Modern Review

MODERN REVIEW
GROSS ANATOMY OF BRAIN
The nervous system is most important system in the body. All other
system directly or indirectly remains under the influence of it. The nervous
system consists of –

A. Central nervous system (CNS)

B. Peripheral nervous system (PNS)

Central nervous system

A. Brain

B. Spinal cord

It occupies the central axis of the body.

Peripheral nervous system

This part lies out side the CNS i.e. in the periphery. The nerve
fibers in the limbs, trunk, head and neck, as well as sympathetic pera
sympathetic are there in PNS.

The neuron and neuralgia (The specialized cells) are present in

CNS. The structural and functional unit of nervous system is neuron. The
brain contains 1000 billions neuron approximately. The number of neuron
in the body is fixed and it does not increase from the number which is
produced in the intra uterine life. It means neuron if damaged due to
certain reason, function of it can not be regained. In fact as the age
advances some neurons dies spontaneously and at old age approximately
60% of neurons remains alive. The loss of brain matter is more in males
then females in ageing process with the increase of age the length of
neuron increases in relation with the length of body. It does not mean that
their number increases. There are somatic and visceral nerves in the
body. The somatic nerves supply somatic structures and visceral nerves
supply the visceral organs. In same way there are motor and sensory
nerves. The motor nerve means a nerve which supply information from
brain to periphery, we call them efferent nerve also. The sensory nerve
bring information from periphery to brain and these are also called afferent

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nerves. The motor nerves are responsible for all type movements in the
body.

Our Forefathers in neo anatomy thought that human brain looks

some what like a tree and they named individuals parts accordingly.
Besides there are some eponymcal (named after the discover)
nomenclatures.

As a tree has a stem so also the brain has a stem and called the
brain stem the brain stem is made up of from below upwards

1. Medulla

2. Pons

3. Midbrain

The brain stem is connected with two massive lobes, each being
called cerebral hemisphere (hemi=half, hence half a sphere) the two
cerebral hemispheres are separated by a space in which the flax cerebri
invigilates. The two cerebral hemispheres are connected with each other
by a structure called carpus callosum which consists of nerve fibers.

CEREBRAL CORTEX

The most superficial part of each cerebral hemisphere is called the

cerebral cortex and is 2-4 mm thick. Underneath the cortex lies the sub
cortical matter the cortex mostly consists of nerve cell bodies (soma/
perikaryon) with some nerve fibers and has a grey appearance hence it is
also called "cerebral grey matter."

The sub cortical matter mostly consists of nerve fibers (efferent,

coming from the cortex as well as afferents going to the cortex) the nerve
fibers are white in appearance and hence it is called "sub cortical white
matter' within the sub cortical white matter there are masses of grey
matter consisting of sub cortical nuclear masses. These nuclear masses
consist of nerve cell soma, packed up densely, together with their axons
and dendrites an example of sub cortical nuclear mass is the "basal
ganglia".

The cortical gray matter sends efferent to many areas of the brain
and most notably to the anterior horn cell of the spinal cord these efferent

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thus controls or in influence other parts of the brain as well as the anterior
horn cell of the spinal cord the cortical gray matter also receives various
sensory (afferent) fibers.

The sub cortical nuclear mass also sends efferent to various other
parts of the brain and receive various afferent impulses.

The cerebral hemispheres are most massive in the human beings.

The total surface area of cerebral cortex in man is about 2,200 sq cm, of
which major parts lie within the sulci. The cortex itself is only about 2-4
mm thick and microscopically is divided into six layers by von Economo as
follows-

1. Molecular (also called plexiform) layer

2. External granular layer

3. External pyramidal layer

4. Internal granular layer

5. Internal pyramidal (also called ganglionic) layer

6. Multiform (polymorphic cell) layer

The names of these layers are self expressive. The plexi form or
molecular (the most superficial) layer consists mostly of transversely
situated (horizontal) nerve fibers these fibers -are derived from various
sources like the pyramidal cells of the inner layers of cortex from thalamus
and so on external granular layer consist mostly of small pyramidal cells
whereas the internal granular layer consists mostly of stellate cells. The
pyramidal layers (3,5) contains large pyramidal cells, cells of the layer 5
being larger than cells of the layer 3.

Two bands of Bail larger, outer (external) and inner (internal)

consisting of transversely (horizontally) placed fibers are also found. They
are found in layer 4 and 5 respectively.

This classical six layered structure is not found every where in the
cortex. Local variations occur. Some important local variation is stated
below.

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1. In area 4 (motor cortex) the pyramidal cells predominate but the

internal granular layer is deficient. This type of cortex, is therefore
called 'agranular cortex'

2. In the occipital cortex, the pyramidal cell layers are deficient but the
internal granular layers are dominant and the cortex is called
"granular cortex"

3. In the limbic lobe, the number of layers of cortex is less than six,
such areas of cortex where the number of the layers is less than six
are called "allocortex" the six layered areas are called "neocortex"
(Allo=old, Neo= New)

Allocortex is found in the brains of animals in the lower rungs of

evolution as well as in man, but neocortex is more and more developed as
the animal is in the scale of evolution more and more advanced and is
best developed in man.

Organization (Function arrangement of neurons)

Cortical neurons are arranged in vertical rows. Each row consist of

about 100 neurons. The longitudinal axis of each such row is
perpendicular to the surface of the cortex. Each such vertical row
constitutes an unit and individual rows are assembled into larger units by
associating with adjacent vertical rows. Such larger units are perhaps
modifiable when one considers the large number of neurons in our brain.
The possible numbers of such larger units and the continuous
modifications of such larger units makes one two under stand what a
fantastically complex structure the brain is.

THE MAJOR LOBES

The cerebral cortex has several areas and the areas can be
classified is several ways.

