Download Ocular Manifestations of Neuro II

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Pathophysiology Paper Chase
02/26/02 8-9AM
Ocular Manifestations of Neuro II
Dr. Luis Serrano
Las vias supranucleares
A. Parte encima de núcleo, tiene que ver con control cortical, eso
movimiento, usualmente lo que hace control de arriba hace que los dos
mueve a la vez hacia mismo lado
B. Donde esta lesion, después hace su diagnostico diferencial de que lesiones
estan a esta nivel
OCULOMOTOR CONTROL SYSTEMS (Video)
A. The purpose of the oculomotor system is to serve vision
B. The saccades: perceives accurate target
C. Pursuit
1. slow movement on slowly moving target
2. at higher speeds saccades takes over
D. Vergence
1. alignment visual axes for binocular vision
2. Think convergence and divergence
E. Vestibular
1. Stability of image if head moves
2. Turn head side to side
F. Repeated pursuit of rapid fixation if see train passing
Spinocerebellar degeneration: saccadic defect
A. To look from side to side to see
B. Eye movement slower than head movement
Congenital ocular motor apraxia
A. head thrusts replace horizontal movements of eyes
B. does not turn eyes, but pass the head past object to view
C. rather than turn eyes, thrust head past object, doll’s head controversion,
eyes deviated to opposite side, maintain fixation head turn back and eyes
fix on object
D. read with difficulty and some head turns
Progressive supranuclear palsy (PSP)
A. Poor prognosis, dystonic rigidity neck upper torso, down gaze involved,
saccadic system involved, vergence may also be impaired, intact
horizontal persuit, little vertical pursuit
B. Horizontal saccades slow, vertical saccades are absent
C. Doll’s head movements are intact
OCULOMOTOR CONTROL SYSTEM (video 2)
Sacades
A. Eye movements serve vision, without vision no need for eye movements
B. Purpose of eye movements is to acquire objects of regard onto our fovea,
then if the objects move, to keep the objects on the fovea
C. The saccadic system probably arises cortically from area 8
Pathophysiology Paper Chase 02/26/02 8-9AM Ocular Manifestations of Neuro II Dr.
Luis Serrano
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D. Cells fire prior to all saccades whether they are random saccades firing all
time, or visually guides
E. Frontal eye fields can evoke saccades if stimulation with only 10
microamps
F. Conclusion: the frontal eye fields clearly are the cerebral cortical
generator of saccades movements
G. Saccade pathway through white matter at junction of midbrain and pons,
then to PPRF, then innervate left lateral rectus and right medial rectus
generating movement to the left
H. Occipital saccades: occipital saccades get direct axis to the brainstem via
the superior folliculus, don’t travel from occipital to parietal areas, to
review the structures involved in the saccadic eye movement pathways,
they receive from supplemental prefrontal areas and visual areas (most
saccades stimulated visually) project to saccade generating sites in
midbrain for horizontal and pons for vertical
I. Pontine: centro de integracion de arriba para movimientos conjugados
J. Substantia nigra and superior pathways are inhibitory to the superior
folliculus, which receives direct input from occipital lobe, and projecting
to the nuclei in the pons, so through either direct or indirect saccades are
generated
K. Pontine paramedian reticular formation (PPRF)
L. Lesion frontal eye field, gaze contralateral palsy, temporary if frontal eye
field (FEF) lesion and superior colliculus (SC) lesion, block saccades
M. Primary saccadic generation center: contralateral frontal
Smooth pursuit
A. Posterior, occipital lobe, area 17 in striate cortex, visual area 1, where
vision is primarily received, there are two areas in the parietal posterior
temporal region, which have been discovered important, areas middle
temporal (MT) visual area, and immediately above it MST (medial
superior temporal area), in posterior bank of superior temporal sulcus
B. MT lesion bilateral pursuit defect (field specific)
C. MST lesion produce low gain ipsilateral pursuit
D. Striate cortex acts on project to extrastriatal visual areas (MT, MST, and
posterior parietal region) project ipsilaterally to dorsolateral pontine
nuclei, then to cerebellum flocculus and dorsal vermis, then to vestibular
nuclei
E. The saccadic pathway doesn’t go into cerebellum, it goes directly from
cerebral hemisphere to brainstem
F. Gain is the ratio of output (eye movement) to input (target movement), the
input is speed of moving target, output is the eye movement attempting to
move the eye
G. Pursuit abnormality: ipsilateral low gain, with lesion of parietal lobe,
brainstem, or cerebellum
H. Clinical in posterior hemisphere lesion
1. Contralateral hemianopsia
2. permanent ipsilateral pursuit deficit
Pathophysiology Paper Chase 02/26/02 8-9AM Ocular Manifestations of Neuro II Dr.
