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GLA Y3S1 > Neurology > Flashcards

Neurology Flashcards

1
Q

what are the risk factors for stroke

A

hypertension
diabetes
smoking
hypercholesterolaemia
AF

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2
Q

what are the two main types of stroke

A

ischaemic and haemorrhage

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3
Q

how do you determine the location of an ischemic stroke

A

if its in large vessels look for cortical signs

if its in small vessels there won’t be any

if its in the posterior circulation there will be cranial nerve findings and crossed signs

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4
Q

what are some right brain cortical signs

A

right gaze preference
and left sided neglect

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5
Q

what are some left sided brain cortical signs

A

left gaze preference
aphasia

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6
Q

what are the features of a MCA stroke

A

arm weakness more than leg weakness
LMCA cognitive: aphasia
RMCA: neglect and topographical difficulty and apraxia, constructional impairment and anosognosia

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7
Q

what are the features of a ACA stroke

A
  • leg weakness is greater than arm weakness, grasp
  • cognitive: muteness, preservation and abulia
  • personality change if its bilateral
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8
Q

what are the features of a PCA stroke

A

hemianopia
cognitive: memory loss/confusion and Alexia

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9
Q

what are some potential findings in a brainstem stroke

A
  • double vision
  • fascial numbness and or weakness
  • slurred speech
  • difficulty walking and ataxia and vertigo and nausea an vomitting and hoarseness
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10
Q

where are ICH typically located

A

spontaneous rupture of a small artery deep in the brain typically in the basal ganglia

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11
Q

airway investigation in ICH

A

if GCS less that 8 then INTUBATE
avoid hyperventilation or hypoventialltion
NBM until swallow assessment completed as there is a high aspiration risk
begin mobilisation as soon as clinically safe

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12
Q

what sort of imaging would you perform

A

non-contrast CTH - good at identifying aneurysms, AVMs and Tumours

MRI - superior for showing underlying structural lesions however there are contraindications as patients may have internal metal you dont know about

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13
Q

what is the acute treatment of stroke

A

tPa
window of delivery within 4.5 hours and it decreases the disability risk by 30%

CANNOT GIVE IN HAEMORRGAHE
or recent surgery
coagulopathy
SBP less than 185 or DBP more than 110

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14
Q

what are some secondary causes of headache

A

thunderclap headaches
high pressure headaches
low-pressure headaches
the neuralgia’s

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15
Q

initial examinations of a patient with headache

A

blood pressur, urine dipstick, pregnancy test, temperature, weight
GCS? MSE?

could palpate the skull and neck and greater occipital nerves, TMJ and temporal arteries and nuchal rigidity

EYES - papillooedema
horners?
fascial sensation?

cranial nerves

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16
Q

what investigations could be performed in a patient presenting with headache

A

blood pressure
ECG
urinalysis
bloods (ESR, CRP, FBC, UE, Thyroid)
CT/MRI BRAIN
lumbar puncture

angiogram CT

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17
Q

who do you image
SSSNOOPPP

A

systemic symptoms
secondary risk factors
seizures
neurological symptoms
onset
older
progression
papolloedema
precipitated by cough, exertion, sleep or valsalvs

CSF
change in nature of headache
systemic symptoms
focal neurological defect

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18
Q

diagnostic criteria for a tension headache

A

at least 10 episodes of headaches
lasts from 30 mins to 7 days
bilateral location
pressing or tightening
mild or moderate intensity
not aggravated by physical routine
no nausea and vomitting

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19
Q

what is the pathophysiology of migraines

A

there is an interaction between primary afferent nociceptive neurone/trgeminovascular system/brainstem/thalamus/hypothalamus/cortex

calcitonin gene related peptide
NOT a primary vascular problem

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20
Q

migraine diagnosis criteria

A
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21
Q

what are the phases migraine

A
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22
Q

what are the key elements of aura

A
  • evolves
  • 5-60 mins
  • positive and negative elements
  • fully reversible
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23
Q

acute treatment of migraine

A
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24
Q

some examples of prophylactic therapy

A

lifestyle advice and triggers
identify and treat a medication overuse headache
give medication prophylaxis if they have more than 4-5 disabling headaches per month
use headache diarires
always review meds after 3 months
if effective continue for 6 - 12 months

