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Background: Poststroke fatigue is a prevalent issue among stroke survivors, significantly impeding functional recovery and diminishing their quality of life. Aim: This prospective cohort study aims to investigate the association between poststroke fatigue and the extent of functional recovery in survivors of ischemic and hemorrhagic strokes. Additionally, it seeks to delineate the temporal progression of poststroke fatigue in these two stroke subtypes. Methods: We assessed a cohort of 79 patients recovering from acute ischemic or hemorrhagic strokes. Poststroke fatigue was quantified using the Fatigue Severity Scale (FSS) and the Numeric Rating Scale (NRSfatigue). Patients' condition was evaluated using the National Institute of Health Stroke Scale (NIHSS), and functional independence levels were determined using the Barthel Index for Activities of Daily Living (BIADL) and the Modified Rankin Scale (MRS). Depressive mood and pain were measured using the Beck Depression Inventory (BDI) and the Numeric Rating Scale for pain (NRSpain), respectively. Results: Our primary findings indicate that the early manifestation of clinically significant fatigue (CSF) is predictive of a poorer trajectory in functional independence levels during recovery. Furthermore, we observed differing patterns of fatigue progression between ischemic and hemorrhagic strokes. Fatigue tends to ameliorate over time in hemorrhagic stroke cases, paralleling functional recovery, while it remains stable over time in ischemic stroke cases. Conclusion: Our results underscore the detrimental impact of early poststroke fatigue on long-term outcomes. Furthermore, they highlight the imperative of managing poststroke fatigue, particularly during the subacute phase of stroke recovery. [ABSTRACT FROM AUTHOR]

Background: Information for treatment or hospital derivation of prehospital seizures is limited, impairing patient condition and hindering patients risk assessment by the emergency medical services (EMS). This study aimed to determine the associated factors to clinical impairment, and secondarily, to determine risk factors associated to cumulative in‐hospital mortality at 2, 7 and 30 days, in patients presenting prehospital seizures. Methods: Prospective, multicentre, EMS‐delivery study involving adult subjects with prehospital seizures, including five advanced life support units, 27 basic life support units and four emergency departments in Spain. All bedside variables: including demographic, standard vital signs, prehospital laboratory tests and presence of intoxication or traumatic brain injury (TBI), were analysed to construct a risk model using binary logistic regression and internal validation methods. Results: A total of 517 patients were considered. Clinical impairment was present in 14.9%, and cumulative in‐hospital mortality at 2, 7 and 30‐days was 3.4%, 4.6% and 7.7%, respectively. The model for the clinical impairment indicated that respiratory rate, partial pressure of carbon dioxide, blood urea nitrogen, associated TBI or stroke were risk factors; higher Glasgow Coma Scale (GCS) scores mean a lower risk of impairment. Age, potassium, glucose, prehospital use of mechanical ventilation and concomitant stroke were risk factors associated to mortality; and oxygen saturation, a high score in GCS and haemoglobin were protective factors. Conclusion: Our study shows that prehospital variables could reflect the clinical impairment and mortality of patients suffering from seizures. The incorporation of such variables in the prehospital decision‐making process could improve patient outcomes. [ABSTRACT FROM AUTHOR]

• tSMS is a portable, inhibitory, non-invasive brain stimulation technique. • Repeated sessions of home-based tSMS of the motor cortex are feasible and safe. • tSMS may provide subjective benefit for the treatment of levodopa-induced dyskinesias. [ABSTRACT FROM AUTHOR]

(1) Background: The aim was screening the performance of nine Early Warning Scores (EWS), to identify patients at high-risk of premature impairment and to detect intensive care unit (ICU) admissions, as well as to track the 2-, 7-, 14-, and 28-day mortality in a cohort of patients diagnosed with an acute neurological condition. (2) Methods: We conducted a prospective, longitudinal, observational study, calculating the EWS [Modified Early Warning Score (MEWS), National Early Warning Score (NEWS), VitalPAC Early Warning Score (ViEWS), Modified Rapid Emergency Medicine Score (MREMS), Early Warning Score (EWS), Hamilton Early Warning Score (HEWS), Standardised Early Warning Score (SEWS), WHO Prognostic Scored System (WPSS), and Rapid Acute Physiology Score (RAPS)] upon the arrival of patients to the emergency department. (3) Results: In all, 1160 patients were included: 808 patients were hospitalized, 199 cases (17%) required ICU care, and 6% of patients died (64 cases) within 2 days, which rose to 16% (183 cases) within 28 days. The highest area under the curve for predicting the need for ICU admissions was obtained by RAPS and MEWS. For predicting mortality, MREMS obtained the best scores for 2- and 28-day mortality. (4) Conclusions: This is the first study to explore whether several EWS accurately identify the risk of ICU admissions and mortality, at different time points, in patients with acute neurological disorders. Every score analyzed obtained good results, but it is suggested that the use of RAPS, MEWS, and MREMS should be preferred in the acute setting, for patients with neurological impairment. [ABSTRACT FROM AUTHOR]

