STROKE MECHANISMS

A stroke occurs when there is interruption of the blood supply to a particular area of the brain,
ultimately leading to cell injury and cell death. Strokes can be classified as either:
ischemic or hemorrhagic.

ISCHEMIC STROKES
Ischemic strokes are the most common, accounting for up to 80% of strokes, and occur when there is an
occlusion of a blood vessel impairing the flow of blood to the brain. Ischemic strokes are divided into:
 Thrombotic
 Embolic
 Systemic Hypoprofusion

THROMBOTIC STROKE
In thrombotic stroke, a thrombus or clot gradually builds up in the artery, eventually occluding it and
disturbing blood flow to tissue downstream from the thrombus. Since blockage of the artery is gradual,
onset of thrombotic strokes is generally slower than that of embolic strokes. Three primary influences
predispose to the formation of thrombi, the so-called Virchow Triad:
Endothelial Injury Stasis or Turbulent Blood Flow Hypercoagulability

atherosclerosis turbulence over atherosclerotic genetic hypercoagulable states (factor V leiden,

plaques protein C deficiency, etc.)

stasis in aneurysms acquired hypercoagulability (prolonged

vasculitis immobilization, cancer, prosthetic cardiac valves,
heparin induced thrombocytopenia)
endocardial injury stasis in noncontractile
following MI endocardium following MI

hypertension
stasis due to atrial fibrillation
bacterial endotoxins
stasis due to vascular occlusion
from sickle-cell anemia

EMBOLIC STROKE

In an embolic stroke, a piece of material (or embolus) travels from a distant location and lodges in the
blood vessel, occluding it. The most common type of embolus is a blood clot. Because the blockage
arrives from another location, the onset of embolic strokes is usually quicker than that of thrombotic
strokes. As well, because of this, treatment of the stroke must also include determining the source of
the embolus so as to prevent further emboli. Because a blood clot is the most common type of embolus,
all of the risk factors listed above for thrombotic stroke (Virchow Triad) also apply to embolic strokes.

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NOTE: although a blood clot is the most common type of embolus, other types do exist. A few of the
most common are listed below:

 fat (from bone marrow in a broken bone)

 air (from accidental injection)
 cancer cells metastasizing from a distant site
 bacteria (i.e. in bacterial endocarditis)

SYSTEMIC HYPOPROFUSION

In systemic hypoperfusion, blood flow is decreased to all areas of the body. This most commonly occurs
due to failure of the heart to pump blood (such as in a cardiac arrest) or because of loss of blood
through bleeding. Because the reduction in blood flow is global, all parts of the brain are affected,
particularly watershed areas. Watershed areas are those areas of the brain that lie between the
territories of the major arteries. These areas are supplied by the smallest vessels and therefore are most
susceptible to damage if the blood supply is decreased.

HEMORRHAGIC STROKES
Although less common (~15% of strokes), hemorrhagic (or bleeding) strokes can be much more serious.
This is because in addition to the interruption of blood supply to the target tissue, the hemorrhage
(bleed) can also cause increasing intracranial pressure which can physically impinge on brain tissue,
further impairing perfusion of the cerebrum.
There are many causes of cerebral hemorrhage, the most common of which are listed below:
 chronic arterial hypertension
 aneurysm
 vascular malformation (a-v malformation, cavernoma, telangectasias, venous angioma)
 abnormally fragile vessels (amyloid angiopathy, vasculitis, sickle-cell anemia)
 bleeding diatheses (anticoagulants, fibrinolytics, thromocytopenia, leukemia, hemophilia)
 drug use
 head trauma (primary hemorrhagic contusion, shear injury, vascular avulsion)
 hemorrhage into preexisting lesions (primary brain tumors, metastases, granulomas)
 secondary hemorrhage into pre-existing infarct

TIA
DEFINITION

The most common cause of short-term neurological episodes is a transient ischemic attack, or TIA. A
TIA is defined as a neurological deficit lasting less than 24 hours, caused by brain ischemia. In fact, the
more typical duration for a TIA is about 10 minutes; longer deficits probably produce at least some
permanent brain damage.