1. Functionally e.g. -

A. Sensory cortex (sensory cortex again can be subdivided into

somatosensory, auditory, visual olfactory sensory areas)

B. Motor areas (motor, premotor frontal eye field, occipital eye field,
second motor area and so on)

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C. Association areas of cortex

2. Anatomically e.g.

A. Frontal

B. Parietal

C. Temporal

D. Occipital lobes

In early part of the 20th century, around 1909 Brodman divided the
entire cortex of each cerebral hemisphere into several areas, now called
Boardman’s area. Each hemisphere contains a total of 47 such areas. The
original idea that each area has an absolutely selective function is over
simplification. Thus Boardman’s area 4 is predominantly a motor area no
doubt, but motor responses can be obtained even when post central gyrus
is stimulated.

Frontal lobe

The major areas in this lobe are (I) area 4 (motor area) (II) area 6
(Premotor area) (III) Frontal eye field (area 8) (IV) supplementary motor
area (V) prefrontal cortex (areas 9, 10,11& 12) and (VI) Broca's area (area
44) The part of the frontal lobe that lies anterior to the area 8 is called
prefrontal or orbit frontal lobe. A complete picture of functions of area 6 is
yet to come stimulations of area 6 produces movement (as in stimulations
of area 4) no doubt, but the intensity of the stimulus has to be much
greater than that for area 4. Further, destruction of area 4 (keeping area 6
intact) does not abolish all voluntary motor activities. Some are retained
although these remnant movement are crude. Electro-stimulation of the
frontal eye field (area 8 which lies in front of the area 6) causes conjugate
movements of the eye particularly towards the opposite side. There fore
area 8 appears to be mainly responsible for the voluntary (but not the
reflex) eye movement it may also be responsible for the saccadic
movements of the eye ball.

Area 44 in the dominant hemisphere is the motor area for speech

(also called Broca's area) the dominant area for right handed person's left
hemisphere, whereas for left handed person, it is the right hemisphere. On
suitable electro stimulation of the prefrontal lobe.

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I. Autonomic changes (eg. BP, heart rate, gastro intestinal secretion

and motility) can be elicited. The area is some how related to

II. Pain perception – It is connected with limbic system and thus

associated with

III. Emotion – The ability to judge a situation and make small plans are
also associated with this areas. Thus this region influences,
autonomic fibers, emotions, pain perception and higher faculties

Parietal lobe

Major areas of these lobes are:

I. Primary sensory area (somesthetic area 1) or Broadmann's area 3,

1, 2 or the post central gyrus.

II. Secondary somatic area or somatic area II

III. And somesthetic association area

Primary somesthetic area (Brodmann's 3,1,2 is the highest area of

general conscious, sense perception, fibers conveying impulses by spino
thalamic tract, lemniscal system etc,.(touch, pain temperature senses etc.)
after relaying in the thalamus, end here, and thus we become aware of the
specific senses. There is a somatotropic mapping, called sensory
homunculus which describes pictorially, which area of somesthetic area I
is responsible for sense perception from which area of the body.

However, numerous interconnections exist between area 4 and

area 3,2,1 so that stimulation of primary sensory area may cause motor
response, or stimulation of motor area (area 4) can elicit sense perception
therefore, area 4 should be considered as an unit tied up with primary
sensory area and these two area, taken together, constitute the sensory
motor cortex.

Somesthetic area II (SII) lies below the area for face of somesthetic
area I, so that it is buried in the lateral sulcus. Therefore there are two
(dual) representation for each sensory perception from each field of the
body although it appears somesthetic area I alone would have been
sufficient. Exact function of SII is not clear. It appears that for our ability to
learn via various somesthetic senses (e.g. touch) the presence of an intact

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SII is necessary. SII receives input from 2 sources, viz (I) from SI (Post
central gyrus) and (II) directly from thalamus.

Somato sensory association area (area 5 and 7 of Broad mann) lies

posterior to the somesthetic area I, in the parietal lobe. Its major function
appears to be as follows.

I. Various sensory inputs reach the posterior part of parietal lobe, also
called posterior parietal lobe (= areas 5 & 7 of Brodmann = somato
sensory association area) and all these inputs are integrated
(=synthesized) thus inputs from SI, olfactory, auditory, visual area
of the brain etc. reach here and are integrated (=synthesized). This
integration produces a motive and the motive in turn can lead to an
action.

II. Another function of this (i.e. posterior parietal lobe) area is that its
presence is necessary for maintenance of body image.

III. The parietal lobe also contains angular gyrus destruction of angular
gyrus causes agraphia (=inability to write) which is a form of
aphasia.

OCCIPITAL LOBE

Major area of this lobe are -

I. Primary visual area (area 17)

II. Visual association area (area 18)

III. Occipital eye field (area 19)

The primary visual area, area 17 (also called visuosensory area or

area striata) in short it is the highest area for perception of visual senses.
Area 18 is the area where visual sense are interprets and integrated in the
light of past experience for example, there is a light and area 17 sees the
light. It is area 18 which interpretes that the light is from a candle stick thus
this can be viewed as a homologue of stereognosis.

In the anterior part of the lateral surface of occipital lobe, lie the
occipital eye field stimulation of this area causes (a) Movement of the eye
and (b) visual hallucination (frontal eye field stimulation) which causes
only movement of the eyes but no hallucination.

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TEMPORAL LOBE

I. Primary auditory area, in the gyrus of Heschl (area 41) which is

situated in the floor of the lateral suclus plus a small part of he
superior temporal gyrus.

II. In area 41 sound is heard while in the wernicke's area the sound is
interpreted.

The brain stem of midbrain, pons and medulla from above below.
The medulla is continued below as the spinal cord. The cerebellum, small
brain lies under the occipital lobe and dorsal to the brain stem. The
cerebellum by mean of three pairs peduncles (superior, middle or inferior)
is connected with the brain stem. The lower portion of the dorsal side of
the brain stem also forms the floor of the 4th ventricle.

On the superior (cephalic) surface of the midbrain are the two

thalami (one thalamus on each side of the mid line). The dorsal side of the
thalamus bulges to form what is known as the pulvinar. Close to the
pulvinar lies the lateral geniculate body (LGB), On the ventral inferior
aspects of the thalami, lies the hypothalamus from the middle of the
hypothalamus hangs the pituitary gland.

