In this board review book entitled Comprehensive Board Review in Neurology, the author covers 13 areas he apparently believes are the most important to neurology residents studying for the ABN examination. Covered are neuroanatomy, vascular disease, seizures, myelination disorders, tumors (brain), headaches and other pain syndromes, psychiatry, movement disorders, nerve disease, muscle disease, infections of the CNS, metabolic and development diseases, and systemic diseases of the nervous system.

Key areas are covered in each chapter. For example in tumors of the nervous system the important points (at least relative to a Board exam) for all the varieties of tumors are covered. This reviewer is struck by 2 aspects—one is that there are far more histologic sections than there are MR images of the brain (only a highly calcified oligrodendroglioma and a meningioma are shown), whereas there are eleven histopathologic sections. This seems a bit unbalanced in terms of what a neurologist needs to know in his/her practice.

While there is material on the spine in places, it appears disproportionately small in total amount and small in contrast to what a neurologist should known about spine disease and low back pain (2 pages); neuronal ceroid lipofuscinosis is given the same amount of space. But, who knows? Maybe these esoterica are given more weight in the Neurology Board exams.

In any event, for a neuroradiologist, the book is a nice review of the major topics in neurology.

A Case-Based Approach to PET/CT in Oncology, edited by Dr. Victor Gerbaud (Director of the Nuclear Medicine and Molecular Imaging Program at Brigham and Women’s Hospital in Boston, Harvard Medical School), with contributing physicians from around the world, is an introduction text for PET/CT in oncologic applications. As the title suggests, this is its primary focus, told through case-based presentations.

The book is divided into two main sections. Section One provides a detailed but not overly complex overview of PET concepts. The first chapter begins with the obligatory refresher of radioactive decay and positron formation, followed by a description of the basic physics of PET and PET/CT acquisition and image generation, with a helpful explanation of attenuation correction, artifacts, and SUV indexes. The second chapter describes in further detail the different PET probes in oncology, primarily FDG, but also provides an introduction to other labeling agents used in research, or to a lesser degree, in clinical practice. The third chapter is a rather detailed discourse on PET/CT information systems, data storage, DICOM basics, and image registration. By far the most useful and relevant chapter in this section for general radiologists is the fourth chapter, describing the physiologic distribution of FDG in normal and abnormal states. This chapter provides a nice table and examples of normal images detailing the normal uptake and SUV values for the different organs of the body, and it explains the common imaging variances in uptake one can observe in day-to-day clinical practice (such as cardiac activity, skeletal activity, and brown adipose tissue).

Section Two is the “case-based” section of the book. Each chapter of this section is broken up into organ-specific (such as brain, esophagus) or site-specific (head and neck, gastrointestinal tract) areas. Every case is presented in the order of a clinical scenario, acquisition and processing parameters, imaging findings, diagnosis and follow up, discussion and teaching points, and take home messages. Each clinical case has accompanying images related primarily to the PET images and fused PET/CT images, with other imaging modalities such as MRI making an occasional appearance when relevant to the case. There are over 120 cases presented in the book, and while it is clear a lot of effort and research went into creating this section, with many educational cases and teaching points throughout the book, there are issues within each case that can make finding the key teaching points somewhat of a search mission. For instance, the acquisition and processing parameters take up one to two paragraphs in each case, including full disclosure of the FDG dose, CT parameters, reconstruction parameters, and so on. In this reader’s opinion, this is somewhat distracting from the primary focus of the case, and this information might have been better served in an appendix or index at the end of the book. Secondly, the imaging findings are presented in the form of a fully dictated report, which in many cases contains discussion of imaging findings not presented in the images or related to a different body part, or sometimes, a list of vague differentials that appear out of place in a case presentation. The discussion and teaching points sections are of variable quality, likely due to multiple author contributions, with some cases discussing outcomes and follow-up imaging studies never visualized in the case, while other cases provide educational discussions on staging classifications, prognosis, and pitfalls, which are very informative. The take-home message section provides 3 or 4 bullet points packed with clinically relevant information helpful not just for the interpretation of the images but also for enhancing the reader’s knowledge of when PET imaging can improve patient care.

For neuroradiologists, the 2 chapters relating to “PET imaging of the Brain” and the “Head, Neck and Thyroid” are of most relevance. While there are interesting topics, such as dynamic PET imaging of the brain for tumor recurrence, and a few cases on other PET radiotracers in brain imaging, there is just not enough content in this book to justify addition to the neuroradiology library. This begets the question, who is this book aimed at?

The preface states it is a useful resource for practicing radiologists, nuclear medicine physicians, and in-training residents and fellows. Certainly, that statement would be true for Section One of the book. However, there are design elements in the case-based section of the book that serve to limit its target audience. For instance, many other case-based review books present the imaging findings at the start of the case, with or without a brief history, allowing the reader to self-examine the case. However, in this book the images are unpredictably spread across pages, displacing text such that cases cannot be taken as unknowns, which hinders its practicality as a self-assessment tool. Secondly, as mentioned above, each case image description and discussion can be unnecessarily long, with many teaching points embedded in the text, which also serves to prevent the book’s serving its potential as a quick-read study aid/board preparation book. As PET/CT plays such an important part in nuclear medicine training programs at present, it would be surprising to find a program that did not encounter many of these cases as part of their standard training, although, this would be a very good refresher for those who do not actively practice oncologic imaging. This book therefore probably offers the highest yield for the general radiologist who is commencing, or is currently involved in, PET/CT imaging and is looking for a brief reference source, and this may be one group of people who would benefit from the “dictation style” of the findings section.

