The collateral ligaments are best visualized by coronal MR images (Fig. 6-27). The medial collateral ligament appears as a narrow low–signal-intensity band extending from the medial epicondyle of the femur to an attachment on the anteromedial aspect of the tibia 5 to 6 cm below the joint line. It is overlaid at its tibial attachment by the tendons of the pes anserinus, which are separated from it by an intervening anserine bursa that is not visualized unless it is inflamed. Deep to the tibial collateral ligament, the medial capsular ligament, sometimes called the deep portion of the tibial collateral ligament, has femoral and tibial attachments close to the joint interval and deep attachments to the medial meniscus, referred to as the meniscofemoral and meniscotibial or coronary ligaments. Valgus and rotary stresses can injure the medial capsular ligament or the tibial collateral ligament, usually in that order (39). In a complete rupture (i.e., grade III injury), MRI can show discontinuity, serpentine ligamentous borders, and edema within adjacent connective tissues. In a partial tear (i.e., grade II injury) or in the case of microtears confined to the ligament substance (i.e., grade I injury), the ligament may show no discontinuity, but the overlying subcutaneous fat typically demonstrates edema and hemorrhage, which is indicated by moderate signal intensity on T1-weighted images and high signal intensity on T2-weighted images. Injury to the tibial collateral ligament is commonly associated with injuries to the anterior cruciate ligament and medial meniscus.

FIGURE 6-27. Tibial collateral ligament tear (MCL). A: Coronal T2-weighted fat suppressed sequences of grade I injury. There is edema (short arrows) overlying the intact fibers of the MCL (long arrow). B: Normal MCL (arrow).

The lateral collateral complex commonly refers to the lateral supporting structures of the knee, whose main components are the iliotibial tract, the lateral collateral ligament, the long head of the biceps femoris, and the popliteofibular ligament. These structures are best seen on axial and coronal MR images as a low–signal-intensity band extending somewhat obliquely from the lateral femoral epicondyle to the fibular head. The lateral collateral ligament is usually injured by varus and rotary stresses to the knee, although its frequency of injury is less than that of the tibial collateral ligament. The MRI findings of the injured fibular collateral ligament are similar to those for the tibial collateral ligament.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice

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.

Refferences

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.

Refferences

brain imagingSource: Physical Medicine and Rehabilitation - Principles and Practice

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.

Refferences

Source: Physical Medicine and Rehabilitation - Principles and Practice