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PubMed2004

Patchy villous atrophy of the duodenum in childhood celiac disease.

OBJECTIVES: Patchy villous atrophy of the duodenal mucosa has been described in adults with untreated celiac disease (CD) but not in children. The authors evaluated the presence and the distribution of villous atrophy in children with celiac disease to see whether this histologic pattern exists in children. METHODS: We studied 95 children at diagnosis (Group 1) and seven during gluten challenge (Group 2). We measured anti-endomysium antibodies (EMA) by immunofluorescence on monkey esophagus, antihuman-tissue transglutaminase autoantibodies (anti-tTG Abs) by radioimmunoprecipitation, and HLA-DQ2/DQ8 heterodimers by polymerase chain reaction using specific primers. During upper intestinal endoscopy, at least five duodenal biopsy samples were obtained, one from the duodenal bulb and four from the distal duodenum. RESULTS: Thirteen of 95 (13.7%) patients in Group 1 and in 3 of 7 (42.9%) in Group 2 had patchy villous atrophy of the duodenum. In all 16 patients, villous atrophy of the bulb was present. In four children from Group 1, villous atrophy was observed only in the bulb samples. EMA, anti-tTG Abs, and HLA-DQ2/DQ8 heterodimers were present in all patients. Fourteen of 16 had symptomatic CD, and two were silent, detected during screening in subjects at risk for CD. CONCLUSIONS: This is the first study demonstrating that children with CD may have patchy villous atrophy of the duodenum. The bulb mucosa may be the only duodenal area involved, both at diagnosis and after gluten challenge. Therefore, multiple endoscopic biopsies should always be performed, not only in the distal duodenum, but also in the bulb.

Adolescent↗

PubMed2001

Gastric corpus atrophy following eradication of Helicobacter pylori.

BACKGROUND: Atrophic gastritis can develop in patients with Helicobacter pylori infection leading to a reduction in basal acid output. Whether the atrophy that develops is reversible is controversial. OBJECTIVE: To investigate the effect of H. pylori eradication in infected subjects who had developed atrophy of the corpus mucosa. METHOD: Ten H. pylori positive patients with corpus atrophy were identified at oesophagogastroduodenoscopy (OGD). They received eradication therapy with amoxicillin, clarithromycin and omeprazole. Repeat OGD with biopsy was performed at least 3 months later. Fasting plasma gastrin was measured at baseline and at re-endoscopy. H. pylori eradication was confirmed by 13C urea breath testing. RESULTS: Median time to re-endoscopy was 5 months. There was improvement in corpus atrophy in 50% of patients after H. pylori eradication, and a significant reduction in plasma gastrin (P = 0.03). The index patients had a significant diminution of basal acid output compared to controls. CONCLUSION: Corpus atrophy as defined by the Sydney System is reversible in some patients after H. pylori eradication. Improvement in atrophy is associated with a fall in fasting plasma gastrin levels. This may have implications in the prevention of gastric carcinoma.

Adult↗

PubMed1996

Isolated infraspinatus atrophy in a collegiate volleyball player.

PURPOSE: To describe a case of isolated infraspinatus atrophy due to suprascapular nerve entrapment by a labral ganglion cyst in a volleyball player and to propose a mechanism for its formation. CASE SUMMARY: A female volleyball player was evaluated for shoulder pain and found to have atrophy of the infraspinatus muscle. Magnetic resonance imaging (MRI) showed a loculated ganglion cyst impinging on the suprascapular nerve. DISCUSSION: Several etiologies for isolated infraspinatus atrophy in volleyball players are cited in the literature. It is suggested here that the rapid deceleration in the volleyball spike can result in a superior labral lesion (SLAP), which can lead to ganglion cyst formation. These ganglion cysts can then cause isolated infraspinatus atrophy by impinging on the suprascapular nerve at the spinoglenoid notch. RELEVANCE: In one study, isolated infraspinatus atrophy was found in 12% of elite volleyball players. Since infraspinatus atrophy may result from impingement of the suprascapular nerve by ganglion cysts and not just traction injuries, imaging studies, such as an MRI, should be considered in the evaluation of these patients.

Adult↗

PubMed2002

Enteral feeding and gut atrophy.

