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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Musculoskeletal Imaging

Musculoskeletal Imaging (21)

The advent of the multidetector CT (MDCT) scanner has increased the applicability of this imaging technique for the assessment of the musculoskeletal system. This technology allows for the acquisition of large data set in the axial plane that can be reconstructed in multiple planes of imaging with the use of multiplanar reconstruction (MPR) algorithm. 


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Spine and Spinal Cord Imaging

Spine and Spinal Cord Imaging (8)

It is clear, after multiple research studies to assess the usefulness of imaging in low back pain, that uncomplicated acute low back pain is a benign, self-limited condition that does not warrant any imaging studies. The vast majority of patients are back to their usual activities within 30 days. Radiographic evaluation of the lumbar spine includes frontal and lateral radiographs. These are indicated in the evaluation of back pain and weight loss, after mild trauma in patients older than 50 y/o, in patients with unexplained fever, immunosuppression, history of cancer, prolonged use of steroids and focal neurologic, or disabling symptoms. Oblique views are useful for the assessment of defects to the pars interarticularis when suspecting spondylolysis and for the evaluation of the nerve root foramina. The relative radiation dose level for a routine radiographic examination of the lumbar spine is between 1 and 10 mSv (56). Although plain radiographs remain valuable for detecting many types of spine fractures and degenerative changes, the high resolution of osseous and soft-tissue structures provided by CT and MRI has made these modalities invaluable for the diagnosis of degenerative, traumatic, neoplastic, and infectious diseases of the spinal column and spinal cord. 


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Brain Imaging

Brain Imaging (10)

The following section will be dedicated to brain imaging relevant to rehabilitation. Emphasis is placed on the imaging of ischemic and hemorrhagic strokes, head trauma, and common degenerative diseases. The imaging of brain neoplasms and infections will not be covered in this section, as it is beyond the scope of this text. 

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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).


Source: Physical Medicine and Rehabilitation - Principles and Practice

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.


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.


Source: Physical Medicine and Rehabilitation - Principles and Practice

One of the common indications for MRI of the hip is to are the standard radiographs performed for the assessment determine the presence of ischemic necrosis. This is bone of hip joint abnormalities (26). The presence of osteoarthri death produced by a compromised blood supply. It also has tis, bone tumors, and soft-tissue calcifications can be assessed been called avascular necrosis, osteonecrosis, or aseptic necrosis. Predisposing factors that should raise the physician’s index of suspicion include corticosteroid therapy, alcoholism, known hip trauma, chronic pancreatitis, Gaucher’s disease, sickle cell disease, exposure to hypobaric conditions, subcapital fractures, childhood septic arthritis or osteomyelitis of the hip, and congenital hip dislocation (27). If undetected early, the disease can progress and finally undergo irreversible collapse of the femoral head. MRI has been demonstrated to be even more sensitive and specific than bone scintigraphy for the early diagnosis of ischemic necrosis of the femoral head (28–31).

On T1-weighted MRI, the foci of ischemic necrosis of the femoral head appear as homogeneous or heterogeneous well-delimited or diffuse areas of decreased signal intensity in the shape of rings, bands, wedges, or crescents, or in an irregular configuration (Fig. 6-18A–C) (32–33). The low signal intensity is caused by death of marrow fat and replacement of the marrow by a fibrous connective tissue. Some cases show a lower signal band surrounding the lesion, and this has been attributed to healing sclerotic bone at the interface between normal and necrotic bone. On T2-weighted images, many cases show a double-line sign with a high–signal-intensity zone just inside of a low–signal-intensity margin. This is thought to be produced by granulation tissue surrounded by sclerotic bone (31–33).


FIGURE 6-18. A: Frontal radiograph on patient with advanced left hip AVN. There is sclerosis to the femoral head and collapse (arrow) to the articular surface. Bilateral ischemic necrosis of the femoral head in a different patient. B: coronal T1-weighted, serpiginous areas of decreased signal intensity are well demarcated within the subchondral marrow. C: coronal T2-weighted fat suppressed images. There is edema within the right femoral head (arrowheads) on the right femoral head. The left femoral heads demonstrates a serpiginous area of increased signal intensity. These findings are characteristic of AVN.


