1. Dr. Parag P Moon
Senior resident
Dept Of Neurology

2. Definition of TBI
 “An insult to the brain, not of degenerative or
congenital nature caused by an external physical force
that may produce a diminished or altered state of
consciousness, which results in an impairment of
cognitive abilities or physical functioning. It can also
result in the disturbance of behavioral or emotional
functioning.”

3. Pathophysiology of
Head Injury
 Mechanism of Injury
 Blunt Injury
 Motor vehicle collisions
 Assaults
 Falls
 Penetrating Injury
 Gunshot wounds
 Stabbing
 Explosions

4. Head Injury-Pathophysiology
 Primary injury
 Irreversible cellular injury as a direct result of the injury
 Prevent the event
 Secondary injury
 Damage to cells that are not initially injured
 Occurs hours to weeks after injury
 Prevent hypoxia and ischemia

5.  Primary mechanical injury to axons and blood vessels
results from rotational and translational accelerations.
 Rotational acceleration causes diffuse shearing/stretch
of axonal and vascular cell membranes, increasing
their permeability (“mechanoporation”)

6.  Intracellular calcium influx triggers proteolysis,
breakdown of the cytoskeleton, and interruption of
axonal transport
 Accumulation of b amyloid precursor protein, the
formation of axonal bulbs (retraction balls), secondary
axotomy, and an inflammatory response.

8. Two types of brain injury occur
 Closed brain injury
 Open brain injury

9. Closed Head Injury
 Resulting from falls, motor vehicle crashes, etc.
 Focal damage and diffuse damage to axons
 Effects tend to be broad (diffuse)
 No penetration to the skull

10. Open Head Injury
 Results from bullet wounds, etc.
 Largely focal damage
 Penetration of the skull
 Effects can be serious

11. Cerebral Contusion
Most common Focal brain
Injury
Sites  Impact site/ under
skull #
Anteroinferior frontal
Anterior Temporal
Occipital Regions
Petechial hemorrahges 
coalesce  Intracerebral
Hematomas later on.

12. Specific Head Injuries
 Skull Fractures
 Basilar Fracture
 Most common-petrous portion of temporal bone, the
EAC and TM
 Dural tear
 CSF otorrhea
 CSF rhinorrhea
 Battle Sign
 Raccoon Sign
 CSF testing
 Ring sign, glucose or CSF transferrin
 Should be started on prophylactic antibiotics
 Ceftriaxone 1-2 gm
 Hemotympanum
 Vertigo
 Hearing loss
 Seventh nerve palsy

13. Specific Head Injuries
 Scalp Lacerations
 May lead to massive blood loss
 Small galeal lacerations may be left alone
 Skull Fracture
 Linear and simple comminuted skull fractures
 Exploration of wound
 Prophylactic antibiotics are controversial
 Occipital fractures have a high incidence of other injury
 If depressed beyond outer table-requires NS repair

14. Specific Head Injuries
 Traumatic Subarachnoid Hemorrhage
 Most common CT finding in moderate to severe TBI
 If isolated head injury, may present with headache,
photophobia and meningismus
 Early tSAH development triples mortality
 Size of bleed and outcome
 Timing of CT
 Nimodipine reduces death and disability by 55%

16. Specific Head Injuries
 Epidural Hematoma
 Occurs in 0.5% of all head injuries
 Blunt trauma to temporoparietal region
 middle meningeal artery involved most commonly
(66%)
 Eighty percent with associated skull fracture
 May occur with venous sinus tears
 classically associated with a lucid interval
 Classic presentation only 30% of the time

17. Diagnosis
 CT is diagnostic
 Initial Ct Hyperdense Lentiform collection beneath
skull
 Actively bleeding- Mixed densities
 Severe anemia- isodense/hypodense
 Untreated EDH imaging over days Hyperdense
Isodense Hypodense w.r.t. brain

19. Treatment
Non surgical Surgical
Minimal / no symptoms
Should be located outside of Temporal or
Post fossae
Should be < 40 ml in volume
Should not be associated with intradural
lesions
Should be discovered 6 or more hours
after the injury

20. Specific Head Injuries
 Subdural Hematoma
 Sudden acceleration-deceleration injury with tearing of
bridging veins
 Common in elderly and alcoholics
 Associated with DAI
 Classified as acute, subacute or chronic
 Acute <2 weeks
 Chronic >4 weeks

22.  Rx- larger- urgent removal
 Small with mass effect/ significant change in
conscious/ focal deficits-Removed
 Small with significant brain injuries + mass effect out
of proportion to size of clot-Non operative approach


