NEUROTRAUMATOLOGY
Eva Vlčková
INCIDENCE
• TRAUMATIC BRAIN INJURIES : Incidence about 150 per 100.000 per year
• SPINAL CORD INJURIES: Incidence about 4 per 100.000 per year
Frequent cause of major disability
• occur at all ages
• peak is in young adults between the ages of 15 and 24 years
• Men are affected three or four times as often as women
• The major cause: motor vehicle accidents
In older adults falls
MAJOR CAUSE OF DEATH AND DISABILITY
• a major cause of death:
• especially in young adults younger than the age of 24 years)
• trend toward an increase of mortality rates from TBI among populations
aged older than 65 years.
• deaths have increased over the past decade
• a major cause of disability (mainly spinal cord injuries).
TYPES OF TBI
• skull fractures
• cerebral concussion and axonal-shearing injury (diffuse axonal injury)
• parenchymal contusion and intracerebral hematoma
• subdural hematoma (acute or chronic)
• epidural hematoma
• traumatic subarachnoid hemorrhage
SKULL FRACTURES
• linear, depressed, or comminuted types
• CLOSED (= SIMPLE, the broken bone doesn´t break the skin)
• OPEND (= COMPOUND, the scalp over the fracture is lacerated)
• = IMPORTANT MARKERS OF A POSSIBLY SERIOUS BRAIN INJURY
• rarely cause problems by themselves (the prognosis depends more on the nature and
severity of injury to the brain than on the severity of injury to the skull).
• LINEAR FRACTURES (80%) – incidate the need to perform CT (mostly otherwise normal),
• most common in the temporoparietal region, where the skull is thinnest
• Nondisplaced linear fractures are managed conservatively
DEPRESSED OR COMMINUTED FRACTURES
• IN DEPRESSED F. one or more fragments of bone are displaced inward, compressing
the underlying brain
• In 85% of cases, they are open and liable to:
become infected
leak cerebrospinal fluid (CSF)
underlying brain injury
tearing, compression, or thrombosis of underlying venous dural sinuses.
• In COMMINUTED F., there are multiple, shattered bone fragments, which may or
may not be displaced
• Even when closed, most of them require surgical exploration for debridement,
elevation of bone fragments, and repair of dural lacerations.
CEREBRAL CONCUSSION AND
AXONAL-SHEARING INJURY
• Frequent symptom of TBI = LOSS OF CONSCIOUSNESS at the moment of impact
• It is caused by acceleration–deceleration movements of the head, which result in
the stretching and shearing of axons
• The mechanism: transient functional disruption of the reticular activating system
caused by rotational forces on the upper brain stem
• the term CONCUSSION is used when the alteration of consciousness is brief (e.g.,
<6 hours),
• patients may be COMPLETELY UNCONSCIOUS or remain awake but appear DAZED;
• most RECOVER SPONTANEOUSLY WITHIN SECONDS OR MINUTES, rather than hours,
• some have RETROGRADE OR ANTEROGRADE AMNESIA surrounding the event.
• Only 5% of patients who sustained a concussion have an intracranial hemorrhage on CT
DIFFUSE AXONAL INJURY
• The term DIFFUSE AXONAL INJURY (DAI) is applied to traumatic coma lasting more
than 6 hours
• no other cause of coma is identified by CT or MRI
• common symptom = autonomic dysfunction (e.g., hypertension, hyperhidrosis,
hyperpyrexia), which may reflect brain stem or hypothalamic injury.
• those who recover may be left with severe cognitive and motor impairment,
including spasticity and ataxia
• the most important cause of persistent disability after traumatic brain damage.
PARENCHYMAL CONTUSION
• CEREBRAL CONTUSIONS are focal parenchymal hemorrhages that result from
scraping and bruising of the brain as it moves across the inner surface of the skull
• With lateral forces, contusions may occur at the site of the blow to the head (coup lesions) or
at the opposite pole as the brain impacts on the inner table of the skull (contrecoup lesions).
• The most common sites of contusion are the inferior frontal and temporal lobes, where brain
tissue comes in contact with irregular protuberances at the base of the skull
• Less frequently, the contusions may result of cuts from the sharp edges of
depressed skull fragments
• Contusions are mostly small and multiple, usually cortical
• Resemble bruised and bloodied brain tissue
• Contusions are often managed conservatively, recovery from one or more small
contusions may be excellent.
