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PubMed2000

A voxel-based morphometry study of semantic dementia: relationship between temporal lobe atrophy and semantic memory.

The cortical anatomy of 6 patients with semantic dementia (the temporal lobe variant of frontotemporal dementia) was contrasted with that of a group of age-matched normal subjects by using voxel-based morphometry, a technique that identifies changes in gray matter volume on a voxel-by-voxel basis. Among the circumscribed regions of neuronal loss, the left temporal pole (Brodmann area 38) was the most significantly and consistently affected region. Cortical atrophy in the left hemisphere also involved the inferolateral temporal lobe (Brodmann area 20/21) and fusiform gyrus. In addition, the right temporal pole (Brodmann area 38), the ventromedial frontal cortex (Brodmann area 11/32) bilaterally, and the amygdaloid complex were affected, but no significant atrophy was measured in the hippocampus, entorhinal, or caudal perirhinal cortex. The degree of semantic memory impairment across the 6 cases correlated significantly with the extent of atrophy of the left anterior temporal lobe but not with atrophy in the adjacent ventromedial frontal cortex. These results confirm that the anterior temporal lobe is critically involved in semantic processing, and dissociate its function from that of the adjacent frontal region.

Aged↗

PubMedDate not supplied

[Is there any correlation between cerebral atrophy, EEG abnormalities and epileptic attacks in patients with multiple sclerosis?].

Among 100 patients with MS, in 65 patients CT examination revealed cerebral atrophy (in 58 cortical and subcortical atrophy, in 7 patients only cortical). In 25 (25%) patients with cerebral atrophy EEG findings were focal type of paroxysmal activity. Only five patients with paroxysmal discharges had epileptic fits. Mean age in these 5 patients was 47 years, mean duration of the disease 17 years. This means that seizures in MS patients appeared in late period of the disease and no correlation was between cerebral atrophy and epileptic seizures. Paroxysmal discharges occurred more often in EEG examination, than clinical seizures.

Adult↗

PubMed2000

Cerebellar atrophy following acute phenytoin intoxication.

A 25-year-old woman was admitted to our hospital with encephalopathy and clinical signs of cerebellar dysfunction. She had recently received an overdose of phenytoin. On admission, plasma phenytoin level was high (50 microg/ml, therapeutic range 10-20 mg/ml). Magnetic resonance imaging showed no signs of cerebellar atrophy. The patient's neurological condition improved rapidly after withdrawal of phenytoin. Eight months later, the neurological examination disclosed minimal cerebellar disorders and magnetic resonance imaging showed cerebellar atrophy. Cerebellar atrophy due to acute phenytoin intoxication is very unusual but few cases have been reported. The present clinical and radiological findings suggest that short-term phenytoin overdose alone may cause cerebellar atrophy.

Acute Disease↗

PubMed2000

[Gyrate atrophy of the choroid and retina: a case report].

BACKGROUND: Gyrate atrophy of the retina and choroid is a rare disease, with recessive autosomal transmission, characterized by progressive chorioretinal atrophy causing blindness. It results from a congenital deficit in aminotransferase ornithine. CASE REPORT: The authors present the case of a young patient aged 15 years old consulting for a progressive fall of visual acuity with hemeralopia. Eye funduscopy showed regions of confluent rounded chorioretinal atrophy. The visual field, the electroretinogram and the retinal angiography were all alterated. Gyrate atrophy of the retina and choroid was evocated. DISCUSSION: It is a systemic and rare metabolic disease where ocular features are dominating. Differencial diagnosis are pigmentary retinopathies. Cataract and/or myopia are often joined to the retinal lesions. General signs could consist in muscular weakness, thin and rare hairs and mental retardation. More than; visual fields, electroretinogram, retinal angiography that are alterated; the plasmatic dosage of the ornithine is often high. The treatment is based on the dietetics with uncertain results. The genic therapy would be the treatment of future.

Adolescent↗

PubMed2000

Optic atrophy in association with cobalamin C (cblC) disease.

PURPOSE: To report the association of optic atrophy with cobalamin C (cblC) disease. METHODS: Descriptive case reports on three patients, two of whom were siblings. RESULTS: All three patients with cblC disease exhibited bilateral optic atrophy with decreased visual acuity. Of the two siblings, the younger sister had received cobalamin supplements from birth and the mother had been given cobalamin supplements prenatally. CONCLUSION: These three cases confirm the association of optic atrophy with cblC disease. Early treatment with cobalamin supplements does not appear to prevent the development of optic atrophy.

