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.

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.

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.

Impression:
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.

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)
Types:
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.

Investigations:
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.

Scheuermanns-disease-lumbar-variant

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.

References:
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.

DDs: 
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. 

Findings:

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


HYPERTROPHIC PACHYMENINGITIS

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.

DDs
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.
Neoplasm
- Lesion in adjacent bony calvarium common in metastasis
- Lymphoma often associated with systemic disease.
Infection/inflammation
- 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.

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. 

Discussion:
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.

Functional MRI

Functional magnetic resonance imaging (fMRI) is a MRI procedure that measures brain activity by detecting associated changes in blood flow. The primary form of fMRI uses the blood-oxygen-level-dependent (BOLD) contrast.
This is a type of specialized brain scan used to map neural activity in brain by imaging the change in blood flow (hemodynamic response) related to energy use by brain cells.
It is non invasive, does not require to ingest substances or be exposed to radiation. The procedure is similar to MRI but uses the change in magnetization between oxygen-rich and oxygen-poor blood as its basic measure. The resulting brain activation can be presented graphically by color-coding the strength of activation across the brain or the specific region studied.
FMRI is used both in the research world, and to a lesser extent, in the clinical world.
Brain activity mapping enables revealing of the areas of neuronal activation in response to tests, motor, sensor, and other stimuli. Until recently, similar mapping was performed with the help of radionuclide methods: PET and SPECT imaging.
Functional MRI (fMRI) is based on increase of brain haemodynamics in response to cortical neuronal activity due to certain stimulus (Ramsey 2002; Pouratian et al. 2003; Sunaert 2006).
BOLD EPI-GRE registers hyperintense MR signal from active areas of the brain cortex. The registration time of one MR image is about 100 ms. fMRI signal intensity, registered by physiological load, is compared with the intensity, registered in the event of its lack. During MRI examination, the stimulation periods (duration of 30 s) alternate with control periods

fMRI neuronal activity maps of cortical motor center activation in a patient with intrinsic tumour of the paracentral area, imposed on a T1 image

(without stimulation) of the same duration. The total number of scans registered during the examination reaches 20,000. This method of stimulus presenting is called a block paradigm. The areas of statistically significant MR signal increasing during activation, revealed in the course of subsequent mathematical processing of images, correspond to areas of neuronal activity. They are marked with colour—this way the neuronal activity maps are built and these maps are imposed on T1 MRI sequences. Map construction methods subtract images obtained during neuron stimulation from control images obtained in the absence of stimulation. The subtracted image is imposed on a control scan according to its location, and areas of increased neuronal activity are marked with colour. The revealed functionally significant areas could be “imposed” on a T1 MRI sequence of the same section or on a three-dimensional (3D) brain model, and thus it is possible to estimate the ratio between the affected area (tumour) and functionally active brain areas, for example, motor, sensory or visual cortex.

Clinical Application of fMRI

Neuronal activity mapping enables planning the surgical approach and studying of the pathophysiological processes in brain. This method is used in neurosurgery in studying cognitive functions. Its perspective is in revealing the epileptic foci. Currently, fMRI is an integral part of MRI protocol in patients with brain tumours located close to the functionally important brain areas. In the majority of cases, the examination results adequately reflect the location of sensomotor, speech and acoustical areas of brain cortex.
In cases in which fMRI can locate active cortical areas, in 87% of cases there is a correspondence with the results of intraoperational electrophysiological methods, within 1-cm limits, and in 13% of cases, within 2 cm. This is evidence of the high accuracy of the fMRI technique (Nennig et al. 2007).
Performing fMRI (currently it is conducted for somatosensory and visual cortices) and tractography with mapping of the functionally active cortical areas, pyramidal or optic tracts.
Imposition of these maps over 3D brain images is promising within the framework of one MRI examination for patients with brain tumours. Based on these data, neurosurgeons plan the interventional approach and estimate the volume of neoplasm resection, and radiologists assess the areas of radiation and its distribution in tumour.

Reference : V. N. Kornienko · I. N. Pronin, Diagnostic Neuroradiology.

Vascular territories of Brain stem and Infarct correlation

The arteries of the brain stem form four groups of penetrating parenchymal vessels; the anteromedial, anterolateral, lateral and posterior arterial groups.
Each group irrigates the corresponding anteromedial, anterolateral, lateral or posterior territory within the substance of the brain stem.

