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Table 1 Pediatric case reports of primary leptomeningeal melanoma and neoplastic meningitis mimicking tuberculous meningitis

From: NRASQ61K mutated primary leptomeningeal melanoma in a child: case presentation and discussion on clinical and diagnostic implications

Reference Makin, 1999 Nicolaides, 1995 Selcuk, 2008 Demir, 2010 Kosker, 2014 Erdogan, 2014 Our patient
Diagnosis Primitive leptomeningeal melanoma Primitive leptomeningeal melanoma Atypical Teratoid Rhabdoid Tumor Spinal low-grade neoplasm Primary diffuse leptomeningeal gliomatosis Primary spinal leptomeningeal gliomatosis Primitive leptomeningeal melanoma
Age and Sex 5,5 years, Male 5 years, Male 6 years, Female 8 years, Female 3 years, male 3 years, male 2 years, Female
Onset signs and symptoms 13-week history of headaches, vomiting, and weight loss followed by acute deterioration of conscious level 3-month history of vomiting, anorexia, and weight loss, 1-month history of headaches and pyrexia, acute deterioration of conscious level 2-months history of confusion, headache, vomiting, aphasia, and right
History of headache, nausea, fever, and vomiting, followed by double vision 3-month history of strabismus and 1-week history of headache and restlessness Deviation of left eye, weakness, lack of appetite, headache and behavioral change 1-week history of vomiting
Imaging at onset CT: diffuse meningeal enhancement CT: diffuse meningeal enhancement MRI: marked leptomeningeal involvement and basal meningitis MRI: communicating hydrocephalus, diffuse leptomeningeal
enhancement at basal cisterns
MRI: leptomeningeal infiltration, prominent around the Sylvian fissure and at the level of the basal cisterns MRI: diffuse leptomeningeal enhancement, predominantly involving the basal cisterns and hydrocephalus MRI: enhancement of the cervical and basal meninges and cranial nerves, in addition to a small focal enhancement anterior to the pons
CSF analysis at onset - Protein 1.5 g/dL
- Glucose 0.7 mmol/L
- No cells
- Protein 1.5 g/L
- Glucose 0.5 mmol/L
(serum glucose 5 mmol/L)
- Leukocytes 36/mm3
- Protein 40.8 mg/dL
- Glucose 36 mg/dL
(serum glucose 136 mg/dL)
- Lymphocytes 350/mm3
- Protein 242 mg/dL
- Glucose 74 mg/dL
(serum glucose 116 mg/dL)
- 10 × 5 cells (60 % lymphocyte, 40 % PMNL)
- Protein 9.2 mg/dL
- Glucose 102 mg/dL
(serum glucose 136 mg/dL)
- Leukocytes 470/mm3 (90 % lymphocyte, 10 % PMNL)
- Protein elevated
- Glucose normal
- Protein 62 mg/dL
- Glucose 83 mg/dL
(serum glucose 133 mg/dL)
- Leukocytes 2/mm3
CSF cyto-morphological examination ND - 1st sample: negative
- 2nd sample: positive for malignant cells
Negative ND Negative Negative - 1st sample:
- 2rd sample: positive for malignant cells
Time delay between onset of symptoms and definitive diagnosis 3 months 3 months UNK 4 months 10 months 4 months 10 weeks
Chemotherapy Vincristine, carboplatin, and etoposide Chemotherapy according to local protocol (not specified) Not done (parent’s refusal) Cisplatin and etoposide; radiotherapy Vincristine, carboplatin, and etoposide; (parents refused radiotherapy) Vincristine and carboplatin Temozolomide, cis-platinum, vindesina and peginterferon alfa-2b; radiotherapy
Outcome Dead 6 months after diagnosis Unknown Dead 3 months after onset Alive after 19 months follow-up Alive after 18 months follow-up Unknown Dead 11 months after diagnosis
  1. CSF, cerebrospinal fluid, CT computed tomography, MRI magnetic resonance imaging, ND not done, UNK unknown, PMNL polymorphonuclear leukocytes