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Phase 2a Medicine - Riona COPY > Neurology > Flashcards

Neurology Flashcards

1
Q

Where is the motor cortex?

A

Pre-central gyrus

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2
Q

Where is the sensory cortex?

A

Post-central gyrus

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3
Q

What are the stretch receptors in muscles called?

A

Muscle spindles

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4
Q

What are muscle spindles innervated by?

A

Gamma motor neurones

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5
Q

What is the middle layer of the cerebellum?

A

Purkinje cell layer

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6
Q

What is the only output element of the cerebellum?

A

Purkinje cell

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7
Q

What are the 4 main fibres?

A
  • ) A alpha
  • ) A beta
  • ) A gamma
  • ) C fibres
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8
Q

Give 3 facts about A alpha fibre

A
  • ) Large
  • ) Myelinated
  • ) Proprioception
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9
Q

Give 3 facts about A beta fibre

A
  • ) Large
  • ) Myelinated
  • ) Light touch, pressure, vibration
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10
Q

Give 3 facts about A gamma fibre

A
  • ) Thin, small
  • ) Myelinated
  • ) Pain, cold sensation
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11
Q

Give 3 facts about C fibres

A
  • ) Thin, small
  • ) Unmyelinated
  • ) Pain, warm sensation
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12
Q

What does a stroke in the R hemisphere present as?

A

Mania

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13
Q

What does a lesion in the orbitofrontal cortex cause?

A

Disinhibited behaviour

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14
Q

What does the cavernous sinus contain?

A 
O TOM CAT
Oculomotor
Trochlear
Ophthalmic branch
Maxillary branch
Carotid artery, internal
Abducens
Trochlear (again)
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15
Q

Define weakness/paresis

A

The impaired ability to move a body part in response to will

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16
Q

Define paralysis

A

The ability to move a body part in response to will is completely lost

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17
Q

Define ataxia/incoordination

A

Willed movements are clumsy, ill-directioned or uncontrolled

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18
Q

Define involuntary movements

A

Spontaneous movement of a body part independently of will

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19
Q

Define apraxia

A

Disorder of consciously organised patterns of movement/impaired ability to recall acquired motor skills

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20
Q

Define a motor unit

A

Basic functional unit of muscle activity

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21
Q

What 3 things make up a motor unit?

A
  • ) LMN
  • ) Axon
  • ) Several supplied muscle fibres
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22
Q

What is the final common pathway?

A

The way by the CNS controls voluntary movement

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23
Q

Give 4 things we need to know in a headache history

A
  • ) Types/number
  • ) Time
  • ) Pain
  • ) Associations
  • ) Triggers
  • ) Response
  • ) Between attacks
  • ) Changes in attacks
  • ) Red flags for brain tumours
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24
Q

What is the most common type of headache?

A

Tension

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25
Q

Give 2 symptoms of a tension headache

A
  • ) Bilateral
  • ) Non-pulsatile
  • ) Scalp muscle tenderness
  • ) No N&V
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26
Q

How do we treat a tension headache (other than painkillers)?

A
  • ) Massage

- ) Antidepressants

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27
Q

Who are cluster headaches more common in?

A
  • ) Smokers

- ) Men

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28
Q

Give 3 symptoms of a cluster headache

A
  • ) Rapid onset excruciating pain around one eye that may become watery ad bloodshot with lid swelling
  • ) Lacrimation
  • ) Facial flushing
  • ) Rhinorrhoea
  • ) Miosis +/- ptosis
  • ) Unilateral pain, almost always same side
  • ) 15-180 mins
  • ) 1/2 a day, often nocturnal
  • ) Pain free periods of months/years
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29
Q

How do we treat an acute cluster headache?

A
  • ) 100% O2

- ) Sumatriptan

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30
Q

Who should we not give O2 in a cluster headache?

A

COPD

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31
Q

Give 2 preventative treatments of cluster headaches

A
  • ) Avoid alcohol
  • ) Corticosteroids short term
  • ) Verapamil
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32
Q

What is the classic presentation of a migraine?

A

Visual or other aura lasting 15-30 mins followed within 1hr by unilateral, throbbing headache

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33
Q

Give the 2 other presentations of a migraine

A
  • ) Isolated aura with no headache
  • ) Episodic severe headaches without aura, often premenstrual, usually unilateral with N&V +/- photophobia/phonophobia
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34
Q

What is a prodrome? Give an example

A

Precedes headache by hours/days

  • ) Yawning
  • ) Cravings
  • ) Mood/sleep change
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35
Q

What are 3 types of aura?

A
  • ) Visual - chaotic distorting, jumbling, dots, zigzags, lines
  • ) Somatosensory - paraesthesiae spreading from fingers to face
  • ) Motor - dysarthria and ataxia, ophthalmoplegia, hemiparesis
  • ) Speech - dysphasia, paraphasia
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36
Q

Give 5 partial triggers for a migraine

A

CHOCOLATE

  • ) Chocolate
  • ) Hangovers
  • ) Orgasms
  • ) Cheese/caffeine
  • ) Oral contraceptives
  • ) Lie-ins
  • ) Alcohol
  • ) Travel
  • ) Exercise
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37
Q

Give an association of a migraine

A
  • ) Obesity

- ) Fhx

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38
Q

What are the diagnostic criteria of a migraine if there is no aura? (5)

A
  • ) 5 or more attacks
  • ) Lasting 4-72 hours
  • ) N&V
  • ) Or P/P
  • ) Any 2 of unilateral, pulsating, impairs/aggravated by routine activity
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39
Q

Give 2 preventative treatments for migraines

A
  • ) Avoid triggers
  • ) Ensure analgesic rebound headache not there
  • ) Propranolol or topiramate
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40
Q

What is the treatment for an acute migraine attack?

A
  • ) Oral triptan and NSAID/paracetamol

- ) Anti-emetics even without N&V

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41
Q

Give 2 CIs for triptan use

A
  • ) IHD
  • ) Coronary spasm
  • ) Uncontrolled HTN
  • ) Recent lithium
  • ) SSRIs
  • ) Ergot use
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42
Q

Give 2 non-pharmacological treatments for migraines

A
  • ) Hot/cold packs
  • ) Rebreathing into bag
  • ) Acupuncture
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43
Q

Give 3 symptoms for trigeminal neuralgia

A
  • ) Paroxysms of intense stabbing pain
  • ) Lasts seconds
  • ) In trigeminal nerve distribution
  • ) Unilateral
  • ) Mandibular or maxillary typically
  • ) Face screws up with pain
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44
Q

Give 2 triggers for trigeminal neuralgia

A
  • ) Washing area
  • ) Shaving
  • ) Eating
  • ) Talking
  • ) Dental prostheses
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45
Q

Who is the typical patient with trigeminal neuralgia?

A

> 50 male

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46
Q

Give 2 secondary causes of trigeminal neuralgia

A
  • ) Compression of trigemini root (inflammation, tumour)
  • ) MS
  • ) Zoster
  • ) Skull base malformation
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47
Q

What is the treatment for trigeminal neuralgia?

A
  • ) Carbamazepine
  • ) Lamotrigine
  • ) Phenytoin
  • ) Gabapentin
  • ) Microvascular decompression
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48
Q

What part of the brain does the middle cerebral artery supply?

A

Lateral

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49
Q

What part of the brain does the anterior cerebral artery supply?

A

Anterior and medial

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50
Q

What part of the brain does the posterior cerebral artery supply?

A

Posterior

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51
Q

Give 3 symptoms of a MCA stroke

A
  • ) Contralateral arm and leg weakness
  • ) Contralateral sensory loss
  • ) Hemianopia
  • ) Aphasia
  • ) Dysphasia
  • ) Facial droop
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52
Q

Give 3 symptoms of a PCA stroke

A
  • ) Contralateral homonymous hemianopia
  • ) Cortical blindness with bilateral involvement of occipital lobe branches
  • ) Visual agnosia
  • ) Prospagnosia
  • ) Dyslexia, anomic aphasia, colour naming and discrimination problems
  • ) Unilateral headaches
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53
Q

Give 3 symptoms of a posterior circulation stroke

A
  • ) Motor deficits
  • ) Dysathria and speech impairment
  • ) Vertigo, N&V
  • ) Visual disturbances
  • ) Altered consciousness
  • ) High mortality, locked in syndrome
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54
Q

What can a posterior circulation stroke cause?

