Reynaldo B. Sta. Mina, Jr., M.D.

NEUROTRAUMA
MED 721 (CLINICAL NEUROLOGY)
 CONTENTS
▪ Learning Objectives  Clinical Features
 Diagnosis and Investigations
▪ Introduction
 Imaging
▪ Head Injury  Treatment
 Definition and Epidemiology  Surgical Treatment
 Etiology and Clinical Features  Cervical Spine
 Thoracic and Thoracolumbar Spine
 Diagnosis and Investigations  Chronic SCI
 Treatment  Prognosis
 YouTube video links
▪ YouTube video links
▪ Concussion
 Definition and Etiology
▪ Clinical Cases
 Clinical Features ▪ Main Reference
 YouTube video links ▪ Related Readings
▪ Spinal Cord Injury
 Definition and Etiology
 Complete SCI
 Incomplete SCI
 LEARNING OBJECTIVES

▪ To define traumatic brain injury or head injury, and

know its epidemiology
▪ To get familiarized with Glasgow Coma Scale and
its significance in clinical practice
▪ To identify the different types of head injury and
know their epidemiology, etiology,
pathophysiology, clinical features, investigations,
treatment, and prognosis
▪ To understand the clinical correlations related to
such disorders
INTRODUCTION
▪ Traumatic brain injury (TBI) is a major public health problem
affecting more than 1.4 million people per year in the United
States and the leading cause of death in those under 45 years of
age.
▪ Resultant direct and indirect medical costs are approximated at
$60 billion per year.
▪ About 500,000 patients require hospital treatment for TBI every
year in the United States, representing 200–300 patients per
100,000 population.
▪ Eighty percent of TBI patients have a mild injury and the
remaining 20% a moderate (10–15%) or severe TBI (5%).
▪ In recent decades improvements in pre-hospital care, especially
airway management, triage to a Level 1 trauma center, prompt
computed tomographic (CT) imaging, removal of significant
intracranial hemorrhagic collections, and avoidance of secondary
insults (hypotension, hypoxemia) has reduced severe TBI
mortality to about 30%. This has occurred without an increase in
those severely disabled or vegetative.
▪ Guidelines for the management of severe TBI
have been widely adopted in the United States
and updated in 2007.
▪ Management of increased intracranial pressure
(ICP) remains a challenge in severe TBI, and
noninvasive neurophysiologic monitoring of
moderate and mild TBI is a realistic goal.
▪ Following spinal injuries, timely realignment,
decompression, and internal fixation are
routinely performed, but spinal cord injury often
remains irreversible or only shows minimal
improvement with corticosteroid treatment.
HEAD INJURY
DEFINITION AND EPIDEMIOLOGY
▪ Despite intensive treatment disability or death occurs in the
majority of patients with severe coma-producing TBI, and
physical and neuropsychologic disabilities are frequent in those
with moderate and mild injuries.
▪ The Glasgow Coma Scale (GCS) is widely used to quantify
severity of injury.
 Patients who open their eyes spontaneously, follow commands, and are
fully oriented score all 15 points.
 Patients who do not open their eyes spontaneously or to stimuli, and
cannot verbalize or move any extremities have the lowest score of 3.
 The patient’s best responses are taken.
 A comatose patient is referred to as a severe TBI and defined as having a
GCS score equal or less than 8, a moderate injury is usually lethargic and
has a GCS of 9–12, and mild injury has less alteration in consciousness
and a GCS of 13–15.
▪ Severe TBI carries an overall mortality of about 30%.
▪ Approximately 10–20% of moderate injuries will
deteriorate into coma, with serious morbidity or death in
just under 10%.
▪ Additionally the severe and moderate injuries yield large
numbers of disabled survivors (20–30%).
▪ In the United States, of the approximately 400,000 patients
admitted awake and alert each year following a mild TBI,
about 1.5% or 6000 will deteriorate and die.
▪ Extreme caution is necessary in that any patient with a GCS
of 13, an abnormal CT brain scan, skull fracture or skull
puncture has a risk similar to that of moderate injuries and
should not be considered a mild head injury.
▪ In terms of prognosis after severe TBI, motor score is most
valuable, and, when combined with patient age and
pupillary response, the motor score is as reliable as the
complete GCS score.
ETIOLOGY AND CLINICAL FEATURES
▪ Head injuries may be classified as closed (blunt) or open
(penetrating).
▪ A closed head injury, with or without fracture but intact dura,
usually results from vehicular injury, blunt assault, or fall.
▪ Open injury is associated with dural penetration due to a gunshot
or stab wound, compound depressed skull fracture from an
angulated object, or basal skull fracture with cerebrospinal (CSF)
leakage.
▪ Focal brain injuries, often precipitated by translational or linear
acceleration–deceleration phenomena, result from inertial
movements of the brain within the skull that may tear venous or
small arterial structures resulting in subdural hemorrhage.
▪ The basifrontal and temporal lobes may strike the rough skull
base, resulting in frontal and temporal contusions and cortical
lacerations associated with local brain swelling.
▪ Focal skull injuries include depressed, linear, and basal skull
fractures, or sutural diastases.
TIPS!
▪ A chronic subdural hematoma can mimic
stroke, either a cerebrovascular accident (CVA)
or a transient ischemic attack (TIA), and
sometimes a tumor (when papilledema is
present).
▪ Focal lesions may be coup (directly under the impact site)
or contrecoup (distant diametrically opposed to the
impact).