SYMPTOMS

The symptoms of a TIA depend on the artery being occluded. Carotid TIAs can present
as unilateral weakness, motor or sensory disturbances of the face or upper or lower limb, dysphasia,

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or homonymous hemianopsia. "Amaurosis fugax" refers to transient monocular blindness due to a
carotid TIA involving the territory of the ophthalmic artery. In contrast, vertebrobasilar TIAs present
with bilateral or side alternating weakness, motor and sensory disturbances, as well as varying degrees
of homonymous visual impairment, gait ataxia, diplopia, dysphagia, dysarthria and dizziness. It should
be noted that isolated symptoms of dizziness, dysequilibrium, tinnitus, transient amnesia, and drop
attacks are generally not due to TIA.

CAUSES

The most likely cause of a TIA is the blockage of the cerebral blood vessel by
an embolus or thrombus that then subsequently dissolves, allowing blood flow to resume before
permanent damage occurs (see Stroke Mechanisms). Another possibility is vasospasm leading to
temporary narrowing of the blood vessel lumen.

COURSE

A diagnosis of TIA is usually made after the symptoms have passed. When an ischemic neurological
deficit is only a few minutes old, the likelihood that it will revert to normal within 24 hours and thus be
termed a TIA is 50%. After 2 hours, the probability is only 10%.

Motor Pathways
The descending tracts are the pathways by which motor signals are sent from the brain to lower motor
neurones. The lower motor neurones then directly innervate muscles to produce movement.

The motor tracts can be functionally divided into two major groups:

Pyramidal tracts – These tracts originate in the cerebral cortex, carrying motor fibres to the spinal cord
and brain stem. They are responsible for the voluntary control of the musculature of the body and face.

Extrapyramidal tracts – These tracts originate in the brain stem, carrying motor fibres to the spinal cord.
They are responsible for the involuntary and automatic control of all musculature, such as muscle tone,
balance, posture and locomotion

Pyramidal tracts
There are no synapses within the descending pathways. At the termination of the descending tracts, the
neurones synapse with a lower motor neurone. Thus, all the neurones within the descending motor
system are classed as upper motor neurones. Their cell bodies are found in the cerebral cortex or the
brain stem, with their axons remaining within the CNS.

Upper Lower
Motor Cortex
Motor Motor Muscle
of the brain
Neurone Neurone

Figure 7 : Motor Nervous System, descending tracts are represented in Red color (Upper Motor Neurone).

These pathways are responsible for the voluntary control of the musculature of the body and face.

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Functionally, these tracts can be subdivided into two:

 Corticospinal tracts – supplies the musculature of the body.

 Corticobulbar tracts – supplies the musculature of the head and neck.

Corticospinal Tracts
The corticospinal tracts begin in the cerebral cortex, from which they receive a range of inputs:

 Primary motor cortex

 Premotor cortex
 Supplementary motor area

They also receive nerve fibres from the somatosensory area, which play a role in regulating the activity
of the ascending tracts.

After originating from the cortex, the neurones

converge, and descend through the internal capsule (a
white matter pathway, located between the thalamus
and the basal ganglia). This is clinically important, as the
internal capsule is particularly susceptible to
compression from hemorrhagic bleeds, known as a
‘capsular stroke‘. Such an event could cause a lesion of
the descending tracts. After the internal capsule, the
neurones pass through the crus cerebri of the midbrain,
the pons and into the medulla. In the most inferior
(caudal) part of the medulla, the tract divides into two:

The fibres within the lateral corticospinal tract

decussate (cross over to the other side of the CNS).
They then descend into the spinal cord, terminating in
the ventral horn (at all segmental levels). From the
ventral horn, the lower motor neurones go on to supply the muscles of the body.

The anterior corticospinal tract remains ipsilateral, descending into the spinal cord. They then decussate
and terminate in the ventral horn of the cervical and upper thoracic segmental levels.

Corticobulbar Tracts
The corticobulbar tracts arise from the lateral aspect of the primary
motor cortex. They receive the same inputs as the corticospinal tracts.
The fibres converge and pass through the internal capsule to the
brainstem. The neurones terminate on the motor nuclei of the cranial
nerves. Here, they synapse with lower motor neurones, which carry the
motor signals to the muscles of the face and neck.

Clinically, it is important to understand the organisation of the

corticobulbar fibres. Many of these fibres innervate the motor neurones
bilaterally.

