MR imaging offers valuable information regarding the analysis of spinal lesions, as the location (posterior and lateral in multiple sclerosis, anterior in arterial infarction) and the size (short segment in multiple sclerosis or long segment in ischemia or neuromyelitis optica) can suggest the incriminated pathology.
The vast majority of lesions are isointense or hypointense on T1WI, but hemorrhagic, fatty or melanotic elements appear hyperintense. T2WI and STIR (short tau inversion recovery) usually show hyperintensity of the lesion. For a better appreciation of the hemorrhagic components, the T2* sequence is very useful (in trauma, tumors, vascular malformations). Diffusion restriction can appear in the presence of cord ischemia or abscesses. Gadolinium-enhanced T1WI is very useful and can show injury enhancement (different patterns) or not.
Degenerative cervical myelopathy is a progressive compression of the spinal cord, due to the age-related modifications of disks, vertebrae, or ligaments.
The most common pathologies that cause spinal canal stenosis, which can lead to myelopathy, are bulging discs, subluxation of the vertebral bodies (atlanto-axial instability, found in rheumatoid arthritis), facet joint arthropathy, prominent posterior osteophytes, ligamentum flavum hypertrophy or posterior ligament ossification (OPLL). The most commonly affected sites of compression are C5-C6 or C6-C7, but myelopathy can appear at any level. Symptoms and signs depend on the level and degree of spinal compression. There may be tingling, loss of fine movements in the hands, spasticity in the lower limbs, loss of balance, bladder incontinence, pain, weakness, and sensory deficits. MRI shows clearly the cause and the effects on the spinal cord (intramedullary hyperintensity on T2WI/STIR close to the site of compression, which may involve more than 3 segments affected).
OPLL represents an inflammatory degenerative disease. Minor calcifications may be seen with difficulty on MRI. The differential diagnosis is made with osteophytic compression, but in this case, the osteophytes are present only at the disc space. Other differential diagnoses are calcified herniated discs or a calcified meningioma (does not extend longitudinally, and is round). OPLL is often associated with DISH, ankylosing spondylitis, or ossification of the ligamentum flavum.
Acute disseminated encephalomyelitis, multiple sclerosis, transverse myelitis and optic neuromyelitis are inflammatory and demyelinating diseases, and the differential diagnosis between them must be well known because the prognosis and treatment are different.
Acute disseminated encephalomyelitis represents an inflammatory pathology of the central nervous system with white matter and spinal cord damage, caused by vaccination or viral infection. The most commonly affected are the cervical and dorsal segments. The spinal cord is not swollen (differential diagnosis with transverse myelitis), but there is complete spinal cord implication. The majority of patients with spinal damage have also brain lesions: bilateral symmetric white matter lesions that can affect grey matter, basal ganglia or pons, with hypointensity on T1WI and hyperintensity on T2WI, with different patterns of enhancement.
Multiple sclerosis is a common chronic demyelinating malady, with unknown etiology and different patterns: relapsing-remitting, secondary progressive, primary progressive or benign type. The McDonald criteria are very important for the multiple sclerosis diagnosis (dissemination in time or space of the lesions, positive oligoclonal bands in CSF, clinical history). Involvement of the spinal cord appears in 90% of cases. Myelopathy appears mostly in the cervical and thoracic spinal cord (very rare at the conus-a clue in the diagnosis of MOGAD), with less than two segments involved (short segments). The lesions can be single or at multiple levels. Some predictive locations of the spinal cord lesions in MS are: posterolateral, lateral, posterior or centrally, with nodular, ring or patchy enhancement in acute phase (edema may be present in case of active lesions).
Optic neuromyelitis (Devic’s syndrome) represents an immune demyelinating condition, a combination between the presence of optic neuritis and myelitis that affects the optic nerves and the spinal cord. Identification of immunoglobulin G/aquaporin 4 antibody is pathognomonic for optic neuromyelitis. Optic neuritis is unilateral/bilateral. MRI could show central longitudinal demyelinating cervicothoracic lesion (more than three spinal segments affected, with confluent lesions), which are hypointense on T1WI, hyperintense on T2WI, with patchy enhancement. Most specific cerebral lesions are periventricular-high aquaporin 4 concentration, cerebellar or affecting the cranial nerves, but without cerebral white matter lesions (like in MS).
Infections are another incriminating agent in the development of myelopathy. The origin can be from the lungs, genitourinary, the skin, digestive system or musculoskeletal, and some possible infectious agents are viral (herpes, polio, varicella zoster), bacterial (mycobacterium tuberculosis, borrelia), fungi or parasites (toxoplasma). The symptoms are severe, motor or sphincter dysfunction, fever or meningism. MRI shows central extensive myelopathy, with edema, most commonly cervicodorsal.
