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Phase 3a conditions list flashcards > Neurology - part 1 > Flashcards

Neurology - part 1 Flashcards

1
Q

What are two methods of investigation problems with the peripheral nervous system (2)?

A
  • EMG
  • Nerve conduction studies
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2
Q

What are two findings in a nerve conduction study?

A
  • Decreased amplitude/ smaller waves = axon loss (e.g. MND, peripheral neuropathy)
  • Delayed signal = demyelination (e.g. GBS)
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3
Q

What are two findings in electromyography?

A
  • Myopathy = decreased action potential duration and amplitude
  • Neuropathy = increased action potential duration and amplitude
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4
Q

What is a myopathy vs neuropathy?

A
  • Myopathy = problem with the muscle (e.g. muscular dystrophy)
  • Neuropathy = problem with the nerve (e.g. MND)
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5
Q

What are 3 ways of investigating problems with the CNS?

A
  • EEG (electroencephalogram)
  • MRI/ CT
  • LP
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6
Q

What is NCCT first line for (3)?

A
  • Stroke
  • ICH
  • Raised ICP
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7
Q

What is a contrast CT useful for?

A

Brain abscess

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8
Q

What are some differences in of PNS and CNS lesions in terms of presentation (2)?

A
  • PNS = back pain?, bi-lateral,
  • CNS = headache?, uni-lateral, visual changes
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9
Q

What is a lateralising sign?

A

Lesion affecting a single hemisphere (e.g. pronator drift, homonymous hemianopia, u/l weakness)

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10
Q

What are 3 important tracts to know about and where do they decussate?

A
  • (DCML) dorsal column medial lemniscal (medulla)
  • Spinothalamic (1-2 spinal levels above)
  • Corticospinal (medulla)
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11
Q

What does the DCML carry (4)?

A
  • Proprioception
  • Fine touch
  • Vibration
  • 2 point discrimination
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12
Q

What does spinothalamic tract carry (3)?

A
  • Lateral = pain + temperature
  • Anterior = crude touch
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13
Q

What does the corticospinal tract carry (1)?

A

Motor signals to muscles

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14
Q

What nerve roots are responsible for the key reflexes?

A
  • Bicep = C5/6
  • Tricep = C7
  • Knee = L4
  • Ankle = S1
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15
Q

What nerve roots are responsible for the key dermatomes (6)?

A
  • C6 = thumb
  • C7 = middle + palm
  • C8 = little
  • T10 = bellybuT-TEN
  • L5 = big toe (largest of the five)
  • S1 = heel + sole
    think of body doing splits with arms out
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16
Q

What are the nerve roots responsible for the key myotomes (5)?

A
  • C5/6 = elbow flexion + shoulder abduction
  • C7 = wrist flex, elbow extend
  • C8 = hand flexion
  • L5 = dorsiflexion
  • S1 = plantar flexion
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17
Q

What are two common causes of foot drop?

A
  • Common peroneal nerve lesion = MC
  • L5 radiculopathy
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18
Q

How could you differentiate between common peroneal nerve lesion and L5 radiculopathy (2)?

A
  • Common peroneal = ankle jerk absent, weak eversion
  • L5 radiculopathy = ankle jerk present, weak inversion
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19
Q

What is a stroke?

A

A sudden infarct in the blood supply to part of the brain with symptoms lasting more than 24 hours

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20
Q

What are the two categories of stroke?

A
  • Haemorrhagic (15%)
  • Ischemic (85%)
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21
Q

What presentation is suggestive of a stroke?

A

Any sudden onset neurological symptom

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22
Q

What is ischemia vs infarction?

A
  • Ischemia = inadequate blood supply
  • Infarction = complete blockage of blood –> tissue death
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23
Q

What are the causes of a stroke (7)?

A
  • Thrombus (+atherosclerosis)
  • Embolus + infective endocarditis
  • Shock
  • Vasculitis
  • Trauma
  • Aneurysm
  • Anticoagulants
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24
Q

What might cause a stroke in young people (6)?

A
  • ADPKD (berry aneurysms)
  • Congenital heart malformations
  • COCP
  • Blood clotting disorders
  • Cocaine
  • Infective endocarditis
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25
Q

Which congenital heart malformations increase the risk of stroke (3)?

A
  • ASD
  • VSD
  • Patent foramen ovale
    allow embolus from systemic circulation to enter the left ventricle and go to brain
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26
Q

What type of stroke affects the deep brain structures?

A

Lacunar stroke

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27
Q

What is a TIA?

A

A temporary neurological dysfunction lasting less than 24 hours caused by ischemia, but without infarction

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28
Q

What are some typical symptoms of a stroke (6)?

A
  • Limb weakness
  • Facial weakness
  • Dysphasia
  • Visual field defect
  • Sensory loss
  • Ataxia and vertigo
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29
Q

What are some risk factors for an ischemic stroke (13)?

A
  • Smoking
  • Hypertension
  • AF
  • Previous stoke/ TIA
  • Diabetes
  • Obesity
  • Raised cholesterol
  • Family history
  • Vasculitis
  • Thrombophilia
  • COCP
  • Migraines (with aura)
  • Older age
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30
Q

What are the Bamford/ Oxford stroke classifications (4)?

A
  • Total anterior circulation stroke
  • Partial anterior circulation strokes
  • Posterior circulation stroke
  • Lacunar stroke
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31
Q

How does a total anterior circulation stroke present (3)?

A
  • Unilateral sensory/ motor loss
  • Homonymous hemianopia
  • Higher cortical function loss e.g. dysphasia
    Need all 3 for this classification
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32
Q

How does partial anterior circulation stroke present?

A

2 out of 3 of the criteria for a TACS

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33
Q

How does a posterior circulation stroke present (3)?

A
  • Isolated vision change
  • Cerebella Sx
  • Contralateral CN palsy
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34
Q

How does a lacunar stroke present (3)?

A
  • Pure motor stroke
  • Pure sensory stroke
  • Ataxic hemiparesis
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35
Q

What would be the presentation of an ACA stroke (2)?

A
  • Lower limb&raquo_space;» upper limb
  • Behavioural change
    sensory and motor deficit
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36
Q

What would be the presentation of an MCA stroke (4)?

A
  • Upper limb&raquo_space;» lower limb
  • Face droop (forehead spared)
  • Brocca/ wernicke aphasia (in dominant hemisphere)
  • Ipsilateral gaze deviation
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37
Q

How does PCA stroke present (2)?

A
  • Contralateral homonymous hemianopia (with macular sparing)
  • Visual agnosia
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38
Q

What is webers stroke?

A

Branches of PCA that supply the midbrain blocked

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39
Q

What is the presentation of webners stroke (2)?

A
  • Ipsilateral CN 3 palsy (down and out)
  • Contralateral hemiplegia (upper + lower)
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40
Q

What is Wallenberg stroke?

