Calcification of trochlear apparatus of orbit

A 50 yo female with left side weakness advised Non contrast CT for Brain to rule out any intra cranial bleed or infarction.

Finding:

No bleed or infarct on CT study of Brain.

A dense nodular calcification noted in the superior-nasal quadrant of the right orbit. Clinically right eye vision and movement normal.  No history of trauma to right eye.

Final diagnosis:

Unilateral calcification of trochlear apparatus of right orbit_ noted an incidental finding.

Calcification of trochlear apparatus of Obit.

Syn: Calcified Trochlea of the Superior Oblique Muscle.

The trochlear apparatus of the eye is a cartilaginous structure with a synovium lined sheath that permits unimpeded movement of the superior oblique muscle.

It is not clear yet the accurate location of calcification whether its cartilage, the synovial sheath, or the tendon.

Hart et al. in his study reported an association between calcification of the trochlear apparatus and DM, reviewed some 159 CT scans of patients and observed trochlear calcifications in 12% of patients with a significant correlation between diabetic patients under 40 years of age and the presence of calcification in the trochlear apparatus. The trochlear calcification on CT is a benign condition may serve as a marker for diabetes in young patients. Trochlear calcifications are observed frequently in persons more than 50 years old. When it is present in patients younger than 40 years, it is strongly associated with diabetes.
Another thing which is observed in these studies is trochlear calcifications were more prevalent in male patients and none of the patients in these studies had symptoms related to their trochlear calcification.

Studies conducted later, results were In contrast to the findings of Hart et al, did not find a significant correlation between patients under 40 years of age with DM and the presence of trochlear apparatus calcifications. Even there was no increase in trochlear calcifications with advancing age or the presence of systemic disease indicating that trochlear calcifications is not suggestive of a degenerative process and occur regardless of chronic medical disease.

Left parietal cyst MRI

MRI findings:

A left temporo parietal cystic lesion.
Lesion is multi locular, its difficult to mention whether the lesion is intra axial or extra axial as it is insinuating in brain parenchyma.
Content of cyst is clear fluid, iso intense to Csf.
No restricted diffusion on Dw images.
Lesion has thin imperceptible wall.
No solid component.
No peri lesional odema.
Significant mass effect_ mid line shift with sub falcine as well as uncal herniation. Mid brain compression.

Imaging wise possible DDs : Arachnoid cyst >  Neuroglial Cyst.

Pt operated, left parietal craniotomy with complete excision of lesion.

Histopathology Report

Specimen : Excisional biospy.
Gross appearance : The specimen consist of soft wrinkled pieces of dull grey white tissue _ cyst wall.
Microscopy : Sections shows a benign cystic lesion comprising delicate membranous fibrous connective tissue cyst wall lined by meningothelial cells, at places seen to form focal aggregates. There is no evidence of cytological atypia.

Final Diagnosis : Arachnoid cyst. 

Congenital Bilateral Perisylvian Syndrome MRI

This MRI brain axial T2w image shows bilateral deep wide vertically running clefts in the region of Sylvian fissures lined by thick gyri.

Imaging diagnosis : Congenital Bilateral Perisylvian Syndrome.

Syn :
Opercular syndrome,
Foix-Chavany-Marie syndrome,
Worster-Drought syndrome,
Bilateral symmetrical polymicrogyria

The term “perisylvian” refers to the area (“peri” = about or around) of the sylvian fissure (lateral sulcus), which acts as the brain’s language and speech center. It is basically an organization anomaly in which the neurons reach their final destination in the cortex but are distributed abnormally.

The syndrome is one of a group of congenital neurological diseases characterized by slack muscles of the face and tongue, chewing and swallowing difficulties, delayed or abnormal speech and language development, epilepsy, and in certain cases, impairment of cognitive function and impaired mobility. Similar disorders were described first by the French neurologists Charles Foix, Jan Alfred Chavany and Julien Marie in 1926, and later by the English physician Cecil Charles Worster-Drought in 1956.

Causes:
Genetic factors are very important, and there are families in which more than one person has the syndrome, although the symptoms may vary from person to person. Linked with a mutation on the long arm of the X chromosome (Xq27.2-q27.3 and Xq28). Disorders caused by mutations in genes on the X chromosome primarily affect boys.
Acquired, the Perisylvian syndrome may also be acquired, for example from a local malfunction in the blood circulation of the brain, or an infection in the relevant area of the temporal lobe during the foetal stage like congenital cytomegalovirus infection. In these cases the condition is not hereditary.