PARENCHYMAL CONTUSIONS
INTRACEREBRAL HEMATOMA
• May occute when rotational forces lead to tearing
of small- or medium-sized vessels within the
parenchyma
• Hematoma is the focal collection of blood clots
that displaces the brain
• located mostly in the deep white matter
• The large, parenchymal hematomas with mass
effect may require surgical evacuation.
SUBDURAL HEMATOMA
• usually arise from a venous source, with blood filling the potential
space between the dural and arachnoid membranes
• the bleeding is usually caused by movements of the brain within the skull that
leads to stretching and tearing of “bridging” veins that drain from the surface of
the brain to the dural sinuses.
• Mostly located over the lateral cerebral convexities, less frequenty in posterior
fossa, between hemispheres, along tentorium usw.
• CT = high-density, crescentic collection along the hemispheric convexity
• Most important risk factors:
• elderly or alcoholic patients with cerebral atrophy (SDH may result from trivial
impact or even only whiplash),
• coagulopathy (incl. oral anticoagulants) – associated with increased risk of death
SUBDURAL HEMATOMA
ACUTE SUBDURAL HEMATOMA
• ACUTE SUBDURAL HEMATOMAS - symptomatic within 72 hours of injury,
• most patients have neurologic symptoms from the moment of impact
• Most frequent after falls or assaults, relatively less common after car accidents
• Half of all patients with an acute SDH lose consciousness at the time of injury
• half of those who awaken lose consciousness for a second time after a “lucid interval”
of minutes to hours as the subdural hematoma grows in size
• the most common focal neurologic signs (each occuring in 1/2 to 2/3 of patients):
• Hemiparesis (usually contralateral) and pupillary abnormalities (mostly ipslateral)
• Sometimes the other way round (because uncal herniation may lead to compression of
the contralateral cerebral peduncle or third cranial nerve against the tentorial edge)
CHRONIC SUBDURAL HEMATOMA
• Become symptomatic after 21 days
• In 25% to 50% of cases, there is no recognized episode of head injury. In many
cases, chronic SDH results from trivial trauma
• Risk factors same as in acute SDH (cerebral atrophy, alcoholism, bleeding
disorders or use of anticoagulant medication and age - after age 50 years).
• The blood clott usually liquefies into a HYGROMA
• In most the cases, the symptoms are minimal (because the brain
accommodates the gradual buildup of mass effect) and may be restricted to
altered mental status
• CT typically shows an isodense or hypodense, crescent-shaped mass that
deforms the surface of the brain
TREATMENT OF ACUTE X CHRONIC SDH
• Symptomatic acute and chronic SDHs with significant mass effect should be
evacuated.
• In acute SDH, the blood is clotted and the surgical evacuation usually
requires a large-window craniotomy.
• Outcome after surgical evacuation depends primarily on the severity of
the initial deficit and the interval from injury to surgery.
• Liquefied chronic SDHs are usually evacuated with drainage of the
collections via a series of burr holes.
• Smaller, minimally symptomatic, subdural hematomas are managed
conservatively.
EPIDURAL HEMATOMA
• Rare complication of TBI - occurs in less than 1% of all TBI cases
• Bleeding into the epidural space
• Generally caused by a tear in the wall of one of the meningeal arteries, usually the
middle meningeal artery,
• in 15% of patients, the bleeding arises from a dural sinus.
• Seventy-five percent of patients are associated with a skull fracture.
• Most epidural hematomas are located over the convexity of the hemisphere in the middle
cranial fossa (occasionally in the anterior or posterior fossa).
• In most cases, the hematoma is ipsilateral to the site of impact.
• primarily a problem of young adults; rarely seen in the elderly because the dura becomes
increasingly adherent to the skull with advanced age.
EPIDURAL HEMATOMA
• in one-third of patients, proceeds from an immediate loss of
consciousness caused by concussion to a lucid interval and then to a relapse into
coma, with hemiplegia as the epidural hematoma expands.
