Download Anatomy of Cerebral Arteries

“ЗАТВЕРДЖЕНО”
на методичній нараді кафедри
нервових хвороб, психіатрії
та медичної психології
“______” _______________ 2008 р.
Протокол № _____
Зав. кафедри нервових хвороб, психіатрії
та медичної психології
професор
В.М. Пашковський
.
METHODOLOGICAL INSTRUCTION № 16
THEME: SYNDROMES OF BLOOD CIRCULATION DISTURBANCES. ISCHEMIC
STROKE
Modul 2. Special neurology
Сontents modul 3. Cerebrovascular diseases. Paroxysmal diseases. Cephalargy. Sleep
disorders. Neurointoxications. Traumatic lesions of nervous system.
Subject:
Nervous deseases
Year 4
Medical faculty
Hours 2
Author of methodological instructions
MD Filipets O.O.
Chernivtsy 2008
1. Scientific and methodological substantiation of the theme.
Diseases of the blood vessels are the most important neurological problem of adults
in the world and especially in Ukraine. Stroke ranks first as the cause of death in the
adult population in Ukraine and probably the first as the cause of chronic functional
incapacity. According to the Report of the WHO in 1998 approximately 8 million
people in the world dead from cancer, other 6 million – dead from infection diseases
and about 14 million people died from strokes.
2. Aim: to study anatomy of cerebral and spinal blood circulation, circle of
Willis, clinical characteristics and the main neurological signs of cerebral circulation
impairments in carotid, vertebral and spinal arteries. To study etiology and
pathogenesis of acute and chronic disturbances of cerebral circulation, clinical
characteristics and main neurological signs of TIAs.
1.
2.
3.
4.
5.
6.
7.
8.
Students must know:
Anatomy of cerebral and spinal blood circulation, circle of Willis.
Examination program for patients with disturbances of cerebral circulation.
Clinical characteristics and main vascular symptoms of the cerebral circulation
impairments in carotid, vertebral and spinal arteries.
Etiology and pathogenesis of ischemic strokes.
Clinical classification of cerebrovascular diseases.
Clinical characteristics and main vascular symptoms of the acute disturbances of
the cerebral circulation.
Clinical characteristics and main vascular symptoms of the acute disturbances of
the spinal circulation.
Examination program for these patients.
1.
2.
3.
4.
Students should be able to:
Examine the patient with acute and chronic disturbances of the cerebral
circulation.
Examine the patient with acute disturbances of the spinal circulation.
Make a correct topical diagnosis.
Make a correct clinical diagnosis.
Student should gain practical skills:
1. To determine types of acute disorders of the cerebral
circulation.
2. To determine Carotid or Vertebrobasilar vessels distribution
3. To determine pathological focus in acute phase
4. To find the reasons to cause disorders of cerebral
circulation
5. To formulate the diagnosis
6. To administer emergency treatment of ischemic stroke
4. Integration (basic level).
Subjects
Anatomy
Gained skills
Knowledge of structure and blood supply of
brain and spinal cord.
Histology
Hystological structure of brain cortex
Physiology
Pathologic physiology
Knowledge of physiology of blood circulation
and pathological mechanisms it’s dysfunction.
Subject
Because the nervous system is incapable of storing essential nutrients (oxygen,
glucose) yet has one of the highest metabolic rates of any organ in the body,
continuous circulation of blood is essential for the sustained health and proper
functioning of neural tissue. The vascular system provides the anatomy for the
circulation of blood. If circulation is interrupted for even short periods of time,
individual structures and the systems within which they operate begin to exhibit signs
of alteration in function. Prolonged occlusion of circulation results in disease and
death to the affected tissue. This infarction is referred to as a stroke or cerebrovascular
accident and is accompanied by specific neurological signs and symptoms that
correspond to the functions controlled by the damaged area.
Metabolism in the nervous system is aerobic or oxidative, and therefore requires
a constant supply of oxygen. Although the brain constitutes only 2 percent of body
weight, it receives 15 percent of cardiac output and uses 20 percent of the oxygen
consumed by the body at rest. Metabolic needs, both the delivery of nutrients and
removal of by-products, are met by the cerebrovascular system.
