Stroke/TIA Flashcards
(76 cards)
1
Q
What are the important parts of a stroke history?
A
- focal neurological symptoms of acute onset <– important!
- LOC & Headache <– typical!
- contiguous parts of the body affectged concurrently (no spread - that would be more like seizure)
- negative vs positive symptoms (flashes/prickles/extra movements)
- RF’s (CVS etc)
- FHx, ETOH and rec drugs
2
Q
what should be looked at on stroke examination?
A
- Inspection – obvious hemiparesis, facial weakness, neglect of one side.
- Inspection – look for xanthoma, stigmata of endocarditis, marfanoid appearance, skin lesions of Fabry’s.
- Pulse – atrial fibrillation
- BP – hypertension
- CVS – murmurs, carotid and renal bruits, evidence of periph. vasc. disease
- Neuro – Full exam! Or enough to calculate NIH Stroke Scale score!!
3
Q
What parts of a neuro exam should be done in stroke?
A
- Cranial nerves – full exam. Check for visual inattention.
- Fundoscopy – hypertensive/diabetic retinopathy.
- PNS – check for drift!
- Gait
- Cerebellar exam.
- Cortical signs – inattention, apraxia, dysphasia
- Speech – dysarthria or dysphasia. Check for fluency, repetition, articulation. Can they follow 1,2 and 3 stage commands?
4
Q
What is the definition of a stroke
A
- sudden interruption in vascular supply to the brain
- result in rapidly developing focal neurological deficit; (e.g. acute onset)
- >24hrs
5
Q
Which strokes are more common out of ischaemic and haemorrhagic?
A
ischaemic = 85%
haemorrhagic = 15%
6
Q
out of ischaemic strokes which of thrombotic or embolic is more common? & what are causes of both?
A
embolic (80%) is more common –>
- cause: left heart AF
- infective endocarditis
- long bone #’s (the haemorrhagic shock and systemic inflammation can precipitate an ischaemic stroke)
- non-thrombotic embolism: fat, air, amniotic fluid
thrombotic (20%)
- rupture of atherosclerotic plaque in an ICA & thrombus –> embolism
- rarely: due to atheromatous rupture of cerebral artery with occlusion at site (less affected by atherosclerosis)
7
Q
What are the risk factors for ischaemic stroke vs haemorrhagic?
A
Both RF:
- age,
- HTN
Ischaemic:
- smoking,
- hyperlipidaemia,
- AF
Haemorrhagic:
- ArterioVenous Malformation
- anticoagulation
8
Q
apart form thrombolic or embolic stroke what else causes ischaemic strokes?
A
- Systemic hypo-perfusion e.g. cardiac arrest –> watershed infarcts
- Cerebral venous sinus thrombosis - results in venous congestion & hypoxia which damages brain tissue
- Cryptogenic - unknown cause 1/3rd of strokes are these
- Anti-phospholipid syndrome
- Thrombophilia
- Arterial dissection (sudden onset, more common in young on straining)
9
Q
What are the caues of haemorrhagic strokes?
A
- HTN
- AVMs
- (Aneurysmal)
- CAA (cerebral amyloid angiopathy e.g. degenerative vasculopathy)
- Anti-coagulation therapy/ haemophilia
- Recreational drugs
10
Q
Which of white or grey matter dies quicker in ischaemic stroke?
A
GREY MATTER IS HIGHLY METABOLICALLY ACTIVE, DIES QUICKER
TIME IS BRAIN - each minute stroke is untreated, destroyed is:
- 1.9 million neurons
- 14 billion synapses
- 12 km (7.5 miles) of myelinated fibres
- The ischemic brain ages 3.6 years each hour without treatment
11
Q
What occurs if you get perfusion failure of the brain?
A
the ischaemic cascade
- energy failure –> no ATP produced, lactic acid & CO2 build up = acidosis –> ion gradients dissipate from Na/K+ pump failure
- –> mambrane depolarisation and large scale NT release (including toxic-in-high-conc. glutamate!)
- –> excitotoxic injury and oxidaive stress from 10x normal glutamate conc = NMDA receptor overstimulation
- –> large Ca2+ influx = cell apoptosis
point of no return = when membrane integrity is compromised and water leaks into the cell = cytotoxic oedema
12
Q
What is an ischaemic penumbra?