Age of Onset↗

PubMed2001

Loss and atrophy of layer II entorhinal cortex neurons in elderly people with mild cognitive impairment.

Layer II of the entorhinal cortex contains the cells of origin for the perforant path, plays a critical role in memory processing, and consistently degenerates in end-stage Alzheimer's disease. The extent to which neuron loss in layer II of entorhinal cortex is related to mild cognitive impairment without dementia has not been extensively investigated. We analyzed 29 participants who came to autopsy from our ongoing longitudinal study of aging and dementia composed of religious clergy (Religious Orders Study). All individuals underwent detailed clinical evaluation within 12 months of death and were categorized as having no cognitive impairment (n = 8), mild cognitive impairment (n = 10), or mild or moderate Alzheimer's disease (n = 11). Sections through the entorhinal cortex were immunoreacted with an antibody directed against a neuron-specific nuclear protein (NeuN). Stereological counts of NeuN-immunoreactive stellate cells, their volume, and the volume of layer II entorhinal cortex were estimated. Cases exhibiting no cognitive impairment averaged 639,625 +/- 184,600 layer II stellate neurons in the right entorhinal cortex. Individuals with mild cognitive impairment (63.5%; p < 0.0003) and mild or moderate Alzheimer's disease (46.06%; p < 0.0017) displayed significant losses of layer II entorhinal cortex neurons relative to those with no cognitive impairment but not relative to each other (p > 0.33). There was also significant atrophy of layer II entorhinal cortex neurons in individuals with mild cognitive impairment (24.1%) and Alzheimer's disease (25.1%). The volume of layer II was also reduced in individuals with mild cognitive impairment (26.5%), with a further reduction in those with Alzheimer's disease (46.4%). The loss and atrophy of layer II entorhinal cortex neurons significantly correlated with performance on clinical tests of declarative memory. Atrophy of layer II entorhinal cortex and the neurons within this layer significantly correlated with performance on the Mini Mental Status Examination. These data indicate that atrophy and loss of layer II entorhinal cortex neurons occur in elderly subjects with mild cognitive impairment prior to the onset of dementia and suggests that these changes are not exacerbated in early Alzheimer's disease.

Aged↗

PubMed2001

Hyperostosis cranii ex vacuo in adults: a consequence of brain atrophy from diverse causes.

Hyperostosis cranii ex vacuo is diffuse thickening of the bones of the cranium occurring after successful ventricular shunting in hydrocephalic children, presumably as a compensatory phenomenon. We present three adults with severe brain atrophy and correspondingly severe skull thickening. In each, the cause of cerebral atrophy was well defined, and none had undergone ventricular shunting. In two, brain atrophy resulted from different temporally discrete insults sustained in adult life, ischemic in one and traumatic in the other. In the third case. progressive brain atrophy resulted from a primary neurodegenerative disorder, Hallervordan Spatz disease. Our observations suggest that hyperostosis cranii ex vacuo is a more general phenomenon than has been previously recognized, and point to a relationship between dynamic changes in brain size and skull thickness. We suggest that such relationships should be taken into account in anthropometric evaluation of the skull.

Adult↗

PubMed2000

Brain and spinal cord atrophy in multiple sclerosis.

Until recently, atrophy of the brain and spinal chord was thought to occur late in the course of multiple sclerosis (MS) or as a result of rare, fulminant disease. Now atrophy is known to occur early and likely indicates destructive and irreversible pathologic change that may be subclinical. Central nervous system atrophy from MS now can be measured accurately over short time intervals. Atrophy may become an important prognostic indicator in MS and is being evaluated as a treatment outcome measure in population studies, and possibly in the future, in individuals.

Atrophy↗

PubMed1997

Muscle atrophy and hormonal regulation in women in 120 day bed rest.

It is known, that exposures to real and simulated weightlessness results in pronounced reduction of the cross-sectional area (CSA) of slow-twitch(ST) and fast-twitch(FT) fibers of mammalian muscle. After space flights of various durations, head-down tilt bedrest, and 7-days of dry immersion sufficient [correction of isufficient] reductions of CSA of both fiber types were observed in man and in the majority of these cases the atrophy levels of ST and FT fibers were similar. It is well-known, that elevated contractile activities of muscle system attenuate muscle atrophy development. It remains still unclear which fiber type is more susceptible to training effects. Among physiological mechanisms involved in the process of microgravity-induced atrophy development which are supposed to be the most important are the profound decrease of a mechanical tension of muscle fibers in situ and alterations in hormonal control of muscle protein metabolism. But it is not known yet if the hormonal changes in the course of exposure to gravitational unloading match somehow the time-course of muscle fiber size reduction. The aim of the study was to investigate the time-course of muscle fiber atrophy development and changes in plasma hormone levels in the course of long-duration BR with and without high-intensity locomotor interval physical training.

