Intracranial hypotension

A case of mild headache with history of lumbar puncture 2 days back shows mild diffuse dural thickening with enhancement, bilateral thin layer of sub dural effusion, enlargement and rounding up of superior sagittal sinus, mild diffusion enlargement of pituitary. Consistent with clinical diagnosis of post lumbar puncture intracranial hypotension. There is no sagging of Brain stem. 

Intracranial Hypotension Imaging 

Reduction of intracranial pressure due to reduction in Csf volume.
Clinically characterized by headache marked in upright posture - postural headache. 
May have isolated abducens nerve palsy, necks stiffness, hearing loss. 
The condition may be spontaneous or secondary to lumbar puncture. Other cause include neurosurgical procedure, dehydration, trauma. Lumbar puncture is most common cause among all. 


Imaging findings in Intracranial Hypotension
- Diffuse thickening of the pachymeninges with enhancement, 
- Engorgement of dural venous sinuses. 
- Enlargement of the pituitary.
- Subdural effusion / hematoma. 
- Sagging brain stem. 


Most of these findings are the result of vascular dilation to compensate for sudden depletion of Csf volume, the explanations are based on Monro Kellie hypothesis, which states that the sum of the volumes of intracranial blood, CSF, and brain tissue remain constant in an intact cranium. Accordingly increased intracranial blood volume compensates for acute loss of CSF. Dilation of the venous side of circulation contributes a lot due to its high compliance and capacitance. 


Meningeal enhancement is thick, linear, without nodularity and involves the pachymeninges without evidence of involvement of the leptomeninges. 


Dura matter, the innermost layer composed of fibroblasts with inter digitating processes that create spaces in between. Extravasation of fluid occur into this layer, in these spaces, in response to increased dural vasculature as the dura lacks blood brain barrier and tight junctions.These extravasations explains dural thickening as well as contrast extravasation and enhancement. Tight junctions in arachnoid and pia mater prevent the similar contrast accumulation, explaining enhancement is limited to the dura. Though it is a frequent finding, abnormal meningeal enhancement is not the rule as cases are reported which are still symptomatic but enhancement that resolved earlier where as in certain typical cases MR images never revealed enhancement at any stage of disease. 


Sub dural effusions occur when the extravasation continue even after meningeal thickening and enhancement, to the point of fluid accumulation in the subdural space as supported by studies in which effusions were not seen in the absence of meningeal enhancement represent more advanced stage of the condition. These sub dural effusions are typically thin, crescentic, often bilateral.


Subdural hematoma occur when effusion get complicated with bleed in subdural space due to rupture of the bridging veins traversing sub dural space in response to traction by ongoing extravasation and effusion.


Descent of cerebellar tonsils with sagging of brain stem, an associated effacement of prepontine cistern, obliteration supra chiasmatic cistern with inferior displacement of the optic chiasm result from reduction of normal Csf buoyancy due to reduced csf volume and represent most advanced stage of disease and severe Csf volume depletion, occurs after all other compensatory mechanisms have exhausted.


Isolated 6th nerve palsy reported in considerable amount of cases. In fact it is the most common nerve among all to get affected due to its longer intracranial course. Often get encountered at inisura when there is sagging of mid brain with antero posterior elongation. 


Engorgement of dural venous sinuses seen as enlarged and round dural venous sinuses which are normally triangular in shape on cross sections.


Pituitary enlargement reflects simple compensatory venous hyperaemia.


Regression in these imaging findings often parallels clinical improvement of these, reversal of pituitary enlargement occurs first. 

Reference : Intracranial Hypotension Syndrome: A Comprehensive Review: Imaging Studies; Neurosurg Focus. 2003;15(6) © 2003 American Association of Neurological Surgeons. 

Post polio unilateral Psoas atrophy

Incidental finding in MRI Lumbar spine of a 30 year old male complaining of mild low backache. He is a known case of poliomyelitis involving left lower limb during childhood. On neurological examination left lower limb wasting, hypotonia and areflexia.  

MRI Lumbar spine axial sections show severe atrophy of left side Psoas consistent with past history of Poliomyelitis.


Post polio unilateral Psoas atrophy 

Cause of the muscle atrophy in Polio is still not completely clear, likely due to the premature degeneration of surviving motor neurons. Poliovirus has a predilection for the motor neurons of the anterior horns of the spinal cord, cell death followed by distal wallerian degeneration, denervation of muscles resulting in muscle weakness and atrophy.

Relevant investigations:  Detection of Oligoclonal immunoglobulin G and M bands in Csf  and demonstration of Poliovirus like RNA sequences in Csf  by Polymerase chain reaction.

DDx: other causes of unilateral psoas atrophy with associated atrophy of other para spinal muscles need to be excluded like scoliosis,  neoplasms, spondylosis with spinal stenosis. In normal or asymptomatic individuals, mild asymmetry of Psoas is a common finding appears to be a benign anatomical variant.

Rx :  No specific and successful treatment. Steroids, human growth hormone, pyridostigmine, Modafanil and bromocriptine all have been disappointing. Role of subcutaneous insulinlike growth factor-1  and IV immunoglobulin is doubtful.

References:  
The late effects of Polio: Information For Health Care Providers, Commonwealth Department of Community Services and Health. ISBN 1-875412-05-0. Archived from the original on June 25, 2008. Retrieved 2008-08-23.
Post-poliomyelitis Syndrome: Case Report and Review of the Literature, KH Lin,  YW Lim,
W. Michael Scheld, Richard J. Whitley, Christina M. Marra..Infections of the Central Nervous System .
Gonzalez H, Sunnerhagen KS, Sjoberg I, Kaponides G, Olsson T, Borg K. Intravenous immunoglobulin for post-polio syndrome: a randomised controlled trial. Lancet Neurol. Jun 2006;5(6):493-500.

Hemangioblastoma

Imaging findings:

A cystic mass with mural nodule at the floor of posterior cranial fossa.

Cyst is insinuating and descending down at foramen magnum, has clear fluid iso intense to Csf with thin imperceptible wall non enhancing on post contrast.

The eccentric round solid mural nodule, iso dense on CT, with intense homogenous enhancement on MR Post contrast T1. Flow voids in the mural nodule and adjacent to it. Imaging finding are very typical of a Hemangioblastoma. 

Significant mass effect on medulla and Pons with obstructive hydrocephalus.

