- Pictorial Review
- Open Access
Primary central nervous system post-transplant lymphoproliferative disorders: the spectrum of imaging appearances and differential
© The Author(s). 2019
- Received: 10 December 2018
- Accepted: 25 February 2019
- Published: 11 April 2019
Central nervous system post-transplant lymphoproliferative disorder (CNS-PTLD) is a rare disease that presents with non-specific signs and symptoms. The purpose of this article is to present the imaging appearances of CNS-PTLD by magnetic resonance imaging. We highlight the differential diagnostic considerations including primary central nervous system lymphoma, glioblastoma, cerebral abscess, and metastatic disease. This is an important topic to review since in daily practice the diagnosis of CNS-PTLD is often not initially considered when present due to its rarity and the lack of radiologists’ familiarity with the disease.
Knowing the unique imaging features of CNS-PTLD narrows the differential diagnosis, facilitates the diagnostic work-up, and optimizes making the diagnosis. Advanced MRI data for CNS PTLD is limited but is promising for helping with narrowing the differential diagnosis.
- Central nervous system
- Post-transplant lymphoproliferative disorders
- Clinical features
There is a tendency for CNS-PTLD lesions to be ring enhancing, have ill-defined enhancing margins, multifocal, supratentorial, and lobar in location.
The solid areas of CNS-PTLD lesions often have restricted diffusion likely related to hypercellularity.
Perfusion analysis would demonstrate a lower maximum relative cerebral blood volume in CNS-PTLD.
CNS-PTLD shares conventional imaging characteristics with multiple other disease processes including PCNS lymphoma, GBM, metastatic disease, abscess, and other infections.
It is important to know the clinical history and to consider the diagnosis of CNS-PTLD to facilitate the diagnosis.
Central nervous system post-transplant lymphoproliferative disorder (CNS-PTLD) is a rare disorder due to immunosuppression secondary to solid organ, stem cell, or bone marrow transplantation [1, 2]. Cases begin to appear as early as 6 weeks in the first year after transplantation but most cases take years to present after transplantation and the attendant immunosuppression. Viral factors have been strongly associated with CNS-PTLD and the strongest association is with Epstein-Barr virus (EBV). The neurological symptoms that patients present with are quite variable. The symptoms are related to general neurological dysfunction as well as specific signs and symptoms related to the location of the CNS lesions. Early consideration for CNS-PTLD is paramount to institute an appropriate work-up and to determine the needed therapy. Since an early step in the work-up is often neuroimaging, a radiologist aware of the imaging characteristics of CNS-PTLD and the differential diagnosis can positively impact patient care.
MR imaging features CNS PTLD vs AIDS CNS Lymphoma and PCNS lymphoma
AIDS CNS Lymphoma
Status post-transplant of solid organ, stem cell, or bone marrow
HIV positive patient
Elderly patient, Wiskott-Aldrich syndrome, ataxia-telangiectasia, severe-combined or common-variable immunodeficiency, rheumatoid arthritis, and systemic lupus erythematosus
Multifocal more common than unifocal
Unifocal more common than multifocal
Lobar predominantly, numerous basal ganglia and thalamic lesions, less commonly abuts CSF surface
Basal ganglia and corpus callosum
Periventricular, abutting CSF surface
Margin of enhancement
Elevated compared to lymphoma, will still have focal areas of restricted diffusion
Slightly elevated compared to normal white matter but lower than in toxoplasmosis
Lower and more homogeneous
Limited data, likely overall low (Fig. 2)
Low to mildly elevated, leakage pattern very suggestive
Increased choline, lipid and lactate
Decreased NAA, Cr
Increased choline, lipid and lactateDecreased NAA, Cr
Intratumoral susceptibility signal
Peripheral pattern of punctate hypointensities, tendency to bleed
Not reported, there is a tendency to bleed more than PCNS lymphoma
Minimal signal changes
The neurological symptoms in CNS-PTLD can be nonspecific and are quite variable. The non-specific symptoms include headache, confusional states/mental status changes, and seizure [3, 4]. Headaches are reported as a more common symptom in some studies [3–5]. Also, seizure can present with focal symptoms (e.g., motor, sensory, vision, or memory changes) indicating the lesion location. Reported focal neurological symptoms include hemiparesis, difficulty walking, ataxia, aphasia, dysarthria, facial droop, vertigo, and diplopia [3–5].
