Central cord syndrome resulting from cervical hyperextension trauma. This patient presents with the classic features of central cord syndrome, the most prevalent incomplete spinal cord injury. It typically occurs in older individuals with pre-existing cervical spondylosis who sustain a hyperextension injury. The mechanical compression of the cervical cord between hypertrophied osteophytes anteriorly and the buckled ligamentum flavum posteriorly causes disproportionate damage to the central region of the spinal cord. Because the cervical somatotopic fibres of the corticospinal tracts are arranged medially within the cord, the upper extremities suffer much more profound motor impairment than the lower extremities. Sacral sensation and perianal tone are typically spared. Anterior cord syndrome results from hyperflexion or anterior spinal artery ischaemia, producing bilateral paraplegia and loss of pain and temperature with dorsal column preservation. Brown-Sequard syndrome manifests as ipsilateral motor and dorsal column loss with contralateral pain and temperature loss. Complete cord transection produces total motor and sensory loss below the lesion without sacral sparing.

Q: A 26-year-old motorcyclist sustains a complete T2 spinal fracture dislocation following a high-speed crash. In the trauma bay, his Glasgow Coma Scale score is 15. His blood pressure is 76/44 mmHg, heart rate is 48 beats per minute, respiratory rate is 18 breaths per minute, and oxygen saturation is 98% on room air. Neurological evaluation demonstrates flaccid paraplegia below the T2 dermatome with absent rectal tone. His skin is warm, pink, and dry over all four extremities. After infusing two litres of intravenous Hartmann's solution, his blood pressure remains 78/46 mmHg and his heart rate is 50 beats per minute. Which of the following is the most appropriate next management step?

Exclude haemorrhage, support perfusion with monitored vasopressor treatment and obtain spinal/critical-care advice. Bradycardia and hypotension after cervical cord injury can suggest neurogenic shock, but haemorrhage and other causes must be excluded. Avoid hypotension and use individual monitored targets with spinal/critical-care advice. Current weak guidance suggests MAP lower limit 75–80 and avoiding active augmentation above 90–95 for 3–7 days, rather than a compulsory identical target for every patient.

Q: A 42-year-old woman is brought to the emergency department after a low-speed rear-end motor vehicle collision. She was wearing her seatbelt and stepped out of the vehicle at the scene without assistance. She currently reports mild neck stiffness and severe right thigh pain from an isolated closed, mid-shaft femur fracture with visible thigh deformity. She is alert and oriented with a Glasgow Coma Scale score of 15, no neurological deficits, and no history of alcohol or substance use. Palpation of the posterior cervical spine reveals no tenderness. How should her cervical spine be managed?

Maintain full cervical immobilization and obtain a formal cervical computed tomography. Under both the Canadian C-Spine Rule and the NEXUS (National Emergency X-Radiography Utilization Study) criteria, clinical clearance of the cervical spine without neuroimaging is permissible only if five specific criteria are fulfilled: no posterior midline cervical tenderness, no focal neurological deficit, normal level of alertness, no intoxication, and no painful distracting injuries. A closed, deformed mid-shaft femur fracture is a major painful distracting injury that impairs the patient's ability to reliably perceive and report cervical spine tenderness. Consequently, her cervical spine cannot be cleared clinically. She must remain immobilized in a cervical collar with spinal precautions and undergo definitive computed tomography (CT) of the cervical spine. Asking her to actively rotate her neck before ruling out a distracting injury or fracture is unsafe and violates validated cervical clearance protocols. Plain radiographs have substantially lower sensitivity than CT and are no longer first-line imaging in adult trauma centers.

Key Takeaways

Uncal herniation can produce an ipsilateral dilated pupil.
Hyperventilation is a short-term rescue measure for active herniation, not routine TBI treatment.
Spinal reflex findings alone do not establish that a cord injury is complete.

Last updated: October 2026

Brain Herniation Syndromes

Uncal (Lateral Transtentorial) Herniation: The medial temporal lobe (uncus) herniates over the free edge of the tentorium cerebelli. Compresses the ipsilateral cranial nerve III (oculomotor), causing an ipsilateral fixed and dilated pupil (unopposed sympathetic mydriasis). Compression of the ipsilateral cerebral peduncle produces contralateral hemiparesis. (Rarely, compression of the contralateral peduncle against Kernohan's notch causes paradoxical ipsilateral hemiparesis).
Cushing's Triad: A late, life-threatening physiological response to impending brainstem herniation:
- Hypertension with widened pulse pressure (sympathetic surge to overcome elevated ICP).
- Bradycardia (reflex baroreceptor vagal response to hypertension).
- Irregular / ataxic respirations (brainstem distortion and medullary ischaemia).

