Principles of Assessment and Evaluation

Principles of Assessment and Evaluation (46)

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Imaging Techniques Relative to Rehabilitation

Imaging Techniques Relative to Rehabilitation (39)

 A brief presentation of imaging techniques of interest to the physiatrist must necessarily be selective. Because the diagnosis and initial treatment of fractures are primarily the responsibility of the orthopedic surgeon, with the rehabilitation professional typically involved only later in the course, a full discussion of fractures is not presented in this chapter. Only those fractures that bring patients under the long-term care of the physiatrist are included (e.g., vertebral fractures with the potential to damage the spinal cord). Similarly, tumors and infectious processes are de-emphasized. Rather, emphasis is placed on imaging degenerative musculoskeletal processes, spine and head trauma, stroke, and degenerative central nervous system (CNS) diseases commonly seen by the physiatrist. We will also cover imaging in sport medicine as this is a rapidly changing area in radiology and review the current applications of diagnostic ultrasound in the evaluation of musculoskeletal disorders.

In the past two decades, computed tomography (CT) and magnetic resonance imaging (MRI) have become the most sophisticated imaging modalities for evaluating the musculoskeletal system and the CNS. Therefore, this chapter focuses mainly on the recent applications of CT and MRI in the imaging of musculoskeletal and neural pathology of interest to the physiatrist. In the final section, we will introduce some relatively new imaging technologies of interest to the physiatrist, including advanced MRI methods and ultrasound imaging (USI).

The role of plain film examinations in the assessment of abnormalities of specific joint disorders is well established in the medical literature. A brief review of the most commonly performed radiographic examinations of the extremities will be done when addressing the specific subject. 

 

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The Physical Examination

The Physical Examination (4)

The hallmark of medicine has always been the physical examination. Perhaps more than the actual diagnosis, the process by which the physician arrives at his or her conclusion has defined the "art" of medicine. Much has been written about the techniques by which this art is performed, and much more will continue to be written. Each generation will take from the past and apply these techniques to the future of medicine.

The physical examination is an extension of the history and extends the doctor-patient relationship initially established during the history. The skill with which the examination is performed instills a sense of confidence in the patient that the examiner knows what he or she is doing. This confidence in the physician has a positive outcome on the patient's ability to recover. Finally, the physical examination serves to narrow the list of diagnostic possibilities.

In a specialty like physiatry, in which the whole person is evaluated in terms of function, there is no adjunct more important than the physical examination. The examination provides the foundation to formulate a plan to improve a person's function. Importantly, though, in looking at function, each piece must be applied to the whole person. The examination of one joint must be applied to the whole picture of the patient, and an understanding of functional biomechanics will enable the physician to include in the physical examination other structures that may indirectly contribute to the impairment.

The focus on function and application to the whole person in physiatry can be best seen in understanding the concept of the kinetic chain. No one joint, bone, or muscle acts alone in the body. An ankle sprain can lead to low-back pain. Lowback pain can affect the serve of a tennis professional. Lateral epicondylitis can alter shoulder mechanics and lead to rotator cuff impingement. It is because of these relationships that the physiatrist must perform a thorough examination. It is this comprehensive manner that sets apart the physiatric approach from others. A thorough knowledge of the neuromuscular system and an understanding of functional biomechanics will narrow the focus of the examination so it can be done in a time-efficient manner. The relationship between the different joints and regions must be understood. In addition, a complete understanding of the muscles and their innervation is required.

An understanding of the muscle kinesiology and biomechanics is very important in the physical examination. Each muscle functions across one or more joints to provide motion or stabilization. One example would be the hamstrings. When the foot is planted, the hamstrings act in their primary function as powerful hip extensors. However, with the foot off the ground, they can become knee flexors. With a patient prone and the knee bent at 90 degrees, the gluteus maximus acts as the primary extensor because of the shortened hamstrings. Place the knee in full extension, and the hamstrings will once again act as hip extensors. We will look further into these types of relationships in the physical examination.

In today's medicine, there exists a tremendous amount of information to digest. The number of articles indexed in MEDLINE has grown in size from 1,098,000 citations in 1970 to 11,761,000 in 2000. The modern physician must have an understanding of the body down to a microcellular level. In addition, access to modern tests like magnetic resonance imaging (MRI) is achieved by a greater number of patients. Any test has its limitations, and in the example of the MRI, these can be multiple false-positive findings (1). The MRI should be used to confirm not make a diagnosis. Many physician referrals are generated from a radiologist's interpretation of a study, often without physical examination findings consistent with the results of the study. It is at this point that the well-trained physiatrist can be the link using evidence-based medicine as it applies to diagnosis, history, and physical examination.

Whole texts are dedicated to the physical exam. Due to the limits of one chapter, this will be an introduction to the physical examination and kinesiology of the cervical spine, shoulder, lumbar spine, and knee. That said, the reader should be able to approach any joint in the manner laid out here to aid in his or her diagnosis. Examination of any joint should be performed in a systematic approach. As the examination begins, the clinician should make sure that the area to be examined is properly exposed for evaluation and the patient appropriately draped. We have focused on the major joints seen in our practice—the cervical and lumbar regions of the spine, the shoulder, and the knee. Other joints will be addressed in chapters in this text. We will now address the physical examination, and the kinesiology of the muscles and joints will be explained. For reference, the dermatomes, myotomes, and sclerotomes are illustrated in Chapter 21.

It is the task of the physiatrist to perform a thorough physical examination to confirm his or her diagnosis derived from the history and additional information. It even is more important today, because of the additional tests modern technology has advanced, to understand physical examination maneuvers and their diagnostic relevance.

