Nuero--brain Herniation

Welco Everyon

Brain Herniation Department of Neurosurgery,The First Affiliated Hospital of Zhengzhou University Xu Bin

Cerebral falx and tentorium of cerebellum divided the whole cranial cavity into three tunes, which communicated each other.

When there is an occupying lesion in one tune, the pressure of the tune must be higher than contiguous tune, which result in migration of cerebral tissues from one part in body to another. This is called herniation.

Brain herniation is a condition in which a portion of the brain is displaced because of increased pressure inside the skull. Increase in pressure results in progressive damage to brain tissue that may include life-threatening damage to the brainstem.

These are generally complications of mass effect whether from tumor, trauma or infection. We will discuss the imaging findings, clinical characteristics and possible complications involved in brain herniations. The key to recognizing all herniations of the brain is evaluation of the cisterns.

According to position of lesions, it is mainly composed of tentorial herniation and foramen magnum herniation.Tentorial hernation also called tentoral incisure of cerebellar herniation or temporal herniation of hippocampal herniation.Foramen magnum herniation also called tonsil of cerebellar herniation.

Large rightsided subdural hematoma producing right to left midline shift and right uncal (red arrow) herniation.

Tentorial and Tonsillar Herniation Two

common types: – Tentorial: medial portion of the temporal lobe herniates into the tentorial notch and compresses the midbrain, cerebral peduncle and third nerve – Tonsillar: herniation of the cerebellar tonsils through the foramen magnum Etiology can include cerebral edema, space occupying lesions (abscesses, tumors, hematomas), hydrocephalus,et al

Tentorial Herniation Definition: Cerebral tissues of temporal lobe are squeezed to posterior cranial fossa through tentorial incisure.

Transtentorial herniations occur when the brain traverses across the tentorium at the level of the incisura. These can be divided into ascending and descending transtentorial herniations.The latter is common.So we emphasis on discussing it.

Descending transtentorial herniations are a larger category caused by mass effect in the cerebrum which pushes the supratentorial brain tissue through the incisura to the posterior fossa.

Ascending transtentorial herniation is caused by mass effect in the posterior fossa which leads to brain extending through the incisura in an upward.

Clinical Manifestation 1. Severe headache: caused by IIP. 2. Disturbance of consciousness, drowsiness, especially coma,et al. The reticular formation of midbrain is involved.

3. Pupillary Alteration,from one pupil dilated to bilateral pupils dilated:Due to involvement of the third cranial nerve. 4.Motor disturbance, hemiplegia, decerebrate rigidity:pyramidal tract of brain stem is involved.

5.Vital signs disorder: Cushing’s response All of them are very important and must be kept in mind, because the diagnosis is based on these clinical findings.

These clinical situation may be isolated or occur together. Ipsilateral pupil dilatation occurs as the parasympathetic fibers, which are located around the outer aspect of the third nerve, are compressed by the uncus. This leads to dysfunction of the parasympathetic fibers with subsequent unopposed sympathetic responds. This will dilate the ipsilateral pupil.

Contralateral hemiparesis occurs with compression of the ipsilateral cerebral peduncle. Since the cortical spinal tracts decussate (cross over) below the mid brain in the level of pons, the hemiparesis is contralateral.

In some cases, an ipsilateral hemiparesis can occur with a contralateral dilated pupil or oculomotor paresis. This occurs when the lateral translation of the brainstem is so great as to push the midbrain and cerebral peduncles all the way across the perimesencephalic cistern, so that the opposite (contralateral) third nerve and cerebral peduncle are pressed against the opposite

This phenomenon is called a Kernohan’s notch - a hemorrhage that occurs in the contralateral cerebral peduncle (image shows damage of the right peduncle with hemorrhage centrally from Durette hemorrhage).

Thus causing ipsilateral hemiparesis. This neurologic sign can be termed a "false localizer", since it can be confusing or misleading for lateralization of the inciting lesion's location.

