Traumatic Brain Injury

1. Traumatic Brain Injury
TBI
Dr Mukesh Sah, MD
UK
Dr. Mukesh Sah

2. Epidemiology
• Motor vehicle collision-related TBIs
• the most common causes in developing countries
• highest in Asia
• Fall-related TBIs
• the most common causes in developed countries
• Europe had the highest percentage
• Sport-related TBIs
• Highest in North America, followed by Oceania
• Fall-related TBIs
• Europe had the highest percentage
Dr. Mukesh Sah

3. Epidemiology
• Men were at higher risk of TBI than women.
• The average age at the time of TBI ranged from 27 to 59.67 years while
the median age ranged from 29 to 45 years
Dr. Mukesh Sah

4. Definitions
• Cerebral Concussion
= a complex pathophysiological process affecting the brain, induced by
traumatic biomechanical forces
= implies a violent shaking or jarring of the brain and a resulting
transient functional impairment such as loss of consciousness, memory
loss, alteration of mental state or personality, or focal neurologic deficits
that heals by itself within time and not associated with structural
abnormality as evidenced on neuroimaging
= it is a reversible traumatic paralysis of nervous function
Dr. Mukesh Sah

5. Definitions
• Cerebral Contusion
= a bruising of cerebral tissue with or without interruption of its
architecture associated with loss of consciousness
= Associated with more severe pathology in the brain such as extradural,
subdural, subarachnoid, and intracerebral hemorrhages, variable
degrees of vasogenic edema that increases during the first 24 to 48 h,
and zones of infarction due to vascular spasm caused by subarachnoid
blood surrounding basal vessels
Dr. Mukesh Sah

6. •Mechanisms of Concussion
1. Due to vasoparalysis or an arrest of circulation by
an instantaneous rise in intracranial pressure
2. The brain is subjected to shearing stresses set up
by rotational forces mainly in the sagittal plane
centered at its point of tethering in the high midbrain
and subthalamus. The torque at the level of the upper
reticular formation would explain the immediate loss
of consciousness
• More favored explanation
Dr. Mukesh Sah

7. Clinical Manifestations of Concussion
• immediate abolition of consciousness, suppression of
reflexes (falling to the ground if standing), transient
arrest of respiration, a brief period of bradycardia, and
fall in blood pressure following a momentary rise at
the time of impact
•Brief tonic extension of the limbs, clonic convulsive
movements lasting up to about 20 seconds and other
peculiar movements may occur immediately after the
loss of consciousness
Dr. Mukesh Sah

8. Clinical Manifestations of Concussion
•if these abnormalities are sufficiently intense, death
may occur at the moment of impact, presumably from
respiratory arrest
•Usually the vital signs return to normal and stabilize
within a few seconds while the patient remains
unconscious.
Dr. Mukesh Sah

9. Cerebral Contusion
•a bruising of cerebral tissue with or without
interruption of its architecture associated with
loss of consciousness
•Areas that are commonly involved are the
frontal and temporal lobes because of the
presence of the petrous bone, sphenoid wing
and orbital ridge
Dr. Mukesh Sah

10. Dr. Mukesh Sah

11. Cerebral Contusion
•Two types
1. coup lesions
= are contusions of the surface of the brain
beneath the point of impact
2. contrecoup lesions
= are more extensive lacerations and
contusions on the side opposite the site of
impact
Dr. Mukesh Sah

12. Dr. Mukesh Sah

13. Dr. Mukesh Sah

14. Dr. Mukesh Sah

15. GCS Score
•< 7 score = indicative of severe head
injury associated with a poor clinical
state
•8 to 12 score = moderate injury
•13 to 15 score = mild injury
Dr. Mukesh Sah

16. Group of patients after head trauma
1. Minor Head Injury
 Patients Who Are Conscious or Are Rapidly
Regaining Consciousness
2. Severe Head Injury
 Patients Who Have Been Comatose from
the Time of Head Injury
Dr. Mukesh Sah

17. 1. Patients Who Are Conscious or Are
Rapidly Regaining Consciousness
•the most frequently encountered in clinical situation
•two degrees of disturbed function within this category
1. the patient was not unconscious at all but only
stunned momentarily or “saw stars”
= injury is insignificant but there is always the
possibility of a skull fracture or later develop epidural
or subdural hematoma
Dr. Mukesh Sah

