Skull & Contents
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Conventional
Radiography
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Although conventional radiology of the skull has been largely replaced by CT and MRI, skull radiography is used sufficiently that a radiologist must be familiar with the radiologic features of the normal pediatric and adult skull as seen on today's standard (AP, lateral, and occipital) projections, including the coronal, sagittal, lambdoidal and spheno-squamosal sutures common to both, as well as the innominate and mendosal sutures and the spheno-occipital synchondrosis peculiar to newborn children and infants; inner table vascular grooves, such as anterior and posterior divisions of the middle meningeal artery, the spheno-parietal venous groove, the transverse and sigmoid dural venous sinuses and intra-diploic vascular channels and lakes.
Physiologic intra-cranial calcifications may be visible in the pineal gland, habenular commissure, falx, dura, choroid plexus of the lateral ventricles, and the clino-petrosal ligament.
Skull fractures, vascular grooves, and intra-diploic vascular channels are recognizable by their distinctive radiographic characteristics and the predictable anatomic locations of the sutures, the inner table arterial grooves, and dural sinus channels.
Artifacts,
particularly on the lateral skull radiograph may mimic pathologic abnormality.
I. Indications for Head Radiography
Skull radiography is rarely indicated for non-traumatic intracranial signs and symptoms. Traumatic skull radiographic indications occur slightly more frequently, and include penetrating foreign body(s); depressed skull fracture; and a limited (AP and lateral) radiographic examination of the skull of children with mild - moderate blunt head trauma requiring head CT in order to document a lineal, non-depressed skull fracture that might not be recorded on CT. That a linear, non-depressed skull fracture, of and by itself, does not alter patient management is a commonly accepted tenet. The obvious fallacy of this tenet is that such fractures may cause an epi- or subdural hematoma or other intracranial injury which can only be seen on head CT. Whether CT is necessary in the face of a non-depressed skull fracture is a clinical decision based upon the neurologic status of the patient.
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Computed
Tomography (CT)
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CT is the imaging standard of care for cranial and intracranial pathology. Multislice CT provides a complete examination of the head in approximately 15 seconds after the patient is properly positioned, is noninvasive, and the current indications for head CT, both trauma and non-trauma are lenient (see Table 1).
The most common application
of head CT, by far, is without IV contrast. While only a single CT examination
is performed from the skull base to the vertex, images are presented at different
window settings for bone, brain, and blood. The CT technique used in the
Memorial Hermann Hospital Emergency Center is as follows:
Head CT Protocol
(GE Lightspeed Scanner)
Patient Preparation: Requesting physician must fill out a clinical history and indication sheet for all non-trauma head CTs.
Patient Position: Supine IV Contrast: None Quiet respiration Reconstruction/
Reformat:None
Scanner Parameters:Collimation Table Feed Start Stop Gantry Tilt
Filming:
ExtentBrain Subdural Bone
I. Indications for Head CT
(A) Non-trauma, (without IV Contrast) Loss of consciousness (LOC) actual or observed "Found down" without obvious cause Change of mental status "Worst headache of my life" First seizure Possible cerebral metastasis HIV with headache (B) Non-trauma, (with IV contrast) Follow-up known brain pathology (C) Trauma, (without IV contrast) Penetrating, all Blunt LOC, observed or documented Visable signs of head trauma Cephalhematoma Laceration Racoon-eyes Battle sign Hemotympanum Depressed skull fx Abnormal mentation Unequal or abnormal pupils
"Syncope" ("syncopal episode") is not an indication for head CT.
