Lecture 2 - Sensory Physiology 2 PDF

NHN3127 Physiology Sensory system II  Pain sensation Pain is unpleasant sensation for body protection. It occurs when there is tissue damage. Damaged tissue releases a variety of chemicals including: bradykinin, prostaglandins, substance P, K+ , and H+ , which...

NHN3127 Physiology Sensory system II  Pain sensation Pain is unpleasant sensation for body protection. It occurs when there is tissue damage. Damaged tissue releases a variety of chemicals including: bradykinin, prostaglandins, substance P, K+ , and H+ , which initiate the inflammatory response.  Pain Receptors Pain receptors (nociceptors) are free nerve endings. They are of three types: 1. Mecahnosensitive pain receptors (they are stimulated by strong mechanical stimuli). 2. Thermosensitive pain receptors (they are stimulated by extreme thermal stimuli). 3. Chemosensitive pain receptors (they are stimulated by histamine and strong acids).  Pain Receptors Distribution: More: in skin, periosteum, arteries, joint surface, falx& tentorium cerebelli and cranial sinuses. Less: in deep tissue Absent: in liver parenchyma, lung alveoli and brain (pain insensitive) Nerve fibers: A delta & C fibers Adaptation: slowly or non adaptive receptors.  Type of Pain (Origin) Somatic Visceral pain pain Cutaneous Deep pain pain  I-Cutaneous Pain On application of a painful stimulus on the skin, one first feels fast pricking pain followed by aching or burning pain (the slow pain). Fast pain Slow pain Character Pricking , well localized Burning, poorly localized Afferent fibers Small myelinated Unmyelinated (A delta) (C fiber) Neurotransmit Glutamate Substance P ter Onset 0.1 sec after the stimulus 1 sec after the stimulus Duration Short Long Associated Flexor withdrawal reflex Increase muscle tone reflexes Perception Cerebral cortex Thalamus  II-Deep pain Deep pain is a slow pain originating from deep structures of musculoskeletal (.e.g. muscles, tendons, ligaments and periosteum). Deep pain is dull aching, poorly localized, associated with nausea and vomiting. It is transmitted by unmyelinated C fibers and can be referred to the skin. Causes of deep pain are; 1. Ischemia of skeletal muscle. 2. Muscle spasm. 3. Joint inflammation.  III-Visceral pain Characters: It is a slow pain that arise from the viscera. It is poorly localized (because the number of pain receptors in the viscera is few). The pain is usually dull aching , burning or colicky. It is carried by unmyelinated C fibers. Causes: ischemia, due to accumulation of metabolites spasm or over distension of a hollow viscus chemical irritation.e.g. perforated peptic ulcer  III-Visceral pain The visceral pain signal initiates the following responses (during its flow in the spinothalamic tract from the diseased viscus to the cerebral cortex) : 1. Spasm of the skeletal muscles overlying the diseased viscus. (muscle guarding). 2. Autonomic reflexes; Bradycardia, decrease in ABP 3. Emotional affect.e.g. malaise, depression and bad mood because ascending pain fibers send signals to the limbic system. It is referred to the area of skin that has the same origin of the diseased viscus in the embryonic life (=Referred pain).  Referred Pain Pain originating in a visceral structure perceived as being from an area of skin innervated by the same segmental level as the visceral afferent. (Dermatomal role of referred pain). Mechanism of referred pain  It is due to the convergence of the visceral pain fiber with the somatic pain fiber that carries pain from the skin area that developed with this viscus from the same embryonic segment.  When this pain signal reaches the cerebral cortex , it will project pain (interpret its origin) to the skin and not to the diseased viscus. Examples of referred pain; 1. Anginal pain: Referred to the left shoulder and the left arm. 2. Gastric pain : Referred to the superior epigastrium above the umbilicus. 3. Gall bladder pain : Referred to the right shoulder. 4. Renal pain : Referred to the inguinal region and the testis. 5. Appendicular pain: referred to the umbilicus. 6. Teeth pain: referred to head. Examples of referred pain  Headache Brain is insensitive to pain Pain sensitive intracranial structure: 1. Arteries; especially middle meningeal artery 2. veins; venous sinuses 3. nerves 4. Dura; at the base of the brain and tentorium  Headache Causes of intracranial headache: 1. Meningeal irritation; meningitis, brain tumor. 2. Migraine headache; abnormal vascular phenomenon. Vasospasm of cerebral vessels (ischemia, prodromal symptoms) followed by vasodilatation (due to accumulation of metabolites) leads to severe headache. 3. Hypertension; expansion of cerebral vessels 4. Constipation; absorption of toxin leads to meningeal irritation  Headache Causes of extracranial headache: 1. Muscle spasm. 2. Irritation of nasal sinuses. 