Neuroanatomy — Spinal Cord

Anatomic Organization and Segmentation

• The spinal cord consists of gray matter (centrally located, butterfly-shaped in cross-section) containing neuronal cell bodies, and white matter (peripherally located) containing myelinated and unmyelinated axons organized into tracts
• Gray matter is divided into dorsal (posterior) horns (sensory processing), ventral (anterior) horns (motor neurons), and intermediate zones (autonomic regulation); the substantia gelatinosa (lamina II) mediates pain transmission via the spinothalamic tract
• Spinal cord segments do not correspond to vertebral levels: cervical segments align with their vertebrae, but thoracic and lumbosacral segments are displaced rostrally; the conus medullaris terminates at L1-L2 vertebral level while the filum terminale (continuation of dura) extends to the coccyx
• Dorsal root ganglia (sensory ganglia) are located in the intervertebral foramina and contain unipolar neurons that bifurcate into peripheral and central branches
• The cauda equina (below L2) represents lumbar, sacral, and coccygeal nerve roots descending in the subarachnoid space

Major Ascending (Sensory) Tracts and Their Functions

• Dorsal Column-Medial Lemniscus System (ipsilateral, uncrossed at level of lesion): transmits discriminative touch, vibration sense, and proprioception; first-order neurons synapse in the nucleus gracilis (lower body, fasciculus gracilis) and nucleus cuneatus (upper body, fasciculus cuneatus) at the medulla; second-order axons decussate (cross) at the medulla as internal arcuate fibers to form the medial lemniscus; lesions produce sensory level with preserved pain/temperature below the lesion
• Spinothalamic Tract (crossed contralateral, crosses at level of entry ±2 segments): transmits pain and temperature sensation; first-order neurons synapse in the dorsal horn substantia gelatinosa; second-order neurons cross in the ventral white commissure and ascend as the spinothalamic tract (lateral for body, anterior for face); lesions produce suspended sensory level (cape-like distribution) at the level of cord involvement with loss of pain/temperature but preserved dorsal column sensation
• Spinocerebellar Tracts (dorsal and ventral): convey unconscious proprioception to the cerebellum for motor coordination; lesions produce truncal ataxia and incoordination
• Tectospinal and Vestibulospinal Tracts: mediate balance and postural reflexes

Major Descending (Motor) Tracts and Their Functions

• Corticospinal Tract (lateral, crossed at medullary pyramid ~90%): originates from motor cortex (Brodmann area 4), descends through the internal capsule, cerebral peduncle, and brainstem, and decussates at the medullary pyramids; synapses with lower motor neurons in the ventral horn; lesions produce contralateral upper motor neuron (UMN) signs: hyperreflexia, spasticity, Babinski sign, and weakness
• Anterior (Ventral) Corticospinal Tract (uncrossed, ~10% of fibers): crosses at the spinal level via the ventral white commissure; lesions produce ipsilateral UMN signs at the level of lesion
• Rubrospinal, Reticulospinal, and Vestibulorespinal Tracts: originate from brainstem nuclei and mediate postural control, balance, and reflexes

Spinal Cord Blood Supply and Vascular Territories

• Anterior Spinal Artery (ASA) (single, midline): supplies the anterior 2/3 of the spinal cord including ventral horns and spinothalamic tracts; arises from vertebral arteries and receives radicular arteries (particularly the artery of Adamkiewicz, typically at T9-L2 on the left)
• Posterior Spinal Arteries (PSAs) (paired, lateral to dorsal roots): supply the posterior 1/3 of the spinal cord including dorsal columns and dorsal horns; receive multiple small radicular arteries
• Spinal Cord Watershed Zones (T1-T4 and L1-L2): regions of reduced collateral perfusion vulnerable to ischemia
• Radicular Arteries: segmental vessels that accompany nerve roots; flow may be disrupted by disk herniation, aortic disease, or surgical procedures
• Venous Drainage: via anterior and posterior spinal veins and radicular veins; thrombosis or congestion can cause venous infarction