The ventricles

Each cerebral hemisphere contains, within its sub cortical white

matter, lateral ventricle containing some fluid called the CSF. The medial
wall of the lateral ventricle is formed by septum pellucidum. In between the
two thalami, lies the 3rd ventricle. The CSF of the lateral ventricles
escapes through a foramen (foramen of Monroe) and comes into the 3rd
ventricle. The floor of the 3rd ventricle is formed by the hypothalamus.
Running longitudinally through the midbrain and upper part of the pons is
a tunnel, called the aqueduct of sylvius. The CSF from the 3 rd ventricle
escapes into the aqueduct of sylvius to enter the 4th ventricle, whose floor,
as mentioned above is formed by the dorsal sides of the pons and
medulla. The central canal of the spinal cord is a continuation of the 4th
ventricles.

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Cerebral circulation

Knowledge of the anatomy and physiology of the cerebral

circulation is essential in order to understand how symptoms and signs
are produced by its disorders and the principles upon which treatment
must be based.

THE BLOOD SUPPLY OF THE BRAIN

The brain receives its blood from four arteries, the two internal
carotids and the two vertebral. The right internal carotid springs from the
right common carotid, a branch of the branchio cephalic trunk, the left from
the common carotid, which springs from the aorta. The vertebral arteries
are derived from the subclavians. The vertebral arteries unite to from the
basilar, which bifurcates into the two posterior cerebral arteries. From the
basilar, short and long perforating branches, as well as its terminal
branches, provide critical brainstem perfusion.

The circle of willis is formed as follows. The posterior

communicating artery on either side joins the internal carotid to the
posterior cerebral and the circle is completed in front by the anterior
communicating artery which units the two anterior cerebrals, branches of
the internal carotid.

The principal branches of the internal carotid artery are:

 The ophthalmic artery – From which the central artery of the retina
is derived.

 Posterior communicating artery – Supplies optic chiasm, pituitary,

hypothalamic region, lower part of the anterior third of the posterior
limb of the internal capsule, parts of the lateral nucleus of the
thalamus the anterior third of the crus cerebri and part of the
midbrain including the sub thalamic nucleus.

 The anterior choroidal artery – Supplies the choroids plexus. Also

distributed to the optic tract, posterior two thirds of the posterior
limb of the internal capsule, part of lentiform nucleus, anterior third
of the crus cerebri etc.

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 The interior cerebral artery – Its gives off the following branches :

 Basal branches of which the most important is the Heubner's artery

which supplies the anterior part of the caudate nucleus, anterior
1/3rd of the putamen and the inferior half of the anterior limb of the
internal capsule.

The anterior communicating artery unit the two anterior cerebrals.

Gives off cortical branches to medial and superior surfaces of the

frontal and parietal lobes. The most important branch supplies the
Para central lobule containing the leg area of the motor cortex.

 The middle cerebral artery – It supplies the frontal, parietal and

superior surfaces of the temporal lobe. Its penetrating branches
supply the putamen, outer globus pallidus, genu and posterior limb
of the internal capsule.

The vertebral arteries run upwards in a bony canal in the cervical

spine. They fuse at the level of the junction between the pons and the
medulla to form the basilar artery. The basilar artery terminates at the
upper border of the pons by dividing into the two posterior cerebrals. It
supplies with blood the pons and part of the midbrain and through the
superior cerebellar and anterior inferior cerebellar arteries that part of the
cerebellum not supplied by the vertebral arteries.

The physiological importance of the circle of Willis lies in the

anastomotic circulation, which it provides. The internal carotid artery and
the basilar artery share the blood supply to each cerebral hemisphere in
such away than there is normally no interchange of blood between them.
The opposing streams of the two arteries meet in the posterior
communicating artery at a 'dead point', at which the pressure of the two is
equal. Consequently they do not mix. Similarly the territories of the two
internal carotid arteries meet at a "dead point" in the middle of the anterior
communicating artery. If however, both internal carotids or both vertebral
arteries are occluded, blood passes forwards or backwards respectively
from the pair, which are still patent. There is then a functioning
anteroposterior anastomosis in each posterior communicating artery.
Similarly occlusion of one internal carotid artery leads to its territory being

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invaded by the basilar supply through the posterior communicating artery,

and from the opposite internal carotid through the anterior communicating
artery.

There is a further anastomotic circulation in the brain, namely the

distal anastomoses which exist between the three major cerebral arteries
at the periphery of their cortical fields of supply. No cerebral artery
becomes an end artery appears until it has entered the brain substance,
but once within the brain no artery appears ever to join another.

Auto regulation

The brain possesses, to a high degree, the property of auto

regulation by which the blood flow and hence the oxygen concentration is
maintained within narrow limits despite wide fluctuations in systemic
pressure. Two factors are principally responsible. First, there is the
response of the arteriolar walls to changes in the intraluminal pressure so
that arterioles constrict with a raised intraluminal pressure and dilate with
a fall. Second, biochemical factors, mainly a rise in CO2, lead to arteriolar
and capillary dilation but at low levels hypoxia also causes dilation,
possibly by release of lactic acid as anaerobic glycolysis occurs.

The normal cerebral blood flow is 50-60 ml/100g. of brain per

minute and remains nearly constant as a result of the fluctuation of
cerebrovascular resistance by auto regulation until the mean arteriolar
pressure falls to 50 mm. Auto regulation also aids the survivals of a locally
ischemic region of the brain, by increasing the diameter of vessels
adjoining the area and thus by means of collaterals compensates for the
lack of blood in the ischemic region.

VENOUS DRAINAGE OF BRAIN

Characteristics of the veins

1. Vein walls are without muscles.

2. The vein are without valves.

3. Some of them open into cranial venous sinuses against the

direction of blood flow.

