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The 3-minute reading column is updated once every two weeks, and highlights the wonderful cases of the past two weeks for everyone to learn and discuss
.
There are thunderous breakfast case studies for medical pulse nerves five working days a week, 3 short and succinct small cases every day, and 3 knowledge points every day
.
The collision of everyone's thoughts has produced countless sparks of wisdom.
They often wander in the group and gain new gains every day
.
Author: Lu Zhijie Case provided: Lu Huadong, Zhao Fengzhu, Zhao Haotian, Shao Mingtao, Lu Dandan, He Zhongyan, Cui Bo, Yu Hao, Zhao Yanping, Shi Dan, Ou Kaiyun, Liu Xinjian, Zhang Jingyan, Wang Jintao, Zhang Min, Case compilation of Dong Caixia, Song Guijun, Wang Jinqin, Li Yutao, Chen Haiting and others: Wang Shang, Miao Pingping, Zhou Ming, Fang Jingnian, Liu Xinjian, Liu Zhihong, Li Zhangxia, Liang Jiahui, Tan Lin, Zhao Qiong, Liu Liquan and other case 1 female patients, 65 years old The main reason was "fever for 4 days and confusion for 2 days"
.
Test: blood routine WBC: 9.
24X109/L, cerebrospinal fluid WBC: 102X106/L, protein 0.
52g/L
.
MRI of the head showed: the left thalamus, hippocampus, cerebral peduncle, and bilateral lateral ventricles had long T1 long T2 signals in the anterior and posterior horns, and the left thalamic lesions showed limited sand-like diffusion
.
Diagnosis: Japanese encephalitis
.
Discussion: Japanese encephalitis is a flavivirus encephalitis, the most common viral encephalitis in Asia, with a fatality rate of up to 60%.
The lesions involve the thalamus and brainstem, especially the substantia nigra, basal ganglia, and cortex.
And the cerebellum
.
MRI often manifests as bilateral thalamic lesions, with or without hemorrhage
.
According to the author's experience, the thalamus lesions of JE are not completely symmetrical, and one side is often more serious.
Combined with the clinical manifestations of infection, it is not difficult to distinguish from other symmetrical thalamus involvement
.
Case 2 is a 6-year-old girl with headache, poor spirits, increased sleep, and fatigue for 2 weeks
.
Cerebrospinal fluid WBC 52×106/L (70% mononuclear, 30% polynuclear), protein 0.
54g/L, sugar 2.
52mmol/L
.
MRI of the head showed: the left basal ganglia, the third ventricle, the bilateral thalamus occipital, the left occipital lobe, the frontal lobe, and the temporal cortex FLAIR high signal, no enhancement
.
Case 3, a 33-year-old male, chief complaint: progressive binocular vision loss for 10 days
.
MRI showed that the bilateral subcortical and deep white matter mostly diverged in flaky, round oval FLAIR hyperintensity
.
The basal ganglia and lateral ventricles were also affected
.
No reinforcement sequence is given
.
Case 2 and Case 3 diagnosis: MOG antibody-related disease (MOG-AD)
.
Case analysis: MOG antibody disease can be said to be a "net red disease" of neuroimaging, with strong clinical and imaging heterogeneity
.
Brain MRI manifestations are more diverse, the most common is ADEM-like changes, mainly scattered on the T2 image of the cortex/subcortex, deep nuclei and fibrous tracts of high signal.
After enhancement, the focus line and nodular enhancement can be seen
.
Compared with NMOSD, MOG-AD is more prone to leptomeningeal enhancement, cortical lesions, and deep nucleus lesions such as the thalamus
.
Domestic scholars reported that the proportion of subcortical white matter lesions and large-area lesions in MOG-AD was significantly higher than that of NMOSD
.
About 30% of patients can also involve subtentorial structures, and have symptoms of brainstem encephalitis such as dysarthria, diplopia, intractable hiccups, and peripheral facial palsy.
When the cerebellum is involved, it shows ataxia and nystagmus
.
It has been reported that cortical encephalitis has also become a characteristic manifestation of MOG antibody-related diseases, mostly manifested as seizures with or without encephalopathy
.
Some scholars call it FLAMES (FLAIR hyperintense cortical lesions in MOG associated Encephalitis with Seizures)
.
Case 2 is mainly involving the deep nucleus + cortex, and case 3 is mainly ADEM-like distribution, with a wide range of lesions and non-specific location
.
It is difficult to diagnose without antibody detection .
MOG antibody disease is a new "universal imitator" after neurosyphilis, and everyone should remain vigilant in clinical practice
.
