Multiple Sclerosis Flashcards

1
Q

Definition of MS

A

A chronic, progression disease of the CNS (brain, optic nerves, spinal cord) that affects sensation, movement and body functions

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2
Q

What are the 4 types of MS

A

Relapsing-remitting (RRMS)
Primary Progressive (PPMS)
Secondary Progressive (SPMS)
Progressive Relapsing

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3
Q

Relapsing-Remitting (RRMS)

A

Around 85% of MS cases

  • Suffer distinct attacks of symptoms which then fade away partially or completely
  • Periods between relapses characterised by a lack of disease progression
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4
Q

Primary Progressive (PPMS)

A

5-10%

  • Symptoms gradually get worse over time
  • Does not experience acute attacks
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5
Q

Secondary Progressive (SPMS)

A

Proceeds RRMS, occurs in 65% RRMS

  • Sustained build up of disability, independent of any ‘relapse’.
  • Develops into SPMS after 15 years of being diagnosed of MS
  • Less recovery following attacks, persistently worsening functioning during and between attacks, and/or fewer attacks accompanied by progressive disability
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6
Q

Progressive Relapsing

A

Gradual progression of disability from the onset of the disease, accompanied by one or more acute relapses, with or without full recovery

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7
Q

Causes of MS

A

Auto immune disorder where immune system attacks its own healthy tissue.

  • Autoimmune response destroys myelin sheath that surrounds CNS nerves
  • Unknown reason
  • Myelin sheath assists with conduction of messages from brain along the nerves
  • With MS, myelin sheaths scarred, causing messages from brain to become slowed or blocked
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8
Q

Risk Factors of MS

A
  • Age: any age, most commonly between 15 and 60
  • Gender: Women 2 x more likely than men
  • Family Hx: Higher risk if parent or sibling has MS
  • Certain infections: Epstein-Barr
  • Race: White people - Asian, African, Native American lowest risk
  • Climate: More common in countries with cooler climates
  • Certain autoimmune diseases: Thyroid disease, type 1 diabetes, inflammatory bowel disease
  • Smoking

MS IS NOT CONTAGIOUS OR INFECTIOUS

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9
Q

Epidemiology- Incidence of MS

A
  • 134 diagnosed in NZ each year
  • Male to female ratio 1:3
  • 1 in 1000 in NZ has MS
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10
Q

Epidemiology - Prevalence of MS

A
  • About 3000 living with MS in NZ (2006)
  • 75% women and 25% men
  • Overall prevalence is 71.9 per 100,000
  • Maori have substantially lower prevalence
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11
Q

Pathophysiology of MS

A

Demyelination of CNS:

  • Destruction of oligodendrocytes (myelinate CNS) and reactive astrogliosis
  • Immune cell infiltration across main blood barrier
  • Promotes inflammation, demyelination, gliosis and neuroaxonal degeneration
  • Disrupts neural signalling
  • Activated T helper cells recruit additional immune cells which increases the immune response
  • These destroy the lymphotoxin and TNF alpha that damage the oligodendrocytes
  • B cells, auto anti bodies and complement factors enter the CNS once the inflammation process has started causing additional damage to the CNS
  • T cells are part of the immune system however sometimes they do more harm than good
  • Begin to attack our CNS
  • T cell secrete cytokines which results in B cells and macrophages
  • B cells transform into plasma cells and release antibodies that attack the myelin
  • Macrophages release nitric oxide chemicals onto the myelin causing further damage to CNS
  • The longer this occurs, the more difficult it is for our nerve cells to carry nerve signals
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12
Q

What produces myelin?

A

Oligodendrocytes

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13
Q

Your patient has noticed a significant increase in muscle tone - what are the most important factors to check?

A

Does the patient have an infection, fever or untreated pain?

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14
Q

Most common lesion location of MS

A

Plaques that result from MS can be anywhere in the CNS
- Majority tend to be in the white matter around the lateral ventricles of cerebellum, BG, brainstem, Motor cortex, cerebral peduncles, spinal cord and optic nerve

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15
Q

Lesions in Grey White junction of associative, limbic, prefrontal cortex

A

Correlated with COGNITIVE DYSFUNCTION…

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16
Q

How is the Limbic System affected?

A

Inappropriate behaviour (impulsive, lack of insight, making off remarks), inappropriate emotional response (increased aggression and violent behaviour), changes to mood (depression), limited awareness of risks (poor judgement)

17
Q

How is the Prefrontal cortex affected?

A

May impact movement initiation, increased difficulty choosing goals, planning goals and executing plans + monitoring results
- may also have difficulty with independent living

18
Q

Lesions located in frontal lobes, dorsal midbrain, pons, parietal and temporal lobes associated with…?

A

Bowel and bladder dysfunction

19
Q

How is the frontal lobe affected?

