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Med 1 UBC Winter 2020 > Week 22: Brainstem and Multiple Sclerosis > Flashcards

Week 22: Brainstem and Multiple Sclerosis Flashcards

1
Q

Conjunctiva

A

Transparent mucous membrane that lines the inner surface of the eyelids and surface of the globe up to the cornea. Responsible for producing tears. Tear film has 3 layers: protein layer, aqueous layer, fat layer. COnunctiva has goblet cells that produce mucous protein for tea film.

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2
Q

Sclera

A

structural support of the eye. Collagen bundles. It is responsible for the white colour of the eye and when eaten away by disease the pigmented eye below can be seen.

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3
Q

Cornea

A

Transparent avascular dome-shaped layer anterior to the iris and pupil. Refracts light - 2/3 of the eye’s refractive power. 5 layers: epithelium, bowman’s layer, stroma, descemet’s membrane, endothelium

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4
Q

what is the role of the endothelial layer of the cornea?

A

the endothelium pumps out fluid from the cornea. It is responsible for fluid and solute regulation. If it isn’t working then the cornea is no longer transparent.

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5
Q

Hypopyon

A

Collection of white blood cells settled in a flat layer of the anterior chamber

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6
Q

Anterior chamber

A

the space between the iris and the cornea

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7
Q

iris

A

2 layers: anterior stroma (iris colour, muscles) and posterior epithelium (produces awueous humour). Controls pupil size with circular and radial muscles.

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8
Q

Lens

A
  • bioconvex, avascular, transparent - enclosed by a capsule - suspended by zonules, which are connected to ciliary muscles. Ciliary bodies control how tight or lose the zonules are, thuse controlling how convex the lens is.
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9
Q

When the lens is more convex, improves focus of…..

A

near objects

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10
Q

Aging lens

A

Becomes cloudy - cataracts Becomes less elastic - unable to focus on nearby things as well.

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11
Q

Aging lens

A

Becomes cloudy - cataracts Becomes less elastic - unable to focus on nearby things as well.

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12
Q

Ciliary body

A

A ring-shaped thickening of tissue fromt he root of the iris to the vitreous body. Ciliary muscle is responsible for changing the shape of the lens. Ciliary epithelium produces aqueous humour (just as the back of the iris does).

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13
Q

Aqueous Humour

A

Transparent, watery fluid. SImilar to plasma but low in protein concentrations. Role is to provide oxygen and nutrients to the lens and cornea and then remove metabolic waste.

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14
Q

Process of production and drainage of aqueous humour

A

Produced by ciliary body, goes to posterior chamber, through the pupil to the anterior chamber, goes through the angle (bewteen iris and posterior part of cornea) and then it is absorbed by the trabecular meshwork (lymphatic system), goes to schlen’s caanal (veins) and then goes to episcleral veins.

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15
Q

Glaucoma

A

optic neuropathy (damages the nerve) in a typical pattern of nerve damage and visual field losses. If not treated properly, you will eventually lose vision. Looks like tunnel vision.

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16
Q

Vitreous body

A

Clear gel that fills the space between the lens and the retina. Liquifies and collapses with age; you get floaters which are little bits of remaining jelly floating in the liquid later in life, which produce shadows.

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17
Q

Optic nerve is made up of

A

afferent fibres of retinal ganglion cells.

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18
Q

Optic nerve surrounded by

A

oligodendrocytes, microglia, astrocytes, and meninges (pia, arachnoid, dura mater)

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19
Q

Optic disc

A

The hole where the optic nerve exits the eye. Retinal vessels enter/exit the eye here too. There are no photoreceptors here - a blind spot.

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20
Q

Myopia =

A

near-sightedness

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21
Q

hyperopia =

A

far-sightedness

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22
Q

Astigmatism =

A

The front of the eye isn’t perfectly spherical.

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23
Q

Presbyopia

A

reading glasses because your lens can’t accommodate for near vision anymore.

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24
Q

From the cortex to the eye, list the components necessary to initiate eye movement. Ex: look to left

A
  • The horizontal gaze centre (paramedian pontine reticular formation) in the pons sends a fibre to the abducens nucleus. Here it synapses with left CN VI (abducens nerve) and with a highly myelinated neuron that will coordinate with right eye
  • CN VI stimulates the lateral rectus of the left eye to abduct it.
  • The neurons coordinated with the right eye crosses over and travels up through the medial longitudinal fasciculus to the oculomotor nucleus, where it synpases with CN III, which innervates the medial rectus of the right eye
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25
Q

Is control of pursuitments ipsilateral or contralateral?

A

Pursuit is ipsilateral. If you want to look R, information comes from the right frontal eye field.

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26
Q

Where is the vertical gaze centre?

A

The midbrain

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27
Q

What would result from damage to one optic nerve?

