Dementia With Lewy Bodies And Dementia In Parkinson’S Disease

As dementia with Lewy bodies chronic cognitive deterioration is called, the (so-called. Lewy bodies) by cellular inclusions is characterized in the cytoplasm of cortical neurons. A dementia in Parkinson’s disease is a cognitive decline, which is characterized by Lewy bodies in the substantia nigra; it develops in late Parkinson’s disease.

Dementia is a chronic, global, usually irreversible deterioration of cognition. Dementia with Lewy bodies is the third most common form of dementia. The age is typically> 60 years at the start.

As dementia with Lewy bodies chronic cognitive deterioration is called, the (so-called. Lewy bodies) by cellular inclusions is characterized in the cytoplasm of cortical neurons. A dementia in Parkinson’s disease is a cognitive decline, which is characterized by Lewy bodies in the substantia nigra; it develops in late Parkinson’s disease. Dementia is a chronic, global, usually irreversible deterioration of cognition. Dementia with Lewy bodies is the third most common form of dementia. The age is typically> 60 years at the start. Lewy bodies are spherical, eosinophilic, neuronal cytoplasmic inclusions which are formed from units of ?-synuclein, a synaptic protein. They occur in the cortex of some patients with primary dementia with Lewy bodies. The neurotransmitter levels and the neural connections between the striatum and neocortex are disturbed. Lewy bodies are also found in the substantia nigra of patients with Parkinson’s disease; dementia (dementia in Parkinson’s disease) may develop in the disease process itself late. About 40% of patients with Parkinson’s disease develop a dementia in Parkinson’s disease, usually after the age of 70 and about 10 to 15 years after diagnosis Parkinson’s disease. As Lewy bodies occur both in dementia with Lewy bodies as well as dementia in Parkinson’s disease, some experts, the two disorders could be part of a generalized Synukleinopathie affecting the central and peripheral nervous system believe. Lewy bodies are sometimes encountered in patients with Alzheimer’s dementia, patients with dementia with Lewy bodies may have neuritic plaques and neurofibrillary tangles. Dementia with Lewy bodies, Parkinson’s disease and Alzheimer’s disease show significant overlaps. Further research is needed to clarify the relationship. Both dementia with Lewy bodies and dementia in Parkinson’s disease has a progressive course with a poor prognosis. Dementia should not be confused with delirium although the perception is impaired in both. A usually helps dementia from delirium to differentiate: Dementia mainly affects memory, is usually caused by anatomical changes in the brain shows a slow start and is usually irreversible. A Dellir mainly concerns the attention is usually caused by an acute illness or drug or drug toxicity (sometimes fatal) and is often reversible. Other characteristics contribute to distinguish dementia and delirium see Table: Differences Between Delirium and Dementia *). Symptoms and signs of dementia with Lewy bodies, the initial cognitive deterioration in Lewy body dementia similar to that of other dementias (Dementia: Symptoms and complaints); it comprises a deterioration of memory, attention and executive function and behavioral problems. Extrapyramidal symptoms (typically including rigidity, bradykinesia, and gait instability) come (also Overview of the Movement and Cerebellar Disorders see) on. In Lewy body dementia (unlike Parkinson’s disease), the distance between the occurrence of cognitive and extrapyramidal symptoms maximum of one year. When dementia with Lewy bodies is in the early stages no tremor before, a rigidity of the core muscles with gear instability occurs early, and the deficits are more symmetrical: Also, the extrapyramidal symptoms from those of Parkinson’s disease differ. Repeated crashes are frequent. The fluctuation in cognitive function is a relatively specific feature of dementia with Lewy bodies. Guard periods with coherent thinking and orientation can change with periods of confusion and lack of response to questions, usually over an interval of days to weeks, but sometimes during the same call. Memory is impaired, but the impairment more by deficits in alertness and attention seems to be due to the memory storage; Therefore, the reproduction of the short-term learned is less affected than the memory span (ability to 7 digits forward and repeat 5 digits backward). Patients can stare at the distance for a long time. Excessive daytime sleepiness is common. The visuospatial abilities and visuokonstruktiven (tested with “block design”, the clock test or Figurennachzeichnen) more than other cognitive areas are affected. Visual hallucinations are common and often threatening, unlike the benign hallucinations in Parkinson’s disease. Auditory, olfactory and tactile hallucinations are less common. Delusions occur in 50-65% of patients and are often complex and bizarre in comparison to the simple pursuit of ideas that are common in Alzheimer’s dementia. Autonomic dysfunction is often, and from unexplained syncope may result. The autonomic dysfunction may occur with or after the onset of cognitive deficits simultaneously. An extreme sensitivity to antipsychotics is typical. Many patients have a REM (rapid eye movement) sleep behavior disorder, d. H. a parasomnia, which is characterized by vivid dreams without the normally occurring physiological paralysis of skeletal muscles during REM sleep. Consequently, the dreams can be acted out, sometimes the bed partner wird.Demenz injured in Parkinson’s disease In the dementia in Parkinson’s disease begins (unlike in dementia with Lewy bodies), the cognitive impairment that leads