#17 - Motor Pathways I: Spinal Systems Flashcards

1
Q

Internal Capsule Parts (3) and what they house

A
  1. Anterior Limb
    • Frontopontine fibers
  2. Genu
    • Corticobulbar fibers
  3. Posterior limb
    • Corticospinal fibers
    • All corticopontine fibers other than frontopontine
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2
Q

Corticobulbar Fibers leaving the pons go to CN nuclei…

A

V, VII

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3
Q

Corticobulbar Fibers leaving the medulla go to CN nuclei…

A

IX, X, XII

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4
Q

Corticobulbar Fibers leaving the foramen magnum to the SC go to CN nuclei…

A

XI

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5
Q

5 descending motor systems that reach the spinal cord

A
  1. Corticospinal system: neurons from primary motor cortex to spinal cord
  2. Reticulospinal system: neurons from brainstem reticular formation to spinal cord
  3. Vestibulospinal system: neurons from brainstem vestibular nuclei to spinal cord
  4. Tectospinal System: neurons from midbrain tectum (superior colliculus) to spinal cord
  5. Rubrospinal system: neurons from red nucleus to spinal cord
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6
Q

Pyramidal vs Extrapyramidal

A
  • Pyramidal: only the corticospinal (and corticobulbar) tracts
  • Extrapyramidal: all other motor tracts
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7
Q

Reticulospinal Tracts

A
  • Brainstem Reticular Formation to SC
  • Modulation of muscle tone, switch on SPG
    1. Pontine (medial) reticulospinal tract (MRST)
  • Origin: pontine tegmentum
  • Spinal course: anterior funiculus
  • Targets: mostly interneurons
  • Functions: facilitates anti-gravity, extensor muscles and increases muscle tone (gamma motor system)
  1. Medullary (lateral) reticulospinal tract (LRST)
  • Origin: medullary reticular formation
  • Spinal course: lateral funiculus
  • Targets: mostly interneurons
  • Functions: suppresses extensor muscle activity and reduces muscle tone (gamma motor system)
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8
Q

Vestibulospinal Tracts

A

Brainstem Vestibular Nuclei to SC

  1. Lateral vestibulospinal tract
    • Origin: Lateral vestibular nucleus (ipsilateral)
    • Target: Ipsilateral intermediate zone and medial motor neuron groups (black dots)
    • Function: excites gamma motor neurons, which increase tone in trunk and proximal limb extensors, maintaining upright posture (vestibulo-spinal reflex: spreading arms out)
  2. Medial vestibulospinal tract
    • Origin: Medial vestibular nucleus (bilateral)
    • Target: bilateral intermediate zone and medial motor neuron groups (white dots) for neck and shoulder muscles, ends at T1
    • Function: maintenance of head in upright position (vestibulo-collic reflex)
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9
Q

Tectospinal Tract

A
  • Origin: superior colliculus (midbrain tectum) to SC
  • Crosses immediately in the midbrain!
  • Targets: axial alpha motor neurons controlling neck muscles
  • Function: reflexive head turn toward/away from visual or auditory stimulus
    • Is velocity-dependent: at most velocities, the reflex will turn the head toward a novel stimulus, but above threshold velocities, the tectospinal activation is protective, turning the head away form the fast-approaching stimuli
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10
Q

Rubrospinal Tract

A
  • Red Nucleus to SC
  • Tract is most like the corticospinal tract in function
  • Origin: red nucleus (midbrain), which gets inputs from numerous cortical areas iand cerebellum
  • Suggests that M1, red nucleus, and cerebellum form a recurrent network involved in the feedback control of voluntary actions (since M1 also receives info from cortex and cerebellum)
  • Decussates immediately in midbrain!
  • Targets: intermediate zone interneurons that synapse on distal limb alpha motoneurons in neck and upper limb only
  • Function: facilitates flexor activity (like corticospinal tract) in cervical spinal cord, but only in a coarse manner; we care about it in terms of abnormal posturing.
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11
Q

Decorticate Posture

A
  • Lesion is in the rostral midbrain or higher, above the red nucleus
    • RN is spared, so damage is rostral to midbrain
  • Rubrospinal biased flexion overrides vestibulospinal and reticulospinal biased extension, but only for the upper limb = we only see upper limb flexion
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12
Q

Decerebrate Posture

A
  • Lesion of the upper pons, so damage to red nucleus itself
    • RN is bilaterally damaged, so damage involves the midbrain or down to the mid-pons
    • If damage extends further caudal, the LVST could also be damaged and we’d see other probs
  • Activity in the intact vestibulospinal system (arising lower down in pontomedullary region) is biased for extension, causing rigidity of all four limbs
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13
Q

