CU-MA-PSY-SEM-IV-Clinical Disorders II (1) Revised

MASTER OF ARTS IN PSYCHOLOGY SEMESTER IV CLINICAL DISORDERS-II

CHANDIGARH UNIVERSITY Institute of Distance and Online Learning SLM Development Committee Prof. (Dr.) H.B. Raghvendra Vice- Chancellor, Chandigarh University, Gharuan, Punjab:Chairperson Prof. (Dr.) S.S. Sehgal Registrar Prof. (Dr.) B. Priestly Shan Dean of Academic Affairs Dr. Nitya Prakash Director – IDOL Dr. Gurpreet Singh Associate Director –IDOL Advisors& Members of CIQA –IDOL Prof. (Dr.) Bharat Bhushan, Director – IGNOU Prof. (Dr.) Majulika Srivastava, Director – CIQA, IGNOU Editorial Committee Prof. (Dr) Nilesh Arora Dr. Ashita Chadha University School of Business University Institute of Liberal Arts Dr. Inderpreet Kaur Prof. Manish University Institute of Teacher Training & University Institute of Tourism & Hotel Management Research Dr. Manisha Malhotra Dr. Nitin Pathak University Institute of Computing University School of Business © No part of this publication should be reproduced, stored in a retrieval system, or transmitted in any formor by any means, electronic, mechanical, photocopying, recording and/or otherwise without the prior written permission of the authors and the publisher. SLM SPECIALLY PREPARED FOR CU IDOL STUDENTS 2 CU IDOL SELF LEARNING MATERIAL (SLM)

First Published in 2021 All rights reserved. No Part of this book may be reproduced or transmitted, in any form or by any means, without permission in writing from Chandigarh University. Any person who does any unauthorized act in relation to this book may be liable to criminal prosecution and civil claims for damages. This book is meant for educational and learning purpose. The authors of the book has/have taken all reasonable care to ensure that the contents of the book do not violate any existing copyright or other intellectual property rights of any person in any manner whatsoever. In the event, Authors has/ have been unable to track any source and if any copyright has been inadvertently infringed, please notify the publisher in writing for Corrective action. 3 CU IDOL SELF LEARNING MATERIAL (SLM)

CONTENT Unit 1 – Neurocognitive Disorders ........................................................................................ 5 Unit 2 – Parkinson's Diseases .............................................................................................. 40 Unit 3 – Delirium ................................................................................................................ 68 Unit 4 – Pica and Rumination.............................................................................................. 89 Unit 5 – Food Addiction.................................................................................................... 107 Unit 6 – Case Studies ........................................................................................................ 129 Unit 7 – Internet Addiction................................................................................................ 143 Unit 8 – Sex Addiction...................................................................................................... 164 Unit 9 – Case Studies ........................................................................................................ 193 4 CU IDOL SELF LEARNING MATERIAL (SLM)

UNIT 1 – NEUROCOGNITIVE DISORDERS STRUCTURE 1.0 Learning Objectives 1.1 Introduction 1.2 Neurocognitive Disorders 1.3 DSM Criteria 1.4Incidence of Neurocognitive Disorders 1.5 Prevalence of Neurocognitive Disorders 1.6 Co-morbidity of Neurocognitive Disorders 1.7 Causes of Neurocognitive Disorders 1.8 Prognosis of Neurocognitive Disorders 1.9 Treatment of Neurocognitive Disorders 1.10 Summary 1.11 Key Words 1.12 Learning Activity 1.13 Unit End Questions 1.14 References 1.0 LEARNING OBJECTIVES After studying this unit, you will be able to,  Explain the nature and symptoms of Neurocognitive Disorders  Describe the incidence and prevalence of Neurocognitive Disorders  Explain the co-morbidity of Neurocognitive Disorders  State the causes of Neurocognitive Disorders  Explain the prognosis of Neurocognitive Disorders  State the treatment for Neurocognitive Disorders 1.1 INTRODUCTION Henry was a 56-year-old businessman when he was hospitalized for cervical disk surgery. Because he was busy as well as anxious about the surgery, he had canceled two previous 5 CU IDOL SELF LEARNING MATERIAL (SLM)

admissions. Henry drank heavily but did not appear to have problems from his drinking. Surgery went well, and in the first couple of days recovery seemed normal. “During the third postoperative night, though, Henry became quite restless and could not sleep. The next day he appeared severely fatigued. The next night his restlessness worsened, and he became fearful. Later in the night, he thought that he saw people hiding in his room, and shortly before dawn he told the nurse that he saw strange little animals running over his bed and up the curtains. By morning rounds, the patient was very frightened, lethargic, and distractible. He was incoherent when he tried to talk about the night before. He knew who he was and where he was but did not know the date or when he had had his surgery. During that day his mental status fluctuated, but by nightfall he had become grossly disoriented and agitated. At this point, psychiatric consultation was obtained.” The consultant diagnosed Henry with delirium, probably due to several factors: withdrawal from alcohol, use of strong analgesics, and the stress of the operation. The treatment consisted of a reduction in pain medications, a family member present at all times, along with 50 mg of chlorpromazine (Thorazine) three times daily and 500 mg of chloral hydrate at bedtime. Treatment reversed his confusion within 2 days, and he was able to return home in a week with no symptoms. As we age, physiological changes are inevitable, and there may be emotional and mentalchanges as well. Many of these may influence social interactions. In contrast to the esteemin which they are held in most Asian countries, older adults are generally not treated well inthe United States. The process of growing old is feared by many, even abhorred. Perhaps ourlack of regard for older adults stems from our own deep-seated fear of growing old. The oldperson with serious infirmities is an unwelcome reminder that we all may one day walk withan unsteady gait, see less clearly, taste food less keenly, and experience more physical illness. The social problems of aging may be especially severe for women. Even with the consciousness raisingof the past decades, our society does not readily accept women with wrinkles andsagging bodies. Although men with gray hair at the temples are often seen as distinguished,signs of aging in women are not valued in the United States and many other countries. Thecosmetics and plastic surgery industries make billions of dollars each year exploiting the fearinculcated in women about looking their age. According to some experts, however, beingfemale confers certain mental health benefits as people age. The old are usually defined as those over the age of 65, an arbitrary point set largely bysocial policies rather than any physiological process. To have some rough demarcation points,gerontologists usually divide people over age 65 into three groups: the young-old, those aged 65 to 74; the old-old, those aged 75 to 84; and the oldest-old, those over age 85. 6 CU IDOL SELF LEARNING MATERIAL (SLM)

1.2 NEUROCOGNITIVE DISORDERS Brain is considered as the most complex organ that the human body possesses. It is involved in almost every aspect of our lives- eating, balancing, standing, running, sleeping or even falling in love. So, whether it’s a physical illness or mental illness, brain is involved in it in some or the other way. If, we go by the anatomy of brain, it is protected and covered by a thick outer cover called dura mater (the “hard mother” of the brain). It is further encased by skull which is very hard in itself. Even though it is highly protected, it is vulnerable to damage and when there is a brain damage, it may result in various cognitive changes. Changes in cognitive functioning are considered to be the most obvious signs of brain damage. The location and extent of the damage determine what problems the patient will have. As you are aware, the brain is highly specialized. Although the two hemispheres are closely interrelated, they are involved in somewhat different types of mental processing. At the risk of oversimplifying, it is generally accepted that functions that are dependent on serial processing of familiar information, such as language and solving mathematical equations, take place mostly in the left hemisphere for nearly everyone. Conversely, the right hemisphere appears to be generally specialized for grasping overall meanings in novel situations; reasoning on a nonverbal, intuitive level; and appreciating of spatial relations. Even within hemispheres, the various lobes and regions mediate specialized functions. Although none of these relationships between brain location and behavior can be considered universally true, it is possible to make broad generalizations about the likely effects of damage to particular parts of the brain. Damage to the frontal areas, for example, is associated with one of two contrasting clinical pictures: (1) being unmotivated and passive and with limited thoughts and ideas or (2) featuring impulsiveness and distractibility. Damage to specific areas of the right parietal lobe may produce impairment of visual-motor coordination, and damage to the left parietal area may impair certain aspects of language function, including reading and writing, as well as arithmetical abilities. Damage to certain structures within the temporal lobes disrupts an early stage of memory storage. Extensive bilateral temporal damage can produce a syndrome in which remote memory remains relatively intact but nothing new can be stored for later retrieval. Damage to other structures within the temporal lobes is associated with disturbances of eating, sexuality, and emotion. Occipital damage produces a variety of visual impairments and visual association deficits, the nature of the deficit depending on the particular site of the lesion. For example, a person may be unable to recognize familiar faces. Unfortunately, many types of brain disease are general and therefore diffuse in their destructive effects, causing multiple and widespread interruptions of the brain’s circuitry. 7 CU IDOL SELF LEARNING MATERIAL (SLM)

Fig 1.1Neurocognitive Disorders Impairments Associated With Brain Disorders The following types of difficulties are often the consequences of brain disease, disorder, or damage. 1. Impairment of memory. The individual has trouble remembering recent events, although memory for past events may remain more intact. Some patients with memory problems may confabulate—that is, invent memories to fill in gaps. In severe instances, no new experience can be retained for more than a few minutes. 2. Impairment of orientation. The individual may not know where he or she is, what the day is, or who familiar people are. 3. Impairment of learning, comprehension, and judgment. The individual’s thinking becomes clouded, sluggish, or inaccurate. The person may lose the ability to plan with foresight or to understand abstract concepts and hence to process complex information (described as “thoughtimpoverishment”). 4. Impairment of emotional control or modulation. The individual is emotionally overactive: laughing, crying, or flying into a rage with little provocation. 8 CU IDOL SELF LEARNING MATERIAL (SLM)

5. Apathy or emotional blunting. The individual is emotionally underactive and seems indifferent to people or events. 6. Impairment in the initiation of behavior. The individual lacks self-starting capability and may have to be reminded repeatedly about what to do next, even when the behavior involved remains well within the person’s range of competence. This is sometimes referred to as “loss of executivefunction.” 7. Impairment of controls over matters of propriety and ethical conduct. The individual may manifest a marked lowering of personal standards in areas such as appearance, personal hygiene, sexuality, or language. 8. Impairment of receptive and expressive communication. The individual may be unable to comprehend written or spoken language or may be unable to express his or her own thoughts orally or in writing. 9. Impaired visuospatial ability. The individual has difficulty coordinating motor activity with the characteristics of the visual environment, a deficit that affects graphomotor (handwriting and drawing) and constructional (e.g., assembling things) performance. Most elderly people do not have cognitive disorders. Indeed, the prevalence of cognitiveimpairment has declined among people over the age of 70 in the United States in the last15 years, perhaps because of improvements in diet, medical care, and education levels overtime. Nonetheless, cognitive disorders account for more hospital admissionsand inpatient days than any other geriatric condition. We will examinetwo principal types of cognitive disorders: dementia, a deterioration of cognitive abilities, anddelirium, a state of mental confusion. For each, we will consider the clinical description as wellas causal factors and treatment. 1.2.1 Dementia Dementia is a descriptive term for the deterioration of cognitive abilities to the point that functioningbecomes impaired. As we will discuss, there are many different causes for dementia. Difficultyremembering things, especially recent events, is the most common symptom of dementia. Peoplemay leave tasks unfinished because they forget to return to them after an interruption. The personwho had started to fill a teapot at the sink leaves the water running. As the dementia progresses, aparent is unable to remember the name of a daughter or son and later may not even recall that he orshe has children or recognize them when they come to visit. Hygiene may become poor because theperson forgets to bathe or dress adequately. People with dementia also may get lost, even in familiarsurroundings. Judgment may become faulty, and the person may have difficulty comprehending situationsand making plans or decisions. People with dementia may lose control of their impulses; theymay use coarse language, tell inappropriate jokes, shoplift, and make sexual advances to strangers. Theability 9 CU IDOL SELF LEARNING MATERIAL (SLM)

