Posterior Spinal Artery Syndrome(PSAS)

Posterior spinal artery syndrome (PSAS), also known as posterior cord syndrome or dorsal cord syndrome, is a rare form of incomplete spinal cord injury. It arises from occlusion or compromise of one or more posterior spinal arteries, which supply the dorsal columns and dorsal horns. As a result, patients experience selective loss of proprioception, vibration sense, and fine touch below the level of the lesion, while motor function and pain/temperature pathways—carried by the anterior and anterolateral tracts—remain intact en.wikipedia.orgradiopaedia.org.

Posterior Spinal Artery Syndrome (PSAS), also known as posterior cord syndrome, is a rare form of incomplete spinal cord injury characterized by infarction or lesion of the paired posterior spinal arteries supplying the dorsal (posterior) columns, posterior horns, and posterolateral portions of the lateral columns of the spinal cord. These arteries arise from the vertebral arteries and run the length of the cord, providing blood flow critical for proprioception and fine touch transmission. When one or both posterior spinal arteries become occluded—due to thromboembolism, trauma, compression by tumors or herniated discs, or inflammatory conditions such as vitamin B₁₂ deficiency and tertiary syphilis—the result is selective loss of vibration and proprioceptive sensation below the level of injury, while motor function (mediated by the anterior corticospinal tracts) and pain-temperature sensation (spinothalamic tracts) are often preserved en.wikipedia.orgosmosis.org.

PSAS accounts for less than 1% of all spinal cord injury syndromes and is frequently under-recognized due to its predominantly sensory presentation. On imaging, it may manifest as hyperintense signals in the dorsal cord on T2-weighted MRI, but early changes can be subtle, leading to diagnostic delays en.wikipedia.orgradiopaedia.org.

Types

1. Unilateral PSAS
   Occurs when a single posterior spinal artery is occluded, resulting in hemilateral dorsal column dysfunction. Patients typically present with loss of vibration and proprioception on one side below the lesion, while the opposite side remains spared en.wikipedia.orgradiopaedia.org.

2. Bilateral PSAS
   Involves occlusion of both posterior spinal arteries or a common posterior pial plexus, producing symmetrical sensory deficits in vibration and position sense. A clear sensory level may be noted, below which tactile discrimination is lost on both sides radiopaedia.orguptodate.com.

3. Segmental PSAS
   Results from interruption of a single radicular artery supplying one spinal segment. This leads to a focal band of dorsal column loss at the corresponding level, often transient if collateral vessels partially compensate for the occlusion radiopaedia.orguptodate.com.

Causes

1. Thromboembolic occlusion
   Emboli from proximal atherosclerotic plaques can lodge in the posterior spinal artery, abruptly cutting off blood flow and causing dorsal cord infarction radiopaedia.orguptodate.com.

2. Atherosclerosis of vertebral arteries
   Progressive plaque buildup in vertebral arteries may extend into posterior spinal branches, leading to chronic narrowing and episodic ischemia of the dorsal columns radiopaedia.orguptodate.com.

3. Arterial dissection
   Dissection of the aortic or vertebral artery can interrupt flow into posterior spinal arteries, resulting in acute dorsal cord ischemia and sensory deficits radiopaedia.orgpmc.ncbi.nlm.nih.gov.

4. Fibrocartilaginous embolism
   Disc material dislodged during trauma can embolize into spinal arteries, producing sudden infarction of the dorsal columns radiopaedia.orgpmc.ncbi.nlm.nih.gov.

5. Systemic hypotension
   Severe drops in blood pressure may create watershed infarctions in areas supplied by posterior spinal arteries, particularly at the thoracic levels uptodate.comradiopaedia.org.

6. Vasculitis
   Conditions such as giant cell arteritis or Takayasu arteritis can inflame and occlude spinal arteries, leading to PSAS uptodate.comamboss.com.

7. Cardiac embolism
   Atrial fibrillation or infective endocarditis may shower thrombi into the spinal vasculature, occluding posterior spinal arteries uptodate.compmc.ncbi.nlm.nih.gov.

8. Hypercoagulable states
   Disorders like antiphospholipid syndrome or malignancy-associated coagulopathy increase thrombosis risk in small spinal vessels uptodate.compmc.ncbi.nlm.nih.gov.

9. Sickle cell disease
   Vaso-occlusive episodes can affect spinal arteries, causing intermittent dorsal column ischemia and sensory loss uptodate.comjournals.lww.com.

10. Diabetes mellitus
    Chronic microangiopathy narrows small spinal vessels, predisposing to insidious dorsal column compromise uptodate.comjournals.lww.com.

11. Iatrogenic injury
    Spinal surgery or instrumentation may inadvertently damage posterior spinal artery branches, leading to segmental PSAS radiopaedia.orgajnr.org.

12. Radiation therapy
    High-dose spinal irradiation induces endothelial damage and fibrosis, causing delayed vascular occlusion of PSA branches uptodate.comjournals.lww.com.

13. Tumor compression
    Intradural or extradural masses such as meningiomas can press on and compromise posterior spinal arteries uptodate.compmc.ncbi.nlm.nih.gov.

14. Infectious endarteritis
    Neurosyphilis or tuberculosis may inflame spinal arteries, occluding blood flow to the dorsal cord osmosis.orgpubmed.ncbi.nlm.nih.gov.

15. Radiation myelopathy
    Vascular injury from radiation leads to late-onset PSAS by progressive arterial damage journals.lww.com.

