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AA Y4 Finals cards NE > Neurology > Flashcards

Neurology Flashcards

1
Q

describe the underlying pathologies seen in Parkinson’s?

A
  • degeneration of dopamine receptors in substantia nigra

- accumulation of lewy bodies in substantia nigra and rest of brain

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2
Q

describe the tremor seen in Parkinson’s?

A

resting, pill rolling tremor

tremor improves on voluntary movement - this is the opposite of a cerebellar tremor, which gets worse on movement

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3
Q

what is one of the 1st signs of PD?

A

change in gait

small, shuffling steps with reduced arm movement

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4
Q

what sleep disorder is associated with PD?

A

REM sleep disorder

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5
Q

if a clinical exam isn’t enough to diagnose PD, what other scan can be done?

A

SPECT scan

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6
Q

what is the gold standard Mx of PD?

A

levodopa and carbidopa

levodopa is used if px is having motor issues

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7
Q

describe the effect of levodopa on PD?

A

it has a diminishing effect with actions lasting 5-10 years

therefore, it’s use is delayed until significant disability

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8
Q

name 3 other classes of drugs that can be used prior to levodopa in PD?

A

dopamine agonists: roprinirole

COMT inhibitors

MOAB inhibitors

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9
Q

which medication should be used to Tx levodopa associated nausea?
Why?

A

domperidone

it is selective to peripheral dopamine receptors so won’t prevent the activity of levodopa in the brain

metoclopramide should be avoided as it lacks peripheral selectivity

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10
Q

name 5 forms of Parkinsonism?

A
  • progressive supranuclear Palsy
  • multi system atrophy
  • corticobasal degeneration
  • vascular Parkinson’s
  • dementia with lewy bodies
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11
Q

which form of Parkinson’s lacks a tremor?

A

progressive supra nuclear palsy

also presents with a vertical gaze palsy and early postural instability

truncal rigidity more prominent than limb rigidity

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12
Q

which form of Parkinson’s has a hot crossed bun sign on MRI?

A

Multi System Atrophy

due to cerebellar and pontine atrophy

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13
Q

describe features associated with Muti system atrophy?

A
  • pyramidal signs
  • onset in 6th or 7th decade
  • ataxia and cerebellar signs
  • jerky, postural tremor
  • early autonomic disturbance (bladder dysfunction and postural hypotension)
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14
Q

describe the distribution of weakness and rigidity in cortico-basal degeneration?

A

rigidity and weakness affecting only 1 limb

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15
Q

describe the characteristics of vascular Parkinson’s?

where is most affected?

A

predominantly affects the lower limbs

associated with prominent gait disturbance

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16
Q

name 3 drugs that can induce Parkinson’s?

A
  • metoclopramide
  • antipsychotics
  • amiodarone
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17
Q

compare the tremor seen in Parkinson’s and cerebellar dysfunction?

how can they be differentiated?

A

parkinson’s: resting tremor

cerebellar dysfunction: intention tremor

resting tremors are abolished by movement, intention tremors are made worse by movement

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18
Q

name 5 causes of a postural tremor?

A
  • anxiety
  • alcohol withdrawal
  • benign essential tremor
  • thyrotoxicosis
  • drugs (salbutamol, caffeine, lithium, valproate, TCAs)
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19
Q

describe the characteristics of a postural tremor?

A

absent at rest but present on maintained posture such as holding arms out

key feature is that it doesn’t get worse on movement

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20
Q

what is 1st line medication to treat a benign essential tremor?

A

propranolol

BETs are made better by alcohol consumption

AD inheritance

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21
Q

give 4 possible causes of an intention tremor?

A
  • cerebellar disease - stroke, haemorrhage, MS

- Wilson’s disease

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22
Q

what 2 blood tests must always be done in a patient presenting with a tremor?

A

thyroid function tests

copper/ceruloplasmin

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23
Q

what is the definition of dystonia?

A

involuntary, sustained muscle spasms

results in abnormal posturing and repetitive movements

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24
Q

what condition can cause focal dystonia (dystonia limited to single muscle groups) in the eyes and jaw?

A

myasthenia gravis

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25
Q

how is acute dystonia managed?

A

anti-spasmodics (baclofen)

botox (focal dystonia)

anti-cholinergic (procyclidine)

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26
Q

describe the pathology seen in Huntington’s disease?

A

AD neurodegenerative disease associated with CAG expansion in chromosome 4

disease is definitely seen if >4 repeats

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27
Q

name 4 early signs of Huntington’s?

A

clumsiness
chorea
irritability
agitation and depression

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28
Q

which type of chorea is seen in children and develops after a strep throat infection?

A

sydemans chroea

self limiting

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29
Q

describe the triad of symptoms seen in cruetzfeldt jakobs disease?

