Brainstem Disorders
Dan Gold, DO Assistant Professor of Neurology, Ophthalmology, Neurosurgery, Otolaryngology – Head & Neck Surgery The Johns Hopkins University School of Medicine
Brainstem Disorders Dan Gold, DO Assistant Professor of Neurology, - - PowerPoint PPT Presentation
Brainstem Disorders Dan Gold, DO Assistant Professor of Neurology, Ophthalmology, Neurosurgery, Otolaryngology Head & Neck Surgery The Johns Hopkins University School of Medicine Relevant Financial Disclosures I have no financial
Dan Gold, DO Assistant Professor of Neurology, Ophthalmology, Neurosurgery, Otolaryngology – Head & Neck Surgery The Johns Hopkins University School of Medicine
disclose.
SACCADIC DYSMETRIA & OCULAR LATEROPULSION
Is the lateral medullary lesion on the right or the left?
RIGHT
LEFT
Left lateral medullary lesion
R L
R L
Disruption of climbing fibers (ICP)
Simple spike (inhibitory) discharge of Purkinje cells increases
R L
Increased Purkinje firing increased fastigial inhibition
Inhibition of fastigial nucleus…
R L
…Decreased excitation of contra IBN
R L
Decreased inhibition of left VIth N & PPRF results in
structures, bias towards the left
PEARL: End result with L Wallenberg is L hypermetria & L ocular lateropulsion
R L
NYSTAGMUS
Unidirectional Nystagmus
Peripheral SCC imbalance Central SCC imbalance
Semicircular canals (SCC) – angular acceleration detectors
Unopposed L PC + L HC + L AC Result is mixed left- beating mixed horizontal-torsional nystagmus
PEARL: At the level of the labyrinth/8th N & medulla, nystagmus can be UNIDIRECTIONAL & indistinguishable
Torsional Nystagmus
PEARL: Pure TORSIONAL nystagmus is almost always central Can you have pure torsional nystagmus from a peripheral lesion?
Gaze-Evoked Nystagmus
PEARL: MVN-NPH responsible for horizontal gaze-holding GAZE-EVOKED NYSTAGMUS Wernicke’s encephalopathy
VESTIBULO-OCULAR REFLEX
Abnormal Head Impulse Test (HIT) to the RIGHT
Damage to horizontal SCC fibers in 8th nerve
Abnormal Head Impulse Test (HIT) to the LEFT
Damage to horizontal SCC fibers synapsing in the MVN
PEARL: While an abnormal (+) HIT is almost always indicative of a peripheral etiology, certain central localizations (vestibular nucleus) can cause this finding
UTRICULAR-OCULAR REFLEX
Utricle – linear acceleration detector, responds to translation & head tilt
Physiologic Ocular Tilt Reaction (OTR)
1) Head tilts right 2) Right eye elevates & Left eye depresses 3) Ocular counter-roll towards left ear
Pathologic OTR from Wallenberg on LEFT (PEARL: caudal to decussation of utricle-ocular motor fibers, ipsi- hypotropia)
PEARL: Although a “peripheral” skew is possible, it is rare and usually small. Presence of a skew should be considered central until proven
What we won’t talk about
NYSTAGMUS
MLF lesions – PEARL: Torsional nystagmus is ipsiversive & vertical components can be dissociated
Why?
dissociated vertical components
How can the ipsiversive torsional nystagmus be explained? Semicircular Canal Pathways
Slow (contraversive) torsional phase towards right ear & Fast (ipsiversive) torsional phase toward left ear
PEARL: Left MLF injury damages PC & AC pathways originating in Right Labyrinth
R L R L
PEARL: Ipsiversive torsional nystagmus can be generated by vertical (posterior & anterior) SCC asymmetry
Skew deviation with Left hypertropia (PEARL: rostral to decussation of utricle-ocular motor fibers, ipsi-hypertropia)
What produces dissociated vertical components? 1) Semicircular Canal Pathways
Stimulate R PC (BPPV) activate R SO, L IR
Slow phase down/towards left ear Fast phase up/towards right ear
Torsional towards left ear; more DB OS
Weaker L IR Stronger L SR upward slow phase more DB OS (ipsilesional to MLF)
Torsional towards left ear; more UB OD
Weaker R SR Stronger R IR downward slow phase more UB OD (contralesional to MLF)
What produces dissociated vertical components? 2) Utricle-ocular motor Pathways
Left MLF lesion causes Left hypertropia & Right hypotropia
Skew (OS) – slow phase up; fast phase down Skew (OD) – slow phase down; fast phase up
PEARL: Fast phases UB OD, DB OS “Jerky see-saw”
VESTIBULO-OCULAR REFLEX
3 pathways for anterior SCC 1 pathway for posterior SCC
PEARL: Abnormal HIT (VOR) in the planes of the posterior canals Normal HIT (VOR) in the planes of the anterior canals
MS patient with bilateral MLF lesions
Central tegmental tract
Guillain-Mollaret’s triangle
CTT normally inhibits IO
CTT injury IO hypertrophy & spontaneous discharges
indistinguishable from “peripheral” nystagmus
nystagmus
canals
related to central tegmental tract pathology
nystagmus is present!