Lesions Brain Stem Infarct

Neuro Block 7 Session 3 1. Explain the differences between the lateral and medial motor pathways. What are the different tracts within these 2 pathways? Lateral: • Movement of contralateral limbs, goal directed movement • Corticospinal: distal limb • Rubrospinal: flexors in proximal limb • Motor nuclei: flexors more central than extensors Medial: • Automatic posture adjustments, eye movements, more axial muscles • Anterior corticospinal: motor for bilateral axial and girdle muscles • MVST: VOR and eye coordination • LVST: balance and posture • Reticulospinal: posture, gait movement (decerbate posture) • Tectospinal Tract: coordination of head and eye movement and forward gaze

2. Lateral Corticospinal Tract: • Fine motor movement excites flexors and inhibits extensors • Goal directed movements that are internally generated (not reflex) and improve with practice •

Cortex corona radiata posterior limb of interior capsule (face medial/ant; leg lateral/posterior) cerebral peduncle (midbrain) anterolateral pons pyramids (medulla) decussation (85% fibers cross) lateral which matter spinal cord  synapse into motor nuclei (especially cortical/lumbar)

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Lesion o Above pyramids: (UMN) contralateral weakness o Below pyramids: (LMN) ipsilateral weakness

3. Lesions of the lateral corticospinal tract at the following anatomical locations result in what type of deficits?: Cortex: contralateral Post. limb of internal capsule: contralateral hemiplegia Weber Syndrome: cerebral peduncle lesion—usually due to PCA occlusion • Affect lateral corticospinal tract and CN III • Contralateral paralysis of arm, leg, tongue, lower face • CN III damage ipsilateral ptosis, pupil dilation, lateral strabismus

Medial Medullary Syndrome: • Vertebral artery or PICA stroke • Contralateral hemiparesis of arm, leg • CN XII: ipsilateral tongue paresis and atrophy • Medial lemniscus: contralateral loss of fine touch

Cervical Corticospinal: • Ipsilateral hemiparesis/paralysis of upper and lower limbs • In acute stage, no UMN symptoms but eventually yes Thoracic Corticospinal: • Ipsilateral lower limb only Brown-Sequard Syndrome: hemisection • Ipsilateral paresis/paralysis • UMN lesion, spastic paralysis • (+) Babinski contralateral? • Sensory: loss of pain and temp (anterolateral) contralateral • Loss of fine touch (dorsal column medial lemniscus) ipsilateral

4. Rubrospinal Tract: • Cortex and cerebellum indirectly influence motor activity via red nucleus • Excitement of motor neurons to proximal flexors • Contralateral cerebellar nuclei/ ipsilateral cerebral cortex (Xdecorticate lesionX)  red nuclei  cross immediately via ventral tegmentum decussation descends via lateral funiculus via corticospinal tract  ends on alpha LMN and gamma LMN

5. Rubrospinal tract lesions result in which type of deficits? -Decorticate Posturing: (w/lesion) • Arms flex in, legs extend when you lesion cortex red nucleus fibers -Bendekit’s Syndrome: unilateral red nucleus lesion • CN III damage: ipsilateral ptosis etc. • Contralateral tremor

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Contralateral hemianesthesia if medial lemniscus affected CN III goes through red nucleus

6. Lateral Vestibulospinal Tract: • Balance and posture using vestibular input • CN VIII has input for 4 vestibular nuclei (pons and medulla) • Also input from flocculus and nodulus • CN VIII/Flocculonodular LVST nuclei ipsilateral laminae VII and VIII in all spinal levels excite alpha and gamma LMN of neck and limb extensors (especially proximal antigravity) 7. Lesions of the lateral vestibulospinal tract result in which deficits? • Lesion to CN VIII or CN VIII nucleus  falling to ipsilateral side (lose extensor input) -Lateral Medullary Syndrome (of Wallenbuerg): • PICA or vertebral occlusions • Loss of nucleus ambiguous • Dysphagia, dysarthyia, decreased Gag, ipsilateral • Ipsilateral loss of pain and temp to face due to CN V • Horners: ptosis (drooping), myosis (pupils constrict), anhydrosis (can’t sweat) due to descending sympathetic fiber loss ipsilateral • Loss of VIII vertigo, vomiting, nystagmus • Contralateral loss of pain and temp of body (spinothalamic lesion), all others ipsilateral

