Bilateral ICA hypoplasia

A 22 yo female with history of mild headache came for MRI evaluation of Brain.

Routine parenchymal sequences shows:

No significant signal abnormality in brain parenchyma.

However axial T2 sections at the level of sella show non visualization of normal T2 flow voids of cavernous portion of ICA in para sellar region on either side.
So, followed by MR Angiography of Brain and Neck.

Non contrast MR Angiography 3 D TOF for Brain and 2 D TOF for neck shows:

1. Non visualization of cervical portion of ICAs on either side except a small stem at its origin.
2. Intra cranial ICA petrous portion show marked diffuse narrowing with non visualization of its cavernous and supra clinoid portions.
3. Both the MCAs and ACAs filled via posterior circulation via PComs, predominantly via dominant right PCom. Dominant Basilar and Vertebrals.

Congenital hypoplasia or Acquired stenosis?

In this case the non visualization of ICAs on MR Angio can be secondary to congenital hypoplasia or acquired severe stenosis at its origin. But here it appears to be the Congenital hypoplasia as patient is asymptomatic for the particular finding, dominant right PCom and Vertebro basilar system taking care of intra cranial blood supply. Axial CT sections at the level of base of skull show smaller caliber of carotid canal which corresponds to petrous portion of intra cranial ICAs supports Congenital Hypoplasia. Agenesis is unlikely as in Agenesis the carotid canals would have been completely absent.

Final impression: Bilateral hypoplastic ICAs. 

Discussion: 

Agenesis, aplasia, and hypoplasia of ICAs are rare congenital anomalies.
Incidence is less than 0.01% of the population.
May be unilateral or bilateral. Unilateral is more common than bilateral with left sided predominance by ~3:1.
Collateral blood flow in these cases most commonly through the circle of Willis, less commonly via persistent embryonic vessels and in rare occasions from transcranial collaterals from ECA, allowing these patients to remain asymptomatic or discovered incidentally. 
Recognition of these anomalies and differentiating them form acquired causes of non visualisation of artery on MR Angiography sequences is important for diagnosis and further planning.

Etiology: 

The exact cause of these developmental anomalies has not been established and is out of imaging consensus. The postulated causes include an intra uterine insult to the developing embryo. The mechanical and hemodynamic stresses placed on the embryo like exaggerated neck folding of the embryo or constriction by amniotic bands.

Differentiating Agenesis from Aplasia: 

Absence of artery that is non visualisation of normal flow voids of artery on parenchymal sequences or flow related signal on Angiography is a general term.

Agenesis is complete failure of an organ to develop.

Aplasia is lack of development (but its precursor did exist at one time), and

Hypoplasia as incomplete development.

In Aplasia of ICA, a tiny fibrous band may be the only remnant of the ICA which may not be depicated on angiography alone. To differentiate Aplasia from Agenesis, evaluation of the skull base can be of great help. Axial CT sections bone window images are the best. The presence or absence of the carotid canal on skull base sections can be used for distinguishing aplasia from agenesis. As presence of the ICA or its precursor is a prerequisite for development of the carotid canal at 5 to 6 weeks of gestation, demonstrating presence of carotid canal on skull base sections rules out Agenesis. Demonstrating the smaller size of carotid canal compared to opposite side can be used to differentiate hypoplasia from acquired causes of reduced caliber of ICA that is stenosis.

Reference:

Congenital Absence of the Internal Carotid Artery: Case Reports and Review of the Collateral Circulation; Curtis A. Given IIa, Frank Huang-Hellingera.

Similar Case : ICA unilateral congenital hypoplasia

Unilateral Abnormal Enhancement of 6th CN in Lateral Rectus Palsy

A 14 yo male, relatives complaining about his sudden recent onset squint and trying to correlate this finding with a history of trauma. On clinical examination right lateral rectus palsy.
MRI advised with clinical diagnosis of right side 6th Cranial Nerve palsy.
MRI study of Brain routine sequences were normal including 3D FIESTA (Steady state free precession (SSFP) sequence.
Due to strong clinical suspicion, MRI study was repeated with thin axial sections of SPGR T1 sequence after injection of intra venous contrast.

Contrast enhanced SPGR T1 sequence show a faint abnormal enhancement along cisternal portion of right side Abducens nerve consistent with clinical diagnosis of 6th Nerve palsy - Post traumatic.
No abnormal enhancement in the region of left side 6th CN.

