes UMN dystonia (spontaneous excess contraction even at rest), abnormal muscle synergy

abnormal muscle synergies

reticulospinal tract provides voluntary control of paretic limb post stroke, consists of abnormal synergies that mainly affect proximal joints
activation of muscle groups that are unable to achieve the desired result

clonus

involuntary, repeating, rhythmic muscle contractions
unsustained clonus fades after a few beats even with maintained muscle stretch
sustained clonus >5 beats always pathologic, produced when lack of UMN control allows activation of oscillating neural networks in SC

clasp-knife response

paretic muscle is slowly and passively stretched, resistance drops at specific point in ROM, change in resistance similar to opening pocketknife
type II and Ib afferents elicit
autogenic inhibition: GTO, with increased tendon stretch muscle becomes inhibited so resistance drops

rigidity

velocity independent increase to passive motion
associated disorders: severe brainstem lesions, basal ganglia disorders
mechanism: increased activation of LMNs

gamma motor loop

gamma MN innervates intrafusal muscle fibers in muscle spindle, spindle has Ia afferents that can cause alpha MN to fire (DTR)
stimulation of muscle spindle → Ia afferents fire → alpha MN fires

decerebrate rigidity

aka gamma rigidity
lesion between sup and inf colliculi interrupts bilat CS, corticoreticular, and rubrospinal
VST and somatosensory input is spared, reticulospinal spared but lose drive to lat RST which causes increased excitability of gamma MN due to loss of inhibition
posture: extension of all 4 limbs

decerebellate rigidity

aka alpha rigidity
same lesion as decerebrate plus lesion of anterior cerebellum which increases excitability of vestibular nuclei d/t loss of purkinje cells
posture: same as decerebrate but even more rigidity, cutting dorsal root does not abolish rigidity so vestibulospinal tracts directly affect alpha MN

decorticate rigidity

lesion above superior colliculi, rubrospinal now intact so UE has some flexion tone
posture: LE ext, UE flex
can progress to decerebrate which is a bad sign meaning lesion has extended

paresis

partial loss of voluntary contraction, occurs in UMN lesions as a consequence of inadequate facilitation of LMNs
common after stroke, spastic CP, TBI, incomplete SCI

paralysis

complete loss of voluntary contraction, occurs in muscles innervated by LMNs below the level of a complete spinal cord lesion
muscles can still move spontaneously/reflexively but no volitional mvmt

disorder of LMNs

trauma, infection, degenerative or vascular disorders, tumors
affected muscles undergo loss of reflexes, atrophy, flaccid paralysis, fibrillations

fibrillations

single muscle fibers spontaneously fire off, cannot palpate/sense

fasciculations

spontaneous contractions of single motor unit, can palpate/sense

UMN syndrome

can cause paresis or paralysis, loss of fractionation of movement, abnormal reflexes, velocity-dependent hypertonia

loss of fractionation of movement

fractionation is ability to activate individual muscles independently of other muscles, fine motor control
interfere with fine movements such as hand dexterity in UE or dorsiflexing in LE

abnormal cutaneous reflexes

babinski’s sign: ext of great toe accompanied by fanning of other toes

cocontraction

simultaneous contraction of antagonist muscles, stabilizes joints to allow for precise movements and standing on unstable surfaces
if it remains too long can become problematic