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3a Exam > Neurology > Flashcards

Neurology Flashcards

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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
Where do you test movement in the following myotomes on the arm? C5-T1
C5: Shoulder abduction C6: Elbow flexion C7: Elbow extension C8: Finger flexion T1: Finger abduction
26
Where do you test movement in the following myotomes on the leg? L2-S2
L2: Hip flexion L3: Knee extension L4: Ankle dorsiflexion L5: Extension of big toe S1: Ankle plantar flexion S2: Knee flexion
27
What muscles does the radial nerve innervate?
Triceps and finger extensors
28
What muscles does the median nerve innervate?
LOAF: Lateral 2 lumbricals Oppenens brevis Abductor pollicis brevis Flexor pollicis brevis
29
What muscles does the ulnar nerve innervate?
Intrinsic muscles of the hand, lumbricals, hypothenar and interossei
30
What nerve is responsible for: Finger flexion? Finger extension? Finger abduction?
Median Radial Ulnar
31
What is the most common winged scapula nerve lesion?
Long thoracic nerve (serratus anterior)
32
What nerve is responsible for the following movements? Knee extension Knee flexion Ankle dorsiflexion Big toe extension Ankle plantar flexion
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
33
Name some foot drop differentials?
Muscle: myopathy Nerve: peroneal nerve, sciatic nerve Root: L4/5 Anterior horn: MND Brain: parasaggital mengingioma
34
Which lobe is Brocas area in and what is its function?
Frontal lobe of the dominant hemisphere (left) Speech production
35
Which lobe is Wernicke's area in and what is its function?
Temporal lobe (left) side of the brain Speech comprehension
36
What is a subdural haemorrahage?
Vessel rupture below the dura mater
37
What is the most common cause of subdural haemorrhage?
Trauma
38
What is a extradural haemorrhage?
Bleeding above the dura mater
39
What can cause a extradural haemorrhage?
Serious head trauma: around the eye
40
What is a subarachnoid haemorrhage?
Berry cerebral aneurysms at points of bifurcation in the circle of Willis i.e ACA, PCA or MCA
41
What is the clinical presentation of brain haemorrhages?
Reduced GCS Focal neurological symptoms: upgoing plantars, muscle weakness, hemiparesis and sensory problems Headache (severe) N&V Seizures Confusion
42
What spcifically indicates a extradural haemorrhage?
Pupil asymmetry (CN III compression)
43
What spcifically indicates a subdural haemorrhage?
Late signs/symptoms
44
What spcifically indicates a subarachnoid haemorrhage?
Sudden-onset Thunderclap headache Occipital
45
How do extradural, subdural and epidural haematomas look on a non-contrast CT scan?
Extradural: biconvex Subdural: crescent Subarachnoid: hyperdense areas in subarach space
46
How are extradural haemorrhages managed?
Decompression: if required Sit up in bed Surgery: evacuation of blood + bleeding lesion ligation
47
What is the management of subdural haemorrhages?
Caniostomy Craniotomy Mannitol (reduces ICP)
48
What is the management of subarachnoid haemorrhages?
**Nimodipine**: CCB prevents vasospasms **Endovascular coiling**
49
What is Multiple Sclerosis?
Autoimmune CNS demyelination via chronic inflammation Peripheral nerves spared 20-40yr onset
50
What may be the first manifestation of MS?
Optic Neuritis (reduced visual acuity_
51
Describe 5 features of Optic Neuritis
1) Reduced visual acuity over days 2) Pain moving eyes 3) Exacerbated by heat/exercise 4) Afferent pupillary defect 5) Dyschromatopsia (especially red)
52
What is Lhermitte's phenomenon?
Neck flexion → electric shock running down spine
53
What is Uhthoffs phenomenon?
Temperature increase worsens symptoms e.g. hot bath
54
What is the clinical presentation of MS?
**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
How is MS diagnosed?
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
What is the management of Ms? Acute? Chronic?
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
What are the 4 types of MS?
1) Clinically isolated syndrome (CIS) 2) Relapsing-remitting 3) Primary progressive 4) Secondary progressive
58
What is Clinically Isolated Syndrome MS?
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
What is Secondary Progressive MS?
Relapsing-remitting → progressive worsening of neurological functioning
60
What is Primary Progressive MS?
Symptoms worsen from onset No relapses or remissions
61
What is Relapsing-Remitting MS?
Episodes (relapses) followed by recovery (remitting) During remissions, there may be no symptoms or disease progression
62
What is the Glasgow Coma Scale?
Describes the level of consciousness in a person following a traumatic brain injury
63
How is the GCS scored?
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
Describe the GCS scoring
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
What would the following GCS scores mean? <8 3 15
<8= coma 3= min score 15= max score
66
What is giant cell arteritis?
Temporal arteritis Vasculitis: immune-mediated inflammatory condition of the medium-large arteries
67
Typical Giant Cell Arteritis features?
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
How is GCA diagnosed?
CRP + ESR FBC Temporal artery US: - Wall thickening - Stenosis - Occlusion
69
How is giant cell arteritis managed?
Corticosteroids (prednisolone): prevents irreversible visual loss Aspirin
70
What is myasthenia gravis?
Acquired autoimmune condition Affects postsynaptic NMJ Abs against AChR in skeletal muscle Results in weakness of the muscles
71
What are 7 clinical presentations of Myasthenia Gravis?