A

Hydrocephalus through blockage of 4th ventricle

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55
Q

What is a stroke?

A

Infarction or bleeding into the brain, manifesting with sudden onset focal CNS signs

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56
Q

Give 3 causes of a stroke

A

-) Small vessel occlusion/cerebral microangiopathy/thrombosis
-) Atherothromboembolism (carotids)
-) CNS bleeds (aneurysm, trauma, anticoagulation)
-) Cardiac emboli
-) Sudden BP drop
-) Carotid artery dissection
-) Vasculitis
-) SAH
ETC

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57
Q

Give 3 risk factors for a stroke

A
  • ) HTN
  • ) Smoking
  • ) DM
  • ) Heart disease
  • ) Peripheral vascular disease
  • ) High PCV
  • ) Carotid bruit
  • ) Combined pill
  • ) Hyperlipidaemia
  • ) Alcohol
  • ) Increased clotting
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58
Q

What does PCV stand for?

A

Packed cell volume

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59
Q

What is embolic stroke?

A

Death of cell bodies, well defined territory, no recovery

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60
Q

What is a haemorrhagic stroke?

A

Compression of the internal capture, large territory, possible complete recovery

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61
Q

Give 2 pointers to bleeding

A
  • ) Meningism
  • ) Severe headache
  • ) Coma
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62
Q

Give 2 pointers to ischaemia

A
  • ) Carotid bruit
  • ) AF
  • ) Past TIA
  • ) IHD
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63
Q

Give 2 signs of a cerebral infarct

A
  • ) Depends on site
  • ) Contralateral sensory loss or hemiplegia
  • ) Initially flaccid, becoming spastic
  • ) Dysphasia
  • ) Homonymous hemianopia
  • ) Visuo-spatial deficit
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64
Q

Give 2 signs of a brainstem infarct

A

-) Quadriplegia
-) Disturbances of gaze and vision
-) Locked in syndrome
Very varied

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65
Q

Give 2 signs of a lacunar infarct

A
  • ) Ataxic hemiparesis
  • ) Pure motor
  • ) Pure sensory
  • ) Sensorimotor
  • ) Dysarthria/clumsy hand
  • ) Cognition/consiousness not in thalamic stroke
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66
Q

Where does a lacunar infarct occur? (4)

A
  • ) Basal ganglia
  • ) Internal capsule
  • ) Thalamus
  • ) Pons
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67
Q

What do we use to estimate the risk of stroke in AF patients?

A

CHA2DS2-VASc

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68
Q

Give the parts of CHA2DS2-VASc (8)

A
  • ) Congestive heart failure
  • ) HTN
  • ) Age >75 (2 points)
  • ) DM
  • ) Stroke prior, TIA (2 points)
  • ) Vascular disease
  • ) Age 65-74
  • ) Female
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69
Q

Give 3 tests we do for a stroke

A
  • ) HTN
  • ) ECG - AF
  • ) Echo
  • ) Carotid doppler US - for stenosis
  • ) MRI/CT
  • ) Vasculitis tests - ESR, ANA+
  • ) Prothrombin states, hyper viscosity, bleeding disorders
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70
Q

Give 3 treatment steps for stroke

A
  • ) Protect airway
  • ) Maintain homeostasis
  • ) Screen swallow
  • ) CT/MRI if thrombolysis/haemorrhage considered, unusual presentation
  • ) Antiplatelet agents (not haemorrhagic stroke), aspirin, clopidiogrel long term
  • ) Thrombolysis (not haemorrhage)
  • ) Thromboectomy
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71
Q

What is the agent for thromboylsis, and when must it be done?

A

Within 4.5 hours, alteplase

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72
Q

Give 2 ways to prevent a stroke

A
  • ) Stop smoking
  • ) Control BP
  • ) Move around/exercise
  • ) DM
  • ) Hyperlipidaemia
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73
Q

How do we treat hyperlipidaemia?

A

Statins

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74
Q

Who do we give anticoagulants to?

A

AF and prosthetic heart valves

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75
Q

How do we detect hypertension? (3)

A
  • ) Retinopathy
  • ) Nephropathy
  • ) Cardiomegaly on CXR
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76
Q

What is a transient ischaemic attack?

A

An ischaemic (usually embolic) neurological event with symptoms lasting <24hours

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77
Q

What is the major risk factor with a TIA?

A

STROKE

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78
Q

What symptom occurs when the retinal artery is occlude?

A

Amaurosis fungax

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79
Q

Are global events (syncope, dizziness) typical of TIAs?

A

No

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80
Q

What suggests a critical intracranial stenosis?

A

Multiple highly stereotyped/crescendo TIAs

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81
Q

Give 3 cause of a TIA

A
  • ) Atherothromboembolism from carotid
  • ) Cardioembolism
  • ) Hyperviscosity
  • ) Vasculitis
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82
Q

Give 3 tests we do in a TIA

A
  • ) FBC, ESR, U&ES, glucose, lipids
  • ) CXR
  • ) ECG
  • ) Carotid doppler +/- angiography
  • ) CT/diffusion weighted MRI
  • ) Echocardiogram
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83
Q

What is amaurosis fungax?

A

Unilateral progressive vision loss ‘like a curtain descending’

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84
Q

Give 3 parts of the treatment of a TIA

A
  • ) Control CV risk factors
  • ) Antiplatelet drugs (aspirin, then clopidogrel)
  • ) Anticoagulation indications (if cardiac source of emboli)
  • ) Carotid endarterectomy is >70% stenosis
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85
Q

What is the ABCD2 risk score?

A

Risk of stroke following a suspected TIA

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86
Q

What makes up the ABCD2 score?

A
  • ) Age >60
  • ) BP high
  • ) Clinical features (unilateral weakness 2, speech 1)
  • ) Dyration of symptoms (>1hr 2, <1hr 1)
  • ) DM
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87
Q

Give 2 secondary causes of damage in a head injury

A
  • ) Hypoxia

- ) Infection

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88
Q

What is an injury under the site of impact called? (head injury)

A

Coup

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89
Q

What is an injury opposite the site of impact called? (head injury)

A

Contrecoup

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90
Q

What builds up in axonal injury?

A

Amyloid precursor protein

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91
Q

Give 3 causes of brain swelling

A
  • ) Congestive brain swelling
  • ) Vasogenic oedema
  • ) Cytotoxic oedema
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92
Q

What is congestive brain swelling?

A

Vasodilation and increased cerebral blood volume

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93
Q

What is vasogenic oedema?

A

Extravasation of oedema fluid from damaged blood vessels

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94
Q

What is cytotoxic oedema

A

Increased water content of neurones and glia

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95
Q

Why does herniation occur?

A

Parts of the brain are squashed from one compartment to another

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96
Q

Give a long term effect of head injury

A

Chronic traumatic encephalopathy

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97
Q

Give 4 criteria for brainstem death

A
  • ) Pupils
  • ) Corneal reflex
  • ) Caloric vestibular reflex
  • ) Gag reflex
  • ) Respirations
  • ) Response to pain
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98
Q

What is a subarachnoid haemorrhage?

A

Spontaneous bleeding into the subarachnoid space, often catastrophic

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99
Q

What is the typical age of presentation of a SAH?

A

35-65

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100
Q

Give 3 symptoms of a SAH

A
  • ) Sudden onset excruciating headache (thunderclap)
  • ) Vomiting
  • ) Collapse
  • ) Seizures
  • ) Coma
  • ) Possible preceding sentinel headache
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101
Q

Give 3 signs of a SAH

A
  • ) Neck stiffness
  • ) Kernig’s sign (leg extension)
  • ) Retinal, subhyaloidand vitreous bleeds
  • ) Focal neurology at presentation may suggest site of aneurysm
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102
Q

Give 2 causes of a SAH

A
  • ) Berry aneurysm rupture
  • ) Arteriovenous malformations
  • ) Encephalitis, vasculitis, tumour, idiopathic
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103
Q

Give 3 risk factors for a SAH

A
  • ) Previous aneyrysmal SAH
  • ) Smoking
  • ) Alcohol misuse
  • ) High BP
  • ) Bleeding disorders
  • ) SBE
  • ) Family history
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104
Q

Give 2 associations with berry aneurysms

A
  • ) Polycystic kidneys
  • ) Aortic coarctation
  • ) Ehlers-Danlos
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105
Q

Give 2 places a berry aneurysm can occur

A
  • ) Posterior communicating with internal carotid
  • ) Anterior communicating with anterior cerebral artery
  • ) Bifurcation of middle cerebral artery
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106
Q

Give 2 tests for a SAH

A
  • ) Urgent CT

- ) Consider LP >12hr after headache (yellow due to Hb breakdown)

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107
Q

What is the treatment for a SAH?

