Monday 31 December 2012

Brachial plexus injury MRI

A 20 Yrs Male. 
Clinical Details  : About 8 days ago sustained a fall off a bike. Thereafter has noted weakness of the right arm. No past history.
Examination shows weakness of supraspinatus, infraspinatus, rhomboids, deltoid, biceps, wrist extension. Mild weakness of wrist flexion. Normal triceps. Sensations are impaired especially from C5 to C6.

MRI study of cervical spine shows mild loss of normal cervical lordosis.
Spinal cord and exiting nerve roots normal.
MRI FOR BRACHIAL PELXUS performed with Coronal STIR, Cor FIESTA, Axial T2, STIR and MR Myelography.
This axial T2w MRI study of Brachial plexus shows:
T2 hyper intensity of fluid between right side anterior and middle scalene muscles attributed to odema / hematoma, the region corresponds to the course of Brachial plexus. Injury to right side Brachial plexus possible here.

Thursday 20 December 2012

Empty Sella MRI

MRI Brain
This mid sag T2w section shows:
Roomy hypophyseal fossa occupied by Csf. 
Pituitary flat at the floor near posterior wall of sella with an abnormal height less than 2mm.

Saturday 15 December 2012

Congenitally Absent 6th CN on MRI in Duane's Retraction Syndrome

A 6 month old baby with congenital left side abduction deficit.
Clinical diagnosis: Duane's Retraction Syndrome.
MRI Brain performed for 6th CN with MRI Orbit.
Sequences planned are FSE T1W, FSE T2W, FLAIR, and DW images show no significant abnormality in Brain parenchyma and region of cavernous sinuses.
Axial and Coronal T1 T2 STIR for orbit show normal optic nerves and extra occular muscles.
On Axial FIESTAs for Cranial Nerves 6th CN not visualized on left side. Cisternal portion of Right side normal 6th CN nerve marked with arrow. Rest of the CNs normal, particularly facial and trigeminal nerves. Normal symmetric cisternal portions of bilateral occulomotor nerves.

Cisternal portion of left side 6th CN not visualized - Congenitally absent.
Consider the diagnosis Duane's Retraction Syndrome (DRS) clinically.

NB: Characteristic diagnostic signs of DRS (congenital abduction deficit accompanied by retraction of the globe on attempted adduction) might not be manifested in early childhood or may be difficult to evaluate, a successful demonstration of absence of the abducens nerve on MRI strongly suggests DRS in children with abduction deficit - Reference: AJNR 2005 26: 702-705 MR Imaging in DRS, Jae Hyoung Kim.

Duane's Retraction Syndrome

Syn: Duane's syndrome (DS)
A rare, congenital disorder of eye movement characterized by the inability of the eye to abduct, to move outwards. The condition involves neural pathways associated with the sixth cranial nerve.
DRS was first described by Jakob Stilling in 1887 and Siegmund Türk in 1896 and subsequently named after Alexander Duane who discussed the disorder in more details in 1905. Other names for this condition include Eye Retraction Syndrome, Sausage Eye, Retraction Syndrome, Congenital retraction syndrome and Stilling-Turk-Duane Syndrome.

As described by Duane, the characteristic features of the syndrome are:
1. Limitation of abduction (outward movement) of the affected eye.
2. Less marked limitation of adduction (inward movement) of the same eye.
3. Retraction of the eyeball on adduction, associated narrowing of the palpebral fissure (eye closing)
4. Poor convergence.
5. A face turn to the side of the affected eye to compensate for the movement limitations of the eye(s) and to maintain binocular vision.
6. Eye is 45゚ to left or right, resulting in "correct movement", but wrong placing of eye. (i.e. when an unaffected eye looks to the right, the affected eye looks straight forward, and when the unaffected eye looks straight forward, the affected eye looks to the left)

DRS is a miswiring of the eye muscles, causing some eye muscles to contract when they are not not supposed to contract and other eye muscles not to contract when they are supposed to contract.
Alexandrakis G and Saunders state that in most cases, the abducens nucleus and nerve are absent or hypoplastic, the lateral rectus is innervated by inferior division of the oculomotor nerve. This misdirection of nerve or mis wiring results in opposing muscles being innervated by the same nerve at  the same time. Thus, on attempted abduction, stimulation of the lateral rectus via the oculomotor nerve will be accompanied by stimulation of the opposing medial rectus via the same nerve. Thus, co-contraction of the muscles takes place, limiting movement and resulting in retraction of the eye into the socket.

