# Neurology: Spinal Cord Tracts, Dermatomes, Myotomes, Reflexes & Spinal Cord Syndromes

> Clinical neurology and neuroanatomy of ascending and descending spinal cord tracts (DCML, spinothalamic, corticospinal, spinocerebellar), somatotopic lamination, UMN vs LMN signs, Brown-Séquard, syringomyelia, ASA/central cord/SCD/ALS/SMA syndromes, dermatomes, myotomes, reflexes, and cauda equina vs conus medullaris.

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- **Level:** advanced
- **Languages:** en → en
- **Total Cards:** 32

## Flashcards (32 Cards)

| # | Front (Term / Prompt) | Back (Definition / Answer) | Example | Multiple-Choice Options |
| :--- | :--- | :--- | :--- | :--- |
| 1 | Which specific spinal cord structure is destroyed in Poliomyelitis and Spinal Muscular Atrophy (SMA), and what physical exam findings result? | Selective destruction of the lower motor neurons in the anterior (ventral) horn of the spinal cord; Poliomyelitis causes asymmetric flaccid paralysis and areflexia, while SMA (autosomal recessive SMN1 deletion on chromosome 5q; treated with SMN-restoring therapies nusinersen, risdiplam, or onasemnogene abeparvovec gene therapy) causes symmetric proximal hypotonia ('floppy baby'), tongue fasciculations, and areflexia with intact sensation. |  |  |
| 2 | What is Autonomic Dysreflexia in a patient with a chronic spinal cord injury at or above T6, and what triggers it? | A noxious stimulus below the lesion (most commonly bladder distension/blocked Foley catheter or fecal impaction) triggers uninhibited sympathetic spinal reflexes below T6, causing life-threatening malignant hypertension and pounding headache with baroreceptor-mediated reflex bradycardia and flushing/diaphoresis ABOVE the lesion. Immediate management: sit the patient upright (orthostatic BP drop), loosen tight clothing, unkink/irrigate or replace the urinary catheter, check for fecal impaction using topical lidocaine jelly, and give rapid-acting antihypertensives (nitroglycerin paste, nifedipine) if hypertension persists. |  |  |
| 3 | How are the Lateral Corticospinal Tract and the Spinothalamic Tract somatotopically laminated from medial to lateral within the spinal cord white matter? | In both the lateral corticospinal tract and the spinothalamic tract, Cervical (upper extremity) fibers are located MEDIALLY, while Sacral/Lumbar (lower extremity) fibers are located LATERALLY (unlike the dorsal columns, where sacral/lower extremity fibers in fasciculus gracilis are medial). |  |  |
| 4 | How do the Dorsal Spinocerebellar Tract and Ventral Spinocerebellar Tract reach the ipsilateral cerebellum? | The Dorsal Spinocerebellar Tract (arising from Clarke's column C8–L2) ascends ipsilaterally and enters via the Inferior Cerebellar Peduncle; the Ventral Spinocerebellar Tract decussates in the spinal cord, ascends contralaterally, enters via the Superior Cerebellar Peduncle, and decussates a second time within the cerebellum to terminate ipsilaterally. |  |  |
| 5 | What is the role of Renshaw cells in the spinal cord ventral horn, and which toxin selectively blocks their neurotransmitter release? | Renshaw cells are inhibitory interneurons excited by collateral branches of alpha motor neurons that release glycine back onto the same and neighboring motor neurons (recurrent inhibition); Tetanospasmin (Clostridium tetani toxin) cleaves SNARE proteins in Renshaw cells, blocking glycine/GABA release and causing spastic paralysis, trismus (lockjaw), and opisthotonos. |  |  |
| 6 | In a posterolateral lumbar disc herniation at the L4–L5 intervertebral disc space, which spinal nerve root is compressed, and why? | The L5 spinal nerve root is compressed; because lumbar nerve roots exit the intervertebral foramen beneath the pedicle of their corresponding vertebra (L4 root exits high in the L4–L5 foramen), a posterolateral disc herniation at L4–L5 misses the exiting L4 root and compresses the traversing L5 root descending to the L5–S1 foramen. |  |  |