There are two possible systems of nomenclature.
1 . Foix and Hillemand Classification 

The penetrating branches arising from the surface vessels are divided into PM (paramedian), SC (short circumferential), and LC (long circumferential) vessels.

2.  Gillilan and Lazorthes et al. Classification

AM (anteromedial)
AL (anterolateral)
L (lateral) and
P (posterior) group.

Reference : Duvernoy’s Atlas of the Human Brain Stem and Cerebellum

Examples: 

Ax T2wi, Left side Medullary Infarction, Vascular territory : Antero Medial group / Para Median branches.

Ax FLAIR, Left side Medial Medullary Infarction, Vascular territory : Antero Lateral group / Short circumferential branches.

Ax T2wi, Left side medullary infarction, Vascular territory : Lateral group / Short circumferential branches.

Ax T2wi, Left side medullary infarction, Vascular territory : Posterior group / Long circumferential branches.

Ax T2wi, Midline medullary infarction, Vascular territory : Bilateral Antero Medial group / Para median branches.

Ax T2wi, Pontine infarction on left side, Vascular territory : Antero Medial group / Para median branches.

Ax T2wi, Pontine infarction on left side, Vascular territory : Antero Lateral group / Short circumferential branches.

Ax T2wi, Pontine infarction, Vascular territory : Bilateral Antero Medial group / Para median branches.

Ax T2wi, Pontine infarction, Vascular territory : Antero Lateral group / Short circumferential branches.

Ax T2wi, Pontine infarction and adjacent cerebellar infarct, Vascular territory : Posterior group / Long circumferential branches.

Ax T2wi, Mid brain infarction, Vascular territory : Antero Medial group / Para median branches.

Ax T2wi, Infarction involving mesencephalic mid brain, Vascular territory : Bilateral Antero Medial group / Para median branches.

Ax Diffusion, Recent Mid brain infarction, Vascular territory : Antero Lateral group / Short circumferential branches.

Nodular calcification Spinal cord

A 35 yo female with right upper limb tingling numbness.

Findings:
Sagittal T2 and T1w images show an abnormal intra medullary low signal intensity nodular calcification at the level of C3 vertebral body, in right half of cord on axial T2w MR images, better seen on non contrast CT section. Lesion is non enhancing on post contrast sagittal Fat sag T1 and axial T1 section , appears to be a benign lesion and needs follow up imaging. Clinically appears to be significant for patients right sided tingling numbness. 

Baastrup’s Disease : Interspinous Odema / Neo-arthrosis

Sagittal T1 T2 and STIR images of lumbar region spine shows:
Degenerative changes marked at L4-5 with reduced height of disc and degenerative intra discal vacume phenomenon. An abnormal linear hyper intensity of an inter spinous odema noted at the same level. 

Baastrup’s Disease

Syn: Kissing Spines Disease, intraspinous odema, intraspinous neo-arthrosis.

Baastrup’s Disease is a type of pseudo / neo-arthrosis between adjacent spinous processes.
Common in lumbar region at L4-5.

Extreme forward flexion may result in supraspinous and intraspinous ligaments sprain with development of a spur. Repeated extension interferes with the healing. An interspinous bursae may develop due to an associated supraspinous ligament laxity and intraspinous ligament breakdown. The interspinous ligament degenerates with aging resulting in the formation of a cavity, the adjacent spinous processes keep coming in contact with each other during extension and result in formation of a joint which precede pain.
Risk Factors are degenerative disc disease, Athletics, Hyper lordosis, Paraspinal muscle atrophy, Pars interarticularis defect.
Clinically characterized by localized interspinous or spinous process pain without a referral pattern, pain present for many years with progressive worsening over time.

Imaging: 
Lateral view LS spine radiograph may demonstrate sclerotic changes or flattening of adjacent spinous processes.
MRI sagittal T2 and STIR images are needed assess interspinous edema.
Bone scan with SPECT can detect increased osteoblastic activity that is associated with reactive sclerosis.

Treatment: Bed rest in semi upright sitting position, Surgical cavity resection, Surgical fusion.