Clinical presentation:
The most common symptoms are impairments of the mobility of the tongue and throat (pseudobulbar palsy), epilepsy and mild cognitive impairment.
In serious forms of the disease, neonates may have problems sucking and swallowing.
May not become apparent till the child starts eating solids. It can be difficult to chew, move food around in the mouth, and swallow. Drooling is common.
Child is slow to start talking or has speech difficulties. The most common symptoms are paralysis or impaired motor capacity of the organs necessary for speech (dysarthria) and difficulties coordinating movements (dyspraxia) of the mouth.
Unclear and slurred speech, as well as problems forming certain sounds, are signs of dysarthia whith as associated drooling and swallowing difficulties. Problems in moving the tongue and the mouth mean that children with the syndrome cannot purse their lips or whistle. Oral motor problems, which commonly cause difficulties eating, drinking and speaking, remain throughout life.
Oral motor problems may affect the growth of the lower jaw, which may be smaller than normal (micrognathia). Misalignment of the teeth (malocclusion) may mean that it is difficult to close the mouth completely and that the lower jaw protrudes.
Dyspraxia may be oral or verbal. Oral dyspraxia means that it is difficult to exert voluntary control over movements of the tongue and lips. Verbal dyspraxia means that it is difficult to form words, despite the relevant organs having normal functionality. The symptoms are the result of abnormalities in areas of the brain controlling the motor skills necessary for speech. In verbal dyspraxia it is difficult to make a connection between sounds and syllables, which is necessary to form words. The degree of severity varies. Less severe disabilities give rise to problems with multi-syllable and longer sentences, which become more difficult to formulate the longer they get. Severe dyspraxia may mean that the child cannot form syllables or words.
Other language and communication problems may also occur, including difficulties with grammar and phonology (speech sounds). Children with the syndrome may have specific reading and writing problems (dyslexia). Speech comprehension, however, does not appear to be affected.
Most individuals with this syndrome have epilepsy. Seizures may present as infantile spasms during the child’s first two years of life and develop into other, difficult to treat, forms of epilepsy as the child gets older. In infantile spasms the child experiences a series of short, sudden, cramp-like jerks of the arms, or wider, uncontrolled movements of the arms.
Physical disability characterized by stiffness in the arms, legs and neck. Stiff, malformed joints make it difficult to walk, and to move in general. Require special aids or a wheelchair.
Mild cognitive impairment and hyperactivity may also present. Individuals with intellectual disability require more time to understand and learn new skills.

Diagnosis: 
The diagnosis is based on observation of the symptoms, as well as finding structural abnormalities on CT and MRI.

Treatment and Rehabilitation: 
There is no cure for Perisylvian syndrome.
Training in oral motor skills and swallowing at an early stage.
Exercises to the muscles of the tongue.
Training in closing the mouth will help prevent deformities of the lower jaw.
Child may need to be fed with the help of a PEG (percutaneous endoscopic gastrostomy), a procedure where a feeding tube is inserted into the stomach directly through the abdominal wall.
Their epilepsy is often difficult to control as the nature of the attacks varies greatly. Medication is prescribed on the basis of type of seizure, EEG results and the effects of the medication.
Surgery may sometimes be used to control epileptic attacks. A vagus nerve stimulator can be an alternative if other measures fail. The vagus nerve is one of the twelve cranial nerves originating in the brain. In an operation the stimulator is placed under the left collar bone and it sends electric impulses to the brain with the help of an electrode placed around the vagus nerve in the neck. These impulses can reduce epileptic activity and attacks.
Speech therapist to assesses and treats chewing and swallowing problems, drooling and communication difficulties.
Treatment usually requires mutli-disciplinary teamwork. The major hospitals in Sweden have specialist teams (dysphagia and nutrition teams) for assessing and treating speech, eating and swallowing difficulties.
Dental treatment for chewing and oral hygiene in the form of dental braces.

