Neuro Chapter 7 (276-297)
Main Somatosensory Pathways
 Somatosensory – sensations of touch, pain, temp, vibration, and proprioception (joint position sense)
 Posterior column-medial lemniscal pathway conveys proprioception, vibration sense, and fine touch
 Anterolateral pathways include spinothalamic tract and other associated tracts that convey pain, temp sense,
and crude touch
 Sensory neuron cell bodies in DRG; each DRG cell has stem axon that bifurcates, resulting in process that carries
sensory info from periphery and second process that carries info to spinal cord through dorsal nerve roots
o Peripheral region innervated by sensory fibers from single nerve root level = dermatome
Posterior Column-Medial Lemniscal Pathway
 Large-diameter, myelinated axons carrying info about proprioception, vibration sense, and fine touch; enter
spinal cord via medial portion of dorsal root entry zone
 Many axons enter ipsilateral posterior
columns to ascend all the way to
posterior column nuclei in medulla
 Remember somatotopic organization of
posterior columns by picturing fibers
adding on laterally from higher levels as
posterior columns ascend (medial
portion (gracile fasciculus) carries
information from legs and lower trunk
and more lateral cuneate fasciculus
carries info from upper trunk and arms)
 First-order sensory neurons that have
axons in gracile and cuneate fasciculi
synapse onto second-order neurons in
nuecleus gracilis and nucleus cuneatus
 Axons of second-order neurons
decussate as internal arcuate fibers and
form medial lemniscus on other side of
medulla
 Medial lemniscus initially has vertical orientation then occupies progressively more lateral and inclined position
as it ascends in brainstem; somatotopic organization assumes vertical position in medulla such that feet
represented more ventrally and inclines again in pons and midbrain so arms represented more medially and legs
mor laterally (little person lies down)
o Reversal in somatotopic orientation: for medial lemniscus in pons and midbrain, feet are lateral, while in
posterior columns, feet are medial
 Medial lemniscus axons terminate in ventral posterior lateral nucleus (VPL) of thalamus; neurons of VPL project
through posterior limb of internal capsule in thalamic somatosensory radiations to reach primary somatosensory
cortex in postcentral gyrus
 Synaptic inputs to primary somatosensory cortex from both face and body occur mainly in cortical layer IV and
deep portions of layer III, with some inputs reaching layer VI
Spinothalamic Tract and other Anterolateral Pathways
 Smaller-diameter and unmyelinated axons carrying info about pain and temp; enter via dorsal root entry zone
o Axons make first synapses immediately in gray matter of spinal cord, mainly in dorsal horn marginal
zone (lamina I) and deeper in dorsal horn (in lamina V)
o Some axon collaterals ascend or descend a few segments in Lissauer’s tract before entering central gray
 Axons from second-order sensory neurons in central gray cross over in spinal cord anterior (ventral )
commissure to ascend in anterolateral white matter; takes 2-3 spinal segments for decussating fibers to reach
opposite side, so lateral cord lesion will affect contralateral pain and temp sensation beginning few segments
below level of lesion
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Somatotopic organization with feet most laterally represented (fibers from anterior commissure add on medially
as anterolateral pathways ascend in
spinal cord)
o When they reach medulla,
anterolateral pathways located
laterally, running in groove
between inferior olives and
inferior cerebellar peduncles;
then enter pontine tegmentum to
lie just lateral to medial lemniscus
in pons and midbrain
 Anterolateral pathways consist of
spinothalamic, spinoreticular, and
spinomesencephalic tracts
o Spinothalamic tract mediates
discriminative aspects of pain and
temp sensation such as location
and intensity of stimulus
 Major relay for spinothalamic tract is
ventral posterior lateral nucleus (VPL) of
thalamus (separate neurons than from
posterior column-medial lemniscal
pathway)
 From VPL, info travelling in spinothalamic tract conveyed via thalamic somatosensory radiations to primary
somatosensory cortex in post-central gyrus
 Pain and temp sensation for face carried by trigeminothalamic tract
 Spinoreticular tract terminates on medullary-pontine reticular formation, which in turn projects to intralaminar
thalamic nuclei (centro-median nucleus); intralaminar nuclei project diffusely to entire cerebral cortex and
involved in behavioral arousal
 Spinomesencephalic tract projects to midbrain periaqueductal gray matter and superior colliculi; periaqueductal
gray participates in central modulation of pain
 Anterolateral pathways can convey some crude touch sensation
 If you step on a tack, spinothalamic tract makes you realize “something sharp is puncturing my foot”;