A Glomus jugulare, a benign tumour with typical salt and pepper appearance noted as an incidental finding near left side jugular foramen.

Hemangioblastoma
A highly vascular tumor.
An intra axial posterior fossa mass with cyst and an enhancing mural nodule is a diagnostic clue.
Currently classified as meningeal tumor of uncertain histogenesis (WHO, 2000)
Locaion:
90% posterior fossa (m/c) in that 80% cerebellar hemispheres, 15% Vermis, 5% in other places  fourth ventricle, medulla.
10% Supratentorium.
In ~ 60% of cases mass present as cyst + mural nodule and in ~ 40% of cases only as a solid nodule.
Imaging:
Cyst is clear, density on CT and signal intensity on MRI same as that of Csf, non enhancing thin imperceptible wall.
Mural nodule on CT may be iso to hyper dense, intense and homogenous enhancement. On MRI hypo to iso intense on T1, hyperintense on T2 and FLAIR. May see flow voids within the nodule with adjacent vascular feeders on T2w images, intense and homogenous enhancement on T1 images implies to its highly vascular nature. May show low signal intensity hemosiderin staining on GRE if associated to with any bleed.

Presentation is usually with headache, dysequilibrium, dizziness may be due to its mass effect and hydrocephalus.
Age : for sporadic: 40-60 yr and for familial : can occur at younger age. Slight male predominance.


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

Gradenigo's syndrome MRI

Syn: Gradenigo Lannois syndrome.
A rare complication of otitis media and mastoiditis involving petrous apex of temporal bone.

Clinically characterised by triad of Ear Discharge, Diplopia, Hemifacial pain.
1  Suppurative otitis media explains ear discharge and pain.
2. Trigeminal nerve (5th CN) involvement explains Trigeminal neuralgia - pain in the distribution of the trigeminal nerve  manifest with hemicranial headache, hemi facial pain.
3. Abducens nerve (6th CN) involvement explains ipsilateral Lateral rectus palsy and Lateral gaze palsy manifest with reproducible Diplopia.

In these patients infection spread from suppurative otitis media to the petrous apex may be via pneumatised air cell tracts, through vascular channels, or as a result of direct extension through fascial planes and giving rise to apical petrositis.
Trigeminal nerve and ganglia lies very close to petrous apex separated by a dura and Abducene nerve lies medial to the trigeminal ganglion.
Extradural inflammation secondary to apical petrositis may form a soft tissue plegmon involve the above mentioned cranial nerves and give rise to symptom triad of Gradenigo’s syndrome.
Early recognition of condition is important to prevent intracranial complications like Meningitis, Intracranial abscess, Spread to skull base and involvement of IX, X, XI cranial nerves (Vernet’s syndrome), Prevertebral/parapharyngeal abscess, Spread to sympathetic plexus.

Case : A 45 yo female with left side ear discharge since 2 weeks with left sided headache and squint clinically. On examination left ear drum perforation with purulent discharge. Left lateral rectus palsy. 

Left side Mastoiditis, Otitis media and Petrositis.

An associated abnormal  adjacent enhancing soft tissue with focal dural enhancement.

The soft tissue extending in left side cavernous sinus explains left side 6th CN involvement and lateral rectus palsy, in left side Meckel's cave explains left side 5th CN involvement. 

A triad of Otitis media, left hemi cranial headache and left lateral rectus palsy consistent with Gradenigo's syndrome. 

Radiation induced spinal cord injury

A case with history of radiotherapy 12 months back for an inoperable Ca oesophagus. Details of radiation dose and fractionation not available. Now complaining of left side slowly progressive hemi paresis since last 3months.

MRI Sagittal T1 and STIR screening of whole spine shows radiotherapy induced fatty marrow in cervico dorsal region, diffusely bright on T1 with signal suppression of STIR. 

Axial T2w section at D9-10 disc level show a faint focal abnormal intra medullary T2 hyper intensity confined to left half of cord implies to Gliosis consistent with clinical diagnosis of
Delayed Radiation induced myelitis.

Radiation induced spinal cord injury
Radio therapy is commonly used as a primary or adjuvant therapy for malignancies.
Necrosis of adjacent normal tissues is one of the major complications.
Radiation induced spinal cord injury is rare occurs when the spinal cord is included within the radiation field, high total radiation dose or high radiation doses per fractionation.
First recognized in the mid-1940s, shortly after the introduction of megavoltage radiotherapy.

There are three types of presentations of radiation induced spinal cord injury.
1. Transient subacute myelopathy,
2. Delayed progressive myelopathy, and
3. Selective lower motor neuron syndrome, rare.

Transient sub acute myelopathy
Most common, mild and transient form.
Often seen after cranio spinal irradiation for primary CNS tumors, treatment of lymphomas or extra neural tumours of the head, neck, or thorax.
Latent period of 1 to 30 months with the peak onset at 6 months.
Characterised by paresthesia along spine extending down to the limbs.
Spinal cord may be normal on MRI.
Resolves gradually over 1 to 9 months.
No obvious documentation of any additional risk for delayed myelopathy in the affected individuals.

Delayed radiation myelopathy
Severe and often irreversible form,
After latent intervals of 12 to 14 months.
Presents with numbness in lower limbs followed by weakness and sphincter dysfunction. Pain is not a prominent feature.
Spontaneous improvement is rare.
MRI may show changes in cord.

Selective lower motor neuron syndrome
A rare syndrome due to selective damage to lower motor neurons, anterior horn cells believed to be the primary site of damage.
After latent period of 4 to 14 months.
Slowly progressivey over several months and then stabilizes.
No spontaneous improvement.

Nobody would like to damage spinal cord but the difficulty is there is no precise threshold of spinal cord for radiation induced injury. The accepted or tolerated dose is again different and necessarily low in patients who receive a second course of radiation, concurrent radiation plus chemotherapy.
Worrisome thing is patients with radiation myelopathy are permanently neurologically disabled and there is no proven effective treatment.                    

References:
Radiation myelopathy Edward J Dropcho MD,
MRI of radiation myelitis: a report of a case treated with hyperbaric oxygen, F. Calabrò and J. R. Jinkins.

Absent Acom

The anterior communicating artery connects the two anterior cerebral arteries along mid line.
Absence of Acom is a rare anatomical variation, seen in less than 5% of cases.
The two ACAs join together directly.

