RADIOLOGICAL EXAMINATION OF THE BRAIN AND SPINAL CORD.
Imaging of the skull, spine and central nervous system utilises techniques which permit a remarkable accuracy in pathological and anatomical diagnosis.
These include:
1. Simple X-ray and tomography
2. CT
3. MRI
4. Ultrasound
5. Angiography
6. Myelography and radiculography
7. Isotope scanning.
The newer techniques have helped to change radically the accuracy of diagnosis, the prognosis and the treatment in many neurological conditions. This is particularly so in the field of tumours and vascular lesions where the introduction of CT in 1972 initiated a new era in radiological diagnosis.
PLAIN FILMS
The need for plain skull films in diagnosis has virtually disappeared. They may show:
• calcification: glioma, meningioma, anteriovenous malformation, post-
infective foci:
pituitary fossa enlargement; lytic bone deposits; fractures;
• Plain spine films are initially utilized in the evaluation of trauma, they are
generally not helpful in back pain.
Fig. Lateral (A) and PA (B) skull films of child with raised intracranial pressure and marked suture diastasis involving the coronal and sagittal sutures.
ULTRASOUND
The neonatal brain can be imaged through the open anterior fontanelle for intraventricular haemorrhage, hydrocephalus or other suspected intracranial pathology. Carotid Doppler studies are used for the diagnosis of carotid stenosis.
COMPUTED TOMOGRAPHY (CT)
A typical brain study is carried out using 5-
Fig. 10.2 Sections through a normal brain CT.
Each brain study of approximately 14 sections requires careful analysis but with practice it should be possible to spot major abnormalities at a glance. Compare the two sides with each other while looking through the series paying special attention to:
• midline shift;
• localized area of altered density;
• presence of mass lesion.
Cerebrospinal fluid appears black. Recent haemorrhage and haematoma appear white.
MAGNETIC RESONANCE IMAGING (MRI)
MRI scans demonstrate the brain using a multiplanar facility in axial, coronal and sagittal planes with excellent views of the posterior fossa, as there are no bone artefacts. It is a particularly sensitive investigation in the detection of tumours such as pituitary adenomas and acoustic neuroma. MRI is superior to CT in many situations including:
• lesions of pituitary fossa;
• spinal cord;
• visualization of demyelinating plaques in multiple sclerosis;
• differentiation of grey and white matter;
• identification of the lesional causes of epilepsy.
|
|
Fig. Sections through a normal brain MR scan.
Instead of axial scanning in CT, two projections are usually utilized: axial and either coronal or sagittal. The appearances vary with the type of pulse sequence e.g. onTI the CSF appears black (low signal) whereas onT2 it appears white (high signal). Both sequences are usually used for a study
|
|
Fig. 10.1 MRI: vertebral collapse of TI2 causing early spinal cord compression
Choice of investigation
Nearly all patients with suspected intracranial lesions are now examined first by CT or MRI with or without a preliminary simple skull X-ray. In many cases this will establish the diagnosis or, if tumour is suspected, will exclude the possibility of tumour.
Angiography still has a valuable role to play, particularly in the elucidation of vascular lesions and has expanded its role in interventional procedures. It may also be occasionally required to further elucidate the pathology and blood supply of a tumour shown at CT or MRI. Isotope scanning once widely practised for tumour localisation is now obsolete for this purpose, but has new applications for functional and metabolic imaging by positron emission tomography (PET) and single photon emission tomography (SPET).
In neonates and small infants it is possible to examine the brain and ventricles by ultrasound using the ‘window’ provided by the open fontanelle and many lesions can thus be diagnosed. Unfortunately the technique cannot be used in the same way for adults and older children because of the skull barrier. However, Doppler ultrasound is used in adults for screening carotid bifurcations in suspected atheromatous stenosis.
Fig. 12.1 Ultrasound coronal section in an infant showing hydrocephalus. V = dilated lateral ventricle.
MRI has proved superior to CT in the demonstration of demyelinating diseases such as MS, and is also superior in the delineation of many posterior fossa lesions. As techniques improve it is likely to further supplant CT.
Plain radiography
Plain radiography of the skull may show evidence of a cerebral tumour either in a general manner or, less commonly, in a manner permitting accurate localisation. The general evidence of cerebral tumour consists of changes in the skull induced by the chronic raised intracranial pressure. In children the most important of these is suture diastasis; in the adult it is thinning or erosion of the dorsum sellae. So-called ‘increased convolutional markings’ or ‘copper beating’ of the skull vault is now generally considered to be of little diagnostic importance.
Fig. Diagram of the sellar changes in raised intracranial pressure in the adult, (a) to (f) show progressive changes from slight in (b) to gross in (f).
Localising evidence of the presence of a cerebral tumour may manifest as local erosion of the bony skull; thus a pituitary adenoma may expand and ‘balloon’ the sella, and an acoustic neurinoma may expand and erode an internal auditory meatus. Both these changes can be demonstrated by plain X-rays as can erosions in the skull vault by metastases. Lateral displacement of the calcified pineal gland is another important radiological sign often observed in adults with tumours in a cerebral hemisphere. Local bony thickening or hyperostosis is not infrequently seen with meningiomas, particularly in their common parasagittal or sphenoidal ridge localization.
Primary brain tumours cause neurological symptoms due to distortion, pressure and displacement of adjacent structures. Even meningiomas or other benign tumours can cause a severe neurological deficit from the effect of expansion of the tumour in a confined space.
|
|
Fig. Meningioma growing through the skull vault. Note the sun-ray spiculation and the enlarged vascular channels of the skull vault. (A) Lateral view. (B) PA view.
Fig. Glioma: CT scan pre- and post-contrast showing a large frontal mass
|
|
|
|
.Fig. Astrocytoma: coronal MRI in a child with a posterior fossa mass (arrow).
Fig. Meningioma: CT scan pre- and post-contrast showing uniform enhancement.
Intracranial calcification is seen with a small proportion of intracranial tumours. Cerebral gliomas form about half the tumours seen in clinical practice; about 7% of these will show calcification in the tumour enabling a localisation to be made on plain X-ray. Meningiomas calcify in some 10% of cases, whilst craniopharyngiomas, presenting in children, show calcification in over 70% of cases. Tumour calcification has to be distinguished from the calcification seen in various other conditions. The calcification in many of these is pathognomonic, for instance, the sinuous tramline occipital calcification seen in the Sturge-Weber syndrome or the ring calcification seen in a small proportion of cerebral aneurysms.
Fig. Heavily calcified craniopharyngioma growing upwards and forwards from the sella
Although plain X-rays are helpful in some cases and may prove diagnostic in a few, further specialised investigation is essential with most suspected tumours for accurate localisation and for further assistance towards diagnosis before a neurosurgeon performs a craniotomy. Generally speaking, the primary method of investigation will be the least traumatic and invasive. This will be CT scanning or MRI.
ARTERIOGRAPHY
Arteries of the cerebral circulation may be visualized by:
• digital subtraction angiography (DSA) with contrast injection in the superior vena cava or aortic arch;
• selective injection of contrast into the carotid and vertebral arteries;
• magnetic resonance angiography (MRA): Demonstrates cerebral arterial or venous circulation and likely to replace conventional contrast angiography in some situations.
Arteriography is useful in evaluation of aneurysms and arteriovenous malformations.
Fig. 12.6 Large aneurysm which presented as a suprasellar mass. (A) Lateral view. (B)AP view.
MYELOGRAPHY
Since the introduction of MRI, this investigation is now needed infrequently, mainly in patients for whom MRI is contraindicated. Water-soluble contrast medium is introduced into the theca usually by means of a lumbar puncture. Views of the lumbar theca in lateral, anteroposterior and oblique projections demonstrate the spinal cord and nerve roots.
TYPES OF PRIMARY NEOPLASMS
Glioma. The commonest primary intracranial tumour and most frequent cause of pathological intracranial calcification; >50% of primary intracranial tumours are gliomas: astrocytoma, glioblastoma, oligodendroglioma and ependymoma. On CT, the tumour appears as an area of altered density, with surrounding oedema and mass effect. Significant enhancement usually follows intravenous contrast.
Meningioma. Meningiomas represent 15-20% of primary brain tumours. They are benign, well-defined lesions, arising from any part of the meningeal covering of the brain, frequent sites being the falx, parasagittal region, sphenoid wing and the convexity of the hemispheres. CT or MRI show well-defined lesions enhancing strongly and diffusely after intravenous contrast.
Acoustic neuroma. Arise in or near the internal auditory canal, and may feature widening and erosion of the canal. MRI is more sensitive than CT in its detection.
Pituitary tumour. Plain films may show pituitary fossa enlargement or erosion. However, tumours such as prolactinomas are usually < I cm in diameter and CT or preferably MRI is required for diagnosis.
Cerebellar tumour. The majority of intracranial tumours in children occur below the tentorium cerebelli: medulloblastoma is the most common intracranial tumour with ependymoma the next most frequent.
METASTASES
Metastases are some of the commonest malignant cerebral lesions, involve any part of the brain and may be single or multiple. CT or MRI often cannot reliably distinguish between a primary neoplasm or a solitary secondary tumour, but the clinical setting may help. Multiple lesions are almost certainly metastases. Secondaries to the brain are commonly from bronchial, breast and gastrointestinal neoplasms.
RADIOLOGICAL FEATURES
Metastases can be haemorrhagic, cystic or calcified and they may cavitate; surrounding oedoema is invariably present. After intravenous contrast, CT almost always shows enhancement of either the whole lesion or around the periphery, due to breakdown of the blood-brain barrier.
TREATMENT
• Palliative:
dexamethasone reduces oedema and relieves headache; radiotherapy.
• Surgical resection occasionally for a solitary metastasis.
Fig. Multiple metastases on a contrast enhanced CT scan (arrows)
Fig. CT scan in generalized cerebral Fig. CT scan of localized frontal
atrophy with enlarged sulci and cerebral atrophy in a child
ventricles.
CEREBRAL ATROPHY
Atrophic changes in the brain are usually idiopathic. Causes include:
• degenerative conditions;
• trauma;
• drugs;
• infection (end stage);
• congenital conditions.
Correlation between atrophic changes and clinical features is poor.
RADIOLOGICAL FEATURES
• Irreversible loss of brain substance results in enlargement of the CSF spaces: the ventricles, basal cisterns, cerebral and cerebellar sulci. Ventricular dilatation may also be noted in hydrocephalus. However, in hydrocephalus, the ventricles dilate with relatively normal sulci whereas in atrophy there is usually both ventricular and sulcal enlargement.
• Alzheimer’s disease: usually diffuse atrophy with relative sparing of cerebellum; the temporal lobes may be severely affected.
• Pick’s disease: circumscribed lobar atrophy.
Other dementias: usually non-specific diffuse atrophy as in Alzheimer’s disease.
CEREBRAL INFARCT
Fig. CT scan: haemorrhagic middle-cerebral artery infarct (arrow).
Fig. CT scan: middle-cerebral artery infarct with extensive low density.
Fig. MRI: left middle-cerebral artery infarct.
Infarction of the brain results from a deficient cerebral circulation from thrombosis or an embolic event and clinically presents as a stroke. Predisposing factors include hypertension, diabetes, a family history and the many causes of atherosclerotic disease or emboli. Symptoms and signs vary depending on the site of infarction.
• A transient ischaemic attack (TIA) produces a focal neurological deficit in which complete recovery of function occurs within 24 hours.