Most patients are diagnosed by the age of 10 years, more common in girls. Around 10–20% of cases are familial. Duane syndrome can be associated with extraocular problems (so-called "Duane's Plus"), including cervical spine abnormalities (Klippel-Feil syndrome), Goldenhar syndrome, autism, heterochromia, and thalidomide-induced embryopathy.

The majority of patients remain symptom free, able to maintain binocularity with only a slight face turn. Amblyopia is uncommon, if present, rarely dense.
Duane syndrome cannot be cured, as the "missing" cranial nerve cannot be replaced.
Surgical intervention recommended only when patient is unable to maintain binocularity or a cosmetically unsightly or uncomfortable head posture in order to maintain binocularity. The aims of surgery is to place the eye in a more central position. Again surgery is not needed during childhood and is appropriate later in life, as head position may change further presumably due to progressive muscle contracture.

Sunday 9 December 2012

Os Odontoideum MRI

An uncommon craniovertebral (CV) junction abnormality characterized by a separate ossicle superior to the dens.
Separation of the odontoid process from rest of the body of the axis was first described in a post mortem specimen In 1863.
Giacomini coined the term os odontoideum for this condition in 1886.

The entity is clinically important because a mobile or insufficient odontoid process renders the transverse ligament ineffective at restraining atlantoaxial motion.
Many cases detected incidentally, others are diagnosed when become symptomatic.

There is continuing controversy over its etiology. Initially, os odontoideum was thought to represent a congenital failure of fusion of the dens to the remainder of the axis. Now its clear that failure of the secondary ossification center of the dens to fuse with the base of the odontoid represents a separate entity known as persistent ossiculum terminale and the Os odontoideum actually represents a previous fracture of the odontoid synchondrosis before its closure at age 5-6 years. There is high incidence of Oo in Morquio syndrome, Multiple epiphyseal dysplasia, Down’s Syndrome.

Size/shape vary with smooth cortical borders (the differentiating point from fracture)
Orthotopic – In normal position at tip of dens.
Dystopic – Displaced towards base of occiput where it may fuse with clivus or anterior ring of C1.

Xray: Open-mouth, anterior-posterior, and flexion-extension lateral radiograph may demonstrate a Gap separating the OO and axis proper. An associated hypertrophy of anterior arch of C1
CT with sagittal CT reconstruction give more detail into the atlanto-axial junction
MRI to evaluate spinal cord for any compression.
Fluoroscopy to show instability

Differential Diagnosis include Persistent ossiculum terminale, True hypoplasia of odontoid peg, Neurocentral synchondrosis, Odontoid fracture nonunion.

Oo predisposes to increased risk of cranio-vertebral junction trauma.
Pt may present with acute neurological dysfunction. Torticollis, localized pain, neurovascular compromise signs.
If cord compression may require neurosurgery.

Conjoined Nerve Root MRI

MRI Lumbar spine
Axial T1w images at the level of L4-5 disc show asymmetrical appearance of thecal sac due to conjoined L5 and S1 nerve root on left side.
In first section, only right side L5 nerve root has emerged out. There is no corresponding L5 nerve root on left.
In second section an ovoid out pouching from thecal sac on left side due to combined exit of L5 and S1 nerve root. Same separate and single L5 nerve root in lateral recess on right.
In last section on left side both L5 and S1 nerve root seen intra spinally in lateral recess. The same separate L5 nerve root in right lateral recess. The right S1 nerve root is about to emerge seen as a small bulge from thecal sac on right side.

Conjoined nerve root

Syn: Composite nerve root sleeve.
A type of developmental anomaly involving nerve root.
The term conjoined nerve root actually refers to the roots of 2 adjacent segments, arising at the same level from the thecal sac, enveloped by a common root sleeve.
Nerve roots usually exit separately at expected neural foraminal levels. Occasionally both the nerve roots exit through the same usually the lower foramen.
It is the commonest nerve root developmental anomaly of the cauda equina.
Often unilateral.
Most common location is lumbar spine in that commonly involves L5 and S1 nerve root.
The incidence in cadaveric studies is about 8% and 6% in MRI study.

