Author: letters

letters
Letters to the Editor • American Journal of Neuroradiology

Beginning with the February 2010 issue, Letters to the Editor and any applicable replies are now posted on AJNR Blog after their publication in the online journal. Comments on published letters and replies are encouraged.

Regarding “Cerebral Angiography for Evaluation of Patients with CT Angiogram-Negative Subarachnoid Hemorrhage: An 11-Year Experience”

X. Wu, V.B. Kalra, H.P. Forman
Department of Diagnostic Radiology

C.C. Matouk
Department of Neurology and Neurosurgery

G. Mongelluzzo, R. Liu, A. Malhotra
Department of Diagnostic Radiology

Yale School of Medicine
New Haven, Connecticut

We would like to thank Heit et al1 for their study “Cerebral Angiography for Evaluation of Patients with CT Angiogram-Negative Subarachnoid Hemorrhage: An 11-Year Experience” on the utility of digital subtraction angiography in patients with negative findings on CT angiography and subarachnoid hemorrhage. This is a laudable effort in addressing an issue with great heterogeneity in literature. However, we would like to raise a few questions regarding the article.

First, the statement that all patients with negative findings on CTA should be considered for DSA should be viewed with caution, especially for patients with perimesencephalic hemorrhage (pSAH). The authors reported that 2 aneurysms and 1 case of vasculitis were identified on DSA as causes of pSAH, which were initially missed on CTA. Heit et al1 stated in the “Materials and Methods” section that if an aneurysm was identified by DSA after negative findings on CTA, the CTA was reviewed retrospectively. However, the results of that review were not available in the article. It would be helpful to know the number of cases with positive findings that could be retrospectively seen on CTA with the hindsight of the DSA results. On the other hand, in our own review of the literature, we found very few and questionable cases of pSAH in which imaging was of utility after initial negative findings on CTA.2

The authors quoted Delgado Almandoz et al3 to support the utility of follow-up DSA after negative findings on CTA because 1 aneurysm was detected on follow-up. On careful review of that article, in particular Fig 3B (the initial DSA that …

T1-Weighted Dynamic Contrast-Enhanced MRI Is a Noninvasive Marker of Epidermal Growth Factor Receptor vIII Status in Cancer Stem Cell–Derived Experimental Glioblastomas

L.S. Politi

Neuroimaging Research, Hematology/Oncology Division
Boston Children’s Hospital/Dana Farber Cancer Institute
Boston, Massachusetts

Radiology Department
University of Massachusetts Medical School
Worcester, Massachusetts

Neuroradiology Unit and CERMAC
Vita-Salute San Raffaele University and IRCCS San Raffaele Scientific Institute
Milan, Italy

G. Brugnara, A. Castellano, M. Cadioli, L Altabella

Neuroradiology Unit and CERMAC
Vita-Salute San Raffaele University and IRCCS San Raffaele Scientific Institute
Milan, Italy

M. Peviani

Neuroimaging Research, Hematology/Oncology Division
Boston Children’s Hospital/Dana Farber Cancer Institute
Boston, Massachusetts

Neuroradiology Unit and CERMAC
Vita-Salute San Raffaele University and IRCCS San Raffaele Scientific Institute
Milan, Italy

S. Mazzoleni

Neural Stem Cell Biology Unit, Division of Regenerative Medicine, Stem Cells and Gene Therapy
IRCCS San Raffaele Scientific Institute
Milan, Italy

A. Falini

Neuroradiology Unit and CERMAC
Vita-Salute San Raffaele University and IRCCS San Raffaele Scientific Institute
Milan, Italy

R. Galli

Neural Stem Cell Biology Unit, Division of Regenerative Medicine, Stem Cells and
Gene Therapy
IRCCS San Raffaele Scientific Institute,
Milan, Italy

We read with great interest the article by Arevalo-Perez et al,1 describing the potential value of T1-weighted dynamic contrast-enhanced MR imaging (DCE-MR imaging) as a biomarker for epidermal growth factor receptor variant III (EGFRvIII) mutation in patients with glioblastoma (GBM). In this retrospective study, the authors showed that EGFRvIII-positive tumors, compared with GBMs lacking the mutation, presented with a statistically significant increase in perfusion values of the contrast transfer coefficient (Ktrans) and plasma volume (Vp). We agree with the authors’ findings, and we also share some of their concerns; as the authors clearly stated in their discussion, both the genetic test performed on the tumor samples and the biopsy location may have induced some bias in their results. Specifically, the genetic test did not account for other mutations on the EGFR gene, which may also correlate to altered perfusion …

Hypothalamic Adhesions: Asymptomatic, Incidental, or Not?