PURPOSE OF REVIEW: Because of the hypothesis that enteral feeding prevents intestinal mucosal atrophy and bacterial translocation, when fasting or malnutrition is present, nutrition support by the enteral route is usually preferred, if it is available. If nutrients are provided only parenterally intestinal mucosal mass falls dramatically in rats, but the relevance of this finding to humans has not been documented. This article reviews findings in the last 2 years relating to this dilemma. RECENT FINDINGS: Most work continues to be done in rats and pigs, two species that demonstrate mucosal atrophy with fasting. The earlier demonstration of effects of administration of hormones and glutamine have been corroborated, but proper controls for hormones (related peptides) or glutamine (most importantly glutamate) have usually not been included. In humans mucosal atrophy does not occur except modestly (approximately 10% decrease in thickness) in some reports during catabolic conditions, such as in critical-care units. Even so, no evidence for reversal by enteral feeding has as yet been provided. On the other hand, evidence for specific gene adaptation with or without mucosal atrophy has begun to appear in animals and humans. SUMMARY: The focus on mucosal atrophy has obscured the adaptation that may occur simultaneously to minimize the atrophy. Attention to gene adaptation during fasting and malnutrition may provide evidence, in future, for appropriate therapeutic interventions.

Adaptation, Physiological↗

PubMed2003

Spinal muscular atrophies reveal motor neuron vulnerability to defects in ribonucleoprotein handling.

PURPOSE OF REVIEW: Many forms of spinal muscular atrophy, a pure lower motor neuron disease, have been characterized clinically but the molecular basis of most of these is unknown. In this article we review recent developments in our understanding of the spinal muscular atrophies and how this knowledge has revealed important new insights into the causes of motor neuron vulnerability which may ultimately lead to novel therapies for this untreatable group of disorders. RECENT FINDINGS: The identification of the genetic basis of two forms of autosomal recessive spinal muscular atrophy has revealed that lower motor neurons appear to have a specific vulnerability to defects in RNA metabolism. Most notably, the survival motor neuron protein, deficient in the most common form of spinal muscular atrophy, plays a multifunctional role in ribonucleoprotein metabolism and pre-messenger RNA splicing. The role of this protein in motor neurons is currently under intense study. The identification of two other spinal muscular atrophy-causing genes has provided support for the central role of components of the RNA metabolic pathway in determining motor neuron survival. SUMMARY: Understanding the molecular basis of lower motor neuron vulnerability in disorders such as spinal muscular atrophy will ultimately allow these disabling disorders to be treated. In addition we can expect to learn much about basic neuronal biology and about the pathways that are relevant to more common neurodegenerative disorders such as amyotrophic lateral sclerosis.

Animals↗

PubMedDate not supplied

Fine structure of muscle in human disuse atrophy: significance of proximal muscle involvement in muscle disorders.

The universal occurrence of weakness of skeletal musculature on disuse, however produced, and the paucity of published reports on the fine structural changes in human disuse atrophy, prompted the present investigation. The quadriceps muscle of a leg immobilized in plaster cast (for fracture) and of the opposite non-immobilized limb was biopsied in four adult males, after periods of immobilization from 50 to 75 days. These 8 muscle specimens were examined for histopathological changes, and muscle fibre diameters were measured by micrometry from paraffin sections. The histograms revealed a larger proportion of small fibres (less than 20 micron) and a smaller proportion of large fibres (greater than 40 micron) in the immobilized limb compared to the opposite. Thus, light microscopy showed only atrophic changes. This was confirmed by electronmicroscopy, where atrophy of few to several muscle fibres was seen in the form of loss of myofibrils, collapse and folding of the basement membrane and prominence of glycogen or muscle nuclei. The atrophic change was more severe in the immobilized limbs, but it was also noticeable in all the non-immobilized limbs. Degenerative changes, especially disorganization and breakdown of myofibrils, and fragmentation of plasma membrane, were also seen in occasional atrophied muscle fibres, again more frequently in the immobilized limb. Lipofuscin was often found accumulated in muscle fibres and occasionally in endothelial cells of intramuscular blood vessels; the latter showed prominent pinocytotic vesicles or thickened basement membrane. It is concluded that both atrophy and degeneration of fibres of proximal muscles can occur as non-specific consequences of disuse of the limb in man, that degeneration is a latter and more severe change, that muscles even of the non-immobilized leg are subjected to disuse atrophy during bed-rest, and that the proximal muscles in man seem to have a natural susceptibility to atrophy and degeneration in any muscular disorders.

