Medicine, at once, is a science and not a pure science. Strictly speaking, it is a science-based practical science. I believe many neurologists share the same feeling: many diseases can be roughly identified in textbooks, but there are always differences here and there. In clinical practice, each patient is an individual, and the same etiology can show completely different symptoms depending on various environmental factors and physical differences. Even the most common thrombosis of the internal carotid artery system may present with mild or severe syndromes due to the patient’s congenital vascular variation, collateral circulation compensation, and cellular tolerance to ischemia and hypoxia; mitochondrial encephalomyopathy may appear as KSS, CPEO, MELAS, MERRF, Leigh disease, Leber optic atrophy, mitochondrial gastrointestinal encephalomyopathy due to the difference of mutated genes Rheumatoid arthritis can appear as a collection of different organs involved in joints, skin, meninges, peripheral nerves, etc., and HIV infection can involve all systems and organs of the body. Faced with a diagnostic puzzle like a code combination, how to really grasp the pulse of the disease to get the real answer is always a problem that neurology practitioners need to face every moment. Personally, I believe that neurologists go through the following stages in the process of gradually forming diagnostic thinking – needle in a haystack, a leaf in the eye, step by step, and a leaf in the eye. Stage 1: Finding a needle in a haystack. Often, when a beginner in neurology is confronted with a patient, the receiving physician has not yet been able to form his or her own clinical judgment, and can only start from the patient’s most primitive complaints, the most basic symptoms, signs, and positive test results, and with the help of textbooks and various professional books, search for the most similar diseases to the patient from the vast spectrum of diseases. Although it is possible to find the real cause of the disease, such a diagnosis is time-consuming and laborious, and even if we can find a series of similar diseases, we will still struggle with where to go. For example, if a patient has “double vision” as the main complaint, a large number of diseases need to be considered, from extraocular muscles, neuromuscular junction, peripheral nerves below the oculomotor nuclei, oculomotor nuclei around the midbrain conduction duct, medial longitudinal bundle, and the brain bridge to measure the visual center, and even the so-called “double vision” of some patients. In addition, when it comes to emergency patients or when a patient has an emergency, how can the physician on duty have time to go through the books behind closed doors to find the most correct answer? As the saying goes, if you don’t understand the essence of the disease, you will only end up looking at flowers in the fog, and the more you look, the more you see. Stage 2: Blindness. When a neurologist has been exposed to a series of diseases, he or she gradually has his or her own ideas and opinions, and is able to diagnose and manage a large number of diseases. At this time, the doctor, already have their own experience and confidence, often in the initial diagnosis will have some eyebrows, know how to further diagnosis and treatment of patients, but this time is also the most likely to make mistakes. The so-called “do not know the true face of the mountain, only the edge of the mountain”, because not out of the fog to see the full picture of the disease, so easy to be confused by some clues, misleading. For example, a young patient with multiple intracranial white matter lesions, and the patient also has multiple occurrences in time, so the diagnosis of “multiple sclerosis” is gladly made, followed by hormonal shock, immune regulation, without knowing that the diagnosis of multiple sclerosis, first of all, it is necessary to exclude other similar diseases, such as atrial mucinous tumor The diagnosis of multiple sclerosis, first of all, needs to exclude other similar diseases, such as atrial mucinous tumor, lymphoma, connective tissue disease (SLE, SSS), Binswanger’s disease, nodal disease, central nervous system vasculitis, etc.; a patient with “lace” sign on cranial MRI, regardless of the presence of cognitive impairment, extrapyramidal pathology, cerebellar disorders and other symptoms, is directly given the diagnosis of “CJD”. A patient with acute symmetric distal limb weakness and numbness, who also has a history of suspected infection before the disease, seems to have “Guillain-Barré syndrome A patient with acute symmetric distal limb weakness and numbness, who also had a history of suspected infection prior to the disease, seemed to have a solid diagnosis of “Guillain-Barré syndrome,” but the patient was unexpectedly from the forest and had tick-bite paralysis. A good neurologist should avoid taking the diagnosis out of context and should scan the whole picture of the disease before drawing his or her own conclusions and thinking more about diseases that may be similar. The knowledge base is like a net. Only when the net is large and crisscrossed, can the net be kept intact. Stage 3: Step by step. A physician who can use such thinking to look at neurological diseases can already be titled as excellent. Physicians who have reached this stage have a more complete overview of the etiology, initiation, progression, prognosis, and possible differential diagnosis of the disease, and organize it in their own form, so as to carry out clinical treatment, and are no longer “seeing the trees but not the forest”, but are well aware of “looking across the mountains to the side They are aware of the fact that “the mountains are different from the peaks, and the heights are different from the distances”. They often know that some patients with cerebrovascular disease can appear in the form of “attack-remission-attack-remission” rather than the textbook acute onset of disease, due to rapid recanalization of emboli or reversal of blood flow disorders. CNS demyelinating lesions can appear as occupancies (demyelinating pseudotumors), symmetrical white matter lesions (Murburg type), and not just parietal ventricular “comb” lesions. Each symptom, sign, and test result has a corresponding cause, which, when brought together, ultimately points to the culprit of the disease. A patient with multiple intracranial occupancies, epileptic seizures, and a preference for spicy hot food often corresponds to parasitic infections (cysts mostly); a patient with peripheral neuropathy who has dry lips, a desire to cry, and multiple cysts in the lungs needs to consider dry syndrome; the AIDP variant is not only Fisher syndrome, but also acute autonomic insufficiency; an occupancy near the midline, a slightly high CT scan The first consideration is mitochondrial encephalopathy if there is diabetes mellitus and seizures at a young age, and if there is a combination of short stature and visual impairment. When we are familiar with each of the characteristics of the disease, we will be comfortable in the diagnosis process. Stage 4: a leaf to know the autumn. This is the “patent” of masters and titans. The clinical experience and solid knowledge of neurology have created the realm of knowing the autumn with one leaf. When he sees “speech disorder” with difficulty in opening the mouth, he can consider tetanus; when he finds a paraplegic or mentally retarded patient with obvious swelling of Achilles tendon, the diagnosis of cerebral tendon xanthoma is ready to be made; when he sees a patient with episodic disorder of consciousness, he needs to consider urea circulation disorder and hyperammonemia; when he sees a young Parkinson’s patient whose occupation is welding, he should first consider manganese poisoning. Manganese toxicity should be considered. At this stage, there is really no trick in the hand and no trick in the heart, and he can send and receive freely, which is admired by the world!