Reflex Arcs and Local Circuits

• Monosynaptic Reflexes: one synapse between sensory and motor neurons (e.g., patellar reflex); polysynaptic reflexes involve multiple interneurons (e.g., withdrawal reflex)
• Renshaw Cells: inhibitory interneurons that provide negative feedback to motor neurons, preventing excessive motor output
• Recurrent Inhibition: feedback mechanism maintaining motor neuron excitability within physiologic ranges

Autonomic Organization in the Spinal Cord

• Sympathetic Preganglionic Neurons: located in the intermediolateral column (IML) from T1-L2 segments; regulate vascular tone, sweating, and sphincter control
• Parasympathetic Preganglionic Neurons: located in the sacral parasympathetic nucleus (S2-S4); innervate pelvic and perineal organs
• Lesions at T1-L2 produce Horner's syndrome (if involving sympathetic outflow) or autonomic hyperreflexia in chronic spinal cord injury

Traumatic Causes

• Spinal Cord Injury (SCI): primary traumatic insult from vertebral fracture-dislocation, penetrating trauma, or severe contusion; secondary injury involves hemorrhage, edema, ischemia, free radical formation, and inflammatory cascade over hours to days; most common cause of spinal cord pathology in patients under 65 years
• Traction Injuries: nerve root avulsion from high-velocity trauma (motorcycle accidents, birth trauma producing Erb's palsy)

Vascular Causes

• Spinal Cord Infarction (Myelomalacia): anterior spinal artery syndrome from aortic aneurysm repair, aortic dissection, thrombosis of radicular arteries, or hypotension; presents with acute paraplegia and loss of pain/temperature sensation with preserved dorsal column function ("anterior cord syndrome")
• Spinal Cord Hemorrhage (Hematomyelia): from arteriovenous malformations (AVM), cavernous hemangiomas, anticoagulation, or trauma
• Epidural Hematoma: venous bleeding between dura and vertebral column causing progressive myelopathy
• Spinal Dural Arteriovenous Fistula (SDAVF): abnormal arteriovenous connection in the dura causing venous hypertension and cord ischemia

Compressive Myelopathy (Extrinsic)

• Extradural Lesions: herniated intervertebral disk (most common), spondylosis, metastatic disease, lymphoma, epidural abscess, hematoma
• Intradural Extramedullary Lesions: meningioma, schwannoma/neurofibromatosis, neurofibroma, myxopapillary ependymoma, arachnoiditis
• Degenerative Disk Disease and Spondylosis: progressive narrowing of spinal canal causing cervical myelopathy (most common in elderly)

Intramedullary Lesions

• Syrinx (Syringomyelia): fluid-filled cavity within the cord from post-traumatic injury, tethered spinal cord, Chiari malformation, or idiopathic causes; produces "cape-like sensory level" and pain
• Spinal Cord Tumors: ependymoma and astrocytoma (most common intramedullary), hemangioblastoma in von Hippel-Lindau disease, spinal metastases
• Demyelinating Disease: multiple sclerosis, transverse myelitis (idiopathic or associated with MOG/aquaporin-4 antibodies)
• Spinal Cord Infarction: central cord syndrome from hyperextension injury with cord contusion

Infectious Causes

• Viral Myelitis: enterovirus, herpes simplex, varicella-zoster, HIV-associated myelopathy
• Bacterial: tuberculosis (Pott's disease with epidural abscess), syphilis (tabes dorsalis affecting dorsal roots and columns), Lyme disease
• Fungal and Parasitic: coccidioidomycosis, aspergillosis, echinococcosis (rare in developed countries)

Metabolic and Degenerative Causes

• Vitamin B12 Deficiency: affects dorsal and lateral columns causing subacute combined degeneration with dorsal column signs (vibration/proprioception loss) plus pyramidal signs (Babinski, hyperreflexia, spasticity)
• Copper Deficiency: mimics B12 deficiency
• Adrenomyeloneuropathy: X-linked disorder causing progressive myelopathy
• Amyotrophic Lateral Sclerosis (ALS): degeneration of motor neurons affecting ventral horn and corticospinal tracts

