Neurology Flashcards
what are the risk factors for stroke
hypertension
diabetes
smoking
hypercholesterolaemia
AF
what are the two main types of stroke
ischaemic and haemorrhage
how do you determine the location of an ischemic stroke
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
what are some right brain cortical signs
right gaze preference
and left sided neglect
what are some left sided brain cortical signs
left gaze preference
aphasia
what are the features of a MCA stroke
arm weakness more than leg weakness
LMCA cognitive: aphasia
RMCA: neglect and topographical difficulty and apraxia, constructional impairment and anosognosia
what are the features of a ACA stroke
- leg weakness is greater than arm weakness, grasp
- cognitive: muteness, preservation and abulia
- personality change if its bilateral
what are the features of a PCA stroke
hemianopia
cognitive: memory loss/confusion and Alexia
what are some potential findings in a brainstem stroke
- double vision
- fascial numbness and or weakness
- slurred speech
- difficulty walking and ataxia and vertigo and nausea an vomitting and hoarseness
where are ICH typically located
spontaneous rupture of a small artery deep in the brain typically in the basal ganglia
airway investigation in ICH
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
what sort of imaging would you perform
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
what is the acute treatment of stroke
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
what are some secondary causes of headache
thunderclap headaches
high pressure headaches
low-pressure headaches
the neuralgia’s
initial examinations of a patient with headache
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
what investigations could be performed in a patient presenting with headache
blood pressure
ECG
urinalysis
bloods (ESR, CRP, FBC, UE, Thyroid)
CT/MRI BRAIN
lumbar puncture
angiogram CT
who do you image
SSSNOOPPP
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
diagnostic criteria for a tension headache
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
what is the pathophysiology of migraines
there is an interaction between primary afferent nociceptive neurone/trgeminovascular system/brainstem/thalamus/hypothalamus/cortex
calcitonin gene related peptide
NOT a primary vascular problem
migraine diagnosis criteria
what are the phases migraine
what are the key elements of aura
- evolves
- 5-60 mins
- positive and negative elements
- fully reversible
acute treatment of migraine
some examples of prophylactic therapy
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
some examples of medicational prophylaxis in migraines
propanolol
topiramate
amitriptyline
candesartan
flunarazine
what would you use after initial prophylactic medications failed
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
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
bradykinesia
slowness in initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions
clinical features of Parkinson’s
bradykinesia and at least one of the following:
- muscular rigidity
- 4-6 Hz rest tremor
- postural instability
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
what are some common causes of Parkinson’s
drug induced
MSA
Lewy body dementia
PSP
CBD
Vascular Parkinsonism
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
what is the pharmacological aim of drug management of parkinsons
to restore dopamine levels
what is the clinical aim of drug management in parkinsons
to improve motor symptoms/improve quality of life
what are the PD drug classes
L-dopa
Dopamine agonists
MAO-B inhibitors
COMT-inhibitors
what are some adverse effects L-dopa preparations (dopa decarboxylase inhibitor)
peripheral: nausea, vomiting, postural hypotension
Central: confusion and hallucinations
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
side effects of dopamine agonists
day time somnolence
impulse control disorders (pathological gambling and hyper sexuality)
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
example of a MAOB inhibitor
selegiline and rasagiline
examples of COMT inhibitors
what are some motor complications of advanced PD
on off fluctuations and l-dopa induced dyskinesia
axial complications of advanced PD
gait difficulties
change in posture
poor balance/falls
speech and swallowing difficulties
cognitive problems in advanced PD
dementia and hallucinations and psychosis
other treatment options besides tablets for PD
apomorphine pen injections or subcutaneous pump
intrajeunal duodopa infusion
Depp brain stimulation surgery
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
what are the 3 implantable components of DBS
brain leads containing electrodes in the distal end
neurostimulator (implantable pulse generator IPG)
extension wires
emergencies in PD
parkinson-hyperpyrexia syndrome
acute psychosis
falls
DBS failure
consider bone health
exercise
advanced care planning
support groups
what are some causes of seizures
faints
fits metabolic cause
psychiatric
trauma
what is the basic science behind an action potential
what is the definition of a seizure
it is a sustained and synchronised electrical discharge in the brain causing symptoms or signs
what causes excitation in a neurone
EAA
Action on NMDA/AMPA/Kainate
Na/Ca influx
what causes the inhibition of an action potential in a neurone
GABA/Glycine
Action of GABA-R
Cl- influx
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
what is the definition of epilepsy
a tendency to have recurrent unprovoked seizures
what are the three classifications of epilepsy
focal epilepsy - localised onset (stroke or scarring or an abscess)
genetic generalised - generalised onset
uncertain
localised onset epilepsy treatment
lamotrigine, carbamazepine, levetiracetam
treatment for generalised onset epilepsy
valproate, levetiracetam and lamotrigine
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
ilness work
the work that patients and their families have to do to understand and live with chronic illness
what is treatment work
tasks that need to be performed to manage health and follow treatments set by healthcare providers
patient capacity
the degree to which patients can cope with management of their illness and their lives
give four factors which influence treatment burden
interacting with others
enacting management strategies
reflecting on management
making sense of treatments and planning care
way of tackling non compliance with medications
ways of tackling appointment non attendance
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
What is important in the background history of dementia
vascular disease such as stroke, trauma, cancer and major mental health issues
what is important in the drug history in dementia
prescribed drugs (care anti-cholinergic elderly), illicit drugs and alcohol
what are the two main bedside assessments used to assess cognitive function
Folstein MMSE
addenbrookes cognitive assessment
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
what are the three facets of executive function
behavioural aspect - orbitofrontal
attention/working memory - dorsolateral prefrontal cortex
Motivation/goal driven - anterior cingulate
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
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
what are the three types of memory
semantic
episodic and working
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
what is the typical disease pathology in Alzheimers
hippocampus = episodic memory
cortical = visuospatial
global atrophy = language centres = language
semantic memory
this is general knowledge
marked reduction in verbal fluency category and impairment of regular words (dyslexia)
what does visuospatial involve
where and what
accurately localise objects
what is processed in the dorsal stream
position of object in space (dyspraxia)
what is processed in the ventral stream
object recognition (visual agnosia)
fascial recognition (prosopagnosia)
language disorders
