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A TO REVISE - PHASE 3A > NEURO TO DO > Flashcards

NEURO TO DO Flashcards

1
Q

STROKE
What vessels can be affected in total anterior circulation syndrome (TACS)?

A
  • ACA, MCA, carotid
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2
Q

STROKE
What vessels can be affected in a partial anterior circulation syndrome (PACS)?

A
  • ACA, MCA, carotid (same vessels as TACS)
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3
Q

STROKE
What vessels can be affected in a posterior circulation syndrome (POCS)?

A
  • PCA, vertebrobasilar artery or branches
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4
Q

STROKE
What vessels can be affected in lacunar syndrome (LACS) and what does that mean?

A
  • Perforating arteries so no higher cortical dysfunction or visual field abnormality, subcortical stroke
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5
Q

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

A
  • Cerebellar: ataxia, nystagmus
  • Ipsi: dysphagia, facial numbness + CN palsy
  • Contra: limb sensory loss
  • Posterior inferior cerebellar artery
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6
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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7
Q

STROKE
What criteria must be met for a total anterior circulation syndrome (TACS)?

A

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 criteria must be met for a partial anterior circulation syndrome (PACS)?

A
  • 2/3 of the criteria for TACS:
  • Hemiplegia (unilateral ± sensory deficit of face, arm leg)
  • Homonymous hemianopia
  • Higher cerebral dysfunction (dysphasia, visuospatial disturbance)
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9
Q

STROKE
What criteria must be met for a posterior circulation syndrome (POCS)?

A

One of the following –
- Cranial nerve palsy + contralateral motor/sensory deficit
- Bilateral motor/sensory deficit
- Conjugate eye movement disorder (e.g. gaze palsy)
- Cerebellar dysfunction (ataxia, nystagmus, vertigo)
- Isolated homonymous hemianopia + cortical blindness

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10
Q

STROKE
What criteria must be met for a lacunar syndrome (LACS)?

A

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
What areas can be affected in lacunar syndrome (LACS)?

A
  • Thalamus, basal ganglia, internal capsule
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12
Q

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

A
  • C7–T1
  • Elbow trauma or fracture, elbow arthritis
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13
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 when grip paper between thumb + index finger

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14
Q

NEUROPATHY
What are the sensory signs of ulnar neuropathy?

A
  • Sensory loss 1.5 fingers ulnar side on dorsal + palmar aspects
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15
Q

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

A
  • C5-T1
  • Compression against humerus
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16
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
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17
Q

NEUROPATHY
What causes brachial plexus neuropathy?
Presentation?

A
  • Trauma, radiotherapy or heavy rucksack
  • Pain, paraesthesia + weakness in affected arm in variable distribution
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18
Q

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

A
  • C3–5
  • Lung cancer, myeloma, thymoma
  • Orthopnoea with raised hemidiaphragm on CXR
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19
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
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20
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
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21
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
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22
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
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23
Q

SPEECH ISSUES
What is dysphasia?
What is it seen in?

A
  • Impairment of language caused by brain damage (area affected dictates type)
  • Stroke
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24
Q

SPEECH ISSUES
What are the features of Broca’s dysphasia?
What area is affected?

A
  • Expressive dysphasia so reading + writing impaired, malformed words + non-fluent speech BUT comprehension intact (can follow commands)
  • Frontal lobe of dominant hemisphere (often left)
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25
Q

SPEECH ISSUES
What are the features of Wernicke’s dysphasia?
What area is affected?

A
  • Receptive dysphasia so cannot respond to requests (comprehension issues) BUT fluent speech production (albeit replies inappropriate)
  • Temporal lobe dominant hemisphere
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26
Q

SPEECH ISSUES
What is dysarthria?
What is it seen in?

A
  • Difficulty in speech articulation due to weakness of speech-related musculature so slurred
  • Cerebellar disease, stroke, pseudobulbar palsy (MND), bulbar palsy (GBS, MND)
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27
Q

SPEECH ISSUES
What is pseudo?
What is pseudobulbar dysarthria?

A
  • Affects UMN
  • Slow, nasal, effortful ‘hot potato’ voice
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28
Q

SPEECH ISSUES
What is dysphonia?
What is it seen in?

A
  • Difficulty in speech volume due to weakness of resp muscles or vocal cords
  • MG, GBS, Parkinson’s (mixed dysphonia + dysarthria)
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29
Q

SPEECH ISSUES
What is bulbar?
What is bulbar dysarthria?

A
  • Affects LMN of CN9–12
  • Nasal speech due to paralysis of palate
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30
Q

STROKE
What are some important differentials of stroke?

A
  • Metabolic (hypo or hyperglycaemia, electrolytes)
  • Intracranial tumours, hemiplegic migraine
  • Infection (meningitis)
  • Head injury, seizure (focal > Todd’s paralysis)
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31
Q

STROKE
What classification system can be used for strokes?

A
  • Oxford stroke (Bamford) classification
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32
Q

TIA
What is it essential to do in someone who has had a TIA?

A

Assess their risk of having stroke in the next 7 days = ABCD2 score

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33
Q

TIA
What do the scores from ABCD2 mean?

A
  • ≥4 or crescendo TIAs = specialist assessment within 24h (give aspirin 300mg OD)
  • ≤3 = specialist assessment within 1 week, ?brain imaging
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34
Q

STROKE
What tools can be used to identify stroke?

A
  • FAST = Facial drooping, Arms floppy, Slurred speech, Time critical (999)
  • ROSIER = Recognition Of Stroke In Emergency Room
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35
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 (squishing) in cortical infarction
  • Hypodense basal ganglia may be seen in deep vessel infarcts
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36
Q

STROKE
How would a haemorrhagic stroke appear on CT head?

A
  • Acute = hyperdense
  • Subacte = isodense
  • Chronic = hypodense
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37
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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38
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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39
Q

STROKE
What other management is given for ischaemic strokes?

A
  • Control BP
  • 300mg aspirin OD 2w post-stroke + then lifelong 75mg clopidogrel
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40
Q

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

A
  • Antiplatelets (lifelong clopidogrel or aspirin + dipyridamole if cardiac disease)
  • Anticoagulation if have AF but wait 2w post-stroke
  • Manage co-morbidities (HTN, DM)
  • Cholesterol >3.5mmol/L diet + 80mg atorvastatin
  • VTE assessment + monitor for infection
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41
Q

STROKE
When assessing whether to anticoagulate a patient, what scores could you use?

A
  • CHA2DS2-VaSc (risk of stroke due to AF)
  • HAS-BLED (risk of serious bleeding)
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42
Q

STROKE
What is the CHA2DS2-VaSc score

A
  • Congestive heart failure
  • HTN
  • Age 65-74 (1), ≥75 (2)
  • Diabetes
  • Prev stroke/TIA (2)
  • Vascular disease
  • Sex female
  • 1 = consider anticoagulation, ≥2 = anticoagulate
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43
Q

STROKE
What is the HAS-BLED score?

A
  • HTN >160mmHg
  • Abnormal liver/renal function
  • Stroke
  • Bleeding Hx or predisposition
  • Labile INR
  • Elderly >65y
  • Drug/alcohol use
  • ≥3 = high risk of bleeding
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44
Q

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

A
  1. tissue ischaemia - less blood, O2 and nutrients can reach the tissue due to bleeding loss -> cell death
  2. raised ICP - fast flowing arterial blood is pumped into the cranial space
  3. space occupying lesion - puts pressure on the brain
  4. brain irritates meninges - these inflame causing meningism symptoms. This can obstruct CSF outflow -> hydrocephalus
  5. vasospasm - bleeding irritates other vessels -> ischaemic injury
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45
Q

SAH
What are the causes of SAH?

A
  • Traumatic injury
  • Berry aneurysm rupture
    (70-80%) - at common points round Circle of Willis
  • Arteriovenous malformations (15%) - abnormal tangle of blood vessels connecting arteries and veins
  • Idiopathic (15-20%)
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46
Q

SAH
What conditions are linked to SAH?

A
  • Polycystic kidneys
  • coarctation of aorta
  • Ehlers-Danlos syndrome
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47
Q

SAH
What are some symptoms of SAH?

A
  • sudden onset excruciating headache - thunderclap, worst headache, typically occipital
  • sentinel headache - before main rupture, sign of warning leak
  • nausea
  • vomiting
  • collapse
  • loss of/depressed consciousness
  • seizures
  • vision changes
  • coma - can last for days
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48
Q

SAH
What are some signs of SAH?

A
  • signs of meningeal irritation
    1. Kernig’s sign (can’t straighten leg past 135 degrees)
    2. neck stiffness
    3. Brudzinski’s sign (Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed)
  • retinal, subhyaloid and vitreous bleeds
    • worse prognosis
    • with/without papilloedema
  • neurological signs - e.g. 3rd nerve palsy
  • increased BP
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49
Q

SAH
What is the management of SAH?

A
  • NIMOPIDINE for 3 weeks -> CCB which prevents vasospasm so reduces cerebral ischaemia
  • surgery = endovascular coiling
  • IV fluids - maintain cerebral perfusion
  • ventricular drainage for hydrocephalus
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50
Q

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

A
  • Often fractured temporal/parietal bone leads to blood accumulating between bone + dura mater over minutes to hours

After a lucid interval there is:
- rapid rise in ICP
pressure on the brain
- midline shift
- tentorial herniation
- coning

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51
Q

EDH
What do the ventricles do to prolong survival in someone with an extradural haematoma?

A
  • Ventricles get rid of their CSF to prevent the rise in ICP
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52
Q

EDH
What is the clinical presentation of EDH?

A
  • initial injury followed by lucid period
  • period of rapid deterioration
  • rapid decline in GCS
  • increasing severe headache
  • vomiting
  • seizures
  • hemiparesis
  • coma
  • UMN signs
  • ipsilateral pupil dilation
  • bilateral limb weakness
  • deep and irregular breathing - due to coning
    late signs = bradycardia and raised BP (cushing’s reflex)
  • death from respiratory arrest
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53
Q

EDH
what are the signs of ICP ± focal neurology in EDH?

A
  • Increasingly severe headache,
  • vomiting,
  • confusion + seizures ± hemiparesis with brisk reflexes
  • upgoing plantars
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54
Q

EDH
What are some differentials for EDH?

A
  • Epilepsy,
  • CO poisoning,
  • carotid dissection
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55
Q

EDH
What is the management for EDH?

A

STABILISE PATIENT

URGENT SURGERY

clot evacuation
ligation of bleeding vessel
IV MANNITOL
- to reduce ICP

airway care
- intubation and ventilation

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56
Q

SDH
What is the most common cause of subdural haematoma (SDH)?

A
  • Rupture of a vein running from hemisphere to the sagittal sinus of the dural venous sinuses (bridging veins) that’s beneath the dura leading to haematoma between arachnoid + dura mater
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57
Q

SDH
What is the pathophysiology of a SDH?

A
  1. bleeding from bridging veins into the subdural space forms a haematoma
  2. then bleeding stops
  3. weeks/months later the haematoma starts to autolyse - massive increase in oncotic and osmotic pressure. Water is sucked in and haematoma enlarges
  4. gradual rise in ICP over weeks
  5. midline structures shift away from side of clot - causes tentorial herniation and coning
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58
Q

SDH
What are the symptoms of SDH?