Spinal Drop Metastasis from Choroid Plexus Papilloma MRI

A 16 y o female patient, known case of posterior fossa mass _ Operated 2 years back.
Here are few snaps of Pre operative MRI Brain images showing lesion at the floor of posterior cranial fossa with caudal protrusion through foramen magnum.

Previous histo pathology report noted mentioning it to be Choroid Plexus Papilloma.

Now patient presented with backache and bilateral lower limb weakness, MRI Brain with spine screening done with contrast.
The Post Opeative MRI Brain shows:
E/o mid line sub occipital craniotomy, complete excision of lesion.
No obvious recurrent or residual lesion on post contrast T1.
Complete regression of hydrocephalus.

The Post Operative MRI Spine shows spinal drop metastasis.

Description of findings:

MRI Sagittal T2w images shows an intra medullary lesions in cervical cord, mild expansion of cord, non enhancing on post contrast fat sat T1.
Similar lesions on surface of spinal cord through out its length and completely filling thecal sac in lumbar region, an abnormal enhancement along surface of cord and nerve roots of cauda equina on post contrast fat sat T1 consistent with Spinal Drop Metastasis from Posterior fossa Choroid Plexus Papilloma.

Discussion: 

Choroid plexus papillomas (CPPs) are typically considered as benign tumors, with a favorable long-term prognosis. The standard treatment for a CPP is complete surgical resection and is thought to be curative.
Drop metastasis of CPP into the spinal subarachnoid space is rare.
In our case 16 year-old female who presented with back pain and lower limb weakness 2  years after removal of a posterior fossa CPP due to its spinal drop metastasis.
CPP can spread via cerebrospinal fluid pathways and cause spinal drop metastasis. Therefore, it is necessary to evaluate the whole spine in addition to brain, pre operatively as well as with post operative periodic follow-up MRIs in patients with CPP.

Choroid Plexus Papilloma MRI

A 1 y o male with headache, signs of raised ICT. 

On Admission CT followed by MRI Brain with Contrast.

This CT and MRI study of Brain shows an intra ventricular ovoid solid frond like well defined lesion in right lateral ventricle.
Lesion is isodense on CT with faint specks of calcifications.
Restricted diffusion on Dw MRI Images.
Avid homogeneous enhancement on post contrast T1w MRI.
No adjacent parenchymal invasion.

Imaging diagnosis given was Choroid Plexus Papilloma, moderate communicating hydrocephalus due to over production of Csf.

HISTOPATHOLOGY REPORT

Specimen : Excisional biopsy, right lateral ventricle mass.

Gross appearance : Multiple irregular soft to friable soft pieces of dull gray tan tissue, together measuring ~ 44x4x29mm. The cut section thru the larger piece appears papillary.

Microscopy : Benign neoplasm of probable choroid plexus epithelia comprising predominantly complex and branching neoplastic papillae lined by single layer of low cuboidal epithelia - devoid of significant cellular pleomorphism nor increased mitosis. In few foci the epithelia show focal stratification and crowding. The sub epithelial cord substance of the papillae appears focally odematous with congested blood vessels and sparse lymphocytic infiltrates. There is no evidence of cytological anaplasia.

Histopathological diagnosis : Choroid Plexus Papilloma.

Choroid Plexus Papilloma (CPP)

Imaging findings:
Location wise most common i.e ~ 50% in  atrium of lateral ventricle, left> right, ~ 40%  fourth ventricle.
~ 10%  third ventricle (roof) and ~ 5%  multiple sites.
• Morphology: Well delineated, lobulated intra ventricular cauliflower like mass, frond like surface projection.
Benign, slowly growing tumor often larger at the time of presentation.
Solid density on CT and signal intensity on MRI.
Foci of calcification best seen on CT.
Intense homogenous enhancement on post contrast T1.
CSF seeding of lesions is known.

Clinical Presentation: 
Age: Lateral ventricular CPPs common in infants and children where as fourth ventricular CPPs common in adults.
Most common signs/symptoms are of raised ICT, Macrocrania, bulging fontanelle, vomiting, headache, ataxia.

DD: 
Imaging wise difficult to differentiate from Choroid plexus carcinoma (CPCA)
Heterogeneous enhancement, invasion of adjacent brain parenchyma goes in favor of CPCA.

Reference : DI Osborn.

CV Junction Meningioma MRI

A 40 y o female with progressive lower limb weakness. 