A. Vossough, S.A. Nabavizadeh
University of Pennsylvania

Children’s Hospital of Philadelphia
Philadelphia, Pennsylvania

The term “hypothalamic adhesion” was first described in 2008 as a common associated finding (48%) in Chiari II malformation by the neuroradiology group at the Hospital for Sick Children in Toronto.1 It has been subsequently presented outside the context of Chiari II in a number of radiologic meetings by us and other groups since 2010 and has been variously referred to as hypothalamic adhesions, hypothalamic fusion bands, interhypothalamic adhesions, intrahypothalamic adhesions, transhypothalamic connections, and even asymptomatic hypothalamic hamartomas. We do not prefer the term “interhypothalamic” because anatomically, there is only 1 hypothalamus that extends to both sides via the tuber cinereum and floor of the third ventricle. Routine use of high-resolution imaging facilitates the detection of this imaging finding, and it is expected that more reports of this finding and its potential association will follow.

In 2014, the presence of this finding was reported in the American Journal of Neuroradiology (AJNR) to be highly associated with other malformations and abnormalities in most instances, in a small case series of 13 patients.2 The authors proposed that it may be a form fruste of holoprosencephaly, given the prevalence of midline abnormalities. Ahmed et al3 recently reported in the AJNR that most patients with this finding are asymptomatic and that these are often incidental findings. So what is the practitioner to do with these seemingly conflicting results? How would the neuroradiologist explain the significance of this finding to referring physicians and patients, given that it is so sparsely reported in the literature? Every time we describe this finding in our clinical radiology reports, we receive these inevitable enquiries from our colleagues. These questions could only be explained with further cumulative experience in the field, a …

Cooling Catheters for Selective Brain Hypothermia

T.K. Mattingly
Neurosurgical Associates
Richmond, VA

D.M. Pelz, S.P. Lownie
London Health Sciences Centre
London, Ontario, Canada

We read with interest “Endovascular Cooling Catheter for Selective Brain Hypothermia: An Animal Feasibility Study of Cooling Performance” by Cattaneo et al.1 The authors achieved mild brain hypothermia by using a novel indwelling cooling catheter. We appreciate the authors’ acknowledgment of our work in selective brain cooling.2However they may have misunderstood the TwinFlo catheter evaluated in our study (ThermopeutiX, San Diego, California). The TwinFlo inner coaxial balloon catheter is 9.5F, with an inner diameter of 2.0 mm (0.080 inches). This is well within the lumen size needed to perform simultaneous mechanical stent-retriever thrombectomy during selective brain cooling.

Reduction in brain metabolic demand is related to the depth of hypothermia.3 Brain cooling using the authors’ device was only mild (−4.2°C to −4.5°C) and took >2 hours to achieve. On the other hand, endovascular cold blood perfusion seems better able to achieve the very low temperatures (25°C–26°C) necessary to avert ischemic stroke and can do so very rapidly (<30°C in a median of 15 minutes). We demonstrated a substantial reduction in stroke volume in our large-animal model, despite starting cooling well into the reperfusion phase and after 3 hours of focal ischemia.

Disclosures

Thomas K. Mattingly—RELATED: Grant: Heart and Stroke Foundation,* ThermopeutiX,* Comments: HSF GIA 7273; ThermopeutiX provided the TwinFlo catheters and assisted in data collection on catheter performance. Stephen P. Lownie—Travel/Accommodations/Meeting Expenses Unrelated to Activities Listed: Vice-President, Canadian Neurosurgery Society. *Money paid to the institution.

References

Cortical Superficial Siderosis Presumed due to Cerebral Amyloid Angiopathy: Minimum Standards for Rating and Reporting

A. Charidimou
J. Philip Kistler Stroke Research Center
Department of Neurology
Massachusetts General Hospital Stroke Research Center
Harvard Medical School
Boston, Massachusetts

With great interest, I read the recent article by Inoue et al1 on the diagnostic significance of cortical superficial siderosis (cSS) for Alzheimer disease in a memory clinic setting. In line with other recent studies on the topic, the authors found cSS in 12 of 347 (3.5%) patients in the memory clinic, a prevalence much lower compared with pathologically proved cerebral amyloid angiopathy (CAA) (approximately 50%), but still higher than the 1% prevalence seen in population-based studies. Not surprisingly, in the current study, cSS was found to be associated with strictly lobar microbleeds,1 a putative marker of CAA.

