Hypoperfusion of the motor cortex associated with parkinsonism in dementia with Lewy bodies
Introduction
Dementia with Lewy bodies (DLB) is recognized as the second major form of dementia in the elderly. The main symptoms of DLB are visual hallucinations, fluctuating cognitive impairment, and parkinsonism [1]. This clinical entity is clinically and neuropathologically different from Alzheimer's disease (AD). However, a definite diagnosis can only be made post-mortem based on neuropathological findings. Recently, various in vivo imaging studies, using modalities such as FDG-positron emission tomography (PET) [2], [3], [4], [5] and single photon emission computed tomography (SPECT)[1], were performed to aid in establishing criteria for DLB diagnosis. These studies have established that DLB is characterized by low glucose metabolism and decreased regional cerebral blood flow (rCBF) in the parietal, temporal, and occipital lobes, and with relative sparing of the paracentral regions such as the motor and sensory cortices. In particular, the lower activity in the occipital cortex distinguishes DLB from AD [6], [7], [8], [9]. Meanwhile, Parkinson's disease with dementia (PDD) is a confusing clinical entity that shows predominant parkinsonism rather than cognitive impairment, including memory disturbance. The guidelines proposed in the Consortium on DLB International Workshop (CDLBIW) [10] recommend that the 1-year rule be used to distinguish between PDD and DLB [1]. However, because PDD and DLB show remarkably convergent neuropathology at autopsy, clear discrimination between the 2 clinical phenotypes is difficult; therefore, DLB, PD, and PDD could be classified as ‘Lewy body (LB) disease’ or ‘Alpha-synucleinopathy’ [1], [11]. However, the term ‘LB disease’ is confusing because of the various methods of disease onset. There should be some reason why DLB and PD have different symptoms at onset. Parkinsonism in DLB would be the key for diagnosing LB disease.
In this study, we aimed to clarify the difference in rCBF patterns between patients with DLB with parkinsonism (DLB-P) and those with DLB without parkinsonism (DLB-nonP), using N-isopropyl-p-[123I] iodoamphetamine (IMP) and SPECT.
Section snippets
Methods
Forty-four probable DLB patients, comprising 13 patients without parkinsonism and 31 patients with parkinsonism, and 16 normal controls were included in this study. We retrospectively selected subjects from among the patients admitted to the infirmary at our institution for evaluating dementia from April 2004 to March 2007. Subjects were matched for sex, age, and Mini-Mental State Examination (MMSE) score. All the patients were examined by neurologists and psychiatrists, and underwent standard
Data analysis
The SPECT scan was initiated in the resting state with eyes closed, 15 min after each patient was administered an injection of 111 MBq (3 mCi) of N-isopropyl-p-[123I] iodoamphetamine (IMP). All SPECT scans were performed using a rotating dual-headed gamma camera (GAMMA View SPECT 2000 H, Hitachi, Tokyo, Japan) with a low-energy-general purpose (LEGP) collimator. Projection data were obtained at 15 s/step × 64 view (2 rotations of 360°). A Ramachandran filter was used for SPECT image reconstruction,
Results
DLB-P patients showed greatly decreased rCBF in the occipital lobes, cingulate cortex, and frontal lobes as compared to the normal controls (Fig. 1A, Table 1). DLB-nonP patients showed a relatively localized decrease in rCBF in the occipital lobes and anterior cingulate cortex (Fig. 1B, Table 1). rCBF in the bilateral M1 and left SMA was significantly decreased in the DLB-P patients as compared to that in the DLB-nonP patients (Fig. 2A, Table 2). rCBF in the right temporal cortex and right
Discussion
The decrease in CBF observed in the occipital lobe of DLB patients is consistent with the results of previous SPECT studies [12], [13] and PET studies [2], [14]. In addition, we found significant differences in the rCBF pattern between the DLB-P and DLB-nonP groups. The CBF in the M1 and SMA was significantly decreased in the DLB-P group as compared to that in the DLB-nonP group. In PD patients, M1 and SMA play important roles as output factors during the process of movement reduction, which is
Conclusion
There are two different clinical entities involved in DLB. DLB-P patients showed significantly decreased CBF in the motor cortex. Similar hypoactivities in the M1 and SMA are also seen in the early stages of Parkinson's disease. The SPECT imaging might be useful in not only diagnosing DLB but also subtyping of DLB. This result will help when diagnosing DLB in the context of LB disease and in fulfilling the criteria for DLB.
References (30)
- et al.
Glucose hypometabolism and neuropathological correlates in brains of dementia with Lewy bodies
Exp Neurol
(2000) - et al.
Functional anatomy of the basal ganglia. I. The cortico-basal ganglia-thalamo-cortical loop
Brain Res Brain Res Rev
(1995) - et al.
Deactivation of thalamocortical activity is responsible for suppression of parkinsonian tremor by thalamic stimulation: a 99mTc-ECD SPECT study
Clin Neurol Neurosurg
(2001) - et al.
Cognitive- and motor-related regions in Parkinson's disease: FDOPA and FDG PET studies
Neuroimage
(2004) - et al.
Diagnosis and management of dementia with Lewy bodies: third report of the DLB Consortium
Neurology
(2005) - et al.
Regional cerebral glucose metabolism in dementia with Lewy bodies and Alzheimer's disease
Neurology
(1998) - et al.
Alzheimer's disease versus dementia with Lewy bodies: cerebral metabolic distinction with autopsy confirmation
Ann Neurol
(2001) - et al.
Comparison of FDG-PET and IMP-SPECT in patients with dementia with Lewy bodies
Ann Nucl Med
(2004) Neuroimaging as a diagnostic tool in dementia with Lewy bodies
Dement Geriatr Cogn Disord
(2004)- et al.
Regional cerebral blood flow difference between dementia with Lewy bodies and AD
Neurology
(1999)