Head Injury.pptx

1
HEAD INJURY AND NEUROLOGICAL EVALUATION
Presenter:
Dr. Harjeet Yadav
PG
Dept. of OMFS
Moderator:
Dr. Alok Bhatnagar
Professor
Dept. of OMFS

CONTENTS
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 Introduction
 Epidemiology
 Association Between Maxillofacial Trauma And Head Injury
 Etiology
 Pathophysiology
 Classification
 Symptoms
 Complications and Challenges
 Scalp Injuries
 Skull Vault Fractures
 Skull Base Fractures
 Coup & Contrecoup Injuries
 Concussion
 Contusion
 Cerebral Laceration
 Cerebral Hematoma
 Diffuse Axonal Injury
 Patient Assessment
 Neurological Evaluation
 Neurodiagnostic Evaluation
 Severity Of Head Injury
 Management
 Conclusion
 References

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 HEAD INJURY is a broad term that describes a vast array of
injuries that occur to the scalp, skull, brain, and underlying
tissue and blood vessels in the head.
 TRAUMATIC BRAIN INJURY is defined as non-degenerative,
non-congenital insult to the brain from an external mechanical
force, possibly leading to permanent or temporary impairment
of cognitive, physical, and psychosocial functions, with an
associated diminished or altered state of consciousness.
 The terms HEAD INJURY and BRAIN INJURY are often used
interchangeably.
INTRODUCTION
Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology
Updated: Mar 27, 2019
Author: Segun Toyin Dawodu,

EPIDEMIOLOGY
GLOBAL SCENARIO
• 69 million individuals are estimated to suffer each year.
• Proportion of TBIs resulting from RTA is greatest in Africa and Southeast Asia (56%) and lowest in
North America (25%).
INDIAN SCENARIO
• More than one lakh lives are lost every year with over 10 lakh suffering from serious head injuries.
• RTAs are the leading cause (60%), followed by falls (20%-25%) and violence (10%).
• Alcohol involvement is known to be present among 15%-20% cases
4
Estimating the global incidence of traumatic brain injury.
Dewan MC et al
J Neurosurg. 2018 Apr 1:1-18
Epidemiology of traumatic brain injuries: Indian scenario.
Gururaj G.
Neurol Res. 2002 Jan;24(1):24-8. Review

Association Between Maxillofacial Trauma And Head Injury:
• According to Keenan et al., patients with maxillofacial fractures have a higher risk of
intracranial haemorrhage when compared to patients without maxillofacial fractures due to
trauma.
• Haug and associates revealed that 17.5% patients with facial fractures had some form of
closed head injury whereas almost 10% sustained a severe intracranial injury.
• A ten year analysis by Erik and associates, suggests that maxillofacial trauma has an
association with traumatic brain injury that requires neurosurgical intervention, with an
incidence rate of 8.1%.
5
Choonthar MM, Raghothaman A, Prasad R, Pradeep S, Pandya K. Head Injury- A Maxillofacial Surgeon's Perspective. J Clin Diagn Res. 2016.

ETIOLOGY
• Road traffic accidents
• Falls
• Sports Injury
• Assault
• Gun Shot
• Miscellaneous
6

CEREBRAL AUTOREGULATION
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• Cerebral autoregulation is a homeostatic process
• In healthy adults, changes in mean arterial pressure (MAP) between 50 and 150 mmHg results in little or no
change in Cerebral blood flow.
• This adaptive mechanism maintains constant CBF by vasodilation or decreasing cerebrovascular resistance.
• However, under traumatic conditions, autoregulation is lost, resulting in a linear relationship of BP to cerebral
blood flow.
• Therefore, maintenance of adequate BP is of vital importance for brain survival.
Cerebral Autoregulation
S.-H. Yang, R. Liu, in Primer on Cerebrovascular Diseases (Second Edition), 2017

MONRO-KELLIE PRINCIPLE
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• Named after Edinburgh doctors Alexander Monro and George
Kellie.
• The pressure–volume relationship between Intracranial pressure
(ICP), CSF, blood, and brain tissue, and cerebral perfusion
pressure (CPP) is known as the Monro–Kellie doctrine or
hypothesis.
• It states that the cranial compartment is inelastic and that the
volume inside the cranium is fixed. The cranium and its
constituents create a state of equilibrium, such that any increase
in volume of one of the cranial constituents must be compensated
by a decrease in volume of another.
• The principal buffers for increased volumes include CSF and, to a
lesser extent, blood volume. These buffers respond to increases in
volume of the remaining intracranial constituents.
Mokri B (June 2001). "The Monro-Kellie hypothesis: applications in CSF
volume depletion".
Neurology. 56 (12): 1746–8.