to deal with abstract ideas deteriorates, and disturbances in emotions are common, includingsymptoms of depression, flatness of affect, and sporadic emotional outbursts. Delusions and hallucinationscan occur (American Psychiatric Association, 2000). People with dementia are likely to showlanguage disturbances as well, such as vague patterns of speech. Despite intact sensory functioning,they may also have trouble recognizing familiar surroundings or naming common objects. Episodesof delirium, a state of mental confusion (discussed in detail later), may also occur. The course of dementia may be progressive, static, or remitting, depending on the cause.Many people with progressive dementia eventually become withdrawn and apathetic. In theterminal phase of the illness, personality loses its sparkle and integrity. Relatives and friendssay that the person is just not himself or herself anymore. Social involvement with others keepsnarrowing. Finally, the person is oblivious to his or her surroundings.Most dementias develop very slowly over a period of years; subtle cognitive and behavioraldeficits can be detected well before the person shows any noticeable impairment. The early signs of decline noted before functional impairmentis present have been labeled as mild cognitive impairment. 1.2.2 Alzheimer's disease (AD) The German psychiatrist Alois Alzheimer first described the disorder that bears his name in 1907. He wrote of a 51-year-old woman who had a “strange disease of the cerebral cortex” that manifested as progressive memory impairment and other behavioral and cognitive problems, including suspiciousness. He called the disorder an “atypical form of senile dementia”; thereafter, it was referred to as Alzheimer’s disease. Alzheimer's disease (AD) and other dementias incur huge costs to society, to the families of those affected, and to the individuals themselves. Costs to society includeboth direct costs to health and social services and indirect economic costs in terms of lost productivity, as careers are taken out of the workplace, and the economiccosts to those families caring for or funding the care of their relative. Increasingly, as treatments become available, these costs are targets for change and are part ofthe cost–benefit analysis of new compounds, especially the largest single direct cost, that of the provision of nursing and other forms of continuing care. Apart fromthe financial cost to families there is the emotional impact resulting in distress and psychiatric morbidity. As the population ages, these costs pose substantial social and economic problems. Although lifespan itself has remained static, the numbers of elderly in bothdeveloped and developing societies is increasing rapidly. In the developed world the sharpest projected growth is in the very elderly cohort—precisely the one that isat most risk of AD. Within the developing world the total number of elderly people is projected to rise substantially, reflecting to a large part better child health andnutrition. For countries in South America and Asia, with large and growing populations, the costs involved in caring for people with dementia in the future will 10 CU IDOL SELF LEARNING MATERIAL (SLM)

becomean increasing burden on health and social services budgets. In the absence of such services families will inevitably shoulder the main part of providing care, although the very process of development is associated with increasing urbanization and, to some degree, a diminution of the security provided by extended family structures. 1.2.3 Dementia with Lewy Bodies Lewy bodies are clumps of protein that can form in the brain. When they build up, they can cause problems with the way the brain works, including your memory, movement, thinking skills, mood, and behavior. These problems can keep a person from doing everyday tasks or taking care of yourself, a condition called dementia. Lewy body dementia (LBD) is one of the most common types of dementia, after Alzheimer’s disease. It usually happens to people who are 50 or over. Lewy body dementia causes a progressive decline in mental abilities. People with Lewy body dementia might have visual hallucinations and changes in alertness and attention. Other effects include Parkinson's disease signs and symptoms such as rigid muscles, slow movement, walking difficulty and tremors. Lewy body dementia may not cause short-term memory loss like Alzheimer’s. People with both conditions have trouble with thinking, alertness, and paying attention. But in Lewy body dementia, those problems come and go. The disease can also cause hallucinations, often in the first few years someone has Lewy body dementia. People with Alzheimer’s usually don’t have hallucinations until the later stages. People with Lewy body dementia also often act out their dreams and make violent movements when they’re asleep. It’s called REM sleep behavior disorder. Sometimes, it’s the first sign that someone has Lewy body dementia. Lewy body dementia is a progressive disease, meaning symptoms start slowly and worsen over time. The disease lasts an average of five to eight years from the time of diagnosis to death but can range from two to 20 years for some people. How quickly symptoms develop, and change varies greatly from person to person, depending on overall health, age, and severity of symptoms. 1.2.4Vascular Dementia Each year, 500,000 people die from strokes (any diseases or traumas to the brain that result in restriction or cessation of blood flow). Although stroke is the third-leading cause of death in the United States, many people survive, but one potential long-term consequence can be severely debilitating. Vascular dementia is a progressive brain disorder that is a common cause of dementia. The word vascular refers to blood vessels. When the blood vessels in the brain are blocked or damaged and no longer carry oxygen and other nutrients to certain areas of brain tissue, damage results. MRI scans of Diana’s brain showed a number of damaged areas, or multiple infarctions, left by a stroke several years earlier; this was one probable cause of her dementia. 11 CU IDOL SELF LEARNING MATERIAL (SLM)

Because multiple sites in the brain can be damaged, the profile of degeneration—the particular skills that are impaired—differs from person to person. DSM-IV-TR lists as criteria for vascular dementia the memory and other cognitive disturbances that are identical to those for dementia of the Alzheimer’s type. However, certain neurological signs of brain tissue damage, such as abnormalities in walking and weakness in the limbs, are observed in many people with vascular dementia but not in people in the early stages of dementia of the Alzheimer’s type. However, this distinction between vascular dementia and dementia of the Alzheimer’s type is controversial and the two types may overlap more than previously thought. In comparison with research on dementia of the Alzheimer’s type, there are fewer studies on vascular dementia, perhaps because of its lower incidence rates. The prevalence of vascular dementia is approximately 1.5% in people 70 to 75 years of age and increases to 15% for those over the age of 80. The risk for men is slightly higher than among women, in contrast with the higher risk among women for Alzheimer’s type dementia, and this has been reported in many developed and developing countries. The relatively high rate of cardiovascular disease among men in general may account for their increased risk of vascular dementia. The onset of vascular dementia is typically more sudden than the onset for the Alzheimer’s type, probably because the disorder is the result of stroke, which inflicts brain damage immediately. The outcome, however, is similar for people with both types: Ultimately, they will require formal nursing care until they succumb to an infectious disease such as pneumonia, to which they are susceptible because of weakening of the immune system. 1.2.5Huntington’s Disease Huntington’s disease is a genetic disorder that initially affects motor movements, typically in the form of chorea, involuntary limb movements. People with Huntington’s disease can live for 20 years after the first signs of the disease appear, although skilled nursing care is often required during the last stages. Just as with Parkinson’s disease, only a portion of people with Huntington’s disease go on to display dementia—somewhere between 20% and 80%— although some researchers believe that all patients with Huntington’s disease would eventually display dementia if they lived long enough. Dementia resulting from Huntington’s disease also follows the subcortical pattern. The search for the gene responsible for Huntington’s disease is like a detective story. For some time, researchers have known that the disease is inherited as an autosomal dominant disorder, meaning that approximately 50% of the offspring of an adult with Huntington’s disease will develop the disease. Since 1979, behavioral scientist Nancy Wexler and a team of researchers have been studying the largest known extended family in the world afflicted by Huntington’s disease, in small villages in Venezuela. 12 CU IDOL SELF LEARNING MATERIAL (SLM)

The villagers have cooperated with the research, partly because Wexler herself lost her mother, three uncles, and her maternal grandfather to Huntington’s disease, and she, too, may develop the disorder. Using genetic linkage analysis techniques, these researchers first mapped the deficit to an area on chromosome 4 and then identified the elusive gene. Finding that one gene causes a disease is exceptional; research on other inherited mental disorders typically points to multiple gene (polygenic) influences. 1.2.6 Dementia Due to Traumatic Brain Injury Major or mild NCD due to traumatic brain injury (TBI) is caused by an impact to the head, or other mechanisms of rapid movement or displacement of the brain within the skull, as can happen with blast injuries. Traumatic brain injury is defined as brain trauma with specific characteristics that include at least one of the following: loss of consciousness, posttraumatic amnesia, disorientation and confusion, or, in more severe cases, neurological signs (e.g., positive neuroimaging, a new onset of seizures or a marked worsening of a preexisting seizure disorder, visual field cuts, anosmia, hemiparesis) (Criterion B). To be attributable to TBI, the NCD must present either immediately after the brain injury occurs or immediately after the individual recovers consciousness after the injury and persist past the acute post- injury period. The cognitive presentation is variable. Difficulties in the domains of complex attention, executive ability, learning, and memory are common as well as slowing in speed of information processing and disturbances in social cognition. In more severe TBI in which there is brain contusion, intracranial hemorrhage, or penetrating injury, there may be additional neurocognitive deficits, such as aphasia, neglect, and constructional dyspraxia. 1.2.7Substance-Induced Dementia Prolonged drug use, especially combined with poor diet, can damage the brain and, in some circumstances, can lead to dementia. This impairment unfortunately lasts beyond the period involved in intoxication or withdrawal from these substances. As many as 7% of individuals dependent on alcohol meet the criteria for dementia. DSM-IV-TR identifies several drugs that can lead to symptoms of dementia, including alcohol, inhalants such as glue or gasoline (which some people inhale for the euphoric feeling they produce), and sedative, hypnotic, and anxiolytic drugs. These drugs pose a threat because they create dependence, making it difficult for a user to stop ingesting them. The resulting brain damage can be permanent and can cause the same symptoms as seen in dementia of the Alzheimer’s type. The DSM-IV-TR criteria for substance induced persisting dementia are essentially the same as those for the other forms of dementia; they include memory impairment and at least one of the following cognitive disturbances: aphasia (language disturbance), apraxia (inability to carry out motor activities despite intact motor function), agnosia (failure to recognize or identify objects despite intact 13 CU IDOL SELF LEARNING MATERIAL (SLM)

sensory function), or a disturbance in executive functioning (such as planning, organizing, sequencing, and abstracting). 1.2.8Substance/Medication Induced Dementia Mild neurocognitive disorder due to substance/medication use and major neurocognitive disorder due to substance/medication use are the diagnostic names for two alcohol- or drug- induced major neurocognitive disorders―\"major\" obviously being the more severe form. Unlike the problems with mental functioning that happen during intoxication or with a hangover the morning after alcohol use—that pass fairly quickly—mild neurocognitive disorder continues to cause difficulty with mental functioning on an ongoing basis. For some people, it can impact their day-to-day functioning permanently. Approximately 10 percent of all dementia cases are related to alcohol consumption, making it the second leading cause of dementia. Medication-induced dementia is a cognitive impairment of language, memory, and comprehension originating from or complicated by prescription or over-the-counter (OTC) medications. With the wide range of possible drugs that could contribute to the condition and the variance of symptoms, it is difficult to gather concrete evidence for the condition. Sufferers usually display symptoms similar to those of Alzheimer's disease, especially lethargy and depression. 1.2.9 Dementia Due to HIV Infection Not many people are aware that cognitive impairment is sometimes the first symptom of untreated HIV. While symptoms vary among individuals, slower mental processing, difficulty with complex tasks, and difficulty concentrating/learning new information are among the most common early signs. When HIV becomes active in the brain, significant alterations of mental processes occur thus leading to a diagnosis of neurocognitive disorder due to HIV infection. HIV-associated neurocognitive disorders (HAND) are neurological disorders associated with HIV infection and AIDS. HAND may include neurological disorders of various severity. HIV-associated neurocognitive disorders are associated with a metabolic encephalopathy induced by HIV infection and fueled by immune activation of macrophages and microglia. These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of AIDS dementia complex (ADC) are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterized by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal loss. 14 CU IDOL SELF LEARNING MATERIAL (SLM)

1.2.10 Dementia Due to Other General Medical Conditions Neurocognitive disorders that may be partially reversible can happen because of other types of medical conditions. The diagnostic category used to specify these conditions is major or mild neurocognitive disorder due to another medical condition. There are hundreds of conditions that can lead to cognitive problems in people. Some of these conditions may be reversible and others may not be fully reversible. Some of the most common are: normal Pressure Hydrocephalus (NPH), disruption of Hormones (as there are many hormonal imbalances that can result in cognitive disorders including problems with insulin and with an excess or deficiency of thyroid hormone), nutritional problems, infections. The side effects of many medications can include a disruption of a person’s thinking. Sensory Deficits can also be mentioned, as the often unrecognized, but common issue in elderly people that contributes to the idea that they have cognitive problems is hearing loss. 1.3 DSM CRITERIA OF NEUROCOGNITIVE DISORDER The hallmark of dementia is memory impairment. In progressive dementias, short-term memory is affected initially. Patients have particular difficulty in learning new information, as shown by their inability to recall three objects after 5 minutes or even after just two distractions. Long-term memory may be affected, and patients may not recall important past personal information. Other cognitive areas may be impaired, including abstract thinking, judgment, personality, and language. In a typical case of Alzheimer's disease, the onset is so insidious that family members have difficulty estimating when the impairment began. According to DSM-IV, the essential features of dementia include memory impairment, impairment in at least one other cognitive domain (e.g., language and visual-spatial skills), and significant disturbance of work or social functioning or both resulting from cognitive deficits. These features cannot occur exclusively during the course of a delirium. Dementia of the Alzheimer's type is defined as a dementia syndrome that is gradual in onset and progression and without another identifiable and sometimes treatable cause. A definite diagnosis of dementia of the Alzheimer's type can be made only by histopathological examination of brain tissue, generally after the patient's death. A work group on the diagnosis of this disorder established by the National Institute of Neurological and Communicative Disorders and the Alzheimer's Association specified criteria that provide a guide for the diagnosis of possible and probable Alzheimer's disease. Possible Alzheimer's disease includes dementia syndromes in which an additional disease (e.g., tumor or cerebral thrombosis) may be implicated. Probable Alzheimer's disease is similar to progressive dementia of the Alzheimer's type. A complete history from someone who knows the patient well, physical and neurological examinations, and a mental status examination are essential in the diagnostic evaluation. 15 CU IDOL SELF LEARNING MATERIAL (SLM)

