Sunday, 21 June 2015

Spinal Epidermoid cyst MRI

Clinically: A 30 y o male with neurogenic bladder. 
video

Findings:

This MRI lumbar spine show a spinal intra dural cystic signal intensity well defined lesion hypo intense on T1, hyper intense on T2 with restricted diffusion on Dw images. 
An associated expansion and scalloping of bony spinal canal. 
Lesion is confined to spinal canal and not extending out of neural foramen. 
Lesion is non enhancing on post contrast, except thin rim of enhancement on post contrast T1. 

Imaging diagnosis : Spinal Epidermoid Cyst.

Urinary bladder show diffuse wall thickening, irregularity with trabeculations attributed to associated Neurogenic bladder. 

Spinal Epidermoid Cyst

They are usually extra medullary but rarely can be intra medullary. They may be congenital or acquired.
Spinal epidermoid cysts are uncommon.

Unlike intracranial epidermoid cysts, which are almost always congenital in origin, most of spinal epidermoid cysts are acquired. Although present since birth, congenital epidermoid tumours often do not present until the second to fourth decade of life.
Males are more commonly affected than females.

Spinal epidermoid cysts may asymptomatic and discovered incidentally. If symptomatic, motor disturbances, pain, sensory disturbances, and bowel or bladder dysfunction may be present.
Congenital spinal epidermoids result from anomalous implantation of ectodermal cells during closure of the neural tube between the third and fifth week of embryonic life.
Acquired spinal epidermoids are a late complication of lumbar puncture, resulting from implanted epidermal elements into the spinal canal. The time interval between lumbar puncture and tumour diagnosis ranges from 1 to more than 20 years. Acquired spinal epidermoids are generally extramedullary and situated near a vertebral interspace.

Congenital epidermoids usually occur at the conus or cauda equina. Acquired cysts are found in the lower lumbar region.
Epidermoid cysts are commonly associated with spinal malformations such as spina bifida and hemivertebrae.
On CT, a well circumscribed mass, hypodense (similar to CSF),  minimal to no enhancement on post contrast, calcification is rare. Associated osseous changes include an expanded spinal canal, laminar thinning and vertebral body scalloping. 
On MRI typical signal characteristics include hypointense (similar to CSF) on T1, hyperintense (similar to CSF) on T2 and slightly hyperintense compared to CSF on FLAIR due to incomplete signal suppression. On T1 C+ (Gd) no enhancement or a thin rim of capsular enhancement. Characteristic bright signal on Diffusion with corresponding low intensity on ADC map. Signal intensity may be homogeneous or heterogeneous according to the variable water, lipid and protein composition of the cyst.

Spinal epidermoid cysts are slow growing.
Surgery is the treatment of choice, complete excision.
If the cyst wall is tightly adherent to the cord parenchyma, the wall should be left in place, however this leads to a risk of recurrence.

Differential diagnosis include spinal arachnoid cyst which lacks brightness of restricted diffusion on DWI, complete signal suppression on FLAIR. Vertebral anomalies uncommon.
Spinal dermoid cyst usually contains fatty elements, less likely to demonstrate diffusion restriction on DWI, patients are usually younger than 20 years of age.
Spinal neurenteric cyst common in thoracic and cervical regions, ventral to spinal cord with associated vertebral anomalies. 

AVM with bleed and ischemic complications on MRI

Clinical Details  : Two months ago suffered from a left basal ganglionic bleed. Had to have decompression done. PResently has a power of grade 0 on the right arm and right leg but speech is fairly well preserved. 
Presently on Ecosprin gold, Omnacortil. Pantocard.

Advised MRI for better evaluation

video

MRI Brain with MR Angiography of Brain Report

Sequences planned are FLAIR, T2w*GRE and DW images.
Non Contrast Enhanced intracranial Angio performed with 3D TOF and Neck Angio performed with 2D TOF sequence. The study viewed in row as well as 3D reconstructed images.

A focal Gliosis  with hemosiderin staining on GRE involving left thalamus, adjacent basal ganglia, insula and temporal lobe_ Chronic resolved hematoma with areas of chronic ischemic infarcts in left MCA cortical branches territory. 
An associated changes of distal wallerian degeneration on left side. 
An obvious high flow vascular malformation _ AVM noted, left pcom appears to be the feeder. 
Sparisty of cortical branches of left MCA. 