A
- an ischaemic penumbra is a poorly perfused area surrounding a necrotic core
- in the necrotic core is <20% normal perfusion
- in the ischaemic penumbra is 20-40% normal flow
- the core will expand if perfusion is not restored
- the neurons in the ischaemic penumbra are viable for ~24hrs and can potentially be salvaged
- they (IP) are a good target for neuroprotective therapies
13
Q
In strokes you would see UMN lesions & focal neurology based on arterial supply
you would expect to see what else with the signs of UMN lesions of hyperreflexia, spascticity & up going plantars?
A
Pyramidal weakness
- extensors weak > flexors (flexed position) in UL
- so in LL = extended position as flexors weaker > extensors there
NB: remember upgoing plantars are normal if baby is <6m old
overall: UMN lesion: pyramidal weakness, hyperreflexia, spasticity, up going plantars (normal <6months)
14
Q
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get leg weakness?
A
Anterior cerebral
(has inner 1o motor cortex e.g. leg bit supply)
15
Q
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get face and arm weakness?
A
middle cerebral artery
(as does the outer segment of 1o motor cortex not the inner bit where legs are thers ACA, the rest is MCA)
16
Q
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get face, arm and leg weakness?
A
Lacunae
17
Q
In stroke depening on the arterial blood supply you get different focal neurology.
What weakness do you get if the PCA is affected?
A
none
you get hemianopia
(e.g. PC supplies occipital lobe)
NB: nor do you get any dysphasia, inattention or neglect.
MCA is the only other artery where you get hemianopia - if MC then the eyes look at the lesion e.g. eye deviation towards
18
Q
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get dysphasia?
A
Middle cerebral artery only
19
Q
What artery is affected if a patient has inattention/neglect?
A
20
Q
Where is the main language dominant hemisphere in 85% of people and TF what syx would a stroke on this side cause?
A
>85% of people are left language dominant (e.g. ?RHanded)
TF in assuming a dominant side stoke on LHS you would get
- dysphasia - total/expressive/receptive
- right sided weakness + hemisensory loss
if you were dominant on LHS but had a RHS stroke (non-dominant side). You would get:
- sensory inattention
- hemispatial neglect
- Lef-sided weakness + hemisensory loss
NB: so either side you have a stroke in you get hemisensory loss and weakness. but depending on if its dominant = dysphasia and if non-dom you get sensory inattention and hemispatial neglect.
21
Q
What are the general symptoms of a LHS stroke (assume dominant) vs a RHS stroke (assume non-dominant)
A
LHS stroke (dom)
- VERBAL - dysphasia & aphasia
RHS stroke (non-dom)
- VISUO-SPATIAL - sensory inattention & hemisensory neglect
22
Q
if the brocas area is affected in the LHS/dominant lobe what type of dysphasia so you get?
A
Non-fluent dysphasia
- cannot EXPRESS what they mean, but can understand you
23
Q
If Wernickes area on LHS stroke/dominant is affected what type of dyspphasia do you get?
A
fluent dysphasia also called receptive dysphasia
they talk and can express words
but cannot UNDERSTAND language & self monitor what they are saying
24
Q
If someone has a non dominant (e.g. RHS stroke) in brocas area what type of problem do they get?
A
they dont understand: Non-verbal expressive communication
- e.g. gesticulations, facial expressions and subtle intonation, expressing meaning by ‘tone of voice’ (sarcasm?)
25
if someone has a non dominant lesion in wernickes e.g. RHS stroke. What problems do they get?
AMUSIA a.k.a. Problems understanding speech intonation,
we convey a lot of meaning using tone of voice and this is lost on people with non-dominant Wernicke lesions --\> They are blind to the music of speech and misunderstand what is being said, even though their comprehension of grammar and syntax (left hemisphere) is unaffected.
26
How do you get CONDUCTION APHASIA (a disconnection syndrome)?
e.g. where is the lesion to cause this...
a stroke or lesion on the **dominant** e.g. LHS, **arcuate fasiculus**
--\> the white matter bundle connecting the anterior (brocas) and posterior (werinickes) language areas
**- they cant talk**
(no connection between understanding and expressing)
27
dyslexia is problems reading
--\> alexia if the ability is lost completely
How do you get this problem?
a LHS/dominant stroke in the fusiform gyrus
the fusiform gyrus = complex pattern recognition
28
the fusiform gyrus = complex pattern recognition
a problem/stroke/lesion in the dominant lobe = dyslexia/alexia
What condition do you get if it is in the non-dominant lobe?
problems with facial recognition called
**_prosopagnosia_**
29
A sudden focal neurology and reduced level of consciousness
typically + a known history of HTN
leads you to consider what dx?
