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PUBLISHED DATE: - 30-11-2024
DOI: -
https://doi.org/10.37547/TAJMSPR/Volume06Issue11-06
PAGE NO.: - 35-40
MORPHO-HISTOLOGICAL CHARACTERISTICS
OF CHANGES AFTER BRAIN INJURIES
(LITERATURE REVIEW)
Sh. Kholikov
Phd, Andijan State Medical Institute Assistant, Department Of Medical
Biology And Histology, Uzbekistan
INTRODUCTION
Brain injuries make up 30-40% of all injuries and
cause disability in 25-30% of cases. [15]. More than
90% of those who died were found to be caused by
ischemic damage of the brain during histological
examination(19). The cause of death remains
unexplained in one-third of 70-72% of brain injury
deaths after traumatic brain injury [20]. Clinical
observations
and
computer
tomographic
examinations revealed that 3-25% of patients
develop acute cerebral blood circulation disorders,
that is, secondary cerebral stroke [20,25,26].
In the Russian Federation, the number of deaths
due to injuries ofbrain in second place, accounting
for 15.8%, and this indicator is a ratio of 6:9 among
the working-age population [15].
Traumatic brain injuries are one of the leading
causes of death and the leading cause of disability
in people under the age of 35. In economically
developed countries, the increase in motor
vehicles and the automation of work processes are
leading to an increase in the incidence of traumatic
brain injuries. For example, in the United States,
there are 180 to 250 cases per 100,000 people, and
in Europe, up to 235 cases, of which 1.6 million are
hospitalized, of whom 66,000 die. According to the
World Health Organization, traumatic brain
injuries are predominantly chronic diseases, the
consequences of which are irreversible, require
long-term rehabilitation, and ultimately result in
disability. [18]
Complete general criteria for the correct
assessment of the severity and consequences of
brain damage in patients after head injuries have
not been developed [15].
RESEARCH ARTICLE
Open Access
Abstract
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The most common cause of dislocation syndromes
in head injuries is injuries accompanied by
intracranial hemorrhage. The cause of these
pathological processes in head injuries is a
condition such as damage to the brain stem. As we
know, we study primary and secondary forms of
brain stem injuries separately. Primary changes
include contusions, compression and rupture of
the stem, diffuse axonal injuries, and hemorrhage
into the stem. Secondary changes include damage
to the structure of the stem, compression of the
brain with a hematoma, swelling and congestion of
the brain, pathological changes in blood circulation
and
cerebrospinal
fluid
circulation.
The
occurrence and development of the above changes
result in clinical manifestations associated with
dislocation syndrome [4]. After head injuries,
intracerebral hypertension, systemic hypotension,
cerebral edema, brain compression with focal
hematomas, and the development of pathologies in
small blood vessels (vasospasm) cause ischemic
processes in the brain.
In traumatic brain injuries, the primary
pathological changes in the brain are necrosis and
dystrophy. Histological examination reveals
rupture of axons of the corpus callosum, brain
stem, cerebellar peduncle, internal capsules,
rupture of blood vessels in sections, and the
appearance of hemorrhagic infarction foci in
numerous subcortical formations, less often in the
peduncle [17].
In the late stages, post-traumatic necrosis may
develop.
Histological
examination
reveals
circulatory disorders (white and red infarction
foci,
edematous
effusions,
perivascular
encephalolysis),
inflammatory
processes
(purulent and hemorrhagic effusions), and
compression of adjacent tissues with the resulting
scars [19].
Changes in neural tissue, such as demyelination
and neuronal cell damage, are characteristic
pathological conditions observed after traumatic
brain injury [19].
In traumatic brain injury, signs of secondary
intracranial and extracranial brain injury must
develop for primary brain damage. Intracranial
changes include changes such as brain hematoma
compression,
impaired
hemo-
and
microcirculation, cerebral edema, intracranial
infection, and hydrocephalus. Extracranial changes
include signs such as hypoxemia, arterial
hypotension, anemia, impaired blood-brain
barrier permeability, and impaired neurohumoral
control.
The system that undergoes the main pathogenetic
changes in the acute period of traumatic brain
injury is the dysfunction of the central nervous
system [1,3,9,13]. Pathological conditions such as
contusions, hematomas, dislocations, and brain
contusions cause dysfunction of the central
nervous system [4,16].
Clinical and pathogenetic changes in injuries are
manifested depending on the location of the lesion
and the nature of the central nervous system
damage [5,28]. Depending on the time of the lesion,
the lesion is divided into manifestations of
resistance to changes, and depending on the
changes in the surrounding tissue, inflammation,
edema and secondary hemorrhage. Focal changes
cause various pathological changes depending on
their location. General cerebral symptoms develop
from varying degrees of change in consciousness
to a state of unconsciousness. The development of
cerebral edema begins with a period of “colorful
interval” and progresses to profound impairment
of consciousness [19].
