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Orthoptics III > 5 Supranuclear disorders - HORIZONTAL > Flashcards

5 Supranuclear disorders - HORIZONTAL Flashcards

1
Q

What is the main function of a saccade and what speed is it?

A

To bring an object of interest onto the fovea
Fast

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2
Q

What is the main function of nystagmus (quick phase) and what speed is it?

A

To direct eyes onto oncoming visual scene and reset eyes after rotation.
Fast

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3
Q

What is the main function of the smooth pursuit and what speed is it?

A

To hold a slow-moving target on the fovea
Slow

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4
Q

What is the main function of optokinetic movement and what speed is it?

A

To hold images steady on the retina during sustained head rotation.
Slow

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5
Q

What is the main function of vestibular movement and what speed is it?

A

To hold images steady on the retina during brief head rotation.
Slow

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6
Q

What is the main function of vergence movements and what speed is it?

A

To move the eyes in opposite directions to maintain bifoveal fixation and a single image
Slow

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7
Q

What are the three cell types present in the horizontal gaze brainstem pathway?

A

Excitatory burst cells
Inhibitory burts cells
Omnipause neurons

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8
Q

What is the action of the excitatory burst cells?

A

Generate ipsilateral horizontal saccades

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9
Q

What is the action of the inhibitory burst cells?

A

Decrease firing rate of contralateral VIth motor neurons and internuclear neurons

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10
Q

What is the action of the omnipause neurons?

A

Inhibit both burst cells.

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11
Q

What is the role and location of the frontal eye fields?

A

Role - Production of saccades on opposite side of side of the stimulus, selects target and commands movement
Location - Frontal cortex

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12
Q

What is the role and location of the Parietal-temporal-occipital region?

A

Role - production of smooth pursuit movements
Location - Cerebral cortex, includes portions of patietal, temporal and occipital lobes. End of Sylvian fissure

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13
Q

What is the role and location of the Paramedian pontine reticular formation (PPRF)?

A

Role - Generating horizontal conjugate gaze
Location - Brainstem

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14
Q

What is the role and location of the medial longitudinal fasciculus (MLF)?

A

Role - facilitates yoked eye movements, important connection through the MLF links contralateral abducens nucleus with ipsilateral medial rectus subnucleus
Location - Fibre tract that extends from spinal cord to oculomotor nucleus

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15
Q

What is the role and location of the Rostral Interstitial Nucleus of the MLF (riMLF)?

A

Role - Generate vertical conjugate fast movements up, down and torsional, but most important in generating downgaze. Vertical and torsional gaze holding.
Location - Mesencephalon at rostral termination of MLF. Adjacent to interstitial nucleus of Cajal.

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16
Q

What is the role and location of the posterior commissure and the nucleus of the posterior commissure?

A

Role - important in generating upward gaze movements
Location - Dorsal to the riMLF

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17
Q

What is the role and location of the superior colliculus?

A

Role - Both ocular motor and sensory function. Generates visually directed saccades independently (may play a role in smooth pursuits)
Location - Dorsal surface of midbrain, below the thalamus.

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18
Q

What is the role and location of the cerebellum?

A

Role - Modulation of all types of eye movement. Long term adaptation to compensate for ocular motor dysmetria. Gaze holding, smooth pursuit, combo head and eye tracking, saccade size, adjustment of vestibulo-ocular reflex
Location - level of the brainstem under the occipital lobe.

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19
Q

What is the route of saccade action?

A

Start: contralateral frontal eye fields (frontal lobe)
→ superior colliculus
→ PPRF
→ horizontal gaze centre (VIth nerve nucleus)
→ ipsilateral LR and contralateral MR (via MLF)

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20
Q

What is the route of smooth pursuit action?

A

Start: ipsilateral parieto-occipital lobe
→ superior colliculus
→ PPRF
→ horizontal gaze centre
→ ipsilateral LR and contralateral MR (via MLF)

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21
Q

What lesions lead to horizontal conjugate gaze deficits?

A
  • Cerebral cortex or pontine lesions
22
Q

What are examples of conjugate gaze limitations?

A

o Unilateral gaze palsy
o Saccadic palsy
o Palsy of Smooth pursuit
o Bilateral gaze palsy
o Conjugate gaze deviation
o Ocular motor apraxia

23
Q

What are some features of a unilateral horizontal gaze palsy?

A

Eyes deviated to opposite side
Mild damage = selective, slow ipsilateral saccades, min limitation, spared pursuit,
Severe lesion = complete ipsilateral saccadic and pursuit palsy large
 lesion leads of deficient VOR and neural integrator, gaze evoked nystagmus towards intact contralateral field and affected vestibular nuclei
Normal gaze to contralateral side
Full vertical gaze
Normal VOR (Doll’s head) but VOR does not improve movement if VIth nuclear lesion
May be long lasting

24
Q

What is the aetiology behind unilateral horizontal gaze palsies?

A

Ipsilateral pontine lesion – affecting PPFR rostral to VIth nucleus
CVA tumour, MG
Compression from external tumour

25
Q

Name some differential diagnosis of unilateral horizontal gaze palsies

A

o Duane’s syndrome
o One and a half syndrome

26
Q

What are features of unilateral saccadic palsies?

A

o Eyes slowly deviate towards side of lesion
o Contralateral saccadic palsy/paresis
o Loss of fast phase OKN
o Pursuit bilaterally impaired, more towards side of lesion
o Intact VOR
o Improve with time, subtle defects remain
o Difficulty maintaining gaze away from affected frontal cortex – small corrective saccades gaze paretic nystagmus

27
Q

What is the aetiology behind unilateral saccadic palsies?

