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Cerebral infarction is one of the most common diseases in the nervous system, different parts of the brain infarction will appear completely different signs and symptoms, and according to the patient's symptoms, signs and accurate positioning diagnosis is a necessary skill for neurologists, this article, the author summarizes the positioning points of common pontine syndrome, let's first look at a case to familiarize.
1 Patient imaging results (provided by the author) 7
years of previous cerebral infarction history, no obvious sequelae, 7 years history of hypertension, blood pressure up to 180/mmHg, type 2 diabetes mellitus for more than 2 years, self-reported poor blood sugar control, denial of coronary heart history, family history, personal history is not special
.
▌Physical examination:
clear mind, lack of fluency in speech, reaction, double pupils are equal to circles, sensitive to light reflection, both eyeballs gaze to the left, right eye abduction can not be, horizontal tremor, right forehead line becomes shallow, right eye closure is weak, right nasolabial fold becomes shallow, the mouth corner of the teeth is left, the tongue is extended to the right, the muscle tone of the limbs is normal, the muscle strength of the left limb is grade 3, The muscle strength of the right limb is grade 5, the left biceps and triceps tendon reflexes are more active than the right side, and the bilateral babinskin sign is negative, and the meningeal irritation sign is negative
.
Biochemical items: total protein 58.
3g/L, albumin 37.
g/L, fasting blood glucose 19.
39mmol/L, triglycerides: 3.
88mmol/L, high-density lipoprotein 1.
11mmol/L, low-density lipoprotein 3.
33mmol/L, homocysteine 17.
00μmol/L, glycated hemoglobin 10.
9mm/L
。 There were no obvious abnormalities
in hematuria and stool routine, six thyroid functions, all male tumors, and five coagulation.
Positioning diagnosis:
Fig.
2 Positioning diagnosis
summary, contralateral hemiplegia (pyramidal tract involvement); Inability to abduct the eyeball on the side of the lesion (abductor nerve involvement); Paralysis of staring at the lesion side of both eyes is Fowier syndrome
in pontine infarction.
Qualitative diagnosis: The patient is an elderly man with a history of high-risk factors for cerebrovascular diseases such as cerebral infarction, hypertension, and diabetes, and the head DWI on admission indicates acute or subacute cerebral infarction of the pons, so it is characterized as ischemic cerebrovascular disease
.
In terms of treatment, comprehensive treatment
such as anti-platelet aggregation, lipid lowering and plaque stabilization, anticoagulation, opening collateral circulation, removing oxygen free radicals, controlling blood pressure and blood sugar, activating blood and removing stasis are given.
There are more pontine syndromes, and it is more difficult to remember, and the following is sorted out according to its typical symptoms and signs, so as to facilitate memory
.
We can sort
by location.
From front to back, damage to the ventrolateral part of the pons may present with abductor nerve and facial nerve palsy-hemiplegia syndrome (Millard-Gubler syndrome), damage in the ventral medial part of the pons may present with Fowel syndrome, damage in the dorsolateral part of the pons may present with Raymond-Cestan syndrome, and bilateral lesions at the base of the pons , locked-in syndrome may occur [1].
the plane of the lower pons.
Fig.
3 Ventrolateral pontine syndrome[2]
(1) involves dilated nerve root fibers, and the lesion is paralyzed laterally abducted and the eyeball cannot be abducted, and is in the internal oblique position
.
(2) Subnuclear paralysis of the facial nerve is involved, that is, complete facial paralysis
on the lesion side.
(3) Involvement of the pyramidal tract, causing central paralysis
of the contralateral upper and lower limbs.
(4) Involving the medial thalamus and the myelothalamic tract, because the two intersect in the medial thalamic system of the medulla oblongata and intersect in front of the white matter of the spinal cord, respectively, it causes the deep sensation of the contralateral limb of the lesion to decrease or disappear; Superficial sensation in the contralateral heminess diminishes or disappears
.
The causes of Millard-Gubler syndrome are often inflammatory foci, tumors (glial nodules, gliomas), plaques of multiple sclerosis
.
Cerebrovascular disease is less
commonly caused.
In conclusion, the lesion is located in the ventrolateral part of the pons, close to the medulla oblongata, and damages the abductor nerve, facial nerve, pyramidal tract, spinosamic tract, and medial thalamus
.