18. Patients Who Are Conscious or Are Rapidly
Regaining Consciousness
2. consciousness was temporarily abolished for a few
seconds or minutes
the patient may have an amnesia for events
immediately preceding and following the injury
•Both has post-traumatic syndrome consisting of
headache, giddiness, fatigability, insomnia, and
nervousness which may appear soon after or within a
few days of the injury
Dr. Mukesh Sah

19. Patients Who Are Conscious or Are Rapidly
Regaining Consciousness
• Criteria that justify obtaining a cranial CT following seemingly minor
forms of head trauma
1. head injury associated with prolonged loss of consciousness
2. severe and persisting headache
3. with nausea and vomiting
4. with confusional state
5. presence of neurologic signs
6. elderly patients
Dr. Mukesh Sah

20. Other associated clinical phenomena
• Delayed Fainting after Head Injury
• Transient Traumatic Paraplegia and Transient Blindness
• Delayed Hemiplegia
• Fat Embolism
Dr. Mukesh Sah

21. Delayed Fainting after Head Injury
•Following an accident, the injured person, after
walking about and seemingly normal, may turn
pale and fall unconscious to the ground
•Recovery occurs within a few seconds or
minutes
•Due to vasodepressor syncopal attack, possibly
related to pain and emotional upset
Dr. Mukesh Sah

22. Transient Traumatic Paraplegia and
Transient Blindness
•Transient Traumatic Paraplegia = occurs with falls or
blows on top of the head, both legs may become
temporarily weak and numb, with wavering bilateral
Babinski signs and sometimes with sphincteric
incontinence
•Transient Traumatic Blindness = occurs with blows to
the occiput, disappear after a few hours
Dr. Mukesh Sah

23. Delayed Hemiplegia
• Mostly occurred some hours after a relatively minor athletic or more
severe injury, developed a massive hemiplegia, homonymous
hemianopia, or aphasia (with left-sided lesions)
• Causes :
1. dissection of the internal carotid artery
2. a mural thrombus forms in the carotid after a blow to the neck which
in turn may shed an embolus to the anterior or middle cerebral artery
3. late evolving epidural or subdural hematoma
Dr. Mukesh Sah

24. Fat Embolism
• Due to fractures of large bones
• Occurs 24 to 72 hrs after the injury
• an acute onset of pulmonary symptoms (dyspnea and hyperpnea)
followed by coma with or without focal signs or seizures due to systemic
fat embolism first of the lungs and then of the brain
• In the brain, the fat emboli cause widespread petechial hemorrhages,
involving both white and gray matter and a few larger infarcts
• Petechial rashes in the thorax
• Mortality rate = 10 %, due to underlying injuries
• Most patients recover spontaneously in 3 or 4 days
Dr. Mukesh Sah

25. 2. Patients Who Have Been Comatose from
the Time of Head Injury
• Pathologic Evidences
1. Increased intracranial pressure
2. cerebral contusions, lacerations, subarachnoid hemorrhage, zones of
infarction
3. scattered intracerebral hemorrhages, both at the point of injury and on
the opposite side and in the corpus callosum
4. diffuse axonal type of injury
5. ischemic and hemorrhagic lesions in the upper midbrain and lower
thalamic region
Dr. Mukesh Sah

26. Patients Who Have Been Comatose from
the Time of Head Injury
• three clinical subgroups can be recognized
1. Death = cerebral and other bodily injuries are severe and
incompatible with survival
2. Vegetative and minimally conscious patients
= the patients remain permanently comatose, stuporous, or
profoundly reduced in their cerebral capacities
3. Patient with residual neurologic signs = improvement sets in within a
few days or a week or two, followed by variable degrees of recovery
Dr. Mukesh Sah

27. Patients Who Have Been Comatose from
the Time of Head Injury
• The effects of contusion, hemorrhage, and brain swelling often become
evident within 18 to 36 hrs after the injury and then may progress for
several days
• If the patients survive this period, their chances of dying from
complications of these effects—such as increased intracranial pressure,
herniations of the temporal lobe, subdural hemorrhage, hypoxia, and
pneumonia—are greatly reduced
Dr. Mukesh Sah

28. Patients Who Have Been Comatose from
the Time of Head Injury
• Mortality rate
• 20 % in those who reach the hospital in coma
• occurs in the first 12 to 24 hrs
• due to direct injury to the brain and other non-neurologic injuries
• Of those alive at 24 hrs,
• the overall mortality falls to 7 to 8 %
• after 48 h, only 1 to 2 % succumb
Dr. Mukesh Sah

