ACQUIRED CENTRAL NERVOUS

SYSTEM VASCULAR DISORDERS

A SEMINAR PRESENTED BY
DR.OFFIAH,SAU

ON THE
21ST DAY OF JUNE
2006.
 OUTLINE:
• Introduction:
• Components of CNS
• Embryogenesis
• Arterial Circulation
• Vascular Disorders
• Vascular pathology
• Acquired CNS Vascular Disorder
• Non-Acquired CNS Vascular Disorder
• Classifications of Acquired CNS Vascular Disorders
• Traumatic
• Non-Traumatic
COMPONENTS OF CNS
 EMBRYOGENESIS
• The human brain and spinal cord are ectodermal derivatives.
• The early embryologic portions of the developing brain are
the prosencephalon, mesencephalon, and rhombencephalon.
• The prosencephalon gives rise to the telencephalon, which
will become the two cerebral hemispheres, and the
diencephalon, which is composed mainly of thalamus and
hypothalamus.
• The mesencephalon becomes the midbrain.
• The rhombencephalon gives rise to the metencephalon,
which is composed of pons and cerebellum, and the
myelencephalon, which becomes the medulla oblongata.
• The spinal cord evolves from the remaining part of the
primitive neural tube.
CEREBRAL ARTERIAL
CIRCULATION
 VASCULAR DISORDERS
• Vascular Pathology
• Blood vessels share many similarities with a water hose.
• Vascular pathology usually arises when there is:
• Abnormalities in the flowing blood (as seen in Embolization and
Thrombosis),
• Likeage due to breakdown of wall (as seen in Amyloid
Angiopathy, Trauma),
• Intraluminal Obstruction to blood flow (as seen in
Atherosclerosis),
• Extraluminal Obstruction to blood flow (as seen in Intracranial
Tumors) and
• When there is Ballooning of arterial wall (as seen in
Aneurysms).
• There is a supply and demand relationship between blood supply and
tissue metabolism
• Inadequate vascular supply or increased demand can both tip this
relationship.
• Inadequate vascular supply can be:
• Focal as seen in:
• Systemic as seen in:
• Hypotension
• Shock
• Pathologic increase in demand
• Inefficient use in fuel-mitochondrial disorder
• Inefficiency in using Oxygen-glycogen storage diseases
 Acquired CNS Vascular Disorders
• Cerebrovascular diseases include some of
the most common and devastating
disorders.
• The incidence increases with age.
• Most cerebrovascular diseases are
manifest by the abrupt onset of a focal
neurologic deficit, as if the patient was
“struck by the hand of God”.
• This is defined clinically as stroke or transient
ischaemic attack depending on the duration of
neurologic deficit.
• Stroke is a clinical term that describes a
syndrome of rapidly evolving or sudden onset,
non-epileptic, neurologic deficit that lasts more
than 24 hours.
• Thus laboratory studies including brain imaging
are used to support the clinical diagnosis.
 A case study
• A 70 year old cocaine addict male was sitting on a
bar stool when he was noted to suddenly fall to the
floor. He was unable to arise and the paramedics
were called. When they arrived, he was able to
answer questions and he stated that he had a severe
headache. Upon arrival to the hospital the admitting
physical examination demonstrated a right
hemiparesis. The patient became increasingly
somnolent after admission.
• In spite of supportive care, the patient became
comatose and died two hours after admission.
WHAT ARE THE POSSIBILITIES?