to dementia, typically 10 15 years after the onset of motor symptoms. The dementia in Parkinson’s disease can affect multiple cognitive areas incl. Attention, memory and visuospatial constructive and executive functions. Impaired executive functions occur in dementia in Parkinson’s disease typically earlier and are more common than in Alzheimer’s disease. Psychiatric symptoms (eg. As hallucinations, delusions) seem to be less frequent and / or less pronounced than in dementia with Lewy bodies. In dementia in Parkinson’s disease postural instability and gait disorders are more common, the motor deterioration is faster and crashes occur more often than in Parkinson’s disease without dementia. Diagnosis Clinical criteria Neuroradiological imaging to rule out other disorders The diagnosis is clinical, but sensitivity and specificity are low. A general diagnosis of dementia requires each of the following: cognitive or behavioral (neuropsychiatric) symptoms that interfere with the ability to function at work and perform usual daily activities. These symptoms represent a decline of previous functional levels. These symptoms can be explained not by delirium or major mental disorder. To Abklärungder cognitive function includes the recording of the patient’s medical history and by a person who knows the patient, plus an examination of the mental state at the bedside or if the investigation at the bedside remains inconclusive, formal neuropsychological examination (dementia: assessment of cognitive function). The diagnosis of dementia with Lewy bodies is considered to be likely if two or three of the following features are present and is considered to be possible if only one exists: Perception fluctuations Visual hallucinations parkinsonism An additional probability is in repeated falls, syncope, REM sleep disorder and sensitivity to antipsychotics. A symptom overlap of dementia with Lewy bodies and dementia in Parkinson’s disease can complicate the diagnosis. If motor deficits (z. B. tremor, bradykinesia, rigidity) progress and are more severe than cognitive impairment, dementia is usually diagnosed with Parkinson’s disease. If early cognitive impairment (particularly impaired executive function) and behavioral disorders dominate, dementia is usually diagnosed with Lewy bodies. Because patients have impaired alertness with Lewy body dementia often that is characteristic of delirium as for dementia, a study should be carried out on delirium especially on common causes, such as pharmaceuticals, particularly anticholinergics, psychoactive substances and opioids dehydration infection CT and Although MRI show characteristic changes, but they are at the beginning helpful to exclude other causes of dementia. PET -labeled with fluorine-18 (18F) deoxyglucose (fluorodeoxyglucose or FDG) and single photon emission computed tomography (SPECT) with 123I-FP-CIT (N-3-fluoropropyl-2?-carbomethoxy-3?- [4-iodophenyl] -tropane), an fluoroalkyl analog of cocaine can contribute to the identification of dementia with Lewy bodies, but they are not routinely performed. The definitive diagnosis requires autopsy examination of brain tissue. Treatment Supportive treatment Treatment is usually supportive. For example, the environment should be bright, be friendly, familiar and designed so that it reinforces the orientation (z. B. placement of large clocks and calendars in the room). Measures to ensure the safety of the patient (eg., Signal monitoring systems for patients who walk) should be initiated. Disturbing symptoms can be treated. Drug cholinesterase inhibitors may improve cognitive function to some extent and be helpful in some patients. Rivastigmine, a cholinesterase inhibitor may be used in the treatment of dementia with Lewy bodies and dementia in Parkinson’s disease. (Editor’s note: The recommendation of the German guidelines is: For the antidementive treatment of Lewy body dementia is no approved or adequately documented medication There is evidence for efficacy of rivastigmine on behavioral symptoms An appropriate treatment trial may be considered particular needs… attention is drawn to the following fact: the treatment of Lewy body dementia rivastigmine is an off-label treatment and the difficulty of off-label use is adequate to consider) an initial dose of 1.5 mg two times a day po. can be increased 2 times daily as needed for up to 6 mg, which is attempted to improve cognition. Other cholinesterase inhibitors can also be used. In about half of patients, the extrapyramidal symptoms anti-Parkinson drugs improve, but the psychiatric symptoms may worsen. If such drugs are necessary, levodopa should be preferred. In dementia with Lewy bodies deteriorate conventional antipsychotics, even in very low doses extrapyramidal symptoms acutely sooner and should be avoided whenever possible. Conclusion Since both occur in dementia with Lewy bodies as well as dementia in Parkinson’s disease Lewy bodies, some experts suggest that the two diseases are part of the same Synukleinopathie affecting the central and peripheral nervous system. Start from dementia with Lewy bodies when the dementia developed almost simultaneously with Parkinson’s symptoms and if the dementia of fluctuations in cognition, loss of attention, psychiatric symptoms (eg visual hallucinations. Complex, bizarre delusions ) and autonomous dysfunction is accompanied. Walk out of a dementia in Parkinson’s disease when the dementia begins years after the development of Parkinson’s symptoms, particularly when impaired executive functions occur early. Consider the use of rivastigmine and sometimes of other cholinesterase inhibitors in trying to improve cognition.

Health Life Media Team

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