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It is only for medical professionals to read.
Different symptoms of the same disease: midbrain infarction is manifested as Wernekink's commissure syndrome.
1 case of midbrain important anatomical structures include the superior colliculus, inferior colliculus and substantia nigra, as well as the red nucleus and the oculomotor nucleus And medial longitudinal beam (see Figure 1).
The most common manifestation of midbrain infarction is diplopia and paralysis of the contralateral limb.
Figure 1: Midbrain anatomy The midbrain infarction case shared with you today, in addition to the common extraocular muscle palsy, is also accompanied by bilateral limb ataxia and slurred speech.
Next, let the Xinhua Hospital affiliated to Dalian University get nervous Director of Internal Medicine Tang Wei, let's analyze the special brainstem syndrome! Case presentation: A 45-year-old male was admitted to the hospital with dizziness, nausea, vomiting and slurred speech for 20 hours.
When the patient was playing cards with a friend 20 hours ago, the patient suddenly experienced dizziness, nausea and vomiting, non-jetting, with slurred speech, double vision, difficulty in completing fine movements, unconscious disturbance, no limb numbness, no headache, convulsions, and noness Diarrhea.
In the local hospital, there was no obvious abnormality in the head CT, and the outpatient was admitted to the hospital with a "dizziness investigation".
Previously healthy, denying history of high blood pressure and diabetes.
Physical examination: Consciousness, poem-like language, varying in tone, explosive.
The calculation power is normal.
Bilateral pupils are 3mm, equal circle, slightly slow to light reflection, diplopia, limited adduction in both eyes, and sufficient movement in other directions.
I cranial nerve (-).
Extremities muscle strength and muscle tension are normal, bilateral finger nose test, rotation test, heel knee tibia test are positive, Romberg sign cannot cooperate, deep and shallow sensation is normal, autonomic nerves are normal, abdominal wall reflex (-), extremity tendon reflex (+++ ), meningeal irritation sign (-), bilateral pathological sign (-).
Auxiliary examination: MRI of the head showed: acute midbrain infarction, DWI showed high signal in front of the aqueduct at the lower part of the right midbrain level, and low signal in ADC phase (see Figure 2).
Figure 2: MRI of the head; DWI shows the high signal in front of the aqueduct at the lower part of the right midbrain level, and the ADC phase low signal localization diagnosis: the patient mainly presents with bilateral trunk and limb ataxia and dysarthria.
No deep sensory impairment, no frontal lobe damage and other manifestations, so it is consistent with bilateral cerebellar ataxia.
Diplopia, limited adduction in both eyes, is located in bilateral medial rectus nucleus damage.
Qualitative diagnosis: middle-aged man with acute onset, bilateral cerebellar ataxia and nuclear ophthalmoplegia.
There are risk factors for high blood pressure and smoking in the past.
There were no signs of high density on the admission cranial CT.
DWI showed high signal in the front of the aqueduct at the lower part of the right midbrain level and low signal in ADC phase.
The diagnosis was acute midbrain infarction and Wernekink's commissure syndrome.
Discussion 1.
Anatomy of Wernekink's commissure The nerve fibers from the cerebellar dentate nucleus pass through the upper foot of the cerebellum, and cross to the contralateral red nucleus in the midbrain aqueduct in front of the midbrain aqueduct.
This crossing is called the Wernekink commissure.
The impulses of the cerebral cortex reach the pontine nucleus on the same side as the cortex through the cortical pons, and then the pontine nucleus sends out the pontine cerebellar tract, which passes through the midfoot of the cerebellum to the contralateral neocerebellum.
Then the new cerebellum sends out fibers, after being replaced by the dentate nucleus, it leaves the cerebellum through the upper foot of the cerebellum, reaches the midbrain, crosses through the midbrain Wernekink junction to reach the contralateral red nucleus, passes through the red nucleus-thalamus (preventral nucleus, ventrolateral (Nucleus)-cortical tracts to inhibit the voluntary movement of the cortex (see Figure 3), so as to achieve braking and coordination, and prevent excessive movement of the limbs.
The pathway between the neocerebellum and the Wernekink commissure (one side of the new cerebellum, dentate nucleus → upper foot of the cerebellum → before the Wernekink commissure) will have ipsilateral limb ataxia after injury.
After Wernekink commissure, the pathway to the cortex is damaged (after Wernekink commissure → red nucleus → ventral prothalamic nucleus and abdominal intermediate nucleus → cortex) after injury, contralateral limb ataxia will occur, and Wernekink commissure lesions will appear double Ataxia of the lateral limbs.
Figure 3: Anatomy of the Wernekink commissure in the coronal position Figure 4: Anatomy of the Wernekink commissure of the midbrain Figure 5: Anatomy of the Wernekink commissure in a cross section of the midbrain 2.
