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Med 4 > CNS Week 3 Movement Disorders > Flashcards

CNS Week 3 Movement Disorders Flashcards

1
Q

What type of disease is huntingtons

A

An inherited neurological disorder
The gene was the first to be discovered on chromosome 4

Autosomal dominant inheritance with full penetration with expansion in the disease range (if you live long enough you will get huntingtons)

Is a trinucleotide repeat disorder - repeating CAG

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2
Q

What is the biological effect of huntington gene

A

HD gene codes for the huntingtin protein (HTT)
Well preserved function present in almost all livng things (absence of HTT causes embryonic death)

Mutated HTT has a gain of function effect as it is toxic to certain cell types especially in the brain

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3
Q

Effect of HTT protein on the brain

A

HTT is neurotoxic
Kills cells in different ways (striatum affected first)
Also widespreaf cell death throughout the brain

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4
Q

Age of onset of huntingtons disease

A

Typically between 30-50

However now recognised it can occur at any age

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5
Q

What causes the age at which huntingtons occurs

A

50% of age of onset relates to CAG repeat number

The other 50% relates to other genetic factors and potentially environmental factors

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6
Q

Life expectancy after diagnosis of huntingtons

A

20 years

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7
Q

Clinical features of huntingtons

A

Neurological- chorea (extra uncontrolled movements), dystonia, dysarthria, dysphagia

Cognitive- progressive dementia of frontal lobe type, loss of empathy, lack of insight, loss of verbal fluency, loss of ability to sequence

Psychiatric features- depression, anxiety, psychosis

Non neurological features- high metabolic rate and weight loss

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8
Q

Diagnosis of huntingtons if asymptomatic

A

A positive gene does not designate onset of the disease but only a pre symptomatic carrier status

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9
Q

Diagnosis of huntingtons disease

A

Relies on presence of a movement disorder in conjunction with a positive gene test
There may be psychiatric prodrome, but diagnosis cannot rest on this as this is common in those with positive predictive test

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10
Q

Early clinical features of huntingtons

A

Chorea
Psychiatric features
Frontal lobe features

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11
Q

Mid disease features of huntingtons

A

Marked chorea, dystonia, falls, declining mobility, frontal lobe dementia and loss of verbal fluency, swallowing difficulties, behavioural issues and psychiatric features

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12
Q

Late features of huntingtons disease

A

Anarthric, severe swallowing problems, immobile weight loss

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13
Q

Social aspects of huntingtons disease

A

DVLA notifiable condition - usually cant drive for ling

Usually fail to continue to work beyond early stages related to chorea but also frontal lobe features

Very high levels of career strain

Family dynamic- people are aware their children are at risk

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14
Q

Treatment of huntingtons

A

No treatment which stops the cell death of brain cells

Chorea- responds to dopamine blocking drugs
Psychiatric medications - neuroleptics, antidepressants

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15
Q

Disadvantages of huntington medication

A

Can cause side effects as it is long term which can be difficult to distinguish from symptoms of huntingtons itself

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16
Q

Non medical treatment of huntingtons

A

Annual speech and swallowing assesments
Regular weight checks, fortified diet supplements
Social care aspects to support family
CPN may be needed for significant psychiatric issues

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17
Q

How is pre symptomatic testing in huntingtons carried out

A

Possible to test asymptomatic carriers ages >18
Through genetic counselling service

High levels of morbidity in those who test gene positive - high levels of depression

Methods of IVF whihc allow pretty good guarantee of unaffected child without the need for test

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18
Q

What is huntingtons disease

A

An autosomal dominant inherited genetic condiiton causing a slowly progressive disease with a movement disorder, frontal lobe dementia and psychiatric problems

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19
Q

How many protein coding genes are there in humans

A

20,000

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20
Q

What is autosomal dominant inheritance

A

One parent is affected with a disease due to a mutation in the relevant gene. As it is dominant he only needs one copy of the gene for it to be present and there is a 50% chance of his offspring inheriting it

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21
Q

What is autosomal recessive inheritance

A

Both copies of the gene need to be mutated to have the disease eg 2 parents that are both carriers so have one copy of the gene
25% chance of offspring having the disease, 50% of them being carriers and 25% chance of being unaffected

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22
Q

What are triplet repeats

A 
Repetitive sequences common in the genome eg CAG 
Often polymorphic (length varies) 
Changes in length can impact gene function
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23
Q