Joseph H. Feinberg and Peter J. Moley

Source: Physical Medicine and Rehabilitation - Principles and Practice
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The cruciate ligaments are best visualized by sagittal or oblique sagittal MR images that display the full length of the ligaments (Fig. 6-24A). On straight sagittal images, the slender nature of the anterior cruciate ligament and its oblique course cause a volume-averaging effect that averages fat signal intensity about the ligaments with the normal low signal intensity of the ligament so that the anterior cruciate ligament frequently does not appear as a complete signal void. Furthermore, straight sagittal images typically fail to demonstrate the anterior cruciate ligament’s femoral attachment because of its oblique orientation in both sagittal and coronal planes. Oblique sagittal images that parallel the ligament show the full thickness and length of the anterior cruciate ligament without subjecting it to partial volume averaging (44). In the extended position of the knee, which is typically used for MR images, the anterior cruciate ligament is normally taut. The posterior cruciate ligament is a thicker ligament and is therefore well visualized on straight sagittal MR images (Fig. 6-24B). It can be visualized as a signal void structure from its attachment to the posterior tibial intercondylar area to its attachment on the medial femoral condyle. With the knee extended, the posterior cruciate ligament is visualized as thick and posteriorly bowed. It straightens with knee flexion. Axial images can be very helpful to evaluate the femoral insertion of the anterior and the posterior cruciate ligaments.

FIGURE 6-24. Normal cruciate ligaments. A: An oblique sagittal MRI parallel to the anterior cruciate ligament demonstrates excellent visualization of all borders and attachments of the anterior cruciate ligament (arrow ). B: A T2-weighted MRI of the posterior cruciate ligament (arrow ), which is normally posteriorly bowed when the knee is extended.

The MRI appearance of an anterior cruciate ligament injury depends on the site and degree of disruption, as well as on the age of the tear. A complete tear may be visualized as a discontinuity of the ligament (Fig. 6-25A–D). In the acute complete tear, the interval between the torn ends of the ligament is often occupied by a mass of intermediate signal intensity on T1-weighted images that appears hyperintense on T2-weighted images (45). At other times, the torn ligament may present as a fusiform or irregular soft-tissue mass of intermediate signal intensity on T1-weighted images that appears hyperintense on T2-weighted images. These fluid masses are usually a combination of edema and hemorrhage, and there may be an associated joint effusion. If the ligament tears from its femoral attachment, the axial images will show fluid signal between the lateral femoral condyle and the expected ligament insertion. In partial tears there is no complete discontinuity, but the ligament that appears intact on a T1-weighted image may show a hyperintense signal on T2-weighted images, or the ligament may display an interrupted or concave anterior or posterior margin when the knee is extended (42). In chronic anterior cruciate ligament deficiency, there may be a complete absence of the ligament, or there may be only remnants remaining in its usual location. Some secondary signs of anterior cruciate ligament injury may be present. These include a forward shift of the tibia and an anterior bowing or buckling of the posterior cruciate ligament caused by the position of the knee within the coil, which duplicates the knee position of an anterior drawer or Lachman test (39).

FIGURE 6-25. Acute ACL injury; spectrum of findings. A: Sagittal PD and B: Sagittal PD fat suppressed sequences. The arrow demonstrates the torn ACL resting against the tibial spine. There is diffuse marrow edema with increased signal intensity on the T2-weighted sequence. C: Axial T2-weighted fat suppressed sequence. The long arrow is pointing to the ACL fibers. There is edema anterior to the ACL (short arrow) within the intercondylar fossa. The arrowheads demarcate an area of marrow edema within the lateral femoral condyle. D: There is bone marrow edema within the posterior tibial plateau (long arrow) and the anterior femoral condyle (short arrow), tipical contusion pattern in ACL injuries. There is a small radial tear to the free inner margin of the lateral meniscus (arrowhead) secondary to the compression injury.

On T1-weighted MR images, partial tears of the posterior cruciate ligament typically appear as foci of increased signal intensity within the normal black signal void of the ligament. These appear hyperintense on T2-weighted images. With complete tears, a frank discontinuity is visualized with an intervening fluid mass that becomes hyperintense on T2-weighted images (Fig. 6-26). The gap between the ends of a completely torn posterior cruciate ligament can be exaggerated by imaging the knee in flexion, which tenses the posterior cruciate ligament.

FIGURE 6-26. Sagittal T1-weighted image of a chronic PCL tear. The arrow points to the thickened posterior cruciate ligament. Intermediate signal intensity is replacing the normal hypointensity of the ligament.

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Source: Physical Medicine and Rehabilitation - Principles and Practice

Subarachnoid and intraventricular hemorrhage can be spontaneous, as in the case of a bleeding aneurysm or arteriovenous malformation, or secondary to trauma. CT is the imaging modality of choice for evaluating these types of hemorrhages because it detects the hemorrhage from its onset as a hyperdensity. However, subarachnoid hemorrhage is not as radiodense as epidural or subdural hemorrhage because the blood will be diluted by CSF. Unless blood replaces at least 70% of the CSF, the subarachnoid hemorrhage remains isodense to adjacent gray matter (82). When the volume of blood is sufficient to make the hemorrhage hyperdense, it accumulates in the extensions and expansions of the subarachnoid space. Subarachnoid hemorrhage appears as linear radiodensities within the sulci or fissures or as larger aggregations in the basal cisterns (Fig. 6-86). MRI will not visualize a very early hemorrhage when oxyhemoglobin, a nonparamagnetic substance, is the primary constituent, and thus CT is the study of choice in the very early stages. Subarachnoid and intraventricular hemorrhage can cause communicating hydrocephalus by virtue of red blood cells blocking the arachnoid granulations, the CSF resorption sites.

FIGURE 6-86. Subarachnoid hemorrhage secondary to a right middle cerebral artery aneurysm. CT shows this condition as hemorrhagic radiodensities within sulci and cisterns (arrow ).

Aneurysms and arteriovenous malformations can be detected directly by contrast-enhanced CT and MRI, or by their flow void characteristics on non–contrast-enhanced MR images (Fig. 6-87A,B).

FIGURE 6-87. A: CT of an anterior cerebral artery aneurysm (arrow ) that produced a subarachnoid hemorrhage with secondary hydrocephalus. B: Axial collapse image of a time of flight (TOF) MR angiogram in a different patient. The arrow points to a large aneurysm arising from the left anterior communicating artery.

