I understand that the information contained here regarding
ischemic and hemorrhagic stroke is somewhat elaborate but some of you out there
will want to comprehend “what is a stroke” better. If you are like me, you would
want all the nitty-gritty details of the condition that is afflicting you,
your father, your mother, your friend… So here it is. I
must warn you though, this may look to some of you (and me) like a textbook
chapter.
There are two broad categories of stroke, hemorrhagic stroke
and ischemic stroke; and these are diametrically opposite conditions: hemorrhagic stroke is characterized by too much blood within the closed cranial cavity,
while ischemic stroke is characterized by too little blood to supply an
adequate amount of oxygen and nutrients to a part of the brain.
Each of these categories can be divided into subtypes that
have somewhat different causes, clinical pictures, clinical courses, outcomes,
and treatment strategies. As an example, intracranial hemorrhage can be caused
by intracerebral hemorrhage (ICH, also called parenchymal hemorrhage), which
involves bleeding directly into brain tissue, and subarachnoid hemorrhage
(SAH), which involves bleeding into the cerebrospinal fluid that surrounds the
brain and spinal cord.
This entry will review the classification and causes of
stroke.
DEFINITIONS — Stroke is classified into two major
types:
- Brain
ischemia due to thrombosis, embolism, or systemic hypoperfusion
- Brain
hemorrhage due to intracerebral hemorrhage or subarachnoid hemorrhage
A stroke is the acute neurologic injury that occurs as a
result of one of these pathologic processes. Approximately 80 percent of
strokes are due to ischemic cerebral infarction and 20 percent to brain
hemorrhage.
An infarcted brain is pale initially. Within hours, the gray
matter becomes congested with engorged, dilated blood vessels and minute
petechial hemorrhages. When an embolus blocking a major vessel migrates, lyses,
or disperses within minutes to days, recirculation into the infarcted area can
cause a hemorrhagic infarction and may aggravate edema (swelling) formation due
to disruption of the blood-brain barrier.
A primary intracerebral hemorrhage, or hemorrhagic stroke,
damages the brain directly at the site of the hemorrhage by compressing the
surrounding tissue. Physicians must initially consider whether the patient with
suspected cerebrovascular accident is experiencing symptoms and signs
suggestive of ischemia or hemorrhage.
The great majority of ischemic strokes are caused by a
diminished supply of arterial blood, which carries sugar and oxygen to brain
tissue. Another cause of stroke that is difficult to classify is stroke due to
occlusion of veins that drain the brain of blood, cerebral venous sinus
thrombosis. Venous occlusion causes a back-up of fluid resulting in brain
edema, and in addition it may cause both brain ischemia and hemorrhage into the
brain.
BRAIN ISCHEMIA — There are three main subtypes of
brain ischemia:
- Thrombosis
generally refers to local obstruction of an artery. The obstruction may be
due to disease of the arterial wall, such as arteriosclerosis, dissection,
or fibromuscular dysplasia; there may or may not be superimposed
thrombosis.
- Embolism
refers to particles of debris originating elsewhere that block arterial access
to a particular brain region. Since the process is not local (as with
thrombosis); further events may occur if the source of embolism is not
identified and treated.
- Systemic
hypoperfusion is a more general circulatory problem, manifesting itself in
the brain and perhaps other organs.
Blood disorders are an uncommon primary cause of stroke.
However, increased blood coagulability can result in thrombus formation and
subsequent cerebral embolism in the presence of an endothelial lesion located
in the heart, aorta, or large arteries that supply the brain.
Transient ischemic attack (TIA) is defined clinically by the
temporary nature of the associated neurologic symptoms, which last less than 24
hours by the classic definition. The definition is changing with recognition
that transient neurologic symptoms are frequently associated with brain damage.
