Lecture 23: Traumatic Brain Injury

Types of skull fracture

Basal skull fracture

the absence of fracture does not mean the absence of brain injury

basal skull fracture easy to miss on CT

occult signs of basal skull fracture (revealed by PE):

leakage of CSF (otorrhea, rhinorrhea)

signs of cranial nerve damage (esp. I, VII, VIII)

characteristic accumulations of blood:

postauricular ecchymosis (Battle’s sign):

bruising over the mastoid process as a

result of extravasation of blood along the path of the posterior auricular artery or sigmoid sinus; indicative of fracture of middle cranial fossa

periorbital ecchymosis (raccoon eyes):

purplish discoloration around the eyes

following fracture of the frontal portion

of the skull base

Basal skull fractures and cranial nerve injuries

Contusion Overview

contusion

contusion

contusion

Contusions in gross anatomy

most commonly injured areas are orbitofrontal and anterior temporal lobes

contusion of occipital lobes and cerebellum rare due to smooth inner table of skull posteriorly

focal neurological deficits related to the site of impact

contused cortex diffusely swollen and hemorrhagic

lesions enlarge over several hours as a result of further hemorrhage

contusions typically involve crests of

gyri; often superficial, involving only

gray matter but may extend into

underlying white matter

Contusion CT findings

lesions appear as edematous regions of cortex and subcortical white matter admixed with areas of increased density representing leaked blood

early response: within hours post-trauma, bleeding points in the contused area may appear small and innocuous

over time, may coalesce and appear as a single large clot or may appear as multiple contusions adjacent to bony prominences

delayed hematomas and edema are common sequelae that may develop up to days later

the mass effect of contusional swelling, if sufficiently large, becomes a major factor in the genesis of tissue shifts and elevated ICP

craniotomy and decompression of the swollen brain relieves the ICP, but has no effect on the focal neurological deficit

Acute brain contusion

smaller, subtle, right temporal cortical

contusion (short arrow) is noted, as

well as a small, left frontal subdural

hematoma (long arrow)

Acute brain contusion

subacute contusion

subacute contusion

acute subdural hematoma

acute subdural hematoma

acute subdural hematoma

intracranial lesions often associated with intracranial bleeding (typically related to meninges); SDH is the most common post-traumatic bleed; may be unilateral or bilateral

typically results from tearing of bridging veins

usually present in combination with other mechanisms of injury (contusions, diffuse axonal injury)

CT findings: hyperdense, crescent-shaped

patients may be stuporous or comatose on admission or they may be alert

if comatose: typically, immediate coma that deepens progressively; high overall mortality

disturbances of consciousness and mentation (inattentiveness, confusion, apathy) are more prominent than focal or lateralizing signs

aphasia possible, but rarely observed

homonymous hemianopia seldom observed because the optic radiation deep and not easily compressed

subacute SDH

subacute SDH

lot is initially hyperdense but becomes slowly more isodense after a period of one or more weeks

may be difficult to detect, except by the tissue shift that it causes

CT findings: isodense, clotted blood beginning to liquefy

generally related to mass effects (i.e., tissue shifts)

focal signs, when present, consist of mild hemiparesis (usually not complete paralysis)

dilation of ipsilateral pupil is a fairly reliable indicator of the side of the lesion

if the condition progresses, patient becomes stuporous or comatose

hemiparesis, dilation of I/L pupil, and

depressed consciousness = classic clinical triad of herniation

chronic SDH

chronic SDH

chronic SDH

traumatic etiology often less clear (especially in elderly)

if bilateral, no shift of tissue (effacement) apparent; mass effect can

produce herniation; compress upper brainstem

CT findings: uniform hypodense (if no further bleeding)

symptoms and signs develop over weeks and progressively worsen (mainly associated with elevated ICP)

headaches

light-headedness

slowness in thinking

apathy and drowsiness

unsteady gait

occasionally, seizures

epidural hematoma

epidural hematoma

epidural hematoma

typically arises with a temporal or parietal fracture and laceration of the middle meningeal artery, or, less commonly, a tear in a dural venous sinus

initial loss of consciousness may be brief, followed by a lucid interval before rapid neurological decline

CT findings: hyperdense, lens-shaped with smooth inner margin

signs and symptoms appear over a few hours (increase ICP)

headache of increasing severity

vomiting

drowsiness

confusion

aphasia

seizures (may be unilateral)

hemiparesis with slight hyperreflexia, Babinski

progression of signs indicates herniation and worsening of prognosis:

coma

hemiparesis becomes bilateral with spasticity and Babinski

ipsilateral pupil may dilate and be nonresponsive

decerebrate posturing may appear

intracerebral hemorrhage

intracerebral hemorrhage

intracerebral hemorrhage

intracerebral hemorrhage

intracerebral (or intraparenchymal) hemorrhage

hemorrhages associated with coup-contrecoup injuries; shearing forces produce bleeding within underlying white matter as well as in gray matter contused areas

