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Case Reports / Journal of Clinical Neuroscience 21 (2014) 1054–1056
Table 1 Liver functions tests and pancreatic enzymes during the course of hospitalization
Day Day Day Day Day
1 (admission) 3 4 5 7 (discharge)
AST (U/L)
ALT (U/L)
Alkaline phosphatase (U/L)
Total bilirubin (mg/dL)
Amylase (U/L)
Lipase (U/L)
1115 785 330 100 35
1083 808 444 376 45
250 267 209 202 68
2.7 2.6 NA 2.6 2.7
439 324 NA 219 41
721 663 NA 310 153
ALT = alanine aminotransferase, AST = aspartate aminotransferase, NA = not available.
nal symptoms when seen by her primary care physician 4 months later. 3. Discussion This report illustrates the development of acute pancreatitis and elevated liver enzymes after rapid titration of oral LEV in a patient with no known risk factors. Possible causes of acute pancreatitis and hepatitis in adults are numerous and include infection, metabolic derangements, multisystem disease and hereditary, idiopathic or medication-related events. In the absence of objective evidence for an organic disease, a cause-relation argument points to LEV as the likely offender. In addition, this is also supported by the accelerated clinical and laboratory improvement after discontinuation of LEV. Abnormal liver function tests and pancreatitis were vaguely reported in post-marketing LEV experience in the drug prescribing information [2]. There was, however, no mention of the number of cases, LEV dosage, severity of condition, or natural course. To our knowledge the medical literature refers to a single case of acute pancreatitis, in an adolescent with autism. This occurred at a dose of 1000 mg of LEV and was preceded by complaints of intermittent abdominal pain when taking phenytoin, which could have been the initial trigger [3]. One other patient with fulminant liver failure was possibly attributed to a therapeutic dose of LEV [4]. The simultaneous occurrence of both pancreatic and hepatic abnormalities has not been reported to our knowledge.
Serious idiosyncratic adverse effects of newer AED are rare. They tend to occur during early titration periods and less commonly during maintenance periods. In our patient, the mild symptoms rapidly started after initiation of LEV, culminating in severe symptoms with rapidly escalating doses, suggesting both dose and time dependent relationships. It is also possible that drug toxicity may have contributed to this reaction which could possibly happen at higher therapeutic doses. This explanation is however less likely as no classic signs of clinical toxicity were present. In addition, LEV blood levels were unavailable to test this possibility. Conflicts of interest/disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Briggs DE, French JA. Levetiracetam safety profiles and tolerability in epilepsy patients. Expert Opin Drug Saf 2004;3:415–24. [2] Union Chimique Belge (UCB). Keppra prescribing information. Georgia:Union Chimique Belge; 2011. [3] Almeida DM, Jean MR, Chystsiakova A, et al. Levetiracetam-associated acute pancreatitis in an adolescent with autism: a case report. Pancreas 2013;42:177–8. [4] Tan TC, de Boer BW, Mitchell A, et al. Levetiracetam as a possible cause of fulminant liver failure. Neurology 2008;71:685–6.
http://dx.doi.org/10.1016/j.jocn.2013.10.002
Intraneural fibroma of the median nerve at the wrist Anthony M. Burrows a, Andrew L. Folpe b, Doris E. Wenger c, Robert J. Spinner a,⇑ a b c
Department of Neurologic Surgery, Mayo Clinic, 200 First Street SW, Gonda 8-214, Rochester, MN 55901, USA Department of Anatomic Pathology, Mayo Clinic, Rochester, MN, USA Department of Radiology, Mayo Clinic, Rochester, MN, USA
a r t i c l e
i n f o
Article history: Received 1 October 2013 Accepted 9 October 2013
a b s t r a c t Distal median neuropathy from carpal tunnel syndrome is the most well known lesion affecting the median nerve. Mass lesions may affect the nerve at the wrist. We present to our knowledge the first histologically confirmed case of an intraneural fibroma. Ó 2013 Elsevier Ltd. All rights reserved.
Keywords: Carpal tunnel Median nerve Peripheral nerve
⇑ Corresponding author. Tel.: +1 507 284 2376; fax: +1 507 284 5206. E-mail address: [email protected] (R.J. Spinner).
