INTRODUCTION

Cavernous angiomas belong to a group of intracranial vascular malformations that are developmental malformations of the vascular bed. These congenital abnormal vascular connections frequently enlarge over time. The lesions can occur on a familial basis. Patients may be asymptomatic, although they often present with headaches, seizures, or small parenchymal hemorrhages.

In most patients cavernous angiomas are solitary and asymptomatic. In recent times, increasing MR imaging has detected several such asymptomatic cases and has prompted a study into the genetics and natural history of this condition.

It is now known that cavernous angiomas have a genetic basis. Familial forms of cavernous angiomas are associated with a set of genes called CCM genes (cerebral cavernous angioma).

This is a case report describing the phenotypic expression of a familial form of cavernous angioma.

CASE REPORT

A 54-year-old man was referred for MRI Brain with complaints of headache and seizures. A cranial CT scan revealed few hyperdense lesions.

A subsequent cranial MR scan revealed several lesions with features representing cavernous angiomas.

The patient was offered counseling and treated conservatively. Genetic testing was not possible due to the high prohibitive cost. However, screening of the family members by MRI was recommended.

Cranial MR imaging of the immediate family members was performed. Four brothers of the patient and his mother were found to have multiple cavernous angiomas.

The father, youngest brother and his younger sister were found not to have any such lesion. Both the children of the patient were also found to be free of these lesions. Incidentally, a meningioma was found in the father of the patient.

DISCUSSION

Cavernous angiomas are typically discrete multilobulated lesions that contain hemorrhage in various stages of evolution. Because they are lobulated and dark red to blue, the lesions grossly resemble small mulberries. They are said to be vascular hamartomas made up of endothelium lined sinusoids not sepertated by neural tissue. Several theories have been proposed to explain their pathogenesis, however, none has proven to be wholly accurate.

Cavernous angiomas may occur anywhere in the central nervous sytem but the most common site is the supreatentorial neuroparenchyma (about 80%).

. A genetic basis for this disease has been established. The three genes associated with familial CCM are CCM1 (KRIT1) CCM2, both of which have been located on chromosome 7q and CCM3 (PDCD10) which has been located on chromosome 3 (1,2). Familial CCM is inherited in an autosomal dominant manner. The occurrence of asymptomatic vascular lesions may prevent recognition of an autosomal dominant pattern of inheritance in a family. The proportion of cases caused by de novo gene mutations is unknown. Each child of an individual with CCM has a 50% chance of inheriting the mutation.

Molecular genetic testing and prenatal testing is available in certain centers.

Familial cerebral cavernous malformation is defined as the occurrence of CCMs in at least two family members, and/or the presence of a disease-causing mutation in one of the genes associated with CCM and/or the presence of multiple CCMs (gene CCM).

Diagnosis of cerebral cavernous angiomas is difficult. Most patients are asymptomatic and diagnosis is incidental. The common presenting symptoms include seizures, focal neurological deficits, chronic headaches and intracranial hemorrhage (3).

MRI is the imaging technique of choice as of today. Both spin echo and gradient recall echo sequences are useful in demonstrating cavernous angiomas. However, gradient echo images have proven to be better than spin echo images (3). In the screening of family described above the Gradient echo T2W images revealed more angiomas than the spin echo sequences. Contrast injection is usually not required.

MRI findings of cerebral cavernous angiomas are quite typical (4,5,6). On MR images they appear as popcorn-like, smoothly circumscribed, well-delineated complex lesions. The core is formed by multiple foci of mixed signal intensities, which represents hemorrhage in various stages of evolution (7). A low signal intensity hemosiderin ring that completely surrounds the lesion is a common finding. The low signal intensity more prominent or ‘blooms’ on T2 weighted and gradient echo images.

The interspersed fibrous-containing elements demonstrate mild hypointensity on both T1- and T2-weighted images because they contain a combination of calcification and hemosiderin.

When multiple cavernous malformations are identified in one patient, a detailed neurologic family history should be sought to identify the mode of inheritance (3). MR imaging can then pick up such lesions in asymptomatic relatives during family screening. It is important to counsel the family members who are found to have these angiomas regarding the risk of hemorrhage and advice changes in their lifestyle.