may include petechial hemorrhages or larger confluent areas of hemorrhage

bleeding occurs in subcortical white matter of one lobe of the brain or in deeper structures such as basal nuclei or thalamus

similar to hypertensive brain hemorrhage (hemorrhagic stroke)

altered consciousness: stupor progressing to coma

hemiplegia, Babinski (unilateral or bilateral)

dilated pupil

stertorous and irregular respirations

stertor: noisy inspiration occurring in

coma or deep sleep (i.e., snoring)

traumatic subarachnoid hemorrhage

traumatic subarachnoid hemorrhage

Acute subdural hematoma

Subfalcine herniation

expanding supratentorial lesion presses the cerebral hemisphere

medially against the falx cerebri

particularly prominent in acute SDH; associated with midline shift

compression of cingulate gyrus, pericallosal, and callosomarginal

arteries

midline hemorrhage with cingulate

gyrus necrosis secondary to ACA infarct

Central herniation

CN Vi

Clivus

Uncus

Uncal herniation

expanding mass lesion located laterally in one cerebral hemisphere forces the medial edge of the temporal lobe to herniate over the free tentorial edge into the tentorial notch

PCA compressed between uncus and tentorium

key clinical presentation: CN III dysfunction (ipsilateral pupil fixed and

dilated); decreased level of consciousness; hemiplegia (may be

ipsilateral or contralateral)

Clinical triad: “blown” pupil hemiplegia coma

herniation syndromes summary

diffuse axonal injury

CT: widespread or patchy damage to the white matter and cranial nerves

Acute gliding brain contusion

gliding contusion is caused by displacement of cortical gray matter during angular acceleration of the head

most of the damage at junction between gray and white matter (account for ~2/3 of DAI lesions)

acute DAI

acute DAI

acute DAI

acute DAI

acute DAI

the brain is either normal or shows petechial hemorrhages in the corpus callosum (most vulnerable area because of falx cerebri) or brainstem due to tearing of blood vessels

Diffuse axonal injury

overall decrease in gross brain weight due to:

decreased volume of white matter

atrophy of the corpus callosum

compensatory dilation of the lateral ventricles

Microscopic changes: axonal swellings (retraction bulbs; particularly common in

corpus callosum, fornix, internal capsule, and brainstem)

Concussion

Pneumocephalus

Pneumocephalus

pneumocephalus: air within intracranial cavity

due to trauma or neurosurgical procedure (e.g., decompression)

can be acute (< 72 hours post-trauma) or delayed (> 72 hours post-trauma)

potential route for entry of bacteria into the cranium

tension pneumocephalus: when pneumocephalus results in increased ICP that leads to neurological deterioration (through mass effect)

headaches, nausea, vomiting, irritability, dizziness, seizures;

diminished level of consciousness; altered sensorium (inability to concentrate or think clearly) and CSF rhinorrhea or otorrhea

CT: subdural hypodensity of frontal area most common; followed by occipital and temporal areas

Mount Fuji sign: bi-frontal subdural collections that separate the frontal lobes

Post-concussion syndrome

Chronic traumatic encephalopathy

neurodegenerative disorder resulting from cumulative effects of repeated cerebral injuries

clinical features (progressive):

early deteriorations in attention, concentration, memory

disorientation and confusion

progresses to lack of insight, poor judgement, and overt dementia

dysarthric speech, dysphagia, ocular abnormalities (ptosis)

movements are slow, still, and uncertain, especially involving the legs

wide-based, shuffling gait

plantar reflexes may be extensor unilaterally or bilaterall

Chronic traumatic encephalopathy Imaging

Chronic traumatic encephalopathy

brown staining indicates tau pathology

Axotomy Overview

axotomy (damage to the axon) causes the neuronal cell body to undergo chromatolysis, characterized by:

cell swelling

nucleus moves to an eccentric position

fragmentation of RER (“loss” of Nissl substance)

increase in protein and RNA synthesis (e.g., GAP-43)

chromatolysis is reversible if successful regeneration occurs; if successful regeneration does not occur, the neuron will die because the cell body is deprived of target-derived trophic factors

if the injury damages the neuron cell body directly, the cell will die

Axotomy and chromatolysis

Axotomy and chromatolysis

Axotomy

results in division of the axon into two segments

proximal stump: remains attached to cell body

remains attached to the cell body; attempted growth and formation of retraction bulbs (characteristic histological feature of DAI)

distal stump: becomes disconnected from cell body; becomes detached from the cell body; undergoes Wallerian degeneration:

axon terminal degeneration

myelin fragmentation

phagocytosis of cellular debris (neutrophils, macrophages)

transneuronal degeneration

of pre- and post-synaptic neurons

synaptic stripping: retraction of presynaptic axon terminals from the dendrites or cell body of chromatolytic neurons; replaced by glial cells (microglia or astrocytes); decreases synaptic activity and impairs functional recovery

functional effect on post-synaptic neuron depends on the importance of the lost input to that cell; target cell may atrophy and die