Adenosine Triphosphatases↗

PubMed1997

Effect of estrogen on the development of disuse atrophy of bone and muscle induced by tail-supension in rats.

Rat tail-suspension induces disuse atrophy of muscles and bones in hindlimbs. In the present investigation we studied how ovariectomy and estrogen substitution affect the development of the disuse atrophy induced by suspension. Five-week old female Wistar rats were ovariectomized and divided into two groups. One group received intramuscular injection of estradiol dipropionate once a week (OVX-E2 group), and the other received a vehicle injection (OVX group). After the third injection, each group was further divided into two groups, tail-suspended and non-suspended. After 7 days of tail-suspension, a significant decrease in the wet weight of femurs and their Ca and Pi content was observed in the OVX group. However, no significant change in those parameters was observed in the E2 group. In both E2 and OVX groups, a significant decrease in the wet weight of soleus and gastrocnemius muscles was demonstrated after the suspension. This demonstrated that estrogen administration to ovariectomized rats prevents the development of disuse bone atrophy but not that of muscle atrophy, suggesting that estrogen plays important roles in bone remodeling.

Animals↗

PubMedDate not supplied

[Cervical collar therapy for juvenile muscular atrophy of distal upper extremity (Hirayama disease): results from 38 cases].

BACKGROUND: Juvenile muscular atrophy of distal upper extremity is a peculiar type of cervical myelopathy affecting young people characterized by localized amyotrophy in the forearm and hand that is initially progressive, and then stabilized in a few years. The anterior horn cell damage may be induced by forward displacement of the lower cervical dural sac and spinal cord on neck flexion. We proposed that the forward displacement was one of pathogenic factors, and reported that therapeutic intervention using a cervical collar in order to minimize neck flexion halted the progressive weakness in some patients. OBJECTIVE: To examine effectiveness of cervical collar treatment for this disease and to investigate clinical and radiological profiles that predict a favorable outcome before treatment. METHODS: Thirty-eight patients who had progressive illness within 5 years after onset underwent cervical collar therapy (treatment group). Forty-five patients in a previous case series without any therapeutic intervention made up a control group. The duration of progressive phase of illness was compared between the two groups. In the treatment group, the time interval from onset and the measurements of cervical cord atrophy and its flattening on neck flexion at the introduction of treatment by CT-myelography or MRI were analyzed with respect to prognosis. RESULTS: All the patients in the treatment group showed no further progression after introduction of treatment. The duration of the progressive period was shorter in the treatment group (mean 1.8 +/- 1.2 years) than in the control group (mean 3.2 +/- 2.3 years) (p < 0.005). In the treatment group, 15 of 31 patients within 2.5 years after the onset showed not only stabilization but also improvement of muscular weakness or cold paresis. Five of 7 patients who had no or mild cord atrophy at the introduction showed improvement after treatment. CONCLUSION: Cervical collar therapy induces a premature arrest of this disease. Improvement is expected in patients who have shorter duration of illness and have mild cord atrophy in a neutral neck position. Early diagnosis and therapeutic intervention may minimize the functional disability of young patients.

Adolescent↗

PubMed2001

Multiple system atrophy: cellular and molecular pathology.

Multiple system atrophy is an adult onset neurodegenerative disease, featuring parkinsonism, ataxia, and autonomic failure, in any combination. The condition is relentlessly progressive and responds poorly to treatment. Death occurs on average six to seven years after the onset of symptoms. No familial cases of multiple system atrophy have been reported, and no environmental factors have been robustly implicated as aetiological factors. However, analytical epidemiological studies are hampered because the condition is relatively rare. The discovery of the glial cytoplasmic inclusion (GCI) in 1989 helped to define multiple system atrophy as a clinicopathological entity, and drew attention to the prominent, if not primary, role played by the oligodendrocyte in the pathogenesis of the condition. Subsequently, GCIs were shown to be positive for alpha-synuclein, with immunostaining for this protein indicating that white matter pathology was more widespread than had previously been recognised. The presence of alpha-synuclein in GCIs provides a link with Parkinson's disease, dementia with Lewy bodies, and neurodegeneration with brain iron accumulation, type 1 (or Hallervorden-Spatz syndrome), in which alpha-synuclein is also found within Lewy bodies. This has led to the term "synucleinopathy" to embrace this group of conditions. The GCIs of multiple system atrophy contain a range of other cytoskeletal proteins. It is unknown how fibrillogenesis occurs, and whether there is primary oligodendrocytic dysfunction, which then disrupts the neurone/axon as a consequence of the glial pathology, or whether the oligodendrocytic changes merely represent an epiphenomenon. Further research into this devastating condition is urgently needed to improve our understanding of the pathogenesis, and also to produce new treatment approaches.

