Tuesday 21 February 2012

IVY sign in major vessel stenosis

A  7yo patient came for MRI Brain with history ... no need to mention here as it was not specific and i am sure it was not related to patient's imaging findings. 
Only Axial FLAIR images of patient were abnormal with a subtle finding. Rest of the MRI study including Diffusion and GRE were absolutely normal.
Guess !! the finding.
Faint serpigenous high signal in right peri sylvian cortical sulci are the cortical branches of right MCA with sluggish flow attributed to IVY sign.
and that's his angio... 
Click image to enlarge. 
3 D TOF Non contrast MR Angiography of brain shows severe right MCA proximal main stem stenosis with sparsity of cortical branches of right MCA compared to left. 

'IVY' sign
Normally cortical branches of major intra cranial vessels which travel along hemispheric cortical sulci are not visualised on FLAIR.
Due to any reason if the flow in these cortical branches hampered, the slow flow in these cortical branches or the cortical collaterals developed thereby , reflect high signal on FLAIR, relatively higher than that of adjacent normal isointense brain parenchyma and seen as serpigenous hyperintensities in the region of cortical sulci on FLAIR attributed to IVY sign. 

IVY sign is reported in following conditions.
Moya Moya disease or major intra cranial vessel stenosis lead to cortical branches with slow flow or development of collaterals with sluggish flow.
Early ischemia thrombus in cortical branches may reflect high signal on FLAIR

To see similar cases with other causes of IVY sign : Click here

Sunday 19 February 2012

Cranial Nerves Normal MRI Anatomy

1st CN - Olfactory Nerve
2nd CN - Optic Nerve
3rd CN-  Occulomotor Nerve, 4th CN - Trochlear Nerve
5th CN - Trigeminal Nerve
6th CN - Abducens Nerve, 7 8 th CN Complex - Facial and Vestibulochoclear Nerve
9th CN - Glassopharyngeal Nerve, 10th CN Vagus Nerve
11th CN - Spinal Accessory Nerve, 12th CN - Hypoglossal Nerve
Cranial Nerves

Cranial nerves can be thought of as modified spinal nerves, since the general functional fibre types found in spinal nerves are also found in cranial nerves but are supplemented by special afferent or efferent fibre. 
The 12 pairs of cranial nerves are identified either by name or by Roman or Arabic numeral.

Olfactory Nerve (CN I or 1)
Conveying information concerning olfaction, or smell. Bipolar cells in the nasal mucosa give rise to axons that enter the cranial cavity through foramina in the cribriform plate of the ethmoid bone. These cells and their axons, totaling about 20 to 24 in number, make up the olfactory nerve. Once in the cranial cavity, the fibres terminate in a small oval structure resting on the cribriform plate called the olfactory bulb. The functional component of olfactory fibres is special visceral afferent. Injury or disease of the olfactory nerve may result in anosmia, an inability to detect odours.

Optic Nerve (CN II or 2)
Rods and cones in the retina of the eye receive information from the visual fields and, through intermediary cells, convey this input to retinal ganglion cells. Ganglion cell axons converge at the optic disc, pass through the sclera, and form the optic nerve. Optic nerve from each eye enters the skull via the optic foramen, and they join to form the optic chiasm. At the chiasm, fibres from the nasal halves of each retina cross, while those from the temporal halves remain uncrossed. In this way the optic tracts, which extend from the chiasm to the thalamus, contain fibres conveying information from both eyes. Injury to one optic nerve therefore results in total blindness of that eye, while damage to the optic tract on one side results in partial blindness in both eyes.
Since the subarachnoid space around the brain is continuous with that around the optic nerve, increases in intracranial pressure can result in papilledema.

Oculomotor Nerve (CN III or 3)
The oculomotor nerve arises from two nuclei in the rostral midbrain. These are (1) the oculomotor nucleus, the source of general somatic efferent fibres to superior, medial, and inferior recti muscles, to the inferior oblique muscle, and to the levator palpebrae superious muscle, and (2) the Edinger-Westphal nucleus, which projects general visceral efferent preganglionic fibres to the ciliary ganglion. The oculomotor nerve exits the ventral midbrain,
pierces the dura mater, courses through the lateral wall of the cavernous sinus, and exits the cranial cavity via the superior orbital fissure. Within the orbit it branches into a superior ramus (to the superior rectus and levator muscles) and an inferior ramus (to the medial and inferior rectus muscles, the inferior oblique muscles, and the ciliary ganglion). Postganglionic fibres from the ciliary ganglion innervate the sphincter pupillae muscle of the iris as well
as the ciliary muscle. Oculomotor neurons project primarily to orbital muscles on the same side of the head. A lesion of the oculomotor nerve will result in paralysis of the three rectus muscles and the inferior oblique muscle (causing the eye to rotate downward and slightly outward), paralysis of the levator palpebrae superious muscle (drooping of the eyelids), and
paralysis of the sphincter pupillae and ciliary muscles (so that the iris will remain dilated and the lens will not accommodate).

