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PubMed1992

Vaccine efficacy for reducing turbinate atrophy and improving growth rate in piggeries with endemic atrophic rhinitis.

Two vaccines, based on formalin-killed whole cells of toxigenic Pasteurella multocida type D and Bordetella bronchiseptica combined with a partially toxoided cell extract of P multocida, were prepared with Freund's incomplete adjuvant (vaccine 1) or by alum precipitation (vaccine 2). Each was tested for safety and efficacy in reducing the severity of nasal turbinate atrophy and improving the growth rate of pigs in three Western Australian commercial piggeries with endemic atrophic rhinitis. In safety experiments with vaccine 1, no adverse clinical effects were observed in vaccinated sows or their progeny. Piglets receiving vaccine 2 showed no injection site abnormalities, pyrexia or turbinate atrophy. In field trials, vaccine 1 significantly reduced the prevalence of moderate to severe nasal turbinate atrophy (Done score 3 to 5) when used in two piggeries (A and B). Progeny from vaccinated sows in piggery B also grew significantly faster than controls. When vaccine 2 was used in piggery A at a later date and in another piggery (C), growth rate was not improved in either piggery and the prevalence of moderate to severe turbinate atrophy was reduced only in piggery C.

Adjuvants, Immunologic↗

PubMed1980

Computer densitometry of retinal nerve fibre atrophy. A pilot study.

Lack of nerve fibre layer opacity and a granular appearance of the retina are important funduscopic signs in optic atrophy. In this pilot study serially obtained fundus photographs from a case with developing optic atrophy where subjected to computer densitometry. A monotonic increase in local density variations was found during evolution of optic atrophy. The change in density variations closely followed the funduscopic change in nerve fibre layer opacity. This method makes it possible to detect and quantify diffuse atrophy of the retinal nerve fibre layer.

Adult↗

PubMed1983

Histopathology of eye, optic nerve and brain in a case of dominant optic atrophy.

Histopathology of eye, optic nerve and brain was performed in a patient with typical signs and symptoms of dominant optic atrophy. He belonged to a previously-reported family of 152 members in which optic atrophy was demonstrable in 14 persons, and probably present in a further 8 cases. In the eyes, fibrosis of the retinal ganglion cell layer and disc was found. Ultrastructural examination showed a few remaining cells in this layer, heavy fibrosis and in particular a highly condensed inner limiting membrane. The optic nerves, the optic chiasm and optic tracts showed an increased content of collagen tissue and a decreased number of neurofibrils and myelin sheaths. In the lateral geniculate body there was massive loss of ganglion cells, fibrillary gliosis and a great quantity of fine granular lipid in the cytoplasm of the ganglion cells. No changes in the calcarine cortex were observed. Examination of the intracranial part of both vestibulocochlear nerves showed a decreased number of neurofibrils and myelin sheaths. It is concluded that the histopathological changes of the visual system are similar to those in Leber's disease, but less pronounced. The study confirms earlier theories that dominant optic atrophy is a primary degeneration of the ganglion cell layer in the retina, with ascending optic atrophy.

Aged↗

PubMed1987

Progression of gyrate atrophy of the choroid and retina. A long-term follow-up by fluorescein angiography.

Fundus fluorescein angiograms of 21 gyrate atrophy patients were evaluated. In 16 of 21 patients between 2 to 13 angiograms were taken during the follow-up which extended from 1.6 to 13.4 years. In 5 of 21 patients the fluorescein angiography was done once. Optic disc drusen occurred in 3 patients. Optic disc atrophy was not observed. Some attenuation occurred in the retinal arteries in the far-advanced stages. Up to the midretinal venous phase 5 of 13 patients had a markedly increased visibility of the larger choroidal vessels in areas of ophthalmoscopically intact retina. Pigment epithelial window defects presented in 17 of 21 patients. In 4, they were seen to enlarge into patches of chorioretinal atrophy during this long-term follow-up. Contrary to the general notion, the macula was affected frequently, i.e. in 9 of 21 patients; In 6 the pigment epithelial window defects presented in the macula, one had bilateral cystoid macular oedema, and in 2 patients the patches of chorioretinal atrophy were central.