Emergency Medical Management of Elevated ICP

Positioning: Elevate the head of the bed to $30^\circ$ with the neck in a neutral midline position to maximize internal jugular venous drainage. Ensure endotracheal tube ties are not constrictive.
Ventilation: Maintain normocapnia ( $PaCO_2 35\text{ to }40\text{ mmHg}$ ). Hyperventilation ( $PaCO_2 30\text{ to }35\text{ mmHg}$ ) causes cerebral vasoconstriction and reduces ICP, but can worsen cerebral ischaemia; it is strictly reserved as an emergency, short-term temporizing bridge during active herniation while moving to the operating theatre.
Hyperosmolar Therapy:
- Mannitol 20%: $0.5\text{ to }1.0\text{ g/kg}$ IV bolus. Acts via osmotic diuresis and plasma expansion. Requires an intact blood-brain barrier; avoid in hypotensive patients (causes osmotic hypovolaemia). Monitor serum osmolarity (keep $< 320\text{ mOsm/kg}$ ).
- Hypertonic Saline (3%): $250\text{ mL}$ IV bolus (or $2\text{ to }3\text{ mL/kg}$ ). Expands intravascular volume and lowers ICP; preferred in hypotensive trauma patients.
Target Physiology: Avoid pyrexia (target normothermia $< 37.5^\circ\text{C}$ ), prevent seizures (prophylactic levetiracetam or phenytoin for 7 days in severe TBI), and maintain blood glucose between $6.0\text{ and }10.0\text{ mmol/L}$ .

Spinal Trauma, Clinical Clearance & Cord Syndromes

Clinical Cervical Spine Clearance Rules

Radiological imaging of the cervical spine is unnecessary if the patient meets all criteria under validated clinical decision rules:

Cervical clearance rules: NEXUS requires no midline tenderness, intoxication, altered alertness, focal neurological deficit or painful distracting injury. The Canadian C-spine rule is a different staged rule for an appropriate alert stable patient. Do not call the NEXUS five criteria the Canadian rule.
1. No posterior midline cervical spine tenderness.
2. No focal neurological deficit.
3. Normal level of alertness ( $GCS = 15$ ).
4. No evidence of intoxication (alcohol, drugs).
5. No painful, distracting injury (e.g., long-bone fracture, large burn, visceral injury).
Canadian C-Spine Rule (CCSR): In alert, stable patients, imaging is mandated if any high-risk factor is present (age $\ge 65$ , dangerous mechanism, paresthesias in extremities). If low-risk factors allow range of motion assessment (simple rear-end collision, sitting in ED, ambulatory at any time, delayed onset of pain, absence of midline tenderness), the patient is asked to actively rotate the neck $45^\circ$ left and right. Inability to do so mandates imaging.

Spinal Cord Injury Syndromes

Complete versus incomplete injury: Classify using a careful neurological examination including sacral sensation and voluntary anal contraction, repeated as spinal shock evolves. Absent early reflexes alone do not prove anatomical transection. Protect the spine and obtain urgent imaging/specialist assessment.
Anterior Cord Syndrome: Caused by hyperflexion injuries or anterior spinal artery occlusion. Disruption of the anterior two-thirds of the cord. Characterized by bilateral loss of motor function (corticospinal tracts) and bilateral loss of pain and temperature sensation (spinothalamic tracts) below the lesion. Proprioception, vibratory sensation, and light touch (posterior dorsal columns) are completely preserved.
Central Cord Syndrome: The most common incomplete cord injury, typically seen in older adults with pre-existing cervical spondylosis following hyperextension injuries (e.g., face impact). Characterized by disproportionately greater motor impairment in the upper extremities compared to the lower extremities, variable sensory loss below the lesion, and sacral sensory sparing.
Brown-Séquard Syndrome: Hemisection of the spinal cord, classically from penetrating stab wounds. Characterized by ipsilateral loss of motor function (corticospinal) and ipsilateral loss of proprioception/vibration (dorsal column), combined with contralateral loss of pain and temperature sensation (spinothalamic tract) beginning 1 to 2 segments below the level of the lesion.

Neurogenic Shock vs Spinal Shock

Neurogenic Shock: A true haemodynamic, distributive shock state resulting from the loss of descending sympathetic autonomic vascular tone following cervical or upper thoracic spinal cord injury (typically at or above T6).
- Clinical Triad: Hypotension, relative/paradoxical bradycardia (due to loss of sympathetic accelerator fibres T1–T4 and unopposed vagal tone), and warm, dry, vasodilated peripheries.
Acute spinal cord injury: Avoid hypotension and obtain urgent spinal/retrieval advice. The 2024 guideline suggests a lower MAP limit of 75–80 and avoiding active augmentation beyond 90–95 mmHg for 3–7 days; these are weak recommendations requiring individual haemodynamic management, not a fixed national prescription of 85–90 for exactly seven days.
Spinal Shock: A transient, neurophysiological state characterized by the temporary loss or depression of all reflex activity below the level of spinal injury (flaccid paralysis, areflexia, absent bulbocavernosus reflex). It is not a circulatory shock state. It resolves over days to weeks, marked by the return of the bulbocavernosus reflex and the subsequent emergence of spasticity and hyperreflexia.

