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Computed tomography of spinal cord atrophy.

Spinal cord atrophy takes on several different forms which correlate closely with specific clinical features. The majority of them, however, can be categorized into three distinct patterns, diffuse (transverse myelopathy), hemi- (Brown-Sequard syndrome), or anterior (anterior spinal artery syndrome) atrophy. Until recently, the differential diagnosis had been made solely on the neurological examination. We present three cases of spinal cord atrophy, one in each category. Spinal computed tomography with metrizamide appears to be a reliable supporting diagnostic method for spinal cord atrophy.

Atrophy↗

[Brain atrophy in chronic alcoholism. Clinical and computer tomographic study].

Fifty chronic alcoholics (37 men and 13 women, ages 26--55, mean age 39.9 years) with different clinical syndromes (alcoholic psychosis, alcoholic encephalopathies) were studied by computerized cranial tomography. Cerebral atrophy was detected in 96% of all cases. Combined cortical and subcortical signs were encountered in almost all cases. Cortical atrophy seemed to be detectable more easily by CT than by pneumencephalography. The computerized tomographic findings were studied in their relations to age, sex, duration of abuse, clinical syndromes, frequency of relapse (and seizures, too), etc. Cerebral atrophy was correlated primarily with the subjects' age and the duration, and less with the intensity of alcoholism. The most distinct changes were found in delirium syndromes and, in cases with relapse of psychosis, especially in combination with seizures. Wernicke-Korsakow encephalopathies showed the widest third ventricles when combined with repeated syndromes of withdrawal in their case histories. Computerized tomographic examinations of ten patients during acute psychosis as well as 4 weeks later showed identical findings; transitory changes, e.g., cerebral edema, were not detected. Computerized cranial tomography appears to be extremely useful to study the numerous open questions concerning the pathogenetic role of age, duration, and severity of abuse with cerebral atrophy.

Adult↗

Antioxidant enzyme systems in skeletal muscle atrophied by immobilization.

To clarify the mechanism of oxidative stress in skeletal muscle atrophied by immobilization, we investigated the change of antioxidant enzyme activities in a typical slow red muscle, the soleus. Atrophied soleus muscles were collected from male Wistar rats (16 weeks old), one ankle joint of which had been immobilized in the fully extended position for 7 days. Also, soleus muscles were collected from intact age-matched rats as control. The activities of Mn-containing superoxide dismutase (Mn-SOD), Cu,Zn-containing superoxide dismutase (Cu,Zn-SOD), Se-dependent glutathione peroxidase (Se-GSHPx), glutathione S-transferase (GST), catalase, and glutathione reductase (GSSGRx) were measured. The activities of Cu,Zn-SOD, GST, and GSSGRx were significantly higher in atrophied muscles, while the others were unchanged. Increased Cu,Zn-SOD and unchanged Mn-SOD levels might reflect increased generation of superoxide anions in the cytoplasm rather than in the mitochondria. Owing to the enhancement of Cu,Zn-SOD and the unaltered Se-GSHPx and catalase activities, hydrogen peroxide is thought to be increased in the cytoplasm. Because there is also an increase of iron in the microsomes of atrophied muscles, the production of hydroxyl radicals, the most aggressive of radicals, might consequently be elevated.

Animals↗

Role of iron in oxidative stress in skeletal muscle atrophied by immobilization.

To clarify the role of iron in oxidative stress in skeletal muscle atrophied by immobilization, we investigated the effect of deferoxamine--an iron-chelating agent. Deferoxamine, iron-saturated deferoxamine and double-distilled water (control) were administered subcutaneously from the 4th day after immobilization via osmotic pumps to male Wistar rats (14 weeks old), one ankle joint of which was immobilized in the extended position. After 12 days' immobilization, soleus--typical slow red muscles were collected from both hind limbs and their levels of thiobarbituric acid-reactive substance (TBARS) and glutathione were measured. Deferoxamine suppressed the increase of TBARS and glutathione disulfide in atrophied muscle while iron-saturated deferoxamine did not, which strongly suggests that the iron-chelating action of deferoxamine suppressed the increased oxidative stress. This means that iron plays a very important role in increasing oxidative stress in atrophied muscle. In addition, deferoxamine decreased the degree of atrophy, an effect thought to be mediated by the suppression of oxidative stress.

Animals↗

Incipient atrophy of cornea. Experimental study.