A

dementia

ataxia

myoclonus

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30
Q

what is the median age of onset of MND?

A

60 y/o

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31
Q

what is the pathology behind MND?

A

a selective loss of motor neurones in either the motor cortex, CN nuclei and anterior horns of the spinal cord

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32
Q

what is the primary symptom in MND?

A

muscle weakness

muscle weakness usually begins as focal and progressively spreads to become generalised

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33
Q

what is typically found on neuro exam in MND?

A

fasciculations
absence of sensory symtoms

mixed UMN and LMN signs
wasting of small hand muscles

muscle weakness - usually affects the limbs (esp upper) 1st, then spreads - can also start in bulbar or thorax muscles 1st

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34
Q

how can MND be distinguished from other neurological conditions?

A
  1. it doesn’t affect the eyes (myasthenia does)

2. no sensory loss or sphincter dysfunction (MS and neuropathies do)

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35
Q

describe the typical UMN and LMN distribution in ALS MND?

A

LMN signs in arms

UMN signs in legs

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36
Q

where does ALS MND usually start and how does it spread?

A

predominantly starts in the hands and then spreads to affect limbs and bulbar muscles

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37
Q

name 5 classic symptoms seen in ALS MND?

A
  1. weak hand grip and shoulder abduction
  2. stumbling gait and foot drop
  3. muscle wasting
  4. drooling and dysarthria (slow slurred speech)
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38
Q

which form of MND has the worst prognosis?

A

progressive bulbar

there is progressive bulbar muscle weakness with subsequent limb involvement

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39
Q

describe the typical presentation of progressive bulbar MND?

A

drooling

dysphagia

progressive dysarthria

aspiration pneumonia

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40
Q

how can progressive spinal muscular atrophy be differentiated from ALS MND?

A

it is purely lower motor neurone

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41
Q

which form of MND is associated with loss of Benz cells in the motor cortex and only has UMN signs?

A

primary lateral sclerosis

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42
Q

what drug can prolong life by around 3 months in MND?

A

riluzole - an anti glutamine drug

mainly used for ALS

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43
Q

what other medication can be used to manage symtoms in MND?

A

analgesia
anti cholinergic for drooling

BiPAP at night
baclofen for spasticity
speech therapy

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44
Q

what pathology is seen in myasthenia gravis?

A

NMJ disease

an AI condition associated with the production of antibodies against nicotinic receptors at the NMJ

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45
Q

name the antibodies seen in MG?

A

anti-AchR and anti MuSK

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46
Q

what other diseases is MG associated with?

A

disease of the thymus, SLE and rheumatoid

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47
Q

which things worsen muscle weakness in myasthenia gravis?

A

pregnancy, emotion, exercise

drugs: BBs, opiates, gentamicin and tetracyclines

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48
Q

describe findings on neuro exam in myasthenia gravis?

A

normal sensation and reflexes

normal muscle appearance and tone

CK levels also normal

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49
Q

what is the 1st muscle group usually affected in MG?

A

extra ocular - causes double vision and ptosis (main way to differentiate it from MND)

followed by bulbar (dysphagia, difficulty chewing etc)

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50
Q

describe thymus involvement seen in MG?

A

younger patients: thymic hyperplasia

older patients: thymic atrophy or tumours

when investigating, always do a CT thorax to assess thymus

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51
Q

what is mainstay management of MG?

A

anti-cholinesterase: pyrostigmine

thymus abnormality: thymectomy

relapses: immunosupression (prednisolone)

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52
Q

how does the pathology behind Lambert eaton myasthenic syndrome differ from MG?

A

in Lambert eaton syndrome, there isnt enough ACh being released from pre synaptic calcium channels

in MG, the antibodies attack the post synaptic nicotinic receptors

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53
Q

name 2 causes of Lambert eaton syndrome?

A

autoimmune

paraneoplastic syndromes (especially small cell LC)

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54
Q

compare the characteristics of the muscle weakness in MG and LEMS?

A

LEMS: muscle weakness improves with exercise whereas it gets worse in MG

LEMS: hyporeflexia, with improvement of reflexes on exercise

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55
Q

what imaging is necessary in LEMS?

A

CT CAP to screen for malignancy (small cell lung cancer)

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56
Q

what is used to manage LEMS?

A

3,4 diaminopyradine

IV Igs

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57
Q

what 2 things is botulism usually associated with?

A

IVDU or penetrative wounds

the toxin blocks the release of ACh from presynaptic terminals

causes flaccid paralysis

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58
Q

which drugs can cause muscle weakness?

A

statins

steroids

alcohol

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59
Q

describe the seizure seen in a syncopal episode?

A

fall to ground and LOC

no movement or brief, symmetrical clonic jerks in the absence of tonic contraction

no associated incontinence or tongue biting

whole event lasts approx 2 mins

rapid recovery and no prolonged symptoms

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60
Q

what name is given to LOC that occurs due to transient arrhythmias causing reduced CO?