Adult↗

PubMed1978

Brain atrophy and intellectual impairment in heavy drinkers--a clinical, psychometric and computerized tomography study.

The frequency of cerebral and cerebellar atrophy was assessed by computerized tomography (CT) in 26 heavy drinkers. Findings were correlated with clinical deficits, with the results of psychometric testing using the Wechsler Adult Intelligence Scale (WAIS), and with the alcoholic history and nutritional status. Cerebral atrophy was present in 19 cases (73%), 16 of whom also had cerebellar atrophy. There was a good correlation between the degree of cerebral hemisphere atrophy and age and length of drinking history, but a poor correlation between neurological deficits and atrophy. Impairment of visuo-spatial and visuo-motor functions with sparing of other non-dominant hemisphere functions and of verbal skills was the characteristic pattern found with the WAIS in 18 subjects; four showed a more global depression of intellectual function. The degree of cerebral hemisphere atrophy correlated significantly with the impairment of non-dominant hemisphere functions but not with total IQ.

Adult↗

PubMed1989

Influence of improved drinking habits on brain atrophy and cognitive performance in alcoholic patients: a 5-year follow-up study.

In the period 1977-1979, a sample of consecutively admitted alcoholic in-patients was studied with CT scan of the brain and neuropsychological tests. A subsample of 52 patients met the following criteria: age less than 46 years, no history of severe head injury or focal signs of traumatic brain damage, and no history of liver disease, drug abuse, or long-lasting anticonvulsant therapy. However, 72% of the patients showed brain atrophy and 49% intellectual impairment as compared to 16% and 13%, respectively, in an age-matched sample of men from the general population. Five years later, after excluding patients with head trauma, serious alcoholic liver disease and drug abuse, 37 patients were reinvestigated. Sixteen patients were abstinent or had greatly improved drinking habits during the 5-year follow-up period and 21 were still drinking. Alcohol abstinence was found to be associated with a regress of cortical atrophy and central atrophy as assessed by the width of the 3rd ventricle. However, the recovery was not complete as compared with the prevalence of atrophy in the sample from the general population. Among the patients a significant improvement in one cognitive test and a trend to improvement in some other tests associated with improved drinking habits was observed. Regression of central atrophy as assessed by a decreased diameter of the 3rd ventricle was associated with improvement in the very same cognitive tests. The results suggest that both atrophy of the brain and cognitive ability can improve in alcoholics who give up drinking.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2002

Is gadolinium enhancement predictive of the development of brain atrophy in multiple sclerosis? A review of the literature.

BACKGROUND AND PURPOSE: Several studies have demonstrated that brain atrophy can be detected over relatively short intervals from the earliest stages of multiple sclerosis (MS). Reviewing the published data, the authors highlight some hypothetical pathological mechanisms proposed as determinants of brain atrophy. METHODS: Using the terms multiple sclerosis, MRI (magnetic resonance imaging), and brain atrophy, 181 citations were identified. The authors considered only studies with prospective designs with natural-course MS patients and/or placebo-treated patients of therapeutic trials, in which patients underwent baseline and follow-up scans with a T1-weighted gadolinium diethylenetriamine penta-acetic acid sequence (0.1 mmol/kg body weight), and correlation analyses between Gd enhancement activity and brain atrophy progression. RESULTS: Five hundred thirty-two patients of 5 natural history studies and 5 therapeutic trial studies participated in the review process. The main observation was that in patients with a relapsing-remitting (RR) disease course, there was a correlation between Gd enhancement activity and brain atrophy progression. This correlation was not influenced by any other demographic and clinical additional data considered in the review process. CONCLUSIONS: Examination of the pathological mechanisms proposed in the reviewed studies led the authors to believe that inflammation is only in part responsible for the development of brain atrophy. This conclusion may have an implication for the strategies of tissue protection advocated in the early stages of the RR course and strengthen recent evidence indicating that anti-inflammatory immunomodulatory agents and immunosuppressive treatments, which predominantly act against the inflammatory component of disease activity, may not have similar effects on progressive tissue loss, either in RR or progressive MS.

Atrophy↗

PubMed1977

Atrophy of optic nerve fibres in compression of the chiasm. Prognostic implications.