Source: Physical Medicine and Rehabilitation - Principles and Practice

MRI can serve as an adjunct diagnostic tool for CTS when the clinical or neurophysiologic findings are equivocal. The carpal tunnel is a fibro-osseous space with little fat that contains the flexor tendons and the median nerve. The flexor retinaculum composes the volar aspect of the tunnel and normally shows slight palmar bowing. The median nerve courses through the tunnel within its volar and radial aspect, and it can be differentiated from the adjacent tendons because it shows relative higher signal intensity. The carpal tunnel and its contents are best evaluated in the axial plane and should be scrutinized at three standard locations.

  1. Distal radioulnar joint before the median nerves enter the tunnel.
  2. Proximal tunnel, at the level of the pisiform.
  3. Distal tunnel, at the level of the hook of the hamate.

FIGURE 6-13. Normal wrist anatomy as seen on T1-weighted MR images. Axial MR images are at the levels A: of the distal radioulnar joint, B: the proximal and C: the distal carpal tunnel. D: Longitudinal MRI through the median nerve within the carpal tunnel. C, capitate; FDP, flexor digitorum profundus; FDS, flexor digitorum superficialis; FR, flexor retinaculum; H, hamate; L, lunate; MN, median nerve; PDN, palmar digital branches of the median nerve; R, radius; T, trapezium; U, ulna; UA, ulnar artery; UN, ulnar nerve. Note fracture through the base of the hook of the hamate (arrow in B).

There are four universal findings of CTS visible by MRI regardless of etiology (21):

  1. Swelling of the median nerve (i.e., pseudoganglion) in the proximal part of the carpal tunnel at the level of the pisiform. Best evaluated by comparing the size of the median nerve at the level of the distal radioulnar joint with its size at the proximal tunnel.
  2. Increased signal intensity of the edematous median nerve on T2-weighted images.
  3. Palmar bowing of the flexor retinaculum, determined by a bowing ratio of more than 15%. The bowing ratio is calculated by drawing a line from the trapezium to the hook of the hamate on the axial plane. The distance from this line to the flexor retinaculum is divided by the previously calculated length.
  4. Flattening of the median nerve in the distal carpal tunnel at the level of the hamate (Fig. 6-14A–D). MRI also has the potential to establish the cause of CTS. Some of the etiologies visualized by MRI include traumatic tenosynovitis, rheumatoid tenosynovitis, a ganglion cyst of a carpal joint, excessive fat within the carpal tunnel, a hypertrophied adductor pollicis muscle in the floor of the carpal tunnel, and a persistent median artery (23).

FIGURE 6-14. Axial FSE T2-weighted fat suppressed images (A, B, C) and sagittal T1-weighted image in a patient with carpal tunnel syndrome. A, B: There is a normal size to the nerve within the tunnel (arrowheads). C: There is thickening, increased girth and increased signal intensity proximal to the flexor retinaculum (arrowheads). D: Note tapering to the nerve as it approaches the carpal tunnel in the sagittal view (arrowheads).

MRI also provides a means of postoperative evaluation of those patients in whom the symptoms persist, to ensure that the flexor retinaculum has been completely incised and that there are no other complicating postoperative factors producing continuing discomfort. When the flexor retinaculum has been completely incised, the incision site is well documented by MRI and the contents of the carpal tunnel are typically displaced forward (Fig. 6-15A). If the distal part of the flexor retinaculum has been incompletely incised, this can be demonstrated by MRI, and the preoperative MRI findings of CTS will persist (Fig. 6-15B and C).

