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(Radiology. 2000;216:31-38.)
© RSNA, 2000

Neuroradiology

Corticobasal Degeneration: Evaluation of Cortical Atrophy by Means of Hemispheric Surface Display Generated with MR Images1

Hajime Kitagaki, MD, Nobutsugu Hirono, MD, Kazunari Ishii, MD and Etsuro Mori, MD

1 From the Neuroimaging Research/Radiology Service (H.K., K.I.) and Clinical Neurosciences/Neurology and Neurorehabilitation Services (E.M., N.H.), Hyogo Institute for Aging Brain and Cognitive Disorders, Himeji, Japan. Received May 4, 1999; revision requested July 14; revision received August 31; accepted September 20. Address correspondence to H.K., Department of Radiology, Shimane Medical University, 89-1 Enya-Cho Izumo 693-8501, Japan. (e-mail: kitagaki@shimane-med.ac.jp).


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
PURPOSE: To determine the characteristics of cortical atrophy in corticobasal degeneration and Alzheimer disease by using a hemispheric surface display generated with magnetic resonance (MR) images.

MATERIALS AND METHODS: The magnitude and extent of cortical atrophy were evaluated with MR hemispheric surface display and volumetric measurement in three groups: 17 patients with corticobasal degeneration, 17 matched patients with Alzheimer disease, and 17 matched healthy control subjects.

RESULTS: The extent and magnitude of cortical atrophy were larger in the group with corticobasal degeneration than in the group with Alzheimer disease. The parasagittal and paracentral regions were significantly more atrophic in patients with corticobasal degeneration than in patients with Alzheimer disease (P < .05). The mean hemispheric-to-total intracranial volume ratios were significantly smaller in the patients with corticobasal degeneration (61%) and those with Alzheimer disease (64%) than in control subjects (69%). Asymmetry of hemispheric volume was significantly larger in the group with corticobasal degeneration than in the control group.

CONCLUSION: The extent of cortical atrophy in corticobasal degeneration is more widespread than was previously thought. Parasagittal and paracentral atrophy is a distinctive feature of corticobasal degeneration and distinguishes it from Alzheimer disease.

Index terms: Alzheimer disease, 13.83 • Brain, atrophy, 13.83 • Brain, MR, 13.121412, 13.121419 • Brain, PET, 13.12163 • Brain, SPECT, 13.12162 • Brain, volume, 13.12144 • Dementia, 13.83 • Magnetic resonance (MR), image processing, 13.121419, 13.12144 • Magnetic resonance (MR), three-dimensional, 13.121419 • Magnetic resonance (MR), volume measurement, 13.12144


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Corticobasal degeneration, or cortical-basal ganglionic degeneration, is a slowly progressive neurodegenerative disease characterized by a peculiar combination of extrapyramidal and cortical symptoms, including rigidity of the trunk and extremities, dystonias, apraxias, cortical sensory losses, the alien limb phenomenon, and myoclonus. Histopathologic features include atrophy of the frontoparietal cortex; neuronal losses and gliosis in the cortex, basal ganglia, and substantia nigra; and the presence of swollen, achromatic neurons. Asymmetric clinical presentation and asymmetric involvement at gross and microscopic pathologic examination have been emphasized.

This pattern of atrophy has been demonstrated by means of neuroimaging studies. Radionuclide studies, which provide information about cortical dysfunction, are reported to be useful in the diagnosis of corticobasal degeneration. Computed tomography and magnetic resonance (MR) imaging, which demonstrate structural changes, also have a role in evaluating clinical-pathologic correlation and in the diagnosis. Results of several studies of single cases or case series have demonstrated high-grade cerebral atrophy in corticobasal degeneration, which may be bilateral or asymmetric and involve the frontoparietal region contralateral to the side that was first affected and that is most severely affected (1–7). However, to our knowledge, there are no neuroimaging studies systematically and quantitatively documenting the cortical atrophy in corticobasal degeneration. The in vivo pattern of cortical involvement and the role of neuroimaging in the assessment remain to be determined, as cortical or neuropsychologic symptoms are central and distinctive features in this disorder.

We developed software that automatically extracts the brain matter from thin-section coronal MR images and generates volumes and three-dimensional volume-rendered images of the cerebral hemisphere, brainstem, cerebellum, and calvaria (8–11). In one of these studies (8), we evaluated the precise anatomic location of the cortical atrophy in frontotemporal dementia and Alzheimer disease by using these three-dimensional reconstructed MR images and determined the utility of this software.

