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Neurology Flashcards

1
Q

Stroke

Pathophysiology

A
  • A sudden interruption in the vascular supply of the brain

- Ischaemic or haemorrhagic

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2
Q

Ischaemic stroke

Problem?

A
  • Blockage in the blood vessels stops blood flow
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3
Q

Ischaemic stroke

Proportion

A

85%

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4
Q

Ischaemic stroke

Subtypes

A
  • Thrombotic stroke - thrombosis from large vessels, e.g. carotid
  • Embolic stroke - AF cause of an emboli forming in the heart
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5
Q

Ischaemic stroke

Risk factors

A
  • General CVS RFs: age, HTN, smoking, hyperlipidaemia, DM
  • CVS disease: angina, MI, PAD
  • Previous stroke/TIA
  • Cardio embolism RF = AF
  • Carotid artery disease
  • Vasculitis
  • Thrombophilia
  • Combined contraceptive pill
  • Family history
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6
Q

Haemorrhagic stroke

Problem?

A

Blood vessel bursts leading to reduction in blood flow

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7
Q

Haemorrhagic stroke

Proportion?

A

15%

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8
Q

Haemorrhagic stroke

Subtypes

A
  • Intracerebral haemorrhage: bleeding within the brain

- Subarachnoid haemorrhage: bleeding on the surface of the brain

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9
Q

Haemorrhagic stroke

Risk factors

A
  • CVS RFs
  • Previous stroke/TIA
  • AV MALFORMATION
  • Anticoagulation therapy
  • Aneurysm (Berry’s)
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10
Q

What features might help differentiate haemorrhagic strokes from ischaemic strokes?

A

More common in haemorrhagic strokes:

  • Decrease in level of consciousness
  • Headache
  • Nausea and vomiting
  • Seizures in 25%
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11
Q

General features of a stroke

e.g. public

A

Face - ‘Has their face fallen on one side? Can they smile?’
Arms - ‘Can they raise both arms and keep them there?’
Speech - ‘Is their speech slurred?’
Time - ‘Time to call 999 if you see any single one of these signs.’

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12
Q

Stroke

Investigations

A
  • NON-CONTRAST CT SCAN
  • MI
    The main cause for urgency is to see whether a patient may be suitable for thrombolytic therapy to treat early ischaemic strokes
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13
Q

Stroke

Immediate management

A
  • Admit
  • Exclude hypoglycaemia
  • Immediate CT to exclude primary intracerebral haemorrhage
  • Aspirin mg STAT (after CT) and continued for 2 weeks (start long-term antithrombotic treatment after this if still in hospital, before if already discharged)
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14
Q

Ischaemic stroke

Thrombolysis criteria

A
  • Ischaemic stroke, NOT haemorrhagic (CT)
  • Present within 4.5 hours of onset
  • No previous intracranial haemorrhage or uncontrolled HTN
  • Not pregnant
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15
Q

Ischaemic stroke

Thrombolysis drug?

A
  • Alteplase
  • Is a tissue plasminogen activator
  • Can reverse stroke if given in time
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16
Q

Ischaemic stroke

Thrombectomy

A
  • Mechanical removal of the clot
  • If occlusion is confirmed on imaging
  • Depends upon location
  • Depends on time since onset - not used after 24 hrs
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17
Q

Caution in stroke treatment

A
  • Do not want to lower the BP as risk reducing perfusion to the brain
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18
Q

Stroke

What is the ROSIER score?

A

EXCLUDE HYPOGLYCAEMIA FIRST then assess:

  • Loss of consciousness/syncope (-1)
  • Seizure activity (-1)

New acute onset of:

  • Asymmetric facial weakness (+1)
  • Asymmetric arm weakness (+1)
  • Asymmetric leg weakness (+1)
  • Speech disturbance (+1)
  • Visual field defect (+1)

A stroke is likely if > 0

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19
Q

Stroke

What do you need to exclude before starting management?

A

Hypoglycaemia

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20
Q

How would an acute ischaemic stroke appear on non-contrast CT?

A
  • Low density in the grey and white matter of the territory
  • May take time for these changes to develop
  • Hyperdense arteries may be seen - tends to be visible immediately
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21
Q

How would an acute haemorrhagic stroke appear on non-contrast CT?

A
  • Hyperdense material (blood) surrounding by low density (oedema)
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22
Q

Relative CIs to thrombolysis? (5)

A
  • Concurrent anticoagulation (INR > 1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery/trauma in preceding 2 weeks
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23
Q

Absolute CIs to thrombolysis? (11)

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke/traumatic brain injury in previous 3 months
  • LP in preceding 7 days
  • GI haemorrhage in preceding 3 weeks
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled HTN (> 200/120 mmHg)
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24
Q

Thrombectomy

Pre-stroke functional status recommendations

A
  • Less than 3 on the modified Rankin scale

- And a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)

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25
Q

Thrombectomy

Types and who to offer to

A

Thrombectomy within 6 hrs of onset, together with IV thrombolysis (if within 4.5 hrs) for:
- Acute ischaemic stroke
AND
- Confirmed occlusion of the PROXIMAL ANTERIOR CIRCULATION (CTA or MRA evidence)

Thrombectomy asap who were known to be well 6-24 hrs earlier (including wake-up strokes):
- Confirmed occlusion of PROXIMAL ANTERIOR CIRCULATION (CTA or MRA)
AND
- Potential to salvage brain tissue, as shown by imaging, e.g. CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

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26
Q

Thrombectomy

Who might you consider this for

A

(Together with IV thrombolysis (if within 4.5 hrs):
- Last known to be well up to 24 hrs earlier (including wake-up strokes
AND
- Acute ischaemia stroke and confirmed occlusion of PROXIMAL POSTERIOR CIRCULATION (basilar or posterior cerebral artery)
AND
- Potential to salvage brain tissue, as shown by imaging, e.g. CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

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27
Q

Secondary prevention of ischaemic stroke

A
  • 1st line = Clopidogrel
  • If CI –> Aspirin + MR dipyridamole
  • Monotherapy with MR dipyridamole if aspirin CI
  • Statins
  • Carotid endarterectomy or stenting if carotid artery disease
  • Treat modifiable RFs - HTN, DM
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28
Q

When might you consider carotid artery endarterectomy

A
  • Stroke or TIA in the carotid territory and are not severely disabled
  • Should only be considered if:
    • Carotid stenosis > 70% according ECST criteria
    • (or > 50% according to NASCET criteria)
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29
Q

Long-term post-stroke medications

A
  • Clopidogrel 75 mg OD

- Atorvastatin 80 mg - not immediately started

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30
Q

What might stroke rehab involve?

A
  • Nurses
  • SALT
  • Dieticians
  • Physio
  • OT
  • Social services
  • Optometry and ophthalmology
  • Psychology
  • Orthotics
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31
Q

Fluid management in stroke

A
  • Must remain normovolaemic
  • Hypovolaemia can worsen the ischaemic penumbra, as well as increase risk of other complications such as infection, deep vein thrombosis, constipation and delirium
  • Over-hydration can also complicate matters by leading to cerebral oedema, cardiac failure and hyponatraemia
  • Oral hydration is preferable in those who are able
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32
Q

Glycaemic control in stroke

A
  • Carefully monitor, particularly if NBM
  • Those with hyperglycaemia have increased mortality
  • Maintain 4-11 mmol/L in those with acute stroke
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33
Q

Why does hyperglycaemia cause increased mortality in stroke?

A

Likely due to increased tissue acidosis from anaerobic metabolism, free radical generation, and increased blood brain barrier permeability post injury

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34
Q

Blood pressure management in stroke

A

Only use antihypertensive meds in stroke if:

  • Hypertensive encephalopathy
  • Hypertensive nephropathy
  • Hypertensive cardiac failure/myocardial infarction
  • Aortic dissection
  • Pre-eclampsia/eclampsia

In these cases use intravenous labetalol, nicardipine and clevidipine as first-line agents

In candidates from thrombolytic therapy -> reduce to 185/110 mmHg

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35
Q

What are the 3 main clinical criteria to be assessed in stroke?