A

stokes Adams attacks

pre attack, patient complains of palpitations

fall to ground with LOC, pallor and slow or absent pulses

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61
Q

how many epileptic events are need to occur before a diagnosis can be made?

A

need to have at least 2 episodes

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62
Q

during epileptic seizures, what 2 features are commonly seen?

A

tongue biting and urinary incontinence

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63
Q

describe the post-ictal period in epilepsy?

A

slow recovery associated with confusion, headache, muscle ache and temirpory weakness

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64
Q

partial/focal seizures occur due to isolated, increased activity in only 1 hemisphere.

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

A

both present with localised symptoms of any nature

simple: no loss of awareness and no post ictal period
complex: LOC, aura, post ictal symtoms present

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65
Q

A focal seizure occurring in which lobe is most associated with a Hx of febrile convulsions?

A

temporal lobe

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66
Q

describe characteristics of a temporal lobe focal seizure?

A 
dysphasia 
de ja vu 
flashbacks 
odd tastes or smells 
visual/auditory hallucinations 
lip smacking, chewing, swallowing
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67
Q

describe characteristics of a frontal lobe focal seizure?

A

dysphasia
posturing movements
head and leg movements
subtle changes in behaviour

Jacksonian seizure: twitching movements of upper limbs that then spread to the face and lower limbs

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68
Q

describe characteristics of an occipital lobe focal seizure?

A

visual phenomena such as spots, lines and flashes

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69
Q

a focal seizure in which lobe of the brain is most likely to cause numbness and tingling?

A

parietal lobe

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70
Q

compare consciousness in focal and generalised seizures?

A

focal: may occur without LOC
generalised: there is always LOC

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71
Q

what often triggers a generalised seizure?

A

flashing lights or sleep deprivation

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72
Q

when during a tonic clonic seizure will tongue biting occur?

A

during the tonic phase

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73
Q

when during a tonic clonic seizure will the eyes roll into back of head and will breathing restart?

A

the clonic phase

asymmetrical convulsile jerks

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74
Q

what are 1st line mx of absence seizures?

A

sodium valproate or ethosuximide

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75
Q

how is a myoclonic seizure different from a tonic clonic?

what condition are myoclonic seizures seen?

A

myoclonic has the clonic jerks but without the tonic contraction

juvenile myoclonic epilepsy

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76
Q

in generalised seizures, when should anti epileptic drugs be started?

A

after the 2nd seizure

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77
Q

what is the 1st line medication given for absence, myoclonic and tonic clonic seizures?

A

sodium valproate

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78
Q

what is the 1st line Tx for focal seizures?

A

1st line: carbamazepine

2nd line: lamotrigine, levetiracetam, sodium valproate

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79
Q

sodium valproate is generally 1st line for generalised seizures.

In which patient groups is it contraindicated?

what should be given instead?

A

contraindicated in younger women - it is highly teratogenic

instead, give lamotrigine

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80
Q

epilepsy occurs due to either too much excitation (glutamate) or not enough inhibition (GABA).

what is the mechanism of action of sodium valproate?

A

increases GABA activity

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81
Q

name some key side effects of sodium valproate?

A 
nausea 
tremor 
weight gain 
liver failure 
thrombocytopenia 
oedema 
pancreatitis 
encephalopathy 
teratogenic
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82
Q

what is the main problem with lamotrigene?

A

it takes several months to titrate to effect

it can be used in both focal and generalised seizures

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83
Q

name side effects seen in lamotrigine?

A
  • maculopapular rash
  • Steven johnson syndrome
  • DIC
  • diplopia and photosensitivity
  • tremor and agitation
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84
Q

why is carbamazepine not used in generalised epilepsy?

A

it may may seizures worse

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85
Q

name some side effects of levetiracetam?

A
  • leucopenia
  • drowsieness
  • double or blurred vision
  • impaired balance
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86
Q

which anti-epileptic is a P450 inhibitor?

A

carbamazepine

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87
Q

how long must you not drive for following 1st unprovoked/isolated seizure?

A

cant drive car for 6 months and HGV for 5 years

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88
Q

when can a patient with established epilepsy qualify for a driving licence?

A

if they have been free from any seizure for 12 months

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89
Q

which forms of contraception are affected in patents on anti-epileptics?

A
  • POP
  • COCP efficacy reduced
  • larger doses of morning after pill required
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90
Q

Give the 3 definitions of status epilepticus?

A
  1. seizure lasting > 5mins
  2. multiple seizures within 30 minutes
  3. 2nd seizure occurs before full neuro recovery from the last one
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91
Q

describe the management of status epilepticus?