P. Alcaide-Leon^a
aMR Unit
Department of Radiology
Passeig de la Vall d’Hebron
Barcelona, Spain

À. Rovira^b
bHospital Universitari Vall d’Hebron
Barcelona, Spain

We read with great interest the recent study published in the American Journal of Neuroradiology on November 22, 2012, entitled “T1-Weighted Dynamic Contrast-Enhanced MR Evaluation of Different Stages of Neurocysticercosis and Its Relationship with Serum MMP-9 Expression.”¹

In the Materials and Methods section, the authors describe their dynamic contrast-enhanced (DCE) study protocol as follows: “A series of 384 images during 32 time points for 12 sections were acquired (temporal resolution, 5.65 seconds).” However, 32 time points × 5.65 seconds of temporal resolution results in a 3-minute-long DCE-MR study. The specific pharmacokinetic model and the postprocessing software used for calculation of the transfer constant (K^trans); rate constant between extracellular extravascular space and blood plasma (K_ep); and leakage space (V_e) are not stated in the article.

We have been using DCE-MR imaging as a part of our tumor protocol since 2010. We usually perform a 4-minute DCE study. With a study of this length, the washout phase is not usually reached in brain tumors. Inflammatory lesions such us neurocysticercosis are known to wash out much later than tumors as the result of their low permeability surface area product (PS).

In their article published in 1991, Tofts and Kermode² generated families of tracer concentration in tissue [Ct(t)] curves from their equation and demonstrated that for fixed permeability, increasing V_e has no effect on the initial slope but does affect the maximum concentration reached and delays the time to peak enhancement. From this assessment, we infer that reaching the washout phase is needed to obtain V_e and K_ep.

To confirm our hypothesis, we performed a 14-minute DCE study in a patient with pilocytic astrocytoma. Maximum enhancement is reached at 5.8 minutes, and a slow washout curve then begins. We performed 2 different K_ep calculations: the first one by use of the first 3 minutes of the DCE study and the second one by use of the whole 15-minute sequence. Resulting K_ep values are as different as K_ep (3-minute DCE): 0.50 minutes⁻¹ and K_ep (14-minute DCE): 0.13 minutes⁻¹. T1 kinetic analysis was based on the 2-compartment extended pharmacokinetic model of Tofts and Kermode by use of nordicICE software (NordicImagingLab, Bergen, Norway) (Figs 1 and 2).

To sum up, the effect of not collecting for long enough to reach the washout phase would be that V_e and K_ep would be imprecise (ie, poor repeatability), and the performance of those biomarkers would be compromised. Available DCE software provides K_ep and V_e maps even without the data needed to support those calculations, and we should be aware of this fact.

Acknowledgments

We thank Professor Paul Tofts for his help.

References

1. Gupta RK, Awasthi R, Garg RK, et al. T1-weighted dynamic contrast-enhanced MR evaluation of different stages of neurocysticercosis and its relationship with serum MMP-9 expression. AJNR Am J Neuroradiol 2012 November 22, 2012 [Epub ahead of print] » Search Google Scholar
2. Tofts PS, Kermode AG. Measurement of the blood-brain barrier permeability and leakage space using dynamic MR imaging, 1: fundamental concepts. Magn Reson Med 1991;17:357–67 » Medline

Reply

Published online before print March 28, 2013, doi: 10.3174/ajnr.A3578
AJNR 2013 34: E60

R.K.S. Rathore^a
aDepartment of Mathematics and Statistics
Indian Institute of Technology, Kanpur, India

R.K. Gupta^b
bDepartment of Radiology and Imaging
Fortis Memorial Research Institute
Gurgaon, India

We thank Paula Alcaide-Leon and Álex Rovira for their interest in our work.¹ In a given a time-series model involving a number of parameters, it is reasonable to expect that a determination of the parameters by using very few time points may result in erroneous estimates due to noise in the data. However, if one uses enough time points, the computations are expected to be relatively error-free; the inclusion of too many time points need not result in any better estimates.

Furthermore, if the model describes the data (ie, it is applicable), the variability in the parameter estimates using variable time points should only be random. A systematic variation in estimated parameter with respect to variable time points is indicative of an inadequacy of the model to describe the data.

The generalized tracer kinetic model (GTKM) given by
is a 2-compartment model used by the commenting authors.

To resolve the persistence of uptake, researchers are using a model that assumes unidirectional exchange (ie, from the capillary plasma to the extracellular extravascular space [EES]^2⇓–4), which essentially consists of the Patlak model:
describing a pure contrast uptake voxel.

