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*Only for medical professionals to read and refer to the Neurological Archives: classic cases, layer by layer analysis! Not much to say, let's look at this case first! The case patient is a 32-year-old male patient who was admitted to the hospital because of "right limb weakness with speech inability for one month".
History of present illness: The patient had no obvious cause before 1 month, and the right limbs were not able to move well, he could not understand other people's words, and he could not express himself.
He rushed to the local hospital to see a doctor.
There was no abnormality in the head CT examination.
After 1 week of treatment with "cerebral infarction", there was no significant improvement.
Brain MRI showed multiple cerebral infarctions in the left basal ganglia and left frontal, parietal, and temporal lobes.
There were no obvious abnormalities in brain MRA and DSA.
The patient had a tonic-clonic seizure during the hospitalization, which lasted for about 5 minutes and then resolved.
Afterwards, the patient's aphasia symptoms significantly worsened.
Repeated head MRI showed multiple subacute cerebral infarctions in the left frontal, parietal, temporal, and occipital lobes, and bilateral parieto-occipital infarctions.
There are multiple small nodular high-density shadows under the cortex.
Past history: The patient has a previous physical fitness and no history of hypertension, diabetes, coronary heart disease, etc.
Family history: No family history.
Nervous system examination: incomplete mixed aphasia, eye movement in all directions, middle tongue extension, no angle of mouth, right limb muscle strength level 4, left limb muscle strength level 5, normal muscle tone.
The right tendon is hyperreflexive, and the right Chadock sign is positive.
The limbs feel normal, without meningeal irritation.
How to locate and diagnose qualitatively at this stage? ▌ Location diagnosis: epileptic seizures indicate cerebral cortex damage; aphasia indicates cortex or subcortical white matter damage in the dominant hemisphere; right limb weakness, tendon hyperreflexia, and positive pathological reflex, suggesting damage to the pyramidal tract in the left cerebral hemisphere.
▌ Qualitative diagnosis: Acquired disease should be considered first if the patient is young and has no family history; if the onset is acute and hemiplegia appears, cerebrovascular disease should be considered first, and MRI of the brain is also confirmed as cerebral infarction.
Atherosclerosis is one of the most common causes of stroke in young people, but this patient has no factors that lead to atherosclerosis.
Brain MRA and DSA also ruled out atherosclerosis in the patient.
Dissecting aneurysms, moyamoya disease, and fibromuscular dysplasia can also cause similar clinical manifestations, but cranial DSA excludes the possibility of these diseases.
Inflammatory vascular diseases include infectious arteritis (syphilis, tuberculosis, Brucella, herpes simplex) and systemic arteritis.
DSA can find segmental arterial stenosis and can find corresponding antibodies.
This patient does not have these characteristics.
Mitochondrial encephalomyopathy with hyperlactic acidemia and stroke-like seizures (MELAS) can also cause epilepsy, limb weakness, etc.
The brain MRI examination often reveals large areas of cortical necrosis in the posterior part of the brain.
The image of this patient does not match.
Genetic examination of MELAS patients Most of the mitochondrial DNA gene mutations can be found.
Young patients with stroke also need to look for the cause of cardiogenic stroke, including valvular heart disease, atrial fibrillation, acute myocardial infarction, atrial myxoma, etc.
, and heart-related examinations are often required to confirm or rule out the diagnosis.
According to the preliminary analysis, perform auxiliary examinations and hematological examinations: hemoglobin (Hb) 84 g/L (normal value 110-150 g/L), erythrocyte sedimentation rate (ESR) 57mm/L, c-reactive protein (CRP) 33 mg/L ( Normal value 0-10mg/L).
Liver and kidney function, rheumatism series, normal coagulation function, negative serum tuberculosis antibody, negative syphilis antibody, and negative Brucella agglutination test.
Cerebrospinal fluid examination: protein is slightly higher than 0.
67 g/L (normal <0.
45), cell count is normal, glucose and chloride levels are normal, no oligoclonal bands, no abnormal cells.
Brain MRI: multiple cerebral infarctions in the left basal ganglia, left frontal, parietal, and temporal lobes.
Craniocerebral MRA: No obvious abnormalities.