16. Vertebral artery occlusion
    Atherosclerotic narrowing of vertebral arteries can secondarily impair PSA perfusion pubmed.ncbi.nlm.nih.govuptodate.com.

17. Minor trauma
    Hyperextension injuries may stretch and occlude small PSA branches, triggering acute PSAS pmc.ncbi.nlm.nih.govradiopaedia.org.

18. Disc herniation
    Herniated material can compress radicular arteries feeding the dorsal cord radiopaedia.orgradiopaedia.org.

19. Arteriovenous malformations
    AVMs near the dorsal cord create a steal phenomenon, chronically under-perfusing PSA territories uptodate.comsciencedirect.com.

20. Smoking
    Tobacco-induced endothelial injury accelerates spinal arterial atherosclerosis and thrombosis uptodate.comjournals.lww.com.

Symptoms

1. Loss of vibration sensation
   Patients cannot detect tuning fork vibrations on bony prominences, reflecting dorsal column damage osmosis.orgphysio-pedia.com.

2. Impaired proprioception
   Difficulty perceiving limb position without visual cues leads to uncoordinated movements osmosis.orgphysio-pedia.com.

3. Sensory ataxia
   Dorsal column dysfunction produces unsteady gait and poor limb coordination osmosis.orgphysio-pedia.com.

4. Positive Romberg sign
   Standing with feet together and eyes closed causes swaying or falls due to lost proprioceptive feedback osmosis.orgphysio-pedia.com.

5. Two-point discrimination impairment
   Patients cannot distinguish two closely spaced stimuli, indicating dorsal column loss osmosis.orgphysio-pedia.com.

6. Dysesthesia
   Abnormal unpleasant sensations—burning or “pins-and-needles”—occur in affected dermatomes osmosis.orgphysio-pedia.com.

7. Tactile agnosia
   Loss of stereognosis prevents object recognition by touch alone osmosis.orgphysio-pedia.com.

8. Loss of fine touch
   Patients fail to perceive light tactile stimuli across dermatomes osmosis.orgphysio-pedia.com.

9. Gait disturbances
   Wide-based, high-stepping, or staggering gait patterns arise from sensory ataxia osmosis.orgphysio-pedia.com.

10. Impaired graphesthesia
    Inability to identify letters or numbers traced on the skin indicates dorsal column compromise osmosis.orgphysio-pedia.com.

11. Reduced vibratory threshold
    Graded tuning fork testing reveals decreased vibration detection thresholds osmosis.orgphysio-pedia.com.

12. Heaviness or clumsiness
    Patients describe their limbs as “heavy blocks” when walking without visual cues osmosis.orgphysio-pedia.com.

13. Worsened imbalance in darkness
    Low-light environments exacerbate gait instability due to reliance on vision osmosis.orgphysio-pedia.com.

14. Poor heel-to-toe walking
    Uneven stepping on a straight line indicates dorsal column dysfunction osmosis.orgphysio-pedia.com.

15. Impaired barognosis
    Inability to perceive weight differences in objects held in hand reflects dorsal column loss osmosis.orgphysio-pedia.com.

16. Loss of kinesthesia
    Patients cannot detect passive movement of joints, showing large-fiber sensory loss osmosis.orgphysio-pedia.com.

17. Dermatomal numbness
    Band-like sensory loss corresponds to the level of posterior column involvement osmosis.orgphysio-pedia.com.

18. Reflex changes
    Absent abdominal or cremasteric reflexes may occur if dorsal horns are affected osmosis.orgphysio-pedia.com.

19. Fine motor difficulty
    Tasks like buttoning or writing become challenging without precise sensory feedback osmosis.orgphysio-pedia.com.

20. Preserved pain/temperature
    Spinothalamic pathways remain intact, so pain and temperature sensation are usually spared osmosis.orgphysio-pedia.com.

Diagnostic Tests

Physical Exam Tests

1. Vibration testing
   A 128 Hz tuning fork placed on bony landmarks assesses large-fiber dorsal column function osmosis.orgphysio-pedia.com.

2. Proprioception assessment
   Examiner passively moves joints while patient reports limb position to test dorsal column integrity osmosis.orgphysio-pedia.com.

3. Romberg’s sign
   Standing feet-together with eyes closed; positive if patient sways or falls due to loss of proprioception osmosis.orgphysio-pedia.com.

4. Gait analysis
   Observation of walking pattern—wide-based, high stepping—indicates sensory ataxia from dorsal column lesions osmosis.orgphysio-pedia.com.

5. Light touch testing
   Cotton swab stroking assesses A-beta fibers conveying tactile information through the dorsal columns osmosis.orgphysio-pedia.com.

6. Pinprick testing
   Sharp stimuli distinguish preserved spinothalamic function from impaired dorsal columns osmosis.orgphysio-pedia.com.

7. Temperature discrimination
   Warm and cold stimuli confirm intact anterolateral pathways despite dorsal column involvement osmosis.orgphysio-pedia.com.

8. Deep tendon reflexes
   Assessment helps differentiate PSAS (often preserved or brisk reflexes) from anterior cord syndromes osmosis.orgphysio-pedia.com.

Manual Tests

1. Tuning fork test
   Manually applied tuning fork evaluates vibration sense and large-fiber function osmosis.orgphysio-pedia.com.

2. Two-point discrimination
   Determines minimal distinguishable distance between two stimuli on the skin osmosis.orgphysio-pedia.com.

3. Graphesthesia
   Tracing shapes on the skin to assess cortical and dorsal column processing osmosis.orgphysio-pedia.com.