▪ Significant parenchymal contusional hemorrhages, either
primary or delayed in onset, may require surgical removal .
▪ Extradural (epidural) hematomas (EDH)
 Result from a focal impact almost always associated with a
nearby skull fracture and stripping of the dura from the inner
table of the skull .
 The hematoma forms a lens shape as blood fills into this space
and causes further stripping of the dura from the skull.
 A lucid interval may be present; however, clinical deterioration
can be rapid.
 Underlying brain damage is usually more severe with an acute
subdural hematoma (mortality >50%) rather than an EDH.
 The mortality of acute EDH continues to decrease in recent
decades as outcome is largely related to triage and timely
decompression by craniotomy.
▪ Posterior fossa skull fractures and
hematomas
 Particularly dangerous due to the proximity of the
brainstem
 Result from impacts to the back of the head.
 The presence of any skull fracture must be taken
seriously in any patient and increases the
likelihood of a significant acute or delayed
intracranial hematoma by a factor of about 400 in
a conscious patient and a factor of 20 in a
comatose patient.
▪ Diffuse axonal injury (DAI)
 Consists of scattered shearing of white matter axons,
histologically appearing days after injury as swollen retraction
balls of axoplasm.
 Their distribution is centripetal and magnitude related to the
force of injury.
 Extension of these white matter shearing lesions, from sites of
relative tethering such as the corpus callosum down into the
brainstem, is believed to represent an increasing degree of injury
related to rotational or angular acceleration–deceleration of the
skull and brain.
 Hemorrhages into the deeper gray matter or ventricles also often
signify DAI .
 The severity of injury in a primate model correlates with a clinical
continuum from simple cerebral concussion to prolonged
traumatic unconsciousness.
 Experimental evidence suggests that the axonal injury may not
be complete at onset, but progresses in the hours after injury.
This raises the hope of partial reversal by pharmacologic means if
such agents could be identified.
▪ Head injury as a result of blunt assault or fall results more
often in focal injuries such as cerebral contusions and
subdural hematomas, whereas vehicular injuries more
often result in diffuse head injuries.
▪ Severe focal, diffuse, or penetrating injuries such as
gunshot wounds are often associated with brain swelling
and increased ICP.
▪ A ‘blast injury’ force as seen in proximity to a discharging
explosive device may result in concussion or prolonged
unconsciousness even without skull penetration by
fragments or shrapnel.
▪ High intensity shock waves consisting of advancing wave-
fronts are believed to cause secondary complex
interference patterns, which may result in diffuse
physiologic or actual mechanical tissue disruption. This
mechanism may result in neuropsychologic deficits and
post-traumatic stress disorders (PTSD).
CT scan showing acute subdural hemorrhage with underlying parenchymal injury. Note the
displacement of ventricles and midline shift.
CT scan showing large delayed onset hemorrhagic contusion evident 2–3 days after injury
with adjacent areas of contusion and significant mass effect.
CT scan showing the typical lens-shaped acute extradural hematoma (EDH) of the parietal
region. Note the associated midline shift. EDH is associated with the best prognosis
among all the intracranial hemorrhages (traumatic or otherwise) when evacuated at an
appropriate time.
MRI scan (FLAIR image) showing diffuse axonal injury with the typical shear trauma to
corpus callosum. Other areas usually show various degrees of petechial hemorrhages.
DIAGNOSIS AND INVESTIGATIONS
▪ An adequate airway, usually by endotracheal
intubation, must be promptly established in
combative or struggling patients.
▪ This includes all severe (GCS 8 or less), possibly
some moderately (GCS 9–12) head injured
patients, those with respiratory distress, or a
borderline patient with any significant
intracranial abnormality of CT scan of the brain.
▪ Attention to airway, ventilation, and circulatory
stability is necessary before adequate diagnosis
and treatment can be carried out.
▪ Secondary insults may occur minutes, hours, or days
after injury and compound the primary brain injury
in about 30% of severe injuries.
▪ These insults include hypotension (systolic blood
pressure <90 mmHg), hypoxia (PO2 <60 mmHg),
carbon dioxide retention (PCO2 >45 mmHg) and
anemia (hematocrit <30%), all known to worsen
brain swelling, ICP, morbidity, and mortality.
▪ Hyperglycemia and hyperthermia are to be avoided.
▪ Injury to visceral organs, or long bone fractures, may
contribute to blood loss hypovolemia, hypotension,
and increased morbidity.
▪ The patient’s level of consciousness may be
depressed secondary to hypotension, and
abdominal/pelvic ultrasound or diagnostic
peritoneal lavage take priority over a CT scan of
the head in this circumstance.
▪ Other diagnoses may be present such as
intoxication, anoxic insult, metabolic
encephalopathy, post-ictal state, or status
epilepticus.
▪ Nonconvulsive status epilepticus may occur and
require prolonged electroencephalogram
monitoring to capture and monitor adequately.
▪ Following respiratory and circulatory stabilization, rapid
neurologic assessment is performed including the GCS and
pupillary light responses.
▪ It is not always possible to examine the patient before
muscle paralyzing agents or sedation with hypnotics such
as propofol, or benzodiazepines have been given.
