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Phase 2a > Neurology > Flashcards

Neurology Flashcards

1
Q

What are cerebrovascular accidents?

A

Transient ischemic attack
Stroke

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2
Q

What is a transient ischemic attack?

A

Sudden onset neurological deficit , lasting <24hr without infarction.

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3
Q

What are the causes of a TIA?

A

Carotid thrombosis-emboli
- thrombosis
emboli from AF

  • 90% ICA
    -10% Vertebral
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4
Q

What are the risk factors of a TIA?

A
  • smoking
    -T2DM
    -HTN
    -AF
    -Obesity
    -VSD
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5
Q

What is the presentation of a TIA?

A

Focal neurology:
-Anterior cerebral artery =weak numb contralateral leg
-Middle cerebral artery= weak numb contralateral side of the body, face drooping w/ forehead spared, dysphasia ,(temporal)
-Amaurosis fugal
-Posterior CA= vision loss
-Vertebral artery = cerebellar syndrome; ataxia, nystagmus , tremor with the Romberg test (sensory +ataxia)
CN lesions 3-12

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6
Q

What is Amaurosis Fugax?

A

Emboli passes into retinal, ophthalmic or ciliary artery, low blood flow to retina due to occlusion

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7
Q

What is the vision loss seen seen in posterior cerebral artery ichemia?

A

contralateral homonymous hemianopia with macular sparing - occipital affected

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8
Q

What is the diagnosis of TIA?

A

Clinically made - use scoring systems:
FAST- face arms speech time

ABCD2 scoring
-Diffusion weighted MRI?CT
-Carotid imaging - doppler USS

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9
Q

What is the acute treatment for a TIA?

A

Aspirin 300mg

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10
Q

What is prophylaxis treatment for a TIA?

A

Clopidogrel 75mg + atorvastatin 80mg

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11
Q

What is hemiparesis?

A

weakness of an entire side of the body

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12
Q

What is affected if a patients is unable to understand speech or is having trouble speaking?

A

inability to understand - (Wernickes)
or speech (Broca’s)

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13
Q

What is a stroke?

A

Focal neurological deficit lasting 24hr< with infarction

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14
Q

What are the types of stroke?

A

Ischemic -85%
Haemorrhagic-15%

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15
Q

What is an ischemic stroke?

A

Essentially long TIA
- carotid throbs-emboli
-thrombosis
-AF embolism

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16
Q

What is a haemorrhage stroke?

A

Brain bleeds - trauma , HTN, Berry aneurysm rupture

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17
Q

What are the risk factors of a stroke?

A

HTN, smoking, obesity, T2DM, AF, TIA

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18
Q

Why is atrial fibrillation a risk factor for stroke?

A

Due to stasis ob blood in atria which thromboses and can embolise to carotids

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19
Q

What is the presentation of a stroke?

A

Focal neurology like TIA!!
- raise ICP t
-pronator drift -stroke sign

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20
Q

How can a haemorrhage stroke cause an increase in ICP?

A

Bleeding/ cerebral oedema causes increase in pressure on the brain structures and causes a midline shift

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21
Q

What are the signs of increased ICP?

A

Ipsilateral pupillary dilation - down and out
Headache, vomiting
Papilloedema
cushings reflex
midline shift
CN6 palsy
LOC

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22
Q

What are the complications of ICP?

A

Tentorial herniation + coning

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23
Q

What is the body’s repsonse/reflex to raised ICP?

A

Cushings reflex

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24
Q

What is cushings reflex?

A

Hypertension
Bradycardia
Irregular breathing

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25
Q

What causes Cushing reflex?

A

Increase in ICP , ICP exceeds arterial blood pressure pushes on arterioles and they start to compress leading to reduced cerebral blood flow–> activates sympathetic system-> alpha 1 adrenergic receptors activated causing vasoconstriction + HTN
HTN detected by barroreceptors –>activation of para-sympathetic and therefore muscarinic 2 receptors to lower heart rate (bradycardia)
Irregular breathing caused by ICP and HTN pressing on respiratory centre

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26
Q

What is Lacunar stroke?

A

common type of ischemis stroke of lenticulostraite arteries (supply deep brain structures)–> ischemia to BG ,internal capsule + thalamus

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27
Q

What is pronator drift?

A

Ask patient to lift arms to ceiling ; pronators take over , arm on affected side will pronate + palm faces down

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28
Q

What is the diagnosis of a stroke?

A

non contrast CT head = ischemic- mostly normal
Haemorrhage - hyper dense blood
Needed to distinguish

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29
Q

What is the treatment for ischemic stroke?

A
  1. presents within 4.5 hours = clot buster (thrombolysis) ? IV alteplase
  2. Aspirin 300mg for 2 weeks
    + lifelong clopidogrel 75mg
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30
Q

What is the treatment for a haemorrhagic stroke?

A

Neurosurgery referral
IV mannitol for increased ICP

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31
Q

What is an intracerebral haemorrhage?

A

Sudden bleeding into brain tissue due to a rupture of a blood vessel within the brain
This can lead to infarction and raised ICP.

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32
Q

What are the types of intracerebral haemorrhages?

A

-subarachnoid
-subdural
-extradural

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33
Q

What is a subarachnoid haemorrhage?

A

spontaneous bleeding into the subarachnoid space usually due to a berry aneurysm circle of willis rupture

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34
Q

Where is the subarachnoid space?

A

Between the arachnoid and Pia mater

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35
Q

What are the risk factors of a subarachnoid haemorrhage?

A

HTN, Traumua, increasing age, FHX, known aneurysm

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36
Q

What is the presentation of a subarachnoid haemorrhage?

A
  • occipital thunderclap headache
    -sudden onset
    -may have had sentinel headache - warning symptom that precedes the rupture of aneurysms
  • worst headache of your life
    -mennigism -mimics meningitis kernig + Brudzinksi signs
    -Low GCS score
    -CN3 palsy - fixed dilated pupi
    -CN6 palsy- signs go increased ICP
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37
Q

What is Kernig sign?

