Craniocerebral trauma

Skull fractures
Concussion,Contusion Extradural
and subdural haematoma

Department of Neurology, DM
LF UPJŠ Košice 6.12.2018.
 Brain/head injury
• Brain and spinal cord injuries and post-traumatic conditions are a
serious medical and socio-economic problem (permanent
consequences, disability, financial costs, ...)

• Most often in: - Traffic accidents

- Sports
- Occupational accidents

• Craniocerebral injury is damage to the skull, brain, or both, an injury

mechanism
• Craniocerebral injury- splitt into :
open and closed                      
focal and diffuse
primary and secondary
 Brain/head injury - mechanism of
action
• Translating - head collision with second body
• Acceleration - linear or rotary

• The patient may also fall as a result of the disease condition:

– Syncope
– Epileptic seizure
– Intoxication
– Stroke
 Introduction: Craniocerebral Injuries
• Effect of an external force on the skull and the
brain tissue with permanent or transient
impairment of brain functions

1. CLOSED
2. OPEN - impairment of the dura mater integrity
 Skull fractures
• Types: open and closed
• Fracture lines - the most common temporal and skull base area
Skull fractures- Location:
• Skull vault fractures:
– Cracks (fissurae) – linear, partial (affect only lamina interna) and complete
– sharp/fritter and impressive/sqeeze fractures - by a sharp object with a risk of brain damage

• Skull base fractures: serious prognosis !

– Brain base injury, hypothalamus, brain stem and cranial nerves injury
– „Eyeglasses-like“ hematoma
– Processus mastoideus ecchymosis – Battle sign
– Risks/complications:
- neuroinfection (purulent meningitis, brain abscess)
- CSF fistula
- IC hypotension syndrome (CFS)
- n. I and n.II., N.VII. injury
- deafness
Skull fractures - diagnosis
- Clinical physical evaluation- palpation- local pain, edema, or bone decline
- Skull X-ray or brain/skull CT (bone window)
- Liquorrhoea nasalis (CSF leakage through broken meninges)
- Otorrhea
 Skull fractures- therapy
• Linear skull fractures (fissurae calvae)
• Mostly without clinical symptoms and requiring no surgical treatment
• Observation to exclude the development of extracerebral hematoma

• Impressive skull fractures with significant bone dislocation

• surgical repositioning of debris
• under great impression - rupture of the dura and brain contusion
• for skull base fractures - ATB coverage is recommended (risk of
pathogens /bacterias entry from oropharynx and airways – meningitis,
encephalitis, ...)
 1. BRAIN CONCUSSION
(COMMOTIO CEREBRI, MILD TRAUMATIC BRAIN INJURY- MTBI)

• Definition:
• 1. Reversibile global brain function failure (transient lost of synaptic funtion)
- generalised asynapsia, reticular formation dysfunction
- disturbance of consciousness
- revised definition from 2008
• 2. Brain injury caused by external mechanical energy on the head area
associated with a subsequent CNS disorder

• Appearance: 70 – 90 % of all cranio-cerebral injuries

• men are twice as likely to be affected
• the most at risk is the age group 15 – 24 years

• Reasons: traffic accidents and falls

• in which the brains are shuffled back and forth
• Mechanism of mTBI: Sharp acceleration or deceleration of head
movement leads to Diffuse Axonal Injury- DAI = Functional or
structural traumatic damage to the axons of brain white matter,
mainly reticulo-cortical pathways

• Loss of consciousness in mTBI - correlates with axonal damage,

may also have image of qualitative change of consciousness
(disturbance of the outer world perception)
 DAI
• DAI is major cause of prolonged coma after TBI, probably due to
disruption of ascending reticular connections to cortex
• Stretched axons = functional, reversible impairment
• Sheared axons = their ascend. and descendent degeneration,
permanent damage
 MTBI - MILD TRAUMATIC BRAIN INJURY
• always comes suddenly
• duration of symptoms - different (a few seconds to hours)

• Injury mechanism:
– either by moving the head that is stopped by the motionless object or the
impact of the moving object on the head
– direct attack on the head, face, neck, or any part of the body with inertial
force transfer to the brain region
Unconsciousness and retrograde amnesia without the presence and evident
structural brain lesion, which will take off without consequences
 MTBI : Clinical picture
• Neurological evaluation + score of GCS (Glasgow Coma Scale)
• mTBI: GCS 13 – 15 and duration of unconsciousness (if present)
within 30 minutes