Aged↗

PubMed2002

Brain atrophy in mild or moderate traumatic brain injury: a longitudinal quantitative analysis.

BACKGROUND AND PURPOSE: Although mild or moderate traumatic brain injury (TBI) is known to cause persistent neurologic sequelae, the underlying structural changes remain elusive. Our purpose was to assess decreases in the volume of brain parenchyma (VBP) in patients with TBI and to determine if clinical parameters are predictors of the extent of atrophy. METHODS: We retrospectively assessed the total VBP in 14 patients with mild or moderate TBI at more than 3 months after injury and in seven patients at two time points more than 3 months apart. VBP was calculated from whole-brain MR images and then normalized by calculating the percent VBP (%VBP) to correct for intraindividual variations in cranial size. Clinical parameters at the time of trauma were evaluated for potential predictors of atrophy. Findings were compared with those of control subjects of similar ages. RESULTS: In the single time-point analysis, brain volumes, CSF volumes, and %VBP were not significantly different between patients and control subjects. In the longitudinal analysis, the rate of decline in %VBP (0.02 versus 0.0064 U/day, P =.05) and the change in %VBP between the first and second time points (-4.16 +/- 1.68 versus -1.49 +/- 1.7, P =.022 [mean +/-SD]) were significantly greater in patients. Change in %VBP was significantly greater in patients with loss of consciousness (LOC) than in those without LOC (P =.023). CONCLUSION: Whole-brain atrophy occurs after mild or moderate TBI and is evident at an average of 11 months after trauma. Injury that produces LOC leads to more atrophy. These findings may help elucidate an etiology for the persistent or new neurologic deficits that occur months after injury.

Adult↗

PubMed2002

Dietary bile acids inhibit potentially elemental diet-induced small intestinal atrophy in rats.

The mechanism responsible for elemental diet (ED)-induced small intestinal atrophy is still unknown. However, it is possible that bile acids in the gut lumen influence this process. The aim of this study was to evaluate the effects of oral bile acid administration during ED feeding. Specific pathogen-free male Sprague-Dawley rats, 10 weeks old, were fed an ED only, ED plus 0.1% (w/w) hyocholic acid, or ED plus 0.1% (w/w) hyodeoxycholic acid ad libitum for 4 weeks. The control rats were fed standard chow ad libitum for 4 weeks. After 4 weeks, the wet weight and whole length of the small intestine, and the mucosal diamine oxidase (DAO) and alkaline phosphatase (ALP) activities were measured. Microscopic histological observation was also performed. ED feeding induced atrophy and elevations in the mucosal DAO and ALP activities in the small intestine. Hyocholic acid and hyodeoxycholic acid administration both tended to inhibit these alterations. In conclusion, ED feeding induced atrophy and elevations in the mucosal DAO and ALP activities in the small intestine. Oral bile acid administration may prevent this atrophy and the elevations in mucosal DAO and ALP activities, which may lead to new therapeutic strategies in patients managed with ED.

Administration, Oral↗

PubMed2001

[Effects of kidney reinforcing and blood circulation activating Chinese medicine on morphological structure of mammary glands in models of mammary atrophy and hyperplasia in female rats].

OBJECTIVE: To study the effects and mechanism of Kidney reinforcing and blood circulation activating Chinese medicine (K&B) on morphologic structure of mammary glands in female rat models of mammary atrophy and mammary hyperplasia. METHODS: The models of mammary gland atrophy and hyperplasia were established respectively by ovariectomy and diethylstilbestrol injection to observe the changes of gland's weight index, structure, estradiol receptor (ER) and progesterone receptor (PR) after treated by K&B. RESULTS: (1) K&B could ameliorate the atrophied structure of mammary gland with significant increase of weight index (P < 0.01), raise the number of ER and PR in mammary tissue and nuclei (P < 0.01, P < 0.05), normalize the ratios of ER and PR in plasma and those in nucleus (EnR/EcR and PnR/PcR). (2) K&B could also improve or restore the proliferated structure of mammary gland and its weight index as well as the EnR/EcR and PnR/PcR ratios. CONCLUSION: K&B has the effects in preventing and improving the mammary gland atrophy induced by hyposecretion of sexual hormone and promoting the development of mammary gland in adult rats. Although both K&B and estrogen can improve the development of mammary gland, their mechanisms are different. There is a bright future of K&B in treating underdevelopment of mammary gland.

