Sensory System II PDF

Central Nervous System Sensory system II 1  Intended Learning Objectives: By the end of this course the student will be able to: ▪Define pain sensation and its mechanism. ▪List three types of pain receptors ▪List different types of pain. ▪Compare betwe...

Central Nervous System Sensory system II 1  Intended Learning Objectives: By the end of this course the student will be able to: ▪Define pain sensation and its mechanism. ▪List three types of pain receptors ▪List different types of pain. ▪Compare between fast and slow pain. ▪Identify referred pain and its mechanism. ▪Enumerate intracranial and extra cranial causes of headache. ▪Recognize pain control system. ▪Enumerate Lesions of Sensory system. 2 Sensory system 3  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. 4  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). 5  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. 6  Types of pain Types of pain Cutaneous Deep Visceral pain pain pain 7  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 fiber Small myelinated (A delta) Unmyelinated (C fiber) 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 8  Reaction to Pain Motor Emotional Autonomic Arousal Reaction Reaction Reaction Reaction Fast: withdrawal acute pain: mild: increase Pain pathway gives reflex screaming & HR & increase collateral to (cutaneous pain) anxiety ABP reticular formation and non-specific thalamic nuclei to enhance Slow: increase sever: decrease wakefulness & chronic pain: muscle tone HR & decrease alertness depression (visceral pain) ABP 9  II-Deep pain Deep pain is a slow type of pain originating from deep structures (.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. 10  III-Visceral pain Characters: It is a slow type of pain that arise from the viscera. It is poorly localized (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 11  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. 12  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). 13  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 it (interpret its origin) to the skin and not to the diseased viscus. 14  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. 15  Headache It is a very common condition that most people will experience many times during their lives. The main symptom of a headache is pain in your head or face. which can differ greatly regarding pain type, severity, location and frequency. Brain is insensitive to pain Pain sensitive intracranial structure are: 1. Arteries; especially middle meningeal artery 2. veins; venous sinuses 3. nerves 4. Dura; at the base of the brain and tentorium 16  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 17  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 18 Sensory system Pain Control 19  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. Much of the incoming information is reduced or even abolished by inhibition from: collaterals from other ascending neurons (e.g., lateral inhibition) or pathways descending from higher centers in the brain (analgesia system). 20 Pain inhibition 21  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 22 Pain-Analgesia 23 Pain-Analgesia 24 Pain-Analgesia 25  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) 26 27  THE THALAMUS ✓ It is a subcortical mass of grey matter at the lateral wall of the third ventricle. ✓ There are two thalami, one of each cerebral hemisphere. ✓ It operates in close association with the cerebral cortex. ✓ All sensory signals ascending to cortex must pass through the thalamus except olfaction. Thalamic Nuclei: Each thalamus consists of 5 groups of nuclei that are classified according to their situation into: anterior, posterior, lateral, medial and ventral groups. From the functional point of view, they are classified into: A) Non specific nuclei: These include mainly midline and intralaminar nuclei they receive signals from reticular formation and project to the whole cortex. B) Specific nuclei: 28  THE THALAMUS B) Specific nuclei: These include: 1. Ventral nuclei: Ventro-lateral: concerned with voluntary movement, they receive signals from both cerebellum and basal ganglia. Ventro-posterior: its lateral part(VPLNT) receives the spinal and medial lemnisci, while its medial part (VPMNT) receives the trigeminal lemniscus. 2. Dorsal nuclei: Dorso-lateral: for integrative function and language, it projects to the cortical association areas. Dorso-medial: for thinking and autonomic function, it projects to frontal lobe and hypothalamus. 3. Anterior nuclei: Concerned with recent memory and emotions. They receive signals from hypothalamus and mamillary body, and discharge to the limbic system. 4. Lateral geniculate body: Projects visual impulses to the visual cortex in the occipital lobe. 5. Medial geniculate body: Projects auditory impulses to the auditory area in the temporal lobe. 29  THE THALAMUS Functions of the thalamus: It conveys all sensations to the cerebral cortex (except smell), Its nuclei are relay stations in the pathways of: Somatic sensations from the opposite side of the body (Epicritic sensations) Visual signals. Auditory signals. The intralaminar and middle nuclei are the center for crude sensations (protopathic sensations) and slow pain from the opposite side. 30 Sensory system 31  I- Peripheral nerves lesions : 1. Lesion of 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. 32  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: 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. 33  II- Spinal cord lesions: 3. Tabes dorsalis (Syphilitic disease): Slow degeneration in the dorsal columns and posterior roots of the spinal cord Results in impairment of vibration & proproceptive sensation and progressive ataxia. Positive Romberg's sign: the patient maintains his erect position by visual impulses i.e. if he closes his eye, he falls. 34  II- Spinal cord lesions: 4. Brown Sequard syndrome (Hemisection of the spinal cord) 35  II- Spinal cord lesions: 4. Brown Sequard syndrome At the level of the lesion: on the Above the level of the Below the level of the lesion same side lesion: on the same side Sensory: loss of all On the same side: Fibrous tissue 1-Sensory: loss of fine touch, sensations at the in spinal cord pressure, vibration & kinesthesia corresponding (posterior column) dermatome —>irritation 2-Motor: upper motor neuron Motor: Lower motor hypersthesia. lesion (UMNL) i.e. spastic paralysis, hyper-reflexia & +ve Babinski sign neuron lesion i.e. flaccid On opposite side: paralysis (loss of reflexes) 1-Sensory: loss of pain, temperature, crude touch (spinothalamic column). So, touch is not lost but decreased in both sides. 2-Motor: No loss 36  III- Thalamic syndrome: Cause: thrombosis of the thalmogeniculate 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 37 38