Spinal Cord and Peripheral Nerve Disorders - Cheat Sheet
Your 30-minute exam survival guide for spinal cord injury, peripheral nerve disorders, and life-threatening emergencies. Focus on trauma levels, shock types, autonomic dysreflexia triggers, and protective sensation loss.
SPINAL CORD INJURY (SCI) - LEVELS AND CLASSIFICATION
Important facts
- C3, C4, C5 KEEP THE DIAPHRAGM ALIVE — injuries above C4 threaten ventilation and require mechanical support
- Cervical injury = tetraplegia; thoracic/lumbar injury = paraplegia (RULE FOR LEVEL)
- Primary injury: direct trauma (compression, contusion, laceration, transection)
- Secondary injury: occurs hours after trauma (edema, hemorrhage, ischemia) — THIS IS PREVENTABLE with early stabilization
- Phrenic nerve (C3–C5) innervates the diaphragm — high cervical injuries → respiratory compromise
- Central cord syndrome: greater motor weakness in UPPER extremities than lower (common in hyperextension injuries in elderly)
- Anterior cord syndrome: loss of motor + pain/temperature with PRESERVED position and vibration sense
- Brown-Séquard syndrome (cord hemisection): ipsilateral motor loss + position sense loss; contralateral pain/temperature loss
Key definitions
Tetraplegia (Quadriplegia)
Example
Motor vehicle accident with C5 injury causes arm and leg paralysis.
Impairment of all four limbs; caused by cervical spinal cord injury (C1–C8).
Paraplegia
Example
Dive into shallow water causing T10 injury results in bilateral leg paralysis.
Impairment of lower limbs only; caused by thoracic or lumbar spinal cord injury.
Complete Injury
Example
Complete transection at T5 = no movement or sensation below waist.
Total loss of motor and sensory function below the level of injury.
Incomplete Injury
Example
Brown-Séquard syndrome preserves ipsilateral motor but loses contralateral pain/temperature.
Preservation of some motor or sensory function below the injury level.
Diagrams to know
- Spinal cord cross-section showing motor (ventral) and sensory (dorsal) tracts
- Cervical, thoracic, lumbar, and sacral levels with their functional outcomes
- Central cord syndrome: motor weakness pattern (upper > lower)
EMERGENCY & ACUTE MANAGEMENT OF SCI
Important facts
- FIRST PRIORITY: Immobilize the spine immediately — cervical collar + backboard
- SECOND PRIORITY: Assess and secure airway WITHOUT hyperextending neck
- Use jaw-thrust (NOT head-tilt chin-lift) for airway in suspected cervical injury
- Maintain mean arterial pressure (MAP) for cord perfusion — prevent hypotension that worsens ischemia
- High-dose corticosteroids: historically used but NOW CONTROVERSIAL and NOT routinely recommended
- Surgical decompression and stabilization: indicated if progressive neurological deficit or instability
- Keep patient NPO until surgery cleared
- Monitor for respiratory failure in high cervical injuries — be ready for intubation and ventilator support
Key definitions
Log-Rolling
Example
Five staff members log-roll patient from stretcher to bed without twisting the spine.
Technique to move SCI patient while maintaining neutral spine alignment; all staff move together as one unit.
Jaw-Thrust Maneuver
Example
Use in C4 SCI patient requiring intubation to avoid extending the injury.
Airway opening technique that does NOT hyperextend the neck; preferred for suspected cervical injury.
Diagrams to know
- Log-rolling technique with staff positioning
- Jaw-thrust vs. head-tilt chin-lift comparison
SPINAL SHOCK vs NEUROGENIC SHOCK - THE CRITICAL DISTINCTION
Important facts
- Spinal shock = NEUROLOGIC (reflexes gone); Neurogenic shock = HEMODYNAMIC (BP/HR changes)
- Spinal shock appears IMMEDIATELY after injury and resolves over days to weeks
- Neurogenic shock: classic triad = HYPOTENSION + BRADYCARDIA + WARM/DRY SKIN
- Neurogenic shock occurs ONLY with T6 OR ABOVE injury (high thoracic/cervical)
- Hypovolemic shock by contrast: tachycardia + cold, clammy skin (OPPOSITE of neurogenic shock's warm skin)
- Neurogenic shock management: IV fluids CAUTIOUSLY (risk of overload), vasopressors to restore vascular tone, atropine for symptomatic bradycardia
- Spinal shock resolves → spasticity returns (reflexes reappear and become hyperactive)
- Neurogenic shock may persist longer than spinal shock in high injuries
Key definitions
Spinal Shock
Example
Immediately after T8 injury: legs flaccid, no patellar reflex, bowel/bladder inert.
