HEAD INJURIES
 US: ~10 million head injuries occur annually
- 20%: Serious enough to cause brain damage
 Chief cause of death in men >35 years
- Accidents, usually motor vehicle collisions
- 70%: Involve head injury
 IMPORTANT considerations
1. Spinal injury often accompanies head injury, and
care must be taken in handling the patient to prevent
compression of the spinal cord d/t instability of the
spinal column;
2. Intoxication is frequently associated with traumatic
brain injury, thus, testing for drugs and alcohol should
be carried out when appropriate;
3. Additional injuries, including rupture of abdominal
organs, may produce vascular collapse, shock, or
respiratory distress that require immediate attention
TYPES OF HEAD INJURIES
CONCUSSION
 Minor injury
 Past definition: Immediate and transient loss of con-
sciousness associated with a short period of amnesia
 Other definition: Dazed or confused, or feel stunned,
or “star struck”
 Current definition: All such cognitive and perceptual
changes experienced after a blow to the head
 Severe concussion
- May precipitate a brief convulsion
- Autonomic signs: facial pallor, bradycardia,
faintness with mild hypotension, or sluggish pupil
lary reaction
- Most patients quickly return to a neurologically
normal state
 Mechanics of a typical concussion
- Sudden deceleration of the head when hitting a
blunt stationary object
- Anterior-posterior movement of the brain within
the skull
- D/t inertia and rotation of the cerebral
hemispheres on the fulcrum of the rela
tively fixed upper brainstem
- Loss of consciousness
- Transient electrophysiologic dysfunction
of the reticular activating system in the
upper midbrain that is at the site of rota
tion
- Transmission of a wave of kinetic energy
throughout the brain
 Diagnostics
- (-) Gross and light-microscopic changes
- (+) Biochemical and ultrastructural changes,
e.g. mitochondrial ATP depletion and local dis
ruption of the BBB
- Normal CT and MRI
- Patients may have skull fracture, an intracranial
hemorrhage, or a brain contusion
Harrison’s Principles of Internal Medicine, 19th ed.
 Retrograde and anterograde amnesia
- Brief period characteristic of concussion
- Recedes rapidly in alert patients
- Extent of retrograde amnesia = Severity of injury
- Unknown mechanism
 Hysterical post-traumatic amnesia
- Not uncommon after head injury
- Should be suspected if
(+) Inexplicable behavioral abnormalities, e.g.
recounting events that cannot be recalled on
later testing, a bizarre affect, forgetting one’s
own name, or a persistent anterograde deficit
that is excessive in comparison with the degree of
injury
 A single, uncomplicated concussion only infrequently
produces permanent neurobehavioral changes in
patients who are free of preexisting psychiatric and
neurologic problems
 Mechanism of blast injury effect to the brain
- A problem mainly in military medicine
- Causes symptoms associated with concussion
- Energy of a blast wave ca enter the cranium
through the openings of the orbits, auditory ca
nals, and foramen magnum
- Not consistent changes in cerebral imaging
studies, but with subtle indications of tissue disrupt
tion
CONTUSION, BRAIN HEMORRHAGE,
AND AXONAL SHEARING LOSS
Contusion
 Surface bruise of the brain
 With varying degrees of petechial hemorrhage, ede-
ma, and tissue destruction
 Mechanisms
- D/t mechanical forces that displace and com
press the hemispheres forcefully
- D/t deceleration of the brain against the inner
skull
- Coup lesion: Under a point of impact
- Contrecoup lesion: Antipolar area, as
the brain swings back
- May be d/t trauma sufficient to cause pro
longed consciousness
 Blunt deceleration impact
- E.g. against an automobile dashboard or from
falling forward onto a hard surface
- Causes contusions on the orbital surfaces of the
frontal lobes and the anterior and basal portions
of the temporal lobes
 Lateral forces
- E.g. Impact on an automobile door frame
- Contusions on the lateral convexity of the hemi
sphere
LVLabsan / MD-MPAIII
 HEAD INJURIES