Three-dimensional imaging and hemispheric volumetric measurement are suitable for the assessment of degenerative cortical atrophy for the following reasons: (a) cortical atrophy can be inspected only from the surface and thus differs from other common neurologic disorders that affect the inside of the brain, such as hemorrhage, infarction, and tumor; (b) the precise anatomic identification of the loci of the atrophy is beneficial for understanding the neurologic and neuropsychologic symptoms; and (c) hemispheric atrophy can be quantitatively expressed with simultaneously generated volumes. In this study, to delineate the extension of cortical atrophy in corticobasal degeneration, we compared patients with corticobasal degeneration with healthy people and with patients with Alzheimer disease, the most common cause of brain atrophy and cognitive impairment, by using three-dimensional reconstruction of MR images.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Patients and Control Subjects
All of the patients in this study were admitted to our hospital (Hyogo Institute for Aging Brain and Cognitive Disorders, Himeji, Japan) from January 1, 1994, to December 31, 1997, for cognitive disorders, and they were examined comprehensively by both neurologists and psychiatrists and underwent routine laboratory tests, electroencephalography, and standardized neuropsychologic examinations, including the Mini-Mental State Examination (MMSE) (12) and Alzheimer Disease Assessment Scale (ADAS) (13). Neuroimaging included MR imaging of the brain and MR angiography of the neck and head. In addition, cerebral glucose metabolism or cerebral blood flow images were obtained by means of positron emission tomography (PET) with 2-[fluorine 18]fluoro-2-deoxy-D-glucose or with the carbon 15 dioxide steady-state method or by means of single photon emission computed tomography (SPECT) with iodine 123 iodoamphetamine or with technetium 99m ethyl cysteinate dimer. Both the diagnostic tests and three-dimensional MR angiography were performed during a 4-week hospital stay for the patient.

All procedures of this study strictly adhered to the clinical study guidelines of the ethics committee of our institute and were approved by the internal review board. After a complete description of the study to both the patients and their relatives or to the healthy volunteers, written informed consent was obtained.

Patients with corticobasal degeneration.—Seventeen patients (eight women and nine men; age range, 52–75 years; mean age, 64.1 years ± 6.5 [SD]) with corticobasal degeneration were examined in this study. All of them fulfilled a modified version of the clinical diagnostic criteria proposed by the corticobasal degeneration multicenter case-control study (4). Our criteria included a progressive course of an asymmetric parkinsonism that did not benefit from levodopa therapy; the presence of either a dystonic limb or focal myoclonus; the presence of ideomotor apraxia, alien limb phenomenon, or cortical sensory loss; and the absence of resting tremor, autonomic disturbance, or laboratory evidence of other disorders. The criteria reportedly have a high specificity (14,15) and have been used often in recent clinical studies (16,17). We excluded patients with complications of other neurologic diseases or evidence of focal brain lesions on MR images. Three patients had vertical gaze palsy. The mean duration of illness was 3.0 years ± 1.4. The mean MMSE score was 20.9 ± 5.2, and the mean ADAS score was 25.8 ± 11.5. Neurologic signs and symptoms in each of the patients are summarized in Table 1.


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  		TABLE 1. Neurologic Signs and Symptoms in Patients with Corticobasal Degeneration
 
Patients with Alzheimer disease.—Seventeen patients (eight women and nine men; age range, 52–74 years; mean age, 63.7 years ± 6.2) with Alzheimer disease were from the same cohort of patients admitted to our hospital for examination and were matched for sex, age, and dementia severity (MMSE score) to those with corticobasal degeneration. Inclusion criteria included (a) probable Alzheimer disease according to the criteria of the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association, or NINCDS/ADRDA (18), and (b) hypoperfusion in the parietal, medial temporal, or both lobes on PET or SPECT scans (19). Patients with complications of other neurologic diseases or evidence of focal brain lesions on MR images were not included. All the patients underwent examinations similar to those the patients in the group with corticobasal degeneration underwent. The mean duration of illness was 3.3 years ± 1.7. The mean MMSE score was 20.2 ± 4.9, and the mean ADAS score was 23.1 ± 12.5.

Control subjects.—Seventeen sex- and age-matched healthy volunteers (eight women and nine men; age range, 54–80 years; mean age, 63.8 years ± 6.5) were recruited from the community. All subjects had normal physical and neurologic examination results, no history of psychiatric or neurologic disorders, and no abnormal findings on MR images. They scored 28 or more on the MMSE. Both the MMSE and three-dimensional MR imaging were performed within the same 2 weeks.