• Because of the acuteness of the symptoms, one

should think of a vascular problem, either due to
trauma:
• This man could have suffered a skull fracture
and epidural or subdural hemorrhage upon
hitting the floor,
TRAUMA

• This man could have suffered a skull fracture

and epidural and\ or subdural hemorrhage
upon hitting the floor.
• Bleeding into subdural and epidural spaces is
principally produced by trauma.
HAEMORRHAGIC STROKE

• This produces neurologic symptoms by

producing a mass effect on neural
structures or from toxic effects of blood
itself.
• Intracranial haemorrhages are classified by
their location (Lobar and Ganglionic) and
the underlying vascular pathology.
EPIDURAL HAEMORRHAGE
BRIDGING VEINS
SUBDURAL HAEMORRHAGE
NON-TRAUMA

• Haemorrhagic Stroke
• Intraparenchymal, intraventricular, and
subarachnoid haemorrhage are usually non-
traumatic.
Hypertensive Brain Haemorrhage
Complication of cocaine
Ruptured Intracranial Aneurysms
SUBARACHNOID HAEMORRHAGE
Ischaemic Stroke

• This is caused by a reduction in blood flow

that lasts longer than several seconds.
• Neurologic symptoms are manifest within
seconds because neurons lack glycogen, so
energy failure is rapid.
• The reduction is either focal or generalized.
 Pathophysiology of Ischaemic Stroke
• Acute occlusion of an intracranial vessel causes reduction in blood flow to the
brain region it supplies.
• The magnitude of flow reduction is a function of collateral blood flow and this
depends on individual vascular anatomy and the site of occlusion.
• A fall in cerebral blood flow to zero causes death of brain tissue within 4 to 10
minutes;
• values less than 16 to 18 mL\100g tissue per minute cause infarction within an
hour; and values less than 20 mL\100g tissue per minute cause ischaemia
without infarction unless prolonged for several hours or days.
• If blood flow is restored prior to a significant amount cell death, the patient may
experience only transient symptoms.
• Tissue surrounding the core region of infarction is ischaemic but reversibly
dysfunctional and is referred to as the ischaemic penumbra that will eventually
infarct if no change in flow occurs, and hence saving the ischaemic penumbra is
the goal of thrombolytic therapy.
Pathogenesis of Ischaemic Stroke
Arterial
Arterial Occlusion
Occlusion

Ischaemia

Mitochondrial
Glutamate Energy failure damage
release

Apoptosis
Ca2+ \Na+ influx
Glutamate
receptor Free radical
iNOS formation
 Proteolysis

Membrane and cytoskeletal

breakdown

Cell Death
Focal ischaemia

• Focal ischaemia or infarction is usually

caused:
• by thrombosis of the cerebral vessels
themselves or
• by emboli from a proximal arterial source
or the heart.
THROMBOSIS
Cerebral Infarction
Valvular Vegetations
Old Cerebral Infarct
Embolism
Lacunar Infarcts
 Generalized Ischaemia
• A generalized reduction in cerebral blood flow
due to systemic hypotension usually produces
syncope.
• If low cerebral blood flow persists for a longer
duration, then infarction in the border zones
between the major cerebral distributions may
develop.
• In more severe instances, global hypoxia –
ischaemia causes widespread brain injury; the
constellation of cognitive sequelae that ensue
is called hypoxic - ischaemic encephalopathy.
Watershed Infarctions
Red Nuclei
Causes of Ischaemic Stroke 1
• Lacunar stroke (small vessel)
- Large vessel thrombosis
- Thrombosis
- Dehydration
• Embolic occlusion
- Artery-to-artery
- Carotid bifurcation
- Aortic arch
• Cardioembolic
- Atrial fibrillation
- Mitral thrombosis
- Myocardial infarction
- Dilated cardiomyopathy
• Valvular lesion
- Mitral stenosis
- Mechanical valve
- Bacterial endocardiatis
Causes of Ischaemic Stroke 2

• Hypercoagulable disorders
-Protein C deficiency
-Protein S deficiency
-Antithrombin III deficiency
-Polycythemia vera
-Systemic malignancy
-Disseminated intravascular coagulopathy
• Vasculitis
-Primary CNS vasculitis
-Systemic Vasculitis
-Meningitis
• Drugs
-Cocaine
-Amphetamine
Venous thrombosis and
infarction1
• Etiology
-Inherent coagulopathy
-Oral contraceptives
-Pregnancy
-Dehydration
-Nephrotic syndrome
Venous thrombosis and
infarction2
• Distribution
-Superior sagittal sinus
-Lateral sinus
-Straight sinus