Adolescent↗

PubMed2005

The survival of motor neurons protein determines the capacity for snRNP assembly: biochemical deficiency in spinal muscular atrophy.

Reduction of the survival of motor neurons (SMN) protein levels causes the motor neuron degenerative disease spinal muscular atrophy, the severity of which correlates with the extent of reduction in SMN. SMN, together with Gemins 2 to 7, forms a complex that functions in the assembly of small nuclear ribonucleoprotein particles (snRNPs). Complete depletion of the SMN complex from cell extracts abolishes snRNP assembly, the formation of heptameric Sm cores on snRNAs. However, what effect, if any, reduction of SMN protein levels, as occurs in spinal muscular atrophy patients, has on the capacity of cells to produce snRNPs is not known. To address this, we developed a sensitive and quantitative assay for snRNP assembly, the formation of high-salt- and heparin-resistant stable Sm cores, that is strictly dependent on the SMN complex. We show that the extent of Sm core assembly is directly proportional to the amount of SMN protein in cell extracts. Consistent with this, pulse-labeling experiments demonstrate a significant reduction in the rate of snRNP biogenesis in low-SMN cells. Furthermore, extracts of cells from spinal muscular atrophy patients have a lower capacity for snRNP assembly that corresponds directly to the reduced amount of SMN. Thus, SMN determines the capacity for snRNP biogenesis, and our findings provide evidence for a measurable deficiency in a biochemical activity in cells from patients with spinal muscular atrophy.

Animals↗

PubMed2004

Optical coherence tomography analysis of axonal loss in band atrophy of the optic nerve.

AIMS: To measure axonal loss in patients with band atrophy of the optic nerve caused by optic chiasm compression using optical coherence tomography and to evaluate its ability in identifying this pattern of retinal nerve fibre layer (RNFL) loss. METHODS: Twenty eyes from 16 consecutive patients with band atrophy of the optic nerve and permanent temporal hemianopia due to chiasmal compression, and 20 eyes from an age and sex matched control group of 16 healthy individuals, were studied prospectively. All patients were submitted to an ophthalmic examination including perimetry and evaluation of the RNFL using optical coherence tomography. Mean RNFL thickness around the optic disc was compared between the two groups. RESULTS: The mean (SD) peripapillary RNFL thickness of eyes with band atrophy was 101.00 (9.89) microm, 62.21 (12.71) microm, 104.89 (12.60) microm, and 50.13 (16.88) microm in the superior, temporal, inferior, and nasal regions, respectively. The total RNFL mean was 79.94 (7.17) microm. In the control group, the corresponding values were 140.10 (16.06) microm, 86.50 (12.17) microm, 144.60 (15.70) microm, and 97.94 (16.02) microm. The total RNFL mean was 117.72 (9.53) microm. The measurements were significantly different between the two groups. Measurements in each of twelve 30 degrees divisions provided by the equipment also showed significantly different values between eyes with band atrophy and normal controls. CONCLUSIONS: Optical coherence tomography was able to identify axonal loss in all four quadrants as well as in each of the twelve 30 degrees segments of the disc. Thus, it seems to be a promising instrument in the diagnosis and follow up of neuro-ophthalmic conditions responsible for RNFL loss, even if predominantly in the nasal and temporal areas of the optic disc.

Adult↗

PubMed1986

Iris atrophy in sickle cell disease.

Iris atrophy, of unknown origin and believed to be secondary to the vaso-occlusive process of sickle cell disease, has been observed in 25 eyes of 22 patients (two SS disease, 20 SC disease). The crude prevalence was highest in males with SC disease, in whom 14.7% of patients were affected. Iris atrophy was closely associated with proliferative sickle retinopathy in the same eye. Analysis of haematological indices failed to reveal any significant differences between patients with and without iris atrophy. The characteristics and distribution of iris atrophy are described as well as the histopathology in one 68-year-old male patient with SS disease.

Adolescent↗

PubMed2004

Quadriceps atrophy: to what extent does it exist in patellofemoral pain syndrome?

