Specialty: Anatomy

Primary Motor Cortex (M1)

Location: Precentral gyrus (Brodmann area 4)

Organization:

• Motor Homunculus: Somatotopic representation with disproportionate areas based on motor control precision
  • Medial: Lower limb and foot (paracentral lobule)
  • Lateral convexity: Upper limb, hand (largest representation)
  • Inferior: Face, tongue, larynx (fine motor control)
• Cortical Layers:
  • Layer V: Contains Betz cells (giant pyramidal neurons); give rise to ~3% of corticospinal fibers
  • Layer III: Smaller pyramidal neurons contribute majority of corticospinal tract
• Function: Direct control of voluntary movements; activation generates contralateral movement

Premotor Areas

Premotor Cortex (PMC)

Location: Anterior to M1 (Brodmann area 6, lateral)

Function:

• Planning and sequencing of movements
• Externally guided movements (visual cues)
• Bilateral movements and proximal muscle control
• Lesions cause apraxia, especially for learned motor sequences

Supplementary Motor Area (SMA)

Location: Medial surface of frontal lobe (Brodmann area 6, medial)

Function:

• Internal generation of movements (self-initiated)
• Planning complex, sequential movements
• Bilateral coordination
• Lesions cause motor neglect, difficulty initiating movements

Frontal Eye Fields (FEF)

Location: Posterior middle frontal gyrus (Brodmann area 8)

Function:

• Voluntary saccadic eye movements
• Contralateral gaze deviation (drives eyes to opposite side)
• Acute lesion: Eyes deviate toward lesion (can’t look away)
• Seizure focus: Eyes deviate away from lesion (forced gaze)

Lateral Corticospinal Tract (Pyramidal Tract)

Function: Voluntary control of distal limb muscles (especially fine finger movements)

Pathway:

1. Origin:
   • 30% from primary motor cortex (M1, area 4)
   • 30% from premotor and supplementary motor areas (area 6)
   • 40% from primary sensory cortex (areas 3, 1, 2) – modulates sensory feedback
2. Corona Radiata: Fibers converge as they descend through centrum semiovale
3. Internal Capsule:
   • Posterior limb: Corticospinal and corticobulbar fibers
   • Somatotopic organization: Face anterior, arm middle, leg posterior
   • Genu: Corticobulbar fibers to lower face
4. Cerebral Peduncle:
   • Middle 3/5 of crus cerebri in ventral midbrain
   • Face fibers medial, leg fibers lateral
5. Basis Pontis:
   • Descends through ventral pons
   • Scattered among pontine nuclei
   • Gives off corticobulbar fibers to motor cranial nerve nuclei
6. Medullary Pyramids:
   • Forms distinct pyramidal elevations on ventral medulla
   • Contains ~1 million axons
7. Pyramidal Decussation:
   • At cervicomedullary junction (foramen magnum level)
   • 85-90% of fibers cross to form lateral corticospinal tract
   • 10-15% remain ipsilateral as anterior corticospinal tract
8. Lateral Corticospinal Tract in Spinal Cord:
   • Descends in lateral funiculus (dorsolateral white matter)
   • Fibers progressively peel off medially to synapse on ventral horn
   • Synapse on alpha motor neurons (directly) and interneurons (indirectly)

Anterior Corticospinal Tract

Function: Control of axial and proximal limb muscles

Pathway:

• 10-15% of fibers that remain uncrossed at pyramidal decussation
• Descends in anterior funiculus of spinal cord
• Most fibers eventually cross at segmental level via anterior white commissure
• Terminates primarily in cervical and upper thoracic levels
• Bilateral control of trunk and proximal muscles

Corticobulbar Tract

Function: Control of muscles of face, head, and neck via cranial nerves

Pathway and Innervation:

Cranial Nerve	Function	Cortical Innervation	Clinical Pearl
CN III, IV, VI	Eye movements	Bilateral	Cortical lesions don’t cause diplopia
CN V	Mastication	Bilateral	Jaw deviation rare with unilateral lesion
CN VII (upper)	Frontalis, orbicularis oculi	Bilateral	Forehead spared in cortical lesions
CN VII (lower)	Lower face	Contralateral only	Lower face weak in cortical lesions
CN IX, X	Palate, pharynx, larynx	Bilateral	Unilateral cortical lesion: mild dysarthria only
CN XI	SCM, trapezius	Complex (ipsilateral SCM)	SCM weakness ipsilateral to cortical lesion
CN XII	Tongue	Contralateral	Tongue deviates toward weak side

Rubrospinal Tract

Origin: Red nucleus (magnocellular part) in midbrain tegmentum

Pathway:

• Crosses immediately in ventral tegmental decussation (of Forel)
• Descends contralaterally near lateral corticospinal tract
• Well-developed in animals; rudimentary in humans
• Controls flexor tone in upper extremities

Vestibulospinal Tracts

Lateral Vestibulospinal Tract

• Origin: Lateral vestibular nucleus (Deiters’ nucleus)
• Course: Descends ipsilaterally in anterior funiculus
• Function: Facilitates ipsilateral extensor tone; maintains upright posture
• Clinical: Important for decerebrate rigidity

Medial Vestibulospinal Tract

• Origin: Medial vestibular nucleus
• Course: Descends bilaterally in medial longitudinal fasciculus (MLF)
• Function: Head and neck position; coordination with eye movements
• Terminates: Cervical cord only

Reticulospinal Tracts

Pontine (Medial) Reticulospinal Tract

• Origin: Pontine reticular formation
• Course: Descends ipsilaterally in anterior funiculus
• Function: Facilitates extensors, inhibits flexors
• Clinical: Contributes to decerebrate rigidity

Medullary (Lateral) Reticulospinal Tract

• Origin: Medullary reticular formation
• Course: Descends bilaterally in lateral funiculus
• Function: Facilitates flexors, inhibits extensors
• Clinical: Opposes pontine reticulospinal; balance of both maintains normal tone

Tectospinal Tract

• Origin: Superior colliculus (optic tectum)
• Function: Reflex turning of head and neck toward visual/auditory stimuli
• Course: Crosses in dorsal tegmental decussation; descends to cervical cord only

Upper Motor Neuron (UMN) Signs

Definition: Lesion anywhere from motor cortex to anterior horn cell

Clinical Features:

Feature	Finding	Mechanism
Weakness	Pattern: Extensors > flexors (arm); Flexors > extensors (leg)	Loss of corticospinal facilitation
Tone	Spasticity (velocity-dependent); “clasp-knife”	Unopposed vestibulo/reticulospinal
Reflexes	Hyperreflexia; clonus	Loss of descending inhibition
Babinski	Upgoing toe (extensor plantar)	Pyramidal tract dysfunction
Atrophy	Minimal (disuse only); late finding	Lower motor neuron intact
Fasciculations	Absent	Lower motor neuron intact

Lower Motor Neuron (LMN) Signs

Definition: Lesion of anterior horn cell, nerve root, peripheral nerve, or neuromuscular junction

Clinical Features:

Feature	Finding	Mechanism
Weakness	Flaccid; follows myotome/nerve distribution	Direct loss of motor neuron
Tone	Hypotonia or flaccidity	Loss of muscle innervation
Reflexes	Hyporeflexia or areflexia	Reflex arc interrupted
Babinski	Absent (downgoing or mute)	Reflex arc interrupted
Atrophy	Prominent and early (weeks)	Denervation
Fasciculations	Often present	Spontaneous motor unit firing

Cortical Lesions

Middle Cerebral Artery (MCA) Stroke

• Pattern: Contralateral face and arm weakness > leg (leg area spared in medial cortex)
• Additional: Sensory loss, aphasia (dominant), neglect (non-dominant)
• Gaze: Eyes deviate toward lesion (away from hemiparesis)