At least the adult siblings  may be screened by Axial GRE sequence to detect the angiomas.

Screening asymptomatic family members may raise cost issues. The insurance companies and government agencies may not reimburse these costs. This scenario would be different in different countries. However if these siblings are screened only using Axial GRE the cost and the time required on the MR scanner may be minimised. This Cost of screening may be worth if asymptomatic carriers of the angiomas are detected!

REFERENCES:

1. Liquori CL, Berg MJ, Siegel AM, et al. Mutations in a gene encoding a novel protein containing a phosphotyrosine-binding domain cause type 2 cerebral cavernous malformations. Am J Hum Genet Dec 2003;73(6):1459-64.
2. Craig HD, Gunel M, Cepeda O, et al. Multilocus linkage identifies two new loci for a mendelian form of stroke, cerebral cavernous malformation, at 7p15-13 and 3q25.2-27. Hum Mol Genet Nov 1998;7(12):1851-8.
3. Brunereau L, Labauge P, Tournier-Lasserve, Laberge S, Levy C, Houtteville, J. Familial Form of Intracranial Cavernous Angioma: MR Imaging Findings in 51 Families. Radiology Jan 2000;214:209-216.
4. Hallam DK, Russell EJ. Imaging of angiographically occult cerebral vascular malformations. Neuroimaging Clin N Am May 1998;8(2):323-47.
5. Hauck EF, Barnett SL, White JA, Samson D. Symptomatic brainstem cavernomas. Neurosurgery Jan 2009;64(1):61-70; discussion 70-1.
6. Ide C, De Coene B, Baudrez V. MR features of cavernous angioma. JBR-BTR Dec 2000;83(6):320.
7. Novak V, Chowdhary A, Abduljalil A, et al. Venous cavernoma at 8 Tesla MRI. Magn Reson Imaging Nov 2003;21(9):1087-9.

A 39-year-old man with history of tingling sensation on the left half of Face.

MRI revealed a solitary lesion in the splenium of the corpus callosum, hyperintense on T2/FLAIR and hypointense on T1W images. There is diffusion restriction.

This lesion was presumed demyelinating in view of h/o upper respiratory tract infection. At 6-week follow up MRI the lesion resolved completely.

Various etiologies have been reported for transient splenial lesions like:

• Seizures
• Sudden withdrawal of antiepileptic drugs
• Brain infarction
• Multiple sclerosis
• Cerebral trauma
• Neoplasm
• Adrenoleukodystrophy
• AIDS dementia complex
• Infections like influenza, measles, herpes,  Salmonella, mumps, adenovirus, varicella zoster, Legionnaires disease, rotavirus, HIV, tubercular meningitis
• Hypoglycemia
• Marchiafava-Bignami syndrome
• Hemolytic-uremic syndrome with encephalopathy

In absence of significant history of any of these conditions, how do we report this lesion and how often follow it up with MR?

However, I want to bring attention to the authors’ representative figure 1 (page 46).  The follow-up hemorrhage 23 hours later appears on this single slice to be petechial in nature, and not a space occupying hematoma as stated by the authors, and certainly not one that would be categorized as parenchymal hematoma type 2 (PH2) by ECASS criteria.  PH2 must be a space occupying hematoma of >30% of the infarct zone with substantial mass effect attributable to the hematoma.  Unless, this slice is presented only for illustration purposes, and the remainder of the follow-up scan does show more extensive hemorrhage, I believe the hemorrhage depicted here should be categorized as hemorrhagic infarction type 2 (HI2) by ECASS criteria.  The associated mass effect/midline shift is to be expected as edema from a rather large infarct.  This is an important issue because only parenchymal hematomas are relevant clinically, while hemorrhagic infarctions do not portend poor prognosis (and may even be epiphenomenal, reflecting revascularization).

FIGURE 1
FLAIR	T2
Postcontrast	Perfusion image
DWI with ADC	Spectroscopy

These were our differential diagnoses. Do you want to add any other differential diagnosis?

