C-Fibers & Touch

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OverviewModelIon ChannelsMemory | C-Fibers & Touch | Mysteries

The issue of peripheral or sensory neuropathy is bound up in the question of touch. Touch is the least explored of our special senses. As an introduction to the issues raised here, it is worth reading Touch – The Science of Hand, Heart, and Mind by David J. Linden (2015).

Touch by David J Linden

The notes here are taken from this book.

The degree to which touch is entangled with our emotions is written into the language – we say some people are ‘tactless’, their touch is poor, they have no feel for the issues or the people.

Even more than is the case with other senses, by the time we perceive touch it has been blended with other sensory input, plans for action, expectations and emotion. And touch exists within a social context – who is touching us and when, will shape whether a given touch will feel emotionally positive or negative.

Our skin is a social organ, responsive to social touch, probably in order to promote trust and cooperation.

The mechanics of touch

Different sensors in the skin are tuned to extract different aspects of information from the tactile world. Information converges from skin to brain through:

  • Serial Processing in the brain extracts increasingly complex touch information.
  • Parallel Processing segregates complex touch information into different streams for action.

Glabrous vs. hairy skin

The body contains both hairy and non-hairy (glabrous) skin. Even skin which would often be thought of as smooth and non-hairy often contains tiny hairs. The only true glabrous skin is found on the palms of the hands, inner sides of the fingers, soles of the feet, lips, nipples and parts of the genitals.

Mechanoreceptors

Glabrous skin contains four different sensors that respond to mechanical pressure for fine manipulation of objects. Two of these are in the shallowest parts of the dermis, while the other two are located deeper. Two send signals only at the beginning and end of a touch stimulus, while the other two provide continuous information throughout the stimulus.

Meissner’s Corpuscle
(Shallow. Brief signal)
Low-frequency vibration, grip control.

Merkel Disk Receptor
(Shallow. Persistent signal)
Edges of objects, form and texture. High density in lips and fingertips. Low density on other glabrous regions. Very low density on hairy skin.

Pacinian Corpuscle
(Deep. Brief signal)
High-frequency vibration, remote sensation through tools.

Ruffini Ending
(Deep. Persistent signal)
Skin stretching

Meissner’s Corpuscles and Merkel Disks decrease with age, reducing our spatial acuity.

A-fibers & C-fibers

A-fibers and C-fibers offer two touch systems that work together, each influencing the other. Between them they allow powerful multisensory and emotional modulation relating to situational and social contexts. This is why the same touch from a stranger ‘feels’ different to the touch of a partner.

Hair deflection can give rise to multiple sensations – fast discriminative emotionally neutral signal (A-beta, A-delta) and slow diffuse, pleasant signal (C-tactile).

C-tactile fibers function as caress detectors that innervate the hairy skin and project through a pathway to the posterior insula and areas of the cortex involved in social cognition (the superior temporal sulcus, medial prefrontal cortex and anterior cingulate cortex).

The posterior insula has been implicated in emotional processing within the brain. It also receives highly processed visual information.

Note: Adults with autism have an aversion to certain social touch. They rate caress as less pleasant compared to control – the more severe the illness, the less the activation of the social control centers.

A-fibers

  • Large myelinated – fast signals
  • Deliver factual aspects of touch
  • A-alpha: Very fast information from sensors in muscles, joints, tendons. Help form an image of where you are in space ie. proprioception.
  • A-beta: Fast signals from Merkels and Meissners allow for fine tactile discrimination. Correlations between intensity of stimuli and response strength.
  • A-delta: Smaller and less myelinated, therefore medium speed signals – pain and temperature sensations.

C-fibers

  • Small unmyelinated – slow signals
  • Designed to integrate information slowly and to discern emotional tone of touch.
  • Some pain and temperature sensations
  • A particular type of C-fiber called C-tactile fibers appear to be tuned for interpersonal touch ie. ‘caress sensors’. They are only found in hairy skin – wrapped around hair follicles. They react to an optimal intensity/speed of stimuli.

Sexual touch

Context is key to sensory experience ie. there is a difference between sensation and perception. If there is a mismatch between our expectation and the sensation itself, this creates a sense that something is ‘at odds’ and therefore our perception of that sensation is altered.

Although glabrous skin eg. lips and fingertips has a high density of mechanoreceptors, the glans and clitoris have very few. However, they have a high density of free nerve endings which transduce temperature, pain and inflammation. They also have specialized genital end bulbs or mucocutaneous end-organs (a coiled axon wrapped by non-neuronal encapsulating cells). The pathway of electrical signals from these genital end bulbs to the spinal cord and brain is still unknown.

Nerves

Touch sensation from the genital region passes through three different nerves (four inc. vagus) on the way to the spinal cord and brain, and each nerve can carry information from several different parts of the genital region ie. convergence and divergence of touch signals.

  • Pudendal nerve – most important for sexual sensation
  • Pelvic nerve
  • Hypogastric nerve
  • Vagus nerve (direct to brain stem, bypassing spinal cord)

Touch signals from the pelvis are carried to the brain along different pathways in the spine and brain stem depending on touch modality (fine discriminative, caress, temp, etc).

