scholarly journals Evaluation of Cognition and Cortical Excitability in Huntington’s Disease

2018 ◽  
Vol 45 (2) ◽  
pp. 176-181 ◽  
Author(s):  
Nitish Kamble ◽  
M. Netravathi ◽  
B.C. Nagaraju ◽  
Abhishek Lenka ◽  
Keshav Kumar ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cortical Excitability ◽  
Short Interval ◽  
Silent Period ◽  
Conduction Time ◽  
Resting Motor Threshold ◽  
Significant Difference ◽  
Significant Impairment

AbstractBackground: Recent advances in neurophysiological techniques have contributed to our understanding of the pathophysiology of Huntington’s disease (HD). Studies of the motor cortical excitability and central motor pathways have shown variable results. Objectives: Our aims were to evaluate the cortical excitability changes in HD using transcranial magnetic stimulation (TMS) and correlate the changes with cognitive impairment. Methods: The study included 32 HD patients and 30 age- and gender-matched controls. The demographic and clinical profiles of the patients were recorded. All subjects were evaluated by TMS and resting motor threshold (RMT), central motor conduction time (CMCT), silent period (SP), short-interval intracortical inhibition (SICI), and intracortical facilitation were determined. A battery of neuropsychological tests was administered to all subjects. Results: The mean age of the patients was 42.1±14.1 years, and that of controls 39.4±12.4 years (p=0.61). There was no significant difference in RMT and CMCT between the two groups. There was a mild prolongation of the contralateral SP in HD, but it was not significant. SICI was significantly reduced in HD (p<0.0001). A significant impairment in attention, verbal fluency, executive function, visuospatial function, learning, and memory was observed in HD patients. However, there was no correlation between cortical excitability changes and cognitive impairment. Conclusions: TMS is a valuable method of evaluating cortical excitability changes in HD. These patients have reduced SICI and significant impairment of cognition in multiple domains.

Cortical dysfunction underlies disability in multiple sclerosis

2011 ◽  
Vol 18 (4) ◽  
pp. 425-432 ◽  
Author(s):  
Steve Vucic ◽  
Therese Burke ◽  
Kerry Lenton ◽  
Sudarshini Ramanathan ◽  
Lavier Gomes ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cortical Excitability ◽  
Short Interval ◽  
Motor Evoked Potential ◽  
Intracortical Inhibition ◽  
Progressive Multiple Sclerosis ◽  
Conduction Time ◽  
Cortical Function ◽  
Resting Motor Threshold ◽  
Cortical Dysfunction

Background: Gray matter atrophy has been implicated in the development of secondary progressive multiple sclerosis (SPMS). Cortical function may be assessed by transcranial magnetic stimulation (TMS). Determining whether cortical dysfunction was a feature of SPMS could be of pathophysiological significance. Objectives: Consequently, novel paired-pulse threshold tracking TMS techniques were used to assess whether cortical dysfunction was a feature of SPMS. Methods: Cortical excitability studies were undertaken in 15 SPMS, 25 relapsing–remitting MS patients (RRMS) and 66 controls. Results: Short interval intracortical inhibition (SPMS 3.0 ± 2.1%; RRMS 12.8 ± 1.7%, p < 0.01; controls 10.5 ± 0.7%, p < 0.01) and motor evoked potential (MEP) amplitude (SPMS 11.5 ± 2.2%; RRMS 26.3 ± 3.6%, p <0.05; controls 24.7 ± 1.8%, p < 0.01) were reduced in SPMS, while intracortical facilitation (SPMS -5.2 ± 1.9%; RRMS -2.0 ± 1.4, p < 0.05; controls -0.9 ± 0.7, p < 0.01) and resting motor threshold were increased (SPMS 67.5 ± 4.5%; RRMS 56.0 ± 1.5%, p < 0.01; controls 59.0 ± 1.1%, p < 0.001). Further, central motor conduction time was prolonged in SPMS (9.1 ± 1.2 ms, p < 0.001) and RRMS (7.0 ± 0.9 ms, p < 0.05) patients compared with controls (5.5 ± 0.2 ms). The observed changes in cortical function correlated with the Expanded Disability Status Scale. Conclusion: Together, these findings suggest that cortical dysfunction is associated with disability in MS, and documentation of such cortical dysfunction may serve to quantify disease severity in MS.

scholarly journals Clinical and Electrophysiological Hints to TMS in De Novo Patients with Parkinson’s Disease and Progressive Supranuclear Palsy

2020 ◽  
Vol 10 (4) ◽  
pp. 274
Author(s):  
Francesco Fisicaro ◽  
Giuseppe Lanza ◽  
Mariagiovanna Cantone ◽  
Raffaele Ferri ◽  
Giovanni Pennisi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Progressive Supranuclear Palsy ◽  
De Novo ◽  
Cortical Excitability ◽  
Motor Evoked Potentials ◽  
Silent Period ◽  
Small Sample ◽  
Conduction Time ◽  
Resting Motor Threshold