FIGURE 6-15. Postoperative MR of carpal tunnel syndrome. A: Axial T1-weighted image. There has been release to the flexor retinaculum (short arrow). The median nerve insinuates through the surgical defect. B: Axial T2-weighted fat suppressed image. The median nerve (arrow) has intermediate signal and is better delineated. C: Patient with failed carpal tunnel release. There is a linear area of decreased signal intensity (short arrow) which was found to represent a fibrous band at surgery. The median nerve (long arrow) is flattened underneath the fibrous band. (A and B; courtesy of Zehava Rosenberg, NY. C; courtesy of Mark Kransdorf, FL.) OTHER WRIST ABNORMALITIES

MRI can visualize postincisional neuromas as lobulated masses in the typical location of the palmar cutaneous branches of the median nerve. Other peripheral nerve tumors such as schwanomas (Fig. 6-16) and neurofibromas can be well recognized as well. It can also demonstrate tenosynovitis involving any of the tendons crossing the wrist. MRI also displays marrow abnormalities such as ischemic necrosis of the proximal fragment of a scaphoid fracture and avascular necrosis of the lunate, where the marrow shows reduced signal intensity (24). MRI has the ability to evaluate the integrity of the intrinsic/extrinsic ligaments of the wrist and the triangular fibrocartilage complex (TFCC) (25). The TFCC, scapholunate, and lunotriquetral ligaments are best evaluated with MR arthrography (Fig. 6-17).

FIGURE 6-16. Coronal T2-weighted sequence in a 72-year-old patient with a palpable hypothenar mass. There is a rounded soft tissue mass (arrow) within the ulnar nerve proximal to the retinaculum representing a shwannoma of the ulnar nerve. Courtesy of Dr. Mark Kransdorf, Jacksonville Fla.

FIGURE 6-17. A coronal T1-weighted image of the wrist shows intermediate signal intensity and increased distance to the scapholunate interval (arrow), representing a scapholunate ligament tear.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Plain film radiographic examination of the elbows should be the initialevaluation forpatients withchronicelbowpain. Radiographs can be useful for the assessment of calcium within the joint compartment or periarticular soft tissues. Standard frontal and lateral radiographs are used for the routine evaluation of the elbow joint. Radiographic examination of the elbow has a minimal RRL.

MRI has not been applied to the evaluation of elbow pathology as extensively as it has been to other large joints (17). However, improving imaging techniques and the use of surface coils permit superb visualization of the bony, ligamentous, muscular and neurovascular structures around the elbow. Common elbow injuries evaluated with MRI are usually related to sports (weightlifting, throwing, and racquet sports) or compartmental nerve entrapment.

FIGURE 6-9. Normal elbow as seen on T1-weighted MR images. A: The axial MRI displays the ulna (U), radius (R), annular ligament (AL), radial collateral ligament (RCL), brachial artery (BA), biceps tendon (BT), forearm flexor muscles (FM), forearm extensor muscles (EM), ulnar nerve (UN), and radial nerve (RN). B: The coronal MRI displays the humeroulnar joint (HUJ), humeroradial joint (HRJ), radial collateral ligament (RCL), ulnar collateral ligament (UCL), forearm flexor muscles (FM), and forearm extensor muscles (EM). C: The sagittal MRI through the humeroulnar joint demonstrates the biceps tendon (BT), brachialis (Br), and triceps (T).

Axial MRI views of the elbow region permit good visualization of the biceps, brachialis, triceps, and all the extensor and flexor muscles of the forearm (Fig. 6-9A). High–signalintensity fat planes and low–signal-intensity intermuscular septa permit clear delineation of each muscle and their tendons of insertion or origin. Axial images clearly depict brachial, ulnar, and radial arteries and all the subcutaneous and deep veins. They also allow identification of the ulnar nerve within the cubital tunnel and the radial nerve in the brachioradialisbrachialis interval and under the supinator muscle’s arcade of Frohse, where it is commonly entrapped. The median nerve is visualized at all its common elbow entrapment sites, including under the bicipital aponeurosis, between the heads of the pronator teres, and under the fibrous arch of the flexor digitorum superficialis.

The humeroulnar, humeroradial, and proximal radioulnar joint spaces and articular cartilages are well visualized on both coronal and sagittal MR images (Fig. 6-9B and C). The low–signal-intensity ulnar collateral, radial collateral, and annular ligaments are depicted on both axial and coronal MR images. Sagittal images delineate the anterior and posterior subsynovial fat pads.