Table 1 Salzman-Turner Criteria for post-traumatic head CT
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Low
risk
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Intermediate
risk
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High
risk
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CT
unnecessary unless change in mental status
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Attending
physician decision regarding need for CT
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CT mandatory
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Glasgow
coma scale (GCS) 13 - 15
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GCS
9 - 12
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GCS
<8
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Unwitnessed
loss of consciousness (LOC)
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Altered
mental status
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Witnessed
LOC
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Only
1 neurologic sign or symptom
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Nausea,
vomiting
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Focal
neurologic deficit
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Otherwise
asymptomatic
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Major
facial trauma
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Abnormal
pupils
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Polytrauma
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Any
sign of basilar skull fracture
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Clinically
suspected skull fracture
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Skeletal
Anatomy
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I. Skull Base
The skull base is divided into the anterior cranial fossa defined by the frontal bone anteriorly and the margins of the lesser wing of the sphenoid, posteriorly; the middle fossa defined by the free margin of the lesser sphenoidal wings anteriorly and the petrous pyramids of the temporal bone, posteriorly; and the posterior cranial fossa extending from the petrous pyramids anteriorly to the occipital bone, posteriorly.
(A) Anterior Cranial Fossa - The anterior cranial fossa contains the frontal sinuses anteriorly, the lesser sphenoidal wings which, together with the orbital plate of the frontal bone, bilaterally form the orbital roofs with the midline structures, the crista galli, the cribriform plate and the planum sphenoidale, between. The planum sphenoidale, the superior surface of the body of the sphenoid bone, is continuous with the tuberculum sellae, the anterior surface of the hypophyseal (pituitary) fossa, which is a middle cranial fossa structure.
(B) Middle Cranial Fossa - The middle cranial fossa contains, centrally, the hypophyseal fossa bounded anteriorly by the tuberculum and anterior clinoid processes, medially by the floor of the hypophyseal fossa and posteriorly, the dorsum sellae and its posterior clinoids. Bilaterally, the floor of the middle cranial fossa contains three constant foraminae from lateral to medial and from posterior to anterior - the foramen spinosum, the foramen ovale, and the foramen rotundum containing the maxillary nerve and the irregularly marginated, rectangular, obliquely situated foramen lacerum which is not a true foramen, being covered by thin fibrous tissue. The anterior portion of the lateral wall of the middle fossa is the greater sphenoidal wing. The middle meningeal artery runs along the inner table of its base with its superiorly extending anterior and posteriorly extending posterior division. The remainder of the lateral wall of the middle fossa is made up of the squamosal portion of the temporal bone, which includes the mastoid process and mastoid air cells and the external auditory canal. The petrous pyramid contains the tympanic membrane (ear drum-head), the bones of the middle ear (incus, malleus, stapes), and the inner ear containing the cochlea.
(C) Posterior Cranial Fossa - The posterior cranial fossa is bounded anteromedially by the dorsum sellae, which is continuous with the clivus; anterolaterally by the posterior surface of the petrous pyramids; laterally by the parietal bones and posteriorly by the occipital bone. The largest opening of the skull and of the occipital bone is the foramen magnum, through which passes the medulla oblongata, the spinal cord (spinal medulla). The midsagittal plane of the anterior arc of the foramen magnum is the basion and its posterior counterpart, the opisthion The basion is a fundamentally important landmark in assessing the occipito-atlantal relationship. The internal auditory (acoustic) meatus is located on the posteromedial aspect of the petrous pyramid. The jugular foramen is lateral to the foramen magnum bilaterally. The jugular foramen transmits the jugular vein, which is the anterior extension of the superior sagittal sinus and its continuation anteriorly as the transverse sinus and sigmoid sinus. The inner table grooves for these sinuses may be visible by both conventional radiography and CT.
Constant openings in the cranial fossae include:
Anterior: cribriform plate foramina Middle: optic canal superior orbital fissure foramen spinosum foramen ovale foramen rotundum (foramen lacerum) hiatus for the greater and lesser petrosal nerves Posterior: foramen magnum internal auditory meatus jugular foramen hypoglossal canal
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Brain
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As stated at the very outset, this Primer is purposefully designed to provide beginning radiology residents with the basic principles, protocols, techniques, and to illustrate the imaging anatomy sufficiently to enable the resident to recognize alterations in that anatomy consistent with traumatic or non-traumatic pathology. To that end, the basic intracranial anatomy shown on axial images from the skull base to the vertex is illustrated in Figures B1 to B13. Obviously much more complete and detailed neuroimaging anatomy will be learned in the neuroradiology rotations.
