Head (Brain) Injury

[John]

Head (Brain) Injury

Head Injury and Epilepsy

Describe the meninges

Describe the site of formation and passage of cerebrospinal fluid

Describe the determinants of intracranial pressure

Describe the causes of tentorial hemiation of the brain

Define hydrocephalus

Define consciousness and the levels of consciousness

Describe the role of the reticular activating system in consciousness

Describe primary and secondary brain injuries due to trauma

Describe the mechanism of brain damage in coup‑contrecoup injuries

Differentiate between the location, manifestations and morbidity of epidural, subdural and intracerebral haematoma

Describe the different types of traces on an electroencephalogram (EEG)

Explain the difference between seizure activity and epileptic seizure

Name four or more causes of seizures other than epilepsy

Describe the origin of seizure activity in partial and generalised forms of epilepsy

Describe the clinical manifestations of epilepsy

This Session
Skull
CSF
Circulation
Brain stem
Head injury
Assessment

Structure of the Skull
Bones fused
Oopenings allow passage of blood vessels and nerves
Largest opening is the foramen magnum

Production and Circulation of Cerebrospinal Fluid (CSF)

Production from choroid plexus
One in each ventricle

CSF provides buoyancy, protection & chemical stability to Brain

CSF circulates through the subarachnoid spaces and ventricles
CSF is reabsorbed from the arachnoid villi into the Sagittal Sinus

Circulation of the Brain
Arterial supply (arterial pressure)

Venous sinuses and veins

Brain Stem
Respiratory centres
Cardiac centres
Cranial nerves
Reticular activating system

Head Injury Risk
Males, ages 15 to 30 years
Low/median income
Peak - evenings, nights weekends
Alcohol
Causes: 
    motor vehicle accident, falls, assaults,
    sport-related injuries

Injury
Primary injury      -  from the impact
Secondary injury  -  hypoxia, hypercapnia, hypotension (ischemia), intracranial hypertension (high ICP)
Acceleration
Deceleration
Rotational injuries

Injury
Primary Injury
    Direct tissue damage from traumatic mechanism
    (eg. Contusion, tissue shearing, haemorrhage)

Secondary injury
    Occurs minutes to hours after the primary injury
    Ischemia from elevated ICP and/or systemic hypotension
    Metabolic toxins
        the subsequent brain swelling, infection, or cerebral hypoxia.

Open Head Injury

Fractures associated with Open Head Injury
    Depressed
         when bone fragments are embedded  into the brain tissues.
   Comminuted
         splintered or multiple fracture
   Basilar
         CSF leakage from nose and ears
         (i.e. rhinorrhea and otorrhea)
   Most often from bullet or knife wounds

Closed Head Injury

Caused by ‘blunt’ trauma
    Concussion
         Mild Concussion  – cortical dysfunction
         Classic Concussion  – loss consciousness
         No physical evidence
                         -  a momentary interruption of brain function with or

                            without loss of consciousness.

Caused by ‘blunt’ trauma
     Contusion
        Cortical bruise
        Usually due to violent anterior
        posterior displacement
        Contusion at point of contact is “coup”
        Contusion opposite is “contre coup”
            A injury of a part without a break in the skin, characterized

            by swelling, discoloration, and pain.
    Laceration
            An injury in which the skin is torn or its continuity is disrupted.
Acceleration & Deceleration Injuries

A. A focal area of cerebral injury (coup contusion) at the point of impact. The cerebral hemispheres float in the cerebrospinal fluid.

