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MRI initially provided two types of images

MRI initially provided two types of images, designated T1 and T2. For brain tumors, the former generally showed a well-demarcated area of low density, and the latter showed bright whiteness that encompassed a more extensive region owing to the signal of the surrounding brain edema. With the availability for general usage in 1988 of gadolinium contrast for MRI, a new set of criteria of usage and differential diagnostic considerations in brain imaging have quickly evolved. T1 gadolinium imaging is the most precise way to image a brain tumor, and patients can often be followed up during and after treatment with that type of study alone. Such an approach is easier for patients because it reduces the length of time otherwise spent on T2 scanning. Now and then, T2 images are useful. For example, T2 images, besides showing the extent of edema, also delineate the demyelinating effects of radiation on white matter. FLAIR images, a variant of T1, are even better for this.


Metastases These are remarkably variable.
Some enhance brightly and solidly with gadolonium. Others are in ring
configuration. Many are invisible with contrast CT.
Acoustic neuromas These are invariably intensely
contrasted by gadolinium, even more reliably than by CT.
Meningiomas Same as for acoustic neuromas.
Pituitary adenomas These always enhance less than
the normal pituitary gland. MRI is superior in every way to CT,
especially when thin slices and magnified views are ordered.
Glioblastoma These are almost always in ring
Anaplastic astrocytomas These are sometimes solidly
bright; they are often patchy, may be noncontrasting, and may look like
low-grade astrocytoma.
Low-grade astrocytomas These do not enhance. They are
often invisible by CT or are imaged only as vague low density.
Oligodendrogliomas These generally do not enhance
unless anaplastic and are often invisible on CT unless they are
Primary brain lymphomas These usually exhibit
homogeneous enhancement and are smoothly rounded. Periventricular
location is common. They are multiple in about a fourth of cases. This
lesion does not often look like glioblastoma but is easily mistaken for
metastases if multiple.

Cerebral angiography seldom is used in the diagnosis of brain tumors. In a few circumstances, neurosurgeons, in preparation for surgery, require a more precise knowledge of the pattern and position of blood vessels, which can be obtained only by angiography. The procedure is also used to embolize highly vascular meningiomas or to study cerebral dominance by injection of barbiturate into the carotid artery (the Wada test) in left-handed individuals who are to have surgery near language areas. Preoperative determination of cerebral localization helps surgeons to plan the extent of surgery and to avoid creation of postoperative language deficits in the patient.

Examination of the spinal fluid has limited indication in the diagnosis of brain tumors. One is to rule out an inflammatory disorder mimicking a brain tumor. Another is to establish the diagnosis of benign intracranial hypertension in patients with uninformative MRIs. In addition, spinal fluid cytology may be useful for determining instances of malignant meningitis secondary to metastatic neoplasms in association with spinal spread of medulloblastoma in some children and in identifying primary lymphomas of the brain in cases in which MRI changes are ambiguous.

The routine electroencephalogram (EEG) has no role in the diagnosis of brain tumors and does not assist in the choice of anticonvulsant drugs for patients with brain tumor. However, specialized intraoperative neurophysiologic techniques, such as depth electrode studies and intraoperative monitoring, may be useful in identifying and removing epileptogenic areas adjacent to brain tumors or to avoid resection of critical brain regions adjacent to tumors.

Positron emission tomography (PET) is able to quantify biochemical functions, such as oxygen and glucose utilization, within tumors as well as in normal brain tissue. PET scanning is a powerful research tool of limited availability for routine clinical purposes. Its spatial resolution is inferior to that of both CT and MR. In patients with brain tumors who develop recurrent symptoms after radiation therapy, PET can differentiate, with about 70% accuracy, radiation-induced injury from tumor recurrences. These disorders often appear identical on MRI.