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Groups of veins

A. External cerebral vein

B. Internal cerebral vein

C. Terminal vein

A. External cerebral vein

In contains following -

1. Superior cerebral veins

2. Superficial middle cerebral vein

3. Deep middle cerebral vein

4. Inferior cerebral vein

5. Anterior cerebral vein

B. Internal cerebral vein –

They are two in number

1. Right internal cerebral vein

2. Left internal cerebral vein

C. Terminal vein

Its contains

1. Great cerebral vein

2. Basal vein one each side

Ultimately all vein drain into cranial veinous sinus and which in turn
drain into internal jugular vein.

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HEMIPLEGIA
Hemiplegia described in Modern Medicine can be related with
Pakshaghata described in Ayurveda and the same is considered in the
current study also.
ETYMOLOGY
The word ‘Hemiplegia’ is derived from two words ‘Hemi’ and
‘Plegia’. The meaning of both these terms are:-
Hemi = Half Plege = Stroke
i.e. Hemiplegia means loss of strength or voluntary movement on
either side of body.
Definition
The term Hemiplegia applied to voluntary muscles signifies loss of
power of voluntary contraction, due to interruption, (whether functional or
organic) in any motor part of cerebral cortex down to the muscle fibre. This
excludes pathology of muscles or any such type.
Hemiplegia
A unilateral brain lesion producing paralysis of contralateral side of
the body including face, trunk and limbs is known as hemiplegia or
ipsilateral (Trunk may be less affected due to bilateral connection).
Diplegia
A bilateral cerebral or a high cervical lesion produces diplegia or
double hemiplegia, the limbs on both side being affected.
Monoplegia
Paralysis of a single limb resulting from a cerebral lesion is termed
cerebral monoplegia. Spinal or peripheral monoplegia is less common.
Paraplegia
Paralysis of the limbs resulting from a lesion of a spinal cord is
called paraplegia, usually affecting both legs alone. It must be
distinguished from cerebral diplegia in which the face is also affected.
Brachial Paraplegia
In rare cases both arms may be paralyzed from a spinal region,
with little or no affection of legs.

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Cross or Alternate Hemiplegia

There is a paralysis of some parts on one side and of others on the

contra lateral side. E.g. Millard – Gubler syndrome.

Clinically, the most commonly encountered type is hemiplegia.

Condition milder in form than above is known as hemiparesis,
characterized by weakness on either side of the body. Before having clear
knowledge of hemiplegia, it is essential to acquaint ourselves with applied
knowledge of normal Cerebral Circulation as well as the Pyramidal Tract
as both share basic pathology in the emergence of the disease.

CAUSES OF CEREBROVASCULAR ACCIDENT

Stroke is the clinical term for acute loss of circulation to an area of

the brain, resulting in ischemia and a corresponding loss of neurologic
function. Classified as either hemorrhagic or ischemic, strokes typically
manifest with the sudden onset of focal neurologic deficits, such as
weakness, sensory deficit, or difficulties with language. Ischemic strokes
have a heterogeneous group of causes, including thrombosis, embolism,
and hypo perfusion, whereas hemorrhagic strokes can be either
intraparenchymal or subarachnoid. The list of causes of different groups of
stroke are as follows.

Causes of thrombotic stroke

a. Arterial – Cerebral atherosclerosis, collagen disease pressure

effect of tumour, severe dehydration, acute fibrile illness of children,
carotid artery occlusion vertebro basilar in sufficiency. Syphilitic
endarteritis

b. Venous – Cortical thrombophlebitis, post partum or post operative

thrombophlebitis.

Cases of embolic strokes – Embolisms are usually from,

a. Heart – Atrial fibrillation, myocardial infarction, infective

endocarditis. Mitral stenosis aneurysm of aorta.

b. Arteries = Detachment of an atheromatous plaque usually from the

aorta or the carotid artery. Atheroma of internal cortid.

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c. Veins – Thrombophlebitis usually from the veins of lower limb and

pelvis.

d. Miscellaneous – Post cardiac surgery, caisson's disease.

Causes of hemorrhagic stroke – Hemorrhage are usually from the

rupture of

a. Berry's aneurisms

b. Atherosclerotic vessel

c. Angiomatous malformation

d. Hypertensive encephalopathy

e. Trauma

f. Whooping cough

Risk factors of strokes

The American strokes Association has identified several factors

that increase the risk of stoke. The more risk factors a person has, the
greater the chance that he will have a stroke.

Medical condition that increase stroke risks

 Transient ischemic attacks (TIAS): TIAS are "mini strokes". They

are strong predictors of stroke. A person who's had one or more
TIAS is almost 10 times more likely to have a stroke than someone
of the same age and sex who hasn't.

 High blood pressure: Hypertension is the one of the leading risks

of stroke. The effective treatment of high blood pressure is key
reason for the accelerated decline in the death rates of stroke.

 Diabetes mellitus: Diabetes is independent risk factor for stroke.

 Heart disease: People with heart disease have more than twice
the risk of stroke as those whose hearts work normally. Atrial
fibrillation in particular raises the risk for stroke. Recent MI is also
major cause of death among stroke survivors.

 Carotid artery disease: Atherosclerosis of carotids artery can lead

to stroke. Carotid bruit is an indication for carotid artery disease.

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 High red blood cell count: A moderate or marked increase in the

red blood cell count is a risk factor for stroke. The reason is that
more RBCs thicken the blood and make clots more likely.

Controllable risk factors and life style choices

 Smoking: Recent studies have shown cigarette smoking to be an

important factor for stroke.

 Obesity, elevated cholesterol and elevated lipids.

 Physical inactivity: A sedentary lifestyle.

 Excessive alcohol intake.

 Illegal drug use: Intravenous drug abuse carries a high risk of

stroke from cerebral emboli.

 Oral contraceptive pills: It increases the risk of venous

thromboembolism.

Uncontrollable Risk factors

 Increasing age: Stroke is more common in people over 50 years.

 Sex: Latest data show that, over all the incidence and prevalence
of stroke area more common in man.

 Heredity and Race: The chance of stroke is greater in people who

have a family history of stroke. African – Americans and Hispanic
Americans are at higher risk than white Americans. This may be
due in part of hypertension and dietary difference.

