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Results for “Multiple System Atrophy”

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PubMed1998

Twenty-four-hour blood pressure profile and blood pressure responses to head-up tilt tests in Parkinson's disease and multiple system atrophy.

OBJECTIVE: To investigate the 24 h blood pressure profile in patients with Parkinson's disease with intact autonomic function or with autonomic failure and patients with multiple system atrophy (MSA), and to assess whether these patients exhibit posture-related variations in blood pressure. PATIENTS AND METHODS: We studied 24 patients with Parkinson's disease (11 with autonomic failure) and 13 patients with MSA (all with autonomic failure). Autonomic failure was determined by autonomic tests. An oscillometric recorder was used for ambulatory blood pressure monitoring. Tilt-table tests were performed with a head-up tilt position of 60 degrees. RESULTS: An alteration in the normal 24 h blood pressure profile was observed in 82% of Parkinson's disease patients with autonomic failure and in 85% of those with multiple system atrophy, but not in the patients with intact autonomic function. Head-up tilt tests revealed a significantly higher supine blood pressure in Parkinson's disease patients with autonomic failure and in those with MSA than in Parkinson's disease patients with intact autonomic function. Tilting resulted in a marked fall in blood pressure in patients with MSA; in Parkinson's disease patients with autonomic failure, the fall was comparatively slighter. CONCLUSIONS: We conclude that autonomic failure contributes to the alterations in the day-night blood pressure profile that may possibly be ascribed to postural dysregulation of blood pressure. We hypothesize that nocturnal hypertension is a risk factor in the development of additional cerebrovascular disease in patients with Parkinson's disease or MSA who are affected by autonomic failure.

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PubMed2002

Characteristic MRI findings in multiple system atrophy: comparison of the three subtypes.

We reviewed MRI findings in 29 patients with probable multiple system atrophy (MSA) to see whether there were common and or less common neuroradiological findings in the various clinical subtypes. We divided the patients into three clinical subtypes according to initial and predominant symptoms: 14 with olivopontocerebellar atrophy (OPCA), eight with the Shy-Drager syndrome (SDS) and seven with striatonigral degeneration (SND). The patients showed atrophy of the brain stem and cerebellum, high signal on T2-weighted images of the base of the pons and middle cerebellar peduncles, high and low signal on T2-weighted images of the putamen and atrophy of frontal and parietal lobes. The degree of atrophy of the middle cerebellar peduncle and cerebellum was greater in OPCA patients and a high-signal lateral rim to the putamen more frequent in SND. However, all findings were observed in all subtypes, and the degrees of atrophy of the putamen and pons and the frequency of high signal in the base of the pons were similar in the subtypes. We also found atrophy of the cerebral hemispheres, especially the frontal and parietal lobes, but its degree was not significantly different in the various subtypes. Our findings suggest that, although MSA can be divided clinically into three subtypes, most of the features on MRI are common and overlap in the subtypes, independently of the clinical presentation.

Brain↗

PubMed2004

Comparison of magnetic resonance imaging in subtypes of multiple system atrophy.

Some abnormal findings in routine MRI have been proposed as helpful discriminators for distinguishing multiple system atrophy (MSA) from Parkinson's disease (PD). However, what the most distinguishing MRI findings for MSA-p (parkinsonism dominant) or MSA-c (cerebellar dominant) are separately has not been systematically analyzed. To determine what the most helpful discriminators for MSA-p or MSA-c are and whether those findings are correlated with the presence of parkinsonism or cerebellar dysfunction, we compared 10 previously reported MRI findings in 36 patients with probable MSA-p, 27 patients with probable MSA-c and 30 patients with PD separately. In our results, hyperintense rim and putaminal atrophy among supratentorial parameters and the parameters of infratentorial atrophy were significantly prominent in MSA-p comparing to PD. Hyperintense rim showed the highest specificity in MSA-p patients (90.0%) with relatively suboptimal sensitivity (72.2%). In MSA-c, all infratentorial parameters had strong discriminating power comparing to PD. Signal increase in the middle cerebellar peduncle showed the highest specificity (100%) and had fair sensitivity (85.2%) in MSA-c. Compared between MSA-p and MSA-c, supratentorial parameters were not valid to differentiate MSA-c from MSA-p except for putaminal atrophy. On the contrary, infratentorial parameters were good for distinguishing MSA-c from MSA-p except dilatation of the fourth ventricle. Parkinsonism was not correlated with a hyperintense rim, but cerebellar symptoms were correlated with signal increase in the middle cerebellar peduncle. Our findings suggest the characteristic MRI can be helpful for differentiating MSA-p and MSA-c from PD, respectively, although they do not reflect the presence or lateralization of parkinsonism.