References:
Haig AJ, Harris A, Quint DJ. Baastrup’s disease correlating with diffuse lumbar paraspinal atrophy: a case report. Arch Phys Med Rehabil. 2001 Feb;82(2):250-2.
Mitra R, Ghazi U, Kirpalani D, Cheng I. Interspinous ligament steroid injections for the management of Baastrup’s disease: a case report. Arch Phys Med Rehabil. 2007 Oct;88(10):1353-6.
Panagos A. Rehabilitation Medicine Quick Reference-Spine (ed. Buschbacher R.M.) New York: Demos Publishing; 2010. p. 20-21.

Unidentified bright objects (UBO) of NF1

A 09 yo male complaining of generalized tonic-clonic seizures since 2years.
Neurological examination normal.
General examination revealed multiple cafe-au-lait spots and axillary freckling.

MRI brain shows faint T2 hyper intensities in left basal ganglion, tectum of mid brain and right half of Pons non enhancing on post contrast, suggestive of unidentified bright objects (UBO) of NF1. 

UBOs are 'T2 hyper intense foci' or focal areas of high signal intensity (FASI), seen in 60-80 percent of patients with Neurofibromatosis Type I (NF1). These lesions typically appear around 3 yr, increase in number and size until 10-12 yr, and then decrease or even disappear. Common locations include basal ganglia, thalami, dentate nucleus of cerebellum and brainstem. Pathologically, these lesions correspond to vacuolar changes in the myelin sheath.
Even though these lesions generally do not cause neurological symptoms they have been correlated with learning disabilities.
A study conducted on 100 has revealed a strong relationship between cognitive and behavioural problems with these focal areas of high signal intensity (FASI or UBO) in children with NF1. The long term effects of these hyper intensities not yet documented.

Reference : NEUROFIBROMATOSIS TYPE I: NEUROPSYCHOLOGY AND MRI CORRELATES, R Feldmann. M Oelerich, T Allkemper, U Wiegard, M Pietsch, J Weglage

Department of Pediatrics, and Department of Radiology, University of Münster, Germany.

ICA Aneurysm

Sellar meningioma

A young female with visual deficit, previous CT report mentions a sellar supra sellar iso dense enhancing mass. Possibility given was Macro adenoma.

Pt refereed for further evaluation by MRI.

Sagittal T2w images show a sellar supra sellar soft tissue signal intensity well circumscribed mass.Pituitary seen separately in at the floor of hypophyseal fossa. Lesion show homogenous enhancement, a focal dural tailing anteriorly on sagittal post contrast T1 w images.

Radiological diagnosis: Sellar meningioma.

Take home massage is all sellar supra sellar masses are not macro adenoma or Craniopharyngioma. Never play on front foot while reporting CT. Always entertain DDs for sellar supra sellar masses on CT and advise MRI for further evaluation as MRI can demonstrate sellar anatomy better than CT due to its high resolution and multi planner imaging capability compared to CT. MRI can demonstrate pituitary separately in hypophyseal fossa which rules out Macroadenoma as in this case of sellar supra sellar meningioma.

Hemangioblastoma MRI

A 50 yo female with headache and giddiness.

Findings:

Axial T2w image show a mixed signal intensity posterior fossa mass with cystic as well as solid component. Solid component is near tentorium intensely enhancing on post contrast T1. Flow voids in this solid component and adjacent to it is very typical of a Hemangioblastoma. 

Mass effect on medulla and Pons with obstructive hydrocephalus.

Radiological and histopathological diagnosis : Hemangioblastoma.

Hemangioblastoma

A highly vascular tumor.

An intra axial posterior fossa mass with cyst and an enhancing mural nodule is a diagnostic clue.

Currently classified as meningeal tumor of uncertain histogenesis (WHO, 2000)

Locaion:

90% posterior fossa (m/c) in that 80% cerebellar hemispheres, 15% Vermis, 5% in other places  fourth ventricle, medulla.

10% Supratentorium.

In ~ 60% of cases mass present as cyst + mural nodule and in ~ 40% of cases only as a solid nodule.

Imaging:

Cyst is clear, density on CT and signal intensity on MRI same as that of Csf, non enhancing thin imperceptible wall.