Intracranial haemorhage
30
What is the name of the stroke classification system that considers anatomical location?
Bamford classification (anatomical location)
31
Which stroke type in Bamford classification section requires:
* All three of -
* Unilateral hemiparesis and/or hemisensory loss -
* Lower limbs & genitalia
* Upper limbs & face
* Homonymous hemianopia (optic tracts course whole brain)
* Higher cognitive dysfunction e.g. dysphasia, visuospatial disorder
Total anterior circulation stroke (TACI) --\> (ACA + MCA)
* ACA - lower limbs & genitalia
* MCA - upper limbs & face
32
Which stroke type in the Bamford classification (anatomical location requires):
Two of -
* Unilateral hemiparesis and/or hemisensory loss -
* Homonymous hemianopia (optic tracts course whole brain)
* Higher cognitive dysfunction e.g. dysphasia, visuospatial disorder (e.g. general dom vs non-dom respectively syx)
Partial anterior circulation stroke
cann be (ACA or MCA) (PACI)
33
which stroke type in bamford classification involves:
* One of the following + no loss of higher function e.g. dysphasia
* Pure sensory stroke
* Purse motor stroke
* Sensori-motor stroke
* Ataxic hemiparesis
* Can also get "dysarthria clumsy hand syndrome"
Lacunar infarction (LACI)
AKA perforating arteries o:
* _Internal capsule_ - relays to motor region of frontal lobe
* hence pure motor syx?
* _thalamus_ - how sensory nerves transmit signals from spinal cord --\> brain
* hence pure sensory syx?
* _Basal ganglia_ - voluntary motor movements, cognition
* hence ataxis hemiparesis (LL\>UL affected)
[overall: hence sensori-motor stroke]
34
What screening tools for stroke are there?
1. FAST - facial weakness, arm & leg weakness, speech problems, time to call 999
2. ROSIER - recognition of stroke in the ER
3. MRS - modified rankin scale = neurological disability score
4. NIHSS - national insitute of health stroke scale (assesses stroke severity on the acute setting)
35
What scoring system does this show and at what threshold?
this is the ROSIER e.g. recognition of stroke in the ER
used AFTER EXCLUDING HYPOGLYCAEMIA
then **any score \>0 means its likely to be a stroke**
36
What scoring system is this?
when is it completed?
this is the **NIHSS**
**complete on admission**
national institutes of health stroke scale **= severity of stroke in the acute setting**
37
There are initial investigations to do in ?stroke then there are also follow up investigations.
What initial investigations should be done?
1. **ABCDE** approach - 2x large bore cannulae
2. **Bloods** - FBCs, U&E, glucose (exclude hypoglycaemia), cholesterol levels
3. **ECG** (?AF)
4. **CXR** - lung pathology, surrogate marker for disease elsewhere e.g. lung cancer - clue to a pro-thrombotic pt
5. **CTH** +/- **CTAngiography** (for cereb. BV's) (within 1hr) - exclude haemorrhage
Other imaging not done in acute, only if diagnosis questionable - MRI (DWI/PWI)
38
in ?stoke a CTH +/- CTA should be done within 1hr to exclude haemorrhage.
On CT what colour is acute blood?
**Acute blood is white**
4x things white on CT:
1. blood,
2. bone,
3. metal,
4. contrast
39
Diffusion scans looking at molecular diffusion e.g. water in the brain. What would be seen in DWI MRI of acute ischaemic stroke?
in ischaemic stroke you can use MRI (CTH+/-CTA is for acute w/i 1hr ?haemorhage)
an acute ischaemic stroke on diffusion MRI will show a **hyperdense** area
ADC map (shows diffusion better) - **black drop** out matching DWI
40
If MRI DWI and ADC map are used in acute ischaemic stroke what can you use to show chronic ischaemic stroke/infarct?
\>6hrs old ischaemic stroke
= use FLAIR sequence to increasingly show infarct
(e.g. if FLAIR doesnt show it then it is \<6hrs old)
41
What are these bloods:
HIV, ANA, ANCA, dsDNA, anticardiolipin ab, lupus anticoagulant
used for in stroke?