▪ Unilateral pupil enlargement (midposition 4–5 mm or
dilated >5 mm) in an obtunded patient, with or without
fixation to light, is highly localized and indicative of
ipsilateral tentorial herniation unless proved otherwise.
▪ Cerebellar, lower cranial nerve, or precipitous respiratory
abnormalities (tonsillar herniation) may be found with
posterior fossa injuries.
▪ Doll’s eye maneuver or cold calorics with head elevation should
only be performed if the status of the cervical spine and tympanic
membranes can be determined.
▪ Patients must be stimulated and the best responses recorded,
such as: follows commands, responds to voice, light pain,
moderate pain, or deep pain.
▪ Asymmetries, decorticate or decerebrate responses, flaccid no
extremity response, DTRs, and plantar responses are recorded.
▪ Sensory examination is only possible in awake, cooperative
patients.
▪ Trauma patients are usually kept in a rigid collar, despite normal
cervical spine studies, until the neck can be cleared clinically or
ligament injury ruled out with magnetic resonance imaging
(MRI).
▪ Concern is given to CSF leakage from the nose (rhinorrhea)
indicative of cribriform or anterior fossa fracture, or ear
(otorrhea) suggestive of temporal bone fracture.
▪ Antibiotic administration is controversial, but a spinal drain
is often indicated when leaks persist after several days.
▪ Rigidity of the neck may indicate a cervical spine fracture
(present in about 5–8% of severe TBI, and 10–15% of severe
facial fractures), occipital fracture, or tonsillar herniation.
▪ Patients with a concussion or mild head injury who present
for medical attention should at least receive plain skull X-
rays, and any patient with a GCS score less than 15, focal
neurologic signs, headache, vomiting, skull fracture, or
significant scalp swelling should receive a plain CT scan of
the head. Further treatment will usually depend upon the
CT scan results.
▪ MRI brain scans are usually unnecessary and inconvenient
in the earlier stages of TBI diagnosis and treatment.
▪ In the subacute phase, characteristic MRI findings can often
establish a suspected diagnosis of DAI.
TREATMENT
▪ In the early resuscitation phase, elevated ICP or
transtentorial–uncal herniation is suggested by clinical
findings such as anisocoria or pupillary dilatation, motor
posturing, or progressive level of consciousness
deterioration not attributed to extracranial factors.
▪ Emergency treatment of suspected herniation or elevated
ICP consists of intubation and hyperventilation, and rapid
intravenous administration of mannitol (i.e. 1 g/kg) or
hypertonic saline solution (variable concentrations given) as
the patient is emergently sent for a CT brain scan.
▪ Patients are brought promptly to surgery for significant
subdural or epidural hematomas (usually equal or greater
than 1 cm) or parenchymal contusions (equal or greater
than 30 ml in the temporal or posterior fossa), and/or a
midline shift of 0.5 cm or greater.
▪ Similarly, compound depressed skull fractures exceeding
the thickness of the skull and penetrating injuries may
require acute or subacute surgery.
▪ Post-traumatic subarachnoid hemorrhage in the basal cisterns,
fissures, cortical sulci, or on the tentorium are a frequent finding
in all forms of TBI, but uncommonly associated with vasospasm
and specific treatment is not required.
▪ Patients with nonsurgical lesions on an initial CT scan require a
repeat CT scan, often as early as 4–6 hours later, to detect
enlarging or evolving lesions such as hemorrhagic cerebral
contusions.
▪ Subsequent observation in the intensive care unit and placement
of an ICP monitor is recommended according to US guidelines
updated in 2007 for patients with:
 A GCS score of 8 or less, with an abnormal but nonsurgical CT scan, or
 A normal scan with two or three of the following:
 Age over 40
 Motor posturing, or
 Systolic blood pressure <90 mmHg.
▪ Head elevation is routinely in the range of 30°.
▪ ICP monitoring with a ventricular catheter is preferred in
that ventricular CSF drainage may be used as a first choice
to control elevated ICP (>20 mmHg) before resorting to
mannitol (0.25–0.50 g/kg), hyperventilation (PCO2 30–35
mmHg), or second-tier therapies such as barbiturate coma,
hypothermia, or decompressive hemicraniectomy (an
option in the acute or subacute period to control refractory
increases in ICP).
▪ ICP management may be augmented by cerebral perfusion
pressure (CPP = mean arterial blood pressure minus ICP)
management.
▪ The CPP is ideally maintained between 50 and 60 mmHg, in
that CPP >70 mmHg has been associated with adult
respiratory distress syndrome (ARDS).
▪ Patients who maintain elevated ICP (<20 mmHg)
require follow-up CT brain scans for enlarging or
evolving lesions, including hydrocephalus.
▪ Other helpful invasive cerebral monitoring
modalities include brain tissue oxygen content,
pH, lactate, and temperature monitoring.
▪ Cerebral blood flow with estimations of
hyperemia or ischemic desaturation as well as
cerebral metabolic rate of oxygen consumption
can be obtained with a jugular bulb venous
catheter.
▪ ICP monitors are generally discontinued after
ICP has normalized for 24–48 hours.
▪ Those patients who have required ventricular
drainage for 5–10 days may develop
hydrocephalus and require a shunting
procedure.
▪ Anticonvulsants are continued post-injury in
patients having a seizure, but only for 1 week
in those without significant cortical or
hemispherical lesions considered at risk of a
seizure.
YouTube Video Links