A

can’t extend leg when knee is flexed

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38
Q

What is Brudzinski sign?

A

when neck elevated knees automatically flex

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39
Q

What is GCS?

A

Glasgow coma scale - measures consciousness
15 - normal
8- comatose
3-unresponsive

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40
Q

What is the diagnosis of subarachnoid haemorrhage ?

A

Diagnostic CT head - a star shape
Positive = Do a CT angiogram to see extent
Negative = lumbar puncture - wait 12hr as results are most sensitive then
Positive sign is that you will see xanthochromia (yellowish CSF due to RBC haemolysis)

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41
Q

What is the treatment of subarachnoid haemorrhage?

A

1st line - neurosurgery ; end-vascular coiling
Nimodipine - CCB so reduces vasospasm and BP

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42
Q

What is a subdural haemorrhage?

A

Bleeding into subdural space due to a rupture of a bridging vein from shearing and deceleration injuries

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43
Q

What is the subdural space?

A

the space between dura mater and arachnid mater

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44
Q

What are the risk factors of subdural haemorrhage ?

A
  • trauma
    -child abuse
    -cortical atrophy - dementia
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45
Q

What is the presentation of subdural haemorrhage?

A

Gradual onset with latent period
- bleeding is small ; accumulation + autolysis of blood - haematoma grows gradually - Sx after days/weeks/months
-Sx of raised ICP; Cushing triad + fluctuating GCS + papillodema
-focal neurology later

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46
Q

What is the diagnosis of subdural haemorrhage?

A

NCCT Head = banana or crescent shaped haematoma ,
crosses suture lines, unilateral, midline shift

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47
Q

What is the treatment for subdural haemorrhage?

A

Surgery; Burr hole + craniotomy
IV mannitol to lower ICP

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48
Q

What is the extradural space?

A

space between dura mater and skull bone

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49
Q

What is an extradural haemorrhage?

A

Bleeding into extradural space usually after trauma to middle meningeal artery / temporal bone

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50
Q

What is the epidemiology of extradural haemorrhage?

A

typically young adults 20-30
As you age the risk decreases as dura mate more firmly adhered to skull

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51
Q

What is a risk factor of extradural haemorrhage?

A

head trauma

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52
Q

What is the pathology of extra dural haemorrhage ?

A

Initial event –> lucid interval ‘I feel fine’ –> after weeks rapid deterioration due to raised ICP as the clot becomes haemolysed and takes up water therefore increases volume of skull; rises ICP

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53
Q

What is the presentation of extra dural haemorrhage?

A

Low GCS - confusion
Raised ICP signs - cushings triad, papillodema

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54
Q

What is the diagnosis pf extradural haemorrhage?

A

NCCT head - Lens shaped hyper dense bleed
-confined to suture lines
-midline shift
-unilateral

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55
Q

What is the treatment of extradural haemorrhage?

A
  • urgent surgery - clot evacuation
    -IV mannitol for raised ICP
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56
Q

What is a complication of extradural haemorrhage ?

A

Death from respiratory arrest
- tonsillar herniation + coning of brain= compressed respiratory centres
- due to untreated raised ICP

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57
Q

What are primary headaches?

A

-migraine
-cluster
-tension
-drug overdose
-Trigeminal neuralgia)

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58
Q

What are secondary causes of headaches?

A

Due to an underlying condition:
-GCA
-Infection
-SAH
-Trauma
-Cerebrovascular disease
-Eye, ear, sinus pathology

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59
Q

What is a migraine?

A

Episodes of recurrent throbbing headache +/- aura , often with vision change

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60
Q

What is the epidemiology of migraines?

A
  • most common cause of episodic headache
    -F>M
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61
Q

What are the triggers of a migraine?

A
  • chocolate
    -hangovers
    -orgasms
    -cheese
    -oral contraceptives
    -alcohol
    -exercise
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62
Q

What is the pathology of migraines?

A

Prodome (days before attack)
- mood change
Aura (part of attack, minutes before headache)
- visual phenomena; zig zag lines
Throbbing headache lasting 4-72hr - migraine

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63
Q

What is the presentation of a migraine?

A

2< of:
- unilateral pain
-throbbing
-motion-sicknss
-mod-severely intense +

1< of:
- N+V
-Photophobia/ phonophobia

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64
Q

What is the diagnosis of a migraine?

A

clinical - unless other pathology suspected

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65
Q

What is the treatment of Migraine?

A

Acute - oral triptan (Sumatriptan) or Aspirin (900mg)

Prophylaxis- Bb - propanolol
or TCA- amitriptyline

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66
Q

What is a cluster headache?

A

Unilateral periorbital pain with autonomic features. 15-60mins

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67
Q

What is the epidemiology of a cluster headache?

A
  • most disabling primary headache
    -rare-ish
    -many headaches clustered in a small amount of time
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68
Q

What are the risk factors of cluster headaches?

A

male
smoking
genetics (auto dom link)

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69
Q

What is the presentation of a cluster headache?

A

Crescendo (rising in severity) unilateral periorybital excruciating pain, may affect temples too
Autonomic features:
-conjunctival infection + lacrimation
-Ptosis (droopy eyelids)
-miosis (dilated unilateral pupil)
-rhinorrhoea

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70
Q

What is the diagnosis of cluster headaches?

A

clinically 5< similar attacks confirms diagnosis

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71
Q

What is the treatment of cluster headaches?

A

Acute - triptans (sumatriptan)
Prophylaxis - CCB- verapamil

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72
Q

What is a tension headache?

A

Bilateral generalised headache, radiated to neck

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73
Q

What is the epidemiology of tension headaches?

A
  • most common primary headache
  • triggered by stress
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74
Q

What is the presentation of tension headaches?

