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Fig. 5.70. A. A 25-year-old African complained of backache ans was found to have a left paravertebral abscess and erosion of the medial end of left tenth rib (arrowhead). B A T 1-weighted coronal MR scan showed bilateral abscesses and low-intensity signals from the marrow of T 8 and T 9. C The T 1-weighted sagittal MR scan showed the large abscess anteriorly and posteriorly, with destruction of the vertebral bodies and compression of the cord (arrow). D After 6 weeks of antituberculous treatment the abscess is much smaller and the cord is less compressed (arrow). It was realized more than 30 years ago (Konstam) that many of the neurological signs are caused by the abscesses rather than the spinal deformity. CT and MRI have confirmed this dramatically. (Courtesy of Dr. Peter Corr, Durban) E Apart from pressure on the cord from an abscess, there may be a tuberculoma, as shown at the level of C 4 in a different patient, a child. This is an intravenous gadolinium-enhanced T 1-weighted MR scan. (From Cremin and Jamieson 1995).

Wherever the abscess presents, there should be careful imaging of the whole spine, starting preferably with isotope scintigraphy. Paravertebral abscesses occur at all levels and may be present on one side only, on both sides symmetrically or asymmetrically, or only in front of the spine without any lateral extension. Some may be dumb-bell in shape, protruding wherever space permits. They vary considerably in size and shape. When there is an anterior spinal abscess, underneath the spinal ligaments, the anterior edge of the vertebral bodies may become concave because of the transmitted aortic pulsation. The vertebral cartilages are not affected and the pressure absorption of the body may be minimal or considerable, so that it resembles the concavity caused by an aortic aneurysm. MRI is the best way to demonstrate what is actually happening, and CT is also suitable for this purpose.

A psoas abscess may connect with any part of the bowel, may be extensive and surround the kidney or the liver, or may burst through the skin onto the surface almost anywhere (Fig. 5.71). In many cases sinography is required, but careful technique is essential. The examination should be carried out under aseptic conditions and under fluoroscopic control. The sinus should be blocked by using the largest catheter that can be inserted; a balloon catheter will often help in achieving a tight connection. Pus should be aspirated, if possible, and pressure on the surrounding tissue or the suspected site of the abscess may help this drainage. Contrast material should then be injected and considerable pressure may be required if the full extent of the abscess is to be visualized. The case illustrated in (Fig. 5.71A and B) was a patient who presented with a sinus in the left side of the lower abdomen, without any obvious etiology. The only organism cultured from it was E. coli. A barium enema and an upper gastrointestinal series with a follow-through examination did not show any connection to any part of the bowel.

Two limited sinograms were performed before the patient was referred to the author, who blocked the sinus and, using considerable pressure, showed the abscess extending up the left psoas and surrounding the left kidney, across the midline between T12 and L1, and then coursing down the right psoas to connect posteriorly with the cecum. This was, therefore, a sinus draining from the left lower abdomen and yet connected with the cecum on the opposite side through a tuberculous abscess of the spine. (A very similar case has been seen in an American who has never been near the tropics!)

Paravertebral tuberculous abscesses shrink and often show calcification as they heal and fibrose (Fig. 5.72). Unfortunately, calcification does not always indicate sterility. There may be active caseous material contained within the fibrotic bag.

Fig. 5.71 A-D. Psoas abscesses can be very extensive and have unexpected connections. This young African has a persistent left flank sinus contaminated with E. coli. A The sinogram from the left lower flank, close to the iliac crest, showed that the fistula was connected to an enlarged left perirenal tuberculous abscess, which had started in a tuberculous infection between the 12th thoracic and first lumbar vertebrae. The abscess had also drained down in the right psoas and connected with the cecum, which was the source of the E. coli infection. B The lateral view of the same patient shows contrast running in front of the vertebrae, above and below the infection. This demonstrates how anterior abscesses can transmit aortic pulsation and also the etiology of the anterior bone bridging which occurs when the periosteum and anterior spinal ligaments are lifted. The aortic pulsation can bow the front of the vertebrae, as is shown in C in a much older patient with advanced aortic athromatous calcification. A previous tuberculous infection has resulted in fusion and increased density of the two lower thoracic vertebrae. D Another African patient with a fistula connecting the terminal ileum with a paraspinal abscess, which originated in lower thoracic tuberculosis. It is not always possible to demonstrate these fistulae with a barium gastrointestinal series. E. coli contamination is usually sufficient proof, even if the actual fistula cannot be imaged. (C courtesy of Dr. Harold Jacobson).

Fig. 5.72 A-E. Tuberculous abscesses of the lower spine. Thoracic and lumbar abscesses track along the psoas and can present at the inguinal region. When they heal, they often calcify. A Well-defined, heavily calcified abscess starting at the lower thoracic region in a patient with severe kyphosis. B Bilateral loculated and less densely calcified psoas abscesses. C A unilateral calcified psoas abscess in the lumbar region. There is bridging between the upper lumbar vertebrae, well above the visible abscess. D, E Sonograms of a right psoas abscess, displacing the kidney, in an African patient from Zimbabwe. RK right kidney. (A courtesy of Dr. Harold Jacobson; D, E courtesy of Dr. Sam Mindel).

Fig. 5.73 A-D. Myelography in tuberculous paraplegia. Where scanning is not available, there is no contraindication to myelography under fluoroscopic control. A There is narrowing of the disc space between the second and third lumbar vertebrae, but the myelogram shows distortion not only at this level, but also one space above. B A patient with thoracic paraplegia. Myelography shows long irregular defects, between the tenth and 12th thoracic vertebrae. C Myelography in a kyphotic patient can be difficult. In spite of the angle, in this patient there was no obstruction on myelography: it can be difficult to retain the contrast at the level of the curve when it flows freely in either direction. D The myelogram may show complete block. (D courtesy of Dr. Harold Jacobson).

Fig. 5.74 A, B. Postoperative spinal tuberculosis. It is very difficult to assess healing, which may take years. These are the postoperative images of a 2-year-old girl from the Pacific Islands. A The lateral radiograph shows the graft across the infected and wedged thoracic vertebrae (T 9-11). B T 2-weighted MRI shows the residual abscess and granulation tissue and the exact extent of the bone destruction. (Courtesy of Dr. Cheryl Sisler, Hawaii).

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Fig.5.75 A-G. The case history of spinal tuberculosis. A young man from Saudi Arabia had been complaining of pain between his shoulder blades for some months before he came to hospital one weekend, with rapidly developing'paraplegia. Plain radiography (A) showed wedging of two upper thoracic vertebrae. Myelography (B) showed almost complete block at this level and CT scan (C) showed destruction of the vertebra, particularly on the right side, and of the medial end of the rib at the same level. Fluid was present in the right side of the chest. D-G Pre- (D) and postgadolinium (E-G) MR scans show the full extent of the paraspinal abscess, and of the epidural granulomatous tissue. The findings on the CT scan are confirmed but shown more dearly. Subsequent surgical decompression revealed both caseation and granulomatous tissue with M. tuberculosis on direct smear microscopy. The patient made a good recovery. (Courtesy of Dr. Frank McGuiness, Ryadh).