On admission MRI Brain and Cervical spine screening done.

This MRI sagittal T2w images and Post contrast fat sat T1w images shows an extra axial solid signal intensity lesion, iso intense on T2w images at foramen magnum causing foramen magnum stenosis and significant cord compression. Intense homogeneous enhancement of lesion on post contrast with dural tailing.

Imaging diagnosis : CV Junction / Foramen Magnum Meningioma.

Neuroimaging During Pregnancy

During pre, there are some alterations in physiological state of pregnancy which leads to variety of neurological problems.
Pregnant patient with neurologic problems carries both diagnostic and therapeutic challenges.
The physicians often require some form of neuro imaging as part of their ongoing evaluation.

Safety of CT and MRI during pregnancy.
Whenever the imaging study in a pregnant patient is considered, risks to the fetus must be balanced with the health of mother.

CT ?
Off course carries risk of radiation to fetus.
The harmful effects of radiation depend on the stage of gestation, the total dose of radiation, and the rate.
As per animal studies, highest sensitivity appears to be during the period prior to conception when developing embryo has not yet been implanted in the uterus, during these first 2 week there is all-or-nothing effect that is either no effect or demise of the embryo.
During organogenesis, 3rd to 8th wk after conception, risks to the developing embryo is variable ranges from congenital malformations to growth retardation or neonatal death.
During the fetal period of development, 6 weeks after conception to birth, irradiation is unlikely to result in gross malformations. However, may result in mental retardation.
As per available data, the dose required to have mental retardation is 12–20 rad which is far higher than the dose achieved in today’s diagnostic procedures.
The fetal radiation dose during CT Brain of mother is less than 0.01 rad, whereas CT abdomen is 0.25–2.5 rad which is far low.
Some believe than there is increase risk of childhood cancer like leukemia but the figures from recent studies mention that there is extremely small added risk for children of patients who have undergone diagnostic imaging during pregnancy. Even multiple CT of the abdomen would only minimally increase the natural risk of childhood cancer.

Now what if patient is found pregnant after CT study is done? 
1. She should she be informed of the fetal radiation.
2. She and her family needs to counseled that exposure to less than 5 rad …is not associated with definite risk of spontaneous abortion, cong malformations, or mental retardation. This over concern should not prevent medically necessary procedures from being performed.

MRI ?
As far as neuroimaging i e Brain and Spine in concerned MRI often preferable to CT and is considered to be safe during pregnancy.
But one should delay elective MRI if possible as its believed that there is a strong magnetic field, minimal increase in body temperature, and there is lot of noise that may affect developing chochlea of fetus.
Intra venous Contrast ?
The problem is that we don’t have well-controlled studies in pregnant women, but animal studies have failed to show association of teratogenicity or mutagenicity with use of contrast.
However CT contrast is rated as a class B drug where as MRI contrast is rated as a class C drug by the FDA so  better avoid both unless no alternative exists.
Contrast during Lactation ?
Let it be CT or MRI, estimated delivery of contrast from mother to baby via breast milk is extremely low so there is no need to stop breast feeding following CT or MRI Contrast.


Neurologic Diseases Associated With Pregnancy

Pregnancy causes changes in the hemodynamic, endocrine, and hematologic systems, which may predispose to stroke during pregnancy.
Neuroimaging features of stroke are not going to change in pregnant and non pregnant pt.

Cerebral Venous Thrombosis
Presentation is often headache, seizures, encephalopathy, papilledema, or focal neurologic deficits.
MRI is investigation of choice as there is no radiation, its high Resolution and have MR Venography option which is possible without contrast. No need of keeping patient Nil by mouth (NBM).
MRI can elegantly demonstrate thrombosed dural venous sinus or deep cerebral vein. Associated infarction and intraparenchymal hemorrhage.

Thrombosed superior sagittal sinus, note low signal intensity thrombus on GRE.  

Thrombosed right parietal para sagittal cortical veins with low signal intensity thrombus on GRE

 A case of deep cerebral venous thrombosis_ bilateral thalamic venous infarcts. Thrombosed straight sinus not visualised on MR Venogram. 

