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YEAR 4 - CCC > Primary care - Neurological > Flashcards

Primary care - Neurological Flashcards

1
Q

What is epilepsy?

A

a group of disorders characterised by a tendency for recurrent epileptic seizures (at least 2 unprovoked seizures occurring >24 hours apart)

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2
Q

What causes epilepsy?

A

2/3rd = idiopathic

1/3rd have identified cause:
Space-occupying lesion e.g. neoplasm
Head injury or cortical scarring from previous head injury
CNS infections
Stroke
Hippocampal sclerosis after febrile convulsion
Vascular malformations

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3
Q

What are some triggers of seizures?

A

Stress
Flashing lights
Alcohol/alcohol withdrawal

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4
Q

Describe the different elements of a partial seizure

A

Prodrome (hours/days) - change in mood/behaviour

Aura - focal seizure (commonly from temporal lobe), deja vu, strange smells, flashing lights

Post-ictal phase - headache, confusion, myalgia, temporary weakness, dysphasia

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5
Q

What is a focal seizure?

A

Start in one area of one side of the brain

Often seen with underlying structural disease

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6
Q

What are generalised seizures?

What are the different types and how do they present?

A

Involve both hemispheres of the brain

  1. Absence seizures - brief (less than 10 sec) pauses e.g. stares into space for 5 seconds then resumes talking, common in childhood
  2. Tonic-clonic - LOC, stiff limbs (tonic) then jerk (clonic). Tongue biting, incontinence. Post-ictal confusion and drowsiness
  3. Myoclonic - sudden jerk of a limb/trunk/face
  4. Atonic - all muscles relax and drop to floor, no LOC
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7
Q

What investigations should you do in epilepsy?

A

Anti-epileptic levels - check compliance

EEG

  • Asymmetry or slowing suggests underlying structural abnormalities
  • Sharp waves or spike wave complexes suggest neuronal hyperexcitability
  • Many children with epilepsy will have a normal EEG

MRI - if focal onset or if seizures continue with medication

ECG - in all patients with altered consciousness

LP - if infection suspected

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8
Q

What are DVLA guidelines related to seizures?

A

Inform DVLA:
• 1st unprovoked seizure – stop driving for 6 months.
• Epileptic seizure – stop driving until seizure-free for 1 year.
• No HGV driving until seizure free and no meds for 10 years

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9
Q

What are 1st and 2nd line treatments for focal/partial seizures? What are important factors when prescribing AEDs?

A

1st line - carbamazepine or lamotrigine

2nd line - sodium valproate

Extra info:
Prescribe brand name - changing brand has 10% risk of worse seizure control

AEDs can only be prescribed following confirmed diagnosis (usually after second
seizure)

Patients on AEDs are entitled to free prescriptions

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10
Q

What are 1st line treatment for all generalised seizures?

A

Sodium valproate

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11
Q

What type of seizures should you avoid carbamazepine in ?

A

Absence
Myoclonic

can worsen them

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12
Q

Which anti-epileptic drug must be strictly avoided in pregnancy?
Which is preferred?
What must be thought about in terms of contraception?

A

Sodium valproate is the most teratogenic

Lamotrigine is preferred

Anti-epileptic drugs are P450 enzyme inducers so they make progesterone-only contraception unreliable.
Oestrogen-containing contraceptives lower lamotrigine levels so need increased dose.

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13
Q

What are the side effects of sodium valproate?

A

vALPROATE

Appetite increase - weight gain
Liver failure
Pancreatitis
Reversible hair loss - grows back curly
Oedema
Ataxia
Teratogenicity, thrombocytopenia, tremor
Encephalopathy
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14
Q

Which drug should you avoid if taking sodium valproate?

A

Aspirin - it displaces sodium valproate from its binding sites which increases the adverse effects

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15
Q

When is carbamazepine contraindicated?

A

AV node conduction abnormalities - can cause AV block

Bone marrow depression - can cause agranulocytosis

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16
Q

Define stroke and TIA - specifying the differences

A

Stroke = sudden onset of focal/global neurological disturbance lasting over 24 hours. Causes irreversible cell damage + death.

