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Medicine Phase 2a Neuro > Peer-Teaching 2 > Flashcards

Peer-Teaching 2 Flashcards

1
Q

Examples of primary headaches

A

Migraine
Cluster Headache
Tension-type headache
Trigeminal neuralgia

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2
Q

Examples of secondary headaches

A

Subarachnoid haemorrhage
Giant cell arteritis
Meningitis
Medication overuse

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3
Q

Patient presents with serious headache, what can neuroimaging (MRI or CT) be used to rule out?

A

Mass lesions

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4
Q

Describe presentation of a migraine

A

Unilateral (can be bilateral)
Throbbing / Pulsetile
Can be associated with Aura
Lasts 4-72 hours
Moderate to Severe pain
Can have many triggers

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5
Q

Common migraine triggers

A 
CHOCOLATE:
Chocolate
Hangovers
Orgasms
Cheese
Oral contraceptive Pill
Lie-ins
Alcohol
Tumult (loud noises)
Exercise
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6
Q

Cause of migraine

A

Changes in brainstem blood flow -> unstable trigeminal nerve nucleus and nuclei in the basal thalamus -> release of vasoactive neuropeptides (CGRP and substance P) -> neurogenic inflammation; vasodilatation and plasma protein extravasation

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7
Q

Types of migraines

A

Migraine without aura
Migraine with aura
Migraine variant

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8
Q

How is migraine variant characterised

A

by unilateral motor or sensory symptoms resembling a stroke

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9
Q

*Diagnostic criteria of migraine without aura

A 
A: At least 5 attacks fulfilling B,C&D
B: Lasting between 4-72 hours
C: ≥2 of the following:
Unilateral
Pulsating
Moderate/Severe pain
Aggravation by (or avoidance of) routine physical activity
D: ≥1 of the following:
Nausea and/or vomiting
Photophobia and phonophobia
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10
Q

*Diagnostic criteria of migraine with aura

A

A: At least 2 attacks fulfilling B&C
B: ≥1 reversible aura symptom
-Visual – zigzags, spots
-Unilateral sensory – tingling, numbness
-Speech – aphasia
-Motor weakness (known as “hemiplegic migraine” so rule out stroke & TIA)
C: ≥2 of the following 4:
- ≥1 aura symptom spreads gradually over ≥5 minutes and/or ≥2 aura symptoms occurring in succession
-Each aura symptom lasts 5-60 minutes
- ≥1 aura symptom is unilateral
-Aura accompanied/followed within 60 minutes by headache

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11
Q

Conservative Treatment of migraine

A

Avoid triggers

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12
Q

Treatment of migraine: acute attacks

A

Mild - NSAID +/- anti-emetic

Severe - Oral triptan (e.g. Sumatriptan)

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13
Q

Treatment of migraine: prophylaxis

A

1st line - Propranolol (Beta-blocker) or Topiramate (Anti-convulsant)
2nd line - Acupuncture
3rd line - Amitriptyline (Tricyclic antidepressant)

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14
Q

1st line prophylaxis for migraine

A

Propranolol (Beta-blocker)
OR
Topiramate (Anti-convulsant)

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15
Q

Presentation of tension headaches

A

Typically bilateral (band around the head)
Tight/Pressing
Lasts anywhere from minutes to days
Mild to moderate pain
Can be associated with photophobia or phonophobia

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16
Q

Cause of tension headache

A 
MC SCOLD
Missed meals
Conflict
Stress
Clenched jaw
Overexertion
Lack of sleep
Depression
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17
Q

Diagnostic criteria of tension headache

A

A: Lasts from 30 minutes to 7 days
B: At least 2 of the following 4 characteristics:
Bilateral location
Pressing or tightening (non-pulsating) quality
Mild or moderate intensity
Not aggravated by routine physical activity such as walking or climbing stairs
C: Both of the following
No nausea or vomiting
No more than one of photophobia or phonophobia

