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Lewy Body Dementia, Its Symptoms and Treatment
Definition
Lewy body dementia (LBD) is ranked as the second most frequently observed type of dementia after Alzheimers disease. LBD occurs as the so-called Lewi bodies, i.e. alpha-synuclein aggregates of protein, start developing in nerve cells in the substantia nigra or cortex of the brain (Walker et al. 519). As a result, the respective functions of the identified parts of the brain are inhibited or impaired to a considerable degree. This phenomenon manifests itself in the patients ability to think coherently, memorize different types of data (i.e., visual, audial, etc.), and control their movement (Arkun et al. 176). Unless addressed in a timely and efficient manner, the disorder leads to a rapid drop in the patients mental capacities (Walker et al. 521).
Diagnosis and Symptoms
Seeing that the cortex is usually affected, the patient is likely to experience issues with movement control (e.g., difficulty when walking, coordinating ones movements, etc.). Cognitive issues faced by the patient, particularly, difficulty remembering important information, lack of attention, frequent confusion, etc., should also be viewed as the signs of LBD. Problems with the autonomous nervous system (ANS), such as uncontrollable changes in pulse, blood pressure, etc., may also be considered a sign of a developing LBD. The patient is also likely to have trouble sleeping. To be more specific, when being in the rapid eye movement (REM) phase, the patients may be prone to acting out their dreams, their movements preceding the image that they see in their dream (Postuma et al. 835).
Visual hallucinations should also be viewed as one of the signs of LBD when observed together with some of the symptoms mentioned above. Similarly, delusions that may occur in patients can also be the symptom of a progressing LBD. There is a propensity for most of the hallucinations to be based on the patients fears, although not all of them are linked to personal phobias (Urwyler et al. 354).
The disorder can be diagnosed by assessing the patients muscle tone, eye movements, reflexes, and walking abilities. Put differently, a neurological examination is a must. Afterward, blood tests, brain scans, and the evaluation of the patients mental abilities must be carried out. Finally, sleep evaluation and the further detection of movements in the REM phase (the Multiple Sleep Latency Test) should be viewed as a possible tool for diagnosing the problem (Ferman et al. 79).
Possible Causes or Risk Factors
As stressed above, the accumulation of protein synuclein aggregates can be viewed as the primary cause of LBD. The plaques and tangles that develop in the brain contribute to the deterioration of the relevant functions of the corresponding parts of the brain, primarily, the ones related to motor functions and cognitive abilities (Recasens et al. 357). As a result, LBD occurs.
The fast pace of the disease progress can be explained by the fact that cell-to-cell transmission can be observed in most of the instances of LBD. Particularly, the rogue protein is transferred to the corresponding nerve cells, thus, causing LBD. Therefore, it will be crucial to develop the therapeutic tools that could help inhibit the transmission process successfully (Urwyler et al. 356).
Possible Treatments of the Clinical Condition
Since the disease is caused primarily by the plaques in the patients brain, cholesterol inhibitors as the means of addressing the specified issue can be suggested as a part of the treatment. The muscle tissues can be addressed with the help of carbidopa-levodopa (Sinemet) and similar medications used to manage Parkinsons disease (Diaz et al. 494). As far as the behavioral issues are concerned, therapies aimed at creating the environment in which the patient will feel comfortable can be suggested. Furthermore, therapies for managing the issues associated with hallucinations, as well as side effects of the medications, may be advised (Boot 47).
References
Arkun, Knarik, et al. Effect of Lewy Bodies on Mitochondrial DNA Copy Numbers and Deletion Burden in Parkinsons Disease Substantia Nigra Neurons. Alzheimers Disease & Parkinsonism, vol. 5, no. 1, 2015, pp. 175-179.
Boot, Brendon. Comprehensive treatment of dementia with Lewy bodies. Alzheimers Research & Therapy, vol. 7, no. 1, 2015, pp. 45-53.
Diaz, Shanna V., et al. A 63-Year-Old Man with Lewy Body Dementia and Multiple Symptoms. Psychiatric Annals, vol. 45, no. 1, 2015, pp. 493-494.
Ferman, Tanis, et al. Abnormal Daytime Sleepiness in Dementia with Lewy Bodies Compared to Alzheimers Disease Using the Multiple Sleep Latency Test. Alzheimers Research & Therapy, vol. 6, no. 9, 2014, pp. 76-84.
Postuma, Ronald B., et al. Risk factors for neurodegeneration in idiopathic rapid eye movement sleep behavior disorder: A multicenter study. Annals of Neurology, vol. 77, no. 5, 2015, pp. 830-840.
Recasens, Ariadna, et al. Lewy Body Extracts from Parkinson Disease Brains Trigger A-Synuclein Pathology and Neurodegeneration in Mice and Monkeys. Annals of Neurology, vol. 75, no. 3, 2014, pp. 351-362.
Urwyler, Peter, et al. Visual Hallucinations in Eye Disease and Lewy Body Disease. The American Journal of Geriatric Psychiatry, vol. 24, no. 5, 2016, pp. 350-358.
Walker, Douglas G., et al. Altered Expression Patterns of Inflammation-Associated and Trophic Molecules in Substantia Nigra and Striatum Brain Samples from Parkinsons Disease, Incidental Lewy Body Disease and Normal Control Cases. Frontiers in Neuroscience, vol. 9, no. 1, 2016, pp. 507-524.
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