Case 4 The patient was 33 years old, male, blurred vision for 2 months; found that white blood cells were low for half a year, 1-2*10^9/L, serum syphilis (+), ratio 1:1, cerebrospinal fluid syphilis (-), nucleated cells 6.
The pressure protein is normal
.
MRI showed: bilateral bridge arms, right thalamus, bilateral occipital subcortical white matter T2/FLAIR hyperintensity, mildly limited diffusion, no obvious enhancement
.
Supplementary information: HIV (+), CD4+ T cell count 2/ul, cerebrospinal fluid JC virus (+)
.
Diagnosis: Progressive multifocal leukoencephalopathy (PML)
.
PML is a rare disease in which the lytic infection of John Cunningham virus (JCV, a type of human papillary polyoma vacuolar virus) leads to the progressive destruction of oligodendrocytes in the central nervous system (CNS)
.
Usually in the case of systemic immunosuppression, dormant systemic JCV infection is reactivated
.
PML typically manifests as progressive cortical symptoms, such as paresis, cognitive decline, sensory impairment, gait disturbance, coordination difficulties, hemianopia, or aphasia
.
MRI usually manifests as single or multiple asymmetric white matter lesions, which are large in size, mostly involving arcuate fibers (U-shaped fibers), and space-occupying is rare
.
Typical PML lesions are not limited to the distribution area of a single vessel, and can fuse, involving multiple brain white matter
.
The lesion showed low signal on T1WI, high signal on T2WI and FLAIR, and there was generally no perifocal edema
.
The boundary of PML lesions toward the white matter side is unclear, but the boundary toward the cortex side is clear
.
The lesions are generally not enhanced
.
Case 5, a 58-year-old male patient, suffered a sudden syncope
.
Head MRI and monitoring ECG showed no obvious abnormalities
.
Perfect the vertebrobasilar artery CTA: CTA prompt: The left styloid process is too long (about 44mm), adjacent to the internal carotid artery
.
Diagnosis: Eagle syndrome/styloid hyoid syndrome/styloid-carotid syndrome
.
Case analysis: The normal length of the styloid process is about 2.
5 cm.
Any styloid process that exceeds 2.
5 cm may be considered too long
.
About 4% of the general population occasionally experience styloid process lengthening, but only about 4% of patients have symptoms attributable to styloid process lengthening; therefore, the true incidence is about 0.
16%, and the ratio of women to men is 3: 1
.
Excessively long styloid process can cause two major types of clinical manifestations: First, the elongated styloid process will compress the cranial nerve, the most common is the glossopharyngeal nerve, followed by throat and neck pain
.
Second, the styloid process may compress the internal carotid artery, which can cause a transient ischemic attack or compress the sympathetic nerves along the artery, leading to a series of symptoms such as syncope
.
It can be treated conservatively (mean effect) or surgery (not easy)
.
Case 6 is a male patient, 45 years old, with general fatigue for 2 weeks
.
Physical examination: dysarthria, ataxia, vertical and horizontal nystagmus
.
Head MRI showed: FLAIR high signal at the top of the cerebellar hemispheres and lateral temporal lobe on both sides, with mild diffusion limited
.
Supplementary medical history: The patient has long-term heavy alcohol abuse and low blood thiamine levels
.
Diagnosis: Wernicke encephalopathy (WE) involving the cerebellum
.
Case 7 is a 53-year-old male with main complaint: dizziness and unstable walking for 1 month
.
A history of heavy drinking for more than 20 years
.
Head MRI showed that the entire corpus callosum was diffusely restricted and ADC reversed, suggesting cytotoxic edema
.
Diagnosis: Primary corpus callosum degeneration (MBD)
.
Case analysis of 6 and 7: Alcoholism is a common cause of thiamine deficiency, and the latter is the direct cause of acute and chronic alcoholic encephalopathy.
Acute injuries include wernicke encephalopathy and primary corpus callosum degeneration
.
The former is manifested in neuropathology and imaging as lesions of the periventricular, hypothalamic nucleus, tectorial plate, and thalamus.
The main clinical manifestations are ophthalmoplegia, nystagmus, ataxia, and confusion
.
The cerebellum is not a common site of acute WE.
In chronic alcoholic encephalopathy, cerebellar atrophy is common
.
The main manifestation of MBD is cytotoxic edema involving the corpus callosum.
The lesions are symmetrical and do not conform to the anterior distribution of the brain
.
Simple involvement of the corpus callosum is type I, and deep white matter is type II
.
The following figure shows the corresponding relationship between the injury site and the clinic
.
