Clinical Diagnosis Of Corticobasal Degeneration Research Articles

Difficulties in the clinical diagnosis of corticobasal degeneration

Difficulties in the clinical diagnosis of corticobasal degeneration

Efficient RT-QuIC seeding activity for \u03b1-synuclein in olfactory mucosa samples of patients with Parkinson\u2019s disease and multiple system atrophy

BackgroundParkinson’s disease (PD) is a neurodegenerative disorder whose diagnosis is often challenging because symptoms may overlap with neurodegenerative parkinsonisms. PD is characterized by intraneuronal accumulation of abnormal α-synuclein in brainstem while neurodegenerative parkinsonisms might be associated with accumulation of either α-synuclein, as in the case of Multiple System Atrophy (MSA) or tau, as in the case of Corticobasal Degeneration (CBD) and Progressive Supranuclear Palsy (PSP), in other disease-specific brain regions. Definite diagnosis of all these diseases can be formulated only neuropathologically by detection and localization of α-synuclein or tau aggregates in the brain. Compelling evidence suggests that trace-amount of these proteins can appear in peripheral tissues, including receptor neurons of the olfactory mucosa (OM).MethodsWe have set and standardized the experimental conditions to extend the ultrasensitive Real Time Quaking Induced Conversion (RT-QuIC) assay for OM analysis. In particular, by using human recombinant α-synuclein as substrate of reaction, we have assessed the ability of OM collected from patients with clinical diagnoses of PD and MSA to induce α-synuclein aggregation, and compared their seeding ability to that of OM samples collected from patients with clinical diagnoses of CBD and PSP.ResultsOur results showed that a significant percentage of MSA and PD samples induced α-synuclein aggregation with high efficiency, but also few samples of patients with the clinical diagnosis of CBD and PSP caused the same effect. Notably, the final RT-QuIC aggregates obtained from MSA and PD samples owned peculiar biochemical and morphological features potentially enabling their discrimination.ConclusionsOur study provide the proof-of-concept that olfactory mucosa samples collected from patients with PD and MSA possess important seeding activities for α-synuclein. Additional studies are required for (i) estimating sensitivity and specificity of the technique and for (ii) evaluating its application for the diagnosis of PD and neurodegenerative parkinsonisms. RT-QuIC analyses of OM and cerebrospinal fluid (CSF) can be combined with the aim of increasing the overall diagnostic accuracy of these diseases, especially in the early stages.

Diagnoses of corticobasal syndrome and corticobasal degeneration

Experts use the term corticobasal syndrome (CBS) for patients with a clinical diagnosis of corticobasal degeneration (CBD), and reserve CBD for those whose conditions have been diagnosed on the basis of neuropathological analyses. Several studies demonstrated that patients with CBD may also present with progressive supranuclear syndrome (PSPS), aphasia, Alzheimer disease-like dementia or behavioral change, suggesting that CBS is merely one of the presenting phenotypes of CBD. Although previous CBD diagnostic criteria reflected only CBS, the international consortium proposed new diagnostic criteria for CBD in 2013 (Armstrong's criteria). The new criteria include 4 CBD subtypes; CBS, frontal behavioral-spatial syndrome (FBS), nonfluent/agrammatic variant of primary progressive aphasia (naPPA)，and PSPS. These subtypes were combined to create 2 sets of criteria: more specific clinical research criteria for probable CBD (cr-CBD) and broader criteria for possible CBD that are more inclusive but have a higher chance to detect other tau-based pathologies (p-CBD). Two studies have already revealed that the sensitivity and specificity of the criteria were not high. Because therapeutic interventions that target abnormally-phosphorylated tau have started, further refinement of the criteria is needed via biomarker researches with prospective study designs.

