Brain mechanism of Touch & Pain

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Touch is special – a handshake, a kiss, a baptism.  It provides our first contact with the world.  Arrays of receptors throughout our bodies are tuned to different aspects of the somatosensory world – touch, temperature and body position – with yet others for the sensations of pain. 

The power of discrimination varies across the body surface, being exquisitely sensitive at places such as the tips of our fingers.  Active exploration is important as well, pointing to important interactions with the motor system.  Pain serves to inform and to warn us of damage to our bodies.  It has a strong emotional impact, and is subject to powerful controls within the body and brain.

Brain mechanism of Touch & Pain

It begins in the skin

Embedded in the dermal layers of the skin, beneath the surface, are several types of tiny receptors.  Named after the scientists who first identified them in the microscope, Pacinian and Meissner corpuscles, Merkel’s disks and Ruffini endings sense different aspects of touch.  All these receptors have ion channels that open in response to mechanical deformation, triggering action potentials that can be recorded experimentally by fine electrodes. 

Some amazing experiments were conducted some years ago by scientists who experimented on themselves, by inserting electrodes into their own skin to record from single sensory nerves.  From these and similar experiments in anaesthetised animals, we now know that the first two types of receptor adapt quickly and so respond best to rapidly changing indentations (sense of vibration and flutter), Merkel’s disk responds well to a sustained indentation of the skin (sense of pressure), while Ruffini endings respond to slowly changing indentations.

An important concept about somatosensory receptors is that of the receptive field.  This is the area of skin over which each individual receptor responds.  Pacinian corpuscles have much larger receptive fields than Meissner’s corpuscles. Together, these and the other receptors ensure that you can feel things over your entire body surface.  Once they detect a stimulus, the receptors in turn send impulses along the sensory nerves that enter the dorsal roots of the spinal cord.

The axons connecting touch receptors to the spinal cord are large myelinated fibres that convey information from the periphery towards the cerebral cortex extremely rapidly. Cold, warmth and pain are detected by thin axons with “naked” endings, which transmit more slowly.  Temperature receptors also show adaptation.

There are relay stations for touch in the medulla and the thalamus, before projection on to the primary sensory area in the cortex called the somatosensory cortex.  The nerves cross the midline so that the right side of the body is represented in the left hemisphere and the left in the right.

The input from the body is systematically “mapped” across the somatosensory cortex to form a representation of the body surface.  Some parts of the body, such as the tips of your fingers and mouth, have a high density of receptors and a correspondingly higher number of sensory nerves. 

Areas such as our back have far fewer receptors and nerves. However, in the somatosensory cortex, the packing density of neurons is uniform.  Consequently, the ‘map’ of the body surface in the cortex is very distorted.  Sometimes called the sensory homunculus, this would be a curiously distorted person if it actually existed with its complement of touch receptors spread at a uniform density across the body surface.

Pain

Although often classed with touch as another skin sense, pain is actually a system with very different functions and a very different anatomical organisation.  Its main attributes are that it is unpleasant, that it varies greatly between individuals and, surprisingly, that the information conveyed by pain receptors provides little information about the nature of the stimulus (there is little difference between the pain due an abrasion and a nettle sting).  The ancient Greeks regarded pain as an emotion not a sensation. 

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Recording from single sensory fibres in animals reveals responses to stimuli that cause or merely threaten tissue damage – intense mechanical stimuli (such as pinch), intense heat, and a variety of chemical stimuli.  But such experiments tell us nothing directly about subjective experience.

Molecular biological techniques have now revealed the structure and characteristics of a number of nociceptors.  They include receptors that respond to heat above 460 C, to tissue acidity and – again a surprise – to the active ingredient of chilli peppers. 

The genes for receptors responding to intense mechanical stimulation have not yet been identified, but they must be there. Two classes of peripheral afferent fibres respond to noxious stimuli: relatively fast myelinated fibres, called Α Αδ δfibres, and very fine, slow, non-myelinated C fibres. 

Both sets of nerves enter the spinal cord, where they synapse with a series of neurons that project up to the cerebral cortex.  They do so through parallel ascending pathways, one dealing with the localisation of pain (similar to the pathway for touch), the other responsible for the emotional aspect of pain. 

A life without pain?

Given our desire to avoid sources of pain, such as the dentist, you might imagine that a life without pain would be good.  Not so.  For one of the key functions of pain is to enable us to learn to avoid situations that give rise to pain.  Action potentials in the nociceptive nerves entering the spinal cord initiate automatic protective reflexes, such as the withdrawal reflex.  They also provide the very information that guides learning to avoid dangerous or threatening situations.

Another key function of pain is the inhibition of activity – the rest that allows healing to occur after tissue damage. Of course, in some situations, it is important that activity and escape reactions are not inhibited.  To help cope in these situations, physiological mechanisms have evolved that can either suppress or enhance pain.  The first such modulatory mechanism to be discovered was the release of endogenous analgesics.  Under conditions of likely injury, such as soldiers in battle, pain sensation is suppressed to a surprising degree – presumably because these substances are released.

Animal experiments have revealed that electrical stimulation of brain areas such as the aqueductal gray matter causes a marked elevation in the pain threshold and that this is mediated by a descending pathway from the midbrain to the spinal cord.  A number of chemical transmitters are involved including endogenous opioids such as met-enkaphalin.  The pain-killer morphine acts on the same receptors at which some of the endogenous opioids act.

The converse phenomenon of enhanced pain is called hyperalgesia.  There is a lowering of the pain threshold, an increase in the intensity of pain, and sometimes both a broadening of the area over which pain is felt or even pain in the absence of noxious stimulation.  This can be a major clinical problem.  Hyperalgesia involves sensitisation of the peripheral receptors as well as complex phenomena at various levels of the ascending pain pathways.  These include the interaction of chemically mediated excitation and inhibition. 

The hyperalgesia observed in chronic pain states results from the enhancement of excitation and depression of inhibition.  Much of this is due to changes in the responsiveness of the neurons that process sensory information.  Important changes occur in the receptor molecules that mediate the action of the relevant neurotransmitters.  In spite of the great advances in our understanding of the cellular mechanisms of hyperalgesia, the clinical treatment of chronic pain is still sadly inadequate.

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