• A stroke is one in which the neurological deficit persists.
• A lacunar infarct occurs as a result of occlusion of small intracerebral arteries.
RADIOLOGICAL INVESTIGATIONS
• CT/MRI of brain.
• Carotid artery imaging: magnetic resonance angiography (MRA)/ Doppler ultrasound.
• Invasive arteriography should be avoided, but will occasionally be necessary.
RADIOLOGICAL FEATURES
The most useful role of CT/MRI is to confirm the presence of an infarct and to exclude haemorrhage or other abnormalities, thus expediting treatment with aspirin or anticoagulants.
• CT: may be and remain entirely normal, but most substantial infarcts that are going to be seen are visible within the first 24 hours. Initial abnormalities are often subtle. Loss of grey/white-matter differentiation evolves into reduced density, normally in an arterial supply territory, often with mild mass effect for the first few days and giving way to localized atrophic changes. About 15% develop haemorrhage, seen as an area of increased density.
• MRI: in association with MRA, is accurate and may demonstrate an occluded or stenosed vessel. The pattern and distribution of infarction is similar to CT.
EXTRACEREBRAL HAEMORRHAGE
Haemorrhage into the subdural or epidural space usually follows trauma. Neurological deterioration after a head injury should raise the suspicion of a haematoma whether or not there is a skull fracture. Chronic subdural haematoma may be found in the elderly, with blood accumulating slowly in the subdural space, possibly from a ruptured vein.
RADIOLOGICAL FEATURES
On CT, a subdural collection initially shows an area of peripherally placed crescentic fluid collection, lying adjacent to the cranial vault; it is seen as an area of altered density usually with a concave inner margin whereas an epidural haematoma has a convex inner border.
A recent haemorrhage is visualized as increased density (white) but subsequently this decreases to finally appear as an area of low density (black). Mass effect, with midline shift, indicates a significant subdural collection.
MRI is accurate for diagnosis and uses the same criteria as CT for differentiating a subdural from an epidural haematoma.
Fig. CT brain: recent right subdural haematoma (arrows) with a significant midline shift.
|
|
|
Fig. MRI brain: subdural haematomas (arrows) in a 3-week-old infant.
SUBARACHNOID HAEMORRHAGE
A subarachnoid haemorrhage is usually spontaneous, often the result of a ruptured aneurysm. Other causes include anticoagulant therapy and trauma. Sudden excruciating headache, nausea and vomiting, loss of con-ciousness or fits are the usual presenting symptoms. Hydrocephalus, either obstructive or communicating, is a recognized complication.
RADIOLOGICAL FEATURES
|
|
CT scanning is the investigation of choice, detecting recent haemorrhage more precisely than MRI. CT may show blood in the cisterns, fissures or ventricles. Arteriography is required in spontaneous subarachnoid haemorrhage to detect the source and site of bleeding, but should only be carried out if the patient is suitable for surgical intervention. Intracranial aneurysms are discovered in approximately 70% of cases. Unruptured aneurysms <4-
Fig. CT brain: subarachnoid haemorrhage with blood in the sulci, third ventricle and the posterior horn of the left lateral ventricle.
Fig. Arteriogram: aneurysm of the right middle-cerebral artery (arrow).
CAROTID ARTERY STENOSIS
Internal carotid artery stenosis may be either asymptomatic, present with transient ischaemic attacks (TIAs) or a stroke. In 30—40% of patients with TIAs, progression to a stroke results from distal infarction or embolization. The carotid artery may occlude totally without causing any symptoms.
RADIOLOGICAL INVESTIGATIONS
Colour Doppler ultrasound; arteriography.
RADIOLOGICAL FEATURES
• Colour Doppler accurately defines the stenosis, blood flow characteristics and alteration in peak velocities.
• MRA delineates the carotid arteries and any associated stenoses without the use of contrast material.
• Arteriography, either intravenous with computer subtraction or intraarterial readily shows the anatomical abnormality, though the latter should be avoided if possible, because of the risk of serious complications. The stenosis is usually found at the origin of the internal carotid artery.
|
|
Fig. Arteriogram demonstrating a critical stenosis at the origin of the left internal carotid artery.
ACROMEGALY
Acromegaly results from an excessive secretion of growth hormone, usually from a pituitary adenoma. Approximately half the adenomas are < I cm in diameter.
RADIOLOGICAL INVESTIGATIONS
Plain films: lateral skull, hands and soft tissue of heel; MRI; CT
RADIOLOGICAL FEATURES
MRI is the investigation of choice in order to demonstrate a pituitary adenoma. A plain lateral skull may feature:
• enlarged pituitary fossa: late stages only;
• protruding mandible (prognathism);
• prominent sinuses.
Hands: become broad and spadelike.
Lateral heel: soft-tissue hypertrophy is best assessed by means of the heel pad thickness. In acromegaly, this is often >
|
|
Fig. Acromegaly with protruding mandible and enlarged pituitary fossa. Compare with the pituitary fossa of a normal lateral skull.
|
|
Fig. Spondylolisthesis at L4/L5
|
|
Fig. Internal fixation to stabilize the abnormality.
RADIAL DIAGNOSTIC OF DISEASES OF THE BRAIN
AND SPINAL CORD
Over the past five years, advances in magnetic resonance imaging (MRI) have revolutionized the ability to visualize the brain and its coverings. Exceptional contrast resolution, multiplanar capability, and the lack of known harmful effects combine to make MRI, in the majority of circumstances, the preferred technique for the initial diagnostic evaluation of patients with neurologic disease. On going developments in magnetic resonance techniques that link the acquisition of physiologic and biochemical information to the display of morphology will soon further enhance the value of this technique as a diagnostic method. In spite of these advantages, however, computed tomography (CT) will continue to be the most widely applied tool for diagnostic imaging of the brain because of its widespread availability, accuracy, speed, and the easy ability to evaluate uncooperative or critically ill patients.
Skull radiography no longer has any meaningful role in the diagnostic evaluation of patients suspected of having neurologic disease. The technique is insensitive and nonspecific. It is also redundant, because even when abnormalities are seen on skull radiographs it is rare that the findings provide sufficient information on which to base patient management. Even though skull radiography no longer plays a role in clinical practice, knowledge of skull anatomy is essential for proper interpretation of CT and magnetic resonance scans of the brain. This knowledge may be facilitated through the study of multiple projections of skull radiographs, which provides a means for correlating the spatial relationships of structures seen on cross-sectional images.
THE CHOICE OF A DIAGNOSTIC TECHNIQUE
When available, MRI is the technique of choice for the initial diagnostic evaluation of the great majority of patients with neurologic disease. Important exceptions where CT remains the technique of choice for initial examination are 1) evaluation of patients after acute trauma; 2) evaluation of patients suspected of having an acute subarachnoid or parenchymal hemorrhage; and, 3) evaluation of patients with diseases affecting primarily the skull base or calvarium.
The array of techniques available with which to perform an MRI examination of the brain is too large and complex for discussion in this chapter. If one is to achieve optimal results from the examination, however, each scan should be tailored to maximize information that can be brought to bear on a particular case. Careful consideration must be given to the choice of pulse sequences and timing parameters used for each study, because depending on factors such as the age of the patient and the type of pathology suspected greatly influences the appearance of the images obtained. One of the great advantages of MRI over other imaging techniques is its ability to depict changes in chemical makeup of tissue. To maximize information obtained from a particular examination, one must not only have some understanding of the changes occurring with various disease states but also understand how images obtained from these altered tissues are affected by variation in MRI pulse sequences. Generally, every initial examination of the brain should include as a minimum one set of T1, proton density, and T2-weighted images.
With modern devices there are also many different ways to perform a CT scan, and as with MRI, each scan should be tailored to optimize information that may influence a particular case. Proper evaluation of some lesions, for example, requires the use of thin sections and special reconstruction algorithms and variation in the plane of section in which the scan is taken.
INTRACRANIAL CALCIFICATION
Certain structures within the skull are found with considerable frequency to contain calcium or other mineral deposits. Calcification of the dura and choroid plexus and mineralization of basal ganglia structures in the elderly are without known clinical significance. In other instances the presence of these deposits provides a valuable clue to the presence of an abnormality and its etiology. CT is the most sensitive technique for the recognition of intracranial calcifications. MRI is not a sensitive technique for the detection of calcification, nor does it allow calcifications to be distinguished from air, rapidly flowing blood, or hemosiderin.
INTRACRANIAL TUMORS
Calcification occurs commonly in many intracranial diseases and its presence is often an important indication of underlying pathology. There is, however, with few exceptions, little diagnostic specificity in the type of calcification occurring as the result of intracranial pathology. In general, one obtains much more indication of the etiology of abnormal calcification from a careful analysis of its location and the characteristics of adjacent parenchyma (i.e. CT density or MRI signal intensities, the presence or absence of mass effect, or enhancement), than from attempting to characterize the features of the calcifications. Calcifications may mimic enhancement or hemorrhage on CT scans and air or rapidly flowing blood on MRI examinations; however, a careful analysis of CT density levels, anatomic location, and a comparison of enhanced and non-enhanced scans usually allows accurate recognition of most calcifications.
SPECIAL PROCEDURES
The rationale for the use of intravenous contrast medium in CT scanning of the brain is two-fold. First, administration of intravenous contrast medium increases the sensitivity of the technique for detection of active areas of abnormality in the blood-brain barrier (BBB). Second, CT scans done after administration of intravenous contrast medium allow improved definition of both vascular and dural structures. The use of paramagnetic intravenous contrast medium in conjunction with MR examinations also increases the sensitivity of the technique for detection of some disease processes. Like intravenous iodine-containing contrast media, the paramagnetic contrast medium used in MRI accumulates in areas of BBB disruption, and, because of its T-1 shortening effect, results in the appearance of enhancement (i.e., increased signal intensity). Unlike CT, widespread dural enhancement is not a normal feature of contrast enhanced MR examinations. Contrast administration is indicated in evaluation of many but not all patients with other vascular abnormalities such as suspected aneurysm or arteriovenous malformations, as well as for studies performed because of suspected neoplasms, and infectious or inflammatory disorders. The routine use of a precontrast or nonenhanced CT scans before an enhanced scan has, in my experience, not been useful and is recommended only for the evaluation of lesions thought to have hemorrhagic or calcified components.
ANGIOGRAPHY
Angiography remains an important tool ieuroradiology; however, as is the case with plain skull films and more recently with CT, many of the indications for cerebral angiography have been eliminated because of the information provided by MRI and MR angiography. The primary indication for cerebral angiography is for the evaluation of patients with vascular disease of all types (atherosclerosis, aneurysms, arteriovenous malformations and fistulas, arteritis and posttraumatic vascular lesions), either intra- or extracranial. Only occasionally is angiography required as part of the diagnostic assessment of neoplasms or other neurologic diseases.
Conventional film-screen angiography is performed by rapidly injecting an iodine-containing contrast medium into one of the arteries supplying the brain or its coverings and then obtaining a series of roentgenograms in rapid sequence. The site of injection, the volume of contrast medium used, and the filming sequence employed all depend on the specific problem under evaluation.
Digital subtraction techniques allow one to perform angiography following either an intravenous or an intraarterial injection of contrast medium at a smaller volume and concentration than would be possible if film-screen techniques were employed. Intraarterial digital subtraction angiography allows procedures to be carried out in less time and at less expense than with conventional methods, with, generally, an insignificant loss of spatial resolution.