Normal dopamine transporter SPECT in neuropathologically confirmed corticobasal degeneration

The role of dopamine transporter imaging in the diagnosis of corticobasal syndrome (CBS) is unclear. In the largest clinical study so far, Cilia et al. [1] presented data from 36 patients with clinically probable corticobasal degeneration (CBD) with [I]FP-CIT (CIT-SPECT) and compared the results to patients with Parkinson’s disease and healthy controls. Their results showed high variability in dopamine transporter binding, and four of the clinically probable CBD patients had normal scans. As the authors acknowledged, the interpretation of the findings was limited by the lack of pathological confirmation of the diagnoses. There is one previously reported patient with ante mortem CIT-SPECT and post mortem confirmation of CBD diagnosis. O’Sullivan et al. [2] reported a 65-year-old woman who had typical symptoms and a clinical diagnosis of CBD together with normal CIT-SPECT 4 years after clinical onset. Here we report a 70-year-old woman, who was referred to a neurologist in 2006 due to symptoms in her left upper extremity that had started 6 months earlier. She complained that her left arm was making ‘‘strange movements’’ and she was not always aware of where her left arm was. The family history was unremarkable. A 1.5 T MRI scan of the brain in 2006 did not show clinically significant findings. Clinical examination showed bilateral apraxia and mild rigidity in the upper extremities, her left arm moved constantly during examination and there was left-sided dysdiadochokinesia. The patient also had mild hypokinesia and walking slowness. A diagnosis of CBS was suspected. CIT-SPECT was performed approximately 9 months after symptom onset and the striatal binding was visually estimated as normal although a retrospective semi-automated analysis (BRASS, Hermes Medical Solutions, Stockholm, Sweden) showed some asymmetry (Fig. 1a). Two years later the disease had clearly progressed: the patient was unable to walk without help, her left arm was now rigid without involuntary movements, and the right arm was constantly moving during examination. There was flexion contracture in the left hand, general hypokinesia and clear hypomimia and rigidity. Levodopa treatment was initiated at a dose of 300 mg/day. This dose did not have significant effects on clinical symptoms, and the patient died 7 months later before dose increases were possible. At autopsy, acute bronchopneumonia was found to be the immediate cause of death. In the neuropathological examination, the macroscopic findings included cerebral atrophy (brain weight 1,240 g), with the most atrophic gyri present in the frontal lobes. There was pallor of the substantia nigra and locus coeruleus. Microscopic examination showed widespread pathology of the cortex. This included neuronal loss, mild vacuolation and ballooned achromatic neurons. Additionally, astrocytic plaques were present (Fig. 1b). In the substantia nigra, there was a loss of pigmented neurons, and V. Kaasinen (&) M. Paivarinta Division of Clinical Neurosciences, Department of Neurology, University of Turku and Turku University Hospital, POB 52, 20521 Turku, Finland e-mail: valtteri.kaasinen@tyks.fi

Imaging-Pathologic Correlation in Corticobasal Degeneration

The clinical diagnosis of corticobasal degeneration (CBD) is often difficult due to varied clinical manifestations. In 4 patients with neuropathologically confirmed CBD, characteristic imaging findings and correlations with neuropathologic features were evaluated. Furthermore, imaging findings in CBD were compared with neuropathologically confirmed progressive supranuclear palsy (PSP) for a differential diagnosis. Four patients with neuropathologically confirmed CBD were studied. We evaluated the area of the tegmentum in the midsagittal plane, subcortical white matter (SCWM) abnormality, asymmetric cerebral atrophy, and signal-intensity abnormality in the subthalamic nuclei on MR imaging and compared them with histopathologic findings. Then, MR imaging findings in CBD were compared with those in 13 patients with PSP. On MR imaging, 3 patients had asymmetric cerebral atrophy extending to the central sulcus. On midsagittal sections, the mean midbrain tegmentum area was 66 mm(2), being markedly smaller than normal, but there was no significant difference between PSP and CBD. All patients had signal-intensity abnormalities of the SCWM, constituting primary degeneration neuropathologically; however, no diffuse signal-intensity abnormality in the SCWM existed in the 13 patients with PSP. In 3 patients, T1-weighted images showed symmetric high signal intensity in the subthalamic nuclei. Neuropathologically, these areas showed characteristic CBD. MR imaging signal-intensity changes also existed in 4 patients with PSP; however, subthalamic nucleus degeneration was more severe in PSP than in CBD. In cases with midbrain tegmentum atrophy and signal-intensity changes in the subthalamic nuclei, the differential diagnosis distinguishing CBD from PSP based on MR imaging alone was difficult. White matter lesions and asymmetric atrophy can be useful for a differential diagnosis.