Superior Ophthalmic Vein

The orbital veins drains orbit, forms important anastomotic channels between the intracranial
and extracranial venous systems.
The number of orbital veins is variable; they are maximum three in numbers.
1. Superior ophthalmic vein (SOV), the largest and the most consistent of the three orbital veins, originates near the trochlea below the medial orbital roof, and travels posteriorly and medially to enter the cavernous sinus. The direction of flow in the ophthalmic veins is from extracranial to intracranial. The reversal of flow should raise suspicion of intracranial venous hypertension. The SOV anastomoses with the supraorbital vein and the angular vein.
2. Inferior ophthalmic vein (IOV). is smaller than the SOV, it is connected to the SOV via several anastomotic vessels and also drains into the cavernous sinus or directly drain into the superior ophthalmic vein.
3. Medial ophthalmic vein. May be present.

SOV Dilatation
Dilatation of SOV is primarily reported in carotid-cavernous fistula, unilateral as well as bilateral. There are many other causes of unilateral / bilateral SOV dilatation.
Any intracranial pathology that causes raised ICT like severe diffuse cerebral odema causes bilateral SOV dilatation.
Unilateral causes of SOV dilatation are Ophthalmic Graves disease, Tolosa-Hunt syndrome, inflammation at the apex of the orbit, Oribital Peri orbital Vascular malformation, Orbital pseudo tumor, cavernous sinus tumour or thrombosis, retrocavernous meningiomas etc.

Imaging for SOV dilatation 
Dilatation of SOV can be demonstrated on CT as wel as MR imaging.
MRI is the investigation of choice.
Along with demonstration of dilated SOV, associated findings like extraocular muscle enlargement, intra or peri orbital space occupying lesion, Vascular malformation, Cavernous sinus if any can also be evaluated, which can contribute in etiological diagnosis of enlarged SOV, in a better way than any other investigation.
Dilated SOV seen as tubular signal void on thin Axial T2 sections at the roof of bony orbit.
On coronal T2 sections seen as a round flow void, cranial to eye ball just under the superior rectus muscle extending towards orbital apex.
Diameters of the SOVs, is measured by using coronal MR images sections and were positively correlated with raised CSF pressure.

A case of post traumatic Carotico Cavernous Fistula with bilateral orbital proptosis and dilatation of Superior Ophthalmic Veins marked on left side.

Diagnostic criteria for SOV dilatation
Diameter of 2.5mm or more considered as abnormal.

Pathophysiology behind positive correlation between SOV dilatation and raised ICT
In studies conducted, SOV diameter determined on the basis of the MR imaging in pts with normal and raised ICT on lumbar punctures was positively correlated with raised ICP. The exact mechanism for the positive correlation between the diameter of the SOV and the ICP is uncertain. It is suggested that an increased ICP impairs the pressure gradient for venous return from the extracranial SOV to the intracranial cavernous sinus. The SOV is valveless and directly connected to the cavernous sinus. Therefore, it is easily influenced by hydrodynamic changes in the intracranial CSF and is consistent with Bernoulli-Poiseuille equation. The diameters are reversed to normal after the reversal of cerebral swelling or raised ICT.

References:
Imaging diagnosis of enlarged superior ophthalmic vein; Wei R, Cai J, Ma X, Zhu H, Li Y.
Diameter of the Superior Ophthalmic Vein in Relation to Intracranial Pressure; Jiing-Feng Lirng, Jong-Ling Fuh, Zin-An Wu, Shiang-Ru Lu, and Shuu-Jiun Wang.
Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt.

Artery of Bernasconi and Cassinari

Branches of the cavernous portion of ICA are highly variable.
The most consistent branches are the posterior and lateral trunks.
The Posterior trunk, also known as the meningohypophyseal artery arises from the posterior bend of the cavernous ICA, gives Tentorial artery, the most consistent branch of the posterior trunk.
Tentorial artery has two branches.
1. Basal tentorial artery, travels laterally along the border between the tentorium and the petrous ridge. Anastomoses with the middle meningeal artery and the dural arteries of the posterior fossa.
2. Marginal artery of the tentorium, travels posteriorly along the medial edge of the tentorium. The artery may arise directly from the ICA.

This Marginal artery of the tentorium is also known as artery of Bernasconi and Cassinari.

Reference : Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt.

Artery of Davidoff and Schecter

A small meningeal branch from P1 segment of PCA to supply part of the inferior surface of the tentorium near mid line.
Enlarged in cases of adjacent pathological processes like Hemangioblastoma, Meningioma or Dural AV fistula. The artery is identified as a feeder on Angiography followed by selective microcatheter embolization of artery.

Reference : Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt.

Anterior Choroidal Artery Infarct

AChA, the anterior choroidal artery originates from the supra clinoid portion of internal carotid artery just after giving off PCom.

Supply choroid plexus of the lateral ventricle and third ventricle, optic chiasm and optic tract, internal capsule,lateral geniculate body, globus pallidus, tail of the caudate nucleus, hippocampus, amygdala, substantia nigra red nucleus and crus cerebri. 

AChA constitutes a special vascular territory have etiology and prognosis different from that of typical hemispheric or deep infarcts.

Vasular terriotory of AchA confined to posterior para ventricular corona radiata region extending caudally along posterior limb of internal capsule and adjacent part of medial temporal lobe. 

Anterior Choroidal Artery territory infarct.
NOTE AN ASSOCIATED  INFARCT OF CHOROID PLEXUS OF ADJACENT RIGHT LATERAL VENTRICLE WITH INCREASED SIGNAL ON DIFFUSION 

AChA syndrome, was first described by Foix et al, consist of contra lateral hemiplegia, contra lateral hemi hypoesthesia, and homonymous hemianopsia.

Hemi plegia or paresis is due to involvement of the posterior limb of the internal capsule, the most constant finding.

Hemi hypoesthesia or hemisensory loss is due to involvement of the ventral postero lateral nucleus of the thalamus and 

Hemianopsia secondary to involvement of the lateral geniculate body.

A syndrome of acute pseudo bulbar mutism has been described in patients with bilateral AChA infarctions.

Principal cause or etiology of AChA infarct varies from lesion to lesion. Smaller lesions are associated with small-vessel disease with chronic hypertension being the single most important risk factor. Large AChA infarcts shows association with an embolic source. Other causes include carotid artery stenosis. Associated with relatively younger age groups, male and diabetic. Cause of AchA infarct is evaluated and individualized in every case, so that treatment is directed towards the risk factors like small-vessel disease, embolism etc. 

