Lobe Atrophy Research Articles

Hepatocellular carcinoma: CT appearance of parenchymal changes after percutaneous ethanol injection therapy.

To evaluate the changes in surrounding liver parenchyma after treatment of hepatocellular carcinoma (HCC) and borderline malignant lesions with percutaneous ethanol injection (PEI). The authors reviewed the findings at computed tomography (CT) and CT during arterial portography (CTAP) obtained before and after PEI therapy for 32 lesions in 26 patients with HCC or adenomatous hyperplasia. Two surgically resected specimens were also histologically examined. In 10 (77%) of 13 lesions, decreased portal vein-related enhancement indicative of reduced portal blood flow in the periphery of the tumor was found at CTAP. Mild atrophy (concave liver surface), segmental atrophy, and lobar atrophy were found in 40%, 17%, and 3%, respectively. Histologic examination of the resected specimens revealed organized thrombi in the peripheral portal vein in the surrounding liver. PEI may cause decreased portal blood flow and atrophy in the noncancerous liver parenchyma that surrounds the tumor being treated.

Progressive language disorder due to lobar atrophy

Progressive language disorder due to lobar atrophy

Evaluation of Adaptive Changes by Non-Invasive Imaging in Hepatic Vein Outflow Obstruction

Hepatic vein outflow obstruction induces remarkable changes of intra–hepatic blood circulation; the significance of these changes remains uncertain. Six patients with obstruction of the hepatic veins were evaluated by duplex Doppler ultrasound and computed tomography. The adaptive changes secondary to obstruction were analyzed and their significance was correlated with the clinical findings. Four patients presenting unilateral hepatic vein occlusion had unilateral reversed portal flow. Two of them, with lobar liver atrophy and contralateral compensatory hypertrophy required operation; the other two, with normal appearance of the liver, benefitted from conservative treatment. Two patients with bilateral hepatic vein occlusion, intra-hepatic bypasses, bilateral lobar atrophy and caudate lobe hypertrophy, received operations. Intrahepatic unilateral portal flow reversal compensates for unilateral hepatic outflow obstruction. The combination of complete or subtotal hepatic vein obstruction and atrophy–hypertrophy complex predicates advanced disease despite flow reversal or spontaneous shunt.

Non-Alzheimer degenerative dementias

The explosion of research aimed at exploring degenerative dementias in the past 20 years has produced a great deal of knowledge concerning not only Alzheimer's disease but also other conditions referred to as non-Alzheimer degenerative diseases. The conditions reviewed here fall broadly into two main categories: diseases with focal (lobar) atrophy and diffuse Lewy body disease. These conditions, which are described more and more often in centers around the world, represent entities different from Alzheimer's disease not only from a clinical and pathological viewpoint, but also in terms of genetics and perhaps even in terms of therapeutic responses. In view of the numerous therapeutic trials currently underway, the distinction between Alzheimer's disease and non-Alzheimer degenerative diseases has acquired new importance.

What is needed for resective epilepsy surgery from a neurosurgical point of view?

Invasive versus non-invasive epileptogenic zone definition was analyzed in a series of 89 patients operated on for drug-resistant epilepsy. In the group of 69 cortical resections, 26% needed invasive recordings, 13.5% when foreign-tissue lesions had been detected by MRI and 32% when were absent. In this last group temporal resections had invasive EEG recordings in 23.5% versus 54.5% when the epileptogenic zone was extratemporal. In a group of 43 temporal resections with more than one year follow-up MRI has detected some abnormality in 84%. Excluding focal lesions, MRI detected hippocampal/temporal lobe atrophy in 66% of the cases in agreement with other noninvasive tests and in 4% contralateral to the epileptogenic zone located by subdural strips. The outcome analysis showed that 85% of the patients with MRI-EEG agreement were seizure free in contrast to only 43% when MRI was non-lateralizing. Future studies has to be oriented to better understand the epileptic process of patients without MRI abnormalities.

Absence of protease-resistant prion protein in dementia characterized by neuronal loss and status spongiosus.

Dementia characterized by neuronal loss and status spongiosus (DNLS) is a non-Alzheimer degenerative process which is characterized by Pick-like lobar atrophy with neuronal depletion and gliosis of the cerebral cortex, corpus striatum, medial thalamus, and substantia nigra and the absence of neuronal inclusions. To further investigate the cause and pathogenesis of DNLS, we probed cerebral homogenates from three cases of DNLS for protease-resistant prion protein to determine if DNLS could be a variant of a human prion disease. Limited proteolysis of prion proteins and guanidine thiocyanate treatment of cortical homogenates was used to enrich potential abnormal prion protein immunoreactivity. Although protease-resistant prion protein was detected in a case of sporadic Creutzfeldt-Jakob disease no abnormal prion protein was found in the cases of DNLS. We conclude that DNLS is not a human prion disease and remains an important dementia of uncertain etiology.