A
  • ) Fluids and maintaining cerebral perfusion
  • ) Nimodipine
  • ) Endovascular coiling or surgical clipping
  • ) Catheter or CT angiography before intervention
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108
Q

What is nimodipine?

A

Calcium antagonist that reduces vasospasm and consequent morbidity from cerebral ischaemia

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109
Q

Give 3 complications of a SAH

A
  • ) Rebleeding
  • ) Cerebral ischaemia
  • ) Hydrocephalus
  • ) Hyponatraemia
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110
Q

Where does the bleeding occur in a subdural haematoma?

A

Bridging veins between cortex and venous sinuses (vulnerable to deceleration injury)

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111
Q

Define haemorrhage

A

The leakage of blood from a blood vessel due to lack of integrity in the vessel wall or clotting mechanism

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112
Q

Define haematoma

A

The accumulation of leaked blood inside the body within tissue planes.

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113
Q

What does a subdural haematoma cause?

A

1) Gradual rise in ICP
2) Shift in midline structures away from side of clot
3) Eventual tentorial herniation and coning

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114
Q

What do more subdural haematomas occur from?

A

Trauma (often minor and forgotton)

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115
Q

Give 2 risk factors for a subdural haematoma

A
  • ) Elderly (atrophy makes bridging veins more vulnerable)
  • ) Falls (epilepsy, alcoholics)
  • ) Anticoagulation
  • ) Shaken babies?
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116
Q

Give 3 symptoms of a subdural haematoma

A 
-) Fluctuating level of consciousness
\+/-
-) Insidious physical/intellectual slowing
-) Sleepiness
-) Headache
-) Personality change
-) Unsteadiness
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117
Q

Give 3 signs of a subdural haematoma

A
  • ) Increased ICP
  • ) Seizures
  • ) Localising neurological symptoms occur late
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118
Q

Give 2 differential diagnoses of a subdural haematoma

A

Stroke, dementia, CNS masses

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119
Q

What does a CT/MRI show in a subdural haematoma?

A

Clot +/- midline shift, crescent shaped collection of blood over 1 hemisphere

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120
Q

What does the sickle shape differentiate a subdural haematoma from on a CT/MRI?

A

Subdural blood from extradural haemorrhage

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121
Q

What is the treatment of a subdural haematoma?

A
  • ) Reverse clotting abnormalities

- ) Craniotomy/burr hole washout on >10mm or with midline shift >5mm

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122
Q

What is an extradural haematoma also known as?

A

Epidural haematoma

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123
Q

What pattern is typical of extradural bleeds?

A

Lucid interval - deteriorating consciousness after any head injury that initially produced no loss of consciousness/drowsiness

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124
Q

What causes an extradural haematoma?

A
  • ) Fractured temporal/parietal bone causing laceration of middle meningeal artery after trauma to temple just lateral to eye
  • ) Any tear in a dural venous sinus
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125
Q

Give 3 clinical features of an extradural haematoma (initially)

A
  • ) Lucid interval
  • ) Decreasing GCS
  • ) Increasingly severe headache
  • ) Vomiting
  • ) Confusion
  • ) Seizures
  • ) +/- hemiparesis with brisk reflexes and an upping plantar
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126
Q

Give 3 clinical features of an extradural haematoma (if bleeding continues)

A
  • ) Ipsilateral pupil dilates
  • ) Coma deepens
  • ) Bilateral limb weakness develps
  • ) Deep and irregular breathing
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127
Q

What is death due to in an extradural haematoma?

A

Respiratory arrest

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128
Q

Give 2 differential diagnoses for an extradural haematoma

A
  • ) Epilepsy
  • ) Carotid dissection
  • ) CO poisoning
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129
Q

What does a CT show in an extradural haematoma?

A

Biconvex/lens shaped haematoma as tough dural attachments keep it localised

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130
Q

What test is CI in an extradural haematoma?

A

LP

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131
Q

What may an XR show in an extradural haematoma?

A

Fracture lines crossing the course of the middle meningeal vessels

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132
Q

What is the management of an extradural haematoma?

A

Clot evaluation +/- ligation of the bleeding vessel

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133
Q

What is epilepsy?

A

The recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures

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134
Q

What are convulsions?

A

The motor signs of electrical discharges

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135
Q

What are the elements of a seizure? (3)

A
  • ) Prodrome
  • ) Aura
  • ) Post-ictal
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136
Q

What is a prodrome?

A

Change in mood or behaviour hours or days before

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137
Q

What is an aura?

A
  • ) Implies a focal seizures often from the temporal lobe

- ) Strange feeling in gut, deja vu, strange smells, flashing lights

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138
Q

What occurs post-ically?

A
  • ) Headache, confusion, myalgia
  • ) Temporary weakness after a focal seizure in the motor cortex
  • ) Dysphasia following a focal seizure in the temporal lobe
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139
Q

Give 3 structural causes of epilepsy

A
  • ) Cortical scarring
  • ) Developmental
  • ) Space-occupying lesion
  • ) Stroke
  • ) Hippocampal sclerosis
  • ) Vascular malformations
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140
Q

Give 2 non-structural causes of epilepsy

A
  • ) Tuberous sclerosis
  • ) Sarcoidosis
  • ) SLE
  • ) PAN
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141
Q

What are the 2 main classifications of seizures?

A
  • ) Focal

- ) Generalised

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142
Q

What is a focal seizure?

A

Originating within networks linked to one hemisphere and often seen without underlying structural disease

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143
Q

What is a generalised seizure?

A

Simultaneous onset of widespread electrical discharge throughout bilaterally distributed networks with no localising features

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144
Q

Give 3 subtypes of a focal seizure

A
  • ) Without impairment of consciousness (simple)
  • ) With impairment of consciousness (complex)
  • ) Evolving to a bilateral, convulsive seizure (secondary generalised)
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145
Q

Give 4 subtypes of a generalised seizure

A
  • ) Absence
  • ) Tonic-clonic
  • ) Myoclonic
  • ) Atonic (akinetic)
  • ) Infantile spasms
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146
Q

Describe tonic-clonic

A

Tonic - limbs stiffen

Clonic - limbs jerk

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147
Q

Give 3 localising features of a temporal lobe focal seizure

A
  • ) Automatisms (lip smaking, fumbling, fiddling, complex actions)
  • ) Dysphasia
  • ) Deja vu
  • ) Emotional disturbance (sudden terror, panic, anger, elation, derealisation)
  • ) Hallucinations (smell, taste, sound)
  • ) Delusional behaviour
  • ) Bizarre associations
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148
Q

Give 3 localising features of a frontal lobe focal seizure

A
  • ) Motor features (posturing/peddling legs)
  • ) Jacksonian march
  • ) Motor arrest
  • ) Subtle behavioural disturbances
  • ) Dysphasia/speech arrest
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149
Q

Give 2 localising features of a parietal lobe focal seizure

A
  • ) Sensory disturbances (tingling, numbness, pain)

- ) Motor symptoms

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150
Q

Give a localising feature of an occipital lobe focal seizure

A

Visual phenomena (spots, lines, flashes)

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151
Q

What is a Jacksonian march? (seizures)

A

Spreading focal motor seizure with retained awareness, often starting with face/thumb

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152
Q

When should we suspect non-epileptic attack disorder? (pseudo seizures)

A
  • ) Gradual onset
  • ) Prolonged duration
  • ) Abrupt termination
  • ) Closed eyes +/- resistance to eye opening
  • ) Rapid breathing
  • ) Fluctuating motor activity
  • ) Episodes of motionless unresponsiveness
  • ) Tests normal
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153
Q

Give 3 provoking causes for seizures

A
  • ) Trauma
  • ) Stroke
  • ) Haemorrhage
  • ) Increased ICP
  • ) Alcohol/benzodiazepine withdrawal
  • ) Metabolic disturbance
  • ) Infection
  • ) High temp
  • ) Drugs
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154
Q

Give 2 tests for epilepsy

A
  • ) EEG
  • ) MRI
  • ) Drugs screen, LP
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155
Q

What type of seizure is it if it begins with focal features and then generalises?

