Amirsys has taken their brilliant concept of medical education for neuroradiology one step further by the publication of the newest in their series, Diagnostic Pathology: Neuropathology. For someone (like this reviewer) who has had the classic textbook by Russell and Rubenstein Pathology of Tumors of the Central Nervous System on his bookshelf for years, this new textbook, authored by 7 neuropathologists led by Drs. Peter Burger and Bernd Scheithauer, brings new life and relevance to neuropathology. What more can one say about the incredible importance that Amirsys has had in bringing new concepts in educational material to radiologists in general, and to neuroradiologists in particular? Understand that this book is far more than a text on CNS tumors: it includes both neoplastic and non-neoplastic conditions and furthermore uses, as appropriate, representative MR images to make more pertinent the associated pathologic features. The pathology shown is predominately histopathology, but gross anatomic images are illustrated in many sections.

The Neoplastic part of the book is divided into (a) Brain/Spinal Cord (infiltrative astrocytic neoplasms – 6 chapters; oligodendroglioma neoplasms – 3 chapters; localized astrocytic neoplasms – 4 chapters; tumors of ependyma and related cells – 7 chapters; choroid plexus neoplasms – 2 chapters; neuronal and glioneuronal neoplasms – 11 chapters; pineal parenchymal neoplasms – 3 chapters; embryonal neoplasms – 5 chapters; germ cell neoplasms – 3 chapters; hemangioblastoma – 1 chapter; lymphoma and hematopoietic neoplasms – 6 chapters; metastatic neoplasms – 1 chapter); (b) Sellar Region (adenohypophyseal neoplasia and hyperplasia – 10 chapters; neurohypophyseal and hypothalamic neoplasms – 3 chapters; craniopharyngioma – 2 chapters; miscellaneous neoplasms – 3 chapters); (c) Meninges – 10 chapters; (d) Cranial, Spinal, Peripheral nerves – 11 chapters; and (e) Familial Tumor Syndromes – 6 chapters. The non-neoplastic portion of the book is divided into (a) Benign Cysts – 9 chapters and (b) infectious, inflammatory, and reactive lesions (21 chapters, which include MS, bacterial/viral/ fungal/parasitic infections, other inflammatory conditions such as sarcord, Rasmussen’s, pseudotumors, etc., and reactive conditions and non-inflammatory pseudotumors). The third section deals with Vascular Malformations (8 chapters), while the fourth section deals with cortical dysplasia.

The last part of the book is unique to radiology texts (at least to this reviewer): it has an antibody index and a molecular factors index. In the former index there is a list of over 200 antibodies, their alternative names, and, importantly, under what pathological condition in the book where it is mentioned/described. So as just one example, the book describes capase-1 in the table as promoting maturation of IL by proteolytic cleavage, mentions its role in inflammation, and refers the reader to HIV encephalitis. When one goes to HIV encephalitis and reads the portion under microscopic pathology, one sees the immunoreactivity listed for a number of entities, including capase-1. In the latter index, the many molecular factors are listed, where their chromosomal location is centered, and again where in the book a description or mention of the factor is located is centered. These 2 long tables are excellent and will be helpful as one reads papers where these factors (either antibody or molecular) are mentioned.

For the major part of the book, in a format which is familiar to most radiologists, each disease is described under bullet points concerning terminology, etiology, clinical issues, pathological findings, differential diagnosis, and references.

Of course, in a book so encompassing, it is impossible for a review like this to do it justice; nonetheless, a few examples will suffice. An intracranial tumor that is rarely encountered, a solitary fibrous tumor, is shown and described fully with its MR, gross pathology, and microscopic features, including those that are of the hemangiopericytoma type (news to me!). Here the terminology is described under “definitions,” where we learn this is a spectrum of lesions, the clinical issues, image findings (briefly), and where ancillary tests are mentioned. As expected the macroscopic and microscopic features along with immunohistochemical features are beautifully shown. A differential diagnosis for every disease is listed, and one should know that this is pathologic differential, not an imaging differential.