NEUROLOGIC phenomenon: temporary loss of ALL reflex activity, motor function, sensation, and autonomic function below the injury level; causes flaccid paralysis and absent reflexes (including bowel/bladder).
Neurogenic Shock
Example
C7 injury patient: BP 80/50, HR 42, warm and dry skin — NOT cold/clammy like hypovolemic shock.
HEMODYNAMIC phenomenon: occurs with injuries AT OR ABOVE T6; loss of sympathetic tone → hypotension, bradycardia, warm/dry skin (vasodilation).
Diagrams to know
- Spinal shock timeline (onset to resolution)
- Neurogenic shock hemodynamic cascade (T6 injury → sympathetic loss → vasodilation)
ONGOING NURSING CARE FOR SCI - COMPLICATIONS AND PREVENTION
Important facts
- PREVENTION FOCUS: immobility complications (pressure injuries, DVT, contractures, respiratory compromise)
- Reposition every 2 hours and provide meticulous skin care to prevent pressure injuries
- DVT prophylaxis: sequential compression devices, anticoagulation, early mobilization
- Respiratory care: incentive spirometry, assisted coughing (manually compress abdomen) for high injuries lacking abdominal muscle control
- Bowel program: scheduled evacuation, adequate fiber and fluids, stool softeners, digital stimulation if needed — prevents impaction (dysreflexia trigger)
- Bladder program: intermittent catheterization on schedule is GOLD STANDARD long-term management
- Neurogenic bladder: spastic bladder (upper motor neuron — T12 or above) empties involuntarily; flaccid bladder (lower motor neuron — S2–S4) fails to empty
- Range-of-motion exercises EVERY DAY to prevent contractures
- Manage orthostatic hypotension during mobilization: gradual sitting, tilt table, compression stockings, abdominal binders
- Psychosocial adjustment and interdisciplinary rehabilitation (PT, OT, social work, psychology) are ESSENTIAL to functional recovery and quality of life
Key definitions
Spastic (Reflex) Bladder
Example
L2 injury: bladder contracts on filling and empties without voluntary control.
Bladder that empties involuntarily when full after spinal shock resolves; results from intact reflex arc below the injury.
Flaccid Bladder
Example
S3 injury: bladder overdistends, cannot empty, requires catheterization.
Bladder that fails to contract and empty; results from damage to sacral reflex arc (S2–S4).
Neurogenic Bladder
Example
Any SCI patient requires a bowel and bladder management program to prevent complications.
Loss of normal bladder control after SCI due to interruption of autonomic pathways; can be spastic or flaccid depending on injury level.
Intermittent Catheterization
Example
Every 4–6 hours for patient with C6 SCI.
Preferred long-term method: scheduled catheterization to empty bladder on a regular schedule; prevents overdistension, infection, and dysreflexia triggers.
Diagrams to know
- Bowel program schedule (timing of laxatives, manual disimpaction)
- Bladder management decision tree (spastic vs. flaccid management)
AUTONOMIC DYSREFLEXIA — THE TRUE EMERGENCY
Important facts
- OCCURS ONLY IN: SCI at or ABOVE T6 (high thoracic/cervical), AFTER spinal shock resolves (reflexes have returned)
- MANIFESTATIONS (SCARY SIGNS): sudden SEVERE pounding headache, SEVERE hypertension (often SBP >200), bradycardia, profuse sweating and flushing ABOVE injury level, pallor and coolness BELOW injury, nasal congestion, blurred vision, anxiety/sense of doom
- MOST COMMON TRIGGER: Distended bladder (blocked/kinked catheter, urinary retention) — THIS IS #1
- OTHER TRIGGERS (in order): fecal impaction/constipation, pressure injuries, tight clothing, skin irritation (ingrown toenails, burns), menstrual cramps
- PATHOPHYSIOLOGY: Noxious stimulus → reflex arc → sympathetic discharge BELOW injury → massive vasoconstriction → hypertension → brain receives signal but CANNOT send descending inhibition across cord → EMERGENCY
- DANGER: Sudden hypertension → stroke, seizures, myocardial infarction, death if not treated IMMEDIATELY
Key definitions
Autonomic Dysreflexia (Hyperreflexia)
Example
Blocked catheter → full bladder → sudden severe hypertension (SBP >200), pounding headache, bradycardia in C5 injury patient.
