Metastatic prostate cancer mimicking chronic subdural hematoma: a case report and review of the literature.
This case reports documents a patient presenting with a chronic subdural hematoma on computed tomography (CT) findings but at the time of craniotomy was discovered to have metastatic prostate cancer.
A 71-year-old man with a past medical history of prostate cancer presented to the emergency department complaining of a two to three week history of headache with concomitant dizziness. He reported falling about three weeks prior to admission. This patient was diagnosed with prostate cancer three months prior to presentation in the emergency department with an elevated prostate-specific antigen (PSA) of 151 ng/mL. Transrectal ultrasound biopsy revealed Gleason 4+3 adenocarcinoma in a 63 gram gland involving 85% of right cores and 70% of left cores. Based on the Kattan Nomogram, his likelihood of non-organ confined prostate cancer was 79%. Despite counseling, he refused further metastatic work up including bone scan or CT scan of his abdomen and pelvis. Moreover, he refused treatment of his prostate cancer.
On initial examination in the emergency room, he complained of dizziness. On neurologic examination, he had a normal mental status and had no focal deficits except bilateral hypoacusis, which he stated was chronic. On rectal exam he had a firm, lobulated prostate, with normal sphincter tone. The CT scan of the head without contrast demonstrated a mixed isodense/hypodense lesion over the left convexity. The isodense component was lateral and the hypodense component was medial abutting the cortical surface (Figure 1). This lesion was associated with a local mass effect of the left hemisphere and mild midline shift. In evaluating the patient's presentation and imaging, neurosurgical consulting physicians diagnosed the patient as having a subacute/chronic subdural hematoma with membrane formation.
The patient was symptomatic and his imaging revealed evidence of a midline shift; neurosurgery recommended evacuation of the presumed subdural hematoma. The patient was taken to the operating room for burr hole evacuation of the left subdural hematoma. Two burr holes were placed over the frontal and parietal convexities. The dura appeared normal in both cases. Upon opening the frontal dura, no frank blood was encountered. However, a smooth, tan, firm mass was found layered in the subdural space. The dura was then opened in the parietal burr hole and similar findings were noted. Due to the intraoperative findings, the burr holes were joined to make a larger craniotomy incision for further exploration of the lesion. After removing the bone flap and extending the dural opening, the lesion was found to be extra-axial and extended at a fairly constant thickness over a broad area of the convexity. Multiple areas were biopsied and the intraoperative frozen section was consistent with neoplasm. The en-plaque lesion was adherent to the underlying cortical surface and thus no attempt was made to extensively resect the tumor. The patient did well postoperatively with improvement of his dizziness. Final pathology was consistent with metastatic adenocarcinoma of the prostate. Postoperatively, magnetic resonance images indicated homogenous enhancement of the subdural mass (Figure 2).
[FIGURE 1 OMITTED]
The patient was started on nonsteroidal antiandrogen treatment for three weeks postoperatively prior to induction of luteinizing hormone-releasing hormone (LHRH) agonist. The bone scan performed revealed extensive skeletal metastasis consistent with "superscan." The patient was eventually treated with whole brain radiation for symptoms with a total of 3000 cGy and dizziness resolved. The patient eventually became hormone refractory on complete hormone ablation and was started on Samarium-153 with a brief duration of PSA response. Now at 25 months followup from original presentation, PSA has begun to rise again and patient plans to start docitaxel based chemotherapy in the near future.
Chronic subdural hematomas most commonly occur in the elderly and can present clinically months or even years after a seemingly trivial head injury. They are usually diagnosed by a noncontrasted CT scan of the head. Occasionally, alternate lesions are encountered during surgery. Notable ones are subdural empyemas, meningiomas, lymphomas of the cranial vault, metastatic lesions, sarcoidosis, and histiocytosis. While few cases of metastatic prostate cancer mimicking subdural hematomas have been reported, there have been no cases reported of patients with classic presentations of subdural hematoma involving the entire subdural space.
