LO: Processing of Sensory Information

1. Describe pain, nociceptors and proprioception

Pain: feeling of sore, aching, throbbing, suffering

Nociceptors (otherwise known as pain receptors): respond to potentially damaging stimuli that result in pain. They are especially common in the superficial portions of the skin, in joint capsules, within the periostea of bones, and around the walls of blood vessels. Other deep organs and most visceral organs have few nociceptors.

Nociception is the sensory process that provides the signal to trigger pain

Nociceptors are free, branching, unmyelinated nerve endings that signal that the body is being damaged or at risk of being damaged. Their activation leads to the conscious experience of pain

There are different types of nociceptors that respond to different stimuli;

o Polymoidal: respond to mechanical, thermal and chemical stimulio Mechanical: respond to strong mechanical pressureo Thermal: respond to extremes of temperature – extreme heat or extreme coldo Chemical: histamine and other chemicals

Stimulation of the dendrites of the nociceptors causes depolarization and an action potential to be created. This signal is then sent down the neuron, and onto target cells by the process of movement of ions (using ion channels) and ultimately by releasing neurotransmitters to the receptors on the target cell (Mealear covers this in her LO)

The initial stimulation comes from substances released from the damaged cells that open ion channels – proteases to break down kininogen to form bradykininactivates ionic conductance, ATP and K+ ions

An important neuropeptide (which functions as a neuron transmitter and neuromodulator, altering the excitability of the dorsal horn ganglion) is substance P. It is associated with inflammatory processes and pain and becomes important when we look at pain prevention/treatment

There two types of axons associated with nociception – Type A delta and Type C fibres (as opposed to the touch reflex which uses myelinated A beta fibres)

(touch pathway and the pain pathway also differ in that the pain pathway crosses the midline straight away, in the dorsal root axon, but the touch, vibration, two-point discrimination and proprioception pathway does not cross over until much higher up in the dorsal column nuclei)

The A delta and C fibres bring information to the CNS at a different rate;o The A delta fibres are slightly myelinated and create the first pain, which is sharp

and fast. These will quickly reach the CNS and often trigger a somatic reflex. They are also relayed to the primary sensory cortex and therefore receive conscious attention, causing the patient to be able to localize the source of the pain

o This is followed by the second pain, which is duller, but longer lasting, which is caused by activation of the C fibres. The Type C fibres carry sensations of slow pain, (burning or aching pain), and cause a generalized activation of the reticular formation and thalamus. Therefore, the individual will be aware of pain, but will only have a general idea of where it is.

Small diameter fibres have cell bodies in the segmental dorsal root ganglia and enter dorsal horn of spinal cord

Fibres travel up and down spinal cord in the zone of Lissauer and synapse in the substantia gelatinosa

Descending Pain Control Pathways Emotion, stress or determination can suppress feelings of pain Neurons in the midbrain called the periventricular and periadaqueductal gray matter

(PAG) implicated in pain suppression. PAG sends information to the raphe nuclei, which projects axons down the spinal cord, where they depress the activity of the nociceptive neurons

Endogenous Opiates The endogenous opioids bind the opioid receptors in the brain and the brain

manufactures endogenous morphine-like substances called endorphins Endorphins and their receptors are distributed widely in the CNS and concentrated in

areas processing nociceptive information Endorphins prevent nociceptive signals through dorsal horn and higher brain levels

where pain is perceived This is achieved by the inhibition of the activity of substance P, thereby stopping the

transduction of the pain (substance P is really important in terms of creating the action potential and the initial sending of a signal)

This kicks in for the longer term management of pain, whereas the descending pain control pathways is more for the immediate response (after the first stimuli)

Hyperalgesia Hyperalgesia is a reduced threshold for pain, increased intensity of pain stimuli or even

spontaneous pain Primary hyperalgesia: within damage area Secondary hyperalgesia: when the tissue surrounding the primary site of injury becomes

supersensitive

When skin is damaged: sensitizing chemicals such as bradykinin, prostaglandins and substance P are released: making nociceptors more sensitive and therefore more readily stimulated

Substance P causes vasodilation (swelling of the blood capillaries) and histamine release from mast cells

Trigeminal pain pathway Pain information from face and head takes a path to the thalamus Small diameter fibres in trigeminal nerve synapse first in spinal trigeminal nucleus of

brain stem Axons cross and ascend to thalamus in the trigeminal lemnisus

Proprioceptors occur in skeletal muscles, tendons, joints, and ligaments and in CT coverings of bone and muscles (and potentially the equilibrium receptors of the inner ear as well). Proprioceptors constantly advise the brain of our body movements by monitoring how much the organs containing these receptors are stretched.

In joints, the mechanosensitive axons respond to changes in the angle, direction and the velocity of movement of the joint. It appears that the information from the joint receptors is combined with the information from the muscle spindles and Golgi tendon organs (in the skeletal muscles) and skin receptors in order to estimate joint angle.

(Interesting note: adaption is the reduction in sensitivity in the presence of constant stimuli. There are receptors which are fast-adapting receptors (eg. thermoreceptors). Nociceptors are slow-adapting sensors, hence why pain sensation reminds you of an injury long after the damage has occurred.)

2. Understand the mechanisms of referred pain and lower back pain

Visceral afferents travel along same pathways as somatic pain fibres and therefore within the spinal cord there is mixing of the 2 inputs into the single spinal cord section (this is what they refer to when they a ‘cross talk’). Therefore, pain arising in the viscera is often perceived as somatic pain in origin.

Referred pain usually follows the dermatome rule, “area of skin where pain is felt usually innervated by the same spinal segment as the affected organ”.

An example of this is where a heart attack causes the sensation of pain that radiates into the superior thoracic wall and along the medial aspect of the left arm. This is because the same spinal segment (T1 – T5) innervates both the heart and the regions to which the pain signal is going to. The brain interprets such inputs as coming from the somatic pathway.

There are a variety of different causes of back pain; Musculoskeletal pain: well localized and aggravated by movement Spinal cord lesion: pain will occur in dermatomal distribution Osteoporosis (with crush fractures), carcinoma, leukaemia: can cause progressive

and unremitting back pain

Crush fracture of a vertebral body will cause pain maybe with a sudden onset and the perhaps dermatomal pain will develop