A
  • Fluctuating GCS
  • Headache
  • Confusion - may fluctuate
  • Drowsiness
  • physical and intellectual slowing
  • personality change
  • unsteadiness
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59
Q

SDH
What are some signs of SDH?

A
  • raised ICP - seizures
  • localising neurological signs (unequal pupils, hemiparesis)
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60
Q

SDH
What is the management of SDH?

A

SURGERY
1* = irrigation via burr-hole craniostomy
2* = craniotomy

IV MANNITOL - to reduce ICP

address cause of trauma

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61
Q

EPILEPSY
Define epilepsy

A

Recurrent, spontaneous, intermittent abnormal electrical activity in part of the brain, manifesting seizures

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62
Q

EPILEPSY
What are the causes of epilepsy?

A
  1. Idiopathic (2/3)
  2. cortical scarring
  3. tumour
  4. stroke
  5. alzheimers dementia
  6. alcohol withdrawal
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63
Q

EPILEPSY
What are some differentials of epilepsy?

A
  • Cardiac = postural or cardiogenic syncope
  • Non-epileptic attack disorder, hypoglycaemia, TIA
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64
Q

EPILEPSY
What investigations would you do in epilepsy?

A
  • Mostly clinical Dx, witnessed seizure Hx crucial

Electroencephalogram (EEG) = supports diagnosis

MRI/ CT head = rule out space-occupying lesions

Bloods
FBC, Ca2+, electrolytes, U&Es, LFTs, blood glucose = rule out metabolic disturbances

Genetic testing
If suspected genetic cause -> juvenile myoclonic epilepsy

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65
Q

EPILEPSY
what is the treatment for generalised tonic-clonic epilepsy?

A

1st line = Sodium Valproate for Males & women unable to childbear,

2nd line = Lamotrigine to females of childbearing potential for myoclonic

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66
Q

EPILEPSY
what is the treatment for absence (petit mal) epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Ethosuximide to females of childbearing potential

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67
Q

STATUS EPILEPTICUS
What are some causes of status epilepticus?

A
  • Poor adherence #1
  • Infections (meningitis, encephalitis)
  • Worsening of primary cause of epilepsy (e.g. brain tumour growing)
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68
Q

STATUS EPILEPTICUS
What is the clinical presentation of status epilepticus?

A
  • Convulsions tend to occur for 2–3m
  • Followed by slow activity or rest period + then more convulsions
  • The whole process continues although individual seizures do not
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69
Q

STATUS EPILEPTICUS
What are the complications of status epilepticus?

A
  • 10% mortality
  • Long-term morbidity after episode, esp. if hypoxic brain injury occurred (rhabdomyolysis, metabolic acidosis, renal failure)
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70
Q

STATUS EPILEPTICUS
What is the initial management for status epilepticus?

A
  • ABCDE approach (Secure airway, high conc oxygen, assess cardiorespiratory function)
  • Establish IV access
  • Measure capillary glucose + correct immediately
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71
Q

STATUS EPILEPTICUS
What investigations might you do for aetiologies of status epilepticus?

A
  • FBC, U+Es, Ca2+, Mg+, LFTs, INR, AED levels, CK
  • Blood cultures
  • Toxicology screen
  • CT head to rule out organic causes
  • LP if imaging -ve
  • EEG useful
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72
Q

STATUS EPILEPTICUS
What is the step-wise management of status epilepticus?

A
  • IV lorazepam 4mg if fitting >5m – repeat after 10m if persists
  • IV phenytoin (regular ECG/BP), phenobarbital or sodium valproate
  • No response to step 2 within 30m then anaesthesia + ICU admission as anaesthesia will stop but v dangerous
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73
Q

STATUS EPILEPTICUS
What considerations should be made in status epilepticus?

A
  • Community – buccal midazolam or rectal diazepam as step 1
  • If ?alcohol related treat with IV thiamine or Pabrinex
  • If medication not working or no response ?non-epileptic
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74
Q

LOC
What are the potential causes of LOC?

A

CRASH
- Cardiogenic (more alarming)
- Reflex (neurally mediated)
- Arterial
- Systemic
- Head

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75
Q

LOC
How might cardiogenic LOC present/causes?

A
  • Transient arrhythmias (SVT, WPW, Brugada, long QT)
  • Bradyarrhythmias like complete heart block > asystole
  • Structural (aortic stenosis, hypertrophic cardiomyopathy) where may have palpitations, dyspnoea + CP
    BLACKOUT ON EXERCISE IS CARDIOGENIC UNTIL PROVEN OTHERWISE
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76
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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77
Q

NEAD
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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78
Q

NEAD
what is the management of NEAD?

A

correct Dx vital,
speak to pt,
reassure them,
wait for seizure to pass,
CBT,
avoid AEDs as can be fatal if mistreated excessively (respiratory depression)

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79
Q

PARKINSON’S DISEASE
What is the pathophysiology of Parkinson’s disease?

A

destruction of dopaminergic neurones (in substantia nigra) –> reduced dopamine supply –> thalamus inhibits –> decrease in movement + symptoms
Lewy body formation in basal ganglia

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80
Q

PARKINSON’S DISEASE
What are the causes of Parkinson’s disease?

A
  • Unknown, some genetic link, typically 70y/o M
  • Haloperidol (dopamine blockade)
  • Metoclopramide + domperidone (anti-emetics which blockade dopamine)
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81
Q

PARKINSON’S DISEASE
What are the cardinal features of Parkinson’s disease?

A
  • BRADYKINESIA (slow, difficult initiating movement, small movements)
  • RIGIDITY (pain, problems turning in bed) – cogwheel rigidity with tension in arm that gives way to movement in small increments (little jerks)
  • RESTING TREMOR – ‘pill-rolling’
  • Shuffling gait, small steps + postural instability (stooped)
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82
Q

PARKINSON’S DISEASE
what are the clinical features of Parkinson’s disease

A

● Often an insidious onset

impaired dexterity,
fixed facial expressions,
foot drag
● Common associated symptoms:

dementia,
depression,
urinary frequency,
constipation,
sleep disturbances
- Smaller writing (micrographia)
- Hypomimia

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83
Q

PARKINSON’S DISEASE
How can you differentiate Parkinson’s resting tremor from benign essential tremor ?

A
  • Asymmetrical vs symmetrical
  • 4–6Hz vs 5–8Hz
  • Worse at rest vs improves at rest
  • Improves with intentional movement vs worse with intentional movement
  • No change with alcohol vs improves with alcohol (also Rx = propranolol)
  • Parkinson’s vs. autosomal dominant condition
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84
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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85
Q

PARKINSON’S DISEASE
What is progressive supranuclear palsy?

A
  • Early falls, cognitive decline or both sides being equally affected
  • Occurs above nuclei of CN3, 4 + 6 so difficulty moving eyes
  • Impaired vertical gaze (down worse = issues reading or descending stairs)
  • Ocular cephalic reflex present (caused by supranuclear issue) where they tilt/turn their head to look at things rather than moving eyes
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86
Q

PARKINSON’S DISEASE
What is multiple system atrophy?

A
  • Neurones in multiple systems in the brain degenerate
  • Degeneration in basal ganglia > Parkinsonism
  • Degeneration in other areas > early autonomic (postural hypotension + falls, bladder/bowel dysfunction) + cerebellar (ataxia) dysfunction
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87
Q

PARKINSON’S DISEASE
What is corticobasal degeneration?

A
  • Early myoclonic jerks, gait apraxia, agnosia + alien limb
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88
Q

PARKINSON’S DISEASE
What investigations would you do in Parkinson’s disease?

A

DaTscan

Functional neuroimaging - PET

Can confirm by reaction to levodopa

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89
Q

PARKINSON’S DISEASE
What are some complications of Parkinson’s disease?

A
  • Infections
  • Falls
  • Depression
  • Aspiration pneumonia
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90
Q

HUNTINGTON’S DISEASE
What is the pathophysiology of Huntington’s disease?

A
  • Less GABA causes less regulation of dopamine to striatum causing increased dopamine levels resulting in excessive thalamic stimulation and subsequently increased movement (chorea)
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91
Q

HUNTINGTON’S DISEASE
What is the inheritance pattern of Huntington’s disease?

A
  • Autosomal dominant inheritance with 100% penetrance
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92
Q

HUNTINGTON’S DISEASE
How does Huntington’s disease present?

A

● Main sign is hyperkinesia
● Characterised by:
○ Chorea, dystonia, and incoordination
● Psychiatric issues
● Depression
● Cognitive impairment, behavioural difficulties
● Irritability, agitation, anxiety

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93
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), high risk of suicide with diagnosis
  • MRI HEAD - shows atrophy of striatum
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94
Q

HUNTINGTON’S DISEASE
What is the management of Huntington’s disease?

A

poor prognosis - no treatment
● Benzodiazepines/valproic acid - chorea
● SSRIs = depression
● Haloperidol = psychosis

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95
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.
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96
Q

HEADACHES
How does a cluster headache present and how long does it last?

A
  • 15m–3h
  • Rapid onset excruciating pain around one eye
  • Pain is unilateral, often nocturnal
  • Eye may be bloodshot, lid swelling, miosis, ptosis + lacrimation
  • ‘Cluster’ of attacks in a day then remission for weeks/months
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97
Q

HEADACHES
How does a tension headache present?

A
  • 30m– 7 days
  • Bilateral, non-pulsatile headache ± scalp tenderness
  • Pressing/tight-band like sensation
  • Mild–moderate intensity
    (Med overuse headache is similar)
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98
Q

HEADACHES
How does a sinusitis headache present?

A
  • Facial pain behind nose, forehead + eyes, pain on leaning forward
  • Tenderness over affected sinus
  • Post-nasal drip, common with coryza
  • Pain lasts 1–2w, viral
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99
Q

HEADACHES
How does acute glaucoma present?

A
  • Constant aching pain rapidly develops around 1 eye, radiates to forehead, markedly reduced vision, visual halos, N+V
  • Signs = red, congested eye, cloudy cornea, dilated non-responsive eye (may be oval shaped)
  • Can be precipitated by dilating eye-drops, emotions or sitting in dark
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100
Q

HEADACHES
How can you diagnose cluster headaches?

A

≥5 classical headaches

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101
Q

HEADACHES
What is the acute management of cluster headaches?

A
  • S/c triptans
  • 15L 100% oxygen via non-rebreathe mask for 15 minutes
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102
Q

HEADACHES
What is the management of tension headaches?

A
  • Reassure, stress relief (Exercise, avoid triggers, massage)
  • Simple analgesia like paracetamol (<15d/m) or complex analgesia (<10d/m)
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103
Q

HEADACHES
What is the management of sinusitis headache?

A
  • Nasal irrigation w/ saline
  • Prolonged Sx with steroid nasal spray
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104
Q

HEADACHES
What is the management of acute glaucoma?

A
  • Immediate expert help + IV acetazolamide (carbonic anhydrase inhibitor)
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105
Q

TRIGEMINAL NEURALGIA
What is the pathophysiology of trigeminal neuralgia?
What is affected?