In the non-tumoral section, take herpes simple encephalitis as an example. A high quality artist’s drawing imbeds in our mind the temporal lobe, cingulate cortex, and insular cortex involvement. The text reminds us that HSE1 is more common in immunocompetent as compared to immunocompromised patients, describes the epidemiology, the clinical issues, the microscopic pathology, the associated ancillary tests and the differential. What follows are MR images of   florid HSE cases and a series of 16 histopathology images showing different stages and forms of this infection (acute, hemorrhagic, microglial clusters, neutrophilic infiltrates, red dead neurons, plasmacytoid lymphocytes, intracellular viral particles, immunopositive stain, CD68 positive macrophages, late-stage HSE with tissue cavitation). This type of in-depth description is found in every disease included in the book.

Of course the book cannot cover every entity with which we deal; enumerating diseases not included would require a long list, so the reader should not expect to see or have discussed all the diseases we encounter. Nonetheless, a very large majority of neuropathological diseases are included.

This reviewer’s strong advice is that every neuroradiologist ought to own his/her own copy of this wonderful textbook. Certainly it ought to be in every Departmental library. If you are uncertain as to whether this book should be in your personal library, make sure you look through it at the next meeting you attend. You will be sold. Remember that, as in all books in this series, you can access the online version with a unique license key.

In summary, this is an outstanding textbook which can expand and deepen one’s understanding of neuropathology and, as a result, improve one’s practice of neuroradiology.

A new entry into the popular format of case-based publications is the recently published (2012) softcover book Neuroradiology Cases: Cases in Radiology written by Drs. Eskey, Belden, Pastel, Vossough and Yoo. This 416-page book is divided into 3 sections (brain/spine/ENT) and unabashedly has the aim of appealing to those preparing for the ABR examination. Therefore, as one would expect, the cases are classic in imaging. The concept is pattern recognition with minimal interrogation in terms of advanced techniques.

The format is straightforward: 192 cases are shown with selected images and a brief history on the right hand page, and the overleaf repeats some of the images with one or two additional images (labeled appropriately). The case discussion for each includes findings, differential diagnosis, pertinent teaching points, clinical management, and references (or what is called “further reading”). This allows for self-testing and studying the entity under consideration.

The images are of good quality, and the selection of cases is appropriate; a number of them are challenging, considering that the authors are aiming this text toward residents studying for the boards. One has to wonder, however, given all the quiz material available on the internet, whether on a society website or from a University, why these types of books continue to be published.

The cases themselves are straightforward, and the abnormalities are obvious. But as we all know, real-life radiology doesn’t present us with a couple of images that are blatantly abnormal and from which we then make a diagnosis.

That being said, there is instructive and worthwhile material here. Just to name a few: infarcts secondary to a meningitis, “chasing the dragon,” adult HIE, small subdural empyemas, fenestral otosclerosis, incomplete partition of the cochlea, PXA, MSA, interhemispheric epidermoid cyst, spinal cord infarction, ATM, SCD, labyrinthitis ossificans, orbital rhabdomyosarcoma, PHPV, inflammatory adenitis (AML), ocular melanoma, kernicterus, anencephaly on prenatal sonography (do they really show OB VS in Neuro?), methanol toxicity, PKAN, RCVS, etc. Overall, the discussions and teaching points are well written and distill the information to the essentials.

Putting aside the review of this book for a second, this reviewer believes what really needs to be published is a compendium of cases where the findings are subtle; such a book could be called Easily Missed Diagnoses: Neuroradiology. Here is where most concern for the everyday practice of neuroradiology lies.

In summary, for this genre of books, the text reviewed here is good and could be one passed from resident to resident as a preparation for the Boards (written and oral).

Clinical Correlation of a New MR Imaging Method for Assessing Lumbar Foraminal Stenosis • H.-J. Park, S.S. Kim, S.-Y. Lee, N.-H. Park, M.-H. Rho, H.-P. Hong, H.-J. Kwag, S.-H. Kook, and S.-H. Choi
Two different systems for grading foraminal stenosis, the Wildermuth (degree of fat obliteration) and the Lee system (type of stenosis, degree of fat obliteration, and nerve root compression) were assessed and correlated with clinical findings. Interobserver agreement was greater with the Lee system. Both systems had good correlation with clinical symptoms, especially for older patients, but the Lee system was better for younger subjects. Although both systems performed well, the Lee system was slightly better.

