| Clinical Profile |
| Findings |
| Discussion |
| Pathology |
| Variants |
| On MRI |
| Differential Diagnosis |
| Suggested Reading |
 |
| Clinical Profile |
| Findings |
| Discussion |
| Pathology |
| Variants |
| On MRI |
| Differential Diagnosis |
| Suggested Reading |
|
H/O diminished vision on the right side, headaches,
giddiness, gait imbalance, neck pain, paresthesias in all four limbs and a weak grip
since two months.
There are hyperintense lesions on the T2W and GRASS images within
the cervical spinal cord, centrally and peripherally at the C2 and C5 vertebral levels.
Similar lesions are noted within the dorsal spinal cord at the D9 and D12/L1 vertebral
levels on the T2W sagittal images.
This patient also had lesions in the brain.
Multiple sclerosis is a primary demyelinating disorder (myelinoclastic
disease-myelin destruction whereas there is relative sparing of the axons).
Patients usually present with weakness, numbness and tingling of one or more extremities,
hyperreflexia, focal motor deficits, radicular pain, Brown-Sequard syndrome, Lhermitte's
syndrome, gait disturbance or visual impairment or diplopia. They usually have a
relapsing/remitting pattern. Severe spinal cord affliction is more common with the chronic
progressive type.
The exact etiology is unknown. One of the prevailing views is that an initial viral infection is subsequently followed by an auto-immune reaction with a resultant attack on the myelin. The MS plaques are usually found in the white matter of the cerebrum, cerebellum, brain stem, spinal cord and the optic nerves, chiasm and tracts. CSF may show the presence of oligoclonal bands.
The distribution of MS plaques within the spinal cord is variable. However the earliest lesions are found within the cervical cord. Grossly the plaques are elongated and may extend longitudinally over several centimeters. They have a tendency to be confluent. Usually plaques are found to involve the posterior and lateral segments of the cord and they do not respect boundaries between grey and white matter and specific white matter tracts. The plaques are usually wedge shaped with it's apex pointing to the centre of the cord.
Acute MS plaques
There is destruction of the myelin with axonal sparing. Usually they occur in a perivenular distribution. Neuroglial infiltration, perivascular mononuclear cells/lymphocytes and lipid phagocytosis are also seen. Interstitial edema is noted. White matter is more severely involved than the grey matter. There is a transient break in the blood-cord barrier.
Chronic MS plaques
They usually show gliosis, atrophy and cavitation. Remyelination may be
noted. A thin rim of active myelin breakdown with perivenous lymphocytic cuffing is noted
at the edge of the chronic active plaque. Gliosis is noted at the edge of the chronic
inactive plaque.
Classic-Charcot Type:
Most common form (discussed above).
Acute-Marburg Type:
In younger patients. Usually preceded by fever and has a
relentless course. May be the terminal event in classic MS.
Neuromyelitis Optica-Devic's disease:
Acute onset of spinal cord and optic nerve demyelination.
Diffuse Sclerosis-Schilder Type:
Seen in children. Psychiatric problems are more common. There is
confluent, asymmetric demyelination involving both cerebral and cerebellar hemispheres and
brain stem.
Concentric Sclerosis-Balo Type:
Has a concentric or lamellar pattern. Areas of demyelinated and
myelinated (? remyelination) white matter alternate. Is progressive and seen in young
people.
MS plaques are seen to have well-defined margins. They are hypointense on the T1W images and hyperintense on the T2W, Proton and GRASS images. Larger lesions have a tendency to coalesce and form confluent lesions.
The plaques usually involve the posterior and lateral segments of the cord and they do not respect boundaries between grey and white matter and specific white matter tracts. The plaques are usually wedge shaped with it's apex pointing to the centre of the cord.
Acute lesions may be associated with significant cord expansion which is quite nonspecific on MR.
Focal cord enlargement with increased signal on the T2W, Proton and GRASS images.
The plaques are sharply defined and there is no edema in chronic cord lesions.
Spinal cord atrophy may be seen with chronic disease.
Contrast enhancement is usually homogenous. However a patchy or peripheral (rim like) enhancement pattern may be seen.
There is a decrease in the mass effect after 3 to 4 weeks with near complete resolution of the swelling after 8 weeks.
Brain lesions are usually seen in patients with spinal cord lesions.
Tumors:
To be considered in patients who have a normal brain study and a spinal cord lesion. Primary tumours (astrocytoma or ependymoma), lymphoma or intramedullary metastases may be considered. Increased or unchanged swelling at the end of 3 months would favour a tumour and a biopsy should be considered.
Transverse Myelitis:
Difficult to definitely distinguish it from MS. Furthermore transverse myelitis is known to relapse. Acute transverse myelitis may be the presenting neurologic episode in MS. Immune mediated myelitis usually shows a dramatic response to steroid therapy.
Miscellaneous:
Spinal cord ischemia, contusion and granulomatous infectious processes may be difficult to distinguish from MS in the initial phase.
In MS the time course of the imaging and clinical findings and the findings on paraclinical studies would help in reaching the right diagnosis.