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3a Exam > Neurology > Flashcards

Neurology Flashcards

1
Q

Define dementia

A

A progressive neurological disorder impacting cognition → functional impairment.

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2
Q

Define pseudo-dementia?

A

Cognitive impairments 2° to a mental illness e.g. depression/anxiety

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3
Q

What is the clinical presentation of dementia?

A

PROGRESSIVE DECLINE:
1) Cognitive impairment (memory, language, attention)
2) Psychiatric changes (personality, emotional control, social behaviour, agitation, hallucinations and delusions)

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4
Q

What could Alzheimers disease be caused by?

A

Amyloid plaques + neurofibrillary tangles

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5
Q

What is Vascular dementia caused by?

A

Cerebrovascular infarcts: most commonly in the white matter of both cerebral hemispheres.

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6
Q

What is frontotemporal dementia caused by?

A

Focal degeneration of the frontal & temporal lobes due to tau protein deposition

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7
Q

What is Lewy body dementia?

A

Lewy body (alpha-synuclein) deposition in cerebral cortex neurons

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8
Q

What is the pathological difference between Lewy Body Dementia and Parkinson’s?

A

Lew bodies in:
Cerebral Cortex= Lewy body dementia
Substantial nigra= PD

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9
Q

What is the typical onset for the following 4 types of dementia?
1) Alzheimers
2) Vascular
3) Lewy body
4) Frontotemporal

A

Alzheimers: Gradual + progressive onset

Vascular: Abrupt (after stroke) or gradual (stepwise deterioration following multiple strokes)

Lewy body: Insidious onset + progressive with fluctuations

Frontotemporal: Insidious onset (50s/60s) then rapid progression

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10
Q

What is the clinical presentation for the following 4 types of dementia?
1) Alzheimers
2) Vascular
3) Lewy body
4) Frontotemporal

A

Alzheimer’s: memory, depression, language, visuospatial skills and behavioural signs

Vascular: focal neurological signs and vascular disease

Lewy body: visual hallucinations and Parkinsonism (tremors, falls and shuffling gait)

Frontotemporal: disinhibition, poor judgement, decreased motivation and socially inappropriate

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11
Q

What can be seen on a CT/MRI in Alzheimers Dementia?

A

Beta-amyloid plaques
Neurofibrillary tangles
Atrophy
Reduced cortical ACh

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12
Q

What may be seen on a CT/MRI in Frontotemporal Dementia?

A

Frontal/temporal atrophy
Picks cells

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13
Q

What may be seen on a CT/MRI in Vascular Dementia?

A

Blood vessels changes
Vascular infarcts

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14
Q

What may be seen on a CT/MRI in Lewy body Dementia?

A

Lewy bodies in cortex of midbrain
Generalised atrophy

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15
Q

List 5 tools used to assess cognition

A
  • Addenbrookes cognitive examination-III (ACE-III)
  • Montreal cognitive assessment (MoCA)
  • Abbreviated mental test score (AMT)
  • 6 item cognitive impairment test (6CIT)
  • GP assessment of cognition (GPCOG)
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16
Q

What is the main investigative screening tool used for dementia?

A

ACE-III screening tool

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17
Q

What 5 cognitive domains does the ACE-III screening tool assess in dementia?

A
  1. Attention
  2. Memory
  3. Fluency
  4. Language
  5. Visiospatia
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18
Q

What MMSE scores supports dementia?

A

/30
≤24= dementia
21-25 = mild
0-20 = moderate
<10 = severe

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19
Q

What is the management of Alzheimers Dementia?

A

No cure
Acetylcholinesterase inhibitors e.g. Donepezil
NMDA antagonist e.g. Memantine
Treat depression and aggression/agitation

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20
Q

What is the management of Lewy body dementia?

A

No cure
Acetylcholinesterase inhibitors: e.g. donepezil
NMDA antagonist e.g. Memantine
RF reduction: e.g. high BP, high cholesterol, diabetes and smoking.
Levodopa
Physiotherapy

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21
Q

What is the management of vascular dementia?

A

No cure
Management of risk factors: e.g. high BP, high cholesterol, diabetes and smoking.
Acetylcholinesterase inhibitors: e.g. donepezil (only used in mixed dementia)
Improve/maintain cognitive function: structured group cognitive stimulation programmes, exercise, aromatherapy, therapeutic music/dancing and massage.
Aspirin
Advanced care planning
End of life care

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22
Q

What is the management of frontotemporal dementia?