COMMON COMPLICATIONSAND CHALLENGES
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 Seizures
 Infections
 Nerve damage
 Post Traumatic Hydrocephalus
 Cognitive disabilities
 Language difficulties
 Personality changes
 Sensory problems
 Post-concussion syndrome
 Psychosocial problems
 Coma and Death

SCALP INJURIES
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• Scalp injuries are usually the result of direct
impact.
• May manifest as abrasion, bruising,
laceration, subcutaneous hemorrhage or
edema (caput succedaneum); subgaleal
hemorrhage or a subperiosteal hemorrhage
(cephalohematoma).
SHORT PRACTICE of SURGERY Bailey & Love’s 27th EDITION, 2018

Subgaleal hematoma
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• Scalp bleeding in the potential space between the periosteum and the galea
aponeurosis.
• Rupture to emissary veins which drain the scalp veins into the dural sinuses.
• Superficial to the periosteum, able to cross suture lines and canvas the
entire skull.
• A fluctuant scalp mass with increasing head circumference may be seen on
palpation.
• Management consists of vigilant observation over days to detect
progression. Fluid bolus may be required if blood loss is significant and
patient becomes tachycardic. Transfusion may be necessary.
Dr Jeremy Jones et al

SKULL VAULT FRACTURES
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 Closed linear fractures are managed conservatively.
 Open or comminuted fractures should be considered
for debridement and antibiotic therapy.
 Depressed fractures involve inward displacement of
a bone fragment by at least the thickness of the
skull.
• Usually open fractures, and are associated with a
high incidence of infection, neurological deficit
and late-onset epilepsy.
• Require exploration and elevation, especially
where intracranial air is present indicating a
breach in the dura mater.
 Fractures that involve the air sinuses should be
managed as open fractures.

SKULL BASE FRACTURES
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 Battle’s sign, periorbital bruising and blood in
ears/nose/ mouth, otorrhoea, rhinorrhea
 May be complicated by pituitary dysfunction, arterial
dissection or cranial nerve deficits, with anosmia,
facial palsy or hearing loss typically.
 CSF leak generally resolves spontaneously but
persistent leak can result in meningitis so repair may
be required.
 Blind nasogastric tube placement is contraindicated in
these patients.

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Basilar Skull Fractures
RACHEL BRIDWELL

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• Broad spectrum antibiotics.
• Head elevation to 30 degrees.
• Avoid blowing of nose.
• If leak persists for more than 72 hours then, lumbar
drain may be effective in reducing intra-cranial
pressure.
• Surgical repair
Management of CSF Leak:

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COUP & CONTRECOUP INJURIES
• Coup injury occurs at the site of impact and Contrecoup
injury occurs at sites remote from, and classically
opposite to the actual impact site on the head.
• Contrecoup injuries classically occur when the moving
head strikes a stationary object, as the skull and brain
accelerate and then decelerate out of synchrony with each
other.
• Classic evidence of both is intracerebral hemorrhage or
contusion in a focal area noted on CT scan or MRI scan.
• Contrecoup injury has also been considered to play a role
in visual abnormalities following minor head injuries.
Contrecoup Brain Injury
William N. Payne; Andrew N. Payne.

CONCUSSION
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 A clinical syndrome characterized by immediate and
transient alteration in brain function, including
alteration of mental status and level of consciousness,
resulting from mechanical force or trauma.
 Symptoms:
• Prolonged headache
• Visual disturbances
• Dizziness
• Nausea or vomiting
• Impaired balance
• Confusion
• Memory loss
• Ringing ears
• Difficulty concentrating
• Sensitivity to light
• Loss of smell or taste AMERICAN ASSOCIATION OF NEUROLOGICAL SURGEONS
The standard treatment for concussion is
rest. For headaches, acetaminophen can
be taken.

