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(2) Tri B - Clinical opthalmology > Week 3 - Neuro 2.1 > Flashcards

Week 3 - Neuro 2.1 Flashcards

1
Q

What is Internuclear Ophthalmoplegia?

A

• INO is a lesion of the Medial Longitudinal Fasciculus (MLF) (find diagram)
• It results in a palsy of the Medial Rectus muscle
• With dissociated gaze evoked nystagmus of the abducting eye
(Ataxic Nystagmus)

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2
Q

What are the pathways involved with Internuclear Ophthalmoplegia?

A

• To look to the left, the right frontal eye field sends a signal to the left PPRF
• The left PPRF innervates the left VI (abducens) nucleus, which controls the left lateral rectus and causes the left eye to abduct. (Gaze left)
• Also, the left VIN nucleus innervates the right IIIN (oculomotor) nucleus, which controls the right medial rectus muscle. Causing the right eye to adduct (Gaze left)

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3
Q

Which tract is damaged in Internuclear Ophthalmoplegia? (INO)

A

• MLF (medial longitudinal fascicules) is tract connecting VIN nucleus to contralateral 3rd nerve nucleus
• In INO there is damage to the MLF giving deficit in adduction
- convergence is usually still intact

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4
Q

What are the two types of INO?

A

• Unilateral
• Bilateral

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5
Q

What is the Aetiology/cause of INO?

A

• Multiple sclerosis (common)
• Stroke - basilar artery occlusion (2nd common)
• Tumour rarely causes INO

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6
Q

What are the presenting signs if INO?

A

• Exophoria/tropia in primary position
- This will increase on attempted adduction

• Impaired/slowed saccades are useful when differentiating a Unilateral INO from an asymmetric bilateral INO
• Ataxic nystagmus on lateral gaze

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7
Q

What are the differential diagnosis of INO?

A

• Myasthenia gravis
Look for fatigue, variability, ptosis, Cogan’s lid twitch, involvement of the vert muscles

• Medial Wall Blow out fracture
History of trauma, enophthalmos, mechanical restriction of abduction

• Duanes Retraction Syndrome
Looking for restriction of abduction ad characteristic palpebral fissure changes
- Infranuclear Medial Rectus Palsy (Partial IlIrd Nerve Palsy)
- very rare

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8
Q

What is the summary of INO?

A

• Ipsilateral MR palsy
• Saccades more affected than pursuit
• Convergence may be intact
• Ataxic nystagmus
• Skew Deviation - ipsilateral hypertropia
• Bilateral has gaze evoked vert nystagmus and impaired vert smooth pursuit

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9
Q

what is recovery with INO?

A

• Adduction can recover quite quickly in MS patients
• Ataxic nystagmus may take longer
• This can be a sign when examining a patient with previous episodes of INO

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10
Q

What is one and a half syndrome?

A

Unilateral INO and ipsilateral horizontal gaze palsy

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11
Q

What is the aetiology of the one and a half?

A

• Extensive lesion of the caudal (lower) lesion of the Pons
• Affecting the horizontal gaze centre and the adjacent MLF
• Bilateral Medial Rectus Palsy and One Lateral Rectus Palsy (Gaze palsy + INO)
• cause: MS, Stroke, Tumour

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12
Q

How does one and a half present?

A

• Unilateral Internuclear ophthalmoplegia
• Ipsilateral Gaze Palsy
• Preserved abduction of contralateral eye
• Ataxic Nystagmus
• Paralytic pontine exotropia
• Intact vertical motility and Convergence
• Vestibular ocular reflex (VOR) usually intact

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13
Q

What is parinaud’s syndrome’s other names?

A

• Dorsal Midbrain Syndrome (where it is in the brain)
• Posterior Commissure Syndrome
• Sylvian Aqueduct Syndrome
• Nystagmus Retractorius Syndrome

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14
Q

What are the clinical features of parinaud’s syndrome? (Pt.1)

A

• Loss of upward saccadic movement with normal vertical pursuit.
• Convergence Retraction “Nystagmus’ - best seen using OKN drum on downward rotatior
There is a characteristic rhythmical convergence movement of both eyes with retraction of the globe.
• Light/Near dissociation - usually dilated pupils that react only to accommodation and not to light.