TIA = less than 24 hour neurological dysfunction caused by ischaemia without evidence of acute infarction

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17
Q

What heart diseases particularly predispose you to ischaemic stroke?

A

AF
Infective endocarditis
Valve disease
Heart failure

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18
Q

What can cause a haemorrhagic stroke?

A

Rupture of an aneurysm
High blood pressure
Head injury

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19
Q

What is the most common cause of ischaemic stroke in young people?

A

Carotid artery dissection - usually caused by hitting their chin and hyperextending their neck, rupturing the carotid artery

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20
Q

What symptoms point more towards a bleed than ischaemia?

A

Meningism
Severe headache
Coma
Seizure

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21
Q

What does the ACA supply?

How would an anterior cerebral artery stroke present?

A

ACA supplies frontal + medial cerebrum

Contralateral leg weakness - foot drop
Contralateral leg sensory loss
Frontal lobe behavioural abnormalities
Facial sparing

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22
Q

What does the MCA supply?

How would an MCA infarct present?

A

Lateral cerebrum

Contralateral hemiparesis
Contralateral homonymous hemianopia if optic radiation involved
Dysphasia if dominant hemisphere
Visuospatial disturbance if non-dominant

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23
Q

What makes up the anterior circulation of the brain?

A

Internal carotid arteries
Middle cerebral artery
Anterior cerebral artery

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24
Q

How would a total anterior circulation stroke (TACS) present?

A 
Hemiparesis (but with sparring of the forehead)
Hemisensory loss
Homonymous hemianopia
Visuo-spatial deficit
Dysphasia
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25
Q

What does the PCA supply?

How would a PCA infarct present?

A

Occipital lobe

Weakness
Coordination issues
Ataxia
Diplopia

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26
Q

What makes up the posterior circulation of the brain?

A

Vertebral arteries (branches from the subclavian arteries. In the cranium, the 2 vertebral arteries form the basilar artery)
Basilar artery
Posterior cerebral artery
Posterior communicating artery

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27
Q

How does a posterior circulation stroke (POCS) present?

A 
Cerebellar dysfunction
Loss of consciousness 
Homonymous hemianopia (superficial branch of posterior cerebral artery to occipital lobe)
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28
Q

What symptoms are in cerebellar dysfunction?

A

DANISH

Dysdiadokinesia
Ataxia
Nystagmus
Intention tremor
Slurred speech/Scanning dysarthria (monotonous voice) 
Hypotonia/hyporeflexia
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29
Q

What are the causes of cerebellar syndrome?

A

PASTRIES

Posterior fossa tumour
Alcohol
MS
Trauma
Rare
Inherited
Epilepsy medication
Stroke
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30
Q

What is the first thing that should be done in suspected stroke?

A

CT head within 1 hour in order to rule out haemorrhage - don’t want to thrombolyse or anticoagulate if bleeding

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31
Q

What is the acute management of an ischaemic stroke?

A

Give alteplase within 4.5 hours once haemorrhage is excluded

If post-4.5 hours, given aspirin 300mg for 2 weeks

Thrombectomy (particularly with large artery occlusion in proximal anterior circulation)

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32
Q

What is alteplase?

A

Recombinant tissue plasminogen activator

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33
Q

What causes a unilateral progressive vision loss ‘like a curtain descending’?

A

amaurosis fugax = TIA of retinal artery

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34
Q

What is the acute management of a haemorrhagic stroke?

A

prothrombin and vitamin K to normalise clotting

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35
Q

What must be assessed in all stroke patients? Describe how this is done

A

Swallow assessment (stroke water swallow screen)

  1. Give the patient 3 x 5ml teaspoons of water
  2. Give patient 6 sips of water from an open cup
  3. Give patient minimum 50ml water in an open cup

If at any point they cough, choke, gurgle, dribble stop the assessment and keep patient nil by mouth and refer to SALT

If they passed the assessment, commence oral fluids and observe closely with first meal

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36
Q

What does a CT head look like in acute/chronic ischaemia?

A

Acute - thrombus/embolus may be visible as hyper-dense segment of a vessel

Chronic - hypo-dense area with negative mass effect (midline shift towards infarct)

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37
Q

What does a CT head look like in extradural/subdural/subarachnoid haemorrhagic strokes?

