I am MD medicine resident I am going to present a case of spinal cord so please give detail of case presentation on spinal cord and suggest what questions with answer that can be asked by examiner and what are the differential diagnosis

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Here is a complete, senior-resident-level case presentation on Multiple Sclerosis with Spinal Cord Lesion, structured for a ward round or viva.

CASE PRESENTATION: Multiple Sclerosis with Spinal Cord Involvement

PART 1 - CASE PRESENTATION SCRIPT

Presenting Complaint

"I am presenting a 28-year-old female, a school teacher, who presented to the neurology OPD with complaints of progressive weakness and numbness in both lower limbs for 3 weeks, along with urinary urgency and difficulty walking for the past 10 days."

History of Present Illness

The patient was in her usual state of health until 3 weeks ago when she noticed gradual onset of tingling and numbness starting in the feet and ascending to mid-thigh level bilaterally. Over the next 10 days, she developed progressive weakness of both lower limbs - initially difficulty climbing stairs, then difficulty walking on flat ground, eventually requiring support to walk.

She developed urinary urgency and urge incontinence 10 days ago. She denies bowel incontinence but reports constipation.

She reports that symptoms worsen significantly during a hot bath or in warm weather (Uhthoff's phenomenon) - a hallmark that she herself described as "my legs give out whenever I take a hot shower."

First episode (elicit this carefully): On directed questioning, she recalls a self-resolving episode 18 months ago of painful blurring of vision in the right eye lasting 3 weeks, which resolved completely without treatment. She did not seek medical attention at that time. This is consistent with a prior episode of optic neuritis.

No history of fever, rash, joint pain, photosensitivity, oral ulcers, or genital ulcers. No family history of neurological disease.

Past History

No prior hospitalizations
No diabetes, hypertension, or tuberculosis
Non-smoker, no alcohol use

Menstrual/Obstetric History

Regular cycles; no pregnancies (relevant as MS often improves during pregnancy and flares postpartum)

Examination Findings

General: Alert, cooperative, mildly anxious. Vitals stable. No pallor, icterus, cyanosis, or lymphadenopathy.

Higher Mental Functions: Normal

Cranial Nerves:

Visual acuity: Mildly reduced in right eye (6/18); right eye relative afferent pupillary defect (RAPD) positive - suggesting prior optic neuritis with incomplete recovery
Fundus: Mild temporal pallor of right optic disc
Eye movements: Internuclear ophthalmoplegia (INO) on lateral gaze - right eye adduction lag with nystagmus in the abducting left eye - indicating a left MLF lesion. (This is highly characteristic of MS)
Other cranial nerves intact

Motor System (Lower Limbs):

	Right	Left
Tone	Increased (spasticity)	Increased (spasticity)
Power	3/5 (hip, knee, ankle)	3/5 (hip, knee, ankle)
Reflexes	Brisk (3+)	Brisk (3+)
Plantar	Extensor (Babinski +)	Extensor (Babinski +)

Sensory System:

Sensory level: T6 level bilaterally (pin prick and temperature reduced below T6)
Vibration and joint position sense: Reduced at ankles and knees bilaterally (posterior column involvement)
Lhermitte's sign: Positive - patient reports electric shock-like sensation down the spine on neck flexion

Cerebellar: Mild dysmetria on finger-nose test (suggesting additional cerebellar/brainstem lesion)

Bladder: Suprapubic fullness; post-void residual elevated on ultrasound

EDSS (Expanded Disability Status Scale) estimated: 5.0 - able to walk ~200 meters without aid, but with significant disability

Summary Statement

"To summarize, this is a 28-year-old female presenting with her second neurological episode - the current episode involving bilateral spastic paraparesis with a T6 sensory level, posterior column signs, INO, and bladder dysfunction; with a prior episode of right optic neuritis 18 months ago. The clinical picture is consistent with Relapsing-Remitting Multiple Sclerosis (RRMS) with a spinal cord lesion, satisfying the 2017 McDonald criteria for dissemination in space and time."

PART 2 - INVESTIGATIONS

MRI Brain and Spine (Most Important)

MRI Findings in MS:

Brain: Periventricular T2/FLAIR hyperintense lesions (ovoid, oriented perpendicular to ventricles - "Dawson's fingers"), juxtacortical and infratentorial lesions
Corpus callosum: Calloso-septal interface lesions ("dot-dash" pattern on sagittal FLAIR)
Brainstem: MLF lesion (explaining INO)
Spine (key feature): T2 hyperintense lesion(s) in the cervical cord, typically:
- Short segment (<3 vertebral segments) - distinguishes MS from NMO
- Peripheral/dorsal location in cross-section (not central like NMO)
- May show gadolinium enhancement during acute relapse
- Lesions often seen in the posterior and lateral columns

Dissemination in Space (DIS) on MRI: ≥1 T2 lesion in ≥2 of 4 areas: periventricular, cortical/juxtacortical, infratentorial, spinal cord

Dissemination in Time (DIT) on MRI: Simultaneous presence of gadolinium-enhancing AND non-enhancing lesions OR new T2 lesion on follow-up MRI

(Source: 2017 McDonald Criteria - Thompson AJ et al., Lancet Neurol 2018;17:162-173, as referenced in Goldman-Cecil Medicine)

CSF Analysis

Parameter	Finding in MS
Appearance	Clear, colorless
Cells	Normal or mildly elevated lymphocytes (5-50 cells)
Protein	Normal or mildly elevated
Glucose	Normal
Oligoclonal bands (OCBs)	Present in CSF but absent in serum (in >95% of MS patients)
IgG index	Elevated (>0.7)
Myelin basic protein	May be elevated during acute relapse

Key point: OCBs must be in CSF but NOT in serum to be specific for intrathecal IgG synthesis. They are not diagnostic alone but support the diagnosis.

