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

diminish the functional abilities of individuals with Parkinson's disease. Motor symptoms and frequent co-occurrence of depression or apathy can make functional impairment worse. 2.7 CAUSES OF PARKINSON’S DISEASE To date, despite decades of intensive study, the causes of Parkinson’s disease remainunknown. Many experts think that the disease is caused by a combination ofgenetic and environmental factors, which may vary from person to person.Scientists have identified aging as an important risk factor; there is a two tofour percent risk for Parkinson’s disease among people over age 60, compared with one to twopercent in the general population. Genetic Factors The vast majority of Parkinson’s disease cases are not directly inherited. About 15 to 25percent of people with Parkinson’s disease report having a relative with the disease. Inlarge population studies, researchers have found that people with an affectedparent or sibling have about twice the risk of developing Parkinson’s disease compared tosomeone without an affected relative. However, even with a positive familyhistory, the risk of developing Parkinson’s disease is less than 10 percent. Researchers have discovered several gene mutations that can cause thedisease directly, but these affect only a small number of families. Some ofthese mutations involve genes that play a role in dopamine cell functions.Parkinson’s has developed at an early age in individuals with mutationsin genes for parkin, PINK1, LRRK2, DJ-1, and glucocerebrosidase, amongothers. However, genetic testing is not currently recommended as part of theevaluation of a person with Parkinson’s disease. Because genetic forms of a disease can be studied in great detail in thelaboratory, and because understanding the rare genetic forms of Parkinson’s disease may help us to understand more common forms of the disease, genetics iscurrently the subject of intense research. Environmental Factors Some scientists have suggested that Parkinson’s disease may result fromexposure to an environmental toxin or injury. Epidemiological research hasidentified several factors that may be linked to Parkinson’s, including ruralliving, well water, manganese and pesticides. Some studies have demonstrated that prolonged occupational exposure tocertain chemicals is associated with an elevated risk of PD. These include theinsecticides permethrin and beta- hexachlorocyclohexane (beta-HCH), theherbicides paraquat and 2,4-dichlorophenoxyacetic acid and the fungicidemaneb. In 2009, the US Department of Veterans Affairs added Parkinson’sto a list of diseases possibly associated with exposure to Agent Orange. A synthetic neurotoxin agent called MPTP can also cause immediate andpermanent parkinsonism. The compound was discovered in the 1980sin individuals who injected 51 CU IDOL SELF LEARNING MATERIAL (SLM)

themselves with a synthetic form of heroincontaminated with MPTP. Cases of MPTP- induced Parkinson’s in the generalpopulation are exceedingly rare. It is noted that a simple exposure to an environmental toxin is never enough tocause Parkinson’s. Most people exposed to a toxin do not develop the disease.In fact, there is no conclusive evidence that any environmental factor, alone,can be considered a cause of the disease. However, environmental factors havebeen helpful in studying laboratory models of Parkinson’s. Scientists continueto pursue these clues to understand why Parkinson’s disease occurs. 2.8 PROGNOSIS OF PARKINSON’S DISEASE Each person with Parkinson’s experiences the disease differently. Some people experience tremor as their primary problem while others may instead suffer from frequent falls, muscle rigidity or slowness of movement. Some people with Parkinson’s have a very stable course with little progression over many years while others develop disability earlier in the disease. Physicians cannot accurately predict the course of Parkinson’s for any individual, and must instead focus on reducing a person’s symptoms, preventing complications and improving his or her quality of life. 2.9 TREATMENT OF PARKINSON’S DISEASE The management of patients with Parkinson’s disease requirespatience and persistence. The patient’s concerns and expectationsmay be very different from yours. It may take time to reacha shared understanding and objectives. Specialist nurses andpatient groups like the Parkinson ’s disease Society are a hugehelp with this. Non-drug treatments should be sought wherepossible, and advice from speech therapists, physiotherapists,occupational therapists and dieticians is often required. 2.9.1 Drug Treatment The goal of medical management of Parkinson's disease (PD) is to control signs and symptoms for as long as possible while minimizing side effects. Medical therapy generally provides good control of symptoms for 4 to 6 years, though disability continues to progress despite best medical management, and many patients develop long-term complications. Such complications include motor fluctuations and dyskinesia associated with long-term levodopa therapy. Other common causes of disability in later stage disease include postural instability and dementia. A key consideration in the treatment of elderly patients is that they are more susceptible to side effects from medication. Older people are more likely than younger individuals to be taking more prescribed and over the counter medication for a range of diseases. Medication prescribed for one condition can worsen another and side effects from medication can be mistaken as a new disease process and lead to further unnecessary prescribing. Cognitive 52 CU IDOL SELF LEARNING MATERIAL (SLM)

impairment and delirium, both of which commonly develop as side effects of drug therapy, reduce compliance with drug treatment. Drug schedules should be altered gradually. Side-effectsfrom the drugs are common, making regular consultationsimportant. As the illness evolves, drug schedules can becomequite complicated, needing clear explanation and writtenconfirmation. The mainstay of drug treatment is to boost dopaminergicactivity in the nigrostriatal pathway, either by giving levodopawhich can be turned into dopamine within the remaining neurons in the substantia nigra or by giving dopamine agonistswhich mimic the effect of dopamine in the striatum.Less potent benefits can be obtained from drugs whichinhibit the metabolism of dopamine by monoamine oxidasetype B and catechol-O-methyl transferase, and from drugs thatmodify other neurotransmitters in the striatum such as amantadineand anticholinergics. Levodopa Levodopa combined with a peripheral decarboxylase inhibitor (PDI) is the gold standard of drug treatment for PD. It usually provides the greatest symptomatic improvement with the fewest side effects. Ehringer and Hornykiewicz demonstrated that P1 is associated with decreased striatal dopamine concentration, but dopamine is not useful as a therapeutic agent because it does not cross the blood—brain barrier. Carlsson et al. had already reported that the administration of the dopamine precursor, levodopa, and reversed reserpine induced parkinsonism in rats. Levodopa was subsequently demonstrated to improve signs and symptoms of P1. Levodopa is a large neutral amino acid, with a serum half-life of approximately one hour. It is primarily absorbed in the proximal small bowel by a saturable, carrier mediated transport system. The stomach is capable of absorbing levodopa only to a limited extent. Meals and anticholinergic medications slow gastric emptying and delay levodopa absorption. In older patients, gastric stasis results in slower gastric emptying and increased duodenal levodopa absorption. In addition, first pass metabolic decarboxylation of levodopa in the gastrointestinal tract is reduced iii older individuals. Because of these age associated changes levodopa bioavailability is as much as 20% greater in the elderly. Levodopa treatment was developed in the 1960s and remainsthe most powerful treatment for Parkinson’s disease. Levodopa is absorbed from the gut, crosses the blood–brain barrier and isconverted into dopamine by the enzyme dopa-decarboxylase.It is given with a dopa- decarboxylase inhibitor which does notcross into the brain. This prevents the levodopa from being convertedinto dopamine in the body (where it would cause nauseaand vomiting) without interfering with the production ofdopamine in the brain. Most patients initially respond brilliantly to levodopatherapy. There are three subsequent problems:  Wearing off: the response becomes shorter and less marked. 53 CU IDOL SELF LEARNING MATERIAL (SLM)

 Dyskinesia: each dose produces involuntary choreamovements.  On–off effect: the transition between lack of response (off) andresponse (on) becomes rapid. Dopamine agonists There are five orally active dopamine agonist drugs available to treat PD: the ergot agonists — bromocriptine, pergolide, and cabergoline, and the non-ergot agonists — pramipexole and ropinirole. Bromocriptine is an ergot alkaloid synthetic cyclic derivative of lysergic acid, with both pre and postsynaptic effects. It was originally developed as a prolactin inhibitor but was also found to have antiparkinsonian activity. Pergolide is a semisynthetic clavine ergoline agonist that stimulates both Dl and D2 receptors. It is roughly 10 times more potent than bromocriptine on amg formg basis and is a strong D2 receptor agonist and a weak Dl receptor agonist. Pergolide is effective as monotherapy in early disease and as an adjunct to levodopa/PDI in advanced disease. Cabergoline is an ergot dopamine agonist with strong D2 and weak Dl receptor affinity. Its plasma half-life is approximately 65 hours, thereby allowing once a day dosing. Cabergoline is introduced at a dose of 0.5mg/day and slowly escalated to a maximum dose of 4—5 mg/day. Pramipexole is a synthetic amino benzathiazol non-ergot agonist that binds with high affinity to the D2 family of dopamine receptors, especially the D3 receptor. It has little affinity for Dl, 5HT, muscarinic, or adrenergic receptors. Pramipexole is rapidly absorbed and reaches peak concentration in about two hours. It is 15% bound to plasma protein. The half-life is approximately eight hours in young volunteers and 12 hours in elderly volunteers. Ropinirole is a non-ergoline dopamine agonist that binds selectively to D2 receptors with little affinity for Dl, 5HT, muscarinic, or adrenergic receptors. It is rapidly absorbed and extensively metabolized by the liver. The elimination half-life of ropinirole is approximately six hours. Maximal plasma concentration is reached after approximately one and a half hours in fasting patients and after approximately four hours when taken with meals. Ropinirole clearance is reduced by 30% in elderly patients. COMT inhibitors Two inhibitors of catechol-O-methyltransferase (COMT), tolcapone and entacapone, have been developed and are available in some countries for clinical and trial use. COMT is one of the primary enzymes responsible for the catabolism of levodopa. When a COMT inhibitor is added to levodopa/PDI therapy, striatal dopamine levels are increased for longer. Central COMT inhibition might further maintain striatal dopamine levels by blocking the central metabolism of dopamine to homovanillic acid. COMT inhibitors reduce 'off time, improve 54 CU IDOL SELF LEARNING MATERIAL (SLM)

motor function, and allow levodopa dose reductions in advanced patients with motor fluctuations on levodopa. 2.9.2 Surgical Interventions Ablative Surgeries Ablative surgical interventions for PD involve stereotactic lesions in the globus pallidus, thalamus, or subthalamic nucleus to reduce motor symptoms. Cognitive and emotional outcomes after ablative procedures for PD in the 1950s and 1960s are sparsely documented. Wilkinson and Tröster pointed out that outcomes from early and more recent studies are difficult to compare for a variety of reasons. In general, however, modern studies reveal that ablative procedures such as pallidotomy, thalamotomy, and sub-thalamotomy (especially unilateral) are relatively safe from a cognitive perspective. With regard to unilateral pallidotomy, declines in verbal fluency performance have been reported in approximately 75% of outcome studies that included a measure of verbal fluency. Postoperative decrements on measures of attention, memory, and executive functions (typically mild and transient) have been reported more occasionally, and significant cognitive complications even more rarely. Preexisting cognitive impairment, advanced age, and dominant hemisphere surgery have been proposed to increase the risk for postoperative cognitive decline. Few formal neuropsychological studies of bilateral pallidotomy have been undertaken, despite the observation that the most frequent adverse events among such patients are declines in speech and cognition. Some suggest that cognitive declines after bilateral pallidotomy may be limited in scope and severity, or that some gains in memory might be observed, but others report marked morbidity. Although early studies examining outcomes after thalamotomy reported decrements in language and memory with regularity, modern thalamotomy is associated with minimal risk of cognitive morbidity. Initial reports of the apparent cognitive safety of sub-thalamotomy remain to be confirmed by larger, controlled studies. Deep Brain Stimulation Non-ablative surgical procedures for treatment of PD involve either unilateral or bilateral implantation of high-frequency stimulation electrodes into deep brain nuclei. Studies detailing neuropsychological outcomes after unilateral globus pallidus (GPi) deep brain stimulation (DBS) have supported the neurobehavioral safety of this technique, although a few studies have demonstrated minor postoperative declines in verbal fluency. The majority of studies indicate that even bilateral GPi stimulation is cognitively well tolerated, although in isolated cases, cognitive declines can occur. There are few studies evaluating cognitive outcomes after thalamic DBS, but preliminary findings suggest that this procedure is associated with minimal cognitive morbidity up to one 55 CU IDOL SELF LEARNING MATERIAL (SLM)