NEOPLASMS
The term “brain tumor,” as used here, includes those neoplasms that occur within the brain parenchyma, those that arise from the meninges or cranial nerves, and those that originate from adjacent structures such as the skull or pituitary gland. These lesions have been classified by a variety of methods, their anatomic location and cell origin being the basis of the most common classification. Precise anatomic localization of an intracranial neoplasm is of fundamental importance in that through use of this information, one has the best hope of being specific about the diagnosis, and, thus, the prognosis of the lesion. The wide availability of CT has made this technique the procedure of choice for the initial evaluation of patients suspected of having a brain tumor. Because of its increased contrast sensitivity and multiplanar capabilities, MRI is rapidly eroding the role of CT in this regard.
There is no routine CT method that optimizes the capabilities of the technique for detection of all brain tumors. If properly used CT is, however, quite sensitive and can detect the great majority of these lesions; it can also provide information that in many instances allows accurate prediction of the tumor’s origin. MRI is more sensitive than CT for the detection of neoplasms and also allows more precise localization of their anatomic extent. When available, MRI is the technique of choice for initial diagnostic evaluation of such patients. Unless contraindicated, the administration of intravenous contrast medium is indicated for both CT and MR scans performed for study of suspected brain tumor. Noncontrast CT scans are not routinely required. MRI examinations are best performed both with and without intravenous contrast administration.
Some tumors of the central nervous system (CNS) tend to have a predilection for certain anatomic sites while others occur throughout the intracranial space. It is thus useful to identify a lesions location and to define whether it is within (intraaxial) or outside (extra-axial) the brain. Nearly 70% of tumors in adults are supratentorial, while the reverse is the case in children. The most common primary tumors of the adult are astrocytomas and glioblastomas; in children, at least half of all such lesions are astrocytomas of the cerebellum or brain stem. In general an extraaxial location of a neoplasm implies a more favorable prognosis than does an intraparenchymal location. The incidence of various intracranial tumors as listed by Potts is as follows: gliomas, 43%; meningiomas, 15%; pituitary adenomas, 13%; acoustic neuromas, 6.5%; congenital tumors, 4%; blood vessel tumors, 3%; and miscellaneous, 9%. These figures vary somewhat depending upon the source (i.e., surgical versus autopsy series).
SUPRATENTORIAL TUMORS
EPENDYMOMA
Ependymomas comprise about 5% of all supratentorial gliomas. The duration of symptoms at the time of diagnosis is usually relatively short, being less than one year in many cases. The average age at the time of diagnosis in supratentorial ependymomas is reported to be 30 years. Infratentorial ependymomas occur most frequently in children and adolescents and are much more common than are the supratentorial variety.
Many supratentorial ependymomas probably arise from ependymal cell rests situated about the margins of the lateral ventricles; they frequently occur near the atrium of one of the lateral ventricles. Ependymomas often contain small, scattered, punctate, calcified deposits, which may be visible on unenhanced CT scans. On these scans, ependymomas most often are isodense or slightly hyperdense as compared with the adjacent normal brain. Cystic changes frequently occur and at times the lesion may appear to be almost entirely cystic. Most ependymomas are enhanced to some degree following administration of intravenous contrast medium. These neoplasms show no specific signal characteristics on MRI. Nonetheless, the multiplanar capabilities of MRI are advantageous in demonstrating the location and pathway of spread of these tumors.
MENINGIOMAS
Meningiomas are extraaxial tumors that arise from the arachnoid; the great majority of them are benign. The common locations of meningiomas include sites along the superior sagittal sinus, particularly in the posterior frontal and parietal areas and adjacent to the convexities of the cerebral hemispheres a short distance away from the midline. Other frequent sites for development of these tumors are in the region of the tuberculum sellae or just anterior to the tuberculum along the olfactory groove, along the edges of the sphenoidal ridge, and somewhat less frequently, along the margins of the falx cerebri and the tentorium. Grossly, meningiomas vary in shape from a globular configuration to a flat type of growth, the so-called meningioma en plaque.
Meningiomas usually receive a major portion of their blood supply from the arteries that supply the normal dura at the site from which they arise. Aggressive or malignant types of this tumor may also parasitize the vasculature of the adjacent brain. Meningiomas that arise from or adjacent to the dural sinuses may invade and obstruct these structures. Most meningiomas that arise near bone exhibit some type of osseous response, most often hyperostosis (i.e., hypertrophy). They may invade the bone and occasionally will extend through it to form a hyperostotic density along the outer table of the skull. In other instances, extensive bone destruction is apparent; rarely, the bone overlying a meningioma is completely destroyed with a soft-tissue mass bulging externally.
Tumors that cause a pure hyperostotic type of bone reaction tend to recur infrequently, while those that cause a destructive or mixed bone reaction recur much more often. In 60% to 65% of patients with meningiomas, changes seen on plain films of the skull will strongly suggest both the diagnosis and location of the tumor; nevertheless, these studies are not indicated because they do not allow assessment of the tumors size and thus are not of value in deciding on management. Likewise, angiography provides typical findings but is now rarely used for diagnostic purposes. Depending upon the size, location, and likely vascularity of the tumor, angiography may be indicated to decide whether removal will be facilitated by preoperative embolization. Initial assessment of all these features is best performed with CT or MRI. Although CT is accurate in the diagnosis of meningiomas, having a specific diagnostic rate of 86% and an overall accuracy rate of 96% in one series, the superior contrast sensitivity and multiplanar capabilities of MRI have now made this method the preferable technique for evaluation of patients with these tumors. MRI allows more precise assessment of the extent, location, and vascularity of these tumors than does CT.
Calcification within meningiomas is found in 15% to 20% of cases. The calcium deposits typically are in the form of small punctate densities that are rather uniformly distributed throughout the tumor mass. These sandlike deposits are known as psammoma bodies and are in part responsible for the homogeneous increase in attenuation values that are typical of the unenhanced CT appearance of these lesions. Some very slow-growing meningiomas form densely calcified masses, which may have little if any soft-tissue component.
On unenhanced CT scans, most meningiomas are homogeneous and have slightly increased attenuation values. The degree of edema surrounding them varies greatly; some lesions cause marked edema of the adjacent brain and others do not. This feature depends in part on their rate of growth. Scans usually show a relationship of the tumor to an adjacent dural structure, and often some reaction of the overlying bone can be seen. Following intravenous contrast administration, the typical meningioma is enhanced in a homogeneous manner and has very well-defined margins. Slow-growing, heavily calcified lesions may not show any enhancement; aggressive or malignant lesions often show inhomogeneous enhancement. Primary lymphomas of the CNS may closely simulate the CT appearance of meningiomas.
On MRI studies, meningiomas are typically isointense to slightly hypointense with the adjacent brain on T1weighted images, and slightly to markedly hyperintense on proton density and T2-weighted images. Most of these tumors have sharply defined margins and heterogeneous signal intensities. Early reports of a superiority of CT over MRI for detection of some of these tumors have not proven to be accurate. The ability to do brain imaging in multiple projections without the presence of artifact created by bone in the calvarium greatly improves the ability to define the full extent of these lesions, especially when they involve the skull base. Most meningiomas enhance significantly following administration of paramagnetic contrast medium. Enhancement of the meninges adjacent to the bulk of the tumor mass is a useful diagnostic sign.
The angiographic findings of the typical meningioma are quite characteristic: the major arterial supply is from dural arteries; tumor vessels are usually uniform so that opacification is relatively constant throughout the tumor; and the arterial branches surround the tumor in an arclike manner, sending small tributaries toward the center of the mass. Nonetheless, angiography is not required in the diagnostic evaluation of meningiomas unless there is concern about the ability at surgery to control the arterial supply because of the location of the lesion. In these instances, a preoperative embolization procedure may be required.
COLLOID CYST
Colloid cysts develop in the anterior portion of the third ventricle, usually arising from the roof. Because of its location, the lesion may block either one or, as is more often the case, both of the interventricular foramina, thereby causing hydrocephalus. In some instances obstruction is intermittent. This tumor shows no predilection for either sex and usually becomes manifest during adult life.
As seen on unenhanced CT scans, colloid cysts characteristically appear as well-demarcated, symmetrical, midline masses of increased density, located at the level of the interventricular foramina. On contrast scans, the mass, particularly its outer margins, may become enhanced slightly.
Tumors that obstruct the interventricular foramen cause enlargement of the lateral ventricles, the third ventricle remaining normal in size. An occasional colloid cyst that is isodense with the adjacent brain has been reported; these may be difficult to visualize without the use of CT scans performed following injection of water-soluble contrast medium into the ventricular system. Astrocytomas that originate from the tissue around the interventricular foramen can usually be distinguished from colloid cysts because they typically are poorly defined, have indistinct margins, and are either isodense or hypodense or unenhanced CT scans.
Because the diagnosis of a colloid cyst depends primarily upon the recognition of its location and the ability to discern that the adjacent brain is normal, the multiplanar nature of MRI alone makes it the technique of choice for evaluation of these lesions. The contents of colloid cysts are variable; therefore, their signal characteristics on MRI are not specific.
Because colloid cysts are benign lesions that cause symptoms only as a result of the hydrocephalus they produce, it is important that they be recognized so that appropriate treatment may be attempted. Treatment may either be removal of the cyst or decompression of the hydrocephalus without cyst removal.
EPIDERMOID TUMOR
Epidermoids are congenital lesions derived from ectoderm. They are found more frequently as intradiploic lesions in the bones of the skull than as intracranial lesions; both are uncommon. There is no age or sex predilection. Desquamation of cholesterol-containing debris from the lining of this tumor accounts for its slow growth. Symptoms usually occur as the result of compression of adjacent neural structures. The most common location for an epidermoid is the cerebellopontine angle cistern. Other sites of occurrence are the juxtasellar area, in one of the lateral ventricles or the fourth ventricle. The CT density of an epidermoid is the same as or slightly lower than that of cerebrospinal fluid. Calcification of the tumors margins is uncommon but when it occurs it is one feature that helps in distinguishing epidermoids from arachnoid cysts which on CT scan may otherwise closely resemble each other. Characteristically, the surface of an epidermoid is rough and nodular, and some are cauliflower like with deep clefts. Arachnoid cysts are smooth. Epidermoids do not enhance after administration of intravenous contrast medium. On MRI, epidermoids tend to have signal intensities that are slightly hyperintense to CSF on all pulse sequences. The signal intensities from epidermoids are often heterogeneous.
LIPOMA
Lipomas, lesions derived from mesoderm, occur infrequently. Like dermoids, they usually occur in the midline, the most common locations being the corpus callosum, the vermis, and the quadrigeminal cistern. The majority of lipomas are incidental findings. When they occur in the corpus callosum they are often associated with callosal agenesis. The fat density of these lesions gives them a characteristic appearance on both CT scans and MRI. Calcification is frequent in their periphery, especially in lipomas that occur in the corpus callosum.
INFRATENTORIAL TUMORS
ASTROCYTOMA
Astrocytoma is the most common primary infratentorial and supratentorial tumor. Astrocytomas of the brain stem and cerebellum account for as many as 50% of childhood tumors in some series. These tumors range in their biologic behavior from very slow-growing, diffusely infiltrating lesions to rapidly spreading malignant lesions that result in death within a few months after symptoms become apparent. Their radiographic appearance depends primarily on their histologic nature but also is influenced by their location.