Additional Investigations

Test	Reason
Visual Evoked Potentials (VEP)	Prolonged P100 latency (>100ms) with preserved amplitude = demyelination of optic nerve
Somatosensory EPs	Demonstrate subclinical posterior column involvement
AQP4-IgG (anti-aquaporin-4)	Rule out NMOSD
MOG-IgG	Rule out MOGAD
ANA, anti-dsDNA, APLA	Rule out SLE/CNS vasculitis
Serum B12, methylmalonic acid	Rule out SACD
HTLV-1 serology	Rule out tropical spastic paraparesis
VDRL/TPHA	Rule out neurosyphilis
ACE level, chest X-ray	Rule out neurosarcoidosis
HIV	Rule out HIV myelopathy

PART 3 - DIAGNOSIS & CRITERIA

2017 McDonald Criteria (most commonly asked)

For one attack with one lesion (Clinically Isolated Syndrome):

DIS: ≥1 T2 lesion in ≥2 of 4 CNS areas, OR ≥2 MRI lesions + positive CSF OCBs
DIT: Simultaneous Gd+ and non-enhancing lesion, OR new T2 lesion on follow-up, OR positive CSF OCBs

This patient: Prior optic neuritis (first attack) + current cord episode (second attack, different site) = 2 attacks + 2 lesion sites = MS diagnosis established clinically without waiting for MRI criteria

PART 4 - TREATMENT

Acute Relapse Management

IV Methylprednisolone 1g/day x 3-5 days - shortens duration of relapse but does not change long-term outcome
Oral taper after IV is optional (not routinely recommended)
Physiotherapy: Passive and active rehabilitation

Disease-Modifying Therapy (DMT)

Platform/Moderate Efficacy (1st line):

Interferon beta-1a / beta-1b (SC or IM injection)
Glatiramer acetate
Teriflunomide (oral)
Dimethyl fumarate (oral)

High Efficacy DMTs (2nd line / aggressive early):

Natalizumab (anti-VLA-4; risk: PML with JC virus seropositivity)
Fingolimod (S1P receptor modulator; risk: bradycardia at first dose, macular edema)
Alemtuzumab (anti-CD52; risk: secondary autoimmunity)
Ocrelizumab (anti-CD20; also approved for PPMS)
Cladribine (oral; annual pulses)

Symptomatic Management

Symptom	Treatment
Spasticity	Baclofen, tizanidine, physiotherapy
Bladder urgency	Oxybutynin, tolterodine
Bladder retention	Intermittent self-catheterization
Fatigue	Amantadine, modafinil, energy conservation
Neuropathic pain	Gabapentin, pregabalin
Depression	SSRI (note: IFN-β may worsen depression)
Erectile dysfunction	Sildenafil

PART 5 - EXAMINER QUESTIONS & MODEL ANSWERS

Q1. What is the single most characteristic sign that points to MS rather than any other cause of myelopathy?

Internuclear ophthalmoplegia (INO) in a young patient is almost pathognomonic of MS. It results from a lesion in the medial longitudinal fasciculus (MLF) and manifests as ipsilateral adduction failure with contralateral abducting nystagmus. Bilateral INO in a young patient = MS until proven otherwise.

Q2. What is Lhermitte's sign and its significance?

Lhermitte's sign is an electric shock-like sensation radiating down the spine and into the limbs, precipitated by neck flexion. It indicates posterior column (dorsal column) involvement, particularly in the cervical cord. It is not specific to MS but is highly characteristic, occurring in up to 40% of MS patients. It represents mechano-sensitivity of demyelinated axons.

Q3. What is Uhthoff's phenomenon?

Worsening of neurological symptoms with rise in body temperature (exercise, hot bath, fever). It occurs because demyelinated axons have a very narrow temperature tolerance for conduction - a small rise in temperature blocks conduction in already demyelinated axons. It is characteristic of MS and helps distinguish it from a structural lesion. It is NOT a relapse; symptoms resolve as temperature normalizes.

Q4. How does an MS spinal cord lesion differ radiologically from NMO?

Feature	MS	NMOSD
Length	Short (<3 vertebral segments)	Long (≥3 segments = LETM)
Location in cord	Peripheral/posterolateral	Central gray matter, central canal
MRI pattern	Asymmetric, small, discrete	Extensive, "bright spotty" lesions
Gadolinium	Mild, peripheral enhancement	Intense, extensive enhancement
Brain lesions	Periventricular, Dawson's fingers	Area postrema, hypothalamus, periaqueductal
AQP4-IgG	Negative	Positive in 70-80%
MOG-IgG	Negative	Some NMOSD-like phenotypes

Q5. What are oligoclonal bands? What is their significance?

Oligoclonal bands (OCBs) are distinct bands of IgG visible on isoelectric focusing of CSF. They represent intrathecal immunoglobulin synthesis by B-cell clones within the CNS. They are present in the CSF but NOT in the serum of the same patient - this pattern confirms intrathecal production. Found in >95% of MS patients. They are not specific to MS (also seen in neurosyphilis, CNS vasculitis, CNS lymphoma, viral encephalitis), but their presence strongly supports MS when clinical and MRI criteria are near-satisfied. The 2017 McDonald criteria incorporated CSF OCBs as a substitute for DIT in certain scenarios.

Q6. What is the IgG index and how is it calculated?

IgG Index = (CSF IgG / CSF albumin) ÷ (Serum IgG / Serum albumin). Normal is <0.7. A raised IgG index >0.7 indicates intrathecal IgG synthesis. It is less specific than OCBs but provides quantitative evidence of CNS inflammation.

Q7. Explain the EDSS scale and how you assess it.

The Kurtzke Expanded Disability Status Scale (EDSS) ranges from 0 (normal) to 10 (death from MS). It is based on the examination of 8 functional systems (pyramidal, cerebellar, brainstem, sensory, bowel/bladder, visual, cerebral, and other). Key clinical anchors:

0: Normal exam

1.0-1.5: Minimal signs, no disability

3.0: Moderate disability but fully ambulatory

5.0: Impaired but can walk ~200m without aid

6.0: Requires unilateral walking aid >100m

6.5: Bilateral walking aid required

7.0: Wheelchair bound

10: Death from MS

Q8. What are the MS subtypes and their natural history?

Subtype	Description
RRMS	85-90% of cases; distinct relapses with full or partial recovery; eventually converts to SPMS
SPMS	Secondary progressive; follows RRMS; gradual accumulation of disability with or without superimposed relapses
PPMS	~10-15%; progressive from onset without relapses; more equal sex ratio; older onset; spinal cord predominant; ocrelizumab approved
PRMS	Progressive from onset with superimposed relapses (less common, sometimes classified under PPMS)
CIS	Clinically Isolated Syndrome; first demyelinating event; high risk of converting to MS if MRI lesions present
RIS	Radiologically Isolated Syndrome; incidental MRI MS-like lesions without clinical symptoms

Q9. What DMT would you choose for this patient and why?

For a young woman with RRMS who has had two relapses with residual disability (EDSS 5.0), most current guidelines favor high-efficacy therapy early ("treat to target") rather than stepping up from platform therapy.

Preferred options in a young woman of childbearing age:

Natalizumab (highly effective; monthly IV; check JC virus antibody index before starting; contraindicated if JC+ with high index)

Ocrelizumab (B-cell depletion; 6-monthly infusions; effective and well-tolerated)

Dimethyl fumarate or Teriflunomide (oral; moderate efficacy; safer in terms of infections)

Avoid: Alemtuzumab and Cladribine (teratogenic potential, complex safety profiles) unless other options fail.