A
  • Compression of trigeminal nerve results in demyelination + excitation of the nerve resulting in erratic pain signalling
  • Affects all 3 ophthalmic (V1), maxillary (V2) + mandibular (V3) branches but V3 mostly
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106
Q

TRIGEMINAL NEURALGIA
What are the causes of trigeminal neuralgia?

A

Compression of trigeminal nerve by a loop of vein or artery
Aneurysms
Meningeal inflammation
Tumours

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107
Q

TRIGEMINAL NEURALGIA
What is the clinical presentation of trigeminal neuralgia?

A
  • Paroxysms of intense, stabbing pain, lasting seconds in the trigeminal nerve distribution (knife-like shooting pain with no neuro deficit)
  • Mostly unilateral, face screws up in pain
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108
Q

TRIGEMINAL NEURALGIA
How would you diagnose trigeminal neuralgia?

A
  • Clinically with ≥3 attacks with pain in ≥1 division + classical Sx
  • ?CT/MRI head to exclude secondary causes
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109
Q

TRIGEMINAL NEURALGIA
How would you manage trigeminal neuralgia?

A

Carbamazepine - suppresses attacks
Less effective options = phenytoin, gabapentin and lamotrigine
Surgery = microvascular decompression, gamma knife surgery

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110
Q

MIGRAINE
What is the pathophysiology of migraines?

A
  • Changes in brainstem blood flow leads to unstable trigeminal nerve nucleus + nuclei in basal thalamus
  • Leads to release of vasoactive neuropeptides CGRP + substance P > neurogenic inflammation > vasodilation + plasma protein extravasation leading to pain propagating all over the cerebral cortex
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111
Q

MIGRAINE
What are the triggers of migraines?

A

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

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112
Q

MIGRAINE
Describe the pain of a migraine

A
  • Unilateral
  • Throbbing
  • Moderate/severe pain
  • Aggravated by physical activity
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113
Q

MIGRAINE
What is the acute management of migraines?

A
  • PO (or nasal in paeds) triptan like sumatriptan plus paracetamol or NSAID
  • Antiemetic like metoclopramide or prochlorperazine if vomiting occurs
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114
Q

MIGRAINE
What is the prophylaxis for migarines?

A
  • Propranolol or topiramate are first line
  • Topiramate is teratogenic + can reduce efficacy of hormonal contraceptives though
  • Also, amitriptyline, botulinum toxin or acupuncture.
  • 400mg OD of riboflavin (B2) may help
  • NOT gabapentin
  • Avoid indentified triggers (?headache diary)
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115
Q

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

A
  • Relentless + unexplained destruction/degeneration of UMN + anterior horn cells in the brain + spinal cord
  • Motor cortex = UMN signs
  • Anterior horn cells = LMN signs
  • Cranial nerve nuclei = mixed signs
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116
Q

MND
What is the cause of MND?

A
  • Most spontaneous + idiopathic with no FHx
  • Rare familial cases with SOD-1 implication (suggests free radicals like smoking, pesticides + heavy metals) can cause MN destruction
  • M>F, 60y/o, associated with frontotemporal dementia
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117
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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118
Q

MND
What is ALS?
What is a long-term consequence?

A
  • Loss of motor neurones in motor cortex + anterior horn of cord so mixed signs
  • Long term consequence is progressive spastic tetraparesis
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119
Q

MND
What is progressive bulbar palsy?
What does it affect?
What does it need to be differentiated from?

A
  • Only affects CN 9–12 (brainstem motor nuclei) so LMN of them
  • Primarily affects muscles of talking, chewing, tongue palsy + swallowing
  • Progressive pseudobulbar palsy = destruction of UMN so same as bulbar but small spastic tongue with no fasciculations
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120
Q

MND
What is…

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

A

i) Anterior horn cells affected so LMN signs only, distal > proximal
ii) Loss of cells in motor cortex so UMN signs only

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121
Q

MND
What is the general clinical presentation of MND?

A
  • Insidious + progressive muscle weakness affecting limbs, trunk, face + speech
  • Often first noticed in upper limbs, may be fatigue when exercising
  • May have stumbling spastic gait, weak grip + clumsiness
  • Dysarthria, dysphagia, emotional lability in pseudobulbar palsy
  • NO SENSORY SYMPTOMS
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122
Q

MND
What are UMN signs?

A

Hypertonia or spasticity,
brisk reflexes
upgoing plantars,
muscle wasting

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123
Q

MND
What are some important differentials of MND and how can they be differentiated?

A
  • Cervical spine lesion as may present with UMN signs
  • Myasthenia gravis but MND NEVER affects eye movements
  • Multiple sclerosis but MND NEVER affects sphincters or sensation
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124
Q

MND
What are some investigations for MND?

A

Head/spine MRI
Blood tests = muscle enzymes, autoantibodies
Nerve conduction studies
EMG
Lumbar Puncture

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125
Q

MND
What medication may be given in MND?

A
  • RILUZOLE – Na+ blocker inhibits glutamate release
  • Drooling - ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
  • Dysphagia: NG tube
  • Spasms: ORAL BACLOFEN
  • Non-invasive ventilation
  • Analgesia e.g. NSAIDs - DICLOFENAC
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126
Q

MULTIPLE SCLEROSIS
What is the pathophysiology of MS?

A
  • Inflammation leads to infiltration of immune cells + damages the myelin causing focal loss
  • Demyelination heals poorly leaving thinner, inefficient myelin
  • Initially relative preservation of axons but as neurodegenerative, eventually axonal loss leading to fixed + progressive deficits
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127
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
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128
Q

MULTIPLE SCLEROSIS
What is a clinically isolated syndrome?

A
  • First episode of demyelination + neuro Sx – not diagnosis as does not meet criteria
  • More likely to develop MS if lesions on MRI
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129
Q

MULTIPLE SCLEROSIS
What are the 4 types of MS?

A
  • Relapsing remitting (most common)
  • Secondary progressive
  • Primary progressive
  • Benign
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130
Q

MULTIPLE SCLEROSIS
What is relapsing remitting MS?

A
  • Characterised by episodes of Sx in attacks (relapses)
  • Followed by periods of stability (remission)
  • May accumulate disability if don’t fully recover
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131
Q

MULTIPLE SCLEROSIS
What is secondary progressive MS?

A

Initially RR but now progressive worsening of Sx + incomplete remissions

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132
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 on MRI) and time (>1m apart)

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133
Q

MULTIPLE SCLEROSIS
What are the symptoms of MS?

A

DEMYELINATION –
- Diplopia (CN VI)
- Eye movement pain (optic neuritis, v common)
- Motor weakness
- nYstagmus
- Elevated temp worsens
- Lhermitte’s sign
- Intention tremor
- Neuropathic pain
- Ataxia
- Talking slurred (dysarthria)
- Impotence
- Overactive bladder
- Numbness

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134
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is the pattern of motor weakness?

A

i) Pyramidal pattern so extensors weaker than flexors in upper limb, flexors weaker than extensors in lower

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135
Q

MULTIPLE SCLEROSIS
What are some signs of MS?

A
  • UMN = spastic paraparesis, brisk reflexes, hypertonia
  • Sensory = loss of sensation, cerebellar signs
  • Relative afferent pupillary defect
  • Internuclear ophthalmoplegia
  • Optic atrophy (pale optic disc) in chronic MS
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136
Q

MULTIPLE SCLEROSIS
What is relative afferent pupillary defect?

A
  • Seen on swinging light test (retina or optic nerve lesion –afferent issue)
  • The affected and normal eye appears to dilate when light is shone on the affected eye
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137
Q

MULTIPLE SCLEROSIS
What is internuclear ophthalmoplegia?

A
  • CN VI/medial longitudinal fasciculus lesion
  • Disorder of conjugate lateral gaze with;
    – Decreased adduction of ipsilateral eye
    – Nystagmus on abduction of contralateral eye
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138
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
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139
Q

MULTIPLE SCLEROSIS
What is the management of MS relapses?
How does this affect disease prognosis?

A
  • IV methylprednisolone
  • Shortens acute relapses but no overall effect on prognosis
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140
Q

MULTIPLE SCLEROSIS
What is the management of MS remissions?

A
  • First line = beta-interferons (1b) to decrease # relapses + lesions on MRI but SEs = depression, flu Sx + miscarriage
  • 2nd line = DMARDs (monoclonal antibody) - natalizumab, dimethyl fumarate
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141
Q

MULTIPLE SCLEROSIS
What is the general symptomatic management for MS?

A

Spasticity
- BACLOFEN (GABA analogue, reduces Ca2+ influx)
- TIZANIDINE (alpha-2 agonist)
- BOTOX INJECTION (reduces ACh in neuromuscular junction)

urinary incontinence = catheterisation

incontinence
- DOXAZOSIN (anti-cholinergic alpha blocker drugs

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142
Q

MENINGITIS
What are the bacterial causes of meningitis?

A

N. meningitidis
S. pneumoniae
H. influenzae

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143
Q

MENINGITIS
What are the viral causes of meningitis?

A

Enterovirus (most common viral)
HSV
CMV
Varicella zoster virus

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144
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
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145
Q

MENINGITIS
What are some differentials of meningitis?

A
  • Malaria
  • Encephalitis
  • SAH
  • Septicaemia
  • Tetanus
  • Dengue fever
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146
Q

MENINGITIS
What investigations would you do for meningitis?

A

Blood cultures (pre LP)
Bloods - FBC, U+E, CRP, ESR, serum glucose, lactate
Lumbar puncture (contraindicated with raised ICP)
CT head - exclude lesions
Throat swabs - bacterial and viral

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147
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) ++ neutrophils
v) Gram stain

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148
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

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149
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

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150
Q

MENINGITIS
What are some complications following meningitis?

A
  • Hearing loss is key complication
  • Seizures + epilepsy
  • Sepsis or abscess
  • Hydrocephalus
  • Cognitive impairment + learning disability
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151
Q

MENINGITIS
What is the management of bacterial meningitis

A
  • IV cefotaxime
    • amoxicillin to cover listeria (potential contraction in birth) in <3m
  • Dexamethasone to reduce frequency + severity of neurological sequelae
  • Adjust treatment according to sensitivities
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152
Q

ENCEPHALITIS
What are the viral causes of encephalitis?

A

Herpes simplex (most common)
CMV
Epstein Barr
varicella zoster
HIV
measles
mumps

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153
Q

ENCEPHALITIS
What is the clinical presentation of encephalitis?

A

begins with features of viral infection:
- fever, headaches, myalgia, fatigue, nausea

progresses to:

personality & behavioural changes
decreased consciousness, confusion, drowsiness
focal neurological deficit - hemiparesis, dysphagia
seizures
raised ICP and midline shift
coma

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154
Q

ENCEPHALITIS
What are the differentials of encephalitis

A
  • Meningitis
  • Stroke
  • Brain tumour
  • Hypoglycaemia, SLE, hypoxic brain injury, DKA
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155
Q

ENCEPHALITIS
What investigations would you do for encephalitis?

