Here, we will draw the posterior column pathway, the anterolateral system (which includes, most notably, the spinothalamic tract), and the lateral corticospinal tract.
First, draw an axial cross-section through the spinal cord.
Next, label the origin and termination points of our pathway; label the right peripheral nerve and the left cerebral hemisphere’s primary motor cortex and primary sensory cortex.
Now, label the posterior column of the right side of the posterior white matter. Posterior column fi bers ascend the spinal cord ipsilateral to their side of origin. Next, label the anterolateral system bundle on the left side of the spinal cord — the anterolateral system fi bers ascend the spinal cord contralateral to their side of origin. Finally, draw the lateral corticospinal tract on the right side of the spinal cord — the lateral corticospinal tract fi bers descend the spinal cord contralateral to their side of origin.
Next, let’s label cell bodies for each pathway and then draw each pathway’s course. We will abbreviate the cell bodies for each pathway as follows: posterior column pathway cell body as PCP, anterolateral system cell body as ALS, and lateral corticospinal tract cell body as CST.
Show that the fi rst cell body (the fi rst-order sensory neuron) for the posterior column pathway lies in the dorsal root ganglion. Th is cell body is pseudo-unipolar:
indicate that it projects a single axon bundle over a very short distance, which divides into a peripheral process (the peripheral nerve) and a central process (the poste-rior nerve root). Next, show that the second-order sen-sory neurons lie in the gracile and cuneate nuclei in the medulla. Th en, draw the third-order sensory neuron in the contralateral thalamus. Now, draw the posterior column pathway, itself. Indicate that the central process enters and ascends the posterior column without form-ing a synapse in the spinal cord and that it instead fi rst synapses in the gracile and cuneate nuclei in the medulla.
Next, show that the gracile and cuneate nuclei send decussating fi bers across the medulla via the internal arcuate fasciculus; these fi bers ascend the brainstem via
the medial lemniscus and synapse in the third-order neuron in the ventroposterior lateral nucleus of the thal-amus. Finally, indicate that the thalamus projects to the sensory cortex.
Now, let’s draw the cell bodies and fi ber pathway for the anterolateral system. Indicate that the fi rst-order neuron lies within the dorsal root ganglion; then, show that the second-order neuron lies within the dorsal horn of the spinal cord; and fi nally, show that the third-order neuron lies within the contralateral thalamus (also within the ventroposterior lateral nucleus). Now, draw the anterolateral system pathway, itself. Show that ante-rolateral system central processes project from the dorsal root ganglion to the dorsal horn. Th ese inputs ascend and descend a variable number of spinal cord levels before synapsing in the spinal cord. Th en, show that at or near their level of entry into the spinal cord, the antero-lateral system fi bers decussate via the ventral commissure and bundle in the anterolateral spinal cord, where they ascend the spinal cord and brainstem to synapse in the thalamus. Finally, show that the thalamus projects to the sensory cortex. Note that whereas the posterior column pathway ascends the spinal cord ipsilateral to its side of origin, the anterolateral system ascends the spinal cord contralateral to its side of origin.
Lastly, let’s draw the cell bodies and pathway for the lateral corticospinal tract. Indicate that the fi rst-order neuron lies in the motor cortex, most notably, but also in the premotor and sensory cortices, and then that the second- order neuron lies within the contralateral ante-rior gray matter horn of the spinal cord. Now, show that lateral corticospinal fi bers descend from the motor cortex through the ipsilateral brainstem, decussate within the medullary pyramids at the cervicomedullary junction, and then descend through the spinal cord in the lateral corticospinal tract to synapse in spinal motor neurons. Th en, show that motor neurons project nerve fi bers via the anterior nerve root, which joins the poste-rior nerve root to form a mixed spinal nerve. 2 , 4 – 12
Ventral commissure Peripheral
Nerve
Posterior column Gracile &
cuneate nuclei
Anterolateral system fiber
Lateral corticospinal tract
Motor neuron
Internal arcuate fasciculus
(1PCP)
(2PCP)
(1CST)
Primary sensory cortex
Corticospinal tract
Medial lemniscus
Thalamus
(2ALS)
(2CST)
Cervico-medullary junction Primary motor cortex
Anterolateral system (1ALS)
Posterior column pathway - PCP Anterolateral system - ALS Lateral corticospinal tract - CST
(3 PCP)(3ALS)
Posterior column fiber
(Right)
(Left)
Axon Posterior nerve root
Anterior nerve root Spinal
nerve
D R AW I N G 7 - 4 Major Ascending & Descending Tracts
Spinocerebellar Pathways (Advanced)
Here we will draw the spinocerebellar pathways, which carry proprioceptive sensory information to the cerebel-lum for the coordination of movement and the mainte-nance of posture. Th e spinocerebellar pathways comprise the posterior, anterior, and rostral spinocerebellar tracts, and the cuneocerebellar tract. Except for the cuneocere-bellar tract, all of the spinocerecuneocere-bellar tracts synapse within the spinal cord (generally within the intermedi-ate zone of the gray matter) prior to reaching the cerebel-lum. Th e posterior and anterior spinocerebellar pathways are the best understood of these pathways; we will draw them fi rst.