CT scan of chest, abdomen and pelvis were done in search of primary tumor. On CT chest, there were bilateral asymmetric hilar adenopathy and lower lobe predominant nodular densities. The overall chest findings were not typical for sarcidosis. Bronchoscopy-guided biopsy of the hilar nodes revealed non-caseating granulomas. CT of the abdomen and pelvis were unremarkable.

A diagnosis of sarcoidosis was presumed and the patient was put on steroids. Patient got better clinically and an MRI after 5 days revealed significant improvement of the T2 signal abnormality and mass effect. There was no appreciable change in the size of the enhancing lesion. Patient was discharged home with the diagnosis of sarcoidosis and was advised to continue steroids.

FIGURE 2
T2	Post contrast

2 weeks later the patient came back with new onset diplopia as a result of left 6th nerve palsy. MRI at this point showed interval enlargement of the mass, FLAIR abnormality and enhancement. Central T2 hypointense area was more heterogeneous. At this point of time, atypical infection was on the top of our differential diagnoses.

FIGURE 3
FLAIR	T2
Post contrast

Due to relatively rapid progression of clinical symptoms, the lesion was biopsied. It was fungal abscess due to blastomycosis!!

Blastomyces dernatitidis is the causative agent for blastomycosis. Blastomycosis is an uncommon, but potentially serious fungal infection, endemic in Mississippi and Ohio River basins and in the regions of Great Lakes and the St Lawrence River. Occasionally. it can be found in non-endemic areas as well. There is no predilection for any age, sex, race or occupation but it occurs more frequently in the immunocompromised hosts, particularly in AIDS patients. It primarily affects the lungs. CNS dissemination accounts for 5-10% of extrapulmonary blastomycosis and is usually manifested as intracranial mass lesion, abscess of the spinal cord or epidural abscess and meningitis in rare cases. Cerebellum is most commonly involved, but it can involve any area of brain. Multiple lesions throughout the brain mimicking multiple cerebral metastases has also been described in literature. CSF analysis is not very sensitive for the diagnosis as is the CSF culture. CNS blastomycosis is usually treated with Amphotericine B in combination with oral azoles.

References:

1. Bariola JR, Perry P, Pappas PG, et al. Blastomycosis of the central nervous system: a multicenter review of diagnosis and treatment in the modern era. Clin Infect Dis 2010;50:797-804.

2. Borgia SM, Fuller JD, Sarabia A, El-Helou P. Cerebral blastomycosis: a case series incorporating voriconazole in the treatment regimen. Med Mycol 2006;44:659-64.

2. U-King-Im JM, Fox AJ et al.    Characterization of Carotid Plaque Hemorrhage: A CT Angiography and MR Intraplaque Hemorrhage Study. Stroke 2010;41:1623-1629.  The authors did not find mean plaque density to be a useful factor for prediction of MR defined IPH. There was significant overlap between the mean plaque densities between the hemorrhagic and the nonhemorrhagic plaque groups. They did find a strong in vivo association between CTA plaque ulceration and IPH as defined by MR-IPH.

3. Raybaud C.  The corpus callosum, the other great forebrain commissures, and the septum pellucidum: anatomy, development, and malformation.  Neuroradiology (2010) 52:447–477.  This is a massive review.  I suggest a very large caffeinated drink prior to attempted reading.  Some things don’t change: the physiological role of the indusium griseum is still unknown.

4. Hassan AE, Zacharatos, H et al.  A Comparison of Computed Tomography Perfusion-Guided and Time-Guided Endovascular Treatments for Patients with Acute Ischemic Stroke. Stroke 2010; 41:1673-1678.  69 patients underwent CT-P-guided and 127 patients underwent time guided endovascular treatment.  CT-P guided endovascular treatment (compared with conventional time-guided endovascular treatment) was not associated with improved short-term outcomes.  Very interesting counterpoint to the utility of CTP, especially given the recent negative press concerning radiation dosage.

5. Ebinger M., et al. Clinical and Radiological Courses Do Not Differ Between Fluid-Attenuated Inversion Recovery-Positive and Negative Patients With Stroke After Thrombolysis.  Stroke 2010;41:1823-1825.  No significant difference was found in terms of lesion growth or neurological changes after thrombolysis between FLAIR-positive and FLAIR-negative patients. Thrombolysis should not be withheld solely based on FLAIR lesion visibility.

