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FINALS > Neuro > Flashcards

Neuro Flashcards

1
Q

STROKE

What is a stroke?

A
  • Stroke represents a sudden interruption in the vascular supply of the brain leading to neurological deficit with associated infarction of CNS tissue.
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2
Q

STROKE

What are the two main causes of stroke and how do they cause a stroke?

A
  • Ischaemic (85%)

- Haemorrhagic (15%)

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3
Q

STROKE

What are the causes of ischaemic strokes?

A
  • Cardiac (atherosclerosis, AF, infective endocarditis)
  • Vascular (aortic or vertebral dissection)
  • Haem (sickle cell, polycythaemia)
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4
Q

STROKE

What are the causes of haemorrhagic stroke?

A

Intracerebral haemorrhage
- Trauma, AVM
- Cerebral amyloid angiopathy
- Small vessel disease due to chronic HTN
SAH (trauma, berry aneurysm, AVM)
Anticoagulants, tumours + substance abuse (secondary causes)

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5
Q

STROKE

Give an example of how chronic HTN can cause a stroke.

A
  • Charcot-Bouchard aneurysms most often in the basal ganglia
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6
Q

STROKE

What are the risk factors for strokes?

A
  • HTN = biggest
  • CV = hypercholesterolaemia, smoking, AF, IHD, DM
  • Previous TIA, carotid artery stenosis
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7
Q

STROKE
What vessels can be affected in TACS?
What criteria must be met for a TACS?

A
  • ACA, MCA, carotid
    All three Hs –
  • Hemiplegia (unilateral ± sensory deficit of face, arm leg)
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disturbance)
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8
Q

STROKE
What vessels can be affected in PACS?
What criteria must be met for a PACS?

A
  • ACA, MCA, carotid (same vessels as TACS)

- 2/3 of the criteria for TACS

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9
Q

STROKE
What vessels can be affected in POCS?
What criteria must be met for a POCS?

A
  • PCA, vertebrobasilar artery or branches
    One of the following –
  • Cerebellar dysfunction
  • Conjugate eye movement disorder (e.g., gaze palsy)
  • Bilateral motor/sensory deficit
  • Cranial nerve palsy with contralateral motor/sensory deficit
  • Isolated homonymous hemianopia + cortical blindness
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10
Q

STROKE
What vessels can be affected in LACS and what does that mean?
What areas can be affected in LACS?
What criteria must be met for a LACS?

A
  • Perforating arteries so no higher cortical dysfunction or visual field abnormality, subcortical stroke
  • Thalamus, basal ganglia, internal capsule
    One of following –
  • Pure sensory stroke (thalamus)
  • Pure motor stroke (posterior limb of internal capsule)
  • Sensori-motor stroke
  • Ataxic hemiparesis
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11
Q

STROKE

How would a brainstem/basilar artery infarct present?

A
  • Locked in syndrome – complete paralysis BUT eye movement + awareness preserved
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12
Q

STROKE
How would lateral medullary/Wallenberg’s syndrome present?
What vessel is implicated?

A
  • Ipsi: ataxia, nystagmus, dysphagia, facial numbness + CN palsy
  • Contra: limb sensory loss
  • Posterior inferior cerebellar artery
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13
Q

STROKE
How would lateral pontine syndrome present?
What vessel is implicated?

A
  • Similar to Wallenberg’s but ipsilateral facial paralysis + deafness
  • Anterior inferior cerebellar artery
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14
Q

STROKE

What is Weber’s syndrome

A

Ipsilateral CN3 palsy + contralateral hemiparesis

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15
Q

STROKE

What is a transient ischaemia attack (TIA)?

A
  • Transient neurological dysfunction secondary to cerebral ischaemia without infarction, usually self-resolving
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16
Q

STROKE

What risk assessment tool can be used to calculate a person’s risk of having a stroke within the next 48h?

A

ABCD2

  • Age >60 (1)
  • BP >140/90mmHg (1)
  • Clinical features (unilateral weakness = 2, speech disturbance = 1)
  • Diabetes (1)
  • Duration (≥60m = 2, 10–59m = 1)
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17
Q

STROKE

What do the scores from ABCD2 mean?

A
  • ≥4 = specialist assessment within 24h (give aspirin 300mg OD)
  • ≤3 = specialist assessment within 1 week, ?brain imaging
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18
Q

STROKE

What investigation is crucial for the management of stroke and why?

A
  • Non-contrast CT head to exclude haemorrhagic before treatment given.
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19
Q

STROKE

How would an ischaemic stroke appear on CT head?

A
  • Hypodensity in region affected with hyperdense vessel

- Loss of grey-white matter differentiation + sulcal effacement (loss of sulci definition) in cortical infarction

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20
Q

STROKE

How would a haemorrhagic stroke appear on CT head?

A
  • Acute = hyperdense
  • Subacte = isodense
  • Chronic = hypodense
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21
Q

STROKE

What is the gold standard imaging for stroke if nothing can be seen on CT head?

A
  • Diffusion-weighted MRI head as shows changes within minutes + higher sensitivity for infarcts
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22
Q

STROKE

What bloods may be taken in suspected stroke?

A
  • FBC, ESR + clotting screen (vasculitis, clotting disorders)
  • U+Es, LFTs, Ca2+ (electrolytes)
  • Blood glucose (hypo)
  • TFTs, lipid profile
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23
Q

STROKE

What other investigations may you do in stroke?

A
  • ECG 72h tape to look for paroxysmal AF
  • ECHO to check for endocarditis or CHD
  • CTA/MRA or carotid doppler USS to look for dissection or carotid stenosis
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24
Q

STROKE

What are some potential complications following a stroke?

A
  • Raised ICP
  • Aspiration pneumonia due to dysphagia, pressure sores
  • Cognitive impairment
  • Long-term disability
  • VTE due to immobility
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25
Q 
STROKE
What is the most crucial management for ischaemic strokes?
What timeframe?
Mechanism of action?
Drug?
A
  • Thrombolysis with IV tPA (tissue plasminogen activator)
  • Within 4.5 hours
  • Converts plasminogen > plasmin so promotes breakdown of fibrin clot
  • Alteplase (tPA) or can use streptokinase
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26
Q

STROKE
What must be done after alteplase treatment?
What are the benefits of alteplase?
What are the risks of alteplase?

A
  • Repeat CT head after 24h to check for haemorrhagic transformation
  • Improves chance of independence on discharge, benefit decreases with time (time=brain), risk of death same
  • Haemorrhage (1 in 20), reaction to tPA
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27
Q

STROKE

What are some contraindications to treatment with alteplase?

A
  • Haemorrhagic stroke
  • Recent surgery
  • GI bleeding
  • Pregnancy
  • Hx of intracranial haemorrhage
  • Active cancer
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28
Q

STROKE

What other treatment can be given in ischaemic stroke either alongside alteplase or after the time frame?

A
  • Thrombectomy (mechanical retrieval of clot)
  • Proximal anterior circulation stroke within 6h (with IV alteplase if <4.5h) or within 24h if potential to salvage brain tissue
  • Proximal posterior circulation stroke within 24h (with IV alteplase if <4.5h) if potential to salvage brain tissue
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29
Q

STROKE

What other management is given for ischaemic strokes?

A
  • 300mg aspirin OD 2w post-stroke + then lifelong 75mg clopidogrel
  • New AF = anticoagulate after 2w
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30
Q

STROKE

What is the management of a haemorrhagic stroke?

A
  • Stop + reverse anticoagulants
  • Aggressive BP control (140–160mmHg systolic)
  • Surgical decompression (either endovascular clipping or coiling)
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31
Q

STROKE

What lifestyle advice should be given post-stroke?

A
  • Smoking + alcohol cessation
  • Improve diet + exercise
  • Cannot drive for 1m post-stroke or 1y if HGV driver
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32
Q

STROKE

What medication and general management may be given in stroke prevention?

A
  • Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
  • Manage co-morbidities (HTN, DM)
  • Statins (high dose post stroke)
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33
Q

STROKE
What treatment may be considered after a TIA?
How would you assess suitability?

A
  • Carotid endarterectomy if >70% carotid artery stenosis within 2w of Sx (TIA/stroke)
  • Carotid doppler USS
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34
Q

SAH

What is the pathophysiology of a subarachnoid haemorrhage (SAH)?

A
  • Intracranial haemorrhage with presence of blood in the subarachnoid space.
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35
Q

SAH

What is the most common cause of SAH?

A
  • Saccular/berry aneurysm rupture (80%)
  • Commonest sites at bifurcations:
  • Junction of anterior communicating/cerebral arteries
  • Junction of posterior communicating with internal carotid
  • Trifurcation of MCA
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36
Q

SAH
What are some other causes of SAH?
What conditions are linked to SAH?
What are some risk factors for SAH?

A
  • Congenital arteriovenous malformations (15%), trauma
  • Polycystic kidneys, coarctation of aorta + Ehlers-Danlos syndrome
  • Smoking, alcohol misuse, HTN, bleeding disorders, FHx of SAH
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37
Q

SAH

What are some symptoms of SAH?

A
  • Sudden onset excruciating headache, often occipital (thunderclap)
  • Can occur on exertion (weightlifting, sex)
  • Vomiting, seizures, drowsiness
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38
Q

SAH

What are some signs of SAH?

A
  • Meningism – neck stiffness, photophobia, +ve kernig’s (pain/unable to extend leg at knee when it’s bent)
  • Focal neurology (CN III palsy, other CN palsies)
  • Retinal, subhyaloid + vitreous bleeds on fundoscopy
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39
Q

SAH
What are some complications of SAH?
What is the most common cause of morbidity?

