Brain anatomy

Mechanism of injury in head trauma

Directtrauma by compression or
crushing.
Acceleration-Deceleration Injuries
Brain has inertia. For example, when a person falls backwards onto a
hard floor, the back of the persons head hits the floor and stops. The
brain, however, is still moving until it strikes the inside of the skull. If
the brain gets bruised, there is bleeding, also called a hemorrhage.
This bleeding causes further damage to the brain.
The skull does not need to strike an object in order for the brain to get
injured. There are many situations in motor vehicle crashes where the
forces are transmitted through the brain without the skull hitting the
dashboard, windshield, steering wheel or window.
Coup/Contrer-Coup Injuries: Related to acceleration-deceleration injuries
(e.g injury to temporal lobe in contralateral temporal trauma)
 Head Trauma
1-Skull fractures.
2-Extradural ,subdural & subarachinoid.
3-Cerebral contusion& intraventricular Hge.
4-Diffuse Axonal Injury (DAI).
5-Related Brain edema & herniation.
 Skull Fracture
A skull fracture is a break in the skull bone
and generally occurs as a result of direct
impact .
Uncomplicated skull fractures themselves
rarely produce neurologic deficit, but the
associated intracranial injury may have
serious neurologic sequelae.
 Four major types of skull fractures may
occur:
(1) linear,
(2) depressed,
(3) diastatic,
(4) basilar.
Linear skull fractures
Depressed skull fractures

Petr Cech
 Basilar skull fractures
Most basilar fractures
occur at 2 specific
anatomic locations
namely, the temporal
region and the occipital
condylar region.
 Other Types
Ping-pong skull
fractures .

Birth fractures (Caput

succedaneum or
cephalohematoma ).

