Aging & Cognition Ladan Ghazi Saidi, Ph.D., Assistant Professor, Department of Communication Disorders, COE, University of Nebraska at Kearney 2018 Nebraska Speech-Language-Hearing Association Fall Convention September 27-28, 2018 at the Holiday Inn & Conference Center in Kearney, Nebraska Copyright 2017 Ghazi-Saidi Aging: Normal vs Pathological Gerontology: Aging and its process. Looks at different aspects of healthy aging: Biological, Neurobiological, Psychological, Social Geriatrics: Aging related Diseases and Disorders Aging often includes changes to vision, hearing, taste, smell, skin, hair, weight & changes to Brain: 10% loss of weight No widespread loss of neurons! (Frontal, Parietal, Striate) Loss in Basal ganglia: (loss of Acetylcholine) Memory Hub of motor activity: - initiating - integrating movements Loss of cells in hippocampus (not necessarily associated with memory loss) Ventricles (Hollow spaces filled with CSF) enlarge White matter changes (Myelination: communication channel for the brain's information processing gray matter) may be related to processing seed As the brain becomes smaller as a result of the gradual, life-long loss of brain cells, subarachnoid space increases in size to fill the space White matter changes in appearance with aging. The reason for these changes is unclear, but it may be related to the normal slowing of information processing in the brain with age Changes to the structure of the brain is variable and individualized, Example: Changes to Memory Reasons: Diabetes, Heart conditions, Risk of stroke, Smoking, History of Trauma, High Blood Pressure, Inflammation Normal cognitive changes at aging: Memory, Attention, Perception, Intelligence, Brain changes, Everyday functioning in familiar environments vs unfamiliar environments. Language: No changes in normal aging unless impacted by other cognitive functions Aging: Normal vs Pathological Cognitive Changes Age-associated memory impairment: Primarily episodic memory and noun retrieval; Not disabling or Non-Progressive Mild cognitive impairment: Significant episodic memory impairment; Not disabling ; Generally progressive 1
Dementia: Disabling memory or executive dysfunction Normal aging memory process: Ability to recall specific events, reductions in processing speed & Attention Free recall > cued recall > recognition recall, Hippocampus encoding is aided by prefrontal cortex and other cortical regions become able to support the memory (Lots and lots of repetition spread out over many years causes this transition) Semantic memory and remote memories tend to be more resilient, and less affected by brain damage, aging, or the initial stages of AD More information on Normal vs Pathological memory loss can be found at: https://www.helpguide.org/articles/alzheimers-dementia-aging/age-related-memory-loss.htm Different types of attention decline, except for Sustained attention: o Attention switching >Divided attention > Selective attention > Sustained attention Fluid Intelligence decline since speed of processing decline, working memory declines, perceptual processing declines and inhibition decreases Crystalized intelligence includes word & world knowledge, therefore increases Neuroplasticity: The ability of the brain to change; neuroplasticity happens at aging to increase compensation (positive) and as a result of disorders (negative). Pathological Aging The most common aging disorders that include speech and language impairment include disorders that cause damage to cortical and subcortical brain structures. Damage to the cortical structures, such as the case in AD impairs the explicit memory, thus language impairment would be in relation to memory loss and learning new information. Damage to the subcortical structures such as PD impairs motor processing and executive functions, which may lead to dysarthria or apraxia of speech. There is constant interaction among brain areas that are involved in language processing and other cognitive processes such as memory, executive functions, attention and visuospatial processing. AD: Assessing progression, Neuropsychological screenings and tests, Brain volume and metabolism, Imaging of beta-amyloid build-up Early markers ability to intervene in very early stages of disease and monitor the impact of these interventions. AD & Language: Language deficit manifestation: word retrieval, Object naming, Verbal fluency: semantic (e.g animals) < phonological (f, a or s), Short term memory impairment, Episodic memory, Articulation and grammar, Progressive Mute AD: Communication windows: Ability to respond to the environmental stimuli Touch!, Facial expression Smile, Tone (emotion: anger, frustration, kindness, firmness, persuasion, etc) energetic, happy tone, Familiar vs unfamiliar faces, Music AD: Communication tips: Maintain eye contact, Address by name, Use simple sentences, One idea at a time, Slow down, Use visual cues & gestures, Yes / no question rather than WH, Consider & support emotions (e.g. embracement, love, frustration, etc), Swallowing issues 2