Case Reports / Journal of Clinical Neuroscience 21 (2014) 1054–1056
1. Case report A 36-year-old laborer presented to our clinic with a right wrist mass. The mass had initially developed rapidly 1 year prior to his presentation but the mass had remained stable in size since that time. After the mass developed, he reported intermittent paresthesias of the right thumb, index, middle, and occasionally, the ring finger. He had the additional history of bilateral median neuropathies relieved by bilateral carpal tunnel releases 8 years prior to his presentation. His mass was felt to be a ganglion cyst by another physician and was surgically explored 2 months prior to his presentation. This surgery was aborted when the mass was visualized and no biopsy was taken. On examination, his wrist had a large mobile mass proximal to the wrist crease with a small area of wound dehiscence (Fig. 1A). Tinel’s sign was present with percussion of the mass. He had 4/5 strength in opponens pollicis and abductor pollicis brevis but no extrinsic finger weakness. He had intact two point sensation in his radial digits. Electromyography showed right median neuropathy at the wrist, with both focal slowing and mild axonal loss across the mass. MRI demonstrated a mass in the median nerve with fascicles draped around the margins of the mass. It had a thick peripheral rim of low signal intensity. It had predominantly intermediate signal on T1-weighted images with minimal patchy internal
1055
enhancement. The mass demonstrated marked heterogeneous signal on T2-weighted images (Fig. 1B, C). He underwent general anesthesia and tourniquet compression and his wrist was opened along the axis of the mass and utilizing the previous carpal tunnel scar. The median nerve was identified proximally and followed around the mass through the carpal tunnel with a thickened epineurium. A plane around the mass was developed preserving the displaced fascicles (Fig. 1D, E). The mass was resected en bloc with no distinct neural origin. The thickened epineurium was resected as well. A complex skin closure was needed despite removal of the mass. The patient tolerated the procedure and had intact sensation and thumb abduction immediately following the procedure. Pathological evaluation showed a heavily collagenized, hypocellular, cytologically bland fibroblastic spindle cell proliferation showing limited expression of CD-34, but wihtout immunoreactivity to smooth muscle actins, S-100 protein, or the perineurial markers epithelial membrane antigen, GLUT-1, or claudin 1, consistent with a fibroma (Fig. 1F, G). 2. Discussion Carpal tunnel syndrome is the most well known cause of distal median neuropathy. Other intrinsic or extrinsic lesions affecting the median nerve at the wrist have been reported, including extra-
Fig. 1. (A) Pre-perative photograph. (B) T2-weighted axial MRI demonstrates heterogeneous signal with displaced fascicles (white arrows). (C) T1-weighted sagittal MRI shows displaced fascicles (white arrows) and heterogeneous content. (D) Intraoperative photograph showing the intraneural mass, the epineureum is reflected. (E) Intraoperative photograph. A traversing fascicle is secured with the superior vessel loop and the mass is being mobilized from the median nerve. (F) Gross sections of the mass show heterogeneous content. (G) The pathology specimen shows a heavily collagenized, hypocellular, cytologically bland fibroblastic spindle cell proliferation on hematoxylin and eosin staining (original magnification 5).
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Case Reports / Journal of Clinical Neuroscience 21 (2014) 1056–1058
neural tendon sheath fibromas, giant cell flexor sheath tumors, and intraneural lipomas [1–5]. Extraneural tendon sheath fibromas are an unrelated myeloproliferative process. In this patient, the mass arose intraneurally and developed rapidly with resulting median neuropathy. To the best of out knowledge, this is the first reported case of a histologically confirmed intraneural fibroma. Given these findings, intraneural fibromas should be included in the differential diagnosis of median neuropathy with a mobile wrist mass. Conflicts of interest/disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication.
