Head and Spinal Cord

Injuries
Presentation by:
 Samuel Mulate
 Semehar Fesseha
 Simret Uffo
 Tsige Sitotaw

Moderator: Dr Abenezer Tirsit

Date: july 31, 2025
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Outline
Head Injuries
•Basic head anatomy
•Definitions and types (scalp injury, skull fracture, TBI)
•Brain injury types: concussion, contusion, DAI, hematomas
•Pathophysiology (ICP, cerebral edema, axonal injury)
•Clinical features, red flags, GCS classification
•Assessment and management strategies

Spinal Cord Injuries

•Anatomy of the spine and spinal cord
•Epidemiology and causes (traumatic vs non-traumatic)
•Pathophysiology (primary and secondary injury)
•Classification and special syndromes (e.g., Brown-Séquard)
•Clinical evaluation and imaging
•Acute management, surgery, and rehabilitation

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Objectives
• Explain the anatomy relevant to head and spinal cord injuries.
• Define and differentiate types of head and spinal injuries.
• Understand the pathophysiological processes involved in these injuries.
• Identify key clinical features, red flags, and injury severity.
• Describe the initial assessment, including GCS and ATLS principles.
• Outline the general management, including when surgical intervention is
needed.
• Recognize common spinal cord injury syndromes and their clinical
presentations.
• Appreciate the role of rehabilitation and long-term care.
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Head injuries
Head injury is trauma to the scalp, skull, or
brain caused by an external force, potentially
resulting in physical damage, neurological
dysfunction, or altered consciousness

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 Anatomy of head
Scalp

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Soft tissue

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Brain hemorrhage

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 pathophysiology
Cerebral Blood Flow (CBF)
The brain depends on a constant supply of glucose and oxygen.
Brain Injury can cause:
• Hypoperfusion
• Ischemia
Raised intracranial pressure (ICP) after trauma can reduce CBF.

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 Intracranial pressure (ICP)

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Intracranial Pressure (ICP)
Normal ICP = 7–15 mmHg

Because the skull is rigid, an increase in the volume of one component

must be compensated by a decrease in another, or intracranial
pressure (ICP) will rise(The Monro-Kellie Doctrine ).

Trauma leads to bleeding and swelling → increased intracranial pressure →

compression of brain tissue → reduced blood flow → risk of brain herniation.

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 Neuronal Function & Axonal Injury
Neurons are highly sensitive to mechanical shearing forces (e.g., in
diffuse axonal injury) and electrolyte imbalance and energy failure
Trauma disrupts:
• Synaptic transmission
• Neurotransmitter release
• Can cause seizures, coma, or permanent cognitive deficits

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 Cerebral Edema
Swelling of brain tissue due to fluid accumulation after trauma can
result from a leaky blood-brain barrier (vasogenic edema) or cell
injury (cytotoxic edema).
This swelling increases intracranial pressure, reduces blood flow to
the brain, and may lead to brain herniation if not treated promptly.

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Types of Head Injury
Head injuries can be classified into:
• Scalp injuries
• Skull fractures
• Brain injuries
• Concussion
• Contusion
• Diffuse Axonal Injury
• Intracranial Hematomas (EDH, SDH, SAH)

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SCALP INJURY
• The most minor type of head trauma
• Scalp is highly vascular profuse bleeding
• Major complication is infection
• Types include
• Hematoma
• Avulsion
• Laceration
• Abrasion

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Skull injury
Type of Skull Injury Description Key Features / Signs Severity / Management
Often minor; heals
Linear Fracture Simple break in skull bone No bone displacement
without surgery
Depressed Fracture Bone pushed inward May press on brain Often requires surgery
- Battle’s sign (bruising
Fracture at skull base behind ears) Serious; risk of brain
Basilar Fracture
(near eyes, ears, nose) - Raccoon eyes injury & infection
- CSF leak from nose/ear
Fracture along skull Sutures widen (common Needs monitoring; rare in
Diastatic Fracture
sutures in infants) adults
Open wound, brain Emergency; high risk of
Penetrating Injury Object penetrates skull
exposure brain damage