B. Rapid deceleration or less commonly, acceleation, causes the cortex to forcefully impact into the anterior ad middle fossa causing injury to the side of the brain opposite the site of injury

C. the position of a contrecoup contusion is determined by the direction of force and the intracranial anatomy.

Brain Stem Injury

•

Poor prognosis
Immediate dysfunction,
     loss of consciousness,
     pupillary changes,
     posturing,
     cranial nerve deficits,
     changes in vital functions

Diffuse Axonal Injury
Shear damage is microscopic
Common cause of brain damage after Traumatic Brain Injury

Small haemorrhages and associated swelling of brain tissue

How things evolve after a Head Injury
Brain is enclosed
Blood, brain tissue and CSF contribute to ICP
Normal = 10 - 15 mm Hg in lateral ventricles
Brain edema, Brain tumour or bleeding increases ICP

Monroe Kellie Hypothesis
BRAIN      80%
BLOOD     10%
CSF         10%

As ICP increases
Initially compensated by displacement of CSF
ICP increases
    ⇒ cerebral blood flow decreases
    ⇒ tissue hypoxia
    ⇒ decrease in pH and increase in CO2 level
This leads to cerebral vasodilation, oedema & further increases in ICP. This cycle continues
CNS ischaemic response
Ultimately, brain can herniate

Signs & Symptoms of

Increased ICP
LOC change
Pupil change
Motor dysfunction
Headache
Change in Breathing Pattern

Vomiting
Positive Babinski reflex
Blurred vision, diplopia
Seizures
Loss of brain stem reflexes
Cushing reflex

Treatment
Reduce ICP surgically or with mannitol (osmotic diuretic)

Types of Hematoma

Epidural
Subdural
Intracerebral

Epidural Haematoma
Between skull & dura
Usually due to torn middle meningeal artery
Skull usually fractured
Dura slowly separates
Arterial bleed

Intracerebral Haematoma
2/3 ruptured aneurysms
Also caused by penetrating injuries
CSF often contains blood
Rapid progression as arterial bleed
More frequent in older persons and alcoholics

Subdural Haematoma
Between dura and arachnoid
Common in victims of child abuse
Dura attached to skull, pia to Brain
Bridging veins shear
Bleeding is slower than epidural
Absence of blood in CSF doesn’t negate subdural haematoma
Clinically manifest as:
     Acute 

     Chronic

Acute and Chronic Subjural Haematoma

Based on time interval until appearance of symptoms after injury
Acute (within 24 hr)
Subacute (2-10 days)
Chronic (possible weeks)

Acute Subdural Haematoma
Symptoms seen within 24 hours

Progresses rapidly and carry high mortality due to secondary injuries from inc. ICP

Similar symptoms to Epidural haematoma due to ICP

Chronic Subdural Haematoma
Develop weeks after injury
Clot is encapsulated by fibroblasts
Encapsulated cells gradually lyse and the contained fluid develops high osmotic pressure
Draws fluid from surrounding tissue, increasing volume (& ICP)

Chronic Subdural Haematoma
Affects older persons with cerebral atrophy
Minor fall causes subdural haemorrhage 
     often subclinical

Clot liquification over next 2-4 weeks results in a process of clot expansion and development of signs and symptoms of a mass
Effects may resemble brain tumour or stroke
Treatment usually surgical
Most patients make excellent recovery unless elevated ICP leads to secondary injury or herniation

Characterization of TBI
Clinical severity is graded using GCS
     Mild, GCS 13-15 

         normal to lethargic, mildly disoriented
     Moderate, GCS 9-12

         lethargic to obtunded, follows commands with arousal, confused

     Severe, GCS 3-8

         comatose, no eye opening or verbalization. 

         does not follow commands

         motor exam:  ranges from localizing to posturing

Glasgow Coma Scale

Eye Opening Response
Spontaneous--open with blinking at baseline           4 points
To verbal stimuli, command, speech                       3 points
To pain only (not applied face)                              2 points
No response                                                       1point

Verbal Response
Oriented                                                               5 points
Confused conversation, but able to answer questions  4 points
Inappropriate words                                                3 points
Incomprehensible speech                                         2 points

no response                                                           1 point

Motor Response
Obeys commands for movement                               6 points
Purposeful movement to painful stimulus                  5 points
Withdraws in response to pain                                 4 points
Flexion in response to pain (decorticate posturing)      3 points
Extension response in response to pain (decerebrate posturing)  

                                                                           2 points
no response                                                           1 point