References: 

"Artery, anterior choroidal." Stedman's Medical Dictionary, 27th ed. (2000). ISBN 0-683-40007-X 

Victor, Maurice and Allan H. Ropper. Adams and Victor's Principles of Neurology. (2001). ISBN 0-07-067497-3

Helgason C, Caplan LR. Anterior choroidal artery-territory infarction: Report of cases and review. Arch Neurol 1986;43:681-686.

Infarcts in the anterior choroidal artery territory, Anatomical distribution, clinical syndromes, presumed pathogenesis and early outcome, R. M. M. Hupperts1,0, J. Lodder1, E. P. M. Heuts-van Raak1 and F. Kessels. 

Anterior Choroidal Artery Territory Infarction: A Small Vessel Disease. Askiel Bruno, MD, Neill R. Graff-Radford, MBBCh, MRCP, Jos6 Biller, MD, and Harold P. Adams Jr., MD

Acute ischemic stroke in anterior choroidal artery territory, Angel Ois

Recurrent artery of Heubner Infarct

Syn: Long central artery, Medial striate artery.

A largest medial lenticulostriate perforating branch arising from ACA.
Arises from the A2 segment in most ~57–78% of cases, may arise from A1 segment in up to ~17% of cases and from the ACA-A-comm junction in 35% of cases.
Called ‘Recurrent’ because it takes U turn after its origin, goes ‘back’ laterally over A1, parallel to A1 and in opposite direction of A1, towards the terminal ICA, so it often looks like a smaller artery running alongside and above the relatively bigger A1.

Ascends up to enter the lateral anterior perforated substance to supply head of caudate nucleus, anterior limb of the internal capsule and the anterior third of the putamen.
The artery is not large enough to be seen on MR Angiography, usually seen on DSA. Often encountered during surgery of the A1 - Acom complex, occlusion of the vessel possible during retraction of the frontal lobe.
Isolated infarction in the vascular territory of this artery can be clinically silent or produce a hemiparesis that is most prominent in the face and upper extremity.

Infarct in territory of Recurrent artery of Heubner involving caudate nucleus, anterior limb of the internal capsule and the anterior third of the putamen 

Reference: Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt. 

Posterior cerebral artery

PCA divided four segments.
P1: extend from its origin from the basilar artery to the junction with the P com.
P2 From the Pcom to the posterior aspect of the midbrain.
P3 From the posterior aspect of the midbrain to the calcarine fissure.
P4 The terminal branches of the PCA distal to the anterior limit of the calcarine fissure.


Branches
PCA branches divided into three categories:
1. Perforating branches, to the brainstem and thalamus, arise from the P1 and P2 segments.
2. Ventricular branches, originate mostly from the P2 segment.
3. Cortical branches, arise from the P2, P3, and P4 segments.

P1 segment
Aka precommunicating, mesencephalic or horizontal segment, lies immediately superior to the oculomotor and trochlear nerves. The average length is 6.6 mm.

Branches: 
Perforators
1. Direct perforating branches (aka posterior thalamoperforating arteries) from the P1 segment pass directly into the brainstem. These are termed the posterior thalamoperforators to distinguish them from the anterior thalamoperforators, which arise from the P-comm artery.
2. Circumflex arteries. The circumflex arteries (aka peduncular, mesencephalic, or tegmental thalamoperforating arteries) arise from the P1 and P2 segments and encircle the midbrain. Subdivided into short and long circumflex arteries.
Posteromedial choroidal artery. This vessel usually arises from the P2 segment, may arises from the P1 segment.
Meningeal branch, aka artery of Davidoff and Schecter, a small branch from P1 segment to supply a midline strip of the inferior surface of the tentorium may be enlarged by pathological processes.

Variations. 
Asymmetry of P1 segments common, being present in ~50% of angiograms. When a fetal PCA is present, the ipsilateral P1 is typically hypoplastic or absent.
Persistent carotid–vertebrobasilar anastomoses, the PCA may be supplied by branches from the carotid system.
True anomalies of the P1 segment are uncommon, includs duplication, fenestration  and a bilateral shared origin of the PCA and SCA.
Congenital absence of the P1 is rare.
Artery of Percheron, a single prominent perforating branch that supplies both the thalami and mesencephalic mid brain.

P2 segment
Aka ambient segment is relatively long, ~ 50 mm in length, travels around the lateral aspect of the midbrain within the ambient cistern, parallel and inferior to the basal vein of Rosenthal. Other adjacent structures are the trochlear nerve, the free edge of the tentorium, and the superior cerebellar artery.
Branches
Perforators
1. Thalamogeniculate arteries, supply the posterior half of the lateral thalamus, the posterior limb of the internal capsule.
2. Peduncular perforating arteries pass directly into the cerebral peduncle and supply multiple structures within the
3. Circumflex arteries.
Posteromedial choroidal artery, often arises from the P2 segment, may arise from P1 segment.
Hippocampal artery.
Inferior temporal arteries, anterior, middle and posterior temporal artery.
Parieto-occipital artery.
Calcarine artery.
Splenial artery.

P3 segment

Aka quadrigeminal segment, extends in a medial and posterior direction ~ 40mm in length.
The PCA often divides into its two terminal branches, the calcarine and parieto-occipital arteries between

Branches
Parieto-occipital artery.

P4 segment
Includes two main terminal branches of the PCA, the calcarine artery and parieto-occipital artery,

Branches
Calcarine artery, travels posteriorly and medially within the calcarine fissure to reach the occipital pole.
Splenial artery, aka posterior pericallosal artery arises from the parieto-occipital artery in 62% of cases, but may arise from the calcarine (12%), travels superiorly around the splenium of the corpus callosum to anastomoses with the pericallosal artery.

Reference: Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt. 

Middle cerebral artery

MCA is divided into four segments.
M1 - From ICA to the bifurcation.
M2 - From the MCA bifurcation to the circular sulcus of the insula.
M3 - From the circular sulcus to the superficial aspect of the sylvian fissure
M4 - Cortical branches.

M1 segment
Aka horizontal segment or sphenoidal segment.
Arises from ICA and travels in lateral direction, parallel to the sphenoid wing and terminates by dividing into the M2 segments.  The division point of the MCA main stem is considered by most clinicians to be the M1/M2 junction. The MCA bifurcates in 71% of cases, trifurcates in 20% of cases and divides into four branches in 9% of cases.
The M1 segment averages ~16 mm in length.