Cardiac ultrasound: a 4.
7cm×2.
4cm mass echo can be seen in the left atrium, which is thrown to the ventricle during diastole, and returns to the atrium during systole.
The surface of the tumor is not smooth, indicating the presence of atrial myxoma.
Figure 1: The patient's brain MRI and MRAA.
The brain MRI showed that the blood supply area of the left anterior cerebral artery was scattered with high signal, and the blood supply area of the left middle cerebral artery was scattered with high signal (yellow dotted arrow).
B.
Brain MRA shows that the left anterior cerebral artery (red solid arrow), the left middle cerebral artery (red dotted arrow), and the intracranial segment of the left internal carotid artery (green arrow) have no obvious stenosis.
Figure 2: The patient’s cardiac echocardiography showed a 4.
7cm×2.
4cm mass echo in the left atrium, suggesting the presence of atrial myxoma.
What is the patient's final diagnosis? Combined with the patient's clinical manifestations, imaging examinations, cerebrospinal fluid and cardiac ultrasound examinations, the patient's final diagnosis was: left atrial myxoma caused multiple cerebral embolism.
Discussion Atrial myxoma is the most common primary cardiac tumor, accounting for about 50% of primary cardiac tumors.
Atrial myxoma is common in women, with a male-to-female ratio of 2:3, and it usually occurs between 30 and 60 years old, with an average age of 43 years.
The clinical manifestations of atrial myxoma are divided into three categories: ①Symptoms of mitral valve obstruction (65%): The tumor affects blood circulation in the heart cavity, resulting in various degrees of blood flow obstruction, resulting in a series of symptoms, such as palpitations, shortness of breath, Syncope and even heart failure.
②Arterial embolism symptoms (31%): Left atrial myxoma often causes systemic embolism.
The size of the tumor embolus and the embolization site are different, causing different symptoms.
Cerebral embolism mostly enters the anterior half of the basal artery ring, and middle cerebral artery embolism is the most common.
For this patient, multiple cerebral embolism is considered due to the shedding of a large tumor thrombus.
③ Systemic symptoms (34%): Patients with atrial myxoma often have fever, weight loss, loss of appetite, and joint pain.
Laboratory tests often find anemia and fast erythrocyte sedimentation rate.
Systemic symptoms may be related to the degeneration, bleeding, necrosis and autoimmune reaction of atrial myxoma.
.
For cerebral infarction in young people without risk factors for stroke, the possibility of atrial myxoma leading to cardiogenic cerebral embolism should be considered.
Cardiac ultrasonography is the first choice for atrial myxoma, and it is very important to understand the size, shape, and location of atrial myxoma.
Cerebral embolism caused by atrial myxoma is the most common form of thrombus shedding.
A small part of the emboli may originate from the tumor tissue itself.
Thrombolytic therapy can be considered for cerebral embolism at the very early stage (<6h).
The thrombolytic effect depends on the composition of the embolus.
Once the atrial myxoma is diagnosed, it should be surgically removed as soon as possible, and the echocardiography should be reviewed regularly to be alert to the possibility of atrial myxoma recurrence.
References: 1.
Lee VH, Connolly HM, Brown RD Jr.
Central nervous system manifestations of cardiac myxoma.
Archieves of neurology,2007,64:1115-1120.
2.
Yufe R,Karpati G,Carpenter S.
Cardiac myxoma:a diagnostic challenge for the neurologist.
Neurology,1976,26:1060-1065.
3.
Zhang Hong, Xie Zhongxiang, Che Fengyuan.
A case report of hyperacute thrombolysis of atrial myxomatous cerebral embolism.
Chinese Journal of Stroke.
2020, 15 (1): 89 .
-92.
4 Yuan cloud editor, "Neurology difficult cases" Beijing Science and technology Press text starting: the medical profession Neurology channel author: Liny paper review: Deputy Director Li Tu Ming, MD, editor: Mr.
Lu Li copyright notice paper original for reprint Welcome to contact for authorization-End-Call for papers.
Welcome to submit papers to the editor’s mailbox: yxjsjbx@yxj.
org.
cn.