Anatomy of Cerebral Arteries
The cerebral arterial system consists of carotid and vertebrobasilar divisions,
both of which emanate from the aortic arch. The carotid system supplies arterial
blood to the vast majority of the cerebral hemispheres. It is derived from the left and
right internal carotid arteries, with each cerebral hemisphere being supplied by the
ipsilateral internal carotid artery. Both internal carotid arteries enter the ventral
surface of the brain immediately adjacent to the optic chiasm. After passing through
the carotid canal located in the petrous portion of the temporal bone, each internal
carotid artery bifurcates into anterior and middle cerebral arteries. The anterior
cerebral artery branches profusely through the medial longitudinal fissure and
supplies the inferior surface of the frontal lobe and medial aspect of the frontal and
parietal lobes, as well as the anterior corpus callosum. Smaller penetrating branches
supply the deeper cerebrum, diencephalon, limbic structures, head of the caudate
nucleus, and anterior limb of the internal capsule. The middle cerebral artery
ascends through the lateral fissure and supplies blood to almost the entire lateral
surface of the hemisphere, including motor, sensory, auditory, association, and
speech areas of the frontal, parietal, occipital, and temporal lobes as well as the
insula. Important penetrating branches of the middle cerebral artery, the lenticulostriate arteries, supply the putamen, outer globus pallidus, body of the caudate
nucleus, and posterior limb of the internal capsule.
The vertebrobasilar system supplies the brain stem and inferior surface of the
temporal and occipital lobes. Each vertebral artery arises from a subclavian artery,
enters the cranium through the foramen magnum, and gives off two branches. The
first descends and forms the anterior spinal artery while the second forms the
posterior inferior cerebellar artery. The vertebral arteries ascend along the anterior
surface of the medulla to the junction of the medulla and pons, where they join to
form the basilar artery. The basilar artery ascends along the anterior surface of the
pons, giving rise to the anterior inferior cerebellar arteries, inferior auditory arteries,
and superior cerebellar arteries as it ascends. At the top of the pons, the basilar
artery bifurcates, giving rise to the posterior cerebral arteries, which supply the
inferior surface с the temporal lobes, inferior and medial surfaces of the occipital
lobes, and posterior corpus callosum. Smaller penetrating branches of the posterior
cerebral arteries supply parts of the thalamus, subthalamic nuclei, and midbrain.
The choroidal arteries arise from both the carotid and vertebrobasilar
systems. The anterior choroid artery arises from the middle cerebral artery and
supplies the choroid plexus of the lateral ventricles hippocampus, and parts of the
globus pallidus a posterior limb of the internal capsule. The posterior choroidal
artery arises from the posterior cerebral artery and supplies the choroid plexus
of the ventricle and dorsal surface of the thalamus.
Throughout the cerebral arterial system, pressure equalized by a series of
anastomoses (communication between two vessels). The circle of Willis is probably
the largest and best-known anastomosis in the brain. It plays an important part in
equalizing the pressure and distributing the blood from the carotid and
vertebrobasilar systems. The anterior сommunicating artery connects the left and
right anterior cerebral arteries, and the posterior communicating artery connects the
middle and posterior cerebral arteries in each hemisphere.
Middle Cerebral Artery Syndrome
The middle cerebral artery is the most common site of cerebrovascular
accident. If the stroke occurs close to the vessel's origin, the symptoms are severe
and very disabling. Middle cerebral artery syndrome includes a contralateral
weakness (hemiplegia), hemisensory deficit, homonymous hemianopia, and,
depending on the hemisphere involved, either aphasia if the dominant hemisphere is
involved or impaired spatial perception if the nondominant hemisphere is involved.
Muscle tone is usually decreased at first (hypotonia or flaccidity) but gradually
increases over days or weeks to spasticity with increased deep tendon reflexes.
Sensory deficits are most severe for proprioceptive and discriminative modalities.
Impairments include two-point discrimination, the ability to recognize objects by
their sensory qualities (stereognosis), and perception of a touch stimulus if another is
presented simultaneously to the uninvolved extremity (extinction). The arm and
particularly the hand are usually involved more than the leg, but not in every case.
When the deep penetrating vessels supplying the internal capsule are involved, the
face, hand, and foot are afflicted equally. Destruction of lateral corticospinal tract
fibers accounts for the prominent involvement of the hand, while the loss of
corticobulbar fibers projecting to cranial nerves accounts for facial involvement. The
involvement of upper motor neurons is reflected in a positive Babinski sign, which is
usually present from the onset.
Depending on the hemisphere involved, the syndrome includes either
disturbance of language or impaired spatial perception. Lesion of the left opercular
(perisylvian) cortex produces aphasia. Lesion of the frontal opercular region (Broca's
area) produces difficulty with speech production and writing while preserving
speech comprehension (productive aphasia). Lesion of the posterior superior temporal
gyrus (Wernicke's area, 22) produces difficulty with speech comprehension and
reading (receptive aphasia). Extensive opercular damage may produce a particularly
disabling global aphasia (a combination of productive and receptive aphasia).
Lesion of the right middle cerebral artery produces difficulties with spatial
perception, including copying simple diagrams (constructional apraxia) and dressing
(dressing apraxia). Apraxia is difficulty in performing learned movements in the
absence of loss of power, sensation, or coordination. Clients may fail to recognize their
hemiplegia (anosognosia), the left side of their body (hemineglect), or any external
object left of their own midline (hemi-inattention).
