L2: Cerebrovascular Disorders Flashcards
Notes in Cerebral Arterial Circulation
Blood Supply of the Brain
- The carotid system.
- The vertebrobasilar system.
The Carotid System
Course of MCA
Lateral surface of cerebral hemisphere
(in sylvian sulcus).
What does MCA supply?
Lateral aspect of anterior 3/5th of
cerebral hemisphere.
Course of ACA
Medial surface of cerebral hemisphere (around corpus callosum) to parieto-occipital sulcus
What does ACA supply?
Medial aspect of anterior 3/5th of cerebral hemisphere & upper edge of lateral surface.
Vertebrobasilar System
What does PCA supply?
Supply posterior 2/5th of the cerebral hemisphere (Whole occipital lobe and the Posterior part of the temporal lobe).
The 3 major cerebral arteries (ACA &MCA &PCA) give off 2 types of branches: ………
- Superficial or Cortical branches: supply pia matter & the cortex.
- Basal or Central branches: supply its central part (white matter & basal ganglia).
Circle of Willis
Diseases of the Nervous brain vessels include:
- Stroke
- TIA
Def of Stroke
- Rapidly developing clinical symptoms and/or signs of focal loss of brain function lasting more than 24 hours or leading to death with no apparent cause other than that of vascular origin.
Incidence of Stroke
- Stroke is the commonest cerebrovascular disease.
- Sometimes called a “brain attack”.
Types of Stroke
Incidence of Cerebral Venous Thrombosis
- < 2% of all strokes.
- Predominantly affects young adults and children.
- Accounts for up to 50% of strokes during pregnancy and Puerperium
Pathogenesis of Ischemic Stroke
Sudden Thrombotic or Embolic occlusion of a cerebral artery.
Causes of Ischemic Stroke
Thrombotic Causes of Ischemic Stroke
Embolic Causes of Ischemic Stroke
Hematological Causes of Ischemic Stroke
Risk Factors for Ischemic Stroke
Non Modifiable & Modifiable
Non-Modifiable RF for Ischemic Stroke
Modifiable RF for Ischemic Stroke
Prognosis of Ischemic Stroke
Depends upon:
- Site & size of the infarction.
- Age.
- Other comorbidities.
Clinical Features of Ischemic Stroke
- Focal loss of neurological function
- Negative in quality
- Rapidly developing
- Maximal at onset
Clinical Features of Ischemic Stroke
- Focal Loss of neurological Function
Clinical Features of Ischemic Stroke
- Focal Loss of neurological Function (In Carotid System)
Unilateral signs e.g.
a. Hemiplegia,
b. Hemi-hypoesthesia,
c. Hemianopia
d. Aphasia (if the left hemisphere is involved).
Clinical Features of Ischemic Stroke
- Focal Loss of neurological Function (In Veretbrobasilar System)
Bilateral signs
a. Motor and sensory signs (hemiplegia may also be found)
b. Disturbance of cranial nerves and cerebellum.
The commonest involved artery is the ……. which supply the internal capsule
MCA & its central branches
The MCA supplies: …….
- Lateral portions of frontal and parietal lobes
- Superior part of the temporal lobe
So, its blockage May damage the following structures: …….
So, its blockage May damage the following structures:
1) Primary Motor Cortex
2) Primary somatosensory cortex
3) Broca’s area
4) Optic radiations
Occlusion of PICA →
Lateral medullary syndrome
Clinical Features of Ischemic Stroke
- Negative in Quality
Clinical Features of Ischemic Stroke
- Rapidly Developing
The onset of the focal neurological symptoms and signs is sudden or acute
Clinical Features of Ischemic Stroke
- Maximal at Onset
- The focal neurological symptoms and signs are maximal at onset (i.e. evolving over minutes to hours in all of the affected body parts) rather than progressive (evolving over days to weeks and migrating from one body part to another).
INVx in Ischemic Stroke
- 1st Line INVx
- Urgent Plain CT
- Duplex Carotid US
- ECG & Echo
- Specialized INVx
INVx in Ischemic Stroke
- 1st Line INVx
- Full blood count & ESR
- PT, INR and PTT
- Plasma glucose
- Plasma urea & electrolytes
- Plasma cholesterol
- Urine analysis
INVx in Ischemic Stroke
- 1st Line INVx (Significance)
- These investigations may reveal important modifiable risk factors & may suggest the cause of stroke (e.g. polycythemia, thrombocythemia, infective endocarditis
INVx in Ischemic Stroke
- Urgent plain CT
INVx in Ischemic Stroke
- Duplex Carotid US
When a carotid ischemic event is suspected.