Rest of the both intra cranial as well as extra cranial vessels show normal flow related signals on 3D reconstructed images of Non Enhanced 3D TOF and 2D TOF sequences.

Impression: 

Chronic resolved hematoma with chronic infarcts in left MCA cortical branches territory.
An obvious high flow vascular malformation / AVM noted, left pcom appears to be the feeder. 
Sparisty of cortical branches of left MCA compared to right.

Needs DSA for better evaluation / confirmation. 

Tuesday, 16 June 2015

Atypical Trigeminal Neuralgia MRI

Clinical details: right side trigeminal neuralgia.


MRI BRAIN FOR TRIGEMINAL NERVES

Multi planner multi echo MRI study of brain has been performed. Sequences planned are FSE T1W, FSE T2W, FLAIR, T2w *GRE and DW images. FIESTA for cranial nerves.
Pc t1

This MRI Brain shows:
Abnormal T2 hyper intensity in right half of Pons at the entry point of right side trigemninal nerve, and adjacent right side trigeminal nerve_ significant for patients clinical complaints.
There is faint high signal on DW images in corresponding region.
No abnormal enhancement on post contrast T1.

Possibilities given were Demyelination, Ischemia.

He was prescribed
Amytryptiline 25 mg HS
Wyselon 20mg daily for 5 days, 10 mg for next 5 day and then stop
Gabapentine 300mg BD

During follow up after 2 weeks
He was clinically improved by 75 % which goes in favor of Demyelination.
During this follow up, MRI imaging shows lesion is same in size without any significant change on T2w images. The faint hyper intensity which was seen in previous MRI was reduced.
Advised further follow up imaging.

Current clinical status after 2 months, 100% improved.

There are persuasive evidences that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem at the entry point of nerve. However in most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein.

Tuesday, 2 June 2015

Unilateral Optic Nerve Aplasia

Clinically a premature baby, Ophthamological evaluation revealed abnormally small Optic disc on right side. Advised MRI for further evaluation. 
MRI brain shows absent right side optic nerve, its intra cranial as well as intra orbital portion.
Left side optic nerve normal in caliber and signals, left half of optic chiasm and bilateral optic tracts normal. No associated anomalies of corpus callosum or septum pellucidum. Pituitary gland normal, no posterior lobe ectopia.

Impression: Congenital Unilateral Optic Nerve Aplasia.

Optic Nerve Aplasia 

A rare developmental anomaly characterized by the congenital absence of the optic nerve, central retinal vessels and retinal ganglion cells.
Aplasia is often unilateral, generally associated with otherwise normal brain development while bilateral optic nerve aplasia is usually accompanied by severe and widespread CNS malformations.
The pathogenesis of optic nerve aplasia may be due to defective formation of the embryonal fissure, failure of the mesenchymal anlage of the hyaloid system to enter the embryonal fissure, or primary agenesis of the retinal ganglion cells.

Optic nerve hypoplasia is seen ophthalmoscopically as an abnormally small optic nerve head. A peripapillary ring around a small optic disc is the hallmark, but is not always present. ONH may be associated with tortuosity of the retinal vasculature. A relative afferent pupil defect adds weight to the diagnosis.

ONH is commonly asymptomatic and may first be detected by identification of visual field loss or observation of the optic nerve head.

Associations,
1. Isolated ONH.
2. Absent septum pellucidum.
3. Posterior pituitary ectopia (commonly associated with endocrine dysfunction).
4. Migrational anomalies in the cerebral hemispheres (for example, thinning of the corpus callosum, which is predictive of neurodevelopmental problems). Other associated brain abnormalities include porencephaly, schizencephaly, intracranial arachnoid cyst, and intracranial epidermoid cyst.

Septo-optic dysplasia comprise any combination of ONH, pituitary gland hypoplasia, and midline abnormalities of the brain. Recent studies have shown that in SOD, key mutations have been identified in Hesx-1, a protein that is involved in the mediation of normal development of the forebrain and the eyes during embryogenesis.