Please specify: [Submission] Hospital + Department + Name Contributions are in the form of word files, and the remuneration is favorable.
Editor WeChat: chenaFF0911
History of present illness: The patient had no obvious cause before 1 month, and the right limbs were not able to move well, he could not understand other people's words, and he could not express himself.
He rushed to the local hospital to see a doctor.
There was no abnormality in the head CT examination.
After 1 week of treatment with "cerebral infarction", there was no significant improvement.
Brain MRI showed multiple cerebral infarctions in the left basal ganglia and left frontal, parietal, and temporal lobes.
There were no obvious abnormalities in brain MRA and DSA.
The patient had a tonic-clonic seizure during the hospitalization, which lasted for about 5 minutes and then resolved.
Afterwards, the patient's aphasia symptoms significantly worsened.
Repeated head MRI showed multiple subacute cerebral infarctions in the left frontal, parietal, temporal, and occipital lobes, and bilateral parieto-occipital infarctions.
There are multiple small nodular high-density shadows under the cortex.
Past history: The patient has a previous physical fitness and no history of hypertension, diabetes, coronary heart disease, etc.
Family history: No family history.
Nervous system examination: incomplete mixed aphasia, eye movement in all directions, middle tongue extension, no angle of mouth, right limb muscle strength level 4, left limb muscle strength level 5, normal muscle tone.
The right tendon is hyperreflexive, and the right Chadock sign is positive.
The limbs feel normal, without meningeal irritation.
How to locate and diagnose qualitatively at this stage? ▌ Location diagnosis: epileptic seizures indicate cerebral cortex damage; aphasia indicates cortex or subcortical white matter damage in the dominant hemisphere; right limb weakness, tendon hyperreflexia, and positive pathological reflex, suggesting damage to the pyramidal tract in the left cerebral hemisphere.
▌ Qualitative diagnosis: Acquired disease should be considered first if the patient is young and has no family history; if the onset is acute and hemiplegia appears, cerebrovascular disease should be considered first, and MRI of the brain is also confirmed as cerebral infarction.
Atherosclerosis is one of the most common causes of stroke in young people, but this patient has no factors that lead to atherosclerosis.
Brain MRA and DSA also ruled out atherosclerosis in the patient.
Dissecting aneurysms, moyamoya disease, and fibromuscular dysplasia can also cause similar clinical manifestations, but cranial DSA excludes the possibility of these diseases.
Inflammatory vascular diseases include infectious arteritis (syphilis, tuberculosis, Brucella, herpes simplex) and systemic arteritis.
DSA can find segmental arterial stenosis and can find corresponding antibodies.
This patient does not have these characteristics.
Mitochondrial encephalomyopathy with hyperlactic acidemia and stroke-like seizures (MELAS) can also cause epilepsy, limb weakness, etc.
The brain MRI examination often reveals large areas of cortical necrosis in the posterior part of the brain.
The image of this patient does not match.
Genetic examination of MELAS patients Most of the mitochondrial DNA gene mutations can be found.
Young patients with stroke also need to look for the cause of cardiogenic stroke, including valvular heart disease, atrial fibrillation, acute myocardial infarction, atrial myxoma, etc.
, and heart-related examinations are often required to confirm or rule out the diagnosis.
According to the preliminary analysis, perform auxiliary examinations and hematological examinations: hemoglobin (Hb) 84 g/L (normal value 110-150 g/L), erythrocyte sedimentation rate (ESR) 57mm/L, c-reactive protein (CRP) 33 mg/L ( Normal value 0-10mg/L).
Liver and kidney function, rheumatism series, normal coagulation function, negative serum tuberculosis antibody, negative syphilis antibody, and negative Brucella agglutination test.
Cerebrospinal fluid examination: protein is slightly higher than 0.
67 g/L (normal <0.
45), cell count is normal, glucose and chloride levels are normal, no oligoclonal bands, no abnormal cells.
Brain MRI: multiple cerebral infarctions in the left basal ganglia, left frontal, parietal, and temporal lobes.
Craniocerebral MRA: No obvious abnormalities.
Cardiac ultrasound: a 4.
7cm×2.