Anterior Cerebral Artery Syndrome
Lesion of the anterior cerebral artery causes hemiparesis and sensory deficits in
the contralateral lower extremity. Effects are similar to those found following lesion
of the middle cerebral artery but restricted to the lower extremity due to the
somatotopic organization of the cerebral cortex. Bilateral lesion of the anterior
cerebral artery may also produce profound changes in personality, including apathy,
akinesia, and muteness.
Posterior Cerebral Artery Syndrome
The symptoms associated with lesion of the posterior cerebral artery are
contralateral homonymous hemianopia with or without a hemiparesis. Thalamic
involvement may produce contralateral hemisensory disturbances including
spontaneous pain and dysesthesia (thalamic pain syndrome). Involvement of the
subthalamic nucleus may cause severe chorea in the proximal segments of the
contralateral upper extremity (hemiballism). Bilateral lesion may cause cortical
blindness and memory disorders. However, posterior cerebral artery syndrome is
quite variable because of several anastomotic connections with the middle cerebral
artery that vary between individuals.
Lacunar Syndrome
The smaller penetrating arteries that originate from the larger vessels are
particularly susceptible to damage caused by hypertension. Because these vessels lack
anastomotic interconnections, occlusion of individual vessels causes small (less than
1.5 cm in diameter) strokes (lacunes). A lacune in the internal capsule that affects
only corticospinal fibers will cause pure contralateral hemiparesis with little or no
sensory loss. A lacune in the ventral posterior nucleus of the thalamus produces a
pure contralateral sensory loss with little or no motor, visual, language, or spatial
disturbance. Most lacunes are asymptomatic; however, if bilateral and numerous,
they may cause a characteristic syndrome (etat lacunaire), which includes
progressive dementia, shuffling gait, and pseudobulbar palsy.
Brain Stem Syndromes
Most brain stem strokes follow occlusion of the vertebral or basilar arteries and
the resulting symptoms and signs are variable; however, two classic syndromes exist.
Lateral medullary (Wallenberg) syndrome results from lesion of large branches of the
vertebral or basilar arteries supplying the lateral brain stem and cerebellum.
Symptoms usually include loss of pain and temperature sensation on the ipsilateral
face and contralateral body, ipsilateral limb ataxia, vertigo, nystagmus, and Horner's
syndrome with ipsilateral ptosis, miosis, dilation of facial blood vessels, and facial
anhidrosis (lack of sweating). Medial brain stem syndrome results from lesion of the
penetrating branches of the basilar or vertebral arteries in the caudal pons.
Symptoms usually include ipsilateral abducens palsy (medial deviation of the eye)
and a contralateral hemiplegia.
Venous Drainage of the Brain
Veins of the brain have thin walls that contain no smooth muscle or valves.
They cross the subarachnoid space to join the dural venous sinus system. The venous
drainage of the brain is divided into superficial and deep systems. The superficial
system is located in the subarachnoid space and follows the contour of the
hemispheres, with major vessels protected inside the medial longitudinal and lateral
fissures. The superior sagittal sinus follows the medial longitudinal fissure and
drains blood from the cortex and superior white matter located near the midline. It
empties directly into the transverse sinuses. The superficial middle cerebral vein
follows the lateral fissure and drains blood from the superficial region of the lateral
aspect of the hemisphere. It empties into the transverse sinus via the inferior
anastomotic vein. The superior sagittal sinus and superficial middle cerebral veins
are connected by anastomotic veins running between the two.
The deep venous system drains blood from the deep white matter and nuclei
of the brain. The internal cerebral vein drains the deep parts of its hemisphere
originating as the thalamostriate and choroid veins. Numerous smaller veins join to
form the internal cerebral vein as it courses below the corpus callosum and empties
into the straight sinus via the great cerebral vein. The basal vein drains the inferior
and medial aspects of its hemisphere. It originates as the anterior cerebral vein,
which accompanies the anterior cerebral artery. It is then joined by the deep middle
cerebral vein and several smaller veins as it courses posteriorly and empties into the
straight sinus via the great ventral vein. The inferior sagittal sinus drains the medial
aspect of the cerebral hemispheres superior to the internal cerebral vein and empties
into the transverse sinuses by way of the straight sinus. The transverse sinuses are
continuous with the sigmoid sinuses, which return the blood to general circulation by
way of the jugular veins. The cavernous sinus drains blood from the region of the
hypothalamus and empties into the sigmoid sinuses and jugular veins via the superior
and inferior petrosal sinuses.
