DWI Scans Research Articles

Aplicação da ressonância magnética no acompanhamento da cirurgia do colesteatoma

A tomografia computadorizada e ressonância magnética (RM) com seqüências convencionais têm baixa especificidade para a diferenciação entre tecido de granulação e recidiva de colesteatoma. OBJETIVO: Avaliar a aplicação da RM com sequência de difusão e pós-contraste T1 tardio na detecção de recidiva de colesteatoma. MATERIAL E MÉTODO: Realizado estudo transversal prospectivo de dezessete pacientes estudados no pós-operatório de colesteatoma utilizando RM de 1.5 T com seqüência difusão, T1, T2 e pós-contraste T1 tardio nos planos coronal e axial. Dois radiologistas avaliaram e decidiram em consenso a presença de foco de hipersinal na difusão e T2, iso/hipossinal em T1 e ausência de impregnação pelo contraste como suspeitos de recidiva de colesteatoma. Os achados da revisão cirúrgica foram comparados com o resultado da RM. RESULTADOS: Onze dos doze casos de recidiva de colesteatoma apresentaram hipersinal na difusão. Todos os pacientes com tecido de granulação na cavidade cirúrgica não apresentaram alteração de sinal na difusão. Um paciente com abscesso no conduto auditivo interno também apresentou hipersinal na difusão. A sensibilidade, especificidade, valor preditivo positivo e negativo foram respectivamente 91,6%, 60%, 84,6% e 75%. CONCLUSÃO: A seqüência de difusão combinada com pós-contraste tardio pode ser útil na diferenciação entre tecido de granulação e recidiva de colesteatoma.

The role of magnetic resonance imaging in the postoperative management of cholesteatomas

SummaryConventional CT and MRI scans have low specificity when it comes to differentiating granulation tissue from relapsing cholesteatoma.Aimthis paper aims to analyze the use of DWI and delayed post-contrast T1-weighed imaging in the detection of recurring cholesteatomas.Materials and methodthis is a cross-sectional prospective study that looked at 17 cholesteatoma patients postoperatively. All patients underwent diffusion magnetic resonance imaging at 1.5T, T1, T2, and delayed post-contrast T1 and images were produced from both coronal and axial planes. Two radiologists assessed the images and decided consensually that the presence of hyperintensive signal in DWI on T2, iso/ hypointensive signal on T1, and absence of contrast uptake were indicative of relapsing cholesteatoma. Surgical review findings were compared to DWI scans.Resultseleven of the twelve cases of recurring cholesteatoma presented hyperintensive signal in the DWI scans. None of the patients with granulation tissue in the surgical wound presented hyperintensive signal in the DWI scans. A patient with an abscess in the internal acoustic meatus also presented a hyperintensive signal in the DWI scans. Sensibility, specificity, positive predictive value and negative predictive value were 91.6%, 60.0%, 84.6%, and 75.0%, respectively.ConclusionDWI combined with delayed post-contrast T1 SE sequence proved to be useful in the differential diagnosis of granulation tissue and recurring cholesteatoma.

Creutzfeldt-Jakob disease: Which diffusion-weighted imaging abnormality is associated with periodic EEG complexes?

Clinical diagnosis of CJD remains important due to lack of access to a genetic or histopathological diagnosis. Using current WHO criteria, diagnostic certainty can be increased from "possible" to "probable" CJD if periodic complexes are recorded on EEG. To study the correlation between patterns of MRI-DWI hyperintensity and typical EEG findings among patients with CJD. Demographics, clinical findings, MRI-DWI and EEG findings of CJD patients were retrospectively reviewed. A total of 14 patients ranging in age from 35 to 81 years were identified. All had dementia and cerebellar ataxia. Psychiatric manifestations were seen in 5 patients. Seven patients had both cortical and striatal DWI changes, five had isolated cortical DWI changes and two had isolated striatal DWI changes. All twelve patients with cortical DWI changes also had periodic EEG changes. In ten, periodic EEG was recorded within seven days of the DWI. The two patients with isolated striatal DWI changes did not develop periodic EEG complexes despite serial EEG recordings, 40 and 88 days from their respective DWI scans. Serial EEGs are not useful for patients with isolated striatal DWI hyperintensity but will increase diagnostic certainty from "possible" to probable" CJD for patients with cortical DWI hyperintensity.