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Disc herniation is typically preceded by degenerative changes in the mucopolysaccharides of the nucleus pulposus, which produce fibrillation of the collagen (60). This eventually causes dehydration and loss of disc volume. As a result, the nucleus pulposus no longer serves as a normal load-dispersing mechanism, and excessive stress is borne by the annulus fibrosus. This produces annular fissuring and tears that can culminate in herniation of the nucleus pulposus. The loss of the load-diffusing function of the normal disc also causes facet joint degeneration and marginal osteophytosis of the vertebral body ends by virtue of the increased loads these joints must bear.

Cervical disc herniation occurs with less frequency than lumbar disc herniation. About 90% of cervical disc herniations occur, in order of decreasing frequency, at C5-6, C6-7, and C4-5 (61,62). On CT examination, a herniated cervical disc appears as a dense soft-tissue mass protruding from the disc space centrally or paracentrally into the spinal canal or posterolaterally into the neural foramen (Fig. 6-51).

FIGURE 6-51. CT evaluation of a herniated C5-6 nucleus pulposus. An axial CT myelogram shows a radiodense protrusion of the C5-6 disc (arrow ) that distorts the left anterior aspect of both the thecal sac and the spinal cord.

On T1-weighted MR images, the herniated cervical disc appears as a posterior extension of the moderate signal intensity of the disc into the low–signal-intensity region of the thecal sac (Fig. 6-52A,B). Because the spinal cord appears as a relatively high–signal-intensity structure outlined by the low–signal-intensity CSF, the relationship of the herniated disc to the spinal cord can be visualized directly by MRI. On T2-weighted MR images, the degenerated disc appears as a narrowed disc interval. The disc herniation appears as a moderate– to low– signal-intensity impingement on the now high–signal-intensity CSF. The posterior margin of the herniated disc may have a to determine its probability of causing a patient’s myelopathic very-low-signal-intensity margin interfacing with the CSF. This findings (Fig. 6-53A,B). It is sometimes difficult to differentiate may be a posterior longitudinal ligament elevated by the herni-lateral herniations of the disc into the neural foramen from osteoated disc, or it may be fragments of the posterior part of the phytic encroachments by MRI because they may both demon- annulus fibrosus (61). T2-weighted images also permit evalua-strate low signal intensity. In these circumstances, CT provides tion of the relationship of the herniated disc to the spinal cord good differentiation between bone and soft-tissue density.

FIGURE 6-52. A: T2*-weighted axial MRI of the cervical spine shows a left posterolateral herniated C6-7 nucleus pulposus (between arrow) indenting the thecal sac (arrowhead ) and extending into the ostium of the ipsilateral nerve root foramina. B: A T2-weighted left parasagittal MRI shows the disc fragment (arrow ) impinging upon the intermediate–signal-intensity thecal sac (arrowheads) and low–signal-intensity posterior longitudinal ligament.

FIGURE 6-53. A: Axial T2-weighted image at the C4-5 level demonstrates a bilobed protrusion contained in the midline by the posterior longitudinal ligament. Note complete obliteration of the normal CSF signal anterior to the cord, posterior displacement, and compression of the cord. B: The herniated disc elevates the posterior longitudinal ligament, compresses the cervical cord, which demonstrates increased signal intensity as a sign of myelopathy.

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All parts of both menisci are well visualized by MRI. Sagittal MR images provide good views of the anterior and posterior horns and a fair view of the body of both menisci. In more central sections, both horns of the menisci appear as wedge- shaped signal voids contrasted on their superior and inferior surfaces by the moderate signal intensity of the hyaline cartilage on the articular surfaces of the femur and tibia. In more peripheral sections, where the images are tangential to the circumference of the menisci, they appear bow tie shaped (Fig. 6-22). Coronal MR images provide the best visualization of the bodies of both menisci.

FIGURE 6-22. Sagittal MR images through a normal peripheral menisci. The anterior and the posterior (arrow ) horns appear wedge (triangular) in shape.

There are three types of meniscal findings visualized by MRI (16,39,40). One is the presence of small globular or irregular high–signal-intensity foci confined to the interior of the meniscus. This is considered to be an early type of mucoid degeneration. A second type of meniscal MRI finding is the presence of a linear region of increased signal intensity within the meniscus that does not extend to either the femoral or tibial articular surface of the meniscus but may extend to the meniscocapsular junction. Histologically, this represents fragmentation and separation of the fibrocartilage and is considered by many to be an intrameniscal tear. The significance of the globular or linear signals that do not extend to either articular surface of the meniscus is not fully agreed on (41).

Frank meniscal tears are demonstrated by MRI as linear or irregular areas of signal intensity that extend to one or both articular surfaces of the meniscus (Fig. 6-23). The high signal intensity is produced by synovial fluid in the crevices within the meniscus. These meniscal tears can be horizontal, vertical, or complex. Bucket-handle tears are vertical tears where the inner meniscal fragment is displaced toward the intercondylar notch (Fig. 6-23C,D). At times, repeated trauma or chronic degeneration may cause a gross distortion of meniscal shape, and the meniscus may then appear to have a truncated apex or to be grossly small with a free fragment.

FIGURE 6-23. Meniscal tears. A: T1-weighted MRI of a horizontal tear (arrow ) at the posterior horn of the medial meniscus that extends to its tibial articular surface. B: Coronal PD-weighted image of a bucket-handle tear. There is a displaced fragment from the lateral meniscus into the intercondylar fossa (arrow ). C: Sagittal FSE-PD fat suppressed sequence of a double “PCL sign.” The displaced fragment from a bucket handle tear (arrow ) projects anterior to the PCL. D: Sagittal PD fat suppressed sequence through the lateral tibiofemoral joint demonstrates the double delta sign. The displaced anterior horn from a large flap injury is projecting anterior to the posterior horn.

