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Phase 2a > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the three types of brain haemorrhage we need to know?

A

Subarachnoid
Subdural
Extradural

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2
Q

What is a subarachnoid haemorrhage?

A

Spontaneous arterial bleed into the subarachnoid space

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3
Q

What is the leading cause of subarachnoid haemorrhage?

A

Saccular (‘berry’) aneurysms

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4
Q

Give some risk factors for subarachnoid haemorrhage

A

Hypertension
Smoking
PKD

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5
Q

What is a subdural haemorrhage?

A

Traumatic venous bleed into the subdural space

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6
Q

What is the leading cause of subdural haemorrhage?

A

Head trauma

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7
Q

Give some types of people who are more susceptible to subdural haemorrhage and explain why

A

Elderly and alcoholics

Because prone to accidents/cerebral atrophy means veins are more susceptible to damage and therefore rupture

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8
Q

What is a extradural haemorrhage?

A

Traumatic arterial bleed into the extradural space (from middle meningeal artery)

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9
Q

What is the leading cause of extradural haemorrhage?

A

Head trauma

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10
Q

Describe the investigation of brain haemorrhage

A

CT head:

  • Subarachnoid = white 5 pointed star shape
  • Subdural = white crescent shaped mass
  • Extradural = white lentiform shaped mass

Lumbar puncture for SUBARACHNOID ONLY - performed 12 hours after onset of symptoms, shows xanthochromia (immediately = blood)

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11
Q

Describe the symptoms and signs of brain haemorrhage

A

Symptoms due to raised intracranial pressure:

  • Headache
  • Seizures
  • Nausea and vomiting
  • Loss of consciousness

Signs:
- Papilloedema (due to raised ICP)

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12
Q

Describe the management of brain haemorrhage

A

Neurosurgery

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13
Q

Types of headache and facial pain…

A 
Tension headache
Migraine
Cluster headache
Giant cell arteritis
Trigeminal neuralgia
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14
Q

Compare the clinical presentation of tension headache and migraine

A

Tension headache:

  • Bilateral pain
  • Lasts minutes to days
  • Feeling of tightness/pressure all around the head
  • No associated features to suggest migraine (visual/GI disturbance)

Migraine:

  • Unilateral, throbbing pain
  • Lasts hours to days
  • Headache associated with visual symptoms (e.g. photophobia) and/or GI symptoms (e.g. nausea/vomiting)
  • Migraine may be preceded by a aura, e.g. flashing lights, tingling/numbness
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15
Q

What are the triggers for migraine?

A

CHOCOLATE

C - chocolate
H - hangovers
O - OCP
C - caffeine
O - orgasms
L - lie-ins
A - alcohol
T - travel
E - exercise
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16
Q

What are the triggers for a tension headache?

A

Stress
Concentrated visual effort
Fumes
Loud noise

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17
Q

How are tension headaches/migraines diagnosed?

A

Diagnosis is clinical

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18
Q

Describe the management of tension headaches

A

Conservative:

  • Stress relief
  • Reassurance

Pharmacological:
Short-term analgesia, e.g. paracetamol, ibuprofen (take care not to cause medication overuse headache!)

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19
Q

Describe the management of migraines

A

Conservative
- Avoid triggers

Pharmacological
Acute attacks:
- Mild: NSAID +/- antiemetic
- Severe: Sumatriptan

Prophylaxis:

  • Beta blockers OR
  • Valproate OR
  • Amitriptyline
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20
Q

Describe the clinical presentation of cluster headaches

A
  • Rapid onset, severe, short lived headaches (average 15 mins up to 3 hours)
  • Pain usually starts around one eye/temple (unilateral)
  • Associated symptoms include eye redness/lacrimation, miosis (pupil constriction) and/or ptosis (eyelid drooping) and rhinorrhoea
  • Multiple attacks over period of weeks/months with periods of remission in between
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21
Q

Describe the management of cluster headaches

A

Pharmacological:

  • Acute attacks: sumatriptan (serotonin agonist) and 100% oxygen
  • Prophylaxis: verapamil (CCB)
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22
Q

What is giant cell arteritis?

A

Granulomatous inflammation of blood vessel walls, in particular the extradural arteries

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23
Q

Describe the symptoms of giant cell arteritis

A

Headache
Tender scalp
Jaw claudication
Loss of vision

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24
Q

Describe the investigation of giant cell arteritis

A

Bloods:
ESR/CRP raised

Temporal artery biopsy showing granulomatous inflammation is diagnostic

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25
Q

Describe the management of giant cell arteritis

A

Immediately start high dose oral steroids (e.g. prednisolone) if GCA is suspected
Temporal artery biopsy must be taken within 7 days of starting steroids

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26
Q

Describe the symptoms of trigeminal neuralgia

Give some triggers for these symptoms

A
  • Sharp, stabbing pain lasting only a few seconds
  • Unilateral, within distribution of trigeminal nerve (side of face)

Triggers:

  • Washing face
  • Shaving
  • Eating
  • Talking
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27
Q

What causes trigeminal neuralgia?