Towards discrimination of infarcts from artifacts in DWI scans

Objective Accurate and rapid quantification of infarcts from DWI scans is critical in acute ischemic stroke. Acquisition artifacts lead to hyperintense regions in DWI MR scans resulting in false positives. Discriminating infarcts and artifacts helps in reducing infarct segmentation errors.

Atypical Clinical Picture in a Patient with Benign Occipital Epilepsy: Diagnostic Contribution of Morpho-Functional MR

Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) is a maternally inherited disease due to mitochondrial DNA (mtDNA) point mutations. The clinical phenotype varies in relation to the systems affected, age at onset and disease severity. The characteristic signs of MELAS are nausea and vomiting due to acidosis, headache, epilepsy, ataxia or generalized weakness, ophthalmoplegia, motor and sensory focal neurological deficits. The clinical course may improve due to partial regression of the typical lesions, but the prognosis is usually adverse. A 19-year-old man with a diagnosis of benign occipital epilepsy and resumption of seizure activity with focal occipital attacks since the age of 14 years came to our attention for the recent onset of drug-resistant electroclinical seizures of long duration with complex symptoms, where the dominant clinical feature was an intense, persistent bilateral periorbital migraine with nausea and vomiting, scintillation scotomata and blurring of vision. MR studies were performed at our institution in the immediate post-seizure phase and then at one week, three and six months. The acute-phase morphological scans showed a right cortical-subcortical area with altered signal in the occipitopolar region that was hypointense on T1 and hyperintense on T2 and FLAIR, with cortical thickening and effacement of the sulci. Contrast-enhanced scans did not demonstrate BBB alterations. The DWI scans showed a right temporo-occipital cortical area with higher signal intensity. In the subsequent examinations the area with altered signal shrank gradually and significantly in parallel with improvement in clinical conditions. The diagnostic hypothesis of benign occipital epilepsy was consistent neither with the clinical course, characterized by persistent headache, visual disturbance and refractoriness to antiepileptic drugs, nor with the temporal-occipital cortical MR findings, which resembled ischemic lesions but displayed a non-territorial pattern as well as reversibility over time. These elements guided in the diagnosis of MELAS, which was subsequently confirmed by identification of the typical gene mutation. On DWI the stroke-like lesions of MELAS are seen more frequently as focal hyperintense areas compared with healthy parenchyma. Such high signal intensity likely corresponds to T2 shine-through rather than cytotoxic edema. Indeed, several studies have demonstrated that in acute-phase scans of MELAS stroke-like lesions DWI hyperintensity is associated with increased ADC values that are not associated with restricted water diffusivity, reflecting the metabolic rather than anoxic-ischemic nature of these changes. In the present case, morphological MR associated with DWI was very helpful in guiding the diagnosis by demonstrating some pathognomonic features of MELAS stroke-like lesions such as cortical-subcortical involvement of the posterior hemispheres, the non-territorial pattern, lesion reversibility and the pathophysiological role of vasogenic edema in inducing an increase in extracellular water and thus in diffusion values.