What do longer triplet repeat sequences lead to

A

Longer repeats = more severe disease phenotype

Several severe neuromuscular and neurodegenerative disorders associated with changes in repeat length

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24
Q

Huntington disease allele repeat sizes

A 
Normal <27 
Intermediate 27-35 
Range of partial penetrance 36-39 
Classic HD 40-65 
Juvenile HD >65 (can be up to 250 repeats)
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25
Q

What is type 1 myotinic dystrophy

A

Myotonic myopathy with associated abnormalities in other organs:
Myotonia: difficulty in relaxing clenched hands
Muscular dystrophy
Cataracts
Testicular atrophy
Frontal balding
Cardiac conduction defects

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26
Q

Triplet repeat causing myotonic dystrophy type 1

A

Expansion of a CTG nucleotide repeat in the 3’ UTR of the DMPK gene

DMPK is expressed mainly in muscles and CNS
CTG repeats are transcribed into mRNA but not translated into protein

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27
Q

Myotonic dystrophy type 1 allele repeat sizes

A

5-35 stable (no DM)
36-50 may be unstable (no DM)
51-150 unstable (no, minimal or classical DM)
>150 unstable (classical, juvenile or congenital DM)

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28
Q

What is the location of the CAG expansion that causes huntingtons

A

CAG expansion in exon 1 of the HTT gene

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29
Q

What is the location of the CTG expansion that causes myotonic dystrophy

A

CTG expansion in the 3’UTR (non coding region) of the DMPK gene (gain of fucntion)

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30
Q

Describe triplet repeat instability

A

Repeats can expand due to errors in DNA replication and repair - account for normal variation in repeat length

Beyond a certain size, repeats become unstable and more likely to expand
Full expansion mutations can be inherited from unaffected parents with an intermediate or premutation allele

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31
Q

What is repeat anticipation

A

Repeat instability means repeats can expand in subsequent generations

An intermediate repeat or a small expansion can increase in size in subsequent generations
Results in a more severe phenotype in child than in the parent

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32
Q

Parent of origin within myotonic dystrophy

A

Maternal transmission
Large expansions in the CTG repeat occur almost exclusively on maternal transmission
Female carriers of unstable repeat sizes >46 CTGs more likely to have children with larger expansions

(Expansion occurs in the oocyte)

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33
Q

Parent of origin in huntingtons disease

A

Large expansions in the CAG repeat occur almost exclusively on paternal transmission

Male carriers of unstable repeat sizes (>27 CAGs) are more likely to have children with larger expansions

(Expansion occurs during spermatogenesis)

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34
Q

What is the polymerase chain reaction used for

A

Method to amplify DNA
Uses DNA template strand eg genomic DNA extracted from patient blood sample
Requires primers - short stretches of DNA that are complimentary to the sequence being amplified

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35
Q

How can PCR be used to detect triplet repeat expansions

A

Primers flanking (either side) of the CAG repeat region
2 primer pairs used
HD1 + HD3
And HD2 + HD5

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36
Q

Describe the PCR reaction using the HD1 and HD3 pair

A

Amplification across the CAG repeat
HD1 primer is fluorescently labelled
PCR fragment sizes can be detected by capillary electrophoresis

Samples with known allele sizes included as controls

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37
Q

What does it mean if the HD1 +HD3 PCR testing is positive

A

Single allele detected so patient may be homozygous for this repeat size
Patient may have an expansion that is not detectable by this method

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38
Q

Define genetic counselling

A

The process by which patients or relatives at risk of a disorder that may be hereditary are advised of the consequences of the disorder, the probability of developing or transmitting it and the ways this may be prevented, avoided or ameliorated

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39
Q

Aims of genetic counselling

A

Understand the clinical features of a condition and its management
Understand the inheritance of the disorder
Understand the options for managing the risks
Make the best possible non judgemental adjustment to the disorder

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40
Q

What are the core principles in genetic counselling

A

Autonomy of the individual or couple

Patients right to full and complete information in a form they understand

Preservation of confidentiality (even when seeing members of the same family)

Aimed at facilitative decision making with time to explore all options

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41
Q

What is autosomal dominant

A

Heterozygotes with one copy of the abnormal gene are affected

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42
Q

What is autosomal recessive

A

Homozygotes with 2 copies of the abnormal gene are affected

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43
Q

What is X linked recessive

A

Males with one copy of the abnormal gene on the X chromosome are affected

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44
Q

What is penetrance

A

Can be complete or incomplete

The proportion of individuals with the gene who are affected often dependent on age of assessment eg if you have huntingtons and live long enough it will be expressed