Growing skull fractures

(leptomeningeal cyst,
traumatic meningocele,
cerebrocranial erosion,
cephalhydrocele,
meningocele, and spuria.
 Epidural Hematoma
An epidural hematoma is usually associated
with a skull fracture. It often occurs when
adirect impact fractures the calvarium .
The fractured bone lacerates a dural artery
(middle meningeal artery) or a venous
sinus.
On CT, the hematoma forms a hyperdense
biconvex mass. It is usually uniformly high
density but may contain hypodense foci due
to active bleeding.
Comment on midline shift .
Natasha Richardson
March 2009
 Subdural Hematoma
Deceleration and acceleration or rotational
forces that tear bridging veins can cause an acute
subdural hematoma so it occurs in cases of wide
subdural space(old age & children)
Causes of subdural are:in minimal trauma in old age,
child abuse and ventricular decompression, may
occur in patients receiving anticoagulants or patients
with a coagulopathy condition.
The blood collects in the space between the
arachnoid matter and the dura matter, Because the
subdural space is not limited by the cranial sutures,
blood can spread along the entire hemisphere and
into the hemispheric fissure, limited only by the
dural reflections .
We have 3 major types :
Acute, subacute & chronic
 Acute Subdural Hematoma
Crescent shaped;
Hyperdense, may contain hypodense foci
due to serum, CSF or active bleeding
 In children, subdural
hematomas occurring
along the posterior
interhemispheric fissure
and the tentorium have
been described as
common findings following
violent nonaccidental
shaking (ie, shaken baby
syndrome) .
 Subacute Subdural Hematoma
Subacute SDH may be difficult to visualize by CT
because as the hemorrhage is reabsorbed it
becomes isodense to normal gray matter. A
subacute SDH should be suspected when you
identify shift of midline structures without an
obvious mass. Giving contrast may help in difficult
cases because the interface between the hematoma
and the adjacent brain usually becomes more
obvious due to enhancement of the dura and
adjacent vascular structures. Some of the notable
characteristics of subacute SDH are:
- Compressed lateral ventricle
& or midline shift
- Effaced sulci .
 Chronic Subdural Hematoma
Chronic SDH becomes
low density as the
hemorrhage is further
reabsorbed. It is
usually uniformly low
density but may be
loculated. Rebleeding
often occurs and
causes mixed density
and fluid levels.
 Subarachnoid Hemorrhage
A subarachnoid hemorrhage occurs with
injury of small arteries or veins on the
surface of the brain. The ruptured vessel
bleeds into the space between the pia and
arachnoid matter. The most common cause
of subarachnoid hemorrhage is trauma .
In the absence of significant trauma, the
most common cause of subarachnoid
hemorrhage is the rupture of a cerebral
aneurysm.
 When traumatic,
subarachnoid hemorrhage
occurs most commonly
over the cerebral
convexities or adjacent to
otherwise injured brain
(i.e. adjacent to a cerebral
contusion)
If there is a large amount
of SAH particularly in the
basilarcisterns,sulci&fissure
s the physician should
consider whether a
ruptured aneurysm led to
the subsequent trauma.
 Cerebral Contusion
Brain contusions commonly are identified in patients with
traumatic brain injury (TBI) .
The second mechanism is related to countercoup acceleration or
deceleration ,which causes the brain to strike the skull. In an
event in which the head is in motion, cortical injury occurs
adjacent to the floor of the anterior or posterior cranial fossa, the
sphenoid wing, the petrous ridge, the convexity of the skull, and
the falx or tentorium. The inferior frontal and temporal lobes are
particularly vulnerable
Cerebral contusions are the most common primary intra-axial
injury. They often occur when the brain impacts an osseous ridge
or a dural fold. The foci of punctate hemorrhage or edema are
located along gyral crests. The following are common locations:
- Temporal lobe - anterior tip, inferior surface, sylvian region
- Frontal lobe - anterior pole, inferior surface
- Dorsolateral midbrain
- Inferior cerebellum
 On CT, cerebral contusion appears as an ill-defined
hypodense area mixed with foci of hemorrhage.
Adjacent subarachnoid hemorrhage is common.
After 24-48 hours, hemorrhagic transformation or
coalescence of petechial hemorrhages into a
rounded hematoma is common
CT scans often demonstrate progression over time in
the size and number of contusions and the amount
of hemorrhage within the contusions
MRI findings typically demonstrate the lesions from
the onset of injury, but many facilities cannot
perform MRI on an emergent basis
On MRI, contusions are isointense to hyperintense
on T1-weighted and hyperintense on T2-weighted
image& The signal intensity is increased in the
affected region on DWIs .
 Diffuse Axonal Injury
Diffuse axonal injury is often referred to as "shear
injury". It is the most common cause of significant
morbidity in CNS trauma. Fifty percent of all primary
intra-axial injuries are diffuse axonal injuries .
When shearing forces occur in areas of greater
density differential, the axons suffer trauma;
this results in edema and in axoplasmic leakage
(which is most severe during the first 2
weeks following injury). The exact location of the
shear-strain injury depends on the plane of rotation
Immediate loss of consciousness is typical of these
injuries .
 The true extent of axonal injury typically is worse than
that visualized using current imaging techniques The CT
of a patient with diffuse axonal injury may be normal
despite the patient's presentation with a profound
neurological deficit .
With CT, diffuse axonal injury may appear as ill-
defined areas of high density or hemorrhage in
characteristic locations.
One or more small intraparenchymal (petechial)
hemorrhages less than 2 cm in diameter,
located in the cerebral hemispheres at the grey
white interface as well as corpus callosum
&brainstem.
One may also observe small focal areas of low
density on CT scans; these correspond to areas of
edema
 Stage I - This involves the parasagittal regions of the
frontal lobes, the periventricular temporal lobes, and,
less likely, the parietal and occipital lobes, internal and
external capsules, and cerebellum.
Stage II - This involves the corpus callosum in addition
to the white-matter areas of stage I. Most commonly,
the posterior body and splenium are involved; however,
the process is believed to advance anteriorly with
increasing severity of disease. Both sides of the corpus
callosum may be involved; however, involvement more
frequently is unilateral and may be hemorrhagic. The
involvement of the corpus callosum carries a poorer
prognosis.
Stage III - This involves the areas associated with stage
II, with the addition of brainstem involvement. A
predilection exists for the superior cerebellar peduncles,
medial lemnisci, and corticospinal tracts .
 Intraventricular Hemorrhage

