ObjectiveTo improve clinicians’ understanding and diagnosis and treatment of bilateral thalamic infarction caused by thrombosis of the rectus sinus. Methods To summarize the clinical manifestations, imaging characteristics, treatment and prognosis of a case of bilateral thalamic infarction caused by thrombosis of the rectus sinus, and review the relevant literature at home and abroad in the past 5 years to further explore its clinical and imaging characteristics. Results: All patients had risk factors for cerebrovascular disease, acute onset of the disease, with sudden onset of impaired consciousness and unequal size of both pupils as the main manifestations; there are reports in the literature on the onset of drowsiness, unresponsiveness, mental changes, ptosis, diplopia, diplopia, blurred vision, etc., with few motor and sensory deficits; there are significant imaging changes, and most of the clinical symptoms improved significantly after anticoagulant therapy was given. As a special type of cerebrovascular disease, cerebral venous sinus thrombosis (CVST) has various etiologies and lacks specific symptoms and characteristics, therefore, the clinical misdiagnosis rate, mistreatment rate and mortality rate are high, which seriously affects the prognosis. Rectus sinus thrombosis is even rarer in clinic, often sudden onset of disease, the condition is dangerous, easy to misdiagnose as other diseases, recognize its clinical manifestations and imaging characteristics are very important for diagnosis and treatment, we found a typical case, and review the relevant literature at home and abroad in the past 5 years, reported as follows. Clinical data The patient, male, 62 years old, a farmer, was admitted to the hospital on March 30, 2013, mainly due to “drowsiness for 7 days”. He had a history of hypertension for more than 10 years, did not take medication regularly, and was addicted to smoking and alcohol abuse. Physical examination: BP167/96mmHg; drowsiness, bilateral pupils 3mm in diameter, sensitive to light, bilateral angle of the mouth is roughly symmetrical, neck seems to have resistance, limb muscle strength grade V, bilateral Babinski’s sign (+). Brain CT showed bilateral thalamic hypodensity, preliminary diagnosis of “acute ischemic cerebrovascular disease, hypertension (very high-risk group), urgent investigation of blood glucose 8.9 mmol / L, electrolytes and blood and coagulation routine is normal, homocysteine 57 mmol / L, given to oxygen absorption, the application of antiplatelet aggregation drugs, free radical scavengers, activate blood circulation and eliminate blood stasis drugs, prevention of complications and other treatments. etc. On April 2, the condition worsened, lethargy, bilateral lateral pupil 3mm, light reaction sensitivity, limb muscle strength about grade 4, brain MRI (DWI) showed bilateral thalamic infarction (Figure 1); MRA was normal, so except for the arterial infarction, consider venous infarction, improve the head CTV examination showed the development of rectus sinus and the left side of the transverse sinus and sigmoid sinus abnormally, the lumbar spinal puncture cerebrospinal fluid pressure of 360mmH2O, the cerebrospinal fluid routine has nuclear Cells 14 × 106 / L cerebrospinal fluid biochemical protein 3.5 g / L, consider the straight sinus thrombosis, given low molecular heparin and warfarin anticoagulation treatment, gradually adjust the INR to 2-3, April 30 consciousness clear, fluent language, limb muscle strength is generally normal, walking is not stable, the patient’s reaction is slow, spontaneous language is less, hospitalized for 30d better discharge. The patient was discharged from the hospital after 30d of hospitalization. 6 months after discharge, the patient’s slow reaction was reduced, his memory was significantly improved, and his eye movements were free. The patient had the following characteristics: (1) elderly patients with risk factors for cerebrovascular disease; (2) acute onset of the disease, gradual aggravation, double pupils of equal size, light responsive, lethargy, normal muscle strength of the limbs; (3) gradual restoration of consciousness after systematic treatment, quadriplegia is not obvious; (4) craniocerebral CT found bilateral thalamus hypodense shadows, craniocerebral MRI showed bilateral thalamus abnormal signals. mra was normal, ctv was visible. The rectus sinuses were poorly visualized. The patient had an acute onset of illness and was admitted to the hospital after a detailed history and physical examination to rule out gas, pesticide, drug and poison poisoning, and an urgent blood glucose check to rule out hypoglycemic coma and hyperosmolar coma, ketoacidotic coma. Acute cerebral infarction was considered at the time of admission, but there were questions: if it was a large cerebral infarction caused by embolization of the MCA-M1 segment of the episcleral lesion, cerebral edema compression of the ipsilateral and contralateral motoneurons caused bilateral pupil changes, disappearance of light reflex, and the possibility of cerebral herniation, which could explain the impaired consciousness, but the patient’s paralysis was not obvious and unsupportive; if it was a brainstem infarction, it could be associated with impaired consciousness, and respiration could be altered, but the patient’s respiration The patient’s respiration was stable. Brain MRI showed abnormal signals in bilateral thalamus, but MRA was normal, so the arterial infarction was excluded, and venous thrombosis was considered, and CTV examination of the head was perfected, which showed venous thrombosis, and reviewing the literature [1-6], the patient was suffering from rectus sinus thrombosis. Intracranial venous sinus thrombosis is related to the special anatomical characteristics of the intracranial venous system and its etiology is complex, including infectious or non-infectious two categories. Infection is a definite cause, and non-infectious factors include oral contraceptives, migraine, peripheral venous thrombosis, postpartum and pregnancy anemia, and other factors affecting hemoglobinopathies protein C deficiency, protein S deficiency, hyperhomocysteinemia leading to a tendency to thrombosis, and other unexplained causes [7]. In our patient, hyperhomocysteinemia was associated with the mechanism of occurrence of intracranial venous sinus thrombosis, most of which had an acute or subacute onset with a wide spectrum of clinical symptoms and nonspecific manifestations. Straight sinus thrombosis may involve bilateral thalamus, midbrain conduit periaqueductal gray matter, with or without midbrain lesions. Cranial CT shows bilateral thalamus and midbrain hypodensity changes, and brain MRI examination shows bilateral thalamus long T1 and long T2 signals and Flair high signals, and the diagnosis of straight sinus thrombosis is mainly based on the typical clinical manifestations and MRV or CTV manifestations [8]. Intracranial venous sinus thrombosis has many causes, complex and variable clinical manifestations, lack of specificity, but if there is a headache with delayed onset or progressive aggravation accompanied by focal symptoms and signs of imaging findings of localized or diffuse cerebral swelling bilateral lesions asymmetric, especially hemorrhagic infarcts located in the vicinity of the midline, not in accordance with the distribution of blood vessels, which should be particularly vigilant, as soon as possible for MRI + MRV or DSA examination to clarify the Diagnosis. There are reports of rare cancerous venous sinus thrombosis, and it should be noted that venous sinus thrombosis due to tumor should be routinely excluded after the patients are elderly and clearly diagnosed as venous sinus thrombosis. Early diagnosis and treatment affect the prognosis. The etiology of the patient’s condition and the impairment of consciousness at the time of presentation and imaging features such as extensive venous sinus occlusion, poor collateral circulation and hemorrhagic infarction are the most important factors in determining the prognosis. However, large-scale clinical studies are lacking.