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Neurology & Psychiatry > L5 MND > Flashcards

L5 MND Flashcards

1
Q

MND defintion

A

it is a neurodegenerative disease resulting in progressive muscular paralysis through neuron degeneration in the primary motor corext, corticospinal tracts, brainstem and spinal cord

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2
Q

MND characteristics

A
  • degeneration of upper and lower motor neurons leading to muscle weakness
  • clinical heterogeneity with unknown etiology
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3
Q

what is the life expentancy of MND

A

4-5 years from first symptom

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4
Q

how long is the average diagnostic delay

A

14 months

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5
Q

what are some possible reasons for a diagnostic delay

A
  • shortage of neurologist appointments
  • lack of availability of testing (MRI) appointments
  • some people don’t want to follow up on their symptoms
  • lack of education and awareness among some GPs and the public
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6
Q

what are two other terms for MND

A
  • Amyotrophic Lateral Sclerosis (ALS)
  • Lou Gehrig’s Disease
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7
Q

where in the world is the term MND more commonly used

A
  • Ireland
  • UK
  • Australia
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7
Q

where in the world is the term ALS more commonly used

A
  • US
  • Canada
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8
Q

where in the world may the term Lou Gherig’s disease be used

A

US

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9
Q

which two adult-onset neurodegenerative disoders are more common than MND

A
  • MS
  • PD
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10
Q

what does incidence mean

A

new cases being diagnosed over a period of time

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11
Q

what is the incidence of MND

A

2.6-3 cases per 100,000

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12
Q

what does prevalence mean

A

number of people currently diagnosed

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13
Q

what is the prevalence of MND

A

7 per 100,000

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14
Q

what is the age of onset

A

can be as early as the second decade but typically in the early 60s

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15
Q

what is the male to female risk ratio

A

1/350:1/400

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16
Q

what charity in Ireland serves the population of people with MND

A

Irish Motor Neurone Disease Association (IMNDA)

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17
Q

how many cases of MND are currently registered with the IMNDA

A

275

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18
Q

in what hospital is the specialist MND clinic located

A

Beaumont hospital

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19
Q

is there a cure for MND

A

no, there is no cure, remission or effective drug treatments for MND

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20
Q

what is the lifetime risk for MND

A

1 in 2000

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21
Q

what is the prognosis for MND

A
  • 50% live less than three years after diagnosis
  • 20% live five years or more after diagnosis
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22
Q

what is the peak incidence for MND

A

55-75 with slight male predominance

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23
Q

what percentage of MND cases are sporadic

A

90%

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24
Q

what percentage of cases are inherited or familial

A

10-15%

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25
Q

how many genes have been identified for familial MND

A

over 30

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26
Q

what gene is associated with 50% of familial cases in ireland

A

C9orf72 repeat expansion

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27
Q

what gene is responsible for 2% of ALS cases

A

CuZnSOD mutation

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28
Q

Which systems does MND not affect

A

autonomic and sensory

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29
Q

what is one way to differentiate MND from PD and MS

A

sensory and autonomic systems are not affected in MND unlike in MS and PD

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30
Q

which motor neurons are resistant to degeneration in MND

A

the eye movment motor neurons (CN III, IV & VI)

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31
Q

why is there no sphincter involvement in MND

A
  • autonomic system is not affected
  • incontinence can be a problem, but that is more due to requiring assistance to toilet than with the sphincter
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32
Q

what does UMN involvment sometimes cause in MND

A

emotional lability

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33
Q

what percentage of people with MND experience changes in cognition

A

60%

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34
Q

what type of cognition changes are experienced in people with MND

A
  • personality changes
  • irritability
  • obsessions
  • poor insight
  • defitics in frontal executive tests
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35
Q

what percentage of people with MND develop fronto-temporal dementia

A

10%

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36
Q

what subtypes are there of MND

A
  • amyotrophic lateral sclerosis
  • primary lateral sclerosis
  • progressive muscular atrophy
  • progressive bulbar palsy
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37
Q

what are the clinical features of amyotrophic lateral sclerosis

A

both upper and motor neuron signs in multiple spinal segments

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38
Q

what is the most common form of adult-onset MND

A

amyotrophic lateral sclerosis

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39
Q

what is the median survival of amyotrophic lateral sclerosis

A

3-5 years

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40
Q

what are the clinical features of primary lateral sclerosis

A

upper motor neuron signs only

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41
Q

what is the course of primary lateral sclerosis

A
  • many patients eventually develop clincial or electrophysiological signs of LMN involvement
  • ALS develops in up to 77% within 3-4 years
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42
Q

what is the median survival of primary lateral sclerosis

A

for those who remain with a diagnosis of PLS, median survival is 20 years or more

