Browse Tag: Cerebral edema

The Cushing Reflex.

The Cushing Reflex

Progressive hypertension associated with bradycardia and diminished respiratory effort is a specific response to acute, potentially lethal rises in ICP. This response is called the Cushing reflex, and its occurrence indicates that the ICP has reached life-threatening levels. The Cushing reflex can occur whenever ICP is increased, regardless of the cause. The full triad of hypertension, bradycardia, and respiratory irregularity is seen in only one third of cases of life-threatening increased ICP.


Cerebral herniation occurs when increasing cranial volume and ICP overwhelms the natural compensatory capacities of the CNS. Increased ICP may be the result of posttraumatic brain swelling, edema formation, traumatic mass lesion expansion, or any combination of the three. When increasing ICP cannot be controlled, the intracranial contents will shift and herniate through the cranial foramen.


The most common clinically significant traumatic herniation syndrome is uncal herniation, a form of transtentorial herniation (Fig. 31-5) (Figure Not Available) . Uncal herniation is often associated with traumatic extraaxial hematomas in the lateral middle fossa or the temporal lobe. The classic signs and symptoms are caused by compression of the ipsilateral uncus of the temporal lobe on the U-shaped edge of the tentorium cerebelli as the brain is forced through the tentorial hiatus. As compression of the uncus begins, the third cranial nerve is compressed. Anisocoria and a sluggish light reflex in the dilated pupil develop on the side ipsilateral to the expanding mass lesion. This phase may last for minutes to hours, depending on how rapidly the expanding lesion is changing. As the herniation progresses, compression of the ipsilateral oculomotor nerve eventually causes ipsilateral pupillary dilatation and nonreactivity.

Initially in the uncal herniation process, the motor examination can be normal, but contralateral Babinski’s responses develop early. Contralateral hemiparesis develops as the ipsilateral peduncle is compressed against the tentorium. With continued progression of the herniation, bilateral decerebrate posturing eventually occurs; decorticate posturing is not always seen with the uncal herniation syndrome. In up to 25% of patients, the contralateral cerebral peduncle is forced against the opposite edge of the tentorial hiatus. Hemiparesis is then detected ipsilateral to the dilated pupil and the mass lesion. This is termed Kernohan’s notch syndrome and causes false localizing motor findings.

As uncal herniation progresses, direct brain stem compression causes additional alterations in the level of consciousness, respiratory pattern, and the cardiovascular system. Mental status changes may initially be quite subtle, such as agitation, restlessness, or confusion. This is soon replaced with lethargy and progression to frank coma. The patient’s respiratory pattern may initially be normal, followed by sustained hyperventilation. With continued brain stem compression, an ataxic respiratory pattern develops. The patient’s hemodynamic status may change, with rapid fluctuations in blood pressure and cardiac conduction. Herniation that is uncontrolled progresses rapidly to brain stem failure, cardiovascular collapse, and death.

Cerebral edema

Cerebral edema is an increase in brain volume caused by an absolute increase in cerebral tissue water content.Diffuse cerebral edema may develop soon after head injury. Vasogenic edema arises from transvascular leakage caused by mechanical failure of the tight endothelial junctions of the BBB. Vasogenic edema is frequently associated with focal contusions or hematomas. It eventually resolves as edema fluid is reabsorbed into the vascular space or the ventricular system.

Cytotoxic edema is an intracellular process that results from membrane pump failure. It is very common after head injury and is frequently associated with posttraumatic ischemia and tissue hypoxia. Normal membrane pump activity depends on adequate CBF to ensure adequate substrate and oxygen delivery to brain tissue. If the CBF is reduced to 40% or less of baseline, cytotoxic edema begins to develop. If CBF drops to 25% of baseline, membrane pumps fail and cells begin to die. Congestive brain swelling can contribute to cytotoxic edema if it becomes severe enough to increase ICP and reduce CPP so that cerebral circulation cannot be maintained.

Alteration in Consciousness

Consciousness is a state of awareness of the self and of the environment and requires intact functioning of the cerebral cortices and the reticular activating system (RAS) of the brain stem. An altered level of consciousness is the hallmark of brain insult from any cause and results from an interruption of the RAS or a global event that affects both cortices.

A patient who has sustained TBI commonly has an altered level of consciousness. Head-injured patients may be hypoxic from injury to respiratory centers or from concomitant pulmonary injury. Hypotension from other associated injuries can compromise CBF and affect consciousness. Global suppression may be present as a result of an intoxicating substance consumed before the injury. With increasing ICP from brain swelling or an expanding mass lesion, brain stem compression and subsequent RAS compression can occur.

Patients with altered levels of consciousness require careful monitoring and observation. Reversible conditions that can alter mental status, such as hypoxia, hypotension, hypoglycemia, should be corrected as they are identified.

The management of patients with brain metastases

As far as the management of patients with brain metastases, generally we don’t instantly go to the use of steroids unless the patient needs them. If the patient needs them, meaning that they have significant symptoms of increased cerebral edema, then we recommend starting out at high doses of steroids, such as 4 mg four times a day, but within an aggressive taper. The patients are going to need to be on long term steroids. Viagra professional works faster and lasts longer than you’ve ever known. If you are not able to wean them off the steroids then one should consider Pneumocystis prophylaxis which usually consists of a double strength Bactrim three times per week. There is no data to support the routine use of anticonvulsants and thus we only recommend anticonvulsants in patients who have already had a seizure. If patients are on anticonvulsants, one has to worry about a relatively high rate of Dilantin/Tegretol reactions, particularly in the setting of receiving radiation therapy where there is this syndrome of Dilantin-steroid taper where patients develop this inflammatory red rash on their skin which tends to progress to a Stevens-Johnson-like syndrome. So anticonvulsants are not a benign drug.

As far as the standard treatment for patients with brain metastases, particularly multiple brain metastases, radiation therapy remains the main form of treatment. There have been a number of studies, including several RTOG studies, that have tried to define the optimal dose. It appears that the optimal dose is somewhere between 20-40 gray. What has become clear however is that the standard way that radiation therapy used to be given – which is in 3 gray fractions or higher – can result in a significant amount of neuro-cognitive deficits if patients live long enough; meaning usually at least a year. Thus for patients who have relatively good prognostic factors, who you think might otherwise actually live for a year or longer, if you are going to treat them with external beam radiation therapy as far as whole brain radiation, one should significantly consider the use of lower fraction sizes, such as 2 to 2.5 grays in order to try to reduce the chances of long term significant neuro-cognitive sequelae.

How about the treatment of single brain metastasis? That represents a more questionable and changing area of management in these patients. If one looks at the data by CT scan one can see that approximately 50% of patients have brain metastasis of single lesions. However, when one uses more selective MRI scans the number reduces down to approximately 30% of patients with brain metastasis. The average or median diameter of these lesions is approximately 2.5 centimeters. About 5-10% of these are invasive, which means that 90-95% of these tumors are that type I CNS lesion that I talked about earlier, where almost all the tumor cells reside locally. This is the reason that surgery can offer a significant benefit for patients with brain metastasis. Another important area to recognize is that approximately 11% of patients with brain metastasis have no known systemic primary and just as importantly, approximately 15% of lesions seen on MRI scans in patients with known systemic cancer are not brain metastasis so one cannot just innocently assume that an abnormality on a scan represents metastasis in the brain.