A
  1. Unilateral hemiparesis and/or hemisensory loss of face, arm, leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction, e.g. dysphasia
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36
Q

Total anterior circulation infarct

Vessels involved

A

Involves middle and anterior cerebral arteries

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37
Q

Total anterior circulation infarct

Presentation

A

All 3 of primary criteria are present

  1. Unilateral hemiparesis and/or hemisensory loss of face, arm, leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction, e.g. dysphasia
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38
Q

Partial anterior circulation infarct

Vessels involved

A

Smaller arteries of anterior circulation

e.g. upper or lower division of middle cerebral artery

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39
Q

Partial anterior circulation infarct

Presentation

A

2 of the criteria are present:

  1. Unilateral hemiparesis and/or hemisensory loss of face, arm, leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction, e.g. dysphasia
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40
Q

Lacunar infarct

Vessels involved

A

Perforating arteries around the internal capsule, thalamus and basal ganglia

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41
Q

Lacunar infarct

Presentation

A

Presents with one of the following:

  1. Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg, or all three
  2. Pure sensory stroke
  3. Ataxic hemiparesis

Strong association with HTN

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42
Q

Posterior circulation infarct

Vessels involved

A

Vertebrobasilar arteries

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43
Q

Posterior circulation infarct

Presentation

A

Present with one of the following:

  1. Cerebellar or brainstem syndromes
  2. Loss of consciousness
  3. isolated homonymous hemianopia
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44
Q

Lateral medullary syndrome

Vessels involved

A

Posterior inferior cerebellar artery

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45
Q

Lateral medullary syndrome

Presentation

A
  • aka Wallenberg’s syndrome
  • Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
  • Contralateral: limb sensory loss

Cerebellar signs, contralateral sensory loss & ipsilateral Horner’s

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46
Q

Weber’s syndrome

Presentation

A

MIDBRAIN STROKE

  • Ipsilateral III palsy
  • Contralateral weakness
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47
Q

Stroke presentation by anatomy

Anterior cerebral artery

A
  • Contralateral hemiparesis and sensory loss

- Lower extremities > upper

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48
Q

Stroke presentation by anatomy

Middle cerebral artery

A
  • Contralateral hemiparesis and sensory loss
  • Upper extremities > lower
  • Contralateral homonymous hemianopia
  • Aphasia
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49
Q

Stroke presentation by anatomy

Posterior cerebral artery

A
  • Contralateral homonymous hemianopia with macular sparing

- Visual agnosia

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50
Q

Stroke presentation by anatomy

Weber’s (branches of posterior cerebral that supply midbrain)

A
  • Ipsilateral CN III palsy

- Contralateral weakness of upper and lower extremity

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51
Q

Stroke presentation by anatomy

Posterior inferior cerebellar artery

A
  • Ipsilateral: facial pain and temperature loss
  • Contralateral: limb/torso pain and temperature loss
  • Ataxia, nystagmus
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52
Q

Stroke presentation by anatomy

Anterior inferior cerebellar artery

A
  • Symptoms are similar to Wallenberg’s (see above)
    BUT
  • Ipsilateral: facial paralysis and deafness
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53
Q

Stroke presentation by anatomy

Retinal/ophthalmic artery

A

Amaurosis fugax

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54
Q

Stroke presentation by anatomy

Basilar artery

A

‘Locked-in’ syndrome

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55
Q

Wernicke’s

Location of Wernicke’s and supply?

A
  • Superior temporal gyrus

- It is typically supplied by the inferior division of theleft MCA

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56
Q

Wernicke’s

Presentation if lesion?

A
  • Receptive aphasia
  • This area ‘forms’ the speech before ‘sending it’ to Broca’s area
  • Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent - ‘word salad’
  • Comprehension is impaired
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57
Q

Broca’s

Location and supply?

A
  • Inferior frontal gyrus

- It is typically supplied by the superior division of theleft MCA

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58
Q

Broca’s

Presentation if lesion?

A
  • Expressive dysphasia
  • Speech is non-fluent, laboured, and halting
  • Repetition is impaired
  • Comprehension is normal
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59
Q

Alteplase

MoA

A
  • A tissue plasminogen activator

- Converts plasminogen to the proteolytic enzyme plasmin, which lyses fibrin as well as fibrinogen

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60
Q

Transient ischaemic attack

Definition

A

A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction

Replaced the previous time-based definition

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61
Q

Transient ischaemic attack

Features

A

Possible features include:

  • unilateral weakness or sensory loss.
  • aphasia or dysarthria
  • ataxia, vertigo, or loss of balance
  • visual problems
    • sudden transient loss of vision in one eye (amaurosis fugax)
    • diplopia
    • homonymous hemianopia
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62
Q

Transient ischaemic attack

What tool is used to assess likelihood of having a TIA?

A

ABCD2 prognostic score

Though no longer recognised by NICE

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63
Q

Transient ischaemic attack

Investigations

A
  • Do not do CT unless clinical suspicious of an alternative diagnosis that CT could detect
  • MRI - diffusion-weighted and blood sensitive is preferred
  • Done on same day if possible
  • Carotid imaging –> URGENT carotid doppler unless they are not a carotid endarterectomy candidate
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64
Q

Transient ischaemic attack

Initial management

A

Give aspirin 300 mg immediately UNLESS:

 - Bleeding disorder/on anticoagulant - need immediate admission for imaging to exclude a haemorrhage
 - Already taking low-dose aspirin regularly - just continue this
 - Aspirin is CI - discuss with team

Advise the person not to drive until they have been seen by a specialist.

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65
Q

Transient ischaemic attack

Initial management

A
  • Clopidogrel = 1st line (or aspirin and dipyridamole if CI)
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66
Q

What is a crescendo TIA?

A
  • A crescendo TIA is where there are two or more TIAs within a week
  • This carries a high risk of developing in to a stroke
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67
Q

Bell’s Palsy

Definition

A

Acute, unilateral, idiopathic, facial nerve paralysis

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68
Q

Bell’s Palsy

Epidemiology

A
  • Aetiology is unknown - role of herpes simplex is investigated
  • Peak = 20-40 yrs old
  • More common in pregnancy
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69
Q

Bell’s Palsy

Features

A
  • LOWER motor neuron facial nerve palsy = FOREHEAD AFFECTED
  • Post-auricular pain (may precede paralysis)
  • Altered taste
  • Dry eyes
  • Hyperacusis (reduced tolerance to sound)
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70
Q

Bell’s Palsy

Management

A
  • Oral prednisolone within 72 hours of onset of Bell’s palsy
  • Either continue 50 mg for 10 days or 60 mg for 5 days (followed by 5-day reducing regime of 10 mg a day)
  • Lubricating eye drops
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71
Q

Bell’s Palsy

Follow-up

A
  • Ophthalmology review for exposure keratopathy if develop pain in the eye
  • If no signs of improvement in paralysis after 3 months then refer urgently to ENT
  • Refer to plastic for more long-standing weakness
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72
Q

Bell’s Palsy

Prognosis

A
  • Most people with Bell’s palsy make a full recovery within 3-4 months
  • If untreated around 15% of patients have permanent moderate to severe weakness
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73
Q

Encephalitis

Features

A
  • Fever
  • Headache
  • Psych symptoms
  • Odd behavior
  • Seizures
  • Vomiting
  • Focal features, e.g. aphasia
  • Peripheral lesions, e.g. cold sores (have no relation to the presence of HSV encephalitis)
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74
Q

Encephalitis

Pathophysiology

A
  • HSV-1 responsible for 95% of cases in adults
  • Typically affects temporal and inferior frontal lobes
  • Primarily the temporal!! (esp if viral)
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75
Q

Encephalitis

Investigations

A

-CSF: lymphocytosis, elevated protein
- PCR for HSV
- Neuroimaging:
- medial temporal and inferior frontal changes, e.g.
petechial haemorrhages
- normal in 1/3rd of patients
- MRI is better
- EEG pattern: lateralised periodic discharges at 2 Hz

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76
Q

Encephalitis

Management

A
  • IV aciclovir should be started in all cases

The prognosis is dependent on whether aciclovir is commenced early. If treatment is started promptly the mortality is 10-20%. Left untreated the mortality approaches 80%

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77
Q

Wernicke’s encephalopathy

Pathophysiology

A
  • Neuropsychiatric disorder
  • Caused by thiamine (B1) deficiency
  • Commonly seen in alcoholics
  • Rarer causes: persistent vomiting, stomach cancer, dietary deficiency
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78
Q

Wernicke’s encephalopathy

Features

A

Classic triad:

  • Nystagmus/ophthalmoplegia
  • Ataxia
  • Confusion/altered GCS

Also peripheral sensory neuropathy

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79
Q

Wernicke’s encephalopathy

Investigations

A

Petechial haemorrhages occur in a variety of structures in the brain including the mamillary bodies and ventricle walls

  • Decreased red cell transketeloase
  • MRI
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80
Q

Wernicke’s encephalopathy

Management

A

Urgent replacement of thiamine (B1!!!)