A

PICA infarct
lateral medullary syndrome

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41
Q

What is the presentation of Wallenberg stroke (4)?

A
  • Ipsilateral spinothalamic face loss (pain + temp)
  • Contralateral spinothalamic limb/ torso loss
  • Nystagmus
  • Ataxia
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42
Q

What is a basilar artery stroke known as?

A

Locked in syndrome
carries blood to brain stem

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43
Q

How does a retinal artery stroke present?

A

Amaurosis fugax
transient loss of vision

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44
Q

How does a Benedikt stroke present?

A

Wallenberg + gait disturbance (red nucleus infarct)

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45
Q

How does an AICA stroke present?

A

Wallenberg + hearing loss + ipsilateral facial paralysis
no dysphasia
lateral pontine syndrome

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46
Q

What tool can be used to assess the likelihood of a stroke (2)?

A
  • FAST (community)
  • ROSIER tool (ED)
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47
Q

How is a patient presenting with a stroke managed (5)?

A
  • BG testing (exclude hypoglycaemia)
  • Immediate NCCT head
  • Aspirin 300mg (for 2 weeks)
  • Thrombolysis < 4.5 h
  • Thrombectomy < 6h
  • Consider diffusion weighted MRI
  • Carotid doppler USS
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48
Q

How is a TIA managed (3)?

A
  • Aspirin 300mg (daily)
  • Referral for specialist assessment within 24 hours (or within 7 days if > 7 days since symptoms resolved)
  • Diffusion weight MRI scanning
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49
Q

What are the specialist treatments offered to those with an ischemic stroke (2)?

A
  • Thrombolysis (alteplase)
  • Thrombectomy
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50
Q

How should blood pressure be managed in those with ischemic strokes?

A

Only treated in hypertensive emergency or to reduce risks associated with IV thrombolysis
reducing BP can reduce perfusion to brain

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51
Q

What are some complications of those with ischemic stroke (5)?

A
  • Haemorrhagic transformation
  • Cerebral oedema
  • Seizures
  • Aspiration pneumonia
  • Long-term complications
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52
Q

What is haemorrhagic transformation in those with ischemic stroke?

A

Damaged tissue during ischemic stroke allows bleeding from the brain

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53
Q

What underlying causes of stroke are assessed in those who have had a TIA/ stroke (2)?

A
  • AF (using ECG)
  • Carotid artery stenosis (using USS)
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54
Q

How can carotid artery stenosis be managed (2)?

A
  • Carotid endarterectomy (when > 70% stenosed)
  • Angioplasty (balloon dilation) and stenting
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55
Q

When is thrombolysis offered to those with stroke?

A

4.5 hours within onset of symptoms (slightly different for those who have woken up with stroke)

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56
Q

What are some contraindications to thrombolysis (4)?

A
  • Previous haemorrhagic stroke
  • Recent major surgery
  • Active internal bleeding
  • Uncontrolled hypertension
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57
Q

When is thrombectomy offered for those with a stroke?

A

Usually within 6 hours, sometimes up to 24 hours if imaging is favourable

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58
Q

How are strokes/ TIAs managed long term (3)?

A
  • Clopidogrel daily - P2Y12 inhibitor (or aspirin + dipyridamole)
  • Atorvastatin
  • BP + diabetes control
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59
Q

What are the 4 types of intracranial haemorrhage?

A
  • Extradural haemorrhage
  • Subdural haemorrhage
  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
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60
Q

Which intracranial haemorrhage constitute a stroke (2)?

A
  • Subarachnoid haemorrhage
  • Intracerebral haemorrhage
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61
Q

Where does a subdural haemorrhage bleed between?

A

Dura mater and arachnoid mater

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62
Q

Where does an extradural haemorrhage bleed between?

A

Skull and dura mater

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63
Q

What shape is a subdural haemorrhage on CT?

A

Banana shaped

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64
Q

What shape is a extradural haemorrhage on CT?

A

Lemon shaped

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65
Q

What percentage of strokes do intracerebral and subarachnoid haemorrhages account for?

A

10-20%

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66
Q

What are some risk factors for intracerebral haemorrhage (7)?

A
  • Head injuries
  • Hypertension
  • Aneurysms
  • Anticoagulants
  • Bleeding disorders/ thrombocytopenia
  • Brain tumours
  • Alcoholism
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67
Q

What are the signs/ symptoms of intracerebral haemorrhage (5)?

A
  • Headache
  • Seizures
  • Vomiting
  • Reduced GCS
  • Focal neurological symptoms
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68
Q

What values is the GCS between?

A

3-15

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69
Q

What are the scores allocated to eyes in GCS (4)?

A
  • Spontaneous opening
  • Speech
  • Pain
  • No response
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70
Q

What scores are allocated to verbal response in GCS (5)?

A
  • Orientated
  • Confused
  • Inappropriate words
  • Incomprehensible sounds
  • No response
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71
Q

What scores are allocated to motor response in GCS (6)?

A
  • Obeys command
  • Localises pain
  • Withdraws from pain
  • Abnormal flexion to pain
  • Extension to pain
  • No response
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72
Q

What GCS score needs intubation?

A

8/15 or less

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73
Q

Damage to which blood vessel usually causes an extradural haemorrhage?

A

Middle meningeal artery

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74
Q

Damage to which region of the head often results in damage to the middle meningeal artery and therefore an extradural haemorrhage?

A

Temporal bone fracture

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75
Q

What age patient is usually affected by extradural haemorrhage?

A

Younger patients (20-30)

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76
Q

What is the typical presentation of a patient with extradural haemorrhage?

A

Head trauma and ongoing headache initially with symptoms improving then rapid worsening

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77
Q

Damage to which blood vessel usually causes an subdural haemorrhage?

A

Bridging veins

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78
Q

What age is typically affected by a subdural haemorrhage (2)?

A
  • Older patients
  • Babies (shaken baby)
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79
Q

What are some risk factors for subdural haemorrhage (3)?

A
  • Head trauma
  • Dementia
  • Alcoholism
    *both cause brain atrophy - causing arachnoid to pull away from dura
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80
Q

What time period do subdural haemorrhages usually come on over?

A

Longer time period than extradural as usually caused by bleeding from veins

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81
Q

How are subdural and epidural haemorrhages managed (3)?

A
  • Correct clotting abnormalities, stabilise BP
  • Craniotomy
  • Burr holes
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82
Q

How does an intracerebral haemorrhage present?

A

Similar to an ischemic stroke but with a headache

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83
Q

What is the presentation of a patient with a SAH?

A

Sudden onset occipital headache ‘thunderclap headache’

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84
Q

What are some other symptoms of SAH other than headache (3)?

A
  • Meningism (hhotophobia, neck stiffness, vomiting)
  • Raised ICP Sx (CN3, 6 palsy, cushings triad)
  • Neurological symptoms
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85
Q

What are some risk factors for SAH (12)?