A
  • Blood culture + CSF serology for viral PCR
    MRI - shows areas of inflammation, may be midline shifting
    EEG - periodic sharp and slow wave complexes
    lumbar puncture
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156
Q

ENCEPHALITIS
What would the CSF look like in encephalitis for…

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

A

i) Clear
ii) Raised
iii) Normal/low
iv) + lymphocytes

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157
Q

ENCEPHALITIS
What is the management of encephalitis?

A

IV Acyclovir immediately - even before investigation results
Primidone = anti-seizure medication if needed
IV benzylpenicillin if meningitis is suspected

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158
Q

BRAIN ABSCESS
What are the most common causative organisms?

A
  • Staph. aureus + strep. pnuemoniae
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159
Q

BRAIN ABSCESS
What is the management of brain abscess?

A
  • CT guided aspiration via burr hole or craniotomy + abscess cavity debridement
  • Craniotomy usually if no response to aspiration or if reoccurs
  • Abx with IV ceftriaxone + metronidazole, ICP Mx with dexamethasone
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160
Q

BRAIN DEATH + COMA
What is a coma?

A

Unarousable unresponsiveness

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161
Q

BRAIN DEATH + COMA
In terms of clinical presentation in brain death and coma, what are some…

i) focal neurological deficits?
ii) brainstem signs?

A

i) Asymmetry of motor function, tendon reflexes + plantar responses
ii) Pupil size (pinpoint vs. dilated + pupillary reactions), eye movements, corneal reflexes, cough + gag reflexes, ice cold water in ears > nystagmus

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162
Q

BRAIN DEATH + COMA
What are lateralising signs?
Give an example of one

A
  • Signs that occur from one hemisphere of the brain but not the other, helps to localise pathology
  • Fixed dilated pupil (CN3 palsy)
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163
Q

BRAIN DEATH + COMA
Explain the pathophysiology of a third nerve palsy?

A
  • CN3 comes out of brainstem + goes over apex of petrous part of temporal bone as it goes through cavernous sinus to supply eye so susceptible to damage if brain swollen, bleeding + trauma.
  • Outside CN3 are parasympathetic fibres which constrict pupil so if damaged > fixed + dilated
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164
Q

BRAIN DEATH + COMA
What is the main differential of a third nerve palsy?
How can they be differentiated?

A
  • Blind eye
  • Blind eye will not give contralateral responsiveness but other causes will + if you shine light in good eye then dilated pupil will restrict
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165
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
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166
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
  • BEST eye, verbal + motor response – 15 max, 3 min
  • ‘GCS ≤8 = intubate’ secure airway as may be unable to maintain on own
  • GCS >8 is greatest prognostic indicator in patients with traumatic brain injury
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167
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

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168
Q

BRAIN DEATH + COMA
What are the components of ‘verbal’ in GCS?

A

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

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169
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 = flexion to pain
M2 = extension to pain
M1 = no response

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170
Q

BRAIN DEATH + COMA
What is abnormal flexion to pain?
What does it indicate?

A
  • Decorticate posturing – arm adducted + flexed, wrist flexed, internal rotation, plantar flexed + stiff appearance
  • Indicates significant damage to cerebral hemispheres, internal capsule + thalamus
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171
Q

BRAIN DEATH + COMA
What is abnormal extension to pain?
What does it indicate?

A
  • Decerebrate posturing – arms + legs extended, head extension, plantar flexion, internal rotation, pt rigid with teeth clenched
  • Indicates brainstem damage + so lesions in cerebellum or midbrain
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172
Q

BRAIN DEATH + COMA
What does the progression from decorticate to decerebrate posturing suggest?

A
  • Uncal (transtentorial) or tonsillar brain herniation ‘coning’
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173
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 if trauma
  • Management in ICU
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174
Q

MYASTHENIA GRAVIS
What is the pathophysiology of myasthenia gravis?

A
  • Anti-ACh receptor antibodies (IgG) interfere with NMJ via depletion of working post-synaptic receptor sites for ACh to bind to leading to fewer action potentials firing, blocking excitatory effect of ACh on receptors (all or nothing principle)
  • Both B + T cells implicated
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175
Q

MYASTHENIA GRAVIS
What is the aetiology of myasthenia gravis?

A
  • Associated with autoimmune disease (RA, SLE)
  • If <40y: F>M, thymic hyperplasia
  • If >60y: M>F, thymoma
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176
Q

MYASTHENIA GRAVIS
What is the main symptom of myasthenia gravis?

A
  • Fatiguable weakness of muscles which improves with rest
  • Affects ocular, bulbar + proximal limb muscles
  • Dysphagia + dysarthria (bulbar)
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177
Q

MYASTHENIA GRAVIS
What will patients with myasthenia gravis struggle with?

A
  • Hairs, chairs + stairs (proximal muscle weakness)
  • Speech, mastication, face + neck weakness
  • Resp muscles (breathing difficulty + dysphagia dangerous features which indicates advancing disease)
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178
Q

MYASTHENIA GRAVIS
What are the signs of myasthenia gravis?

A
  • Ptosis, diplopia (extra-ocular muscle weakness)
179
Q

MYASTHENIA GRAVIS
What are some clinical signs of myasthenia gravis?

A
  • Repeated blinking = ptosis
  • Repeated abduction of one arm 20x + compare to other side
180
Q

MYASTHENIA GRAVIS
What antibodies are implicated in myasthenia gravis?

A
  • Anti-AChR antibodies (90%)
  • Muscle-specific tyrosine kinase (MuSK, esp. males)
  • Low density lipoprotein receptor-related protein 4 (rare)
181
Q

MYASTHENIA GRAVIS
What investigations would you do for myasthenia gravis?

A

mostly clinical examination
positive tensilon test
anti-AChR antibodies
TFTs
EMG
CT of thymus
crushed ice test - ice is applies to ptosis for 3 mins, if it improves it is likely to be myasthenia gravis

182
Q

MYASTHENIC CRISIS
What is the main complication of myasthenia gravis?

A
  • Myasthenic crisis
183
Q

MYASTHENIC CRISIS
What are the causes of myasthenic crisis?

A
  • Infection (resp), natural disease cycle, under/overdosing meds
184
Q

MYASTHENIC CRISIS
What is the management of myasthenic crisis?

A
  • Urgent review by neurologists + anaesthetists
  • Monitor breathing with serial FVC measurements
  • NIV, BiPAP or intubation + ventilation
  • Immunomodulatory therapies (IVIg or plasmapheresis)
185
Q

MYASTHENIA GRAVIS
What is the management of myasthenia gravis?

A
  • Acetylcholinesterase inhibitors like pyridostigmine or rivastigmine
  • Immunosuppression with prednisolone (acute) or azathioprine to suppress antibody production
  • Thymectomy if thymoma or anti-AChR +ve disease
  • Plasmapheresis for severe relapsing cases
186
Q

GUILLAIN-BARRE
What is Guillain-Barré syndrome (GBS)?

A
  • Acute inflammatory demyelinating polyneuropathy which targets Schwann cells
187
Q

GUILLAIN-BARRE
What is the pathophysiology of GBS?

A
  • B cells produce antibodies against the antigens on the pathogen causing the preceding infection and these antibodies also match proteins on the nerve cells leading to demyelination and potentially axonal degeneration
188
Q

GUILLAIN-BARRE
What is Miller-Fisher syndrome?

A
  • GBS variant which affects CNS + eye muscles
  • Characterised by ophthalmoplegia + ataxia
189
Q

GUILLAIN-BARRE
What are the causes of GBS?

A
  • Often triggered by preceding illness 4w before symptoms

Bacteria
- Camplylobacter jejuni
- Mycoplasma

Viruses
- CMV
- EBV
- HIV
- Herpes zoster

190
Q

GUILLAIN-BARRE
What is the clinical presentation of GBS?

A
  • Acute symmetrical, progressive, ascending muscle weakness.
  • Peripheral neuropathy or neuropathic pain
  • Absent tendon reflexes early in disease
  • Back or leg pain is very common in initial stages
  • Proximal muscles (trunk, resp) more affected + cranial nerves (esp. VII)
  • Autonomic –urinary retention, diarrhoea, sweating, BP changes
191
Q

GUILLAIN-BARRE
What are some differentials for GBS?

A
  • Other causes of neuromuscular paralysis = hypokalaemia, polymyositis, botulism
  • Cord compression, transverse myelitis
192
Q

GUILLAIN-BARRE
What are the investigations for GBS?

A

Nerve Conduction Studies (NCS) = diagnostic -> shows slowing of conduction
Lumbar Puncture at L4 = raised protein and normal WCC (cyto-protein dissociation)
bloods - FBC, U&E, LFT, TFT
Spirometry = respiratory involvement
ECG

193
Q

GUILLAIN-BARRE
What is the main treatment for GBS?

A
  • IVIg reduces duration + severity of paralysis but C/I if IgA deficiency as would cause anaphylaxis
  • Plasma exchange
  • Intubation, ventilation + ICU admission in severe cases in resp failure
194
Q

BRAIN TUMOURS
What are acoustic neuromas?
What are they associated with?

A
  • Tumours of Schwann cells that occur around cerebellopontine angle surrounding the auditory nerve that innervates inner ear
  • Slow growing but eventually grow large enough to produce Sx
  • Usually unilateral, bilateral associated with neurofibromatosis type 2
195
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, recent new onset suggest sinister aetiology)
196
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the frontal lobe?

A

Personality + intellect change, hemiparesis, expressive dysphasia

197
Q

BRAIN TUMOURS
Other than surgery, what management is there for brain tumours?

A
  • Radio/chemotherapy – stereotactic radiotherapy (gamma knife)
  • Medical – dexamethasone or mannitol to reduce cerebral oedema but can cause insomnia so give in mornings
  • AEDs for seizures
  • Palliative care involvement
198
Q

NEUROPATHY
What are the peripheral nerve causes of muscle weakness?

A
  • Peripheral neuropathy = lots of nerves affects all over body, often symmetrical + systemic causes
  • Mononeuropathy = 1 nerve affected, usually due to entrapment
  • Mononeuritis multiplex = various, individual nerve defects all over the place, randomly
199
Q

NEUROPATHY
What is the pathophysiology of mononeuritis multiplex?

A
  • Inflammation of vasa nervorum can block off blood supply to nerve causing sudden deficit
200
Q

NEUROPATHY
What are the causes of peripheral neuropathy?

A

ABCDE –
- Alcohol
- B12 deficiency
- Cancer + CKD
- Diabetes + drugs (isoniazid, amiodarone)
- Every vasculitis

201
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

202
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
203
Q

NEUROPATHY
What is the generic clinical presentation of mononeuropathy?

A

Individual nerve deficits in isolation, mostly upper limb nerves affected at compression points

204
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
205
Q

NEUROPATHY
What is the most common mononeuropathy?

A
  • Carpal tunnel syndrome
206
Q

NEUROPATHY
What muscles does the median nerve innervate?

A

LLOAF –
- Lateral lumbricals x2
- Opponens pollicis
- Abductor pollicis brevis
- Flexor pollicis brevis

207
Q

NEUROPATHY
What is the clinical presentation of carpal tunnel syndrome?