Hyaline vascular Castleman disease associated with POEMS syndrome and cerebral infarction

Dear Editor, In 2006, a 42-year-old Chinese woman was admitted to the Endocrine Department of our hospital because of diarrhea for 5 months and chilly for 1 month. She was diagnosed of hyperthyroidism 2 months before admission and was treated with antithyroid drugs. Her prior medical history was unremarkable, with no history of diabetes, smoking, alcohol, or HIV. On admission she was suffering from diarrhea, was experiencing progressive fatigue and chill, night sweats, weight loss, and edema. Positive physical examination revealed multiple small peripheral lymph nodes, hepatomegaly, splenomegaly, hyperpigmentation, paraesthesia in four limbs and pitting edema of the lower extremities. Laboratory tests on admission showed HbsAg (+), HbcAb (+), HbeAb (+) and HIVAb (−). The fibrinogen level was 0.35 g/dl (normal 0.2–0.4 g/dl). Blood biochemistry indicated hypoalbuminemia and hyperglobulinemia. Immunoelectrophoresis showed a polyclonal increase in serum immunoglobulin (IgG 22.7 g/l, IgA 48.3 g/l, IgM 0.66 g/l) with a monoclonal IgA kappa. Ultrasonic examination indicated pericardial effusion. Needle electromyogram test was performed. Slow conduction velocity on sensory nerve and motor nerve was confirmed. Blood routine was normal. Cervical lymph node biopsy diagnosed of Castleman disease (hyaline vascular type) (Fig. 1). Then she was admitted to the Hematology Department because of Castleman disease associated with POEMS syndrome. One day after admission, the patient suffered from mental anomaly, gradually occurred left hemiplegia, and coma. Findings of physical examination revealed fever, hyperpigmentation, ascites, dysarthria, tetraparesis, and areflexia of both legs. The fibrinogen level was 0.412 g/dl. Neither polycythemia nor thrombocythemia was detected. The MRI and DWI scans showed a large area of acute cerebral infarction including right frontal lobe and parietal lobe, left frontal lobe, extending to the cortex and subcortex (Fig. 2). After treatment with dexamethasone 10 mg/day, cerebrospinal fluid pressure lowered; after supportive treatment for 7 days, the consciousness of the patient improved. She became drowsy and could respond to our call. Physical examination showed no fever or ascites, no edema or lymphadenectasis; she could raise her right limbs by herself. The fibrinogen level dropped to normal (0.29 g/dl). Ultrasonic examination indicated no pericardial effusion or splenohepatomegalia. Castleman disease is a rare pathologic process of unknown etiology, characterized by reactive proliferation of lymphoid tissue [1]. The clinical features of Castleman disease are classified into two categories, localized and multicentric. The localized form usually presents in young adults with localized masses in the mediastinum, neck, or, less commonly, intra-abdominal masses. Systemic symptoms are rare with localized Castleman disease (LCD). In contrast, multicentric Castleman disease (MCD) presents with polylymphadenopathy and frequently multi-organ involvement and is associated with systemic features. MCD is less common than LCD and follows a more aggressive natural history. The histology of Castleman disease is similarly divided into two subgroups: the hyaline vascular type and the plasma cell type. The former is found in 90% of LCD, but rarely in MCD and associated with systemic clinical manifestations. The latter is found in only Ann Hematol (2007) 86:59–61 DOI 10.1007/s00277-006-0188-z

Prediction of Outcome in New-Born Infants with Arterial Ischaemic Stroke Using Diffusion-Weighted Magnetic Resonance Imaging