A
  • 50% die suddenly or soon after haemorrhage
  • Rebleeding
  • Obstructive hydrocephalus
  • Hyponatraemia
  • Cerebral ischaemia due to vasospasm #1 cause of morbidity
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40
Q

SAH

What are some important investigations for SAH?

A
  • CT head gold standard (95% sensitivity on day 1) – white star-shaped lesion as blood fills gyro patterns around brain + ventricles
  • Lumbar puncture if CT -ve after 12h to allow Hb to break down – xanthochromia (yellow due to bilirubin) confirms
  • CT angiography to locate aneurysms before surgical procedures
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41
Q

SAH

What is the management of SAH?

A
  • Neurosurgery ASAP (endovascular coiling vs. surgical clipping which requires craniotomy)
  • Maintain cerebral perfusion with IV fluids but ensure SBP <160mmHg
  • PO nimodipine for 3w to reduce vasospasm + prevent morbidity
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42
Q

EDH
What is the pathophysiology of extra-dural haematoma (EDH)?
What is the offending vessel?

A
  • Often fractured temporal/parietal bone 2º to traumatic head injury leads to blood accumulating between bone + dura mater
  • Middle meningeal artery
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43
Q

EDH

What is the natural clinical presentation of EDH?

A
  • May be initial LOC
  • Lucid interval pattern where pt appears to improve but then rapid decrease in GCS from rising ICP
  • Signs of increased ICP ± focal neurology develop
  • Ipsilateral pupil dilation
  • Cushing’s reflex and triad is a late sign
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44
Q

EDH

What is Cushing’s reflex and triad

A
  • Reflex = bradycardia and hypertension

- Triad = irregular breathing too

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45
Q

EDH

What are the investigations for EDH?

A

Non-contrast CT head –
- Hyperdense biconvex haematoma ± midline shift
- Haematoma IS limited by cranial sutures bound by dura mater
Skull XR may show fracture lines crossing course of middle meningeal artery

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46
Q

EDH

What investigation is contraindicated in EDH and why?

A
  • Lumbar puncture
  • Drop in CSF pressure in spinal column will speed up brain herniation through the foramen magnum > brainstem compression + respiratory arrest
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47
Q

EDH

What is the management for EDH?

A
  • Neurosurgical transfer for clot evacuation ± ligation of bleeding vessel
  • IV mannitol if increased ICP (osmotic diuresis)
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48
Q

SDH

What is the pathophysiology of subdural haematoma (SDH)?

A
  • Rupture of bridging veins beneath dura leading to haematoma between arachnoid + dura mater
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49
Q

SDH

What causes a SDH and who are at risk of SDH?

A
  • Often minor trauma in alcoholics + elderly on anticoagulation as prone to falls + atrophied brains with stretched bridging veins, also shaken babies.
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50
Q

SDH

What is the clinical presentation of SDH?

A
  • Headache
  • N+V
  • Confusion
  • May have focal neurology
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51
Q

SDH

What are the investigations for SDH?

A

Non-contrast CT head shows concave shaped haematoma ± midline shift –

  • Acute (<14d) = hyperdense
  • Chronic (>14d) = hypodense
  • Acute-on-chronic (rebleed) = both/mixture
  • Haematoma is NOT limited by cranial sutures
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52
Q

SDH

What is the management of SDH?

A
  • Small = clot evacuation via burr hole

- Large = craniotomy

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53
Q

EPILEPSY

What is epilepsy?

A
  • Recurrent tendency to have unprovoked seizures
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54
Q

EPILEPSY

What are the causes of epilepsy?

A
  • 2/3rd idiopathic, FHx
  • Alcohol/drugs including withdrawal
  • SOL = tumour, abscess, bleeds
  • Infection = meningitis, encephalitis
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55
Q

EPILEPSY

What is a focal/partial seizure?

A
  • Start in a specific area on one side of the brain
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56
Q 
EPILEPSY
What is a...
i) simple-partial seizure?
ii) complex-partial seizure?
iii) secondary generalised seizure?
A

i) Consciousness + awareness is preserved (e.g. foot twitch)
ii) Without consciousness or awareness
iii) Focal > generalised seizure

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57
Q 
EPILEPSY
How would a partial seizure present in...
i) frontal lobe?
ii) temporal lobe?
iii) parietal lobe?
iv) occipital lobe?
A

i) Motor = Jacksonian march, Todd’s paresis, dysphagia
ii) déjà/jamais-vu, automatisms (chewing, lip smacking), emotional distress, hallucinations
iii) Tingling + numbness
iv) flashing lights, eyelid fluttering, eye movements

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58
Q

EPILEPSY
What is…
i) Jacksonian march?
ii) Todd’s paresis?

A

i) Starts on one side of body then “marches” over a few seconds to affect larger parts of body like entire hand, foot or facial muscles + may generalise
ii) Focal weakness in a part or all of the body after a seizure

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59
Q

EPILEPSY
What is a generalised seizure?
What are the 4 main types?

A
  • Diffuse activity across both hemispheres

- Absence seizures, tonic-clonic seizures, myoclonic seizures + atonic (akinetic) seizures/drop attacks

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60
Q

EPILEPSY

Explain what an absence seizure is and any key features

A
  • Brief <30s pauses where activity stops (still, no talking, stares)
  • Begins in childhood, may progress to tonic-clonic later
  • EEG = 3Hz generalised spike, symmetrical
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61
Q

EPILEPSY

Explain what a tonic clonic seizure is.

A
  • Tonic = vague warning, rigid, pt falls + may verbalise, LOC
  • Clonic = convulsions, bilateral rhythmic muscle jerks, irregular breathing, may bite tongue (lateral) or urinary incontinence
  • Post-ictal = drowsy, confused, irritable
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62
Q

EPILEPSY

Explain what a myoclonic seizure is.

A
  • Brief, sudden muscle contractions like jerk of a limb, face or trunk
  • Usually remains awake, can occur in juvenile myoclonic epilepsy
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63
Q

EPILEPSY

Explain what an atonic (akinetic) seizure/drop attack is.

A
  • Brief, sudden loss of muscle tone causing a fall but no LOC
  • Typically begin in childhood, ?Lennox-Gastaut syndrome
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64
Q

EPILEPSY

What investigations would you do in epilepsy?

A
  • Mostly clinical Dx, witnessed seizure Hx crucial
  • Exclude organic causes (FBC, U+Es, LFTs, glucose, ECG)
  • Electroencephalogram (EEG) often sleep deprived or hyperventilate to provoke
  • ?Neuroimaging (CT/MRI head) if focal neurology + concerned about SOL
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65
Q

EPILEPSY

Compare the management of generalised seizures and focal seizures

A
  • Generalised 1st line = sodium valproate, 2nd line = lamotrigine, carbamazepine (for TC only as can exacerbate absent + myoclonic)
  • Focal 1st line = carbamazepine, 2nd line = lamotrigine, sodium valproate or levetiracetam
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66
Q

EPILEPSY

What is the management of absence seizures?

A
  • 1st line = ethosuximide or sodium valproate
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67
Q

EPILEPSY

What driving advice should be given to patients regarding seizures and established epilepsy?

A
  • Cannot drive for 6m following seizure + must inform DVLA

- Established epilepsy must be seizure free for 12m before driving

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68
Q

STATUS EPILEPTICUS

What is status epilepticus?

A
  • Medical emergency where a seizure does not self-limit – seizures lasting >5m or ≥2 within a 5-minute period
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69
Q

STATUS EPILEPTICUS
What are some causes of status epilepticus?
When might status epilepticus be the first presentation of epilepsy?

A
  • Poor adherence #1
  • Infections (meningitis, encephalitis)
  • Worsening of primary cause of epilepsy (e.g. brain tumour growing)
  • First presentation of epilepsy = alcoholics
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70
Q

STATUS EPILEPTICUS

What is the initial management for status epilepticus?

A
  • ABCDE > anaesthetists review airway

- IV access = ABG (glucose), FBC, U&E, CRP, Ca, phosphate, magnesium, AED levels

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71
Q

STATUS EPILEPTICUS

What is the stepwise management of status epilepticus?

A
  • 1 = IV lorazepam 4mg (buccal midazolam or rectal diazepam if no IV access)
  • 2 = repeat 1 after 10m
  • 3 = IV phenytoin (cardiac monitoring), levetiracetam or valproate in critical care
  • 4 = general anaesthetic
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72
Q

STATUS EPILEPTICUS

What might you consider after the acute management of status epilepticus?

A
  • CT head, LP for ?cause
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73
Q

LOC

What are the potential causes of LOC?

A

CRASH

  • Cardiogenic (more alarming)
  • Reflex (neurally mediated)
  • Arterial
  • Systemic
  • Head
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74
Q

LOC
How might cardiogenic LOC present/causes?
In the presentation, what suggests cardiogenic LOC?

A
  • Transient arrhythmias (SVT)
  • Bradyarrhythmias like complete heart block
  • Structural (aortic stenosis, hypertrophic cardiomyopathy)
  • BLACKOUT ON EXERCISE IS CARDIOGENIC UNTIL PROVEN OTHERWISE*
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75
Q

LOC

How might reflex LOC present?

A
  • Vasovagal syncope = intense fear like watching surgery, needles > faint
  • Situational syncope = coughing, post-micturition
  • Carotid sinus syncope = hypersensitive baroreceptors cause excessive reflexive bradycardia on minimal stimulation (turn head, shaving, reaching high)
  • Postural hypotension (iatrogenic autonomic failure)
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76
Q

LOC
How might…

i) arterial
ii) systemic
iii) head

LOC present?