A
  • Hypertension
  • Smoking
  • Alcohol
  • Cocaine
  • Family history
  • Sickle cell
  • Connective tissue disorders
  • ADPKD
  • Neurofibromatosis
  • Aged 45-70
  • Women
  • Black
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86
Q

How is a SAH investigated?

A

CT head = hyperlattenuation in SAS
most reliable within 6 hours

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87
Q

What can be performed if CT head is negative for SAH?

A

Lumbar puncture

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88
Q

How long after symptoms should a lumbar puncture be performed for a SAH?

A

More than 12 hours

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89
Q

What would a lumbar puncture show for those with SAH (2)?

A
  • Xanthocromia
  • Raised red cell count
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90
Q

How can the source of the bleeding in a SAH be located?

A

CT angiogram

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91
Q

How is a SAH managed (2)?

A
  • Aneurysm coiling or clipping
  • Neurosurgery
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92
Q

What are 2 complications of a SAH?

A
  • Vasospasm
  • Hydrocephalus
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93
Q

How is vasospasm treated in those with SAH?

A

Nimodipine (CCB)

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94
Q

How is hydrocephalus treated (in those with SAH) (2)?

A
  • Therapeutic lumbar puncture
  • Shunt (ventriculoperitoneal/ external)
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95
Q

How is raised intracranial pressure treated in those with intracranial haemorrhage?

A

Mannitol

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96
Q

What is the most common cause of a head injury in the UK?

A
  • RTA = mc
    also alcohol + drugs
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97
Q

What criteria might suggest a patient with a head injury would need a scan (6)?

A
  • Persistently reduced GCS (<15)
  • Vomited on more than 1 occasion
  • Seizure/ focal neurological deficit
  • Battle sign (fluid from ear/ nose)
  • > 65
  • Dangerous mechanism of injury
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98
Q

A fracture in which part of the skull may cause CSF to leak from nose?

A

Basilar skull fracture (base of skull)

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99
Q

What are some complications of head injuries (4)?

A
  • Epilepsy
  • Mood disorders
  • Personality changes
  • Focal neurological deficits
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100
Q

What is dementia?

A

Progressive condition that causes irreversible impairment in memory, cognition, communication or personality

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101
Q

What are the main types of dementia (4)?

A
  • Alzheimers (60%)
  • Vascular dementia
  • Lewy body dementia
  • Fronto-temporal dementia
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102
Q

What term is often used to describe symptoms similar to dementia but not as severe?

A

Mild cognitive impairment

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103
Q

What age would be considered early onset for dementia?

A

< 65

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104
Q

What are some differential diagnoses for dementia (8)?

A
  • Delirium
  • Medication use
  • Psychiatric conditions e.g. depression/ bereavement
  • Parkinsons
  • Brain tumours
  • Hyper(para)thyroidism
  • Cushings
  • Nutritional deficiencies
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105
Q

What medications can cause symptoms of dementia in particular (3)?

A
  • Anticholinergics (urological drugs e.g. Oxybutynin)
  • Antihistamines
  • TCA
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106
Q

What nutritional deficiencies may cause dementia like symptoms in particular (2)?

A
  • B12 deficiency
  • Thiamine (B1) deficiency - Wernicke-Korsakoff syndrome
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107
Q

What are some risk factors for developing dementia (5)?

A
  • Sedentary lifestyle
  • Lack of mental stimulation
  • Obesity
  • High BP
  • High BG
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108
Q

What are 2 specific risk factors for the development of Alzheimers?

A
  • Downs syndrome
  • Family history
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109
Q

What are the general signs/ symptoms of dementias (4)?

A
  • Forgetful (events/ names)
  • Asking same questions
  • Difficult remembering words
  • Impaired decision making
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110
Q

What is the general progression of symptoms in dementia?

A

Slow and insidious worsening of symptoms and ability to function

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111
Q

What are the prominent features of Alzheimers?

A
  • Agnosia - can’t recognise
  • Apraxia
  • Aphasia
  • Dysphagia
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112
Q

What is the pattern of memory loss in Alzheimers?

A

Short term memory worse affected

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113
Q

What is a prominent feature of vascular dementia?

A

Stepwise decrease in functioning/ symptoms
symptoms vary depending on the area of the brain affected

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114
Q

What type of person is typically affected by vascular dementia?

A

Stereotypically unhealthy patient - overweight, smokes, drinks

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115
Q

What is a prominent feature of fronto-temporal dementia (2)?

A
  • Frontal = thinking and memory
  • Temporal = speech and language
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116
Q

What is a prominent feature of Lewy body dementia (2)?

A
  • Parkinsonism
  • Hallucinations
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117
Q

What is the pathophysiology of Alzheimers dementia?

A

Beta amyloid proteins accumulate as plaques and tau neurofibrillary triangles –> death of brain cells

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118
Q

How is Alzheimers managed with medication (2)?

A
  • Cholinesterase inhibitors
  • Memantine
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119
Q

What are 3 examples of cholinesterase inhibitors used for Alzheimers?

A
  • Galantamine
  • Donepezil
  • Rivastigmine
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120
Q

What causes Lewy body dementia?

A

Lewy body accumulation in the cortex

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121
Q

What is the main constituent of Lewy bodies?

A

Alpha synuclein

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122
Q

What is Lewy body dementia an umbrella term for?

A
  • Dementia with Lewy bodies (memory affected first)
  • Parkinsons disease dementia (movement affected first)
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123
Q

What is the difference between Parkinson’s disease and dementia with Lewy bodies?

A

Likely due to the location of accumulation of Lewy bodies
considered a spectrum of disorders

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124
Q

The collection of which protein leads to fronto-temporal dementia?

A

Tau protein/ pick body

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125
Q

What sometimes causes frontotemporal dementia?

A

Autosomal dominant mutation in tau protein

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126
Q

What is frontotemporal dementia associated with?

A

ALS (15-20% of those with ALS develop FTD)

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127
Q

How are those with dementia initially managed in primary care (2)?

A
  • Exclude physical cause (bloods, CXR MSU)
  • Referral to memory clinic
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128
Q

How are those with dementia investigated in secondary care (2)?

A
  • ACE (addenbrookes cognitive examination)
  • MRI
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129
Q

What would an MRI show in those with dementia (2)?

A
  • Atrophy of brain
  • Lack of structural pathology
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130
Q

How are those with dementia managed (5)?

A
  • Lasting power of attorney
  • Advanced decisions
  • Antidepressants
  • Antipsychotics (risperidone)
  • Benzos (for crisis management)
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131
Q

What are some associated behavioural and psychological symptoms of dementia (6)?

A
  • Depression
  • Anxiety
  • Agressions
  • Agitation
  • Hallucinations
  • Sleep disturbances
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132
Q

What is delirium?

A

Acute fluctuating disturbance in mental function

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133
Q

What are the signs/ symptoms of delirium (6)?

A
  • Agitation
  • Confusion
  • Drowsiness
  • Hallucinations
  • Delusions
  • Memory problems
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134
Q

What are the causes of delirium?

