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PubMed1977

Effects of low- and high-passage influenza virus infection in normal and nude mice.

A human isolate of type A Hong Kong influenza virus (H3N2) was adapted to mice by serial passage. Lung homogenates from mice who received low passage levels contained about the same quantity of virus (10(6.2-6.95) 50% tissue culture infective doses/ml) as those from mice who received high passage levels (10(5.95-6.45) 50% tissue culture infective doses/ml); however, death occurred only in animals given high-passage virus. Passage 3 (P3) and passage 9 (P9) viruses were selected as representative of low-passage and high-passage viruses, respectively. Although minimal differences were detected in infectivity for rhesus monkey kidney tissue cultures and mice, P9 virus was at least 10,000 times more lethal for mice (mean lethal dose = 10(4.2)). Infection with P3 virus was accompanied by minimal bronchitis and bronchiolitis only, whereas P9-infected animals exhibited marked bronchitis, bronchiolitis, and pneumonia. Striking thymic cortical atrophy was also demonstrable in the P9-infected animals and, although virus was more commonly recovered from thymuses from these animals, immunofluorescent studies revealed only a few cells containing influenza virus antigens. To further explore the participation of thymus-derived lymphocytes in influenza, athymic nude mice and furred immunocompetent littermates were given 500 50% mouse infectious doses of P9 virus. Nude mice exhibited an increased survival time and, in contrast to the extensive lung pathology seen in furred littermates, manifested minimal cellular infiltration and no tissue destruction in lungs. Brains from nude mice exhibited encephalomalacia with lymphocytic perivascular cuffing, which was not seen in furred animals. Virus was recovered from brains of 6 of 13 nude mice and 1 of 10 furred animals. The contrasting models suggest that thymus-dependent cells play a significant role in the inflammatory response to influenza virus infection and should prove useful for probing host-virus interactions which characterize influenza virus virulence.

Acute Disease↗
PubMed1981

Television-induced formed visual hallucinations and cerebral diplopia.

A 65-year-old man with ischaemic encephalomalacia following surgery for an aortic arch aneurysm experienced episodes of stereotyped formed visual hallucinations uniquely provoked by television viewing. In addition he noted vertical diplopia of cerebral origin. These symptoms are discussed in the light of what is known about visual hallucinations, television-induced epilepsy, and cerebral polyopia.

Aged↗
PubMed1988

Transient global amnesia and left frontal haemorrhage.

A patient developed spontaneous, acute, dominant frontal lobe haemorrhage neighbouring on a zone of pre-existing post-traumatic encephalomalacia manifesting clinically as transient global amnesia. Amnesia can be secondary to disease of the frontal lobe, affecting pathways interconnecting the basal forebrain and hippocampus of the temporal lobe.

Aged↗
PubMed1987

Caprine arthritis-encephalitis in the Basque country, Spain.

A goat herd severely affected by arthritis was studied. The most representative clinical signs consisted of articular swelling, mainly of the carpal joints, and the subsequent locomotor disorders. Some goats also showed signs of central nervous system involvement. Examinations of joint fluid revealed an increased number of mononuclear blood cells, mostly lymphocytes. Gross and microscopic articular lesions were of inflammatory and degenerative types. Periarticular connective tissue, synovial bursae, tendons and tendon sheaths were predominantly affected. Inflammatory lesions were those of a chronic hyperplastic tenosynovitis with fibrosis of the connective tissue components. Degenerative changes consisted mainly of necrosis and mineralisation of articular-related structures. Histological lesions in the central nervous system were those of a nonpurulent encephalitis initially located in periventricular areas, but in one case extensive encephalomalacia was also seen. Of the 80 animals sampled 82.5 per cent showed seropositive reactions against an ovine progressive pneumonia virus antigen. None was seropositive to brucella and titres to chlamydia were low. Attempts to isolate chlamydia and mycoplasma from affected joints and several organs failed. Different bacteria were recovered from a few samples but did not seem significant. Syncytium-forming viral particles were isolated from several organs, mainly the lungs, synovial membranes and lymphoid tissue of almost all the slaughtered animals. These particles were identified as lentiviruses by electron microscopy. The clinical signs, lesions serological results and microbiological findings, led to a diagnosis of caprine arthritis-encephalitis. This syndrome has not been recognised in Spain previously.

Animals↗
PubMed1992

Some unusual diseases in the birds of Victoria, Australia.