Trochlear Nerve (CN IV or 4)
The fourth cranial nerve is unique for three reasons. First, it is the only cranial nerve to exit the dorsal side of the brainstem. Second, fibres from the trochlear nucleus cross in the midbrain before they exit, so that trochlear neurons innervate the contralateral (opposite side) superior oblique muscle of the eye. Third, trochlear fibres have a long intracranial course before piercing the dura mater. The trochlear nucleus is located in the caudal midbrain; the functional component of these cells is general somatic efferent. After exiting at the dorsal side of the midbrain, the trochlear nerve loops around the midbrain, pierces the dura mater, and passes through the lateral wall of the cavernous sinus. It then enters the orbit through
the superior orbital fissure and innervates only the superior oblique muscle, which rotates the eye downward and slightly outward. Damage to the trochlear nerve will result in a loss of this eye movement and may produce double vision (diplopia).

Trigeminal Nerve (CN V or 5)
The trigeminal nerve is the largest of the cranial nerves. It has both motor and sensory components, the sensory fibres being general somatic afferent and the motor fibres being special visceral efferent. Most of the cell bodies of sensory fibres are located in the trigeminal ganglion, which is attached to the pons by the trigeminal root. These fibres convey pain and thermal sensations from the face, oral and nasal cavities, and parts of the dura mater and nasal
sinuses, sensations of deep pressure, and information from sensory endings in muscles.  Trigeminal motor fibres, projecting from nuclei in the pons, serve the muscles of mastication (chewing). Lesions of the trigeminal nerve result in sensory losses over the face or in the oral cavity. Damage to the motor fibres results in paralysis of the masticatory muscles; as a result, the jaw may hang open or deviate toward the injured side when opened. Trigeminal neuralgia, or tic douloureux, is an intense pain originating mainly from areas supplied by sensory fibres of the maxillary and mandibular branches of this nerve.
The trigeminal ganglion gives rise to three large nerves: the ophthalmic, maxillary, and mandibular.

Abducens Nerve (CN VI or 6)

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.

Facial Nerve (CN VII or 7)
The facial nerve is composed of a large root that innervates facial muscles and a small root (known as the intermediate nerve) that contains sensory and autonomic fibres. From the facial nucleus in the pons, facial motor fibres enter the internal auditory meatus, pass through the
temporal bone, exit the skull via the stylomastoid foramen, and fan out over each side of the face in front of the ear. Fibres of the facial nerve are special visceral efferent; they innervate the small muscles of the external ear, the superficial muscles of the face, neck, and scalp, and
the muscles of facial expression. The intermediate nerve contains autonomic parasympathetic) as well as general and special sensory fibres. Preganglionic autonomic fibres, classified as general visceral efferent, project from the superior salivatory nucleus
in the pons. Exiting with the facial nerve, they pass to the pterygopalatine ganglion via the greater petrosal nerve (a branch of the facial nerve) and to the submandibular ganglion by way of the chorda tympani nerve (another branch of the facial nerve, which joins the lingual branch of the mandibular nerve). Postganglionic fibres from the pterygopalatine ganglion innervate the nasal and palatine glands and the lacrimal gland, while those from the submandibular ganglion serve the submandibular and sublingual salivary glands. Among the sensory components of the intermediate nerve, general somatic afferent fibres relay sensation from the caudal surface of the ear, while special visceral afferent fibres originate from taste
buds in the anterior two-thirds of the tongue, course in the lingual branch of the mandibular nerve, and then join the facial nerve via the chorda tympani branch. Both somatic and visceral afferent fibres have cell bodies in the geniculate ganglion, which is located on the facial nerve as it passes through the facial canal in the temporal bone. Injury to the facial nerve at the brainstem produces a paralysis of facial muscles known as Bell palsy as well as
a loss of taste sensation from the anterior two-thirds of the tongue. If damage occurs at the stylomastoid foramen, facial muscles will be paralyzed but taste will be intact.