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PubMed1999

Prevalence of progressive supranuclear palsy and multiple system atrophy: a cross-sectional study.

BACKGROUND: The prevalence of progressive supranuclear palsy (PSP) and multiple system atrophy (MSA) in the general population is unknown. Clinicopathological studies of patients diagnosed as having Parkinson's disease suggest that the two disorders may be underdiagnosed. We investigated the population prevalence of these disorders. METHODS: We screened computerised records of 15 general practices in London, UK, for patients with specific diagnostic labels suggestive of Parkinson's disease or parkinsonism and all patients who had ever received antiparkinsonian medication. We assessed eligible patients by review of records, interview, physical examination, and video recordings of neurological signs for independent diagnostic confirmation. We diagnosed parkinsonian disorders according to published criteria and further reviewed patients with atypical features after 1 year. FINDINGS: The participation rate was 84%. The age-adjusted prevalence for PSP was 6.4 per 100,000 (five probable and one possible case [95% CI 2.3-10.6]) and for MSA 4.4 per 100,000 (two probable and two possible cases [1.2-7.6]). An additional four atypical patients were identified at 1 year but did not fulfil criteria for PSP or MSA. INTERPRETATION: Our results suggest that the true prevalence of PSP and MSA has been underestimated, since many patients in the community remain undiagnosed or misdiagnosed.

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PubMed1998

Multiple system atrophy with severe involvement of the motor cortical areas and cerebral white matter.

We report multiple system atrophy (MSA) of 14 years' duration in a 75-year-old woman. Postmortem examination revealed pathological changes typical of MSA. Furthermore, neuronal loss with astrocytosis in the primary motor and premotor cortices, especially in the fifth and sixth layers, and extensive myelin and axonal loss in the frontal and parietal white matter were evident. There were numerous ubiquitin-positive oligodendroglial inclusions, which are characteristic of MSA, in these cortical and white matter lesions. These findings suggest that the motor cortical areas and cerebral white matter are sites of significant involvement in the MSA disease process and that inclusion-bearing oligodendroglial alterations contribute to the white matter degeneration.

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PubMed2004

Alpha-synuclein immunoreactivity in neuronal nuclear inclusions and neurites in multiple system atrophy.

We examined neuronal and oligodendroglial nuclear inclusions and neurites in the pontine base of multiple system atrophy brains using an antibody to alpha-synuclein. Immunohistochemistry showed alpha-synuclein positive inclusions in the nuclei of some neurons and oligodendroglia. Immunoelectron microscopy showed that the labeled inclusions were composed of bundles of tightly packed straight filaments with a diameter of 10-20 nm. The filaments were similar, if not identical, in morphology and immunoreactivity, to those found in the soma of neurons and oligodendrocytes with glial cytoplasmic inclusions. In addition, similar immuno-positive filaments were found in dendrites or unmyelinated axons, but not in myelinated axons. The functional significance of these inclusions in terms of transcriptional and axonal dysfunction is unknown.

Actin Cytoskeleton↗

PubMed2007

Multiple system atrophy in a patient with the spinocerebellar ataxia 3 gene mutation.

The cerebellar variant of multiple system atrophy (MSA-C) has overlapping clinical features with the hereditary spinocerebellar ataxias (SCAs), but can usually be distinguished on a clinical basis. We describe a patient who developed a sporadic, late-onset, rapidly progressive neurodegenerative disorder consistent with MSA-C. Genetic testing, however, showed an abnormal expansion of one allele of the spinocerebellar ataxia 3 (SCA3) gene. The clinical impression of MSA-C was confirmed by identification of numerous alpha-synuclein-containing glial cytoplasmic inclusions on autopsy. These findings suggest that abnormal expansion of the SCA3 gene may be a risk factor for the development of MSA-C.

Alleles↗

PubMed2025

Distinct spatial transcriptomic patterns of substantia Nigra in Parkinson disease and Parkinsonian subtype of multiple system atrophy.