spinothalamic intralaminar projections and spinoreticular tract say “ouch, that hurts”; spinomesencephalic tract
leads to pain modulation to think “that feels better” later
Somatosensory Cortex
 From thalamic VPL and VPM nuclei, somatosensory info conveyed to primary somatosensory cortex in
postcentral gyrus; primary somatosensory cortex somatotopically organized with face most laterally and leg
most medially
 Info from primary somatosensory cortex conveyed to secondary somatosensory association cortex in Sylvian
fissure, along superior margin in parietal operculum region
 Further processing of somatosensory info occurs in association cortex of superior parietal lobule
 Primary somatosensory cortex and somatosensory association cortex have lots of connections with motor cortex
 Lesions of somatosensory cortex and adjacent regions produce cortical sensory loss
Central Modulation of Pain
 Gate control theory – sensory inputs from large-diameter, nonpain A-β fibers reduce pain transmission through
dorsal horn (why shaking your hand after hitting your thumb with hammer temporarily helps pain)
 Periaqueductal gray receives inputs from hypothalamus, amygdala, and cortex, and inhibits pain transmission in
dorsal horn via relay in region at pontomedullary junction (rostral ventral medulla or RVM); includes
serotonergic neurons of raphe nuclei that project to spinal cord, modulating pain in dorsal horn
o RVM sends inputs mediated by substance P to locus ceruleus, which sends noradrenergic projections to
modulate pain in spinal cord dorsal horn
o Histamine contributes to modulation of pain through H3 receptors
 Opiate medications exert analgesic effects through receptors located on peripheral nerves and neurons in spinal
dorsal horn; opiate receptors and endogenous opiate peptides found in high concentrations at key points in pain
modulatory pathways; enkephalin-containing neurons and dynorphins-containing neurons concentrated in
periaqueductal gray, RVM, and spinal cord dorsal horn; β-endorphin-containing neurons concentrated in regions
of hypothalamus that project to periaqueductal gray
Thalamus
 Nearly all pathways that project to cerebral cortex do so via synaptic relays in thalamus
 Thalamus also conveys nearly all other inputs to cortex, including motor inputs from cerebellum and basal
ganglia, limbic inputs, widespread modulatory inputs involved in behavioral arousal and sleep-wake cycles, etc.
 Some thalamic nuclei have specific topographical
projections to restricted cortical areas, while
others project more diffusely; nuclei typically
receive dense reciprocal feedback connections
from cortical areas to which they project;
corticothalamic projections outnumber
thalamocortical projections
 Thalamus located in diencephalon with
hypothalamus and epithalamus (contains
habenula, parts of pretectum, and pineal body)
 Thalamus divided into medial nuclear group,
lateral nuclear group, and anterior nuclear group
by internal medullary lamina; nuclei located
within internal medullary lamina itself called
intralaminar nuclei
o Midline thalamic nuclei lie adjacent to third ventricle, several of which are continuous with and
functionally very similar to intralaminar nuclei
o Thalamic reticular nucleus forms extensive but thin sheet enveloping lateral aspect of thalamus
 Most of thalamus made up of relay nuclei – receive inputs from numerous pathways and project to cortex
o Projections to primary sensory and motor areas most localized; lie mainly in lateral thalamus
o All sensory modalities (except smell) have specific relays in lateral thalamus
o VPL and VPM project to primary
somatosensory cortex
o Visual info relayed in lateral geniculate
nucleus (LGN)
o Auditory info relayed in medial
geniculate nucleus (MGN) [lateral light,
medial music]
o Motor pathways leaving cerebellum
and basal ganglia have specific thalamic
relays in ventral lateral (VL) nucleus en
route to motor, premotor, and
supplementary motor cortex
 Widely projecting (nonspecific) thalamic relay
nuclei – visual and other sensory inputs to
pulvinar relayed to large regions of parietal, temporal, and occipital association cortex involved in behavioral
orientation toward relevant stimuli
o Diffuse relays of limbic inputs and other info involved in cognitive functions occur in mediodorsal
nucleus (MD) as well as midline and intralaminar thalamic nuclei
 MD serves as major thalamic relay for info traveling to frontal association cortex
 Intralaminar nuclei lie within internal medullary lamina; receive inputs from numerous pathways and have
reciprocal connections with cortex
o Main inputs and outputs from basal ganglia
o
Divided into caudal intralaminar nuclei (centromedian nucleus; involved mainly in basal ganglia circuitry)
and rostral intralaminar nuclei (have input and output connections with basal ganglia)
 Rostral intralaminar nuclei relay inputs from ascending reticular activating systems (ARAS) to
cortex, maintaining alert conscious state