year after surgery. Indeed, subtle and limited cognitive improvements might be witnessed after thalamic DBS. The majority of DBS procedures now target the subthalamic nucleus (STN). Modest decrements in verbal fluency are the most commonly reported adverse cognitive sequelae associated with STN DBS. Findings regarding possible postoperative declines and/or improvements in global cognitive abilities, memory, attention, and executive functions are less consistent. When considered in the context of the important benefits of surgery on motor functions, mood state, and quality of life, the cost of possible minor and/or transient cognitive declines in a minority of well-selected patients seems to be overshadowed by the benefits. Preliminary evidence indicates that elderly patients (older than 69 years), as well as those patients displaying presurgical cognitive deficits, might be at greater risk for neurobehavioral morbidity after STN DBS. The advantages of DBS compared to lesion surgeries include no destructive lesion in the brain, the ability to adjust stimulation parameters to increase efficacy or reduce adverse effects, the performance of bilateral procedures with increased safety and reduced adverse effects, and the reversibility of the system to accommodate the potential use of future therapies. The disadvantages include cost of the system, time and effort involved in programming the system, repeat surgeries related to device complications, the use of general anesthesia for IPG and extension wire implantation, and battery replacement every three to five years. Transplantation Fetal mesencephalic tissue transplantation studies have indicated variability in neurocognitive outcomes among individual patients, but, given small sample sizes, the source of variability is difficult to identify. A recent double-blind study comparing patients, having undergone sham surgery and embryonic tissue implantation, failed to find significant differences in cognitive functioning between the groups. The strategy of stem cell approaches to PD is to hormonally induce stem cell differentiation into nigrostriatal dopaminergic neurons or their precursors and then to transplant them into patients. The hope is that these transplanted cells will survive, re-innervate the striatum, and functionally replace dopaminergic cells that have been lost as a result of disease progression. These goals result in considerable challenge and complexity. The ideal stem cell source would have the capacity for indefinite clonal expansion to allow a small number of donor sources to be utilized to treat a much larger number of patients. This expansion would have to be free of genetic mutation and would have to cease once transplantation took place. The cells would also require the capacity for controlled differentiation into phenotypically appropriate dopaminergic neurons. For example, the generated neurons should not only produce dopamine but also must have the similar capacity for regulation and other aspects of functionality as native neurons. 56 CU IDOL SELF LEARNING MATERIAL (SLM)

During production, not all stem cells would be expected to differentiate into the same progeny cells. Although some cells may form neurons, others may form glial cells. A mechanism through which to select neurons from this heterogeneous background of surrounding cells in culture would be required. Of course, proper functioning of transplanted neurons may require the presence of supporting cells, which would also need to be produced and sustained in the transplanted tissue. The transplanted stem cells would have to cease to divide or to differentiate in an uncoordinated or uncontrolled fashion once transplantation had taken place. Otherwise, the transplant might either become a tumor, if growth continued, or lose functionality over time, if differentiation progressed. Methods to ensure that the transplanted cells are not rejected by the recipient would also have to be developed. As described earlier, immunological rejection may have been a critical factor in the failure of fetal transplantation studies. Finally, and most importantly, transplantation of these cells would have to result in the substantial improvement or reversal of the symptoms of PD. Loss of dopaminergic neurons is associated with bradykinesia, rigidity, postural instability and tremor. These symptoms might be expected to improve with stem cell transplantation. However, additional nondopaminergic symptoms such as dementia, autonomic dysfunction, depression, and sleep disturbance would likely remain. Furthermore, stem cell therapies should not produce disabling dopamine- associated side effects, such as troubling dyskinesia. As with any invasive or complex therapy, serious consideration will have to be given to cost relative to changes in patient quality of life. Despite these substantial challenges, several different stem cell types have been considered and studied. 2.9.3 Physiotherapy The deficiency of dopamine in Parkinson’s disease (PD) leads to several problems. One key problem is the interruption of smooth, coordinated muscle function. This in turn can affect complex tasks such as speech, mobility, and coordinated use of the limbs. PD is a progressive neurodegenerative disorder, which can be treated with various medications and surgical procedures. However, since this condition is progressive, it invariably affects functional activities such as mobility and activities of daily living at some point. There are two main factors that often impact functional activities in patients with PD. One is the direct result of the neurodegenerative process and its effect on coordination and other neurological functions. The other is the myriad of indirect effects related to neurological deficits and debilitation. Some of these secondary problems include problems such as decreased activity, deconditioning, depression, weight gain, joint pain and contractures, cognitive problems, drooling, constipation, and poor hygiene. These in turn lead to further disability and impairment. PD is more prevalent in older persons and, often, these patients have other comorbid conditions such as osteoarthritis, hypertension, diabetes, and 57 CU IDOL SELF LEARNING MATERIAL (SLM)

cardiovascular disease. All of these comorbidities can worsen with deconditioning and further impact functional status. The focus of rehabilitation interventions in patients with PD is to maintain and possibly improve function. Although physical therapy (PT) and occupational therapy (OT) may have little or no impact on the progression of PD, they can have a very significant effect on quality of life, functioning, and prevention of secondary problems. Posture Assessment Sitting and standing posture are observed with attention to trunk flexion, forward head, or uneven lower extremity weight-bearing. Postural deficits alter the body’s center of gravity during movement. Postural deficits also create muscle imbalances due to overly tight and overly stretched muscles that can contribute additional impairment to the rigidity and weakness, usually accompanying PD. Amplitude Training A specific form of physical therapy for Parkinson’s disease is called LSVT BIG training. (LSVT is Lee Silverman Voice Treatment. LSVT LOUD is therapy to amplify the voice.) “It’s meant to help patients with Parkinson’s increase what we call ‘amplitude of movement,’” says Padilla-Davidson. In LSVT BIG, you make over exaggerated physical movements, like high steps and arm swings. It’s a way to retrain the muscles and slow down the progression of hypokinesia, the increasingly smaller, more shuffling movements that happen with Parkinson’s. Ask your doctor or physical therapist about LSVT BIG. Reciprocal Patterns Reciprocal movements are side-to-side and left-to-right patterns, such as swinging your arms while taking steps as you walk. Parkinson’s disease may affect these patterns. Your therapist may help you reinforce reciprocal patterns by the use of a recumbent bicycle (a stationary bike in which you sit in a reclined position) or elliptical machine (in which you use your arms and legs). On your own, says Padilla-Davidson, “Practice walking, keeping in mind the swinging of your arms. It may help to chant or sing to keep the rhythm.” Dance classes and tai chi are also useful. Balance Work Normal balance, explains Padilla-Davidson, is an interplay among what you see (visual feedback), your inner ear (which helps you orient yourself) and how your feet sense the ground beneath them. Parkinson’s disease can affect this balance system, making your gait (how you walk) unstable, which in turn may make you fearful to be in public or crowded spaces. Gait training (practice walking) can help. Exercises that aim to improve balance should be guided by a physical therapist, who can work with you to understand any issues with balance and teach you ways to compensate. Stretching and Flexibility 58 CU IDOL SELF LEARNING MATERIAL (SLM)

It’s common for patients with Parkinson’s disease to develop tight hip flexor, hamstring and calf muscles. To counteract that stiffness, it’s best to stretch at frequent intervals throughout the day, rather than just once, says Padilla-Davidson. Ask a qualified trainer or therapist who specializes in Parkinson’s to show you how. Strength Training Muscles naturally weaken with age, so strength training is important for everyone. But research suggests that muscle weakness is a bigger problem for patients with Parkinson’s disease, says Padilla-Davidson. Depending on what stage of the disease you are in, a therapist might have you do resistance exercises with light dumbbells or a resistance band (a kind of thick rubber band). Pool-based classes, using the water’s resistance to strengthen muscles, can also be a good fit, she says. 2.9.4 Exercise Postural instability is created by a pattern of weakness, muscular tightness, and standing alignment changes that diminish the patient’s ability to control their center of gravity during transfers and gait. A common presentation is that of a stooped forward posture of the upper body with tight anterior chest wall musculature and a crouched lower body posture. A series of stretching exercises designed to diminish kyphosis of the thoracic spine and increase flexibility in the pectoralis major and minor muscles can lead to improved upper body posture and upper limb function. In the lower aspect of the body, strengthening of the lumbar paraspinal musculature and stretching of the hamstring and hip flexor muscles can be used to improve posture. It is important not only to stretch the key muscles in patients with poor posture, but to also strengthen the appropriate muscles to achieve good biomechanical alignment. To improve muscle length, therapists use several techniques, including heat and cold modalities, stretching postures, bracing, strengthening of antagonist muscles, and proper positioning of the affected limb. Frequently, thoracic extension and scapular stabilization exercises are utilized to assist with correcting a kyphotic posture, and abdominal, paraspinal, and pelvic girdle strengthening exercises are used to help improve trunk control. Difficulty with bed mobility and transfers is usually the result of trunk rigidity and core weakness. These problems are tackled by exercises to increase trunk flexibility and segmental mobility, and core muscle strengthening of the abdominals, paraspinal, and pelvic girdle muscles. Manual muscle testing is performed for all major muscle groups of the extremities, cervical spine, and core stabilization musculature. Weakness in PD patients tends to be due to deconditioning and other comorbidities. An endless list of available exercises to consider for overall health promotion exists (i.e., weight lifting, conditioning, isometric/Pilates, aerobic, stretching, martial arts, specific sports, 59 CU IDOL SELF LEARNING MATERIAL (SLM)

etc.). Exercise can positively impact any person’s health and in particular a person with PD by increasing muscle strength (thereby increasing one’s ability to get up, walk, swallow, speak, and breath), flexibility (reducing muscle rigidity/joint stiffness and increasing range of motion), and bone density (reducing the risk of a limb fracture related to falling). Additional benefits include enhanced cardiovascular and respiratory function and subsequent blood flow and delivery of oxygen and nutrients to the brain. Exercise may also increase daily energy levels, reduce emotional and mental stress, improve mood by raising endorphin levels, and result in better sleep patterns. Many controlled, randomized clinical studies of the benefits of exercise in the elderly can be found in the medical literature. Exercises that improve balance and promote more efficient body movement such as yoga and tai chi may be of particular interest to persons with PD. A randomized, single-blind, controlled study of 30 persons with PD found that those who practiced tai chi regularly over three months had an 18 times greater reduced risk of falling compared with the control group. Similar benefits have been reported with smaller open-label studies along with numerous anecdotal reports of the benefits of yoga for PD. There is also animal data from the 6- hydroxydopamine mouse model of PD suggesting the possible neuroprotective role of aerobic exercise by increasing the production of endogenous neurotrophic factors in the brain. Human clinical studies with newly diagnosed PD patients are examining whether aerobic exercise can increase neurotrophic. 2.9.5Alternative Treatments Traditional Chinese Medicine Traditional Chinese Medicine (TCM) has existed for thousands of years, long before Western medicine. Rather than following the disease model of Western medicine, TCM focuses on a symptom approach such that a person with PD who has mostly tremor would be evaluated and treated differently than another person whose symptoms were mostly gait and balance difficulty with no tremor. The specific symptoms of the individual signal a deficiency in the body fluids/blood that is unable to properly nourish the energy flow or “chi” or “Qi” of the entire organism. There are three main symptom approaches under TCM (5). The first is Qi and blood deficiency, which is believed to arise from anger, emotional stress, frustration, and resentment. The second is phlegm-fire-agitating wind (yang), which is the result of poor diet, in particular eating greasy, fried, sweet, sugary foods and alcohol. The third is kidney and liver (yin) deficiency, which results from a lack of rest and overwork as well as part of the aging process and a subsequent overall imbalance of the natural body rhythm. PD is thought primarily to occur from a yin or liver and kidney deficiency. The liver, as all organs in TCM, is thought to function through energy channels or meridians that connect to all other body parts. The liver is believed to regulate normal body movement 60 CU IDOL SELF LEARNING MATERIAL (SLM)

such that when it is deficient, the body develops tremor, stiffness, and slowed, uncoordinated motor function. A physician of TCM often referred to as a Doctor of Oriental Medicine would prescribe specific treatments to strengthen yin deficiency, reduce overactive wind, restore blood circulation, and unclog phlegm obstruction which would likely involve a particular diet, specific herbs, acupuncture, proper rest, and exercise (Tai Chi and Qi Gong breathing) all with the ultimate goal of restoring proper “chi,” the life energy source. Ayurvedic Medicine Ayurvedic medicine is the traditional medical system in India, which has existed for over 5000 years. The term Ayurveda literally means science of life or life knowledge. PD is documented to have existed in ancient India and was called “Kampavata.” Similar to the TCM system, physical illness is thought to result from emotional imbalance, unhealthy lifestyle, and toxins that ultimately upset the balance of the three doshas or regulatory systems of a person (5). These three doshas are vata, which symbolizes physical movement, pitta, which represents heat, metabolism, and energy, and kapha, which stands for physical structure and balance. Although all three systems may be affected in PD, therapy focuses heavily upon treatment of the vata disturbance through oleation with massage along with enemas and ingestion of oils. Proper harmony of the three doshas is achieved by specific diet and nutrition, a number of herbs, meditation, breathing exercises, massage, and yoga poses. Stress reduction with a peaceful environment that is not overstimulating along with daily meditation, yoga, and techniques to reduce internal stress is the foundation of a complete Ayurvedic program. All of these modalities, not just one, are necessary to practice on a daily basis, thus requiring an entire lifestyle change for a holistic health program. Naturopathy Naturopathic doctors exist in large numbers in Europe, but are growing in the United States with established four-year accredited naturopathic schools and now over 1000 naturopaths practicing in America. Naturopathy incorporates many of the modalities of TCM and Ayurveda, such as acupuncture, herbs, nutrition, massage, and homeopathy with the goal of achieving a balance between one’s physical, emotional, mental, and spiritual health by allowing the body and mind to heal itself through its own natural mechanisms. Homeopathy The practice of homeopathy was founded in the late 1800s. It is based upon the theory that “like cures like” or the law of similar. This law states that the body’s ability to heal itself and fight an illness is stimulated by orally ingesting very minute amounts of a homeopathic remedy containing a substance that at higher concentrations would cause the very symptoms the person wants to get rid of. For instance, if a particular substance is known to cause tremor, diluting it several hundred or thousand-fold is believed to trigger the body to reject or lessen the tremor. The belief is that the remedy stimulates the body to use its own natural healing mechanisms. 61 CU IDOL SELF LEARNING MATERIAL (SLM)

