# Lecture 8: Spinal Cord Anatomy and Pathways ## Unit 2.5: Neuroscience --- ## Learning Objectives By the end of this lecture, students will be able to: 1. Describe the gross anatomy and organization of the spinal cord 2. Explain the blood supply to the spinal cord 3. Describe the major ascending and descending tracts 4. Explain spinal cord syndromes and their clinical presentations 5. Describe the dermatomes and myotomes 6. Explain the evaluation and localization of spinal cord lesions --- ## Lecture Outline ### I. Gross Anatomy The spinal cord represents the caudal continuation of the central nervous system, extending from the foramen magnum to approximately the L1-L2 vertebral level in adults. This cylindrical structure measures approximately 45 centimeters in length and serves as the primary conduit for information traveling between the brain and the body. The cord terminates in a tapered structure called the conus medullaris, which marks the transition from spinal cord proper to the collection of nerve roots known as the cauda equina. The filum terminale, a slender fibrous extension of the pia mater, anchors the conus to the coccyx and maintains cord position within the vertebral canal. Two prominent enlargements along the cord's length reflect increased gray matter volume serving the limbs. The cervical enlargement spans C4 through T1 and contains the motor neurons and sensory processing circuits for the upper extremities via the brachial plexus. The lumbar enlargement, extending from L1 through S2, similarly serves the lower extremities through the lumbosacral plexus. The spinal cord contains thirty-one segments corresponding to the paired spinal nerves: eight cervical, twelve thoracic, five lumbar, five sacral, and one coccygeal. Because the spinal cord is shorter than the vertebral column, an important discrepancy exists between vertebral levels and corresponding spinal cord segments. In the cervical region, vertebral and spinal levels correspond closely. However, in the thoracic region, adding two to the vertebral level approximates the spinal segment at T1-T6, and adding three applies for T7-T9. At T10, spinal segments L1-L2 are located, while T12 corresponds to L5 segments, and the lumbar vertebrae contain sacral cord segments. A comprehensive anatomical illustration of spinal cord gross anatomy displayed across four panels. Panel A shows a posterior view of the complete spinal cord within the opened vertebral column, with color-coded regions indicating cervical (blue), thoracic (green), lumbar (yellow), and sacral (orange) segments. The cervical and lumbar enlargements appear as prominent swellings, labeled with their corresponding vertebral levels. Panel B provides a detailed view of the cord termination, showing the conus medullaris at L1-L2 vertebral level, the filum terminale extending downward, and the cauda equina nerve roots cascading like a horse's tail through the lumbar cistern. Panel C presents a correlation chart comparing vertebral levels to spinal cord segments, with arrows showing how the discrepancy increases moving caudally. Panel D illustrates a cross-section at the lumbar cistern level showing nerve roots floating in cerebrospinal fluid, demonstrating why lumbar puncture can be safely performed below L2. --- ### II. Cross-Sectional Anatomy Examination of the spinal cord in cross-section reveals the characteristic butterfly or H-shaped gray matter surrounded by white matter organized into distinct columns. The gray matter contains neuronal cell bodies, dendrites, and synapses, while the white matter consists of myelinated axon tracts carrying information longitudinally. The dorsal horn receives sensory input from peripheral receptors via the dorsal root ganglia. Neurons within the dorsal horn process and relay sensory information, with different laminae handling specific modalities. The ventral horn contains motor neurons whose axons exit through the ventral roots to innervate skeletal muscle. The intermediate zone houses interneurons that integrate sensory and motor activity and coordinate reflexes. At thoracolumbar levels T1 through L2, a lateral horn appears containing preganglionic sympathetic neurons. Similarly, sacral segments S2 through S4 contain parasympathetic motor neurons in this location that control pelvic visceral function including bladder, bowel, and sexual organs. The gray matter is organized into ten laminae of Rexed, numbered from dorsal to ventral. Lamina I, the marginal zone at the dorsal horn tip, receives pain and temperature afferents. Lamina II, the substantia gelatinosa, plays a critical role in pain modulation and serves as