Brief standardized mental status tests (e.g., the Mini-Mental State Examination) are useful to quantify the degree of cognitive impairment, and more extensive neuropsychological batteries provide details on the nature of the cognitive deficits. On examination, the patient may show apraxia (inability to carry out motor commands, even though comprehension and motor function are intact), agnosia (inability to recognize objects, despite intact sensory function), or difficulties in visual-spatial skills (inability to copy two-dimensional and three- dimensional figures or to assemble blocks). A variety of behavioral changes may accompany the cognitive deficits, including paranoia, agitation, insomnia, anxiety, and depression. 1.3.1 Criteria for Major Neurocognitive Disorder (Dementia) A. Evidence of significant cognitive decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning and memory, language, perceptual-motor, or social cognition) based on: 1. Concern of the individual, a knowledgeable informant, or the clinician that there has been a significant decline in cognitive function; and 2. Substantial impairment in cognitive performance, preferably documented by standardized neuropsychological testing or, in its absence, another quantified clinical assessment. B. The cognitive deficits interfere with independence in everyday activities (i.e., at a minimum, requiring assistance with complex instrumental activities of daily living such as paying bills or managing medications). C. The cognitive deficits do not occur exclusively in the context of a delirium. D. The cognitive deficits are not better explained by another mental disorder (e.g., major depressive disorder, schizophrenia). Differential diagnosis The differential diagnosis of Alzheimer's disease can be a problem. Most potential biological markers are still in a development phase, and the clinician is left with conventional methods of evaluation: the patient's history, a physical examination, and laboratory tests. The history provides important information, and several informants should be sought for corroboration. Even with the most thorough evaluation, diagnostic errors do occur. Clinical researchers who have neuropathological confirmation of diagnosis report accuracy rates ranging from 65 percent to more than 90 percent, even though other progressive dementias (such as Pick's disease) can rarely be distinguished on clinical grounds alone. Vascular dementia is estimated to account for 10 to 20 percent of the dementias of old age. Classically, the disorder is characterized by a sudden onset of illness and stepwise decline in cognitive function, rather than the insidious onset and gradually progressive course of Alzheimer's disease. Focal neurological signs and association with hypertension in many patients may also help differentiate between these two dementias. The clinical signs and symptoms, coded and given weighted scores, have been used widely to help differentiate 16 CU IDOL SELF LEARNING MATERIAL (SLM)

multi-infarct dementia from dementia of the Alzheimer's type. Although the validity of the scale has been questioned, searching for these features can help clarify the patient's clinical profile (Table 51.3e–1). An expanded scale has been developed aimed at correcting the methodological shortcomings of the early instrument. Nonetheless, the frequent coexistence of these two dementias (estimated at about one third of all dementias) impairs diagnostic accuracy. 1.3.2 Diagnostic Criteriafor Dementia of the Alzheimer’s Type A. The development of multiple cognitive deficits manifested by both 1. Memory impairment (impaired ability to learn new informationor to recall previously learned information) 2. One (or more) of the following cognitive disturbances: a. Aphasia (language disturbance) b. Apraxia (impaired ability to carry out motor activities despiteintact motor function) c. Agnosia (failure to recognize or identify objects despite intactsensory function) d. Disturbance in executive functioning (i.e., planning, organizing,sequencing, abstracting) B. The cognitive deficits in criteria A1 and A2 each cause significantimpairment in social or occupational functioning and represent asignificant decline from a previous level of functioning. C. The course is characterized by gradual onset and continuing cognitivedecline. D. The cognitive deficits in criteria A1 and A2 are not due to any ofthe following: 1. Other central nervous system conditions that cause progressivedeficits in memory and cognition (e.g., cerebrovasculardisease, Parkinson’s disease, Huntington’s disease, subduralhematoma, normal-pressure hydrocephalus, brain tumor) 2. Systemic conditions that are known to cause dementia (e.g.,hypothyroidism, vitamin B12 or folic acid deficiency, niacin deficiency, hypercalcemia, neurosyphilis, HIV infection) 3. Substance-induced conditions E. The deficits do not occur exclusively during the course of adelirium. F. The disturbance is not better accounted for by another Axis I disorder(e.g., major depressive disorder, schizophrenia). Specify if: With behavioral disturbance 17 CU IDOL SELF LEARNING MATERIAL (SLM)

1.3.3 Diagnostic Criteria for Dementia with Lewy Bodies A. The criteria are met for major or mild neurocognitive disorder. B. The disorder has an insidious onset and gradual progression. C. The disorder meets a combination of core diagnostic features and suggestive diagnostic features for either probable or possible neurocognitive disorder with Lewy bodies. For probable major or mild neurocognitive disorder with Lewy bodies, the individual has two core features, or one suggestive feature with one or more core features. For possible major or mild neurocognitive disorder with Lewy bodies, the individual has only one core feature, or one or more suggestive features. 1. Core diagnostic features: a. Fluctuating cognition with pronounced variations in attention and alertness. b. Recurrent visual hallucinations those are well formed and detailed. c. Spontaneous features of Parkinsonism, with onset subsequent to the development of cognitive decline. 2. Suggestive diagnostic features; a. Meets criteria for rapid eye movement sleep behavior disorder. b. Severe neuroleptic sensitivity. D. The disturbance is not better explained by cerebrovascular disease, another neurodegenerative disease, the effects of a substance, or another mental, neurological, or systemic disorder. 1.3.4Diagnostic Criteriafor Vascular Dementia A. The development of multiple cognitive deficits manifested by both 1. Memory impairment (impaired ability to learn new informationor to recall previously learned information) 2. One (or more) of the following cognitive disturbances: a. Aphasia (language disturbance) b. Apraxia (impaired ability to carry out motor activities despiteintact motor function) c. Agnosia (failure to recognize or identify objects despite intactsensory function) d. Disturbance in executive functioning (i.e., planning, organizing,sequencing, abstracting) B. The cognitive deficits in criteria A1 and A2 each cause significantimpairment in social or occupational functioning and represent asignificant decline from a previous level of functioning. 18 CU IDOL SELF LEARNING MATERIAL (SLM)

C. Focal neurological signs and symptoms (e.g., exaggeration ofdeep tendon reflexes, extensor plantar response, pseudobulbarpalsy, gait abnormalities, weakness of an extremity) or laboratoryevidence indicative of cerebrovascular disease (e.g., multiple infarctionsinvolving cortex and underlying white matter) that arejudged to be etiologically related to the disturbance. D. The deficits do not occur exclusively during the course of adelirium. With delirium: If delirium is superimposed on the dementia. With delusions: If delusions are the predominant feature. With depressed mood: If depressed mood (including presentationsthat meet full symptom criteria for a major depressive episode)is the predominant feature. A separate diagnosis of mooddisorder due to a general medical condition is not given. Uncomplicated: If none of the above predominates in the currentclinical presentation. Specify if: With behavioral disturbance 1.3.5 Diagnostic Criteria for Dementia Due to Traumatic Brain Injury A. The criteria are met for major or mild neurocognitive disorder. B. There is evidence of a traumatic brain injury—that is, an impact to the head or other mechanisms of rapid movement or displacement of the brain within the skull, with one or more of the following: 1. Loss of consciousness. 2. Posttraumatic amnesia. 3. Disorientation and confusion. 4. Neurological signs (e.g., neuroimaging demonstrating injury; a new onset of seizures; a marked worsening of a preexisting seizure disorder; visual field cuts; anosmia; hemiparesis). C. The neurocognitive disorder presents immediately after the occurrence of the traumatic brain injury or immediately after recovery of consciousness and persists past the acute post- injury period. 1.3.6 Diagnostic Criteria for Substance/Medication-Induced Dementia A. The criteria are met for major or mild neurocognitive disorder. B. The neurocognitive impairments do not occur exclusively during the course of a delirium and persist beyond the usual duration of intoxication and acute withdrawal. C. The involved substance or medication and duration and extent of use are capable of producing the neurocognitive impairment. 19 CU IDOL SELF LEARNING MATERIAL (SLM)

D. The temporal course of the neurocognitive deficits is consistent with the timing of substance or medication use and abstinence (e.g., the deficits remain stable or improve after a period of abstinence). E. The neurocognitive disorder is not attributable to another medical condition or is not better explained by another mental disorder. 1.3.7 Diagnostic Criteria for Dementia Due to Huntington’s Disease A. The criteria are met for major or mild neurocognitive disorder. B. There is insidious onset and gradual progression. C. There is clinically established Huntington’s disease, or risk for Huntington’s disease based on family history or genetic testing. D. The neurocognitive disorder is not attributable to another medical condition and is not better explained by another mental disorder. 1.3.8 Diagnostic Criteria for Dementia Due to HIV Infection A. The criteria are met for major or mild neurocognitive disorder. B. There is documented infection with human immunodeficiency virus (HIV). C. The neurocognitive disorder is not better explained by non-HIV conditions, including secondary brain diseases such as progressive multifocal leukoencephalopathy or cryptococcal meningitis. D. The neurocognitive disorder is not attributable to another medical condition and is not better explained by a mental disorder. 1.3.9Diagnostic Criteriafor Dementia Due to Other GeneralMedical Conditions A. The development of multiple cognitive deficits manifested by both 1. Memory impairment (impaired ability to learn new informationor to recall previously learned information) 2. One (or more) of the following cognitive disturbances: a. Aphasia (language disturbance) b. Apraxia (impaired ability to carry out motor activities despiteintact motor function) c. Agnosia (failure to recognize or identify objects despite intactsensory function) d. Disturbance in executive functioning (i.e., planning, organizing,sequencing, abstracting) B. The cognitive deficits in criteria A1 and A2 each cause significantimpairment in social or occupational functioning and represent asignificant decline from a previous level of functioning. 20 CU IDOL SELF LEARNING MATERIAL (SLM)

C. There is evidence from the history, physical examination, or laboratoryfindings that the disturbance is the direct physiological consequenceof one of the general medical conditions listed below. D. The deficits do not occur exclusively during the course of adelirium.  Dementia due to HIV disease  Dementia due to head trauma  Dementia due to Parkinson’s disease  Dementia due to Huntington’s disease  Dementia due to Pick’s disease  Dementia due to Creutzfeldt-Jakob disease  Dementia due to (indicate the general medical condition not listedabove) For example, normal-pressure hydrocephalus, hypothyroidism,brain tumor, vitamin B12 deficiency, intracranial radiation 1.4 INCIDENCE OF NEUROCOGNITIVE DISORDER The prevalence of dementias is not precisely known. Estimates varydepending on the age range of the population studied and whetherthe individuals sampled were in the general community, acute carefacilities, or long-term nursing institutions. A review of 47 surveysof dementia conducted between 1934 and 1985 indicated thatthe prevalence of dementia increasedexponentially by age, doublingevery 5 years up to age 95 years, and that this condition wasequally distributed among men and women, with Alzheimer’s dementia(AD) much more common in women. A National Institute of Mental Health Multisite EpidemiologicalCatchment Area study revealed a 6-month prevalence rate for milddementia of 11.5 to 18.4% for persons older than 65 years livingin the community. The rate for severe dementiawas higher for the institutionalized elderly: 15% of the elderly inretirement communities, 30% of nursing home residents and 54%of the elderly in state hospitals. Studies suggest that the fastest growing segment of theUS population consists of persons older than the age of 85 years,15% of whom are demented. Half of the USpopulation currently lives to the age of 75 years and one quarterlives to the age of 85. A study of 2000 consecutiveadmissions to a general medical hospital revealed that9% were demented and, among those, 41% were also delirious onadmission. The cost of providing carefor demented patients exceeds $100 billion annually (about 10%of all health care expenditures), and the average cost to familiesin 1990 was $18 000 a year. 21 CU IDOL SELF LEARNING MATERIAL (SLM)

