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Phase 2a Resits > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a TIA?

A
  • sudden onset

- brief episode of neurological deficit

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2
Q

Pathophysiology of TIA

A
  1. temporary, focal cerebal ischaemia
  2. lack of O2 and nutrients to brain
  3. without infarction → no irreversible cell death
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3
Q

Features of a TIA

A
  • symptoms are maximal at onset
  • usually lasts 5-15 mins
  • classical definition = lasts <24hrs
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4
Q

Risk factors for TIA

A
  • age
  • HTN
  • smoking
  • diabetes
  • a fib
  • the pill
  • males
  • black people
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5
Q

Causes of a TIA

A

atherothromboembolism from carotid artery

cardioembolism

  • in a fib
  • after an MI
  • valve disease/prosthetic valve

hyperviscosity

hypoperfusion

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6
Q

Presentation of a TIA

A
  • amaurosis fugax
  • aphasia
  • hemiparesis
  • hemisensory loss
  • hemianopic visual loss
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7
Q

What symptoms do not indicate a TIA on their own?

A
  • syncope
  • dizziness
  • temporary loss of consciousness
  • temporary memory loss
  • gradual onset
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8
Q

What scoring tool measures the risk of a stroke after a TIA?

A

ABCD2 score

  • age
  • BP
  • clinical features
  • duration of TIA
  • DM
  • gives 2 day risk
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9
Q

Investigations for TIA

A
  1. diffusion weighted MRI/CT brain
  2. carotid imaging → doppler US then angiography if stenosis found
  • bloods
  • ECG
  • echo
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10
Q

Management of TIA

A
  • loading dose 300mg aspirin
  • control BP/cholesterol
  • no driving for 1 month
  • antiplatelet therapy = daily 75mg aspirin
  • anticoagulation if AF
  • carotid endarterectomy
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11
Q

What is a stroke?

A
  • rapid onset neurological deficit
  • lasting over 24hrs
  • poor blood flow to brain → cell death
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12
Q

What are the 2 types of stroke?

A

ischaemic 85%
- blood clot in blood vessel to brain

haemorrhagic 15%
- bleed in small blood vessel in/around brain

urgent CT/MRI to determine type → guides treatment

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13
Q

Risk factors for ischaemic stroke

A
  • age
  • male
  • HTN
  • smoking
  • diabetes
  • recent/past TIA
  • IHD/AF
  • the pill
  • black/asian
  • PVD
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14
Q

Causes of ischaemic stroke

A
  • small vessel occlusion by thrombus
  • atherothromboembolism
  • cardioembolism
  • hyperviscosity
  • hypoperfusion
  • vasculitis
  • fat emboli from long bone fracture
  • venous sinus thrombosis
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15
Q

Presentation of cerebral infarcts

A

depends on site

ACA
- contralateral weakness and sensory loss of lower limb

MCA

  • contralateral motor weakness/sensory loss
  • speech issues
  • contralater hemiplegia
  • UMN facial weakness
  • dysphagia
  • homonymous hemianopia
  • visuo-spatial deficit
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16
Q

Presentation of brainstem infarcts

A

depends on site

  • quadriplegia
  • facial numbness/paralysis
  • vision disturbances
  • speech impairment
  • vertigo → N&V
  • locked-in syndrome
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17
Q

What are lacunar infarcts?

A
  • small infarcts
  • occlusion of a single perforating artery supplying a subcortical area

occurs in

  • internal capsule
  • basal ganglia
  • thalamus
  • pons
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18
Q

Presentation of lacunar infarcts

A

depends on site → one of:

  • sensory loss
  • unilateral weakness
  • ataxic hemiparesis
  • dysarthria
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19
Q

Management of ischaemic strokes

A
  • exclude haemorrhagic stroke
  • loading dose 300mg aspirin
  • antiplatelet therapy → 300mg aspiring daily for 2 weeks then clopidogrel
  • anticoagulation if AF
  • thrombolysis → IV alteplase within 4.5hrs
  • mechanical thrombectomy

acute stroke unit

  • rehabilitation
  • swallowing/feeding support
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20
Q

What are the 4 types of haemorrhagic stroke?

A
  • intracerebral haemorrhage
  • subarachnoid haemorrhage
  • extradural haemorrhage
  • subdural haemorrhage
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21
Q

What is an intracerebral haemorrhage?

A
  • sudden bleeding into brain tissue
  • rupture of blood vessel in brain
  • leads to infarction (O2 deprivation)
  • pooling blood increases ICP
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22
Q

Risk factors for intracerebral haemorrhage

A
  • HTN
  • age
  • alcohol
  • smoking
  • diabetes
  • anticoagulation
  • thrombolysis
  • secondary to ischaemic stroke
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23
Q

Pathophysiology of increased ICP

A
  • pressure on skull/brain/blood vessels
  • CSF obstruction
  • midline shift
  • tentorial herniation
  • coning
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24
Q

Presentation of intracerebral haemorrhage

A

similar to ischaemic stroke

pointers to haemorrhage

  • sudden loss of consciousness
  • severe headache
  • meningism
  • coma
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25
Q

Investigations for intracerebral haemorrhage

A
  • same as ischaemic stroke

- CT/MRI brain = essential

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26
Q

Management of intracerebral haemorrhage

A
  • stop anticoagulants immediately → reverse effects with clotting factor replacement
  • BP control
  • reduce ICP → mechanical ventilation, IV mannitol
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27
Q

What is a subarachnoid haemorrhage?