Branches: 
Lateral lenticulostriate branches, approximately 80% of the lenticulostriate perforators that arise from the MCA, arise from the M1 segment, on an average are 10 in number, enter the anterior perforated substance to supply the anterior commissure, internal capsule, caudate nucleus, putamen, globus pallidus, and substantia innominata.
Anterior temporal artery, typically arises near the midpoint of the M1 segment. Less commonly, it arises from the inferior division (an M2 segment) or as part of an M1 trifurcation, supplies the anterior temporal lobe.

Variations: 
MCA duplication, consists of a large MCA branch arising from the ICA proximal to the ICA bifurcation,  in 0.2–2.9% of cases, the anamolous vessel travels parallel and inferior to the main M1 segment and primarily supplies the anterior temporal lobe.
Accessory MCA, arises from the ACA and runs parallel to the M1 segment, and has a frequency of 0.3–4.0%, supplies the orbitofrontal area and should be not be confused with a large recurrent artery of Heubner.
Aplasia, is rare.
Fenestration. 

M2 segments
Aka insular segments, extend from the main division point of the M1 segment, over the insula within the sylvian fissure and terminate at the circular sulcus of the insula.
There are two, superior and inferior divisions. Cortical area supplied by the superior division usually extends from the orbitofrontal area to the posterior parietal area. Cortical area supplied by the inferior division usually extends from the temporal pole to the angular area.
The M2 segments number from six to eight vessels at the point of transition into the M3 segments.

M3 segments
Aka opercular segments, begin at the circular sulcus of the insula and end at the surface of the sylvian fissure.
These vessels travel over the surface of the frontal and temporal opercula to reach the external surface of the sylvian fissure. The M3 branches, together with the M2 vessels, give rise to the stem arteries, which in turn give off the cortical branches. There are usually eight stem arteries per hemisphere, and each one typically gives rise to one to five cortical branches.

The M4 branches
Aka cortical branches,begin at the surface of the sylvian fissure and extend over the surface of the cerebral hemisphere. The smallest cortical branches arise from the anterior sylvian fissure and the largest ones emerge from the posterior sylvian fissure.

The cortical branches of MCA can be grouped according to which lobe they supply;
1. Frontal lobe. Orbitofrontal, prefrontal, precentral, and central arteries
2. Parietal lobe. Anterior and posterior parietal arteries and angular artery
3. Temporal lobe. Temporopolar, anterior, middle and posterior temporal arteries,
and temporooccipital artery
4. Occipital lobe. Temporo-occipital artery.

The cortical branches can also be grouped according to which M2 segment they arise from;
1. Superior division. Orbitofrontal, prefrontal, precentral, and central arteries.
2. Inferior division. Temporopolar, temporo-occipital, angular, and anterior, middle, and posterior temporal arteries.
3. Dominant division (these branches may arise from either division, and usually come off of the larger of the MCA divisions). Anterior and posterior parietal arteries.

Reference: Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt. 

Anterior cerebral artery

On either side ICA divides into ACA which travel anteromedially and MCA which travel laterally.
ACA includes three segments A1, A2 and A3.
A1. From ICA to anterior communicating artery.
A2. From anterior communicating artery to the origins of the pericallosal and supramarginal arteries.
A3. Distal ACA or cortical branches.


A1 segment and Acom complex
The A1 segment also known as precommunicating segment, extends from the ICA bifurcation to its junction with the anterior communicating Artery. It travels superior to the optic chiasm or optic nerves and inferior to the anterior perforated substance.

In most cases, the A1- Acom complex assumes one of the four configurations.
A) Single or duplicated Acom forms a bridge between the ACAs.
B) A single large branch arising from the A com
C) Absent A-com and the two ACAs join together directly.
D) Azygos ACA.

Single or duplicated Acom forms a bridge between the ACAs. 

A single large branch arising from the A com 

Absent A-com and the two ACAs join together directly 

Azygos ACA.

A1 Branches: 
Perforating branches of A1 divided into superior and inferior branches.
i. Approximately 2–15 superior branches are medial lenticulostriate arteries that travel superiorly and posteriorly into the anterior perforated substance and supply the anterior hypothalamus, septum pellucidum, anterior commissure, fornix, and the anterior striatum.
ii. Inferior branches supply the optic chiasm and optic nerves.
Acom branches
Perforating branches of the Acom divided into subcallosal, hypothalamic and chiasmatic branches, according to their vascular territories.  The subcallosal branch is usually single and the largest branch of the A com, supplies the septum pellucidum, columns of the fornix, corpus callosum and lamina terminalis.
Recurrent artery of Heubner, most often an A2 branch, may arise from the A1 segment in upto 17% of cases and from the ACA-A-comm junction in 35% of cases.

Variations 
A1 variants
Asymmetry:The left and right A1 segments are asymmetric in size in upto 80% of cases. About 10% of the A1 vessels are hypoplastic.
Absence:Absence of one A1 segment is seen in 1–2% of cases.
Infraoptic ACA:  The A1 segment may travel inferior to or through the optic nerve, rare.
Fenestration of A1 segment.
Accessory ACA: An atypical branch of the ICA courses under the optic nerve and ACA to give rise to the orbitofrontal and frontopolar arteries.
Anomalous origin of A1 from the cavernous ICA or from the contralateral ICA.
Acom variants
A normal Acom, is a single vessel which forms a link between two ACAs, is present in only about 40% of cases.
Anomalous Acom anatomy is present in the remaining 60% of cases. Some 227 A-comm artery complex variations or pattern have been described. These patterns included plexiform (i.e., multiple complex vascular channels, 33%), dimple (i.e., incomplete fenestration, 33%), fenestration (21%), duplication (18%), string (18%), fusion (12%), median artery of the corpus callosum (6%), and azygos ACA (3%). The Acom is absent in some 5% of cases.

A2
The A2 segment travels in a vertical direction, adjacent to the genu of the corpus callosum, extend from the Acom to its division into the pericallosal and callosomarginal arteries. Averages 43 mm in length.
The left and right A2 segments usually travel together in the interhemispheric fissure. Right A2 is more often (~72% of cases) anterior to the left A2 in the sagittal plane.

