Stroke, Head Trauma and conciousness

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Stroke, Head Trauma and conciousness. Amy Wood, Haddy Cosh, Vishal Chauhan, Asfand Baig , Stewart O’Conner. Definition. Definition. a syndrome of rapid onset of cerebral deficit (usually focal) Lasting > 24 hours or leading to death and no cause apparent other than a vascular one. - PowerPoint PPT Presentation

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Stroke, Head Trauma and conciousness

Amy Wood, Haddy Cosh, Vishal Chauhan, Asfand Baig, Stewart O’Conner

Definition

Definition a syndrome of rapid onset of cerebral

deficit (usually focal) Lasting > 24 hours or leading to death and

no cause apparent other than a vascular one

Stroke Risk Factors Non Modifiable

Modifiable

Stroke Risk Factors Non Modifiable

Age Male FHx Race – black/

hispanic

Modifiable HT IHD AF DM Hypercholesterola

emia Smoking Alcohol

Types

Types Ischaemia/ embolism causing cerebral infarct

– 80%

Intracebral Haemorrhagic – 15%

Causes -Haemorrhagic

Causes -Haemorrhagic Ruptured aneurysm Trauma (subarachnoid/intracerebral) Dissection (carotid/vertebral)

Causes - Ischaemic

Causes - Ischaemic Cerebral Thrombosis Cerebral Emboli

Give examples Lacunar

Symptoms - General

Symptoms - General Weakness/Paralysis or numbness on

contralateral side Vertigo/dizziness Headache Visual loss/blurred vision Faintness Confusion Speech problems Difficulty swallowing Cognitive problems Memory problems Consciousness alterations BUT…DEPENDS ON SITE

Stroke Syndromes

Stroke Syndromes TACS - Total Anterior Circulation Syndrome PACS - Partial Anterior Circulation Syndrome LACS - Lacunar Syndrome POCS - Posterior Circulation Syndrome

What are the differences between them?

Syndrome Symptoms Artery

TACS Higher DysfunctionsDysphasiasVisuospatial problemsHomonymous HemianopiaMotor/Sensory Deficits

ICA, MCA, (ACA)

PACS 2/3 Similar to TACIPartial motor/sensory deficitsHigher dysfunction alone

MCA, (ACA)

LACS Pure Motor or Sensory or Sensorimotor lossAtaxic Hemiparesis

Small vessels (Perforating arteries)

POCS Cranial nerve palsy & contralateral motor/sensory deficitBilateral motor or sensory deficitCerebellar signsEye Movement deficits/isolated homonymous

hemianopia

Vertebral

PCA

Extras - watershedsSyndrome Symptoms Artery

Watershed ACA-MCA

"Man-in-a-Barrel" SyndromeAphasia

Internal Carotid Artery occlusion

Watershed MCA-PCA

Visual Processing ICA

Susceptibility to ischaemia:• Systemic BP drop• ACA-MCA occlusion of carotid

TIA

TIA Sudden focal deficit – usually only a few

seconds Presentation very similar to stroke Amaurosis fugax??

<24 hours with complete recovery

Issue: after 1 hour ischaemic damage has already occurred

High risk of recurrence and full stroke

Causes- TIA

Causes- TIACarotid artery insufficiency – 80%Veterbrobasilar Insufficiency – 20%

Circle of Willis – collateral supplies

Management1. Assessment/ diagnosis

Location Subtype Cause

2. Acute intervention 3. Secondary prevention

Reduce risk factors

Assessment and Diagnosis

Assessment: Diagnosis Clinically usually

FAST

Imaging - <3hrs CT

Available Exclude haemorrhage

MRI If brainstem or cerebellar symptoms

Urgent CT required

Acute intervention

Acute intervention Admit to Acute Stroke Unit for assessment

Iscahaemic – Thrombolysis rTPA within 3 hrs of symptoms

Haemorragic – emergency surgery

Antiplatelet drugs (Aspirin 150-300mg) if infarct Contraindicated if haemorrhage!!