The nerve root anomaly itself does not cause symptoms.
Usually asymmptomatic.
Symptomatic patient present with radiculopathy. Conjoined nerve roots are more prone to compression by degenerative processes of disc or facetal joint.
It is important to know about this normal anatomical variation as it may be confused with disk herniations, possible with poor quality MR images. Axial slices should be contiguous over several segments. Typical signs include asymmetry of the anterolateral corners of the dural sac, excess extradural fat between the asymmetric dura and the nerve root, parallel course of the affected nerve roots at the disc level

MRI is the investigation of choice. Associated findings may be enlarged or asymmetric neural foramen or lateral recesses, hypoplastic or absent pedicle. Association mentioned with vertebral anomalies such as vertebral arch defects, spondylolisthesis, spina bifida, absence of the ipsilateral facet joints.

Natural history and prognosis is asymptomatic patients requires no treatment. Rare symptomatic patient with pain referable to conjoined nerve root may require surgery. Symptomatic undiagnosed cases of conjoined nerve root are one cause of failed back syndrome. 

Vertebral venous plexuses MRI

Axial section through the body of a thoracic vertebra, showing the intra osseous veins draining basivertebral vein in Y’ / ‘V’ shape configuration.
Basivertebral veins are tortuous vascular channels in the vertebral bodies, unite with the longitudinal prevertebral veins anteriorly and the anterior epidural venous plexus posteriorly. These intra osseous veins should not be mistaken for a compression fracture in cases of asymmetry.

Scheuermann's disease MRI

MRI Cervico Dorsal region spine sagittal T2w images show multiple and contiguous involvement of vertebral bodies in dorsal region.
Antero posterior elongation of vertebral bodies.
Associated Schmorl's nodes, end plate irregularity and disc space narrowing.
Reduced height with anterior wedging of D5, exaggerated kyphosis.
Findings are Classical of Scheuermann's disease.

Scheuermann's disease
A k a Scheuermann kyphosis.
A common condition resulting in kyphosis of the thoracic or thoracolumbar spine.
Low back pain in adolescents, the Schueurmann's disease must be considered.
A plain Xray film is sufficient for diagnosis.
Incidence : ~ 0.4 to 8% of the general population.
Strong hereditary predisposition present (Autosomal dominant).
Adolescent males.
M = F

The most common and classical form of Scheuermann's disease occurs in thoracic region.
The Lumbar variant of Scheuermann's occurs in lumbar or dorso lumbar region.

Imaging wise Diagnostic criteria for classical Schuermann's:
- Degree of kyphosis, for dorsal region should be more than 45 degree (normal 25 - 40 deg) and for dorso lumbar region more than 30 degree (normal 0 deg)
- Multiple and contigenous involvement of vertebral bodies, at least 3 adjacent vertebrae demonstrating wedging.
- Antero posterior elongation of vertebral bodies.
- Associated Schmorl's nodes.
- End plates irregularity which are normally flat.
- Disc space narrowing.

Lumbar Scheuermann's Disease

Type I or classic Lumbar Schuermann's shows hallmark wedging deformities of the vertebrae similar to Thoracic Scheuermann's kyphosis.
Type II or atypical Lumbar Schuermann's does not have a wedging deformity of the vertebrae. Instead the vertebrae maintain their normal squared shape. Severity of kyphosis is also mild. This variant is known as "acute traumatic intraosseous disc herniation." This is characterized by a history of a traumatic event – usually a fall – and includes a fracture of the bony endplate with disc material herniating into the bone.


The true cause of Schuerman's disease is not known.
Proposed theories include mechanical compression during growth, acute disc injuries, hormonal variations, and genetic factors as the cause. None is proven.

Treatment is symptomatic.
Surgery for severe kyphosis.

Ali RM, Green DW, Patel TC. Scheuermann's kyphosis. Curr. Opin. Pediatr. 1999;11 (1): 70-5.
Lowe TG. Scheuermann disease. J Bone Joint Surg Am. 1990;72 (6): 940-5.

Central Pontine Myelinolysis

A 60 y o female with altered consciousness accompanying with a file of previous hospital admission and lab reports mentioning abnormal levels of Na and K. 

On Admission MRI T2w images show T2 hyperintensity confined to centre of Pons. No abnormal restricted diffusion on Dw images.
MR Angiogram of Brain show no significant major vessel stenosis or occlusion.
Basilar normal.
Recent lab reports mentions normal Na+. Slightly raised Cl-

Imaging diagnosis: Central Pontine Myelinolysis (CPM) / Osmotic Demyelination.

Follow up MR Images after 1 month show:
Foci of Gliosis in Pons.
No abnormal enhancement on post contrast T1 supports clinical and imaging diagnosis of CPM.