Other factors

 Season & climate: Stroke deaths occur more often during periods
of extremely hot or cold temperature.

 Socioeconomic factors: There's some evidence that people of

lower income and educational levels have higher risk for stroke.

 Vit. B deficiency increases stroke risk.

 Air pollution may increase stroke (Oct. 2003 – Journal of American

heart association)

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 Sleeping for more than eight hours at night, snoring and daytime
drowsiness is associated with an increased risk for stroke. (Feb.
2001, American stroke Association's 26th International stroke
conference).

 Low potassium intake may increase risk for stroke. (Aug. 13, 2002
– journal of American academy of Neurology).

PRODROMAL SYMPTOMS
Cerebral thrombosis

Premonitory symptoms are common and exist for hours, days or

months before the onset of paralysis. They are given names as TIA.

Transient cerebral ischemic attacks

Since the aim of treatment in CVD is the prevention of a major

stroke, the management of the TIA may be considered first. TIA are the
episodes indicating ischemia of some parts of cerebral hemisphere or the
brain stem. They are defined as episodes of temporary and focal cerebral
dysfunction of vascular origin leaving no persistent neurological deficit and
lasting less than 24 hours. Attacks indicating ischemia in the distribution of
one carotid artery are often referred to as episodes of carotid insufficiency,
those involving the brainstem as vertebro basilar insufficiency. In carotid
artery disease the transient warning attacks consist of monocular
blindness, hemiplegia, hemianesthesia, disturbances of speech and
language, confusion, etc. In vertro-basilar system the prodromata take the
form of episodes of dizziness, diplopia, numbness, and impaired vision in
one or both visual fields, dysarthria.

Cerebral embolism

Premonitory symptoms are absent in this type of CVA. Onset in

instantaneous, hemiplegia developing in few seconds and minutes.
However cases of less sudden onset, resembling that of 'Stroke in
evolution' have been described. A convulsion may occur at onset and
there is sometimes headache.

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Cerebral hemorrhage

The onset is usually sudden like a bolt from blue without any
prodromal symptoms. But the patient may be known to be hypertensive
and there may have been premonitory symptoms such as transitory
speech disturbance or attacks of weakness of a limb. Severe headache,
vomiting, loss of consciousness and convulsion are accompanied at the
onset.

Intravranial aneurysms may produce symptoms by compressing

the structures in their vicinicty. Patients may suffer from recurrent
headaches, typical migraine, convulsions, TIAs. SAH from a cerebral
angioma may occur without previous warning but is more often preceded
by symptoms and signs of the cerebral lesion.

Sign and symptoms of cerebrovascular accident

The signs and symptoms of stroke depend upon the following

factors:

 Nature of vascular lesion.

 Duration of ischemia

 Region of the brain supplied by the effected vessel

 Status of the collaterals to that regions

 Vulnerability of neurons of that region

Clinical picture as per the nature of lesion

As earlier mentioned there are three basic lesion of brain manifest

as cerebrovascular accident v.i.z. ischemia, infraction and hemorrhage.
Each lesion manifests its characteristic clinical presentation. The
presenting features of each type of lesion are tabulated below.

S.No. Cerebral hemorrhage Thrombosis Embolism

1. Age Usually above 40 year Young or aged Young or aged
Females
2. Sex Male predominant Males or females
predominate
3. Onset During emotion, During sleep No such

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excitement or exertion
Rapidity of
4. Rapid Less rapid Stormy
onset
Headache
Premonitory hemisparsis
5. Headache Nothing
symptoms transient aphasia
etc.
Symptoms at Convulsive
6. Vomiting No such
onset seizure
Unconscious Gradually deepening Patient may be
7. Transient
ness unconsciousness dazed
May or may not May or may
8. BP Always high
be high not be
9. Convulsion Usually absent Rare Common
Neck
10. Frequent Absent Absent
stiffness
May be
irregular and
11. Pulse Slowed down No change rapid due to
auricular
fibrillation
There may be
evidence of
May show evidences of auricular
May or may not
12. Heart left ventricular fibrillation,
be involved
hypertrophy coronary
thrombosis or
mitral stenosis
13. Leucocytosis Common Absent Absent
May not detect May not detect
14. CT/MRI Can detect within minute
for 2-4 days for 2-4 days
Residual
Usually good but
hemiplegia
residual
15. Prognosis Bad persists
hemiplegia
recurrence is
persists
common

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Clinical picture as per duration of ischemia

If ischemia is of short duration and circulation restored immediately
then the patient develops neurologic deficit for a short period usually less
than 24 hours. This is called transient ischemic attack.
If the ischemia is permanent and lasts for long duration then the
patient's neurologic deficit become persistent and it is called as completed
stroke.
If the ischemia progresses in a stuttering manner over days then
the focal deficit continue to worsen after about 6 hours from onset. This is
called evolving stroke.
Clinical presentation as per the site of lesion
The following are some distinctive symptoms of lesions of the
corticospinal tract at different points in its course-
Cortical lesion
Cortical corticospinal lesions produce monoplegia or paralysis of
even smaller muscle group, Aphasia (if dominant cortex is involved),
cortical sensory loss. Jacksonain fits may occur if the lesion is in or near
the cortex.
Sub cortical lesion
Weakness predominates in one limb but the whole of the opposite
side is affected, impairment of postural sensibility and tactile discrimination
by involvement of thalamocortical sensory fibers; crossed homonymous
hemiapnoia by damage to optic radiation.
Internal capsule
It is the commonest site and presents with a pure motor and
isolated hemiplegia, hemi anesthesia if lesion in the posterior one third of
internal capsule. Sometimes homonymous hemiapnoia on the same side
may be present.
Lesion in the midbrain: Lesion in the midbrain produces
 Weber's syndrome: IIIrd nerve palsy with crossed hemiplegia.
 Benedict's syndrome: IIIrd nerve affection on the side of lesion with
tremors, hypertonia and ataxia on opposite side.
 Facial diplegia of the supranuclear type.

