Student’s Name
Institution Affiliation
 
 
 
 
 
 
 
 
 
 
 
Overview of the Central Nervous System
The central nervous system (CNS) is the most important part of the body in the implementation and coordination of their functions. CNS is made of the brain and the spinal cord. The peripheral nervous system is part of the nervous system that connects the ventral nervous system with the rest of the body. The meninges, which is a system of membranes covers the brain and spinal cord. In addition, both the brain and the spinal cord are suspended in the cerebrospinal fluid (Makino et al., 1996). Further, the skull and the bones of the vertebral column offer this organs protection.
This system has a wide and integrated connection of neurons that are supported by the neuroglia. The interior section of the central nervous system is organized into the white matter (WM) and the gray matter (GM). The latter is made up of nerve fibers that are embedded in neuroglia. On the other hand, the former has nerve cells embedded in neuroglia (Parke & Watanabe, 1985). Finally, the many brain neurons are connected to the neurons in the body through synapses. Through this integrated network, the CNS is able to coordinate all the functions of the body.
Spinal Cord Anatomy and Functioning
The spinal cord is found in the vertebral canal and is continuous carnally with the medulla. The vertebrae and its associated ligaments protect the spine. In addition, the cerebrospinal fluid (CSF) and the meninges provide added protection. The spinal cord does not lie adjacent to the bones; rather, the meninges, fat, fluid, and venous plexus protect it from these rough surfaces (Darby, nd, 72).
While the vertebrae column grows in length, the spinal cord lags and eventually it extends from the foramen magnum, to the lower part of the first lumbar, or to the upper part of the second lumbar vertebrae (Darby, nd, 67). It ends with fibrous extension, which is called the filum terminate. In addition, the spinal cord has a varying width of between 13 mm the cervical and lumbar region and 6.4 mm in the thoracic region. The cervical enlargement between C5 and T1, which provides sensory inputs go to the arms. On the other hand, the lumber enlargement between L1 and S3 provides sensory and motor inputs for the legs.
The spinal cord is made of 31 segments that contain sensory nerve root and motor nerve root. These nerve roots merge into 31 bilaterally symmetrical pairs of spinal nerves. Noteworthy, these spinal roots, nerves, and ganglia form part of the peripheral nervous system. All spinal nerves, except the first seven, leave below their corresponding vertebrae (Darby, nd., 86-87). In particular, C1 to C7 exit above the vertebrae, whereas C8 nerves and subsequent nerves exit below the vertebrae. The muscles and skin have an independent connection with a spinal nerve fiber.
Internal Structure of the Spinal Cord: Gray Matter and White Matter
The internal structure is composed of the gray matter, white matter, and tiny central canals that are filled with the cerebral spinal fluid. A single layer of cells called the ependymal layer surrounds the canal. The ependymal layer is surrounded by the gray matter. The shape and size of the gray matter depend on the spinal cord level. The ratio between the gray matter and the white matter is always greater at the lower levels than at the higher levels (Darby, n.d). Generally, the difference in color is because lower levels have less ascending and descending nerve fibers. The dorsal horn is comprised of sensory nuclei, whose function is to process and receive incoming somatosensory information.
The pelvic organs, as well as the autonomic neurons innervating visceral, make the intermediate column and the lateral horn. The nerve cells in the gray matter are multipolar. In fact, most them are Golgi type 1 and Golgi type 2 nerve cells. The cells of the spinal cord are also grouped in terms of function. In this manner, they are categorized as root cells, column cells, and propriospinal cells. The column cells are located in the dorsal gray horn and are confined within the CNS. On the other hand, the propriospinal cells are spinal interneurons and have all their axons in the spinal cord proper.