Preeclampsia and Eclampsia
A multisystem disorder seen in the later stages of pregnancy / in the first 6 to 8 weeks after delivery.
Exact etiology is not clear, but the circulating toxins released from the placenta believed to cause vascular pathology.
Preeclampsia, a less-severe form of the disorder, occurs in ~5% of pregnancies, characterized by hypertension and proteinuria. Clinically usually asymptomatic, may present with headaches, sudden or unusual severe edema, visual changes.
Eclapsia , a severe form characterized by seizures.
MRI findings of preeclampsia and eclampsia are same, the combined term used in imaging diagnosis is Hyper tensive encephalopathy /  Posterior reversible encephalopathy.

MRI Brain axial FLAIR images show bilateral fronto parietal T2 white matter hyper intensities without restricted diffusion, and with normal MR Venogram of Brain which is very typical of  Posterior Reversible Encephalopathy

HELLP, a severe form seen in ~ 10% of patients and is a life-threatening condition characterized by hemolytic anemia, elevated liver enzymes, and low platelet count.
This low platelet count can lead to intra parenchymal bleed without any CVT on MR Venogram.

A typical case of HELLP, low platelet count and raised liver enzymes. 
MRI Brain shows left frontal bleed with left fronto parietal sub dural hematoma. Normal MR Angiography and Venography of Brain, done to rule out any associated vascular malformation.

Postpartum Angiopathy
A reversible cerebral vasoconstriction syndrome involves medium-sized intracranial arteries.
Patient often present with thunderclap headache, acute as well as focal neurologic deficits.
MRI Brain with MR Angio investigation of choice.  No contrast. No NBM.
MRI may demonstrate recent infarcts along border zones. Stenosis / vessel occlusion on MR Angio.

MRI Brain diffusion shows multiple recent infarcts along bilateral cortical border zones. MR Angiography of Brain shows multifocal intracranial stenosis. 

Meningioma
Meningiomas may dramatically increase in size during pregnancy as some of them represent hormonal receptors.
Presentation depends on its size and location, varies from elevated intracranial pressure, visual impairment with optic nerve atrophy to seizure.

A known case of Sphenoid wing meningoma.

Now admitted with recent onset seizures while pregnant, the on admission repeat MRI Brain shows same left side Sphenoid wing meningioma, but this time it was marginally increased in size with marked perilesional odema which was absent in previous MRI. 

Choriocarcinoma with Metastasis 
A malignant trophoblastic tumor.
May occur after a normal pregnancy, or can be seen in the context of abortion, molar or ectopic pregnancy.
Can metastasize to the liver, lung, or in 10% of cases to the brain.
Choriocarcinoma and its mets a highly vascular tumor and therefore very susceptible to bleed.
Presentation may be headache, focal neurologic deficits, seizures, encephalopathy, raised ICT.

A case of Choriocarcinoma with hemorrhagic metastasis in Brain

Pituitary Apoplexy
During pregnancy the pituitary gland tends to grow in size and some time it outstrips its vascular supply leading to hemorrhagic and/or ischemic changes.
Presentation is usually sudden headache, nausea, or vomiting, loss of consciousness.
Due to the close proximity of the pituitary gland to the optic chiasm and cranial nerves III, IV, and VI may present with  multiple CN Palsy.

A case of pituitary apoplexy showing enlargement of pituitary with bleed on MRI mid sagittal non contrast T1w section. 

Sheehan syndrome
A hypopituitarism secondary to severe blood loss and hypo volemic shock during labour resulting in Ischemia and necrosis of pituitary .
On MRI, lack of normal enhancement on post contrast images is a diagnostic clue.
Once bleed or ischemia resolves, on follow-up imaging one may find Empty sella due to loss of tissue volume.

MRI Brain, mid sag T2w sections shows Roomy hypophyseal fossa occupied by Csf. 

Pituitary flat at the floor near posterior wall of sella with an abnormal height less than 2mm.

Lymphocytic Hypophysitis
An autoimmune condition of the pituitary occurs in late pregnancy or the postpartum period due to Lymphocytic infiltration of the pituitary gland, infundibulum.
Enlargement of pituitary gland with abnormal enhancement on MRI is a diagnostic clue.

Wernicke's Encephalopathy
Caused by thiamine deficiency.
Common in chronic alcoholics however pregnant patients with hyperemesis gravidarum due to malnutrition due to nausea and vomiting and increased fetal metabolic demand for thiamine, land up with thiamine deficiency.