Vestibulocochlear Nerve (CN VIII or 8)
This cranial nerve has a vestibular part, which functions in balance, equilibrium, and orientation in three-dimensional space, and a cochlear part, which functions in hearing. The functional component of these fibres is special somatic afferent; they originate from receptors located in the temporal bone. Vestibular receptors are located in the semicircular canals of the ear, which provide input on rotatory movements (angular acceleration), and in the utricle and saccule, which generate information on linear acceleration and the influence of gravitational pull. This information is relayed by the vestibular fibres, whose bipolar cell bodies are located in the vestibular (Scarpa) ganglion. The central processes of these neurons exit the temporal bone via the internal acoustic meatus and enter the brainstem alongside the facial nerve. Auditory receptors of the cochlear division are located in the organ of Corti and follow the spiral shape (about 2.5 turns) of the cochlea. Air movement against the eardrum initiates action of the ossicles of the ear, which, in turn, causes movement of fluid in the spiral cochlea. This fluid movement is converted by the organ of Corti into nerve impulses that are interpreted as auditory information. The bipolar cells of the spiral, or Corti, ganglion branch into central processes that course with the vestibular nerve. At the brainstem, cochlear fibres separate from vestibular fibres to end in the dorsal and ventral cochlear nuclei. Lesions of the vestibular root result in eye movement disorders (e.g., nystagmus), unsteady gait with a tendency to fall toward the side of the lesion, nausea, and vertigo. Damage to the cochlea or cochlear nerve results in complete deafness, ringing in the ear (tinnitus), or both.

Glossopharyngeal Nerve (CN IX or 9)
The ninth cranial nerve, which exits the skull through the jugular foramen, has both motor and sensory components. Cell bodies of motor neurons, located in the nucleus ambiguus in the medulla oblongata, project as special visceral efferent fibres to the stylopharyngeal muscle. The action of the stylopharyngeus is to elevate the pharynx, as in gagging or swallowing. In addition, the inferior salivatory nucleus of the medulla sends general visceral efferent fibres to the otic ganglion via the lesser petrosal branch of the ninth nerve; postganglionic otic fibres innervate the parotid salivary gland. Among the sensory components of the glossopharyngeal nerve, special visceral afferent fibres convey taste sensation from the back third of the tongue via lingual branches of the nerve. General visceral afferent fibres from the pharynx, the back of the tongue, parts of the soft palate and eustachian tube, and the carotid body and carotid sinus have their cell bodies in the superior and inferior ganglia, which are situated, respectively, within the jugular foramen and just outside the cranium. Sensory fibres in the carotid branch detect increased blood pressure
in the carotid sinus and send impulses into the medulla that ultimately reduce heart rate and arterial pressure; this is known as the carotid sinus reflex. 

Vagus Nerve (CN X or 10)
The vagus nerve has the most extensive distribution in the body of all the cranial nerves, innervating structures as diverse as the external surface of the eardrum and internal abdominal organs. The root of the nerve exits the cranial cavity via the jugular foramen. Within the foramen is the superior ganglion, containing cell bodies of general somatic afferent fibres, and just external to the foramen is the inferior ganglion, containing visceral afferent cells. Pain and temperature sensations from the eardrum and external auditory canal and pain fibres from the dura mater of the posterior cranial fossa are conveyed on general somatic afferent fibres in the auricular and meningeal branches of the nerve. Taste buds on the root of the tongue and on the epiglottis contribute special visceral afferent fibres to the superior laryngeal branch. General visceral afferent fibres conveying sensation from the lower pharynx, larynx, trachea, esophagus, and organs of the thorax and abdomen to the left (splenic) flexure of the colon converge to form the posterior (right) and anterior (left) vagal
nerves. Right and left vagal nerves are joined in the thorax by cardiac, pulmonary, and esophageal branches. In addition, general visceral afferent fibres from the larynx below
the vocal folds join the vagus via the recurrent laryngeal nerves, while comparable input from the upper larynx and pharynx is relayed by the superior laryngeal nerves and by pharyngeal branches of the vagus. A vagal branch to the carotid body usually arises from the inferior ganglion. Motor fibres of the vagus nerve include special visceral efferent fibres arising from the nucleus ambiguus of the medulla oblongata and innervating pharyngeal constrictor muscles and palatine muscles via pharyngeal branches of the vagus as well as the superior laryngeal nerve. All laryngeal musculature (excluding the cricothyroid but including the muscles of the vocal folds) are innervated by fibres arising in the nucleus ambiguus. Cells of the dorsal motor nucleus in the medulla distribute general visceral efferent fibres to plexuses or ganglia serving the pharynx, larynx, esophagus, and lungs. In addition, cardiac branches
arise from plexuses in the lower neck and upper thorax, and, once in the abdomen, the vagus gives rise to gastric, celiac, hepatic, renal, intestinal, and splenic branches or plexuses.  Damage to one vagus nerve results in hoarseness and difficulty in swallowing or speaking. Injury to both nerves results in increased heart rate, paralysis of pharyngeal and laryngeal musculature, atonia of the esophagus and intestinal musculature, vomiting, and loss of visceral reflexes. Such a lesion is usually life-threatening, as paralysis of laryngeal muscles may result in asphyxiation.