Inflammatory and Autoimmune Causes

• Transverse Myelitis: acute inflammatory demyelination across one spinal cord segment; associated with MS, NMO spectrum disorders, viral infection, or idiopathic
• Neuromyelitis Optica Spectrum Disorder (NMOSD): aquaporin-4 antibody-associated recurrent transverse myelitis with optic neuritis
• Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): can affect proximal nerve roots and spinal cord
• Sarcoidosis: granulomatous inflammation affecting spinal cord and meninges

Toxic and Metabolic Causes

• Lathyrism: neurolathyrogens in grass pea causing spastic paraplegia
• Konzo: cassava-derived cyanogenic glucosides causing spastic paraplegia
• Nitrous Oxide (N2O) Abuse: inactivates vitamin B12 mimicking B12 deficiency myelopathy
• Radiation Myelopathy: delayed necrosis months to years after spinal radiation therapy

Congenital and Developmental Causes

• Tethered Spinal Cord: abnormal attachment of the filum terminale or intraspinal mass preventing normal cord mobility causing progressive myelopathy (especially in children with neural tube defects)
• Chiari Malformation: herniation of cerebellar tissue into the spinal canal causing syrinx and progressive myelopathy
• Spinal Dysraphism: incomplete closure of spinal canal with various sequelae depending on severity
• Vascular Malformations: AVM and cavernous hemangioma with risk of hemorrhage

Acute Presentation (Hours to Days)

• Acute Paraplegia or Tetraplegia: sudden onset weakness; paraplegia affects lower extremities (thoracic/lumbar cord lesion) while tetraplegia affects all four limbs (cervical cord lesion); flaccid paralysis initially (spinal shock phase lasting hours to weeks) followed by development of spasticity and hyperreflexia
• Acute Sensory Level: sharp demarcation of sensory loss at the level of cord lesion; ascending level may indicate progressive edema or hemorrhage
• Acute Back or Neck Pain: severe pain at level of injury, especially with fracture or epidural hematoma; radicular pain in distribution of affected roots
• Bowel and Bladder Dysfunction: acute urinary retention or incontinence; fecal incontinence
• Respiratory Compromise: if cervical (C3-C5) or high thoracic lesion affecting phrenic nerve innervation or intercostal muscles; acute respiratory failure possible with C1-C2 lesions
• Loss of Temperature Sensation ("suspended sensory level"): cape-like distribution due to spinothalamic tract involvement; classically seen with syrinx causing loss of pain/temperature while preserving dorsal column function

Chronic Progressive Presentation (Weeks to Months/Years)

• Progressive Weakness and Spasticity: initially flaccid paralysis transitions to spasticity with hyperreflexia and Babinski signs (extensor plantar response); upper extremities typically affected first in cervical myelopathy
• Sensory Loss: may be discriminative touch and proprioception loss (dorsal column) or pain/temperature loss (spinothalamic), depending on lesion location
• Gait Disturbance: spastic gait with scissoring (legs crossing); ataxic gait if cerebellar tracts involved; asymmetric weakness producing steppage gait if anterior horn cells affected
• Lhermitte's Sign: electric shock-like sensation down the spine with neck flexion; suggests demyelinating disease or posterolateral cord compression
• Radicular Pain: burning or sharp pain radiating into the distribution of nerve root(s); often precedes motor/sensory deficits in compressive myelopathy
• Paresthesias and Dysesthesias: abnormal sensations; neuropathic pain is common in spinal cord lesions

Syndrome Presentations Based on Location and Pattern

Complete Transection

• Total loss of motor, sensory, and autonomic function below the level of lesion
• Spinal shock phase: initial flaccid paralysis, areflexia, loss of all reflexes below lesion (lasts days to weeks)
• Recovery phase: gradual return of reflexes and spasticity; usually no recovery of motor or sensory function if truly complete

Anterior Cord Syndrome** (Anterior Spinal Artery Syndrome)

• Pathology: infarction of anterior 2/3 of spinal cord affecting ventral horns and spinothalamic tracts
• Motor loss: paralysis due to motor neuron involvement
• Sensory loss: loss of pain and temperature sensation below lesion (spinothalamic); preserved vibration and proprioception (dorsal columns intact)
• Autonomic: loss of autonomic control (sphincters, sweating)
• Prognosis: generally poor with minimal recovery

