🏥 Spinal Cord Diseases (Myelopathies): Syndromes and Rehabilitation

Spinal cord diseases (Myelopathies) result from damage, compression, or inflammation of the spinal cord, causing neurological deficits below the level of the lesion. This guide details the classification, the distinct clinical cord syndromes, and the phased physiotherapy approach essential for managing both traumatic and non-traumatic myelopathy.

1. 📚 Classification and Etiology (Causes)

Definition

Myelopathy specifically refers to dysfunction of the spinal cord itself, resulting in Upper Motor Neuron (UMN) signs below the lesion level, often with sensory loss and autonomic changes.

A. Based on Etiology (Key Categories)

Category	Examples	Key Feature
Traumatic	Spinal Cord Injury (SCI), Fractures, Dislocations (Road accidents, falls).	Acute onset, often leads to Spinal Shock.
Degenerative	Cervical Spondylotic Myelopathy (CSM), Disc Herniation.	Chronic, progressive compression (most common non-traumatic cause).
Infectious	Tuberculosis (Pott’s spine), Epidural Abscess.	Requires urgent anti-microbial treatment and stabilization.
Inflammatory/Autoimmune	Transverse Myelitis, Multiple Sclerosis (MS), Neuromyelitis Optica (NMO).	Acute/subacute onset, often high degree of recovery potential.
Vascular	Anterior Spinal Artery (ASA) Infarction.	Acute, painful onset, specific incomplete cord syndrome.

2. 🔬 Pathophysiology: Tract Damage and Neurological Level

[Image of Spinal Cord Cross Section showing ascending and descending tracts]

The Damage Pattern

The location of the damage within the spinal cord determines the clinical picture (level and type of deficit):

• Descending Tracts (Corticospinal): Damage leads to Motor Deficits (weakness, paralysis) and UMN signs (spasticity, hyperreflexia) below the lesion level.
• Ascending Tracts:
  • Dorsal Columns: Loss of Proprioception and Vibration Sense (causes sensory ataxia).
  • Spinothalamic Tracts: Loss of Pain and Temperature Sensation.
• Autonomic: Disruption of sympathetic/parasympathetic outflow $\rightarrow$ Bladder, bowel, sexual dysfunction, and Autonomic Dysreflexia.

3. ⭐ Incomplete Spinal Cord Syndromes (Exam Critical)

These syndromes result from partial damage, usually due to trauma, and present distinct, asymmetrical patterns of motor and sensory loss.

Syndrome	Pathology	Key Motor/Sensory Pattern
Central Cord	Damage to center (most common in Cervical hyperextension injury).	Motor loss: Upper Limbs > Lower Limbs. Variable sensory loss.
Anterior Cord	Damage to anterior 2/3rds (e.g., Anterior Spinal Artery Infarction).	Loss of Motor and Pain/Temperature below lesion. Proprioception Preserved.
Brown-Sequard	Hemi-section of the cord (e.g., penetrating trauma/tumor).	Ipsilateral Motor Paralysis and Proprioception Loss. Contralateral Pain and Temperature Loss.
Posterior Cord	Damage to posterior columns (rare, e.g., B12 deficiency).	Loss of Proprioception and Vibration. Motor function preserved.

Conus Medullaris and Cauda Equina

• Conus Medullaris Syndrome (L1–L2): Damage to the terminal end of the spinal cord. Presents as Symmetric lower limb weakness and early, prominent bladder/bowel dysfunction (UMN signs may be mixed LMN/UMN).
• Cauda Equina Syndrome (L3–S5): Damage to the nerve roots below the conus. Presents as LMN Paralysis, severe Saddle Anesthesia, and urinary retention. NEUROSURGICAL EMERGENCY.

4. 🚩 Clinical Features and Autonomic Dysfunction

Motor and Sensory Signs

• Motor: Weakness/paralysis, UMN signs (Spasticity, Hyperreflexia, Babinski). Flaccidity may persist if the lesion is at the conus or due to Spinal Shock.
• Sensory Level: A distinct horizontal line on the trunk marking the transition from normal to impaired sensation $\rightarrow$ vital for locating the lesion level.