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Lesion in the pons – It produces

 Millard – Gubbler syndrome: Paralysis of lateral rectus, with or
without LMN type of facial paralysis on one side with crossed
hemiplegia.
 Foville's syndrome: Similar to Millard Gubbler syndrome except that
instead of lateral rectus paralysis, there is conjugate ocular
deviation to side of the lesion.
 Horner's syndrome: Paralysis of the ocular sympathetic may result
from a lesion in the tegmentum of the pons.
Lesions in the medulla – It produces
 Many variety of crossed hemiplegia in unilateral medullary lesion.
 In midline lesion: Unilateral paralysis of half of the tongue, crossed
hemiplegia, loss of postural sensibility is found.
 Lesion in lateral part of medulla: Vocal cord paralysis, Horner's
syndrome, trigeminal analgesia, thermo anesthesia, and some
cerebellar deficiency – all on the side of the lesion with loss of
appreciation of pain, heat and cold in the limbs and trunk on the
opposite side.
Lesion in thalamus: It produces thalamic syndrome characterized by;
 Fleeting hemiparesis of hemiplegia on the opposite side of the
lesion.
 Impairment of superficial & loss of deep sensation on opposite side.
 Elevation of threshold to cutaneous, tactile and painful stimuli.
 Intolerable, spontaneous pains & hyperpathia on the opposite side.
 Ataxia, tremor and / or choreoathetoid movements on the opposite
side.

Lesion in the spinal cord

Unilateral lesion of the cortico-spinal tract below the medulla and 5th
cervical spine produces spinal hemiplegia with paralysis of muscles
innervated by cranial nerves.

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PATHO PHYSIOLOGY OF STROKE

There are two major categories of brain damage in stroke –

Ischemia and Hemorrhage, which result in the destruction of brain tissue
via abnormalities in the brain's blood supply. Ischemic stroke is a
consequence of a lack of blood flow where brain tissue is starved of
oxygen and vital nutrients. Hemorrhagic stroke is the rupture of a blood
vessels and the subsequent release of blood into the extra vascular space
with in the cranium.

Either kind of stroke can occur anywhere in the brain and

consequences range from minimal disability to paralysis or death.
Ischemic stroke account for 80-86% of all stroke whereas hemorrhagic
stroke accounts for 14-20%.

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EMBOLIC STROKE

Heart Major arteries Systemic veins

Embolic Material

Pieces of thrombus Fat Air Bone marrow Atheromatus Clumps of Bacteria

material

Cerebral arteries

Impaction or blockage of blood vessels

Ischemia of the brain area deprived of blood supply

If blood seeps into the infarcted area

K+ moves to extra cellular space

Hemorrhagic infarction Ca++ moves into the cells (Nerve cells)

O2 free radical production

Lipid Peroxidation

Cell damage

Decreased O2

Anaerobic glycolysis

Lactic acid accumulation

Acidosis

Cell damage

Raised levels of neurotransmitter glutamate

Increases Na++ and Ca++ influx into cells

Influx of water and Cl-

Swelling of cells

Oedema

Cell death
Infraction

Ingestion of Necrotic debris by Macrophages

Shrinkage of volume of infracted tissue Glial scar formation at chronic stage

Frank cavity

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THROMBOTIC STROKE

Age over Diabetes

40 yrs. Genetic Familial Hyperlipidaemia Hypertension Mellitus

Obesity

Lack of
ENDOTHELIAL INJURY
Exercise

Hypertrophy of Tunica Media Alcohol

Atheroscelotic Plaque formation

Infections

Platelets afhere to the plaque cervices

Deposition of fibrin, thrombin etc

Formation of clot

Narrowing of lumen of the blood vessels

Decreased perfusion to the brain

Ischemia

INFARCTION

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HAEMORRHAGIC STROKE

Hypertension

Hypertrophy of Tunica Media in

Small arteries and arterioles

Degeneration of Tunica Media

Micro Aneurysms
Atherosclerosis

Brittle vessels

RUPTURE OF VESSEL

Explosive entry of Blood into

Brain parenchyma

Neurons are structurally disrupted and white

matter Parts are split apart

Forms circular or oval mass which disrupts Bleeding dissects into Death in 40%
tissue and grows in volume Ventricles and enters CSF within 3-4 days

Adjacent brain tissue is displaced

and compressed

Blood clot solidifies causing swelling

Of adjacent tissue

If Patients survives May cause transtentorial

conning

Clot is absorbed
Death

Clot is replaced by Haemosiderin lined

Slit like neurological scar

Cavity of yellow serous fluid

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Ischemic

Ischemia can be further subdivided into three different

mechanisms: thrombosis, embolism and decreased systemic perfusion.

Thrombosis

Thrombosis refers to an obstruction of blood flow due to a localized

occlusive process within one or more blood vessels. The lumen of the
vessel is narrowed or occluded by an alternation in the vessel wall or by
superimposed clot formation. The commonest type of vascular pathology
is atherosclerosis in which fibrous and muscular tissue overgrow in the
subintima, and fatty materials form plaques that can encroach on the
lumen. Next, platelets adhere to the plaque crevices and form clumps that
serve as nidi for the deposition of fibrin, thrombin and clot. Atherosclerosis
affects chiefly the larger extra cranial and intracranial vessels.

 Occasionally clot forms within the lumen because of primary

haematological problems.

 In hypertensive patients, increased arterial tension leads to

hypertrophy of the media of small arteries and arterioles and
deposition of fibrinoid material to the vessel wall, sometimes with
atherosclerosis, is seen.

 Lacunar infarcts are among the commonest cerebrovascular

lesions. When small arteries or arterioles already thickened as a
result of hypertension are occluded by thrombus or embolus from
larger anterosclerotic vessels, this may cause areas of micro
infarction, which ultimately lead to small slit-like cavities known as
lacunas. Some affected vessels show lipohyalinosis. In sever
hypertension multiple lacunas may be found in putamen, pons,
thalamus, internal capsule etc.