A
  • ABCDE

1st line: IV lorazepam (2-4mg, max dose = 2)

2nd line: phenytoin

3rd line: general anaesthesia

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92
Q

what do non-epileptic attack disorder have a strong association with?

A

past trauma - early childhood sexual abuse

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93
Q

describe a non-epileptic attack disorder?

A

excessively long- they last 10-20 mins

coordinated, symmetrical, large movements

normal breathing and awareness throughout

no associated tongue biting/incontinence

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94
Q

what is the Mx of non epileptic attack disorder?

A

consoling and psychological therapy

anti-convulsants make the attacks worse!

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95
Q

name common places for demyelination to occur in MS?

A

optic nerve, spinal cord, cerebellum and peri ventricular white matter

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96
Q

are UMN or LMN signs seen in MS?

A

UMN - spasticity, brisk reflexes, +ive babinski

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97
Q

name ophthalmic signs seen in MS?

A

nystagmus, RAPD (optic neuritis), internuclear opthalmaplegia

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98
Q

compare relapse remitting and secondary progressive MS?

A

both have relapses, but the difference is whether total recovery is seen in between relapses.

RR: complete recovery seen in between relapses

SP: incomplete recovery seen and acute relapses superimposed - this leads to steady neurological decline

99
Q

what will majority of patients with relapse remitting MS go onto develop?

A

secondary progressive MS

they will not recover fully in between relapses, so will gradually decline

100
Q

how do primary and secondary progressive MS differ from one another?

A

primary MS: no periods of remission following onset of symptoms (it doesn’t relapse)

secondary MS: relapses with incomplete recovery

101
Q

what diagnostic criteria for MS shows dissemination in time and place?

A

2 episodes of symptoms suggestive of MS at last >1 hour and are 30 days apart

102
Q

what bloods would you request when investigating possible MS?

A

FBC, LFT
auto antibodies
metabolic: B12, folate and copper
infection: HIV, syphilis

103
Q

what is seen on LP in MS?

A

oligoclonal bands of IgG

104
Q

what can be seen on MRI in MS patients?

A

optic neuritis and plaques of demyelination

105
Q

how are relapses of MS managed?

A

IV steroids (methylprednisolone)

plasma exchange (to remove autoantibodies)

106
Q

name the 3 1st line disease modifying drugs used in MS?

A
  • B interferon
  • Capaxone
  • Tecfidera
107
Q

what is used to manage spasticity in MS?

A

1st line: baclofen/gabapentin, physio, OT

108
Q

compare the changes in sensation that are seen in large sensory and small sensory neuropathies?

A

large sensory neuropathy: vibration and proprioception decreased

small sensory: pin prick and temperature decreased

109
Q

which nerve roots are affected in carpal tunnel syndrome?

A

median nerve

C6-T1 nerve roots

110
Q

which neuropathy causes a wrist drop and can occur die to damage in humeral shaft fractures?

A

radial nerve (C5-T1)

111
Q

which nerve can be compressed under the inguinal ligament, causing burning thigh pain?

A

lateral cutaneous nerve of the thigh (also called meralgia parasthetica)

112
Q

what is the mainstay investigation for mononeuropathies?

A

nerve conduction studies

113
Q

in a patient with weak plantarflexion and unable to stand up on tip toes, which nerve root is affected?

A

S1 nerve root

114
Q

what is a mono neuritis multiplex?

A

when 2 mononeuropathies in different locations develop at the same time

115
Q

name 5 causes of mononeuritis multiplex?

A 
diabetes
rheumatoid 
carcinomatosis 
vasculitis (wegners, PAN) 
infection (HIV)
116
Q

is the demyelination in guillian barre syndrome central, peripheral or both?

how will this present?

A

peripheral

LMN signs - loss of reflexes

117
Q

describe guillan barre syndrome?

A

acute, AI, inflammatory demyelinating peripheral neuropathy

118
Q

what does guillian barre syndrome commonly occur secondary to?

A

occurs within a few weeks of infection (URTI or GI infection)

119
Q

describe the typical presentation of guillan barre syndrome?

A

ascending muscle weakness, starting in the lower limbs and spreading

usually over a 4 week period
can spread to all 4 limbs and respiratory muscles

120
Q

name some associated symptoms of guillian barre syndrome?

A

back/leg pain initially

sensory loss

autonomic dysfunction

CN symptoms

loss of reflexes

121
Q

describe the course of guillian barre syndrome?

A

gradual and increasing paralysis over a 4 week period

then recovery phase starts and full recovery seen in majority of patients

122
Q

describe investigations done in guillian barre syndrome?

what would be expected findings?

A

nerve conduction: slowed conduction

LP: increased protein with normal white cells

123
Q

how is gguillian barre syndrome managed?

A
  • IV Ig
  • plasmaphoresis
  • +/- ventilatory support
124
Q

describe Charcot-marie tooth disease?