INVx in Ischemic Stroke
- ECG & Echo
When a potential Cardioembolic source is suspected
INVx in Ischemic Stroke
- Specialized INVx
When the cause of stroke remains uncertain e.g.:
1. MRI and MRA of the brain.
2. Transcranial Doppler.
3. Tests for collagen vascular disease.
4. Angiography, etc.
Acute TTT of Ischemic Stroke
- Emergency Care
- Throbolytic TTT
- Neuroprotective TTT
- Prevention of Complications
Def of Ischemic Penumbra
- Zone of reversible ischemia around core of irreversible infarction
- Salvageable in first few hours after ischemic stroke onset.
Penumbra is damaged by ……
- Hypoperfusion
- Hyperglycemia
- Fever
- Seizure
TTT of Ischemic Stroke
Modern therapy for ischemic stroke includes:
- Acute treatment: to reduce morbidity and mortality.
- Rehabilitation: to reduce disability and dependence.
- Prevention: to reduce stroke recurrence.
Emergency Care of Ischemic Stroke
- Airway
- Breating
- Circulation
Emergency Care of Ischemic Stroke
- Airway
To protect against air way obstruction
- Suction of Nasal and pharyngeal secretions may be needed.
- Endotracheal intubation may be needed.
Emergency Care of Ischemic Stroke
- Breathing
To protect against air way hypoventilation, and aspiration.
- Pulse oximetry or arterial blood gases
- Supplemental oxygen & ventilatory assistance.
- A feeding tube is placed if there is oropharyngeal dysfunction
- Mild hypothermia …… the brain
- Mild hyperthermia …… the outcome.
- protects
- Worsens
Emergency Care of Ischemic Stroke
- Circulation
Emergency Care of Ischemic Stroke
- Circulation (Blood Pressure Monitoring)
Emergency Care of Ischemic Stroke
- Circulation (cardiac Monitoring)
To guard against MI & arrhythmia.
- If the patient was taking hypotensive drugs before the stroke → …….
- If BP does not fall after a 1-2w → ……
- Continue them in the same dose.
- use ACE inhibitors. (gradual & permanent lowering to <140/85 (target))
- If systolic BP was >220 mmHg or diastolic BP was >120 mmHg → ……
use LV. labetalol or sodium nitroprusside (urgent but slow lowering of BP is indicated)
Thrombolytic Therapy of Ischemic Stroke
Recombinant Tissue Plasminogen Activator (Actilyse)
Thrombolytic Therapy of Ischemic Stroke
- Aim
To recanalize the occluded artery and re-perfuse the ischemic brain tissue
Thrombolytic Therapy of Ischemic Stroke
- Dose
0.9 mg/kg I.V.
Thrombolytic Therapy of Ischemic Stroke
- Precautions
- It carries the risk of major bleeding, hence should be used carefully and only in the presence of facilities to handle bleeding complication
Thrombolytic Therapy of Ischemic Stroke
- Indications
Thrombolytic Therapy of Ischemic Stroke
- CI
Neuroprotective Therapy of Ischemic Stroke
- Aim
Preventing or limiting the brain tissue damage that occurs in the area of reduced cerebral blood flow.
Neuroprotective Therapy of Ischemic Stroke
- Examples
Prevention of Complications in Ischemic Stroke
Prevention of Complications in Ischemic Stroke
- Brain Edema
- Fluid restriction for 24-48 hours.
- Mannitol 20% solution 0.25 - 1 gm / kg over 30-60 minutes
Prevention of Complications in Ischemic Stroke
- Pneumonia
- Prevention of aspiration.
- Chest exercise & early mobilization.
Prevention of Complications in Ischemic Stroke
- DVT
Low doses of unfractionated or LMW heparin for Bed ridden patients.
Prevention of Complications in Ischemic Stroke
- depression
Antidepressants
Prevention of Complications in Ischemic Stroke
- Electrolyte Disturbance & Nutritional Deficiency
- Adequate LV. fluids.
- Tube feeding (after 3 days).
Prevention of Complications in Ischemic Stroke
- Prssurte Sores
- Skin cleaning.
- Frequent positional changes.
- Frequent change of bed sheets.
- Special mattress.