Differential diagnosis of brain tumors

Patients who present with symptoms and signs of increased intracranial pressure or a first convulsive seizure need to be hospitalized. Diagnosis and treatment measures must be started at once; it may be unsafe to wait. Those who present with focal neurologic impairment and who do not have symptoms of increased intracranial pressure may reasonably be evaluated in the outpatient setting for other conditions that are often considerations in the differential diagnosis of brain tumor. The tempo of evolution of symptoms and signs of focal neurologic impairment, much more than their severity, governs urgency of evaluation. The tempo also strongly influences diagnostic considerations. Although an occasional brain tumor may manifest with such rapid onset of hemiparesis or aphasia that a stroke is mimicked, most do not. Associated aspects of the history, such as recent head trauma, previous episodes of reversible neurologic impairment, or recent infection and fever, should direct attention to diagnostic alternatives such as subdural hematoma, multiple sclerosis, or cerebral abscess. Simply stated, it is the careful history, not the neurologic examination, that usually points to the alternative diagnoses.


Brain imaging by MRI or CT scans is an indispensable component of the modern diagnosis of the presence, but not the type, of brain tumors. One type of tumor can look like another or even resemble a non-neoplastic mass lesion, such as a brain abscess, fungal infection, parasitic invasion, demyelinating disease, or stroke. For definitive diagnosis and adequate treatment planning, one must obtain a tissue diagnosis whenever possible. This can be made either by direct surgical biopsy or, in the case of some non-neoplastic conditions, by judging CT or MRI responses to particular therapies.

MRI is almost always superior to CT scanning in diagnosing intracranial mass lesions. MRI outlines posterior fossa structures and tumors with a clarity that CT cannot achieve because of x-ray distortions caused by the bony structure of that region. In several types of tumor, particularly the low-grade gliomas, MRI may show extensive brain infiltration in cases that fail to produce any image abnormality on CT or, at most, show a vague area of low density. Although either MRI or CT should be used with contrast enhancement in cases of suspected brain tumor, the passage of such contrast agents beyond the blood-brain barrier into the tissue does not necessarily imply the presence of a histologically malignant tumor. For example, although malignant gliomas almost always show contrast enhancement, so do meningiomas, which are entirely benign if they can be fully removed surgically.

CT scans done without contrast enhancement are of little value in the diagnosis of brain tumors or other mass lesions. Although it is true that hemorrhage, calcifications, hydrocephalus, and shift can be well seen on a non-contrast CT scan, the interpretation of even these conditions is tentative because each can have an underlying causative structural abnormality, such as a brain tumor, which may fail to appear on a non-contrast CT study. Allergy to CT dye is rare and is readily manageable. Currently available non-ionic CT dyes have an extremely low incidence of side effects. Currently used CT dyes carry little risk of causing renal dysfunction in normally hydrated patients who are not known to have kidney disease.


Hematomas, especially in tumors
that have a tendency to bleed, such as melanoma
Abscesses, including fungal
Parasitic infections, such as
Vascular malformations,
especially those without arteriovenous shunts
Solitary large plaques of
multiple sclerosis
Progressive strokes (rare)

Initial evaluation


Brain tumors present in two patterns, not necessarily mutually exclusive. One consists of nonfocal symptoms of increased intracranial pressure, such as headaches, nausea, vomiting, confusion, and lethargy. The other consists of symptoms or signs of focal brain dysfunction, such as hemianopia, hemiparesis, cranial nerve palsies, or focal seizures. Such signs of focal brain dysfunction may have convincing localizing value even before an image of the brain is made by computed tomography (CT) or magnetic resonance imaging (MRI).

Some tumors that arise in neurologically “silent” areas, such as the parietal or frontal association cortices, may produce only nonfocal generalized symptoms of headache, confusion, behavioral change, or, eventually, a seizure, despite growing to a considerable size. Although the capacity to reach early diagnosis by CT or MRI has greatly reduced the numbers of patients in whom symptoms of increased intracranial pressure represent initial complaints, examples still remain, especially in association with fast-growing tumors and in children. The latter are particularly likely to have tumors in the posterior fossa that tend to obstruct spinal fluid pathways earlier than do supratentorial tumors. The tempo with which a brain tumor grows also influences the presenting symptoms. Despite the fixed space within the skull (once infantile sutures have closed), the human brain possesses a remarkable capacity to make room for a slowly growing tumor. Because of this, and even allowing for the relative rapidity of growth of aggressive brain tumors, such as glioblastomas, the patient usually appears better clinically than might be expected from the degree of abnormality seen on CT or MRI scan.


