BACKGROUND Patients with thalamic infarction experience abnormal blockages of multinuc-leated vessels,affecting the body and thereby the thalamus.Most patients with thalamic infarction have an adverse prognosis,which ...BACKGROUND Patients with thalamic infarction experience abnormal blockages of multinuc-leated vessels,affecting the body and thereby the thalamus.Most patients with thalamic infarction have an adverse prognosis,which seriously affects their safety.Therefore,it is essential to analyze the independent risk factors that influence the prognosis of patients with thalamic infarction and develop corresponding preventive measures.AIM To explore the effect of non-high-density lipoprotein cholesterol(non-HDL-C)and Homocysteine(Hcy)levels in cognitive impairment in thalamic infarction.METHODS From March 2019 to March 2022,80 patients with thalamic infarction were divided into a group with cognitive impairment[Montreal Cognitive Assessment(MoCA)score<26;35 patients]and a group with normal cognitive function(MoCA score of 26-30;45 patients)according to the MoCA score.In addition,50 healthy people in the same period were selected as the control group.A correlation between the non-HDL-C and Hcy levels and the MoCA score and receiver operating characteristic curve was observed,and the serum non-HDL-C and Hcy levels were analyzed for the diagnosis of cognitive impairment in patients with thalamic infarction.According to the Modified Rankin Scale(MRS)score,80 patients with thalamic infarction were divided into a good prognosis group(MRS score≤2)and a poor prognosis group(MRS score>2).RESULTS The non-HDL-C and Hcy levels were significantly higher in the group with cognitive impairment than in the group with normal cognitive function(P<0.05).There was no significant difference in the non-HDL-C level between the control group and the group with normal cognitive function(P>0.05).The MoCA scores of the group with cognitive impairment were significantly lower than those of the group with normal cognitive function and the control group(P<0.05).There was a significant difference between the control group and the group with normal cognitive function(P<0.05).The non-HDL-C and Hcy levels were correlated with the MoCA score(P<0.05),cognitive impairment[areas under the curve(AUC)=0.709,95%confidence interval(95%CI):0.599-0.816],the non-HDL-C level,and could predict cognitive impairment in patients with thalamic infarction(AUC=0.738,95%CI:0.618-0.859).Hcy combined with non-HDL-C levels can predict cognitive impairment in patients with thalamic infarction(AUC=0.769,95%CI:0.721-0.895).RESULTS There were 50 patients in the good prognosis group and 30 patients in the poor prognosis group.Compared with the good prognosis group,in the poor prognosis group,the National Institutes of Health Stroke Scale(NIHSS)score,non-HDL-C level,Hcy level,large-area cerebral infarction,atrial fibrillation,and activated partial prothrombin time were statistically significant(P<0.05).The non-HDL-C level,the Hcy level,the NIHSS score,extensive cerebral serum,and atrial fibrillation may all be independent risk factors for poor prognosis in patients with thalamic infarction(P<0.05).CONCLUSION Non-HDL-C and Hcy levels are positively correlated with cognitive impairment in patients with thalamic infarction.Non-HDL-C and Hcy levels can be used in the diagnosis of cognitive impairment in patients with thalamic infarction,and the combined detection effect is better.The main factors affecting the prognosis of patients with thalamic infarction are the non-HDL-C level,the Hcy level,the NIHSS score,large-area cerebral infarction,and atrial fibrillation.Clinically,corresponding preventive measures can be formulated based on the above factors to prevent poor prognosis and reduce mortality.展开更多
We investigated the effects of ipsilateral versus bilateral limb-training on promotion of endogenous neural stem cells in the peripheral infarct zone and the corresponding cerebral region in the unaffected hemisphere ...We investigated the effects of ipsilateral versus bilateral limb-training on promotion of endogenous neural stem cells in the peripheral infarct zone and the corresponding cerebral region in the unaffected hemisphere of rats with cerebral infarction. Middle cerebral artery occlusion was induced in Wistar rats. The rat forelimb on the unaffected side was either wrapped up with tape to force the use of the paretic forelimb in rats or not braked to allow bilateral forelimbs to participate in training. Daily training consisted of mesh drum training, balance beam training, and stick rolling training for a total of 40 minutes, once per day. Control rats received no training. At 14 days after functional training, rats receiving bilateral limb-training exhibited milder neurological impairment than that in the ipsilateral limb-training group or the control group. The number of nestin/glial fibrillary acidic protein-positive and nestin/microtubule-associated protein 2-positive cells in the peripheral infarct zone and in the corresponding cerebral region in the unaffected hemisphere was significantly higher in rats receiving bilateral limb-training than in rats receiving ipsilateral limb-training. These data suggest that bilateral limb-training can promote the proliferation and differentiation of endogenous neural stem cells in the bilateral hemispheres after cerebral infarction and accelerate the recovery of neurologic function. In addition, bilateral limb-training produces better therapeutic effects than ipsilateral limb-training.展开更多
