Functional brain imaging in pure akinesia with gait freezing: [¹⁸F] FDG PET and [¹⁸F] FP‐CIT PET analyses

Abstract

Pure akinesia with gait freezing (PAGF) has characteristic features, including freezing of gait and prominent speech disturbance without rigidity or tremor. The purpose of this study was to investigate changes in brain glucose metabolism and presynaptic dopaminergic function in PAGF. By using [(18)F] fluorodeoxyglucose (FDG) PET, 11 patients with PAGF were compared with 14 patients with probable progressive supranuclear palsy (PSP), 13 patients with Parkinson's disease (PD), and 11 normal controls. [(18)F] N-(3-fluoropropyl)-2beta-carbon ethoxy-3beta-(4-iodophenyl) nortropane (FP-CIT) PET was performed in 11 patients with PAGF and with 10 normal controls. The PAGF patients showed decreased glucose metabolism in the midbrain when compared with normal controls. PSP patients showed a similar topographic distribution of glucose hypometabolism with additional areas, including the frontal cortex, when compared with normal controls. The FP-CIT PET findings in patients with PAGF revealed severely decreased uptake bilaterally in the basal ganglia. These findings suggest that both PAGF and PSP may be part of the same pathophysiologic spectrum of disease. However, the reason why PAGF manifests clinically in a different manner needs to be further elucidated.

Clinical Significance of F-18 FP-CIT Dual Time Point PET Imaging in Idiopathic Parkinson’s Disease

“…Park et al [17] reported that SOR was 3.1±0.6 for the caudate nucleus and 3.2 ±0.7 for the putamen on 90-min FP-CIT PET imaging, whereas SOR was 4.48±1.51 for the caudate nucleus, 4.98±0.72 for the anterior putamen and 5.03±0.72 for the posterior putamen in this study. A relativity higher uptake value in our study is probably due to a difference in the average age of the control group (72± 6.0 vs. 70.3±10.2) and dose of the radiotracer [fixed dose of 185 MBq vs. 149-259 MBq (3.7 MBq/kg)] between the two studies.…”

Acoustical Analysis of Speech in Progressive Supranuclear Palsy

“…In the latter ones, the underlying tau pathology is less severe and features a more restricted distribution. [6][7][8] Moreover, there is an overlap to other clinically defined entities, such as PSP-corticobasal syndrome and PSPprogressive nonfluent aphasia, in which the cortical involvement of tau pathology is more severe. 9,10 The heterogeneity of PSP has recently been examined in detail in postmortem series to define pathological surrogate parameters based on the extent and pattern of tau pathology to distinguish RS from PSP-P. 11,12 Differences were most striking in the cerebral cortex, pons, caudate, and some cerebellar regions, whereas the subthalamic nucleus and substantia nigra were affected similarly both in RS and PSP-P. 11,12 The involvement of brainstem and midbrain structures in both subtypes of PSP probably influences the clinical manifestation of dysarthria, which is often an early and prominent symptom of PSP 13 and had already been described by Richardson et al 1 as pseudobulbar palsy.…”

Differentiation between idiopathic and atypical parkinsonian syndromes using three-dimensional magnetic resonance spectroscopic imaging

“…For PSP (subtype Richardson syndrome), many morphological MRI studies described typical midbrain atrophy patterns, such as humming bird10 and morning glory signs,11–17 which are only slightly present in the PSP parkinsonism subtype. In other PSP subtypes, such as pure akinesia with gait freezing or PSP with corticobasal syndrome, these features have not been observed 18 19. For MSA, a number of signs have been reported using routine MRI which include putaminal atrophy, hypointensity and slit sign, as well as atrophy of the pons and of the middle cerebellar peduncle, dilatation of the fourth ventricle and the hot cross bun sign 9 20…”