the anatomical substrate for gate control theory. Laminae III and IV constitute the nucleus proprius handling tactile information. Laminae V and VI in the neck of the dorsal horn integrate multimodal sensory information. Lamina VII, the intermediate zone, contains Clarke's nucleus at thoracolumbar levels for proprioceptive relay to the cerebellum. Lamina VIII and IX occupy the ventral horn, with lamina IX containing the alpha and gamma motor neurons organized somatotopically. Lamina X surrounds the central canal. The white matter is divided into three columns or funiculi. The dorsal column lies between the dorsal horns and contains the fasciculus gracilis medially carrying lower body sensory information and the fasciculus cuneatus laterally carrying upper body information. The lateral column between dorsal and ventral horns contains the lateral corticospinal tract and spinothalamic tract. The anterior column between ventral horns carries the anterior corticospinal tract and vestibulospinal fibers. Several nuclei deserve special mention. The substantia gelatinosa in lamina II modulates pain transmission through interneurons that release enkephalins and GABA. Clarke's nucleus, present from T1 to L2, relays proprioceptive information to the cerebellum via the posterior spinocerebellar tract. Onuf's nucleus in the sacral cord controls the external urethral and anal sphincters, making it particularly important in maintaining continence. A detailed cross-sectional anatomy illustration of the spinal cord shown across four panels. Panel A displays an annotated cervical cord cross-section with the butterfly-shaped gray matter clearly demarcated into dorsal horn, intermediate zone, and ventral horn, with color-coded Rexed laminae numbered I through X. The surrounding white matter shows the dorsal, lateral, and anterior columns with major tracts labeled. Panel B compares cross-sections at cervical, thoracic, lumbar, and sacral levels, demonstrating how the ratio of gray to white matter changes and how the lateral horn appears only at thoracolumbar levels. Panel C provides a magnified view of the dorsal horn showing the substantia gelatinosa and its role in pain modulation, with small interneurons illustrated releasing enkephalins. Panel D shows the ventral horn motor neuron organization with the somatotopic arrangement indicating that medial neurons supply axial muscles while lateral neurons supply distal limb muscles. --- ### III. Blood Supply The spinal cord receives its arterial supply from the vertebrobasilar system through three longitudinal arteries supplemented by segmental contributions. Understanding this blood supply is essential for recognizing vascular syndromes and avoiding iatrogenic injury during surgical procedures. The anterior spinal artery forms from the junction of branches from each vertebral artery at the level of the foramen magnum. This single midline vessel descends along the anterior median fissure and supplies the anterior two-thirds of the spinal cord, including the ventral horns, corticospinal tracts, and spinothalamic tracts. The posterior spinal arteries, typically paired vessels arising from the vertebral arteries or PICA, supply the posterior one-third of the cord including the dorsal columns and dorsal horns. These longitudinal arteries are relatively small and require supplementation from radicular arteries at each segmental level. Most radicular arteries supply only the nerve roots, but several larger radiculomedullary arteries actually reach and augment the longitudinal arterial system. The most important of these is the artery of Adamkiewicz, also called the great radicular artery, which typically arises from the left side between T9 and L2 in most individuals. This vessel provides the dominant blood supply to the lumbar cord and conus medullaris. The mid-thoracic cord, approximately T4 through T8, represents a watershed zone between the territories supplied by vertebral artery branches above and the artery of Adamkiewicz below. This region is particularly vulnerable to hypoperfusion during systemic hypotension or aortic surgery. Clamping of the aorta during thoracoabdominal aneurysm repair can compromise the artery of Adamkiewicz origin, potentially causing devastating cord infarction. Venous drainage occurs through anterior and posterior spinal veins that drain into the internal vertebral venous plexus, also known as Batson's plexus. This valveless system communicates with the external vertebral plexus and pelvic veins, providing a potential route for metastatic spread of pelvic and abdominal malignancies to the spine. The anterior spinal artery syndrome