References [1] Okubo T, Saito T, Mitomi H, et al. Intraneural lipomatous tumor of the median nerve: three case reports with a review of literature. Int J Surg Case Rep 2012;3: 407–11. [2] Tiong WH, Ismael TS, Regan PJ. Fibroma of tendon sheath: a rare cause of carpal tunnel syndrome. J Hand Surg 2006;31:579–80. [3] Chalmers RL, Mandalia M, Contreras R, et al. Acute trigger wrist and carpal tunnel syndrome due to giant-cell tumour of the flexor sheath. J Plast Reconstr Aesthet Surg 2008;61:1557. [4] Evangelisti S, Reale VF. Fibroma of tendon sheath as a cause of carpal tunnel syndrome. J Hand Surg 1992;17:1026–7. [5] Garrido A, Lam WL, Stanley PR. Fibroma of a tendon sheath at the wrist: a rare cause of compression of the median nerve. Scand J Plast Reconstr Surg Hand Surg 2004;38:314–6.
http://dx.doi.org/10.1016/j.jocn.2013.10.002
Primary leptomeningeal melanocytosis presenting as chronic meningitis Michael C. Honigberg c,⇑, Efstathios Papavassiliou b,c, Yehuda Z. Cohen a,c a
Division of Infectious Diseases, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA Division of Neurosurgery, Department of Surgery, Beth Israel Deaconess Medical Center, Boston, MA, USA c Tosteson Medical Education Center, Harvard Medical School, 260 Longwood Avenue, Boston, MA 02115, USA b
a r t i c l e
i n f o
Article history: Received 17 October 2013 Accepted 18 October 2013
Keywords: CSF protein elevation Leptomeningeal melanocytic neoplasm Meningeal melanocytosis Primary leptomeningeal melanocytosis
a b s t r a c t We report a patient with primary leptomeningeal melanocytosis presenting as chronic meningitis. A previously healthy 27-year-old man presented with 2 months of severe headaches and photophobia. A lumbar puncture was notable for a highly elevated cerebrospinal fluid (CSF) protein level without pleocytosis. Imaging at the time of admission suggested only meningitis without the presence of parenchymal lesions. On the basis of the CSF findings, early meningeal biopsy was performed, leading to the diagnosis of a meningeal melanocytic neoplasm. Early meningeal biopsy should be considered in patients with meningitis when the CSF profile suggests the possibility of a central nervous system neoplasm. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction Primary leptomeningeal melanocytosis is a rare central nervous system (CNS) neoplasm with an estimated incidence of 1 in 10 million [1]. It can have a variety of clinical presentations, including headache, neck pain, symptoms of increased intracranial pressure, focal neurologic deficits, and seizures [2,3]. We report a previously healthy young man who presented with chronic meningitis and was ultimately found to have primary leptomeningeal melanocytosis.
2. Case report A 27-year-old man originally from El Salvador was transferred to our hospital with confusion and 2 months of headache. Seven weeks previously, he had presented to an outside hospital with 2 weeks of severe headache as well as nausea, vomiting, and mild photophobia. A lumbar puncture (LP) was performed and the results are shown in Table 1. An infectious workup was negative. The patient was discharged with presumed aseptic meningitis. He continued to have daily headaches with nausea and vomiting. One week prior to admission, he presented to the same outside hospital and underwent a second LP (Table 1). A tuberculin skin ⇑ Corresponding author. Tel.: +1 703 980 4521; fax: +1 617 735 4527. E-mail address: [email protected] (M.C. Honigberg).
test was positive and cerebrospinal fluid (CSF) mycobacterial culture was sent. He was discharged without a clear diagnosis. Six days later, the patient was transferred to our institution with confusion and lethargy. MRI of the head with contrast showed diffuse leptomeningeal enhancement without parenchymal lesions (Fig. 1A, B). A third LP was performed, and the patient was scheduled for meningeal biopsy (Table 1). Intra-operatively, multiple black and gray spots were visualized on the dura (Fig. 2). Pathology revealed a melanocytic neoplasm in the subarachnoid and Virchow-Robin spaces with significant atypia and a high mitotic index, consistent with a primary CNS melanocytic meningeal tumor or metastatic melanoma. A lesion on the patient’s right leg was concerning for melanoma; however, biopsy revealed a benign nevus. The patient was diagnosed with primary leptomeningeal melanocytosis. He received whole-brain radiation without neurologic improvement. Repeat head MRI on hospital day 45 demonstrated progression of disease (Fig. 1C, D). The patient died on hospital day 53.
3. Discussion In this young man from El Salvador with chronic meningitis, a broad differential diagnosis was considered, including infectious etiologies such as tuberculosis (TB) meningitis. However, based on the CSF findings, early meningeal biopsy was performed, establishing the diagnosis of leptomeningeal melanocytosis.