A2 Branches
Perforating branches penetrate the gyrus rectus and olfactory sulcus.
Recurrent artery of Heubner, also known as the medial striate artery or long central artery.  Thelargest medial lenticulostriate perforator branch from ACA. Arises from the A2 segment in most (57–78%) cases, may arise from A1 segment in up to 17% of cases and from the ACA-A-comm junction in 35% of cases. Called ‘Recurrent’ because it takes U turn after origin, goes ‘back’ laterally over A1, parallel to A1, in opposite direction of A1, towards the terminal ICA, so it often looks like a smaller artery running alongside and above the relatively bigger A1.
Orbitofrontal artery, this artery runs close to the midline in an anterior direction to the gyrus rectus, olfactory bulb and medial aspect of the inferior frontal lobe.
Frontopolar artery, this artery travels anteriorly and superiorly towards the frontal pole.

Variations 
Azygos ACA, a single unpaired A2 segment that arises from the junction of the A1s. It is present in < 1% of the general population. Commonly associated with terminal aneurysm in ~41% of cases.  Associated with holoprosencephaly.
Duplicated A2.
Superior anterior communicating artery, an anomalous communicating vessel between the ACAs near the corpus callosum.

A3
‘A3’ include all the ACA cortical branches distal to the origin of the pericallosal and callosomarginal arteries. Some authors have further subdivided the distal ACA into A4 and A5 segments.
The distal ACA branches have extensive anastomoses with distal branches of the MCA and PCA with a watershed zones inbetween which is most vulnerable to ischemia during hemodynamic failure.

A3 Branches 
Pericallosal artery, the pericallosal artery comprises the main trunk of the ACA as it passes posteriorly over the corpus callosum, gives off multiple small branches 'short callosal arteries'  that travel laterally along the corpus callosum and anastomoses with the splenial artery the 'posterior pericallosal branch', a branch of the PCA.
Callosomarginal artery, is the second largest distal branch of the ACA, after the pericallosal artery. It travels superiorly over the cingulate gyrus to run in a posterior direction within the cingulate sulcus.
Frontal branches are Anterior frontal, middle frontal and posterior frontal. These branches arise from the pericallosal or the callosomarginal artery, are identified according to which part of the superior frontal gyrus they supply.
Paracentral artery, supply the paracentral lobule.
Parietal arteries, the final and most distal branches of the ACA, anastomose with the parietooccipital branch of the PCA. They can be divided into Superior parietal and inferior parietal artery.

Cortical ACA Branches:
Orbitofrontal Artery.
Frontopolar Artery.
Internal Frontal Branches (Anterior, Middle, and Posterior).
Paracentral Artery.
Parietal Arteries (Superior and Inferior).

Reference: Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt. 

Circle of Willis Anatomy

The circle of Willis is the ring of interconnecting vessels that encircles the pituitary infundibulum and provides important collateral circulation between the carotid territories and the vertebro basilar system.

It is actually a heptagon, a seven sided structure, not a circle.
Although it bears the name of Thomas Willis, named in honor of Willis by his student Lower who actually described this structure for first time.

Vessel contributing in formation of Circle of Willis are ICA from either side and PCAs from Basilar. Right and left ACA A1 segments anteriorly from ICAs on either side and Acom in between.
Pcoms from ICA on either side.
Right and left PCA P1 segments posteriorly from PCAs on either side.

A complete well-developed and symmetric circle is found in <50% of cases.
In some 60% of cases, at least one component of the circle is relatively hypoplastic and diminished in its capacity to provide collateral flow.
Sources of asymmetry in the circle of Willis.
Vessel: Variant and incidences
A1 segment: Hypoplastic in 10%; Absent in 1–2%1
Acom: Absent in 5%
Pcom: Hyperplastic (Fetal) in 18–22%; Hypoplastic in 34%; Absent in 0.6%
ICA: Hypoplastic in 0.079%; Absent in 0.01%
P1 segment: Hypoplastic in 15–22% ; Absence is Rare.

Asymmetry of the circle of Willis results in significant asymmetry of flow and is an important factor in the development of intracranial aneurysms and atypical ischemic stroke.

Reference: Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt. 

Carotid siphon

The carotid siphon is an S-shaped part to the ICA; it begins at the posterior bend of the cavernous ICA and ends at the ICA bifurcation.
Cavernous and supra clinoid portions of the ICA forms carotid siphon. Cavernous portion contributes greater part of the carotid siphon, the cavernous portion consist of sub segments as (a) Posterior vertical, (b) Posterior bend, (c) Horizontal, (d) Anterior bend, and (e) Anterior vertical.

The siphon can have an open or a closed configuration.
A closed siphon anatomy can be attributed to exaggerated tortuosity of the ICA, can be seen in patients with advanced age or fibromuscular dysplasia. Clinical significance is during the endovascular navigation where it becomes difficult to negotiate catheter in such close configuration turn.

Haughton's view
During DSA 'Haughton view' is used to open up the carotid siphon and to prevent overlapping of MCA branches within the Sylvian fissure. This view is also helpful for imaging of ICA and MCA aneurysms, PCom origin and anterior choroidal artery.
The lateral arc is positioned as if the patient’s head is tilted away from the side of the injection and away from the xray tube. In simple words the X-ray tube should touch the shoulder on the side of interest.

Reference: 
Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt.

Carotid - Vertebrobasilar Anastomoses

These are transient connections which appear during embryonic development between the carotid and vertebro basilar circulations. These embryonic anastomotic connections usually disappear as the posterior communicating arteries develop.
In rare cases these vessels persist into adulthood.
From superior to inferior, these persistent fetal vessels are:
1. Fetal PCA, the most common of all with prevalence of ~20% of genernal population.
2. Trigeminal, named after the cranial nerve it parallels.
3. Otic,
4. Hypoglossal, named after the cranial nerve it parallels.
5. Pro atlantal intersegmental artery.

1. Persistent Fetal PCA
Normally the posterior communicating artery arises from the ICA just proximal to the ICA bifurcation joins PCA at the junction of p1 and p2 segments. Fetal PCA or  Persistent fetal origin of PCA defined as a prominent P com that gives rise to or continues as PCA p2 segment and onwards with same diameter.  Ipsilateral PCA p1 segment is usually hypoplastic or may be absent.




