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Neurology > Movement disorders > Flashcards

Movement disorders Flashcards

Parkinsons Epilepsy MS

1
Q

What is motor neuron disease

A

In motor neurone disease (MND), motor nerves become damaged and eventually stop working. Therefore, the muscles that the damaged nerves supply gradually lose their strength.

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2
Q

Key features of UMN signs

A
  • Spasticity: increased muscle tone
  • Weakness: Lower limb: flexors weaker than extensors, upper limp extensors weaker than flexors
  • Hyperreflexia
  • Up going plantars
  • Clonus
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3
Q

If there is a lesion of the spinal cord, what might you expect to see

A
  • UMN weakness
  • Sphincter symptoms
  • sensory level
  • bilateral motor signs
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4
Q

If there is a lesion in the motor cortex, what might you expect to see

A
  • UMN weakness
  • Frontal signs
  • Dysphasia
  • Hemianopia
  • Disturbance of higher sensory function
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5
Q

If someone is displaying LMN signs, where is the lesion

A
  • In the anterior horn cell

- distal to the anterior horn cell: root, plexus, peripheral nerve

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6
Q

What are LMN lesions characterised as

A
  • Decreased muscle tone
  • weakness and wasting - muscle atrophy
  • Arreflexia
  • Muscle fasciculations
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7
Q

What is the most common form of MND

A

AML: Amyotrophic lateral sclerosis (ALS)

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8
Q

when does MND usually develop

A

Usually 55-79, rarely before 40
Men more than women
Not usually inherited

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9
Q

Symptoms of MND

A
  • UMN signs
  • Poor co-ordination and balance - stiff gait
  • Painful muscle spasms
  • head drop
  • slurred quiet speech
  • NO SENSORY SIGNS
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10
Q

Investigations of MND

A
  • Mainly clinical
  • EMG: ongoing chronic denervation
  • MRI will be normal
  • Nerve conduction studies will be normal
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11
Q

Management of MND

A
  • Neurology referral
  • supportive care
  • may eventually require resp help - BiPAP
  • muscle relaxants
  • carbocysteine for mucus
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12
Q

What is multiple sclerosis

A

Multiple sclerosis (MS) is a chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system. This is caused by an inflammatory process involving activation of immune cells against the myelin.

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13
Q

What are the causes of MS

A

Growing evidence for the influence of:

  • Multiple genes
  • Epstein–Barr virus (EBV)
  • Low vitamin D
  • Smoking
  • Obesity
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14
Q

What are the signs and symptoms of MS

A
  • Symptoms generally progress over 24 hours and can last days to weeks
  • Optic neuritis
  • Eye movement abnormalities
  • Focal weakness
  • Focal sensory changes
  • Ataxia
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15
Q

What is optic neuritis

A
  • most common presentation of multiple sclerosis
  • demyelination of the optic nerve and loss of vision in one eye
  • Central scotoma. This is an enlarged blind spot.
  • Pain on eye movement
  • Impaired colour vision
  • Relative afferent pupillary defect
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16
Q

What focal sensory symptoms may someone with MS experience

A

Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign

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17
Q

What is the management of optic neuritis

A
  • urgent ophthalmology referral - 24hrs
  • Steroids: recovery 2-6 weeks
  • 50% develop MS over next 15 years
  • Change on MRI will help to predict this
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18
Q

What is Lhermitte’s sign

A
  • electric shock down the spine and into the limbs when flexing the neck
  • indicates disease in the dorsal column of cervical spinal cord
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19
Q

What focal weakness can patients with MS experience

A

Bells palsy
Horners syndrome
Limb paralysis
Incontinence

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20
Q

What is sensory ataxia

A
  • loss of the proprioceptive sense

- positive Romberg’s test

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21
Q

What s cerebellar ataxia

A
  • problems with the cerebellum coordinating movement.

- suggests cerebellar lesions.