The following unusual diseases were diagnosed in birds submitted to the Veterinary Research Institute, Victoria, between 1978 and 1987: the viral diseases beak and feather disease of psittacines, infectious laryngotracheitis in peafowls, a papovavirus-like inclusion body disease in psittacines, and pox; chlamydiosis; the bacterial diseases actinomycosis, listeriosis and mycobacteriosis; the fungal diseases favus, yeast infections and systemic zygomycosis; the protozoan diseases cryptosporidiosis, hexamitiasis, suspected leucocytozoonosis, sarcosporidiosis, toxoplasmosis, trichomoniasis and an unidentified protozoan-like organism which caused pneumonia in ducks; a variety of parasites; the metabolic disorders curled-toe paralysis in pheasant poults, encephalomalacia and parenchymatous goitre; toxicity due to dimetridazole and the ingestion of the leaves of the tobacco tree; and other non-infectious conditions including asphyxiation, burns, cataracts, cerebellar degeneration and atrophy, cystic right oviducts and exertional rhabdomyolysis.

Animals↗
PubMed1997

Caprine enterotoxaemia associated with cerebral microangiopathy.

Cerebral microangiopathy is described in naturally occurring clostridial enterotoxaemia in two goats. The two cases were selected from the files of two diagnostic laboratories in Australia, on the basis that the clinical syndrome and history were consistent with a diagnosis of enterotoxaemia, and that the diagnosis was confirmed by the identification of epsilon toxin in the intestinal contents. The lesions consisted of acute perivascular proteinaceous exudate in the brain and bilaterally symmetrical foci of encephalomalacia were observed in one of the goats. These brain lesions confirm that Clostridium perfringens type D enterotoxaemia may produce histologically detectable brain changes in goats.

Animals↗
PubMed2004

Clinicopathological findings in sheep from Sardinia showing neurological signs of disease.

Histopathological and bacteriological examinations were performed on 178 brains from Sardinian sheep which were showing neurological signs. The sheep represented the total number of sheep with neurological syndromes submitted for diagnostic investigations over a three-year period in Sardinia. Scrapie was detected in 57 cases, cerebrocortical necrosis in 25, intoxication by a typical Mediterranean plant (Cistus species) was suspected in 25, coenurosis was detected in 11 cases, Listeria monocytogenes in eight cases and focal symmetrical encephalomalacia in six cases. Non-suppurative inflammatory changes were observed in three of the brains and suppurative changes were noted in two. Lesions restricted to the spinal cord were found in three cases. In the remaining 38 cases there were no significant neuropathological changes.

Animals↗
PubMed2003

Prospective brain imaging evaluation of children with sickle cell trait: initial observations.

PURPOSE: To determine whether sickle cell trait (hemoglobin AS) is associated with abnormalities in the brain of asymptomatic children. MATERIALS AND METHODS: Magnetic resonance (MR) imaging and MR angiography were performed prospectively in 26 siblings (eight girls, 18 boys; mean age, 10.5 years) of patients with sickle cell disease. Two neuroradiologists, blinded as to whether a child had hemoglobin AS or AA, reviewed images obtained in siblings. With MR imaging, lacunae, loss of white matter volume, encephalomalacia, or leukoencephalopathy was identified. With MR angiography, arterial stenosis, occlusion, or tortuosity was identified. Images with definite or possible abnormalities were mixed with randomly selected images and were referred to a third neuroradiologist for a completely blinded review. In cases in which all neuroradiologists concurred, a score was assigned that indicated the sibling had an abnormality. MR angiographic findings were assigned a score for tortuosity with a new quantitative scale. RESULTS: Among 26 siblings screened, 21 children had sickle cell trait. Among these 21 children, two had mild abnormalities at MR imaging (sample prevalence rate, 10% [95% CI: 1%, 29%]), and four had arterial tortuosity (sample prevalence rate, 19% [95% CI: 5%, 42%]). When children with sickle cell trait were compared with 31 control subjects without the trait, arterial tortuosity was significantly more common in children with sickle cell trait (P =.014). Among children with sickle cell trait, percentage of hemoglobin S was significantly greater in children who had tortuosity than percentage of hemoglobin S in children who had normal blood vessels at MR angiography (P <.03). CONCLUSION: Findings suggest that greater percentage of hemoglobin S is associated with mild vasculopathy. This vasculopathy may explain some of the excess risk of stroke among African Americans.