It can be said to have a drink, and it hurts the body and the brain when drunk
.
Case 8 is a female patient, 32 years old, a worker
.
He was admitted to the hospital for 1 week due to poor speech and numbness and weakness of both lower limbs
.
Head MRI: bilateral subcortical white matter is extensively affected, T2 hyperintensity, limited diffusion, and U-shaped fibers are involved
.
Diagnosis: benzene poisoning
.
Benzene is an organic solvent that can cause acute or chronic poisoning
.
Benzene toxic encephalopathy means that a large amount of benzene or xylene quickly enters the body in a short period of time, causing severe organic and functional damage to the CNS
.
Urophenol determination, especially >10mg/L, suggests benzene exposure.
The normal value of domestic urophenol: 132-253umol/L (12.
4-23.
8mg/L)
.
Typical imaging findings: Head CT, especially magnetic resonance examination, FLAIR sequence, diffuse symmetrical high signal, showing characteristic "sunflower"-like vasogenic edema, enhanced without enhancement
.
Case 9 The patient is 18 years old and male.
The chief complaint: dizziness, slurred speech, and unsteady walking for 7 days
.
Head MRI: Diffuse FLAIR hyperintensity in the pons, showing gravel-like and pepper-like enhancement
.
Re-examination after hormone therapy: the lesions were significantly reduced
.
Diagnosis: steroid hormone-responsive chronic lymphocytic inflammation with peri-pontine enhancement syndrome (CLIPPERS)
.
Case analysis: CLIPPERS is a very rare inflammatory disease of the central nervous system that is effective for corticosteroid therapy.
The pathological changes mainly involve the pons, cerebellum and spinal cord.
Pathologically, it is mainly infiltrated by CD3+ T lymphocytes.
The enhanced lesions on MRI "Curve-like" and "pepper-salt"-like special enhancements, the lesions spreading to the supratentorial are rare, and in most cases the lesions are located in the cerebellum and brain stem
.
References: [1] Zhao Cong, Li Zhuyi.
Research progress in diseases related to myelin oligodendrocyte glycoprotein antibody[J].
Chinese Journal of Neuroimmunology and Neurology,2021,28(01):71-74 .
[2] Maria R.
Bokhari et.
Eagle Syndrome.
StatPearls.
[3] Nat Rev Neurol.
2011.
5; 7(5):284-94.
.
There are thunderous breakfast case studies for medical pulse nerves five working days a week, 3 short and succinct small cases every day, and 3 knowledge points every day
.
The collision of everyone's thoughts has produced countless sparks of wisdom.
They often wander in the group and gain new gains every day
.
Author: Lu Zhijie Case provided: Lu Huadong, Zhao Fengzhu, Zhao Haotian, Shao Mingtao, Lu Dandan, He Zhongyan, Cui Bo, Yu Hao, Zhao Yanping, Shi Dan, Ou Kaiyun, Liu Xinjian, Zhang Jingyan, Wang Jintao, Zhang Min, Case compilation of Dong Caixia, Song Guijun, Wang Jinqin, Li Yutao, Chen Haiting and others: Wang Shang, Miao Pingping, Zhou Ming, Fang Jingnian, Liu Xinjian, Liu Zhihong, Li Zhangxia, Liang Jiahui, Tan Lin, Zhao Qiong, Liu Liquan and other case 1 female patients, 65 years old The main reason was "fever for 4 days and confusion for 2 days"
.
Test: blood routine WBC: 9.
24X109/L, cerebrospinal fluid WBC: 102X106/L, protein 0.
52g/L
.
MRI of the head showed: the left thalamus, hippocampus, cerebral peduncle, and bilateral lateral ventricles had long T1 long T2 signals in the anterior and posterior horns, and the left thalamic lesions showed limited sand-like diffusion
.
Diagnosis: Japanese encephalitis
.
Discussion: Japanese encephalitis is a flavivirus encephalitis, the most common viral encephalitis in Asia, with a fatality rate of up to 60%.
The lesions involve the thalamus and brainstem, especially the substantia nigra, basal ganglia, and cortex.
And the cerebellum
.
MRI often manifests as bilateral thalamic lesions, with or without hemorrhage
.
According to the author's experience, the thalamus lesions of JE are not completely symmetrical, and one side is often more serious.
Combined with the clinical manifestations of infection, it is not difficult to distinguish from other symmetrical thalamus involvement
.
Case 2 is a 6-year-old girl with headache, poor spirits, increased sleep, and fatigue for 2 weeks
.
