Somatosensory Systems
Chapter 7 Blumenfeld
Robert Altman PGY 3
Neurology, McGill University
Oct 2009
Overview

Overview key afferent pathways

Focusing on central course in spinal cord and brain




Introduction to the thalamus
Neurology of bladder & bowel function




Dorsal Column Medial Lemniscal (DCML)
Spinothalamic and other anterolateral pathways
VERY brief
Clinical examples
Take-home messages
Jeopardy-Style Trivia, Round 2!
General Principals



Somatotopy respected in spinal
cord, brainstem relay nucleii and
cortex
Aids with localizability of lesions
Touch is shared in both
pathways



Discriminative
Crude
DRG; pseudo-unipolar neuron
Sensory Neuron Types
NAME
A- (I)
DIAMETER (µm)
13-20
RECEPTORS
SENSORY
MODALITY
Yes
Muscle spindle, golgi
tendon organ
Proprioception
Proprioception, superficial
touch, deep touch,
vibration, touch
MYELINATED
A-β (II)
6-12
Yes
Muscle spindle, Meissner’s
corpuscule, Merkel’s
receptor, Pacinian
corpuscule, Ruffini ending,
Hair receptor
A-δ (III)
1-5
Yes
Bare nerve ending
Pain, temperature (cool)
0.2-1.5
No
Bare nerve ending
Pain, temperature
(warm), itch
C (IV)
DCML
DCML

Most axons do not perform their 1st synapse until at n. gracilis or cuneatus
in lower medulla (i.e. 1st order)








Somatotopy mnemonic
Lemniscus = tract
Gracile = thin
Cuneate = wedge
T6
Internal Arcuate fibers
Medial Lemniscus




2nd order neurons run to VPL
Vertical
Lateral / inclined position in upper brainstem
VPL
Posterior limb of IC to reach areas 3, 1, 2 of primary SS cortex

Primarily layer IV > III > VI
6 layers of the neocortex
Layer
Name
Function
Molecular Layer / Plexiform Layer
Dendrites and axons from
other layers
Small Pyramidal Layer / External Granular
Layer
Cortical-cortical connections
III
Medium Pyramidal layer / External Pyramidal
Layer
Cortical-cortical connections
IV
Granular Layer / Internal Granular Layer Input from thalamus
I
II
V
VI
Large Pyramidal Layer / Internal Pyramidal
Layer
Outputs to subcortical
structures besides thalamus
e.g. from giant cells of Betz
in motor cortex
Polymorphic Layer / Multiform Layer
Cortical-Thalamic
connections (Outputs to
Thalamus)
Layers I through VI vary in thickness in different cortical regions. Layer IV is most pronounced in the
sensory projection cortex and layer V is most pronounced in the primary motor cortex (pre-central gyrus).
Sensory Homonculus
Anterolateral Systems
Anterolateral Systems

First synapse is immediate in the spinal cord






Dorsal horn of lamina I (marginal zone)
Lamina V
Lissauer’s tract allows some axon collaterals to ascend or
descend 2-4 segments before entering in central gray
Second order neurons than traverse anterior commisure
(over 2-3 spinal segments)  clinical correlation to
spinal lesions
Somatotopy (see next slide)
Once reaches brainstem, remains lateral (b/w olives and
ICP)
Anterolateral Systems

Anterolateral system

Spinothalamic (I, V)



Spinoreticular (II, VII, VI, VIII)



Discriminative aspects of pain, location, intensity
Synapse on VPL (different area than DCML), relay to specific
SSC target (Brodmann 3,1,2)
Emotional and arousal aspects of pain
Ultimately RF projects to IL thalamic nuclei (centromedian),
which then project diffusely to the entire cerebral cortex
(behavioural arousal)
Spinomesencephalic


To PAG, SC
Pain modulation
Central Pathways Involved in Pain
Modulation

Spinal cord circuits



Gate theory (A-β)
TENS
“Long range” modulatory inputs


PAG (MB) receives diffuse inputs from hypothalamus,
amygdala, cortex
Relays to nucleus raphe-magnus in RVM (rostral ventral medulla)


Subsequently relays (via 5HT neurons) to dorsal horn, acting as pain
modulator
Also relays to locus ceruleus (rostral pons) via substance P, which in
turn relay NE projections to dorsal horn, acting as pain modulator
The Cerebral Signature for Pain Perception and Its Modulation, Neuron 55, August 2, 2007
J Bone Joint Surg Am.
2006;88:58-62.
Opiods

Receptors found on peripheral nerves and
diffusely in pain modulating system.