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SECOND IMPACT SYNDROME
• It is claimed that while symptomatic following a head injury, patients may be
especially vulnerable to repeat impacts.
• It is proposed that in the context of disordered cerebral autoregulation, a second
minor injury may trigger a form of malignant cerebral oedema refractory to
treatment.
POSTCONCUSSIVE SYNDROME
• Symptoms persisting for a prolonged period after injury.
• Headache, dizziness and disorders of hearing and vision.
• Difficulty with concentration and recall, insomnia, emotional lability, fatigue,
depression and personality change.

CEREBRAL CONTUSIONS
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• Bruising of brain tissue.
• Occur predominantly where brain is in contact with the irregularly ridged
bone, i.e. At the inferior frontal lobes and temporal poles.
• ‘Coup contre-coup’ contusions
• Appear heterogenous on CT, reflecting their composition of injured brain
matter interspersed with acute blood.
• Numerous small contusions from broken capillaries that occur in grey
matter are called Multiple Petechial Hemorrhages Or Multifocal
Hemorrhagic Contusion.

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Hallmarks of a Contusion
• Changes in cognition such as alterations in personality, or reduction in intelligence.
• Difficulty understanding speech.
• Memory challenges.
• Localized numbness or tingling.
• Difficulty coordinating movements
• Difficulty speaking.
• Problems with attention.
Treatment aims to prevent cerebral swelling.
• Measures include prevention of hypotension, hyponatremia and hypercapnia.
• Increased ICP might require surgery for evacuation.
Khoshyomn S, Tranmer BI (May 2004). "Diagnosis and management of
pediatric closed head injury". Seminars in Pediatric Surgery.

CEREBRAL LACERATION
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• Occurs when the tissue of the brain is mechanically cut
or torn.
• The pia-arachnoid membranes are torn over the site of
injury in laceration and are not torn in contusion
• Patients may have a lucid interval
• The level of consciousness decreases as the laceration
bleeds and blood begins to build up within the skull
• Frequently accompany skull fractures
• If bleeding and swelling in the brain are minor, patient
is kept under observation
• If bleeding is severe, patient is admitted to an ICU

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The injury is a contusion if two thirds or less of the
tissue involved is blood and a hemorrhage otherwise.
Khoshyomn S, Tranmer BI (May 2004). "Diagnosis and management of
pediatric closed head injury". Seminars in Pediatric Surgery.

EPIDURAL / EXTRADURAL HEMATOMA
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• A neurosurgical emergency.
• Results from rupture of an artery, vein or venous sinus, in
association with a skull fracture.
• Classical - Fracture of the thin squamous temporal bone,
with associated damage to the middle meningeal artery.
• Transient loss of consciousness, subsequent lucid interval
with headache but without any neurological deficit.
• There is contralateral hemiparesis, reduced conscious level
and ipsilateral pupillary dilatation, the cardinal signs of
brain compression and herniation.

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• On CT, appear as a lentiform, hyperdense lesion
between skull and brain, constrained by the adherence
of the dura to the skull.
• Compression of surrounding brain and midline shift.
• Areas of mixed density suggest active bleeding.
• A skull fracture will usually be evident.
• Extradural hematoma mandates immediate evacuation
in deteriorating or comatose patients or those with
large bleeds.

ACUTE SUBDURAL HEMATOMA
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It is encountered in two broadly distinct contexts
Firstly, high-energy injury mechanisms can
result in the rupture of cortical surface vessels.
This results in expanding hematoma with rapid
deterioration and raised ICP, without the lucid
interval.
These collections require prompt evacuation,
typically by craniotomy or craniectomy.

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Second group of patients, older and often
anticoagulated, a lower-energy injury leads to venous
bleeding around the brain.
The resulting hematoma may be acute or chronic
subdural hematoma
Bleeds of significant size require urgent evacuation.
Smaller bleeds in neurologically stable patients may be
managed conservatively
Right-sided acute subdural hematoma (hyperdense).
The substantial midline shift is seen.

CHRONIC SUBDURAL HEMATOMA
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It is a common cause of acute neurological
deterioration in the elderly.
Cerebral atrophy results in stretching of cortical –
dural bridging veins, which are vulnerable to
rupture.
The resulting hematoma can expand over days or
weeks by osmosis, ultimately producing
symptoms of raised ICP or focal deficits.
History of recent injury, but especially in the
context of antiplatelet or anticoagulant
medication.
Bilateral chronic subdural hematomas: the left is mixed density, the
hypodense material representing old blood and the higher density
indicating more recent bleeding. The bleed on the right is isodense,
indicating intermediate age.

