Nervous System IV - Peripheral

Upper Motor Neurons

carry motor information within the CNS, typically start in the frontal lobe, completely contained within CNS, synapse on LMNs, originate in cortex, direct or indirect

Direct UMNs

carry motor information that is fast and precise (finely coordinated speech and finger movements)

Indirect UMNs

carry motor information for controlling reflexes, posture, muscle tone

Lower Motor Neurons

carry motor information within the PNS, originate in brain stem/SC, synapse directly on muscle fibers, cell BODIES contained in CNS, but axons join PNS

Nucleus

where LMN cell bodies aree/where UMN/LMN synapses occur, usually in SC or brainstem

Pyramidal decussation

crossing point where contralateral control happens, all spinal cord UMNs cross here, but UMNs in brainstem cross elsewhere

located at most inferior part of medulla

UMN Innervation to LMN

Contralateral: CN XII

Bilateral: CN V, IX, X, XI

Special for VII: Upper face is bilateral, lower face is contralateral

Descending fibers/tracts

Corticobulbar tract, corticospinal tract, rubrospinal tract

Ascending fibers/tracts

Spinothalmic tract

Corticobulbar tract

from cortex to brainstem, descending motor pathway of UMNs, corona radiata → internal capsule → branches of brainstem for LMN synapse

Corticospinal tract

from cortex to spine, starts in motor strip/precentral gyrus, descends through internal capsule → spinal cord

Rubrospinal tract

from brainstem to spine

Spinothalmic tract

ascends from periphery → spinal cord → thalamus → sensory strip

Spinal Cord

continuous with medulla, ipsilateral control, exits vertebrae at transverse foramen, ends as the cauda equina

Spinal Cord Signaling

Motor: Out from ventral (anterior) side

Sensory: In from dorsal (posterior) side

Phrenic Nerve

cervical spinal roots C3, C4, and C5, innervates diaphragm (motor and sensory), sensory innervation for pericardium and parietal pleura

Flaccid dysarthria

caused by damage to LMN or to muscle, features weakness or erduced muscle tone

breathiness (RLN of X), hypernasality (IX, X), imprecise consonants (VII, IX, X, XII), monopitch (RLN/SLN of X)

Spastic dysarthria

caused by damage to direct/indirect UMNs bilaterally, features excessive muscle tone/spasticity at velopharynx (less closure), larynx (hyperadduction), makes speech slow and effortful

Ataxis dysarthria

caused by damage to cerebellar control circuit, affects artic and prosody, impairs coordination of movement PATTERNS, leads to inaccurate and slow movements, slurred speech

Hypokinetic dysarthria

caused by damage to basal ganglia, often seen in Parkinson’s, features rigidity, decreased mobility, reduced rate or rapid and accelerating rate, difficulty initiating movement

Hyperkinetic dysarthria

caused by damage to basal ganglia, has prominent effects on prosody, leads to production of abnormal, rhythmic or irregular and unpredictable, rapid or slow INVOLUNTARY movements

Apraxia of speech

phonetic-motoric speech disorder, problems with planning, leads to distortions of speech, difficulty with co-articulation, extension of consonants, vowels, time between sounds/syllables/words, errors consistent in location only