6. Soto-Pérez-de-Celis, E.  The Death of Leon Trotsky. Neurosurgery 67:417-423, 2010. In 1940, a Stalinist agent wounded Trotsky in the head with an ice axe in his house in Coyoacán, Mexico, where he was living in exile.  His assassin, Frank Jacson, after his release from prison, spent his time between Cuba and the Soviet Union, where he received the nation’s highest distinction, the Hero of the Soviet Union medal.  That Stalin, what  a guy.

7. Cloyd JM et al. En Bloc Resection for Primary and Metastatic Tumors of the Spine: A Systematic Review of the Literature. Neurosurgery 67:435-445, 2010. Median time to total recurrence for primary tumors was 113 months and for metastatic tumors was 24 months.  En bloc tumor excisions are highly complex and technically demanding procedure with average operating time of 12.1 hours, estimated blood loss of 3.7 L, and complication rate of 36.3%.  The comments are worth reading, and give a nice summary of current thinking regarding en bloc resection vs. lesion resection with chemo and radiation.

8. Scoccianti S., et al. Patterns of Care and Survival in a Retrospective Analysis of 1059 Patients with Glioblastoma Multiforme Treated Between 2002 and 2007.  Neurosurgery 67:446-458, 2010. Median survival was 9.5 months, and actuarial overall survival rates at 1, 2, and 5 years were 62.3%, 24.8%, and 3.9%, respectively.  Patient characteristics associated with a better prognosis included younger age at diagnosis, single lesion, absence of focal symptoms at diagnosis, and higher preoperative KPS score. One small glimmer of hope is the percentage of patients with long term survival (4-year 6.8%; 5-year 3.9%).

9. Pitt D., et al.  Imaging Cortical Lesions in Multiple Sclerosis with Ultra–High-Field Magnetic Resonance Imaging. Arch Neurol 2010; 67(7):812-818. This is a detailed assessment of the sensitivity of 3-D T2*GRE and 3-D inversion recovery WM attenuated turbo-field-echo (TFE) sequences at 7 T in formalin-fixed MS brains in three patients evaluating cortical demyelination. 46% (T2*GRE) and 42% (WHATTFE) of histologically confirmed lesions were seen on prospective scoring. These scores improved to 93% and 82%,respectively, on retrospective scoring. Lesion visibility was partially determined by size as all undetected lesions had a diameter of 1.1 mm or less.  Very impressive image quality.

10. Fisher CG, Vaccaro AR.  The Highest Level of Evidence in a High Impact Journal: Is This the Final Verdict? Spine 2010; 35 (15): E676-E677.  More fodder for the vertebroplasty debate.  They do make an interesting comparison to femur fractures: The natural history of femur fractures is healing by 6 to 12 months regardless of treatment. The goal of internal fixation is early mobilization and pain control.  The authors ask the question: Would anyone for go internal fixation of a femur fracture because of the equivocal long-term fracture healing?

11. Thompson PM, Martin MG, Wright MJ. Imaging genomics. Current Opinion in Neurology 2010, 23:368–373.  Nice reference list for an area of research to which I pay little (or no) attention.

12. Mirzayan MJ et al. Extended Long-Term (>5 Years) Outcome of  Cerebrospinal Fluid Shunting in Idiopathic Normal Pressure Hydrocephalus. Neurosurgery 67:295-301, 2010. Fifty-one patients (mean age of 70) were included after confirmation of the diagnosis by extensive clinical and diagnostic investigations. Surgery included ventriculoatrial or ventriculoperitoneal shunting with differential pressure valves. Shunt-related mortality was negligible and the main cause of death was vascular comorbidity. Nice table summarizing the literature regarding long-term follow-up studies after shunting in iNPH.

13. Langner S et al. Perfusion CT scanning and CT angiography in the evaluation of extracranial-intracranial bypass grafts. J Neurosurg July 9, 2010. Perfusion CT allows monitoring of hemodynamic changes after bypass surgery. The combination of both modalities enables noninvasive anatomical and functional analysis of superficial temporal artery–middle cerebral artery anastomoses using a single CT protocol.  Didn’t we know this already? We use both all the time in our by-pass population.