▪ Glasgow Coma Scale

 https://www.youtube.com/results?search_query=
glasgow+coma+scale
▪ Traumatic Brain Injury
 https://www.youtube.com/results?search_query=t
raumatic+brain+injury
▪ Epidural Hematoma vs Subdural Hematoma
 https://www.youtube.com/results?search_query=
epidural+vs+subdural+hematoma
▪ Diffuse Axonal Injury
 https://www.youtube.com/results?search_query=
diffuse+axonal+injury
CONCUSSION
DEFINITION AND ETIOLOGY
▪ Concussion is a frequently encountered form of mild head injury and the
most common form of head injury in athletic injuries.
▪ The term cerebral concussion has been used interchangeably with mild
TBI.
▪ Approximately 250,000 concussions occur yearly in the US in football
alone.
▪ Classic cerebral concussion was defined as a loss of consciousness (LOC),
usually brief, and associated with retrograde and post-traumatic
(anterograde) amnesia.
▪ By such definition, full consciousness is regained by 24 hours, and the
condition may be accompanied by abnormal microscopic neuronal
changes.
▪ In recent decades cerebral concussion has come to be defined as a
physiologic dysfunction secondary to a minor head injury without
associated pathologic changes in the brain.
▪ A cerebral concussion is often a consequence of sudden angular
acceleration–deceleration head motions that usually accompany,
but may be independent of, impact to the head.
▪ Helmets greatly absorb impacts to the head, have virtually
eliminated skull fracture, significantly reduce focal impact brain
injury, but cannot eliminate concussion.
▪ A five- to tenfold increase in extracellular potassium
concentration lasting 3–5 minutes is associated with a concussion
producing loss of consciousness, resulting in nerve action
potential failure and LOC.
▪ Excitatory amino acids such as glutamate are believed to open
gated channels resulting in the ionic flux.
▪ Occasionally the process requires several seconds or longer,
allowing some purposeful action before collapse.
CLINICAL FEATURES
▪ With cerebral concussion, confusion is more frequently
found than LOC, clearly indicating a problem of cerebral
processing, affecting orientation, higher thought
processes, and memory.
▪ There may be disturbances of vision, unsteadiness, vacant
stare, a foggy state, delayed responses, slurred speech, and
emotional outbursts.
▪ Symptoms of headache, especially with exertion and
dizziness, are common, and nausea and vomiting may
occur.
▪ Simple concussion is completely reversible and unless
repetitive, is not believed to be associated with
neurological sequelae.
▪ In order to categorize, study, and treat concussion several classification
schemes have been devised, such as the American Academy of
Neurology Practice Parameter Grading System For Concussion.
▪ Grading the severity of concussion has been helpful in both treating
athletic injuries and prognostication regarding the safe return to
sporting activity.
▪ Athletes should not return to contact sports while significant residual
symptoms persist.
▪ Repeated concussions can result in cumulative cytoarchitectual and
gross structural brain damage, usually manifesting as increasing severity
and duration of symptoms with successive concussions.
▪ In recent years, professional athletes from several contact sports were
forced to retire due to repeated concussions.
▪ Some suffer from problems such as headaches, slurred speech, visual
problems, depression, or dementia.
▪ Adolescents, high school or college students who experience multiple
concussions are strongly encouraged to discontinue contact sports.
▪ A rare and controversial issue is the second impact syndrome
(SIS).
▪ This involves the athlete who suffers a concussion and returns to
the contact sport (minutes to weeks later) to experience a second
head injury before recovery from the earlier concussion.
▪ This may result in death or severe disability from malignant brain
swelling.
▪ It is believed that the first concussion caused a focal or diffuse
abnormality in cerebral vascular regulation leading to excessive
blood congestion, and a second injury occurred before this
congestion has recovered.
▪ The SIS has been reported in high school age as well as adult
contact sport athletes, highlighting the risks of persistent signs
and symptoms in the return to contact sports.
▪ Neuropsychologic testing appears to be effective in
obtaining useful data on the short-term and long-term
effects of concussion and mild TBI, and is useful to those
involved in decisions involving athletes.
▪ Brief but concise neuropsychologic tests batteries,
administered to the contact sport athlete before the season
begins, and similar testing after a concussion, is sensitive to
document the absence of a lingering effects before return
to play.
▪ Conditions that may mimic recurrent concussion symptoms
in the contact sport athlete include a previously
asymptomatic or undiagnosed Chiari malformation, basilar
invagination, hydrocephalus, arachnoid cyst, or migraine
headaches.
YouTube Video Link

