HEARING LOSS and DEMENTIA: CONNECTING the DOTS the Participant Will Be Able To: Identify Age-Related Sensorineural Hearing Loss Presented By: and Dementia
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2/15/2019 LEARNING OBJECTIVES HEARING LOSS AND DEMENTIA: CONNECTING THE DOTS The participant will be able to: Identify age-related sensorineural hearing loss Presented by: and dementia. Distinguish hallmark signs and causes of Dr. Diana Blakeney-Billings, CCC-A Assistant Professor – Alabama A&M University dementia. CSD Department Differentiate dementia from other neurologic diseases and syndromes. and Co-presenter: Mrs. Kaci W. McAfee, BS, SLP-A CHRONIC CO-MORBIDITIES OF HEARING LOSS Psychosocial Physiological Conditions Age-related hearing loss has contributed to faster Consequences declines in other disorders. Hypertension Cognitive Disorders Dementia/cognitive disorders Cardiovascular Disease (Dementia/Alzheimer’s Untreated hearing loss is an independent variable Arthritis Disease) Balance disorders Hypertension, diabetes, and ototoxic drugs Chronic kidney disease Communication Hearing loss can threaten health outcomes Stroke Disorders particularly older aged adults. Falls Depression Older adults with hearing loss develop brain Diabetes Infectious diseases shrinkage faster. Cancer Quality of Life AGE RELATED HEARING LOSS (ARHL) CAUSES OF ARHL Chronic health condition Most Common – inner ear changes from aging Presbycusis Central changes impact perceiving auditory verbal Gradual process and nonverbal stimuli Certain medications Bilateral high frequency sensorineural loss, Morphological alterations (stria vascularis) symmetrical Central Auditory Pathway Degeneration Peripheral and central pathology Genetics Progressively impacts mid to low frequencies Environmental exposure to noise Poor speech understanding in noise Metabolic disorders Lifestyle choices Hyperacusis and tinnitus present Smoking – hypertension Absent or undetected otoacoustic emissions Lack of exercise/diet - obesity Noise exposure dependent on hearing loss severity Dietary habits 1 2/15/2019 ARHL PATHOPHYSIOLOGY CENTRAL AUDITORY SYSTEM –AGING Schuknecht’s 1974 Classification system based on: MECHANICS Audiometric pattern of hearing loss Inner ear vasculature abnormalities Animal and human studies investigation on Hair cells and membrane abnormalities Thorough case history and temporal bone analysis patho-physiological changes associated with aging. (Yamasoba, et al., 2013) Four Classifications - 1974 Sensory Metabolic or Strial Neural Cochlear conductive (Blevins, Deschler, & Kunins, 2018; Jayakody et al., 2018) CHANGES IN CENTRAL AUDITORY SYMPTOMS PATHWAY (CAP) FROM ARHL Neuroimaging results show changes in : Understanding family/friends/medical professionals (poor socialization) Gray matter volume decline in middle and superior Unable to follow directions temporal gyri, primary auditory cortex, both medial and superior frontal gyrus, occipital lobe, and the Unable to hear phones, warning alarms, hypothalamus doorbells Both gray and white matter decline near auditory Leads to feelings of isolation cortex Can hear but “can’t understand” Secondary pathophysiological change in CAP, and other brain areas not related to auditory stimuli Leads to depression processing. A hearing loss that goes untreated can contribute to depression, isolation, and cognitive decline. Balance/fall issues (Jayokody, et al., 2018) CHARACTERISTICS OF ARHL LIN ET AL., 2013 STUDY Objective: to determine an association between Hearing deficits with competing background hearing loss and cognitive decline. noise. Subjects: 1984 older adults with a mean age of 77.4 years old. ARHL patients hear fine in one-on-one in quiet. Baseline showed no cognitive impairments. Cocktail party effect – difficulty in social settings Method: – isolation. Used the Modified Mini-Mental State Examination Test [3MS] with score greater or less than 80 and puretone Women’s voices harder to hear than men. average at 500 to 4000 Hz in the ear with better hearing. Results: The majority of a soundwaves energy lies in the 1162 patients with hearing loss of 25 dB PTA showed lower and mid-frequencies in human speech. declines annually in 3MS (41%). High frequencies carry the consonants that give 32% greater declines with the Digit Symbol substitution scores than subjects with normal hearing at baseline. meaning to words. Some are soft sounds. Conclusion: Central hearing loss isn’t corrected with hearing Cognitive decline is associated with hearing loss. aids A correlations between cognitive decline and peripheral and central hearing loss exist (p. 293). 