Arterial Supply to the Spinal Cord
In the spinal cord, arterial blood is supplied by one anterior and two posterior
arteries, which extend the length of the spinal cord. The anterior spinal artery is
located in the anterior medial fissure. It arises from a small descending branch of each
vertebral artery that unites and descends along the ventral surface of the pons,
medulla, and cervical spinal cord. In the thoracic, lumbar, and sacral regions, blood is
supplied by a series of radicular arteries (root-like beginning of arteries) that arise
outside the central nervous system. The junction between spinal and radicular arteries
creates two zones (upper thoracic and lumbar levels) where the spinal cord is most
susceptible to ischemia (local and temporary reduction in blood flow due to
obstruction of circulation). Caudally, the anterior spinal artery also serves the cauda
equina. At each segmental level, sulcal branches from the anterior spinal artery
penetrate and supply the anterior two thirds of the spinal cord, including the lateral
horns, anterior horns, and anterior funiculi, bilaterally.
The posterior spinal arteries are paired structures. Each arises from a small
branch of the ipsilateral vertebral artery and extends the length of the spinal cord
adjacent to the posterior lateral sulcus. A series of posterior radicular arteries
contribute to posterior spinal arteries in the thoracic, lumbar, and sacral regions. The
posterior spinal arteries distribute blood to the posterior one third of the spinal cord,
including the posterior horns and posterior funiculi, bilaterally.
Venous Drainage of the Spinal Cord
The venous drainage of the spinal cord has a distribution similar to that of the
arterial supply. Like the arterial system, a variable number of anterior and posterior
radicular veins form the basis of the system. The anterior radicular veins form a
distinct anterior medial vein and paired anterolateral trunks that extend the length of
the spinal cord. The posterior radicular veins form a posterior medial vein as well as
smaller, paired posterolateral trunks that extend the length of the spinal cord. As with
the arteries, a meningeal plexus of veins connects the longitudinal trunks. From the
anterior spinal vein, sulcal branches pass through the anterior medial fissure, where
they drain blood from the lateral horns, anterior horns, and anterior funiculi,
bilaterally. Sulcal branches from the posterior radicular veins also drain the posterior
horns and posterior funiculi, bilaterally.
Vascular Supply and Clinical Aspects of Peripheral Nerves
The arterial blood supply to peripheral nerves is derived from rich anastomotic
plexuses of small penetrating arterioles that originate from peripheral arteries of the
body. Small branches from peripheral arteries penetrate the protective covering of the
nerve and project longitudinally inside of the nerve. Different regional arteries
form anastomotic chains within the peripheral nerve that extend the length of the
nerve. Because of the rich anastomosis derived from several different sources,
ischemic vascular disease of peripheral nerves is rare. When it occurs, such disease is
usually due to direct compression of a nerve.
Etiology and Pathology Ischemia and infarction. When blood supply is
interrupted for 30 seconds, brain metabolism is altered. After 1 minute, neuronal
function may cease. After 5 minutes, anoxia initiated a chain of events that may
culminate in cerebral infarction; however, if blood is restored quickly enough, the
damage may be permanent.
Whether a permanent vascular lesion actually causes symptoms and signs depends
on its location and the collateral arteries with which a person is born or that develop
over time to circumvent it. Their adequacy depends on many factors, especially the
rate of development of the obstruction.
The reasons and risk factors.
There are many risk factors that cause development of cerebral circulation
disturbances . They are: physiological, behavioral and environmental factors .
All of those increase risk of cerebrovascular diseases of nervous system.
The risk factors are not the reasons of disease, but they show a connection with
etiological reasons of the disease.
The most common causes of ischemia:
1. Clinical evidence of atherosclerosis - it is the reason in 75 % of all cases of
acute neurologic deficit as a result of disturbances of cerebral circulation
(arterial occlusion).
2. Hypertension - the frequency of arterial hypertension is about 72%.
3. Combination of atherosclerosis and hypertension.
Except these main reasons it is necessary to mention others which can reduce
cerebral circulation:
1. Symptomatic (renovascular) arterial hypertension (for example, renal
diseases);
2. Diseases of heart (inherent and congenital heart valvular defects, cardiac
arrhythmias, rheumatic heart disease, atrial fibrillation, mural thrombus
after myocardial infarction, bacterial and marantic endocarditis, atrial
myxoma, cardiosclerosis, angina pectoris, cardiac insufficiency, ischemic
heart disease and etc);
3. Infectional and infectionial-alergic diseases of vessels (rheumatic disease,
syphilis, tuberculosis, systemic diseases, fibromuscular dysplasia,
poliarteritis nodosa etc) by drain occlusion of the veins;
4. Systemic hypotension;
5. Vasomotor dystonia;
6. Diseases of blood (polycythemia, leukemia, hemophilia ets) - by contituents of
the blood that are too viscous to be propelled through the system.