A

Focal

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156
Q

Give 2 triggers for a seizure

A
  • ) Alcohol
  • ) Stress
  • ) Fevers
  • ) Sounds
  • ) Lights
  • ) Reading
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157
Q

What are the non-pharmacological treatment options for epilepsy?

A
  • ) Relaxation, CBT
  • ) Surgical resection
  • ) Vagal nerve/deep brain stimulation
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158
Q

When should we start someone on anti-epileptic drugs?

A

After 2 or more seizures/high risk of recurrence

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159
Q

What do we give for focal seizures? (1st/2nd line)

A

1) Carbamazepine or lamotrigine

2) Levetiracetam, oxcarbazepine, or sodium valproate

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160
Q

What do we give for generalised tonic-clonic seizures? (1st/2nd line)

A

1) Sodium valproate or lamotrigine

2) Carbamazepine, clobazam, levetiracetam or topiramate

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161
Q

What do we give for absence seizures? (1st/2nd line)

A

1) Sodium valproate or ethosuximide

2) Lamotrigine

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162
Q

What do we give for myoclonic seizures? (1st/2nd line)

A

1) Sodium valproate
2) Levetiracetam or topiramate
- ) Avoid carbamazepine and oxcarbazepine

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163
Q

What do we give for tonic or atonic seizures?

A

Sodium valproate or lamotrigine

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164
Q

What is dementia?

A

A neurodegenerative syndrome with progressive declines several cognitive domains

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165
Q

What is the usual initial presentation of dementia?

A

Memory loss over months/years

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166
Q

How do we diagnose dementia?

A
  • ) History
  • ) Cognitive testing (AMTS)
  • ) Examination for physical cause
  • ) Medication review
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167
Q

What tests do we do in dementia?

A
  • ) Bloods for reversible/organic causes
  • ) MRI can identify reversible pathologies or underlying vascular damage
  • ) PET functional imaging
  • ) EEG
  • ) HIV, syphilis, autoantibodies
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168
Q

Give 3 subtypes of dementia

A
  • ) Alzheimer’s disease
  • ) Vascular dementia
  • ) Lewy body dementia
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169
Q

What is vascular dementia?

A

The cumulative effect of many small strokes

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170
Q

How does vascular dementia present?

A

Sudden onset and stepwise deterioration

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171
Q

What do we look for in diagnosing vascular dementia?

A
  • ) High BP
  • ) Past strokes
  • ) Focal CNS signs
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172
Q

How does Lewy body dementia present?

A
  • ) Fluctuating cognitive impairment
  • ) Detailed visual hallucinations
  • ) Parkinsonism
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173
Q

Give 3 other causes of dementia

A

-) Alcohol/drug abuse
-) Repeated head trauma
-) Pellagra
-) Whipple’s disease
-) Huntington’s
-) CJD
-) Parkinson’s
-) HIV
Etc

174
Q

When should we suspect AD? (2)

A
  • ) >40

- ) Persistent, progressive, global cognitive impairment

175
Q

In what disorder does AD present earlier in?

A

Down’s syndrome

176
Q

Give 4 symptoms of AD

A
  • ) Visuo-spatial skill affected
  • ) Memory loss
  • ) Verbal abilities affected
  • ) Executive function (planning) effected
  • ) Anosognosia
  • ) Irritability later
  • ) Mood disturbance later
  • ) Behavioural change later
  • ) Psychosis later
  • ) Agnosia later
177
Q

What is anosognosia?

A

The loss of the ability to gain feedback about one’s own condition or impairments

178
Q

What accumulates in AD?

A

Beta-amyloid peptide

179
Q

What is beta-amyloid peptide?

A

A degradation product of amyloid precursor protein

180
Q

What does the accumulation of beta-amyloid peptide result in? (4)

A
  • ) Progressive neuronal damage
  • ) Neurofibrillary tangles
  • ) Increased numbers of amyloid plaques
  • ) Loss of neurotransmitter ACh
181
Q

What parts of the brain are most vulnerable to neuronal loss in AD? (4)

A
  • ) Hippocampus
  • ) Amygdala
  • ) Temporal neocortex
  • ) Subcortical nuclei
182
Q

Give 3 risk factors for AD

A
  • ) 1st degree relative with AD
  • ) Down’s syndrome
  • ) Homozygosity for apolipoprotein E E4 allele
  • ) Vascular risk factors
  • ) Decreased physical/cognitive activity
  • ) Depression, loneliness
  • ) Smoking
183
Q

How do we manage AD?

A
  • ) Acetylcholinesterase inhibitors
  • ) Antiglutamatergic treatment
  • ) Antipsychotics (severe non-cognitive only)
  • ) BP control
184
Q

Give 2 examples of an acetylcholinesterase inhibitor

A
  • ) Donepezil
  • ) Rivastigmine
  • ) Galantamine
185
Q

Give an example of an antiglutamatergic treatment

A

Memantine (NMDA antagonist)

186
Q

Give the extrapyramidal triad of Parkinsonism

A
  • ) Tremor
  • ) Hypertonia
  • ) Bradykinesia
187
Q

Describe the tremor in parkinsonism

A
  • ) Worse at rest

- ) Often ‘pill-rolling’ of thumb over fingers

188
Q

Describe the hypertonia in parkinsonism

A

Rigidity and tremor gives ‘cogwheel rigidity’ felt during rapid pronation/supination

189
Q

Describe the bradykinesia in parkinsonism

A
  • ) Slow to initiate movement
  • ) Actions slow and decrease in amplitude with repetition
  • ) Blink rate, micrographic
  • ) Gait is shuffling, pitched forwards, reduced arm swing, freezing at obstacles/doors
190
Q

Give 2 causes of parkinsonism

A
  • ) Parkinson’s disease

- ) Drugs, trauma, encephalopathy, copper toxicity, HIV

191
Q

What is the pathogenesis of PD? (2)

A
  • ) Loss of dopaminergic neurons in the substantial nigra

- ) Associated with Lewy bodies in the basal ganglia, brainstem, cortex

192
Q

What is the mean age of onset of PD?

A

60

193
Q

Give 3 clinical features of PD

A
  • ) Parkinsonism triad
  • ) Autonomic dysfunction (postural hypotension, constipation, urinary frequency/urgency, dribbling of saliva)
  • ) Sleep disturbance
  • ) Reduced sense of smell
  • ) Neuropsychiatric complications
194
Q

Is PD symmetrical?

A

No

195
Q

How do we treat PD?

A
  • ) Symptom control
  • ) Deep brain stimulation (dopamine responsive)
  • ) Surgical ablation of overactive basal ganglia circuits
  • ) Postural exercises and weightlifting
196
Q

Give 4 medications we can give in PD

A
  • ) Levodopa
  • ) Dopamine agonists
  • ) Apomorphine
  • ) Anticholinergics
  • ) MAO-B inhibitors
  • ) COMT inhibitors
197
Q

Should we start medication early or late in PD, and why?

