Name : Zainal Muttaqin

Date of Birth : 24 November 1957

Address : Jl. Permata Semeru B-27 Semarang
50234, Indonesia
Education
1983 - : Graduated from Medical Faculty,
Diponegoro University, Semarang
1987 - 1994 : Ph.D. Degree in Neurosurgery, and
Neurosurgical training at Department of
Neurosurgery, Hiroshima University
School of Medicine, Hiroshima, Japan
1994 now : Several trainings and courses in
Skullbase Dissection and Epilepsy
Surgery
 Working Experiences
1984 1987 : Teaching Neurophysiology at
Medical Faculty, Diponegoro
University
1995 - now : Teaching Neurophysiology,
Neuroradiology, and Neurosurgery
at Medical Faculty, Diponegoro
University, Semarang
Special Interest :
Epilepsy, Neuroimaging, Transcranial Doppler
Sonography, Skullbase Tumors
 Head Injury Up-date:

intracranial patophysiology and

the Role of CT Scan

Zainal Muttaqin, M.D., Ph.D.

Department of Neurosurgery,
Medical Faculty, Diponegoro University
Back ground

9 HI ranks highest as cause of death in 15-45 Y-old

9 Most death and disability due to Cerebral Ischemia
9 Ischemia after HI most often related to: High ICP,
systemic hypotension, and hypoxia-hypoxemia
9 High ICP after HI caused by: intracranial hematoma,
contused parenchyma, and hyperemic condition
(congestion or swelling)
9 Role of CT: showing High ICP, not just showing the
presence or absence of intracranial hematoma
9Name : Zainal Muttaqin
9Date of Birth : 24 November 1957
9Address : Jl. Permata Semeru B-27
Semarang 50234, Indonesia
9Education
91983 - Graduated from Medical Faculty,
Diponegoro University, Semarang
91987 - 1994 Ph.D. Degree in Neurosurgery, and
Neurosurgical training at
Department of Neurosurgery,
Hiroshima University School of
Medicine, Hiroshima, Japan
91994 now Several trainings and courses in
Skullbase Dissection and Epilepsy
Surgery
Risk of hematomas after HI

9 HI severity: 2% in Mild, 9-10% in moderate, and 50%

in severe head injuries
9 In Mild HI, presence of fracture line increases the risk
7-10 times, risk is 32% in the presence of lucid interval
9 Age: in > 50 Y, risk is 3-4 times higher than < 30 Y
9 HI biomechanic: low speed injury (fall, domestic and
sport injuries) produces focal lesion more often, while
high speed road-traffic injuries produces diffuse
axonal injuries (DAI) more often
Intracranial hematomas after HI
Epidural Subdural Intracerebral

Presence of fracture line :

Location of Hematomas
9 Patient with temporal or
temporo-parietal lesion
has higher risk of
brainstem compression
and transtentorial her
niation despite normal
ICP (located closer to
the tentorial hiatus), so
that prompt and early
evacuation of the mass
lesion should be Lt Frontal EDH Rt Temporal EDH
considered GCS 12 GCS 4 (died in 1 H)
Diffuse Axonal Injury (DAI)
Among patients with severe HI, only 50% related to presence of

focal hematomas ( EDH, SDH, ICH/contusion )

9 Introduced by Strich (1956), then successfully reprodu

ced experimentally by Genarelli (1982)
9 Patient with obvious neurologic deficit or loss of
consciousness without significant lesion on CT scan
9 Radiology: presence of hemorrhagic lesion without
mass effect (tissue tear or petechial hemorrhage), in
subcortical white matter, corpus callosum, basal
ganglia, or brainstem
9 Other fetaures: diffuse edema, t-SAH, and IVH
DAI : CT features
 head accelleration
or deceleration