▪ Concussion
 https://www.youtube.com/results?search_query=
concussion
SPINAL CORD INJURY
DEFINITION AND ETIOLOGY
▪ Spinal stability is the ability of the spinal column to limit
displacement of its segments under physiological loads, so as to
prevent damage or irritation of the neural structures, and to
prevent irreversible deformity or pain due to structural changes.
▪ Biomechanical instability refers to the ability of spine to resist
forces in experimental settings or controlled environment ex
vivo.
▪ Acute spinal cord injury (SCI) is a devastating injury affecting
many young, productive individuals with a male preponderance.
▪ The average age is 37.6 years which has increased over the last
four decades, likely due to increased longevity and associated
accidental falls.
▪ The most common cause for acute SCI is a motor vehicle
accident in industrialized countries, falls, and pedestrian
injuries.
▪ Gunshot SCI is unfortunately common in the US and
exceeds the number of sport injuries, which have been
reduced due to protective and preventive measures.
▪ SCI is expensive to the person, family, and the nation.
▪ An average 15,000 people sustain SCI per year in the US,
and a young individual with high cervical SCI will incur
medical costs in the range of $740,000 the first year and
$135,000 each year of survival5.
▪ About 400,000 people are living with the effects of SCI in
the US.
COMPLETE SCI
▪ These injuries produce a complete paraplegia or a complete
tetraplegia.
▪ Loss of motor and/or sensory function for more than three
segments below the level of injury is termed complete SCI.
▪ Only about 3% of injuries with complete SCI at the initial
physician examination may regain some function within 24
hours.
▪ Complete paraplegia is permanent loss of motor and nerve
function at T1 level or below, with loss of sensation and
movement in the legs, bladder, bowel, and perineum.
▪ Arms and hands retain normal function.
▪ Some people may retain partial trunk movement.
▪ Complete tetraplegia is characterized by loss of hand and
arm movement as well.
▪ Some may require an artificial ventilator to support
respiratory function.
▪ Partial hand and arm movements may by retained in some.
INCOMPLETE SCI
▪ These are far more common than complete SCI and the
patients retain some sensory and motor function below the
level of injury.
▪ Have the best chances for recovery.
▪ Avoiding a second injury during transfers is all the more
important.
▪ This is determined after the period of spinal shock has
subsided, which is usually 6–8 weeks post-injury.
 Anterior cord syndrome: an incomplete SCI characterized by
damage to the anterior part of the spinal cord, resulting in
impaired temperature, touch, and pain sensations below the level
of injury.
 Central cord syndrome: characterized by damage of the central
part of the spinal cord, with loss of function in upper extremities
predominantly and some variable weakness in the lower limbs.
The hands may be maximally involved and sensory loss minimal.
 Posterior cord syndrome: this results in impaired coordination
due to damage to the posterior columns of the spinal cord.
 Brown–Sequard syndrome: usually found secondary to a
stab wound and results in damage to one-half of the spinal
cord or hemisection, resulting in impaired loss of
movement but preserved sensation on one side of the body
and preserved motor function with sensory loss on the
other half of the body. Incomplete Brown–Sequard may be
found in some anterior cord syndromes.
 Conus medullaris syndrome: this results from injury to the
sacral portions of the spinal cord resulting in saddle
anesthesia, loss of bladder/bowel function, with weakness
of lower extremities. Recall that the spinal cord usually
terminates at the L1 level.
 Cauda equina syndrome: characterized by injury to the
nerves located below the L1 region of the spine, resulting in
partial or complete loss of sensation. In some cases, these
nerve roots can regenerate and recover function.
CLINICAL FEATURES
▪ The American Spinal Injury Association (ASIA) provides a scoring
system and a scale for measuring the disability.
▪ Both the score and scale are extensively used in clinical and
research settings.
▪ The clinical picture is a result of the level of injury, mechanism,
and severity.
▪ In a severe injury with spinal shock, all reflexes below the lesion
are lost, including the bulbocavernous, cremasteric, and
abdominal reflexes, with motor as well as sensory deficits
accompanied by hyporeflexia.
▪ Gradually the reflexes may return, and deep tendon reflexes
become brisk.
▪ A complete and flaccid paralysis becomes spastic over a period of
time.
▪ In a high cervical lesion, respiratory compromise because of
phrenic nerve denervation and diaphragm paralysis is seen.
▪ Sphincter tone is lost and sacral functions are compromised.
▪ Spinal shock results in hypotension and bradycardia
due to loss of sympathetic tone (contrary to the
hypovolemic shock more commonly seen in trauma,
with hypotension and tachycardia).
▪ Spinal shock can be due to a mixed expression of
loss of sympathetic tone, loss of muscle tone due to
paralysis, and blood loss.