The actual situation, however, appears to be best described by the 3-compartment leaky tracer kinetic model (LTKM)⁵:
presented in Rathore et al^6,7 and Sahoo et al.⁸

LTKM reduces to GTKM if the leakage space is absent (λ^tr = 0); and it reduces to the Patlak model in the absence of a permeable space (k^tr = 0).

The systematic variability of the tracer kinetic parameters using GTKM and its cessation using LTKM is considered at length in Sahoo et al.⁵

In short, it not necessary to prolong the observations until the washout phase, and a study of approximately 3 minutes is quite adequate. What is needed is to use the correct model in which the constancy of the parameters is restored to its original state. For further discussion of LTKM, readers may refer to Sahoo et al.⁵

We used only an in-house-developed code for our computations.

References

1. Gupta RK, Awasthi R, Garg RK, et al. T1-weighted dynamic contrast-enhanced MR evaluation of different stages of neurocysticercosis and its relationship with serum MMP-9 expression. AJNR Am J Neuroradiol 2012 Nov22. [Epub ahead of print] » Search Google Scholar
2. Sourbron SP, Buckley DL. Tracer kinetic modeling in MRI: estimating perfusion and capillary permeability. Phys Med Biol 2012;57:R1–33 » CrossRef » Medline
3. Li KL, Zhu XP, Checkley DR, et al. Simultaneous mapping of blood volume and endothelial permeability surface area product in gliomas using iterative analysis of first-pass dynamic contrast enhanced MRI data. Br J Radiol 2003;76:39–50 » Abstract/FREE Full Text
4. Patlak CS, Blasberg RG, Fenstermacher JD. Graphical evaluation of blood-to-brain transfer constants from multiple-time uptake data. J Cereb Blood Flow Metab 1983;3:1–7 » Medline
5. Sahoo P, Rathore RK, Awasthi R, et al. Subcompartmentalization of extracellular extravascular space (EES) into permeability and leaky space with local arterial input function (AIF) results in improved discrimination between high- and low-grade glioma using dynamic contrast-enhanced (DCE) MRI. J Magn Reson Imaging 2013 Feb 6. [Epub ahead of print] » Search Google Scholar
6. Rathore RKS, Sahoo P, Awasthi R,et al. A modified generalized tracer kinetic model for perfusion parameters in DCE-MRI for high grade intracranial mass lesions. In: Proceedings of the Nineteenth Annual Meeting of the International Society of Magnetic Resonance in Medicine, Montreal, Quebec, Canada; May 6–13, 2011 » Search Google Scholar
7. Rathore RKS, Gupta RK, Sahoo P, et al. DCE-MRI using a three compartment leaky tracer kinetic model (LTKM) for whole body applications. In: Proceedings of the Twentieth Annual Meeting of the International Society of Magnetic Resonance in Medicine, Melbourne, Australia; May 5–11, 2012 » Search Google Scholar
8. Sahoo P, Awasthi R, Rathore RKS, et al. Effects of AIF selection and pharmacokinetic model selection on discrimination of chronic infective from chronic inflammatory knee arthritis using DCE-MRI. In: Proceedings of the Twentieth Annual Meeting of the International Society of Magnetic Resonance in Medicine. Melbourne, Australia; May 5–11, 2012 » Search Google Scholar

Y. Shibata^a
aDepartment of Neurosurgery
University of Tsukuba
Mito Medical Center
Ibaraki, Japan

I read with great interest the article by Hilario et al.¹ The authors retrospectively analyzed the MR imaging data from the first 30 days after injury in 108 patients with severe head trauma and found that the presence of posterior and bilateral brain stem injuries were poor prognostic signs. Although they analyzed the location of the brain stem lesions, they did not analyze the volume or depth of the brain stem lesions. In their study, the median time between trauma and MR imaging was 17 days, with a maximum of 30 days. We previously investigated the MR imaging findings of traumatic primary brain stem injury.² In our study, MR imaging was carried out within 6 days, generally 2 days after the injury.² Superficial dorsal brain stem injury was found to be an indicator of a good prognosis, whereas only deep dorsal brain stem injury was related to a poor prognosis. Small lesions may disappear in a few days after injury. Most of the injuries in Hilario et al’s series of patients had affected the posterior dorsolateral aspect of the midbrain. Hilario et al’s study may have underestimated the lesion size and presence of brain stem injury. They did not extensively discuss the cause of unilateral injuries with a good prognosis, except for the possibility of supratentorial herniation, and they did not discuss the clinical and MR imaging findings of supratentorial herniation. Our study excluded secondary brain stem injury associated with cerebral herniation and evaluated only “primary” brain stem injury. We discussed 2 mechanisms of brain stem injury: primary brain stem injury that occurs after a direct impact of the brain stem against the tentorial free edge, and brain stem injury associated with diffuse axonal injury. Direct focal brain stem injuries caused by an impact against the free tentorial edge have been pathologically and radiologically recognized.^3,4 It is sometimes difficult to differentiate these 2 mechanisms of injury; however, the brain stem lesion size and the location and supratentorial lesion findings are helpful. Hilario et al’s report did not discuss the mechanism of brain stem injury. I believe that differentiating these 2 mechanisms of brain stem injury is therefore critical for accurately diagnosing and understanding traumatic brain stem injuries. In Hilario et al’s study, nonhemorrhagic injuries showed the highest positive predictive value for a good outcome, though no explanation was discussed. Obviously, the presence of no injuries would be most predictive of a good outcome.