A

Rubber band, tight around head. Bilateral pain, feel it in trapezius too
- mild to mod severely
-no motion sickness, photophobia, aura

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75
Q

What is the diagnosis of tension headaches?

A

Clinical from Hx

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76
Q

What is the treatment for tension headaches?

A

Simple analgesia - Aspirin or paracetamol

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77
Q

Why would a patient avoid opiates?

A

Risk of dependence

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78
Q

What is trigeminal neuralgia ?

A

Unilateral pain in 1< trigeminal branches

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79
Q

What are the risk factors of trigeminal neuralgia ?

A

MS (20x more likely)
Increasing age
Female

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80
Q

What are the triggers of trigeminal neuralgia ?

A

eating, shaving, talking, brushing teeth

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81
Q

What is the presentation of trigeminal neuralgia?

A

Electric shock pain (secs -2min) in V1/2/3

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82
Q

What is the diagnosis of trigeminal neuralgia?

A

Clinical 3< attacks with symptoms

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83
Q

What is the treatment of trigeminal neuralgia?

A

Carbamazepine - anticonvulsant

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84
Q

What is giant cell arteritis?

A

Large vessel vasculitis

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85
Q

What is the pathology of giant cell arteritis?

A

50 year old - caucasian women - presents with unilateral tender scalp, intermittent jaw claudication
- worst case Amaurosis Fugax

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86
Q

What is the diagnosis of giant cell arteritis?

A

Temporal artery biopsy -> big sample as many skip lesions
- granulomatosis non caseating inflammation of intimal + media with skip lesions
- Raised ESR/CRP
-nomocytic nomochromic anemia (of chronic disease)

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87
Q

What is the treatment of giant cell arteritis?

A

Corticosteroids - prednisolone
- if signs of amaurosis fugax - high dose IV methylprednisolone

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88
Q

What is Parkinson’s disease?

A

Progressive movement disorder due to degeneration of dopamine - producing neurons in the substantia nigra

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89
Q

What is the epidemiology of Parkinson’s disease?

A
  • 2nd most common neurodegenerative disorder after dementia
    -more common in males, peak onset 55-65
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90
Q

What are the risk factors of Parkinson’s disease?

A

FHx, males, increasing age, smoking seems to be protective ?

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91
Q

What is the pathology of Parkinson’s disease?

A

To initiate movement - nigrostriatal pathway signals striatum to stop firing to substantia niagra pars reticularis therefore stop movement inhibition

Degenrated substantia Niagara pars compacta, less dopamine to striatum - harder to initiate movement

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92
Q

What is the presentation of Parkinson’s disease?

A

Cardinal Sx = Bradykinesia , resting tremor , Rigidity, postural instability
- anosmia, constipation
-shuffling gait , pill rolling thumb
- typically asymmetrical

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93
Q

What is the diagnosis of Parkinson’s disease?

A

Clinical - Bradykinesia + 1< other cardinal Sx

DaTSCAN - reduced dopamine supply
Head CT - SN atrophy

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94
Q

What is the treatment of Parkinson’s?

A

Levodopa - increase amount of dopamine in CNS + carbidopa

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95
Q

What is the problem with L-DOPA?

A

L-DOPA usually works very well but soon the body becomes resistant to it, effects wear off therefore don’t give LDOPA to mild Sx

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96
Q

What is Ddx of Parkinson’s ?

A

Lewy body dementia - associated with Parkinson’s

Parkinson Sx then dementia= Parkinson dementia
Parkinson Sx after dementia = Lewy body dementia with Parkinsonism

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97
Q

What is Dementia?

A

Neurodegenerative disorder; reduced cognition (memory, judgement, language) over time

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98
Q

What are the risk factors of dementia?

A

-Depression
-reduced activity
-Downs

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99
Q

What are the causes of dementia?

A

Alzheimer’s - 60%
Vascular -20%
Lewy body- 10%
Fronto temporal -5%

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100
Q

What is Alzheimers disease?

A

Accumulation of beta amyloid plaques (breakdown product of amyloid precursor protein) and neurofibrillary tangles in cerebral cortex. This increases cortical scarring and brain atrophy and reduces Ach transmitters

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101
Q

What is the risk factors of Alzheimer’s disease?

A

Downs - inevitable ; APP gene mutation
-ApoE4 allele in familial alzheimers late onset

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102
Q

What are amyloid plaques?

A

clusters that form in the space between nerve cells

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103
Q

What are neurofibrillary tangles?

A

Knots of the brain cells

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104
Q

What is the presentation of Alzheimers disease?

A

Agnosia - can’t recognise things
Apraxia -cant do basic motor skills
Aphasia - can’t talk as well as normal
-amnesia

  • gradual onset / steady decline
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105
Q

What is vascular dementia?

A

Cerebrovascular damage - stroke,TIA

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106
Q

What is the presentation of vascular dementia?

A

UMN signs + general decline in cognition
Stepwise decline with short periods of stability

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107
Q

What is Lewy body dementia?

A

Lewy bodies (alpha synuclein + ubiquitin aggregates) accumulate in cortex. Associated with parkinons

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108
Q

What is the presentation of Lewy body?

A

Fluctuating cognitive function
Parkinsonism

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109
Q

What is front-temporal dementia?

A

Specific degeneration of frontal and temporal lobes of the brain

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110
Q

What are the risk factors of fronto temporal dementia ?

A

FHx-Autosomal dominant change in Tau protein , chromosome 17
- Motor neurone disease

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111
Q

What is the presentation of fronto-temporal dementia?

A

speech; language mostly = temporal more so affected

Thinking+memory affected= frontal more so

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112
Q

What is the diagnosis of dementia?

A

Mini mental state exam
>25 - normal
18-25 - impaired
<17 -severely impaired
Brain MRI - cortical atrophy

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113
Q

What is the treatment of dementia?

A

Conservative ; social stimulation, exercise
For alzheimers - Rivastigmine (Acetylcholinesterase inhibitor- stops the enzyme breaking down Ach)

Vascular - antihypertensives - ramipril

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114
Q

What is Huntington’s disease?

