1. Brainstem Stroke Annegret Dahlmann-Noor
Consultant in Paediatric Ophthalmology and Strabismus
Wales and West Vision Conference
26 June2015

2. Eye movement problems after stroke
Background
Incidence: Each year in England, approximately 110,000 people have a first or recurrent stroke and a further 20,000 people have a transient ischaemic attack Wales: 11,000 have a first or recurrent stroke per year, of which 6,000 new stroke events More than 900,000 people in England are living with the effects of stroke, with half of these being dependent on other people for help with everyday activities

3. Vision and eye movement problems after stroke
Sensory (afferent): visual field defects
Ocular motility (efferent): double vision from limitation of eye movements jumping images from nystagmus head turns to compensate for gaze palsy
Processing: Charles Bonnet, palinopsia

4. Background Most strokes are ischaemic (80-85%), some are haemorrhagic
Eye movement problems after stroke
Background
Most strokes are ischaemic (80-85%), some are haemorrhagic
Two main blood supplies to the brain:
Carotid
Vertebral/basilar arteries

5. Eye movement problems after stroke
Background
27% of ischaemic strokes affect the vertebral/basilar arteries Symptoms of brainstem stroke: vertigo - dizziness double vision/binocular visual disturbance generalised weakness

6. Blood supply to brainstem and cerebellum
Eye movement problems after stroke
Blood supply to brainstem and cerebellum
Posterior cerebral artery
Branches of bifurcation of basilar artery: III ncl/fasc
Superior cerebellar artery: IV ncl/fasc
Anterior inferior cerebellar artery: VI ncl/fasc
Posterior inferior cerebellar artery
Vertebral artery

7. Superior cerebellar artery
Eye movement problems after stroke
Superior cerebellar artery
Branches of basilar artery

8. Branches of basilar artery and of anterior inferior cerebellar artery
Eye movement problems after stroke
Branches of basilar artery and of anterior inferior cerebellar artery
Paramedian branches of basilar artery

9. Eye movements Smooth pursuit: eyes follow a moving target
Eye movement problems after stroke
Eye movements
Smooth pursuit: eyes follow a moving target
Saccades: gaze rapidly jumps from one fixation point to another
Vergence eye movements: eyes do not move in parallel, but in relation to each other: convergence: when looking at something close up
Vestibulo-ocular reflex (VOR): the signal triggering eye movements comes from the balance organ (labyrinth), which keps the image of the visual surroundings stable on the retina during head movements
Optokinetic reflex: triggered by moving visual targets, consists of smooth pursuit and saccades
Gaze holding: ability to keep the eyes in an eccentric position

10. The players: the team on the ground
Eye movement problems after stroke
The players: the team on the ground
Six muscles on each eye
Move eye horizontally, vertically, and tilt it in- and outwards

11. The players: the middle management
Eye movement problems after stroke
The players: the middle management
Vertical eye movements
Interstitial nucleus of Cajal (INC)
Rostral interstitial nucleus of the MLF (riMLF)
Horizontal eye movements
Parapontine reticular formation (PPRF)
Abducens nucleus
The runner: Medial longitudinal fasciculus (MLF)

12. The players Vertical eye movements Interstitial nucleus of Cajal
Eye movement problems after stroke
The players
Vertical eye movements
Interstitial nucleus of Cajal
Rostral interstitial nucleus of the MLF
Horizontal eye movements
Paramedian pontine reticular formation
Abducens nucleus

13. The players: the supreme controls
Eye movement problems after stroke
The players: the supreme controls
Frontal eye field: sends signals to the third nerve nucleus on the same side, and the paramedian pontine formation on the opposite side: horizontal saccades, and to the rostral interstitial nucleus of the MLF (riMLF) for vertical saccades
Parietal eye field: production of smooth pursuit eye movements, also participates in the production of saccades (more to novel visual stimuli rather than to remembered targets)
Paramedian pontine reticular formation: excitatory burst neurons that start the “pulse”
From: Oculomotor Dysfunction in Amyotrophic Lateral Sclerosis:  A Comprehensive Review Arch Neurol. 2011;68(7): doi: /archneurol

14. The action: midbrain Oculomotor nucleus Trochlear nucleus
Eye movement problems after stroke
The action: midbrain
Oculomotor nucleus
Trochlear nucleus
Rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF)

15. Presentation title to go here
Fourth cranial nerve

16. Fourth cranial nerve MRI courtesy of Dr Indran Davagnanam
Presentation title to go here
Fourth cranial nerve
MRI courtesy of Dr Indran Davagnanam

17. Third cranial nerve infarct
Presentation title to go here
Third cranial nerve infarct

18. Oculomotor nerve paresis
Presentation title to go here
Oculomotor nerve paresis
lack of adduction: eye deviated outwards
lack of elevation: eye deviated downwards
lid droop (ptosis)