4. Stereognosis
   Identification of common objects by touch alone tests higher-order dorsal column function osmosis.orgphysio-pedia.com.

5. Barognosis
   Differentiation of object weights held in hand evaluates dorsal column pathways osmosis.orgphysio-pedia.com.

6. Kinesthesia test
   Passive joint movements with patient reporting direction assess proprioceptive tracts osmosis.orgphysio-pedia.com.

7. Tactile localization
   Patient points to site of light touch with eyes closed, evaluating spatial accuracy of sensation osmosis.orgphysio-pedia.com.

8. Vibration threshold
   Graded tuning forks determine the lowest amplitude of vibration perceived osmosis.orgphysio-pedia.com.

Lab and Pathological Tests

1. Complete blood count (CBC)
   Screens for anemia, infection, or systemic contributors to cord ischemia uptodate.compmc.ncbi.nlm.nih.gov.

2. Erythrocyte sedimentation rate (ESR)
   Elevated ESR indicates systemic inflammation or vasculitis affecting spinal vessels uptodate.compmc.ncbi.nlm.nih.gov.

3. C-reactive protein (CRP)
   High CRP levels point to acute inflammatory states that may precipitate vascular occlusion uptodate.compmc.ncbi.nlm.nih.gov.

4. Vitamin B₁₂ level
   Deficiency can mimic PSAS by causing dorsal column degeneration uptodate.compmc.ncbi.nlm.nih.gov.

5. Syphilis serology (RPR/VDRL)
   Detects neurosyphilis, which can involve the posterior cord vasculature uptodate.compmc.ncbi.nlm.nih.gov.

6. Folate level
   Low folate impairs vascular health and neuronal function uptodate.compmc.ncbi.nlm.nih.gov.

7. Autoimmune panel
   ANA and related markers identify systemic vasculitides affecting spinal arteries uptodate.compmc.ncbi.nlm.nih.gov.

8. Coagulation studies
   Tests for antiphospholipid antibodies and clotting factors assess thrombophilia risks uptodate.compmc.ncbi.nlm.nih.gov.

Electrodiagnostic Tests

1. Somatosensory evoked potentials (SSEPs)
   Record cortical responses to peripheral stimuli, evaluating dorsal column conduction osmosis.orgradiopaedia.org.

2. Motor evoked potentials (MEPs)
   Assess corticospinal tract function, demonstrating preserved motor pathways in PSAS osmosis.orgradiopaedia.org.

3. Nerve conduction studies
   Measure peripheral nerve function to exclude neuropathies mimicking central sensory loss osmosis.orgradiopaedia.org.

4. Electromyography (EMG)
   Evaluates muscle electrical activity, ruling out primary muscle or lower motor neuron diseases osmosis.orgradiopaedia.org.

5. H-reflex testing
   Examines monosynaptic reflex arcs, often preserved in PSAS, helping differentiate it from anterior cord syndromes osmosis.orgradiopaedia.org.

6. F-wave studies
   Assess proximal nerve conduction and can localize lesions to roots or central pathways osmosis.orgradiopaedia.org.

7. Central motor conduction time
   Transcranial magnetic stimulation evaluates spinal conduction; normal results support isolated dorsal column involvement osmosis.orgradiopaedia.org.

8. Sensory nerve action potentials
   Measure peripheral sensory fiber responses to distinguish peripheral from central deficits osmosis.orgradiopaedia.org.

Imaging Tests

1. MRI T2-weighted imaging
   Reveals hyperintense signals in dorsal columns indicative of infarction or edema radiopaedia.orgpmc.ncbi.nlm.nih.gov.

2. Diffusion-weighted imaging (DWI)
   Detects acute ischemic changes earlier than conventional MRI sequences radiopaedia.orgpmc.ncbi.nlm.nih.gov.

3. MR angiography
   Noninvasively visualizes posterior spinal arteries to identify stenosis or occlusion radiopaedia.orgpmc.ncbi.nlm.nih.gov.

4. CT angiography
   Provides detailed 3D images of spinal vasculature for detecting anatomical variants or blockages radiopaedia.orgpmc.ncbi.nlm.nih.gov.

5. Digital subtraction angiography
   Gold-standard invasive study of spinal arteries, guiding potential endovascular treatments radiopaedia.orgpmc.ncbi.nlm.nih.gov.

6. CT myelography
   Shows spinal cord contour changes and flow disturbances when MRI is contraindicated radiopaedia.orgpmc.ncbi.nlm.nih.gov.

7. Doppler ultrasound
   Assesses vertebral artery flow velocities to infer PSA perfusion status radiopaedia.orgpmc.ncbi.nlm.nih.gov.

8. Functional MRI
   Advanced research tool evaluating spinal perfusion and functional integrity of dorsal columns radiopaedia.orgpmc.ncbi.nlm.nih.gov.

Non-Pharmacological Treatments for PSAS

Rehabilitation and supportive therapies are the cornerstone of PSAS management. Below are 30 evidence‐based, non-drug interventions categorized into physiotherapy/electrotherapy, exercise therapies, mind-body approaches, and educational self-management.

A. Physiotherapy & Electrotherapy Modalities

1. Thermotherapy (Heat Therapy)
   Description: Application of moist heat packs or paraffin wax to the paraspinal muscles.
   Purpose: To reduce muscle spasm, increase tissue extensibility, and relieve pain.
   Mechanism: Heat increases local blood flow, raises tissue temperature, and decreases muscle spindle activity, promoting relaxation physio-pedia.com.