A

Contralateral frontal lobe lesion
 CVA – haemorrhage or infarct
 Tumour

28
Q

What is a differential diagnosis of unilateral saccadic palsies?

A

o Episodic saccadic palsy = epilepsy

29
Q

What are some features of a smooth pursuit palsy?

A

o ‘Cog wheel’ pursuit
o Corrective saccade
o Slow phase OKN affected when stripes rotated towards lesion
o Parietal-occipital lesion – contralateral HH

30
Q

What is the aetiology behind smooth pursuit palsies?

A

Lesion in parieto-occipital lobe damage
 CVA or tumour

31
Q

What are features of a bilateral gaze palsy?

A

o Loss of saccadic movement to both sides
o Loss of smooth pursuit
o Intact VOR

32
Q

What is the aetiology of a bilateral gaze palsy?

A

o Bilateral pontine lesions restricted to PPRF or VIth nerve nucleus

33
Q

What are differential diagnosis of bilateral gaze palsies?

A

o CPEO
o TED
o MG
o Bilateral IIIrd and VIth

34
Q

What are features of ocular motor apraxia (acquired balints syndrome)?

A

o Difficulty initiating voluntary horizontal saccades
o Difficulty initiating reflexive saccades and smooth pursuit in all directions
o Simultanagnosia
o Optic ataxia
o Frequently have associated dementia and visual field defects

35
Q

What is the aetiology behind ocular motor apraxia (acquired balints syndrome)?

A

Extensive bilateral cerebral disease – parieto-occipital

36
Q

What are the features of ocular motor apraxia (congenital)?

A

o Present in infancy
o Apparent visual inattention
o Once develop head control characteristic head thrusts and excessive blinking occur
o Inability to execute voluntary saccades
o Vertical saccades and pursuit not affected
o Head thrust: manoeuvre to change fixation
o Excessive blinking

37
Q

What is the aetiology behind ocular motor apraxia (congenital)?

A

o Associated with CNS disorders
 agenesis of corpus callosum
 Collicular abnormalities
 Cerebellar vermian dysplasia (e.g. Joubert syndrome)

38
Q

What are features of spasm near reflex?

A

 Variable esotropia
 Pseudo VIth nerve palsy
 Signs of dorsal midbrain syndrome
 Fasicular IIIrd nerve palsy
 Skew deviation

39
Q

What is the aetiology behind spasm near reflex?

A

 Usually psychogenic
 Rarely: head trauma, dorsal midbrain syndrome, lesion in brainstem, lesion in diencephalon, intoxication, Wernicke’s encephalopathy

40
Q

What is the differential diagnosis for spasm near reflex?

A

 Bilateral VIth nerve palsies

41
Q

What are features of convergence insufficiency?

A

 NPC less than 10cm
 Or can only be maintained at 10cm with effort
 Diplopia
 Asthenopic symptoms
 Blurred vision
 Exophoria at near

42
Q

What is the aetiology behind convergence insufficiency?

A

 Primary – no other cause found
 Secondary – Parkinson’s, PSP, INO

43
Q

What are the two differential diagnosis for convergence insufficiency?

A

 Exophoria – convergence weakness type
 Accommodation insufficiency or fatigue

44
Q

What are the features of convergence paresis/paralysis?

A

 Diplopia at near, or closer than infinity for paralysis
 Fatiguability while reading/near visual task
 Asthenoptic symptoms
 Blurred vision at near
 Does not respond to orthoptic exercises
 Exotropia/phoria at near (constant XT within infinity for paralysis)

45
Q

What is the aetiology behind convergence paresis/paralysis?

A

 Age
 Less commonly, dorsal midbrain syndrome, Parkinson’s, MS, encephalitis, Cholinergic drugs, morphine, ocular inflammation, alcohol

46
Q

What are the differential diagnosis for convergence paresis/paralysis?

A

 Decompensated exophoria
 Primary exotropia
 Secondary exotropia
 Accommodation insufficiency or fatigue
 Uncorrected hypermetropia
 Intermittent exotropia, simulated by accommodation

47
Q

What are the features of divergence paresis/paralysis?

A

 Can occur in isolation or in association with other neurological signs
 Uncrossed diplopia
 Concomitant esotropia, Distance>Near
 Normal ocular movements, full abduction
 Paresis – defective negative fusional amplitudes
 Paralysis – absent negative fusional amplitudes
 Associated convergence weakness reported (Roper-Hall & Burde, 1987)

48
Q

What is the aetiology of divergence paresis/paralysis?

A

 Lack of agreement of location of divergence centre – agree in brainstem
 Intracranial tumour, raised ICP, infection, Miller-fisher syndrome and vascular disease

49
Q

What are differential diagnosis of divergence paresis/paralysis?

A

 Acquired VIth nerve palsy
 Convergence spasm
 TED
 Esophoria with divergence weakness
 Distance esotropia

50
Q

What are some features of Wernike’s Encephalopathy?

A

 Triad: Ophthalmoplegia, confusion and gait ataxia
 Abduction weakness
 Gaze-evoked nystagmus
 INO
 Upbeat nystagmus
 Impaired VOR
 Horizontal and vertical gaze palsies that may progress t complete ophthalmoplegia
 Bilateral but may be asymmetric

51
Q

What is the aetiology for Wernike’s Encephalopathy?

A

 Lesions occur throughout brainstem, thalamus, hypothalamus, cerebellum
 Thiamine B1 deficiency
 Most commonly seen in alcoholics

Orthoptics III (13 decks)

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