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Rita Bella,
Raffaele Ferri,
Giuseppe Lanza,
Mariagiovanna Cantone,
Manuela Pennisi, Valentina Puglisi,
Luisa Vinciguerra,
Concetto Spampinato,
Tommaso Mazza,
Giulia Malaguarnera,
Giovanni Pennisi
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ABSTRACT: Vascular Cognitive Impairment-no dementia (VCI-ND) is a condition at risk for future dementia and should be the target of preventive strategies. Recently, an enhanced intracortical facilitation observed in VCI-ND patients was proposed as a candidate neurophysiological marker of the disease process. The aim of this study was to monitor the excitability of the motor cortex and the functioning of excitatory/inhibitory intracortical circuits in patients with VCI-ND after a follow-up period of approximately two years, in order to pick out early markers of disease progression into dementia. Nine patients and nine age-matched controls were re-evaluated for single and paired pulse TMS measures of cortical excitability, as well as for neuropsycological and functional assessment. Compared to the first evaluation, patients showed a decrease of the median resting motor threshold (rMT). Patients exhibited a significant worsening at Stroop Color Word Test Interference scores without substantial functional impairment. Our study represents the first evidence of a decrease of rMT in VCI-ND patients during the progression of cognitive impairment. This result might be considered an index of motor cortex plasticity and interpreted as a compensatory mechanism for the loss of motor cortex neurons.
Neuroscience Letters 12/2012; · 2.11 Impact Factor
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ABSTRACT: Recently, neuropathological studies have shown an important motor cortex involvement in Alzheimer’s disease (AD), even in
its early stages, despite the lack of clinically evident motor deficit. Transcranial magnetic stimulation (TMS) studies have
demonstrated that cortical excitability is enhanced in AD patients. This cortical hyperexcitability is believed to be a compensatory
mechanism to execute voluntary movements, despite the progressive impairment of associative cortical areas. At present, it
is not clear if these motor cortex excitability changes might be the expression of an involvement of intracortical excitatory
glutamatergic circuits or an impairment of inhibitory cholinergic and, to a lesser extent, gabaergic activity. Although the
main hypothesis for the pathogenesis of AD remains the degeneration of the basal forebrain cholinergic neurons, the development
of specific TMS protocols, such as the paired-pulse TMS and the study of the short-latency afferent inhibition, points out
the role of other neurotransmitters, such as gamma-amino-butyric acid, glutamate and dopamine. The potential therapeutic effect
of repetitive TMS in restoring or compensating damaged cognitive functions, might become a possible rehabilitation tool in
AD patients. Based on different patterns of cortical excitability, TMS may be useful in discriminating between physiological
brain aging, mild cognitive impairment, AD and other dementing disorders. The present review provides a perspective of these
TMS techniques by further understanding the role of different neurotransmission pathways and plastic remodelling of neuronal
networks in the pathogenesis of AD.
KeywordsTranscranial magnetic stimulation–Cortical excitability–Aging–Alzheimer’s disease–Neurotransmission–Neuroplasticity
Acta Neurovegetativa 04/2012; 118(4):587-598. · 2.73 Impact Factor
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ABSTRACT: Recently, neuropathological studies have shown an important motor cortex involvement in Alzheimer's disease (AD), even in its early stages, despite the lack of clinically evident motor deficit. Transcranial magnetic stimulation (TMS) studies have demonstrated that cortical excitability is enhanced in AD patients. This cortical hyperexcitability is believed to be a compensatory mechanism to execute voluntary movements, despite the progressive impairment of associative cortical areas. At present, it is not clear if these motor cortex excitability changes might be the expression of an involvement of intracortical excitatory glutamatergic circuits or an impairment of inhibitory cholinergic and, to a lesser extent, gabaergic activity. Although the main hypothesis for the pathogenesis of AD remains the degeneration of the basal forebrain cholinergic neurons, the development of specific TMS protocols, such as the paired-pulse TMS and the study of the short-latency afferent inhibition, points out the role of other neurotransmitters, such as gamma-amino-butyric acid, glutamate and dopamine. The potential therapeutic effect of repetitive TMS in restoring or compensating damaged cognitive functions, might become a possible rehabilitation tool in AD patients. Based on different patterns of cortical excitability, TMS may be useful in discriminating between physiological brain aging, mild cognitive impairment, AD and other dementing disorders. The present review provides a perspective of these TMS techniques by further understanding the role of different neurotransmission pathways and plastic remodelling of neuronal networks in the pathogenesis of AD.
Acta Neurovegetativa 01/2011; 118(4):587-98. · 2.73 Impact Factor