A

Unilateral blindness

28
Q

What would result from severing the optic chiasm in the middle

A

bitemporal hemianopia (lost lateral half of each eye field)

29
Q

What would result from severing the right optic tract?

A

homonymous hemianopia (loss of left visual field from both eyes)

30
Q

what would result from severing the right temporal (meyer’s loop) optic radiations?

A

homonymous superior quadrantanopia (lost upper left visual field from both eyes)

31
Q

what would result from severing the left parietal (superior) optic radiations

A

congruous partial or complete hononymous inferior quadrantanopia (lost botton left visual field from both eyes)

32
Q

Internuclear Opthalmoplegia (INO)

A
  • DIsorder of the MLF that is a common presenting symptom in MS.
  • The patient complains of double vision at end gaze because their eyes aren’t lining up
  • Characterized by ipsilateral adduction weakness and contralateral adducting nystagmus.
  • Occurs because horizontal gaze in the contralateral eye is mediated by the MLF. The MLF is one of the most myelinated tracts in the body so it is one of the first to suffer from demylemination in MS.
  • Convergence is maintained (uses convergence centre in the midbrain)
33
Q

Explain the dual innervation of the face

A

The facial nerve has an upper motor neuron in the cortex that crosses over and synapses at its nucleus in the pons with a LMN that innervates the ipsilateral side of the face.

  • The top half of the face’s LMN gets stimulation from both the left and the right cortex.
  • The bottom half of the face’s LMN only gets innervation from the contralateral cortex.
  • This means that a stroke to the left cortex may lead to facial droop ONLY on the lower half of the right face. A lesion to both left LMNs leaving the pons would result in a full left facial droop
34
Q

What lesion would cause a the bottom of the left face to droop? What lesion would cause the whole left side of the face to droop?

A
35
Q

How does the romberg test work? What does it tell us?

A

The patient is to stand with eyes closed for at least 15 seconds. If they fall it is a positive sign.

Balance is maintained by vision, vestibular, and proprioceptive (dorsal columns) systems. You need 2 of 3 intact to stay balanced. The Romberg test removes vision. When the patient falls, it tells us that they have a deficit in either their proprioceptive or vestibular system.

36
Q
A
37
Q

What are the cardinal manifestation of MS? (4)

A
  1. Optic Neuritis
  2. Transverse Myelitis
  3. Brainstem inflammation (INO; Ataxia)
  4. Multifocal lesions
38
Q

What is transverese myelitis

A

Inflammation of the spinal cord that causes rising numbness from toes to trunk. This is often a presenting symptom of MS. It is often transient. The patient ma describe an “MS hug” - feel like there is a band around them.

39
Q

What does brainstem inflammation look like as a presenting symptom in MS?

A

Brainstem inflammation includes:

  • Intranuclear Opthalmoplegia (INO) - double vision at end gaze resulting from an attack of the MLF
  • Ataxia - trouble with balance and coordination
40
Q

Uhthoff’s phenomenon

A

Describes exacerbation of MS symptoms when they are hot. The pt may describe onset of symptoms when taking a shower - i.e., optic neuritis flares up.

41
Q

L’Hermitte’s phenomenon

A

An electric shock sensation that some patients with MS experience. Often short and intermittent.

42
Q

What is Optic Neuritis

A

Monocular vision loss that is often a presenting symptom in MS.

It is the result of acute inflammation, demyelination, and a conduction block in the optic nerve.

The patient may describe seeing a bull’s eye distribution of bluriness in their central vision.

The physician may observe a relative afferent pupillary defect.

43
Q

Relative afferent pupilary defect: What is it and what is it a sign of?

A

A clinical sign where both eyes contract well when light is shined in one of them, but when you shine the light in the other eye, they don’t contract as much. This suggests that the second optic nerve has been compromised.

May be a sign of MS or temporal (giant cell) arteritis.

44
Q

What are some tests for MS? (3)

A
  1. MRI and a good history
  2. Lumbar puncture (for oligoclonal banding)
  3. Visual evoked potential (look for slowed transmission of information to the brain)
45
Q

What are the diagnostic criteria for MS? COnsider both relapsing remitting and primary progressive

A

MacDonald Criteria: dissemination in space and time

  1. Relapsing Remitting MS
    • 2 attacks or evidence of lesions, based on history and/or clinical evidence (MRI; follow up MRI)
  2. Primary Progressive
    • Progressive disability over more than 1 year
    • 2 or more of…
      • 1+ lesion(s) in periventricular, juxtacortical and/or infratentorial white matter
      • 2+ spinal cord lesions
      • oligoclonal bands in CSF
46
Q

What is the best imaging modality for MS

A

MRI

47
Q

What causes MS?

A

The cause remains poorly understood. Combination of genes and environmental factors. Vitamin D deficiency is recognized as a significant risk factor.