Enkephalins*
dynorphin*
β-endorphins**
Thalamus
Brief overview
Thalamus

Master relay center







Sensory
Motor
Cerebellar
Basal ganglia
Limbic
Behaviour, arousal, sleep-wake cycle
Dense reciprocal feedback connections between
cortex and thalamus.

Corticothalamic projections outnumber
thalamocortical!
Thalamus


Diencephalon
Divided by internal medullary lamina






Medial
Lateral
Anterior
Intralaminar nuclei
Midline thalamic nuclei
Thalamic reticular nucleus
3 chief functions
1.
Relay


2.
3.
Specific
Nonspecific (widely projecting)
Intralaminar
Reticular
Relay Nuclei




Lie mainly in lateral thalamus
All primary sensory modalities have relays in the lateral thalamus en
route to their specific cortical target, with one exception*
Reciprocal innervation w/ cortex
Examples:
Relay Nucleus
Lateral
Group
In
Out
Function
VPL
Medial lemniscus,
spinothalamic
Somatosensory cortex
Somatosensory spinal
input
*
VPM
Trigeminal lemniscus,
trigeminothalamic
tract, taste
Somatosensory
cortex, taste
Somatosensory CN input
and taste
*
LGN
Retina
Primary visual cortex
Vision
MGN
Inferior colliculus
Primary auditory
cortex
Audition
VL
Internal GP, deep
cerebellar nucleii, SN
(ParsR)
Motor, premotor and
supplementary motor
Relays BG and cerebellar
inputs to cortex
*
VA
SN (ParsR), internal
GP, deep cerebellar
nucleii
WIDESPREAD to
frontal lobe ->
prefrontal, premotor,
motor, supplementary
motor
Relays BG and cerebellar
inputs to cortex
***
Tectum
(extrageniculate visual
pathway), other
sensory input
P-T-O association
Behaviour orientation
toward relevant visual and
other stimuli
**
w/ anterior nuclei
**
w/ pulvinar
**
Maintain alert, conscious
state
***
Pulvinar
Lateral dorsal
Lateral
posterior
Ventral medial
Midbrain reticular
formation
Widespread to cortex
*
*
Relay
Nucleus
In
Out
Function
Medial group
Mediodorsal /
dorsomedial
Amygdala, olfactory
cortex, limbic cortex, BG
Frontal cortex
Limbic pathways, major relay
to frontal cortex
Mammillary bodies,
hippocampal formation
Cingulate gyrus
Limbic pathways
Amygdala, hippocampus,
limbic cortex
Limbic pathways
**
Anterior group
Anterior nucleus
*
Midline Thalamic group
Paraventricular,
parataenial,
intermediodorsal,
rhomboid, medial
ventral
Hypothalamus, basal
forebrain, amygdala,
hippocampus
**
Within the internal medullary lamina
Intralaminar
Nuclei
Rostral intralaminar nuclei;
central medial nucleus,
paracentral nucleus, central
lateral nucleus
Caudal intralaminar nuclei;
Centromedian nucleus,
parafascicular nucleus
Reticular
Nucleus
Reticular nucleus
Intralaminar
Nuclei
In
Out
Function
Rostral intralaminar nuclei;
Deep cerebellar nuclei,
GP, brainstem, ARAS,
sensory pathways
Cerebral cortex, striatum
Maintain alert consciousness;
motor relay for basal ganglia
and cerebellum
Caudal intralaminar nuclei;
GP, ARAS, sensory
pathways
Striatum, cereral cortex
Motor relay for BG
Cerebral cortex,
thalamic relay and
intralaminar nuclei,
ARAS
Thalamic relay and
intralaminar nuclei
central medial nucleus,
paracentral nucleus, central
lateral nucleus
Centromedian nucleus,
parafascicular nucleus
***
Reticular
Nucleus
Reticular nucleus
***
Regulates state of other
thalamic nuclei
Clinical Concept – dysfunction in
sensory pathways



Negative = anasthesia, loss of sensation
Positive = added sensation
Localizability of symptom description
“numb”
Victor and Adams
Central Disturbance & Other

Parietal lobe or primary SSC


Thalamic


LHermitte’s sign
Radicular



Dejerine-Roussy
Cervial cord


Contralateral numb tingling or pain
Symptoms (dermatomal) reproduced by maneuvers that stretch
or compress the NR
Spurling’s maneuver
Focal or diffuse pripheral n disease

Pain, numbness, tingling, etc…
Spinal Cord Lesions

Myelopathies



Etiology multifactorial



Compressive
Non-Compressive
VINDICATE, VITAMIN CD etc….
Most common causes = compressive due to trauma,
metasteses, degenerative changes
Clinically evident by sensory level, motor dysfunction,
reflex abnormalities, b/b incontinence, fever?