14. Barkovich AJ.  Current concepts of polymicrogyria.  Neuroradiology 52: 479-487, 2010.  Everything you need to know in one place….’nuff said.

15. Tubbs RS et al.  Retroclival Epidural Hematomas: A Clinical Series. Neurosurgery 67:404-407, 2010. As Dr. Heger noted in the comments section, 25% of their patients experience occipital cervical dissociation and required stabilization surgery underscores the need for a high index of suspicion for spinal instability in all cases of REDH. 5 of the 6 surviving patients had minimal to no neurologic deficit on long term follow-up indicates that the prognosis from this lesion may be good.

16. Rutherford MA, et al. Magnetic resonance imaging of white matter diseases of prematurity. Neuroradiology (2010) 52:505–521.  Excellent review article with loads of images.  Highly recommended.

Every year in the United States, more than three quarters of a million people have a stroke, and approximately every 3 minutes someone dies from a stroke. A significant portion of stroke victims are young, and left with a devastating handicap for the rest of their lives. The monetary and societal costs of stroke represent a major economic challenge to the healthcare system.  With stroke – as with heart attack – rapid treatment is essential to limit the extent of irreversible brain injury (“time-is-brain”), and rapid determination of the cause and degree of existing brain injury can be critical in deciding treatment.

CT perfusion imaging is a quick, widely available test that displays information about blood flow to the brain that can help diagnose, treat, and predict outcome in stroke patients.  When MRI is not readily available or contraindicated, CT perfusion imaging provides the best possible estimate of brain tissue likely to die without urgent, advanced therapies, including arterial “clot busting” drugs and blood clot retrieval devices.  CT perfusion imaging can also help classify reversible brain injury (“transient ischemic attacks”) that – like cardiac angina – may not require such immediate, aggressive treatment, as well as evaluate brain injury caused by arterial spasm due to bleeding from aneurysm rupture.

Published protocols for performing CT perfusion imaging at “as low a radiation dose as reasonably achievable” – a principle endorsed by the American College of Radiology and American Society of Neuroradiology – have circulated in the medical community for over a decade.  Strict protocol rules and oversight radiation protection personnel at most medical centers ensure that optimal image quality is maintained with a total radiation exposure often considerably lower than the current FDA recommended maximum dose.  Indeed, in an early, highly quoted study that compared different scanning protocols, it was shown that image quality is actually improved when CT perfusion is obtained at a lower average X-ray beam energy than is standard for routine CT imaging.

In all of medicine – and especially for stroke – the potential risks of any diagnostic test or therapeutic procedure (however rare) must be weighed against the very real benefits of preventing death or severe disability.  We believe, and the medical literature supports, that CT perfusion imaging, when appropriately performed, is justified and provides safe, valuable information that can substantially contribute to the management of acutely ill patients in an emergency setting.  Recent advances in scanner hardware and software, and the ongoing efforts of industry, offer the promise of further, significant reductions in CT radiation dose. The radiology community is committed to work hard towards this goal of reducing CT radiation dose, and continuing to offer the best imaging care to our patients.

References:

Janet C Miller, D. Phil., et al. CT Perfusion Imaging of the Brain. Radiology Rounds: A Newsletter for Referring Physicians from the Massachusetts General Hospital Department of Radiology. Volume 8, Issue 6, June 2010. http://www.mghradrounds.org/index.php?src=gendocs&ref=2010_june

Wintermark M, Lev MH. FDA investigates the safety of brain perfusion CT. AJNR Am J Neuroradiol. 2010 Jan;31(1):2-3.

Latchaw RE, Alberts MJ, Lev MH, Connors JJ, Harbaugh RE, Higashida RT, Hobson R, Kidwell CS, Koroshetz WJ, Mathews V, Villablanca P, Warach S, Walters B; American Heart Association Council on Cardiovascular Radiology and Intervention, Stroke Council, and the Interdisciplinary Council on Peripheral Vascular Disease. Recommendations for imaging of acute ischemic stroke: a scientific statement from the American Heart Association. Stroke. 2009 Nov;40(11):3646-78.