Imaging findings of descending transtentorial herniations include ipsilateral ambient cistern widening and ipsilateral prepontine cistern widening. A contralateral temporal horn is also widened. These findings occur as the ipsilateral, lateral ventricle is compressed with subsequent dilatation of the contralateral ventricle to maintain the same volume.

ipsilateral ambient cistern widening

ipsilateral prepontine cistern widening

contralateral temporal horn is also widened

The ipsilateral cistern is widened because of the fact that the brain stem is inferiorly contiguous with the spinal cord leading to a long rigid structure as shown in the coronal CT image.

Note the mass on the right with widening of the ipsilateral, right ambient cistern. As the supratentorial brain shifts to the right, the superior aspect of this long column of mid brain and cord also shifts to the right.

This will narrow the contralateral cistern and widen the ipsilateral cistern at the anterolateral aspects of the brain stem.

Uncal herniation is a subset of descending transtentorial herniations. The uncus is displaced into the suprasellar cistern. The usual six pointed star appearance of the suprasellar cistern then becomes truncated on the ipsilateral side of the herniation. Coronal imaging can also demonstrate uncal herniation either by CT or MRI.

usual six pointed star appearance of the suprasellar cistern

truncated on the ipsilateral side of the herniation

This CT scan demonstrates a Durette hemorrhage, descending transtentorial shift to the left, widening of the contralateral, right temporal horn and a residual ipsilateral ambient cistern (left) still remaining. The uncus is also filling the left aspect of the suprasellar cistern.

Complications of descending transtentorial herniations include occipital infarction. The posterior cerebral artery becomes compressed as the ipsilateral uncus and parahippocampal gyrus compresses the artery against the ipsilateral cerebral peduncle.

The gross specimen associated with the CT of occipital infarcts demonstrates the excellent correlation. This can occur unilaterally or bilaterally depending on the extent of injury and amount of mass effect. Generally, an ipsilateral occipital infarct will appear first followed by contralateral infarction.

Another complication of descending transtentorial herniation includes Durette hemorrhage. This is due to pontine perforators which are displaced downward by mass effect.

The basilar artery sends these perforators posteriorly into the pons. As the pons shifts inferiorly, these perforators are stretch and can cause hemorrhage within the brain stem or pons.

Sagittal and axial MRI demonstrates the hemorrhage in the dorsal lateral pons.

Kernohan’s notch is another type of hemorrhagic damage caused by transtentorial herniation. This is due to compression of the contralateral cerebral peduncle against the incisura. If this occurs, it leads to ipsilateral hemiparesis since the cortical spinal tracts become damaged.

The gross specimen demonstrates hemorrhage in the left central midbrain from Durette hemorrhage and cortical damage with some hemorrhage at the right cerebral peduncle consistent with Kernohan’s notch. There is also a left uncal herniation.

Foramen Magnum Herniation Defination: Cerebellar tonsil is squeezed to cervical vertebral canal through foramen magnum and compresses the medulla oblongata and cervical spinal cord.

Clinical Manifestation A neurologic examination would show an impaired level of consciousness. Depending on the severity of the herniation, one or several brainstem reflexes and cranial nerve functions will be impaired. The patient would show an inability to breathe consistently, and heart rhythms would be irregular.

❂1. Severe headache:

the manifestation of IIP ❂2. Sudden arrest of

respiration: respiratory center in medulla is involved.

❂3. Disturbance of consciousness:

This always happened later than. ❂4. Neck

stiffness and head tilt from impaction of the foramen magnum. ❂5.

Bradycardia and wide pulse pressure.

Clinical symptomatology maybe subtle in foramen magnum herniation until the patient becomes obtunded. Patients with a Chiari malformation may have little or no clinical symptomatology or may demonstrate Lhermitte’s phenomenon.

This is changed or dysesthesia in the arms or legs with forward bending of the head. This is postulated to occur as the anterior spinal tracts within the ventral spinal cord, become compressed against the bone of the posterior vertebral bodies.