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
What autoantibodies are involved in myasthenia gravis?
Acetylcholine receptor antibodies (AChR) Muscle-specific tyrosine kinase (MuSK) antibodies
73
How is Myasthenia Gravis diagnosed?
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
How is myasthenia gravis treated?
Pyridostigmine (reversible acetylcholinesterase inhibitor) Corticosteroid (prednisolone)
75
What is Huntington's disease?
Autosomal dominant Degeneration of CNS neurons
76
How does Huntingtons occur?
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
What condition is due to a CAG repeat?
Huntingtons
78
Signs of Huntingtons?
**Asymptomatic until age 30-50** **Progressive worsening of symptoms** Prodromal phase: cognitive, psychiatric or mood problems Chorea  Eye movement disorders Dysarthria Dysphagia Dementia
79
What is Progressive Supranuclear Palsy?
A Parkinson’s-plus syndrome
80
What is the clinical presentation of Progressive Supranuclear Palsy (PSP)?
Brain cell damage due to tau protein accumulation
81
What is the clinical presentation of Progressive Supranuclear Palsy?
- 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
What is the most common cause of head tremor? (titubation)
Essential tremor
83
What may relieve an essential tremor? What medication can be given?
Alcohol Rest Propanolol
84
What is motor neurone disease?
Upper and lower motor neurone degeneration in the CNS
85
What is the most common motor neuron disease?
Amyotropic lateral sclerosis (ALS)
86
What are the clinical features of motor neurone disease?
Starts up, then goes down MND does NOT affect eye movement (differentiate from myesthenia gravis) Signs of LMN disease: everything goes down Reduced tone Reduced reflexes Fasciculations Muscle wasting Signs of UMN disease: everything goes up Increased tone/spasticity Brisk reflexes Upgoing plantar responses NO SENSORY SIGNS Sphincters unaffected
87
How is a Hoffmans sign elicited?
Flick the middle finger nail: Flexion of ipsilateral thumb or index = positive sign = UMN pathology
88
Give 4 signs of UMN weakness
1. Increased muscle tone 2. Hyperreflexia 3. Spasticity 4. Minimal muscle atrophy
89
Give 5 signs of LMN weakness
1. Decreased muscle tone 2. Hyporeflexia 3. Flaccid 4. Muscle atrophy 5. Fasciculations
90
What is the management of ALS?
Riluzole Baclofen
91
Which type of MND has the worst prognosis?
Progressive bulbar palsy: difficulty swallowing / speech / respiratory insufficiency
92
What are red flags for headaches?
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
What is Giant Cell Arteritis?
Temporal arteritis Vasculitis: immune-mediated inflammatory condition of the medium-large arteries
94
Who does GCA tend to affect?
Females >males Scandinavians >50 yrs
95
What is the clinical presentation of Giant Cell Arteritis?
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
What Anaemia is seen in Giant Cell Arteritis?
Normocytic Normochromic
97
How is Giant Cell Arteritis investigated?
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
What is the management of Giant Cell Arteritis?
Corticosteroids (prednisolone): prevents irreversible visual loss Aspirin
99
What is the main complication of Giant Cell Arteritis?
BLINDNESS
100
What is the difference between a facial palsy caused by an upper or lower motor neurone lesion?
Upper motor neurone lesion spares the upper head e.g 'wrinkle forehead/raise eyebrows'
101
What is Bells Palsy? What is the classic triad?
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
At what age are you more likely to get Myasthenia Gravis?
Women: <40 Men: >60
103
What muscles are weakened in Myasthenia Gravis?
Weakness of extra-ocular muscles causing: 1) Diplopia 2) Ptosis (droopy eyelid)
104
What is a Myasthenic Crisis?
Weakness of breathing muscle = life threatening
105
What type of hypersensitivity reaction is Myasthenia Gravis and Multiple Sclerosis?
MG: type II (antibody mediated- AChR/MuSK) MS: type IV (cell-mediated- T cells)
106
What is Charcots Neurological Triad?
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
What visual defects are caused within the Optic Chiasm?
Bitemporal hemianopia
108
What is Cauda Equina?
Sudden spinal stenosis at L2/L3
109
Give 5 signs of Cauda Equina
1. Bilateral sciatic: pain radiates down leg to foot 2. Saddle anaesthesia 3. Bladder/bowel dysfunction 4. Erectile dysfunction 5. Leg weakness
110
What is polypharmacy?
A large number of unnecessary medications (4+)
111
How often should a patient be repositioned to prevent pressure sores?
Normal risk: every 6 hrs High risk: every 4hrs
112
Give 3 treatment options for malnutrition
1. Encouraging food and drink intake 2. ONS: yoghurts, milkshakes, juices etc 3. Enteral feeding 4. Parenteral feeding
113
Define refeeding syndrome
Electrolyte imbalance from reintroducing food after starvation (>10 days)
114
What is the clinical presentation of Re-feeding syndrome?
Drop in phosphate due to rapid initiation of food →: ▪ Rhabdomyolysis ▪ Respiratory/cardiac failure ▪ Hypotension ▪ Arrhythmias ▪ Seizures
115
What is the management of re-feeding syndrome?
Slow refeeding Thiamine Monitor : - Hypophosphatemia - Hypokalaemia - Hyperglycaemia - Hypermagnesemia
116
Define frailty
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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