The gray matter is surrounded by the white matter, which is composed of unmyelinated and myelinated nerve fibers, that transfer information along the cord. Further, the white matter is divided into the dorsal column and the ventral column. The spinal cord has crossing nerve fibers at its center that are from the spinothalamic tracts, anterior corticospinal tracts, and spinocerebellar tracts (Darby, n.d). The long ascending nerve fibers originate from the column cells while the long descending nerve fibers are from the brain stem nuclei and the cerebral cortex. They also spread to synapse found in the different spinal cord’s Rexed layers. The ascending tracts are found in all the columns of the short nerve fibers interconnecting the various spinal cord levels, while the descending tracts are in only the lateral and the anterior columns.
Functions of the Spinal Cord
Motor Organization
Through the corticospinal tract, the spinal cord acts as an important link for the upper neutrons signals that originate from the cerebral cortex and the primitive brainstem motor nuclei. Through the crus cerebri and the medullary pyramids, the cortical upper motor neurons, which originate from Brodmann area 1,2,3,4, and 6, descend to the posterior limb of the internal capsule. These axons synapse with the ventral horns of the lower motor neuron of the spinal cord. The lower motor neurons are made up of the lateral corticospinal tract and the anterior cortical spinal tract (Fox, Beall, Bhattacharyya, & Sakae, 2011, 358). The lateral tract contains dorsal lateral (DL) lower motor neurons, which are used in distal limb movements. The anterior corticospinal tract synapses on lower ventromedial motor neurons. These motor neurons control postural muscles of the axial skeleton.
Spinocerebellar tracts
Proceptive information passes through the spinal cords to the rest of the body. Below L2, the proprioceptive information uses the ventral spinocerebellar tract to travel in the spinal cord. The sensory receptors transfer this information to the spinal cord. In the spinal cord, the axons synapse and the secondary travels up to the superior cerebellar peduncle after they decussate (Fox, Beall, Bhattacharyya, & Sakae, 2011, 358). Motor information travels from the brain to the spinal cord using the descending spinal cord tracts.
Somatosensory Organization
This functionality uses three different neurons to get information from the sensory receptors to the cerebral cortex. These neurons are categorized as primary, secondary, and tertiary sensory neurons. Somatosensory is divided into the anterolateral system and the dorsal column-medial leminiscus tract. In the dorsal column-medial leminiscus tract, a primary neuron enters the spinal cord and the dorsal column. At this level, the axon travels in the fasciculus gracillis or fasciculus cuneatus till the lower medulla where it fasciculus and synapses with a secondary neuron in any of the dorsal column nuclei. The secondary neurons, which are known as internal arcuate fibers, then terminate in the ventral posterolateral nucleus (VPL) of the thalamus. At this location, they synapse with tertiary neurons. From this point, they ascend upwards and through the internal capsule until they reach the primary sensory cortex (Fox, Beall, Bhattacharyya, & Sakae, 2011, 358).
In the anterolateral system, the primary neurons axons enter the spinal cord, ascend through the Lissauer’s tract, and synapse at the substantia gelatinosa. After synapsing, the seconday axons decussate and move to the anterior lateral portion of the spinal cord of the spinothalamic tract (Fox, Beall, Bhattacharyya, & Sakae, 2011, 358). They then move to the VP where they synapse on tertiary neurons. Later, these neurons travel to the primary sensory cortex through the posterior limb of the internal capsule.
Spinal Cord Diseases
            Given the importance of the spinal cord, diseases that affect its functionality extremely hinder the activities of the individual. There are various diseases of the spinal cord such as multiple sclerosis, amyotrophic lateral sclerosis (ALS), lupus, spinal bifida, spinal stenosis, syringomyelia (SM) and transverse myelitis.
Lupus is a chronic disease that causes swelling to various parts of the body. Worse still, it is characterized with symptoms of anemia, arthritis, and fever, which make it difficult to detect the disease (Constantinescu et al., 2011). Although the disease can be life-threatening, modern medications and antibiotics, as well as exercise have made it easy for individuals to live with it.