• Clinical picture must meet at least one of the following criteria :

• confusion and / or disorientation
• Unconsciousness of up to 30 minutes (may or may not be) - DAI
• Post-traumatic amnesia up to 24 hours (the lost memory of the event)
• Other transient! neurological symptomatology – focal neurological
deficit, convulsion and detected intracranial lesion, not required
neurosurgical intervention
• Areflexia, bradycardia and hypotension, nauzea. Gradually, the patient takes over, is disoriented, can not
make simple commands, confused, behavior changes, slow reactions, incoherent speech, motion
coordination disorder, restlessness, crying (disappear within minutes)
 MTBI - DIAGNOSIS
• History + neurological (without focal symptoms/deficit) +  traumatological investigation
• transient (several hours) may be pyramidal irritation symptoms or tendon jerk hyperreflexia

mTBI - 3 categories by risk:

– 1 ) GCS 15, without serious and with maximum 1 less serious risk factor, after head injury without
brain injury, who can be released without head and brain CT scan for home observation unless
another reason for hospitalization is known
– 2 ) GCS 15 with serious or multiple minor risk factors
– 3 ) GCS 13–14, required brain CT

• Brain CT : usually a negative finding!!!

• Brain MRI : changes in tissue signal (hypersignal) in corpus callosum, subcortical white matter, in the
thalamus and brainstem
 MTBI – DIFFERENTIAL DIAGNOSIS

• Other states of short-term loss of consciousness:

• Epileptic seizure
• Syncope
• Arhytmia
• Intoxication
• Diabetic coma
 MTBI – THERAPY
• 1) In the case of negative brain CT and negative neurological
findings and amnesia up to maximally 60 minutes - patient may
be released

• 2) Indications for patient observation:

– Focal neurological deficit
– GCS < 15 points + prolonged posttraumatic amnesia/ agitation
– Headache of high intensity
– Persisting vomitus
– Liquorrhea with suspected skull base fracture
– Polytrauma
– Koagulaopathy
– Alcohol or drug intoxication
– Suspected non- traumatic damage
 MTBI – THERAPY
• Acute state:
• physical and mental relax until symptoms disappear, followed by gradual
loading
• analgetics (inappropriate non-steroidal anti-inflammatory drugs, ASA-risk of
bleeding higher + opiates - effect on consciousness)

• Prognosis : generally favorable

• spontaneous disappearance of post-mTBI symptoms

• Profylaxy:
• use of helmets (bicycles, motorbikes), education of adults and children about
the brain injury risks and consequences
• adjustment of risk working practices in individual jobs
 POST-CONCUSSION SYNDROME
IN 50% MTBI
• Occurs when trying to start a normal personal and working life after head injury
• Symptoms retreat within a few days or weeks
• Improvement after mTBI – within 3 to 12 months
• 5 -20% - 1 or more symptoms are persistent even one year after the injury
• Somatic and vegetative: headache, dizziness, nausea, vomiting, smell deficit, insomnia, rapid tiredness,
pathological fatigue, visual problems, hypersensitivity to light and noise
• Cognitive: disturbance of attention, memory, slowing of thinking, faults in executive functions, decreased
performance
• Emotional: lability, attention disturbance, depression, anxiety, nervousness, apathy
• Occurenece: either immediately after the concussion or with latency of a few days after
the accident
• Substrate: unknown, 2-12 months, EEG – slight patologic pattern
• Chronic traumatic encephalopathy - Repeated head injuries ! (boxers, epileptic falls,
physically abused persons) can trigger a neurodegenerative cascade - progressive tau-
pathies
2. Contusio cerebri – cerebral contusion
• Definition: focal/multifocal crush of
brain tissue that results from non-
penetrating head trauma
• Structural brain injury/damage