results from occlusion of this vessel, producing bilateral motor loss from corticospinal tract involvement, bilateral pain and temperature loss from spinothalamic tract damage, but preserved proprioception and vibration sense because the dorsal columns receive separate posterior spinal artery supply. Spinal epidural hematomas, whether spontaneous or related to anticoagulation or procedures, can compress the cord and require urgent surgical decompression. A comprehensive illustration of spinal cord blood supply across four panels. Panel A shows the arterial system with the anterior spinal artery descending along the cord's anterior surface as a single midline vessel, paired posterior spinal arteries posteriorly, and the vertebral arteries converging at the brainstem. Panel B demonstrates the artery of Adamkiewicz arising from a left intercostal artery at approximately T10, with its characteristic hairpin turn as it ascends to join the anterior spinal artery, labeled as the dominant supply to the lumbar cord. Panel C illustrates the watershed zone at T4-T8, with shading indicating the area of vulnerability during hypotension and a diagram showing cross-clamping during aortic surgery. Panel D presents cross-sections showing the territories supplied by anterior versus posterior spinal arteries, with the anterior two-thirds and posterior one-third clearly demarcated and corresponding clinical deficits listed for each territory. --- ### IV. Ascending Tracts The major ascending sensory pathways convey information from peripheral receptors to the cerebral cortex for conscious perception and to the cerebellum for motor coordination. These tracts differ in the type of sensory information they carry, their course through the cord, and their site of decussation. The dorsal column-medial lemniscus pathway conveys fine touch, vibration sense, and proprioception with high spatial and temporal resolution. First-order neurons in the dorsal root ganglia send their central processes into the ipsilateral dorsal column without synapsing, making this a two-neuron relay to the cortex. Fibers from lower body segments travel in the medially-positioned fasciculus gracilis, while upper body fibers join laterally in the fasciculus cuneatus. These fibers ascend to the nucleus gracilis and nucleus cuneatus in the lower medulla, where they synapse on second-order neurons. These second-order neurons send axons that cross the midline as the internal arcuate fibers, forming the medial lemniscus which ascends through the brainstem to the ventral posterolateral nucleus of the thalamus. Third-order neurons project from VPL to the primary somatosensory cortex. The spinothalamic tract, the anterolateral system's main component, conveys pain, temperature, and crude touch information. First-order neurons synapse immediately upon entering the cord in the dorsal horn, primarily in laminae I, II, and V. Second-order neurons cross the midline through the anterior white commissure within one to two segments above their entry level, then ascend in the anterolateral quadrant of the cord. This tract terminates primarily in VPL thalamus, with collaterals to the insula and anterior cingulate cortex mediating the emotional aspects of pain. The spinocerebellar tracts convey unconscious proprioceptive information to the cerebellum for motor coordination. The posterior spinocerebellar tract carries information from the lower body via Clarke's nucleus, remaining ipsilateral and entering the cerebellum through the inferior cerebellar peduncle. The anterior spinocerebellar tract also carries lower body proprioception but crosses twice, once in the cord and once in the cerebellum via the superior cerebellar peduncle, ultimately providing ipsilateral cerebellar input. The cuneocerebellar tract similarly conveys upper body proprioception through the inferior cerebellar peduncle. Additional ascending tracts include the spinoreticular tract contributing to arousal and the affective component of pain, the spinomesencephalic tract projecting to the periaqueductal gray for pain modulation, and the spinotectal tract mediating reflexive head turning toward stimuli. A comprehensive illustration of ascending spinal cord tracts displayed across four panels. Panel A shows the dorsal column-medial lemniscus pathway from receptor to cortex, with first-order neurons in the DRG projecting to the ipsilateral dorsal column, second-order neurons in the medullary nuclei crossing as internal arcuate fibers to form the medial lemniscus, and third-order neurons from VPL thalamus reaching S1 cortex. The somatotopic organization shows gracilis medially and cuneatus