8. Medial Vestibulospinal Tract (MVST): • Coordination of eye movements • VOR: keeps eyes focused on stationary objects whole head moves • Project bilateral within MLF to inhibit alpha and gamma LMN’s that control neck and axial movements (MLF= medial longitudinal fasiculus) • Project superiorly to CN III, IV, VI nuclei (through MLF) -VOR: • Interruption of MLF  comatose patients eyes will move with head (doll’s eyes) -PPRF: • Paramedian pontine reticular formation • Coordinates incoming CN III information

9. Lesions of the MVST: -INO: (internuclear opthalmoplegia) • Unilateral MLF lesion, lesioned side can’t move (can’t adduct eye) • Opposite side has abducting nystagmus • MS, tumor, pons infarct is cause -Loss of CN VI nucleus: • Lesion R. Vi nucleus • R. medial deviation (can’t abduct) • L. lateral deviation (can’t adduct) • If lesion on right, can’t look right with other eye 10. Corticotectal Tract/Tectospinal Tract: • Facilitates reflexive eye movement and head turning with attention grabing • Associated with upward gaze • Retina, visual cortex superior colliculi tectospinal fibers dorsal tegmentum (decussation) MLF  C. Spine, LMN for head turning (CN XI nuclei) • Retina, visual cortex superior colliculi  PPRF MLF upward gaze (CN III) 11. Lesions of the corticotectal tract: -Parinauds: • Lesion at superior colliculi • Lose upward gaze • Cause: pineal gland tumor and hydrocephalus • Pupils don’t constrict with light, do constrict with accommodation • Eyelid retraction • Ptosis • Convergence retraction nystagmus 12. Reticulospinal Tracts: • Posture and ANS • Inhibit or excite axial motor neurons • Influence voluntary or reflexive movements -Medullary (lateral) RST: • Medullary is Mellow (relaxing) • Inhibit spinal and cranial LMN’s

-Pontine (medial) RST: • Pontine pumps up (excitatory); contraction • Facilitates LMN to axial muscle and leg extensors to maintain posture

13. Lesion of the reticulospinal tract: -Decerebrate Posturing: • Arms extended • Back arched • Legs extended • Toes curled • Lesion caudal to red nuclei, loss of LRST • Removal of cortical excitation, lose inhibition, so increase muscle tone (because MRST is still intact) • Increase extensor MN activity; arms adducted and medially rotated 14. Corticonuclear/Corticobulbar Tract: • UMN corresponds to CN’s • Precentral gyrus corona radiata genu of internal capsule cerebral peduncle bilateral CN V, X, XI and contralateral CN VII, XII • **Know her diagrams!!! 15. Lesions of the corticobulbar tract: -Internal Capsule lesion: • Corticonuclear CN defects if genu lesioned • If posterior limb also lesioned contralateral hemiplagia -Pseudobulbar Palsy: • Bilateral corticobulbar lesion (central) • MS, ALS, brain stem infarct • Dysphagia, dysarethmia, tongue paresis, loss of emotional control -Bells Palsy: • CN VII lesion (peripheral) • Ipsilateral muscle hemiplegia **Distinction: can’t wrinkle forehead with Bell’s Palsy, can with stroke (UMN) -UMN corticonuclear lesion: (central) • Contralateral loss of lower face motor • Contralateral loss of tongue movement -Peripheral CNXII lesion: • Tongue deviates toward affected side 16. What is locked-in syndrome?

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Infarct in ventral pons: affects bilateral corticospinal tracts No cortical input to CN’s or spinal cord Absent motor function Maintain sensation and cognition Fully aware Spared eye opening and vertical eye movements (rostral midbrain and tegmentum) o Lose horizontal eye movement from pons