BACKGROUND: Quadriceps atrophy is a commonly cited accompaniment to patellofemoral pain syndrome (PFPS), yet there is little valid, objective evidence for its existence. OBJECTIVE: To investigate atrophy and weakness of the quadriceps femoris muscle group in patients with PFPS using measures of cross-sectional area and peak extension torque. METHODS: A total of 57 patients with insidious onset of PFPS and 10 healthy control subjects had ultrasound scanning of the quadriceps femoris. The scans were analysed using computerised planimetry to estimate the cross-sectional area of the quadriceps femoris. Lower limb peak torque was also measured using a Biodex dynamometer. RESULTS: The mean of % differences revealed a 3.38% (95% confidence interval (CI) 1.3 to 5.45) difference in cross-sectional area (CSA) between the affected and unaffected limb in PFPS patients and a 1.31% (95% CI 0.06 to 2.55) difference in the dominant and non-dominant limb of the control group; the between-groups difference was not significant (p = 0.409). There was a 18.4% (95% CI 13 to 23.8) difference between the affected and unaffected limb in peak torque in PFPS patients and a 7.6% (95% CI 3.2 to 12) difference between the dominant and non-dominant limb in the control group; the between-groups difference was significant (p = 0.002). CONCLUSIONS: The mean of % differences of 3.38% quadriceps atrophy between limbs was considerably less than the only other study using ultrasound scanning on the quadriceps in PFPS and was not significant between the groups. There were greater and more significant between-group differences in lower limb peak torque indicating that muscle strength may not be related to muscle size. These results help to re-appraise of the amount of quadriceps atrophy in PFPS.

Adult↗

PubMed2004

Acetylated sialic acid residues and blood group antigens localise within the epithelium in microvillous atrophy indicating internal accumulation of the glycocalyx.

BACKGROUND: Microvillous atrophy, a disorder of intractable diarrhoea in infancy, is characterised by the intestinal epithelial cell abnormalities of abnormal accumulation of periodic acid-Schiff (PAS) positive secretory granules within the apical cytoplasm and the presence of microvillous inclusions. The identity of the PAS positive material is not known, and the aim of this paper was to further investigate its composition. METHODS: Formaldehyde fixed sections were stained with alcian blue/PAS to identify the acidic or neutral nature of the material, phenylhydrazine blocking was employed to stain specifically for sialic acid, and saponification determined the presence of sialic acid acetylation. The specificity of sialic acid staining was tested by digestion with mild sulphuric acid. Expression of blood group related antigens was tested immunochemically. RESULTS: Alcian blue/PAS staining identified a closely apposed layer of acidic material on the otherwise neutral (PAS positive) brush border in controls. In microvillous atrophy, a triple layer was seen with an outer acidic layer, an unstained brush border region, and accumulation within the epithelium of a neutral glycosubstance that contained acetylated sialic acid. Blood group antigens were detected on the brush border, in mucus, and within goblet cells in controls. In microvillous atrophy they were additionally expressed within the apical cytoplasm of epithelial cells mirroring the PAS abnormality. Immuno electron microscopy localised expression to secretory granules. CONCLUSIONS: A neutral, blood group antigen positive, glycosubstance that contains acetylated sialic acid accumulates in the epithelium in microvillous atrophy. Previous studies have demonstrated that the direct and indirect constitutive pathways are intact in this disorder and it is speculated that the abnormal staining pattern reflects accumulation of glycocalyx related material.

ABO Blood-Group System↗

PubMed1998

Clinical features, molecular genetics, and pathophysiology of dominant optic atrophy.

Inherited optic neuropathies are a significant cause of childhood and adult blindness and dominant optic atrophy (DOA) is the most common form of autosomally inherited (non-glaucomatous) optic neuropathy. Patients with DOA present with an insidious onset of bilateral visual loss and they characteristically have temporal optic nerve pallor, centrocaecal visual field scotoma, and a colour vision deficit, which is frequently blue-yellow. Evidence from histological and electrophysiological studies suggests that the pathology is confined to the retinal ganglion cell. A gene for dominant optic atrophy (OPA1) has been mapped to chromosome 3q28-qter, and studies are under way to refine the genetic interval in which the gene lies, to map the region physically, and hence to clone the gene. A second locus for dominant optic atrophy has recently been shown to map to chromosome 18q12.2-12.3 near the Kidd blood group locus. The cloning of genes for dominant optic atrophy will provide important insights into the pathophysiology of the retinal ganglion cell in health and disease. These insights may prove to be of great value in the understanding of other primary ganglion cell diseases, such as the mitochondrially inherited Leber's hereditary optic neuropathy and other diseases associated with ganglion cell loss, such as glaucoma.

