Spinal Cord Functional Anatomy (Spinal Cord Disorders 2015)

Educational Objectives

The goal of this program is to improve diagnosis and treatment of disorders of the spinal cord. After hearing and assimilating this program, the clinician will be better able to:

1. Diagnose neurologic disorders by localizing lesions of the spinal cord.

Summary

Transverse anatomy: Gray matter — divided into three columns; anterior gray horn associated with motor neurons and posterior gray horn with sensory neurons; lateral horn contains autonomic and cerebellar nuclei; white matter — also has three columns; anterior column contains anterior commissure, with crossing pain and temperature fibers, and some corticospinal fibers that innervate axial muscles of trunk; lateral column contains ascending pain and temperature fibers from contralateral body and descending corticospinal fibers to ipsilateral muscles; posterior columns convey ipsilateral vibration and proprioception.

Injuries: Lateral injuries to cord often involve corticospinal tract and cause ipsilateral spasticity or upper motor neuron weakness and contralateral impairment of pain and temperature sensation; posterior column involvement leads to ipsilateral impairment of vibration and proprioception; injuries to anterior horn cause ipsilateral flaccid or lower motor neuron weakness.

Somatotopic organization: In lateral corticospinal and anterolateral spinothalamic tracts, fibers to and from rostral segments of the body located most medially and to and from caudal segments most laterally; when process such as expanding syrinx affects central cord and spreads outward, cervical segments often involved first and sacral segments last; conversely, process that affects cord from external surface may involve sacral segments early and cervical segments later; patients with cervical spondylosis and cord compression often have lower extremity spastic weakness and little involvement of upper extremities.

Longitudinal anatomy: Pain/temperature sensory level of spinal cord most useful indicator of location of cord lesion; motor findings include flaccid weakness at site of injury (segmental weakness — most reliable, if present) and spastic weakness at lower levels; anterior spinal artery supplies anterior two-thirds of spinal cord; paired posterior spinal arteries supply posterior columns; anterior spinal artery more prone to thrombotic and embolic events; patients with stroke of spinal cord related to anterior spinal artery present with bilateral weakness and impaired sensory perception of pain and temperature, but vibration and proprioception spared because posterior columns supplied by posterior spinal arteries.

Bilateral sensorimotor syndromes of hands: Spinal cord problem rostral to cervical enlargement may mimic peripheral nerve disease.

Numb "clumsy hand” syndrome: Presents with dense sensory impairment in glove distribution, particularly affecting position sense; motor function of hand and sensory function elsewhere relatively spared; such phenomena reported most often in patients with cervical spondylotic myelopathy; often associated with compression at C3 to C4 but may also occur with lesion at cervicomedullary junction; postulated mechanisms include extrinsic cervical compression causing ischemia in borderzone between superficial and deep arterial supply (watershed area), especially in cuneate fasciculus in upper cervical cord.

Atrophic hand syndrome: Most often reported with high cervical lesions; patients present with atrophy and weakness in intrinsic muscles of hand; manifestations suggest lower motor neuron process at C8 or T1, but more proximal or rostral cervical myotomes spared; syndrome typically due to extrinsic spondylotic compression above C5; mechanism hypothesized to involve compression of venous plexus, with resulting congestion caudally, and damage to anterior horns of C8 and T1 due to hypoxia (lower motor neuron process that occurs several levels caudal to site of compression).

“Man in a barrel” syndrome: Presents with weakness of hands and arms; anterolateral sensory tracts cross in anterior commissure (area affected when lesions such as syringomyelia affect central spinal cord); fibers from rostral segments found medially and from caudal segments laterally; hence, processes of central spinal cord tend to affect fibers from cervical segments first and caudal segments later; suspended sensory level may be observed because crossing fibers in anterior commissure for lower cervical and upper thoracic regions involved, and may result in “cape distribution” of pain and temperature sensory loss; combination of weakness of hands and arms preceding involvement of lower extremities and suspended sensory level specific for process of central spinal cord.

Spinocerebellar tracts: Spinal cord carries conscious and unconscious proprioceptive information; conscious information reaches thalamus and sensory cortex; unconscious information travels in spinocerebellar tracts and helps cerebellum to plan and fine-tune movements; located laterally to corticospinal tracts and involved in processes affecting lateral columns; assessed via tests for truncal and appendicular ataxia; when spinocerebellar tracts affected, corticospinal tracts usually also involved, and weakness may overshadow ataxia.

Conus medullaris and cauda equina syndromes: Conus medullaris — patients present with early dysfunction of bladder, saddle anesthesia, symmetric sensory symptoms, and mild symmetric weakness, with pain absent or developing late in course; cauda equina — presents with early radicular pain, asymmetric findings, such as radicular weakness and sensory loss weakness usually more profound than in patients with conus medullaris syndrome; bladder dysfunction occurs later in course of cauda equina syndrome; external compressive processes (eg, disc herniation, epidural metastasis, epidural abscess) can cause either syndrome; cytomegalovirus, herpes simplex virus 2, and schistosomiasis may affect conus and cauda equina; management — acute onset of either syndrome requires urgent imaging; clinical examination unlikely to reliably differentiate between them.

Neuroanatomy of urinary bladder: Sensory input from bladder and urethra passes through sacral nerve roots and up spinal cord to frontal and pontine micturition centers; frontal micturition center in medial frontal region triggers pontine micturition center, which then initiates voiding reflex; parasympathetic motor neurons in lateral horns of S2 through S4 activate detrusor muscle; voluntary somatic relaxation of urethral sphincter leads to reflex inhibition of sympathetic input to bladder neck, which causes contraction and further activation of parasympathetic detrusor; once flow initiated, these reflexes contribute to further contraction of detrusor; when flow stops, another reflex (mediated through urethra) causes contraction of sphincter; parasympathetic system main driver of autonomic component of bladder control; frontal micturition center voluntarily oversees these functions.

Bilateral weakness: Cervical compressive lesions — due to lateral arrangement of fibers to caudal segments of body in corticospinal and spinocerebellar tracts, such lesions may present with lower extremity spasticity and gait ataxia without apparent involvement of upper extremities; imaging (including cervical region) should be performed, even if upper extremities appear intact; symmetric flaccid weakness — patients with this presentation often suspected of having Guillain-Barré syndrome; however, spinal cord process involving anterior horn may present similarly; bladder dysfunction tends to occur early in cord processes and late in Guillain-Barré syndrome.

Readings

Cho TA. Spinal cord functional anatomy. Continuum (Minneap Minn) 2015;21(1).

Disclosures

For this program, the following was disclosed: Dr. Cho has received compensation as a consultant for OptumInsight, Inc. Unlabeled Use of Products/Investigational Use Disclosure: Dr. Cho reports nothing to disclose. To view disclosures of planning committee members with relevant financial relationships, visit: audiodigest.org/continuumaudio/committee. All other members of the planning committee report nothing to disclose.

Acknowledgements

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

CA040101

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.