neuro volume 1 Flashcards
discuss ischaemic stroke + risk factors
85% of all strokes
cerebral infarction due to insufficient cerebral blood flow.
is a syndrome not a disease
most likely thrombotic - RF= Male, older, FHx, smoking, booze, HTN, DM, hyperlip, CVD, PVD, obesity.
Embolic- AF, Rheumatic heart disease, carotid stenosis
discuss the vascular territories and the smyptoms they will give
ACA- contralateral sensory + motor function of legs
MCA- contralateral sensory + arms and face motor function. Bocas, Wernicks, Parietal (visuospatal deficits) temporal- contralateral homonymous hemianopia.
PCA= occipital lobe -visual loss, macula sparing.
investigations of ischaemic stroke + RX
urgent neuroimaging- CT/ MRI then CTA
rule out haemorrhagic strokes
FBC, U+E, ESR, Check blood pressure.
carotid doppler
SALT for swallow
cardiac assessment - ECG (AF) Echo for emboli/ valve issues.
Rx: ABCDE
300mg aspirin + PPI
Alteplase (thrombolysis) within 4.5 hours
thrombectomy is less than 6 hours (NIHSS score less than 6)
2’ prevention- aspirin for 2/52 post stroke
switch to clopidogrel after 2/52
statin if approp
aim for BP <130/80
carotid endarterectomy is stenosis >50%
epidemiology of stroke + complications of stroek
100,000 in the uk each year
38 000 deaths (11% of all deaths)
common in older lower levels of education people.
DVT, haemorrhagic transformation of ischaemic stroke (more common in larger infarcts + if alteplase has been given)
alteplase related orolingual oedema
depression
fatigue
aspiration pneumonia
what is a TIA
transient episode or neurological dysfunction- caused by brain, spinal, retinal ischaemia. resolves in 24 hours, but in most cases in less than 1 hour.
there is no tissue based injury - no ischaemic lesion seen on brain imaging.
risk of recurrent stroke is high (10%) in 1st 7/7. starting 2’ prevention immediately once TIA diagnosis is confirmed.
epidemiology of TIA + risk factors. what flow rates are needed in the brain for it to thrive, survive, and die
each year 2000 people have their 1st TIA episode. 190 per 100 000 (age adjusted)
risk factors- as per ischaemic stroke
normal flow is 50ml/100g/ min
20-50 ml/100g/min the brain can extract more O2 and manage
below 15 neuronal death will occur.
early in ischaemic neuronal injury- cytotoxic oedema causes influx of water to intracellular space- observable as hyperintensity on MRI. - complete by 2 hours, not present at 15 mins.
diagnosis of a TIA
anyone with sudden onset focal neuro deficit which resolves should be suspected - espesh if cannot be explained by other condition
treat as a stroke until the symptoms have completely resolved.
no reliable test to tell you its a tia, so FAST or other stroke tool
in clinic Ix:
glucose, FBC + platelet, prothrombin, INR, partial thromboplastin time, fasting lipid, serum electrolytes. ECG, inc 24 hour tape.
Rx: loading dose aspirin (300) + PPI
refer to a TIA clinic- to be seen within 24 hours of symptoms
Duel antiplateles (aspirin + clopidogrel) for 21 days, or aspirin + tricagrelor for 30 days.
single antiplatelet Rx is enough after that.
consider statin, anticoagulant.
discuss intraparenchymal haemorrhage
bleeding into the brain parenchyma (but not the ventricles)
accounts for 10-20% of all strokes. - 2nd most common form
incidence increases after age 55, slight male predominance.
most often occurs to hypertensive damage - eventual bursting and bleeding. (primary) - or 2’ is trauma, tumor, EVM etc.
presents with the classical symptoms of stroke
Ix + management of intra-parenchymal haemorrhage
ABCDE approach initially
then
Ct without contrast - hyperdense within the parenchyma (gold standard)
complete neuro exam to assess deficits.
FBC for the usuals
consider MRI is patient suitable- can be bleeding as a result of tumour
Mx: control blood pressure
discuss with neurosurg- surgical evacuation, craniectomy
neuroprotective measures, reverse coagulopathys
prognosis of Intra parenchymal haem
POOR
30 day mortality of 20-60%
prognostic factors: GCS at presentation, location, age, anticoag use + presence of interventricular extension
Cerebral venous sinus
thrombosis overview
a very rare condition- thrombosis of the cerebral veins/ sinuses. can lead to sig morbidity and mortality. - variable in presentation, challenging diagnosis - onset to hospital admission is usually 4 days, diagnosis is 7.
S+S: headache (mimic migranes but inc in severity over days), benign intercranial hypertension, subarach haemorrhage, focal neuro deficit especially cranial nerve 6 , seizures, meningoencephalitis.
aetiology + epidemiology of cerebral venous sinus overview
any prothrombotic state can dispose you to developing this.