Scanning, Paraplegia, and Myelography

As already mentioned, MRI is the ideal way to examine a patient with a tuberculous spine. A T 1-weighted scan shows tuberculous spondylitis as an area of low signal intensity where there is normally a higher intensity from the bone marrow, adjacent to the end plate of the vertebra. On a T 2-weighted scan these lesions have a high intensity. Liquid pus also yields a high-intensity signal on a T 2-weighted scan. MRI gives an accurate image of the spinal cord compression associated with intraspinal abscesses. At surgery, almost all patients with paraplegia will have at least a small abscess; even if it has not been visualized on plain radiography, it will probably be clearly seen on MRI (Fig. 5.73). Paraplegia indicates that there is about 50%-60% extradural compression above the conus, provided there is no vertebral instability. Peripheral nerves below the cauda or extraspinal nerves are not likely to be affected by compression. In some cases of paraplegia, the cord will appear to be intact, in which case there is likely to be a vascular deficit, a toxic reaction, or, as MRI can demonstrate (by showing a high-intensity focus on a T 2-weighted scan), damage to the cord, probably due to prolonged compression. This focal myelitis has a poor prognosis and the paraplegia is likely to be irreversible. However, as Konstam demonstrated, rest and drug therapy may relieve paraplegia which is of short duration, and simple decompression, either by needle aspiration or surgery, may be all that is needed in the early stages. Whenever any intervention is planned, it is a wise precaution to have the patient already on antituberculous therapy to obviate the risk of tuberculous septicemia.

Whatever method of imaging is used, it is essential that the whole cord or spinal canal is examined because the obstruction may not occur at the site of the obvious bone lesion, but rather be above or below it, depending on the extent of the fluid, necrotic tissue displacement, or granulation tissue.

If MRI is not available, myelography, with or without CT, is a very useful investigation and should be performed as early as possible and always before surgery to localize the exact site of any obstructions (Fig. 5.74). There are no contraindications to myelography although in some patients the kyphosis may make it extremely difficult. Where there is a double curve, careful manipulation of the patient (especially in the lateral decubitus position) may permit the column of contrast material to travel throughout the length of the spinal canal. Sometimes this is technically impossible, even when there is no blockage, because of severe spinal angulation. Fortunately, paraplegia is less often due to kyphosis or bony deformity than to an abscess or soft tissue pressure. The decision as to whether myelography needs to be repeated during treatment should be based on the clinical examination.

Following surgery in patients with spinal tuberculosis it is very difficult to assess healing, which may take years. Again, MRI is the best method for this purpose (Fig. 5.75).

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Fig. 5.76 A-D. Skeletal tuberculosis. The pelvis. Infection of the sacroiliac joints can be destructive and then, as healing occurs, become sclerotic and fused. A Widening and irregularity of the left sacroiliac joint. B Sclerosis on the iliac side of the right sacroiliac joints. C In another patient there is infection on both sides of the sacroiliac joint, particularly the sacrum. D Extensive destruction of a right sacroiliac joint in a different African patient. The infection must have spread through the right ilium, which is becoming sclerotic. The joint is widened throughout its length. The right hip joint is narrowed and probably also infected. (A, C courtesy of Dr. Harold Jacobson).

Differential Diagnosis

Theoretically any type of bone infection may cause a paravertebral abscess. In practice, the majority of spinal abscesses in the tropics are tuberculous; if there is active pulmonary tuberculosis, the possibility of spinal infection also being tuberculous is enhanced. It is unusual for a pyogenic or typhoid infection to cause a large paravertebral abscess, and even less often do such abscesses point to the surface as occurs with tuberculosis. On MRI, pyogenic disc infection usually has a high intensity on T 2-weighted scans, but in tuberculosis less than one third show this. However, pyomyositis (tropical myositis) can present in this way, usually without any osseous lesion (see Chap. 30). Brucellosis may also produce a paravertebral abscess (see Chap. 32). There may be paravertebral thickening in lymphoma (particularly in Burkitt's lymphoma) which may resemble an abscess, and the bony destruction may also be very confusing because Burkitt's lymphoma may involve a vertebral body or a pedicle (see Chap. 41). Sometimes the differential diagnosis is impossible with any method of imaging, but in the majority of cases there will be other evidence of Burkitt's or other lymphoma to establish the correct diagnosis. Wedging, particularly wedging and fusion of two or three vertebrae, is very uncommon in any infection other than tuberculosis.

Because tuberculous osteomyelitis in the tropics (even in patients without AIDS) is often an acute disease, it is difficult to differentiate from other infections and the clinical condition of the patient may be very important when giving a radiological opinion. Nontuberculous spinal infections usually cause more severe clinical symptomatology than tuberculosis, with more systemic reaction, a higher pyrexia, and a raised white cell count, but none of these criteria are absolute and biopsy or aspiration and culture are essential.

The differential diagnosis of tuberculosis from acute trauma is seldom difficult, if only because of the clinical history. Trauma does not cause as much bone loss and destruction as tuberculosis. Long standing cases need serial review, both clinical and radiological. In the majority of such problem patients the etiology is of no immediate clinical significance, permitting a more cautious approach. Scintigraphy or other imaging survey of the rest of the spine may show other involved vertebrae and allow the differentiation between trauma and infection.

In all patients, the possibility of malignancy will have to be excluded, particularly when the bone destruction involves the pedicles. Many malignant tumors cause paravertebral swelling resembling an abscess; obtaining a tissue specimen, either through needle aspiration or biopsy, becomes essential. Most errors are made because the possibility of tuberculosis is overlooked in the elderly or in the very young.

Fig. 5.77 A-G. Tuberculosis of the ischium and symphysis pubis. In the early stages most tuberculous lesion in the ischium are ill-defined lucent areas; they later become sclerotic. A A lucent focus of infection in the left ischium, with some early surrounding sclerosis. B A more destructive lesion closer to the hip in another patient, with some loose bone fragments. C There are foci on both sides on the symphysis and in the left ischiurn. D Both sides of this symphysis have been infected, the joint is widened, and there is a central sequestrum. An African from Zimbabwe. E A different patient from the same country in which a similar infection has healed causing sclerotic fusion across the symphysis. F There is a lytic area of infection above the acetabulum in this child from South Africa, but the hip joint remains normal. G An isotope scan at the same patient shows that the iliac infection is more extensive than seen on the radiograph. Tuberculosis is the proven cause in all these cases. (A-C courtesy of Dr. Harold Jacobson; F, G from Cremin and Jamieson 1995).