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22
Q

How do you diagnose MS

A
  • symptoms have to be disseminated in time and space

- one episode of symptoms and nothing on MRI suggests clinically isolated syndrome

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23
Q

What is relapsing-remitting MS

A
  • most common pattern at initial diagnosis
  • characterised by episodes of disease and neurological symptoms followed by recovery
  • symptoms occur in different areas with different episodes
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24
Q

What is secondary progressive MS

A
  • relapsing-remitting disease at first, but now there is a progressive worsening of symptoms with incomplete remissions
  • Symptoms become more and more permanent.
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25
Q

What is primary MS

A
  • worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remission
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26
Q

How do you diagnose MS

A
  • Clinical picture
  • LP
  • MRI
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27
Q

What is the management of chronic MS

A
  • Involve MDT team
  • disease modifying drugs and biologic therapy
  • Treat symptoms
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28
Q

How do you treat acute flares of MS

A
  • Methylprednisilone:
  • 500mg orally daily for 5 days
  • 1g intravenously daily for 3–5 days where oral treatment has failed previously or where relapses are severe
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29
Q

What symptomatic treatments can be given for MS

A
  • Exercise to maintain activity and strength
  • Neuropathic pain: amitriptyline or gabapentin
  • Depression: SSRIs
  • Urge incontinence: anticholinergic medications such as tolterodine or oxybutynin (although be aware these can cause or worsen cognitive impairment)
  • Spasticity: baclofen, gabapentin and physiotherapy
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30
Q

What is Huntington’s Chorea

A
  • autosomal dominant genetic condition that causes a progressive deterioration in the nervous system
  • Patients are usually asymptomatic until symptoms begin around aged 30 to 50.
  • Affects parts of the brain meaning it doesn’t work properly
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31
Q

What is the genetics behind Huntington’s chorea

A

“trinucleotide repeat disorder” that involves a genetic mutation in the HTT gene on chromosome 4.

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32
Q

What is anticipation

A

successive generations have more repeats in the gene, resulting in:
- Earlier age of onset
- Increased severity of disease
Associated with trinucleotide repeat disorders i.e Huntingtons

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33
Q

What is the common presentation of Huntington’s Chorea

A
  • nsidious, progressive worsening of symptoms
  • begins with cognitive, psychiatric or mood problems
  • Chorea (involuntary, abnormal movements)
  • Eye movement disorders
  • Speech difficulties (dysarthria)
  • Swallowing difficulties (dysphagia)
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34
Q

How do you diagnose Huntington’s Chorea

A
  • genetic test for the faulty gene

- pre-test and post-test counselling

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35
Q

What is the management plan for Huntington’s Chorea

A
  • Effectively breaking bad news
  • MDT:
  • SALT
  • Genetic counselling regarding relatives, pregnancy and children
  • Advanced directives
  • End of life care planning
36
Q

Medications which may help the movement disorder aspect of Huntington’s chorea

A
  • Antipsychotics (e.g. olanzapine)
  • Benzodiazepines (e.g. diazepam)
  • Dopamine-depleting agents (e.g. tetrabenazine)
37
Q

What is the prognosis of Huntington’s Chora

A
  • Life expectance is around 15-20 years after the onset of symptoms.
  • As the disease progresses patients become more susceptible and less able to fight off illnesses.
  • Death is often due to respiratory disease (e.g. pneumonia).
  • Suicide is a more common cause of death than in the general population.
38
Q

What is Charcot Marie Tooth

A
  • inherited disease affecting peripheral motor and sensory nerves
  • various types
  • dysfunction in the myelin or the axons
  • majority AD
  • Symptoms usually < 10 years but onset can be delayed >40 yrs
39
Q

Features of Charot Marie Tooth to particular look for in OSCEs

A

High foot arches (pes cavus)
Distal muscle wasting causing “inverted champagne bottle legs”
Weakness in the lower legs, particularly loss of ankle dorsiflexion
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

40
Q

What are the key causes of peripheral neuropathy

A 
A – Alcohol
B – B12 deficiency
C – Cancer and Chronic Kidney Disease
D – Diabetes and Drugs (e.g. isoniazid, amiodarone and cisplatin)
E – Every vasculitis
41
Q

Main symptoms of charcot marie tooth

A

muscle weakness in their feet, ankles, legs and hands
an awkward way of walking (gait)
highly arched or very flat feet
numbness in the feet, arms and hands

42
Q

what is the management of Charcot marie tooth

A
  • No cure or meds to slow progression
  • Neurologists and geneticists to make the diagnosis
  • Physiotherapists
  • Occupational therapists
  • Podiatrists: insoles and other orthoses
  • Orthopaedic surgeons to correct disabling joint deformities
43
Q

What is myasthenia Gravis

A

Myasthenia graves is an autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.
Typical patients are either a woman under the age of 40 or a man over the age of 60.

