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CHAPTER 3 SENSORY SYSTEMS Disorders of sensory systems • Deficits – Sensory organ – Sensory nerves – Central nervous system • Hyperactivity – Central neuropathic pain – Tinnitus – Tingling • Normal response that is redirected – Pain from touch – Dizziness and vertigo from head movements Disorders of sensory systems • Reduced sensitivity – Hearing loss – Visual impairment • Incorrect response – Hyperacusis – Distorted sounds – Allodynia – Hyperpathia Disorders of sensory systems • Impaired conduction of the physical stimulus to the receptors • Impaired function of receptors • Impaired function of sensory nerves • Impaired or changed function of the central nervous system Reduced sensitivity • Often caused by disorders of the sense organs • Injury to afferent nerves Hyperactive sensory disorders • Increased sensation of physical stimuli • Altered sensation of physical stimuli • Sensation without any physical stimulation General organization of sensory systems • Conduction of the physical stimulus to the receptors • Sensory receptors • Sensory nerves • Central nervous system Sensory transduction • A physical stimulus generates a receptor potential • The receptor potential is a graded potential • The receptor potential is conducted electrotonically to the spike generation site Bipolar receptor cells (taste) Initiation of nerve impulses • Occurs at the first node of Ranvier Two different types of receptors, with bipolar nerve fibers Sensory transduction (mechanoreceptor in a muscle) Central nervous system HUMAN Mouse Chick Auditory nervous system Ascending auditory pathways P rimary audit ory cort ex Midline Ret icular format ion Vent ral t halamus MGB Inferior colliculus Cochlea AN LL Cochlear nucleus From: Møller, 2005 Two different ascending sensory pathways have been identified: • The classical systems • The non-classical systems Classical auditory pathways Non-classical auditory pathways From: Møller: Sensory Systems, 2003 Non-classical auditory pathways Receive input from the somatosensory system Use the dorsal part of the MGB From: Møller, 2005 The classical ascending pathways • The number of nuclei is different in different sensory systems • Use ventral thalamic nuclei that project to primary sensory cortices • Neurons processes only input from of one sensory modality Visual system Classical ascending pathways Non-classical ascending pathways A B External eye muscles Midline Primary visual cortex Extrastriate cortex Primary visual cortex Other regions of the CNS T halamus Pulvinar T halamus Superior colliculus T halamus LGN LGN Pretectal nucleus Light reflexes Retinal ganglion cells Retinal ganglion cells SCN and hypothalamus From: Møller, 2005 The nonclassical pathways • Use dorsal and medial thalamic nuclei that project to secondary cortices and to other parts of the CNS • Receive input from more than one sense Somatosensory pathways Classical pathways Non-classical pathways Pain pathways Limbic system Association cortex SII "WHAT" SI cortex "WHERE" Thalamus dorsal Thalamus ventral Medial lemniscus Reticular formation AROUSAL Anterior lateral tract Fig 3.3 From: Møller, 2005 Cerebral cortex Thalamus Trigeminal ganglion Midbrain Motor nuclei RF Brainstem Spinalcord Processing after primary sensory cortices • Integration of input from different sensory systems occurs in association cortices • Parallel processing • Stream segregation The neocortex has six layers Simplified diagram of the connections to and from the different layers of the cerebral cortex From: Møller: Sensory Systems, 2002 Maps Tonotopic Somatotopic SURFACE VIEW LOWER BODY IS REPRESENTED NEAR THE MIDLINE Tonotopic organization in the CN of a cat, as an example of tonotopic organization in the auditory system Tonotopic organization in the CN of a cat, as an example of tonotopic organization in the auditory system Parallel processing Stream segregation Parallel processing: Cochlear nucleus Function of sensory nervous systems • Processing