Tuberculosis of Bones and Joints (Nonspinal)

Tuberculous Arthritis

A tuberculous infection of a joint can occur at any stage, but is more common in the younger age groups. Even babies from 6 months onwards may present with quite severe skeletal infection. The joints most affected in order of frequency are the hips, knees, ankles elbows, wrists, sacroiliac joints, and shoulders (Fig. 5.76, 5.77). In 98% of HIV-negative patients the tuberculin skin test will be positive. The way in which tuberculosis affects a joint depends on whether the original focus is in the synovium or in the adjacent bone. Spread of the infection from bone into a joint is more common and has a poorer prognosis.

Nontuberculous mycobacteria may cause arthritis and bone infection. This is uncommon, but may become more frequent in patients with AIDS. Mycobacterium kansasii has been known to infect knee joints, and M. intracellulare has infected the shoulder, the spine, and, in one patient, both wrists. The differential diagnosis will only be made by joint aspiration or synovial tissue culture.

Synovial Tuberculosis

Patients will first complain of either slight pain or stiffness in the affected joint, and of limitation of movement. In the early stages pain is minimal and it is only as the joint swells that it becomes significant. In many cases there will be a dull, ill-defined ache, often worse at night, but in developing countries such discomfort is often ignored, and it is not until the disease has progressed further that the patient seeks help.

In the beginning, it will be difficult to detect any clinical abnormality to account for the symptoms. Later there will be edema and swelling around the joint, with some limitation of passive movement and increase in local temperature; an effusion often develops early and aspiration of the fluid usually shows it to be clear or straw-colored with few cells; it is sterile on culture. The diagnosis may have to be presumptive, because it may not be possible to find any positive proof of tuberculosis. At this stage, scintigraphy is a reliable way of excluding bone infection; ultrasonography and MRI, and to a lesser extent CT, can be useful in demonstrating the soft tissue changes. Radiographically the joints may be entirely normal in the early stages, and it may take 2-6 weeks before there are positive radiological findings (Fig. 5.78).

The earliest change is loss of clarity of the bones forming the joint; their margins become hazy and difficult to define. There is a mild generalized osteoporosis but not localized bone destruction. The joint space may be widened because of the effusion. Progress of the infection is slow, but a little more rapid once the radiological changes have developed. The osteoporosis becomes more pronounced and there will be soft tissue swelling around the joint. It may be difficult to define any bone erosion because of the osteoporosis and the variable change in bone density. Eventually foci of bone destruction become more definite as the cartilage is destroyed. At this stage the radiological appearance is "ghost-like;" particularly when compared with the opposite normal side. If only the synovium is involved, and if treatment is adequate, the disease shows no further progress but slowly heals with a return of the joint towards normality. In the majority of cases, however, there is permanent damage to the cartilage and occasionally to the underlying bone which may lead to degenerative arthritis. When the synovial involvement has been severe, the joint may eventually ankylose.

Fig. 5.78 A-F. Tuberculosis of the hip. The earliest evidence of infection may be an effusion into the joint. A The CT scan did not show any bone lesion but there were M. tuberculosis in the effusion. B In other patients there may be soft tissue swelling, osteoporosis, and loss of bone definition, as can be seen by comparison with the normal left hip. C A different but similar infected hip in which the ill-defined, hazy appearance of the joint and the soft tissue swelling around the acetabulum, particularly medially, are clearly shown. D-F The same patient (an African from Zimbabwe) over a period of 3 years. D There is soft tissue swelling and an effusion in the hip joint with destruction of the acetabulum and femoral head. E Six months later there is less fluid and the bone density is improving: in spite of the bone destruction, there are no sequestra. F Two years later the joint has fused: there will be shortening of the limb and there is significant deformity of the right side of the pelvis. (A courtesy of Dr. Cheryl Sisler, Hawaii).

Osteoarticular Tuberculosis

Scintigraphy is a very useful way of locating tuberculous bone infection and ensuring that it is not multifocal. In the majority of patients, tuberculous infection of a joint is due to spread from a focus within an adjacent bone. An effusion is evidence of this spread but may also occur before actual cartilage destruction has taken place. The bony focus may be close to the articular surface, a few millimeters away from it, or in the metaphysis. The very early bone focus (as well as the soft tissue involvement) can be shown by MRI, and the extent of marrow replacement can be assessed. Gadoliniumenhanced T 1-weighted images show differential rim enhancement. Such foci can be single or multiple, and although they are usually opposite one another on opposing sides of the joint, they need to be so closely related. On plain radiographs or CT, the lesion within the bone appears as an area of decalcification, without any definite edge and of no particular shape. This slowly spreads up the shaft, but also across the epiphysis into the joint. At this stage clinical symptoms will be minimal. Some patients may complain of a dull ache or "spasm" in the joint or occasionally some swelling. Careful clinical examination may show some restriction of movement, but this may be so slight that there is little suspicion of an underlying osteomyelitis.

As the infection bursts into the joint, there will be a considerable reaction, with fluid and tuberculous debris in the joint space. The sacroiliac joints can be the most difficult to assess on plain radiography. Scintigraphy can be helpful but the uptake ratio between the sacroiliac joint and the os sacrum can vary with age. In any joint, CT and MRI provide more definite evidence of bone destruction on either side of the joint, and of subsequent joint involvement. Clinically, at this stage, there is no doubt that a limb joint is abnormal. It will be painful, swollen, and immobile.

The disease progresses with further destruction and disorganization; the soft tissues, already swollen, become involved with the tuberculous process, best shown by MRI or CT. The joint may subluxate. In weight-bearing joints such as the hip (one of the most commonly affected: (Figs. 5.78, 5.79), involvement of the acetabulum may lead to rupture of the femoral head into the pelvis, particularly where treatment has been delayed and weight bearing has been continued. CT and MRI, and occasionally ultrasonography, can show a soft tissue mass within the pelvis when this occurs. There will usually be multiple, very small sequestra within the mass. The margin of the infected lesion in the bone will probably show reactive sclerosis. Angiography has been used to show the soft tissue mass, which is usually vascular, but it is unlikely that this will provide much useful information.

As healing occurs, the joint space usually narrows; the bones increase in density but do not remodel and the deformity persists. Ankylosis is almost inevitable and may in fact be beneficial because it often permits limited use of the limb. The entire process may take months, even with adequate drug therapy, and the principal imaging problem is to assess the progress of healing, because the changes occur slowly and are often minimal. Ankylosis may become complete, but because of fibrous tissue rather than bony fusion. In such cases the infection may be quiescent but not fully healed. As with all other types of tuberculosis, experience must be combined with careful clinical judgment and continuous observation of the patient to obtain the best end result.