HIV, ANA, ANCA, dsDNA, anticardiolipin ab, lupus anticoagulant
are follow up stroke bloods specifically for --\> **_young stroke bloods_**
42
What bloods do you do in stroke for follow up
(excluding Young stroke bloods - HIV, ANA, ANCA, dsDNA, anticardiolipin ab, lupus anticoagulant)?
**FBC**, **U&E**, Cr, LFTs, CRP, ESR, TFTs, **Chol**, **Glu**, HbA1C, sometimes cardiac troponin,
the ones in **bold** are bloods you did as part of your inital stroke Ix - repeat these **(FBC, U&E, Chol, Glu)**
& so added in is:
* creatinine
* LFT
* CRP, ESR
* TFT
* HBA1C
* +/- caradiac troponin
43
As well as follow up bloods what other follow up ?stroke investigations need to be done?
1. **Carotid USS ?**stenosis
2. **Echo**?source of embolus - multi-territorial stroke think embolic (e.g. lot of bits coming off 1 thing, AF, infective, #'s)
3. **24hr tape**?paroxysmal AF
4. **MRI** at this point if indicated
44
What is the supportive management of stroke?
**ABCDE** & supportive management
* **BM, fluid, O2 & temp maintenance** (only lower BP in acute phase if hypertensive encephalopathy)
* Assess **swallowing** - aspiration risk
* **Nutrition** - early NG tube for feeding & medication
* **Fever** - treat with paracetamol but screen for infection
* **DVT** prophylaxis - thigh length IPCs (Intermittent Pnuemonatic Compressions) (CLOTS3 trial)
45
Management of stroke (ischaemic) is thrombolytic therapy
up till how many hour of onset can you use thrombolytic therapy?
\<4.5hrs from onset
\<3 hours IF DIABETIC
46
Thrombolytic therapy has to be done within 4.5 hrs from onset or within 3hrs of onset if diabetic. What other criteria need to be met for thrombolytic therapy?
no haemorrhage of CT (within 1 hr - would see white acute blood)
BP \<185/110
47
Thrombolytic therapy criteria:
(\<4.5hrs onset (\<3hr if diabetic), no haemorrhage on CT, BP \<185/110):
what drug is recommended by NICE for thrombolysis and what are the risks/benefits - what medications do you have to avoid for 24hrs?
**Alteplase (tPA)** recommended by NICE
Risks: *haemorrhage, hypotension (monitor)*
Benefits: **no effect on mortality,** but **effect on disability** - **1 in 8 cured, 1 in 3 get better,** _1 in 18 get worse_
**_No anti-platelets for 24 hours following intravenous thrombolysis_** to avoid bleeding complications
48
In what situations can thrombolysis never occur... e.g. absolute contraindications to thrombolysis?
_CNS problems_
* - Previous intracranial haemorrhage (**ICH**)
* - **Seizure** at onset of stroke
* - Intracranial **neoplasm**/ **aneurysm**
* - Suspected subarachnoid haemorrhage **(SAH)**
* - Pmhx: **Stroke** or traumatic **brain** **injury** in preceding 3 months
* - **Lumbar puncture** in preceding 7 days
_GI-_
* **GI** haemorrhage in preceding 3 weeks
* Oesophageal varices
General:
* Active bleeding
* Uncontrolled hypertension \>200/120mmHg
* Pregnancy
NB: so NEVER in a pregnant woman or conditions where bleeding has happened recently or currently happening or likely to happen (Hight HTN). Dont do if think it could be seizure too.
49
What do these criteria realte to?
* Concurrent anticoagulation (INR \>1.7)
* Haemorrhagic diathesis (inc. suseptibility to bleed)
* Active diabetic haemorrhagic retinopathy
* Suspected intracardiac thrombus
* Major surgery / trauma in preceding 2 weeks
these are the **relative** contraindications to thrombolysis....
* - Concurrent anticoagulation (INR \>1.7)
* - Haemorrhagic diathesis
* - Active diabetic haemorrhagic retinopathy
* - Suspected intracardiac thrombus
* - Major surgery / trauma in preceding 2 weeks
50
IN certain patients with stroke you can do a thrombectomy...
thrombectomy is done within \<6hrs onset of stroke, often thrombolysis is done first (alteplase) then consider intra-arterial thrombectomy (IAT)
what certain patients/times can you do this?