Detection of Microhemorrhage in Posterior Reversible Encephalopathy Syndrome Using Susceptibility-Weighted Imaging • A.M. McKinney, B. Sarikaya, C. Gustafson, and C.L. Truwit
Hemorrhage in posterior reversible encephalopathy syndrome occurs in 15-17% of patients but can be underestimated by using conventional MRI. Thus, these authors used SWI to study 31 patients with PRES and found that microbleeds were present in nearly 65% and subarachnoid hemorrhage in 10%. In some patients, microhemorrhages persisted after PRES resolved and in others these developed after its onset. Although the clinical significance of these small bleeds is not known, they could be caused by endothelial cell damage.

Susceptibility-Weighted Imaging in Patients with Pyogenic Brain Abscesses at 1.5T: Characteristics of the Abscess Capsule • P.H. Lai, H.C. Chang, T.C. Chuang, H.W. Chung, J.Y. Li, M.J. Weng, J.H. Fu, P.C. Wang, S.C. Li, and H.B. Pan
The rim of cerebral abscesses is dark on T2 presumably due to the accumulation of oxygen radicals in inflammatory cells. Because DWI is more sensitive to susceptibility effects than other MRI sequences, these authors used it to evaluate 14 abscesses. DWI agreed with previous observations detecting mild hypointensity in most abscess rims, compatible with the presence of paramagnetic substances due to oxygen free radicals from phagocytosis. SWI provides another means of establishing the diagnosis and helping us to understand the pathophysiology of abscesses.

Fellows’ Journal Club

Practice Patterns and Opening Pressure Measurements Using Fluoroscopically Guided Lumbar Puncture • A.S. Abel, J.R. Brace, A.M. Mckinney, A.R. Harrison, and M.S. Lee
Here is an article that offers evidence-based information regarding different protocols used for fluoroscopically guided lumbar punctures. The data were obtained via Web-based anonymous questionnaires sent to neuroradiologists. From 577 responses the following information can be gleaned: most neuroradiologists place the patient prone, use a 22-gauge needle, and access the L2-3 or L3-4 spaces. The techniques for measuring pressure vary widely and only a minority of neuroradiologists rotate their patients for this purpose. The authors recommend developing a uniform protocol for opening pressure measurement.

Differentiation of Tumefactive Demyelinating Lesions from High-Grade Gliomas with the Use of Diffusion Tensor Imaging • C.H Toh, K.-C. Wei, S.-H. Ng, Y.-L. Wan, M. Castillo, and C.-P. Lin
Although perfusion and MRS have been used to differentiate tumefactive demyelinating lesions from gliomas, this article explores the use of DTI for this purpose. The authors measured fractional anisotropy inside the lesions, at their periphery, and in the perilesional zone in 8 TDLs and 13 gliomas. Fractional anisotropy in the peripheral enhancing portions of the lesions was higher in TDLs than in gliomas, whereas in the perilesional zones fractional anisotropy was higher in gliomas. Thus, DTI was helpful in differentiating between these 2 lesions.

Acute Effects of Alcohol on the Human Brain: Diffusion Tensor Imaging Study • L.M. Kong, W.B. Zheng, G.P. Lian, and H.D. Zhang
Is DTI helpful in assessing the effects of acute alcohol ingestion on the brain? Sixteen healthy volunteers were given either low or high doses of alcohol in the form of wine and DTI measurements were obtained at 0.5, 1, 2, and 3 hours after its initiation. No abnormalities were seen by conventional MRI but low ADC values were found in the frontal lobe, thalamus, and middle cerebellar peduncle especially at 1 and 2 hours. Breath alcohol measurements reached their peak at 30 minutes. DTI is thus better than breath measurements for detection of acute alcohol-induced changes.

