A review of the neuroimaging studies of alcoholism]

In this article, we reviewed brain damage seen in patients with alcohol dependence briefly focusing on neuroimaging studies. In uncomplicated alcoholic patients, a high incidence of cortical shrinkage and ventricular dilatation were reported using brain CT scans. In older alcoholics, prefrontal gray matter deficits were especially marked when compared with younger alcoholics. Reversibility of brain shrinkage is a common neuroimaging finding in patients with alcohol dependence and a study by Gazdinski et al. reported more rapid brain tissue gain during the first month of sobriety than in the following months. Another MRI study using deformation-based morphometry revealed significant shrinkage in the frontal and temporal lobes within 1 week of abstinence of alcoholic patients. This study followed participants for 8 months longitudinally and revealed that abstaining alcoholics recovered tissue volumes significantly faster than nonalcoholic controls in the parietal and frontal lobes and this study also revealed that when abstaining alcoholics were compared with relapsed alcoholics, additional regions with significantly greater recovery in abstainers were the temporal lobes, thalamus, brainstem, cerebellum, corpus callosum, anterior cingulate, insula, and subcortical white matter. Finally we introduced a MR spectroscopy (MRS) study on alcoholic patients. This study using proton MRS indicated that with short-term abstinence, cerebellar choline and frontomesial N-acetylaspartate (NAA) were significantly increased. Findings showing that a cerebellar choline increase and a frontomesial NAA increase were detected at stable water integrals and creatine concentrations, serum electrolytes and red blood cell indices suggest that early brain recovery through abstinence does not simply reflect rehydration. This might indicate that even the adult brain has capacities for regrowth and further understanding of the mechanisms of recovery of alcoholics' brains may result in a valuable model of brain regeneration with relevance for other disorders.     

Pontine glioblastoma multiforme initially presenting with leptomeningeal gliomatosis

A 49-year-old female presented with diffuse leptomeningeal gliomatosis as the initial manifestation of pontine glioblastoma. Magnetic resonance imaging initially revealed diffuse leptomeningeal enhancement caused by metastatic deposits, predominantly along the basal cistern and bilateral sylvian fissures. The primary pontine lesion appeared as hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging, but with no enhancement by gadolinium-diethylenetriaminepenta-acetic acid. There was no diffuse enlargement of the pons. The patient died 11 months after the initial presentation. The primary lesion in the pons was histologically confirmed at autopsy. Diffuse enhancement of leptomeningeal dissemination may occur as the initial manifestation of non-enhanced pontine glioblastoma.     

Apoptosis and microglial activation in influenza encephalopathy

During influenza epidemics in Japan, the number of children with acute encephalopathies and encephalitis has recently increased. Although the pathophysiologies remain unclear, there is usually brain edema with evidence of damage to the blood-brain-barrier (BBB). We investigated the glial reaction and apoptosis in brains of eight such cases comprising two of acute necrotizing encephalopathy and six of influenza encephalopathy, and compared the results with those in five control brains. Apoptosis, evidenced by chromatin condensation and fragmentation in hematoxylin sections, in situ end labeling of fragmented DNA (TUNEL) and DNA laddering, was observed in neurons and glial cells in four brains with influenza encephalopathy. In the TUNEL-positive brains, the increase in microglia was greater than in the TUNEL-negative brains. Immunoreactivity for active-caspase 3, demonstrated by immunohistochemistry, and the overexpression of a caspase-cleaved fragment of poly(ADP-ribose) polymerase, demonstrated by Western blotting, indicated that activation of caspase 3 is involved in the apoptotic pathway in the brains of influenza encephalopathy cases. Apoptosis or specific pathological processes that cause apoptosis may give rise to aggravated encephalopathy.     

Apocrine carcinoma of the vulva in a band-like arrangement with inflammatory and telangiectatic metastasis via local lymphatic channels

BACKGROUND: Primary adenocarcinomas of the vulva have been classified as sweat gland carcinomas, extramammary Paget's disease, and primary breast carcinomas of the vulva. They share some common histopathologic features. METHODS: We describe a 72-year-old Japanese woman with apocrine carcinoma of the vulva and local lymphatic metastasis. RESULTS: The patient presented with a bruise on her inguinal area. Physical examination revealed a 4 cm x 7 cm, dark-red, irregularly elevated tumor on the left labium majora. Dome-shaped, flesh-colored, small papulovesicles were scattered on the abdomen, accompanied by erythema and induration. The lesion showed a band-like arrangement. General examination revealed multiple bone metastases, particularly in the spine. Microscopic examination revealed a moderately differentiated adenocarcinoma with signet ring cells. A few pagetoid clear cells were present in the hypertrophic epidermis. The peripheral papulovesicles demonstrated the same histopathologic view as in inflammatory and telangiectatic, metastatic breast carcinoma. Tumor cells were positive for various ductal and glandular markers. Estrogen and progesterone receptors were not expressed. Ultrastructural findings suggested differentiation towards apocrine or mammary glands because of the presence of an apocrine process and electron-dense mucous granules. The patient died in spite of combination chemotherapy and irradiation therapy. CONCLUSIONS: We report a rare case of apocrine carcinoma of the vulva in a band-like arrangement with local lymphatic metastasis which showed the clinical and histopathologic characteristics of inflammatory and telangiectatic carcinoma.     

Intrinsic angiotensin II-generating system in human pancreatic cancer tissues

To clarify whether an intrinsic angiotensin II-generating system exists in human advanced pancreatic cancer tissues, we measured angiotensin II concentration and angiotensin converting enzyme (ACE) activity in tissues of normal pancreas, pancreatic cancers, colon cancers and hepatocellular carcinomas. After the surgically resected specimens were homogenized, angiotensin II concentration and ACE activity in tissues were measured using the florisil method and Kasahara's method, respectively. Tissue angiotensin II levels in pancreatic cancers (n = 13) were significantly higher than those of normal pancreas (n = 7), colon cancers (n = 7), or hepatocellular carcinomas (n = 7). However, there was no significant difference in tissue ACE activity between them. This study provides in vivo evidence of ACE-independent angiotensin II-generating system in human pancreatic cancer tissues and suggests that this locally-formed angiotensin II influences the microenvironment of pancreatic cancer tissues in a paracrine fashion.