44
Q

What is closely associated with Myasthenia Gravis

A
  • thymoma (tumours of the thymus gland)
  • 10-20% of patients with myasthenia gravis have a thymoma
  • 20-40% of patients with a thymoma develop myasthenia gravis.
45
Q

What autoantibodies are involved in myasthenia gravis

A
  • acetylcholine receptor antibodies: 85%
  • muscle-specific kinase (MuSK) (10%)
  • Low-density lipoprotein receptor-related protein 4 (LRP4) (5%)
46
Q

What is the characteristic features of myasthenia gravis

A
  • weakness that gets worse with muscle use and improves with rest
  • Symptoms are typically minimal in the morning and worst at the end of the day
47
Q

What is the main presentation of myasthenia gravis

A
  • Extraocular muscle weakness causing double vision (diplopia)
  • Eyelid weakness causing drooping of the eyelids (ptosis)
  • Weakness in facial movements
  • Difficulty with swallowing
  • Fatigue in the jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
48
Q

How can you illicit fatiguability in a patient with myasthenia gravis

A
  • Repeated blinking will exacerbate ptosis
  • Prolonged upward gazing will exacerbate diplopia on further eye movement testing
  • Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
49
Q

Investigations for Myasthenia gravis

A
  • Check for a thymectomy scar.
  • Test the forced vital capacity (FVC)
  • test for autoantibodies
  • CT/MRI of thymus gland for thymoma
  • edrophonium test
50
Q

What an edrophonium test

A
  • IV dose of edrophonium chloride/neostigmine:
  • Edrophonium block enzymes and stop the breakdown of acetylcholine
  • level of acetylcholine at the neuromuscular junction increases
  • briefly and temporarily relieves the weakness.
51
Q

What is the management of Myasthenia gravis

A
  • Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine)
  • Immunosuppression (e.g. prednisolone or azathioprine) suppresses the production of antibodies
  • Thymectomy can improve symptoms even in patients without a thymoma
  • monoclonal antibodies
52
Q

How to Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine work

A

ncreases the amount of acetylcholine in the neuromuscular junction and improve symptoms

53
Q

What is a myasthenic Crisis

A
  • Severe complication resulting in an acute worsening of symptoms, often triggered by another illness such as a respiratory tract infection
  • can lead to respiratory failure as a result of weakness in the muscle of respiration
54
Q

Management of myasthenic crisis

A
  • non-invasive ventilation with BiPAP
  • full intubation and ventilation.
  • immunomodulatory therapies such as IV immunoglobulins and plasma exchange.
55
Q

What is Parkinson’s Disease

A

progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movement. The symptoms are characteristically asymmetrical, with one side affected more than the other

56
Q

What is the classic Parkinsonian Triad

A

Resting tremor
Rigidity
Bradykinesia

57
Q

What type of tremor is associated with Parkinsons

A
  • Unilateral, pill rolling tremor
  • more pronounced when resting and improves on voluntary movement
  • worsened if the patient is distracted
58
Q

What is meant by cogwheel rigidity

A
  • Rigidity is a resistance to passive movement of a joint. If you take their hand and passively flex and extend their arm at the elbow, you will feel a tension in their arm that gives way to movement in small increments (like little jerks).
59
Q

What is bradykinesia

A

Bradykinesia describes how their movements get slower and smaller:

  • micrographia
  • Shuffling gait
  • Difficulty initiating movement
  • Difficulty turning
  • Hypomimia
60
Q

What are other features of Parkinson’s Disease

A 
Depression
Sleep disturbance and insomnia
Loss of the sense of smell (anosmia)
Postural instability
Cognitive impairment and memory problems
61
Q

What type of dementia is associated with Parkinson’s Disesae

A
  • Lewy body dementia
  • progressive cognitive decline
  • visual hallucinations, delusions, disorders of REM
62
Q

What is Multiple system atrophy

A
  • neurones of multiple systems in the brain degenerate.
  • degeneration of the basal ganglia lead to a Parkinson’s presentation.
  • degeneration in other areas lead to autonomic dysfunction and cerebellar dysfunction (causing ataxia).
63
Q

What happens in autonomic dysfunction

A

postural hypotension
constipation
abnormal sweating
sexual dysfunction)