A case of Wernike's Encephalopathy, MRI Brain Axial FLAIR images at the level of brain stem shows typical peri aqueductal involvement of mid brain and hypothalamic T2 hyper intensities. 

Characterized by triad of Acute encephalopathy, Ataxia, and Ophthalmoplegia or Coma alone.
With early diagnosis, can be rapidly reversed with IV high dose of thiamine and fatal if left untreated.
MRI is investigation of choice.

Multiple Sclerosis
Commonly affects 20 to 50 Years females i e reproductive  age group.
Nothing specifically different in the neuroimaging of pregnant / non preg MS patients however pregnancy, affect the relapse rate, as relapses decrease in frequency throughout pregnancy  but increase in the postpartum period.
Increased estriols level during pregnancy result in  T2 mediated immune shift in MS.
MRI investigation of choice.

Case of MS, MRI Brain Axial and Sagittal T2w images of Brain showing plaques of demyelination in bilateral fronto parietal peri ventricular white matter, involving corpus callosum. Sagittal T2 w images of spine of same patient shows faint T2 hyper intensities of demyelination involving cervico dorsal cord.

Pregnancy-related Back Pain
Backache is common during pregnancy cause can be  hormone-induced laxity of spinal ligaments, Gravid uterus exerting pressure on the lumbosacral plexus or increased lordosis in pregnancy.
MRI is the best, can visualize spine , spinal cord as well as nerve roots which is not possible with CT.
Better post pone MRI too.
But Strong indications for MRI are cauda equina syndrome, acute weakness, radiating pain, bowel bladder involvement.
MRI may reveal Disc herniation causing cord, cauda equina or nerve root compression and cord demyelination in patient of lower limb weakness.

MRI Lumbar spine sagittal and axial T2 w images at L5-S1 show a left para central disc extrusion causing obvious compression of left traversing S1 nerve root in lateral recess. 

MRI Dorsal spine sagittal and axial T2w images shows a focal disc protrusion causing cord compression.

MRI Cervico dorsal spine, sagittal T2w images show abnormal multi segmental contiguous intramedullary T2 hyper intensity suggestive of cord demyelination. 

Epidural hematoma can occur rarely in association with pregnancy, either spontaneous related to increased abdominal pressure during delivery or as a complication of epidural anesthesia.

MRI Lumbar spine, Sag T1 and T2w images : Case of posterior spinal epidural hematoma causing significant canal stenosis at L2-3 disc level with marked compression over thecal sac and nerve roots of cauda equina. 

Conclusion
As far as safely is concerned MRI is safe than CT. However post pone both CT as well as MRI if possible.
As far as Neuro imaging is concerned the treating physician, radiologist should be aware of these conditions which are common during pregnancy. Even the MRI technician should be trained for this to do necessary changes in a given study depending upon the findings while doing MRI like running Angio or Veno sequence as and when required.

Post Laminectomy site Adhesion / Herniation of Cord MRI

A post operative case came for follow up imaging. Clinical details not available.

This MRI Dorsal spine shows:
E/o laminectomy, faint intra medullary T2 hyper intensity of focal cord Gliosis.
Focal posterior displacement of cord at laminectomy site.
MRI repeated in prone position, cord is persistently seen displaced posteriorly at laminectomy site _ possible with adhesion or herniation.

Anterior Thoracic Spinal Cord Adhesion and Herniation on MRI

A 30 y male presented with intermittent backache, mild progressive paraplegia. Anterior spinal cord dysfunction on neurological examination. No obvious dorsal column involvement. 

MRI spine shows anterior thoracic cord displacement with flattening. Wide sub arachnoid space dorsal to cord iso intense to Csf.

Imaging wise possible DD:
1. Posterior Arachnoid cyst.

2. Idiopathic Anterior Spinal Cord Herniation / Adhesion.

ANTERIOR SPINAL CORD HERNIATION / ADHESION

In a study of middle aged patients of both sexes presenting with chronic progressive anterior cord dysfunction with imaging demonstration of anterior thoracic cord displacement is either by a posterior arachnoid cyst or anterior dural adhesion / herniation. Cord thinning was frequently found without signal abnormality in cord.

