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Showing posts with label spinal cord diseases. Show all posts
Showing posts with label spinal cord diseases. Show all posts

Thursday, December 16, 2010

intramedullary ependymoma



A)intramedullary
B)subdural
C)epidural

intra-medullary neoplasm


sub-dural hygroma


epi-dural hematoma


Tuesday, July 6, 2010

MRI T1, precontrast showing solitary myeloma involving the second cervical vertebra,notice the T1 hypointensity.
D.D.:
Spinal metastases.

Tuesday, June 8, 2010

pre (a) and post (b) contrast sagittal T1 weighted images of the cervical spine showing a 2 cm predominantly low signal area in the anterior cervical spinal cord with patchy tubular enhancement and focal dural thickening consistent with AVM .


http://www.google.com.eg/imgres?imgurl=http://www.ispub.com/ispub/ijra/volume_5_number_2_29/high_cervical_spinal_cord_vascular_malformation_masquerading_as_guillian_barre_syndrome_a_case_report/spine-fig2.jpg&imgrefurl=http://www.ispub.com/ostia/index.php%3FxmlPrinter%3Dtrue%26xmlFilePath%3Djournals/ijra/vol5n2/spine.xml&usg=__6WdViDjaXcnTq7Bkie8jDX6gOus=&h=592&w=931&sz=60&hl=en&start=3&sig2=t_W5FAD60isrT67Nh9Q8tw&itbs=1&tbnid=w2a4jZvmCvPr_M:&tbnh=93&tbnw=147&prev=/images%3Fq%3D,mr%2BIntra-medullary%2Bvascular%2Bmalformation%2B(AVM).i%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1&ei=kAsOTPmsLov-4AbSltD3DA

As the older names imply, spina bifida and cranium bifidum share a failure of bone fusion in the posterior midline of the skull (cranium bifidum) or the vertebral column (spina bifida). The result is a bony cleft through which the meninges and varying quantities of brain or spinal cord tissue protrude. In cranium bifidum, the neural herniation is termed encephalocele and can consist of brain parenchyma and meninges or only of meninges. These form the wall of a saclike cyst filled with cerebrospinal fluid (CSF). Posterior encephaloceles may contain only supratentorial structures, only posterior fossa structures, or both. In spina bifida, the herniation is called meningocele or meningomyelocele, depending on whether the meninges herniate alone or together with spinal cord parenchyma and nerve roots. The traditional names spina bifida and cranium bifidum are now less frequently used than in the older literature because of the recognition that the bony cleft may not be the primary defect in all cases, but instead that the pathogenesis may involve neural induction of mesodermal tissues in the dorsal midline, including leptomeninges, dura mater, and bone.

Spina bifida occulta is a minor fusion failure of the posterior vertebral arches unaccompanied by herniation of meninges or neural tissue. Spina bifida cystica collectively designates meningocele, meningomyelocele, and other cystic lesions (FIGURE). Similarly, in the head, cranium bifidum comprises meningocele, a herniation of meninges containing only CSF, and the more commonly occurring encephalocele, in which the sac contains neural and glial tissue. Rachischisis refers to a severe condition with an extensive defect of the craniovertebral bone with exposure of the brain, spinal cord, and meninges. Myeloschisis is another defect in the tissues over the lower spinal cord. Neural tissue is exposed at the surface as a flat, red lesion with a velvety appearance over the sacral region, without protruding as a myelomeningocele sac.
meningocele meningomyelocele

myelocystocele myelocele


Drawings of various forms of spinal dysraphic lesions (spina bifida cystica). A: Meningocele. Through the bony defect (spina bifida), the meninges herniate and form a cystic sac filled with spinal fluid. The spinal cord does not participate in the herniation and might or might not be abnormal. B: Myelomeningocele. The spinal cord is herniated into the sac and ends there or can continue in an abnormal way further downward. C: Myelocystocele or syringomyelocele. The spinal cord shows hydromyelia; the posterior wall of the spinal cord is attached to the ectoderm and is undifferentiated. D: Myelocele. The spinal cord is araphic; a cystic cavity is in front of the anterior wall of the spinal cord.


http://www.google.com.eg/imgres?imgurl=http://www.msdlatinamerica.com/ebooks/ChildNeurology/files/5fcff0a7a0e5332caecf1ba18773d10c.gif&imgrefurl=http://www.msdlatinamerica.com/ebooks/ChildNeurology/sid398771.html&usg=__ZgHjoeZbwMSVuUVd5qOmeAqge1Q=&h=480&w=405&sz=113&hl=en&start=9&sig2=MA-qBTVzVvIDsdkXFlSN1g&itbs=1&tbnid=n8KdUngJ4OqbcM:&tbnh=129&tbnw=109&prev=/images%3Fq%3Dspinal%2Bdysraphism,mri%26hl%3Den%26sa%3DX%26gbv%3D2%26tbs%3Disch:1&ei=jwUOTICOM5WL_AbryMXMDA
Severe medullary contusion opposite C5 and C6 vertebrae with cord edema extending upwards until the level of C2 with visibility of small area of medullary hemorrhage opposite the vertebral body of C6 and the spinal cord is swollen at the level of the injury. However, no evidence of cord rupture. Severe injury to the C5-C6 intervertebral disc which is torn with posterior displacement of the posterior portion and inferior displacement of the anterior portion along the anterior aspect of C6 vertebra.