A

i) Vertebrobasilar insufficiency (TIA, CVA)
ii) Hypoglycaemia
iii) Epilepsy, NEAD, anxiety (hyperventilation)

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77
Q

LOC
How might syncope present in terms of…

i) patient?
ii) triggers?
iii) prodrome?
iv) ictal?
v) post-ictal?

A

i) Older, co-morbidities or young + FHx of young deaths
ii) Posture, exertion, metabolic
iii) Pale, clammy, palpitations, CP, ‘going dark’
iv) Floppy, seconds, eye closed ± few jerks
v) Rapid recovery, seconds

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78
Q

LOC
How might NEAD present in terms of…

i) patient?
ii) triggers?
iii) prodrome?
iv) ictal?
v) post-ictal?

A

i) Younger, F>M, social/personal stressors, psych Hx, deprivation, abuse
ii) Heightened emotion, stress or panic
iii) No warning, upset/panic, aware of impending seizure
iv) Thrashing/asymmetrical, long (up to 1h), pelvic thrusting, violent, back arching, eyes + mouth forcibly closed, crying, ?distractible, tongue biting (tip), waxing/waning
v) unusually rapid, emotional ± amnesia

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79
Q

LOC
What investigations would you do for LOC?
How can NEAD and a true epileptic seizure be differentiated?

A
  • CV + neuro exam, vital signs esp (LSBP)
  • FBC, U+Es, glucose, LFTs, TFTs (normal CK + prolactin in NEAD)
  • 24h 12-lead ECG + ECHO
  • EEG + CT/MRI if necessary
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80
Q

LOC
What is the driving advice for LOC?
Management of NEAD?

A
  • No driving until cause known or until blackout free for 1y

- NEAD = correct Dx vital, speak to pt, reassure them, wait for seizure to pass, CBT, avoid AEDs

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81
Q

PARKINSON’S DISEASE

What is the pathophysiology of Parkinson’s disease?

A
  • Progressive loss of dopaminergic neurones from the pars compacta of the substantia nigra leading to decreased levels of dopamine within the basal ganglia which regulates movement
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82
Q

PARKINSON’S DISEASE
What is the epidemiology of Parkinson’s disease?
What are the causes of Parkinson’s disease?
What can exacerbate it?

A
  • Typically 70y/o M

- Haloperidol + metoclopramide (dopamine blockade)

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83
Q

PARKINSON’S DISEASE

What are the cardinal features of Parkinson’s disease?

A

Triad –

  • Bradykinesia (slow movements, difficult initiating)
  • Rigidity (pain, problems turning in bed) – cogwheel rigidity
  • Resting tremor – ‘pill-rolling’
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84
Q 
PARKINSON'S DISEASE
What is the distribution of the symptoms?
What happens to the gait?
What daily tasks may they struggle with?
What might you notice on their face?
A
  • Asymmetrical (one side worse)
  • Shuffling gait, small steps + postural instability, reduced arm swing
  • Problems doing up buttons, smaller writing (micrographia)
  • Hypomimia
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85
Q

PARKINSON’S DISEASE

What are some pre-motor symptoms of Parkinson’s disease?

A
  • Anosmia
  • Depression/anxiety
  • Sleep disturbance = REM sleep behaviour disorder
  • Autonomic features = postural hypotension, ED
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86
Q

PARKINSON’S DISEASE
How can you differentiate Parkinson’s resting tremor from benign essential tremor in terms of…

i) side?
ii) frequency?
iii) effect of rest?
iv) effect of intentional movement?
v) alcohol?
vi) cause?

A

i) Asymmetrical vs symmetrical
ii) 3–5Hz vs 5–8Hz
iii) Worse at rest vs improves at rest
iv) Improves with intentional movement vs worse with intentional movement
v) No change with alcohol vs improves with alcohol (also Rx = propranolol)
vi) Parkinson’s vs. autosomal dominant condition

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87
Q

PARKINSON’S DISEASE

What are 4 differential diagnoses to consider in Parkinson’s disease?

A

Parkinson’s plus syndromes –

  • Progressive supranuclear palsy
  • Multiple system atrophy
  • Lewy Body dementia
  • Corticobasal degeneration
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88
Q

PARKINSON’S DISEASE
Where is affected in progressive supranuclear palsy?
How does progressive supranuclear palsy present?
What signs may be present on examination?

A
  • Above nuclei of CN3, 4 + 6
  • Postural instability + early falls
  • Vertical gaze impairment (down worse) = difficulty reading or descending stairs
  • Ocular cephalic reflex = tilt head to look at objects rather than moving eyes
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89
Q

PARKINSON’S DISEASE
What is multiple system atrophy?
How does it present?

A
  • Neurones in multiple systems in the brain degenerate (incl basal ganglia)
  • Early autonomic features = ED, postural hypotension + cerebellar signs
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90
Q

PARKINSON’S DISEASE

What is Lewy Body dementia associated with?

A
  • Visual hallucinations

- Fluctuating cognitive impairment

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91
Q

PARKINSON’S DISEASE

What is corticobasal degeneration?

A
  • Spontaneous limb activity

- Alien limb

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92
Q

PARKINSON’S DISEASE
How would you diagnose Parkinson’s disease?
What are some histological features in Parkinson’s disease?
What other imaging might be used?

A
  • Clinical Dx
  • Lewy bodies (alpha-synuclein + ubiquitin), loss of dopaminergic neurones in the substantia nigra
  • Idiopathic Parkinson’s disease shows normal MRI head + SPECT (if unclear)
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93
Q

PARKINSON’S DISEASE

What options are there for managing Parkinson’s disease under specialist guidance?

A
  • Co-careldopa, co-beneldopa = increase amount of dopamine in CNS
  • Bromocriptine, cabergoline = dopamine receptor agonist
  • Entacapone + selegiline = inhibit enzymatic breakdown of dopamine
  • Deep brain stimulation
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94
Q

HUNTINGTON’S DISEASE

What is the pathophysiology of Huntington’s disease?

A
  • AD inherited CAG trinucleotide repeat expansion in the HTT gene on chromosome 4 > mutant huntingtin protein which causes neuronal loss in the striatum (caudate nucleus + putamen) of basal ganglia = depleted inhibitory GABA
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95
Q

HUNTINGTON’S DISEASE
What 2 unique genetic features are seen in Huntington’s disease?
When do symptoms normally present?

A
  • 100% penetrance (all affected) = ≥36 repeats
  • Anticipation = more repeats in successive generations > earlier, more severe onset
  • Middle age
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96
Q

HUNTINGTON’S DISEASE
Huntington’s disease shows anticipation.
What does this mean?
When do symptoms typically occur?

A
  • Successive generations have more repeats leading to earlier age of onset + increased severity of disease
  • Around middle age
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97
Q

HUNTINGTON’S DISEASE
What is the clinical presentation of Huntington’s disease?
What is the cause of fatality in HD?

A
  • Cognitive disturbance = subcortical dementia (visuospatial + executive difficulties)
  • Neuropsych = depression, psychosis
  • Motor = chorea, eye movement disorders, dysphagia
  • Respiratory disease #1, suicide
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98
Q

HUNTINGTON’S DISEASE

What investigations would you do for Huntington’s disease?

A
  • Genetic testing with pre- + post-test counselling (cannot give to children have to be old enough to decide themselves)
  • MRI head shows atrophy of striatum
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99
Q

HUNTINGTON’S DISEASE

What is the management of Huntington’s disease?

A
  • No cure so Sx control
  • Chorea = tetrabenazine (dopamine depleting agent) is licensed
  • SSRIs = depression
  • Antipsychotics = psychosis, aggression
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100
Q

HEADACHES

What are the two types of headaches and give some examples?

A
  • Primary (no underlying cause) such as migraine, cluster + tension (most common)
  • Secondary due to an underlying cause e.g., meningitis, SAH
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101
Q

HEADACHES

What are some common causes of headaches and their epidemiology + causes?

A
  • Cluster – 30–50M smokers
  • Tension – missed meals, stress, dehydration
  • Med overuse – commonest secondary, often analgesia overuse
  • Sinusitis + acute glaucoma
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102
Q

HEADACHES

How does a cluster headache present?

A
  • 15m–2h
  • Rapid onset excruciating pain around one eye
  • Eye may be bloodshot, lid swelling, miosis, ptosis + lacrimation
  • ‘Cluster’ of attacks in a day then remission for weeks/months
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103
Q

HEADACHES

How does a tension headache present?

A
  • 30m–days
  • Bilateral, non-pulsatile headache ± scalp tenderness
  • Pressing/tight-band like sensation
  • Mild–moderate intensity
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104
Q

HEADACHES

What is the acute and prophylactic management of cluster headaches?

A
  • S/c triptans + high flow 100% oxygen via non-rebreather (about 15m)
  • Verapamil is first line, avoid triggers (alcohol), ?short course prednisolone may break cycle during clusters
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105
Q

HEADACHES

What is the management of tension headaches?

A
  • Reassure, stress relief (exercise, avoid triggers)

- Analgesia (paracetamol, NSAIDs)

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106
Q

HEADACHES

What is the management of medication overuse headache?

A
  • Gradual withdrawal of analgesia
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107
Q

TRIGEMINAL NEURALGIA
What is the pathophysiology of trigeminal neuralgia?
What is affected and which one mostly?

A
  • Compression of trigeminal nerve = erratic pain signalling

- Affects all 3 ophthalmic (V1), maxillary (V2) + mandibular (V3) branches but V3 mostly

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108
Q

TRIGEMINAL NEURALGIA
What are the causes of trigeminal neuralgia?
What is the typical patient?
What are some triggers?

