-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
*For medical professionals only
.
Cerebral herniation refers to the compression of brain tissue, blood vessels and cranial nerve structures caused by compression of brain tissue driven by a pressure gradient into physiological spaces (cerebellar foramen hiatus, occipital foramen, cerebral subsickle herniation, etc.
) or pathological apertures (such as surgical decompression windows), resulting in compression of brain tissue, blood vessels and cranial nerve structures
.
according to the location and contents.
(1) Patients with hooked gynia
can have oculomotor nerve compression and contralateral hemiplegia (ipsilateral cerebral foot compression) in the early stage, and compression of the posterior cerebral artery can also be combined with occipital lobe infarction, which mostly occurs in cerebral hemisphere stroke
.
(2) Patients with central hernia
have impaired consciousness and respiratory changes, and pupil changes appear relatively late, mostly secondary to midline or deep brain mass lesions, and can also be seen in diffuse intracranial hypertension
.
.
.
Large-scale infarction is one of the important causes of clinical herniation, so early identification of its risk can help avoid serious conditions
such as cerebral herniation in patients.
Large-scale cerebral infarction refers to cerebral hemispheric infarction ≥ infarction of in the middle cerebral artery supply area, or cerebral infarction with a diameter of > 3 cm
.
For patients with infarction in the middle cerebral artery supply area, if neurological deficits and aggravated consciousness disorders occur in the early stage, malignant middle cerebral artery infarction may occur, which quickly endangers the patient's life
.
Therefore, there should be a high suspicion of ischemic stroke with hemiplegia, hemiplegia, hemiplegia, gaze disturbance, head-eye separation, and aphasia (dominant hemisphere) with a high suspicion of cerebral hemisphere-large cerebral infarction
.
A NIHSS score of > 15 or a NIHSS score of 2>0 in the dominant hemisphere, or disappearance of the basal cistern or midline displacement on imaging in the early onset indicates a higher risk
of malignant cerebral edema.
Patients with 6 points ≥ modified EDEMA model are at high risk of malignant cerebral infarction, so surgical indications such as decompression of the bone flap should be actively evaluated
.
Table 1.
Malignant cerebral edema risk prediction model[2] (can be enlarged).
of increased intracranial pressure Brain herniation is mainly due to the displacement of part of the brain tissue due to intracranial pressure difference, so it is necessary to clarify the cause of
increased intracranial pressure.
Intracranial causes are mainly caused by increased brain tissue volume, intracranial mass lesions, increased intracranial blood volume, or increased
cerebrospinal fluid due to angiogenic edema or cytotoxic edema.
At the same time, it should be noted that extracranial hypoxemia can also lead to increased intracranial pressure in patients
.
Table 2.
Causes of increased intracranial pressure[3].
of cerebral herniation, it is mainly targeted to reduce intracranial pressure, in addition, we can also use osmotic diuretics such as mannitol, hyperventilation, hypothermia and other methods
.
However, we need to be aware that long-term, high-dose infusion of osmotic diuretics such as mannitol may cause adverse drug reactions
such as prerenal renal dysfunction and osmotic encephalopathy.
Therefore, for patients with refractory intracranial hypertension and even possible herniation, surgical treatment such as decompression of the bone flap can be considered
.
Table 3.
Treatment of increased intracranial pressure [3] (can be viewed in enlarge).
.
Paradoxical herniation is characterized by progressive neurological deterioration, flap collapse at the site of skull defect, midline displacement, and brainstem compression, mainly weeks to months
after skull resection.
For patients with flap collapse syndrome after decompression surgery, if there are symptoms such as dyskinesia, cognitive impairment, decreased alertness, headache, etc.
, emergency CT is required to drain abnormal brain herniation, especially for patients with mild supine symptoms but worsening upright symptoms, orthostatic CT may detect and objectively evaluate abnormal herniation and midline bias
that are not obvious in the supine imaging mode.
In terms of treatment, for such patients, we need to pay attention to the cause of low intracranial pressure, so it is necessary to increase intracranial pressure by fluid resuscitation, etc
.
, and emergency can be treated with cranioplasty.
If cranioplasty is not possible due to infection, etc.
, external fixation frame scalp traction can also be a viable modality
.
Where to see more neurological clinical knowledge?
Come to the "doctor's station" and take a look 👇
This article analyzes cerebral herniation from multiple perspectives
, such as clinical manifestations, risk identification, etiology analysis, and treatment steps.
.
Cerebral herniation refers to the compression of brain tissue, blood vessels and cranial nerve structures caused by compression of brain tissue driven by a pressure gradient into physiological spaces (cerebellar foramen hiatus, occipital foramen, cerebral subsickle herniation, etc.
) or pathological apertures (such as surgical decompression windows), resulting in compression of brain tissue, blood vessels and cranial nerve structures
.
1
Clinical manifestations01
Structures such as hippocampal gyrus and hook gyrus on the medial temporal lobe of the cerebellar tomeroplastic hernia or midline and deep brain tissues are squeezed into the cerebellar tostorial hiatus, which can be divided into lateral type (hook gyranium hernia) and central type (central herniation)according to the location and contents.
(1) Patients with hooked gynia
can have oculomotor nerve compression and contralateral hemiplegia (ipsilateral cerebral foot compression) in the early stage, and compression of the posterior cerebral artery can also be combined with occipital lobe infarction, which mostly occurs in cerebral hemisphere stroke
.
(2) Patients with central hernia
have impaired consciousness and respiratory changes, and pupil changes appear relatively late, mostly secondary to midline or deep brain mass lesions, and can also be seen in diffuse intracranial hypertension
.
