Wednesday, 15 April 2015

Frontal subcortical white matter cystic lesions MRI

A 30 y o male with headache.
MRI Brain with contrast shows:






Multiple T2 hyper intense well defined cystic foci in right frontal sub cortical white matter.
Lesions are iso intense to Csf on all pulse sequences.
No abnormal enhancement on post contrast T1.
No obvious restricted diffusion or hemosiderin staining on GRE in corresponding region.
No significant mass effect.
No adjacent white matter Gliosis.
No obvious calcification on CT sections.
Rest of the MRI brain within normal limits.

These appears to be benign lesions, and incidental finding not related to patient's headache.
Possibility given was Enlarged peri vascular spaces ( ' V R Spaces') and advised EEG correlation.
EEG was unremarkable.

Follow up imaging after 6 month revealed no change which again favors imaging diagnosis of Enlarged peri vascular spaces.

Bilateral Hypertrophic Olivary Degeneration MRI

A 50 y o was admitted after acute onset of unconsciousness. On admission MRI brain reveled hypertensive Pontine bleed extending in adjacent mid brain. His clinical condition gradually improved.

On follow up after 6 month pt was alert, dysartric, bilateral dysmetria of the arms without paresis, bilateral horizzontal gaze paresis. No palatal myoclonus.

During this 6mth follow, MRI  shows;
A resolved chronic Pontine bleed with,
New bilateral and symmetric T2 hyper intense foci with mild swelling in the region of inferior olivary nuclei of medulla suggestive of bilateral hypertrophic inferior olivary degeneration. 

Hypertrophic olivary degeneration ( HOD)

Hypertrophic olivary degeneration is a rare finding secondary to focal lesions of the brain stem involving Guillain–Mollaret triangle.

The three corners of the triangle are:
1.             Red nucleus.
2.             Inferior olivary nucleus
3.             Contralateral dentate nucleus.

In CNS the degeneration of an anatomical structure is usually characterized by neuronal loss replaced by proliferation of glial elements.
Unique to the inferior olivary nucleus is transneuronal degeneration resulting in hypertrophy.
Clinical presentation is Palatal myoclonus, a classically described feature.
Interruption of either of the connections between the dentate nucleus and contralateral red nucleus (dentatorubral tract, superior cerebellar peduncle) or the connection between the red nucleus and ipsilateral inferior olivary nucleus (central tegmental tract) leads to changes in the olive.
In short hypertrophic olivary degeneration can be caused by any lesion involving the above mentioned structures, it is typically seen with focal lesions involving the ipsilateral central tegmental tract, the contralateral superior cerebellar peduncle, or the dentate nucleus.
Isolated lesions of the inferior cerebellar peduncle do not cause HOD, as anatommically there are no direct connections between the inferior olivary nucleus and the contralateral dentate nucleus.

Pathologically, cell body enlargement, vacuolation of the cytoplasm, astrocytic hyperplasia and proliferation, demyelination, and fibrillary gliosis have been described.

Hypertensive bleeding is a relatively common cause of pontine haemorrhages resulting in hypertrophic olivary degeneration.

Imaging wise the inferior olivary nucleus or nuclei gets larger and increases in T2 signal intensity. Typically, within a few months T2 signal increases and lasts 3-4 years, whereas hypertrophy occurs later (at about one year), and resolves by 3-4 years.
On imaging DDs include infarction, demyelination, Neoplastic, metastases, lymphoma, infection, including tuberculoma.

T2 hyperintense non enhancing lesion that is accompanied by enlargement of the olivary nucleus, particularly if bilateral and symmetric, as our patient, can be explained only by hypertrophic olivary degeneration. Typically T 2  hyperintensity is evident on follow up imaging  the signal abnormality was absent in the on admission MR imaging. In the next few months the patient could complain palatal myoclonus which is not evident now.

Most commonly a lesion involving central tegmental tract causes unilateral olivary degeneration. Our patient is having bilateral hypertrophic degeneration from lesion located in the midbrain and Pons.

Sunday, 5 April 2015

MELAS

A 15 y o male with altered sensorium. 

Here is CT Brain study. 


CT study of Brain shows bilateral symmetric chronic lacunes in bilateral caudate nuclei.
Rest of the CT brain normal.
No associated atrophy or cortical involvement.