Astrocytomas of the brain stem occur most frequently in children but are not unusual in adults. They account for about one third of all infratentorial tumors. They may originate at any level of the brain stem, but are most common in the pons. Rapidly growing, diffusely infiltrating tumors (fibrillary astrocytomas) are more common than the slow-growing varieties. Because of diffuse infiltration of these tumors, large segments of the brain stem are often found to be abnormal. At the time of diagnosis, the clinical signs and symptoms produced by brain-tem astrocytomas are often mild when compared with the large size of the tumor. It is not uncommon to observe a low-grade astrocytoina involving the entire brain stem and even extending into both the cervical portion of the spinal cord and the cerebellum. Astrocytomas commonly form exophytic extensions along the surface of the brain stem, and, occasionally, can simulate an extraaxial mass lesion. In very low-grade lesions, the only indication of the presence of an abnormality may be distortion of the shape and increase in the size of the involved brain stem segment. The use of low-dose, intrathecal, water-soluble contrast medium in conjunction with CT scanning has been of great value in the early detection of such tumors. Because of improvements in the capability of CT scanning and the development of MRI, this technique is now seldom if ever needed. Calcification in brain-stem astrocytomas is not observed as frequently as in the case of similar supratentorial tumors. Following the administration of intravenous contrast medium, there is a variable pattern; higher-grade or malignant tumors tend to enhance intensely while those that are less aggressive enhance slightly or not at all.
MRI is more sensitive than CT for detection of both the presence and the extent of these tumors. On T1 weighted images, most of these lesions are hypointense: on T2 images they are hyperintense. Small cystic changes are not uncommon. As is the case with CT scanning, enhancement following intravenous contrast administration is variable.
Astrocytomas arising in the cerebellum are a common CNS tumor of childhood. Two major types of cerebellar astrocytoma exist. The most frequent is the pilocystic variety, which is well demarcated, benign, and often cystic. Less common is the diffusely inflltrative (fibrillary) variety that is poorly defined and often malignant. Calcification is unusual in either the solid or the cystic variety of this tumor. Most of the lesions of either type arise in the cerebellar hemispheres.
On CT scans the cystic pilocystic astrocytoma is seen as a well-circumscribed mass with attenuation values that are similar to those of cerebrospinal fluid. On MRI, signal intensities from the cystic portion of the tumor are similar to those of cerebrospinal fluid. Often there is a mural nodule that enhances after administration of intravenous contrast medium. Solid varieties of these tumors are isodense on CT scans performed without intravenous contrast medium; on MRI they are hypointense on T1-weighted images and hyperintense on T2-weighted scans.
The infiltrating variety of cerebellar astrocytoma (fibrillary astrocytoma) has an appearance on both CT and MRI that is similar to that of its brain-stem counterpart.
HEMANGIOBLASTOMA
These benign tumors, found mostly in adults, occur most often in the cerebellum. They also occur regularly, however, in the brain stem and spinal cord; supratentorial occurrences are rare. These neoplasms are sometimes associated with the von Hippie-Lindau disease, and, in this setting, the chance of their being multiple increases significantly. As many as half of all hemangioblastomas are mostly cystic; the remainder are divided between those that are partially cystic and solid and those that are entirely solid. Regardless of whether they are cystic or solid, hemangioblastomas have extensive vascularity. The cystic variety typically has a well-defined mural nodule that receives its blood supply from adjacent pial vessels. At times the vascularity of these tumors is so extensive that they may simulate arteriovenous malformations. Calcification is usually not seen.
As seen on unenhanced CT scans, these tumors vary in appearance depending primarily upon whether they are cystic or solid. Lesions that are largely cystic appear as well-defined masses, the attenuation values of which are similar to those of cerebrospinal fluid. Careful observation will usually reveal an area along the margin of the mass that is isodense as compared with the adjacent brain; this represents the mural nodule. Solid hemangioblastomas are most often isodense. Likewise, on MRI, the cystic portion of a hemangioblastoma typically has signal characteristics that are the same as those of cerebrospinal fluid. Solid portions of these tumors are usually hypointense to adjacent brain on T1-weighted scans and hyperintense on T2-weighted images. Following administration of intravenous contrast medium, the solid portion of a hemangioblastoma enhances intensely both on CT and MRI. On the basis of CT findings alone it may be difficult or even impossible to distinguish a cystic cerebellar hemangioblastoma from a cystic cerebellar astrocytoma. Angiography usually allows this differential to be made, since the mural nodule of a cystic hemangioblastoma typically has enlarged feeding arteries and draining veins, a feature not common in astrocytomas of this nature. Because of its ability to portray vascular structures, MRI is probably more sensitive than is CT in allowing this distinction to be made without the use of angiography.
MEDULLOBLASTOMA
These malignant tumors, which originate solely in the cerebellum, are the most common posterior fossa tumors of childhood and are unusual in adults. They spread both by direct extension and by dissemination of tumor cells throughout the subarachnoid space. The great majority of childhood medulloblastomas occur in the vermis along the roof of the fourth ventricle. Most medulloblastomas in adults originate more laterally in one of the cerebellar hemispheres. It is unusual for a medulloblastoma to have a significant cystic component, the majority of them being composed of densely cellular tissue; likewise, calcification within these tumors is atypical. With increasing length of survival of patients with these as well as some other malignant tumors of the CNS, there are increasing reports of extraneural metastases particularly to lymph nodes and bone. Osseous metastases from medulloblastomas occur chiefly in the axial skeleton and may be osteolytic, osteoblastic, or of mixed type. Because most medulloblastomas originate in the cerebellar vermis and grow into the fourth ventricle, obstructive hydrocephalus is common and is frequently the cause of the initial complaint.
On unenhanced CT scans the most typical appearance of a medulloblastoma is a midline vermian mass with attenuation values that are slightly higher than those of the adjacent brain. Except for their location, tumors that originate in the cerebellar hemispheres have a similar appearance. On enhanced CT scans medulloblastomas show an intense increase in their density and are seen to have sharply defined margins. Both the subarachnoid and subependymal metastases of these tumors enhance following administration of intravenous contrast medium.
As with other posterior fossa tumors, MRI is superior to CT for depicting the origin and full extent of these lesions. Probably because of their dense cellularity and scant cytoplasm, most medulloblastomas are of somewhat lower signal intensity on T2-weighted images than are most other primary brain tumors. Both the primary lesion and its parenchymal and subarachnoid metastases enhance markedly after administration of paramagnetic contrast medium.
SCHWANNOMA
Schwannomas are benign tumors that occur along the course of cranial, spinal, and peripheral nerves. The previous designation of these tumors as neuromas or neurilemmomas is misleading and should not be used. The discussion that follows is limited to those tumors that involve the cranial nerves.
Schwannomas are primarily tumors of adults and occur considerably more often in females than in males, a 2:1 ratio being reported in some series. The eighth cranial nerve is most frequently involved; most of the other tumors occur on the fifth nerve. There is no explanation for the tendency of these tumors to occur in sensory nerves almost exclusively. Of those schwannomas that originate from the eighth cranial nerve approximately 75% involve the vestibular division, usually its intracanalicular portion. Because of their location, eighth-nerve schwannomas often produce signs and symptoms when they are quite small. These include a characteristic hearing loss, tinnitus, vertigo, and dizziness. Large eighth-nerve lesions may also cause dysfunction of the fifth and seventh cranial nerves. Schwannomas account for the great majority of tumors that occur in the cerebellopontine angle.
The appearance of an acoustic schwannoma on an unenhanced CT scan depends primarily on its size. Large lesions are visible because of obliteration of the ipsilateral cerebellopontine angle cistern, displacement of the brain stem and fourth ventricle, and widening of the contralateral cerebellopontine angle cistern. Small lesions may be occult or may manifest themselves only by enlargement of the ipsilateral internal auditory canal. Following administration of intravenous contrast medium, schwannomas enhance significantly. Very small tumors that are confined to the internal auditory canal may not, however, be visualized on even the best routine CT scans. MRI is, therefore, recommended over CT as the technique of choice for the evaluation of patients suspected of having a cerebellopontine angle lesion. Except when MRI or modern CT devices are not available, there is now no longer a place for complex motion tomography or CT following placement of air in the subarachnoid space in the evaluation of acoustic schwannomas.
Most schwannomas are well seen on thin-section (
Except for location, schwannomas of the other cranial nerves appear similar on MRI and CT scan to those of the eighth nerve. MRI is also the technique of choice for evaluation of these lesions.
Neurofibromas are pathologically distinct from schwannomas; however, on the basis of imaging features, differentiation is not possible. Almost all neurofibromas occur in association with von Recklinghausens disease; bilateral eighth nerve tumors as well as multiple tumors of other cranial nerves are common.
METASTATIC TUMORS
Metastasis of a remote primary tumor to the brain, its coverings, and the skull is common. Most metastatic tumors arise as the result of hematogenous spread; the initial tumor implants thus tend to occur in the distribution of end arteries, that is, at the gray-white matter junction and in the distribution of deep perforating arteries. Common primary sources are tumors of the lung, breast, colon, kidney, skin, and paranasal sinuses. Carcinomas of the breast and lung account for over half of all metastatic brain tumors. There is wide variability in the CT and MR appearance of metastatic brain tumors. Among factors that influence this variation are the primary source of the tumor (i.e., its cellularity); vascularity and biologic behavior; the number and location of the tumor(s) within the brain; and whether previous treatment has been directed to the area of the tumor.
On unenhanced CT scans, metastatic tumors most often are seen as multiple (solitary metastases also occur commonly, 0% to 40%), fairly discrete areas of isodensity or slight hyperdensity surrounded by low density that extends along and through the white matter. The low density abnormality is believed to be a reflection of edema, and in the majority of metastatic tumors it is substantial. For reasons that are not clear, however, some metastases produce almost no edema, and, when isodense with the adjacent brain, may be occult on scans performed without the use of intravenous contrast. Except for metastases from primary osseous tumors, especially osteogenic sarcomas, calcification is unusual in untreated metastatic brain tumors. Some metastatic tumors show a tendency to hemorrhage spontaneously; these include melanoma, renal cell carcinoma, and choriocarcinoma.
As is the case on unenhanced CT scans, the appearance of metastatic brain tumors on scans performed following the use of intravenous contrast medium varies. Most metastases will be enhanced to some degree, but the pattern that they exhibit shows great variability; enhancement may be ringlike, diffuse (either homogeneous or inhomogeneous), or only in scattered areas with no apparent particular distribution. Tumors in individuals being treated with corticosteroids may not become enhanced because of the medication s stabilizing effect on the BBB. Metastases to the brain may involve the subarachnoid space because of meningeal involvement. This may occur either as an isolated phenomenon or may be seen in association with parenchymal tumors. These meningeal implants appear on contrast-enhanced CT as either areas of nodular high density or as generalized enhancement occurring along the subarachnoid cisterns, fissures, and sulci. Melanoma is one tumor that is particularly prone to this type of involvement.
MRI is more sensitive than CT for the detection of CNS metastatic tumors and is thus the technique of choice for evaluating patients suspected of having such disease. While many metastatic tumors can be recognized ooncontrast-enhanced scans, the use of intravenous contrast medium increases detection of small and peripheral tumor deposits. As is the case on CT scans, the appearance of metastatic tumors on MRI is variable. Typically, however, the tumor is seen as an area of hypointensity on T1-weighted images and heterogeneous hyperintensity on T2-weighted images. Surrounding most metastatic tumors is edema, which has less signal variation (i.e., it is more homogeneous than the tumor itself). Hemorrhage, cystic change, and necrosis are all common in metastatic tumors and account for the variable signal intensities of these lesions. Most metastases enhance following administration of intravenous contrast medium; as with CT, the pattern of enhancement is variable.