Contraception counseling: Teriflunomide is teratogenic (requires washout with cholestyramine before pregnancy). Natalizumab may be continued into early pregnancy or switched to glatiramer acetate. Ocrelizumab should be stopped 6 months before planned pregnancy.

Q10. What is the risk of PML with natalizumab?

PML (Progressive Multifocal Leukoencephalopathy) is caused by reactivation of JC (John Cunningham) polyomavirus in the setting of immune suppression from natalizumab. Risk stratification:

JC antibody negative: Very low risk (~1:10,000)

JC antibody positive, index <0.9: Low risk (~1:1,000)

JC antibody positive, index >1.5 + >2 years of treatment + prior immunosuppression: Very high risk (~1:100 or more)

MRI surveillance every 3-6 months in high-risk patients. If PML is suspected, withhold natalizumab and consider plasma exchange to rapidly eliminate drug.

Q11. How does MS affect pregnancy and vice versa?

During pregnancy: Relapse rate typically decreases by ~70% in the third trimester due to immunological shift toward tolerance (Th2/regulatory immune phenotype)

Postpartum: Significant increase in relapse rate in the first 3-6 months after delivery; plan for early reinstitution of DMT

MS does not increase obstetric complications; vaginal delivery is preferred

Breastfeeding: Glatiramer acetate and interferons are generally considered acceptable; most oral DMTs should be avoided while breastfeeding

Q12. What is the difference between a relapse and a pseudo-relapse?

A true relapse (also called exacerbation or attack) is a new neurological symptom or worsening of an existing symptom lasting >24 hours in the absence of fever or infection, occurring at least 30 days after a previous relapse. It must represent a new lesion or reactivation of an existing lesion.

A pseudo-relapse is worsening of pre-existing symptoms due to intercurrent infection, fever (Uhthoff's phenomenon), metabolic disturbance, extreme fatigue, or heat. No new MRI lesion is found. It resolves when the precipitant is treated. Urinary tract infections are the most common cause in MS patients.

PART 6 - DIFFERENTIAL DIAGNOSIS

Primary Differential Diagnoses for a Young Patient with Myelopathy

Diagnosis	Key Distinguishing Features
Neuromyelitis Optica Spectrum Disorder (NMOSD)	LETM (≥3 segments), area postrema involvement (intractable hiccups/vomiting), AQP4-IgG positive, severe attacks with poor recovery, simultaneous optic neuritis
MOGAD (MOG antibody disease)	MOG-IgG positive, often better recovery, LETM or short lesions, optic neuritis common, cortical encephalitis possible
Subacute Combined Degeneration (SCD)	B12 deficiency; posterior column >> lateral column; dorsal column involvement, absent vibration/JPS, megaloblastic anemia, B12 very low, no relapses
CNS Vasculitis (SLE/APLA)	Young woman, ANA/anti-dsDNA/APLA positive, systemic features (rash, arthritis, photosensitivity, serositis), CSF inflammatory but OCBs absent
Neurosarcoidosis	Hilar adenopathy, elevated ACE, skin/eye involvement, enhancing meningeal thickening on MRI, non-caseating granulomas on biopsy
Spinal Cord Compression	Cervical spondylosis, disc herniation, epidural abscess, metastatic disease; NO brain lesions; MRI shows structural compression; no relapses
Spinal AVM/Dural AVF	Progressive myelopathy, flow voids on MRI, no brain lesions, spinal angiography diagnostic
Tropical Spastic Paraparesis (HTLV-1)	Endemic areas, HTLV-1 serology positive, insidious progression, no relapses, spastic paraparesis with minimal sensory involvement
HIV Vacuolar Myelopathy	HIV positive, posterior column involvement, subacute course
Lyme Neuroborreliosis	Endemic area, tick exposure, erythema migrans, facial palsy, Borrelia serology positive
CNS Lymphoma	Older patients, immunocompromised, large enhancing lesions, periventricular distribution can mimic MS
Hereditary Spastic Paraplegia (HSP)	Family history, no relapses, pure spastic paraparesis, genetic testing
Adrenoleukodystrophy	Young males, adrenal insufficiency, very long chain fatty acids elevated, confluent white matter lesions
Metachromatic Leukodystrophy	Arylsulfatase A deficiency, diffuse white matter disease, peripheral neuropathy, cognitive decline

Memory Aid for Differentials (STINVM + HALO)

S - SLE/CNS vasculitis
T - TSP (HTLV-1), Toxoplasmosis (HIV)
I - Infective (TB, Neurosyphilis, Brucella, Lyme)
N - NMO spectrum disorder / MOGAD
V - Vascular (AVM, dural AVF, anterior spinal artery infarct)
M - Metabolic (B12/SCD, Copper deficiency)
H - Hereditary (HSP, Adrenoleukodystrophy)
A - Autoimmune/Sarcoid
L - Lymphoma/Leprosy
O - Other structural (cervical spondylosis, disc, tumor)

Quick Reference: Why This Is MS and Not Something Else

Feature	Favors MS
Young woman, 2nd-3rd decade	Yes
Relapsing-remitting course	Yes
Optic neuritis as first attack	Classic
Spinal cord lesion (short, <3 segments)	Classic
INO on examination	Near pathognomonic
Uhthoff's phenomenon	Classic
Lhermitte's sign	Classic
Multiple brain lesions (Dawson's fingers)	Diagnostic
OCBs in CSF only	Supportive
Negative AQP4/MOG antibodies	Rules out NMO/MOGAD

Sources: Goldman-Cecil Medicine 26e (International), Harrison's Principles of Internal Medicine 22e (2025), Bradley and Daroff's Neurology in Clinical Practice - all accessed via the medical textbook library. McDonald Criteria referenced: Thompson AJ et al., Lancet Neurol 2018;17:162-173.

I am MD medicine resident I am going to present a case of spinal cord so please give detailed history and examination of case presentation on spinal cord lesions and suggest what questions with answer that can be asked by examiner and what are the differential diagnosis

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Here is a complete, professor-round / fellowship-level guide covering ALL major spinal cord syndromes - structured as case presentations with detailed history, examination, examiner Q&A, and differentials.

COMPLETE SPINAL CORD CASE PRESENTATIONS

For MD Medicine Residents - Senior/Fellowship Level

HOW TO PRESENT ANY SPINAL CORD CASE: THE UNIVERSAL FRAMEWORK

Before diving into individual syndromes, every spinal cord case presentation must answer these 5 questions:

Level of lesion - What spinal segment is involved?
Side of lesion - Unilateral / bilateral / central?
Tracts involved - Which columns/tracts are affected? (Posterior, lateral, anterior)
Onset - Acute (seconds-hours), subacute (days-weeks), or chronic (months-years)?
Etiology - Compressive or non-compressive?