Prevention of Complications in Ischemic Stroke
- Seizures
Anticonvulsant medications
Prevention of Complications in Ischemic Stroke
- Urosepsis
Indwelling catheters are used only when absolutely indicated and for the shortest possible time
Rehab in Ischemic Stroke
Should start as soon as the diagnosis of stroke is established and includes:
1. Physiotherapy.
2. Speech therapy.
3. Occupational therapy.
Prevention of 2ry Ischemic Stroke
Prevention of 2ry Ischemic Stroke
- Aggresive Control of RF
Avoid smoking.
Lipid lowering.
Control of diabetes.
Treatment of hypertension.
Prevention of 2ry Ischemic Stroke
- Antiplatlet Therapy
For thromboembolic ischemic strokes. e.g.
Aspirin 75-150 mg daily
Clopidogrel 75 mg daily.
Prevention of 2ry Ischemic Stroke
- Anticoagulant Therapy
Prevention of 2ry Ischemic Stroke
- Carotid endarterectomy
For patients with severe carotid stenosis (>70%) and non-disabling ischemic symptoms
Types of Hemorrhagic Stroke
- ICH
- SAH
Causes of Intracerebral Hemorrhage
Most common Causes of Intracerebral Hemorrhage
Hypertension
Hematological Disorders Causing Intracerebral Hemorrhage
Vascular Malformations Causing Intracerebral Hemorrhage
Saccular or Mycotic aneurysms.
Arteriovenous malformations.
Cavernous angiomas.
Inflammatory Vessel Diseases Causing Intracerebral Hemorrhage
Granulomatous Angitis.
Polyarteritis Nodosa.
Incidence of 1ry (Hypertensive) Intracerebral Hemorrhage
This is the commonest spontaneous intracerebral hemorrhage.
Pathogenesis of 1ry (Hypertensive) Intracerebral Hemorrhage
It is due to ……. in the cerebral arteries
chronic hypertension & degenerative changes
- Extravasated blood forms a mass (hematoma) → disrupts and compresses the adjacent brain tissue.
- If the hemorrhage is large, → displacement of the midline structures to the opposite side → compression the reticular activating system and respiratory centers → coma & death.
- In the first hours and days following the hemorrhage, edema accumulates around the clot and adds to the mass effect.
..
Sites of 1ry (Hypertensive) Intracerebral Hemorrhage
Most common Site of 1ry (Hypertensive) Intracerebral Hemorrhage
Putamen
“The most common type of ICH” lenticulostriate artery”
Most Dangerous Site for 1ry (Hypertensive) Intracerebral Hemorrhage
Thalamus
CP of ICH
..
CP of ICH
- Time of Symptoms
In the majority of cases, the hemorrhage has its onset while the patient is up and active.
CP of ICH
- Onset
Abrupt onset of symptoms over minutes, hours or a day or Depending on the size of the ruptured artery
CP of ICH
- General
- Specific
General CP of ICH
Clinical manifestations of increased intracranial pressure
- Headache
- Vomiting
- Depressed level of consciousness and
- Seizures (in some cases)
Specifc CP of ICH
clinical manifestations which are related to the site of the hematoma
- Putaminal
- Lobar
- Thalamus
- Cerebellar
- Pontine
CP of Putaminal Hemorrhage
CP of Lobar Hemorrhage
CP of Thalamic Hemorrhage
CP of Cerebellar Hemorrhage
CP of Pontine Hemorrhage
Dx of ICH
Dx of ICH
- Clinically
Dx of ICH
- Brain CT
- CT is reliable and superior to MRI in early detection of intracerebral hemorrhage (white mass).
- The surrounding edema is hypodense.
Dx of ICH
- Brain MRI
MRI is particularly useful for brainstem hemorrhages.
Dx of ICH
- Others
As PT, PPT, Platelet count, Liver functions etc.
Prognosis of ICH
TTT of ICH
TTT of ICH
- Emergency Care
to protect against Airway obstruction, Hypoventilation, & Aspiration (ABC)
TTT of ICH
- Control of BP
Carried out cautiously & slowly (see before).
TTT of ICH
- Control of ICP
Rapid treatment of intracranial HTN improves the outcome of patients with ICH.
- Controlled hyperventilation to PCO2 (25-30 mmHg).
- IV mannitol (0.25-1 gm/kg).
- Dexamethasone.
TTT of ICH
- Prevention & TTT of Comp
as seizures, pneumonia etc. (see before).