A.J. da Rocha^a and A.C. Martins Maia Jr^b
aDivision of Neuroradiology

B.C. Oliveira Valério^b
bDivision of Neurology
Santa Casa de Misericórdia de São Paulo
São Paulo, Brazil

We read the article by Carrara et al,¹ entitled “A Distinct MR Imaging Phenotype in Amyotrophic Lateral Sclerosis: Correlation between T1 Magnetization Transfer Contrast Hyperintensity along the Corticospinal Tract and Diffusion Tensor Imaging Analysis,” with great interest. The possible recognition of a distinct phenotype of amyotrophic lateral sclerosis (ALS) based on typical corticospinal tract (CST) hyperintensity on T1-weighted images with magnetization transfer contrast (T1 MTC) reinforces the applicability of MR imaging in confirming upper motor neuron (UMN) involvement in ALS. However, previous reports have described false-negative MR imaging results that were attributed to progressive CST degeneration in the advanced stages of the disease.^2,3 Nevertheless, to the best of our knowledge, this theoretic “pseudonormalization” has never been documented in the MR imaging follow-up of a patient with ALS.

We describe imaging follow-up of a young-adult patient with ALS (a 20-year-old woman) who was examined in the 6th and 30th months after the initial clinical manifestations of UMN involvement. The MR imaging protocol included T1 MTC (TR/TE, 512 ms/minimum full; MT pulse, 1200 Hz; off resonance). For quantitative assessment, we obtained axial proton density sequences (TR/TE, 2200/30 ms) with and without MTC to determine the magnetization transfer ratios (MTRs). All MR images were obtained in the same 1.5T scanner with identical parameters for monitoring. On the first MR imaging scan, there was a marked abnormal CST hyperintensity on the T1 MTC images, which became almost inconspicuous on follow-up MR imaging (Fig 1). The MTRs of a 3-mm-diameter circular region of interest were measured in the bilateral CST in the subcortical precentral regions, the posterior segment of the internal capsules, and the extramotor bilateral frontal white matter (Table). It is possible to realize a significant reduction of MTR values in all different regions, consistent with the findings of the conventional sequence.

Our findings are consistent with those previously reported and reinforce the utility of T1 MTC sequences for the early diagnosis of UMN degeneration based on qualitative analysis of the CST.⁴ The typical hyperintensity on T1 MTC likely reflects the abnormalities that are restricted to the CST in the initial UMN degeneration events in definite ALS. This likely reflects the abnormalities that are restricted to the CST in the initial UMN degeneration events in definite ALS. However, pseudonormalization limits this sequence applicability in advanced ALS, likely as a consequence of the gliosis that is secondary to axonal loss and CST degeneration.^2,3 Our quantitative results support this argument to explain the pseudonormalization documented on T1 MTC signal intensity. Disease progression is presumably followed by some changes in the microstructural tissue environment that modify the exchange basis of magnetization transfer; furthermore, this progression leads to widespread abnormalities beyond the CST limits, as confirmed on DTI.³ As shown here, MTR is useful to estimate the structural damage in different brain regions, including motor and extramotor ALS progression, particularly in advanced stages of UMN compromise in patients with ALS.^2,3

References

1. Carrara G, Carapelli C, Venturi F, et al. A distinct MR imaging phenotype in amyotrophic lateral sclerosis: correlation between T1 magnetization transfer contrast hyperintensity along the corticospinal tract and diffusion tensor imaging analysis. AJNR Am J Neuroradiol 2012;33:733–39 » Abstract/FREE Full Text
2. Charil A, Corbo M, Filippi M, et al. Structural and metabolic changes in the brain of patients with upper motor neuron disorders: a multiparametric MRI study. Amyotroph Lateral Scler 2009;10:269–79 » CrossRef » Medline
3. Agosta F, Chio A, Cosottini M, et al. The present and the future of neuroimaging in amyotrophic lateral sclerosis. AJNR Am J Neuroradiol2010;31:1769–77 » Abstract/FREE Full Text
4. da Rocha AJ, Oliveira AS, Fonseca RB, et al. Detection of corticospinal tract compromise in amyotrophic lateral sclerosis with brain MR imaging: relevance of the T1-weighted spin-echo magnetization transfer contrast sequence. AJNR Am J Neuroradiol 2004;25:1509–15 » Abstract/FREE Full Text