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TYPES OF SKULL FRACTURE

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Basillar skull fracture
 Anterior cranial fossa
• Nasal bleeding
• Orbital hematoma (Raccoon eyes)
• Cerebrospinal fluid rhinorrhea
Middle cranial fossa
• Orbital hematoma
• Bleeding from the ear
• Cerebrospinal fluid otorrhea
Posterior cranial fossa
• Bruising over the suboccipital region, which develops after a day or two (Battle’s sign)

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Traumatic brain injury
• Is a serious medical issue that affects how your brain works
• Can occur from minor impacts or blows to the head, large blows from
significant impact, and penetrating injuries to the head.
• Can also occur secondary to rapid acceleration and deceleration of
the brain without impact.
• Can be classified into mild, moderate, and severe categories based on
GCS.
• Can be primary and secondary.
• Can be focal or diffuse.

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Types of brain injury
 Primary Brain Injury
• The initial damage to the brain that occurs at the time of trauma.
• Irreversible—occurs instantly due to mechanical forces.

Secondary Brain Injury

• Damage that develops hours to days after the primary injury.
• Caused by physiological and biochemical responses to the primary injury.
• Preventable or treatable with early intervention

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Types of brain injury
Feature Focal Injury Diffuse Injury

Widespread (many brain

Location Localized area
regions)

Rotational or deceleration
Cause Direct impact
forces

DAI, concussion, hypoxic

Examples Contusion, hematoma
injury

Imaging Often visible on CT/MRI May be subtle or invisible

Often associated with

Outcome Depends on location
severe disability

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Concussion
• Temporary neuronal dysfunction due to non penetrating trauma.
• Normal head CT; there is no apparent parenchymal damage
• Deficit resolve over minutes to hours.
• Clinical features include:
• Confusion
• Amnesia – specially amnesia of the event is very common
• Loss of consciousness
• Headache
• Dizziness
• Nausea and vomiting
• Delayed verbal expression
• Inability concentrating
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 Concussion grading according to
Colorado grading system
• Grade 1 Head trauma patients with confusion only

• Grade 2 Patients with amnesia

• Grade 3 Patients who lose consciousness

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Contusion
• Bruise of the brain

• It is due to break down of small vessels and extravasation blood into the brain

• The frontal, occipital and temporal lobes are commonly involved

• On CT scan, the contused areas appear bright

• Frequently associated with edema

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…
 Coup injury:
• Occurs under the site of impact with an object
Countercoup injury:
• Occurs on the side opposite to the area that was hit.
• Occurs with deceleration of the brain against the skull

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Diffuse axonal injury
• Shearing (tearing) of the brain's long connecting nerve fibers (axons)

• Usually causes coma and injury to many different parts of the brain.

• Is associated with poor outcomes.

• No specific cure, focus is on minimizing secondary injury and complications

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Grades of DAI

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Intracranial hematoma:
A. Extradural Hematoma
• Accumulation of blood between the skull and dura

• Associated with tear in the middle meningeal artery due to temporal bone
fracture

• Is neurosurgical emergency

• Has classical three stage clinical presentation (seen only 20%).

• Brief loss of consciousness, then lucid interval followed by sudden
deterioration.
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MANAGEMENT
Conservative (Monitor in ICU)
Only if:
• Small hematoma (<30 mL), no shift, GCS > 8,
no deficits
Surgical Indications (Craniotomy)
Do surgery if:
• Hematoma > 30 mL
• GCS ≤ 8 with unequal pupils
• Midline shift > 5 mm
• Neurological deterioration

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Subdural Hematoma
• Accumulation of blood between dura and subarachnoid

• Occurs from tearing of bridging veins.

• It can be acute , sub acute and chronic.