A 
Primary = idiopathic
Secondary = e.g. compression of trigeminal nerve by intracranial vessels or a tumour, multiple sclerosis
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28
Q

Describe the investigation of trigeminal neuralgia

A

MRI to exclude secondary causes

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29
Q

Describe the management of trigeminal neuralgia

A

Pharmacological:

Carbemazepine

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30
Q

Brain tumours are classed as being either…

A

Primary

Secondary

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31
Q

What is the most common histopathological type of malignant primary brain tumour?

A

Glioma

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32
Q

Which primary cancers commonly lead to brain metastases?

A 
Lung
Prostate
Breast
Thyroid
Kidney
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33
Q

What are the symptoms/signs of a brain tumour?

A

Symptoms:

  • Focal neurological deficit
  • Symptoms of raised ICP (headache, seizure, nausea and vomiting, loss of consciousness)

Signs:
- Papilloedema (due to raised ICP)

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34
Q

Describe the investigation of a brain tumour

A

CT/MRI head

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35
Q

Describe the management of a brain tumour

A

Neurosurgery to remove mass lesion if possible
Radiotherapy
IV dexamethasone to reduce cerebral oedema
Anti-convulsants (if having seizures)

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36
Q

What is the definition of ‘transient ischaemic attack’?

A
  • Focal, sudden-onset, neurological deficit lasting less than 24 hours
  • Complete clinical recovery
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37
Q

What are the causes of TIA?

A
  • Thromboembolism from carotid arteries
  • Cardioembolism, e.g. post-MI, AF
  • Hyperviscosity, e.g. polycythaemia
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38
Q

What visual syndrome is associated with TIA?

Describe its pathophysiology and it symptoms

A

Amaurosis fugax:

  • Thromboembolism passes into retinal artery
  • ‘curtain descending over field of vision’
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39
Q

Describe the investigation of TIA

A
  • Diagnosis is clinical
  • Brain imaging: MRI
  • Carotid artery imaging: carotid doppler and CT angiography (stenosis)
  • Risk of stroke assessed using ABCD2 score

ABCD2:

  • Age > 60
  • BP > 140/90 mmHg (either systolic or diastolic)
  • Clinical features (unilateral weakness or speech disturbance without weakness)
  • Duration of symptoms < 10 mins, 10-59 mins, > 1 hour
  • Diabetes
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40
Q

Describe the conservative, pharmacological and interventional management of TIA

A

Conservative:
- Smoking cessation, regular exercise etc.

Pharmacological:

  • Aspirin 300 mg should be started immediately and continued long term (75 mg daily)
  • Start statin if high cholesterol

Interventional:
- Carotid endarterectomy to remove plaque build up if stenosis > 70%

41
Q

What types of stroke are there?

A

Ischaemic

Haemorrhagic

42
Q

What are the causes of ischaemic stroke?

A

Thromboembolism from carotid arteries
Cardioembolism, e.g. post-MI, AF
Hyperviscosity, e.g. polycythaemia

43
Q

What are the causes of haemorrhagic stroke?

A

Chronic HTN (Charcot-Bouchard aneurysms)
AV malformations
Over-anticoagulation

44
Q

Describe the symptoms of an ischaemic, posterior circulation stroke

A
  • Horner’s syndrome = miosis, ptosis, anhydrosis, enophthalmos
  • Cerebellar syndrome = headache, vomiting, vertigo, ataxia
45
Q

Describe the symptoms of an ischaemic anterior circulation stroke

A
  • Anterior cerebral artery = personality/mood changes
  • Middle cerebral artery = contralateral loss of motor/sensory function of upper limbs, aphasia
  • Posterior cerebral artery = contralateral hemianopia
46
Q

Describe the investigation of stroke

A

CT head to distinguish between ischaemic and haemorrhagic

47
Q

Describe the management of ischaemic stroke

A
  • If patient presents within 4.5 hours = thrombolysis (IV alteplase = tissue plasminogen activator)
  • 2nd line = aspirin for 2 weeks, then clopidogrel OD
48
Q

Describe the management of haemorrhagic stroke

A
  • Control BP with beta blockers

- Use beriplex if warfarin related bleed

49
Q

What are the contraindications to thrombolysis?

A
  • Time of onset more than 4.5 hours ago/time of onset unknown
  • Haemorrhage
  • Low platelet count
  • Recent major surgery
50
Q

What is meningitis?