of sensory input at the peripheral level – Convergence (spatial integration) – Interplay between inhibition and excitation Spatial integration: Receptive field of a dorsal column nucleus cell Convergence of input to a secondary neuron Lateral inhibition Central processing of sensory information • Each stage enhances or suppress specific Information Parallel processing: The same information is processed in different structures Stream segregation: Different kinds of information is processed in different structures (“What” and “Where”) Processing after primary sensory cortices • Integration of input from different sensory systems occurs in association cortices Stream segregation Cortical circuitry Dorsal stream “where” Ventral stream “what” From: Møller: Sensory Systems, 2003 Sensory information can reach other regions than sensory regions Motor systems Memory Emotional brain (limbic system) Two different routes to the Amygdala from a sensory system Arousal and plasticity Cortex AAF "High Route" AI Association cortices Polymodal association cortex Other cortical areas AII Nucleus basalis Amygdala "Low Route" AL Dorsal medial MGB ICX ICC DC ABL ACE Thalamus Endocrine Ventral MGB Autonomic Behavioral From: Møller, 2005 Connections from a sensory system to the amygdala “the high route” From: Møller: Sensory Systems, 2003 Connections from a sensory system to the amygdala “the low route” From: Møller: Sensory Systems, 2003 Connections from the amygdala From: Møller: Sensory Systems, 2003 Hypoactive sensory disorders • Loss of sensitivity – Hearing loss – Poor vision – Numbness – Loss of vestibular (balance) function -10 0 10 20 30 40 50 60 70 80 90 100 110 0.125 0.25 0.5 0.75 1 1.5 Frequency in kHz 2 3 4 6 8 NOISE IMMISSION LEVEL HEARING LEVEL AT 4 kHz Genetic, epigenetic and environmental Causes (and a stochastic component ?) Courtesy of M. Charles Liberman Age-related hearing loss Normal variations in hearing loss of 70 year old individuals Number 100 4000 Hz. Women Number 100 90 90 80 80 70 70 Left Ear Right Ear 60 50 50 40 30 30 20 20 10 10 0 0-9 20-29 40-49 60-69 80-89 10-19 30-39 50-59 70-79 90-99 dB Left Ear Right Ear 60 40 0 4000 Hz. Men 0-9 20-29 40-49 60-69 80-89 10-19 30-39 50-59 70-79 90-99 dB Variations in speech discrimination in 70 year old individuals % 100 % 100 Men 70 years old N=179 N=197 75 75 50 50 Left Ear Right Ear 25 0 Women 70 years old Left Ear Right Ear 25 •92% 76-88%<76% <48% deaf 0 •92% 76-88%<76% <48% deaf Hearing loss in Ménière's disease -10 0 10 20 30 40 50 60 70 80 90 100 110 0.125 0.25 0.5 0.75 1 1.5 Frequency in kHz 2 3 4 6 8 A Effect of surgical injuries to the auditory nerve: -10 0 I 10 20 30 40 50 60 70 80 90 Large decrease in speech discrimination II 100 110 0.125 0.25 0.5 0.75 1 1.5 2 3 4 6 8 Frequency in kHz I: Pre-op Discr.=96% AS II: 5 days post-op Discr.=0% AS B -10 0 10 I 20 30 40 50 60 70 80 II 90 100 110 0.125 0.25 0.5 0.75 1 1.5 2 Frequency in kHz I: Pre-op Discr.=80% AS II: 7 days post-op Discr.=30% AS 3 4 6 8 Hyperactive sensory disorders • • • • • Tinnitus Paresthesia Phosphenes Phantom sensations Central neuropathic pain Subjective and objective tinnitus • Different forms of tinnitus have very different effects on an individual’s life Similarities between chronic pain and severe tinnitus There are many forms of tinnitus • Mild tinnitus: Does not interfere noticeably with everyday life • Moderate tinnitus: May cause some annoyance and may be perceived as unpleasant • Severe tinnitus: Affects a person’s entire life in major ways Patients’ own perception varies between mild, moderate and severe (disabling) Important to have words for disorders • We cannot think about matters that do not have names • The same words is used to describe very different forms of tinnitus and pain • Using the same names for fundamentally different disorders is a disadvantage in treating these disorders How prevalent is severe tinnitus? Some statistics show 50 million people have tinnitus in the USA The prevalence of severe (bothersome) tinnitus is infrequent at young age; it reaches 12-14% for people at age 65 according to one study How prevalent is severe pain? Some pain was reported by 86% of individuals above the age of 65 (Iowa study, 1994) The prevalence of severe pain was 33% for people at age 77 and above (Swedish study, 1996) Severe tinnitus affects a person’s entire life in major ways • Prevents or disturbs sleep • Interferes with or prevents Intellectual work • Often accompanied by altered perception of sound Severe pain affects a person’s entire life in major ways • Prevent or disturb sleep • Interfere with or prevents intellectual work • May cause suicide May involve limbic structures causing affective reactions Often accompanied by abnormal sensations from touch Severe tinnitus is often accompanied by altered perception of sound • Sounds are distorted • Sounds have exaggerated loudness (hyperacusis) • Sounds are unpleasant • Sounds are painful and arouse fear (phonophobia) Little is known about the cause of subjective tinnitus • Noise exposure • Ototoxic antibiotic • Acoustic tumors The sympathetic nervous system is involved in some forms of severe tinnitus Some forms of tinnitus can be cured by sympathectomy Deprivation of sound can cause changes in neural processing such as change in temporal integration • Expression of neural plasticity The anatomical location of the abnormality that cause chronic pain and tinnitus may be different from that to which the pain or the tinnitus is referred The abnormal neural activity that causes symptoms are not generated at the location where the symptoms are felt Examples: • Phantom pain • Tinnitus with severed auditory nerve The tinnitus in some patients can be modulated by stimulation of the somatosensory systems (such as by electrical stimulation of the median nerve) “cross-modal” interaction Non-classical auditory pathways Receive input from the somatosensory system Use the dorsal part of the MGB From: Møller, 2005 Other signs of involvement of the somatosensory system •Gaze related tinnitus •Neck muscles and tinnitus •TMJ and tinnitus •Sensation of sound from touching the skin Connections between spinal C2 segment and the dorsal cochlear nucleus Can explain why electrical stimulation of the skin behind the ears can modulate tinnitus Symptoms and signs of neuropathic pain and severe tinnitus • Strong emotional components • Depression • High risk of suicide Severe tinnitus is often associated with affective (mood) disorders • Depression • Phonophobia The amygdala is involved in fear and other mood disorders Connections from the auditory system to the amygdala • Cortical-cortical connections (the “high route”) • Subcortical connections (the “low route”) Arousal and plasticity Cortex AAF "High Route" AI Association cortices Polymodal association cortex Other cortical areas AII Nucleus basalis Amygdala "Low Route" AL Dorsal medial MGB ABL ACE Thalamus Endocrine Ventral MGB Autonomic Behavioral ICX ICC DC Fig 3.7 From: Møller, 2005 CONCLUSION ACTIVATION OF NON-CLASSICAL ASCENDING SENSORY PATHWAYS CAN CAUSE SYMPTOMS AND SIGNS OF SEVERAL DISEASES Neural plasticity play greater role in generating symptoms and signs than previously assumed • Plastic changes are reversible • Treatments without medicine and surgery may alleviate pain and tinnitus Therapy There is no treatment for tinnitus that is comparative to common pharmacological treatment of pain. Treatment of tinnitus has been mainly benzodiazepines (GABAA agonists) Reversal of neural plasticity • “TENS” (transderm electric nerve stimulation) has been used for many years in treatment of chronic pain • Recently sound stimulation in various forms have been introduced in treatment of severe tinnitus Stimulation of somatosensory system can relieve tinnitus • Electrical stimulation – of the ear and – of the skin behind the ears have been used to treat tinnitus • Electrical stimulation of the auditory cortex is in a stage of development • Few systematic studies of efficacy have been published