1.5 PREVALENCE OF NEUROCOGNITIVE DISORDER Dementias are the most common causes of psychopathology in elderly persons. Dementia of the Alzheimer's type accounts for about 60 percent of old-age dementias. It is estimated to afflict from 5 to 10 percent of people age 65 and accounts for the most striking rise in dementia incidence in the very old. Dementia of the Alzheimer's type and related dementias cost society each year an estimated $100 billion, which includes both direct costs (i.e., actual dollar expenditures) and indirect costs (i.e., resource losses not involving dollar expenditures). The greatest risk factor for developing dementia is age—the incidence and prevalence of the disease double every 5 years after age 60. An estimated 4 million U.S. citizens suffer from Alzheimer's disease. As the baby-boom generation (born in the 1950s and 1960s) moves into the age group of 60 years and older, Alzheimer's disease will become an even greater public health problem. By the year 2040, 14 million Americans could be affected if current trends remain unabated. Moderate to severe dementia in a population aged 65 years or older is consistently reported at approximately 5 percent. Within that age group the exponential curve is pronounced so that the prevalence in the subgroup aged 65 to 69 years is 1.5 to 2 percent; in the subgroup aged 75 to 79 years it is 5.5 to 6.5 percent; and in the subgroup aged 85 to 89 years it is 20 to 22 percent. Dementia of the Alzheimer's type is the most common dementing disorder in clinical and neuropathological prevalence studies reported from North America, Scandinavia, and Europe. Prevalence studies from Russia and Japan show vascular dementia to be more common in those countries. It remains unclear whether those apparent clinical differences reflect true etiological distinctions or inconsistent uses of diagnostic criteria. Dementia of the Alzheimer's type becomes more common with increasing age; among persons older than 75 years, the risk is six times greater than the risk for vascular dementia. There is a suggestion of higher rates of dementia of the Alzheimer's type in females and higher rates of vascular dementia in males. In geriatric psychiatric patient samples, dementia of the Alzheimer's type is a much more common etiology (50 to 70 percent) than vascular dementia (15 to 25 percent). Studies of the incidence of dementia have been plagued by widely differing methodology and results. Again, there is an exponential increase in incidence with age, although some reports have noted a leveling off starting around age 75 years. 1.6 CO-MORBIDITY OF NEUROCOGNITIVE DISORDER World-wide there are an estimated 35.6 million people with dementia. By 2050 it has been estimated that this number will rise to more than 115 million. Dementia is primarily a disease of old age and it often coexists with other conditions of old age. Evidence suggests that 22 CU IDOL SELF LEARNING MATERIAL (SLM)

amongst people with dementia there is a high prevalence of comorbid medical conditions and related complaints. In addition, there is evidence to support an association between the dementia syndrome including Alzheimer’s disease and cardiovascular risk factors, such as hypertension and hyper cholesterol. Comorbidity amongst people with dementia presents particular challenges for primary and secondary care. Certain comorbid medical conditions may exacerbate the progression of dementia. For example, cognitive decline may be accelerated in older people with type 2 diabetes. Moreover, the presence of dementia may adversely affect and complicate the clinical care of other conditions and be a key factor in how patients’ needs are anticipated and specialist and emergency services are used. It may also undermine patients’ abilities to self- manage chronic conditions and engage in health maintenance activities. Despite this, little is known about the effects of comorbidity on processes and quality of care, patient experience, or how services are adapting to address the particular needs of this population. A review of qualitative research on the experience of diagnosis and treatment of dementia found very little evidence relating to the experiences of people diagnosed with dementia who have an accompanying comorbid condition. There is also a lack of research on patients’ views on the ways in which multiple conditions affect their health, well-being and clinical care. The aim of this review was to identify the extent, range and nature of research activity relating to dementia and comorbidity, in particular the prevalence of co-morbidity amongst people with dementia, systems and structures that currently exist for the care of people with dementia who have comorbid medical conditions, and the experiences of people with dementia who have comorbid medical conditions and their family careers. 1.7 CAUSES OF NEUROCOGNITIVE DISORDER As our technology for studying the brain advances, so does our understanding of the many and varied causes of dementia. Biological Influences Cognitive abilities can be adversely compromised in many ways. As you have seen, dementia can be caused by a number of processes: Alzheimer’sdisease, Huntington’s disease, Parkinson’s disease, head trauma,substance abuse, and others. The most common cause of dementia,Alzheimer’s disease, is also the most mysterious. Because ofits prevalence and our relative ignorance about the factors responsiblefor it, Alzheimer’s disease has held the attention of manyresearchers, who are trying to find the cause and ultimately atreatment or cure for this devastating condition. Findings from Alzheimer’s research seem to appear almostdaily. We should be cautious when interpreting the output of thisfast-paced and competitive field; too often, as you have seen inother areas, findings are heralded prematurely as conclusive andimportant. Remember that “discoveries” of a single gene for bipolardisorder, schizophrenia, and alcoholism were 23 CU IDOL SELF LEARNING MATERIAL (SLM)

later shown tobe based on overly simplistic accounts. Similarly, findings fromAlzheimer’s research are sometimes too quickly sanctioned asaccepted truths before they have been replicated, an essential validationprocess. Psychological and Social Influences Research has mostly focused on the biological conditions thatproduce dementia. Although few would claim that psychosocialinfluences directly cause the type of brain deterioration seen inpeople with dementia, they may help determine onset and course.For example, a person’s lifestyle may involve contact with factorsthat can cause dementia. You saw, for instance, that substanceabuse can lead to dementia and, as we discussed previously, whether a person abuses drugs is determined by acombination of biological and psychosocial factors. In the case ofvascular dementia, a person’s biological vulnerability to vasculardisease will influence the chances of strokes that can lead to thisform of dementia. Lifestyle issues such as diet, exercise, andstress influence cardiovascular disease and therefore help determinewho experiences vascular dementia. Cultural factors may also affect this process. For example,hypertension and strokes are prevalent among African Americansand certain Asian Americans, which may explain why vascular dementia is more oftenobserved in members of these groups. In an extreme example,exposure to a viral infection can lead to dementia similar in formto Creutzfeldt- Jakob disease through a condition known as kuru.This virus is passed on through a ritual form of cannibalism practicedin Papua New Guinea as a part of mourning. Dementia caused by head trauma and malnutrition arerelatively prevalent in preindustrial rural societies. Not getting enough of vitaminsB9 and B12 in particular seems to lead to dementia, althoughthe process is as yet unknown. These findings suggest that occupationalsafety (such as protecting workers from head injuries)and economic conditions influencing diet also affect the prevalenceof certain forms of dementia. It is apparent that psychosocialfactors help influence who does and who does not developcertain forms of dementia. Brain deterioration is a biological processbut, as you have seen throughout this text, even biologicalprocesses are influenced by psychosocial factors. Psychosocial factors themselves influence the course of dementia.Recall that educational attainment may affect the onset ofdementia. Having certain skills mayhelp some people cope better than others with the early stages ofdementia. As you saw earlier, Diana’s mother was able to carry onher day-to-day activities by making maps and using other tricksto help compensate for her failing abilities. The early stages ofconfusion and memory loss may be better tolerated in cultureswith lowered expectations of older adults. In certain cultures, includingthe Chinese, younger people are expected to take the demandsof work and care from older adults after a certain age, andsymptoms of dementia are viewed as a sign of normal aging. Dementia may go undetected for years in thesesocieties. 24 CU IDOL SELF LEARNING MATERIAL (SLM)

Much remains to be learned about the cause and course ofmost types of dementia. As you saw with Alzheimer’s disease andHuntington’s disease, certain genetic factors make some individualsvulnerable to progressive cognitive deterioration. In addition,brain trauma, some diseases, and exposure to certain drugs, suchas alcohol, inhalants, and sedative, hypnotic, and anxiolyticdrugs, can cause the characteristic decline in cognitive abilities. We also noted that psychosocial factors can help determine whois subject to these causes and how they cope with the condition.Looking at dementia from this integrative perspective should helpyou view treatment approaches in a more optimistic light. It maybe possible to protect people from conditions that lead to dementiaand to support them in dealing with the devastating consequencesof having it. We next review attempts to help from bothbiological and psychosocial perspectives. The prevalence of comorbid conditions in people with dementia is high. Whilst current evidence suggests that people with dementia may have poorer access to services the reasons for this are not clear. There is a need for more research looking at the ways in which having dementia impacts on clinical care for other conditions, how process of care and different services can adapt to the needs of people with dementia and comorbidity, and what interventions might improve access to services and the physical health of people with dementia. Clinical guidance should consider the particular needs of those with dementia and comorbid health conditions. 1.8 PROGNOSIS OF NEUROCOGNITIVE DISORDER The course of a particular dementia is influenced by its etiology.Although historically the dementias have been considered progressiveand irreversible, there is, in fact, significant variationin the course of individual dementias. The disorder can be progressive,static, or remitting. In addition to the etiology, factors that influence the courseof the dementia include: i. the time span between the onset andthe initiation of prescribed treatment, ii. the degree of reversibilityof the particular dementia, iii. the presence of comorbid psychiatricdisorders, and iv. the level of psychosocial support. Theprevious distinction between treatable and untreatable dementiashas been replaced by the concepts of reversible, irreversible andarrestable dementias. Most reversible cases of dementia are associatedwith shorter duration of symptoms, mild cognitive impairmentand superimposed delirium. Specifically, the dementiascaused by drugs, depression and metabolic disorders are mostlikely to be reversible. Other conditions such as normal pressurehydrocephalous, subdural hematomas and tertiary syphilis aremore commonly arrestable. 25 CU IDOL SELF LEARNING MATERIAL (SLM)

Although potentially reversible dementias should be aggressivelyinvestigated, in reality, only 8% of dementias are partiallyreversible and about 3% fully reversible (Kaufman, 1990b).There is some evidence to suggest that early treatment of dementedpatients, particularly those with Alzheimer’s type, withsuch agents as donepezil, which acts as an inhibitor of acetylcholinesterase,and galantamine may slow the rate of progressionof the dementia. 1.8.1 Prognosis for Neurocognitive Disorders The course of NCD varies across etiological subtypes, and this variation can be useful in differential diagnosis. Some subtypes (e.g., those related to traumatic brain injury or stroke) typically begin at a specific time and (at least after initial symptoms related to inflammation or swelling subside) remain static. Others may fluctuate over time (although if this occurs, the possibility of delirium superimposed on NCD should be considered). NCDs due to neurodegenerative diseases like Alzheimer's disease or frontotemporal lobar degeneration typically are marked by insidious onset and gradual progression, and the pattern of onset of cognitive deficits and associated features helps to distinguish among them. NCDs with onset in childhood and adolescence may have broad repercussions for social and intellectual development, and in this setting intellectual disability (intellectual developmental disorder) and/or other neurodevelopmental disorders may also be diagnosed to capture the full diagnostic picture and ensure the provision of a broad range of services. In older individuals, NCDs often occur in the setting of medical illnesses, frailty, and sensory loss, which complicate the clinical picture for diagnosis and treatment. When cognitive loss occurs in youth to midlife, individuals and families are likely to seek care. NCDs are typically easiest to identify at younger ages, although in some settings malingering or other factitious disorders may be a concern. Very late in life, cognitive symptoms may not cause concern or may go unnoticed. In late life, mild NCD must also be distinguished from the more modest deficits associated with \"normal aging,\" although a substantial fraction of what has been ascribed to normal aging likely represents prodromal phases of various NCDs. In addition, it becomes harder to recognize mild NCD with age because of the increasing prevalence of medical illness and sensory deficits. It becomes harder to differentiate among subtypes with age because there are multiple potential sources of neurocognitive decline. 1.8.2 Prognosis for Alzheimer’s Disease Major or mild NCD due to Alzheimer's disease progresses gradually, sometimes with brief plateaus, through severe dementia to death. The mean duration of survival after diagnosis is approximately 10 years, reflecting the advanced age of the majority of individuals rather than the course of the disease; some individuals can live with the disease for as long as 20 years. Yate-stage individuals are eventually mute and bedbound. Death most commonly results from aspiration in those who survive through the full course. In mild NCD due to Alzheimer's 26 CU IDOL SELF LEARNING MATERIAL (SLM)