Central Pontine Myelinolysis 
Syn : Osmotic Demyelination Syndrome, ODMS.
An acute demyelination caused by rapid shift in serum osmolarity.
Classic setting is rapid correction of hyponatremia.
ODMS may occur in Normonatremic patients (Reports with normal Na+ levels are known).
CT; may be normal. May show faint hypodensity confined to center of Pons. Non enhancing on post contrast.
MRI; T2 hyperintensity confined to center of Pons seen in ~50% of cases. Diffusion may be normal or may show faint high signal.
May involve basal ganglia and cerebral white matter without Pontine involvement is called Extra Pontine Myelinolysis. Pontine and Extra Pontine involvement together is pathognomic for ODMS.

Infarct: Usually off midline and unilateral as commonly occur due to occlusion of perforators arising from basilar. May affect centre of Pons and extending to periphery if there is complete basilar occlusion, restricted diffusion on Dw images, an associated basilar occlusion on MR Angio.
Neoplasm: Imaging Pontine Glioma may confuse with CPM. Clinically CPM has acute debilating course. Pontine Glioma pt will be young, clinically stable with slow progressive symptoms, without any history of hospital admission or osmotic corrections. Follow up can help, if lesion increases in size goes in favour of Glioma.

Compression fracture with cord contusion

A young male with history of road traffic accident. 
MRI lumbar spine
Sagittal STIR and T2w image with axial T2w image at the level of L1 shows: 
L1 compression fracture with hyper intense marrow odema on STIR. 
Retropulsion of posterior fragment causing canal stenosis, cord compression.
A focal T2 hyper intense cord contusion and cord odema.
L5 show a superior sub chondral collapse with hyper intense marrow odema on STIR. 
Adjacent intervening discs are uninvolved. 

Idiopathic Hypertrophic Patchymeningitis

A 40 yo female with moderate continuous headache not responding to anelgesics. Neurological examination normal. Advised CT study of Brain. 
Plain CT study of Brain shows hyper density along inter hemispheric fissure and tentorium.
MRI study of brain Axial Post contrast SPGR T1 w images show dural thickening along inter hemispheric fissure and tenotorium. No significant signal abnormality in rest of the brain parenchyma. MR Venogram of Brain normal. 

Imaging wise : Idiopathic Hypertrophic Patchymeningitis. 

Csf examination normal.
Pt is responding to steroids.

Similar Cases: 
Case 1
Case 2


Syn : Dural pseudotumor, Idiopathic cranial hypertrophic pachymeningitis (ICHP) is diffuse dural thickening without known etiology like neoplasm or infection.

Imaging wise best diagnostic clue is thickened enhancing meninges "turn the corner" under temporal lobes in continuous line from vertex on coronal sections.
CT often normal. May show hyper density along inter hemispheric dura and tentorial leaflets. Brain parenchyma show normal attenuation pattern.
MRI is the investigation of choice, shows dural thickening often bilateral follows inner calvarium, extends along falx, tentorium may extend into lACs, along spinal cord with enhancement on post contrast T1w.
Dural thickening has to be more than 2 mm, may be more than 1 cm.
Usually smooth, linear, diffusely thickened dura. Less commonly nodular, focal soft tissue mass like lesions.
Signals on MRI are often iso to hyper intense on T2w images. In cases of densely fibrosing pseudotumor may appear profoundly hypointense.
Invasive variety may show encroachment of dural venous sinus with abnormal MR Venogram, dural venous sinuses showing poor flow related signals.

Diffusely thickened dura is nonspecific finding and can be seen in a spectrum of following identifiable disorders:
- Congenital (mucopolysaccharidoses)
- Iatrogenic (surgery, shunti post-LP meningeal enhancement rare & should be diagnosis of exclusion)
- Trauma (chronic SDH)
- Spontaneous intracranial hypotension
- Infection (TB, HTLV- 1, indolent infections such as pseudomonas, syphilis, rhinoscleroma, fungal.
- Inflammatory (rheumatoid, sarcoid, Wegener, pseudotumor)
- Neoplasm (meningiomatosis, lymphoma, mets)
- Hematologic (monoclonal plasma cell hyperplasia, extramedullary hematopoiesis)
- Other causes fibrosing inflammatory pseudotumors, fibrosclerosis)
- Idiopathic.

Histopathological findings of ICHP
Meningeal fibrosis.
+/- Inflammatory cells (lymphocytes, plasma cells)
May have multinucleated giant cells
No bacteria, fungi, neoplastic cells.