7. Renal diseases.
8. Diseases of endocrine glands (pancreas);
9. Diabetes mellitus;
10. Extero- and endogenic toxic defeat (renal and hepar insufficiency, alcohol
toxemia, early toxemia of pregnancy);
11. Traumatic vessels defect (subdural hemorrhage, epidural hemorrhage,
parenchymatous hemorrhage, ventricular hemorrhage);
12. Compression of vessels (for example, by arthritis of the cervical spine);
13. Anomaly (inherent and congenital) of Villis circle (stenosis and occlusion of
magistral cerebral and neck artery, congenital defects of cerebral vessels such
as aneurysm, closed loop, stenosis);
14. Tumors cerebri.
15. Cerebral arterial spasm is a debated cause of ischemia, but is incriminated in
migraine and may be a major complication of subarachnoid hemorrhage.
Pathology. The following steps occur in the evolution of an infarct:
1. local vasodilatation
2. stasis of the blood column with segmentation of the red cells are followed by
3. edema
4. necrosis of brain tissue.
Although most infarct are pale, a "red infarct" is occasionally caused by local
hemorrhage into the necrotic tissue. Grey matter tends to have petechial
hemorrhages and white matter tends to have pale (ischemic) infarction. Hemorrhagic
infarct probably occurs when the occluding clot or embolus breaks up and migrates,
restoring flow through the infarcted area. If the interruption is sufficiently prolonged
and infarction results, the brain tissue first softens, then liquefies; a cavity finally
forms when the debris is removed by the phagocytic microglia. In attempts to fill the
defect, astroglia in the surrounding brain proliferate and invade die softened area,
and new capillaries are formed. If the area is large, the cavity may collapse or
become the site for the formation of small multilacular cysts that are filled with clear
fluid.
Many patients have multiple infarctions. Small cysts infarcts, or lacunas, are the
most common form of infarction. They usually occur in the basal ganglia, internal
capsule, and basis pontis, and less commonly in the centrum semiovale or
cerebellum. Lacunas result from occlusions of perforating arteries damaged by
longstanding hypertension or diabetes mellitus.
Embolism. Cerebral embolism is the term used to describe occlusion of an artery
by a fragment of clotted blood, neoplasm, fat, air, or other foreign substance. The
course of the disorder is similar to that described for infarction, except that an
element of vasospasm may be superimposed. Most emboli are sterile; but some may
contain bacteria if emboli arise secondary to subacute or acute bacterial
endocarditis or if there is a lung infection. Infected emboli may result in arteritis with
or without mycotic aneurysm formation, brain abscess, localized encephalitis or
meningitis.
Air embolism usually follows injuries or surgical procedures involving the
lungs, the dural sinuses, or jugular veins. It !may also occur as a result of the release
of nitrogen bubbles into the general circulation following a rapid reduction in
barometric pressure. Fat embolism is rare and almost always arises from a bone
fracture.
In children, cerebral emboli are commonly associated with valvular heart disease
(rheumatic or congenital) and superimposed endocarditis. In adults, atrial
fibrillation or myocardial infarction is the usual cause. Thrombi in the left atrium
may dislodge during fibrillation or after cardio version has restored more forcefulaid rhythmic contractions. After myocardial infarction, a portion of the clot that
forms on the necrotic endocardium may cause transient ischemic attack (TIAs) or
stroke, depending on the rapidity with which blood flow is reconstituted.
Recurrent emboli in the lungs may cause pulmonary hypertension with a
resultant inversion of the pressure gradient across the foramen ovale. As a
consequence, subsequent emboli may traverse the foramen to the left side of the
heart and then to the brain - a "paradoxical" embolus. Other rare causes of cerebral
embolism are atrial myxoma, marantic endocarditis, and prolapse of the mitral valve.
The most common sings of emboli are TIAs, which result from micro embolisms
arising from atherosclerotic plaques on the aortic-cranial arteries. These plaques form
nodes for clots, which may break off or ulcerate, discharging their contents of
cholesterol and calcium into the bloodstream.
The arterial bed in which, the embolus lodges constricts and may go into spasm.
Tissue becomes ischemic, resulting in infarction unless the embolus fragments and
migrates further. If the embolus lyses, blood flow is restored and a hemorrhagic
infarction may follow. Except when an embolus contains bacteria, the pathologic
changes in the brain are the same as those of infarcts due to atherothrombosis.
Cerebral emboli are often multiple and are often associated with emboli in arteries in
other parts of the body.
Clinical considerations.
The frequency of symptomatic cerebrovascular disease depends in part of age,
sex, and geographic location and whether the data were gathered clinically, by
CT, or at autopsy. It is therefore misleading to be too specific about the incidence of
the several forms. In the prospective Framingham study of 35 000 people, 59 % of
strokes were due to atherothrombosis, 15 % to hemorrhage, and 14 % to embolism.