  • IV Pabrinex for 5 days
  • Followed by oral thiamine
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81
Q

What is Korsakoff’s syndrome?

A
  • If WE is not treated Korsakoff’s syndrome may develop as well
  • This is termed Wernicke-Korsakoff syndrome and is characterised by the addition of antero- and retrograde amnesia and confabulation in addition to the WE symptoms
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82
Q

Multiple system atrophy

Features

A
  • Parkinsonism
  • Cerebellar signs
  • Autonomic disturbance
    • erectile dysfunction: often an early feature
    • postural hypotension
    • atonic bladder
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83
Q

Multiple sclerosis

Pathophysiology

A
  • Myelin covers the axons of neurones in CNS, helps the electrical impulse move along quicker
  • Made up of Schwann cells in peripheral nervous system and oligodendrocytes in CNS
  • MS typically only affects CNS, so oligodendrocytes
  • Inflammation of the myelin and infiltration of immune cells that cause damage to the myelin
  • Affects the way electrical signals travel along the nerve
  • In early disease, re-myelination can occur and symptoms can resolve. In the later stages of the disease, re-myelination is incomplete and symptoms gradually become more permanent
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84
Q

Multiple sclerosis

Epidemiology

A
  • 3x more common in women
  • Typically presents in young adults (< 50 yrs)
  • Symptoms tend to improve in pregnancy and post-partum period
  • Much more common at higher latitudes (5 times more common than in tropics)
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85
Q

Multiple sclerosis

Genetics

A
  • Monozygotic twin concordance = 30%

- Dizygotic twin concordance = 2%

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86
Q

Multiple sclerosis

Causes

A

Might be influenced by a combination of:

  • Multiple genes
  • Epstein–Barr virus (EBV)
  • Low vitamin D
  • Smoking
  • Obesity
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87
Q

Multiple sclerosis

Features

A

Lesions are disseminated in time and space
75% have significant lethargy

  • Optic neuritis = most common
  • Optic atrophy
  • Eye movement abnormalities
  • Focal weakness: bells palsy, horners syndrome, limb paralysis
  • Focal sensory symptoms: trigeminal neuralgia, numbness, paraesthesia (pins + needles)
  • LHERMITTE’S SIGN: electric shock sensation that travels down the spine and into limbs when flexing neck. It indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column.
  • UTHOFF’S PHENOMENON: worsening of vision following rise in body temperature
  • Ataxia
  • Sexual dysfunction
  • Intellectual deterioration
  • Urinary incontinence

When a patient presents with symptoms of a clinical “attack” of MS, for example, an episode of optic neuritis, there are usually other lesions of demyelination at the same time throughout the central nervous system, most of which are not causing symptoms.

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88
Q

Multiple sclerosis

What features might you see if the 6th cranial nerve (abducens) was affected?

A

6th nerve - double vision

  • Internuclear ophthalmoplegia:
    The internuclear nerve fibres are responsible for coordinating the eye movements to ensure the eyes move together. Ophthalmoplegia means a problem with the muscles around the eye.
  • Conjugate lateral gaze disorder:
    When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct. For example, in a lesion affecting the left eye, when looking to the left, the right eye will adduct (move towards the nose) and the left eye will remain in the middle as the muscle responsible for making it move laterally is not functioning.
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89
Q

Multiple sclerosis

Disease patterns

A

Clinically isolated symptoms:
- MS can not be diagnosed with a single episode as can not be convinced by ‘disseminated in time and space’

Relapsing-remitting (85%):
- Acute attacks (1-2 months) followed by periods of remission

Secondary progressive
- Relapsing-remitting patients who have deteriorated and have developed neurological signs between relapses

Primary progressive (10%)

  • Progressive deterioration from the onset
  • More common in older people
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90
Q

Multiple sclerosis

Investigations

A
  • MRI scans can demonstrate typical lesions
  • Lumbar puncture of CSF
  • Visual evoked potentials
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91
Q

Multiple sclerosis

What would be seen on MRI?

A
  • High signal T2 lesions
  • Periventricular plaques
  • Dawson fingers: often seen on FLAIR images - hyperintense lesions perpendicular to corpus callosum
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92
Q

Multiple sclerosis

What would be seen in CSF?

A
  • Oligoclonal bands (and not in serum)

- Increased intrathecal synthesis of IgG

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93
Q

Multiple sclerosis

How does optic neuritis present?

A
  • Central scotoma. This is an enlarged blind spot.
  • Pain on eye movement
  • Impaired color vision
  • Relative afferent pupillary defect
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94
Q

Multiple sclerosis

What would you see on a visual evoked potential?

A
  • Delayed

- But well preserved waveform

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95
Q

Multiple sclerosis

How do you treat optic neuritis?

A
  • Treated with steroids
  • Recovery takes 2-6 weeks
  • 50% of optic neuritis patients will go on to develop MS within next 15 years
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96
Q

Multiple sclerosis

Management focus

A
  • No cure - focus is on reducing frequency and duration of relapses
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97
Q

Multiple sclerosis

Acute management

A
  • High dose steroids –> IV Methylprednisolone
  • 500mg orally daily for 5 days
  • 1g IV OD for 3–5 days where oral treatment has failed previously or where relapses are severe
  • Shortens the length of acute relapse
  • Do not alter degree of recovery (e.g. whether they return to baseline)
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98
Q

Multiple sclerosis

Disease-modifying drugs

A
  • Beta-interferon can reduce relapse rate
  • Natalizumab (recombinant monoclonal antibody)
  • Fingolimod
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99
Q

Multiple sclerosis

Symptom management

A
  • Exercise to maintain activity and strength
  • Neuropathic pain can be managed with medication such as amitriptyline or gabapentin
  • Depression can be managed with antidepressants such as SSRIs
  • Urge incontinence can be managed with anticholinergic medications such as tolterodine or oxybutynin (although be aware these can cause or worsen cognitive impairment)
  • Spasticity can be managed with baclofen, gabapentin and physiotherapy
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100
Q

Myasthenia gravis

Pathophysiology (of the majority)

A
  • Myasthenia gravis is an autoimmune disorder resulting in insufficient functioning acetylcholine receptors
  • Acetylcholine receptor antibodies (ACh-R) bind to the post-synaptic junction receptors, preventing acetylcholine from stimulating the receptor and triggering muscle contraction
  • As the muscles are used more, more of the receptors get blocked up (worse on exercise/speech etc when muscles are being used)
  • These antibodies also activate the complement system within the neuromuscular junction, leading to damage to cells at the postsynaptic membrane. This further worsens the symptoms.
  • Antibodies to acetylcholine receptors are seen in 85-90% of cases
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101
Q

Myasthenia gravis

Pathophysiology in the minority

A
  • Seen in 15% of cases
  • Two antibodies: One against muscle-specific kinase (MuSK) and antibodies against low-density lipoprotein receptor-related protein 4 (LRP4).
  • MuSK and LRP4 and important proteins for the creation and organisation of the acetylcholine receptor. - Destruction of these proteins by autoantibodies leads inadequate acetylcholine receptors
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102
Q

Myasthenia gravis

Epidemiology

A
  • Affects men and women at different ages
  • Typically women < 40 yrs and men > 60 yrs
  • More common in women
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103
Q

Myasthenia gravis

A key association

A

THYMOMA (tumour of thymus gland)

  • 10-20% of patients with myasthenia gravis have a thymoma
  • 20-40% of patients with a thymoma develop myasthenia gravis
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104
Q

Myasthenia gravis

Other associations

A
  • Autoimmune disorders - pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
  • Thymic hyperplasia in 50-70%
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105
Q

Myasthenia gravis

Features

A
  • DIPLOPIA - extraocular muscle weakness:
  • Proximal muscle weakness: face, neck, limb-girdle
  • PTSOSIS
  • Dysphagia
  • Fatigue in jaw when chewing
  • Slurred speech
  • Progressive weakness with repetitive movements
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106
Q

Myasthenia gravis

Examination

A
  • Repeated blinking will exacerbate ptosis
  • Prolonged upward gazing will exacerbate diplopia on further eye movement testing
  • Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
  • Check for a thymectomy scar.
  • Test the forced vital capacity (FVC).
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107
Q

