Conf.Dr.

Mohan Dumitru

POSTTRAUMATIC CRANIOCEREBRAL PATHOLOGY

CRANIOCEREBRAL WOUNDS

They are focal primary traumatic effects (open direct craniocerebral

trauma) characterized by a gap between the endocranial space and the
external environment.
The concerned anatomical structures in the craniocerebral wound are:
the scalp (contused, linear, punctiform wounds-according to the nature of
the traumatic agent) + the calvaria (recessed fractures, comminutive
fractures, etc.) + dura mater (direct laceration) + encephalon (direct
laceration).
According to the size and location, the clinical examination of the
craniocerebral wounds can show:
- Focal neurological signs (caused by affected cerebral zones or due to
some associated focal primary effects – intracranial hematomas, etc);
- Signs of meningeal irritation (secondary to subarachnoid hemorrhage
or to the septic element);
- The alteration of consciousness in various degrees.
The craniocerebral wound diagnosis is determined based on:
- Local clinical exam – most of the time it is enough for craniocerebral
wounds; one can notice a wound of the scalp of different shapes and
sizes, with bone splinters and lacerated brain;
- Cranium radiography in standard incidences – gives details on the
extension of the cranium fracture, splinter elements, their intrusion or
extrusion degree;
- Cerebral CT-scan – gives details about extension of the lesion, the
presence of associated lesions (contusion, intracerebral hematoma,
laceration, etc.).
The main wound types caused by fire arms are:
- Tangent craniocerebral wounds in case of high speed projectiles,
which due to their tangent trajectory, the dura mater can be
dilacerated and the subjacent brain suffers a contusion.
- The most frequent wounds are the blind craniocerebral penetrating
wounds, characterized only one orifice (the penetration orifice of the
traumatic agent) resulting in a orifice-like cranial fracture with
canalicular cerebral laceration.

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 - Transfixant craniocerebral wounds caused by high speed projectiles
result in an orifice-like fracture at the place of impact and a extrusive
fracture exiting the cranium, and the lacerations tract is canalicular
progressively growing from the place of penetration to that of the
exit.
- Ricochet craniocerebral wounds are rare, the projectile strikes the
cranium at a certain angle, it does not have enough penetration
power and thus it causes a unleveled shrapnel (splinter) cranial
wound on the impact spot.
Clinically one observes development of the level of consciousness
into coma and neurological syndrome of location. Most frequently a
intraparenchymal hematoma appears in the area of the cerebral laceration.
The craniocerebral wound is considered a neurosurgical
emergency.
Treatment. In case of craniocerebral wounds the treatment is as
follows:
- Removal of the bone splinter and the lacerated brain;
- Smoothening of the calvaria fracture edges down to the normal dura
mater;
- Suture of the dural edges if possible, if not duraplasty with wide
fascia or artificial dura, firm suture of the scalp wound in 2 layers.
The surgical treatment must be completed with pre and postoperative
antibiotherapy. The anticonvulsive medication (carbamazepine, phenytoin) is
mandatory.

CRANIAL FRACTURES

Cranial fractures are primary posttraumatic effects frequently

associated to craniocerebral trauma. They can be classified according to the
suprajacent tegument integrity in closed fractures (the teguments being
intact) or open fractures (the suprajacent scalp is wounded).
The anatomical location of the fracture spot classifies the fractures
into two categories: skullcap fractures and base of the cranium fractures.
According to the type of wound the fractures are classified as:
- Linear fractures;
- Diastatic fractures;
- Dehiscent fractures;
- Unleveled fractures;
- Comminutive fractures.

