Quantitative Electroencephalography in Frontotemporal Dementia with Methylphenidate Response: A Case Study

2004 ◽  
Vol 35 (2) ◽  
pp. 108-111 ◽  
Author(s):  
Harold W. Goforth ◽  
Lukasz Konopka ◽  
Margaret Primeau ◽  
Amity Ruth ◽  
Kathleen O'Donnell ◽  
...  
2014 ◽  
Vol 26 (12) ◽  
pp. 2023-2026 ◽  
Author(s):  
W. F. Fick ◽  
J. P. van der Borgh ◽  
S. Jansen ◽  
R. T. C. M. Koopmans

ABSTRACTA problematic and disturbing behavior which can develop in people with dementia, is vocally disruptive behavior (VDB). To date, the study of VDB is underdeveloped and with only a limited knowledge base. Medications commonly used in VDB have limited benefits and specific risks in patients with dementia. This report details the case of a patient with frontotemporal dementia with VDB, which responded very well by providing a lollipop. Subsequently, we pose theory-based hypotheses in order to try to explain the beneficial effect of this intervention. This may contribute to a better understanding of VDB and possible treatment strategies.


2019 ◽  
Vol 13 (3) ◽  
pp. 356-360
Author(s):  
Leonardo Cruz de Souza ◽  
Luciano Inácio Mariano ◽  
Renata Freire de Moraes ◽  
Paulo Caramelli

ABSTRACT Alzheimer's disease (AD) has heterogeneous clinical presentations. Amnestic progressive disorder leading to dementia is the most typical, but non-amnestic presentations are also recognized. Here we report a case of frontal variant of AD. A right-handed woman, aged 68 years, was referred for progressive behavioral disorders and personality changes. She had a corroborated history of dietary changes, hyperorality, impulsivity, affective indifference and apathy, with functional impairment. Cognitive assessment yielded severe executive deficits. Positron emission tomography with fluorodeoxyglucose showed marked hypometabolism in frontotemporal regions, with relative preservation of parietal regions. CSF AD biomarkers showed low Aβ42, high Tau and high P-Tau. The patient fulfilled criteria for probable behavioral variant frontotemporal dementia. However, considering the AD pathophysiological signature on CSF biomarkers, a diagnosis of frontal variant of AD was established. In the perspective of disease-modifying therapies, it is important to identify atypical Alzheimer presentations, as these patients may be candidates for specific treatments.


Author(s):  
Thomas Benke ◽  
Christoph Scherfler ◽  
Elfriede Karner ◽  
Florian Dazinger ◽  
Evelin Donnemiller

2014 ◽  
Vol 29 (6) ◽  
pp. 510-510 ◽  
Author(s):  
M. Sarno ◽  
A. Bure-Reyes ◽  
M. Rosado ◽  
R. Curiel ◽  
E. Crocco

2011 ◽  
Vol 23 ◽  
pp. 231-232
Author(s):  
Chinar Dara ◽  
Kathleen Kortte ◽  
Cameron Davis ◽  
Elisa Ochfeld ◽  
Melissa Newhart ◽  
...  

2019 ◽  
Vol 09 (01) ◽  
Author(s):  
Elmar Weiler ◽  
Rainer Wiegand ◽  
Klaus Brill ◽  
Dieter Schneider

2000 ◽  
Vol 15 (5) ◽  
pp. 277-283
Author(s):  
Bess Mehring ◽  
Judy C.Y. Lin ◽  
Dahlia Wilson ◽  
Carol F. Lippa

In motor neuron disease (MND) cases associated with dementia, neurons often contain ubiquitin-positive, taunegative cytoplasmic inclusions that are numerous in the granule cell neurons of the hippocampal complex. Dot or threadlike ubiquitinated neurites are also observed in the surrounding neuropil and in other frontotemporal regions. Cases of frontotemporal dementia (FTD) with identical appearing ubiquitinated deposits have been described in FTD cases lacking signs of MND. The underlying pathobiology of these cases remains obscure. We describe a case from a familial FTD kindred and use immunohistochemistry to evaluate the hippocampal ubiquitin-positive cytoplasmic granule cell inclusions in relationship to the threads and dots that surround them. Ubiquitin-positive threads were more numerous in the overlying molecular layer of the dentate gyrus (DG) compared with the underlying polymorphic layer, suggesting that threads are formed primarily in the dendrites of the affected granule cells. In contrast, dot-like inclusions were uniformly distributed. Using antibodies to synapticterminal specific proteins, we observed loss of perforant pathway synapses in the outer molecular layer of the DG. The numbers of thread-and dot-like inclusions were no greater in the region of synaptic loss than in the layer that lacked detectable synaptic loss. Similarly, ubiquitinated aggregates were more numerous in rostral sections, and they tended to cluster, whereas synapse loss was uniform. These findings expand upon previous data by suggesting that formation of these ubiquitinated aggregates relate to an inherent susceptibility in the granule cell neuron, rather than solely to a deafferentation effect. This study contributes to our understanding of what might be a common pathological process underlying FTD and MND cases with ubiquitinated inclusions.


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