Spina bifida occurs when the spinal column does not close completely during pregnancy. Consequently, there is fluid on the brain, which causes motor and sensory impairment, depression, learning disabilities, and incontinence (Constantinescu et al., 2011). Individuals who have worked in the army can have babies with this disease, especially if they were exposed to Agent Orange.
Spinal stenosis occurs when there is a constriction of the nerves due to an overgrown bone. Generally, this disease can be detected through a CT scan, MRI, and blood tests. Its treatment is done through therapy, medication, or surgery to relieve the pressure on the nerves.
Syringomyelia (SM) is a spinal cord disorder that is caused by the growth of a cyst in the spinal cord. An accident, tumor, or a disease may trigger this disease. Fluids flow into the spinal cord and cause a cyst to grow. The cyst damages the nerve fibers through the force that it applies on their walls. Initial symptoms include headaches, muscle weakness, and loss of sensitivity (Constantinescu et al., 2011). If left untreated, the cyst can lead can cause scoliosis, osteoporosis, and advanced SM. Surgery is an effective method of stopping the growth of the cyst. Moreover, cysts can be drained to ease the pain in the spinal cord.
Transverse myelitis refers to a group of diseases that cause the spinal cord to swell. Normally, they are caused by a neural injury, which may cause infections to occur in less than a day (Constantinescu et al., 2011). These diseases have no known cause, and while full recovery is possible, most of those infected become paralyzed.
Multiple Sclerosis
Multiple sclerosis is a central nervous disease that is usually crippling. However, it is not fatal. It is a common neurological disease among young adults. Although the real cause of the disease is unknown, it is widely believed that it is due to abnormalities in the body’s immune system, which make it attack itself (Constantinescu et al., 2011). The symptoms of the disease include paralysis, fever, blindness, tremors, and numbness. Since the disease has no known treatment, medication normally involves managing the underlying symptoms.
Multiple Sclerosis Overview
Multiple sclerosis (MS) is a potentially disabling disease that affects the central nervous system, which is the brain and the spinal cord. This disease damages the insulating cover of the nerve cells, the myelin. As a result, the communication system in the nerves is disrupted. Given that the disease is caused by the damage to the myelin, the severity of the disease varies depending the level of damage. Symptoms may include double vision, blindness, muscle weakness, loss of sensation, and paralysis.
Normally, MS is known through the underlying symptoms. Moreover, it does not have any known cure. The treatment of this disease also entails treating the underlying symptoms, and preventing new attacks. In addition, patients are taught how to manage the symptoms.
Multiple Sclerosis of the Spinal Cord
            MS of the spinal cord is a demyelinating disease that affects the spinal cord. Most patients who have MS experience it in the spinal cord. Notably, the cervical spinal cord is more likely to be involved than the lower areas. MS of the spinal cord  normally exhibits >= 1 foci of increased signal on T2- weighted images with or without a decrease in the signal in the spinal cord on T1-weighted images. In the earlier stages, the images show cord edema and selling. Later on, the disease imaging reveals cord atrophy.
Clinical Presentation of MS Stages and Microstructural Changes in MS
Although MS is normally detected in early adulthood, such as between 20 and 30 years, the disease actually starts in early childhood. At this stage, the symptoms of the disease are extremely mild and difficult to detect. Generally, a combination of vitamin D deficiency, genetic susceptibility, and viral infection are the most common reasons. The deficiency in vitamin D levels ensure that the child’s viral infection is not well controlled, which leads to the development of a huge number of memory immune cells. These memory immune cells are reactive to both the myelin protein as well as to the virus. Their negative effects start to occur when the child is between and 20-30 years. During this period, since there is a vitamin D deficiency, the Pre-Clinical MS (PCMS) activate the myelin-sensitive memory cells (Fox et al., 2011). Over time, these reactions cause inflammations in various parts of the brain and the spinal cord. The repeated bouts of these attacks lead to the emergence of the relapsing-remitting MS (R-R MS).