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 The linear fracture is associated to both side of the skull (unlike the
fissure that only affect one side of the skull). Linear fractures can be single
or multiple and are located in various places (frontal, temporal, parietal,
frontotemporal, etc).
The diastatic fractures occur at the level of the cranial sutures
determining the separation (disjunction) of the two. It can occur at any age
but it is more frequent in children.
The dehiscent fractures refer to those that have from several
millimeters up to 1cm gap between the bone edges of the fracture.
The unleveled fractures refer to displacement of one the edges (or
splinters) of the fracture over a distance at least equal to the thickness of the
skullcap at the level of the impact. Unleveled fractures can be extrusive or
intrusive. In case of extrusive unleveled fracture the bone fragments are
projected over the skullcap. Whilst in the case of the intrusive unleveled
fracture the bone fragments are projected under the skullcap. The unleveled
fracture is often called depressed fracture.
The comminutive fractures of the skullcap refer to 2 or several linear
tracts intersecting. These linear fractures radiate from the impact spot of the
traumatic agent.

CEREBROSPINAL FLUID FISTULA

A CSF fistula refers to a traumatic lesion resulted from a

communication between the subarachnoid spaces and the external
environment. The lesions affects a cranial component (bone defect) and a
meningeal component (dura mater and arachnoid defect).
According to the location and means of leaking of the CSF there are
several types of CSF fistulas, the main being:
- rhinorrhoea refers to CSF leak through one or both of the nostrils,
most frequently the lesion being located on the level of the cibriform
plate of the ethmoid bone;
- otorrhoea refers to CSF leak through one or both of the auditory
canals, the lesion being in the petrous portion of the temporal bone;
- oral cavity CSF leak ororrhoea refers to the CSF leak through the
mouth and occurs in dehiscent fractures of the base of the skull;
- craniocerebral wound CSF leaks.
Clinically the ear, nose or mouth CSF leak is the pathognomonic sign.
Quantity-wise the leak may be:
- continuous and abundant CSF leak in case of severe CCT which
require surgical intervention to prevent a purulent meningitis,
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 - minor and intermittent CSF leak in case of a craniodural fracture
only; requires surgical intervention as well,
- CSF leak that occurs in the same time as the trauma; it is minor and
it lasts for a few days, then it stops.
The treatment of CSF fistulas or leaks has a triple objective:
suppressing the liquid leak, preventing secondary meningoencephalitis and
treatment of the main meningoencephalitis. Conservative treatment refers to
drainage of the CSF, antibiotherapy and administering macromolecular
solutions. The surgical treatment closes off the CSF fistula by closing the
traumatic dural injury.

CEREBRAL CONCUSSION

It is a primary posttraumatic diffuse effect. It refers to sudden and

reversible changes in the patient’s general condition usually with headaches,
dizziness, vertigo, amnesia and loss of consciousness which can last from
several minutes to 6 hours. It does not have a cerebral anatomical lesional
layer, the phenomenon occurring due to some functional disorder, that a
sudden depolarization of the neuron membrane of the reticular formation of
the brain stem.
The clinical aspect of the cerebral concussion is characterized by
confusions, disorientation, amnesia (retrograde, anterograde) and loss of
consciousness.
The diagnosis of the cerebral concussion is exclusively clinical. Up to
now there are no means of investigation (image or other) that can record the
modifications that occur in cerebral concussion.
The correct medical behavior towards the cerebral concussion patients
(which represent most of the CCT patients) is usually the following:
- For minor cases, with no loss of consciousness, a normal
neurological exam and normal cranium radiography, the patients do
not require hospitalization and the medication is symptomatic;
- For patients with a history of posttraumatic amnesia, loss of
consciousness and a normal neurological examination it is
recommended supervision of the patients for a few days in a
neurosurgical ward. The treatment should be analgesics and
sedatives.