A

spontaneous bleeding into subarachnoid space

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28
Q

Risk factors for SAH

A
  • HTN
  • known aneurysm
  • previous aneurysmal SAH

conditions associated with berry aneurysms

  • PKD
  • coarctation of aorta
  • connective tissues diseases
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29
Q

Causes of SAH

A
  • aneurysmal rupture → Berry aneurysms
  • ateriovenous malformations
  • idiopathic
  • traumatic injury
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30
Q

Pathophysiology of SAH

A
  • tissue ischaemia
  • raised ICP
  • space-occupying lesion → puts pressure on brain
  • blood irritates meninges → can obstruct CSF outflow
  • vasospasm
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31
Q

Complications of SAH

A
  • rebleeding

- hyponatraemia

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32
Q

Symptoms of SAH

A
  • sudden onset excruciating headache → thunderclap, occipital
  • N&V
  • collapse
  • loss of consciousness
  • vision changes
  • coma
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33
Q

Signs of SAH

A

signs of meningeal irritation

  • neck stiffness
  • Kernig’s sign
  • Brudzinski’s sign
  • retinal, subhyaloid, vitreous bleeds
  • focal neurological signs
  • high BP
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34
Q

Investigations for SAH

A

ASAP brain CT
- star shaped sign

lumbar puncture

  • only if normal ICP
  • xanthochromia → yellowish CSF

MR/CT angiography to find source of bleeding

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35
Q

Management of SAH

A
  • IV fluids
  • ventricular drainage if hydrocephalus
  • nimodipine reduces vasospasm
  • surgery if aneurysm → endovascular coiling/surgical clipping
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36
Q

What is a subdural haematoma?

A
  • bleeding into subdural space
  • rupture of bridging vein
  • usually due to head trauma
  • massive latent interval
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37
Q

Risk factors of subdural haematoma

A
  • babies → traumatic injury
  • brain atrophy → dementia, elderly, alcoholics
  • prone to falls
  • anticoagulants
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38
Q

Pathophysiology of subdural haematoma

A
  • bleeding forms haematoma then stops

weeks/months later

  • haematoma autolyses → increase in oncotic/osmotic pressure → water sucked in → haematoma enlarges
  • rise in ICP
  • midline structures shifted away from side of clot
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39
Q

Symptoms of subdural haematoma

A
  • fluctuating levels of consciousness
  • drowsiness
  • headache
  • confusion
  • insidious physical/intellectual slowing
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40
Q

Signs of subdural haematoma

A
  • raised ICP
  • seizures
  • localising neurological signs
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41
Q

Investigations for subdural haematoma

A

CT scan

  • haematoma → banana shaped
  • midline shift

MRI

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42
Q

Management of subdural haematoma

A

surgery

  • remove haematoma → clot evacuation
  • craniotomy
  • burr hole washout

IV manittol

reverse clotting abnormalities

address cause

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43
Q

What is an extradural haematoma?

A
  • bleeding into extradural space
  • after trauma to temple → fracture → rupture of MMA
  • lucid interval
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44
Q

Risk factors for extradural haematoma

A
  • young people

- male

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45
Q

Pathophysiology of extradural haematoma

A

after lucid interval

  • rise in ICP
  • pressure on brain
  • midline shift → tentorial herniation/coning
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46
Q

Presentation of extradural haematoma

A

after lucid interval

  • rapidly declining GCS
  • headache
  • vomiting
  • seizures
  • coma
  • deep/irregular breathing → coning
  • death → respiratory arrest
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47
Q

Investigations for extradural haematoma

A

CT scan

  • haematoma → lemon shaped
  • midline shift

skull xray → fracture lines

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48
Q

Management of extradual haematoma

A
  • stabilise
  • urgent surgery → clot evacuation/ligation of bleeding vessel
  • IV mannitol
  • airway care
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49
Q

What are the red flags for headaches?

A
  • worst headache ever
  • other neurological signs
  • onset >50
  • severe, quick onset
  • abnormal pattern of migraine
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50
Q

What is a migraine?

A
  • recurrent throbbing headache
  • often preceded by an aura
  • associated with N&V, visual changes

most common cause of episodic headache

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51
Q

Risk factors for migraines

A
  • family history
  • female
  • age → first in adolescence
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52
Q

Causes of migraines

A

CHOCOLATE

  • chocolate
  • hangovers
  • orgasms
  • cheese
  • oral contraceptives
  • lie-ins
  • alcohol
  • tumult
  • exercise
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53
Q

Presentation of migraine

A

prodrome

  • yawning
  • craving
  • mood/sleep changes

aura

  • precedes attack, variety of symptoms
  • visual disturbances
  • parasthesia
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54
Q

Diagnosis of migraine

A

2+ of:

  • unilateral pain
  • throbbing-type pain
  • moderate to severe intensity
  • motion sensitivity

and 1+ of:

  • N&V
  • photo/phonophobia
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55
Q

Investigations for migraine

A
  • bloods
  • CT/MRI → look for red flags
  • lumbar punture
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56
Q

Management of migraines

A

conservative = avoid triggers

mild

  • NSAIDs → naproxen/ipubprofen
  • antiemetic

severe = oral triptans eg sumatriptan

  • not if IHD, uncontrolled HTN
  • SE → arrythmias, angina
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57
Q

Prophylaxis of migraines

A
  • beta blockers
  • acupuncture
  • amitriptyline = TCA
  • topiramate = anticonvulsant
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58
Q

What are cluster headaches?