2. Cryotherapy (Cold Therapy)
   Description: Use of ice packs or cold compresses over the injured segment.
   Purpose: To decrease inflammation, swelling, and acute pain during the first 48–72 hours post-injury.
   Mechanism: Cold constricts blood vessels, reduces metabolic rate in tissues, and slows nerve conduction, diminishing pain signals physio-pedia.com.

3. Transcutaneous Electrical Nerve Stimulation (TENS)
   Description: Low-voltage electrical currents delivered via skin electrodes.
   Purpose: To modulate pain and improve comfort during rehabilitation.
   Mechanism: Activates Aβ fibers that inhibit nociceptive signal transmission at the dorsal horn (“gate control” theory) and may stimulate endorphin release physio-pedia.com.

4. Interferential Current Therapy (IFC)
   Description: Two medium-frequency currents intersecting to produce a low-frequency effect.
   Purpose: To provide deeper pain relief and reduce edema compared to conventional TENS.
   Mechanism: The beat frequency penetrates deeper tissues, leading to analgesia through similar gating and endorphin mechanisms physio-pedia.com.

5. Therapeutic Ultrasound
   Description: High-frequency sound waves applied with a transducer over the spine.
   Purpose: To enhance tissue healing, reduce inflammation, and improve flexibility.
   Mechanism: Mechanical vibrations produce deep-heat, increasing cell permeability, collagen extensibility, and local circulation physio-pedia.com.

6. Low-Level Laser Therapy (LLLT)
   Description: Non-thermal laser light applied to injured tissues.
   Purpose: To accelerate nerve and tissue repair and reduce pain.
   Mechanism: Photobiomodulation stimulates mitochondrial activity, increasing ATP production and modulating inflammatory mediators physio-pedia.com.

7. Neuromuscular Electrical Stimulation (NMES)
   Description: Electrical currents that elicit muscle contractions.
   Purpose: To prevent atrophy, improve muscle strength, and re-educate paralyzed muscles.
   Mechanism: Direct activation of motor neurons enhances muscle fiber recruitment and promotes neuroplasticity physio-pedia.com.

8. Pulsed Electromagnetic Field Therapy (PEMF)
   Description: Application of time-varying magnetic fields to the spine.
   Purpose: To support tissue repair and reduce neuropathic pain.
   Mechanism: Alters ion binding at the cell membrane, modulates inflammatory cytokines, and enhances microcirculation physio-pedia.com.

9. Short Wave Diathermy (SWD)
   Description: High-frequency electromagnetic energy generating heat in deep tissues.
   Purpose: To relieve muscle spasm and improve joint mobility.
   Mechanism: Tissue heating increases blood flow, enzyme activity, and collagen extensibility physio-pedia.com.

10. Extracorporeal Shock Wave Therapy (ESWT)
    Description: Acoustic shock waves focused on soft tissue.
    Purpose: To promote regeneration and reduce chronic pain.
    Mechanism: Stimulates angiogenesis, disrupts pain receptors, and facilitates release of growth factors physio-pedia.com.

11. Biofeedback
    Description: Real-time visual or auditory feedback of muscle activity.
    Purpose: To enhance patient awareness and voluntary control of muscle activation.
    Mechanism: Provides sensory feedback that helps retrain neuromuscular pathways and reduce maladaptive patterns physio-pedia.com.

12. Magnetotherapy
    Description: Static magnetic fields applied via magnetized pads.
    Purpose: To alleviate neuropathic pain and support tissue healing.
    Mechanism: Magnetic fields may influence ion transport and cellular signaling, modulating pain perception physio-pedia.com.

13. Iontophoresis
    Description: Delivery of anti-inflammatory medications (e.g., dexamethasone) through the skin via low-level electrical current.
    Purpose: To target analgesics or anti-inflammatories directly to the lesion site.
    Mechanism: Electrical repulsion drives charged drug molecules through the skin into underlying tissues physio-pedia.com.

14. Traction Therapy
    Description: Application of longitudinal pull to decompress the spinal segments.
    Purpose: To reduce mechanical compression on the cord or nerve roots and relieve pain.
    Mechanism: Gently separates vertebral bodies, increasing intervertebral space and improving blood flow physio-pedia.com.

15. Vibration Therapy
    Description: Localized or whole-body vibration platforms.
    Purpose: To stimulate muscle activation and improve proprioception.
    Mechanism: Vibratory stimuli activate muscle spindles and mechanoreceptors, enhancing neuromuscular coordination physio-pedia.com.

B. Exercise Therapies

16. Core Stabilization Exercises
    Description: Low-level activation of deep trunk muscles (e.g., transversus abdominis).
    Purpose: To support spinal alignment and reduce stress on injured segments.
    Mechanism: Reinforces feed-forward activation of stabilizer muscles, improving load distribution physio-pedia.com.

17. Balance Training
    Description: Tasks on unstable surfaces (e.g., foam pads).
    Purpose: To restore proprioceptive feedback and prevent falls.
    Mechanism: Challenges sensory integration, enhancing vestibular and somatosensory inputs physio-pedia.com.

18. Gait Training
    Description: Treadmill or overground walking with assistance.
    Purpose: To recover walking capacity and endurance.
    Mechanism: Repetitive task-specific practice promotes central pattern generator activation and neuroplasticity physio-pedia.com.