Like other areas of the body, the pelvis tactile signals form a relay connection in the thalamus, then the neocortex, and are represented in the primary somatosensory region.

Orgasm

  1. Unique experience – not just an intense form of touch sensation.
  2. Most reliable way of achieving (but not the only way) is touch signals from genital stimulation carried through sensory nerves to the spinal cord and brain.
  3. Orgasm occurs in the brain, not the genitals.

Touch signals from all four nerve sources can contribute to orgasm.

Brain circuitry

Based on the results of brain scans, orgasm contains the following neurological features:

  • Activation of touch sense from genitals (somatosensory cortex)
  • Deactivation of fear/vigilance (amygdala)
  • Activation of pleasure circuit (ventral tegmental area – responsible for ‘pleasurable’ emotional feeling, nucleus accumbens and dorsal stratum.
  • Activation of motor control center (cerebellar nuclei)
  • Deactivation of areas involved in ‘slow decision making’ (lateral orbitofrontal cortex and anterior temporal pole).

The discriminative sense of genital touch is mediated by activation of the somatosensory cortex, but this is not pleasurable in itself. Pleasurable emotional feeling is produced only when the ventral tegmental area dopamine neurons are activated.

Individual variation in sexual sensation

While sexual sensation is broadly the same in every person, it has been speculated that there may be subtle differences which might account for individual variation in preferred sexual activities. Discussion has centered around:

  • Minor differences in the fine structure of the nerves in different parts of the genital region.
  • Variation in the parts of the brain that are activated by sexual touch.
  • Difference in the electrical or chemical signaling of the neuron.
  • Difference in the properties of ion channels or neurotransmitter receptors affecting the function of the neurons involved in the sexual touch circuit.

Persistent Genital Arousal Disorder (PGAD)

Persistent Genital Arousal Disorder (PGAD) can cause a genital response in the absence of sexual desire. There is no single well-defined cause of PGAD and it isn’t known whether there are changes in nerve endings in the skin of the genital region. Various causes have been reported:

  • Entrapment of pudendal or pelvic nerve
  • Vascular problem relating to blood flow to pelvis
  • Tarlov cyst on dorsal root ganglia
  • Medication

Pain and emotion

Pain is transmitted in two stages resulting from the different speeds at which the nerve fibers convey their signals.

  • Primary pain from A-beta & A-delta fibers is fast and discriminative. It elicits an immediate withdrawal response.
  • Secondary pain from C-fibers is slower and poorly localised. It elicits a demand for attention (prevention of further injury).

There are three main categories of pain sensor:

  1. Mechanical
  2. Thermal
  3. Polymodal

When tissue is injured, a number of actions occur:

  • Damaged cells release compounds called prostanoids, which affect TRVP1 recptors on the endings of C-type pain fibers.
  • They can also activate white blood cells like mast cells and macrophages, causing them to release bradykinin – this reduces the temperature threshold of TRPV1.
  • Macrophages also release other compounds like the proteins TNF-alpha and NGF, which sensitize C-type pain fibers.
  • Activated mast cells release histamine which targets blood vessels to dilate them and make them slightly porous to blood plasma (hence redness/swelling).
  • C-fibers also signal back on a positive feedback loop.

Helpful for pain

  • Aspirin / ibuprofen – inhibits production of prostanoids.
  • Antihistamine – blocks action of histamine on receptors of nerve terminals and blood vessels.
  • Rheumatoid arthritis medications interfere with TNF-alpha signalling.
  • Drugs for persistent pain that disrupt the action of NGF are being tested.
  • Compounds extracted from pineapple and aloe can interfere with the action of bradykinin.

Factors affecting perception of pain

  • Cognitive and emotional factors can dull or heighten pain perception.
  • There is an overlap in the brain’s emotional pain circuitry in response to social rejection and physical pain.
  • Fight / flight
  • Expectation / anticipation can heighten pain
  • Feedback loop ie. negative emotion enhances the perception of pain, which then feeds negative thoughts and anxiety about the pain.

Interventions that might help break the cycle (primarily through reducing anxiety):

  • Benzodiazepines
  • Mindfulness meditation
  • Naltrexone – blocks ‘mu-opioid’ receptors

Persistent pain

This is produced by changes to endings of pain sensing fibers and alterations at synapses in the spinal cord (where these fibers contact neurons of the spinal dorsal horn).

Glutamate is involved in the propagation of pain signals through the spinal cord. When synapses are repeatedly stimulated, as with persisting pain, they become stronger and more efficient. These changes in the spinal cord can endure for months or years, like memories, even when the inflammatory response and nerve endings have returned to normal – ie. chronic pain.

Itch

There are a number of itch triggers, one of which is histamine. It has been speculated that itch might be a unique form of touch sensation, rather than just a particular type of pain. Experiments with genetically engineered mice have implicated NPPB and MrgprA3 as neurons that might be dedicated to the processing of itch sensation, though there may also be others.