disease, impairments increase over time, and functional status gradually declines until symptoms reach the threshold for the diagnosis of major NCD. The onset of symptoms is usually in the eighth and ninth decades; early-onset forms seen in the fifth and sixth decades are often related to known causative mutations. Symptoms and pathology do not differ markedly at different onset ages. However, younger individuals are more likely to survive the full course of the disease, while older individuals are more likely to have numerous medical comorbidities that affect the course and management of the illness. Diagnostic complexity is higher in older adults because of the increased likelihood of comorbid medical illness and mixed pathology. 1.8.3 Prognosis for Dementia with Lewi Bodies Dementia with Lewi Bodies is a gradually progressive disorder with insidious onset. However, there is often a prodromal history of confusional episodes (delirium) of acute onset, often precipitated by illness or surgery. The distinction between Dementia with Lewi Bodiesentia, in which Lewy bodies are primarily cortical in location, and major or mild NCD due to Parkinson's disease, in which the pathology is primarily in the basal ganglia, is the order in which the cognitive and motor symptoms emerge. In Dementia with Lewi Bodies, the cognitive decline is manifested early in the course of illness, at least a year before the onset of motor symptoms (see the section \"Differential Diagnosis\" for this disorder). Disease course may be characterized by occasional plateaus but eventually progresses through severe dementia to death. Average duration of survival is 5-7 years in clinical series. Onset of symptoms is typically observed from the sixth through the ninth decades of life, with most cases having their onset when affected individuals are in their mid-70s. 1.8.4 Prognosis for Vascular Dementia Major or mild vascular Dementia can occur at any age, although the prevalence increases exponentiallyafter age 65 years. In older individuals, additional pathologies may partly accountfor the neurocognitive deficits. The course may vary from acute onset with partialimprovement to stepwise decline to progressive decline, with fluctuations and plateaus ofvarying durations. Pure subcortical major or mild vascular Dementia can have a slowly progressivecourse that simulates major or mild Dementia due to Alzheimer's disease. 1.8.5 Prognosis for Dementia Due to Traumatic Brain Injury The severity of a Traumatic Brain Injury is rated at the time of injury/initial assessment as mild, moderate, or severe according to the thresholds in Table below. Severity ratings for traumatic brain injury Injury characteristic Mild Moderate Severe Loss of consciousness <30 minutes 30 minutes-24 >24 hours 27 CU IDOL SELF LEARNING MATERIAL (SLM)

hours Posttraumatic amnesia <24 hours 24 hours-7 >7 days days Disorientation and confusion at initial 13-15 9-12 3-8 assessment (Glasgow Coma Scale Score) The severity rating of the Traumatic Brain Injury itself does not necessarily correspond to the severity of the resulting Dementia. The course of recovery from Traumatic Brain Injury is variable, depending not only on the specifics of the injury but also on cofactors, such as age, prior history of brain damage, or substance abuse, that may favor or impede recovery. 1.8.6 Prognosis for Substance/Medication Induced Dementia Substance use disorders tend to commence during adolescence and peak in the 20s and 30s. Although longer history of severe substance use disorder is associated with greater likelihood of Neuro Cognitive Disorders, the relationships are not straightforward, with substantial and even complete recovery of neurocognitive functions being common among individuals who achieve stable abstinence prior to age 50 years. Substance/medication-induced major or mild Neuro Cognitive Disorders is most likely to become persistent in individuals who continue abuse of substances past age 50 years, presumably because of a combination of lessened neural plasticity and beginnings of other age-related brain changes. Earlier commencement of abuse, particularly of alcohol, may lead to defects in later neural development (e.g., later stages of maturation of frontal circuitries), which may have effects on social cognition as well as other neurocognitive abilities. For alcohol-induced Neuro Cognitive Disorders, there may be an additive effect of aging and alcohol-induced brain injury 1.8.7 Prognosis for Dementia Due to Huntington’s Disease The average age at diagnosis of Huntington's disease is approximately 40 years, although this varies widely. Age at onset is inversely correlated with CAG expansion length. Juvenile Huntington's disease (onset before age 20) may present more commonly with bradykinesia, dystonia, and rigidity than with the choricmovement’s characteristic of the adult-onset disorder. The disease is gradually progressive, with median survival approximately15 years after motor symptom diagnosis. Phenotypic expression of Huntington's disease varies by presence of motor, cognitive,and psychiatric symptoms. Psychiatric and cognitive abnormalities can predate the motorabnormality by at least 15 years. Initial symptoms requiring care often include irritability,anxiety, or depressed mood. Other behavioral disturbances may include pronounced apathy,disinhibition, impulsivity, and impaired insight, with apathy often becoming moreprogressive over time. Early movement symptoms may involve the 28 CU IDOL SELF LEARNING MATERIAL (SLM)

appearance of fidgetinessof the extremities as well as mild apraxia (i.e., difficulty with purposeful movements),particularly with fine motor tasks. As the disorder progresses, other motor problems includeimpaired gait (ataxia) and postural instability. Motor impairment eventually affectsspeech production (dysarthria) such that the speech becomes very difficult to understand, which may result in significant distress resulting from the communication barrier in the context of comparatively intact cognition. Advanced motor disease severely affects gaitwith progressive ataxia. Eventually individuals become non-ambulatory. End-stage motordisease impairs motor control of eating and swallowing, typically a major contributor tothe death of the individual from aspiration pneumonia. 1.8.8 Prognosis for Dementia Die to HIV Infection A Neuro Cognitive Disorder due to HIV infection can resolve, improve, slowly worsen, or have a fluctuating course. Rapid progression to profound neurocognitive impairment is uncommon in the context of currently available combination antiviral treatment; consequently, an abrupt change in mental status in an individual with HIV may prompt an evaluation of other medical sources for the cognitive change, including secondary infections. Because HIV infection preferentially affects subcortical regions over the course of illness, including deep white matter, the progression of the disorder follows a \"subcortical\" pattern. Since HIV can affect a variety of brain regions, and the illness can take on many different trajectories depending on associated comorbidities and consequences of HIV, the overall course of a Neuro Cognitive Disorder due to HIV infection has considerable heterogeneity. A subcortical neurocognitive profile may interact with age over the life course when psychomotor slowing and motor impairments such as slowed gait may occur as a consequence of other age-related conditions so that the overall progression may appear more pronounced in later life. In developed countries, HIV disease is primarily a condition of adults, with acquisition via risky behaviors (e.g., unprotected sex, injection drug use) beginning in late adolescence and peaking during young and middle adulthood. In developing countries, particularly sub- Saharan Africa, where HIV testing and antiretroviral treatments for pregnant women are not readily available, perinatal transmission is common. The Neuro Cognitive Disorder in such infants and children may present primarily as neurodevelopmental delay. As individuals treated for HIV survive into older age, additive and interactive neurocognitive effects of HIV and aging, including other Neuro Cognitive Disorder s (e.g., due to Alzheimer's disease, due to Parkinson's disease), are possible. 1.8.9 Prognosis for Dementia Die to Other General Medical Conditions Typically the course of the NCD progresses in a manner that is commensurate with progression of the underlying medical disorder. In circumstances where the medical disorder is treatable (e.g., hypothyroidism), the neurocognitive deficit may improve or at least not progress. When the medical condition has a deteriorative course (e.g., secondary progressive 29 CU IDOL SELF LEARNING MATERIAL (SLM)

multiple sclerosis), the neurocognitive deficits will progress along with the temporal course of illness. 1.9 TREATMENT OF NEUROCOGNITIVE DISORDER For many of the disorders discussed in other chapters, treatmentprospects are fairly good. Clinicians can combine various strategiesto reduce suffering significantly. Even when treatment doesnot bring expected improvements, mental health professionalshave usually been able to stop problems from progressing. This isnot the case in the treatment of dementia. One factor preventing major advances in the treatment of dementiais the nature of the damage caused by this disorder. Thebrain contains billions of neurons, many more than are used.Damage to some can be compensated for by others because ofplasticity. However, there is a limit to where and how many neuronscan be destroyed before vital functioning is disrupted. Researchersare closing in on how to use the brain’s natural processof regeneration to potentially reverse the damage caused in dementia. Currently, however, with extensivebrain damage, no known treatment can restore lost abilities. Thegoals of treatment therefore become (1) Trying to prevent certainconditions, such as substance abuse, that may bring on dementia; (2) Trying to delay the onset of symptoms to provide better qualityof life; and (3) Attempting to help these individuals and their caregiverscope with the advancing deterioration. Most efforts intreating dementia have focused on the second and third goals,with biological treatments aimed at stopping the cerebral deteriorationand psychosocial treatments directed at helping patientsand caregivers cope. A troubling statistic further cloud the tragic circumstancesof dementia: More than 23% of caregivers of people withdementia—usually relatives—have the symptoms characteristicof one or more anxiety disorders and 10% are clinically depressed. Compared with the public, thesecaregivers use more psychotropic medications (designed to reducesymptoms of various psychological disorders) and reportstress symptoms at 3 times the normal rate. Caring for peoplewith dementia, especially in its later stages, is clearly a tryingexperience. In fact, there is some evidence to suggest that thestress associated with caring for a person with dementia may place the caregiver at greatly increasedrisk for developing dementia themselves. As a result,clinicians are becoming increasinglysensitive to the needs of these caregivers,and research is now exploring interventionsto assist them in caring forpeople with dementia. Biological Treatments Dementia resulting from known infectious diseases, nutritionaldeficiencies, and depression can be treated if it is caught early.Unfortunately, however, no known treatment exists for 30 CU IDOL SELF LEARNING MATERIAL (SLM)

most typesof dementia that are responsible for the vast majority of cases.Dementia caused by stroke, HIV, Parkinson’s disease, or Huntington’sdisease is not currently treatable because there is no effectivetreatment for the primary disorder. However, exciting researchin several related areas has brought us closer to helpingindividuals with these forms of dementia. A substance that mayhelp preserve and perhaps restore neurons—called glial cell– derivedneurotrophic factor—may someday be used to help reduceor reverse the progression of degenerative brain diseases. Researchers are also looking into the possiblebenefits of transplanting stem cells (fetal brain tissue) into thebrains of people with such diseases. Initial results from thesestudies are still preliminary but appear promising. Dementia brought on by strokes may now be more preventable bynew drugs that help prevent much of the damage inflicted by theblood clots characteristic of stroke.Most current attention is on a treatment for dementia of the Alzheimer’stype, because it affects so many people. Here, too,however, success has been modest at best.Several other medical approaches are being explored to slowthe course of Alzheimer’s disease, but initial excitement generatedby these approaches has waned with the findings from researchers. For example, most of you have heard of using Ginkgobiloba (maidenhair) to improve memory. Initial research suggestedthat this herbal remedy may produce modest improvementsin the memory of people with Alzheimer’s disease, butother studies have not replicated this benefit. Similarly, the effects of vitamin E have been evaluated. One large study found that among individuals with moderatelysevere impairment, high doses of the vitamin (2,000 internationalunits per day) delayed progression compared to a placebo, but it did not prevent the development of the disease. Further research, in fact, indicates that taking high doses of vitaminE may actually increase mortality and therefore this interventionis no longer recommended. Modestslowing of the progression of the disease also may be obtainedby introducing exercise to patients. To date, however, no medical interventionsare available that directly treat and therefore stop the progressionof the conditions that cause the cerebral damage in Alzheimer’sdisease. Medical interventions for dementia also include the useof drugs to help with some associated symptoms. A variety ofantidepressants—such as serotonin-specific reuptake inhibitors—are commonly recommended to alleviate the depression and anxietythat too often accompany the cognitive decline. Antipsychoticmedication is sometimes used for those who become unusuallyagitated. Next, we describe psychosocialapproaches that are used with medication to address the varietyof problems that accompany memory difficulties. Psychosocial Treatments 31 CU IDOL SELF LEARNING MATERIAL (SLM)