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45
Q

What is variable expressivity

A

Variation in expression

The degree to which a disorder is expressed in an individual - different complications are common in autosomal dominant conditions

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46
Q

What is reduced penetrance

A

Common in cancer predisposition syndromes

Not everyone who inherits the mutation develops cancer in their lifetime

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47
Q

Benefits of predictive tests

A

Reduce uncertainty

Screening / surgery / treatment to reduce the risk of the conditon

Pregnancy options

Plan life eg career

Information for relatives

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48
Q

Problems with predictive tests

A

Further uncertainty

Financial implications eg insurance and mortgages

May restrict career choices eg army

Survivor guilt

Information about relatives risk

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49
Q

Clinical features of huntington disease

A

Movement disorder - involuntary movements, abnormal gait, psychiatric disturbances, personality changes, depression, apathy, aggression, cognitve decline (early onset dementia)

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50
Q

Symptoms of migraines

A 
Severe throbbing headache, unilateral at first but may spread to the opposite side 
Sonophobia 
Photophobia 
Pallor 
Perspiration 
Vomitting
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51
Q

Symptoms of a stroke

A

Motor and sensory deficits in face (cranial nerves V and VII); unilateral, bilateral or alternating V and VII

Abnormal eye movements

Dysphagia (cranial nerve X)

Vertigo, atiaxia, motor and sensory deficits which may be unilateral or alternating

Headache
Vomitting

Altered consciousness

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52
Q

What are the 3 phases of an epileptic seizure

A

Tonic phase: epileptic cry, incontinence, cyanosis, generalised stiffening of body and limbs

Clonic phase: incontinence, cyanosis, clonic jerks of limbs, body and head, salivary frothing, eye blinking

Postictal stupor: drowsy, sleepy, confused, limbs and body limp, salivary drooling, unresponsive

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53
Q

What is parkinsons disease chemically

A

Lack of dopamine in the substantia nigra

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54
Q

Stages of parkinsons disease

A

Stage 1: unilateral involvement, blank facies, affected arm in semiflexed position with tremor; patient leans to unaffected side
Stage 2: bilateral involvement with early postural changes; slow shuffling gait with decreased excursion of legs
Stage 3: pronounced gait disturbances and moderate generalised disability: postural instability with tendency to fall
Stage 4: significant disability; limited ambulation with assistance
Stage 5: complete invalidism; confined to bed or chair cannot stand or walk eevn with assistance

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55
Q

What is bradykinesia

A

Slowness of initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions (symptom of parkinsons)

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56
Q

What is multiple sclerosis

A

A chronic condition with low incidence but high prevalence

Dissemination of CNS inflammatory demyelinating lesiosn in space and time
No cure but treatments are available

57
Q

What is myasthenia gravis

A

An autoimmune disorder of the neuromuscular junction

Fluctuating skeletal muscle weakness
Typically presenting with ptosis, diplopia or bulbar symptoms

Myasthenic crisis is a medical emergency characterised by neuromuscular respiratory failure
Spontaneous or precipitated by infection, surgery or medication
Requires early diagnosis and respiratory monitoring

58
Q

What is guillain barre syndrome

A

Acute immune mediated polyneuropathy

  • progressive muscle weakness
  • reduced or absent tendon reflexes
  • from mild weakness to complete paralysis of limb, facial, respiratory and bulbar muscles
  • autonomic nervous system dysfunction
59
Q

What is a DALY

A

Disability adjusted life years

One year lost due to ill health, disability or early death

60
Q

Role of the motor cortex

A

Integrates information and produces motor signals

61
Q

Role of the basal ganglia

A

Receives sensory and motor cortical informatino and helps plan movement by feeding back to the cortex via the thalamus (initiates voluntary movement)
Prevents unwanted movement, is involved in learning movement and associated reward

62
Q

Role of the cerebellum

A

Receives infromation from the body and assists with dynamic coordination of movement balance and posture

63
Q

What is the basal ganglia

A

A group of sub cortical grey matter structures that are part of the extra pyramidal motor systems

Does not initiate movement but helps plan movement by integrating cortical input and feeding back to the cortex via the thalamus through a direct and indirect pathway

64
Q

What can injury to or CNS dysfunction of the basal ganglia cause

A

Abnormal involuntary movements (dyskinesias)
Slowed voluntary movement (bradykinesia)
Ridged postures (dystonia)
Struggle to move (akinesia)