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 Anticoagulation should be reversed
 Conservative management, with administration of
corticosteroids, can be considered for small bleeds
without symptoms or with headache alone.
 For the majority, drainage is performed using burr
holes.
 Urgency is dictated by the clinical condition of the
patient
 If clinically stable, a delay of 7–10 days may be
considered to allow platelet function to normalise
after withdrawal of aspirin/clopidogrel.
A superficial layer demonstrating residual hematoma after
evacuation of the CSDH, and a deep layer indicating recurrence :
DOUBLE-CRESCENT SIGN
Double-crescent sign as a predictor of chronic subdural hematoma recurrence
following burr-hole surgery
Koichi Miki MD et al

TRAUMATIC SUBARACHNOID HEMORRHAGE
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• Classic sign includes thunderclap headache which is a
feeling of being kicked on the head
• It is not usually associated with significant vasospasm,
which characterises aneurysmal subarachnoid
hemorrhage
• May present with photophobia and meningitis
• Managed conservatively

DIFFUSEAXONAL INJURY
35
• Seen in high-energy accidents, usually renders the
patient comatose.
• Result of traumatic shearing forces that occur when the
head is rapidly accelerated or decelerated
• Mechanical breaking of the axonal cytoskeleton,
decerebration or decortication
• It is strictly a pathological diagnosis made at
postmortem, but haemorrhagic foci in the corpus
callosum and dorsolateral brainstem on CT may be
suggestive, although the CT often appears normal.
• MRI is more sensitive than CT scans, but MRI may also
miss DAI
• DAI currently lacks a specific treatment

ASSESSMENT
Rule of “Three S”:
1. Simple to facilitate
2. Systematic
3. Standardized
36
Oral & maxillofacial trauma vol.1 3rd edition; Raymond J. Fonseca

HISTORY
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 History taking should include a witnessed account of the injury if possible.
 Red flag signs and symptoms:
• Loss of consciousness at any time.
• GCS <15 on initial assessment.
• Focal neurological deficit.
• Retrograde or anterograde amnesia.
• Persistent headache.
• Vomiting or seizures post injury.
 Previous neurosurgical intervention, use of anticoagulants, clotting disorders or alcohol excess,
patients aged > 65 years have a higher incidence of intracerebral haemorrhage following minor
falls.
https://www.gponline.com/emergency-medicine-assess-manage-head-
injuries/neurology/article/1016967

39
• In the setting of trauma, a neurologic
examination is focused on identifying and
assessing the function of vital portions of CNS
• This typically includes a physical examination
and a review of the patient's medical history,
but not deeper investigations such as
neuroimaging.
• Both a screening as well as investigative tool
• Primary focus on testing patient’s mental status,
CN, sensory exam, motor exam, and reflexes.
Clark A, Mesfin FB. Trauma Neurological Exam. [Updated 2019 May 11]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019

40
Mental Status
• The mental status examination assesses the level of consciousness or alertness, which then
permits a more detailed examination of cognitive function.
• Consciousness is awareness of the internal and external environments.
• An individual with a normal level of consciousness is “awake or can be easily awakened”,
“alert”, and “oriented”.
• Abnormal or depressed consciousness exists on a continuum ranging from mild sleepiness to
an unarousable unresponsive state (termed “coma”).
• Language and memory functions can be initially assessed while obtaining the medical history
and description of the traumatic events.

41
(Jennet and Teasdale in 1974)

42
When compared to GCS, the AVPU classification of alertness has been suggested to correspond in the following manner:
Alert = 15 GCS
Voice Responsive = 12 GCS
Pain Responsive = 8 GCS
Unconscious= 3 GCS
(Kelly, Upex and Bateman, 2004)

43
Sensory, Motor, and Reflexes
• The sensory exam, motor exam, and reflex testing of the extremities are important to
help identify the location and extent of an injury.
• Sensation changes, muscle weakness, or alterations in reflexes noticed during the post-
traumatic neurologic examination can be used to localize impairment to a potential
single peripheral nerve, peripheral plexus, or spinal nerve level.