A

Inflammation of the meninges

51
Q

What causes meningitis?

A
  • Infective: bacteria, e.g. strep pneumoniae, neisseria meningitidis; virus, e.g. EBV
  • Non-infecive, e.g. paraneoplastic, autoimmune (e.g. SLE, vasculitis)
52
Q

Describe the symptoms and signs of meningitis

A

Symptoms:

  • Fever
  • Headache
  • Nausea and vomiting
  • Stiff neck
  • Photophobia

Signs:

  • Non-blanching rash
  • +ve Kernig’s signs (inability to allow full extension of the knee when the hip is flexed 90 degrees)
53
Q

Describe the investigation and management of acute bacterial meningitis

A
  • Immediately administer IM benzylpenicllin
  • Immediately start patient on cephalosporin, e.g. cefotaxime if suspect meningitis
  • Bloods/lumbar puncture –> MC+S, use results to direct Abx
54
Q

Who must be notified when there is a case of meningitis?

55
Q

What is encephalitis?

A

Inflammation of the brain

56
Q

What causes encephalitis?

A
  • Infective: viral, e.g. herpes simplex virus, varicella zoster virus
  • Non-infective, e.g. paraneoplastic, autoimmune (e.g. SLE, vasculitis)
57
Q

Describe the investigation of encephalitis

A
  • CSF analysis shows raised lymphocyte count

- Viral serology

58
Q

Describe the management of encephalitis

59
Q

What is shingles?

A

Shingles (also known as herpes zoster) is caused by reactivation of varicella zoster virus, the same virus which causes chickenpox (which has been dormant in dorsal root ganglion)

60
Q

Describe the symptoms of shingles

A

Rash/pain in dermatomal distribution that does not cross midline

61
Q

Describe the management of shingles

62
Q

Give some causes of epilepsy

A
  • Idiopathic (most cases)

- Structural causes, e.g. brain tumour

63
Q

What is the most common symptom of epilepsy?

64
Q

How are seizures classified?

A
  • Generalised seizure

- Partial/focal seizure

65
Q

What is a generalised seizure?

Give an example of a type of generalised seizure and describe the symptoms

A

Generalised seizure = bilateral abnormal electrical activity with bilateral motor manifestations and impaired consciousness

Type of generalised seizure: tonic clonic seizure
Characterised by:
- Loss of consciousness
- Limbs suddenly stiffen (tonic) then jerk uncontrollably (clonic)
- Common ictal symptoms: tongue biting, urinary incontinence
- Common postictal symptoms: drowsiness, confusion

66
Q

What is a partial seizure?

A

Abnormal electrical activity in one specific area of the brain

67
Q

Describe the diagnosis of epilepsy

A

Diagnosis is made clinically from detailed description of eye-witness account or from video evidence

68
Q

Describe the management of generalised and partial seziures

A 
Generalised = Sodium valproate 
Partial = carbemazepine

Lamotrigine can be used for either as alternative

69
Q

Describe the pathophysiology of Parkinson’s disease

A
  • Depletion of dopaminergic neurons in substantia nigra

- Prescence of Lewy bodies

70
Q

What are the three characteristic features of Parkinson’s disease?

A
  1. Resting tremor
  2. Rigidity (increase in muscle tone in limbs and trunk)
  3. Bradykinesia (difficulty initiating movement, slow speech, progressive fatiguing/reduction in amplitude of repetitive movements, dysdiadochokinesa)

Other features:

  • Stoop
  • Shuffling gait
  • Reduced arm swing on one side
71
Q

Give some non-motor features of Parkinson’s disease

A
  • Neuropsychiatric problems: depression/anxiety/impulsive behaviour
  • Sleep problems: insomnia
  • GI/autonomic symptoms: excess saliva, excess sweating, constipation
72
Q

Describe the diagnosis of Parkinson’s disease

A
  • Diagnosis is clinical

- CT/MRI head shows atrophy of substantia nigra

73
Q

Describe the management of Parkinson’s disease

A

Pharmacological:

  1. Increase the amount of dopamine in the CNS by using a dopamine precursor, e.g. levodopa, co-careldopa
  2. Mimic the action of dopamine using dopamine agonists, e.g. ropinirole
  3. Inhibit enzymatic breakdown of dopamine
  4. Tremor management using an anticholinergic, e.g. amantadine
74
Q

List the causes of peripheral neuropathy

A

DAVID

D -diabetes
A - alcohol
V - vitamin B12 deficiency
I - infective (Guillian Barre)
D - drugs (e.g. isoniazid)
75
Q

What is multiple sclerosis?