BACKGROUND Hemichorea usually results from vascular lesions of the basal ganglia.Most often,the lesion is contralateral to the affected limb but rarely,it may be ipsilateral.The pathophysiology of ipsilateral hemichor...BACKGROUND Hemichorea usually results from vascular lesions of the basal ganglia.Most often,the lesion is contralateral to the affected limb but rarely,it may be ipsilateral.The pathophysiology of ipsilateral hemichorea is still poorly understood.We review the literature on hemichorea due to ipsilateral cerebral infarction and explore possible mechanisms for its occurrence.CASE SUMMARY A 72-year-old woman presented with complaints of involuntary movements of the muscles of the left side of the face and mild weakness of the right limbs.Her symptoms had started suddenly 1 d earlier.After admission to the hospital,the involuntary movements spread to involve the left limbs also.Magnetic resonance imaging revealed a left thalamic infarction.The patient’s hemichorea subsided after treatment with haloperidol(2 mg per time,3 times/d)for 3 d;the hemiparesis resolved with rehabilitation physiotherapy.She is presently symptom free and on treatment for prevention of secondary stroke.We review the literature on the occurrence of ipsilateral hemichorea following thalamic infarction and discuss the possible pathomechanisms of this unusual presentation.CONCLUSION Ipsilateral hemichorea following a thalamic stroke is rare but it can be explained by structure of the extrapyramidal system.The thalamus is a relay station that exerts a bilateral control of motor function.展开更多
In multiple trauma, blunt carotid artery injuries (BCAIs) have occasionally been reported. However, bilateral blunt carotid artery occlusions (Grade 4 BCAIs) associated with multiple trauma are rare, and delays in dia...In multiple trauma, blunt carotid artery injuries (BCAIs) have occasionally been reported. However, bilateral blunt carotid artery occlusions (Grade 4 BCAIs) associated with multiple trauma are rare, and delays in diagnosis and treatment result in a lethal outcome. Here, we report our experience with bilateral carotid artery occlusions. A 76-year-old female suffered multiple traumas in a motor vehicle accident. On arrival at our hospital, she presented in a coma, with left mydriasis and unreactive pupils. Computed tomography (CT) showed bifrontal intracranial epidural hematoma and fractures of the facial bone and anterior skull base, and osteoplastic craniotomy was urgently undertaken for the epidural hematoma. However, the comatose state and unreactive pupils persisted during the post-operative course. Serial head CT findings showed progressive bilateral ischemic changes, and radiological examinations revealed bilateral internal carotid artery occlusions. We speculated that bilateral Grade 4 BCAIs had induced progressive cerebral infarctions. The patient partially responded to anticoagulation therapy with heparin infusion, but died of multiple organ failure on day 15. When bilateral progressive ischemic changes are observed in a patient with severe traumatic brain injury, bilateral Grade 4 BCAIs should be considered in the differential diagnosis. CT angiography as part of whole-body CT at admission may be effective for preventing delays in diagnosis and treatment of bilateral Grade 4 BCAIs.展开更多
BACKGROUND Diabetic ketoacidosis(DKA)is a serious complication of type 1 diabetes mellitus(T1DM).Very rarely does DKA lead to cerebral edema,and it is even rarer for it to result in cerebral infarction.Bilateral inter...BACKGROUND Diabetic ketoacidosis(DKA)is a serious complication of type 1 diabetes mellitus(T1DM).Very rarely does DKA lead to cerebral edema,and it is even rarer for it to result in cerebral infarction.Bilateral internal carotid artery occlusion(BICAO)is also rare and can cause fatal stroke.Moreover,case reports about acute cerebral infarction throughout both internal carotid arteries with simultaneous BICAO are very scarce.In this study,we present a patient with BICAO,T1DM,hypertension,and hyperlipidemia,who had a catastrophic bilateral cerebral infarction after a DKA episode.We briefly introduce BICAO and the mechanisms by which DKA results in cerebral infarction.CASE SUMMARY A 41-year-old woman presented with ischemic stroke that took place 3 mo prior over the left corona radiata,bilateral frontal