Clinical Neurology

Cerebrovascular Disorders


Cerebrovascular disease is a designated group of conditions that can lead to cerebrovascular event/s, i.e. stroke. These events affect the blood supply and vessels to the brain. With a blockage, malformation, or hemorrhage happens, this prevents brain cells from getting enough oxygen, which can cause brain damage. Cerebrovascular diseases can develop in different ways. These include deep vein thrombosis (DVT) and atherosclerosis.

Types of cerebrovascular disease: Stroke, transient ischemic attack, aneurysms, and vascular malformations

In the U.S. cerebrovascular disease is the fifth most common cause of death.

Cerebrovascular Disorders

The Brain

  • Makes up ~2% of the body weight
  • Accounts for ~10% of the body’s oxygen use
  • Accounts for ~20% of the body’s glucose use
  • Receives ~20% of the cardiac output
  • Per minute, requires ~50-80cc of blood per 100g of grey matter brain tissue and ~17-40cc of blood per 100g of white matter
  • If blood supply to the brain is <15cc per 100g of tissue, per minute, neurologic dysfunction occurs
  • As with all tissues, the longer there is ischemia, the more likely there is to be cell death and necrosis
  • The brain depends on a constant, uninterrupted supply of oxygen and glucose
  • 3-8 minutes of cardiac arrest can result in irreversible brain damage!

Autoregulation In The Brain

  • Systemic hypotension causes reactive cerebral vasodilation to allow more blood flow to the brain
  • The brain can extract enough oxygen from the brain if systolic pressure is 50 mmHg
  • Atherosclerotic narrowing can produce reactive vasodilation to attempt to reduce excess pressure
  • Increased blood pressure can result in vasoconstriction, reducing likelihood of hemorrhage
  • If systolic pressure averages >150 mmHg for prolonged periods, this compensation may fail
  • Labelled hypertensive encephalopathy

Blood Supply To The Head

Collateral Circulation

  • In slowly developing occlusion such as atherosclerotic thrombosis, collateral circulation has time to develop
  • Circle of Willis connects the carotid and basilar systems
  • Anterior and posterior communicating arteries provide collateral supply
  • Anastomoses between main cerebral and cerebellar arteries in some people
  • Internal and external carotid artery connection via the ophthalmic & maxillary arteries

Circle Of Willis

  • Connects the vertebrobasilar system with the internal carotid system
  • While providing helpful collateral circulation, is also the most susceptible area to Berry Aneurysms which can lead to hemorrhagic stroke

Blood Supply To The Brain

Maxillary & Ophthalmic aa.

Cerebrovascular Disorders

  • ~700,000 adults in the US have a stroke each year
  • Third most common cause of death in the US
  • ~2 million people are disabled due to stroke
  • By far more common in persons of advanced age
  • Occlusive/Ischemic Disease
  • 80% of all strokes
  • Most common site of occlusion is at the internal carotid artery just above the bifurcation of the common carotid a.
  • Atherothrombotic
  • Embolic
  • Small vessel
  • Hemorrhagic Disease

Occlusive/Ischemic Stroke

  • Can be due to artery OR vein occlusion
  • Artery occlusion is much more common
  • Due to lack of blood & oxygen supply reaching a particular area of the brain
  • Sudden onset of neurologic deficits, correlating to the distribution of a specific artery
  • Deficits will differ depend on which artery’s distribution has been disrupted

Venous Occlusion

  • Hyperviscocity
  • Dehydration
  • Thombocytosis
  • Elevated red or white blood cells counts
  • Polycythemia
  • Hypercoagulability
  • Elevated homocysteine
  • Prolonged immobility or airplane travel
  • Genetic clotting factor disorders
  • Pregnancy
  • Cancer
  • Hormone replacement & OCP use


  • Neurologic deficits may be transient or develop slowly over time
  • Possible causes/types:
  • Dissection of the tunica intima and tunica adventitia
  • Can occur in younger patients with connective tissue disorders
  • Inflammatory materials deposit & build up in the vessel walls
  • Oxidized LDLs deposit in vessel walls


  • Neurologic deficits likely to have sudden onset
  • Dislodged tissue from dissection of the tunica intima and tunica adventitia
  • Any dislodged thrombus can become an embolus blocking/closing the lumen of smaller vessels

Small Vessel

  • Lipohyalinosis
  • Vessel wall micro-trauma & ballooning
  • Amyloid Angiopathy
  • Accumulation of amyloid proteins in vessel walls
  • More common in patients >65 years old
  • Causes narrowing (leading to ischemia) but can also cause vessel fragility (leading to hemorrhage)
  • Associated with Alzheimer’s disease
  • Inflammatory
  • Spasmotic

Risk Factors For Occlusive Stroke

  • Hypertension
  • Diabetes Mellitus
  • Cardiac abnormalities
  • Right-left shunts (Patent foramen ovale, VSD, tetralogy of fallot, etc)
  • Atrial fibrillation
  • Valve disease/artificial heart valves
  • Advanced age
  • Obesity
  • Hyperlipidemia
  • Especially high LDL and low HDL
  • Sedentary lifestyle
  • Cigarette/Tobacco smoking
  • High oxidation status
  • Elevated homocysteine
  • Contributed to by low folic acid, B6 & B12 statuses
  • Interacts with LDL cholesterol
  • Hyperviscocity and hypercoagulability states as shown on previous slide