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Extrapyramidal Tracts
The extrapyramidal tracts originate in the brainstem, carrying motor fibres to the spinal cord. They are
responsible for the involuntary and automatic control of all musculature, such as muscle tone, balance,
posture and locomotion. There are four tracts in total. The vestibulospinal and reticulospinal tracts do
not decussate, providing ipsilateral innervation. The rubrospinal and tectospinal tracts do decussate,
and therefore provide contralateral innervation

 Vestibulospinal Tracts
There are two vestibulospinal pathways; medial and lateral. They arise from the vestibular
nuclei, which receive input from the organs of balance. The tracts convey this balance
information to the spinal cord, where it remains ipsilateral. Fibres in this pathway control
balance and posture by innervating the ‘anti-gravity’ muscles (flexors of the arm, and extensors
of the leg), via lower motor neurones.
 Reticulospinal Tracts
The two recticulospinal tracts have differing functions:
1. The medial reticulospinal tract arises from the pons. It facilitates voluntary movements,
and increases muscle tone.
2. The lateral reticulospinal tract arises from the medulla. It inhibits voluntary movements,
and reduces muscle tone.
 Rubrospinal Tracts
The rubrospinal tract originates from the red nucleus, a midbrain structure. As the fibres
emerge, they decussate (cross over to the other side of the CNS), and descend into the spinal
cord. Thus, they have a contralateral innervation. Its exact function is unclear, but it is thought
to play a role in the fine control of hand movements
 Tectospinal Tracts
This pathway begins at the superior colliculus of the midbrain. The superior colliculus is a
structure that receives input from the optic nerves. The neurones then quickly decussate, and
enter the spinal cord. They terminate at the cervical levels of the spinal cord. The tectospinal
tract coordinates movements of the head in relation to vision stimuli.

Clinical Relevance: Upper Motor Neurone Lesion

Upper motor neurone lesions are also known as supranuclear lesions.

Damage to the Corticospinal Tracts: The pyramidal tracts are susceptible to damage, because they
extend almost the whole length of the central nervous system. As mentioned previously, they
particularly vulnerable as they pass through the internal capsule – a common site of cerebrovascular

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accidents (CVA). If there is only a unilateral lesion of the left or right corticospinal tract, symptoms will
appear on the contralateral side of the body.

The cardinal signs of an upper motor neurone lesion are:

1. Hypertonia – an increased muscle tone

2. Hyperreflexia – increased muscle reflexes
3. Clonus – involuntary, rhythmic muscle contractions
4. Babinski sign – extension of the hallux in response to blunt stimulation of the sole of the foot
5. Muscle weakness

Damage to the Corticobulbar Tracts: Due to the bilateral nature of the majority of the corticobulbar
tracts, a unilateral lesion usually results in mild muscle weakness. However, not all the cranial nerves
receive bilateral input, and so there are a few exceptions:

Hypoglossal nerve: a lesion to the upper motor neurones for CN XII will result in spastic paralysis of the
contralateral genioglossus. This will result in the deviation of the tongue to the contralateral side.

Note: this is in contrast to a lower motor neurone lesion, where the tongue deviates towards the
damaged side.

Facial nerve: a lesion to the upper motor neurones for CN VII will result in spastic paralysis of the
muscles in the contralateral lower quadrant of the face.

Damage to the Extrapyramidal Tracts: Extrapyramidal tract lesions are commonly seen in degenerative
diseases, encephalitis and tumours. They result in various types of dyskinesias or disorders of
involuntary movement.

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ANTERIOR CEREBRAL ARTERY

The Anterior Cerebral Artery (ACA) supplies the frontal, pre-

pre-frontal and
supplementary motor cortex, as well as parts of the primary motor and
primary sensory cortex. ACA infarcts are rare because of the collateral
circulation provided by the anterior communicating artery.

Figure 1:: Superficial branch

MOTOR CORTEX SUPPLEMENTAL MOTOR AREA

(Lower Limb) (Dominant Hemisphere)

Controls movement of the contralateral lower Functions with Broca’s area

rea in the initiation of
limb. speech.

SENSORY CORTEX PREFRONTAL CORTEX

(Lower Limb)

Functions in volition, motivation, and planning

Receives sensory input from the contra lateral and organizing of complex behavior
lower limb.
LOCATION OF DEFICIT
INFARCT

Left ACA Right leg upper motor neuron weakness due to damage to motor cortex and right leg cortical
sensory loss due to damage to sensory cortex. Grasp reflex, frontal lobe behavioral abnormalities,
and transcortical aphasia can also be seen if the prefrontal cortex and supplemental motor areas are
involved.