Corticopontine System

A
  • Largest descending motor control system in the CNS
  • Cortical input to ipsilateral pons (which then goes to contralateral cerebellum via MCP)
  • Conveys motor plan and integrates sensory data to the cerebellum
  • Makes up the majority of internal capsule
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14
Q

Sections of Internal Capsule and their contents

A
  • Anterior limb: Frontopontine fibers
  • Genu: corticobulbar fibers
  • Posterior limb:
    • Corticospinal fibers
    • Temporopontine fibers
    • Parietopontine fibers
    • Occipitopontine fibers
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15
Q
A
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16
Q

Hand Muscle Motoneuron Location

A
  • Dorsal part of C7-T1 ventral horn
  • Direct innervation from corticospinal tract
    • Thought to allow individual, fractionated had, forearm movements
17
Q

Lateral Corticospinal Fiber Targets, Function

A
  • 80% end in intermediate zone
  • 20% end on alpha motor neurons, particiularly in dorsolateral part of ventral horn
  • Function:
    • Strongest influence on flexor muscle groups
    • Make adaptive CPG modifications
    • Excites whatever it lands on (including inhibitory interneurons)
18
Q

MRST

A
  • Pontine (medial) reticulospinal tract (MRST)
  • Origin: pontine tegmentum
  • Spinal course: anterior funiculus
  • Targets: mostly interneurons
  • Functions: facilitates anti-gravity, extensor muscles and increases muscle tone (gamma motor system)
19
Q

LRST

A
  • Medullary (lateral) reticulospinal tract (LRST)
  • Origin: medullary reticular formation
  • Spinal course: lateral funiculus
  • Targets: mostly interneurons
  • Functions: inhibits extensor muscle activity and reduces muscle tone (gamma motor system)
20
Q

Tectum

A
  • Inferior colliculi
    • Maps sounds in space
    • Sends info to superior colliculus
  • Superior colliculi
    • Maps retinotopic info
    • Integrates auditory & visual stimuli
    • Drives tectospinal tract for reflexive head movement
21
Q

UMN Lesion Symptoms

A
  • Spasticity
    • Paresis
    • Hypertonia
    • Hyperreflexia
  • Clonus
  • Babinski sign
22
Q

LMN Lesion Symptoms

A
  • Almost always ipsilateral
  • Paralysis = loss of movement
  • Paresis = diminution of movement
  • Hypotonia = decrease in muscle tone
  • Hyporeflexia = decreased reflexes
  • Areflexia = absent reflexes
  • Fasciculations = spontaneous activity of muscle fibers at rest
  • Muscle atrophy
23
Q

Spasticity vs Rigidity

A
  • Spasticity = pyramidal damage (corticospinal tract)
    • Combination of paresis, hyperreflexia, and hypertonia
    • Variable features that distinguish it from extrapyramidal rigidity:
      • More resistance in one direction (increased tone in flexors with corticospinal tract damage)
      • Velocity dependent (more noticeable with fast movements)
  • Rigidity = extrapyramidal damage
    • Rigidity is a kind of hypertonia
    • Indicates damage to basal ganglia or vestibulospinal tracts
      • When BG only are involved, a “cogwheel” effect can be seen; circular, jerking rigidity in flexion and extension in the background tremor, that continues throughout an entire range of movement
    • Muscles are stiff, but rigidity features same resistance to all directions of movement (flexion and extension)
    • Is not velocity dependent
24
Q

Clonus

A
  • A pattern of involuntary and rhythmic muscle contraction resulting from lesion in descending motor pathways
  • Two widely accepted hypotheses:
    • Caused by hyperactive stretch reflexes via self-excitation, producing rhythmic stimulation of LMN
    • Caused by CPG activity arising as a consequence of peripheral sensory events, producing the rhythmic effect
  • May be seen at ankle, knee, wrist, jaw, and elbow, or any muscle with a frequency of 5-8 Hz.
25
Q

Hyperreflexia Explanation

A
  • UMN lesion symptom
  • Due to loss of supraspinal inputs to neurons that inhibit alpha/gamma motor neurons
    • Loss of excitatory corticospinal fiber innervation to inhibitory interneurons, which inhibit alpha/gamma motor neurons via spindle type II pathways, results in exaggerated stretch reflex
    • Fast adapting type Ia fibers encode changes in muscle length and velocity without temporally precise reference to immediate length
  • BASICALLY: Both supraspinal inputs and type Ia pathways work to inhibit the type II alpha/gamma motor neurons. So, if you take away the supraspinal input, there’s less inhibition, so you see hyperreflexia.