Abnormal Cranial Nerve Enhancement on MRI

MRI is a valuable tool in evaluation of cranial Nerves and detecting the diseases of the cranial nerves. Contrast enhanced MRI increases the ability of MRI to detect such abnormalities. Abnormal cranial nerve enhancement on MRI may sometimes be the only finding of an underlying disease.
Layers of connective tissue sheaths of cranial nerves are endoneurium, perineurium, and epineurium. The blood-nerve barrier of cranial nerves is formed by the combined actions of tight junctions in the endothelium of the endoneural capillaries and tight junctions in perineurium.
Various insults like neoplasm, autoimmune disease, inflammation, demyelination, ischemia, trauma, radiation can disrupt this blood-nerve barrier, allowing leakage and accumulation of intra venous contrast material with resultant enhancement along the cranial nerves.

References : MRI of Cranial Nerve Enhancement, Farhood Saremi, Mohammad Helmy, Sahar Farzin, Chi S. Zee and John L.


Normal Anatomy of Abducens Nerve (VI or 6th CN)

Divided into four portions:
1. Nuclear portion
2. Cisternal portion
3. Cavernous sinus portion
4. Orbital portion

The Nuclear or intra parenchymal portion is its nucleus in the caudal pons, the abducens nerve exits the brainstem at the pons-medulla junction.
Cisternal portion is the part of nerve after emerging from pons in prepontine cistern. It courses superiorly with the anterior inferior cerebellar artery anterior to it, and the pons posteriorly, pierce the dura at the medial most portion of the petrous apex, passing through the inferior petrosal sinus in Dorello's canal. It is its oblique course and relatively fixed anchor in Dorello's canal which makes it prone to stretching when raised ICP from any space occupying lesion.
Cavernous sinus portion is within the cavernous sinus, the abducens nerve is located inferolateral to the internal carotid artery, medial to the lateral wall of the sinus.
Orbital portion is after having entered the orbit through the tendinous ring. It supplies the lateral rectus. Damage to the abducens nerve results in lateral rectus palsy, a tendency for the eye to deviate medially, may result in double vision.


Related articles:
how-to-plan-mri-for-cranial-nerve
cranial-nerves-normal-mri-anatomy

Diagnostic Criteria for Orbital Proptosis

Proptosis is defined as an abnormal protrusion of eyeball. 

Owing to the rigid bony structure of the orbit with only anterior opening for expansion, any increase in orbital contents taking place from the side or from behind will displace the eyeball forward.  Proptosis can be the result from varies disease processes including infections, inflammations, Tumours, trauma, metastases, endocrine lesions, vascular lesion, orbital - extra orbital osseous lesions.

Proptosis can be measured Clinically as well as Radiologically.

How to Measure Proptosis Radiologically ?

Both CT and MRI can be used.

Plane of the scan or axial sections must be parallel to the plane passing through the optic nerve head and lens.

Eyelids should be open with the patient looking straight ahead without eye movements. 

Interzygomatic line is drawn first, a straight line connecting the anterior margins of zygomatic processes, at the level of median portion of the globe or orbit. 

The distance from posterior sclera margin to Interzygomatic line (IZL) , Normal is 9.9mm +/- 1.7mm (Reference : Robert A.Nugent, Rod I.Belkin, Janet M. Niegel, Jack Rootman et al, Correlation of CT and clinical findings. Radiology, 177(3):675-82. Dec 1990)

Other measurements includes thickness of recti, the superior rectus muscle group (comprising of superior rectus muscle and the elevator muscle of the upper eyelid) and inferior rectus muscle best measured coronal and sagittal planes. The horizontal diameters of the lateral and medial recti are best measured on axial plane.

References: 

Thyroid ophthalmopathy revisited ; Karina Freitas Soares Machado; Marcelo de Mattos Garcia.

Szucs-Farkas Z, Toth J, Balazs E, et al. Using morphologic parameters of extraocular muscles for diagnosis and follow-up of Graves' ophthalmo pathy: diameters, areas, or volumes? AJR Am J Roentgenol. 2002;179:1005-10. 