ANATOMY PRIMER (Must Know for Viva)

Tract	Location in Cord	Function	Lesion Findings
Dorsal columns (posterior)	Posterior	Vibration, proprioception, fine touch (ipsilateral)	Loss of vibration/JPS ipsilateral
Lateral corticospinal tract	Lateral	Motor (ipsilateral)	UMN weakness ipsilateral
Lateral spinothalamic tract	Anterolateral	Pain, temperature (contralateral, 2-3 levels below)	Loss of pain/temp contralateral
Anterior spinothalamic	Anterior	Crude touch (bilateral)	Rarely lost alone
Anterior horn cells	Central gray	LMN motor (segmental)	Wasting, fasciculations at level

SYNDROME 1: TRANSVERSE MYELITIS

History

Model Case: 28-year-old male presents with 5 days of progressive weakness in both lower limbs, started after a mild febrile illness 2 weeks ago.

Chief Complaint: "My legs are getting weak and I cannot feel my bladder."

History of Present Illness:

Onset: Subacute, over 5-7 days, progressive
Both lower limbs affected simultaneously (bilateral) - started as heaviness, progressing to inability to walk
Band-like tightness around the abdomen (sensory level symptom - patients describe it as "tight belt around the waist")
Paresthesias (tingling/burning) in both lower limbs, ascending from feet
Urinary urgency progressing to urinary retention - patient cannot feel when bladder is full
Constipation (bowel involvement)
No back pain (unlike compression)
Preceding febrile illness 2 weeks prior (post-infectious demyelination trigger)
No prior similar episode (if first episode - possible idiopathic TM; if prior episode - consider MS or NMO)
Ask specifically: Any visual blurring (MS/NMO), any joint pains/rash/photosensitivity (SLE), any genital ulcers (Behcet's)

Systemic Review:

Ask about vaccinations (post-vaccination TM rare but recognized)
IV drug use / sexual history (HIV, syphilis)
Travel history (tropical infections)
Family history (MS, NMOSD)

Examination

Vitals: Stable. May have urinary retention on bladder scan.

General: No pallor, no lymphadenopathy, no rash

Neurological:

Higher mental functions: Normal

Cranial nerves: Normal (no cranial nerve involvement distinguishes cord from brainstem)

Motor System (Lower Limbs):

Tone: Initially flaccid/reduced (spinal shock phase, first few days), then becomes spastic
Power: 1-2/5 bilaterally in all muscle groups
Reflexes: Initially absent (spinal shock), later brisk/exaggerated
Plantars: Bilateral extensor (Babinski positive)
No involvement of upper limbs (if thoracic level)

Sensory Examination - CRITICAL:

Sensory level - test pin-prick starting from feet, moving upward. Note the level where sensation returns. A clear horizontal sensory level is the hallmark of transverse myelitis.
If level at T6: Reduced pain/temperature from T6 downward
Vibration and position sense: Also reduced below the level (posterior column involved)
Saddle area sensation: Check perianal sensation

Autonomic:

Bladder: Suprapubic fullness, catheter drainage may be needed
Bowel: Absent anal tone
Absent bulbocavernosus reflex (early)

Sensory Level Summary:

Level	Clinical landmark
C4	Shoulder level
T4	Nipple level
T6	Xiphisternum level
T10	Umbilicus level
T12/L1	Groin crease

Investigations

Test	Expected Finding
MRI spine with gadolinium	T2 hyperintense lesion spanning >3 vertebral segments (LETM if NMO), central cord involvement, may enhance
MRI brain	Rule out MS brain lesions
CSF analysis	Lymphocytic pleocytosis (10-200 cells), mildly elevated protein, normal glucose, may have OCBs
AQP4-IgG (anti-aquaporin-4)	Positive in NMOSD (most important to check)
MOG-IgG	Positive in MOGAD
ANA, anti-dsDNA, APLA	Rule out SLE/CNS vasculitis
Anti-Ro, Anti-La	Rule out Sjogren's myelitis
VDRL/TPHA	Rule out neurosyphilis
HIV serology
HTLV-1 serology	If endemic area
VEP	If MS suspected
Serum B12	Baseline
Urine culture	UTI often complicates bladder dysfunction

Treatment

Acute: IV methylprednisolone 1g/day x 3-5 days
Refractory: IV immunoglobulin or plasma exchange (PLEX)
If NMOSD confirmed: Long-term immunosuppression (azathioprine + oral steroids; or rituximab; or newer agents: eculizumab, satralizumab, inebilizumab)
Bladder care: Intermittent catheterization; treat UTI aggressively
Rehabilitation: Early physiotherapy

SYNDROME 2: SUBACUTE COMBINED DEGENERATION (SCD) - Vitamin B12 Deficiency

History

Model Case: 52-year-old strict vegetarian male, presenting with 3 months of tingling and numbness in both hands and feet, difficulty walking in the dark, and progressive weakness.

Key History Points:

Onset: Insidious, subacute (weeks to months) - NO acute episodes/relapses
Tingling/paresthesias starting in fingertips and toes (peripheral neuropathy component)
Difficulty walking in the dark or on uneven ground (loss of proprioception - sensory ataxia)
Weakness of lower limbs (lateral column involvement)
Lhermitte's sign may be present (electric shock on neck flexion)
Cognitive symptoms: Irritability, memory difficulty, personality change (in advanced cases)
Visual blurring (optic nerve involvement in severe cases)

Dietary/Metabolic History (Critical):

Strict vegetarian or vegan for years?
Previous gastric surgery (gastrectomy, bariatric surgery = loss of intrinsic factor)
Pernicious anemia history (autoimmune parietal cell destruction)
Chronic proton pump inhibitor use (impairs B12 absorption)
Nitrous oxide exposure (dental anesthesia, recreational - inactivates B12)
Medications: Metformin (reduces B12 absorption), phenytoin, colchicine
Crohn's disease, terminal ileal resection (site of B12 absorption)
Fish tapeworm (Diphyllobothrium) infestation (consumes B12)
Alcoholism (poor nutrition)

No history of relapses and remissions (key differentiator from MS)

Examination

General: Pallor (megaloblastic anemia), mild jaundice (hemolysis from ineffective erythropoiesis), smooth tongue (atrophic glossitis - beefy red tongue)

Classic Signs - "Combined" degeneration means BOTH posterior AND lateral columns:

Posterior Column Signs:

Vibration sense: Absent or severely impaired at ankle, then knee (128 Hz tuning fork)
Joint position sense: Absent (patient cannot detect movements of toes/fingers)
Romberg's sign: Positive - patient sways and falls with eyes closed
Sensory ataxia: Wide-based gait, stamping gait

Lateral Column (Corticospinal) Signs:

Power: 3-4/5 lower limbs
Tone: Increased (spasticity)
Reflexes: Diminished or absent (peripheral neuropathy component suppresses reflexes despite UMN lesion - very characteristic combination)
Plantars: Extensor (Babinski positive) - the combination of absent ankle jerks + extensor plantar is HIGHLY CHARACTERISTIC of SCD

Peripheral Neuropathy (Glove-and-stocking pattern):

Reduced pin-prick and temperature distally
Absent ankle jerks

No sensory level (unlike transverse myelitis - the sensory loss is distal/peripheral, not at a segmental horizontal level)

Cognitive: Irritability, mild cognitive impairment (in advanced cases)

Key Examination Clue: Absent ankle reflexes + positive Babinski sign in the same patient - this paradoxical combination strongly suggests SCD or motor neuron disease.

Investigations

Test	Finding
CBC	Macrocytic anemia (MCV >100), hypersegmented neutrophils (>5 lobes in >5% = diagnostic of megaloblastic change), thrombocytopenia
Serum B12	Low (<200 pg/mL is deficient; 200-300 = borderline)
Serum homocysteine	Elevated (sensitive, elevated before B12 drops)
Methylmalonic acid (MMA)	Elevated (most specific for functional B12 deficiency)
Serum folate	Normal (to distinguish from folate deficiency myelopathy)
Anti-parietal cell antibodies	Positive in pernicious anemia (90%)
Anti-intrinsic factor antibodies	Positive in pernicious anemia (60%) - more specific
LDH, indirect bilirubin	Elevated (ineffective erythropoiesis)
Peripheral smear	Macro-ovalocytes, hypersegmented neutrophils
MRI spine	T2 hyperintensity in posterior columns (inverted V sign), cervical > thoracic cord
Nerve conduction study	Sensorimotor axonal neuropathy
Schilling test	(Rarely done now) assesses B12 absorption

MRI finding: "Inverted V sign" - T2 bright signal in posterior columns resembling inverted V on axial image is characteristic of SCD.

Treatment

IM Vitamin B12 (Cyanocobalamin/Hydroxocobalamin) 1000 mcg daily x 7 days, then weekly x 4 weeks, then monthly lifelong
Oral high-dose B12 (1000-2000 mcg/day) - effective even in pernicious anemia due to passive absorption
Do NOT give folate alone - may worsen neurological manifestations of B12 deficiency
Treat underlying cause (dietary counseling, treat pernicious anemia)
Physiotherapy for gait rehabilitation

SYNDROME 3: SPINAL CORD COMPRESSION (Cervical Spondylotic Myelopathy / Metastatic)

History - Two Sub-Types:

A. Cervical Spondylotic Myelopathy (CSM) - Most Common Chronic Compression

Model Case: 62-year-old male, office worker, presenting with 6 months of neck pain radiating to both arms, difficulty buttoning shirts, unsteady gait, and recently developed urinary urgency.

History Points:

Neck pain (often absent or mild - do not dismiss without it)
Clumsy hands: Dropping objects, difficulty with fine motor tasks (buttoning, writing) - indicates posterior column + corticospinal involvement in cervical cord
Lhermitte's sign: Electric shock down spine on neck flexion - cervical posterior column involvement
Lower limb stiffness, dragging gait (spastic paraparesis)
Urinary urgency/hesitancy (late sign)
Worsening with neck position (flexion or extension aggravates)
Insidious onset over months - NO acute episodes (unlike MS)
Occupational history (heavy manual labor, repetitive neck movements)

B. Metastatic Spinal Cord Compression (MSCC) - Oncological Emergency

Model Case: 55-year-old known case of carcinoma breast, presenting with 3 weeks of severe mid-back pain that is worse lying down, with progressive leg weakness and urinary retention.

Key History:

Back pain - constant, severe, worse with recumbency (unlike mechanical pain), worse with Valsalva
Prior history of malignancy (breast, lung, prostate, kidney, thyroid - the common ones)
Weight loss, anorexia (systemic cancer symptoms)
Progressive bilateral leg weakness
Bladder/bowel dysfunction (late sign - if already present, nerve recovery is poorer)
Time course: Days to weeks of progressive neurological decline

Examination (Common to both compression types)

Level-specific LMN signs AT level, UMN below:

Cervical cord compression:

Wasting and weakness of small muscles of hand (C8/T1 LMN)
Inverted supinator reflex (tap BR tendon → finger flexion instead of elbow flexion; indicates C5-6 lesion)
Hoffmann's sign: Flick middle finger distal phalanx → reflex flexion of thumb and index finger (UMN sign)
Brisk knee and ankle jerks, bilateral extensor plantars
Sensory loss in hands + reduced vibration sense below cervical level
Lhermitte's sign on examination

Thoracic cord compression:

Normal upper limbs
Sensory level in thorax (find level by testing pin prick from feet upward)
Bilateral spastic paraparesis
Brisk knee and ankle jerks, bilateral Babinski
Bladder/bowel involvement

Examination tip for examiners: Always check for a "sensory level" - the level at which sensation RETURNS as you test upward from the feet. This correlates with the level of compression.

Investigations

Test	Finding
MRI spine (URGENT - within 4 hours if MSCC suspected)	Disc/spondylosis compressing cord; epidural tumor, vertebral collapse
X-ray spine	Osteophytes, disc space narrowing, vertebral collapse
CT spine	Better bony detail
Myelography	If MRI unavailable
If malignancy:	PSA, CA-125, mammogram, CT chest/abdomen/pelvis
Bone scan	Metastatic disease
Biopsy	If primary unknown

Treatment

CSM: Cervical decompression surgery (laminectomy/laminoplasty/ACDF) - surgery preferred over conservative in moderate-severe myelopathy

MSCC (Oncological Emergency):

Dexamethasone 16mg IV STAT then 4mg 6-hourly - reduces cord edema
Urgent neurosurgery / radiotherapy within 24 hours
Radiotherapy for radiosensitive tumors (lymphoma, myeloma)
Surgery for single level, unknown primary, radioresistant tumor, spinal instability
Analgesia, bladder care

SYNDROME 4: BROWN-SEQUARD SYNDROME (Spinal Hemisection)

History

Model Case: 25-year-old male brought with stab wound to the left side of the neck, presenting with weakness of the left leg and inability to feel pain in the right leg.