19. Flexibility Exercises
    Description: Gentle stretching of paraspinal and lower-limb muscles.
    Purpose: To maintain range of motion and prevent contractures.
    Mechanism: Sustained stretch reduces muscle stiffness and improves collagen elasticity physio-pedia.com.

20. Endurance Training
    Description: Low-impact aerobic activities (e.g., cycling).
    Purpose: To enhance cardiovascular fitness and support spinal cord perfusion.
    Mechanism: Increases heart rate and systemic circulation, improving oxygen delivery to neural tissue physio-pedia.com.

C. Mind-Body Practices

21. Yoga
    Description: Combined postures, breathing, and meditation.
    Purpose: To reduce pain, improve flexibility, and enhance mind-body awareness.
    Mechanism: Gentle stretching and focused breathing modulate the autonomic nervous system, decreasing muscle tension physio-pedia.com.

22. Mindfulness Meditation
    Description: Non-judgmental focus on present sensations and thoughts.
    Purpose: To improve pain coping and reduce anxiety or depression.
    Mechanism: Alters brain regions involved in pain modulation (e.g., anterior cingulate cortex) through neuroplastic changes physio-pedia.com.

23. Tai Chi
    Description: Slow, flowing movements coordinated with breath.
    Purpose: To enhance balance, proprioception, and mental focus.
    Mechanism: Integrates vestibular and proprioceptive cues, promoting neural reorganization physio-pedia.com.

24. Biofeedback-Assisted Relaxation
    Description: Feedback of physiological signals (e.g., heart rate) to guide relaxation.
    Purpose: To lower sympathetic arousal and reduce spasticity.
    Mechanism: Increases parasympathetic activity and downregulates muscle tone via cortical control physio-pedia.com.

25. Guided Imagery
    Description: Visualization of calming scenes or successful movement.
    Purpose: To manage pain and enhance motor planning.
    Mechanism: Activates similar cortical networks as actual movement, facilitating motor learning physio-pedia.com.

D. Educational & Self-Management Strategies

26. Pain Neuroscience Education
    Description: Teaching patients the biology of pain and injury.
    Purpose: To reduce fear-avoidance and empower active coping.
    Mechanism: Cognitive reframing decreases central sensitization and promotes engagement in therapy physio-pedia.com.

27. Ergonomics & Posture Training
    Description: Instruction on neutral spine positioning during daily activities.
    Purpose: To minimize mechanical stress and prevent re-injury.
    Mechanism: Optimizes load bearing through proper alignment, reducing nociceptive input physio-pedia.com.

28. Self-Monitoring Diaries
    Description: Logs of pain levels, activities, and triggers.
    Purpose: To identify patterns and adjust behaviors accordingly.
    Mechanism: Increases self-awareness and enables data-driven adjustments to treatment physio-pedia.com.

29. Goal-Setting & Action Planning
    Description: Collaborative establishment of short- and long-term rehabilitation goals.
    Purpose: To enhance motivation and track progress.
    Mechanism: Provides structured feedback loops that reinforce adherence and self-efficacy physio-pedia.com.

30. Assistive Technology Training
    Description: Instruction on using devices (e.g., walkers, orthoses).
    Purpose: To maximize independence and safety in daily tasks.
    Mechanism: Facilitates optimal biomechanical support and compensates for lost function physio-pedia.com.

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Pharmacological Treatments: Key Drugs

Below are 20 evidence-based medications used in PSAS management, organized by therapeutic class. Each entry includes dosage recommendations, drug class, optimal timing, and common side effects.

1. Aspirin (Antiplatelet)

   • Dosage: 75–325 mg orally once daily (morning).

   • Class: Cyclooxygenase (COX) inhibitor.

   • Use-Time: Initiate immediately post-event to prevent recurrent infarction.

   • Side Effects: Gastrointestinal irritation, bleeding, tinnitus. emedicine.medscape.com

2. Clopidogrel (Antiplatelet)

   • Dosage: 75 mg orally once daily.

   • Class: P2Y₁₂ ADP receptor antagonist.

   • Use-Time: Add-on for aspirin-resistant patients or when dual therapy indicated.

   • Side Effects: Bleeding, rare thrombotic thrombocytopenic purpura. emedicine.medscape.com

3. Heparin (Anticoagulant)

   • Dosage: 80 units/kg IV bolus, then 18 units/kg/hr infusion (adjust per aPTT).

   • Class: Indirect thrombin and factor Xa inhibitor.

   • Use-Time: Acute management of thrombotic occlusion in select cases.

   • Side Effects: Hemorrhage, heparin-induced thrombocytopenia. emedicine.medscape.com

4. Warfarin (Anticoagulant)

   • Dosage: 2–5 mg orally once daily (adjust to INR 2–3).

   • Class: Vitamin K antagonist.

   • Use-Time: Secondary prevention when cardioembolic source identified.

   • Side Effects: Bleeding, warfarin skin necrosis. emedicine.medscape.com

5. Rivaroxaban (Anticoagulant)

   • Dosage: 20 mg orally once daily with evening meal.

   • Class: Direct factor Xa inhibitor.

   • Use-Time: Alternative to warfarin for long-term anticoagulation.

   • Side Effects: Bleeding, elevated liver enzymes. emedicine.medscape.com

6. Tissue Plasminogen Activator (tPA) (Thrombolytic)

   • Dosage: 0.9 mg/kg IV (10% bolus, remainder over 60 min), within 3–4.5 hrs of symptom onset.

   • Class: Fibrinolytic agent.

   • Use-Time: Acute ischemic event (select patients).