1. Edema/ swelling
2. Bleeding / haematoma
3. Hypoxic-ischemic changes

• Contusion at the point of crush - par coup

• In the opposite direction to the crush side -
par contre coup – these are more serious
and clinically significant
 2. Contusio cerebri – cerebral contusion
• Local or multiplicit (multifocal) cerebral contusions
• On the hemisheral surface: Temporal lobe, Frontal lobe
• In the deep brain structures: Periventricular areas, Basal ganglia
• The degree of brain tissue damage is different: petechial bleeds until extensive lacerations
• Characteristic sign – multifocal lesions!
• Contused tissue = necrosis, edema and bleeds = followed by postmalatic necrosis = healing
by cerebromeningeal scar, +/- uncousciousness, focal neurological deficit
• The first 24-48 hours brain edema is worsening
 2. Cerebral contusion
• Clinical symptoms and disease course: depends on the extent and
location of lesions
• totally asymptomatic ... up to heavy contusions with unconsciousness

• Clinically manifested brain contusion:

• always present disorder of consciousness (qualitative and quantitative) and
focal neurological deficit (hemiparesis, aphasia, agnosia, epileptic seizures)

• qualitative consciousness changes – prefrontal syndrome = behavioral

disturbance, affectivity change, restless, loss of orientation in space, lack of
criticism and deliberation
• sleepiness can be alternated with restlessness, agitation and confusion state
 2. Cerebral contusion
• In the beginning, unconsciousness may be present - usually longer! as in brain
concussion (mTBI) (hours to days)
• an amnesia for head injury is always present

A) lucide interval (short wakefulness) may occur and the development of the focal
symptoms due to perifocal edema continues = again a disturbance of
consciousness arise
B) in many cases the lucide interval is missing = the patient is unconscious from
the beginning

• GCS ≤ 7 = serious state, poor prognosis

• GCS ≥ 9 = better prognosis (the border is GCS = 8 points)
 2. Cerebral contusion - diagnosis
• History + clinical neurological and traumatological
investigation
• Brain CT: hyperdense places of brain crushing, dynamic pattern–
enlargement a few days after injury- unpredictable (surrounding
edema)
• Brain CT should be repeated 24 - 48 hours
• Scars (glial scars), posttraumatic necrosis, pseudocysts

• Patient monitoring /ICU: continual observation and

vital function monitoring, neurological state changes,
vital function correction (BP, heart freq., respiration
parameters, pO2 saturation), X-ray cervical spine,
fundoscopy (optic disc n.II. edema = brain edema)
 2. Cerebral contusion – Therapy and prognosis
• Ensuring vital functions - ventilation and circulatory functions
• positioning of the head and neck - optimal head with an elevation of 30 - 45
degrees
• Therapeutic approach: symptomatic or surgical
• Antiedematous therapy – manitol, anti-convulsants, decubites profylaxy
• Intracranial pressure monitoring – in a case of malign brain edema is
indiated decompressive partial craniectomy
• Fyziotherapy

• Prognosis: different
• depends on the extent of brain damage
• GCS score
• in many cases - sustained focal deficit
cognitive and psychiatric disorders, posttraumatic epilepsy
 Gunshot wound and stab brain
injuries
• Penetrating injuries= gunshot injuries
• Perforating injuries = stab injuries
• are an open type of head injury
• an injury to the skull and the brain by penetrating
subject – e.g. rod, knife, cutting and stab object

• The extent of the brain injury depends on

the kinetic energy of the penetrating
object
 Gunshot wound brain injury
• The range and severity depend on the velocity, caliber and character of the
projectile and the trajectory of the shot (the higher the kinetic energy of the shot,
the greater the destruction of the tissue)
• Usually extensive brain tissue devastation is present
• Gunshot brain injuries - two types
• Perforating gunshot wound – the projectile penetrates the skull and the brain, creates a fire channel
with fragments of bone and flies out of the head
• Penetrating gunshot wound – the projectile penetrates the skull and the brain, but it is trapped
intracranially
• Complications (may be fatal): brain edema, neuroinfection-meningitis,
meningoencephalitis, cerebral abscess
 Gunshot wound brain injury
• Diagnosis:
• Inspection of the entry site /shot
• X-ray, CT scan – skull injury, bone fragments in the fire channel and
locating the projectile (at the aperture) - brain tissue damage, brain
contusion around the fire channel and hematoma

• Therapy: surgical + antibiotics (14 days)