Accessory Nerve (CN XI or 11)
The accessory nerve is formed by fibres from the medulla oblongata (known as the cranial root) and by fibres from cervical levels C1–C4 (known as the spinal root). The cranial root originates from the nucleus ambiguus and exits the medulla below the vagus nerve. Its fibres join the vagus and distribute to some muscles of the pharynx and larynx via pharyngeal and recurrent laryngeal branches of that nerve. For this reason, the cranial part of the accessory
nerve is, for all practical purposes, part of the vagus nerve. Fibres that arise from spinal levels exit the cord, coalesce and ascend as the spinal root of the accessory nerve, enter the cranial cavity through the foramen magnum, and then immediately leave through the jugular foramen. The accessory nerve then branches into the sternocleidomastoid muscle, which tilts the head toward one shoulder with an upward rotation of the face to the opposite side, and the trapezius muscle, which stabilizes and shrugs the shoulder.

Hypoglossal Nerve (CN XII or 12)
The hypoglossal nerve innervates certain muscles that control movement of the tongue. From the hypoglossal nucleus in the medulla oblongata, general somatic efferent fibres exit the cranial cavity through the hypoglossal canal and enter the neck in close proximity to the accessory and vagus nerves and the internal carotid artery. The nerve then loops down and forward into the floor of the mouth and branches into the tongue musculature from underneath. Hypoglossal fibres end in intrinsic tongue muscles, which modify the shape of the tongue (as in rolling the edges), as well as in extrinsic muscles that are responsible for changing its position in the mouth. A lesion of the hypoglossal nerve on the same side of the head results in paralysis of the intrinsic and extrinsic musculature on the same side. The tongue atrophies and, on attempted protrusion, deviates toward the side of the lesion.

Reference : The brain and the nervous system / edited by Kara Rogers.

Related article:  MRI Planning Protocol for Cranial Nerves

Acute MCA infarct Limitations of CT

A 32 yo male with sudden left sided weakness since 4 hrs. 
CT study of Brain shows faint hypodensity involving right basal ganglia and adjacent insular cortex - a subtle and subjective finding. 
CT immediately followed by MRI Brain Diffusion with Non contrast 3 D TOF MR Angiography of Brain shows
An acute infarct with restricted diffusion involving right basal ganglia, adjacent insular cortex and right peri sylvian cerebral cortex. Area of involvement corresponds to right MCA proximal main stem territory.
No significant mass effect.
No hemorrhagic transformation.
On MR Angiography right ICA - MCA not visualized implies to occlusion. Right ACA filled from contra lateral anterior circulation via Acom.

Imaging diagnosis : Acute infarct right MCA proximal main stem territory secondary to right ICA - MCA occlusion.

CT in acute ischemic stroke: 
Infarcted tissue on CT seen as an area of low attenuation due to cytotoxic edema that develops in the region of infarct as a result of ATP ionic pump failure. An increase of water content of brain tissue by 1% will decrease CT attenuation by ~2.5 HU.
Hypoattenuation on CT is highly specific for irreversible ischemic brain damage if it is detected within first 6 hours, and implies to larger volume infarct, more severe symptoms, less favorable clinical courses and proneness for hemorrhage.
Therefore if infarct is seen on CT means bad news.
No hypodensity on CT is a good sign indicates reversible ischemic brain damage.
On CT 60% of infarcts are seen within 3-6 hrs and virtually all are seen in 24 hours. The overall sensitivity of CT to diagnose stroke is 64% and the specificity is 85%.
Diffusion Weighted MR Imaging (DWI) in acute ischemic stroke: 
The most sensitive sequence for acute ischemic stroke, works on principle of restriction of Brownian motion of extracellular water due to imbalance caused by ion pump failure and cytotoxic edema.
Comparison of diffusion-weighted MRI and CT in acute stroke.
On DWI the acute lesion identified correctly in all instances and on CT it was identified correctly in 42 to 63% of patients.
Sensitivity for detection of more than 33% MCA involvement was better for DWI (57 to 86%) than for CT (14 to 43%), whereas specificity obviously high with MRI Diffusion.

Diffusion is the most sensitive and specific sequence. Not even compared to CT, more practicle compared to CT and MRI Perfusion imaging  in acute ischemic stroke where time is very precious. Each second represent one neuron. 