Image above sensory level (2-4 levels)
And even if you suspect LS pathology, try and get whole spine
imaged
Spinal Shock





Acute flaccid paralysis
Absent DTR
Hypotension
Sphincter / tone flaccidity
Rule of thumb = 80% of patients treated for CC
after they are nonambulatory remain so.
However, 80% treated before losing mobility,
remain so for the remainder of their lives.
Clinical Examples
Contra or ipsi, sensory loss, motor loss, other…

Primary somatosensory cortex






Primary vs “cortical” sensory loss
VPL or VPM or Thalamic somatosensory
radiations
Lateral Pons or lateral medulla
Medial medulla
SC
NR / Peripheral n.
Spinal Cord Syndromes

Transverse Cord Lesion
Brazis, Localization in
Clinical Neurology, 5th ed
Spinal Cord Syndromes

Brown-Séquard Syndrome
The Brown-Sequard
syndrome is
characteristically
produced by
extramedullary
lesions
Brazis, Localization in
Clinical Neurology, 5th ed
Spinal Cord Syndromes

Central Cord*
Typically due to Chiari type I and type II or Dandy-Walker
malformations, or as a late sequel to traumatic paraplegia
or tetraplegia, spinal trauma, spinal cord tumors,
arachnoiditis
Brazis, Localization in
Clinical Neurology, 5th ed
Syringomyelia

The classic presentation is a central cord syndrome
consisting of a dissociated sensory loss and
areflexic weakness in the upper limbs.

Loss of pain and temperature sensation with sparing of
touch and vibration in a distribution that is "suspended"
over the nape of the neck, shoulders, and upper arms
(cape distribution) or in the hands.

Begins asymmetrically with unilateral sensory loss in the hands
that leads to injuries and burns that are not appreciated by the
patient.
Syringomyelia


Muscle wasting in the lower neck, shoulders, arms, and hands
with asymmetric or absent reflexes in the arms reflects
expansion of the cavity into the gray matter of the cord.
As the cavity enlarges and further compresses the long tracts






Spasticity and weakness of the legs
Bladder and bowel dysfunction
Horner's syndrome
Facial numbness and sensory loss from damage to the descending
tract of the trigeminal nerve (C2 level or above).
In cases with Chiari malformations, cough-induced headache and
neck, arm, or facial pain are reported.
Extension of the syrinx into the medulla, syringobulbia, causes
palatal or vocal cord paralysis, dysarthria, horizontal or vertical
nystagmus, episodic dizziness, and tongue weakness.
Spinal Cord Syndromes

Central Cord & Sacral Sparing
http://www.neuroanatomy.wisc.edu/SClinic/Myelo/Myelbase.htm
Intramedullary and
Extramedullary Syndromes


Intramedullary vs Extramedullary processes
 Intra or external to cordcompresses the spinal cord or its
vascular supply.
The differentiating features are only relative and serve as clinical
guides.
 With extramedullary lesions, radicular pain is often prominent,
and there is early sacral sensory loss (lateral spinothalamic tract)
and spastic weakness in the legs (corticospinal tract) due to the
superficial location of leg fibers in the corticospinal tract.
 Intramedullary lesions tend to produce poorly localized burning
pain rather than radicular pain and spare sensation in the perineal
and sacral areas ("sacral sparing"), reflecting the laminated
configuration of the spinothalamic tract with sacral fibers
outermost; corticospinal tract signs appear later.
Spinal Cord Syndromes

Posterior & Postero-Lateral Cord
•SCD (cobalamin B12
deficiency)
•vacuolar myelopathy
associated with AIDS
• HTLV-1 associated
myelopathy (tropical spastic
paraparesis)
• extrinsic cord compression
(e.g., cervical spondylosis)
•copper deficiency myelopathy
Brazis, Localization in
Clinical Neurology, 5th ed
Spinal Cord Syndromes