Other meniscal abnormalities well visualized by MRI include discoid meniscus, meniscal cysts, and abnormalities involving the postoperative meniscus. In discoid meniscus, typically involving the lateral meniscus, there is a continuous bridge of meniscal tissue between the anterior and the posterior horns in the central part of the joint. Meniscal cysts are usually associated with underlying horizontal meniscal tears through which synovial fluid collects at the meniscocapsular junction (42). They show high signal intensity on T2-weighted images. MRI also can be used to evaluate the postmeniscectomy patient with continuing or recurrent symptomatology (39). It can detect an incompletely excised meniscal tear, retained meniscal fragments, or a tear developing within the residual part of the meniscus. MR arthrography with gadolinium can be helpful to distinguish between retears and old healed tears that might still show increased signal intensity on T2-weighted images (43). .

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A stroke is considered truly hemorrhagic if blood is found within the first 24 hours after initial symptoms. When blood is noted after this time, it is usually hemorrhagic transformation of an ischemic stroke, which is due to reperfusion injury.

Hypertension is the most common cause of intraparenchymal hemorrhage, which can also be caused by ruptured aneurysm, arteriovenous malformation, and more rarely, by infarction, neoplasms, blood coagulation defects, and cerebral arteritis (81). Common hemorrhage sites include the putamen and the thalamus, which receive their major blood supply from the lenticulostriate and the thalamogeniculate arteries, respectively.

Because freshly extravasated blood is more radiodense than gray or white matter, an acute hemorrhagic stroke is well visualized by CT as a hyperdense region usually conforming to an arterial distribution (Fig. 6-84A,B). The radiodensity of the blood clot increases over 3 days because of clot retraction, serum extrusion, and hemoglobin concentration. The extruded serum may form a hypodense rim around the hyper- dense clot (Fig. 6-84C). As edema develops over 3 to 5 days, the hypodense rim may increase. Eventually, the hyperdensity of the clot gradually fades and usually disappears by 2 months, leaving only a narrow hypodense slit to mark the site where hemorrhage took place (Fig. 6-84D).

FIGURE 6-84. CT evaluation of early and evolving hemorrhagic strokes. A: Recent hemorrhagic stroke has occurred in the distribution of the right posterior cerebral artery, which appears hyperdense (arrows). B: A massive hypertensive hemorrhage involving most of the interior of the left cerebral hemisphere with intraventricular hemorrhage, midline shift to the right, and herniation of the left hemisphere under the falx cerebri. C: A 5-day-old hemorrhagic stroke involving the lenticular nucleus shows a hyperdense hemorrhagic center (arrow ) and a hypodense edematous rim (arrowhead). D: The same stroke patient displays replacement of the hyperdense hemorrhage with a narrow hypodense interval (arrows) several months later.

The appearance of hemorrhage by MRI depends on the state of the hemoglobin in the hemorrhage (81). The oxyhemoglobin present in a fresh hemorrhage is nonparamagnetic; therefore, very early hemorrhage is not detected by MRI. Within a few hours, the oxyhemoglobin will be converted to deoxyhemoglobin, which is a paramagnetic substance. Intracellular deoxyhemoglobin will cause acute hemorrhage to appear very hypointense on T2-weighted images and slightly hypointense or isointense on T1-weighted images (Fig. 6-85A). By 3 to 7 days, intracellular deoxyhemoglobin is oxidized to methemoglobin as the clot enters the subacute phase. Although a subacute hemorrhage has several subphases in which the signal intensity of methemoglobin varies, in general methemoglobin appears hyperintense on both T1- and T2-weighted images (Fig. 6-85B). Because the conversion to methemoglobin begins at the periphery of the clot, early in the subacute phase a hemorrhage can have a hyperintense margin and a central hypointense region still containing deoxyhemoglobin. Eventually the entire region of subacute hemorrhage becomes hyperintense. Over several months, the methemoglobin is gradually resorbed and the clot develops a rim of hemosiderin- containing macrophages. Hemosiderin is hypointense on both T1- and T2-weighted images. Therefore, a chronic hemorrhage of several months duration often has a hyperintense methemoglobin center and a hypointense hemosiderin rim. Because the hemosiderin deposits remain indefinitely, an old hemorrhage of several years duration shows up as a totally hypointense area. Gradient-echo sequences have recently been added to many brain MRI protocols, as they are very sensitive in the detection of degrading blood products, which appear as areas of hypointensity. As can be seen, CT provides the very earliest information about cerebral hemorrhage, whereas MRI is the better technique for determining hemorrhage age.

FIGURE 6-85. MRI evaluation of hemorrhagic stroke. A: An acute hemorrhagic stroke involving the occipital lobe appears hypointense (arrow ). B: In the subacute phase, the same area appears hyperintense (arrow ).

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brain imagingSource: Physical Medicine and Rehabilitation - Principles and Practice

The intervertebral disc space is a cartilaginous joint with a central nucleus pulposus surrounded by an annulus fibrosus. Degenerative change in the nucleus pulposus is termed inter-vertebral osteochondrosis (Fig. 6-49A,B). Early signs of disc disease may include loss of fluid signal within the nucleus pulposus (dehydration), which results in decreased signal within the central portion of the disc on T2-weighted images, and blurring of the transition between the nucleus pulposus and the annulus fibrosus. This is followed later by narrowing of the intervertebral disc, which sometimes results in vertebral body end-plate degenerative changes. These end-plate changes are referred to as Modic changes (58). Modic type I changes are characterized by signal of edema, that is decreased signal on T1-weighted images and increased signal on T2-weighted images. Type II changes (Fig. 6-50A,B) follow the signal characteristic of fat, with intermediate to increased signal on T1-weighted images and increased signal on T2-weighted images. This is the most common type of reactive end-plate changes appreciated on degenerative osteochondrosis. Type III changes represent osseous sclerosis, characterized by decreased signal on both the T1- and the T2-weighted images.