• Prognosis:
• always very severe damage
• total mortality - 90 % (up to 70% of patients die before hospital treatment)
 Stab brain injuries
• sharp object – a stick, needle, knife, sword, fork ... with low speed
• narrow fracture of the skull + puncture channel with bloody brain tissue in the area of ​the
puncture canal and its surroundings
• there is no concentration zone of coagulatting necrosis, nor diffuse brain damage around the
puncture channel
• degree of disability and prognosis depend on the location and depth of penetration

• Prefrontal area – personality changes, relatively good prognosis

• Temporal lobe – risk of injury of important structures- thalamus, brainstem, Willis circle
vessels, cranial nerves - high mortality!
• The penetrating object under the first aid principles is not removed from the wound - the
wedged object creates a tamponade of important vessels
 Stab brain injuries
• Diagnosis
– Brain CT - clarifies the depth and magnitude of brain damage
– CT brain- bone window - useful for indicating skull plastic surgery or
removal of bone fragments, foreign body from brain tissue
– AG brain vessels – suspected vascular posttraumatic complications

• Therapy- perforating brain injuries - surgical

– craniotomy and with the revision of the punch or fire channel
– drainage of bloody brain tissue
– removing available foreign bodies and bone fragments
– maximal carefully review and treatment of the speech and visual cortex!
– antibiotics - an infection profylaxy
 Stab brain injuries
• 35 % - complications : neuroinfections, inflammatory-
type complications, especially if the puncture canal
passes through the paranasal sinuses
– meningoencephalitis
– abscess
– ventriculitis

• 30 % - complications with brain vessels damage

– pseudoaneurysm –up to 50 % of them bleed
during the first week and lead to death in 30-50 %
of cases
– vazospasms
– vessel occlusion
– arterio-venous fistula

• Because of these complications and their high

mortality, it is recommended to perform an AG
-angiographic examination as soon as possible
 Secondary brain injuries

• Primary head injury can cause secondary brain

injury

1.Epidural bleeding
2.Subdural bleeding
3.Intracerebral traumatic bleeding
4.Traumatic subarachnoidal bleeding
 Epidural haematoma
• Arterial bleeding between skull bone and dura mater after
head injury
• Source: most common a. meningea media at the fracture site
(with patietal and temporal bone fractures)
• arterial bleeding (high pressure) does not have tendency to
stop spontaneously
• up to 75% - a skull fissure is present
• supratentorial localisation, rarely infratentorialy (venous sinus)
 Epidural haematoma
• Small hematoma - may be asymptomatic
Larger hematomas - progressive character:

• Typical disease course: initial coma (DAI) – lucid interval (few hours) -
development of rapid progression uncousciousness + focal brain
symptoms/deficit – sy ICH + brain herniation (temporal conus) and
craniocudial deterioration (occipital conus) – death
• Posterior fossa hematoma - occipital conus, respiratory failure
• Syndrome ICH- intracranial hypertension
• Epileptic seizure
Epidural haematoma: diagnosis and
treatment
• History + neurological evaluation
• Skull X ray – fissura, fracture crossing
a.meningea media
• Brain CT: typical convex shape lens-like
hyperdense lesion- hematoma

• Treatment:
• surgery, urgent blood aspiration-
evacuation + revision of affected artery
and dural space
• In most cases life-saving procedure
• progressive expansion of hematoma with
compression of the brain, the risk of brain
cones - does not delay!
• Without therapy- fatal brainstem
compression /brain herniation- temporal
and occipital conus/
 Subdural haematoma
• Traumatic venous bleeding between dura mater and  arachnoidea
• Source: rupture of brain bridging veins (surface veins of the brain in the section
prior to sinus entry) or of the pial vessels
• Most often - frontal and parietal, in 15-20% of cases it is on both sides
• Venous bleeding – low pressure, slow, may stop spontaneously
• size varied - from small cloaks to large
• Occurrence: the most at risk: old people with atrophy of the brain

Classification – disease course:

» acute
» subacute
» chronic
 Acute subdural haematoma
• Focal neurological deficit- similar to epidural hematoma
• the most common type of traumatic intracranial bleeding
• manifests itself within 24-48 hours after injury
• development of focal symptoms from direct hematoma to brain
pressure or brain herniation (coma), may also be associated
with cerebral contusion
• may coincide with the image of epidural hematoma with lucid
interval and focal symptoms, but the dynamics of consciousness
disorder is not so dramatic