To investigate transcriptomic signatures of Parkinson's disease (PD) and the Parkinsonian subtype of Multiple System Atrophy (MSA-P) in substantia nigra pars compacta (SNpc), we conducted transcriptome analysis using in-situ hybridization on paraffin-embedded SNpc tissues from post-mortem brains. The study included 2 MSA-P patients, 2 PD patients, and 2 healthy controls (HC), with 12 regions of interest (ROIs) selected from the dorsal to ventral and medial to lateral aspects of the SNpc. A total of 72 ROIs from 6 participants were analyzed, and differentially expressed genes (DEGs) were identified by comparing MSA-P, PD and HC groups. The MSA-P group showed 88 upregulated DEGs and 326 downregulated DEGs (adjusted 𝑝<0.05) compared to HC. The downregulated DEGs were significantly enriched in pathways related to ribosomal translation, immune processes, mitochondrial function, and autophagy. Notably, the dorsomedial quadrant was uniquely linked to antigen presentation, while other quadrants showed downregulation of protein synthesis. The PD group exhibited 165 upregulated DEGs and 350 downregulated DEGs (adjusted 𝑝<0.05) compared to HC, with downregulated DEGs associated with ribosomal translation, mitochondrial function, and the ubiquitin-proteasome system. In both MSA-P and PD, the upregulated DEGs were not associated with any pathways or biological process in gene enrichment analysis. In network propagation analysis, amyloid precursor protein was the most significant network hub among DEGs in both MSA-P and PD. Comparing the transcriptomic signatures of SNpc between MSA-P and PD, we found immune/inflammation, mitochondrial function and neural signaling related genes were significantly downregulated in MSA-P compared to PD. Overall, the transcriptomic signature of the SNpc in MSA-P and PD revealed overlapping but distinct features, including alterations in protein synthesis, immune processes, mitochondrial function, and protein degradation systems. Future studies with larger cohorts and functional validation are needed to further elucidate these findings.

Humans↗

PubMed2003

Reciprocal accumulation of beta-synuclein in alpha-synuclein lesions in multiple system atrophy.

Alpha-Synuclein is a major component of neuronal and glial cytoplasmic inclusions in multiple system atrophy (MSA), one of the alpha-synucleinopathies. Recent studies have shown that beta-synuclein, a homolog of alpha-synuclein, inhibits alpha-synuclein aggregation in vitro. We immunohistochemically examined the MSA brain, using specific antibodies against alpha-synuclein and beta-synuclein. alpha-synuclein-positive filamentous aggregates were frequently found in neurons in the pontine and inferior olivary nuclei. No abnormal accumulation of alpha-synuclein was noted in Purkinje cells. In contrast, beta-synuclein accumulation occurred extensively in Purkinje cells, and only minimally in pontine and olivary neurons. Thus, neuronal alpha-synuclein inclusions appear to occur only rarely in neurons in which beta-synuclein accumulates. These findings support the possibility that beta-synuclein is a negative regulator of alpha-synuclein aggregation.

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PubMed1999

[Neuronal kinases in glial cytoplasmic inclusions in patients with multiple system atrophy].

Glial cytoplasmic inclusions (GCI) occur characteristically in the cytoplasms of oligodendrocytes of brains with multiple system atrophy. We examined whether proline-directed protein kinases, which have been found in several neuronal inclusion bodies such as neurofibrillary tangles and Lewy bodies, are associated with GCI. We unexpectedly have observed cdk 5 and MAPK in GCI. These kinases were not immunolabeled in coiled bodies which are oligodendroglial inclusion bodies in brains with progressive supsranuclear palsy and Alzheimer's disease. We also found microtubule-associated protein 2 in oligodendrocytes in brains with MSA, which have not been observed in normal controls or neurological disease controls. Cdk 5 and MAP 2 are principally neuronal proteins. MAPK have been found in neuronal somata and some astrocytes, but not in oligodendrocytes. Thus, the present results suggest that oligodendrocytes in MSA harbor an abnormal phenotypic nature in terms of the aberrant expressions of the principally neuronal proteins.

Brain↗

PubMed2002

Abnormalities of rate-corrected QT intervals in Parkinson's disease-a comparison with multiple system atrophy and progressive supranuclear palsy.