A relationship between the degree of atrophy of retinal nerve fibres and visual field defect has been described in postoperative steady-state patients (Lundström & Frisén 1976). The same factors were studied prior to surgery in six patients with compression of the chiasm due to chromophobe adenoma. In five eyes the field defect was excessive in relation to the degree of atrophy. After surgery the visual field defects improved to a level corresponding to the degree of atrophy in these eyes. In the remaining seven eyes there was a close correspondence between the atrophy and the visual field defect already before surgery. The visual field defects remained unchanged in these eyes. Provided that atrophy does not increase after surgery, simultaneous preoperative evaluation of retinal nerve fibre atrophy and visual field defect allows an accurate prediction of prognosis for improvement.

Adenoma, Chromophobe↗

PubMed1985

Clinical trials of vitamin B6 and proline supplementation for gyrate atrophy of the choroid and retina.

Five patients with gyrate atrophy of the choroid and retina were examined ophthalmologically, especially ophthalmoscopically, to evaluate trials of vitamin B6 (pyridoxine) or supplementary proline. The oral administration of vitamin B6 was tried in two patients. The vitamin did not alter the serum ornithine level and the progression of chorioretinal atrophy in one patient (case 2). Despite a reduced serum ornithine level following vitamin B6 administration, chorioretinal atrophy progressed gradually in another patient (case 3). Supplementary proline was tried in four patients. Despite the supplementation the serum proline level did not increase, and the chorioretinal atrophy progressed in one patient (case 2) who received both vitamin B6 and proline. Supplementary proline minimised the progression of gyrate atrophy in the youngest patient (case 1) and halted the progression in two others (cases 4 and 5). Supplementary proline may possibly lessen the progression of chorioretinal lesions in gyrate atrophy.

Adolescent↗

PubMed1987

Iris atrophy with hypoperfusion and microneovascularisation.

A series of 17 patients with stromal atrophy, hypoperfusion, and microneovascularisation of the iris investigated in the Glaucoma Investigation and Research Unit are described, and their iris angiograms were compared with those of normal irides of patients in the same age group seen in general clinics. In all but one of the 17 cases this iris atrophy was associated with glaucoma or ocular hypertension, which appeared to be secondary to the iris changes. The condition was bilateral and presented a typical slit-lamp appearance, with subtle evidence of microneovascularisation. There was neither history nor clinical evidence of previous trauma, heterochromia, or intraocular inflammation. The commonest form of iris atrophy affected the inner third of the iris stroma in a patchy manner, often with sparing above. However, diffuse atrophy occurred in two cases, and there were two cases of 'senile tears' of the iris. Some accompanying atrophy of the pigment epithelium was usual but less prominent. The changes on fluorescein angiography of the iris included the late appearance of dye with a long arteriovenous circulation time, fewer arteries than normal with sectorial hypoperfusion, leakage of dye from the pupil margin and peripupillary neovascularisation, stromal tufts, and sometimes more complex stromal microneovascularisation. An expanded prominent lesser vascular circle was a common feature of the condition. The condition is bilateral and distinct from other forms of iris atrophy. In all cases the iris changes appeared to be secondary to the vascular hypoperfusion and were not consistently associated with evidence of gross vascular disease. All patients had grey (blue) irides, and this may be an aetiological factor. The condition appears common enough to form a significant group of glaucoma patients and to be a separate clinical entity.

Aged↗

PubMed2003

Quantitative analysis of axonal loss in band atrophy of the optic nerve using scanning laser polarimetry.