A
  • Pain
  • Infection
  • Nutrition
  • Constipation
  • Hydration status
  • Medications
  • Environvment/ electrolytes
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135
Q

What medications commonly cause delirium (5)?

A
  • Benzos
  • Opioids
  • Anticholinergics
  • Dopaminergics
  • Steroids
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136
Q

What might make a diagnosis of delirium more likely in terms of presentation (3)?

A
  • Hallucinations (esp. visual)
  • Altered consciousness (hyperalert/ drowsiness)
  • Agitation more common (looking round room, fidgety)
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137
Q

What is the second most common neurodegenerative condition after dementia?

A

Parkinsons disease

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138
Q

What is the underlying cause of parkisnons disease?

A

Loss of dopamine producing neurones in the substantial nigra pars compacta

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139
Q

What protein accumulation causes the death of these neurones in PD?

A

Alpha synuclein aggregating to form Lewy bodies

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140
Q

What is the mechanism by which parkinsons makes it more difficult to initiate movement?

A

Decrease in nigrostriatal pathway neurones –> less GABA-ergic inhibition (via indirect pathway) –> gross cortex inhibition –> more difficult to initiate movement

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141
Q

What are some risk factors for PD (3)?

A
  • Family history
  • Male (2:1)
  • Older age
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142
Q

What is protective against PD?

A

Smoking

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143
Q

What medications can cause parkinonism or exacerbate parkinsons (2)?

A
  • Antipsychotics (especially typical)
  • Metoclopramide (antiemetic)
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144
Q

What is a feature of drug induced parkinsonism?

A

Bilateral resting tremor

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145
Q

What are the 4 typical symptoms of parkinsons disease?

A
  • Bradykinesia
  • Resting tremor
  • Rigidity
    + Postural instability (not part of the triad, but a key symptom
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146
Q

What is the typical feature/ presentation of symptoms in PD?

A

Asymmetrical symptoms with one side affected much more than the other

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147
Q

What are some symptoms of PD when walking (3)?

A
  • Stooped posture
  • Reduced arm swing
  • Shuffling gait
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148
Q

What are two types of rigidity found in parkinsons disease?

A
  • Cogwheel = jerky
  • Lead pipe = smooth tremor throughout
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149
Q

What are some other features of PD other than the 4 main features (7)?

A
  • Depression
  • Sleep disturbance (REM sleep disorders)
  • Postural instability
  • Loss of sense of smell
  • Cognitive impairment/ memory problems
  • Constipation
  • Autonomic symptoms (e.g. postural hypotension)
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150
Q

What are the features of a tremor in parkinsons disease (3)?

A
  • 4-6 hertz (pill rolling)
  • Asymmetrical (worse on one side)
  • Resting
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151
Q

What is a key differential to the tremor seen in PD?

A

Benign essential tremor

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152
Q

What are the features of benign essential tremor when compared to PD?

A
  • Higher frequency 6-12 Hz
  • Intention tremor
  • Symmetrical
  • Improves with alcohol
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153
Q

How is PD diagnosed?

A

Clinically by a specialist

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154
Q

How is more mild PD treated (3)?

A
  • Da agonist
  • Monoamine oxidase - B inhibitors
  • Levodopa
155
Q

What is an example of a dopamine agonist used for PD?

A

Bromocriptine

156
Q

What is an example of a MAOB-i used for parkinsons?

A

Selegiline

157
Q

How do MAOB-i work?

A

Prevent the breakdown of dopamine

158
Q

What is a complication of long term use of dopamine agonists?

A

Pulmonary fibrosis

159
Q

What medication is used in more severe PD?

A

Levodopa

160
Q

What medications are levodopa combined with to prevent its breakdown/ metabolism (2)?

A
  • COMT inhibitors
  • Peripheral decarboxylase inhibitors - always combined with this
161
Q

What is an example of a COMT inhibitor?

A

Entacapone

162
Q

What is an example of a peripheral decarboxylase inhibitor?

A

Carbidopa

163
Q

What treatments are offered to those with PD where initial medications are ineffective (2)?

A
  • Deep brain stimulation
  • Apomorphine (dopamine agonist) sub cut infusion
164
Q

What is a side effect of levodopa (4)?

A
  • Postural hypotension
  • Confusion
  • Psychosis
  • Dyskinesia/ chorea
165
Q

What can be given for those with PD who develop dyskinaesia due to levodopa?

A

Amantadine (glutamate antagonist)

166
Q

What is a phenomena seen in those who take levodopa for a long time?

A

“On-off phenomena” motor fluctuations throughout the day

167
Q

Overall what is the typical treatment of parkinsons (3)?

A
  1. Levodopa + decarboxylase inhibitor (co-careldopa)
  2. COMT inhibitors, DA agonists
  3. DBS
168
Q

What two conditions are similar to PD but important differentials especially in those not responding to treatments?

A
  • Progressive supranuclear palsy (PSP)
  • Corticobasal degeneration
169
Q

How is essential tremor treated (5)?

A
  • Propanolol = 1st
  • Primidone
  • Gabapentin
  • Botox injections
  • Beep brain stimulation
170
Q

What are 3 primary causes of headaches?

A
  • Migraine
  • Tension headache
  • Cluster headache
171
Q

What are some other (secondary) causes of headache (8)?

A
  • Meningitis/ infection
  • Sinusitis
  • Giant cell arteritis
  • Intracranial haemorrhage
  • Medication overuse headache
  • Glaucoma
  • Pre-eclampsia
  • Raised ICP
  • Trigeminal neuralgia
172
Q

What is the most common type of primary headache disorder?

A

Tension headache

173
Q

What type of pain is felt in tension headaches?

A

Bilateral tight band around sides of head - temples, occipital region and neck

174
Q

What are other associated symptoms with a tension headache?

A

There are not really any
no N+V, motion sickness or visual changes

175
Q

What are some triggers for tension headaches (5)?

A
  • Stress
  • Alcohol
  • Dehydration
  • Stagnant head/ neck position
  • Lack of sleep
176
Q

How can the symptoms of tension headaches be treated medically?

A

Analgesics - paracetamol, Ibuprofen

177
Q

What can be used to treat for chronic/ frequent tension headaches?

A

Amitriptyline

178
Q

What is the most common type of recurrent primary headache disorder?

A

Migraine

179
Q

Which gender is most commonly affected by migraines?

A

Females

180
Q

What age do migraines typically begin?

A

< 40 year olds
most common in young adults/ adolescents

181
Q

What are the types of migraine (4)?

A
  • Migraine with aura
  • Migraine without aura
  • Silent migraine
  • Hemiplegic migraine
182
Q

What is a silent migraine?

A

Migraine that does not cause a headache only an aura

183
Q

What are the 5 stages of a migraine?

A
  • Prodrome
  • Aura
  • Headache
  • Resolution
  • Postdrome
184
Q

What does a prodrome refer to in the development of a migraine?