| 7 | How do you clinically distinguish Conus Medullaris Syndrome (S3–S5 cord lesion at L1–L2) from Cauda Equina Syndrome (L2–S5 nerve root compression below L2)? | Conus Medullaris: sudden-onset, symmetric perianal ('saddle') anesthesia, early urinary/fecal incontinence and impotence, minimal radicular leg pain, and mixed UMN/LMN signs (preserved knee reflex, absent ankle reflex); Cauda Equina: gradual, asymmetric severe radicular leg pain, asymmetric flaccid leg weakness, late bowel/bladder dysfunction, and pure LMN signs (loss of both knee and ankle reflexes). |  |  |
| 8 | What tracts are damaged in Friedreich Ataxia, what is its genetic basis, and what non-neurological complication is the leading cause of death? | Autosomal recessive GAA trinucleotide repeat expansion in the frataxin (FXN) gene on chromosome 9 causing mitochondrial iron overload; degenerates the spinocerebellar tracts, dorsal columns, lateral corticospinal tracts, and dorsal root ganglia (ataxia, loss of vibration/proprioception, spastic weakness, absent DTRs, pes cavus, kyphoscoliosis); hypertrophic cardiomyopathy is the leading cause of death. |  |  |
| 9 | Which spinal nerve roots mediate the Biceps, Brachioradialis, Triceps, Patellar (Knee), and Achilles (Ankle) deep tendon reflexes? | Biceps reflex: C5 (and C6); Brachioradialis reflex: C6; Triceps reflex: C7; Patellar (quadriceps) reflex: L4 (and L3); Achilles (gastrocnemius-soleus) reflex: S1 (and S2). |  |  |
| 10 | What sensory modalities are carried by the Dorsal Column–Medial Lemniscus (DCML) pathway, and where do its first-, second-, and third-order neurons synapse and decussate? | Fine discriminative touch, vibration, conscious proprioception, and two-point discrimination; 1st-order neurons (DRG) ascend ipsilaterally in fasciculus gracilis/cuneatus and synapse in nucleus gracilis/cuneatus (caudal medulla); 2nd-order axons decussate as internal arcuate fibers to ascend in the contralateral medial lemniscus and synapse in the VPL thalamus. |  |  |
| 11 | Why does a high cervical Brown-Séquard hemisection (above T1) also produce an ipsilateral Horner Syndrome? | Because first-order hypothalamospinal sympathetic fibers descend ipsilaterally through the lateral funiculus of the cervical cord before synapsing in the ciliospinal center of Budge (intermediolateral cell column at C8–T2). |  |  |
| 12 | Which myotomes (spinal nerve roots) are tested by shoulder abduction, elbow flexion, wrist extension, elbow extension, finger flexion, and finger abduction? | C5: shoulder abduction (deltoid) and elbow flexion (biceps); C6: wrist extension (extensor carpi radialis); C7: elbow extension (triceps) and wrist flexion; C8: finger flexion (flexor digitorum); T1: finger abduction/adduction (interossei). |  |  |
| 13 | What are the key anatomical landmarks for the C4, T4, T10, L1, L4, L5, S1, and S2–S4 dermatomes? | C4: clavicles/shoulder tips; T4: nipples; T10: umbilicus; L1: inguinal ligament; L4: medial malleolus and knee cap; L5: dorsum of foot and great toe web space; S1: lateral malleolus, sole of foot, and small toe; S2–S4: perianal / saddle area. |  |  |
| 14 | What are the afferent and efferent nerves and spinal segments for the Cremasteric Reflex and the Anal Wink Reflex? | Cremasteric reflex (L1–L2): stroking the medial thigh (femoral branch of genitofemoral / ilioinguinal nerve) causes ipsilateral testicular elevation (genital branch of genitofemoral nerve); Anal wink reflex (S2–S4): perianal pinprick causes external anal sphincter contraction via the pudendal nerve. |  |  |
| 15 | What is Spinal Shock, and how does the clinical presentation of an acute complete spinal cord transection evolve over time? | Immediately after acute spinal cord transection, spinal shock causes transient flaccid paralysis, complete areflexia, and urinary retention below the lesion due to sudden loss of descending tonic facilitation; over weeks, spinal interneuron reorganization leads to classic UMN spasticity, hyperreflexia, clonus, and spastic neurogenic bladder. |  |  |