FIGURE 6-49. A: Sagittal T2WI of the lumbar spine demonstrating different stages of intervertebral osteochondrosis. Normal disk (ND) demonstrates increased signal to the nucleus pulposus and normal height. With early degeneration (ED), the nucleus pulposus loses signal in part related to the decreased water content of the intervertebral disc but preserves the intervertebral height. With advanced degeneration (AD), there is near complete loss to the normal signal of the intervertebral disk and early traction osteophyte formation (TO). Note herniated disk (DH) at the L5-S1 segment. B: Advanced degenerative osteochondrosis on a different patient. There is loss of the intervertebral disk height, Schmorl’s node formation (SN) representing end-plate herniation and moderate traction osteophyte formation (arrow).

FIGURE 6-50. Sagittal T1- (A) and T2- (B) weighted images with degenerative osteochondrosis of the cervical spine. There is decreased T2 signal to most intervertebral discs, decreased disc height throughout, annular bulge, and traction osteophytosis. Note increased signal to the inferior end plate of C5 both on the T1- and T2-weighted images (arrows) characteristic of Modic type II changes.

When the disc becomes degenerated, it may undergo tearing of the annulus fibrosus collagen bundles, which is often a precursor to herniation of the nucleus pulposus, particularly at the posterolateral aspect of the disc. Protrusion is herniation of the nucleus pulposus that is contained by the annulus. In the axial plane, it usually demonstrates a base broader than the height against the parent disc (59). Extrusion is defined as a herniation of the nucleus pulposus beyond the fibers of the

The loss of the load-diffusing function of the normal disc also causes facet joint osteoarthrosis and marginal osteophytosis of the vertebral body ends (spondylosis deformans) by virtue of the increased loads these joints must bear.

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Source: Physical Medicine and Rehabilitation - Principles and Practice

Another hip region imaging application of potential interest to physiatrists involves the use of technetium bone scanning to evaluate recently described “thigh splints” caused by exaggerated stride length by short female basic trainees in the unisex-oriented military (34). Seven cases of thigh pain in female recruits at one military base were imaged after administration of technetium-99, with the expectation of finding stress fractures. Instead, the scans showed longitudinal linear accentuation sites in the upper or middle femur that were consistent with periosteal elevation and corresponded with the sites of insertion of one or more of the adductor muscles (Fig. 6-21). The reason these findings occur only in female trainees is explained by a Saunders and colleagues’ classic description of pelvic rotation as the first of their six determinants of gait (35). Because the shorter female recruits had to march with taller males, their stride had to be lengthened to maintain straight lines of march, and exaggerating the normal pelvic rotation lengthens stride. The adductor muscles are important pelvic rotators, and their overuse apparently produced avulsion and elevation of the periosteum adjacent to their femoral insertions.

FIGURE 6-21. Thigh splint sites demonstrated by technetium-99 scintigraphy. The accentuation sites (arrowheads) correspond to the insertions of the adductor longus and magnus muscles.

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Femoroacetabular impingement is another cause of hip pain that may initially have a non–specific clinical presentation; however, a thorough physical evaluation should be able to identify this condition. Pain can be elicited on physical exam by passive movement of the thigh into full flexion, adduction, and internal rotation (34). Radiographs often help to identify anatomical variations such as dysplasia of the femoral neck (Fig. 6-19) or acetabular overcoverage. MR arthrography (Fig. 6-20) can be a helpful imaging study for evaluating the consequences of femoroacetabular impingement as well as thoroughly evaluating the abnormal anatomy. Intra-articular contrast helps to better delineate hyaline cartilage defects as well as labral tears. These findings, along with the clinical evaluation, help guide the appropriate treatment plan.

FIGURE 6-19. Lateral radiograph of the left hip. There is a bump along the superior margin of the left femoral head-neck junction that

Transient regional osteoporosis presents with a low– signal-makes for an aspherical configuration of the femoral head. This is intensity lesion on T1-weighted images that is similar to isch-characteristic of Cam-type femoroacetabular impingement. emic necrosis, but it typically involves both femoral head and neck and becomes hyperintense on T2-weighted images, suggesting the presence of edema. MRI demonstrates osteoarthritic subchondral sclerosis as low–signal-intensity zones in the subchondral marrow of both the femoral head and acetabulum. MRI also has been found to be very useful for identifying stress or occult fractures. These appear as low–signal-intensity areas containing an oblique or wavy line of still lower signal intensity, representing the actual fracture site. On T2-weighted images, these areas become hyperintense, suggesting that they are edema. MRI also can identify many types of soft-tissue abnormalities about the hip, including synovial cysts, periarticular bursitis, soft tissue masses and articular abnormalities such as synovial chondromatosis.

FIGURE 6-20. A: Coronal T1 MR arthrogram. There is an intermediate signal intensity subcortical cyst (herniation pit) related to pressure erosion from the incongruent joint (large arrow). A labral tear (short arrow) and remodeling to the superior acetabulum (arrowhead) are well appreciated. B: Coronal PD fat suppressed with intra-articular contrast. The subcortical cyst is hyperintense (large arrow). The labral tear is better delineated (short arrow).

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Cerebral ischemia can be produced by thrombosis of large extracranial or small intracerebral vessels, emboli originating from atherosclerotic plaques or thrombi within more proximal vessels or the heart. In addition, decreased perfusion of systemic origin, such as shock, decreased cardiac output, or respiratory failure can also cause cerebral ischemia with or without infarction,

Cerebral ischemia can be completely or partially reversible, or irreversible leading to neuronal cell death, commonly known as infarction. Once blood flow to the brain is decreased or interrupted for a sufficient period of time, usually in a well- defined vascular territory, the chemical pumps within the neuronal cell membranes cease to function adequately disturbing the normal electrolyte homeostasis. Extracellular water subsequently rushes into the affected neuronal cells. This cascade of events initially causes neurons to halt cellular function in an attempt to survive. This “stunned” cell population is potentially salvageable with prompt reperfusion. If adequate reperfusion does not occur in a timely fashion, irreversible neuronal cell deaths will occur. Edema related to infarction involves both gray and white matter and has certain CT and MRI findings.