Anterior Cord
Anterior Spinal Artery Syndrome
•Back of neck pain of sudden onset
•Rapidly progressive flaccid and areflexic
paraplegia
•Loss of pain and temperature to a sensory
level
•Preservation of JPS and vibration sensation
•Urinary incontinence
Brazis, Localization in
Clinical Neurology, 5th ed
The other “anterior cord” diseases
•Autosomal recessive spinal
muscular atrophies (I,II,III)
•Adult onset of spinal muscular
atrophy
•hexosaminidase deficiency
• poliomyelitis (postpolio
syndrome)
•postirradiation syndrome
Brazis, Localization in
Clinical Neurology, 5th ed
The other “anterior cord” diseases
•Degeneration of AHC (and in the motor
nuclei of the brainstem) and in the
corticospinal tracts.
•Progressive diffuse lower motor neuron
signs (progressive muscular atrophy,
paresis, and fasciculations) are
superimposed on the signs and symptoms
of upper motor neuron dysfunction
(paresis, spasticity, and extensor plantar
responses).
•Bulbar or pseudobulbar impairment
•explosive dysarthria, dysphagia,
emotional incontinence, and tongue
spasticity, atrophy, or weakness
•Bowel / bladder unaffected
•“Intact” mentation
Brazis, Localization in
Clinical Neurology, 5th ed
Anatomy of Bowel and Bladder
Function

Complex interplay between sensory, motor (voluntary and
involuntary) and autonomic pathways at multiple levels of the
nervous system


Frontal “micturition inhibiting area”, sensorimotor sphincter control
area, BG, vermis, pontine micturition center
S2-S4

Sensory (bladder, rectum, urethra, genetalia)





Ascends via posterior & anteralateral columns
Motor (AHC  pelvic floor, Onuf’s nucleus =sphincteromotor
nucleus  urethral and anal sphincters)
Parasympathetics  detrusor contraction
Sympathetics T11-L1 (inermediolateral cell column) detrusor
relaxation, bladder neck contraction
Need bilateral pathways involved to get clinical syndrome
Bladder Function
VOIDING
DETRUSOR REFLEX
1.
Voluntary
relaxation of EUS
2.
Inhibition if
sympathetics to
bladder neck
3.
Parasympathetic
activation for
detrusor
contraction
4.
Self-perpetuates
Bladder Function
STORAGE
URETHRAL REFLEX
1.
Voluntary
relaxation of EUS
2.
Inhibition if
sympathetics to
bladder neck
3.
Parasympathetic
activation for
detrusor
contraction
4.
Self-perpetuates
5.
When urine
stops, urethral
sphincters
contract
triggering
detrusor
relaxation
Summary
1.
The cerebral loop


2.


concerned with the voluntary control of the sphincters and pelvic floor
urethral afferents to pudendal motor neurons
maintains the sphincter tone when the detrusor is inactive
The detrusor reflex loop


5.
motor cortex to pudendal motor neurons
The urethral reflex loop

4.
initiates and inhibits switching between filling and voiding states
Corticospinal pathways

3.
involving the brainstem, cerebral cortex, and basal ganglia structures
detrusor afferents to pudendal motor neurons
sphincter relaxation when the detrusor is active
The cord loop


brainstem structures to the conus medullaris
coordinates detrusor and sphincter contraction and relaxation
Lesion Location & Clinical
Syndrome

Bilateral medial frontal lesion (parasaggital meningioma)


Removal of conscious control over sphincter/bladder, when to initiate/halt
voiding, with intact reflex arc
Below pontine micturition center, above conus




Interrupt pathways that are inhibitory to the detrusor and those that coordinate
normal sphincter-detrusor activity
Flaccid, acontractile evolves over wks to months
Reflex contraction of uretheral sphincterretention
Detrusor-sphincter dyssnergia; increased and uncoordinated, antagonistic


Examples: TM, MS, trauma
Peripheral nerves or S2-S4


Flaccid, areflexic resembling acontractile type
Overflow + stress incontinence


Eg. DB, conus or cauda lesion
Due to


Loss of parasympathetics
Loss of afferents from urethra and bladder
Bowel Function


Also mediated by medial frontal lobes
Players:





Internal smooth sphincter + GI motility
(parasympathetics)
External striated sphincter (Onuf)
Pelvic floor muscles (S2-S4 AHC)
Etiologies: damage at any level
Acute lesions flaccid sphincter and loss of
sacral PS  constipation
Take Home