Wintermark M, Rowley HA, Lev MH. Acute stroke triage to intravenous thrombolysis and other therapies with advanced CT or MR imaging: pro CT. Radiology. 2009 Jun;251(3):619-26.

Wintermark M, Maeder P, Verdun FR, Thiran JP, Valley JF, Schnyder P, Meuli R. Using 80 kVp versus 120 kVp in perfusion CT measurement of regional cerebral blood flow. AJNR Am J Neuroradiol. 2000 Nov-Dec;21(10):1881-4.

Broad expert consensus on the minimum requirements for CT perfusion scan acquisition can be found in Table 2 (page E25) of the following paper, which can be freely downloaded from PubMed:

Wintermark M, Albers GW, Alexandrov AV, Alger JR, Bammer R, Baron JC, Davis S, Demaerschalk BM, Derdeyn CP, Donnan GA, Eastwood JD, Fiebach JB, Fisher M, Furie KL, Goldmakher GV, Hacke W, Kidwell CS, Kloska SP, Köhrmann M, Koroshetz W, Lee TY, Lees KR, Lev MH, Liebeskind DS, Ostergaard L, Powers WJ, Provenzale J, Schellinger P, Silbergleit R, Sorensen AG, Wardlaw J, Wu O, Warach S. Acute stroke imaging research roadmap. AJNR Am J Neuroradiol. 2008 May;29(5):e23-e30.

The loss of CSF volume explains the usual complaint of orthostatic headache, relieved by lying down, and the characteristic MRI findings: 1) thickening of the dura, enhancing after contrast medium administration, 2) subdural fluid collections, 3) sagging of the brain, 4) dilatation of the venous structures, which includes enlargement of the dural sinuses and veins, enlargement of the pituitary gland, and, in the spinal canal, engorgement of the epidural plexuses. All these features are explained by the Monro-Kellie doctrine: in a closed compartment, such as the intracranial cavity and spinal canal, which contains nervous tissue, blood, and CSF, the loss of one component is compensated by the equivalent increase of the other ones. Therefore, if a dural leakage causes a loss of CSF, an increase in nervous tissue or blood must compensate for that loss to re-establish the equilibrium. Obviously, the easiest compensation comes from an increase in blood, and specifically venous blood because the veins may dilate passively more than the arteries. In peculiar cases, the nervous tissue may participate in the compensation through swelling of the brain (Savoiardo et al. Brain 2007).

Most of the authors who have published papers on SIH, have shifted their emphasis from the loss of pressure in the closed system (intracranial hypotension) to the actual loss of volume of CSF. We agree that the loss of volume of CSF rather than its decreased pressure should be emphasized and pointed out in the denomination of this condition because it is more correct in terms of pathophysiology. However, the term “CSF hypovolemia”, that has been used by most authors, is wrong. We would like to point out again why this is so.

The suffix “emia” in “hypovolemia”, indicates blood, as in glycemia, uremia, and so on. Therefore, “CSF hypovolemia” means “decreased (hypo) volume (vol) of the blood (emia) of the CSF” which is a total nonsense. There is no “blood of the CSF”; moreover, we have seen that venous blood increases (“hypervolemia”) to compensate for the loss of CSF.

According to dictionaries, “hypovolia” exists and should be the correct term. However, since “hypovolia” has never been used and is unknown to most of us, we propose using “CSF loss of volume” or “decreased volume of CSF” rather than “CSF hypovolia”. In our opinion, “CSF hypovolemia” remains a misnomer and should be banned. This is probably a lost cause, but we think it’s worth using the precise terms.

We thank Dr. Neeraj Kumar and Dr. Mauricio Castillo for discussing this matter.

Mario Savoiardo and Marina Grisoli
Department of Neuroradiology
Foundation IRCCS Istituto Neurologico Carlo Besta
Milan, Italy

E-mail:
msavoiardo@istituto-besta.it
mgrisoli@istituto-besta.it

Savoiardo M, Minati L, Farina L, et al. Spontaneous intracranial hypotension with deep brain swelling. Brain 2007;130:1884-93.