Frontotemporal Dementia: Other names: Pick's disease; (Arnold Pick,1892); first described a patient with distinct symptoms affecting language. Frontotemporal disorders, Frontotemporal degenerations, Frontal lobe disorders. Portions of the Frontal & Temporal lobes shrink (atrophy). Signs and symptoms vary (depending on the brain area affected) and progressively worsen over years, and include Deterioration in: Behavior, Personality, Language disturbances, Alterations in muscles, Motor functions. Eventually, people require 24-hour care. Can affect younger adults (under 60); impacts life and family. Cause: Accumulation of the protein tau & the protein TDP43; Preference to target the frontal and temporal lobes (unknown reasons); Degeneration of the frontal, temporal and insular regions, causes problems with Decision-making, Behavior, Emotion, Language. FTD: Variants: Behavioral variant frontotemporal dementia (bvftd); Motor Variant; Primary Progressive Aphasia (PPA) PPA: Semantic variant primary progressive aphasia (svppa); Non-fluent/agrammatic variant primary progressive aphasia (nfvppa); Logopenic variant primary progressive aphasia (LV-PPA) The bvftd: Gradual changes in behavior, Disregard for social conventions, Impulsivity, Apathy, Loss of sympathy or empathy, Repetitive or compulsive movements, Dietary changes, Poor insight, planning and assessment, Prominent changes in personality, Interpersonal relationships. The motor variant: Gradual weakness or slowing of movement, General weakening of muscles, stiffness, uncoordinated and slowing of movements (arms, legs, face, tongue or neck), Fasciculations (muscle twitches), Dysphagia, Slowing of particular eye movements, Dysarthria (slurred speech, nasal or breathy speech), Spasticity (tight and stiff muscles), Hyperreflexia (exaggerated reflexes), Outbursts of laughing or crying that may not be appropriate to the situation or which may appear when the patient is mounting an effort to speak PPA: 1) Semantic variant primary progressive aphasia (svppa): Comprehension and Production of sentences/words, Problems with word-understanding, Forgetting the names of familiar objects, The principal feature is a loss of word meaning, even of common words. When asked to bring an orange, for example, the person may appear puzzled and may ask what an "orange" means, Speech has less nouns and is therefore somewhat empty of meaning, It sounds perfectly fluent because of liberal use of fillers, Changes of personality and behavior are frequent. Agitation, display of excessive friendliness to strings, change of dietary habits, etc. 2) Non-fluent/agrammatic variant primary progressive aphasia (nfvppa): Hesitant and effortful ungrammatical speech, Better at reading and writing, Eventually may lead to mutism, Difficulty swallowing, Problems with word-order and word-production, Effortful speech and reduced in quantity, Sentences become gradually shorter, Word-finding hesitations become more frequent, Occasionally giving the impression of stammering or stuttering, Pronouns, conjunctions and 3
articles are lost first, Word-order may be abnormal, especially in writing or e-mails, Words may be mispronounced or used in the reverse sense (e.g., "he" for "she" or "yes" for "no"), Word understanding is preserved but sentence comprehension may suffer if the sentences are long and grammatically complex. 3) Logopenic variant primary progressive aphasia (LV-PPA): Impaired repetition, naming difficulty. Problems with word-finding & impaired object naming. Fluent speech during causal small talk but breaks into mispronunciations and word-finding pauses when a more difficult or precise word needs to be used, Circumlocutions, Using less apt or simpler word as well as to insert fillers such as "the thing that you use for it," "you know what I mean,", Spelling errors, Understanding long and complex sentences can become challenging, Preserved single word comprehension, Impaired repeating phrases and sentences. Assessment of FTD: Medical history and detailed neurological examination, Neuroimaging: where and how extensive, Lumbar puncture (spinal tap), Neuropsychological examination (Language, Behavior, Memory, Executive, Visual-spatial functions). Treatment of FTD: Currently no treatments to slow or stop the progression of the disease, FTD research is expanding, Important for caregivers and families to think about: Long-term management