Autonomic Dysfunction (Critical for Safety)

• Autonomic Dysreflexia (AD): A potentially life-threatening emergency in lesions above T6. Noxious stimulus (e.g., full bladder, skin pressure) causes massive sympathetic surge $\rightarrow$ severe, sudden Hypertension and headache.
• Orthostatic Hypotension: Loss of sympathetic control below T6 leads to failure of vasoconstriction, causing dizziness/fainting upon standing.
• Bladder/Bowel/Sexual Dysfunction.

5. 🔬 Investigations and Management

A. Investigations

• MRI Spine: The Gold Standard. Excellent for visualizing soft tissues (cord, discs, tumors, inflammatory lesions).
• CT Scan: Superior for bony trauma and fracture screening.
• Laboratory Tests: $B_{12}$ levels, ESR/CRP (for inflammation), Autoimmune panels.

B. Medical and Surgical Management

• Traumatic: Emergency spinal decompression and stabilization.
• Inflammatory (e.g., Transverse Myelitis): High-dose corticosteroids, plasma exchange, or immunosuppressants.
• Degenerative (CSM): Surgical decompression (anterior cervical discectomy and fusion - ACDF) if compression is severe and progressive.

6. 🛠️ Physiotherapy Management: Phased Approach

Management is adapted to the ASIA Impairment Scale (AIS) and the stability of the spine.

A. Early Phase (Acute/Immobilization)

• Positioning & PROM: Strict Passive ROM to prevent contractures (especially hip flexors, ankle plantarflexors). Use of splints (AFO, resting hand splints).
• Respiratory Care: Chest Physiotherapy and breathing exercises (essential in cervical/high thoracic lesions).
• Pressure Relief: Hourly turning and specialized cushions to prevent Pressure Sores.
• Bed Mobility: Log-rolling techniques to maintain spinal alignment.

B. Subacute Phase (Functional Reintegration)

• Strengthening: Focus on preserved and partially innervated muscles. Strengthen the upper body aggressively for transfers and manual wheelchair propulsion (especially in paraplegia).
• Spasticity Management: Prolonged stretching, weight-bearing activities (standing frame), and positioning. Avoid stimuli that trigger spasticity or AD.
• Gait Training (Incomplete Lesions): Use of parallel bars, harness systems (Bodyweight-Supported Treadmill Training - BWSTT), or robotic assistance for high-repetition, task-specific training.
• Balance: Sitting balance training (with and without hand support).

C. Chronic Phase (Community and Adaptation)

• Adaptive Skills: Advanced wheelchair skills, independent transfers, and ADL training using assistive devices.
• Pain Management: TENS for neuropathic pain.
• Fitness: Aerobic conditioning for general health and fatigue management.

7. 💡 Patient Education and Long-Term Care

Education empowers the patient for lifetime self-management:

• Skin Integrity: Lifelong vigilance for pressure sore prevention.
• Autonomic Dysreflexia (AD): Recognition of early symptoms (throbbing headache, flushed skin) and immediate response (sit up, check catheter/bowel).
• Adaptive Technology: Selection of appropriate orthotics (e.g., KAFO), manual or power wheelchair, and home modifications.
• Bladder/Bowel Programs: Training in intermittent catheterization and bowel protocols.

8. 📈 Prognosis

• Complete SCI: Very poor prognosis for functional motor recovery below the lesion.
• Incomplete SCI: Highly variable. Patients with Brown-Sequard or Central Cord Syndrome generally have better functional outcomes than those with Anterior Cord Syndrome.
• Non-Traumatic: Prognosis depends heavily on the cause (e.g., B12 deficiency treated early often reverses deficits, while chronic CSM may only stabilize after surgery).

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❓ Frequently Asked Questions (FAQs)

Q: What is Spinal Shock and how does it affect initial assessment?

A: Spinal Shock is a state that occurs immediately post-SCI, characterized by temporary loss of all neurological function, including reflexes and tone, below the level of the lesion. It can last days to weeks. This makes initial assessment (e.g., determining UMN vs. LMN) unreliable until shock resolves.

Q: Why is Central Cord Syndrome characterized by greater upper limb weakness?