Transient Ischemic Attack (TIA)

  • Fully reversible episodes of neurologic deficit due to vascular insufficiency generally lasting no more than 30 minutes at a time
  • Occasionally can last 24 hours or more
  • Half of patients who suffer from a complete occlusive stroke previously had transient ischemic attack(s)
  • 20-40% of patients with TIA go on to have complete stroke
  • In is important to identify patients with TIAs to that they can be appropriately managed and modifiable risk factors reduced

History of Transient Neurologic Deficit In Patient > 45 y/o

  • DDx
  • TIA most likely dx
  • Migraine
  • Focal seizures
  • BPPV
  • Meniere’s
  • Demyelinating diseases
  • Temporal arteritis
  • Hypoglycemia
  • Tumor
  • Arteriovenous malformations

Carotid Artery Disease

  • High pitched systolic bruit heard over the carotid artery may indicate carotid stenosis
  • Requires duplex ultrasound evaluation
  • Lesions narrowing the lumen >70% can possibly cause ischemia
  • Many carotid occlusions do not cause ischemia due to slow development allowing for collateral circulation to be developed as well
  • Fast forming occlusions or emboli can produce problems with <70% stenosis
  • Surgical intervention should be considered for patients with >70% stenosis and symptoms of TIA

Occlusive Stroke

  • If there is an onset of definitive substantial neurologic deficit, the patient should have a CT to rule out hemorrhage
  • If hemorrhage is ruled out, tissue plasminogen activator should be given within the first 4.5 hours
  • It should not be given later than this because it can increase risk of bleeding during reperfusion of brain tissue
  • After this initial period, focused thrombolysis or mechanical extraction of the embolus

Intracranial Hemorrhage

  • Approximately 20% of stroke cases
  • Severe HA or vomiting suggest hemorrhage over occlusion
  • Two types
  • Spontaneous intracranial hemorrhage
  • Hypertension
  • Arterial aneurysms
  • Arteriovenous malformations
  • Bleeding disorders
  • Vessel weakening due to amyloid angiopathy
  • Traumatic

Aneurysm Sites

  • Intraparenchymal hemorrhage
  • 50% – Lenticulostriate branches of the middle cerebral artery
  • Affects the putamen and external capsule
  • 10% – Penetrating branches of the posterior cerebral artery
  • Affects the thalamus
  • 10% – Penetrating branches of the superior cerebellar artery
  • Affects the cerebellum
  • 10% – Paramedian branches of the basilar artery
  • Affects the basilar pons
  • 20% – Various vessels affecting areas of white matter
  • Subarachnoid hemorrhage
  • Berry aneurysms at communicating artery junctions

Bleeding Disorders

  • Thrombocytopenia
  • Leukemia
  • Excess anticoagulant therapies

Risk Factors For Hemorrhagic Stroke

  • Hypertension
  • Arterial aneurysms
  • Arteriovenous malformations
  • Bleeding disorders
  • Vessel weakening due to amyloid angiopathy
  • Head trauma

Signs Of Stroke: Teach Patients F.A.S.T

Common Transient Symptoms

  • Vertigo
  • Bilateral blurring or loss of vision
  • Ataxia
  • Diplopia
  • Bilateral or unilateral sensory and motor deficits
  • Syncope
  • Weakness in the distribution of a motor cranial nerve one side of the head with a contralateral hemiparesis (medial brainstem damage)
  • Damage to a sensory cranial nerve & Horner’s syndrome on one side of the head and loss of contralateral pain and temperature sensation in the body (lateral brainstem damage)

Long-Term Symptoms Depend On Area Affected

  • Monocular visual obscuration (amaurosis fugax) that is due to retinal ischemia
  • Contralateral hemiparesis
  • Hemisensory deficit
  • Visual field deficits
  • Dysphasia
  • Receptive aphasia (Wernicke’s area lesion)
  • Expressive aphasia (Broca’s areas lesion)
  • Contralateral neglect (on-dominant parietal lobe lesion)
  • Problemswithinitiationofmovement(Supplementarymotorcortex lesion)
  • Difficulty with voluntary gaze to the contralateral side (Frontal eye field lesions)
  • Short-term memory deficits(medial temporal lobes lesioned)

Brain-Stem Syndromes syndromes/common-stroke- syndromes-chapter-9-textbook-of- stroke-medicine.html

Stroke Recovery

  • Rehab needs depend upon the area of brain tissue that was affected by the stroke
  • Speech therapy
  • Restriction of functioning limbs
  • Balance and gait exercises
  • Encourages neuroplastic restructuring
  • Symptoms may improve within the first 5 days due to reduction in edema
  • Edema may cause herniation through the foramen magnum which can cause brainstem compression and death – patients with this problem may require craniectomy (last resort)


Alexander G. Reeves, A. & Swenson, R. Disorders of the Nervous System. Dartmouth, 2004.
Swenson, R. Cerebrovascular Disorders. 2010

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The information herein on "Cerebrovascular Disorders" is not intended to replace a one-on-one relationship with a qualified health care professional or licensed physician and is not medical advice. We encourage you to make healthcare decisions based on your research and partnership with a qualified healthcare professional.

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