http://www.google.com.eg/imgres?imgurl=http://www.ispub.com/ispub/ija/volume_19_number_2/problems_faced_during_anesthesia_in_morbidly_obese_patient_with_cervical_injury_presented_for_fixation_in_prone_position/obese-fig1.jpg&imgrefurl=http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_19_number_2/article_printable/problems_faced_during_anesthesia_in_morbidly_obese_patient_with_cervical_injury_presented_for_fixation_in_prone_position.html&usg=__OmGkowHq0mz-qxFeb2ApKH0RqZc=&h=523&w=689&sz=41&hl=en&start=3&sig2=h5504esCWaa5V3l7gF6efw&itbs=1&tbnid=udqgkQ-3yBHf7M:&tbnh=106&tbnw=139&prev=/images%3Fq%3Dspinal%2Bcord%2Bcontusion,mri%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1&ei=QAMOTOXFKtf__Qbtk8W6DA
Guillain-Barré syndrome. T1-weighted postcontrast axial MR image of the cauda equina shows smooth, diffuse enhancement of the lumbar nerve roots. There is preferential involvement of the ventral roots, which is very suggestive of Guillain-Barré syndrome.


http://www.google.com.eg/imgres?imgurl=http://download.imaging.consult.com/ic/images/S1933033208703963/gr2-midi.jpg&imgrefurl=http://imaging.consult.com/image/topic/dx/Brain%2520and%2520Spine%3Ftitle%3DGuillain-Barre%2520Syndrome%2520(Spine)%26image%3Dfig2%26locator%3Dgr2%26pii%3DS1933-0332(08)70396-3&usg=__-5VAeTBmiID2yMO0OvIRadhS8qA=&h=192&w=200&sz=5&hl=en&start=4&sig2=8BblKz_g9ujZriV7hNrVvw&itbs=1&tbnid=X0pR1IU0BYuPIM:&tbnh=100&tbnw=104&prev=/images%3Fq%3DGuillain-Barre%2Bsyndrome,mri%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1&ei=gfINTO2eIYfs4gaay6XuDA

Sunday, June 6, 2010

Note that the lesions above do not enhance with contrast.

ADEM (acute disseminated encephalomyelitis): an inflammatory, demyelinating disorder, primarily of children, typically occurs after an infection (often a URI) or vaccination. It often presents as encephalopathy and multifocal neurologic deficits. An LP may show a mild leukocytosis and elevated protein (as in this case), but may be normal. MRI is key to the diagnosis and shows subcortical white matter hyperintensity on T2, with basal ganglia, brainstem, and spinal cord also commonly affected. Enhancement is unusual and suggestive of infection. Accepted treatment is with high dose steroids, followed by an oral taper. Other experimental immunosuppresive therapies have been tried. Prognosis is generally good, with 60-90% having a complete recovery. Traditionally considered monophasic in nature, multiple episodes are often reclassified as multiple sclerosis.

http://www.google.com.eg/imgres?imgurl=http://www.stanford.edu/~jen1917/adem.jpg&imgrefurl=http://www.stanford.edu/~jen1917/cases.htm&usg=__Zq2Xyb6wPABqueDdFwVe5yInj6w=&h=899&w=750&sz=40&hl=en&start=4&sig2=pSzptUZwTh62NEdhqWAXew&itbs=1&tbnid=iEhvaha0x3Q34M:&tbnh=146&tbnw=122&prev=/images%3Fq%3DADEM%2BDISEASE%26hl%3Den%26sa%3DG%26gbv%3D2%26tbs%3Disch:1&ei=ao0LTOauLtL24AbP9_1x

Saturday, June 5, 2010




Cervical spinal cord MRI in the sagittal plane of a 28-year-old woman with polyphasic neuromyelitis optica. (A) T1-weighted image showing thickening of the cord from C7 to T2 with patchy areas of subtle intraparenchymal hyperintensity. (B) T1-weighted image, post gadolinium contrast administration, showing several enhancing lesions from C7 to T2. (C) T2-weighted image showing a contingous area of increased signal intensity spanning from C6 to T3.









MRI (Magnetic Resonance Imaging) is the leading diagnostic tool used in determining SM. The MR imager takes pictures of body structures, such as the brain and spinal cord, in vivid detail. MRI Testing will show the syrinx in the spine or any other conditions, such as the presence of a tumor. MRI is safe, painless, and informative and has greatly improved the diagnosis of syringomyelia.
What is syringomyelia?

Syringomyelia is a disorder in which a cyst forms within the spinal cord This cyst called a syrinx expands and elongates over time destroying the center of the cord Since the spinal cord connects the brain to the nerves in the extremities this damage may result in pain weakness and stiffness in the back shoulders arms or legs Other symptoms may include headaches and loss of the ability to feel extremes of hot or cold especially in the hands and disruption in body temperature SM may also adversely affect sweating sexual function and bladder and bowel control.