Case Reports / Journal of Clinical Neuroscience 21 (2014) 1054–1056
Table 1 Liver functions tests and pancreatic enzymes during the course of hospitalization
Day Day Day Day Day
1 (admission) 3 4 5 7 (discharge)
AST (U/L)
ALT (U/L)
Alkaline phosphatase (U/L)
Total bilirubin (mg/dL)
Amylase (U/L)
Lipase (U/L)
1115 785 330 100 35
1083 808 444 376 45
250 267 209 202 68
2.7 2.6 NA 2.6 2.7
439 324 NA 219 41
721 663 NA 310 153
ALT = alanine aminotransferase, AST = aspartate aminotransferase, NA = not available.
nal symptoms when seen by her primary care physician 4 months later. 3. Discussion This report illustrates the development of acute pancreatitis and elevated liver enzymes after rapid titration of oral LEV in a patient with no known risk factors. Possible causes of acute pancreatitis and hepatitis in adults are numerous and include infection, metabolic derangements, multisystem disease and hereditary, idiopathic or medication-related events. In the absence of objective evidence for an organic disease, a cause-relation argument points to LEV as the likely offender. In addition, this is also supported by the accelerated clinical and laboratory improvement after discontinuation of LEV. Abnormal liver function tests and pancreatitis were vaguely reported in post-marketing LEV experience in the drug prescribing information [2]. There was, however, no mention of the number of cases, LEV dosage, severity of condition, or natural course. To our knowledge the medical literature refers to a single case of acute pancreatitis, in an adolescent with autism. This occurred at a dose of 1000 mg of LEV and was preceded by complaints of intermittent abdominal pain when taking phenytoin, which could have been the initial trigger [3]. One other patient with fulminant liver failure was possibly attributed to a therapeutic dose of LEV [4]. The simultaneous occurrence of both pancreatic and hepatic abnormalities has not been reported to our knowledge.
Serious idiosyncratic adverse effects of newer AED are rare. They tend to occur during early titration periods and less commonly during maintenance periods. In our patient, the mild symptoms rapidly started after initiation of LEV, culminating in severe symptoms with rapidly escalating doses, suggesting both dose and time dependent relationships. It is also possible that drug toxicity may have contributed to this reaction which could possibly happen at higher therapeutic doses. This explanation is however less likely as no classic signs of clinical toxicity were present. In addition, LEV blood levels were unavailable to test this possibility. Conflicts of interest/disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication. References [1] Briggs DE, French JA. Levetiracetam safety profiles and tolerability in epilepsy patients. Expert Opin Drug Saf 2004;3:415–24. [2] Union Chimique Belge (UCB). Keppra prescribing information. Georgia:Union Chimique Belge; 2011. [3] Almeida DM, Jean MR, Chystsiakova A, et al. Levetiracetam-associated acute pancreatitis in an adolescent with autism: a case report. Pancreas 2013;42:177–8. [4] Tan TC, de Boer BW, Mitchell A, et al. Levetiracetam as a possible cause of fulminant liver failure. Neurology 2008;71:685–6.
http://dx.doi.org/10.1016/j.jocn.2013.10.002
Intraneural fibroma of the median nerve at the wrist Anthony M. Burrows a, Andrew L. Folpe b, Doris E. Wenger c, Robert J. Spinner a,⇑ a b c
Department of Neurologic Surgery, Mayo Clinic, 200 First Street SW, Gonda 8-214, Rochester, MN 55901, USA Department of Anatomic Pathology, Mayo Clinic, Rochester, MN, USA Department of Radiology, Mayo Clinic, Rochester, MN, USA
a r t i c l e
i n f o
Article history: Received 1 October 2013 Accepted 9 October 2013
a b s t r a c t Distal median neuropathy from carpal tunnel syndrome is the most well known lesion affecting the median nerve. Mass lesions may affect the nerve at the wrist. We present to our knowledge the first histologically confirmed case of an intraneural fibroma. Ó 2013 Elsevier Ltd. All rights reserved.
Keywords: Carpal tunnel Median nerve Peripheral nerve
⇑ Corresponding author. Tel.: +1 507 284 2376; fax: +1 507 284 5206. E-mail address: [email protected] (R.J. Spinner).
