SNS.pdf - Bailey Gwyn

Overview

The Somatic Nervous System governs voluntary movement and conscious somatic sensation. Its efferent limb runs from upper motor neurons (UMNs) in the cortex to lower motor neurons (LMNs) in the brainstem and anterior horn of the spinal cord, projecting to skeletal muscle via the neuromuscular junction. The afferent limb relays touch, vibration, proprioception, pain, temperature, and crude touch from peripheral receptors to cortex through exquisitely organized ascending pathways.

Core Components

Motor: Corticospinal & corticobulbar tracts → LMNs → motor units.
Sensory: Dorsal column–medial lemniscus (DCML), spinothalamic (ALS), trigeminothalamic pathways.
Segmental circuits: Reflex arcs (monosynaptic & polysynaptic), central pattern generators.

Key Functions

Skilled movement, posture, and muscle tone.
Discriminative touch, vibration, joint position, pain & temperature.
Protective and postural reflexes; sensorimotor integration.

Descending Motor Pathways

Tract	Origin → Course → Termination	Function	Lesion Pattern
Corticospinal (Pyramidal)	Primary motor cortex (precentral gyrus) → internal capsule → cerebral peduncle → medullary pyramids (≈85–90% decussate) → lateral corticospinal tract → LMNs.	Fine voluntary movement; fractionated distal control.	UMN signs (spasticity, hyperreflexia, Babinski, weakness with minimal atrophy) contralateral to a supramedullary lesion.
Corticobulbar	Motor cortex face area → internal capsule genu → brainstem motor nuclei (bilateral except lower facial nucleus, hypoglossal partial).	Voluntary control of cranial motor (face, tongue, pharynx, larynx).	Contralateral lower facial weakness (forehead sparing); dysarthria, tongue deviation away from lesion (UMN).
Extrapyramidal (rubro/reticulo/vestibulo)	Brainstem nuclei → spinal interneurons & LMNs.	Tone, posture, gross automatic movements, head/eye positioning.	Imbalance of tone & postural reflexes; axial/appendicular instability.

UMN vs LMN: UMN lesions → spasticity, hyperreflexia, Babinski; LMN lesions → flaccid weakness, hyporeflexia/areflexia, fasciculations, atrophy.

Ascending Sensory Pathways

Modality	Pathway	Primary Relay	Clinical Lesion
Fine touch, vibration, proprioception	DCML: Dorsal roots → gracile/cuneate fasciculi → dorsal column nuclei (caudal medulla) → decussate as internal arcuate fibers → medial lemniscus → VPL thalamus → S1.	VPL (body), VPM (face for trigeminal)	Ipsilateral loss below medullary decussation (spinal lesion); contralateral loss above (brainstem/cortical).
Pain & temperature	Spinothalamic (ALS): DRG → Lissauer’s tract → dorsal horn → decussate segmentally (anterior commissure) → ascend contralaterally → VPL.	VPL	Contralateral loss beginning ~1–2 segments below lesion (“cape” distribution in syringomyelia at C8–T1).
Face sensations	Trigeminal pathways: principal nucleus (touch) & spinal trigeminal nucleus (pain/temp) → decussate → trigeminothalamic → VPM → S1 face area.	VPM	Facial sensory loss ± corneal reflex changes (CN V afferent; VII efferent).

Spinal Reflexes & Segmental Circuits

Monosynaptic

Stretch (myotatic): muscle spindle → Ia afferent → α-LMN; maintains tone & posture.
Jendrassik maneuver augments reflex by central facilitation.

Polysynaptic

Golgi tendon: Ib afferent limits excessive tension.
Flexor withdrawal / crossed extensor: protective, intersegmental.

Key Deep Tendon Reflexes (DTR)

Biceps	C5–C6 (musculocutaneous)
Brachioradialis	C6
Triceps	C7–C8
Knee (patellar)	L3–L4 (femoral)
Ankle (Achilles)	S1–S2 (tibial)
Plantar response	Corticospinal integrity (Babinski)

Motor Unit & Neuromuscular Junction (NMJ)

A motor unit comprises a single α-LMN and all innervated muscle fibers. Recruitment and rate coding scale force. Fiber types: Type I (slow, oxidative) vs Type II (fast, glycolytic). Chronic denervation → fiber type grouping (reinnervation) & atrophy.

