16
Volume 04 Issue 04-2022
The American Journal of Medical Sciences and Pharmaceutical Research
(ISSN
–
2689-1026)
VOLUME
04
I
SSUE
04
Pages:
16-18
SJIF
I
MPACT
FACTOR
(2020:
5.
286
)
(2021:
5.
64
)
(2022:
6.
319
)
OCLC
–
1121105510
METADATA
IF
–
7.569
Publisher:
The USA Journals
ABSTRACT
Traumatic brain injury is a sudden damage to the bones of the skull and brain by various mechanical agents. Diffuse
axonal injury is a type of traumatic brain injury resulting from a closed brain injury. Traumatic brain injury is the leading
cause of death and disability worldwide.
KEYWORDS
Diffuse axonal injury, immunohistochemical reaction, white matter, corpus callosum.
INTRODUCTION
Diffuse axonal injury of the brain is diffuse damage to
the axons and affects the white matter tracts of the
brain. Its development is based on the tension and
rupture of axons (long processes of nerve cells) in the
white matter of the hemispheres and brain stem. This
type of injury is characterized by a long multi-day coma
Research Article
FORENSIC EVALUATION OF DIFFUSE AXONAL INJURY
Submission Date:
April 05, 2022,
Accepted Date:
April 15, 2022,
Published Date:
April 28, 2022 |
Crossref doi:
https://doi.org/10.37547/TAJMSPR/Volume04Issue04-04
Iskandarov Alisher Iskandarovich
MD Professor, Tashkent Pediatric Medical Institute, Uzbekistan
Yakubov Khayot Hamidullaevich
Candidate Of Medical Sciences, Tashkent Pediatric Medical Institute, Uzbekistan
Ismatov Abrorkhon Askarovich
Assistant, Tashkent Pediatric Medical Institute, Uzbekistan
Journal
Website:
https://theamericanjou
rnals.com/index.php/ta
jmspr
Copyright:
Original
content from this work
may be used under the
terms of the creative
commons
attributes
4.0 licence.
17
Volume 04 Issue 04-2022
The American Journal of Medical Sciences and Pharmaceutical Research
(ISSN
–
2689-1026)
VOLUME
04
I
SSUE
04
Pages:
16-18
SJIF
I
MPACT
FACTOR
(2020:
5.
286
)
(2021:
5.
64
)
(2022:
6.
319
)
OCLC
–
1121105510
METADATA
IF
–
7.569
Publisher:
The USA Journals
from the moment of injury. In this case, the following
symptoms are expressed: paresis of the reflex upward
gaze, eye separation along the vertical or horizontal
axis, bilateral depression or loss of pupillary reaction to
light. Gross violations of the frequency and rhythm of
breathing are often observed. At the same time,
changes in muscle tone are extremely diverse, mainly
in the form of diffuse hypotension. Pyramid-
extrapyramidal paralysis of the extremities often
found, asymmetric paresis is characteristic. Vegetative
disorders are prominent: arterial hypertension, high
fever, hyperhidrosis (sweating), hypersalivation
(increased salivation). A distinctive feature of the
clinical course of diffuse axonal damage is the
transition from a prolonged coma to a persistent
vegetative state, the onset of which is evidenced by
spontaneous opening of the eyes or in response to
various stimuli, but there are no signs of tracking, fixing
the gaze, or following at least elementary instructions.
The vegetative state lasts from several days to several
months and is characterized by the appearance of a
new class of neurological signs - symptoms of
functional or anatomical separation of the cerebral
hemispheres and the brain stem.
The largest white matter tract, the corpus callosum, is
particularly vulnerable to diffuse axonal injury. The
fibers of the corpus callosum have high anisotropy and
unidirectional coherence. The study of its damage is
important given the enormous role of this structure in
providing interhemispheric transmission of auditory,
visual, sensory and motor information related to a
variety of cognitive processes. The most common
mechanism involves acceleration and deceleration of
movement, resulting in shear forces in the white
matter tracts of the brain. This leads to microscopic
and gross damage to the axons of the brain at the
junction of gray and white matter. Diffuse axonal injury
usually affects the white matter tracts of the corpus
callosum and brainstem. The axonal parts of neurons
have mechanical destruction of the cytoskeleton,
which leads to proteolysis, edema, and other
microscopic and molecular changes in the structure of
neurons. Comparative analyzes of data from patients
in a coma with severe diffuse axonal damage, the
results of the analysis show that extensive changes in
the structure of the corpus callosum and corticospinal
tracts occur in the first 2–17 days after severe diffuse
brain damage. The most sensitive indicator of pathway
damage is fractional anisotropy. Diffuse axonal injury
leads to axonal degeneration, causing a more
significant decrease in anisotropy from 2–3 weeks after
injury. Thus, primary brain damage, and in particular
diffuse axonal damage, is a trigger for degenerative
changes in axons and myelin sheaths of the white
matter of the brain, leading to their destruction and
atrophy 2–3 months after the injury.
