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phase 2a clinical > neuro > Flashcards

neuro Flashcards

1
Q

nerve malfunction: demyelination

A
  • schwann cell damage leads to myelin sheath disruption
  • results in marked slowing of conduction
  • seen for example- in guillain-barre syndrome
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2
Q

nerve malfunction: axonal degeneration

A
  • axon damage causes the nerve fibre to die back from periphery
  • conduction velocity initially remains mortal because axonal continuity is maintained in surviving fibres
  • typically occurs in toxic neuropathies
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3
Q

nerve malfunction: compression

A
  • focal demyelination at point of compression causes disruption of conduction
  • typically occurs in entrapment neuropathies
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4
Q

nerve malfunction: infarction

A

-micro infarction of vasa nervorum occurs in diabetes and arteritis

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5
Q

nerve malfunction: infiltration

A

infiltration occurs by inflammatory cells in leprosy and granulomas such as sarcoid and neoplastic cells

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6
Q

nerve malfunction: wallerian degeneration

A

process that results when a nerve fibre is cut and distal part of the axon that is separated from neurone’s cell body degenerates

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7
Q

neuropathy

A

pathological process affecting a peripheral nerve or nerves

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8
Q

mononeuritis multiplex

A

means that several individual nerves are affected

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9
Q

mononeuropathies

A

process affects a single nerve

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10
Q

carpal tunnel syndrome

A

most common mononeuropathy and entrapment neuropathy

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11
Q

carpal tunnel syndrome: pathology

A

results from pressure and compression on the median nerve as it passes through carpal tunnel in the wrist

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12
Q

carpal tunnel syndrome: epidemiology

A

more common in females
females have narrower wrists but same sized tendons
usually in those >30 y/o

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13
Q

carpal tunnel syndrome: causes

A

usually idiopathic

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14
Q

carpal tunnel syndrome: associations

A 
hypothyroidism
diabetes mellitus
pregnancy (3rd trimester)
amyloidosis
obesity
rheumatoid arthritis
acromegaly
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15
Q

carpal tunnel syndrome: risk factors

A

diabetes

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16
Q

carpal tunnel syndrome: presentation

A
  • aching pain in hand and arm, especially at night

- paraesthesiae (tingling or prickling) in thumb, index, middle + 1/2 ring fingers, and palm

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17
Q

carpal tunnel syndrome: differentials

A

peripheral neuropathy
motor neurone disease
MS

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18
Q

carpal tunnel syndrome: electromyography

A

shows slowing of conduction velocity in median sensory nerves across carpal tunnel
helps confirm lesion site and severity

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19
Q

carpal tunnel syndrome: phalen’s test

A

patient can only maximally flex wrist for 1 minute

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20
Q

carpal tunnel syndrome: tinel’s test

A

tapping on the nerve at the wrist induces tingling

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21
Q

carpal tunnel syndrome: treatment

A

wrist splint at night
local steroid injection
decompression surgery

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22
Q

mononeuropathies: ulnar nerve (C7-T1)

A

vulnerable to elbow trauma

compression mostly occurs at epicondylar groove at point where nerve passes between 2 heads of flexor carpi ulnaris

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23
Q

mononeuropathies: ulnar nerve (C7-T1) signs

A

weakness/wasting of:

  • medial wrist flexors
  • interossei
  • medial 2 lumbricals
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24
Q

mononeuropathies: ulnar nerve (C7-T1) treatment

A

rest and avoiding pressure on the nerve

night time soft elbow splinting

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25
Q

mononeuropathies: radial nerve (C5-T1)

A

nerve opens the fist

it may be damaged by compression against the humerus

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26
Q

mononeuropathies: radial nerve (C5-T1) signs

A 
test for wrist and finger drop
muscles involved= BEST
Brachioradialis
Extensor
Supinator
Tricep
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27
Q

mononeuropathies: phrenic nerve (C3-5)

A

consider phrenic palsy if orthopnoea (SOB while lying flat) with raised hemidiaphragm on CXR

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28
Q

mononeuropathies: phrenic nerve (C3-5) causes

A 
lung cancer
myeloma
thymoma
cervical spondylosis
phrenic nucleus lesion
thoracic surgery
HIV
muscular dystrophy
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29
Q

mononeuropathies: sciatic nerve (L4-S3)

A

damaged by pelvic tumours or fractures to pelvis or femur

lesions affect the hamstrings and all muscles below knee- foot drop

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30
Q

mononeuropathies: common peroneal nerve (L4-S1)

A

originates from sciatic nerve above the knee

often damaged as it winds around the fibular head due to trauma or sitting cross-legged

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31
Q

mononeuropathies: common peroneal nerve (L4-S1) signs

A

foot drop
weak ankle dorsiflexion
sensory loss over dorsum of foot

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32
Q

polyneuropathies

A

diffuse, symmetrical disease usually commencing peripheral

can be motor, sensory, sensorimotor and autonomic

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33
Q

polyneuropathies: classification

A

acute or chronic
sensory/motor/autonomic/mixed
demyelination, axonal degeneration or both

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34
Q

polyneuropathies: causes

A

metabolic- diabetes, renal failure, hypothyroidism
malignancy- paraneoplastic syndromes
inflammatory- guillain-barre syndrome, sarcoidosis
infections- leprosy, HIV, syphilis

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35
Q

polyneuropathies: sensory neuropathy presentation

A

numbness
affects extremities first
difficulty handling small objects
signs of trauma

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36
Q

polyneuropathies: motor neuropathy presentation

A

often rapidly progressive
weak or clumsy hands
difficulty walking and breathing

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37
Q

cranial nerve 3 lesions

A

oculomotor palsy
ptosis- dropping eyelids
fixed dilated pupil
eye down and out

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38
Q

cranial nerve 3 lesions: causes

A

raised intracranial pressure
diabetes
hypertension
giant cell arteritis

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39
Q

cranial nerve 6 lesions

A

abducens palsy

innervate lateral rectus muscle thus eyes will be adducted

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40
Q

cranial nerve 6 lesions: causes

A

MS
wernicke’s encephalopathy
pontine stroke

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41
Q

cranial nerves 3, 4 & 6 lesions

A

non functioning eye

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42
Q

cranial nerves 3, 4 & 6 lesions: causes

A

stroke
tumours
wernicke’s encephalopathy

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43
Q

cranial nerve 5 lesions

A

trigeminal palsy
jaw deviates to side of lesion
loss of corneal reflex
caused by trigeminal neuralgia, herpes zoster

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44
Q

cranial nerve 7 lesions

A

facial palsy

facial droop and weakness

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45
Q

cranial nerve 7 lesions: causes

A

bells palsy= most common lesion
fractures of petrous bones
middle ear infections

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46
Q

cranial nerve 8 lesions

A

vestibulocochlear palsy
hearing impairment
vertigo and lack of balance

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47
Q

cranial nerve 8 lesions: causes

A

skull fracture
toxic drug effects
ear infections

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48
Q

cranial nerves 9 & 10 lesions

A

glossopharyngeal and vagus palsy

gag reflex issues, swallowing issues, vocal issues

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49
Q

autonomic neuropathy

A

sympathetic and parasymp neuropathies may be isolated or part of a generalised sensorimotor peripheral neuropathy

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50
Q

autonomic neuropathy: causes

A

diabetes
guillain-barre
HIV
SLE

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51
Q

autonomic neuropathy: sympathetic presentation

A

postural hypotension- faints on standing, eating or hot bath
ejaculatory failure
reduced sweating

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52
Q

autonomic neuropathy: parasymp presentation

A

erectile dysfunction
constipation
nocturnal diarrhoea
urine retention

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53
Q

polyneuropathy: diagnosis

A

FBC, ESR, glucose, U&E, LFT, TSH, B12
CXR
urinalysis
lumbar puncture

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54
Q

polyneuropathy: treatment

A

treat the cause
foot care and shoe choice
splinting of joints

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55
Q

Nerve root lesion @ L2: Pain, weakness, reflex affected

A

pain- across upper thigh
weakness- hip flexion and adduction
reflex- N/A

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56
Q

Nerve root lesion @ L3: Pain, weakness, reflex affected

A

pain- across lower thigh
weakness- hip adduction, knee extension
reflex- knee jerk

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57
Q

Nerve root lesion @ L4: Pain, weakness, reflex affected

A

pain- across knee to medial malleolus
weakness- knee extension, foot inversion, dorisflexion
reflex- knee jerk

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58
Q

Nerve root lesion @ L5: Pain, weakness, reflex affected

A

pain- lateral shin to dorsum of foot and great toe
weakness- hip extension and abduction, knee flexion
reflex- great toe jerk

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59
Q

Nerve root lesion @ S1: Pain, weakness, reflex affected

A

pain- posterior calf to lateral foot and little toe
weakness- knee flexion, foot and toe plantar flexion
reflex- ankle jerk

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60
Q

focal scalp lesions

A

contusions

lacerations

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61
Q

focal skull lesions: fracture

A

implies considerable force
high risk of haematoma, infection and aerocele
pointed objects cause localised fractures
flat surfaces cause linear fractures

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62
Q

focal meninges lesions: extradural haematoma

A

10% of severe injuries, 15% of fatal ones
associated with skull fracture
occurs slowly over hours

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63
Q

focal meninges lesions: extradural haematoma causing death

A

brain displacement
raised intracranial pressure
herniation
infection

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64
Q

focal meninges lesions: subdural haematoma

A

usually due to tears in bridging veins- cross subdural space from superior surface of brain to midsagittal sinus
occurs slowly

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65
Q

focal meninges lesions: traumatic subarachnoid haematoma causes

A

contusions
base of skull fracture
vertebral artery dissection
intraventricular haemorrhage

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66
Q

focal brain lesions: contusions

A

superficial bruises on the brain
coup or contre coup
haemorrhagic then brown and soft for days-weeks and then indented or cavitated after months

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67
Q

focal brain lesions: lacerations

A

when contusion is sufficiently severe to teat the pia mater

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68
Q

focal brain lesions: haemorrhage

A

cerebral or cerebellar haemorrhage
superficial- due to severe contusion
deep- related to diffuse axonal injury

