Functional MRI

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

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

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

Clinical Application of fMRI

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

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

Vascular territories of Brain stem and Infarct correlation

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

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

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

2.  Gillilan and Lazorthes et al. Classification

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

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

Examples: 

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

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

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

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

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

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

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

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

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

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

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

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

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

Nodular calcification Spinal cord

A 35 yo female with right upper limb tingling numbness.

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

Baastrup’s Disease : Interspinous Odema / Neo-arthrosis

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

Baastrup’s Disease

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

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

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

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

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

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

Unidentified bright objects (UBO) of NF1

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

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

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

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

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

ICA Aneurysm

Sellar meningioma

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

Pt refereed for further evaluation by MRI.

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

Radiological diagnosis: Sellar meningioma.

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

Hemangioblastoma MRI

A 50 yo female with headache and giddiness.

Findings:

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

Mass effect on medulla and Pons with obstructive hydrocephalus.

Radiological and histopathological diagnosis : Hemangioblastoma.

Hemangioblastoma

A highly vascular tumor.

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

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

Locaion:

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

10% Supratentorium.

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

Imaging:

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

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

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

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

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

Similar case:

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

Hirayama Disease MRI

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

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

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

Discussion

Hirayama et al first reported this disease in 1959.

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

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

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

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

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

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

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

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

Fatty filum terminale MRI

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

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

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

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

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