lobe,and parietal lobe with right hemiplegia and Broca’s aphasia.She had a history of hypertension for 5 years,hyperlipidemia for 4 years,hyperthyroidism for 3 years,and T1DM for 31 years.The first brain magnetic resonance imaging not only revealed the aforementioned ischemic lesions but also bilateral internal carotid artery occlusion.She was admitted to our ward for rehabilitation due to prior stroke sequalae.DKA took place on hospital day 2.On hospital day 6,she had a new massive infarction over the bilateral anterior cerebral artery and middle cerebral artery territory.After weeks of aggressive treatment,she remained in a coma and on mechanical ventilation due to respiratory failure.After discussion with her family,compassionate extubation was performed on hospital day 29 and she died.CONCLUSION DKA can lead to cerebral infarction due to several mechanisms.In people with existing BICAO and several stroke risk factors such as hypertension, T1DM,hyperlipidemia, DKA has the potential to cause more serious ischemic strokes.展开更多
BACKGROUND: Following ischemia, apoptosis is observed at the ipsilateral ventropostenor thalamic nucleus and substantia nigra, which are distant from, but connected to, the ischemic cerebral cortex, in animals with n...BACKGROUND: Following ischemia, apoptosis is observed at the ipsilateral ventropostenor thalamic nucleus and substantia nigra, which are distant from, but connected to, the ischemic cerebral cortex, in animals with normotension. However, secondary brain damage in hypertension has not been clearly investigated. OBJECTIVE: The present study determined whether neuronal apoptosis is associated with neuronal loss in the ipsilateral ventroposterior thalamic nucleus and substantia nigra following cortical ischemia in adult hypertensive rats. Results should provide options for determining a time window for anti-apoptotic therapy. DESIGN, TIME AND SETTING: All experimental procedures in this randomized, controlled trial were conducted at the Neurological Laboratory of the First Affiliated Hospital of Sun Yat-sen University of China between October 2006 and July 2008. MATERIALS: Monoclonal primary antibodies specific to mouse anti-rat microtubule-associated protein 2 and glial fibrillary acidic protein were respectively purchased from Sigma Chemical, USA and BD Pharmingen, USA. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) detection kits were purchased from Roche Applied Science, Switzerland and Upstate, USA, respectively. METHODS: A total of 64 male, Sprague Dawiey rats, aged 60-90 days, were equally and randomly divided into middle cerebral artery occlusion and sham surgery groups. Renovascular hypertension was established in both groups by renal artery occlusion. Right distal middle cerebral artery occlusion was performed by electrocoagulation in the middle cerebral artery occlusion group. MAIN OUTCOME MEASURES: Microtubule-associated protein 2 and glial fibrillary acidic protein were detected by immunohistochemistry, and apoptotic cells were observed by TUNEL assay. The stainings were separately detected in the ipsilateral ventroposterior thalamic nucleus and substantia nigra. RESULTS: During the 4 weeks following distal middle cerebral artery occlusion in renovascular hypertensive rats, microtubule-associated protein 2 expression gradually, but significantly, decreased (P 〈 0.05). Expression of glial fibrillary acidic protein increased significantly in the ipsilateral ventroposterior thalamic nucleus and substantia nigra (P 〈 0.05) and reached a peak at 4 weeks. In addition, number of apoptotic cells was significantly increased in both areas compared with the sham controls (P 〈 0.05), with a peak at 2 weeks. CONCLUSION: Results suggested that neuronal loss in the ipsilateral ventroposterior thalamic nucleus and substantia nigra following distal middle cerebral artery occlusion in hypertensive rats could be a secondary event resulting from apoptosis. The temporal apoptosis profile provides options for determining a time window for anti-apoptotic therapy at 2 weeks after stroke.展开更多
To the Editor:Bilateral medial medullary infarction(MMI)is a rare stroke subtype.[1]usually leads to quadriplegia,sensory disturbance,hypoglossal palsy,bulbar paralysis,etc.[2]We encountered a patient with rapidly pro...To the Editor:Bilateral medial medullary infarction(MMI)is a rare stroke subtype.[1]usually leads to quadriplegia,sensory disturbance,hypoglossal palsy,bulbar paralysis,etc.[2]We encountered a patient with rapidly progressive tetraparesis and diffusion-weighted imaging(DWI)exhibited a“heart appearance”sign in the bilateral ventral medulla.Computed tomography angiography(CTA)demonstrated that the left vertebral artery(VA)was hypoplastic and there was an atherosclerotic stenosis in the V4 segment.展开更多
基金The study was reviewed and approved by the Institutional Review Board of Chaohu Hospital Affiliated to AnhuiMedical University,Approval No.KYXM-202208-011.