On the basis of CT or MRI scan findings alone it is impossible to predict with accuracy the primary source of a metastatic tumor. Likewise, a solitary metastasis cannot reliably be distinguished from a primary neoplasm of the brain.
SUBDURAL HEMATOMA
Bleeding into the subdural space is a frequent complication of head injury; when it occurs, the result is the formation of a subdural hematoma. These lesions are most common over the convexity of the cerebral hemisphere, but may develop at any site over the surface of the brain. They occur infrequently, however, in the posterior fossa. Bilateral subdural hematomas are not uncommon, occurring in approximately 20% of patients. The early use of CT scanning in patients suffering acute head trauma has significantly reduced the previously high mortality rate associated with acute subdural hematomas.
The appearance of a subdural hematoma on CT scan depends on several important factors: the age of the lesion, whether repeated episodes of bleeding have occurred, whether the lesion is unilateral or bilateral, and the level of the patient s hematocrit at the time of the injury. It is most useful to divide subdural hematomas into those that are hyperdense, isodense, and hypodense in relation to the adjacent area of the brain. In general, blood within the subdural space in the early stages of its presence is hyperdense; over a period of two to six weeks it becomes isodense, and weeks hypodense, as compared with the CT values present in a healthy brain. Extensive variation in this sequence occurs as the result of rebleeding into a subdural collection, a frequent occurrence, as well as because of differences in the attenuation values of blood caused by variations in the hematocrit levels.
Using CT scan criteria it is thus impossible to accurately classify subdural hematoma as acute, subacute, or chronic. In the majority of instances, however, hyperdense subdural collections have occurred recently, isodense lesions will have been present for at least several days, and hypodense lesions are likely to be of a chronic nature.
With the exception of those instances in which the patient has a very low hematocrit, subdural hematomas studied with CT soon after their occurrence appear as hyperdense collections having a crescentic configuration. The degree of mass effect present in association with these lesions is almost always greater than that which can be accounted for on the basis of the size of the hematoma, a reflection of the underlying brain injury that accompanies most such injuries. The medial margin of very large lesions may be straight or even convex, thus somewhat simulating an epidural collection. If scans are performed soon after the injury or if there are disorders of the coagulation system, the subdural collection may be inhomogeneous, a phenomenon thought to be due to the presence of incomplete clotting within the hematoma.
Although they are encountered infrequently, it is important to be aware of the existence of the isodense subdural hematomas because they may be occult on even high quality CT scans. Unilateral effacement of cortical sulci, asymmetries in the gray-white matter junction, ventricular asymmetries, and unilateral mass effect are all signs that usually serve to alert one to the presence of a unilateral, isodense, subdural hematoma. Bilateral lesions of this nature may be more difficult to recognize. In older adults, the presence of a “super normal” appearing scan (i.e., one in which the cortical sulci and ventricular system appear like those of a much younger person), is one clue that such lesions may be present. The administration of intravenous contrast medium is valuable in that it results in opacification of dural margins and cortical vessels, thereby allowing good definition of the margins of the brain.
Chronic subdural hematomas usually appear on CT scans as well-defined crescentic collections, the attenuation values of which are hypodense as compared with those of the adjacent area of the brain. As is the case with acute lesions, a very large chronic subdural hematoma may have a straight or even concave medial margin. Episodes of rebleeding may be indicated by inhomogeneous densities within the hematoma. Occasionally, sedimentation levels are seen in dependent portions of such lesions. Calcification of the margins of these lesions occurs frequently.
On MRI, subdural hematomas that appear hypodense on CT will have high-signal intensity on T1-weighted images because of the hemoglobin that they contain. Because of its sensitivity in detecting blood degradation products of different ages, MRI is more sensitive than CT for identification of subdural hematomas that have undergone multiple episodes of bleeding. These lesions are seen as having multiple collections with signal intensities characteristic of hemoglobin breakdown products of different ages. The membranes separating these areas have low-signal intensities on images made with all pulse sequences.
SUBDURAL HYGROMA
A subdural hygroma represents the accumulation of clear fluid in the subdural space. It may be observed following head trauma, in which case it represents either the residual of an old subdural hematoma, or an injury of the arachnoid membrane that has allowed accumulation of cerebrospinal fluid in the subdural space. The mechanisms causing those that are noted in the absence of trauma are poorly understood. Subdural hygromas are usually not symptomatic, and with time they resolve spontaneously. Except for their size, subdural hygromas appear similar on CT scan to the description given for chronic subdural hematomas. These lesions should not be confused with atrophic changes, because the CT scan appearance of the two conditions is quite different. Atrophy produces widening of the cortical sulci, and the involved gyri are not significantly displaced away from the margin of the calvarium. Subdural hygromas represent mass lesions and as such displace the brain away from the skull margin; the adjacent gyri and sulci are effaced and obliterated.
EPIDURAL HEMATOMA
Epidural hematomas occur as a result of injury to meningeal vessels, and are most often the result of arterial rather than venous disruptions. The most common location of an epidural hematoma is over the lateral surface of one of the cerebral hemispheres; however, like subdural hematomas, they may occur in other places as well.
Except for the rare instances in which they occur in the presence of severe anemia or severe recent blood loss, epidural hematomas are hyperdense on CT scans. Because they occur peripheral to the dura, which is the periosteum of the inner table of the calvarium, they are more restrained than subdural collections. This is the explanation for their typical biconvex configuration; it also accounts for the observation that they sometimes cross the midline, not being limited as are subdural hematomas by dural attachments. On CT scans, as is the case in subdural hematoma, areas of inhomogeneity within an epidural hematoma indicate either incomplete clotting or active bleeding. Angiography is no longer performed in the evaluation of patients with either subdural or epidural hematomas.
BRAIN ABSCESS
Brain abscesses occur most frequently because of hematogenous dissemination of infectious agents from a distant site (most often the lung). They may also result, however, from the direct spread of an infection from a location such as a paranasal sinus or the middle ear. Abscesses that develop from the hematogenous spread of microorganisms occur most frequently in the cerebral hemispheres, along the corticomedullary junction and in the basal ganglia. A wide variety of organisms has been associated with brain abscesses; none of these produce totally characteristic radiographic findings. Immunosuppression, cyanotic heart disease, and pulmonary arteriovenous fistulae predispose patients to the development of brain abscess. The ability to define the extent and characteristics of a brain abscess with CT, MRI, and ultrasound, as well as the use of these methods as guides for the surgical treatment of abscesses that do not respond to medical therapy have greatly reduced the high morbidity and mortality previously associated with these lesions.
During the course of its development, a brain abscess evolves through a number of stages. Initially, it is a poorly defined area consisting of small, scattered foci of inflammation (i.e., cerebritis); when mature, it is a well-demarcated, encapsulated lesion, the central portion of which consists of suppurative material and tissue debris. The appearance of a brain abscess on CT, MRI, or ultrasound depends primarily on the stage in its development during which the study is performed.
On CT scans, early lesions may be seen only as areas of hypodensity, with little, if any, enhancement occurring after administration of intravenous contrast medium. Over time, as neovascularity and a collagen capsule develop, however, a pattern of ring enhancement will become apparent. The ring or margin of an incompletely encapsulated abscess becomes thicker and shows increased intensity of enhancement on scans performed 30 to 45 minutes following intravenous contrast administration. The margin of a mature abscess does not show this pattern and often may even decrease in intensity on delayed scans. Except in immunocompromised patients or individuals who are taking corticosteroids, studies done before the onset of treatment usually show extensive vasogenic edema surrounding the area of a brain abscess. Except in the immunocompromised patient, multiple abscesses are unusual. On ultrasound examination, an abscess appears as a hypoechoic area surrounded by an echogenic rim.
MRI is superior to CT for evaluation of patients with brain abscesses because of its increased contrast sensitivity (i.e., better detection of edema and characterization of the various elements of an abscess), the lack of associated artifact from bone at the skull base, and, because of its multiplanar capability, its superior ability to detect subtle mass effect. The abscess capsule is its hallmark and this is best characterized on either contrast-enhanced or T2-weighted MRI scans. The thin, relatively smooth capsule enhances uniformly. On T2-weighted scans it is hypointense as compared with gray matter. Often, adjacent, smaller, so-called satellite capsules are present, particularly along the margin of an abscess that faces one of the lateral ventricles. Healing of an abscess is indicated by a decrease in its size; it is important in this regard to emphasize that on both CT and MRI, enhancement of the capsule may persist for some time despite adequate treatment.
SUBDURAL AND EPIDURAL EMPYEMA
Although suppurative infections in the subdural or epidural space are uncommon, it is important that they be recognized, because if untreated they are associated with high mortality. Most infections of this nature occur in association with osteomyelitis of the skull, sinusitis, meningitis, or penetrating trauma. In general, on CT scans these lesions appear as areas of hypodensity over the surface of the brain; they may extend into the interhemispheric fissure or along the margins of the tentorium. They are, unless very small, associated with mass effect. Following administration of intravenous contrast medium, variable enhancement is seen about the margins of both subdural and epidural empyemas. Hypodensity is often present within the brain adjacent to this type of infection. Subdural empyemas, like subdural hematomas, are limited by the attachments of the dura; this may be the only way to distinguish an epidural from a subdural suppurative process.
BRAIN INFARCTION
Brain infarction may occur as the end result of a large number of pathologic processes, by far the most common of which is atherosclerosis. Approximately 60% of ischemic brain infarcts are etiologically related to atherosclerotic disease of the extracranial segment of the internal carotid artery. A significant percentage of all embolic brain infarctions also result from emboli that originate within the heart. Other causes of brain infarction, besides atherosclerotic vascular disease, include other primary arterial diseases such as fibromuscular hyperplasia, arterial dissections, and arteritis; venous occlusive disease and a host of more unusual diseases such as septic and tumor embolizations may also be associated with infarction of the brain.
Although CT continues to be the most commonly employed imaging technique for evaluation of patients with suspected strokes, MRI has been shown to be a superior method both in permitting earlier detection of ischemic changes and in allowing identification of infarcts not visible on CT scans. These advantages arise from the superior ability of MRI to detect edema and its freedom from artifact caused by the bone and air at the skull base. Most symptomatic infarctions can be recognized with MRI within 12 to 24 hours of their occurrence. MRI is especially useful in demonstrating ischemic changes that involve the brain stem or cerebellum. In most instances, the use of intravenous contrast medium is not required for the diagnosis of infarct, either with CT scanning or MRI. The suggestive evidence that the use of contrast-enhanced CT scans in evaluation of cerebral infarcts is associated with increased damage to neural structures provides added incentive to avoid contrast administration when possible.
The CT scan findings seen following an infarct depend on the size of the abnormality, whether the infarct is associated with hemorrhage, the amount of time that has elapsed between the occurrence of the infarct and the CT scan, and, to a lesser degree, the location of the infarct within the brain. CT scans performed in the initial 24 hours following a nonhemorrhagic infarct may be normal, especially if the lesion is small or if it is located in the brain stem or cerebellum. In typical examples, scans performed after an interval of more than 24 hours show an area of reduced density that can be related to a single vascular distribution. The character of the infarct evolves from an area of poorly defined inhomogeneous reduced density, which causes mass effect, to one with no mass effect, sharp margins, and homogeneous attenuation values approaching those of cerebrospinal fluid. The subarachnoid space and ventricle adjacent to an old infarct are usually dilated. These changes have a variable time course; however, it is highly unusual for an infarct to have significant mass effect after it has been present for two weeks, and within three weeks its margins should be clearly defined. If intravenous contrast medium is given, a variable pattern of enhancement may be seen from four to five days following occurrence of the infarct for as long as six weeks after its origin. Although the configuration of abnormal enhancement in a brain infarct often assumes a gyral pattern, this is not specific and may be seen iumerous other pathologic conditions. The distribution of abnormal enhancement does not correlate with the amount of brain parenchyma that will ultimately be destroyed.