LIFE-THREATENING emergency occurring in SCI at/above T6 after spinal shock resolves; uncontrolled sympathetic response to noxious stimulus below injury level that brain cannot regulate.
Diagrams to know
- Autonomic dysreflexia reflex arc and pathophysiology
- Trigger checklist (bladder → bowel → skin)
AUTONOMIC DYSREFLEXIA — PRIORITY INTERVENTIONS (EXACT ORDER)
Important facts
- STEP 1 — IMMEDIATE: Raise head of bed / SIT PATIENT UPRIGHT to use gravity to lower blood pressure (ORTHOSTATIC EFFECT) — this is FIRST because it acts fastest
- STEP 2: Loosen tight clothing, catheter attachments, or any constrictive devices
- STEP 3: FIND AND REMOVE THE TRIGGER in this order:
- → CHECK URINARY CATHETER FIRST (most common): look for kinks, clots, or blockage; straighten tubing; if still blocked, perform catheterization (use ANESTHETIC lubricant to avoid worsening dysreflexia); monitor for large urinary return indicating retained urine
- → CHECK BLADDER: if no catheter in place, may need to catheterize if patient cannot void
- → CHECK FOR FECAL IMPACTION (second most common): perform manual disimpaction using ANESTHETIC lubricant (because digital stimulation can trigger dysreflexia); do NOT use soap suds enema (too stimulating)
- → CHECK SKIN: inspect for pressure injuries, ingrown toenails, tight dressings, or other irritants
- STEP 4: Monitor blood pressure every 5–15 minutes (CONTINUOUSLY if very high)
- STEP 5: If blood pressure REMAINS DANGEROUSLY HIGH after removing trigger (SBP still >180–200), give RAPID-ACTING ANTIHYPERTENSIVE:
- → Nifedipine (sublingual, FAST-acting calcium channel blocker)
- → Nitrates (nitroglycerin paste, IV nitroglycerin)
- → Other options: hydralazine, labetalol
- STEP 6: Document trigger found, time onset, BP readings, interventions, and response
- PATIENT EDUCATION: Teach patient and caregivers early signs (headache, sweating, feeling "different"), when to call for help, and PREVENTION importance
Diagrams to know
- Autonomic dysreflexia intervention flowchart (in priority order)
HERNIATED INTERVERTEBRAL DISC
Important facts
- MOST COMMON LOCATIONS: lumbar spine (L4–L5, L5–S1) accounts for majority of herniated discs; cervical spine also common
- LUMBAR PRESENTATION: low back pain + sciatica (leg pain, numbness, tingling), weakness in leg, diminished reflexes, positive straight-leg-raise test
- CERVICAL PRESENTATION: neck pain and arm pain, weakness, paresthesia in arm/hand
- DIAGNOSIS: MRI is gold standard for visualizing disc herniation and nerve root compression; CT if MRI contraindicated; X-ray does not show disc but shows bone changes
- CONSERVATIVE MANAGEMENT (first-line): limited rest (NOT prolonged bed rest), physical therapy, heat/cold, NSAIDs, muscle relaxants, analgesics, proper body mechanics, avoiding aggravating positions
- Most patients improve with conservative management over weeks to months
- SURGERY (discectomy, laminectomy, spinal fusion) indicated for: persistent neurological deficits NOT improving with conservative care, progressive weakness, CAUDA EQUINA SYNDROME (emergency)
- CAUDA EQUINA SYNDROME IS SURGICAL EMERGENCY: bowel/bladder dysfunction + saddle anesthesia + bilateral leg weakness = OPERATE WITHIN HOURS to prevent permanent paralysis and loss of bowel/bladder control
- POSTOPERATIVE CARE: log-rolling, maintain spinal alignment, neuro checks (motor, sensory, reflexes), monitor for CSF leak (clear drainage from incision), monitor for infection; after fusion, avoid twisting and heavy lifting (6–12 weeks)
Key definitions
Herniated Disc
Example
L4–L5 disc herniation compresses L5 nerve root, causing right leg pain and weakness.