 Clinical signs of contusion = Location and size of le- Diffuse Axonal Injury (DAI)
sion
- Often no neurologic abnormalities  Presence of widespread multifocal axonal damage in
- Injured regions are later sites of gliotic scars that both hemispheres
may produce seizures - Proposed to explain persistent coma and the
Moderately sized-contusions (+) Hemiparesis of gazeprefer- vegetative state after closed head injury
ence - Alternative explanation: Small ischemic hemor
rhagic lesions in the midbrain and thalamus
Large bilateral contusions (+) Stupor with extensor pos-
turing  Deep white matter lesion with widespread mechani-
Frontal lobe contusions (+) Taciturn state cal disruption, or shearing, of axons at the time of im-
pact
- Most characteristic: Small areas of tissue injury in
Temporal lobe contusions (+) Delirium or an aggressive the corpus callosum and dorsolateral pons
combative syndrome
 CT scan
 Acute contusions easily visible on CT and MRI scans - Visualize only severe shearing lesions that con
- CT: Inhomogeneous hyperdensities tain blood, usually in the corpus callosum and
- T2 and fluid-attenuated inversion recovery centrum semi-ovale
(FLAIR) MRI sequences: Hyperintensities
(+) Surrounding localized brain edema
(+) Subarachnoid bleeding

 Special MRI sequences

 Blood in the CSF d/t trauma may provoke a mild in-
flammatory reaction
 Contusions acquire a surrounding contrast enhance-
ment and edema which may be mistaken for tumor or
abscess
 Plaques jaunes
- Chronic, scarred, hemosiderin-stained depress
sions on the cortex
- D/t glial and macrophage reactions
- Main source of post-traumatic epilepsy
Brain Hemorrhage
 Torsional or shearing forces within the brain cause
hemorrhage of the basal ganglia and other deep re-
gions
 Large hemorrhage after minor trauma = Bleeding di-
athesis or cerebrovascular amyloidosis
 Deep cerebral hemorrhages may not develop until
several days after the injury
(+) Sudden neurologic deterioration in a coma
tose patient
(+) Sudden rise in ICP
- May detect small amounts of blood
 Diffusion tensor imaging
- Demonstrate numerous such lesions throughout
the white matter
SKULL FRACTURES
 D/t a blow to the skull that exceeds the elastic toler-
ance of the bone
- 2/3: Accompanied by intracranial lesions
- May increase chances of an underlying subdue
ral or epidural hematoma
 Fractures = Markers of the site and severity of injury
(+) Torn arachnoid membrane
- Fractures provide potential pathways for
entry of bacteria to the CSF with a risk of
meningitis and for leakage of CSF out
ward through the dura
(+)CSF leakage
- Severe orthostatic headache d/t low
ered CSF pressure