44
CT
• Contiguous slices from vertex to foramen
Magnum.
• Extend to C3 if upper spine # suspected
• Brain, Blood and Bone windows
• Can miss # running parallel to CT slice
and located at vertex.
Indications
• Penetrating head trauma
• Basilar/ depressed skull #
• Posttraumatic seizure
• Severe head injury
In addition anyone with,
• Altered level of consiousness
• Focal deficits
• Persistent headaches/ repeated emesis
MRI • Better than CT in subacute and chronic phases
of injury to detect contusions/shearing in white
matter/corpus callosum
• Invaluable in spinal cord injury
Cerebral angiography • Carotid/vertebrobasilar dissections/occlusions
• Pesudoaneurysms
Textbook of Neurosurgery vol 2; Wilkins
NEURODIAGNOSTIC EVALUATION

45
SEVERITY OF HEAD INJURY
A Needs Review of Caregivers for Adults With Traumatic Brain Injury
Fed Pract. 2017 December;34(12):42-48
Author(s): Elisabeth M. Moy Martin et al

47
Emergency Neurological Life Support: Traumatic Brain Injury
Neurocritical Care, 2015
Rachel Garvin, Chitra Venkatasubramanian, Angela Lumba-Brown,

48
a)Restoration of blood pressure and oxygenation:
• Hypotension (SBP < 90 mmHg) or hypoxia (apnea, cyanosis or SPO2 < 90%) must be corrected
immediately
• MAP > 90 mmHg, through the infusion of fluids to attempt to maintain Cerebral Perfusion Pressure >
70 mmHg.
• Patients with GCS < 9 who are unable to maintain their airway or who remain hypoxemic despite
supplemental O2 require endotracheal intubation.
• PaO2 > 100 mm Hg.
• PCO2 = 35 to 40 mm Hg.
Head Injuries
Maj A Pushkarna·, Brig HS Bhatoe, VSM" Col SM Sudambrekar

49
• GCS 3-8, with abnormal CT scans
• Comatose patients with normal CT scans have a
much lower incidence of intracranial hypertension
unless they have two or more of the following
features:
• age over 40
• unilateral or bilateral abnormal motor
posturing
• a systolic blood pressure of less than 90
• Routine ICP monitoring is not indicated in patients
with mild or moderate head injury.
• ICP monitoring devices are usually continued for
≤1 week; with daily examination for glucose,
protein, blood cell count, Gram stain, culture and
sensitivity.
b) Indications for intracranial pressure monitoring:
Head Injuries

50
• An absolute ICP threshold that is uniformly applicable is
unlikely to exist.
• Current data, however, supports 20-25 mmHg as an upper
threshold above which treatment to lower ICP should
generally be initiated.
• Mannitol is effective (INITIAL BOLUS - 0.25 to 1g/kg, then
0.25-0.5g/kg every 2-6 hr)
• Indications to its use prior to ICP monitoring are signs of
herniation or neurological worsening.
• Hypovolemia should be avoided by fluid replacement
• Fluids: Only isotonic or hypertonic fluids (Ringer lactate,
0.9% Saline, 5% DNS)
c) Intracranial pressure treatment threshold:
Head Injuries
Management of Raised Intracranial Pressure, Naveen Sankhyan et al
Indian J Pediatr (2010)

51
d) Use of barbiturates in the control of intracranial hypertension:
• High-dose barbiturate therapy is efficacious in lowering ICP
• Utilization of barbiturates for the prophylactic treatment of ICP is not indicated.
e) Analgesia and Sedation :
• Narcotics, such as morphine, fentanyl and remifentanil, should be considered first line therapy
since they provide analgesia, mild sedation and depression of airway reflexes in patients who are
mechanically ventilated
• For sedation it is preferable to use agents with minimal effect on blood pressure.
• Short acting benzodiazepines (e.g. midazolam)
• If sedatives are not completely effective, then a neuromuscular blocking agent (e.g. Pancuronium,
atracurium, vecuronium) may be required.
Head Injuries
Management of Raised Intracranial Pressure, Naveen Sankhyan et al
Indian J Pediatr (2010)

f) Role of antiseizure prophylaxis following head injury:
• Prophylactic use of phenytoin, carbamazepine, phenobarbital or valproate, is not recommended
for preventing late post-traumatic seizures.
• Anti -convulsants may be used to prevent early PTS in patients at risk.
• Routine seizure prophylaxis later than 1 week following head injury is not recommended.
g) Nutrition:
• Replace 140% of resting metabolism expenditure in non-paralyzed patients and 100% in
paralyzed patients using enteral or parenteral formulas containing at least 15% of calories as
protein by day 7 after injury.
Head Injuries

