 Hello everyone, I am Dr. Parimal Phuket. I am one of the directors and constituent radiologist at Precision Scan and Research Centre in Nagpur. Today we are going to discuss the imaging of brachial plexus. The clinical investigations of brachial nerve lesions are routinely involved in nerve conduction studies and EMG. The role of imaging is traditionally limited to excluding vocal nerve lesions or extensive completions. MRI, because of its excellent soft tissue imaging, can identify structural changes in the nerves as well as the secondary neurogenic proliferation which occurs in the subtle muscles. This greatly enhances its use in differential diagnosis of peripheral nerve lesions. Before moving on to the imaging part, let us first revise the cost-sectional anatomy of our peripheral nerve. Each peripheral nerve has got a covering called epineurium, inside which there are multiple bundles of fascicles, which are separated by the intervening fat as shown here. Each fascicle has got a covering of sheep called as perineurium and inside which there are multiple bundles of mildly red axons. These axons are separated by thin sheeps called as indoneurium. So we got indoneurium, the perineurium and epineurium. This is a fat saturated T2-80-metre sciatic nerve which clearly shows this anatomy. These small hyperenters areas are the nerve fascicles which are in turn separated by these black dots, which is the suppressed fat, intervening fat between the fascicles. This is a fat saturated sequence, so the fat is going to appear black here. When we speak of nerve injuries, we generally follow the seton and the simple line classification, which divides the nerve injuries in different categories. Going on from the least severe to the most severe, we have got neuropraxia, axon remasses, neuron remasses, and nerve transfection. The simplest of injuries is neuropraxia, which means nerve stretching or edema. There is no loss of continuity in the axons. The axons are intact. Mildly issued around the axon might be restricted, but the epineurium, the endoneurium, and the perineurium all are intact. These patients potentially have worked rapid and concrete recovery with no rate of surgery. They don't have an incipital or valentine degeneration. Moving on to the next type, which is slightly more severe, axon remasses. In axon remasses, we have got partial disruption of some of the axons. The endoneurium might be disrupted, however, the nerve fascicles are intact and the perineurium is intact. So these patients will have some mild neuro deficit, most of them will have concrete recovery, some of them will have mild neuro deficit. Again, surgery is not largely indicated in these patients. Moving on to the next type, the neuron remasses. Now, this is a slightly severe form of injury in which there is partial nerve tear. So there will be disruption of the axons as well as some of the nerve fascicles. They will be breached in the endoneurium as well as the perineurium. But the epineurium will be intact, so the nerve structure is generally maintained. These are patients who will need surgery many a times. They might have some permanent neuro deficit and a security of valentine degeneration. And moving on to the most severe type, nerve transaction, there will be complete breach in the penalty of the nerve so that there is break in the epineurium. These are patients who will require surgery immediately after the injury to have a good recovery. So these patients are likely to have permanent neuro deficit and a security of valentine degeneration. So why do we need to do imaging of patients who will be able to do the surgery? And what do we tell the surgeons after doing the imaging? So this is an illustration showing the different forms of injury. The image on the bottom here shows neuropraxia. The nerve rootlets are intact. The nerve itself is intact. There is some stretch in the axons for edematostring in the nerve. These patients have complete recovery. Second image here shows axon tuberculosis. There is partial disruption of some of the axons. However, the nerve epineurium is intact. These are patients who will generally have some deficit. But good recovery is possible. Surgery generally is not indicated for these patients. The third image here, you can see that there is complete nerve transaction. So this is a severe form of injury. This will be severe axon neurotomyosis or nerve transaction. There is a complete breach in the epineurium. Again, these are the patients who should be subjected to early surgery to have a good prognosis. The fourth image here shows what we call as nerve root abolition. So you can see that the mental nerve rootlets here are adverse from the insertion on the cord. These again are patients who will need surgery on a urgent basis to have a good prognosis. So when we do imaging of these patients with brachial plexus injury, almost 10% of patients will have severe injury in the form of nerve divulging or nerve transaction. And 90% of patients will have less severe or minor injury in the form of neuropaxia or axon neurosis. So these 90% of patients generally don't need surgery. 