A
  • Aching pain in hand + arm (especially at night)
  • Paraesthesia in radial 3.5 digits relieved by dangling hand over edge of bed + shaking (wake + shake)
  • Difficulty with precision grip
  • Sensory loss (radial 3.5 digits palmar + fingertips dorsally)
  • Wasting of thenar eminence (APB, FPB + OP)
208
Q

NEUROPATHY
What investigations can you do for carpal tunnel syndrome?

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
209
Q

NEUROPATHY
What is the management of carpal tunnel syndrome?

A
  • Splinting
  • Analgesia
  • Local steroid injection ± decompression surgery
210
Q

NEUROPATHY
What does a CN1 lesion cause?

A
  • Anosmia
211
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

212
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
213
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)
214
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
215
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
216
Q

NEUROPATHY
What does a CN6 lesion cause?

A
  • Issues abducting eye beyond midline as innervates lateral rectus
217
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

218
Q

NEUROPATHY
What is Bell’s palsy?

A
  • CN7 lesion with complete facial paralysis, hyperacusis,
  • Differentiate from stroke as no forehead sparring as LMN
  • Often post-viral (HSV), treat with pred + eye care
219
Q

NEUROPATHY
What does a CN8 lesion cause?

A
  • Sensorineural deafness
  • Tinnitus, vertigo, nystagmus
220
Q

NEUROPATHY
What does a CN9/10 lesion cause?

A
  • Swallow, gag + cough issues
  • Uvula deviated away from side of lesion
221
Q

NEUROPATHY
What does a CN11 lesion cause?

A
  • Weakness turning head to contralateral side
222
Q

NEUROPATHY
What does a CN12 lesion cause?

A
  • Tongue deviation towards side of lesion
223
Q

NEUROPATHY
What are the investigations used in neuropathy?

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
224
Q

CORD COMPRESSION
What is myelopathy?

A

Injury to the spinal cord due to severe compression resulting in UMN signs + specific symptoms based on compression

225
Q

RADICULOPATHY
How does radiculopathy present?

A
  • Sharp, shooting pain within distribution of nerve, weakness + loss of sensation
226
Q

CORD COMPRESSION
What are the aetiologies of spinal cord compression?

A
  • Malignancy (mostly secondary, 5Bs = breast, bronchus, byroid, bidney, brostate)
  • Infection (epidural abscess), spinal osteophytes
  • Disc prolapse (slower onset), haematoma (warfarin)
  • Lumbar degeneration due to trauma or age (conservative Mx or steroid injections)
  • Myeloma
227
Q

CORD COMPRESSION
What are the symptoms of spinal cord compression?

A
  • Weakness of legs with UMN signs (contralateral spasticity + hyperreflexia)
  • Sudden/progressive onset weakness = emergency
  • Sensory loss below certain level
  • Numbness/tingling may have stabbing pain
  • Bladder + anal sphincter involvement is a later manifestation (hesitancy, frequency, painless retention)
228
Q

CORD COMPRESSION
What are the signs of spinal cord compression?

A
  • Motor, reflex + sensory level = normal ABOVE lesion
  • LMN signs = AT level
  • UMN signs = BELOW level
  • Tone + reflexes usually reduced in acute cord compression
  • ?Sign of infection like tender spine, pyrexia
229
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
230
Q

CORD COMPRESSION
What are the differentials for spinal cord compression?

A
  • Transverse myelitis (inflammation of both sides of one section of spinal cord)
  • MS
  • Trauma
  • Dissecting aneurysm
231
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 spine gold standard
  • If mass, ?biopsy/surgical exploration
232
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
233
Q

CORD COMPRESSION
What can cause cauda equina syndrome?
How does it present?

A
  • Mostly malignancy, disc prolapse (L4/5, L5/S1), trauma
  • Back pain, early urinary retention + constipation, saddle anaesthesia, decreased sphincter tone, mixed UMN/LMN leg weakness, erectile dysfunction, asymmetrical paralysis of legs
234
Q

CORD COMPRESSION
What is the management of spinal cord compression?

A
  • Malignancy = stat dexamethasone + consider chemo, radio, surgery
  • Epidural abscess = surgical decompression + Abx
  • Cauda equina = surgery for emergency pressure relief
  • Degenerative cervical myelopathy = urgent spinal surgery referral for surgical decompression
235
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)
236
Q

ANTERIOR CORD SYNDROME
What is anterior cord syndrome?

A
  • Anterior spinal artery occlusion or compression
  • Bilateral spastic paresis (lateral corticospinal)
  • Bilateral loss of pain + temp (lateral spinothalamic)
237
Q

SPINAL CORD INJURY
What is posterior cord syndrome?

A
  • Trauma or posterior spinal artery occlusion
  • Loss of fine touch, proprioception + vibration (DCML)
238
Q

SPINAL CORD INJURY
What is central cord syndrome?

A
  • Hyperextension injury, often elderly with underlying cervical disease
  • Sensory + motor deficit (upper extremities > lower)
239
Q

MYOPATHY
What are myopathies?

A
  • Neuromuscular disorders where the primary Sx is muscle weakness due to dysfunction of muscle fibres
240
Q

MYOPATHY
What are the aetiologies of myopathies?

A
  • inflammatory
  • metabolic
  • inherited
  • polio
  • drugs - steroids, statins
241
Q

MYOPATHY
How do myopathies present?

A
  • Symmetrical proximal pattern of muscle weakness (hairs, stairs + chairs)
  • Weakness > wasting
  • Reflexes + sensation normal, no fasciculations
242
Q

MYOPATHY
How does myotonic dystrophy present?

A
  • type 1 = distal weakness more prominent
  • type 2 = proximal weakness more prominent.
  • May have cataracts, testicular atrophy, cardiac lesions (heart block, cardiomyopathy), DM
243
Q

MYOPATHY
What are the investigations for myopathies?

A
  • CRP/ESR, creatinine kinase elevated
  • Autoantibodies (anti-Jo-1), EMG, genetics + muscle biopsy
244
Q

MYOPATHY
What is the management of myopathies?

A
  • Remove causative agent (statins, steroids)
  • Immunosuppression (steroids, azathioprine) if inflammatory cause.
245
Q

MYOPATHY
What is the general supportive management of myopathies?

A
  • OT = aids + adaptations to help live with condition
  • Physio = prevent contractures
  • Renal protection = myoglobin can cause kidney damage
  • Diet = ideally low BMI with good nutrition
246
Q

HYDROCEPHALUS
What is hydrocephalus?

A
  • Abnormal build-up of CSF around the brain causing compression to nearby brain tissue as the ventricles dilate
247
Q

HYDROCEPHALUS
What is the purpose of CSF?

A
  • Protects brain from damage
  • Removes waste products from the brain
  • Provides brain with nutrients to function properly
248
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
249
Q

HYDROCEPHALUS
What are the 3 types of hydrocephalus?

A
  • Obstructive (non-communicating) = structural pathology blocking flow of CSF with dilatation superior to site of obstruction
  • Non-obstructive (communicating) = imbalance of CSF production/absorption
  • Normal pressure = unknown, can develop after head injury or stroke, >60s
250
Q

HYDROCEPHALUS
What are some causes of obstructive hydrocephalus?

A

Tumour,
acute haemorrhages,
developmental abnormalities (aqueduct stenosis)

251
Q

HYDROCEPHALUS
How does hydrocephalus present?

A
  • Signs of raised ICP
  • Headache (worse in morning or lying down)
  • N+V, papilloedema, blurred vision
252
Q

HYDROCEPHALUS
How does normal pressure hydrocephalus present?

A

‘Wet, wacky, wobbly’ –
- Urinary incontinence, dementia + abnormal gait (apraxia)
Trouble walking (feels like the feet are stuck to the ground)
Poor balance
Falling
Changes in the way you walk
Forgetfulness and confusion
Mood changes
Depression
Difficulty responding to questions
Loss of bladder control

  • Sx come on gradually + similar to Alzheimer’s so difficult to diagnose
253
Q

HYDROCEPHALUS
What are the investigations for hydrocephalus?

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)
254
Q

HYDROCEPHALUS
What is the management of hydrocephalus?

A
  • An external ventricular drain (EVD) is used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside
  • Ventriculoperitoneal shunt = surgically implanted into brain to drain excess fluid (may become blocked or infected)
  • Endoscopic third ventriculostomy = hole made in floor of 3rd ventricle to allow trapped CSF to escape to be reabsorbed
255
Q

IIH
What is idiopathic intracranial hypertension (IIH)?

A
  • Build up of CSF pressure around the brain causing signs of raised ICP
  • Associated with obese young women
256
Q

IIH
What are the causes of IIH?

A
  • Primary = idiopathic
  • Secondary (often causing chronic intracranial HTN) = brain tumour, chronic SDH, meningitis/encephalitis, venous sinus thrombosis, drugs (nitrofurantoin, vitamin A)
257
Q

IIH
What is the clinical presentation of IIH?

A
  • Presents as if mass but none found
  • Signs of raised ICP (headache, papilloedema + enlarged blind spot)
  • Blurred vision, narrowed visual fields ± diplopia
  • Consciousness + cognition preserved
258
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)
259
Q

IIH
What is the management of IIH?

A
  • # 1 weight loss (topiramate can be used + has benefit of weight loss)
  • Acetazolamide
  • Surgery = optic nerve sheath decompression + fenestration to prevent damage
  • Lumboperitoneal or ventriculoperitoneal shunt
260
Q

NEURO PHARMACOLOGY
Give some examples of anti-epileptic drugs (AEDs).
What is their mechanism of action?

A
  • Carbamazepine, valproate, lamotrigine, levetiracetam, phenytoin, ethosuximide.
  • Inhibit voltage-gated Na+ channels which prevents excitability of neurones > reduced firing > stops seizure, some promote GABA release
261
Q

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

i) carbamazepine?
ii) valproate?
iii) lamotrigine

A

i) Blurred vision, headache, drowsiness – agranulocytosis, aplastic anaemia, P450 inducer
ii) Teratogenic, hepatitis, hair loss, tremor, weight gain – some interactions with antidepressants
iii) Blurred vision, headache, drowsiness – Steven-Johnson syndrome + risk of leukopenia

262
Q

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

i) phenytoin?
ii) levetiracetam?
iii) ethosuximide?

A

i) Megaloblastic anaemia (folate), osteomalacia, teratogenic, P450 interactions – Steven-Johnson syndrome
ii) Headache, drowsiness – some interactions with antidepressants
iii) Night terrors, rashes

263
Q

NEURO PHARMACOLOGY
What is the mechanism of action of Levodopa?

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
264
Q

NEURO PHARMACOLOGY
What are the side effects of Levodopa?

A
  • Postural hypotension
  • Confusion
  • Dyskinesias (abnormal movements)
  • Effectiveness decreases with time (even with dose increase)
  • On-off effect
  • Psychosis
265
Q

NEURO PHARMACOLOGY
A side effect of high dopamine are dyskinesias.
What is dystonia?
What is chorea?
What is athetosis?

A
  • Excessive muscle contraction > abnormal postures/movements
  • Abnormal involuntary movements may be jerky
  • Involuntary twisting or writhing movements, usually in fingers/hands/feet
266
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 (more than levodopa), postural hypotension
  • ECHO, ESR, creatinine + CXR prior to Rx
267
Q

NEURO PHARMACOLOGY
What are some adverse effects of dopamine receptor agonists?