A dorsal arachnoid cyst is one of the most important entities included in the differential diagnosis of idiopathic spinal cord herniation. If findings on standard MR images are equivocal, phase-contrast MR imaging or CT myelography may be helpful for detecting the free flow of CSF and excluding an arachnoid cyst.
If it’s an obvious posterior Arachnoid cyst, needs decompression for sure. Cases without appreciable Arachnoid cyst can be associated with either anterior spinal cord herniation or adhesion. 

Mechanisms leading to anterior spinal cord herniation described in literatures are congenital anterior dural defects, duplication and rarely trauma. A dural defect cannot be demonstrated on MRI, although absent visualization did not exclude a defect at surgery.

A typical case of anterior spinal cord herniation from AJNR

In patients in whom no defect is found at surgery; instead, the cord can be anteriorly tethered by arachnoid or dentate adhesions. The thoracic anterior spinal cord adhesion syndrome (TASCAS) is a novel term to describe patients presenting in this way. 

The frequency with which adjacent disc abnormality is seen in surgical case report supports the role of disc disease in the aetiology of TASCAS. One possible mechanism would involve inflammatory change, incited by a diseased disc, causing adhesions with the adjacent dura. The anterior cord surface becomes tethered by associated arachnoid and/or dentate ligament adhesions. Subsequent disc resorption could result in formation of a dural retraction pocket predisposing to progressive pathological cord displacement and subsequent herniation. Other factors may also be contributory, such as the relatively anterior position of the cord in the mid-thoracic spine due to the normal physiological thoracic kyphotic status, bringing the spinal cord into close apposition with the discovertebral complexes.

MRI is considered sufficient for the diagnosis of Posterior Arachnoid cyst Vs Anterior Cord herniation / Adhesion in most cases. Use of three-dimensional volume T2* sequences (such as CISS /FIESTA) as in this case provide high-resolution images which aid the decision making while limiting the need for invasive procedures.
Even with these high-resolution series, the exact nature of the abnormality can only really be defined at surgery. In any case, the decision whether to operate or not is ultimately made on clinical rather than radiological grounds. 

If a surgical approach is to be contemplated, the anterior aspect of the cord should be visualized intra operatively, regardless of the degree of radiological certainty in the pre-operative differentiation between hernia or adhesion.

Appropriate initial imaging studies in Neuro as per clinical problems

                      Clinical problem                                             Modality

Fractures / Bony lesions of Skull	CT brain with bone window
Major head trauma	CT (neurologically unstable); MRI (neurologically stable)
Mild head trauma	Observe; CT (if persistent headache)
Acute hemorrhage (Bleed)	Non contrast CT
Suspected intracerebral aneurysm or AV Malformations	MRI Brain with (3D TOF Non Contrast) MR Angiography
Hydrocephalus	Non contrast CT < MRI
Transient Ischemic Attack	Non contrast CT, MRI if vertebro basilar findings; consider carotid Doppler if bruit present.
Recent giddiness and walking imbalance	MRI Brain with 3D TOF Non Contrast MR Angiography
Acute stroke (suspected hemorrhagic)	Noncontrast CT
Acute stroke (suspected non hemorrhagic)	MRI Brain with (3D TOF Non Contrast) MR Angiography
Multiple sclerosis	MRI Brain and Whole Spine screening for Cord
Tumor or metastases	MRI with Contrast
Aneurysm (chronic history)	3D TOF Non Contrast MR Angiography or Contrast CT Angiography
Abscess	Contrast CT / MRI
Preoperative for cranial surgery	Contrast angiography
Meningitis	Lumbar tap; CT Brain only to exclude complications
Seizure (new onset or poor therapeutic response)	MRI (Epilepsy protocol)
Seizure (febrile or alcohol withdrawal without neurologic deficit)	CT / MRI sos
Neurologic deficit with known primary tumor elsewhere	MRI if associated sensorineural findings
Vertigo (if suspect acoustic neuroma or posterior fossa tumor)	MRI with thin sections for Cranial Nerve imaging
Headache	CT Brain covering Para nasal sinuses
Dementia	Nothing, or MRI Brain
Alzheimer’s disease	Nuclear medicine SPECT scan
Sinusitis	CT / MRI Brain with limited axial sections to cover sinuses

Reference: Mettler, Essentials of Radiology, 2nd ed.