Animals↗

PubMedDate not supplied

[Progressive encephalopathy with oedema, hypsarrhythmia and optic atrophy (PEHO syndrome). A case report].

INTRODUCTION: Progressive encephalopathy with oedema, hypsarrhythmia and optic atrophy (PEHO syndrome) is a pathological process that begins in the first months of life and quickly leads to a very serious encephalopathy. We report the case of an infant suffering from PEHO syndrome and discuss its pathogenesis. CASE REPORT: A 4 year old male, the son of parents who were not blood related, with no pre or perinatal background of interest, who, from the first month, was seen to have a moderate retardation in psychomotor development and generalised hypotonia. These clinical signs increased progressively over the next months. From the age of 6 months onwards infantile spasms were observed, together with an EEG displaying hypsarrhythmic characteristics, slight facial oedema as well as in the hands, abnormal ocular movements and loss of vision with optic atrophy. In the neuroimaging serial studies, MRI showed a progressive atrophy of the brain stem and the cerebellum associated with cortical atrophy, hypoplasia of the corpus callosum and retarded myelination. CONCLUSIONS: Diagnosis of PEHO syndrome is essentially clinical with the help of neuroimaging, since there is no biological or genetic marker. The case described fulfils the criteria required for diagnosis of PEHO syndrome. The existence of cases in the family suggests that PEHO syndrome is due to a genetically based neurodevelopmental disorder. To our knowledge this is the first case reported in Spain.

Abnormalities, Multiple↗

PubMedDate not supplied

[Mixed hypotonia, neurological regression and atrophy of the cerebellum: manifestations that suggest infantile neuroaxonal dystrophy].

INTRODUCTION: Infantile neuroaxonal dystrophy (INAD), or Seitelberger disease, is a neurodegenerative disease of unknown origin which is transmitted by autosomal recessive inheritance. Clinically, it courses with psychomotor stagnation and regression that begins at the age of one or two years, associated to hypotonia with mixed clinical features (segmentary and suprasegmentary) that progresses towards spastic tetraplegia and progressive optic atrophy and dementia; this leads to death before the age of ten years. AIMS. To present the case of a 30 month old child with INAD, in whom a N acetylgalactosaminidase deficiency and mitochondrial cytopathy were ruled out. CASE REPORT: Male aged 30 months with an initial overall retardation, and later regression, of psychomotor acquisitions. In the physical exploration the patient displayed serious neurological involvement with mixed hypotonia, muscular hypotrophy with generalised weakness and mild bilateral horizontal nystagmus. Complementary explorations with neuroimaging revealed a slight increase in the subarachnoid space, with atrophy of the vermis and cerebellar hemispheres. Neurophysiological tests (EMG and ENG), which were initially normal, later showed signs of denervation in the EMG, and the ENG revealed a decreased amplitude of motor responses, with preservation of conduction speed. Histological tests showed the presence of axons with axoplasm expanded by the inclusion of typical tubulovascular structures. CONCLUSION: The clinical features of our patient met all the criteria to satisfy a diagnosis of INAD, and he displayed a classic form of the disease. INAD must be considered when the clinician is faced with: 1. A clinical picture of stagnation and later regression of psychomotor development before the age of two years; 2. Hypotonia, muscular atrophy and initial overall areflexia, with later progression towards pyramidalism; 3. Initially normal EMG findings, with later signs of denervation; 4. Cerebellar atrophy (hemispheres and vermis); 5. Visual deficit, and 6. Histopathological proof of characteristic findings.

Atrophy↗

PubMed2003

[The effect of retabolil and support loads on atrophied muscles in suspended rats].

In experiments with rats histological and morphometric methods were employed to study effects of anabolic steroid rhetabolil and a combination of rhetabolil with predetermined support loads on development of atrophy in m. soleus and m. gastrocnemius. Muscular atrophy was provoked by tail suspension of rats for a period of 30 days. Rhetabolil was injected once a week I/M at a total dose of 10 mg per 100 g of the body mass. The experiment showed that this dose of rhetabolil had no effect on atrophy development; neither it amplified the favorable effect of support loads observed in earlier experiments with injection of small doses of rhetabolil. A supposition was made that the anti-atrophy effects of rhetabolil combined with the support loads are dose dependent. It was concluded that large doses of rhetabolil do not activate anabolic processes in the load-deprived muscles.

Anabolic Agents↗