Cerebrospinal fluid WBC 52×106/L (70% mononuclear, 30% polynuclear), protein 0.
54g/L, sugar 2.
52mmol/L
.
MRI of the head showed: the left basal ganglia, the third ventricle, the bilateral thalamus occipital, the left occipital lobe, the frontal lobe, and the temporal cortex FLAIR high signal, no enhancement
.
Case 3, a 33-year-old male, chief complaint: progressive binocular vision loss for 10 days
.
MRI showed that the bilateral subcortical and deep white matter mostly diverged in flaky, round oval FLAIR hyperintensity
.
The basal ganglia and lateral ventricles were also affected
.
No reinforcement sequence is given
.
Case 2 and Case 3 diagnosis: MOG antibody-related disease (MOG-AD)
.
Case analysis: MOG antibody disease can be said to be a "net red disease" of neuroimaging, with strong clinical and imaging heterogeneity
.
Brain MRI manifestations are more diverse, the most common is ADEM-like changes, mainly scattered on the T2 image of the cortex/subcortex, deep nuclei and fibrous tracts of high signal.
After enhancement, the focus line and nodular enhancement can be seen
.
Compared with NMOSD, MOG-AD is more prone to leptomeningeal enhancement, cortical lesions, and deep nucleus lesions such as the thalamus
.
Domestic scholars reported that the proportion of subcortical white matter lesions and large-area lesions in MOG-AD was significantly higher than that of NMOSD
.
About 30% of patients can also involve subtentorial structures, and have symptoms of brainstem encephalitis such as dysarthria, diplopia, intractable hiccups, and peripheral facial palsy.
When the cerebellum is involved, it shows ataxia and nystagmus
.
It has been reported that cortical encephalitis has also become a characteristic manifestation of MOG antibody-related diseases, mostly manifested as seizures with or without encephalopathy
.
Some scholars call it FLAMES (FLAIR hyperintense cortical lesions in MOG associated Encephalitis with Seizures)
.
Case 2 is mainly involving the deep nucleus + cortex, and case 3 is mainly ADEM-like distribution, with a wide range of lesions and non-specific location
.
It is difficult to diagnose without antibody detection .
MOG antibody disease is a new "universal imitator" after neurosyphilis, and everyone should remain vigilant in clinical practice
.
Case 4 The patient was 33 years old, male, blurred vision for 2 months; found that white blood cells were low for half a year, 1-2*10^9/L, serum syphilis (+), ratio 1:1, cerebrospinal fluid syphilis (-), nucleated cells 6.
The pressure protein is normal
.
MRI showed: bilateral bridge arms, right thalamus, bilateral occipital subcortical white matter T2/FLAIR hyperintensity, mildly limited diffusion, no obvious enhancement
.
Supplementary information: HIV (+), CD4+ T cell count 2/ul, cerebrospinal fluid JC virus (+)
.
Diagnosis: Progressive multifocal leukoencephalopathy (PML)
.
PML is a rare disease in which the lytic infection of John Cunningham virus (JCV, a type of human papillary polyoma vacuolar virus) leads to the progressive destruction of oligodendrocytes in the central nervous system (CNS)
.
Usually in the case of systemic immunosuppression, dormant systemic JCV infection is reactivated
.
PML typically manifests as progressive cortical symptoms, such as paresis, cognitive decline, sensory impairment, gait disturbance, coordination difficulties, hemianopia, or aphasia
.
MRI usually manifests as single or multiple asymmetric white matter lesions, which are large in size, mostly involving arcuate fibers (U-shaped fibers), and space-occupying is rare
.
Typical PML lesions are not limited to the distribution area of a single vessel, and can fuse, involving multiple brain white matter
.
The lesion showed low signal on T1WI, high signal on T2WI and FLAIR, and there was generally no perifocal edema
.
The boundary of PML lesions toward the white matter side is unclear, but the boundary toward the cortex side is clear
.
The lesions are generally not enhanced
.
Case 5, a 58-year-old male patient, suffered a sudden syncope
.
Head MRI and monitoring ECG showed no obvious abnormalities
.
Perfect the vertebrobasilar artery CTA: CTA prompt: The left styloid process is too long (about 44mm), adjacent to the internal carotid artery
.
Diagnosis: Eagle syndrome/styloid hyoid syndrome/styloid-carotid syndrome
.
Case analysis: The normal length of the styloid process is about 2.
5 cm.
Any styloid process that exceeds 2.
5 cm may be considered too long
.
About 4% of the general population occasionally experience styloid process lengthening, but only about 4% of patients have symptoms attributable to styloid process lengthening; therefore, the true incidence is about 0.