   • Side Effects: Intracranial hemorrhage, bleeding. pubmed.ncbi.nlm.nih.gov

7. Methylprednisolone (Corticosteroid)

   • Dosage: 30 mg/kg IV over 15 min, then 5.4 mg/kg/hr for 23 hrs (controversial).

   • Class: Glucocorticoid.

   • Use-Time: Historically used in acute spinal cord injury; now individualized.

   • Side Effects: Hyperglycemia, infection, GI ulceration. emedicine.medscape.com

8. Baclofen (Muscle Relaxant)

   • Dosage: 5–10 mg orally TID, may titrate to 80 mg/day.

   • Class: GABA_B receptor agonist.

   • Use-Time: Manage spinal-level spasticity and cramps.

   • Side Effects: Sedation, weakness emedicine.medscape.com.

9. Tizanidine (Muscle Relaxant)

   • Dosage: 2–4 mg orally every 6–8 hrs (max 36 mg/day).

   • Class: α₂-adrenergic agonist.

   • Use-Time: Alternative for spasticity unresponsive to baclofen.

   • Side Effects: Hypotension, dry mouth, sedation. emedicine.medscape.com

10. Diazepam (Muscle Relaxant)

    • Dosage: 2–10 mg orally or IV every 6–8 hrs.

    • Class: Benzodiazepine.

    • Use-Time: Short-term relief of severe spasms.

    • Side Effects: Drowsiness, dependence. emedicine.medscape.com

11. Gabapentin (Neuropathic Pain Agent)

    • Dosage: Initial 300 mg orally at bedtime, titrate up to 1,800 mg/day in divided doses.

    • Class: GABA analogue (modulates calcium channels).

    • Use-Time: Treat dysesthetic pain from dorsal column injury.

    • Side Effects: Dizziness, somnolence nature.com.

12. Pregabalin (Neuropathic Pain Agent)

    • Dosage: 75 mg orally BID, may increase to 300 mg/day.

    • Class: α₂δ ligand.

    • Use-Time: Adjunct for neuropathic pain refractory to gabapentin.

    • Side Effects: Dizziness, edema mayoclinic.org.

13. Amitriptyline (Neuropathic Pain Agent)

    • Dosage: 10–25 mg orally at night, titrate up to 100 mg.

    • Class: Tricyclic antidepressant.

    • Use-Time: Off-label for chronic neuropathic pain and dysesthesias.

    • Side Effects: Anticholinergic effects, sedation.

14. Duloxetine (Neuropathic Pain Agent)

    • Dosage: 30 mg orally once daily, may increase to 60 mg/day.

    • Class: SNRI.

    • Use-Time: Neuropathic pain and mood symptoms.

    • Side Effects: Nausea, insomnia.

15. Vitamin B₁₂ (Cyanocobalamin)

    • Dosage: 1,000 µg IM weekly for 4 weeks, then monthly.

    • Class: Water-soluble vitamin.

    • Use-Time: Correct B₁₂ deficiency–induced demyelination.

    • Side Effects: Rare injection site pain osmosis.org.

16. Penicillin G (Antibiotic)

    • Dosage: 18–24 million U/day IV infusion for 10–14 days.

    • Class: β-lactam antibiotic.

    • Use-Time: Treat neurosyphilis (tabes dorsalis) causing dorsal column damage.

    • Side Effects: Allergic reactions, GI upset osmosis.org.

17. GM-1 Ganglioside (Neuroprotective Agent)

    • Dosage: 100 mg IV daily for 4 weeks (research use).

    • Class: Glycosphingolipid.

    • Use-Time: Experimental for neuronal repair after SCI.

    • Side Effects: Rare hypersensitivity link.springer.com.

18. Erythropoietin (RhEpo) (Neuroprotective Agent)

    • Dosage: 5,000 U/kg IV daily for 3 days (research protocols).

    • Class: Hematopoietic growth factor.

    • Use-Time: Investigational to reduce apoptotic cell death post-injury.

    • Side Effects: Hypertension, thrombosis en.wikipedia.org.

19. Nimodipine (Vasodilator)

    • Dosage: 60 mg orally every 4 hrs for 21 days.

    • Class: Dihydropyridine calcium channel blocker.

    • Use-Time: Off-label to prevent vasospasm after spinal infarction.

    • Side Effects: Hypotension, headache.

20. Minocycline (Anti-inflammatory Agent)

    • Dosage: 200 mg orally loading, then 100 mg BID for 7 days.

    • Class: Tetracycline antibiotic with anti-inflammatory properties.

    • Use-Time: Experimental to reduce microglial activation and secondary injury.

    • Side Effects: Photosensitivity, vestibular symptoms.

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Dietary Molecular Supplements

Emerging evidence suggests certain nutrients may support neural repair and modulate inflammation in spinal cord injury contexts, including PSAS.

1. Omega-3 Polyunsaturated Fatty Acids (EPA/DHA)

   • Dosage: 2–4 g daily mixed EPA/DHA.

   • Function: Anti-inflammatory, promotes membrane fluidity.

   • Mechanism: Increases pro-resolving lipid mediators, reduces cytokine-mediated damage. pmc.ncbi.nlm.nih.govpubmed.ncbi.nlm.nih.gov

2. Alpha-Lipoic Acid (ALA)

   • Dosage: 600 mg orally once daily.

   • Function: Antioxidant, mitochondrial support.