A

No cure
Exercise, physiotherapy, speech and language therapy, and behaviour modification.
Serotonin reuptake inhibitors (SSRI): for behaviour (decreases disinhibition, anxiety, impulsivity and repetitive behaviours)
Atypical anti-psychotics: for agitation and behaviour

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23
Q

Where do you test sensation in the following dermatomes on the arm?
C5-T2

A

C5: Over deltoid

C6: Index finger

C7: Middle finger

C8: Little finger

T1: Inside arm

T2: Apex of axilla

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24
Q

Where do you test sensation in the following dermatomes on the leg?
L2-S2

A

L2: Anterior medial thigh

L3: Over knee

L4: Medial tibia

L5: Dorsum of foot running to big toe

S1: Lateral heel

S2: Popliteal fossa

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25
Q

Where do you test movement in the following myotomes on the arm?

C5-T1

A

C5: Shoulder abduction

C6: Elbow flexion

C7: Elbow extension

C8: Finger flexion

T1: Finger abduction

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26
Q

Where do you test movement in the following myotomes on the leg?

L2-S2

A

L2: Hip flexion

L3: Knee extension

L4: Ankle dorsiflexion

L5: Extension of big toe

S1: Ankle plantar flexion

S2: Knee flexion

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27
Q

What muscles does the radial nerve innervate?

A

Triceps and finger extensors

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28
Q

What muscles does the median nerve innervate?

A

LOAF:
Lateral 2 lumbricals
Oppenens brevis
Abductor pollicis brevis
Flexor pollicis brevis

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29
Q

What muscles does the ulnar nerve innervate?

A

Intrinsic muscles of the hand, lumbricals, hypothenar and interossei

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30
Q

What nerve is responsible for:

Finger flexion?

Finger extension?

Finger abduction?

A

Median

Radial

Ulnar

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31
Q

What is the most common winged scapula nerve lesion?

A

Long thoracic nerve (serratus anterior)

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32
Q

What nerve is responsible for the following movements?

Knee extension

Knee flexion

Ankle dorsiflexion

Big toe extension

Ankle plantar flexion

A

Knee extension: femoral L3

Knee flexion: sciatic/tibial L5, S1/2

Ankle dorsiflexion: peroneal L4

Big toe extension: peroneal L5

Ankle plantar flexion: tibial S1

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33
Q

Name some foot drop differentials?

A

Muscle: myopathy

Nerve: peroneal nerve, sciatic nerve

Root: L4/5

Anterior horn: MND

Brain: parasaggital mengingioma

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34
Q

Which lobe is Brocas area in and what is its function?

A

Frontal lobe of the dominant hemisphere (left)
Speech production

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35
Q

Which lobe is Wernicke’s area in and what is its function?

A

Temporal lobe (left) side of the brain
Speech comprehension

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36
Q

What is a subdural haemorrahage?

A

Vessel rupture below the dura mater

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37
Q

What is the most common cause of subdural haemorrhage?

A

Trauma

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38
Q

What is a extradural haemorrhage?

A

Bleeding above the dura mater

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39
Q

What can cause a extradural haemorrhage?

A

Serious head trauma: around the eye

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40
Q

What is a subarachnoid haemorrhage?

A

Berry cerebral aneurysms at points of bifurcation in the circle of Willis i.e ACA, PCA or MCA

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41
Q

What is the clinical presentation of brain haemorrhages?

A

Reduced GCS
Focal neurological symptoms: upgoing plantars, muscle weakness, hemiparesis and sensory problems
Headache (severe)
N&V
Seizures
Confusion

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42
Q

What spcifically indicates a extradural haemorrhage?

A

Pupil asymmetry (CN III compression)

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43
Q

What spcifically indicates a subdural haemorrhage?

A

Late signs/symptoms

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44
Q

What spcifically indicates a subarachnoid haemorrhage?

A

Sudden-onset Thunderclap headache
Occipital

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45
Q

How do extradural, subdural and epidural haematomas look on a non-contrast CT scan?

A

Extradural: biconvex
Subdural: crescent
Subarachnoid: hyperdense areas in subarach space

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46
Q

How are extradural haemorrhages managed?

A

Decompression: if required
Sit up in bed
Surgery: evacuation of blood + bleeding lesion ligation

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47
Q

What is the management of subdural haemorrhages?