Type Time after injury CT Appearance Severity Management
Acute <72 hours Hyperdense (bright) Very severe Emergency surgery
Surgery or
Subacute 3–21 days Isodense Moderate
observation
Chronic >21 days Hypodense (dark) Mild-slow Burr hole drainage

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Subarachnoid Hemorrhage
• Bleeding into the space between subarachnoid membrane and pia matter

• Can occur spontaneously (ruptured cerebral aneurysm which is the most

common cause) or due to head trauma

• Signs and symptom include sudden onset severe headache, loss of consciousness,
hemiparesis seziure, nausea or vomiting, meningismus

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Management
• Secure aneurysm –coiling (endovascular) or clipping (surgery)

• Prevent rebleeding – early repair, bed rest

• Prevent vasospasm – nimodipine (60 mg q4h for 21 days)

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 General Assessment and
management

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Clinical assessment
ATLS (Advanced Trauma Life Support)
I. Primary Survey (ABCDE approach)

II. Resuscitation
• Begin oxygen therapy.
• Establish IV access.
• Start fluid resuscitation (e.g. crystalloids or blood products if
needed).
• Control hemorrhage (internal or external). Secondary Survey

III. Secondary Survey

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History

• Mechanism
• Loss of Consciousness
• Vomiting, seizures, amnesia, headache
• Drug use / alcohol / anticoagulants
• Past neuro history

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Physical Examination

• Scalp & skull (Laceration, swelling, fractures)

• Pupils (Size, reactivity)
• Cranial nerves
• Motor and sensory
• Signs of basal skull fracture
• CSF leak (rhinorrhea/otorrhea)
• Battle's sign, raccoon eyes

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GCS & TBI Classification

Typical
GCS Score Severity Clinical Features Prognosis
Management
May have brief LOC
Observe; CT if red
13–15 Mild TBI or amnesia, normal Usually good
flags present
neuro exam
Confusion, longer Admit, CT scan,
9–12 Moderate TBI LOC, vomiting, may neuro obs, consider Variable
have focal signs ICU
Coma, abnormal
Intubate, neuro ICU, High risk of
≤8 Severe TBI pupils/posture, risk
urgent neurosurgery complications
of herniation

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Red Flags for Urgent Imaging

• GCS <15 after 2 hours

• Repeated vomiting (≥2 episodes)
• Seizures after injury
• Focal neurologic deficit
• Signs of skull fracture (e.g. CSF leak)
• Age ≥65 or on anticoagulants

Order a CT Head immediately

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General Management

Prevent Secondary Brain Injury

• Oxygen: SpO₂ >94%
• BP: SBP ≥100 mmHg
• Head elevation (30°)
• Avoid hypoglycemia, hyperthermia
Medical Management:
• Seizure prophylaxis (e.g. phenytoin)
• Osmotherapy: mannitol or hypertonic saline
• Avoid steroids (CRASH trial → ↑ mortality)
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Neurosurgical Emergencies

• EDH >30 mL
• SDH >10 mm or midline shift >5 mm
• GCS drop >2 points
• Fixed, dilated pupil (suggests herniation)
• Depressed/open skull fractures

• Craniotomy or craniectomy needed urgently

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Spinal cord Injury
• Spinal cord injury is damage to the spinal cord or cauda equina
resulting in partial or complete loss of motor, sensory, and/or
autonomic function below the level of the lesion

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Introduction (Anatomy of the Spine and Spinal
Cord)

The spine is composed of 33 vertebrae grouped as:

• Cervical (C1–C7)
• Thoracic (T1–T12)
• Lumbar (L1–L5)
• Sacral (S1–S5, fused)
• Coccygeal (1–4, fused)
The spinal cord is part of the central nervous system, beginning at the
foramen magnum and ending around L1–L2 (conus medullaris),
followed by the cauda equina.
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Epidemiology
Incidence: ~40–80 cases per million people annually
worldwide
•Gender: ~80% occur in males
•Age:
•Young adults (15–30 years) → trauma (e.g., MVAs)
•Elderly (>65) → falls, degenerative disease
Common Causes:
•Motor vehicle accidents (~40%)
•Falls (~25–30%)
•Violence (~10–15%)
•Sports (~10%)
Level of Injury:
•Cervical: most common (~50–60%)
•Thoracic/lumbar: ~30%
•Sacral/cauda equina: ~10%

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Major Spinal Cord Tracts
• There are three key long tracts in the spinal cord that are clinically
relevant in localizing and diagnosing spinal cord injuries:
1. Corticospinal Tract (Motor Tract)
2. Dorsal Column-Medial Lemniscal Pathway (DCML)
3. Spinothalamic Tract (Anterolateral System)

