Overview of the Brain and it’s CT Images
Brain herniation is also called Cerebral herniation, Brain herniation refers to displacement of a portion of the brain from its normal position through openings in the inelastic dura secondary to focal or diffuse intracranial pressure. Recognition of the CT signs of brain herniation on the emergent head CT is critical to proper patient management. The types of brain herniations are schematically illustrated.”:a) ” Subfalcial (cingulate) herniation ; b) uncal herniation ; c) downward (central, transtentorial) herniation ; d) external herniation ; e) tonsillar herniation.Types a, b, & e are usually caused by focal, ipsilateral space occupying lesions, ie., tumor or axial or extra-axial hemorrhage.”
Types of brain herniation
- Transtentorial (uncal) herniation
- Subfalcine herniation
- Central herniation
- Upward transtentorial herniation
- Tonsillar herniation
Transtentorial (uncal) herniation:
- Ipsilateral 3rd cranial nerve (often first) and posterior cerebral artery.
- As herniation progresses, the ipsilateral cerebral peduncle.
- In about 5% of patients, the contralateral 3rd cranial nerve and cerebral peduncle.
- Eventually, the upper brain stem and the area in or around the thalamus.
Subfalcine herniation:
Central herniation:
The posterior 3rd ventricle becomes compressed. Upward herniation also distorts the mesencephalon vasculature, compresses the veins of Galen and Rosenthal, and causes superior cerebellar infarction due to occlusion of the superior cerebellar arteries.
Upward transtentorial herniation:
Tonsillar herniation:
Symptoms and Signs
- dilated pupils
- headache
- drowsiness
- difficulty concentrating
- high blood pressure
- loss of reflexes
- seizures
- abnormal posturing.
- cardiac arrest
- loss of consciousness
- coma
Causes of brain herniation
A brain herniation is typically the result of swelling in the brain. The swelling puts pressure on brain tissues (referred to as increased intracranial pressure), causing the tissue to be forced away from its normal positon.
The most common causes of a brain herniation include:
- head injury leading to a subdural hematoma (when blood collects on the brain’s surface beneath the skull) or swelling (cerebral edema)
- stroke
- brain hemorrhage (bleeding in the brain)
- brain tumor
- abscess (collection of pus) from a bacterial or fungal infection
- buildup of fluid in the brain (hydrocephalus)
- brain surgery
- a defect in brain structure called Chiari malformation
Diagnosis brain herniation
CT or MRI
Treatment brain herniation
- Immediate stabilization (airway, breathing, circulation, or ABCs)
- Admission to an intensive care unit (ICU)
- Supportive measures, including control of ICP
- Treatment of underlying disorder.
Treatment of brain herniation is similar to treatment of coma.
Hypotension must be corrected. Patients are admitted to the ICU so that respiratory and neurologic status can be monitored.
Patients must be stabilized. Airway, breathing, and circulation must be ensured immediately.
If increased ICP is suspected, incubation should be done via rapid-sequence oral intubation (using a paralytic drug) rather than via nasotracheal intubation; nasotracheal intubation in a patient who is breathing spontaneously causes more coughing and gagging, thus increasing ICP, which is already increased because of intracranial abnormalities.
If ICP is increased, intracranial and cerebral perfusion pressure should be monitored (see Intracranial Pressure Monitoring), and pressures should be controlled. The goal is to maintain ICP at ≤ 20 mm Hg and cerebral perfusion pressure at 50 to 70 mm Hg. Cerebral venous drainage can be enhanced (thus lowering ICP) by elevating the head of the bed to 30° and by keeping the patient’s head in a midline position.
Measures to control Intracranial Pressure Monitoring (ICP) include
- Sedation: Sedatives may be necessary to control agitation, excessive muscular activity (eg, due to delirium), or pain, which can increase Intracranial Pressure Monitoring
- Hyperventilation: Hyperventilation causes hypocapnia, which causes vasoconstriction, thus decreasing cerebral blood flow globally.
- Hydration: Isotonic fluids are used. Providing free water through IV fluids (eg, 5% dextrose, 0.45% saline) can aggravate cerebral edema and should be avoided. Fluids may be restricted to some degree, but patients should be kept euvolemic. If patients have no signs of dehydration or fluid overload, IV fluids with normal saline can be started at 50 to 75 mL/h. The rate can be increased or decreased based on serum sodium, osmolality, urine output, and signs of fluid retention (eg, edema).
- Diuretics: Serum osmolality should be kept at 295 to 320 mOsm/kg. Osmotic diuretics (eg, mannitol) may be given IV to lower ICP and maintain serum osmolality. These drugs do not cross the blood-brain barrier. They pull water from brain tissue across an osmotic gradient into plasma, eventually leading to equilibrium. Fluid and electrolyte balance should be monitored closely while osmotic diuretics are used. A 3% saline solution is another potential osmotic agent to control ICP.
- Blood pressure (BP) control: Systemic antihypertensives are needed only when hypertension is severe (> 180/95 mm Hg). How much BP is reduced depends on the clinical context. Systemic BP needs to be high enough to maintain cerebral perfusion pressure even when ICP increases.
- Corticosteroids: Corticosteroids are effective only for tumors and sometimes abscesses of the brain when vasogenic edema (due to disruption of the blood-brain barrier) is present. Corticosteroids are ineffective for cytotoxic edema (due to cell death and breakdown) and can increase plasma glucose, exacerbating cerebral ischemia.