A

Change in mood/ fatigue up to days before an attack

185
Q

What does an aura refer to in the development of a migraine?

A

Neurological changes in the minutes before an attack

186
Q

What are the most common areas an aura may affect in the development of migraines (4)?

A
  • Visual = MC
  • Sensory (parasthaesia)
  • Speech (dysphasia)
  • Motor (weakness)
187
Q

What are some common visual changes associated with migraines with aura (3)?

A
  • Sparks in vision
  • Blurred vision
  • ‘QR code’ vision
188
Q

What is a migraine that causes motor symptoms known as?

A

Hemiplegic migraine

189
Q

What are the symptoms of a hemiplegic migraine (3)?

A
  • Unilateral limb weakness
  • Ataxia
  • Reduced consciousness
190
Q

What is an important condition to rule out in those with migraines and associated symptoms?

A

Stroke/ TIA

191
Q

What can sometimes cause the abrupt end to symptoms of migraines (2)?

A
  • Vomiting
  • Sleeping
192
Q

What is the types of pain experienced in a migraine?

A

Unilateral moderate - severe throbbing headache
may come on quickly or gradually

193
Q

What are some associated symptoms with migraines (other than headache) (5)?

A
  • Nausea/ vomiting
  • Photo/phono/osmo phobia
  • Aura
  • Motion sickness
  • Facial weekness
194
Q

What are some triggers for migraines (8)?

A
  • Stress
  • Over/under sleeping
  • Caffeine
  • Chocolate
  • Alcohol
  • Dehydration
  • Menstruation
  • Exercise/ orgasm
195
Q

How are migraines managed acutely first line?

A

Triptans (e.g. sumatriptan) + NSAID/ paracetamol

196
Q

What is the mechanism of triptans?

A

Serotonin receptor agonist
various effects including cranial vasoconstriction

197
Q

What are some contraindications for triptans (3)?

A
  • Hypertension
  • CAD
  • Stroke
    things vasoconstriction would negatively affect
198
Q

How are migraines treated prophylactically (2)?

A
  • 1st = Propanolol
  • 2nd = TCAs e.g. amitriptyline
199
Q

What is given as migraine prophylaxis first line in asthmatics?

A

Topiramate

200
Q

What is important to check in females diagnosed with migraines?

A

Take them off oral contraceptive pill

201
Q

What type of pain is felt in those with cluster headaches?

A

Severe unilateral pain, usually around the eye

202
Q

What is the pattern of attacks seen in cluster headaches?

A

Periods of pain 15min - 3hours, 3-4 times per day, for 4-12 weeks, followed by a period of pain free lasting weeks, months or years

203
Q

What are some risk factors for cluster headaches (4)?

A
  • Male
  • 30-50
  • Genetics/ family history
  • Smoking
204
Q

What are some other features of cluster headaches other than pain (4)?

A
  • Ptosis
  • Red, swollen watery eye
  • Rinorrhoea
  • Miosis
205
Q

How are cluster headaches treated acutely (2)?

A
  • SC triptans (sumatriptan)
  • High flow oxygen 100%
206
Q

How are cluster headaches treated with prophylaxis?

A

Verapamil (CCB)

207
Q

What is the presentation of a patient with trigeminal neuralgia?

A

Shooting/ stabbing/ electric shock pain usually on ONE side of the face

208
Q

Where can trigeminal neuralgia affect?

A

Any combination of the trigeminal nerve branches:
* V1 ophthalmic
* V2 maxillary
* V3 mandibular

209
Q

What condition is trigeminal neuralgia associated with?

A

Multiple sclerosis

210
Q

What are some other risk factors for trigeminal neuralgia other than multiple sclerosis (2)?

A
  • Female
  • Older age
211
Q

What is the treatment for trigeminal neuralgia?

A
  • 1st = Carbamazepine
  • Surgical intervention
212
Q

What is the most common secondary headache?

A

Medication overuse headache

213
Q

How many days per months should analgesia be taken for a headache to be termed a medication overuse headache?

A

15/ 30 days
10/30 for opiates

214
Q

What often precedes sinusitis?

A

Viral infection

215
Q

Where is pain felt in sinusitis?

A

Areas above the eyebrows and below the eyes

216
Q

When might sinusitis need to be treated?

A

After 10 days

217
Q

How is sinusitis treated (2)?

A
  • Steroid nasal spray
  • Penicillin V (phenoxymethylpenicillin)
218
Q

What is giant cell arteritis?

A

Large cell vasculitis mainly affecting temporal artery

219
Q

What are some risk factors for GCA (3)?

A
  • Female
  • > 50 years
  • Caucasian
220
Q

What are the signs/ symptoms of GCA (3)?

A
  • Jaw claudication
  • Temporal tenderness
  • Amaurosis fugax
221
Q

How is GCA investigated (2)?

A
  • Bloods = raised ESR
  • Temporal artery biopsy = granulomas + skip lesions
222
Q

How is GCA treated (2)?

A
  • IV methylprednisolone (if vision loss)
  • PO prednisolone (if no vision loss)
223
Q

What is an epileptic seizure?

A

Transient episodes of abnormal electrical activity in the brain

224
Q

What is another type of seizure (not epileptic)?

A

Non-epileptic seizure (functional seizure)

225
Q

What are some causes of non-epileptic seizures (5)?

A
  • Psychological
  • Syncope
  • Hypoglycaemia
  • Arrhythmias
  • Functional neurological disorder
226
Q

What are two ways to differentiate non epileptic seizures from epileptic seizures?

A
  • Epileptic = eyes open
  • Non-epileptic = injuries less common
227
Q

What defines epilepsy (in terms of when the seizures happen)?

A

2 or more unprovoked seizures that occur more than 24 hours apart

228
Q

What are some causes of seizures (8)?

A
  • Epilepsy (idiopathic)
  • Vascular
  • Infections
  • Fever
  • Metabolic/ electrolyte disturbances
  • Trauma
  • Eclampsia
  • Autoimmune disease e.g. SLE
229
Q

What are some conditions associated with epilepsy (5)?

A
  • Brain tumours
  • NFM1
  • Dementia
  • Cerebral palsy
  • History of trauma/ infection
230
Q

What are the features of an epileptic seizure (3)?

A
  • Eyes open
  • Synchronous movements
  • Can happen at night
231
Q

What is thought may be a cause of epilepsy?

A

Imbalances between the inhibitory GABA and excitatory glutamate neurotransmitters

232
Q

How long does an epileptic seizure typically last?

A

< 2 minutes

233
Q

What can lower the seizure threshold in those with epilepsy (4)?

A
  • Hypoglycaemia
  • Alcohol
  • Stress + lack of sleep
  • Medications (e.g. ciprofloxacin, lithium, TCAs)
234
Q

What are the phases of epileptic seizures (4)?