Manifested as: 1 lateral abduction nerve palsy; 2 contralateral central hemiplegia; 3 Contralateral hemisensory impairment
may occur.
of the lesion.
Fig.
4 Pontine ventral medial syndrome[2]
(1) Contralateral hemiplegia (pyramidal tract involvement) (2) Inability to abduct the eyeball on the lesion side (abductor nerve involvement)
(3) Paralysis of the gaze of both eyes to the side of the lesion (the result of damage to the abductor nerve nucleus or its root fibers and PPRF, because the abductor nerve nucleus and root fibers and PPRF participate in the sympathic fixation mechanism of the two eyes, not paralysis of the medial rectus muscle of the contralateral eyeball, because when the two eyes are cohesive, the contralateral eyeball can still adduct.
The cause of Fowwer's syndrome is cerebrovascular disease most common, because there is less collateral circulation in the paramedian artery, and cerebral infarction is predisposed to
.
Can also be caused
by tumors and inflammation.
.
Involving vestibular, span, facial nerve nuclei, medial longitudinal tract, cerebellar midfoot, medial thalamus and other structures, seen in the upper cerebellar artery or inferior anterior cerebellar artery blockage, manifested as:
(1) vertigo, nausea, vomiting, nystagmus (vestibular nerve nucleus damage);
(2) The affected side of the eyeball cannot be abducted (abductor nerve damage);
(3) Lateral muscle paralysis (facial nerve nuclear damage);
(4) Inability to fixate on the affected side of both eyes (damage to the pontine lateral visual center and medial longitudinal tract);
(5) Cross-cutting sensory disorders, that is, ipsilateral pain, loss of temperature perception (trigeminal nerve spinal tract damage), contralateral migraine pain, temperature loss or loss (lateral fascicular tract damage of the myelochalus);
(6) Decreased or lost sense of touch, position, and vibration of the contralateral body (medial thalamus damage);
(7) Horner sign on the affected side (sympathetic descending fiber damage);
(8) Hemibody ataxia on the affected side (damage to the cerebellar middle foot, the lower cerebellar foot and the anterior fascicular fascicular tract of the spinal cord).
Fig.
5 Pontine undercover syndrome[2].
the bilateral pons.
Bilateral cortical pontine tracts, cortical medullary tracts and corticospinal tracts are interrupted, thus causing cranial nerve motor nuclei or subnuclear palsy and quadriplegia
in and below the pons.
(1) III.
and IV of the midbrain are not damaged to the cranial nerve motor nucleus and its fibers, and the cortical brainstem fibers and medial longitudinal tract of the III and IV brain nerve motor nuclei are not damaged, so the patient can flash his eyes and move his eyes up and down
.
(2) If the bilateral parapontine median reticular structure and the dilduction nucleus or its nerve roots are involved, there will be horizontal co-directional movement disorders of both eyes (unable to look sideways).
(3) Because the vertical fixation of both eyes is mainly dominated by the superior midbrain thalamus or the anterior area of the parietal cover, the area is not affected, so the patient can do up and down eye movements
.
(4) The cause of this syndrome is mostly cerebrovascular disease, with the ventral basilar artery occlusion on the ventral side of the pons being the most, followed by pontine hemorrhage (paramedian artery).
Others can be seen in pontine tumors, inflammation, multiple sclerosis, heroin overdose, etc
.
The above are the four common syndromes in pontine syndrome, which can be quickly localized
clinically according to the symptoms and signs after involvement.
There are also some rare syndromes, such as facial thalumus syndrome, Gasperini syndrome, etc.
, which need to be further studied and studied
.
Where to see more about ponnt syndrome?
Come to the "Doctor Station" and take a look 👇
Qualitative, positioning diagnosis this article is all about!
Cerebral infarction is one of the most common diseases in the nervous system, different parts of the brain infarction will appear completely different signs and symptoms, and according to the patient's symptoms, signs and accurate positioning diagnosis is a necessary skill for neurologists, this article, the author summarizes the positioning points of common pontine syndrome, let's first look at a case to familiarize.
Case data review
The patient, Zhang Moumou, male, 63 years old, was admitted to the hospital
mainly due to "dizziness with unfavorable left limb movement for 12 hours".