* Patients with **ischaemic** stroke due to
* proximal **MCA**,
* carotid Terminus
* distal MCA & basilar occlusion (evidence for latter two less robust)
* Patients presenting **within 6 hours**
* Patients with **significant neurological deficit (NIHSS ≥ 6)**
* **Minimal ischaemia visible** on brain imaging at time of presentation
51
Pt admission to stroke units has shown to
↓s mortality, ↓s dependency, ↓s need for institutional care, NNT = 20
why/how?
on a stroke unit there is dedicated medical and nursing treatment
* Early mobilisation & physiotherapy
* Speech & language therapy (within first few days)
* Good nutrition & hydration (+ nasogastric or parenteral feeding if necessary)
* Prompt & aggressive treatment of complications (e.g. infection, PE, UTI, aspiration)
* Venous thrombus embolism –IPCs, intermittent pneumatic compression stockings
52
What medications are used for pt optimisation post stroke?
* **_Aspirin_ 300mg PO/d** ASAP
or if had thrombolysis cant have anti-platelets for 24h after so give Aspirin 300mg PO 24hrs later if haemorrhage is excluded
**--\> for 2x weeks!**
* **then --\> _clopidogrel_ 75mg** daily (anticoagulants) after 2wks - minimise risk haemorrhagic transformation
* **after 48h from onset if cholesterol is \>3.5mmol/l give _statin_ -** prevents risk of haemorrhagic transformation (e.g. after thrombolytic therapy)
53
When may a decompressive hemicraniectomy surgery be needed in stroke?
_in ischaemic stroke can have malignant MCA syndrome:_ (RF in young patients, distal carotid/MI)
which **comes from an MCA stroke** --\> space occupying cerebral oedema --\> **80**% mortality due to **herniation**!
SSx: rapid neuro deterioration: gaze deviation, hemplegia, **visual field defect**, aphasia, neglect, early/rapid neurological deterioration, **headache**, **vomiting**, **drop in GCS** *(like having another stroke)*
Decompressive hemicraniectomy = removal of large **bone** flap on **side** of stoke and **dura** opened to relieve pressure
54
Another surgery possible for ischaemic stroke (as well as decompressive hemcraniectomy for malignany MCA syndrome) is *posterior fossal decompression.*
## Footnote
*What is this for?*
large cerebellar infarction
e.g. drop in GCS due to pressure on brainstem
--\> do posterior fossal decopmression
NB: there are no RCTs on this though
55
What do the following criteria indicate?
* NIHSS\>15, (severity of stroke in acute setting; on admission)
* reduction in level of consciousness to 1 or more on NIHSS
* pre stroke mRS \<2 (modified rankin scale for neurodisability)
* clinical deficit indicating infarction in MCA terriotory e.g. UL & face hemiparesis/sensory loss
* signs on CT of infarction on \>50% MCA territory
these are the RCP guidelines ofr malignant MCA syndrome --\> neurosurgery for decompressive hemicraniectomy
56
After a patient has a stroke what should they be doing for LIFE?
* _Conservative_: smoking, diabetic control, hypertension, high cholesterol & AF
* _Medical_: **Clopidogrel 75mg OD for life** (or dipyridamol 200mg BD + aspirin 75mg OD)
* Or if stroke + AF = **apixaban/DOAC**
* Surgery: Carotid endarterectomy and angioplasty
* should only be considered if **carotid stenosis \>50%** (OR \>70%)
* recommend if patient has suffered stroke or TIA in the **carotid** territory and are **not severely disabled**
* ****carotid territory = the retina, anterior and lateral cerebral hemisphere.
57
the Conservative managment of a post-stroke patient involves watching their:
* smoking,
* diabetic control,
* hypertension,
* high cholesterol
* & AF
what medical treatment can happen for BP, cholesterol, AF?
For correction of medical RFs for secondary prevention (post stroke):
1. BP - **ACEI** first line
2. Cholesterol - **atorvastatin** 80mg (after 2d)
3. AF - **DOAC** or warfarin (after 2wks)
4. **DM** - aim for best control possible
58
What do these definitions describe:
new definition = **transient** episode of neurological dysfucntion caused by **ischaemia without infarction**
Old definition = focal neurology that resolves within 24 hours, typically ~1hr;
Transient Ischaemic attack (TIA)
!
59
by definition a TIA is a transient episode of neurological dysfunction caused by ischaemia WITHOUT infarction
is a TIA medically important?
how do we assess this?