Tuberculous spondylodiscitis is typically found in the anterior and inferior parts of the vertebral body (hypointense T1WI, hyperintense T2WI-edematous changes), with subligamentous spread, abscess, avascular necrosis, destruction of the vertebral body, granuloma formation, involvement of the discs (hyperintense T2WI). Posterior elements involvement can spread to spinal canal, with epidural abscess and spinal cord compression. Gadolinium-enhancement can have a rim pattern. A rare entity is intramedullary tuberculous infection often found in HIV-positive patients. The spinal cord in iso/hyperintense on T1WI, hypo/isointense on T2WI (with surrounding edema), with solid/ring enhancement.
Toxoplasmosis is a parasitic infection, often found in AIDS patients, where spinal cord implication is usually associated with cerebral infection. Paralysis can appear during the course of the disease. A hypointense T1WI/ hyperintense T2WI lesion, gadolinium-enhancing, can be seen in the spinal cord.
Variable types of tumors can compress the spinal cord, whether intradural (intraspinal: astrocytoma, hemangioblastoma, ependymoma or extraspinal: meningioma, schwannoma, arachnoid cyst, paraganglioma) or extradural (bone metastasis, lymphoma, meningioma).
The most frequently found intramedullary tumor in pediatric population is astrocytoma, a commonly low-grade tumor (cervicodorsal region). MRI shows a large diffuse lesion, hypointense on T1WI, hyperintense on T2WI, with cystic/necrotic/hemorrhagic zones, with or without enhancement. Intense enhancement may be seen in pilocytic astrocytoma. On the other hand, high grade astrocytoma is heterogenous with vividly patchy enhancement.
Ependymoma is located in the cervical spinal cord, and may be present with a specific “cap sign” (hypointense on GE T2WI-hemosiderin cap due to chronic hemorrhage) or with cystic areas. These tumors are large, well defined, with vividly and homogeneous enhancement.
Hemangioblastoma is a benign tumor, which can present as a tumor with small subpial nodule with intramedullary edema or as a small nodule with enormous intramedullary cystic zones. In can be associated with von Hippel-Lindau syndrome. The nodule is isointense on T1/T2WI, with intense enhancement. MRI can show enlarged vessels (feeding arteries and draining veins).
Schwannomas are solitary well-encapsulated lesions, located intradural extramedullary. MRI shows intermediate signal or slight hypointense on T1WI and with high signal on T2WI, with or without cystic or calcified areas. Gadolinium-enhancement is homogenous and intense. Hemorrhage can appear in some cases.
Meningiomas are benign intradural tumors with a dural base, with predilection for the thoracic region. MRI shows an isointense T1WI/T2WI lesion, with homogenous and strongly enhancement, with a specific “dural tail”.
Paragangliomas are large relatively benign tumors with rich vascularity, with “flow voids” on T2WI, that can erode the bony canal.
Myelopathy of vascular origin is due to arteriovenous malformations (intraspinal, epidural), cavernomas, telangiectasias, and arteriovenous fistulae. Dural arteriovenous malformations show tortuous vessels with gadolinium enhancement, without flow void. Cavernous malformations are isointense on T1WI/T2WI, with a hemosiderin component. Infarction is another cause of vascular myelopathy, which can appear mostly at thoraco-lumbar level (the blood supply is poor), with serious symptoms like bowel/bladder incontinence, and motor and sensory deficits of lower extremities. The spinal cord can be enlarged (tumor-like), but the acute symptoms are helpful for the diagnosis. It can be the result of: dissecting aneurysm, aortic surgery, arteritis, vascular malformations, hypotension, meningitis, or disk herniation. MRI shows hyperintense signal on T2WI in the spinal cord, sometimes with enhancement. The pathognomonic appearance is hyperintense “pencil-like” strip on T2WI, with enhancement, in the anterior horns of the spinal cord (“owl-eye”), with restricted diffusion. Rarely, it can appear in the posterior part of the spinal cord.
A complication of B12 deficiency represents the subacute combined degeneration, with lesions at the cervical or upper dorsal spinal cord, brain, optic tracts and peripheral nerves. Paresthesias of the upper and lower extremities, spasticity, weakness at the lower limbs can be present. MRI shows extensive longitudinal hypersignal on T2WI in the posterior/lateral columns. Myelopathy found in copper deficiency is located centrally, with features similar to B12 deficiency.