At the level of the middle-posterior cranial fossae (Image B1), the 4th ventricle, which lies between the pons, anteriorly, and the cerebellum, posteriorly, is the communication pathway for flow of cerebrospinal fluid (CSF) from the aqueduct, superiorly, and the central canal of the medulla, inferiorly. The basalar artery, formed by the junction of the two vertebral arteries, lies anterior to the pons and gives rise to the two posterior cerebral arteries.
The axial image rostral to the petrous pyramids (Image. B2) shows the frontal and temporal lobes and the cerebellum. The pituitary gland is located in the hypophyseal (pituitary) fossa of the sella, anterior to the dorsum sellae.
The middle cerebral artery, which lies in the Sylvian fissure arises from the cavernous portion of the internal carotid artery.
The perimesencephalic cistern surrounds the brain stem which consists of the pons, medulla and the mesencephalon.
The faint, bilateral, obliquely situated density with a sharply defined lateral margin is the tentorium cerebelli.
Images above the sella show the five-pointed suprasellar cistern which contains with in it the pituitary gland and the superior portion of the internal carotid artery. The triangular shaped midline posterior aspect of the suprasellar cistern is the interpeduncular fossa. At these higher levels, the posterior-most portion of the perimesenteric cistern is called the quadrigeminal cistern. The aqueduct, connecting the fourth and third ventricles extends rostrally through the midbrain.
The CT images above the suprasellar cistern show intracranial anatomy which is peculiar to the level of the image as well as the level-dependent appearances of the same anatomic structures, eg., the lateral ventricles. These observations become apparent in studying images B5 - B13.
An axial image through the inferior aspects of the anterior and posterior portions of the third ventricle, for example (Image B5), would also show the confluence of sinuses and the superior vermus of the cerebellum, all structures unique to this level of image. The anterior horn of the lateral ventricle, the caudate head, the anterior limb of the internal capsule, the lentiform nucleus, the external capsule, the insular cortex and the straight sinus are also visible on this and subsequent higher slices.
More superiorly (Image B8), at the level of the roof of the 3rd ventricle, the anterior portion of the bodies of the lateral ventricles are separated by the septum pellucidum, and the posterior horns by the splenum of the corpus callosum. The olive-shaped caudate head (nucleus) is always found in the concavity of the anterior horn of the lateral ventricle.
Rostral to the ventricular system and the forebrain structures (Image B11), the cerebral sulci and gyri and the falx throughout the length of the interhemispheric fissure, become visible.
The sagittal sinus is typically visable on the superior-most image of the brain (Image B13). Physiologic dural calcifications may be present.
At the conclusion of this chapter, it seems appropriate to include typical CT examples of a few intracranial abnormalities commonly encountered in emergency radiology practice such as, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, shear injury, intracerebral hemorrhage, brain herniation, hydrocephalus, cerebral infarction (stroke), and diffuse brain edema.
EPIDURAL HEMATOMA
Epidural hematoma (EDH) is the accumulation of blood between the dura and the inner table of the skull. Normally, because the periosteal surface of the dura is densely adherent to the inner table of the skull, no epidural space exists. Blunt trauma to the head, with or without skull fracture, may cause the dura to separate from the inner table. The separation may occur on the side of the trauma (“coup”) or the contra lateral side (“contra-coup”). The source of bleeding into the traumatically created epidural “space” may be from dural sinuses, intradiploic veins, meningeal vessels or, most commonly, from injury to the middle meningeal artery or its anterior or posterior branches. The classic CT appearance of an epidural hematoma is a sharply defined, biconcave, high-attenuation density interposed between the inner table of the skull and the brain. The mass compresses the brain and may cause compression or obliteration of the ipsilateral lateral ventricle and a midline shift. The hematoma is limited in extent by the sutural dural attachments.