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 CEREBRAL CONTUSION

It is a primary posttraumatic effect with direct implication of the

encephalon.
Etiopathogeny. Cerebral contusion can be caused by any type of CCT.
The traumatic lesional effect is caused by a direct vascular disorder or
distance vasomotor reflexes that create various degrees of extravasation of
the vascular matter in the parenchyma which lead to hypoxia and
hemorrhagic lesions. Anatomopathologically, the cerebral contusion lesion is
composed of hemorrhagic foci, lacerated cerebral parenchyma, tissue
necroses and perilesional edema.
The clinical forms of cerebral contusion:
- Minor cerebral contusion – alteration of the level of consciousness,
lasting from a few minutes to 1 hour with or without minor
neurological signs, with remissive character.
- Moderate cerebral contusion may be diffuse or may be predominant
on one cerebral hemisphere. The abolishing of the state of
consciousness takes several hours and it has accompanying
neurological signs (balance disorders, motor deficit) and other
symptoms like headache and vomiting followed by partial or total
remission.
- Severe cerebral contusion has as its main clinical manifestation a
state of coma of various degrees which may last for several days or
even weeks and is associated with focal neurological
symptomatology.
- contrecoup contusion – occurs on the opposite side of the impact
spot, being caused by the shock waves generated by a direct
deceleration mechanisms.
Paraclinical investigations.
The CT-scan can determine the impact lesion, degree of contusion and
the association with other traumatic lesions. On the Ct-scan the contusion
focus looks like a hyperdense area circumscribed by a hypodense area
represented by perilesional vasogenic edema.
Cerebral contusion treatment is the treatment of the clinical context to
which the trauma belongs, that is minor, moderate or severe. In minor and
moderate cerebral contusion the treatment is symptomatic – antiedemic,
antiemetic, antithermic, sedative and anticonvulsivant. The severe cerebral
contusion requires a complex medical treatment in the intensive care unit,
with vital functions monitoring. The surgical treatment is only indicated for

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severe contusion of large dimensions which causes intracranial hypertension
that show up on the CT-scan.

CEREBRAL LACERATION

Cerebral laceration is a destructive lesion which refers to the lack of

continuity on the surface of the cerebral parenchyma. The lesional focus
affects the cortex and the subjacent white matter and it is composed of a
mixture of cerebral parenchyma that has several tissue necrosis zones,
hemorrhagic foci and edema.
There are 2 types of cerebral laceration: direct and indirect.
Direct cerebral laceration is a destructive lesion of the parenchyma
determined by the penetration of: a foreign body (bullet, splinter) or bone
splinters from the internal skullcap which have sunk into the cortex.
Indirect cerebral laceration is the result of the shift of the cerebral
mass towards the endocranial or dural surface. Through this mechanism the
accelerated motion of the brain causes it to suddenly stop when reaching the
hard surface; the brain does not simultaneously stop and it continues its
kinetic inertia of acceleration for a fraction of time and thus the brain is
thrown on the craniodural structures leading to its laceration.
Clinically the general condition of the patient can be drastically
altered. The level of consciousness is frequently modified (confusion,
obnubilation, agitation, drowsiness). According to the affected cerebral area
there may occur focal neurological deficits. The meningeal irritation
syndrome may also occur frequently.
There may be signs of brain stem injury: decerebration rigidity, uni or
bilateral mydriasis, disorders of the vegetative functions.
The diagnosis may be done by CT-scanning. The CT-scan shows a
intraaxial lesion with mixed density – hyperdense areas inlayed with
hypodense areas.
Treatment is complex, both medical and surgical.
Direct cerebral laceration requires immediate neurosurgical
intervention.
Indirect cerebral lacerations of small and medium sizes are usually
treated symptomatically, since there is a possibility of slow resorption of the
laceration focus.
In case of cerebral lacerations that show signs of intracranial
hipertension on the CT-scan require neurosurgical intervention.