A
  • episodic headaches with pain free periods

- most disabling primary headache

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59
Q

Risk factors for cluster headaches

A
  • smoking
  • alcohol
  • male
  • 20-40
  • autosomal dominant gene
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60
Q

Presentation of cluster headaches

A

pain

  • rapid onset excruciating
  • classically around the eye
  • can be temples and forehead
  • unilateral, localised to one area
  • rises to a crescendo over few minutes
  • lasts 15-160mins, 1/2 x a day
  • watery bloodshot eye
  • facial flusing
  • rhinorrhoea
  • miosis +/- ptosis
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61
Q

Management of cluster headaches

A
  • 15L 100% O2 for 15mins via non-rebreather mask

- triptans → sumatriptan

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62
Q

Prevention of cluster headaches

A
  1. verapamil CCB
  • prednisolone
  • stop smoking/drinking
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63
Q

What is a tension headache?

A
  • most common chronic daily headache

- can be episodic or chronic

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64
Q

Triggers of tension headaches

A
  • stress
  • sleep deprivation
  • bad posture
  • hunger
  • eyestrain
  • anxiety
  • noise
  • clenched jaw
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65
Q

Presentation of tension headaches

A

1+ of:

  • bilateral
  • pressing/tight and non-pulsatile
  • mild/moderate intensity
  • +/- scalp tenderness

no aura, vomiting, sensitiy to movement

can have pressure behind eyes

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66
Q

Management of tension headaches

A
  • avoid triggers
  • symptomatic relief → aspirin, PCM, ibuprofen
  • analgesia no more than 6days/month → can cause medication overuse headaches
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67
Q

What is epilepsy?

A
  • recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain
  • manifesting in seizures
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68
Q

Criteria for diagnosing epilepsy

A

1 of:

  • at least 2 unprovoked seizures more than 24hrs apart
  • one unprovoked seizure and probability of future seizures
  • diagnosis of an epilieptic syndrome
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69
Q

What is a seizure?

A
  • convulsions
  • motor signs of abnormal electrical discharges
  • epileptic seizures = convulsions due to epileptic syndromes
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70
Q

Causes of epilepsy

A
  • idiopathic
  • cortical scarring
  • tumours/space-occupying lesions
  • strokes
  • alzheimer’s
  • alcohol withdrawal → delirium tremens
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71
Q

Risk factors for epilepsy

A
  • family hisotry
  • premature babies
  • abnormal cerebral blood vessels
  • drugs eg cocaine
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72
Q

What are the components of a seizure?

A
  • prodrome
  • aura
  • post-ictal
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73
Q

What is prodrome?

A
  • precedes seizures by hrs/days

- weird feeling eg mood/behaviour changes

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74
Q

What is aura?

A
  • part of seizure
  • patient is aware, often precedes other manifestations
  • eg strange feeling, deja vu, strange smells, flashing lights
  • can imply partial seizure
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75
Q

What is post-ictal

A
  • period after seizures
  • headache, confusion, myalgia, sore tongue
  • post-ictal Todd’s palsy
  • dysphagia after temporal lobe seizure
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76
Q

What is post-ictal Todd’s palsy

A

temporary weakness after focal seizure in motor cortex

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77
Q

What are the types of seizures?

A
  • primary generalised seizures
  • partial focal seizure
  • partial seizure with secondary generation
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78
Q

What are primary generalised seizures?

A
  • whole cortex affected
  • bilateral and symmetrical motor manifestations
  • loss of consciousness/awareness
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79
Q

Types of primary generalised seizures

A
  • tonic = high tone → rigid/stiff limbs
  • clonic = muscle jerking
  • tonic clonic = muscle jerking and rigidity
  • myoclonic = isolated jerking
  • atonic = loss of muscle tone
  • absence = childhood, goes blank → risk of developing tonic clonic
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80
Q

What are the 3 types of partial focal seizures?

A
  • single lobe features
  • simple partial seizure
  • complex partial seizure
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81
Q

Features of single lobe feature seizures

A
  • underlying structural disease
  • limited to one lobe
  • progress to generalised seizures
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82
Q

Features of simple partial seizures

A
  • does not affect consciousness/memory
  • no post-ictal signs
  • motor/sensory/autonomic/pyschic signs
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83
Q

Features of complex partial seizures

A
  • memory affected
  • mainly temporal lobe
  • post-ictal confusion = common if temporal
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84
Q

Characteristics of temporal lobe seizures

A
  • memory, understanding speech/emotion
  • aura
  • anxiety/out of boy experiences
  • automatisms
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85
Q

Characteristics of frontal lobe seizures

A
  • motor, thought processing
  • jacksonian march
  • post-ictal Todd’s palsy
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86
Q

Characteristics of parietal lobe seizures

A
  • sensation

- sensory disturbances → tingling/numbness

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87
Q

Characteristics of occipital lobe seizures

A
  • vision

- visual phenomena eg spots, lines, flashes

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88
Q

Diagnosis of epilepsy

A
  • EEG → supports diagnosis
  • MRI/CT head → exclude space-occupying lesions
  • bloods → exclude metabolic disturbances
  • genetic testing
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89
Q

Management of epilepsy

A
  • sodium valproate
  • if fertile female = lamotrigine
  • myoclonic = levetiracetam/topiramate
  • absence = ethosuximide
  • partial = lamotrigine/carbamazepine
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90
Q

What is status epilepticus?