Myasthenia gravis

Investigations

A
  • Test for antibodies (ACh-R, MuSK, LRP4)
  • CT or MRI of thymus gland
  • Normal CK
  • Single fibre electromyography: high sensitivity (92-100%)
  • Edrophonium test / tensilon test:
    • IV edrophonium chloride or neostigmine is given
    • Blocks breakdown of existing acetylcholine
    • Briefly and temporarily relieves weakness
    • Establishes a diagnosis
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108
Q

Myasthenia gravis

Long-term management

A
  • Long-acting acetylcholinesterase inhibitors (e.g. pyridostigmine)
  • Immunosuppressions (Pred or Azathioprine)
  • Thymectomy if required
  • Monoclonal antibodies - rituximab (if other Tx not effective)
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109
Q

Myasthenia gravis

What is a myasthenic crisis

A
  • Acute severe worsening of symptoms
  • Can be life threatening
  • Often triggered by another illness, e.g. RTI
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110
Q

Myasthenia gravis

Management of a crisis

A
  • Plasmapheresis
  • IV immunoglobulins
  • May need NIV with BiPAP or full intubation and ventilation
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111
Q

Myasthenia gravis

Drugs that may exacerbate it

A
  • Penicillamine
  • Quinidine, procainamide
  • Beta-blockers
  • Lithium
  • Phenytoin
  • Antibiotics: gentamicin, macrolides, quinolones,
  • Tetracyclines
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112
Q

Myasthenia gravis

Something to consider with anaesthesia

A

MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses
E.g. Suxamethonium

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113
Q

Brain abscess

Causes

A
  • Extension of sepsis from middle ear or sinuses
  • Trauma or surgery to the scalp
  • Penetrating head injuries
  • Embolic events from endocarditis
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114
Q

Brain abscess

Presentation

A
  • Headache (dull, persistent)
  • Fever (though may be absent and not usually the pyrexia seen in other abscesses)
  • Focal neurology, e.g. oculomotor nerve palsy or abducens nerve palsy (2ndry to raised ICP)
  • Nausea, papilloedema, seizures
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115
Q

Brain abscess

Investigations

A
  • CT
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116
Q

Brain abscess

Management

A
  • IV antibiotics –> CEPHALOSPORIN and METRONIDAZOLE
  • ICP –> Dexamethasone
  • Surgery: craniotomy and abscess cavity is debrided
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117
Q

Cerebral palsy

Definition

A
  • Disorder of movement and posture due to NON-PROGRESSIVE lesion of the motor pathways in the developing brain
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118
Q

Cerebral palsy

Causes

A
  • Antenatal (80%), e.g. cerebral malformation and congenital infection (rubella, toxoplasmosis, CMV), trauma during pregnancy
  • Intrapartum (10%): birth asphyxia/trauma, pre-term birth
  • Postnatal (10%): intraventricular haemorrhage, meningitis, head-trauma, severe neonatal jaundice
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119
Q

Cerebral palsy

Presentation

A
  • HAND PREFERENCE BEFORE 18 MONTHS
  • Abnormal tone in early infancy (increased or decreased)
  • Delayed motor milestones
  • Abnormal gait
  • Feeding difficulties
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120
Q

Cerebral palsy

Associated non-motor problems

A
  • Learning difficulties (60%)
  • Epilepsy (30%)
  • Squints (30%)
  • Hearing impairment (20%)
121
Q

Cerebral palsy

Classifications

A

Spastic (70%):

  • Also known as pyramidal CP
  • Hemiplegia, diplegia or quadriplegia
  • Increased tone from damage to UMNs

Dyskinetic:

  • Also known as extrapyramidal CP
  • Damage to basal ganglia and substantia nigra
  • Athetoid movements and oro-motor problems

Ataxic:

  • Damage to cerebellum
  • Typical cerebellar signs

Mixed:
- A mix of some or all of the above

122
Q

Cerebral palsy

Classic OSCE presentation

A
  • They will have signs of an upper motor neurone lesion, with good muscle bulk, increased tone, brisk reflexes and slightly reduced power.
  • Power may be normal.
  • Look for athetoid movements that indicate extrapyramidal (basal ganglia) involvement.
  • Test for coordination to look for cerebellar involvement.
123
Q

Cerebral palsy

Differentials for UMN lesions

A
  • Acquired brain injury

- Tumour

124
Q

Cerebral palsy

Management

A
  • MDT approach: physio, OT, SALT, dieticians
  • Spasticity: oral diazepam, oral/intrathecal baclofen, botulinum toxin type A, orthopaedic surgery
  • Anticonvulsants
  • Analgesia
125
Q

Essential tremor

Genetics

A
  • Autosomal dominant
126
Q

Essential tremor

Epidemiology

A
  • Most common in older age
127
Q

Essential tremor

Features

A
  • FINE tremor
  • Affecting all the voluntary muscles
  • Symmetrical
  • More prominent on voluntary movement
  • Worse if arms outstretched
  • Worse when tired, stressed, after caffeine
  • Improved by alcohol and rest (absent during sleep)
  • Most common cause of head tremor (titubation)
  • May also see jaw tremor and vocal tremor
128
Q

Essential tremor

Management

A
  • Propanolol = 1st line (non-selective beta-blocker)

- Primidone (barbiturate anti-epileptic)

129
Q

Chronic fatigue syndrome

Epidemiology

A
  • More common in females

- Past psych Hx not shown to be RF

130
Q

Chronic fatigue syndrome

Diagnosis

A
  • Diagnosed after at least 4 months of disabling fatigue affecting mental and physical function more than 50% of the time
  • In absence of other disease which may explain symptoms
131
Q

Chronic fatigue syndrome

Features

A

Fatigue = central features

  • Sleep problems - insomnia, hypersomnia, unrefreshing sleep, disturbed sleep cycle
  • Muscle/joint pain
  • Headaches
  • Painful lymph nodes without enlargement
  • Sore throat
  • Cognitive dysfunction, e.g. difficulty thinking, inability to concentrate, impairment of short-term memory
  • Physical or mental exertion makes symptoms worse
  • General malaise or ‘flu-like’ symptoms
  • Dizziness
  • Nausea
  • Palpitations
132
Q

Chronic fatigue syndrome

Investigations

A

Perform a large number of screening bloods to exclude other pathology:

  • FBC
  • U&Es
  • LFTs
  • Glucose
  • TFTs
  • ESR
  • CRP
  • Calcium
  • CK
  • Ferritin (only in young people)
  • Coeliac screen
  • Urinlaysis
133
Q

Chronic fatigue syndrome

Management

A
  • CBT
  • Graded exercise therapy (formal supervised programme)
  • ‘Pacing’ (organising activities to avoid tiring)
  • Low-dose amitriptyline
  • Referral to pain management clinic
134
Q

Raised ICP

Normal ICP?

A

7 - 15 mmHg in adults in supine position

135
Q

Raised ICP

Causes

A
  • Idiopathic intracranial hypertension
  • Traumatic head injuries
  • Infection, e.g. meningitis
  • Tumours
  • Hydrocephalus
  • Brain abscesses
136
Q

Raised ICP

Features

A
  • Headache - worse on bending down, coughing etc.
  • Vomiting
  • Reduced GCS
  • Papilloedema
  • Cushing’s triad
137
Q

Raised ICP

What is Cushings triad?

A
  • Widening pulse pressure
  • Bradycardia
  • Irregular breathing
138
Q

Raised ICP

Investigations

A
  • CT/MRI to investigate the cause
  • Invasive ICP monitoring
    • catheter placed in lateral ventricles to monitor the pressure
    • may also be used to collect CSF samples and drain small amounts of fluid to relieve pressure
139
Q

What is the cut off to determine if further treatment is required to raised ICP?

140
Q

Raised ICP

Management

A
  • Treat underlying cause
  • Head elevation to 30 degrees
  • IV mannitol
  • Controlled hyperventilation
  • Removal of CSF
141
Q

What is controlled hyperventilation and what is its goal in raised ICP? What is the issue with it?

A
  • Aim is to reduce pCO2 → vasoconstriction of the cerebral arteries → reduced ICP
  • Leads to rapid, temporary lowering of ICP.
  • Caution needed as may reduce blood flow to already ischaemic parts of the brain
142
Q

Methods for removing CSF in raised ICP?

