STROKE ,HEALTHY

A stroke , previously known medically as a cerebrovascular
accident (CVA) , is the rapidly developing loss of brain function(s) due to disturbance in the blood supply to the brain. This can be due to ischemia (lack of blood flow) caused
by blockage ( thrombosis, arterial embolism ), or a haemorrhage (leakage of blood).[1] As a result, the affected area of the brain is
unable to function, which
might result in an inability to move one or more limbs
on one side of the body , inability to understand or formulate speech, or an inability to see one side of the visual field .[2] A stroke is a medical emergency and can cause permanent neurological damage, complications, and
death. It is the leading
cause of adult disability in
the United States and Europe and the second leading cause of death worldwide. [3] Risk factors for stroke include old age, hypertension (high blood pressure), previous stroke
or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation .[2] High blood pressure is the most
important modifiable risk factor of stroke. [2] A silent stroke is a stroke that does not have any
outward symptoms, and
the patient is typically
unaware they have
suffered a stroke. Despite
not causing identifiable symptoms, a silent stroke
still causes damage to the
brain, and places the
patient at increased risk
for both transient ischemic attack and major stroke in the future. Conversely,
those who have suffered a
major stroke are at risk of having silent strokes. [4]In a broad study in 1998,
more than 11 million
people were estimated to
have experienced a stroke
in the United States.
Approximately 770,000 of these strokes were
symptomatic and 11 million
were first-ever silent MRI
infarcts or hemorrhages. Silent strokes typically
cause lesions which are detected via the use of
neuroimaging such as MRI. Silent stroke are estimated
to occur at five times the
rate of symptomatic stroke. [5][6] The risk of silent stroke increases with
age but may also affect
younger adults and
children, especially those with acute anemia.[7][5] An ischemic stroke is
occasionally treated in a
hospital with thrombolysis (also known as a "clot
buster"), and some
hemorrhagic strokes
benefit from neurosurgery . Treatment to recover any lost
function is termed stroke rehabilitation , ideally in a stroke unit and involving health professions such as speech and language
therapy , physical therapy and occupational therapy . Prevention of recurrence
may involve the
administration of antiplatelet drugs such as aspirin and dipyridamole, control and reduction of hypertension , and the use of statins. Selected patients may benefit from carotid endarterectomy and the use of anticoagulants.[2] Definition The traditional definition of
stroke, devised by the World Health Organization in the 1970s,[8] is a "neurological deficit of
cerebrovascular cause that
persists beyond 24 hours
or is interrupted by death
within 24 hours". This
definition was supposed to reflect the reversibility of
tissue damage and was
devised for the purpose,
with the time frame of 24
hours being chosen
arbitrarily. The 24-hour limit divides stroke from transient ischemic attack , which is a related
syndrome of stroke
symptoms that resolve
completely within 24 hours.[2] With the availability of treatments
that, when given early, can
reduce stroke severity,
many now prefer
alternative concepts, such
as brain attack and acute ischemic
cerebrovascular
syndrome (modeled after heart attack and acute coronary syndrome respectively), that reflect
the urgency of stroke
symptoms and the need to act swiftly. [9] Classification A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke Strokes can be classified
into two major categories:
ischemic and hemorrhagic. [10] Ischemic strokes are those that are caused by
interruption of the blood
supply, while hemorrhagic
strokes are the ones which
result from rupture of a blood vessel or an abnormal vascular
structure. About 87% of
strokes are caused by
ischemia, and the
remainder by hemorrhage.