文摘BACKGROUND Patients with thalamic infarction experience abnormal blockages of multinuc-leated vessels,affecting the body and thereby the thalamus.Most patients with thalamic infarction have an adverse prognosis,which seriously affects their safety.Therefore,it is essential to analyze the independent risk factors that influence the prognosis of patients with thalamic infarction and develop corresponding preventive measures.AIM To explore the effect of non-high-density lipoprotein cholesterol(non-HDL-C)and Homocysteine(Hcy)levels in cognitive impairment in thalamic infarction.METHODS From March 2019 to March 2022,80 patients with thalamic infarction were divided into a group with cognitive impairment[Montreal Cognitive Assessment(MoCA)score<26;35 patients]and a group with normal cognitive function(MoCA score of 26-30;45 patients)according to the MoCA score.In addition,50 healthy people in the same period were selected as the control group.A correlation between the non-HDL-C and Hcy levels and the MoCA score and receiver operating characteristic curve was observed,and the serum non-HDL-C and Hcy levels were analyzed for the diagnosis of cognitive impairment in patients with thalamic infarction.According to the Modified Rankin Scale(MRS)score,80 patients with thalamic infarction were divided into a good prognosis group(MRS score≤2)and a poor prognosis group(MRS score>2).RESULTS The non-HDL-C and Hcy levels were significantly higher in the group with cognitive impairment than in the group with normal cognitive function(P<0.05).There was no significant difference in the non-HDL-C level between the control group and the group with normal cognitive function(P>0.05).The MoCA scores of the group with cognitive impairment were significantly lower than those of the group with normal cognitive function and the control group(P<0.05).There was a significant difference between the control group and the group with normal cognitive function(P<0.05).The non-HDL-C and Hcy levels were correlated with the MoCA score(P<0.05),cognitive impairment[areas under the curve(AUC)=0.709,95%confidence interval(95%CI):0.599-0.816],the non-HDL-C level,and could predict cognitive impairment in patients with thalamic infarction(AUC=0.738,95%CI:0.618-0.859).Hcy combined with non-HDL-C levels can predict cognitive impairment in patients with thalamic infarction(AUC=0.769,95%CI:0.721-0.895).RESULTS There were 50 patients in the good prognosis group and 30 patients in the poor prognosis group.Compared with the good prognosis group,in the poor prognosis group,the National Institutes of Health Stroke Scale(NIHSS)score,non-HDL-C level,Hcy level,large-area cerebral infarction,atrial fibrillation,and activated partial prothrombin time were statistically significant(P<0.05).The non-HDL-C level,the Hcy level,the NIHSS score,extensive cerebral serum,and atrial fibrillation may all be independent risk factors for poor prognosis in patients with thalamic infarction(P<0.05).CONCLUSION Non-HDL-C and Hcy levels are positively correlated with cognitive impairment in patients with thalamic infarction.Non-HDL-C and Hcy levels can be used in the diagnosis of cognitive impairment in patients with thalamic infarction,and the combined detection effect is better.The main factors affecting the prognosis of patients with thalamic infarction are the non-HDL-C level,the Hcy level,the NIHSS score,large-area cerebral infarction,and atrial fibrillation.Clinically,corresponding preventive measures can be formulated based on the above factors to prevent poor prognosis and reduce mortality.