This is similar in theory to how allergy shots or vaccines are believed to work. Homeopaths use herbs, minerals, or animal products which they crush and dissolve in grain alcohol or lactose and then store and refer to as the “mother of tincture.” They then dilute the tincture typically into 1:10 or 1:100. These remedies are prescribed to be taken several times daily for short periods for a few days. Homeopathy was very popular in the 1800s in the United States before the development of pharmaceutical companies. It remains heavily practiced in Europe and is regaining popularity in the United States with an estimated 3000 practitioners and over 25 homeopathic schools in the United States. Chiropractic Chiropractic theory is similar to TCM and Ayurveda in that it views the body as having an innate ability to heal itself and naturally adapt to changes in its internal and external environments to maintain a natural state of health. Chiropractic practitioners focus on the nervous system knowing that the brain sends messages through the spinal cord to all the organs, muscles, blood vessels, and cells of the body. The nervous system helps to coordinate and regulate a vast array of chemical reactions that affect how a person thinks, feels, sleeps, digests food, physically moves, etc. Chiropractic theory is based upon the belief that when bones of the spine become misaligned they block normal flow and communication of the nervous system to the entire body and thereby result in impairment of normal body function that leads to a variety of physical symptoms and possibly the development of disease states. Chiropractic literally means “to be done by hand” and it was founded in 1895 with the theory that all diseases are caused by spinal subluxations and restoration of nerve flow is essential to healing. Spinal manipulation is the primary therapy performed by chiropractors with the goal of manually realigning the vertebral bodies in order to restore communication of the nervous system with the entire body and thereby restore normal body function and rid the body of disease. 2.10 SUMMARY  Parkinson’s disease (PD) is a chronic, progressive neurodegenerative conditionpredominately affecting the people over the age of 50, and estimated to affect 1percent of the population aged 65 and over It is the secondmost commonly occurring neurodegenerative condition after Alzheimer’s disease.  Parkinson’s disease is a degenerative disorder of the central nervous system mainly affecting the motor system.  Early in the course of the disease, the most obvious symptoms are movement-related; these include shaking, rigidity, slowness of movement and difficulty with walking and gait. 62 CU IDOL SELF LEARNING MATERIAL (SLM)

 Later, thinking and behavioral problems may arise, with dementia commonly occurring in the advanced stages of the disease, whereas depression is the most common psychiatric symptom.  Other symptoms include sensory, sleep, and emotional problems. Parkinson’s disease is more common in older people, with most cases occurring after the age of 50; when it is seen in young adults, it is called young onset Parkinson’s disease.  Life expectancy for those with Parkinson’s disease is a littleshorter than most of the general population but if a person is diagnosed withParkinson then the disease may thus be lived with for many years  Parkinson’s disease in most people is idiopathic (having no specific known cause). However, a small proportion of cases can be attributed to known genetic factors. Other factors have been associated with the risk of developing Parkinson’s disease, but no causal relationships have been proven.  A number of environmental factors have been associated with an increased risk of Parkinson’s, including pesticide exposure, head injuries, and heavy metals exposure.  There is no cure for Parkinson’s disease, but medications, surgery, and multidisciplinary management can provide relief from the symptoms. There is some evidence that speech or mobility problems can improve with rehabilitation, although studies are scarce and of low quality.  Regular physical exercise with or without physiotherapy can be beneficial to maintain and improve mobility, flexibility, strength, gait speed, and quality of life.  However, when an exercise program is performed under the supervision of a physiotherapist, there are more improvements in motor symptoms, mental and emotional functions, daily living activities, and quality of life compared to a self- supervised exercise program at home. 2.11 KEY WORDS  Aetiology: The study of the origins of disease: physical, mental or emotional.  Aphasia: Loss of ability to use language (especially the ability to speak) because of brain damage.  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.  Group therapy: Psychotherapy involving several people at the same time. The assumption is that people can benefit from the experiences and companionship of other people. 63 CU IDOL SELF LEARNING MATERIAL (SLM)

 Huntington’s disease: Is a fatal progressive, neurodegenerative genetic disorder with symptoms that include typical changes in movement, changes in personality, and cognitive decline  Neurocognitive Disorders: Involves a loss of cognitive ability due to brain damage, disease or impairment and comprises of delirium, dementia and amnestic and other cognitive disorders.  Psychotherapy: The use of psychological techniques to treat psychological disturbances. 2.12 LEARNING ACTIVITY 1. Explain the process of assessment undertaken in order to diagnose a child with Parkinson’s disease? ___________________________________________________________________________ ___________________________________________________________________________ 2. Explain the process of treatment provided to a child with Parkinson’s disease? ___________________________________________________________________________ ___________________________________________________________________________ 2.13 UNIT END QUESTIONS A. Descriptive Questions Short Questions 1. Who is the person after whom Parkinson’s disease is named? 2. What do you mean by bradykinesia? 3. What do you mean by brady phasia? 4. What is the nature of tremors experienced by patient’s suffering from Parkinson’s disease? 5. What is incidence of Parkinson’s disease? 6. What is prevalence of Parkinson’s disease? 7. What are the common medications used to treat the symptoms of Parkinson’s disease? Long Questions 1. Explain the symptoms of Parkinson’s disease in detail. 2. What is the DSM 5 criteria for Parkinson’s disease? 64 CU IDOL SELF LEARNING MATERIAL (SLM)

3. Explain the different co-morbid conditions for Parkinson’s Disease. 4. Write in detail about the prognosis of Parkinson’s disease. 5. What are the different non pharmacological treatment for Parkinson’s Disease? B. Multiple Choice Questions 1. Antiviral drug found to have anti-Parkinson's properties: a. procyclidine b. amantadine c. pergolide d. reserpine 2. Parkinson disease is marked by a lack of which chemical in the brain? a. Serotonin b. Norepinephrine c. Dopamine d. GABA 3. What was Parkinson's Disease originally referred to? a. The Shaking Palsy b. Parky's Rattle c. Shakesons d. Shake Disorder 4. The average age of onset of Parkinson's is about ____________ years a. 52 b. 55 c. 58 d. 60 5. The characteristic tremor of Parkinson’s disease usually involves ________ 65 CU IDOL SELF LEARNING MATERIAL (SLM)

a. Hands b. Feet c. Eyes d. Jaw Answers 1-b, 2-c, 3-a, 4-d, 5-a 2.14 REFERENCES Textbooks  Ahuja N (2002). A short text book of Psychiatry. (5th edn). 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  Domjan Michael (2010). The Principles of Learning and Behavior (6th Edt) 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.  Emery, R.E., &Oltmans, T.F. (1998). Abnormal Psychology (2nd ed.). Upper Saddle River, NJ: Prentice-Hall, Inc. 66 CU IDOL SELF LEARNING MATERIAL (SLM)

 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 67 CU IDOL SELF LEARNING MATERIAL (SLM)

UNIT 3 – DELIRIUM 68 STRUCTURE 3.0 Learning Objectives 3.1 Introduction 3.2 Delirium 3.3 DSM criteria for Delirium 3.4 Incidence of Delirium 3.5 Prevalence of Delirium 3.6 Co-morbidity of Delirium 3.7 Causes of Delirium 3.8 Prognosis of Delirium 3.9 Treatment of Delirium 3.10 Summary 3.11 Key Words 3.12 Learning Activity 3.13 Unit End Questions 3.14 References 3.0 LEARNING OBJECTIVES After studying this unit, you will be able to,  Explain the nature and symptoms of Delirium  Describe the incidence and prevalence of Delirium  Explain the co-morbidity of Delirium  State the causes of Delirium  Explain the prognosis of Delirium  State the treatment for Delirium CU IDOL SELF LEARNING MATERIAL (SLM)

3.1 INTRODUCTION Delirium, also known as acute confusional state or acute organic brain syndrome, is a medical condition that results from various causes. It involves severe confusion and rapid changes in brain function as well as a specific cluster of symptoms involving a disturbance in mental abilities and abrupt changes in the brain. It can interfere with sleep, concentration and attention, and cognitive functioning. Delirium differs from dementia in that it develops relatively abruptly and is potentially reversible with treatment of the underlying medical condition that is causing it. Delirium can be a side effect of certain medications, medical conditions, or have other causes such as alcohol withdrawal or surgery. Mrs. Patterson was 75 years old when she was admitted to the hospital. A widow who lived alone, she had broken her leg, and she needed a routine operation. The operation was successful. However, shortly afterward, Mrs. Patterson began to show signs of confusion. She had problems with awareness and attention, and she had no idea of what had happened to her or why she was in the hospital. During the day, she seemed agitated and aimlessly wandered around. She was unable to focus enough to watch television or to read. She was also unable to recognize friends and relatives who came to visit her. On several occasions, nursing staff saw her staring at an imaginary spot on the ceiling of her room and having conversations with imaginary people. Mrs. Patterson refused to take any medications. She would knock her meals onto the floor when they were brought to her. Between these outbursts, Mrs. Patterson was able to calm down, sleeping for short periods of about 30 minutes at a time. However, at night, she could hardly sleep at all. Instead, she wandered around the hospital ward. She went into the rooms of other patients, waking them up, and sometimes even trying to get into their beds. On a number of occasions, she was found in her nightdress, trying to leave the hospital. However, the staff always stopped her and carefully escorted her back to her room. Mr. John Mr. J., an older gentleman, was brought to the hospital emergency room. He didn’t know his own name, and at times he didn’t seem to recognize his daughter, who was with him. Mr. J. appeared confused, disoriented, and a little agitated. He had difficulty speaking clearly and could not focus his attention to answer even the most basic questions. Mr. J.’s daughter reported that he had begun acting this way the night before, had been awake most of the time since then, was frightened, and seemed even more confused today. She told the nurse that this behavior was not normal for him and she was worried that he was becoming senile. She mentioned that his doctor had just changed his hypertension medication and wondered whether the new medication could be causing her father’s distress. Mr. J. was 69 CU IDOL SELF LEARNING MATERIAL (SLM)

