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Опубликовано Nelas в 18 Март, 2010 - 20:51
Мужчина, за 50. Несколько лет тому назад прооперирован по поводу лимфомы желудка с последующей химиотерапией. В последнее время появились головные боли и расстройства памяти и небольшие психические нарушения. Была выполнена МРТ. Очень хотелось бы услышать мнение коллег, желательно поподробнее, так как я сама МРТ не занимаюсь.
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Поскольку заключение по МРТ не соответсвовало анамнезу и клиническому течению, было назначено КТ.
Натив
С усилением:
Внутримозговые гематомы (поздняя подострая стадия), слева - с компрессией заднего рога левого бокового желудочка. Множественные очаги демиелинизации в белом веществе головного мозга и перивентрикулярно - вероятно дисциркулятоного характера и как проявление микроангиопатии..Смешанная заместительная гидроцефалия. На МРА - отсутствует визуализация интракраниального сегмента левой позвоночной артерии. Связь вышеописанных гематом с магистральными сосудами головного мозга не определяется..
Поздняя подострая стадия - это сколько недель? С чем нужно дифференцировать? Дело в том, что анамнеза и клиники кровоизлияния нет.
Поздняя подострая - соответствует 1-2 неделям. По контуру гематом гипоинтенсивный ободок по Т2 ВИ - откладывется гемоседерин. Могу предположить ранее существовавшие кавернозные ангиомы, а теперь произошло кровоизлияние??? но почему одновременно? А раньше пациент никогда МРТ не делал?
Гемосидерин по периферии откладывается не только в гематомах. Столько кровоизлияний в мозг - головными болями и снижением памяти не отделаешься. Те же самые кавернозные ангиомы (без разрыва и формирования внутримозговой гематомы) гипоинтенсивны по периферии, но они неоднородны по структуре за счет мелких кровоизлияний и скоплений крови в разных стадиях метаболизма в кавернах. Кровоизлияния в метастазы - мне кажется, это наиболее вероятный вариант, хотя опять нет выраженного перифокального отека!!! Метастазы меланомы, по литературным данным, гиперинтенсивны на МРТ Т1 и Т2 ВИ. Тоже не исключено, а может, даже так оно и есть. Одной фразой - многоочаговое поражение головного мозга, более вероятно, вторичного (метастатического) характера.
Спасибо, Тамара, спасибо, Анна. Метастазы меланомы отпадают, так как на КТ они высокой плотности, такой же как свежая гематома. Метастазы вполне вероятны. А как насчет вторичных лимфом, ведь у больного была лимфома желудка? Может кто-нибудь имеет опыт? Я знаю, что распады в лимфомах бывают, особенно при СПИДе. А кровоизлияния?
Одна из немногих лимфом, что видела.
Конечно, когда в анамнезе есть онкология, первая мысль о метастазах. Но возможно это просто вн/мозговая инсульт- гематома правой височной доли с прорывом в боковой желудочек, в поздней подострой ст. на фоне гипертензивного криза, в заднем роге левого желудочка свернутая кровь.
Все возможно. Но кровоизлияние с прорывом в желудочки без клинических проявлений, на мой взгляд, очень маловероятно. А чем объяснить накопление контраста по периферии?
Это лимфома. Наличие описанных выше полиморфных изменений в паренхиме головного мозга вкупе с утолщенной и контрастно усиленной эпендидимой желудочков, говорит в пользу лимфомы.
eMedicine
CNS Lymphoma:
Computed Tomography
Findings
Nonenhanced CT images typically show focal nodular areas of high attenuation, representing high tumor cellularity, with ill-defined margins and little surrounding vasogenic edema (see Image 1). Corresponding contrast-enhanced CT images usually demonstrate marked and diffuse enhancement of the lesions (see Image 2).16,17
In patients with AIDS-related immunocompromise, lymphomas often appear as ring-enhancing lesions (see Image 3) because of central areas of necrosis. The enhancing ring typically appears thick and nodular.
