the somatosensory system ch7 blumenfield by: laurence poliquin-lasnier r2 neurology

The Somatosensory SystemCH7 Blumenfield

By: Laurence Poliquin-Lasnier

R2 neurology

Outline

• Sensory neuron• Main somatosensory pathways

– Posterior column-medial lemniscus– Spinothalamic tract

• Somatosensory cortex• Central modulation of pain• Thalamus• Spinal cord syndromes• Bladder, bowel and sexual function

Main somatosensory pathways

• Posterior column-medial lemniscus– Proprioception, vibration, fine

discriminative touch

• Spinothalamic tract– Pain, temperature, crude touch

• Via unipolar sensory neuron

Unipolar sensory neuron

Sensory neuron fiber types

NameDiameter (µm)

Myelinated Receptors Sensory mdality

A- (I) 13-20 Yes Muscle spindle, golgi tendon organ Proprioception

A-β (II) 6-12 Yes

Muscle spindle Proprioception,

Meissner’s corpuscule Superficial touch

Merkel’s receptor Superficial touch

Pacinian corpuscule Deep touch, vibration

Ruffini endings Deep touch, vibration

Hair receptor Touch, vibration

A-δ (III) 1-5 Yes Bare nerve ending Pain, temperature (cool)

C (IV) 0.2-1.5 No Bare nerve ending Pain, temperature (warm), itch

Sensory neuron

• Sensory neuron cell body located in dorsal root ganglia

• A peripheral region innervated by sensory fibers from a single nerve root = dermatome

Outline




Posterior column-Medial lemniscus


• Large myelinated axons

• Proprioception, vibration, fine touch


Ascend through:• Gracile Fasciculus: legs + lower trunk• Cuneate Fasciculus: arms, neck, trunk above

T6• 1st order sensory neuron synapses synapse

onto 2nd order neurons in the nucleus gracilis and nucleus cuneatus at th level of the medulla

• Axons of these 2nd order neurons decussate as internal arcuate fibers and form the medial lemniscus on the other side of the medulla


• 2nd order neurons synapse into the ventral posterior lateral (VPL) nucleus of the thalamus

• 3rd order neurons then project to the posterior limb of the internal capsule to reach the primary somatosensory cortex in the post-central gyrus

Sensory homunculus

Outline




Spinothalamic tract

SpinothalamicTract

• Small diameter• Unmyelinated• Pain and

temperature

Spinothalamic tract

• Enter spinal cord via dorsal root ganglia• 1st order neuron synapse in the grey matter of the

dorsal horn marginal zone (lamina1) and deeper in the dorsal horn (lamina 5)

• Some axon collaterals ascend or descend for a few segments in lissauer tract before entering the central gray

• 2nd order neuron cross over in the spinal cord anterior commissure to ascend in the anterolateral white matter

• It takes 2-3 spinal segments for the decussating fibers to reach the opposite side ( so sensory level of spinal cord lesion starts a few levels below the lesion)

Spinothalamic tract

• Anterolateral pathway reaches medulla• Run between the olives and the inferior

cerebellar peduncles• Enters pontine tegmentum• 2nd order neuron synapses in the thalamus to 3rd

order neuron• 3rd order neuron to somatosensory cortex in the

postcentral gyrus• Secondary somatosensory association cortex in

parietal operculum (somatotopic organization) and association area in posterior parietal lobule

Anterolateral pathway: 3 tracts

• Spinothalamic (I, V)– Discriminative aspects of pain, location, intensity– Synapse on VPL (different area than DCML),

relay to specific SSC target (Brodmann 3,1,2)• Spinoreticular (VI, VII, VIII)

– Emotional and arousal aspects of pain– Reticular formation projects to intralaminar

thalamic nuclei (centromedian), which then project diffusely to the entire cerebral cortex (behavioural arousal)

• Spinomesencephalic (I, V)– To periaqueductal grey and superior colliculi– Pain modulation

Outline




Central modulation of pain

• Gate control theory• Sensory input from large diameter non pain A-β fibers

reduce pain transmission through the dorsal horn• Periaqueductal gray receives input from: hypothalamus,

amygdala, cortex• Inhibits pain transmission in the dorsal horn via relay in

rostral ventral medulla (RVM)• RVM includes serotonergic neurons of the raphe nuclei

that project to the spinal cord and modulate pain• RVM sends input (via substance P) to the locus

ceruleus to spinal cord dorsal horn (via NE)