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25
Q

some examples of medicational prophylaxis in migraines

A

propanolol
topiramate
amitriptyline
candesartan
flunarazine

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26
Q

what would you use after initial prophylactic medications failed

A
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27
Q

what history features would make you think of a secondary cause for a headache

A

worse on lying flat
worse in the morning
persistent nausea and vomitting worse on valsalva
worse on physical exertion
transient visual obscurations with change in posture

optic disc swelling
impaired visual acuity
restricted visual fields
3rd nerve palsy
6th nerve palsy
focal neurological signs

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28
Q

thunderclap headache

A

onset within one minute and lasts more than an hour
MEDICAL EMERENCY
CAUSES:
- intercerebral haemorrhage
arterial dissection
cerebral venous sinus thrombosis
ischaemia stroke
bacterial meningitis

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29
Q

bradykinesia

A

slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions

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30
Q

clinical features of Parkinson’s

A

bradykinesia and at least one of the following:
- muscular rigidity
- 4-6 Hz rest tremor
- postural instability

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31
Q

what are some of the non motor symptoms of Parkinson’s

A

dementia
depressio
urinary urgency and nocturia
speech difficulties
restless leg syndrome
reduced olfactory function
hallucinations and delusions
erectile dysfunction
anxiety
excessive salvation
constipation

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32
Q

what are some common causes of Parkinson’s

A

drug induced
MSA
Lewy body dementia
PSP
CBD
Vascular Parkinsonism

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33
Q

what are some red flags in parkinsons patients which may make you think it isn’t Parkinsons

A

rapid gait impairment requiring a wheelchair within 5 years
no progression of their motor symptoms
marked bulvar dysfunction within 5 years

34
Q

what is the pharmacological aim of drug management of parkinsons

A

to restore dopamine levels

35
Q

what is the clinical aim of drug management in parkinsons

A

to improve motor symptoms/improve quality of life

36
Q

what are the PD drug classes

A

L-dopa
Dopamine agonists
MAO-B inhibitors
COMT-inhibitors

37
Q

what are some adverse effects L-dopa preparations (dopa decarboxylase inhibitor)

A

peripheral: nausea, vomiting, postural hypotension
Central: confusion and hallucinations

38
Q

dopamine agonists

A

Ropinirole

  • longer half life than L-dopa and less effacious

there are fewer motor complications can be used as a monotherapy in early PD

39
Q

side effects of dopamine agonists

A

day time somnolence
impulse control disorders (pathological gambling and hyper sexuality)

40
Q

enzyme inhibitors - the two types

A

MAO-B = can be prescribed in early disease as a monotherpy

COMT = results in longer L-dopa half-life and therefore a longer duration of action
Co-prescribed with L-dopa (stalevo is the combined tablet)

side effects are dopinergic and diarrhoea

41
Q

example of a MAOB inhibitor

A

selegiline and rasagiline

42
Q

examples of COMT inhibitors

A
43
Q

what are some motor complications of advanced PD

A

on off fluctuations and l-dopa induced dyskinesia

44
Q

axial complications of advanced PD

A

gait difficulties
change in posture
poor balance/falls
speech and swallowing difficulties

45
Q

cognitive problems in advanced PD

A

dementia and hallucinations and psychosis

46
Q

other treatment options besides tablets for PD

A

apomorphine pen injections or subcutaneous pump
intrajeunal duodopa infusion
Depp brain stimulation surgery

47
Q

what does DBS

A

allows electrical stimulation of target nucleus most commonly the STN

provides a targeted, adjustable, non-destructive and reversible way of modulating pathological brain circuits

48
Q

what are the 3 implantable components of DBS

A

brain leads containing electrodes in the distal end
neurostimulator (implantable pulse generator IPG)
extension wires

49
Q

emergencies in PD

A

parkinson-hyperpyrexia syndrome
acute psychosis
falls
DBS failure

consider bone health
exercise
advanced care planning
support groups

50
Q

what are some causes of seizures

A

faints
fits metabolic cause
psychiatric
trauma

51
Q

what is the basic science behind an action potential

A
52
Q

what is the definition of a seizure

A

it is a sustained and synchronised electrical discharge in the brain causing symptoms or signs