Harrison’s Principles of Internal Medicine, 19th ed. LVLabsan / MD-MPAIII

 HEAD INJURIES
 Most fractures are linear and extend from the point of
impact toward the base of the skull
Basilar skull fractures
 Often extensions of adjacent linear fractures over the
convexity of the skull
 May occur independently owing to stresses on the
floor of the middle cranial fossa or occiput
 Usually parallel to the petrous bone or along the
sphenoid bone and directed toward the sella turcica
and ethmoidal groove
 May cause CSF leakage, pneumocephalus, and de-
layed cavernous-carotid fistulas
 Associated features
- Hemotympanum: Blood behind the tympanic
membrane
- Battle sign: Ecchymosis over the mastoid pro
cess
- Raccoon sign: Periorbital ecchymosis
 CSF may leak through the cribriform plate or the adja-
cent sinus and cause CSF rhinorrhea
- Persistent rhinorrhea and recurrent meningitis =
Surgical repair of torn dura underlying the fracture
- Diagnostics to identify site of leak
- Installation of water-soluble contrast into
the CSF followed by CT with the patient in
various positions
- Injection of radionuclide compounds or
fluorescein into the CSF and insertion of
absorptive nasal pledgets
Sellar fractures
 May be radiologically occult or evident only by an air
-fluid level in the sphenoid sinus
 Fractures of the dorsum sellae = 6th or 7th nerve pal-
sies or optic nerve damage
Petrous bone fractures
 Along the long axis of the bone: Associated with faci-
al palsy, disruption of ear ossicles, and CSF otorrhea
 Transverse petrous fractures: Less common; Almost
always damage the cochlea or labyrinths and facial
nerve
 May cause external bleeding from the ear
Frontal bone fractures
 Usually depressed, involving the frontal and paranasal
sinuses and the orbits
 Depressed fractures
- Compound
- May be asymptomatic because the impact en
ergy is dissipated in breaking the bone
- Some have underlying brain contusions
 Management
- Debridement and exploration of compound
fractures to avoid infection
- Simple fractures do not require surgery
Harrison’s Principles of Internal Medicine, 19th ed.
CRANIAL NERVE INURIES
 Most often injured cranial nerves
- Olfactory nerve
- Optic nerve
- Oculomotor nerve
- Trochlear nerve
- First and second branches of trigeminal nerve
- Facial and auditory nerves
Anosmia and Loss of taste
 Loss of taste: Loss of perception of aromatic flavors,
with retained elementary taste perception
 ~10% of people with serious head injuries, particularly
from falls on the back of the head
 Result of displacement of the brain and shearing of
the fine olfactory nerve filaments that course through
the cribriform bone
 Bilateral anosmia for several months: Poor prognosis
Optic nerve injuries
 Partial injuries d/t closed trauma = Blurring of vision,
central or paracentral scotomatas, or sector defects
 Direct orbital injury = Short-lived blurred vision for close
objects d/t reversible iridoplegia
Trocheal nerve damage
 Indicated by diplopia limited to downward gaze and
corrected when the head is tilted away from the side
of the affected eye
Facial nerve injury
 D/t basilar fracture: Present immediately in up to 3% of
severe injuries, and may be delayed for 5-7 days
 Usually d/t fractures of the petrous bone, particularly
the less common transverse type
 Delayed facial palsy (>1 week): Good prognosis
Vestibulocochlear nerve injury
 D/t fracture of the petrous bone
 (+) Loss of hearing, vertigo, and nystagmus immedi-
ately after injury
 Deafness: Rare; Must be distinguished from blood in
the middle ear or disruption of the middle ear ossicles
 Dizziness, tinnitus, and high-tone hearing loss: D/t
cochlear concussion, most typically after blast injury
SEIZURES
 Convulsions: Uncommon
 Brief period of tonic extensor posturing or a few clonic
movements of the limbs just after the moment of im-
pact
 Cortical scars from contusions: Highly leptogenic and
may later manifest as seizures
 Severity of injury = Risk of future seizures
(+) Brain injury, subdural hematoma, or prolonged
loss of consciousness: 17% risk of seizures
(+) Mild injury: <2% risk of seizures, usually within 5
years to decades
LVLabsan / MD-MPAIII
(+) Penetrating injuries: Higher risk of epilepsy
 HEAD INJURIES

SUBDURAL AND EPIDURAL HEMATOMAS

 Hemorrhages
- Subdural: Beneath the dura
- Epidural: B/w the dura and skull
 Mass effect and raised ICP may be life-threatening
 Management: Identify rapidly by CT or MRI scan and remove them when appropriate

SUBDURAL HEMATOMA
ACUTE SUBDURAL HEMATOMA CHRONIC SUBDURAL HEMATOMA EPIDURAL HEMATOMA
ETIOLOGY
- Direct cranial trauma: Minor; Not re- - Hx of trauma may or may not be elicited - Evolve more rapidly than subdural
quired for acute subdural hemorrhage - Injury may be trivial and forgotten, par- hematomas
to occur, especially in the elderly and ticularly in the elderly and those with clot- - ~10% of severe head injuries
those taking anticoagulant ting disorders - Less often associated with underlying
medications cortical damage than subdural hema-
- May be d/t acceleration force tomas
- Larger hematomas: Venous origin

- Lucid interval lasting minutes to hours
before coma supervenes, but most are
drowsy or coma tose from the moment
of injury
- Unilateral headache and slightly en-
larged pupil on the side of the hemato-
ma
- Larger hematomas: Stupor or coma,
hemiparesis, and unilateral pupillary
enlargement
- Subacutely evolving syndrome:
Drowsiness, headache, confusion, or
mild hemiparesis, usually in alcoholics
and in the elderly and often after only
minor or unnoticed trauma
SYMPTOMS
- Headache: Common but not invariable; - Most patients are unconscious when
Fluctuates in severity, sometimes with first seen
changes in head position - Most characteristic: “Lucid interval” of
- Slowed thinking, vague change in per- several minutes to hours before coma
sonality, seizure, or a mild hemiparesis supervenes
- Bilateral chronic subdural hematoma:
Initial clinical impression ~stroke, brain tu-
mor, drug intoxication, depression, or a
dementing illness; With low tolerance for
surgery, anesthesia, and drugs that de-
press the nervous system; drowsiness or
confusion persists post-operatively
- Drowsiness, inattentiveness, incoherence
of thought
- Brief episodes of hemiparesis or aphasia