ultimately diagnosed as having substance-induced delirium (a reaction to his new medication); once the medication was stopped, he improved significantly over the course of the next 2 days. Delirium can occur in a person of any age. However, the elderly are at particularly high risk, perhaps because of brain changes caused by normal aging that lead to reduced “brain reserve.” As described in the case of Mrs. Petersen, delirium is very common in the elderly after they have had surgery, with patients over 80 being particularly at risk. At the other end of the age spectrum, children are also at high risk of delirium, perhaps because their brains are not yet fully developed. In addition to advanced age, other risk factors for delirium include dementia, depression, and tobacco use. People with delirium appear confused, disoriented, and out of touch with their surroundings. They cannot focus and sustain their attention on even the simplest tasks. There are marked impairmentsin memory and language. Mr. J. had trouble speaking; he was not only confused but also couldn’t remember basic facts, such as his own name. As you saw, the symptoms of delirium do not come on gradually but develop over hours or a few days, and they can vary over the course of a day. 3.2 DELIRIUM Delirium, also known as acute confusional state, is an organically caused decline from a previous baseline mental functioning that develops over a short period of time, typically hours to days. Delirium is a syndrome encompassing disturbances in attention, consciousness, and cognition. Delirium may also involve other neurological deficits, such as psychomotor disturbances (e.g., hyperactive, hypoactive, or mixed), impaired sleep-wake cycle, emotional disturbances, and perceptual disturbances (e.g., hallucinations and delusions), although these features are not required for diagnosis. Delirium is caused by an acute organic process, which is a physically identifiable structural, functional, or chemical problem in the brain that may arise from a disease process outside the brain that nonetheless affects the brain. Delirium may result from an underlying disease process (e.g., infection or hypoxia), a side effect of a medication, withdrawal from drugs, over-consumption of alcohol, usage of hallucinogenic deliriants, or from any number of factors affecting one’s overall health (e.g., malnutrition, pain, etc.). In contrast, fluctuations in mental status/function due to changes in primarily psychiatric processes or diseases (e.g., schizophrenia or bipolar disorder) do not, by definition, meet the criteria for delirium. Delirium may be difficult to diagnose without the proper establishment of a person’s usual mental function. Without careful assessment and history, delirium can easily be confused with a number of psychiatric disorders or chronic organic brain syndromes because of many overlapping signs and symptoms in common with dementia, depression, psychosis, etc. Delirium may manifest from a baseline of existing mental illness, baseline intellectual 70 CU IDOL SELF LEARNING MATERIAL (SLM)

disability, or dementia, without being due to any of these problems. Delirium is distinguished from dementia (chronic organic brain syndrome), which describes an acquired (non- congenital) and usually irreversible cognitive and psychosocial decline in function. The disorder known as delirium is characterized by impairedconsciousness and cognition during the course of several hours ordays. Delirium is one of the earliest-recognized mental disorders:Descriptions of people with these symptoms were written morethan 2,400 years ago (Solai, 2009). Consider the case of Mr. J. Types of Delirium There are actually three main types as well as delirium tremens which is related to alcoholism. Hyperactive Delirium This type of delirium tends to involve restlessness, agitation, rapid mood swings or hallucinations. It may result in a patient refusing to cooperate with a caregiver. Hypoactive Delirium This type of delirium tends to involve reduced activity, being sluggish, becoming drowsy, or appearing to be in a daze. Persons with this type of delirium will often sleep more and may miss some meals. Mixed Delirium The mixed delirium type involves symptoms of both hyperactive and hypoactive delirium. A person with this type of delirium may switch back and forth between the two different states of hyperactive delirium and hypoactive delirium. Clinical Features According to DSM-IV-TR, the primary feature of delirium is adiminished clarity of awareness of the environment (AmericanPsychiatric Association, 1994). Symptoms of delirium are characteristicallyglobal, of acute onset, fluctuating and of relativelybrief duration. In most cases of delirium, an often overlooked prodromeof altered sleep patterns, unexplained fatigue, fluctuatingmood, sleep phobia, restlessness, anxiety and nightmares occurs. A review of nursing notes for the days before the recognized onsetof delirium often illustrates early warning signs of the condition.Several investigators have divided the clinical featuresof delirium into abnormalities of 1) arousal, 2) language andcognition, 3) perception, 4) orientation, 5) mood, 6) sleep and wakefulness,and 7) neurological functioning (Kaplan et al., 1994). The state of arousal in delirious patients may be increasedor decreased. Some patient’s exhibit marked restlessness, heightenedstartle, hypervigilance and increased alertness. This patternis often seen in states of withdrawal from depressive substances(e.g., alcohol) or 71 CU IDOL SELF LEARNING MATERIAL (SLM)

intoxication by stimulants (phencyclidine, amphetamine,lysergic acid diethylamide). Patients with increasedarousal often have such concomitant autonomic signs as pallor,sweating, tachycardia, mydriasis, hyperthermia, piloerectionand gastrointestinal distress. These patients often require sedationwith neuroleptics or benzodiazepines. Hypoactive arousalstates such as those occasionally seen in hepatic encephalopathyand hypercapnia are often initially perceived as depressed or dementedstates. The clinical course of delirium in any particularpatient may include both increased and decreased arousal states. Many such individuals display daytime sedation with nocturnalagitation and behavioral problems (sun downing).Perceptual abnormalities in delirium represent an inabilityto discriminate sensory stimuli and to integrate current perceptionswith past experiences. Consequently, patients tend to personalizeevents, conversations and so forth that do not directlypertain to them, become obsessed with irrelevant stimuli andmisinterpret objects in their environment. The misinterpretationsgenerally take the form of auditory and visual illusions. Patients with auditory illusions, for example, might hear thesound of leaves rustling and perceive it as someone whispering about them. Paranoia and sleep phobia may result. Typical visualillusions are that intravenous tubing is a snake or worm crawlinginto the skin, or that a respirator is a truck or farm vehicle aboutto collide with the patient. The former auditory illusion may leadto tactile hallucinations, but the most common hallucinations indelirium are visual and auditory. Orientation is often abnormal in delirium. Disorientationin particular seems to follow a fluctuating course, with patientsunable to answer questions about orientation in the morning, yetfully oriented by the afternoon. Orientation to time, place, personand situation should be evaluated in the delirious patient. Generally,orientation to time is the sphere most likely impaired, withorientation to person usually preserved. Orientation to significantpeople (parents, children) should also be tested. Disorientation toself is rare and indicates significant impairment. The examinershould always reorient patients who do not perform well on anyportion of the orientation testing of the mental status examination,and serial testing of orientation on subsequent days is important. Language and Cognition Patients with delirium frequently have abnormal production andcomprehension of speech. Nonsensical rambling and incoherentspeech may occur. Other patients may be completely mute.Memory may be impaired, especially primary and secondarymemory. Remote memory may be preserved, although thepatient may have difficulty distinguishing the present from thedistant past. Mood Patients with delirium are susceptible to rapid fluctuations inmood. Unprovoked anger and rage reactions occasionally occurand may lead to attacks on hospital staff. Fear is a common 72 CU IDOL SELF LEARNING MATERIAL (SLM)

emotionand may lead to increased vigilance and an unwillingnessto sleep because of increased vulnerability during somnolence.Apathy, such as that seen in hepatic encephalopathy, depression,use of certain medications (e.g., sulfamethoxazole [Bactrim]) andfrontal lobe syndromes, is common as is euphoria secondary tomedications (e.g., corticosteroids, DDC, zidovudine) and drugsof abuse (phencyclidine, inhalants). Neurological Symptoms Neurological symptoms often occur in delirium. These includedysphagia as seen after a CVA, tremor, asterixis (hepatic encephalopathy,hypoxia, uremia), poor coordination, gait apraxia,frontal release signs (grasp, suck), choreiform movements, seizures, Babinski’s sign and dysarthria. Focal neurological signsoccur less frequently. Sleep–Wakefulness Disturbances Sleeping patterns of delirious patients are usually abnormal.During the day they can be hypersomnolent, often falling asleepin midsentence, whereas at night they are combative and restless.Sleep is generally fragmented, and vivid nightmares are common.Some patients may become hyper vigilant and develop asleep phobia because of concern that something untoward mayoccur while they sleep. 3.3 DSM CRITERIA FOR DELIRIUM 3.3.1 DSM Criteria for Delirium due to… [Indicate the General MedicalCondition] A. Disturbance of consciousness (i.e., reduced clarity ofawareness of the environment) with reduced ability tofocus, sustain, or shift attention. B. A change in cognition (such as memory deficit disorientation, language disturbance) or thedevelopment of a perceptual disturbance that is notbetter accounted for by a preexisting, established, orevolving dementia. C. The disturbance develops over a short period of time(usually hours to days) and tends to fluctuate during thecourse of the day. D. There is evidence from the history, physicalexamination, or laboratory findings that the disturbanceis caused by the direct physiological consequences of ageneral medical condition. Coding note: If delirium is superimposed on a preexistingdementia of the Alzheimer’s type or vascular dementia,indicate the delirium by coding the appropriate subtype ofthe dementia, e.g., 290.3 dementia of the Alzheimer’s type,with late onset, with delirium. Coding note: Include the name of the general medicalcondition on Axis I, e.g., 293.0 delirium due to hepaticencephalopathy; also code the general medical conditionon Axis III. 73 CU IDOL SELF LEARNING MATERIAL (SLM)

3.3.2 DSM Criteria for Substance Intoxication Delirium A. Disturbance of consciousness (i.e., reduced clarity ofawareness of the environment) with reduced ability tofocus, sustain, or shift attention. B. A change in cognition (such as memory deficit,disorientation, language disturbance) or thedevelopment of a perceptual disturbance that is notbetter accounted for by a preexisting, established, orevolving dementia. C. The disturbance develops over a short period of time(usually hours to days) and tends to fluctuate during thecourse of the day. D. There is evidence from the history, physicalexamination, or laboratory findings of either (1) or (2): (1) the symptoms in criteria A and B developed duringsubstance intoxication (2) medication use is etiologically related to thedisturbance Note: This diagnosis should be made instead of a diagnosisof substance intoxication only when the cognitivesymptoms are in excess of those usually associated withthe intoxication syndrome and when the symptoms aresufficiently severe to warrant independent clinical attention. Note: The diagnosis should be recorded as substanceinduceddelirium if related to medication use. Code: [specific substance] intoxication delirium: (291.0 alcohol; 292.81 amphetamine [or amphetaminelikesubstance]; 292.81 cannabis; 292.81 cocaine; 292.81hallucinogen; 292.81 inhalant; 292.81 opioid; 292.81phencyclidine [or phencyclidine-like substance]; 292.81sedative, hypnotic, or anxiolytic; 292.81 other [or unknown]substance [e.g., cimetidine, digitalis, benztropine]) 3.3.3 DSM Criteria for Substance Withdrawal Delirium A. Disturbance of consciousness (i.e., reduced clarity ofawareness of the environment) with reduced ability tofocus, sustain, or shift attention. B. A change in cognition (such as memory deficit,disorientation, language disturbance) or the developmentof a perceptual disturbance that is not better accountedfor by a preexisting, established, or evolving dementia. C. The disturbance develops over a short period of time(usually hours to days) and tends to fluctuate during thecourse of the day. D. There is evidence from the history, physicalexamination, or laboratory findings that the symptomsin criteria A and B developed during, or shortly after, awithdrawal syndrome. Note: This diagnosis should be made instead of a diagnosisof substance withdrawal only when the cognitive symptomsare in excess of those usually associated with the 74 CU IDOL SELF LEARNING MATERIAL (SLM)

withdrawalsyndrome and when the symptoms are sufficiently severe towarrant independent clinical attention. Code: [specific substance] withdrawal delirium: (291.0 alcohol; 292.81 sedative, hypnotic, or anxiolytic;292.81 other [or unknown] substance) 3.4 INCIDENCE OF DELIRIUM The incidence of delirium tremens, for example, is found in 1% of all alcoholics, but in 5% of hospitalized alcohol abusers. Improvement of the delirium occurs when the offending agent is reintroduced or a cross-sensitive drug (e.g., a benzodiazepine or alcohol withdrawal) is employed. Delirium is estimated to be present in as many as 30% of older adults who are admitted into acute care facilities such as emergency rooms. It is most prevalent among older adults, people undergoing medical procedures, cancer patients, and people with acquired immune deficiency syndrome (AIDS). Delirium subsides relatively quickly. Once thought to be only a temporary problem, more recent work indicates that the effects of delirium may be more lasting. Some individuals continue to have problems on and off; some even lapse into a coma and may die. Concern by medical professionals is increasing—perhaps because of the increased number of adults living longer – leadingsome to recommend that delirium be included as one of the “vital signs” (along with heartbeat, breathing rate, temperature, and blood pressure) that physicians routinely check when seeing older adults. 3.5 PREVALENCE OF DELIRIUM Delirium can occur in a person of any age. However, the elderly are at particularly high risk, perhaps because of brain changes caused by normal aging that lead to reduced “brain reserve.” Estimates of the prevalence of delirium vary widely with the age of the population studied. However, somewhere between 10 and 51 percent of patients who have had surgery will experience delirium; patients who have had cardiac surgery seem to be at especially high risk. The presence of delirium is also a bad prognostic sign. Delirium is correlated with cognitive decline, longer hospital stays, more health problems, and increased mortality; 25 percent of elderly patients with delirium die within the following 6 months The overall prevalence of delirium in the community is low, but delirium is common in hospitalized patients. Lipowski (Saito, 1987) reported studies of elderly patients and suggested that about 40% of them admitted to general medical wards showed signs of delirium at some point during the hospitalization. Because of the increasing numbers of elderly in this country and the influence of life-extending technology, the population of hospitalized elderly is rising; and so is the prevalence of delirium. 75 CU IDOL SELF LEARNING MATERIAL (SLM)

