The Nervous System, Somatic Sensations, Pain, Headache and Thermal Sensations
Pain Sensation: fast and Slow Pain Classification
- Fast Pain
- Slow Pain
- All pain receptors are free nerve endings
Three types of Stimuli
- Pain receptors are activated by mechanical, thermal and chemical stimuli
- Mechanical and thermal stimuli - fast pain
- Chemical stimuli - slow pain
- No adaptation, progressively greater as the pain stimulus continues, this is called hyperalgesia
Two separate pathways of Pain transmission
- A-delta fibers fast - 6 to 30m/s - Mechanical and thermal stimuli
- C-Fibers slow - 0.5 to 2m/s
- neospinothalamic tract - A-delta fibers
- paleospinothalamic tract - C-fibers
- The neospinothalamic tract is used in pain localisation
- Activity in the paleospinothalamic system may impart unpleasant perception of pain.
- paleospinothalamic pathway
- The periaqueductal gray
- the periadueductal gray of the midbrain and the rostral pons receives input from the ascending pain pathways in addition to descending projections from the hypothalamus and other forebrain regions.
- The nucleus raphe magnus (serotonin) and nucleus paragigantocellularis (noradrenalin)
- in the medulla receive input from the periaqueductal gray and the project to neurons in the spinal cord dorsal gray
- The dorsal horn, enkephalin interneurons receive input from the descending serotenergic raphe magnus axons , and the latter from direct synaptic contact with incoming pain fibers.
- primary afferent depolarisation (or presynaptic inhibition)
- the effect is to interrupt the transmission of the pain signals over these incomming primary sensory fibers. This effect is thought to be mediated by calcium channel blockade in the membrane of the sensory fiber terminal. Other serotonergic fibers exert more conventional postsynaptic inhibitory effects on their synapses with those dorsal horn neurons that process pain signals.
- The descending noradrenergic axons from the medullary reticular formation, may lead to the interuption of pain transmission at the level of the dorsal horn.
- The Role of the Periaqueductal Gray in Pain Perception
- Neurons in the periaqueductal grey and the nucleus raphe magnus - have opiate receptors on their surface membranes.
- When stimulated by exogenous opiods or endogenous endorphins and enkephalins the pain suppression circuitry is activated and this leads to the reduction of pain perception.
- Pain Sensation: Inhibited by Certain type of tactile Stimulation
- Activation of the large, rapidly conducting tactile sensory fibers of the dorsal roots appears to suppress the transmission of pain signals in the dorsal horn, probably through lateral inhibitory circuits.
- This explains why pain is relieved by message
- Electrical Stimulation: Pain Relief
- Stimulating electrodes implanted on the spinal cord dorsal columns or the thalamus or periaqueductal gray reduces chronic pain. The level of stimulation can be regulated up or down by the patient to effectively manage the pain.
- Referred Pain: Distant From the Stimulus
- signals that originate from the visceral organ or tissue -
- heart pain referred to the left jaw and neck or the left arm.
- Leakage of gastric secretions from a perforated or ulcerated GIT may directly stimulate the endings of the peritonium and lead to painful sensation in the body wall.
- Appendicitis - central abdomial pain or pain in the RFI
- Clinical Abnormalities of Pain and Other Sensations
- Hyperalgesia - heightened sensitivity to painful stimuli
- Thalamic pain syndrome: Interruption of the blood supply or damage to the ventrobasal thalamus - somatosensory region may cause thalamic pain syndrome.
- Initially there is a loss of sensation on the contralateral body surface. Eventually sensation returns - poorly localised and appears to be pain. Even the slightest touch is excruciating pain - hyperpathia.
- Herpes Zoster (Shingles) - viral infection of the dorsal root ganglion or cranial nerve sensory ganglion
- Segmental pain and a severe skin rash over the area served by the afferent ganglion.
- Trigeminal neuralgia - severe lancinating pain in the cutaneous distribution of one of the three main branches of the trigeminal nerve.
- May also be caused by pressure of a blood vessel on the trigeminal nerve in the cranial cavity - requires surgical intervention
- Brown-Sequard Syndrome - extensive damage to the Right or Left half of the spinal cord
- Transaction of the anterolateral system
- loss of pain and temperature sensation contralaterally that begins a few segments caudal to the level of the lesion
- On the Ipsilateral side there is a loss of dorsal column sensations beginning at about the level of the lesion and extending through all levels caudal to the lesion. Loss of sensation to all in the dermatomes that correspond to the location of the cord lesion.
- Headache results when pain from deeper structures is referred to the surface of the head:
- The source of the pain stimuli may be intra- or extracranial
- The brain is insensitive to pain -
- when somatosensory structures are damaged, sensation of pins and needles
- Except for
- TIC DOULOUREUX
- THALAMIC PAIN SYNDROME
- Pain from structures above the tentorium cerebrei - pain is referred to the frontal frontal portion of the head
- Pain from structures below the tentorium cerebrei - pain is referred to the occipital part of the brain.
- Pressure on the venous sinuses and stretching of the dura or blood vessels and cranial nerves passing through the dura lead to the sensation of headache.
- Meningeal inflammation typically produces pain that involves the entire head.
- If a small volume of CSF is removed (20 ml) and the patient is not recumbent, gravity will cause the brain to "sink"; this leads to stretching of the meninges, vessels and cranial nerves, resulting is a diffuse headache.
- The headache that follows an alcoholic binge is though to be the direct toxic irritation of alcohol on the meninges.
- Constipation may cause a headache as a result of direct toxic effect of circulating metabolic substances or from circulatory changes relating to loss of fluid from the gut.
- Migraine headaches - may be the result of vascular phenomena. Prolonged unpleasant emotions or anxiety produces spasm in the brain arteries and leads to local ischemia in the brain. Prodromal visual or olfactory symptoms. The resultant prolonged spasm and ischemia, the vascular muscle wall looses its capability to maintain tone. The pulsations of circulating blood arteries stretches (dilates) and relaxes the vascular wall and this stimulates pain receptors in the vascular wall or in the meninges surrounded by entry points of vessels into the brain or cranium. The result is an intense pulsating headache.
THERMAL SENSATIONS
- Changes in Temperature: Three types of receptors
- Pain receptors - perceive pain
- Specific Warmth receptors - not clearly identified - free nerve endings
- The cold receptor - identified as small nerve endings, the tips of which protrude to the basal epidermal cells. Signals are transmitted via A-delta type sensory fibers. There are 3-10x as many cold receptors as there are warm receptors, density varies from 10-15 per square centimetre on the lips to 3-15 receptors per square centimeter on the fingers.
- Cold and Warm Receptors: Temperature in range of 7 degrees to 50 degrees Celsius
- Temperatures below 7 degrees and above 50 degrees activate pain receptors, the perception is pain and not warm or cold.
- The cold receptor, When exposed to extremely cold temperature, temperature decrease, it is strongly stimulated initially but after the first few seconds the generation of action potentials falls off dramatically. The decrease in the generation of action potentials - progresses more slowly over the next 30 minutes.
- This explains why cold and warm receptors respond to the steady state temperature
- Thermal receptors are stimulated by the change in the nerve fiber metabolic rate - induced by the temperature change. For every change in 10 degrees there is a doubling of the intracellular chemical reaction.
- Thermal signals are transmitted through the central nervous system in parallel with pain signals.
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