2. Persistent Trigeminal Artery
The next most common.
Extends from the cavernous ICA to the upper part of the basilar artery and often perforates the dorsum sella.
The vertebrobasilar system proximal to the upper basilar artery may be hypoplastic, with the primitive trigeminal artery supplying most of the flow to the PCAs and the SCAs.
Two main variants.
Saltzman Type I. The persistent trigeminal artery supplies the PCA and SCA territories. The posterior communicating arteries and the basilar artery proximal to the anastomosis are hypoplastic.
Salzman Type II. The PCAs are supplied by the posterior communicating arteries, and the persistent trigeminal artery joins the basilar artery at the level of the SCAs.
Clinical significance is association with intracranial aneurysms. May have an intrasellar component and should not be mistaken for a pituitary mass.

3. Persistent Otic aArtery
Rarest of all carotid-basilar anastomosis.
Extends from the petrous ICA to the basilar system via the internal auditory canal.


4. Persistent Hypoglossal Artery
Common carotid-basilar anastomosis next to trigeminal.
Extends from the cervical ICA to the basilar artery via the hypoglossal canal.
The ipsilateral vertebral artery is usually hypoplastic.
May be associated with an aneurysm.

5. Proatlantal Intersegmental Artery
Extends from the cervical ICA or ECA to the vertebrobasilar system via the foramen magnum.
Relatively rare.
Associated with aplasia or hypoplasia of the vertebral arteries in 50% of cases.

Reference: Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt.

Internal carotid artery Anatomy

Among various classification available for describing the portions of ICA the most simple and widely used is based on the description by Gibo and colleagues.
ICA on either side divided in to four segments or portions.
1. Cervical
2. Petrous
3. Cavernous
4. Supraclinoid

1. Cervical portion 
This portion begins at the carotid bifurcation (usually at the level of C3) and ends at the skull base and usually has no branches. The ICA receives approximately 80% of flow from the CCA.
Further divided into two divisions.
a. Carotid bulb, a focal dilation of the ICA at the origin, ~ 7.4 mm in diameter, compared to 7.0 mm diameter for the CCA.
b. Ascending cervical segment ~4.7mm diameter which remains relatively constant throughout its course.

2. Petrous portion 
The petrous portion extends from the opening of the carotid canal in the skull base to the posterior edge of the foramen lacerum. The proximal portion is vertical followed by horizontal portion with a genu portion which is a bend in the vessel of ninety degree.

3. Cavernous portion
The cavernous segment is S-shaped, extends through the cavernous sinus, is surrounded by areolar tissue, fat, postganglionic sympathetic fibers and the interconnecting venous chambers of the cavernous sinus. The ICA rests directly against the lateral surface of the body of the sphenoid bone in a groove called the carotid suclus. Further divided into five sub segments.
a. Posterior vertical,
b. Posterior bend,
c. Horizontal,
d. Anterior bend,
e. Anterior vertical.

4. Supraclinoid portion 
The supra clinoid portion further divided into three sub segments.
a. Clinoidal segment,
b. Ophthalmic segment and
c. Communicating segment.
The clinoidal segment comprises a tiny wedge-shaped part of the ICA between the proximal and distal dural rings. The anterior clinoid process lies superior and lateral to the clinoidal ICA, over the part of widest separation between the dural rings.
The Ophthalmic segment is the most proximal intradural part of the ICA and extends from the distal dural ring to the origin of the posterior communicating artery gives the ophthalmic artery, which arises from the anterior aspect of the ICA medial to the anterior clinoid process.
The communicating segment begins just proximal to the origin of the posterior
communicating artery and ends with the bifurcation of the ICA into the ACA and the MCA. Gives off posterior communicating artery.

Reference: 
Handbook of Cerebrovascular Disease and Neurointerventional Technique.  Mark R. Harrigan, John P. Deveikis and Agnieszka Anna Ardelt

Salt and Pepper sign

The term is used to describe the speckled appearance of the tissue.
Used in many instances in radiology as well as even some pathology textbooks and journals mentions this term while describing the tissue but most commonly used while described the tissue during MRI interpretation.

* Vascular tumours

Highly vascular tumours such as a paragangliomas which contain flow void and areas of haemorrhage they are Glomus tympanicum , Glomus jugulare , pheochromocytoma and , carotid body tumour.
‘Salt' represents the hyperintensity of mass due to areas of hemorrhages in these hypervascular tumors.
‘Pepper' represents multiple black dots due to signal void of vessels.
The appearance is seen on T1 w images, may be seen on T2w images. Such lesions show ‘blooming’ low signal intensity hemosderin staining on T2*GRE, intense enhancement on post contrast due to the hyper vascularity of the mass.
* Vertebral haemangioma
A less common usage for the term is for vertebral haemangiomas which have a courser black and white dotted appearance especially on axial T2 and T1 images (salt = fat, pepper = coarsened trabeculae).
* Sjogren syndrome
The parotid gland in Sjogren's syndrome has also been described with this appearance, due to a combination of punctate regions of calcification (pepper) and fatty replacement (salt)

Glomus jugulare 
Rare, slow-growing, hypervascular, benign but locally invasive tumor.
Seen at Cp angle near jugular foramen of the temporal bone.
Represent small collections of paraganglionic tissue, derived from embryonic neuroepithelium admixed with autonomic nervous system, found in the region of the jugular bulb.
Globus jugulare is a part of group Paraganglioma, also referred to as chemodectomas or nonchromaffin paragangliomas. Paragangliomas are found at other sites also, including the middle ear (glomus tympanicum), the carotid body (carotid body tumor), and the vagus nerve in proximity to the inferior (nodosum) vagal ganglion (glomus vagale tumor, glomus intravagale tumor).
Association of glomus jugulare is reported with Pheochromocytoma, parathyroid adenoma, and thyroid carcinoma.
Histologically Glomus jugulare described as dense matrix of connective tissue among nerve fascicles.
Expand within the temporal bone via the pathways of least resistance such as air cells, vascular lumens, skull base foramina and the eustachian tube. Spares the ossicular chain.
Often noted as an incidental finding. May go unnoticed due  to non specific and insidious onset symptoms. Predominantly occur in female, common during their fifth and sixth decades of life, more common on the left side.

A 40 yo female presented with hydrocephalus due to mass effect of a Hemangioblastoma (H) at the floor of posterior fossa. The Glomus jugulare tumor (G) with typical salt and pepper appearance on T1w images noted as an incidental finding.