53
Q

what causes excitation in a neurone

A

EAA
Action on NMDA/AMPA/Kainate
Na/Ca influx

54
Q

what causes the inhibition of an action potential in a neurone

A

GABA/Glycine
Action of GABA-R
Cl- influx

55
Q

what are the two types of seizures

A

generalised tonic-clonic seizures (bilaterally convulsive)
partial seizures:
- loss of awareness
- motor phenomena
- sensory phenomena
- psychological phenomena
- cognitive phenomena

56
Q

what is the definition of epilepsy

A

a tendency to have recurrent unprovoked seizures

57
Q

what are the three classifications of epilepsy

A

focal epilepsy - localised onset (stroke or scarring or an abscess)
genetic generalised - generalised onset
uncertain

58
Q

localised onset epilepsy treatment

A

lamotrigine, carbamazepine, levetiracetam

59
Q

treatment for generalised onset epilepsy

A

valproate, levetiracetam and lamotrigine

60
Q

what is treatment burden

A

workload of healthcare for individuals managing long term health conditions and the impact on wellbeing

results due to workload volume and care deficiencies

high levels can lead to poor adherence, disengaging from health services and poorer QOL

61
Q

ilness work

A

the work that patients and their families have to do to understand and live with chronic illness

62
Q

what is treatment work

A

tasks that need to be performed to manage health and follow treatments set by healthcare providers

63
Q

patient capacity

A

the degree to which patients can cope with management of their illness and their lives

64
Q

give four factors which influence treatment burden

A

interacting with others
enacting management strategies
reflecting on management
making sense of treatments and planning care

65
Q

way of tackling non compliance with medications

A
66
Q

ways of tackling appointment non attendance

A
67
Q

what is the definition of dementia

A

progressive cognitive decline with the cognitive behavioural impairment involving a minimum of two of the following domains
- memory
- executive function
- language
- apraxia/visuospatial

MUST INTERFERE WITH THE ABILITY TO FUNCTION AT WORK OR USUAL ACTIVITIES
REPRESENT A DECLINE FROM PREVIOUS LEVELS OF FUNCTIONING AND PEFORMING AND NOT BE EXPLAINED BY DELIRIUM OR MAJOR PSYCHIATRIC DISORDER

68
Q

What is important in the background history of dementia

A

vascular disease such as stroke, trauma, cancer and major mental health issues

69
Q

what is important in the drug history in dementia

A

prescribed drugs (care anti-cholinergic elderly), illicit drugs and alcohol

70
Q

what are the two main bedside assessments used to assess cognitive function

A

Folstein MMSE
addenbrookes cognitive assessment

71
Q

ACE-r examines what and what is its purpose

A
  • executive function
  • memory
  • language
  • visuospatial

its purpose is to assess severity and the pattern of impairment

72
Q

what are the three facets of executive function

A

behavioural aspect - orbitofrontal
attention/working memory - dorsolateral prefrontal cortex
Motivation/goal driven - anterior cingulate

73
Q

what is attention/concentration/orientation

A

this is the component of consciousness which allows filtering of information to allow one to focus on particular stimuli

pathological processes include delirium and often depression

can test with orientation and the series 7s in the ACEr

74
Q

if you have impaired behaviour and judgment (dysexecutive disorders) what kind of dementia are you most likely to have

A

this disinhibited behaviour is often associated with front-temporal dementia

75
Q

what are the three types of memory

A

semantic
episodic and working

76
Q

how do you test episodic memory in the acer

A

anterograde memory is with the address learning and retrograde memory is with the famous historical figures

77
Q

what is the typical disease pathology in Alzheimers

A

hippocampus = episodic memory
cortical = visuospatial
global atrophy = language centres = language

78
Q

semantic memory

A

this is general knowledge

marked reduction in verbal fluency category and impairment of regular words (dyslexia)

79
Q

what does visuospatial involve

A

where and what
accurately localise objects

80
Q

what is processed in the dorsal stream

A

position of object in space (dyspraxia)

81
Q

what is processed in the ventral stream

A

object recognition (visual agnosia)
fascial recognition (prosopagnosia)

82
Q

language disorders

A

GLA Y3S1 (13 decks)

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