3. Error of refraction; spasm of ciliary & extraocular muscles 4. Otitis media 5. Toothache 6. Systemic disorders; like anemia Pain Control  Pain Control All sensory signals are subject to extensive modification at the various synapses along the sensory pathways before they reach higher levels of the central nervous system. Gate control theory: pain stimuli transmitted by afferent pain fibers are reduced or even blocked by gate mechanism located at the Posterior Horn Of Spinal Cord. The gate control inhibition has two mechanisms: A. Lateral inhibition = collaterals from other ascending sensory neurons or B. Analgesia system = pathways descending from higher centers in the brain (= descending pain pathway). A. Pain control (lateral inhibition)  B. Pain-Analgesia This results partly from a capability of the brain itself to suppress input of pain signals to the nervous system by activating a pain control system, called an analgesia system. Brain has built in analgesic system Suppresses transmission in pain pathways as they enter spinal cord Depends on presence of opiate receptors Endogenous opiates – endorphins, enkephalins, dynorphin  Pain-Analgesia The components of the opioid analgesic system of the brain are: 1.The periaqueductal grey and periventricular area of the mesencephalon in the upper pons (Enkephalin) 2.The raphe magnus nucleus located in the lower pons and upper medulla (serotonin) 3.Pain inhibitory complex located in the dorsal horn of the spinal cord (Enkephalin) Pain-Analgesia Pain-Analgesia Pain-Analgesia I- Peripheral nerves: 1. Lesion of single peripheral nerve: loss of all sensation in the area of supply 2. Diffuse lesion of all peripheral nerves (peripheral neuritis): loss of sensations from the distal parts of the limbs i.e. gloves & Socks loss of sensation especially pain sensation. 3. Lesions of the dorsal root: loss of sensations from the corresponding dermatomes. 4. Hyperalgesia: hypersensitivity to pain occurs in the inflamed skin due to presence of inflammatory mediators. It occurs in the area of injury and area around it (area of redness). Non painful stimuli (e.g. touch) become painful, due to hypersenesitivty of pain receptors. It occurs in normal skin area which surrounding the flare. Pain sensation is intense & prolonged, due to Facilitation of pain transmission II- Spinal cord lesions: 1. Herpes zoster: It is a virus which infects dorsal root ganglion -->excitation of pain neuronal cells-->severe pain in the dermatomal segment supplied by infected ganglion. The virus migrates to the cutaneous terminals —>rash & vesicles. 2. Syringomyelia: Widening of the central canal of the spinal cord (usually cervical) Damage: spinothalamic tracts (pain, temperature & crude touch fibers) as they cross immediately in front of central canal (Jacket sensory loss). The sensations carried in the dorsal column are not affected i.e. dissociation of cutaneous sensations occur.  II- Spinal cord lesions: 3. Tabes dorsalis (3rd stage Syphilitic disease): Slow degeneration in the dorsal columns and posterior roots of the spinal cord Results in impairment of vibration & proprioceptive sensation  progressive sensory ataxia. Positive Romberg's sign: the patient maintains his erect position by visual impulses i.e. if he closes his eye, he falls. II- Spinal cord lesions: 4. Brown Sequard syndrome (Hemisection of the spinal cord) At the level of the lesion: on the same side Sensory: loss of all sensations at the corresponding dermatome Motor: Lower motor neuron lesion i.e. flaccid paralysis (loss of reflexes) Below the level of the lesion: On the same side: Sensory: loss of fine touch, pressure, vibration & kinesthesia (posterior column) Motor: upper motor neuron lesion (UMNL) i.e. spastic paralysis, hyper-reflexia & +ve Babinski sign On opposite side: Sensory: loss of pain, temperature, crude touch (spinothalamic column). So, touch is not lost but decreased in both sides. Motor: No loss Brown Sequard syndrome (Hemisection of the spinal cord) continued  Carried by spinothalamic (Crude touch, Due to complete destruction of Posterior Carried Painbyand dorsal Horn Cells column leminiscus (Tactile and Temperature proprioceptive sensations) sensations)  Increased Carried by Carried by tone a. Spastic spinothalamic dorsal column Paralysis, b. No muscle (crude touch, leminiscus (fine atrophy, Carried by Paincolumn dorsal and c. Exaggerated touch, pressure, deep reflexes, leminiscus Temperature (Tactile and d. Positive vibration,…etc) Babiniski`s sign proprioceptiv sensations) e sensations)  III- Thalamic syndrome: Cause: thrombosis of the thalamogeniculate branch of posterior cerebral artery. This artery supplies posteroventral & lateral ventral nucleus of thalamus. Effects: 1) Loss of all sensations on opposite side of the body 2) Return of some crude sensations. 3) Return of pain after few months (thalamic pain) Characters of thalamic pain: Increase threshold i.e. needs stronger stimulus to produce it, Once produced, it is very severe. 4) Ataxia: mixed ataxia due to: a/Loss of proprioceptive sensations. b/Cutting of connection between cerebellum & cortex. This connections passes through the lateral ventral nucleus. 5) Emotional disturbances IV- Brain stem lesions: Loss of all sensations on opposite side V- Cortical lesions: A) The person loses ability for: 1) Fine but not crude localization. 2) Judgement of critical degrees of pressure. 3) Judgement of close weights. 4) Judgement of stereognosis & texture of material. 5) Orientation of different parts of the body to each other B) Temperature sensation is moderately affected. C) Pain sensation is poorly affected.