I really got surprised when I noted the clinical history.
Patient was a known case of MELAS, laboratory Studies with abnormal reports of Serum lactic acid, serum pyruvic acid, cerebrospinal fluid (CSF) lactic acid, and CSF pyruvic acid noted.

Imaging findings are actually atypical for MELAS.

The typical radiographic features of MELAS includes multiple acute and chronic infarcts in multiple vascular territories, may be either symmetrical or asymmetrical. Parieto-occipital and parieto-temporal involvement is most common. Associated basal ganglial calcification and atrophy.

MELAS (mitochondrial encephalopathy with lactic acidosis and stroke-like episodes) is one of many mitochondrial disorders, only inherited from the mother, characterised by 'stroke-like' episodes, typically in childhood or early adulthood. 90% present before 40 years of age.
Clinical presentation usually has a relapsing remitting course with or without superimposed accretion of permanent deficits.
Clinical presentation is characterized by stroke like episodes, encephalopathy, seizures, dementia, lactic acidosis, muscle weakness, deafness. 

Astrocytoma vs Ependymoma

These common spinal cord neoplasms, differentiating Astrocytoma vs Ependymoma imaging wise is challenging, sure differentiation is out of imaging consensus however the combination of following set of findings can be used to give a more likely possibility of one over other.
Again it is one of favorite questions in FRCR 2A.

Astrocytomas are common in Children, Thoracic region, Eccentric lesion in spinal cord, Ill defined margins, Long segment involvement , No to faint enhancement on post contrast. 

Ependymomas are common in Adult, Cervical region, Central location in spinal cord, Well defined margins, Short segment involvement of cord, Avid enhancement on post contrast, Associated with cord syrinx, intralesional Bleed and Spinal canal remodeling.  

Cholesteatoma vs Cholesterol Granuloma


This is one of favorite questions in FRCR 2A exam. 

Appearances of Infarct on Diffusion and ADC with time


This is one of favorite questions in FRCR 2A exam. 

Toxoplasmosis Vs Lymphoma

It’s some times challenging to differentiate Toxoplasmosis Vs Lymphoma imagingwise as both of these are common in immune compromised patients, again its one of favorite questions in FRCR 2A.

Sure differentiation is out of imaging consensus however the combination of following set of findings can be used to give a more likely possibility of one over other.

Hypo dense to hyper dense lesion on CT, involvement of Basal ganglia, intra lesional bleed or hemosiderin staining on MRI GRE, Multiplicity of lesions, Rim enhancement on Contrast, an associated eccentric nodule goes in favor of Toxoplasmosis over Lymphoma.

Whereas hyper dense lesion on CT,  involvement of Peri ventricular white matter, an associated sub ependymal spread of lesion, Single lesion, Homogenous enhancement in immune component and rim enhancement in immune compromised goes in favor of Lymphoma over Toxoplasmosis.

Saturday, 4 April 2015

Occipital Encephalocele MRI


Discal Cyst MRI Lumbar Spine

A 44-year-old male with low backache with left lower  limb radiating pain, straight leg raising test positive at 40 degrees in the left leg. Rest of the neurological examinations normal.


MRI revealed a well defined spherical extra dural cystic lesion with low signal intensity on T1 and high signal intensity on T2 antero lateral to thecal sac at L4-5 level. 

Imaging wise possibility of discal cyst was given compressing left traversing L5 nerve root in lateral recess.
Left partial hemilaminectomy at L4-5 revealed blue colored cyst compressing the left traversing L5 nerve root. The cyst contained serous fluid without blood. A connection between the cyst and the disc was identified, and the cyst was removed at the base of the connection by dissecting the annulus fibrosus.
Histopathological examination of the cyst revealed fibrous connective tissue with hemosiderin deposits without lining cell layers, no disc materials.
The patient's low back pain and radiating pain in the left leg improved remarkably immediately after surgery.

Discal Cyst

The discal cyst is a new clinical entity and it communicates with the intervertebral disc. More and more cases are now diagnosed with advent of MRI. Histologically, intraspinal cysts of the facet are referred to as synovial cysts. Although the difference between discal cysts and synovial cysts is based on the presence of lining cells.  The clinical symptoms of patients with discal cysts are indistinguishable from those of patients with a typical disc herniation manifesting as a unilateral single nerve root lesion. MRI and discography are useful for obtaining a presumptive diagnosis of this disease.