A
  • continuous seizure lasting over 5mins OR
  • repeated seizures with no recovery in between
  • treatment = IV lorazepam then phenytoin
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91
Q

What are features of non-epileptic seizures?

A
  • metabolic disturbances
  • longer
  • don’t occur in sleep
  • no incontinence/tongue biting
  • pre-ictal anxiety signs
  • no muscle pain
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92
Q

What is meningitis?

A
  • inflammation of the meninges
  • almost always due to infection
  • notifiable disease
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93
Q

Risk factors for meningitis

A
  • students
  • travel
  • immunocompromised
  • pregnancy
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94
Q

Causes of bacterial meningitis

A
  • neonates = group B strep
  • children <2 = strep pneumoniae
  • 2-50 = n.meningitis, s.pneumoniae
    50+ = s.pneumoniae, listeria meningitis

acute emergency

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95
Q

Causes of viral meningitis

A
  • enterovirus

- HSV

96
Q

Causes of fungal meningitis

A
  • cryptococcus

- candida → immunocompormised HIV

97
Q

Why is Neisseria meningitidis important?

A
  • can cause meningococcoal septicaemia
  • non blanching purpuric rash
  • necrosis
  • high mortality
98
Q

Symptoms of meningitis

A
  • triad → fever, headache, neck stiffness
  • purpuric rash
  • photo/phonophobia
  • papilloedema
  • raised ICP
  • seizures
99
Q

Signs of meningitis

A
  • Kernig’s +ve
  • Brudzinski’s +ve
  • glass test → blanching/non-blanching rash
100
Q

What is Kernig’s sign?

A

resistance to extension of leg while hip is flexed

101
Q

What is Brudzinski’s sign?

A

flexion of hips and knees in response to neck flexion

102
Q

Treatment of meningitis

A
  • ABCDE and support
  • empiric therapy = IV benylpenicillin
  • asses GCS
  1. ceftriaxone/cefotaxime
    - add IV benzylpenicillin for rash
    - if penicillin allergy = chloramphenicol
    - if immunocompromised = amoxicillin/ampicillin
103
Q

Prophylaxis for meningitis

A
  • rifampicin and ciprofloxacin

- viral = acyclovir

104
Q

What is Guillain-Barre syndrome?

A
  • acute polyneuropathy → rapid damage of peripheral nerves
  • results in demyelination/axonal degeneration
  • common cause = post-GI infection
105
Q

What infections commonly cause GBS

A
  • campylobacter jejuni
  • EBV
  • CMV
  • mycoplasma
  • HIV
106
Q

Symptoms of GBS

A
  • weakness
  • paraesthesia
  • hyporeflexia
  • sudden onset toe-nose weakness
  • absent reflexes
  • pain in legs, back
  • sensory loss in lower extremities
  • urinary hesitancy
107
Q

Investigations for GBS

A
  • bloods
  • lumbar puncture → protein in CSF
  • spirometry
  • ECG
  • slow conduction velocities
108
Q

Treatment for GBS

A
  • IV Ig
  • plasma exchange
  • LMW heparin → DVT prophylaxis
  • avoid corticosteroids
109
Q

What is Parkinson’s disease?

A
  • destruction of dopaminergic neurons
  • too little dopamine
  • affects ventral tier of zona compacta in substantia nigra
110
Q

Causes of Parkinson’s

A
  • drug induced → dopamine antagonists
  • encephalitis
  • exposire to toxins eg manganese
111
Q

Presentation of Parkinson’s

A
  • bradykinesia
  • resting tremor
  • rigidity
  • parkinsonian gait
  • sleep disorders
  • depression
  • monotonous voice
  • difficulty with fine/repetitive movement
  • cog-wheel walk

b-amyloid plaques

112
Q

Diagnosis of Parkinson’s

A

clinical diagnosis
1. diagnosis of Parkinsonian syndrome
2. exclusion criteria
3 supportive criteria

DaTscan

113
Q

Treatment of Parkinson’s

A

young onset, biologically fit

  • Da agonist = ropinirole
  • MOA-B inhibitor = rasagiline
  • L-DOPA = co-careldopa

biologically frail, comorbidities

  • L-DOPA
  • MOA-B inhibitor
114
Q

What is Huntington’s disease?