laterally. Panel B illustrates the spinothalamic tract with first-order neurons synapsing in the dorsal horn, second-order neurons crossing in the anterior white commissure and ascending contralaterally, and termination in VPL. A small inset shows that lesions produce contralateral deficits one to two levels below the lesion. Panel C demonstrates the spinocerebellar tracts, comparing the ipsilateral posterior tract via ICP with the double-crossing anterior tract via SCP, both conveying proprioceptive information to the cerebellum. Panel D presents a cross-section showing the spatial organization of all major ascending tracts color-coded within the white matter columns. --- ### V. Descending Tracts The descending motor pathways transmit commands from the brain to lower motor neurons and interneurons in the spinal cord. These tracts can be divided into lateral pathways controlling voluntary limb movement and medial pathways controlling posture and axial muscles. The corticospinal tract represents the primary pathway for voluntary, skilled movement. Approximately sixty percent of fibers originate in the primary motor cortex, with additional contributions from premotor areas, supplementary motor area, and sensory cortex. These fibers descend through the posterior limb of the internal capsule, occupy the middle portion of the cerebral peduncle, traverse the basis pontis, and form the pyramids in the medulla. At the cervicomedullary junction, eighty-five to ninety percent of fibers cross at the pyramidal decussation to form the lateral corticospinal tract, descending in the lateral funiculus to synapse on motor neurons and interneurons. The remaining ten to fifteen percent continue ipsilaterally as the anterior corticospinal tract, crossing at segmental levels before terminating. The rubrospinal tract originates in the red nucleus of the midbrain, crosses immediately in the ventral tegmental decussation, and descends in the lateral funiculus just anterior to the lateral corticospinal tract. This pathway facilitates flexor motor neurons and may contribute to recovery after corticospinal tract injury, though its importance in humans remains debated. The reticulospinal tracts influence posture and muscle tone through connections with motor neurons and interneurons. The pontine or medial reticulospinal tract descends ipsilaterally from the pontine reticular formation, facilitating extensor muscles and maintaining upright posture. The medullary or lateral reticulospinal tract inhibits extensor activity, balancing the pontine influence. The vestibulospinal tracts maintain balance and coordinate head and eye movements. The lateral vestibulospinal tract originates in the lateral vestibular nucleus and descends ipsilaterally through the entire cord, powerfully facilitating extensor muscles to maintain upright posture against gravity. The medial vestibulospinal tract from medial vestibular nuclei descends bilaterally only to cervical levels, coordinating head position with vestibular input. A comprehensive illustration of descending spinal cord tracts across four panels. Panel A traces the corticospinal tract from motor cortex through the internal capsule, cerebral peduncle, and pyramid, showing the pyramidal decussation where 85-90% of fibers cross to form the lateral corticospinal tract and 10-15% remain ipsilateral as the anterior corticospinal tract. Panel B shows cross-sections at cervical level with the lateral versus medial motor system organization, demonstrating how lateral pathways control distal limb muscles while medial pathways control axial muscles. Panel C illustrates the reticulospinal system with the pontine tract facilitating extensors (shown with plus signs) and the medullary tract inhibiting extensors (shown with minus signs), explaining the mechanism of decerebrate posturing when pontine influences predominate. Panel D demonstrates the vestibulospinal tracts maintaining balance and facilitating extensor tone, with a diagram showing how lateral vestibular nucleus activation produces extension of ipsilateral limbs. --- ### VI. Dermatomes and Myotomes Dermatomes represent the cutaneous areas innervated by sensory fibers from a single spinal nerve root. Although dermatomal maps show discrete boundaries, substantial overlap exists between adjacent dermatomes, meaning that loss of a single nerve root produces a smaller area of sensory deficit than the full dermatomal distribution. Key dermatomal landmarks provide clinical shortcuts for rapid sensory level assessment. The C4 dermatome covers the shoulder in a cape-like distribution. C5 covers the lateral arm, C6 includes the thumb, C7 the