Cranial Nerves MRI Planning Protocol

MRI is the imaging modality of choice when any cranial nerve pathology is suspected.
The routine MRI Brain sequences augmented by a 3 D Gradient Echo Steady- State sequences such as FIESTA or FISP are sufficient to demonstrate most of the pathologies of cranial nerves. Intravenous gadolinium-DTPA may be required occasionally and provides additional diagnostic information.
The protocol that we follow in our institute on 1.5 Tesla GE Signa Excite for MRI evaluation of Cranial Nerves is “MRI BRAIN FOR CRANIAL NERVES” includes routine MRI Brain sequences followed by FIESTA.

Routine Brain includes: Axial T1 SPGR, FLAIR, T2w, Dwi,T2*GRE, Coronal T2, Sagittal T2.
For Cranial Nerves axial 3 D FIESTA.
In selected cases Contrast enhanced T1 SPGR axial sos coronal and sagittal.

How to plan MRI FIESTA for Trigeminal Nerve and 7th-8th Cranial Nerve complexes ? 

 Slab Oriented at right angle to vertical axis of brain stem covering whole brain stem.

What is FIESTA ?
FIESTA stands for 'Fast Imaging Employing Steady State Acquisition', provides images of fluid filled structures with very short acquisition times, uses the T2 steady state contrast mechanism to provide high SNR (Signal / Noise Ratio) images with strong signal from fluid tissues while suppressing background tissue for contrast and anatomic detail of small structures. In addition, the ultra short TR and TE enable extremely short acquisition times – shorter than FSE – and the images can be post processed using MIP, volume rendering, or 3D navigator techniques.

What is Steady State Free Precession Imaging (SSFP) ? 
Steady state free precession (SSFP) imaging is a Gradient Echo MRI technique which uses steady states of magnetizations achieved by a series of radiofrequency (RF) irradiation and natural relaxation behaviors of spins. So the influencing factors include: the flip angles of RF pulses, repetition time (TR) of pulse repeats, the relaxation time constants including longitudinal (T1) and transverse (T2) ones, plus if gradient moments (i.e. the integral of gradients with time) in one TR are zero, etc.
In general, SSFP MRI sequences are based on a (low flip angle) gradient-echo MRI sequence with a short repetition time which in its generic form has been described as the FLASH MRI technique.

Commercial names for Steady-State Free Precession (SSFP)
GE : FIESTA  (Fast Imaging Employing Steady-stateAcquisition)
Siemens : FISP (Fast Imaging with Steady-statePrecession)
Philips: FFE (Fast Field Echo), b-FFE (Balanced Fast Field Echo)

Usefulness of FIESTA:
This protocol and the FIESTA sequence is useful for evaluation of Trigeminal Nerve in Trigeminal Neuralgia, Facial and Vestibulo choclear Nerves in IAC for any space occupying lesion or Vascular loop, Abducens nerves for Lateral rectus palsy and in addition Hypoglossal and Glassopharyngeal Nerves.

Related Article : Cranial nerves normal MRI Anatomy

Spinal Epidural Hematoma MRI

A 26 yo male with sudden onset backache and chest pain for last 2 days. An associated bilateral upper limb tingling numbness. Both lower limb weakness is of sudden onset and non progressive.

Power: Rt arm 4-5, Lt arm 4-5, Rt leg 0, Lt leg 0.

No history of trauma or any heavy weight lifting. 

BT CT PT and other related caugulation profile normal.

On admission MRI dorsal region spine done with contrast. 

MRI Findings: 

A focal posterior epidural lentiform shaped collection extending from C6-7 to D2-3 disc level

Collection is hypo intense on sagittal T2 images with low signal intensity 'blooming'on GRE. No significant enhancement within the collection on post contrast T1 and fat sat T1. Thin enhancement noted along the normal dura.

Significant cord compression with focal cord edema.

Imaging wise Diagnosis: Possible DDs given were as Epidural Hematoma more likely than Abscess.

Post operative findings:

Operated with C6-D3 Laminectomy, posterior epidural hematoma / blood clot evacuated with coagulation of dural AV fistula along left D2 root.

Final Diagnosis : Posterior epidural hematoma secondary to Spinal Dural AV Fistula - Malformation.

Discussion:

In this case possibility of Epidural hematoma is more likely due to sudden onset of symptoms clinically, low signal intensity of collection on T2w and T2*GRE, iso to hyper intensity on T1w images, non enhancing on post contrast on imaging, thought there no history of history of trauma and normal coagulation profile. So one should entertain a possibility of Hematoma for a spinal Epidural lesion as Epidural Hematoma can present without history of trauma and moreover blood has variable signal and enhancement pattern on MRI.