Patient Positioning during MRI

Here through this case I’m trying to discuss importance of proper patient positioning during the MRI and certain modifications as per the case.
This is a 75 y o male with severe kyphotic deformity, even he was not able to extend his hip and knee.  When made to sleep on MR table could not place his head in Brain coil due to kyphosis.
We can’t use force to make him straight.
Proper packing is important is such case so that patient can lie, provided he should be conformable.
So what we did is some medications, in the packing to supports his trunk.
First made an elevator of pillows on the table sloping towards gantry to raise his lumbar region and pelvis to negotiate his inability to place his head in brain coil.  Yes with this he could do that. Needed one more support of pillow below his thigh and knee to support his fixed flexed hip and knees.
With this we could perform at least necessary sequences like Diffusion , FLAIR and Non contrast 3 D TOF for Brain Angio.

Take home notes... 
Due to deformities or severe spasm patient may not be able to lie strength supine on table, needs additional packing in certain areas to negotiate the deformity and to support body portions, making patient conformable during the study.  

UL Basal ganglia T1 hyperintensity

Left basal ganglionic T1 hyperintensity.
No obvious low signal intensity hemosiderin staining on T2*GRE.
3D TOF Non contrast MR Angiography of brain and neck show no significant major vessel stenosis or occlusion particularly on left side.
Clinical details not available.

There are many causes of basal ganglionic signal abnormality.
Cases of unilateral signal abnormality very uncommon than bilateral and causes are very typical.

DDs for unilateral basal ganglionic T1 hyperintensity in this case include Meth Hb staining due to haemorrhage or hemorrhagic transformation in an infarct,  Hyperglycemia associated Hemi chorea-ballism.
In this case haemorrhage with Meth Hb staining is unlikely as there is no any low signal intensity hemosiderin staining on T2*GRE images. Infarct with hemorrhagic transformation unlikely as there is no significant major vessel stenosis or occlusion on MR Angio.
Hyperglycemia associated Hemi chorea-ballism (Non-ketotic hyperglycemia ) is possible and needs further evaluation of pts blood sugar levels and clinically for any Hemichorea or hemiballismus.

The triad of Hemichorea, Hyperglycemia and Unilateral high signal in basal ganglia on T1 MRI Brain is considered to be a unique syndrome, reported with Non-ketotic hyperglycemia.

Discectomy and Fusion Cage MRI

MRI Cervical region spine Sagittal T1, Sagittal T2 with Axial T2w image : E/o Anterior cervical discetomy at C3-4 and C5-6 with susceptibly artefact due to cage implanted in the disc space for interbody fusion.
At C4-5 disc show posterior protrusion with significant cord compression.

Anterior cervical discectomy with disc cage assisted interbody fusion: 
Anterior cervical discectomy (ACD) is an effective and safe approach for nerve root or spinal cord compression caused by disc herniation, allows direct visualization of the entire inter space and wide decompression of the anterior aspect cervical spinal cord and nerve roots. It may be undertaken in cases of multilevel disease and interbody fusion may be performed if required on the same setting.
Cervical inter body fusion after discectomy needed for preservation of the physiological lordosis and stability of the cervical spine. Fusion rates decrease significantly when more than one level undergoes surgery so some authors recommended the addition of a plate system to improve results in past.
In newer studies, cages are used for inter body fusion, the disc cages have a load-sharing function and stabilize the spine to increase segmental stiffness, thus achieving fusion rates similar to those associated with bone grafts, even in multilevel disease.
Interbody fusion cages are hollow metal implants that restore physiological disc height, allowing bone growth within and around them, thus stimulating bone fusion.

In anterior cervical discectomy, an incision is made in the front of the neck which allows the surgeon to remove the damaged and protruding disc and associated bone spurs in order to relieve any pressure on the spinal cord and nerve roots. After the disc is removed, the gap that has been created between the two bones is then typically filled with a piece of bone graft (obtained from a cadaver or from the patient’s pelvis) or with a titanium cage device.  The goal of the procedure is with preservation of height of disc space and to cause the two bones to grow and fusion together resulting in a complete loss of motion at the surgical level.
Subsidence of disc cage into the adjacent VBs, cage dislocation, nonunion-related instability, and painful pseudarthrosis.
MRI Safety: 
Patients who have metallic devices implanted in spine like pedicle screws or disc cages can have MRI scan done, but the image quality and information often hampered due to susceptibility artifact by the metal device. Artifact is much more of a problem if stainless steel implants are used for the fusion. Recently, titanium implants have been used for most fusions and stainless steel has almost out dated in most of the institution for the sake of follow up post operative MRI study.