29. SPECIFIC TRAUMATIC CRANIAL LESIONS
• Acute Epidural Hemorrhage
• Acute and Chronic Subdural Hematomas
• Subdural Hygroma
• Cerebral Contusion
• Traumatic Intracerebral Hemorrhage
• Diffuse Axonal Injury
Dr. Mukesh Sah

30. Acute Epidural Hemorrhage (EDH)
•arises from a temporal or parietal fracture and
laceration of the middle meningeal artery or vein
•Less often due to a tear in a dural venous sinus
•Hematoma is situated between the skull and dura
•lens shaped hyperdense lesion on CT scan
Dr. Mukesh Sah

31. Acute Epidural Hemorrhage (EDH)
• Lucid interval = transient loss of consciousness after a hard blow to the
head then regain consciousness
• A few hours later, headache of increasing severity develops, with
vomiting, drowsiness, confusion, aphasia, seizures (which may be focal),
hemiparesis with slightly increased tendon reflexes, and a Babinski sign
• As coma develops, the hemiparesis may give way to bilateral spasticity
of the limbs and Babinski signs
• pupil dilates on the side of the hematoma
• Death comes at the end of a comatose period and is due to respiratory
arrest if no surgery
Dr. Mukesh Sah

32. Dr. Mukesh Sah

33. Acute epidural hematoma
Dr. Mukesh Sah

34. Recommendations
• EDH > 50 ml = should be surgically evacuated regardless of the patient’s
GCS score
• EDH < 30 ml and with <15mm thickness and with < 5mm midline shift in
patients w/ a GCS score >8 w/o focal deficit can be managed non-
operatively with serial CT scan and close neurological observation
• It is strongly recommended that patients with an acute EDH in coma
(GCS score <9) with anisocoria should undergo surgical evacuation as
soon as possible
• craniotomy provides a more complete evacuation of the hematoma
Dr. Mukesh Sah

35. Acute subdural hematoma
• Acute, rapidly evolving subdural hematomas are due to tearing of
bridging veins
• Hematoma between the dura and arachnoid
• Hyperdense crescentic lesion
• Symptoms are caused by compression of the brain by an expanding clot
of fresh blood
• venous bleeding is usually arrested by the rising intracranial pressure
Dr. Mukesh Sah

36. Stages of Subdural Hematoma
• Acute
1st 2-3 days
• Subacute
3-14 days
• Chronic
>14 days
Dr. Mukesh Sah

37. Dr. Mukesh Sah

38. Acute Subdural Hematoma
Dr. Mukesh Sah

39. Chronic Subdural Hematomas
• the traumatic etiology is often less clear
• In elderly and in those taking anticoagulant drugs, head injury may be
trivial and may even forgotten
• main symptoms
= weeks after a trivial injury follows headaches, light-headedness,
slowness in thinking, apathy and drowsiness, unsteady gait, and
occasionally a seizure
• Differential diagnosis
• a vascular lesion (stroke), drug intoxication
• brain tumor , depressive illness
• Alzheimer disease
• progression of symptoms = due to gradual expansion of the hematoma
Dr. Mukesh Sah

40. Chronic Subdural Hematoma
Dr. Mukesh Sah

41. Chronic Subdural Hematomas
•focal signs
1. Hemiparesis = ipsilateral
Kernohan-Woltman sign = the hemiparesis may sometimes be
ipsilateral to the clot, as a result of compression of the contralateral
cerebral peduncle against the free edge of the tentorium by horizontal
displacement of the midbrain
2. Homonymous hemianopia due the involvement of the
geniculocalcarine pathway
• If the condition progresses, the patient becomes stuporous or comatose,
but this course is often interrupted by fluctuations of awareness
Dr. Mukesh Sah

42. Chronic Subdural Hematoma
Other manifestations
• Dilatation of the ipsilateral pupil is a reliable indicator of the side of the
hematoma
• Convulsions occur occasionally, most often in alcoholics or in patients
with cerebral contusions
• Internuclear ophthalmoplegia
• transient disturbances of neurologic function simulating transient
ischemic attacks (TIAs) may occur
Dr. Mukesh Sah