Normal dural enhancement
- Thin less than 2 mm,
- Discontinuous, most prominent at convexity, less intense than cavernous sinus.
Chronic subdural hematoma
- May contain loculated foci of old hemorrhage
- May show calcification.
- Lesion in adjacent bony calvarium common in metastasis
- Lymphoma often associated with systemic disease.
- Sarcoid often has other lesions, diffuse non focal dural thickening is less common than focal dura based masses
- TB is meningitis lepto meningeal pattern of involvement is more common than patchy meningeal involvement.
- Sinus disease seen in Wegener, Rheumatoid arthritis, SLE, Sjogren
Intracranial hypotension
- Associated finding are sagging midbrain on sagittal sections with tonsillar herniation.
- Dural venous engorgement.
Dural sinus occlusion
- Engorgement of collateral venous channels may thicken dura

Clinical Presentation: 
Any age; peak 3rd-5th decades.
Most common complaint is Headache.
Cranial neuropathy: Progressive sensorineural hearing loss, hoarseness, optic neuropathy, Tolosa-Hunt syndrome.
Uncommonly seizures.

Prognosis and Treatment: 
Variable course.
Some are benign, require no treatment.
Specific diagnosis may require biopsy.
Corticosteroid therapy. Recurrence may occur with steroid tapering
Immunosuppressants (e.g., methotrexate, azathioprine)

Reference : Diagnostic imaging Osborn.

Saturday 1 December 2012

Pseudomeningocele with Nerve root Avulsion on MRI

A middle aged male with history of trauma due to a motor vehicle accident. 
Now complaints of Right arm weakness and parasthesias. A “frostbite” sensation which progressed to a sharp right shoulder and neck pain with a burning sensation.
There is typical history of impact caused his head to flex on left, to the contralateral side. 
MRI Sag T2 right ward section
Coronal FIESTA
MRI Sag T2 right far lateral section for end on view of neural foramen show abnormal T2 hyper intensity in the region of neural foramen at C6-7 and C7-D1 level with non visualization of normal punctate iso intense dots of nerve roots. Cystic outpouching noted iso intense to Csf along the course of corresponding right sided exiting nerve roots on Coronal FIESTA can be attributed to pseuomeningoceles. Redundant nerve roots noted just at the top of these pseudo meningoceles implies to an associated Nerve root avulsion. 

Diagnosis: Traumatic Pseudomeningocele with Nerve root avulsion. 

Pseudomeningoceles represent a tear in the meningeal sheath that surrounds the nerve roots and extravasation of CSF into the neighboring tissues. Because they are filled with fluid, they are easily identifiable on T2-weighted MR images and MR Myelography, does not require any intra thecal contrast.
MR can adequately demonstrate the traumatic pseudomeningoceles however myelography and CT myelography remain the gold standard. In another recent study, neurosurgeons when asked which method they prefer and use to evaluate the avulsed brachial plexus before surgery. Eighty percent prefer post myelography CT, 20% prefer MRI, and 41% use both methods, whereas the remaining participants expressed no preference. As per Volle et al. the sensitivities of cervical myelography, CT myelography and MR are 100%, 45% and 6% respectively, for demonstration of nerve root avulsions. Xray and CT myelography not only show the level of avulsion but also documented overall size and morphology of the associated pseudomeningocele. The difficulty with MR imaging is it can demonstrate pseudomeningocele as an indirect evidence of nerve root avulsion. But the fact is that Pseudo meningocele can occur without root avulsion and root avulsions may occur without pseudomeningoceles.
Recent advances in high resolution MR imaging with steady state sequences may allow evaluation of exiting nerve root avulsion. In infants, the use of MRI is recommended because post myelography CT is a minimally invasive procedure, needs contrast and radiation exposure. Adequate information can be provided by noninvasive MRI. MR myelography is helpful in depicting pseudomeningoceles in a fashion similar to conventional myelography, but it is a supplemental method because most of the lesions are identifiable on MRI.

Brain Abscess MRI

A 50 yo male with headache and recent onset left sided weakness. 
This MRI study of Brain shows:
A right parietal space occupying lesion.
Lesion has a thick walls, peripheral enhancement along its wall of uniform thickness, central non enhancing necrotic core showing restricted diffusion on Dw images.
Marked T2 hyper intense perilesional vasogenic odema and mass effect.

Imaging wise DDs given were Abscess and Glioma.
Steriotactic biospy of lesion performed.
Histopathological diagnosis : Abscess.