A

Pre-motor area
- Trunk instability, difficulty with anticipatory strategies for balance, external cues,

Supplementary motor area
- trouble with initiation, using internal cues

Broca’s area
- Problem with fluency of language (expressive aphasia, can’t plan sentence to communicate what you’re thinking)

20
Q

How is the dorsal midbrain affected?

A

Parinaud’s syndrome - inability to move eyes up and down (paralysis of up gaze)

21
Q

How is the pons affected?

A

Sleep disturbances, sensory problems, arousal dysfunction, locked-in syndrome (consciously away of what is going on BUT unable to move any part of the body except the eyes)

22
Q

How is the parietal affected?

A

Loss of discriminative somatosensation (localisation, size, shape, texture, 2pts, proprioception)

23
Q

How is the temporal affected?

A

Loss of localisation of sounds

24
Q

Lesions located at Corpus Callosum, Inferior / superior longitudinal fascicles, occipitofrontal fascicles, corticospinal tracts

A

Correlated with coordination impairment

25
Q

How is the corticospinal tract affected?

A

Loss of voluntary motor function bilaterally at level of lesion and below (dermatomes affected: C6 onwards)

26
Q

For more progressive and chronic forms of MS, where is there damage?

A

Damage to the axon

27
Q

Benign MS

A

One or two relapses and remission resulting in full recovery and no disability

28
Q

Clinical Features of MS

A

Bladder dysfunction - failure to empty

Constipation or loss of control of the bowels

Fatigue (80% of people with MS)

Pain

Spasticity - feelings of stiffness and wide range of involuntary muscle spasms

Dysarthria (slurring, unclear articulation of words, difficulty controlling loudness) + Dysphonia (hoarseness, breathlessness, nasality, poor control of pitch) + Swallowing problems (dysphagia)

Difficulty to concentrate and poor memory (difficulty to organise, plan, focus)

Visual - sudden onset of double vision, poor contrast, eye pain, heavy blurring

Emotional changes - severe depression, mood swings, irritability, episodes of uncontrollable laughing and crying

Heat sensitivity - elevated core temp can alter effective conduction of nerve impulses causing fatigue

29
Q

Diagnosis of MS

A

NO single set of symptoms

1) Medical Hx and Neurological exam
2. MRI - detects presence of MS plaques or scarring, cannot differentiate between old and new lesions
3) Visual Evoked Potential (VEP) - recordings of NS electrical response to stimulation of specific sensory pathways (demyelination will cause slower response time)
4) Lumbar puncture - can detect levels of certain immune system proteins
5) Blood tests - can rule out other conditions

30
Q

What is the first line of treatment for MS?

A

Medication

31
Q

What types of medications to treat MS?

A

Gilenya - reduces relapses and disability progression in RRMS

Aubagio Teriflunomide - Interfares with WBC’s

Tecfidera Dimethyl Fumerate - reduces inflammation in brain caused by MS + helps protect cells that form myelin against attacks

Tysabri Naralizymab - Locks onto T cells and stops them from crossing blood-brain barrier

Stem Cell transplant - targets stem cells, replace or repair damaged cells or tissues

Stem cell transplant autologous haematopoietic stem cell transplant (AHSCT) - reset immune system so stops attacking person’s own CNS

Diet and Nutrition

Exercise - helps manage symptoms and disease progresison

Medicinal Cannabis

32
Q

Prognosis of MS

A

The longer you can maintain a healthy brain = the better the prognosis
- SELDOM life or death issues BUT QoL issues

33
Q

Prognosis of RRMS (88%)

A

Some people have been known to go many years or decades without new relapses

  • A relapse doesn’t mean that you disability will progress as in most cases following a relapse and a period of recovery there will be no lasting damage
  • Some cases - depending on severity and localisation of new brain lesions disability progression may occur
34
Q

Prognosis of PMS (12%)

A

Disability will occur much faster

- Men tend to progress faster than women by 38%

35
Q

Influencing factors for prognosis (factors suggesting a better disease course)

A
  1. Diagnosed at young age (20-30s)
  2. New relapses in first years after diagnosis
  3. Complete recovery from relapses with no long-term damage
  4. Long intervals between relapses
  5. Symptoms that are sensory in nature (numbness and tingling)
36
Q

Differential diagnosis of MS

A

SHOULD NOT rush to diagnose MS

  • Gullian Barre Syndrome (attacks myelin sheath in lower motor neurons)
  • Spinal cord neoplasms
  • Schilder disease
  • Sarcoidosis
37
Q

Outcome Measures for MS

A
  • Expanded Disability Status Scale (EDSS) GOLD STANDARD (0-10, scoring in 0.5 increments)
  • Neurologic Rating Scale (NRS) (8 categories of 22 parameters, -10 - 100)
  • Multiple Sclerosis Impact Scale (MSIS)