The intensive care unit, geriatric psychiatry ward, emergency department, alcohol treatment units and oncology wards have particularly high rates of delirium. Massie and colleagues (Lipowski, 1987) reported that 85% of terminally ill patients studied had symptoms that met criteria for delirium, as did 100% of post cardiotomy patients in a study by Theobald (Lipowski, 1989). Overall, it is estimated that 10% of hospitalized patients are delirious at any particular point in time. Older adults are more likely than others to develop delirium. At any given time, 0.4% of adults over the age of 18 may be delirious; among those 55 years of age or older, the prevalence almost triples, to 1.1%. Among elderly patients in hospitals, 10–15% are delirious when admitted and 10–40% may be diagnosed with delirium during their stay. Among residents in nursing homes who are age 75 and older, up to 60% may be delirious at any point in time. Up to 80% of terminally ill patients will become delirious, particularly when they are close to death 3.6CO-MORBIDITY OF DELIRIUM Many medical conditions that impair brain function have beenlinked to delirium, including intoxication by drugs and poisons;withdrawal from drugs such as alcohol and sedative, hypnotic,and anxiolytic drugs; infections; head injury; and various othertypes of brain trauma. DSM-IV-TRrecognizes several causes of delirium among its subtypes. Thecriteria for delirium due to a general medical condition include adisturbance of consciousness (reduced awareness of the environment)and a change in cognitive abilities such as memory andlanguage skills, occurring over a short period and brought aboutby a general medical condition. Other subtypes include the diagnosisreceived by Mr. J.—substance-induced delirium—as well asdelirium due to multiple causes and delirium not otherwise specified. The rise in the use of drugs such as Ecstasy (methylenedioxymethamphetamine)is of particular concern because of suchdrugs’ potential to produce delirium. The last twocategories indicate the oftencomplex nature of delirium. That delirium can be brought on by the improper use of medicationis a particular problem for older adults, because they tendto use prescription medications more than any other age group.The risk of problems among the elderly is increased further becausethey tend to eliminate drugs from their systems less efficiently than younger individuals. It is not surprising, then, thatadverse drug reactions resulting in hospitalization are almost6 times higher among elderly people than in other age groups. And it is believed that delirium is responsiblefor many of the falls that cause debilitating hip fractures inthe elderly. Although there has been someimprovement in the use of medication among older adults withphysicians using more care with drug dosages and the use ofmultiple drugs, improper use continues to produce serious sideeffects, including symptoms of delirium.Because possible 76 CU IDOL SELF LEARNING MATERIAL (SLM)

combinations of illnesses and medications areso numerous, determining the cause of delirium is extremely difficult.Delirium may be experienced by children who have high feversor who are taking certain medications and is often mistakenfor noncompliance. It often occurs duringthe course of dementia; as many as 50% of people with dementiasuffer at least one episode of delirium. Because many of the primary medical conditions can betreated, delirium is often reversed within a relatively short time.Yet, in about a quarter of cases, delirium can be a sign of the endof life. Factors other than medical conditions can trigger delirium.Age itself is an important factor; older adults are more susceptible delirium to developing delirium as a result of mild infections or medicationchanges. Sleep deprivation, immobility,and excessive stress can also cause delirium. 3.7 CAUSES OF DELIRIUM The cause of delirium may lie in intracranial processes, extracranialones, or a combination of the two. The most common etiologicalfactors are as follows (Francis et al., 1990).Infection InducedInfection is a common cause of delirium in hospitalized patientsand typically, infected patients will display abnormalities in hematologyand serology. Vital signs are noted except in persons(elderly, chronic alcohol abusers, chemotherapy patients, thosewith HIV spectrum disease) who may not be able to mount thetypical response. Bacteremic septicemia (especially that causedby gram-negative bacteria), pneumonia, encephalitis and meningitisare common offenders. The elderly are particularly susceptibleto delirium secondary to urinary tract infections. 3.7.1 Metabolic and Endocrine Disturbances Metabolic causes of delirium include hypoglycemia, electrolytedisturbances and vitamin deficiency states. The most commonendocrine causes are hyper function and hypo function ofthe thyroid, adrenal, pancreas, pituitary and parathyroid. Metaboliccauses may involve consequences of diseases of particularorgans, such as hepatic encephalopathy resulting from liverdisease, uremic encephalopathy and post dialysis delirium resultingfrom kidney dysfunction, and carbon dioxide macros isand hypoxia resulting from lung disease. The metabolic disturbanceor endocrinopathy must be known to induce changesin mental status and must be confirmed by laboratory determinationsor physical examination, and the temporal course ofthe confusion should coincide with the disturbance (Francis etal., 1990). In some individuals, particularly the elderly, braininjured and demented, there may be a significant lag time betweencorrection of metabolic parameters and improvement inmental state. 77 CU IDOL SELF LEARNING MATERIAL (SLM)

3.7.2 Low-perfusion States Any condition that decreases effective cerebral perfusion cancause delirium. Common offenders are hypovolemia, congestiveheart failure and other causes of decreased stroke volume such asarrhythmias and anemia, which decreases oxygen binding. Maintenanceof fluid balance and strict measuring of intake and outputare essential in delirious states. 3.7.3 Intracranial Causes Intracranial causes of delirium include head trauma, especiallyinvolving loss of consciousness, post concussive states and hemorrhage;brain infections; neoplasms; and such vascular abnormalitiesas CVAs, subarachnoid hemorrhage, transient ischemicattacks and hypertensive encephalopathy. 3.7.4 Postoperative States Postoperative causes of delirium may include infection, atelectasis,and post pump confusion from maintenance on a heart–lungmachine, lingering effects of anesthesia, thrombotic and embolicphenomena, and adverse reactions to postoperative analgesia.General surgery in an elderly patient has been reported to be followedby delirium in 10 to 14% of cases and may reach 50% aftersurgery for hip fracture (Lipowski, 1989). 3.7.5 Sensory and Environmental Changes Many clinicians underestimate the disorienting potential of anunfamiliar environment. The elderly are especially prone to developenvironment-related confusion in the hospital. Individualswith preexisting dementia, who may have learned to compensatefor cognitive deficits at home, often become delirious once hospitalized.In addition, the nature of the intensive care unit oftenlends itself to periods of high sensory stimulation (as during a“code”) or low sensory input, as occurs at night. Often, patientsuse such external events as dispensing medication, mealtimes,presence of housekeeping staff, and physicians’ rounds to markthe passage of time. These parameters are often absent at night,leading to increased rates of confusion during night-time hours.Often, manipulating the patient’s environment (see section ontreatment) or removing the patient from the intensive care unitcan be therapeutic. 3.7.6 Substance Intoxication Delirium The list of medications that can produce the delirious state isextensive (Table 32.9). The more common ones include suchantihypertensives as methyldopa and reserpine, histamine(H2) receptor antagonists (cimetidine), corticosteroids, antidepressants,narcotics (especially opioid) and nonsteroidal analgesics,lithium carbonate, digitalis, baclofen, anticonvulsants,antiarrhythmics, colchicine, bronchodilators, benzodiazepines,sedative- hypnotics and anticholinergics. Of the narcotic analgesics,meperidine can produce an agitated delirium with tremors,seizures and myoclonus. 78 CU IDOL SELF LEARNING MATERIAL (SLM)

These features are attributed toits active metabolite normeperidine, which has potent stimulantand anti-cholinergic properties and accumulates with repeatedintravenous dosing. In general, adverse effects of narcotics aremore common in those who have never received such agentsbefore (the narcotically naive) or who have a history of a similarresponse to narcotics. Lithium-induced delirium occurs at blood levels greaterthan 1.5mEq/L and is associated with early features of lethargy,stuttering and muscle fasciculations. The delirium may take aslong as 2 weeks to resolve even after lithium has been discontinued,and other neurological signs such as stupor and seizurescommonly occur. Maintenance of fluid and electrolyte balanceis essential in lithium-induced delirium. Facilitation of excretionwith such agents as aminophylline and acetazolamide helps, buthemodialysis is often required. Principles to remember in cases of drug-induced deliriuminclude the facts that 1) blood levels of possibly offending agentsare helpful and should be obtained, but many persons can becomedelirious at therapeutic levels of the drug, 2) drug-induceddelirium may be the result of drug interactions and polypharmacyand not the result of a single agent, 3) over-the-counter medicationsand preparations (e.g., agents containing caffeine or phenylpropanolamine)should also be considered, and 4) delirium canbe caused by the combination of drugs of abuse and prescribedmedications (e.g., cocaine and dopaminergic antidepressants). The list of drugs of abuse that can produce delirium is extensive.Some such agents have enjoyed a resurgence after yearsof declining usage. These include lysergic acid diethylamide, psilocybin(hallucinogenic mushrooms), heroin and amphetamines.Other agents include barbiturates, cannabis (especially dependenton setting, experience of the user and whether it is laced withphencyclidine [“superweed”] or heroin), jimsonweed (highly anticholinergic)and mescaline. In cases in which intravenous useof drugs is suspected, HIV spectrum illness must be ruled out asan etiological agent for delirium. The physical examination of a patient with suspected illicitdrug-induced delirium may reveal sclerosed veins, “pop” scarscaused by subcutaneous injection of agents, pale and atrophic nasalmucosa resulting from intranasal use of cocaine, injected conjunctivaand pupillary changes. Toxicological screens are helpfulbut may not be available on an emergency basis. 3.7.7 Substance Withdrawal Delirium Alcohol and certain sedating drugs can produce a withdrawaldelirium when their use is abruptly discontinued or significantly reduced. Withdrawal delirium requires a history of use ofa potentially addicting agent for a sufficient amount of time toproduce dependence. It is associated with such typical physicalfindings as abnormal vital signs, pupillary changes, tremor, diaphoresis,nausea and vomiting, and diarrhea. Patients generally complain of abdominal and leg cramps, insomnia, nightmares,chills, hallucinations (especially visual) and a general feeling of“wanting to jump out of my skin”. Some varieties of drug withdrawal,although uncomfortable, are not life threatening (e.g.,opioid withdrawal). Others such as alcohol withdrawal deliriumare potentially fatal. 79 CU IDOL SELF LEARNING MATERIAL (SLM)

Withdrawal delirium is much more commonin hospitalized patients than in patients living in the community. 3.8 PROGNOSIS OF DELIRIUM After elimination of the cause of the delirium, the symptoms gradually recede within 3 to 7 days. Some symptoms in certain populations may take weeks to resolve. The age of the patient and the period of time during which the patient was delirious affect the symptom resolution time. In general, the patient has a spotty memory for events that occurred during delirium. These remembrances are reinforced by comments from the staff (“You’re not as confused today”), or the presence of a sitter, or use of wrist restraints. Patient should be reassured that they were not responsible for their behavior while delirious, and that no one hates or resents them for the behavior they may have exhibited. As mentioned earlier, delirious patients have an increased risk of mortality in the year following their first episode. Patients with underlying dementia show residual cognitive impairment after resolution of delirium, and it has been suggested that a delirium may merge into a dementia.Delirium significantly worsens prognosis and is associated with increased mortality at discharge and at 12 months. A significant proportion of patients with delirium during their hospital admission continued to demonstrate symptoms of delirium at discharge, 6-month, and 12-month follow-up. Resolution of symptoms may take longer in patients with poor premorbid cognitive function, incorrect or incomplete diagnosis of contributing factors, and structural brain diseases treated with large doses of psychoactive medications prior to the onset of acute medical illness.Delirium can be life-threatening if left untreated. But with the right care and treatment, people can recover. 3.9 TREATMENT OF DELIRIUM Determining the cause of delirium will guide the treatment plan in most cases. Beyond that, best practices for delirium include ensuring the patient is comfortable, safe, and has his or her physical and emotional needs met. This may include nutritional support, pain management, and, in some cases, medications to help manage mood or dangerous behaviors. Loved ones are often an important part of delirium treatment, as they can comfort the patient and help them keep calm during a confusing time. Delirium is a true medical emergency, and its underlying cause must be identified and managed. Most cases of delirium are reversible, except when the delirium is caused by a terminal illness or by severe brain trauma. Treatment involves medication, environmental manipulations, and family support. The medications that are used for most cases are neuroleptics. These are the same drugs that are used to treat schizophrenia. 80 CU IDOL SELF LEARNING MATERIAL (SLM)

