#17 - Motor Pathways I: Spinal Systems Flashcards
Internal Capsule Parts (3) and what they house
- Anterior Limb
- Frontopontine fibers
- Genu
- Corticobulbar fibers
- Posterior limb
- Corticospinal fibers
- All corticopontine fibers other than frontopontine
Corticobulbar Fibers leaving the pons go to CN nuclei…
V, VII
Corticobulbar Fibers leaving the medulla go to CN nuclei…
IX, X, XII
Corticobulbar Fibers leaving the foramen magnum to the SC go to CN nuclei…
XI
5 descending motor systems that reach the spinal cord
- Corticospinal system: neurons from primary motor cortex to spinal cord
- Reticulospinal system: neurons from brainstem reticular formation to spinal cord
- Vestibulospinal system: neurons from brainstem vestibular nuclei to spinal cord
- Tectospinal System: neurons from midbrain tectum (superior colliculus) to spinal cord
- Rubrospinal system: neurons from red nucleus to spinal cord
Pyramidal vs Extrapyramidal
- Pyramidal: only the corticospinal (and corticobulbar) tracts
- Extrapyramidal: all other motor tracts
Reticulospinal Tracts

- 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)
- 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)
Vestibulospinal Tracts
Brainstem Vestibular Nuclei to SC
- 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)
- 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)
Tectospinal Tract
- 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
Rubrospinal Tract
- 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.
Decorticate Posture
- 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
Decerebrate Posture
- 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
Corticopontine System
- 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
Sections of Internal Capsule and their contents
- Anterior limb: Frontopontine fibers
- Genu: corticobulbar fibers
- Posterior limb:
- Corticospinal fibers
- Temporopontine fibers
- Parietopontine fibers
- Occipitopontine fibers


Hand Muscle Motoneuron Location
- Dorsal part of C7-T1 ventral horn
- Direct innervation from corticospinal tract
- Thought to allow individual, fractionated had, forearm movements
Lateral Corticospinal Fiber Targets, Function
- 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)
MRST
- 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)
LRST
- 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)
Tectum
- 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
UMN Lesion Symptoms
- Spasticity
- Paresis
- Hypertonia
- Hyperreflexia
- Clonus
- Babinski sign
LMN Lesion Symptoms
- 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
Spasticity vs Rigidity
- 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
Clonus
- 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.
Hyperreflexia Explanation
- 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.