The essence of the process in which the corneal tissue disappears in atrophy of the eye has not yet been studied. The authors of this investigation studied the changes in cornea as they developed after a gross perforating injury to the eye in rabbit. They found that the diameter of the cornea had grown smaller by 2 mm and its radius by 0.5 mm. The tensile strength of the cornea had decreased and hydration increased. Histologically there were but little changes and histochemically a decreased amount of acid mucopolysaccharides was ascertained in the corneal stroma. Incorporation of radioactive sulphate (Na2-35SO4) in vivo disclosed decreased biosynthesis of glycosaminoglycans. Clinically, even though the eye ball atrophied, complete atrophy with flattening and complete diminution, as in the human eye, never developed. The question arises whether the six-months period was sufficient for rabbit cornea to develop clinically similar atrophy as in human cornea or whether the clinical features are principally different in the two species. Foci of ossification, as found in atrophic eye balls, which are known to develop after a long time, would be evidence of the second alternative.

Animals↗

Primary and secondary testicular atrophy.

1. (a) Primary and secondary testicular atrophy is caused by ischaemia, most frequently after intrauterine and prepuberal testicular torsion. (b) After standard orchiopexy, and especially after orchiopexy in high undescended testis, secondary testicular atrophy is frequent. (c) The histological condition of a cryptorchid testis does not predict atrophy. Immediate detorsion and/or prophylactic fixation as well as subtle technique in orchiopexy are essential. 2. Sympathetic orchiopathy of a unilateral atrophic testis was not proven in cryptorchidism and testicular torsion. There is considerable evidence of primary bilateral disease. 3. Testicular atrophy as an aetiological factor in the development of testicular tumor remains open to debate.

Atrophy↗

Periventricular hyperintensity on magnetic resonance imaging correlated with brain ageing and atrophy.

Fifty-two patients with cerebrovascular risk factors without neurological abnormalities were reviewed with respect to periventricular hyperintensity (PVH) on T2-weighted magnetic resonance imaging (MRI); brain atrophy was also assessed by CT and T1-weighted MRI. Extensive PVH showed a stronger correlation with age-related atrophy than mild or absent PVH. The relative volume of brain affected by PVH, calculated by computer, also correlated with brain atrophy, especially ventricular enlargement. The effects of PVH on brain ageing and atrophy is discussed.

Aged↗

Radiological study of the brain at various stages of human immunodeficiency virus infection: early development of brain atrophy.

One hundred and one persons infected with human immunodeficiency virus (HIV-1), in whom other central nervous system infections or diseases were excluded, underwent brain CT and/or MRI at various stages of HIV-1 infection: 29 were asymptomatic (ASX), 35 had lymphadenopathy syndrome (LAS), 17 had AIDS-related complex (ARC), and 20 had AIDS. A control group of 32 HIV-1-seronegative healthy persons underwent brain MRI. The most common finding was brain atrophy, found in 9% of controls, and 31% of ASX cases, 29% of LAS, 59% of ARC and 70% of AIDS. Even the difference between the ASX or LAS groups and controls was significant. The changes were bilateral and symmetrical, and they were more severe at later stages of infection. Infratentorial atrophy was seen in the early stages; supratentorial atrophy became more pronounced at ARC, and generalized atrophy was typical of AIDS. Non-specific small hyperintense foci were found on MRI in 13% of controls and 6-15% of the infected groups. Larger, diffuse, bilateral white matter infiltrates were detected in 4 demented patients with AIDS. Four patients with AIDS and 1 with LAS had focal hyperintense lesions in the internal capsules, lentiform nuclei or thalamus, often bilateral on MRI. One patient with AIDS, examined with CT only, had low density in the lentiform nucleus. Loss of brain parenchyma can occur at an early stage of HIV-1 infection, and the atrophic process becomes more intense at later stages (ARC and AIDS). Parenchymal infiltration, seen as hyperintense areas on MRI, is most often associated with severe clinical symptoms, in the later stages of the disease.

Acquired Immunodeficiency Syndrome↗

Interobserver variability in CT assessment of brain atrophy.

To assess interobserver variability in estimation of brain atrophy based on CT, four neuroradiologists examined CT brain images of 150 consecutive patients without focal lesions. An independent neuroradiologist made the following quantitative measurements: frontal horn index, subarachnoid space area and the ratio between subarachnoid space area and inner skull space area. Level of agreement was fair for the presence (k = 0.24), slight for the degree (mild, moderate, severe) (k = 0.24) and moderate for the type (cortical, subcortical, mixed) of atrophy (k = 0.59). There was a highly significant correlation between the number of observers agreeing and quantitative measurements. We concluded that neuroradiologists' subjective estimation of brain atrophy alone is not reliable. Quantitative measurements would be needed in cases where the presence of brain atrophy might determine clinical decisions.

Adult↗

White matter magnetic resonance imaging hyperintensity in Alzheimer's disease: correlations with corpus callosum atrophy.