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43
Q

what are the clinical signs of progressive muscular atrophy

A

lower motor neuron signs only

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44
Q

what is the course of progressive muscular atrophy

A

variable evolution to ALS

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45
Q

what is the median survival of progressive muscular atrophy

A

5 years, though a subset survive 20 years or more

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46
Q

what are the clinical features of progressive bulbar palsy

A

speech and swallowing are affected initially due to LMN involvement of CN IX, X, XII

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47
Q

symtoms of progressive bulbar palsy

A
  • dysarthria, dysphagia and dysphonia
  • aspiration pneumonia is usually the terminal event
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48
Q

what is the median survival of progressive bulbar palsy

A

2-3 years

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49
Q

what is an example of a disease which has similar traits to MND

A

Kennedy’s Disease

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50
Q

what is Kennedy’s disease

A

A slowly progressive disorder of the motor neurons caused by a genetic mutation. It is a rare form of muscular atrophy which leads to weakness.

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51
Q

Can women get Kennedy’s disease

A

no, it only affects men though women may carry the genetic mutation

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52
Q

Kennedy’s disease prognosis

A

compatible with a normal lifespan

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53
Q

cognitive changes which may be present in MND

A
  • executive function
  • fluency
  • language
  • social cognition
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54
Q

changes in behaviour associated with MND

A

apathy & loss of sympathy

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55
Q

in MND, what are cognitive changes associated with

A
  • agressive disease
  • genetic mutations
  • non-compliance
  • increased caregiver burden
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56
Q

what percentage of people with MND develop cognitive impairment within the spectrum of fronto-temporal dementia

A

5-15%

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57
Q

examples of cognitive and behavioural tests which can be administered to an MND population

A
  • ALS Brief Cognitive Assessment
  • ALS Cognitive Behavioural Screen
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58
Q

hypothesised causes of MND

A
  • Genetic factors
  • Traumatic events
  • Toxic exposures.
  • Viral infections.
  • Excitotoxicity - toxins interacting with glutamate receptor resulting in cellular calcium overload.
  • Oxidative stress causing motor neuron damage.
  • Speculation about a link with elite athleticism.
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59
Q

some symptoms of initial presentation of MND

(exact presentation will depend on the type of MND)

A
  • Stumbling.
  • Foot drop.
  • Loss of dexterity.
  • Weakened grip.
  • Cramps and fasciculations.
  • Voice changes.
  • Swallowing difficulties.
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60
Q

what does loss of upper motor neurones result in

A
  • Muscle weakness
  • Stiffness
  • Slowness of movement
  • Spasticity
61
Q

clinical features of UMN lesions

A
  • increased tone in limbs
  • muscular weakness
  • brisk tendon reflexts
  • extensor plantar responses
62
Q

what does loss of LMNs result in

A
  • muscle weakness and wasting
  • cramping and twitching
63
Q

clinical features of LMN lesions

A
  • muscle atrophy
  • fasiculations
  • muscle weakness
  • reduced/absent tendon reflexes
64
Q

examples of conditions which can mimic MND

A
  • Kennedy’s disease
  • Spinal muscular atrophy
  • Myaesthenia gravis
65
Q

three different sites of onset for MND

A
  1. Limb/spinal
  2. Bulbar
  3. Respiratory
66
Q

what is the most common pattern (site) of onset

A

limb/spinal, accounting for 60-70% of cases

67
Q

features of limb/spinal onset MND

A
  • assymetrical symptoms
  • upper limb presentation is more common
  • symptoms include cramps fasciculations, stiffness & stumbling
  • will ultimately present with bulbar symtpms
68
Q

what is the least common site of onset

A

respiratory

69
Q

features of respiratory onset

A
  • Respiratory failure due to motor neuron loss.
  • Inspiratory muscles preferentially affected.
  • Decreased lung vital capacity (<50% predicted).
  • Symptoms include mild dyspnoea (shortness of breath) on exertion, morning sleepiness, and headaches.
70
Q

examples of pulmonary function tests

A

Spirometry, SNIP, ABGs TOSCA.