   • Mechanism: Scavenges reactive oxygen species, upregulates glutathione pathways. pubmed.ncbi.nlm.nih.govpubmed.ncbi.nlm.nih.gov

3. Vitamin D₃ (Cholecalciferol)

   • Dosage: 2,000 IU orally daily (adjust per serum 25(OH)D).

   • Function: Modulates immune response, supports myelination.

   • Mechanism: Enhances anti-inflammatory cytokines, promotes oligodendrocyte differentiation. pubmed.ncbi.nlm.nih.gov

4. Acetyl-L-Carnitine

   • Dosage: 1,000 mg orally BID.

   • Function: Supports mitochondrial energy production, nerve repair.

   • Mechanism: Transports fatty acids into mitochondria, modulates neurotrophic factors. verywellhealth.com

5. Coenzyme Q₁₀

   • Dosage: 200 mg orally daily.

   • Function: Antioxidant, mitochondrial electron transport.

   • Mechanism: Reduces oxidative stress, supports ATP generation. verywellhealth.com

6. Magnesium

   • Dosage: 400 mg elemental magnesium orally daily.

   • Function: NMDA receptor modulation, muscle relaxation.

   • Mechanism: Blocks excitotoxic calcium influx, reduces neuronal apoptosis. verywellhealth.com

7. Curcumin

   • Dosage: 500 mg standardized extract orally BID.

   • Function: Anti-inflammatory, antioxidant.

   • Mechanism: Inhibits NF-κB signaling, reduces lipid peroxidation. verywellhealth.com

8. Resveratrol

   • Dosage: 150 mg orally daily.

   • Function: Sirtuin activation, neuroprotection.

   • Mechanism: Enhances mitochondrial function, reduces microglial activation. verywellhealth.com

9. B-Complex Vitamins

   • Dosage: Standard B-complex once daily.

   • Function: Cofactors for neuronal energy metabolism.

   • Mechanism: Support myelin synthesis and nerve conduction velocity. verywellhealth.com

10. N-acetylcysteine (NAC)

    • Dosage: 600 mg orally BID.

    • Function: Precursor to glutathione, antioxidant.

    • Mechanism: Replenishes intracellular GSH, reduces oxidative damage. verywellhealth.com

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Advanced Regenerative and Supportive Therapies

These emerging interventions aim to modulate bone health, promote repair, or reconstruct neural networks after spinal cord injury.

1. Alendronate (Bisphosphonate)

   • Dosage: 70 mg orally once weekly.

   • Function: Prevent bone mineral density loss in SCI-associated osteoporosis.

   • Mechanism: Induces osteoclast apoptosis, slowing bone resorption. ncbi.nlm.nih.govnature.com

2. Zoledronic Acid (Bisphosphonate)

   • Dosage: 5 mg IV once yearly or single dose at 10–12 weeks post-injury.

   • Function: Attenuate rapid bone loss after acute SCI.

   • Mechanism: Potent inhibition of osteoclast-mediated bone resorption. ncbi.nlm.nih.govpmc.ncbi.nlm.nih.gov

3. Pamidronate (Bisphosphonate)

   • Dosage: 30–90 mg IV every 3–4 months.

   • Function: Maintain bone density in chronic SCI.

   • Mechanism: Reduces osteoclast activity via bisphosphonate binding to bone matrix. ncbi.nlm.nih.gov

4. Teriparatide (PTH Analog)

   • Dosage: 20 µg subcutaneously daily for up to 24 months.

   • Function: Anabolic agent improving bone formation and motor recovery.

   • Mechanism: Stimulates osteoblast differentiation and function; may enhance spinal tissue repair. mdpi.com

5. GM-1 Ganglioside (Regenerative Glycolipid)

   • Dosage: 100 mg IV daily for 4 weeks (experimental).

   • Function: Promote axonal regrowth and neuroprotection.

   • Mechanism: Enhances mitochondrial health and axonal sprouting. link.springer.com

6. Mesenchymal Stem Cells (MSCs)

   • Dosage: 1–5×10⁶ cells/kg intrathecal or intravenous (Phase I/II trials).

   • Function: Support neuronal survival and remyelination.

   • Mechanism: Differentiate into neural lineages and secrete trophic factors. frontiersin.org

7. Stem Cell-Derived Exosomes

   • Dosage: Equivalent to exosomes from 1×10⁶ MSCs IV weekly for 4 weeks (investigational).

   • Function: Cell-free regenerative therapy.

   • Mechanism: Deliver microRNAs and proteins that modulate inflammation, promote angiogenesis, and repair the blood-spinal cord barrier. stemcellres.biomedcentral.com

8. Erythropoietin (RhEpo)

   • Dosage: 5,000 U/kg IV daily ×3 days (research).

   • Function: Neuroprotective and anti-apoptotic agent.

   • Mechanism: Activates JAK2 pathways to reduce neuronal apoptosis and inflammation. en.wikipedia.org

9. Intranasal Olfactory Ensheathing Cell Implantation

   • Dosage: Autologous nasal mucosa cells implanted during surgery (1st-in-human trial).

   • Function: Form a “nerve bridge” to promote axonal migration.

   • Mechanism: Provide a supportive scaffold and secrete neurotrophic factors. theaustralian.com.au

10. Platelet-Rich Plasma (PRP)

    • Dosage: 3–5 mL perilesional injection once weekly for 4 weeks (experimental).

    • Function: Enhance local regeneration and reduce inflammation.

    • Mechanism: Delivers concentrated growth factors (PDGF, TGF-β, VEGF) to injured tissue.