MRI has the capability of directly visualizing degenerative or traumatic abnormalities of the annular and the radial and ulnar collateral ligamentous complexes. A sprain appears in MRI as thickened or thinned ligament with surrounding highT2 signal intensity. The collateral ligaments may show degeneration in association with adjacent epiocondylosis. The affected ligament commonly shows thickening and intermediate signal intensity. Full thickness of avulsion ligamentous tears appears as discontinuities of the low–signal-intensity ligament. The T2-weighted images disclose hyperintense edema and hemorrhage between the torn ends of the ligament extending into the joint interval and adjacent soft tissues. A partial thickness tear appears as high T2 fluid signal intensity within an uninterrupted ligament (Fig. 6-10).

FIGURE 6-10. Coronal MR T1WI with intra-articular contrast in a 22-year-old baseball player with medial elbow pain. There is a partial tear (arrowhead) at the insertion of the ulnar collateral ligament into the coronoid process of the ulna. Note the minimal amount of contrast extending between the bone cortex and the distal ligament attachment.

MRI also provides good visualization of the sites of muscle injury and denervation about the elbow (18) (Fig. 6-11A,B). Acute muscle denervation is demonstrated by increased T2-weighted signal intensity within the specific muscle group supplied by the injured or the affected nerve. Increased intramuscular T2-weighted signal intensity is due to muscle edema. Chronic muscle denervation is demonstrated by increased intramuscular T1-weighted signal intensity, related to muscle atrophy and fatty infiltration. Acute muscle injuries presents with intramuscular edema and hemorrhage. Increased thickening, increased signal intensity, and discontinuity of tendon fibers are the findings commonly observed in tendon tears (Fig. 6-12A,B).

FIGURE 6-11. Impingement to the anterior interosseous branch of the median nerve, Kiloh Nevin Syndrome. Axial STIR (short tau inversion recovery sequence) at the level of the distal forearm. On this fat suppressed sequence there is increased signal intensity to the fibers of the flexor pollicis longus muscle as can be appreciated with acute (stage I) or subacute (stage II) impingement. (Courtesy of Zehava Rosenberg, NY.)

FIGURE 6-12. Sagittal A and axial B FSE T2-weighted fat suppressed images of the distal arm in a patient with a complete biceps tear. A: The tendon free margin is retracted (long arrow in A). B: There is significant edema (arrow- heads) surrounding the retracted tendon (long arrow). B, biceps muscle; Br, brachialis muscle.

MRI has the ability to demonstrate tendinosis involving the common extensor and flexor tendon origins from the lateral and medial aspects of the humerus with findings similar to those described in tendinosis about the shoulder. It also can display abnormalities of the radial and ulnar collateral ligament complexes.


Source: Physical Medicine and Rehabilitation - Principles and Practice

Tendinitis and rupture also can involve the subscapularis, infraspinatus, and teres minor, or biceps tendons, although far less commonly than the supraspinatus. Early tendinitis involves an increased signal intensity area within the tendon. This can progress to frank rupture of the tendon with a high–signalintensity area at the site of the tear on T2-weighted images and may be associated with joint effusion. A complete tear will eventually cause muscle retraction and later atrophy.

Calcific tendinosis (Fig. 6-8) of the supraspinatus is a common clinical entity most commonly affecting middle age persons. It is slightly more common in females and can affect multiple tendons in the body. It is however far more frequently in the supraspinatus. Although the exact etiology is unknown, it is felt to be secondary to chronic ischemia of the tendon fibers.


FIGURE 6-8. Calcific tendinosis of the infraspinatus tendon. A: Axial T1WI and B: coronal oblique T2WI with fat suppression demonstrating a focal area of decreased signal within the fibers of the distal infraspinatus (arrow). Note high–signal-intensity fluid within the posterior joint (*). C: Sagittal oblique T1WI shows the calcification within the posterior fibers of the infraspinatus.

Increased high-intensity fluid about the biceps tendon on T2-weighted MR images can be produced by either a biceps tenosynovitis or a shoulder joint effusion because the tendon sheath normally communicates with the shoulder. Rupture of the biceps tendon is demonstrated by absence of the biceps tendon within the intertubercular sulcus and by distal retraction of the muscle, which is seen on imaging the arm (16). Dislocation of the biceps tendon is identified by medial displacement of the biceps tendon out of the intertubercular sulcus.