A

Huntington’s disease is an autosomal dominant neurodegenertive disorder with full penetrance characterised by the lack of inhibitor neurotransmitter GABA. The cause of chorea

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115
Q

What is the aetiology of HD?

A

CAG repeats on chromosome 4, affecting gene HTT

The more trinucleotide repeats, the earlier + more severe Sx present ; Anticipation.

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116
Q

What is the presentation of Huntington’s disease?

A

Chorea, dementia, psychiatric issues, depression

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117
Q

What is Chorea?

A

A continuos flow of involuntary jerky movements

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118
Q

What is the diagnosis of Huntington’s disease?

A

Clinical
FHx of earlier + more severe Huntington’s
Genetic test if over 35 repeats

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119
Q

What is the treatment for HC?

A

Extensive counselling
DA antagonist - Tetrabenazine

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120
Q

What is Multiple Sclerosis?

A

Chronic autoimmune , T cell mediated inflammatory disorder against myelin basic protein of oligodendrocytes leading to multiple plaques of demyelination, occurring sporadically over years

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121
Q

What are the risk factors of MS?

A

females
20-40
Autoimmune disease- FHx
EBV

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122
Q

What are the types of MS?

A

Relapsing/ remitting
Primary Progressive
Secondary Progressive

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123
Q

What is relapsing-remitting?

A

Most common
- clearly defined disease relapses with full or partial
recovery with residual deficits
-periods between disease relapses have no increase in disability between bouts
- incomplete recovery

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124
Q

What is primary progressive?

A

Gradual deterioration without recovery

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125
Q

What is secondary progressive ?

A

Relapsing-remitting -> primary progressive - 75% R-R causes evolve to this

126
Q

What are the symptoms of Multiple sclerosis ?

A

Parasthesia - tingling and numbness
Blurred vission
Uhtoffs phenomenon - Sx exacerbated with heat, after a shower

127
Q

What are the signs of MS?

A

Optic Neuritis- inflamed optic nerve, can’t see red properly
Internuclear opthalmoplegia - lateral gaze impaired - damaged medial longitudinal fasciculus
Brainstem signs(displopia, dysarthria , vertigo), Sensory signs ( impaired proprioception, Paraesthesia)
UMN signs = Lhermitte Phenomenon , Charcot neurological triad

128
Q

What is Lhermitte phenomena ?

A

UMN sign
- electric shock sensation with neck flexion

129
Q

What is Charcot neurological triad?

A
  • dysarthria - struggle soaking due to muscles
    -Nystagmus - miscommunication between eye and brain
    -Intention tremor
130
Q

What is the diagnosis of Multiple sclerosis?

A

Mcdonald Criteria = 2< attacks disseminated in time and space - separate events + different part of CNS affected

Diagnostic = MRI brain + cord- shows dissemination in space (where there is white demyelination)
- delayed conduction speed
-LP may show oligoclonal IgG bonds - CNS inflammation

131
Q

What is the treatment for multiple sclerosis ?

A

Acutely - IV Methylprednisolone
Prophylaxis - Beta interferon
DMARD

132
Q

What is motor neurone disease?

A

Progressive degeneration of motor neurones in the brain and spinal cord, causing UMN and LMN signs

133
Q

What is the main motor spinal tract?

A

Corticospinal - UMN from precentral gyrus which has - Decussation (lateral , 90% fibres) and no decussation (anterior, 10% fibres)

134
Q

What is the organisation of movement?

A
  1. Idea of movement - association cortexes, pre motor cortex
    2.Activation of UMNs - in motor cortex
  2. Impulse via corticospinal tract to LMN
    4.Modulation by
    -cerebellum - fine tuning
    -Basal ganglia - green signal to move
  3. Movement + somatosensory info obtained by sensory tracts
135
Q

What is a UMN lesion?

A

Lesion from precentral gyrus to anterior spinal cord
-everything goes up

136
Q

What are the signs of a UMN lesion?

A
  1. Hypertonia; rigidity, spasticity
  2. Hyperreflexia
    3.No fasciculations
    4.Babinski Positive -occurs when stimulation of the lateral plantar aspect of the foot leads to extension (dorsiflexion or upward movement) of the big toe
  3. Arms: Flexor muscles stronger> than extensors
    Legs: Extensor> flexers
137
Q

What is a LMN lesion?

A

Lesions from anterior spinal cord to the muscles innervated
-everything goes down

138
Q

What are the signs of a LMN lesion?

A
  1. Hypotonia ;flaccid +muscle wasting
  2. Hypoflexia
  3. Fasciculations
    4.Babinski negative
    5.Generally low power
139
Q

What are the risk factors of motor neurone disease?

A

Male
FHx -SOD-1 mutation
Increasing age

140
Q

What does motor neurone disease never affect?

A

Eye muscles –> MS+MG do
Sensory function –> MS+ polyneuropathies do

141
Q

What are the classification of MND?

A
  1. Amyotrophic lateral sclerosis
    2.Progressive lateral sclerosis
    3.Progressive muscular atrophy
    4.Progressive bulbar palsy
142
Q

What is Amyotrophic lateral sclerosis?

A
  • most common
    -UMN +LMN signs
    -Can progress to bulbar palsy
143
Q

What is primary lateral sclerosis?

A

UMN signs only

144
Q

What is progressive muscular atrophy?

A

LMN signs only

145
Q

What is progressive bulbar palsy?

A

-Cn 9-12 affected
-weak prognosis - increases risk of respiratory failure
- causes dysarthria, dysphagia , chocking

146
Q

What are the Sx of MND?

A

mixed UMN +LMN signs
- no eye, sensory, cerebellar or parkinson signs

147
Q

What is the diagnosis of MND?

A

Mainly clinical - LMN +UMN signs in 3 regions
Electromyography - shows fibrillation potentials - abnormal pattern

148
Q

What is the treatment of MND?

