Neville Russell

Cellular Blue Nevus (“Melanocytoma”) of the Spinal Meninges: Electron Microscopic and Immunohistochemical Features

A primary cellular blue nevus (melanocytoma) of the spinal canal in a 21-year-old woman is reported. Light microscopic examination revealed a melanotic neoplasm with histological patterns resembling schwannoma, dermal nevi, and neuroblastic-like tumor. The ultrastructural features of the neoplastic cells were similar to those in dermal blue nevi and melanomas. There was no evidence of arachnoidal cell differentiation. Immunohistochemistry revealed positive reactions for S-100 protein and neuron-specific enolase in many cells and no reactions for glial fibrillary acidic protein, cytokeratins, epithelial membrane antigen, 70-kD neurofilament protein, or Leu-7. Vimentin was strongly positive in the melanocytic cells as well as in the arachnoidal cells of involved meninges. The ultrastructural and immunohistochemical features support the nevoid nature of this tumor, which is frequently mislabeled as melanotic meningioma.

Intracarotid Chemotherapy with a Combination of 1,3-Bis(2-chloroethyl)-1-nitrosourea (BCNU), cis-Diaminedichloroplatinum (Cisplatin), and 4'-O-Demethyl-1-O-(4,6-O-2-thenylidene-β-D-glucopyranosyl)epipodophyllotoxin (VM-26) in the Treatment of Primary and Metastatic Brain Tumors

Thirty-seven patients with intracranial primary or metastatic tumors were treated with an intraarterial combination of BCNU, cisplatin, and VM-26 to determine the efficacy, toxicity, and maximal tolerated doses for the combination. A transfemoral fluoroscopic approach was used to catheterize temporarily the internal carotid or vertebral artery. Thirteen of 19 (68%) evaluable primary brain tumors and 9 of 16 (56%) evaluable brain metastases responded. The response rate was lower in patients previously treated with both cranial irradiation and i.v. chemotherapy than in patients less heavily pretreated (54% vs. 82%), although even patients previously treated i.v. with all three of the study drugs responded. All five patients with both extracranial and intracranial evaluable tumor deposits experienced a greater response of their intracranial than of their extracranial tumor. Ipsilateral retinal and neurological toxicity were dose-limiting, with major toxicity (permanent decreased vision or hemiparesis) occurring in five of nine (56%) patients receiving doses of BCNU greater than or equal to 100 mg/m2 plus cisplatin, 60 mg/m2 plus cisplatin, 60 mg/m2, plus VM-26, 175 mg/m2. Only 9% of the patients treated with a lower VM-26 dose developed permanent severe toxicity, and the doses that we now recommend are: BCNU, 100 mg/m2; cisplatin, 60 mg/m2; and VM-26, 150 mg/m2. The response rate was also dose-related (100% at the highest doses tested vs. 57% at the lower doses).(ABSTRACT TRUNCATED AT 250 WORDS)

Intraparenchymal epithelial (Enterogenous) cyst of the medulla oblongata

Intraparenchymal solitary cyst of the medulla oblongata was diagnosed on MRI examination in a 66-year-old woman with a nine year history of progressive brainstem dysfunction and three negative CT scan examinations. Craniotomy and drainage of the cyst to the IVth ventricle led to remarkable clinical recovery. Biopsy of the wall of the cyst revealed an epithelial lining with tonofilaments, desmosomes and surface coating on ultrastructural examination. Immunohistochemistry demonstrated positive reactions of epithelium for keratins, cytokeratins, epithelial membrane antigen and Ulex Europeus lectin, indicating endodermal origin of the cyst.

Cisplatin plus cytosine arabinoside in adults with malignant gliomas

SummaryA combination of cisplatin and cytosine arabinoside was used to treat 21 patients with glioblastomas and 5 patients with recurrent grade 11 gliomas. Cisplatin 60–100 mg/m2 was given I.V. in 250 ml 0.45% saline and preceded by 500 ml dextrose 5% in 0.45% saline. Mannitol 50 g was given I.V. concurrently with the cisplatin. Cytosine arabinoside 500–1000 mg/m2 was given by rapid I.V. infusion immediately after the cisplatin. Of 25 evaluable patients, 10 (40%) experienced objective tumor shrinkage on CT scan, and 6 (24%) stabilized. There were 2 complete remissions. Patients who had had no prior treatment had a higher response rate (58%) than those previously treated (23%). Myelosuppression occurred in some patients 2–3 weeks after treatment. Gastrointestinal toxicity (vomiting and diarrhea) was dose-limiting. Two patients had possible neurological toxicity. Recommended doses for further studies are cisplatin 90 mg/m2 and cytosine arabinoside 900 mg/m2.