Monitor/prevent complications Physiological monitoring for first 72 hours to

maintain CO and supply to brain HR, Temperature, BP, O2 sats, Blood sugar, ECG

Acute intervention

Complications

Complications Post-stroke pain/thalamic pain

1 week- 6 months after stroke Anywhere in spinothalamic system Contralateral side referral of pain Burning + sharp Hyperalgesia & Allodynia

Treat as for neuropathic pain TCAs

Layers of the brain

a) Pia materb) Arachnoid mater c) Dura mater d) Superior sagittal

venous sinus e) Skull f) Falx celebri g) Subarachnoid space

Pia

Arachnoid

Dura

Subarachnoid – arteries

Subdural – Bridging veins

Epidural – Meningeal arteries

Normal CT

Usually going to be symmetrical Ventricles symmetrical and equally full

Midline Shift Coup injury –

injury on same side of force

Contra coup– injury on the opposite side on injury

If you see midline shift, you have a high pressure situation

Case 1 Young lady hit on the side of head by a glass at a gig,

seemed to recover , Found slumped 50 minutes later Ix?

CT/MRI, x-ray if fracture Where may she have been hit?

Pterion What bones converge here?

frontal, parietal, sphenoid, temporal What does this area cover?

Middle meningeal artery Type of intracranial haemorrhage?

extradural (epi) Type of blood characterises this?

Arterial Why passed out?

raised ICP Rx

surgical

Extradural haematoma:

Midline shift

Lenticular shape

This can be middle meningeal artery – pterion bone breaks

Cerebral perfusion pressure = mean arterial pressure – ICP

Extradural haematoma you give Mannitol – 100mL at 20% Diuretic

Case 2 Old alcoholic man had a fall in the park now noticed to be very

drowsy with low consciousness Ix:

CT/MRI Likely haematoma?

Subdural Other symptoms?

Headache, confusion, N/V, tinnitus, speech and visual problems, dizziness, weakness

Where is the bleed likely to be? bridging veins

Type of blood? venous

Rx depends on size + growth rate: often conservative (body reabsorbs), sometimes burr-hole drainage

Acute or Chronic

Subdural Haematoma:

Runs along the surface of the brain, underneath the dura

Depending on the GCS score of the patient you may need to remove it

Midline shift

Subarachnoid Haemorrhage Sudden onset severe

headache, often at the back of the head, Neck stiffness, Impaired consciousness (drowsiness / coma), Cranial nerve signs, Hemiplegia

The bleeding occurs as the result of rupture of aneurysm (80%) and AV malformations (15%) or trauma

Contusion (bruise)

Intra- axial As bruise swells, pressure goes up – all features

of raised ICP (coma) If you remove them you need to do a craniotomy

Diffuse Axonal InjuryRTAs / shaken baby syndrome

If a rotational force is applied, the axons are damaged and you can have damage very far away from the original injury – diffuse axonal injury

Small contusions all over the brain

The worse it looks on the CT scan, the worse the injury in the patient – especially if you see an injury in the brainstem

DAI doesn’t look as bad on CT as some of the other ones, but can be much worse

Le fort Fractures

Blow-Out Fractures

With a mass lesion why do you not get an immediate loss of consciousness?

Due to an ability to Compensate! Intra cranial vol = vol CSF + vol Brain + vol

blood + vol Mass lesion Skull can’t expand Compensation – 10-20 ml CSF in to lumbar

cisterns Compensation exceeded Increase in ICP

herniation

What are the 3 key symptoms of raised ICP?

Papilloedema

Headache

Nausea and Vomiting

Label diagram

Name two areas of the brain that can be damaged, leading to loss of consciousness?

Compression of reticular formation from herniation

Large damage to cortical regions

How unconscious are they?

What is the main tool that we use to measure this?

Glasgow Coma scale

“Patient has Glasgow coma score of 9”

What’s wrong with this?

It’s more useful to say:

GCS = V1 E3 M5V3 E3 M3 etc.

They are different situations that may need managing differently

Three indicators of change of brain function in the unconscious patient?

Reaction to painful stimulus – (part of Glasgow Coma scale)

Vestibulo-ocular reflex E.g Caloric test, doll’s head

test

Size and reaction of pupils

What are the three components of consciousness? Alertness - upper brainstem reticular formation

- wakefulness

Awareness - cerebral cortex state of awareness and interaction with environment

Attention - limbic system and frontoparietal association areas - affect, mood, attention, motivation pay attention to

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