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Surgical Interventions

1. Decompressive Laminectomy: Surgical removal of lamina to relieve spinal cord compression and restore blood flow.

2. Posterior Spinal Fusion: Stabilizes vertebral segments after traumatic instability to prevent further cord injury.

3. Tumor Resection: Excision of compressive mass causing posterior cord syndrome, followed by stabilization.

4. Disc Herniation Discectomy: Removal of herniated intervertebral disc impinging on the posterior cord vessels.

5. Meningeal Decompression: Lysis of arachnoid adhesions in post-infectious compressive cases.

6. Vascular Bypass or Stenting: Revascularization in proximal vertebral artery atherosclerosis leading to PSAS.

7. Intrathecal Catheter Placement for Baclofen Pump: Delivers spasticity-relieving medication directly to the CSF space.

8. Duroplasty with Expansion Graft: Expands the dural sac to relieve chronic ischemia.

9. Stem Cell Transplantation Surgery: Implantation of stem cells into the lesion site under microsurgical guidance.

10. Neuroprosthetic Implantation: Surgically positioned electrodes for long-term FES in cases of persistent motor deficits.

Each procedure carries its own risk–benefit profile but aims to relieve compression, restore perfusion, or facilitate regeneration.

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Prevention Strategies

1. Maintain Cardiovascular Health: Control hypertension and hyperlipidemia to reduce thrombotic risk.

2. Avoid Neck Hyperflexion: Use proper protective gear in high-risk sports.

3. Treat B₁₂ Deficiency Promptly: Screen high-risk populations (e.g., older adults).

4. Screen for Syphilis in At-Risk Groups: Early penicillin therapy to prevent tabes dorsalis.

5. Optimize Glycemic Control in Diabetes: Reduce microvascular ischemic events.

6. Bone Health Management: Ensure adequate calcium and vitamin D to prevent osteoporotic fractures complicating SCI.

7. Tobacco and Alcohol Cessation: Both increase vascular and degenerative risks.

8. Ergonomic Lifting Techniques: Prevent disc herniation and traumatic compression injuries.

9. Regular Neurological Check-ups: Early detection of sensory changes for timely intervention.

10. Vaccinations: Prevent infections (e.g., herpes zoster) that can cause compressive myelopathies.

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When to See a Doctor

• Sudden Onset of Sensory Loss or Ataxia: Especially if accompanied by new neck or back pain.

• Progressive Numbness or Tingling: Worsening over days to weeks, suggesting compressive etiologies.

• Development of Incontinence or Urinary Retention: Indicative of spinal cord involvement.

• Severe, Unrelenting Pain: Not relieved by conservative measures.

• Falls or Recurrent Instability: Due to proprioceptive deficits.

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What to Do and What to Avoid

Do:

1. Follow a structured rehab program.

2. Use assistive devices (canes, walkers) as prescribed.

3. Monitor skin integrity to prevent pressure ulcers.

4. Maintain hydration and nutrition.

5. Engage in regular cardiovascular exercise (as tolerated).

Avoid:

1. Rapid neck manipulation (e.g., high-impact sports).

2. Smoking and excessive alcohol.

3. Prolonged immobility without position changes.

4. Unsupervised heavy lifting.

5. Abrupt cessation of prescribed medications.

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Frequently Asked Questions

1. What causes Posterior Spinal Artery Syndrome?
   PSAS arises from infarction, compression, or demyelination of the posterior spinal arteries, often due to trauma, vascular occlusion, tumors, or nutritional deficiencies en.wikipedia.orgosmosis.org.

2. How is PSAS diagnosed?
   Diagnosis relies on clinical exam (loss of vibration/proprioception), MRI showing posterior column signal changes, and vascular imaging if infarction is suspected.

3. Can you recover from PSAS?
   Recovery depends on etiology and timeliness of treatment. Early decompression or vascular reperfusion improves outcomes; rehabilitation maximizes functional gains.

4. Is motor function affected?
   Usually preserved, as corticospinal tracts lie anteriorly. However, severe lesions may produce segmental weakness.

5. What is the prognosis?
   Varies: vascular infarcts often result in permanent sensory deficits, while compressive or inflammatory causes may partially reverse.

6. Are steroids recommended?
   High-dose methylprednisolone is controversial; evidence is stronger in traumatic SCI than vascular infarcts emedicine.medscape.com.

7. When is surgery indicated?
   In cases of mechanical compression (tumors, disc herniation) or to place intrathecal pumps for spasticity management.

8. Can supplements help?
   Omega-3, ALA, vitamin D, and other antioxidants have shown modest benefits in preclinical spinal injury models pubmed.ncbi.nlm.nih.gov.

9. What role does physical therapy play?
   It is central to regaining balance and coordination, exploiting neuroplasticity through task-specific training.

10. Is PSAS hereditary?
    No; it is typically acquired rather than genetic.

11. How long is rehabilitation?
    Often lifelong; intensive rehab is recommended initially, followed by maintenance programs.

12. Can PSAS recur?
    If underlying vascular risk factors are uncontrolled, infarcts may recur in spinal or cerebral vessels.

13. Are there ongoing research trials?
    Yes—stem cell, exosome, and neuroprotective agent trials are active globally bmcmedicine.biomedcentral.com.

14. What assistive devices help?
    Canes, walkers, ankle–foot orthoses, and balance platforms support safe mobility.

15. How to prevent falls?
    Incorporate vision, vestibular, and proprioceptive training; remove home hazards; use appropriate footwear and devices.

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: July 06, 2025.

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