Dementia with Lewy bodies (DLB) is the second most common cause of dementia in the elderly after Alzheimer’s disease (AD) in the spectrum of degenerative diseases of the central nervous system, with diffuse Lewy bodies, Aβ deposition, and neurofibrillary tangles as the main pathological features; fluctuating cognitive dysfunction, realistic and vivid visual hallucinations, and spontaneous symptoms of Parkinson’s disease syndrome as clinical features. Typical DLB also usually has an insidious onset, progresses slowly, and takes several years to eventually develop into full-blown dementia. Early presentation is similar to that of AD, with cognitive impairment of a temporoparietal type, i.e., predominantly memory, language, and visuospatial skills, but in contrast to the natural progression of cognitive impairment in AD, which is comprehensive, progressive, and irreversibly decompensated, cognitive impairment in DLB patients appears to fluctuate markedly over time, with fluctuating cycles that can be weeks or even within a single day. As mentioned earlier, the misdiagnosis rate of DLB can be as high as 80%, and the most frequently misdiagnosed disorder is AD. If patients change doctors frequently, or if both doctors and patients ignore such fluctuations, they are highly likely to be misdiagnosed. This reflects from one side the importance of looking back at the development pattern of a disease from a higher level for diagnosis, and from another side the danger of static observation of a disease at a certain point of time for diagnosis. However, in actual clinical practice, misdiagnosis is common due to the awareness of both doctors and patients, the medical system, the disease itself, and the customs. Therefore, the best strategy to avoid misdiagnosis of DLB as AD is detailed observation and long-term follow-up by professional staff. If we compare DLB to a white fox in the snow, only a professionally trained hunter (doctor) can detect and kill it through long-term and patient follow-up, especially the observation of footprints in the snow and the movements of the white fox when it moves. In fact, this is the final diagnosis of many chronic degenerative diseases occurring in the central nervous system! A second clinical feature of DLB is vivid and distinct visual hallucinations. In the psychiatric concept, hallucinations can be broadly divided into two categories: real and pseudo hallucinations. As a result, they are convinced of the content of their visual hallucinations, and because they are often accompanied by various delusions of victimization, patients often have facial expressions and body movements that match the content of the hallucinations and delusions. For example, patients who see a burglar entering their dormitory in the middle of the night often describe with horror the footsteps, the sound of prying, and the physical characteristics and movements of the burglar. It is often seen in clinical practice that medical procedures are initiated because of the various “creepy” and “unnecessary” visual hallucinations of DLB patients that disrupt the peaceful lives of family members and neighbors. However, due to a lack of expertise, many patients are often misdiagnosed with schizophrenia and do not begin to reflect on the diagnosis until symptoms of cognitive impairment and Parkinson’s-like symptoms begin to emerge or are recognized. Since DLB and AD both have insidious onset and slow progression, the exact time of onset is difficult to project, and comprehensive collection and dynamic analysis of patient history, symptoms, signs and other information is essential to reduce such misdiagnosis. In addition the high sensitivity to neuroleptics and antipsychotics and the dramatic efficacy of DLB patients help to distinguish them from other types of dementia. A third clinical feature of patients with DLB is the tendency to misdiagnose extrapyramidal symptoms as rigid Parkinson’s disease. Such as myotonia, decreased movement, and bradykinesia, but the most classic tremor symptoms of Parkinson’s disease are less common. These symptoms can occur simultaneously with dementia symptoms or sequentially, and there are reports of diagnostic significance of two sets of symptoms occurring sequentially within a year. Of particular diagnostic interest is the fact that levodopa is virtually ineffective for Parkinson’s-like symptoms in patients with DLB. Therefore, when making the differential diagnosis, clinicians may try experimental treatment with levodopa medication, which supports Parkinson’s disease or Parkinson’s syndrome if effective and DLB if ineffective. Some other symptoms in DLB patients are also a cause of misleading clinicians’ wrong diagnosis. For example, myoclonus and chorea-like movements can be misdiagnosed as other extrapyramidal disorders such as dystonia and chorea; frequent falls or syncope can be misdiagnosed as epilepsy, transient ischemic attack, and upright hypotension; sleep disorders and autonomic symptoms can be misdiagnosed as various affective disorders. However, with a comprehensive analysis and some necessary laboratory and neuroimaging examinations, it is not difficult to find that none of these diseases can explain all the symptoms of DLB patients. In conclusion, the rich, diverse and variable nature of DLB symptoms is the direct cause of its easy misdiagnosis. Sometimes it is like a snow fox lying still in the snow, and it takes a wise and patient hunter to capture it. At the treatment level, the principles of treatment for DLB are similar to those of other dementias, which mainly focus on improving patients’ cognitive function, relieving psycho-behavioral symptoms and improving social life skills through medication. However, clinically, antipsychotic medications and motor rehabilitation training often become the focus of treatment because of the patient’s prominent psycho-behavioral symptoms and extrapyramidal symptoms.