Multicentric tumors are known in ~ 3-10% of sporadic cases and in 25-50% of familial cases.
Metastases from glomus tumors occur in approximately 4% of cases, includes lung, lymph nodes, liver, vertebrae, ribs, and spleen.
CE MRI is investigation of choice, characteristic salt and pepper appearance on T1 and T2-weighted images.

Thornwaldt's cyst MRI

Syn: Pharyngeal bursa, Thornwaldt bursa, Tornwaldt cyst.
A cystic density / signal intensity lesion at the roof of nasopharynx.
A developmental cyst, represent potential space developing in the nasopharynx at the point where the notochord retains its union with the pharyngeal ectoderm.

MRI is investigation of choice, signal intensity on MRI varies on both T1 and T2 weighted images depending up on its protein content and if any associated haemorrhage in the lesion.

The lesion is a mucosal cyst situated in the mid line between the longus capitus muscles, without associated inflammatory changes or edema in the surrounding soft tissues or without any adjacent bone involvement.

DDs:
Usually nil due to its typical location and imaging appearance. May include normal / prominent adenoidal tissue with cystic degeneration, mucous retention cyst.

Age group is second or third decades, no sex predilection.
Clinical symptoms:
Most often asymptomatic. Noted as an incidental findings on CT / MRI.
Symptoms may include postnasal drip, halitosis, headaches, eustachian tube dysfunction resulting in earache.

References:
1. Weissman JL. Thornwaldt cysts. Am J Otolaryngol 1992; 13: 381–5.
2. Miyahara H, Matsunaga T. Tornwaldt's disease. Acta Otolaryngol Suppl (Stockh) 1994; 517: 36–9.
3. Ikushima I, Korogi Y, Makita O, Komohara Y, Kawano H et al. MR imaging of Tornwaldt's cysts.AJR 1999; 172: 1663–5.
4. Goodwin RW. Tornwaldt's disease. Characteristics headaches syndrome and etiology. Laryngoscope 1944; 54: 66–75.
5.Chong VF, Fan YF. Radiology of the nasopharynx: pictorial essay. Australas Radiol 2000; 44: 5–13.
6. Battino RA, Khangure MS. Is that another Thornwaldt's cyst on MRI? Australas Radiol 1990; 34: 19–23.

Vein of Trolard MR Venogram of Brain

Syn:  Superior Anastamotic Vein.
The vein of Trolard, is a part of the superficial venous system of the brain, often located in post central sulcus, connects superficial middle cerebral vein of Sylvius to superior sagittal sinus.

Also important know here about vein of Labbé, the inferior anastomotic vein crosses the temporal lobe, connects the superficial middle cerebral vein of Sylvius to the ipsilateral lateral sinus.
The dominance of these anastomotic veins is dictated by the relative size of the superficial middle cerebral vein and the other anastomotic vein. There is inverse relationship between the size of the superficial middle cerebral vein, the anastomotic vein of Trolard and the vein of Labbé, as all three shares a same drainage area.

Clinical significance:
Surgery : Important to know about these vein , to preserve the vein during lobectomy or Decompressive craniecotmy.
Thrombosis : isolated thrombosis of this vein is known where MR Venogram may show controversial findings like normal superior sagittal sinus with an adjacent hemorrhagic venous infarct which may be otherwise mistaken for a hemorrhagic contusion.

Vein of Labbe MR Venogram Brain

Named after 17th century French surgeon Charles Labbé who described it in his 3rd year of medical school.

The vein is a part of the superficial venous system of the brain, crosses the temporal lobe from sylvian fissure to end in ipsilateral lateral sinus mostly at the junction of transverse and sigmoid sinus. Exact location in temporal region is variable may be anterior temporal, middle temporal or posterior temporal of which middle temporal is most common. The structural anatomy of the vein itself is also variable, with a dominant single channel, multiple branching channels and even venous lakes having been described.

Vein of Labbé is also known as Inferior anastomotic vein, connects the superficial middle cerebral vein of Sylvius from sylvinan fissure to the lateral sinus.

Also important know here about Vein of Trolard, also known as superior anastomotic vein, often located in post central sulcus, connects the superficial middle cerebral vein of Sylvias from sylvian fissure to the superior sagittal sinus.

The dominance of these anastomotic veins is dictated by the relative size of the superficial middle cerebral vein and the other anastomotic vein. There is inverse relationship between the size of the superficial middle cerebral vein, the anastomotic vein of Trolard and the vein of Labbé, as all three shares a common drainage area. 

Clinical significance:

Surgery : Important to know about the vein and to preserve the vein during Temporal lobectomy for temporal lobe epilepsy or Decompressive craniecotmy.

Thrombosis : isolated thrombosis of this vein is known where MR Venogram may show controversial findings like normal or congenital absent ipsilateral lateral sinus with a hemorrhagic venous infarct which may be otherwise mistaken for hemorrhagic contusion. 

Intradiscal Vacuum Phenomenon

Sagittal T1 and T2 w images show intradiscal vacuum phenomenon at L4-5. 

Gas in the disc space first analysed by Ford in 1977, is an ~ 90% nitrogen combined with oxygen, carbon dioxide and other traces of gases.
VP is described in every segment of the spine including the disc space, Schmorl nodes, vertebral  body, the epidural and intradural spaces and facetal joints.
Intradiscal VP is commonest, observed in  up to 20% elderly individuals.
Most of the articles related to intra discal VP are based on plain radiographs and CT findings, although MRI being the preferred diagnostic method for spine, suffers a reduced sensitivity in detecting gas.
Intradiscal VP can be marginal or central. An anterior marginal VP means a crack in the peripheral fibres of the annulus fibrosus caused by a traumatic or degenerative process. A central VP can be found in many conditions characterized by the development of horizontal intra discal clefts. Disc degeneration is the commonest cause of a centrally positioned VP.
On MRI intra discal vaccum phenomenon is seen as a streak of signal void (‘z’ black) on T1 as well as T2 w images. Most commonly seen in lumbar region. Associated with degenerative changes in the disc like disc desiccation, reduced disc height with endplate sclerosis, modic changes, marginal osteophytosis and adjacent segment degeneration.

Sagittal reformatted images of spiral CT study at L5-S1 level shows Grade I anterior subluxation of L5 off S1, break in L5 pars on either side. Height of disc space reduced. Degenerative intra discal vacuum phenomenon noted as a 'Z'black air density in the disc space.  

Reference: The spectrum of vacuum phenomenon and gas in spine, B. Coulier