Some hemorrhages develop inside areas of
ischemia ("hemorrhagic
transformation"). It is
unknown how many
hemorrhages actually start as ischemic stroke. [2] Ischemic Main articles: Cerebral infarction and Brain ischemia In an ischemic stroke,
blood supply to part of the
brain is decreased, leading
to dysfunction of the brain
tissue in that area. There
are four reasons why this might happen: 1. Thrombosis
(obstruction of a
blood vessel by a
blood clot forming
locally) 2. Embolism
(obstruction due to
an embolus from
elsewhere in the body, see below),[2] 3. Systemic
hypoperfusion
(general decrease in
blood supply, e.g., in shock)[11] 4. Venous thrombosis . [12] Stroke without an obvious
explanation is termed
"cryptogenic" (of
unknown origin); this
constitutes 30-40% of all ischemic strokes. [2][13] There are various
classification systems for
acute ischemic stroke. The
Oxford Community Stroke
Project classification (OCSP,
also known as the Bamford or Oxford classification)
relies primarily on the initial
symptoms; based on the
extent of the symptoms,
the stroke episode is
classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar infarct (LACI) or posterior circulation infarct (POCI). These four entities predict
the extent of the stroke,
the area of the brain
affected, the underlying
cause, and the prognosis. [14][15] The TOAST (Trial of Org 10172 in Acute Stroke Treatment)
classification is based on
clinical symptoms as well as
results of further
investigations; on this
basis, a stroke is classified as being due to (1)
thrombosis or embolism
due to atherosclerosis of a large artery, (2) embolism
of cardiac origin, (3) occlusion of a small blood
vessel, (4) other
determined cause, (5)
undetermined cause (two
possible causes, no cause
identified, or incomplete investigation). [2][16] Hemorrhagic Main articles: Intracranial hemorrhage and intracerebral hemorrhage CT scan showing an intracerebral hemorrhage with associated intraventricular hemorrhage. Intracranial hemorrhage is
the accumulation of blood
anywhere within the skull
vault. A distinction is made
between intra-axial hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the
brain). Intra-axial
hemorrhage is due to intraparenchymal
hemorrhage or intraventricular hemorrhage (blood in the ventricular
system). The main types of
extra-axial hemorrhage
are epidural hematoma (bleeding between the dura mater and the skull), subdural hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of the hemorrhagic stroke
syndromes have specific
symptoms (e.g., headache, previous head injury). Signs and symptoms Stroke symptoms typically
start suddenly, over
seconds to minutes, and in
most cases do not progress
further. The symptoms
depend on the area of the brain affected. The more
extensive the area of brain
affected, the more
functions that are likely to
be lost. Some forms of
stroke can cause additional symptoms. For example, in
intracranial hemorrhage,
the affected area may
compress other structures.
Most forms of stroke are
not associated with headache, apart from subarachnoid hemorrhage
and cerebral venous
thrombosis and
occasionally intracerebral
hemorrhage. Early recognition Various systems have been
proposed to increase
recognition of stroke by
patients, relatives and
emergency first
responders. A systematic review, updating a previous systematic review
from 1994, looked at a
number of trials to
evaluate how well
different physical examination findings are able to predict the
presence or absence of
stroke. It was found that
sudden-onset face
weakness, arm drift (i.e., if
a person, when asked to raise both arms,
involuntarily lets one arm
drift downward) and
abnormal speech are the
findings most likely to lead
to the correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these
is present). Similarly, when
all three of these are
absent, the likelihood of
stroke is significantly
decreased (– likelihood ratio of 0.39).[17] While these findings are not
perfect for diagnosing
stroke, the fact that they
can be evaluated relatively
rapidly and easily make
them very valuable in the acute setting. Proposed systems include FAST (stroke) (face, arm, speech, and time),[18] as advocated by the Department of Health
(United Kingdom) and The Stroke Association , the American Stroke Association
(www.strokeassociation.o
rg) , National Stroke
Association (US
www.stroke.org), the Los
Angeles Prehospital Stroke Screen (LAPSS) [19] and the Cincinnati Prehospital
Stroke Scale (CPSS).[20] Use of these scales is recommended by professional guidelines.[21] For people referred to the emergency room , early recognition of stroke is
deemed important as this
can expedite diagnostic
tests and treatments. A
scoring system called
ROSIER (recognition of stroke in the emergency
room) is recommended for
this purpose; it is based on
features from the medical
history and physical examination. [21][22] Subtypes If the area of the brain
affected contains one of
the three prominent central nervous system
pathways —the spinothalamic tract , corticospinal tract , and dorsal column (medial lemniscus), symptoms may include: hemiplegia and muscle weakness of the face numbness reduction in sensory or
vibratory sensation initial flaccidity
(hypotonicity), replaced
by spasticity
(hypertonicity),
hyperreflexia, and
obligatory synergies. [23] In most cases, the
symptoms affect only one
side of the body
(unilateral). Depending on the part of the brain
affected, the defect in the
brain is usually on the
opposite side of the body.