There is tendency for atheromatous plaques to form at branching

and curves of the cerebral arteries. The most frequent side are in the ICA
at the carotid sinus in the cervical part of the vertebral arteries and at their
junction to form the basilar at the main bifurcation of the MCA, in the PCA
as they wind around the midbrain and in the ACA as they curve over
corpus callosum.

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Embolism

An embolus is a foreign body that is transported from one part of

the circulatory system to another where it becomes impacted. The process
is known as embolism. Approximately 99% of all emboli are pieces of a
dislodged thrombus, hence the common term thromboembolism. Other
forms of emboli are fat, air tumor, bone marrow, atheromatous materials
and clumps of bacteria. Embolic material typically originates in the heart
(valves, endocardium, arterial or ventricular clots or tumors). Major
arteries (eg- aorta carotid and vertebral) or systemic vein. In contrast to
thrombosis embolic luminal blockage is not due to localized process
originating within the blocked vessel.

Brain embolism is essentially a manifestation of heart disease. Any

region of the brain may be affected; the territory of the MCA, particularly
the upper division is most frequently involved. The arteries of the left side
of the brain are embolized more often than those of right, chiefly the MCA.
Large embolic masses can block large vessels (sometimes the carotid in
the neck); while tiny fragment may reach vessels as smaller 0.2 mm in
diameter. The embolic material may remain arrested and plug the lumen
solidly but in many cases it breaks up into fragments, which enter smaller
vessels and disappear completely. Because of the rapidity with which
embolic occlusion develops, there is not much time for collateral influx to
become established. Following impaction of an embolus, a thrombus
usually form in the vessel and may spread distally or less frequently
proximally and the area of brain deprived of blood supply is infracted. If an
embolus impacts and then moves on, arterial blood may then enter the
infracted area. Thus embolism is the commonest causes of hemorrhagic
infraction. When the embolus is infected meningitis or cerebral abscess
may develop, or when the infection is of low virulence, embolism may be
followed by infective softening of the vessel wall and aneurysm formation-
mycotic aneurysm.

Fat embolism may occur as the result of fat globules being set free
into the circulation after the fracture of one of the long bone, passing
through the pulmonary circulation and so reaching the brain. In an
embolism, gas bubbles may appear in the arterial circulation of the CNS in

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caission disease or air can enter the circulation accidentally during cardiac
surgery, venous catherizations etc.
Decreased systemic perfusion
In this circumstance, diminished flow to brain tissue is due to low
systemic perfusion pressure. The most common causes are cardiac pump
failure and systemic hypotension. In such cases, the lack of perfusion is
more generalized than in localized thrombosis or embolism and affects the
brain diffusely and bilaterally. Poor perfusion is most critical in border zone
or so called water shed regions at the periphery of the major vascular
supply territories. Asymmetrical effects can result from preexisting
vascular tensions causing an uneven under perfusion.

LOCAL BRAIN EFFECT OF ISCHEMIA BY ALL THREE ABOVE

MENTIONED MECHANISM
When blood flow into a brain region is reduced, survival of the
tissue at risk usually depends on the duration of compromised blood flow
and the availability of collateral circulation to the cells. Generally, the
sooner circulation is restored to occluded neural tissue; the more likely
ischemic damage can be reversed. Prolonged vascular blockage results in
irreversible ischemic damage and cell death, an event termed infraction.
Surrounding the core of infracted neural tissue is a region with
reduced, (but not entirely blocked), cerebral blood flow (CBF). This
marginally per fused area is called the ischemic penumbra. Infracted
neural tissue is characterized by local CBF below 10ml/100g/min (normal
CBF is appro. 50ml/100g/min.). Where as CBF in the penumbra is
presumed to be 10-20ml/100 g/ min. Scientists believe that infracted
tissue cannot be saved but that the ischemic penumbra represents
potentially reversibly damaged neural tissue.
When neurons are rendered ischemic, a number of biochemical
changes occurs which potentiate and enhance cell death: k+ moves
across the cell membranes into the extra cellular space and Ca++ moves
into the cell which ultimately leads to mitochondrial failure. Decreased O2
availability leads to production of oxygen free radicals, which causes
peroxidation of fatty acid and severely damage the cell function. With
deceased oxygen availability, anaerobic glycolysis leads to accumulation

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of lactic acid and a decrease in pH. The resulting acidosis also greatly
impairs cell metabolic functions. In regions of ischemia, concentrations of
excitatory neurotransmitters specially glutamate is increased which
causes vulnerable neuron to receive toxic exposure to glutamate and
there by increasing the likelihood of cell death. Glutamate entry opens
membranes and increase Na + & Ca ++ influx into the cells. Large influxes
of Na+ are followed by entry of chloride ions and water, causing cell
swelling and oedema. In chronic phase, glial scars form and macrophages
gradually ingest the necrotic tissue debris within the infract leading to
shrinkage of the volume of the infracted tissue or a frank cavity.
These aforementioned local metabolic changes cause a self
perpetuating cycle of changes that lead to increasing neuronal damage
and cell death.
Intracranial hemorrhage
This is the third most frequent cause of stroke. There are four
varieties of intracranial hemorrhage – extradural, subdural, subarachnoid
and intracerebral. The first two are invariably traumatic.
Intracerebral hemorrhage
The term intracerebral hemorrhage describes bleeding directly into
the brain substance. The commonest cause of intracerebral arterials
hemorrhage is rupture of an atheromatous artery in a hypertensive
individual. Hypertension cause medial hypertrophy in small arteries and
arterioles, which lead to degeneration of media and produces a thickened
but brittle vessel. Bleeding diatheses, vascular malformations, rupture of
saccular aneurysm and vasculapathies such as amyloid degeneration or
segmental lipohyalinosis can also cause bleeding into the brain. The
degree of damage will depend on the location, rapidity, volume and
pressure of the bleeding.
The extravacations forms a roughly circular or oval mass, which
disrupts the tissue and grows in volume as the bleeding continues;
adjacent brain tissue is displaced and compressed. Intracerbral
hemorrhages are at first soft and dissect along white matter fiber tracts.
When bleeding dissects into the ventricles or onto the surface of the brain,
blood is introduced into the cerebrospinal fluid. The blood clots solidifies,
causing swelling of adjacent brain tissues. Later the clots is absorbed, and
it replaced by a neuroglial scar or by a cavity containing yellow serous