Saturday 18 February 2012

Thyroid Ophthalmopathy MRI

A 45 y o male with bilateral orbital proptosis clinically more on left side.  Found to be restless. No visual field defect.
MRI study shows:
Bilateral proptosis, marked on left side.
On axial sections diffuse enlargement of recti, confined to muscle belly. Tendinous portions spared.
Predominantly inferior rectus, medial rectus and superior rectus involved, more on left side compared to right.

Imaging wise diagnosis: Thyroid Ophthalmopathy.
Advised T3, T4 and TSH in further evaluation.

Syn : Thyroid associated Orbitopathy.
The commonest cause of proptosis in adults, most frequently associated with Grave’s disease  with female preponderance.
Clinical presentation includes predominantly proptosis and diplopia.
Patholophysiology is enlargement of the extraocular muscles and increase retro orbital fat. The exact mechanism is unknown, antibodies to thyroid stimulating hormone (TSH) appear to cross react with antigens in the orbit resulting in infiltration by activated T lymphocytes with subsequent release of inflammatory mediators. The muscles are infiltrated with inflammatory cells and mucopolysccaride deposition.
MRI is investigation of choice due to its excellent soft tissue resolution.
Diffuse enlargement is usually confined to muscle belly. Along with diffuse enlargement signal abnormality may be obvious, T1 and T2 hyper intensity can attributed to fatty infiltration and inflammation. Tendinous portions of recti typically spared.
Bilateral (80%) and symmetric (70%) involvement is typical.
Severity of involvement of  extra-ocular muscles is as Inferior > medial > superior > lateral. (Mnemonic: I'M SLOW)

Cauda Equina Tumor

MRI Lumbar spine: 
In spinal canal, there is an intra dural single well circumscribed ovoid mass below conus among the nerve roots of cauda equina at the level of L2-3 disc, iso intense to cord on T1 and slightly hyper intense to cord on T2w images.
Not extending out of neural foramen.
Nerve roots of cauda equina displaced on either side of the lesion and compressed by the side of mass.
No marked remodelling of bony spinal canal.

Imaging wise possible DDs: Nerve sheath tumor > Meningioma.
Histopathology: Nerve sheath tumor - Schwannoma. 

Duplication of fetal PCA MRA

3 D TOF Non Contrast MR Angiography of Brain shows:
Non visualisation of left MCA from its origin along with its cortical branches implies to occlusion.
Left PCA has fetal origin - a common anatomical variation but in that it shows Duplication, two fetal PCAs on left side seen arising from ICA - a rare normal anatomical variation. 

Hypoxic Ischemic Encephalopathy MRI

A 7 y o male with delayed mile stone. Birth history significant father mentions delayed cry. NICU admission after birth for 1month.
CT study of Brain

...... Honestly I may pass it off normal if in hurry.
Somehow i was not very convinced with the normal CT looking at patient and requested relatives to get his MRI done.
And that's his MRI...
MRI Axial FLAIR images show bilateral symmetrical T2 hyperintensity involving thalami and Perirolandic cortex consistent with Perinatal Hypoxic Ischemic Brain Insult. 
Take home notes...
It may not be possible every time but as far as possible, keep habit of seeing patient clinically and give a second look to the study. 
My Boss has taught this to me and he always insist me to do so. 
It really works !!!

Hypoxic Ischemic Encephalopathy

HIE, formerly peri natal or birth asphyxia – a cerebral hypoperfusion injury.

Imaging wise best diagnostic clue is Gliosis involving peri rolandic cortex or para sagittal border zones, bilateral and often symmetric involvement. Basal ganglia damaged if ischemic event is profound and acute. Associated findings may be microcephaly, secondary craniosynostosis, cerebral cortical and mid brain atrophy.

Patient with this finding often are term neonates with significant birth history like fetal distress prior to delivery, low Apgar score, required resuscitation at birth, metabolic acidosis (cord pH less than 7), Neurological abnormalities in first 24 hours. Maternal infection, pre-eclampsia and diabetes.

Seek inborn errors of metabolism if apparent HIE with normal Apgar OR if more than 1 HIE child in a family. Other causes can be Inherited prothrombotic disorders leading to arterial or venous occlusions are Protein CIS deficiencies, factor V Leiden mutation, antiphospholipid antibodies.

Epidemiology up to 2/1,000 (0.2%) live births.