A
  • ) Late
  • ) Efficacy of therapy reduces with time, requiring larger and more frequent dosing with worsening SEs and response fluctuations
198
Q

What is levodopa? (PD)

A

Dopamine precursor

199
Q

What should levodopa be given with? (PD)

A

Dopa-decarboxylase inhibitor (to stop conversion to dopamine in peripheral NS)

200
Q

Give an example of a dopamine agonist (PD)

A
  • ) Ropinirole

- ) Pramipexole

201
Q

Give 2 side effects of a dopamine agonist (PD)

A
  • ) Tiredness
  • ) Hypersexuality
  • ) Gambling
  • ) Nausea
  • ) Hallucinations
202
Q

What is apomorphine? (PD)

A

Potent dopamine agonist

203
Q

When do we use apomorphine? (2) (PD)

A
  • ) SC to even out end of dose effects

- ) Rescue pen for one off freezing

204
Q

Give an example of an anticholinergic (PD)

A
  • ) Benzhexol

- ) Orphenadrine

205
Q

Who should we use anticholinergics on? (PD)

A

Young - causes confusion in elderly

206
Q

Give an example of a MAO-B inhibitor (PD)

A
  • ) Rasagiline

- ) Selegiline

207
Q

Give an example of a COMT inhibitor (PD)

A
  • ) Entacapone

- ) Tolcapone

208
Q

What is Huntington’s disease? (HD)

A

Incurable, progressive, autosomal dominant, neurodegenerative disorder

209
Q

What are the prodromal phase symptoms in HD?

A
  • ) Irritability
  • ) Depression
  • ) Incoordination
210
Q

What are the later symptoms in HD?

A
  • ) Chorea
  • ) Dementia
  • ) +/- Fits and death
211
Q

What is the pathology of HD?

A

Atrophy and neuronal loss of striatum and cortex

212
Q

What is the genetic basis of HD?

A

Expansion of CAG repeat on chromosome 4

213
Q

How do we treat chorea in HD?

A

Dopamine antagonists such as tetrabenzine

214
Q

What is multiple sclerosis? (MS)

A

Inflammatory plaques of demyelination in the CNS disseminated in space and time (multiple sites, >30d between attacks)

215
Q

What does poorly healing demyelination cause in MS?

A

Axonal loss

216
Q

Which gender does MS occur more in?

A

Females

217
Q

Is MS an autoimmune disease?

A

Yes, T cell mediated

218
Q

What is the prevalence of MS geographically?

A

More common the further away from the equator you go

219
Q

What is the mean age of onset in MS?

A

30

220
Q

What sort of progression is the in MS?

A

Relapsing and remitting

221
Q

How does MS present?

A
  • ) Usually monosymptomatic
  • ) Unilateral optic neuritis
  • ) Numbness/tingling in limbs, leg weakness
  • ) Brainstem/cerebellar symptoms (diplopia, ataxia)
  • ) ED, anorgasmia, urine retention, incontinence
  • ) Charcot’s triad
222
Q

What may worsen symptoms in MS?

A

Heat (hot bath/exercise)

223
Q

How do we diagnose MS? (3)

A
  • ) 2 or more attacks/relapses
  • ) 2 or more clinical lesions
  • ) Exclusion of other conditions
224
Q

What does the CSF show in MS?

A

Oligoclonal bands of IgG on electrophoresis that are not present in the serum (CNS inflammation)

225
Q

What does an MRI show in MS?

A

Plaque detection

226
Q

What evoked potentials are there in MS?

A

Delayed visual, auditory, somatosensory

227
Q

How do we manage MS? (4)

A
  • ) Lifestyle advice (avoid stress)
  • ) Disease modifying drugs
  • ) Treat relapses
  • ) Symptom control
228
Q

What disease modifying drugs do we give in MS? (3)

A
  • ) Dimethyl fumarate
  • ) Alemtuzumab (monoclonal antibody against T cells)
  • ) Natalizumab (monoclonal antibody against VLA-4 receptors that allow immune cells to cross the BBB)
229
Q

What drug to we give to treat relapses in MS?

A

Methylprednisolone

230
Q

What do we give for spasticity symptom control in MS?

A

Baclofen or gabapentin

231
Q

What do we give for tremor symptom control in MS?

A

Botulinum toxin type A injections

232
Q

What do we give for urgency/frequency symptom control in MS?

A
  • ) Teach intermittent self-catheterisation if >100mL residual
  • ) Tolterodine if <100mL residual
233
Q

What do we give for fatigue symptom control in MS?

A

Amantadine, CBT, exercise

234
Q

What is myasthenia gravis? (MG)

A

Autoimmune disease mediated by antibodies to nicotinic acetylcholine receptors on the post-synaptic side of the NMJ

235
Q

What type of immune cells are implicated in MG?

A

B and T cells

236
Q

What is the presentation of MG?

A
  • ) Slowly increasing or relapsing muscular fatigue

- ) Muscle groups affected in order: extraocular > bulbar > face > neck > limb girdle > trunk

237
Q

Give 3 signs of MG

A
  • ) Ptosis
  • ) Diplopia
  • ) Myasthenic snarl
  • ) Peek sign of orbicularis fatigability
  • ) Voice fades on counting
238
Q

Give 3 things symptoms are exacerbated by in MG

A
  • ) Pregnancy
  • ) Decreased K+
  • ) Infection
  • ) Over treatment
  • ) Change in climate
  • ) Emotion
  • ) Exercise
  • ) Gentamicin
  • ) Opiates
  • ) Tetracycline
  • ) Quinine
  • ) Beta blockers
239
Q

Give 2 differential diagnoses of MG

A
  • ) Polymyositis/other myopathies
  • ) SLE
  • ) Takayasu’s arteritis
  • ) Botulism
240
Q

What is MG associated with when <50?

A

Commoner in females, associated with thymic hyperplasia

241
Q

What is MG associated with when >50?

A

Commoner in males, associated with thymic atrophy or thymic tumour

242
Q

What do tests show in MG? (4)

A
  • ) Anti-AChR antibodies increased in 90%
  • ) MUSK antibodies if -ve
  • ) EMG shows decremental muscle response to repetitive nerve stimulation +/- single fibre jitter
  • ) Ptosis improves by >2mm after ice application to eyelid
243
Q

What does MUSK stand for?

A

Muscle specific tyrosine kinase

244
Q

How do we treat symptoms in MG?

A

Anticholinesterase (e.g. pyridostigmine)

245
Q

What can we use to treat relapses of MG?

A

Prenisolone (with osteoporosis prophylaxis)

246
Q

What surgery can we do for MG?

A

Thymectomy

247
Q

What is a myasthenia crisis?

A

A life threatening weakness of respiratory muscles during a relapse

248
Q

What is motor neurone disease? (MND)

A

A cluster of neurodegenerative diseases characterised by a selective loss of neurons

249
Q

Where is the selective loss of neurones in MND? (3)

A
  • ) Motor cortex
  • ) Cranial nerve nuclei
  • ) Anterior horn cells
250
Q

How do we distinguish MND from MS and polyneuropathies?

A

MND has no sensory loss or sphincter disturbance

251
Q

How do we distinguish MND from myasthenia?

A

MND never affects eye movements

252
Q

What are the 4 clinical patterns of MND?

A
  • ) ALS/amyotrophic lateral sclerosis
  • ) Progressive bulbar palsy
  • ) Progressive muscular atrophy
  • ) Primary lateral sclerosis
253
Q

Where and what is ALS?

A
  • ) Loss of motor neurons in motor cortex and anterior horn of cord
  • ) UMN and LMN signs
254
Q

What is progressive bulbar palsy?

A

Only affects cranial nerves IX-XII

255
Q

Where and what is progressive muscular atrophy?

A
  • ) Anterior horn lesion
  • ) LMN signs only
  • ) Distal muscle groups affected before proximal
256
Q

Where and what is primary lateral sclerosis?

A
  • ) Loss of Betz cells in motor cortex
  • ) Mainly UMN sighs
  • ) No cognitive decline
  • ) Marked spastic leg weakness and pseudo bulbar palsy
257
Q

What is the median age at onset of MND?

A

60

258
Q

Give 4 presenting features of MND

A
  • ) Stumbling spastic gait
  • ) Foot drop
  • ) Proximal myopathy
  • ) Weak grip
  • ) Shoulderabduction
  • ) Aspiration pneumonia
  • ) UMN signs
  • ) LMN signs
  • ) Bulbar signs
259
Q

Give 2 UMN signs of MND

A
  • ) Spasticity
  • ) Brisk reflexes
  • ) Increased plantars
260
Q

Give 2 LMN signs of MND

A
  • ) Wasting

- ) Fasciculation of tongue, abdomen, back, thigh

261
Q

Give a bulbar sign of MND

A

Speech or swallowing affected

262
Q

What are the diagnostic criteria for definite MND?