A

AD hereditary condition

progressive distal muscle wasting in the legs - gives champagne bottle shaped legs

usually occurs around puberty

motor loss with associated lower limb weakness

foot drop and high stepping gait

125
Q

how is charcot Marie tooth disease managed?

A

physio +/- surgery

126
Q

what bloods would you request for a peripheral neuropathy?

A

FBC, U&Es, LFT, TFT, HbA1c and glucose, B12/folate

autoantibody screen

vitamin and nutrient levels

toxicology screen

127
Q

what is the most common viral cause of meningitis?

A

echo virus

128
Q

compare the onset of viral meningitis to bacterial?

A

viral tends to have a more insidious onset compared to bacterial

129
Q

what is the most common cause of bacterial meningitis in <10y/o?

A

H. Influenzae

130
Q

compare the causative in bacterial meningitis in 10-21 year olds and those > 21?

A

10-21 y/o: meningococcal

> 21: pneumococcal

131
Q

in a suspected meningitis in a patient with an altered level of consciousness, focal neurological signs, papillodema or immunosupression, what must be done prior to LP?

A

a CT brain

need to rule out raised ICP prior to LP

132
Q

compare the cell type, protein and glucose level on LP in a patient with viral vs bacterial meningitis

A

viral: lymphocytes, normal protein, normal glucose
bacterial: neutrophils, high protein, low glucose

133
Q

what is the 1st line Tx for meningitis?

A

ceftriaxone or cefotaxime

134
Q

in which patient groups with meningitis should amoxicillin be added as initial Tx?

A

> 60 y/os or immunocompromised should also get amoxicillin

135
Q

if pneumococcal cause of meningitis is suspected, what other medication should be given?

A

dexamethasone

given with or just before 1st dose of ABs

136
Q

how can one compare between encephalitis and meningitis?

A

cerebral function reminds normal in patient with meningitis

there is often an altered mental status in encephalitis

137
Q

how should a case of encephalitis be treated?

A

IV acyclovir to cover herpes simplex infection

138
Q

describe the treatment time windows for an acute stroke?

A

<4.5 hrs from onset = thrombolysis

<6 hours from onset = thrombectomy

not suitable for thrombectomy = treatment dose aspirin

139
Q

why are antiparkinson’s drugs classed as “critical” medicines?

A

stopping them abruptly can cause significant worsening of symptoms

they should not be stopped on acute admissions, sick days or holidays

139
Q

why are antiparkinson’s drugs classed as “critical” medicines?

A

stopping them abruptly can cause significant worsening of symptoms

they should not be stopped on acute admissions, sick days or holidays

140
Q

what blood test can be used to differentiate between a true seizure and a pseudoseizure?

A

prolactin

raised prolactin 10-20 mins following an episode suggests a general tonic clonic seizure rather than a non-epileptic pseudo seizure

141
Q

which nerve supplies the extensor muscle group in the hand?

A

the radial nerve

142
Q

which nerve allows for adduction of the fingers?

A

the ulnar nerve

143
Q

what is the hallmark finding of MG?

A

fatiguability - painless muscle weakness that is improved with rest

144
Q

compare the nerve roots affected in klumpke’s and erb’s palsy?

A

klumpke’s: C8-T1

erb’s: C5-6

klumpke’s occurs due to traction injuries or during delivery

145
Q

describe the appearance of the arm in erb’s palsy?

A

arm is pronated and medially rotated (waiter’s tip appearance)

146
Q

how should a suspected TIA be managed?

A

aspirin 300mg immediately and specialist review within 24 hours

147
Q

how long should patients recieve aspirin following an ischemic stroke?

A

300mgg once daily for 14 days

148
Q

which form of headache is completely responsive to Tx with indomethacin?

A

paroxysmal hemicrania

149
Q

compare the findings on CT between an acute and chronic subdural haematoma?

A

acute: blood appears white on CT
chronic: low blood is “hypodense (dark)” on CT

150
Q

what is used to treat cerebral oedema in patients with brain tumours?

A

dexamethasone

151
Q

which class of antibiotics are known to increase risk of ideopathic inter cranial hypertension?

A

tetracyclines

so is the COCP

152
Q

name 3 symptoms common in a temporal lobe seizure?

A
  • motionless staring
  • lip-smacking
  • post-ictal dysphasia
153
Q

which condition classically presents with ascending weakness?

A

guillian barre syndrome

the ascending weakness presents following an infection

patients with GBS have abnormal nerve conduction studies

154
Q

which infection classically causes guillian barre syndrome?

A

campylobacter jejuni

155
Q

compare when IV dexamethasone and mannitol would be used?

A

both used to treat raised ICP

dexamethasone used to Tx raised ICP 2ndary to vasogenic oedema (from infection or neoplasm)

mannitol is used in patients with raised ICP 2ndary to brain trauma

156
Q

why is CN6 (abducens nerve) susceptible to damage early in the course of raised ICP?