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69
Q

focal brain lesions: infection

A

predominantly due to skull fracture

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70
Q

diffuse brain lesions: diffuse axonal injury

A

clinicopathological syndrome of widespread axonal damage

can be caused by variety of processes

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71
Q

diffuse brain lesions: diffuse vascular injury

A

usually a result of near immediate death

multiple petechial haemorrhages throughout brain

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72
Q

diffuse brain lesions: hypoxia-ischaemia

A

often causes infarction and damage

likely in pts. with evident hypoxia, hypotension and/or raised intracranial pressure

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73
Q

diffuse brain lesions: swelling

A

occurs in 75% of pts.

causes raised intracranial pressure

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74
Q

diffuse brain lesions: congestive brain swelling

A

vasodilation and increased cerebral blood volume

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75
Q

diffuse brain lesions: vasogenic oedema swelling

A

extravasation of oedema fluid from damaged blood vessels

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76
Q

diffuse brain lesions: cytotoxic oedema swelling

A

increased water content of neurons and glia

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77
Q

coup vs. contre coup injuries

A

coup= occurs under site of impact from an object

contre coupe= occurs on side opposite area that was hit

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78
Q

traumatic axonal injury

A

focal or widespread
usually involves acceleration and deceleration of the head
mild= recovery of consciousness, variable severity of deficit
severe= unconscious from impact, can remain so or severe disability

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79
Q

meningitis

A

inflammation of the meninges

can be infective or non-infective (drugs, autoimmune)

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80
Q

encephalitis

A

inflammation of the brain

usually viral

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81
Q

encephalopathy

A

reduced level of consciousness/diffuse disease of brain substance
usually non-infective with multiple aetiologies

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82
Q

polyradiculopathy

A

inflammation of nerve roots e.g. cauda equina

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83
Q

myelitis

A

inflammation of spinal cord

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84
Q

meningitis: epidemiology

A

occurs in people of all age groups but more common in infants/elderly
meningococcal disease is notifiable to public health england

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85
Q

meningitis: aetiology; adults and children

A

neisseria meningitides- gram negative diplococci

streptococcus pneumoniae/pneumococcus

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86
Q

meningitis: aetiology; pregnancy/older adults

A

listeria monocytogenes- found in cheese so why theyre told to avoid

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87
Q

meningitis: aetiology; neonates

A

escheria coli

group b haemolytic streptococcus

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88
Q

meningitis: aetiology; immunocompromised

A

cytomegalovirus
TB
HIV
herpes simplex virus

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89
Q

meningitis: risk factors

A 
intrathecal drug administration
immunocompromised
elderly
pregnant
crowding- uni students
diabetes
IV drug abuse
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90
Q

bacterial meningitis: pathophysiology

A

typically sudden
N. meningitides is transmitted by droplet spread
pia-arachnoid is congested with polymorphs
layer of pus forms which can form adhesions causing cranial nerve palsied and hydrocephalus

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91
Q

bacterial meningitis: meningococcal septicaemia pathophsyiology

A

bacteria invades into blood

presence of endotoxin in bacteria causes inflammatory cascade

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92
Q

chronic meningitis: pathophysiology

A

e.g. TB

brain is covered in a viscous grey-green exudate with numerous meningeal tubercles

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93
Q

viral meningitis: pathophysiology

A

predominantly lymphocytic inflammatory CSF reaction w/o pus formation
little of no cerebral oedema unless encephalitis develops

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94
Q

bacterial meningitis: presentation

A

triad= headache, neck stiffness and fever
sudden onset
intense malaise, rigor, photophobia and vomiting
irritable
seizures and CNS signs
papilloedema

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95
Q

bacterial meningitis: papilloedema

A

swelling of optic disc on fundoscopy
usually bilateral
can occur over hours to weeks
caused by raised intracranial pressure

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96
Q

viral meningitis: presentation

A

triad
benign, self limiting condition lasting 4-10 days
headache may follow for some months

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97
Q

chronic meningitis: presentation

A

mycobacterium tuberculosis
long history and vague symptoms of headache, anorexia and vomiting
signs of meningeal triad are often absent or late

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98
Q

meningitis: differentials

A

aseptic meningitis- due to tumour
sub-arachnoid haemorrhage
encephalitis

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99
Q

meningitis: investigations

A

blood culture before lumbar puncture
FBC, U&E, CRP and serum glucose
throat swab

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100
Q

meningitis: investigations; lumbar puncture

A

@L4
send for microscopy and sensitivity
can give headache, paresthesia, CSF leak and damage to spinal cord

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101
Q

meningitis: lumbar puncture results; TB

A

lymphocytes
raised protein
low/normal glucose

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102
Q

meningitis: lumbar puncture results; Virus

A

lymphocytes
normal protein
normal glucose

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103
Q

meningitis: lumbar puncture results; bacteria

A

neutrophil polymorphs
raised protein
low glucose

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104
Q

meningitis: investigations; CT head

A 
exclude lesions such as tumours
to do CT before lumbar puncture:
- >60y/o
-immunocompromised
-history of CNS disease
-new onset of seizures
-GCS <14
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105
Q

meningitis: investigations; non- blanching petechial or purpuric rash

A

purpuric rash +signs of sepsis= meningococcal septicaemia
immediate IV benzylpenicillin or IV cefotaxime
don’t do lumbar puncture, instead of blood cultures

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106
Q

bacterial meningitis: treatment

A

if suspect bacterial- start antibiotics before tests come back
IV cefotaxime
if immunocompromised then add IV amoxicillin to cover listeria
consider steroids, dexamthasone to reduce oedema

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107
Q

encephalitis: epidemiology

A

infections are most frequent in children and elderly- mainly viral cause
more common in immunocompromised

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108
Q

encephalitis: viral aetiology

A 
herpes simplex virus 1 and 2
varicella zoster
epstein barr
HIV
mumps and measles
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109
Q

encephalitis: non viral aetiology

A

bacterial meningitis
TB
malaria

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110
Q

encephalitis: risk factors

A

extremes of age

immunocompromised

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111
Q

encephalitis: pathophysiology

A

disease which mostly affects the frontal and temporal lobes resulting in decreased consciousness, confusion and focal signs

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112
Q

encephalitis: general presentation

A

whole brain affected- problems with consciousness
can be abrupt in onset
triad= fever, headache and altered mental status

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113
Q

encephalitis: early presentation

A

begins with features of viral infection

fever, headache, myalgia, fatigue and nausea

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114
Q

encephalitis: progressive presentation

A 
personality and behavioural changes
decreased consciousness, confusion and drowsiness
hemiparesis, dysphasia
seizures
coma
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115
Q

encephalitis: differentials

A

meningitis
stroke
brain tumour

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116
Q

encephalitis: MRI

A

shows area of inflammation and swelling, generally in temporal lobes in HSV

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117
Q

encephalitis: electroencephalography

A

shows periodic sharp and slow wave complexes

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118
Q

encephalitis: lumbar puncture

A

CSF shows elevated lymphocyte count

viral detection by CSF, PCR is highly sensitive for herpes simplex and varicella zoster

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119
Q

encephalitis: treatment

A

if viral then immediate treatment with anti-viral- IV aciclovir
anti seizure medication- primidone

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120
Q

herpes zoster

A

shingles
virus remains latent in sensory ganglia
caused by reactivation of varicella zoster (chicken pox) usually within the dorsal root ganglia

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121
Q

herpes zoster: epidemiology

A

90% of children exposed to chicken pox before age of 16

can affect all ages but seen in elderly

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122
Q

herpes zoster: aetiology

A

varicella zoster virus

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123
Q

herpes zoster: risk factors

A

increasing age
immunocompromised
HIV
bone marrow transplants

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124
Q

herpes zoster: pathophysiology

A

viral infection affecting peripheral nerves
when latent virus is reactivated in dorsal root ganglia it travels down the affected nerve via sensory root- dermatomal distribution
result in perineural and intramural inflammation

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125
Q

herpes zoster: presentation

A

pain and paresthesia in dermatomal distribution
malaise, myalgia, headache and fever
rash

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126
Q

herpes zoster: rash presentation

A

consists of papules and vesicles restricted to same dermatome
neuritic pain
crust formation and drying occurs over next week w/ resolution in 2-3 weeks
infectious until lesions are dried

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127
Q

herpes zoster: differentials

A

before rash:
pain in chest or abdo pain- cholecystitis or renal stones
cluster headaches or migraine

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128
Q

herpes zoster: diagnosis

A

rash is virtually diagnostic

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129
Q

herpes zoster: treatment

A

oral antiviral therapy w/i 72 hours of rash onset (aciclovir x5 daily)
topical antibiotic for secondary infection of rash
analgesia for pain

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130
Q

herpes zoster: post herpetic neuralgia

A

pain lasting more than 4 months after shingles
occurs in 10%
burning, intractable pain
responds poorly to analgesics

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131
Q

herpes zoster: post herpetic neuralgia treatment

A

tricyclic antidepressant- amitriptyline
anti-epileptic- gabapentin
anti-convulsant- carbamezapine

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132
Q

tetanus: pathology

A

inoculation through skin with clostridium tetani spores- found in soil
bacteria produce toxins such as tetanolysin- tissue destruction
tetanospasmin- clinical tetanus

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133
Q

tetanus: pathogenesis

A

tetanospasmin can travel retrogradely along axons

interferes with neurotransmitter release, increased neuron firing, unopposed muscle contraction and spams

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134
Q

tetanus: generalised presentation

A

risus sardonicus- abnormal, sustained spasm of facial muscles that appears to produce grinning
opisthotonos- spasm of muscles causing backward arching of the head, neck and spine

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135
Q

tetanus: localised presentation

A

e.g.

injury to R hand, 2 days later unopposed flexion of fingers and spasm in forearm

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136
Q

tetanus: prevention

A

better than cure

vaccinate

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137
Q

tetanus: symptomatic treatment

A

supportive- muscle relaxants, paracetamol
immunoglobulin to mop up toxin
metronidazole to clear residual bacteria