Source: Physical Medicine and Rehabilitation - Principles and Practice

For the assessment of shoulder instability and labral tears, it is imperative that intra-articular contrast medium be injected in order to be able to evaluate the entire articular labrum, glenoid fossa, and capsular mechanism (12). Axial MR images provide the best visualization of the anterior and posterior glenoid labra, capsule, and lower rotator cuff muscles (Fig. 6-1). Anteriorly, the moderate–signal-intensity subscapularis muscle belly and its low–signal-intensity tendon are visualized. The tendon fuses with the low–signal-intensity anterior capsule as it courses to its insertion on the lesser tubercle. The fibrocartilaginous anterior and posterior labra appear as low–signal-intensity triangular or rounded areas attached to the glenoid rim. The higher–signalintensity intra-articular contrast opposed the hyaline cartilage surfaces of the glenoid and humeral head. The posterior capsule is visualized as a low-intensity area blending with the deep surface of infraspinatus and teres minor muscles as they extend to their insertions on the greater tubercle of the humerus. The long tendon of the biceps is demonstrated as a round, low– signal-intensity area within the bicipital groove.

Shoulder instability and the associated disruption of the anterior capsular mechanism can cause chronic shoulder pain and disability. The instability may be caused by an acute traumatic

episode or can occur with no history of a traumatic event. Both recurrent traumatic subluxation and nontraumatic instability are typically associated with disruption of the anterior capsular mechanism. Anteriorly, where most instability occurs, this mechanism includes the subscapularis muscle and tendon, the anterior joint capsule, three underlying glenohumeral ligaments, the synovial lining, and the anterior labrum. With instability, the labrum shows tears, separation from the glenoid rim, or degeneration (13). Also frequently present are medial stripping of the capsule from its normal attachment to the labrum and glenoid rim, an enlarged fluid-filled subscapular bursa secondary to joint effusion, attenuation of the glenohumeral ligaments, and injury or laxity of the subscapularis muscle or tendon.

By MRI, labral tears may be visualized as discrete linear areas of increased signal intensity within the normal signal void of the labrum (Figs. 6-6 and 6-7). These areas show moderate intensity on T1-weighted images and high intensity on T2-weighted images. With recurrent dislocation or subluxation, the labrum can become fragmented or attenuated.

FIGURE 6-6. SLAP lesion and posterior labral tear in a patient with history of posterior instability. A: Coronal oblique T1-weighted fat suppressed MR arthrogram demonstrates increased signal intensity within the BLC extending on the biceps tendon (arrowhead) characteristic of a type IV SLAP lesion. B: Axial T1-weighted MR arthrogram demonstrates increased signal within the posterior labrum (arrowhead ). There is a cyst within the posterior aspect of the spinoglenoid notch with high–signal-intensity contrast extending into the cyst.

FIGURE 6-7. Bankart lesion. A: Axial T1-weighted images of a left shoulder MR arthrogram demonstrate the fibrocartilaginous Bankart lesion of the anterior glenoid labrum (arrow). B: Coronal T1-weighted fat suppression demonstrates the inferior (short arrow) and the superior (long arrow) extensions of the labral tears.

Capsular detachment from the scapula (i.e., stripping) is visualized by T2-weighted MRI as an area of high–signalintensity fluid dissecting medially from the glenoid rim. With trauma to the subscapularis tendon, there can be medial retraction of the muscle-tendon junction when the tendon is completely ruptured. Chronic atrophy of the subscapularis muscle belly is identified by high–signal-intensity fatty replacement. The glenoid marrow underlying a labral detachment may show pathologically decreased signal intensity even before the plain film radiograph shows an osseous Bankart lesion. MRI and CT can be used to visualize Bankart fractures of the anterior glenoid and the Hill-Sachs compression deformity of the posterolateral humeral head (14,15) and are both useful in the assessment of the extent of a Hill-Sachs defect in patients with engaging lesions. Patients with the rarer posterior instability show similar posterior labral, capsular, and muscular defects.