The patient felt dizzy with unfavorable left limb activity when working 12 hours ago, manifested as a sense of unclear brightness of the head, the left upper limb can still be lifted but the object cannot be held, the left lower limb walks and drags, does not accompany headache, does not accompany nausea and vomiting, does not accompany limb numbness and pain, does not accompany consciousness impairment, incontinence, in order to seek diagnosis and treatment, in our hospital's emergency department, head CT showed that the right pons brain low density opacity
.
Head DWI: pontine acute or subacute cerebral infarction
.
No significant stenosis or occlusion of cranial MRA was seen (Figure 1).
For further diagnosis and treatment, it is admitted to our department
.
1 Patient imaging results (provided by the author) 7
years of previous cerebral infarction history, no obvious sequelae, 7 years history of hypertension, blood pressure up to 180/mmHg, type 2 diabetes mellitus for more than 2 years, self-reported poor blood sugar control, denial of coronary heart history, family history, personal history is not special
.
▌Physical examination:
clear mind, lack of fluency in speech, reaction, double pupils are equal to circles, sensitive to light reflection, both eyeballs gaze to the left, right eye abduction can not be, horizontal tremor, right forehead line becomes shallow, right eye closure is weak, right nasolabial fold becomes shallow, the mouth corner of the teeth is left, the tongue is extended to the right, the muscle tone of the limbs is normal, the muscle strength of the left limb is grade 3, The muscle strength of the right limb is grade 5, the left biceps and triceps tendon reflexes are more active than the right side, and the bilateral babinskin sign is negative, and the meningeal irritation sign is negative
.
Biochemical items: total protein 58.
3g/L, albumin 37.
g/L, fasting blood glucose 19.
39mmol/L, triglycerides: 3.
88mmol/L, high-density lipoprotein 1.
11mmol/L, low-density lipoprotein 3.
33mmol/L, homocysteine 17.
00μmol/L, glycated hemoglobin 10.
9mm/L
。 There were no obvious abnormalities
in hematuria and stool routine, six thyroid functions, all male tumors, and five coagulation.
How to locate and qualitatively diagnose?
Positioning diagnosis:
Fig.
2 Positioning diagnosis
summary, contralateral hemiplegia (pyramidal tract involvement); Inability to abduct the eyeball on the side of the lesion (abductor nerve involvement); Paralysis of staring at the lesion side of both eyes is Fowier syndrome
in pontine infarction.
Qualitative diagnosis: The patient is an elderly man with a history of high-risk factors for cerebrovascular diseases such as cerebral infarction, hypertension, and diabetes, and the head DWI on admission indicates acute or subacute cerebral infarction of the pons, so it is characterized as ischemic cerebrovascular disease
.
In terms of treatment, comprehensive treatment
such as anti-platelet aggregation, lipid lowering and plaque stabilization, anticoagulation, opening collateral circulation, removing oxygen free radicals, controlling blood pressure and blood sugar, activating blood and removing stasis are given.
4 common pontine syndromes, what are the positioning points of each?
There are more pontine syndromes, and it is more difficult to remember, and the following is sorted out according to its typical symptoms and signs, so as to facilitate memory
.
We can sort
by location.
From front to back, damage to the ventrolateral part of the pons may present with abductor nerve and facial nerve palsy-hemiplegia syndrome (Millard-Gubler syndrome), damage in the ventral medial part of the pons may present with Fowel syndrome, damage in the dorsolateral part of the pons may present with Raymond-Cestan syndrome, and bilateral lesions at the base of the pons , locked-in syndrome may occur [1].
01 Ventrolateral pontine syndrome
the plane of the lower pons.
Fig.
3 Ventrolateral pontine syndrome[2]
(1) involves dilated nerve root fibers, and the lesion is paralyzed laterally abducted and the eyeball cannot be abducted, and is in the internal oblique position
.
(2) Subnuclear paralysis of the facial nerve is involved, that is, complete facial paralysis
on the lesion side.
(3) Involvement of the pyramidal tract, causing central paralysis
of the contralateral upper and lower limbs.
(4) Involving the medial thalamus and the myelothalamic tract, because the two intersect in the medial thalamic system of the medulla oblongata and intersect in front of the white matter of the spinal cord, respectively, it causes the deep sensation of the contralateral limb of the lesion to decrease or disappear; Superficial sensation in the contralateral heminess diminishes or disappears
.
The causes of Millard-Gubler syndrome are often inflammatory foci, tumors (glial nodules, gliomas), plaques of multiple sclerosis
.
