Acute Disseminated Encephalomyelitis (ADEM)

Acute disseminated encephalomyelitis (ADEM) is an immune mediated disease of brain. It usually occurs following a viral infection but may appear following vaccination, bacterial or parasitic infection, or even appear spontaneously. It involves autoimmune demyelination.Full recovery is seen in 50 to 75% of cases, ranging to 70 to 90% recovery with some minor residual disability, with an average time to recover of one to six months.MRI is highly sensitive in detecting white matter lesions and the lesions described are rather extensive and subcortical in location. Involvement of the deep gray matter, particularly basal ganglia, is more frequent. Use of high-dose methylprednisolone, plasma exchange, and IVIG are based on the analogy of the pathogenesis of ADEM with that of multiple sclerosis (MS). Differentiation of ADEM from the first attack of MS is important from prognostic as well as therapeutic point of view. This differentiation is more relevant to India where the incidence of MS is low.

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Dermoids Here and There

Intracranial Dermoids:
Most dermoid tumors have signal intensity characteristics similar to fat—that is, they are hyperintense on T1-weighted images and hypointense on T2-weighted images. Fat-suppression techniques may be helpful in confirming the presence of fat in the lesion. Centrally, dermoid tumors may appear inhomogeneous due to the presence of hair follicles, calcifications, and cellular debris.Rupture of a dermoid tumor can result in fat droplets in the subarachnoid spaces or ventricles.


Spinal Dermoids:
The most frequent site of these tumors is in an extramedullary location; a few may lie in the substance of the cord itself. Complications of the cyst include secondary infection, particularly when associated witha dermal sinus. Rarely these lead to chemical meningitis from the cholesterol-laden keratin released in the subarachnoid space from a ruptured cyst leading to a foreign body type of reaction.


Presacral Dermoid:
A unilocular cystic mass located at or near the midline, with signal intensity similar to that of fat, is highly suggestive of a dermoid tumor.

Submitted by Dr MGK Murthy (Elbit Medical Diagnostics)

Chordoma

Large expansile infiltrative lesion in the S1 and S2 vertebral bodies with pre and paravertebral and epidural components with consequent neural compromise and spinal canal narrowing.
Chordomas are rare tumors that arise from embryonic notochordal remnants along the length of the neuraxis at developmentally active sites.Chordomas are rare neoplasms. As primary intracranial neoplasms, they only constitute 0.2% of all CNS tumors. Chordomas generally occur in 3 locations, which are, in descending order of frequency, the sacrum, intracranially at the clivus, and along the spinal axis.CT scan or MRI studies are indicated to evaluate the extent of the tumor and to identify the tissues that the chordoma has infiltrated.The 5-year survival rate is estimated to be 51%, and the 10-year survival is estimated to be 35%. Factors that may improve prognosis are young age, complete resection, and the addition of radiation therapy in incompletely resected tumors.

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Coexistent Carcinomas

Known case of prostatic carcinoma with increased PSA levels and osteoblastic metastasis in the spine. Interestingly this patient also had para-aortic adenopathy and a testicular swelling. This could well represent metastatic lymphadenopathy but the question of coexistent prostatic and testicular carcinomas should be raised. The incidence of coexistent malignancies is high in the elderly.

Malignant chacracteristics of a breast lesion

MRI - Sensitivity - 93% Specificity - 70%
1. Opacity
2. Enhancement pattern : patchy
- invasive: pheripheral or rim
- DCIS : linear
3. Type 3 time intensity curve
- early steep rise within 5 mts with a 70% increase in SI
- rapid washout
4. Tumour recurrence – radiation fibrosis does not enhance after 18 mts

Ultrasound :
Poorly reflective
Ill defined
Heterogenous internal echo pattern
Absent farwall echoes
Posterior acoustic shadowing
Taller than wide


Mammography:UOQ - 50% Retroareolar 18%
Opacity - stellate,spiculated,comet tail
- high density
- nonhomogenous
- wide halo
Asymmetric Density
Microcalcification – 30% of cases
- < 0.5 mm & > 5 particles per cc
- segmental, cluster distribution
- pleomorphic : linear, branching, punctate
- eccentric location in opacity

Local Gigantism of Right Ankle and Foot

Large diffuse irregular hypertrophy of the soft tissues involving the distal leg, ankle and foot on the right side. No evidence of phleboliths or signs of arteriovenous fistulae or fat elements. The differential here for local gigantism would include Klippel Trenaunay Syndrome and Plexiform Neurofibromatosis.
Klippel-Trenaunay syndrome (KTS) is defined by the presence of a combined vascular malformation of the capillaries, veins, and lymphatics, congenital venous abnormalities, and limb hypertrophy. Most patients with KTS can be treated conservatively with compression stockings or pneumatic pumps. Compression stockings decrease edema, act as a barrier for minor trauma, and reduce venous insufficiency.
Surgical Care - Servelle reported successful surgical intervention (resection or ligation of abnormal blood vessels) in more than 700 patients with KTS. Most medical centers have tried to avoid surgical intervention. Surgical treatment can be complicated by infection, lymph seepage, and skin breakdown. Intravenous sclerotherapy has been proposed as an alternative to surgical intervention in KTS and to embolization in PWS. Reports exist of the use of a sclerosant in microfoam.
Clinicians at all centers agree that a leg length discrepancy of more than 2.0 cm warrants epiphysiodesis. Hypertrophied digits with severe deformity and infection may require amputation.

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Posterior Reversible Encephalopathy Syndrome (PRES)

Multiple illdefined irregular altered signal intensity areas involving both parietoccipital regions in parasagital location.
Posterior Reversible Encephalopathy Syndrome (PRES) or Reversible Posterior leukoencephalopathy syndrome (RPLS) is an increasingly recognized neurologic disorder with characteristic computed tomographic (CT) and magnetic resonance (MR) imaging findings, and it is associated with a multitude of diverse clinical entities. These include acute glomerulonephritis, preeclampsia and eclampsia, systemic lupus erythematosus, and thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome, as well as drug toxicity from agents such as cyclosporine, tacrolimus, cisplatin, and erythropoietin. Most, but not all, cases manifest with acute to subacute hypertension, and seizures are also frequent. Classic CT findings are those of bilaterally symmetric low attenuation in the posterior parietal and occipital lobes, whereas MR imaging demonstrates hyperintensity on T2-weighted images in the same distribution.
Two pathophysiologic mechanisms for RPLS have been proposed. One postulates cerebral vasospasm with resulting ischemia within the involved territories, whereas the other posits a breakdown in cerebrovascular autoregulation with ensuing interstitial extravasation of fluid. Diffusion MR imaging can be used to discriminate between these two possibilities, as the cytotoxic edema of cerebral ischemia demonstrates decreased water mobility, whereas vasogenic edema due to cerebrovascular autoregulatory dysfunction results in increased water mobility.

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