Combined intraommaya methotrexate, cytosine arabinoside, hydrocortisone and thio-TEPA for meningeal involvement by malignancies

Twenty-three adult patients with meningeal involvement by a variety of malignancies were treated with the intra-Ommaya combination of methotrexate, hydrocortisone, cytosine arabinoside, and thio TEPA. Whole brain irradiation was also administered to most patients who had not previously received it. Most patients demonstrated improvement of cerebrospinal fluid parameters, but only 50% of the patients experienced neurological improvement. Patients who did not receive cranial irradiation and performance status 4 patients were less likely to respond than were patients who did receive cranial irradiation as part of their treatment and patients who were performance status 0–3. Four patients developed possible and 2 patients developed probable or definite serious neurological complications. Another 4 patients developed less severe, reversible neurological toxicity. It is possible (but still uncertain) that this regimen is more toxic than other less intensive regimens, and further studies should be undertaken cautiously.

Feasibility study of intraarterial vs intravenous cisplatin, BCNU, and teniposide combined with systemic cisplatin, teniposide, cytosine arabinoside, glycerol and mannitol in the treatment of primary and metastatic brain tumors

Sixteen patients with intracerebral tumors received intraarterial cisplatin, teniposide, and BCNU combined with intravenous cisplatin, teniposide, and cytosine arabinoside. Oral glycerol and intravenous mannitol were given along with the intravenous chemotherapy in an attempt to increase drug delivery to tumor by augmenting tumor blood flow. Thirteen additional patients were treated with the same regimen, but received all the chemotherapy intravenously. Of the 16 patients receiving intraarterial chemotherapy (median survival, 14 weeks), none responded, 5 (31%) were stable for > 8 weeks, 8 (50%) failed, and 3 (19%) were unevaluable due to early death. Of the 13 patients receiving all their treatment intravenously (median survival, 13 weeks), 3 (23%) responded, 1 (8%) was stable, 7 (54%) failed, and 2 (15%) were unevaluable due to early death. In the patients receiving intraarterial chemotherapy, toxicity included ipsilateral retinal toxicity (2 patients), ocular pain or headache (10), periorbital swelling and flushing (6), increased brain edema with focal neurological deficits and drowsiness (5), and catheter-related carotid artery thrombosis followed by fatal herniation (1). Myelosuppression was worse in patients who received all their treatment intravenously than in those receiving intraarterial chemotherapy (p < 0.05). Neutropenic sepsis developed in 4 patients on the intraarterial arm (1 fatal) and in 5 patients on the intravenous arm (2 fatal). Other toxic effects were similar whether or not patients received intraarterial treatment or only intravenous treatment. Overall, toxicity of this regimen was excessive, and response rates were lower than would have been expected with single agent therapy.

Hypopituitarism resulting from an intrasellar carotid aneurysm.

We report a 74 year old lady who presented with an exceedingly rare combination of an internal carotid artery aneurysm which was almost entirely intrasellar and associated with hypopituitarism but no neurological deficits. Such a lesion could be misdiagnosed as a pituitary tumour with serious consequences, if surgery is attempted without prior carotid angiography.

Epidural hematoma: report of seven cases with delayed evolution of symptoms.

Epidural hematomas occasionally have a prolonged clinical course with gradual evolution of the neurologic symptoms. Seven such cases are reviewed in this report. Although the clinical course is insidious, there are certain features which should signal the presence of a slowly expanding hematoma. After an apparently minor head injury, the patient who is usually in the younger age group, develops headache. This persists and is accompanied by other non-specific neurologic symptoms which may lead to a mistaken diagnosis of post-concussion syndrome. Papilledema and focal neurologic deficits eventually appear. Definitive diagnosis is made by the CT scan, although contrast enhancement may be necessary to confirm the nature of the lesion. The treatment is craniotomy and evacuation of the hematoma before serious neurologic deterioration occurs.

Atypical subependymoma of the spinal cord: ultrastructural and immunohistochemical studies.

A 76-year-old woman with a 2-year history of progressive weakness of the left arm and leg underwent a laminectomy for an intradural, extramedullary, pedunculated subependymoma involving the meninges and spinal nerve roots at C7-T1. Eight months later, another operation was necessary for an intramedullary neoplasm at C3-T4. This latter tumor consisted of small, poorly developed cells, large atypical astrocytes, and ependymal cells. Neither ependymal rosettes nor papillary formations were present. Ultrastructural studies showed some features of ependymal differentiation of the large astrocytic cells. This case illustrates an unusual pattern of extramedullary and intramedullary presentations of subependymoma and a spectrum of cellular differentiation of neoplastic subependymal glia.

Interhemispheric subdural hematoma

Although relatively uncommon, interhemispheric subdural hematoma (ISDH) occurs more frequently than was suspected before the advent of computerized tomographic (CT) scanning. When its mass is sufficiently large to compress the medial cerebral hemisphere, specific focal neurological abnormalities may occur. These include weakness of the contralateral leg, or contralateral hemiparesis with the leg being weaker than the arm. On the unenhanced CT scan ISDH is seen as a crescent shaped, midline hyperdensity. Treatment is dictated by the clinical course. Evacuation of the hematoma by parasagittal craniotomy is recommended if the symptoms are pronounced.