65
Q

What structures make up the basal ganglia

A 
Caudate nucleus 
Putamen 
Globus pallidus 
Subthalamic nucleus 
Substantia nigra
66
Q

What are the 2 parts of the substantia nigra

A

Pars reticulata (SNr)

Pars compacta (SNc)

Dark cells in the midbrain

67
Q

What do the caudate nucelus and putamen make up

A

Neostriatum

68
Q

2 parts of the globus pallidus

A

Internal (Gpi)

External (Gpe)

69
Q

Major inputs of the basal ganglia

A 
Cerebral cortex (corticostriate) 
Thalamus (thalamostriate) 
Brain stem (SNc- nigtostriate)
70
Q

Maojr outputs of the basal ganglia

A

Thalamic nuclei
The cortex (via thalamus)
And brain stem

71
Q

What are the striatal afferents

A

Corticostriatal (glutamatergic)

Thalamostriatal (glutamatergic)

Nigrostriatal (dopaminergic)

72
Q

Where do the striatal afferents synapse

A

They synapse onto the medium spiny neurons (90% of cells in the striatum- GABAergic)

73
Q

What are the striatal efferents

A

Medium spiny neurons

Striatopallidal (GABAergic)
- direct and indirect

Striatonigral (GABAergic)

74
Q

What type of neurotransmitters are glutamate and dopamine

A

Glutamate - excitatory

Dopamine - excitatory or inhibitory depending on which receptor its binded to

75
Q

What is the globus pallidus

A
  • internal (GPi) and external (GPe) segments
  • input to both GABAergic projection neurons
  • output from both GABAergic
76
Q

What is the major output structure of the basal ganglia

A

GPi

77
Q

What is the direct pathway of movement

A

Cerebral cortex releases glutamate which is absorbed by the striatum and activity increases
More GABA is released to the internal globus pallidus
Activity decreases in the global pallidus internal
Activity of the thalamus is increased due to reduced tonic level of activity
More glutamate is released and movement is turned on

78
Q

Role of dopamine in the direct pathway of movement

A

Dopamine released from the substantia nigra pars reticulata onto dopamine 1 receptor. This switches the neurons on and reduces movement

79
Q

What is the indirect pathway of movement

A

Glutamate released by the cerebral cortex into the striatum. Striatum is excited so more GABA is released and absorbed into the globus pallidus external (activity reduces)
Less GABA is released so there is less inhibition of the substantia nigra
More glutamate is released to the globus pallidus internal
More GABA is released and inhibits the thalamus and turns movement off

80
Q

Role of dopamine in the indirect pathway

A

Inhibits neuroon (switches off the indirect pathway)

81
Q

What are the symptoms of the disruptions of the basal ganglia

A

Slowness of voluntary movement / postural reflexes (bradykinesia)

Muscular rigidity

Lack of movement (akinesia)

Abnormal involuntaty movements (dyskinesia)

82
Q

What is the role of the basal ganglia

A

Facilitate context appropriate voluntary behaviour and movement

Inhibit inappropriate involuntary movement

83
Q

Pathology of huntingtons disease

A

10-20% reduction in brain weight (atrophy)
Decreased striatal volume and cell death
Loss of GABA containing medium spiny neurons in the striatum
1st: enkephalin containing MSN
Later stage: substance P containing
Cholinergic interneurons of the striatum are spared

Decreased cortical volume and cell death

84
Q

Symptoms of parkinsons disease

A 
Tremor 
Bradykinesia 
Rigidity 
Mask like expression 
Postural instability 
Microphagia (small writing) 
Shuffling gait

Later:
Depression
Dementia
Endocrine dysfunction (constipation)

85
Q

What are lewy bodies

A

Inclusions in neurones with core of a-synuclein

(Aggregate to form fibrils and may contribute to dementia seen in 50% of parkinson patients

86
Q

Causes of PD

A
  • Oxidative stress
  • 15% of patients have a first degree relative with PD
  • genetic causal factors - familial PD is rare
  • PARK1 or SNCA gene codes a-synuclein ; autosomal dominant early onset PD with lewy bodies and marked rigidity
  • PINK1 and PARK7 gene mutations also cause autosomal recessive forms of PD
  • drug induced neurodegeneration - MPTP (environmental toxin) synthetic heroin causes immediate parkinsonism when injected
87
Q

Diagnosis of parkinsons disease using PET scan

A

Used to visualise and quantify dopaminergic neurones using radioactive ligands which bind to dopamine transporter proteins