Causes to elicit in history:

Trauma (stab wounds, penetrating injuries) - most common cause
Herniated cervical disc (unilateral compression)
Spinal cord tumor (intradural-extramedullary: meningioma, neurofibroma)
Multiple sclerosis (unilateral cord lesion)
Epidural hematoma / abscess
Spinal cord herniation
Cervical manipulation (iatrogenic)

Symptoms:

Weakness and stiffness on ONE side of the body below the lesion
Loss of pain and temperature on the OPPOSITE side (contralateral) below lesion
Loss of vibration/position sense on the same side (ipsilateral) as weakness
Patients often describe: "My right leg is numb to touch but my left leg can't feel hot or cold"
If cervical: May describe Horner's syndrome on the ipsilateral side (ptosis, miosis, anhidrosis)

Examination - The Classic Pattern

This is one of the most asked syndromes in viva. The key is the dissociation between sides.

Finding	Side	Explanation
UMN weakness (spastic)	Ipsilateral to lesion	Lateral corticospinal tract (uncrossed)
Loss of vibration and proprioception	Ipsilateral to lesion	Dorsal columns (uncrossed, cross at medulla)
Loss of pain and temperature	Contralateral to lesion	Spinothalamic tract (crosses 2-3 segments above entry)
At level of lesion: LMN weakness, ipsilateral band of anesthesia	Ipsilateral	Anterior horn cells + entering sensory root
Horner's syndrome (if cervical)	Ipsilateral	Ciliospinal center of Budge (C8-T2)

Memory Aid: "BS syndrome - BruiSe on one side, Burn on the other"

You feel bruised (touch/proprioception lost) on the same side as weakness
You can't feel the burn (pain/temperature lost) on the opposite side

SYNDROME 5: ANTERIOR SPINAL ARTERY SYNDROME (Anterior Cord Syndrome)

History

Model Case: 65-year-old male, sudden onset (within minutes) of bilateral leg weakness and inability to feel pain, after an abdominal aortic aneurysm repair surgery.

Key Historical Features:

Acute onset (minutes to hours) - stroke-like presentation
Sudden bilateral leg weakness/paralysis
Loss of pain and temperature below the lesion
Preserved vibration and position sense (this is the key - posterior columns spared)
Bladder and bowel incontinence
Back pain at onset (in many patients)
Precipitants: Aortic surgery (cross-clamp, stent), aortic dissection, hypotension, embolism (disc material, air, thrombus), vasculitis

High-risk situations to ask:

Recent cardiovascular surgery (aortic aneurysm repair, CABG)
Aortic dissection
Cardiac arrest / prolonged hypotension
Trauma with disc herniation compressing anterior cord
Fibrocartilaginous embolism (young patients after exercise)
Arteriovenous malformation of cord

Examination - Classic "Anterior 2/3" Pattern

Function	Result
Motor power	Paralyzed (bilateral, UMN)
Pain/Temperature (spinothalamic)	ABSENT bilaterally below level
Vibration/Proprioception (dorsal columns)	PRESERVED (posterior 1/3 spared)
Reflexes	Initially absent (spinal shock), then hyperreflexia
Plantars	Bilateral extensor
Bladder/Bowel	Affected

The Hallmark: Complete motor paralysis + loss of pain/temperature + INTACT vibration and position sense

Acute phase: Flaccid paralysis (spinal shock) - do not be misled into thinking it is LMN lesion. Over days-weeks, this converts to spasticity.

Investigations

Test	Finding
MRI spine (DWI sequences)	Restricted diffusion in anterior cord (similar to brain stroke); "pencil-like" T2 hyperintensity in anterior cord
MRA/CT angiography aorta	Identify aortic pathology
Echocardiogram	Embolic source
CSF	Usually normal (no inflammation)

SYNDROME 6: SYRINGOMYELIA

History

Model Case: 22-year-old male, presenting with 2 years of painless burns on both hands (burned himself while cooking without noticing), wasting of small muscles of both hands, and more recently weakness of lower limbs.

Characteristic Symptoms:

"Cape distribution" sensory loss - bilateral loss of pain and temperature over shoulders, upper arms, and upper chest (like a cape/shawl), with PRESERVED touch and vibration = suspended/dissociated sensory loss
Painless injuries - burns, cuts, wounds not felt in hands; trophic changes in hands
Weakness and wasting of hands and arms (anterior horn cell involvement)
Lower limb spasticity (later - when syrinx expands to involve lateral columns)
Neck/back pain (distension of syrinx, associated Chiari malformation)
Headache worse on coughing/straining (Chiari I malformation association)
Scoliosis (often first sign in children)
Bladder dysfunction (late)

Associated Conditions to Ask:

Chiari malformation (most common cause - 50-60%)
History of previous spinal cord trauma
Intramedullary tumor history
Spinal meningitis, adhesions
Tethered cord

Examination - Central Cord Pattern

The Key Pattern: Lesion starts centrally (crossing spinothalamic fibers in anterior commissure are damaged first):

Finding	Explanation
Bilateral loss of pain and temperature (cape distribution - shoulders, arms, upper chest)	Crossing spinothalamic fibers in anterior commissure damaged
PRESERVED vibration, proprioception, fine touch	Dorsal columns spared initially
LMN signs in upper limbs at level (wasting, weakness, fasciculations, absent reflexes)	Anterior horn cells involved
UMN signs in lower limbs (if advanced)	Lateral corticospinal tracts compressed
Horner's syndrome (unilateral)	Ciliospinal center at C8-T1 damaged
Scoliosis	Often visible on inspection
Trophic changes: Charcot joints, painless ulcers, burned/scarred hands	Sensory denervation

Dissociated sensory loss = Pain/temperature lost, vibration/touch preserved in the same area - this is PATHOGNOMONIC of syringomyelia.

Chiari signs to look for:

Downbeat nystagmus
Ataxia
Dysarthria
Occipital headache worse on Valsalva

Investigations

Test	Finding
MRI spine (T1 and T2)	CSF-filled cavity (hypointense on T1, hyperintense on T2) within cord, often extending over many segments. MRI of craniocervical junction to look for Chiari malformation
MRI brain	Chiari malformation (cerebellar tonsils descent >5mm below foramen magnum in Chiari I)
CT myelography	If MRI unavailable
Nerve conduction study	Denervation changes in upper limbs

Treatment

Treat the cause: Chiari I - posterior fossa decompression (suboccipital craniectomy)
Syringosubarachnoid or syringoperitoneal shunt if persistent after decompression
Cervical traction if arachnoid adhesions are cause
Rehabilitation

SYNDROME 7: NEUROMYELITIS OPTICA SPECTRUM DISORDER (NMOSD)

History

Model Case: 35-year-old female presenting with 1 week of complete inability to walk, urinary retention, and 3 months ago she had a sudden painful loss of vision in the left eye requiring hospitalization.