TIAs accounted for 0.9 % of strokes and other causes accounted for 3 %. Although
cerebrovascular disorders may occur at any age, at any time, in either sex, and in all
races, each of these factors affects the incidence and prevalence of the various
types of cerebrovascular disease. Except for embolic causes, stroke is uncommon
before the age of 40. The incidence of cerebral infarction is greatest between ages
60 and 80. Cerebral hemorrhage occurs most frequently among people between the
ages of 40 and 60. The incidence of cerebral embolism and primary subarachnoid
hemorrhage is more evenly spread, but is highest in the fifth and sixth decades of life.
Cerebral infarction is not accidental occurrence, as the common but poorly
chosen term "cerebral vascular accident" implies; rather it is the end result of a
chain of events set in motion decades before the stroke. Epidemiologic
investigations are now identifying susceptible persons and the factors that predispose
those persons to disturbances of cerebral circulation. Known components of the
stroke-phone profile are contained in the following list:
Age
Sex
Race
Cigarette smoking
Alcohol abuse
Hyperlipidemia (elevated blood lipids)
- abnormal cholesterol (below age 50)
- beta lipoprotein and possibly endogenous triglyceride and pre-beta lipoprotein
Hyperglycemia (evidence of impaired glucose utilization)
Hypertension
Erytrocytosis (high hematocrit)
Hyperurecemia (gout)
Personality type
Chronic stress
Transient ischemic attacks or previous cerebral infarction
Cardiac abnormalities
- electrocardiography abnormalities indicating leit ventricular hypertrophy
- myocardial infarction
- cardiac dysrhythmias - particularly atrial fibrillation
- X-ray evidence of cardiac enlargement - particularly if accompanied by EKG
evidence of left ventricular hypertrophy
- Congestive heart failure
Clinical evidence of atherosclerosis
- angina pectoris
- intermittent claudicating of legs
- arterial bruits
Combination of three or more factors increases risk of development of acute
neurological deficit.
Premonitory and initial symptoms.
Although the several types of cerebrovascular disease differ slightly in mode
of onset, symptoms, and clinical course, clinical data alone often fail to identify its
cause in an individual patient. Therefore, the symptoms of the various causes of
stroke shall be discussed together.
Patient with cerebrovascular disease are usually asymptomatic until the disorder
reaches an advanced stage. Premonitory symptoms are infrequent. When they occur,
they may be so nonspecific that they are not recognized as sings of an impending
stroke. Headache, dizziness, drowsiness, and confusion may be present for minutes
or hours before the ictus.
The transient ischemic attack (TIA) is an acute neurological deficit that clears
completely. As the name indicates, transient ischemic attacks are thought to result
from ischemia too brief to cause infarction. TIAs and infarction are caused by the
same mechanisms as embolism or thrombus, and the syndromes are essentially the
same except for duration.
TIAs have been defined as syndromes that last less than 24 hours. There are two
types of TIA. In one type, the TIA usually lasts about 10 minutes and never lasts
more than an hour. These attacks show a low frequency of intracranial arterial
branch occlusions attributable to embolism, and a high frequency (about 50 %) of
severe stenosis or occlusion of major arteries. The other type of TIA lasts longer
than an hour and is ttore often associated with angiographically demonstrable
intracranial embolism. These attacks have a low frequency of severe stenosis or
occlusion of major arteries. They represent part of the spectrum of symptomatically
short-lived ischemic strokes.
A TIA is important to recognize because it may be a warning that a more
catastrophic and permanent neurological deficit is imminent. In some instances
treatment is available that will help to prevent the impending stroke. Between onehalf to two-thirds of people with thrombotic strokes give a history of a previous
TIA, and at least 20 % to 30 % of patients with TIAs will go on to have a stroke.
The symptom complex TIA represents a variety of pathophysiologic processes,
some better understood than others. The following points should be established in
the patient with a TIA.
Although both types of TIAs imply increased risk of stroke, it is mainly the brief
attacks that are associated with atherosclerotic occlusive disease, which is a
surgically correctable arterial disease.
TIA may occur in carotid or vertebrobasilar territory. The differential points
between these two types of TIAs are:
TIAs in carotid distribution. Two types of TIA syndromes occur in carotid artery
region:
1. Transient monocular blindness (TMB) in the eye on the same side as a
narrowed internal carotid artery (amaurosis fugax). Patient may report a
"shade coming down" over his eye. In over 95 % of cases, it develops within
Seconds as a sudden painless darkness or blurring that affects vision
uniformly or from above downward in window-shade fashion. Vision is
restored after a few minutes, like the clearing of atmospheric fog.
Variants of TMB are rare enough to question whether they are really sings
of arterial stenosis. In cases where repeated TMBs occur, the clinical
syndrome is almost always the same.