 Reticular nucleus – only nucleus of thalamus that doesn’t project to cortex; receives inputs mainly from other
thalamic nuclei and cortex and projects back to thalamus
o Consists of almost pure population of inhibitory GABAergic neurons; regulates thalamic activity
Paresthesias
 Lesions of posterior column-medial lemniscal pathways described as tingling numb sensation, feeling of tight
band-like sensation around trunk or limbs, or sensation similar to gauze on fingers when trying to feel things
 In lesions of anterolateral pathways, often sharp, burning, or searing pain
 Lesions of parietal lobe or primary sensory cortex may cause contralateral numb tingling; can have pain
 Dejerine-Roussy syndrome – lesions of thalamus causing severe contralateral pain
 Lhermitte’s sign – electricity-like sensation running down back into extremities on neck flexion; lesion in C-spine
 Lesions of nerve roots produce radicular pain that radiates down limb in dermatomal distribution; accompanied
by numbness and tingling; provoked by movements that stretch nerve root
 Peripheral nerve lesions cause pain, numbness, and tingling
 Dysesthesia – unpleasant, abnormal sensation
 Allodynia – painful sensations provoked by normally nonpainful stimuli
 Hyperpathia or hyperalgesia – enhanced pain to normally painful stimuli
Spinal Cord Lesions
 In acute, severe lesions, often initially phase of spinal shock characterized by flaccid paralysis below lesion, loss
of tendon reflexes, decreased SNS outflow to vascular smooth muscle causing moderately decreased BP, and
absent sphincteric reflexes and tone
o Spasticity and UMN signs develop over weeks to months
o Some sphincteric and erectile reflexes may return, often without voluntary control
o Acute traumatic spinal cord lesions may have improved outcome if treated within first 8 hours with high
doses of steroids
 Chronic myelopathy (spinal cord dysfunction) often seen with degenerative disorders of spine; spine and nerve
roots compressed, so combo of UMN and LMN signs mimicking motor neuron disease can happen
 If tumors treated with radiation after patient loses ambulation, 80% can’t get it back; reverse is true
 Infarction of spinal cord due to anterior spinal artery occlusion leads to anterior cord syndrome

Patients with myelitis usually present with spinal cord dysfunction that develops relatively quickly
o MRI often shows T2 bright areas, and CSF has elevated WBC (usually lymphocytic)
Sensory Loss: Patterns and Localization
 Primary somatosensory cortex – deficit is contralateral to lesion; discriminative touch and joint position sense
often most severely affected, but all modalities may be involved
o Sometimes all primary modalities relatively spared, but cortical sensory loss present (decreased
sterognosis (perceiving and understanding form of object by touch) and graphesthesia (ability to feel
writing on skin)
o Associated deficits from involvement of adjacent cortical areas may include UMN-type weakness, visual
field deficits, or aphasia
 VPL, VPM, or thalamic somatosensory radiations – deficit contralateral to lesion; may be more noticeable in
face, hand (lips and fingertips), and foot than trunk or proximal extremities
o All sensory modalities may be involved, sometimes with no motor deficit
o Larger lesions may be accompanied by hemiparesis or hemianopia caused by involvement of internal
capsule; lateral geniculate; or optic radiations

Lateral pons or lateral medulla – lesion involves anterolateral pathways and spinal trigeminal nucleus on same
side; causes loss of pain and temperature sensation in body opposite lesion, and loss of pain and temp sensation
in face on same side as lesion
 Medial medulla – lesion involves medial lemniscus, causing contralateral loss of vibration and joint position
sense
Spinal Cord Syndromes
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Transverse cord lesion – all motor and sensory pathways either partially or completely interrupted; often
sensory level (diminished sensation in all dermatomes below level of lesion)
Hemicord lesions (Brown-Séquard syndrome) – damage to lateral corticospinal tract causes ipsilateral UMN-type
weakness; interruption of posterior columns causes ipsilateral loss of vibration and proprioception; interruption
of anterolateral systems causes contralateral loss of pain and temp sensation
Central cord syndrome – in small lesions, damage to spinothalamic fibers crossing in ventral commissure causes
bilateral regions of suspended sensory loss to pain and temperature; produce cape distribution
o With larger lesions, anterior horn cells damaged, producing LMN deficits at level of lesion
o Because anterolateral pathways compressed from medial surface by large lesions, there may be near
complete loss of pain and temp sensation except for sacral sparing
Posterior cord syndrome – cause loss of vibration and proprioception below level of lesion; with larger lesions
there may be encroachment on lateral corticospinal tracts, causing UMN-type weakness