71
Q

what is not recommended for people with MND who have respiratory presentation

72
Q

examples of respiratory symptoms which occur in advanced stages of the disease

A
  • Shortness of breath on exertion (SOBOE)
  • Daytime sleepiness
  • Fatigue
  • Headache
  • Orthopnoea
  • Weak cough/sniff
  • Nocturnal restlessness/sweating
73
Q

what are the features of bulbar onset MND

A

changes in speech, swallowing and oro-motor functions

74
Q

what percentage of people with MND present with bulbar features at diagnosis

75
Q

what percentage of people with MND present with bulbar features during advanced stages of the disease

76
Q

what is bulbar onset MND associated with

A
  • shorter survival
  • faster functional decline
  • reduced quality of life
  • increased support needs
77
Q

examples of direct MND symptoms

A
  • weakness
  • fasciculations
  • spasticity
  • dysarthria
  • dysphagia
  • dyspnoea
  • emotional lability
78
Q

examples of indirect MND symptoms

A
  • psychological difficulties
  • constipation
  • sleep disorders
  • drooling
  • pain
  • secretions
  • hypoventilation
79
Q

why is diagnosis of MND difficult

A
  • there is no one disease-specific test
  • the disease represents a heterogenous group of disorders
80
Q

what is diagnosis of MND based on

A
  • patient’s report
  • observation over time
  • diagnostic tests
  • response to intervention
81
Q

what criteria are used in the diagnosis of MND

A

Gold Coast Critera (Shefner et al., 2020)

82
Q

what does the Gold Coast Criteria state

A

diagnosis can be reached if there is evidence of UMN and LMN dysfunction in one body region or if there is evidence of LMN dysfunction in at least two body regions

83
Q

diagnostic tests for MND

A
  1. Needle Electromyography (EMG).
  2. Nerve conduction studies.
  3. Chest X-ray.
  4. Autoantibody screening.
  5. Thyroid function tests.
  6. Creatine kinase levels.
  7. Biochemical screen.
  8. Full blood count.
84
Q

diagnostic tools for bulbar presentation of MND

A
  • cranial nerve examination
  • needle EMG in genioglossus, sternocleidomastoid & trapezius muscles
  • cranial nerve MRI of bulbar regions
  • auditory perceptual assessment of dysarthria types
  • frenchay dysarthria assessment
  • videoflouroscopy
  • EAT-10
  • 3oz swallow test
  • voluntary cough test
85
Q

cranial nerve examination

A

identifies bulbar motor LMN and UMN signs → weakness, fasciculations, atrophy, tone, reflexes

86
Q

advantages of cranial nerve examianation

A
  • well established
  • easy to perform
  • reliability of items established in stroke, structural disorders and mixed neurological populations
  • validated with respect to detection of dysphagia with VFSE.
87
Q

disadvantages of cranial nerve examination

A
  • not sufficiently standardised
  • subjective
  • measurement proportions have not been evaluated in MND
88
Q

needle EMG in genioglossus, sternocleidomastoid & trapezius muscles

A

Indicates acute and chronic denervation in selected muscles & LMN changes

89
Q

advantages of needle EMG in genioglossus, sternocleidomastoid & trapeziuz muscles

A
  • well established
  • helpful in the exclusion of mimics
  • able to detect subclinical involvement
  • can be quantitative
90
Q

disadvantages of needle EMG in genioglossus, sternocleidomastoid & trapezius muscles

A
  • invasive
  • not well standardised across clinics
  • requires substantial training
  • low sensitivity due to difficulty with relaxation
  • commonly qualitative
90
Q

cranial nerve MRI of bulbar regions

A

Rules out neurological mimics, tongue and pharyngeal pathology.

91
Q

advantages of cranial nerve MRI of bulbar regions

A
  • widely available; noninvasive
  • potentially sensitive to prodromal stages of bulbar disease
92
Q

disadvantages of cranial nerve MRI of bulbar regions

A
  • qualitative
  • not formally assessed with respect to clinical utility in the diagnosis of early stages of bulbar disease.
93
Q

auditory perceptual assessment of dysarthria types

A

Detection of UMN vs LMN signs in speech/voice tasks; rating specified dimensions of voice/speech quality on a Likert scale

94
Q

advantages of auditory perceptual assessment of dyarthria types

A

well established method in dysarthria assessment in SLT

95
Q

disadvantages of auditory perceptual assessment of dysarthria types

A
  • specific set of MND-relevant items is not established
  • may not be equally sensitive to all dysarthria severities
  • requires specialised training; not well utilised in neurology
  • lengthy
  • low reliability for some items
96
Q

frenchay dysarthria assessment

A

Comprehensive assessment of bulbar structure and function.