Anterior Cerebral Artery (ACA) Stroke

• Pattern: Contralateral leg weakness > arm and face (medial motor cortex affected)
• Additional: Abulia, grasp reflex, urinary incontinence
• Bilateral: Akinetic mutism if both SMA areas affected

Subcortical Lesions

Internal Capsule Stroke (Lacunar)

• Pattern: Pure motor hemiparesis; face = arm = leg (all fibers together)
• Location: Posterior limb of internal capsule
• Cause: Lenticulostriate artery occlusion (hypertensive vasculopathy)
• Key: No sensory, visual, or language deficits (pure motor)

Brainstem Lesions

Weber Syndrome (Medial Midbrain)

• Ipsilateral: CN III palsy (ptosis, dilated pupil, “down and out” eye)
• Contralateral: Hemiparesis (cerebral peduncle involvement)
• Cause: Posterior cerebral artery or perforating branches

Millard-Gubler Syndrome (Ventral Pons)

• Ipsilateral: CN VI and VII palsy (can’t abduct eye; facial weakness including forehead)
• Contralateral: Hemiparesis (corticospinal tract in basis pontis)

Medial Medullary Syndrome

• Ipsilateral: CN XII palsy (tongue deviates toward lesion)
• Contralateral: Hemiparesis (pyramid); loss of vibration/proprioception (medial lemniscus)

Spinal Cord Lesions

Brown-Séquard Syndrome (Hemisection)

• Ipsilateral: UMN weakness below lesion; loss of vibration/proprioception
• Contralateral: Loss of pain/temperature 1-2 levels below
• At level: LMN weakness in corresponding myotome

Anterior Spinal Artery Syndrome

• Bilateral: Flaccid paraplegia or quadriplegia; loss of pain/temperature
• Spared: Vibration, proprioception (dorsal columns)
• Cause: Aortic surgery, hypotension, atherosclerosis

Central Cord Syndrome

• Pattern: Arms > legs (central corticospinal fibers to arms affected first)
• Hands: Often profound weakness; sacral sparing common
• Cause: Hyperextension injury in setting of cervical stenosis
• Sensory: “Cape” distribution pain/temperature loss (crossing spinothalamic fibers)

Conus Medullaris Syndrome

• Motor: Mixed UMN/LMN (early hyperreflexia, then areflexia)
• Sensory: Saddle anesthesia; perianal numbness
• Autonomic: Bladder/bowel dysfunction (early and severe)
• Pain: Minimal or absent

Cauda Equina Syndrome

• Motor: Pure LMN (flaccid, areflexic)
• Sensory: Asymmetric, radicular pattern
• Autonomic: Bladder/bowel dysfunction (late)
• Pain: Severe radicular pain (prominent)

Decerebrate vs Decorticate Posturing

Feature	Decorticate	Decerebrate
Lesion Level	Above red nucleus (cortex/internal capsule)	Below red nucleus (midbrain/pons)
Upper Extremities	Flexed, adducted	Extended, pronated
Lower Extremities	Extended	Extended
Mechanism	Loss of cortical inhibition; rubrospinal intact	Loss of rubrospinal; unopposed vestibulospinal
Prognosis	Better than decerebrate	Worse prognosis

Amyotrophic Lateral Sclerosis (ALS)

Pathology: Degeneration of both upper and lower motor neurons

Clinical Features:

• UMN signs: Spasticity, hyperreflexia, Babinski sign
• LMN signs: Weakness, atrophy, fasciculations
• Distribution: Can start in limbs (limb-onset) or bulbar (bulbar-onset)
• Spared: Extraocular movements, bladder/bowel function, sensation
• Split hand: Preferential wasting of thenar/first dorsal interosseous vs hypothenar

Diagnostic Criteria (El Escorial):

• Evidence of LMN degeneration (clinical, EMG, or neuropathology)
• Evidence of UMN degeneration (clinical)
• Progressive spread within or between regions
• Absence of other disease processes

Primary Lateral Sclerosis (PLS)