A
  • Pulmonary retroperitoneal + cardiac fibrosis
  • Bromocriptine associated with gambling + other inhibition disorders (e.g. sexual)
268
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
269
Q

NEURO PHARMACOLOGY
Why are dopamine receptor agonists + COMT/MAO-B inhibitors used in Parkinson’s disease?

A
  • Delay use of levodopa + then used in combination to reduce levodopa dose as levodopa is most effective treatment
270
Q

NEURO PHARMACOLOGY
Examples of triptans.
Mechanism of action?
Used for?

A
  • Sumatriptan, naratriptan
  • 5-HT (serotonin) receptor agonists + act on smooth muscle in arteries > vasoconstriction, peripheral pain receptors > inhibit activation of pain receptors (vasoactive peptides) + reduce neuronal activity in CNS
  • Abort migraines when start to develop
271
Q

NEURO PHARMACOLOGY
What are some SEs + C/Is of triptans?

A
  • Dizziness, dry mouth, sleepy, nausea
  • C/I in CVD
272
Q

DIZZINESS/VERTIGO
What is vertigo?
What is it characterised by?

A
  • Hallucination of movement, often rotary, of the pt/their surroundings
  • Spinning, tilting, veering sideways, feeling as if being pushed/pulled
  • Always worse with movement, relief on lying or sitting still
  • Difficulty walking or standing
  • N+V, pallor, sweating
273
Q

DIZZINESS/VERTIGO
What is benign paroxysmal positional vertigo (BPPV)?
What is it caused by?
What is the treatment?

A
  • Brief vertigo on head movements (rolling in bed) due to disruption of debris in semi-circular canal of ears (canalolithiasis)
  • Idiopathic, secondary to head trauma, labyrinthitis
  • Reassurance, Epley manoeuvre
274
Q

ACUTE LABYRINTHITIS
What is acute labyrinthitis?

A
  • Inflammation of labyrinth + damage to vestibular + auditory end organs
275
Q

MENIERE’S DISEASE
What is Ménières disease?

A
  • Increased pressure in endolymphatic system due to increased volume of inner ear.
276
Q

DIZZINESS/VERTIGO
What is the management of dizziness/vertigo?

A
  • Tilt-table test + Dix-Hallpike manoeuvre
  • FBC, ESR/CRP, U+Es, LFTs, TFTs to exclude causes
  • MRI head if ?acoustic neuroma or other brain issue
  • Sx relief with anti-emetic (prochlorperazine), dizziness use antihistamine cinnarizine
277
Q

STROKE
What are the various classifications of strokes?

A
  • Total anterior circulation stroke (TACS)
  • Partial anterior circulation stroke (PACS)
  • Posterior circulation syndrome (POCS)
  • Lacunar syndrome (LACS)
278
Q

SAH
What are some risk factors for SAH?

A

Hypertension
Known aneurysm
Previous aneurysmal SAH

Smoking
Alcohol
Family history
Bleeding disorders

  • associated with berry aneurysms:
    • Polycystic Kidney Disease
    • Coarctation of aorta
    • Ehlers-Danlos syndrome & Marfan syndrome
279
Q

EDH
Which vessels most commonly are affected in extradural haematomas?
which other vessels can be affected?

A
  • Middle meningeal artery
  • 25% venous if fracture disrupts the venous sinuses
280
Q

EDH
What causes an EDH?

A

Traumatic head injury (typically to temple, just lateral to eye e.g. punch) - often the temproal bone

281
Q

EDH
What are some complications of EDH?

A
  • Brainstem compression can cause deep + irregular breathing,
  • death may follow period of coma due to respiratory arrest
282
Q

SDH
what are the risk factors of SDH?

A
  • Elderly - brain atrophy, dementia
  • Frequent falls - epileptics, alcoholics
  • Anticoagulants
  • babies - traumatic injury (“shaking baby syndrome”)bridging veins stretched so more likely to rupture,
283
Q

EPILEPSY
Define seizure

A

Paroxysmal event in which changes of behaviour, sensation, cognition + consciousness caused by excessive, hypersynchronous neurological discharges in the brain

284
Q

EPILEPSY
What is Todd’s paresis?

A

Focal weakness in a part or all of the body after a seizure

285
Q

EPILEPSY
What are the 4 main types of generalised seizure?

A
  • Absence seizures,
  • tonic-clonic seizures,
  • myoclonic seizures
  • atonic (akinetic) seizures/drop attacks
286
Q

EPILEPSY
what is the treatment for generalised tonic/atonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Lamotrigine to females of childbearing potential

287
Q

STATUS EPILEPTICUS
When might status epilepticus be the first presentation of epilepsy?

A

First presentation in alcohol abuse (most commonly) or acute brain problem (stroke, trauma, infections, hypoglycaemia)

288
Q

NEAD
What is NEAD?

A

Episodes of movement, sensation or experience that resemble epileptic seizures but without ictal cerebral discharges, physical manifestation of psychological distress

289
Q

NEAD
How can NEAD and a true epileptic seizure be differentiated?

A
  • Vital signs including lying-standing BP
  • FBC, U+Es, glucose, LFTs, TFTs (normal CK + prolactin in NEAD)
  • 24h 12-lead ECG + ECHO
  • EEG + CT/MRI if necessary
290
Q

TRIGEMINAL NEURALGIA
What are some triggers?

A

Washing affected area, shaving, eating, talking + dental prostheses

291
Q

MND
What are some complications of MND?

A
  • UTI, pneumonia + respiratory failure (common cause of death), constipation, pressure sores
292
Q

MULTIPLE SCLEROSIS
What is benign MS?

A

Relapses + Remissions but overall progress will never worsen

293
Q

MULTIPLE SCLEROSIS
What is primary progressive MS?

A

Gradually worsening of disease from point of diagnosis without any RR

294
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Lhermitte’s sign?

A

Neck flexion causes electric shock sensation down spine

295
Q

MULTIPLE SCLEROSIS
In terms of the symptoms of MS, what is Uhthoff’s phenomenon?

A

symptoms worsening in heat e.g. in the shower/exercise

296
Q

MULTIPLE SCLEROSIS
What is the criteria for treatment of MS remissions?

A
  • 2 relapses in past 2y
297
Q

MENINGITIS
What are the aseptic causes of meningitis?

A

MS.
HSV2, SLE, sarcoidosis + skull # can cause recurrent aseptic meningitis

298
Q

ENCEPHALITIS
What are the non-viral causes of encephalitis?

A

Bacterial meningitis
TB
Malaria
Lyme’s disease

299
Q

BRAIN DEATH + COMA
What is brain death?

A

Irreversible cessation of all brain function, usually from widespread injury to brain indicated by lack of brainstem signs

300
Q

BRAIN DEATH + COMA
What is a persistent vegetative state?

A

State of wakefulness with sleep-wake cycles but no detectable awareness

301
Q

MYASTHENIA GRAVIS
What medications can exacerbate myasthenia gravis?

A

Abx, CCBs, beta-blockers, lithium + statins

302
Q

BRAIN TUMOURS
How do acoustic neuromas present?

A

Classic Sx = hearing loss, tinnitus, balance issues, decreased facial sensation

303
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the temporal lobe?

A

Receptive dysphasia, amnesia

304
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the parietal lobe?

A

Hemisensory loss, dysphasia

305
Q

BRAIN TUMOURS
What focal signs would you get if the tumour was located in the occipital lobe?

A

Contralateral visual defects

306
Q

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

A

Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Slurred speech, Hypotonia (DANISH)

307
Q

NEUROPATHY
What can cause mononeuritis multiplex?

A

Inflammatory or immune mediated vasculitis like granulomatosis with polyangiitis, polyarteritis nodosa, RA or sarcoidosis

308
Q

RADICULOPATHY
What is radiculopathy?

A

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

309
Q

RADICULOPATHY
What is the most common radiculopathy?

A

Sciatica (L5) = lower back pain that travels to buttocks + down back of thigh to calf

310
Q

MYOPATHY
What are dystrophies?

A

If they’re inherited = dystrophies

311
Q

MYOPATHY
How do myopathies compare to neuropathies?

A

Weakness is proximal in muscle disease (nerves = distal)

312
Q

MENIERE’S DISEASE
How does it present?

A

Recurrent attacks in clusters of vertigo lasting >20m, fluctuating/perm sensorineural hearing loss (uni/bilateral), tinnitus + sense of fullness or pressure in one or both ears

313
Q

MENIERE’S DISEASE
What causes it?

A

Idiopathic, trauma, endo

314
Q

MENIERE’S DISEASE
How is it managed?

A

Bed rest, reassurance

315
Q

ACUTE LABYRINTHITIS
How does it present?

A
  • Abrupt onset severe vertigo, N+V, may have hearing loss or tinnitus + nystagmus towards side opposite to lesion
  • Severe vertigo subsides in days, full recovery 3-4w
316
Q

ACUTE LABYRINTHITIS
What are the causes?

A

Usually viral, ?vascular lesion

317
Q

CEREBRAL PALSY
what are the causes?

A
  • antenatal = prematurity, multiple births, TORCH
  • perinatal = asphyxia during delivery
  • postnatal = hyperbilirubinaemia, neonatal sepsis, resp distress, meningitis, head injuries, seizures
318
Q

CEREBRAL PALSY
what are the symptoms?

A
  • delay in motor/speech/cognitive development
  • retention of primitive reflexes
  • spasticity/clonus
  • toe walking/knee hyperextension
  • scissoring
  • crouched gait
  • contractures
319
Q

CEREBRAL PALSY
what are the investigations?

A

MRI brain - periventricular leukomalacia, congenital malformation, stroke or haemorrhage

320
Q

CEREBRAL PALSY
what is the management?

A
  • OT, physio and speech therapy
  • orthoses
  • adaptive equipment
321
Q

BELL’S PALSY
what are the causes?

A

viral infection - reactivation of herpes simplex virus 1 (HSV1)

this leads to swelling of CN VII

322
Q

BELL’S PALSY
what is the pathophysiology?

A

reactivation of HSV-1 results in destruction of ganglion cells and infection of schwann cells leading to demyelination and neural inflammation

323
Q

BELL’S PALSY
what are the symptoms?

A

unilateral LMN facial weakness
altered taste
post auricular pain - pain behind ears

324
Q

BELL’S PALSY
what is the management?

A
  • corticosteroid
  • eye drops
  • ?antivrials
325
Q

BELL’S PALSY
what are the investigations?

A
  • can be clinical diagnosis
  • ENoG
  • needle EMG
326
Q

NEUROFIBROMATOSIS
what are the clinical signs of NF1?

A
  • cafe-au-lait spots on the skin
  • pea-sized lumps under skin
  • skeletal abnormalities
  • tumour on optic nerve
327
Q

NEUROFIBROMATOSIS
what are the clincial signs of NF2?

A
  • acoustic neuromas
  • family history
  • meningioma, schwannoma, juvenile cortical cataracts or glioma
328
Q

NEUROFIBROMATOSIS
what are the causes of neurofibromatosis 1 and 2?