• Diagnosis: brain CT - semilunar shape of haematoma

• Therapy:
• Large hematomas- urgent surgery, blood evacuation
• Small hematomas- observation
 Subacute subdural hematoma
• manifests itself within 3 weeks of injury

• more frequent in older age

• dominated progressive consciousness

disorder, headache, dizziness and light palsy/
hemiparesis
 Chronic subdural haematoma
• Slow progressive or persistent symptoms
• Less severe disease course and symptoms
• The onset of several weeks to months after the head injury
• Chronic headache, ICH syndrome, hemiparesis, psychic changes,
apathy, balance disorders, speech disorder (aphasia), epileptic seizures
• Occurrence: chronic alcoholics, people with blood clotting disorder, infants
• In the elderly - even after the banal head injury
• Can be undiagnosed or silent!
• Unrecognized - an image of progressive dementia, incontinence, walking
disorders, and can be mistakenly evaluated as Alzheimer's disease, brain
tumor in the frontal region
• Often slight head injury
• Haematoma- blood/Hb metabolic changes are osmotic active – water,
lesion enlargement = hygroma
• Complications: ICH syndrome, brain herniation
 Chronic subdural haematoma: diagnosis
and therapy
• Diagnosis: History + neurol. evaluation
• Brain CT - typical moon shape hematoma /hyperdensity
• Chronic stage- hypodensity (hygroma)

• Therapy:
• relatively rigid capsula even after evacuation of the hygroma it can be repeatedly filled
with fluid - require open operation with removing of the hematoma sleeve
• Small SH – conservative approach- observation
• Surgery indications:
• hematoma thickness 10-12 mm, taking into account the degree of cerebral atrophy and
the manifestations of hematoma expansion to surrounding structures
• Urgent surgery: posterioir fossa (infratentorial) hematoma- risk of brainstem compression

• Prognosis- depends on hematoma volume and brain compression

• Generally good prognosis
 Intracerebral traumatic bleeding
• Intracerebral traumatic hematoma
• Focal symptoms
• occurs at the time of injury or delay -6 hours apart
• usually with heavy head injuries

• Cause: rupture or vessel wall distention

• Localized on the head injury side, contralateral, or both sides
• Mainly frontal lobe, temporal lobe
• may be combined with bone fracture, subdural hematoma, brain
contusion and diffuse axonal injury

• Clinical picture: focal neurological symptoms

small hematomas - asymptomatic
large hematomas - ICH syndrome, conus of the brain
• Diagnosis: brain CT
 Traumatic subarachnoidal
haemorrhage (SAH)

• Associated with cranial injuries

• Often accompanied by brain contusion
Clinical picture: meningeal syndrome,
ICH sy, hydrocephalus
•
Diagnosis:
CT brain
AG
• CSF - finding a blood in a CSF
 Postraumatic syndromes
1. Brain edema and ICH syndrome
Brain congestion, neuroinfection (meningitis, brain
abscess), likvorhea
2. Epileptic seizures and posttraumatic epilepsy
3. Hydrocephalus
4. Posttraumatic syndrome, irritability, instability,
diziness, sleep problems, emotions, mood, ...
5. Dementia pugilistica
6. Posttraumatic parkinsonism
ICH syndrome
Brain herniation

• Head elevation up to 30o

• Slight hypothermia
• Arterfic. hyperventilation
• Antiedematous th – Manitol,
Kortikoids ?

• Dekompressive surgery
• Hematoma evacuation
• Decompressive craniectomy
 Posttraumatic complications
Hydrocephalus
• slowed CSF reabsorption after brain injury
• communicating normotensive hydrocephalus - cognitive impairment (dementia),
walking disorder and incontinence, DG: Brain CT
Treatment: surgery = temporary or permanent shunt - ventriculoperitoneal drainage
with removal CSF from the ventricle into the peritoneal abdominal cavity

Epileptic seizures
• 5-10% of patients with craniocerebral trauma
• Early post-traumatic epileptic seizures (within 1-2 weeks of injury) – symptomatic
• Late - the development of epilepsy
• brain injury have a 29-fold higher risk of developing epilepsy than a normal population
• Cause: hematomas, contusive lesions, fragments of bone with impression
The greatest risk of late seizures - 0.5-2 years from head injury and <10 GCS
Treatment: anti-convulsants (2 weeks after head / brain injury)