It is possible to make the diagnosis of CNS-PTLD with cerebral spinal fluid (CSF) sampling only. Positive CSF PCR for EBV is highly suggestive of the diagnosis and the CSF PCR for EBV can be positive even when PCR on the peripheral blood is negative . Caution is advised in evaluating the CSF by PCR when the blood is positive for EBV. CSF cytological analysis is usually positive in fewer cases but in some small series, a majority of patients have positive CSF cytology [3–5, 7]. Flow cytometric analysis can assist in making the diagnosis of PTLD in the CSF. However, overall, the CSF analysis including CSF cytological analysis usually results in non-specific findings. Biopsy is almost always required for a definitive diagnosis .
The survival is quite variable with some patients dying within the first month but many patients survive for years [3–7]. The treatment almost invariably involves decreasing or withdrawal of immunosuppressive therapy in the first instance [3, 4, 7, 12]. This must be balanced with not causing rejection of the transplanted organ. Corticosteroids are used routinely. Treatment with chemotherapy or radiotherapy should be strongly considered and the therapies utilized have been rather heterogeneous [3, 4, 7, 12]. However, after multivariate analysis, Cavaliere et al. only found age to be predictive of survival . Methotrexate has more commonly been used intravenously with less common utilization intrathecally [3, 4, 12]. There have also been promising results utilizing rituximab with cranial radiation . There is a trend for improved progression-free survival in patients receiving rituximab and/or cytarabine . More patients are being treated with antiviral therapies with mixed results. Mortality is very high in non-responders to immunosuppressive therapy modification and failures of treatment with first modality .
Identifying the imaging characteristics of CNS-PTLD can aid in the diagnosis and help differentiate CNS-PTLD from several differential diagnostic considerations. A neuroimaging exam can be used to detect the lesion(s), demonstrate the neuroanatomical areas involved, and associated complications such as brain herniation. The MRI or CT examinations should be performed with and without intravenous contrast. Contrast greatly helps to define the lesions in CNS-PTLD. MRI is superior to CT in sensitivity and for detailed analysis of CNS-PTLD lesions. An MRI protocol to best delineate and characterize the brain lesions should include T2-weighted/T2 fluid-attenuated inversion recovery (FLAIR), T1-weighted pre contrast, a gradient-echo or susceptibility-weighted imaging sequence, diffusion-weighted/diffusion tensor imaging (DWI), and the post-contrast T1-weighted images. Perfusion-weighted imaging (PWI) should also be useful to help differentiate CNS-PTLD from other potential diagnostic considerations.
Numerous authors have found lesions to be multifocal with predominantly lobar location [3, 5, 6, 12]. Predominant multifocal disease has been reported in 61% to 88% cases [3, 5, 6, 12]. An exception is Evens et al. who reported that 63% of cases had one lesion . There is a greater amount of variability with the described location of CNS-PTLD lesions. Evens et al. described a minority of cases to have deep involvement of the basal ganglia, brainstem, cerebellum, and/or periventricular involvement . However, the basal ganglia can be frequently involved and even the second most common location (39%) [3, 6]. Although, others have found the periventricular location to be the second most common location and at least one periventricular lesion being seen in 72% of cases [5, 12]. Usually lesions are less commonly reportedly in the corpus callosum, thalami, and periventricular locations [4–6]. Rarely, lesions are present in isolation in non-lobar locations including infratentorially or in the spinal cord. Rare presentations are generally found to include cerebral lymphomatosis and associated or isolated meningeal contrast enhancing lesions . However, there has been concurrent meningeal enhancement reported in over 50% of patients and meningeal/ependymal enhancement in 40% of patients [3, 5].
The CT density of CNS-PTLD lesions has a wide reported variation. Lesions on CT have been reported to be hyper, iso, or hypoattenuating [12, 15, 16]. The presence of hypodensity in the lesions differs from what has been described for PCNS lymphoma [17, 18]. However, mild hyperdensity might be present due to hypercellularity or to the presence of hemorrhage [16, 19].