R-R MS is characterized by well defined and separate attacks. In fact, it is at this stage that most individuals visit hospitals and are diagnosed with MS. Additionally, the amplified severity of the attacks is due to the increased autoimmune activity. These attacks lead to inflammations of the brain, which causes demyelination and nerve damage (Fox et al., 2011). In general, the greater the axon damage, the more likely the patient will have long-term disability. The extensive damage to the myelin and nerves is the main cause of disability.
The final stage is the Secondary Progressive MS (SPMS). This stage is characterized by a steady increase in disability and few distinct attacks. At this stage, there is a slow but continuous degeneration of the long axon stands (Fox et al., 2011). As a result, fewer brain impulses reach the muscles. In turn, this translates to increased disability. In order to limit the chances of occurrence of this disease, parents should ensure that their children have an adequate supply of vitamin D.
Animal Models of MS Such as EAE
According to Constantinescu et al. 1084, EAE is an autoimmune animal model of inflammatory diseases of the CNS, which is similar to MS. EAE has been effectively used in major scientific fields. Ivanov et al. 2006, reported that it is an essential in vivo validation model. In particular, it was effectively used in the discovery of ROR-ᴕ (RORC) as a master transcription factor for the Th17 cell development. According to Sabin and Wright, human beings were the first species to experience EAE on animal models.
Gold et al. (2006), stated that EAE has been used to provide models of acute monophasic chronic progressive CNS inflammation and relapsing-remitting. Active EAE is induced by the immunization with CNS tissue or myelin peptides, like proteolipid protein (PLP) and myelin basic protein (MBP) (Stromenes and Goverman, 2006a). Normally, the disease occurs after 9-12 days.
Alvord et al. (1985), found that chronic relapsing-remitting disease can be induced in guinea pigs by immunization with MBP or using CNS tissue homogenate. Stomnes and Goverman, (2006b) also found out that adoptive EAE (AT-EAE) can be induced by the transfer of pathogenic myelin-specific CD4 T cells, which have been generated from the donor animal by active immunization. Pettnellu and McFarlin (1981), reported that AT-EAE is an essential variable in the “effector phase” of myelin-reactive T cells diseases.
Adoptive transfer of cells has enabled the analysis of inflammatory molecules in different aspects of disease development and regulation using gene-targeted donor or recipient animal strains such as C57BL/mice. Lassmann 2007, found out that there is a variation in the lesion of different animal strains. For instance, C57BL/6 mouse immunization with MOG35-55 in CFA can result in monophasic or a chronic brought about by the EAE.
Vanderlugt et al. (2000), found out that inducing EAE in a SJL/J mouse through immunization with PLP138-151 lead to relapsing-remitting disease. In this case, typical lesions appeared in the optic nerve, cerebellum, spinal cord, and cerebral cortex. Tanum et al. (2000), found out that syngeneic spinal cord tissue can be used to induce EAE that is characterized by demyelination and spinal cord lesions with subpial inflammatory and perivascular infiltration.
Clinical Diagnosis and Assessment of MS in Clinical Patients
Ordinarily, the clinical diagnosis of patients with MS is done using DW-MRI by analyzing the significance of damage to the white matter pathways on the inside and outside the matter lesions. According to Yu et al., (2012), there is a correlation between the FA reduction and cognitive impairment in the cognitively relevant tracts. Similarly, Bodini et al. (2014), reported that there is a relationship between the damage in the callosal fibers and the occurrence of MS. Generally, a low FA along the entire corpus callosum is associated with poor verbal and processing of information.
According to Dineen et al. (2009), there is an association between fornix FA with controls. Generally, low fornix FA levels are correlated to low visual memory. Further, a research by Bodini et al. (2009), showed that there is a quantitative relationship between reduced FA and increased atrophy of the gray matter. Therefore, the analysis of the underlying symptoms using an MRI scan is essential in diagnosing and assessing for the presence of MS.