A

Caniostomy
Craniotomy
Mannitol (reduces ICP)

48
Q

What is the management of subarachnoid haemorrhages?

A

Nimodipine: CCB prevents vasospasms
Endovascular coiling

49
Q

What is Multiple Sclerosis?

A

Autoimmune CNS demyelination via chronic inflammation
Peripheral nerves spared
20-40yr onset

50
Q

What may be the first manifestation of MS?

A

Optic Neuritis (reduced visual acuity_

51
Q

Describe 5 features of Optic Neuritis

A

1) Reduced visual acuity over days
2) Pain moving eyes
3) Exacerbated by heat/exercise
4) Afferent pupillary defect
5) Dyschromatopsia (especially red)

52
Q

What is Lhermitte’s phenomenon?

A

Neck flexion → electric shock running down spine

53
Q

What is Uhthoffs phenomenon?

A

Temperature increase worsens symptoms e.g. hot bath

54
Q

What is the clinical presentation of MS?

A

Any neurological sign can be present in MS:
However NEVER involves LMN
Optic neuritis: loss of vision in one eye (CNII demyelination)

Diplopia: CNVI demyelination
Gaze paralysis: CNVI

Lhermitte’s phenomenon

Uhtoff’s phenomenon

Ataxia

Focal sensory symptoms: trigeminal neuralgia

Focal weakness: honers syndrome

55
Q

How is MS diagnosed?

A

MRI: CNS lesions causing symptoms that:
- Last >24 hours
- Are disseminated in space (clinically or on MRI)
- Are disseminated in time (>1 month apart)

56
Q

What is the management of Ms?
Acute?
Chronic?

A

No cure

Relapse/Acute:
Steroids (methylprednisolone may induce remission)

Chronic:

Disease-modifying drugs: maintain remission

  • Beta-interferon: decreases inflammatory cytokine levels
  • Monoclonal antibodies: alemtuzumab (anti-CD52) and natalizumab (anti-α4𝛃1-integrin).

Pain: gabapentin (anti epileptic)

Prevent relapse: Glatiramer

57
Q

What are the 4 types of MS?

A

1) Clinically isolated syndrome (CIS)
2) Relapsing-remitting
3) Primary progressive
4) Secondary progressive

58
Q

What is Clinically Isolated Syndrome MS?

A

First episode of demyelination (clinical presentation)
Not MS yet- does not fulfil space and time criteria!
MS diagnosis IF MRI shows lesions and ANOTHER attack occurs

59
Q

What is Secondary Progressive MS?

A

Relapsing-remitting → progressive worsening of neurological functioning

60
Q

What is Primary Progressive MS?

A

Symptoms worsen from onset
No relapses or remissions

61
Q

What is Relapsing-Remitting MS?

A

Episodes (relapses) followed by recovery (remitting)
During remissions, there may be no symptoms or disease progression

62
Q

What is the Glasgow Coma Scale?

A

Describes the level of consciousness in a person following a traumatic brain injury

63
Q

How is the GCS scored?

A

1) Eye opening (E) 4
2) Verbal response (V) 5
3) Motor response (M) 6

The score may be expressed as e.g. ‘GCS 12 = E2 V4 M6’

64
Q

Describe the GCS scoring

A

Motor response:
6. Obeys commands
5. Localises to pain
4. Withdraws from pain
3. Abnormal flexion to pain (decorticate posture)
2. Extending to pain
1. None

Verbal response:
5. Orientated
4. Confused
3. Words
2. Sounds
1. None

Eye opening:
4. Spontaneous
3. To speech
2. To pain
1. None

65
Q

What would the following GCS scores mean?
<8
3
15

A

<8= coma

3= min score

15= max score

66
Q

What is giant cell arteritis?

A

Temporal arteritis

Vasculitis: immune-mediated inflammatory condition of the medium-large arteries

67
Q

Typical Giant Cell Arteritis features?

A

Rare <50yrs
Severe unilateral headache around temple and forehead
Scalp pain when brushing hair: superficial temporal artery ischaemia
Jaw claudication: mandibular artery ischaemia
Blurred/diplopia
Irreversible painless complete sight loss can occur rapidly: opthalmic (retinal) artery ischaemia
Amaurosis fugax

68
Q

How is GCA diagnosed?

A

CRP + ESR
FBC
Temporal artery US:
- Wall thickening
- Stenosis
- Occlusion

69
Q

How is giant cell arteritis managed?