Clinical comparison: Intracranial Haemorrhages Compared

Vessel Involved: Extradural (Epidural) Haematoma: Middle meningeal artery (pterion fracture); Acute Subdural Haematoma: Cortical bridging veins; Chronic Subdural Haematoma: Cortical bridging veins (atrophied brain); Traumatic Subarachnoid Haemorrhage: Small superficial cortical / pial vessels
Mechanism: Extradural (Epidural) Haematoma: Direct focal blow to temple / pterion; Acute Subdural Haematoma: High-energy deceleration / rotational shear; Chronic Subdural Haematoma: Trivial trauma in elderly / alcohol misuse; Traumatic Subarachnoid Haemorrhage: Blunt trauma, rupture of small vessels
CT Morphology: Extradural (Epidural) Haematoma: Hyperdense, biconvex (lentiform); Acute Subdural Haematoma: Hyperdense, crescentic (concavoconvex); Chronic Subdural Haematoma: Hypodense / isodense, crescentic; Traumatic Subarachnoid Haemorrhage: Hyperdensity in cerebral sulci / cisterns
Suture Lines: Extradural (Epidural) Haematoma: Limited by sutures; does not cross sutures; Acute Subdural Haematoma: Crosses suture lines; limited by falx/tentorium; Chronic Subdural Haematoma: Crosses suture lines; limited by falx/tentorium; Traumatic Subarachnoid Haemorrhage: Follows subarachnoid space and sulci
Classic Course: Extradural (Epidural) Haematoma: Loss of consciousness $\rightarrow$ lucid interval $\rightarrow$ coma; Acute Subdural Haematoma: Immediate coma, rapid neurological decline; Chronic Subdural Haematoma: Insidious cognitive decline, gait ataxia, headache; Traumatic Subarachnoid Haemorrhage: Severe headache, photophobia, meningism

Primary references (checked 7 October 2026): Acute spinal cord haemodynamic guidance.

Test Your Knowledge

A 74-year-old man with known severe cervical spondylosis presents following a mechanical ground-level fall in which he struck his forehead against a table, causing a hyperextension injury to his neck. Neurological examination reveals marked flaccid weakness and loss of dexterity in both upper limbs (grade 1/5 motor strength), with relatively preserved motor strength in both lower limbs (grade 4/5 motor strength). Sensation to pinprick is diminished over both shoulders and forearms, but perianal sensation and voluntary anal sphincter tone are intact. Which of the following spinal cord syndromes is present?

Anterior cord syndrome due to thrombosis of the anterior spinal artery

Central cord syndrome resulting from cervical hyperextension trauma

Brown-Sequard syndrome resulting from lateral cord hemisection injury

Complete spinal cord transection causing functional paraplegia below C5

Test Your Knowledge

A 26-year-old motorcyclist sustains a complete T2 spinal fracture dislocation following a high-speed crash. In the trauma bay, his Glasgow Coma Scale score is 15. His blood pressure is 76/44 mmHg, heart rate is 48 beats per minute, respiratory rate is 18 breaths per minute, and oxygen saturation is 98% on room air. Neurological evaluation demonstrates flaccid paraplegia below the T2 dermatome with absent rectal tone. His skin is warm, pink, and dry over all four extremities. After infusing two litres of intravenous Hartmann's solution, his blood pressure remains 78/46 mmHg and his heart rate is 50 beats per minute. Which of the following is the most appropriate next management step?

Administer an immediate bolus of intravenous atropine followed by transvenous cardiac pacing

Infuse four units of un-crossmatched packed red blood cells via rapid blood infuser

Exclude haemorrhage, support perfusion with monitored vasopressor treatment and obtain spinal/critical-care advice

Initiate high-dose intravenous methylprednisolone according to the acute spinal cord protocol

Test Your Knowledge

A 42-year-old woman is brought to the emergency department after a low-speed rear-end motor vehicle collision. She was wearing her seatbelt and stepped out of the vehicle at the scene without assistance. She currently reports mild neck stiffness and severe right thigh pain from an isolated closed, mid-shaft femur fracture with visible thigh deformity. She is alert and oriented with a Glasgow Coma Scale score of 15, no neurological deficits, and no history of alcohol or substance use. Palpation of the posterior cervical spine reveals no tenderness. How should her cervical spine be managed?

Clinically clear the cervical spine and remove all precautions without imaging

Request plain anteroposterior, lateral, and open-mouth odontoid radiographs

Instruct the patient to actively rotate her neck 45 degrees bilaterally to test range

Maintain full cervical immobilization and obtain a formal cervical computed tomography

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