YES
After TIA have a _high risk of stroke_ **particularly** in the _first few days after_
_risk stratify--\>_ although now not recommended by nice: ABCD2 score
* 4+ is a high risk of future stroke
* **a**ge over 60 - (1)
* **b**lood pressure \>140/90 - 1()
* **cl**inical features max 2pts - unilateral weakness (2) or speech dist. w/o weakness - (1)
* duration of tia - \>60m = (2), \>10-60= (1) and \<10 = (0)
* diabetes = (1)
60
TIA brings a high risk of stroke particularly in the first few days pot-tia
what should be done for a pt who has a tia?
if pt is on warfarin/doac or has a bleeding disorder --\> admit for CTH --\> to rule out ICH
if had \>1 TIA --\> admit for assessment/observation
**aspirin 300mg daily** (CI: unless bleeding disorder/on anticoag or already taking aspirin)
61
What is the secondary prevention of TIA?
* Clopidogrel 75mg OD (as 1st line as in stroke) (or aspirin + dupyridamole if cannot tolerate)
* Carotid endarterectomy if \>50% stenosis (some people say \>70%)
(same as for stroke: + lifestyle e.g. smoking, DM control, HTN (ACEi), cholesterol (atorvostatin) &AF (doac/warfarin after 2wks))
62
TIA clinics exist for specialist assessment and investigations. What happens at these appointements?
patients at lower risk are notmally seen within 7d and those at higher risk within 24h what defines these?
Appointment: Within 24hrs for patients at high risk (ABCD2 \>3) or had TIA in last 7d ; w.i 7d for patients at lower risk.
At appt:
* Carotid Doppler (ultrasound) [for carotid endarterectomy = \>50% stenosis]
* MRI and CT techniques are also valuable and improving
* 24hr ECG
* Echo??
63
What is the emergency management for intracerebral haemorrhage?
**_General_** haemorrhagic --\> reverse anticoagulants, neurosurgical referral
* resuscitation + ABCDE
* CTh --\> white hyper intensity (acute blood)
**_Medical_**:
* BP lowering - do 1o ICH w/in 6hrs if SBP\>150m (RCP stroke guidance)
* reverse anticoagulants
* prevent complications - thigh-length pneumatic compression stockings, nutrition (as per stroke care unit)
**_Surgical:_**
* posterior fossa bleed - posterior fossa decompresion
* hydrocephalus (decompressive hemicarniectomy)
64
Warfarin and Dibigatran are both anticagulants.
If a patient is on these and having an intracerebral haemorrhage, how do you reverse them?
Warfarin:
* _**vit K + prothrombin** complex concentrate_ (factors 2,7,9,10)(PCC)
* --\> after PCC infusion **repeat INR 30mins, 4-6hr, daily**
Dibigatran:
* **_idarucizumab_**
65
A _pregnant_ lady or another pt with a _tendency to clot_ experiences f_ocal neurological deficits_ and _seizures_, she had also just been experiencing _signs of raised ICP_ including
* high pressure headache
* sudden onset,
* double vision,
* pulsatile tinnitus,
* papilloedema,
* visual obscuration ,
* seizure.
WHat is going on?
venous stroke
--\> cerebral venous sinus thrombosis
makes up ~1% of stroke, 85% make full recovery if diagnosed early
66
Venous stroke/cerebral venous sinus thrombosis symptoms inlcude:
## Footnote
**raised ICP** (high-pressure headache - sudden onset, double vision, pulsatile tinnitus, papilloedema, visual obscuration, seizures) **due to obstruction or**
**focal neurological deficits and seizures due to venous infarction and venous haemorrhage**
**_how may sagittal sinus thrombosis particularly present with?_**
* _May present with **seizures** and **hemiplegia**_
* Parasagittal _biparietal_ or _bifrontal_ haemorrhagic infarctions are sometimes seen
* 50% of patients have **isolated** sagittal sinus thromboses
* the other **50**% have **coexistent** lateral/transverse sinus thromboses and cavernous sinus thromboses
67
Venous stroke/cerebral venous sinus thrombosis symptoms inlcude:
* raised ICP (high-pressure headache - sudden onset, double vision, pulsatile tinnitus, papilloedema, visual obscuration, seizures) due to obstruction or
* focal neurological deficits and seizures due to venous infarction and venous haemorrhage
**_how may cavernous sinus thrombosis particularly present with?_**
cavernous sinus thrombosis = eye stuff (as drains eye veins)
1. _Periorbital oedema_
2. _Ophthalmoplegia_: 6th nerve damage typically occurs before 3rd & 4th
3. Trigeminal nerve involvement may lead to hyperaesthesia of _upper face and eye pain_
4. _Central retinal vein thrombosis_
* Other causes of cavernous sinus syndrome:
* local infection (e.g. _sinusitis_), neoplasia, trauma
68
A patient presents with 6th/Abducens and 7th/facial nerve palsy what venous stroke syndrome is likely to give this?