MRI provides a means for demonstrating ischemic changes in the brain earlier than any other imaging technique, abnormalities having been shown in as little as one hour following experimental arterial occlusion. On T1-weighted images, areas of infarction are seen as an area of decreased signal intensity with a loss of the normal signal differences between gray and white matter. On T2-weighted images, areas of infarction appear as high-signal intensity. In pathologic studies, small areas of hemorrhage into infarcts are very common; these small hemorrhages are ofteot apparent on high-resolution CT scans, but are frequently seen on MRI studies. Depending upon the stage of evolution of the hemorrhage, their signal intensities are variable, ranging from predominantly low-signal intensities on both T1 and T2-weighted images in acute hemorrhages, to high-signal intensities on T1 and T2-weighted images in subacute hemorrhages, and then again to low signal intensities in longstanding hemorrhages. For details of the evolution of the pattern of MRI signal intensities in parenchymal hemorrhages, see the following section.
NONTRAUMATIC INTRACRANIAL HEMORRHAGE
Most intracranial hemorrhages are the result of trauma and have been discussed in a previous section. Non-traumatic causes of intracranial hemorrhage include hypertension, aneurysms, and vascular malformations. Careful analysis of the CT scan and MRI findings often allows determination of the likely cause of a nontraumatic hemorrhage.
HYPERTENSIVE HEMORRHAGES
Hypertension is an important etiologic factor in intracranial hemorrhages. If chronic, it results in the presence of structural arterial changes that in themselves predispose to the development of hemorrhages. The presence of elevated blood pressure is also thought to increase the risk of hemorrhage from other nonrelated vascular abnormalities such as aneurysms and arteriovenous malformations.
Hypertensive hemorrhages occur most often in the external capsule. This location is followed in frequency by the thalamus, the internal capsule, the cerebellum and pons, and the lobar white matter of the cerebral hemispheres. Hematomas of this nature frequently rupture into the ventricular system, but rarely are seen in association with subarachnoid hemorrhage. This feature helps in distinguishing these lesions from traumatic hematomas in which the opposite combination is the case. Although the use of contrast-enhanced CT scans is usually not indicated in evaluation of these lesions, it should be noted that as they resolve, hematomas of any nature may be enhanced to simulate closely other mass lesions (i.e., neoplasms and inflammatory abnormalities).
As is the case for hematomas of any etiology, hypertensive hemorrhages appear on CT scans as areas of high density with sharply defined borders. Unless there is still active bleeding or impairment of coagulation, the density of a hematoma is homogeneous. Acutely, on CT scans, edema is not seen in association with a hypertensive hematoma. Over a period of several days following the initial hemorrhage, however, edema develops and low density is commonly seen peripheral to the margin of a hypertensive hematoma. Over a period of several weeks, the density of a hematoma changes from high density to isodense and finally to hypodense, the end stage being an area of encephalomalacia having attenuation values similar to those of CSF.
The MRI appearance of a hematoma is variable depending upon a large number of interrelated factors. These include, among others, the age of the hemorrhage, and, thus, the stage of degradation of both its cellular (erythrocytes) and noncellular (hemoglobin) elements; its location (i.e., parenchymal, subarachnoid, subdural, or epidural); the presence or absence of an associated abnormality (i.e., an arteriovenous malformation or neoplasm); and, the magnetic field strength and pulse sequence used to obtain the image. A complete description of these variables and their effects on the MR image is beyond the scope of this text.
In spite of the complexities and variations associated with the MRI appearance of hemorrhages, however, several relatively consistent observations are noteworthy. On MR scans performed within several hours of the onset of a hemorrhage, a hematoma not associated with an underlying lesion appears similar to most other brain lesions (i.e., slightly hypointense on T1-weighted images and hyperintense on T2-weighted images). During the first 24 hours, this appearance changes so that the hematoma is of definite low-signal intensity on both T1 and T2-weighted images. Unlike on CT scans, surrounding edema (high-signal intensity on T2-weighted sequences) may often be visualized on MR images obtained during this stage of a hematoma’s evolution. During the first week after its occurrence, a hematoma becomes of predominant high-signal intensity on both T1 and T2-weighted images. This change in signal intensity from low to high is due to the development of methemoglobin within the lesion and occurs gradually from the periphery of the hematoma to its center, so that there is a steady replacement of low-signal areas by high-signal areas. The rim of a hematoma at this stage of evolution is seen as a sharply defined zone of very low-signal intensity; this is the result of accumulation of hemosiderin, the end product of hemoglobin degradation. After several weeks or even months, a hematoma loses its mass effect and assumes signal intensities similar to those of the adjacent brain and CSF. Small areas of both high- and low-signal intensity may persist, however, almost indefinitely.
SPONDYLOLISTHESIS
Spondylolisthesis refers to a slip of one vertebra on another, usually forwards but may occasionally be backwards. It may be degenerative (associated with severe osteoarthritis of the posterior facet joints, usually L4/L5), congenital, or posttraumatic, resulting in a defect in the pars interarticu-laris of the neural arch. It is often asymptomatic.
RADIOLOGICAL FEATURES
The slip is best demonstrated on a lateral projection of the lumbar spine and there may be an associated loss of disc space.The commonest affected levels are L4/L5 and L5/SI. CT/MRI evaluate the theca and any bony canal narrowing.
TREATMENT
• Conservative.
• Surgical: for a severe slip, internal fixation stabilizes the vertebra.
LUMBAR VERTEBRAL DISC PROLAPSE
Disc degeneration commonly occurs in the lower lumbar spine. Prolapse is due to extrusion of soft disc material from the nucleus pulposus and characterized by sciatic pain radiating from the buttock down the leg.
• L4/L5 prolapse (20% of cases): compression of the L5 root may result in foot drop and sensory loss of the outer aspect of the leg.
• L5/SI prolapse (70% of cases): SI root compression may cause an absent ankle jerk, with tingling and loss of sensation at the outer aspect of the foot.
RADIOLOGICAL FEATURES
• Plain films. Disc space narrowing, often with osteophyte formation, is best seen in the lateral projection.
• CI. Sensitive examination for posterior and lateral disc herniation in the lumbar spine. Demonstrates also hypertrophic degenerative changes in the facet joints which may cause bony canal stenosis.
• MRI. Distinguishes the nucleus pulposus from the annulus fibrosus with accurate diagnosis of degenerative discs. Degenerative disc disease is extremely common and must be correlated with clinical symptoms.
• Myelography. Injection of contrast into the spinal theca via a lumbar puncture, previously a common examination, but now almost obsolete.
|
|
Fig. MRIscan demonstrating a prolapsed disc at L4/L5 with posterior deviation of the theca (arrow).
|
|
Fig. Typical degenerative changes in the lumbar spine with disc space narrowing.
THE SPINE AND SPINAL CORD
The methods recently used for investigation of the spine and spinal cord include:
1. Simple X-rays
2. Radioisotopes
3. Myelography and radiculography
4. CT and computed myelography (CM)
5. MRI
6. Spinal angiography.
Fig. Prolapsed L3/4 intervertebral disc. Radiculogram. (A) Anteroposterior. (B) Right posterior oblique projections. The disc substance impresses the right anterolateral aspect of the contrast column at L3/4 disc level. The right 3rd lumbar root is compressed against the pedicle of the corresponding vertebra and the 4th lumbar root is deviated medially.
A plain X-ray of the spine, like a plain X-ray of the skull, will often provide helpful information as to the cause of a neurological disability. Inflammatory lesions such as tuberculosis of the spine may be demonstrated, as may neoplastic lesions such as secondary deposits involving the bony spine. Congenital anomalies may also be demonstrated, and these, particularly in the cervical region, are now being increasingly recognised in association with neurological disorders.
The value of radiology in the diagnosis of fractures and dislocations of the spine is self-evident.
Evidence of disc lesions may also be shown by plain X-ray. The importance of lumbar disc protrusions as the major cause of sciatica has long been known. The role of the cervical disc in the production of brachial neuritis and of pyramidal signs in the elderly is also well recognised. Evidence of these disc lesions is usually present on plain X-ray, but the radiological findings of disc narrowing and adjacent bony sclerosis or lipping must be carefully correlated with the clinical aspects of the problem since disc degeneration without significant symptoms is common in the middle-aged and elderly.
Evidence of the presence of an intraspinal tumour may occasionally be seen in a plain X-ray, manifesting itself as erosion of adjacent vertebral pedicles or vertebral body.
Fig. 12.30 CT following a laminectomy which failed to cure the patient. There is a large lateral disc herniation occluding the right intervertebral foramen and compressing the right 5th lumbar nerve root (T). The left root is shown exiting the foramen (^). (B) shows the plane of section through L5-S1.
Radioisotopes are useful in identifying lesions of the bony spine, particularly multiple metastases and their use in this context has been described above (Ch. 6).
Spinal angiography is used for the diagnosis of the rare vascular lesions involving the cord. These include angiomas and dural AV fistulas. It is also diagnostic for the rare haemangioblastoma of the spinal cord.
Myelography and radiculography once widely practised, have been largely superseded by MR. They were performed with water-soluble low osmolar contrast media such as Niopam. These can demonstrate both intramedullary and extramedullary tumours affecting the cord and cauda equina. They can also demonstrate disc protrusions.
CT shows bony lesions in greater detail than simple X-ray and will also show disc lesions. However computed myelography (CM) is necessary for it to define the spinal cord and most lesions involving it. CT requires the introduction of only a small amount of Niopam by lumbar puncture shortly before examination by CT. It can also be performed following a more formal myelogram or radiculogram.
Fig. Sagittal MRI study shows ovoid tumour lying anterior to the spinal cord behind C2 (neurofibroma).
MRI is now the primary investigation of choice in the diagnosis of most lesions affecting the spinal cord and in many lesions affecting the bony spine. Intramedullary lesions of the cord are particularly well defined including tumours both solid and cystic. Syringomyelia is also easily diagnosed, and degenerative and inflammatory lesions can be recognised.
MRI also offers a non-invasive method for diagnosing disc protrusions.
Fig. MRI showing deposit in upper lumbar vertebra Anterior extension displacing aorta. Posterior extension compressing spinal cord. Hodgkins disease.
RADIAL DIAGNOSTICS OF DISEASES OF THE SKELETAL SYSTEM
The most common indications for obtaining radiographs of the skeletal system are:
· trauma
· back pain
· joint symptoms – pain, stiffness, swelling.
Congenital skeletal anomalies and variants are relatively common and should not be mistaken for acquired disease. These variants are usually discovered coincidentally and almost never cause symptoms.
