Spinal Cord Descending Pathways Flashcards

1
Q

Descending Motor Tracts

A
  • originate from cerebral cortex and brainstem
  • functions: control movement, muscle tone, spinal reflexes, spinal autonomic functions, modulation of sensory transmission to higher centers
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2
Q

General Pathway of Primary Motor Cortex

A

-projects down –> crosses over –> goes down to level it needs to be in anterior horn –> acts on neuron that’s already down there (doesn’t cross over) –> acts on peripheral nerve –> acts on muscle –> contraction

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3
Q

General Organization of Motor Systems

A

-cerebral cortex and brainstem have interactions with thalamus, pons, cerebellum and basal ganglia in modification of movement

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4
Q

Apraxia

A

-normal strength but difficulty performing motor plan –> can’t put all the pieces together

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5
Q

Motor and Somatosensory Cortical Areas

A
  • primary motor cortex-Brodmann’s Area 4
  • motor association cortex-higher order motor planning and projects to primary motor cortex: supplementary motor area-Brodmann’s Area 6; premotor cortex-Brodmann’s Area 6 (both of these are in front of precentral gyrus)
  • primary somatosensory cortex: Brodmann’s Areas 3, 1, 2
  • somatosensory association cortex: receives inputs form primary somatosensory cortex: parietal association cortex-Brodmann’s Areas 5, 7; secondary somatosensory area
  • lesions in these areas present with contralateral symptoms
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6
Q

Medial Motor System

A
  • travels in anteromedial spinal cord columns to synapse on medial ventral horn motor neurons and interneurons
  • controls proximal axial and girdle muscles for tone, balance, orienting movements of head and trunk and automatic gait
  • consists of: anterior corticospinal tract, vestibulospinal tracts, reticulospinal tracts, tectospinal tract
  • lateral controls more distal extremities while medial controls more trunk/axial skeleton
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7
Q

Anterior Corticospinal Tract

A
  • control of bilateral axial and girdle muscles
  • originates in primary motor cortex
  • terminates cervical and upper thoracic spinal cord
  • runs ipsilaterally and acts a little bilaterally
  • stays ipsilateral going down anterior-medial motor column in SC, synapses on medial aspect of ventral horn, some crosses over and acts on interneurons to supply other side of trunk
  • it is the uncrossed corticospinal fibers going down-don’t decussates at medulla keeping our trunk upright
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8
Q

Vestibulospinal Tract

A
  • positioning of head and neck
  • controls limb extensor tone to maintain posture
  • balance
  • originates at vestibular nuclei of pons/medulla
  • runs entire cord
  • runs ipsilaterally and contralaterally
  • received input from cerebellum and ear
  • lots of cross innervation
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9
Q

Reticulospinal Tract

A
  • automatic posture and gait-related movements
  • originates: pontine and medullary reticular formation
  • runs entire cord
  • runs ipsilaterally
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10
Q

Tectospinal Tract

A
  • coordination of head and eye movements
  • originates at superior colliculus
  • terminates at cervical cord
  • decussates at midbrain
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11
Q

Lateral Motor System

A
  • travels in lateral column of spinal cord and synapse on lateral groups of ventral horn motor neurons and interneurons
  • controls movement of extremities
  • consists of lateral corticospinal tract (rapid dextrous movement at individual digits or joints) and rubrospinal tract
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12
Q

Lateral Corticospinal Tract

A
  • aka pyramidal tract: triangular shape in medulla
  • movements of contralateral limbs
  • originates in primary motor cortex and other frontal and parietal areas
  • runs entire cord
  • most fibers cross over (pyramidal decussation) at junction between medulla and spinal cord
  • lesions above decussation would produce contralateral weakness
  • lesions below would produce ipsilateral weakness
  • middle 1/3 of basis pedunculi is where lateral corticospinal tract runs
  • in medulla it runs in pyramids
  • decussates at cervicomedullary junction where brainstem ends and goes through foramen magnum
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13
Q

Corticospinal Course

A
  • cerebral cortex to corona radiata
  • descend into internal capsule
  • continues into midbrain cerebral peduncles “feet of brain”
  • basis pedunculi-ventral portion: middle 1/3 contains corticospinal and corticobulbar fibers
  • descend thru ventral pons to ventral medulla to form medullary pyramids
  • at cervicomedullary junction decussates to lateral white matter columns of cord forming lateral corticospinal tract
  • descends and enters gray matter of spinal cord to synapses on anterior horn cells
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14
Q

Internal Capsule

A
  • looks like two V’s with points facing in
  • thalamus and caudate medial
  • globus pallidus and putamen are lateral
  • 3 parts: anterior limb separates head of caudate from gp and putamen, genu transition between (at level of foramen of monro), posterior limb separates thalamus from gp and putamen (corticospinal tract lies in this limb)
  • lesion in this area can cause weakness in contralateral body or more selective
  • gp and putamen are part of basal ganglia
  • head of caudate is in floor of lateral ventrical
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15
Q

Corticobulbar

A
  • fibers projecting from cortex out to brainstem (bulb)
  • called corticobulbar rather than corticospinal because they project to the bulb
  • acts on neurons in brainstem (CN are in brainstem –> supply face)
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16
Q

Rubrospinal Tract

A
  • control of tone of limb flexor muscles in contralateral side
  • originates at red nucleus of the midbrain and receives connections from the cerebral cortex and the cerebellum
  • terminates at ventral horn synapsing with motor neurons
  • decussates in midbrain immediately
  • doesn’t start in cortex
  • a little more anterior than lateral corticospinal tract
17
Q