A

Extra-dural

  • “Egg-stradural” - egg-shaped (lentiform-shaped) hyperdensity with positive mass effect
  • Usually arterial (needs pressure to tear dural away from skull)

Subdural

  • Sliver - venous bleed between dura and arachnoid
  • Crescent-shaped hyperdensity adjacent to skull with positive mass effect

Subarachnoid
- Central hyperdensity with loss of sulci and gyri

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38
Q

What is the long term management post-stroke?

A

HALTSS
• Hypertension: anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke
• Antiplatelet therapy: clopidogrel 75 mg OD lifelong
○ In patients with ischaemic stroke secondary to atrial fibrillation - warfarin (target INR 2-3) or a DOAC (rivaroxaban/apixaban) is initiated 2 weeks post-stroke
• Lipid-lowering therapy: high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke)
• Tobacco: offer smoking cessation support.
• Sugar: screened for diabetes and managed appropriately
- Surgery: patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy

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39
Q

How do you assess stroke risk in someone with TIA?

A

ABCD2

Age>60 - 1
BP > 140/90 - 1
Clinical features (unilateral weakness, speech difficulty) - 2
Duration > 60 min - 2
Diabetes - 1
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40
Q

How do you differentiate between extradural and subdural haematoma on CT head?

A

Extradural haematoma

  • lens shape of bleeding
  • can’t cross sutures of skull
  • can cross midline

Subdural haematoma

  • crescent shape of bleeding
  • can cross sutures of skull
  • can’t cross midline
41
Q

How do you differentiate between extradural and subdural haematoma with symptoms?

A

Extradural haematoma - LOC then lucid interval then 2nd LOC

Subdural haematoma - slow progression + confusion

42
Q

What is the pathophysiology of MS?

A

Autoimmune inflammatory disorder of CNS
Characterised by formation of patches of demyelination which heal intermittently causing relapsing/remitting symptoms
Prolonged demyelination causes axonal loss and progressive symptoms
NEVER affects peripheral nerves

43
Q

What virus is multiple sclerosis sometimes linked to?

A

EBV - antibodies produced by B cells + T cells directed against EBV nuclear antigens may be redirected to attack CNS myelin due to molecular mimicry

44
Q

Who is more likely to get MS?

A

Females in their 30s

Caucasians

45
Q

How does MS usually first present?

A

Unilateral optic neuritis - pain on eye movement and rapid decrease in central vision

46
Q

What investigation is done for MS and what does it show?

A

MRI - shows brain and spinal cord plaques in periventricular white matter

Sensitive but not specific

47
Q

What are some other symptoms/signs of MS?

A 
Trigeminal neuralgia
Numbness/tingling in limbs
Leg weakness - transverse myelitis
Brainstem symptoms - ataxia, diplopia 
Symptoms worsened by heat = Uhthoff's phenomenon
48
Q

If MS affects the autonomic system, how would this present?

A
  • Loss of control over bladder
  • Faecal incontinence
  • Impotence
  • Loss of thermoregulation - sweating, pyrexia, hypothermia
49
Q

What is the diagnostic criteria for MS called?

A

McDonald Criteria

50
Q

How do you treat an acute flare of MS?

A

Prednisolone 500mg/day for 5 days (with omeprazole)

51
Q

What is used in mild/moderate relapsing-remitting MS?

A

DMARDs

  • Dimethyl fumarate
  • Monoclonal antibodies (alemtuzumab/natalizumab)
52
Q

What is motor neurone disease?

A

A group of neurological disorders affecting neurones in spinal cord, brainstem and motor cortex

Affects upper and lower motor neurons

53
Q

What are UMN signs?

A 
Weakness
Spasticity
Hypertonia
Hyperreflexia i.e. brisk reflexes
Upgoing plantar reflex
54
Q

What are LMN signs?

A

Weakness
Hypotonia
Hyporeflexia
Fasciculation

55
Q

What symptoms never appear in motor neurone disease?

A

Eye movement problems

Sensory loss

56
Q

What is amyotrophic lateral sclerosis (ALS)?