Some skeletal disorders do not produce radiographically detectable abnormalities early in their course and this may lead to diagnostic errors. This is particularly important in skeletal trauma and in bone infection (osteomyelitis); metastatic deposits from non-skeletal primary tumours may also cause symptoms without producing radiographically detectable bone abnormalities. Specific examples of skeletal trauma and their diagnostic problems are discussed later. In all these situations radionuclide imaging may give important information. Bone-seeking isotopes are concentrated in areas of bone repair where osteoblastic activity is at its most intense. Fractures, infectious and even tumours provoke a reparative response and thus, even at an early stage, radionuclide imaging may be positive (localised ‘hot spots’ of concentrated isotope) when radiographs are negative. This fact has important medicolegal implications, particularly in skeletal trauma.
Radiographic bone abnormalities fall into a few broad descriptive categories. Bone is either destroyed (lysis) or laid down (sclerosis). The former causes loss of bone density and the latter results in increased bone density. The underlying pathological process may nevertheless be very different. Many disorders cause a combination of the two processes, giving a ‘mixed’ radiographic picture. In view of this apparent limited range of radiographic abnormalities, many other factors are taken into account when the diagnosis is made – the extent of skeletal involvement, associated joint or soft tissue signs, the age of the patient, etc.
Many disorders affecting the skeleton cause widespread loss of bone density – osteopenia or osteoporosis. The severity of the demineralisation is difficult to assess from plain radiographs except in extreme cases, and several alternative methods of measuring bone density are in common use. Biochemical assessment of bone metabolism, especially calcium phosphate and alkaline phosphatase levels, are also important diagnostic aids. In several conditions, such as osteomalacia and hyperparathyroidism, they are much more sensitive than radiographic assessment, it is important to correlate clinical, radiological, biochemical and haematological findings in all complex bone disorders. If bone biopsy becomes an important element of the diagnostic process, this can be carried out under radiological control – fluoroscopy or CT.
Not all bone disorders arise primarily in the skeleton; there are many systemic or multisystem disorders that affect bone maturation and metabolism. Likewise, joint symptoms may be a manifestation of a variety of non-articular disorders.
Growth and development of the skeleton
Calcification and ossification of the underlying osteoid matrix and cartilage occurs in a predictable progression throughout intrauterine life and during infancy and childhood. The skeleton becomes fully mature between 16 and 18 years of age, when longitudinal bone growth ceases. Using plain radiography the skeleton can be ‘aged’ on the basis of the pattern of ossification of the skeleton; radiographs of the non-dominant hand and wrist allow accurate assessments of bone age to be made between the ages of 18 months and complete skeletal maturation. In infancy, radiographs of the knees and feet are particularly useful for ‘dating’ some of the earliest epiphyses to ossify.
This maturation process may be affected in several ways, either by specific bone disorders or by systemic or generalised disease. Inherited disorders, such as some of the chromosomal syndromes, also affect skeletal development. The radiographic pattern of abnormal development is often distinctive and diagnostic, although radio-graphic skeletal surveys deliver a significant dose of radiation to young children and should not be carried out without full consultation. Normal bone modelling is dependent on normal physical development – ‘floppy’ babies tend to have straight spines or to develop abnormal curvatures. Non-weight-bearing affects the development of the pelvis and lower limbs particularly -poor muscle tone or control produces thin ‘spindly’ and demineralised bones. This occurs in children with severe neurological disorders such as cerebral palsy.
Bone is a dynamic structure; throughout childhood osteoblastic activity is intense and exceeds osteoclastic activity. This is particularly apparent in radionuclide imaging of the skeleton – the bone ends (i.e. the metaphyses) show intense isotope uptake, often enough to obscure pathological lesions such as osteomyelitis or skeletal injury. Longitudinal bone growth occurs at the metaphysis and periosteal activity along the diaphysis (or shaft) of the bone contributes to circumferential growth.
Long bones develop from three distinct components: the epiphysis (sub-articular bone ends), the metaphysis, incorporating the epiphyseal plate, and the diaphysis or bone shaft. By the age of 16-18 years virtually all the epiphyses have fused with the diaphyses and longitudinal growth ceases. Bone repair, e.g. after a fracture, then becomes predominantly the function of the periosteum.
Premature fusion of the epiphyses may occur under certain circumstances –inflammatory joint disorders in childhood and traumatic involvement of the epiphyseal growth plate are examples. Premature fusion results in early cessation of longitudinal growth and there may be generalised short stature if the fusion is caused by multiple affected arthritic joints, or isolated stunted growth in the case of trauma.
Table. 1 summarises the most important disorders that affect these key areas of the developing skeleton. Rare inherited disorders (bone dysplasias and chromosomal disorders) cause a variety of specific abnormalities at one or more sites (a combination of epiphyseal and metaphyseal abnormalities, for example). These may result in severe growth retardation and dwarfism. A radiographic survey of the skeleton is an important part of the genetic assessment and counselling process in these circumstances.
Table 1 Disorders affecting growth and development of the skeleton
|
Site |
Abnormalities and their significance |
|
Epiphysis |
Delayed development – epiphyses small and fragmented. .Inherited dysplasia, but hypothyroidism is an important cause. Long-term complication is premature degenerative change, especially in weight-bearing joints. Bone age assessment often impossible. |
|
Metaphysis |
Dysplasias, metabolic disorders, infiltrations, infections. All these may cause significant and possibly permanent impairment of bone growth and development. Inherited deficiency of alkaline phosphatase may cause severe deformities. Acquired rickets on the other hand may be reversed, leading to normal bone development. Trauma (in child abuse) causes microfractures. |
|
Diaphysis |
Commonly affected by trauma. Repair process depends on periosteum. Some fractures fail to heal and unite, causing pseudoarthrosis. This is a recogised feature of neurofibromatosis. Stress or fatigue fractures occur in the diaphysis. Transverse or chalk-stick fractures indicate abnormal underlying bone (osteopetrosis, for example). Multiple fractures in osteogenesis imperfecta may cause severe deformities and limb shortening |
Table 2 Examples of the distribution of lesions in some common skeletal disorders
|
Disorder |
Distribution |
|
Paget’s disease |
Skull – may be predominantly lytic lesion but later sclerotic with thickened vault. Pelvis – thickened bone with coarse trabecular pattern and increased density. Limb bone – subarticular sclerosis and coarse trabeculation extending into diaphysis |
|
Hyperparathyroidism |
Hands – acro-osteolysis, subperiosteal bone resorption, cartilage calcification, bone cysts. Chest – erosion of the lateral ends of the clavicles; generalised abnormality of bone trabeculation. Abdomen – nephrocalcinosis |
|
Osteomalacia |
Looser’s zones in clavicles, scapulae, pubic rami. Deformed pelvis. Bowed lower limbs |
|
Myelomatosis |
Skull – multiple lytic lesions. Chest – expanding rib lesions Spine – ostoopenia, collapsed vertebrae. Limbs – endosteal erosion due to intramedullary expanding lesions. |
Table 3 Locally destructive bone lesions
|
Causes |
Radiological features |
|
Well-defined margins e.g. bone ‘cysts’ Often detected in childhood Humerus – present with pathological fracture fibrous cortical defects Superficial lesions; no significance; usually disappear enchondroma Hands; may have flecks of calcification eosinophil granuloma Skull and elsewhere, solitary or multiple sarcoidosis Hands; associated soft tissue swelling
Note: Some of these lesions may be discovered coincidentally, and there is some overlap in the radiological appearances. The site of the lesion is important in determining the likely diagnosis. |
|
|
Poorly defined margins e.g. metastases, myelomatosis Multiple, variable appearance but may be solitary initially primary bone tumours Localised but variable soft tissue extension infection Osteomyelitis tends to occur at ends of bones in the young, but there may be predisposing circumstances – trauma, diabetes, surgery, etc. Note: Considerable overlap in radiological signs. Skeletal survey, radionuclide studies, and bone biopsy may be necessary to resolve the problem. |
|
Analysing radiographic abnormalities in the skeleton
· Fractures and their consequences- displacement, angulation, healing nonunion and evidence of surgical intervention – form a well-defined group of radiological appearances. Trauma to joints – dislocations, associated bony injuries – also give characteristic signs. It is important to rule out an underlying bone lesion or a generalised abnormality that predisposes to fractures.
· Non-traumatic disorders of the skeleton require a more systematic approach, involving the following stages.
-Identification of the type of lesion –destructive, sclerotic, localised or widespread, involving joints and/or soft tissues.
-Assessment of the full extent of the lesion(s). This may eventually require the use of other imaging techniques such as CT or MRI.
–Determination of the extent of the abnormality in the skeleton as a whole and whether any lesion may be accessible for biopsy.
-Consideration of the general health of the patient, the mode of presentation, the patient’s age, evidence of systemic ill health. The differential diagnosis in cases where a tumour is being considered depends to a large extent on the patient’s age. Childhood tumours such as
– Some bone lesions have very characteristic appearances, e.g. rickets, and little or no corroborative radiological evidence is necessary. Conversely, acroosteolysis (dissolution of the tufts of the terminal phalanges) occurs in a variety of conditions and full clinical and biochemical assessment is necessary.
–Evidence of growth retardation with specific clinical features (e.g. abnormal facial appearance, low-set ears, supernumerary teeth, poly- or syndactyly) are very suggestive of a dysplastic or dysmorphic syndrome and full clinical, radiological, biochemical and genetic assessment is usually carried out.
This is not an exhaustive list but it illustrates the important elements of the analysis of radiographic bone or joint abnormalities. The ‘geographical’ distribution of the lesion(s) in the skeleton as a whole is a useful discriminator.
When planning further radiographic assessment, Table 4 illustrates some of the most common sites of involvement in a few well-known skeletal disorders.
Table 4 Locally sclerotic lesions
|
Causes |
Radiological features |
|
Anatomical variants e.g. ‘bone islands’ |
Incidental finding – pelvis, femora mainly. |
|
Degenerative joint disease |
Qsteophytes may produce localised sclerosis around joints. |
|
Infection |
Chronic osteomyelitis. Mixed pattern of lysis and sclerosis, periosteal new bone, deformity. |
|
Tumours e.g. benign osteoma Skull, very dense osteoid osteoma Usually limb bone, child or adolescent, pain (nocturnal). Intense sclerosis if sited in or near cortex
osteogenic sarcoma Characteristic bone-forming tumour with extension into soft tissues and intense periosteal response May cause ‘ivory vertebra’. Usually mixed lesion) lymphoma Usually multiple but may be solitary. Prostate and metastasis breast are most common sources |
|
|
Miscellaneous disorders e.g. bone infarct Osteonecrosis, e.g. in divers. Usually medullary, long bones. Geographical area of increased density Pagets disease Skull, pelvis, etc. Thickened bone with coarse trabecular pattern trauma Healing fractures or stress fractures may produce localized sclerosis with no visible fracture line post-radiotherapy Form of osteonecrosis, e.g. ribs after breast cancer treatment. |
|
Types of bone abnormality
It is convenient to classify bone lesions along the following lines to arrive at a reasonable list of differential diagnoses:
locally destructive (e.g. infections, tumours)
locally sclerotic (e.g. chronic infection, some tumours, avascular necrosis)
widespread loss of density (e.g. osteoporosis, metabolic bone disorders, e.g. hyperparathyroidism, steroid therapy)
widespread increased density (e.g. some metastatic tumours, myelofibrosis, fluorosis)
mixed lesions (e.g. Paget’s disease, chronic infection)
bone growth and modelling abnormalities (e.g. bone dysplasias, neurofibromatosis, trauma)
· primary joint disease affecting adjacent bony structures (e.g. inflammatory joint disease, some synovia! tumours)
soft tissue disorders that affect joints (e.g. collagen diseases, soft tissue tumours or infections that invade or compress adjoining bone)
miscellaneous radiological features (e.g. periosteal reaction, intraarticular calcification, soft-tissue calcification).