issues, Identify a team of experts who can help with difficult medical, financial and emotional challenges, Knowledgeable team about FTD: Physician speech and language pathologists, occupational and physical therapists, neuropsychologists, nurses (especially home-care nursing), social workers and genetic counselors. PPA may benefit during the course of their illness by acquiring new communication strategies from speech-language pathologists. Some families have also learned new strategies through participation in Aphasia Community Groups. Carrying identification cards and other materials that can help explain the person s condition to others. ID cards are available from the National Aphasia Association website. Some communication-assistive devices may also be helpful. Non-verbal techniques for communicating such as Gesturing or Pointing to pictures, Therapy may target all modalities. Parkinson s disease: Early Symptoms, Motor impairment, Muscle weakness, Slow movement, Tremors, Masked Faces Later Symptoms: Flat affect, Memory problems, Poor problem-solving and abstract reasoning Speech symptoms: Soft voice, Slurred speech, Mumbled or rapid speech, Monotone, Breathy or hoarse vocal quality, Lack of facial gestures, Word finding difficulty, Challenges participating in fast paced conversations, Possibility of Coughing or choking while eating, Not enjoying socialization Language symptoms: Treatment: L-Dopa and other pharmaceutical options, Surgery: Dopamine cell implantation & Deepbrain stimulation Healthy Aging: A continual process of change (does not begin at a particular point in time); Cognitive declines around 30 but noticeable around 50 4
Healthy Aging: Healthy and active aging is a process to achieve physical, mental and social well-being throughout one s life particularly in the later years; Goal: A life free of Disease & disability with high physical & cognitive function and active engagement with life in old age Contributing factors: Behavioral: smoking, alcohol, exercise, diet, drugs; Environmental: pollution, home safety, rural/urban; Socioeconomic: family, community, income, literacy; Personal: biology, genetics, coping mechanisms; Services: primary care, health promotion, disease prevention. It is easier (and MUCH less expensive) to prevent an illness than it is to treat it. By taking action early to prevent or treat a condition, we stand a much greater chance of minimizing the long-term deleterious effects of many conditions which can have the cumulative effect of shortening our life span and/or interfering with our quality of life. Cognitive Reserve: Cognitive reserve may be mediated by: efficiency/capacity of existing brain networks, ability to enlist new networks, or compensatory networks. Influencing cognitive reserve may delay or reverse the effects of aging or brain pathology Brain Reserve: Size, Neuronal count, Synapse count, Connectivity, Threshold: burden of pathology, enhancing neuronal capacity, Compensatory, Enriched brain vasculatories: enhanced blood flow & delivery Neuropsychological studies both behavioral and neuroimaging studies have proved that both languages are active at all times. Selecting the Correct language and Language switching requires cognitive control (Hernandez, 2009). Picture naming and semantic fluency are slower in bilinguals but they are better at executive tasks and episodic memory. Also, white matter hold up better over time in bilinguals (Luk 2011). The hypothesis is that juggling creates a need to negotiate competition across the two languages so that the use of each language is controlled to enable fluent performance. These control processes may include inhibition of the L1 or more dominant language with enduring consequences for native language use. A life of resolving cross-language competition appears to confer a range of positive consequences for cognition and changes to the brain networks that reflect the way in which control mechanisms are engaged. This builds stronger cognitive reserve to enable fluent performance. Bilingualism delays the onset of Alzheimer's-type dementia by four years (Bialystok, 2004; 2007). Language experience may provide protection to the brain. Bilinguals resist more to the pathology, so when the symptoms appear, the disease is severely advanced. Two individuals who appear the same clinically, whether demented or non-demented, can have widely divergent levels of underlying age-related neural changes or AD pathology. The clinical diagnosis of normal aging, MCI or AD may be accompanied by very minimal pathology or more than enough to meet pathological criteria for AD. Measuring CR therefore becomes an important component of diagnosing and characterizing aging and dementia. 5