Chromosome Mapping↗

PubMed2004

Pontine atrophy precedes cerebellar degeneration in spinocerebellar ataxia 7: MRI-based volumetric analysis.

BACKGROUND AND OBJECTIVE: Spinocerebellar ataxia 7 (SCA7) is characterised by cerebellar ataxia and visual loss. The aim of the present study was to elucidate the magnetic resonance imaging (MRI) findings characteristic of patients with SCA7. METHODS: Twenty patients with SCA (eight SCA3, three SCA6, and nine SCA7) and 20 control subjects underwent an MRI-based volumetric analysis. RESULTS: The pontine volume in patients with SCA7 was decreased by a greater amount than in patients with other types of SCA (p<0.01), whereas the cerebellar volume was not different from that in other types of SCA (p>0.05). Pontine atrophy was a consistent finding in all patients with SCA7 regardless of the degree of cerebellar atrophy or the severity or duration of illness. In contrast, cerebellar atrophy was not found in those with a short duration of illness or mild ataxia, but became prominent as the severity and duration of illness progressed. CONCLUSIONS: Our study suggests that neurodegeneration is ongoing during the life of individuals with SCA7, and that the primary pathology in these individuals involves the brainstem rather than the cerebellum. In addition, pontine atrophy is a prominent, consistent finding in SCA7, and may help in establishing the clinical diagnosis of SCA7.

Adult↗

PubMed2004

Cerebral atrophy in myotonic dystrophy: a voxel based morphometric study.

Brain involvement in myotonic dystrophy type 1 (DM1) is characterised by cortical atrophy and white matter lesions. We compared the magnetic resonance imaging derived grey matter maps of 22 DM1 patients with those of matched, healthy controls using voxel based morphometry to evaluate the extension of global and regional cortical atrophy in DM1, as well as its relationships with clinical and genetic features. Patients had significantly reduced brain tissue volumes. Grey matter volume was inversely correlated with age; this inverse correlation was significantly stronger in DM1 than in controls. Neither the clinical and genetic characteristics nor white matter lesions were correlated with cortical atrophy. Grey matter atrophy was located mainly in the bilateral frontal and parietal lobes, in the bilateral middle temporal gyrus, and in the left superior temporal and occipital gyrus.

Adult↗

PubMed1971

Vasopressin test in cases of optic atrophy and optic neuritis.

The vasopressin test gave pathological results in 12 cases of optic atrophy and normal results in three cases. One of the patients with a pathological response had Leber's disease and three had tobacco-alcholic amblyopia, while in the rest the optic atrophy was of uncertain origin. In the cases with normal results the aetiology was also unclear. The Metopirone test was normal in 13 cases and pathological in only one case of optic atrophy. In three out of five patients with optic neuritis the vasopressin test gave pathological responses. The high frequency of pathological vasopressin tests in patients with optic lesions indicates a simultaneous disturbance of the hypothalamo-hypophyseal function. The background to this might be a disturbed vascular supply. The vasopressin test was of no help in diagnosing tumours as a cause of optic atrophy.

Adolescent↗

PubMed1989

Non familial juvenile distal spinal muscular atrophy of upper extremity.

An uncommon variety of non familial, juvenile onset, spinal muscular atrophy with asymmetric distal upper extremity affection is described. One hundred and two patients with a one to 14 year follow up are analysed. Spinal muscular atrophies with a distal distribution are rare. However, in the past three decades, previously unrecognised varieties of neurogenic muscular atrophy have been described in Asia (Japan, India, Sri Lanka and Singapore) under a variety of names. These provide interesting data for discussion of Asian neurogenic muscular atrophies with distal affection, in the context of diseases of the motor neuron.

Adolescent↗

PubMed1993

Familial progressive aphasia: its relationship to other forms of lobar atrophy.