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 Major Spinal Cord Tracts
Side Affected
Tract Modality (Spinal Cord Key Clinical Signs
Lesion)
Corticospinal Voluntary motor Ipsilateral below lesion Spastic paralysis, Babinski

Proprioception, vibration, Sensory ataxia, positive

Dorsal columns Ipsilateral below lesion
fine touch Romberg

Contralateral, 1–2 levels Loss of pain/temp

Spinothalamic Pain, temperature
below sensation

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Pathophysiology
• SCI involves primary mechanical damage and secondary biochemical injury
A. Primary Injury
• Immediate disruption of axons, blood vessels, and cell membranes due to trauma (fracture,
dislocation, compression, or laceration)
B. Secondary Injury
• Occurs over hours to days:
• Ischemia and reduced perfusion
• Inflammation: neutrophils, macrophages infiltrate
• Excitotoxicity: excessive glutamate release
• Free radical production
• Apoptosis and demyelination
• Edema causing further compression
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Classification
By Cause
1. Traumatic SCI
• Involves sudden mechanical force causing injury to spinal elements:
• Fracture–dislocation: vertebral body fractures with displacement
(common in cervical and thoracolumbar spine)
• Hyperflexion/extension injury: cervical spine vulnerable (e.g., whiplash)
• Axial compression: leads to burst fractures (e.g., diving into shallow water)
• Penetrating injuries: stab wounds or gunshots → usually incomplete, may
cause hemisection (→ Brown-Séquard syndrome)

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By Cause

2. Non-Traumatic SCI
• Infections: spinal TB (Pott's disease), epidural abscess (Staph aureus)
• Tumors: compressive (e.g., metastasis to vertebral column from
breast/lung/prostate)
• Vascular: anterior spinal artery infarct (→ anterior cord syndrome)
• Degenerative: spondylotic myelopathy, disc herniation
• Autoimmune/Demyelinating: MS, transverse myelitis

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By Anatomical Level
Level Structures Involved Typical Deficits

Quadriplegia/tetraplegia, respiratory
Cervical (C1–C8) Arms + legs (UMN) compromise (C3–C5 affects
diaphragm), neurogenic shock

Thoracic (T1–T12) Trunk + legs Paraplegia, possible autonomic

dysreflexia (T6 and above)

Lumbar (L1–L5) Legs + bladder/bowel LMN leg weakness, areflexia,

incontinence

Sacral (S1–S5) Perineum, bladder, anal sphincter Saddle anesthesia,

bowel/bladder/sexual dysfunction

Conus Medullaris End of spinal cord (L1–L2) Mixed UMN + LMN signs, early
bladder/bowel involvement

LMN pattern, asymmetric leg

Cauda Equina (below L2) Lumbosacral nerve roots weakness, severe radicular pain, saddle
anesthesia, areflexia
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Special Injury Syndromes
1. Central Cord Syndrome
• Mechanism: Hyperextension injury (common in elderly with cervical
spondylosis)
• Anatomy: Damage to central portion of spinal cord (corticospinal
tract fibers for upper extremities are more medial)
• Clinical Features:
• Arm weakness > leg weakness
• Variable sensory loss
• Urinary retention may occur
• Prognosis: Good; leg function often returns first
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Special Injury Syndromes
2. Anterior Cord Syndrome
• Mechanism: Infarct (anterior spinal artery) or flexion/compression
injury
• Anatomy: Anterior 2/3 of spinal cord affected (corticospinal +
spinothalamic tracts)
• Clinical Features:
• Bilateral motor paralysis
• Loss of pain and temperature
• Proprioception/vibration preserved (dorsal columns spared)
• Prognosis: Poor; motor function rarely returns
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Special Injury Syndromes
3. Brown-Séquard Syndrome
• Mechanism: Hemisection (e.g., stab wound, lateral mass fracture)
• Anatomy:
• Ipsilateral corticospinal + dorsal column damage
• Contralateral spinothalamic tract damage
• Clinical Features:
• Ipsilateral motor paralysis + loss of proprioception
• Contralateral loss of pain and temperature (1–2 levels below)
• Prognosis: Good; most regain functional mobility