Draw an axial cross-section through the spinal cord.
In the corner of the diagram, write the words “tract” and
“origin.” We will list the origin of each spinocerebellar pathway as we complete our diagram. First, indicate that the posterior spinocerebellar tract originates from aff er-ents of the lower trunk and lower limb. Now, to draw the posterior spinocerebellar tract course, draw a peripheral nerve and show its central process synapse in the inter-mediate zone of the spinal cord from T1 to L2 in a region called the dorsal nucleus of Clarke. Th e majority of the posterior spinocerebellar tract aff erent fi bers arise from below the L2 spinal level, ascend in the posterior funicu-lus, and then make their synapse in the dorsal nucleus of Clarke. Now, show that the dorsal nucleus of Clarke projects via the ipsilateral inferior cerebellar peduncle to enter the cerebellum.
Next, let’s draw the anterior spinocerebellar tract.
Indicate that it originates from aff erents of the lower limb. Th en, to draw the anterior spinocerebellar tract course, show the central process of a peripheral nerve fi ber synapse at the L3 to L5 levels of the spinal cord.
Th e course of the anterior spinocerebellar tract is quite long and involves a double decussation. Indicate that the
anterior spinocerebellar tract projects from L3 to L5 across midline within the ventral commissure, ascends the spinal cord and brainstem within the anterior spi-nocerebellar tract, enters the cerebellum within the supe-rior cerebellar peduncle, and then decussates again within the cerebellum to terminate on its side of origin (although a small portion of fi bers terminate in the contralateral cerebellum and do not make this last decussation). Th us, through this double decussation, the anterior spinocere-bellar tract remains ipsilateral to its side of origin. Note that, generally, the inferior and middle cerebellar pedun-cles are the infl ow pathways into the cerebellum and the superior cerebellar peduncle is the outfl ow pathway for fi bers from the cerebellum — the anterior spinocerebellar pathway is an important exception to this rule.
Now, let’s draw the cuneocerebellar tract. Indicate that the cuneocerebellar tract originates in the upper limb and upper trunk. Th en, just beneath the inferior cerebellar peduncle, label the lateral cuneate nucleus (aka accessory cuneate nucleus) — the fi rst synapse of the cuneocerebellar tract. Next, to draw the cuneocerebellar tract course, show the central process of a peripheral nerve fi ber enter the posterior column and directly ascend the spinal cord to the lateral cuneate nucleus.
Th en, indicate that the cuneocerebellar fi bers project from the lateral cuneate nucleus through the ipsilateral inferior cerebellar peduncle to enter the cerebellum.
Finally, let’s draw our last pathway, the rostral spinoc-erebellar tract. Indicate that it originates in the upper limb. Th en, to draw the rostral spinocerebellar tract course, show the central process of a peripheral nerve synapse at the C4 to C8 spinal levels. Indicate that along a poorly described course, fi bers project from the C4 to C8 spinal levels to the cerebellum via the ipsilateral infe-rior cerebellar peduncle. 2 , 4 – 12
Anterior spino-cerebellar tract Inferior
cerebellar peduncle
Superior cerebellar peduncle Cerebellum
Posterior spino-cerebellar tract Lateral cuneate nucleus
Cuneo-cerebellar tract
C4 to C8 T1 to L2
L3 to L5 Rostral
spino-cerebellar tract (from C4 to C8)
TRACT ORIGIN Posterior Lower limb &
lower trunk Anterior Lower limb Cuneo- Upper limb &
upper trunk Rostral Upper limb
D R AW I N G 7 - 5 Spinocerebellar Pathways
Spinal Cord Disorders
Case I
Patient presents with years of progressive “lightning-like”
pain in the lower extremities. Exam reveals profound lower extremity loss of vibration/proprioception sensation with preserved pain/temperature sensation and preserved strength in the lower extremities. Th ere is arefl exia in the lower extremities. Th e upper extremities are normal.