A

NF1 = neurofibromin 1 (autosomal dominant)
NF2 = neurofibromin 2 (autosomal dominant)

329
Q

NEUROFIBROMATOSIS
what is the treatment for NF1 and NF2?

A
  • no cure
  • pain management
  • growths can be surgically removed
330
Q

NARCOLEPSY
what are the clinical features?

A
  • excessive daytime sleepiness/sleep attacks
  • cataplexy
  • hypnagogic/hypnopompic hallucinations
  • sleep paralysis
  • excessive fatigue/impaired memory
331
Q

NARCOLEPSY
what are the investigations?

A
  • actigraphy and sleep diary
  • overnight polysomnography
  • multiple sleep latency test (MSLT)
332
Q

NARCOLEPSY
what is the management?

A

1st line = sleep hygiene + lifestyle changes
can also consider pharmacotherapy
- modafinil
- pitolisant
- sodium oxybate

333
Q

CORD COMPRESSION
How is spinal stenosis managed?

A

MRI + canal decompression surgery

334
Q

CORD COMPRESSION
How does spinal stenosis present?

A
  • Spinal claudication > pain in buttocks/legs when walking
  • pain eased by bending forward as canal opens
  • negative straight leg raise
335
Q

RADICULOPATHY
what are the causes?

A
  • intervertebral disc prolapse
  • degenerative diseases of the spine
  • fracture (trauma or pathological)
  • malignancy (metastatic)
  • infection (extradural abscesses, osteomyelitis)
336
Q

RADICULOPATHY
what is the management?

A

analgesia - amitryptyline, pregabalin, gabapentin
physiotherapy
surgery in emergencies

337
Q

RADICULOPATHY
what is the management?

A

analgesia - amitryptyline, pregabalin, gabapentin
physiotherapy
surgery in emergencies

338
Q

WERNICKE-KORSAKOFF SYNDROME
what is it?

A
  • includes wernicke’s encephalopathy and korsakoff’s syndrome
  • it is a spectrum (wernicke’s = acute, korsakoff’s = chronic)
339
Q

WERNICKE-KORSAKOFF SYNDROME
what are the clinical signs?

A
  • mental confusion/amnesia
  • vision problems
  • coma
  • tremor
  • ataxia
  • hypothermia
  • low blood pressure
340
Q

WERNICKE-KORSAKOFF SYNDROME
what is the cause?

A

vitamin B1 (thiamine) deficiency - most commonly caused by alcoholism

341
Q

WERNICKE-KORSAKOFF SYNDROME
what is the management?

A

B1 (thiamine) replacement and proper nutrition/hydration

342
Q

MYASTHENIC CRISIS
What are the clinical features?

A
  • Resp failure or death
343
Q

MYASTHENIC CRISIS
what are the complications?

A

Resp failure or death

344
Q

CATAPLEXY
what is it?

A

sudden muscle weakness triggered by strong emotions such as laughter, anger and surprise

345
Q

CATAPLEXY
what happens during an attack?

A
  • slurred speech
  • impaired eyesight (double vision, unable to focus)
  • hearing and awareness are undisturbed (remain conscious)
346
Q

CATAPLEXY
what are the causes?

A
  • 75% of people with narcolepsy have cataplexy
  • it is rare for cataplexy to be only symptom
347
Q

CATAPLEXY
what is the management?

A

sodium oxybate
tricyclic antidepressants (clomipramine)
SSRIs

348
Q

SAH
what is the appearance of SAH on CT head?

A

white star-shaped lesion as blood fills gyro patterns around brain + ventricles

349
Q

EDH
what is the appearance of EDH on non-contrast head CT?

A

lens shaped haematoma = LEMON SHAPE
doesn’t cross suture lines
shows midline shift

350
Q

SDH
What causes water to be sucked up into a subdural haematoma 8-10 weeks after a head injury?

A

Clot starts to break down and there is massive increase in oncotic pressure –> water is sucked up by osmosis into the haematoma

351
Q

SDH
what is the appearance of SDH on non-contrast head CT?

A

crescent shaped haematoma = BANANA SHAPE (clot turns from white to grey over time)
unilateral
shows midline shift

352
Q

EPILEPSY
What is the emergency treatment for epilepsy?

A

ABCDE
check glucose
RECTAL/IV DIAZEPAM or LORAZEPAM
IV PHENYTOIN loading
mechanical ventilation

353
Q

EPILEPSY
what is the treatment for generalised myoclonic epilepsy?

A

Sodium Valproate for Males & women unable to childbear,

Levetiracetam/Topiramate to females of childbearing potential

354
Q

BELL’S PALSY
how do you tell the difference between bell’s palsy and a stroke?

A
  • stroke = forehead still innervated - forehead sparing
  • Bell’s palsy = both forehead and lower face are affected on one side
355
Q

PARKINSON’S DISEASE
Give 2 histopathological signs of Parkinson’s disease

A
  1. Loss of dopaminergic neurones in the substantia nigra
  2. Lewy bodies
356
Q

PARKINSON’S DISEASE
What surgical treatment methods are there for Parkinson’s disease?

A

Deep brain stimulation of the sub-thalamic nucleus

Surgical ablation of overactive basal ganglia circuits

357
Q

HUNTINGTON’S DISEASE
What is the triplet code that is repeated in Huntington’s disease?

A

Trinucleotide expansion repeat of CAG in HTT gene on chromosome 4
- >35 = HD

358
Q

HUNTINGTON’S DISEASE
what are the signs of Huntington’s disease?

A

Abnormal eye movements
Dysarthria
Dysphagia
Rigidity
Ataxia

359
Q

HEADACHES
What is the prophylactic management of cluster headaches?

A

1st line = Verapamil
- avoid triggers (alcohol)
- short course prednisolone may break cycle during clusters

360
Q

MIGRAINE
What other symptoms may a patient with a migraine experience other than pain?

A

Nausea
Photophobia
Phonophobia
Aura

361
Q

MIGRAINE
What is the diagnostic criteria for a migraine?

A

classified as with or without aura
at least 2 of:
unilateral pain (usually 4-72hrs)
throbbing-type pain
moderate > severe intensity
motion sensitivity
plus at least 1 of:

  • nausea/vomiting
    -photophobia/phonophobia

there must also be a normal examination and no attributable cause

362
Q

MIGRAINE
How does triptan work?

A

Selectively stimulates 5-hydroxytryptamine (serotonin) receptors in the brain

363
Q

MND
does MND affect UMN or LMN?

A

both UMN and LMN can be affected

364
Q

MND
Does MND cause sensory loss or sphincter disturbance?

A

No (clinical feature of MS)

365
Q

MND
What are LMN signs?

A

Hypotonia + muscle wasting,
reduced reflexes,
fasciculations (particularly tongue)

366
Q

MND
What is the diagnostic criteria for MND?

A

LMN + UMN signs in 3 regions

El Escorial criteria

Presences of LMN and UMN degeneration and progressive history
Absence of other disease processes

367
Q

MULTIPLE SCLEROSIS
What are the differential diagnosis’s of MS

A

SLE
Sjogren’s
AIDS
Syphilis

368
Q

MENINGITIS
What are the bacterial causes of meningitis in neonates?

A

E.coli
Group B strep - strep agalactiae

369
Q

MENINGITIS
What can cause meningitis in immunocompromised patients?

A

CMV
Cryptococcus
TB
HIV
herpes simplex

370
Q

MENINGITIS
Give 4 potential adverse effect of a lumbar puncture

A

Headache
Paraesthesia
CSF leak
Damage to spinal cord

371
Q

ENCEPHALITIS
Name the main triad of symptoms of encephalitis

A

Fever + headache + altered mental state

372
Q

MYASTHENIA GRAVIS
What can weakness due to myasthenia gravis be worsened by?

A

Pregnancy
Hypokalaemia
Infection
Emotion
Exercise
Drugs

373
Q

GUILLAIN-BARRE
When is IV immunoglobulin contraindicated in the treatment for Guillain-Barre syndrome?

A

If a patient has IgA deficiency - can cause severe allergic reaction

374
Q

NEUROPATHY
What is the generic clinical presentation of mononeuritis multiplex?

A

Subacute presentation (months rather than years), painful, asymmetrical sensory + motor neuropathy

375
Q

NEUROPATHY
What is the pathophysiology of carpal tunnel syndrome?

A

Inflammation of carpal tunnel leads to entrapment of the median nerve

376
Q

NEUROPATHY
What are the causes of carpal tunnel syndrome?

A

Idiopathic but associated with local tumours, DM + RA

377
Q

ANTERIOR CORD SYNDROME
what are the causes?

A
  • iatrogenic - thoracic and thoracoabdominal AA repair
  • aortic dissection
  • atherothrombotic disease
  • emboli
  • vasculitis
378
Q

ANTERIOR CORD SYNDROME
what are the symptoms?

A
  • acute motor dysfunction
  • loss of pain and temperature sensation below level of infarction
  • autonomic dysfunction - neurogenic bowel/bladder
  • acute onset back pain
379
Q

ANTERIOR CORD SYNDROME
what are the investigations?

A

MRI - ‘owls eyes’ hyperintensities in anterior horns

lumbar puncture, CSF testing, blood and urine to rule out other causes

380
Q

ANTERIOR CORD SYNDROME
what is the treatment?

A
  • IV fluids to increase intravascular volume
  • vasopressor medications to increase systemic vascular resistance
  • lumbar drain to remove CSF

symptomatic management
- mechanical ventilation
- catheterisation

381
Q

HORNER’S SYNDROME
what is the pathophysiology of horner’s syndrome?

A

unilateral damage to the sympathetic chain

382
Q

HORNER’S SYNDROME
what is the pathophysiology of horner’s syndrome?

A

unilateral damage to the sympathetic chain

383
Q

HORNER’S SYNDROME
what are the causes of 1st order horner’s syndrome?

A

stroke, tumours of hypothalamus, spinal cord lesions

384
Q

HORNER’S SYNDROME
what are the causes of 2nd order horner’s syndrome?

A

tumours of upper chest cavity, trauma to the neck

385
Q

HORNER’S SYNDROME
what are the causes of 3rd order horner’s syndrome?

A

lesions to carotid artery, middle ear infections, injury to base of the skull

386
Q

HORNER’S SYNDROME
what are the clinical features of horner’s syndrome?

A

MAPLE

Miosis
Anhydrosis
Ptosis
Loss of ciliospinal reflex
Endophthalmos (sunken eyeball)

387
Q

HORNER’S SYNDROME
what are the investigations for horner’s syndrome?

A

clinical examination

MRI - detect lesions

388
Q

HORNER’S SYNDROME
what is the treatment for horner’s syndrome?

A

treat underlying cause

389
Q

BULBAR PALSY
what is it?

A

refers to a set of signs and symptoms linked to the impaired function of the lower cranial nerves, typically caused by damage to their lower motor neurons or to the lower cranial nerve itself
CN 9, 10, 11 and 12

390
Q

BULBAR PALSY
what ar ethe causes?

A
  • brainstem tumours and strokes
  • ALS
  • GBS
391
Q

BULBAR PALSY
what are the causes?

A
  • brainstem tumours and strokes
  • ALS
  • GBS
392
Q

BULBAR PALSY
what are the symptoms?