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138
Q

rabies: pathology

A

caused by rabies lyssavirus, formerly rabies virus
kills 35-50 thousand/yr
inoculation through skin with saliva of rabid animals
travels retrogradely along nerves

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139
Q

rabies: incubation

A

depends on size and site of inoculation

min 2 weeks, max 2 years

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140
Q

rabies: presentation

A

paresthesia at bite site
reaches CNS- furious or paralytic presentation
once symptomatic, invariably fatal, >99.9%

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141
Q

rabies: treatment

A

managed with sedatives

prophylaxis- PrEP (vaccination) or PEP

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142
Q

dementia

A

a syndrome caused by a number of brain disorders which cause memory loss, difficulties with thinking, problem solving or language as well as difficulties with activities of daily living

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143
Q

dementia: epidemiology

A

rare under 55 y/o
prevalence rises with age
AD more common in females than males

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144
Q

alzheimer’s dementia: aetiology

A

50%
most common cause
degeneration of cerebral cortex
accumulation of beta-amyloid peptide, a degradation product of amyloid precursor protein- results in progressive neuronal damage

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145
Q

vascular dementia: aetiology

A

25%
brain damage due to cerebrovascular disease, either major stroke, multiple smaller unrecognised strokes
presents with signs of vascular pathology

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146
Q

lewy-body dementia: aetiology

A

15%
deposition of abnormal protein with neurones in brain stem and neocortex
associated with parkinson’s

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147
Q

fronto-temporal dementia: aetiology

A

specific degeneration/atrophy of frontal and temporal lobes of the brain
behavioural and personality change, early preservation of episodic memory and spatial orientation

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148
Q

dementia: risk factors

A 
family history
age
down's syndrome
alcohol use, obesity, high BP
atherosclerosis
depression
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149
Q

alzheimer’s dementia: presentation

A

insidious onset with steady progression over years
short term memory loss is usually the most prominent early symptoms
slow disintegration of personality and intellect
decline in language skills

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150
Q

vascular dementia: presentation

A

stepwise deterioration with declines followed by short periods of stability
history of TIAs and/or strokes
evidence of arthropathy

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151
Q

dementia: presentation of Lewy bodies

A 
fluctuating cognition with pronounced variation in attention and alertness
persistent memory loss
impairment in attention
depression and sleep disorders
visual hallucinations
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152
Q

dementia: differentials

A

substance abuse
hypothyroidism
huntington’s

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153
Q

dementia: investigations

A

mini mental state examination commonly used to screen for cognitive function
MRI to see atrophy

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154
Q

dementia: prevention

A

no specific therapy
healthy behaviour- smoking cessation, good diet, low alcohol
>6 leisure activities lowers risk

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155
Q

dementia: supportive care

A

socially active- sees friends and families
cognitively active
specialist memory service

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156
Q

multiple sclerosis

A

chronic autoimmune, T-cell mediated inflammatory disorder of the CNS in which there are multiple plaques of demyelination w/i brain and spinal cord

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157
Q

multiple sclerosis: epidemiology

A

begins early adulthood, typically 20-40 y/o
more common in females
more common in white populations

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158
Q

multiple sclerosis: aetiology

A

not understood

combination of genetics and environment

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159
Q

multiple sclerosis: pathophysiology

A

autoimmune mediated demyelination at multiple CNA sites- targeting oligodendrocytes
thought to be T cell mediated- activate B cells to produce auto-antibodies against myelin
myelin sheath regenerates but it is less efficient and when exposed to high heat conduction decreases drastically

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160
Q

types of multiple sclerosis: relapsing & remitting

A

80%- most common
symptoms occur in attacks with onset over days and typically recovery- partial or complete
periods of good health or remission are followed by sudden symptoms or relapses

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161
Q

types of multiple sclerosis: secondary progressive

A

follows from relapsing and remitting (75% of RR get secondary)
late stage that consists of gradually worsening symptoms with fewer remissions

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162
Q

types of multiple sclerosis: primary progressive

A

gradually worsening disability w/o relapses or remissions

typically presents later and is associated with fewer inflammatory changes on MRI

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163
Q

multiple sclerosis: presentation

A 
usually initially monosymptomatic 
symptoms may worsen with heat
numbness and tingling in limbs
leg weakness
trigeminal neuralgia
constipation
intension tremor
amnesia
sexual dysfunction
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164
Q

multiple sclerosis: unilateral optic neuritis presentation

A

pain in one eye on eye movement

reduced central vision

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165
Q

multiple sclerosis: brainstem demyelination presentation

A

diplopia, vertigo, facial numbness, dysarthria or dysphagia

clumsy/useless hand or limb due to loss of proprioception

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166
Q

multiple sclerosis: differentials

A

hereditary spastic paraplegia
cerebral variant of SLE
sarcoidosis
HIV

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167
Q

multiple sclerosis: investigations

A

requires 2+ attacks affecting different parts of CNS- 2 lesions disseminated in time and space
exclude differentials with inflammatory markers, auto-antibodies, calcium and LFTs

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168
Q

multiple sclerosis: MRI brain and spinal cord

A

diagnostic
95% have periventricular lesions
over 90% show discrete white matter abnormalities

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169
Q

multiple sclerosis: lumbar puncture

A

CSF examination shows oligoclonal IgG bands in over 90% of cases- not specific to MS

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170
Q

multiple sclerosis: electrophysiology investigation

A

visual evoked potential studies

delayed nerve conduction suggests demyelination

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171
Q

multiple sclerosis: acute relapse treatment

A

IV methylprednisolone
<3 days can shorten relapse
use steroid sparingly and aim to use less than twice a year

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172
Q

multiple sclerosis: treatment for frequent relapse

A

SC interferon 1B or 1A are anti-inflammatory cytokine and reduce relapses by 30% in active remitting MS and reduce lesion accumulation
dimethyl fumarate
monoclonal antibodies

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173
Q

multiple sclerosis: monoclonal antibodies

A

disease modifying agents
IV alemtuzumab- targets T cells
IV natalizumab- against VLA-4 receptors that allow autoimmune cells to cross BBB

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174
Q

multiple sclerosis: symptomatic treatment

A

urinary urgency/frequency- self catheterisation
incontinence- anti cholinergic alpha blocker (doxazosin)
spasticity- physio, baclofen, botox injection

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175
Q

epilepsy: definition

A

recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain
manifests as seizures
chronic disorder- at least 2 seizures to be diagnosed

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176
Q

epilepsy seizure definition

A

paroxysmal/unprovoked event in which changes in behaviour, sensation or cognitive are caused by excessive, hypersynchronous neuronal discharges in the brain

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177
Q

epilepsy: epidemiology

A

common
highest at extremes of age- <20 y/o or >60 y/o
can go into remission

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178
Q

epilepsy: aetiology

A 
2/3rds idiopathic
often familial
stroke
space occupying lesion- tumour
alcohol withdrawal
cortical scarring
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179
Q

epilepsy: risk factors

A 
family history
premature babies
abnormal blood vessels in brain
alzheimers
use of drugs- cocaine
stroke/tumour/infection
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180
Q

epilepsy: elements of a seizure

A

prodome
aura
post-ictally

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181
Q

epilepsy pathophysiology: prodome

A

lasting hours or days
may rarely precede the seizure
not part of seizure, results in change of mood/behaviour

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182
Q

epilepsy pathophysiology: aura

A

part of seizure
patient is aware and may precede its other manifestations
strange feeling in gut, deja vu, strange smells/lights
implies focal seizure often but not necessarily temporal lobe

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183
Q

epilepsy pathophysiology: post-ictally

A 
after seizure
headache
confusion
myalgia
temporary weakness if its in motor cortex
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184
Q

epilepsy pathophysiology: primary generalised

A

simultaneous onset of electrical discharge throughout whole cortex
no localising features referable to one hemisphere
bilateral, symmetrical manifestations
loss of consciousness

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185
Q

epilepsy pathophysiology: partial/focal seizures

A

features referable to part of one hemisphere/lobe

often seen with underlying structural disease

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186
Q

epilepsy presentations: generalised tonic-clonic seizure

A

often no aura
loss of consciousness
tonic= rigid, stiff limbs, falls to floor
clonic=bilateral, rhythmic muscle jerking, seconds to minutes
eyes open and tongue often bitten
incontinence

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187
Q

epilepsy presentations: typical absence seizure

A

usually disorder of childhood
ceases activity, stares and pales for a few seconds
often don’t realise anything happened
tend to develop tonic-clonic in later life

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188
Q

epilepsy presentations: myoclonic seizure

A

sudden isolated jerk, face or trunk
patient may be thrown suddenly to ground
violently disobedient limb

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189
Q

epilepsy presentations: tonic seizure

A

sudden sustained increased tone with cries/grunts

not followed by jerking

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190
Q

epilepsy presentations: atonic seizure

A

sudden loss of muscle tone and cessation of movement

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191
Q

epilepsy presentations: simple partial seizure

A

not affecting consciousness or memory
awareness if unimpaired in motor, sensory, autonomic or psychic focal seizures
no post-ictal

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192
Q

epilepsy presentations: complex partial seizure

A

affect awareness or memory before, during or immediately after seizure
commonly arise from temporal lobe- speech, memory and emotion
post-ictal confusion

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193
Q

epilepsy presentations: partial seizure w/ secondary generalisation

A

in 2/3rds of patients with partial seizures the electrical disturbance starts focally then spreads
causes a secondary generalised seizure- usually convulsive

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194
Q

epilepsy presentations: temporal lobe involvement

A 
aura 80%
deja-vu
auditory hallucinations
funny smells
anxiety
out of body experience
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195
Q

epilepsy presentations: frontal lobe involvement

A

motor features such as posturing or movement of leg
Jacksonian march= seizure marches up or down motor homunculus starting in face or thumb
post-ictal Todd’s palsy= paralysis of limbs involved