23.  Cranial neuropathies occur in about 10% of admitted
and 30% of severe injuries.
 Frontal injury, basal skull fracture, and pressure effects
account for most
 Anosmia – frontal injury

24.  Visual symptoms result from oculomotor dysfunction,
refractive error shifts, damage to the cornea and
intraocular structures, visual field loss caused by
anterior and posterior visual pathway damage.
 Traumatic optic neuropathies-at the entry and exit of
the optic canal

25.  Auditory disturbance-
1. Fracture of petrous temporal bone(longitudinal)
2. Hemotympanum
3. Tympanic membrane perforation
 Facial nerve palsies -longitudinal or transverse petrous
temporal fractures

26. Concussion
• No structural injury to brain
• Level of consciousness
 Variable period of unconsciousness or confusion
 Followed by return to normal consciousness
• Retrograde short-term amnesia
 May repeat questions over and over
• Associated symptoms
 Dizziness, headache, ringing in ears, and/or nausea
Head Trauma - 26

27. Diffuse axonal injury
•Hallmark of severe traumatic Brain
Injury
•Differential Movement of Adjacent
regions of Brain during acceleration
and Deceleration.
•DAI is major cause of prolonged
COMA after TBI, probably due to
disruption of Ascending Reticular
connections to Cortex.
•Angular forces > Oblique/ Sagital
Forces

28. The shorn Axons
retract and are evident
histologically as
RETRACTION BALLS.
Located
predominantly in
1. CORPUS
CALLOSUM
2. PERIVENTRICULA
R WHITE MATTER
3. BASAL GANGLIA
4. BRAIN STEM

29. Grading of DAI
 Grade I-Hemisphere DAI
 Grade II-Additional posterior callosal
 Grade III-Dorsolateral midbrain

30. MRI
 T2 weighted , FLAIR, T2* gradient echo MRI
sequences early and late post-injury.
 Markers of DAI
1. number and volume of lesions resulting from
contusions and large deep haemorrhages (T1, T2,
FLAIR, and T2*)
2. Residual haemosiderin of microvascular shearing
injuries(T2*)
3. Degree of atrophy

31.  Diffusion tensor imaging (DTI)-reveal evidence of loss
of neuronal and glial cells (increased diffusivity) and
parallel fibre tracts (reduced anisotropy)
 Spectroscopy may show a reduction in N-acetyl
aspartate, consistent with neuronal loss

32. Post traumatic amnesia
 Confused and disorientated
 Lack the capacity to store and retrieve new
information
 Duration of PTA, not of retrograde amnesia, is a useful
predictor of outcome
 Treated with haloperidol and oral resperidone with
benzodiazapine

33. Level Of Consciousness
 Glasgow Coma Scale

34. Children's Coma Scale
Ocular response Verbal response Motor response
Opens eyes spontaneously
4
Smiles, orientated to
sounds, follows objects,
interacts.
5
Infant moves spontaneously or
purposefully 6
EOMI, reactive pupils
( opens eyes to speech) 3
Cries but consolable,
inappropriate
interaction 4
Infant withdraws from touch 5
EOM impaired, fixed pupils
(opens eyes to painful stimuli)
2
Inconsistently
inconsolable, moaning
3
Infant withdraws from pain 4
EOM paralyzed, fixed pupils
( doesn’t open eyes)
1
Inconsolable, agitated
2
Abnormal flexion to pain for an
infant (decorticate response) 3
No verbal response
1
Extension to pain (decerebrate
response) 2
No motor response 1

35. Levels of TBI
 Mild TBI
 Glascow Coma Scale score
13-15
 Moderate TBI
 Glascow Coma Scale score
9-12
 Severe TBI
 Glascow Coma Scale score
8 or less

36. Head Injury-Initial Evaluation
and Management
 Prevent Secondary Brain Injury
 Hypoxemia
 Hypotension
 Anemia
 Hyperglycemia
 Evacuation of mass
 Maintainance of MAP above 90mm of Hg
 Airway control with cervical spine immobilization
 Orotracheal Rapid Sequence Intubation

37. Non invasive methods for ICP
 Audiological tech- displacement of TM and perilymphatic
pressure as a correlate of ICP
 Infrared light- thickness of CSF from reflected light as a
correlate of ICP
 Arterial BP wave contours and blood flow velocity –
mathematical model
 Changes In optical nerve head with optical coherent
tomography
 IOP as correlate of ICP =With ICP cutoff of 20mmhg it has
Specificity of 0.7 and sensitivity of 0.97