A
  • Prodrome
  • Aura
  • Ictal event
  • Post-ictal period
235
Q

What are symptoms of a prodrome before a seizure (3)?

A
  • Changes in mood
  • Changes in sensation
  • Changes in behaviour
236
Q

What are the symptoms of an aura associated with a seizure (5)?

A
  • Change in smell/ taste
  • Lip smacking
  • Visual changes
  • Sensory disturbances
  • Deja vu
  • Sudden emotional changes
    the beginning of the seizure - a focal seizure that then spreads to become a generalised seizure
237
Q

How long does a prodrome last before a seizure?

A

Days before the seizure

238
Q

How long does an aura last before a seizure?

A

Minutes/ seconds

239
Q

What are the symptoms associated with the post-ictal period after a seizure (4)?

A
  • Confusion
  • Drowsiness
  • Headache/ body ache
  • Emotional changes
240
Q

How long does the post-ictal period last?

A

Minutes to hours

241
Q

How are epileptic seizures classified depending on the part of the brain they affect (2)?

A
  • Generalised - bilateral, often lose consciousness
  • Focal - features confined to one region
242
Q

What are the main types of generalised seizures?

A
  • Tonic clonic
  • Absence
  • Myoclonic
  • Tonic
  • Atonic
  • Clonic
243
Q

What is the presentation of a patient with a tonic clonic seizure?

A

Loss of consciousness, muscles tense –> repeated jerking of muscles

244
Q

What other symptoms may the patient have during a tonic clonic seizure (4)?

A
  • Tongue biting
  • Incontinence
  • Groaning
  • Irregular breathing
245
Q

What is the presentation of a patient with an absence seizure?

A

Period of loss of consciousness and awareness for 10-20 seconds

246
Q

Who is most commonly affected by absence seizures?

A

Children, most adults have grown out of them

247
Q

What is the presentation of a myoclonic seizure?

A

Sudden brief muscle jerks affecting any part of the body, usually remain conscious

248
Q

What is the presentation of atonic seizures?

A

Sudden brief loss of muscle tone, consciousness maintained

249
Q

What is the presentation of tonic seizures?

A

Sudden stiffening of muscles, resulting in a fall if standing (around 20 seconds) - sometimes lose consciousness

250
Q

What is the presentation of a clonic seizure?

A

Repeated rhythmic muscle jerking in the upper body/ face (last a few minutes) - sometimes lose consciousness

251
Q

What is a feature of absence seizures on an EEG?

A

3 Hz spike

252
Q

What are the two types of focal seizures?

A
  • Simple
  • Complex
253
Q

What is the difference between a simple and complex focal seizure?

A
  • Simple = remain aware
  • Complex = lose awareness
254
Q

What are the symptoms of a focal seizure in each hemisphere of the brain?

A
  • Temporal = repeated movements + dysphasia
  • Frontal = repeated muscle twitching/ paralysis
  • Parietal = paraesthesia
  • Occipital = visual changes
255
Q

What two neurological phenomena sometimes occur with frontal lobe seizures?

A
  • Todds paralysis
  • Jacksonian marching (twitching along the motor homunculus)
256
Q

What extra brain structure is often involved in complex focal seizures?

A

Basal ganglia

257
Q

What are some differentials for epileptic-seizures (6)?

A
  • Vasovagal syncope (fainting)
  • Hemiplegic migraine
  • Psychogenic non epileptic seizures
  • Arrhythmias
  • Hypoglycaemia
  • TIA/ stroke
258
Q

How is epilepsy investigated (5)?

A
  • EEG
  • MRI/ CT
  • ECG
  • Serum electrolyte
  • BG
259
Q

What blood marker is commonly raised in those with epileptic seizures?

A

Prolactin

260
Q

How are generalised seizures treated (2)?

A
  • Sodium valproate (in all except women who may become pregnant)
  • Lamotrigine/ levetiracetam (for women of childbearing age)
261
Q

How are focal seizures treated?

A
  • 1st = Lamotrigine or levetiracetam
  • 2nd = carbamazepine
262
Q

What medication is first line in those with absence seizures?

A

Ethosuximide

263
Q

What medication is first line for myoclonic seizures (2)?

A
  • Male = sodium valproate
  • Female = levetiracetam
264
Q

What medication is first line for tonic or atonic (2)?

A
  • Male = sodium valproate
  • Female = lamotrigine
265
Q

What are some other important steps to take in the management of people with epilepsy (2)?

A
  • Cannot drive until seizure free for 1 year (must tell DVLA)
  • Advise not to swim/ operate heavy machinery
266
Q

In what way is sodium valproate teratogenic?

A

Increases likelihood of neural tube defects

267
Q

What is a side effect of lamotrigine?

A

Stephen Johnson syndrome

268
Q

What is a side effect of ethosuxamide?

A

Agranulocytosis (like clozapine)

269
Q

What AED has lots of different side effects and isn’t used very much any more?

A

Phenytoin

270
Q

What is important to tell women on AEDs?

A

Lots of them interact with hormonal contraceptives
the same goes with some other medications

271
Q

What is a severe complication of those who have seizures?

A

Status epilepticus

272
Q

What is status epilepticus?

A
  • Seizure lasting more than 5 minutes
    or
  • Multiple seizures without regaining consciousness
273
Q

How is status epilepticus treated (5)?

A
  1. ABCDE management
  2. IV lorazepam/ other benzo
  3. IV lorazepam (after 5 min)
  4. IV levetiracetam/ phenytoin/ valproate
  5. Phenobarbital/ general anaesthesia
274
Q

What is multiple sclerosis?

A

Autoimmune condition causing demyelination in the CNS

275
Q

What type hypersensitivity is MS?

A

Type 4

276
Q

What cell is attacked in MS?

A

Oligodendrocytes

277
Q

Who is typically affected by MS (2)?

A
  • Younger adults especially
  • Women (<40)
278
Q

What phase is often used to describe MS and can be useful in radiological and clinical diagnosis?

A

Disseminated in space and time
lots of parts of the body affected at different points in time

279
Q

What are some causes/ risk factors/ precipitating factors of MS (7)?

A
  • Smoking
  • EBV/ other infections
  • Obesity
  • Genetics
  • Vitamin D deficiency
  • Other autoimmune diseases
  • Female
280
Q

How quickly do symptoms of MS come on at initial presentation?

A

Over 24 hours

281
Q

How long do symptoms last at initial MS presentation?

A

Days to weeks, then improve

282
Q

What is the most common presentation of MS?

A

Optic neuritis

283
Q

What are the symptoms/ signs of optic neuritis (4)?

A
  • Unilateral reduced vision
  • Pain (with eye movement)
  • Loss of colour vision (especially red)
  • Relative afferent pupillary defect
284
Q

What is a relative afferent pupillary defect?

A

Pupil of affected eye constricts more when shining light in the contralateral eye than the affected eye

285
Q

How should optic neuritis be managed?