Conventional Magnetic Resonance Imaging
The conventional MRI has led to an improved noninvasive imaging of lesions in the central nervous system (CNS), which has led to advancement in the study of MS. Basically, most infections of MS result in formation of lesions such as inflammation, edema, and demyelination, which result in an increase in the water content. As a result, MR images have hyperintense T2 weighted images and hypointense T1 weighted images (Robinson et al., 2010, 240). Additionally, the use of superparamagnetic iron oxide nanoparticles (SPIO) contrast reagents may be used to enhance the images of anatomical regions such as the spinal cord. In addition, the MRI of in vitro labeled cells with magnetic contrast reagents provides an essential method of monitoring the migration of labeled cells and their contribution to pathological mechanisms. Essentially, SPIO-contrast reagents create a hypointense signal on T2 weighted images due to a shortening of the T2 and T2 * relaxation time constants (Robinson et al., 2010, 241).
MRI Studies of MS in Patients and Animal Models
Robinson et al., 2010, 245, performed an MRI scan on on a sample of mice. The detection of gray and white matter inflammation demonstrated the ability of the MRI to monitor lesion formation in each distinct anatomical region. In the study, a 10:3 μg/mL Fe/ProS was used to increase the intracellular iron almost 50 times to 0.7 pg iron. The research was able to detect gadolinium-enhanced lesions in the EAE brain of the mice without the onset of clinical symptoms. Importantly, these results correlated with others from published works. Moreover, although intracellular ferrous ions can be poisonous, labeling them with a 10:3 μg/mL Fe/ProS does not increase the reactive oxygen species ROS. In addition, hypointense regions were observed in T2 weighted MRI due to transfected ferritin in mouse brain. Therefore, although SPIO is dissolved, the intracellular labeling with Fe/ProS provides a long-term tracking by MRI (Sykova & Jendelova 2005).
Using various MRI techniques such as DW-MRI, MS damages can be detected. Theaudin et al., 2012 found out that MRI may underestimate the size of the MS lesions. In his study, he found out that MRI showed lower levels of FA and ADC than those detected in the normal appearing white matter. The results also indicated that higher FA and reduced radial diffusivity may have better outcomes. According to Setzer et al., (2010), the tractography fibers can be traced through inactive, T2 hyperintense MS plaques. Further, Renoux et al. (2006), said that a decrease in FA values was similar to the T2 abnormalities in patients with myelitis.
 
 
 
 
 
References
Alvord EC, Jr, Driscoll BF, Kies MW (1985). Large subpial plaques of demyelination in a new form of chronic experimental allergic encephalomyelitis in the guinea pig. Neurochem Pathol, 3: 195–214.
Bodini, B., & Ciccarelli, O. (2014). Diffusion MRI in neurological disorders. Amsterdam, Netherlands: Elsevier Publishing.
Bodini, B., Ciccarelli, O. (2009). Diffusion MRI in neurological disorders. In: Johansen-Berg, H., Behrens, T.E.J. (Eds.), Diffusion MRI: From Quantitative Measurement to In-vivo Neuroanatomy. Academic Press, pp. 175–204.
Caverzasi, E., Papinutto, N., Castellano, A., Zhu, A., Scifo, P., Riva, M., Bello, L., Falini, A., Bharata, A., & Henry, R (2016). Neurite Orientation Dispersion and Density Imaging Color Maps to Characterize Brain Diffusion in Neurologic Disorders. Journal of Neuroimaging, 26 (1), 494-498).
Chang Y, Jung TD, Yoo DS, Hyun JK. (2010). Diffusion tensor imaging and fiber tractography of patients with cervical spinal cord injury. J Neurotrauma. 27 (11):2033-2040.
Cohen-Adad J, El Mendili MM, Morizot-Koutlidis R, Lehericy S, Meininger V, Blancho S, Rossignol S, Benali H, Pradat PF. (2013). Involvement of spinal sensory pathway in ALS and specificity of cord atrophy to lower motor neuron degeneration. Amyotroph Lateral Scler Frontotemporal Degener, 14:30–38.