BRAIN HEMORRHAGE — There are two main subtypes of
hemorrhage stroke:
- Intracerebral
hemorrhage refers to bleeding directly into the brain parenchyma
- Subarachnoid hemorrhage refers to bleeding into the cerebrospinal fluid within the
subarachnoid space that surrounds the brain
Intracerebral hemorrhage — Bleeding in
intracerebral hemorrhage (ICH) is usually derived from arterioles or small
arteries. The brain bleeding is directly into the brain parenchyma, forming a
localized hematoma (clot). Accumulation of blood occurs over minutes or hours;
the hematoma gradually enlarges by adding blood at its periphery like a
snowball rolling downhill. The hematoma continues to grow until the pressure
surrounding it increases enough to limit its spread or until the hemorrhage
decompresses itself by emptying into the ventricular system or into the
cerebrospinal fluid (CSF) on the pial surface of the brain.
The most common causes of hemorrhagic stroke are
hypertension, trauma, bleeding diatheses, amyloid angiopathy, illicit drug use
(mostly amphetamines and cocaine), and vascular malformations. Less frequent
causes include bleeding into tumors, aneurysmal rupture, and vasculitis.
The earliest symptoms of hemorrhagic stroke relate to
dysfunction of the portion of the brain that contains the hemorrhage. As
examples:
- Bleeding
into the right putamen and internal capsule region causes left limb motor
and/or sensory signs
- Bleeding
into the cerebellum causes difficulty walking
- Bleeding
into the left temporal lobe presents as aphasia
The neurologic symptoms usually increase gradually over
minutes or a few hours. In contrast to brain embolism and SAH, the neurologic
symptoms related to hemorrhagic stroke may not begin abruptly and are not
maximal at onset.
Headache, vomiting, and a decreased level of consciousness
develop if the hematoma becomes large enough to increase intracranial pressure
or cause shifts in intracranial contents. These symptoms are absent with small
hemorrhages; the clinical presentation in this setting is that of a gradually
progressing stroke.
ICH destroys brain tissue as it enlarges. The pressure
created by blood and surrounding brain edema is life-threatening; large
hematomas have a high mortality and morbidity. The goal of treatment is to
contain and limit the bleeding. Recurrences are unusual if the causative
disorder is controlled (eg, hypertension or bleeding diathesis).
Subarachnoid hemorrhage — The two major causes of
SAH are rupture of arterial aneurysms that lie at the base of the brain and
bleeding from vascular malformations that lie near the pial surface. Bleeding
diatheses, trauma, amyloid angiopathy, and illicit drug use are less common.
Rupture of an aneurysm releases blood directly into the
cerebrospinal fluid (CSF) under arterial pressure. The blood spreads quickly
within the CSF, rapidly increasing intracranial pressure. Death or deep coma
ensues if the bleeding continues. The bleeding usually lasts only a few seconds
but rebleeding is very common. With causes of SAH other than aneurysm rupture,
the bleeding is less abrupt and may continue over a longer period of time.
Symptoms of SAH begin abruptly in contrast to the more
gradual onset of ICH. The sudden increase in pressure causes a cessation of
activity (eg, loss of memory or focus or knees buckling). Headache is an
invariable symptom and is typically instantly severe and widespread; the pain
may radiate into the neck or even down the back into the legs. Vomiting occurs soon
after onset. There are usually no important focal neurologic signs unless
bleeding occurs into the brain and CSF at the same time (meningocerebral
hemorrhage). Onset headache is more common than in ICH, and the combination of
onset headache and vomiting is infrequent in ischemic stroke.
Approximately 30 percent of patients have a minor hemorrhage
manifested only by sudden and severe headache (the so-called sentinel headache)
that precedes a major SAH. The complaint of the sudden onset of severe headache
is sufficiently characteristic that a minor SAH should always be considered.
The goal of treatment of SAH is to identify the cause and
quickly treat it to prevent rebleeding. The other goal of treatment is to
prevent brain damage due to delayed ischemia related to vasoconstriction of
intracranial arteries; blood within the CSF induces vasoconstriction, which can
be intense and severe. The treatment of SAH will be discussed separately.
In the next articles I will try to go over each of the
specific types of strokes, risk factors for stroke, stroke medications, stroke
rehab, and, most importantly, prevention of stroke.