  • Frontal lobe
  • Generalized
  • Focal motor
    seizures (contralateral)
  • Expressive aphasia
    (dominant side)
  • Behavioral changes
  • Dementia
  • Gait disorders,
  • Basal ganglia
  • Hemiparesis (contralateral)
  • Movement disorders
  • Parietal lobe
  • Receptive aphasia
    (dominant side)
  • Spatial
    disorientation (nondominant side)
  • Cortical sensory
    dysfunction (contralateral)
  • Hemianopia (contralateral)
  • Occipital lobe
  • Hemianopia (contralateral)
  • Visual disturbances
  • Temporal lobe
  • Complex partial
    (psychomotor) seizures
  • Generalized
  • Behavioral changes
  • Olfactory and
    complex visual auras
  • Corpus callosum
  • Dementia (anterior)
  • Behavioral changes
  • Asymptomatic (mid)
  • Thalamus
  • Sensory loss (contralateral)
  • Behavioral changes
  • Language disorder
    (dominant side)
  • Midbrain/pineal
  • Paresis of vertical
    eye movements
  • Pupillary
  • Precocious puberty
  • Sella/optic nerve/pituitary
  • Endocrinopathy
  • Bitemporal
  • Monocular visual
  • Pons/medulla
  • Cranial nerve
  • Ataxia, nystagmus
  • Weakness, sensory
  • Spasticity
  • Cerebellopontine angle
  • Deafness (ipsilateral)
  • Loss of facial
    sensation (ipsilateral)
  • Facial weakness (ipsilateral)
  • Ataxia
  • Cerebellum
  • Ataxis (ipsilateral)
  • Nystagmus

Osmotic Agents

Additional therapy for increased ICP includes the use of osmotic diuretics, such as mannitol. In the face of deepening coma, pupil inequality, or other deterioration of the neurologic examination, mannitol may be life saving. Mannitol (0.25 to 1.0 gm/kg) can effectively reduce cerebral edema by producing an osmotic gradient that prevents the movement of water from the vascular space into the cells during membrane pump failure and draws tissue water into the vascular space. In effect, this reduces brain volume and provides increased space for an expanding hematoma or brain swelling. The osmotic effects of mannitol occur within minutes of its administration and peak at about 60 minutes after the bolus has been administered.

The ICP-lowering effects of a single bolus may last for 6 to 8 hours. Mannitol has many other neuroprotective properties. It is an effective volume expander in the presence of hypovolemic hypotension and therefore may maintain systemic blood pressure required for adequate cerebral perfusion. It also promotes CBF by reducing blood viscosity and microcirculatory resistance. Mannitol reduces RBC deformity and therefore improves oxygen carrying capacity. It is an effective free radical scavenger, reducing the concentration of oxygen free radicals that may promote cell membrane lipid peroxidation.

Pancreatic cancer information

Emergency Department


Rapid sequence induction (RSI) for intubation is an effective method for securing the airway in combative or agitated patients.


If hypotension is detected at any time in the course of the emergent management of a head-injured patient, a cause should be sought other than the head injury. Hypotension is rarely caused by head injury except as a terminal event, but important exceptions include profound blood loss from scalp lacerations and pediatric patients with relatively small circulating blood volumes. In small children, hemorrhage into an epidural or subgaleal hematoma can produce profound hypovolemic shock. In the presence of concomitant spinal cord injury, spinal cord hypotension may occur. This is rare and can be differentiated from hypovolemic hypotension by its nonresponsiveness to fluid administration.