A

Presents as UMN in legs and LMN signs in arms

It may be familial - associated with Ch21

50% of cases of MND

57
Q

What is the prognosis of MND?

A

Rapidly progressive

Death usually results from ventilatory failure 3-5 years post-diagnosis

58
Q

What are the types of MND?

A

Amyotrophic lateral sclerosis (ALS)
Bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

59
Q

What is the difference between progressive muscular atrophy and primary lateral sclerosis?

A

Progressive muscular atrophy - only LMN affected

Primary lateral sclerosis - only UMN affected

60
Q

What is the only licensed drug for MND?

A

Riluzole - prolongs life by 3 months; requires LFT monitoring

61
Q

What is the pathophysiology of Parkinson’s disease?

A

Loss of dopaminergic neurons in substantia nigra in the brainstem
Therefore, there is a deficiency of dopamine and relative excess of ACh

62
Q

Name some differential diagnoses for Parkinsonism and how can you differentiate them from Parkinson’s

A
  1. Lewy-body dementia - MMSE (in LBD the dementia symptoms are present first)
  2. Multiple system atrophy - would have poor response to levodopa
  3. Progressive supranuclear palsy
  4. Benign essential tremor - ask them to draw something
63
Q

What can cause drug-induced Parkinsonism and how can you tell difference from Parkinson’s disease?

A

Parkinson’s disease is asymmetrical; drug-induced more likely to be symmetrical

Psychosis tranquilisers

  • Phenothiazines
  • Thioxanthes
  • Butyrophenones
  • Haloperidol

Metoclopramide

64
Q

What is the extrapyramidal triad of Parkinsonism?

A
  1. Tremor - ‘pill-rolling’, 4-6Hz resting tremor
  2. Hypertonia - cogwheel rigidity during pronation/supination
  3. Bradykinesia - slow to initiate movement, festinating gait, decreased arm swing, mask-like face
65
Q

Describe a Parkinsonian gait

A

Hesitant - difficulty initiating + turning
Shuffling - small steps
Festinating - walks faster and faster to not fall over
Lack of arm swing
Stooped posture
Unsteadiness

66
Q

What sign is seen with glabella tap in Parkinson’s?

A

Myerson’s sign - blinking fails to cease with tapping on forehead

67
Q

What is the first line medication given to Parkinson disease patients under 65 years with no significant comorbidities?

A

Dopamine receptor agonist

  • bromocriptine
  • pergolide
68
Q

What type of drug are Sinemet and Madopar?

A

Levodopa = dopamine precursor

69
Q

What do you have to give levodopa drugs with?

A

Dopa-decarboxylase inhibitor (carbidopa) to prevent peripheral conversion to dopamine which reduces nausea and lowers the dose required

70
Q

What are some side effects of levodopa?

A
  • Dyskinesia
  • Dystonia (painful)
  • Psychosis
  • Nausea + vomiting

The efficacy reduces over time, which requires much larger doses –> more side effects.

71
Q

What are some side effects of dopamine agonists?

A
  • Compulsive behaviour e.g. gambling, hypersexuality
  • Drowsiness
  • Nausea
  • Hallucinations
72
Q

What is myasthenia gravis?

A

Autoimmune disease that affects the antibodies to nicotinic acetylcholine receptors on muscle fibres (LMN)

73
Q

How does myasthenia gravis present?

A

Starts with weakness of extraocular muscles

Proximal weakness that gets worse throughout the day and improves with rest

74
Q

What visual problem is typical of myasthenia gravis?

A

Mild bilateral ptosis exacerbated by prolonged upward gaze - this is due to fatiguability, which shows that it is a motor problem

75
Q

What can occur in a myasthenic crisis (acute attack of myasthenia gravis)?

A

Respiratory failure

76
Q

What is the most sensitive test for myasthenia gravis?

A

Serum acetylcholine receptor antibody (90% sensitive)

77
Q

What tumour is myasthenia gravis associated with?

A

Thymoma (10-15% patients)

78
Q

What investigation is required for all new diagnoses of myasthenia gravis?

A

CT chest to rule out thymoma

79
Q

What is the main differential diagnosis for myasthenia gravis?