References

1. Hilario A, Ramos A, Millan JM, et al. Severe traumatic head injury: prognostic value of brain stem injuries detected at MRI. AJNR Am J Neuroradiol 2012;33:1925–31 » Abstract/FREE Full Text
2. Shibata Y, Matsumura A, Meguro K, et al. Differentiation of mechanism and prognosis of traumatic brain stem lesions detected by magnetic resonance imaging in the acute stage. Clin Neurol Neurosurg 2000;102:124–28 » CrossRef » Medline
3. Clifton G, McCormick W, Grossman R. Neuropathology of early and late deaths after head injury. Neurosurgery 1981;8:309–14 » Medline
4. Firsching R, Woischneck D, Diedrich M, et al. Early magnetic resonance imaging of brainstem lesions after severe head injury. J Neurosurg 1998;89:707–12 » CrossRef » Medline

Reply

Published online before print March 28, 2013, doi: 10.3174/ajnr.A3577
AJNR 2013 34: E57

A. Hilario^a and A. Ramos^a
aDepartment of Radiology

A. Lagares^b
bDepartment of Neurosurgery
Hospital 12 de Octubre
Madrid, Spain

We are grateful for the interest of Dr Shibata in our work and appreciate his comments. Although we are partially in agreement with them, we cannot ascertain why he has not noticed, by reading our work, that we obtained similar conclusions. We retrospectively analyzed data from 108 patients with severe head injury defined by a Glasgow Coma Scale (GCS) score of ≤8 at admission or deterioration in the first 48 hours after injury who underwent an MR imaging examination in the first 30 days after trauma.¹ From this group of patients with severe trauma, we selected those presenting with identifiable brain stem lesions on MR imaging (51 patients). Imaging was performed in the subacute stage of trauma on a 1.5T scanner. The MR imaging protocol consisted of T1, T2, FLAIR, and gradient-echo T2 images in the 3 orthogonal planes. Data were obtained by using 4-mm-thick sections with a 1-mm skip.

Our series is somewhat different from that presented by Shibata et al,² because they just included 17 patients with brain stem injury having all degrees of head injury (GCS scores of 14–3; five patients having mild or moderate head injury). In their series, MR imaging was performed within the first 6 days after trauma by using a 0.5T scanner. Images of continuous 10-mm sections in transaxial planes were obtained by using only T1- and T2-weighted images.

Although the series are different, conclusions are in some aspects similar. As Dr Shibata pointed out, this study and previous publications of our work group^3,4 state that the best predictor of good outcome is the presence of no injuries detectable at MR imaging. However, as stated by the work of Shibata et al,² the mere presence of a brain stem injury does not determine a poor outcome. If there is an identifiable injury in the brain stem, the combination of nonhemorrhagic, anterior, and unilateral injuries determines a better outcome. The mechanism of that injury would be most probably related to direct contusion of the cerebral peduncle, as we stated in our article. Patients presenting with bilateral, hemorrhagic, and posteriorly located brain stem lesions experienced a worse outcome. Our results are not in disagreement with the data published by Shibata et al, in which only superficial (n = 3) and ventrally located lesions had a good prognosis. Lesions situated dorsally but in a deep location or those superficial but associated with a supratentorial diffuse axonal injury (DAI) had a poor prognosis. Of course, lesions present in the subacute stage of trauma are most probably related to a more severe injury.

In the series of Shibata et al,² MR imaging was performed in the acute stage. They acknowledged that superficial lesions detectable in the first days after trauma can disappear or diminish in most patients. In their series, MR imaging was repeated later after injury in 8 patients, and in 5 of them, superficial lesions had disappeared. Therefore, most probably, we are not detecting, at MR imaging, superficial lesions not related to DAI but identifying only deep posteriorly located lesions related to severe DAI.

We do not agree with Dr Shibata’s comments on the lack of information regarding the origin of brain stem injuries because this is discussed in our article. In our series, all patients with brain stem injury had supratentorial lesions related to DAI, such as corpus callosum and subcortical white matter lesions. Therefore, most patients would have primary brain stem injury and not secondary brain stem damage due to supratentorial herniation. In our series, only those lesions located anteriorly had a better prognosis; as we stated, these are most probably related to direct contusion of the mesencephalon with the dura of the tentorium. Posterior brain stem lesions, deeply located and related to other diffuse axonal injuries, had a poor prognosis. We pointed out that nonhemorrhagic lesions have a better prognosis so that we could show that not all brain stem injuries determine a poor prognosis. Hemorrhagic lesions show a worse prognosis because they are related to more intense and greater damage to such important and delicate structures.