A

MDT management
Rituzole - blocks glutamergic transmission
Supportive - breathing support

149
Q

What are the primary brain tumours?

A

-Gliomas
-Meningioma
-Acoustic neuroma

150
Q

What are Meningiomas?

A

Tumour growing from the cells of the meninges in the brain + spinal cord

151
Q

What is acoustic neuroma?

A

Tumour of the Schwann cells surrounding the auditory nerve

152
Q

What are gliomas and what are the types?

A

Tumour of the glial cells in the brain or spinal cord.
- Astrocytoma -mc especially in kids
-oligodendroglioma
-ependymoma

153
Q

What are the secondary brain tumours?

A

NSCLC- mc +SCLC
Breast
Melanoma
Renal cell carcinoma
Gastric cancer

154
Q

What is the grading system of astrocytomas?

A

WHO classification 1-4
1- benign
2- low grade astrocytoma
3- Anaplastic astrocytoma
4- Gliobastoma multiforme - bad prognosis

155
Q

What is the presentation of brain tumours?

A

Raised ICP; couching triad (increased PP/ HTN, bradycardia, irregular breathing) ,Papillodema, CN6 palsy
-Focal neuroogy
-Epileptic seizures
-Lethargy and weight loss

156
Q

What is the diagnosis of brain tumours ?

A

MRI head= locate tumour, then biopsy (determine grade)
- no LP as raised ICP - massive CI

157
Q

What is the treatment of brain tumours?

A

Surgery - remove tumour if possible and low ICP
+ chemo
Steroids - dexamethasone

158
Q

Where does the spinal cord extend from and to?

A

C1 to L1/2

159
Q

At what level is the conus medullar is and Cause Equine ?

A

L3

160
Q

What is Cauda Equine?

A

Lumbar and sacral nerve roots group together to form cauda equine

161
Q

What is Hemiplegia?

A

Paralysis of one side of body - brain lesion

162
Q

What is paraplegia?

A

paralysis of both legs - cord lesion

163
Q

What is the DCML?

A

Dorsal column medial lemniscus - ascending
Dorsal root - medulla then decussates
-fine touch, 2 point discrimination , proprioception

164
Q

What is spinothalamic tract?

A

Ascending
-Decussates 1-2 spinal levels above entry
- pain + temperature

165
Q

What is the corticospinal tract?

A

Descending UMN; decussates at medulla - ventral root
- motor

166
Q

What does a spinal cord lesion cause?

A

Ipsilateral Sensory signs
Contralateral Motor signs

167
Q

What reflex is at L3/4?

A

Knee reflex

168
Q

What reflex is at L5?

A

Big toe jerk

169
Q

What reflex is at S1?

A

Ankle jerk

170
Q

What are the causes of spinal cord compression/ myelopathy?

A
  • Vertebral body neoplasms ! mc- mets from lung, breast , RCC, melanoma
    -Spinal pathology - disc prolapse/ herniation
171
Q

What is the presentation of spinal cord compression?

A

-Progressive leg weakness with UMN signs
-Sensory loss BELOW lesion as ascending send info up

172
Q

What is the diagnosis of spinal cord compression?

A

If suspect; MRI cord ASAP
CXR if malignancy suspected

173
Q

What is the treatment of spinal cord compression?

A

Neurosurgery + laminectomy / microdisectomy

174
Q

What is Cauda Equina syndrome?

A

Compression of cauda equina

175
Q

What are the causes of cauda equina syndrome?

A

Lumbar herniation

176
Q

What is the presentation of Cauda Equina syndrome?

A
  • Leg weakness with LMN signs
    -Saddle anaesthesia - perioneal numbness
  • Bladder/ bowel dysfunction + sphincter involvement common
177
Q

What is the diagnosis of Cauda equina syndrome?

A

MRI cord - diagnostic + testing nerve roots/ reflexes

178
Q

What is the treatment for Cauda equina syndrome?

A

Neurosurgery - microdisectomy

179
Q

What is the Brown sequard syndrome?

A

Condition associated with hemisection (damage) to half of the spinal cord

180
Q

What is the presentation of Brown sequard syndrome?

A
  • ipsilateral motor weakness (UMN)
    -ipsilateral DCML dysfunction - proprioception , 2point discrimination
    -Contralateral spinothalamic dysfunction - paint + temp sensation
181
Q

What are the types of peripheral neuropathy?

A

Mononeuropathy = affects single nerve
Polyneuropathy= multi systemic
Mononeuritis multiplex= several individual nerves

182
Q

What is peripheral neuropathy?

A

Peripheral neuropathy is a type of nerve damage that can cause pain, numbness or weakness.

183
Q

What are the causes of peripheral neuropathy?

A

T2DM
Surgery
B12 deficiency
Infection
chronic disease
Gullen Barre syndrome

184
Q

What are the mechanisms of peripheral neuropathy?

A
  • Demyelintaion- Schwann cell damage , slower conduction
    -Axonal damage
    -Nerve compression - focal demyelination at point of compression
    -Wallerian degeneration - nerve cut distally dies
    -Vasa nervorum infraction
185
Q

What are the causes of mononeuritis multiplex?

A
  • wegeners
    -AIDs
    -RA
    -T2DM
    -Sarcoidosis
    -leprosy
    -carcinomas
186
Q

What are the types of mononeuropathy?

A

Carpal tunnel syndrome
Peroneal neuropathy
Ulnar neuropathy

187
Q

What are the types of polyneuropathy?

A

MS
Guillen Barre

188
Q

What is carpal tunnel syndrome?

A

Pressure on median nerve passing through carpal tunnel
- nerve roots C6-T1

189
Q

What are the RF/Causes of carpal tunnel syndrome?

A

F>M
Hypothyroidism; acromegaly ; pregnancy
RA
Obesity

190
Q

What is the presentation of carpal tunnel syndrome?