▪ Chronic SCI findings vary again depending upon the
initial presentation, respiratory support,
immobilization, urinary dysfunction, urinary tract
infection, pulmonary problems, and decubitus
ulcers. These are also the usual causes of death.
▪ A central cervical spinal cord injury is difficult to
evaluate during an acute phase especially with
obtunded sensorium.
▪ Degenerative changes in the cervical spinal cord
must make the clinical picture very suspect.
DIAGNOSIS AND INVESTIGATIONS
▪ Like in any acute trauma condition, cardiorespiratory function
takes priority and the patient has to be stabilized initially.
▪ All trauma patients, especially the unconscious, are considered as
spinal injured, unless proven otherwise.
▪ Stabilization procedures have to keep this in mind, especially
intubation in a high cervical spinal cord injury or transfers in an
unstable cervical and/or thoracic spine trauma.
▪ Effective treatment of hypotension is essential to maintain
perfusion to the spinal cord, with or without spinal shock.
▪ A complete neurologic examination has to follow careful history-
taking, eliciting the mechanics of injury.
▪ It is important to ask if the patient had been able to walk after
the injury or paralysis was sudden and complete.
▪ A delay implies instability issues or developing hematoma in the
canal.
▪ Not uncommonly, patients with an incomplete SCI or cervical
fracture without SCI will describe a several minute period,
immediately after injury, of inability to move their extremities.
▪ Sensory and motor examination provides the
injury level to the spinal cord while sphincter
examination is essential for the sacral
functions.
▪ Physical examination of the spine can provide
details about the surface landmarks and
gross displacements of spinal segments.
IMAGING
▪ Cervical, thoracic, and lumbosacral plain films are usually routinely
obtained. Radiographs and high resolution CT/MRI scans provide
information regarding the nature and mechanics of the spinal cord
injury.
▪ While in some cases SCI exists without radiological abnormality
(SCIWORA), the usual patient has fractures, fracture dislocations, or
instability due to ligamentous injury sometimes seen as subluxation.
▪ MRI is excellent in providing the succinct details of spinal cord status and
has prognostic significance.
▪ A long segment spinal cord edema usually has a bad prognosis as does a
hemorrhage into the cord substance with contusion.
▪ In awake patients with or without polytrauma, clearance of the cervical
spine is usually provided following dynamic X-rays, CT scans, or MRI
scans.
MRI (T2 image) showing the fracture dislocation of the cervical spine which is usually
associated with complete spinal cord injury.
A displaced cervical spine at C4 and C5, mostly ligamentous injury. A subluxation
usually has incomplete SCI. (MRI-T2 sequence.)
▪ A CT with dynamic flexion/extension views and a MRI with
or without X-rays may be indicated in unconscious patients
within 48 hours to clear the patient.
▪ High resolution CT of spine with reconstructions provides
greater detail regarding the body and ligamentous
instability in the obtunded patient.
▪ Both CT and MRI help in the diagnosis of ligamentous
instability which may not be obvious in the resting position
of the spine in an unconscious patient.
▪ SCI exists without radiological abnormality and radiological
abnormality can exist without SCI. Thus both clinical and
radiological examinations are crucial.
TREATMENT
▪ Both complete and incomplete SCI require acute and chronic management
protocols.
▪ Acute care includes stabilization of cardiorespiratory function, management of
spinal shock, and immobilization of the unstable spinal injury.
▪ Spinal shock with hypotension and bradycardia requires aggressive treatment
using pressors in order to maintain normal perfusion to the damaged neural
tissue.
▪ Secondary damage due to ischemia must be prevented by normalization of
blood pressure.
▪ High-dose methyl prednisolone treatment is offered as an option according to
the guidelines provided by both the American Association and Congress of
Neurological Surgeons.
▪ According to the reviewer, the evidence suggested ‘harmful side-effects are
more consistent than any suggestion of clinical benefits’.
▪ A total of 639 manuscript titles and abstracts on corticosteroids and human SCI
published between 1966 and 2001 were included in the study.
▪ There is no convincing evidence to support that methyl prednisolone
administration within 8 hours of acute cervical SCI improved neurological
recovery.
▪ A significant increase in severe medical complications was noted when the
administration continued for 24 hours.
 SURGICAL TREATMENT
 Following external immobilization during the emergency care and clinico-
radiologic evaluations, indications for internal fixation of the spinal
column are assessed.
 Diagnostics and implant technology have improved tremendously over
the past decade, and newer internal surgical stabilization techniques have
been introduced.
 The goals of surgical intervention in acute SCI are stabilization of spinal
column and decompression of spinal cord.