Alzheimer's disease: Report of two autopsy cases with a clinical diagnosis of corticobasal degeneration

Alzheimer's disease (AD) is the most common cause of dementia in the elderly. Corticobasal degeneration (CBD) is a rare neurodegenerative disease affecting adults, being characterized clinically by a combination of extrapyramidal signs and focal cortical syndromes. In both diseases, tau deposits are a characteristic neuropathological feature. We report two new patients with autopsy-proven AD, in whom clinical diagnoses of CBD were made during life. The ages of the patients at onset were 52 and 67 years, and the disease durations were 9 and 15 years, respectively. At autopsy, both cases exhibited marked cortical atrophy with evident neuronal loss in the convex areas of the frontal and parietal lobes. Immunohistochemically, AT8-positive neurofibrillary tangles (NFTs) and Abeta-positive senile plaques (SPs) were widespread and abundant in the cerebral cortex (Alzheimer pathology stage VI/C of Braak and Braak), leading us to the final pathological diagnosis of AD. No tau lesions suggestive of CBD were observed, and the deep gray matter areas, including the substantia nigra, were unremarkable (exceptionally, only mild neuronal loss was noted in the putamen in case 2). These findings further strengthen the idea that in AD, neurodegeneration with tau and Abeta deposits may begin in the fronto-parietal neocortical areas, which are often preferentially affected in CBD, earlier than, or as early as the medial temporal lobe, and that extrapyramidal signs, such as rigidity and tremor, can occur in the absence of neuronal loss in the basal ganglia and substantia nigra.

Diffusion-weighted brain imaging study of patients with clinical diagnosis of corticobasal degeneration, progressive supranuclear palsy and Parkinson's disease

Diffusion-weighted brain imaging study of patients with clinical diagnosis of corticobasal degeneration, progressive supranuclear palsy and Parkinson's disease

Diffusion-weighted brain imaging study of patients with clinical diagnosis of corticobasal degeneration, progressive supranuclear palsy and Parkinson's disease

Corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) are two neurodegenerative disorders within the category of tauopathies, which must be considered in differential diagnosis of Parkinson's disease. Although specific clinical and neuroradiological features help to guide the clinician to a likely diagnosis of Parkinson's disease, CBD or PSP, differential diagnosis remains difficult. The aim of our study was to analyse apparent diffusion coefficient (ADC(ave)) maps from patients with clinical diagnosis of CBD (corticobasal syndrome, CBS), classical phenotype of PSP (Richardson's syndrome, RS) and Parkinson's disease (PD) in order to identify objective markers to discriminate between these groups. Thirteen Parkinson's disease patients, 10 RS patients, 7 CBS patients and 9 healthy volunteers were recruited and studied in a 1.5 T MR scanner. Axial diffusion-weighted images were obtained and the ADC(ave) map was generated. Regions of interest (ROIs) included mesencephalon, corpus callosum and left and right superior cerebellar peduncle (SCP), thalamus, caudate, putamen, pallidus, posterior limb of internal capsule, frontal and parietal white matter. Histograms of ADC(ave) were generated for all voxels in left and right cerebral hemispheres and in left and right deep grey matter regions separately, and the 50th percentile values (medians) were determined. The ratio of the smaller to the larger median value (symmetry ratio) was calculated for left and right hemispheres and for left and right deep grey matter regions (1 = perfect symmetry). Putaminal ADC(ave) values in CBS and RS were significantly greater than those in Parkinson's disease and healthy volunteers, but could not distinguish CBS from RS patients. In CBS patients, the values of the medians of cerebral hemispheres histograms were significantly higher than those in RS, Parkinson's disease and healthy volunteers, while the hemispheric symmetry ratio in CBS (0.968, range 0.952-0.976) was markedly reduced compared with RS (0.993, range 0.992-0.994), Parkinson's disease (0.991, range 0.988-0.993) and healthy controls (0.990, range 0.988-0.993). The hemispheric symmetry ratio differentiated CBS patients from RS and Parkinson's disease patients with a sensitivity and specificity of 100%. In RS patients, the ADC(ave) values of the SCPs were significantly greater than those in Parkinson's disease and healthy volunteers. Our findings confirm that putaminal ADC(ave) values evaluation provides a good discrimination between Parkinson's disease and atypical parkinsonisms, including RS and CBS. Furthermore, diffusion-weighted imaging, by detecting the brain microstructural correlates of the typical asymmetric signs and symptoms in CBS and the SCP involvement in RS, was shown to aid characterization and differentiation of atypical parkinsonism.