Adolescent↗
PubMed2003

Brain imaging findings in pediatric patients with sickle cell disease.

PURPOSE: To determine prevalence of imaging abnormalities in the brain of children with sickle cell disease (SCD) and to identify clinical and methodological factors that influence prevalence estimate. MATERIALS AND METHODS: Magnetic resonance (MR) imaging and MR angiographic findings for 185 patients with SCD examined at St Jude Children's Research Hospital since 1993 were reviewed. At least two readers independently reviewed images. Standard MR imaging criteria were used to identify lacunae, loss of white matter volume, encephalomalacia, or leukoencephalopathy. Patients were assigned grades to indicate limited or extensive abnormalities. Standard MR angiographic criteria were used to identify arterial tortuosity (limited vasculopathy) and stenosis or occlusion (extensive vasculopathy). Findings were evaluated as a function of patient clinical status (including stroke) and diagnosis. Recent methods (T1- and T2-weighted MR imaging plus fluid-attenuated inversion recovery [FLAIR] at 3-mm section thickness) were compared with older methods (T1- and T2-weighted MR imaging without FLAIR at 5-mm section thickness). RESULTS: At mean age of 10 years, overall prevalence of infarction, ischemia, or atrophy in patients with SCD was 44% (82 of 185), and prevalence of vasculopathy was 55% (102 of 185), without evidence of a significant referral bias. Twenty-six of 27 patients with clinical stroke had abnormal findings at imaging, but even if patients with stroke were excluded, 35% (56 of 158) had a "silent infarction" (MR imaging-visible injury without clinical stroke), and 49% (78 of 158) had abnormal findings at MR angiography. Patients with clinically severe disease had more abnormalities at MR imaging (P <.001) and MR angiography (P <.004) than did patients with milder disease. Severe vasculopathy was more prevalent in patients with hemoglobin SS than in those with hemoglobin SC (P <.001). Recent imaging methods showed more abnormalities than did older methods (P <.01). With newer methods, 43% (29 of 67) of patients had extensive abnormalities, whereas with older methods, 28% (33 of 116) had extensive abnormalities. CONCLUSION: Prevalence of ischemic brain injury in pediatric patients with SCD is substantially higher than was previously reported, in part because of improvements in imaging methods.

Anemia, Sickle Cell↗
PubMed1984

Intracranial hemorrhage in the hypoxic-ischemic infant: ultrasound demonstration of unusual complications.

Seven neonates (four preterm and three term) with severe hypoxic-ischemic parenchymal brain changes are presented to illustrate the kinds of parenchymal lesions demonstrable on ultrasound, to show the similarity of parenchymal lesions in preterm and term infants, and to correlate the severe neurologic deficits with the parenchymal changes. The lesions demonstrated are periventricular leukomalacia, large-vessel infarction, isolated parenchymal hemorrhage, multiple cystic encephalomalacia, and parenchymal atrophy. Parenchymal changes should be sought in such infants during any stage of their disease.

Brain↗
PubMed1985

Intracranial calcification in the infant and neonate: evaluation by sonography and CT.

This study reports the sonographic and computed tomography (CT) findings in seven infants and neonates with intracranial calcifications and a spectrum of underlying disorders, including toxoplasmosis, cytomegalic inclusion disease, transverse/straight sinus thrombosis, and probable anoxia. Neurotropic infectious disease usually produced clumped or subependymal calcifications accompanied by sometimes bizarre ventricular configurations and prominent periventricular cystic encephalomalacia. Sonography failed to identify prospectively intracranial calcifications in two of the three patients without infection, although calcifications were visible in retrospect. Overall, CT provided optimum visualization of intracranial calcifications.

Brain Diseases↗
PubMed1998

Serial radiography in the infant shaken impact syndrome.