Constantinescu CS, Farooqi N, O’Brien K, Gran B. 2011. Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS). Br J Pharmacol 164:1079–1106.
Darby, S. nd. General anatomy of the spinal cord. Clinical anatomy of the spine, spinal cord, and ANS.  
DeBoy, C., Zhang, J., Dike, S., Shats, I., Jones, M., Reich, D., & Calabresi, P. (2007). High resolution diffusion tensor imaging of axonal damage in focal inflammatory and demyelinating lesions in rat spinal cord. Brain, 130 (1), 2199-2210.
Dineen, R.A., Vilisaar, J., Hlinka, J., et al., 2009. Disconnection as a mechanism for cognitive dysfunction in multiple sclerosis. Brain, 132, 239–249.
Ferizi, U., Schneider, T., Panagiotaki, E., Nedjati-Gilani, G., Zhang, H., Wheeler-Kingshott, C.A., Alexander, D. (2014). A ranking of diffusion MRI compartment models with in vivo human brain data. Magn. Reson. Med. 72, 1785–1792.
Fox, R., Beall, E., Bhattacharyya, P., & Sakae, K. (2011). Advanced MRI in Multiple Sclerosis: Current Status and Future Challenges. Neurology Clinic, 29 (1): 357-380.
Gold R, Linington C, Lassmann H (2006). Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research. Brain 129: 1953–1971.
Grussu, F., Schneider, T., Zhang, H.,  Alexander, D., & Wheeler-Kingshott, C. (2015). Neurolmage. 111, 590-601.
Hagmann, P., et al. (2013). Understanding diffusion MR imaging techniques: From scalar diffusion-weighted imaging to diffusion tensor imaging and beyond: RadioGraphics, 26, S205-S203.
Hendrix, P., Griessenauer, C., Cohen-Adad, J., Rajasekaran, S., Cauley, K., Shoja, M., Pezeshik, P., & Tubbs, S. (2015). Spinal diffusion tensor imaging: A comprehensive review with emphasis on spinal cord anatomy and clinical applications. Clinical Anatomy, 28, 88-95.
Kern, K.C., Ekstrom, A.D., Suthana, N.A., et al., (2012). Fornix damage limits verbal memory functional compensation in multiple sclerosis. NeuroImage, 59, 2932–2940.
Kim, J.H., Loy, D.N., Liang, H.F., Trinkaus, K., Schmidt, R.E., Song, S. (2007). Noninvasive diffusion tensor imaging of evolving white matter pathology in a mouse model of acute spinal cord injury. Magn. Reson. Med. 58, 253–260.
Loy DN, Kim JH, Xie M, Schmidt RE, Trinkaus K, Song SK. (2007). Diffusion tensor imaging predicts hyperacute spinal cord injury severity. J Neurotrauma, 24:979–990.
Lukas, C., Sombekke, M.H., Bellenberg, B., Hahn, H.K., Popescu, V., Bendfeldt, K., Radue, E.W., Gass, A., Borgwardt, S.J., Kappos, L. (2013). Relevance of spinal cord abnormalities to clinical disability in multiple sclerosis: MR imaging findings in a large cohort of patients. Radiology, 269, 542–552.
Makino M et al. (1996). Morphometric study of myelinated fibers in human cervical spinal cord white matter. Spine, 21(9), 1010-1016.
Mohammadi, S., Freund, P., Feiweier, T., Curt, A., Weiskopf, N. (2013). The impact of post processing on spinal cord diffusion tensor imaging. Neuroimage, 70, 377–385.
Parke WW & Watanabe R. (1985). The intrinsic vasculature of the lumbosacral spinal nerve roots. Spine, 10, 508-515.
Rajasekaran S, Kanna RM, Karunanithi R, Shetty AP. (2010). Diffusion tensor tractography demonstration of partially injured spinal cord tracts in a patient with posttraumatic Brown Sequard syndrome. J Magn Reson Imaging 32:978–981.