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 EXTRADURAL HEMATOMA (EDH)

Epidural/extradural hematoma is a circumscribed blood collection

which develops between the endocranium and the dura mater, its etiology is
usually traumatic having a compressive effect over the encephalon.
Etiology is traumatic and the sources of the bleeding are: arterial
(middle meningeal artery) and venous (superior longitudinal sinus, lateral
sinuses). The topography may be: typical in the temporal fossa (Gerard-
Marchand area) or atypical affecting any region of the cranium even the
posterior fossa. The cerebral infliction is caused by the compressive effect of
the hematoma on the brain. The volume of a hematoma varies from 50-150
ml, sometimes even above 200 ml.
The clinical aspect (tableau) of the EDH has 3 stages:
- loss of consciousness - posttraumatic;
- the patient is gaining back his consciousness;
- period of aggravation – sudden alteration of the level of
consciousness. Focal neurological signs (speaking disorders,
hemiparesis) and signs of intracranial hypertension; it is very
quick.
Paraclinical investigations. The CT-scan shows the area, the type and
the volume of the hematoma as well as the shifting of the ventricular system.

In the CT-scan the hematoma appears as a hyperdense collection under the

form of a biconvex lens. The cerebral angiography indicates the area and
even the nature of the extraaxial lesion by revealing the aspect of ‘vascular
void’.
Clinical forms.
- Over-acute – occurs after a CCT that causes epidural arterial
hemorrhage by rupturing the base of the middle meningeal artery,
the neurological evolution and the level of consciousness
deteriorate rapidly and in almost 100% of the cases it leads to
death;
- Acute – occurs after a CCT that causes arterial hemorrhage of one
of the meningeal branches and it is the most frequent form;
- Subacute – it has 2 stages clinically: loss of consciousness –
regaining of consciousness with minimal symptomatology then the
neurological state worsens and the coma progressively sets in;
- Chronic – clinically it takes more time and it refers to losing
consciousness and regaining it in about 7 to 21 days then the state

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 patients condition progressively worsens, slowly leading to the
setting in of the coma.
The treatment of the EDH is in most cases surgical especially when
there is a GCS < 8 with focal neurological signs, uni or bilateral mydriasis
and shift of the anatomical structures of the medial line > 5 mm. EDH is
considered a neurosurgical emergency. The surgical intervention consists of
craniotomy focused on the area of the hematoma, ablation of the hematoma
and the hemostasis of the source of bleeding.

SUBDURAL HEMATOMA (SDH)

The subdural hematoma is a blood collection of traumatic etiology

that develops between the dura mater and the arachnoid, having a
compressive effect on the encephalon. It is usually unilateral having a
tendency to spread all over the cerebral hemisphere.
Subdural hematomas are classified according to the age of the blood
collection:
- Acute - occurs in day1-3 from the CCT;
- Subacute - (day 3-21) has a thin parietal membrane;
- Chronic - (after day 21) has visceral and parietal membranes, they
are perfectly anatomically delimited.
Acute and subacute SDH
The acute and subacute SDH always occurs posttraumatically,
subsequent to moderate or severe CCTs and cause lesions of the laceration
or contusion type.
The pathology of these blood collection that occur in the subarachnoid
space may be explained by the direct rupture of the contusioned cortical
vessels; in case of arterial sources the SDH occurs suddenly, hence the acute
clinical forms, whilst in the case of venous sources the SDH has a slow
evolution hence the subacute clinical forms.
Morphopathology. The acute SDH contains fluid blood mixed with
blood clogs. In the acute cases these blood collections are not perfectly
delimited, whilst the subacute forms are layered with fibrin and sometimes
even a very thin internal membrane.
The clinical aspect depends on the clinical form of the blood
overflow:
The acute SDH sets in and leads to coma immediately after the CCT
with major neurological signs of location. The source of the hemorrhage
represents the rupture of the cortical arteries affected by the laceration focus,
usually frontotemporal.
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 The subacute SDM results in a superficial posttraumatic coma with
discrete neurological signs of location. The source of the hemorrhage
represented in these cases is represented by the frontotemporal cerebral
contusion causing causes a subdural blood extravasation which grows
slowly and progressively with a compressive effect over the cerebral
parenchyma.
Paraclinical investigations. The cerebral CT-scan give information
regarding the location, volume, type and age of the blood overflow. In case
of acute SDH the blood collections appears hyperdense, hemispheric in the
shape of a half moon, whilst in the case of subacute SDH the blood
collection appears isodense, thus it is hard to distinguish from the brain. The
cerebral angiogram reveals the existence of SDH marked by concave-convex
vascular void with maximum frontotemporal width.
The surgical treatment of the acute and subacute SDH must be applied
only after the stabilization of the vital functions of the patient, having as a
result the removal of the hematoma by craniotomy or craniectomy and
hemostasis of the sources of the bleeding.
Chronic SDH
The chronic SDH is a hemolysed blood collection which usually
occurs in seniors as a result of a mild CCT.
The chronic SDH are caused by the rupture of the corticodural veins
which go from the cerebral cortex to the superior longitudinal sinus, passing
through the subarachnoid space, with a fixed end on the dura mater and a
mobile cerebral end. This overflow may be uni or bilateral.
Morphopathology. The chronic is covered by a capsule with parietal
and visceral membranes. The parietal membrane (external) is fibrous , thick
(1-3mm), vascularized. The visceral membrane (internal) is conjunctive,
thin, completely avascular.
The clinical aspect may be considered typical: after a mild CCT
(sometimes with no loss of consciousness), the patient has a perfectly lucid
time span of 3-12 weeks. In this interval there may be signs like: intermittent
headache, vertigo, rare vomiting. After this time span the focal neurological
syndrome (contralateral faciobranchial paresis) and the intracranial
hypertension syndrome (headache, vomiting, papilar edema) settle in
gradually and slowly. Gradually contralateral and then ipsilateral settles in, t
and so do drowsiness, temporal and space disorientation and gatisms.
Paraclinical investigations. Cerebral CT-scan indicates a hypodense
collection located unilaterally or bilaterally on the whole of the cerebral
convexity. The angiogram indicates vascular void.