Protrusion of nucleus pulposus through annulus fibrosus, compressing spinal nerve root.
Sciatica
Example
Sharp pain from low back down right buttock and posterior leg.
Pain radiating down the leg from compression of sciatic nerve or L5–S1 nerve roots.
Positive Straight-Leg-Raise Test
Example
Leg pain at 30° hip flexion suggests L5–S1 nerve root involvement.
Patient pain reproduction when examiner raises extended leg; indicates nerve root compression.
Cauda Equina Syndrome
Example
Massive disc herniation at L4–L5 → urinary retention, fecal incontinence, bilateral leg paralysis, saddle numbness.
Surgical EMERGENCY: compression of multiple nerve roots in lumbar spine causing bowel/bladder dysfunction, saddle anesthesia, and bilateral leg weakness.
Diagrams to know
- Intervertebral disc anatomy (nucleus pulposus, annulus fibrosus, nerve root compression)
- Straight-leg-raise test demonstration
PERIPHERAL NEUROPATHY
Important facts
- MOST COMMON CAUSE: diabetes mellitus (hyperglycemia damages nerves over time)
- OTHER CAUSES: chronic alcohol use, vitamin B12 deficiency, chemotherapy (vincristine, cisplatin), HIV, uremia, hypothyroidism
- PRESENTATION: numbness, tingling, burning pain in feet and hands (distal distribution), weakness, diminished or absent reflexes; onset gradual (days to months); worse at night
- TYPES: sensory neuropathy (most common), motor neuropathy (weakness), autonomic neuropathy (orthostatic hypotension, gastroparesis, urinary retention)
- DIAGNOSIS: clinical history + examination (monofilament testing, vibration sense, reflexes) + nerve conduction studies and electromyography (EMG) to confirm and assess severity; investigate underlying cause (blood glucose, HbA1c, vitamin B12, thyroid function)
- CENTRAL DANGER: Loss of protective sensation → patient cannot feel injuries (burns, cuts, pressure) → unnoticed wounds → infections → amputation (especially in diabetes)
- DIABETIC FOOT COMPLICATIONS: foot ulcers (neuropathic ulcers are PAINLESS, occurring over pressure areas) → cellulitis, osteomyelitis, gangrene → amputation if untreated
- MANAGEMENT: treat underlying cause (tight glycemic control in diabetes is ESSENTIAL), pain management, protection from further injury
Key definitions
Peripheral Neuropathy
Example
Diabetic neuropathy: numbness and burning pain in both feet starting at toes.
Damage to peripheral nerves causing sensory, motor, and autonomic dysfunction; typically DISTAL and BILATERAL.
Stocking-Glove Distribution
Example
Feet and hands lose sensation in "sock" and "glove" areas respectively.
Characteristic sensory loss pattern in neuropathy: loss starts in toes and fingers, progresses proximally in symmetric pattern.
Protective Sensation
Example
Monofilament test: inability to sense 10-gram monofilament in foot indicates loss of protective sensation.
Ability to feel pain and pressure; loss of this is the PRIMARY DANGER in neuropathy (patient cannot detect injuries).
Diagrams to know
- Stocking-glove sensory loss pattern diagram
- Neuropathic pain pathways vs. nociceptive pain
PERIPHERAL NEUROPATHY — PHARMACOTHERAPY AND PATIENT TEACHING
Important facts
- NEUROPATHIC PAIN: ordinary pain relievers (acetaminophen, NSAIDs, opioids) are OFTEN INEFFECTIVE — need agents that target nerve pain specifically
- FIRST-LINE AGENTS for neuropathic pain: gabapentin or pregabalin (both safe, well-tolerated)
- SECOND-LINE AGENTS: tricyclic antidepressants (amitriptyline) or duloxetine
- GABAPENTIN: titrate slowly to minimize side effects (dizziness, drowsiness); renal dosing needed
- PREGABALIN: similar to gabapentin; also used for fibromyalgia and post-herpetic neuralgia
- AMITRIPTYLINE: anticholinergic side effects (dry mouth, constipation, urinary retention); contraindicated in glaucoma or cardiac arrhythmias; avoid in elderly (fall risk)
- DULOXETINE: generally well-tolerated; monitor for serotonin syndrome if combined with other serotonergic agents
- TOPICAL AGENTS: lidocaine patch, capsaicin cream for localized pain (limited by cost and availability in PH)
- PATIENT EDUCATION — PROTECTION AND DAILY INSPECTION: (THIS IS CRITICAL TO PREVENT AMPUTATION)
- → EXAMINE FEET DAILY: look for blisters, cuts, redness, calluses, cracks, signs of infection
- → WEAR PROTECTIVE FOOTWEAR: well-fitting shoes with cushioning; NEVER go barefoot (risk of unnoticed injury)
- → TEST WATER TEMPERATURE with thermometer or elbow BEFORE bathing (numb feet cannot sense hot water burns)
- → MAINTAIN FOOT HYGIENE: wash feet daily, dry thoroughly (especially between toes), trim nails straight across (NOT too short), do NOT self-treat calluses or corns
- → CONTROL BLOOD GLUCOSE: tight glycemic control is THE KEY to preventing progression of neuropathy and complications
- → REPORT PROMPTLY: any wound, redness, ulcer, or sign of infection to healthcare provider
- → FOLLOW-UP: regular foot exams with provider (every 3–6 months in diabetes)
Key definitions
Gabapentin
Example
Dosing typically 300–3600 mg/day in divided doses for diabetic neuropathy.