A
  • progressive neurodegenerative disorder with 100% penetrance
  • loss of main inhibitory neurotransmitter GABA
  • cell loss within basal ganglia and cortex
115
Q

Pathophysiology of Huntington’s

A
  • less GABA = less regulation of dopamine to striatum

- increased dopamine → excessive thalamic stimulation → increased movement (chorea)

116
Q

Inheritance of Huntington’s

A
  • autosomal dominant

- increased in CAG repeats on chromosome 4

117
Q

Presentation of Huntington’s

A
  • hyperkinesia
  • chorea
  • dystonia
  • incoordination
  • psychiatric issues
  • depression
  • cognitive impairment, behavioural difficulties
  • irritability, agitation, anxiety
118
Q

Investigations for Huntington’s

A
  • MRI/CT → loss of striatal volume
  • genetic testing
  • tests for SLE, thyroid disease, Wilson’s, dementia
119
Q

Treatment for Huntington’s

A
  • poor prognosis
  • most common cause of death = pneumonia then suicide
  • benzodiazepines/valproic acid for chorea
  • SSRIs for depression
  • haloperidol, risperidone for psychosis
120
Q

What is Alzheimer’s

A
  • most common type of dementia
  • EC deposition of b-amyloid plaques
  • tau-containing IC neurofibrillary tangles
  • damaged synapses
  • atrophy
121
Q

Risk factors of Alzheimer’s

A
  • over 65
  • Down’s
  • reduced cognitive activity
  • depression/loneliness
  • ApoE E4 allele homozygosity
122
Q

Presentation of Alzheimer’s

A
  • memory → episodic and semantic
  • language → difficulty understanding/finding words
  • attention/concentration issues
  • psychiatric changes
  • disorientation
123
Q

Diagnosis of Alzheimer’s

A
  • mini-mental state examination
  • bloods
  • memory clinic assessment
  • MRI
124
Q

Treatment of Alzheimer’s

A
  • no cure
  • supportive therapy
  • medications to manage symptoms → AChEi
125
Q

What is frontotemporal dementia

A
  • progressive dementia
  • atrophy of frontal and temporal lobes
  • loss of neurons but no plaque formation
  • 50% dominant inheritance
126
Q

Presentation of frontotemporal dementia

A

often tends to be insidious and progressive

  • behavioural issues
  • progressive aphasia
  • semantic dementia

Picks bodies

127
Q

Investigations for frontotemporal dementia

A
  • bloods
  • FBC and LFTS for encephalopathy
  • MMSE
  • MRI
128
Q

Treatment for frontotemporal dementia

A
  • no cure
  • supportive therapy
  • SSRIs → behaviour symptoms
  • levodopa/carbidopa if Parkinson’s symptoms
  • stop exacerbating drugs
129
Q

What is vascular dementia?

A

result of multiple, small infarcts

130
Q

Risk factors for vascular dementia

A
  • smoking
  • history of TIAs
  • AF
  • HTN
  • T1DM
  • hyperlipidaemia
  • obesity
  • coronary heart disease

one stroke doubles risk of vascular dementia

131
Q

Presentation of vascular dementia

A
  • stepwise progression → periods of stable symptoms then sudden increase in severity
  • visual disturbances
  • UMN signs
  • attention deficit
  • depression
  • incontinence

if infarct was subcortical → dysarthria, pakinsonisms

132
Q

Investigations for vascular dementia

A
  • full history → previous stroke/TIA
  • cognitive impairment screen
  • medication review
  • MRI → previous infarcts
133
Q

Treatment for vascular dementia

A
  • supportive therapy
  • SSRIs/anti-psychotics to control symptoms
  • prognosis 3-5yrs
134
Q

What is dementia with Lewy Bodies?

A
  • characterised by Lewy bodies in brainstem and neocortex
  • substantia nigra depigmentation and amyloid deposits
  • on a spectrum
135
Q

Presentation of dementia with Lewy Bodies

A
  • initial presentation = dementia
  • Parkinsonisms
  • visual hallucinations
  • sleepless disorders/restless leg syndrome
136
Q

Diagnosis of dementia with Lewy Bodies

A

presence of dementia with 2 of:

  • fluctuating attention/concentration
  • recurrent visual hallucinations
  • spontaneous Parkinsonism
  • SPECT/PET scan → low dopamine transporter uptake in basal ganglia
  • MMSE
  • bloods
  • MSU → urine infection
137
Q

Treatment for dementia with Lewy Bodies

A
  • supportive therapy
  • cholinesterase inhibitors for cognitive decline
  • avoid neuroleptic drugs
138
Q

What is multiple sclerosis?

A
  • cell mediated autoimmune condition
  • repeated episodes of inflammation of nervous tissue in brain and SC → DC4 mediated destruction
  • results in loss of myelin sheath in CNS
139
Q

What are the types of MS?

A

relapse-remitting MS

secondary progressive MS

  • follows from relapsing-remitting
  • gradually worsening symptoms
  • fewer remissions

primary progressive MS

  • from beginning of disease
  • symptoms develop and worsen over time

acute attacks followed by periods of remyelination → these periods become shorter/less frequent

140
Q

Symptoms of MS

A
  • pyramidal weakness
  • spasric paraparesis
  • changes in sensation
  • fatigue
  • chronically increasing bladder movement
  • cognitive impairment
  • dizziness
  • depression
141
Q

Signs of MS

A
  • UMN signs
  • loss of colour vision
  • Lhermitte sign
  • Uhthoff phenomenon
142
Q

Diagnosis of MS

A
  • symptoms disseminated in time and space
  • GOLD STANDARD = MRI → GD-enhancing plaques
  • lumbar puncture
  • McDonald criteria
  • bloods
143
Q

Treatment of MS

A
  • notify DVLA
  • supportive care

relapses

  • acute = methylprednisolone
  • chronic = DMARDs, biologicals
144
Q

What is motor neurone disease?