43. How to diagnose
• CT Scan or MRI
Acute epidural hematoma Acute subdural hematoma
Dr. Mukesh Sah

44. Stages of Subdural Hematoma
Acute subacute chronic
Dr. Mukesh Sah

45. Treatment of Subdural Hematoma
• Acute hematoma = burr holes and evacuate the clot
• Treatment of larger hematomas, particularly after several hours have
passed and the blood has clotted, wide craniotomy to permit control of
the bleeding and removal of the clot
• Thin, crescentic clots can be observed and followed over several weeks
and surgery undertaken only if focal signs or indications of increasing
intracranial pressure arise (headache, vomiting, and bradycardia)
• Small subdural hematomas causing no symptoms, surgery is not
indicated
Dr. Mukesh Sah

46. Treatment of Subdural Hematoma
•In chronic hematomas, a craniotomy must be
performed and an attempt made to strip the
membranes that surround the clot
•This diminishes the likelihood of
reaccumulation of fluid
Dr. Mukesh Sah

47. Recommendations
• Thickness >10mm or a midline shift >5 mm on Cranial CT scan = should
be surgically evacuated regardless of GCS.
• A patient’s GCS <9 with an SDH less than 10mm thick and midline shift
<5mm should undergo surgical evacuation of the lesion
• if the GCS score decreases between the time of injury and hospital
admission by 2 or more points and the patient presents with asymmetric
or fixed dilated pupils or the ICP exceeds 20mm Hg surgery is indicated
Dr. Mukesh Sah

48. Subdural Hygroma
• An encapsulated collection of clear or xanthochromic fluid in the
subdural space that form after an injury as well as after meningitis
• presumably due to a ball-valve effect of an arachnoidal tear that allows
cerebrospinal fluid to collect in the space between the arachnoid and
the dura seen in patients with brain atrophy
• Occasionally a hygroma originates from a tear in an arachnoidal cyst
• It may be difficult to differentiate a long-standing subdural hematoma
from hygroma, and some chronic subdural hematomas are probably the
result of repeated small hemorrhages that arise from the membranes of
hygromas
Dr. Mukesh Sah

49. Cerebral Contusion
• Due to severe closed head injury
• With associated surrounding edema and if sufficiently large, lead the
genesis of tissue shifts (herniation) and raised intracranial pressure
• the contused area has the tendency to swell or to develop into a
hematoma which may give rise to clinical deterioration hours to days
after the injury, sometimes abrupt in onset
Dr. Mukesh Sah

50. Dr. Mukesh Sah

51. Cerebral Contusion
Dr. Mukesh Sah

52. Contusion Hematoma
Dr. Mukesh Sah

53. Traumatic Intracerebral Hemorrhage
•One or several intracerebral hemorrhages may be
apparent immediately after head injury
•The bleeding is in the subcortical white matter of one
lobe of the brain or in deeper structures, such as the
basal ganglia or thalamus.
•The injury is nearly always severe; blood vessels as
well as cortical tissue are torn
Dr. Mukesh Sah

54. Traumatic Intracerebral Hemorrhage
•The clinical picture is similar to that of hypertensive
brain hemorrhage (deepening coma with hemiplegia,
a dilating pupil, bilateral Babinski signs, stertorous and
irregular respirations).
•It may be manifest by an abrupt rise in blood pressure
and increase intracranial pressure.
Dr. Mukesh Sah

55. Traumatic Intracerebral Hemorrhage
Dr. Mukesh Sah

56. Diffuse Axonal Injury
• represent a degeneration of nerve fibers that had been stretched or torn
by the shear stresses set up during rotational acceleration of the head
• the degeneration of white matter can be remarkably diffuse, with no
apparent relationship to focal destructive lesions
• The extension of the diffuse axonal injury throughout the cerebral white
matter is the main cause of persistent unconsciousness in patients with
no significant contusions or hemorrhages
Dr. Mukesh Sah

57. Dr. Mukesh Sah

58. Dr. Mukesh Sah

59. SEQUELAE OF HEAD INJURY
• Post-traumatic Epilepsy
• Autonomic Dysfunction Syndrome in Traumatic Coma
• “Punch-Drunk” Encephalopathy (Dementia Pugilistica)
• Posttraumatic Hydrocephalus
• Posttraumatic Nervous Instability (Post-concussion Syndrome)
Dr. Mukesh Sah

60. Epilepsy after trauma
3 types
•immediate epilepsy
•early epilepsy
•posttraumatic epilepsy
Dr. Mukesh Sah

61. Epilepsy after trauma
Immediate Epilepsy
• generalized seizure that occur within moments after the injury
• a brief tonic extension of the limbs, with slight shaking movements
immediately after concussion, followed by awakening in a mild
confusional state
• is the result of arrest of cerebral blood flow or a transient brainstem
dysfunction
• have a good prognosis
• Does not require long term treatment
Dr. Mukesh Sah