Nonenhanced CT is the initial study of choice in patients with suspected stroke, as it is readily available, can be performed quickly, and is highly sensitive in the detection of cerebral hemorrhage. On nonenhanced CT, edema related to a cerebral infarction appears as a hypodense or low attenuation area, which means that it appears darker than expected. Early nonenhanced CT signs of ischemic cerebral infarction in the MCA territory are as follows:

(1) Obscuration of the lentiform nucleus, sometimes referred to as the disappearing basal ganglia sign, which can be seen as early as 2 hours after symptom onset (77) (Fig. 6-70).

FIGURE 6-70. Obscuration of the lentiform nucleus. Nonenhanced CT shows effacement of the left lentiform nucleus (arrowhead). Compare with normal lentiform nucleus on the right (arrowhead).

(2) Insular ribbon sign, which refers to hypoattenuation of the insular cortex (Fig. 6-71).

FIGURE 6-71. Insular ribbon sign. CT changes of slight hypodensity, loss of normal gray-white matter differentiation, and effacement of overlying cortical sulci in the region of the right insula (arrow ).

(3) Hyperdense MCA sign, which refers to a fresh thrombus within the artery and can be seen as soon as 90 minutes after the event (Fig. 6-72). It is important to note that this sign implicates occlusion and not necessarily infarction. Nevertheless, nonenhanced CT is usually negative during the first few hours after an ischemic infarct, and it is only later that areas of hypoattenuation can be identified with associated effacement of the adjacent cortical sulci (Fig. 6-73).

FIGURE 6-72. MCA hyperdense sign. Tubular hyperdensity at location of the left middle cerebral artery, compatible with intraluminal thrombus.

FIGURE 6-73. Postinjury edema has peaked and the infarcted area is shown as a distinct hypodensity conforming to the territory of the right middle cerebral artery.

Edema reaches its peak at 3 to 5 days, and by this time non–contrast-enhanced CT typically demonstrates a well- defined hypodense area that usually corresponds to the vascular territory of one of the cerebral arteries or its branches. With large infarctions, brain swelling can eventually lead to brain herniation or obstructive hydrocephalus, which can be life threatening (Fig. 6-74A,B). With subsequent degeneration and phagocytosis of the infarcted brain tissue, there is volume loss that causes an increase in size of the overlying cortical sulci and underlying ventricles (78). When the infarction is caused by a systemically induced general reduction in brain perfusion, the infarcted areas correspond to the border zones between the territories of the major cerebral arteries because perfusion is most tenuous here (Fig. 6-75). Emboli can at times be directly visualized by noncontrast CT as hyperdensities within arteries. It is important to note that hemorrhage can not only occur de novo related to a hemorrhagic infarct, but that it can also occur within an ischemic infarct, as a consequence of reperfusion injury due to blood-brain barrier breakdown. When the latter occurs, it appears as a hyperdense mass within the hypodense edema of the infarct (Fig. 6-76).

FIGURE 6-74. A: Axial CT scan examination with large left subdural hematoma (arrowheads) and early subfalcine herniation (long arrow). B: Coronal multiplanar reformatted image (MPR) demonstrates to a better advantage the mass effect and the subfalcine herniaton (long arrow). The subdural hematoma has a lentiform shape (short arrow).

FIGURE 6-75. Axial diffusion weighted images (DWI) of an acute watershed infarct at the left superior frontal lobe. Increase signal intensity (arrow) represents restricted diffusion.

FIGURE 6-76. There is a hyperdense region at the left basal ganglia and thalamus surrounded by hypodense rim of edema, compatible with hemorrhagic transformation of an ischemic stroke. Patient had suffered an ischemic stroke 12 days earlier.

Injection of intravenous (IV) contrast provides no brain enhancement in the first day or two after a stroke. Contrast enhancement must await sufficient damage to the blood-brain barrier. It reaches its peak at 1 to 2 weeks and usually ceases to occur after 2 or 3 months (79). The greatest vascular damage to intact vessels is at the periphery of the infarct. Therefore, contrast-enhanced CT frequently visualizes a contrast-enhanced ring about the infarcted area or in the immediately adjacent cortical gyri, a phenomenon known as luxury perfusion (Fig. 6-77A,B).

FIGURE 6-77. Axial CT images of the brain of patient with small focal areas of low attenuation representing lacunar infarcts within the right inferior basal ganglia (A) and within the caudate nucleus (B).

Conventional MRI is more sensitive and specific than CT for the detection of acute ischemic brain infarcts, within the first few hours after the onset of symptoms. On MRI, the edema of an early infarct is of low signal intensity on T1-weighted images with corresponding high signal intensity on FLAIR (fluid-attenuated inversion recovery) and T2-weighted images (Fig. 6-78A,B). In addition, there is loss of gray-white matter differentiation, sulcal effacement, and mass effect analogous to CT imaging findings. With the administration of IV gadolinium-diethylenetriamine pentaacetic acid (DTPA), a damaged blood-brain barrier can often be visualized as a hyperintense area on T1-weighted images. MRI is more sensitive than CT at detecting lacunar infarcts, which are small infarcts of less than 1.5 cm (78) typically located in the basal ganglia, periventricular areas, and at the brain stem (Fig. 6-79A,B). Lacunar infarcts are most commonly caused by hypertension or diabetes-induced arteriolar occlusive disease of the deeply penetrating arteries, such as the lenticulostriate branches of the middle cerebral arteries. MRI is also superior to CT in detecting ischemic infarcts of the posterior cranial fossa, because MR images are not degraded by osseous structures. Another powerful tool in the imaging stroke arsenal is diffusion-weighted MR imaging (DWI). The concept here is that water molecules normally move within tissues in a random fashion known as Brownian motion. As was discussed earlier, acute stroke produces an electrolyte imbalance, which causes water molecules to rush into the intracellular compartment, where free random motion is no longer possible and therefore falling into a state of restricted diffusion. DW images reflect restricted diffusion as a signal increase, which corresponds with a signal drop in its accompanying sequence, the apparent diffusion coefficient (ADC) map. The combination of increased signal in the DW images and decreased signal in the ADC map is compatible with an infarct in the appropriate clinical setting, as other entities such as viscous abscesses and dense masses such as lymphomas can have a similar restricted diffusion pattern (Fig. 6-80A,B). One of the key features of DWI of acute cerebral ischemia is that it becomes positive as soon as 30 minutes after the insult and can remain positive for 5 days or more (80).