64
Q

What are the Parkinson’s Plus syndrome

A
  • Multiple system atrophy
  • Progressive Supranuclear Palsy
  • Corticobasal Degeneration
65
Q

How do you diagnose Parkinson;s DIsease

A

MAde on clinical assessment

Can get MRI

66
Q

What is the Management of Parkinson’s Disease

A
  • No cure so aim to minimise treatment
  • Levodopa
  • COMT inhibitors
  • MOB inhibitors
  • Dopamine agonists
67
Q

What is levodopa

A

synthetic dopamine given orally to boost their own dopamine levels. It is usually combined with a drug that stops levodopa being broken down in the body before it gets the chance to enter the brain

68
Q

What are peripheral decarboxylase inhibitors

A

drug that stops levodopa being broken down in the body before it gets the chance to enter the brain

69
Q

What are examples of levodopa and peripheral decarboxylase inhibitors

A

Co-benyldopa (levodopa and benserazide)

Co-careldopa (levodopa and carbidopa)

70
Q

What is the main side effect of dopamine

A

If dose is too high you can get dyskinesia which are abnormal movements associated with excessive motor activity

71
Q

Examples of dyskinesia

A

Dystonia
Chorea
Athetosis

72
Q

What is dystonia

A

This is where excessive muscle contraction leads to abnormal postures or exaggerated movements.

73
Q

What is chorea

A

These are abnormal involuntary movements that can be jerking and random.

74
Q

What is athetosis

A

These are involuntary twisting or writhing movements usually in the fingers, hands or feet.

75
Q

How do monoamine oxidase B inhibitors work

A

Monoamine oxidase enzymes break down neurotransmitters such as dopamine, serotonin and adrenaline. The monoamine oxidase-B enzyme is more specific to dopamine and does not act on serotonin or adrenalin. These medications block this enzyme and therefore help increase the circulating dopamine.

  • Selegiline
  • Rasagiline
76
Q

What is Lambert-Eaton myasthenic syndrome

A
  • progressive muscle weakness with increased use as a result of damage to the neuromuscular junction.
  • symptoms tend to be more insidious and less pronounced than in myasthenia gravis.
  • Typically occurs in patients with small cell lung cancer that creat autoantibodies to voltage-gated calcium channels
77
Q

What is the presentation of Lambert-Eaton Myasthenic syndrome

A
  • proximal muscle weakness
  • double vision: intraocular muscle weakness
  • ptosis
  • Oropharyngeal muscles causing slurred speech and swallowing problems (dysphagia)
  • Progressively worsens with muscle use
78
Q

what is the management of Lambert-Eaton Myasthenic syndrome

A
  • diagnose underlying malignancy
  • Amifampridine
  • Immunosuppressants (e.g. prednisolone or azathioprine)
  • IV immunoglobulins
  • Plasmapheresis
79
Q

What is Amifampridine

A

allows more acetylcholine to be released in the neuromuscular junction synapses. It works by blocking voltage-gated potassium channels in the presynaptic cells, which in turn prolongs the depolarisation of the cell membrane and assists calcium channels in carrying out their action

80
Q

What is benign essential tremor

A
  • relatively common condition associated with older age.

- fine tremor affecting all the voluntary muscles.

81
Q

What areas tend to be affected by benign essential tremor

A
  • hands
  • head
  • jaw
  • vocal
82
Q

What are the features of Benign essential tremor

A 
Fine tremor
Symmetrical
More prominent on voluntary movement
Worse when tired, stressed or after caffeine
Improved by alcohol
Absent during sleep
83
Q

What are the differential diagnose’ of benign essential tremor

A
  • Parkinson’s disease
  • Multiple sclerosis
  • Huntington’s Chorea
  • Hyperthyroidism
  • Fever
  • Medications (e.g. antipsychotics)
84
Q

What is the management of benign essential tremor

A
  • Doesn’t need treatment unless causing functional of psychological distrubance
  • Propranolol (a non-selective beta blocker)
  • Primidone (a barbiturate anti-epileptic medication)
85
Q

Side effects of Levo Dopa

A
  • dyskinesia (involuntary writhing movements),
  • ‘on-off’ effect
  • dry mouth
  • anorexia
  • palpitations
  • postural hypotension
  • psychosis
  • drowsiness
86
Q

Hints that may suggest MND

A

fasciculations
the absence of sensory signs/symptoms*
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common

Neurology (9 decks)

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