02
Occipital foramen hernia cerebellar tonsils and adjacent cerebellar tissue hernia into the upper end of the spinal canal through foramen magnum occipital hernia, patients often have posterior occipital pain, impaired consciousness, and can be combined with posterior cranial nerve involvement, more common in patients with posterior fossa mass lesions or diffuse intracranial hypertension.
03
The suprateural occuporial mass of the subfalcial hernia of the brain leads to a pressure gradient between the left and right supratentorial cranial cavities, resulting in the relocation of the cingulate band to the subcranial sickle of the brain, and patients often present with headache and weakness of the contralateral lower extremity, and infarction of the anterior cerebral artery supply area may occur, which may also be accompanied by other types of hernia.
2
Large-scale cerebral infarction Brain herniation risk recognitionLarge-scale infarction is one of the important causes of clinical herniation, so early identification of its risk can help avoid serious conditions
such as cerebral herniation in patients.
Large-scale cerebral infarction refers to cerebral hemispheric infarction ≥ infarction of in the middle cerebral artery supply area, or cerebral infarction with a diameter of > 3 cm
.
For patients with infarction in the middle cerebral artery supply area, if neurological deficits and aggravated consciousness disorders occur in the early stage, malignant middle cerebral artery infarction may occur, which quickly endangers the patient's life
.
Therefore, there should be a high suspicion of ischemic stroke with hemiplegia, hemiplegia, hemiplegia, gaze disturbance, head-eye separation, and aphasia (dominant hemisphere) with a high suspicion of cerebral hemisphere-large cerebral infarction
.
A NIHSS score of > 15 or a NIHSS score of 2>0 in the dominant hemisphere, or disappearance of the basal cistern or midline displacement on imaging in the early onset indicates a higher risk
of malignant cerebral edema.
Patients with 6 points ≥ modified EDEMA model are at high risk of malignant cerebral infarction, so surgical indications such as decompression of the bone flap should be actively evaluated
.
Table 1.
Malignant cerebral edema risk prediction model[2] (can be enlarged).
3
Causesof increased intracranial pressure Brain herniation is mainly due to the displacement of part of the brain tissue due to intracranial pressure difference, so it is necessary to clarify the cause of
increased intracranial pressure.
Intracranial causes are mainly caused by increased brain tissue volume, intracranial mass lesions, increased intracranial blood volume, or increased
cerebrospinal fluid due to angiogenic edema or cytotoxic edema.
At the same time, it should be noted that extracranial hypoxemia can also lead to increased intracranial pressure in patients
.
Table 2.
Causes of increased intracranial pressure[3].
4
The treatment of increased intracranial pressure For the treatmentof cerebral herniation, it is mainly targeted to reduce intracranial pressure, in addition, we can also use osmotic diuretics such as mannitol, hyperventilation, hypothermia and other methods
.
However, we need to be aware that long-term, high-dose infusion of osmotic diuretics such as mannitol may cause adverse drug reactions
such as prerenal renal dysfunction and osmotic encephalopathy.
Therefore, for patients with refractory intracranial hypertension and even possible herniation, surgical treatment such as decompression of the bone flap can be considered
.
Table 3.
Treatment of increased intracranial pressure [3] (can be viewed in enlarge).
5
Paradoxical cerebral herniation for the intracranial pressure increased, so that the treatment of cerebral herniation, decompression of the bone flap is a common surgical method, however, we need to pay attention to the decompression of the bone flap atmospheric pressure is higher than the intracranial pressure, combined with gravity, the pressure difference will cause the intracranial contents to collapse, and finally make the brain parenchyma through the cerebellar curtain notch or occipital foramen hernia, forming abnormal brain herniation.
Paradoxical herniation is characterized by progressive neurological deterioration, flap collapse at the site of skull defect, midline displacement, and brainstem compression, mainly weeks to months
after skull resection.
For patients with flap collapse syndrome after decompression surgery, if there are symptoms such as dyskinesia, cognitive impairment, decreased alertness, headache, etc.
, emergency CT is required to drain abnormal brain herniation, especially for patients with mild supine symptoms but worsening upright symptoms, orthostatic CT may detect and objectively evaluate abnormal herniation and midline bias
that are not obvious in the supine imaging mode.
In terms of treatment, for such patients, we need to pay attention to the cause of low intracranial pressure, so it is necessary to increase intracranial pressure by fluid resuscitation, etc
.
, and emergency can be treated with cranioplasty.
If cranioplasty is not possible due to infection, etc.
, external fixation frame scalp traction can also be a viable modality
.
References:
[1] HE Jiawei, YANG Qi, ZHANG Liang, et al.
Research progress of abnormal cerebral herniation[J].
Chinese Journal of Neuromedicine,2022,21(3):291-293.
) DOI:10.
3760/cma.
j.
cn115354-20210911-00595.
[2] Neurocritical Collaborative Group of Neurology Branch of Chinese Medical Association, Neurology Special Committee of Neurology Branch of Chinese Medical Doctor Association.
Chinese expert consensus on monitoring and treatment of large-area infarction in cerebral hemispheres[J].
Chinese Medical Journal,2017,97(9):645-652.
) DOI:10.
3760/cma.
j.
issn.
0376-2491.
2017.
09.
003
[3] Neurocritical Collaborative Group of Neurology Branch of Chinese Medical Association, Neurology Professional Committee of Neurologist Branch of Chinese Medical Doctor Association.
Chinese expert consensus on the monitoring and treatment of refractory intracranial hypertension[J].
Chinese Medical Journal,2018,98(45):3643-3652.
) DOI:10.
3760/cma.
j.
issn.
0376-2491.
2018.
45.
004
Where to see more neurological clinical knowledge?
Come to the "doctor's station" and take a look 👇