FIGURE 6-78. Subacute ischemic infarct. A: Axial CT image demonstrates an area of decreased attenuation (arrow) within the head of the caudate nucleus. B: Axial proton density (PD) sequence. There is increased signal intensity (arrow) due to restricted diffusion characteristic of an infarct.

FIGURE 6-79. Lacunar infarcts. A: CT shows multiple bilateral lacunar infarcts as small hypodense areas (arrows). B: By MRI, these infarcts are shown as multiple hyperintense areas (arrows).

FIGURE 6-80. Ischemic infarct. Restricted diffusion is shown as increased signal intensity in the diffusion-weighted image (A) with corresponding signal drop in the ADC map (B) (large arrows).

Nonenhanced CT is highly sensitive in detecting intracranial bleeds, which, in the setting of an ischemic stroke, represents hemorrhagic transformation. In MR imaging, T2*-weighted gradient-echo sequences depict areas of hemorrhage as focal regions of low signal intensity, secondary to a phenomenon known as blooming (Fig. 6-81).

FIGURE 6-81. Axial gradient echo T2* image shows an irregular area of signal drop with surrounding high–signal-intensity edema at the left superior parietal lobe, compatible with a hemorrhagic stroke.

As was stated before, cerebral ischemia can be reversible. Tissue that is potentially salvageable with prompt recanalization is referred to as penumbra. The goal of modern stroke imaging is not merely to document an infarct and exclude hemorrhage, but rather to differentiate infarcted from salvageable tissue (penumbra) in an effort to guide thrombolytic therapy and save as much brain tissue as possible. CT and MR imaging techniques that are currently being used with this purpose in mind will be briefly discussed. CT perfusion is a technique in which a bolus of contrast is injected into the patient with simultaneous imaging of a slice of tissue, usually chosen at the level of the basal ganglia, because it represents the three major vascular territories: Anterior, middle, and posterior cerebral arteries. The three main parameters obtained and compared throughout the slice are cerebral blood volume (CBV), cerebral blood flow (CBF), and mean transit time (MTT). In general terms, a mismatch between these parameters usually represents tissue suffering reversible ischemia or penumbra. MR perfusion is a contrast-dependent technique also utilized to determine the amount, if any, of salvageable brain tissue. In general terms, when a perfusion defect matches a diffusion defect, irreversible infarction has occurred. On the other hand, a perfusion- diffusion mismatch represents an area of reversible ischemia or penumbra, where infarction can possibly be avoided with timely thrombolytic treatment.

CTA is a technique that uses IV contrast to image extracranial and intracranial blood vessels. Different methods are utilized to reconstruct the arterial system, in an attempt to identify the cause of the patient’s symptoms, usually an obstructing thrombus or embolus, which is seen as a cut-off in one or various vessels. CTA information is commonly used to guide intra-arterial or mechanical thrombolysis in stroke centers. Just as in CTA, MRA can also be performed following injection of IV contrast. Nevertheless, MRI has the added bonus of being able to perform angiograms without having to inject contrast material based on the MR properties of flowing blood; a useful proposition in patients with renal insufficiency. Contrast-enhanced MRA findings are analogous to CTA findings, nevertheless in non–contrast-enhanced (time-of-flight) MRAs, normal vessels are depicted as a flow void and intra- arterial thrombus is seen as an area of increased signal intensity (Fig. 6-82).

FIGURE 6-82. Right middle cerebral artery thrombosis by MRA. Arrow points to vessel cut off.

Cerebral venous thrombosis is caused by aseptic or septic etiologies, and can lead to infarction in a nonarterial distribution. This rare cause of infarction has characteristic imaging features. Whether the thrombosis involves a deep cerebral vein or a dural venous sinus, the thrombus can be detected on a noncontrast CT as a hyperdensity within the vein (81). The hyperdensity may have a hypodense center, implying a residual lumen. In a contrast-enhanced CT, a thrombus appears as a filling defect, with tortuous dilated collateral venous channels occasionally demonstrated around the thrombosed vein. By MRI, while the thrombus is still in the oxyhemoglobin stage, which is isodense to brain tissue, it can be suspected

by the absence of the normal flow void in that vessel. In the deoxyhemoglobin stage the thrombus is hypointense on T1, and in the later methemoglobin stage it becomes hyperintense on T1-weighted images. The venous thrombus typically does not proceed to the hemosiderin phase because it usually lyses spontaneously and flow is reestablished. Contrast and non– contrast-enhanced MR venography techniques can also be utilized to diagnose venous thrombosis (Fig. 6-83).

FIGURE 6-83. Deep venous thrombosis. Sagittal noncontrast T1-weighted image. Arrow points to a thrombus-filled hyperintense superior sagittal sinus. Arrowhead points to a thrombus filled hyper- intense straight sinus.

A stroke-like clinical presentation frequently encountered in the ER is a transient ischemic attack (TIA). A TIA is a functional neurologic disturbance usually lasting a few minutes, which clears completely within 24 hours. TIAs typically produce no CT or MRI findings, yet one third of these patients eventually will suffer a cerebral infarction, 20% of them within the first month after the episode. Some stroke centers perform an MRI to all patients who suffered a TIA, as occasionally acute infarcts are actually found.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice
 

CT and MRI provide complementary information about degenerative diseases of the spine. MRI is often the modality of choice in assessing degenerative changes within the spine due to its superior soft-tissue contrast. CT has superior spatial resolution and provides better conspicuity of osseous and calcified structures. The advent of MDCT technology allows for superb reconstruction in the sagittal and the coronal planes that allows for better depiction of pathologic processes and hardware evaluation in the post–operative spine (57). MRI permits noninvasive visualization of the spinal cord and subarachnoid space within the spinal canal and the nerve roots within the neural foramina. Discrimination of these structures by CT requires injection of intrathecal contrast agents. MRI has a superior ability to evaluate intramedullary abnormalities. It also offers direct multiplanar imaging capabilities.