Central modulation of pain

• Opiate receptors and endogenous opiate peptides located at key points in the pain modulatory pathways– Enkephalin and dynorphin -> PAG,

RVM, dorsal column – β-endorphin -> hypothalamus

Outline




Thalamus

• Major sensory relay station• Deep gray matter structure part of the

diencephalon• Convey different types of input to the

cortex– Sensory– Motor from cerebellum and basal ganglia– Limbic– Modulatory inputs involved in aroual and

sleep-wake cycle

Thalamus

• Divided by internal medullary lamina (a Y shaped structure) into:– Medial nuclear group– Lateral nuclear group– Anterior nuclear group

• Nuclei within internal medulary lamina called intralaminar nuclei

Thalamus

Thalamus

• 3 categories of nuclei:– Relay nuclei– Intralaminar nuclei– Reticular nucleus

Thalamus: 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 -> olfaction

• Reciprocal innervation w/ cortex

Thalamus: Relay nuclei -> Lateral nuclear group

Relay Nucleus 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

Pulvinar Tectum (extrageniculate visual pathway), other sensory input

P-T-O association Behaviour orientation toward relevant visual and other stimuli

Lateral dorsal w/ anterior nuclei

Lateral posterior

w/ pulvinar

Ventral medial Midbrain reticular formation

Widespread to cortex Maintain alert, conscious state

Thalamus: Relay nuclei -> other groups

Relay Nucleus IN Out Function

Medial group

Mediodorsal/dorsomedial

Amgdala, olfactory cortex, limbic cortex, BG

Frontal cortex Limbic pathways, major relay to frontal cortex

Anterior group

Anterior nucleus Mammilary bodies, hippocampal formation

Cingulate gyrus Limbic pathways

Midline thalamic group

Paraventricular, paratenial, intermediodorsal, rhomboid, medial ventral

Hypothalamus, basal forebrain, amygdala, hippocampus

Amygdala, hippocampus, limbic cortex

Limbic pathways

Thalamus

In Out Function

Intralaminar nuclei (within internal medullary lamina)

1) Rostral intralaminar nuclei:Central medial nucleus, paracentral nucleus, central lateral nucleus

Deep cerebellar nuclei, GP, brainstem, ARAS, sensory pathways

Cerebral cortex, striatum

Alert consciousness, motor relay for BG and cerebellum

2) Caudal intralaminar nuclei: Centromedian nucleus, parafascicular nucleus

GP, ARAS, sensory pathways

Cerebral cortex, striatum

Motor relay for BG

Reticular nucleus(only one not projecting to cortex)

Cerebral cortex, thalamic relay and intralaminar nuclei, ARAS

Thalamic relay and intralaminar nuclei

Regulates state of other thalamic nuclei

Clinical concept: dysfunction in pain pathways

• Negative symptom = sensory loss• Positive symptoms = paresthesias =

added sensation• Dysesthesia = unpleasant abnormal

sensation• Allodynia = painful sensation provoked by

minor stimulus eg.: light touch• Posterior column: tingling, numb, tight

band, walking on clouds• Anterolateral: sharp, burning pain

Outline




Spinal cord lesions

Spinal shock:• Flaccid paralysis below the lesion• Loss of DTR• Autonomic dysfunction

– Decreased sympathetic outflow to vascular smooth muscles -> Hypotension

– Absent sphincter tone• Over weeks to months, spasticity and UMN signs

develop

Cord compression:• If non-ambulatory at tx, 80% remain so• If ambulatory at tx, 80% will remain mobile

Sensory loss: patterns and localization

• Primary somatosensory cortex– Contralateral face, arm, leg, trunk– Two point discrimination, extinction, stereognosis,

graphestesia• Thalamus (VPL or VPL)

– Contralateral face, arm, leg, trunk– Relative preservation of cortical features

• Lateral pons and medulla• Pain and temperature• Ipsi face and contra hemibody

• Medial medulla– Medial lemniscus = vibration, position sense

Spinal cord syndromes

• Transverse cord syndrome

• Sensory level with loss of all sensory modalities

• DDx: trauma, tumor, MS, transverse myelitis


• Hemicord syndrome• “Brown-Sequard”• Damage to lateral

corticospinal tract = ipsi UMN weakness

• Damage to post. column = ipsi loss of vibration and position sense

• Damage to anterolateral system = contra pain and temperature• May have a strip of 1-2 segments of ipsi loss of pain and temp caused by damage to post horn cell before their axons have crossed over