A number of patients with Parkinson's disease (PD) and multiple system atrophy (MSA), in whom sudden death does occur occasionally, have QT or rate-corrected QT (QTc) interval prolongation on electrocardiogram (ECG). Although these QT or QTc interval abnormalities are likely related to autonomic dysfunction, the pathophysiology remains unknown. The aim of this study was to compare the degree of QTc interval prolongation among akinetic-rigid syndromes, namely PD and related disorders, and to evaluate the relationship between QTc prolongation and severity of autonomic dysfunction. Thirty-four patients with PD, 22 with MSA, 11 with progressive supranuclear palsy (PSP) and 30 healthy controls underwent standard autonomic function tests, and electrocardiography variables (RR, QT and QTc intervals) were measured by an ECG recorder with an automated analyzer. The relationship between QTc interval and cardiovascular reflex tests were also analyzed. Orthostatic hypotension and decreased heart rate in response to respiratory stimuli were prominent in MSA, while these were relatively mild in PD. Unlike the RR and QT intervals, the QTc interval significantly differed among all groups (p<0.01). The QTc interval was significantly prolonged in PD (409+/-17 ms; p<0.001) and MSA (404+/-14 ms; p<0.05) compared with healthy controls (394+/-19 ms). Neither autonomic dysfunction nor QTc interval prolongation was evident in PSP. QTc intervals and cardiovascular reflexes did not correlate, except for Valsalva ratio. The QTc interval was obviously prolonged in PD patients to an extent that could not be accounted for simply by autonomic dysfunction levels. MSA patients showed slightly prolonged QTc intervals in spite of marked cardiovascular autonomic dysfunction. Abnormalities of the QTc may reflect the degeneration of cardioselective sympathetic and parasympathetic neurons that cannot be fully captured by cardiovascular autonomic function tests.

Adult↗

PubMed2005

When is Onuf's nucleus involved in multiple system atrophy? A sphincter electromyography study.

BACKGROUND: External anal sphincter (EAS) electromyography (EMG) abnormalities can distinguish multiple system atrophy (MSA) from Parkinson's disease in the first five years after disease onset. However, the prevalence of the abnormalities in the early stages of MSA is unknown. OBJECTIVES: To present EAS-EMG data in the various stages of MSA. METHODS: 84 patients with "probable" MSA were recruited (42 men, 42 women; mean age 62 years (range 47 to 78); mean disease duration 3.2 years (0.5 to 8.0; <1 year in 25%); 50 cerebellar form (MSA-C), 34 parkinsonian form (MSA-P)). EAS motor unit potential (MUP) analysis and EMG cystometry were carried out in all patients. RESULTS: The overall prevalence of neurogenic change of the EAS MUP was 62%-52% in the first year after disease onset, increasing to 83% by the fifth year (p<0.05); it also increased with severity of gait disturbance (p<0.05), storage and voiding disorders, and detrusor sphincter dyssynergy (NS). The neurogenic change was not correlated with sex, age, MSA-P/C, postural hypotension, constipation, erectile dysfunction in men, underactive or acontractile detrusor, or detrusor overactivity. In 17 incontinent patients without detrusor overactivity or low compliance, urinary incontinence was more severe in those with neurogenic change than in those without (p<0.05). CONCLUSIONS: Involvement of Onuf's nucleus in MSA is time dependent. Before the fifth year of illness, the prevalence of neurogenic change does not seem to be high, so a negative result cannot exclude the diagnosis of MSA.

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PubMed2005

Voxel based comparison of glucose metabolism in the differential diagnosis of the multiple system atrophy using statistical parametric mapping.

OBJECTIVE: A differential diagnosis of idiopathic parkinsonian disease (IPD) and multiple system atrophy (MSA) is difficult due to their common signs and symptoms. The aim of this 18F-2-fluoro-2 deoxyglucose (18F-FDG) positron emission tomography (PET) study was to compare the regional cerebral glucose metabolism in MSA with that in IPD by statistical parametric mapping (SPM) and image registration. METHODS: The 18F-FDG PET images of MSA and IPD patients were assessed by SPM and image registration to determine metabolic patterns that may be useful in differentiating between the two groups. Eleven patients with MSA, eight patients with IPD and 22 healthy controls participated in the study. RESULTS: The IPD patients were found to have a significant glucose hypometabolism in comparison with the healthy controls in the prefrontal, lateral frontal, and parietotemporal cortices, and the cingulate and caudate areas (p< or =0.01, 100 voxel-level). In patients with MSA, hypometabolism was observed in the putamen, pons, and cerebellum in comparison with the healthy controls and IPD patients. CONCLUSION: The voxel-based analysis of 18F-FDG PET images showed detailed differences between IPD and MSA, which may be useful in differentiating the two disease entities, as evidenced by the correlation of glucose metabolism with disease severity and dopamine agonist medication. The mapping analysis of 18F-FDG PET images might be a useful adjunctive method of a differential diagnosis for parkinsonism in a clinical setting.