53
h) Antibiotics:
• Broad-spectrum antibiotics should be administered to patients with penetrating injuries.
i) Surgical:
• Prevent infection and relieve/prevent intracranial hypertension.
• ICP monitoring devices placement and relief of ICP with craniotomy, craniectomy or
ventriculostomy
Head Injuries

EMERGENCY “BURR HOLE” CRANIOSTOMY
54
Wilson et al.: Emergency burr holes: “How to do it”.
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2012
Emergency procedure
Indications
• Epidural or subdural hematoma with midline shift on imaging and unequal pupils
on exam.
• GCS < 8
• Anticipated extended time to assessment/treatment by neurosurgeon.
Contraindications
• GCS > 8
• Neurosurgery available in reasonable timeframe
• Lack of imaging
*In absence of imaging, very high clinical suspicion may be enough.

55
Select optimal site based on location of hemorrhage on CT (if unsure, use temporal site)
• Temporal - 2 finger-breadths above and 2 finger-breadths forward of the auditory
canal
• Parietal - over parietal eminence
• Frontal - 10 cm above eye in mid-pupillary line (about 3 cm from sagittal suture)

CONCLUSION
58
Head injury is a devastating condition that
causes major psychosocial complications
and requires a multidisciplinary approach
for treatment to be effective.

REFERENCES
59
1. Traumatic Brain Injury (TBI) - Definition, Epidemiology, Pathophysiology, Segun Toyin Dawodu,
2. Estimating the global incidence of traumatic brain injury. Dewan MC et al. J Neurosurg. 2018 Apr 1:1-18
3. Epidemiology of traumatic brain injuries: Indian scenario. Gururaj G.Neurol Res. 2002 Jan;24(1):24-8. Review
4. Choonthar MM, Raghothaman A, Prasad R, Pradeep S, Pandya K. Head Injury- A Maxillofacial Surgeon's
Perspective. J Clin Diagn Res. 2016;10(1):ZE01–ZE6
5. Cerebral Autoregulation, S.-H. Yang, R. Liu, in Primer on Cerebrovascular Diseases (Second Edition), 2017
6. Mokri B (June 2001). "The Monro-Kellie hypothesis: applications in CSF volume depletion". Neurology.
7. SHORT PRACTICE of SURGERY Bailey & Love’s 27th EDITION, 2018
8. Basilar Skull Fractures, RACHEL BRIDWELL
9. Contrecoup Brain Injury, William N. Payne; Andrew N. Payne
10. AMERICAN ASSOCIATION OF NEUROLOGICAL SURGEONS
11. Khoshyomn S, Tranmer BI (May 2004). "Diagnosis and management of pediatric closed head injury". Seminars
in Pediatric Surgery.
12. Oral & maxillofacial trauma vol.1 3rd edition; Raymond J. Fonseca
13. https://www.gponline.com/emergency-medicine-assess-manage-head-injuries/neurology/article/1016967
14. Clark A, Mesfin FB. Trauma Neurological Exam. [Updated 2019 May 11]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2019
15. Textbook of Neurosurgery vol 2; Wilkins

60
16. A Needs Review of Caregivers for Adults With Traumatic Brain Injury, Fed Pract. 2017 December;34(12):42-48
Author(s): Elisabeth M. Moy Martin et al
17. Head Injuries, Maj A Pushkarna·, Brig HS Bhatoe, VSM" Col SM Sudambrekar
18. Emergency Neurological Life Support: Traumatic Brain Injury, Neurocritical Care, 2015, Rachel Garvin,
Chitra Venkatasubramanian, Angela Lumba-Brown
19. Wilson et al.: Emergency burr holes: “How to do it”.
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine 2012
20. Management of Raised Intracranial Pressure, Naveen Sankhyan et al Indian J Pediatr (2010)

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