The motor cortex shows adaptive functional changes to brain injury from multiple sclerosis

2000 ◽  
Vol 47 (5) ◽  
pp. 606-613 ◽  
Author(s):  
M. Lee ◽  
H. Reddy ◽  
H. Johansen-Berg ◽  
S. Pendlebury ◽  
M. Jenkinson ◽  
...  
2008 ◽  
Vol 14 (7) ◽  
pp. 995-998 ◽  
Author(s):  
G Koch ◽  
S Rossi ◽  
C Prosperetti ◽  
C Codecà ◽  
F Monteleone ◽  
...  

We tested the effects of 5-Hz repetitive transcranial magnetic stimulation (rTMS) over the motor cortex in multiple sclerosis (MS) subjects with cerebellar symptoms. rTMS improved hand dexterity in cerebellar patients ( n = 8) but not in healthy subjects ( n = 7), as detected by a significant transient reduction of the time required to complete the nine-hole pegboard task. rTMS of the motor cortex may be a useful approach to treat cerebellar impairment in MS patients.


Brain Injury ◽  
2014 ◽  
Vol 28 (10) ◽  
pp. 1270-1276 ◽  
Author(s):  
Nick R. Miller ◽  
Alia L. Yasen ◽  
Logan F. Maynard ◽  
Li-Shan Chou ◽  
David R. Howell ◽  
...  

Author(s):  
Ю.В. Гаврилов ◽  
К.З. Деревцова ◽  
Е.А. Корнева

Актуальность. Хроническое нарушение цикла «сон-бодрствование» является частым последствием черепно-мозговой травмы (ЧМТ), однако патогенез этого явления неизвестен. Недоступность прижизненного гистологического анализа пораженных структур головного мозга, полиморфность повреждений при ЧМТ создают определенные трудности для систематического изучения посттравматических нарушений. Большая часть современных исследований сфокусирована на острых изменениях активности клеток мозга после ЧМТ. Проблема изучения отдаленных последствий после перенесенной ЧМТ остается не менее актуальной. Характерные для посттравматического периода нарушения сна существенно влияют на когнитивную активность и вызывают вторичные функциональные изменения, приводящие к последующему снижению трудоспособности и качества жизни людей, перенесших травму. Целью исследования стало изучение нарушений цикла «сон-бодрствование» в течение нескольких недель после ЧМТ у крыс по результатам анализа электроэнцефалограмм. Методы. Для объективной оценки нарушений сна использовали полисомнографию. Проанализированы данные электрофизиологических изменений через 1, 7 и 28 дней после травмы. Результаты. Обнаружено отставленное (через 28 дней) влияние ЧМТ на показатели цикла «сон-бодрствование»: повышение продолжительности сна за счёт возрастания длительности периодов сна в темное время суток в часы активного бодрствования крыс, с соответствующим снижением индекса фрагментации сна. Заключение. Выявленный характер нарушений сна после ЧМТ позволяет приблизиться к пониманию адекватных способов терапии, направленной на нормализацию цикла сон-бодрствование, что поможет снизить развитие посттравматической астении. Background. Chronic disturbance of the sleep-wake cycle is a frequent consequence of traumatic brain injury (TBI) with an unknown pathogenesis. Unavailability of intravital histological analysis of affected brain structures and the polymorphism of TBI complicate systematic study of posttraumatic disorders. Most of current research focuses on acute changes in brain cell activity following TBI. The issue of long-term TBI consequences is still relevant. Sleep disorders typical for the post-traumatic period considerably affect the cognitive function and cause secondary functional changes that lead to impaired working ability. In addition, TBI decreases the patients’ quality of life. Thus, the aim of the study was to evaluate disorders of the sleep-wake cycle during several weeks after TBI in rats using electroencephalographic analysis. Methods. The polysomnography study detected electrophysiological changes at 1, 7, and 28 days after trauma. Results. A delayed (28 days) impact of TBI on indexes of the sleep-wake cycle included an increased sleep duration due to longer sleep periods in the dark time of day, during the hours of rat active waking with a corresponding decrease in the sleep fragmentation index. Conclusion. The identified nature of post-TBI sleep disorders provides better understanding of adequate therapy aimed at normalizing the sleep-wake cycle, which will help reduce the development of post-traumatic asthenia.


2020 ◽  
Vol 34 (3) ◽  
pp. 260-270 ◽  
Author(s):  
Riccardo Iandolo ◽  
Giulia Bommarito ◽  
Laura Falcitano ◽  
Simona Schiavi ◽  
Niccolò Piaggio ◽  
...  