88
Q

Role of dopamine in parkinsons disease

A

As there is less dopamine being released from the substantia nigra the direct pathway is less stimulated so results in reduced movement

89
Q

What is the first line treatment of parkinsons disease

A

Levodopa (L dopa)
A precursor of dopamine

L dopa with peripheral DOPA decarboxylase inhibitor

90
Q

Why cant you use dopamine to treat parkinsons disease

A

Because it does not cross the blood brain barrier

91
Q

Unwanted effects of levodopa

A

Development of dyskinetic movements due to fluctuations of dopamine throughout the day

Rapid fluctuation in clinical state

Nausea and anorexia

Hypotension

Psychotic effects

92
Q

Surgical treatment for parkinsons disease

A

Implantation of deep brain stimulation

Or surgery to implant a tube into the small intestine that releases levodopa

93
Q

Benefits and risks of levodopa

A

More improvement in motor symptoms

More improvement in activities of daily living

More motor complications

Fewer adverse events

94
Q

Benefits and risks of dopamine agonists for treating PD

A

Less improvement in motor symptoms

Less improvement in activities of daily living

Fewer motor complications

More specified adverse events

95
Q

Benefits and risks of monoamine oxidase B inhibitors for treating PD

A

Less improvement in motor symptoms

Less improvement in activities of daily living

Fewer motor complications

Fewer specified adverse events

96
Q

Neuropathology of parkinsons disease

A

Loss of the substantia nigra pars

Alters balance of basal ganglia circuitry to lack of movement

97
Q

Key features of executive dysfunction

A

Normal speech and perception

IQ may be normal

Loss of goal oriented behaviour

Stimulus driven behaviour (eg it is normal to put glasses on your head so a patient will put glasses on even if the context is inappropriate

Deficit in apathy (unable to correct mistakes)

Socially inappropriate behaviour

98
Q

What can cause executive dysfunction

A

Unilateral frontal damage (caused by head injury), degenerative disease, stroke, surgery
Subcortical and cortical damage

99
Q

When is executive function required

A

When the situationr requires a response that competes with a strong habitual response

A novel solution is required or the task is not well learnt (no memories / habit to draw on)

The situation requires error correction or troubleshooting

100
Q

Define executive function

A

A description of psychological processes that underlie flexible goal directed behaviour

101
Q

Purpose of the wisconsin card sorting test

A

Measures the ability to learn concepts and considered a good measure of frontal lobe functioning

102
Q

What is a TIA

A

Transient ischaemic attack -

Symptoms only one hour means more at risk of stroke

103
Q

Define stroke

A

Acute onset of neurological deficits (lasting for more than 24 hours) due to a disturbance in blood supply to the brain

Approx 15million people suffer strokes each year
1/3 die, 1/3 left disabled

104
Q

Non modifiable stroke risk factors

A 
Age (avg between 68-73) 
Atrial fibrillation (2-6 x ) 
Gender (females less likely pre menopause but more severe) 
Ethnicity 
Family history
105
Q

Modifiable stroke risk factors

A 
Hypertension 
Diabetes (6 x inc risk) 
Hyperlipidaemia (high cholesterol) 
Smoking 
Obestiy 
Carotid artery disease 
Atherosclerosis
106
Q

What are the 2 different types of strokes

A

Ischaemic (85%): blocked blood vessels

Haemorrhagic (15%): ruptured blood vessels

107
Q

What are the different types of ischaemic strokes

A

Thrombotic (55%): build up of plaque in the cerebral vessel
(Lacunar occlusion or large vesse occlusion)

Embolic (30%): travelling clot or plaque lodged in major cerebral vessel
(Large vessel occlusion)

108
Q

Haemorrhage Stroke symptoms

A

thunderclap headache, seizures, nausea, unilateral weakness (common in all types of stroke)

109
Q

Anterior circulation stroke symptoms

A 
Hemiplegia / paresis 
Hemisensory loss 
Hemianopia 
Dysphasia 
Aphasia 
(Motor and sensory deficits in the opposite side of the body to where the stroke has occured)
110
Q

Posterior circulation stroke symptoms

A

Dizziness
Unilateral limb weakness (can be bilateral)
Ataxia (broken down coordination - damage to the cerebellum)
Dysarthria (speech, hard to express self)

Harder to diagnose due to more generalised symptoms

111
Q

Non specific stroke symptoms

A 
Confusion 
Drowsiness 
Dizziness 
Nausea 
Double vision 
Incontinence
112
Q

What is a lacunar infarction

A

Commonly occuring in brainstem, thalamus, basal ganglia

Small strategic strokes in penetrating arteries that feed sub cortical structures