Tables 3-6 summarise the most important radiological features of these disorders.
Table .5 Widespread loss of bone density
|
Causes |
Radiological features |
|
Osteoporosis e.g. ‘senile’ or post-menopausal disuse, adjoning inflammation, steroid therapy |
All these conditions produce bone demineralisation, and this may predispose to vertebral collapse, rib fractures; densitometry assessment more accurate than radiographs |
|
Metabolic bone disease e.g. osteomalacia, rickets, hyperparathyroidism |
These disorders produce characteristic radiological signs, but Hyperparathyroidism – bone cysts, sub-periosteal bone resorption, acro-osteolysis, nephrocalcinosis, soft-tissue (articular) calcification Rickets – characteristic flaring, splaying and irregularity of the metaphyses in the growing skeleton. Wide zone of unossified matrix |
|
Infiltration e.g. metastases, myeloma tosis, leukaemia |
Diffuse demineralisation may occur without identifiable localised bone destruction |
|
Haemolytic disorders, e.g. thalassaemia |
Marrow overactivity and overgrowth giving characteristic appearances in the small bones of the hand particularly |
Table.6 Widespread increase in bone density
|
Causes |
Radiological features |
|
Congenital- osteopetrosis |
Rare conditions resulting in characteristic sclerosis of the skeleton and bone fragility resulting in ‘chalk-stick’ fractures. ‘Marble-bone’ disease in its severest form is lethal. Bands or islands of very dense bone affecting all bones. |
|
Acquired e.g. metastases myelofibrosis
fluorosis
sickle-cell disease
|
Usually from prostate or breast. May coalesce to produce dense skeleton Uniformly dense bones. Splenomegaly. Several causes including drug-induced myelosclerosis Endemic areas, e.g. Middle East. Accompanied by soft tissue (ligamentous) ossification Generalised increased density with localised areas of bone infarction, e.g. humeral heads, vertebrae |
Skeletal trauma
Radiographs are used to confirm or exclude fractures, to assess the type and complexity of a fracture and the relationship of bony fragments to each other and to adjoining structures, and to show possible underlying predisposing conditions such as metastatic deposits. Radiographs are also useful in the follow-up of fractures to show healing (or lack of it) and resultant deformity or other complications, e.g. infection.
Similarly, dislocations of joints, even in the absence of a fracture, can be assessed radiographically. Here some additional alternative projections may be necessary, e.g. axial view of the shoulder joint.
The golden rule of fadiography in skeletal trauma is that views in two planes must be obtained to confirm or exclude a fracture, because a fracture line or a deformity may only be visible in one plane.
Transverse (or chalk-stick) fractures of the shafts of long bones usually indicate underlying bone pathology, e.g. Pagef s disease or one of the disorders giving rise to ‘brittle bones’, e.g. osteopetrosis.
Stress or fatigue fractures occur in active individuals, e.g. athletes, and the sites depend on the activity. For example, long distance runners develop undisplaced, incomplete fractures in the upper third of the tibia or in the metatarsals. They are painful and appear as localised areas of increased density on radiographs, with some periosteal reaction and surrounding soft tissue calcification (callus). Pagef s disease also predisposes to incomplete or stress fractures.
Ambulant and adventurous young children often sustain long-bone (usually mid-shaft) fractures, but ion-accidental injury, usually occurring in infancy, fractures occur in unusual sites, e.g. posterior ends of the ribs, scapulae, hand and foot bones, and metaphyses. Fractures may be multiple and of different ages and stages of repair. The ageing of these fractures is often imprecise because of the repetitive nature of the injury. This may account for the abundant amount of callus that forms around the fracture(s) in some cases.
Table 7 Common joint disorders
|
Causes |
Radiological features |
|
Osteoarthritis |
Narrowed joint space, marginal osteophytes, surrounding sclerosis, subchondral cysts Affects spine, hips, knees mainly; also hands – distal interphalangeal joints and first metacarpophalangeal joints in particular. |
|
Rheumatoid arthritis (RA) and Still’s disease (juvenile chronic arthritis) |
Erosive arthropathy, symmetrical involvement usually. Proximal interphalangeal, metacarpo- and metatarsophalangeal joints commonly. Acute phase – soft-tissue swelling, periarticular osteoporosis. Cortical erosions Later – joint subluxation, ‘arthritis mutilans’ Juvenile form – few, if any, erosions; soft-tissue swelling and hyperaemia leading to epiphyseal overgrowth followed by premature fusion. |
|
Gout |
Erosions affecting mainly the interphalangeal joints. Deep, punched out, with less surrounding osteoporosis than in RA. Crystal deposition in joints (sodium biurate). |
|
Psoriasis |
Resembles RA except that distal interphalangeal joints of hands and feet are disproportionately affected. Skin disorders may not be severe or even prominent. |
|
Ankylosing spondylitis |
Sacroiliitis; calcification of longitudinal ligaments to form continuous bridges over discs – ‘bamboo spine’. Causes severe kyphosis in later stages. Synovial joints also affected by seronegative arthritis similar to RA with severe degenerative changes superimposed. |
|
Haemophilia |
Knees, ankles, elbows – chronic or repeated haemarthrosis, with changes similar to juvenile arthritis initially, followed by degenerative changes |
|
Neuropathic joints |
Impaired sensation (diabetes, syringomyelia) leading to severe degenerative changes and total disruption and dislocation of affected joints (Charcot joints). |
Difficult areas in skeletal trauma
Undiagnosed fractures and dislocations can have serious medical and legal consequences and may result in severe deformity and disability. Examples include the following.
Undiagnosed scaphoid fracture: causes chronic pain and may result in osteonecrosis of the bone.
Fractures of the femoral neck may be impacted, with no apparent fracture line radiographically and no deformity. In this circumstance an MRI scan may be diagnostic. Avascular necrosis of the femoral head is a recognised complication and may necessitate prosthetic replacement of the hip joint.
Posterior dislocation of the shoulder or hip joints may not be apparent on standard radiographs and additional projections are necessary for confirmation. Unsuspected fractures of the humeral and femoral heads may be discovered in association with these dislocations.
Complex fracture/dislocations of the wrist, foot and ankle, e.g. translunar dislocation, require radiographs in at least two planes for complete assessment. There are usually associated relatively unimpressive fractures, e.g. of the radial and ulnar styloid processes, which are easily overlooked. Avascular necrosis of bone is a serious long-term complication of many complex fractures, resulting in severe mechanical instability of joints, pain and disability.
Skull fractures and spinal fractures give rise to diagnostic difficulties.
Use of alternative imaging techniques in the skeleton
It will be apparent that in some circumstances plain radiographs of the skeleton are inadequate for the assessment of early phases of damage and repair, whether the cause is trauma, infection or even tumour. In this situation radionuclide studies are very useful because they are more sensitive to increased osteoblastic activity man radiographs. Therefore this technique has become well established in the early detection of bone disease and is particularly useful where the possible complications of that disease are to be avoided. In possible avascular necrosis of bone, ‘cold’ areas on radionuclide scanning confirm the diagnosis, e.g. in the femoral head following a fracture of the neck.
MRI has also become established as an important and sensitive technique for the early detection of bone marrow disease and soft tissue abnormalities adjacent to bone or within joints. Cancellous bone is not visible on MRI scans but the consequences of bone trauma are frequently visible, e.g. paraspinal masses, disruption of joint structures.
Radiology of joint diseases
On clinical grounds alone it may be difficult to distinguish between the different forms of arthritis, although the predominant site of pain and stiffness and the distribution of affected joints may give some indication of the likely diagnosis.
It must be remembered that ‘arthralgia’ is a fairly common accompaniment of a variety of non-articular, systemic disorders. A complete assessment of the clinical history and examination is necessary; other non-radiological investigations may give strong dues as to the likely diagnosis.
The most common form of joint disease is osteoarthritis (or osteoarthrosis), which is a degenerative process. It affects mainly the weight-bearing joints and is due to general wear and tear. Some occupations involving strenuous manual work (e.g. the use of vibrating tools) may predispose to degeneration. Joint disease from an early age and internal mechanical disruption of joints (e.g. following Perthes’ disease) also predispose to premature degenerative change.
Inflammatory joint disease is relatively common; there are numerous variants that mimic rheumatoid arthritis and there are several types that are seronegative but may be an integral part of systemic or multisystem disease. Some are linked with deposition of crystals or haemosiderin in the joints and form part of a metabolic or haematological disorder. The association between inflammatory bowel disease and ankylosing spondylitis and sacroiliitis is well recognised, as is the association between psoriasis and a seronegative erosive arthritis.
The radiological features of joint disorders can be categorised into:
· non-specific: signs of effusion degenerative osteophytes joint space narrowing sub-chrondral ‘cysts’
· specific: erosions, cartilage calcification soft-tissue swelling, periarticular osteoporosis long-term complications such as ankylosis, arthritis mutilans and osteonecrosis.
The radiological features of some of the most common forms of arthritis are summarised in Table 7.
Miscellaenous signs of bone and joint disease:
Periosteal reaction
This has been mentioned several times in this chapter because it is a common accompaniment of bone and joint disease. Periosteal new bone is a reparative response along the shafts of bones and is stimulated by trauma, inflammation, infection and tumours. It causes localised increased density of bone and may produce one of several distinctive radiological patterns – lamellar’, ‘onion skin’, ‘speculated’, etc., and some of these signs have been attributed to specific disorders. It may occur in response to soft tissue inflammation or infection alongside bone and need not therefore signify a primary bone disorder. One very distinctive pattern is seen in patients with certain lung disorders, e.g. carcinoma – hypertrophic pulmonary osteoarthropathy (HPOA), which is a symmetrical periosteal reaction along the femora, tibiae and forearm bones and is associated with severe, constant pain. The aetiology is not known.
Avascular necrosis of bone
This process may be provoked by trauma (resulting ion-union of fractures, e.g. of the scaphoid, femoral head, or talus), barotrauma, ischaemia due to abnormal coagulation in sickle cell disease, or drug therapy, e.g. corticosteroids. The process is not well understood but causes non-uptake of bone-seeking radionuclides, causing ‘cold’ areas in scans. Perthes’ disease is a very specific form of this disorder and occurs in children, usually in boys between the ages of 5 and 8 years. The femoral capital epiphyses become fragmented and small, and later dence. They reform with appropriate therapy (mainly immobilisation) but are usually abnormal in shape and may predispose to premature osteoarthriris. The sclerosis seen in avascular necrosis is due to thickened trabeculae and is attributed to bone repair.
Intra-articular calcification
Degenerative change (osteoarthritis) is associated with calcification of joint fibrocartilage, but cartilage calcification is a prominent feature of pseudo-gout (a crystal deposition arthritis) and metabolic conditions such as hyperparathyroidism, haemochromatosis and ochronosis.
Soft-tissue calcification around joints
Systemic sclerosis (scleroderma) causes calcification in soft tissues related to joints and on pressure points, i.e. the extensor surfaces of joints. The condition may cause a seronegative arthropathy. Extensive paraarticular soft-tissue calcification may occur in paralysed patients and calcium deposition has been seen in patients in renal dialysis, especially around the shoulder joints. These calcifications should not be confused with parasitic calcification, which usually occurs in muscles and is typical of cysticercosis.
