Somatosensory Systems Flashcards
Function of Somatosensory systems
Transmits and processes sensory input/information
Overview of functions
-Cutaneous sensation of touch (discriminating and non-discriminating) from physical contact
-Position sense (proprioception) and movement sense (kinethesis) of the body
-Temperature from objects and the external environment
-Pain (nociception); also many other sensations including: itch, tickle, specific chemical
Receptors & their associated afferent nerves
Cell bodies often in dorsal root ganglion (DRG)
Spinal cord
-Dorsal horn (gray matter)
-Tracts (dorsal columns, spinothalamic tract, spinocerebellar tract, etc.)
Brainstem
Decussation and tracts
Cerebellum
Proprioceptive feedback
Diencephalon
-Thalamus (VPL,VPM, VMpo): primary target of most somatosensory information
-Hypothalamus
Cerebral cortex
Primary & secondary somatosensory areas; insula, cingulate cortex)
Dorsal column/ Medial lemniscus Pathway
Touch (discriminatory), vibration, conscious proprioception from the body
Receptors (via DRG)→dorsal columns→synapse in dorsal column nuclei (brainstem) →fibers decussate & pass through medial lemniscus→VPL (thalamus) →somatosensory cortex
Where do the receptors enter ?
Enter spinal cord near dorsal horn (Lissauer’s tract)
Axons have somatotopic arrangement
- information from the highest spinal level is furthest lateral
- information from the lowest spinal levels in most medial
Fasciculus gracilis in dorsal columns
- from LE (below T6)
- more medial
Fasciculus cuneatus in dorsal columns
- from UE (rostral to T6)
- more lateral
Primary somatosensory cortex (S1)
In postcentral gyrus of parietal lobe
▪ primarily function in localization and discriminatory touch
➢ also conscious propriocetion
▪ somatopically organized
➢ medial to lateral: LE, UE, face
➢ sensory homunculus
Secondary somatosensory cortex (S2)
Primarily functions in texture & roughness
What can result from internal capsule damage?
MS, lacunar stroke, or others
Tabes dorsalis
Damage to dorsal column in late stage neurosyphilis
Friedrich ataxia
➢ degeneration of DRG neurons (and their axons)
➢ damages more than dorsal columns [also corticospinal tract (motor), dorsal spinocerebellar tract (proprioception)]
Is touch destroyed with a loss of complex discrimination?
No, but it is impaired.
You know something is happening (can probably localize stimuli)
Asterognosis
➢ unable to recognize patterns drawn on the skin
➢ unable to recognize object place on skin
➢ unable to recognize objects by manipulation
Sensory ataxia
loss (usually total) of conscious proprioception and kinesthesia
results in:
-steppage gait: high stepping & slapping feet due to loss of proprioception
-Romberg’s sign: sway and fall with eyes closed
Trigeminal nerve (CN V) Pathway
Touch (discriminatory), vibration, conscious proprioception from the face
Receptors (via DRG)→brainstem at mid-pons→synapse in main sensory bucleus of trigeminal nerve →fibers decussate & join medial lemniscus→VPM (thalamus) →somatosensory cortex
Dorsal trigeminal tract
An uncrossed pathway that carries some information
from the inside of the mouth; this info ends up on the same side of the brain as gustatory (taste)
info (gustatory info is also uncrossed)
Pain vs Nociception
-Pain: “An unpleasant sensory and emotional experience associated with actual or potential
tissue damage, or described in terms of such damage” (International Association for the
Study of Pain) {emphasis mine}
-Nociception: “Encoding and processing of harmful (or potentially harmful) stimuli”
▪ in other words – pain is an emotion, while the term nociception is separate from the
emotional aspects of tissue damage (affect)
Two primary spinothalamic pathways: Lateral STT & Anterior STT
-Separate pathways as they pass through the spinal white matter
▪ lateral STT is larger & contains more afferents
➢ classic pain & temperature pathway
▪ anterior STT carries crude touch & deep pressure
-Merge at the brainstem as they adjoin the medial lemniscus
Nociceptors
-Small diameter fibers with moderate (Aδ) or no (C) myelin
▪ Aδ fibers - ‘fast pain’ (pricking, stabbing, bright)
▪ C fibers – ‘slow pain’ (aching, throbbing, etc)
-Specific receptors respond to mechanical (including blood vessel distention, affective touch, itch, tickle), specific chemicals (capscacian, acids, CO2, etc), temperature (specific ranges); and combinations of these (polymodal)
▪ some hypothesized as ergoreceptors (sense energy utilization)
Pain & Temperature (Homeostatic) Sensation from the BODY
Nociceptors–>SC through Lissauer’s tract–>synapse Lamina I (superficial dorsal horn)–>Decussate immediately (origin) + travel in CL Lateral Spinothalamic tract–>Synapse in posterior part of Ventral medial nucleus of the thalamus (VMpo)—>Posterior insula
