Acute Spinal Cord Syndromes

INTRODUCTION

Patients presenting with acute spinal cord syndromes represent true neurologic emergencies. Pathologic damage to the cord is usually incomplete. Therefore, there is opportunity to salvage (and peril of losing) vital cord tissue and function over the ensuing minutes and hours after presentation. As with other neurologic presentations, clinicians must first localize and then differentiate the type of damage in order to initiate the most effective interventions.

DIFFERENTIAL DIAGNOSIS

The differential diagnosis for an acute cord syndrome ranges from mechanical to vascular, infectious, inflammatory, neoplastic, and toxic etiologies (Tables 16.1 and 16.2). A careful history regarding remote or recent trauma, other systemic symptoms, or toxic habits may help narrow your differential. Determining the rate of symptom progression proves critical, as patients whose symptoms reach maximal involvement within minutes are more likely to have a mechanical or vascular cause rather than an infectious, inflammatory, or neoplastic cause.

SPINAL CORD ANATOMY

To aid with localization, recall that the caudal spinal cord segments do not align with the vertebrae bearing the same names. The spinal cord ends around L1, with the roots of the cauda equina below that vertebral level. Additionally, within the cervical cord, the spinal roots exit the spinal canal above the associated vertebral level except for root C8, which exits between C7 and T1. Thereafter, each spinal root exits below the corresponding vertebral body.

MOTOR SYSTEM

The majority of the corticospinal tract, mediating a large proportion of our volitional limb movements, decussates in the medulla before descending in the contralateral lateral corticospinal tract. The minority of motor axons that do not decussate within the medulla form the anterior corticospinal tract. The lower motor neurons, receiving input from corticospinal fibers as well as segmental interneurons, reside within the ventral horn (Fig. 16.1).

SENSORY SYSTEM

Afferent sensory fibers from the dorsal root ganglia enter the spinal cord at the dorsal horn. From there, their course depends on the type of modality being transmitted.

Pain and Temperature

These fibers travel rostrally within Lissauer tract for one or two spinal segments before synapsing within the dorsal horn and crossing to the contralateral anterolateral system. The anterolateral system is composed of the anterior spinothalamic tract, which carries crude touch sensory fibers, and the lateral spinothalamic tract, which carries pain and temperature fibers.

TABLE 16.1 Differential Diagnosis for Acute Spinal Syndromes

Compressive/mechanical
	Trauma
	Disk herniation
	Epidural abscess
	Epidural hematoma
	Epidural neoplasm/metastasis
	Vertebral compression fracture
Vascular
	Ischemic stroke
	Dural arteriovenous fistula
	Arteriovenous malformation
	Cavernous malformation
Inflammatory
	Multiple sclerosis
	Neuromyelitis optica
	Transverse myelitis
	Acute disseminated encephalomyelitis (ADEM)
	Sarcoidosis
	Paraneoplastic
	Systemic lupus erythematosus (SLE)
	Antiphospholipid antibody syndrome (APS)
	Sjögren syndrome
	Mixed connective tissue disease (MCTD)
	Behçet disease
Toxic/metabolic
	Heroin
	Konzo
	Arachnoiditis after angiographic/myelographic contrast agents
	Methotrexate toxicity
	Cytarabine toxicity
	Amphotericin B toxicity
Neoplasm
Infectious
	Viral gray matter/acute flaccid paralysis
		Poliovirus
		Enterovirus
		Coxsackieviruses A & B
		West Nile virus (WNV)
		Japanese encephalitis (JE)
		Tick-borne encephalitis
	Viral white matter/longitudinal myelitis
		Herpes simplex virus (HSV)
		Varicella-zoster virus (VZV)
		Cytomegalovirus (CMV)
		Epstein-Barr virus (EBV)
		Influenza
	Bacterial
		Mycoplasma pneumoniae
		Syphilis
		Tuberculosis
		Lyme
	Fungal
		Cryptococcus neoformans
		Coccidioides immitis
		Blastomycetes dermatitides
		Histoplasma capsulatum
		Candida species
		Aspergillus species
		Zygomycetes
	Parasitic
	Schistosoma species
	Toxoplasma gondii
	Taenia solium (cysticercosis)

TABLE 16.2 Classic Spinal Cord Syndromes

Syndrome	Typical Causes	Clinical Characteristics
Central cord syndrome (syringomyelia)	Underlying cervical spondylosis with hyperextension injury; damage relatively greater to gray than white matter	Weakness in upper extremities > in lower extremities; may have neurogenic bladder dysfunction and varying degrees of sensory loss at or below the lesion (often in a “cape-like” distribution).
Brown-Séquard syndrome	Penetrating trauma (many nonpenetrating injuries show partial asymmetric syndromes)	Ipsilateral motor and vibration/proprioception loss below the lesion, contralateral pain/temperature loss two levels below the lesion
Anterior cord syndrome	Hypotensive event leading to infarct within the midthoracic region, or hyperflexion injury leading to compression of the anterior spinal artery	Bilateral loss of motor, pain/temperature sensation below the lesion with preservation of vibration/proprioception/two-point discrimination
Posterior cord syndrome	B₁₂ deficiency, MS, vascular malformations, atlantoaxial subluxation	Bilateral loss of vibration/proprioception/two-point discrimination with preservation of motor, pain/temperature sensation below the lesion
Cauda equina syndrome	Disk herniation, tumor	Asymmetric lower extremity weakness, patchy impaired sensation to all modalities, loss of deep tendon reflexes as well as bulbocavernosus reflex and anal wink, often with low back and radicular pain
Conus medullaris syndrome	Disk herniation, trauma, tumor	Symmetric sacral > lumbar weakness (may have normal leg strength), saddle anesthesia, bowel/bladder dysfunction
MS, multiple sclerosis.

Vibration, Proprioception, and Two-Point Discrimination

These fibers travel within the ipsilateral dorsal columns to the gracilis and cuneatus nuclei of the lower medulla. Axons from the legs (fasciculus gracilis) are pushed medially by entering axons from the arms (fasciculus cuneatus) (see Fig. 16.1).

AUTONOMIC SYSTEM

Sympathetic

Sympathetic preganglionic neurons are located within the inter-mediolateral nucleus of the thoracic and upper lumbar (L1-L2) spinal cord. Their axons exit via the ventral roots and synapse on the postganglionic sympathetic neurons in the paravertebral ganglia (the “sympathetic chain ganglia”) or the prevertebral ganglia.

FIGURE 16.1 Anatomy of the spinal cord (cross-section). Tract lamination: S, sacral segments; L, lumbar segments; Th, thoracic segments; C, cervical segments. (From Brazis PW, Masdeu JC, Biller J. Localization in Clinical Neurology. 5th ed. Philadelphia: Lippincott Williams and Wilkins; 2007.)

Only gold members can continue reading. Log In or Register to continue