Spinal Epidural hematoma (EDH)

Extra vasation of blood into the epidural space of spine.

Imaging

MRI is best.

Typically lentiform shaped long segmental extra axial collection mass encasing or displacing cord or cauda equina.

Location anywhere along spinal canal, commonly in dorsal region. 

vertical extent variable depending upon severity of bleed, often multi segmental,rarely focal when associated with an adjacent fracture.

On CT, density on CT varies with age of hematoma high density in acute stage to low density in chronic. 

On MRI 

TIWI: Hypo-, iso- or hyperintense (depending on age)

T2WI: Inhomogeneous low (if acute), or high signal (if subacute) intensity.

T2* GRE: low signal.

T1 C+: None to marginal enhancement along the dural outling of collection. Avid enhancement if bleeding is active. 

DSA

Often negative. Rarely, may show AVM or vascular tumor as Source of bleeding. 

DDs

Epidural abscess: Usually vivid enhancement, associated osteomyelitis or paraspinous infection, constitutional signs like fever, pain, chills.

Epidural tumor: Typically quite focal, adjacent bone often involved, Lymphoma may simulate EDH, enhances vividly. 

Etiology

o Spontaneous in 1/3

• Pressure elevation in vertebral venous plexus due to minor exertion, like sit-ups with Valsalva.

• Chiropractic manipulation

o Therapeutic anticoagulation

• Coumadin

• Anti platelet agents

o Instrumentation

• Epidural anesthetic

• Nerve block

• Facet joint injection

• Lumbar puncture

o Vascular malformation

Clinical Presentation

Most common signs/symptoms are intense, knife-like pain.

Associated extremity weakness, sphincter disturbance

Age: 35-70 Gender: Male > Female

Treatment

o Surgical for significant cord compression is decompressive Laminectomy and evacuation of hematoma. 

o Non-surgical for minor neurological signs.

Caudal Regression Syndrome

MRI Sagittal T2w images of lumbo sacral spine shows:
Hypoplastic S1 and S2 with failure of formation of S3 and onwards. 

Cord ending at a higher level at D12-L1 with 'wedge' shaped termination.

No cord tethering.

No terminal cord cyst or syrinx. 

Imaging diagnosis : Caudal Regression, Group I. 

Synonyms: CRS, sacral agenesis, lumbosacral dysgenesis
Definition: Constellation of caudal developmental growth abnormalities with associated regional soft tissue anomalies of Spine.
Imaging wise best diagnostic clue: Lumbosacral dysgenesis with abnormal distal spinal cord.
Affects Lumbosacral spine.
Severity of diminution of caudal spine varies with case, ranging from absent coccyx to lumbosacral agenesis.
With an associated
Unilateral partial or total dysgenesis with oblique lumbosacral joint.
Bilateral total lumbosacral dysgenesis; vertebral column terminates in thoracic spine.
+/- Caudal vertebral bodies often fused.
+/- Severe canal narrowing rostral to last intact vertebra.
+/- Osseous vertebral excrescences, fibrous bands connecting bifid spinous processes, or severe distal dural tube stenosis.

Staging, Grading or Classification Criteria: 
Group 1:
More severe caudal dysgenesis with high-lying, ‘’club or wedge shaped ‘’ terminating cord (decreased number of anterior horn cells of cord, Distal cord hypoplasia with wedging seen in all patients with partial or complete dysgenesis and termination of spinal cord above Ll, Termination of the conus above Ll highly correlated with sacral malformations ending at Sl or above) so this group is associated with severe sacral osseous anomalies.  +/- dilated central canal, conus CSF cyst.
Group 2:
Less severe dysgenesis with low-lying, tapered, distal cord tethered by tight filum.
 (Conus termination below Ll highly correlated with sacral malformations ending at S2 or below) so this group is associated with milder sacral dysgenesis with tethered cord +/-  Lipoma, lipomyelomeningocele, or terminal myelocystocele.

Imaging wise DDs:  
Tethered cord:  Low-lying spinal cord +/- thickened or fatty filum, no caudal dysgenesis.
Closed spinal dysraphism:  Dorsal dysraphism without severe vertebral column agenesis.
Occult intrasacral meningocele : Sacrum thinned and remodelled, sometimes imitating caudal regression.