Pain & Temperature (Homeostatic) Sensation from the FACE
Nociceptors–> CNS through pons via trigeminal nerve (CN V)–> synapse in Ipsilat. spinal nucleus of trigeminal nerve–>Decussate immediately joining CL STT–>synapse in VMpo–>middle insular cortex
Spinoretucular
to reticular formation in brainstem
arousal/alertness caused by pain stimuli
Spinomesencephalic
to PAG (periaqueductal gray….and eventually amygdala)
descending pain modulation
ANS response to painful stimuli
Spinohypothalamic
to hypothalamus
ANS response to painful stimuli
Spinotectal
to superior colliculus
orienting/turning of eyes toward painful stimulus
Allodynia
Previously innocuous stimuli now painful (sensitization)
dysesthesis = unpleasant, abnormal sensation
Hyperglesia
Increased pain (to previous mild painful stimuli)
Analgesia
Loss/reduction of pain sensation
Anesthesia
Loss of sensation
Hypesthesia
Partial loss of touch sensation
Hyperesthesia
Increased touch sensitivity
Centralmodulation
Suppression of pain by descending signals (from PAG and rostral medulla)
Opiates
Increase activity of (particularly) PAG & rostral medulla and dorsal horn
Endogenous opiates
enkephalins, endorphins, dynorphin
▪ made in response to exercise and stress
Exogenous opiates
morphine, heroin, etc
▪ issues with habituation and addiction
Damage to lateral STT system
Trigeminal neuralgia (tic doulourex)
-facial pain syndrome (may be severe)
-thought to be caused by vascular compression leading to demyelination
-affects V2 & V3
-almost always unilateral
Damage to lateral STT system
Anterior cord lesion
-e.g., from damage to anterior spinal artery
-spares dorsal horns & Lisseur’s tracts, but…
-destroys STT (lateral & anterior)
a loss of all pain & temperature caudal to injury
-also destroys many other tracts & ventral horn neurons – so will discuss later
Damage to lateral STT system
Brown-Sequard syndrome
-cord hemisection
-destroys STT (lateral & anterior) on one side
loss of all pain & temp on contralateral side, caudal to injury
-also destroys many other tracts as well as the neurons in the spinal gray matter
3 primary pathways for Proprioception/Kinesthetic Sensory Pathways (unconscious)
Posterior Spinocerebellar Tract (from LE)
Anterior Spinocerebellar Tract (from LE)
Cuneocerebellar Tract (from UE)
Post SCT
Origin: Clarke’s nucleus (T1-L2/3)
Body Region: LE
Major inputs: Mechanoreceptors in muscles, joints, & skin
Midline crossing: None
Peduncle used to enter cerebellum: Inferior
End Target: Vermis
Ant SCT
Origin: Spinal border cells (T12-L5)
Body Region: LE
Major inputs: Mechanoreceptors, movement related interneurons
Midline crossing: Two: one in cord, again in cerebellum
Peduncle used to enter cerebellum: Superior
End target: ?
Cuneocerebellar
Origin: Lateral cuneate nucleus (medulla)
Body Region: UE
Major inputs: Mechanoreceptors in muscles, joints, & skin
Midline crossing: None
Peduncle used to enter cerebellum: Inferior
End Target: vermis
Muscle spindles
Long, thin stretch receptors inside skeletal muscle
▪ sensitive to length and rate of muscle stretch
▪ collection/bundle of intrafusal muscle fibers
▪ as opposed to extrafusal
▪ which are the larger & much more common fibers that generate force/torque to move & control limbs
Muscle spindles are composed of 2 types of intrafusal fibers
Both types have a central, non-contractile region where most receptors are found
▪ nuclear chain fibers
➢ thinner
▪ nuclear bag fibers
➢ have swelling at center
Primary endings (annulospiral)
Wrap around central region
➢ sense onset of stretch; rate of stretch
➢ have lower tonic discharge
▪ rapidly adapting
➢ are Type Ia fibers
▪ larger, faster
Secondary endings (flowerspray)
Found at either side of central regions
➢ less sensitive to changes in stretch, stronger response to continuing stretch = length
▪ slowly adapting, tonic
➢ are Type II fibers
▪ smaller, slightly slower conduction speed
Motor stimulation to muscle spindles, what needs to happen?
If spindles do not contract with the extrafusal fibers, the spindles will be unable to sense stretch in a contracted muscle
Spindles have their own motor neurons in spinal cord, what are they?
gamma motor neurons
* (actually two types: one for chain/another for bag; but who cares?)
* note that alpha motor neurons control extrafusal fibers
▪ match intrafusal & extrafusal contraction
Golgi tendon organs (GTOs)
sense muscle tension/torque
▪ very sensitive
▪ can respond to contraction of just a few muscle fibers
similar to Ruffini endings
found at junction of muscle and tendon
Joint receptors
Pacinian, Ruffini, & Golgi tendon organs
Sense joint position and movement
Usually tonic