A
  • Idiopathic or secondary to tumour or MS
  • 50y/o asian male
  • Washing affected area, shaving, eating, talking + dental prostheses
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109
Q

TRIGEMINAL NEURALGIA

What is the clinical presentation of trigeminal neuralgia?

A
  • Brief paroxysms of intense, electric-shock pain in trigeminal nerve distribution
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110
Q

TRIGEMINAL NEURALGIA
How do you diagnose trigeminal neuralgia?
How do you manage trigeminal neuralgia?

A
  • Clinical diagnosis but CT/MRI head to exclude secondary causes
  • 1st line = carbamazepine
  • ?Microvascular decompression if fails
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111
Q

MIGRAINE
What are the triggers of migraines?
How long do they last for and who are they more common in?

A

CHOCOLATE –

  • Chocolate
  • Hangovers
  • Orgasms
  • Cheese/caffeine
  • Oral contraceptives
  • Lie-ins
  • Alcohol
  • Travel
  • Exercise

F>M

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112
Q

MIGRAINE

Explain the migraine diagnostic criteria

A
  • A = at least 5 attacks which fulfil criteria B–D
  • B = headache attacks 4–72h
  • C = ≥2: unilateral, pulsating, mod–sev pain, physical activity exacerbates
  • D = ≥1 during: N±V, photophobia + phonophobia
  • E = no underlying cause
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113
Q

MIGRAINE

What are three other potential types of migraine?

A
  • Migraine with aura
  • Silent migraine
  • Hemiplegic migraine
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114
Q

MIGRAINE

How does a migraine with aura present?

A

Aura before headache = sparks/lines, blurring, visual defects

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115
Q

MIGRAINE
How does a…

i) silent migraine
ii) hemiplegic migraine

present?

A

i) Migraine with aura but no headache

ii) Stroke mimic = heimplegia, ataxia

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116
Q

MIGRAINE

What is the acute management of migraines?

A
  • PO (or nasal in paeds) 5HT receptor agonists (triptans) like sumatriptan plus paracetamol or NSAID
  • Parenteral antiemetic like metoclopramide or prochlorperazine if vomiting occurs
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117
Q

MIGRAINE

What is the prophylaxis for migraines?

A
  • Propranolol or topiramate are first line
  • Topiramate is teratogenic + can reduce efficacy of hormonal contraceptives though
  • Amitriptyline, botulinum toxin or acupuncture.
  • Riboflavin (B2) 400mg OD may help
  • NOT gabapentin
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118
Q

MND

What is the pathophysiology of motor neurone disease (MND)?

A
  • Degeneration of upper motor neurones + anterior horn cells in brain + spinal cord
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119
Q

MND
What is the most common cause of MND?
What is a rare cause?
What is the epidemiology of MND and what condition is it associated with?

A
  • Most spontaneous + idiopathic with no FHx
  • Rare familial cases with SOD-1 implication (free radicals)
  • M>F, 60y/o, associated with frontotemporal dementia
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120
Q

MND
What are the 4 types of MND?
Best and worse prognosis?

A
  • Amyotrophic lateral sclerosis (ALS)
  • Progressive bulbar palsy (worst prognosis)
  • Progressive muscular atrophy (best prognosis)
  • Primary lateral sclerosis
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121
Q

MND
What is ALS?
How does it typically present?

A
  • Loss of motor neurones in motor cortex (UMN) + anterior horn of cord (LMN) so mixed signs
  • LMN in arms, UMN in legs
122
Q

MND
What is progressive bulbar palsy?
What does it affect?

A
  • Loss of function of brainstem motor nuclei CN 9–12

- Palsy of tongue, muscles of chewing/swallowing + facial muscles

123
Q

MND
What is…

i) progressive muscular atrophy?
ii) primary lateral sclerosis?

A

i) Anterior horn cells (LMN), distal > proximal

ii) Loss of cells in motor cortex (UMN)

124
Q

MND

What is the general clinical presentation of MND?

A
  • UMN = spasticity, brisk reflexes, upgoing plantars, wasting
  • LMN = hypotonia, reduced reflexes, fasciculations (esp. tongue), wasting
125
Q

MND

What are some important features that are absent in MND to help with excluding differentials?

A
  • NO sensory symptoms

- Does not affect eye movements or sphincters

126
Q

MND

What are some investigations for MND?

A
  • Clinical Dx = El-Escorial diagnostic criteria for ALS (Signs in 3 regions)
  • Nerve conduction studies = normal motor conduction (excludes neuropathy)
  • EMG = muscle denervation
  • MRI head/spine for ?structural causes, lumbar puncture for ?inflammatory causes
127
Q

MND

What is a key complication of MND?

A
  • Pneumonia/respiratory failure (common cause of death) due to bulbar palsy
128
Q

MND
What key medication can be given in MND?
What is the mechanism of action?
What is its role in management?

A
  • Riluzole
  • Na+ blocker inhibits glutamate release
  • Prolongs life by 3m
129
Q

MND

What MDT management is given for MND?

A
  • Dysphagia = NG/PEG feeding (drooling = anticholinergics)
  • Spasticity = baclofen or botox injections
  • T2RF = NIV
  • Palliative care (advanced directives, EOL planning)
130
Q

MULTIPLE SCLEROSIS

What is the pathophysiology of multiple sclerosis (MS)?

A
  • Autoimmune disorder leading to CNS demyelination with poor healing resulting in thinner, inefficient myelin, and initial relative axonal preservation which eventually leads to axonal loss + so fixed, progressive deficits
131
Q

MULTIPLE SCLEROSIS

What are some classic sites for MS?

A
  • Periventricular white matter lesions

- Predilection for distinct sites – optic nerves, corpus callosum, brainstem + cerebellar peduncles

132
Q

MULTIPLE SCLEROSIS
What is the epidemiology of MS?
What is MS associated with?

A
  • F>M, young adults

- EBV, low vitamin D + smoking

133
Q

MULTIPLE SCLEROSIS
What is a clinically isolated syndrome?
What might indicate risk of MS?

A
  • First episode of demyelination with neuro signs = not diagnostic
  • More likely to develop MS if lesions are seen on MRI
134
Q

MULTIPLE SCLEROSIS

What are the 4 types of MS?

A
  • Relapsing remitting (most common)
  • Secondary progressive
  • Primary progressive
  • Benign
135
Q

MULTIPLE SCLEROSIS

What is relapsing remitting MS?

A
  • Episodes of Sx in attacks (relapses)
  • Followed by periods of stability (remission)
  • May accumulate disability if don’t fully recover
136
Q

MULTIPLE SCLEROSIS
What is…

i) secondary progressive MS?
ii) primary progressive MS?
iii) benign MS?

A

i) RR initially but begins to have decline in function without remissions
ii) Gradual worsening of disease from point of diagnosis without any remissions
iii) Relapses + remissions but overall progress will never worsen

137
Q

MULTIPLE SCLEROSIS

What is the diagnostic criteria for MS?

A

McDonald criteria –

  • Multiple CNS lesions (≥2)
  • Sx that last >24h
  • Disseminated in space (clinically or MRI) + time (>1m apart)
138
Q

MULTIPLE SCLEROSIS

What are the symptoms of MS?

A

DEMYELINATION –

  • Diplopia (CN VI)
  • Eye movement pain (optic neuritis, #1 presentation)
  • Motor weakness
  • nYstagmus
  • Elevated temp worsens
  • Lhermitte’s sign
  • Intention tremor
  • Neuropathic pain
  • Ataxia
  • Talking slurred (dysarthria)
  • Impotence
  • Overactive bladder
  • Numbness
139
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is meant by…

i) motor weakness?
ii) elevated temp worsens?
iii) Lhermitte’s sign?

A

i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower
ii) Uhthoff’s phenomenon
iii) Neck flexion causes electric shock sensation down spine

140
Q

MULTIPLE SCLEROSIS

What are some signs of MS?

A
  • Relative afferent pupillary defect (RAPD)
  • Internuclear ophthalmoplegia
  • Optic atrophy (pale optic disc) in chronic MS
141
Q

MULTIPLE SCLEROSIS

What is relative afferent pupillary defect?

A
  • Seen on swinging light test (afferent optic nerve issue)

- The affected and normal eye appears to dilate when light is shone on the affected eye

142
Q

MULTIPLE SCLEROSIS

What is internuclear ophthalmoplegia?

A
  • CN VI/medial longitudinal fasciculus lesion
  • Disorder of conjugate lateral gaze with;
    – Decreased adduction of affected eye
    – Nystagmus on abduction of contralateral eye
143
Q

MULTIPLE SCLEROSIS

What are the investigations for MS?

A
  • MRI head + spinal cord to show demyelination plaques = diagnostic
  • Lumbar puncture may show oligoclonal bands of IgG on CSF electrophoresis
  • Evoked potentials = delayed visual, auditory + somatosensory potentials
144
Q

MULTIPLE SCLEROSIS

What is the management of MS relapses?

A
  • IV methylprednisolone
145
Q

MULTIPLE SCLEROSIS

What is the management of MS to maintain remissions?

A
  • First line = beta-interferon + glatiramer

- Second line = natalizumab, dimethyl fumarate

146
Q

MULTIPLE SCLEROSIS

What is the general symptomatic management for MS?

A
  • Spasticity = baclofen or gabapentin
  • Fatigue = amantadine or CBT
  • Bladder dysfunction = USS before anticholinergics
147
Q

MENINGITIS

What are the common causes of bacterial meningitis based on age groups?

A
  • 0–3m = GBS (#1 neonates), E. coli + listeria monocytogenes
  • 3m–60y = Neisseria meningitidis (gram -ve diplococci) + streptococcus pneumoniae (#1 = gram +ve cocci chain)
  • > 60y = N. meningitidis, S. pneumoniae + listeria monocytogenes
148
Q

MENINGITIS

What are the viral causes of meningitis?