Clinical presentation
Mild : Hyperalert/irritable, mydriasis, EEG normal
Moderate: Lethargy, hypotonia, ~ HR, Seizures.
Severe: Stupor, flaccid, reflexes absent; Seizures.
Periventricular leukomalacia (PVL) patient show Lower extremity spasticity.
Unilateral/focal lesions present with Hemiplegia / Hemiparesis.
Parasagittal cystic encephalomalacia show Spastic tetra paresis whereas Bilateral BG damage show Extrapyramidal cerebral palsy.

Reference : Diagnostic imaging Osborn

Secondary Empty Sella MRI

Term Empty sella was first applied by Busch in 1951 to an anatomic finding of severely flattened Pituitary gland against the floor of the sella at autopsy.

Primary Empty Sella Syndrome is an anatomical variation where the wide aperture of the diaphragma sella, through which the pituitary stalk reaches pituitary. When this aperture is wide, the cardio pulmonary pulsations with time make the sella wide with flattening of the pituitary gland at the floor of sella. When an isolated finding has no clinical significance and pt's are usually asymptomatic.

MRI is investigation of choice. Midline sagittal T1 and T2 images show sella occupied by fluid isointense to Csf, infundibular stalk traversing the sellar cavity to the residual pituitary tissue which is flattened at the floor of hypophyseal fossa.
On MRI other findings like slit like ventricles, prominent subarachnoid space around the optic nerves, tortuosity of the optic nerves, compressed dural venous sinuses should be looked for, presence of which may suggest the clinical diagnosis of Idiopathic Intracranial hypertension in symptomatic patients with papillodema clinically.

Secondary empty sella syndrome occurs when the sella is empty because the pituitary gland has been damaged by either Radiotherapy or Surgery.
MRI Sagittal T2 image shows Empty Sella secondary to surgery as pt's previous clinical details reveals operative notes mentioning a pituitary adenoma excised with trans sphenoid approach.   

Thursday 16 February 2012

Focal Cortical Dysplasia MRI

Left side inferior frontal gyrus is thick with poor grey white matter inter phase, convolution pattern is asymmetric compared to opposite side - a subtle and subjective finding of Focal Cortical Dysplasia.

Focal Cortical Dysplasia:
First described in 1971 by Taylor.
A congenital abnormality thought to be secondary to genetic, ischemic, toxic, or infectious insult during cortical development.
A distinct subtype of malformation of cortical development, neurons in corresponding area are larger than normal called balloon cells for their large elliptical shape, displaced nucleus, and lack of dendrites or axons. Often found near the cerebral cortex.
This area causes the signals sent through the neurons to misfire and contributes in seizure activity.
The common cause of intractable epilepsy in children and is a frequent cause of epilepsy in adults.

Venous Angioma

A venous angioma, also referred to as a "developmental venous anomaly" (DVA), a variation of normal.
Usually seen as a little cluster or may seen as single prominent vein.
Angioma on their own don't tend to cause any trouble, except very few (reported) exceptions of bleed, so should generally be left alone.
May be seen isolated or in association with cavernoma, when associated with cavernous malformations (cavernomas) tend to be troublesome, usually present with seizures.
Similar cases: Developmental venous anomaly

Aneurysm DSA

Subarachnoid Hemorrhage - Sentinel Bleed.
Axial Non contrast CT shows a focal hyper dense subarachnoid blood in left parietal cortical sulcus.
Sentinel bleed is a warning bleed due to minor blood leakage, precedes aneurysm rupture by a few hours to a few months, present with sudden focal or generalized headache, should not be overlooked must be screened on time to rule out underlying aneurysm with non invasive MR Angio or DSA.
Subarachnoid Hemorrhage – Massive and diffuse.
Axial Non contrast CT shows diffuse sub arachnoid bleed in basal cistern, interhemispheric fissure and sylvian fissure.

Most common causes of spontaneous SAH are rupture of a saccular (berry) aneurysm (80%) and rupture of an arteriovenous malformation (AVM) (10%). Causes of non aneurysmal SAH include amyloid angiopathy, blood dyscrasias, fibromuscular dysplasia, Moyamoya disease, vasculitis (10%)
As per the Law of La Place, the tension on the wall is proportional to the diameter. Thus, the rate of rupture is directly related to the size of the aneurysm.
Aneurysms usually occur at arterial bifurcations and mostly arise from the anterior circulation of the Circle of Willis (85%).
Left ACA Aneurysm
ACom Aneurysm
Basilar tip Aneurysm
MCA bifurcation Aneurysm
ICA Tip Aneurysm
Pcom Aneurysm

Wednesday 15 February 2012

Primary CNS Vasculitis DSA

A 35 yo male with basal ganglionic infarcts.
Cerebral Angiogram; Right ICA injection (oblique view) showing irregularities involving right ICA cavernous supra clinoid portion and ACA A1 segment; Multiple dilatations and focal narrowings giving "beaded" appearance suggestive of Primary CNS Vasculitis / Arteritis - appears to be HIV associated as meanwhile patient found to be TRIDOT Positive.
HIV’s CNS complications result either from direct HIV infection or as a consequence of opportunistic infections.
HIV related CNS vasculitis is a direct neurological complication of HIV, where intracranial vessels develop aneurysmal dilatations and is associated with either infarction or bleeding.