38. Increased ICP-Management
 Hypertonic Saline
 Improves CPP and brain tissue O2 levels
 Decreased ICP by 35% (8-10 mm HG)
 CPP increased by 14%
 MAP remained stable
 Greatest benefit in those with higher ICP and lower CPP
 Repeated doses were not associated with rebound,
hypovolemia or HTN
 30 mL of 23.4% over 15 minutes
A. Defillo, Hennepin County Medical Center

39. Increased ICP-Management
 Mannitol
 Osmotic agent
 Effects ICP, CBF, CPP and brain metabolism
 Free radical scavenger
 Reduces ICP within 30 minutes, last 6-8 hrs
 Dosage
 0.25-1 gm/kg bolus

40. Increased ICP-Management
 Hyperventilation
 Not recommended as prophylactic intervention
 Never lower than 25 mm Hg
 Reduces ICP by vasoconstriction, may lead to cerebral
ischemia
 Used as a last resort measure
 Maintain PaCO2 at 30-35 mm Hg
• Steroids not recommended

41. Increased ICP-Management
 Barbiturate Coma
 Not indicated in the ED
 Lowers ICP, cerebral metabolic O2 demand
 Anticonvulsants
 Reduce occurrence of post-traumatic seizures
 No improvement in long-term outcome
 ICP Monitoring
 Should be performed on TBI with GCS <9
 Increased ICP may be managed by drainage

42. Treatment of Intracranial Hypertension
May Repeat Mannitol
if Serum Osmolarity
< 320 mOsm/L &
Pt euvolemic
YES
Insert ICP Monitor
Maintain CPP  70 mmHg
Intracranial Hypertension?*
Ventricular Drainage (if available)
Intracranial Hypertension?
YES NO
Mannitol (0.25 - 1.0 g/kg IV)
Intracranial Hypertension?
YES NO
Hyperventilation to PaCO2 30 - 35 mmHg
Intracranial Hypertension?
YES NO
High Dose
Barbiturate therapy
NO
Carefully
Withdraw
ICP Treatment
• Hyperventilation to PaCO2 < 30 mmHg
• Monitoring SjO2, AVDO2, and/orCBF
Recommended
Consider
Repeating
CT Scan
Other Second
Tier Therapies
Second Tier Therapy
*Threshold of 20-25 mmHg may be used. Other values may be substituted in individual
conditions.

43. Cognitive and neuropsychiatric
sequelae
 Personality changes, egocentricity, childishness,
irritability, aggressiveness, poor judgement,
tactlessness, stubbornness, lethargy, disinterest,
reduced drive and initiative, reduced sexual interest
 Low mood, depression,anxiety disorders

44. Epilepsy
 More common with penetrating injury
 In Blunt trauma predicted by depressed skull fracture,
an intracranial clot requiring surgery, and altered
awareness for more than 24 hours associated with
contusion.

45.  Concussive convulsions (occurring seconds after the
impact)
 Immediate epilepsy (occurring up to 12 hours after
injury)
 Early seizures (12 hours to one week post-injury)
 Late epilepsy (more than one week post-injury)

46. 1. Early posttraumatic seizures within min to hours of injury.
1. No radiological intracranial injury noted in many cases
2. Do not progress later epilepsy
3. Most do not need Rx
4. Outcome good.
 Late seizure  >24 hrs after injury
 Visible intracranial injury.
 Penetrating injuries/ depressed #/ SDH/ Lower GCS score
 Long term risk of epilespy high- need Rx for 6-12 mo.

47.  Intravenous phenytoin within 24 hours of high risk
injury prevents early seizures, but not late seizures,
even in high risk patients
 Antiepileptics continued for atleast 1 year

48. Post traumatic headache
 Post-traumatic headache, by definition, starts within
14 days of the injury, or with recovery of awareness,
 If it continues for more than eight weeks it is said to
have become chronic.
 Can be tension or migraine or combination of two
 Local soft tissue injury contribute

49. Predictors of outcome
 Acute predictors—
 admission GCS
 present/absent pupillary responses
 Attendant hypoxic/ischaemic injury
 imaging findings, especially depth of lesion
 biochemical markers
 Duration of coma and PTA

50. On long term outcome affected by
 Increasing age over 50 years, social class, personality,
family support, premorbid caseness, and genetic make
up(at least one apolipoprotein E e4 allele)

51. Thank you

52. References
 HEAD INJURY FOR NEUROLOGISTS: Richard
Greenwood ;J Neurol Neurosurg Psychiatry 2002 73: i8-
i16
 Traumatic brain injury; Emily Gilmore and Steven
Karceski ;Neurology 2010;74;e28-e31
 Guidelines for the Management of Severe
Traumatic Brain Injury:A joint initiative of:The Brain
Trauma Foundation ,The American Association of
Neurological Surgeons ,The Joint Section on
Neurotrauma and Critical Care