Source: Physical Medicine and Rehabilitation - Principles and Practice

The MRI findings of shoulder impingement syndrome and its associated supraspinatus injury are best seen on oblique coronal MR images that visualize the full length of the supraspinatus muscle belly and tendon (Fig. 6-1B). The normal muscle belly displays moderately low signal intensity. The tendon is visualized as an intermediate–signalintensity structure that blends with the low signal intensity of the superior capsule as it courses to its insertion on the greater tubercle of the humerus. The tendon demonstrates smooth tapering from medial to lateral into its insertion in the greater tuberosity. The inferior aspect of the tendon is delimited below by the moderate signal intensity of the hyaline cartilage on the superior aspect of the humeral head. The superior aspects of both the muscle belly and tendon are delimited by a high–signal-intensity subacromial and subdeltoid fat plane. The normal subacromial-subdeltoid bursa is not specifically visualized because its walls are separated only by monomolecular layers of a synovial-type fluid, but it is situated between the supraspinatus tendon and the fat plane. Above the fat plane, the clavicle, acromioclavicular joint, acromion, and deltoid muscle are demonstrated on different oblique coronal sections.

Although rotator cuff impingement is a clinical diagnosis, MRI can provide direct visualization of the constituents to the coracoacromial arch and their relationship to the supraspinatus (Fig. 6-2A and B). Downward slanting of the acromion in the coronal or the sagittal plane, a thickened coracoacromial ligament or inferior osteophytosis within the acromioclavicular joint can exert mass effect upon the supraspinatus. This has been implied as being in part responsible for chronic tears of the supraspinatus.


FIGURE 6-2. A: Coronal oblique T2-weighted pulse sequence with fat suppression demonstrates downward slanting to the acromion (long arrow ), which is against the supraspinatus tendon (*). Note focal area of increased signal at the myotendinous junction of the SsT (short arrow ). B: Sagittal oblique T2WI with fat suppression demonstrates to a better advantage the inferior slanting to the acromion against the SsT (short arrow ). Note focal tendinosis (long arrow ).


FIGURE 6-3. A: T1-weighted MRI of focal supraspinatus tendinosis demonstrating focal thickening and slight increase signal intensity to the tendon (arrow ). B: CoronalobliqueT2-weightedfat suppressed sequence with increased signal intensity within the area of tendinosis (arrowhead ). There is fluid within the adjacent subdeltoid bursa (long arrow ). C: Sagittal oblique T2-weighted fat suppressed image demonstrates the area of increased signal to be within the anterior superior portion of the rotator cuff representing fibers of the supraspinatus tendon (short arrow ).

Neer stated that 95% of rotator cuff tears are associated with chronic impingement syndrome (7) and described three stages in the progression of rotator cuff injury. These can be visualized by MRI (6–10). Stage 1 is characterized by edema and hemorrhage within the supraspinatus tendon characteristic of an early tendinitis. On MRI, there is focal tendon thickening and diffuse moderate increase in signal intensity within the tendon (Fig. 6-3A–C). In stage 2, Neer described both inflammation and fibrosis within the tendon. MRI shows this as thinning and irregularity of the tendon. Stage 3 is a frank tear of the supraspinatus tendon. On MRI, complete tears are noted by a discontinuity of the tendon with a well-defined focus of high signal intensity on T2-weighted images (Fig. 6-4). The most susceptible area is the critical zone of hypovascularity, located about 1 cm from the insertion (11). With small or partial tears, there is no retraction of the muscle-tendon junction, the subacromial-subdeltoid fat plane is commonly obliterated, and fluid may accumulate in the subacromial-subdeltoid bursa, which becomes hyper- intense on T2-weighted images. There also may be effusion of the shoulder joint, which may extend inferiorly along the tendon sheath about the long head of the biceps. With a complete supraspinatus tendon tear, the muscle belly may retract medially, and atrophy may occur as the tear becomes chronic (Fig. 6-5A,B). Muscle atrophy appears as areas of high signal intensity because of fatty replacement within the muscle belly and decreased muscle mass. Finally, the acromiohumeral interval narrows as the humeral head migrates superiorly, because of the loss of supraspinatus restraint to the deltoid’s tendency to sublux the humerus superiorly during abduction.