Central Cord Syndrome

• Pathology: intramedullary lesion affecting central gray matter and crossing spinothalamic fibers
• Motor loss: "cape-like" weakness affecting upper extremities more than lower extremities (sacral fibers are peripheral in spinothalamic tract and spared); upper extremities more affected because central lesion first disrupts crossing fibers for upper body
• Sensory loss: "cape-like" loss of pain and temperature across shoulders, arms, and upper trunk; preserved below
• Preservation: lower extremity strength and sensation relatively preserved; dorsal columns may be spared
• Prognosis: best of the incomplete syndromes; variable recovery depending on etiology

Brown-Sequard

Initial imaging

• Non-contrast CT: first study in trauma — detects fracture, dislocation, and malalignment that MRI reads poorly. Per ACR Appropriateness Criteria, imaging need in blunt trauma is triaged by the NEXUS low-risk criteria or the Canadian C-Spine Rule; a normal CT does not exclude cord injury (SCIWORA in children).
• Plain radiographs: limited role, useful only for gross alignment or hardware.

Confirmatory/gold standard

• MRI of the whole spine without and with gadolinium: the definitive test for cord parenchyma, epidural collections, and compression. Cord signal change is T2 hyperintense; enhancement suggests tumor, inflammation, or abscess.
• Pattern recognition: pencil-like anterior cord T2 signal with owl's-eye anterior horn hyperintensity on axial images in anterior spinal artery infarct; central cavity in syringomyelia (image the craniocervical junction for Chiari I); inverted-V/dorsal column T2 signal in subacute combined degeneration; longitudinally extensive myelitis spanning three or more vertebral segments favors NMOSD, whereas short, dorsolateral, peripheral lesions favor multiple sclerosis.

Immediate stabilization (any acute myelopathy)

• Airway and ventilation first: C3–C5 lesions threaten the phrenic nerve; rising PaCO2 or falling vital capacity mandates intubation before frank failure.
• Spinal immobilization and log-roll precautions until the spine is cleared.
• Hemodynamic support: the AANS/CNS guidelines support maintaining MAP 85–90 mmHg for about the first week after acute traumatic SCI to preserve cord perfusion — vasopressors (norepinephrine) and atropine or chronotropic support for the bradycardia of neurogenic shock.
• VTE prophylaxis with LMWH (enoxaparin) once bleeding risk permits.

Etiology-directed therapy

• Metastatic epidural cord compression: corticosteroid (dexamethasone IV) started immediately, then urgent neurosurgical assessment for decompressive surgery followed by radiotherapy, which outperforms radiotherapy alone in ambulatory outcome (ASTRO/NCCN CNS and bone metastasis guidance).
• Spinal epidural abscess: emergent surgical decompression and drainage plus empiric vancomycin (dosed to a 24-hour AUC/MIC of 400–600 per the 2020 IDSA/ASHP consensus) with an antipseudomonal beta-lactam (cefepime), narrowed by culture — IDSA native vertebral osteomyelitis guidance.
• Cauda equina syndrome: emergent MRI and surgical decompression — a true surgical emergency, not a next-morning problem.
• Acute transverse myelitis/MS relapse: high-dose IV methylprednisolone, with plasma exchange for steroid-refractory disease (AAN).
• NMOSD: acute steroids/PLEX, then maintenance with complement or B-cell/IL-6 directed biologics (eculizumab, inebilizumab, satralizumab) or rituximab.
• Subacute combined degeneration: parenteral cyanocobalamin; stop nitrous oxide exposure.
• Degenerative cervical myelopathy: surgical decompression for moderate–severe or progressive disease (AOSpine/NASS).

Contraindicated or discouraged

• Routine high-dose methylprednisolone in traumatic SCI is not recommended by AANS/CNS (harm outweighs benefit); AOSpine offers it only as a weak option within 8 hours.
• Succinylcholine beyond roughly 48–72 hours post-injury — denervation upregulates acetylcholine receptors and causes lethal hyperkalemia.
• Interferon-beta, natalizumab, and fingolimod in NMOSD — they worsen it.
• Folate alone in B12 deficiency — corrects anemia while the myelopathy progresses.