A

Corticosteroids (prednisolone): prevents irreversible visual loss
Aspirin

70
Q

What is myasthenia gravis?

A

Acquired autoimmune condition

Affects postsynaptic NMJ

Abs against AChR in skeletal muscle

Results in weakness of the muscles

71
Q

What are 7 clinical presentations of Myasthenia Gravis?

A

1) Symptoms better in the morning and worse throughout the day
2) Ptosis
2) Droopy mouth
3) Diplopia
4) Dysphagia
5) Dysarthria (facial muscles)
6) Muscle weakness
7) Dspnoea

72
Q

What autoantibodies are involved in myasthenia gravis?

A

Acetylcholine receptor antibodies (AChR)

Muscle-specific tyrosine kinase (MuSK) antibodies

73
Q

How is Myasthenia Gravis diagnosed?

A

Serum anti- acetylcholine (AchR) receptor
Serum anti- muscle specific Kinase (MuSK) antibodies
Thymomas (tumour)
Tensilon test: drug strengthens muscles so outstretched arms tire less easily

74
Q

How is myasthenia gravis treated?

A

Pyridostigmine (reversible acetylcholinesterase inhibitor)
Corticosteroid (prednisolone)

75
Q

What is Huntington’s disease?

A

Autosomal dominant

Degeneration of CNS neurons

76
Q

How does Huntingtons occur?

A

Autosomal dominant:
1) Chr 4 produces Huntingtin protein
2) Mutation to chr 4 Huntington gene → CAG nucleotide repeats
3) Abnormal Huntingtin protein → neurodegenerative disorder

77
Q

What condition is due to a CAG repeat?

A

Huntingtons

78
Q

Signs of Huntingtons?

A

Asymptomatic until age 30-50
Progressive worsening of symptoms
Prodromal phase: cognitive, psychiatric or mood problems
Chorea
Eye movement disorders
Dysarthria
Dysphagia
Dementia

79
Q

What is Progressive Supranuclear Palsy?

A

A Parkinson’s-plus syndrome

80
Q

What is the clinical presentation of Progressive Supranuclear Palsy (PSP)?

A

Brain cell damage due to tau protein accumulation

81
Q

What is the clinical presentation of Progressive Supranuclear Palsy?

A
  • Falls and balance impairments
  • Lack of interest, behaviour change, thought and memory impairment
  • Hypertonia
  • Dysarthria / Dysphagia
  • Difficult eye and eyelid movements- focusing/ looking up/down
82
Q

What is the most common cause of head tremor? (titubation)

A

Essential tremor

83
Q

What may relieve an essential tremor?
What medication can be given?

A

Alcohol
Rest
Propanolol

84
Q

What is motor neurone disease?

A

Upper and lower motor neurone degeneration in the CNS

85
Q

What is the most common motor neuron disease?

A

Amyotropic lateral sclerosis (ALS)

86
Q

What are the clinical features of motor neurone disease?

A

Starts up, then goes down
MND does NOT affect eye movement (differentiate from myesthenia gravis)

Signs ofLMN disease: everything goes down

Reduced tone

Reduced reflexes

Fasciculations

Muscle wasting

Signs ofUMN disease: everything goes up

Increased tone/spasticity

Brisk reflexes

Upgoing plantar responses

NO SENSORY SIGNS

Sphincters unaffected

87
Q

How is a Hoffmans sign elicited?

A

Flick the middle finger nail:
Flexion of ipsilateral thumb or index = positive sign = UMN pathology

88
Q

Give 4 signs of UMN weakness

A
  1. Increased muscle tone
  2. Hyperreflexia
  3. Spasticity
  4. Minimal muscle atrophy
89
Q

Give 5 signs of LMN weakness

A
  1. Decreased muscle tone
  2. Hyporeflexia
  3. Flaccid
  4. Muscle atrophy
  5. Fasciculations
90
Q

What is the management of ALS?

A

Riluzole
Baclofen

91
Q

Which type of MND has the worst prognosis?

A

Progressive bulbar palsy: difficulty swallowing / speech / respiratory insufficiency

92
Q

What are red flags for headaches?

A

1) Thunderclap: ‘worst headache I’ve ever had’.
2) Worse in the morning
2) Sudden + severe
2) Age >50
3) Neck pain/stiffness, photophobia
4) Fever
5) Papilloedema
6) New onset neuro deficit
7) Vomiting
8) Dizziness and visual disturbances/atypical aura (over an hour)

93
Q

What is Giant Cell Arteritis?