Calcifications do not occur in lymphoma, except rarely in patients who have undergone prior radiation therapy. Hemorrhage in lymphoma is rare. Contrast-enhancing, thickened ependyma may be seen.
Degree of Confidence
In patients with immunodeficiency or immunosuppression, other lesions, such as toxoplasmosis, cryptococcosis, metastasis, and pyogenic abscess, may have the same ring-enhancing appearance as that of CNS lymphoma. Clinical correlation is necessary in diagnosis.
False Positives/Negatives
Although in the proper clinical setting, radiographic findings may suggest CNS lymphoma, such findings are often not pathognomonic. Other lesions, such as toxoplasmosis, abscesses, cryptococcoma, glioma, and metastases, may have a similar appearance.
Magnetic Resonance Imaging
Findings
The classic appearance of CNS lymphoma on nonenhanced T1-weighted MRIs is that of an isointense to isointense-to-hypointense nodule or mass. On T2-weighted MRIs, the appearance is that of an isointense-to-hyperintense mass. On postgadolinium-enhanced T1-weighted MRIs, lymphoma tends to enhance intensely and diffusely. In patients with AIDS-related immunosuppression, a ringlike enhancing pattern is seen most often (see Images 4-5). Often, little or no surrounding vasogenic edema is demonstrated.18
Tumor lesions may cross the midline and may appear as a butterfly tumor involving both cerebral hemispheres. In 30% of patients, leptomeningeal involvement is encountered, usually in secondary systemic lymphoma; in such cases, meningeal involvement is typical. Involvement of the perivascular spaces with contrast enhancement is strongly suggestive of CNS lymphoma (in such cases, lymphoma must be differentiated from sarcoidosis and CNS tuberculosis); involvement of the corpus callosum is also strongly suggestive of CNS lymphoma (in such cases, lymphoma must be differentiated from glioma and metastatic neoplasm). Contrast-enhancing, thickened ependyma may be seen (cytomegalovirus ependymitis in AIDS or metastatic neoplasm such as carcinoma of lung or breast, and ependymal spread of anaplastic glioma must be differentiated).
Contrast-enhancing, thickened ependyma may be seen. If such findings are seen in patients with AIDS, lymphoma must be differentiated from cytomegalovirus ependymitis; if such findings are encountered in patients who do not have AIDS, lymphoma must be differentiated from metastatic neoplasm, such as carcinoma of the lung or breast. In addition, in patients with these findings, lymphoma must be differentiated from ependymal spread of anaplastic glioma.
AJR:
American Roentgen Ray Society
AJR 2005; 184:1679-1685
© American Roentgen Ray Society
Pictorial Essay
CT and MRI Findings of Intracranial Lymphoma
H. Wayne Slone1, Joseph J. Blake, Rajul Shah, Sangeeta Guttikonda and Eric C. Bourekas
1 All authors: Department of Radiology, The Ohio State University Medical Center and The Ohio State University College of Medicine and Public Health, 629 Means Hall, 1654 Upham Dr., Columbus, OH 43210.
Received July 26, 2004; accepted after revision November 8, 2004.
Address correspondence to H. W. Slone (slone-1@medctr.osu.edu' + u + '@' + d + '<\/a>'//-->).
Presented at the 2004 annual meeting of the American Roentgen Ray Society, Miami Beach, FL.
Introduction
Primary CNS lymphoma is the confinement of extranodal lymphoma to the CNS. Classically, lymphomas are divided into Hodgkin's lymphoma and non-Hodgkin's lymphoma, with a primary extranodal presentation in 5% and 30% of cases, respectively. With an increasing incidence in both the immunocompetent and immunocompromised populations, primary CNS lymphoma represents 1% of all lymphomas and as many as 16% of all primary brain tumors [1]. This amplified prevalence makes primary CNS lymphoma an important consideration in the differential diagnosis of brain lesions. This pictorial essay will review the varied CT and MRI appearances of intracranial lymphomas.