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 The treatment is surgical having spectacular outcomes. The extraction
of the hematoma is done by making a loose trepan hole, cleaning the cavity
with normal saline solution and external drainage for 24-48 hours after the
intervention.
INTRAPARENCHYMAL HEMATOMA (IPH)

The posttraumatic IPH is a circumscribed and well delimited blood

collection which develops in the cerebral matter as a result of a focal
contusion or cerebral laceration. It is expansive process with progressive
evolution and compressive effect. Usually it is located in the area of the
sphenoid wing at the level of the temporal and frontal lobe.
Pathogeny. There are 2 types: pure hematoma, in which the blood
collection develops from a slightly traumatically injured cerebral
parenchyma, and the secondary traumatic hematoma which develops in the
cerebral tissue with primary traumatic lesions (contusion).
Symptomatology refers to a major neurological deficit (motor deficit,
hemianopsia) with changes of the level of consciousness, which varies
according to the intensity of the hemorrhage (venous, arterial) and according
to the location of the hematoma.
Paraclinical investigations. CT-scan shows a homogenous hyperdense
and intraparenchymal collection, circumscribed by perilesional edema. Thus
one can estimate the type, location and volume of the intraparenchymal
hematoma.
The treatment is surgical in case of IPH of large size with a mass-
effect. One purpose is to reduce the compressive effect and the other to
perform hemostasis. In diffuse, non-compressive cases the surgical
intervention is postponed as the patient is monitored clinically and
undergoes repeated CT-scan examinations. In these cases the IPH may
gradually dissolve.

HYGROMA OF THE DURA MATER

Hygroma is a fluid collection that is intracranial, traumatic and

circumscribed, located in the subdural space which can be delimited by a
new membrane having a content of xanthochromic liquid (hygroma), or
without a membrane having a clear liquid content (hydroma).
Etiopathogeny. The occurs of the hygroma is conditioned the presence
of a small arachnoid laceration which acts as a valve that allows leaks of
small quantities of CSF to accumulate in the subdural space..