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196
Q

epilepsy presentations: occipital lobe involvement

A

visual phenomena

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197
Q

epilepsy presentations: epilepsy rather than syncope

A 
tongue biting
head turning
muscle pain
loss of consciousness
cyanosis
post-ictally
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198
Q

epilepsy presentations: syncope rather than epilepsy

A

syncope= loss of consciousness due to hypoperfusion to the brain

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199
Q

epilepsy presentations: non-epileptic seizure vs. epileptic

A

non-epileptic= situational, longer, close mouth/eyes, do not result from sleep, no incontinence

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200
Q

epilepsy differential diagnosis

A 
postural syncope
cardiac arrhythmia
TIA
migraine
panic attack
non-epileptic seizure
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201
Q

epilepsy investigations

A

EEG
MRI/CT head
blood tests
genetic testing

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202
Q

epilepsy investigations: electroencephalogram

A

not diagnostic
performed to support diagnosis of epilepsy when history suggests
may help determine seizure type

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203
Q

epilepsy investigations: MRI

A

imaging hippocampus studies epilepsy

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204
Q

epilepsy investigations: CT head

A

used in emergency to look for space occupying lesion

identify or exclude structural abnormalities that could cause symptoms

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205
Q

epilepsy investigations: blood tests

A

done to rule out metabolic cause
discover comorbidities
FBC, electrolytes, Ca2+, renal function

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206
Q

epilepsy treatment

A

generally drugs are not advised after just one fit unless the risk of recurrence is high
drug resistant to drug treatment in 1/3rd of patients

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207
Q

epilepsy treatment: emergency measures

A

ensure they harm themselves as little as possible
check glucose
prolonged seizure (>3min) or repeated are treated with rectal/IV diazepam or loraezepam x2
IV phenytoin loading

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208
Q

epilepsy treatment: for generalised tonic-clonic seizures

A

oral sodium volproate- S/E =weight gain and hair loss
oral lamotrigine- S/E= maculopapular rash, blurred vision
oral carbamazepine- S/E= diplopia, rashes, impaired balance

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209
Q

epilepsy treatment: for absence seizure

A

oral sodium valproate
oral lamotrigine
oral ethosuximide

210
Q

epilepsy treatment: for partial/focal seizure

A

carbamazepine
sodium valproate
lamotrigine

211
Q

epilepsy treatment: neurosurgical

A

if drugs don’t work

if a single defined cause if identified such as hippocampal sclerosis or tumour

212
Q

epilepsy treatment: advice to patients

A

must inform DVLA and cannot drive until they have been free of daytime seizures for at least one year

213
Q

epilepticus

A

repeated seizures with brief periods of recovery can lead to epilepticus
medical emergency
risk of death if generalised tonic-clonic

214
Q

epilepticus: causes

A

abruptly stopping anti-epileptic treatment
alcohol abuse
poor compliance to therapy

215
Q

sudden unexpected death epilepsy

A

more common in uncontrolled epilepsy

can be related to nocturnal seizure-associated apnoea and asystole

216
Q

TIA definition

A

transient ischaemic attack= a brief episode of neurological dysfunction due to temporary focal cerebral ischaemia w/o infarction

217
Q

TIA epidemiology:

A

15% of first strokes are preceded by TIA

more common in males

218
Q

TIA aetiology

A 
small vessel occlusion 
atherothromboembolism from carotid
cardioembolism from microemboli
hyperviscosity
hypoperfusion
219
Q

TIA aetiology: cardioembolism

A

microemboli come from:
mural thrombus post MI or AF
valve disease
prosthetic valve

220
Q

TIA aetiology: hyperviscosity

A

polycythaemia
sickle cell anaemia
extremely raised white cell count
myeloma

221
Q

TIA aetiology: hypoperfusion

A

consider in younger people
cardiac dysrhythmia
postural hypotension

222
Q

TIA risk factors

A 
increased age
hypertension
smoking
diabetes
heart disease
past TIA
excess alcohol
clotting disorder
combined oral contraceptive
223
Q

TIA pathophysiology

A

most common cause is cerebral ischaemia- lack of oxygen and nutrients to brain causes cerebral dysfunction
usually short lived so symptoms last 5-15 mins and resolves itself

224
Q

TIA presentation: carotid artery

A

supplies frontal and medial part of cerebrum
occlusion may cause weak, contralateral symptoms of limbs
hemiparesis (weakness on entire side of body)
dysphasia
amaurosis fugax

225
Q

TIA presentation: amaurosis fugax

A

sudden transient loss of vision in one eye

occurs due to reduction in retinal, ophthalmic or ciliary blood flow leading to temporary retinal hypoxia

226
Q

TIA presentation: vertebrobasilar artery

A 
diplopia- double vision
vertigo
vomiting
ataxia- no control over body 
hemisensory loss
hemianopia vision loss
227
Q

stroke definition

A

cerebrovascular accidents

syndrome of rapid onset of neurological deficit caused by focal, cerebral, spinal or retinal infarction

228
Q

stroke epidemiology

A 
3rd most common cause of death in high income countries
11% of all deaths in UK
leading cause of adult disability
incidence increases with age
more common in males
229
Q

stroke aetiology: ischaemic

A 
80%
small vessel occlusion/thrombosis
cardiac emboli from AF or infective endocarditis 
large artery stenosis
hypoperfusion
vasculitis
hyperviscosity
230
Q

stroke aetiology: CNS bleeds

A 
17%
trauma
aneurysm rupture
anticoagulation
thrombolysis
artery dissection
subarachnoid haemorrhage
231
Q

stroke aetiology: young people

A 
vasculitis 
thrombophilia
subarachnoid haemorrhage
carotid artery dissection
venous sinus thrombosis
232
Q

stroke aetiology: elderly

A 
thrombosis in situ
atherothromboembolism
heart emboli
CNS bleed
sudden drop in BP
233
Q

stroke risk factors

A 
male
black or asian
hypertension
past TIA
smoking
diabetes
increasing age
heart disease
alcohol
AF
hypercholesterolaemia
combined contraceptive
234
Q

stroke pathophysiology: ischaemic

A

arterial disease and atherosclerosis is main pathological process

235
Q

stroke pathophysiology: cardio-embolic stroke

A

AF
cardiac valve disease
infective vegetations due to endocarditis
fat emboli

236
Q

stroke pathophysiology: venous sinus thrombosis

A

very rare
thrombosis in intracranial venous sinuses
cortical infarction, seizures and raised intracranial pressure result

237
Q

stroke pathophysiology: haemorrhagic

A

hypertension resulting in micro aneurysm rupture
cerebral amyloid angiopathy
carotid/vertebral artery dissection

238
Q

stroke presentations: anterior cerebral artery

A

leg weakness
sensory disturbance in legs
gait apraxia
drowsiness

239
Q

stroke presentations: middle cerebral artery

A

contralateral arm and leg weakness
contralateral sensory loss
hemianopia
aphasia- cant understand or produce speech
dysphasia- deficiency in speech generation
facial droop

240
Q

stroke presentations: posterior cerebral artery

A 
contralateral homonymous hemianopia 
cortical blindness
visual agnosia but can see
prosopagnosia- cant see faces
colour naming problems
241
Q

stroke presentations: vertebrobasilar artery

A

more catastrophic due to wide region supplied
locked in is more likely
motor deficits- hemiparesis or tetraparesis
facial paralysis
vertigo
visual disturbance
altered consciousness

242
Q

stroke presentations: lacunar

A

small subcortical strokes
unilateral weakness of face and arm, arm and leg or all three
pure sensory loss

243
Q

stroke presentations: haemorrhage or ischaemic

A

no reliable way to distinguish from presentation
haemorrhage is more associated with severe headache
if on anticoagulants- assume haemorrhage

244
Q

stroke differentials

A

exclude hypoglycaemia
migraine
intracranial lesion
syncope

245
Q

stroke investigations: urgent CT head

A

before treatment
rules out haemorrhage before starting thrombolysis
infarct is seen as low density lesion

246
Q

stroke investigations: pulse, BP, ECG

A

look for AF

be careful treating high BP as fall in 20% can compromise cerebral perfusion

247
Q

stroke investigations: bloods

A

look for thrombocytopenia and polycythaemia in FBC

rule out hypoglycaemia

248
Q

stroke treatment: maximise reversible ischaemic tissue

A

ensure hydration
keep oxygen sats >95%
if ischaemia proceed to thrombolysis

249
Q

stroke treatment: thrombolysis

A

can be given up to 4.5 hours post onset of symptoms
give tissue plasminogen activator- IV alteplase
then antiplatelet therapy- clopidogrel
if time of onset unknown and thrombolysis is unsuitable give aspirin daily for 2 weeks then lifelong clopidogrel

250
Q

stroke treatment: thrombolysis contraindications

A 
recent surgery in last 3 months
recent arterial puncture
history or active malignancy 
evidence of brain aneurysm 
on anticoagulants
clotting disorder
251
Q

treatment for haemorrhagic stroke

A 
frequent GCS monitoring
antiplatelets contraindicated
reverse all anticoagulants
control hypertension
surgery
252
Q

risk management for stroke prevention

A

platelet treatment- aspirin+ dipyridamole/clopidogrel
simvastatin for cholesterol
AF treatment- warfarin
ramipril for BP

253
Q

TIA differentials

A

until full recovery- impossible to differentiate from stroke
hypoglycaemia
intracranial lesion
syncope

254
Q

TIA investigations

A

carotid artery doppler ultrasound to look for stenosis
CT angiography to see extent of stenosis
ECG to look for MI ischaemia or AF

255
Q

TIA investigations: bloods

A 
FBC- polycythaemia
ESR raised in vasculitis
Glucose- hypoglycaemia
creatinine
cholesterol
256
Q

TIA treatment: ABCD2 score risk of stroke

A

Age >60= 1
Blood pressure >140/90= 1
Clinical features- unilateral weakness= 2, speech disturbance w/o weakness= 1
Duration of symptoms- >1hr= 2, 10-59mins= 1
Diabetes= 1

score >6 strongly predicts a stroke and should be referred immediately

257
Q

TIA treatment: antiplatelet drugs

A

aspirin and dipyridamole for 2 weeks, then lower dose
P2Y12 inhibitor long term- clopidogrel
anticoagulant if they have AF or mitral stenosis- warfarin