• The ipsilateral pupil loses reactivity to light because the third cranial nerve is
stretched as the midbrain is displaced contralaterally. Later, it becomes fixed and
dilated as the third nerve is compressed by the hippocampal gyrus as it herniates over
the free edge of the tentorium.
• On CT, epidural blood takes on a bulging convex pattern, because the collection is
limited by firm attachments from the dura to the cranial sutures
• Progression (to herniation and death) may occur rapidly because the bleeding is
arterial.
• The mortality rate approaches 100% in untreated patients and ranges from 5% to 30%
in treated patients (the faster the treatment is, the better is a chance to recover)
• If there is little coexisting brain damage, functional recovery may be excellent.
EPIDURAL HEMATOMA
• Epidural hematoma on
CT
• CT with none window
shows two adjacent
fractures (arrows)
• The anterior one is at
the site of the groove
for the middle
meningeal artery
TRAUMATIC SUBARACHNOID HEMORRHAGE
• Some extravasation of blood into the subarachnoid spaces is to be expected
in any patient with head injury (mostly detecable only by CSF examination).
• with more serious injuries (when larger vessels traversing the subarachnoid
space are torn) focal or diffuse subarachnoid hemorrhage may be detected
by CT (in most the cases over the convexities – note the contrast to
spontaneous SAH, which is mostly distributed in basal cistern)
• Usually little clinical importance
• Large amount of blood in subarachoid space is a negative prognostic factor
• delayed complications of aneurysmal SAH, such as hydrocephalus and
ischemia from vasospasm, are unusual after traumatic SAH
TRAUMATIC SPINAL CORD INJURY
• A sudden event with possibly catastrophic effects
• May create a medical, financial, and social burden for the individual and society
• primarily affects young adults aged between 16 and 30 years, 79% are male
• The most frequent cause: motor vehicle accidents (42%), followed by falls, sport or workrelated
injuries and violence.
• Most injuries occur on the weekends and during the summer months.
• From the neurological point of view, they may lead to:
• Tetraplegia: incomplete (34%) or complete (18%)
• Paraplegia: incomplete (19%) or complete (23%)
• The level of affection identified by the sensory level. Frequent signs of dysautonomia.
• Less than 1% of persons experienced complete neurologic recovery by hospital discharge.
MECHANISM OF ACUTE SCI
• The two step process = involves primary and secondary mechanisms
• The primary mechanism results from the initial mechanical injury due to local
deformation and energy transformation
• Most commonly the combination of the initial impact as well as subsequent persisting
compression.
• Main primary mechanism: the impact of bone and ligament against the spinal cord
from high translational forces, such as that generated by flexion, extension, axial
rotation, or vertebral compression
• The spinal cord may consequently be compressed, stretched, or crushed by fracture
or dislocations
• Injury can result from only the initial impact without ongoing compression (as a
result of severe ligamentous injuries in which the spinal column dislocates and then
spontaneously reduces or when there is preexisting cervical spondylosis or spinal
stenosis)
SCI – SECONDARY MECHANISMS
• Secondary mechanisms result from biochemical cascades that
occur after the initial event
• are a source of ongoing SCI and neurologic deterioration.
• cause the damage to neural tissue on the cellular level
• include the pathologic effects of microvascular changes,
excitatory amino acids, cell membrane destabilization, free
radicals, inflammatory mediators, and neuroglia apoptosis
SCI PATHOLOGY
• solid cord injury – the spinal cord grossly appears normal without evidence
of softening, discoloration, or cavity formation. However, damage to the
cord can be clearly seen on histologic examination
• contusion/cavity - no breach or disruption in the surface anatomy, but the
areas of hemorrhage and necrosis (eventually evolving into cysts) are readily
identified in the cord parenchyma
• laceration - result in clear-cut disruption of the surface anatomy. Most often
caused by penetrating missiles or sharp fragments of bone.