A
  • group of neurodegenerative disorders
  • selective loss of neurones in motor cortex, cranial nerve nuclei, anterior horn cells
  • progressive, ultimately fatal
  • only affects motor, not sensory
145
Q

Risk factors for MND

A
  • smoking

- exposure to heavy metals

146
Q

Types of MND

A
  • ALS → most common
  • PLS
  • PMA
  • PBP
147
Q

Signs and symptoms of MND

A
  • mixed UMN and LMN presentation
  • LMN signs predominate → weakness, atrophy, muscle fasciculations
  • wrist/foot drop
  • wasting in hands
  • gait disorders
  • excessive fatigue
148
Q

Diagnosis of MND

A

El Escorial criteria

149
Q

Treatment of MND

A
  • supportive therapy
  • riluzole slows progression
  • end of life care
150
Q

Features of ALS

A
  • SOD1 gene
  • loss of neurons in motor cortex and anterior horn
  • UMN and LMN signs
  • babinski response
  • asymmetric
  • corticobulbar signs = worse prognosis
151
Q

Features of PBP

A
  • CN 9-12 → UMN and LMN
  • worst prognosis
  • dysphagia
  • flaccid tongue
  • hoarse, nasal speech
152
Q

Features of PMA

A
  • anterior horn cells affected
  • LMN only
  • distal muscles affected then proximal
153
Q

Features of PLS

A
  • rare
  • progressive tetraparesis
  • UMN only
154
Q

What is myasthenia gravis?

A
  • disorder of neuromuscular transmission
  • caused by binding of autoantibodies to component of NMJ → acetylcholine receptor
  • can be inherited
  • 30s for women, 60-70s for men
155
Q

Signs and symptoms of myasthenia gravis

A

muscle weakness

  • worse on exertion, better with rest
  • marked in proximal muscles → small muscles of hand, deltoid, triceps, bulbar, chewing muscles
  • ocular manifestations
  • no muscle wasting
  • seizures
156
Q

Diagnosis of myasthenia gravis

A
  • mostly clinical
  • detect ACh receptor antibodies
  • +ve tensilon test → tensilon improves muscle weakness
157
Q

Treatment of myasthenia gravis

A

treat symptoms

  • AChEis
  • pryidostigmine
  • methotrexate
  • ciclosporin
  • tacrolimus

stop exacerbating drugs

158
Q

What drugs can exacerbate myasthenia gravis?

A
  • ciprofloxacin
  • azithromycin
  • propanolol
  • atenolol
  • verapamil
  • lithium
  • statins
  • chloroquine
  • prednisolone
159
Q

What is syncope

A
  • temporary loss of consciousness
  • due to disruption of blood flow to brain → fall
  • syncopal episodes AKA vasovagal episodes/fainting
160
Q

Causes of primary syncope

A
  • dehydration
  • missed meals
  • extended standing in warm environment
  • vasovagal response to stimuli → surprise, pain, blood
161
Q

Causes of secondary syncope

A
  • hypoglycaemia
  • dehydration
  • anaemia
  • infection
  • anaphylaxis
  • arrhythmias
  • valvular heart disease
162
Q

Signs and symptoms of syncope

A
  • hot/clammy
  • sweaty
  • heavy
  • dizzy/light headed
  • vision going blurry/dark
  • headache
163
Q

Investigations for syncope

A
  • history
  • ECG/24hr ECG
  • echo
  • bloods
164
Q

Management of syncope

A
  • primary = avoid triggers

- secondary = manage underlying pathology

165
Q

What is a nerve lesion?

A
  • damage to a nerve through compression, trauma, infection etc
  • results in interruption of axonal continuity
166
Q

What are the 3 categories of peripheral nerve injuries?

A
  • stretch related
  • lacerations
  • compressions
167
Q

Signs and symptoms of nerve lesions

A

depends on nerve affected

  • numbness/ tingling
  • muscle weakness
  • dropping objects
  • sharp pains
168
Q

Investigations for nerve lesions

A
  • neurological exam

- MRI

169
Q

Treatment of nerve lesions

A
  • splint/braces
  • physical therapy
  • exercise
  • analgesia
  • surgery if severe
170
Q

What is carpal tunnel syndrome?

A
  • compression of median nerve in carpal tunnel
  • median nerve → sensation to thumb/index/middle/half of ring finger
  • causes unknown
171
Q

Presentation of carpal tunnel syndrome

A
  • pins and needles
  • pain in index/middle finger → reaches shoulder
  • numbness
  • weakness, loss of grip
  • worse a night
172
Q

Diagnosis of carpal tunnel syndrome

A
  • based on symptoms
  • nerve conduction test
  • US/MRI
173
Q

Treatment of carpal tunnel syndrome

A
  • pregnancy cases resolve postpartum
  • rest wrist
  • splint
  • steroid injections
  • surgery if severe
174
Q

What is foot drop?

