Late onset encephalopathy is one of the most serious sequelae of acute carbon monoxide poisoning, and because of its long recovery period and lack of specific treatment, most patients are left with varying degrees of neurological impairment, which affects their quality of life. Since the disease is induced by carbon monoxide poisoning, theoretically, if the patient is no longer exposed to carbon monoxide, the disease will not reoccur or worsen, but every year, we encounter some such patients in outpatient clinics or online consultation; the family members describe that the late-onset encephalopathy has been more than 1 or 2 years, and although it is not completely well, it has been stable, but why would it have worsened? And the symptoms are exactly the same as when the late-onset encephalopathy first started, so will the disease recur or not? The following is a recent case of late-onset encephalopathy treated by our department. Patient, female, 61 years old, primary cause: intermittent delayed reaction for 1.5 years, aggravated with walking and eating disorder for 3 months. History: 1.5 years ago, the patient began to have unresponsiveness, reduced speech, difficulty in eating, incontinence, and difficulty in walking, and was diagnosed with carbon monoxide poisoning late onset encephalopathy at a local hospital in a foreign country. The family found that the patient’s condition had worsened in March, with slow response, no speech, further difficulty in walking, broken stride, and increased muscle tone, and the family reduced the medroba back to 62.5mg, 3/day. The patient’s symptoms worsened and he was unable to eat and walk, so he underwent MRI at an outside hospital: paraventricular white matter lesion with partial high signal on DWI, and was admitted to our department for further treatment. Past history: Half a month before the onset of encephalopathy, the patient was diagnosed with acute carbon monoxide poisoning in a foreign hospital. On admission: blood pressure: 130/80mg, negative heart, lung and abdominal examination, clear consciousness, unresponsive, no speech, dull expression, bilateral pupils equal in size and round, sensitive to light reflex, bilateral frontal lines and nasolabial folds symmetrical, slightly increased muscle tension of limbs, normal muscle strength, normal tendon reflex, negative Bartholin’s sign. MRI: T2 and FLAIR high signal with no enhancement in the lateral paraventricular and semi-oval regions bilaterally, no abnormalities in T2*. Carotid ultrasound: mixed plaque was seen in the left common carotid artery. Diagnostic analysis: The patient was clearly diagnosed 1.5 years ago: carbon monoxide poisoning late onset encephalopathy, MRI was done at that time: T2 and FLAIR high signal was seen in bilateral lateral paraventricular and semi-oval areas, MRI was reviewed 10 months ago, and compared with this admission MRI, there was no change in lesion extent, DWI part was slightly higher than before, ventricular size was basically normal, and there was no significant atrophy in each brain lobe. Consider the possible causes: 1, Medobar drug dose and reduce too quickly: the patient since the beginning of late-onset encephalopathy on Medobar, the dose has changed several times, the onset of this May before taking Medobar 62.5mg, 3 / day, after an unknown reason to add to Medobar 250mg, 3 / day, March before the family quickly reduced back to 62.5mg, 3 / day, Medobar is a combination of benserazide and levodopa. The patient had a history of sudden dose increase and decrease, which does not exclude that the change in dopamine delivery leads to aggravation of symptoms. 2. Ischemic cerebral white matter lesions: The patient is an elderly female, although she denied her past history of hypertension, diabetes mellitus and other chronic diseases, but this examination carotid ultrasound shows mixed plaques in the common carotid artery, and nuclear magnetic DWI shows paraventricular white matter lesions. The signal was higher than before, and combined with the symptoms of this attack, cerebral white matter sparing in cerebral small vessel disease could not be excluded. 3, other causes of cerebral white matter demyelination lesions: according to the medical history and the results of the auxiliary examination, other diseases such as multiple sclerosis, inflammation, paraneoplastic syndrome and immune system diseases that cause cerebral white matter degeneration were not supported. 4, late recurrence of encephalopathy: this may be the most concerned issue, although the disease is currently Although the definite cause of the disease is not clear, we currently believe that the disease will not recur except for the re-exposure to carbon monoxide, and after years of case observation, this kind of case is very rare, so we do not consider the onset of the disease is a late recurrence of encephalopathy, but this aggravation is certainly related to the original condition. Treatment process: According to the above analysis, we first increased the medroba from 62.5mg, 3/day to 125mg, 3/day, and added a small amount of baclofen 5mg, 3/day due to the increased muscle tone, and added aspirin, lipid-lowering drugs and blood circulation treatment considering vascular factors. Three days later, the patient’s mental status improved and he could eat on his own initiative, and the gastric tube was removed. Discussion: According to this patient’s diagnosis and treatment process, we believe that the main reason for this patient’s symptom aggravation is related to the rapid adjustment of the dose of Medobar, and we do not exclude the vascular factors that cause ischemic changes, so we must look for other reasons for such patients, especially those who are old and have more underlying diseases, without considering the problem of late recurrence of encephalopathy!