AIMS: To measure axonal loss in patients with band atrophy from optic chiasm compression using scanning laser polarimetry (GDx, Laser Diagnostic Technologies, Inc, San Diego, CA, USA) and to evaluate the ability of this instrument to identify this pattern of retinal nerve fibre layer (RNFL) loss. METHODS: 19 eyes from 17 consecutive patients with band atrophy of the optic nerve and permanent temporal hemianopia due to chiasmal compression, and 19 eyes from an age and sex matched control group of 17 healthy individuals were prospectively studied. All patients were submitted to an ophthalmic examination including Goldmann perimetry and evaluation of the RNFL using scanning laser polarimetry. Mean RNFL thickness around the optic disc were compared between the two groups. The diagnostic performance of the deviation from normal analysis provided by the GDx software was also assessed. RESULTS: The peripapillary RNFL thickness (mean (SD)) of eyes with band atrophy was 47.9 (7.63) micro m, 37.1 (8.48) micro m, 57.0 (9.31) micro m, and 37.2 (8.86) micro m in the superior, temporal, inferior, and nasal regions, respectively. The total average was 43.7 (12.0) micro m. In the control group, the corresponding values were 71.1 (12.2) micro m, 40.4 (10.9) micro m, 85.4 (14.0) micro m, and 49.8 (10.1) micro m. The total average measured 67.9 (11.2) micro m. The measurements from eyes with optic atrophy were significantly different from those in the control group in all regions but the temporal. The deviation from normal analysis provided by the GDx software failed to identify the majority of abnormalities in the temporal and nasal regions of patients with band atrophy. CONCLUSIONS: Scanning laser polarimetry was able to identify axonal loss in the superior, inferior, and nasal regions, but failed to detect it in the temporal region of the optic disc, despite the fact that this area was clearly altered in eyes with band atrophy. This examination also showed poor sensitivity to detect axonal loss in the nasal region when GDx software analysis was used. The results of this study emphasise that RNFL evaluation using scanning laser polarimetry should be interpreted with caution in the study of eye diseases that lead to axonal loss predominantly in the nasal and temporal areas of the optic disc.

Adult↗

PubMed1982

Overwhelming pneumococcal septicaemia in a patient with ulcerative colitis and splenic atrophy.

This report describes a young woman with ulcerative colitis who developed rapidly fatal pneumococcal septicaemia. Necropsy revealed splenic atrophy. This case supports the hypothesis that splenic atrophy might contribute to the morbidity of ulcerative colitis. The occurrence of splenic atrophy in ulcerative colitis is now well established. Splenic atrophy from other causes has been associated with severe bacterial infections, often pneumococcal. It has been suggested that splenic atrophy is most severe when ulcerative colitis is active and may contribute to postoperative morbidity. This case documents overwhelming septicaemia in a patient with splenic atrophy whose colitis was in remission.

Adult↗

PubMed2006

Increased cortical atrophy in patients with Alzheimer's disease and type 2 diabetes mellitus.

BACKGROUND: The risk of Alzheimer's disease (AD) is increased in type 2 diabetes (DM2). This increased risk has been attributed to vascular comorbidity, but other mechanisms, such as accelerated ageing of the brain, have also been implicated. OBJECTIVE: To determine whether AD in patients with DM2 is associated with an increased occurrence of vascular lesions in the brain, by increased cerebral atrophy, or a combination of both. METHODS: In total, 29 patients with AD and DM2 and 58 patients with AD and without DM2 were included in the study. Clinical characteristics were recorded, and a neuropsychological examination and magnetic resonance imaging (MRI) scan were performed. MRI scans were rated for cortical and subcortical atrophy, medial temporal lobe atrophy, white matter lesions, and infarcts. RESULTS: The neuropsychological profiles of the two groups were identical. Patients with AD and DM2 had increased cortical atrophy on MRI (p<0.05) compared with the non-DM2 group. In addition, infarcts were more common (odds ratio 2.4; 95% CI 0.8 to 7.8), but this effect did not account for the increased atrophy. The other MR measures did not differ between the groups. CONCLUSION: The results suggest that non-vascular mechanisms, leading to increased cortical atrophy, are also involved in the increased risk of AD in DM2.

Aged↗

PubMed2006

Cord atrophy separates early primary progressive and relapsing remitting multiple sclerosis.

BACKGROUND AND OBJECTIVE: The onset of multiple sclerosis is relapsing remitting or primary progressive. An improved understanding of the causes of early progressive disability in primary progressive multiple sclerosis (PPMS) could provide mechanistic targets for therapeutic intervention. METHODS: Five magnetic resonance imaging (MRI) parameters that could potentially cause progressive disability were investigated in 43 patients with early PPMS and in 37 patients with early relapsing remitting multiple sclerosis (RRMS): atrophy in brain, both grey matter and white matter; intrinsic abnormality in brain, both grey matter and white matter (measured by the magnetisation transfer ratio (MTR)); and atrophy of the upper cervical spinal cord. Both groups were also compared with controls. RESULTS: Patients with PPMS were older and more likely to be men. Both patient groups had atrophy of brain grey matter and white matter, and intrinsic abnormality in MTR of normal-appearing grey matter and white matter. Cord atrophy was present only in the PPMS (mean cord area: PPMS, 67.8 mm2; RRMS, 72.7 mm2; controls, 73.4 mm2; p = 0.007). This was confirmed by multivariate analysis of all five MRI parameters, age and sex. CONCLUSION: Grey matter and white matter of the brain are abnormal in both early RRMS and PPMS, but cord atrophy is present only in PPMS. This is concordant with myelopathy being the usual clinical presentation of PPMS. Measurement of cord atrophy seems to be clinically relevant in PPMS treatment trials.