FIGURE 6-4. Complete rupture of the supraspinatus tendon is seen in a T2-weighted MRI. There is fluid filling the gap (arrow) and there is retraction to the tendon fibers underneath the acromion.

FIGURE 6-5. Complete rotator cuff tear. A: Coronal oblique T1-weighted image. There is intermediate signal intensity (*) from the inflammatory reaction replacing the normal low signal to the SS tendon. B: The edge (arrow) to the retracted tendon is at the level of the superior labrum. There is increased signal intensity filling the gap of the retracted tendon (long arrow).


Source: Physical Medicine and Rehabilitation - Principles and Practice

Plain film radiographic evaluation of the shoulder should include frontal examinations with internal and external humeral rotation. If there is a question of instability or dislocation, an axillary view, a scapular Y view, or both should be obtained. There have been several reports that recommend the use of a 30-degree caudad-angled radiograph or a suprascapular outlet view for the assessment of the anterior acromion in cases of suspected shoulder impingement. Since these are special views, they must be ordered as routine shoulder radiographs do not include axillary or suprascapular outlet views. The RRL for plain film radiographic examinations of the shoulder is less than 0.1 mSv, which is considered minimal.

MRI has become valuable in evaluating a host of shoulder abnormalities very familiar to the physiatrist. These include impingement syndrome, other rotator cuff abnormalities, instability syndrome, and bicipital tendon abnormalities. It is also useful in demonstrating arthritic changes, occult fractures, ischemic necrosis, and intra-articular bodies. MRI with intra- articular contrast is now considered the modality of choice for the evaluation of labral and capsular pathology. The use of MRI for shoulder evaluation avoids radiation exposure to the nearby thyroid gland, which can occur with CT examinations.The excellent visualization of marrow by MRI permits early diagnosis of ischemic necrosis, infection, and primary or metastatic tumors.

Because of the oblique orientation of the scapula on the chest wall and the consequent anterolateral facing direction of the glenoid, the direct multiplanar imaging capability of MRI provides optimal visualization of all the important shoulder structures. An oblique coronal image parallel to the plane of the scapula provide full-length views of the rotator cuff musculature, especially the supraspinatus and is the best plane for the evaluation of injuries to the biceps-labral complex (BLC) (Fig. 6-1A and B). Coronal oblique images can also provide information about the presence of impingement upon the supraspinatus by the acromion and osteophytes in the presence of acromioclavicular joint osteoarthritis. Oblique sagittal imaging planes parallel to the glenoid provide cross-sectional views of the rotator cuff apparatus and evaluates the anatomical configuration of the coracoacromial arch and the presence of impingement (Fig. 6-1D). Axial imaging planes provide good visualization of the anterior and posterior capsular apparatus, glenoid labrum, bony glenoid rim, and humeral head (Fig. 6-1C).

FIGURE 6-1. Normal shoulder MR images. A: An axial scout film with cursors displays the oblique coronal planes parallel to the plane of the scapula, which allow optimal visualization of the supraspinatus. B: An oblique coronal image demonstrates the supraspinatus muscle belly (SsB), supraspinatus tendon (SsT), subacromial-subdeltoid fat plane (FP), acromioclavicular joint (ACJ), deltoid muscle (D), articular cartilage of humeral head and glenoid (AC), glenoid (G), and humeral head (H). C: An axial image displays humeral head (H), glenoid (G), glenoid labrum (L), the inferior glenohumeral ligament (IGL), deltoid muscle (D), subscapsularis tendon (ScT), and biceps tendon (BT). D: A sagittal section demonstrates good resolution of the coracoacromial ligament (CAL) extending from the coracoid process (CP) to the acromion; coracoid process (CP), supraspinatus (SS), infraspinatus (IS).


Source: Physical Medicine and Rehabilitation - Principles and Practice
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