MR Image Acquisition, Image Processing, and Surface Display
The detailed MR imaging acquisition and image processing is described elsewhere (8). In brief, all studies were performed with a 1.5-T MR unit (Signa Advantage 5; GE Medical Systems, Milwaukee, Wis) with a circularly polarized head coil as both transmitter and receiver. Coronal three-dimensional spoiled gradient-recalled acquisition images were obtained with the following parameters: 14/3 (repetition time msec/echo time msec), a field of view of 220 mm, a 256 x 256 matrix, 124 x 1.5-mm contiguous sections, and a flip angle of 20°. These images covered the whole calvaria and were the source data. The voxel size was (220/256)2 x 1.5, or 1.1 mm3.

The data sets of the spoiled gradient-recalled acquisition images were transmitted directly to a graphic workstation (INDIGO2 Hi-Impact; Silicon Graphics, Mountain View, Calif) from the MR unit and were analyzed by using three-dimensional MR image processing software developed by Kobashi et al (20). The software makes use of a combination of gray-scale (three-dimensional expansion of the region-growing method) and edge-detection (three-dimensional expansion of Sobel filtering) algorithms and some a priori knowledge by which a computer may make unsupervised identification of the cerebral hemisphere, brainstem, cerebellum, and calvaria. This software includes a three-dimensional volume-rendered image of each structure, a two-dimensional reconstruction with optional angles, and volumetric measurements of each structure. The caudal end of the whole brain and calvaria was set manually at the plane intersecting the occipitoatlantal junction, which is the only supervised operation required. The whole procedure took approximately 5 minutes.

Assessment of Cortical Atrophy
The assessment of cortical atrophy is described in detail in our previous article (8). In brief, a three-dimensional volume-rendered image of each cerebral hemisphere was displayed on a high-resolution color monitor. One neuroradiologist (H.K.) blinded to the clinical data and diagnosis rated regional cortical atrophy for each of 66 cortical regions of the lateral and medial hemispheric surface into five categories: normal, nadir of the sulcus invisible with stacked gyri; minimal, nadir of the sulcus visible; mild, bottom of the sulcus widened; moderate, gyrus thinner than sulcus; and severe, very shrunken gyrus with a knife-blade appearance.

The regions included the orbitofrontal cortex, superior frontal gyrus (anterior and posterior for lateral and medial), middle frontal gyrus (anterior and posterior), inferior frontal gyrus (anterior and posterior), cingulate gyrus (anterior and posterior), precentral gyrus (superomedial and inferolateral), postcentral gyrus (superomedial and inferolateral), superior parietal lobule (anterior and posterior for lateral and medial), inferior parietal lobule (anterior and posterior), superior temporal gyrus (anterior and posterior), middle temporal gyrus (anterior and posterior), inferior temporal gyrus (anterior and posterior), parahippocampal gyrus (anterior and posterior), and occipital gyri (anterior and posterior for lateral and medial) of each hemisphere. When one side of a region of the frontal lobe was more atrophic than the other, the score for the more atrophic side was considered representative of the severity of the atrophy for that whole region.

The volumes of the right and left cerebral hemispheres and the total cerebral and total intracranial volumes were determined. We calculated total intracranial volume, hemispheric volume, hemispheric-to-total intracranial volume ratio, and asymmetry index: asymmetry index = absolute value of (left hemispheric volume - right hemispheric volume)/(left hemispheric volume + right hemispheric volume).

Statistical Analysis
Differences among the groups were analyzed by using the Kruskal-Wallis one-way analysis of variance test followed by the post hoc Tukey test with Dunn joint ranking test for nonparametric ordinal data (atrophy rating) (21) and by using one-way analysis of variance and Tukey post hoc analysis for numeric data (volume). Statistical analyses were performed with a statistical software package (STATISTICA version 4.1; StatSoft, Evanston, Ill). The level of statistical significance was set at P less than .05.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
In the experiment to determine the reliability of the atrophy rating, the intraclass coefficients were 0.44–0.93, with a mean value of 0.71 ± 0.13. Test-retest reliability was fairly good (coefficient > 0.60) in most regions except for the orbital regions, temporal lobe, and occipital lobe, where severe atrophy is unlikely to be present.