Mural nodule on CT may be iso to hyper dense, intense and homogenous enhancement. On MRI hypo to iso intense on T1, hyperintense on T2 and FLAIR. May see flow voids within the nodule with adjacent vascular feeders on T2w images, intense and homogenous enhancement on T1 images implies to its highly vascular nature. May show low signal intensity hemosiderin staining on GRE if associated to with any bleed.

Presentation is usually with headache, dysequilibrium, dizziness may be due to its mass effect and hydrocephalus.

Age : for sporadic: 40-60 yr and for familial : can occur at younger age. Slight male predominance.

Closest DD is Pilocytic Astrocytoma; mural nodule show mild to moderate enhancement not this intense, not characterized by flow voids and feeders. Seen in relatively younger age group.

Similar case:

http://www.neuroradiologycases.com/2012/11/hemangioblastoma.html

Hirayama Disease MRI

An 18 yo male with 4 year history of slowly progressive weakness of forearms and hand marked on right side. Neurologic examination revealed atrophic changes in thenar, hypothenar muscles, interossei of the hands, muscles of forearm more on right side. Deep tendon reflexes symmetrically normal. No Babinski sign. Normal pin-prick, vibration and joint position sensation. No extra pyramidal signs.

Previous MRI cervical spine report at other center mentions spinal cord atrophy in lower cervical region. Rest of the spine and spinal cord screening unremarkable.

We performed MRI Cervical spine, sagittal T2w MR images revealed cord atrophy at the C5-6 disc level, a linear signal abnormality in anterior half of cord. The atrophy marked in anterior half of cord, signal abnormality confined to anterior half of cord in the region of either side anterior horn cells marked on right side confirmed on Axial T2w images. Study repeated during flexion with clinical suspicion of Hirayama disease shows marked anterior displacement of the posterior wall of dura with marked flattening of the cord. Flow void noted in this posterior epidural space appears to be the engorged venous plexus due to dural shifting. Clinical presentation and flexion MR imaging findings led to the diagnosis of Hirayama disease. Neck collar was advised to prevent neck flexion and to prevent further progression of disease and disease symptoms with follow up MRI Imaging.

Discussion

Hirayama et al first reported this disease in 1959.

Hirayama disease, a non progressive juvenile spinal muscular atrophy, occurs mainly in young males between the ages of 15 and 25 years. The clinical features include insidious onset, predominantly unilateral upper extremity weakness and atrophy, cold paresis, and no sensory or pyramidal tract involvement.

Pathologic studies have shown the lesions only in the anterior horns of the spinal cord from C-5 to T-1, particularly marked at C-7 and C-8.

Current neuroradiologic techniques have shown forward displacement of the posterior wall of the lower cervical dural canal in neck flexion, which is presumed to be a primary

pathogenetic mechanism of Hirayama disease. The mechanism of this anteriorly displaced dural canal has been explained by Kikuchi et al as a tight dural canal in flexion,

caused by a disproportional length between the vertebrae and the dural canal.

Early diagnosis of disease is necessary, because placement of a cervical collar will prevent neck flexion, which has been shown to stop disease progression. Atrophy on routine nonflexion MR studies especially at the lower cervical cord, should raise the suspicion of Hirayama disease. When this sign is seen, a flexion MR study should be performed to confirm the diagnosis.

Similar case:
http://www.neuroradiologycases.com/2011/08/hirayama-disease.html

Reference : Hirayama Disease: MR Diagnosis, Chi-Jen Chen, Chiung-Mei Chen, Chia-Lun Wu, Long-Sun Ro, Sien-Tsong Chen, and Tsong-Hai Lee, AJNR Am J Neuroradiol 19:365–368, February 1998 

Fatty filum terminale MRI

Syn: Lipoma of the filum terminale, filar lipoma.
A relatively common benign finding on MR imaging of the lumbar spine, seen in ~ 5 % of cases.

On MRI the abnormality typically is thin and linear, extends over only few segments. Signal iso intense to fat on all pulse sequences may show chemical shift artefact on T2* GRE sequences. T1 and T2 hyperintens with signal supression on STIR.