Case Reports / Journal of Clinical Neuroscience 21 (2014) 1054–1056
1. Case report A 36-year-old laborer presented to our clinic with a right wrist mass. The mass had initially developed rapidly 1 year prior to his presentation but the mass had remained stable in size since that time. After the mass developed, he reported intermittent paresthesias of the right thumb, index, middle, and occasionally, the ring finger. He had the additional history of bilateral median neuropathies relieved by bilateral carpal tunnel releases 8 years prior to his presentation. His mass was felt to be a ganglion cyst by another physician and was surgically explored 2 months prior to his presentation. This surgery was aborted when the mass was visualized and no biopsy was taken. On examination, his wrist had a large mobile mass proximal to the wrist crease with a small area of wound dehiscence (Fig. 1A). Tinel’s sign was present with percussion of the mass. He had 4/5 strength in opponens pollicis and abductor pollicis brevis but no extrinsic finger weakness. He had intact two point sensation in his radial digits. Electromyography showed right median neuropathy at the wrist, with both focal slowing and mild axonal loss across the mass. MRI demonstrated a mass in the median nerve with fascicles draped around the margins of the mass. It had a thick peripheral rim of low signal intensity. It had predominantly intermediate signal on T1-weighted images with minimal patchy internal
1055
enhancement. The mass demonstrated marked heterogeneous signal on T2-weighted images (Fig. 1B, C). He underwent general anesthesia and tourniquet compression and his wrist was opened along the axis of the mass and utilizing the previous carpal tunnel scar. The median nerve was identified proximally and followed around the mass through the carpal tunnel with a thickened epineurium. A plane around the mass was developed preserving the displaced fascicles (Fig. 1D, E). The mass was resected en bloc with no distinct neural origin. The thickened epineurium was resected as well. A complex skin closure was needed despite removal of the mass. The patient tolerated the procedure and had intact sensation and thumb abduction immediately following the procedure. Pathological evaluation showed a heavily collagenized, hypocellular, cytologically bland fibroblastic spindle cell proliferation showing limited expression of CD-34, but wihtout immunoreactivity to smooth muscle actins, S-100 protein, or the perineurial markers epithelial membrane antigen, GLUT-1, or claudin 1, consistent with a fibroma (Fig. 1F, G). 2. Discussion Carpal tunnel syndrome is the most well known cause of distal median neuropathy. Other intrinsic or extrinsic lesions affecting the median nerve at the wrist have been reported, including extra-
Fig. 1. (A) Pre-perative photograph. (B) T2-weighted axial MRI demonstrates heterogeneous signal with displaced fascicles (white arrows). (C) T1-weighted sagittal MRI shows displaced fascicles (white arrows) and heterogeneous content. (D) Intraoperative photograph showing the intraneural mass, the epineureum is reflected. (E) Intraoperative photograph. A traversing fascicle is secured with the superior vessel loop and the mass is being mobilized from the median nerve. (F) Gross sections of the mass show heterogeneous content. (G) The pathology specimen shows a heavily collagenized, hypocellular, cytologically bland fibroblastic spindle cell proliferation on hematoxylin and eosin staining (original magnification 5).
1056
Case Reports / Journal of Clinical Neuroscience 21 (2014) 1056–1058
neural tendon sheath fibromas, giant cell flexor sheath tumors, and intraneural lipomas [1–5]. Extraneural tendon sheath fibromas are an unrelated myeloproliferative process. In this patient, the mass arose intraneurally and developed rapidly with resulting median neuropathy. To the best of out knowledge, this is the first reported case of a histologically confirmed intraneural fibroma. Given these findings, intraneural fibromas should be included in the differential diagnosis of median neuropathy with a mobile wrist mass. Conflicts of interest/disclosures The authors declare that they have no financial or other conflicts of interest in relation to this research and its publication.