Liver parenchymal changes after transcatheter arterial embolization therapy for hepatoma: CT evaluation.

We retrospectively reviewed computed tomographic (CT) findings of 118 patients with hepatoma who received sequential follow-up CT after transcatheter arterial embolization (TAE). Thirty-five patients received TAE using Gelfoam particles with cisplatin, 37 patients using Gelfoam particles and iodized oil (Lipiodol) with cisplatin, and 46 patients using iodized oil with cisplatin. Liver atrophy was observed in 33 patients, lobarly or focally, depending on the embolized area. It was frequently associated with portal vein occlusion by the tumor, usage of iodized oil, and repeated embolization therapy. The lobar atrophy was seen in patients who had portal vein occlusion and/or received repeated embolization therapy. The focal atrophy was observed in patients who were administered iodized oil. Infarction developed in four patients who had a thrombus in the portal vein and received peripheral embolization therapy using iodized oil. We conclude that liver parenchymal changes occur frequently in patients who have portal vein occlusion and/or receive peripheral embolization using iodized oil.

Bilateral occipital calcification, epilepsy and coeliac disease: clinical and neuroimaging features of a new syndrome.

Twenty patients affected by bilateral occipital cortical-subcortical calcification (BOC) are described, 19 (95%) had epilepsy. In 8 of 16 cases studied, intestinal biopsy revealed coeliac disease. Fourteen patients had occipital partial epilepsy with a relatively benign outcome, while 4 patients were affected by a severe form of epilepsy, with very frequent, drug-resistant, generalised and partial seizures with mental deterioration. One patient had a single episode of convulsive status epilepticus at four months of age. The neurological examination was normal in all patients. CT showed flocculo-nodular, cortico-subcortical BOC, without enhancement and without lobar or hemispheric atrophy. MRI was normal. The clinical and neuroimaging features of these patients are different therefore from those with the Sturge-Weber Syndrome. The study confirms a high prevalence of coliac disease in patients with BOC, but the relationship between these two pathologies still needs to be clarified.

Progressive language dysfunction and lobar atrophy.

The patterns of language disorder associated with 'progressive aphasia' due to lobar atrophy were compared with the language dysfunction of patients with dementia of frontal lobe type (DFT). The progressive aphasias were characterised primarily by impairment at the structural levels of language: phonology, grammar and semantics, whereas DFT was associated primarily with spontaneity and loss of generative capability. However, there was overlap in language symptomatology, particularly with progression of disease. The findings lend support to the argument that progressive aphasia and DFT represent different clinical manifestations of a common pathology, and form part of the spectrum of lobar atrophies.

Dementia of frontal type and the focal lobar atrophies

Dementia of frontal type(DFT) and the other focal lobar atrophies challenge the clinician to assess patients with dementia thoroughly. DFT presents with characteristic behavioural and personality changes, and operational criteria have recently been devised to assist in the assessment and diagnosis. A significant proportion of cases present with functional psychiatric disorders including mood disturbance. Diogenes syndrome may be a variant of DFT. A number of syndromes associated with focal lobar atrophy of other brain regions have also been described, most common of these is primary progressive aphasia (PPA). Bedside cognitive and formal neuropsychological testing, and neuroimaging—both functional (SPECT) and anatomical—may assist in the diagnosis of these disorders. At post-mortem, non-specific atrophy is present; in DFT, the frontal lobes are affected, and in PPA, the focus of pathology is the dominant temporal lobe. Only a minority of cases show Pick cells and Picks bodies, in the remainder non-specifi...

Preliminary neurochemical findings in non-Alzheimer dementia due to lobar atrophy.

Non-Alzheimer's dementia due to lobar atrophy had choline acetyltransferase activities comparable with control rather than Alzheimer's disease values, based on 3 autopsy proven cases on Pick's disease and biopsies from 3 examples of dementia of frontal lobe type. Muscarinic cholinergic receptors were relatively spared only in Alzheimer's disease. Serotonin receptors were markedly reduced (based on Pick cases) whereas measures that reflected presynaptic serotonergic activity were either not affected or increased. Cerebrospinal fluid and brain tissue measurements suggested that inhibitory interneurones and dopamine release were relatively spared. There was no in vitro evidence of hypometabolism.

The clinical pathological correlates of lobar atrophy.

Three clinical syndromes associated with fronto-temporal cerebral atrophy, studied in one centre are discussed: dementia of frontal type (DFT), DFT and motor neurone disease (MND) and progressive aphasia (PA). The pathological findings in DFT (13 brains), DFT and MND (5 brains) and PA (5 brains) permit a number of clinical pathological groupings. The nosological status of fronto-temporal atrophy is discussed with reference to the literature and it is suggested that a common underlying pathology, including Picks disease as strictly defined by the presence of inclusion bodies, underlies the clinical syndromes, each being determined by the anatomical distribution of the pathology.