First-line medication for neuropathic pain; anticonvulsant that modulates calcium channels and reduces pain signal transmission.
Pregabalin
Example
Dosing 150–600 mg/day in divided doses.
Similar to gabapentin; approved for diabetic peripheral neuropathy and postherpetic neuralgia.
Tricyclic Antidepressants
Example
Amitriptyline 10–50 mg at bedtime for pain relief (also helps with sleep).
Effective for neuropathic pain by blocking reuptake of norepinephrine and serotonin; amitriptyline is most common.
Duloxetine
Example
Dosing 60 mg once or twice daily.
Serotonin-norepinephrine reuptake inhibitor (SNRI); FDA-approved for diabetic peripheral neuropathy.
Diagrams to know
- Neuropathic pain medication algorithm
- Daily foot care checklist
Must remember
- C3, C4, C5 KEEP THE DIAPHRAGM ALIVE — Any SCI above C4 threatens breathing and requires mechanical ventilation; phrenic nerve (C3–C5) innervates diaphragm.
- Cervical SCI = tetraplegia (all 4 limbs); thoracic or lumbar SCI = paraplegia (legs only) — This is the basic level-to-deficit rule.
- SPINAL SHOCK is neurologic (reflexes absent immediately); NEUROGENIC SHOCK is hemodynamic (hypotension + bradycardia + warm/dry skin with T6+ injury) — OPPOSITE of hypovolemic shock.
- LOG-ROLL any suspected SCI patient with spine immobilized in NEUTRAL alignment — never twist the spine; use jaw-thrust (NOT head-tilt chin-lift) for airway in cervical injury.
- AUTONOMIC DYSREFLEXIA (T6+ injury after spinal shock resolves) is an EMERGENCY: sudden severe headache + severe hypertension + bradycardia + sweating above injury. PRIORITY: raise head of bed FIRST, then check bladder (blocked catheter is #1 cause) THEN bowel. Give antihypertensive if BP stays dangerously high after trigger removed.
- CAUDA EQUINA SYNDROME (bowel/bladder dysfunction + saddle anesthesia + bilateral leg weakness) is a SURGICAL EMERGENCY in disc herniation — operate within hours to prevent permanent paralysis.
- INTERMITTENT CATHETERIZATION on schedule is gold-standard long-term bladder management in SCI — prevents overdistension, infection, and dysreflexia triggers. SPASTIC bladder (T12+ injury) needs different management than flaccid bladder (S2–S4 injury).
- PERIPHERAL NEUROPATHY: daily foot inspection + protective footwear + testing water temperature = KEY to preventing amputation. Loss of protective sensation (monofilament test) is the central danger because patient CANNOT feel injuries.
- NEUROPATHIC PAIN (diabetes, chemotherapy, etc.) requires SPECIFIC agents: gabapentin/pregabalin or amitriptyline/duloxetine — ordinary pain relievers are often ineffective. Treat underlying cause (tight glycemic control in diabetes is ESSENTIAL).
- PRESSURE INJURIES, DVT, CONTRACTURES, and RESPIRATORY FAILURE are the major complications of immobility after SCI — prevention through repositioning, DVT prophylaxis, ROM exercises, respiratory care, and early mobilization is ESSENTIAL.
