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1.T1 and T2 weighted spin echo sequences in the sagittal plane.
2.These images represent relatively normal findings for the lumbar spine. There are however, two round cystic lesions observed posterior to S2 within the sacral canal. These lesions demonstrate low signal intensity on T1 and high signal intensity on T2 weighted sequences, isointense to CSF. As axial views are not provided, the relationship to adjacent nerve roots cannot be detailed.
3.Possibly, but unlikely. Tarlov’s cysts are usually asymptomatic, but can cause sensori-motor changes where nerve root compression occurs.
Tarlov’s cysts
Also known as peri-neurial cysts and arachnoid cysts, these lesions represent extradural meningeal cysts with spinal nerve root fibers either within the cyst wall or cyst cavity itself. They may or may not communicate with the subarachnoid space. Approximately one fifth of Tarlov cysts are symptomatic and can produce, a variety of symptoms of nerve root compression . Sacral cysts have been noted to cause sacral radiculopathy, hip, leg, or foot pain, perineal pain, paresthesias, and bowel or bladder dysfunction. Symptoms can be exacerbated by standing, coughing, or other Valsalva maneuvers, because elevated subarachnoid pressure forces CSF from the spinal subarachnoid space through a small ball valve like communication into the perineurial cyst cavity. Tarlov cysts may also cause diffuse poorly localized sacral pain due to pressure on adjacent periosteum and joint capsules and can also result in sacral insufficiency fractures from erosion of the sacrum. The natural history of symptomatic Tarlov cysts is one of progressive enlargement leading to increasing symptoms. The hydrostatic and pulsatile forces of CSF cause Tarlov cysts to grow over time. As the mass enlarges, sensory nerve root filaments are stretched over the periphery of the lesion or are compressed against adjacent bone or other nerve roots, causing pain or other sensory disturbances. Surgical and non-surgical treatment options are available, however risks are associated with all procedures and careful consideration for the degree of disability suffered by the patient should be given.
Where significant bowel or bladder changes are present, surgical resection may be warranted
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1. What are your imaging findings?
A 9.3cm long serpiginous opacity is noted, centrally located in the medullary aspect of the distal femoral shaft. The surrounding trabecular and cortical bone is normal. No effusion or other soft tissue abnormality is identified. Small osteophytes are observed at the medial proximal tibia and distal femur, as well as the superior and inferior articulating surface of the patella. A slight genu varus deformity is present.
2. What is the most likely diagnosis?
This is a classic appearance of a bone infarct. Very mild degenerative joint disease is also present at the medial tibio-femoral compartment and patello-femoral joint.
3. Does this appearance explain the patients’ symptoms?
No, this is an incidental finding on the radiographs, and should be differentiated from other symptom-producing pathologies. In the case of this patient, physical examination revealed local point tenderness over the pes anserine entheses probably due to excessive repetitive loading resultant from medial tibio-femoral compartment laxity, evidenced by greater translation in a valgus stress test at 30o. The diagnosis of pes anserine tendinosis was concluded which responded well to a short course of soft tissue work and ultrasound therapy. Long term rehabilitation of lower limb kinematics was prescribed.
Bone Infarct
Bone infarct, ischaemic necrosis, avascular necrosis and aseptic necrosis all represent terms used to describe the various forms of osteonecrosis. However, the term bone infarct is typically reserved for those cases presenting in a metaphyseal or diaphyseal location, within the medullary cavity of a long bone. Osteonecrosis occurs when there is insufficient or absent blood supply to an area of tissue leading to a state of hypoxia/ischaemia, which, if sustained will result in death to the affected cells.
Aetiology
Interruption of vascular supply to an area of tissue may occur in one or more of three ways:
- Compression – from other structure, or due to an increase in marrow pressure as a result of an increase in the size or number of cells in the region;
- Trauma – severing of blood supply; and/or
- Occlusion – intraluminal, as a result of embolus (fat/air/blood) or atherosclerosis.
Typically, bone infarcts are clinically silent lesions, appearing incidentally on radiographic examinations taken for other reasons; however, they may present as acutely symptomatic lesions owing to an increased intra-osseous pressure, leading to a “bone compartment syndrome” and, as such, the determination of any predisposing conditions is important. Accurate diagnosis is usually established by conventional radiography, the infarct appearing as an irregular or serpiginous, clearly delineated, intramedullary increased density located in the metadiaphyseal region of a long bone. However, magnetic resonance (MR) imaging is the most sensitive in identifying early changes associated with osteonecrosis, including bone infarct and avascular necrosis.
Differential diagnoses for bone infarct on conventional radiographs include:
- Enchondroma. In conventional radiography of a long bone, an enchondroma typically appears as a geographic area of radiolucency, centrally located within the metaphyseal region. Stippled calcification occurs in 50% of cases and may be the most prominent radiographic feature.
- Chondrosarcoma. With a variable radiographic presentation, a low grade central chondrosarcoma may present as an ill-defined area of irregularly scattered calcification, usually occurring in a metaphyseal or diaphyseal location in a long bone. In addition, regions of radiolucency may be noted as well as evidence of endosteal scalloping as progressive destruction and replacement of the bone occurs.
- Calcar. In the region of the proximal femur, a region of radio-opacity may be encountered owing to the additional trabecular bars connecting the medullary cavity and the cortex. This is a normal variant, although may be very hard to distinguish from an enchondroma. However, on a frog-leg view, the calcar is noted to appear as multiple radio-opaque thin linear densities as distinct from an enchondroma, which will tend to appear on all views as stippled calcifications.
Natural History
Bone infarcts usually remain stable, although a spontaneous decrease in size may occur. Complications can occasionally arise, the most severe of which is malignant transformation. Malignant fibrous histiocytoma represents the most common tumour associated with this rare complication. Clinicians must remain aware to the malignant potential and consider this in cases of newly presenting unexplained pain in the region of previously established bone infarction.
Treatment
There is no specific treatment for bone infarcts. In the case of sickle cell crisis, hypotonic fluids, fresh frozen plasma, and partial exchange, transfusions may be indicated. Clinicians should continue to centre their management approach at the primary pain generator and predisposing conditions, but remain astute to the possibility of developing bone pain from malignant change within the bone infarct.
Source: Timchur, et al. A 74 year old woman with knee pain. Clin Chiro 2007 Dec; 10(4) 177-8, 222-6.
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