Two brothers presented with slowly progressive aphasia. One brother, who became behaviourally disturbed only at the end of his illness, was found at necropsy to have predominant left frontotemporal atrophy. The other brother developed severe behavioural disturbances shortly after the onset of language impairment. His brain revealed bilateral frontotemporal atrophy. In both there was non-Alzheimer's disease pathology with the histological features of loss of large cortical nerve cells, spongiform change and mild gliosis. The differential anatomical atrophy supports the view that clinical manifestations of lobar atrophy are dictated by the topographical distribution of a common underlying pathology, linking the syndromes of progressive aphasia to dementia of frontal lobe type (DFT) and DFT with motor neuron disease.

Aphasia↗

PubMed1995

Nerve conduction studies, skeletal muscle EMG, and sphincter EMG in multiple system atrophy.

Although autonomic failure, parkinsonism, and cerebellar and pyramidal signs are well documented in multiple system atrophy, much less is known about the frequency and severity of involvement of the peripheral nervous system. The frequency and nature of peripheral nerve involvement has therefore been determined in 74 patients with multiple system atrophy using nerve conduction studies and skeletal muscle EMG. These findings were compared with those on sphincter EMG. Ninety per cent of the patients had an abnormal sphincter EMG, indicating denervation and reinnervation consistent with anterior horn cell loss in Onuf's nucleus, but only 40% had either abnormal nerve conduction studies (mixed sensorimotor axonal neuropathy in 17.5%) or abnormal skeletal muscle EMG (suggesting partial denervation in 22.5%). These data indicate a remarkable selective vulnerability of the anterior horn cells of Onuf's nucleus innervating external sphincter muscles relative to those supplying skeletal muscle in patients with multiple system atrophy. If this selective pattern of involvement can be explained it may be a clue to pathogenetic mechanisms in multiple system atrophy.

Adult↗

PubMed1996

Attentional functions in multiple system atrophy and Parkinson's disease.

OBJECTIVE: To assess cognitive performances of patients with striatonigral degeneration type multiple system atrophy compared with those of patients with Parkinson's disease. METHODS: The cognitive performances of a group of patients with multiple system atrophy of the striatonigral type were compared with those of matched patients with Parkinson's disease and controls, using tests sensitive to frontal lobe dysfunction. RESULTS: The multiple system atrophy group, when compared with the Parkinson's disease group, showed significant deficits in attention tasks, particularly in the Stroop test. CONCLUSION: There was a consistently greater impairment in attention resources in patients with multiple system atrophy than in patients with Parkinson's disease.

Aged↗

PubMed1996

Progressive biparietal atrophy: an atypical presentation of Alzheimer's disease.

OBJECTIVES: To define the clinical, neuropsychological, and radiological features of bilateral parietal lobe atrophy. METHODS: Four patients underwent a comprehensive longitudinal neuropsychological assessment, as well as MRI and HMPAO-SPECT. RESULTS: The consistent findings in the patients were early visuospatial problems, agraphia of a predominantly peripheral (or apraxic) type, and difficulty with bimanual tasks, all of which outweighted deficits in memory and language until later in the course of the illness. As the disease progressed, impairments in the phonological aspects of language and in auditory-verbal short term memory were often striking, perhaps reflecting spread from the parietal lobe to perisylvian language areas. Three patients went on to develop a global dementia and fulfilled the criteria for a clinical diagnosis of probable Alzheimer's disease; the fourth patient has only recently been identified. Neuroimaging disclosed bilateral parietal lobe atrophy (MRI) and hypoperfusion (SPECT), which was out of proportion to that seen elsewhere in the brain. One patient has died and had pathologically confirmed Alzheimer's disease with particular concentration in both superior parietal lobes. CONCLUSIONS: Bilateral biparietal atrophy is a recognisable clinical syndrome which can be the presenting feature of Alzheimer's disease. Although the label "posterior cortical atrophy" has been applied to such cases, review of the medical literature suggests that this broad rubric actually consists of two main clinical syndromes with features reflecting involvement of the occipitotemporal (ventral) and biparietal (dorsal) cortical areas respectively.

Aged↗