Etiology: 
Normal caudal spine development  includes canalization and retrogressive differentiation.
Anorectal and genitourinary structures form contemporaneously in close anatomic proximity.
Insult prior to fourth gestational week  result in caudal cell mass developmental abnormalities.
Signaling defects by retinoic acid and sonic hedgehog during blastogenesis and gastrulation > Abnormal neural tube, notochord development > impaired migration of neurons and mesodermal
Cells.
Hyperglycemia, infectious, toxic, or ischemic insult postulated to impair spinal cord, vertebral formation.

Genetics: 
Most cases sporadic.
Inherited in the HLBX9homeobox gene (chromosome 7) , HLBX9also expressed in pancreas  so possible association between diabetes hyperglycemia and caudal regression.
Epidemiology:
1/7,500 births (milder forms> severe forms)
15-20% are infants of diabetic mothersi 1% of offspring from diabetic mothers affected.

Associated abnormalities  and anomalies: 
Association with VACTERL(10%), omphalocele, exstrophy bladder, imperforate anus, spinal anomaluies (10%), and Currarino triad syndromic complexes
Common associated abnormalities  Tethered cord (100% of CRS patients with conus terminating
below L1), Thickened filum (65%) +/- dermoid or lipoma.
Other spinal anomalies: Vertebral anomalies (22%), diastematomyelia, terminal hydromyelia (10%), myelomeningocele (35-50%), lipomyelomeningocele (10-20%), terminal myelocystocele (15%), Anterior sacral meningocele.
Cardiac anomalies: Congential cardiac defects (24%), pulmonary hypoplasia.
Genitourinary abnormalities (24%), Renal agenesis/ectopia, hydronephrosis, Mullerian duct malformations, urinary bladder malformation
Anorectal anomalies (particularly anal atresia), Higher the level of anal atresia  >  more severe
lumbosacral dysgenesis, genitourinary anomalies.
Orthopaedic abnormalities: Extreme cases with lower extremity fusion (sirenomelia).

Reference: Diagnostic imaging Spine / Jeffrey S. Ross MD, Michael Brant-Zawadzki, MD, FACR, Kevin R.Moore, MD, Julia Crim, MD, Mark Z. Chen, MD, Gregory L. Katzman, MD,

Chemotherapy induced Acute Cerebellitis

A 60 y o male known case of oesophageal cancer not spread to other organs.
Planned to be treated with chemotherapy plus concurrent external-beam radiation therapy prior to surgery.
He received five courses of chemotherapy with carboplatin and paclitaxel. Now presented with recent onset cerebellar ataxia.

MRI study of Brain shows faint Cerebellar hyper intensity on FLAIR and Diffusion.
Imaging diagnosis: Acute Cerebellitis.
Clinical diagnosis: Chemotherapy induced Acute Cerebellitis / Cerebellar Ataxia.

Discussion: Normally, cells grow and die in a controlled way. Cancer cells keep forming without control. Chemotherapy is drug therapy that can kill these cells or stop them from multiplying. However, it can also harm healthy cells, which causes side effects. During chemotherapy there may be no side effects or just a few. The severity of side effects depend on the type and dose of chemotherapy. Common ones are nausea, vomiting, tiredness, pain and hair loss. Healthy cells usually recover after chemotherapy, so as with drug toxicity, these deficits are usually reversible unless exposure has been heavy and prolonged.

Carboplatin
A post-marketing study of Cerebellitis (Acute cerebellar ataxia) among people who take Carboplatin. The study is created by eHealthMe based on 8 reports from FDA and user community.
Carboplatin has active ingredients of carboplatin.
It is used in cancer, lung cancer - non-small cell, chemotherapy.
Common side effects of Carboplatin include agranulocytosis, nausea, dehydration, nausea and vomiting, fever.
On Aug, 6, 2012; 26,662 people reported to have side effects when taking Carboplatin. Among them, 8 people (0.03%) have Cerebellitis.