The
classic CT appearance of an acute SDH is a crescentric homogenous high-attenuation
mass between the skull and the cerebral cortex without the sutural-dural limitation
characteristic of EDH.
CHRONIC ISODENSE SUBDURAL HEMATOMA
Fig. 2
This man sustained a closed head injury 2 months prior to this CT scan which shows a relatively large right frontal subdural hematoma ( * )made subtle because its density is very close to that of the underlying, compressed cerebral cortex with obliterated sulci (arrows). Minimal right-to-left midline shift is present deep to the hematoma.
Subarachnoid
hemorrhage is blood in the (actual) subarachnoid space, usually due to trauma.
The blood comes from disrupted small vessels that pass through the
arachnoid space, cortical surface vessels, and direct tear of arteries and
veins beneath a fracture or associated with penetrating trauma.
On CT,
the blood appears as a high-attenuation
density in the sulci, the basilar
cisterns and, particularly
the interpeduncular cistern
in the presence of skull base fractures.
Subarachnoid blood
causes the falx to become dense and wide with irregular margins and, covering
the posterolateral surfaces of the sagittal sinus, results in the “pseudodelta”
sign. The “delta” sign represents
a filling defect in the sagittal sinus on contrast-enhanced head CT and is
purported to represent thrombosis of the sagittal sinus. On a non-contrast head CT of a patient with
subarachnoid hemorrhage, the high intensity of the subarachnoid blood covering
the margins of the sagittal sinus relative to the low-intensity of the unenhanced
sinus blood constitutes the “pseudodelta”
sign described by Yeakley
[9].
In Images B26, B27, B28, B29, and B30, see if you can locate some of the following:
| a | subarachnoid hemorrhage |
| b | transtentorial herniation |
| c | intraventricular hemorrhage |
| d | cerebral contusion |
| e | diffuse axonal (shearing) injury |
| g | corpus callosum hemorrhage |
| h | diffuse cerebral edema |
In Images B33, B34, and B35, locate blood in the following:
| a | Sylvian fissure |
| b | interpeduncular cistern |
| c | ambient (perimesencephalic) cistern |
| d | supratentorial blood |
| e | interventricular blood |
The etiology
of diffuse brain edema is protean with trauma and hypertension being the most
common causes in adults and child abuse, strangulation, and aspiration most
common in pediatric patients.
On CT, diffuse cerebral edema is typically manifest by effacement of the cortical sulci, loss of the grey-white interface, and compression of the ventricles.
Diffuse
axonal injury (DAI) is usually the result of an acceleration–deceleration
injury to the head, although it certainly may also occur following direct
blunt trauma to the head in which the brain, lagging behind the speed
of movement of the skull, results in a strain-shearing mechanism that preferentially
tears axons at the gray-white matter junction.
The adjective “diffuse” refers not to the cortical extent of the lesion
but to the fact that the bulk of the injury occurs deep to the cortex.
Consequently, CT typically shows only the “tip of the iceberg” in the
form of small, irregular, high-intensity signals, typically located in the
periphery of the frontal lobes but may involve other lobes as well. The true extent of DAI is best demonstrated
by MRI. The important clinical fact
regarding DAI is that it causes immediate, irreversible, axonal injury leading
to severe post-traumatic dementia.
Intracerebral
hemorrhage is bleeding into the cerebral parenchyma.
The most common causes of this non-traumatic form of intracranial bleed
are hypertension, cerebral aneurysms, and vascular malformations.
Hypertension is the most common cause of intracerebral hemorrhage in adults and one of the common sites is the thalamus. Dissection into the ventricular system occurs in approximately 50% of hypertensive intracerebral bleeds. Intracerebral hemorrhage appears as an area of high attenuation in the cerebral parenchyma on axial non-contrast CT.
Hydrocephalus,
the accumulation of excessive amounts of cerebrospinal fluid (CSF) in the
ventricular system due either to an obstruction of the flow, or impaired resorption,
of CSF, may be communicating
(non-obstructive) when the entire ventricular system is enlarged or non-communicating
(obstructive) when only a part of the ventricular system is involved.