Cognitive and motor assessment in autopsy-proven corticobasal degeneration

To investigate the clinical features of autopsy-proven corticobasal degeneration (CBD). We evaluated symptoms, signs, and neuropsychological deficits longitudinally in 15 patients with autopsy-proven CBD and related these observations directly to the neuroanatomic distribution of disease. At presentation, a specific pattern of cognitive impairment was evident, whereas an extrapyramidal motor abnormality was present in less than half of the patients. Follow-up examination revealed persistent impairment of apraxia and executive functioning, worsening language performance, and preserved memory. The motor disorder emerged and worsened as the condition progressed. Statistical analysis associated cognitive deficits with tau-immunoreactive pathology that is significantly more prominent in frontal and parietal cortices and the basal ganglia than temporal neocortex and the hippocampus. The clinical diagnosis of corticobasal degeneration should depend on a specific pattern of impaired cognition as well as an extrapyramidal motor disorder, reflecting the neuroanatomic distribution of disease in frontal and parietal cortices and the basal ganglia.

Corticobasal degeneration as cause of progressive non‐fluent aphasia: Clinical, radiological and pathological study of an autopsy case

A Japanese male developed gradual loss of spontaneous speech at age 60. Three years later meaningful speech had deteriorated to the point that it had become restricted to monotonous utterances. Neuropsychological examination at age 62 showed that he had severe non-fluent aphasia. A brain MRI demonstrated mild cortical atrophy with ischemic lesions in the cerebral white matter. He was diagnosed as having primary progressive aphasia. At age 63, he was admitted to the hospital to reevaluate the neurological condition. Neurologic examination showed severe non-fluent aphasia, hyperreflexia, snout and sucking reflexes. No alien hand was observed. He was able to walk, dress, wash himself and use chopsticks as well as name real objects. At age 65, 99Tc-hexamethylpropyleneamine oxime single photon emission computed tomography (HMPAO-SPECT) revealed diffuse cerebral hypoperfusion that was particularly prominent in the left frontal lobe. An MRI showed progressive cortical atrophy with the definite atrophy of the left paracentral gyrus. The hippocampal formation and putamen were also atrophic. He died of pneumonia at age 67. The brain weighed 810 g with atrophy of the frontal lobe, globus pallidus, enlargement of the lateral ventricles and depigmentation of the substantia nigra. Microscopic examination showed severe neuronal loss and gliosis in the cerebral cortex, globus pallidus interna and substantia nigra. Ballooned neurons were observed in the cerebral cortex. Gallyas-Braak method revealed numerous astrocytic plaques and argentophilic threads in the cerebrum. Clinical diagnosis of corticobasal degeneration sometimes is difficult in individuals with atypical clinical presentations. More exact clinical and radiological criteria may warrant a diagnosis of corticobasal degeneration.

SU‐FF‐I‐40: Image Registration and Voxel Based Analysis for the Differential Diagnosis of Corticobasal Degeneration and Progressive Supranuclear Palsy

Purpose: This study measured the cerebral glucose metabolism in patients suffering from corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP). PSP and CBD are neurodegenerative disorders that may be accompanied by dementia and parkinsonism as clinical symptoms. The aim was to determine if there was a different metabolic pattern using 18F‐labeled 2‐deoxyglucose (18F‐FDG) positron emission tomography (PET). Method and Materials: The regional cerebral glucose metabolism was examined in 8 patients with a clinical diagnosis of CBD (mean age 69.6 ± 7.8 y; male/female: 5/3), 8 patients with probable PSP (mean age 67.8 ± 4.5 y; male/female: 4/4) and 22 healthy controls. Statistical parametric mapping (SPM) using a voxel by voxel approach (p<0.001, 200 voxel‐level) was used to compare the regional cerebral glucose metabolism between the 3 groups. Results: Compared with the normal controls, asymmetry in the regional glucose metabolism was observed in the parietal, frontal and cingulate in CBD patients. In the PSP patients, the glucose metabolism was lower in the orbitofrontal, middle frontal, cingulated, thalamus and mid brain than their age matched normal controls. A comparison of the two patient groups demonstrated relative hypometabolism in the thalamus, the mid brain in PSP and the parietal lobe in CBD patients. Conclusion: These results suggest that when making a differential diagnosis of CBD and PSP, voxel based analysis of the 18F‐FDG PET images using SPM might be a useful adjunct tool in clinical examinations.