48
Q

What are the risk factors for MS? (5)

A
  1. Age 20-40
  2. caucasian ethnicity (more about where you live)
  3. female (3:1 to males)
  4. Vitamin D deficiency
  5. infection (epstein Barr)

(picture: young white twin sisters getting the D and then getting STIs)

49
Q

Outline pathophysiology of MS

A
  • Unknown why autoimmunity develop
  • Lymphocytes become autoreactive, cross the BBB, recruit macrophages, and start attacking myelin
  • NO is released
  • A self-limiting process of autoimmunity
    • Spreads and then resolves (recruit other cells to clean up the inflammatory process)
  • SUbclinical injury continues to occur between attacks resulting in multiple scars throughout CNS and some axonal destruction
50
Q

Mechanisms of recovery between MS attacks

A

It takes days to get injurded but months to heal.

  • Stop active inflammation
  • Remove NO and cellular debris
  • Insert Na channels
  • Some compensation (via alternate pathways) to keep up function, but these tire over time.
  • Remyelination (hindered by smoking and age)
51
Q

How common is relapsing remitting vs primary progressive MS?

A

70% RR and 20% PP. 10% will start off RR and develop into PP

52
Q

What is the natural course of relapsing remitting MS?

A

Remission between attacks, but not full recovery. Subclinical lesions arise bewteen attacks. Baseline after attacks progressively becomes more impaired. about 10% will progress to primary progressive.

53
Q

What is the natural course of primary progressive MS?

A

Primary progressive shouldb e suspected if there is no remission between attacks. It is a steady decline.

54
Q

How does MS impact pregnancy?

A
  • Reduced relapses during pregnancy
  • Increased relapses for 3-6 mo post-partum
  • return to normal relapse rate 3-6 after birth
55
Q

OVerview of the range of disability/social challenges that MS patients experience

A
  • Fatigue
  • bladder dysfunction
  • sexual dysfunction
  • unemployment
  • pain
  • depression and cognitive dysfunction (associated with neural degeneration and are markers of accumulating disability)
  • trouble concentrating

involving a multidisciplinary team to manage the complex array of symptoms is therefore critical.

56
Q

Life expectancy with MS

A

Reduced by about 7.5 years. Death is most oftenr elated to infection, advanced disability and immobility (aspiration pneumo), chronic respiratory disease

57
Q

Theory of treatment for MS

A

Goal is to prevent new inflammation to maintain brain health.

Drugs act by destroying lymphocytes, interrupting lymphocyte communication and trafficking and increasing immune tolerance.

58
Q

primary treatment options for MS and how effective they are (3)

A

In order of increasing effectiveness

  1. Injectables (IFNs): 30% do well, but many SE so not often used
  2. Oral Pills: 50% decrease in relapse
  3. Monoclonal Antibodies: 80-90% effectiveness
59
Q

Where do the temporal radiations go and what information do they carry?

A

They go to the LOWER primary visual cortex and they carry information from the upper contralateral visual fields

parietal radiations carry information from the lower/contralateral visual vields and bring it to the upper primary visual cortex.

60
Q

relationship between smoking and MS

A

smoking exacerbates the progression of MS

61
Q

what are some presenting symptoms of MS?

A

fatigue, giat, bladder dysfunction, sexual dysfunction, heat intolerance (Utrhoff’s sign), l’hermitte sign (electric jolt), dysarthria, dysphagia, cognitive issues, spasticity/contractions

62
Q

ddx for acute vision loss (4)

A
  1. Amaurosis fugax due to central retinal arteru occlusion
  2. Retinal detachment
  3. Temoral (giant cell) arteritis
  4. Post-operative embolus to occipital lobe
63
Q

Amaurosis fugax

Presentation, cause, risks, management

A
  • Presentation: transient darkening (<10 mins); shade, tunnel, blur effect
  • Cause: hypoperfusion of the nerve; worry about central retinal artery occlusion
  • Risks: Risk of not regaining vision, other ischemic events, neovascularization (new, aberrant blood vessels); 7.5% stroke risk in 7 days
  • Management: find occlusion and give anticoagulation
64
Q

How does a reintal detachment present?

A
  • The patient sees floaters and then a curtain extending over their field of vision
  • Floaters are due to detachment of the vitreous humor. The disturbance of the humor can cause a tear in the retina that leads to retinal detachment
65
Q

Temporal (giant cell) arteritis:

What is it, presentation, diagnosis, treatment

A
  • Medium-large vessel vasculitis
  • Presentation: unilateral vision loss, temoral headache, jaw claudication, relative afferent pupillary defect
  • Diagnosis: ESP and CRP for inflammatory markers
  • treatment: IV steroids for inflammation to prevent further vision loss and vascular occlusion.

Med 1 UBC Winter 2020 (14 decks)

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