In a letter to the editor about this study, Bai et al2 raised a number of important points on cSS definition and detection and opined that the pathogenesis of cSS in the context of CAA is still an unproven hypothesis. They suggested that an, as yet, unidentified bleeding source may account for cSS in the studied cohort instead of CAA.2 Some of these issues deserve further attention. First, ample evidence suggests that cSS detected in older patients (generally older than 50 years of age) in the context of small-vessel disease (including CAA) is quite distinct from the “classic” superficial siderosis of the central nervous system with regard to underlying pathology, pattern, and clinical presentation.3 The classic superficial siderosis of the central nervous system (to which Bai et al are referring), affects mainly the infratentorial regions (brain stem and posterior fossa) and spinal cord and typically presents with progressive sensorineural hearing loss, cerebellar ataxia, and corticospinal tract signs.3 By contrast, published CAA cases with cSS lack these typical clinical manifestations, and cSS is limited to …

Macrocyclic Gadolinium-Based Contrast Agents Do Not Cause Hyperintensity in the Dentate Nucleus

T. Kanda, H. Oba, K. Toyoda, S. Furui
Department of Radiology
Teikyo University School of Medicine
Itabashi-ku, Japan

We wish to comment on the December 2015 article of Ramalho et al1 entitled “Gadolinium-Based Contrast Agent Accumulation and Toxicity: An Update” in theAmerican Journal of Neuroradiology.

First, the authors introduced the study of Stojanov et al,2 in which gadobutrol (Gadavist; Bayer Schering Pharma, Berlin, Germany) was purported to cause hyperintensity in the dentate nucleus. However, this report lacks evidence because no hyperintensity in the dentate nucleus on T1WI could be noted in their presented figure, despite being seen in all other previous reports.3 In addition, Radbruch et al4 performed a replication study in which gadobutrol showed no correlation with hyperintensity in the dentate nucleus on T1WI. An animal study5 also denied the association between gadobutrol and hyperintensity in the dentate nucleus on T1WI. These results demonstrated that macrocyclic gadolinium-based contrast agents do not cause hyperintensity in the dentate nucleus.

Second, our group6 evaluated gadolinium deposition in the dentate nucleus, internal segment of the globus pallidus, frontal cortical lobe, white matter of the frontal lobe, and cerebral white matter. McDonald et al7 evaluated gadolinium deposition in the dentate nucleus, globus pallidus, thalamus, and pons. In addition, they confirmed the presence of extensive gadolinium deposits prominently clustered within the endothelial wall by using x-ray microanalysis. In the article by Ramalho et al, our work is mistaken for the great work of McDonald et al.

These 2 articles6,7 were published at almost the same time. The submission of our article on November 20, 2014, was earlier than that of McDonald et al,7 submitted on January 5, 2015, but the acceptance was on March 24, 2015—namely, later than the acceptance of the …

Regarding “Clinical and Imaging Follow-Up of Patients with Coiled Basilar Tip Aneurysms Up to 20 Years”

A. Malhotra, X. Wu, V.B. Kalra
Department of Diagnostic Radiology

C.C. Matouk
Department of Neurology and Neurosurgery

H.P. Forman
Department of Diagnostic Radiology
Yale School of Medicine
New Haven, Connecticut

We thank van Eijck et al for their effort in addressing the important, relevant question regarding the follow-up on coiled basilar aneurysms in “Clinical and Imaging Follow-Up of Patients with Coiled Basilar Tip Aneurysms Up to 20 Years.”1 However, we would like to raise a few questions regarding the study.

In this long-term follow-up study of patients with coiled basilar aneurysms, the authors concluded that regular and life-long follow-up should be done, possibly with yearly MR imaging, to detect reopening in a timely manner, because even stable occluded aneurysms can reopen and rebleed many years after treatment. However, it is unclear from the data presented how many of the aneurysms reopened or regrew and whether growth was progressive on follow-up. Were all patients with reopening treated? Retreatment statistics may not accurately indicate how many of these aneurysms reopened or regrew unless all of these were retreated. Chalouhi et al2 reported a much higher recanalization rate (17.2% in stented and 38.9% in nonstented aneurysms) versus retreatment rates (7.8% in stented and 27.8% in nonstented aneurysms) in 235 cases of coiled basilar tip aneurysms.

The study provides valuable insight, and it would be very helpful to have a few more questions answered.

In the 9 patients who rebled (and 3 who died), did follow-up imaging help in predicting the event? Did any of these cases show evidence of reopening or regrowth on imaging?

Progressive mass effect was seen in 6 patients and was the cause of death in 5 patients. Four of these had multiple retreatments, and 3 had 5 retreatments. Did repeat coiling have any correlation with progressive mass …

Integrative Analysis of 334 Patients with Blister-Like Aneurysms

L. Yang, X. Huang, X. Tan
Department of Neurology
The Second Xiangya Hospital of Central South University
Changsha, China

H. Zhou
Department of Neurology
The First Xiangya Hospital of Central South University
Changsha, China

H.X. Bai
Department of Radiology
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania

We read with great interest a recent article by Peschillo et al1 on blister-like aneurysms. The authors performed a meta-analysis of 334 patients with blister-like aneurysms who were treated with either an operation or endovascular therapy. The authors found that endovascular treatment had lower morbidity and mortality and provided a better outcome compared with surgical approaches, especially in patients with low Hunt and Hess (HH) scale and Fisher grades. Only the HH and Fisher grades were clear predictors of outcomes in multivariate analysis, but the method of treatment was not.