A
  • Enteroviruses (coxsackie virus) = #1

- HSV, CMV, mumps

149
Q

MENINGITIS

What are the symptoms of meningitis?

A
  • Fever, headache, N+V, photophobia, drowsiness, seizures
150
Q

MENINGITIS

What are the clinical signs of meningitis?

A
  • Meningism
  • +ve Kernig’s = pain or unable to extend leg at knee when it’s bent
  • +ve Brudzinski = involuntary flexion of hips + knees when neck flexed
  • Non-blanching purpuric rash = later sign in meningococcal septicaemia
151
Q

MENINGITIS

What investigations would you do for meningitis?

A
  • Blood cultures + serology (before LP + Abx unless undesirable delay)
  • FBC, U+Es, LFTs, CRP, blood glucose
  • CT head if other signs like papilloedema
  • Lumbar puncture for MC&S with protein, cell count, glucose + viral PCR
152
Q

MENINGITIS
What would you expect the lumbar puncture result for meningitis to be in bacterial causes for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Cloudy/turbid
ii) ++
iii) ––
iv) ++ neutrophil polymorphs
v) Gram stain

153
Q

MENINGITIS
What would you expect the lumbar puncture result for meningitis to be in viral causes for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Clear
ii) Mild + or normal
iii) Mild – or normal
iv) ++ lymphocytes
v) PCR

154
Q

MENINGITIS
What would you expect the lumbar puncture result for meningitis to be in TB causes for…

i) appearance?
ii) protein?
iii) glucose?
iv) white cell count?
v) other?

A

i) Fibrin web
ii) ++
iii) ––
iv) ++ lymphocytes
v) Acid fast bacilli

155
Q

MENINGITIS

When is a lumbar puncture contraindicated in meningitis?

A
  • Signs of raised ICP (risk of coning of cerebellar tonsils)

- Meningococcal septicaemia

156
Q

MENINGITIS

What are some complications following meningitis?

A
  • Sensorineural hearing loss = key complication
  • Seizures, focal neuro deficit
  • Infection = sepsis/abscess
  • Waterhouse-Friderischsen in meningococcal meningitis (adrenal haemorrhage)
157
Q

MENINGITIS
You see a patient in General Practice with a non-blanching petechial rash and organise blue light transfer for hospital.
What immediate treatment should be given whilst awaiting for hospital transfer?

A
  • IM benzylpenicillin
158
Q

MENINGITIS
What is the management of bacterial meningitis depending on the age of the patient?
What additional treatment could you give but when would you not give it?

A
  • <3m = IV cefotaxime + amoxicillin (listeria cover)
  • 3m–50y = IV cefotaxime (or ceftriaxone)
  • > 50y = IV cefotaxime (or ceftriaxone) + amoxicillin
  • IV dex if >3m to reduce complications but NOT in septic shock, meningococcal septicaemia or immunocompromised
159
Q

MENINGITIS

What is the management of viral meningitis?

A
  • Empirical broad spectrum Abx until LP results

- IV aciclovir for HSV

160
Q

MENINGITIS

What prevention can be given for meningitis?

A
  • Childhood vaccination schedule
  • All close contacts should receive PO ciprofloxacin (or rifampicin) prophylaxis if <7d exposure since onset if meningococcal
161
Q

MENINGITIS

Who must you notify about cases of meningitis?

A
  • Public Health England immediately as notifiable disease
162
Q

ENCEPHALITIS
What is encephalitis?
What are the most common causes?

A
  • Inflammation of the brain parenchyma
  • Viral = HSV1 #1, CMV, EBV, mumps
  • Non-viral = any bacterial meningitis, TB, lyme disease
163
Q

ENCEPHALITIS
What is the clinical presentation of encephalitis?
What specific feature may be present in HSV1 encephalitis?

A
  • Fever, headache, altered mental status, personality change
  • Focal neuro deficits + seizures
  • HSV1 associated with temporal lobe = olfactory seizures
164
Q

ENCEPHALITIS

What investigations would you do for encephalitis?

A
  • Blood culture + serology for viral PCR
  • CT head = medial temporal + inferior frontal changes (petechial haemorrhages)
  • LP = lymphocytosis and raised protein
165
Q

ENCEPHALITIS

What is the management of encephalitis?

A
  • Empirical IV ceftriaxone (bacterial cover) + IV aciclovir in all cases
166
Q

BRAIN ABSCESS
What is a brain abscess?
What are the most common causative organisms?

A
  • Pus-filled swelling in the brain

- Staph. aureus + strep. pneumoniae

167
Q

BRAIN ABSCESS

What are the aetiologies of brain abscesses?

A
  • Local spread = otitis media, sinusitis, mastoiditis
  • Penetrating head injuries, trauma or surgery to the scalp
  • Embolic events from infective endocarditis
168
Q

BRAIN ABSCESS

What is the clinical presentation of a brain abscess?

A
  • Fever, headache + focal neurology are the classic triad

- Raised ICP Sx = nausea, papilloedema, seizures

169
Q

BRAIN ABSCESS

What are the investigations for brain abscess?

A
  • CT head shows ring-enhancing lesion ± surrounding oedema

- LP is contraindicated due to raised ICP

170
Q

BRAIN ABSCESS

What is the management of brain abscess?

A
  • CT guided aspiration via burr hole or craniotomy + abscess cavity debridement
  • Abx with IV ceftriaxone + metronidazole
  • ICP Mx with dexamethasone
171
Q

BRAIN DEATH + COMA
What is…

i) coma?
ii) persistent vegetative state?
iii) brain death?

A

i) Unarousable unresponsiveness
ii) State of wakefulness with sleep-wake cycles but no detectable awareness
iii) Irreversible cessation of all brain function with absent brainstem signs

172
Q

BRAIN DEATH + COMA

What are some neurological causes of brain death and coma?

A
  • Trauma
  • Tumours
  • Infection (meningitis, encephalitis)
  • Vascular (haemorrhage)
  • Epilepsy
173
Q

BRAIN DEATH + COMA

What are some metabolic causes of brain death + coma?

A
  • Drugs/poisoning
  • DKA/HHS or hypoglycaemia
  • Septicaemia
  • Hypothermia
  • Hepatic/uraemia encephalopathy due to liver/renal failure
  • CO2 narcosis in COPD
174
Q

BRAIN DEATH + COMA

In terms of clinical presentation in brain death and coma, what are some brainstem signs?

A
  • Pupil size (pinpoint vs. dilated + pupillary reactions)
  • Eye movements, corneal reflexes, cough + gag reflexes
  • Ice cold water in ears > nystagmus
175
Q

BRAIN DEATH + COMA
What are lateralising signs?
Give an example of one and why it occurs

A
  • Signs that occur from one hemisphere of the brain but not the other
  • Fixed dilated pupil (CN3 palsy) due to parasympathetic fibre compression over petrous part of temporal bone
176
Q

BRAIN DEATH + COMA

What are some investigations for brain death and coma?

A
  • Bloods – FBC, cultures, U+Es, Ca2+, phosphate, LFTs, glucose, clotting screen, toxicology (+ alcohol), ABG
  • CT/MRI head, EEG + LP for infection
177
Q

BRAIN DEATH + COMA
What is the Glasgow Coma Scale (GCS)?
What is it based on?
What scores should prompt action?

A
  • Universal consciousness assessment tool in head injury
  • BEST eye, verbal + motor response – 15 max, 3 min
  • ‘GCS ≤8 = intubate’ secure airway
178
Q

BRAIN DEATH + COMA

What are the components of ‘eyes’ in GCS?

A 
E4 = opens spontaneously
E3 = opens to verbal command
E2 = opens to pain
E1 = no response
179
Q

BRAIN DEATH + COMA

What are the components of ‘verbal’ in GCS?

A 
V5 = orientated to TPP, answers appropriately
V4 = confused conversation, odd answers
V3 = inappropriate words (random, abusive)
V2 = incomprehensible sounds (groans)
V1 = no response
180
Q

BRAIN DEATH + COMA

What are the components of ‘motor’ in GCS?

A 
M6 = obeys commands
M5 = localises pain
M4 = withdraws away from painful stimulus
M3 = abnormal flexion to pain (decorticate posturing)
M2 = abnormal extension to pain (decerebrate posturing)
M1 = no response
181
Q

BRAIN DEATH + COMA

What does decorticate posturing indicate?

A

Significant damage to cerebral hemispheres, internal capsule + thalamus

182
Q

BRAIN DEATH + COMA

What does decerebrate posturing indicate?

A
  • Indicates brainstem damage + so lesions in cerebellum or midbrain
183
Q

BRAIN DEATH + COMA

What does the progression from decorticate to decerebrate posturing suggest?

A
  • Uncal (transtentorial) or tonsillar brain herniation ‘coning’ = Cushing’s reflex
184
Q

BRAIN DEATH + COMA

What is the management of brain death + coma?

A
  • ABCDE as emergency
  • Measure vitals, GCS, neuro signs (pupils) + re-check
  • IV access + stabilise c-spine
  • Manage in ICU
185
Q

MYASTHENIA GRAVIS

What is myasthenia gravis?

A
  • Autoimmune disorder against acetylcholine receptors in the neuromuscular junction
186
Q

MYASTHENIA GRAVIS

What is the pathophysiology of myasthenia gravis?

A
  • Autoimmune disorder against acetylcholine receptors in the NMJ leading to depletion of working post-synaptic ACh receptor sites = fewer action potentials
187
Q

MYASTHENIA GRAVIS
What is myasthenia gravis associated with?
What is the epidemiology?