Tuesday 14 February 2012

Moyamoya Disease DSA

Cerebral Angiogram : Left Internal Carotid Artery injection (AP view) show stenosis involving cavernous portion with prominent collateral vessels giving puff of smoke appearance of Moyamoya disease, a rare idiopathic disorder characterized by progressive narrowing of the distal internal carotid arteries and their branches.
It is typically seen in children, although rarely reported in adults.
As the carotid artery is compromised, there is progressive enlargement of the collateral circulation, especially among the lenticulostriate vessels. This results in a characteristic angiographic picture of a blush or "puff of smoke" in the area of the lenticulostriate vessels.
Typically presents with recurrent infarcts where as in some cases, the fragile collaterals can rupture resulting in intra cranial bleed.

Vertebro basilar stenosis DSA

Lateral view showing mid portion basilar stenosis
Towns view showing severe mid basilar stenosis
Left intracranial vertebral stenosis near formation of basilar
Cervical vertebral stenosis at its origin
Posterior circulation stroke
Syn :  Vertebra basilar insufficiency can result from either stenosis or complete occlusion of Vertebral and or basilar.

The posterior circulation consists of the vertebral arteries, the basilar artery, the posterior cerebral arteries and their branches. These arteries, through short penetrating branches and circumferential branches, supply the brainstem (medulla, pons, and midbrain), the thalamus, the hippocampus, the cerebellum, and medial portion of temporal and occipital lobes.
The vertebral arteries originate from the subclavian arteries and course through the vertebral foramina of C6-C2, around the atlas, and through the foramen magnum.  At the pontomedullary junction both vertebral arteries join to create the basilar artery.  The vertebral arteries supply the medulla, the pons and the cerebellum. The distal vertebral arteries and the basilar artery give rise to superior, anterior, posterior, and inferior cerebellar arteries that supply the cerebellum.
The vertebral arteries are prone to stenosis at their origin and at the junction with the basilar artery.
The basilar artery and its branches supply the pons and the cerebellum.  Distally the basilar divides into the posterior cerebral arteries.
Stenosis can occur anywhere along the trunk of the basilar.
The posterior cerebral artery (PCA) supplies portions of the midbrain, the thalamus, medial temporal and occipital lobes.

Clinical presentation: 
Patients may present with a wide variety of syndromes.
Neurological dysfunction includes hemi or quadriparesis, cranial nerve deficits (III-XII), respiratory difficulty, altered sensorium, vertigo and ataxia. Multiple cranial nerve signs indicate involvement of more than one brainstem level.
Patients may present with only hemiparesis, which may progress rapidly to quadriparesis or a locked-in syndrome. The onset of symptoms may not be as abrupt as with anterior circulation strokes.
As the posterior circulation supplies the brainstem, cerebellum, and occipital cortex, the symptoms frequently involve the "5Ds": dizziness, diplopia, dysarthria, dysphagia, and dystaxia.
The hallmark of posterior circulation stroke is “crossed findings,” with cranial findings on the side of the lesion and motor or sensory findings on the opposite side.
The exact symptom complex depends on the precise location of the infarct.

ICA stenosis vs occlusion DSA

ICA stenosis: 
DSAs showing significant ICA stenosis at origin.

Note the sluggish distal filling of the internal carotid artery.

Patients with ICA stenosis often present with transient ischemic attacks, cortical border zone infarcts, amaurosis fugax that is transient monocular blindness which results from reduced blood flow through the ophthalmic artery, the first major branch off the internal carotid artery.
Patient with symptomatic high grade ICA stenosis benefit from stenting compared with conventional medical treatment.

ICA Occlusion: 
DSAs showing complete cut off of ICA at its origin without any distal filling implies to occlusion.

In such patients, the carotid Doppler or MR Angiogram most of the time mentions complete occlusion of ICA. But on DSA there is thin / sluggish distal filling of the internal carotid artery goes in favour of stenosis.
This distinction is important because patients with high grade stenosis benefit from carotid end arterectomy or stenting and those with complete occlusions are not surgical candidates.