Time on Carboplatin when people have Cerebellitis:
< 1 month           Cerebellitis 100.00%
1 - 6 months                            0.00%
6 - 12 months                          0.00%              
1 - 2 years                               0.00%
2 - 5 years                               0.00%
5 - 10 years                             0.00%
10+ years                                0.00%

Age of people (in years) who have Cerebellitis when taking Carboplatin :
0-1       Cerebellitis 0.00%
2-9                        0.00%
10-19                    0.00%
20-29                    0.00%
30-39                    0.00%
40-49                    0.00%
50-59                    0.00%
60+                     100.00%

Paclitaxel
A post-marketing study of Cerebellitis (Acute cerebellar ataxia) among people who take Paclitaxel. The study is created by eHealthMe based on 6 reports from FDA and user community.
Paclitaxel has active ingredients of paclitaxel. It is used in metastases to peritoneum, endometrial cancer, investigation abnormal, endometrial cancer stage iii, transitional cell carcinoma. Common side effects of Paclitaxel include breathing difficulty, fever, agranulocytosis, dehydration, diarrhea.
On Jul, 28, 2012: 14,867 people reported to have side effects when taking Paclitaxel. Among them, 6 people (0.04%) have Cerebellitis.

Age of people (in years) who have Cerebellitis when taking Paclitaxel
0-1      Cerebellitis 0.00%
2-9                       0.00%
10-19                   0.00%
20-29                   0.00%
30-39                   0.00%          
40-49                   0.00%
50-59                  33.33%
60+                     66.67%

References : eHealthMe - Real world drug outcomes http://www.ehealthme.com

6th CN Palsy in Apical Petrositis MRI

A 15 y o male advised MRI with a clinical diagnosis of left Lateral Rectus - 6th CN Palsy.

MRI Post contrast SPGR T1w images at the level of Pons show:

E/o Left side Mastoiditis and Apical petrositis.

An abnormal soft tissue in the region of cisternal portion of left 6th CN where it is entering in Dorello’s canal explains involvement of left 6th CN. 

Note the normal 6th CN on right side. 

After MRI study is over despite of asking leading questions patient refused any kind of ear discharge or ear pain but said yes to mild occasional left facial pain. 

Imaging diagnosis: 6th CN involvement secondary to Apical petrositis. 

Apical petrositis

Involvement of petrous apex is a relatively rare complication that occurs when infectious otomastoiditis extends medially into the petrous apex usually via pneumatized air cells. Initially, intact petrous apex air cells are opacified with purulent exudate. With progressive infection, the epithelium is invaded and destroyed, and the supporting bony trabeculae and inner cortical margins undergo demineralization and resorption. Infection then spreads beyond the air cells to the adjacent marrow space of the petrous apex, essentially forming a localized osteomyelitis of the skull base.

Symptoms variable and depend on the stage of disease. Most patients present with severe otalgia and otorrhea with associated deep facial or retroorbital pain. Occasionally, patients present with the classic Gradenigo triad: otomastoiditis, deep facial pain secondary to trigeminal neuropathy, and lateral rectus palsy and diplopia secondary to sixth cranial nerve palsy. The classic triad is explained by the unique relationship of the petrous apex to Dorello canal (Abducens, 6th CN) and Meckel cave (Trigeminal, 5th CN), may not be present every time as in this case.

Normal Anatomy of Abducens Nerve (VI or 6th CN)

Divided into four portions: 

1. Nuclear portion

2. Cisternal portion

3. Cavernous sinus portion

4. Orbital portion

The Nuclear or intra parenchymal portion is its nucleus in the caudal pons, the abducens nerve exits the brainstem at the pons-medulla junction.

Cisternal portion is the part of nerve after emerging from pons in prepontine cistern. It courses superiorly with the anterior inferior cerebellar artery anterior to it, and the pons posteriorly, pierce the dura at the medial most portion of the petrous apex, passing through the inferior petrosal sinus in Dorello's canal. It is its oblique course and relatively fixed anchor in Dorello's canal which makes it prone to stretching when raised ICP from any space occupying lesion.

Cavernous sinus portion is within the cavernous sinus, the abducens nerve is located inferolateral to the internal carotid artery, medial to the lateral wall of the sinus.

Orbital portion is after having entered the orbit through the tendinous ring. It supplies the lateral rectus. Damage to the abducens nerve results in lateral rectus palsy, a tendency for the eye to deviate medially, may result in double vision.


Cranial-nerves-normal-mri-anatomy

Intracranial extension of Shotgun pellet through orbit

A 30 year male came for follow up imaging with history of accidental shot gun injury to left eye while working in field. There is a small entrance wound scar in the lower left orbital fold. Neurological examination including visual acuity and eye movements are normal.
MRI not done as it is contraindicated in this case.