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18
Q

Classifications of tension headaches

A

Infrequent episodic
Frequent episodic
Chronic
Probable

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19
Q 
Describe what is meant by each of these classifications of tension headaches:
Infrequent episodic
Frequent episodic
Chronic
Probable
A

Infrequent episodic - <1day/month on average (<12 days/year)
Frequent episodic - 1-14 days/month on average for >3 months (≥12 and <180 days/year)
Chronic - ≥15 days/month on average for >3 months (≥180 days/year)
Probable - Tension type headache missing one of the features required to fulfill all criteria and does not fulfill criteria for another headache disorder

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20
Q

Treatments of tension headaches (in order)

A

Reassurance
Stress relief
Avoidance of causes
Medication:
Analgesic - NSAIDs (ibuprofen, diclofenac) or aspirin
Tricyclic antidepressants (Amitriptyline)

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21
Q

Presentation of cluster headache

A

Unilateral orbital, supraorbital or temporal pain
Boring/hot poker characteristic
Lasts between 15-180 minutes
Severe pain
Associated with:
-Ipsilateral eye lacrimation & redness
-Rhinorrhoea (runny nose)
-Miosis and/or ptosis (pupil constriction and drooping of eye-lid)

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22
Q

When do cluster headaches usually occur

A

Middle of the night
OR
Morning hours

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23
Q

Types of cluster headache

A

Episodic - ≥2 cluster periods lasting 7 days to 1 year separated by pain free periods lasting ≥1 month.
Chronic - attack occur for ≥1 year without remission or with remission lasting <1 month.

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24
Q

Treatment of cluster headaches (acute attacks and prophylaxis)

A

Acute attacks - SC Sumatriptan, IM/N Zolmitriptan, 100% Oxygen therapy
Prophylaxis - Verapamil (CCB), Lithium, Corticosteroids

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25
Q

Clinical presentation of trigeminal neuralgia

A

Unilateral pain confined to one or more divisions of the trigeminal nerve.
Electrifying / Lightning / Stabbing pain
Lasts a few seconds
Very severe pain

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26
Q

Triggers of trigeminal neuralgia

A 
Washing affected area
Shaving
Eating
Dental Prostheses
Talking
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27
Q

Aetiology of trigeminal neuralgia

A

Compression of the trigeminal nerve by intracranial vessels or a tumour, MS, skull base malformation, zoster

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28
Q

Diagnostic criteria of trigeminal neuralgia

A

A: ≥3 attacks of unilateral facial pain
B: Pain in ≥1 division of the trigeminal nerve with no radiation
C: ≥3 of the following
Paroxysmal attacks lasting from 1-180 seconds
Severe intensity
Electric shock-like / shooting / stabbing / sharp
Precipitated by innocuous stimuli to the affected side of the face
D: No neurological deficit

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29
Q

1st line treatment of trigeminal neuralgia

A

Carbamazepine (Anti-convulsant)

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30
Q

Medical treatment of trigeminal neuralgia

A

1st line - Carbamazepine (Anti-convulsant)

2nd line - Phenytoin, gabapentin (Analgesics targeted for neuropathic pain)

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31
Q

Surgical treatment of trigeminal neuralgia

A

Microvascular decompression - Relieves pressure on the nerve by blood vessels touching the nerve or wrapped around it

Stereotactic Radiotherapy - Concentrated beam of radiotherapy to deliberately damage the trigeminal nerve where it enters the brainstem

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32
Q

Presentation of giant cell arteritis

A

Usually occurs in people over 50.