Kumar N. Neuroimaging in superficial siderosis: an in-depth look. AJNR Am J Neuroradiol 2010;31:5-14.

Savoiardo M, Grisoli M. Further in-depth look at superficial siderosis (and intracranial hypotension). AJNR Am J Neuroradiol Published June 25, 2010 as DOI 103174/ajnr.A2172

Kumar N. Reply. AJNR Am J Neuroradiol Published June 25, 2010 as DOI 103174/ajnr.A2187

2. Kim KH et al.  Adjacent Segment Disease After Interbody Fusion and Pedicle Screw Fixations for Isolated L4–L5 Spondylolisthesis. Spine 2010;35:625–634. A low postoperative segmental lordotic angle, especially less than 20°, at index level was related with development of clinical ASD in both isthmic and degenerative spondylolisthesis patients.

3. Ribas GC .The cerebral sulci and gyri. Neurosurg Focus 28 (2):E2, 2010.  Very detailed review of the literature regarding the historical, evolutionary, embryological, and anatomical aspects of the cerebral sulci and gyri to establish detailed descriptions of these structures, as well as their groupings in the brain lobes, for microneurosurgical purposes.

4. Diaz FL et al.  Cervical External Immobilization Devices: Evaluation of Magnetic Resonance Imaging Issues at 3.0 Tesla. Spine 2010;35:411–415. Generation 80 and V1 Halo devices exhibited substantial temperature rises with “sparking” evident for the Generation 80 during the MRI procedure. Artifacts were problematic for these devices. The 2 Resolve Ring-based cervical external immobilization devices showed little or no heating and the artifacts were acceptable.

5. Harrop JS et al.  Cervical Myelopathy: A Clinical and Radiographic Evaluation and Correlation to Cervical Spondylotic Myelopathy. Spine 2010;35:620–624.  Nice review of clinical signs.  No patients without cord compression showed myelopathy.  The likelihood of myelopathy increases with the presence of T2 cord signal hyperintensity.

6. Monti MM et al. Willful Modulation of Brain Activity in Disorders of Consciousness. N Engl J Med 2010;362:579-89. Of the 54 patients enrolled in the study, 5 were able to willfully modulate their brain activity demonstrated by fMRI.

7. Ropper AH. Cogito Ergo Sum by MRI. N Engl J Med 2010; Feb 18, 362;7. Editorial accompanying the N Engl J Med article above. (I think, therefore I am).The author reminds us of three important concepts: First, in this study, brain activation was detected in very few patients. Second, activation was found only in some patients with traumatic brain injury, not in patients with global ischemia and anoxia. Third, cortical activation does not provide evidence of an internal “stream of thought”, memory, self-awareness, reflection, synthesis of experience, symbolic representations, anxiety, despair, or awareness of one’s predicament.

8. Kase CS, Nguen TN.  The clinical conundrum of convexal subarachnoid hemorrhage. Neurology 2010;74:874–875.  Editorial. “Convexal” SAH is frequently encountered in clinical practice, and presents at times with acute headache suggestive of SAH, but often it is an unexpected finding on imaging in patients evaluated for a variety of symptoms, including change in mental status, transient focal neurologic deficits, or partial seizures.

9. Kumar S, Goddeau RP et al. Atraumatic convexal subarachnoid hemorrhage:  Clinical presentation, imaging patterns, and etiologies.  Neurology 2010;74:893–899. Reversible vasoconstriction syndrome appears to be a common cause in patients 60 years or younger whereas amyloid angiopathy is frequent in patients over 60.

10. Lovblad K, Baird AE.  Computed tomography in acute ischemic stroke. Neuroradiology (2010) 52:175–187.  Comprehensive review of use of CT imaging and perfusion.

11. Kleiser R, Staempfli P et al.  Impact of fMRI-guided advanced DTI fiber tracking techniques on their clinical applications in patients with brain tumors. Neuroradiology (2010) 52:37–46.  DTI scan can be acquired in a few more scan minutes in the same scan session in which all the other necessary images for the surgery are acquired (anatomical and fMRI data). The data processing is performed offline with dedicated software packages without involvement of the patient.