A

Gradual onset
- weakness of grip + aching hand/forearm
-pain worse at night
-parasthesia of hand
-Wasting of thenar eminence

191
Q

What is the diagnosis of carpal tunnel syndrome?

A

Phalen test - flex fist for 1 minute at wrist +ve = parasthesia and pain

Tinel test = tapping wrist causes tingling
Electromyography diagnostic if above tests uncertain

192
Q

What is the treatment of carpal tunnel syndrome?

A

Wrist splint at night + steroid injection
Last resort - surgical decompression

193
Q

What is radial nerve palsy?

A

Roots C5 - T1
- Presents with classic wrist drop
- radial nerve mostly innervates extensor arm muscles

194
Q

What is the treatment for radial nerve palsy?

A

Splint + simple analgesia

195
Q

What is ulnar nerve palsy ?

A

Roots C8-T1
Presents with classic claw hand

196
Q

What is the treatment for ulnar nerve palsy ?

A

Splint
Simple analgesia

197
Q

What is sciatica?

A

L5/S1lesion

198
Q

What are the causes of sciatica?

A
  • spinal : Intervertebral disc herniation / prolapse
    -Non spinal : piriformis syndrome, tumours, pregnancy
199
Q

What is the presentation of sciatica?

A

Pain from buttock down lateral leg –> pinky toe

Weak plantar flexion + absent ankle jerk

200
Q

What is the diagnosis of sciatica?

A

Exam ; can’t do straight leg raise test without pain
MRI cord to confirm

201
Q

What is the treatment for sciatica?

A

Analgesia + physiotherpay
Neurosurgery

202
Q

What is polyneuropathy?

A

‘Glove and stocking’ distribution ; mostly peripheries affected

203
Q

What are the causes of polyneuropathy?

A

Guillain barre - motor mostly
Diabetic neuropathy- sensory mostly
- vasculitis
-malignancy
-RA
-B-12 deficiency

204
Q

What is the diagnosis of polyneuropathy?

A

Find underlying cause - bloods, serology, ESR/CRP

205
Q

What is the treatment of polyneuropathy?

A

Analgesia + treat underlying cause

206
Q

What is perineal neuropathy?

A

common perineal nerve compressed
- foot drop - ankle dorsiflexion deficit
-sensory deficit over dorsal foot

207
Q

What are the causes of cranial nerve lesions?

A

Tumour
MS
Trauma

208
Q

What is the presentation of CN3 nerve lesion?

A

Ptosis
Down and out eye
Fixed dilated pupil

209
Q

What is the presentation of CN4 nerve lesion?

A

Diplopia looking down
- rare, always due to trauma

210
Q

What is the presentation of CN 5 lesion?

A

Jaw deviates towards affected side
- loss of corneal reflex
-sensory pain/ motor jaw pain V1/2/3

211
Q

What is the presentation of CN 6 lesion?

A

Adducted eye - signs of raised ICP

212
Q

What cranial nerve lesions leads to a non functioning eye?

A

CN 3/4/6

213
Q

What is the presentation of a CN 7 lesion?

A

Facial droop with no forehead sparing
- bell’s palsy , parotid inflammation

214
Q

What is the presentation of a CN8 lesion?

A

Hearing loss
Loss of balance
- skull change, compression, middle ear disease

215
Q

What is the presentation of a CN 9+10 lesion?

A

Impaired gag reflex + swallowing, respiratory, vocal issues

216
Q

What is the presentation of a CN11 lesion?

A

Cant shrug shoulder/ turn heard vs resistance

217
Q

What is CN12 lesion presentation?

A

tongue deviation towards side of lesion

218
Q

What is Myasthenia Gravis?

A

Autoimmune disease against neuromuscular junction post synaptic receptors , nicotinic acetylcholine receptors and muscle specific Kinase

219
Q

What is MG mediated by?

A

Nicotinic acetylcholine receptor antibody- Anti- AchR and muscle specific receptor tyrosine kinase - anti-Musk

220
Q

What is the epidemiology of MG?

A

Females = 40y/o- related to autoimmune disease

Males- 60y/o - related to thymoma - thymes tumour

221
Q

What is the pathology of MG?

A

85% - AntiAchR ; bind to post synaptic receptor + inhibit competitively Act binding. More binding with exertion therefore worse Sx later on

15% AntiMusk; Musk helps synthesise Ach-R therefore anti-musk asks against Musk and therefore there is a low Ach-R expression on post synaptic membrane

222
Q

What is the presentation of MG?

A

-Muscle weakness; worse later on with exertion
-Starts at head and neck–> lower body
-Better with rest
Weak eye muscles = diplopia
Ptosis
Myasthenic snarl
Jaw fatiguability
Swallowing difficulty
Speech fatiguability

223
Q

What is the diagnosis of MG?

A

Serology- Anti AchR +AntiMusk raised
-Tensilon/edrotropium test - administer edrotropium (rapid acting Acetylcholinesterase inhibitor) - positive if results in muscle power in few seconds

224
Q

What is the treatment of MG?

A

1st line - Achase inhibitor ; neostigmine
2nd line - Immunosuppression - steroids

225
Q

What is a complication of MG?

A

Myasthenic crisis- Acute Sx worsening with severe resp weakness

226
Q

What is the treatment for myasthenia crisis?

A

Plasma exchange + IVIg +BiPaP for respiratory failure

227
Q

What is a Ddx of MG?

A

Lambert eaton syndrome

228
Q

What is Lambert eaton syndrome?

A

Paraneoplastic (SCLC) or autoimmune antibodies against pre synaptic Ca++ channels

229
Q

What is the presentation of LES?

A

Sx improve with exertion
Sx( weakness of muscles )start at extremities then move to head and neck + there is autonomic involvement - dry eyes/ mouth

230
Q

What is the treatment of LES?

A

Steroids - prednisolone
+ immunosuppression - IV Ig

231
Q

What is Guillain Barre syndrome?