In most cases is an incidental finding of no clinical significance. However it is considered as one of the causes in tethered cord syndrome and may be associated with tethered cord, where there is associated markedly thickened filum with low lying conus. Location and the size of fatty filum are considered as the important factors for Tethered cord syndrome. The thickened fatty filum terminale (more than 2mm) considered as one of the causes of the tethering. Fat in the filum may represent mesodermal cells that did not properly migrate to their normal position in the process of canalization. The presence of fatty tissue may alter the developmental properties of the filum and may predispose patients to cord tethering. Bursara et al. reported the correlation between the fat and the neural dysfunctions with MRI. They concluded that fat in the filum terminale within 13mm of the conus medullaris was most predictive of neurological deficits. And TCS in adults is caused by the anoxia due to over-stretching of the conus medullaris - See more at h:ttp://www.ispub.com/journal/the-internet-journal-of-spine-surgery/volume-3-number-1/fatty-filum-terminale-on-mri.html#sthash.5KQVStuW.dpuf

In asymptomatic patients, nothing need be done. Difficulty arises in patients who have some symptoms suggesting tethered cord syndrome, but whose conus terminates at a normal level. Controversy as to the benefits of division of a fatty filum in such patients exists.

Imagingwise there is little or no differential when signals of fat is confirmed, however other filum terminale lesions like paraganglioma of the filum terminale and myxopapillary ependymoma can be considered.

Dural AV fistula

Plain CT and MR Axial T2w images show abnormal serpigenous vascular hyper density on CT and T2 flow voids on MRI marked in posterior fossa at the floor and along tentorial dura suggestive of dural AV fistula.
An associated abnormal dilatation of petrosal sinuses noted on MR Angio.

Dural arteriovenous fistula (DAVF)

Dural AVF, a rare, abnormal connectivity between arteries and veins, lies exclusively along dural covering of the brain or spinal cord, and referred accordingly as a cranial DAVF and spinal DAVF.
Cranial DAVF is supplied by branches of the carotid artery (external and internal carotid arteries) and possibly also by branches of the vertebral artery before these arteries penetrate the dura.
The fistula communications seen as serpigenous dilated vessels with T2 flow voids along dura overlying cererebral convexity and along tentorium. Frequently the blood flow in a DAVF is very high, and it may cause blood to flow in the opposite direction of normal over the brain's surface.

Commonly diagnosed in women over the age of 40 years. Unlike AVMs, which are thought to be present from birth, cranial DAVF most often develop later in life following hypoplasia or thrombosis of dural venous sinus particularly superior sagittal sinus.

Cranial DAVF may present with pulsatile tinnitus or pulsatile proptosis, impairment of vision and eye movement, isolated but persistent or progressive headache; hemorrhage
Unfortunately, the diagnosis may be missed or delayed because such lesions occur so rarely, CT may be normal and even in case of MRI, a common practise of inadequate sequences particularly screening protocols used for brain and spine.

Pathogenesis of Dural AV fistula:
Dural AV fistula are shunts between the meningeal arterial networks and the dural venous sinuses. Long standing dural sinus thrombosis result in obstruction in venous outflow which raises intra cranial venous sinus pressure. This venous hypertension leads to ischemia, followed by aberrant angiogenic activity along the Dura. CVT here is the primary event that result in venous hypertension and fistula. Sinus thrombosis may be the primary even as result of turbulent flow in the Dural venous sinus secondary to DAVFs.

Treatment:
Highly challenging, various line of management and materials are under debates.
Intra sinus stenting can relieve raised venous sinus pressure but may increase arteriovenous pressure gradient and shunt flow.
Arterial embolization of DAVF, without correction of venous hypertension can give rise to another fistula.
Intermittent carotid arterial compression.
Percutaneous intra arterial embolization using detachable balloons, isobutylcyanoacrylate, or polyvinyl alcohol particles.
Transvenous embolization with coils or liquid adhesives.
Surgical venous bypass using saphenous vein.
Gamma knife stereotactic surgery.

Similar Case: http://www.neuroradiologycases.com/2011/09/dural-arteriovenous-fistula-davf.html

Spinal cord ischemia in a case of Aortic Dissection

A young male admitted with sudden onset both lower limb weakness with an associated severe backache. Motor loss more than sensory. Advised MRI whole spine screening for spinal cord. 

Day 1 MRI

Findings:

Sagittal T2w images of spine show faint abnormal intramedullary T2 hyper intensity confined to anterior cord in dorsal region.

