Yoshiho Honda

The long-term growth rate of residual acoustic neurinomas

SummaryThe growth rate of 19 residual acoustic neurinomas was examined in a long-term follow-up study (median, 10 years; range, 5 to 17 years) following intracapsular removal. Of these, 10 (53%) had regrowth, three (16%) showed regression, and six (32%) were unchanged. The 10 acoustic neurinomas showing regrowth were divided into two categories, either solid or cystic, according to computed tomographic findings. Five acoustic neurinomas with cyst formation showed rapid regrowth, with the tumour doubling time ranging from 0.15 to 5.0 years (median, 4.5 years), and required re-operation. Five solid tumours showed slow regrowth, with the tumour doubling time ranging from 9 to 34 years (median, 15 years). Although cyst formation is a major factor in rapid regrowth, residual acoustic neurinomas without cyst formation have a slower growth potential. In this study, 74% of the residual acoustic neurinomas have never required re-operation. It is advisable to choose intracapsular removal if there is major risk of neurological deficits.

Long-term follow-up of the residual intracanalicular tumours after subtotal removal of acoustic neurinomas

SummaryWe examined growth potential of residual intracanalicular tumours left from subtotal removal of large acoustic neurinomas. Eleven patients were followed-up by magnetic resonance (MR) imaging. The interval between surgery and MR study ranged from 12 to 29 years (median, 16 years). MR images of two patients showed no evidence of tumour remnant, and in six a small tumour was localized in the internal auditory canal. The other three showed an intracanalicular tumour protruding slightly towards the intracranial portion. This result suggests that the intracanalicular residual tumours have less risk of regrowth after subtotal removal of acoustic neurinomas. It is advisable to choose intracapsular subtotal removal without opening the internal auditory canal in the treatment of acoustic neurinoma, if it is large in size and there is a high risk of nerve injury.

The occurrence of catecholamine neurons in a parietal lobe ganglioglioma

A parietal lobe ganglioglioma in a 2‐year‐old girl was investigated ultrastructurally and immunohistochemically, using antiserum against tyrosine hydroxylase (TH), a rate‐limiting enzyme of the catecholamine (CA)‐synthesizing pathway. The tumor was composed essentially of neuronal and astrocytic cells. Ultrastructurally, numerous dense core vesicles measuring between 56 nm and 136 nm (mean, 90 nm) in diameter were observed in the neuronal cytoplasm and processes. The fact that the TH immunohistochemistry revealed many positive neuronal cells in the tumor tissue was of considerable interest. The implications and possible significance of the presence of CA neurons in this ganglioglioma are discussed.

Pleomorphic xanthoastrocytoma: New ultrastructural observations

A 58 year old woman presented with a right frontal lobe cystic mass diagnosed as pleomorphic xanthoastrocytoma (PXA), in which a reticulin fiber network was not evident but prominent vasculature was noted (angiomatous variant). The patient had a 36 year history of epileptic seizure which had been relatively well controlled with anticonvulsants. An ultrastructural study revealed that the neoplastic astrocytes occasionally contained filamentous inclusions identical to Hirano bodies in their cytoplasm and that, at the periphery of the tumor, pre‐existing axon terminals and synaptic junctions were found in close proximity to neoplastic astrocytes. The former may represent a degenerative process in the constituent neoplastic astrocytes and the latter appears to be of interest when considering the epileptogenic lesions associated with this type of benign tumor.

An anaplastic cytokeratin‐immunopositive xanthomatous tumor involving the pharynx and clivus of a child: An ultrastructural and immunohistochemical study

An autopsy case of an anaplastic xanthomatous tumor involving the pharynx and clivus in a 2 year old girl was investigated ultrastructurally and immunohistochemi‐cally. The tumor was manifested as an epi‐ and subdural mass in the posterior cranial fossa involving the pharynx and clivus. The tumor showed an interlacing fascicular and pleomorphic pattern. The tumor cells contained numerous intermediate filaments, which were mainly tonofilaments, and lipid droplets, but did not have junctional complex. Immunohistochemically, most of the tumor cells were positive for cytokeratin, epithelial membrane antigen and vimentin, and some tumor cells were positive for myoglobin and a‐1 antichymotrypsin, but negative for S‐100, CD‐68 and glial fibrillary acidic protein. These findings suggest that this tumor was derived from epithelial cells, and showed xanthomatous appearance. A discussion of its differential diagnosis was conducted.

Regional Cerebral Blood Flow in Patients with Ischemic Cerebrovascular Disease

Regional cerebral blood flow (rCBF) was measured in 25 patients with transient ischemic attacks (TIA) and 34 patients with reversible ischemic neurological deficits (RIND) or ischemic strokes with full recovery. The rCBF measurements were performed by means of the 133Xe intracarotid injection method, using a scintillation camera and an on-line computer system. The rCBF data were analysed and compared with the computed tomography (CT) and angiographic findings on each patient. There was no significant difference in the average of the mean hemispheric values of rCBF (mean CBF) between TIA and RIND. The averages of mean CBF of TIA or RIND were significantly lower than those of the normal controls, and higher than those of the completed strokes. There was no correlation between the elapsed time from the last attack and the mean CBF in TIA. There was also no correlation between the elapsed time from the onset, or between the presence or absence of hemiparesis and the mean CBF in RIND. CT showed lacunae in 24% of TIA and 32% of RIND, whereas a cortical low density area was shown in only one case in each group. Angiographic abnormalities were found predominantly in the intracranial major arteries, rather than the extracranial carotid artery in both groups. Six patients of TIA (24%) and 6 of RIND (18%) had involvement of their extracranial internal carotid artery. There was no correlation between the mean CBF and angiographic findings. Although the mean CBF did not correlate to CT findings in TIA, it was significantly lower in RIND patients with lacunae on CT scans. Hemispheric pattern of flow distribution (HPFD) was disturbed in 88% of TIA and 74% of RIND. Focal ischemia was shown in only one case with RIND, whereas diffuse ischemia was shown in 2 cases with TIA and 5 cases with RIND. Loss of the hyperfrontal pattern which was thought to represent a mild diffuse cerebral dysfunction, was shown in 44% of TIA and 29% of RIND. Because diffuse involvement of HPFD was shown without reference for the elapsed time from the last attack of TIA or the onset of RIND, the authors support the ‘hemodynamic’ theory as opposed to ‘microembolic’ theory as the cause of TIA or RIND. It is concluded that TIA and RIND have the same causative factors, and the clinical difference of TIA and RIND is the only difference in recovery times between TIA and RIND.