Periprostatic schwannoma mimicking metastatic lymphadenopathy in a case of multifocal prostate carcinoma.
Periprostatic schwannoma diagnosed in conjunction with multifocal prostate carcinoma.
A 67-year-old male was referred to the urology clinic for lower urinary tract symptoms (LUTS) consisting of increased frequency and nocturia as well as a raised serum prostate specific antigen (PSA) level of 12.2 UG/L (normal range: 0 – 4.0) and raised PSA density of 0.24 UG/L/ML. Digital rectal examination was unremarkable and transabdominal bedside ultrasound revealed a prostate volume of 40 ml with intravesical prostatic protrusion. The finding of a raised serum PSA level prompted further investigation with multiparametric magnetic resonance imaging (MpMRI) of the prostate. Anatomical imaging comprised high-resolution T2-weighted (T2w) sequences of the prostate in the axial, coronal and sagittal planes, with functional imaging consisting of diffusion weighted (DWI) sequences (high B-value up to 1800 s/mm2) and dynamic contrast enhanced (DCE) sequences (temporal resolution 5s).
MpMRI revealed a prostate gland volume of 51.8 ml. There were two dominant T2w hypointense masses with marked restricted diffusion and early intense enhancement (PIRADS 5) in both lobes of the prostate gland. The PIRADS 5 mass involving the right lobe anterior peripheral and transition zone at the mid gland measured 2.1 x 4.7 x 1.6 cm with no evidence of extraprostatic extension. The PIRADS 5 mass in the left lobe posterior peripheral zone at the apex and mid gland measured 1.6 x 1.4 x 1.7 cm with broad contact (1.5 cm) on the prostatic capsule but no tumour extension into the periprostatic fat. Enhancement of the left neurovascular bundle was seen, suspicious for neurovascular bundle infiltration. There was an additional 1.8 x 1.5 x 1.3 cm well circumscribed, mild and heterogeneous T2w hypointense lesion in the left periprostatic region adjacent to the neurovascular bundle and abutting the prostatic capsule. This lesion demonstrated restricted diffusion and mild heterogeneous enhancement. In view of the restricted diffusion, differential diagnoses for the periprostatic lesion included an enlarged periprostatic lymph node, an ectopic prostatic adenoma or a neurogenic tumor. Subsequent transperineal MRI-ultrasound fusion targeted biopsy revealed multiple cores of Gleason 4+4 adenocarcinoma from MRI-identified lesions in both lobes of the prostate gland. The patient was offered robotic assisted laparoscopic radical prostatectomy for definitive treatment with en-bloc resection of the periprostatic lesion. Intra-operative findings include an approximately 2 cm rounded well circumscribed extra-prostatic lesion just caudal to the left vascular pedicle at the prostate-vesical junction. The nodular lesion appeared to be embedded within the neurovascular bundle. The lesion was excised en-bloc with the neurovascular tissue in a non-nerve sparing fashion given the radiological finding of probable left neurovascular bundle infiltration by tumour. In this case, although the location of the schwannoma raised suspicion for tumour involvement, its circumscribed and distinct outline was atypical for a malignant process, and its signal and enhancement characteristics also differed from the primary prostate tumour. For example, the schwannoma demonstrated mild and heterogeneous T2w hypointensity with mild heterogenous enhancement. This was in contrast to the primary prostate tumour, which showed marked and homogeneous T2w hypointensity with early intense enhancement. Restricted diffusion reflects hypercellularity and can be seen in schwannomas; it may not necessarily represent malignancy. T2w hypointensity is unusual in schwannomas but possibly related to presence of haemosiderin or calcification. Whole mount histopathological examination of the resected specimen revealed pT2 Gleason 4+4 adenocarcinoma (grade group 4) in both lobes of the prostate gland with a small tertiary component of Gleason pattern 5. There was perineural invasion but no extraprostat
There is bias towards diagnosing periprostatic lesions found on MRI as lymphadenopathy in the setting of prostate carcinoma. This is doubly so when the lesion in question arises close to the neurovascular bundle, a structure often involved by tumour in cases of locally advanced disease. Other differential diagnoses, including lesions of benign aetiology should however be considered if atypical MR imaging features are present, with special attention paid to the border contour and morphology as well as the signal and enhancement characteristics of the lesion. In this case, although the location of the schwannoma raised suspicion for tumour involvement, its circumscribed and distinct outline was atypical for a malignant process, and its signal and enhancement characteristics also differed from the primary prostate tumour. For example, the schwannoma demonstrated mild and heterogeneous T2w hypointensity with mild heterogenous enhancement. This was in contrast to the primary prostate tumour, which showed marked and homogeneous T2w hypointensity with early intense enhancement. Restricted diffusion reflects hypercellularity and can be seen in schwannomas; it may not necessarily represent malignancy. T2w hypointensity is unusual in schwannomas but possibly related to presence of haemosiderin or calcification. This case is unique as we have a high-resolution MRI examination providing us with superior morphological, anatomical and functional information about the incidentally detected periprostatic schwannoma, for which there is a dearth of literature concerning the MRI features. Most described cases of prostatic schwannoma are often within the prostate gland, and imaging features would likely overlap with the heterogeneous MRI appearance of benign prostate hyperplastic nodules in the transition zone. The unique location in the periprostatic soft tissue implies that the schwannoma was most likely arising from the posterolateral neurovascular bundle. Ultimately, the definitive diagnosis of an atypical periprostatic lesion such as a schwannoma is histopathological. However, a careful approach and interpretation of MRI findings will allow for the detection of atypical imaging characteristics and sensible formulation of alternate differential radiological diagnoses. This may alter clinical decision-making as a diagnosis of locally advanced or metastatic disease may deprive the patient of a chance at curative surgical treatment versus a diagnosis without.
Metastatic lymph nodes in prostatic cancer usually demonstrate MRI features similar to the primary cancer. Alternate differential diagnoses including lesions of benign aetiology should be considered if the MR imaging characteristics are atypical and differ from the primary prostate cancer.