Wernekink commissure syndrome Levy.
The lesion is located in the midbrain area in front of the midbrain aqueduct.
The typical clinical manifestations are bilateral cerebellar ataxia, with or without extraocular muscle palsy, palatine myoclonus, and lethargy.
Cerebellar ataxia lesions are not only located in the cerebellum, but the efferent fibers (Figure 4) that are relayed by the dentate nucleus can also be affected as cerebellar ataxia.
If the disease is located in the midbrain Wernekink commissure area .
Case analysis has consolidated the anatomy of the nervous system and deepened the understanding of the disease.
Figure 6: Head MRI axial position Wernekink's commissure syndrome injury area This patient's Wenekink's commissure syndrome is considered to be caused by the occlusion of the median perforating branch of the basilar artery.
Wernekink's commissure syndrome may be accompanied by eye movement disorders and soft palate clonus.
As the bilateral parapontine midline structure sends out ascending fibers to reach the contralateral oculomotor nerve inner rectus subnucleus, and the ascending fibers converge near the Wernekink commissure area.
When the Wernekink commissure area is damaged, the ascending fiber converging area can be affected, and then There is limited adduction in the eyes.
Figure 7: Anatomy of the midbrain oculomotor nucleus 3.
Differential diagnosis (1) Wernicke encephalopathy Wernicke encephalopathy often involves the Wernekink commissure area, and similar manifestations of Wernekink commissure syndrome appear.
This patient had no history of long-term alcohol abuse, gastrointestinal surgery, fasting, and malnutrition, so Wernicke encephalopathy was not considered.
(2) Optic neuromyelitis Optic neuromyelitis can also affect the Wernekink commissure, but generally involves a wider range, such as the medial thalamus, optic nerve, and posterior area.
Patients may have clinical manifestations such as vision changes, spinal cord symptoms, intractable vomiting, and hiccups.
The patient had no similar clinical manifestations, and his symptoms improved after antiplatelet therapy, so neuromyelitis optica was not considered.
(3) Patients with Wenekink's commissure syndrome whose other diseases begin with acute bilateral cerebellar ataxia and eye dysfunction also need to be differentiated from acute cerebellitis, Fisher syndrome, and Bickerstaff brainstem encephalitis.
The patient has no history of pre-infection, unconscious and mental changes, and normal tendon reflexes.
The above diseases can basically be ruled out.
Different symptoms of the same disease: midbrain infarction is manifested as Wernekink's commissure syndrome.
1 case of midbrain important anatomical structures include the superior colliculus, inferior colliculus and substantia nigra, as well as the red nucleus and the oculomotor nucleus And medial longitudinal beam (see Figure 1).
The most common manifestation of midbrain infarction is diplopia and paralysis of the contralateral limb.
Figure 1: Midbrain anatomy The midbrain infarction case shared with you today, in addition to the common extraocular muscle palsy, is also accompanied by bilateral limb ataxia and slurred speech.
Next, let the Xinhua Hospital affiliated to Dalian University get nervous Director of Internal Medicine Tang Wei, let's analyze the special brainstem syndrome! Case presentation: A 45-year-old male was admitted to the hospital with dizziness, nausea, vomiting and slurred speech for 20 hours.
When the patient was playing cards with a friend 20 hours ago, the patient suddenly experienced dizziness, nausea and vomiting, non-jetting, with slurred speech, double vision, difficulty in completing fine movements, unconscious disturbance, no limb numbness, no headache, convulsions, and noness Diarrhea.
In the local hospital, there was no obvious abnormality in the head CT, and the outpatient was admitted to the hospital with a "dizziness investigation".
Previously healthy, denying history of high blood pressure and diabetes.
Physical examination: Consciousness, poem-like language, varying in tone, explosive.
The calculation power is normal.
Bilateral pupils are 3mm, equal circle, slightly slow to light reflection, diplopia, limited adduction in both eyes, and sufficient movement in other directions.
I cranial nerve (-).
Extremities muscle strength and muscle tension are normal, bilateral finger nose test, rotation test, heel knee tibia test are positive, Romberg sign cannot cooperate, deep and shallow sensation is normal, autonomic nerves are normal, abdominal wall reflex (-), extremity tendon reflex (+++ ), meningeal irritation sign (-), bilateral pathological sign (-).
Auxiliary examination: MRI of the head showed: acute midbrain infarction, DWI showed high signal in front of the aqueduct at the lower part of the right midbrain level, and low signal in ADC phase (see Figure 2).
Figure 2: MRI of the head; DWI shows the high signal in front of the aqueduct at the lower part of the right midbrain level, and the ADC phase low signal localization diagnosis: the patient mainly presents with bilateral trunk and limb ataxia and dysarthria.