DAI: axonal stretching

pathomechanism axonal membrane disruption

excitatory amino acid Ca ++ influx

free radical peroxidation
Ca ++ mediated damages

activation of proteases

destruction of cytoskeletons

block of axoplasmic transport

axonal swelling

PA: axonal retraction ball

only in those survived
more than 12 H post-injury

complete axotomy or
secondary axotomy
Severity of DAI

Clinically, concussion or com-

motio cerebri is the mildest
and reversible form of DAI
The severity depends on the
magnitude and duration of
motion
Depth of parenchymal lesion
positively correlated to the
degree and duration of
impaired consciousness
(patient with deeply located The petechial hemorrhage is located
lesion had lower GCS than
deeper in B, means that mechanism
those with cortical and
subcortical lesion
causing DAI is more severe in B
Evaluation of Role of CT scan in HI
9 At first, CT is useful in showing intracranial hematoma
9 Then, CT helps differentiate focal lesion from DAI
9 Since 1990, Traumatic Coma Data Bank (TCDB)
Classification of Head Injury :
9 Based on admission CT
9 Highlighted features related to High ICP (obliteration of cisterns
and ventricles, especially basal cistern, and midline shift) mainly
in cases of diffuse brain injury (DAI : pathological entity)
9 Predict the outcome better than other methods
9 In less severe cases : identify those at risk of cerebral swelling
and death (which clinically look well on admission
CT evidences of elevated ICP
9 Loss of image of third ventricle
9 Loss of image of perimesencephalic cistern
9 In unilateral lesion :
1. Midline shift ( should be visualized at level of Foremen Monro )
2. Dilatation of contralateral ventricles
TCDB Classification of HI based on CT

9 Diffuse Injury I: No visible intracranial pathology on CT

9 Diffuse Injury II: Presence of lesion densities (may include bone
fragment or foreign body) but not more than 25ml, cistern
present, midline shift may present but less than 5mm
9 Diffuse Injury III (swelling): No high or mixed density lesion >
25ml, midline shift <5ml, cistern compressed or absent
9 Diffuse Injury IV (shift): No hugh or mixed density lesion >25ml,
midline shift >5 mm
9 Evacuated Mass : Any lesion surgically evacuated
9 Non Evacuated Mass: high or mixed density lesion > 25ml, not
evacuated ( from Marshall LF, et al. 1991)
TCDB classification (1)
TCDB classification (2)
TCDB classification and prognosis (1)

9 Diffuse Injury I: Normal CT, never

develop high ICP unless there is
systemic complication
9 Diffuse Injury II: Abnormal CT but
normal cistern, low risk of high ICP
and death (as same as diffuse injury I)

9 Diffuse Injury III : With swelling, usually

related to previous occurrence of hypoxia or hypotension
9 Diffuse Injury IV: with midline shift, strong predictor of high ICP; (from
mortality point of view, diffuse injury III and IV are the non-surgical
analog of patient with mass lesion)
TCDB classification and prognosis (2)

9 Average mortality: 36% in severe head injury (16-76%), the lower

the GCS score the higher the mortality
9 Traumatic SAH: increases risk of death twice higher
9 Bad outcomes (vegetative and death): 19.2%, 24.8%, 56.9%, &
75% respectively for diffuse injury I,II, III, IV)
9 Functional outcomes are: 61.6%, 34.5%, 16.4%, and 6.2%
respectively for diffuse injury I, II, III, dan IV
9 In mass lesion (EM and non-EM), bad outcomes were 51.3% and
69.5%, similar as diffuse injury III and IV
Indication for CT evaluation after HI:

9 Decreasing level of consciousness (moderate & severe HI)

9 Fully conscious patient (mild HI, GCS 13-15), in the presence of:
Focal neurologic deficit and/or seizures, with or without linear fractures
Decreasing level of consciousness > 2 GCS score during observation
Difference in pupillary diameter > 1 mm
Depressed fractures more than 1 table ( external table of the depressed
part lies parallel or deeper than the internal table of the normal part )
Penetrating wounds, including depressed fractures or foreign body
GCS < 15 that do not normalized even after 24 H later
Indications for CT evaluation
When a repeat CT scan needed ?
Pittfalls in Imaging of HI
Complication of HI

Tension pneumo-
cephalus
Conclusions

9 Most of death and disability after HI are due to cerebral ischemic

condition, some of which is caused by high ICP
9 The role of CT scan in HI has evolved from just detection of
intracranial hematomas toward detection of high ICP
9 The new HI classification (TCDB) based on CT, put emphasis on
features related to the presence of High ICP and bad prognosis
9 The application of this classification, in combination with GCS,
will improve our understanding on intracranial pathophysiology,
and thus our ability to identify HI patients with risk of high ICP
and bad prognosis, eventhough clinically look well on admission