References [1] Okubo T, Saito T, Mitomi H, et al. Intraneural lipomatous tumor of the median nerve: three case reports with a review of literature. Int J Surg Case Rep 2012;3: 407–11. [2] Tiong WH, Ismael TS, Regan PJ. Fibroma of tendon sheath: a rare cause of carpal tunnel syndrome. J Hand Surg 2006;31:579–80. [3] Chalmers RL, Mandalia M, Contreras R, et al. Acute trigger wrist and carpal tunnel syndrome due to giant-cell tumour of the flexor sheath. J Plast Reconstr Aesthet Surg 2008;61:1557. [4] Evangelisti S, Reale VF. Fibroma of tendon sheath as a cause of carpal tunnel syndrome. J Hand Surg 1992;17:1026–7. [5] Garrido A, Lam WL, Stanley PR. Fibroma of a tendon sheath at the wrist: a rare cause of compression of the median nerve. Scand J Plast Reconstr Surg Hand Surg 2004;38:314–6.
http://dx.doi.org/10.1016/j.jocn.2013.10.002
Primary leptomeningeal melanocytosis presenting as chronic meningitis Michael C. Honigberg c,⇑, Efstathios Papavassiliou b,c, Yehuda Z. Cohen a,c a
Division of Infectious Diseases, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA Division of Neurosurgery, Department of Surgery, Beth Israel Deaconess Medical Center, Boston, MA, USA c Tosteson Medical Education Center, Harvard Medical School, 260 Longwood Avenue, Boston, MA 02115, USA b
a r t i c l e
i n f o
Article history: Received 17 October 2013 Accepted 18 October 2013
Keywords: CSF protein elevation Leptomeningeal melanocytic neoplasm Meningeal melanocytosis Primary leptomeningeal melanocytosis
a b s t r a c t We report a patient with primary leptomeningeal melanocytosis presenting as chronic meningitis. A previously healthy 27-year-old man presented with 2 months of severe headaches and photophobia. A lumbar puncture was notable for a highly elevated cerebrospinal fluid (CSF) protein level without pleocytosis. Imaging at the time of admission suggested only meningitis without the presence of parenchymal lesions. On the basis of the CSF findings, early meningeal biopsy was performed, leading to the diagnosis of a meningeal melanocytic neoplasm. Early meningeal biopsy should be considered in patients with meningitis when the CSF profile suggests the possibility of a central nervous system neoplasm. Ó 2013 Elsevier Ltd. All rights reserved.
1. Introduction Primary leptomeningeal melanocytosis is a rare central nervous system (CNS) neoplasm with an estimated incidence of 1 in 10 million [1]. It can have a variety of clinical presentations, including headache, neck pain, symptoms of increased intracranial pressure, focal neurologic deficits, and seizures [2,3]. We report a previously healthy young man who presented with chronic meningitis and was ultimately found to have primary leptomeningeal melanocytosis.
2. Case report A 27-year-old man originally from El Salvador was transferred to our hospital with confusion and 2 months of headache. Seven weeks previously, he had presented to an outside hospital with 2 weeks of severe headache as well as nausea, vomiting, and mild photophobia. A lumbar puncture (LP) was performed and the results are shown in Table 1. An infectious workup was negative. The patient was discharged with presumed aseptic meningitis. He continued to have daily headaches with nausea and vomiting. One week prior to admission, he presented to the same outside hospital and underwent a second LP (Table 1). A tuberculin skin ⇑ Corresponding author. Tel.: +1 703 980 4521; fax: +1 617 735 4527. E-mail address: [email protected] (M.C. Honigberg).
test was positive and cerebrospinal fluid (CSF) mycobacterial culture was sent. He was discharged without a clear diagnosis. Six days later, the patient was transferred to our institution with confusion and lethargy. MRI of the head with contrast showed diffuse leptomeningeal enhancement without parenchymal lesions (Fig. 1A, B). A third LP was performed, and the patient was scheduled for meningeal biopsy (Table 1). Intra-operatively, multiple black and gray spots were visualized on the dura (Fig. 2). Pathology revealed a melanocytic neoplasm in the subarachnoid and Virchow-Robin spaces with significant atypia and a high mitotic index, consistent with a primary CNS melanocytic meningeal tumor or metastatic melanoma. A lesion on the patient’s right leg was concerning for melanoma; however, biopsy revealed a benign nevus. The patient was diagnosed with primary leptomeningeal melanocytosis. He received whole-brain radiation without neurologic improvement. Repeat head MRI on hospital day 45 demonstrated progression of disease (Fig. 1C, D). The patient died on hospital day 53.
3. Discussion In this young man from El Salvador with chronic meningitis, a broad differential diagnosis was considered, including infectious etiologies such as tuberculosis (TB) meningitis. However, based on the CSF findings, early meningeal biopsy was performed, establishing the diagnosis of leptomeningeal melanocytosis.