62. Epilepsy after trauma
Early Epilepsy
•seizures within the first week of the injury
•more likely to have a complete remission of seizures
than those whose attacks begin a year or so after
injury
Dr. Mukesh Sah

63. Epilepsy after trauma
Posttraumatic epilepsy
• refers to late epilepsy
• seizures that develop several weeks or months after the head injury (1
to 3 months in most cases)
• The interval between head injury and development of seizures is longer
in children.
• The longer the interval, the less certain one is of its relation to the
traumatic incident.
Dr. Mukesh Sah

64. Epilepsy after trauma
In severe head injury,
• patients who escape seizures for 1 year after injury can be 75 % certain
of remaining seizure-free
• patients without seizures for 2 years can be 90 % seizure-free
• for 3 years, 95% seizure-free
In less severely injured
• patients who escape seizures for 2 to 6 months after injury can be 75 %
certain of remaining seizure-free
• patients without seizures for 12 to 17 months can be 90 % seizure-free
• for 21 to 25 months, 95% seizure-free
Dr. Mukesh Sah

65. Post-traumatic Epilepsy
• the most common delayed sequela of craniocerebral trauma
• Incidence =
• 5 % in patients with closed head injuries
• 50 % in compound skull fracture and wound of the brain
• nearly always due to contusion or laceration of the cortex
• also related to the overall severity of the closed head injury
Dr. Mukesh Sah

66. Posttraumatic Epilepsy
Risk of seizures depends upon the severity of head injury:
• Severe injury (loss of consciousness or amnesia for more than 24 h,
including subdural hematoma and brain contusion) = 7 % within 1 year
and 11.5 % in 5 years
• Moderate injury (unconsciousness or amnesia for 30 min to 24 h or
causing only a skull fracture) = 0.7 % within 1 year and 1.6 % in 5 years
• Mild injury (loss of consciousness or amnesia of less than 30 min), the
incidence was not significantly greater than in the general population
Dr. Mukesh Sah

67. Autonomic Dysfunction Syndrome in
Traumatic Coma
• Manifest as an episodic seizures combined with violent extensor
posturing, profuse diaphoresis, hypertension, and tachycardia lasting
minutes to an hour due to excessive sympathetic activity
• A slight fever may accompany the spells
• may be precipitated by painful stimuli or by distention of a viscus, but
often arise spontaneously
• Is likely the result of the removal of suppressive cortical influences,
allowing the hypothalamus to function independently of normal
inhibitory mechanisms
Dr. Mukesh Sah

68. “Punch-Drunk” Encephalopathy
(Dementia Pugilistica)
• Observed in boxers due to cumulative effects of repeated cerebral
injuries
• A parkinsonian and dementing syndrome
• Manifests as a dysarthric speech and a state of forgetfulness,
slowness in thinking, and other signs of dementia
• Movements are slow, stiff, and uncertain, especially those involving
the legs, and there is a shuffling, wide-based gait.
.
Dr. Mukesh Sah

69. Posttraumatic Hydrocephalus
• an uncommon complication of severe head injury
• Initial manifestations are intermittent headaches, vomiting, confusion,
and drowsiness
• Later on, mental dullness, apathy, and psychomotor retardation, by this
time the CSF pressure may have fallen to a normal level (normal
pressure hydrocephalus)
• Due to an adhesive basilar arachnoiditis and secondary blocking of the
aqueduct and fourth ventricle by blood clot and basilar meningeal
fibrosis
• Response to ventriculoperitoneal shunt may be dramatic
Dr. Mukesh Sah

70. Posttraumatic Nervous Instability
(Postconcussion Syndrome)
• also called the posttraumatic syndrome, posttraumatic headache,
traumatic neurasthenia, and traumatic psychasthenia
• Headache is the central symptom, either generalized or localized
• described as aching, throbbing, pounding, stabbing, pressing, or band-
like
• intensifies by mental and physical effort, straining, stooping, and
emotional excitement
• May also complain of dizziness, giddiness or lightheadedness.
• Rest and quiet room tend to relieve it
• symptoms clear up in several weeks in the majority of patients
Dr. Mukesh Sah

71. Thank you
Dr. Mukesh Sah