12. Bello L et al. Intraoperative use of diffusion tensor imaging fiber tractography and subcortical mapping for resection of gliomas: technical considerations. Neurosurg Focus 28 (2):E6, 2010.  Shows the potential usefulness of the routine combined use of DT imaging–FT and subcortical mapping, particularly in patients with low-grade gliomas. These tumors display an infiltrative modality of growth, along short and long connecting fibers, and visualizing the trajectory of the tracts is important for planning and performing surgery.

13. Verhoeven JS et al.  Neuroimaging of autism. Neuroradiology (2010) 52:3–14.  This is an area I have not paid much attention too, so it is convenient to have an all encompassing review available.

14. Chhabra V, Sung E et al.  Safety of magnetic resonance imaging of deep brain stimulator systems: a serial imaging and clinical retrospective study.  J Neurosurg 112:497–502, 2010.  This retrospective MR imaging–based study supports the safety of MR imaging in patients with implanted DBS systems.  Because the indications for DBS continue to expand, it is likely that postoperative MR imaging will remain an important clinical tool.

15. Richards PJ, George J et al. Spine Computed Tomography Doses and Cancer Induction. Spine Volume 35, Number 4, pp 430–433.  Risk ratio for inducing a cancer when CT scanning the whole lumbar spine was about 1 in 3200, which was much less than the risk of CTing the whole dorsal spine (about 1 in 1800) due to the longer coverage required and the anatomic implications of scanning in the region of the cervical dorsal junction.

16. Karppinen J, Solovieva S et al. Modic changes and interleukin 1 gene locus polymorphisms in occupational cohort of middle-aged men. Eur Spine J (2009) 18:1963–1970.  The pathomechanism of LBP due to Modic changes (MC) remains poorly understood. It has been hypothesized that MC is a result of a biomechanically induced inflammation around the intervertebral disc.  This inflammatory etiology is also supported by the finding of an increased number of tumor necrosis factor immunoreactive nerve cells and fibers in endplates with MC, especially in type I changes [30].   This paper shows an association between IL1A gene variation and type II MC replicates a previous finding from a different Finnish geographic area,  confirming the importance of the ILA gene in the pathophysiology of MC.

17. Kim D, Wadley R. Variability in Techniques and Patient Safety Protocols in Discography. Journal of Spinal Disorders & Techniques, 27 January 2010. To improve diagnostic validity and patient safety, the International Spine Intervention Society (ISIS) has published practice guidelines for performing discography (Bogduk N, ed. Practice Guidelines for Spinal Diagnostic and Treatment Procedures. San Francisco: International Spine Intervention Society; 2004:20–46).  The overall compliance with ISIS guidelines is fair to poor with the specialty rank order of compliance greatest to least as follows: Anesthesiology, PMR, and Radiology.

18. Kim HS, Chong HS et al. Vascular Injury in Thoracolumbar Spinal Surgeries and Role of Angiography in Early Diagnosis and Management. Journal of Spinal Disorders & Techniques, 27 January 2010. Of the total 8 arterial injury cases, only 1 of them occurred in the thoracic region and the rest all were seen in the lumbar spine.  Pseudoaneurysm formation in thoracic aorta was seen in 1 case of multiple vertebral fractures, segmental artery was found to be injured in 3 cases of osteotomy for deformities, 2 cases of aortic injury and 1 case of inferior mesenteric artery injury was seen in posterior lumbar interbody fusion. Common iliac artery and vein both were seen to be injured simultaneously in 1 case of lumbar discectomy.

Clinically he was  diagnosed as having sustained a diffuse axonal injury and was treated conservatively.

A brain MRI was performed  one month following injury and a repeat one 1 year later.

Susceptibility WI at the one month interval  showed multiple microhemorrhages in both frontal lobes.

The one year follow-up MRI showed diffuse, symmetric, confluent hyperintensities in the  periventricular WM and these findings were not present on the initial MRI.

The question is whether the WM changes seen at the one-year follow up study are  related to the diffuse  axonal injury. The  microbleeds seen on SWI did not coincide exactly with  the WM changes.