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fluid. During absorption of the clots, gliosis occurs in the wall of the cavity
with phagocytosis of destroyed neural tissue by compound granular
corpuscles.
Hemorrhage may be described as massive, small, slit and
petechial. Massive refers to hemorrhage several centimeters in diameter,
small applies to that 1 to 2 cm in diameter. Slit refers to hypertensive
hemorrhage. Which lies sub cortically at the junction of white and gray
matter, and petechial are pinpoint hemorrhages.
Subaracniod hemorrhage
Here blood leaks out of the vascular bed onto the brain's surface
and is disseminated quickly via the spinal fluid pathway into the spaces
around the brain. The commonest cause is a ruptured aneurysm, which
release blood rapidly at systemic blood pressure, suddenly increasing
intracranial pressure, where as bleeding from other causes is usually
lower and at lower pressures.
PATHOGENESIS OF ATHEROSCLEROSIS
As already mentioned the pathological phenomena manifesting as
stroke are ischemic and hemorrhage. The main cause of ischemic is
atherosclerotic thromboembolism. In case of hemorrhage also the main
cause intracerebral hemorrhage is formation and rupture of micro
aneurysms by continuous hypertension. The major risk factor for
hypertension is also the atherosclerosis. The major cause of sub
arachniod hemorrhage is the rupture of berry's aneurysm and berry's
aneurysm forms as a consequence of developmental defect in tunica
media and atherosclerotic change in the wall arteries. So be it the
ischemia or hemorrhage the main pathological process playing central role
is atherosclerosis.
Atherosclerosis is a specific form of arteriosclerosis affecting
primarily the intima of large and medium sized muscular arteries and is
characterized by fibro fatty plaques or atheromas. Anterosclerosis is not
caused by a single etiological factor but is a multifactorial disease whose
exact pathogenesis is still unkown. However several risk factors has been
implicated for the atherogensis v.i.z.1) – Major constitutional factors like
age 4th decade or more sex - Men affected more than women, Genetic
factor, familial or radical factors, 2)- Major acquired factors which included
hyperlipidemia, hypertension, cigarette smoking, Diabetes mellitus, and 3)

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– Minor risk factors like environmental influence, obesity, oral

contraceptive, Lack of exercise, Type A behavior, Alcohol, Viral infection.
There are many theories which has been postulated by different
scientists to explain the pathogenesis of atherosclerosis. The widely
accepted theory of pathogenesis of atheroma is as follows.
 Endothelial injury or dysfunction – It induced by hypertension,
hemodynamic force, chronic hyper lipidemia, cigarette smoking and
DM.
 Intimate smooth muscle proliferation – Endothelial injury causes
adherence, aggregation and platelet release reaction at the site of
exposure of endothelium. Proliferation on intimal smooth muscle
cells is stimulated by various mitogens, the most important of which
is PDGF, epidermal growth factors, fibroblast growth factors and
transforming growth factors alpha. Proliferation can also be
facilitated by loss of growth inhibitors. Intimal proliferation of smooth
muscle cell is followed by synthesis of matrix protein- collagen,
elastic fiber proteins and proteoglycans.
 Role of monocytes – Though blood monocytes do not possess
receptors for normal LDL, LDL does appear in the monocytes
cytoplasm to form foam cell. Due to endothelial injury plasma LDL
enters to intima and undergoes oxidation.
 For the monocytes oxidized LDL acts to attract, proliferate
immobilize and activate them as well as is readily taken up by
scavenger receptor on the monocyte to transform it to a lipid –
laden foam cell.
 For endothelium, oxidized LDL is cytotoxic.
 Death of foam cell by apoptosis releases lipid to form lipid core of
plaque.
 Thrombosis – Endothelial injury exposes sub endothelial
connective tissue resulting in formation of small platelet aggregates
at the site and causing proliferation of smooth muscles cells. This
causes mild inflammatory reaction which together with foam cells is
incorporated into the atheromatous plaque. The lesions enlarge by
attaching fibrin and cells from the blood so that thrombus becomes
a part of antheromatous plaque.

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Prognosis of cerebrovascular accident

Prognosis depends on the type of stroke, the degree and duration

of obstruction or hemorrhage and the extent of brain tissue death. Most
stroke patients experience some permanent disability that may interfere
with walking, speech, vision, understanding, reasoning or memory.

Thrombosis

Approximately 70% of ischemic stroke patients are able to regain

their independence and 10% recover almost completely. Approximately
25% of patients die as a results of the stroke. When focal ischemic lesions
is within the territory of the internal carotid artery, the greater the extent of
the area of cerebral damage, the worse the outlook. Previous strokes,
unconsciousness, association of sensory loss, hemiplegia are bad signs.
The longer the delays in onset of recovery, the poorer the prognosis.

Cerebral embolism

Cerebral embolism as such is rarely, fatal, unless the embolus

lodges in the internal carotid artery. The immediate mortality of cerebral
embolism is 7-10%. Here the eventual prognosis is determined by the
progress of the condition causing embolism and the gravity of the
underlying illness cardiac failure. MI. malignant growth, etc.

Cerebral hemorrhage

The location of a hemorrhagic stroke is an important factors in the

outcome, and this type generally has a worse prognosis than ischemic
stroke. A cerebral hemorrhage may prove rapidly fatal. A patient with
pontine hemorrhage or capsular hemorrhage which bursts into one lateral
ventricle is unlikely to survive more than a day or two, a progressive
hemorrhage in these sites proving fatal by causing brainstem
compression. If the hemorrhage is continuing there is a progressive
depending of coma, indicated by inability to rouse a formerly responsive
patients and loss of corneal and papillary reflexes.

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