A
  • difficulty lifting front part of foot → toes drag
  • permanent/temporary
  • damage to common peroneal/fibular nerve
175
Q

Causes of foot drop

A
  • injury
  • lower back damage
  • tumour
  • cauda equina syndrome
  • MS
176
Q

Presentation of foot drop

A
  • unilateral symptoms
  • one foot drags across floor
  • tripping
  • numbness/weakness
177
Q

Diagnosis of foot drop

A
  • clinical diagnosis

- find cause using xray/US/CT/MRI/nerve conduction studies

178
Q

Treatment of foot drop

A
  • brace/splint
  • physiotherapy
  • special shoes
  • nerve stimulation
  • surgery
179
Q

Causes of spinal cord compression

A
  • trauma
  • tumours → common spinal metastases = breast, prostate, lung
  • central disc protrusion
  • prolapsed disk
  • infection
  • epidural haematoma
180
Q

Signs and symptoms of spinal cord compression

A

red flag signs

  • loss of bladder/bowel function
  • UMN signs in lower limbs eg clonus
  • LMN signs in upper limbs eg atrophy

symptoms depend on injury type and site

  • paraplegia
  • pain
  • paraesthesia
181
Q

Diagnosis of spinal cord compression

A
  • xray whole spine
  • MRI if indicated
  • renal function
  • Hb → monitor blood loss
182
Q

Treatment of spinal cord compression

A
  • acute = emergency
  • dexamethasone until treatment confirmed
  • catheterisation
  • analgesi
  • surgical decompression
  • chemo
183
Q

What is Brown-Sequard syndrome?

A
  • hemisection of spinal cord
  • most common cause = penetrating trauma
  • most cases = cervical region
184
Q

Signs and symptoms of Brown-Sequard syndrome

A
  • total ipsilateral loss of position, light touch, vibration sensation at lesion level
  • contralateral loss of pain/temperature below lesion
  • sphincter disturbances
  • ipsilateral spastic paraparesis
185
Q

Diagnosis of Brown-Sequard syndrome

A
  • radiographs for trauma
  • MRI for extent of injury
  • neuro exam for level of injury
186
Q

Treatment of Brown-Sequard syndrome

A
  • spine immobilisation
  • steroids decreased swelling
  • therapy
  • surgery
187
Q

What is the cauda equina?

A

formed by nerve roots caudal to spinal cord termination

188
Q

What is cauda equina syndrome?

A

sudden severe compression of cauda equina

189
Q

Causes of cauda equina syndrome

A
  • herniation of lumbar
  • tumours
  • trauma
  • infection
  • late stage ankylosing spondylitis
  • post op haematoma
  • sarcoidosis
190
Q

Presentation of cauda equina syndrome

A
  • sudden onset → hrs
  • saddle paraesthesia
  • bladder/bowel dysfunction
  • sexual dysfunction
  • motor problems
  • lower back pain
  • bilateral LMN weakness, absent ankle reflex
191
Q

Diagnosis of cauda equina syndrome

A
  • medical emergency
  • rectal exam → loss of anal tone/sensation
  • MRI spine
192
Q

Treatment of cauda equina syndrome

A
  • surgical decompression
  • immobilise spine
  • anti-inflammatory agents
  • Abs if infection
  • chemo
193
Q

What is Wernicke’s encephalopathy?

A

depletion of thiamine → vitB1

194
Q

Causes of Wernicke’s

A
  • chronic alcoholism
  • severe starvation
  • prolonged vomiting
195
Q

Presentation of Wernicke’s

A

classic triad

  • confusion
  • ataxia
  • ophthalmoplegia
  • asterixis = liver flap → general sign of metabolic encephalopathy
  • diagnosis = clinical
196
Q

Management of Wernicke’s

A
  • pabrinex → IV b-vitamins incl thiamine

- complication = Korsakoff’s syndrome

197
Q

What is Korsakoff’s sybdrome?

A
  • irreversible
  • long term brain damage due to B1 deficiency
  • decreased ability to acquire new memorites
  • retrogade amnesia
  • confabulation
198
Q

Primary brain tumours

A
  • less common

gliomas

  • astrocytoma
  • oligondendroglioma

others

  • ependymoma
  • meningioma
  • schwannoma
  • craniopharyngiomas
199
Q

Secondary brain tumours

A
  • much more common

originate from

  • non-small cell lung cancer
  • small cell lung cancer
  • breast
  • melanoma
  • renal cell carcinoma
  • GI
200
Q

What is Charcot Marie Tooth?

A
  • heterogenous group of inherited peripheral neuropathies

- autosomal dominant

201
Q

What are the 4 major categories for Charcot Marie Tooth?

A
  • CMT1
  • CMT2
  • CMT3
  • CMTX
202
Q

Signs and symptoms of Charcot Marie Tooth

A
  • muscle weakness in lower limbs
  • highly arched/very flat feet
  • curled toes
  • awkward/high step and difficult using ankle muscles
  • lack of sensation to arms and feet
  • poor circulation → cold peripheries
  • wasting of muscles in lower legs
  • fatigue
203
Q

Diagnosis of Charcot Marie Tooth

A
  • bloods
  • CSF examination
  • MRI brain, SC
  • genetic studies
  • nerve conduction studies
  • nerve biopsy if genetic studies inconclusive
204
Q

Treatment of Charcot Marie Tooth

A
  • no cure
  • supportive therapy
  • analgesia
  • surgical correction of spinal deformity
  • avoid neurotoxic drugs eg vincristine
205
Q

What is DMD?