Depending on the mechanism of occurrence and
clinical signs, it is divided into 2 types, namely
epidural and subdural hematomas. As a result of
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these hematomas, compression of the brain stem is
observed. Compression of the brain stem
manifests a set of symptoms of a diencephalic or
mesencephalo-bulbar type [12] (a state of deep
coma, hypo- or atonia, areflexia, divergence of the
eyeballs, cardiorespiratory disorders). Epidural
hematomas gradually increase in size and acquire
a distinctly delimited area, in which case the dura
mater of the spinal cord is in close contact with the
skull [7]. In epidural hematomas, changes in the
central nervous system gradually develop, and
general cerebral symptoms join. After loss of
consciousness, symptoms of pyramidal system
insufficiency develop: anisoreflexia, weakness, or
paralysis [6]. These processes occur on the
opposite side of the hematoma. Dislocation and
compression occur on both sides if the pyramidal
system is involved. Mydriasis and pupillary light
reflex are absent on the side of the hematoma.
Mydriasis may be accompanied by ptosis of the
upper eyelid.
Subdural hematomas are larger than epidural
hematomas. The rapid appearance of the
hematoma can accelerate the “color interval”
period or completely eliminate it [8]. The main
clinical manifestation in this process is
hypertensive syndrome [10]. Hypertensive
syndrome is caused by compression of the motor
center of blood vessels. Bilirubin formed during
hemolysis affects nerve fibers, causing clonic
convulsions. After the process of cerebral edema,
the meninges are affected, causing meningeal signs
[11].
In the acute phase of traumatic brain injury, the
diffusion
of
noradrenaline,
serotonin,
prostaglandin E into the brain and sympathetic
stimulation result in spasm of arteries and
arterioles, resulting in impaired cerebral blood
flow [2].
Experimental studies have shown that products of
erythrocyte hemolysis have a spasmogenic effect.
In animal studies, the introduction of erythrocyte
hemolysis
products
(oxyhemoglobin,
methemoglobin, and mixtures thereof) into the
blood of animals caused vasospasm. [21,22].
The diffusion of hemolysis products into the blood
leads to the release of prostaglandins from
endothelial cells. This process causes the
spasmogenic
effect
of
hemolysis
[22].
Oxyhemoglobin and other products of hemolysis
inhibit endothelin, which relaxes smooth muscle
fibers by providing them with nitric oxide.
Oxyhemoglobin enhances the release of
endothelin, a protein with strong vasoconstrictive
properties, from endothelial cells [24]. As a result,
the distribution of hemoglobin products damages
perivascular nerves and other factors that have a
synergistic effect on vasoconstruction, increases
the hypoxia process, and affects biologically active
substances such as serotonin and potassium [22].
The calcium in the extracellular space contacts the
smooth muscle layer of the blood vessel, causing
the blood vessel to contract. In the study of the
smooth muscle layer of the blood vessels of the
brain, hemolysis products cause an increase in the
amount of calcium in the extracellular space. As a
result, the blood vessel muscle contracts
spastically and dies. As a result of the relaxation of
the smooth muscles, calcium enters the cell. The
removal of calcium from the cell against the
concentration gradient is carried out by the
calcium-sodium antiporter due to the energy of the
transmembrane sodium gradient, which is
supported by the energy resources of the cell. In
injuries, the release of calcium from the cell is
impaired due to energy deficiency [27].
Transcranial Doppler has been studied to show
that an increase in blood flow velocity of 120 cm/s
is pathological, and an increase of 200 cm/s leads
to a cerebral infarction. During vasospasm, the
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ratio of blood flow velocity in the middle cerebral
artery and internal carotid artery changes. This
ratio has been found to exceed the norm. Based on
this indicator, it is possible to compare the
acceleration of flow due to the development of
hyperperfusion with the acceleration of blood flow
due to vasospasm. The following factors can also
affect the blood flow velocity in blood vessels:
increased intracranial pressure, age, existing
stenoses in blood vessels, increased blood
pressure, circulating blood volume, and
hematocrit. Taking these factors into account and
monitoring them in dynamics allows you to avoid
mistakes [23].
CONCLUSION
In summary, the main areas of change after brain
injuries are the basilar artery (a. basilaris) and the
middle cerebral artery (a. cerebri media), where
excessive calcium ion concentration in the smooth
muscle fibers causes spastic contraction of the
vessels, resulting in the death of myocyte cells,
rupture of blood vessels, and bleeding into
surrounding tissues, with the development of
pathological changes such as necrosis and
dystrophy from primary pathological changes.
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