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 The clinical aspects evolves by focal neurological phenomena with
changes in the level of consciousness, intracranial hypertension and psychic
phenomena.
Paraclinical investigations. The CT-scan shows a extraaxial hypodense
collection, speared all over the area of the cerebral convexity in the shape of
a half moon, with a moderate compressive effect. Most frequently its
location is bifrontal or unilateral hemispheric.
Treatment is applied according to the clinical symptomatology. In
asymptomatic case where the CT-scan shows no shift of the structures on the
medial line, the treatment will be conservatory: diuretics, corticotherapy,
clinical monitoring and CT-scan. If the patient shows focal neurological
signs or intracranial hypertension, and on the CT-scan image appears a shift
of the medal line the surgical treatment is required. The surgical
intervention is similar to that of the subdural hematoma.

CEREBRAL EDEMA

The term cerebral edema (Gr. Oidema = swelling) refers to a abnormal

accumulation of liquid in the cerebral parenchyma, leading to its increase in
volume. According to the pathogenic mechanism there are several types of
cerebral edema: vasogenic, cytotoxic, hydrostatic, interstitial, osmotic, etc.
The vasogenic cerebral edema (traumatic, tumorous, inflammatory)
occurs when the vascular wall is modified and the hematoencephalic barrier
(blood-brain barrier) is affected followed by accumulation of water, proteins
and sodium (Na+) in the interstitial space. Corticotherapy (Dexamethasone
like products) diminishes the vasogenic cerebral edema more efficiently by
lowering the vascular permeability. It is specific to cerebral tumors and
cerebral abscesses but it also occurs in focal lesion trauma like cerebral
contusion, traumatic intracerebral hematomas, cerebral lacerations.
The cytotoxic cerebral edema (anoxic, hypercapnic, from some
intoxications) is intracellular, the affected cell being is usually the astrocyte.
It is considered to be of a metabolic cause whilst the hematoencephalic
barrier is normal. The cytotoxic edema occurs due to hypoxia/ischemia
which causes a negative energetic metabolism that makes the neurolemma
permeable. It occurs often in severe traumas due to the frequency of the
ischemic disorders in these situations.
The morphopathology of the cerebral edema is just one of the aspects
of an extremely complex process which implies a series of biochemical,
histochemical, biophysical (permeability of the blood-brain barrier and of
cellular membrane) factors.
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 In the initial stage, contusion lesions affect the permeability of the
vascular wall causing vasodilation, which can develop into vasoparalysis.
The major and global macroscopic modification is the increase in volume of
the brain, flattening the cerebral gyrus. Microscopically, the cerebral edema
can be: generalized, predominant on one hemisphere or circumscribed.
The clinic of the edema depends on whether it is diffuse or
circumscribed:
- Intracranial hypertension is predominant in the diffuse cerebral
edema,
- In the circumscribed cerebral edema the symptomatology is
dominated by focal neurological signs.
Paraclinical investigations. The diagnosis of the cerebral edema is
done by CT-scan where one can see: total flattening of the cerebral gyri,
shrinking or obliteration of the lateral ventricles and the third ventricle,
obliteration of the perimesencephalic cistern. Another precise and usual
method is that of monitoring the intracranial pressure.
The fallowing measure must be taken in the treatment of cerebral
edema, especially in severe trauma cases:
- hyperventilation – reduces intracranial hypertension by
vasoconstriction and reduces the cerebral blood flow.
- Dehydration using solution like Mannitol 20% (hyperosmolar
solution), Furosemide (diuretic), etc.
- corticotherapy, Cortizone like solution, Dexamethasone.
- Intracranial pressure monitoring – according to its level, the CSF
volume is reduced to normal values of the intracranial pressure.
- Decompressive bone flaps – surgical technique used in some cases; it
refers to massive frontotemporal craniectomy, unilateral or bilateral;
located as close as possible to the temporal-base area and the
opening of the subjacent dura mater; thus a large cranial space is
created leading to a sudden drop in intracranial pressure.

