A juvenile case of frontotemporal dementia: Neurochemical and neuropathological investigations

Nagaoka, Shigeyuki; Arai, Heii; Iwamoto, Norihiko; Ohwada, Jiro; Ichimiya, Yosuke; Nakamura, Makoto; Inoue, Reiichi

doi:10.1016/0278-5846(95)00264-2

Cited by 21 publications

(11 citation statements)

References 7 publications

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“…Pasquier et al [27] in a study of 74 FTD patients reported extrapyramidal symptoms in the first visit of 40% of the patients. Reduction of monoamine metabolites in the CSF of patients with FTD [28] as well as in several brain areas including the basal ganglia and substantia nigra in a juvenile patient with FTD [29] is reported. Another study using PET and [ 11 C]CFT showed a reduction of tracer binding in the caudate nucleus and putamen of 12 patients with FTD [30] .…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Dopaminergic Function in Frontotemporal Dementia Using <sup>123</sup>I-FP-CIT Single Photon Emission Computed Tomography

et al. 2007

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Extrapyramidal symptoms are observed in frontotemporal dementia (FTD). ¹²³I-FP-CIT (DaT scan) single photon emission computed tomography (SPECT) can detect loss of presynaptic dopamine transporters in the striatum. We aimed to evaluate the dopaminergic status of the striatum in patients with FTD using DaT scan. Seven patients (age range 65–76 years), who fulfilled the Neary criteria and in whom the diagnosis of FTD was confirmed by hexamethylpropyleneamine oxime SPECT, were included in the study. The severity of the extrapyramidal symptoms was evaluated by the motor part of the Unified Parkinson’s Disease Rating Scale (UPDRS). SPECT using ¹²³I-FP-CIT was done. A (region – occipital)/occipital ratio was calculated for the striatum, putamen and caudate nucleus. The results were compared with those of the 7 age-matched normal controls. The uptake of the radiotracer in the right and left striatum was reduced to 62% (p = 0.000) and 68% (p = 0.000), respectively, compared to controls. The motor UPDRS score of the patients with FTD showed a negative correlation to the uptake of the radiotracer. The presynaptic dopamine transporter in FTD is impaired, related to the severity of the extrapyramidal symptoms. Since an effective treatment for FTD is still to be established, there is a need for evaluating the efficacy of dopaminergic drugs.

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Section: Discussionmentioning

confidence: 99%

Evaluation of Dopaminergic Function in Frontotemporal Dementia Using <sup>123</sup>I-FP-CIT Single Photon Emission Computed Tomography

et al. 2007

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“…Biopsy-proven non-Picks frontotemporal dementia has been reported twice under the age of 30. A female aged 28 at symptom onset had severe neuronal loss and gliosis with frontotemporal atrophy on CT similar to this case [3]. Another 27-year-old woman had pathological evidence of subcortical gliosis without Pick bodies [4].…”

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confidence: 93%

Non-Picks frontotemporal dementia imitating schizophrenia in a 22-year-old man

Stone

Griffiths

Rastogi³

et al. 2003

Journal of Neurology

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“…31 A SPECT study showed severely reduced presynaptic dopaminergic nerve terminals and mild reduction of postsynaptic D2 receptor binding in the striatum of a patient with FTDP-17. 32 Studies have demonstrated significantly lower CSF levels of HVA and dopamine in FTD and Pick's disease (PiD), 21,33,34 and decreased D2 ligand uptake in frontal cortex. 35 Reports that do not support dopamine abnormalities in FTD include one that failed to demonstrate abnormal levels of CSF HVA, 18 and another that failed to show abnormalities in brain dopamine concentrations.…”

Section: Mechanism Reviewmentioning

confidence: 99%

A systematic review of neurotransmitter deficits and treatments in frontotemporal dementia

2006

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Objective-To evaluate neurotransmitter deficiencies and neurotransmitter-based treatments for frontotemporal dementia (FTD).Methods-The authors conducted a systematic review of the literature on the mechanism and treatment of FTD and a meta-analysis of treatment studies of antidepressants for the behavioral symptoms of FTD.Results-Patients with FTD show deficiencies in the serotonin and dopamine neurotransmitter systems, while the acetylcholine system appears relatively intact. Antidepressant treatment significantly improves behavioral symptoms in FTD, but most studies are small and uncontrolled. Serotonergic treatments appear to improve the behavioral but not cognitive symptoms of FTD.Conclusions-Studies of neurotransmitter deficiencies in frontotemporal dementia (FTD) can be helpful in developing treatments. Treatment studies on FTD are scarce, given the prevalence and severity of this illness. Larger, well-controlled treatment studies are required to reach more definitive conclusions about treatment efficacy. Multicenter studies are likely the best way to complete treatment studies in a timely manner.Frontotemporal dementia (FTD) is increasingly recognized as an important cause of dementia. 1 The symptoms of FTD include behavioral symptoms such as disinhibition, inappropriate social behavior, and apathy. Other symptoms include language and executive dysfunction. 2,3 The behavioral symptoms of FTD can be difficult to manage for caregivers and clinicians.The paucity of pharmacologic trials for FTD is likely due to the only recent clinical definition of the illness, limitations in understanding the biology of FTD, and the difficulty of assembling well-characterized groups of patients.

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A juvenile case of frontotemporal dementia: Neurochemical and neuropathological investigations

Cited by 21 publications

References 7 publications

Evaluation of Dopaminergic Function in Frontotemporal Dementia Using <sup>123</sup>I-FP-CIT Single Photon Emission Computed Tomography

Evaluation of Dopaminergic Function in Frontotemporal Dementia Using <sup>123</sup>I-FP-CIT Single Photon Emission Computed Tomography

Non-Picks frontotemporal dementia imitating schizophrenia in a 22-year-old man

A systematic review of neurotransmitter deficits and treatments in frontotemporal dementia

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