References

1. Hilario A, Ramos A, Millan JM, et al. Severe traumatic head injury: prognostic value of brain stem injuries detected at MRI. AJNR Am J Neuroradiol 2012;33:1925–31 » Abstract/FREE Full Text
2. Shibata Y, Matsumura A, Meguro K, et al. Differentiation of mechanism and prognosis of traumatic brain stem lesions detected by magnetic resonance imaging in the acute stage. Clin Neurol Neurosurg 2000;102:124–28 » CrossRef » Medline
3. Lagares A, Ramos A, Alday R, et al. Magnetic resonance in moderate and severe head injury: comparative study of CT and MR findings: characteristics related to the presence and location of diffuse axonal injury in MR [in Spanish]. Neurocirugia (Astur) 2006;17:105–18 » Medline
4. Lagares A, Ramos A, Perez-Nuñez A, et al. The role of MR imaging in assessing prognosis after severe and moderate head injury. Acta Neurochir (Wien) 2009;151:341–56 » CrossRef » Medline

Diagnostic Accuracy of PET for Recurrent Glioma Diagnosis: A Meta-Analysis • T. Nihashi, I.J. Dahabreh, and T. Terasawa
These authors compared the diagnostic accuracy of PET with that of CT and MRI in the diagnosis of recurrent glioma in 26 previously published articles. PET studies with either FDG or carbon methionine were obtained once glioma recurrence was suspected on CT and/or MRI. Diagnostic accuracies were heterogeneous and studies did not compare PET with other imaging modalities. Despite these limitations, PET with both tracers appears to have a moderately good accuracy as an add-on test for diagnosing recurrent glioma.

Cognitive Impairment in Mild Traumatic Brain Injury: A Longitudinal Diffusional Kurtosis and Perfusion Imaging Study • E.J. Grossman, J.H. Jensen, J.S. Babb, Q. Chen, A. Tabesh, E. Fieremans, D. Xia, M. Inglese, and R.I. Grossman
DTI, diffusional kurtosis, and arterial spin-labeling were used in an attempt to detect abnormalities in 20 patients shortly after mild traumatic brain injury. These patients were also evaluated for attention, concentration, executive functioning, memory, learning, and information processing. At 1 and 9 months after injury, all patients showed significant abnormalities in gray and white matter by using all techniques and thus these methods may be useful in investigating cognitive impairment after brain injury.

Postoperative Changes in Cerebral Metabolites Associated with Cognitive Improvement and Impairment after Carotid Endarterectomy: A 3T Proton MR Spectroscopy Study • H. Saito, K. Ogasawara, H. Nishimoto, Y. Yoshioka, T. Murakami, S. Fujiwara, M. Sasaki, M. Kobayashi, K. Yoshida, Y. Kubo, T. Beppu, and A. Ogawa
This study assessed the use of metabolites seen on MRS as markers of change in cognitive status after carotid artery surgery. MRS and neurocognitive testing were obtained before and after surgery in 100 patients. The results showed that cognition remained unchanged in 80%, improved in 10%, and was impaired in 10% of patients postoperatively and that in these last 2 groups, NAA/Cr correlated well the clinical status. Thus, NAA/Cr may serve as a marker of neurologic status after carotid artery surgery (see accompanying editorial by Lövblad and Pereira).

Fellows’ Journal Club

Diagnostic Evaluation in Patients with Intractable Epilepsy and Normal Findings on MRI: A Decision Analysis and Cost-Effectiveness Study • E. Widjaja, B. Li, and L. Santiago Medina
Here is an investigation designed to determine cost-effectiveness of diagnostic tests on patients with focal epilepsy and normal MRI. Studies compared were PET, ictal SPECT, and MEG, individually and in various combinations. PET + MEG and SPECT were the preferred imaging modalities and PET + MEG was favored when the willingness to pay was less than US $10,000, while SPECT was favored when the willingness to pay was above $10,000.

Angioarchitecture of Brain AVM Determines the Presentation with Seizures: Proposed Scoring System • J.J.S. Shankar, R.J. Menezes, B. Pohlmann-Eden, C. Wallace, K. terBrugge, and T. Krings
This group of authors came up with a scoring system to predict seizures in patients with brain AVMs. They retrospectively reviewed imaging studies of 1299 patients and found 33 with unruptured AVMs and seizures and 45 with unruptured lesions without seizures. Features that predicted seizures included: arterial dilation, pial recruitment, fistula, intranidal aneurysm, pial long draining vein, pseudophlebitic pattern, venous outflow obstruction, and venous ectasia. Because seizures are associated with significant morbidity, AVMs with these features may be targeted for treatment with surgery and/or embolization.

Yield of CT Angiography and Contrast-Enhanced MR Imaging in Patients with Dizziness • S. Fakhran, L. Alhilali, and B.F. Branstetter IV
Which is the preferred imaging modality in patients presenting with isolated dizziness? These authors retrospectively evaluated CTA, contrast-enhanced MRI of the brain, and contrast-enhanced MRI of the internal auditory canals and temporal bones in a large group of patients and showed that all 3 are unlikely to identify significant findings that will lead to a change in clinical management in this situation.

