Physiology of the Brain in the Manifestation of Alzheimer's, Possible Clinical Treatment and Social Care for the Patient - Case Study Example

Clinical Case about CNS Disorder Name Institutional Affiliation Objectives Describe a clinical case basing on the key facts provided. Analyse the diagnosis of the patient. Discuss the physiology of the relevant organ. Discuss the pathophysiology of the disease diagnosed in the case. Explain the possible clinical treatment and social/familial care for the patient. Case Background The patient is a 72 year old retired occupational nurse referred by her GP because of memory problems. Account of husband and daughter confirm she is forgetful, dislikes her past hobbies including reading, and faces difficulties performing routine tasks. Husband has taken over daily household chores including cooking, shopping and household account management. The patient lacks hallucinations, has positive mood, drinks only very occasionally and has no family history of cognitive impairment. She treats her hypertension with bendroflumethazide. Patient’s MMSE (Mini-Mental State Examination) revealed a score of 22 out of 30, losing 3 points for orientation, 3 points for delay recall of three objects, 1 point for attention and calculation, and 1 point for copying a figure of intersecting pentagons. Patient’s physical, neurological examinations and CSF test results were all normal and she showed no signs of extrapyramidal movements. The brain MRI showed hippocampal atrophy, which is consistent with Alzheimer’s disease (AD). Electroencephalogram showed generalised slowing. Analysis of the Clinical Case: Diagnosis The patient has Mild Alzheimer’s disease. This is because of her cognitive impairment revealed by MMSE and the other tests conducted that have helped to rule out other causes of dementia. An MMSE between 19 and 24 points suggest mild cognitive impairment (Lin,et al. 2013). Memory problem is among the first warning signs of AD development and older people from age 65 years with mild cognitive impairment are likelier to develop AD. Other causes of dementia such as Fronto-temporal symptoms begin from around 45 years and patent’s mood is impulsive which lack in this case. The patient’s neurological and physical examinations and the blood tests all came out normal. Normal body movements/no ataxia and no hallucinations helped rule out Lewy Body cause of dementia; progressive manifestation of her symptoms is more consistent with AD than other dementia causes; non hereditary cognitive impairment, normal CSF results, patient’s EEG results ruled out other causes such as Vascular dementia, Hydrocephalus dementia and thyroid disease, pathogenic infections, and Vitamin deficiencies which are reversible causes of dementia (Montez et al. 2009; Palmqvist et al. 2009). Physiology of the Brain in the manifestation of Alzheimer The brain is a complex structure forming a significant part of the central nervous system (CNS) and is in close proximity with major sensory organs for vision, smell, hearing taste and balance (Agrawal, Tyagi, Shukla & Nath 2009). The cerebral cortex/ cerebrum forms the largest part of the human brain and contains billions of interconnected neurons which pass communication signals via axons to target recipient cells enabling communication to other parts of the brain and the body. Four major lobes in the cerebrum perform various functions. The frontal lobe is the centre of reasoning, planning, movement, emotions, problem solving and some parts of speech. The parietal lobe receives sensory input including touch, temperature, pain and pressure. The occipital lobe or visual cortex receives visual senses from the eyes. The temporal lobe is responsible for hearing, speech perception, and some types of memory (Agrawal et al. 2009). At the back of the head is the cerebellum and is responsible for movement, posture and balance. It often takes over learned activities. The hippocampus is responsible for short and long-term memory and forms part of the limbic system (Erickson, Weinstein & Lopez 2012). The function of the brain is dependent on the ability of neurons to transmit electrochemical impulses to target cells, and the ability of these cells to respond to the signals from other cells (Agrawal et al., 2009). Main functions of the brain include information processing, motor control, perception, motivation, learning and memory, homeostasis and arousal. In learning and memory function of the brain, working memory confers the ability of the brain to retain information about the task one is currently engaged in. Episodic memory refers to the ability to recall details of specific events, and evidence points to the hippocampus playing a significant role. Hence, people whose hippocampus has suffered severe damage will show forgetful tendencies and may be unable to form new long-term episodic memories. Pathophysiology of Alzheimer’s Disease AD is an acquired condition of cognitive and behavioural impairment which significantly interferes with social and occupational life and has no known cure. The AD pathology can be characterised as the gradual loss of brain tissue involving several neurotransmitter factors and pathophysiological processes, with key factors being beta amyloid plaques, neurofibrillary tangles and neuronal cell death (Erikson et al., 2012). Plaques and tangles establish in the deeply seated hippocampus structure in the brain. The plaques and tangles also settle in other parts of the cerebral cortex that are used in thinking and decision-making, such as the frontal lobe. Due to the fact that AD is a progressive disease, patients at different stages of the condition may manifest some symptoms differently. As the disease progresses, neurons die in a particular pattern over time (Ritchie et al. 2014). In preclinical AD, the patient results are normal on both MMSE and physical examination. Specific areas of the brain such as the hippocampus and entorhinal cortex may begin to be affected 10 to 20 years prior manifestation of AD symptoms. As the brain cells atrophy, cerebrospinal fluid fills in the space in which the brain tissue occupied previously (Sperling, Karlawish, & Johnson, 2013). In mild AD, clinical symptoms include memory loss, confusion about the location of familiar places, trouble handling money and paying bills, compromised judgement which leads to bad decisions, normal daily activities take longer to accomplish, motivation, spontaneity and sense of initiative are lowered, anxiety increases, and mood and personality changes (Sperling et al., 2013). In moderate AD, damage occurs in cerebral cortex regions that controls