Psychosocial treatments are now receiving a great deal of attentionfor their ability to delay the onset of severe cognitive decline.These efforts focus on enhancing the lives of people with dementia,as well as those of their families. People with dementia can be taught skills to compensate fortheir lost abilities. Recall that Diana’s mother learned on her ownto make maps to help her get from place to place. Diana herselfbegan making lists so that she would not forget important things. Some researchers have evaluated more formal adaptations to helppeople in the early stages of dementia. Michelle Bourgeois created “memory wallets” to help people with dementia carry onconversations. On white index cards inserted into a plastic wallet are printed declarative statements such as, “My husband John andI have 3 children,” or “I was born on January 6, 1921, in Pittsburgh.” In one of her studies, Bourgeois found that adultswith dementia could, with minimal training, use this memory aidto improve their conversations with others. Adaptations such asthese help people communicate with others, help them remainaware of their surroundings, and can reduce the frustration thatcomes with the awareness of their own decline. Cognitive stimulation—encouraging people with dementia topractice learning and memory skills—seems to be an effectivemethod for delaying the onset of the more severe cognitive effectsof this disorder. These activities include wordgames, tests of memory of famous and familiar faces, and practicewith numbers (for example, how much change back youwould receive from a purchase). These types of skill-buildingexercises can maintain cognitive activity and improve the qualityof life in those patients when compared to controls. Individuals with advanced dementia are not able to feed,bathe, or dress themselves. They cannot communicate with orrecognize even familiar family members. They may wander awayfrom home and become lost. Because they are no longer aware ofsocial stigma, they may engage in public displays of sexual behavior,such as masturbation. They may be frequently agitated oreven physically violent. To help both the person with dementiaand the caregiver, researchers have explored interventions fordealing with these consequences of the disorder. For example, some research indicates that a combinationof exercise for patients and instruction for caregivers onhow to handle behavior problems can improve the overall healthand the depression in people with Alzheimer’s disease. Of great concern is the tendency of people with dementia towander. Sometimes they wind up in places or situations that maybe dangerous (for example, stairwells or the street). Often, theperson is tied to a chair or bed, or sedated, to prevent roaming. Unfortunately, physical and medical restrainthas its own risks, including additional medicalcomplications; it also adds greatly to the lossof control and independence that alreadyplague the person with dementia. Psychologicaltreatment as an alternative to restraintsometimes involves providing cues for peopleto help them safely navigate around 32 CU IDOL SELF LEARNING MATERIAL (SLM)

theirhome or other areas. New innovations in surveillancetechnology—creating a “smarthome” that can monitor the location of thepatient and warn caregivers—may providemore piece of mind for those who care forthese patients. At the same time, ethical concernsare being raised about the use of thistechnology because of its ability to invadeprivacy. Someone with dementia can become agitatedand sometimes verbally and physicallyaggressive. This behavior is understandablystressful for people trying to provide care. Inthese situations, medical intervention is oftenused, although many times with only modestresults. Caregivers are often given assertiveness training to helpthem deal with hostile behaviors. Otherwise,caregivers may either passively accept all criticism inflicted bythe person with dementia, which increases stress, or become angry and aggressive in return. This last response is of particularconcern because of the potential for elder abuse. Withholdingfood or medication or inflicting physical abuse is most commonamong caregivers of elderly people who have cognitive deficits. It is important to teachcaregivers how to handle stressful circumstances so that they donot escalate into abusive situations. Not a great deal of objectiveevidence supports the usefulness of assertiveness training for reducingcaregiver stress, and more research is needed to guide futureefforts. In general, families of people with dementia can benefit fromsupportive counseling to help them cope with the frustration,depression, guilt, and loss that take a heavy emotional toll.However, clinicians must first recognize that the ability to adaptto stressors differs among people. One study, for example, foundcultural differences in the coping styles of caregivers. In onearea of rural Alabama, white caregivers used acceptance andhumor as coping strategies, and black caregivers used religionand denial. Another large-scale study of 555 principal caregivers over a3-year period identified a number of steps that can be taken tosupport caregivers through these difficult times. However, despitenumerous studies aimed at supporting caregivers, the results todate remain weak and additional work is needed to determinehow best to support these individuals. Early on, caregivers need basic information on the causesand treatment of dementia, financial and legal issues, and locatinghelp for the patient and the family. As the dementia progresses,and the affected person requires increasing amounts of assistance,caregivers will need help managing behavioral difficulties (wanderingaway or violent outbursts) and developing effectiveways to communicate with the patient. Clinicians also assist thefamily with decisions about hospitalizations and, finally, helpthem adjust during bereavement. Overall, the outlook for slowing (but not stopping) the cognitivedecline characteristic of dementia is optimistic. The bestavailable medications provide some recovery of function, but theydo not stop the progressive deterioration. Psychological interventionsmay help people cope more effectively with the loss ofcognitive abilities, especially in the earlier stages of this 33 CU IDOL SELF LEARNING MATERIAL (SLM)

disorder.In addition, emphasis is placed on helping caregivers—the othervictims of dementia—as the person they care for continues todecline. Prevention Without treatment, we need to rely even more heavily on preventionstrategies for dementia. You can imagine that it is difficultto study prevention efforts for dementia because of the need tofollow individuals for long periods to see whether the effortsare effective. One major study conducted in Sweden—wheresocialized medicine provides complete medical histories of allresidents—looked at many of the risk factors (those factors thatincrease the chance of having dementia) and protective factors(those that decrease the risk) under study today. They looked at the medical recordsof 1,810 participants who were older than 75 at the time andfollowed them for about 13 years. Through interviews and medicalhistories, they came to two major conclusions: control yourblood pressure, and lead an active physical and social life! Thesetwo recommendations came out as the major factors that individualscan change— because you cannot change your genetics,for example—that will decrease the chances of developing dementia.Additional prevention research is ongoing, and there maybe other potentially fruitful research areas that can lead to thesuccessful prevention of this devastating disorder. 1.10 SUMMARY  Most aspects of cognitive functioning remain stable during the normal course of aging. However, fluid intelligence and the related abilities of processing speed, recalling verbal information on demand, maintaining attention, and multitasking do decline in older adults. But these declines do not generally impair daily functioning.  Although older adults are less likely than younger adults to have a psychological disorder, the disorders that are most common among older adults are depression and generalized anxiety disorder. A small percentage of adults develop schizophrenia and have their first psychotic episode after the age of 44. These disorders can lead to impaired cognitive functioning that may superficially resemble symptoms of a cognitive disorder.  Brain injury, most commonly from a stroke, can produce various cognitive deficits that may resemble those related to psychological disorders. Among the deficits that may follow a stroke or a head injury are aphasia (problems with producing and comprehending language), agnosia (problems in interpreting what is perceived), and apraxia (problems in organizing and producing voluntary movements).  Legally prescribed medications or illegal substances can alter awareness, emotional states, and cognitive functioning. A dose that is standard for a younger person can adversely affect an older adult. 34 CU IDOL SELF LEARNING MATERIAL (SLM)

 Neurocognitive disorder is an umbrella term of conditions used to describe impairments in mental functioning. Most of the neurocognitive disorders occurs most commonly in older adults.  Neurocognitive disorders are a group of conditions that frequently lead to impaired mental function. Organic brain syndrome used to be the term to describe these conditions, but neurocognitive disorders is now the more commonly used term.  Neurocognitive disorders were previously referred to as “dementia”. The common symptoms of neurocognitive disorders include impairments in cognitive abilities like language, memory, perception, problem solving, etc.  Neurocognitive disorders are progressive in nature wherein the symptoms become severe as time passes. The broad category of dementia under cognitive disorders is renamed as majorneurocognitive disorder in DSM-5. Due to this renaming the stigma associatedhas reduced to some extent. A major reason for change was that although theterm dementia has been accepted for older adults but it is not consideredappropriate for younger adults with cognitive deficit, for those who have sustaineddamage from certain head injuries. Major Neurocognitive Disorders are characterized by marked deficits in cognitiveabilities such as attention, learning, memory, language, perception, socialcognition and executive functioning. It is important to note that the decline beingdiscussed here is the deterioration from a previously attained level. The onset of cognitive deficits is gradual. Initially, the individual is alert and also attuned tothe environment. 1.11 KEY WORDS  An etiology: The study of the origins of disease: physical, mental or emotional.  Alzheimer's disease: A degenerative form of dementia whose symptoms are similar to senile dementia but which can occur in middle age.  Dementia: A disabling disorder of both cognition and affect which impairs the higher mental processes of learning, thinking, decision-making and, especially, memory and is accompanied by changes in personality and ways of relating to other people.  Depression: One of the most common forms of emotional disturbance which can vary in intensity from an everyday attack of 'the blues ' to a psychotic condition of paralyzing hopelessness.  Face recognition: Concerned with the processes involved in the way we recognize faces.  Hallucination: A perceptual illusion of a vivid experience that has no apparent reality in the external world. 35 CU IDOL SELF LEARNING MATERIAL (SLM)

 Korsakoff's syndrome: A memory disorder involving amnesia, due mostly to alcoholism, first observed by the nineteenth-century Russian neurologist Sergei Korsakoff.  Psychotherapy: The use of psychological techniques to treat psychological disturbances. 1.12 LEARNING ACTIVITY 1. Explain with the help of the case study given in the unit, the DSM criteria for neurocognitive disorders? ___________________________________________________________________________ ___________________________________________________________________________ 2. Explain with the help of the case study given in the unit, the ICD 10 criteria for neurocognitive disorders? ___________________________________________________________________________ ___________________________________________________________________________ 1.13 UNIT END QUESTIONS 36 A. Descriptive Questions Short Questions 1. Define neurocognitive disorder. 2. Name any two types of neurocognitive disorder. 3. What are the primary symptoms of neurocognitive disorder? 4. What are first symptoms of Alzheimer’s disorder? 5. What the reasons for Wernicke Korsakoff’s Syndrome? 6. Which of the neurocognitive disorder which has a genetic causation? 7. What are some of the comorbidities of neurocognitive disorder? Long Questions 1. Explain the different types of neurocognitive disorders in detail. 2. What is DSM 5 criteria for mild moderate neurocognitive disorders? 3. What is DSM 5 criteria for moderate neurocognitive disorders? 4. Explain the causes of neurocognitive disorders? CU IDOL SELF LEARNING MATERIAL (SLM)

5. Explain the prognosis of neurocognitive disorders? 6. What is the pharmacological treatment available for treatment of neurocognitive disorders? 7. What is the non-pharmacological treatment available for treatment of neurocognitive disorders? B. Multiple Choice Questions 1. Which of the following sentence is/ are correct about Dementia? a. In Dementia mental ability declines and interfere the daily life. b. A person suffering from this disease may forget his or her name. c. Alzheimer's disease is a cause of Dementia. d. All the above are correct 2. A much-feared outcome of Alzheimer's disease is a. senile dementia b. general paresis c. paranoia d. functional psychosis 3. Which of the following medical conditions can produce a mild neurocognitive disorder and mild impairments in social/occupational functioning? a. Creutzfeldt-Jakob disease b. Huntington's disease c. HIV d. Parkinson's disease 4. Which of the following are the consequences of vitamin and mineral deficiencies which can lead to dementia and memory disorders in alcohol abuse? a. Creutzfeldt-Jakob disease b. Korsakoff's syndrome c. HIV d. Parkinson's disease 37 CU IDOL SELF LEARNING MATERIAL (SLM)

5. Occasionally, other health conditions may mimic this disease. What are they? a. heredity b. age c. All of these d. Toxins Answers 1-d, 2-a, 3-c, 4-b, 5-c 1.14 REFERENCES Textbooks  Ahuja N (2002). A short text book of Psychiatry. (5th edh). New Delhi: Jaypee Brothers Medical. Publishers (pvt.) Ltd.  American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders, Fourth Edition, Text Revision: DSM-IV-TR. Washington, DC: American Psychiatric Publishing, Inc.  Clifford Morgan, Richard King, John Weisz, John Schopler (2004) Introduction to Psychology, McGraw-Hill, New Delhi  Damjan Michael (2010). The Principles of Learning and Behavior (6th Edn) Wadsworth, Cengage Learning.  Hergenhahn B R (2008). An introduction to the history of psychology, Wadsworth, Cengage Learning.  Robert S. Feldman (2011) Understanding Psychology, McGraw-Hill, New Delhi.  Robert. A. Baron, Psychology, (2008) Prentice Hall India. Reference books  American Psychiatric Association (2000). Diagnostic and statistical manual of mental disorders, Fourth Edition, Text Revision: DSM-IV-TR. Washington, DC: American Psychiatric Publishing, Inc.  Carson, R. C., Butcher, J. N., & Mineka, S. (2002).Abnormal psychology over time. In Fundamentals of abnormal psychology and modern life. New York: Allyn & Bacon. 38 CU IDOL SELF LEARNING MATERIAL (SLM)