This process, either synovial or osteoarticular, may occur in any tuberculous joint and the same pattern will be followed. Variations occur depending on the type and location of the joint, whether or not it is weight bearing, and how much it is used. For example, when foci oppose each other on either side of a joint [usually the knee (Fig. 5.80), but also the elbow, shoulder, and hip, dense areas of bone may be seen ("kissing sequestra"). There is some individual variation depending on the host resistance, but this is more in terms of the time taken for the changes to be complete rather than in the pattern of the disease.

Fig. 5.79 A-F. Tuberculosis of the hip. In some patients the femoral head remains surprisingly intact, while in others it is eventually destroyed. A A cystic lesion in the acetabulum of a young African male: the hip joint is narrowed and irregular. There was also infection in the inferior pubic ramus. B There is destruction of the greater trochanter in this adult African and a cystic lesion in the neck of the femur, spreading into the femoral head. The joint space is not affected. C In this child there is central destruction of the upper end of the left femur, with a periosteal reaction along the shaft. The joint is infected and the femoral head has been dislocated and will never develop properly. D Advanced tuberculosis of the left hip and the left part of the pelvis. The hip joint is fused and there is dense sclerotic bone around the three lytic foci in the left iliac bone. This could be mistaken for a pyogenic infection. E The femoral head has disappeared, the acetabulum is irregular and sclerotic, and there are cystic changes both in the femoral neck and around the joint. The end result will be fusion, and there may be fixed fibrosis already. F The joint has been completely destroyed and dislocated and is surrounded by calcified debris. There will be marked shortening of the right leg and the hip is fixed. (Courtesy of the University of Cape Town Radiology Library).

Tuberculosis of Bones

Osteomyelitis due to the tubercle bacillus is a common condition and need not always involve a joint; in fact it can occur in virtually any bone in the skeleton (Figs. 5.81-5.85). It is most common in childhood but no age is immune; it is frequently multifocal. Scintigraphy is very helpful in identifying the possible multiple sites.

As with pyogenic organisms, the infection most commonly begins in the metaphysis. Its effect on the adjacent joint has already been described. Away from the joint the early changes, localized areas of osteoporosis without any surrounding bone reaction, are often more easily seen than delineated. They have no particular shape, but follow the contour of the bone; in the skull they may be large and apparently spreading. The initial lesion may be seen in the diaphysis, but this is rare. Multiple bones may be infected or the same bone may have foci in different places, not initially connected.

If there is a lesion close to the cortex, expansion is common and cortical thinning occurs. There will be an associated periosteal reaction with a fine lamellar pattern, spreading proximally and distally from the original focus. Ultrasound can identify the edema and the periosteal reaction and be used to guide aspiration biopsy to establish the diagnosis. Both CT and MRI can image the infection, but are unlikely to add much to the accuracy of the diagnosis. This type of reaction is most common in the smaller bones, such as the phalanges (tuberculous dactylitis) and is most frequently seen in children (Figs. 5.86, 5.87). The changes are more marked at this age because the cortex is relatively soft and expansion occurs more easily. The old descriptive term "spina ventosa" (spina=short bone; ventosa=inflated with air) is thus especially appropriate (Fig. 5.86 A).

The radiolucent areas are filled with tuberculous granulation tissue, which causes the expansion. As the cortex expands and thins, subperiosteal new bone is laid down on the outer aspect; this new bone may be layered, quite thick and dense, and sclerotic. Because there is the appearance of an involucrum, the possibility of a pyogenic infection should be considered. The differential diagnosis then depends largely on the patient's clinical condition. In tuberculosis the pain is not marked, pyrexia is minimal, and the whole condition is relatively benign. A pyogenic osteomyelitis causing such a reaction would be acutely painful, swollen, and inflamed, with a generalized systemic reaction which is often absent in the tuberculous variety.

Radiographically detectable sequestration does not often occur in tuberculosis because the blood supply has not been affected, but there are exceptions and tuberculous sequestra do occur without any other associated infection (Fig. 5.82 F). CT may detect very small sequestra when a bone lesion has spread rapidly into the soft tissues, e. g., in the pelvis.

Fig. 5.80 A-H. Tuberculosis of the knee. A The earliest signs of infection may be a large joint effusion and mild generalized osteoporosis, without any visible bone defect. B, C Another African patient from Zimbabwe. The soft tissue swelling and effusion are marked but there is a lytic bone focus in the lower end of the femur and periosteal elevation around the full diameter of the femoral shaft. There is accentuated growth of both the femoral and tibial epiphyses. The lytic bone focus is important in the differential diagnosis, because nonarticular rheumatoid arthritis and hemophilia can both give similar appearances before there is any bone destruction. D Another patient with a lytic bone focus medially in the lower end of the femur, but also in the femoral epiphysis with a slight sclerotic margin. There is a joint effusion. E A tuberculous infection of the patella with a suprapatellar effusion. F, G The end stages of a tuberculous joint infection. In F there were foci on both sides of the joint; the lateral femoral and tibial condyles had been partially absorbed and destroyed. New bone is present on the lateral aspect of the joint with some fragmentation. There is angulation which may progress. The joint will probably fuse, with either fibrous tissue or bony anyklosis, but in some patients it may remain a lax unstable joint. H A healed but badly damaged joint, with partial destruction of the upper end of the tibia, and a lot of new bone and loose fragments. There is calcified debris in the supra-patellar bursa.

In Europe and North America, the same multifocal lytic lesions can occur, but they are better demarcated and cyst-like. They are most common in the long bones of children and young adults; sometimes they are symmetrical. Probably the difference between the tropical and nontropical pattern is related to immunity or more prompt treatment. The "tropical" pattern will be seen in AIDS anywhere and will often be more destructive and spread more rapidly.

In the skull, scapula, and ribs, as well as the long bones, there may be similar lytic foci without any bone response. In the skull this results in quite large, destructive lesions. Solitary skull foci also occur, sometimes with a reactive edge and a central "button" sequestrum. Because these solitary tuberculous foci are associated with a fluctant "cold" abscess they were named "a puffy tumor" by Sir Percival Pott in the eighteenth century.

In the ribs there may be quite a marked periosteal reaction and localized swelling (Fig. 5.85 E, F). Some care has to be taken to differentiate tuberculous osteomyelitis of a rib from a tuberculous abscess tracking around the intercostal space from its origin in the thoracic spine. Such as abscess will also cause swelling, and there may be some local periosteal reaction on adjacent ribs. Ultrasonography (or CT/MRI) may help to track the abscess more accurately and, like scintigraphy, will locate any intrinsic bone focus. Radiographically, in slender bones such as ribs it may not be easy to see the destructive areas within the bone itself, particularly when the periosteal reaction is marked; an exactly similar process can occur in the long bones. Periosteal new bone is not the "hallmark" of pyogenic infection; it can also be seen in tuberculosis.