E. Anagnostou^a, S. Vassilopoulou^a and K. Spengos^a
aDepartment of Neurology
University of Athens
Eginition Hospital
Athens, Greece

S. Lachanis^b
bIatropolis Magnetic Resonance Diagnostic Centre
Athens, Greece

A 32-year-old woman presented with vertical diplopia after a blunt head injury due to a vehicle crash. On examination 2 weeks after the trauma, she had a pupil-involving right third-nerve palsy. The absence of intorsion when looking downward starting from an abducted eye-in-orbit position suggested a concomitant fourth nerve palsy. T1-weighted brain MR imaging revealed marked gadolinium enhancement of the cisternal portion of the right oculomotor nerve (Fig 1). The trochlear nerve could not be visualized on the available scans.

Mechanical compression and/or traction of cranial nerves may develop as a consequence of head trauma. Still, systematic studies of cranial nerve palsies after mild head injury are sparse. In a recent analysis by Coello et al,¹ 11.3% of patients with posttraumatic cranial nerve injuries had an oculomotor nerve palsy; 42.8% of these patients had at least 1 additional cranial nerve involvement. The most commonly associated nerve injury was to the trochlear nerve. Unfortunately, no MR imaging data are available from this study.

Oculomotor nerve enhancement is not uncommon in inflammatory conditions and in ophthalmoplegic migraine.² On the other hand, the presence of cranial nerve enhancement after head injury is not systematically investigated. We could find only 1 case description of nerve enhancement after a presumed mild head injury concerning the hypoglossal nerve.³ Despite the lack of data in the clinical literature, contrast enhancement of injured nerves after traction or compression is well-known from animal experiments.⁴ Neuropathologic findings indicate that the intraneural edema caused by mechanical compression is a vasogenic edema induced by congesting venous blood flow and develops because of increased permeability of capillaries in the endoneurial space. In turn, leakage of endoneurial pressure appears to induce demyelination.⁴ Our case presents pathologic gadolinium enhancement of the third cranial nerve after a minor head injury, which probably reflects a trauma-induced local breakdown of the blood-nerve barrier, with consequent edema formation. Modern MR imaging techniques such as 3D constructive interference in steady state³ may help develop diagnostic algorithms for monitoring and treatment of cranial nerve palsies after head injury.

References

1. Coello AF, Canals AG, Gonzalez JM, et al. Cranial nerve injury after minor head trauma. J Neurosurg 2010;113:547–55 » CrossRef » Medline
2. Mark AS, Blake P, Atlas SW, et al. Gd-DTPA enhancement of the cisternal portion of the oculomotor nerve on MR imaging. AJNR Am J Neuroradiol1992;13:1463–70 » Abstract
3. Sakushima K, Terae S, Tsuji-Akimoto S, et al. Idiopathic hypoglossal nerve laceration detected by high-resolution three-dimensional constructive interference in steady state magnetic resonance imaging. J Neuroimaging2011;21:e177–79 » CrossRef » Medline
4. Kobayashi S, Meir A, Baba H, et al. Imaging of intraneural edema by using gadolinium-enhanced MR imaging: experimental compression injury. AJNR Am J Neuroradiol 2006;26:973–80

K. Wang^a and S. Yuan^a
aDepartment of Neurosurgery
General Hospital of Jinan Military Command
Jinan, China

Published reports have described the elastase-induced aneurysm model in rabbits as easy and reproducible and possessing geometric, pathologic, and hemodynamic features that are similar to those of human cerebral aneurysms.¹ We used a simple surgical technique to produce the elastase-induced aneurysm model in rabbits² and used it to explore the efficacy of new endovascular devices. Recently, we found that 3 rabbits unexpectedly developed a thoracic aortic aneurysms (TAA), which was located in the posterior part of thoracic aorta, in 40 elastase-induced rabbit aneurysm models (Fig 1).