Hydrocephalus is characterized by the ventricles being disproportionately
enlarged relative to the sulci, whereas the ventricular and sulcal dilation
is proportionate in brain atrophy.
The CT appearance of hydrocephalus reflects the pathology described above. The temporal horns of the lateral ventricle are the most sensitive indicators of increased interventricular pressure and a width of >3mm of the temporal horns is said to indicate hydrocephalus. With marked, or increasing, intraventricular pressure, the cortical sulci may become effaced.
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 in Fig. 3:
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.
Lateral
herniation of the cingulate gyrus beneath the falx is called subfalcine or
cingulate herniation and is characterized on axial CT by herniation of the
corpus callosum and the ipsilateral lateral ventricle beneath the falx.
Downward (rostrocaudal, transtentorial) herniation may be lateral or central. Lateral refers to displacement of the medial portion of the temporal lobe (uncus) through the tentorial incisura. When unilateral, uncal herniation is characterized on axial CT by asymmetry of the six-pointed suprasellar cistern and compression of the ipsilateral ambient (perimesencephalic) cistern. Central transtentorial herniation, usually due to massive cerebral edema or large axial or extra-axial hemorrhage, is recognizable on axial CT by severe compression, or obliteration, of the suprasellar cistern, all the cisterns surrounding the midbrain, and the forth ventricle.
SUBFALCINE AND DOWNWARD TRANSTENTORIAL BRAIN HERNIATION
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This patient
sustained a left temporoparietal fracture (g) in a fall 6 weeks prior to this
CT scan indicated because of seizures. The patient has a large right subdural
hematoma
( * ), small bilateral subarachnoid hemorrhages (arrows), intraventricular
hemorrhage (curved arrow), and bilateral frontal lobe shear injuries. The
subdural hematoma has caused massive increase in right sided intracranial
pressure forcing the right lateral ventricle (a) and the corpus callosum (b)
to the left, beneath and lateral to, the free margin of the falx (subfalcine
or cingulate herniation). Obliteration of the suprasellar and ambient (perimesencephalic)
cisterns indicates downward transtentorial herniation.
Cerebral
infarction (“ischemic stroke”) with resultant neurologic dysfunction is a
common reason for emergency center admission. Emboli, usually from the common carotid
bifurcation and the internal carotid artery, are the most common cause of
cerebral infarction. Thrombosis
of major arteries, and most commonly the middle cerebral artery (MCA),
is the second most common etiology. Because
of recent advances in the systemic and local use of thrombolytic agents, which
must be instituted within a 1-5 hour post-ictal “window,” CT is even more
essential in the assessment of patients with non-traumatic, persistant neurologic
deficits.
A major
contribution of head CT in patients with the clinical picture just described
is to exclude intracranial hemorrhage, tumor, or infection as etiology
for the neurologic signs and symptoms.
It is essential to remember that, with ischemic stroke, the head CT obtained
within the first 4-6 hours following the onset of the neurologic deficit may
be normal. Cerebral CT angiography is useful in delineating arterial embolism
or thrombosis. MRI, and particularly
diffusion MR, is the imaging modality of choice because it records
the very earliest pathologic changes of brain infarction.
The early findings of brain infarction on non-contrast head CT include hyperdensity
in the region of the middle or anterior cerebral artery reflective of acute
thrombus; hypodensity of the basilar ganglia, loss of insular cortex, and
hypodensity of the white matter; and slight mass effect.
Only approximately 5% of cerebral infarcts are initially hemorrhagic.
Lacunar infarct
refers to occlusion of an end artery that supplies the white and deep gray
matter, typically of the basilar ganglia.
Because the infarcted area becomes cystic, lacunar infarcts appear
as small hypodense areas most commonly in the basilar ganglia on non-contrast
CT.
Questions
regarding emergency radiology should be directed to Dr.
Harris. Concerns or questions regarding the function or design of
this site should be directed to Thea
Troetscher, RN.
Copyright ©
2000 Harris & Troetscher