Traumatic intraventricular
hemorrhage is associated
with diffuse axonal injury,
deep gray matter injury,
and brainstem contusion.
An isolated intraventricular
hemorrhage may be due
to rupture of
subependymal veins .
 Cerebral Edema
Severe brain edema or
a large intracranial
hemorrhage may
cause downward brain
displacement and
coning, which is
usually fatal
 Stroke
Stroke is a clinical term for sudden, focal
neurological deficit
Hemorrhagic strokes ischemic stroke
due to rupture of a caused by blockage of
cerebral blood vessel blood flow in a major
that causes bleeding cerebral blood vessel,
into or around the usually due to a blood
brain . clot .
account for 16% of all account for about 84%
strokes . of all strokes.
 Hemorrhagic Stroke
Hemorrhagic strokes account for 16% of all strokes
Intracerebral hge is Subarachnoid hge, due
the most common, to rupture of a
accounting for 10% of cerebral aneurysm,
all strokes . accounts for 6% of
strokes overall.
Now Dudes tell me what are the reasons of cerebral
hemorrhage!???
1. Hypertensive hemorrhage .
2. Amyloid angiopathy.
3. Ruptured vascular malformation.
4. Coagulopathy(A fluid level within the hematoma) .
5. Hemorrhage into a tumor .
6. Venous infarction.
7. Drug abuse.
 Subarachnoid Hemorrhage
Common aneurysm locations include the
anterior and posterior communicating arteries,
the middle cerebral artery bifurcation and the
tip of the basilar artery.
Subarachnoid hemorrhage typically presents as
the "worst headache of life" for the patient .
 Ischemic stroke
Ischemic strokes are caused by thrombosis, embolism of
thrombosis, hypoperfusion and lacunar infarctions(1%)
A thrombotic stroke An embolic stroke
(53%)occurs when a (30%) occurs when a
blood clot forms in situ detached clot flows
within a cerebral artery into and blocks a
and blocks or reduces cerebral artery
the flow of blood
through the artery
A CT is 58% sensitive
for infarction within the
first 24 hours (Bryan et
al, 1991). MRI is 82%
sensitive. If the patient
is imaged greater than
24 hours after the event,
both CT and MR are
greater than 90%
sensitive.
After a stroke, edema
progresses, and brain
density decreases
proportionately.
Diffuse Hypodensity and Sulcal
Effacement
Hypodensity in greater
than one-third of the
middle cerebral artery
territory is generally
considered to be a
contra-indication to
thrombolytic therapy.
 Hyperdense Vessel Sign
A hyperdense vessel is
defined as a vessel
denser than its
counterpart and
denser than any non-
calcified vessel of
similar size.
This sign indicates
poor outcome and
poor response to IV-
TPA therapy.
 Basilar Thrombosis
Thrombosis of the
basilar artery is a
common finding in
stroke patients. CT
findings include a
dense basilar artery
without contrast
injection.
Lentiform Nucleus Obscuration
 Subacute Infarction
-Increasing mass effect
- Wedge shaped low
density
- Hgic transformation
After 4 - 7 days the CT
- Gyral enhancement
- Persistent mass effect
In 1-8 weeks:
- Mass effect resolves
- Enhancement may
persist
Chronic Infarction
Case 1
 Gunshot injury leading to brain
contusion,localized subarachnoid
hemorrhage & skull fracture at
the site of the bullet entry
Case 2
 Depressed skull
fracture,pneumocephaly
Case 3
Subacute subdural hematoma
Case 4
Chronic subdural hematoma with
fluid fluid level secondary to new
bleeding &mix of recent and old
blood
Case 5
 Intraventricular
hemorrhage,extending from
intracerebral hge
Case 6
 Ischemic cerebral stroke
Hyperdense vessel sign of MCA
Case 8
Chronic cerebral infarction
Case 9
Brain contusion(TBI)