A

LMN and UMN signs in 3 regions

263
Q

What test excludes structural causes? (MND)

A

Brain/cord MRI

264
Q

What test excludes inflammatory causes? (MND)

A

LP

265
Q

What treatments do we give in MND?

A
  • ) Antiglutamatergic drugs
  • ) Symptom control
  • ) Palliative care
266
Q

Give the main antiglutaminergic drug

A

Riluzole

267
Q

What drug do we give for excess saliva in MND?

A

Antimuscarinic (e.g. propantheline)

268
Q

What drug do we give for spasticity in MND?

A

Baclofen or diazepam

269
Q

What do we give for joint pain and distress in MND?

A

Analgesia

270
Q

What is Guillain-Barre syndrome?

A

An acute inflammatory demyelinating polyneuropathy

271
Q

How does Guillain-Barre syndrome present?

A

Symmetrical ascending muscle weakness a few weeks after an infection

272
Q

Give 3 triggers for Guillain-Barre syndrome

A
  • ) Campylobacter jejuni
  • ) CMV
  • ) Mycoplasma
  • ) Zoster
  • ) HIV
  • ) EBV
  • ) Vaccinations
273
Q

What differentiates Guillain-Barre syndrome from other neuropathies?

A

Proximal muscles are more affected

274
Q

What is the pathology in Guillain-Barre syndrome?

A

Triggers cause antibodies to attack nerves

275
Q

Give 3 signs of autonomic dysfunction

A
  • ) Sweating
  • ) Increased pulse
  • ) BP changes
  • ) Arrhythmias
276
Q

What do nerve conduction studies show in Guillain-Barre syndrome?

A

Slow conduction

277
Q

What does the CSF show in Guillain-Barre syndrome?

A

High protein

278
Q

Give a symptom of Guillain-Barre syndrome

A

Back or limb pain

279
Q

What is the treatment for Guillain-Barre syndrome?

A
  • ) IV immunoglobulin
  • ) Ventilation if needed
  • ) Plasma exchange
280
Q

What is the cause of Creutzfeldt-Jakob disease? (CJD)

A

A prion, misfolded form of a normal protein that can transform other proteins into prion proteins

281
Q

What do lots of prions lead to in CJD?

A

Spongiform changes in the brain

282
Q

How is variant CJD transmitted?

A

Via contaminated CNS tissue affected by bovine spongiform encephalopathy

283
Q

Give 3 causes of CJD

A
  • ) Inherited
  • ) Iatrogenic (contaminated surgical instruments, corneal transplants, blood (vCJD only)
  • ) Sporadic
284
Q

What does the prion protein resist?

A

Sterilisation

285
Q

Give 3 signs of CJD

A
  • ) Progressive dementia
  • ) Focal CNS signs
  • ) Myoclonus
  • ) Eye signs
286
Q

What tests do we do for CJD?

A
  • ) Tonsil/olfactory mucosa biopsy
  • ) CSF gel electrophoresis
  • ) MRI
287
Q

What are mononeuropathies?

A

Lesions of individual peripheral or cranial nerves

288
Q

Give 2 causes of a mononeuropathy

A
  • ) Trauma

- ) Entrapment

289
Q

What is mononeuritis multiplex?

A

2 or more peripheral nerves are affected, usually has a systemic cause

290
Q

What test helps us to define the site in a mononeuropahty?

A

Electromyography

291
Q

How do we treat a mononeuropathy?

A

Rest, splinting, decompression

292
Q

What are the roots of the ulnar nerve?

A

C7-T1

293
Q

How does ulnar nerve mononeuropathy present? (2)

A
  • ) Weakness/wasting of medial wrist flexors, interossei, medial 2 lumbicals, hypothenar eminence
  • ) Sensory loss over medial 1.5 fingers and ulnar side of hand
294
Q

How does radial nerve mononeuropathy present? (2)

A
  • ) Wrist and finger drop

- ) Sensory loss of anatomical snuff box

295
Q

What are the roots of the radial nerve?

A

C5-T1

296
Q

What are the roots of the median nerve?

A

C6-T1

297
Q

What is the most common mononeuropathy?

A

Carpal tunnel syndrome

298
Q

Give 3 clinical features of carpal tunnel syndrome

A
  • ) Aching pain in hand and arm
  • ) Pain especially at night
  • ) Paraesthesiae in thumb, index and middle fingers
  • ) Relieved by dangling hand over edge of bed and shaking
  • ) Sensory loss
  • ) Weakness of abductor pollicis brevis
  • ) Wasting of thenar eminence
  • ) Light touch, 2 point discrimination, sweating may be impaired
299
Q

Give 3 causes of carpal tunnel syndrome

A
  • ) Myxoedema
  • ) Prolonged flexion
  • ) Acromegaly
  • ) Myeloma
  • ) Local tumours
  • ) RA
  • ) Amyloidosis
  • ) Pregnancy
  • ) Sarcoidosis
300
Q

How do we test for carpal tunnel syndrome?

A
  • ) Neurophysiology
  • ) Maximal wrist flexion for 1 minute may elicit symptoms
  • ) Tapping over the wrist may induce tingling
301
Q

How do we treat carpal tunnel syndrome? (3)

A
  • ) Splinting
  • ) Local steroid injection
  • ) Possible decompression surgery
302
Q

What is a polyneuropathy?

A

Motor and/or sensory disorder of multiple peripheral or cranial nerves

303
Q

What is the usual distribution of polyneuropathies? (3)

A
  • ) Symmetrical
  • ) Widespread
  • ) Often worse distally (glove and stocking)
304
Q

How do we classify polyneuropathies?

A
  • ) Chronicity
  • ) Function
  • ) Pathology
305
Q

What are the functional classifications of polyneuropathies?

A
  • ) Sensory
  • ) Motor
  • ) Autonomic
  • ) Mixed
306
Q

What are the pathological classifications of polyneuropathies?

A
  • ) Demyelination
  • ) Axonal degeneration
  • ) Both
307
Q

How do we diagnose a polyneuropathy?

A
  • ) History

- ) Nerve conduction studies

308
Q

What does sensory neuropathy present with?

A
  • ) Numbness
  • ) Paraesthesiae (pins and needles, glove and stocking)
  • ) Difficulty handling small objects
  • ) Signs of trauma or joint deformation
  • ) DM and alcoholic neuropathies typically painful
309
Q

What does motor neuropathy present with?

A

-) Often progressive
-) Weak or clumsy hands
-) Difficulty in walking
-) Difficulty in breathing
) LMN lesion - wasting and weakness
-) Reduced/absent reflexes

310
Q

What do cranial nerve polyneuropathies present with?

A
  • ) Swallowing/speaking difficulty

- ) Diplopia

311
Q

What do sympathetic autonomic neuropathies present with?

A
  • ) Postural hypotension
  • ) Decreased sweating
  • ) Ejaculatory failure
  • ) Horner’s syndrome
312
Q

What do parasympathetic autonomic neuropathies present with?

A
  • ) Constipation
  • ) Nocturnal diarrhoea
  • ) Urine retention
  • ) Erectile dysfunction
  • ) Holmes-Adie pupil
313
Q

Give 4 causes of polyneuropathies

A
  • ) DM
  • ) Renal failure
  • ) Hypothyroidism/glycaemia
  • ) Leprosy
  • ) HIV
  • ) Syphilis
  • ) Lyme disease
  • ) PAN
  • ) RA
  • ) Charcot-Marie-Tooth
  • ) Guillaine-Barre
  • ) Sarcoidosis
  • ) Drugs
  • ) Deficiencies
  • ) Malignancy
314
Q

Give 4 ways we can treat polyneuropathies

A
  • ) Treat cause
  • ) Physio and OT
  • ) Foot care and shoe choice
  • ) Splinting
  • ) Amitriptyline, fluoxetine, gabapentin for neuropathic pain
315
Q

How does a cerebral hemisphere lesion present?

A

Contralateral, unilateral pattern

316
Q

How does a spinal cord lesion present?

A

Bilateral, at a level

317
Q

How does a cerebellum lesion present?

A

Coordination loss, ipsilateral, DANISH symptoms

318
Q

What are the DANISH symptoms?