2. transient hemisphere attack (THA), which affects the region of the middle
cerebral artery:
- Combinations of focal motor and sensory deficits occur, most often involving the
fingers, hand, or forearm (a clumsy "bear's paw" hand), and some-times distorting
language (transient aphasia) or behavior. The syndrome begins suddenly, is
usually maximal at the moment of onset, and subsides slowly in several minutes.
- no focal symptoms such as headache, lightheadedness, dizziness,
forgetfulness, seizures, or behavior are not correctly diagnosed as carotid
territory TIAs.
TMB and THA almost never occur simultaneously, and only occasionally occur at
separate times in the same patient; when TIAs are multiple, the clinical symptoms
usually remain of the same type in the same patient.
Severe ipsilateral internal carotid stenosis or occlusion is present in 50 % of
patient with either TMB or THA that last less than an hour. The frequency is slightly
higher if both types of TIAs occur in the same patient. TMB rarely lasts longer than
10 minutes. THA may last hours. When it does, it is more likely to be due to an
embolus than to significant extracranial carotid stenosis.
In vertebrobasilar TIAs, the variety of symptoms is too large to list, but the
most diagnostically reliable are:
- diplopia (double vision)
- circumoral numbness (around lips or face)
- dysarthria (slurred speech)
- ataxia
Dizziness, syncope, hemiparesis and hemisensory syndromes may effect one or
both sides, loss do not parallel each other in the individual limb as in carotid
disease. These symptoms are more difficult to classify as vertebrobasilar in origin
when they occur alone.
TIAs in carotid territory may be associated with stenosis or ulcerative plaques
at the carotid bifurcation in the neck. When the patient has carotid symptoms,
especially in association with a carotid bruit and/or decreased carotid pulse,
arteriography is usually performed to define the vascular anatomy and to determine
if he is a candidate for carotid endarterectomy. Remember, the carotid must be at
least 80 % to 90 Vo narrowed before the blood flow is, significantly decreased. If the
TIA is caused by emboli from an ulcerated plaque, high-grade stenosis need not be
present. There are patients who have an occluded internal carotid with no
symptoms at all. Moreover, patients may have a carotid bruit. There may be an
occlusion with a palpabre pulse or a decreased pulse in a well-functioning vessel.
TIAs in the vertebrobasilar territory are not well understood. The vertebral
arteries and their origins have a predilection for atheroma development, but it is not
certain what role emboli play in the vertebrobasilar system, or even what
hemodynamic factors may be important. Most serious vertebrobasilar disease is
intracranial, where surgery is not feasible, and the benefit of operation on the
vertebral arteries in the neck is not proved.
In the subclavian steal syndrome the patient has a narrowed subclavian artery
and the arm "steals" blood from the basilar artery via the vertebral artery. There
may be a cervical bruit and difference in blood pressure between the arms. At times
of arm exercise the patient may experience vertebrobasilar insufficiency. In contrast
to other patients with TIAs, those with the subclavian steal syndrome rarely develop
a stroke due to the steal though there may be coexistent serious disease in the
carotid arteries.
Vertigo alone is rarely a, symptom of vertebrobasilar insufficiency ullness other
brainstem sings or symptoms are present. Occasionally a patient may have
vertebrobasilar symptoms when he turns his head, there being secondary to
mechanical factors in the cervical region which alter blood flow.
Emboli from the heart are well-recognized causes of TIAs in both the carotid and
vertebrobasilar systems (more common in the carotid) and are seen in rheumatic
heart disease, atrial fibrillation, mural thrombus after myocardial infarction,
bacterial and marantic endocarditis, atrial myxoma, and with prosthetic valves.
(Don't confuse Stokes-Adams attacks with TIAs).
Cardiac arrhythmias may be associated with TIAs via decreased cardiac output
and may require Holter monitoring for identification. Hypotension may be
associated with TIAs in a patient with compromised cerebral circulation. There is a
smooth clinical continuum from transient ischemia to infarction. At one end is
infarction, caused by a persisting arterial occlusion when collateral vessels fail to
spare the endangered arterial region distal to the occlusion. At the other end is
ischemia, which is caused by the same severe stenosis or occlusion but is either
rapidly relieved or adequately collateralized. Some clinical improvement is the rule
in almost all symptomatic arterial occlusions, but even when function returns to
normal, the attack should not be regarded as a TIA if it lasts longer than 24 hours
because there usually is an infarct due to embolism or thrombosis. If the ischemic
attack lasts more than 24 hours it should be diagnosed as an ischemic stroke. The
term reversible ischemic neurologic deficit (RIND) has been applied to syndromes
that improve within 24 hours but leave some minor neurologic abnormality; these
are also properly regarded as minor ischemic strokes.
Differential diagnosis of TIAs.