Last minute tips
- When you see a patient with acute spine trauma → FIRST thought: immobilize, log-roll, keep spine neutral. When you see cervical injury → SECOND thought: check breathing and prepare for potential intubation using jaw-thrust. These two steps prevent secondary injury.
- If a question asks about a T7 SCI patient with sudden severe headache, hypertension, and sweating → AUTONOMIC DYSREFLEXIA. Action: sit upright FIRST (gravity), check catheter/bladder SECOND (most common cause), then bowel. This is the exact order.
- SPINAL SHOCK resolves (days to weeks), then spasticity returns. NEUROGENIC SHOCK (T6+ injury) may persist longer. On an exam, if you see "flaccid paralysis + absent reflexes" right after injury = spinal shock. If you see "hypotension + bradycardia + warm skin" = neurogenic shock. They can coexist but treat differently.
- Distinguishing incomplete cord syndromes on exam: CENTRAL CORD = upper arms weaker than legs (ask about hyperextension in elderly). ANTERIOR CORD = motor + pain/temperature loss but VIBRATION preserved (very specific). BROWN-SÉQUARD = one-sided weakness + opposite-side pain/temperature loss (hemisection pattern). Each has a clinical fingerprint.
- In peripheral neuropathy exams, expect questions on: (1) daily foot care to prevent amputation, (2) gabapentin/pregabalin as first-line neuropathic pain meds, (3) monofilament test to assess protective sensation, (4) tight glycemic control in diabetes as ESSENTIAL. These four elements appear in nearly every neuropathy question.
Comparison tables
SPINAL SHOCK vs NEUROGENIC SHOCK — QUICK DISTINCTION
| Feature | Spinal Shock | Neurogenic Shock |
|---|---|---|
| Type of Phenomenon | NEUROLOGIC | HEMODYNAMIC |
| Injury Level | ANY level of SCI | T6 or ABOVE only |
| Onset | IMMEDIATE (within minutes of injury) | Immediate but may persist longer |
| Motor Function | Flaccid paralysis (absent motor control) | May have flaccid or spastic depending on level |
| Reflexes | ABSENT (all reflexes gone, including deep tendon and bowel/bladder) | Present (neurogenic shock is hemodynamic, not neurologic) |
| Blood Pressure | Normal (may have hypotension from fluid loss) | HYPOTENSION (loss of sympathetic vasoconstriction) |
| Heart Rate | Normal or tachycardic (if bleeding) | BRADYCARDIA (loss of sympathetic innervation to heart) |
| Skin | Normal (depends on bleeding, temperature) | WARM and DRY (vasodilation from loss of sympathetic tone) ABOVE injury level; pale/cool BELOW |
| Duration | Days to weeks (resolves as reflexes return and spasticity develops) | May persist weeks in high injuries |
| Management | Supportive care, prevent complications, bowel/bladder program, physical therapy | IV fluids (cautious), vasopressors, atropine for bradycardia, treat underlying cause |
INCOMPLETE SPINAL CORD SYNDROMES — RECOGNITION
| Syndrome | Location of Damage | Motor Loss | Sensory Loss | Key Feature / Common Cause |
|---|---|---|---|---|
| Central Cord Syndrome | Center of cord (cross-section) | Greater weakness in UPPER extremities than lower | Bilateral, roughly symmetric | Upper limbs MORE affected than lower; common in hyperextension injuries in elderly |
| Anterior Cord Syndrome | Ventral (anterior) cord | Loss (anterior corticospinal tract) | Loss of pain and temperature (spinothalamic tract); PRESERVED position and vibration (posterior columns) | Most common incomplete syndrome; caused by flexion-rotation injuries or ischemia |
| Brown-Séquard Syndrome | One HALF of cord (hemisection) | IPSILATERAL (same side) loss of motor function and position sense | IPSILATERAL: position and vibration lost; CONTRALATERAL: pain and temperature lost | Rare; caused by penetrating trauma (stab wound) or cord hemisection; most complete recovery of all incomplete syndromes |
| Posterior Cord Syndrome | Posterior columns | Preserved motor function (anterior column intact) | Loss of position sense and vibration (posterior columns); pain/temperature preserved | Rarest incomplete syndrome; usually from dorsal artery occlusion |
SPASTIC (REFLEX) vs FLACCID BLADDER — MANAGEMENT
| Feature | Spastic (Reflex) Bladder | Flaccid Bladder |
