57 research outputs found

    Paradoxically Decreased Signal Intensity on Postcontrast Short-TR MR Images

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    Seven lesions are presented in which short TRfshort TE images obtained immediately after IV administration of gadopentetate dimeglumine demonstrated an apparent decrease in signal intensity compared with precontrast short TRfshort TE images. All seven lesions were hyperintense on precontrast short TRfshort TE images. In four cases in which long TRflong TE scans were also obtained, the lesions were hypointense. This phenomenon may be due to a dominant T2 shortening effect by the contrast material that "overwhelms" T1 shortening even on short TRfshort TE scans. Other compounding factors may include variations in scanning variables, receive and transmit attenuations, or a photographic phenomenon due to window widths and center levels. The use of gadopentetate dimeglumine for evaluating CNS disease has become commonplace. With a standard dose of 0.1 mmolfkg , lesions that show contrast enhancement usually become bright on short TRfTE images. The explanation for this phenomenon is the shortening of T1 relaxation by the paramagnetic contrast agent on adjacent protons. As with any dipolar interaction , T2* shortening also occurs; however, its effect is usually inapparent on the short TR/short TE (T1-weighted) scans. We present seven cases in which there was a decrease in signal intensity after IV administration of contrast material in lesions that were hyperintense on precontrast short TR/short TE scans. Materials and Methods In the past 2 years we have observed seven cases in which there appeared to be a decrease in lesion signal intensity on postcontrast short TR (600-850)/short TE (20/30) images compared with precontrast scans. All scans were obtained on high-field 1.5-T scanners. Standard doses of gadopentetate dimeglumine (Magnevist, Berlex Industries , Wayne, NJ) at 0.1 mmolfkg were administered intravenously followed by immediate (i .e. ,< 5 min) postcontrast short TR scans. In three case

    Variability in Surgical Treatment of Spondylolisthesis Among Spine Surgeons

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    Background There are a multitude of treatments for low-grade lumbar spondylolisthesis. There are no clear guidelines for the optimal approach. Objective To identify the surgical treatment patterns for spondylolisthesis among United States spine surgeons. Methods 445 spine surgeons in the United States completed a survey of clinical/radiographic case scenarios on patients with lumbar spondylolisthesis with neurogenic claudication with (S+BP) or without (S−BP) associated mechanical back pain. Treatment options included decompression, laminectomy with posterolateral fusion, posterior lumbar interbody fusion, or none of the above. The primary outcome measure was the probability of 2 randomly chosen surgeons disagreeing on the treatment method. Results There was 64% disagreement (36% agreement) among surgeons for treatment of spondylolisthesis with mechanical back pain (S+BP) and 71% disagreement (29% agreement) for spondylolisthesis without mechanical back pain (S−BP). For S+BP, disagreement was 52% for those practicing 5 to 10 years versus 70% among those practicing more than 20 years. Orthopedic surgeons had greater disagreement than did neurosurgeons (76% vs. 56%) for S+BP. Greater clinical equipoise was seen for S−BP than for S+BP regardless of surgeon characteristics. For spondylolisthesis without mechanical back pain, neurosurgeons were significantly more likely to select decompression-only than were orthopedic surgeons, who more commonly selected fusion. Conclusions Clinical equipoise exists for the treatment of spondylolisthesis. Differences are greater when the patient presents without associated back pain. Surgeon case volume, practice duration, and specialty training influence operative decisions for a given pathologic condition. Recognizing this practice variation will hopefully lead to better evidence and practice guidelines for the optimal and most cost-effective treatment paradigms

    Brian C. Bowen, MD, PhD

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    Intracranial extramedullary hematopoiesis: a rare cause of headaches

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    Ectopic bone marrow production, known as extramedullary hematopoiesis, may result in symptoms due to compression on normal structures. We present the multimodality imaging findings and subsequent management of a rare case of symptomatic extramedullary hematopoiesis within the calvarium. Case report. A 54-year-old male with a history of myelofibrosis and no previous diagnosis of a headache disorder presented to the emergency department with worsening severe bilateral headaches. A nonenhanced CT of the brain was performed and diffuse extra-axial nodular hyperdensities were visualized. MRI of the brain demonstrated diffuse extra-axial avidly enhancing nodular masses, dural thickening and marked susceptibility. No paravertebral masses, typical for extramedullary hematopoiesis, were present in the chest or abdomen. Although the clinical team considered a biopsy to confirm the diagnosis, we suggested a noninvasive confirmatory test. The subsequent Tc99m sulfur colloid scan corroborated the diagnosis. The patient was then referred to radiation oncology for treatment. In summary, extramedullary hematopoiesis is a hematologic compensatory disorder that rarely occurs within the CNS and may cause neurological compromise due to compression on underlying structures. The diagnosis can be made with noninvasive imaging and treated with low dose radiation therapy

    Acute Lacunar Infarcts in CLIPPERS: Is the Chronic Infiltrative Lymphocytic Perivascular Disease Process to Blame?

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    CLIPPERS (chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids) is a recently described chronic inflammatory disorder involving the brainstem with characteristic imaging findings. Since it was originally described in 2002, only a handful of cases have been reported in the literature. We describe two additional cases of CLIPPERS with characteristic clinical and radiological findings. Besides the previously described MR findings, one of the cases also demonstrated multiple basal ganglia lacunar infarcts, a finding which has not been previously reported. We hypothesize that the lacunar infarcts are caused by this chronic infiltrative perivascular disease process
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