Prostate cancer is the most common cancer in men and the second leading cause of cancer-related death. The age adjusted incidence of prostate cancer is estimated to be 145 per 100,000 in men and is the most common site of cancer in men of all races, (18) with the incidence increasing with age. (15) Interestingly, the prevalence of prostate cancer is consistent throughout the world, but the clinical incidence is much higher in North America. (18) This suggests that dietary and/or environmental influences may play a role in the development of prostate cancer. (15) The median age of diagnosis is 72 years and is usually detected by screening with an annual digital rectal exam and prostate specific antigen levels (PSA) beginning at age 50. About 4% of those diagnosed with prostate cancer will have evidence of metastatic disease at the time of presentation. (11) As with other cancers, prognosis depends on the grade and stage.
Metastatic prostate cancer to the axial skeleton is relatively common. However, intracranial metastasis is quite rare, reported in less than 5% of patients with end stage prostate cancer. (2) Of the intracranial sites affected by metastatic prostate cancer, the dura (67%) is by far the most common, followed by the cerebral cortex (25%) and the cerebellum (8%).13, 16 As with most intracranial metastasis, the clinical manifestations (seizures, headaches, or focal neurologic deficits) are usually due to intracranial hypertension, mass effect, or hemorrhage. (2, 7) Our patient, for example, presented with headaches and dizziness corresponding to the radiographic findings of mass effect and midline shift and presumptive diagnosis of subdural hematoma.
The patient's age, history of a fall three weeks prior to presentation, clinical manifestations, neurological examination, and radiographic findings all suggested subacute/chronic subdural hematoma as the working diagnosis. Classically, subdural hematomas present with radiographic findings of an extra-axial crescent shaped lesion that crosses suture lines. Various other pathologies mimicking subdural hematoma have been reported in the literature. (10) The most common of these are en-plaque meningioma and subdural empyema. (7, 8 16) Given their advanced age, the population that tends to present with chronic subdural hematomas often has a history of cancer. It is not our routine practice to obtain MRI scans on patients that present with what we initially feel is a chronic subdural hematoma; perhaps this preoperative workup should be rethought in patients with a history of cancer. In our case, a preoperative MRI would certainly have raised our suspicion of a subdural neoplasm and allowed us to counsel the patient more effectively regarding the goals of surgical intervention.
[FIGURE 2 OMITTED]
Most deaths due to prostate cancer are from metastatic disease. (15) The mainstay of treatment of metastatic prostate cancer is androgen ablation therapy. (15) The downside of androgen suppression is that many patients will develop hormone-refractory disease.14 For metastatic disease, this therapy is palliative and has produced a progression-free survival of 18 to 20 months and an overall survival of 24 to 36 months. (14)
For patients with evidence of intracranial metastatic prostate cancer average survival is one month without and three and a half months with treatment and the histology or the location of the lesion supra or infratentorial did not alter the survival rate. (6, 17) Treatment for intracranial metastasis from prostate cancer mainly involves surgical debulking and hormonal therapy when possible with radiation treatment. (5, 6 17) Radiation therapy in patients with metastatic prostate cancer to the central nervous system is reserved for those with hormone-refractory disease, painful bone metastases, or for patients with impending spinal cord compression. (14) When surgical resection is not an option, as in our patient, a fractionated radiation paradigm will provide the best chance for local control.
Metastatic disease is commonly seen with prostate cancer. However, disease spread to the subdural space is extremely rare, occurring in less than 1% of patients with metastatic disease. We present a case report of metastatic prostate cancer to the entire hemispheric subdural space that mimics a chronic subdural hematoma. Both metastatic tumors and meningioma should be in the differential diagnosis for convexity subdural lesions; the former especially in the clinical setting of a patient with a history of cancer. This case highlights the fact that extra scrutiny should be applied to intracranial lesions in the presence of cancer history. In hindsight a preoperative MRI would have greatly heightened our suspicion that the lesion was neoplastic rather than hematoma. This would have allowed better preoperative counseling of our patient.
(1.) Batson O. The function of the vertebral veins and their role in the spread of metastases. Ann Surg 1940;112:138-149.
(2.) Confavreux CBN, Cotton F, Tebib JG. Advanced MRI could help to differentiate meningeal carcinomatosis with mass effect from cerebral metastasis in prostate cancer. Bull Cancer 2006;93: E31-5.
(3.) Delaney P. Subdural metastases from prostatic adenocarcinoma. J Neurol Neurosurg Psychiatry 1983;46:186-188.