A
  • Associated with autoimmune disease = RA, SLE, thyroid disorders
  • F>M if <40y, M>F if >60y + associated with thymic hyperplasia mainly but also thymoma
188
Q

MYASTHENIA GRAVIS
What is the cardinal feature of myasthenia gravis?
How might this manifest?

A
  • Fatiguable weakness of muscles which improves with rest
  • Extraocular muscles = diplopia, ptosis
  • Proximal muscle weakness = face/neck/limb girdle (hairs, stairs + chairs)
  • Bulbar muscles = dysphagia, dysarthria + nasal speech
189
Q

MYASTHENIA GRAVIS

What are some signs in myasthenia gravis that might be elicited on examination?

A
  • Repeated blinking > ptosis

- Repeated abduction of one arm 20x + compare

190
Q

MYASTHENIA GRAVIS

What can exacerbate myasthenia gravis?

A
  • Abx (ciprofloxacin), CCBs, beta-blockers, lithium + phenytoin
191
Q

MYASTHENIA GRAVIS

What antibodies are implicated in myasthenia gravis?

A
  • Anti-AChR antibodies (90%)

- Muscle-specific tyrosine kinase (MuSK, esp. males)

192
Q

MYASTHENIA GRAVIS

What other investigations might you do for myasthenia gravis?

A
  • Tensilon/edrophonium test = cholinesterase enzymes > increased ACh in NMJ so briefly relieves weakness
  • EMG = decremental muscle response to repeated nerve stimulation
  • CT chest for thymic hyperplasia/thymoma
193
Q

MYASTHENIA GRAVIS
What is the main complication of myasthenia gravis?
What happens?
What may occur?

A
  • Myasthenic crisis
  • Acute exacerbation with severe muscle weakness leading to difficulty breathing + swallowing
  • May lead to respiratory failure
194
Q

MYASTHENIA GRAVIS

What are the causes of myasthenic crisis?

A
  • Infection (resp)
  • Natural disease cycle
  • Under/overdosing meds
195
Q

MYASTHENIA GRAVIS

What is the management of myasthenic crisis?

A
  • Urgent review by neurologists + anaesthetists
  • Monitor breathing with serial FVC measurements
  • NIV or intubation + ventilation
  • Medical = IVIg or plasmapheresis
196
Q

MYASTHENIA GRAVIS

What is the management of myasthenia gravis?

A
  • Acetylcholinesterase inhibitors like pyridostigmine or rivastigmine
  • Immunosuppression with prednisolone or azathioprine to suppress Ab production
  • Thymectomy if thymoma or anti-AChR +ve disease
197
Q

LAMBERT-EATON
What is the pathophysiology of Lambert-Eaton myasthenic syndrome?
What is the classic cause?

A
  • Ab produced against voltage gated Ca2+ channels in SCLC cells also target those at presynaptic NMJ terminals responsible for releasing ACh
  • Paraneoplastic syndrome of SCLC
198
Q

LAMBERT-EATON
What is the clinical presentation of Lambert-Eaton myasthenic syndrome?
How does this contrast to myasthenia gravis?

A
  • Repeated muscle contractions lead to increased muscle strength
  • Limb-girdle weakness (affects lower limbs first)
  • Hyporeflexia
  • Autonomic = dry mouth, impotence, difficulty urinating
  • Eye symptoms NOT commonly present
199
Q

LAMBERT-EATON

What are the investigations for Lambert-Eaton myasthenic syndrome?

A
  • Autoantibodies against voltage gated Ca2+ channels
  • Tensilon test response is not as noticeable
  • EMG shows incremental muscle response to repeated nerve stimulation
  • CT chest for SCLC
200
Q

LAMBERT-EATON

What is the management of Lambert-Eaton myasthenic syndrome?

A
  • 3,4-diaminopyridine like amifampridine
  • Immunosuppression with prednisolone, azathioprine
  • IVIg or plasmapheresis may be trialled
201
Q

LAMBERT-EATON

What is the mechanism of action of amifampridine?

A
  • Blocks pre-synaptic K+ channels so prevent K+ efflux
  • This prolongs AP in nerve terminal so prolongs opening time of Ca2+ channels
  • This augments ACh release in synaptic cleft
202
Q

GUILLAIN-BARRE

What is Guillain-Barré syndrome (GBS)?

A
  • Ascending inflammatory demyelinating polyneuropathy where antibodies attack Schwann cells of the peripheral nervous system
203
Q

GUILLAIN-BARRE
What is Miller-Fisher syndrome?
How does it present?

A
  • GBS variant which affects CNS + eye muscles

- Characterised by ophthalmoplegia, areflexia, ataxia + descending paralysis

204
Q

GUILLAIN-BARRE

What is the aetiology of GBS?

A
  • Often triggered by preceding illness 4w before symptoms

- Campylobacter jejuni (v common), CMV, EBV

205
Q

GUILLAIN-BARRE
What might be the initial symptoms in GBS?
What is the clinical presentation of GBS?

A
  • Initial = back/leg pain
  • Progressive, symmetrical, ascending muscle weakness + paraesthesia
  • Reflexes reduced/absent
  • CN/autonomic involvement, respiratory muscle weakness
206
Q

GUILLAIN-BARRE

What are the investigations for GBS?

A
  • Monitor FVC
  • Anti-ganglioside antibody (anti-GM1)
  • Nerve conduction studies = slowing of motor conduction velocity (demyelination)
  • LP CSF shows raised protein with normal WCC + glucose
207
Q

GUILLAIN-BARRE

What is the prognosis of GBS?

A
  • 80% fully recover
  • 15% recover with neurological disability
  • 5% die, mostly from PE, resp failure or infection
208
Q

GUILLAIN-BARRE
What is the main medical management of GBS?
What is a contraindication for one of these treatments?

A
  • IVIg but C/I if IgA deficiency as would cause anaphylaxis

- Plasma exchange if ineffective

209
Q

GUILLAIN-BARRE

What is the supportive therapy for GBS?

A
  • VTE prophylaxis with TEDS + LMWH
  • NG or PEG feeding if swallowing issues
  • Ventilation if respiratory respiratory failure
210
Q

BRAIN TUMOURS

What’s the most common type of brain tumour?

A
  • Secondary mets

- Lungs > breast > melanoma > colorectal > RCC

211
Q

BRAIN TUMOURS

Give 4 examples of different brain tumours

A
  • Gliomas
  • Meningiomas
  • Pituitary adenoma
  • Acoustic neuromas
212
Q

BRAIN TUMOURS
What are gliomas?
Give some examples

A
  • Glial cell in origin in the brain or spinal cord
  • Graded 1–4 (1 = most benign, 4 = most malignant glioblastomas)
  • Astrocytomas like glioblastoma multiforme most common (90%)
213
Q

BRAIN TUMOURS

What are meningiomas?

A
  • Benign tumours growing from cells of the meninges in the brain + spinal cord
214
Q

BRAIN TUMOURS

What are the 3 cardinal signs of brain tumours?

A
  • Progressive focal neurological deficit depending on location of tumours
  • Sx of raised ICP
  • Seizures/epilepsy (focal rather than generalised)
215
Q

BRAIN TUMOURS

Why is the neurological deficit progressive in brain tumours?

A
  • Mass effect of tumour + surrounding cerebral oedema as it grows
216
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in…

i) frontal lobe?
ii) temporal lobe?
iii) parietal lobe?
iv) occipital lobe?
v) cerebellum?

A

i) Personality change, hemiparesis, expressive dysphasia
ii) Receptive dysphasia, amnesia
iii) Hemisensory loss, dysphasia
iv) Contralateral visual defects
v) Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia (DANISH)

217
Q

BRAIN TUMOURS

What are some symptoms of raised ICP?

A
  • Headache – worse in morning, coughing, bending forwards or lying
  • N+V
  • Papilloedema (swollen optic disc) on fundoscopy
218
Q

BRAIN TUMOURS
What investigations would you perform for brain tumours?
What might you see with a glioblastoma?

A
  • CT/MRI head (MRI gold standard)
  • MR angiography may be useful to define site or blood supply of mass
  • Solid tumour, central necrosis, contrast-enhanced rim
219
Q

BRAIN TUMOURS

What is the general management of brain tumours?

A
  • Combination surgery, radio + chemotherapy

- Medical = dexamethasone or mannitol to reduce cerebral oedema

220
Q

BRAIN TUMOURS

How do you manage raised intracranial pressure?

A
  • Head elevation to 30º
  • IV mannitol
  • Hyperventilation (reduces PaCO2 = cerebral artery vasoconstriction = reduced ICP)
221
Q

NEUROPATHY
What is the pathophysiology of mononeuritis multiplex?
What can cause mononeuritis multiplex?

A
  • Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit
  • Inflammatory or immune mediated vasculitis like granulomatosis with polyangiitis, polyarteritis nodosa, RA or sarcoidosis
222
Q

NEUROPATHY

What are the causes of peripheral neuropathy?

A

ABCDE –

  • Alcohol
  • B12 deficiency
  • Cancer + CKD
  • Diabetes + drugs (isoniazid, amiodarone)
  • Every vasculitis
223
Q

NEUROPATHY
In terms of peripheral neuropathy, what conditions show a…

i) mostly motor loss?
ii) mostly sensory loss?

A

i) GBS, chronic inflammatory demyelination polyneuropathy (chronic GBS), Charcot-Marie-Tooth disease
ii) DM, CKD, deficiencies

224
Q

NEUROPATHY

What is Charcot-Marie-Tooth disease?