 Emery, R.E., &Oltmans, T.F. (1998). Abnormal Psychology (2nd ed.). Upper Saddle River, NJ: Prentice-Hall, Inc.  Kay J, Tasman A. (2006) Essentials of Psychiatry, Chichester, John R. Wiley and Sons.  Sadock, Benjamin, J., & Virginia A. (2002). Kaplan and Sadock’s Synopsis of Psychiatry: Behavioral Sciences/Clinical Psychiatry (9th ed.). Lippincott Williams &Wilkins.  Sarason I., G & Sarason B. R. (2005).Abnormal psychology: The problem of maladaptive behavior. (11th edn). PHI Learning Private limited.  World Health Organization (1993). The ICD-10 Classification of Mental and Behavioral Disorders Websites  www.simplypsychology.com  http://www.human-memory.net  www.simplypsychology.org  https://psychcentral.com  https://courses.lumenlearning.com  https://www.sparknotes.com 39 CU IDOL SELF LEARNING MATERIAL (SLM)

UNIT 2 – PARKINSON'S DISEASES STRUCTURE 2.0 Learning Objectives 2.1 Introduction 2.2 Parkinson's Diseases 2.3 DSM criteria for Parkinson's Diseases 2.4 Incidence of Parkinson's Diseases 2.5 Prevalence of Parkinson's Diseases 2.6Co-morbidity of Parkinson's Diseases 2.7 Causes of Parkinson’s disease 2.8 Prognosis of Parkinson's Diseases 2.9 Treatment of Parkinson's Diseases 2.10 Summary 2.11 Key Words 2.12 Learning Activity 2.13 Unit End Questions 2.14 References 2.0 LEARNING OBJECTIVES After studying this unit, you will be able to,  Explain the nature and symptoms of Parkinson’s diseases  Describe the incidence and prevalence of Parkinson’s diseases  Explain the co-morbidity of Parkinson’s diseases  State the causes of Parkinson’s diseases  Explain the prognosis of Parkinson’s diseases  State the treatment for Parkinson’s diseases 2.1 INTRODUCTION Parkinson’s disease is rare before the age of 40, but becomes increasing common with age, and affects 1–2% of people over 65 years old. Several genes causing familial Parkinson’s 40 CU IDOL SELF LEARNING MATERIAL (SLM)

disease have been identified, and other genes probably contribute to the risk of developing the disease in those with no family history. Environmental factors that increase the risk of developing Parkinson’s disease include working with pesticides; drinking coffee and smoking cigarettes both reduce the risk. The symptoms and signs of Parkinson’s disease reflect a highly selective pattern of degeneration in the brain. The worst damage occurs in the dopamine-producing neurons of the substantia nigra, and this accounts for many of the abnormalities of movement, referred to as ‘parkinsonism’. These neurons project to the corpus striatum via the nigrostriatal pathway. The consequence of loss of neurons in the substantia nigra is dopamine deficiency in the corpus striatum. This may be unilateral, asymmetrical or symmetrical. 2.2 PARKINSON’S DISEASE Named after James Parkinson, who first described it in 1817,Parkinson’s disease is the second most common neurodegenerativedisorder (after Alzheimer’s disease). It is more often foundin men than in women, and it affects between 0.5 and 1 percentof people between ages 65 and 69 and 1 to 3 percent of peopleover 80 (Toulouse & Sullivan, 2008). However, the actorMichael J. Fox developed Parkinson’s disease when he was only30 years old. His book Lucky Man (2002) offers a moving personalaccount of his struggle with the illness and well describessome of its major symptoms. Parkinson’s disease is a degenerative brain disorder that affects about 1 in every 1,000 people worldwide. Movie and television star Michael J. Fox and former Attorney General Janet Reno both suffer from this progressive disorder. Motor problems are characteristic among people with Parkinson’s disease, who tend to have stooped posture, slow body movements (called bradykinesia), tremors, and jerkiness in walking. The voice is also affected; afflicted individuals speak in a soft monotone. The changes in motor movements are the result of damage to dopamine pathways. Because dopamine is involved in complex movement, a reduction in this neurotransmitter makes affected individuals increasingly unable to control their muscle movements, which leads to tremors and muscle weakness. The course of the disease varies widely, with some individuals functioning well with treatment. It is estimated that about 75% of people who survive more than10 years with Parkinson’s disease develop dementia; conservativeestimates place the rate at 4 to 6 times that found in the generalpopulation. The pattern of impairmentsfor these individuals fits the general pattern of subcortical dementia. Early symptoms of Parkinson’s disease: Commonly non-specific at first  aches and pains  disturbed sleep  anxiety and depression 41 CU IDOL SELF LEARNING MATERIAL (SLM)

 slower dressing  slower walking Early symptoms of Parkinson’s disease: Later more specific  tremor  difficulty turning in bed  stooping or shuffling  softer speech  spidery handwriting Features of Parkinson’s disease There is often a delay in diagnosing Parkinson’s disease. Theearly symptoms of Parkinson’s disease can be vague.The signs are usually asymmetrical, leading to confusion withstrokes and tumors.The core features of Parkinson’s disease are bradykinesia andrigidity. Bradykinesia is a lack of spontaneous movements(often most noticeable as reduced blinking, lack of facial expressionand reduced arm swing when walking), and a slowing ofmovements, especially fine repetitive ones. Rigidity is an increasein tone throughout the full range of movement, unlikespasticity which builds up and then gives way. Rigidity mayhave a constant resistance (like bending a lead pipe) or a judderingfeel (like turning a cogwheel against a ratchet). The rest tremor of Parkinson’s disease (in the limbs, the jawor the lightly closed eyes) is highly characteristic, but 50% ofpatients do not have it at presentation and 20% never get it.Gait disturbance is usually mild in the first few years. Patientsmay then develop difficulty in starting to walk or in stopping(festination) or may abruptly freeze in doorways or crowds. Eventually most patients have falls. The falling is partly aconsequence of slow, stiff muscles or freezing, but partly alsodue to a failure of more complex postural righting reflexesor orthostatic hypotension. It has a very bad effect on qualityof life. Non-motor symptoms are often equally distressing, especiallydepression, dementia and disturbed sleep. Depression hasa prevalence of 30% and should be actively sought andtreated. Dementia is unusual before 70 years but affects manypatients thereafter. Losing the thread of sentences and memoryloss are followed by periods of confusion, often accompaniedby visual hallucination. Sleep may be disrupted forseveral reasons. The most worrying is REM sleepbehavioraldisturbance, in which patients act out their vivid dreams. 2.2.1 Motor signs of Parkinson’s disease The diagnosis of Parkinson’s does not come from a test, but instead requires acareful medical history and a physical examination to detect the cardinal signsof the disease, including: Resting Tremor 42 CU IDOL SELF LEARNING MATERIAL (SLM)

In the early stages of the disease, about 70 percent of people experience aslight tremor in the hand or foot on one side of the body, or less commonlyin the jaw or face. A typical onset is tremor in one finger. The tremor consistsof a shaking or oscillating movement, and usually appears when a person’smuscles are relaxed, or at rest, hence the term “resting tremor.” The affectedbody part trembles when it is not performing an action. Typically, the fingersor hand will tremble when folded in the lap, or when the arm is held loosely atthe side, i.e., when the limb is at rest. The tremor usually ceases when a personbegins an action. Some people with Parkinson’s disease have noticed that they can stop a handtremor by keeping the hand in motion or in a flexed grip. The tremor of Parkinson’s disease can be exacerbated by stress or excitement, sometimes attracting unwantednotice. The tremor often spreads to the other side of the body as the diseaseprogresses, but usually remains most apparent on the initially affected side.Although tremor is the most noticeable outward sign of the disease, not allpeople with Parkinson’s disease will develop tremor. Essential tremor is a neurologic movement disorder in whichtremor is the major symptom, where the tremor is typically anaction tremor, rather than the resting tremor of Parkinson’s disease. Essentialtremor is a different disorder than Parkinson’s disease, but is sometimesmistaken for it, especially early in the disease. Bradykinesia Greek for “slow movement,” bradykinesia is a frequent symptom of Parkinson’s disease and related movement disorders. In addition to a general slowness of movement, the bradykinesia of Parkinson’s disease is typically demonstrated by a reduced or mask-like expression of the face (hypomimia), a decreased blink rate of the eyes, and problems with fine motor coordination (for example, difficulties buttoning a shirt). Having trouble turning over in bed and slow, small handwriting (micrographia) are other signs of bradykinesia. Bradykinesia means “slow movement.” A defining feature of Parkinson’s, bradykinesia also describes a general reduction of spontaneous movement, which cangive the appearance of abnormal stillness and a decrease in facial expressivity.Bradykinesia causes difficulty with repetitive movements, such as fingertapping. Due to bradykinesia, a person with Parkinson’s may have difficultyperforming everyday functions, such as buttoning a shirt, cutting food orbrushing his or her teeth. People who experience bradykinesia may walk withshort, shuffling steps. The reduction in movement and the limited range ofmovement caused by bradykinesia can affect a person’s speech, which maybecome quieter and less distinct as Parkinson’s progresses. Rigidity Rigidity refers to a tightness or stiffness of the limbs or torso. Rigidity, especially in the early stages of PD, may be wrongly attributed to arthritis or orthopedic problems, such as a rotator cuff injury. 43 CU IDOL SELF LEARNING MATERIAL (SLM)

Rigidity causes stiffness and inflexibility of the limbs, neck and trunk. Musclesnormally stretch when they move, and then relax when they are at rest. InParkinson’s rigidity, the muscle tone of an affected limb is always stiff anddoes not relax, sometimes contributing to a decreased range of motion. People with PD most commonly experience tightness of the neck, shoulder andleg. A person with rigidity and bradykinesia tends to not swing his or her armswhen walking. Rigidity can be uncomfortable or even painful. Postural Instability Bradykinesia and postural instability both contribute to walking, or gait, difficulties in Parkinson’s disease, particularly as the disease progresses. A common, early symptom of Parkinson’s disease is a decrease in the natural swing of one or both arms when walking. Later, steps may become slow and small, and a shuffling gait may appear. Gait problems in Parkinson’s disease can also include a tendency to propel forward with rapid, short steps (festination). People with advanced Parkinson’s disease may experience episodes of freezing, in which the feet feel as though they are glued to the floor. One of the most important signs of Parkinson’s is postural instability, atendency to be unstable when standing upright. A person with posturalinstability has lost some of the reflexes needed for maintaining an uprightposture and may topple backwards if jostled even slightly. Some develop adangerous tendency to sway backwards when rising from a chair, standing orturning. This problem is called retropulsion and may result in a backwards fall. People with balance problems may have particular difficulty when pivoting ormaking turns or quick movements.Doctors test postural stability by using the “pull test.” During this test, theneurologist gives a moderately forceful backwards tug on the standingindividual and observes how well the person recovers. The normal response isa quick backwards step to prevent a fall; but many people with Parkinson’s areunable to recover and would tumble backwards if the neurologist were notright there to catch him or her. Freezing Freezing of gait is an important sign of Parkinson’s disease that is not explained by rigidity or bradykinesia. People who experience freezing will normally hesitate before stepping forward. They feel as if their feet are glued to the floor. Often, freezing is temporary, and a person can enter a normal stride once he or she gets past the first step. Freezing can occur in very specific situations, such as when starting to walk, when pivoting, when crossing a threshold or doorway, and when approaching a chair. For reasons unknown, freezing rarely happens on stairs. Various types of cues, such as an exaggerated first step, can help with freezing. Some individuals have severe freezing, in which they simply cannot take a step. Freezing is a potentially serious problem in Parkinson’s disease, as it may increase a person’s risk of falling forward. 44 CU IDOL SELF LEARNING MATERIAL (SLM)