In the tropics this type of "cystic" and periosteal tuberculous bone infection (Fig. 5.81) may be relatively slow and benign, or can be progressive, depending on the host resistance and the rapidity with which treatment is commenced. In young children the imaging changes may appear worse than the clinical condition. When tuberculous osteomyelitis occurs in adolescence and adults, it takes longer to heal and may be more significant. In the skull vault the infection usually spreads outwards; only rarely does it involve the meninges, leading to an intracerebral tuberculous abscess (Fig. 5.95).

Healing follows the same slow pattern already described (Fig. 5.88). The bone density returns; the defect may be filled in with new bone, or may persist for some time. The bone may be sclerotic, heavily trabeculated, or relatively normal. Some areas may be dense, resembling sequestra; the dense sclerosis in some bones, especially in the diaphysis, may mimic a chronic pyogenic (Brodie's) abscess. Healing is more rapid in the long bones and digits than in the flat bones and tends to leave less deformity except when the epiphyseal place has been involved, which commonly results in shortening. Almost all diaphyseal lesions respond well to therapy.

Fig. 5.81 A-G. Tuberculosis in the lower leg. Many tuberculous foci in the long bones are cystic and are often multiple. There is nearly always periosteal reaction. A Multiple cystic foci in the tibia and lower femur. There is minimal periosteal reaction along the upper half of the tibia laterally. B Multiple similar cysts in the tibia and fibula of another patient, with a periosteal reaction in the fibula particularly. Some of the cystic foci have minimal sclerotic but incomplete borders. C A focus of infection in the center of the tibia with a layered periosteal reaction. D An expansile lesion in the fibula, with the ghost of the original shaft running through it. E Tuberculous foci may appear in more than one limb. In this African there is a periosteal reaction around the shafts of tibiae and the left fibula, with several faint foci of infection. G An African child from Kenya with tuberculous foci in both fibulae, the left tibia, and the lower ends of both femora. He also had similar foci in the right humerus, radius, and ulna. This type of tuberculous bone infection usually responds quite well to appropriate treatment (see Fig. 5.88). (B courtesy of Dr. Harold Jacobson ; A, C, D from Cremin and Jamieson 1995).

Fig. 5.82 A-F Tuberculosis around the ankle joint. A Very early infection. There is synovial thickening and a small effusion, as well as a minimal bone defect in the cortex of the upper surface of the talus posteriorly. B Infection of the lower end of the tibia, with an effusion into the ankle joint. There is marked soft tissue swelling. C A large defect medially and posteriorly in the lower end of the tibia with generalized osteoporosis and a small focus in the fibula. The ankle joint is decreased and a focus of infection is seen in the talus posteriorly. There is marked soft tissue swelling, and a joint effusion. D Collapse and destruction of the os calcis with marked soft tissue swelling and generalized osteoporosis. The infection is in the os calcis, but the whole joint will eventually be destroyed. E Cystic and sclerotic tuberculous infection in the posterior two-thirds of the os calcis, only affecting the cortex in one small area of the upper margin, near the tendo Achillis. F A more localized infection of the os calcis, with a sequestrum and extensive disruption of the upper surface. In D-F the differential diagnosis would include pyogenic and mycotic infections. (Courtesy of the University of Cape Town Radiology Library).

Fig. 5.83 A-D. The swollen ankle of a 7-year-old boy from the Pacific Islands. A There is generalized osteoporosis, but it is difficult to be sure that there is any bone focus. B-D MR scans show the joint effusion, and destruction of both the talus and the posterior part of the tibial epiphysis. The unfortunate child had tuberculous meningitis and miliary tuberculosis.

Fig. 5.84 A-H. Tuberculosis of the shoulder. A Acute tuberculosis with marked osteoporosis of all the bones around the shoulder. There is minimal periosteal elevation along the clavicle, but there is no bony defect. B A more chronic infection with multiple lytic areas in the head of the humerus, the clavicle, and the acromion process. The acromioclavicular joint is disrupted, but the shoulder joint is still relatively intact. C Considerable destruction of the head of the humerus in a child. There is left hilar lymphadenopathy. D Cystic tuberculosis in the right shoulder of a middle-aged African. The glenoid is almost destroyed, and filled with multiple cystic lesions. Next to it, the head of the humerus shows similar defects and there is destruction of the articular surface. The joint space is narrowed. The acromion was also affected. E Erosion of the glenoid and humeral head in a child; F, G two CT scans in the same patient showing the defect in the humeral head and the partial destruction of the glenoid (G). H The late stage of tuberculosis; there is calcified debris all around the joint, with partial destruction of the end of the clavicle. The acromion was also involved. The humeral epiphysis is very decalcified. The calcified masses could be mistaken for tumoral calcinosis, but the destruction of the clavicle and acromion provide evidence of infection. (E-G from Cremin and Jamieson 1995).

Fig. 5.85 A-G. Tuberculosis in the arm, scapula, and chest wall. A A lytic defect in the lower end of the humerus, will ill-defined edges, destruction of the cortex, and a minimal periosteal reaction. A similar but earlier lesion is suspected in the head of the radius. B A well-defined lytic focus in the upper end of the humerus, with a smaller, less clear focus in the middle of the shaft. C Periosteal reaction along the radius and ulna, with disruption of the lower end and widening of the upper end of the ulna and some lytic foci in the lower end of the radius. D Lytic destruction and minimal periosteal reaction in the lower part of the scapula. E, F Tuberculosis of the ribs. In E there is cortical destruction and periosteal reaction, and in F the infection is a little more advanced. There is also a pleural reaction. G A CT scan showing tuberculous infection of the left upper chest wall of a 4-year-old child from the Pacific Islands. He had widespread adenopathy, left upper lobe tuberculous infection, and tuberculous foci in the liver. (A progressive primary infection.) (D-F courtesy of Dr. Harold Jacobson; G courtesy of Dr. Cheryl Sisler, Hawaii).

Fig. 5.86 A-F Tuberculosis of the extremities. Infections of the hands and feet produce similar images. A The hand of an infact showing marked periosteal elevation and multiple lytic areas of bone destruction. There is a periosteal reaction along the ulna also. Lytic defects are present without periosteal reaction in some of the digits. B In this child there is also some epiphyseal damage and less periosteal reaction. The infection was by atypical mycobacteria, but this could not be recognized by looking at the images. C Destructive tuberculous osteomyelitis affecting the fourth left metacarpal. D The hand of an older patient with more advanced tuberculosis; the proximal phalanx of the fifth finger has been almost entirely replaced by granulation tissue and there are also multiple lytic foci in the phalanges of the third and fourth fingers. This is an unusual form of tuberculosis and it could be mistaken for multiple enchondromas or even metastases. E Osteomyelitis of the second right metatarsal and F the fibula of the same patient, a young African girl; her hand is shown in C. Her chest x-ray was normal and there were no other bone foci. (A courtesy of Dr. Harold Jacobson; C, E, F courtesy of the University of Cape Town Radiology Library).