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PubMed2007

Diffusion-weighted magnetic resonance imaging differentiates Parkinsonian variant of multiple-system atrophy from progressive supranuclear palsy.

Progressive supranuclear palsy (PSP) and the parkinsonian variant of multiple-system atrophy (MSA-P) may present with a similar phenotype. Magnetic resonance diffusion-weighted imaging (DWI) has been shown to be a sensitive discriminator of MSA-P from Parkinson's disease (PD). We studied 20 PSP, 11 MSA-P, 12 PD patients and 7 healthy controls in order to investigate whether regional apparent diffusion coefficients (rADCs) help distinguish PSP and MSA-P; whether rADCs are correlated with clinical disease severity scores; and the relationship between brainstem and cerebellar volumes and rADCs in PSP and MSA-P. The Unified Parkinson's Disease Rating Scale, Hoehn and Yahr score, Mini Mental State Examination, and frontal assessment battery were recorded in all patients. Regional ADCs were measured in the middle cerebellar peduncle (MCP), caudal and rostral pons, midbrain, decussating fibers of the superior cerebellar peduncle, thalamus, putamen, globus pallidus, caudate nucleus, corpus callosum, frontal and parietal white matter, as well as the centrum semiovale. In MSA-P, rADCs in the MCP and rostral pons were significantly greater than in PSP (P < 0.001 and 0.009) and PD (P < 0.001 and = 0.002). Stepwise logistic regression revealed that the MCP rADC distinguishes MSA-P from PSP with a sensitivity of 91% and a specificity of 84%. Increased brainstem rADCs were associated with motor deficit in MSA-P and PSP. Increased rADCs in the pons and MCP were associated with smaller pontine and cerebellar volumes in MSA-P. rADCs distinguish MSA-P from PSP. These have a clinical correlate and are associated with reduced brainstem and cerebellar volumes.

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PubMed2001

Videourodynamic and sphincter motor unit potential analyses in Parkinson's disease and multiple system atrophy.

OBJECTIVES: Urinary dysfunction is a prominent autonomic feature in Parkinson's disease (PD) and multiple system atrophy (MSA), which is not only troublesome but also a cause of morbidity in these disorders. Recent advances in investigative uroneurology offer a better insight into the underlying pathophysiology and appropriate management for urinary dysfunction. METHODS: twenty one patients with PD (15 men, six women, mean age 64 (49-76), mean disease duration 4 years (1-8 years), median Hoehn and Yahr grade 3 (1-4), all taking 300 mg/day of levodopa (100-500 mg)) and 15 with MSA (eight men, seven women, mean age 59 (48-72), mean disease duration 3 years (0.5-6 years)) were recruited. Videourodynamic and sphincter motor unit potential analyses in the patients with PD and MSA were carried out, looking for distinguishing hallmarks that might be useful in the differential diagnosis of these two diseases. RESULTS: Urinary symptoms were found in 72% of patients with PD and in 100% with MSA. Filling phase abnormalities in the videourodynamic study included detrusor hyperreflexia in 81% of patients with PD and 56% with MSA, and uninhibited external sphincter relaxation in 33% of patients with PD and 33% of those with MSA. However, open bladder neck at the start of filling was not seen in patients with PD but was present in 53% of those with MSA, suggestive of internal sphincter denervation. Sphincter motor unit potential analysis showed neurogenic motor unit potentials in 5% of patients with PD and in 93% of those with MSA, suggestive of external sphincter denervation. On voiding, detrusor-external sphincter dyssynergia was not seen in patients with PD but was present in 47% of those with MSA. Pressure-flow analysis showed that the Abrams-Griffiths number, a grading of urethral obstruction (outflow obstruction >40), in PD (40 in women and 43 in men) was larger than that in MSA (12 in women and 28 in men). Weak detrusor in PD (66% of women and 40% of men) was less common than that in MSA (71% of women and 63% of men). Postmicturition residuals >100 ml were absent in patients with PD but were present in 47% of patients with MSA. CONCLUSION: Patients with PD had less severe urinary dysfunction with little evidence of internal or external sphincter denervation, by contrast with the common findings in MSA. The findings of postmicturition residuals >100 ml, detrusor-external sphincter dyssynergia, open bladder neck at the start of bladder filling, and neurogenic sphincter motor unit potentials are highly suggestive of MSA.

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PubMed2000

Complex motor disturbances in a sequential double lesion rat model of striatonigral degeneration (multiple system atrophy).