IMAGING STUDIES

Harrison’s Principles of Internal Medicine, 19th ed. LVLabsan / MD-MPAIII


SUBDURAL HEMATOMA
ACUTE SUBDURAL HEMATOMA CHRONIC SUBDURAL HEMATOMA
IMAGING STUDIES
- Crescentic collections over the con-
vexity of one or both hemispheres
- Most common: Frontotemporal region
- Less often: Inferior middle fossa or
over the occipital poles
- Interhemispheres, posterior fossa, or
bilateral convexity hematomas: Less
frequent; Difficult to diagnose clinically
- Acute deteriorating patient: Burr
(drainage) holes or an emergency cra-
niotomy
- Small subdural hematomas: May be
asymptomatic and usually do not re-
quire evacuation if they do not enlarge
Harrison’s Principles of Internal Medicine, 19th ed.
HEAD INJURIES
SUBDURAL AND EPIDURAL HEMATOMAS
EPIDURAL HEMATOMA
- Crescentic clots over the convexity of
one or both hemispheres, most commonly
in the frontotemporal region
- CT w/o contrast:
- Initial: Low-density mass over the
convexity of the hemisphere
- 2-6 weeks after initial bleeding:
Clot becomes isodense compared
to adjacent brain and may be
inapparent
- Week-old hematoma: Areas of
blood and intermixed serous fluid
- Bilateral chronic subdural hematoma
- May not be detected in CT d/t
absence of lateral tissue shifts
- Older patient: Hypernormal CT
scan with fullness of the cortical
sulci and small ventricles
- Infusion of contrast material
- Enhancement of the vascular
fibrous capsule surrounding the
collection
- MRI: Identifies subacute and chronic
hematomas
- Very chronic subdural hematomas are
difficult to distinguish from hygromas
- Hygromas: CSF collection from a rent
in the arachnoid membrane
MANAGEMENT
- Clinical observation & serial imaging - Rapid surgical evacuation and liga-
- Minimally symptomatic chronic subdural tion or cautery of the damaged vessel,
hematoma: Glucocorticoids; Surgical usually the middle meningeal artery,
evacuation (often successful) that has been lacerated by an overly-
- Fibrous membranes that grow from the ing skull fracture
dura and encapsulate the collection re-
quire removal to prevent recurrent fluid
accumulation
- Small hematomas: Resorbed, leaving
organizing membranes
LVLabsan / MD-MPAIII
 HEAD INJURIES
CLINICAL SYNDROMES AND TREATMENT OF HEAD INJURY
MINOR INJURY
 Typical concussion syndrome
- Brief loss of consciousness or stunned after a mi
nor head injury
- Becomes fully alert and attentive within minutes
- Complaints: Headache, dizziness, faintness, nau
sea, single episode of emesis, difficulty with con
centration, a brief amnestic period, or slight blur
ring of vision
- Good prognosis with little risk of subsequent de
terioration
 Children: Prone to drowsiness, vomiting, and irritability
 Vasovagal syncope may cause undue concern
 Generalized or frontal headache
- May be migranous (throbbing or hemicranial) or
aching and bilateral
 Persistent severe headache and repeated vomiting
with normal alertness and no focal neurologic signs
- Usually benign
- CT should be obtained
- Longer period of observation
 Imaging tests
- Decision to perform = Clinical signs
- Severe impact: E.g. persistent confusion,
periorbital or mastoid hematoma, re
peated vomiting, palpable skull fracture
- Seriousness of other bodily injuries
- Degree of surveillance that can be an
ticipated after discharge
- Sensitive (but not specific) indicators of intracra
nial hemorrhage that justify CT scanning
- Older age
- 2 or more episodes of vomiting
- >30 minutes of retrograde or persistent
anterograde amnesia
- Seizure
- Concurrent drug or alcohol intoxication
 Management: After several hours of observation, pa-
tient may be accompanied home and observed, with
written instructions to return if symptoms worsen
Concussion in Sports
 Management
- Remove the individual from play immediately
- Avoid contact sports for at least several days
after a mild injury
- Avoid contact sports for a longer period if there
are more severe injuries or if there are protracted
neurologic symptoms, e.g. headache and diffi
culty concentrating
 Younger athletes are particularly likely to experience
protracted concussive symptoms, and a slower return
to play
Harrison’s Principles of Internal Medicine, 19th ed.
 Second impact syndrome
- Diffuse and fatal cerebral swelling following a
second minor head injury
 Dementia pugilistica
- Mental decline in boxers late in their careers
- Delayed progressive cognitive disorder d/t dep
osition of tau protein in cortical neurons
 Chronic traumatic encephalopathy (CTE)
- Brains display deposition of tau protein in the
superficial cortical layers, and particularly in the
depths of sulci within the frontal cortices
INURY OF INTERMEDIATE SEVERITY
 Patients not fully alert or have persistent confusion,
behavioral changes, extreme dizziness, or focal neu-
rologic signs, e.g. hemiparesis
- Management: Admitted to the hospital and
have cerebral imaging
- Usual finding: Cerebral contusion or hematoma
 Common syndromes
Anterior temporal lobe Delirium with a disinclination to be
contusions examined or moved, expletive
speech, and resistance if disturbed
Inferior frontal and Quiet, disinterested, slowed mental
frontopolar contusions state (abulia) alternating with irasci-
bility
Subdural hematoma Focal deficit, e.g. aphasia or mild
or convexity contu- hemiparesis
sion or, less often, ca-
rotid artery dissection
Several types of inju- Confusion and inattention, poor
ries and medial frontal performance on simple mental
contusions and inter- tasks, and fluctuating orientation
hemispheric subdural
hematoma
Labyrinthine concus- Repetitive vomiting, nystagmus,
sion, but occasionally drowsiness, and unsteadiness
d/t posterior fossa
subdural hematoma
or vertebral artery dis-
section
Damage to the medi- Diabetes insipidus
an eminence or pitui-
tary stalk
 Blast injuries are often accompanied by rupture of the
tympanic membranes
 Management: Surgical removal of hematomas
- First week: State of alertness, memory, and other
cognitive functions often fluctuate; Agitation,
somnolence
LVLabsan / MD-MPAIII
 HEAD INJURIES