Background/Objective. Position sense, defined as the ability to identify joint and limb position in space, is crucial for balance and gait but has received limited attention in patients with multiple sclerosis (MS). We investigated lower limb position sense deficits, their neural correlates, and their effects on standing balance in patients with early MS. Methods. A total of 24 patients with early relapsing-remitting MS and 24 healthy controls performed ipsilateral and contralateral matching tasks with the right foot during functional magnetic resonance imaging. Corpus callosum (CC) integrity was estimated with diffusion tensor imaging. Patients also underwent an assessment of balance during quiet standing. We investigated differences between the 2 groups and the relations among proprioceptive errors, balance performance, and functional/structural correlates. Results. During the contralateral matching task, patients demonstrated a higher matching error than controls, which correlated with the microstructural damage of the CC and with balance ability. In contrast, during the ipsilateral task, the 2 groups showed a similar matching performance, but patients displayed a functional reorganization involving the parietal areas. Neural activity in the frontoparietal regions correlated with the performance during both proprioceptive matching tasks and quiet standing. Conclusion. Patients with early MS had subtle, clinically undetectable, position sense deficits at the lower limbs that, nevertheless, affected standing balance. Functional changes allowed correct proprioception processing during the ipsilateral matching task but not during the more demanding bilateral task, possibly because of damage to the CC. These findings provide new insights into the mechanisms underlying disability in MS and could influence the design of neurorehabilitation protocols.


2020 ◽  
Vol 131 (2) ◽  
pp. 566-573 ◽  
Author(s):  
Mario Stampanoni Bassi ◽  
Fabio Buttari ◽  
Pierpaolo Maffei ◽  
Nicla De Paolis ◽  
Andrea Sancesario ◽  
...  

2005 ◽  
Vol 11 (3) ◽  
pp. 316-321 ◽  
Author(s):  
J Liepert ◽  
D Mingers ◽  
C Heesen ◽  
T Bäumer ◽  
C Weiller

We investigated electrophysiological correlates of fatigue in patients with multiple sclerosis (MS). Transcranial magnetic stimulation (TMS) was used to explore motor excitability in three groups of subjects: MS patients with fatigue (MS-F), MS patients without fatigue (MS-NF) and healthy control subjects. All participants had to perform a fatiguing hand-grip exercise. TMS was performed prior to and after the exercise. Prior to the motor task, MS-F patients had less inhibition in the primary motor cortex compared to both other groups. Postexercise, intracortical inhibition was still reduced in the MS-F patients compared to the MS-NF patients. In MS-F patients the postexercise time interval for normalization of the motor threshold was correlated with the fatigue severity. We conclude that MS patients with fatigue have an impairment of inhibitory circuits in their primary motor cortex. The results also indicate that fatigue severity is associated with an exercise-induced reduction of membrane excitability.


2019 ◽  
Vol 13 ◽  
pp. 117906951982588 ◽  
Author(s):  
Shaona Acharjee ◽  
Quentin J Pittman

Multiple sclerosis, and its animal model—experimental autoimmune encephalomyelitis (EAE), is a demyelinating disease causing motor and sensory dysfunction, as well as behavioral comorbidities. In exploring possible functional changes underlying behavioral comorbidities in EAE, we observed increased excitatory drive onto the major cells of the basolateral amygdala. This was associated with increased numbers of dendritic spines. An unexpected finding was that microglial cells at this time were in a “deactivated” state, and further studies suggested that the microglial deactivation was responsible for the increased excitatory drive. This is the first report of microglial deactivation in an inflammatory disease and raises many questions as to the underlying mechanisms and functional relevance.


2018 ◽  
Vol 25 (5) ◽  
pp. 715-726 ◽  
Author(s):  
Quinten van Geest ◽  
Rosa E Boeschoten ◽  
Matthijs J Keijzer ◽  
Martijn D Steenwijk ◽  
Petra JW Pouwels ◽  
...  

Background: The biological mechanism of depression in multiple sclerosis (MS) is not well understood. Based on work in major depressive disorder, fronto-limbic disconnection might be important. Objective: To investigate structural and functional fronto-limbic changes in depressed MS (DMS) and non-depressed MS (nDMS) patients. Methods: In this retrospective study, 22 moderate-to-severe DMS patients (disease duration 8.2 ± 7.7 years), 21 nDMS patients (disease duration 15.3 ± 8.3 years), and 12 healthy controls underwent neuropsychological testing and magnetic resonance imaging (MRI; 1.5 T). Brain volumes (white matter (WM), gray matter, amygdala, hippocampus, thalamus), lesion load, fractional anisotropy (FA) of fronto-limbic tracts, and resting-state functional connectivity (FC) between limbic and frontal areas were measured and compared between groups. Regression analysis was performed to relate MRI measures to the severity of depression. Results: Compared to nDMS patients, DMS patients (shorter disease duration) had lower WM volume ( p < 0.01), decreased FA of the uncinate fasciculus ( p < 0.05), and lower FC between the amygdala and frontal regions ( p < 0.05). Disease duration, FA of the uncinate fasciculus, and FC of the amygdala could explain 48% of variance in the severity of depression. No differences in cognition were found. Conclusion: DMS patients showed more pronounced (MS) damage, that is, structural and functional changes in temporo-frontal regions, compared to nDMS patients, suggestive of fronto-limbic disconnection.


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