70% of them will have complete recovery. And around 30% will have some neurodificit. But the whole idea of imaging patients with brachial plexus injury is to identify this 10% of patients who will need surgery and who can have a good prognosis after surgery. The actual nerve regions was a T2 hyper intense signal at and distance to the region side. This correlates with ballet degeneration and navelima, prolongation of the T2 reaction time and gathering the enhancement of denominated muscle developing parallel to the development of spongebob activity on EMG. And these are the consequences of capital enlargement and increased muscular blood volume. Similarly, when we do imaging of these patients, we also see changes of muscle denomation. These can be acute denomation, muscle denomation or chronic muscle denomation. And how do you differentiate these? So actively denominated muscles show prolongation of T2 reaction time. There will be increased intensity on T2 and star images. But the muscle volume is directly maintained. Whereas in chronically denomated certain muscles, there is apnoxy and fatty degeneration. And these muscles will show increased intensity on T2 and star images. These are patients to different patients with two sequential episodes of foot rock affecting the peroneal nerve distribution. The first image here shows the axial development of the image. And in the peroneous brevis muscle, we are seeing there is hyper intense signal here which suggests fatty degeneration. So this is chronic muscle denomation. Second image, second patient here shows there is edematous changes and slightly increased volume in the peroneous longus muscle. It is hyper intense here on an axial fat saturated T2-rated image suggesting muscle edema and acute muscle denomation. The mental technique of the click-excessive imaging and the sequences that we take, both 155 tisla and tata slime rm machines are good. But as we know, tata slime rm scores over 1.5 tisla in terms of vessel signal to earth ratio and availability of newer 3D imaging sequences. We use specialized RF coils, surface coils or face diacons are used. T1-rated images are good to show detailed anatomy and they are used to define the bone structures and tissue planes surrounding the nerves. Eye resolution and fast pinnacle T2 images are good to express pathology. Fat separation techniques using FS sequences or stir sequence, these will detect early changes of edema, inflammation and they will make the pathology more conspicuous. Gat-enhanced t1-rated imaging is useful for evaluation of peripheral noctimals plus infestation and in identifying adiapathic intramural disorders like parsley, stung, and so on. And very importantly, 3 tisla MR neurography. So, when we speak of MR neurography, we need to take 3D sequences like 3D stir sequence, 3D GRE and now these 3D different sequences. So, this enhance the imaging and will help us in getting reformative images. What are the imaging planes that we take when we image the brachial plexus? Now, we have to keep in mind that the imaging plane should parallel the nerves, the bones of the nerves. So, when we take a coronal sequence, this is the oblique coronal, this is the actual slice here. We are going to take the plane which parallels the nerves as they exit from the neural pharma and travels and know laterally towards the axilla. So, this is the imaging plane to get the coronal images. So, for actual image, the imaging plane should go laterally and infinitely because this is the bones of the nerves. And on sedative, the imaging plane should cut the nerves at right angles. So, if the nerves are passing in this direction, the imaging plane should be so that the nerves are cut in right angles. Coming to the anatomy of brachial plexus, we know that when we speak of brachial plexus, we speak in terms of roots, trunks, divisions, cords and branches. When it comes to roots, we have to speak in two terms, the ganglionic part and the post-ganglic part. So, what does that mean? So, this is an illustration. This is a C5 root section. So, this is a ventral rootlet of C5 nerve. This is the dorsal of the posterior rootlet. Both of them join here to form the C5 nerve. Just before joining, the dorsal or the posterior rootlet has got a ganglion. This is the dorsal ganglion. So, the part before the ganglion is the pre-ganglionic part, the part here called in green. So, this is the ventral rootlet dorsal rootlet of the neon ganglion. This comprises the pre-ganglionic segment and the part in orange is the post-ganglionic segment. So, this is the C5 nerve itself and then it divides into the ventral ribose and dorsal ribose. So, we have to keep in mind that only the ventral ribose of C5, C6, C7, C8 and C1 nerves will come away or will take part in formation of the brachial plexus. The posterior rmi will not take part in the brachial plexus. Sometimes, we have got contributions from the C4 nerve and the D2 nerve. So, this is the action which is very important to image this part also. Generally, when we do brachial plexus imaging, we tend to forget to take action sections or 3D sequences to evaluate the rootlets. So, we have to take a 3D space or fiesta sequence. In this machine, we have a space sequence or a set sequence and the G machine will have a fiesta sequence. So, take a 3D space or fiesta to the existing neutral throne. So, this is the image here which shows the ventral rootlet on the right side. So, this is the right ventral rootlet, the posterior rootlet. This is joined together to form the existing nerve here. This nerve again will be divided into the ventral ribose and the posterior ribose. In nerve divergence, we will see that this segment is lost and there will be a formation of a pseudo-meningosal in this region. We will come to these images later. So, this is the patient who has got nerve divergence involving right-sided C5, C8 nerves. So, we have taken action to be space or fiesta sequence here. So, this is at the level of C5 nerve root. We can see that the ventral and the dorsal rootlets are seen on the left side but they are not seen on the right side. Again, same at the level of neural fragment. The C5 and left-sided rootlets are seen. The right side root is not seen here. Same case at C6 level. At C7 level, same thing here. And additionally, we are seeing that there is a cystic area here in the epidural space in the lateral resist and neural fragment on the right side. This is, in fact, a pseudo-meningosal. So, this is the classical case of nerve diversion with pseudo-meningosal formation on the right side. At the D1 level, we can see both the ventral and dorsal rootlets on the right and left side here. So, the D1 rootlets of the roots are intact.