In contrast to traditional techniques, we used a temporary arcuated aneurysm clip rather than an occlusion balloon to achieve flow arrest in the right common carotid artery (RCCA). When we checked the primary records of the elastase-induction procedure in the 3 cases, we found that the stump of the RCCA had collapsed in the first few minutes after complete filling with elastase had been achieved. We deduced that when the origin of the RCCA was separated from the surrounding tissue in the initial procedure, ≥1 arterial branch originating from the proximal RCCA that was barely visible to the naked eye had split, allowing elastase to leak into the tissue surrounding the thoracic aorta during incubation, ultimately resulting in TAA formation. Thiex et al³recommended avoiding elastase leaking into the branch originating from the proximal RCCA because of the danger of lethal hemorrhage of the trachea.³ We are unable to explain how the leaked elastase came into contact with the thoracic aorta and thereby induced TAA, because the TAAs we have reported here were in the pericardial cavity. It is possible that elastase permeated into the pericardial cavity and concentrated around the posterior part of thoracic aortic artery during the surgical procedure.

The TAAs we found here in rabbits reproduced key features of human TAAs in regard to site-specific phenotypes and pathology. The external surroundings of aneurysms in the pericardial cavity resembled those of the intracranial subarachnoid cavity, and the location is similar to that of human ophthalmic segment aneurysms.

This case report comes from an animal experimental study, which was supported by the China Postdoctoral Science Foundation (grant 20100481521). All procedures of the animal experimental study in this article were approved by the Institutional Animal Care and Use Committee at our hospital.

References

1. Zeng Z, Kallmes DF, Durka MJ, et al. Hemodynamics and anatomy of elastase- induced rabbit aneurysm models: similarity to human cerebral aneurysms? AJNR Am J Neuroradiol 2011;32:595–601 » Abstract/FREE Full Text
2. Wang K, Huang Q, Hong B, et al. Neck injury is critical to elastase-induced aneurysm model. AJNR Am J Neuroradiol 2009;30:1685–87 » Abstract/FREE Full Text
3. Thiex R, Hans FJ, Krings T, et al. Haemorrhagic tracheal necrosis as a lethal complication of an aneurysm model in rabbits via endoluminal incubation with elastase. Acta Neurochir (Wien) 2004;146:285–89, discussion 289 » CrossRef » Medline

Dear Mauricio,

First, let me say how much I enjoyed the 50^th anniversary event. What a wonderful welcome you all gave me!  I am glad that Janet was sitting next to you at the banquet because it was hard for me to move around and meet all my old and new friends there.

You may be aware that I started my neuroradiology training in New Zealand. My mentor there was Dr. Stephen Moor, one of the first trainees of Dr. James Bull at Queen Square when Dr. Bull returned from prison in the Pacific after the war ended. Dr. Moor was my mentor when I started my radiology training in Auckland Hospital and he wrote a supporting letter to Dr. Bull. After I went to London to continue my training I was interviewed by Dr. Bull for a position at the Atkinson Morley.  Later I was told that Dr. Bull “would have given his eye teeth” to get Steve Moor back to London! After 18 months at the AMH, Dr. Bull moved me to Queen Square for a year. Near the end of that time Dr. Bull visited Dr. Taveras in New York at a time when neurosurgical residents were doing most of the neuroradiology special procedures (angiograms and air studies at that time). I moved to the Neurological Institute with Juan Taveras and from there to New York Hospital with John Evans and, after 18 years there, went on to Toronto.

Thank you for your invitation to share some recollections of earlier days of neuroradiology.  Mike Huckman is a friend of many years and he might know whether I would have anything else useful to contribute. Please give him best wishes of Janet and myself if you are in touch with him.