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15
Q

What are the clinical features of parinaud’s syndrome? (Pt.2)

A

• Collier’s sign - bilateral upper eyelid retraction with lid lag
• Papilloedema - children more likely to have hydrocephalus but can be present in adults too.
• Convergence Insufficiency
• Accommodative Insufficiency
•Skew Deviation

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16
Q

What may you see in extensive progressive lesions?

A

• In extensive/progressive lesions you may also see:
- Illrd, IVth and Vith Nerve Palsies
- INO

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17
Q

What would you notice with a pineal mass compression causing superior colliculi restriction or Edinger-Westphal Nucleus restriction?

A

• Pineal mass will compress causes: Increased HBP
• Superior Colliculi restricting upward saccades
• Edinger-Westphal Nucleus (Rostral portion of Oculomotor Nerve) causing light near dissociation of the pupils

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18
Q

what is a progressive supra-nuclear palsy?

A

• Degeneration of the Brainstem Reticular
Formation
• Is a disease of later life
• First described by Steele in 1964 and also known as Steele-Richardson Syndrome
• The vertical gaze palsy differentiates the condition from other Parkinsonian disorders

19
Q

what are progressive supra-nuclear palsy signs?

A

• Impared/slowing of vertical saccades
• Usually affecting downgaze initially
• Then complete loss of vertical saccades
• Late stage may have horizontal gaze disorders. With complete ophthalmoplegia.

• Frequent square - wave jerks have been noted/saccadic intrusions
• Difficulty in voluntary opening the eyelids (Apraxia of lid opening)

20
Q

What is the neurological signs of progressive supra-nuclear palsy?

A

• History or early falls
• Dysphagia with choking
• Symmertical akinetic rigidity
• Absence of tremor
• Frontal Lobe Deficits

• Combination of vertical gaze palsy and axial rigidity limiting neck movement.
- Patients complain of difficulty seeing food on their plate
- Trouble walking downstairs

• Sadly, dementia and death usually occur approx 10yrs after onset

21
Q

What is Myasthenia Gravis?

A

• Myasthenia - Greek for Weak Muscle
• Gravis - Latin for Heavy/severe

22
Q

What is the aetiology of Myasthenia Gravis?

A

• Autoimmune disorder
• Formation of acetylcholine receptor site antibodies
• The antibodies prevent acetylcholine from binding and reduce the effectiveness of the neurotransmitter

• Acetylcholine continues to be released
• This maintains the striated muscle contracture until the stores are drained.
• This then shows the classic early muscle fatigue

23
Q

What are the two types of Myasthenia Gravis?

A

• Systemic
• Ocular

24
Q

What are the features if Myasthenia Gravis?

A

• Characterised by excessive fatigueability of striated muscle
• EOM, facial, bulbar, neck, limb girdle, distal limb and trunk muscles
• 80-90% of patients with general MG have receptor site antibodies in their blood serum, compared to only 40-50% in Ocular MG

25
Q

Which muscles are affected and what are the associations with myasthenia gravis?

A

• When the respiratory muscles are severely affected it can be fatal
• EOM’s may be mostly affected as they have a very high concentration of receptors and an increased sensitivity of the Neuromuscular junction
• It may be associated with other autoimmune diseases Diabetes, Graves’ Orbitopathy and Rheumatoid arthritis

26
Q

What are the symptoms of myasthenia Gravis?

A

• Generally symptoms of MG increase as the day goes on.
• Patients may be symptom free in the morning and only complain of fatigue by the evening

27
Q

What are the ocular symptoms of myasthenia gravis?

A

• Ptosis
• Diplopia
• Inadequate lid closure

28
Q

How is ptosis presented in myasthenia gravis?