We have previously demonstrated with MRI that as well as marked white matter involvement in late-onset Alzheimer's disease (AD), atrophy of the corpus callosum may also be present. This finding prompted us to study possible correlations between atrophy of the corpus callosum and white matter hyperintensity (WMH) and between white matter lesions and the severity of the disease. We compared the corpus callosum and white matter lesions on MRI from 15 AD patients and 15 controls. The white matter lesions were scored according to the Scheltens' rating scale. We found a significant reduction of the area of the corpus callosum and more severe white matter lesions in AD patients than in controls. Both atrophy of the corpus callosum and the severity of lesions depended mainly on the diagnosis of senile dementia of the Alzheimer type and on age but not on the diagnosis of presenile AD. We demonstrated a negative correlation between white matter lesions scores and areas of corpus callosum in AD patients and no correlation between the white matter lesions and the severity of the disease. We demonstrated that white matter lesions including WMH and atrophy of the corpus callosum are more frequent in AD than in controls. The predominance of white matter lesions in senile AD may be explained by the combination of aging and disease processes.

Aged↗

Visual assessment of medial temporal lobe atrophy on magnetic resonance imaging: interobserver reliability.

We conducted an interobserver study to assess agreement on visual rating of medial temporal lobe atrophy on coronal T1-weighted MRI. A total of 100 studies of elderly individuals, using two different MRI techniques (spin echo and inversion recovery sequences), were analysed by four raters (three neurologists and one neuroradiologist) using a five-point rating scale. Complete agreement was found in 37% of the total sample. Interobserver agreement as expressed by kappa values was 0.44 (95% CI = 0.34-0.54) and 0.51 (95% CI = 0.41-0.61) for the two techniques. After dichotomizing medial temporal lobe atrophy into present or absent, a post hoc analysis revealed higher complete agreement (70%), with kappa values of 0.59 (95% CI = 0.51-0.67) and 0.62 (95% CI = 0.48-0.075), for the two techniques (all four raters). From this study we conclude that visual rating of medial temporal lobe atrophy on MRI in the coronal plane yields fair to good agreement among observers. We recommend this type of visual rating for use in clinical settings when a quick judgement on the presence of medial temporal lobe atrophy is needed.

Atrophy↗

Combination of a dual 5-lipoxygenase/cyclooxygenase inhibitor with a glucocorticoid results in synergistic topical antiinflammatory activity without inducing skin atrophy.

Synthetic glucocorticosteroids are widely used in clinical dermatology in the treatment of a number of inflammatory skin disorders. However, cutaneous side effects such as induction of skin atrophy are among the factors that limit the chronic use of this class of agents. We have found that a combination of a dual 5-lipoxygenase/cyclooxygenase inhibitor (9-phenylnonanohydroxamic acid, BMY 30094) and a glucocorticosteroid (hydrocortisone valerate) has synergistic antiinflammatory activity. Topical application of a 0.2% solution of hydrocortisone valerate alone inhibited phorbol ester-induced mouse skin inflammation by 92%. A 1% solution of BMY 30094 alone or a low dose of hydrocortisone valerate (0.005%) had no significant effect on the inflammatory reaction. A combination of 1% BMY 30094 and 0.005% hydrocortisone valerate inhibited the inflammation by 76%. This latter combination produced no signs of skin atrophy in rats after 28 days of application. In contrast, a 0.1% dose of hydrocortisone valerate produced significant skin atrophy. These findings suggest that it is possible to reduce the skin atrophy potential of glucocorticoids while maintaining the antiinflammatory activity using a novel drug combination.

Administration, Cutaneous↗

Hereditary motor and sensory neuropathy (HMSN) and optic atrophy (HMSN type VI, Vizioli).

Clinical and electrophysiological findings are described in three patients with hereditary motor and sensory neuropathy in association with optic atrophy (HMSN VI). The optic atrophy was of the Leber type in a 15-year-old boy. In a 70-year-old patient, as in three members of his family, optic atrophy was associated with tapetoretinal degeneration. In addition to HMSN and optic atrophy a 20-year-old man suffered from sensorineural deafness. Electrophysiological studies indicated a neuronal form of neuropathy, as in HMSN II. Brainstem auditory evoked potentials also revealed subclinical involvement of the central auditory pathways in the patients without hearing defects.

Adolescent↗

The role of MRI in the diagnosis of olivopontocerebellar atrophy.

Under the term of olivopontocerebellar atrophy different nosological pictures are grouped, all characterized by showing clinical signs of deficiency of the structures of the pons and of the cerebellum. The diagnosis of olivopontocerebellar atrophy has been made, until now, by clinical criteria while typical anatomopathological changes are found at the autoptic studies. We describe three patients affected by olivopontocerebellar atrophy, of different types and at different stages of disease. In all cases MRI showed a similar and typical picture of atrophy of the olivary eminences of the medulla oblongata resulting in straightening of the angle usually present on the ventral frontier between pons and medulla oblongata. This diagnostic tool demonstrated thus to be of primary relevance yet in the early phases of the disease.

Aged↗

Clinicopathologic differentiation of atrophy of the pancreatic body and tail aplasia.