258
Q

TIA treatment: control risk factors

A

long term statin- simvastatin
antihypertensives- ace inhibitors, ramipril or angiotensin receptor blocker, candesartan
improve diet
stop smoking

259
Q

subarachnoid haemorrhage

A

spontaneous bleeding in subarachnoid space- between arachnoid layer of meninges and pia mater

260
Q

subarachnoid haemorrhage: epidemiology

A

35-65 y/o

5% of strokes

261
Q

subarachnoid haemorrhage causes: rupture of saccular aneurysms

A

80%
e.g. berry aneurysms
rupture in circle of willis @
junction of posterior communicating artery with internal carotid/ anterior communicating w/ anterior cerebral

262
Q

subarachnoid haemorrhage causes: atriovenous malformation

A

10%
vascular development malformation often with a fistula between arterial and venous systems causing high flow through AVM
and high pressure arterialisation of draining veins

263
Q

subarachnoid haemorrhage: rare causes

A

bleeding disorder
mycotic aneurysms
acute bacterial meningitis
tumours

264
Q

subarachnoid haemorrhage: risk factors

A 
hypertension
known aneurysm
family history
smoking
bleeding disorders
265
Q

subarachnoid haemorrhage: pathophysiology

A

most common cause is ruptured aneurysm
leads to tissue ischaemia
rapid raised ICP as blood acts as space occupying lesion
long term pressure on brain results in deficits

266
Q

subarachnoid haemorrhage: presentation

A 
sudden, sever headache
neck stiffness
vomiting 
depressed level of consciousness
coma
fixed dilated pupils
double vision
267
Q

subarachnoid haemorrhage: differentials

A

must differentiate from migraine
meningitis
cortical vein thrombosis

268
Q

subarachnoid haemorrhage investigations: ABG

A

to exclude hypoxia

269
Q

subarachnoid haemorrhage investigations: heat CT

A

gold standard
detects >90% in first 48 hours
star shaped lesion- blood filling in gyro patterns around ventricles

270
Q

subarachnoid haemorrhage investigations: lumbar puncture

A

if CT normal but SAH suspected
CSF is uniformly bloody early on
becomes xanthochromic (yellow) after several hours- bilirubin

271
Q

subarachnoid haemorrhage: treatment

A

neurosurgeon referral immediately
IV fluids to keep cerebral perfusion
administer calcium blocker to reduce vasospasm and so morbidity from ischaemia

272
Q

subarachnoid haemorrhage treatment: endovascular coiling

A

preferred to surgical clipping since has lower complication rate
promotes thrombosis and ablation of aneurysm
first line treatment where angiography shows aneurysm

273
Q

subarachnoid haemorrhage treatment: surgery

A

intracranial stents and balloon remodelling for wide-necked aneurysms

274
Q

subarachnoid haemorrhage: complications

A

rebleeding
cerebral ischaemia due to vasospasm
hydrocephalus due to blockage of arachnoid granulations
hyponatraemia

275
Q

subdural haemorrhage

A

caused by accumulation of blood in subdural space
between the arachnoid and dura mater
follows rupture of a bridging vein between cortex and venous sinus

276
Q

subdural haemorrhage: epidemiology

A

most common where patient has a small brain- alcoholics or dementia or babies

277
Q

subdural haemorrhage: pathophysiology

A

trauma results in bleeding from bridging veins between cortex and venous sinuses
haematoma forms
weeks later it autolyses due to oncotic/osmotic pressure- water is brought into haematoma causing it to enlarge
slow rise in ICP

278
Q

subdural haemorrhage: risk factors

A 
traumatic head injury
cerebral atrophy
increasing age
alcoholism
anticoagulation
279
Q

subdural haemorrhage: presentation

A

sleepiness
headache
unsteadiness
signs of raised ICP

280
Q

subdural haemorrhage: differentials

A 
stroke
dementia
CNS masses
SAH
extradural haemorrhage
281
Q

subdural haemorrhage investigations: CT head

A

diffuse spreading, hyperdense crescent shaped collection of blood
usually over one hemisphere

282
Q

subdural haemorrhage investigations: MRI head

A

for subacute haematomas and smaller haematomas

283
Q

subdural haemorrhage: treatment

A

refer to neurosurgeons- irrigation/evacuation via burr twist drill and burr hole craniotomy
address cause of trauma

284
Q

extradural haemorrhage

A

collection of blood between dura and bone

suspect this after head injury and conscious level falls or is slow to improve or there is a lucid interval

285
Q

extradural haemorrhage: aetiology

A

traumatic head injury resulting in a fracture

286
Q

extradural haemorrhage: risk factors

A

usually occurs in young adults

rare <2 y/o and >60 y/o

287
Q

extradural haemorrhage: pathophysiology

A

mainly temporal or parietal bone
causes laceration of middle meningeal artery
blood accumulates rapidly over minutes-hours between bone and dura

288
Q

extradural haemorrhage: presentation

A 
sever headache
nausea
vomiting
confusion
decreased GCS
death due resp arrest if surgical intervention not done fast enough
289
Q

extradural haemorrhage presentation: lucid interval

A

period of time between traumatic brain injury and decrease in consciousness
whilst haematoma is still small and there is still some bleeding
can last several hours

290
Q

extradural haemorrhage: differentials

A 
epilepsy 
carotid dissection
carbon monoxide poisoning
meningitis
SAH
291
Q

extradural haemorrhage investigations: CT head

A

shows hyperdense haematoma adjacent to skull- biconvex/lense shaped/lemon shaped

292
Q

extradural haemorrhage investigations: skull x ray

A

may be normal or show fracture lines crossing course of middle meningeal artery

293
Q

extradural haemorrhage: treatment

A

emergency management
IV mannitol if increased ICP
neurosurgery

294
Q

primary brain tumours: epidemiology

A

8/100,000
16th most common adult cancer
2nd most common paediatric cancer

295
Q

primary brain tumours: risk factors

A 
primary tumours more common in affluent groups
ionising radiation
vinyl chloride
immunosuppression
family history
296
Q

primary brain tumours: astrocytomas

A

most common primary brain tumour- 85-90%
glial cell in origin
graded I-IV

297
Q

primary brain tumours: grade I pilocytic astrocytomas

A

good prognosis
completely benign
paediatric tumour mainly

298
Q

primary brain tumours: grade II diffuse astrocytoma

A

prognosis >5yrs
premalignant tumour
nuclear atypia

299
Q

primary brain tumours: grade III anaplastic astrocytoma

A

prognosis 2-5 years
malignant
active growth
mitosis present

300
Q

primary brain tumours: grade IV glioblastoma multiforme

A

<1 year
most common phenotype
active growth, mitotic activity and necrosis
very malignant

301
Q

pathways to malignant gliomas: most common

A

mainly in those <50-60 y/o
initial genetic error is of glucose glycolysis
mutation of isocitrate dehydrogenase I
excess 2-hydroxyglutarate
triggers genetic instability in glial cells and subsequent inappropriate mitosis

302
Q

pathways to malignant gliomas: less common

A

more common in those >50-60 y/o
no IDH-1 mutation
catastrophic genetic mutation
poor prognosis even for low grade

303
Q

primary brain tumours: oligodendroma

A 
most common in 40-50y/o
arise from oligodendrocytes
grow slowly over several years
calcification is common
may have seizures
WHO grade II
all have IDH-1 mutation
304
Q

primary brain tumours: ependymomas

A

arise from ependymal cells

line ventricles and spinal cord

305
Q

primary brain tumours: meningiomas

A

more common in older people and women

benign and arise from arachnoid mater and may grow to a large size

306
Q

primary brain tumours: neurofibromas/schwanomas

A

solid, benign tumours that arise from schwann cells

occur principally in cerebellopontine angle

307
Q

primary brain tumours: medulloblastoma

A 
WHO grade IV
primitive small blue cell
tumour of cerebellum
in childhood
highly malignant but can respond to excision and chemo
308
Q

primary brain tumours: presentation (4 cardinal symptoms)

A

symptoms of raised ICP
progressive neurological deficit
epilepsy/seizures
lethargy

309
Q

primary brain tumours presentation: raised ICP

A

progressive headache
drowsiness
vomiting
papilloedema

310
Q

primary brain tumours presentation: raised ICP- papilloedema

A 
swelling of optic disc due to obstruction of venous return from retina 
loss of crisp optic nerve head margins
venous engorgement 
retinal oedema
haemorrhages
311
Q

primary brain tumours presentation: progressive neurological deficit

A 
depends on region affected
temporal=dysphagia.amnesia
frontal=hemiparesis/personality change/unable to make plans
parietal= hemisensory loss/dysphagia
occipital=contralateral visual defects
cerebellum=DASHING
312
Q

primary brain tumours presentation: progressive neurological deficit (DASHING)

A 
Dysdiaochokinesis
Ataxia
Slurred speech
Hypotonia
Intention tremor
Nystagmus
Gait abnormality
313
Q

primary brain tumours presentation: epilepsy/seizure

A

sinister when of recent onset

314
Q

primary brain tumours: differentials

A

other causes of space occupying lesions

aneurysm, abscess, cyst, haemorrhage, idiopathic intracranial hypertension

315
Q

primary brain tumours investigations: CT/MRI

A

determine size and location of lesion

high grade have irregular edges and high growth rates

316
Q

primary brain tumours investigations: biopsy

A

via skull burr hole

determines cancer grade

317
Q

primary brain tumours investigations: lumbar puncture

A

contraindicated when any possibility of a mass lesion- withdrawing CSF may provoke immediate coning
results in brainstem compression as it passes through foramen magnum

318
Q

primary brain tumours: treatment

A

surgery to remove mass whenever possible
chemo
oral dexamethasone
anticonvulsants for seizures- oral carbamazepine

319
Q

primary brain tumours treatment: chemotherapy for glioma

A

at same time as surgery and then for 6 weeks post op

e.g. temozolomide

320
Q

primary brain tumours treatment: oral dexamethasone

A

most powerful synthetic steroid
rapidly improves brain performance
reduces inflammation and oedema