文摘We investigated the effects of ipsilateral versus bilateral limb-training on promotion of endogenous neural stem cells in the peripheral infarct zone and the corresponding cerebral region in the unaffected hemisphere of rats with cerebral infarction. Middle cerebral artery occlusion was induced in Wistar rats. The rat forelimb on the unaffected side was either wrapped up with tape to force the use of the paretic forelimb in rats or not braked to allow bilateral forelimbs to participate in training. Daily training consisted of mesh drum training, balance beam training, and stick rolling training for a total of 40 minutes, once per day. Control rats received no training. At 14 days after functional training, rats receiving bilateral limb-training exhibited milder neurological impairment than that in the ipsilateral limb-training group or the control group. The number of nestin/glial fibrillary acidic protein-positive and nestin/microtubule-associated protein 2-positive cells in the peripheral infarct zone and in the corresponding cerebral region in the unaffected hemisphere was significantly higher in rats receiving bilateral limb-training than in rats receiving ipsilateral limb-training. These data suggest that bilateral limb-training can promote the proliferation and differentiation of endogenous neural stem cells in the bilateral hemispheres after cerebral infarction and accelerate the recovery of neurologic function. In addition, bilateral limb-training produces better therapeutic effects than ipsilateral limb-training.
基金Department of Education Zhejiang Province Scientific Research Project,No.Y201942038and Zhejiang Province Medical Science and Technology Project,No.2020RC061.
文摘BACKGROUND Hemichorea usually results from vascular lesions of the basal ganglia.Most often,the lesion is contralateral to the affected limb but rarely,it may be ipsilateral.The pathophysiology of ipsilateral hemichorea is still poorly understood.We review the literature on hemichorea due to ipsilateral cerebral infarction and explore possible mechanisms for its occurrence.CASE SUMMARY A 72-year-old woman presented with complaints of involuntary movements of the muscles of the left side of the face and mild weakness of the right limbs.Her symptoms had started suddenly 1 d earlier.After admission to the hospital,the involuntary movements spread to involve the left limbs also.Magnetic resonance imaging revealed a left thalamic infarction.The patient’s hemichorea subsided after treatment with haloperidol(2 mg per time,3 times/d)for 3 d;the hemiparesis resolved with rehabilitation physiotherapy.She is presently symptom free and on treatment for prevention of secondary stroke.We review the literature on the occurrence of ipsilateral hemichorea following thalamic infarction and discuss the possible pathomechanisms of this unusual presentation.CONCLUSION Ipsilateral hemichorea following a thalamic stroke is rare but it can be explained by structure of the extrapyramidal system.The thalamus is a relay station that exerts a bilateral control of motor function.
文摘In multiple trauma, blunt carotid artery injuries (BCAIs) have occasionally been reported. However, bilateral blunt carotid artery occlusions (Grade 4 BCAIs) associated with multiple trauma are rare, and delays in diagnosis and treatment result in a lethal outcome. Here, we report our experience with bilateral carotid artery occlusions. A 76-year-old female suffered multiple traumas in a motor vehicle accident. On arrival at our hospital, she presented in a coma, with left mydriasis and unreactive pupils. Computed tomography (CT) showed bifrontal intracranial epidural hematoma and fractures of the facial bone and anterior skull base, and osteoplastic craniotomy was urgently undertaken for the epidural hematoma. However, the comatose state and unreactive pupils persisted during the post-operative course. Serial head CT findings showed progressive bilateral ischemic changes, and radiological examinations revealed bilateral internal carotid artery occlusions. We speculated that bilateral Grade 4 BCAIs had induced progressive cerebral infarctions. The patient partially responded to anticoagulation therapy with heparin infusion, but died of multiple organ failure on day 15. When bilateral progressive ischemic changes are observed in a patient with severe traumatic brain injury, bilateral Grade 4 BCAIs should be considered in the differential diagnosis. CT angiography as part of whole-body CT at admission may be effective for preventing delays in diagnosis and treatment of bilateral Grade 4 BCAIs.