Day 2 MRI with axial T2

Sagittal T2w image of cervico dorsal region spine with axial T2w images at the level of signal abnormality of spinal cord show same abnormal intramedullary T2 hyper intensity confined to anterior half of cord in dorsal region becoming more obvious on this follow up MRI.

Radio logical diagnosis: Acute Spinal cord Ischemia.
Further evaluation revealed an thoraco abdominal Aortic Dissection on CT Angiography. 


Discussion:

The differential diagnosis of acute onset paraplegia includes spinal cord injury, tumor, infection, Disc herniation, Demyelination or aortic dissection - occlusion. Aortic dissection in acute paraplegia is missed in up to 50% of cases.
Aortic dissection is uncommon, accounts for approximately 1 in 10,000 hospital admissions. The mortality rate is as high as 80% without aggressive treatment. Clinical presentation is commonly a severe painful tearing sensation usually located interscapular or mid-back area. Other common signs and symptoms include cardiovascular collapse, acute myocardial infarction, oliguria, syncope and cold extremities.

Classification of aortic dissection; DeBakey classification divides dissections into 3 types. Type I involves the ascending aorta, aortic arch and descending aorta. Type II involves only the ascending aorta. Type III involves the descending aorta distal to the left subclavian artery.
Stanford classification Type A includes involvement of the ascending aorta and Type B excludes it.

Neurologic sequelae of aortic dissection occur in ~ one third of cases. These sequelae fall into 3 categories: cerebral ischemia, spinal cord ischemia and ischemic peripheral neuropathy.
When the ascending aorta is involved, cerebral ischemia may result, present as a stroke or encephalopathy. Paraplegia with or without sensory loss is a rare phenomenon, occurs in about 2% to 8% of patients, results from dissection of the descending aorta. The clinical picture of motor loss without complete loss of sensation is known as anterior artery syndrome. Painful peripheral neuropathy result when the iliac arteries are involved.

The artery of Adamkiewicz arises from the posterior aspect of the aorta and supplies the anterior aspect of the major portion of spinal cord. This artery is can be involved in the aortic dissection. When involves most areas of the spinal cord receive additional blood flow from the collateral flow. In the thoracic spinal cord, there is a “watershed” area which is especially prone to ischemia.

Conclusion: Acute aortic dissection to be considered in the differential diagnosis of acute onset paraplegia. 

Cavernoma with Bleed

Non contrast CT study of brain shows right frontal Cavernoma with punctate calcifications. An adjacent Gliosis noted. 
MRI study of brain shows right frontal Cavernoma appears to be complicated with bleed which has resolved and is evident by Gliosis with low signal intensity hemosiderin staining on GRE. It is not uncommon for a Cavernoma patient to be asymptomatic, massive bleed in a Cavernoma is known but a rare complication. 


Cavernoma (Cavernous Malformation)
A benign vascular hamartoma, composed of closely packed immature blood vessels with intra lesional micro hemorrhages, without any neuronal tissue.
Best diagnostic clue is "Pop corn ball" like appearance with hemosiderin rim on T2w images.
Occur anywhere in brain. Rare in Spinal cord.
Vary in size from few mms to cms. Average size is between 1 to 5cm.
Usually single solitary, may be multiple, discrete lesions.
MRI is more sensitive and specific for detection of lesion.
Hyper dense on non contrast CT. Punctate Calcifications seen in ~ 50% cases. No to faint enhancement on post contrast.
On MRI lobulated appearance due to multiple locules which show variable signals, depending up on the blood degradation products. T1 bright locules attributed to Meth Hb - a sub acute stage blood degradation product. Low signal intensity hemosiderin rim on T2 images. Low signal intensity blooming on  T2*GRE images. No to faint enhancement on post contrast T1 images.
No to mild peri lesional odema.
No mass effect.

Clinical presentation:
Seizures 50%
Neuro deficit 25%
Asymptomatic 20%, detected as an incidnetal finding.
No intervention is a rule. But need follow up imaging as it may show progression or regression in size. Rarely show massive bleed.
Can affect any age group.
No gender preponderance.
Familial association in Hispanic Americans - Multiple Cavernoma Syndrome, carries higher risk for bleed and re bleed.

Similar cases:
cavernoma
cavernous-malformation
venous angioma with bleed