321
Q

secondary brain tumours: common neoplasms to metastasise to CNS

A 
10x more common than primary
non small cell lung cancer
small cell lung cancer
breast cancer
melanoma
GI
renal cell
322
Q

secondary brain tumours: treatment

A

surgery if <75 y/o
radiotherapy
chemo
palliative care

323
Q

pathology of raised intracranial pressure

A

herniation haemorrhage
tonsillar herniation/coning
local deformity
decreased CSF volume

324
Q

cerebellar disease: ataxia

A

name given to a group of neurological disorders that affect balance, coordination and speech

325
Q

cerebellar disease: signs and symptoms

A 
dysarthria- slurring of speech
dysphagia- difficulty swallowing
clumsiness
intention tremor
unsteadiness
stumbling/falls
nystagmus
limb and gait ataxia
326
Q

cerebellar disease: classification of ataxia

A

congenital ataxia
episodic ataxia- attacks, resolves, reoccurs
autosomal recessive/dominant
sporadic

327
Q

cerebellar disease: autosomal recessive ataxia

A

ataxia of gait and limb
absent reflectors
complications include diabetes and cardiomyopathy

328
Q

cerebellar disease: autosomal dominant ataxia

A

most common in UK
slowly progressive with dysarthria, dysphagia and gait ataxia
stats from late 40s-early 50s

329
Q

cerebellar disease: sporadic ataxia

A

gluten ataxia

toxic effects

330
Q

cerebellar disease: investigations

A

cerebrovascular damage
primary tumours
secondary tumours hydrocephalus
MS

331
Q

neurological disorders and psychiatric presentations

A

cognitive, psychological and behavioural sequelae of CNS disorder depend on:

  • tempo of underlying disorder
  • site of brain affected
  • neurotransmitter system involved
  • individual characteristics
332
Q

neurological disorders and psychiatric presentations: tempo

A 
acute= trauma, drugs and infections. associated with delirium or confusional state
chronic= dementia
333
Q

neurological disorders and psychiatric presentations: site

A

certain brain regions are associated with particular patterns of psychological and behavioural disturbances
e.g. right hemisphere stroke can give rise to mania

334
Q

neurological disorders and psychiatric presentations: neurotransmitter

A

memory impairment in alzheimers= acetyl choline depletion

depression in parkinsons= serotonin, noradrenaline and dopamine depletion

335
Q

neurological disorders and psychiatric presentations: individual characteristics

A

age, gender, education or prior psychiatric history can affect how brain pathology can give rise to symptoms.
e.g. higher levels of education can protect against alzheimer’s

336
Q

inherited neurological disorders: Wilson’s disease

A

disorder of hepatic copper disposition

presents with personality change, mood disturbance, psychosis and cognitive impairment

337
Q

inherited neurological disorders: acute intermittent porphyria

A

metabolic disorder of haem

can give rise to acute psychosis, agitation, mania and depression

338
Q

inherited neurological disorders: neuroacanthocytosis

A

blood contains misshapen red blood cells

associated with anxiety, paranoia, depression, obsessive behaviour

339
Q

presentation of inherited neurological disorders: huntington’s

A 
subcortical dementia
anxiety
depression
personality changes
delusions
apathy
suicidal thoughts
340
Q

presentation of acquired neurological disorders: fronto-temporal dementia

A 
blunting of emotions
anxiety
egocentricity
compulsive behaviour
neglect of personal appearance
341
Q

presentation of acquired neurological disorders: left lobe dysfunction

A

presents with semantic dementia
progressive word finding difficulty
loss of language comprehension
depletion of conceptual knowledge

342
Q

presentation of acquired neurological disorders: right lobe dysfunction

A

prosopagnosia- impaired face recognition

loss of knowledge about people

343
Q

presentation of acquired neurological disorders: vascular

A

confusional states occur in 1/3 of pts. in acute stroke

focal behavioural disturbance caused by cerebral ischaemia can mimic functional disorder

344
Q

presentation of acquired neurological disorders: MS

A

fatigue
depression
mania
psychosis

345
Q

presentation of acquired neurological disorders: HIV associated dementia

A

apathy

social withdrawal

346
Q

presentation of acquired neurological disorders: variant creutzfeldt-jakob disease

A

anxiety or depression
cognitive symptoms develop
varied neurological features including pyramidal, extrapyramidal, cerebellar signs and myoclonus

347
Q

presentation of acquired neurological disorders: hypothyroidism

A 
lethargy
impaired cognition
hallucinations
delusions
often paranoid
348
Q

presentation of acquired neurological disorders: hyperthyroidism

A

anxiety
irritability
delirium
psychosis

349
Q

presentation of acquired neurological disorders: pheochromocytoma

A

chronic anxiety

paroxysmal dear akin to panic

350
Q

presentation of acquired neurological disorders: neoplastic/paraneoplastic

A

depression
paranoia
confusion
disorientation

351
Q

presentation of acquired neurological disorders: trauma

A

delirium
insidious cognitive decline
odd behaviour

352
Q

presentation of acquired neurological disorders: Wernicke’s encephalopathy

A

confusion
ataxia
ophthalmoplegia

353
Q

presentation of acquired neurological disorders: vitamin B12 deficiency

A

cognitive decline

organic psychosis

354
Q

somatisation disorders

A

when physical symptoms are caused by mental or emotional factors
mental or emotional problem is expressed as one or more physical symptom

355
Q

somatisation disorders: somatisation

A

many physical symptoms from different parts of the body

356
Q

somatisation disorders: hypochondriasis

A

fear that the minor symptoms may be due to a serious disease

357
Q

somatisation disorders: conversion disorder

A

a person has symptoms which suggest a serious disease of the brain or nerves such as total loss of vision
they develop quickly in response to stress

358
Q

somatisation disorders: body dysmorphia

A

a person spends a lot of time worried and concerned about their appearance, focussing on an apparent physical defect that others cannot see

359
Q

somatisation disorders: pain disorder

A

a person has persistent pain that cannot be attributed to a physical disorder

360
Q

dissociative disorders

A

a range of conditions that can cause physical or psychological problems
can be short lived, following trauma, and resolve on their own
can last a long time

361
Q

dissociative disorders: of movement or sensation

A

includes convulsions
paralysis
and loss of sensation

362
Q

dissociative disorders: dissociative amnesia

A

periods where they cannot remember information about themselves
may forget a learnt skill

363
Q

dissociative disorders: identity disorder

A

may feel uncertain about their identity and who they are

may feel presence of other identities

364
Q

spinal cord disease: hemiplegia

A

paralysis of one side of the body caused by lesion of brain

365
Q

spinal cord disease: paraplegia

A

paralysis of both legs

always caused by spinal cord lesion

366
Q

spinal cord disease: upper motor neurone signs

A

contralateral to lesion
indicate lesion above anterior horn cell
increased muscle tone

367
Q

spinal cord disease: lower motor neurone signs

A

ipsilateral to lesion
indicate lesion is either in anterior horn cell or distal to anterior horn cell
decreased muscle tone

368
Q

spinal cord disease: spondylolisthesis

A

slippage of one vertebra over the one below
nerve root comes out above the disc
therefore root affected will be one below disc herniation

369
Q

spinal cord disease: spondylosis

A

degenerative disc disease

370
Q

spinal cord disease: myelopathy

A

caused by spinal cord compression

upper motor neurone signs

371
Q

spinal cord disease: radiculopathy

A

caused by spinal root compression
lower motor neurone signs
pain down dermatome
weakness in myotome

372
Q

spinal cord compression

A

compression of spinal cord resulting in upper motor neurone signs and specific symptoms dependent on the location of compression

373
Q

spinal cord compression causes: vertebral body neoplasms

A

most common cause of acute compression

secondary malignancy commonly from lung, breast, prostate, myeloma or lymphoma

374
Q

spinal cord compression causes: disc herniation

A

when centre of disc (nucleus pulposus) has moved through annulus resulting in pressure on nerve root and pain

375
Q

spinal cord compression causes: disc prolapse

A

when nucleus pulposus moves and presses against the annulus but it doesn’t escape outside annulus
can produce a bulge in disc- this results in pressure on nerve causing pain

376
Q

spinal cord compression causes: rare

A

infection- epidural abscess
haematoma- warfarin
primary spinral cord tumour

377
Q

spinal cord compression presentation: sensory loss below level of lesion

A

known as the sensory level

sensation abruptly diminishes 1/2 cord segments below the level of actual anatomical lesion

378
Q

spinal cord compression presentation: L5/S1

A

S1 nerve root compression= sciatica

sensory loss/pain in back of thigh/leg/lateral aspect of little toe

379
Q

spinal cord compression presentation: L4/L5

A

sensory loss/pain in lateral thigh/leg and medial side of big toe

380
Q

spinal cord compression: differentials

A 
transverse myelitis
multiple sclerosis
cord vasculitis
trauma
dissecting aneurysm
381
Q

spinal cord compression: MRI

A

do not delay imaging

identifies the cause and site of compression

382
Q

spinal cord compression: treatment

A

refer to neurosurgeons
epidural steroid injection
surgical decompression
removal of herniated tissue

383
Q

cauda equine syndrome

A

medical emergency

spinal damage at or caudal to L1

384
Q

cauda equine syndrome: epidemiology

A

rare

occurs mainly in adults

385
Q

cauda equine syndrome: aetiology

A 
common cause is lumbar disc herniation @ L4/5 or L5/S1
tumours
trauma
infection
spondylolisthesis
386
Q

cauda equine syndrome: presentation

A 
bilateral sciatica
saddle anaesthesia
bladder/bowel dysfunction
erectile dysfunction
variable leg weakness- flaccid and areflexic
387
Q

cauda equine syndrome: differentials

A

conus medullaris syndrome
vertebral fracture
peripheral neuropathy

388
Q

cauda equine syndrome: investigations

A

MRI to localise lesion
knee flexion test
ankle plantar flexion test

389
Q

cauda equine syndrome: treatment

A

refer to neurosurgeon asap to relieve pressure

390
Q

parkinson’s disease

A

degenerative movement disorder caused by a reduction in dopamine in substantia nigra