19. Midbrain Control of vertical and torsional eye movements
Eye movement problems after stroke
Midbrain
Control of vertical and torsional eye movements
Input from cortex (vertical and torsional saccadic commands and vertical gaze-holding signal)
Input from lower brainstem (vestibular and pursuit signals)
Generation of vertical saccades: rostral interstitial nucleus of the MLF (riMLF): projects bilaterally for eye elevation (superior rectus and inferior oblique), ipsilaterally for eye depression, also projects to the interstitial nucleus of Cajal (INC)
From: T.C. Frohman et al. Neurology 2008;70:e57-e67

20. Midbrain Example: left head tilt
Eye movement problems after stroke
Midbrain
Example: left head tilt
Otoliths (balance organ) trigger signal to extorters (inferior oblique and inferior rectus muscles) in the right eye (cross midline) and to intorters of left eye (superior oblique and superior rectus muscles) in the left eye (double crossing)
plus: torsional fast phases mediated by riMLF
INC: neural integration of vertical and torsional gaze, eye-head coordination during roll movements, and inhibitory burst neurons for vertical eye movements
lesions: intorsion and elevation of the right eye and extorsion and depression of the left eye = skew deviation
From: T.C. Frohman et al. Neurology 2008;70:e57-e67

21. Lesions of vestibular nuclei
Eye movement problems after stroke
Lesions of vestibular nuclei
Lesions of vestibular nuclei, for example lateral medullary infarction (Wallenberg syndrome):
Vestibular imbalance: nystagmus or skew deviation and impairment of gaze holding for all types of conjugate eye movement
Ocular tilt reaction (OTR): skew deviation, hypotropia on same side, lower eye extorsion and head tilt towards side of lesion
Lateropulsion: eyes deviate conjugately towards the side of the lesion if lids are closed, or with saccades
Top: isolated vestibular nucleus infarct.
Bottom: different patient - marked skew deviation T.C. Frohman et al. Neurology 2008;70:e57-e67

22. Dorsal midbrain syndrome
Eye movement problems after stroke
Dorsal midbrain syndrome
Lesions of the riMLF:
loss of upward gaze (vestibulo-ocular reflex and Bell phenomenon may be spared)
slowing of vertical saccades below the horizontal meridian,
convergence weakness,
convergence-retraction nystagmus,
light-near dissociation of pupils,
lid retraction
Patient with dorsal midbrain syndrome
T.C. Frohman et al. Neurology 2008;70:e57-e67

23. Eye movement problems after stroke
Stop and recap
1. Strokes affecting the basilar artery or its brances can affect eye movements, causing double vision and jumping images
2. There are different types of eye movements – smooth pursuit, saccades, vergences, and eye movements in response to changes in head or body position
3. Areas in the cortex trigger saccades (fast eye movements) and pursuits.
4. Centres in the midbrain forward signals to the cranial nerves which innervate the eye muscles that move the eyes vertically and in torsion.
5. Lesions in these pathways can cause loss of saccades and vertical eye movements, and a complex change in vertical and torsional eye movements (skey deviation)

24. Now the easy stuff: horizontal eye movements
Eye movement problems after stroke
Now the easy stuff: horizontal eye movements
Abducens nucleus

25. Horizontal eye movements
Eye movement problems after stroke
Horizontal eye movements
Two types of nerve fibres in the abducens nerve: a) motoneurons to lateral rectus muscle on the same side b) internuclear neurons, which project up the contralateral medial longitudinal fasciculus to contact medial rectus motoneurons of the oculomotor nucleus
=> Conjugate, horizontal eye movements .
Details of the descending projection involved in the volitional control of horizontal saccadic eye movements. Excitatory pathways are shown in orange and the reciprocal inhibitory pathways are shown in blue.
T.C. Frohman et al. Neurology 2008;70:e57-e67

26. Eye movement problems after stroke
Abducens nucleus
Inputs: vestibular and optokinetic inputs from vestibular nuclei
Saccadic commands originate from burst neurons of the pontine and medullary reticular formation
Descending smooth pursuit pathway via cerebellar nuclei to abducens nucleus .
Projections involved in the activation of the left lateral semicircular canal. This figure illustrates the projections involved during the activation of the left lateral semicircular canal.
T.C. Frohman et al. Neurology 2008;70:e57-e67

27. Eye movement problems after stroke
Stop and recap
From the abducens nucleus, signals go the lateral rectus muscle on the same side and medial rectus on the opposite side
Those signals are triggered by messages from the vestibular nuclei (tilting head), cerebellar nuclei (moving body), burst neurons in the PPRF, and the frontal and parietal eye fields.