97
Q

advantages of frenchay dysarthria assessment

A
  • well established method in dysarthria assessment in SLT
  • reliability is establish
98
Q

disadvantages of frenchay dysarthria assessment

A
  • relatively lengthy
  • not specific to MND
  • validation is limited
99
Q

videoflouroscopy

A

Gold standard dysphagia assessment to directly visualise swallow safety and efficiency.

100
Q

advantages of VFS

A
  • well established in MND
  • showed sensitivity to prodromal stage of dysphagia and sensitivity to change.
101
Q

disadvantages of VFS

A
  • requires expensive instrumentation and highly trained personnel
  • involves radiation exposure (although minimal)
  • need for a seperate and additional test.
102
Q

EAT-10

A

self administered screening tool for dysphagia, it has 10 items and is symptom based.

103
Q

advantages of EAT-10

A
  • validated and reliability assessed in a large non-MND cohort
  • differentiates safe vs unsafe swallowers in MND
  • quick and easy
  • low administrative burden for scoring
104
Q

disadvantages of EAT-10

A
  • subjective
  • may not be sensitive to early disease stages
105
Q

3oz swallow test

A

Screening tool for dysphagia; 3oz of water is given to a patient in a cup; pass/fail → fail is an inability to drink without stopping, cough/throat clear, wet voice.

106
Q

advantages of 3oz swallow test

A

validated in general patient populations with very high sensitivity (but poor specificity); quick and easy to use

107
Q

disadvantages of 3oz swallow test

A
  • not validated in MND
  • may miss patients with sensory deficits (ie. silent aspirators) and early signs of dysphagia
  • could overestimate risk of dysphagia.
108
Q

voluntary cough test

A

Screening tool for airway defense physiological capacity using airflow spirometry or peak cough flow meter.

109
Q

advantages of voluntary cough test

A
  • objective, instrumental
  • validity, reliability, sensitivity and specificity relative to VFS have been established in MND
110
Q

disadvantages of voluntary cough test

A
  • requires instrumentation and a trained examiner
  • voluntary cough is mediated differently neurologically to a reflexive cough
  • effort dependent
111
Q

what is an example of an outcome measure used for MND

A

ALS Functional Rating Scale Revised (ALSFRS)
* 12 items rated from 0-4

112
Q

advantages of ALSFRS (1999)

A
  • Has been found to be predictive of aspiration on videoflouroscopy
  • Has been found to be predictive of prognosis.
113
Q

12 items of ALSFRS (1999)

A
  • Speech
  • Salivation
  • Swallowing
  • Handwriting
  • Cutting food and handling utensils
  • Dressing and hygiene
  • Turning in bed and adjusting clothes
  • Walking
  • Climbing stairs
  • Dyspnea
  • Orthopnea
  • Respiratory insufficiency
114
Q

what type of treatment is usually used for MND

A

sypmtom-focused care (as opposed to restorative care)

115
Q

example of a medication used to treat MND

A

Riluzole which extends median survival from 11.8 to 14.8 months

116
Q

examples of a new drugs used for treatment of MND

A

Ellorarxine

117
Q

example of a drug treatment which has been approved in japan

118
Q

example of a drug treatment which may treat bulbar symptoms in MND

119
Q

what is the use of Riluzole based on

A

excitotoxicity theory of MND pathogenesis

120
Q

example of a drug used for treatment of MND due to the SOD1 gene

121
Q

members of the MDT

A

neurologist
gp
MND clinical nurse specialist
SLT
OT
physio
dietician
social worker
palliative care
psychiatry & neuropsychology
respiratory physician

122
Q

neurologist’s role within the MDT

A

diagnosis, disclosure of diagnosis, treatment and symptom management, initiation of respiratory and nutritional interventions, unbiased information regarding research developments

123
Q

GP’s role within the MDT

A

symptom control, drug monitoring, liaison with other teams

124
Q

clinical nurse specialist’s role within the MDT

A

liaison with medical team and coordination of care, home visits, practical advice regarding accessing support services, patient advocacy

125
Q

SLT’s role within the MDT

A

evaluation and monitoring of dysphagia and aspiration, speech therapy and counselling regarding communication devices