391
Q

parkinson’s: epidemiology

A

increasing prevalence with age
more common in males
peak onset 55-65 y/o
non smokers have higher risk

392
Q

parkinson’s: aetiology

A 
idiopathic
drug induced
environmental factors
parkinson genes
oxidative stress and mitochondrial dysfunction
393
Q

parkinson’s: pathophysiology

A
  • substantia nigra usually produces dopamine
  • mitochondrial dysfunction results in progressive degeneration of dopaminergic neurones that project into striatum of basal ganglia
  • less dopamine means thalamus is inhibited
  • a decrease in movement (hence symptoms)
394
Q

parkinson’s: presentation

A 
onset is usually gradual
impaired dexterity
unilateral foot drop
asymmetrical- one side worse than the others
difficulty with fine movements
speech quiet 
drooling of saliva 
depression is common
395
Q

parkinson’s presentation: triad

A

tremor
rigidity
bradykinesia

396
Q

parkinson’s presentation: tremor

A 
worse at rest
often asymmetrical
obvious in hands
improved by voluntary movements
made worse by anxiety
397
Q

parkinson’s presentation: rigidity

A

as extrapyramidal lesion
increased tone in limbs and trunk
resist passive extension throughout movement
can cause pain

398
Q

parkinson’s presentation: bradykinesia/hypokinesia

A

slow to initiate movement and slow, low-amplitude excursions in repetitive actions
reduced blink rate, monotonous hypophonic speech, write smaller

399
Q

parkinson’s presentation: gait

A 
reduced asymmetrical arm swing
narrow gait
stooped postured
small steps
shuffling steps, dragging feet
expressionless face
400
Q

parkinson’s: differentials

A 
benign essential tremor
multiple cerebral infarct
lewy-body dementia
drug-induced, trauma
if suspect early parkinson's but: dementia, incontinence, symmetry, early falls. THEN probably not parkinson's
401
Q

parkinson’s: investigations

A

clinical diagnosis

confirm with response to L-DOPA

402
Q

parkinson’s: treatment

A

aim is compensate for loss of dopamine

physiotherapy for balance, speech and gait problems

403
Q

parkinson’s treatment: L-DOPA

A

gold standar
give alongside decarboxylase inhibitor (co-careldopa) (prevents peripheral conversion of LDOPA, reducing peripheral side effects and maximises dose that crosses BBB)
precursor to dopamine so can cross BBB

404
Q

parkinson’s L-DOPA: side effects

A 
nausea
vomiting
arrhythmia 
psychosis
motor complications
405
Q

parkinson’s L-DOPA side effects: reduced efficacy

A

effect wears off in 5-10 years

so L-DOPA avoided for as long as possible

406
Q

parkinson’s L-DOPA side effects: on-dyskinesias

A

hyperkinetic, choreiform movement when drug works

repetitive, rapid, jerky, well coordinated, involuntary

407
Q

parkinson’s L-DOPA side effects: off-dyskinesias

A

fixed, painful, dystonic posturing
twisting
caused by sustained repetitive muscle contractions

408
Q

parkinson’s L-DOPA side effects: freezing

A

unpredictable loss of mobility

409
Q

parkinson’s treatment: dopamine agonists

A

oral ropinrole

used to delay starting L-DOPA

410
Q

parkinson’s treatment: monoamine oxidase B inhibitors

A

oral selegiline
inhibit MAO-B which break down dopamine- so dopamine remains for longer
used to delay starting L-DOPA

411
Q

parkinson’s treatment: catechol-O-methyl transferase inhibitors

A

oral entacapone

inhibition stops breakdown of dopamine

412
Q

parkinson’s treatment: neuropsychiatric complications

A

depression, dementia, psychosis
SSRI’s- citalopram
antipsychotics- quetiapine

413
Q

huntington’s chorea

A

huntington’s is a cause of chorea and is a neurodegenerative disorder
lack of inhibitory neurotransmitter GABA

414
Q

huntington’s chorea: epidemiology

A

autosomal dominant condition with full penetrance

presents middle age

415
Q

huntington’s chorea: aetiology

A

mutation on chromosome 4

results in repeated expression of CAG sequence

416
Q

huntington’s chorea: risk factors

A

having a parent with Huntington’s

child has 50% risk of getting it

417
Q

huntington’s chorea: pathophysiology

A

repeated CAG leads to translation of expanded polyglutamine repeat sequence
the more CAG is repeated the earlier the onset
progressive cerebral atrophy with marked loss of neurones in caudate nucleus and putamen
specific loss of GABA-nergic and cholinergic neurons

418
Q

huntington’s chorea: presentation

A 
mild psychotic and behavioural symptoms
dysarthria, dysphagia and abnormal eye movements
apathy
dementia
seizures
chorea
419
Q

huntington’s chorea: chorea presentation

A 
relentlessly progressive, jerky, explosive, rigidity
involuntary movements
ceases when sleeping
can't sit still
may begin as general restlessness
420
Q

huntington’s chorea: differentials

A

sydenham’s chorea
wilson’s disease
SLE
stroke of basal ganglia

421
Q

huntington’s chorea: genetic testing

A

shows how many CAG repeats

counselling required due to impact of positive diagnosis

422
Q

huntington’s chorea: CT/MRI

A

shows caudate nucleus atrophy and increased size of frontal horns of lateral ventricles

423
Q

huntington’s chorea: treatment

A

no treatment to prevent progression
counselling
antidepressants
risperidone treats aggression

424
Q

huntington’s chorea: symptomatic management of chorea

A

benzodiazepines
sulpiride- neuroepileptic
tetrabenazine- dopamine depleting agent

425
Q

myasthenia gravis

A

autoimmune disease against nicotinic acetylcholine receptors (AChR) in neuromuscular junction

426
Q

myasthenia gravis: epidemiology

A

more common in females than males UNTIL over 50 is more common in males
peak age of incidence for women = 30 y/o, males = 60 y/o

427
Q

myasthenia gravis: aetiology/risk factors

A

in women, associated with other autoimmune disease and thymic hyperplasia
in men it is associated with thymic atrophy or thymic tumour

428
Q

myasthenia gravis: pathophysiology

A

autoimmune
mediated by antibodies to AChR- interfere with neuromuscular junction via depletion of working post-synaptic sites
achieved by immune complex deposition of anti-AChR IgG and complement at post-synaptic membranes
both T and B cells implicated
blocked excitatory effect- muscle weakness

429
Q

myasthenia gravis: presentation

A

proximal limb muscles, speech and facial expression are commonly affected
ptosis, diplopia and myasthenic snarl on smiling
resp difficulties

430
Q

myasthenia gravis presentation: muscle groups affected

A

in order:

  • extra-ocular
  • bulbar (swallowing/chewing)
  • face
  • neck
  • trunk
431
Q

myasthenia gravis presentation: increasing muscular fatigue

A

worsened by pregnancy, infection, exercise
to elicit:
-ask to count to 50, their voice becomes less audible
-hold your finger up high, ask to keep looking at it with eyes only, can’t keep it up

432
Q

myasthenia gravis: differentials

A

MS
hyperthyroidism
acute guillain-barre syndrome
lambart-eaton myasthenic syndrom

433
Q

myasthenia gravis investigations: serum anti-AChR

A

raised in 90%

if negative then look for muscle specific tyrosine kinase antibodies (anti-MuSK)

434
Q

myasthenia gravis investigations: electromyography and nerve conduction study

A

EMG detects it as muscle cells not properly activated

characteristic decrement occurs in evoked muscle action potential during repetitive stimulation

435
Q

myasthenia gravis investigations: CT of thymus

A

look for hyperplasia/ atrophy/ tumour

436
Q

myasthenia gravis investigations: tensilon test

A

IV edrophonium given
muscle power increases within seconds
rarely used due to side effects

437
Q

myasthenia gravis treatment: symptom control

A

anti-cholinesterase - pyridostigmine

so more ACh remains in neuromuscular junction

438
Q

myasthenia gravis treatment: immunosuppression

A

prednisolone

treat relapse or if there’s no response to pyridostigmine

439
Q

myasthenia gravis treatment: thymectomy

A

removal of thymus if onset < 50 y/o and disease not controlled with anti-cholinesterase

440
Q

myasthenia gravis treatment: myasthenic crisis

A

weakness of the resp muscles during a relapse can be life threatening
monitor FVC
treat with plasmapheresis

441
Q

paresis

A

impaired ability to move a body part in response to will

442
Q

paralysis

A

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

443
Q

ataxia

A

willed movements are clumsy, ill-directional or uncontrolled

444
Q

involuntary movements

A

spontaneous movement of a body part, independently of will

445
Q

apraxia

A

disorder of consciously organised pattern of movement or impaired ability to recall acquired motor skills

446
Q

potential sites of damage along motor pathway

A 
motor nuclei of cranial nerve
motor neurones in spinal cord
spinal ventral roots
peripheral nerves
neuromuscular junction
muscle
447
Q

upper motor neurone signs

A 
upper- everything goes up!
increased muscle tone
brisk reflexes
plantars are upturned on stimulation
upper limb extensor muscles weaker than flexor
lower limb=opposite
448
Q

lower motor neurone signs

A 
lower- everything goes down!
muscle tone reduced
muscle wasting
fasciculation
reflexes depressed
449
Q

motor neurone disease

A

cluster of major degenerative diseases characterised by selective loss of neurones in motor cortex
cranial nerve nuclei and anterior horn cells

450
Q

motor neurone disease: epidemiology

A

more common in males
median age of onset 60 y/o
often fatal in 2-4 years

451
Q

motor neurone disease: aetiology/risk factors

A

no established risk factors

5-10% familial- mutation in free radical scavenging enzyme (SOD-1)

452
Q

motor neurone disease: pathophysiology

A

degenerative condition affecting motor neurones-anterior horn cells
cause both UMN and LMN dysfunction but no sensory or sphincter disturbance, never affects movements