A: The Central Cord Syndrome commonly results from hyperextension in the cervical spine. The corticospinal tract fibers controlling the upper limbs are arranged more medially in the cord, making them more susceptible to compression damage from the central edema or bone fragments compared to the more laterally arranged fibers for the lower limbs.

Q: What is the first immediate action for Autonomic Dysreflexia (AD)?

A: The immediate action is to sit the patient upright (or raise the head of the bed) to lower the blood pressure and prevent stroke. Next, find and remove the noxious stimulus (e.g., check for kinked catheter, full bladder, tight clothes, or pressure sore).

Q: What is the primary imaging modality for diagnosing Cervical Spondylotic Myelopathy (CSM)?

A: Magnetic Resonance Imaging (MRI) is the gold standard for CSM, as it clearly visualizes the soft tissue compression (disc herniation, osteophytes, ligamentum flavum thickening) causing indentation and signal changes (edema/myelomalacia) within the spinal cord.

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🎯 10 Practice MCQs for Spinal Cord Exam

Q1. A patient presents with Ipsilateral loss of motor function and contralateral loss of pain/temperature sensation below the level of the lesion. This syndrome is:

Answer: B). Brown-Sequard syndrome results from hemisection, affecting motor/proprioception (uncrossed) and pain/temperature (crossed) differently.

Q2. The primary cause of mortality in high cervical spinal cord injury (SCI) is:

Answer: A). Lesions C3, C4, C5 "keep the diaphragm alive." High lesions paralyze the diaphragm and intercostals.

Q3. A patient reporting loss of vibration and position sense with a positive Romberg test, but preserved pain and motor function, likely has damage to the:

Answer: C). Proprioception and vibration are carried by the dorsal columns (Posterior Cord Syndrome).

Q4. Autonomic Dysreflexia (AD) is a medical emergency that typically occurs in spinal cord lesions located:

Answer: A). T6 is the key anatomical level for major sympathetic outflow, controlling splanchnic circulation.

Q5. The most common non-traumatic cause of myelopathy in older adults is:

Answer: C). CSM results from chronic compression by degenerative structures (osteophytes, discs, ligaments).

Q6. Which finding is considered the absolute neurosurgical emergency among the following?

Answer: B). Cauda Equina Syndrome requires immediate decompression to prevent permanent bladder/bowel dysfunction.

Q7. The goal of using Bodyweight-Supported Treadmill Training (BWSTT) for an incomplete SCI patient is primarily:

Answer: B). BWSTT provides partial weight-bearing and high-intensity practice to drive spinal locomotor network plasticity.

Q8. Which clinical finding best suggests the onset of permanent spasticity rather than the state of Spinal Shock?

Answer: A). Spinal shock is marked by absent reflexes (areflexia). The reappearance of reflexes (hyperreflexia) signals the resolution of spinal shock and the onset of UMN signs (spasticity).

Q9. A key characteristic of Anterior Cord Syndrome is the preservation of:

Answer: C). ACS is caused by ASA infarct, sparing the posterior columns (dorsal columns) responsible for proprioception/vibration.

Q10. What is the primary role of physiotherapy in the acute (ICU) phase of stable SCI?

Answer: B). Early PT focuses on respiratory support, positioning, and joint protection until the spine is stable and the patient is medically ready for mobilization.

📚 Important Academic References

• Kirshblum, S. C., et al. (2011). International Standards for Neurological Classification of Spinal Cord Injury (revised). The Journal of Spinal Cord Medicine, 34(6), 535–546. (The ASIA Standard).
• Ditunno, J. F., et al. (2009). Spinal cord injury: Functional changes after rehabilitation. Archives of Physical Medicine and Rehabilitation, 90(7), 1083–1092. (Functional outcome prediction).
• McKinley, W. O., et al. (2007). Central cord syndrome: analysis of functional and neurological outcomes. Spinal Cord, 45(3), 184–192. (Clinical Syndrome Analysis).
• O’Sullivan, S. B., & Schmitz, T. J. (2019). Physical Rehabilitation (7th ed.). F.A. Davis Company. (For comprehensive Physiotherapy Assessment and Management).