No deep sensory impairment, no frontal lobe damage and other manifestations, so it is consistent with bilateral cerebellar ataxia.
Diplopia, limited adduction in both eyes, is located in bilateral medial rectus nucleus damage.
Qualitative diagnosis: middle-aged man with acute onset, bilateral cerebellar ataxia and nuclear ophthalmoplegia.
There are risk factors for high blood pressure and smoking in the past.
There were no signs of high density on the admission cranial CT.
DWI showed high signal in the front of the aqueduct at the lower part of the right midbrain level and low signal in ADC phase.
The diagnosis was acute midbrain infarction and Wernekink's commissure syndrome.
Discussion 1.
Anatomy of Wernekink's commissure The nerve fibers from the cerebellar dentate nucleus pass through the upper foot of the cerebellum, and cross to the contralateral red nucleus in the midbrain aqueduct in front of the midbrain aqueduct.
This crossing is called the Wernekink commissure.
The impulses of the cerebral cortex reach the pontine nucleus on the same side as the cortex through the cortical pons, and then the pontine nucleus sends out the pontine cerebellar tract, which passes through the midfoot of the cerebellum to the contralateral neocerebellum.
Then the new cerebellum sends out fibers, after being replaced by the dentate nucleus, it leaves the cerebellum through the upper foot of the cerebellum, reaches the midbrain, crosses through the midbrain Wernekink junction to reach the contralateral red nucleus, passes through the red nucleus-thalamus (preventral nucleus, ventrolateral (Nucleus)-cortical tracts to inhibit the voluntary movement of the cortex (see Figure 3), so as to achieve braking and coordination, and prevent excessive movement of the limbs.
The pathway between the neocerebellum and the Wernekink commissure (one side of the new cerebellum, dentate nucleus → upper foot of the cerebellum → before the Wernekink commissure) will have ipsilateral limb ataxia after injury.
After Wernekink commissure, the pathway to the cortex is damaged (after Wernekink commissure → red nucleus → ventral prothalamic nucleus and abdominal intermediate nucleus → cortex) after injury, contralateral limb ataxia will occur, and Wernekink commissure lesions will appear double Ataxia of the lateral limbs.
Figure 3: Anatomy of the Wernekink commissure in the coronal position Figure 4: Anatomy of the Wernekink commissure of the midbrain Figure 5: Anatomy of the Wernekink commissure in a cross section of the midbrain 2.
Wernekink commissure syndrome Levy.
The lesion is located in the midbrain area in front of the midbrain aqueduct.
The typical clinical manifestations are bilateral cerebellar ataxia, with or without extraocular muscle palsy, palatine myoclonus, and lethargy.
Cerebellar ataxia lesions are not only located in the cerebellum, but the efferent fibers (Figure 4) that are relayed by the dentate nucleus can also be affected as cerebellar ataxia.
If the disease is located in the midbrain Wernekink commissure area .
Case analysis has consolidated the anatomy of the nervous system and deepened the understanding of the disease.
Figure 6: Head MRI axial position Wernekink's commissure syndrome injury area This patient's Wenekink's commissure syndrome is considered to be caused by the occlusion of the median perforating branch of the basilar artery.
Wernekink's commissure syndrome may be accompanied by eye movement disorders and soft palate clonus.
As the bilateral parapontine midline structure sends out ascending fibers to reach the contralateral oculomotor nerve inner rectus subnucleus, and the ascending fibers converge near the Wernekink commissure area.
When the Wernekink commissure area is damaged, the ascending fiber converging area can be affected, and then There is limited adduction in the eyes.
Figure 7: Anatomy of the midbrain oculomotor nucleus 3.
Differential diagnosis (1) Wernicke encephalopathy Wernicke encephalopathy often involves the Wernekink commissure area, and similar manifestations of Wernekink commissure syndrome appear.
This patient had no history of long-term alcohol abuse, gastrointestinal surgery, fasting, and malnutrition, so Wernicke encephalopathy was not considered.
(2) Optic neuromyelitis Optic neuromyelitis can also affect the Wernekink commissure, but generally involves a wider range, such as the medial thalamus, optic nerve, and posterior area.
Patients may have clinical manifestations such as vision changes, spinal cord symptoms, intractable vomiting, and hiccups.
The patient had no similar clinical manifestations, and his symptoms improved after antiplatelet therapy, so neuromyelitis optica was not considered.
(3) Patients with Wenekink's commissure syndrome whose other diseases begin with acute bilateral cerebellar ataxia and eye dysfunction also need to be differentiated from acute cerebellitis, Fisher syndrome, and Bickerstaff brainstem encephalitis.
The patient has no history of pre-infection, unconscious and mental changes, and normal tendon reflexes.
The above diseases can basically be ruled out.