Fig. 5.87 A-E. Tuberculosis of the carpal and tarsal bones in different patients. All show generalized osteoporosis, particularly at the ends of the digits and around the carpal and tarsal joints. No bone foci are visible because the disease is mainly synovial. Bone destruction is likely to occur eventually and fusion will be the end result. A Osteoporosis is well marked. B The wrist of another patient in which bone destruction has started, involving the radius and ulna as well as the metacarpals. The carpus is collapsing. C In this patient the cystic and destructive tuberculous infection could be mistaken for rheumatoid arthritis or even severe gout. D Similar changes in the tarsus: generalized osteoporosis particularly around the joints. There are a few bone foci in the metatarsals. E A more chronic infection at the proximal end of the right first metatarsal and the medial side of the tarsus. The cystic lesions are becoming sclerotic and the joints are fused. There is a periosteal reaction along the shaft of all the metatarsals, but this may be due to the soft tissue reaction rather than local bone infection. This African patient was treated for many months but there was no significant change in his foot. (B courtesy of Dr. Harold Jacobson).

Fig. 5.88 A-D. The healing of tuberculous bone foci. A Cystic changes in the lower end of the femur and the upper end of the tibia, including their epiphyses. Eighteen months following the completion of 6 months of antituberculous treatment, the changes have responded well. They will probably leave only small dense foci. C This young African child had been on treatment for 3 months and the large cystic focus was healing with sclerosis. The periosteal reaction along the medial aspect of the femur has also thickened. Unfortunately, there is considerable disruption of the normal growth pattern of the femoral epiphysis. D A longstanding lesion in the lower end of the femur of another child with a multicystic appearance, periosteal thickening, and widening of the lower end of the femur. In this case the epiphysis is small but otherwise appears normal.

Differential Diagnosis

The differential diagnosis of tuberculous bony lesions can be very difficult, particularly if this possible etiology is not considered early. The patient's clinical condition may help to differentiate tuberculosis from acute pyogenic infections, but even this may not ensure accuracy. The mycotic infections, such as North American blastomycosis, can simulate tuberculosis, particularly in their early stages. The multifocal destructive lesions of histoplasmosis duboisii (see Chapter 6) may resemble the aggressive form of tuberculosis.

In the early stage osteoporosis is more marked in tuberculosis compared with pyogenic infections, but tropical (or AIDS) tuberculosis (unlike tuberculosis in Europe or North America) may behave quite acutely and change can be rapid. Sequestration is not common in tuberculosis, but can occur. Spread of infection across an epiphyseal plate is uncommon in pyogenic infections, but is frequent in tuberculosis. Eosinophilic granuloma may mimic tuberculosis (or vice versa) and infections associated with sickle cell disease, such as typhoid osteomyelitis, may closely resemble tuberculosis in their early stages in the bones of the skull vault or in the spine. Later there tends to be more periosteal reaction and the clinical condition is more acute in nontuberculous infections. The frontoparietal lytic lesions of tuberculosis are usually ill defined, compared with the clearly beveled edge of histiocytosis. Syphilis can produce very similar osteolytic lesions.

Particularly in children it is important to differentiate early rheumatoid arthritis, especially the monarticular variety. Cystic lesions could be mistaken for hydatid disease of bone, but this is uncommon in the midshaft of long bones.

The pattern of tuberculosis is the same in the bones of the skull, and may be found in the sphenoid, mastoid, zygoma, as well as the calvarium (Figs. 5.89-5.95). The maxilla and the mandible can also be involved and the differential diagnosis can be extremely difficult.

Tropical tuberculosis affects the skeleton in many ways, and this possible etiology must be remembered when any bone infection, "acute" or "chronic", is being reviewed.

Fig. 5.89 A, B. Tuberculosis is very frequently multifocal, particularly in patients who have a depressed immune system for any reason. Although multifocal infection is seen most commonly in children as part of the progressive primary tuberculosis, it may also appear in adults, even in old age if the infection is reawakened. A This 10-month-old African baby had widespread skeletal tuberculosis. There are cystic lesions with marked periosteal reaction in almost all the long bones. In the right arm, the lower end of the humerus, the upper end of the radius, and the lower half of the ulna are affected. There is dactylitis of the fifth right metacarpal. There were similar lesions in the left arm. B There cystic lesions in both lower limbs, in each femur; the left is more severely affected and shows a greater periosteal reaction. In the lower legs only the right fibula seems to have escaped. Whenever there is multifocal disease, a radioisotope bone study may reveal unexpected foci. The only reason that this child was brought to a hospital was because of swelling of the left lower leg. (Courtesy of the University of Cape Town Radiology Library).

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Fig. 5.90 A-C. Tuberculosis in the spine may be the clinical reason why a patient comes to hospital, but there are often foci of infection elsewhere. In this small African child there is destruction of the inner ends of the sixth and seventh ribs and the infection has spread along the seventh right rib (A). The right side of the sixth thoracic vertebra has collapsed, although so far the disc space has remained relatively intact. There is a large right paravertebral abscess and a smaller one on the left. It is probable that the rib became infected from the spinal foci, because there is a periosteal reaction along to the anterior ends of both the sixth and seventh right ribs. This child also had two tuberculous foci in the vault of the skull (B) and destruction of the condyle of the mandible (C).

Fig. 5.91 A, B. A young African from Zimbabwe being treated for pulmonary tuberculosis was found to have a swelling around the jaw. There were no local symptoms. There is destruction of the left side of the mandible with multiple granulomas and very little new bone periosteal reaction.

Fig. 5.92 A-C. This young African child had an overwhelming tuberculous infection and presented (A) with multiple cutaneous lesions covering the whole body. The only bone focus was in the upper end of the left humerus (B), seen on the chest radiograph. There was a large cavity almost replacing the right upper lobe, pneumonia, and multiple tuberculous foci throughout both lungs. Young children with lowered immunity may suffer from hematogenous miliary spread and present with papules, erythematous macules, or purpuric lesions over most of the body. The tuberculin skin test is usually negative and the prognosis is often poor, but this child improved after 2 months of treatment (C). The skin lesions are regressing, and there is a thick periosteal reaction around the upper end of the humerus, seen through the shadow of the shoulder.