Consider Takayashu arteritis if the patient is less than 50

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33
Q

Symptoms of giant cell arteritis

A 
Headache
Jaw claudication
Amaurosis fugax
Temporal artery scalp tenderness
Malaise 
Fever
Weight loss
Depression
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34
Q

Signs of giant cell arteritis

A

Palpable, tender and reduced pulsation of the temporal arteries

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35
Q

Gold standard for investigation of giant cell arteritis

A

temporal artery biopsy

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36
Q

Investigations of giant cell arteritis

A

Gold standard - temporal artery biopsy

Bloods - raised inflammatory markers (ESR and CRP)

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37
Q

Treatments of giant cell arteritis

A 
40mg Prednisolone (High dose steroid)
75mg low dose aspirin
PPI (e.g. omeprazole) as both drugs are associated with gastrointestinal toxicity
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38
Q

Acute glaucoma headache describe

A

Severe eye pain, red eyes, cloudy cornea, dilated or unresponsive pupil

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39
Q

What headaches are worse when bending over?

A

Sinusitis

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40
Q

*What medication overused can result in headache

A 
Aspirin
Paracetamol
NSAIDs
Triptans
Opioids
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41
Q

What are oligodendrocytes and Schwann cells

A

Oligodendrocytes - A glial cell that provides myelination of neurons in the CNS
Schwann cells - A glial cell that provides myelination of neurons in the PNS

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42
Q

Most common cause of Parkinsonism

A

Idiopathic Parkinsons disease

43
Q

Other causes of Parkinsonism except Parkinsons disease

A

Vascular parkinsonism
Infections (Encephalitis, CJD)
Toxin induced (Carbon monoxide, drugs)

44
Q

Aetiology of Parkinsons

A

NO KNOWN CAUSE!
Thought to be due to abnormal accumulation of alpha-synuclein bound to ubiquitin which forms lewy bodies in the cytoplasm.
Also thought to be some sort of environmental link

45
Q

Pathophysiology of Parkinsons

A

Neurodegenerative loss of dopamine secreting cells from the substantia nigra. Lack of dopamine causes alteration in neural circuits within basal ganglia that regulates movement

46
Q

*Parkinsons Features and explain what each is

A

Bradykinesia - Problems with daily activities e.g. doing up buttons, micrographia, expressionless face, dysdiadochokinesia
Tremor - Resting, commonly unilateral, Starts in the hands “pill rolling”
Rigidity - Cogwheel like, stooped posture

Gait - Shuffling, reduced arm swing, slow to start
Postural instability - impaired balance, especially when trying to turn

47
Q

Complications of Parkinsons

A

Depression
Dementia
Other psychiatric problems (e.g. hallucinations)
Autonomic problems (Constipation, urinary frequency)

48
Q

Investigations of Parkinsons

A

CT head or MRI head will show atrophy of the substantia nigra

49
Q

*Treatment of Parkinsons

A
  1. Carbidopa/Levodopa tablets to increase amount ofdopamine
  2. Dopamine Receptor Agonists to mimic dopamine e.g. Ropinirole, Pramipexole, Rotigotine
  3. Inhibit enzymatic breakdown of Dopamine
    (all these help manage bradykinesia and rigidity, but not affect the tremor)
  4. Tremor management
50
Q

Why is levodopa given instead of dopamine

A

Dopamine can’t cross the blood-brain barrier but levodopa can and can be converted to dopamine in the CNS

51
Q

How is Levodopa converted to dopamine in body (CNS)

A

Dopa Decarboxylase

52
Q

Why is levodopa given alongside carbidopa

A

Dopa decarboxylase also exists outside the CNS
Carbidopa is a Dopa decarboxylase inhibitor.
Carbidopa can’t cross into the CNS so it doesn’t affect dopamine production in the CNS

53
Q

What enzymes break down dopamine

A

COMT (Catecholamine-O-Methyltransferase)

MAO-B (Monoamine Oxidase-B)

54
Q

What drugs can be given to inhibit the breakdown of dopamine

A

Entacapone and Tolcapone inhibit the action of COMT (Catecholamine-O-Methyltransferase)
Selegiline inhibits the action of MAO-B (Monoamine Oxidase-B)

55
Q

Describe tremor management in Parkinsons

A

Amantadine

Anticholinergic

56
Q

Aetiology of Huntingtons Disease

A

Autosomal dominant inherited condition.
Caused by CAG trinucleotide repeat in huntingtin gene. CAG triplet codes for Glutamine.
Need ≥36 triplet repeats (hence glutamines) to be diagnostic of Huntington’s

57
Q

Pathophysiology of Huntingtons disease

A

Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels and subsequently increased movement

58
Q

Symptoms of Huntingtons

A

1st phase - Depression, incoordination, personality changes

2nd phase - Chorea (Purposeless, dance-like movements), dementia & rigidity

59
Q

Ix of Huntingtons

A

Genetic testing

MRI - Atrophy of the Striatum (Caudate and Putamen)

60
Q

Management of Huntingtons

A

NO CURE!