A

An acute inflammatory demyelinating polyneuropathy affecting the PNS (targets Schwann cells) following an upper respiratory or GIT infection

232
Q

What is the epidemiology of GBS?

A

males 15-30, 50-70 - mc
Acute polyneuropathy - 85% recover - good prognosis

233
Q

What are the causes of GBS?

A

Camylobacter Jejuni -mc + viruses ;CMV,EBV,HZV

234
Q

What is the pathology of GBS?

A

Molecular mimicry - organism antigens are similar to those on the schwann cells
- results in antibody production against schwann cells= leading to demyelination and acute polyneuropathy

235
Q

What is the presentation of GBS?

A

Post infection presents with :
- ascending symmetrical muscle weakness + paralysis
-Loss of deep tendon reflexes
- autonomic involvement - 50%
-Resp failure - 35%

236
Q

What is the diagnosis of GBS?

A

Nerve conduction studies (low conduction)
- Lumbar puncture at L3/4 = raised protein + normal WCC = inflammation and no infection

237
Q

What is the treatment of GBS?

A

IVIg for 5 days + plasma exchange
(CI in IgA deficient patients - allergic reaction)
- also if FVC<0.8 consider ITU

238
Q

What is Wernicke’s encephalopathy?

A

Reversible acute emrgency; severe B1(thiamine) deficiency

239
Q

What is the cause of wernickes encephalopathy?

A

mostly alcohol

240
Q

What is the presentation of WE?

A

Ataxia, confusion, ophthalmoplegia

241
Q

What is the diagnosis of WE?

A

Clinically recognised , supported with macrocytic anemia + deranged LFTs

242
Q

What is the treatment of WE?

A

Pabrinex (Vit B1) for 5 days acutely
Oral thiamine prophylactically

243
Q

What is the complication of WE?

A

Korsakoff syndrome

244
Q

What is korsakoff syndrome?

A

When wernickes is left too long without TX; severe thiamine deficiency
Same Sx with increased memory loss
- irreversible damage

245
Q

What is Duchenne muscular dystrophy?

A

X linked autosomal recessive disorder due to a mutation of the dystrophin gene leading to progressive muscle degeneration and weakness
Muscle replaced with adipose

246
Q

What is the role of dystrophin?

A

protein that helps keep muscles intact

247
Q

What sex is more affected by DMD?

A

males

248
Q

What is the presentation of DMD?

A

Difficulty getting up from lying down - Gower’s sign
Skeletal deformities- scoliosis

249
Q

What is the diagnosis of DMD?

A

Prenatal tests+ DNA genetic test

250
Q

What is the treatment for DMD?

A

purely supportive

251
Q

What is Charcot Mary tooth ?

A

Autosomal dominant condition affecting the PMP22 gene on chromosome 17 causing sensory and motor PNS polyneuropathy

252
Q

What is the presentation of CMT?

A

foot drop - common perineal palsy
Stork legs
Hammer toes
Feet - pes planus - flat feet
-pes cavus - high arched feet

253
Q

What is the diagnosis of CMT?

A

Nerve biopsy, genetic testing

254
Q

What is the treatment of CMT?

A

supportive - physio

255
Q

What is Tetanus?

A

Inoculation through skin with clostridium tetani (gram positive bacillus)

256
Q

What is the pathology of tetanus?

A

tetanospasmin toxin produced - travels along axon and causes involuntary muscle spasms

257
Q

What is the treatment for tetanus?

A

Vaccine

258
Q

What is Herpes Zoster (chicken pox/ shingles)?

A

Varicella zoster virus :90% under 16 have this –> reactivation = shingles
- peripheral nerves attacked via dorsal root (sensory)
Painful rash - confined to a dermatome

259
Q

What is the treatment for Herpes zoster ?

A

Oral aciclovir - anti-viral

260
Q

What is Prion (creutzfield - Jakub disease)?

A

Idiopathic misfolder protein deposited in cerebrum + especially cerebellum
- severe cerebellum dysfunction - sponge like appearance - ataxia, poor memory, behaviour changes
- no Tx

261
Q

What is epilepsy ?

A

Idiopathic recurrent tendency of spontaneous , intermittent abnormal electrical activity in parts of the brain manifesting in seizures. 2< episodes more than 24hr apart

262
Q

What are the components of an epileptic seizure?

A

Prodrome - mood change days/hours before

Aura- minutes before= deja vu, strange feelings , strange smells, lip smacking (not always seen - mostly seen in temporal lobe epilepsy)

Ictal event = seizure

Post octal period

263
Q

What is the presentation of a post ictal period?

A
  • headache
    -confusion
    -Todd’s paralysis - if motor cortex affected , may have temporary paralysis + muscle weakness
    -dyspahsia
    -amnesia
    -sore tongue
264
Q

What are the types of seizures?

A

Generalised
Focal

265
Q

What is a generalised seizure?

A

Electrical charge throughout whole cortex
Bilateral
always associate with loss of consciousness + awareness

266
Q

What are the types of generalised seizures?

A

Tonic-rigidity
Tonic clonic- rigidity + jerking of limbs
clonic - muscle jerking
Atonic- floppy muscles
Absence -childhood - pale +stare blankly for seconds then carryon
Myoclonic - isolated jerk of a limb

267
Q

What are focal seizure?

A

Focal onset that can be referred to a single lobe may progress to generalised

268
Q

What are the types of focal seizures?

A

simple focal
Complex focal

269
Q

What is a simple focal seizure?

A
  • no affect on conscious
    -patient awake + aware
270
Q

What is a complex focal seizure?

A
  • loss of consciousness , patient unaware , post octal period positive
271
Q

What is the presentation of a temporal lobe specific seizure?

A

Aura, dysphasia , post ictal period

272
Q

What is the presentation of. frontal lobe specific seizure ?