Cerebellum and Basal Ganglia

A
  • help refine or modulate output of motor system using multiple feedback systems
  • these don’t project directly to LMN
  • instead project back to motor cortex through thalamus-influencing movement in indirect ways
  • lesions can lead to ataxia
18
Q

UMN vs LMN

A
  • UMN: cross, motor neurons project from cortex down to spinal cord or brainstem; form synapses onto LMN
  • LMN: do not cross, located on anterior horns of central gray matter or in brainstem of motor nuclei; axons project out of CNS via ventral roots of spinal cord or cranial nerves to reach muscles in periphery
19
Q

UMN Lesions

A
  • weakness
  • increased tone-spasticity (velocity dependent)
  • increased reflexes-hyperreflexia
  • abnormal reflexes-babinski positive = lesion, posturing-usually signs before death
  • after acute UMN lesion often flaccid paralysis, decreased tone and decreased DTRs after time tone and reflexes increase
20
Q

LMN Lesions

A
  • weakness
  • atrophy
  • fasciculations (abnormal contractions of muscle-twitches)
  • hyporeflexia
  • hypotonia
21
Q

Spinal Cord Injury

A
  • most commonly caused by trauma, neoplasms, vascular occlusion, or multiple sclerosis
  • lesion may partially or completely interrupt spinal cord
  • may cause damage to ascending tracts, descending tracts, sensory and motor neurons at level of the lesion
22
Q

Complete vs. Incomplete SCI

A
  • A: complte transection
  • B: transection of ventrolateral quadrants
  • C: transection of ventral 2/3 (anterior spinal artery occlusion)
  • D: hemisection (Brown-Sequard)
  • E: normal
23
Q

ALS

A
  • amyotrophic lateral sclerosis
  • Lou Gehrig’s Disease/Wasting Palsy
  • degenerative disease of motor neurons
  • weakness and atrophy of muscles of hands, forearms, and legs spreading to involve most of body and face
  • lose ability to move and breathe
  • results from degeneration of ventral horns and corticospinal tracts
  • begins in middle age and progresses rapidly causing death within 2-5 years
  • no known treatment
24
Q

Transverse Myelitis

A
  • focal spinal cord inflammation
  • primary identifiable causes are SLE, MS or viral infection
  • most cases represent an autoimmune disorder
  • dx: CSF analysis, viral titers, serologies, T2 MRI with Gadolinium enhancement (focal signal abnormality)
  • tx: steroids, immunosuppressive agents, PT
25
Q

Multiple Sclerosis

A
  • autoimmune inflammatory disease affecting CNS myelin

- plaques of demyelination and inflammatory response form scars

26
Q

Neurologic Gait and the PT

A
  • difficulty walking is common result of neurologic impairments
  • understanding the cause of the impairment can help PT examine, evaluate, diagnosis, and form a prognosis and treatment plan for gait disturbances
27
Q

Spastic Gait

A
  • unilateral or bilateral corticospinal tracts
  • stiff-legged circumduction sometimes with scissoring of legs and toe walking, decreased arm swing, unsteady, falling toward side of greater spasticity
  • cortical, subcortical, or brainstem infarcts affecting upper motor neuron pathways; cerebral palsy; degenerative conditions, MS, SC lesions
28
Q

Ataxic Gait

A
  • cerebellar vermis or other midline cerebellar structures
  • wide based, unsteady, staggering, side to side, and falling toward side of worse pathology
  • toxins like alcohol, meds, tumors of cerebellar vermis
29
Q

Vertiginous Gait

A
  • vestibular nuclei, vestibular nerve, or semicircular canals
  • looks similar to ataxic, wide based, unsteady, sway and fall when attempting to stand with feet together and eyes closed
  • toxins like alcohol, infarcts or ischemia of vestibular nuclei, vertigo
30
Q

Frontal Gait

A
  • frontal lobes or frontal subcortical white matter
  • slow, shuffling, narrow or wide based magnetic unsteady
  • hydrocephalus; frontal tumors; bilateral anterior cerebral artery infarcts
31
Q

Parkinsonian Gait

A
  • substantia nigra or other regions of basal ganglia
  • slow, shuffling, narrow based, difficulty initiating walking, stooped forward, en bloc turning, unsteady with retropulsion
  • parkinson’s disease
32
Q

Dyskinetic Gait

A
  • subthalamic nucleus or other regions of basal ganglia
  • unilateral or bilateral dance like, flinging, or writhing movements
  • huntington’s, infarct of subthalamic nucleus or striatum, levodopa side effect
33
Q

Tabetic Gait

A
  • posterior columns or sensory nerve fibers
  • high-stepping, foot-flapping gait difficult in dark or on uneven surfaces
  • posterior cord syndrome; severe sensory neuropathy
34
Q

Paretic Gait

A
  • nerve roots, peripheral nerves, neuromuscular junction, or muscles
  • proximal hip weakness may be waddling, trendelenburg gait, sudden knee buckling, foot drop can cause high stepping
35
Q

Painful Gait

A
  • peripheral nerve or orthopedic injury
  • pain may be obvious based on patients report or facial expression, avoid pressure on affected limb
  • herniated disc, peripheral neuropathy, muscle strain, contusions, fractures
36
Q

Orthopedic Gait Disorder

A
  • bones, joints, tendons, ligaments, and muscles
  • depends on location; peripheral nerve injury or SC-related deficits may be present as well
  • arthritis, fractures, dislocations, contractures, soft tissue injuries
37
Q

Functional Gait Disorder

A
  • psychologically based
  • some times pts say have poor balance yet spontaneously perform highly destabilizing swaying movements while walking without ever falling
  • conversion disorder, factitious disorder