Fig. 5.93 A-C. This African patient came to hospital with a complaint of frequency of micturition. An intravenous urogram showed that he had a tuberculous infection of the spine (A) with almost complete destruction of the 12th thoracic vertebra. There was a large left paravertebral abscess, and destruction and subluxation of the 12th left rib. A large lytic defect was present in the right 10th rib. The patient was started on antituberculous therapy but later complained of a pain in his foot where there was a similar destructive lesion in the third metatarsal (B). The urogram had also shown tuberculous swelling of the left side of the bladder (C) and another incidental finding was almost complete destruction of the right lower pubic ramus. Despite all these lesions, the patient's main complaint was still urinary!

Fig. 5.94 A-D. When the infection is tuberculosis, patients may only complain of part of the infection. This teenage African came to hospital with swollen right orbit (A, B) and was found to have a destructive bone infection of the right orbital margin. Standard tomography (B) showed not only the sclerotic thickening, but a sequestrum within a lytic area above the eye. His chest radiograph (C) showed a primary tuberculous infection, with lymphadenopathy and the lateral radiograph (D) showed that he also had a tuberculous sternum.

Fig. 5.95 A-D. Tuberculosis may affect any part of the skull. A, B Two different views of a lytic area in the frontal bone. C Multiple lytic areas across the skull vault. D Similar foci with surrounding bone reaction suggesting healing or a more chronic infection.

Fig. 5.96 A-H. Plain radiography of the skull may show calcification in tuberculomas or basal meninges. A normal skull radiograph does not, of course, exclude tuberculosis. A Multiple calcified tuberculomas with calcification of the meninges, probably also tuberculous. B Multiple calcified tuberculomas in a child. C Calcification of the basal meninges. D Curvilinear calcification in a tuberculoma in the left occipital region. E, F A calcified tuberculoma which was a chance finding in a patient who suffered a head injury. The depressed fracture had to be elevated and the tuberculoma was removed to confirm the histology. G, H Angiography is not usually helpful in making the diagnosis. However, it may indicate the size of the mass, if scanning is not available. A lateral radiograph (G) shows suture diastasis and a calcified mass. Arteriography (H) shows that this is a avascular and indicates that the size of the tuberculoma is much larger than the calcification would suggest. (G, H courtesy of Dr. L. Handler, Cape Town). None of these radiographs would pernut an accurate diagnosis of tuberculoma.

Tuberculosis of the Central Nervous System

CT and MRI have changed our knowledge of the incidence and significance of tuberculosis of the central nervous system (CNS). It was not possible previously to image satisfactorily the different lesions caused by tuberculosis: plain radiography seldom gives much information or allows an accurate diagnosis (Fig. 5.96), and many foci that cannot be demonstrated with plain radiography are recognized on CT or MRI.

Tuberculomas of the brain probably have a variable geographic distribution, seemingly being more common in India and southern Africa. But this may also reflect the availability of imaging facilities and, particularly with the AIDS epidemic, CNS tuberculosis is likely to become more common. Tuberculosis involves the CNS by hematogenous spread, except in a few cases which result from rupture of cranial osteitis, e.g., from the mastoid or frontal bones. The tubercle bacilli may be seeded anywhere but are most common superficially over cerebral and cerebellar hemispheres and the ventricular system.

Tuberculosis of the central nervous system affects the meninges (which is probably the most important, because it carries a poor prognosis but if treated early may respond) and causes granulomatous masses (tuberculomas) which vary considerably in size and significance. Tuberculous abscesses are probably the result of central necrosis in a tuberculoma. Most tuberculomas respond to treatment, some may resolve spontaneously and the minority calcify. Plain radiography seldom gives much information or allows an accurate diagnosis. CT and MRI are the important imaging methods.

As tuberculosis develops and caseates, involving the meninges, the infection can spread to the subarachnoid space. The most extensive reaction is at the base of the brain, where a thick exudate develops and surrounds the cranial nerves, compressing blood vessels and blocking the foramina of the fourth ventricle. The general inflammatory response also causes raised intracranial pressure.
Two main patterns of CNS tuberculosis develop:

1. Tuberculous meningitis

2. Parenchymal or meningeal mass lesions, tuberculoma

In some patients both varieties develop together, becoming a very complex infection.

Tuberculous meningitis

Tuberculous meningitis as a presenting illness is most common in children and carries a significant mortality and complication rate if not treated early. It is often associated with progressive primary tuberculosis and will also be seen in immunosuppressed patients. Cranial nerve damage may occur and ischemic infarction can occur in any part of the brain: these are the two most common causes of long-term complications. The incidence of infarction is high, perhaps 40%-60%. As the blood vessels become involved with the proliferative arachnoiditis, spasm and occlusion may result in infarction.
Plain radiography has little part to play in the imaging of tuberculous meningitis. Small infants may have suture diastasis as intracranial pressure rises, but this is a nonspecific finding. In babies and if the diastasis is sufficient, ultrasonography can be used to demonstrate the basal meningeal changes and the ventricular dilatation. Most children are too old for ultrasonography to be really useful.

Where available, CT and MRI are the most important imaging modalities (Figs. 5.97, 5.98). Following infarction, CT will show ill-defined hypodense areas, which may enhance with contrast. MRI is more accurate and a contrast enhanced T 2-weighted scan can demonstrate a mass effect and hyperintense areas. These may progress to show cavitation. On T 1-weighted scans these areas are well defined and hypointense.

Hydrocephalus develops in most cases of tuberculous meningitis unless treatment is started very promptly (Fig. 5.99). The obstruction is usually in the basal cisterns or the aqueduct. Immediate surgical shunting may be necessary. The end results, even with treatment, may be fibrosis and continued basal obstruction. Healing may be recognized by lack of contrast enhancement on CT but the end stage is difficult to judge. A small number of cases will resolve completely.

Cerebral arteriography during the active phase of meningitis may show vascular irregularity of the larger vessels basally, probably due to arteritis because of the surrounding inflammation. Sometimes complete obstruction of the vessel can be demonstrated. These findings correlate well with the CT images and it is doubtful whether arteriography is indicated during tuberculous meningitis. Occasionally tuberculous meningitis may form plaques or clusters of thickening around major cerebral vessels, demonstrated by CT. These have not been reported commonly from tropical patients, but this may represent infrequency of scanning rather than absence of the pathology.

It is important to note that the incidence of intracranial tuberculomas complicating tuberculous meningitis is 4%-28%: at least one such case has developed during adequate antituberculous treatment. The presence of an intracranial tuberculoma may be indicated by clinical deterioration and may be thought to be due to a resistant organism. When a clinical change occurs, MRI or CT scanning is indicated.

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Fig. 5.97. A-E. Three important findings on CT scanning of tuberculous meningitis: A basal leptomeningeal enhancement (small arrows); B, C infarction in the basal ganglia (curved arrow) and hydrocephalus. D, E MRI with gadolinium enhancement in another child showing basal leptomeningeal enhancement, as well as a cavitated infarct deep in the left gray matter (arrow) and hydrocephalus. (From Cremin and Jamieson 1995).