Show that the loss of vibration/proprioception sensa-tion with preserved pain/temperature sensasensa-tion and pre-served motor function suggests posterior column spinal
cord involvement. Th e lower extremity arefl exia suggests lower motor neuron involvement, so also show that there is dorsal root involvement. Th e dorsal root involvement causes the lancinating pain — presumably from irritation of the pain/temperature fi bers.
Indicate that this constellation of defi cits suggests a diagnosis of tabes dorsalis (aka syphilitic myelopathy), in which the posterior columns and dorsal roots are aff ected. 15 – 21
Case II
Patient presents with an abrupt onset of interscapular pain, lower extremity weakness, sensory disturbance, and bowel and bladder incontinence. Exam reveals arefl exia of the lower extremities; paraparesis; loss of pain/temperature sensation with preserved vibration/
proprioception sensation in the lower extremities; anal sphincter atonia; and a normal motor, sensory, and refl ex exam in the upper extremities.
Show that the sudden weakness and arefl exia suggests bilateral anterior motor horn cell involvement, and that
the longitudinal loss of pain/temperature sensation sug-gests involvement of the anterolateral system with pres-ervation of the posterior columns.
Indicate that this constellation of defi cits suggests anterior spinal artery ischemia, in which the anterior two thirds of the spinal cord are aff ected. Note that this syndrome variably aff ects the lateral corticospinal tracts. Th e most common site of anterior spinal artery ischemia is at the T4 level. 18 – 22
Case III
Patient presents with sudden weakness on the right side of the body and sensory disturbance. Exam reveals right-side weakness, right-right-side loss of vibration/proprioception sensation, and left -side loss of pain/temperature sensa-tion. Refl exes are absent on the right side and normal on the left .
Show that the right-side hemi-body weakness sug-gests right-side corticospinal tract involvement; that the right-side loss of vibration/proprioception suggests
right-side posterior column tract involvement; that the left -side loss of pain/temperature sensation suggests right-side anterolateral system involvement; and that the right-side arefl exia suggests right-side lower motor neuron involvement, which could occur from either anterior or posterior horn injury.
Indicate that this constellation of defi cits suggests a hemi-cord syndrome involving the right half of the spinal cord, called Brown-Séquard syndrome. 18 – 21
Anterior spinal artery ischemia Brown Sequard syndrome Tabes dorsalis
(Syphilitic myelopathy)
D R AW I N G 7 - 6 Spinal Cord Disorders — Partial
Spinal Cord Disorders (Cont.)
Case IV
Patient presents with a few-month course of progressive burning pain across the shoulders. Exam reveals weak-ness of the upper extremities; absent biceps refl exes with hyperrefl exia of lower extremities; pathologic (ie, posi-tive) Babinski’s; absent pain/temperature sensation across the upper chest and limbs with preserved vibra-tion/proprioception sensation.
Show that the dissociation of loss of pain/temperature sensation with preserved vibration/proprioception sen-sation in a suspended sensory level suggests damage to the crossing anterolateral system fi bers. Show that the loss of strength and arefl exia of the upper limbs in that same seg-ment suggests bilateral anterior motor horn damage.
Indicate that this constellation of defi cits suggests a central cord syndrome, oft en a syringomyelia.
Syringomyelia is a fl uid-fi lled cavity within the spinal cord, which may be limited to a dilatation of the central canal, may extend outside of the central canal, or may be separate from the central canal, entirely. It causes lower motor neuron signs at the level of the lesion, impaired pain/temperature sensation but preserved vibration/proprioception in a segmental distribution (classically, in a cape-like distribution across the arms and upper trunk): a so-called suspended sensory level, and upper motor neuron signs below the level of the lesion. 18 – 21
Case V
Patient presents with a few-month course of trunk and lower limb sensory dysesthesias. Exam reveals hyperre-fl exia throughout except for absent ankle jerks; patho-logic (ie, positive) Babinski’s; loss of vibration/
proprioception sensation in the lower extremities with preserved pain/temperature sensation; and mild, diff use lower extremity weakness.
Show that the loss of vibration/proprioception sensa-tion with preserved pain/temperature sensasensa-tion suggests posterior column involvement. Th en, show that the diff use motor weakness is due to corticospinal tract involvement.