middle finger, and C8 the little finger. On the trunk, T4 lies at the nipple line and T10 at the umbilicus. The L1 dermatome follows the inguinal ligament. L4 supplies the medial leg and foot, L5 covers the lateral leg and dorsum of the foot including the great toe web space, and S1 innervates the lateral foot and heel. The sacral segments S3 through S5 supply the perianal saddle region. Myotomes describe the muscle groups innervated by each spinal segment. Again, individual muscles typically receive innervation from multiple segments, so weakness from single root lesions is often subtle. C5 mediates shoulder abduction through the deltoid, while C5-C6 controls elbow flexion via the biceps. C7 produces elbow extension through the triceps, C8 flexes the fingers, and T1 controls the intrinsic hand muscles enabling finger abduction and adduction. In the lower extremity, L2-L3 flexes the hip through the iliopsoas, L3-L4 extends the knee via the quadriceps, L5 dorsiflexes the ankle through the tibialis anterior, and S1 plantarflexes through the gastrocnemius. These myotomal assignments allow rapid screening of motor function and localization of lesion levels. The deep tendon reflexes integrate these concepts by testing specific segmental levels. The biceps reflex tests C5-C6, the brachioradialis C5-C6, and the triceps C7-C8. The patellar reflex assesses L3-L4, and the Achilles reflex tests S1-S2. Absence or diminution of these reflexes helps localize the level of spinal cord or root pathology. A comprehensive dermatomal and myotomal reference illustration across four panels. Panel A shows anterior and posterior body diagrams with dermatomes color-coded by spinal level, with key landmarks labeled: C4 at shoulders, T4 at nipple line, T10 at umbilicus, L1 at inguinal region, and S3-S5 as saddle. Panel B illustrates dermatomal overlap with a diagram showing that three adjacent dermatomes must be affected before complete sensory loss occurs in a region. Panel C presents the myotomal examination sequence with photographs demonstrating shoulder abduction (C5), elbow flexion (C5-C6), elbow extension (C7), finger flexion (C8), finger spread (T1), hip flexion (L2-L3), knee extension (L3-L4), ankle dorsiflexion (L5), and plantarflexion (S1). Panel D shows the reflex arc diagram with specific spinal levels for each major reflex, including proper hammer technique and expected response. --- ### VII. Spinal Cord Syndromes Recognition of specific patterns of spinal cord injury enables precise localization and guides differential diagnosis and management. These syndromes result from the anatomical arrangement of tracts within the cord. Complete transection produces total loss of all motor and sensory function below the lesion level. In the acute phase, spinal shock causes flaccid paralysis, areflexia, and loss of autonomic function below the injury. This occurs because the isolated spinal cord loses facilitatory descending input and enters a temporarily depressed state. Over days to weeks, spinal shock resolves and is replaced by spastic paralysis with hyperreflexia as spinal circuits recover independent function. Autonomic dysreflexia may occur with lesions above T6, producing dangerous hypertension in response to stimuli below the lesion such as bladder distension. Brown-Séquard syndrome results from hemisection of the spinal cord. The characteristic findings reflect tract organization: ipsilateral upper motor neuron weakness from corticospinal tract disruption, ipsilateral loss of proprioception and vibration from dorsal column involvement, and contralateral loss of pain and temperature from spinothalamic tract damage that crossed below the lesion level. At the lesion level itself, lower motor neuron weakness occurs from ventral horn damage, and ipsilateral segmental sensory loss reflects dorsal horn involvement before fibers cross. Central cord syndrome typically results from hyperextension injuries in patients with cervical spondylosis or from expanding syringomyelic cavities. The hallmark is weakness greater in the upper extremities than the lower extremities, explained by the somatotopic organization of the corticospinal tract where cervical fibers lie medially and are more susceptible to central cord damage. Similarly, crossing spinothalamic fibers for the arms pass through the central cord, producing a suspended or cape-like distribution of pain and temperature loss affecting the upper trunk and arms while sparing the lower body. Anterior cord syndrome occurs from anterior spinal artery occlusion or direct anterior cord compression. Because this vessel supplies the anterior two-thirds of the