Cardinal Features in History:

Simultaneous or sequential optic neuritis + severe transverse myelitis (the classic NMO Devic's syndrome)
Optic neuritis: Usually severe, bilateral, with significant permanent visual loss (unlike MS optic neuritis which is usually mild and recovers well)
Myelitis: Very severe, bilateral paralysis; longitudinally extensive (≥3 vertebral segments)
Area postrema involvement: Intractable hiccups or nausea/vomiting (highly specific for NMO - ask specifically!)
Poor recovery between attacks (unlike MS where recovery is better)
Other features: Diencephalic syndrome (narcolepsy, hypothermia), brainstem features

Epidemiology: Asian and African women > Caucasians; female predominance (9:1); NMO more common than MS in India

Risk Factors:

Personal/family history of autoimmune disease (thyroid disease, SLE, Sjogren's)
Prior infections as triggers

Differentiate from MS:

Worse attacks, worse recovery than MS
Spinal lesion very long (LETM) vs short in MS
Brain lesions atypical: Area postrema, hypothalamus, periaqueductal gray (not Dawson's fingers)
AQP4 antibody positive

Examination

Optic component:

Visual acuity severely reduced (may be hand movements only or worse)
RAPD (Relative Afferent Pupillary Defect) in affected eye
Visual field: Central scotoma or severely constricted field
Fundus: Optic disc pallor (if prior neuritis resolved), disc edema (if acute)

Spinal cord component (LETM pattern - usually cervical-thoracic):

Dense bilateral paraplegia or quadriplegia (very severe, worse than MS)
Complete sensory level (both posterior and lateral column loss)
Bladder/bowel completely dysfunctional
Respiratory involvement if high cervical cord (C3-5) - may need ventilation

Brainstem (if area postrema involved):

Persistent hiccups on history confirmed by observation
Vomiting without explanation
May have eye movement abnormalities

Investigations

Test	Finding
AQP4-IgG (anti-aquaporin-4)	Positive in 70-80% of NMOSD (pathognomonic if positive)
MOG-IgG	Positive in AQP4-seronegative NMOSD (MOGAD); better prognosis
MRI spine	LETM - T2 hyperintensity spanning ≥3 vertebral segments; central gray matter ("bright spotty" lesions); may be contiguous cervical-thoracic
MRI brain	Area postrema lesion (dorsal medulla - pathognomonic); linear periependymal lesions; hypothalamic lesion; typically NO Dawson's fingers
CSF	Pleocytosis (can be neutrophilic, unlike MS which is lymphocytic), elevated protein, OCBs usually ABSENT (in contrast to MS)
VEP	Severely abnormal in acute optic neuritis
ANA, anti-Ro/La	Rule out associated Sjogren's, SLE

Treatment

Acute Attack:

IV methylprednisolone 1g/day x 5 days
Plasma exchange (PLEX) for severe attacks or steroid-unresponsive attacks - more important than in MS

Long-term Immunosuppression (mandatory - unlike MS, NMO attacks can be fatal):

Rituximab (anti-CD20) - preferred in many centers
Azathioprine 2-3 mg/kg/day + low-dose prednisolone
Mycophenolate mofetil
New FDA-approved biologics:
- Eculizumab (anti-complement C5)
- Satralizumab (anti-IL-6R)
- Inebilizumab (anti-CD19)

AVOID MS drugs in NMO - Natalizumab, fingolimod, interferon-beta can WORSEN NMO!

MASTER EXAMINER QUESTIONS & ANSWERS (Common to All Cord Syndromes)

Q1. How do you distinguish UMN from LMN lesion clinically?

Feature	UMN	LMN
Tone	Increased (spasticity - clasp-knife)	Decreased (flaccid)
Power	Reduced (pyramidal pattern)	Reduced (segmental)
Reflexes	Brisk/exaggerated	Absent/diminished
Plantar	Extensor (Babinski +)	Flexor or absent
Wasting	Mild, late	Pronounced, early
Fasciculations	Absent	Present
Distribution	Extensors weak in arm, flexors in leg	Muscle group at root/nerve level

Q2. What is spinal shock and how long does it last?

Spinal shock is the period of flaccid areflexic paralysis immediately after an acute severe spinal cord injury. ALL reflexes are abolished below the level. It lasts 24-72 hours, sometimes up to 3-4 weeks. The bulbocavernosus reflex (squeeze glans penis/clitoris → anal sphincter contraction) is the first reflex to return, signaling end of spinal shock. Absence of this reflex after 48 hours suggests complete cord lesion.

Q3. How do you determine the level of a spinal cord lesion clinically?

The lesion level is one or two segments ABOVE the dermatomal level of sensory loss (because pain/temperature fibers enter, ascend 2-3 segments, then cross to the contralateral spinothalamic tract). Key landmarks:

C5: Shoulder (regimental badge area)

C6: Lateral forearm, thumb

C8/T1: Medial arm, little finger

T4: Nipple line

T6: Xiphisternum

T10: Umbilicus

L1: Inguinal ligament

L4: Medial knee, medial malleolus

S1: Lateral foot, sole

Q4. Describe the "inverted V sign" on MRI. What does it indicate?

The inverted V sign is seen on axial T2 MRI of the cervical/thoracic cord in Subacute Combined Degeneration. It refers to T2 hyperintensity in the bilateral posterior columns forming a shape resembling an inverted "V" (or sometimes described as "rabbit ears"). This reflects selective demyelination of the gracile and cuneate fasciculi due to B12 deficiency. It is diagnostic of SCD when combined with clinical features.

Q5. What is the difference between sensory level (cord lesion) and distal sensory loss (peripheral neuropathy)?

Feature	Spinal Cord (Transverse Myelitis)	Peripheral Neuropathy
Pattern	Horizontal sensory level (clear demarcation)	Distal, glove-and-stocking
Onset	Acute/subacute with progression	Insidious, distal to proximal
Motor	UMN signs (hyperreflexia, Babinski)	LMN signs (hyporeflexia, wasting)
Bladder/Bowel	Involved early (cord)	Rarely involved until late
Lhermitte's sign	May be positive	Absent

Q6. What is dissociated sensory loss? Give examples.

Dissociated sensory loss = loss of one modality with preservation of another in the same area.