 Behavioral changes tend to be worse at night POST-CONCUSSION SYNDROME

- May be treated with small doses of antipsychot
ic medications  State following minor head injury
 (+) combination of fatigue, dizziness, headache, and
SEVERE INJURY difficulty in concentration
 Simulates asthenia and anxious depression
 Patients who are comatose from the moment of injury
 Proposed mechanism for the cognitive symptoms
require immediate neurologic attention and resuscita-
- Subtle axonal shearing lesions or as yet unde
tion
fined biochemical alterations
 Assessment: Done after intubation
 Moderate and severe trauma
- Depth of coma
- Neuropsychological changes, e.g. difficulty with
- Pupillary size and reactivity
attention and memory and other cognitive defi
- Limb movements
cits
- Babinski responses
- Testing scores tend to improve rapidly during the
first 6 months after injury and them more slowly for
 Management
Years
- Transfer to critical care unit: As soon as vital
functions permit and cervical spine x-rays and a
 Management
CT scan have been obtained
- Identification and treatment of each separate
- Hypoxia: Reversed
element of depression, sleeplessness, anxiety, per
- Normal saline: Resuscitation fluid vs. albumin
sistent headache, and dizziness
- (+) Epidural or subdural hematoma or large in
- Care is taken to avoid prolonged use of drugs
tracerebral hemorrhage: Prompt surgery and in
that produce dependence
tracranial decompression
- Headache: Acetaminophen, amitriptyline
- Measurement of ICP with a ventricular catheter
- Dizziness: Vestibular exercises and small doses of
or fiberoptic device: Has not improved outcome
vestibular suppressants, e.g. promethazine
- Hyperosmolar IV solutions: Limit ICP
(Phenergan)
- Removing portions of the skull in order to de
- Difficulty with memory or with complex cognitive
compress the intracranial contents: Successful for
tasks at work may be reassured that these prob
brain swelling after cerebral infarction; Not prov
lems usually improve over 6-12 months, and work
en effective for TBI
load may be reduced in the interim
- Prophylactic antiepileptic medications
- Serial and quantified neuropsychological test
ing: Adjust the work environment to the patient’s
Grading and Prognosis
abilities and to document improvement over time

 Good prognosis: Previously energetic and resilient

individuals
 Patients with persistent symptoms: Possibility of malin-
gering or prolongation as a result of litigation

 >85% of patients with GCS <5 die within 24 h

 Patients <20 y/o, particularly, may make remarkable
recoveries after having grave early neurologic signs
 Poor prognosis
- Older age
- Increased ICP
- Early hypoxia or hypotension
- Compression of the brainstem on CT or MRI
- Delay in the evacuation of large intracranial
hemorrhages
Harrison’s Principles of Internal Medicine, 19th ed. LVLabsan / MD-MPAIII