cord, bilateral motor weakness from corticospinal tract infarction combines with bilateral pain and temperature loss from spinothalamic involvement. Proprioception and vibration sense are characteristically preserved because the dorsal columns receive posterior spinal artery supply. Posterior cord syndrome, rare in isolation, produces loss of proprioception and vibration sense with resultant sensory ataxia. This pattern occurs with posterior spinal artery occlusion, tabes dorsalis, or vitamin B12 deficiency. Motor function and pain and temperature sensation remain intact. A comprehensive spinal cord syndrome illustration across four panels. Panel A shows a complete transection with cross-section diagram indicating all tracts interrupted, alongside clinical photos showing spinal shock phase versus chronic phase with spasticity and hyperreflexia. Panel B illustrates Brown-Séquard syndrome with a hemisection lesion shown in cross-section, arrows indicating ipsilateral motor and proprioceptive loss from uncrossed tracts versus contralateral pain and temperature loss from crossed spinothalamic fibers. Panel C demonstrates central cord syndrome with the central lesion depicted as a dark area, showing how medially-positioned arm fibers in the corticospinal tract are preferentially affected while lateral leg fibers are spared. Panel D compares anterior versus posterior cord syndromes with shaded territories on cross-sections corresponding to the anterior spinal artery and posterior spinal artery supplies, with expected deficits listed for each pattern. --- ### VIII. Spinal Cord Pathology Traumatic spinal cord injury produces deficits determined by the level and completeness of injury. Lesions above C3 are often fatal due to loss of diaphragmatic function from phrenic nerve involvement. C4-C5 injuries cause quadriplegia with variable preservation of shoulder and elbow movement. C6-C7 injuries preserve more upper extremity function, allowing some independent activity. Thoracic injuries produce paraplegia with preserved arm function, and lumbar injuries cause variable lower extremity weakness depending on level and completeness. Subacute combined degeneration results from vitamin B12 deficiency affecting the spinal cord, peripheral nerves, and brain. The characteristic pathology involves demyelination of the dorsal columns and lateral corticospinal tracts, producing a distinctive clinical picture. Patients develop sensory ataxia from proprioceptive loss, with positive Romberg sign and a stamping gait. Upper motor neuron signs including spasticity and hyperreflexia appear from corticospinal tract involvement, though concurrent peripheral neuropathy may paradoxically reduce or abolish ankle reflexes. Associated findings include megaloblastic anemia, cognitive impairment, and peripheral neuropathy with paresthesias. Syringomyelia describes the formation of a fluid-filled cavity or syrinx within the spinal cord, most commonly in the cervical region. Association with Chiari type I malformation is common, where tonsillar herniation disrupts normal cerebrospinal fluid dynamics. The expanding central cavity first damages crossing spinothalamic fibers, producing the classic cape distribution of pain and temperature loss over the shoulders and upper arms while sparing light touch. As the syrinx enlarges, it damages the anterior horns producing lower motor neuron weakness and atrophy in the hands, and eventually involves the lateral columns causing upper motor neuron signs in the legs. Transverse myelitis describes inflammatory demyelination affecting a segment of the spinal cord. Causes include multiple sclerosis, neuromyelitis optica, infectious agents, and idiopathic inflammation. Patients present with rapidly progressive bilateral weakness, a sensory level, and bladder dysfunction. MRI demonstrates cord lesion typically spanning several segments. Treatment involves high-dose corticosteroids, with further therapy directed at the underlying cause. A comprehensive spinal cord pathology illustration across four panels. Panel A demonstrates traumatic injury levels with a spine diagram showing functional outcomes at each level: C3 and above causing respiratory failure, C4-C5 quadriplegia with shoulder function, C6-C7 quadriplegia with arm function, and thoracic causing paraplegia. Panel B illustrates subacute combined degeneration with a cross-section showing dorsal column and lateral corticospinal tract demyelination shaded, alongside clinical features including sensory ataxia posture and the megaloblastic blood smear. Panel C shows syringomyelia with an MRI image demonstrating the central syrinx cavity in sagittal