Luis Serrano
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3. low gain
4. velocity saturation
5. acceleration saturation
patient left cerebral hemispherectomy, oculomotor deficits caused by this
are identical to those caused by large parietoccipital lesions, the problem
of low gain pursuit to the left, normal pursuit to left
bilateral low gain pursuit: bilateral cerebral, basal ganglia, brain stem,
cerebellu, drugs (sedative, anticonvulsants), normal aging, inattentive,
schizophrenia
CNS disease with normal pursuit: none
Slow to no saccade syndrome: congenital ocular motor aprxia,
huntington’s, wilson’s OPCA, PSP, whipple’s, lipid storage disease,
anticonvulsant toxicity, PPRF lesions, peripheral (myasthenia gravis MG,
CPEO, restrictive such as thyroid eye disease)
Video of soldier with difficulty making saccadic eye movements:
watching ping pong game has to move the head, reads by moving the eyes,
blinking between the thrusts, his head moves and his eyes stay still, as he
looks between objects must move head because unable to move eyes, can
voluntarily move eyes, he wills saccade, but outcome is slow eye
movement, when looking down and asks to do that, he substitutes
convergence, because his convergence is normal, and vertical saccades is
normal, pursuit is normal with vertical pursuit, pursuit saturates as velocity
Vertical eye movements, midsagital through brainstem, cajal and
darshuwiz, the rostral MLF for vertical saccadic eye movements, they
receive input from PPRF go to rostral interstitial nucleus of MLF then to
the cajal then to CN III and IV for control of vertical eye movement
Downgaze in lateral aspect of
Upgaze, projection from rMLF to the CNIII, IV, is not direct, it goes up
and decussates in the posterior commisure, then comes down dorsally, so
variety of lesions in midbrain will produce upgaze palsy, lesion of
posterior commissure, or large tegmental lesion on one side of tegmentum
of midbrain
Case: difficulty moving eyes in both vertical directions as well as to the
left, but vestibular ocular is normal because this is midbrain, normal visual
field to right, hemianopsia to the left, lesion to right lateral geniculate
body, curious phenomenon, torsion of eye, extort when eyes open, then
intort when eyes close, rare,
Progressive supranuclear palsy
1. heterogenous degeneration involving the brain stem, basal
ganglia and cerebellum with vertical gaze and pseudobulbar
palsy, nuchal dystonia and dementia
2. asked to move to right, slow, can’t look up or down, vertical gaze
palsy, masked facies is obvious, when asked to pursue
horizontally, he has low gain pursuit bilaterally
3. nuchal rigidity difficult to get vestibulocular movements
Pathophysiology Paper Chase 02/26/02 8-9AM Ocular Manifestations of Neuro II Dr.
Luis Serrano
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4. supranuclear opthalmoplegia with involvement of vertical rather
than orizontal gaze, though horizontal progressively becomes
affected
5. lesions involve the globus pallidus bilaterally, subthalamus
nucleus, midbrain tegmentum, substantia nigrum periaqueductal
grey, which explains all phenomenon
6. 60:40 men:women, average age onset 60, 70% onset between 5065 years, can live up to 20 years
7. treatment frustrating, dopaminergic agonists with bromocriptine,
may reduce rigidity, but no effect on eye movements, usually
frustrating endeavor
S. Oculomyorrhtyhmia: conpendulary convergence nystagmus,
manifestation of central CNS whipple’s disease, have manifestations of
supranuclear palsy, but also curious convergence nystagmus, and
masticatory movement in association with nystagmus, provided make
diagnosis, should make small bowel diagnosis, if treat infection then may
resume ocular function, if no biopsy possible, must treat empirically
Final comments (Dr. Serrano)
A. 4 sistema supranuclear: saccadic que son rapido, pursuit son lento
perseguir objetos de interes, vergence es convergence and divergence
B. eye movements proposito que usted fija, mantiene imagen de interes in
fovea
C. examina paciente, ver todo sistema en accion, que sigua las cosas
lentamente, movimientos rapidos deben ser preciso
D. Condiciones de ganglio basal, parkinson’s
E. Movimientos horizontal al nivel de puente
F. Movimientos vertical al nivel de mesencephalo
G. Movimientos saccadic son de origen contralateral
H. Movimientos pursuit son de origen ipsilateral