Loss of pain/temperature + PRESERVED vibration/proprioception:

Syringomyelia (damage to crossing spinothalamic fibers in anterior commissure)

Anterior spinal artery infarction (spinothalamic lost, dorsal columns spared)

Loss of vibration/proprioception + PRESERVED pain/temperature:

Subacute combined degeneration (posterior column degeneration)

Friedreich's ataxia

Tabes dorsalis

Complete loss of all modalities on one side:

Brown-Sequard (ipsilateral side: motor + proprioception lost; contralateral: pain/temp lost)

Q7. What is autonomic dysreflexia? When does it occur?

Autonomic dysreflexia is a life-threatening syndrome in patients with spinal cord injury at or above T6 (above the splanchnic sympathetic outflow). A noxious stimulus below the level (most commonly: urinary retention, fecal impaction, pressure sore, tight clothing, cold water) triggers massive uncontrolled sympathetic discharge below the lesion. Clinical features: Severe hypertension (systolic can reach 300 mmHg), bradycardia (baroreflex), severe pounding headache, profuse sweating, flushing above lesion, pallor below. Management: Sit patient upright (orthostatic BP drop), find and remove trigger, nitroprusside/nifedipine for acute hypertension.

Q8. Compare MRI findings in all spinal cord syndromes:

Syndrome	MRI Finding
Transverse myelitis (idiopathic)	Central T2 signal, may span 1-3 segments
NMOSD	LETM ≥3 segments, central gray matter, "bright spotty", enhances
MS	Short lesion <3 segments, peripheral/dorsal, Dawson's fingers in brain
SCD (B12 deficiency)	Posterior column T2 hyperintensity, "inverted V sign"
Anterior cord infarct	Anterior cord DWI restriction, "pencil-like" T2
Syringomyelia	CSF-filled cavity in center, T1 dark/T2 bright
Compression	Extrinsic compression, disc/tumor, cord edema

Q9. What are "Red Flags" for spinal cord compression (oncological emergency)?

The NICE Red Flag criteria for MSCC:

New onset back pain in a known cancer patient

Pain worse on lying down / at night (unlike mechanical pain)

Progressive bilateral limb weakness

Bladder/bowel dysfunction (late sign)

Saddle area numbness

Unrelenting thoracic pain (thoracic disc disease is rare; think metastasis)

Management: Do NOT wait for weakness to develop. Treat with dexamethasone IMMEDIATELY and arrange urgent MRI within 4 hours.

Q10. Which spinal cord syndrome has the WORST prognosis for recovery?

Anterior cord syndrome (anterior spinal artery infarct) - has the worst prognosis among incomplete cord syndromes, with <10-15% chance of meaningful motor recovery.

Brown-Sequard - best prognosis of all partial cord syndromes (>90% recovery of ambulation)

Central cord syndrome - intermediate prognosis; lower limbs recover better than upper limbs

NMOSD - often severe permanent disability without aggressive immunosuppression (Source: Miller's Review of Orthopaedics 9th Ed., Bradley & Daroff's Neurology)

MASTER DIFFERENTIAL DIAGNOSIS TABLE - ALL SPINAL CORD LESIONS

(Based on Bradley & Daroff's Box 27.1 + Harrison's + Goldman-Cecil)

Category 1: COMPRESSIVE MYELOPATHY

Cause	Key Feature
Cervical spondylotic myelopathy	Elderly, neck pain, insidious, osteophytes on MRI
Disc herniation (acute)	Sudden onset with movement, radicular pain
Epidural abscess	Fever, back pain, raised inflammatory markers, risk factors (IV drug use, DM)
Epidural hematoma	Anticoagulation, coagulopathy, acute onset
Metastatic spinal cord compression	Known malignancy, night pain, vertebral collapse
Intradural extramedullary tumors	Meningioma (F>M), neurofibroma (NF1), slowly progressive, NF lesions
Intramedullary tumors	Ependymoma (adults), astrocytoma (children), enhancing lesion

Category 2: NON-COMPRESSIVE MYELOPATHY

Cause	Key Distinguishing Feature
Multiple sclerosis	Young woman, relapses, short cord lesions, brain lesions (Dawson's fingers), OCBs positive
NMOSD	Severe attacks, LETM, AQP4-IgG positive, area postrema lesion
MOGAD	MOG-IgG positive, may have LETM or short lesion, better recovery
Idiopathic Transverse Myelitis	Post-infectious, no prior episodes, AQP4/MOG negative
Subacute Combined Degeneration	B12 deficiency, posterior columns, absent ankle jerks + Babinski
Anterior spinal artery infarction	Acute, motor + spinothalamic loss, preserved dorsal columns
Syringomyelia	Dissociated sensory loss, "cape" distribution, wasting of hands
CNS vasculitis (SLE, APLA)	Young woman, systemic features, positive autoantibodies
Neurosarcoidosis	Hilar adenopathy, elevated ACE, leptomeningeal enhancement
Tropical spastic paraparesis (HTLV-1)	Endemic area, HTLV-1 positive, insidious progressive spastic paraparesis
HIV vacuolar myelopathy	HIV positive, posterior > lateral columns, slowly progressive
Tabes dorsalis (neurosyphilis)	Lightning pains, Argyll Robertson pupils, Romberg positive, VDRL positive
Hereditary spastic paraplegia	Family history, pure spastic paraparesis, no sensory level, genetic
Radiation myelopathy	Prior spinal irradiation, delayed onset (months-years), progressive
Paraneoplastic myelopathy	Occult malignancy, anti-Hu/anti-CV2 antibodies
Adrenoleukodystrophy	Young males, adrenal insufficiency, VLCFA elevated

QUICK VIVA RECAP - "What Syndrome Is This?"

Pattern on Exam	Syndrome
Bilateral paraparesis + sensory level + bladder	Transverse Myelitis
Absent ankle jerks + extensor plantar + no sensory level	Subacute Combined Degeneration
One side weak + opposite side cannot feel pain/heat	Brown-Sequard
Both legs paralyzed + can't feel pain + vibration NORMAL	Anterior Spinal Artery
Cape distribution of pain/temperature loss + wasting hands	Syringomyelia
Severe myelitis + optic neuritis + hiccups	NMOSD
Elderly + neck pain + clumsy hands + Hoffmann's sign	Cervical Spondylotic Myelopathy
Cancer patient + back pain + progressive paraparesis	Metastatic Cord Compression (EMERGENCY)

Sources: Bradley & Daroff's Neurology in Clinical Practice (Chapters 26, 27, 28); Harrison's Principles of Internal Medicine 22e (2025); Goldman-Cecil Medicine International Edition; Localization in Clinical Neurology 8e. All accessed from the medical textbook library.

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