A

due to its long, intracranial course

would present with headache, nausea, papilloedema and a diplopia when looking laterally

157
Q

what is the gold standard test for diagnosing venous sinus thrombosis?

A

MR venogram

non contrast CT normal in around 70% of cases

158
Q

which medications can cause neuroleptic malignant syndrome?

how does it present?

A

caused by antipsychotics

presents with hyperthermia, limb rigidity, autonomic instability and altered mental status

raised CK seen in most cases

159
Q

the symptoms of what condition can be described as “wet, wobbly and whacky?”

A

normal pressure hydrocephalus

wet - incontinent
wobbly - ataxia
whacky - dementia

thought to be due to reduced CSF absorption at the arachnoid villi
Tx - ventriculoperitoneal shunting

160
Q

how is guillian barre syndrome treated in hospital?

A

IV immunoglobulin or plasma exchange to remove the antibodies

161
Q

name the 2 nerves responsible for the corneal reflex?

A

corneal reflex = the blink reflex

afferent limb = CN V1

efferent limb = facial nerve (CN7)

162
Q

what sensations are conveyed by the dorsal column?

A

fine touch, proprioception and vibration

163
Q

what neuro condition leads to loss of fine motor function in both upper limbs?

A

degenerative cervical myelopathy

it is a progressive condition, so worsening, deteriorating or new symptoms are warning signs

164
Q

what is an acoustic neuroma?

A

a benign tumour of the vestibulocochlear nerve

165
Q

which nerve is compressed in “Saturday night palsy?”

A

radial nerve

it is compressed against the humeral shaft - possibly due to sleeping with hand draped over a hard chair

166
Q

if a child does not respond to 2 doses of IV lorazepam in an episode of status epilepticus, what should be given next ?

A

IV phenytoin

167
Q

which condition is the cause of horizontal disconjugate eye movement?

A

internuclear opthalmoplegia

there is impaired adduction of the eye on the same side as the lesion

and horizontal nystagmus of the abducting eye on the contralateral side

can be caused by MS

168
Q

which drug used in the management of seizures can cause a megaloblastic anaemia?

A

phenytoin

it alters folate metabolism, causing megaloblastic anaemia

169
Q

describe the headache seen in a migraine?

A

unilateral pulsating headache made worse by movement

associated with at least two of: photophobia, phonophobia or osmophobia

they last 4-72 hours

170
Q

compare when NSAIDs, triptans, propranolol and topiramate are used to treat migraines?

A

acute relief: NSAIDs and triptans

prophylaxis: propranolol and topiramate

in the acute phase in a pregnant women, paracetamol is 1st line

171
Q

what class of drugs are triptans? ie- sumatriptan?

A

serotonin (5-HT) agonists

can reduce symptoms by up to 50%

172
Q

when should prophylactic Tx for migraines be considered?

A

if there is >2 attacks per month causing disability

173
Q

compare the character of tension headaches with migraines?

A

tension headaches: bilateral, not made worse by movement, last 30 mins- 7 days, characteristic pressure or tightness

migraines: unilateral, made worse by movement, last 4-72hours

174
Q

compare the Tx of chronic with acute tension headaches?

A

acute: paracetamol/ NSAIDs
chronic: relaxation techniques or amitriptyline

175
Q

describe the characteristics of a cluster headache?

A

always occurs on same side of head, severe unilateral headache that occurs around the orbit

lasts 0.5-3 hours

attacks tend to come in clusters where multiple attacks happen most days over a 1-3 month period

176
Q

describe how cluster headaches are treated acutely and also prophylactically?

A

acute: high flow O2 1st line, SC triptan 2nd line
prophylaxis: 1st line: verapamil, 2nd line topiramate

177
Q

what is thought to cause trigeminal neuralgia?

A

due to blood vessel dilation compressing the trigeminal nerve as it leaves cranium

178
Q

what medication class are used 1st line in tirgeminal neuralgia?

A

anti-convulsants (carbamazepine, lamotrigine)

surgical intervention is 2nd line

179
Q

how can a stroke (UMN) be differentiated from a bell’s palsy (LMN)?

A

in stroke (UMN), there is preservation of forehead wrinkling

in LMN cases, there is loss of forehead wrinking on affected side

180
Q

how is Bell’s palsy treated?

A

it is a diagnosis of exclusion

if <72 hours since onset - 60mg prednisolone for 5 days

if > 72 hours, no Tx given

majority of patients make full recovery in 3 months

181
Q

what makes up the circle of willis?

A

the basilar artery and 2 internal carotid arteries

182
Q

what artery joins the basilar artery to the internal carotids?

A

the posterior communicating artery

183
Q

what problems are associated with an anterior cerebral stroke?