Adult↗

PubMed1973

Possible neurogenic factor in muscular dystrophy: its similarity to denervation atrophy.

Muscle biopsy specimens from 179 cases of muscular dystrophies and from 140 cases of anterior horn cell disorders (from a total of 1,348 biopsied patients) were examined histologically. There were 72 cases of Duchenne type muscular dystrophy (DMD), five of Becker type MD, four girls with myopathy resembling DMD, 40 with limb-girdle, 10 with facioscapulohumeral, seven with late onset, 13 with congenital, and 28 with unclassifiable muscular dystrophies. Groups of small atrophied muscle fibres were encountered in 42 (23%) of the cases in this group, most frequently in patients with limb-girdle, facioscapulohumeral, and least frequently with DM dystrophy. In the second group there were 25 cases of infantile, 38 of juvenile, and 39 of adult spinal muscular atrophy (SMA); there were 21 patients with motor neurone disease (MND), six with poliomyelitis, and 11 with an unclassifiable type of anterior horn cell disorder. Pseudomyopathic changes were encountered in 43 (30%) of all cases in this group. They were most frequently present among patients with juvenile and adult SMA and in those with MND. The presence of group atrophy in muscular dystrophy is considered significant myopathological evidence of a denervation process. On the other hand, pseudomyopathic changes, variation in fibre size, rounding, central nuclei, and increase in connective tissue occurring in various anterior horn cell disorders are seen not to be specific `myopathic' changes. Thus there was an overlap of pathological reactions in muscles from the dystrophies and the neurogenic atrophies. Comparably atrophied fibres (much less than 2 SDs below the normal mean diameter) and hypertrophied fibres (much more than 2 SDs above the normal mean diameter) were encountered in both dystrophy and neurogenic atrophy, considering the large muscles of the limb. Likewise, the mean fibre diameters were comparable in DMD and in juvenile SMA. The fourth evidence of a neurogenic factor in muscular dystrophy was derived from an examination of SDH preparations of muscle. There was a preponderance of type I muscle fibres in dystrophic muscles compared with specimens from controls, suggesting depletion of type II fibres. It appears that the concept of muscular dystrophy as a primary muscle disease needs to be re-examined.

Adolescent↗

PubMed1996

Early diagnosis and stage classification of vocal cord abductor paralysis in patients with multiple system atrophy.

OBJECTIVES: Vocal cord abductor paralysis (VCAP) is a life threatening complication which may cause nocturnal sudden death in patients with multiple system atrophy. However, the early diagnosis of VCAP is often difficult to make on routine laryngoscopy performed during wakefulness, as stridor, which is the sole symptom of VCAP in the early stage, develops only during sleep. The aim was to investigate laryngeal dysfunction in patients with multiple system atrophy while awake and asleep. METHODS: Seven patients with multiple system atrophy with nocturnal stridor and five control patients were studied. Vocal cord movement was analysed by laryngoscopy while the patients were awake and also during sleep induced by intravenous diazepam. RESULTS: When awake, for the seven patients with multiple system atrophy normal movement of the vocal cords occurred in three, mild abduction restriction in three, and paradoxical movement in one. When asleep, however, all showed obvious paradoxical movement with high pitched inspiratory stridor. In controls, there were no differences in the vocal cord movement between wakefulness and sleep. From these findings, VCAP could be divided into four stages: stage 0 (normal) with normal vocal cord movement during both wakefulness and sleep, stage 1 (mild VCAP) with normal movement during wakefulness and paradoxical movement during sleep, stage 2 (moderately severe VCAP) with abduction restriction during wakefulness and paradoxical movement during sleep, and stage 3 (severe VCAP) with an almost midline position for the vocal cords during both wakefulness and sleep. CONCLUSIONS: Laryngoscopy during sleep can disclose subclinical VCAP, making an early diagnosis of VCAP in patients with multiple system atrophy. Stage 2 of VCAP seems to be a suitable stage for tracheostomy in patients with multiple system atrophy.

Aged↗