Sincerely,

Gordon

This text provides well formed explanations on topics of physics, radiographic exposure, and radiation biology as they are related to the use of digital imaging practices. This text is timely because conventional imaging procedures are increasingly being replaced by the use of computed and direct digital imaging features. Due to this transition into digital imaging procedures, a more accurate presentation is needed in imaging acquisitions. This text has addressed the need to instruct learners in new digital imaging terminology, fundamentals in basic physics and imaging equipment and accessories, radiation protection, and specifics on digital image acquisition.

Text Organization
This text is presented in four (4) sections:

Part I:              The Physics of Radiography

Part II:             Production of Radiographic the Radiographic Image

Part III:           Digital Radiography

Part IV:           Special Imaging Methods

The sections are appropriately introduced in a logical order that any novice learner in radiography would understand. Parts I and II are consistent with the basics of physics, equipment, and image production that would be consistent with either conventional or digital imaging procedures. In appropriate areas, a brief comparison is provided that notes the differences between conventional and digital radiography. The more thorough digital information is provided in Part III, Digital Imaging. Part III provides a complete lecture of digital efficacy from all aspects of physics, radiation protection, and exposure. Part IV, on Special Imaging Methods, is a beneficial feature. Similar texts discuss special imaging modalities briefly, but in this text the author presents a full explanation of each modality and its special applications of digital imaging. This text, as compared to similar works, contains a very thorough analysis which will allow it to be used for several courses in radiology.

Each chapter ends with a conclusion and review questions that are extremely helpful to the reader in summarizing and analyzing learning objectives for that chapter.

The author did an outstanding job of selecting appropriate graphs, charts, illustrations, and pictures. The illustrations are marked and easy to locate for the reading. The information was accurate and fulfilled the purpose of its presentation of digital imaging technology.  The table of contents, appendices, and index are cross-referenced appropriately. The references provided appear to be within the last 10 years. The relevant radiation protection measures (i.e., NCRP suggested standards) are accurate with their most recent publications.

Relevant Audience
This text provides a very complete analysis of subject matter for any student learner in the radiologic sciences. Those studying a complete course of Radiology Technology would benefit most. The information that is provided in the book is consistent with the radiology technology curriculum as presented by the American Society of Radiology Technologists. This text is relevant to the neuroradiology audience.

Workbook
The accompanying workbook provided with this text does attempt to provide the learner with an additional tool for self-study and evaluation of material comprehension. The workbook contains information for other products that are related to digital imaging that could be used as additional resources.

The author failed to use multiple learning approaches in the presentation of the workbook review. The entire workbook uses the fill-in the blank format to answer questions related to chapter information. There are no diagrams or other illustrations within the workbook. The use of multiple-choice questions, matching, and diagrams would have provided a more precise guided learning-tool, since all students learn through different approaches. The author does provide a suggestion as to how the workbook should be used by the student specifically using the Lecture Slides for Radiology in the Digital Age, along with the workbook. This would provide more reinforcement but does require the student to obtain this additional resource.   

Conclusion
The use of this text would be most beneficial to those who are studying in the field of radiographic imaging, and who are expected to function in a digital capacity. The book does provide a very complete analysis of digital imaging, more so for those studying to become Radiology Technologists.

The book is organized in 23 chapters according to commonly performed surgical procedures. The majority of the book contains intraoperative pictures that have been nicely illustrated and augmented by on-lay drawings to further clarify anatomical points and landmarks. There is a minimum of text, but the text is excellent in further describing anatomical features.

The publication in general would be helpful for neuroradiology audience so that they could better understand the sometimes limited anatomical views that surgeons who operate on the spine are faced with. It would probably best benefit a medical student and/or lower year trainee in neurosurgery or orthopedics who has a special interest in spine.

Common surgical procedures are adequately covered, and the introductory chapter, which is excellent, deals with positioning of the patient on the operating room table. The book is clearly unique in that regard and is not easily comparable to other texts on the subject. The legends are suitably descriptive and well labeled.

There are no references, as this represents a surgeon’s guide to other surgeons on surgical approaches and anatomy. It is not technique-focused, nor does it deal with spinal instrumentation.

Again, I would recommend this to colleagues, particularly those interested in spine and its surgical treatment.