INTRACRANIAL HYPERTENSION

Intracranial hypertension is a secondary posttraumatic effect caused

by the increase in the volume of the intracranial mass.
Intracranial hypertension occurs when the intracranial pressure value
exceeds 20 mmHg. The ICH is caused by: cerebral edema, (place)
substitution processes (traumatic or tumorous), hydrocephalon, systematic
arterial hypertension, venous sinuses thrombosis, etc.
The content of the cephalic extremity is comprised of 3 elements:
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 - Cerebral parenchyma – approximately 1500 ml in normal adults;
- CSF – 75ml at the level of the ventricular system and the
subarachnoid spaces in normal adults (the total quantity of the
CSF n the cerebrospinal space is of 150 ml);
- Blood content – the blood from the cerebral arteries and veins.
Considering the fact that the cranial cavity is inextensible, the
intracranial pressure stays constant as long as the sum of the 3 elements stay
constant ( Monro-Kellie rule).
The effects of ICH over the cerebral parenchyma are classified as
mechanical effect and vascular effects.
The mechanical effects of the ICH refer to cerebral herniations caused
by the intracranial expansive processes.
There are 2 systems that help maintain the intracranial pressure within
normal values: the volume of the CSF and the cerebral blood volume. In the
first stage of the increase of intracranial pressure, the first compensatory
mechanisms occurs: the CSF is pushed to the level of the spinal
subarachnoid space. If this mechanisms is exceeded, in the second stage the
cerebral blood volume is shrunken by evacuating the venous blood. The
continuous increase of intracranial pressure will lead to pushing of the
cerebral mass through natural orifices resulting in cerebral herniations:
subfalcin herniation, superior tentorial herniation, central tentorial
herniation, inferior tentorial herniation, foramen magnum herniation.
Vascular effects of the ICH are cerebral ischemia, which occurs due to
a cerebral perfusion pressure drop.
The clinical aspect of the intracranial hypertension: in the
compensatory stage - headache (especially in the morning), nausea, vomiting
(which lowers the intensity of the headaches); in the uncompensatory stage –
when the compensatory mechanisms are exceeded coma, decerebration,
respiratory and circulatory disorders settle in and may have neurologic signs
(shift of part of the brain mass through a natural orifice).
Diagnosis. The main noninvasive method that offers information
regarding intracranial pressure in case of craniocerebral trauma is the CT-
scan.
Another more precise method of investigation of the ICP is invasive
and can be done in 2 manners:
- By using a system of catheters, the intracranial cavity is connected
to an external system of monitoring the intracranial pressure,
through a fluid column (CSF);
- By using electronic monitoring equipment or fiber optic catheters.

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 The treatment for intracranial hypertension can be medical or surgical.
Medical treatment consists of: lifting the head at a 30 degree angle from the
level of the bed to favor the cerebral venous drainage, therapy with Mannitol
20% and Furosemide, hyperventilation, inducing pharmacologic paralysis,
avoiding hypoxia.
When can be applied, the surgical treatment removes the
posttraumatic intracranial expansive process. In extreme situations where the
conservatory treatment does not work, unilateral or bilateral
frontotemporoparietal craniectomy is required.

TRAUMATIC SUBARACHNOID HEMORRHAGE (TSH)

It refers to the presence of blood between the arachnoid membrane

and the pia mater. It occurs in most cases of moderate and severe CCT
usually having a negative prognosis.
Most frequently it occurs due to a posttraumatic effect by rupturing
the blood vessels at the level of the subarachnoid space, caused by the shear
forces of the trauma or the rupture of the pia mater by the laceration focus ,
blood leaking into the subarachnoid space.
Clinically TSH is characterized by: headaches, nausea, dizziness,
vomiting, changes in the level of consciousness, neck stiffness; these usually
occur in patients with a CCT history.
Diagnosis. The CT-scan shows the subarachnoid bleeding as a
hyperdense area located at the level of the sulci on the cerebral convexities,
cerebral cisterns, falx cerebri and the free edges of the tentorial incisures.
The treatment of the TSH is conservatory: bed rest, hemostatic
medication, anthalgics, sedatives and moderate dehydration.

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