lateral/transverse sinus thrombosis...
69
What casues are there of cerebral venous sinus thrombosis?
1. Infective – bacterial & fungal
2. Thrombophilia - Inherited or Acquired thrombophilia – SLE, pregnancy, puerperium
3. Dehydration
4. Inflammatory – Behcet’s, Wegener’s, SLE
5. Haematology – Sickle cell, PRV, Thrombocythemia, PNH
6. Malignancy – Haematological
7. Trauma -Head injury, Neurosurgery, LP
8. Combined OCP (especially if migraine aura)
70
How do you Rx venous stroke / cerebral venous sinus thrombosis?
Confirm diagnosis, usually with **CTV or MRV.**
* **Anticoagulation for 6 months** (even if there is some haemorrhage on CT).
* *Investigate for an underlying cause.*
If untreated, patients may deteriorate due to propagation of venous thrombus or _thrombus can break off and go to lung (pulmonary embolism – think of DVT!)_
71
A patient has experienced these things:
* Stoke in evolution/ completed stroke/ crescendo TIA
* Carotid bruits
* Neurological features
* Amaurosis fugax -
* Internal capusular stroke - dense hemiplegia including face (striate branches of MCA)
* Hemianopia
How do you investigate?
We are Ix for carotid disease:
1. **colour duplex scan (USS)**
* all patients with TIA/CVA within the last 6months,
2. when duplex is inconclusive or difficult due to calcified vessels --\> **MRA or CTA**
72
What is the medical Rx for carotid disease ( need RX as can get amaurosis fugax and stroke/crescendo TIA)
**antiplatelet agent**
(e.g. **clopidogrel**, aspirin, dipyridamole),
* smoking cessation,
* BP optimization,
* DM control,
* statin,
-- **acute thrombolysis** in specialist units if detected early
73
What is amaurosis fugax?
transient monocular visual loss lasting a few seconds or minutes
--\> (central retinal artery occlusion)
74
When should a carotid endarterectomy (unblocking) be done?
Trial data shows that removal of atherosclerotic neck vessels may **reduce the risk of TIA & stroke** – however it is **not recommended** as **primary prevention** in best practice guidelines due to increased risk of precipitation of a cerebral infarct from surgery itself .
Use if
* **Symptomatic \>70% stenosis of ICA** or
* **\>50% stenosis if recent TIA/CVA & high ABCD2** score (age, BP, clinical duration, diabetes = TIA inc risk of stroke is \>4 scoring)
_All patients **presenting with acute TIA/CVA** = Carotid endarterectomy within **2wks** - TIMING IS IMPORTANT_
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What are the complications of carotid endarterectomy?
* (cerebral infarct risk from procedure itself)
* death or major disabling stroke,
* minor stroke with recovery,
* MI,
* wound haematoma,
* damage to hypoglossal nerve, glossopharyngeal nerve,
* facial numbness
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Is carotid endarterectomy done under LA or GA?
where is the insicion made?
any prophylaxis med?
how is cerebral circulation protected?
_Is carotid endarterectomy done under LA or GA?_
* *Increasingly undertaken under LA block*
_where is the insicion made?_
* Incision *anterior to sternomastoid*
* Carotid vessels controlled after dissection
_any prophylaxis med?_
* *IV heparin* prior to trial clamp (if patient awake)
_how is cerebral circulation protected?_
* Protection of cerebral circulation with a *shunt*
* 10% awake pts - without intact Circle of Willis, not enough collateral flow from contralateral carotid
* GA patients - shunt depends on surgeon preference & cerebral monitoring e.g. Doppler of MCA flow
_Closure & post op:_
* Patch closure of arteriotomy common; eversion endarterectomy may avoid the need for patch
* Post-op close monitoring of BP & neurological state