2.2.2 Secondary Motor Symptoms In addition to the cardinal signs of Parkinson’s, there are many other motorsymptoms associated with the disease including:  Micrographia is the name for a shrinkage in handwriting that progressesthe more a person with Parkinson’s writes. This occurs as a result ofbradykinesia, which causes difficulty with repetitive actions.  Drooling and excess saliva result from reduced swallowing movements.  The mask-like expression found in PD, meaning a person’s face may appearless expressive than usual, can occur because of decreased unconsciousfacial movements.  The flexed posture of Parkinson’s disease may result from a combination of rigidityand bradykinesia.  Some people with Parkinson’s experience movements that are too quick, nottoo slow. These unwanted accelerations are especially troublesome in speechand movement.  People with excessively fast speech, tachyphemia, produce arapid stammering that is hard to understand. Those who experience festination, an uncontrollable acceleration in gait, may be at increased risk for falls. 2.2.3 Non-Motor Symptoms of Parkinson’s disease Because Parkinson’s disease is a type of movement disorder, the associated non-motor symptoms can be overlooked. However, there are several common symptoms of Parkinson’s disease that do not primarily involve movement. Some of these non-motor symptoms such as decreased smell, depression, sleep disorders, and constipation can precede motor symptoms by years or even decades. Disturbances in the Sense of Smell A reduced sensitivity to odors (hyposmia) or a loss of smell (anosmia) is often an early symptom of Parkinson’s Disease. This may be due to degeneration of the anterior olfactory nucleus and olfactory bulb, one of the first parts of the brain affected by Parkinson’s. This can happen so gradually that you’re not even aware of it. Sleep Problems Sleep problems are commonly experienced by people with Parkinson’s disease. The inability to fall asleep, or primary insomnia, is less common than the inability to stay asleep, or secondary insomnia. Some people with Parkinson’s disease disrupt the normal sleep-wake cycle by taking catnaps throughout the day; doing this may lead to an inability to sleep at night. Other individuals with Parkinson’s disease have vivid dreams, although these are more typically due to side effects of medications for Parkinson’s disease. People with Parkinson’s 45 CU IDOL SELF LEARNING MATERIAL (SLM)

disease may also talk or thrash in their sleep, particularly during the rapid eye movement (REM) sleep stage (REM sleep behavior disorder). Parkinson's medication can cause excessive daytime sleepiness or sudden onset of sleep. This can be severe for some people, so it's important to get support from your healthcare professionals if this happens. Excessive feelings of sleepiness during the day can also happen if you aren't sleeping well at night. The affect can cause some people to doze off during normal waking hours. Other sleep issues that can affect people with Parkinson's include sleep conditions and difficulty moving in bed. You may also experience mental health problems if you don't sleep well enough. Depression and Anxiety Depression is a fairly common non-motor symptom of Parkinson’s disease. It can range in severity and may improve with Parkinson’s disease treatment, anti-depressant medications, or psychotherapy, such as cognitive behavioral therapy (CBT). Group or family therapy may also help alleviate depression. Anxiety occurs in Parkinson’s disease as well and, like depression, can be mild or severe. In some cases, anxiety may require medication. As with depression, psychotherapy such as CBT can help to address anxiety. Some people with Parkinson’s have anxiety that happens when they’re ‘off’. When a person takes their medication, their symptoms will improve. But these symptoms can sometimes come back before the next dose is due, causing a person’s condition to fluctuate. This is called ‘wearing off’. Fatigue Fatigue is a complex symptom of Parkinson’s disease that is not fully understood. It is known, however, that fatigue is significantly associated with depression and sleep disorders. Cognitive Decline Particularly in more advanced Parkinson’s disease or in older people with Parkinson’s disease, problems with thinking, word finding, and judgment are common. Many individuals report difficulties in multitasking and organizing daily activities. Confusion may also be a side effect of some Parkinson’s disease medications. Many people with Parkinson’s experience fatigue but it’s common in people with other long- term physical health conditions too. We don’t yet fully understand what causes it in Parkinson’s, but it is thought to be linked to chemical changes that happen in the brain. Fatigue in Parkinson’s may also be related to other symptoms or features of the condition. Such as:  The timing and dosage of your medication. This can mean that you feel energetic and capable of doing everyday jobs at certain times of the day, but not at other times. 46 CU IDOL SELF LEARNING MATERIAL (SLM)

 Tremor, stiffness or involuntary movements, which may put stress on your muscles. It means they work harder, often against each other, in order to move or complete a task, and can become fatigued quickly  Slowness of movement (bradykinesia). If you experience this, tasks can take you longer to complete than they used to, leading to fatigue  Stress. Parkinson’s and its symptoms can cause stress at work or home and this can make fatigue worse, particularly true if stress builds up over a period of time Weight Loss Loss of weight is a common symptom of Parkinson’s disease, particularly in the later stages of the illness. If weight loss is significant and unintended, your physician should perform an examination to exclude other medical causes of weight loss. While there can be a great deal of weight loss with Parkinson’s disease, it will typically level off. There are different causes of weight loss in patients with Parkinson’s disease, including decreased appetite (anorexia), swallowing difficulties, gastrointestinal problems such as chronic constipation, or depression. The constant motion of an advanced resting tremor or involuntary movements may burn many calories and can also be the cause of weight loss. Gastrointestinal Issues Disturbances of the gastrointestinal system are common in Parkinson’s disease. Constipation, in particular, occurs frequently because Parkinson’s disease may slow the automatic movement of the digestive system; however, side effects of medications may also contribute to constipation. Reduced swallowing and associated drooling or collection of saliva are often seen in Parkinson’s disease. Nausea and vomiting occur occasionally in untreated Parkinson’s disease, but more often these symptoms are related to medication side effects. Nausea and vomiting are most frequent when treatment for Parkinson’s disease first begins. Lightheadedness Separate from the balance problems of postural instability but contributing to gait problems, lightheadedness or a faint feeling occurs often in Parkinson’s disease. This symptom is related to the body’s inability to quickly regulate blood pressure, particularly when sitting up from a lying position or standing from a sitting position. This phenomenon is known as orthostatic or postural hypotension. Feelings of lightheadedness may also be increased by certain medications for Parkinson’s disease. When severe, lightheadedness may cause black- outs or fainting. Urinary Issues Urinary frequency (the need to urinate often) and urinary urgency (the feeling that one must urinate right away, even if the bladder is not full) are other possible symptoms of PD. These symptoms occur because the normal reflex mechanisms that control the bladder are disrupted. 47 CU IDOL SELF LEARNING MATERIAL (SLM)

Urinary problems may be worse at night, when a person is lying flat. There may also be problems with initiating a urine stream (urinary hesitancy), slowness of urination, and overfill of the bladder. It should be noted that urinary symptoms in older men specifically may be caused by an age-related enlargement of the prostate gland and not Parkinson’s disease. Sexual Concerns Changes in sexual desire, or libido, is another non-motor symptom of Parkinson’s disease that is often under-recognized. Sexual desire may be reduced in some cases because of complex psychological issues. In other cases, a reduced libido can be a direct effect of Parkinson’s disease. Treatment with Parkinson’s disease drugs frequently improves sexual desire and, in some cases, even increases it to a troublesome level. In men, the inability to achieve or maintain an erection (impotence) can occur; however, impotence may also be related to other age-related changes in the body or other conditions. Sweating Excessive sweating is a relatively common sign of Parkinson’s disease, particularly if the disease is untreated. It happens most often in the upper body. Melanoma Individuals with Parkinson’s disease may have an increased risk of melanoma, a serious type of skin cancer. As a result, people with Parkinson’s disease should undergo annual skin examinations with a dermatologist. If you notice any troubling skin lesions, be sure to talk to your physician about them. Most people with Parkinson’s disease will experience both motor and nonmotor symptoms. As the disease progresses, most people will begin to experience more symptoms, though exactly which ones, and how severe they are, will vary from person to person. Talk with your physician about new symptoms as they arise to determine the best treatment. Stages of Parkinson’s By definition, Parkinson’s is a progressive disease. Although some people with Parkinson’s only have symptoms on one side of the body for many years, eventually the symptoms begin on the other side. Symptoms on the other side of the body often do not become as severe as symptoms on the initial side. The stages of Parkinson’s correspond both to the severity of movement symptoms and to how much the disease affects a person’s daily activities. At all stages of Parkinson’s, effective therapies are available to ease symptoms and make it possible for people with Parkinson’s disease to live well. With mild Parkinson’s, movement symptoms, often tremor, occur on one side and may be inconvenient, but do not affect daily activities. Friends may notice changes in a person’s posture, walking ability or facial expression. Regular exercise improves and maintains 48 CU IDOL SELF LEARNING MATERIAL (SLM)

mobility, flexibility, range of motion and balance, and also reduces depression and constipation. With moderate Parkinson’s, movement symptoms occur on both sides of the body. The body moves more slowly and trouble with balance and coordination may develop. “Freezing” episodes — when the feet feel stuck to the ground — may occur. Parkinson’s medications may “wear off” between doses and may cause side effects, including dyskinesias (involuntary movements). Regular exercise, perhaps with physical therapy, continues to be important for good mobility, and balance and occupational therapy may provide strategies for maintaining independence. With advanced Parkinson’s, a person may have great difficulty walking; may be in a wheelchair or bed most of the day. The person is not able to live alone and will need assistance with all daily activities. Cognitive problems may be prominent, including hallucinations and delusions. Balancing the benefits of medications with their side effects becomes more challenging. 2.3 DSM CRITERIA FOR PARKINSON’S DISEASE Often, the diagnosis of Parkinson’s disease is first made by an internist or family physician. Many people seek an additional opinion from a neurologist with experience and specific training in the assessment and treatment of Parkinson’s disease — referred to as a movement disorder specialist. To diagnose Parkinson’s, the physician takes a careful neurological history and performs an examination. Although there are no standard diagnostic tests for Parkinson’s disease, DaTscan, an imaging technology, may provide beneficial insights to help a doctor confirm a Parkinson’s disease diagnosis in the early stages of the disease. The main role of any additional testing is to exclude other diseases that imitate Parkinson’s disease, such as stroke or hydrocephalus. Very mild cases of Parkinson’s disease can be difficult to confirm, even by an experienced neurologist. This is in part because there are many neurological conditions that mimic the appearance of Parkinson’s. The symptoms of Parkinson’s disease can be temporarily reduced by medications, such as Mirapex (pramipexole), that increase the availability of dopamine in the brain. However, once the medications wear off, the symptoms return. Another treatment approach that is now being tried is deep brain stimulation. In the future, stem cell research may also offer some hope for patients with this disease. A. The criteria are met for major or mild neurocognitive disorder. B. The disturbance occurs in the setting of established Parkinson’s disease. C. There is insidious onset and gradual progression of impairment. 49 CU IDOL SELF LEARNING MATERIAL (SLM)

D. The neurocognitive disorder is not attributable to another medical condition and is not better explained by another mental disorder. Major or mild neurocognitive disorder probably due to Parkinson’s disease should be diagnosed if 1 and 2 are both met. Major or mild neurocognitive disorder possibly due to Parkinson’s disease should be diagnosed if 1 or 2 is met: 1. There is no evidence of mixed etiology (i.e., absence of other neurodegenerative or cerebrovascular disease or another neurological, mental, or systemic disease or condition likely contributing to cognitive decline). 2. The Parkinson’s disease clearly precedes the onset of the neurocognitive disorder. 2.4 INCIDENCE OF PARKINSON’S DISEASE The average age at which someone is diagnosed is 60. Incidence of Parkinson’s disease increases with age, but an estimated four percent of people with Parkinson’s disease are diagnosed before the age of 50. This is referred to as young-onset P Parkinson’s disease D. Although symptoms are similar, people with young-onset Parkinson’s disease often face different financial, family and employment concerns. Changes in disease incidence provide a powerful tool to investigate disease risk, disease associations and disease aetiology. Unfortunately, incidence studies of diseases that are relatively infrequent require long-term follow-up of populations and must achieve high levels of disease ascertainment. In PD the best long-term data on the longitudinal study from Rochester, Minnesota. These studies indicate a relatively unchanging age adjusted incidence for PD of around 20/100000 population between the years 1967-1979. However, despite a constant overall incidence, an increasing incidence for disease in older subjects and a falling incidence in younger subjects may have occurred over this time. 2.5 PREVALENCE OF PARKINSON’S DISEASE Worldwide, there are more than 10 million people living with Parkinson’s disease. In the United States (US), as many as one million people live with Parkinson’s, which is more than the combined number of people with multiple sclerosis, muscular dystrophy and ALS. Approximately 60,000 Americans are diagnosed with Parkinson’s disease each year. This number does not reflect the thousands of cases that go undetected. 2.6 CO-MORBIDITY OF PARKINSON’S DISEASE Parkinson's disease may coexist with Alzheimer's disease and cerebrovascular disease, especially in older individuals. The compounding of multiple pathological features may 50 CU IDOL SELF LEARNING MATERIAL (SLM)