A

Temporal arteritis

Vasculitis: immune-mediated inflammatory condition of the medium-large arteries

94
Q

Who does GCA tend to affect?

A

Females >males
Scandinavians
>50 yrs

95
Q

What is the clinical presentation of Giant Cell Arteritis?

A

Myalgia
Fever
Unilateral Headache
Scalp pain when brushing hair: superficial temporal artery ischaemia
Jaw claudication: mandibular artery ischaemia
Diplopia
Irreversible painless complete sight loss can occur rapidly: opthalmic(retinal) artery ischaemia
Amaurosis fugax

96
Q

What Anaemia is seen in Giant Cell Arteritis?

A

Normocytic Normochromic

97
Q

How is Giant Cell Arteritis investigated?

A

Increased ESR
Increased LFTs (ALP)
Increased IgGs and complements
(CK not elevated as no muscle damage)
Temporal artery US:
- Wall thickening
- Stenosis
- Occlusion
Temporal artery biopsy: confirms

98
Q

What is the management of Giant Cell Arteritis?

A

Corticosteroids (prednisolone): prevents irreversible visual loss
Aspirin

99
Q

What is the main complication of Giant Cell Arteritis?

A

BLINDNESS

100
Q

What is the difference between a facial palsy caused by an upper or lower motor neurone lesion?

A

Upper motor neurone lesion spares the upper head e.g ‘wrinkle forehead/raise eyebrows’

101
Q

What is Bells Palsy?
What is the classic triad?

A

Lower motor neurone palsy of the facial nerve (7th)

Causes:
1) Facial droop on one side of the face
2) Flat wrinkles on one side of forehead
3) Can’t close one eyelid

102
Q

At what age are you more likely to get Myasthenia Gravis?

A

Women: <40

Men: >60

103
Q

What muscles are weakened in Myasthenia Gravis?

A

Weakness of extra-ocular muscles causing:

1) Diplopia
2) Ptosis (droopy eyelid)

104
Q

What is a Myasthenic Crisis?

A

Weakness of breathing muscle = life threatening

105
Q

What type of hypersensitivity reaction is Myasthenia Gravis and Multiple Sclerosis?

A

MG: type II (antibody mediated- AChR/MuSK)

MS: type IV (cell-mediated- T cells)

106
Q

What is Charcots Neurological Triad?

A

1) Dysarthria (dysfunctional eating, talking and swallowing)
2) Intention tremor (muscle weakness, spasms, ataxia and paralysis)
3) Nystagmus (optic neuritis, greying of vision, pain and diplopia)

Linked to MS

107
Q

What visual defects are caused within the Optic Chiasm?

A

Bitemporal hemianopia

108
Q

What is Cauda Equina?

A

Sudden spinal stenosis at L2/L3

109
Q

Give 5 signs of Cauda Equina

A
  1. Bilateral sciatic: pain radiates down leg to foot
  2. Saddle anaesthesia
  3. Bladder/bowel dysfunction
  4. Erectile dysfunction
  5. Leg weakness
110
Q

What is polypharmacy?

A

A large number of unnecessary medications (4+)

111
Q

How often should a patient be repositioned to prevent pressure sores?

A

Normal risk: every 6 hrs

High risk: every 4hrs

112
Q

Give 3 treatment options for malnutrition

A
  1. Encouraging food and drink intake
  2. ONS: yoghurts, milkshakes, juices etc
  3. Enteral feeding
  4. Parenteral feeding
113
Q

Define refeeding syndrome

A

Electrolyte imbalance from reintroducing food after starvation (>10 days)

114
Q

What is the clinical presentation of Re-feeding syndrome?

A

Drop in phosphate due to rapid initiation of food →:
▪ Rhabdomyolysis
▪ Respiratory/cardiac failure
▪ Hypotension
▪ Arrhythmias
▪ Seizures

115
Q

What is the management of re-feeding syndrome?

A

Slow refeeding
Thiamine
Monitor :
- Hypophosphatemia
- Hypokalaemia
- Hyperglycaemia
- Hypermagnesemia

116
Q

Define frailty

A

A state of increased vulnerability resulting from an ageing associated decline in reserve and function across multiple physiologic systems.

The ability to cope with everyday stressors is compromised.

3a Exam (9 decks)

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