NMJ Physiology

ACh release → nicotinic receptors → end-plate potential → muscle AP.
Safety factor normally prevents transmission failure; autoantibodies or toxins reduce it.

Disorders

Myasthenia gravis	Anti-AChR (or MuSK); fatigable weakness, ptosis; improves with rest; decrement on RNS.
Lambert–Eaton	Anti-VGCC; proximal weakness, autonomic signs; increment on high-frequency RNS.
Botulism	Presynaptic ACh release blockade; descending paralysis, autonomic dysfunction.

Clinical Localization — Patterns

Level	Findings	Examples
Cortex / Internal Capsule	Contralateral face–arm–leg UMN weakness; aphasia/neglect if dominant/non-dominant hemisphere; cortical sensory loss.	MCA stroke; lacunar infarct (pure motor).
Brainstem	“Crossed” signs: ipsilateral cranial nerve deficits + contralateral body weakness/sensory loss.	Lateral medullary/Wallenberg; medial medullary; pontine lesions.
Spinal Cord	Level-defined UMN signs below + segmental LMN at lesion; sensory level; autonomic involvement.	Anterior cord syndrome; Brown–Sequard; central cord/syrinx.
Root (Radiculopathy)	Dermatomal pain/sensory loss; myotomal weakness; reduced reflex at level.	L5 radiculopathy (foot dorsiflexion), C7 (triceps).
Plexus / Peripheral Nerve	Patchy or nerve distribution deficits; LMN signs; length-dependent sensory loss (stocking–glove).	Brachial plexopathy; diabetic polyneuropathy; carpal tunnel.
NMJ	Fluctuating fatigable weakness; normal sensation; reflexes normal or reduced if severe.	MG, LEMS, botulism.
Muscle (Myopathy)	Proximal > distal weakness; normal sensation; CK often ↑; reflexes preserved until late.	Duchenne/Becker; inflammatory myositis; endocrine myopathy.

Somatic Sensory Exam & Dermatomes

Bedside Modalities

Light touch & vibration (128 Hz tuning fork) → DCML.
Pinprick & temperature → ALS.
Proprioception (joint position); Romberg for DCML integrity.

Common Landmarks

C5 lateral upper arm; C6 thumb; C7 middle finger; C8 little finger.
T4 nipple line; T10 umbilicus.
L4 medial malleolus; L5 dorsum of foot; S1 lateral foot.

Quantitative Tests

Nerve conduction studies (NCS) & EMG for neuropathy/radiculopathy.
Somatosensory evoked potentials (SSEPs) for pathway integrity.
Quantitative sensory testing (QST) in research/selected clinics.

Tip: A “sensory level” strongly localizes to the spinal cord; dissociated loss (pain/temp vs vibration) suggests tract-specific lesions.

Motor Control: Tone, Gait, Coordination

Tone

Spasticity (UMN): velocity-dependent increased tone, clasp-knife.
Rigidity (basal ganglia): cogwheel/lead-pipe, not velocity dependent.
Hypotonia (LMN/cerebellar).

Coordination

Cerebellar ataxia: dysmetria, dysdiadochokinesia, intention tremor.
Sensory ataxia: worsens with eyes closed; positive Romberg.

Gait Patterns

Hemiparetic (circumduction) — UMN unilateral.
Spastic diplegic — scissoring, UMN bilateral.
Steppage — foot drop (L5/peroneal neuropathy).
Ataxic — wide-based (cerebellar or sensory).
Parkinsonian — shuffling, reduced arm swing, festination.

Red Flags & Time-Critical Conditions

Acute focal deficit	Stroke/TIA — activate stroke protocol; thrombolysis/mechanical thrombectomy windows.
Rapid ascending weakness	Guillain–Barré syndrome — monitor respiration (vital capacity), IVIG or plasmapheresis.
Spinal cord compression	Back pain + sensory level + sphincter signs — MRI urgently; steroids if malignant compression.
Myasthenic crisis	Bulbar/respiratory weakness — ICU, NIF/VC monitoring, IVIG/PLEX.

Rehabilitation & Plasticity

Recovery after somatic pathway injury leverages neuroplasticity and task-specific training. Principles include high-repetition practice, intensity progression, multisensory feedback, and minimizing learned non-use. Adjuncts: neuromuscular electrical stimulation, robot-assisted therapy, virtual reality, and spasticity management (stretching, chemodenervation, intrathecal baclofen).