A 
Dysdiadochokinesis
Ataxia
Nystagmus
Intention tremor
Scanning dysarthria
Heel-shin test positivity
319
Q

How does a brainstem lesion present?

A

Weirdly

320
Q

How do peripheral nerve lesions present?

A

Mononeuropathy, polyneuropathy

321
Q

How does a lesion in cranial nerve I present?

A

Cannot smell

322
Q

How does a lesion in cranial nerve II present?

A

Acuity lost, visual fields, reaction to light

323
Q

How does a lesion in cranial nerve III present?

A

Ptosis, large pupil, eye down and out

324
Q

How does a lesion in cranial nerve IV present?

A

Diplopia on looking down and in, head tilting

325
Q

How does a lesion in cranial nerve VI present?

A

Horizontal diplopia on looking out, nystagmus (away from lesion if acute, towards if chronic)

326
Q

How does a lesion in cranial nerve V present?

A

Motor palsy

327
Q

How does a lesion in cranial nerve VII present?

A

Facial nerve lesions - droop and weakness, taste in anterior 2/3 of tongue lost

328
Q

How does a lesion in cranial nerve VIII present?

A

Hearing, balance, vertigo problems

329
Q

How does a lesion in cranial nerve IX present?

A

Gag reflex

330
Q

How does a lesion in cranial nerve X present?

A

Gag reflex, palate pulled to one side on saying ‘Ah’, problems swallowing

331
Q

How does a lesion in cranial nerve XI present?

A

Cannot shrug shoulders against resistance, turn head

332
Q

How does a lesion in cranial nerve XII present?

A

Tongue deviates to side of lesion

333
Q

Give 3 clinical features of a LMN lesion

A

-) Muscle tone normal/reduced (flaccid)
-) Muscle wasting
-) Fasciculation
-) Reflexes depressed/absent
Everything goes down!

334
Q

Give 3 clinical features of an UMN lesion

A

-) Muscle tone increased (spasticity)
-) Tendon reflexes/jaw jerk brist
-) Plantar responses extensor (positive Babinski sign)
-) Characteristic pattern of limb muscle weakness
-) Maybe emotional lability
Everything goes up!

335
Q

What is the characteristic pattern of limb muscle weakness in UMN lesions?

A

Upper limbs - extensor muscles weaker than flexors

Lower limbs - flexor muscles weaker than extensors

336
Q

What does spinal cord compression usually present with?

A

Weak legs

337
Q

Is arm or leg weakness more severe?

A

Leg

338
Q

Give 3 causes of spinal cord compression

A
  • ) Secondary malignancy in spine
  • ) Infection causing abscess
  • ) Disc prolapse
  • ) Cord tumour
  • ) Haematoma
  • ) Myeloma
339
Q

Give 2 signs of spinal cord compression

A
  • ) Normal above lesion
  • ) LMN signs at level
  • ) UMN signs below level
340
Q

Give 2 tests for spinal cord compression

A
  • ) MRI
  • ) Biopsy if mass
  • ) Screening bloods
  • ) CXR
341
Q

How do we treat a malignant cause of spinal cord compression?

A

Dexamethasone IV and consider more specific therapy, possible decompression

342
Q

How may we treat an epidural abscess?

A

Surgical decompression, antibiotics

343
Q

What are the presenting symptoms of cauda equina syndrome? (6)

A
  • ) Leg weakness is flaccid and areflexic (not spastic and hyperreflexic)
  • ) Back pain
  • ) Radicular pain down legs
  • ) Asymmetrical, atrophic, areflexic paralysis of legs
  • ) Sensory loss in root distribution
  • ) Decreased anal sphincter tone
344
Q

Give 3 causes of cauda equina syndrome

A
  • ) Secondary malignancy in spine
  • ) Infection causing abscess
  • ) Disc prolapse
  • ) Cord tumour
  • ) Congenital lumbar disc disease
  • ) Lumbosacral nerve lesions
345
Q

What grade is an anapaestic astrocytoma?

A

III

346
Q

What are the pathogenic steps in the common pathway to a malignant glioma? (5)

A

1) Genetic error of glucose glycolysis
2) Mutation of isocitrate dehydrogenase 1
3) Excessive build up of 2-hydroxyglutarate
4) Genetic instability in glial cells
5) Inappropriate mitosis

347
Q

What is the most frequent brain tumour?

A

Astrocytoma

348
Q

What is a gorilla cell?

A

Tumour cells in other parts of the brain away from the main tumour that can cause recurrence

349
Q

What do we see in the histology of an oligodendroglioma?

A

Fried egg nuclei

350
Q

Give 3 of the most common sites that metastasise to the brain

A
  • ) Lung
  • ) Breast
  • ) Melanoma
  • ) GU/GI tract
  • ) Kidney
351
Q

Give 3 signs of a brain tumour

A
  • ) Increased ICP
  • ) Vomiting
  • ) Headache worse on waking/coughing/bending
  • ) Focal neurological signs
  • ) Ataxia
  • ) Fits
  • ) Nausea
  • ) Papilloedema
  • ) Decreased GCS
  • ) Subtle personality changes
352
Q

What can tumours physically cause in the brain?

A

Mass effect, hernias, coning

353
Q

Why does a papilloedema occur?

A

Prolonged high ICP due to obstruction of venous return from retina

354
Q

How do we diagnose a brain tumour?

A
  • ) CT/MRI
  • ) Biopsy
  • ) Avoid LP before imaging
355
Q

How do we treat a brain tumour?

A
  • ) Remove
  • ) Ventricle peritoneal shunt (for hydrocephalus)
  • ) Chemo/radio
  • ) Temozolomide for glioblastoma
  • ) Mannitol or dexamethasone for cerebral oedema
  • ) Analgesia
  • ) Phenytoin for seizure prophylaxis
356
Q

Does MGMT wild type or mutant indicate a better prognosis?

A

Mutant

357
Q

What is myelitis?

A

Inflammation of the spinal cord

358
Q

What in meningoencephalitis?

A

Inflammation of the brain and meninges

359
Q

What type of virus is rabies?

A

RNA

360
Q

What organism is tetanus caused by?

A

Clostridium tetani

361
Q

What toxin is secreted in tetanus?

A

Tetanospasmin

362
Q

How does tetanus infect?

A

Via dirty wounds

363
Q

How is rabies transmitted?

A

Via the saliva

364
Q

Give 2 symptoms of tetanus

A
  • ) Trismus (lockjaw)
  • ) Sustained muscle contraction
  • ) Involvement of facial muscles
  • ) Paroxysmal generalised spasms
365
Q

Give 2 symptoms of rabies

A
  • ) Rapid, aggressive, odd behaviour
  • ) Hypersalivation
  • ) Hydrophobia
  • ) Fever
  • ) Anxiety, confusion
  • ) Hyperactivity, uncontrollable excitement, hallucinations
  • ) Violent movement
366
Q

What is the prevention for both rabies and tetanus?

A

Vaccinations

367
Q

What is meningitis?

A

Inflammation of the meninges

368
Q

Give 3 causes of meningitis

A
  • ) Meningococcus
  • ) Pneumococcus
  • ) Haemophilus influenzae
  • ) Listeria monocytogenes
369
Q

Give a cause of meningitis in the immunosuppressed

A
  • ) CMV
  • ) Crytococcus
  • ) TB
370
Q

What can viral meningitis be caused by?

A

Enterovirus

371
Q

Give 2 early clinical features of meningitis

A
  • ) Headache
  • ) Leg pain
  • ) Cold hands and feet
  • ) Abnormal skin colour
372
Q

Give 2 late clinical features of meningitis

A
  • ) NECK STIFFNESS
  • ) Photophobia
  • ) Kernig’s sign
  • ) Decreased GCS
  • ) Seizures
  • ) Focal CNS signs
  • ) Non-blanching petechial rash
373
Q

Give 3 tests for meningitis

A
  • ) U&E, FBC, glucose, coagulation
  • ) Blood culture, throat swabs, serology
  • ) LP usually after CT
  • ) CSF for MC&S, gram stain, protein, glucose, virology/PCR, lactate
  • ) CXR for TB
374
Q

What does the CSF fluid appear like in meningitis if it is pyogenic?