2 2/15/2019 EFFECTS OF HEARING AIDS, AURAL REHABILITATION, COCHLEAR IMPLANTS ON DEPRESSION AND COGNITIVE FUNCTION Italian researchers Castiglione, et al., 2016 reviewed effects Older white male smokers showed higher on mental and cognitive decline prevalence of hearing loss and cognitive decline. Method: 125 older adults (> 65 years) with hearing loss (105) and A 30-40% accelerated cognitive decline rate and a normal hearing (20) 24% (Lin et al., 2013) risk increase for 6 study groups based on degree of loss impairment. Rehabilitation with cochlear implants or hearing aids Routine cognitive and hearing assessments (before/after Faster decline in hearing impaired vs. normal rehabilitation) hearing individuals (7.7 years vs. 10.9 years). Digit Span test Stroop color-word test Cognitive load or social isolation can connect Montreal Cognitive Assessment (MoCA) hearing loss and cognitive decline Geriatric Depression Scale mechanistically. . (Castiglione, et., 2016) RELATIONSHIP BETWEEN HYPERACUSIS, TINNITUS, AND SEMANTIC DEMENTIA TAKE AWAY: The Lancet International Commission on Dementia Prevention, Intervention, and Care (Livingston et al., 2017) suggests that one-third of diagnosis of Alzheimer’s Disease (AD) could be prevented or delayed with A 2011 study by Mahoney, et al., evaluated MRI life style changes, early intervention, and adhering to public health strategies (e.g. correcting hearing data from patients with auditory symptoms and impairments). semantic dementia. Current projects that one in 30 Americans will have dementia by 2050 (Taylor & Tysoe, 2015). Hearing loss older adults have a 30-40% greater chance of acquiring dementia or a cognitive decline (i.e. Grey matter in posterior superior portion of memory issues). temporal lobe preserved Older adults with even mild hearing loss untreated will have processing problems. Grey matter in orbitofrontal cortex and medial Prevention could reduce the number of patients with AD by 2050 from 8.8 to 16.2 million (Jayakody et al., geniculate nucleus reduced 2018; Livingston et al., 2017). Mild cognitive impairment (MCI) can be a pre-cursor to dementia. Over a fourth of older adults 65 years and Orbitofrontal cortex atrophy – tinnitus older have MCI (Livingston et al., p. 2689). Hearing loss can cause: Medial geniculate nucleus or auditory thalamus Difficulties attending –working memory Visual and auditory free call tasks atrophy – hyperacusis Longer latency needed for accurate judgements in perception Isolation and depression WHAT IS DEMENTIA? Neurological syndrome caused by different brain diseases. High prevalence among aging population Dementia Congenital Organic Caused by infections and toxicity medicine reactions Symptom severity progress until death (ASHA., (n.d). Dementia) 3 2/15/2019 NEURODEGENERATIVE DISEASES ASSOCIATED WITH DEMENTIA WARNING SIGNS OF DEMENTIA Alzheimer Disease Confusion and memory loss Lewy Body Disease Work problems Vascular pathology (e.g., multi-infarct Dementia) Problems paying bills or housekeeping Frontotemporal lobar degeneration Personality changes Pick’s Disease Primary Progressive Aphasia Depression Huntington’s Disease Problems following simple directions Parkinson’s Disease Trouble expressing wants and needs to others HIV/AIDS or neuroAIDS dementia (Manasco, p.59) Eating and swallowing problems (ASHA. (n.d). Dementia) (ASHA, (n.d). Dementia) ETIOLOGY FROM PROGRESSIVE CHANGES IN FUNCTION OF BRAIN DEMENTIA CHARACTERISTICS Wernicke-Korsakoff Syndrome secondary to Attention Deficits chronic alcohol abuse Easily distracted Traumatic Brain Injury (TBI) Difficulties without input being restricted or Chronic Traumatic Encephalopathy due to simplified repeated trauma (e.g., dementia pugilistica) Decreased information-processing Longer speed-thinking processes than usual Chemotherapy (Kean & Locke, 2008) Learning and Memory Deficits Multiple Sclerosis Episodic memory deficits (e.g., specific Human immunodeficiency virus (AIDS/HIV) autobiographical events, situations, and experiences) Short-term and working memory deficits- rapid forgetfulness recent auditory/visual stimuli (ASHA, (n.d). Dementia) (ASHA, (n.d.). Dementia) COMMON SYMPTOMS COMMON SYMPTOMS (CONT’D) Reasoning and Executive Functioning Deficits Perceptual Deficits Insufficient goal and planning difficulties reliance on others Impediment of completion of familiar activities Loss of recognition of familiar people, common objects, Impaired reasoning and poor judgement sounds, etc. safety concerns Inability to find objects in direct view Inabilities in multi-tasking and complex Lack of inhibition Lack of mental flexibility (ASHA. (n.d.). Dementia) 4 2/15/2019 COMMON SYMPTOMS (CONT’D) COMMON SYMPTOMS (CONT’D) Language Deficits Inability to follow conversations Empty discourse with fewer ideas In bilingual individuals: Repetitious/perseverative language Errors in selecting and maintaining appropriate same question repetition) language during conversation (Friedland