CONCLUSION: Congenital aplasia of the body and tail of the pancreas is derived from a defect of the dorsal pancreatic anlage and should not be considered a type of acquired atrophy of these structures. BACKGROUND: Congenital aplasia of the body and tail of the pancreas radiologically mimics acquired atrophy of the pancreatic body and tail. METHODS: Two patients with radiologically identified aplasia of the body and tail of the pancreas were studied clinicopathologically. RESULTS: An 82-yr-old man was diagnosed radiologically as having both carcinoma of the head of the pancreas and aplasia of the body and tail of the pancreas and underwent pancreatoduodenectomy. Pathologically the carcinoma was distributed in the anterosuperior part of the head of the pancreas, and spread into the duct of Santorini and intraductally to a portion of the main pancreatic duct beyond the junction of the ducts of Santorini and Wirsung. Consequently, obstructive pancreatitis of the body and tail of the pancreas developed, resulting in marked atrophy that mimicked aplasia of the body and tail of the pancreas. A 74-yr-old woman was diagnosed radiologically as having two carcinomas, one of the gallbladder and one of the stomach, and aplasia of the body and tail of the pancreas. During surgery, suspected parenchymal disappearance and fatty replacement in the body and tail of the pancreas were noted. Histologic examination of biopsy specimens from the body portion revealed atrophic pancreatic tissue surrounded by fat. Therefore, these patients had atrophy of the pancreatic body and tail.

Aged↗

[Augmentation of the extremely atrophied maxilla and mandible by autologous calvarial bone transplantation].

Rehabilitation in patients with severe alveolar ridge atrophy of the maxilla or mandible is problematic and can often only be achieved by long-term treatment. In most cases, autologous bone grafting with iliac crest bone has been used to augment severely atrophied upper jaws. In our experience, iliac bone grafts are less useful, since iliac bone appears to be of inferior quality; in elderly osteoporotic women, the bone is soft, indentable, and of poor osteogenic potency. In our department, we have been using only autologous calvarial bone grafts for augmentation of alveolar ridge atrophy since 1993. The bone is removed from the outer table of the skull only, trimmed to the alveolar ridge, und fixed with titanium lag scews. The skull defect created is covered with crushed bone or a titanium mesh to avoid aesthetic problems. Insertion of dental implants follows after a healing period of the bone grafts of 5-6 months. A total of 63 patients underwent calvarial split-graft augmentation; augmentation of the maxilla and mandible was carried out in 15 of these patients, of the maxilla only in eight, and of the mandible only in 40. The investigations 1 year later showed a resorption rate of approximately 10%. This is lower than when using iliac bone grafting. The resorption results were stable between 6 and 12 months after augmentation. Using dental implants (12 patients with 32 implants), the resorption rate was low and constant. We have never seen total loss of bone grafts or intracranial complications. All patients were pleased with the treatment. In our opinion, severe alveolar atrophy of the maxilla or mandible should be compensated for by augmentation with autologous calvarial bone grafts to obtain good long-term results.

Adult↗

Ataxia-telangiectasia: the pattern of cerebellar atrophy on MRI.

We describe MRI of the brain in 19 patients with ataxia-telangiectasia (AT) and correlate the appearances with the degree of neurologic deficit. We examined 10 male and nine female patients; 17 were aged between 2 and 12 years (mean 8 years) but a woman and her brother were 35 and 38 years old, and had a variant of AT. Ataxia was the first recognized sign of the disease in every patient. We detected the following patterns of cerebellar atrophy: in the youngest patient, aged 2 years, the study was normal; in the five next youngest patients 3-7 years of age, the lateral cerebellum and superior vermis showed the earliest changes of atrophy; and all but one of the other patients had moderate to marked diffuse atrophy of vermis and cerebellar hemispheres. There were 12 patients aged 9 years and above; one, who was normal, was 9 years old. The five patients who at the time of examination were unable to walk all had diffuse atrophy involving both vermis and cerebellar hemispheres.

Adult↗

MRI of the intraorbital optic nerve in patients with autosomal dominant optic atrophy.

Measurements of the intraorbital optic nerve were made using high-resolution coronal MRI in 10 adults with autosomal dominant optic atrophy. Comparisons were made with previous studies of 10 normal adult subjects. The cross-sectional diameters of the optic nerve and the perineural subarachnoid space were measured and a ratio of there diameters at anterior, mid and posterior positions along the optic nerve was determined. We found a statistically significant difference in the mean optic nerve: sheath ratio between the control group and patients with autosomal dominant optic atrophy. At anterior, mid and posterior locations along the optic nerve it is significantly smaller in patients with optic atrophy. We have demonstrated that the loss of ganglion cells, previously documented in dominant optic atrophy, is associated with a significant loss of optic nerve tissue and thinning of the nerve along its length.

Case-Control Studies↗