The aim of this study was to assess the additional value of diffusion-weighted magnetic resonance imaging (DW-MRI) compared to conventional magnetic resonance imaging (MRI) in new-born infants with arterial ischaemic stroke, with regard to the prediction of neurodevelopmental outcome. Neonatal DW-MRI data were available in 15 infants with a gestational age of > or = 35 weeks and repeat MRI data were obtained in 12 of the 14 survivors. T(1)- and T(2)-weighted transverse images were obtained as well as 4-mm DWI slices. ADC maps were calculated in manually selected regions on the basis of the DWI scans. All 14 survivors were seen in the follow-up clinic and 12 were > 18 months when last seen. T (2) hyperintensity was detected in the descending white matter tracts at the level of the internal capsule in 7 infants and in only one of these also at the level of the cerebral peduncles. Increased signal intensity (SI) was seen on DW-MRI in 8 infants in the descending white matter tract ipsilateral to the territorial infarct at the level of the internal capsule and in 5 of these also at the level of the cerebral peduncles. ADC maps were available in 12 infants. ADC values were calculated at the level of the cerebral peduncles, using the contralateral side as a reference value. A significantly reduced value was found in 3 of the 5 infants who showed an increased SI on DW-MRI. ADC maps were not available in the other two. Five of the seven infants with abnormalities on DW-MRI/ADC of the corticospinal tracts developed a mild to moderate hemiplegia, one showed an asymmetry of tone and one with only involvement of the anterior part of the internal capsule was normal at follow-up. Wallerian degeneration, seen at the level of the cerebral peduncles and/or the PLIC on the repeat MRI, was seen in the 5 infants who had shown acute changes of the corticospinal tracts in the neonatal period and who went on to develop motor sequelae. Compared to MRI, DW-MRI and ADC maps provided additional, quantitative data of acute corticospinal tract injury at an early time point after the insult, especially at the level of the cerebral peduncles. The presence of increased SI on DW-MRI at the level of the PLIC and the cerebral peduncles in new-born infants with arterial ischaemic stroke is followed by Wallerian degeneration and subsequent development of hemiplegia.

Diffusion-weighted and perfusion-weighted magnetic resonance imaging to monitor acute intra-arterial thrombolysis

Diffusion-weighted and perfusion-weighted magnetic resonance imaging (DWI, PWI) are useful in detecting early cerebral ischemic lesions. Intra-arterial thrombolysis is an effective treatment for some patients with acute thromboembolic occlusion. We evaluated the efficacy of acute thrombolytic therapy by using DWI and PWI in 3 patients who presented with internal carotid artery or middle cerebral artery occlusion. On the initial magnetic resonance imaging scans, the abnormal areas shown by PWI were bigger than those shown by DWI. All patients received thrombolytic therapy within 6 hours after stroke onset. In 1 patient, the hyperintensity area detected by initial DWI scanning diminished after thrombolysis. DWI and PWI may be useful to monitor the effectiveness of intra-arterial thrombolysis.

Thrombolysis with reteplase, an unglycosylated plasminogen activator variant, in experimental embolic stroke

We incorporated diffusion-weighted magnetic resonance imaging (MRI) (DWI) and perfusion-weighted MRI (PWI) to evaluate the efficacy of thrombolysis in experimental embolic stroke using a plasminogen activator, reteplase. Reteplase (rPA) is an unglycosylated plasminogen activator with enhanced fibrinolytic potency. Right internal carotid arteries of 34 rabbits were embolized using aged heterologous thrombi. Baseline DWI and PWI scans 0.5 hours after embolization confirmed successful embolization among 32. Intravenous treatment with rPA (n=11; 1 mg/kg bolus), recombinant tissue plasminogen activator (rt-PA) (n=11; 6 mg/kg bolus over 1 hour), or placebo (n=10) commenced 1 hour after stroke induction. MRIs were performed at 1.75, 3, and 5 hours after embolization. Six hours after embolization, brains were harvested and examined for hemorrhage. Posttreatment areas of diffusion abnormality and perfusion delay were graded using both a semiquantitative scale and percent areas expressed as a ratio of the baseline values. Improved perfusion was seen among the rt-PA, and rPA-treated groups compared with placebo, using a semiquantitative scale (P<.01 rt-PA v controls, P<.05, rPA v controls). DWI scans, however, were not improved with thrombolysis. Cerebral hemorrhage was not increased with thrombolytic treatment, although the incidence of wound site hemorrhage was higher with either rPA or rt-PA. One fatal systemic hemorrhage was observed in each of the thrombolytic-treated groups. Cerebral perfusion was equally improved with either rt-PA or rPA without causing excess cerebral hemorrhage. An advantage of rPA is single-bolus dosing rather than continuous infusion. Use of rPA for stroke treatment should be further explored.