Primary CNS Lymphoma in the Immunocompetent
Most primary CNS lymphomas are of the non-Hodgkin's B-cell type [1]. B-cell primary CNS lymphoma typically presents when the patient is approximately 50 years old and is more frequent in men. The most common presenting symptom is a change in mental status followed by nausea, headache, hemiparesis, cerebellar signs, cranial nerve palsies, and visual disturbances [1, 2]. Cerebrospinal fluid analysis yields a cytologic diagnosis in fewer than half of patients with B-cell primary CNS lymphoma. Neuroimaging reveals solitary lesions that are most commonly located supratentorially in the white matter of the frontal or parietal lobes or in the subependymal regions, but the lesions may also involve the deep gray matter (Figs. 1A, 1B, 1C and 2A, 2B). In 12% of B-cell primary CNS lymphomas, the leptomeninges are involved [1]. CT scans usually show high attenuation, probably because of high cellularity, and virtually all lesions show homogeneous contrast enhancement (Fig. 1A). On MRI, B-cell primary CNS lymphoma lesions are clearly delineated masses that appear isointense to hypointense on T1-weighted images and mostly hypointense on T2-weighted images [1, 2] (Fig. 1B). Nearly all lesions show homogeneous enhancement with contrast material (Fig. 1C). A classic presentation is the lesion that crosses the corpus callosum in a butterfly pattern (Fig. 3A, 3B). Rarely, necrosis, cyst formation, calcification, and hemorrhage can be seen. If steroids are administered, the tumor may shrink and "vanish," compromising the ability to obtain a histologic diagnosis (Fig. 4A, 4B).
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Primary CNS Lymphoma in the Immunocompromised
Immunocompromised patients are at increased risk for developing primary CNS lymphoma. In fact, estimates indicate that nearly 6% of the AIDS population will be afflicted with an intracranial lymphoma [3]. Indeed, primary CNS lymphoma in an HIV-seropositive patient is an AIDS-defining condition. The age at presentation is earlier (fourth decade) in immunocompromised patients than in the immunocompetent, but the cell type (B cell) and presenting signs and symptoms are similar. Neuroimaging reveals a higher frequency of multiple lesions and more often displays irregular margins, heterogeneity, and ring enhancement [1, 3] (Figs. 5A, 5B, 5C and 6A, 6B, 6C). In the immunocompromised population, an important dilemma is the difficulty in distinguishing primary CNS lymphoma from the more common cerebral toxoplasmosis using CT and MRI, because both entities can present with multiple ring-enhancing lesions. Thallium SPECT or PET can aid in this setting, although frequently the patient is treated for presumed toxoplasmosis, and if the patient responds the diagnosis is established.
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Primary Leptomeningeal Lymphoma
Although extension of primary CNS lymphoma into the leptomeninges is common, primary leptomeningeal lymphoma is rare, constituting fewer than 8% of all cases of primary CNS lymphoma [4]. The clinical presentation of primary leptomeningeal lymphoma is similar to that of B-cell primary CNS lymphoma but may also include dizziness, tinnitus, spinal neuropathies, and meningismus. The diagnosis is often elusive because clinical findings are often suggestive of meningoencephalitis or common conditions that cause increased intracranial pressure. Analysis of the cerebrospinal fluid of patients with primary leptomeningeal lymphoma has failed to show a consistent presence of malignant cells. Neuroimaging is often unremarkable or may show nonspecific findings such as hydrocephalus. On occasion, significant imaging findings may include widespread meningeal calcification, discrete masses or densities, and faint meningeal enhancement (Figs. 7A, 7B, 7C and 8). In the absence of other findings, proton-density or FLAIR MRI revealing the presence of high signal intensity in the subarachnoid space may support a diagnosis of primary leptomeningeal lymphoma.
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Metastatic CNS Lymphoma, B-Cell Type
In 5–9% of systemic non-Hodgkin's lymphoma, secondary spread involves the CNS [5], usually in the form of leptomeningeal infiltrates, and has a poor prognosis. Parenchymal lesions, when present, typically result from secondary involvement from the leptomeninges via infiltration of the perivascular spaces (Fig. 9A, 9B).