view, a cross-section showing the syrinx expanding to damage crossing fibers and anterior horns, and a body diagram of the cape distribution sensory loss. Panel D presents transverse myelitis with sagittal and axial MRI images showing cord inflammation, along with the typical clinical presentation timeline. --- ### IX. Spinal Cord vs Cauda Equina Lesions Differentiating between lesions of the conus medullaris and cauda equina is clinically important because they produce different presentations and have different surgical urgency. Conus medullaris syndrome results from damage to the terminal spinal cord segments S3 through S5, located at approximately the L1 vertebral level. Because this region contains parasympathetic neurons and the sacral motor nuclei, bladder and bowel dysfunction occur early and prominently. Motor weakness in the legs is typically minimal because most leg muscles are innervated by higher lumbar segments. Sensory findings include saddle anesthesia affecting the perianal region. Reflexes may show a Babinski sign from upper motor neuron involvement, and the bulbocavernosus and anal wink reflexes are diminished or absent. Cauda equina syndrome results from compression of the nerve roots within the lumbar cistern below L2. Because these are peripheral nerve roots rather than spinal cord, the findings are lower motor neuron in character. Severe radicular pain is typically prominent and often the presenting complaint. Motor weakness is asymmetric and involves multiple myotomes in an LMN pattern with decreased reflexes. Sensory loss is similarly asymmetric. Bladder involvement with urinary retention occurs later than in conus lesions because the sacral roots must be significantly compressed before function is lost. Several features help distinguish these syndromes. Conus lesions present suddenly with symmetric findings and early bladder dysfunction but minimal pain. Cauda equina syndrome develops more gradually with asymmetric findings, prominent radicular pain, and later bladder involvement. However, combined conus-cauda lesions occur when pathology affects both regions. Cauda equina syndrome represents a surgical emergency. Red flag symptoms include saddle anesthesia, urinary retention with overflow incontinence, fecal incontinence, and progressive bilateral leg weakness. When suspected, urgent MRI of the lumbar spine should be obtained. If compression is confirmed, emergent surgical decompression within 24 to 48 hours optimizes the chance of neurological recovery. The most common cause is large central disc herniation, though tumor, epidural abscess, and hematoma must be considered. A comprehensive conus and cauda equina comparison illustration across four panels. Panel A shows a sagittal spine diagram with the conus medullaris at L1 level and cauda equina nerve roots descending through the lumbar cistern, clearly labeled to show the anatomical relationship. Panel B contrasts conus versus cauda equina syndrome features in a side-by-side comparison: conus showing early bladder symptoms, symmetric findings, minimal pain, and sudden onset; cauda equina showing asymmetric weakness, severe radicular pain, late bladder involvement, and gradual onset. Panel C demonstrates the examination findings with perianal sensation testing, rectal tone assessment, and the bulbocavernosus reflex technique. Panel D shows MRI images of both syndromes: an axial image showing conus compression and a sagittal image showing large central disc causing cauda equina compression, with red flag symptoms listed as requiring urgent surgical consultation. --- ### X. Clinical Evaluation Systematic evaluation of suspected spinal cord pathology combines careful history, detailed neurological examination, and appropriate imaging to localize the lesion and identify its cause. The history should establish the pattern and progression of symptoms. The distribution of weakness helps distinguish cord lesions from peripheral causes. Sensory symptoms should be characterized by quality and distribution. Bowel and bladder dysfunction suggests autonomic involvement indicating cord pathology. Back pain, particularly with percussion tenderness, may indicate local structural pathology. The tempo of onset provides diagnostic information: sudden onset suggests vascular causes or trauma, subacute progression suggests inflammatory or compressive causes, and chronic progression suggests degenerative or neoplastic processes. The motor examination documents the pattern and severity of weakness, distinguishing upper motor neuron signs including spasticity, hyperreflexia, and Babinski sign from lower motor neuron signs including