A

Jacksonian March (seizures march up and down motor hornuculus + Todd’s palsy

273
Q

What is the presentation of a parietal lobe specific seizure?

A

paraesthesia - tingling/numbness

274
Q

What is the presentation of an occipital lobe specific seizure?

A

Vision change - spots, lines

275
Q

What is the difference between an epileptic seizure and a non epileptic seizure?

A

Epilepsy - eyes open , can occur at night, situational (what they were doing)

Non- eyes closed, can’t happen at night, can be related to syncope , metabolic disturbances

276
Q

What is syncope?

A

A loss of consciousness for a short period of time due to an insufficient blood supply/02 to brain

277
Q

What is the presentation of syncope?

A

dizzy, light head, from sitting or standing, hypoglycaemia , anemia

278
Q

What investigations would be done for syncope?

A
  • bloods
    -ECG
    -Echocardiogram
279
Q

What is the diagnosis for epilepsy?

A
  • Must have had >2 seizures 24hr part to consider epilepsy

-CT head +MRI (check bleeds, tumours)
Electroencephalogram
-Bloods- rule out metabolic cause

280
Q

What is the treatment for Epilepsy?

A

Sodium valproate Except for women at child bearing age = Lamotrigine

Except Myoclonic = levetiracetom

Absence = ethosuximide

Focal = carbamazepine

281
Q

What are the side effects of carbamazepine?

A

reduce risk of contraception
leukopenia
thrombocytopenia

If pregnant keep using - risk of epileptic damage worse risk than risk of foetus

282
Q

What is a complication of Epilepsy?

A

Status epilepticus

283
Q

What is status epilepticus?

A

epileptic seizures back to back without a break
or seizure lasting over >5mins

284
Q

What is the treatment for a status epilepticus?

A

Benzodiazepines ; Lorazepam IV

285
Q

What is Encephalitis?

A

Viral infection of brain parenchyma

286
Q

What is the epidemiology of Encephalitis?

A

95% cases ; HSV-1 (herpes simplex virus) others CMV,EBV,HIV

287
Q

What are the risk factors of encephalitis?

A

Immunocompromised
Extremes of age

288
Q

What is the presentation of encephalitis?

A

Fever, headache, encephalopathy, Focal neurology - mc place affected is temporal lobe

289
Q

What are the investigations for Encephalitis?

A

CSF- raised lymphocytes, consider PCR
MRI head - unilateral usually temporal encephalitis - midline shift

290
Q

What is the treatment of encephalitis?

A

Aciclovir

291
Q

What is Meningitis?

A

Inflammation of the meninges
Notifiable to PHE

292
Q

What are the main bacterial causes of meningitis?

A

S.pneumonia
N.menningitis
Group B or haem strep - in neonates
Listeria - mc in elderly

293
Q

What are the main viral causes in meningitis?

A

Viral causes -mc - less severe
Entervoiruses
Herpes simplex virus
VZV

294
Q

What are the risk factors of meningitis?

A

-Extremities of age
-Immunocompromised
-Students
-non vaccination

295
Q

What is Neisseria Meningitis?

A
  • gram negative diplococcus
    -vaccines available ; menB+C, men ACWY
    -10% mortality
    -Non blanching purpuric rash
296
Q

What is Streptococcus pneumonia ?

A

-Gram positive diplococcus in chains
-PCV vaccine
-25% mortality

297
Q

What is group B strep?

A
  • gram postive coccus in chains
  • mc cause of neonatal meningitis
  • colonises maternal vagina
298
Q

What is listeria monocytogenes?

A

-Gram positive bacillus
-affects extreme os age , and maternal ladies
-found in cheese

299
Q

What is the presentation of Meningitis?

A

Meningism; Headache , neck stiffness, photophobia
Signs : Kernig (cant extend knee when hip is flexed)
Brudzinski (when neck flexed, knees + hips automatically flex)
Pyrexia

300
Q

What is the diagnosis of Meningitis?

A

LP+CSF analysis from L3/4
CI in raises ICP due to tectorial herniation and coning risk

301
Q

What is a bacterial result of an LP?

A
  1. High opening pressure
  2. Cloudy yellow
    3.Raised neutrophilic
  3. Raised protein
  4. Low plasma glucose
302
Q

What is a viral results of an LP?

A
  1. normal pressure
  2. normal/clear colour
  3. raised lymphocytes
  4. normal protein
  5. Normla serum glucose
303
Q

What is a fungal / TB result of an LP?

A
  1. raised opening pressure
    2.Cloudy colour
    3.Raised lymphocytes
    4.Raised protein
    5.Normal serum glucose
304
Q

What is the treatment of bacterial meningitis?

A

Ceftriaxone/ cefotaxime + steroids -Dexamethasone
- amoxicillin covers listeria

305
Q

What is the treatment for viral meningitis?

A

Nothing if enteroviruses
Aciclovir if HSV,VZV

306
Q

What is the prophylaxis treatment for Meningitis?

A

contact tracing - ciprofloxacin one of dose

307
Q

What is a complication of meningitis?

A

DIC (meningococcal septicaemia)
Waterhouse friderichsen syndrome - adrenal insufficiency caused by intradrenal haemorrhage as a result of meningococcal DIC -disseminated intravascular coagulation)

308
Q

What is the treatment for depression?

A

Selective serotonin reuptake inhibitors - fluoxetine
- prevent the presynaptic neurone from reabsorbing the serotonin so more remains in the synaptic cleft and can stimulate receptors on post synaptic neurone
TCA- Tricyclic Antidepressants - amitriptyline

309
Q

What are the baby checks given ?

A

1- Within first 72hr + heel prick test- check sickle cell/CF/congenital hypothyroid

2 -6+8 weeks later (check arms , eyes, heart, hips

310
Q

What vaccines are given at 8 weeks?

A

5 in 1 IM injection against
-diptheria
tetanus
whooping cough
H.inluenza
poliovirus

Phase 2a (9 decks)

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