A
  • Drain from intraventricular monitor
  • Repeated LP (e.g. in idiopathic intracranial hypertension)
  • Ventriculoperitoneal shunt (e.g. for hydrocephalus)
143
Q

Febrile convulsions

Definition

A
  • Seizures provoked by fever in otherwise normal children
144
Q

Febrile convulsions

Epidemiology

A
  • Occur between 6 months and 5 years

- Seen in 3% of children

145
Q

Febrile convulsions

Features

A
  • Usually occur early on in viral infection as temp rises rapidly
  • Usually brief, lasting < 5 mins
  • Most commonly tonic-clonic
146
Q

Febrile convulsions

Types

A

Simple:

  • < 15 mins
  • Generalised seziure
  • Typically no recurrence within 24 hrs
  • Should be complete recovery withing 1 hour

Complex:

  • 15-30 minutes
  • Focal seizure
  • May reoccur within 24 hrs

Febrile status epilepticus:
- > 30 minutes

147
Q

Febrile convulsions

Management

A
  • Admit to paeds
  • Analgesia - Paracetamol (though do not decrease likelihood of recurrence)
  • Place in safe place, e.g. carpeted floor with pillow under head
  • Place in recovery position
  • CALL 999 IF LASTS > 5 MINS
  • If recurrences, try teaching parents how to use rectal diazepam or buccal midazolam
148
Q

Febrile convulsions

Prognosis

A
  • Typically do not cause lasting damage

- One in three will have another febrile seizure

149
Q

Febrile convulsions

Risk of developing epilepsy?

A
  • 1.8% for the general population
  • 2-7.5% after a simple febrile convulsion (depending on other RFs present)
  • 10-20% after a complex febrile convulsion
150
Q

Muscular dystrophies

Pathophysiology

A
  • X-linked recessive
  • Mutation in gene encoding dystrophin, dystrophin gene on Xp21
  • Dystrophin = part of large membrane associated protein in muscle which connects the muscle membrane to actin, part of the muscle cytoskeleton
151
Q

Duchenne muscular dystrophy

Pathophysiology

A
  • FRAMESHIFT MUTATION –> resulting in 1 or both of the binding sites being lost –> severe form
152
Q

Becker muscular dystrophy

Pathophysiology

A
  • NON-FRAMESHIFT INSERTION in dystrophin gene –> both binding sites are preserved –> milder form
153
Q

Duchenne muscular dystrophy

Presentation

A
  • Progressive proximal muscle weakness from 5 years
  • Calf pseudohypertrophy
  • GOWER’S SIGN: child used arms to stand up from squatted position
  • 30% have intellectual impairment
154
Q

Becker muscular dystrophy

Presentation

A
  • Develops after age of 10 yrs

- Intellectual impairment is much less common than duchennes

155
Q

Duchenne muscular dystrophy

Investigations

A
  • Raised CK

- Genetic testing! (now replaced muscle biopsy)

156
Q

Duchenne muscular dystrophy

Management

A
  • Largely supportive

- No effective Tx

157
Q

Duchenne muscular dystrophy

Prognosis

A
  • Most can not walk by 12 yrs

- Typically survive until 25-30 yrs

158
Q

Duchenne muscular dystrophy

Association

A

Dilated cardiomyopathy

159
Q

List 9 X-linked recessive conditions? (not all neuro)

A
  • Androgen insensitivity syndrome
  • Becker muscular dystrophy
  • Colour blindness
  • Duchenne muscular dystrophy
  • G6PD deficiency
  • Haemophilia A,B
  • Hunter’s disease
  • Lesch-Nyhan syndrome
  • Nephrogenic diabetes insipidus
160
Q

Which tumours most commonly spread to the brain?

A
  • Lung (most common)
  • Breast
  • Bowel
  • Skin (namely melanoma)
  • Kidney
161
Q

Supply of facial nerve

A

Supply = face, ear, taste, tear

  • Face: muscles of facial expression
  • Ear: nerve to stapedius
  • Taste: ANTERIOR 2/3rds of tongue
  • Tear: parasympathetic fibres to lacrimal glands and salivary glands
162
Q

Causes of bilateral facial nerve palsy

A
  • Sarcoidosis
  • Guillain-Barre syndrome
  • Lyme disease
  • Bilateral acoustic neuromas (as in neurofibromatosis type 2)
  • Bell’s palsy is relatively common so it accounts for up to 25% of cases of bilateral palsy, but this represents only 1% of total Bell’s palsy cases
163
Q

Berry aneurysm

Associations

A
  • Adult polycystic kidney disease
  • Ehlers-Danlos syndrome
  • Coarctation of the aorta
164
Q

Subdural haemorrhage

Causes

A
  • Acute = trauma to brain
  • Chronic = primarily in elderly or alcoholics (brain atrophy -> tension on cerebral vein), or shaken baby syndrome (fragile bridging veins)
165
Q

Subdural haemorrhage

Treatment

A
  • Conservative Tx if small or no neuro deficit

- Surgical decompression with burr holes if confusion, neurological deficit or severe imaging findings

166
Q

Subdural haemorrhage

Presentation

A
  • Insidious onset of confusion
  • Neuro deficit
  • Fluctuating consciousness levels
167
Q

Subdural haemorrhage

CT findings

A
  • Crescent shape

- Not limited by suture lines

168
Q

Extradural haemorrhage

Causes

A
  • Most often laceration of MIDDLE MENINGEAL ARTERY

- Often due to temporal head injury

169
Q

Extradural haemorrhage

Presentation

A
  • Fall in consciousness
  • Followed by a LUCID INTERVAL
  • Then second fall in consciousness as expanding haematoma and brain herniation
170
Q

Extradural haemorrhage

CT findings

A
  • Binconvex (lentiform) hyperdense collection

- Limited by suture lines

171
Q

Extradural haemorrhage

Management

A
  • If no neuro deficit -> cautious clinical and radiological observation
  • Definitive Tx = craniotomy and evacuation of haematoma
172
Q

SAH

Complications

A
  • Rebleeding (10%, most common in 1st 12 hrs, repeat CT, high mortality)
  • Cerebral ischaemia due to vasospasm (7-14 days after)
  • Hydrocephalus
  • Seizures
  • Hyponatraemia (due to SIADH)
173
Q

SAH

Tx

A
  • Prompt Tx within 24 hrs
  • Maintain cerebral perfusion (SBP of 160) and bed rest until Tx available
  • Nimodipine (CCB) for 21 days to reduce vasospasm risk
  • Endovascular coiling!!
174
Q

SAH

Investigations

A
  • CT
  • LP if negative CT, 12 hrs after, see xanthochromia
  • Cerebral angiography after diagnosis to find causative vascular lesion
175
Q

Define epilepsy

A

Paroxysmal changes in behaviour, sensation or cognitive processes that are caused by EXCESSIVE, HYPERSYNCHRONOUS, NEURONAL DISCHARGES in the brain

176
Q

Tx for partial/focal seizures

A
  • First-line = CARBAMAZEPINE

- 2nd = lamotrigine, sodium valproate, oxcarbamazepine, topiramate

177
Q

Tx for primary generalised seizures

A

First-line = SODIUM VALPROATE

  • Avoid in pregnancy –> Use lamotrigine
  • others: topiramate, carbamazepine
  • AVOID carbamazepine in tonic/atonic/myoclonic
178
Q

Epilepsy and driving

A
  • Generally cannot drive for 6 months following a single seizure if unprovoked/no structural imaging changes
  • For patients with established epilepsy or multiple unprovoked seizures they must be fit free for 12 months before being able to drive
  • When epilepsy meds are being withdrawn can not drive for 6 months after last dose
  • If not seizures for 5 years generally a full license is restored
179
Q

Epilepsy and pregnancy and breastfeeding

A
  • Lamotrigine and carbamazepine are generally considered safe in pregnancy
  • Breast feeding is generally considered safe for those on antiepileptics
  • It is advised that pregnant women taking phenytoin are given vitamin K in the last month of pregnancy to prevent clotting disorders in the newborn
180
Q

Define status epilepticus

A
  • Single seizure lasting > 5 mins

- OR >= 2 seizures within a 5-min period without returning to normal between

181
Q

Status epilepticus

Management

A
  • ABCDE
  • 1st line in community = PR diazepam or rectal midazolam
  • 1st line in hospital = IV lorazepam
  • Repeat once after 10-20 min
  • if ongoing –> phenytoin or phenobarbital infusion
  • If no response within 45 mins from onset -> general anaesthesia
182
Q