A
  • progressive muscle wasting and weakness
  • X linked recessive
  • results in damage to dystrophin gene → dystrophin strengthens muscle fibres and protects from injury
206
Q

Signs and symptoms of DMD

A
  • presents in early childhood
  • progressive proximal muscular dystrophy with characteristic pseudohypertophy of calves
  • major milestones delayed
  • recurrent falls
  • speech delay
  • fatigue
207
Q

Diagnosis of DMD

A
  1. serum creatinine kinase → v high
  • genetic analysis
  • muscle biopsy with assay for dystrophin protein
  • muscle strength test
  • gait assessment
208
Q

Complications of DMD

A
  • join contractures
  • respiratory failure
  • cardiomyopathies, HF
  • gastric dilation
  • learning difficulties
209
Q

Treatment of DMD

A
  • MDT care
  • vaccines → influenza/pneumococcal
  • physiotherapy
  • vitD/bisphosphonates
  • corticosteroids
  • end of life care
210
Q

What is Lamber Eaton?

A
  • disorder of neuromuscular transmission
  • caused by impaired presynaptic release of acetylcholine
  • caused by autoimmune attack of VG Ca2+ channels
211
Q

Signs and symptoms of Lambert Eaton

A
  • similar to myasthenia gravis
  • can present with small cell lung cancer
  • insidious onset
  • proximal muscle weakness
  • depressed tendon reflexes
  • gait changes
  • dry mouth
  • impotence in males
  • eyelid ptosis
212
Q

Diagnosis of Lambert Eaton

A
  • ACh receptors indicate MG
  • nerve stimulation
  • serum test for VG Ca2+ channels
  • MRI for malignancy
213
Q

Treatment of Lambert Eaton

A
  • treat any cancer
  • AChEi
  • amifampridine → muscle strength
  • immunosuppression
  • surgery
214
Q

What is Amaurosis Fugax?

A

painless, temporary loss of vision in one/both eyes

215
Q

Causes of Amaurosis Fugax

A
  • embolic
  • haemodynamic
  • ocular
  • neurological
  • idiopathic
216
Q

Presentation of Amaurosis Fugax

A
  • black curtain coming down vertically into visual field
  • vision loss/blurring/fogging/dimming
  • lasts seconds to hours
217
Q

Diagnosis of Amaurosis Fugax

A
  • clinical diagnosis
  • full history
  • ophthalmic exam
  • ESR level
  • CT head
218
Q

Treatment of Amaurosis Fugax

A
  • treat underlying cause

- can cause stroke if untreated

219
Q

What are peripheral neuropathies?

A
  • damage to one/more peripheral nerves
  • results in transmission blockages between PNS and CNS
  • can be acute or chronic
220
Q

Causes of peripheral neuropathies

A
  • diabetes = most common
  • dietary deficiencies
  • medication
  • alcohol excess
  • CKD
  • connective tissue disorders
  • inflammatory conditions
  • inherited conditions

axonal degeneration → DM, B12 deficiency, lead poisoning
segmental demyelination → GBS, CMT

221
Q

Sensory symptoms of peripheral neuropathies

A

loss of

  • touch
  • proprioception
  • temperature/pain
  • sensation
  • paraesthesia
  • +ve Romberg test → sensory ataxia
222
Q

Motor symptoms of peripheral neuropathies

A
  • distal weakness
  • proximal weakness
  • muscle wasting
  • fasciculations
  • absent tendon reflexes
223
Q

Diagnosis of peripheral neuropathies

A
  • history
  • bloods
  • nerve conduction studies
  • electromyography
  • nerve biopsy
224
Q

Treatment of peripheral neuropathies

A
  • treat underlying cause
  • pregabalin/gabapentin for pain
  • supportive therapy
225
Q

What is encephalitis?

A
  • inflammation of brain parenchyma due to viral infection

- other causes = TB, lume disease, toxoplasmosis

226
Q

Viruses that cause encephalitis

A
  • most common = HSV1
  • CMV
  • EBV
227
Q

Presentation of encephalitis

A
  • fever
  • headache
  • altered mental status
  • can present with signs of meningitis
  • confusion/drowsiness
  • symptoms of raised ICP
  • if caught late, coma
228
Q

Symptoms of raised ICP

A
  • vertigo
  • nausea
  • headache
  • photophobia
229
Q

Diagnosis of encephalitis

A
  • bloods
  • CSF → viral PCR to detect virus
  • CT/MRI
  • blood cultures/gram stain
230
Q

Treatment of encephalitis

A
  • urgent admission
  • acyclovir
  • stat IV benzylpenicillin
  • careful with fluids → cerebral oedema
231
Q

What is Herpes Zoster?

A
  • shingles
  • painful rash caused by reactivation of nerve infection caused by varicella-zoster virus
  • first presents as chickenpox as a kid
  • remains dormant in dorsal root ganglia
  • travels through peripheral sensory nerves to skin
232
Q

Risk factors of herpes

A
  • immunocompromised
  • HIV
  • malignancy
233
Q

Presentation of herpes

A

rash

  • red, painful
  • dermatomal distribution → cervical, trigeminal, thoracic, lumbar
  • fluid filled blisters
  • stabbing/burning pain
  • fever, headache, fatigue
  • itching
234
Q

Diagnosis of herpes

A
  • PCR
  • CSF analysis
  • bloods
  • diagnosis often clinical
235
Q

Treatment of herpes

A

antiviral therapy

  • acyclovir
  • valacyclovir
  • famiciclovir
  • if immunocompromised → IV acyclovir
  • analgesia
  • antipyretics

Phase 2a Resits (10 decks)

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