TTT of ICH
- Surgical Evacuation
Especially in patients with superficial (lobar hematomas or with cerebellar hemorrhage
Def of SAH
Sudden flooding of the subarachnoid space with arterial blood.
Etiology of SAH
CP of SAH
CP of SAH
- Sex
Both sexes might be affected.
CP of SAH
- Age
Aneurysmal group: usually in the 4th and 5th decades.
Angiomatous group: usually in the 2nd and 3rd decades.
CP of SAH
- Premonitoring Symptoms
usually absent but it can be in the form of:
- Periodic headache.
- Recurrent ophthalmoplegia
- Seizures.
CP of SAH
- Onset
- Sudden, usually during periods of activity Spontaneous but occasionally precipitated by: Physical strain. Straining.
CP of SAH
CP of SAH
- Rapidly Increasing ICP
CP of SAH
- Headache
Severe, worst headache (thunderclap) “felt first in the suboccipital & cervical region”
CP of SAH
- Consciousness
Change in the state of consciousness varying from drowsiness to semi-coma and even coma.
CP of SAH
- Fundus Ex
Fundus examination may show slight Papilledema and Retinal hemorrhage
CP of SAH
- Meningeal Irritation
CP of SAH
- Focal Manifestations
INVx for SAH
- Brain CT
- CSF Examination (If CT Unavailable)
- Angiography (4 Vessels Angiography)
INVx for SAH
- Brain CT
Blood appears in the subarachnoid space.
INVx for SAH
- CSF
INVx for SAH
- Angiography (4 Vessels Angiography)
To localize the site of the aneurysm or angiomatous malformation.
Prognosis of SAH
- Immediate
- 1/2 the cases recover from the acute attack.
- Better prognosis in younger patients & when the coma is neither deep nor prolonged.
Prognosis of SAH
- Late
There is usually no residual disability, but 1/3 of the survivors are liable to suffer from recurrent fatal attacks
TTT of SAH
- Conservative
TTT of SAH
- Surgical
- As early as the general condition of the patient allows angiography, Surgical treatment of the aneurysm should be carried (Excision or Clipping of the aneurysm or feeding vessel) out.
TTT of SAH
- Others
Embolization (coiling) or Stereotactic radiotherapy.
Def of CVT
Thrombosis in the Dural sinuses and / or cerebral veins.
Incidence of CVT
- < 2% of all strokes.
- Predominantly affects young adults and children.
- Accounts for up to 50% of strokes during pregnancy and Puerperium.
Causes of CVT
- Primary idiopathic thrombosis.
- Secondary thrombosis
Causes of CVT
- Secondary thrombosis
Causes of CVT
- Secondary thrombosis (Local Conditions)
Causes of CVT
- Secondary thrombosis (Systemic Disorders)
CP of CVT
CP of CVT
- Intracranial Hypertension
- 25% of patients with intracranial hypertension are due to dural sinus thrombosis.
- Prognosis is good but may cause optic atrophy.
CP of CVT
- Disturbed Conscious level
Due to widespread thrombosis in cerebral veins & dural sinuses.
CP of CVT
- Presentations According to affected Sinus
CP of CVT
- Presentations According to affected Sinus
(Cavernous Sinus)
CP of CVT
- Presentations According to affected Sinus
(Superior Sagittal Sinus)
CP of CVT
- Presentations According to affected Sinus
(Lateral Sinus)
CP of CVT
- Presentations According to affected Sinus
(DVT - Straight Sinus & Its Branches)
Investigations for CVT
Investigations for CVT
- MRV
- Visualize thrombus in the sinuses but less often visualize cerebral veins
Investigations for CVT
- CT Brain
Investigations for CVT
- Cerebral Angiography
Provides the Definitive Diagnosis
Investigations for CVT
- CSF
Non-specific & can be normal
TTT of CVT
Def of TIA
- Acute focal loss of brain function with symptoms lasting less than 24 hours due to inadequate cerebral blood supply
Duration of TIA
- Most TIAs last only 10 seconds to 15 minutes but occasionally as long as 24 hours (followed by complete recovery).
- Episodes that last longer than 1 hour are usually caused by small infarctions.
TIA & Stroke
- TIA is an important predictor of stroke risk.
Pathogenesis of TIA
Symptoms of Carotid TIA
Symptoms of Vertebrobasilar TIA
INVx for TIA
TTT of TIA