A
  • Urgent ophthalmology review
  • High dose steroids
286
Q

What are some other symptoms of MS other than optic neuritis (5)?

A
  • Weakness (incontinence, limb weakness, Horners syndrome)
  • Sensory symptoms (paraesthesia, trigeminal neuralgia)
  • Eye movement abnormalities
  • Ataxia
  • Hyper-reflexia
  • Intention tremor
287
Q

What is a specific sensory sign seen in MS when flexing the neck?

A

Lhermittes sign

288
Q

What other sensory sign is found in MS amongst other neurological conditions?

A

Transverse myelitis - site of inflammation in the spinal cord

289
Q

What eye movement disorder sometimes present in those with MS (2)?

A
  • Intranuclear ophthalmoplegia
  • Horizontal lateral gaze disorder
290
Q

What causes intranuclear ophthalmoplegia (INO)?

A

Lesion in the medial longitudinal fasciculus

291
Q

What is the clinical feature of INO?

A

Impaired adduction on the same side of the lesion and nystagmus in the contralateral abducting eye

292
Q

What is the clinical feature of horizontal lateral gaze disorder?

A

When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct

293
Q

What is the group of 3 signs/ symptoms found in MS known as?

A

Charcots neurological triad

294
Q

What is in charcots neurological triad?

A
  • Nystagmus
  • Dysarthria
  • Intention tremor
295
Q

What are two types of ataxia that may occur in MS?

A
  • Sensory ataxia = due to loss of proprioception (causes +ve Rombergs test)
  • Cerebellar ataxia
296
Q

What are some other causes of optic neuritis other than MS (4)?

A
  • SLE
  • Sarcoidosis
  • Infections e.g. syphilis, Lyme disease
  • Neuromyelitis optica
297
Q

What are the 4 patterns of disease in those with MS?

A
  • Clinically isolated syndrome
  • Relapsing-remitting
  • Primary progressive (never has remission)
  • Secondary progressive (started as relapsing-remitting
298
Q

How is MS investigated (3)?

A
  • MRI
  • Lumbar puncture
  • NCS = decreased velocity (due to demyelination)
299
Q

What would be suggestive of MS on a lumbar puncture?

A

Oligoclonal bands

300
Q

What criteria are sometimes helpful in the diagnosis of MS?

A

Mc Donald criteria

301
Q

How are relapses of MS treated (2)?

A
  • Methylprednisolone
  • Plasmapheresis + IV Ig (if severe)
302
Q

What sometimes precipitates a flare of MS?

A

Infections!!

303
Q

How is MS managed in the long term?

A

Disease modifying drugs

304
Q

What are some disease modifying drugs used to treat MS (3)?

A
  • Natalizumab
  • Glatiramer
  • Beta interferon
305
Q

What is a complication of some of the disease modifying therapies used in MS?

A

Progressive multifocal leukoencephalopathy (reactivation of the JC virus - living in glial cells)

306
Q

What are some differential diagnoses for MS?

A
  • Migraine with aura
  • Stroke
  • Hypoglycaemia/ hypothyroidism
  • Infections
  • Brain tumour
  • Neuromyelitis optica
307
Q

What is neuromyelitis optica?

A

Sister disease to MS with lots of similar symptoms but WORSE
only affects eyes and cord (not brain)

308
Q

What are 3 anterior horn diseases?

A
  • MND = mc
  • Poliomyelitis
  • Spinal muscular atrophy
  • Anterior spinal artery infarct
309
Q

What is the anterior horn of the spinal cord?

A

The place where motor information exits the spinal cord

310
Q

What are the symptoms of anterior horn diseases?

A

Purely motor symptoms

311
Q

What is usually the cause of an anterior spinal artery infarct (2)?

A
  • AAA repair
  • AD repair
312
Q

What are the signs/ symptoms of an anterior spinal artery infarct (2)?

A
  • Bilateral paralysis (below lesion)
  • Bilateral loss of pain + temp
313
Q

How is polio spread?

A

Faeco-oral spread
VERY contagious

314
Q

What is a complication of polio?

A

Attacks anterior horns –> lower motor neurone signs + paralysis

315
Q

What is spinal muscular atrophy?

A

Auto recessive condition causing floppiness that can present at various ages (including in newborns) with progressing muscle weakness

316
Q

What is motor neurone disease?

A

A neurodegenerative disorder that selectively targets motor neurones leading to their degeneration through unknown mechanisms

317
Q

What are some risk factors for motor neurone disease (4)?

A
  • Genetics/ family history
  • Exposure to toxic, viral, heavy metals
  • Smoking thought to increase risk
  • Male
318
Q

What is the typical patient affected by MND?

A

60 y/o male

319
Q

What gene mutation has been associated with MND?

A

SOD-1 gene mutation

320
Q

What condition is MND linked to?

A

Frontotemporal dementia

321
Q

What is the types of MND (4)?

A
  • Amytrophic lateral sclerosis
  • Progressive bulbar palsy
  • Progressive muscular atrophy
  • Primary lateral sclerosis
322
Q

Which neurones are affected in ALS?

A

Upper and lower motor neurones

323
Q

What are the signs/ symptoms of ALS (4)?

A
  • Muscle weakness + waisting
  • Muscle fasciculations
  • Dysarthria/phagia
  • Generalised fatigue
324
Q

What might a patient complain of with ALS to a GP in the initial stages (3)?

A
  • More clumsy
  • Dropping things
  • Tripping over
325
Q

What are the two initial presentations found in those with ALS?

A
  • Bulbar onset symptoms
  • Limb onset symptoms
326
Q

What is the prognosis for those diagnosed with ALS?

A

Poor typically 3-5 year survival

327
Q

What nerves are affected in progressive bulbar palsy?

A

Lower motor neurones of cranial nerves 9, 10, 12

328
Q

What are the signs/ symptoms of PBP (3)?

A
  • Dysphagia
  • Dysarthria
  • Tongue atrophy
    worst prognosis
329
Q

What nerves are affected in progressive muscular atrophy?

A

Lower motor neurones

330
Q

What are the signs/ symptoms of progressive muscular atrophy (3)?

A
  • Muscle weakness
  • Muscle atrophy
  • Fasciculations
331
Q

What nerves are affected in primary lateral sclerosis?

A

Upper motor neurones

332
Q

What are the signs/ symptoms of primary lateral sclerosis (2)?

A
  • Spasticity
  • Weakness
333
Q

How can progressive muscular atrophy be distinguished from ALS and PLS?

A

Absence of:
* Brisk reflexes
* Spasticity
* Babinski

334
Q

How can primary lateral sclerosis be distinguished from ALS and PMA?

A

No muscle atrophy

335
Q

How is MND diagnosed?

A

Clinically after excluding other conditions
EMG (can be abnormal), nerve conduction and MRI can help

336
Q

How is MND managed (2)?

A
  • Riluzole (can slow progression)
  • Supportive care
337
Q

How is spasticity in MND treated?