Delirium brought on by withdrawal from alcohol or other drugsis usually treated with haloperidol or other antipsychotic medications,which help calm the individual. Infections, brain injury, andtumors are given the necessary and appropriate medical intervention,which often then resolves the accompanying delirium. Theantipsychotic drug haloperidol is also prescribed for individualsin acute delirium when the cause is unknown. The recommended first line of treatment for a person experiencingdelirium is psychosocial intervention. The goal of nonmedicaltreatment is to reassure the individual to help him or herdeal with the agitation, anxiety, and hallucinations of delirium. Aperson in the hospital may be comforted by familiar personalbelongings such as family photographs. Also, a patient who is included in all treatment decisions retainsa sense of control. This type of psychosocial treatmentcan help the person manage during this disruptive perioduntil the medical causes are identified and addressed. Some evidencesuggests that this type of support can also delay institutionalizationfor elderly patients. In addition, environmental manipulations that help patients stay oriented, such as good lighting, clear signage, and easily visible calendars and clocks, can be helpful. It is also important that staff members introduce themselves when they work with patients, explain what their role is, and provide reorienting prompts whenever necessary. Some patients, however, especially elderly ones, may still have orientation problems, sleep problems, and other difficulties even months after an episode of delirium. Prevention There is substantial evidence that delirium results in long-term poor outcomes in older persons admitted to hospital. Recent long-term studies showed that many patients still meet the criteria for delirium for a prolonged period after hospital discharge, with up to 21% of patients showing persistent delirium at six months post-discharge. Using a tailored multifaceted approach clinicians can decrease rates of delirium by 27% among the elderly. At least 30–40% of all cases of delirium could be prevented, and high rates of delirium reflect negatively on the quality of care. Episodes of delirium can be prevented by identifying hospitalized people at risk of the condition: those over age 65, those with a known cognitive impairment, those with hip fracture, and those with severe illness. Delirium may be prevented and treated by using non-pharmacologic approaches focused on risk factors, such as constipation, dehydration, low oxygen levels, immobility, visual or hearing impairment, sleep deprivation, functional decline, and removing or minimizing problematic medications. Ensuring a therapeutic environment (e.g., individualized care; clear communication; adequate reorientation and lighting during daytime; promoting uninterrupted sleep hygiene with minimal noise and light at night; minimizing bed relocation; having familiar objects like family pictures; providing earplugs; and providing adequate nutrition, pain control, and assistance toward early mobilization) can also yield benefit toward 81 CU IDOL SELF LEARNING MATERIAL (SLM)

preventing delirium. Research into pharmacologic prevention and treatment is weak and insufficient to make proper recommendations. Preventive efforts may be most successful in assisting people whoare susceptible to delirium. Proper medical care for illnesses andtherapeutic drug monitoring can play significant roles in preventingdelirium. For example, the increasednumber of older adults involved in managed care andpatient counseling on drug use appear to have led to more appropriateuse of prescription drugs among the elderly. Complete recovery from delirium is possible if the underlyingcause is treated promptly and effectively. The patient must be examined thoroughly for all possiblereversible causes of the disorder, such as drug intoxication, infections, fever, and malnutrition,and then treated accordingly. Beyond treating the underlying medical conditions, the mostcommon treatment is atypical antipsychotic medication. It usually takes 1 to 4 weeks for the condition to clear; it takes longer in older peoplethan in younger people. Because of the high rates of delirium in hospitalized older adults, preventive strategies arerecommended to prevent delirium from beginning. In one study of such strategies, researchersrandomly assigned 852 elderly hospitalized patients to receive either standard medical careonly or standard medical care along with an intervention designed to prevent delirium. Thisintervention addressed common risk factors for delirium within the hospital setting, such assleep deprivation, immobility, dehydration, and visual and hearing impairment. Among otherstrategies, medical tests and rounds were scheduled later in the morning to avoid wakingpatients, patients were helped to resume walking soon after surgery, glasses and hearing aidswere returned as soon as possible after medical procedures, and care was given to help patientsconsume enough liquid and calories. The patients who received the intervention were less likelyto develop delirium, and those who did develop delirium recovered more quickly comparedto patients who received standard medical care. The high risk of delirium among people with dementia raises another set of preventionissues. The family of a person with dementia should learn the symptoms of delirium and knowabout its reversible nature so that they do not interpret the onset of delirium as a new stage ofa progressive dementia. With proper diagnosis and treatment, the person can usually returnto the earlier state. The primary treatment of delirium is to identify and ameliorate any causal or contributing medical conditions. As part of that effort, the dosages of all sedatives and other CNS-active medications should be minimized as much as possible. (The exception is sedative-hypnotic or alcohol withdrawal delirium, in which treatment of the underlying problem requires the administration of a cross-tolerant agent such as a benzodiazepine.) Delirious patients may need extra supportive physical care; maintenance of basic functions such as food and fluid intake is crucial to rapid recovery. 82 CU IDOL SELF LEARNING MATERIAL (SLM)

Keeping the patient in an environment that is quiet and free of unnecessary stimulation may help reduce agitation. Frequent cues to orientation may also be helpful. Supportive contacts with the patient, family, and sometimes staff members are necessary to reassure the patient that the new, often frightening behavioral state reflects physical illness and that the patient is not going crazy. Attention may need to be paid to the patient's legal capacity to participate in informed clinical care decisions. The patient with a quiet, hypoactive delirium needs no specific pharmacotherapy. However, many delirious patients show persistent or intermittent psychomotor agitation that may interfere with nursing care or necessary tests and procedures. Control of the agitation is essential to prevent inadvertent self-damage and allow appropriate evaluation and treatment. Physical restraints may be used transiently when necessary. If sedation is desired, the drug of choice is a high-potency antipsychotic agent in relatively low dosages should generally be avoided because they are likely to worsen the delirious state. At times of severe, life- threatening agitation, sedation at nearly any cost becomes necessary, and combinations of antipsychotic agents, benzodiazepines, and opioids have been used. There have been case reports of improvement in or remission of delirious states due to intractable medical illnesses with ECT. Although ECT may rarely be advised by a consultant with expertise in the procedure, routine consideration of ECT for delirium is not advised. 3.10 SUMMARY  Delirium is defined as a transient, usually reversible, cause of mental dysfunction and manifests clinically with a wide range of neuropsychiatric abnormalities.  It can occur at any age, but it occurs more commonly in patients who are elderly and have a previously compromised mental status.  The clinical hallmarks of delirium are decreased attention or awareness and a change in baseline cognition. Delirium often manifests as a waxing and waning type of confusion.  Because delirium is temporary, it’s hard to know exactly how many people develop it. Researchers estimate that hospital delirium affects 15% to 50% of people.  The different types of delirium produce different symptoms. Symptoms tend to start suddenly and get worse over the next few hours or days.  A person with delirium may act like they’re intoxicated. The main symptom is being unable to pay attention. Symptoms tend to become worse in the evening, which is known as sundowning. 83 CU IDOL SELF LEARNING MATERIAL (SLM)

 Healthcare providers look for problems with attention, memory, orientation and visual ability. Providers may ask the person to perform a few simple tasks, such as spelling a short word backward or doing a basic math problem.  In some cases, the person is in the hospital when they develop delirium. If they are not, they will most likely need hospitalization. In a hospital setting, providers can monitor them and keep them from injuring themselves or others.  Providers try to identify the cause of delirium quickly to get the patient treatment as fast as possible. Once providers identify and treat the reason, they can often reverse the delirium.  Treatment for delirium depends on the cause.Treatments may include antibiotics for infections, fluids and electrolytes for dehydration and benzodiazepines for problems due to drug and alcohol withdrawal. Often, treatments for delirium focus on the environment.  The symptoms typically improve in a few days to weeks. But someone who had delirium may have to stay longer in the hospital even after symptoms improve.  They may still have an underlying medical condition or be unable to function completely on their own. 3.11 KEY WORDS  Aetiology: The study of the origins of disease: physical, mental or emotional.  Delirium: An altered state of consciousness characterized by delusions, hallucinations and illusions.  Hallucination: A perceptual illusion of a vivid experience that has no apparent reality in the external world.  Psychotherapy: The use of psychological techniques to treat psychological disturbances. 3.12 LEARNING ACTIVITY 1. Explain the process of assessment undertaken in order to diagnose a person with delirium? ___________________________________________________________________________ ___________________________________________________________________________ 2. Explain the process of treatment provided to a person with delirium? ___________________________________________________________________________ ___________________________________________________________________________ 84 CU IDOL SELF LEARNING MATERIAL (SLM)

3.13 UNIT END QUESTIONS A. Descriptive Questions Short Questions 1. What is delirium? 2. What are the key characteristics of Delirium? 3. What is orientation? 4. What is the incidence of delirium? 5. What is the prevalence of delirium? Long Questions 1. What are the symptoms of Delirium? 2. What are the causes of delirium? 3. What are the comorbidities of delirium? 4. What is the treatment for delirium? 5. Write in detail about the DSM criteria for Delirium? B. Multiple Choice Questions 1. Delirium is characterized by: a. Insomnia b. A gradual worsening of memory c. A sudden confusion or worsening of confusion that develops over a short time period d. Agitation 2. A disturbance of consciousness caused by a medical condition that develops over a very short period of time and is characterized by a change in cognition (such as a memory deficit or disorientation) and a reduction in the ability to focus, shift, or sustain attention, is known as a. Korsakoff's syndrome b. delirium c. HIV-associated dementia. d. Alzheimer's disease 85 CU IDOL SELF LEARNING MATERIAL (SLM)

3. Delusional thinking is characteristic of a. fugue b. conversion disorder c. obsessive-compulsive disorder d. psychosis 4. DSM stands for a. diagnostic and statistical manual b. diagnostic schedule of medicine c. depressive scale modalities d. doctor of surgical medicine 5. Which of the following is not a hallucinogenic? a. Cannabis b. MDMA c. LSD d. Antibiotics Answers 1-c, 2-b, 3-d, 4-a, 5-d 3.14 REFERENCES Textbooks  Ahuja N (2002). A short text book of Psychiatry. (5th edn). 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 86 CU IDOL SELF LEARNING MATERIAL (SLM)

 Domjan Michael (2010). The Principles of Learning and Behavior (6th Edt) 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  AIDS Surveillance Report (2002) Centers for Disease Control, February.  American Psychiatric Association (1994) Diagnostic and Statistical Manual of Mental Disorders, 4th edn. APA, Washington DC, pp. 123–174.  Kaplan H, Sadock B and Grebb J (1994) Kaplan and Sadock’s Synopsis of Psychiatry, 7th edn. Williams & Wilkins, Baltimore.  Karp H (1984) Dementia in adults, in Clinical Neurology, Vol. 3 (eds Baker AB and Baker LH). Harper & Row, New York, pp. 1–32.  Lipowski ZJ (1987) Delirium (acute confusional states). JAMA 258, 1789–1792.  Lipowski ZJ (1989) Delirium in the elderly patient. New Engl J Med 320, 578–582.  Torres R, Mittal D and Kennedy R (2001) Use of quetiapine in delirium. Psychosomatics 42, 347–349.  Ahuja N (2002). A short text book of Psychiatry. (5th edn). 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.  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.  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. 87 CU IDOL SELF LEARNING MATERIAL (SLM)

 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 88 CU IDOL SELF LEARNING MATERIAL (SLM)

