Craniopharyngiomas are histopathologically classified as adamantinomatous type (AD) and squamous‐papillary type (SP). However coexistence of a mixed type seen on histopathologic specimens has not been reported. In this report, a patient diagnosed with mixed type craniopharyngioma is presented and the etiology and pathologic features are discussed.
Increased creatine kinase isoenzyme BB (CK-BB) has been observed in sera from patients with brain injuries and occasionally in sera from patients with malignancy. We report here that, in two patients with giant cell tumor of bone (GCT), preoperative serum CK-BB increased to approximately 20 and 90 U/L, but in postoperative serum the CK-BB decreased to normal values. That the tumors contained CK-BB was indicated by electrophoretic analysis and immunohistochemical staining. Furthermore, serum CK-BB was detectable in five additional cases of GCT and in cultured tumor cells from a patient with GCT by an electrophoretic method. These results suggest that CK-BB may be a marker for GCT.
An 8-year-old boy presented complaining principally of headache and vomiting. A single large cystic lesion extending from the suprasellar region to the ventral brainstem was identified, and total extirpation was performed via a right orbitozygomatic, transtemporal transchoroidal fissure approach. The cyst contents resembled motor oil, and no strong adhesions were identified between the tumor and the surrounding tissue except at the site of origin of the tumor, allowing easy dissection. The tumor originated at the junction of the adenohypophysis and the pituitary stalk. Although the histopathological diagnosis was adamantinomatous craniopharyngioma, the cyst walls comprising the majority of the tumor were not thin, fragile tissues formed by squamous metaplasia, but were thick and robust, bearing a close resemblance to unicystic ameloblastoma mixed with solid tissue. The existence of this type of cyst wall represents corroborating evidence that craniopharyngiomas are derived from the oral primordium. The existence of such tumors that can be totally extirpated in a single procedure while preserving hypothalamo-pituitary function may be taken as a warning not to rush at random to perform treatments that might encourage recurrence or regrowth by carrying out cyst fenestration and drug injection with the addition of stereotactic radiotherapy.
The purpose of this study is to determine if intrathecal 2% tetracaine (TC) causes histological changes by its neurotoxicity, and to examine the relationship between the lesions and neurological functions. Twenty-two rats received either 2% TC or 0% TC dissolved in 10% glucose, via an intrathecal catheter terminated at T 13 level. Neurological deficits were evaluated by rat's behavior and paw stimulation test (UCSF). Five days after drug administration, the L 1 spinal cord with the anterior and posterior roots and cauda equina were excised for light and electron microscopy. Four rats out of 8 in 2% TC group showed mild pathological changes induced by neurotoxicity mainly in the posterior roots and slightly in the posterior column. However, there were no significant differences in sensory and behavioral function between the rats who had received 2% TC with lesion and the others with no lesion. As many rootlets enter one segment of the spinal cord, mild and restricted lesions may be difficult to detect by sensory tests. These findings may explain the fact that the patients with transient neurologic symptoms (TNS) are normal by neurological tests.
For the purpose of histopathological diagnosis, so-called “invasive meningioma” is defined as a meningioma that has infiltrated the cerebral parenchyma, and such cortical infiltration raises the risk of recurrence. However, as the definition of “invasive” remains far from clear, we have attempted to redefine it. Tumors that were completely removed from 32 patients between April 2005 and September 2015 and that had been diagnosed as so-called “invasive meningioma” were classified by World Health Organization grade (Group I–III), and then further classified as: true invasion, involving invasion of the brain with breakdown of the pia mater; and pseudo-invasion, involving encroachment into the brain with the pia mater still intact. We then investigated recurrence rates in the brain or dura mater for each group. Rate of recurrence in the brain or dura mater was significantly higher for Group I meningioma classified as true invasion compared to that of the same group classified as pseudo-invasion. We redefined so-called “invasive meningioma” as Group I meningioma exhibiting true invasion, and considered that, when possible, wide resection of the areas of adhesion to the dura mater in addition to tumor extirpation along with the cerebral parenchyma increased the success rate for curative treatment.
Fibrous or transitional meningioma and solitary fibrous tumor (SFT) are frequently difficult to differentiate from each other on the basis of histopathology. It is extremely unusual for a meningioma to exhibit diffuse, strongly positive immunoreactivity for cluster of differentiation 34 (CD34), and this has never been previously reported from a histopathological specimen. A patient with transitional meningioma that exhibited strongly positive for CD34, which has been regarded as characteristic of SFT and is considered to be useful for distinguishing the latter from meningioma, is reported.
Up to now diffuse white matter demyelination of the cerebrum has been reported in only a few cases of mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS). Here we document an autopsy case with this rare neuropathology. Most MELAS cases are diagnosed antemortem by A3243G transition of mitochondrial DNA. While cerebral damage including necrotic foci in the cerebral cortex are common findings in MELAS, prominent white matter involvement best characterizes this MELAS case. There were numerous necrotic foci, varying in size and chronological stage, in the cerebral white matter. In the areas of the white matter without necrotic foci, there was diffuse fibrillary gliosis with the loss of axons and oligodendrocytes. The gliosis was dominant in the deep white matter, sparing the U-fiber. The cerebral cortex showed diffuse cortical atrophy with few scattered necrotic foci. Distribution of the cerebral lesions does not coincide with the territory of blood supply. The vascular wall presented only slight to mild hyalinosis. We assumed a common pathogenesis to the cortical lesions and the white matter change. The pathogenesis of the present diffuse cerebral lesions may not be just secondary to circulatory disturbance but partly due to metabolic abnormality.
Craniopharyngioma is a benign tumor. However, sometimes, this tumor may recur repeatedly even after apparent total resection. This study investigated the requirements for ideal radical treatment, based on a discussion of the long-term clinical course and pathological findings in surgical patients.We performed 81 surgical procedures for 67 patients with craniopharyngioma between February 1990 and December 2015. We classified patients into Groups I-III according to emphasis of surgery in chronological order, so we investigated the tumor recurrence rate and the necessity for postoperative hormonal replacement.Multiple comparison of results from the three groups found significant differences in recurrence rate between Groups I and II (P = 0.0111) and Groups I and III (P = 0.0056). Although there were no differences in recurrence rate between Groups II and III, mortality rate of Group III was lower than that of Group II. No significant difference was seen between any group in terms of hormonal replacement.These results strongly suggest that the radical resection used to treat patients in Group III should be given priority as the procedure for removing craniopharyngioma.