• Pure UMN disease: Spasticity, hyperreflexia, Babinski
• No LMN signs: No atrophy or fasciculations
• Diagnosis: Requires >4 years without LMN signs (may evolve into ALS)
• Prognosis: Better than ALS; slower progression

Progressive Muscular Atrophy (PMA)

• Pure LMN disease: Weakness, atrophy, fasciculations
• No UMN signs: Reflexes normal or reduced; no spasticity or Babinski
• Prognosis: Better than ALS but many eventually develop UMN signs

Spinal Muscular Atrophy (SMA)

Genetics: SMN1 gene deletion (5q13); autosomal recessive

Types:

Type	Onset	Features	Survival
Type 1 (Werdnig-Hoffmann)	0-6 months	Never sit; severe hypotonia; “frog leg” posture	<2 years
Type 2	6-18 months	Sit but never walk; tremor	>2 years
Type 3 (Kugelberg-Welander)	>18 months	Walk then lose ambulation; proximal weakness	Normal lifespan
Type 4	Adulthood	Mild proximal weakness	Normal lifespan

Muscle Strength Testing (MRC Scale)

Grade	Description	Clinical Correlation
0	No contraction	Complete paralysis
1	Flicker of contraction	Visible/palpable but no movement
2	Movement with gravity eliminated	Can move laterally but not lift
3	Movement against gravity	Can lift but not against resistance
4	Movement against some resistance	Weaker than normal
5	Normal strength	Full strength

Key Muscle Testing (Nerve Root Level)

Root	Muscle	Action	Test Position
C5	Deltoid	Shoulder abduction	Resist arm abduction at 90°
C6	Biceps	Elbow flexion	Resist elbow flexion
C7	Triceps	Elbow extension	Resist elbow extension
C8	FDP to middle finger	Finger flexion	Resist DIP flexion of middle finger
T1	Interossei	Finger abduction	Resist finger spreading
L2	Iliopsoas	Hip flexion	Resist hip flexion
L3	Quadriceps	Knee extension	Resist knee extension
L4	Tibialis anterior	Ankle dorsiflexion	Walk on heels
L5	Extensor hallucis longus	Great toe extension	Resist big toe extension
S1	Gastrocnemius	Ankle plantarflexion	Walk on toes; single leg toe raise

Deep Tendon Reflexes

Reflex	Nerve Root	Nerve	Technique
Biceps	C5-C6	Musculocutaneous	Tap biceps tendon in antecubital fossa
Brachioradialis	C5-C6	Radial	Tap brachioradialis ~4cm above wrist
Triceps	C7-C8	Radial	Tap triceps tendon above elbow
Knee (patellar)	L3-L4	Femoral	Tap patellar tendon below kneecap
Ankle (Achilles)	S1-S2	Tibial	Tap Achilles tendon with foot dorsiflexed

Pathological Reflexes (UMN Signs)

• Babinski: Upgoing great toe with fanning of other toes when lateral sole stroked
• Hoffman: Flick distal phalanx of middle finger → thumb and index flex (upper extremity Babinski)
• Clonus: Rapid dorsiflexion of ankle → rhythmic beats (>3 abnormal)
• Jaw Jerk: Hyperactive = bilateral corticobulbar lesion (pseudobulbar palsy)

Mastery of motor pathways requires understanding:

1. Cortical organization: Motor homunculus, premotor areas, motor planning
2. Descending tracts: Corticospinal (pyramidal) and extrapyramidal pathways
3. Decussation points: Pyramidal at cervicomedullary junction; corticobulbar varies by cranial nerve
4. UMN vs LMN signs: Critical for localization
5. Clinical syndromes: Pattern recognition for rapid localization
6. Motor examination: Systematic testing to identify lesion location

The key to motor localization is integrating the pattern of weakness (distribution), associated UMN or LMN signs, and accompanying sensory or cranial nerve findings. This systematic approach enables precise anatomical diagnosis essential for boards and clinical practice.