A
  • Autosomal dominant condition.
  • Characterised by high-arched feet, distal muscle weakness + atrophy (inverted champagne bottle legs), hyporeflexia, foot drop + hammer toes
225
Q

NEUROPATHY

What is the generic clinical presentation of mononeuritis multiplex?

A
  • Subacute presentation (months rather than years), painful, asymmetrical sensory + motor neuropathy
226
Q

NEUROPATHY

What is the generic clinical presentation of peripheral neuropathy?

A
  • Chronic + slowly progressive
  • Starts in legs + longer nerves first (furthest from heart)
  • Sensory/motor/both
  • Glove + stocking distribution
227
Q

NEUROPATHY
What is the most common mononeuropathy?
What is the pathophysiology?
What is the aetiology?

A
  • Carpal tunnel syndrome
  • Inflammation of carpal tunnel leads to entrapment of the median nerve
  • Idiopathic but associated with local tumours, DM + RA
228
Q

NEUROPATHY

What muscles does the median nerve innervate?

A

LLOAF –

  • Lateral lumbricals x2
  • Opponens pollicis
  • Abductor pollicis brevis
  • Flexor pollicis brevis
229
Q

NEUROPATHY

What is the clinical presentation of carpal tunnel syndrome?

A
  • Pain, sensory loss + paraesthesia (esp. night) in radial 3.5 digits, may be relieved by shaking hand (wake + shake)
  • Difficulty with precision grip
  • Wasting of thenar eminence
230
Q

NEUROPATHY
What clinical signs might you elicit on examination?
What investigation might you do in carpal tunnel syndrome and what would it show?

A
  • Phalen’s test = inverse prayer sign, can only maximally flex wrist for 1m
  • Tinel’s test = tapping on nerve at wrist induces tingling
  • Nerve conduction studies = motor + sensory prolongation of AP
231
Q

NEUROPATHY

What is the management of carpal tunnel syndrome?

A
  • Wrist plinting
  • Analgesia
  • Local steroid injection ± decompression surgery
232
Q

NEUROPATHY
Roots of the ulnar nerve?
What causes ulnar neuropathy?

A
  • C7–T1

- Elbow trauma or fracture, elbow arthritis

233
Q

NEUROPATHY

What are the motor signs of ulnar neuropathy?

A

Weakness/wasting of –

  • Interossei (can’t do good luck sign)
  • Medial lumbricals (claw hand)
  • Hypothenar eminence
  • +ve Froment’s sign = thumb bent when holding paper (weak adductor pollicis)
234
Q

NEUROPATHY

What are the sensory signs of ulnar neuropathy?

A
  • Sensory loss 1.5 fingers ulnar side on dorsal + palmar aspects
235
Q

NEUROPATHY
Roots of the radial nerve?
What causes radial neuropathy?

A
  • C5-T1

- Compression against humerus

236
Q

NEUROPATHY
What are the motor signs of radial neuropathy?
What are the sensory signs?

A
  • Wrist + finger drop (weak extension), can’t open first

- Below fingertips on radial 3.5 fingers dorsally, part of thenar eminence

237
Q

NEUROPATHY
What causes brachial plexus neuropathy?
Presentation?

A
  • Trauma, radiotherapy or heavy rucksack

- Pain, paraesthesia + weakness in affected arm in variable distribution

238
Q

NEUROPATHY
Roots of phrenic nerve?
Causes of neuropathy?
Presentation?

A
  • C3–5
  • Lung cancer, myeloma, thymoma
  • Orthopnoea with raised hemidiaphragm on CXR
239
Q

NEUROPATHY
Roots of lateral cutaneous nerve of the thigh?
Causes of neuropathy?
Presentation?

A
  • L2–L3
  • Entrapment under inguinal ligament
  • Meralgia paraesthetica = antero-lateral burning thigh pain
240
Q

NEUROPATHY
Roots of sciatic nerve?
Causes of neuropathy?
Presentation?

A
  • L4–S3
  • Pelvic tumours or pelvic/femoral #
  • M = foot drop, S = loss below the knee laterally
241
Q

NEUROPATHY
Roots of common peroneal nerve?
Causes of neuropathy?
Presentation?

A
  • L4–S1
  • Damaged as winds round fibular head by trauma or sitting cross-legged (classic after night out)
  • M = foot drop, weak ankle dorsiflexion + eversion with high steppage gait, S = loss over dorsal foot
242
Q

NEUROPATHY
Roots of the tibial nerve?
Presentation of neuropathy?

A
  • L4–S3

- M = weak ankle plantar flexion, inversion + toe flexion, S = loss over sole of foot

243
Q

NEUROPATHY

How does an L5 radiculopathy present?

A
  • Loss of inversion (tibial nerve)
  • Foot drop
  • Sensation loss in L5 dermatome
244
Q

NEUROPATHY

What does a CN1 lesion cause?

A
  • Anosmia
245
Q

NEUROPATHY
In terms of the optic nerve, what does a…

i) L optic nerve lesion
ii) Optic chiasma lesion
iii) L optic tract lesion
iv) L Baum’s loop lesion
v) L Meyer’s loop lesion

cause?

A

i) No vision through L eye
ii) Bitemporal hemianopia
iii) Contralateral (R) homonymous hemianopia
iv) Inferior R homonymous quadrantanopia
v) Superior R homonymous quadrantanopia

246
Q

NEUROPATHY
Where is Baum’s loop located?
Where is Meyer’s loop located?
How can you remember which is superior/inferior?

A
  • Parietal lobe
  • Temporal lobe
  • PITS – Parietal Inferior Temporal Superior
247
Q

NEUROPATHY

What does a CN3 lesion cause?

A
  • Tramps’ palsy (eye down + out)
  • Ptosis
  • Fixed dilated pupil (loss of parasympathetic outflow, exclude a surgical 3rd nerve)
248
Q

NEUROPATHY

What does a CN4 lesion cause?

A
  • Vertical diplopia noticed when reading book or going downstairs
  • Defective downward gaze as innervates superior oblique
249
Q

NEUROPATHY

What does a CN5 lesion cause?

A
  • Loss of sensation to face
  • Weak muscles of mastication
  • Loss of corneal reflex (afferent)
  • Jaw deviation to weak side
250
Q

NEUROPATHY

What does a CN6 lesion cause?

A
  • Issues abducting eye beyond midline as innervates lateral rectus
251
Q

NEUROPATHY

What does a CN7 lesion cause?

A

Face, ear, taste, tear –

  • Muscles of expression
  • Stapedius
  • Anterior 2/3rd tongue
  • Parasympathetic fibres to lacrimal + salivary glands
252
Q

NEUROPATHY
What is Bell’s palsy and how does it present?
What causes it?

A
  • CN7 lesion with complete facial paralysis (LMN so no forehead sparing but spares extraocular + mastication muscles) hyperacusis + otalgia
  • Often post-viral (HSV)
253
Q

NEUROPATHY

What is the management of Bell’s palsy?

A
  • PO pred within 72h
  • Eye care = lubricants, artificial tears, tape eye shut
  • Paralysis no improvement after 3w = urgent ENT referral
254
Q

NEUROPATHY

What does a CN8 lesion cause?

A
  • Sensorineural deafness

- Tinnitus, vertigo, nystagmus

255
Q

NEUROPATHY

What does a CN9/10 lesion cause?

A
  • Swallow, gag + cough issues

- Uvula deviated away from side of lesion

256
Q

NEUROPATHY
What does a…

i) CN11 lesion cause?
ii) CN12 lesion cause?

A

i) Weakness turning head to contralateral side

ii) Tongue deviation towards side of lesion

257
Q

NEUROPATHY
What investigations are included in a neuropathy screen?
What investigations are included in a vasculitis screen?

A
  • Neuropathy screen (symmetrical) = FBC, CRP/ESR, U+E, glucose, TFT, B12 + folate
  • Vasculitis screen (asymmetrical) = first 3 + ANA, ANCA, anti-dsDNA, RhF, complement
  • EMG + nerve conduction studies
258
Q

NEUROPATHY

What is the management of neuropathy?

A
  • Sx relief with neuropathic analgesia (gabapentin, pregabalin, amitriptyline)
  • Treat underlying cause
259
Q

CORD COMPRESSION
What is…

i) myelopathy?
ii) radiculopathy?

A

i) Injury to the spinal cord due to severe compression

ii) Sx caused by pinching of a nerve root as they exit the spinal cord

260
Q

CORD COMPRESSION
How does radiculopathy present?
What is the most common radiculopathy?

A
  • Sharp, shooting pain within distribution of nerve, weakness + loss of sensation
  • Sciatica (L5) = lower back pain that travels to buttocks + down back of thigh to calf
261
Q

CORD COMPRESSION

What are the aetiologies of spinal cord compression?

A
  • Malignancy (mostly secondary, 5Bs = breast, bronchus, byroid, bidney, brostate) or myeloma
  • Infection (epidural abscess)
  • Disc prolapse
  • Haematoma (warfarin)
  • Lumbar degeneration + spinal osteophytes due to trauma or age
  • Myeloma
262
Q

CORD COMPRESSION

What are the symptoms of spinal cord compression?

A
  • Back pain (earliest + most common)

- Lower limb weakness + sensory changes (sudden or progressive = red flag)

263
Q

CORD COMPRESSION

What are the signs of spinal cord compression?

A
  • LMN signs = AT level
  • UMN signs = BELOW level
  • Tendon reflexes increased below level of lesion + absent at level
264
Q

CORD COMPRESSION

How does degenerative cervical myelopathy present?

A
  • Pain, loss of motor or sensory function affecting neck, upper or lower limbs
  • Loss of autonomic function
  • Hoffman’s sign +ve
265
Q

CORD COMPRESSION

What are the investigations of spinal cord compression?