CT in lobar atrophy of the liver caused by alveolar echinococcosis.

We reviewed the CT findings of 13 patients with histologically proved alveolar echinococcosis of the liver. Seven of these patients had hilar involvement, which caused dilatation of intrahepatic bile ducts and invasion of the portal vein or portal branches. In two of these patients we found marked atrophy of the right lobe and in one patient marked atrophy of the left lobe in addition to various CT findings previously reported for alveolar echinococcosis of the liver. The occurrence of lobar atrophy of the liver caused by alveolar echinococcosis has not been previously reported. We concluded that, when a mass lesion with hilar infiltration causing lobar atrophy is found in endemic areas, alveolar echinococcosis should be considered in the differential diagnosis in addition to malignant neoplasms.

Clonorchis-associated cholangiocarcinoma: A report of two cases with unusual manifestations

Two cases of Clonorchis-associated cholangiocarcinoma are described along with their cholangio-graphic features to illustrate the spectrum of pathology ascribed to the injurious effects of the flukes on the bile duct epithelium. This includes adenomatous hyperplasia, extensive fibrosis, and carcinoma. The first case was also complicated by hepatic abscesses, left hepatic lobar atrophy, gastrobiliary and biliaro-cutaneous fistulae. The second case features an unusually dilated pancreatic duct containing pancreaticoliths that was found later to consist of hyperplastic bile duct epithelium, presumably carried by worm migration in the biliary tree. Liver sections from both patients showed typical features of hepatic clonorchiasis with the cancer. A knowledge of the wide spectrum of clinical presentation of clonorchiasis, particularly cholangiocarcinoma, might aid Western physicians in averting this serious sequela through prompt eradication of the helminthic infection and early recognition and treatment of its complications.

Liver Atrophy Associated With Monolobar Caroli′s Disease

The association of the atrophy-hypertrophy complex in monolobar Caroli’s disease (Type I) is reported in a 30 year old male who presented with recurrent cholangitis. Ultrasound and CT scan showed localised, right sided, saccular biliary dilatation in a normal sized liver. Severe right lobar atrophy was detected at operation and the resected right lobe weighed only 140 gms. Distortion of the hilar vascular anatomy and posterior displacement of the right hepatic duct orifice were problems encountered at surgery.

Non Alzheimer's disease forms of cerebral atrophy.

Some new and distinct cerebral disorders have emerged, which are much more common than previously supposed and those reviewed here comprise dementia frontal-lobe type (DFT), DFT and motor neuron disease (MND), lobar atrophy and diffuse Lewy body disease

Lobar atrophy with pontine neuronal chromatolysis (“ballooned” neurons)

A 64-year-old man developed progressive dementia over a period of 11 years. Postmortem examination showed severe atrophy of the temporal lobes of the brain with extensive neuronal loss and a remarkable alteration of the neuronal perikaryon—the “ballooned” neuron—restricted to the nuclei of the basis pontis. No neuritic plaques, neurofibrillary tangles, or Pick bodies were seen.

Lobar atrophy with dense-core (brain stem type) Lewy bodies in a patient with dementia

A 62-year-old man presented with memory impairment progressing over 6 years to dementia with near mutism and was diagnosed as having Alzheimer's disease. At autopsy his brain showed lobar atrophy suggestive of Pick's disease and there were spherical intracytoplasmic neuronal inclusions in the fascia dentata, hippocampal pyramidal cell layer, and temporal cortex. Unlike Pick bodies, however, the inclusions were eosinophilic with H&E stains, non-argyrophilic, and failed to react immunohistochemically with antibodies to paired helical filaments or Alz-50. They did label with antibodies to ubiquitin, however, and electron microscopy disclosed dense-cored granular structures with thin filamentous coronas which resembled brain stem-type Lewy bodies. The substantia nigra and locus coeruleus were not affected.

Lobar and segmentai atrophy of the liver

Lobar atrophy of the liver has been recognized as a complication of hepatic and biliary disease for many years. Previously regarded as rare and clinically unimportant, it is now accepted as reasonably common and clinically significant in many patients. Atrophy of liver lobes and, now, also segments, is much more frequently diagnosed because of the routine use of ultrasound and computed tomography scanning in the assessment of hepatobiliary disease, together with its recognition on angiograms and at laparoscopy.

Progressive aphasia due to lobar atrophy : J.S. Snowden, D. Neary, D.M.A. Mann. Department of Neurology, Manchester Royal Infirmary and Department of Pathology, University of Manchester, Manchester M13 9WL, England.

Progressive aphasia due to lobar atrophy : J.S. Snowden, D. Neary, D.M.A. Mann. Department of Neurology, Manchester Royal Infirmary and Department of Pathology, University of Manchester, Manchester M13 9WL, England.