文摘BACKGROUND Diabetic ketoacidosis(DKA)is a serious complication of type 1 diabetes mellitus(T1DM).Very rarely does DKA lead to cerebral edema,and it is even rarer for it to result in cerebral infarction.Bilateral internal carotid artery occlusion(BICAO)is also rare and can cause fatal stroke.Moreover,case reports about acute cerebral infarction throughout both internal carotid arteries with simultaneous BICAO are very scarce.In this study,we present a patient with BICAO,T1DM,hypertension,and hyperlipidemia,who had a catastrophic bilateral cerebral infarction after a DKA episode.We briefly introduce BICAO and the mechanisms by which DKA results in cerebral infarction.CASE SUMMARY A 41-year-old woman presented with ischemic stroke that took place 3 mo prior over the left corona radiata,bilateral frontal lobe,and parietal lobe with right hemiplegia and Broca’s aphasia.She had a history of hypertension for 5 years,hyperlipidemia for 4 years,hyperthyroidism for 3 years,and T1DM for 31 years.The first brain magnetic resonance imaging not only revealed the aforementioned ischemic lesions but also bilateral internal carotid artery occlusion.She was admitted to our ward for rehabilitation due to prior stroke sequalae.DKA took place on hospital day 2.On hospital day 6,she had a new massive infarction over the bilateral anterior cerebral artery and middle cerebral artery territory.After weeks of aggressive treatment,she remained in a coma and on mechanical ventilation due to respiratory failure.After discussion with her family,compassionate extubation was performed on hospital day 29 and she died.CONCLUSION DKA can lead to cerebral infarction due to several mechanisms.In people with existing BICAO and several stroke risk factors such as hypertension, T1DM,hyperlipidemia, DKA has the potential to cause more serious ischemic strokes.
基金Chinese Medical Board of USA, No.CMB00-730the Na-tional Natural Science Foundation of China, No. 30770764, 30973108the Fund of Health Department of Guangdong Province Department of China, No.A2009172
文摘BACKGROUND: Following ischemia, apoptosis is observed at the ipsilateral ventropostenor thalamic nucleus and substantia nigra, which are distant from, but connected to, the ischemic cerebral cortex, in animals with normotension. However, secondary brain damage in hypertension has not been clearly investigated. OBJECTIVE: The present study determined whether neuronal apoptosis is associated with neuronal loss in the ipsilateral ventroposterior thalamic nucleus and substantia nigra following cortical ischemia in adult hypertensive rats. Results should provide options for determining a time window for anti-apoptotic therapy. DESIGN, TIME AND SETTING: All experimental procedures in this randomized, controlled trial were conducted at the Neurological Laboratory of the First Affiliated Hospital of Sun Yat-sen University of China between October 2006 and July 2008. MATERIALS: Monoclonal primary antibodies specific to mouse anti-rat microtubule-associated protein 2 and glial fibrillary acidic protein were respectively purchased from Sigma Chemical, USA and BD Pharmingen, USA. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end-labeling (TUNEL) detection kits were purchased from Roche Applied Science, Switzerland and Upstate, USA, respectively. METHODS: A total of 64 male, Sprague Dawiey rats, aged 60-90 days, were equally and randomly divided into middle cerebral artery occlusion and sham surgery groups. Renovascular hypertension was established in both groups by renal artery occlusion. Right distal middle cerebral artery occlusion was performed by electrocoagulation in the middle cerebral artery occlusion group. MAIN OUTCOME MEASURES: Microtubule-associated protein 2 and glial fibrillary acidic protein were detected by immunohistochemistry, and apoptotic cells were observed by TUNEL assay. The stainings were separately detected in the ipsilateral ventroposterior thalamic nucleus and substantia nigra. RESULTS: During the 4 weeks following distal middle cerebral artery occlusion in renovascular hypertensive rats, microtubule-associated protein 2 expression gradually, but significantly, decreased (P 〈 0.05). Expression of glial fibrillary acidic protein increased significantly in the ipsilateral ventroposterior thalamic nucleus and substantia nigra (P 〈 0.05) and reached a peak at 4 weeks. In addition, number of apoptotic cells was significantly increased in both areas compared with the sham controls (P 〈 0.05), with a peak at 2 weeks. CONCLUSION: Results suggested that neuronal loss in the ipsilateral ventroposterior thalamic nucleus and substantia nigra following distal middle cerebral artery occlusion in hypertensive rats could be a secondary event resulting from apoptosis. The temporal apoptosis profile provides options for determining a time window for anti-apoptotic therapy at 2 weeks after stroke.
文摘To the Editor:Bilateral medial medullary infarction(MMI)is a rare stroke subtype.[1]usually leads to quadriplegia,sensory disturbance,hypoglossal palsy,bulbar paralysis,etc.[2]We encountered a patient with rapidly progressive tetraparesis and diffusion-weighted imaging(DWI)exhibited a“heart appearance”sign in the bilateral ventral medulla.Computed tomography angiography(CTA)demonstrated that the left vertebral artery(VA)was hypoplastic and there was an atherosclerotic stenosis in the V4 segment.