Axial CT images of the normal cervical and lumbar spine (Figs. 6-44 and 6-45) provide good visualization of all osseous elements, including the facet joints. In the cervical spine, the uncovertebral joints (i.e., Luschka) are well depicted with coronal reformatted and sagittal oblique images. Sagittal oblique images through the lumbar spine provide excellent anatomical reconstruction of the pars interarticularis for the assessment of spondylolysis. Soft-tissue windows typically permit visualization of the moderate radiodensity of the soft- tissue structures, such as the intervertebral disc, ligamentum flavum, and thecal sac. Sagittal images provide assessment of anatomical alignment, intersegmental instability and allows for adequate evaluation of foraminal stenosis. The epidural fat contains the internal vertebral venous plexus, which can be enhanced by a circulating bolus of contrast material to improve visualization of soft-tissue encroachments into the spinal canal, such as herniated discs. Introduction of contrast material into the subarachnoid space (i.e., CT myelography) delimits the contained spinal cord and the nerve roots (Fig. 6-46).

FIGURE 6-44. MDCT of the normal cervical spine. A: Bone window CT of the cervical spine in the axial plane at the level of C5-6 displays normal facet joints (short arrow) and Luschka joints (long arrow). B: Coronal multiplanar reformatted images (MPR) through the level of the uncovertebral joints (arrow). C: Midplane sagittal reconstructed images of the cervical spine shows mild reverse of the normal lordosis that could be secondary to spasm or associated to positioning. Note adequate alignment and no intersegmental subluxations. D: Sagittal oblique MPR demonstrates the nerve root foramina, uncovertebral joints, and facet joints.

FIGURE 6-45. Normal lumbar spine CT. A: Axial soft-tissue window CT of L5 demonstrating thecal sac (T), L5 nerve root (NR) within the lateral recess, epidural fat (E), and ligamentum flavum (LF). B: Bone windows axial through the same level demonstrate the sclerotic margins of the facet joint and the right sacroiliac joint. C: Midplane sagittal reconstruction (MPR image). Normal homogeneous trabecular pattern. Note intervertebral space distance and anatomical alignment of the anterior and posterior surface to the vertebral bodies. D: The density of the nucleus pulposus (NP) and annulus fibrosus (AF) can be appreciated. Note decreased attenuation to the CSF in the thecal sac. E: Oblique reconstruction through the posterior elements demonstrating the normal facet joints and pars interarticularis.

 

FIGURE 6-46. Metrizamide CT myelogram at L1 level delimiting the spinal cord (SC), nerve roots (NR) arising from the cord, and the contrast-enhanced CSF.

The introduction of MDCT technology allows for the acquisitions of multiple thin cut images in the axial plane that can be reconstructed in the sagittal and the coronal planes. The high spatial resolution of the acquired data allows for near-perfect isometric reconstruction in different planes. In addition, computer-generated volume rendering images provide superb 3D images of the spine (Fig. 6-47A–C).

Sagittal T1-weighted MR images of the cervical, thoracic, or lumbar spine provide excellent noninvasive survey to evaluate patients with suspected regional spinal pathology. Midsagittal T1-weighted images display the high–signal-intensity marrow of the vertebrae bordered by low–signal-intensity cortical bone. Structures displaying very low signal intensity include the peripheral part of the annulus fibrosus of the intervertebral disc, all ligaments, the dura, and the cerebrospinal fluid (CSF), and these are usually indistinguishable from each other (Fig. 6-48A–C). The nucleus pulposus, and probably the inner portion of the annulus fibrosus, shows moderate signal intensity. The spinal cord and the nerve roots display moderate signal intensity, which is well contrasted against the low–signal-intensity CSF. Collections of epidural fat, which are largest at lumbar levels, produce high signal intensity on T1-and T2-weighted images. On T2-weighted MR images, CSF and the normal well-hydrated nucleus pulposus assume high signal intensity.

FIGURE 6-47. Volume rendering images of the normal lumbar spine. A: Coronal (frontal) projection. Arrow points to a hypoplastic right transverse process, a normal anatomical variant. B: Sagittal (lateral) view, note relationship of pars interarticularis (PI) to the facet joint (FJ) and root foramina (RF). C: Midplane sagittal view through the central canal. Facet joint (FJ), pars interarticularis (PI), and pedicle (P).

FIGURE 6-48. MRI of the normal spine and spinal cord. A: A T2-weighted axial MRI at the L5-S1 disk level shows the thecal sac (T) as an area of high signal intensity, the nerve roots (S1, S2) within the posterior thecal sac are of low signal intensity. Note the ligamentum flavum (LF), and fluid within the facet joints (FJ) with high–signal-intensity fluid. B: T1-weighted midsagittal MRI of the lumbosacral spine displays the nucleus pulposus (NP) of the intervertebral discs, spinal cord (SC), conus medullaris (CM), and nerve roots of the cauda equina (CE) as areas of moderate signal intensity. Cerebrospinal fluid (CSF) is of low signal intensity, and epidural fat (E) is hyperintense. C: T2-weighted midsagittal MRI of the lumbosacral spine demonstrates the increased intensity of the nucleus pulposus (NP) and CSF. peripheral annulus. In the axial plane, it can demonstrate a narrower base in relationship to the height of the herniation. A sequestered or free fragment is an extruded disc without contiguity to the parent disc. The majority of disc herniation are central or paracentral (subarticular) in location.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice
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