16%, and the ratio of women to men is 3: 1
.
Excessively long styloid process can cause two major types of clinical manifestations: First, the elongated styloid process will compress the cranial nerve, the most common is the glossopharyngeal nerve, followed by throat and neck pain
.
Second, the styloid process may compress the internal carotid artery, which can cause a transient ischemic attack or compress the sympathetic nerves along the artery, leading to a series of symptoms such as syncope
.
It can be treated conservatively (mean effect) or surgery (not easy)
.
Case 6 is a male patient, 45 years old, with general fatigue for 2 weeks
.
Physical examination: dysarthria, ataxia, vertical and horizontal nystagmus
.
Head MRI showed: FLAIR high signal at the top of the cerebellar hemispheres and lateral temporal lobe on both sides, with mild diffusion limited
.
Supplementary medical history: The patient has long-term heavy alcohol abuse and low blood thiamine levels
.
Diagnosis: Wernicke encephalopathy (WE) involving the cerebellum
.
Case 7 is a 53-year-old male with main complaint: dizziness and unstable walking for 1 month
.
A history of heavy drinking for more than 20 years
.
Head MRI showed that the entire corpus callosum was diffusely restricted and ADC reversed, suggesting cytotoxic edema
.
Diagnosis: Primary corpus callosum degeneration (MBD)
.
Case analysis of 6 and 7: Alcoholism is a common cause of thiamine deficiency, and the latter is the direct cause of acute and chronic alcoholic encephalopathy.
Acute injuries include wernicke encephalopathy and primary corpus callosum degeneration
.
The former is manifested in neuropathology and imaging as lesions of the periventricular, hypothalamic nucleus, tectorial plate, and thalamus.
The main clinical manifestations are ophthalmoplegia, nystagmus, ataxia, and confusion
.
The cerebellum is not a common site of acute WE.
In chronic alcoholic encephalopathy, cerebellar atrophy is common
.
The main manifestation of MBD is cytotoxic edema involving the corpus callosum.
The lesions are symmetrical and do not conform to the anterior distribution of the brain
.
Simple involvement of the corpus callosum is type I, and deep white matter is type II
.
The following figure shows the corresponding relationship between the injury site and the clinic
.
It can be said to have a drink, and it hurts the body and the brain when drunk
.
Case 8 is a female patient, 32 years old, a worker
.
He was admitted to the hospital for 1 week due to poor speech and numbness and weakness of both lower limbs
.
Head MRI: bilateral subcortical white matter is extensively affected, T2 hyperintensity, limited diffusion, and U-shaped fibers are involved
.
Diagnosis: benzene poisoning
.
Benzene is an organic solvent that can cause acute or chronic poisoning
.
Benzene toxic encephalopathy means that a large amount of benzene or xylene quickly enters the body in a short period of time, causing severe organic and functional damage to the CNS
.
Urophenol determination, especially >10mg/L, suggests benzene exposure.
The normal value of domestic urophenol: 132-253umol/L (12.
4-23.
8mg/L)
.
Typical imaging findings: Head CT, especially magnetic resonance examination, FLAIR sequence, diffuse symmetrical high signal, showing characteristic "sunflower"-like vasogenic edema, enhanced without enhancement
.
Case 9 The patient is 18 years old and male.
The chief complaint: dizziness, slurred speech, and unsteady walking for 7 days
.
Head MRI: Diffuse FLAIR hyperintensity in the pons, showing gravel-like and pepper-like enhancement
.
Re-examination after hormone therapy: the lesions were significantly reduced
.
Diagnosis: steroid hormone-responsive chronic lymphocytic inflammation with peri-pontine enhancement syndrome (CLIPPERS)
.
Case analysis: CLIPPERS is a very rare inflammatory disease of the central nervous system that is effective for corticosteroid therapy.
The pathological changes mainly involve the pons, cerebellum and spinal cord.
Pathologically, it is mainly infiltrated by CD3+ T lymphocytes.
The enhanced lesions on MRI "Curve-like" and "pepper-salt"-like special enhancements, the lesions spreading to the supratentorial are rare, and in most cases the lesions are located in the cerebellum and brain stem
.
References: [1] Zhao Cong, Li Zhuyi.
Research progress in diseases related to myelin oligodendrocyte glycoprotein antibody[J].
Chinese Journal of Neuroimmunology and Neurology,2021,28(01):71-74 .
[2] Maria R.
Bokhari et.
Eagle Syndrome.
StatPearls.
[3] Nat Rev Neurol.
2011.
5; 7(5):284-94.