UNIT 4 – PICA AND RUMINATION STRUCTURE 4.0 Learning Objectives 4.1 Introduction 4.2 Pica and Rumination 4.3 DSM Criteria for Pica and Rumination 4.4 Incidence of Pica and Rumination 4.5 Prevalence of Pica and Rumination 4.6 Co-morbidity of Pica and Rumination 4.7 Causes of Pica and Rumination 4.8 Prognosis of Pica and Rumination 4.9 Treatment of Pica and Rumination 4.10 Summary 4.11 Key Words 4.12 Learning Activity 4.13 Unit End Questions 4.14 References 4.0 LEARNING OBJECTIVES After studying this unit, you will be able to,  Explain the nature and symptoms of  Describe the incidence and prevalence of  Explain the co-morbidity of  State the causes of Neurocognitive Disorders  Explain the prognosis of  State the treatment for 4.1 INTRODUCTION Pica refers to persistent consumption of nonnutritive, nonfood items that is inappropriate for the individual’s developmental age. Pica may occur in association with a number of medical 89 CU IDOL SELF LEARNING MATERIAL (SLM)

conditions, including during normal pregnancy. The disorder should not be assigned if it is occurring in the context of another mental or medical condition or disorder unless it is so severe that it warrants additional clinical attention. The only changes recommended to the DSM-IV criteria for pica were minor alterations to the wording of the criteria for clarification and to make clear that the disorder could be assigned to the behavior of adolescents and adults as well as children. Patients should be queried regarding pica, the consumption of nonfood items. The diagnosis of pica is characterized by a persistent ingestion of one or more nonnutritive, nonfood substances (e.g., chalk, soap, cloth, nails, paper, and soil) over a period of at least 1 month. Although this behavior may occur in patients with other psychiatric disorders (e.g., developmental disorders, autism, schizophrenia) or medical conditions (e.g., pregnancy), a separate DSM-5 diagnosis of pica is made when the severity of the eating behavior warrants specific clinical management. Rumination refers to the persistent, repeated regurgitation of food that has already been swallowed. Relatively little is known about this phenomenon. Rumination occurs among some individuals with AN and BN, but in such cases, an additional diagnosis of rumination disorder is not assigned. As in the case of pica, the only changes recommended to the DSM- IV criteria for rumination disorder were for the purpose of clarification and to make clear that this disorder can be assigned to individuals across the life span. Patients should be queried regarding pica, the consumption of nonfood items. The diagnosis of pica is characterized by a persistent ingestion of one or more nonnutritive, nonfood substances (e.g., chalk, soap, cloth, nails, paper, and soil) over a period of at least 1 month. Although this behavior may occur in patients with other psychiatric disorders (e.g., developmental disorders, autism, schizophrenia) or medical conditions (e.g., pregnancy), a separate DSM-5 diagnosis of pica is made when the severity of the eating behavior warrants specific clinical management or a medical condition and the severity of the behavior necessitates clinical attention, then a DSM-5 diagnosis of rumination disorder is warranted. 4.2 PICA AND RUMMINATION Pica Pica refers to behaviorally and culturally inappropriate eating of non-nutritional substances for at least 4 weeks. It is most often associated with poverty related nutritional deficiencies and mental retardation. Because mouthing of objects is still common in toddlers between 1 and 2 years, the diagnosis of pica should be made only if the behavior is persistent and inappropriate for the child’s developmental level. The diagnosis of pica should be explored in children with accidental poisoning, with lead intoxication, or with worm infestation. Young children with signs of malnutrition or iron deficiency should also be considered for the diagnosis of pica. 90 CU IDOL SELF LEARNING MATERIAL (SLM)

The assessment should include the history of the child’s development in general, and feeding in particular. Special attention should be given to other oral activities that the child may use for self-soothing and relief of tension. In addition, the home environment and the parents’ relationship with each other and with the child need to be explored to assess the parents’ availability to nurture and supervise the child. Above all, mother and child should be observed during a meal and during play to gain a better understanding of their relationship and how the symptoms of pica can be understood in the context of that relationship. If the diagnosis of pica is established, it is critical that the child undergo a thorough physical examination to rule out any of the complications associated with this disorder, such as nutritional deficiencies (especially iron deficiency), lead poisoning, intestinal infections (toxoplasmosis or intestinal parasites), or gastrointestinal bezoars. Rumination Rumination disorder is characterized by the repeated regurgitation and rechewing of food occurring for at least one month with prior normal functioning. As in the case of feeding disorder of infancy and early childhood, these behaviors cannot be the result of a medical condition affecting the gastrointestinal tract. Similarly, this diagnosis is not made in the presence of anorexia nervosa or bulimia nervosa. Most frequently, infants who ruminate come to the attention of professionals because of “frequent vomiting” and weight loss. Some infants ruminate primarily during the transition to sleep when left alone, and their ruminatory activity might not be readily observed. However, these infants are frequently found in a puddle of vomitus, which should raise suspicion of rumination. Other infants can be observed to posture with the back arched, to put the thumb or whole hand into the mouth, or to suck on the tongue rhythmically to initiate the regurgitation of food. Most of the regurgitated food is initially vomited, but gradually the infant appears to learn to hold more of the food in the mouth to rechew and reswallow. “Experienced” ruminators appear to be able to bring up food through repeated tongue movements. They learn to rechew and reswallow the food without losing any of it. Their rumination can be inferred only from the movements of their cheeks and foul oral odor because of the frequent regurgitation. In addition to taking a thorough medical history, it is important to explore the onset of vomiting and the social context under which the symptoms developed. An acute medical illness or a stressor in the parents’ life is frequently associated with the onset of vomiting. When exploring the stressors in the mother–infant relationship, one needs to be careful neither to alienate the mother nor to add additional stress to the relationship. It is best to observe the infant in various situations with the mother, with other caretakers and alone in the crib during the transition to sleep. 91 CU IDOL SELF LEARNING MATERIAL (SLM)

These observations will help in understanding the severity of the rumination, and whether it is situational or pervasive. In addition to assessing the rumination in the infant, the mother– infant relationship and the mother’s life circumstances need to be evaluated because the mother’s ability to soothe and to stimulate her infant is critical for successful intervention. 4.3 DSM CRITERIA FOR PICA AND RUMMINATION 4.3.1 DSM criteria for Pica A. Persistent eating of nonnutritive, nonfood substances over a period of at least 1 month. B. The eating of nonnutritive, nonfood substances is inappropriate to the developmental level of the individual. C. The eating behavior is not part of a culturally supported or socially normative practice. D. If the eating behavior occurs in the context of another mental disorder (e.g., intellectual disability [intellectual developmental disorder], autism spectrum disorder, schizophrenia) or medical condition (including pregnancy), it is sufficiently severe to warrant additional clinical attention. Coding note: The ICD-9-CIVI code for pica is 307.52 and is used for children or adults. The ICD-10-CM codes for pica are (F98.3) in children and (F50.8) in adults. Specify if: In remission: After full criteria for pica were previously met, the criteria have not been met for a sustained period of time. 4.3.2 DSM criteria for Rumination A. Repeated regurgitation of food over a period of at least 1 month. Regurgitated food may be re-chewed, re-swallowed, or spit out. B. The repeated regurgitation is not attributable to an associated gastrointestinal or other medical condition (e.g., gastroesophageal reflux, pyloric stenosis). C. The eating disturbance does not occur exclusively during the course of anorexia nervosa, bulimia nervosa, binge-eating disorder, or avoidant/restrictive food intake disorder. D. If the symptoms occur in the context of another mental disorder (e.g., intellectual disability [Intellectual developmental disorder] or another neurodevelopmental disorder), they are sufficiently severe to warrant additional clinical attention. Specify if: In remission: After full criteria for rumination disorder were previously met, the criteria have not been met for a sustained period of time. 92 CU IDOL SELF LEARNING MATERIAL (SLM)

4.4 INCIDENCE OF PICA AND RUMMINATION Incidence of Pica The prevalence of pica is difficult to establish because of differences in definition and the reluctance of patients to admit to abnormal cravings and ingestion. An incidence of pica greater than 50% is considered normal in children aged 18 to 36 months. Pica is thought to decrease with age; one study showed that about 10% of children older than 12 years engage in pica.8 Persistence of excessive hand-to-mouth movements observed in pica is abnormal in children older than 36 months. Although the onset of pica can occur at any age, it most commonly emerges during childhood. Pica appears to be more common among pregnant women and children with developmental and intellectual disabilities. It often occurs along with other disorders such as autism spectrum disorder, obsessive-compulsive disorder, and attention-deficit/hyperactivity disorder. Incidence of Rumination Rumination syndrome can affect children and adults. In a study that surveyed 2163 children and adolescents, 110 (5 percent) fulfilled clinical criteria for rumination syndrome. There are limited data on the prevalence of rumination syndrome in adults. In two population-based studies, rumination syndrome had a prevalence of 0.8 to 0.9 percent of adults in the general population. In patients with fibromyalgia or eating disorders, the prevalence of rumination syndrome may be as high as 7 to 8 percent. 4.5 PREVALENCE OF PICA AND RUMMINATION Prevalence of Pica Pica is a common, but frequently missed problem. The onset of pica is usually during the toddler age between 12 and 24 months. Because infants commonly mouth objects, it is difficult to make the diagnosis in young infants. Estimates of the prevalence of pica among institutionalized mentally retarded individuals range from 10 to 33%. Children with pica are more susceptible to malnutrition, anemia, diarrhea or constipation, and worm infestation. It has been noted that pica is highest in a group of children hospitalized for accidental poisoning and that more than 60% of mothers with children with pica have pica themselves. There is limited research on pica. It is believed to be rare among healthy children in the US. Less than 10% of US children older than 12 years of age meet diagnostic criteria for pica. One study reported a high prevalence of pica among children in treatment for sickle cell anemia and another study showed high rates among school-aged children in Africa. 93 CU IDOL SELF LEARNING MATERIAL (SLM)

The practice of eating dirt is culturally sanctioned in some African countries and may continue among AfricanAmericans as a culturally normative practice based on their heritage. Data show that pica is more prevalent among African and African American females who are pregnant. The eating of dirt by AfricanAmerican women may be considered a cultural practice. It may be a learned behavior that provides social and psychological benefits. When pica behavior is a culturallysupported practice, it would not be diagnosed as a mental disorder. Prevalence of Rumination Rumination disorder appears to be uncommon, occurring more often in boys than in girls and also in individuals with mental retardation. 4.6 CO-MORBIDITY OF PICA AND RUMMINATION Because of the frequent occurrence of mood disturbance and substance abuse among individuals with eating disorders, symptoms of these and other psychiatric disorders should be reviewed during the clinical assessment of concerns related to eating and weight. Specific questions about the use of drugs and alcohol, both currently and in the past, should be asked directly in a nonjudgmental fashion. The clinician should be mindful of patients’ potential reluctance to disclose such information and should assume an open, curious stance. Individuals at significantly low weight almost invariably endorse depressive symptoms, because such symptoms are associated with the pathophysiology of starvation and malnutrition. Anxiety disorders, obsessive-compulsive and related disorders, and trauma- and stressor- related disorders may also be comorbid with eating disorders. Once again, it may be difficult to accurately attribute symptoms to one disorder or another, and clinicians should be aware that eating disorders. The clinician should also be alert for indications of personality disorders, which are relatively common among individuals with eating disturbances. Personality traits commonly associated with eating disorders include perfectionism, impulsivity, and novelty seeking. 4.6.1 Co-morbidity for Pica Disorders most commonly comorbid with pica are autism spectrum disorder and intellectual disability (intellectual developmental disorder), and, to a lesser degree, schizophrenia and obsessive-compulsive disorder. Pica can be associated with trichotillomania (hair pulling disorder) and excoriation (skin-picking) disorder. In comorbid presentations, the hair or skin is typically ingested. Pica can also be associated with avoidant/restrictive food intake disorder, particularly in individuals with a strong sensory component to their presentation. When an individual is known to have pica, assessment should include consideration of the possibility of gastrointestinal complications, poisoning, infection, and nutritional deficiency. 94 CU IDOL SELF LEARNING MATERIAL (SLM)