We commend the authors for performing a meta-analysis of this type of aneurysm because it is a rare disease with imprecise definition and no existing guidelines on optimal management.2 However, we have significant concerns about the methodologies and results. First, the authors did not specify how they handled the data in their meta-analysis. It seems that the authors performed an integrative analysis of individual patients pooled from each individual study instead of a “meta-analysis.” If this is the case, did the authors exclude a study because it did not specify clinical presentation, method of treatment, or outcome? The exact criteria used for study inclusion were not clear; this problem increases the potential for publication bias. A previous systematic review of 331 patients showed that results from multivariate analysis were influenced by the number of cases in a single study and the journal Impact Factor.3

Second, for studies that did not provide information on HH or Fisher grade, did the authors …

Asymptomatic Interhypothalamic Adhesions in Children

M.T. Whitehead and G. Vezina
Department of Neuroradiology
Children’s National Medical Center
Washington, DC

We have several comments regarding the article “Asymptomatic Interhypothalamic Adhesions in Children.”1 We agree with the main message of the article: Referable hypothalamic–pituitary axis symptoms are rare in patients with interhypothalamic adhesions. However, because symptoms can be present on occasion, it is prudent to exclude endocrinopathy on clinical grounds. We have encountered a few cases of patients with interhypothalamic adhesions and pituitary axis disturbances, one associated with Kallmann syndrome2; 2 with septo-optic dysplasia; and 1, with abnormal weight gain.

We agree with the authors’ theory that interhypothalamic adhesions may be the result of “incomplete hypothalamic cleavage, failed apoptosis, or abnormal neuronal migration” and acknowledge the association with “gray matter heterotopia.” Therefore, additional midline abnormalities would be expected. However, the authors did not identify additional abnormalities in most patients. Nonetheless, concurrent gray matter heterotopia was present in 40%, a considerably large percentage of patients, and they proposed that heterotopia associated with interhypothalamic adhesions may be part of an unknown genetic disorder.

All portions of the brain, including the midline, must be carefully examined in patients with interhypothalamic adhesions because they represent a potential marker for brain malformation. Additional midline anomalies/abnormalities are quite common in our experience.24 These may be subtle and insignificant (hypoplasia of the falx, underrotated hippocampi, and so forth) or obvious and potentially of great consequence (malformations of brain development).24 Indeed, review of Fig 1 demonstrates subtle midline anomalies not mentioned in the article, including hypogenesis or volume loss of the splenium (Figs 1A and E) and a partially fenestrated, persistent cavum septum pellucidum (Fig 1D).1 In normal brains, the callosal splenium is typically equal to or larger in …

In Reply to Antiplatelet Therapy Prior to Temporary Stent-Assisted Coiling

B. Gory
FHU IRIS, Department of Interventional Neuroradiology

Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon
Lyon, France

F. Signorelli
Department of Neurosurgery

Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon
Lyon, France

Department of Experimental and Clinical Medicine
University Magna Græcia
Catanzaro, Italy

F. Turjman
FHU IRIS, Department of Interventional Neuroradiology

Hôpital Neurologique Pierre Wertheimer, Hospices Civils de Lyon
Lyon, France

We would like to thank Drs Almekhlafi and Goyal for their comments1 concerning our article, “Temporary Solitaire Stent-Assisted Coiling: A Technique for the Treatment of Acutely Ruptured Wide-Neck Intracranial Aneurysms.”2

Almekhlafi et al noticed that we performed the procedures without preadministering antiplatelet therapy, and they would like to caution against the wide adoption of this technique without pretreatment with antiplatelet agents. They reported the endovascular treatment of 10 aneurysms (6 unruptured and 4 ruptured) in 8 patients by using temporary stent-assisted coiling. One of their patients with an unruptured aneurysm was not pretreated with dual antiplatelet therapy and presented with a procedural in-stent thrombosis with no clinical sequelae.

An antiplatelet regimen is usually administered before stent placement in selective cases. However, in our article,2 we reported our experience in a different situation (acutely ruptured aneurysms). In this setting, to the best of our knowledge, it seems clear that adverse events happen more commonly and clinical outcomes are likely to be worse than those achieved without stent assistance3; thus, we did not use antiplatelet therapy in our series. Recently, Bechan et al4 compared the rate of stent-placement complications in acutely ruptured versus unruptured aneurysms, and they have shown that the morbidity and mortality increased. Application of dual antiplatelet therapy in stent-assisted coiling of acutely ruptured aneurysms is associated with an increased risk of hemorrhagic complications following shunt placement,5 especially in middle cerebral …