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Fig. 5.98 A-D. A 9-year-old girl from the Pacific Islands with tuberculous meningitis. A Contrast-enhanced CT scan shows edema in the right temporal lobe and inflammatory reaction in the basal cisterns and sylvian fissures, with has enhanced. B, C T 1-weighted MR images with contrast show similar enhancement of the basilar cisterns and the sylvian fissures, encasing the middle cerebral arteries. D Another child; a right carotid angiogram shows nearly complete occlusion of the artery as it traverses the meninges. An alternative collateral supply has been derived from the middle meningeal artery (long arrows), the ophthalmic artery (short arrows), and the posterior system (curved arrows). (A-C courtesy of Dr. Cheryl Sisler, Hawaii; D from Cremin and Jamieson 1995).

Tuberculomas

Any granuloma may develop into a tuberculoma, forming a mass anywhere on or within the meninges. A tuberculoma can be single and nodular, or there may be more than one (Fig. 5.100). Provided they are treated, almost all will resolve without residual imaging abnormality; untreated many will continue to become calcified granulomas (Figs. 5.96, 5.100 A, B). A few, during development, may become tuberculous cerebral abscesses. These have thin walls and are smooth but can be multiloculated. They are indistinguishable from pyogenic abscesses except histologically. Many have surrounding edema which can be demonstrated by CT (hypodense) and T 2-weighted MRI (hyperintense) (Fig. 5.101).

The tuberculoma without central necrosis is hypodense on CT and hyperintense on T 1-weighted MR scans. T 2-weighted scans show hypointensity. On both CT and MRI there is contrast enhancement. If there is central necrosis, this does not enhance and there will be a ring mass (Fig. 5.101 C, D). The central necrosis of tuberculoma may have two origins. The granulation tissue may undergo necrosis or it may result from cellular components which can be caseous or quite liquefied, more like pus. Both types of necrosis may be present in the same abscess and will react differently on CT and MRI. When due to a granuloma, the necrotic area does not enhance, is hyperdense on CT, and is hypointense on T 2-weighted MRI. When liquid, it is hypodense on CT and hyperintense on T 2-weighted MRI (Fig. 5.102).

Some tuberculomas under treatment may resolve in 3 or 4 months, but others may take over a year. Of those which are treated, about 5% probably calcify; this is a surprisingly small figure, because CT and MRI scans undertaken for other reasons have shown granulomas in patients with no previous history or knowledge of a CNS tuberculous infection: natural resistance must result in calcification more often than occurs with therapy.

Cerebral arteriography can demonstrate the mass lesion of a tuberculoma, depending on its size and situation. They are almost all avascular, but a small minority have a ring blush.

The differential diagnosis for tuberculous meningitis in the early stages includes any progenic infection. Tuberculomas can be mistaken for an intracranial neoplasm, or almost any other disease process causing mass lesions in the brain (such as subacute trauma, hemorrhage, pyogenic abscesses, or hydatid disease).

Careful clinical history, the clinical examination, and a high index of suspicion are very important. Mycotic infections can give rise to identical clinical and imaging findings (see Chapter on Taeniasis, Cysticerosis).
Tuberculosis of the skull vault results in multifocal, lytic, and well-circumscribed fluctuant swellings (Fig. 5.95). The majority are symptom free, and they almost always occur under the age of 20 years. A few may discharge to the surface and then become secondarily infected. Internal extension is very common.

These are the "puffy tumours" described by Sir Percival Pott. The soft tissue swelling can be quite significant. They can be imaged with ultrasonography, CT, or MRI. It is important to distinguish them from histiocytosis or a low-grade pyogenic infection. These and other tuberculous lesions within the bones of the skull have been described and shown in (Fig. 5.84-5.95).

Fig. 5.99 A-F Ventricular dilatation is common with tuberculous meningitis, but is not always permanent. A A 14-month-old boy from the Pacific Islands with tuberculous meningitis and positive CSF culture for M. tuberculosis; a nonenhanced CT shows ventricular enlargement. B With contrast there is enhancement of the basilar cisterns and sylvian fissures. C A 23-month-old girl, also from the Pacific Islands, was treated successfully for tuberculous meningitis when she was 6 months old. The enhanced CT scan shows persistent ventricular enlargement, but there is no enhancement of the basal cisterns. D The lateral, third and fourth ventricles, also enlarged, showing that there is communicating hydrocephalus. E This is ,the admission CT scan of another child with active tuberculous meningitis, already on treatment. F A repeat scan of the same child 1 month later. Another scan after 3 months did not show any significant change. (E, F from Cremin and Jamieson 1995).

Fig. 5.100 A-F. Tuberculous granulomas. A The lateral radiograph of the skull of a 35-year-old man from the Pacific Islands who had tuberculous meningitis when he was 19 year old. There is a group of calcified granulomas (arrows) which are better seen on the nonenhanced CT (B: arrows). There are more than would be expected from the plain radiograph. C The contrast-enhanced CT scan of another child from South Africa showing that the granuloma has a hypodense center and surrounding edema (arrow). D T 2-weighted MR scan of the same patient shows that the caseous necrotic center is T 2 hyperintense, the rim of the granuloma is hypointense (arrow), and the edema is T 2 hyperintense. E Several granulomas (arrows) are shown on a contrast-enhanced CT of another patient. There is also basal enhancement and hydrocephalus. F A gadolinium-enhanced T 1-weighted MR scan of another patient shows a cluster of granulomas in the left occipital lobe. (A, B courtesy of Dr. Cheryl Sisler, Hawaii; C-F from Cremin and Jamieson 1995).

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Fig. 5.101 A-D. Some tuberculomas have been described as "gummatous" and become quite large. A T 2-weighted MR scan of a large tuberculoma. There is hyperintense edema surrounding a predominantly hypointense granuloma. B On a T 1-weighted MR scan, the tuberculoma is isointense. C, D Gadolinium enhanced MR scans of another patient show that the central necrosis is hypointense but there is strong rim enhancement. Both tuberculomas imaged in the same way. (From Cremin and Jamieson 1995).

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Fig. 5.102 A-C. Tuberculous abscesses do not image in the same way as tuberculomas. A A contrast-enhanced CT scan shows rim enhancement with a hypodense center. There is also a group of enhancing granulomas posterior to the abscess. B A T 2-weighted MR scan without enhancement shows that the abscess has a hypointense rim and a hyperintense center. C A T 1-weighted MR scan of the same patient, with gadolinium enhancement, shows that the center of the ab scess is hypointense and the wall of the abscess enhances.(From Cremin and Jamieson).

 

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