• Central cord syndrome• Suspended sensory loss to pain and temp• Cape-like pattern if cervical cord• Suspended dermatomes if at other level• LMN deficit if damage to anterior horn cells


• May get sacral sparing as spinothalamic tract = more medial cervical region and more lateral sacral region

• Causes of central cord syndrome:• Spinal cord contusion, post-traumatic

syringomyelia, intrinsic spinal cord tumor


• Posterior cord syndrome• Loss of vibration and position

sense below the lesion• May get UMN weakness if it

encroaches lateral corticospinal tract

• Causes: trauma, extrinsic compression, MS, Vitamin B12 deficiency, tabes dorsalis (tertiary syphilis), HTLV-1


• Anterior cord syndrome• Damage to anterolateral

pathway = loss of pain and temp below lesion

• Damage to anterior horn cell may produce LMN weakness at the level of the lesion

• If larger lesion, corticospinal tract involved -> UMN weakness

Spinal cord syndrome

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

Outline




Anatomy of bowel, bladder and sexual 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, genitalia)• Ascends via posterior & anterolateral columns

– Motor• ant. horn cell pelvic floor• Onuf’s nucleus =sphincteromotor nucleus urethral and

anal sphincters contraction– Parasympathetics detrusor contraction

• Sympathetics T11-L1 (intermediolateral cell column) detrusor relaxation, bladder neck contraction

• Need bilateral pathways involved to get clinical syndrome

Bladder function: detrusor reflex (voiding) and urethral reflex (storage)

1. Voluntary relaxation of external urethral sphincter

2. Inhibition of sympathetics to bladder neck (relaxes)

3. Parasympathetic activation for detrusor (dome) contraction

4. Self-perpetuate as long as urine flows

5. When urine stops, , urethral sphincters contract triggering detrusor relaxation

Detrusor reflex mediated by intrinsic spinal cord circuits, pontine micturition center, cerebellar and BG pathways

Incontinence

• Lesions affecting bilateral medial frontal micturition centers result in reflex activation of pontine and spinal micturition centers when the bladder is full

• Normal emptying but not under voluntary control

• Causes of frontal type incontinence: hydrocephalus, parasagittal meningioma, traumatic brain injury, neurodegenerative disorders

Incontinence

• Lesion below pontine micturition center but above conus (S2-S4)– Flaccid, acontractile (atonic) bladder -

>retention– Evolves over months into hyperreflexic spastic

bladder -> retention 2ary dyssynergia and feeling of urgency 2ary reflex bladder contractions

• Peripheral nerve lesion or lesion at S2-S4– Flaccid atonic bladder ->overflow incontinence– Loss of parasympathetic outflow to detrusor or

loss of afferent sensory information

Bowel function

• Also mediated by medial frontal lobes• 3 components:

– Internal smooth muscle sphincter + GI motility (parasympathetics)

– External striated sphincter (Onuf)– Pelvic floor muscles (S2-S4 anterior horn

cells)• Etiologies: damage at any level• Acute lesions flaccid sphincter and loss

of sacral PS constipation

Sexual function

• Sensation from genitalia -> S2-S4 via pudendal nerve

• Female:– Parasympathetic: lubricating mucus from

bartholin gland– Sympathetic: vaginal blood flow, secretions

• Male:– Both sympa and parasympa control erection– Sympa = ejaculation

Summary

• Sensory neuron: unipolar• Main somatosensory pathways

– Posterior column-medial lemniscus (vib, position, fine touch)

– Spinothalamic tract (pain and temp)• Somatosensory cortex: somatotopic• Central modulation of pain• Thalamus

– Relay nuclei– Intralaminar nuclei– Reticular nucleus

• Spinal cord syndromes• Bladder, bowel and sexual function

the somatosensory system ch7 blumenfield by: laurence poliquin-lasnier r2 neurology

Documents

unipolar sensory neuron

spinothalamic tract

temperature slide

sensory homunculus slide

medulla slide

fine touch slide

dermatome slide

itch slide