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
some examples of medicational prophylaxis in migraines
propanolol topiramate amitriptyline candesartan flunarazine
26
what would you use after initial prophylactic medications failed
27
what history features would make you think of a secondary cause for a headache
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
28
thunderclap headache
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
29
bradykinesia
slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions
30
clinical features of Parkinson's
bradykinesia and at least one of the following: - muscular rigidity - 4-6 Hz rest tremor - postural instability
31
what are some of the non motor symptoms of Parkinson's
dementia depressio urinary urgency and nocturia speech difficulties restless leg syndrome reduced olfactory function hallucinations and delusions erectile dysfunction anxiety excessive salvation constipation
32
what are some common causes of Parkinson's
drug induced MSA Lewy body dementia PSP CBD Vascular Parkinsonism
33
what are some red flags in parkinsons patients which may make you think it isn't Parkinsons
rapid gait impairment requiring a wheelchair within 5 years no progression of their motor symptoms marked bulvar dysfunction within 5 years
34
what is the pharmacological aim of drug management of parkinsons
to restore dopamine levels
35
what is the clinical aim of drug management in parkinsons
to improve motor symptoms/improve quality of life
36
what are the PD drug classes
L-dopa Dopamine agonists MAO-B inhibitors COMT-inhibitors
37
what are some adverse effects L-dopa preparations (dopa decarboxylase inhibitor)
peripheral: nausea, vomiting, postural hypotension Central: confusion and hallucinations
38
dopamine agonists
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
side effects of dopamine agonists
day time somnolence impulse control disorders (pathological gambling and hyper sexuality)
40
enzyme inhibitors - the two types
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
example of a MAOB inhibitor
selegiline and rasagiline
42
examples of COMT inhibitors
43
what are some motor complications of advanced PD
on off fluctuations and l-dopa induced dyskinesia
44
axial complications of advanced PD
gait difficulties change in posture poor balance/falls speech and swallowing difficulties
45
cognitive problems in advanced PD
dementia and hallucinations and psychosis
46
other treatment options besides tablets for PD
apomorphine pen injections or subcutaneous pump intrajeunal duodopa infusion Depp brain stimulation surgery
47
what does DBS
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
what are the 3 implantable components of DBS
brain leads containing electrodes in the distal end neurostimulator (implantable pulse generator IPG) extension wires
49
emergencies in PD
parkinson-hyperpyrexia syndrome acute psychosis falls DBS failure consider bone health exercise advanced care planning support groups
50
what are some causes of seizures
faints fits metabolic cause psychiatric trauma
51
what is the basic science behind an action potential
52
what is the definition of a seizure
it is a sustained and synchronised electrical discharge in the brain causing symptoms or signs
53
what causes excitation in a neurone
EAA Action on NMDA/AMPA/Kainate Na/Ca influx
54
what causes the inhibition of an action potential in a neurone
GABA/Glycine Action of GABA-R Cl- influx
55
what are the two types of seizures
generalised tonic-clonic seizures (bilaterally convulsive) partial seizures: - loss of awareness - motor phenomena - sensory phenomena - psychological phenomena - cognitive phenomena
56
what is the definition of epilepsy
a tendency to have recurrent unprovoked seizures
57
what are the three classifications of epilepsy
focal epilepsy - localised onset (stroke or scarring or an abscess) genetic generalised - generalised onset uncertain
58
localised onset epilepsy treatment
lamotrigine, carbamazepine, levetiracetam
59
treatment for generalised onset epilepsy
valproate, levetiracetam and lamotrigine
60
what is treatment burden
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
ilness work
the work that patients and their families have to do to understand and live with chronic illness
62
what is treatment work
tasks that need to be performed to manage health and follow treatments set by healthcare providers
63
patient capacity
the degree to which patients can cope with management of their illness and their lives
64
give four factors which influence treatment burden
interacting with others enacting management strategies reflecting on management making sense of treatments and planning care
65
way of tackling non compliance with medications
66
ways of tackling appointment non attendance
67
what is the definition of dementia
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
What is important in the background history of dementia
vascular disease such as stroke, trauma, cancer and major mental health issues
69
what is important in the drug history in dementia
prescribed drugs (care anti-cholinergic elderly), illicit drugs and alcohol
70
what are the two main bedside assessments used to assess cognitive function
Folstein MMSE addenbrookes cognitive assessment
71
ACE-r examines what and what is its purpose
- executive function - memory - language - visuospatial its purpose is to assess severity and the pattern of impairment
72
what are the three facets of executive function
behavioural aspect - orbitofrontal attention/working memory - dorsolateral prefrontal cortex Motivation/goal driven - anterior cingulate
73
what is attention/concentration/orientation
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
if you have impaired behaviour and judgment (dysexecutive disorders) what kind of dementia are you most likely to have
this disinhibited behaviour is often associated with front-temporal dementia
75
what are the three types of memory
semantic episodic and working
76
how do you test episodic memory in the acer
anterograde memory is with the address learning and retrograde memory is with the famous historical figures
77
what is the typical disease pathology in Alzheimers
hippocampus = episodic memory cortical = visuospatial global atrophy = language centres = language
78
semantic memory
this is general knowledge marked reduction in verbal fluency category and impairment of regular words (dyslexia)
79
what does visuospatial involve
where and what accurately localise objects
80
what is processed in the dorsal stream
position of object in space (dyspraxia)
81
what is processed in the ventral stream
object recognition (visual agnosia) fascial recognition (prosopagnosia)
82
language disorders