Cerebrovascular disease is less
commonly caused.
In conclusion, the lesion is located in the ventrolateral part of the pons, close to the medulla oblongata, and damages the abductor nerve, facial nerve, pyramidal tract, spinosamic tract, and medial thalamus
.
Manifested as: 1 lateral abduction nerve palsy; 2 contralateral central hemiplegia; 3 Contralateral hemisensory impairment
may occur.
02 Pontine ventromedial syndrome
of the lesion.
Fig.
4 Pontine ventral medial syndrome[2]
(1) Contralateral hemiplegia (pyramidal tract involvement) (2) Inability to abduct the eyeball on the lesion side (abductor nerve involvement)
(3) Paralysis of the gaze of both eyes to the side of the lesion (the result of damage to the abductor nerve nucleus or its root fibers and PPRF, because the abductor nerve nucleus and root fibers and PPRF participate in the sympathic fixation mechanism of the two eyes, not paralysis of the medial rectus muscle of the contralateral eyeball, because when the two eyes are cohesive, the contralateral eyeball can still adduct.
The cause of Fowwer's syndrome is cerebrovascular disease most common, because there is less collateral circulation in the paramedian artery, and cerebral infarction is predisposed to
.
Can also be caused
by tumors and inflammation.
03 Pontine undercover syndrome
.
Involving vestibular, span, facial nerve nuclei, medial longitudinal tract, cerebellar midfoot, medial thalamus and other structures, seen in the upper cerebellar artery or inferior anterior cerebellar artery blockage, manifested as:
(1) vertigo, nausea, vomiting, nystagmus (vestibular nerve nucleus damage);
(2) The affected side of the eyeball cannot be abducted (abductor nerve damage);
(3) Lateral muscle paralysis (facial nerve nuclear damage);
(4) Inability to fixate on the affected side of both eyes (damage to the pontine lateral visual center and medial longitudinal tract);
(5) Cross-cutting sensory disorders, that is, ipsilateral pain, loss of temperature perception (trigeminal nerve spinal tract damage), contralateral migraine pain, temperature loss or loss (lateral fascicular tract damage of the myelochalus);
(6) Decreased or lost sense of touch, position, and vibration of the contralateral body (medial thalamus damage);
(7) Horner sign on the affected side (sympathetic descending fiber damage);
(8) Hemibody ataxia on the affected side (damage to the cerebellar middle foot, the lower cerebellar foot and the anterior fascicular fascicular tract of the spinal cord).
Fig.
5 Pontine undercover syndrome[2].
04 Locked-in syndrome
the bilateral pons.
Bilateral cortical pontine tracts, cortical medullary tracts and corticospinal tracts are interrupted, thus causing cranial nerve motor nuclei or subnuclear palsy and quadriplegia
in and below the pons.
(1) III.
and IV of the midbrain are not damaged to the cranial nerve motor nucleus and its fibers, and the cortical brainstem fibers and medial longitudinal tract of the III and IV brain nerve motor nuclei are not damaged, so the patient can flash his eyes and move his eyes up and down
.
(2) If the bilateral parapontine median reticular structure and the dilduction nucleus or its nerve roots are involved, there will be horizontal co-directional movement disorders of both eyes (unable to look sideways).
(3) Because the vertical fixation of both eyes is mainly dominated by the superior midbrain thalamus or the anterior area of the parietal cover, the area is not affected, so the patient can do up and down eye movements
.
(4) The cause of this syndrome is mostly cerebrovascular disease, with the ventral basilar artery occlusion on the ventral side of the pons being the most, followed by pontine hemorrhage (paramedian artery).
Others can be seen in pontine tumors, inflammation, multiple sclerosis, heroin overdose, etc
.
The above are the four common syndromes in pontine syndrome, which can be quickly localized
clinically according to the symptoms and signs after involvement.
There are also some rare syndromes, such as facial thalumus syndrome, Gasperini syndrome, etc.
, which need to be further studied and studied
.
References:
[1] GAO Ben, LIU Jing, ZHANG Xu, et al.
Stroke and Neurological Diseases,2019,26(06):759-763.
)
[2] Malla G,Jillella D V.
Pontine Infarction[J].
2022.
Where to see more about ponnt syndrome?
Come to the "Doctor Station" and take a look 👇