453
Q

motor neurone disease presentation: amyotrophic lateral sclerosis

A 
UMN and LMN
most common 
loss in motor cortex and anterior horn of the cord 
split hand sign 
cramps common
wrist and foot drop
454
Q

motor neurone disease presentation: progressive muscular atrophy

A

LMN only
present with weakness, wasting and fasciculation
distal muscle before proximal

455
Q

motor neurone disease presentation: progressive bulbar pasty

A

LMN only
lower cranial nerves and nuclei initially
dysarthria, dysphasia, nasal regurgitation of fluids
LMN lesion of tongue

456
Q

motor neurone disease presentation: primary lateral sclerosis

A

UMN only
least common
loss of Betz cells in motor cortex
no cognitive decline

457
Q

motor neurone disease: differentials

A 
MS
polyneuropathies
myasthenia gravis
diabetic amotrophy
guillain-barre
spinal cord tumours
458
Q

motor neurone disease investigations: clinical findings

A

definite: LMN+UMN signs in 3 regions
probable: UMN+LMN in 2 regions
probable: LMN+UMN in 1 region/UMN in more than 1 region… w/ EMG showing acute denervation in >2 limbs
possible: LMN+UMN in 1 region

459
Q

motor neurone disease investigations: brain/cord MRI

A

helps exclude structural causes

460
Q

motor neurone disease investigations: lumbar puncture

A

exclude inflammatory causes

461
Q

motor neurone disease investigations: nerve conduction studies

A

denervation of muscles due to degenerative of LMN confirmed by EMG

462
Q

motor neurone disease treatment: anti-glutamatergic drugs

A

oral riluzole
sodium channel blocker that inhibits glutamate release
prolongs life by 3 months
but raises LFTs

463
Q

motor neurone disease treatment: drooling

A

drooling due to bulbar palsy

oral propantheline or amitriptyline

464
Q

motor neurone disease treatment: dysphagia

A

blend food
nasogastric tube
percutaneous catheter gastrostomy

465
Q

motor neurone disease treatment: spasms

A

oral baclofen

466
Q

guillain-barre syndrome

A

acute inflammatory demyelinating ascending polyneuropathy
affects peripheral nervous system- schwann cells
follows upper resp tract or GI infection

467
Q

guillain-barre syndrome: epidemiology

A

more common in males
peak ages= 15-35 y/o and 50-75 y/o
most common acute polyneuropathy

468
Q

guillain-barre syndrome: aetiology

A 
campylobacter jejuni
cytomegalovirus
mycoplasma
zoster
HIV
epstein-barr virus
469
Q

guillain-barre syndrome: risk factors

A

history of resp/GI infection 1-3 weeks prior to onset

vaccinations have been implicated

470
Q

guillain-barre syndrome: pathophysiology

A

infectious organisms share same antigens as those on schwann cells- leads to autoantibody mediated nerve cell damage
reduction in peripheral nerve conduction follows- acute polyneuropathy

471
Q

guillain-barre syndrome: presentation

A
  • 1-3 weeks post infection, symmetrical ascending muscle weakness
  • all limbs then affected, can lead to paralysis
  • proximal muscles are more affected- trunk/resp/CN 7
  • pain common
472
Q

guillain-barre syndrome: differentials

A

other causes of acute paralysis:

  • hypokalaemia
  • stroke
  • brainstem compression
  • encephalitis
  • vasculitis
  • myasthenia gravis
473
Q

guillain-barre syndrome: nerve conduction studies

A

diagnostic if matches clinical examination

show slowing of conduction, prolonged distal motor latency

474
Q

guillain-barre syndrome: lumbar puncture

A

done at L4

CSF has raised protein but normal white cell count

475
Q

guillain-barre syndrome: spirometry

A

monitors FVC if resp involvement

decreased FVC indicates the need to admit to ITU

476
Q

guillain-barre syndrome: treatment

A

ventilate to improve FVC
IV immunoglobulin for 5 days- decreases severity of paralysis
plasma exchange
low molecular weight heparin and compression stockings

477
Q

headache

A

a symptom of many different illnesses and medications

478
Q

headache classification

A

primary secondary and other (trigeminal neuralgia/facial pain)

479
Q

primary headaches

A

no underlying cause

migraine, cluster and tension

480
Q

secondary headaches

A

underlying cause

meningitis, SAH, giant cell arteritis, medication

481
Q

secondary headache red flags

A 
HIV or immunosuppressed
fever
thunderclap
seizure
suspected meningitis/encephalitis
482
Q

migraines

A

recurrent throbbing headache often preceded by an aura and associated with vomiting and visual changes

483
Q

migraines: epidemiology

A

most common cause of episodic/recurrent headache
more common in females
90% onset before 40 y/o

484
Q

migraines: causes CHOCOLATE

A 
Chocolate
Hangovers
Orgasms
Cheese
Oral contraception
Lie-ins
Alcohol
Tumult (loud noise)
Exercise
485
Q

migraines: risk factors

A

females
adolescence
genetic component- family history

486
Q

migraines: pathophysiology

A
  • genetics play a role in causing neuronal-hyper-excitability
  • changes in brainstem blood flow lead to an unstable trigeminal nerve nucleus in basal thalamus
  • self propagating wave spread across cerebral cortex
  • release of inflammatory mediators which act on trigeminal nerve nucleus
487
Q

migraines without aura: presentation

A 
attacks for 4-72 hours
at least 2 of:
unilateral/pulsing/moderate-severe pain/aggravated by physical activity 
during, at least one of:
nausea/vomiting/photophobia
488
Q

migraines with auras: presentation

A

at least 2 attacks
aura precedes attack by minutes
visual= chaotic cascading/jumbling/distorting lines/dots. Black hole in field. hemianopia
tingling/prickling face

489
Q

general migraines: features

A

at least 2 of:
unilateral pain/throbbing pain/moderate-severe/motion sensitivity
at least 1 of:
nausea/vomiting/photophobia

490
Q

migraines: differentials

A

tension headache
medication
brain tumour

491
Q

migraines: investigations

A

mainly clinical

examine eyes for papilloedema, BP, head and neck

492
Q

migraines: when to perform neuroimaging

A 
worst headache/thunderclap
change in pattern
abnormal neuro exam
onset > 50 y/o
epilepsy
493
Q

migraines: lumbar puncture investigations

A

worst headache/thunderclap
rapid onset/progressive
neuroimaging should precede to rule out mass/lesion/raised ICP

494
Q

migraines: acute treatment

A

NSAIDs- avoid ibuprofen

triptans- sumatriptan

495
Q

migraines: prevention

A

if more than 2 attacks/month or acute treatment needed 2x/week
beta blocker- propranolol
amitriptyline

496
Q

tension headaches

A

most chronic daily and recurrent headaches are tension headaches

497
Q

tension headaches: epidemiology

A

can be episodic, <15 days/month

or chronic >15/month

498
Q

tension headaches: aetiology

A 
stress
sleep deprivation
hunger
eyestrain
anxiety 
noise
499
Q

tension headaches: presentation

A 
without vomiting
not affected by exercise
tight band sensation
pressure behind eyes
30 mins-7 days
500
Q

tension headaches: pain presentation

A

bilateral
pressing/tight non-pulsatile
mild/moderate intensity
scalp muscle tenderness

501
Q

tension headaches: differentials

A

migraine
cluster headache
giant cell arteritis
drug induced

502
Q

tension headaches: investigations

A

clinical diagnosis from history

503
Q

tension headaches: symptomatic treatment

A 
aspirin
paracetamol
NSAIDs
no opioids
amitriptyline
504
Q

cluster headaches

A

most disabling headache disorders

505
Q

cluster headaches: epidemiology

A

rare 1/1000
more common in males
affects adults, 20-40 y/o
common in smokers

506
Q

cluster headaches: risk factors

A

smoker
male
autosomal dominant gene has a role

507
Q

cluster headaches: pathophysiology

A

unknown

may be due to superficial temporal artery smooth muscle, hyper-activity to serotonin

508
Q

cluster headaches: presentation

A

abrupt onset
excruciating pain around one eye/temple/forehead
facial flushing
miosis/ptosis
pain is strictly unilateral and almost always affects same side
last 4-12 weeks

509
Q

cluster headaches: differentials

A

migraine

510
Q

cluster headaches: investigations

A

clinical diagnosis

at least 5 headaches fulfilling typical presentation

511
Q

cluster headaches: treatment

A

analgesics unhelpful

triptan- SC sumatriptan. reduce vascular inflammation

512
Q

cluster headaches: presentation

A

calcium channel blocker- verapamil
avoid alcohol
corticosteroids may help- prednisolone

513
Q

trigeminal neuralgia

A 
CN5= motor and sensory 
.1=ophthalmic
.2= maxillary
.3=mandibular
chronic debilitating condition resulting in intense and extreme episodes of pain
514
Q

trigeminal neuralgia: epidemiology

A

peak incidence 50-60 y/o

more common in females

515
Q

trigeminal neuralgia: aetiology

A

mainly due to compression of trigeminal nerve by a loop of vein or artery
local pathology= aneurysms, meningeal inflammation, tumours

516
Q

trigeminal neuralgia: fifth nerve lesion causes

A

w/i brainstem= tumour, MS, infarction
cerebellopontine angle= acoustic neuroma, tumour
petrous bone=spreading middle ear infection
cavernous sinus= aneurysm of internal carotid

517
Q

trigeminal neuralgia: pathophysiology

A

hypertension

triggered by washing affected area/shaving/eating/talking

518
Q

trigeminal neuralgia: presentation

A

compression of the trigeminal nerve results in demyelination and excitation of the nerve resulting in erratic pain signalling

519
Q

trigeminal neuralgia: pain presentation

A 
almost always unilateral
3 attacks required
reoccurring in paroxysmal attacks from seconds to minutes
severe intensity
electric shock like
precipitated by innocuous stimuli
520
Q

trigeminal neuralgia: differentials

A 
giant cell arteritis/temporal arteritis should be excluded
dental pathology
temporomandibular joint dysfunction
migraine
cluster
521
Q

trigeminal neuralgia: investigations

A

need 3 attacks with unilateral face pain
based on history
MRI to exclude secondary causes

phase 2a clinical (8 decks)

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