REQUIREMENTS: M.D. with a residency in radiology, neurology, or neurosurgery.  Additional degree in Biomedical Engineering, Computer Science, Physics, Cognitive Neuroscience is helpful, but not required. Candidates must be able to work independently. Programming experience is desired. Good organizational skills is a must.

The Massachusetts General Hospital is an equal opportunity and affirmative action employer.

CONTACT: Please email Dr. Steven Stufflebeam with a cover letter and CV to sms at nmr.mgh.harvard.edu. Two letters of recommendation will be required.  If you have any questions please email Dr. Stufflebeam or call (617) 726-0963.

Neuroradiology Neuropathology Conference, April 2013 (PPT)

Anatomic MR Imaging and Functional Diffusion Tensor Imaging of Peripheral Nerve Tumors and Tumorlike Conditions • A. Chhabra, R.S. Thakkar, G. Andreisek, M. Chalian, A.J. Belzberg, J. Blakeley, A. Hoke, G.K. Thawait, J. Eng, and J.A. Carrino
In this study 29 patients underwent anatomic and functional imaging (DWI and DTI) of peripheral nerve masses in an attempt to improve their characterization. ADC values were lower in malignant tumors, the involved nerves had lower fractional anisotropy, and DTI showed differences between benign and malignant tumors. The authors concluded that tractography and fractional anisotropy provide insight into neural integrity while low diffusivity indicates malignancy.

Diagnostic Yield of Catheter Angiography in Patients with Subarachnoid Hemorrhage and Negative Initial Noninvasive Neurovascular Examinations • J.E. Delgado Almandoz, B.M. Crandall, J.L. Fease, J.M. Scholz, R.E. Anderson, Y. Kadkhodayan, and D.E. Tubman
These authors explored the diagnostic yield of DSA in patients with SAH and previously negative CTA or MRA. A total of 55 patients who presented with diffuse SAH, perimesencephalic SAH, or sulcal SAH received CTA (n= 47) or MRA (n= 8). Despite normal findings on CTA or MRA, DSA showed vascular lesions in 11% of patients with diffuse SAH and in 1 patient with sulcal SAH. The investigators concluded that DSA is a valuable tool in patients with diffuse or sulcal SAH in whom previous noninvasive examinations are negative.

Screening Cervical Spine CT in the Emergency Department, Phase 2: A Prospective Assessment of Use • B. Griffith, M. Kelly, P. Vallee, M. Slezak, J. Nagarwala, S. Krupp, C.P. Loeckner, L.R. Schultz, and R. Jain
Here, the number of unnecessary CT cervical studies despite proper application of NEXUS criteria was assessed. The authors also tried to determine indications for ordering studies in the absence of guideline criteria. Of 507 CT studies, only 5 (1%) were positive while 81 of the 502 patients with negative findings (16%) were imaged despite meeting all NEXUS criteria for non-imaging. The most common indications for the studies were a dangerous mechanism of injury and subjective neck pain. Strict application of NEXUS criteria may result in considerable reduction of screening CT studies of the cervical spine.

Fellows’ Journal Club

Clopidogrel Hyper-Response and Bleeding Risk in Neurointerventional Procedures • C. Goh, L. Churilov, P. Mitchell, R. Dowling, and B. Yan
Patients may respond to antiplatelet medication in 2 ways: resistance leading to higher incidence of ischemic events and hyper-response resulting in bleeds. Here, 47 patients treated with clopidogrel were tested for P2Y12 receptor-mediated platelet inhibition. Clopidogrel hyper-response was more common in patients with major (n=10) than in those with minor bleeds. Of 7 patients defined as hyper-responders, 43% had major bleeding complications. Thus, hyper-response to clopidogrel is associated with increased risk of major hemorrhage. (See the related article by Comin and Kallmes.)

Neuroradiology Critical Findings Lists: Survey of Neuroradiology Training Programs • L.S. Babiarz, S. Trotter, V.G. Viertel, P. Nagy, J.S. Lewin, and D.M. Yousem
These authors questioned neuroradiology fellowship programs about the availability of “critical findings” lists and, if available, how these are distributed to trainees and whether they were vetted by corresponding clinical departments. Over one-half of programs responded and 41% had such lists. The lists were distributed during orientation, sent or made available electronically, and posted in work areas. Less than 25% of lists were developed with input from other departments. The most common entities found in the lists were: brain hemorrhage, acute stroke, cord compression, brain herniation, and spine fracture.

Traumatic Intracranial Hematomas: Prognostic Value of Contrast Extravasation • L. Letourneau-Guillon, T. Huynh, R. Jakobovic, R. Milwid, S.P. Symons, and R.I. Aviv
Contrast extravasation in hematomas predicts their growth and thus these authors assessed the prognostic value of this sign. Sixty patients with cerebral hematomas received CTA and/or perfusion CT within 24 hours of admission and then a follow-up CT at 72 hours. Fifty percent of patients showed contrast extravasation and this finding predicted poor in-hospital outcome. Recognition of contrast extravasation achieved a near perfect interobserver agreement.