A

Autoimmune demyelination (T cell mediated) affecting the CNS only

76
Q

Describe the clinical presentation of multiple sclerosis

A

Relapsing-remitting pattern (at least 2 clinically distinct episodes with period of remission in between)

Common presentations:

  • Optic neuritis (inflammation of optic nerve resulting in blurred vision and unilateral eye pain)
  • Spinal cord lesions (tingling/numbness)
  • Other symptoms: spasticity, tremor, urinary incontinence
77
Q

Describe the investigation of MS

A
  • Clinical diagnosis based on symptoms and relapsing remitting pattern
  • MRI showing plaques disseminated in time and space
78
Q

Describe the management of MS

A

Pharmacological:

  • Acute attacks: steroids
  • Prophylaxis: B interferon
  • Symptom control: beta blockers for tremor, baclofen for spasticity, oxybutynin for incontinence
79
Q

What is Huntington’s chorea? Characteristics, age of onset…?

A
  • Autosomal dominant degenerative CNS condition
  • Characterised by chorea (abnormal, involuntary movement), dementia and personality/mood changes (e.g. aggression, depression)
  • Onset 4th/5th decade (although children of affected parents may develop symptoms at an earlier age - this is known as anticipation)
80
Q

Describe the pathophysiology of Huntington’s chorea

A

Loss of GABA and cholinergic neurons

81
Q

Describe the investigation of Huntington’s chorea

A
  • Genetic testing (CAG repeat)
82
Q

Describe the management of Huntington’s chorea

A

NO CURE

  • Mx of chorea: benzodiazepine
  • Depression: SSRI
  • Aggression: Risperidone
83
Q

What is myasthenia gravis - describe its pathophysiology

A

Destruction of ACh postsynaptic receptor sites at NMJ by IgG autoantibodies

84
Q

What are the symptoms of myasthenia gravis

A

Weakness and fatiguability (worse at end of day)

85
Q

Describe the investigation of myasthenia gravis

A
  • Electromyography shows fatiguability

- CT = thymus gland hyperplasia

86
Q

Describe the management of myasthenia gravis

A
  • Pyridostigmine (acetylcholinesterase inhibitor) and steroids (immunosuppression)
  • May need ciclosporin, methotrexate etc. in severe disease
87
Q

What is an upper motor neurone?
What is a lower motor neurone?
What is motor neurone disease (MND)?

A
  • Upper motor neurone: motor neurone which begins in the motor cortex and terminates in the medulla
  • Lower motor neurone: motor neurone which begins in the spinal cord and terminates at the neuromuscular junction
  • Motor neurone disease: degeneration of motor neurones in the brain, brainstem and spinal cord; degeneration may affect UMN only, LMN only or both
88
Q

Describe the symptoms that would be present with UMN lesion(s)

A
  • Muscle tone increased (spasicity)
  • Reflexes brisk
  • +ve Babinski sign (extensor plantar response)
  • Pyramidal pattern weakness (upper limbs - extensors weaker than flexors, lower limbs - flexors weaker than extensors)
89
Q

Describe the symptoms that would be present with LMN lesion(s)

A
  • Muscle tone reduced
  • Reflexes decreased/absent
  • Muscle wasting
  • Fasciculation
90
Q

Which type of motor neurone disease is most common?

Does this affect UMNs/LMNs? - and therefore what is the clinical picture?

A

ALS - amyotrophic lateral sclerosis
Affects UMNs and LMNs
Mixed clinical picture of UMN and LMN symptoms

91
Q

Describe the investigation of MND

A
  • Clinical diagnosis confirmed by electromyography

- Raised creatinine kinase due to muscle breakdown

92
Q

Describe the management of MND

A
  • Slowing disease progression: Riluzole (Na channel blocker)
  • Symptom control, e.g. baclofen for spasticity
  • May need palliative intervention, e.g. tracheostomy, ventilator etc.
93
Q

What is Guillian Barre syndrome?

A

Acute, demyelinating, inflammatory polyneuropathy affecting peripheral nerves as a result of viral infection

94
Q

Give some examples of viruses which can cause Guillian Barre syndrome

95
Q

Describe the symptoms of Guillian Barre syndrome

A

Acute ascending muscle weakness following viral infection

96
Q

Describe the investigation of Guillian Barre syndrome

A

Lumbar puncture shows raised protein count but normal WCC

97
Q

Describe the management of Guillian Barre syndrome

A

Usually self-limiting
Treat viral infection
Supportive therapy in mean time

98
Q

What are the different types of dementia?

A
  • Alzheimer’s
  • Vascular dementia
  • Lewy body
  • Frontotemporal
99
Q

What class of drug is used in Alzheimer’s disease?

A

Acetylcholinesterase inhibitor, e.g. donepezil

Phase 2a (16 decks)

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