How to differentiate CNS PTLD from other pathologies
◦ High perfusion in the enhancing mass
◦ More commonly will be a single enhancing lesion, around 2/3 of the time
◦ More common involvement of the corpus callosum
◦ Peritumoral region can have abnormalities indicating tumor (increased perfusion, restricted diffusion, tumor spectroscopy)
◦ High diffusion signal centrally with relative restricted ADC
◦ Low diffusion signal in the rim with elevated ADC
◦ Thin smooth rim of enhancement with thin rim of low T2 signal
◦ Smooth rim of hypointensity on susceptibility weighted images
◦ Spectroscopy—amino acids present in the abscess cavity ((valine, leucine and isoleucine; 0.9 ppm), acetate (1.9 ppm), alanine (1.5 ppm), and succinate (2.4 ppm))
◦ High perfusion in the enhancing mass
◦ Tend not to occur in the basal ganglia, thalami, or periventricular locations
A common signature feature of PCNS lymphoma is marked associated restricted diffusion in the mass lesions secondary to hypercellularity. The ADC values in PCNS lymphoma are typically lower and more homogeneous than in CNS-PTLD . The ADC and FA values measured in the solid enhancing components of lymphoma are significantly decreased compared to GBM . The perfusion of PCNS lymphomas are relatively low with reported rCBVs 1.29 ± 0.18 to 2.74 ± 0.87 [29–31]. The variation in the rCBVs measured likely relates to the analysis technique but the rCBV values are consistently found to be significantly lower than in high-grade gliomas. The signal recover of the perfusion curve is also significantly higher (rising above baseline) in PCNS lymphoma than in high-grade gliomas [31–33]. This leakage pattern does not prove PCNS lymphoma but it is an important diagnostic clue . Spectroscopy can show the presence of lipid and/or lactate, increased Cho/Cr, and decreased NAA/Cho . However, this pattern can be seen with GBM and metastatic disease. A massively elevated lipid peak and a markedly elevated Cho/Cr ratio has been found to be more suggestive of PCNS lymphoma than glioma . The spectral pattern might help to differentiate from abscesses which often demonstrate a number of amino acids peaks not seen in PCNS lymphoma.
Glioblastoma (GBM) WHO grade IV is the most common primary intraparenchymal tumor, is typically ring enhancing, and can have a similar appearance to CNS-PTLD. GBM mostly occurs in the cerebral hemispheres and rarely in the posterior fossa or spinal cord. GBMs are a common mass lesion to involve the corpus callosum and this is a less common characteristic of CNS-PTLD. Predominantly, GBMs presents as single masses but multifocal or multicentric disease can occur around 33% of the time. Typically, GBM presents as a large heterogeneous mass with central necrosis and concave shaggy enhancing margin. GBMs occur in all age groups but has a peak incidence in the 7th and 8th decades. GBM is a diagnostic consideration for many ring-enhancing brain lesions with surrounding edema as seen with CNS-PTLD. However, GBM can infrequently present as a solid enhancing mass with necrosis only present at pathological analysis. ITSS signal changes are often found in GBMs and could represent microhemorrhages or calcifications . Massive hemorrhage can occur and this will obscure the underlying tumor.
DWI and ADC analysis of the abscess cavity are also very useful [44–47]. Abscesses tend to have cavities of relative restricted ADC and high diffusion signal, whereas the necrotic cavities of tumors have higher ADC values . The opposite is true for the rims of these lesions with higher ADC values in the rims of abscesses and lower ADC values in the rims of tumors. The diffusion characteristics of the rims of abscesses and tumors offer the better diagnostic differentiation between these entities. The reason is even though the central cavities of tumors usually have lower signal on DWI and elevated ADC values, the presence of hemorrhage and the debris within necrotic components of tumors can result in elevated DWI signal and lower ADC values that mimic the appearance of an abscess.
On PWI, abscesses typically have mildly elevated CBV [44, 46, 48, 49]. This makes PWI less useful for differentiating an abscess from lymphoma or likely CNS-PTLD. The abscess MR spectrum does not have elevated choline but has elevated amino acids from 0.9–2.4 ppm ((valine, leucine and isoleucine; 0.9 ppm), acetate (1.9 ppm), alanine (1.5 ppm), and succinate (2.4 ppm)) . This spectrum when present helps identify an abscess cavity.
The imaging characteristics of metastatic disease overlap significantly with CNS-PTLD. Many cases of metastatic disease in the brain are ring enhancing with multiple lobar lesions but single metastatic brain lesions are not uncommon. These features are similar to CNS-PTLD. However, metastatic disease is not as commonly present in the basal ganglia, thalami, and periventricular locations as CNS-PTLD. CNS-PTLD and metastatic disease both often have ring enhancement that is heterogeneous. PCNS lymphoma is a usually a more solid homogeneously enhancing disease process.
CNS-PTLD is a complicated disease process that affects immunosuppressed post-transplant individuals. Being able to accurately help differentiate this diagnosis through imaging is vital and helps optimize making an early diagnosis (Tables 1 and 2). Given the rarity of the diagnosis, the consideration of CNS-PTLD is often lacking on initial imaging interpretations. Advanced imaging characteristics likely will help to diagnosis CNS-PTLD but our review of the literature demonstrates a paucity of information pertaining to these techniques. CNS-PTLD shares imaging characteristics with multiple other disease processes including PCNS lymphoma, GBM, metastatic disease, abscess, and other infections. Even though definitive diagnosis will often come down to biopsy, imaging characteristics will help distinguish the disease processes.
We thank Dr. Justin Cramer for his thoughtful proofreading and insightful suggestions.
All authors read and approved the final manuscript.
The authors declare that they have no competing interests.
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