A

contralateral weakness and sensory loss in the legs (hemiparesis)

184
Q

what problems are associated with an middle cerebral stroke?

A

contralateral sensory and motor loss of the face and arms (hemiparesis)

homonymous hemianopia (contralateral)

aphasia

185
Q

what problems are associated with a posterior cerebral artery stroke?

A

homonymous hemianopia with macular sparing

186
Q

what does a stroke in the ophthalmic artery cause?

A

amaurosis fugax

187
Q

what is the most common cause of haemorrhage stroke?

A

uncontrolled hypertension

others include: trauma, aneurysm, clothing disorders and tumours

188
Q

what accounts for 20% of strokes under the age of 40?

A

carotid artery dissection

189
Q

name 4 things that a carotid artery dissection would present with?

A
  1. focal neurological deficits
  2. pain in the neck or face
  3. Horner’s syndrome (dilated pupil and droopy eyelid)
  4. lower CN symptoms: facial weakness, visual loss, dysarthria
190
Q

name the 3 signs that are used to diagnose a total anterior circulation stroke (TACS) or a partial anterior circulation stroke (PACS)?

A
  1. hemiparesis (sensory and motor loss in face, arms or leg)
  2. homonymous hemianopia
  3. dysphasia/ other signs of visuospatial problems
3/3 = TACS
2/3= PACS
191
Q

name signs of a posterior circulation stroke?

A
  1. isolated homonymous hemianopia
  2. LOC
  3. cerebellar/brainstem signs (ataxia, facial weakness, nystagmus, diplopia)
192
Q

what is the definition of a lacunar stroke?

how does it present?

A

multiple small vessel infarcts in the basal ganglia and thalamus

purely sensory stroke

ataxic hemiparesis

unilateral weakness +/- sensory loss in face, arms or legs

193
Q

what imaging is 1st line in acute phase of stroke?

A

non contrast CT brain

194
Q

if a patient is presenting after 1 week of stroke like symptoms, what imaging is 1st line?

A

MRI

also used for mild deficits that suggest a small lesion

195
Q

how is ischemic stroke treated if presentation < 4.5 hours?

A

thrombolysis +/- thrombectomy

196
Q

name the 2ndary prevention for ischemic stroke?

A

1st line: clopidogrel

2nd line: aspirin + dipyridamole

197
Q

compare Broca’s and wernicke’s dysphasia?

A

broca’s = broken speech - it is non-fluent. comprehension normal, repetition impaired

wernicke’s: language comprehension is impaired. speech is fluent

198
Q

which form of Parkinson’s is known to have autonomic disturbance?

A

multi system atrophy

presents with erectile dysfunction, postural hypotension and an atonic bladder (requires catheter sometimes)

199
Q

what is the cushing reflex?

what is it due to?

A

bradycardia + hypertension with a wide pulse pressure

it is a physiological nervous system response to raised ICP

200
Q

which patients are most at risk of a medication overuse headache?

A

those using opioids and triptans

201
Q

which spinal tracts are compressed in syringomyelia?

A

the spinothalamic tracts

results in loss of sensation of pain, temperature and non-discriminative touch

202
Q

which neurocutaneous syndrome presents with hypopigmentation and subungual fibromas?

A

tuberous sclerosis

203
Q

broadly speaking, how can tuberous sclerosis be differentiated from neurofibromatosis?

A

both are neurocuteneous conditions

tuberous sclerosis tends to cause hypOpigmented (lighter) spots

NF tends to cause hyPERpigmented (darkened) spots

204
Q

name and compare the appearance of the cutaneous manifestations seen in neurofibromatosis and tuberous sclerosis?

A

NF: hyper pigmented cafe au lait spots

tuberous sclerosis: hypo pigmented ash leaf macules

205
Q

what is the most common type of cancer to spread to the brain?

A

lung cancer

206
Q

compare the most likely causes of upper and lower quadrant bitemporal hemianopia?

A

upper bitemporal hemianopia- inferior chiasmal compression = pituitary tumour

lower bitemporal hemianopia - upper chiasmal compression = craniopharyngioma

207
Q

damage to which nerve can cause weakness of foot dorsiflexion and foot eversion?

A

common peroneal nerve

208
Q

what is the most characteristic feature of a common peroneal nerve lesion?

A

foot drop

a high stepping gait develops to compensate for foot drop

209
Q

describe the tremor seen in an essential tremor?

A

postural tremor: worse if arms are outstretched

improved by alcohol and rest

propranolol is 1st line

210
Q

what is the 1st line management of ocular myasthenia gravis?

A

pyridostigmine

a long acting AChesterase inhibitor

211
Q

in a patient with status epilepticus, what 2 causes should be ruled out first, ASAP?

A

hypoxia and hypoglycaemia

212
Q

what is the strongest risk factor for developing a bells palsy?