T.M. Ryan^a, E.C. Kavanagh^a and P.J. MacMahon^a
aDepartment of Radiology
Mater Misericordiae University Hospital
Dublin, Ireland

We read with great interest the recent article by Miller et al¹ regarding lateral decubitus positioning for cervical nerve root block by using CT image guidance to minimize effective radiation dose and procedural time.

The technique of cervical foraminal injection is outlined in the “Materials and Methods ” section. The authors state, “A slow 1-mL injection of iohexol diluted in 1-mL 1% lidocaine was used in all cases to identify inadvertent direct vessel puncture.” We ask the authors in how many cases did they identify inadvertent direct vessel puncture with the aid of contrast?

From the >1000 procedures we have performed by using the technique outlined in this article, we have never identified vessel puncture with contrast CT. The reason for this is likely to be 2-fold: First, should the contrast be injected intravascularly, it is likely to be washed away by the time CT is performed. Second, it is possible that the given vessel enters the cord at a different level and is therefore not imaged.

In this sense, we believe that contrast administration gives the radiologist a false sense of security. Real-time imaging such as digital subtraction angiography would be needed to reliably exclude inadvertent direct vessel puncture. However, we believe that such measures are also unnecessary on the basis of current best evidence in the literature (case series,² animal experimentation,³ and in vitro microscopy⁴). Dexamethasone sodium phosphate is likely safe if inadvertently injected intravascularly.

On this basis, we propose that this procedure can be made even safer in 2 ways: By eliminating the administration of contrast, the possibility of an adverse reaction is avoided. Furthermore, the number of imaging series could be reduced to give an even lower effective radiation dose and a shorter procedural time.

References

1. Miller TS, Fruauff K, Farinhas J, et al. Lateral decubitus positioning for cervical nerve root block using CT image guidance minimizes effective radiation dose and procedural time. AJNR Am J Neuroradiol 2013;34:23–28 » Abstract/FREE Full Text
2. Scanlon GC, Moeller-Bertram T, Romanowsky SM, et al. Cervical transforaminal epidural steroid injections: more dangerous than we think? Spine 2007;32:1249–56 » CrossRef » Medline
3. Okubadejo GO, Talcott MR, Schmidt RE, et al. Perils of intravascular methylprednisolone injection into the vertebral artery: an animal study. J Bone Joint Surg Am 2008;90:1932–38 » CrossRef
4. Derby R, Lee SH, Date ES, et al. Size and aggregation of corticosteroids used for epidural injections. Pain Med 2008;9:227–34 » CrossRef » Medline

Reply

Published online before print March 14, 2013, doi: 10.3174/ajnr.A3546
AJNR 2013 34: E46

T. Miller^a and A. Brook^a
aMontefiore Medical Center
Department of Radiology and Neuroradiology
Albert Einstein College of Medicine
Bronx, New York

We appreciate the comments submitted by Timothy Martin Ryan, Eoin C. Kavanagh, and Peter J. MacMahon regarding the use of contrast before CT-guided cervical nerve root block. The group certainly has extensive experience with the procedure. In our cases, we did not show an instance of inadvertent direct vessel contrast uptake with the contrast injection. However, we were able to visualize the extent of foraminal or epidural contrast with each injection.

The intent to decrease procedural time and radiation dose by skipping a step is valid, but eliminating the contrast step would be of little incremental value. The accepted safety profile of nonparticulate steroid formulations is growing, and we are believers. We agree that the contrast injection is unlikely to demonstrate intravascular injections. We have begun to rely on the contrast injection to document the location of the injectant. If we see poor perineural or epidural contrast, the needle can be adjusted to allow better medication deposition. Regardless, this process also allows us to document injectant localization.

Although the concern over contrast reaction is plausible, with 1-mL injections, we have yet to elicit a reaction. We concede that it is possible to generate a reaction even with such small volumes; however, we believe that the benefit outweighs the minimal risk. Contrast can be omitted for patients with known contrast allergy, pretreatment can be used, or gadolinium-based agents (off-label) may be substituted for iodinated contrast.

Lidocaine is much more useful for determining intravascular medication injection. Untoward patient reaction signals an inadvertent vascular injection. In such cases, the procedure can be terminated or the needle can be adjusted and the injection can be repeated. This choice is dependent on the patient’s reaction and recovery.

In summary, we agree with the notion that nonparticulates should be the standard of care and that imaging after contrast in CT is of limited utility in demonstrating intravascular contrast. The contrast documents injectant localization and allows us to adjust the injection to maximize localization of the medication. The potential for contrast reaction is minimal, and we believe that another benefit of contrast injection is to document injectant flow. Therefore, we are not yet ready to abandon contrast injections for small incremental reductions in potential contrast reaction, radiation exposure, or procedure time.