It is mainly the sudden less of onset and the focal sings that give these
syndromes the popular term stroke, and help to distinguish cerebrovascular disease
frcn other neurologic disorders. Hypertension, arteriosclerosis, or other evidence of
vascular disease is commonly present, but only the disappearance of symptoms
within minutes or hours permits the separation of TIA from stroke. In the acute
state, considerations of differential diagnosis apply equally to TIA and stroke.
Sudden onset also characterizes trauma, epilepsy, and migraine.
Migraine is increasingly appreciated as a major source of difficulty in the
diagnosis of TIA. Migraine may begin in middle age; the. aura alone, without
headache, is commonly experienced by those who suffer from chronic migraine.
When symptoms are visual and diagnosis of transient mononuclear blindness is
considered, the differential diagnosis from migraine is the easiest: migraine
typically produces a visual disorder that marches across the vision of both eyes as
an advancing thin scintillating line that takes 5 to 15 minutes to pass out of
vision. Subsequent unilateral pounding headache need not occur, but makes the
diagnosis certain. It is difficult to diagnose migraine as a cause of symptoms of
hemisphere dysfunction because the auras of classic migraine only rarely include
motor, sensory, language, or behavior elements. TIA rarely marches from one limb
to another like the visual disorder of migraine. Until the matter is clarified, a
diagnosis of migraine should probably not be seriously considered as 1 an
explanation for transient hemisphere attacks unless the patient is young, has
repeated attacks, experiences classic visual migraine auras at other times, and has a
pounding headache contralateral to the sensory or motor symptoms in the hours
after the attack. Nevertheless, older people do experience migraine's phenomena,
and there may not always be prominent headache symptoms.
Keep in mind that focal seizures may produce transient neurologic symptoms
(numbness, leg or arm weakness) which may persist for hours. Obtain an EEG if
seizures are suspected.
Some systemic factors are known to be associated with TIAs. Well-recognized
ones are anemia, polycythemia, thrombocytosis, and hypoglycemia.
Self assessment:
Tests for self-assessment:
1. The deficit signs of anterior cerebral artery distribution.
2. The deficit signs of median cerebral artery distribution.
3. The deficit signs of posterior cerebral artery distribution.
4. The deficit signs of vertebrobasilar distribution.
5. Venous drainage of the Brain.
6. Venous drainage of the Spinal cord.
7. Clinical classification of cerebrovascular diseases.
8. Name the causes of ischemia?
9. Clinical differentiated signs between transient ischemic attack and ischemic
occlusive stroke.
10.Name the pathogenesis of infarct.
11.Name the premonitory and initial symptoms of strokes.
12.What are the differentiated signs between transient ischemic attack and
ischemic occlusive stroke?
13.What are the main signs of TIAs in carotid distribution?
14.What are the main signs of TIAs in vertebrobrobasilar distribution?
Tests
1. What are the main causes of strokes
a) atherosclerosis;
b) hypertensive disease;
c) atherosclerosis and hypertensive disease;
d) age, sex and race;
e) chronic stress.
2. What are the differentiated signs between transient ischemic attack and ischemic occlusive
stroke
a) Local neurological signs are absent;
b) Local neurological signs may be present for minutes or hours before stroke;
c) Local neurological signs may be present for minutes or hours but not more than 24 hours;
d) TIA and ischemic stroke haven’t differentiated signs;
e) If the local neurological signs are present – it is ischemic stroke;
a)
b)
c)
d)
e)
3. The acute period of ischemic stroke lasts for:
1 day;
3-5 days;
10-15 days;
30-35 days;
2-3 months.
Real-life situations:
1.
Verbal production of the patient is deceleated, blocked and impaired. Where is the
focus of the stroke
2.
The patient has headache which spread all over the head, a loss of sensation ad
strength of movements in the left extremities. Examination has revealed central hemiparesis in the
left side. There is increased muscular tone and tendon reflexes and Babinski sign on the paralysed
limb. Where is the focus of the stroke
References:
1.
Basic Neurology. Second Edition. John Gilroy, M.D. Pergamon press. McGraw Hill
international editions, medical series. – 1990.
2.
Clinical examinations in neurology /Mayo clinic and Mayo foundation. – 4th edition. –
W.B.Saunders Company, Philadelphia, London, Toronto. – 1976.
3.
McKeough, D.Michael. The coloring review of neuroscience /D.Michael McKeough/ 2nd ed. – 1995.
4.
Neurology for the house officer. – 3th edition. – howard L.Weiner, MD and Lawrence P.
Levitt, MD, - Williams&Wilkins. – Baltimore. – London. – 1980.
5.
Neurology in lectures. Shkrobot S.I., Hara I.I. Ternopil. – 2008.
6.
Van Allen’s Pictorial Manual of Neurologic Tests. – Robert L. Rodnitzky. -3th edition. –
Year Book Medical Publishers, inc.Chicago London Boca Raton. - 1981.