A

• Usually the first presenting sign of MG
• Bilateral but Asymmetrical
• Ptosis increases throughout the day

29
Q

How is the Ptosis assessed in myasthenia gravis?

A

• Ptosis should increase with continued elevation or repeated up/down gaze, with extreme cases the lids drop in primary position

30
Q

How does diplopia present in myasthenia gravis?

A

• Dipopia can be Hor/Vert/Both and will vary throughout the day
• MG may cause any type of muscle palsy

31
Q

What muscles can be affected causing diplopia?

A

• Limited elevation is the most common
• Pseudo INO
• Isolated IR Palsy
• Pseudo gaze palsy
• Pseudo 3rd, 4th, 6th nerve palsies
- In fact pseudo anything!!!

32
Q

How can the orbiculares test be done in myasthenia gravis?

A

Ask the patient to close their eyes tightly and then examiner tries to open them, whilst they keep them shut

33
Q

What are the systemic signs of Myasthenia Gravis?

A

• All dependant on which muscle groups are affected
• Ensure that you ask for signs of general MG in case History
• Difficulty chewing/swallowing aw Muscles)
• Difficulty speaking (Bulbar Muscles)

34
Q

What are the four differentiations of Adult myasthenia gravis?

A

• Ocular - that does not become generalised after 2 years since onset
• Mild/Mod Generalised MG - Ocular signs before the disease spreads to skeletal and bulbar muscles
• Acute Fulminating MG - Rapid onset with early involvement of respiratory muscles
• Late Severe MG - Can develop in the ocular or mild group, 2 years after onset

35
Q

What tests can be done to improve a ptosis?

A

• Ice pack test
• Lowering temp can improve symptoms
• Ice pack applied to the eyelid can improve the ptosis

36
Q

What blood test can be done and their results for Myasthenia Gravis?

A

• Serum blood testing for acetylchoine receptor site antibodies
• 80-90% seen in General MG
• 40-50% seen in Ocular MG
• Do not exclude MG if -ve blood result

37
Q

What is electro Electromyography? (MGO)

A

• carried out to record the electrical activity of the skeletal muscles
• Single or multipe muscle fibres may be tested
• Nerve supply to the muscles are electronically stimulated and muscle activity is then recorded

38
Q

How are patients with Myasthenia gravis managed?

A

• The Ophthamologist may trial a longer acting antichoinesterase drug for example pyridostigmine/mestinon
• CT scan of the thymus gland, as the thymus can be enlarged in MG
• If the gland is enlarged (Thymoma) it can be removed. Thus eliminating the B-cells that can produce the acetylcholine receptor antibody

39
Q

What is the ocular management of myasthenia gravis?

A

• Fresnel prisms
• Ptosis props
• occlusion
• Botox
• strabismus surgery under local anaesthesia with adjustable

40
Q

What is Chronic progressive external opthalmoplegia?

A

• Mitochondrial disorder
• Associated with Kearns Sayre Syndrome

41
Q

What is CPEO’s Clinical features?

A

• Progressive symmetrical loss of motility.
• Usually upgaze is the first to be affected
• Ptosis and Obicularis weakness
• Normal pupils and accommodation

• Diplopia is not commonly complained of as symmetrical and very slowly progressive
• Final stages have virtually no eye movements with +ve FDT due to secondary fibrosis

42
Q

What is the Kearns Sayre Syndrome?

A

• CPEO (In Childhood)
• Fine pigmentary retinopathy
• Heart conduction block

43
Q

What is the differential diagnosis for Kearns Sayre Syndrome?

A

• Myasthenia
• Graves
• Supra-nuclear Gaze Palsy
• Multiple Nerve Palsies

44
Q

How is Kearns Sayre Syndrome investigated?

A

• Fundoscopy
• Electro cardiogram
• Orthoptic assessment to include Uniocular fields of fixation
• Ptosis Props /Fresnels

(2) Tri B - Clinical opthalmology (10 decks)

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