|---|---|---|
| Nerve Involvement | Upper motor neuron (UMN) damage; reflex arc INTACT but disconnected from brain | Lower motor neuron (LMN) damage; reflex arc DAMAGED (S2–S4 nerve damage) |
| SCI Level | T12 (thoracic 12) or ABOVE | S2–S4 (sacral) or BELOW |
| Bladder Function | Involuntary emptying when full; contracts reflexively | Fails to contract and empty; over-distends; large residual volume |
| Pressure | HIGH intrabladder pressure (reflex contraction) | LOW intrabladder pressure (no contraction) |
| Management | Trigger voiding (abdominal tap, tapping above pubis, urge), scheduled catheterization, antimuscarinic meds to decrease bladder pressure if needed | Intermittent catheterization on schedule (every 4–6 hours); monitor for overdistension and reflux |
| Complication Risk | High pressure → reflux nephropathy, upper UTI, autonomic dysreflexia | Overdistension → reflux, upper UTI; but LOWER dysreflexia risk |
DIABETIC NEUROPATHY: PAIN MEDICATION SELECTION
| Medication Class | Examples | Mechanism | Advantages | Disadvantages / Watch Out |
|---|---|---|---|---|
| Anticonvulsants | Gabapentin, Pregabalin | Modulate calcium channels, reduce excitatory neurotransmitter release | First-line, well-tolerated, few drug interactions, renal dosing (good for CKD patients on dialysis) | Titrate slowly (dizziness, drowsiness), renally cleared (adjust in renal failure) |
| Tricyclic Antidepressants | Amitriptyline, Nortriptyline | Block reuptake of norepinephrine and serotonin | Inexpensive, also improve sleep | Anticholinergic side effects (dry mouth, constipation, urinary retention), contraindicated in glaucoma, cardiac arrhythmias; avoid in elderly (fall risk from orthostasis) |
| SNRIs | Duloxetine | Block reuptake of serotonin and norepinephrine | FDA-approved for diabetic neuropathy, well-tolerated | Monitor for serotonin syndrome if combined with other serotonergic drugs (SSRIs, tramadol, MAOIs) |
| Topical Agents | Lidocaine patch, Capsaicin cream | Local anesthetic, substance P depletion | Localized effect, minimal systemic absorption | Limited effectiveness, expensive, not widely available in PH, capsaicin causes burning sensation initially |
Diagrams
AUTONOMIC DYSREFLEXIA - PRIORITY INTERVENTION FLOWCHART
Step-by-step decision flowchart for autonomic dysreflexia emergency management, emphasizing the exact priority order: raise head of bed FIRST, then check bladder (blocked catheter = most common trigger), then bowel, then skin. Includes decision points for ongoing assessment and antihypertensive use.
SPINAL CORD INJURY - COMPREHENSIVE CONCEPT MAP
Comprehensive mind map showing the hierarchical relationships of SCI concepts: injury levels with corresponding deficits, injury types (complete vs. incomplete syndromes), acute emergency management priorities, early complications (spinal shock vs. neurogenic shock), autonomic dysreflexia triggers and management, and long-term management strategies including bowel/bladder programs, complication prevention, and rehabilitation focus.
HERNIATED DISC DECISION TREE - MANAGEMENT PATHWAY
Decision tree for herniated disc management, illustrating the pathway from diagnosis through conservative management, the red flag (cauda equina syndrome) requiring emergency surgery, and postoperative care priorities. Emphasizes that most herniated discs improve with conservative care but cauda equina requires urgent intervention.
SCI RECOVERY TIMELINE - SPINAL SHOCK TO SPASTICITY
Timeline showing the progression from acute SCI through spinal shock resolution to chronic spasticity, illustrating when reflexes return, when autonomic dysreflexia risk begins, and the ongoing nature of neurogenic bladder/bowel management and complication prevention.
PERIPHERAL NEUROPATHY - ASSESSMENT AND MANAGEMENT
Comprehensive flowchart for peripheral neuropathy management, from initial assessment through monofilament testing and confirmatory testing, identification and treatment of underlying cause (especially tight glycemic control in diabetes), neuropathic pain medication selection, and critical patient education on foot protection to prevent ulcers and amputation.