language, speech, reasoning, conscious thought and sensory processing. The patient is unable to learn new things, or carry out complex tasks (Erikson et al., 2012). Statements and movements are repetitive, and they experience occasional muscle twitches. They may behave impulsively and this is exhibited through behaviour such as use of vulgar language or undressing in public. They may also experience hallucinations, paranoia, delusions and suspiciousness. Perceptual-motor problems become apparent, for instance, getting out of a chair, or setting the table. In severe Alzheimer’s disease, plaques and tangles have occurred throughout the brain and the brain tissue has shrunk immensely. The patient is unable to communicate and is entirely dependent on others for basic care needs (Erikson et al., 2012). Other signs and symptoms include difficulty in swallowing, extreme weight loss, seizures, skin infections, increased sleeping, lack of bladder and bowel continence, and grunting, moaning or groaning consistently. In the end-stage AD, patient may stay in bed all of the time. Death often occurs as a result of other opportunistic illnesses such as aspiration pneumonia. Although plaques and tangles are defining components of AD, they are not unique to the condition as they can also be found in normal aging and in some neurodegenerative disorders. However, in AD, they are localized to regions in the brain that are consistent with the clinical symptoms (Palmqvist et al., 2009). During AD pathogenesis, tau proteins are affected by electrolyte imbalance, which disrupts their bonds to microtubules making the structure weak and collapsed (Montez et al., 2009). The number of cholinergic neurons usually reduces significantly during severe and end stage AD. Possible clinical treatment and social/familial care for the patient The patient can be treated with acetylcholinestratse inhibitors (AChE) -Donepezil, Tacrine, Rivastigmine, and Galantiminem which are approved for mild to moderate AD. A non-competitive glutamate receptor antagonist mentamine can be used at moderate to severe AD (Lin et al., 2013). The AChE work by inhibiting acetylcholinestrase enzyme which is responsible for cleaving acetylcholine at the post synaptic moment; hence the drugs help to retain the acetylcholine in the synapse for longer (Sperling, et al., 2013). Pharmacotherapy for other symptoms may be included, where possible, for example, the patient will need an anti-depressant, and it is advised to avoid tricyclic antidepressants or other anti-cholinergics, as they may have a negative effect on cognition (Lin et al., 2013). In regards to familial and social care, the elderly adult should be assisted by the spouse or adult children. Worth noting that caring for an elderly person with AD is demanding as AD’s burden on the family is high from every dimension. The burden can contribute to psychiatric manifestations such as depression, anxiety or fear for the patient’s condition; hence the family members should be involved in cognitive behavioural therapy (CBT) with patient. The patient should be encouraged to participate in memory enhancement strategies such as lists, reminder notes and possessions reorganisation is helpful. Multi-sensory stimulation and reminiscence therapy can help the patient refresh her memory and for the brain to hold onto the recall feature for as long as possible. Changes can be made on the living environment and her daily activities simplified to ensure that she is able to cope with the progressing disability. The patient’s carer should encourage oral nutrition for as long as possible. Therapeutic use of music, exercise, massage, meditation and restorative forms of exercises such as yoga can help the patient to relax, focus, and deal better with confusion and anxiety (Erickson et al., 2012). The family can help identify and join relevant support groups in the community, not only for the patient but also for families living with people with AD (Erickson et al., 2012). Carers should target to promote independence for the patient where possible and palliative care should fair. Decisions involving nutritional support should be considered within both ethical and legal frameworks. Summary AD is a progressive disease affecting the brain and the patient losses cognitive abilities as the disease progresses. In addition to treatment using AChE inhibitors to delay symptom progression, love, understanding, patience, care and ability to teach and support the patient on coping with her condition with exercises and relaxation are helpful. References: Agrawal, R., Tyagi, E., Shukla, R., & Nath, C (2009) A study of brain insulin receptors, AChE activity and oxidative stress in rat model of ICV STZ induced dementia. Neuropharmacology, 56(4), 779-787. doi:10.1016/j.neuropharm.2009.01.005. Erickson, K. I., Weinstein, A. M., & Lopez, O. L (2012) Physical activity, brain plasticity, and alzheimer's disease. Archives of Medical Research, 43(8), 615-621. doi:10.1016/j.arcmed.2012.09.008. Lin, J. S., O'Connor, E., Rossom, R. C., Perdue, L. A., Burda, B. U., Thompson, M., & Eckstrom, E. (2013) Screening for Cognitive Impairment in Older Adults: An Evidence Update for the US Preventive Services Task Force. Agency for Healthcare Research and Quality, 14-05198-EF-1. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK174643/pdf/TOC.pdf Montez, T., Poil, S., & Jones, B. F. (2009) Altered temporal correlations in parietal alpha and prefrontal theta oscillations in early-stage alzheimer disease. Proceedings of the National Academy of Sciences of the United States of America [H.W.Wilson - GS], 106(5), 1614. Retrieved from http://www.jstor.org.ezp01.library.qut.edu.au/stable/40272426 Palmqvist, S., Hansson, O., Minthon, L., Londos, E., Institutionen för kliniska vetenskaper, M., Psychiatry/Primary Care/Public Health, . . . Lund University. (2009) Practical suggestions on how to differentiate dementia with lewy bodies from alzheimer's disease with common cognitive tests. International Journal of Geriatric Psychiatry, 24(12), 1405-1412. doi:10.1002/gps.2277 Ritchie, C., Smailagic, N., Noel‐Storr, A. H., Takwoingi, Y., Flicker, L., Mason, S. E., & McShane, R. (2014) Plasma and cerebrospinal fluid amyloid beta for the diagnosis of Alzheimer's disease dementia and other dementias in people with mild cognitive impairment (MCI). Cochrane Database Systematic Review, 10(6). http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD008782.pub4/pdf Sperling, R. A., Karlawish, J., & Johnson, K. A. (2013; 2012) Preclinical alzheimer disease-the challenges ahead. Nature Reviews.Neurology, 9(1), 54. doi:10.1038/nrneurol.2012.241 Read More