 The timing of such intervention is unclear and several prospective studies
are being conducted.
 Early surgery is, however, indicated in cases of incomplete SCI, since
decompression would facilitate the recovery of the neural structures.
 In complete SCI such an emergency procedure may not produce the
desired outcome, while operative stress on an unstable patient could be
counter-productive.
 A stable patient is considered for surgical intervention which could be
anterior, posterior, or combined.
 This decision is based upon the location of compressive elements and the
instability, along with the degree of instability.
 In several instances the surgeon may make a selection based on the
familiarity of an approach and condition of the patient.
 Indications for emergency surgery (applicable to the
incomplete lesions of spinal cord):
 Progression of neurologic deficits.
 Complete subarachnoid block radiographically (MRI or
myelography).
 Myelogram, CT, or MRI showing bone fragments or
soft tissue elements in the spinal canal producing
spinal cord compression.
 Compression of an important nerve root requiring
decompression.
 Penetrating trauma or compound spinal injury.
 Nonreducible fracture displacement due to locked
facets producing spinal cord compression.
 Acute anterior spinal cord syndrome secondary to disc
herniation or fracture/dislocation.
 Cervical spine
 Preoperative traction is helpful in achieving closed reduction of
the displaced segments. In a seriously ill patient with medical
contraindications, a reducible injury may be externally
immobilized in a halo traction device: for a reducible C1–2
injury, halo immobilization is useful in patients over 60 years
of age, and a type III odontoid fracture that traverses the body
of C2 vertebra heals very well.
 A ruptured transverse ligament with atlanto-axial dislocation
(AAD) with a displacement of more than 6 mm is preferably
treated with internal fixation by transarticular screws and
posterior C1–2 fusion.
 Most unstable spine injuries below C2 are treated by anterior
decompression and internal fixation by screw–plate systems.
 A single level injury may need bone graft and plate fixation,
while a burst fracture may require more extensive
decompression and fusion techniques including posterior
stabilization.
 Posterior lateral mass screw–plate/rod fixation has been used
extensively for long segment fixation.
Radiograph showing hangman’s fracture with severe displacement of fracture segments at
C2–3.
The hangman’s fracture in 262 was reduced using cervical traction. This injury can heal
in a Halo external immobilization or surgical internal fixation. Note the posterior gap
between C1 and C2 due to bilateral fracture of C2 pedicles.
 Thoracic and thoracolumbar spine
 As the thoracic, thoracolumbar, and lumbar spine injuries
are the more common injuries, several advancements in
hardware technology have expanded the indications for
stabilization.
 The surgical route can be anterior, posterior, or in some
cases circumferential.
 Surgical treatment with internal fixation of upper
thoracic spine is more complicated since suitable
hardware is not easily available and the cervicothoracic
junction is difficult to approach from the front.
 A posterior long segment rod fixation through laminar or
pedicle hooks is useful in some instances.
 Anterolateral approach via a thoracotomy for the mid-
thoracic spine is practiced to place an anterior plate with
bone-packed cages filling the intervetebral spaces.
 CHRONIC SCI
 Rehabilitation and disability management through
physiotherapy and occupational therapy improves the
outcome of these patients, especially those with
incomplete SCI.
 Complete injuries require management of airway,
pulmonary complications, decubitus ulcers, and
complications resulting from immobility.
 Bladder and bowel care requires attention and patients
are taught to accommodate changes in life-style to
prevent further complications.
 Long-standing SCI can lead to a variety of pain
syndromes, autonomic dysreflexia, syringomyelia, and
spasticity that need specialized treatments.
PROGNOSIS
▪ An incomplete SCI has a potential for good recovery and the
advances in technology along with the paramedical support
systems have yielded encouraging results.
▪ However, despite these advances acute SCI has mortality of up to
20%.
▪ Mortality is higher with acute complete or severe incomplete
cervical SCI, where respiratory paralysis sets in early.
▪ In the subacute phase, ARDS or gastric bleeding may be
encountered.
▪ Among those with incomplete SCI, the central cord syndrome
and Brown–Sequard syndrome, many regain independent
mobility by the end of the first year.
▪ Anterior cervical cord syndrome usually has a poorer recovery.
▪ C4–C5 edema is a frequent indicator for a poor prognosis.
▪ Complete SCI is not reversible.
▪ A complete SCI without improvement after 72 hours is very
unlikely to show functional recovery and only one-third of
complete cervical SCI requiring ventilator support survive 5 years.
MRI (T2) scan showing spinal cord edema at C4 and C5, a frequent indicator of poor
prognosis.
YouTube Video Links

