Clinical Correlations - Pyramidal Tracts and Motor Neurons

pyramidal tract controls

voluntary movement via corticospinal and corticobulbar tracts

pyramidal tract originates in the

brain cortex

extrapyramidal tract controls

involuntary movement and maintenance of posture - motor modulation

extrapyramidal tracts originate in the

brainstem

decorticate rigidity of extrapyramidal tract

injury at superior border of red nucleus disturbing descending corticopsinal and rubrospinal tracts

decorticate rigidity posture

flexion of the upper extremities and extension of lower extremities

decerebrate rigidity of extrapyramidal tract

injury at superior border of the pons causes lateral ventrospinal tract and reticulospinal tract to overactivate extensor motor neurons with inhibition of cortex and basal ganglia

decerebrate rigidity posture

extensor muscles of all limbs and muscles of neck and trunk to have increased tone

holmes tremor

resting and intention postural tremor with slow freqeuncy and large amplitude

holmes tremor occurs from

lesions in basal ganglia, brainstem CVA (extrapyramidal tract)

upper motor neuron

first system of relay from the cortex to periphery - activates LMN

UMN are found in the

precentral gyrus and terminate in the spinal cord/brainstem

clinical symptoms of UMN lesions

weakness, spasticity, clonus, co-contraction and hyperreflexia

injuries of UMN occur in the

central nervous system (CVA, TBI, malignancy, neurodegenerative disorders)

spasticity

increase in muscle resistance to velocity dependant passive stretch

UMN spasticity is often seen in

flexors of UE and extensors of LE

clonus

rhythmic, involuntary muscle contraction with swift dorsiflexion stretch

co contraction

simultaneous contraction of antagonist and agonist muscle around a joint (stiff)

UMN lesions impact the rate of

rapid alternating movements

hyperreflexia of deep tendon reflexes

due to decreased modulation via descending inhibitory pathways

examples of hyperreflexia of UMN lesion

babinski sign and hoffman's reflex

assessments of lesions are

fatiguable with repeated testing

babinski sign is

normal in peds, not normal in adults

circumduction gait could be seen with

UMN lesion to compensate for LE extensor tone

lower motor neuron

directly innervates skeletal muscle via impulses to spinal peripheral nerves or cranial nerves

cell bodies of LMN are in

anterior horn of spinal cord and cranial nerve nuclei

clinical symptoms of LMN lesions

muscle atrophy, fasciculations, hyporeflexia, decreased tone, negative babinski sign, flaccid paralysis

atrophy in LMN vs UMN

LMN atrophy is immediate and drastic wasting, UMN is disuse atrophy over time

diagnoses of LMN lesions can include

peripheral nerve injury, spinal muscular atrophy, guillain barre syndrome, polio, radiculopathy

fasciculations

Involuntary contractions or twitchings of muscle fibers

ALS

selective degeneration of motor neurons and motor tracts - could have LMN and UMN symptoms

two ways ALS presents itself

limb onset and bulbar onset

limb onset with ALS

weakness begins in body

bulbar onset ALS

weakness begins with face/mouth

UMN and LMN signs

weakness of body, face, muscles of respiration, atrophy, fasciculations/fibrillations, hyperreflexia/hyporeflexia, abnormal reflexes and spasticity

UMN facial nerve has two parts

one innervates top part of the face, one innervates bottom part of the face

UMN upper face nuclei

bilaterally innervated from the cortex

UMN lower face nuclei

contralaterally innervated from the cortex

LMN after synapse in CN VII

effects both upper and lower face

lower motor neuron lesion (facial nerve)

lesion in CN VII after nucleus, weakness of face ipsilateral to lesion, cant close eyelid, decreased lacrimal and salivary gland production (bells palsy)

upper motor neuron lesion (facial nerve)

lesion in the cortex, preservation of muscles of facial expression in upper 1/2 of face, weakness in lower 1/2 of face contralateral to lesion