Right ACA Left leg upper motor neuron weakness due to damage to motor cortex and left leg cortical type
sensory loss due to damage to sensory cortex. Grasp reflex, frontal lobe behavioural abnormalities
and left hemineglect can also be seen if the prefrontal cortex and non-dominant
dominant association cortex
are involved.

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MIDDLE CEREBRAL ARTERY
The Middle Cerebral Artery (MCA) is the most common site of stroke. MCA
infarcts occur in two general regions: superficial
divisions and lenticulostriate branches.

Figure 2:: Left Superficial Division

MOTOR CORTEX BROCA'S AREA

Movement of right head, neck, trunk and arm. Expressive speech area.
Integration with other language areas.
SENSORY CORTEX
WERNICKE'S AREA

Sensation from right head, neck, trunk and arm.

Receptive speech area.
Integration with other language areas.

Figure 3: Right Superficial Division

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MOTOR CORTEX SENSORY CORTEX

Movement of left head, neck, trunk and arm. Sensation from left head,, neck, trunk and arm

Figure 1.2: Lenticulo-Striate Branches

Figure 4.1: Lenticulo- Striate Branches

STRIATUM (Caudate and Putamen) INTERNAL CAPSULE (Genu)

Receives cortical inputs relayed to basal ganglia.

Contains descending fibers of the corticobulbar
Functions in direct and indirect pathways for
tract.
initiation and control of movement.
GLOBUS PALLIDUS
INTERNAL CAPSULE (Anterior Limb)

Contains corticopontine and thalamocortical fibers. Site of origin of output from the basal ganglia to
substantia nigra and thalamus.
Functions in direct and indirect pathways for
initiation and control of movement.

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Clinical Syndromes
LOCATION OF
INFARCT DEFICIT

Left MCA Right face and arm upper motor weakness due to damage to motor cortex, expressive
Superficial (Broca’s) aphasia due to damage to Broca’s area. There may also be right face and arm
Division cortical-type
type sensory loss if the infarct involves the sensory cortex. Other deficits
include receptive (Wernicke’s) aphasia due to damage to Wernicke’s area.

Right MCA Left face and arm upper motor weakness due to damage to motor cortex.
Superficial Left hemineglect (variable) due to damage to non-dominant
non dominant association areas. There may also
Division be left face and arm cortical type sensory loss if the infarct involves the sensory cortex.

Left MCA Right pure upper motor hemiparesis due to damage to the basal ganglia (globus pallidus and
Lenticulostriate striatum) and the genu of the
the internal capsule on the left side. Larger infarcts extending to the
Branches cortex may produce cortical deficits such as aphasia.

Right MCA Left pure upper motor hemiparesis due to damage to the basal ganglia (globus pallidus and
Lenticulostriate striatum)
tum) and the genu of the internal capsule on the right side. Larger infarcts extending to
Branches the cortex may produce cortical deficits such as aphasia.

POSTERIOR CEREBRAL ARTERY

The Posterior Cerebral Artery (PCA) supplies the occipital lobe, the inferior part
part of the temporal lobe,
and various deep structures including the thalamus and the posterior limb of the internal capsule.

Figure 5.2 : Superficial Branch

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OCCIPITAL LOBE SPLENIUM OF CORPUS CALLOSUM

Primary and secondary visual areas.

Carries commissural fibers connecting right
Functions in the sensation and interpretation of
and left visual association
visual input.

Thalamus

Figure 6: Deep Branch

Relay center for descending and ascending information.

Functions in integration
integration of cerebral cortex with the rest of the
central nervous system.

CLINICAL SYNDROMES
LOCATION OF DEFICIT
INFARCT

Left PCA Right homonymous hemianopsia due to damage to left visual cortex in the occipital lobe.
Extension to the splenium of the corpus collusom therefore interfering with comunication
between the two visual association areas can cause dyslexia without agraphia. Larger infarcts
involving the internal capsule and thalamus may cause right hemisensory loss and right
hemiparesis due to disruption
disruption of the ascending and descending information passing through
these structures.

Right PCA Left homonymous hemianopsia due to damage to right visual cortex in the occipital lobe. Larger
infarcts involving the internal capsule and thalamus may cause left hemisensory loss and left
hemiparesis due to disruption of the ascending and descending information passing through
these structures.

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