126
Q

OT’s role within the MDT

A

optimisation of patient’s environment, advice regarding safety awareness, adaptive and splinting devices, activity modification, driving, energy conservation, home modification

127
Q

dietician’s role within the MDT

A

evaluation of nutritional status and the need for tube feeding, management of dysphagia, management of enteral feeding

128
Q

physio’s role within the MDT

A

evaluation of muscle strength and function, advice regarding walking aids and orthoses, safety awareness

129
Q

social worker’s role within the MDT

A

advice and counselling regarding employment, change in lifestyle and financial issues, support for carers

130
Q

palliative care’s role within the MDT

A

symptom control, pain management, maintenance of quality of life, preservation of dignity

131
Q

psychiatry and neuropsychology’s role within the MDT

A

evaluation and management of cognitive impairment/dementia, adjustment disorders, anxiety and depression

132
Q

respiratory physician’s role within the MDT

A

assessment of respiratory dysfunction, initiation of non-invasive ventilation.

133
Q

three areas of MND which involve SLT input

A
  1. Speech/communication
  2. Swallowing
  3. Sialorrhea
134
Q

type of dysarthria found in those with MND

A

mixed flaccid-spastic dysarthria

135
Q

symptoms associated with dysarthria in MND

A
  • Strangled voice quality (spastic).
  • Vocal cord paresis.
  • Soft palate involvement.
  • Nasal regurgitation.
  • Weak cough.
  • Drooling.
  • Tongue fasciculations.
136
Q

patient report of symtoms of swallowing difficulty in MND

A
  • Difficulty clearing mucous.
  • Choking on dry/crumbly food.
  • Avoidance of chewy meat or skinned fruit.
  • Small sips to avoid coughing.
  • Nasal regurgitation.
  • Blender use and social restrictions.
137
Q

patient report of symptoms of communication difficulty in MND

A
  • Nasal quality, slurred speech.
  • Weak, breathy, or strained voice.
  • Shortness of breath while speaking.
  • Saliva catching during speech.
138
Q

symptoms of flaccid dysarthria on an oro-facial exam

A
  • Flaccid dysarthria
  • Nasal speech
  • Nasal regurgitation
  • Absent jaw jerk
  • Reduced/absent gag reflex
  • Lingual atrophy
  • Fasciculations
139
Q

features of spastic dysarthria on an oro-facial exam

A
  • Spastic dysarthria
  • Emotional lability
  • Brisk jaw jerk
  • Hypersensitive gag reflex
  • Shrunken immobile tongue
140
Q

3 strategies in dysarthria management

A
  1. Education - informing the patient and their family of course and treatment of dysarthria.
  2. Compensation - implementation of compensatory strategies to enhance intelligibility.
  3. AAC - use of AAC devices (voice banking and eye gaze) to promote communication.
141
Q

what is message banking

A

patient records messages to be able to play once speech deteriorates

142
Q

what is voice bamking

A

patient records their voice to be able to create new messages with the recorded voice when their speech ability has deteriorated

143
Q

where do MND patients get their voice/message banking devices

144
Q

considerations for implementing AAC

A
  • Upper limb function.
  • Literacy and computer skills.
  • Cognition and social acceptability.
  • Timing and prognosis.
145
Q

goal of dysphagia management

A

Safe and efficient oral intake with emphasis on patient’s quality of life.

146
Q

dysphagia management in MND

A
  • Compensatory strategies over active exercises (due to fatigue concerns).
  • Emerging evidence for EMST (Expiratory Muscle Strength Training).
147
Q

when should tube feeding be introduced in MND

A
  • Should be introduced proactively (not as crisis intervention).
  • Consider when weight loss exceeds 5% and before respiratory involvement.
148
Q

is the recommendation for PEG or RIG in MND

A
  • PEG (Percutaneous Endoscopic Gastrostomy) vs. RIG (Radiologically Inserted Gastrostomy).
    • Recommendation is for RIG as they do not require sedation, which as we know is risky for those with respiration features.
149
Q

how is sialorrhea managed

A
  1. Behavioural changes.
    • Neck brace
    • Beep reminders.
  2. Education.
  3. Anticholinergic medications.
    • Hyoscine patch (can have side effects).
  4. Botox injections.
  5. Radiation therapy.
  6. Portable suction devices.

Neurology & Psychiatry (9 decks)

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