| 16 | What is Central Cord Syndrome, what mechanism of injury causes it, and why does it produce greater motor weakness in the upper extremities than the lower extremities? | Acute hyperextension injury of the neck in an older patient with cervical spondylosis/stenosis causing central spinal cord contusion; because the lateral corticospinal tract is laminated with cervical (arm/hand) fibers medially and lumbar/sacral (leg) fibers laterally, upper extremity weakness is disproportionately worse than lower extremity weakness. |  |  |
| 17 | Which spinal cord tracts degenerate in Subacute Combined Degeneration (SCD), what nutritional or toxic etiologies cause it, and how does it present? | Demyelination of the Dorsal Columns, Lateral Corticospinal Tracts, and Spinocerebellar Tracts caused by Vitamin B12 (cobalamin) deficiency, nitrous oxide ('whippit') abuse, or copper deficiency; presents with symmetric paresthesias, loss of vibration/proprioception (sensory ataxia / positive Romberg sign), and spastic paraparesis with hyperreflexia/Babinski sign. |  |  |
| 18 | In a cervical disc herniation at the C5–C6 intervertebral disc space, which spinal nerve root is compressed, and why? | The C6 spinal nerve root is compressed; because there are 8 cervical nerve roots and 7 cervical vertebrae, cervical roots C1–C7 exit ABOVE their similarly numbered vertebra (and C8 exits between C7 and T1), so a C5–C6 disc herniation compresses the C6 root. |  |  |
| 19 | What spinal structures are degenerated in Tabes Dorsalis, what infection causes it, and what are its classic clinical signs? | Degeneration of the dorsal roots and dorsal columns caused by tertiary neurosyphilis (Treponema pallidum); presents with lancinating pain, sensory ataxia (wide-based stamping gait, positive Romberg sign), Charcot neuropathic joints, absent deep tendon reflexes (due to dorsal root loss), and Argyll Robertson pupils. |  |  |
| 20 | How do the C6, C7, and C8 dermatomes distribute across the digits of the hand? | C6 supplies the thumb and radial forearm; C7 supplies the index and middle fingers; C8 supplies the ring and little fingers and the ulnar border of the hand. |  |  |
| 21 | How do you clinically differentiate an Upper Motor Neuron (UMN) lesion from a Lower Motor Neuron (LMN) lesion on motor examination? | UMN lesion: spastic paralysis, hyperreflexia, clonus, clasp-knife spasticity, and positive Babinski sign (upgoing plantar reflex); LMN lesion: flaccid paralysis, hyporeflexia/areflexia, profound early muscle atrophy, fasciculations, and downgoing or absent plantar reflex. |  |  |
| 22 | What is Amyotrophic Lateral Sclerosis (ALS), what tracts/cells degenerate, and what genetic mutation accounts for the most common familial form? | Progressive neurodegeneration of BOTH upper motor neurons (primary motor cortex and corticospinal tract) and lower motor neurons (brainstem cranial nerve nuclei and spinal ventral horn) with spared sensory and extraocular function (and frequent frontotemporal dementia overlap); >95% of sporadic cases show cytoplasmic TDP-43 inclusions, while familial cases are most commonly caused by C9orf72 hexanucleotide repeat expansion or SOD1 mutation (treated with riluzole, edaravone, or tofersen for SOD1-ALS). |  |  |
| 23 | What sensory modalities are carried by the Spinothalamic Tract (Anterolateral System), and where do its fibers synapse and decussate? | Pain, temperature (lateral spinothalamic), and crude touch/pressure (anterior spinothalamic); 1st-order neurons (DRG) enter Lissauer's tract and synapse in the ipsilateral dorsal horn (substantia gelatinosa); 2nd-order axons decussate via the anterior white commissure within 1–2 spinal segments above entry and ascend contralaterally to the VPL thalamus. |  |  |