• massive compression - often accompanied by severe vertebral body
fractures or dislocations
BASIC TYPES OF INCOMPLETE SCIs (spinal cord syndromes
based on horizontal and partly vertical localization)
• central cord syndrome (mostly in cervical region loss of motion and sensation
mainly in arms and hands, the most common)
• anterior cord syndrome (resulting in loss of function of the anterior two-thirds of
the spinal cord. The region affected includes the descending corticospinal tract,
ascending spinothalamic tract, and autonomic fibers. It is characterized by a
corresponding loss of motor function, loss of pain and temperature sensation, and
hypotension)
• posterior cord syndrome (the least common – less than 1% of SCIs, posterior column
dysfunction – vibration, discrimination and proprioception is impaired)
• conus medullaris syndrome (motor and sensory deficits in lower legs + autonomic
dysfunction, combination of upper and lower motor neuron signs)
• cauda equina syndrome
• Brown-Séquard Syndrome, which is characterized anatomically by a hemicord injury
with ipsilateral proprioceptive and motor loss and contralateral pain and
temperature sensation loss below the level of the lesion
Source: wikipedia
CLINICAL PICTURE OF SCI
(based on vertical localisation)
• Cervical – thoracic – lumbar – sacral, particular segment
• Sensory level + autonomic impairment + motor dysfunction:
• Tetraplegia (cervical segments):
• spastic in UE if rostral C segments are affected,
• In lesions at or above C4 ventilation is usually impaired due to
diaphragm palsy
• In lesions at or below C5, the paresis is flaccid in the affected
segment (and spastiv below, while no signs of abnormity are
apparent above the level of the affected segment)
• Paraplegia (thoracic or lumbar)
• Spastic in lesions affecting thoracic or rostral lumbar segments
• Flaccid at the segment of affection
• + epiconus, conus or cauda equina syndrome
Source: Ambler et al., Clinical neurology
SCI IMAGING
• There are several recommendations available allowing to decide if any imaging
examination is necessary
• In general, the imaging is not necessary in case of:
• no relevant clinical signs and symptoms (incl.neck or back pain)
• + no risk factors (motor vehicle accidents, falls from 6 ft or more, altered mental
status with an unknown mechanism of injury) are present
• In low risk patients (no neurological signs or symptoms, only neck or back pain or
limited extend of spinal cord movement), the lateral and AP X-ray may be used.
• However, due to its ease of use and superior sensitivity, most centers go directly to
(cervical) spine CT as the initial imaging study of choice.
• MR is the best technique for imaging the spinal cord itself. IN SCIs, it should be
performed mainly in case of neurologic deficit with normal x-rays or in the lack of
correlation between a neurologic deficit and x-ray findings.
SCI MANAGEMENT
• Prehospital trauma protocols are critical to prevent further injury to the spinal cord
• Any patient with suspected SCI should be immobilized with a hard cervical collar and/or
a rigid head-strap/backboard until definitive neurosurgical assessment can take place.
• Treatment of hypoxia and hypotension, proper monitoring of vital signs, and transfer to
an appropriate trauma center will affect ultimate outcomes positively.
• On arrival to the trauma center, a rapid assessment should be undertaken to assess the
status of the airway, respiratory, and circulatory (ABC) systems, followed by a cursory
assessment of the neurologic status (“disability”)
• The acute management of patients with SCI is primarily directed at medical stabilization
to prevent secondary injury and to permit the accurate clinical and radiographic
diagnosis of spinal cord and column pathology
SCI MANAGEMENT
• neural element decompression and spinal stabilization within 24 hours may improve
neurologic recovery in patients with deficits and spinal cord compression
• there has been no demonstrated increased risk of neurologic deterioration from early
surgery
• Management of vital functions and autonomic dysfunction
• High-dose methylprednisolone has long been considered a potential neuroprotective
agent in SCI, with the potential of reducing tissue injury by inhibiting lipid peroxidase
and free radical production. Several studies performed showed only small (if any)
benefit. Due to a trend towards more serious complications associated with steroid use,
current guidelines do not recommend administration of methylprednisolone (MP) for the
treatment of acute SCI [Level 1].
• Early rehabilitation
THANKS FOR YOUR ATTENTION
• Main source of information:
• Badjatia N, Parikh GY, Mayer SA. Traumatic Brain Injury. In Lewis ED, Mayer
SA, Rowland LP. Merritt's Neurology, 13th edition. LWW 2015.
• Mandigo CE, Kaiser MG, Angevine PD. Traumatic Spinal Cord Injury. In Lewis
ED, Mayer SA, Rowland LP. Merritt's Neurology, 13th edition. LWW 2015