A
  • PR to assess loss of sphincter control
  • Screening bloods (FBC, CRP/ESR, B12, LFT, U+Es)
  • MRI WHOLE spine gold standard
266
Q

CORD COMPRESSION

What is the main complication of spinal cord compression?

A
  • Cauda equina syndrome

- Cord compression below the level of the termination of the spinal cord at L1/2 vertebral level = medical emergency

267
Q

CORD COMPRESSION
What can cause cauda equina syndrome?
What are the red flag symptoms for cauda equina?
How is it managed?

A
  • Mostly malignancy, disc prolapse (L4/5, L5/S1), trauma
  • Lower back pain, bilateral sciatica, saddle anaesthesia, decreased anal tone, urinary dysfunction, bowel dysfunction (incont or retain)
  • Urgent MRI whole spine, dexamethasone STAT ± surgical decompression
268
Q

CORD COMPRESSION
What is spinal stenosis?
How does it present?
How is it managed?

A
  • Narrowing of lower spinal canal due to OA osteophytes
  • Spinal claudication > pain in buttocks/legs when walking, pain eased by bending forward (canal opens), sitting better than standing, uphill better than downhill
  • MRI spine + canal decompression surgery
269
Q

CORD COMPRESSION
What is the management of malignant spinal cord compression?
What is the management of epidural abscess?
What is the management of degenerative cervical myelopathy?

A
  • Malignancy = stat dexamethasone + consider chemo, radio, surgery
  • Epidural abscess = surgical decompression + Abx
  • Degenerative cervical myelopathy = urgent spinal surgery referral for surgical decompression
270
Q

SPINAL CORD INJURY

What is Brown-Sequard syndrome?

A
  • Lateral hemisection of spinal cord
  • Ipsilateral weakness below the lesion (lateral corticospinal)
  • Ipsilateral loss of fine touch, proprioception + vibration (DCML)
  • Contralateral loss of pain + temp (lateral spinothalamic)
271
Q

MYOPATHY

What are the aetiologies of myopathies?

A
  • Inflammatory = polymyositis, dermatomyositis
  • Inherited = Duchenne, Becker’s muscular dystrophy, myotonic dystrophy
  • Endo = Cushing’s, thyrotoxicosis
  • Drugs = alcohol, statins
272
Q

MYOPATHY

How do myopathies present?

A
  • Symmetrical proximal pattern of muscle weakness (hairs, stairs + chairs)
  • Weakness > wasting
  • Reflexes + sensation normal, no fasciculations
273
Q

MYOPATHY

How does myotonic dystrophy present?

A
  • Autosomal dominant

- Bilateral ptosis, cataracts, dysarthria, cardiac involvement

274
Q

MYOPATHY

What are the investigations for myopathies?

A
  • CRP/ESR, creatinine kinase elevated

- Autoantibodies (anti-Jo-1), EMG, genetics + muscle biopsy

275
Q

MYOPATHY

What is the management of myopathies?

A
  • Remove causative agent (statins, steroids)

- Immunosuppression (steroids, azathioprine) if inflammatory cause.

276
Q

HYDROCEPHALUS

What is hydrocephalus?

A
  • Abnormal build-up of CSF around the brain causing compression to nearby brain tissue as the ventricles dilate
277
Q

HYDROCEPHALUS

What is the usual flow of CSF in the brain?

A
  • Lateral ventricles
  • Foramen of Munro
  • 3rd ventricle
  • Cerebral aqueduct
  • 4th ventricle
  • Subarachnoid space (Medially by foramen of Magendie, Laterally by Luschka)
  • Dural sinus via arachnoid granulations
278
Q

HYDROCEPHALUS

What are the 3 types of hydrocephalus?

A
  • Obstructive (non-communicating)
  • Non-obstructive (communicating) = imbalance of CSF production/absorption
  • Normal pressure = unknown, can develop after head injury or stroke, >60s
279
Q

HYDROCEPHALUS
What are some causes of…

i) obstructive
ii) non-obstructive

hydrocephalus?

A

i) Tumour, acute haemorrhages, developmental abnormalities
ii) Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage) or increased CSF production (choroid plexus tumour) but very rare

280
Q

HYDROCEPHALUS

How does hydrocephalus present?

A
  • Signs of raised ICP
  • Headache (worse in morning or lying down)
  • N+V, papilloedema, blurred vision
281
Q

HYDROCEPHALUS
What are the investigations for hydrocephalus?
What do you need to be careful about?

A
  • CT head = enlarged ventricles
  • MRI head if suspected underlying lesion
  • LP is both diagnostic + therapeutic (caution in obstructive as difference in cranial/spinal pressures can cause brain herniation)
282
Q

HYDROCEPHALUS
What is the management of hydrocephalus?
What is a potential complication?

A
  • Ventriculoperitoneal shunt = surgically implanted into brain to drain excess fluid (may become blocked or infected)
  • Endoscopic third ventriculostomy
283
Q

IIH

What is idiopathic intracranial hypertension (IIH)?

A
  • Buildup of CSF pressure around the brain causing signs of raised ICP
284
Q

IIH

What are some risk factors?

A
  • Obesity, female, pregnancy, drugs (COCP, tetracyclines, vitamin A)
285
Q

IIH

What is the clinical presentation of IIH?

A
  • Presents as if mass but none found
  • Headache, blurred vision
  • Papilloedema
  • Enlarged blind spot ± CN 6 palsy
286
Q

IIH

What are the investigations for IIH?

A
  • Routine bloods + CT head to exclude organic causes

- LP to exclude infection = increased opening pressure (can be therapeutic)

287
Q

IIH

What is the management of IIH?

A
  • First line = weight loss, if not = acetazolamide
  • Surgery = optic nerve sheath decompression + fenestration if visual Sx
  • Lumboperitoneal or ventriculoperitoneal shunt
288
Q

DVS THROMBOSIS
What is dural venous sinus thrombosis (DVS thrombosis)?
What can it lead to?
What causes it?

A
  • Blood clot in the dural venous sinuses which drain blood from the brain.
  • Cerebral infarction (stroke) but less commonly than arterial
  • Thrombophilias, pregnancy, polycythaemia, sickle cell
289
Q

DVS THROMBOSIS
What is the clinical presentation of DVS thrombosis?
How does sagittal sinus thrombosis present?
How does lateral sinus thrombosis present?
How does cavern

A
  • Headaches (sudden onset), N+V, abnormal vision
  • Sagittal sinus thrombosis (mostly) = seizures + hemiplegia
  • Lateral sinus thrombosis = CN6+7 palsies
290
Q

DVS THROMBOSIS
How does cavernous sinus thrombosis present?
What structures run through the cavernous sinus?

A
  • CN3, 4, CN 5 (V1+V2) + ICA
  • Periorbital oedema
  • Ophthalmoplegia (CN 6 usually before 3 + 4)
  • Hyperaesthesia to upper face + eye pain (CN 5)
291
Q

DVS THROMBOSIS
What are the investigations for DVS thrombosis?
What is the management?

A
  • CT head of superior sagittal sinus thrombosis can show classic empty delta sign
  • MRI venogram gold standard
  • Anticoagulation with LMWH then warfarin
292
Q

NEURO PHARMACOLOGY

What is their mechanism of action of AEDs?

A
  • Inhibit voltage-gated Na+ channels which prevents excitability of neurones > reduced firing > stops seizure, some promote GABA release
293
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) carbamazepine?
ii) valproate?

A

i) P450 INDUCER, SIADH, agranulocytosis

ii) P450 INHIBITOR, teratogenic, weight gain

294
Q

NEURO PHARMACOLOGY
What are some side effects and important information for…

i) lamotrigine?
ii) phenytoin?

A

i) Steven-Johnson syndrome

ii) P450 INDUCER, megaloblastic anaemia, peripheral neuropathy

295
Q

NEURO PHARMACOLOGY
What is the mechanism of action of Levodopa?
What is it combined with?

A
  • Levodopa is dopamine precursor which can cross BBB to be converted to dopamine by dopa-decarboxylase
  • Must be combined with peripheral dopa-decarboxylase inhibitor like carbidopa so levodopa can reach brain
296
Q

NEURO PHARMACOLOGY

What are the side effects of Levodopa?

A
  • Postural hypotension
  • Dyskinesias (abnormal movements)
  • Effectiveness decreases with time
  • On-off effect
  • Psychosis
  • Palpitations
297
Q 
NEURO PHARMACOLOGY
Give some examples of dopamine receptor agonists.
What is the mechanism of action?
What are some side effects?
What monitoring is required?
A
  • Bromocriptine, cabergoline, ropinirole
  • Increases amount of dopamine in CNS
  • Hallucinations, postural hypotension
  • ECHO, ESR, creatinine + CXR prior to Rx
298
Q

NEURO PHARMACOLOGY

What are some adverse effects of dopamine receptor agonists?

A
  • Pulmonary retroperitoneal + cardiac fibrosis

- Impulse control disorders

299
Q

NEURO PHARMACOLOGY
What are COMT + MAO-B inhibitors?
What is the mechanism of action?

A
  • Catechol-o-methyltransferase (COMT) inhibitor = entacapone
  • Monoamine oxidase-B (MAO-B) inhibitor = selegiline
  • Inhibit enzymatic breakdown of dopamine
300
Q

NEURO PHARMACOLOGY
Examples of triptans.
Mechanism of action?
Side effects/contraindications?

A
  • Sumatriptan, naratriptan
  • 5-HT (serotonin) receptor agonists
  • SE = dizziness, dry mouth, fatigue, nausea, C/I in CVD

FINALS (20 decks)

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