Acute foramen magnum herniation clinically can be catastrophic as the brains extrudes through the foramen magnum. Again, this is generally associated with other herniations such as ascending transtentorial herniation depending on the level of the mass.

Imaging findings include on the axial images, cerebellar tonsils at the level of the dens.

In general if the tonsils are located at the level of the dens on the axial images, this generally is an indicator of foramen magnum herniation.

Excessive cerebellar tissue can be seen at the foramen magnum but it may be best to visualize the dens and cerebellum together since the CT gantry angle can yield different appearances at the foramen magnum.

A sagittal MRI is a much easier method of determining if foramen magnum herniation is present as in this patient with a tentorial subdural and shift through the foramen magnum. This is because the association between the inferior aspect of the clivus and inferior aspect of the occipital bone is much easier to demonstrate on the sagittal images.

tentorial subdural and shift through the foramen magnum

This gross specimen also shows a crease on the cerebellar tonsils as they extend through the foramen magnum. Clinical complications would include obturation and death as this progresses.

Treatment of cerebral herniation Brain herniation is a medical emergency! The goal of treatment is to save the patient's life. To help reverse or prevent a brain herniation, the medical team will treat increased swelling and pressure in the brain. This can be accomplished by:

Ⅰ.Nonoperative treatment: 1.Dehydration drug: 20%Mannitol 250ml iv drop q6h– q6h 1g/kg over 15 minutes,Effects last 4-6 hours or other diuretics 2.Cortisone:dexamethasone 10~20mg iv qd, especially in cases where a tumor is involved.

3. A drain placed into the brain to drain off fluid, in the case of a mechanical obstruction causing herniation. 4. Removing the blood if a massive hemorrhage is present and causing herniation, although the outlook in these cases is poor.

5.Keeping the respiratory tract unobstructed: Placing a tube in the airway and mechanically ventilating (forced breathing) at a rapid rate to reduce the levels of carbon dioxide (CO2) in the blood for patients with breathlessness.

Ⅱ.Operative treatment: 1.Removing the etiology: such as resection of tumor, remove of hematoma,et al. 2.Brain ventricle drainage: such as hydrocephalus .

3.Operation of decompression: such as temporal decompression for cerebral edema. 4.Cerebral spinal fluid shunt: such as ventricle-abdominal cavity shunt.

•Expectations (prognosis) Once herniation in the brain's temporal lobe or the cerebellum occurs, death is often inevitable. Herniation of other areas of the brain areas has a more variable outlook.

•Complications Permanent and significant neurologic problems Brain death

The end result of herniation is compression and Duret hemorrhages, as seen here in the pons.

Here is another example of uncal herniation. Also seen with such herniation can be Duret hemorrhages in the brainstem.

Brain Death When ICP increased suddenly and reach to or beyond the mean artery pressure (MAP), brain circulation completely stopped. The patient was deep coma, no autonomous breathing. Applying artificial respiration and some medicine, the heartbeat can be sustained for 1~2 week or so.

Diagnosis standard of brain death (1) No autonomous breathing; (2) deep coma; (3) Bilateral pupil dilation and light reflex disappear; (4) brain stem reflex disappear: such as swallowing reflex, corneal reflex, et al.

(5) the blood pressure must be maintained by medicine, such as dopamine, adrenaline. (6) Electroencephalogram (EEG) display resting potential. (7) to inject atropine 1~3mg intravenously, no heartbeat acceleration was found.

(8) Brain stem auditory evoked potential (BAEP) display resting potential; (9) ICP monitoring found that ICP reach to or beyond the mean artery pressure. When manifestation above-mentioned sustained at least 6 hours and examined by 2 doctors, the diagnosis can be made.

The summary Brain tumor Chronic IIP

Intracranial Hematoma acute IIP

headache, vomiting, headache, vomiting, papilloedema

Cushing’s response Herniation

(Tentorial H or Foramen magnum H) brain death

Questions?