Temporal lobe features of seizures

A
  • Lip-smacking
  • Chewing
  • Fumbling
  • Grabbling
  • Abdo rising sensation or pain
  • Hallucinations
  • Dysphasia
  • Impaired awareness
  • No recollection after
183
Q

Frontal lobe features of seizures

A
  • Assymetrical posturing - extending one arm/leg then another
  • Peddling leg movements
  • Jacksonian march
  • Do NOT lose awareness
  • Post-ictal weakness (Todd’s paresis)
184
Q

Parietal lobe features of seizures

A
  • Paraesthesia
185
Q

Occipital lobe features of seizures

A
  • Floaters

- Flashes

186
Q

Parkinsons

Pathophysiology

A
  • Degeneration of dopaminergic neurons in the SUBSTANTAI NIGRA
  • Decreased dopamine supply to striatum –> motor symptoms
187
Q

Parkinsons

Presentation

A

One side is ALWAYS worse than the other

Cardinal triad:

  • Bradykinesia
  • Resting tremor
  • Rigidity (cogwheel)
  • Depression in 40%
  • Postural instability and hypotension (due to autonomic failure)
188
Q

Parkinsons

Investigations

A
  • Mostly based on history and physical exam
  • SPECT: Lewy bodies
  • Loss of dark substantia nigra
  • DaTSCAN: poor dopamine supply to striatum
189
Q

Describe the tremor in parkinsons

A
  • Most marked at rest
  • Worse when tired or stressed
  • Improves with voluntary movement
  • Typically ‘pill-rolling’
190
Q

Differentiating from drug-induced parkinsons

A

Drug-induced:

  • Motor symptoms are generally rapid onset and bilateral
  • Rigidity and resting tremor are uncommon
191
Q

What might make you reconsider a Parkinsons diagnosis?

A
  • Early incontinence
  • Early dementia
  • Symmetrical
  • Early falls
  • Diplopia (progressive supranuclear palsy)
192
Q

Parkinson’s disease

First-line Tx
MoA
SEs

A
  • Levodopa
  • Given with dopa-decarboxylase inhibitor to stop it being converted into dopamine in peripheral nervous system
  • MoA: synthetic dopamine

SEs:

  • Dyskinesia
  • Dry mouth
  • Anorexia
  • Palpitations
  • Postural hypotension
  • Psychosis
  • Drowsiness
193
Q

Parkinson’s disease

Dopamine agonists

Examples
MoA
Who given to?
SEs?

A
  • Ropinirole, cabergoline, bromocriptine and pramipexole
  • MoA: Acts directly on post-synaptic receptors
  • First-line for < 60 yrs
  • SEs: gambling, hypersexuality
194
Q

Parkinson’s disease

COMT

Examples
MoA

A

COMT: Entacapone
MAO-B: Rasagaline, Selegiline

MoA: Prevent breakdown of dopamine by Catechol-O-Methyl and Monoamino-oxidase in synaptic cleft

195
Q

Parkinson’s medication risks

A

risk of acute akinesia or neuroleptic malignant syndrome if medication is not taken/absorbed (for example due to gastroenteritis) and advise against giving patients a ‘drug holiday’ for the same reason

196
Q

Drug-induced parkinsonism Tx

A

Antimuscarinics:

  • Procyclidine
  • Benzotropine
  • Trihexyphenidyl (benzhexol)
197
Q

Common meningitis causative organisms and their morphology

A
  • Nisseria meningitidis (gram negative diplococcus)
  • Streptococcus pneumoniae (gram positive diplococcus)
  • Listeria monocytogenes (in immunocompromised and babies, gram positive bacilli)
198
Q

Syringomyelia

Causes

A
  • CHIARI MALFORMATION = strong association
  • Trauma
  • Tumours
  • Idiopathic
199
Q

Syringomyelia

Definition

A

A collection of CSF fluid within the spinal cord

- Compression of the spinothalamic tract fibres decussating in the anterior white commissure of the spine

200
Q

Syringomyelia

Features

A

SLOWLY PROGRESSIVE NEURO SYMPTOMS

  • Cape-like
  • Loss of sensation to temp but preservation of light touch, proprioception and vibration
  • E.g. burn hand without realising
  • Spastic weakness
  • Neuropathic pain
  • Upgoing plantars
  • Sometimes autonomic features
201
Q

Syringomyelia

Investigations

A
  • Full spine MRI to exclude tethered cord or tumour

- Brain MRI to exclude Chiari malformation

202
Q

Syringomyelia

Management

A
  • Treat cause of syrinx

- If persistent –> shunt can be placed

203
Q

How would an alcohol withdrawal seizure present

A

s a generalized seizure and involve loss of consciousness

204
Q

How would a psychogenic non-epileptic seizure present?

A

A psychogenic non-epileptic seizure (previously called a pseudoseizure) should be considered in a patient who remains conscious during whole-body convulsions, exhibits no post-ictal state and can remember what happened

205
Q

Typical features of post-LP headache

A
  • Usually develops within 24-48 hours following LP but may occur up to one week later
  • May last several days
  • Worsens with upright position
  • Improves with recumbent position
206
Q

Tx of post-LP headache

A
  • Supportive initially (analgesia, rest)
  • If pain continues for more than 72 hours then specific treatment is indicated, to prevent subdural haematoma
  • Treatment options include: blood patch, epidural saline and intravenous caffeine
207
Q

Typical presentation of neurogenic thoracic outlet syndrome

A
  • Muscle wasting of the hands
  • Numbness and tingling
  • Possibly autonomic symptoms

Subclavian vein compression leads to painful diffuse arm swelling with distended veins

Subclavian artery compression leads to painful arm claudication and in severe cases, ulceration and gangrene

208
Q

Neurogenic thoracic outlet syndrome

Definition

A

A disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet

209
Q

Neurogenic thoracic outlet syndrome

Epidemiology

A

Typically young thin women possessing long neck and drooping shoulders

210
Q

Neurogenic thoracic outlet syndrome

Causes

A
  • Usually Hx of neck trauma (acute or repeated stress)
  • Anatomical abnormalities:
    • Osseous, e.g. CERVICAL RIB
    • Soft tissue, e.g. scalene muscle hypertrophy,
      anomalous bands
211
Q

Which eye defect is most commonly seen in idiopathic intracranial hypertension? How would this present?

A

6th nerve palsy (abducens)
Unable to abduct –> affected eye is adducted
Can sometimes get a third nerve palsy (down and out if herniation)

212
Q

Meningitis

Signs

A
  • Hangover-like headache
  • Leg pain
  • Cold hands and feet
  • Abnormal skin colour
  • Meningism: neck stiffness, photophobia, Kernigs +ve
  • Low GCS
  • Papilloedema
  • Brudinski’s sign
  • Petechial rash (NOT in viral)
213
Q

Meningitis

What is Kernigs sign

A

KERNIG’S SIGN

- Hip at 90 degrees, can’t straighten leg > 135 without pain

214
Q

Meningitis

What is Burdinskis sign

A

BRUDZINSKI’S SIGN

- Flex neck –> patient compromised by flexing hips and knees

215
Q

Meningitis

Investigations

A
  • CT head
  • LP if not raised ICP
    • High opening pressure
    • Send CSF for gram stain
  • Fundoscopy for papilloedema
216
Q

Meningitis

CSF findings

A

Bacterial:

  • High neutrophils
  • High protein
  • Low glucose

Viral:

  • High lymphocytes
  • High/normal protein
  • Normal glucose
217
Q

Meningitis

Management

A

Community –> IM/IV benzylpenicillin

  • CEFOTAXIME
    + Amoxicillin if < 3 months, > 50 yrs or immunocompromised to cover for listeria
    + Dexamethasone
  • If viral –> Acylovir

Do NOT give Dex if:

  • Septic shock
  • Meningococcal septicemia
  • Immunocompromised
  • Meningitis following surgery
218
Q

Meningitis

Prophylaxis

A
  • For close contacts within 7 DAYS before onset
  • First-line = Ciprofloxacin
  • 2nd line = Rifampicin (NOT pregnancy)
219
Q

Encephalitis

Causes

A
  • HERPES SIMPLEX VIRUS 1 + 2
  • VZV, HIV
  • Bacterial
  • Non-infectious prodrome: immunocompromised, hypoglycaemia, hepatic encephalopathy, DKA, drugs
220
Q

Encephalitis

Presentation

A
  • Odd behaviour
  • COnfusion
  • Fever
  • Lethargy
  • Headache
  • SEIZURES
  • History of animal/travel bite
221
Q