On hemispheric surface MR images in the healthy volunteers, as previously described (8), the gyri in the posterior temporal, inferior parietal, and occipital lobes appeared rather packed as compared with those in the other lobes (Fig 1). Although mild atrophy appeared in the paracentral gyri and superior parietal lobule in some of the volunteers, none of the volunteers showed moderate or severe atrophy in any regions.



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  		Figure 1. Three-dimensional volume-rendered images reconstructed from thin-section coronal three-dimensional spoiled gradient-recalled MR images (14/3; field of view, 220 mm; matrix, 256 x 256; 124 x 1.5-mm contiguous sections; and flip angle, 20°) show the appearance of the hemisphere in a healthy 62-year-old man. Note mild cortical atrophy in the lateral parietal cortex (arrows in A). Viewed from A, above; B, below; C, front; D, behind; E, left lateral surface; F, right lateral surface; G, left inner surface of bisected brain; and H, right inner surface of bisected brain.

 
In the patients with Alzheimer disease, atrophy of a mild to moderate degree was almost proportionate in the frontal, temporal, and parietal association cortices (Fig 2). Mild atrophy of the occipital lobes was also noted in some patients with Alzheimer disease; severe focal atrophy was never observed, and the central areas showed only mild atrophy. The distribution of cortical atrophy was similar to that seen with normal aging, although the degree was more intense.



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  		Figure 2. Three-dimensional volume-rendered images reconstructed from thin-section coronal three-dimensional spoiled gradient-recalled MR images (14/3; field of view, 220 mm; matrix, 256 x 256; 124 x 1.5-mm contiguous sections; and flip angle, 20°) show diffuse cortical atrophy in a 74-year-old man with Alzheimer disease. The parietotemporal (arrows in A, E, F) and the frontal (arrowheads in A, E, F) association cortices are moderately atrophic. Viewed from A, above; B, below; C, front; D, behind; E, left lateral surface; F, right lateral surface; G, left inner surface of bisected brain; and H, right inner surface of bisected brain.

 
On the other hand, focal atrophy affecting the frontal and parietal lobes was apparent on hemispheric surface images obtained in the patients with corticobasal degeneration (Figs 3, 4). The central area, especially the postcentral gyrus, was highly atrophic (Table 2). In the frontal lobe, atrophy was concentrated on the lateral and medial surface of the superior frontal gyrus. In the parietal lobe, atrophy severely affected the superior parietal lobule. In contrast, atrophy of the temporal and occipital lobes was mild. Severe atrophy with a knife-blade appearance was recorded in the superior parietal lobule in four patients and in the postcentral gyrus in one patient (Fig 5).



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  		Figure 3. Patient 10. Three-dimensional volume-rendered images reconstructed from thin-section coronal three-dimensional spoiled gradient-recalled MR images (14/3; field of view, 220 mm; matrix, 256 x 256; 124 x 1.5-mm contiguous sections; and flip angle, 20°) show severe frontoparietal atrophy in a 63-year-old woman with corticobasal degeneration. Intense focal atrophy is accentuated in the bilateral superior parietal lobules (arrows in A, D-H). Viewed from A, above; B, below; C, front; D, behind; E, right lateral surface; F, left lateral surface; G, right inner surface of bisected brain; and H, left inner surface of bisected brain.

 


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  		Figure 4. Three-dimensional volume-rendered images reconstructed from thin-section coronal three-dimensional spoiled gradient-recalled MR images (14/3; field of view, 220 mm; matrix, 256 x 256; 124 x 1.5-mm contiguous sections; and flip angle, 20°) show focal cortical atrophy in corticobasal degeneration. Remarkable cortical atrophy is apparent in A, the superior parietal lobules (patient 1; arrows); B, the parasagittal frontoparietal lobes (patient 5; arrows); and C, the left postcentral gyrus (patient 15; white arrow) and superior parietal lobule (black arrow). Viewed from A, above and behind and B, C, oblique left lateral surface.

 

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  		TABLE 2. Severity of Cortical Atrophy in the Frontoparietal Regions
 


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  		Figure 5. Statistical maps show gray areas that represent regions where the atrophy rating was significantly different between two groups (light gray, P < .05; dark gray, P < .01). In all instances, atrophy was more profound in the first of the two groups being compared. AD = group with Alzheimer disease, CBD = group with corticobasal degeneration, NC = control group. The top row shows the left lateral surface of the bisected brain, and the bottom row shows the left inner surface of the bisected brain.