CT study of brain shows a pellet stuck at left petrous apex, the region corresponds to junction of left cavernous sinus and superior petrosal sinus. Streak artifact due to its high density. 

In the present case the left eye appears to be an entry point, going intra cranially through superior orbital fissure appears to have gained entry in left cavernous sinus stuck at the tip of left petrous apex due to resistance in the trajectory of the pellet.


Discussion:

Missile injuries and intracranial extension through bony calvarium or orbit are common but embolisation of the bullet or pellet is rare event. Most of the reports are related to arterial embolisation in that anterior cerebral circulation are relatively common. Posterior cerebral circulation embolisation are rarely mentioned in the literature.
The embolism after penetrating the vessel let it be artery or vein depends on the size of the missile and its velocity. Small size and low velocity are requirements for embolization to occur. Because of the small size and low velocity with the wider area covered at a time by the large number of these pellets, the shotgun wounds are most commonly associated with arterial or venous penetration and embolism. The site of entrance of the missile in cases of embolization to the intracranial circulation is usually the chest or the neck, where it can either enter the heart, aortic arch or the neck vessels.
The treatment of intra cranial extension and embolism of pellet is controversial. Conservative treatment is suggested for such asymptomatic patient. Metallic pellets are not amenable to endovascular removal because of the risk of intimal injury.

Radiation induced Cryptic Vascular malformation

A 50 yo male operated for right parietal Glioma with post operative radiotherapy.

Clinically started worsening after 5th week. 

The follow up CT with MRI FLAIR and T2*GRE.

Non Contrast CT study of brain shows multiple punctuate hyperdense foci are the Radiation induced Cryptic Vascular Malformation

Axial T2*GRE images show  multiple punctuate low signal intensity foci "blooming" related to blood degradation products are the Radiation induced Cryptic Vascular Malformations predominantly the Capillary Telangiectasia

Axial FLAIR image show bilateral confluent peri ventricular T2 white matter hyper intensities suggestive of Radiation induced Leukoencephalopathy 

Radiation induced brain injury

Spectrum of insult includes edema, arteritis, leukoencephalopathy, mineralizing microangiopathy, necrotizing leukoencephalopathy, radiation-induced tumors and Cryptic Vascular Malformations.

Depending up on the time of presentation divided into acute, early delayed injury and late delayed injury:
Acute injury: 1-6 weeks after or during treatment ; Mild and reversible, vasogenic edema.
Early delayed injury: 3 weeks to several months; Edema & demyelination.
Late delayed injury: Months to years after treatment; More severe, irreversible.


Imaging findings:
Radiation injury: Mild focal hypodense / T2 hyper intense vasogenic edema to areas of necrosis.
Radiation necrosis: Irregular enhancing lesion, single or multiple.
Leukoencephalopathy:  Bilateral confluent white matter hypodensity / T2 hyperintensity predominantly involve peri ventricular white matter, sub cortical U fibers involves late.
Mineralizing microangiopathy: Bilateral basal ganglia and sub cortical white matter faint calcification best seen on CT. An associated cerebral cortical atrophy.
Necrotizing leukoencephalopathy:  Areas of white matter necrosis.
Cryptic Vascular Malformation: Best seen on MRI T2* GRE as punctate low signal intensity foci represent capillary Telangiectasia.


Pathological Basis:
Radiation-induced neurotoxicity : Direct radiation induced Glial and WM damage. Sensitivity of oligodendrocytes is more than neurons to radiation induced damage. Effects on fibrinolytic system and immune effects.
Radiation-induced vascular injury: Altered vascular permeability, endothelial and basement membrane damage, accelerated atherosclerosis, telangiectasia and cavernoma formation.
Radiation-induced tumor like sarcoma seen after ~ 5 years, genetic predisposition.

Distinguishing residual/recurrent neoplasm from Radiation induced Necrosis difficult using morphology alone. MRS, PET or SPECT may help delineate recurrent tumour from radiation necrosis.


Reference: DI Anne G Osborn. 

Scheuermann's disease MRI

MRI Dorso Lumbar region spine sagittal T2w images show:
Multiple and contiguous involvement of vertebral bodies, the anterior wedging, antero posterior elongation, associated Schmorl's nodes, end plate irregularity and disc space narrowing.
The exaggerated kyphosis of Classical Scheuermann's is absent. 

Scheuermann's disease
Also known as 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.

Classical Scheuermann's disease MRI

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.

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.