All cases of cerebral infarction and paralysis above, the diagnosis is quite different...

*Only for medical professionals to read and refer to the Neurological Archives: Layer by layer analysis to improve clinical thinking.
I believe everyone has heard of facial paralysis, but do you know that it is just a symptom, not a disease
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Facial paralysis is the same, but there are differences.
Do you know the difference between them? Do you know the cause of facial paralysis in patients with facial paralysis? Today we introduce 2 cases, both of which are cerebral infarction and paralysis.
Why is the first case with 2 diseases, and the second case with 1 disease? Case 1 is a male, 85 years old, with a history of coronary heart disease, hypertension, and diabetes.
He was admitted to the hospital with "slurred speech found 1.
5 hours" as the substitute complaint (the patient had a stroke after waking up, and the specific time of onset is unknown.
The family refused thrombolytic therapy.
Thrombolysis)
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Physical examination: slurred speech, symmetrical forehead lines on both sides, large cleft eyes, strong eyes closed, left nasolabial folds shallow, mouth angle slightly tilted to the right, tongue out in the center, limb muscle strength V, normal muscle tension, Positive Pap sign on both sides
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The head MRI is shown in Figure 1a, 1b: Figure 1a Figure 1b Figure 1: The left frontal punctate infarct was given antiplatelet, lipid-lowering and spot stabilization treatments.
The next day, the slurred speech basically returned to normal, and the angle of mouth was the same as before
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On the 3rd day, the patient felt that his left eye was incompletely closed, and the angle of mouth was more skewed than before
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Physical examination: clear speech, shallow left forehead lines, incomplete closure of left eye, shallow left nasolabial fold, angle of mouth skewed to the right, tongue in the middle, normal muscle tone of limbs, and positive Pap sign on both sides
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Re-examination of head MRI is shown in Figure 2a, 2b: Figure 2a Figure 2b Figure 2: Left frontal lobe and semi-oval center scattered with acute infarction Case 2 Female, 70 years old, previously healthy, with "dizziness, unstable walking for 9 hours "Admitted to the hospital
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Physical examination: clear speech, symmetrical bilateral frontal lines, large cleft eyes, strong eyes closed, large equal circles on both sides, sensitive light reflection, unrestricted eye movement in all directions, no nystagmus, right nasolabial fold Slightly shallow, the tongue is in the middle, the muscle strength of the four limbs is V grade, the muscle tension is normal, the right side limb paresis test is positive, the ataxia is normal, and the bilateral Pap sign is negative
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The head MRI is shown in Figure 3: Figure 3: Acute infarction on the left side of the pons.
Ask the above two cases to have facial paralysis, so what is the difference? Can they all be explained by the same disease? ■ Case 1 In case 1, the upper and lower facial expression muscles are paralyzed, which is called peripheral facial paralysis—refers to facial paralysis (lower motor neuron injury) caused by facial nerve nucleus or the facial nerve segments below it.
The lesion can be located in Intracranial, temporal bones, or parotid glands and other areas where the facial nerve runs
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Peripheral facial paralysis is not an independent disease.
It is a common symptom of many diseases.
The most common disease of peripheral facial paralysis is acute facial neuritis, which is mainly due to the damage of the facial nerve near the stomata foramen
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If the lesion is located in the facial nerve canal, the cord tympanic branch and the stapedial muscle branch are damaged, there will be loss of taste before the tongue, auditory hypersensitivity, peripheral facial paralysis with external auditory canal or tympanic herpes, which indicates that the geniculate ganglion herpes virus infection is called Hunt syndrome
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Secondly, the etiology includes trauma, chronic otitis media, tumor and stroke, etc.
The etiology and location are complicated
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■ Case 2 In case 2, only the facial expression muscles are paralyzed, which is called central facial paralysis—referring to damage to the area above the facial nucleus (upper motor neuron injury)
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The brainstem structure is complex and compact, and the cranial nerve nuclei and upper and lower conduction bundles are densely arranged.
Generally, the brainstem lesions involve the facial nucleus, and the adjacent structures of the lateral nucleus are often involved, often involving other cranial nerve nuclei and/or conduction.
Fiber, the corresponding symptoms appear
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Millard-Gubler syndrome involves the abducens nerve and facial nerve, and manifests as peripheral facial paralysis, abductor nerve palsy, and contralateral hemiplegia
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Foville syndrome is the occlusion of the deep perforating branch of the basilar artery involving the parapontine midline mesh structure and the pyramidal tract.
It is manifested as gaze paralysis toward the lesion side and contralateral hemiplegia
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If both cranial nerves are involved at the same time, it also suggests intra-brain stem disease, because the cranial nerve nuclei are easily affected at the same time because the cranial nerve nuclei are adjacent to each other
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Figure 4 Peripheral facial paralysis vs.
central facial paralysis [1] At this point, the diagnosis is announced.
I believe everyone should be very clear about the diagnosis of the above two cases! The first case was diagnosed as: acute cerebral infarction combined with acute facial neuritis on the left side
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Arteriosclerotic cerebral infarction with facial neuritis refers to facial nerve palsy within 17 days of the onset of cerebral infarction
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It has been reported in the literature that in 8 patients (middle-aged and elderly men are the majority), the onset time of the two diseases is 3-17 days apart, and most of them occur within 10 days.
From the overall prognosis, the disease course is long and the recovery is poor
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After the body suffers from cerebral infarction, the immune function is low and the resistance is reduced, causing viral infections, especially E, B virus, herpes zoster virus and measles virus infection, which invades the facial nerve and causes facial nerve demyelination changes
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In these 8 patients, facial neuritis mostly occurred on the opposite side of the cerebral infarction lesion.
It may be because the contralateral side has been suffering from central facial paralysis, and the function of facial expression muscles is lost or severely inhibited.
At this time, the facial nerve is more likely to be invaded by the virus and form a central nervous system.
Facial paralysis and peripheral facial paralysis mostly occur on the same side
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The second case was diagnosed as: infarction of the blood supply area of ​​the paramedian artery in the upper middle of the pons
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Because the lesion is above the facial nerve nucleus, it can cause central facial and tongue paralysis on the opposite side of the lesion.
This disease often manifests as numbness and weakness of the contralateral limb, central facial and tongue paralysis, and slurred speech
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There are no signs of crossover clinically, and it needs to be differentiated from hemiplegia caused by cerebral hemisphere lesions
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Well, through the above sharing, I believe you must have a better understanding of facial paralysis.
Different disease treatment principles are different.
Correct analysis is the prerequisite for the benefit of patients.
If the diagnosis is wrong, it is likely to cause delays in the condition
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Source: [1] WeChat public account "Medical Mito", a picture to understand Peripheral facial paralysis VS central facial paralysis, 2016-11-08 18:01