 
The regions where cortical atrophy was significantly different among the three groups—patients with corticobasal degeneration versus control subjects, patients with Alzheimer disease versus control subjects, and patients with corticobasal degeneration versus patients with Alzheimer disease—are illustrated on statistical maps in Figure 5. In the patients with corticobasal degeneration, 31 cortical regions, which compose the whole cerebrum except for the medial occipital lobe, were significantly atrophic as compared with those in the control subjects. In the patients with Alzheimer disease, 10 of the 31 cortical regions, including parts of the frontal lobe, lateral temporal lobe, and parietal lobe, were significantly atrophic as compared with those in the control subjects. A comparison of the group with corticobasal degeneration and the group with Alzheimer disease revealed that 11 regions in the central areas and the frontal, temporal, parietal, and occipital lobes were significantly atrophic in the patients with corticobasal degeneration. In particular, atrophy in the central areas was characteristic of corticobasal degeneration.

Table 3 shows the mean values and SDs of the total intracranial volume, hemispheric volume, hemispheric-to-total intracranial volume ratio, and asymmetry index. The mean total intracranial volume was comparable among the three groups. The mean hemispheric volumes and mean hemispheric-to-total intracranial volume ratios were significantly smaller in the group with corticobasal degeneration and in the group with Alzheimer disease than in the control group. Although the mean hemispheric-to-total intracranial volume ratio was smaller in the group with corticobasal degeneration than in the group with Alzheimer disease, the difference did not reach the level of significance (P = .105).


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  		TABLE 3. Volumetric Data for Patients in the Corticobasal Degeneration, Alzheimer Disease, and Control Groups
 
The mean asymmetry index was significantly larger in the groups with corticobasal degeneration and Alzheimer disease than in the control group. Although the mean asymmetry index was larger in the group with corticobasal degeneration than in the group with Alzheimer disease, the difference did not reach the level of significance (P = .215).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Pathology examination results indicate that cortical atrophy in corticobasal degeneration is located mainly in the frontal, parietal, and central regions (1–4). The greatest histologic changes, including neuronal loss with disruption of the normal cortical layering, fibrillary gliosis, and status spongiosus, are found in the parietal and posterior frontal cortex, especially in the precentral and postcentral gyri (4,22). Although results of previous MR imaging studies (5–7) showed asymmetric parietal and frontal cortical atrophy and asymmetric dilatation of the lateral ventricles, results of these studies could not be used to specify the exact location of cortical atrophy. Using MR imaging and computer technology, we documented the extent and the precise anatomic location of the cortical atrophy in corticobasal degeneration in vivo. The results of our atrophy rating in the present study showed that the atrophy was accentuated in the parasagittal and paracentral regions in patients with corticobasal degeneration despite widespread cortical involvement. We also demonstrated quantitatively the asymmetric hemispheric involvement in patients with corticobasal degeneration.

The most important disease to differentiate from corticobasal degeneration is Alzheimer disease, since Alzheimer disease is the most common cause of cognitive impairment in the elderly. Our study results clearly demonstrated that parasagittal frontoparietal and paracentral cortical atrophy in corticobasal degeneration, which has often been emphasized in pathology studies (4,23,24), was an MR imaging sign that could be used to discriminate corticobasal degeneration from Alzheimer disease. Although asymmetry of atrophy in corticobasal degeneration was stressed in the previous studies (1–7) and was also demonstrated in the present volumetric study, we did not note a significant difference between the two groups.

Most of the patients included in this study had early-onset Alzheimer disease. In patients with early-onset Alzheimer disease, asymmetric hemispheric involvement is common (25). This would obscure the difference in asymmetric atrophy between the groups with corticobasal degeneration and Alzheimer disease in this study. In addition, the relatively small number of subjects included in this study might partly explain why we did not obtain a significant difference. Asymmetric hemispheric atrophy is reportedly a hallmark of corticobasal degeneration when compared with progressive vertical gaze palsy and Parkinson disease, both of which also manifest as progressive extrapyramidal syndrome with some cognitive losses (6,7).

Our findings suggest that asymmetric atrophy is not a sign that is seen exclusively in corticobasal degeneration. Nevertheless, asymmetric atrophy accentuated in the parasagittal frontoparietal and paracentral regions would be a useful sign for discriminating corticobasal degeneration from progressive vertical gaze palsy and Parkinson disease, as these disorders lack the pattern of cortical atrophy characteristic of corticobasal degeneration (Fig 6).