▪ Spinal Cord Injury

 https://www.youtube.com/results?search_query=spin
al+cord+injury
▪ Spinal Shock
 https://www.youtube.com/results?search_query=spin
al+shock
▪ Anterior Cord Syndrome
 https://www.youtube.com/results?search_query=ante
rior+cord+syndrome
▪ Central Cord Syndrome
 https://www.youtube.com/results?search_query=cent
ral+cord+syndrome
▪ Posterior Cord Syndrome
 https://www.youtube.com/results?search_query=post
erior+cord+syndrome
▪ Brown-Sequard Syndrome
 https://www.youtube.com/results?search_query=brow
n+sequard+syndrome
▪ Conus Medullaris Syndrome vs Cauda Equina
Syndrome
 https://www.youtube.com/results?search_query=conu
s+medullaris+syndrome+vs+cauda+equina+syndrome
CLINICAL CASES
▪ An otolaryngologist requested an expeditious neurologic
evaluation of a very vigorous octogenarian who was so fit that he
downhill skied 3 weeks earlier; this patient reported recent-onset
sense of “spinning vertigo” and cloudiness of vision, precipitated
by sudden standing or neck extension. Additionally, he was
experiencing new-onset headaches that were becoming
increasingly severe and were awakening him from his sleep.
Concomitantly he was having difficulty with mental
concentration and hand coordination, as well as a feeling of
“weak legs.” On further questioning, he recalled that 7 weeks
earlier he had slipped on the ice, striking his occiput, while
helping to push an auto out of a snow bank.
On examination, he had moderately severe difficulty performing
tandem gait (something most healthy 70-year-olds often cannot
perform, but this was probably abnormal in this athletic man).
The remainder of his neurologic examination was normal. Head
computed tomography (CT) was done.
 Question 1: What is the likely diagnosis?
 Question 2: What do you expect to see in the
patient’s brain scan?
 Question 3: Is this condition compatible with life?
▪ On a rainy morning, this vigorous hypertensive, 68-year-old
musician, went to get something from his car parked on the
slippery driveway. He was next found lying on the ground
barely able to move any extremity with the exception of
some spontaneous, brief dystonic posturing of his right
arm. He had no recall of what occurred. Admission to a local
hospital led to a diagnosis of a brainstem stroke.

When there was no sign of improvement after 48 hours, his

son-in-law, a physician, had him transferred to a tertiary
level hospital. Neurologic examination demonstrated an
alert, articulate gentleman with absolutely normal
brainstem function, full visual fields, and normal optic
fundi. He had a severe spastic quadriparesis, and bilateral
Babinski signs. There was a dense spinal cord level; he had
absolutely no appreciation of touch, temperature, or pin
sensation below the C6 dermatomes.
 Question 1: What is the likely diagnosis?
 Question 2: How do you explain the neurologic
examination findings?
 Question 3: What do you expect to see in the
patient’s spinal cord MRI?
▪ An 18-year-old football player was covering a kickoff when he
crashed into an opposing player after losing his helmet, hitting
the right side of his head against the opponent’s knee. He fell to
the ground and was unconscious for 20 to 30 seconds. He was
then immediately transported to the nearest hospital. Twenty
minutes after the accident, he was alert and conscious without
neurologic deficit, but he had amnesia for the event. He had a
superficial bruise to the scalp on the right. Approximately 1 hour
after the trauma the patient developed a generalized motor
seizure. Lorazepam 4 mg IV stopped the seizure. A CT scan,
performed 100 minutes after the trauma, was unremarkable. He
was then transferred to a larger hospital.
On admission, neurologic examination showed a slight
psychomotor slowing and slurred speech, which was thought to
have been caused by lorazepam administration, in the absence of
other neurologic deficits. The Glasgow Coma Scale score was 15
of 15.
Routine laboratory investigations and electrocardiography were
normal. Eight hours after the trauma, he had nausea, vomiting,
and a headache.
 Question 1: What is the likely diagnosis?
 Question 2: Should this patient have a repeat or
follow-up brain scan?
 Question 3: What is the prognosis for this patient?
MAIN REFERENCE

▪ Hankey’s Clinical Neurology, 2ed, Philip B.

Gorelick et al, Chapter 9, pp 279-289

▪ The contents of this slide presentation are largely lifted from the above reference textbook, with some minor alterations in wordings,
sentence construction and sequence of sentences or paragraphs to suit the needs of the students of AMA School of Medicine. Materials
in the presentation that are not found in the above reference, including pictures and clinical cases , are taken from the references listed
under Related Readings or from various internet sources.
RELATED READINGS

▪ Current Diagnosis and Treatment Neurology,

3ed, John C.M. Brust, Chapter 14, pp 175-198
▪ Clinical Neurology and Neuroanatomy, 1ed,
Aaron L. Berkowitz, Chapter 19, pp 199-200
▪ Adams and Victor’s Principles of Neurology,
11ed, Allan H. Ropper et al, Chapter 34, pp 906-
935 and Chapter 42, pp 1257-1265
▪ Netter’s Neurology, 2ed, H. Royden Jones, Jr. et
al, Chapters 59-60, pp 548-571
▪ Case Files Neurology, 1ed, Eugene C. Toy et al,
pp 71-78