제가 생각하기에 아래 기술한 차이는 증상 발생 초기에 국한됩니다. 증상 발생으로부터 시간이 경과할수록 치매 유형별 증상의 차이가 적어집니다.
알츠하이머에 비해 루이소체 치매에서 visuospatial/visuoconstructive deficit이 뚜렷합니다. 가장 핵심적인 차이입니다.
These studies have consistently shown that the most salient neuropsychological difference between the two disorders is a disproportionately severe visuospatial and visuoconstructive deficit in patients with DLB. This has been shown using tests of visual perception (e.g., segregation of overlapping figures), tests of visual search (e.g., parallel search tasks that usually elicit the pop-out phenomenon), and tests that require drawing simple and complex two-dimensional figures or the construc- PET: positron emission tomography tion of three-dimensional objects (for review, see Salmon & Hamilton 2006). These particularly severe deficits in visuospatial and visuoperceptual abilities are often apparent even when DLB patients perform better than do AD patients on tests of verbal memory (e.g., Lambon Ralph et al. 2001). (중략) Because occipital cortex pathology is rare in pure AD, it is not surprising that the visuoperceptual and visuospatial abilities that may be dependent upon these cortices are disproportionately impaired in patients with DLB.
실행기능과 주의력에서의 문제도 루이소체 치매에서 더 뚜렷합니다.
Patients with DLB often also have disproportionately severe deficits in executive functions and attention in comparison to equally demented patients with pure AD.
기억력 문제는 알츠하이머형 치매에서 더 뚜렷하고, 루이소체 치매는 회상과 재인 과제 모두에서 알츠하이머형 치매보다 나은 결과를 보이기 쉽습니다. 이는 루이소체 치매에서의 기억 기능 문제가 알츠하이머형에서처럼 부호화 실패에 따른 인출 실패라기보다(ex. SVLT 즉각회상 과제에서의 저조한 수행) 실행기능 손상에 따른 인출 문제일 가능성이 상대적으로 더 높을 가능성을 가리킵니다.
The observed differences are consistent with neuropathologic (Lippa et al. 1998) and MRI (Barber et al. 2001, Hashimoto et al. 1998) evidence that medial temporal lobe structures important for memory (e.g., hippocampus, entorhinal cortex, parahippocampal gyrus) are less severely affected in DLB than in AD. A combination of only moderate medial temporal lobe damage and frontostriatal dysfunction might explain the less severe retention deficit and greater impact of deficient retrieval processes in DLB than in AD.
이상의 레퍼런스는 아래 논문입니다. 치매 유형에 따른 신경심리학적 프로파일의 차이를 매우 세부적으로 다룹니다. 교과서에서도 이 정도로 구체적인 설명을 본 적이 없습니다. 관심 있으시다면 꼭 한 번 읽어보시길 바랍니다.
참고로.. 저도 루이소체 치매와 파킨슨병에 수반되는 치매가 헷갈려서 찾아봤습니다. 사실 오늘 글은 파킨슨병에 수반되는 치매를 지닌 환자를 본 이후에 공부한 내용이기도 합니다.
파킨슨병이 먼저 발병하고 수년이 지난 뒤 치매가 발병한 환자를 루이소체 치매라고 부르진 않습니다. 이는 파킨슨병에 수반되는 치매라고 부릅니다. 파킨슨병에 수반되는 치매와 루이소체 치매는 루이소체가 주로 분포하는 위치가 다릅니다. (여기 사진 참고.) 하지만 루이소체 치매와 파킨슨병에 수반되는 치매는 비슷한 증상을 공유합니다. 두 치매를 묶어서 Lewy body dementia라 부르기도 합니다.
Clinically, dementia with Lewy bodies is characterized by progressive dementia with fluctuating cognition, visual hallucinations and parkinsonian features including flexed posture, shuffling gait, rigidity and hyperkinesias (McKeith et al., 2005). Macroscopically, the brain usually shows atrophy that may be diffuse or more severe in the frontotemporal region. The pigmented nuclei of the brainstem show pallor. Microscopically, Lewy bodies, neuronal loss, abnormal neurites, astrocytosis and vacuolation of the cortex may be observed (Figure 2.10b–d). As with PD, the histological hallmark is the Lewy body. The severity of dementia appears to be related to the density of Lewy bodies..(후략) - Clinical Neuropsychology: A Practical Guide to Assessment and Management for Clinicians(2판), 48쪽.
아래는 루이소체 치매와 파킨슨병에 수반되는 치매의 차이입니다.
Dementia with Lewy bodies (DLB) is a type of dementia that causes problems with memory and thinking abilities that are severe enough to interfere with everyday activities. It specifically affects a person’s ability to plan and solve problems, called executive function, and their ability to understand visual information. Dementia always appears first (or around the same time as parkinsonism) in DLB. The motor symptoms of Parkinson’s such as tremor, slowness, stiffness and walking/balance/gait problems usually become more evident as the disease progresses. Visual hallucinations, REM sleep behavior disorder, fluctuating levels of alertness and attention, mood changes and autonomic dysfunction are also characteristic of DLB.
In contrast, Parkinson’s disease dementia (PDD) is a term used for dementia that develops after several or many years of living with Parkinson’s, a disease that is caused by loss of dopamine-producing nerve cells. In nearly all cases of Parkinson’s, people experience motor symptoms in the early stages; some may also have very mild changes in cognition at diagnosis. Over time, non-motor symptoms of Parkinson’s may appear, including cognitive impairment, REM sleep disorder, memory problems, fatigue, anxiety, autonomic dysfunction, pain and more. Most importantly, not all people with Parkinson’s will develop dementia and at this time, it’s impossible to predict which individuals with Parkinson’s will also develop Parkinson’s disease dementia.
댓글