28. How things can go wrong in brainstem stroke
Eye movement problems after stroke
How things can go wrong in brainstem stroke
Abducens nucleus lesions
Medial longitudinal fasciculus lesions
Combined lesions of MLF and abducens nucleus
PPRF lesion

29. How things can go wrong in brainstem stroke
Eye movement problems after stroke
How things can go wrong in brainstem stroke
1. Abducens nucleus lesions: paralysis of lateral rectus muscle on the same side and medial rectus muscle on the opposite side (vergence spared) Usually associated with involvement of adjacent structures: facial nerve fascicle, MLF, paramedian pontine reticular formation

30. How things can go wrong in brainstem stroke
Eye movement problems after stroke
How things can go wrong in brainstem stroke
1. Abducens nucleus lesions: paralysis of lateral rectus on same side and medial rectus muscle on opposite side, vergence spared Usually associated with involvement of adjacent structures: facial nerve fascicle, MLF, paramedian pontine reticular formation
MRI courtesy of Dr Indran Davagnanam

31. MLF 2. MLF lesions: Internuclear ophthalmoplegia (INO):
Eye movement problems after stroke
MLF
2. MLF lesions: Internuclear ophthalmoplegia (INO):
paresis of adduction on the side of the lesion,
abduction overshoot of the contralateral eye
Often accompanied by
skew deviation (disruption of the otolithic-ocular connections),
gaze-evoked vertical nystagmus,
impaired vertical pursuit,
decreased vertical vestibular responses,
small-amplitude saccadic intrusions
Volitional saccadic pathway with a lesion in the right medial longitudinal fasciculus (MLF) that results in an internuclear ophthalmoparesis (INO). Volitional saccadic pathway with a lesion in the right MLF that results in an INO during an attempted saccade to the patient's left. T.C. Frohman et al. Neurology 2008;70:e57-e67

32. Eye movement problems after stroke
INO
INO continued: Usually orthotropic (straight eyes) or exophoric (latent outward drift) in primary position, except when associated with skew deviation Occasionally exotropia (manifest outward strabismus) in bilateral INO (wall-eyed bilateral INO, WEBINO)
T.C. Frohman et al. Neurology 2008;70:e57-e67

33. Eye movement problems after stroke
One and a half
Right internuclear ophthalmoparesis (INO) upon attempted gaze to the left.
T.C. Frohman et al. Neurology 2008;70:e57-e67
3. Combined lesion of one MLF and the adjacent abducens nucleus, or its inputs:
paresis of all conjugate movements except for abduction of the eye on side opposite the lesion: one and a half syndrome
If acute, may present with marked exotropia
Deviated eye (opposite the side of the lesion) may show marked nystagmus

34. Eye movement problems after stroke
PPRF lesions
4. Lesions of the PPRF Loss of saccadic burst neurons: loss of saccades and quick phases of nystagmus to the side of the lesion Pontine lesions may cause unilateral defect of smooth pursuit

35. Eye movement problems after stroke
Stop and recap
Abducens nucleus lesions: loss of abduction same side, loss of adduction opposite side; often involve PPRF as well, so horizontal gaze palsy
Medial longitudinal fasciculus lesions: impaired adduction on the side of the lesion, abduction overshoot of the opposite eye
Combined lesions of MLF and abducens nucleus: affects all horizontal eye movements except for abduction on the side opposite the lesion
PPRF lesion: loss of saccades to the side of the lesion

36. The last part of the talk: cerebellum and cortex stroke
Eye movement problems after stroke
The last part of the talk: cerebellum and cortex stroke

37. Cerebellar infarct Three arteries from the posterior circulation:
Eye movement problems after stroke
Cerebellar infarct
Superior cerebellar artery
Anterior inferior
cerebellar artery
Posterior inferior
Three arteries from the posterior circulation:
Posterior-inferior cerebellar artery
Anterior-inferior cerebellar artery
Superior cerebellar artery
Infarcts often associated with brainstem infarcts, so mixed clinical picture

38. Eye movement problems after stroke
Cerebellar infarct
Posterior-inferior cerebellar artery: acute vertigo and nystagmus, possibly gaze-evoked nystagmus
Anterior-inferior cerebellar artery: vertigo, vomiting, hearing loss, facial palsy, ipsilateral limb ataxia
Superior cerebellar artery: ataxia of gait and limbs and vertigo, saccadic contrapulsion (overshooting of contralateral saccades, undershooting of ipsilateral saccades; attempted vertical saccades are oblique)

39. Cerebral hemispheric lesions
Eye movement problems after stroke
Cerebral hemispheric lesions
acute lesion: eyes often deviated conjugately toward the side of the lesion; often after large stroke involving right post-rolandic cortex; associated with visual hemineglect

40. Cerebral hemispheric lesions
Eye movement problems after stroke
Cerebral hemispheric lesions
chronic lesion: no resting deviation; persistence of gaze deviation
Small-amplitude nystagmus
Deficit of horizontal pursuit when tracking targets moving towards the side of the lesion (OKN)

41. Bilateral Frontoparietal lesions
Eye movement problems after stroke
Bilateral Frontoparietal lesions
Acquired Ocular Motor Apraxia
Loss of voluntary control of eye movements
Preservation of reflex movements, including vestibulo-ocular reflex and quick phases of nystagmus
Can be associated with difficulty in lid opening
Balint syndrome: loss of voluntary eye movements plus disturbance of visual attention

42. Management of ocular motility problems
Eye movement problems after stroke
Management of ocular motility problems
Prism treatment
Occlusion
Ptosis props
Surgery/botulinum toxin

43. Eye movement problems after stroke
Principles of surgery
Enhance muscle action by shortening a paretic muscle, or by transposing a different muscle towards the insertion of a paralytic muscle
Create a matching defect by weakening a muscle, to reduce double vision

44. Presentation title to go here
Thank you