General Information
The pathological process underlying stroke is usually ischemia or hemorrhage due to an arterial lesion.
In this case, we can divide stroke into 2 main groups.
A. Ischemic stroke
B. Hemorrhagic stroke
While 2/3 of all strokes develop due to infarction, 1/3 of them develop due to bleeding.
Etiological Causes in CVA
A. Occlusions (thrombotic atherosclerotic-SLE and non-atheromatous conditions in PAN)
B. Embolization (atheromatous foci, cardiac pathologies, fat-air embolisms)
C. Bleeding (HT, Arteriovenous malformations, SAH, intraparenchymal, anticoagulant therapy)
RISK FACTORS
0 hypertension
0 Oral contraceptives: Previous cerebrovascular accident, Hypotension
0 Obesity
0 Heart diseases
0 Risk factors for atherosclerosis and embolism
Transient Ischemic Attacks (TIA)
They are attacks consisting of focal neurological symptoms that develop due to insufficiency of cerebral blood flow.
Attacks have a sudden onset and resolve within 24 hours or less.
Since these attacks herald larger infarcts, they are stimulating.
The most common amaurosis fugax.
Great Vessel Occlusions - Neurovascular Syndromes
Arteria Carotid Interna (ICA)
1. Amarosis fugax is the most common finding.
• Transient monocular vision loss lasting 3-5 minutes occurs on the lesion side.
• Carotid endarterectomy should be performed in appropriate indications.
2. Hemispheric transient ischemic attacks
• In advanced cases; hemiparesis-plegia, hemihypoesthesia may develop on the opposite side.
• Global aphasia may occur if the dominant hemisphere is affected.
• It comes with middle cerebral artery findings.
Arteria Cerebri Anterior (ACA)
• It joins with the anterior communicating artery soon after its onset.
• Lesions proximal to this level are well tolerated due to the blood flow from the other side. However, the distal occlusions are:
Weakness in the contralateral lower extremity
Cortical sensory loss
It causes sphincter defect.
Akinetic mutism:
Bilateral frontal lobe infarction
Voluntary movement, speech, emotional expressions are completely eliminated.
Bilateral ant. seen in cerebral artery occlusion.
Arteria Serebri Media (MCA)
• It is the largest and most flow-receiving branch of the internal carotid artery.
• It is the most occluded artery.
• Aphasia (if the dominant hemisphere is affected)
• Hemiparesis, hemihypoesthesia, more dominant in the arm on the opposite side
• The patient who cannot use his right hand, has epilepsy, cannot remember the correct words
In the dominant hemisphere → aphasia + right hemiplegia
Nondominant hemisphere → neglect + left hemiplegia
Gerstmann syndrome: It is seen in parietal lobe gyrus angularis lesions due to occlusion of the medial cerebral artery. It is characterized by agraphia, acalculia, right-left discrimination, and finger agnosia.
Vertebrobasilar System
Subclavia-proximal vertebral artery occlusions
Subclavian steal syndrome
1. Coldness, weakness, pain with the use of the arm
2. Dizziness -dizziness
A. Cerebellaris posterior inferior - PICA
Lower level occlusions are tolerated with anastomoses.
Only the posterior inferior cerebellar artery (PICA) is completely dependent on vertebral artery blood flow.
Wallenberg's syndrome (Lateral medullary syndrome)
Findings related to the affected anatomy
1. Vestibular nucleus: Vertigo, nystagmus, vomiting
2. Spinothalamic tract: Loss of pain and temperature sensation on the opposite side
3. Descending sympathetic tract: Ipsilateral Horner's syndrome
4. Ninth and tenth cranial nerve fibers (hoarseness, decreased gag reflex)
5. Olivocerebellar and spinocerebellar tracts: Ipsilateral ataxia
6. Fifth nerve nucleus and fibers
7. Nucleus solitarius: Decreased sense of taste
The corticospinal tract and the 12th cranial nerve (CN) are not affected.
Vertigo, nausea, vomiting, dysphagia, cranial nerve findings
in Wallenberg's syndrome:
sudden syncope
Same side ( ataxia cerebral - Horner's syndrome - hypothermia + pain in the face - laryngopharyngeal palatine paralysis - tinnitus)
Opposite side (loss of heat and pain sensation in half of the body)
Basilar Artery Occlusion
• It mainly feeds the basis pons.
• It usually causes bilateral ischemia.
• In fully seated basillary syndrome after occlusion
Loss of consciousness, coma
Bilateral motor, sensory loss
Cerebellar findings
Cranial nerve findings according to the level
Locked-in syndrome
Bilateral basis pontis lesion -> corticospinal and corticobulbar pathway involvement
Alert patient with quadriparalysis
There are only vertical eye movements
Can't speak, can't make a sound, can't swallow
Clinic where eye opening-closing is healthy
Pain - temperature sense is intact
One-and-a-half syndrome (Fisher's one-and-a-half syndrome)
Unilateral pons lesion
Paramedian reticular formation -PPRF- and medial longitudinal fasciculus and 6. nerve nucleus involvement
In horizontal eye movements, abduction was preserved only in the opposite eye.
Posterior Cerebral Artery Occlusion
• They are the terminal branches of the basilar artery.
• Contralateral homonymous hemianopsia (macular vision is preserved)
• Occlusions at the midbrain level cause ocular anomalies.
• CN III palsy, internuclear ophthalmoplegia, downward-outward deviation of the eyes are seen.
• In occlusions affecting the occipital lobe, the patient has anomic aphasia. (Cannot name objects)
• Alexia without agraphia, visual agnosia, inability to recognize objects on the left side of the visual field
• Bilateral occlusion leads to cortical blindness.
lacunar infarct
• Occlusion of deep penetrating arteries
• A water-filled pond (-lacuna) forms in the feeding area of that artery.
• The effect of chronic hypertension on the vessels plays a role in the etiology.
• It can occur in the thalamus, nucleus caudatus, pons, intemal capsule, most often in the putamen.
Treatment in Cerebrovascular Disease
- Increases cerebral blood flow
• Hypercapnia
• Hyperthermia
• hypoxia
• Hypertension
- In thrombi:
• By-pass may be beneficial in extracranial vessels in the first 6 hours.
• Streptokinase or urokinase can be given to the thrombus with an intracranial catheter.
• TPA (tissue plasminogen activator) is given if the blood pressure is normal in the first 4.5 hours and there is no evidence of hemorrhage on CT.
Contraindications for thrombolytic therapy
• Presence of intracranial hemorrhage in cerebral imaging
• Presence of large infarct area in cerebral imaging
• Presence of AVM and aneurysm
• Blood pressure greater than 185/110 mmHg
• Hematological changes
Platelet count less than 100,000
Heparin administration that causes aPTT elevation in the last 48 hours
Ongoing use of anticoagulants (INR > 1.7 or PT > 15 sec)
• Blood sugar less than 50 mg/dl
• Head trauma in the last 3 months
• History of intracranial bleeding
• Arterial puncture in the area where active bleeding or pressure is not possible
• Relative contraindications
Minor stroke
Initial seizure
Major surgery or trauma in the last 14 days
History of GI and genitourinary bleeding in the last 21 days
Myocardial infarction in the last 3 months
This information differs on the basis of the textbook according to the branches.