(4.) Dolloff NG, Shulby SS, Nelson AV, et al. Bone-metastatic potential of human prostate cancer cells correlates with AKT/PKB activation by a platelet-derived growth factor receptor. Oncogene 2005;24:6848-6854.
(5.) Kabeer MA, Lloyd-Davies E, Maskell G, et al. Metastatic prostate cancer masquerading clinically and radiologically as a primary caecal carcinoma. World J Surg Oncol 2007;5:2.
(6.) Kim S, Chao S, Toms S, et al. Stereotactic radiosurgical treatment of parenchymal brain metastases from prostate adenocarcinoma. Surg Neurol 2008;69:641-646.
(7.) Lath CO, Khanna PC, Gadewar S, et al. Intracranial metastasis from prostatic adenocarcinoma simulating a meningioma. Australas Radiol 2005;49:497-500.
(8.) Lyons MK, Drazkowski JF, Wong WW, et al. Metastatic prostate carcinoma mimicking meningioma. Neurologist 2006;12:48-52.
(9.) N'dri Oka D, Varlet G, Boni N, et al. Dural metastasis of prostatic adenocarcinoma presenting as acute intracranial subdural hematoma: a case report. J Neuroradiol 2000;27:282-284.
(10.) Nemeth AJ, Henson JW, Mullins ME, et al. Improved detection of skull metastasis with diffusion-weighted MR imaging. Am J Neuroradiol 2007;28:1088-1092.
(11.) Ries LAG, Melbert D, Krapcho M, et al (editors). SEER Cancer Statistics Review, 1975-2005, National Cancer Institute. Bethesda, MD. <http://seer.cancer.gov/csr/1975_2005/>.
(12.) Scarrow AM, Rajendran PR, Marion D. Metastatic prostate adenocarcinoma of the duramater. Br J Neurosurg 2000;14:473474.
(13.) Sutton MA, Watkins HL, Green LK, et al. Intracranial metastasis as the first manifestation of prostate cancer. Urology 1996;48:798803.
(14.) Terris MK, Rhee A, Qureshi SM. Prostate cancer: metastatic and advanced disease (2006). Emedicine from WebMD.<http:// www.emedicine.com/med/TOPIC3197.HTM> (accessed 6 June, 2008).
(15.) Tierney LM, McPhee SJ, Papadakis MA. Current medical diagnosis and treatment. McGraw-Hill's Access Medicine. <http://www. accessmedicine.com/popup.aspx?aID=779015&pring=yes> (accessed 6 June, 2008).
(16.) Tomlin JM, Alleyne CH. Transdural metastasis from adenocarcinoma of the prostate mimicking subdural hematoma. Surg Neurol 2002;58:329-331.
(17.) Tremont-Lukats IW, Bobustuc G, Lagos GK. et al. Brain metastasis from prostate carcinoma: the MD Anderson Cancer Center experience. Cancer 2003;98:363-368.
(18.) US Cancer Statistics Working Group. United States Cancer Statistics: 1999-2004 Incidence and Mortality Web-based Report. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention and National Cancer Institute;2007. <www.cdc.gov/uscs>.
Shashikant Patil, MD; Ayme Veron, MD; Pegah Hosseini, MD; Rachel Bates, MD; Benjamin Brown, MD; Bharat Guthikonda, MD; and Rowena DeSouza, MD
Drs. Patil, Veron, Brown, Guthikonda, and DeSouza are affiliated with the Department of Neurosurgery and the Department of Urology at the Louisiana State University Health Sciences Center in Shreveport. Dr. Hosseini is affiliated with the Department of Internal Medicine at Louisiana State University Health Sciences Center in Shreveport. Dr. Bates is affiliated with the Department of Dermatology at Louisiana State University Health Sciences Center in New Orleans.
|Printer friendly Cite/link Email Feedback|
|Author:||Patil, Shashikant; Veron, Ayme; Hosseini, Pegah; Bates, Rachel; Brown, Benjamin; Guthikonda, Bharat;|
|Publication:||The Journal of the Louisiana State Medical Society|
|Article Type:||Case study|
|Date:||Jul 1, 2010|
|Previous Article:||Granular cell tumor of the vulva.|
|Next Article:||Three organ transplant patients infected with 2009 novel H1N1 influenza in early Fall, 2009.|