4cm mass echo can be seen in the left atrium, which is thrown to the ventricle during diastole, and returns to the atrium during systole.
The surface of the tumor is not smooth, indicating the presence of atrial myxoma.
Figure 1: The patient's brain MRI and MRAA.
The brain MRI showed that the blood supply area of the left anterior cerebral artery was scattered with high signal, and the blood supply area of the left middle cerebral artery was scattered with high signal (yellow dotted arrow).
B.
Brain MRA shows that the left anterior cerebral artery (red solid arrow), the left middle cerebral artery (red dotted arrow), and the intracranial segment of the left internal carotid artery (green arrow) have no obvious stenosis.
Figure 2: The patient’s cardiac echocardiography showed a 4.
7cm×2.
4cm mass echo in the left atrium, suggesting the presence of atrial myxoma.
What is the patient's final diagnosis? Combined with the patient's clinical manifestations, imaging examinations, cerebrospinal fluid and cardiac ultrasound examinations, the patient's final diagnosis was: left atrial myxoma caused multiple cerebral embolism.
Discussion Atrial myxoma is the most common primary cardiac tumor, accounting for about 50% of primary cardiac tumors.
Atrial myxoma is common in women, with a male-to-female ratio of 2:3, and it usually occurs between 30 and 60 years old, with an average age of 43 years.
The clinical manifestations of atrial myxoma are divided into three categories: ①Symptoms of mitral valve obstruction (65%): The tumor affects blood circulation in the heart cavity, resulting in various degrees of blood flow obstruction, resulting in a series of symptoms, such as palpitations, shortness of breath, Syncope and even heart failure.
②Arterial embolism symptoms (31%): Left atrial myxoma often causes systemic embolism.
The size of the tumor embolus and the embolization site are different, causing different symptoms.
Cerebral embolism mostly enters the anterior half of the basal artery ring, and middle cerebral artery embolism is the most common.
For this patient, multiple cerebral embolism is considered due to the shedding of a large tumor thrombus.
③ Systemic symptoms (34%): Patients with atrial myxoma often have fever, weight loss, loss of appetite, and joint pain.
Laboratory tests often find anemia and fast erythrocyte sedimentation rate.
Systemic symptoms may be related to the degeneration, bleeding, necrosis and autoimmune reaction of atrial myxoma.
.
For cerebral infarction in young people without risk factors for stroke, the possibility of atrial myxoma leading to cardiogenic cerebral embolism should be considered.
Cardiac ultrasonography is the first choice for atrial myxoma, and it is very important to understand the size, shape, and location of atrial myxoma.
Cerebral embolism caused by atrial myxoma is the most common form of thrombus shedding.
A small part of the emboli may originate from the tumor tissue itself.
Thrombolytic therapy can be considered for cerebral embolism at the very early stage (<6h).
The thrombolytic effect depends on the composition of the embolus.
Once the atrial myxoma is diagnosed, it should be surgically removed as soon as possible, and the echocardiography should be reviewed regularly to be alert to the possibility of atrial myxoma recurrence.
References: 1.
Lee VH, Connolly HM, Brown RD Jr.
Central nervous system manifestations of cardiac myxoma.
Archieves of neurology,2007,64:1115-1120.
2.
Yufe R,Karpati G,Carpenter S.
Cardiac myxoma:a diagnostic challenge for the neurologist.
Neurology,1976,26:1060-1065.
3.
Zhang Hong, Xie Zhongxiang, Che Fengyuan.
A case report of hyperacute thrombolysis of atrial myxomatous cerebral embolism.
Chinese Journal of Stroke.
2020, 15 (1): 89 .
-92.
4 Yuan cloud editor, "Neurology difficult cases" Beijing Science and technology Press text starting: the medical profession Neurology channel author: Liny paper review: Deputy Director Li Tu Ming, MD, editor: Mr.
Lu Li copyright notice paper original for reprint Welcome to contact for authorization-End-Call for papers.
Welcome to submit papers to the editor’s mailbox: yxjsjbx@yxj.
org.
cn.
Please specify: [Submission] Hospital + Department + Name Contributions are in the form of word files, and the remuneration is favorable.
Editor WeChat: chenaFF0911