A

Baclofen

338
Q

How is drooling in MND treated?

A

Hyoscine

339
Q

What type of ventilation is often required in MND?

A

BiPAP

340
Q

What is usually the most suitable way to feed people with MND?

A

Percutaneous endoscopic gastroscopy tube (PEG)

341
Q

What symptoms are never found in those with MND (3)?

A
  • Sensory Sx
  • Eye Sx
  • Sphincters never affected
342
Q

What are the general signs/ symptoms of UMN lesions (3)?

A
  • Increased reflexes
  • Hypertonia / increased spasticity
  • Babinski sign +ve (toes upward)
343
Q

What are the general signs/ symptoms of LMN lesions (5)?

A
  • Atrophy
  • Fasciculations
  • Reduced tone
  • Reduced reflexes
  • -ve Babinski
344
Q

What is Huntington’s chorea?

A

Progressive neurodegenerative genetic disorder characterised by gradual onset of involuntary movements

345
Q

What is the inheritance pattern of Huntington’s chorea?

A

Autosomal dominant

346
Q

What gene and chromosome are affected in Huntington’s?

A

HTT (huntingtin) gene on chromosome 4

347
Q

What is the dysfunction of the DNA in huntingtons chorea?

A

Trinucleotide repeat disorder of CAG

348
Q

How many repeats of CAG are required for people to develop huntingtons?

A

36 or more

349
Q

What changes in the development of huntingtons disease are seen from generation to generation?

A

Anticipation - symptoms present earlier and more severely

350
Q

What are the signs/ symptoms of huntingtons chorea (6)?

A
  • Chorea
  • **Dementia **
  • Psychiatric issues/ depression
  • Dystonia - abnormal muscle tone –> abnormal postures
  • Dysphagia/arthria
  • Rigidity
  • Eye movement disorders
351
Q

What is usually the first symptoms of those with huntingtons?

A

Cognitive decline/ depression

352
Q

What age does huntingtons usually present?

A

30 - 50

353
Q

How is huntingtons investigated?

A
  • Clinical suspicion e.g. symptoms + family history
  • Genetic testing = diagnostic
354
Q

How is huntingtons chorea managed (2)?

A

Symptomatic relief:
* Tetrabenazine for chorea
* Valproic acid for muscle twitching

355
Q

What are the two most common causes of death in huntingtons?

A
  1. Resp arrest
  2. Suicide
356
Q

What are two neuromuscular junction disorders?

A
  • Myasthenia gravis
  • Lambert eaton myasthenia disorder
357
Q

What is myasthenia gravis?

A

Autoimmune condition attacking the neuromuscular junction

358
Q

What is the pathophysiology of MG?

A

ACh receptor antibodies bind to postsynaptic ACh receptors, blocking them and preventing stimulation by ACh

359
Q

As well as AChR antibodies what two other antibodies sometimes cause MG?

A
  • Muscle specific kinase (MuSK)
  • Low-density lipoprotein receptor-related protein 4 (LRP4)
360
Q

What is another mechanism by which ACh receptor antibodies cause symptoms?

A

They activate the compliment system leading to cell damage at postsynaptic membrane

361
Q

What are MuSK and LRP4 proteins important for the creation and organisation of?

A

Acetylcoline receptors

362
Q

What is the key feature of those with MG?

A

Fatiguability - weakness that improve with rest/ worsens with activity

363
Q

Why does MG improve with rest?

A

AChR are cleared from the postsynaptic ACh receptors when resting

364
Q

What two groups of people are most commonly affected by MG?

A
  • Men over 60 (with thyomas)
  • Women under 40 (autoimmune)
365
Q

Which two muscle groups are most commonly affected in MG?

A
  • Small muscles of the head and neck
  • Proximal muscles of the limbs
366
Q

What are the signs/ symptoms of MG (5)?

A
  • Ptosis
  • Diplopia
  • Dysphagia/arthria
  • Weakness in limbs e.g. tripping over
  • Fatigue in jaw when chewing
367
Q

What condition is there a link to with MG?

A

Thymomas (30% develop MG)

368
Q

How can you exacerbate symptoms of MG on a physical examination (3)?

A
  • Repeated blinking exacerbates ptosis
  • Prolonged upward gazing exacerbates diplopia
  • Repeated abduction of one arm will result in unilateral weakness
369
Q

How is MG investigated (3)?

A
  • Antibodies tests (85% have AChR, 10 MuSK, 5 LRP4)
  • CT/ MRI thymus (to look for thymoma)
  • Edrophonium test if any doubt
370
Q

How does edrophonium test work in MG?

A

Edrophonium blocks cholinesterase –> more ACh available at postsynaptic receptor –> weakness of muscle improves

371
Q

How is MG managed (4)?

A
  • Pyridostigmine (cholinesterase inhibitor)
  • Immunosurpression (e.g. azathioprine, prednisolone)
  • Thymectomy - can improve symptoms even if no thymoma
  • Rituximab
372
Q

What is a serious complication of MG?

A

Myasthenia crisis

373
Q

How can severity of myasthenic crisis be monitored?

A

Forced vital capacity (easy test involves counting numbers in 1 breath)

374
Q

How is myasthenic crisis managed (3)?

A
  • NIV/ mechanical ventilation
  • IVIg (against AChR)
  • Plasmapheresis
375
Q

How long does MG last?

A

It is lifelong

376
Q

What is Lambert eaton myasthenic syndrome?

A

Autoimmune condition affecting neuromuscular junction

377
Q

What is the pathophysiology of Lambert eaton syndrome?

A

Antibodies are formed against voltage gated calcium channels and destroy them –> less ACh released into the synapse

378
Q

What is the importance of voltage gated calcium channels in the NMJ?

A

They assist in the release of ACh

379
Q

What condition is usually associated with cases of Lambert eaton myasthenic syndrome?

A

SCLC (paraneoplastic syndrome)
can also occur as a primary autoimmune disorder

380
Q

What are the signs/ symptoms of Lambert eaton myasthenic syndrome?

A
  • Proximal muscle weakness e.g. difficulty climbing stairs
  • Autonomic dysfunction e.g. dry mouth, impotence
  • Reduced/ absent reflexes
381
Q

What is a key feature of Lambert eaton myasthenia syndrome?

A

Muscle strength improves after use

382
Q

How is Lambert eaton myasthenic syndrome investigated (3)?

A
  • Excluding SCLC (CT)
  • Nerve conduction studies/ EMG
  • Blood tests for voltage gated calcium antibodies
383
Q

How is Lambert eaton myasthenic syndrome managed (3)?

A
  • Diaminopyridine (amifampridine)
  • Immunosurpression
  • IVIg/ plamapheresis
384
Q

How does diaminopyradine work?

A

Blocks voltage gated potassium channels in presynaptic membrane –> prolongs depolarisation –> assists calcium channels in carrying out their function

Phase 3a conditions list flashcards (31 decks)

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