Spinal Cord Lesions: Anatomy and Syndromes

• The session will cover deficits that are characteristic of spinal cord lesions
• These include lesions of the anterior, lateral, and posterior column as well as anterior spinal cord syndrome
• Also discussed: syringomyelia and Brown-Séquard syndrome.

Ascending Tracts

• Clinically important ascending tracts send sensory information towards the brain
• They include pathways for vibration, position sense, two-point discrimination, and touch
• Pain and temperature are also sensed
• A key component is the somesthetic cortex, located in the postcentral gyrus of the parietal lobe
• The signals travel from the spinal cord to the brainstem
• Then through the medial lemniscus to the thalamus (diencephalon)
• Then through the thalamocortical relay axon to the somesthetic cortex

Descending Tracts

• Clinically important descending tracts send motor information downwards from the brain
• The descending motor tracts originate in the somatic motor area, specifically the precentral gyrus, located in the frontal lobe
• Descending signals travel from the frontal lobe
• Then through the midbrain (mesencephalon) to the pons
• Then to the Medulla oblongata, Medullocervical junction, and finally the Spinal cord
• The corticobulbar tract is mostly crossed, but also has some uncrossed fibers
• The lateral corticospinal tract, predominantly crossed, with a small portion uncrossed, facilitating movement and motor control

Spinal Cord End

• The spinal cord ends around the L1-L2 vertebral level in adults.
• Understanding this level is vital for procedures like lumbar punctures, to avoid spinal cord injury.

Basic Features of Spinal Cord Disease

• Upper motor neuron (UMN) findings appear below the lesion
• Sensory and motor deficits are seen that can be localized to a specific spinal cord level
• Bowel and bladder dysfunction is common

UMN vs LMN Differences

• Upper motor neuron lesions can result from stroke or spinal cord injury, where lower motor neuron lesions may be caused disk herniation or polio
• With UMNs, muscle tone is initially flaccid, later becoming spastic
• With LMNs, muscle tone is flaccid
• Tendon reflexes are hyperactive in UMN lesions but absent in LMN lesions
• Pathologic reflexes (e.g., Babinski) are present after days to weeks in UMN lesions but always absent with LMN
• Muscle manifestations in UMN include random spasms and atrophy, with LMN lesions, fibrillations and atrophy occur after weeks
• Both lesion types result in weakness or paralysis

Motor Symptoms

• Plegia = complete lesion
• Paresis = some muscle strength preserved
• Tetraplegia (or quadriplegia) is an injury of the cervical spinal cord
  • Patients can often move their arms using segments above the injury (e.g., C7 injury can still flex forearms through C5 segment)
• Paraplegia involves injury to the thoracic or lumbo-sacral cord, including cauda equina
• Hemiplegia involves paralysis of one half of the body
  • Usually seen in brain injuries (e.g., stroke)

Motor Exam

• Muscle strength helps localize the lesion
• Upper cervical lesions result in quadriplegia with impaired respiration
• Lower cervical damage preserves proximal arm strength, but leads to hand and leg weakness
• Thoracic injuries present with paraplegia; paraplegia can also occur with a midline brain lesion
• Tone increases distal to the lesion

Babinski Sign

• Babinski sign is indicative of an upper motor neuron (UMN) syndrome
• In a normal response, the toes flex downward
• In a plantar extensor response (Babinski sign), the toes extend upward

Sensory Exam

• It's important to establish a sensory level
• Examine Dermatomes, noting nipple sensation at T4-5 & the umbilicus at T8-9
• Assess posterior columns for vibration & joint position sense
• Explore spinothalamic tracts for pain & temperature

Spinal Shock

• Spinal shock results in flaccid paralysis and loss of autonomic reflexes, especially with injury above T6.
• Bowel and bladder dysfunction are also observed

Autonomic Disturbances

• Neurogenic bladder - urgency, incontinence, or retention
• Bowel dysfunction - often more constipation, less incontinence
• High cord lesions can disrupt blood pressure control & alter sweating patterns.

Central Cord Syndrome: Case Study 1

• Ascending/descending tracts that may be involved include:
  • With small lesions, the anterolateral spinothalamic tracts are impacted
  • With larger lesions, the cuneatus fasciculus of the dorsal column and medial aspect of the lateral corticospinal tracts are affected

Central Cord Syndrome

• Spinal tracts' somatotopic arrangement goes from medial to lateral, cervical to sacral
  • Central Cord Syndrome affects upper extremities more than lower
• Since the cord's periphery remains, thoracic, lumbar, and sacral functions are retained
  • Bilateral loss of pain and temperature discrimination in upper limbs and upper trunk is observed
• Larger lesions = loss of discriminative touch and conscious proprioception; motor impairments can occur if lateral corticospinal tracts are involved
• A lesion interrupts fibers crossing into the spinothalamic tracts, affecting tendon stretch reflexes
• With enlargement, it affects the intermediolateral columns (impairing autonomic function) and lateral corticospinal tracts

Syringomyelia

• Syringomyelia involves a fluid-filled cavitation in the center of the spinal cord
• The cervical cord is the most common site
  • Loss of pain and temperature related to crossing fibers arises soon after onset.
  • Cape-like sensory loss develops
• See weakness and atrophy with hyporeflexia in the arms
• In later stages, CST involvement leads to brisk reflexes in the legs, spasticity, and weakness
• It may arise as a delayed consequence of trauma or malformation

Anterior Cord Syndrome: Case Study 2

• Ascending and descending tracts that are involved - essentially all except those of the Dorsal Column
• Results in bilateral loss of pain and temperature discrimination and paralysis below the lesion level
• Proprioception and discriminative touch remain intact

Spinal Cord Arteries

• The anterior spinal artery is formed by branches of the vertebral arteries
  • It runs down the anterior median fissure - supplies the anterior two-thirds of the spinal cord
• Posterior spinal arteries originate from the vertebral arteries and descend to supply the posterior one-third of the spinal cord
• Often arising from the posterior inferior cerebellar arteries (PICAs)
• The artery of Adamkiewicz is most commonly found between T9-T12, and can originate anywhere from T8 to L3
  • It originates most commonly on the left side, so injury can lead to paraplegia

Brown-Sequard Syndrome: Case Study 3

• Ascending and descending tracts that are involved - all on one side of the spinal cord
• Dorsal Column damage causes loss of proprioception and discriminative touch ipsilaterally (below the lesion)
• Damage to the Anterolateral Spinothalamic tract causes a loss of crude touch, pain and temperature sense on the contralateral side a few levels below the lesion
  • The difference in affected level occurs because the anteriolateral spinothalamic tracts ascend ipsilaterally several segments before decussating
• Damage to descending tracts causes paralysis ipsilaterally below the lesion

Brown-Sequard Syndrome

• The syndrome has the following characteristics
• Cord hemisection: can be from trauma or tumor
• Dissociated sensory loss:
  • loss of pain/temperature sensation contralaterally
  • involves the crossing of spinothalamic tracts 1-2 segments above where they enter
  • Also have loss of of vibration/proprioception ipsilaterally
  • pathways cross at the brainstem level
  • Weakness and UMN findings ipsilateral to the lesion