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  		Figure 6. Three-dimensional volume-rendered images reconstructed from thin-section coronal three-dimensional spoiled gradient-recalled MR images (14/3; field of view, 220 mm; matrix, 256 x 256; 124 x 1.5-mm contiguous sections; and flip angle, 20°) show brain atrophy in patients with progressive vertical gaze palsy and Parkinson disease. View from oblique left lateral surface. A, Moderate frontal atrophy (arrows) in a 62-year-old woman with progressive vertical gaze palsy (MMSE score, 24; ADAS score, 14). B, Mild diffuse atrophy in a 72-year-old woman with Parkinson disease (MMSE score, 24; ADAS score, 16). Atrophic patterns are different from those in corticobasal degeneration.

 
In a previous study (8) of frontotemporal dementia in which we used the same technique, we found that cortical atrophy in frontotemporal dementia is widespread over the affected hemisphere and is accentuated in the frontal and anterior temporal lobes. Asymmetry of atrophy is also a distinctive feature of frontotemporal dementia. Therefore, the distribution of atrophy in frontotemporal dementia is very similar to that in corticobasal degeneration, although the focus of the atrophy in frontotemporal dementia is different from that in corticobasal degeneration. Severe focal gyral atrophy with a knife-blade appearance, which is characteristic of Pick disease (26), was observed in patients with corticobasal degeneration. Although atrophy with a knife-blade appearance appears in the frontal and temporal lobes in Pick disease, it may appear in the parietal lobe in corticobasal degeneration.

The histologic changes in frontotemporal dementia include neuronal loss, spongiform changes, and astrocytic gliosis in the outer cortical layers and white matter, which are very similar to those in corticobasal degeneration. Neuronal inclusion bodies, so-called corticobasal inclusions, that appear in the brains of patients with corticobasal degeneration mimic Pick bodies that appear in the brains of patients with Pick disease (1). A hypothesis has been made that both corticobasal degeneration and frontotemporal dementia are types of tau disease (27). Results of our studies demonstrated that both disorders affect hemispheres asymmetrically and cause severe focal cortical atrophy with a knife-blade appearance. Apart from the controversy over whether both disorders are different manifestations of the same disease, this similarity suggests a common mechanism between the two disorders. In contrast, it is apparent that the different patterns of cortical involvement in these disorders correspond to their different cognitive and behavioral syndromes.

Although an analysis of the relation between the specific cortical involvement in corticobasal degeneration and the distinct cortical syndrome in corticobasal degeneration is not straightforward because of the diverse types of cortical involvement and the complex combination of clinical syndromes, our study results provide some important clues for cases in which only distinctive clinical syndromes and severely affected sites are considered. Cortical sensory deficits are caused by severe damage in the postcentral gyrus and superior parietal lobule of the opposite side. Myoclonus is likely to be related to the involvement of the precentral gyrus in the opposite side. The involvement of the inferior parietal lobule of the dominant hemisphere is responsible for the ideomotor and ideational apraxias. The alien limb phenomenon in some patients is explained by the involvement of the medial frontal lobe and probably the corpus callosum. Simple nonpurposeful movements seen in other patients, which is also referred to as the alien limb phenomenon, might be related to the involvement of the parietal lobe of the opposite side (3,4), which may cause a differentiation syndrome like the "levitation" phenomenon (28).

Three-dimensional reconstruction of MR images provides the first step in a gross pathologic examination (ie, inspection of a brain specimen before dissection). Detection of cortical atrophy with precise anatomic localization by means of the present system enables us to find the correlation between clinical symptoms and the affected regions and to provide useful additional evidence supporting the clinical diagnosis of the disease. Results of neuroimaging studies have demonstrated the involvement of the basal ganglia (29–33). As our system currently cannot be used to evaluate internal structures, including the basal ganglia, we presently are attempting to improve image acquisition and the associated software. Nevertheless, three-dimensional reconstruction of MR images is a useful complementary tool for evaluating focal cortical atrophy in degenerative dementias and may facilitate the study of brain-behavior relationships and the differentiation of various dementias.


   FOOTNOTES
 
Abbreviations: ADAS = Alzheimer Disease Assessment Scale, MMSE = Mini-Mental State Examination

Author contributions: Guarantor of integrity of entire study, H.K.; study concepts and design, H.K., E.M.; definition of intellectual content, H.K., E.M.; literature research, H.K., N.H.; clinical studies, N.H., E.M.; data acquisition and analysis, H.K., K.I.; statistical analysis, N.H., H.K.; manuscript preparation, editing, and review, H.K., E.M.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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