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Special Injury Syndromes
4. Posterior Cord Syndrome (Rare)
• Mechanism: Trauma, tumor, tabes dorsalis (syphilis)
• Anatomy: Dorsal columns only
• Clinical Features:
• Loss of proprioception and vibration
• Preserved motor and pain/temp
• Ataxic gait, positive Romberg
• Prognosis: Moderate; depends on etiology

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Special Injury Syndromes
5. Conus Medullaris Syndrome
• Mechanism: Injury at L1–L2 (conus terminalis)
• Anatomy: Mixed spinal cord and peripheral nerve involvement
• Clinical Features:
• Symmetric lower limb weakness
• Early bladder and bowel dysfunction
• Variable sensory loss (saddle anesthesia)
• Prognosis: Variable; often incomplete recovery

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Special Injury Syndromes
6. Cauda Equina Syndrome (Surgical Emergency)
• Mechanism: Compression of nerve roots (L2–S5) – e.g., massive disc
herniation, tumor
• Anatomy: LMN only
• Clinical Features:
• Asymmetric leg weakness
• Saddle anesthesia
• Areflexia, especially in ankles
• Bladder and bowel incontinence
• Prognosis: Depends on early surgical decompression (within 24–48 hrs)
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Special Injury Syndromes
Syndrome Motor Sensory Reflexes Key Features

Elderly,
Central cord Arm > leg weakness Variable May be spared hyperextension
injury

Pain/temp lost,
Infarct, worst
Anterior cord Bilateral loss proprioception Absent below lesion
prognosis
spared

Ipsilateral motor Contralateral Ipsilateral Hemisection, good

Brown-Séquard
loss pain/temp loss hyperreflexia prognosis

Loss of
Posterior cord None Normal Ataxia, rare
proprioception

Conus medullaris Mixed UMN + LMN Saddle anesthesia Variable Early bladder/bowel
Cauda equina LMN only Saddle anesthesia Areflexic Surgical emergency
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Approach to a Patient with
Suspected Spinal Injury
Initial Management – ATLS Protocol (ABCDE)
Diagnosis and Evaluation
• Neurological Exam
• Motor strength grading (0–5)
• Sensory testing (light touch, pinprick)
• Rectal exam for tone/sensation
• Use the ASIA chart
Imaging
• X-ray: initial screening
• CT scan: best for bony detail
• MRI: best for cord injury, hematoma, disc herniation
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Definitive Management
A. Immobilization
• Cervical collar, spinal board
• Log-roll for movement
B. Medical Management
• Avoid hypotension/hypoxia
• Maintain MAP 85–90 mmHg for cord perfusion
• Foley catheter to manage retention
• Monitor for autonomic dysreflexia (in T6 and above)

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Definitive Management
C. Steroids
• Controversial: previously used (e.g., methylprednisolone), not routine
now per current guidelines (AANS, CNS)
D. Surgical Intervention
• Decompression (laminectomy, discectomy) if:
• Progressive deficit
• Instability
• Cord compression
• Stabilization with rods/screws

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Rehabilitation and Long-Term
Care
•Physical therapy: to prevent contractures and maintain
strength
•Occupational therapy: for activities of daily living
•Bladder/bowel training
•Psychological support
•Assistive devices: braces, wheelchairs

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Summary
1. Brain injuries can be open or closed, with types like concussion,
contusion, and diffuse axonal injury causing varying degrees of
neurological dysfunction.
2. Spinal cord injuries may be traumatic or non-traumatic and are
classified by level, severity, and completeness.
3. Key spinal tracts affected include corticospinal (motor), dorsal
columns (proprioception), and spinothalamic (pain/temp), with specific
syndromes like central cord or Brown-Séquard showing distinct patterns.
4. Early stabilization, imaging, and sometimes surgery are essential, and
recovery depends on injury type—complete lesions have worse
outcomes than incomplete ones.
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References

Principles of Neurology by Adams & Victor, twelfth edition

Snell’s Clinical Neuroanatomy, Eighth Edition

Bailey & Love’s Short Practice of Surgery. 27th edition

https://www.uptodate.com/

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 Thank you

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