4.6.2 Co-morbidity for Rumination Regurgitation with associated rumination can occur in the context of a concurrent medical condition or another mental disorder (e.g., generalized anxiety disorder). When the regurgitation occurs in this context, a diagnosis of rumination disorder is appropriate only when the severity of the disturbance exceeds that routinely associated with such conditions or disorders and warrants additional clinical attention. 4.7 CAUSES OF PICA AND RUMMINATION 4.7.1 Causes for Pica Organic, psychodynamic, socioeconomic and cultural factors have been implicated in the cause of this disorder. Some authors have suggested that inadequate dietary intake of iron and calcium leading to abnormal cravings may induce pica. Other authors have implicated psychosocial stress, maternal deprivation, parental neglect and abuse, and disorganized and impoverished family situations in the etiology of pica. In certain population groups, cultural acceptance of pica has been considered an important factor in the etiology of this disorder as well. Most helpful clinically is a multifactorial etiology, whereby constitutional, developmental, familial, socioeconomic and cultural factors interact with each other. Children who engage in pica often experience frequent separations from one or both parents followed by replacement of rapidly changing, inadequate caretakers who seemed to encourage oral gratification in response to the child’s distress. These children show a high degree of other oral activities (e.g., thumb-sucking or nail-biting) and may be seeking gratification caused by the lack of parental availability and nurture. Risk Factors Pica often occurs with other mental health disorders associated with impaired functioning (e.g., intellectual disability, autism spectrum disorder, schizophrenia). Iron-deficiency anemia and malnutrition are two of the most common causes of pica, followed by pregnancy. In these individuals, pica is a sign that the body is trying to correct a significant nutrient deficiency. Treating this deficiency with medication or vitamins often resolves the problems. A medical professional should assess if the behavior is sufficiently severe to warrant independent clinical attention (e.g., some people may eat nonfood items during pregnancy, but their doctor may determine that their actions do not indicate the need for separate clinical care). Due to extremely limited research on pica, risk factors are not well-understood. One popular theory is that mineral deficiencies, in particular iron deficiency, can cause pica and that pica is the behavioral response to the deficiency. Much of the evidence comes from case reports that showed a cessation of the behavior after correction of the deficiency.3 Some have proposed that pica may develop in response to stress on top of a dietary deficiency. 95 CU IDOL SELF LEARNING MATERIAL (SLM)

Medical Risks Pica can be associated with significant medical risks depending on the substances ingested and how severe the behavior is. Heavy metals such as lead, mercury (from paper), zinc, and copper can be toxic. Pica can lead to masses of consumed matter in the stomach and gastrointestinal tract, blockages in the intestines, and tears requiring surgery. Pica can also lead to issues including internal parasites, poisoning, choking, respiratory problems, and death. 4.7.2 Causes for Rumination Several authors have attributed rumination to an unsatisfactory mother–infant relationship, (including neglect or lack of stimulation, and sometimes too stressful life situations of the parent. Others have considered rumination a learned behavior that is maintained by special attention by the caregivers to the child’s rumination and, consequently, the rumination has to be unlearned by counter conditioning. The precise cause of rumination syndrome isn't clear. But it appears to be caused by an increase in abdominal pressure. Rumination syndrome is frequently confused with bulimia nervosa, gastroesophageal reflux disease (GERD) and gastroparesis. Some people have rumination syndrome linked to a rectal evacuation disorder, in which poor coordination of pelvic floor muscles leads to chronic constipation. The condition has long been known to occur in infants and people with developmental disabilities. It's now clear that the condition isn't related to age, as it can occur in children, teens and adults. Rumination syndrome is more likely to occur in people with anxiety, depression or other psychiatric disorders. Rumination can be seen along a continuum: a patient may have gastrointestinal disease, such as hiatal hernia or reflux, and little psychiatric illness in the mother–infant relationship at one end of the spectrum; or the converse, a patient might have no reflux and severe psychiatric illness in the mother–infant relationship at the other end of the spectrum. Reflux or a temporary illness associated with vomiting frequently precedes the rumination. At some point, the infant seems to learn to initiate vomiting and turn it into rumination to achieve self- regulation. It appears that in circumstances in which the infant fails to elicit or loses either caring attention or tension-relieving responses from the caretaker, the infant resorts to rumination as a means of self-soothing and relief of tension. 4.8 PROGNOSIS OF PICA AND RUMMINATION 4.8.1 Prognosis of Pica Onset of pica can occur in childhood, adolescence, or adulthood, although childhood onset is most commonly reported. Pica can occur in otherwise normally developing children, whereas in adults, it appears more likely to occur in the context of intellectual disability or other mental disorders. The eating of nonnutritive, nonfood substances may also manifest in pregnancy, when specific cravings (e.g., chalk or ice) might occur. The diagnosis of pica 96 CU IDOL SELF LEARNING MATERIAL (SLM)

during pregnancy is only appropriate if such cravings lead to the ingestion of nonnutritive, nonfood substances to the extent that the eating of these substances poses potential medical risks. The course of the disorder can be protracted and can result in medical emergencies (e.g., intestinal obstruction, acute weight loss, poisoning). The disorder can potentially be fatal depending on substances ingested. In many instances, the disorder is believed to be self-limited and to remit spontaneously after a few months. However, there may be a developmental impact of the disorder in some children. For example, younger children may be somewhat retarded in the use of their speech and show conflicts about their dependency needs and aggressive feelings. Adolescents may evidence some degree of depression, borderline personality disorders, and other forms of disturbed oral activities and the use of tobacco, alcohol, or drugs. There may be a strong relationship between pica in childhood and symptoms of bulimia nervosa in adolescence. 4.8.2 Prognosis for Rumination The onset of rumination is frequently in the first year of life except in individuals with developmental delays, in whom the disorder may occur during later years. Rumination has also been reported to occur in adults with normal intelligence and in association with bulimia nervosa. In some infants and children, the disorder is believed to remit, however, electrolyte imbalance, weight loss, dehydration and death have been reported to result from rumination, and rumination should always be taken seriously. Onset of rumination disorder can occur in infancy, childhood, adolescence, or adulthood. The age at onset in infants is usually between ages 3 and 12 months. In infants, the disorder frequently remits spontaneously, but its course can be protracted and can result in medical emergencies (e.g., severe malnutrition). It can potentially be fatal, particularly in infancy. Rumination disorder can have an episodic course or occur continuously until treated. In infants, as well as in older individuals with intellectual disability (intellectual developmental disorder) or other neurodevelopmental disorders, the regurgitation and rumination behavior appears to have a self-soothing or self-stimulating function, similar to that of other repetitive motor behaviors such as head banging. 4.9 TREATMENT OF PICA AND RUMMINATION Treatment for Pica In treating pica, one must consider the various factors that appear to contribute to the development of pica as well as its complications. It is important to treat the child medically while addressing the psychosocial needs of the child’s family as well. The mothers need to be made aware of the dangers of pica and should be enlisted in providing a childproof environment. This might include removing lead from paint in old substandard housing units or instituting anthelmintic therapy for family pets. A psychoeducational treatment approach 97 CU IDOL SELF LEARNING MATERIAL (SLM)

that, in addition to teaching the mothers the dangers of pica, would also provide social support to help them become more available to their children is preferable. There is no widely-accepted treatment for pica. Current interventions to address pica include surgery as well as nutritional, pharmacological, and behavioral treatments. Surgical interventions may be required when items ingested have caused damage to the body, but they do not address the underlying symptoms. Nutritional supplements such as iron have been used for treatment when underlying nutritional deficiencies or excesses have been identified. Various medications have been tried although there are no conclusive studies on their use. There are limited studies of behavioral interventions for pica. Interventions that seem most likely to be successful in treating pica in children are combination treatments that include reinforcement procedures such as contingent reinforcement and discrimination training.  Contingent reinforcement strategies reward children with food or toys when they do not engage in pica behaviors.  Discrimination training strategies involve teaching children to distinguish between edible and inedible substances and also about the dangers of eating inedible items.  For adults with pica, cognitive behavioral therapy (CBT) may be a useful technique. Such treatment may focus on helping the person to change their thoughts about eating the nonfood item and changing the behavior and replacing it with another coping strategy. Nutritional Treatment Although various factors contribute to the development of pica, a lack of certain nutrients can trigger the desire to eat non-food materials. This connection explains why some women who are pregnant and people with zinc or iron deficiencies may experience symptoms of pica. To combat this cause, nutritional experts like physicians, dietitians and nutritionists test individuals with this condition for missing nutrients and other medical problems associated with pica, such as lead poisoning and indigestible masses in the body. Once the professionals establish physical safety, they will encourage diet changes to compensate for any nutrition deficiencies present. With a balanced diet and adequate vitamins and minerals, pica symptoms tend to diminish quickly. If the person is unable or unwilling to adjust their food intake, the professional may recommend dietary supplements to stabilize and increase nutrients in the body. Behavioral Therapies Some people with pica will see their symptoms quickly diminish with nutritional coaching, diet change and supplements. Others will require mental health therapy to decrease unwanted urges. Mental health treatment for children with pica focuses on: 98 CU IDOL SELF LEARNING MATERIAL (SLM)

 Educating people with pica and their families about the condition, including possible causes, risks and treatment strategies  Creating a safe environment for the child where they will not be injured by consuming chemicals or other hazardous materials  Removing preferred nonfood items from the home  Increasing the supervision so the person cannot eat the nonfood items and blocking any attempts to do so  Using distraction to sway the child toward a desirable behavior  Praising the child for eating healthy food items and discarding nonfood items that they would have previously eaten The cornerstone to childhood treatment of pica is behavior modification. The primary aim of this therapeutic technique is to reinforce desired behaviors through rewards, like food, verbal praise, money, toys and prizes. Parents may also administer punishments, like timeouts or extra chores, to decrease the frequency of pica behaviors. Studies of pica using these behavior modification principles saw a 96 percent reduction in eating nonfood items within weeks of the treatment beginning. For adults with pica, many of the same techniques apply. Friends and family can take turns exposing their loved one to items the person would like to eat and reward them for resisting the urge to consume the items. Medications Currently, there are no medications specifically approved to treat pica, but that does not mean no drug options exist. Researchers and prescribers have begun to find some benefit from medicines. Medications that enhance a chemical in the brain called dopamine might help improve pica symptoms. Medications like Zyprexa, a drug ordinarily used for schizophrenia, may also reduce the urges and impulses to eat nonfood items. Additionally, medications used to manage severe behavioral problems in children may prove effective in treating pica as well. As always, it is essential to discuss all medication options with your physician. Treating Pica and Co-Occurring Disorders Since pica commonly co-occurs with other mental health disorders, it is valuable to receive a thorough evaluation from a mental health specialist to understand what other conditions may be present and the best ways to manage their symptoms. Pica frequently co-occurs with mental health conditions like:  Autism spectrum disorder  Intellectual disabilities 99 CU IDOL SELF LEARNING MATERIAL (SLM)

 Schizophrenia  Obsessive-compulsive disorder  Trichotillomania (hair-pulling disorder)  Excoriation (skin-picking) disorder When mental health conditions co-occur, the individual and treatment providers must take steps to address all symptoms, rather than only focusing on one symptom or one condition. Without a comprehensive approach to pica and co-occurring disorder treatment, there will be limited progress. Treatment for Rumination Diverse theories of etiology have resulted in various proposed methods of treatment. Besides surgical intervention to prevent reflux and the early use of mechanical restraints, treatment has been primarily behavioral or psychodynamic or a combination of both. On the basis of the assumption that rumination is a learned habit reinforced by increased attention for regurgitation, unlearning by counter conditioning has been suggested. Some authors have used electric shock after other methods had failed. A number of alternative procedures of punishment, such as aversive taste stimuli (lemon juice or hot sauce), have been developed. There are difficulties in the use of aversive taste stimuli as punishment. Frequently, the infants are out of reach of the caretakers when they ruminate; consequently, the use of lemon juice or hot sauce is inconsistent, and this delays learning. Some infants appear to become adapted to these aversive taste stimuli. These authors suggest scolding the infant by shouting “No”, placing the infant down, and leaving the room for 2 minutes immediately on initiation of rumination by the infant. If the infant is not ruminating on the caretaker’s return, he or she is to be picked up, washed and played with as a reward. There may be two behavioral causes of rumination: 1) rewardlearning through increased attention for regurgitation, and2) social deprivation. Whereas punishment with time-out may benecessary for the first type, holding the child for 10 to 15 minutesbefore, during and after meals is the treatment of choice for thesecond type. A psychodynamic approach based on the assumptionthat rumination results from a disturbance in the mother–infantrelationship has been advocated. Mothers of ruminating infantsare frequently found to be overwhelmed by their personal lives,which make them unavailable or tense in their relationship withtheir infants. Psychotherapy for the mother and environmentalchanges that produce enhanced mothering have been proposed. After an understanding of the mother’s situation has beengained, treatment is best individualized by use of a combinationof psychodynamic and behavioral interventions to enhance themother–infant relationship in general, and to address the symptomof rumination in particular. 100 CU IDOL SELF LEARNING MATERIAL (SLM)