  1. Chorea - Antipsychotics (Risperidone) as they are Dopamine Receptor Antagonists. Alternatively, tetrabenazine can be used which depletes dopamine.
  2. Depression - SSRI (Sertraline)
  3. Aggressive Behaviour - Antipsychotics (Risperidone)
61
Q

What is Multiple sclerosis

A

Chronic autoimmune T-cell mediated demyelination of the CNS

62
Q

Epidemiology of Multiple Sclerosis

A

Women:Men = 2:1
More common the further from the equator you go (Possible Vit D link)
Usually diagnosed between 20-40 = Disease of the YOUNG

63
Q

Diagnostic criteria of Multiple Sclerosis

A

2 or more attacks of MS with demyelination plaques disseminated in space and time (Old Macdonald Classification)

64
Q

Types of MS progression

A

Relapsing-remitting MS
Primary progressive MS
Secondary progressive MS
Progressive-relapsing MS

65
Q

Describe Relapsing-remitting MS

A

Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission

66
Q

Describe Primary progressive MS

A

Steady increase in disability without attacks

67
Q

Describe Secondary progressive MS

A

Initial relapsing-remitting multiple sclerosis that begins to have decline without periods of remission

68
Q

Describe Progressive-relapsing MS

A

Steady decline since onset with super-imposed attacks

69
Q

Signs and symptoms of MS

A 
DEMYELINATION:
Diplopia
Eye movements painful (Optic Neuritis)
Motor weakness
nYstagmus
Elevated temperature worsens symptoms (Uhthoff’s phenomenon)
Lhermitte’s sign (movement of neck causes shocks in neck)
Intention tremor
Neuropathic pain
Ataxia
Talking Slurred
 Impotence
Overactive bladder
Numbness
70
Q

Investigations of Multiple sclerosis

A

MRI with contrast
Lumbar puncture with CSF electrophoresis
Evoked potentials

71
Q

Define evoked potentials

A

Electrical activity generated in response to sensory or motor stimulus

72
Q

What is seen for each of these investigations of MS:
MRI with contrast
Lumbar puncture with CSF electrophoresis
Evoked potentials

A

MRI with contrast - demyelination plaques
Lumbar puncture with CSF electrophoresis - oligoclonal IgG bands
Evoked potentials - Delayed visual, brainstem, auditory, somatosensory potentials

73
Q

Symptomatic management of MS

A

Tremor - Beta blocker
Spacicity - Baclofen
Neuropathic pain - Gabapentin

74
Q

Management of MS

A

Acute attacks (RRMS) - IV Methylprednisolone (steroid)
Chronic:
1st line = Beta interferon and glatiramer acetate
2nd line = Alemtuzumab or Natalizumab
Symptom management

75
Q

Epidemiology of Motor Neurone Disease

A

More common in men
Most commonly affects people in middle age
Most die within 3 years of diagnosis

76
Q

Aetiology of Motor Neurone Disease

A

Unknown cause but believed to be associated with SOD-1 gene mutation

77
Q

What results from degeneration or destruction of motor neurones in:
Motor cortex
Anterior horn cells
Cranial nerve nuclei

A

Motor cortex = UMN signs
Anterior horn cells = LMN signs
Cranial nerve nuclei = Mixed UMN & LMN signs