DCML
ALS
Thalamus; specific relays
Somatosensory Cortex



Somatotopy!
Lesions localizable and recognizable
Imaging and paraclinical will help determine
etiology of lesion
References



Blumenfeld
Brazis
Pain articles:



Basic Science of Pain, J Bone Joint Surg
Am. 2006;88:58-62.
The Cerebral Signature of Pain and its
Modulation, Neuron, Aug 2nd, Vol 55, 2007
Cord Syndromes Website

http://www.neuroanatomy.wisc.edu/SClinic/My
elo/Myelbase.htm
Merci!
San Francisco, August 2009
Trivia Time
Split into 2 teams.
Scorekeeper needed.
Somatosensory Jeopardy
Multiple
Choice Q’s
The Thalamus
Somatotopy+
Cord
Syndromes 1
Miscellaneous
Points
1
Easy
Easy
2
Medium
Medium
3
Hard
Hard
Easy
Medium
Hard
Easy
Medium
Hard
Easy
Medium
Hard
MCQ 1

Name the different levels that pain
perception is modulated
a)
b)
c)
d)
e)
Peripheral
Spinal
Supraspinal
None of the above
All of the above (excluding choice D)
MCQ 2

Where does the 2nd order neuron in the
DCML system take off from, if I were to
touch my toe?
a)
b)
c)
d)
e)
Clarke’s nucleus
Intermediolateral cell column
Thalamus
Rexed lamina II
Nucleus gracilis
MCQ 3

At which layer in the cerebral neocortex
do most afferents terminate in?
1.
2.
3.
4.
5.
II
III
IV
VI
V
Thalamus 1

What is the broad classification scheme for
thalamic projections?
Thalamus 2

Where does the pulvinar project to?

Bonus

In what condition can we see the “pulvinar sign”
on MRI?
Thalamus 3

Name 5 specific relay nuclei
Somatotopy 1
Place on
schema:
Cervical
Thoracic
Lumbar
Sacral
Somatotopy 2

Which pathway in the ALS convey’s the
emotional and arousal aspects of pain?
Somatotopy 3

What “built-in” system is heavily involved
in intrinsic pain modulation?

Name 4 key players involved in pain control
Cord Syndromes 1





24 yo F, followed in psychiatry for schizoaffective d/o
3 mo Hx “walking on clouds”, can’t feel soles
Mild weakness in LE’s
Impaired JPS, Vib
+ Romberg sign


Where is the lesion?
Ddx?
Cord Syndromes 2



36 yo F, complaining of not feeling the tips of her fingers,
accidentally closed car door on hands several times. Also mentions
some bladder urgency, and incontinence.
On exam: atrophy of neck muscles / scapular girdle and arms,
asymmetrically hyporeflexic UE, spastic catch on R biceps, R
Horner’s syndrome
Where would you place the lesion ?
Sensory exam:
What segment to image first?
How do you explain the Horner’s?
How about the mixed UMN and LMN
syndrome?
Name 4 conditions this can occur in?
Cord Syndromes 3



28 yo M
Complaining of L sided weakness, bladder
fullness – inability to void. O/E brisk DTR’s
on L HB, L sided spacticity
Sensory exam shows to PP/T:
Pathology is 2-3 segments above or
below clinical sensory level?
Intra or extramedullary based on
findings?
Miscellaneous 1




63 yo M
HTN/DB/DLPD
Awoke yesterday with patchy numbness to R
face, hands, feet
O/E




R HB decreased sensation
No weakness appreciated
Reflexes 2+ symmetric UE, LE
Plantars flexor
Where could you propose one lesion to
account for these symptoms? Etiology?
L
VPL
Miscellaneous 2



At what level is Onuf’s nucleus?
What is it’s function?
Bonus: On a completely unrelated
question

Where is the internal arcuate fibers?
Miscellaneous 3








76 F
OA/ Cx and Lx DDD/HTN/DB
Complains of weakness in hands > legs x 2/12
Clumsy hands
Progressive
“zinging” down spine when flexes head forward
Urinary frequency / some urge incontinence
O/E






Decreased PP/T on L from T4 distally
Decreased ST on R T2 distally
Spastic catch R elbow
Mild pyramidal weakness RUE
FDI, hand intrinsic atrophy+
Extensor plantar on R, diffusely brisk DTR’s on R HB
What segment of the CNS would you image?
What do you think is the pathophysiology?

Spondylotic myelopathy