For histological comparison, a set of staining methods
is proposed, which should be used taking into account
the timing of the post-traumatic period. The main ones
are techniques that allow detecting changes in axial
cylinders - silver impregnation according to Bilshovsky
or Glies, myelin sheaths - osmium impregnation
according to Marks to detect early demyelination,
Spielmeier stain to detect late demyelination. If
necessary, examine the bodies of neurocytes - staining
with hematoxylin and eosin, according to Nissl,
microglia
and
astroglia.
Careful
microscopic
examination using neurohistological techniques in full
allows us to determine the morphological substrate of
diffuse axonal damage in the form of many axonal
balls. They were located everywhere in the white
matter of the brain and were direct evidence of
mechanical damage to the axons, because when the
nerve fiber is interrupted, the axoplasm flows out of
the ends of the damaged process and their club-
shaped thickening occurs. After the rupture of the
18
Volume 04 Issue 04-2022
The American Journal of Medical Sciences and Pharmaceutical Research
(ISSN
–
2689-1026)
VOLUME
04
I
SSUE
04
Pages:
16-18
SJIF
I
MPACT
FACTOR
(2020:
5.
286
)
(2021:
5.
64
)
(2022:
6.
319
)
OCLC
–
1121105510
METADATA
IF
–
7.569
Publisher:
The USA Journals
nerve fiber, its distal part undergoes complete
degeneration. This process is referred to as the
Wallerian rebirth. In the area of the axon located
proximal to the site of damage, retrograde changes or
the so-called retrograde degeneration are observed,
which spreads in the central direction towards the cell
div. Histological studies of the brain indicate that
damage to axons in all cases was localized in the
brainstem, corpus callosum, in the area of internal
capsules, even when macroscopic changes were not
found in these structures. In the first days of white
matter lesions, multiple axonal balls were found. Near
them, axons showed signs of initial degeneration, were
uneven, swollen, and perceived color unevenly. Later,
by the end of the 1st week, degenerative changes
spread along the entire length of the damaged axon.
Nerve fibers had a tortuous appearance, varicose
thickenings, fragmented into sections of various
lengths. According to their contours, a large number of
small fat granules of degenerating myelin were
determined. Studies of neurocytes did not reveal
structural changes. During the second week after
injury, in addition to the described changes, signs of
secondary degeneration of the white matter (axons
intact at the time of injury) along the conduction tracts
of the central nervous system near the rupture site
were detected. In places of primary axon breaks, a
moderate macrophage reaction with the formation of
granular balls was determined. When experiencing
trauma, a decrease was observed, and by the end of
the first month, the complete disappearance of axonal
balls. The remains of damaged axons fragmented into
smaller ones and gradually disappeared. Diffuse
proliferation of macrophages was noted, which were
loaded with granules of decaying myelin. At the same
time, the secondary degeneration of nerve fibers along
the conduction tracts became more pronounced.
Depending on the duration of the post-traumatic
period, changes in the bodies of neurocytes were
determined from an “axonal reaction” (“primary
irritation”) to wrinkling, ischemic changes, or severe
illness. Thus, it has been proven that the fact of the
existence of diffuse axonal injury as a special form of
cerebral injury is beyond doubt. These data indicate the
traumatic nature of damage to nerve fibers and
delayed (secondary) damage to neurons. With the
advent of positron emission tomography in clinical
practice, intravital diagnosis of primary axonotomy
became possible, not only in diffuse axonal injury, but
also in other forms of TBI, the genesis of which is
associated with inertial displacement of the brain in the
cranial cavity. It should be noted that the information
obtained fully helps to make a diagnosis in the forensic
evaluation of this condition.
REFERENCES
1.
Adams JH. Brain damage in fatal non-missile
head injury in man. In: Braakman R, ed.
Handbook of Clinical Neurology. Amsterdam,
Netherlands: Elsevier; 1990.
2.
Konovalov A.N., Potapov A.A., Likhterman L.B.
etc. Surgery consequences of traumatic brain
injury. M., 2006
3.
Potapov A.A., Kravchuk A.D., Zakharova N.E.
etc. Traumatic brain injury. 2006
4.
Gentry LR, Godersky JC, Thompson B, Dunn VD.
Prospective
comparative
study
of
intermediate-field MR and CT in the evaluation
of closed head trauma. 1988