| 24 | How does an Upper Motor Neuron (suprasacral, above S2) lesion versus a Lower Motor Neuron (sacral S2–S4 or cauda equina) lesion affect bladder function? | A suprasacral UMN lesion disconnects the pontine micturition center, causing a spastic/hyperreflexic neurogenic bladder (detrusor hyperreflexia and detrusor-sphincter dyssynergia with urge incontinence); a sacral LMN lesion destroys the pelvic splanchnic reflex arc, causing a flaccid/atonic bladder with urinary retention and overflow incontinence. |  |  |
| 25 | What is Syringomyelia, what anatomical malformation is it classically associated with, and what is its pathognomonic neurological finding? | Fluid-filled cavitation (syrinx) expanding from the central canal of the cervical spinal cord (associated with Chiari I malformation or trauma); compresses the crossing fibers of the anterior white commissure first, producing a bilateral 'cape-like' loss of pain and temperature over the shoulders and arms while sparing fine touch/vibration ('dissociated sensory loss'). |  |  |
| 26 | At what spinal cord level does the Fasciculus Cuneatus join the Fasciculus Gracilis in the dorsal columns, and how are they somatotopically arranged? | Fasciculus Gracilis lies medially throughout the cord carrying lower extremity fibers (below T6); Fasciculus Cuneatus lies laterally from T6 and above carrying upper extremity and upper trunk fibers. |  |  |
| 27 | What sensory and motor deficits occur in Brown-Séquard Syndrome (spinal cord hemisection) at the T10 level? | Ipsilateral below T10: spastic paralysis (lateral corticospinal tract) and loss of vibration/proprioception (dorsal columns); Contralateral starting 1–2 levels below T10 (around T12): loss of pain and temperature sensation (spinothalamic tract); plus ipsilateral segment-level LMN and complete sensory loss at T10. |  |  |
| 28 | Which myotomes (spinal nerve roots) are tested by hip flexion, knee extension, ankle dorsiflexion/great toe extension, and ankle plantarflexion? | L2–L3: hip flexion (iliopsoas); L3–L4: knee extension (quadriceps); L4: ankle dorsiflexion (tibialis anterior); L5: great toe extension (extensor hallucis longus) and hip abduction; S1: ankle plantarflexion (gastrocnemius/soleus) and foot eversion. |  |  |
| 29 | How does Neurogenic Shock caused by a high spinal cord injury (above T6) differ hemodynamically from Hypovolemic/Hemorrhagic Shock? | Neurogenic shock interrupts descending sympathetic vasomotor and cardioaccelerator (T1–T4) fibers, producing hypotension accompanied by BRADYCARDIA and warm, flushed dry skin (vasodilation), whereas hypovolemic shock produces hypotension with reflex TACHYCARDIA and cool, clammy pale skin. |  |  |
| 30 | At what vertebral level does the adult spinal cord (conus medullaris) terminate, and at what vertebral level is a lumbar puncture safely performed? | In adults, the conus medullaris terminates at the lower border of L1 or L2 (L3 in newborns); lumbar puncture is performed at the L3–L4 or L4–L5 interspace (located along the supracristal line connecting the iliac crests) to sample CSF from the lumbar cistern without hitting the cord. |  |  |
| 31 | Which vascular territory is infarcted in Anterior Spinal Artery (ASA) Syndrome, what tracts are spared, and what is the classic surgical cause? | Infarction of the anterior two-thirds of the spinal cord (corticospinal tracts, spinothalamic tracts, and ventral/autonomic horns) with COMPLETE SPARING of the dorsal columns (vibration/proprioception intact, supplied by paired posterior spinal arteries); classically caused by thoracic aortic surgery damaging the artery of Adamkiewicz (usually arising at T9–T12). |  |  |
| 32 | Where do the axons of the Lateral Corticospinal Tract originate, decussate, and terminate? | Upper motor neurons originate in the primary motor cortex (layer V pyramidal cells, Brodmann area 4), descend through the posterior limb of the internal capsule, cerebral peduncle, and ventral pons, decussate (85–90%) at the caudal medullary pyramids, and descend in the lateral funiculus to synapse on ventral horn lower motor neurons. |  |  |

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