A

pregnancy

213
Q

what is the main way to differentiate acute alcohol intoxication from wernicke’s encephalopathy?

A

the level of consciousness

in wernicke’s, the patient is conscious and able to follow commands

in acute alcohol intoxication, there would be a profound reduction in conscious level

214
Q

name the condition that presents with confusion, ataxia, nystagmus and opthalmiplegia?

A

wernicke’s encephalopathy

confused patient, but consciousness not impaired

Tx = urgent replacement of thiamine

215
Q

what is the most common complication following meningitis?

A

SNHL

216
Q

in which fracture may a wrist drop be found as a complication?

A

mid shaft humeral fracture

due to compression/damage to the radial nerve

217
Q

which 3 cranial nerves are most likely to be affected in vestibular schwannomas?

A

CN 5, 7 and 8

218
Q

which type of stroke presents with ipsilateral facial pain and temperature loss, and contralateral limb/torso pain and temperature loss? it may also present with ataxia and nystagmus.

A

PICA stroke

posterior inferior cerebellar artery

also known as lateral medullary syndrome

219
Q

which feature suggests a history of the ideopathic form of Parkinson’s?

A

an asymmetrical tremor

220
Q

compare the roles of “grey matter” and “white matter”?

A

grey matter - is where the processing is done

white matter - provides the communication between different grey matter areas

220
Q

where do the pyramidal tracts derive their name from?

A

name is derived from the medullary pyramids of the medulla oblongata, which the pyramidal tracts pass through

221
Q

compare the roles of pyramidal and extra pyramidal tracts?

A

both are motor tracts that enable movement

pyramidal tracts allow conscious control of muscles

extra-pyramidal tracts allow for unconscious, reflexive or responsive control of musculature (tone, balance, posture)

222
Q

name the 2 tracts that the pyramidal tracts are divided into?

A
  1. corticospinal tract
  2. corticobulbar tract

CS tract supples the musculature of the body

CB tract supples the musculature of the head and neck

223
Q

name 4 conditions that classically present due to damage to the extrapyramidal tracts?

A
  1. Parkinson’s disease
  2. Huntington’s disease
  3. multi system atrophy
  4. progressive supra nuclear palsy
224
Q

which class of medication is most associated with extra pyramidal side effects?

A

first generation/typical anti-psychotics

haloperidol and phenothiazine

225
Q

compare how sensation and motor symptoms present in guillian barre syndrome?

A

ascending motor weakness

sensory symptoms tend to be mild with very few signs

226
Q

why is timing of the surgery in degenerative cervical myelopathy important?

A

surgery should be carried out ASAP in DCM as any existing spinal cord damage can be permanent

treatment should ideally be within 6 months of diagnosis

227
Q

what is the key diagnostic test for guilian barre syndrome?

A

lumbar puncture

findings: elevated protein with normal WCC

228
Q

what is the best initial Tx for a patient presenting with a suspected TIA to a GP?

A

give 300mg aspirin now and refer for specialist review within 24 hours

229
Q

which type of stroke commonly occurs as a complication of longterm, poorly controlled hypertension?

A

pontine haemorrhage

230
Q

what is the definition of multi system atrophy?

A

it is a Parkinson’s plus syndrome…

it displays signs of Parkinsonism plus autonomic dysfunction (postural hypotension and erectile dysfunction)

231
Q

why may a patient with myasthenia gravis get distended neck veins and a flushed face?

A

due to superior vena cava obstruction, caused by a thymoma

232
Q

what is 1st line treatment for trigeminal neuralgia?

A

carbamazepine

233
Q

name 2 features specific to progressive supra nuclear palsy that do not occur in multi system atrophy?

A
  1. impairment of vertical gaze

2. frontal lobe dysfunction (out of character behaviour)

234
Q

what will nerve condition studies show in MND?

A

normal motor condition

this helps to exclude a neuropathy as a cause

235
Q

in a painful 3rd nerve palsy, where is the most likely location of the lesion?

A

posterior communicating artery aneurysm

236
Q

which is the only epileptic seizure where sodium valproate is not 1st line Tx?

what should be given in this seizure?

A

focal seizures

give carbamazepine or lamotrigine

237
Q

which drug is almost always associated with Steven-johnson syndrome?

A

carbamazepine

used 1st line for focal seizures

238
Q

what side effect of triptans should all patients be warned about?

A

tightness of the throat and chest

239
Q

what is the management for symptomatic chronic subdural haemorrhages?

A

burr hole evacuation

240
Q

compare the management of chronic and acute subdural haematomas?

A

acute: decompressive craniotomy

chronic (and symtomatic): burr holes

241
Q

describe pulse and BP in cushing’s reflex?

A

bradycardia and hypertension

AA Y4 Finals cards NE (40 decks)

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