Encephalitis

Investigations

A
  • LP: raised protein and lymphocytes, low or normal glucose
  • Contrast CT - white areas of enhancement
    VIRAL HAS TEMPORAL CHANGES
222
Q

Encephalitis

Management

A

ACYCLOVIR within 30 mins of admission for 2 weeks

223
Q

Motor neuron disease

Pathophysiology

A
  • Cluster of major degenerative diseases
  • Degeneration of UPPER AND LOWER motor neurons
  • Sensory neurons are spared !!
  • Does NOT affect ocular muscles
224
Q

Motor neuron disease

Clues towards a diagnosis

A
  • FASCICULATIONS
  • Absence of sensory signs
  • Does NOT affect ocular muscles
  • Mixture of LMN and UMN signs
  • Wasting of small hand muscles
  • No cerebellar signs
  • Abdominal reflexes are usually preserved
  • Sphincter dysfunction if present is a late feature
225
Q

Motor neuron disease

Investigations

A

Clinical diagnosis usually

  • Nerve conduction studies would be NORMAL (help exclude neuropathy)
  • Electromyography: reduced number of action potentials with increased amplitude
  • MRI to exclude cervical cord compression and myelopathy
226
Q

Motor neuron disease

Types

A

ALS (50%) - amyotrophic lateral sclerosis
- LMN in arms and UMN in legs

Primary lateral sclerosis:

  • UMN signs only
  • Loss of Betz cells in motor cortex

Progressive muscular atrophy:

  • LMN signs only
  • Anterior horn cell lesion ONLY
  • Affects distal muscle before proximal
  • Best prognosis

Progressive bulbar palsy:

  • Palsy of tongue, muscle of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
  • Cranial nerves IX - XII (9-12)
  • Worst prognosis
227
Q

MND

Hereditary ALS
Gene and codes for what?

A

Chromosome 21 if familial (codes for superoxide dismutase)

228
Q

MND

Progressive bulbar palsy

A
  • Palsy of tongue, muscle of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
  • Cranial nerves IX - XII (9-12)
  • Jaw jerk = normal or absent
  • Speech = quiet, hoarse, nasally
  • Worst prognosis
229
Q

MND

Poor prognostic factors

A
  • Bulbar palsy or bulbar onset of ALS
  • Increased age
  • Low FVC
230
Q

MND

Management

A
  • Riluzole = anti glutaminergic –> prolongs life by about 3 months. Mainly used in ALS.
  • Resp: BIPAP at night, survival benefit of about 7 months
231
Q

Alzheimer’s dementia

Management
1st line treatment?

A

Acetylcholinesterase inhibitors

  • Donepezil
  • Galantamine
  • Rivastigmine
232
Q

Alzheimer’s dementia

2nd line management, MoA and indications

A

MEMANTINE

  • MoA: NMDA antagonist - binds to glutamate site on NMDA receptor to block glutamate action
  • Moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
  • As an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
  • Monotherapy in severe Alzheimer’s
233
Q

Donezepil

CI and SE

A
  • Relatively contraindicated in patients with bradycardia

- Adverse effects include insomnia

234
Q

Dementia

Tx for self-harm risk/agitation etc

A
  • Antipyschotics
235
Q

Normal pressure hydrocephalus

Presentation

A
  • Urinary incontinence
  • Gait abnormality
  • Dementia/bradyphrenia (mental slowing)
236
Q

Normal pressure hydrocephalus

Investigations

A

Hydrocephalus with ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement

237
Q

Normal pressure hydrocephalus

Management

A
  • Ventriculoperitoneal shunting

- Complications = seizures, infection, intracerebral haemorrhages

238
Q

Hydrocephalus

Presentation

A
  • Headache (typically worse in the morning, when lying down and during valsalva)
  • Nausea and vomiting
  • Papilloedema
  • Coma (in severe cases)
239
Q

Hydrocephalus

Pathophysiology

A
  • Excessive volume of CSF in ventricular system of brain

- Caused by imbalance between CSF production and absorption

240
Q

Hydrocephalus

Presentation in children

A
  • Failure of upward gaze
  • Sunsetting eyes
  • Due to compression of superior colliculus of midbrain
241
Q

Hydrocephalus causes

A

Obstructive:

  • Tumours
  • Acute haemorrhage (SAH/intraventricular)
  • Developmental abnormalities (e.g. aqueduct stenosis)

Non-obstructive:

  • Increased production, e.g. choroid plexus tumour
  • Failure of resorption at arachnoid granulations (meningitis, post-haemorrhage)
242
Q

Hydrocephalus

Investigations

A
  • CT head
  • MRI if suspected underlying lesion
  • LP
243
Q

Hydrocephalus

Managementidi

A
  • External ventricular drain (ECD) in acute, severe, typically in RIGHT lateral ventricle
  • VPS is a long-term CSF diversion that drains CSF into peritoneum
  • If obstructive may require surgery to remove obstruction
244
Q

Hydrocephalus

Caution in obstructive

A

Do NOT do an LP

245
Q

Idiopathic intracranial HTN

Risk factors

A
  • Obesity
  • Female sex
  • Pregnancy
  • Drugs:
    • combined oral contraceptive pill
    • steroids
    • tetracyclines
    • vitamin A
    • lithium
246
Q

Idiopathic intracranial HTN

Features

A
  • Headache
  • Blurred vision
  • Papilloedema
  • Enlarged blind spot
  • Sixth nerve palsy
247
Q

Idiopathic intracranial HTN

Management

A
  • Weight loss
  • DIURETICS –> ACETAZOLAMIDE
  • Topiramate can be used and helps weight loss
  • Repeated LPs
  • Surgery: optic nerve sheath decompression and fenestration may be needed to prevent damage to the optic nerve. A lumboperitoneal or ventriculoperitoneal shunt may also be performed to reduce intracranial pressure
248
Q

Degenerative cervical myelopathy

Presentation

A
  • Pain (neck, limbs)
  • Loss of motor function (holding fork, doing up buttons, arm/leg stiffness/weakness)
  • Loss of sensory function - numbness
  • Loss of autonomic function (urinary incontinence)
  • Hoffman’s sign: reflex test for cervical myelopathy. Flick one finger of patients hand. Positive = reflex twitching of other fingers on same hand.
249
Q

Degenerative cervical myelopathy

Investigations

A
  • MRI of cervical spine

- May show disc degeneration and ligament hypertrophy, with accompanying cord signal change

250
Q

Degenerative cervical myelopathy

Management

A
  • Urgent referral to spinal surgery

- Decompressive surgery

251
Q

Cauda equina syndrome

Causes

A
  • Most common = central disc prolapse, typically at L4/L5 or L5/S1
  • Tumours
  • Infection: abscess, discitis
  • Trauma
  • Haematoma
252
Q

Cauda equina syndrome

Features

A
  • Low back pain
  • Bilateral sciatica
  • Reduced sensation/pins-and-needles in perianal area
  • Decreased anal tone
  • Urinary dysfunction
253
Q

Cauda equina syndrome

Investigations

A
  • Urgent MRI
254
Q

Cauda equina syndrome

Management

A

Surgical decompression

255
Q

MRC power score

A

0: No contraction
1: Flicker of trace of contraction
2: Active movement with gravity eliminated
3: Active movement against gravity
4: Active movement against gravity and resistance
5: Normal power

256
Q

GCS score

A

Eyes 4

1: No opening
2: Open to pain
3: Open on demand
4: Open spontaneously

Verbal 5

1: No response
2: Incomprehensible sounds
3: Inappropriate words
4: Confused
5: Orientated

Motor 6

1: No movement
2: Extension
3: Abnormal flexion
4: Flexion withdrawal from pain
5: Moves to localised pain
6: Obeys commands

257
Q

What is autonomic dysreflexia? Features?

A
  • Sympathetic overdrive
  • Flushing
  • Sweating
  • HTN
258
Q

Which spinal cord lesions can cause autonomic dysreflexia?