o Vitamin B12 deficiency and tabes dorsalis (tertiary syphilis) preferentially affect posterior cord
Anterior cord syndrome – loss of pain and temp sensation below level of lesion; LMN weakness
o With larger lesions, lateral corticospinal tracts may be involved, causing UMN signs
o Incontinence common because descending pathways controlling sphincter function ventrally located
Anatomy of Bowel, Bladder, and Sexual Function
 Sensory info from S2-S4 ascends to higher levels of nervous system through posterior and anterolateral columns
 Voluntary somatic motor fibers arise from anterior horn cells at S2-S4 to control pelvic floor muslces and from
specialized sphincteromotor nucleus of Onuf at S2-S4 to control urethral and anal sphincters
 Pelvic PNS arise from sacral parasympathetic nuclei (S2-S4), and SNS arise from intermediolateral cell column
(T11-L1)
 In general, for lesions to affect bowel, bladder, or sexual function, bilateral pathways must be involved
 Sense of bladder fullness reaches sensory cortex, and micturition initiated by descending pathways from medial
frontal micturition centers that activate detrusor reflex
o Detrusor reflex mediated by intrinsic spinal cord circuits and regulated by pontine micturition center
o Reflex normally initiated by voluntary relaxation of external urethral sphincter, which triggers inhibition
of SNS to bladder neck, causing it to relax, and activation of PNS, causing detrusor muscle contraction
o Sensation of urine flow through urethra activates continued sphincter relaxation and detrusor
contraction
o When flow stops, urethral sphincters contract, triggering detrusor relaxation through urethral reflex
o Flow can be interrupted at any time by voluntary closure of urethral sphincter, which triggers detrusor
relaxation
 Lesions affecting bilateral medial frontal micturition centers result in reflex activation of pontine and spinal
micturition centers when bladder full
o Urine flow and bladder emptying normal, but no longer under voluntary control
 Lesions below pontine micturition center and above conus medullaris levels S2-S4 initially cause flaccid,
acontractile (atonic) bladder, which usually evolves over weeks to months to hyperreflexic (spastic) bladder
o When bladder atonic, reflex contractions of urethral sphincters persist, resulting in urinary retention and
bladder distention; post-void residual volume increased
o In hyperreflexic bladder, detrusor-sphincter dyssynergia often occurs, in which both detrusor and
urethral sphincter tone increased in uncoordinated, at times antagonistic, fashion
 When involuntary reflex bladder contractions occur, there may be sense of urinary urgency or
urge incontinence
 Often residual volume increases because of incomplete emptying, although volume smaller than
with acontractile bladder
 Lesions of peripheral nerves or spinal cord at S2-S4 cause flaccid areflexic bladder or significantly impaired
bladder contractility; result can be due to loss of PNS outflow to detrusor and/or loss of afferent sensory info
from bladder and urethra
o Overflow incontinence present
o Urinary retention and incontinence can also be caused by prostatic hypertrophy, urethral strictures, etc.
 Neurogenic bladder – refers to flaccid or hyperreflexic bladder disorders of neurologic origin
 Fecal continence controlled by descending pathways originating mainly in medial frontal lobes
o Anal sphincter closure maintained by internal anal sphincter innervated by sacral PNS and external anal
sphincter innervated by pelvic nerves arising from Onuf’s nucleus (voluntary), and pelvic floor muscles
innervated by sacral anterior horn cells
o GI motility depends on PNS from S2-S4 for colorectal smooth muscle beyond splenic flexure
o Fecal incontinence caused by diffuse cerebral or medial frontal lesions, spinal cord lesions, or lesions of
sacral nerve roots or pelvic or pudendal nerves
o In acute spinal cord lesions, anal sphincter completely flaccid with loss of sacral PNS outflow, causing
severe constipation
 During sexual arousal, stimuli from sensory modalities with internal psychological factors result in activation of
spinal cord autonomic pathways involved in sexual function
o Sensation from genitalia conveyed by pudendal nerve, reaching S2-S4
o In female, secretion of lubricating mucus by Bartholin’s glands PNS mediated, and increased vaginal
blood flow and secretions SNS mediated
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In male, both PNS and SNS contribute to erection; ejaculation occurs through SNS mediated contraction
of smooth muscle, causing emission of semen into urethra, followed by rhythmic reflex contractions of
striated muscles (pelvic floor, urethral sphincter, bulbospongiosus, etc.) resulting in forceful expulsion
In spinal cord lesions, reflex erection and ejaculation may still occur, but highly variable
Peripheral nerve lesions, higher-order cortical lesions, medications, etc., can all contribute to sexual
dysfunction