78
Q

How are upper limbs affected by MND

A

Reduced dexterity
Stiffness
Wasting of intrinsic muscles of hand

79
Q

How are lower limbs affected by MND

A

Tripping
Strumbling gait
Foot drop

80
Q

MND of Bulbar (Cranial nerve 9-12) symptoms

A

Slurred speach
Hoarseness of voice
Dysphagia

81
Q

Overall symptoms of MND

A

Muscle atrophy

Spasiticity

82
Q

Types of MND

A

Amyotrophic Lateral Sclerosis (ALS)
Primary Lateral Sclerosis (PLS)
Progressive muscular atrophy (PMA)
Progressive Bulbar Palsy (PBP)

83
Q

What is most common type of motor neurone disease

A

Amyotrophic Lateral Sclerosis (ALS)

84
Q

Signs of Amyotrophic Lateral Sclerosis (ALS)

A

UMN+LMN signs

85
Q

Describe Amyotrophic Lateral Sclerosis (ALS)

A

Progressive focal wasting, weakness and fasciculation spreading to other limbs, Cramps, Spasticity and brisk reflexes

86
Q

Signs of Primary Lateral Sclerosis (PLS)

A

UMN signs only

87
Q

Describe Primary Lateral Sclerosis (PLS)

A

Slow progressive tetraparesis and pseudobulbar palsy

88
Q

Signs of Progressive muscular atrophy (PMA) MS

A

LMN signs only

89
Q

Describe Progressive muscular atrophy (PMA)

A

Weakness and fasiculations starting in one limb and progressing to adjacent spinal segments

90
Q

Signs of Progressive Bulbar Palsy (PBP)

A

UMN + LMN + Cranial Nerve IX,X,XI,XII signs

91
Q

Describe Progressive Bulbar Palsy (PBP)

A

Lower cranial nerve nuclei affected causing dysarthria, dysphagia, nasal regurgitation of fluids, choking

92
Q 
UMN lesion:
Weakness
Atrophy
Reflexes
Plantars
Tone
Fasciculation
A 
Weakness - Yes
Atrophy - NO
Reflexes - UP
Plantars - UPgoing
Tone - UP
Fasciculation - NO
93
Q 
LMN lesion:
Weakness
Atrophy
Reflexes
Plantars
Tone
Fasciculation
A 
Weakness - Yes
Atrophy - YES
Reflexes - DOWN
Plantars - DOWNgoing
Tone - DOWN
Fasciculation - YES
94
Q

Investigations of MND

A 
Largely a clinical diagnosis
Electromyography - Denervation of muscles
Bloods - Raised Creatinine Kinase
Nerve Conduction studies
Lumbar puncture
MRI
95
Q

Why is there raised Creatinine kinase in MND

A

Muscle destruction

96
Q

Ix of MND - What is purpose of:
Nerve Conduction studies
Lumbar puncture
MRI

A

Nerve conduction studies - To rule out motor neuropathies
Lumbar puncture - To exclude inflammatory causes
MRI - To rule out lesions

97
Q

Differential diagnosis if no sensory loss

A

Multiple sclerosis

Myelopathy

98
Q

Differential diagnosis if no disturbances in eye movements

A

Myasthentia gravis

Multiple Sclerosis

99
Q

Differential diagnosis if no sphincter disturbances

A

Multiple sclerosis

100
Q

Management of Motor Neurone Disease

A

Riluzole - Anti-glutaminergic sodium channel blocker
Refer to MDT
Symptomatic Management

101
Q

Symptomatic management of MND

A

Dysphagia - NG/PEG tube
Spasticity - Baclofen
Joint pain - Analgesic ladder

102
Q

General features of brain tumours

A

Progressive focal neurological deficit (symptoms vary depending on location of the tumour)
Raised intracranial pressure
Epilepsy (generalised or focal seizures)
General cancer symptoms (weight loss, malaise, night sweats etc)

103
Q

Symptoms resulting from raised intracranial pressure

A

Headaches worse on couching/leaning forward
Vomiting
Papilledema

Medicine Phase 2a Neuro (28 decks)

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