flaccidity, atrophy, fasciculations, and hyporeflexia. The sensory examination systematically tests pin prick and temperature for spinothalamic function and vibration and proprioception for dorsal column function. Identifying a sensory level, below which sensation is diminished, strongly suggests spinal cord pathology. The sensory level is typically one to two segments below the actual cord lesion due to tract lamination. Deep tendon reflexes should be assessed at multiple levels. Hyperreflexia indicates upper motor neuron dysfunction above that level, while areflexia suggests lower motor neuron involvement at or below that level. An inverted reflex, where stimulating one level produces response at a lower level, can help localize the lesion precisely. Rectal examination assesses perianal sensation, sphincter tone, and voluntary contraction, which are critical for evaluating sacral cord function. MRI is the imaging modality of choice for evaluating spinal cord pathology, demonstrating intrinsic cord lesions, compression, and surrounding structures. When MRI is contraindicated, CT myelography provides useful information about compressive lesions. Plain radiographs demonstrate bony alignment and fractures but provide limited information about the cord itself. Localization principles guide the differential diagnosis. A sensory level suggests cord pathology one to two segments above. Bilateral upper motor neuron findings in the legs with normal arms indicate thoracic cord involvement. Lower motor neuron findings in the arms combined with upper motor neuron findings in the legs suggest cervical cord pathology. Pure lower motor neuron findings suggest cauda equina or peripheral nerve involvement. A comprehensive clinical evaluation illustration across four panels. Panel A demonstrates the motor examination sequence with proper technique for assessing power at each myotomal level, alongside photographs showing how to detect upper motor neuron signs including spasticity, clonus, and Babinski sign. Panel B illustrates sensory testing with the dermatomal chart showing where to test each level, proper technique for pin prick and vibration testing, and how to identify a sensory level by progressive testing from abnormal to normal areas. Panel C shows the reflex examination with proper technique and grading scale, plus diagrams explaining inverted reflexes indicating the lesion level. Panel D demonstrates MRI interpretation with sagittal and axial images showing normal anatomy compared with cord compression, intrinsic cord lesion, and cauda equina compression, with key features to identify in each pattern. --- ## Summary The spinal cord extends from C1 to L1-L2, terminating as the conus medullaris with the cauda equina below. Gray matter is organized with dorsal horns for sensory processing, ventral horns for motor output, and lateral horns at T1-L2 for sympathetic function. The blood supply from anterior and posterior spinal arteries supplemented by the artery of Adamkiewicz creates vulnerable watershed zones in the mid-thoracic cord. Ascending tracts include the dorsal columns conveying fine touch and proprioception ipsilaterally before crossing in the medulla, and the spinothalamic tract conveying pain and temperature that crosses within one to two segments in the cord. Descending pathways include the corticospinal tract for voluntary movement that crosses at the pyramidal decussation, and medial pathways including reticulospinal and vestibulospinal tracts for posture and tone. Spinal cord syndromes produce characteristic patterns. Brown-Séquard syndrome from hemisection produces ipsilateral motor and proprioceptive loss with contralateral pain and temperature loss. Central cord syndrome preferentially affects the arms with cape distribution sensory loss. Anterior cord syndrome spares proprioception while affecting motor and pain pathways. Cauda equina syndrome produces LMN findings with radicular pain and represents a surgical emergency. --- ## Key Terms | Term | Definition | |------|------------| | Conus medullaris | Tapered end of spinal cord at L1-L2 | | Cauda equina | Nerve roots below the conus medullaris | | Brown-Séquard syndrome | Hemisection of spinal cord | | Dermatome | Skin area innervated by single spinal segment | | Myotome | Muscles innervated by single spinal segment | | Anterior spinal artery syndrome | Infarction of anterior 2/3 of cord | | Syringomyelia | Fluid-filled cavity in spinal cord | | Sensory level | Highest level of normal sensation | --- *This content is subject to the [MIT License](https://opensource.org/licenses/MIT). © 2024–2026 Hibbert School of Medicine.*