Background: Transcranial magnetic stimulation (TMS) can non-invasively probe cortical excitability in movement disorders, although clinical significance is still controversial, especially at early stages. We compare single-pulse TMS in two prototypic synucleinopathy and tauopathy—i.e., Parkinson’s disease (PD) and Progressive Supranuclear Palsy (PSP), respectively—to find neurophysiological differences and identify early measures associated with cognitive impairment. Methods: 28 PD and 23 PSP de novo patients were age-matched with 28 healthy controls, all right-handed and drug-free. Amplitude and latency of motor evoked potentials (MEP), central motor conduction time, resting motor threshold (rMT), and cortical silent period (CSP) were recorded through a figure-of-eight coil from the First Dorsal Interosseous muscle (FDI), bilaterally. Results: Mini Mental Examination and Frontal Assessment Battery (FAB) scored worse in PSP; PD had worse FAB than controls. Higher MEP amplitude from right FDI in PD and PSP than controls was found, without difference between them. CSP was bilaterally longer in patients than controls, but similar between patient groups. A positive correlation between FAB and rMT was observed in PSP, bilaterally. Conclusions: Despite the small sample size, PD and PSP might share, at early stage, a similar global electrocortical asset. rMT might detect and possibly predict cognitive deterioration in PSP.

The prolonged cortical silent period in patients with Huntington's disease

2001 ◽  
Vol 112 (8) ◽  
pp. 1470-1474 ◽  
Author(s):  
N Modugno ◽  
A Currà ◽  
M Giovannelli ◽  
A Priori ◽  
F Squitieri ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Silent Period ◽  
Cortical Silent Period

The relationship between impairment of voluntary movements and cognitive impairment in Huntington’s disease

2009 ◽  
Vol 256 (10) ◽  
pp. 1629-1633 ◽  
Author(s):  
Jiří Klempíř ◽  
Olga Klempířová ◽  
Jan Štochl ◽  
Nataša Špačková ◽  
Jan Roth
Keyword(s):  
Cognitive Impairment ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Voluntary Movements ◽  
The Relationship

Profiles of motor and cognitive impairment in the transgenic rat model of Huntington's disease

2012 ◽  
Vol 88 (2-3) ◽  
pp. 223-236 ◽  
Author(s):  
Steven A. Fielding ◽  
Simon P. Brooks ◽  
Alexander Klein ◽  
Zubeyde Bayram-Weston ◽  
Lesley Jones ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Rat Model ◽  
Transgenic Rat ◽  
Transgenic Rat Model

scholarly journals Preserved central cholinergic functioning to transcranial magnetic stimulation in de novo patients with celiac disease

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0261373
Author(s):  
Giuseppe Lanza ◽  
Francesco Fisicaro ◽  
Carmela Cinzia D’Agate ◽  
Raffaele Ferri ◽  
Mariagiovanna Cantone ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
De Novo ◽  
Systemic Disease ◽  
Conduction Time ◽  
Healthy Controls ◽  
Resting Motor Threshold ◽  
Significant Difference ◽  
Interstimulus Intervals

Background Celiac disease (CD) is now viewed as a systemic disease with multifaceted clinical manifestations. Among the extra-intestinal features, neurological and neuropsychiatric symptoms are still a diagnostic challenge, since they can precede or follow the diagnosis of CD. In particular, it is well known that some adults with CD may complain of cognitive symptoms, that improve when the gluten-free diet (GFD) is started, although they may re-appear after incidental gluten intake. Among the neurophysiological techniques, motor evoked potentials (MEPs) to transcranial magnetic stimulation (TMS) can non-invasively probe in vivo the excitation state of cortical areas and cortico-spinal conductivity, being also able to unveil preclinical impairment in several neurological and psychiatric disorders, as well as in some systemic diseases affecting the central nervous system (CNS), such as CD. We previously demonstrated an intracortical disinhibition and hyperfacilitation of MEP responses to TMS in newly diagnosed patients. However, no data are available on the central cholinergic functioning indexed by specific TMS measures, such as the short-latency afferent inhibition (SAI), which might represent the neurophysiological correlate of cognitive changes in CD patients, also at the preclinical level. Methods Cognitive and depressive symptoms were screened by means of the Montreal Cognitive Assessment (MoCA) and the 17-item Hamilton Depression Rating Scale (HDRS), respectively, in 15 consecutive de novo CD patients and 15 healthy controls. All patients were on normal diet at the time of the enrolment. Brain computed tomography (CT) was performed in all patients. SAI, recorded at two interstimulus intervals (2 and 8 ms), was assessed as the percentage amplitude ratio between the conditioned and the unconditioned MEP response. Resting motor threshold, MEP amplitude and latency, and central motor conduction time were also measured. Results The two groups were comparable for age, sex, anthropometric features, and educational level. Brain CT ruled out intracranial calcifications and clear radiological abnormalities in all patients. Scores at MoCA and HDRS were significantly worse in patients than in controls. The comparison of TMS data between the two groups revealed no statistically significant difference for all measures, including SAI at both interstimulus intervals. Conclusions Central cholinergic functioning explored by the SAI of the motor cortex resulted to be not affected in these de novo CD patients compared to age-matched healthy controls. Although the statistically significant difference in MoCA, an overt cognitive impairment was not clinically evident in CD patients. Coherently, to date, no study based on TMS or other diagnostic techniques has shown any involvement of the central acetylcholine or the cholinergic fibers within the CNS in CD. This finding might add support to the vascular inflammation hypothesis underlying the so-called “gluten encephalopathy”, which seems to be due to an aetiology different from that of the cholinergic dysfunction. Longitudinal studies correlating clinical, TMS, and neuroimaging data, both before and after GFD, are needed.

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