MRI features of discal cysts are a ventrolateral extradural cyst attached to a lumbar disc with or without rim enhancement on contrast enhanced MRI, occasional extension in lateral recess. These MRI features are the key to differentiating between a discal cyst and lumbar disc herniation. Discography and CT discography provide a connection between the cyst and the corresponding disc, and it is possible to differentiate discal cysts from lumbar disc herniation and other intraspinal cysts. However, need of this differentiation is controversial because the line of management is same for both of them. Removal of the cyst leads to symptom improvement, regardless of its origin.

The pathogenesis of discal cysts is still unclear. Several pathogeneses, such as resorption of a preexisting herniation and hematoma associated with a disc prolapse, have been suggested. Kyo et al. reported a case of discal cyst with an annular defect of the corresponding disc. Jeong and Bendo argued that the underlying pathological mechanism of discal cysts is a subsequent change in a herniated disc material. Tokunaga et al. confirmed the presence of cartilaginous tissue in the cyst wall and thought that the discal cyst might have developed from the absorption process of an intervertebral disc herniation. Chiba et al. proposed that discal cysts arise first from an underlying intervertebral disc injury that causes an annulus fibrosis fissure in the posterior intervertebral disc. Hemorrhage from the epidural venous plexus with a rich blood flow then occurs in the space between the peridural membrane and the vertebral body.
Whatever the pathogenesis may be, a discal cyst is responsible for the development of the symptoms in patients. Most of the discal cysts have been treated surgically. Lee et al. reported a case of recurrence among nine patients of discal cysts who underwent surgery at one year follow-up after the operation. It is suggested that careful long-term follow-up is necessary after surgery.

In 2007, Chou et al. reported a case of spontaneous regression of a discal cyst, patient who was treated with a routine epidural injection and selective nerve root block, and the discal cyst regressed spontaneously after 5 months. However, it is unclear whether steroid injection contributed to the regression of a discal cyst. Nevertheless, it is important to consider that although steroids influence the regression of discal cysts, potential spontaneous regression may also occur in discal cysts.
Standard therapeutic guidelines for discal cysts have not been established because the natural history and the long-term prognosis of discal cysts treated by surgery or percutaneous CT-guided aspiration and steroid injection are still unknown.

Reference : Discal Cyst of the Lumbar Spine J Korean Neurosurg Soc. 2008 Oct; 44(4): 262–264. Jae Ha Hwang, M.D., In Sung Park, M.D.

Temporal Bone Fracture with Facial Nerve Palsy

A middle aged male with h.o. RTA.
Now present with right side Facial nerve palsy and Deafness.

Here is CT study of brain with Bone window images as the level of petrous temporal bone: 

CT study shows non depressed fracture involving occipital bone extending anteriorly to involve petrous bone. The fracture line is running transverse to petrous axis, involving internal auditory canal and vestibule appears to be the cause of patient's right side facial nerve palsy and sensory neural hearing loss. 

Petrous Temporal Bone Fractures

Temporal bone fracture is encountered in 75% of all skull base fractures.
There are 3 subtypes of temporal fractures are longitudinal, transverse, and mixed.

A. Longitudinal fractures occurs in the temporo parietal region and involves the squamous portion of temporal bone, superior wall of the external auditory canal, and the tegmen tympani. These fractures may run either anterior or posterior to the cochlea and labyrinthine capsule, ending in the middle cranial fossa near the foramen spinosum or in the mastoid air cells, respectively. Longitudinal fracture is the most common of the 3 subtypes (70-90%) and associated with conductive deafness due to ossicular chain disruption.

B. Transverse fractures begin at the foramen magnum and extend through the cochlea and labyrinth, involves internal auditory canal, ending in the middle cranial fossa (5-30%), are associated with sensory neural deafness and facial nerve palsy.

C. Mixed fractures have elements of both longitudinal and transverse fractures.

Another classification system of temporal bone fractures has been proposed. This system divides temporal bone fractures into petrous and non petrous fractures; the latter includes fractures that involve mastoid air cells. These fractures do not present with cranial nerve deficits.