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Intravascular Lymphomatosis
With fewer than 50 reported cases, intravascular lymphomatosis is an extraordinarily rare form of large B-cell non-Hodgkin's lymphoma that is characterized by aggressive, intravascular proliferation of lymphoid cells. Proclivity for involvement and subsequent occlusion of CNS vessels often leads to nonlocalizing neurologic deficits and changes in mental status. Because no specific clinical or laboratory findings are associated with intravascular lymphomatosis, the diagnosis is rarely established before histologic examination during autopsy. MRI findings in intravascular lymphomatosis include high-signal deep white matter lesions and infarctlike, high-signal lesions in vascular territories on T2-weighted images. After the administration of contrast material, enhancement can be masslike [6] (Fig. 10A, 10B, 10C). Various patterns of parenchymal and meningeal enhancement may also be seen.
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Primary CNS Lymphoma, T-Cell Type
Primary T-cell lymphoma of the CNS constitutes a small fraction of all primary CNS lymphomas in the immunocompetent population. A threefold higher incidence of T-cell primary CNS lymphoma in Japan compared with the United States has been reported. In a review of 25 cases of T-cell primary CNS lymphoma, Liu et al. [7] reported that T-cell primary CNS lymphoma is similar to B-cell primary CNS lymphoma in clinical presentation and imaging features. Unlike B-cell primary CNS lymphoma, involvement of the cerebrospinal fluid in T-cell primary CNS lymphoma is uncommon. CT and MRI typically show one or more homogeneous masses that uniformly enhance with contrast material [7] (Fig. 11A, 11B). Association with AIDS or other types of immunodeficiency has only rarely been reported.
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Intracranial Hodgkin's Lymphoma
Fewer than 0.5% of patients with Hodgkin's lymphoma have CNS involvement, and most of these cases are late manifestations of disseminated disease outside the CNS. Primary intracranial Hodgkin's lymphoma, with only a few case reports, is perhaps the rarest of all intracranial lymphomas. In the reported cases, neuroimaging usually shows meningeal involvement. Intracranial Hodgkin's lymphoma may mimic meningioma, although parenchymal lesions without meningeal attachment have been reported [8] (Figs. 12A, 12B and 13A, 13B, 13C).
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Conclusion
The CT and MRI findings of intracranial lymphomas can be nonspecific or share common features with other diseases such as demyelinating disorders, other neoplasms, sarcoid, tuberculosis, and toxoplasmosis. Therefore, a definitive diagnosis of primary CNS lymphoma requires histologic assessment. However, a high index of suspicion and the presence of features similar to those illustrated in this article can aid in the diagnosis of intracranial lymphoma.
References
Degree of Confidence
Leptomeningeal extension is depicted better on enhanced MRIs than on CT scans.
False Positives/Negatives
Care should be taken, especially in cases involving ring-enhancing lesions, to differentiate lymphoma from other disorders, such toxoplasmosis, cryptococcosis, gliomas, and metastasis; on MRI, the appearance of these disorders may be similar to that of lymphoma.
Involvement of the corpus callosum is highly suggestive of CNS lymphoma, but such involvement also occasionally occurs with anaplastic glioma and metastatic neoplasm.
Спасибо, Марио. Я написала лимфома, но сомнения замучили.
По-моему похоже на эту картинку.
вопрос, а как обьяснить такой высокий МР-сигнал на нативной Т1 серии ? Кроме того, разве лимфомы не должны гомогенно депонировать контраст по КТ?
Не всегда, я специально привёл выдержки из литературных источников.
Я согласна с Тамарой , очень похоже на подострые гематомы с ярким сигналом метгемоглобина и периферического гипоободком гемосидерина, с симметричной локализацией в базальных отделах затылочно-височных областей , с желудочками они не связаны, итимно прилежат к нижним стенкам. ельзя не учитывать, что пациенткае получала достаточно агрессивное лечение, чо могло спровоцировать развитие постхимиотерапевтического васкулита.