A

Above T6 spinal level

259
Q

Charcot Marie Tooth disease

Features

A
  • History of freq sprained ankles
  • Foot drop
  • High arched feet
  • Hammer toes
  • Distal muscle weakness
  • Distal muscle atrophy
  • Hyporeflexia
  • Stork leg deformity
260
Q

Subacute combined degeneration of the cord

Cause

A
  • B12 deficiency
  • Replacing folate without vitamin B12 can precipitate subacute combined degeneration of the cord in a patient who is vitamin B12 deficient.
  • Always ensure vitamin B12 levels are checked (and replenished) before giving folate for a macrocytic anaemia
  • Dorsal columns and lateral corticospinal tracts due to vitamin B12 deficiency - joint position and vibration sense lost first then distal paraesthesia
  • UMN signs typically develop in the legs, classically extensor plantars, brisk knee reflexes, absent ankle jerks
261
Q

Epilepsy

Infantile spams/Wests syndrome

A
  • Flexion of head, trunk, limbs
  • Hypsarrhythmia on EEG
  • Progressive mental handicap
  • Poor prognosis
262
Q

Epilepsy

Benign Rolandic epilepsy

A
  • Focal symptoms including paraesthesia on one side of child face or mouth
  • ‘Fizzy’ or ‘buzzing’
  • Twitching
  • Usually on waking up
263
Q

Epilepsy

Juvenile myoclonic epilepsy

A
  • Adolescence
  • Infrequent generalised seizures
  • Often in morning/following sleep deprivation
  • Daytime absences
  • Sodium valproaete
264
Q

Petit mal absence seizures

A
  • Onset 4-8 yrs
  • Duration few-30 secs; no warning, quick recovery; often many per day
  • EEG: 3Hz generalized, symmetrical
  • Sodium valproate, ethosuximide
  • Good prognosis: 90-95% become seizure free in adolescence
265
Q

How can you differentiate between pseudoseizures and generalized seizures?

A
  • Elevated serum prolactin 10 to 20 minutes after an episode = true epileptic seizure
  • Tongue biting = true epileptic seizure
266
Q

Gillian-Barre Syndrome

Features

A
  • May start as back/leg pain initially
  • Progressive peripheral polyneuropathy
  • Hyporeflexia
  • Ascending
  • Some mild sensory symptoms
  • Hx of gastroenteritis (classically Campylobacter jejuni)
  • Resp muscle weakness
  • Cranial nerve involvement: diplopia, bilateral facial nerve palsy, oropharyngeal weakness
  • Autonomic involvement
267
Q

Guillain-Barre Syndrome

Investigations

A
  • LP: rise in protein, normal WCC
  • Nerve conduction studies: decreased motor nerve conduction velocity, also prolonged distal motor latency, increased F wave latency
268
Q

Guillain-Barre Syndrome

Management

A
  • IV immunoglobulins
  • Plasma exchange (alternative to IV IG)
  • Supportive care
  • VTE prophylaxis (pulmonary embolism is a leading cause of death)
269
Q

Guillain-Barre Syndrome

Prognosis

A

80% will fully recover
15% will be left with some neurological disability
5% will die

270
Q

Guillain-Barre Syndrome

Pathophysiology

A
  • Molecular mimicry
  • B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection
  • These antibodies also match proteins on the nerve cells
  • They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon.
271
Q

What test might you do in a <55 yr old with unknown cause of stroke?

A

Autoimmune and thrombophilia screening!

272
Q

Migraine

Acute Tx

A
  • Oral triptan and an NSAID
    OR
  • Oral triptan and paracetamol

Can use nasal triptan if 12-17 yrs``

273
Q

Migraine

Prophylaxis

A
  • Topiramate

- Propanolol

274
Q

Parkinsons meds if NBM

A

If a patient with Parkinson’s disease cannot take levodopa orally, they can be given a dopamine agonist patch as rescue medication to prevent acute dystonia

275
Q

Syncope and driving

A
  • Simple faint: no restriction
  • Single episode, explained and treated: 4 weeks off
  • Single episode, unexplained: 6 months off
  • Two or more episodes: 12 months off
276
Q

Neuroleptic malignant syndrome

Features

A
  • pyrexia
  • muscle rigidity
  • autonomic lability: typical features include hypertension, tachycardia and tachypnoea
  • agitated delirium with confusion
277
Q

Neuroleptic malignant syndrome

Investigations

A
  • Raised CK
  • AKI sometimes - 2ndry to rhabdomyolysis
  • Leukocytosis
278
Q

Neuroleptic malignant syndrome

Management

A
  • Stop antipsychotic
  • Transfer to medical ward
  • IV fluids
  • Dantrolene can sometimes be used
279
Q

Ataxia

Location in cerebellar

A

Cerebellar hemisphere lesions cause peripheral (‘finger-nose ataxia’)

Cerebellar vermis lesions cause gait ataxia

280
Q

Creutzfeldt-Jakob Disease

Features

A
  • Dementia (rapid onset)
  • Myoclonus (spasmodic jerky contraction of groups of muscles)
  • Rigidity
281
Q

Creutzfeldt-Jakob Disease

Investigations

A
  • CSF = normal
  • EEH: biphasic high amplitude sharp waves
  • MRI: hyperintense signal in BASAL GANGLIA and THALAMUS
282
Q

Creutzfeldt-Jakob Disease

Pathophysiology

A
  • Rapidly progressive neurological condition caused by prion proteins
  • These proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases
283
Q

Huntington’s

Genetics

A

Autosomal dominant

  • Defect in huntingtin gene on chromosome 4
  • Trinucleotide repeat disorder: repeat expansion of CAG
  • Phenomenon of anticipation (disease presents earlier in successive generations)
284
Q

Huntington’s

Features

A

Triad of motor, cognitive and psychiatric symptoms

  • Motor: impairment of involuntary (chorea) and voluntary movements, reduced manual dexterity, balance problems and falls
  • Cognitive: initially = loss of speed and flexibility in thinking but later develop into global dementia
  • Psychiatric: depression (most common), irritability, anxiety, agitation, and social withdrawal
285
Q

Huntington’s

Management

A
  • Chorea: tetrabenazine
  • Depression: SSRIs
  • Psychosis: Haloperidol
  • Aggression: Risperidone
  • Bilateral stimulation of globus pallidus
  • Counsel patiecnt and family
286
Q

Huntington’s

Pathophysiology

A
  • Degeneration of cholinergic and GABAnergic neurons in the striatum of basal ganglia
287
Q

When can you consider stopping epileptic drugs and over how long?

A
  • If seizure free for > 2 years

- Stopped over 2-3 months

288
Q

What is the Cushing Reflex?

A
  • A physiological nervous system response to increased intracranial pressure that results in HYPERTENSION and BRADYCARDIA
289
Q

Status epilepticus management

A

1 Buccal midazolam/ IV lorazepam
2 IV lorazepam
3 IV phenytoin (phenobarbital if already on regular phenytoin)
4 Rapid sequence induction of anaesthesia using thiopental sodium

290
Q

Trigeminal neuralgia

Red flags requiring specialist referral

A
  • Sensory changes
  • Deafness or other ear problems
  • History of skin or oral lesions that could spread perineurally
  • Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
  • Optic neuritis
  • A family history of multiple sclerosis
  • Age of onset before 40 years
291
Q

Intracranial venous thrombosis

Features

A
  • Headache
  • N+V
  • Reduced consciousness
292
Q

Intracranial venous thrombosis

Ix’s

A

MRI venography (or CT venography)

  • D-dimer level may be elevated
293
Q

Intracranial venous thrombosis

Management

A
  • Anticoagulation (typically LMWH)

- Warfarin generally still used for long-term anticoag

294
Q

Intracranial venous thrombosis

Cavernous sinus thrombosis - presentation

A
  • Causes: local infection, neoplasia, trauma
  • Periorbital oedema
  • Ophthalmoplegia (6th nerve damage before 3rd or 4th)
  • Trigeminal nerve involvement - may lead to hyperaesthesia of upper face/eye pain
  • Central retinal vein thrombosis
295
Q

Intracranial venous thrombosis

Sagittal sinus thrombosis - presentation

A
  • May present with seizures and hemiplegia
  • Parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
  • Empty delta sign on venography
296
Q

Intracranial venous thrombosis

Lateral sinus thrombosis - presentation

A
  • 6th and 7th cranial nerve palsies (abducens, facial)
297
Q

Hyophosphataemia levels

A

Serum phosphate level <0.80 mmol/L:

  • Mild (∼0.64–0.80 mmol/L)
  • Moderate (∼0.32–0.64 mmol/L)
  • Severe (<0.32 mmol/L)
298
Q

Hyophosphataemia Tx

A

Mild to moderate: enteral replacement is required using Phosphate Sandoz® effervescent tablet

Severe or symptomatic: IV phosphate replacement

Finals (21 decks)

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