Recently, it has been suggested that hypotensive patients with penetrating abdominal trauma may have better outcomes if fluids are restricted before operation. These studies did not include head-injured patients. In the case of the head-injured patient, systematic hypotension cannot be tolerated without profound worsening of neurologic outcome; fluids should therefore be delivered to maintain a systolic blood pressure of at least 90 mm Hg. Several laboratory and clinical studies have investigated the effects of the delivery of large amounts of fluid to severely head-injured patients who are hypotensive from other injuries and have not demonstrated clinically significant increases in ICP. Fluids should not be withheld in the hypovolemic hypotensive head trauma patient for fear of increasing cerebral edema and ICP. Hypotension from any cause increases mortality from the head injury by 30%. Hypotension may interfere with the accurate neurologic assessment of the brain-injured patient. Often, when blood pressure is restored, an improved neurologic status is observed.

As many as 60% of patients with severe head injury are victims of multiple trauma. The dramatic presentation of the head injury should not distract the clinician from a thorough search for other life threats.

The ED neurologic assessment should be compared with the initial prehospital examination, focusing on evidence of neurologic deterioration or signs of increasing ICP. If the patient is deteriorating or has signs of increased ICP, active intervention must be initiated in the ED.


Hyperventilation to produce an arterial P CO2 of 25 to 30 mm Hg will temporarily reduce ICP by promoting cerebral vasoconstriction and subsequent reduction of CBF. The onset of action is within 30 seconds and probably peaks within 8 minutes after the P CO2 drops to the desired range. In most patients hyperventilation lowers the ICP by 25%; if the patient does not rapidly respond, the prognosis for survival is generally poor. Prolonged hyperventilation probably loses its effectiveness and therefore is of limited value beyond the acute phase. The partial pressure of carbon dioxide should not fall below 25 mm Hg because this may cause profound vasoconstriction and ischemia in normal and injured areas of the brain. Prophylactic hyperventilation has been associated with worsened neurologic outcome when measured at 3 and 6 months after severe trauma and is therefore not recommended in head-injured patients who are not exhibiting signs of increased ICP.

Central Transtentorial

Central Transtentorial.

The central transtentorial herniation syndrome is demonstrated by rostrocaudal neurologic deterioration caused by an expanding lesion at the vertex or the frontal or occipital pole of the brain. It is less common than uncal transtentorial herniation. Clinical deterioration occurs as bilateral central pressure is exerted on the brain from above. The initial clinical manifestation may be a subtle change in mental status or decreased level of consciousness, bilateral motor weakness, and pinpoint pupils (<2 mm). Light reflexes are still present but often are difficult to detect. Muscle tone is increased bilaterally, and bilateral Babinski signs may be present. As central herniation progresses, both pupils become midpoint and lose light responsiveness. Respiratory patterns are affected and sustained hyperventilation may occur. Motor tone increases. Decorticate posturing, initially contralateral to the lesion, is elicited by noxious stimuli. This progresses to bilateral decorticate and then spontaneous decerebrate posturing. Respiratory patterns that may initially include yawns and sighs progress to sustained tachypnea, followed by shallow slow and irregular breaths immediately before respiratory arrest.


Cerebellotonsillar herniation occurs when the cerebellar tonsils herniate downward through the foramen magnum. This is usually caused by a cerebellar mass or a large central vertex mass causing the rapid displacement of the entire brain stem. Clinically, patients demonstrate sudden respiratory and cardiovascular collapse as the medulla is impinged. Pinpoint pupils are noted. Flaccid quadreplegia is the most common motor presentation because of bilateral compression of the corticospinal tracts. The mortality resulting from cerebellar herniation approaches 70%.

Upward Transtentorial.

Upward transtentorial herniation is occasionally seen as a result of an expanding posterior fossa lesion. A rapid decline in the level of consciousness occurs. These patients may have pinpoint pupils because of compression of the pons. A downward conjugate gaze with the absence of vertical eye movements is also observed.

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.