Indicate that this combination of defi cits is oft en found in subacute combined degeneration due to vitamin B12 defi ciency. Subacute combined degeneration aff ects the posterior and lateral columns. Although not men-tioned, gait ataxia is oft en present in this disorder and may be due to the profound vibration/proprioception sensory loss or due to posterior spinocerebellar tract involvement from lateral column pathology. B12 defi -ciency also oft en causes a superimposed neuropathy, which explains the absent ankle jerks. 18 – 21 , 23 , 24
Case VI ( Advanced )
Patient presents with longstanding gait disturbance and weakness. Exam shows lower extremity arefl exia with preserved upper extremity refl exes; pathologic (ie, posi-tive) Babinski’s; profound ataxia; vibration/propriocep-tion sensory loss out of proporvibration/propriocep-tion to pain/temperature sensory loss; and motor weakness of the upper and lower extremities.
First, show that the mixed refl ex pattern in the pres-ence of pathologic Babinski’s suggests a mixed upper and lower motor neuron disease pattern with pathology of the dorsal nerve roots and dorsal horns. Th en, show that
the vibration/proprioception sensory loss with preserved pain/temperature sensation suggests posterior column involvement. Next, show that the profound ataxia sug-gests spinocerebellar tract involvement. And fi nally, indicate that the motor weakness suggests corticospinal tract involvement.
Indicate that this constellation of defi cits is found in Friedreich’s ataxia, an inherited progressive ataxia with pathology that fi rst appears in the dorsal roots.
Spinocerebellar tract involvement is an important dis-tinguishing feature of this disorder. 18 – 21
(Vitamin B12 deficiency) (often Syringomyelia)
Friedreich’s ataxia Anterior spinal artery ischemia Brown Sequard syndrome Tabes dorsalis
Central cord syndrome Subacute combined degeneration (Syphilitic myelopathy)
D R AW I N G 7 - 7 Spinal Cord Disorders — Partial
Spinal Cord Disorders (Cont.)
Case VII
Patient presents with a several-month course of weak-ness that began in the left arm and has since spread to both arms and legs. Exam reveals asymmetric but diff use upper and lower extremity weakness. Th ere is mixed hyperrefl exia and arefl exia throughout the bilat-eral upper and lower extremities. Th ere are bilateral pathologic (ie, positive) Babinski’s. Sensory exam is normal.
Show that the presence of motor weakness in con-junction with mixed hyperrefl exia and arefl exia with bilateral pathologic Babinski’s and a normal sensory exam suggests both corticospinal tract and anterior motor horn involvement.
Indicate that this constellation of defi cits is oft en found in amyotrophic lateral sclerosis (aka ALS or Lou Gehrig’s disease). 18 – 21
Case VIII (Advanced)
Patient presents with muscle pains and slowly progres-sive muscle wasting. Exam reveals asymmetric lower extremity weakness; hyporefl exia in the lower extremi-ties; the absence of pathologic Babinski’s (ie, negative Babinski's); and normal sensation.
Show that the weakness in conjunction with hypore-fl exia and a normal sensory exam suggests anterior motor horn involvement, only.
Many illnesses cause select anterior horn cell loss.
Indicate that two common illnesses that cause this pathol-ogy are polio syndrome and spinal muscular atrophy. 18 – 21
Case IX ( Advanced )
Patient presents with slowly progressive lower extremity weakness. Exam reveals spastic weakness of the lower extremities more so than the upper extremities; hyper-refl exia; bilateral pathologic (ie, positive) Babinski’s; gait ataxia; and a normal sensory exam.
Show that the weakness in conjunction with spasticity, hyperrefl exia, bilateral pathologic Babinski’s, and a normal sensory exam suggests corticospinal tract involvement.
Indicate that select corticospinal tract involvement suggests a diagnosis of primary lateral sclerosis. 18 – 21
Polio syndrome (Vitamin B12 deficiency) (often Syringomyelia)
Friedreich’s ataxia
Amyotrophic lateral sclerosis Spinal muscular atrophy, Primary lateral sclerosis (aka ALS or Lou Gehrig’s disease)
Anterior spinal artery ischemia Brown Sequard syndrome Tabes dorsalis
Central cord syndrome Subacute combined degeneration (Syphilitic myelopathy)
D R AW I N G 7 - 8 Spinal Cord Disorders — Complete
References
illustrated guide to physiology, pharmacology, and recording techniques ( Springer , 2006 ). spinal cord: its role in motor control and movement disorders ( Cambridge University Press , 2005 ). interpretation based on experimental studies in animals ( Oxford University Press , 2001 ).13 . Campbell , W. W. , DeJong , R. N. & Haerer , A. F. DeJong’s the neurologic examination: incorporating the fundamentals of
neuroanatomy and neurophysiology, 6th ed. ( Lippincott Williams &