This study characterizes paw reaching, stepping and balance abnormalities in a double lesion rat model of striatonigral degeneration, the core pathology underlying levodopa unresponsive parkinsonism associated with multiple system atrophy. Extensive unilateral nigral or striatal lesions induced by 6-hydroxydopamine or quinolinic acid, respectively, produced a similarly marked contralateral paw reaching deficit without further deterioration following a secondary (complementary) lesion of ipsilateral striatum or substantia nigra. Contralateral stepping rates were reduced by unilateral 6-hydroxydopamine lesions without further deterioration following the secondary striatal lesion. In contrast, initial unilateral striatal quinolinic acid injections induced bilateral stepping deficits that significantly worsened contralaterally following the secondary nigral lesion. Contralateral sidefalling rates were significantly increased following primary nigral and striatal lesions. Secondary nigral but not secondary striatal lesions worsened contralateral sidefalling rates. Histological studies revealed subtotal (>90%) depletion of dopaminergic neurons in substantia nigra pars compacta and variable degrees of striatal degeneration depending on the lesion sequence. Animals pre-lesioned with 6-hydroxydopamine showed significantly larger residual striatal surface areas following the secondary striatal quinolinic acid lesion compared to animals with primary striatal quinolinic acid lesions (P<0.001). These findings are in line with previous experimental studies demonstrating that striatal dopamine depletion confers neuroprotection against subsequent excitotoxic injury. Whether loss of dopaminergic neurons protects against the striatal disease process occurring in multiple system atrophy (Parkinson-type) remains to be elucidated. In summary, this is the first experimental study to investigate spontaneous motor behaviour in a unilateral double lesion rat model. Our observations are consistent with a complex interaction of nigral and striatal lesions producing distinct behavioural and histological changes depending on the lesion sequence. Tests of forelimb akinesia and complex motor behaviour appear to provide a reliable tool that will be helpful for monitoring the effects of interventional strategies such as embryonic neuronal transplantation in the rat model of striatonigral degeneration.

Animals↗

PubMed2005

Therapeutic strategies in multiple system atrophy.

This review provides an update on therapeutic principles and their implications for practical management in multiple system atrophy (MSA), a sporadic neurodegenerative disorder characterized clinically by various combinations of dysautonomia, Parkinsonism, or cerebellar ataxia, often associated with other warning features (red flags), and pathologically by cell loss, gliosis, and glial cytoplasmic inclusions in selected multiple regions of the brain and spinal cord. Because of the small number of randomized controlled trials, the management of MSA is largely based on empirical or open-label evidence. Parkinsonism often shows a poor or unsustained response to chronic levodopa therapy, although more patients than previously recognized may experience an initial moderate-to-good dopaminergic response. There is no effective drug treatment for cerebellar ataxia. However, features of dysautonomia such as orthostatic hypotension, urinary retention or incontinence, constipation, and impotence, may often be relieved if recognized by the treating physician. Because no drug treatment consistently benefits patients with this disease in the long-term, palliative therapies are all the more important. Novel symptomatic and neuroprotective therapies are urgently required.

Adrenergic alpha-Antagonists↗

PubMed1999

T1 and T2 in the brain of healthy subjects, patients with Parkinson disease, and patients with multiple system atrophy: relation to iron content.

PURPOSE: To investigate the potential of magnetic resonance imaging for identification and quantification of brain iron in healthy subjects, patients with Parkinson disease, and patients with multiple system atrophy. MATERIALS AND METHODS: Forty-nine subjects were studied at 1.5 T. Regional T1 and T2 values were compared among groups and also with histopathologic estimates of iron concentration. RESULTS: In healthy subjects, interregional T1 and T2 differences in the cortex and basal ganglia showed a good correlation with reported values for iron concentration, and intraregional variations were generally consistent with reported variability of iron concentration. Patients with multiple system atrophy had T1 and T2 shortening in the globus pallidus consistent with reported increases in ferritin-bound iron and changes in the putamen consistent with accumulation of hemosiderin (posterior portion) and neuromelanin (remainder). Both groups of patients had changes in the cortex that are consistent with decreased ferritin concentration and T2 changes in white matter consistent with demyelination. Patients with Parkinson disease also had a (nonsignificant) T2 shortening in the substantia nigra that was suggestive of iron accumulation. CONCLUSION: Most of the T1 and T2 findings appear to be related to changes in iron content and form and may possibly be used as indicators of such changes.

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