What causes Syringomyelia?

• Trauma to the spinal cord or congenital developmental problems of the brain and/or spinal cord may result in SM

o Spinal cord trauma such as a car accident or serious fall may manifest years later as SM

- OR -

o Congenital developmental problems, sometimes undetectable may result in syringomyelia

In either case the condition may lie dormant and undetected for months or years until a symptom or variety of symptoms become bothersome enough to warrant medical attention. Many people with SM are not diagnosed until mid-life.


What are the different forms of Syringomyelia?

Generally, there are two forms of SM. The disorder may be related to a congenital abnormality of the brain called Arnold Chiari malformation. A syrinx may then develop in the cervical region of the spinal cord; this is referred to as communicating syringomyelia. Some people with this form of the disorder also have hydrocephalus (water on the brain), a condition in which CSF accumulates in the skull, or arachnoiditis, in which a covering of the spinal cord is inflamed.

The second major form of SM occurs as a complication of trauma, meningitis, hemmorrhage or tumor. Here, the cyst or syrinx develops in a segment of the spinal cord damaged by one or more of these conditions. The syrinx may start to expand; this is sometimes referred to as noncommunicating syringomyelia.

Presumed spinal cord metastasis in a female patient known to have breast cancer. MRI shows:
- Focal cord expansion with intramedullary enhancing mass,
- Thin enhancing rim along lower anterior cord surface and,
- Enhancing metastatic foci in the bone marrow.
Spinal cord metastases can be:
1-Intramedullary (within the cord): rare.
2-Pial (Superficial, along pial surface): in most of the cases.
Common primary CNS tumors: PNET/medulloblastoma and glioblastoma.
Common primary malignancy outside CNS: lung (70%), breast (11%), melanoma, kidney, lymphoma and leukemia.


Post contrast MRI demonstrates so called “sugar coating” or zuckerguss (German for sugar icing) of the lower portions of the spinal cord in keeping with leptomeningeal metastases.
MR findings in all intramedullary gliomas may be similar. T1WI typically demonstrates fusiform widening of the cord over one or several segments by a soft tissue mass that is iso or slightly hypointense to normal cord. T2WI demonstrates focal areas of increased signal within the enlarged cord segments that represents the tumor and surrounding edema. There is a frequent association of both intratumoral cysts and an adjacent syrinx with astrocytomas (38%) and ependymomas (46%). It is difficult to differentiate cystic tumor from a benign or adjacent syrinx on standard spin-echo sequences, since the signal may vary depending on the fluid characteristics. Gadolinium may help in this regard, as nearly all gliomas can be expected to enhance.

1-moderate spinal cord expansion from T9 to conus.
2-tumor are hypertense in T1&T2.
3-tumor enhances in certain manner in serpentine fashion.

Friday, March 19, 2010












Clinical History: 76-year-old male with a history of back pain and suspicion of infection.
Radiologic Findings: T1-weighted images (Figs. 1 and 2) show, at the T8-9 level, decreased signal intensity in the disc with loss of delineation of the vertebral end plates from the disc. Mild central canal stenosis is noted. A T2-weighted image (Fig.3) demonstrates increased signal intensity in the intervertebral disc with loss of the normal intranuclear cleft of low signal in the center of the disc. Following Gadolinium administration, T1-weighted images (Figs. 4 and 5) show abnormal enhancement of the disc, adjacent vertebral bodies, and anterior epidural and paraspinal soft tissues.
Diagnosis: Discitis with adjacent osteomyelitis.
Discussion: Pyogenic vertebral discitis and osteomyelitis are related to bacterial seeding from hematogenous spread secondary to bacteremia, or extension from surgery, trauma, or from a contiguous infection. Hematogenous spread is the most common cause, primarily related to infections of the genitourinary tract, skin and respiratory tract.
The most common causative organisms are Staphylococcus aureus (60%) and Enterobacter species (30%). Tuberculous and fungal infections tend to spare the intervertebral disc until late in disease. The frequency of location, in decreasing order, is lumbar> thoracic > cervical spine.
Most cases respond to systemic antibiotics, although epidural abscesses may require surgical drainage, especially if there is cord compression.
The differential diagnosis of discitis and osteomyelitis includes degenerative disc disease, which usually shows decreased signal intensity in the disc on the T2-weighted images. Lymphoma and myeloma spare the disc. Postoperative discectomy may normally show enhancement of the disc space and posterior annulus, but enhancement of vertebral marrow is rare.
References: 1. Modic, et al., Radiologic Clinics of North America, Imaging of the Spine, W. B. Saunders.Philadelphia, PA, Vol. 29, No. 4, 1991, pgs. 813-821.
2. Willing, Atlas of Neuroradiology, W. B. Saunders, Philadelphia, PA, 1995, pgs. 545-548.
Submitted by:Rakesh Shah, M.D.Charles F. Lanzieri, M.D. (uhrad.com).