M.P. Menezes^a
aInstitute for Neuroscience and Muscle Research

T. Nowland^b and E. Onikul^b
bDepartment of Radiology
The Children’s Hospital at Westmead
Sydney, New South Wales, Australia

We read with interest the article by Jokhura et al¹ on diffusion-weighted imaging in acute hypoglycemia in adults. Although there is now an increasing amount of literature on the MR imaging changes and outcome in adults with hypoglycemia, there is a paucity of literature that details imaging abnormality with acute hypoglycemia in childhood beyond the neonatal period. We describe the early progression of DWI abnormalities in a child with acute hypoglycemia and prolonged febrile seizure, and we document the poor outcome that is associated with diffuse hemispheric white matter DWI change.

A 4-year-old girl with congenital adrenal hyperplasia presented after a prolonged right focal seizure. She had been previously well with normal intelligence and had previous episodes of hypoglycemia with illness, but none that resulted in a seizure or encephalopathy. She had a fever and vomiting in the 24 hours before presentation. The seizure commenced with right arm twitching that secondarily generalized, despite intramuscular hydrocortisone administered by the mother. The blood glucose level was measured with a hand-held glucometer while the patient was being transported by ambulance and showed a reading of “low.” She was given intramuscular glucagon and had a repeat blood glucose level of 12.5 mmol/L and a temperature of 40.5°C 25 minutes after seizure onset. The seizure lasted for 45 minutes and was terminated with a midazolam infusion and intravenous phenytoin. Subsequent investigations including extensive biochemical and serologic investigations were normal.

The first MR imaging was performed at 28 hours after admission. At that time, she had a Glasgow Coma Scale score of 8, intact brain stem reflexes, brisk reflexes, upgoing plantars, and no decorticate or decerebrate posturing. The MR imaging (Fig 1A, –B) showed diffusion restriction in the cortex with sparing of the temporal and most of the occipital lobes, with corresponding T2 hyperintensity. There was also diffusion restriction in the left hippocampus.

The MR imaging was repeated at 50 hours after admission because of right focal face seizures and deterioration in responsiveness. This showed prominent diffusion restriction and ADC map changes involving both the cortex and subcortical white matter of the frontal and parietal lobes bilaterally, and the left hippocampus, with prominent corresponding T2 hyperintensity (Fig 1C–H). She improved slowly, and, on discharge 48 days after admission, she was significantly disabled with limited functional use of her upper limbs, nonambulatory, nonverbal, and fed through a nasogastric tube.

There were some differences in the early DWI in our child when compared with imaging at presentation in adults, as reported by Jokhura et al. Imaging at 28 hours in our patient showed diffusion restriction only in the cortex, though there was prominent subcortical white matter involvement on DWI at 50 hours. The basal ganglia, internal capsule, centrum semiovale, and corpus callosum remained uninvolved. The diffusion restriction primarily involved the frontal and parietal lobes. This predominantly cortical involvement and predilection for the frontal and parietal cortex has been previously reported in adults and differs from the predominantly occipital involvement reported with neonatal hypoglycemia.^2,3 As reported in adults, diffuse hemispheric cortical and white matter change was predictive of a poor outcome in our patient.^1,2 The acute diffusion restriction seen in the left hippocampus is consistent with hippocampal edema after a prolonged febrile convulsion. Prolonged febrile convulsion in childhood is associated with unilateral diffusion restriction in the hippocampus contralateral to the focal seizure and increase in T2 relaxation time on MR imaging performed early after the convulsion, with resolution on follow-up imaging, indicating that these changes probably are caused by transient hippocampal edema.^4,5

Prolonged ictal activity causes increased glucose requirements in the neuronal and glial cells, which, in combination with the glucose deprivation, causes severe energy failure, resulting in cytotoxic edema and restricted diffusion on DWI imaging. It is likely that the combination of hypoglycemia and prolonged seizure in our patient caused severe cytotoxic edema and neuronal injury in the hemispheric neuronal cells and was responsible for severe injury and poor outcome in this case. Diffuse hemispheric white matter change on DWI should raise the possibility of acute hypoglycaemia in those with unexplained encephalopathy. In conclusion, our case demonstrates the early DWI changes after acute hypoglycemia in childhood encephalopathy. The combination of acute hypoglycemia and prolonged seizures lead to a poor long-term outcome.

References

1. Johkura K, Nakae Y, Kudo Y, et al. Early diffusion MR imaging findings and short-term outcome in comatose patients with hypoglycemia. AJNR Am J Neuroradiol 2012;33:904–09 » Abstract/FREE Full Text
2. Kang EG, Jeon SJ, Choi SS, et al. Diffusion MR imaging of hypoglycemic encephalopathy. AJNR Am J Neuroradiol 2010;31:559–64 » Abstract/FREE Full Text
3. Barkovich AJ, Ali FA, Rowley HA, et al. Imaging patterns of neonatal hypoglycemia. AJNR Am J Neuroradiol 1998;19:523–28 » Abstract
4. Natsume J, Bernasconi N, Miyauchi M, et al. Hippocampal volumes and diffusion-weighted image findings in children with prolonged febrile seizures. Acta Neurol Scand 2007;115:25–28 » CrossRef » Medline
5. Scott RC, Gadian DG, King MD, et al. Magnetic resonance imaging findings within 5 days of status epilepticus in childhood. Brain 2002;125:1951–59 » Abstract/FREE Full Text