Orofacial apraxia in corticobasal degeneration, progressive supranuclear palsy, multiple system atrophy and Parkinson?s disease

To determine whether the assessment of orofacial praxis is useful for the differential diagnosis of parkinsonian syndromes and to understand the neural mechanisms underlying OFA, searching for the respective roles of cortical and subcortical structures. Forty-four patients were assessed: 12 with idiopathic Parkinson's disease (IPD), 8 with multiple system atrophy (MSA), 12 with progressive supranuclear palsy (PSP) and 12 with corticobasal degeneration (CBD). An easy bedside scale was used, exploring single gestures, gestures with noise production and multiple sequential gestures. We searched for group and task effects. Patients with CBD were significantly more impaired than those with IPD, MSA or PSP (p<0.001). Our assessment was unable to distinguish between the IPD, MSA and PSP groups. There was a clear task effect in CBD with a major impairment in multiple sequential gestures (p<0.0001). Assessment of orofacial praxis helps in the clinical diagnosis of CBD. Patients with IPD, MSA and PSP did not present with OFA. We suggest that the deficit in multiple sequential gestures in CBD is related to simultaneous lesions of the parietal lobule and the supplementary motor area.

Impairment of transcallosal inhibition in patients with corticobasal degeneration.

To evaluate the motor function of the transcallosal pathways in patients with clinical diagnosis of corticobasal degeneration (CBD). In a group of 7 patients (4 males, 3 females; mean age 70.6 years) with clinical diagnosis of probable CBD (and in 8 age-matched normal controls) we evaluated the suppression of the ongoing voluntary EMG activity in the opponens pollicis muscle induced by focal transcranial magnetic stimulation (TMS) of the ipsilateral hand motor cortex. Such ipsilateral silent period (iSP) is mediated from one motor cortex to the contralateral side via a transcallosal pathway. In addition, CBD patients were investigated with magnetic resonance imaging (MRI) and neuropsychological assessment. iSP was normal in 4 CBD patients, while it was bilaterally disrupted in the other 3. MRI showed an atrophy of the corpus callosum (middle-posterior part of the trunk) in the CBD patients with iSP disruption. Neuropsychological evaluation showed in patients with iSP impairment a decrease of verbal fluencies associated with an impairment of attentive function. A proportion of CBD patients shows physiological evidence of impaired callosal motor function and atrophy of the corpus callosum on MRI, possibly correlated to dysphasic and cognitive disorders.

Features of Regional Cerebral Glucose Metabolism Abnormality in Corticobasal Degeneration

We studied regional cerebral glucose metabolism in 15 patients with a clinical diagnosis of corticobasal degeneration (CBD), 15 patients with probable Alzheimer’s disease (AD), and 15 healthy controls for 19 brain regions. Asymmetry in regional glucose metabolism was found in the central and frontal cortices in patients with CBD as compared with either the normal controls or the patients with AD. Regional glucose metabolism in CBD patients was significantly lower in the paracentral and superior parietal areas and thalamus than in patients with AD. Relative glucose metabolism in patients with CBD was significantly higher in the posterior cingulate, medial temporal and basal frontal areas, and significantly lower in the paracentral and superior parietal areas than in those with AD. These features of regional glucose metabolic abnormality in CBD may correspond to neurological and cognitive disturbances peculiar to CBD.

Cognitive and magnetic resonance imaging aspects of corticobasal degeneration and progressive supranuclear palsy.

To identify cognitive and MRI features important for the clinical diagnosis of corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP); these diseases share several clinical features and are often difficult to distinguish on clinical grounds. Cognitive functions and MRI characteristics were examined in 16 patients with CBD and 28 patients with PSP, all diagnosed according to current clinical criteria (none was examined by autopsy). MRI findings differed significantly between the two groups: 87.5% of patients with CBD but none with PSP had asymmetric frontoparietal atrophy, whereas 89.3% of patients with PSP but only 6.3% of those with CBD had midbrain atrophy. Cognitive examination showed that ideomotor apraxia (De Renzi's test) was significantly more frequent in CBD, and executive functions (Nelson's test) were significantly more impaired in patients with PSP. MRI findings of asymmetric frontoparietal atrophy in CBD and midbrain atrophy in PSP are the most consistent and useful aids to careful clinical evaluation for differentiating between the two diseases.