A

Lambert-Eaton Myasthenic Syndrome

80
Q

What is the difference in presentation between myasthenia gravis and Lambert-Eaton?

A

Myasthenia gravis

  • Starts with weakness of extraocular muscles
  • Weakness gets worse throughout the day and improves with rest

Lambert-Eaton

  • Starts with weakness of the lower legs
  • Weakness improves with exercise
81
Q

What can trigger a myasthenic crisis?

A

Infection
Surgery
Pregnancy
Medications

82
Q

What is the first line treatment for myasthenia gravis?

A

Anticholinesterase inhibitors e.g. pyridostigmine

83
Q

How does a third cranial nerve palsy present?

A

Ptosis - due to impaired innervation to levator palpebrae superioris

‘Down and out’ pupil - due to unopposed activation of lateral rectus and superior oblique

84
Q

What three conditions can cause a surgical third nerve palsy?

A
  • Aneurysm
  • Tumour
  • Intracranial haemorrhage
85
Q

What three conditions can cause a medical third nerve palsy?

A
  • Diabetes (most common)
  • Hypertension
  • Stroke

(medical lesions affect the blood supply)

86
Q

What is the difference in presentation between a medical and surgical third cranial nerve palsy? Explain why

A

In a ‘medical’ third nerve palsy there is pupil sparing

This is because the parasympathetic (constrictive) fibres run on the outside of the nerve

Medical lesions will affect the blood supply to the inner (motor) fibres of the nerve (the vasa vasorum), leaving the outer parasympathetic fibres intact

87
Q

What cranial nerve does Bell’s palsy affect?

A

The facial nerve (CN 7)

88
Q

Describe the facial weakness in Bell’s palsy

A

Unilateral, lower motor neuron facial weakness

Spares the extraocular muscles and muscles of mastication

89
Q

Aside from facial weakness, what are the other signs of Bell’s palsy?

A

Pain around/behind the ear
Dry mouth due to decreased saliva production
Altered taste
Hyperacusis

90
Q

What is the central component of Bell’s palsy management?

A

Prompt administration of oral steroids - 50mg OD for 10 days then taper

91
Q

What are the two classes of hydrocephalus? Describe the difference

A

Communicating - a failure to reabsorb CSF occurs from an insult to the arachnoid villi (e.g. meningitis or subarachnoid haemorrhage) or increased CSF production (e.g. choroid plexus papilloma)

Non-communicating - something is obstructing the flow through the ventricular system (tumour, haemorrhage, inflammation)

92
Q

Which of the two classes of hydrocephalus is more common?

A

Communicating

93
Q

What are the signs and symptoms of hydrocephalus in adults?

A

Features of increased ICP

  • Headache worse in the morning and leaning forwards
  • Nausea + vomiting
  • Altered GCS
  • Papilloedema
  • 6th nerve palsy
  • Cushing triad (irregular breathing, widening pulse pressure, bradycardia)
94
Q

How is hydrocephalus diagnosed in adults? What is seen?

A

MRI head

  • Enlargement of ventricles seen
  • Communicating hydrocephalus: all ventricles dilated
  • Non-communicating hydrocephalus: ventricles upstream of obstruction are dilated
95
Q

How is hydrocephalus managed?

A

Insertion of a ventriculoperitoneal (VP) shunt - drainage of excess CSF via a cerebral shunt into the peritoneum where it is reabsorbed

96
Q

Who does normal pressure hydrocephalus primarily affect?

A

Elderly people > 60 years

97
Q

What clinical triad characterises normal pressure hydrocephalus?

A

Wet, wacky, wobbly

Urinary incontinence - initially only increased urgency and frequency, but later develops to urge incontinence
Dementia
Ataxic gait - frequent falls, broad-based gait with short steps

98
Q

What causes normal pressure hydrocephalus?

A

Impaired CSF reabsorption- usually idiopathic

99
Q

What is the confirmatory test for normal pressure hydrocephalus?

A

CSF tap test

  • Opening pressure is normal/slightly raised
  • Remove a small amount of CSF fluid
  • Improvement of symptoms after CSF removal confirms NPH

YEAR 4 - CCC (7 decks)

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