1.Herniation of brain (Herniation of brain) basic concept.
It is a life-threatening syndrome caused by intracranial hypertension.
The cranial cavity is divided into three chambers: supratentorial left, right and infratentorial by the cerebral falx and cerebellar curtain.
When the local pressure in the brain increases, the pressure is transferred from high to low, but the cerebral falx and cerebellar curtain prevent the pressure from transferring freely, and can only concentrate on moving to the above-mentioned traffic orifice, so that part of the brain tissue protrudes from the traffic orifice and forms brain herniation. Yu Xin, Department of Neurosurgery, Naval General Hospital
2.The formation of brain herniation
Intracranial lesion → pressure imbalance → pressure gradient → partial displacement of brain tissue → herniation into anatomical foramen (cerebellar curtain notch or occipital foramen) → compression of brain stem and other structures → corresponding symptoms (pupil, consciousness, vital signs, long bundle damage, etc.) → intracranial hypertensive crisis.
3.Characteristics of brain herniation
Cause: Pressure gradient formation
Component: Herniated tissue, anatomical cavity, compressed tissue
Pathological changes/compressed tissue
Reversibility/small
4.Common causes and classification of brain herniation
Common causes.
Intracranial occupancy: hematoma, tumor, abscess, granuloma, etc
Cerebral edema and acute brain swelling
Classification.
Cerebellar curtain herniation
Foramen magnum herniation
Subfalcine herniation
Supratentorial herniation
Pterygoid crest herniation
Composite herniation
5.Cerebellar herniation
1.Surgical anatomy.
Interpeduncular pool: containing the articular N, posterior traffic A, basal A, posterior cerebral A
Circumferential pool: external to the circumferential pool wing, containing the sliding carriage N and posterior cerebral A
Tetrahymenal pool: containing the large V of the brain
2.Pathophysiology
Damage to the motor nerve.
Brainstem changes: ① compression, deformation, and displacement.
② Ischemia, edema, hemorrhage, secondary softening.
CSF circulatory disorders.
Posterior cerebral A embolism.
3. Clinical manifestations
Increased intracranial pressure
Arterial N damage
Cone bundle sign
impaired consciousness
Changes in vital signs
4. Clinical manifestations in each stage.
(1) Early stage.
a:Dizziness, headache, nausea and vomiting, restlessness.
b:Progressive aggravation of disorders of consciousness.
c:Pupillary changes: stimulation of the motoneural nerve, transient pupil narrowing, later the pupil begins to gradually dilate and the reflex to light is blunted.
d:Cone bundle signs: mild contralateral upper and lower limb muscle strength is slightly weaker and muscle tone is increased.
e:Change in vital signs, slight slowing of pulse and respiration.
(2) Typical manifestations of temporal lobe hook gyrus hernia in the middle stage.
(1) Impaired consciousness, progressive aggravation, change from drowsiness to semi-comatose state.
(2) Pupillary changes: the affected side is dilated and the reflex to light is absent. The contralateral side may be normal, but the light reflex is diminished.
③Vital signs: Cushing’s reaction changes appear as follows: deep and slow breathing, slow and strong pulse, elevated blood pressure, and continuous rise in body temperature.
(iv) Cone bundle signs: ipsilateral cerebral peduncle compression, contralateral upper and lower limb paralysis including central facial palsy, increased muscle tone, hyperactive tendon reflexes, and positive pathological reflexes.
(3) Late stage.
(i) Deep coma with no response to all stimuli.
(2) Both pupils are dilated and fixed, the light reflex disappears, and most of the pupils are deactivated.
③The vital center begins to fail, tidal breathing or sigh-like breathing appears, pulse is frequent and weak, blood pressure and body temperature drop, and finally respiratory arrest. If cardiac compressions are performed, assisted breathing, and pressure-raising drugs are given, the heartbeat and blood pressure can still be maintained for a period of time.
5.Treatment principles
Quick dehydration, buy time
Find and remove the cause of the disease as soon as possible
Fan Guifang F 50 Post-traumatic brain herniation
Post-operative CT manifestation
Post-operative MRI
7 months after injury
Vegetative survival state
Dilated right pupil has not recovered
Pupillary reflex
Visual conduction pathway and pupil-to-light reflex pathway
6.Hernia of the foramen magnum of the occipital bone
1.Surgical anatomy
2.Mechanism: small volume of posterior cranial fossa, small cushioning capacity, small occupancy can cause ICP increase, herniation of cerebellar tonsils into the upper cervical spinal canal
3.Pathophysiology
Medulla oblongata compression, life center failure, life-threatening
Obstruction of the middle foramen of the fourth ventricle → obstructive hydrocephalus
Cerebellar tonsil congestion, edema and hemorrhage → increased compression
4.Clinical manifestations (acute)
Symptoms of increased intracranial pressure.
Altered vital signs.
Spinal nerve root compression symptoms: posterior neck pain, forced head position
Posterior group cranial nerve dysfunction.
Cerebellar symptoms.
Cone fasciculus signs.
L late onset of impaired consciousness and pupillary changes
5. Differentiation between foramen magnum herniation and cerebellar tangential herniation.
In occipital foramen magnum herniation, impairment of medullary vital center function (respiration and circulation in vital signs) appears early, while pupillary changes and disorders of consciousness appear late.