3-4 cases per million each year.
significantly increased in post partum/ pregnancy.
3x more common in women.- due to the early age risks (HRT, contraceptive pill, pregnancy)
injury to brain is caused by: thrombus increases venous and cap pressure
decreased cerebral perfusion
ischaemic injury + cytotoxic edema
damaged membrane + swelling.
2nd mechanism resulting in loss of CSF absorption- increased ICP.
investigations for central venous sinus thrombosis + treatment
Valsalva- if headache made worse then indicative.
look for papilloedema + visual symptoms (6th CN palsy)
focal neuro signs- so full neuro exam.
focal seizures
exclude anything serious- imaging can be normal at first but then will show after a few days.
anticoagulate- with heparin then warfarin (inr 2-3)
decompressive hemicraniectomy if looking like it will rupture
thrombectomy provides limited benefit.
presentation of sub arachnoid headache + RF, epidaemiology.
sudden headache peaking within 1-5 mins. lasts more than an hour; typically alongside vomiting, photophobia, and non-focal neurological signs.
Risk factors: HTN, smoking, family history
polycystic kidney disease.
incidence is between 6-8 per 100 000
1.6 more common in women.
2.1 x more common in black people vs white people. 5% of all strokes.
aetiology: 80% are due to ruptured berry aneurisms. 20% from other causes - e.g AV formation.
investigations of sub arachnoid haemorrhage
acute + life threatening early diagnosis + secure aneurism within 48 hours.
Ix: full history
full neuro ax (any pupil changes discuss with neurosurg)
urgent non contrast CT. - within 6 hrs of onset
FBC, clotting, top, glucose
ECG + continuous monitoring.
consider LP if CT (if done after 6 hrs) is inconclusive, wait 12 hrs before LP.
Mx: if GCS <8- secure airway
ABC approach
nimodipine- prevent delayed cerebral ischaemia
stop + reverse anticoagulent
endovascular coiling or surgical clipping / cons mgt
aneurisms that are less than 7mm in diameter and discovered during other things are low risk to rupture, if bigger or exerting mass effect then more at risk of blowing.
sub dural haemorrhage definition
SDH is a collection of blood between the dural and arachnoid coverings of the brain
can progress to herniation if untreated. large variation in reported incidence. caused by trauma/ assault.
risk factors:
head trauma
anticoagulant use
age over 65
signs and symptoms- nausea, decreased verbal response, dec motor response, confusion, headache.- seizures otorrhea, rhinorrhoea are less common but present
1st line Ix is non contrast CT scan.
types of sub dural haemotoma
defined by chronicity- acute < 3 days - hyperdense appearance on CT
Subacute SDH (3-21 days old, heterogeneously hyperdense/isodense)
Chronic SDH (>21 days old, diffusely hypodense)
or acute: chronic
chronic formed by leaking bridging veins +/- osmotic radiant pull into the haematoma from CSF
what to look out for in babies with subdural haemorrhages + management of
shaken baby syndrome
retinal haemorrhage
sub Dural haematoma
brain swelling.
Mx: stop anticoagulation
conservative if <10 mm width and <5 mm midline shift.
craniotomy decompression and burr hole drainage
maintain cerebral perfusion pressure of 60 to 70 mmHg and ICP <22 mmHg (in adults)
Levetiracetam and phenytoin- prophylactic antiepileptics
how many deaths a day are due to epilepsy
3 per day
often young adults
what is the single diagnostic test for epilepsy
there is none! need multiple sources of information.
- was it a seziure
- what type
3 whats the cause
4 was it epilepsy - what impairment is it causing.
definition of seizure
transient occurrence of signa and or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.
signs it was a seziure
usually breif self limiting, stereotyped to that persons seziures
massive inter-individual variation
little intra-individual
spread/ recruitment of anatomically connected groups of neurons
orientated immediately after a feint, not after a seziure takes time to recover, can feel like they have done immense physical exertion.
what causes unprovoked seziures
‘normal’ stuff- like dec sleep, photosensitive
you can have a known cause but it wouldnt ‘normally’ cause a seziure- unlike hypoglycaemia or trauma whicch would cause one.
can be some blurring in the middle, how much booze is enough to give someone a seziure etc etc etc
lots of things can then go on to cause epilepsy- hx of traume, stroke, encephalopahy, tumour.
new epilepsy dfinition
a disorder of the brain charactrised by an enduring predisposition to generate epileptic seizures and by the neurobiologic cognitive psychological and social consequences of tis condition.
any of the following conditions
at least two unprovikes occuring more than 24 hours apart
one unprovoked seziure + possibility of more
management of convulsive status epilepticus
benzoz
diazapam midaz or loraz
aed 40mg/kg valporate
intubate if after 30
