• Sensory & Motor Homunculus
• Upper Motor Neurons (UMNs)
• Lower Motor Neurons (LMNs)
• Monosynaptic Stretch-Reflex (MSR) Arc
• Spinal-Cord Grey \text{vs.} White Matter
• Somatotopy = point-to-point correlation between a body region and its representation within the CNS.
• Numerous CNS nuclei, tracts, and cortical areas preserve this map.
• Pre-central gyrus (primary motor cortex, frontal lobe) houses the Motor Homunculus.
– Distorted figure reflects density of UMNs controlling each body part.
• Post-central gyrus (primary somatosensory cortex, parietal lobe) houses the Sensory Homunculus.
– Larger cortical territory allotted to areas with finer discriminatory touch (e.g., lips, fingertips).
• Clinical significance: a small cortical infarct can yield highly predictable focal motor or sensory losses.
• Grey = neuronal cell bodies, dendrites, proximal axons; organized into dorsal, lateral, and ventral horns.
– Site of synapses for incoming (sensory) and outgoing (motor) info.
• White = myelinated axons grouped into fasciculi/tracts funiculus-by-funiculus.
– Conveys long-distance communication between cord & higher centers.
• MSR arc integrates both: sensory afferent enters dorsal horn, interneuron (if present) sits in grey, efferent LMN exits ventral horn.
• Fasciculus = bundle of axons inside the CNS that share common origin, destination, & modality. Examples:
– Fasciculus Gracilis
– Fasciculus Cuneatus
• Tract = fasciculus whose termini are explicitly known (e.g., Cortico-spinal tract).
• Funiculus = large white-matter region containing multiple fasciculi/tracts.
– Posterior, Lateral, Anterior funiculi.
• Modality: proprioception, vibration, fine/discriminative touch.
• Composed of central-process axons of DRG neurons.
• Two side-by-side fasciculi:
– Fasciculus Gracilis (FG): medial, carries lower trunk & lower-extremity information from T7 and below.
– Fasciculus Cuneatus (FC): lateral, carries upper trunk & upper-extremity information beginning at T6 and above.
• Four-neuron chain:
(1) DRG ➜ \text{FG/FC} (ascend ipsilaterally).
(2) Synapse in medullary nuclei (Nucleus Gracilis or Cuneatus).
(3) Internal-arcuate fibers decussate, ascend as medial lemniscus to thalamus (VPL).
(4) Thalamo-cortical projection to post-central gyrus.
• Lesion rules: ipsilateral loss below lesion until decussation, then contralateral.
• Descending, efferent \sim 10^6 axons.
• Origin: layer 5 pyramidal cells (Betz) of pre-central gyrus.
• Pathway:
– Internal Capsule ➜ cerebral peduncle (midbrain) ➜ basis pontis ➜ medullary pyramids.
– \approx 85\% of fibers decussate at pyramidal decussation in lower medulla, enter contralateral lateral funiculus as LCST.
– Remaining 15\% descend uncrossed as Anterior Corticospinal Tract (ACST); most of these cross at segmental level to supply axial muscles.
• Termination: synapse on LMNs (or interneurons) in ventral horn; LMN axons leave via ventral root to NMJ.
• Functional role: voluntary, fractionated, distal-limb movement.
• Ascending, afferent pain, temperature, crude/light touch.
• Four-neuron chain:
(1) Peripheral receptor ➜ DRG.
(2) Synapse in ipsilateral dorsal horn.
– Axon decussates within 1-2 spinal segments via anterior white commissure.
(3) Ascend contralaterally as STT through medulla, pons, midbrain to thalamus (VPL).
(4) Thalamo-cortical projection ➜ post-central gyrus.
• Lesion: contralateral loss beginning 2 segments below the lesion (because of short ascending propriospinal climb before crossing).
• Dorsal Columns: ipsilateral ascent, cross in medulla, modalities = proprioception/vibration/fine touch.
• LCST: descends contra-laterally after medullary decussation, modality = voluntary limb motor.
• STT: crosses soon after entry, ascends contralaterally, modality = pain/temperature/light touch.
• At lesion level: LMN damage ➜ hypo- or areflexia.
• Below lesion (if tract cut but ventral horn intact): UMN signs ➜ hyper-reflexia, clonus, Babinski.
• Above lesion: normal.
• Sensory: bilateral loss of all modalities below lesion.
• Motor: bilateral flaccid at level, spastic below.
• MSR:
– At level: absent (LMN).
– Below: hyperactive (UMN).
• Ipsilateral motor loss (LCST) with spasticity below lesion.
• Ipsilateral dorsal-column modality loss below lesion.
• Contralateral pain/temp loss (STT) \ge 2 segments below.
• MSR: hyperreflexive ipsilaterally below lesion.
• LMN signs (flaccid paralysis, fasciculations, atrophy) confined to myotome at that level on ipsilateral side.
• Above: normal.
• Below: intact/possible mild weakness if LCST spared.
• Reflexes: absent for muscles innervated at that segment only.
• Sensory: none (dorsal horn/columns intact).
• Pattern depends on which tract(s) are hit; grey horns spared so segmental LMNs survive.
• Segmental LMN loss \pm STT decussating fibers (cape-like loss of pain/temp in syringomyelia).
• Progressive degeneration of UMNs (motor cortex & LCST) + LMNs (ventral horn).
• Mixed picture:
– UMN signs: hyperreflexia, spasticity, Babinski.
– LMN signs: atrophy, fasciculations, hypo-/areflexia.
• Sensory pathways spared ➜ no primary sensory deficit.
• Is the pathway motor or sensory?
• What modality is carried?
• Where does it decussate?
• Ultimate cortical destination?
• Expected clinical deficits if lesioned?
• MSR presentation:
(1) At lesion?
(2) Above lesion?
(3) Below lesion?
• Brown-Séquard at T10: predict proprioception, motor, pain/temp, and reflexes per side.
• Lesion limited to posterior funiculus at C4: sensory ataxia without weakness.
• Ventral-horn poliomyelitis at L3: flaccid paralysis in quadriceps, absent knee-jerk, normal sensation.
• Central cord (syrinx) within cervical enlargement: bilateral "cape" loss of pain/temp with hand weakness.
• ALS progression: explain coexistence of hyperreflexive patellar reflex and wasted hand intrinsic muscles.