MRI Helps in the Early Diagnosis of Corticobasilar Degeneration

We describe MR findings in patients with a clinical diagnosis of corticobasal degeneration (CBD). Five patients with different extrapyramidal symptoms were submitted to MRI. All patients were clinically followed-up for a minimum period of at least 12 months. MRI study was performed on a 0.5 T system (Philips NT 5 II), using conventional SE, TSE and t-FLAIR sequences on axial and coronal planes. In all cases MR showed bilateral parietal cortical atrophy. t-FLAIR sequences demonstrated cortical signal alteration on both parietal and frontal cortex in four cases and on the parietal cortex alone in 1 case. During the follow-up clinical evolution gave rise to the suspicion of CBD. MRI demonstrated parietal cortex atrophy even in those cases in which symptoms at onset were not specific for CBD, thus helping the diagnosis. Moreover MRI, using t-FLAIR sequences suggested CBD diagnosis even in the earlier phases of the disease, in which cortical damage has not yet become evident as atrophy.

Myoclonus in corticobasal degeneration.

Five patients with unilateral myoclonus and a clinical diagnosis of corticobasal degeneration (CBD) were studied. All patients showed enhanced long-loop responses in their myoclonic arms without enlarged somatosensory potentials. The cortical relay time of the long-loop responses was studied in three patients, in two of whom it was < 2 ms, even in the nonmyoclonic arm. Myoclonus in CBD is probably related to an enhanced long-loop reflex whose pathway is unlikely to be the same as that in classic cortical reflex myoclonus.

Accuracy of the clinical diagnosis of corticobasal degeneration: a clinicopathologic study.

The accuracy of the clinical diagnosis of corticobasal degeneration (CBD) is unknown. To determine its diagnostic accuracy, we presented 105 cases with known neuropathologic diagnoses, including CBD (n = 10), progressive supranuclear palsy (PSP, n = 24), Parkinson's disease (n = 15), diffuse Lewy body disease (n = 14), multiple system atrophy (n = 16), postencephalitic parkinsonism (n = 7), Pick's disease (n = 7), Creutzfeldt-Jakob disease (n = 4), Alzheimer's disease (n = 4), vascular parkinsonism (n = 3), and Whipple's disease (n = 1), as clinical vignettes to six neurologists unaware of the autopsy findings. Reliability was measured with the kappa statistics. The neurologists' clinical diagnoses were compared with clinicopathologic diagnoses for sensitivity, specificity, and positive predictive values at first and last clinic visits. The group reliability for the diagnosis of CBD significantly improved from moderate for the first visit (mean = 34 months after onset) to substantial for the last (68 months after onset). For the first visit, mean sensitivity for CBD was low (35%), but specificity was near-perfect (99.6%). For the last visit, mean sensitivity minimally increased (48.3%), and specificity remained stable. False-negative misdiagnoses mainly occurred with PSP. False-positive diagnoses were rare. The extremely low sensitivity of the clinical diagnosis of CBD suggests that this disorder is markedly underdiagnosed. Although the validity of the clinical diagnosis might have been improved if neurologists could have examined these patients, more important is that this disorder was misdiagnosed by the primary neurologists. In our data set, the best predictors for the diagnosis of CBD included limb dystonia, ideomotor apraxia, myoclonus, and asymmetric akinetic-rigid syndrome with late onset of gait or balance disturbances.

MRI in corticobasal degeneration

Corticobasal degeneration is a degenerative disease characterized by asymmetric brain atrophy and clinically by asymmetric onset of an akinetic-rigid syndrome with apraxia, dysarthria and dysphagia. Diagnosis must be confirmed by autopsy. We have investigated the ability of MRI to detect asymmetric atrophy to support the clinical diagnosis and permit differential diagnosis against other degenerative disorders. Ten patients with clinical suspicion of corticobasal degeneration were studied by brain MRI, and the images were reviewed with the side of greater clinical involvement unknown to the reviewer. The original reports of MR scans were also reviewed. MRI demonstrates that cortical atrophy is asymmetric and more marked in the posterior frontal and mainly in the parietal regions on the side contralateral to the clinical symptoms. Asymmetry was rarely detected on the first reading. Our review of MRI findings demonstrates that it is possible to detect asymmetrical parietal atrophy, thus supporting the clinical diagnosis of corticobasal degeneration. It is essential to be aware of the disease and alert for asymmetries in order to discern the more involved side. No abnormalities were detected in the basal ganglia.