Emergencies

• Neurogenic shock: loss of sympathetic outflow from the intermediolateral column in lesions at or above T6 — hypotension with bradycardia and warm, dry, vasodilated skin. The bradycardia distinguishes it from hemorrhagic shock (tachycardia) and from spinal shock, which is a reflex phenomenon, not a hemodynamic one.
• Autonomic dysreflexia: in chronic injuries at or above T6, a noxious stimulus below the lesion (distended bladder, fecal impaction, pressure injury) drives unopposed sympathetic reflex vasoconstriction below, while baroreflex vagal slowing and vasodilation occur only above. Signs: pounding headache, paroxysmal severe hypertension, flushing/sweating above the level, pallor and piloerection below, reflex bradycardia. Risk of intracranial hemorrhage, seizure, and death — sit the patient upright, loosen constricting clothing, catheterize/disimpact, then a rapid short-acting antihypertensive; avoid nitrates if a PDE5 inhibitor was taken recently.
• Ventilatory failure from ascending cord edema in cervical injury — a rising sensory level is the warning sign.

Disease-related

• Post-traumatic syringomyelia: cavitation months to years later; heralded by an ascending sensory level, new cape-like pain/temperature loss, or worsening spasticity — re-image.
• Spasticity and contractures from loss of descending inhibition; treated with baclofen or tizanidine. Abrupt intrathecal baclofen withdrawal (pump failure) causes fever, rigidity, and rhabdomyolysis and is an emergency.
• Neurogenic bladder with detrusor–sphincter dyssynergia: high storage pressures cause hydronephrosis, stones, and urosepsis — the leading long-term cause of morbidity.
• Pressure injuries, heterotopic ossification, DVT/PE, orthostatic hypotension, and refractory neuropathic pain.

Treatment-related

• Corticosteroids: hyperglycemia, infection, GI bleeding, and delayed avascular necrosis; the principal argument against routine steroids in trauma.
• Radiation myelopathy: delayed cord necrosis months to years after spinal radiotherapy, presenting as progressive painless myelopathy with enhancing cord signal.
• Postoperative C5 palsy after cervical decompression — isolated deltoid/biceps weakness, usually self-limited; also dural tear with CSF leak and surgical-site infection.

• Brown-Séquard: hemisection gives ipsilateral UMN weakness and dorsal column loss (crossing occurs in the medulla) with contralateral pain/temperature loss beginning one to two segments below the lesion, because spinothalamic fibers ascend a segment or two before decussating in the ventral white commissure. An ipsilateral LMN band at the level itself is the giveaway.
• Suspended, cape-like loss of pain and temperature with preserved vibration = syringomyelia expanding through the ventral white commissure. Best next step: MRI of the cervical cord and craniocervical junction to find a Chiari I malformation.
• Anterior cord syndrome preserves vibration and proprioception — the posterior spinal arteries are paired and spared. Classic stem: paraplegia after thoracoabdominal aortic aneurysm repair (artery of Adamkiewicz territory).
• Dorsal columns plus lateral corticospinal tracts, with a normal or macrocytic CBC: subacute combined degeneration. Check methylmalonic acid and homocysteine, and ask about nitrous oxide abuse or bariatric surgery. Distractor to avoid: tabes dorsalis also hits dorsal columns but produces areflexia, sensory ataxia, lancinating pains, and Argyll Robertson pupils, not Babinski signs.
• Central cord syndrome: elderly patient, hyperextension fall, spondylosis — upper extremities weaker than lower, with sacral sparing from the lamination of spinothalamic fibers.
• Spinal shock ≠ neurogenic shock. Spinal shock is transient areflexia and flaccidity; neurogenic shock is hypotension with bradycardia from lost sympathetic outflow above T6. Return of the bulbocavernosus reflex signals the end of spinal shock and makes the ASIA grade prognostic.
• Cancer patient with back pain and a new sensory level: give IV dexamethasone immediately and obtain whole-spine MRI — do not wait for imaging to start steroids, and do not image only the painful level.
• Do not reflexively pick high-dose methylprednisolone for acute traumatic SCI; AANS/CNS recommends against it. The correct answers are immobilization, ventilatory support, and MAP augmentation.