Renoux J, Facon D, Fillard P, Huynh I, Lasjaunias P, Ducreux D. (2006). MR diffusion tensor imaging and fiber tracking in inflammatory diseases of the spinal cord. AJNR Am J Neuroradiol, 27:1947–1951.
Robinson, K. et al. (2010). MR Imaging of Inflammation During Myelin-Specific T Cell-Mediated Autoimmune Attack in the EAE Mouse Spinal Cord. Molecular Imaging Biology. 12:240-249.
Roosendaal, S.D., Geurts, J.J., Vrenken, H., et al. (2009). Regional DTI differences in multiple sclerosis patients. NeuroImage 44,1397–1403.
Setzer M, Murtagh RD, Murtagh FR, Eleraky M, Jain S, Marquardt G, Seifert V, Vrionis FD. (2010). Diffusion tensor imaging tractography in patients with intramedullary tumors: Comparison with intraoperative findings and value for prediction of tumor resectability. J Neurosurg Spine, 13:371–380.
Shanmuganathan K, Gullapalli RP, Zhuo J, Mirvis SE. (2008). Diffusion tensor MR imaging in cervical spine trauma. AJNR Am J Neuroradiol, 29:655–659.
Smith, S.A., Jones, C.K., Gifford, A., Belegu, V., Chodkowski, B., Farrell, J.A., Landman, B.A., Reich, D.S., Calabresi, P.A., McDonald, J.W., van Zijl, P.C. (2010). Reproducibility of tract-specific magnetization transfer and diffusion tensor imaging in the cervical spinal cord at 3 tesla. NMR Biomed. 23, 207–217.
Song, S.K., Sun, S.W., Ramsbottom, M.J., Chang, C., Russell, J., Cross, A. (2002). Dysmyelination revealed through MRI as increased radial (but unchanged axial) diffusion of water. Neuroimage, 17, 1429–1436.
Song SK, Sun SW, Ju WK, Lin SJ, Cross AH, Neufeld AH. (2003). Diffusion tensor imaging detects and differentiates axon and myelin degeneration in mouse optic nerve after retinal ischemia. Neuroimage, 20:1714–1722.
Stromnes IM, Goverman JM (2006a). Active induction of experimental allergic encephalomyelitis. Nat Protoc 1: 1810–1819.
Stromnes IM, Goverman JM (2006b). Passive induction of experimental allergic encephalomyelitis. Nat Protoc 1: 1952–1960.
Sykova E, & Jendelova P (2005) Magnetic resonance tracking of implanted adult and embryonic stem cells in injured brain and spinal cord. Ann N Y Acad Sci 1049:146-160.
Tanuma N, Shin T, Matsumoto Y (2000). Characterization of acute versus chronic relapsing autoimmune encephalomyelitis in DA rats. J Neuroimmunol, 108: 171–180.
Theaudin M, Saliou G, Ducot B, Deiva K, Denier C, Adams D, Ducreux D. (2012). Short-term evolution of spinal cord damage in multiple sclerosis: A diffusion tensor MRI study. Neuroradiology. 54:1171–1178.
Vendantam, A, Jirjis, M., Wang, M., Ulmer, J & Kurpad, S. (2014). Diffusion Tensor Imaging of the spinal cord: Insights from animal and human studies. Neurosergery, 74, 1-8.
Yamada K, Sakai K, Akazawa K, Yuen S, Nishimura T. (2009). MR tractography: A review of its clinical applications. Magn Reson Med Sci 8:165–174.
Yu, H.J., Christodoulou, C., Bhise, V., et al. (2012). Multiple white matter tract abnormalities underlie cognitive impairment in RRMS. NeuroImage 59, 3713–3722.
Zhang, H., Schneider, T., Wheeler-Kingshott, C.A., Alexander, D.C. (2012). NODDI: Practical in vivo neurite orientation dispersion and density imaging of the human brain. Neuroimage 61, 1000–1016.