A
  • dysphagia
  • reduced/absent gag reflex
  • slurred speech
  • aspiration of secretions
  • dysphonia
  • dysarthria
  • drooling
  • difficulty chewing
  • nasal regurgitation
  • atrophic tongue
    weak jaw/facial muscles
393
Q

BULBAR PALSY
what are the investigations?

A

MRI
lumbar puncture

394
Q

BULBAR PALSY
what is the treatment?

A
  • no known treatment
  • drooling = riluzole
  • feeding tube
  • SaLT - help chewing
395
Q

STRABISMUS
what is it?

A

where there is misalignment of the visual axes of the eyes; it may be latent or manifest and, if manifest, it may be constant or intermittent

396
Q

STRABISMUS
what are the causes?

A
  • congenital
  • graves (restricted eye movement)
  • myasthenia gravis
  • intra-cranial process (mass, raised ICP, CNS infarction, inflammation of CNS)
397
Q

STRABISMUS
what are the symptoms?

A
  • diplopia
  • eye misalignment
  • amblyopia (decreased vision in an anatomically normal eye)
  • abnormal eye movements
  • visual confusion
  • asthenopia (ocular discomfort)
398
Q

STRABISMUS
what are the risk factors?

A

FHx of strabismus
prematurity
low birth weight
maternal smoking during pregnancy

399
Q

STRABISMUS
what are the investigations?

A
  • cover test
  • simultaneous prism and cover test (SPCT)
  • uncover test (UCT)
  • alternate prism cover test (APCT)
  • Hirschberg test
  • Krimsky test
400
Q

STRABISMUS
what is the management?

A

definitive treatment = extraocular muscle surgery

correction of refractive errors

treatment of amblyopia - eye patch

treatment for diplopia - patch, prisms, high prescription, orthoptic exercises

401
Q

SCIATICA
what is it?

A

nerve pain from an injury or irritation to sciatic nerve which originates in buttock/gluteal region

402
Q

SCIATICA
how is the pain from sciatica described?

A
  • burning
  • electric
  • stabbing

can be constant or it can come and go
worse when sat down
usually unilateral

403
Q

SCIATICA
what are the risk factors?

A
  • previous injury
  • overweight
  • lack of core strength
  • physically demanding job
  • diabetes
  • osteoarthritis
  • inactivity
  • smoking
404
Q

SCIATICA
what are the causes?

A
  • herniated/slipped disc - puts pressure on nerve root
  • degenerative disc disease
  • spinal stenosis
  • spondylolisthesis
  • osteoarthritis
  • trauma
  • cauda equina syndrome
405
Q

SCIATICA
what are the symptoms?

A
  • moderate pain in lower back, buttock and leg
  • numbness/weakness in lower back, buttock, leg or feet
  • pain gets worse with movement
  • pins and needles in legs, toes, or feet
  • loss of bladder or bowel control (due to cauda equina)
406
Q

SCIATICA
what are the investigations?

A
  • physical exam - straight leg raises
  • spinal x-ray
  • MRI/CT
  • nerve conduction velocity
  • electromyography
  • myelogram
407
Q

SCIATICA
what is the management?

A
  • apply ice/hot packs
  • over the counter medications
    • NSAIDs
    • aspirin
    • paracetamol
  • prescription medications
    • muscle relaxants (cyclobenzaprine)
    • tricyclic antidepressants (amitryptyline)
    • gabapentin/pregabalin
  • physical therapy
408
Q

RAISED ICP
what are the causes?

A
  • tumour
  • abscess
  • haemorrhage
  • hydrocephalus
  • strokes that cause brain swelling
409
Q

RAISED ICP
what are the symptoms?

A
  • high BP
  • irregular or slow pulse
  • severe headache
  • weakness
  • cardiac arrest
  • LOC, coma
  • loss of brainstem reflexes (blinking, gagging, pupils reacting to light)
  • respiratory arrest
  • dilated pupils + no movement in one/both eyes
410
Q

RAISED ICP
what are the investigations?

A
  • x-ray of skull + neck
  • head CT
  • MRI head
  • blood tests
411
Q

RAISED ICP
what is the management?

A
  • drain to remove CSF
  • mannitol to reduce swelling
  • intubation
  • surgery to remove part of skull
412
Q

MYOPATHY
what is myotonic dystrophy?

A

autosomal dominant genetic condition causing progressive muscle weakness
most common form of muscular dystrophy to occur in adults

413
Q

MYOPATHY
what are the causes of myotonic dystrophy type 1 and 2?

A

type 1 - DMPK gene mutation on chromosome 19

type 2 = ZNF9 gene on chromosome 3

414
Q

TIA
what are the differential diagnosis’s for a TIA

A

Migraine aura
Epilepsy
Hypoglycaemia
Hyperventilation
retinal bleed
syncope - due to arrhythmia

415
Q

TIA
what is the ABCD2 score?

A

Assesses risk of stoke in the next 7 days for those who have had a TIA

age
BP
clinical features - unilateral weakness, speech disturbance
duration of TIA
presence of diabetes mellitus

416
Q

TIA
What is the treatment for a TIA?

A

immediate treatment = aspirin 300mg and refer to specialist within 24hrs

control CV risk factors

BP control - ACEi (RAMIPRIL) or ARB (CANDESARTAN)
smoking cessation
statin - SIMVASTATIN
no driving for 1 month
antiplatelet therapy
- ASPIRIN 75mg daily (With Dipyridamole)
or
- CLOPIDOGREL daily

anticoagulation (e.g. WARFARIN) for patients with AF

carotid endarterectomy

if >70% carotid stenosis
reduces stroke/TIA risk by 75%

417
Q

HYDROCEPHALUS
what are the causes of normal pressure hydrocephalus?

A

excess fluid builds up in the ventricles, which enlarge and press on nearby brain tissue

  • injury
  • bleeding
  • infection
  • brain tumour
  • brain surgery
418
Q

CHRONIC FATIGUE SYNDROME
what is it?

A

It is a disorder characterized by extreme fatigue or tiredness that doesn’t go away with rest and can’t be explained by an underlying medical condition.

419
Q

CHRONIC FATIGUE SYNDROME
What are the causes?

A

unknown - could be:
- viruses (EBV, rubella, RRV)
- a weakened immune system
- stress
- hormonal imbalances

420
Q

CHRONIC FATIGUE SYNDROME
what are the risk factors?

A
  • sex (female)
  • genetic predisposition
  • allergies
  • stress
  • environmental factors
421
Q

CHRONIC FATIGUE SYNDROME
what are the symptoms?

A
  • severe fatigue that interferes with daily life for >6 months
  • sleep problems
    • feeling unrefreshed after night’s sleep
    • chronic insomnia
  • memory loss
  • reduced concentration
  • orthostatic intolerance
  • muscle pain
  • frequent headaches
  • multi-joint pain without redness or swelling
  • frequent sore throat
422
Q

CHRONIC FATIGUE SYNDROME
what are the differentials?

A

mononucleosis
lyme disease
MS
SLE
hypothyroidism
fibromyalgia
depression
sleep disorders

423
Q

CHRONIC FATIGUE SYNDROME
what are the investigations?

A

rule out all other causes
- bloods - FBC, U+Es, CRP, ESR, TFTs

424
Q

CHRONIC FATIGUE SYNDROME
what is the management?

A

no cure
- pacing activities
- reduce caffeine, nicotine and alcohol
- create sleep routine
- antidepressant medications
- complementary/alternative medicines

425
Q

ESSENTIAL TREMOR
what is it?

A

Progressive, mainly symmetrical, rhythmic, involuntary oscillation movement disorder of the hands and forearms (69% of patients) that is usually absent at rest and present during posture and intentional movements.
it can also involve the voice, head and jaw

426
Q

ESSENTIAL TREMOR
what is the presentation?

A
  • slowly progressive
  • difficulties with writing, eating, drinking, dressing
  • tremor only present with movement
427
Q

ESSENTIAL TREMOR
what are the investigations?

A

clinical diagnosis
- bilateral tremor with normal muscle tone and speed of movement

428
Q

ESSENTIAL TREMOR
what is the management?

A
  • medication - propranolol, primidone
  • deep brain stimulation
  • focused ultrasound thalamotomy with MRI guidance
429
Q

MENIERE’S DISEASE
what is the classical triad of symptoms?

A

vertigo
hearing loss - worse during attacks
tinnitus

430
Q

STROKE
what is the primary prevention of strokes?

A

Risk factor modifcaiton

  • Antihypertensives for HTN
  • Statins for hyperlipiaemia
  • Smoking cessation
  • Control DM
  • AF treatment = warfarin/NOAC’s
431
Q

STROKE
what is the secondary prevention of strokes?

A

2 weeks of aspirin –> long term clopidogrel

432
Q

SAH
give 3 possible complications of a subarachnoid haemorrhage

A
  1. Rebleeding (common = death)
  2. Cerebral ischaemia
  3. Hydrocephalus
  4. Hyponatraemia
433
Q

SDH
what are the differential diagnoses for a subdural haematoma?

A

stroke
dementia
CNS masses (tumour vs abscess)

434
Q

EPILEPSY
what is the diagnostic criteria for eilespy?

A

At least 2 or more unprovoked seizures occurring >24 hours apart

One unprovoked seizure + probability of future seizures

Epileptic syndrome diagnosis

435
Q

EPILEPSY
how do lamotrigine and carbamazepine work?

A

Inhibit pre-synaptic Na+ channels so prevent axonal firing

436
Q

EPILEPSY
how does sodium valproate work?

A

Inhibits voltage gated Na+ channels and increases GABA production

437
Q

EPLILEPSY
give 4 potential side effects of anti-epileptic drugs (AEDs)

A
  1. Cognitive disturbances
  2. Heart disease
  3. Drug interactions
  4. Teratogenic
438
Q

PARKINSONS DISEASE
what is the pathway for dopamine production?

A

Tyrosine –> L-dopa –> Dopamine

439
Q

HYDROCEPHALUS
What are some causes of non-obstructive hydrocephalus?

A
  • Commonly failure of reabsorption of arachnoid granulations (meningitis, post-haemorrhage)
  • increased CSF production (choroid plexus tumour) but very rare
440
Q

HYDROCEPHALUS
What is the pathophysiology of obstructive (non-communicating) hydrocephalus?

A

due to a structural pathology blocking the flow of cerebrospinal fluid. Dilatation of the ventricular system is seen superior to site of obstruction

441
Q

HYDROCEPHALUS
What is the pathophysiology of non-obstructive (communicating) hydrocephalus?

A

due to an imbalance of CSF production absorption

442
Q

DIABETIC NEUROPATHY
what is the management of neuropathic pain?

A
  • 1st line = amitriptyline, duloxetine, gabapentin or pregabalin (if one doesn’t work try another)
  • tramadol for rescue therapy
  • topical capsaicin
443
Q

DIABETIC NEUROPATHY
what are the effects on the GI system?

A
  • gastroparesis
  • chronic diarrhoea (particularly at night)
  • GORD
444
Q

DIABETIC NEUROPATHY
what is the management for gastroparesis?

A

metoclopramide, domperidone or erythromycin

A TO REVISE - PHASE 3A (16 decks)

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