Certain CT and/or MRI abnormalities have been used medicolegally to time intracranial injuries from the infant shaken impact syndrome (ISIS). For example, parenchymal hypodensities on CT scans are said to arise only after 6-48 h have elapsed postinjury, and the presence of chronic or mixed subdural hematomas suggests injury that occured 1-4 weeks prior. However, these statements are based largely upon inference from data obtained in other conditions such as ischemic anoxic injury and chronic subdural hemorrhage in adults. Direct evidence about the evolution of intracranial injuries in infants with ISIS is sparse, and the radiographic changes following ISIS have never been systematically studied on serial imaging studies. One hundred-seventeen serial CT and MRI scans obtained from 33 infants with ISIS were reviewed retrospectively. The exact scan dates and times were obtained directly from the scans. Acute subdural hemorrhage was the most common intracranial abnormality and was present in 27 (81%) of the 33 infants. Other intracranial abnormalities included chronic subdural collections, subarachnoid hemorrhage, epidural hematomas, parenchymal hypodensities, edema and contusions, and atrophy and encephalomalacia. In 15 of the 33 infants, the injury could be timed with reasonable certainty, and the evolution of the radiographic changes followed over time. Six of the 15 infants had evidence of prior cranial trauma such as chronic subdural collections (5 infants) or mild atrophy (1 infant). Of the remaining 9 infants, parenchymal abnormalities such as hypodensities, edema and contusion appeared in virtually all of the initial scans performed approximately 3 h following the report of injury. One 'chronic' subdural collection was absent on the first scan performed 2.75 h postinjury, but appeared on a second scan performed 17 h later, suggesting that some 'chronic' subdural fluid collections may arise much sooner than previously thought. These findings challenge some of the current dogma about the timing of radiographic changes following abuse and are important in timing the alleged abuse for legal purposes.

Battered Child Syndrome↗
PubMed2006

Fetal germinal matrix and intraventricular hemorrhage.

Subependymal germinal matrix with intraventricular hemorrhage (GMIVH) is a common complication associated with delivery in preterm neonates but has rarely been observed in the fetus. Clinical and neuroradiological findings of 5 patients who were diagnosed as having fetal GMIVH with prenatal ultrasonographic examinations (US) and MRI, and postnatal MRI were reviewed retrospectively. During a seemingly uneventful pregnancy, fetal GMIVH occurred at approximately 30-33 weeks of gestation, with the absence of any known factor predisposing to fetal hemorrhage. Routine obstetric US revealed an intraventricular lesion in the enlarged ventricles. Prenatal MRI clearly demonstrated parenchymal change such as intracerebral hematoma adjacent to the subependymal and intraventricular hematoma, and periventricular leukomalacia as well as GMIVH. Although patients without parenchymal destruction (hemosiderin deposit alone) had a favorable neurodevelopmental outcome, encephalomalacia and periventricular leukomalacia contributed to long-term neurodevelopmental deficits. Evaluating parenchymal damage with prenatal MRI can therefore help to predict neurodevelopmental prognosis of the fetus with GMIVH.

Adult↗
PubMed1987

Cytoskeletal immunohistochemistry of Alzheimer's dementia and related diseases. A study with monoclonal antibodies.

Mabs directed against phosphorylated epitopes on the heavy and medium neurofilament protein were used to immunostain histological sections from brains of patients without neurological disease and patients suffering from SDAT, Pick's disease, Parkinson's disease, progressive supranuclear palsy and encephalomalacias of the white matter inducing chromatolysis in the overlying cortex. In normal brains only axons but never perikarya were stained. In the pathological brains, however, swollen neurons with chromatolysis and swollen cells in Pick's disease, NFT in SDAT, Pick bodies in Pick's disease, the centers of Lewy bodies in Parkinson's disease and some tangles in progressive supranuclear palsy were stained. These changes are perikaryal alterations. The results are discussed in relation to the formation of NFT in SDAT, i.e. the PHF as seen by electron microscopy. It is concluded that in spite of the reliable staining of NFT with some of our mabs, with sera directed against PHF, MAPs and other cytoskeletal proteins there is no absolutely specific immunoreaction for PHF. The most similar pattern to that observed in NFTs of SDAT is seen in the Pick bodies of Pick's disease, although these do not consist of PHF when looked at with the electron microscope, and although they behave differently from NFT in some 'conventional' histological stains. From this nonspecificity of the immunoreaction and from the presence of multiple cytoskeletal epitopes in NFT it is concluded that NFT (i.e. PHF) are probably not derived from one particular cytoskeletal element but are reassembled from proteolytic breakdown fragments of several of these elements. In this regard the similarities and dissimilarities with the alterations of Pick's disease might be specially relevant and deserve further studies, especially as the clinical features of SDAT and Pick's disease can be very similar.

Alzheimer Disease↗
PubMed1995

Alpha-tocopherol and phospholipase A2 in liver and brain of chicks posthatching: the influence of dietary fat and vitamin E.