A

Turbid

375
Q

What prophylaxis do we give to close contacts of meningitis?

A

Rifampicin or ciprofloxacin

376
Q

What is the treatment for meningitis? (4)

A
  • ) IV fluids and resus
  • ) <55 cefotaxime IV (or ceftriaxone)
  • ) >55 cefotaxime and ampicillin IV
  • ) Aciclovir if viral suspected
377
Q

What is encephalitis?

A

Inflammation of the brain

378
Q

Give 3 viral causes of encephalitis

A
  • ) HSV1 and 2
  • ) Arboviruses
  • ) CMV
  • ) EBV
  • ) VZV
  • ) HIV
  • ) Measles
  • ) Mumps
  • ) Rabies
  • ) Japanese B encephalitis
  • ) West Nile virus
  • ) Tick borne encephalitis
379
Q

Give 2 non viral causes of encephalitis

A

-) Bacterial meningitis
-) TB
-) Malaria
-) Listeria
-) Lyme disease
-) Legionella
-) Aspergillosis
-) Shistosomiasis
-) Typhus
Etc

380
Q

Give 3 signs and symptoms of encephalitis

A
  • ) Bizarre encephalopathic behaviour or confusion
  • ) Decreased GCS/coma
  • ) Fever
  • ) Headache
  • ) Focal neurological signs
  • ) Seizures
  • ) History of travel/animal bite
381
Q

What investigations do we do for encephalitis?

A
  • ) Bloods
  • ) Contrast enhanced CT
  • ) LP
  • ) EEG
382
Q

What is suggestive of HSV encephalitis on a contrast enhanced CT?

A

Focal bilateral temporal lobe involvement

383
Q

What is suggestive of meningoencephalitis on a contrast enhanced CT?

A

Meningeal enhancement

384
Q

What does a LP show in encephalitis? (3)

A
  • ) High protein
  • ) High lymphocytes
  • ) Low glucose
385
Q

What is the treatment for encephalitis?

A

Aciclovir

386
Q

What does reactivation of the virus that caused chickenpox cause?

A

Shingles

387
Q

How do we treat shingles?

A

Aciclovir

388
Q

Where does the herpes zoster virus lay dormant after infection?

A

Dorsal root ganglia

389
Q

Give 3 symptoms of ataxia

A
  • ) Slurring of speech
  • ) Unsteadiness when walking/worse in dark
  • ) Stumbles and falls
  • ) Swallowing difficulties
  • ) Oscillopsia
  • ) Clumsiness
  • ) Action tremor
  • ) Loss of precision of fine movement/motor skills
  • ) Cognitive problems
390
Q

Give 3 signs of ataxia

A
  • ) Nystagmus
  • ) Dysarthria
  • ) Action tremor
  • ) Truncal ataxia
  • ) Dysdiadochokinesia
  • ) Limb ataxia
  • ) Gait ataxia
391
Q

Give 3 types of inherited ataxia

A
  • ) Autosomal recessive (Freidreich’s)
  • ) Autosomal dominant (SC6, episodic)
  • ) Mitochondrial
  • ) X-linked
392
Q

Give 3 types of acquired ataxia

A
  • ) Toxic (alcohol, lithium, phenytoin)
  • ) Immune mediated (gluten)
  • ) Neurodegenerative
  • ) Idiopathic sporadic
  • ) Vascular/structural
393
Q

Define dermatome

A

The area of skin supplied by a single spinal nerve

394
Q

Define myotome

A

The volume of muscle supplied by a single spinal nerve

395
Q

Give 3 symptoms of Brown-Sequard syndrome

A
  • ) Ipsilateral UMN weakness below lesion
  • ) Ipsilateral loss of proprioception and vibration
  • ) Contralateral loss of pain and temperature
396
Q

Why is there ipsilateral UMN weakness below the lesion in Brown-Sequard syndrome?

A

Corticospinal tract severed

397
Q

Why is there ipsilateral loss of proprioception and vibration in Brown-Sequard syndrome?

A

Dorsal column severed

398
Q

Why is there contralateral loss of pain and temperature in Brown-Sequard syndrome?

A

Spinothalamic tract severed

399
Q

How does the corticospinal tract decussate?

A

Lateral - 85% in medulla

Anterior - 15% stays same side

400
Q

What does the corticospinal tract do?

A

Rapid, skilled, voluntary movement

401
Q

What does the rubrospinal tract do?

A
  • ) Facilitates flexors

- ) Inhibits extensors

402
Q

What does the vestibulospinal tract do?

A
  • ) Facilitates extensors

- ) Inhibits flexors

403
Q

What does the tectospinal tract do?

A

Truncal reflexes from sight

404
Q

What do the fasciclulus gracilis and cuneatus do?

A

Sensation of touch, vibration, conscious muscle/joint sense

405
Q

Where is the fasciculus gracilis from?

A

Leg

406
Q

Where is the fasciculus cuneatus from?

A

Arm

407
Q

What does the spinocerebellar tract do?

A

Sensation of non-conscious muscle/joint sense

408
Q

Where do the tracts decussate in the spinocerebellar tract?

A

Posterior - ipsilateral

Anterior - immediate

409
Q

What does the spinothalamic tract do? (2)

A

Lateral - pain, temperature

Anterior - light touch, pressure

410
Q

What does the spina-olivary tract do?

A

Sensation of proprioception

411
Q

Why do epidural anaesthetics give greater sensory block than motor block?

A

Cell bodies (sensory neurones in dorsal root ganglia) have a higher SA than axons

412
Q

What does Wernicke’s area do?

A

Understands speech, uses correct words

413
Q

What does Broca’s area do?

A

Motor speech, movements

414
Q

What are the 3 layers of the meninges?

A

Dura
Arachnoid
Pia

415
Q

Where does the circle of Willis lie?

A

Subarachnoid space

416
Q

Where do meningeal vessels lie?

A

Extradural space

417
Q

What can compress the optic pathway?

A

Pituitary tumours

418
Q

Name the 12 cranial nerves

A 
I - Olfactory
II - Optic
III - Oculomotor
IV - Trochlear
V - Trigeminal
VI - Abducens
VII - Facial
VIII - Vestibulocochlear
IX - Glossopharnygeal
X - Vagus
XI - Accessory spinal
XII - Hypoglossal
Oh Oh Oh To Touch And Feel Very Good Vaginas And Hymens
419
Q

Which cranial nerves make up the parasympathetic NS?

A

III, VII, IX, X

420
Q

What type of fibre is each cranial nerve?

A 
I - Sensory
II - Sensory 
III - Motor
IV - Motor
V - Both 
VI - Motor
VII - Both
VIII - Sensory
IX - Both
X - Both
XI - Motor
XII - Motor
Some Say Money Matters But My Brother Says Big Breasts Matter Most
421
Q

What is Wilson’s disease?

A

Inherited disorder of copper excretion with excess deposition in liver and CNS

422
Q

Give 2 CNS signs of Wilson’s disease

A
  • ) Psychiatric symptoms
  • ) Personality change
  • ) Mood disturbance
  • ) Psychosis
  • ) Cognitive impairment
423
Q

What is acute intermittent porphyria?

A

A metabolic disorder of haem

424
Q

Give 2 symptoms of acute intermittent porphyria

A
  • ) Acute psychosis
  • ) Agitation
  • ) Mania
  • ) Depression
425
Q

What is neuroacanthocytosis?

A

Blood contains misshapen RBCs - acanthocytes

426
Q

Give 3 symptoms of neuracanthocytosis?

A
  • ) Anxiety
  • ) Paranoia
  • ) Depression
  • ) Obsessive behaviour
  • ) Emotional instability
427
Q

What are somatisation disorders?

A

Physical symptoms are caused by mental/emotional factors

428
Q

What is hypochondriasis?

A

Fear that minor symptoms may be due to serious disease

429
Q

What is dissociative amnesia?

A

Periods where they cannot remember information about themselves/events in their past

430
Q

What is dissociative identity disorder?

A

Feel uncertain about identity, may feel presence of other identities

431
Q

Are you gonna pass phase 2a?

A

Yassssss

Phase 2a Medicine - Riona COPY (17 decks)

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