However, since these
pathways also travel in the spinal cord and any lesion there can also produce
these symptoms, the
presence of any one of
these symptoms does not
necessarily indicate a
stroke. In addition to the above
CNS pathways, the brainstem give rise to most of the twelve cranial nerves. A stroke affecting the brain stem and brain
therefore can produce
symptoms relating to
deficits in these cranial
nerves: altered smell, taste,
hearing, or vision (total
or partial) drooping of eyelid
(ptosis) and weakness of ocular muscles decreased reflexes:
gag, swallow, pupil
reactivity to light decreased sensation
and muscle weakness
of the face balance problems and nystagmus altered breathing and
heart rate weakness in sternocleidomastoid
muscle with inability to turn
head to one side weakness in tongue
(inability to protrude
and/or move from side
to side) If the cerebral cortex is involved, the CNS
pathways can again be
affected, but also can
produce the following
symptoms: aphasia (difficulty with verbal expression,
auditory
comprehension,
reading and/or writing Broca's or Wernicke's area typically involved) dysarthria (motor speech disorder
resulting from
neurological injury) apraxia (altered voluntary movements) visual field defect memory deficits
(involvement of temporal lobe) hemineglect (involvement of parietal lobe) disorganized thinking,
confusion, hypersexual gestures (with
involvement of frontal
lobe) anosognosia (persistent
denial of the existence
of a, usually stroke-
related, deficit) If the cerebellum is involved, the patient may
have the following: trouble walking altered movement
coordination vertigo and or disequilibrium Associated symptoms Loss of consciousness, headache, and vomiting
usually occurs more often
in hemorrhagic stroke than
in thrombosis because of
the increased intracranial
pressure from the leaking blood compressing the
brain. If symptoms are maximal
at onset, the cause is more
likely to be a subarachnoid
hemorrhage or an embolic
stroke. Causes
Thrombotic stroke In thrombotic stroke a
thrombus (blood clot)
usually forms around atherosclerotic plaques. Since blockage of the
artery is gradual, onset of
symptomatic thrombotic
strokes is slower. A
thrombus itself (even if
non-occluding) can lead to an embolic stroke (see
below) if the thrombus
breaks off, at which point
it is called an "embolus."
Two types of thrombosis
can cause stroke: Large vessel disease
involves the common
and internal carotids , vertebral , and the Circle of Willis. Diseases that may form thrombi in the large vessels include
(in descending
incidence):
atherosclerosis, vasoconstriction (tightening of the
artery), aortic, carotid or vertebral artery dissection , various inflammatory
diseases of the blood
vessel wall (Takayasu arteritis , giant cell arteritis , vasculitis), noninflammatory
vasculopathy, Moyamoya disease and fibromuscular
dysplasia. Small vessel disease
involves the smaller
arteries inside the brain:
branches of the circle of Willis, middle cerebral artery, stem, and
arteries arising from
the distal vertebral and basilar artery . Diseases that may form thrombi
in the small vessels
include (in descending
incidence): lipohyalinosis (build-up of fatty hyaline matter
in the blood vessel as a
result of high blood
pressure and aging)
and fibrinoid
degeneration (stroke involving these vessels
are known as lacunar infarcts ) and microatheroma (small
atherosclerotic plaques) .[24] Sickle cell anemia, which can cause blood cells to clump up and block blood
vessels, can also lead to
stroke. A stroke is the
second leading killer of
people under 20 who
suffer from sickle-cell anemia.[25] Embolic stroke An embolic stroke refers to
the blockage of an artery
by an arterial embolus , a travelling particle or debris
in the arterial bloodstream
originating from
elsewhere. An embolus is
most frequently a
thrombus, but it can also be a number of other
substances including fat (e.g., from bone marrow in a broken bone ), air, cancer cells or clumps of bacteria (usually from infectious endocarditis). Because an embolus arises
from elsewhere, local
therapy solves the problem
only temporarily. Thus, the
source of the embolus must
be identified. Because the embolic blockage is sudden
in onset, symptoms usually
are maximal at start. Also,
symptoms may be
transient as the embolus is
partially resorbed and moves to a different
location or dissipates
altogether. Emboli most commonly
arise from the heart (especially in atrial fibrillation ) but may originate from elsewhere
in the arterial tree. In paradoxical embolism , a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into the brain. Cardiac causes can be
distinguished between high and low-risk: [26] High risk: atrial
fibrillation and paroxysmal atrial
fibrillation , rheumatic disease of the mitral or aortic valve disease, artificial heart valves , known cardiac thrombus of the
atrium or ventricle, sick sinus syndrome, sustained atrial flutter , recent myocardial
infarction, chronic
myocardial infarction
together with ejection fraction <28 percent, symptomatic congestive heart failure with ejection fraction
<30 percent, dilated cardiomyopathy , Libman-Sacks
endocarditis , Marantic endocarditis , infective endocarditis , papillary fibroelastoma , left atrial myxoma and coronary artery bypass
graft (CABG) surgery Low risk/potential:
calcification of the
annulus (ring) of the
mitral valve, patent
foramen ovale (PFO),
atrial septal aneurysm, atrial septal aneurysm
with patent foramen
ovale, left ventricular
aneurysm without
thrombus, isolated left
atrial "smoke" on echocardiography (no mitral stenosis or atrial fibrillation), complex
atheroma in the ascending aorta or proximal arch