One of the classical vitamin E deficiency syndromes is nutritional encephalomalacia in broiler chicken. Subject of this study was the influence of dietary fatty acids and vitamin E on phospholipase A2 and alpha-tocopherol concentration in liver, cerebrum and affected cerebellum posthatching. Therefore, chicks were fed either oleic, linoleic or linolenic acid rich fats together with 5, 25, or 125 ppm vitamin E. At the end of 0, 1, 2 and 3 weeks the tocopherol content and phospholipase A2 activity of liver, cerebrum and cerebellum were determined. Dietary fatty acids did not influence tissue alpha-tocopherol and phospholipase A2. In the vitamin E-deficient cerebellum the enzyme activity of cytosolic phospholipase A2 was increased. Due to its low content of vitamin E the cerebellum is the most susceptible tissue to oxidative stress during vitamin E deficiency.

Aging↗
PubMedDate not supplied

Vertebrobasilar insufficiency.

Permanent or transient reduction of the blood flow to the brain is often responsible for dizziness and occasionally sensorineural hearing loss. So far the diagnosis of this condition has been made by angiography, either carotid or vertebral arteriography, but there is a justified reluctance of subjecting unselected patients to this invasive procedure. It is the purpose of this paper to present a new approach to the diagnosis of cerebral vascular insufficiency based on a three-step protocol. The two initial steps are formed by noninvasive techniques and may be used for the selection of those cases requiring additional diagnostic procedures. 1) Cerebral hemodynamic evaluation provides a physiologic assessment of the direct carotid and indirect carotid and vertebral blood flow. It includes ocular plethysmography and ophthalmodynamometry obtained with the patient supine and erect, without and during carotid compression. 2) Computerized tomography allows an evaluation of the brain substance and of the changes produced by vascular insufficiency such as brain atrophy, infarcts and encephalomalacia. A new form of radiographic assessment based on a dynamic evaluation of regional blood flow will be introduced in this paper. 3) Carotid and vertebral arteriograms are performed only on these cases demonstrating a significant cerebral vascular insufficiency by the previous tests and in cases where corrective surgery is contemplated.

Aged↗
PubMedDate not supplied

Arteriolar sclerosis as a cause of presbycusis.

Temporal bones, brains, and kidneys of 40 patients over 50 years of age were studied histopathologically, paying special attention to angiosclerotic changes. The histopathologic findings were correlated with audiometric and manometric records obtained while the patients were alive. A close relation existed among the lumen narrowing of the internal auditory artery, spiral ganglion atrophy, and hearing loss. The angiosclerotic changes of the Willis' circle, encephalomalacia, and hearing loss were also related.

Arteriosclerosis↗
PubMed1993

Clinical signs and lesions in gnotobiotic pigs inoculated with Shiga-like toxin I from Escherichia coli.

Gnotobiotic pigs were used as a model to study the contribution of Shiga-like toxin I to natural disease caused by enterohemorrhagic Escherichia coli in calves and human beings. Eleven 2- to 7-day-old gnotobiotic pigs of either sex, obtained by closed hysterotomy, were injected intramuscularly with graded doses of partially purified Shiga-like toxin I derived from a lysogenized Escherichia coli strain. Four other gnotobiotic pigs were injected with a mock toxin preparation obtained from a nonlysogenized culture of the same E. coli strain. All toxin-injected pigs developed diarrhea, and three displayed signs of neurologic disease. Pigs either died or were euthanatized 2 to 4 days post-inoculation. Necrosis of muscle was grossly evident at the site of injection in all toxin-inoculated pigs. Hemorrhage in the lumen of the small and large intestines and blood in the feces were also evident in two toxin-inoculated pigs. Microscopically, severe necrotizing myositis at the injection site, multifocal encephalomalacia, and mucosal infarcts and hemorrhage in the small and large intestines were seen. In small vessels at lesion sites, endothelial cells were frequently swollen or necrotic. Pigs inoculated with mock toxin did not develop diarrhea or exhibit signs of neurologic disease, and the only apparent lesion was mild microscopic myositis at the injection site in 1/4 pigs. The results of this study indicate that Shiga-like toxin I causes vascular damage and ischemic necrosis in the intestines and brains of gnotobiotic pigs. These lesions are similar to those seen in the intestines of calves and human beings with hemorrhagic colitis and in the brains of human beings with thrombotic thrombocytopenic purpura.

Animals↗