80% clinically silent

Motor hemiplegia syndrome - infarction in the posterior limb of the internal capsule, basal ganglia or pons

113
Q

Which artery is most comminly affected by strokes

A

Middle cerebral artery

114
Q

Symptoms of stroke in the middle cerebral artery

A

Hemiplegia, hemisensory loss, dysphagia

115
Q

How is a stroke identified

A

Neurological examination followed by urgent referral for neuroimaging
Via CT which can detect haemorrhage but is less effective at detecting acute ischaemic stroke

116
Q

What on a CT scan indicates a stroke has occurred

A

Lack of putamen

117
Q

Haemorrhage stroke mortality / outcome

A

45% mortality

30% vasospasm: likely to have ischaemic stroke in the next 7-14 days

118
Q

Haemorrhage stroke treatment

A

Pain management and surgery to repair the bleed with clipping or coiling (microclip over the base of the rupture)

May include lowering blood pressure with labetalol or glycerol trinitrate

119
Q

Treatment of ischemic strokes

A

Thrombolysis with altepase (tissue plasminogen activator).within 3 hours

Thrombectomy with retriever devices within 6hrs (physical removal of clot. Used when TPA is contraindicated or failed)

120
Q

What is the penumbra

A

The area surrounding an ischemic event such as thrombotic or embolic stroke
The area that is at risk of progressing to infarction but is still salvageable if reperfused (located around the infarct core)

121
Q

Why is time crucial in stroke treatment

A

Becuase the core tissue starts to expand into the penumbra at 12-22 ml/100g/min

122
Q

What do the core and the penumbra represent

A

Core represents irreversibly damaged tissue

Penumbra represents potentially salvageable tissue

123
Q

Order of events that are likely to occur after a stroke

A

1) failure of ion pumps, cell depolarisation and swelling
2) excessive glutamate release
3) peri infarct depolarisations
4) inflammatory cells infiltrate the brain
5) apoptosis

124
Q

What is vascular cognitive impairment

A

A heterogeneous group of cognitive phenotypes (mild to severe) that are presumed to share a vascular origin

125
Q

What cerebrovascular pathologies associated with vascular cognitive impairment can be visualised with neuroimaging

A

White matter change

Lacunar infarction

Microbleeds

Enlarged perivascular spaces

Cerebral amyloid angiopathy

126
Q

What happens to nerves in MS

A

The myelin sheath which is a protective membrane that wraps around the axon of a nerve cell is destroyed with inflammation and scarring

127
Q

Cause of right leg numbness

A

Lesion in the left side of the brain (Sensory cortex)

128
Q

Describe inflammatory neurodegeneration in MS

A

Immune mediated pathogenesis is thought to drive neurodegeneration

Early relapsing remitting pahse is more susceptible to treatment

Both inflammation and neurodegeneration are involved throughout the disease course

129
Q

Describe the immunopathology of MS

A

Inflammation is present at all stages of MS, from acute disease through to later chronic disease

Neurodegenerative damage has been correlated with immune mechansims

Brain reserve and repair mechanisms are important in compensating for CNS damage

130
Q

Role of T cells and B cells in MS

A

T cells have been viewed at the centre of MS immunopathology
But B cells also have multiple functions that may contribute to MS pathogenesis in addition to their capacity to differentiate into antibody secreting cells

131
Q

Clinical features suggestive of MS

A 
Onset between 15-50 
Blurred or double vision 
Lhermitte’s sign 
Fatigue 
Heat sensitivity 
Bladder symptoms 
Cognitive or affective changes
132
Q

Central symptoms of MS

A 
Fatigue 
Cognitive impairment 
Depression 
Anxiety 
Unstable mood
133
Q

Visual symptoms of MS

A

Nystagmus
Optic neuritis
Diplopia

134
Q

Musculoskeletal symptoms of MS

A

Weakness
Spasms
Ataxia

135
Q

Sensation symptoms of MS

A

Pain
Hypoesthesias
Paraesthesias

136
Q

Bowel symptoms of MS

A

Incontinece

Diarrhoea or constipation

137
Q

Urinary symptoms of MS

A

Incontinence

Frequent or retention

138
Q

Which neurotransmitters are affected to cuase jerky movements of arms and legs (huntingtons disease)

A

ACh and GABA

Med 4 (12 decks)

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