Preclinical studies have demonstrated that brain-derived neurotrophic factor (BDNF) plays a crucial role in the homeostatic regulation of cortical excitability and excitation/inhibition balance. Using transcranial magnetic stimulation techniques, we investigated whether BDNF polymorphism could influence cortical excitability of the left and right primary motor cortex in healthy humans. Twenty-nine participants were recruited and genotyped for the presence of the BDNF Val66Met polymorphism, namely homozygous for the valine allele (Val/Val), heterozygotes (Val/Met), and homozygous for the methionine allele (Met/Met). Blinded to the latter, we evaluated inhibitory and facilitatory circuits of the left (LH) and right motor cortex (RH) by measuring resting (RMT) and active motor threshold (AMT), short-interval intracortical inhibition (SICI), and intracortical facilitation (ICF). For each neurophysiological metric, we also considered the interhemispheric balance expressed by the laterality index (LI). Val/Val participants (n = 21) exhibited an overall higher excitability of the LH compared with the RH, as probed by lower motor thresholds, lower SICI, and higher ICF. Val/Val participants displayed positive LI, especially for AMT and ICF (all P < 0.05), indicating higher LH excitability and more pronounced interhemispheric excitability imbalance as compared with Met carriers. Our preliminary results suggest that BDNF Val66Met polymorphism might influence interhemispheric balance of motor cortex excitability. NEW & NOTEWORTHY BDNF Val66Met polymorphism might influence interhemispheric balance of motor cortex excitability. Specifically, Val/Val carriers display higher excitability of the left compared with the right primary motor cortex, whereas Met carriers do not show any significant corticomotor excitability imbalance. These preliminary results are relevant to understanding aberrant interhemispheric excitability and excitation/inhibition balance in neurological disorders. [ABSTRACT FROM AUTHOR]

In Parkinson's disease, striatal dopamine depletion produces profound alterations in the neural activity of the cortico-basal ganglia motor loop, leading to dysfunctional motor output and parkinsonism. A key regulator of motor output is the balance between excitation and inhibition in the primary motor cortex, which can be assessed in humans with transcranial magnetic stimulation techniques. Despite decades of research, the functional state of cortical inhibition in Parkinson's disease remains uncertain. Towards resolving this issue, we applied paired-pulse transcranial magnetic stimulation protocols in 166 patients with Parkinson's disease (57 levodopa-naïve, 50 non-dyskinetic, 59 dyskinetic) and 40 healthy controls (age-matched with the levodopa-naïve group). All patients were studied OFF medication. All analyses were performed with fully automatic procedures to avoid confirmation bias, and we systematically considered and excluded several potential confounding factors such as age, gender, resting motor threshold, EMG background activity and amplitude of the motor evoked potential elicited by the single-pulse test stimuli. Our results show that short-interval intracortical inhibition is decreased in Parkinson's disease compared to controls. This reduction of intracortical inhibition was obtained with relatively low-intensity conditioning stimuli (80% of the resting motor threshold) and was not associated with any significant increase in short-interval intracortical facilitation or intracortical facilitation with the same low-intensity conditioning stimuli, supporting the involvement of cortical inhibitory circuits. Short-interval intracortical inhibition was similarly reduced in levodopa-naïve, non-dyskinetic and dyskinetic patients. Importantly, intracortical inhibition was reduced compared to control subjects also on the less affected side (n = 145), even in de novo drug-naïve patients in whom the less affected side was minimally symptomatic (lateralized Unified Parkinson's Disease Rating Scale part III = 0 or 1, n = 23). These results suggest that cortical disinhibition is a very early, possibly prodromal feature of Parkinson's disease. [ABSTRACT FROM AUTHOR]

Essential tremor is the most common movement disorder in adults. In patients who are not responsive to medical treatment, functional neurosurgery and, more recently, transcranial MR‐guided focused ultrasound thalamotomy are considered effective therapeutic approaches. However, the structural brain changes following a thalamotomy that mediates the clinical improvement are still unclear. In here diffusion weighted images were acquired in a cohort of 24 essential tremor patients before and 3 months after unilateral transcranial MR‐guided focused ultrasound thalamotomy targeting at the posteroventral part of the VIM. Microstructural changes along the DRTT were quantified by means of probabilistic tractography, and later related to the clinical improvement of the patients at 3‐months and at 1‐year after the intervention. In addition the changes along two neighboring tracts, that is, the corticospinal tract and the medial lemniscus, were assessed, as well as the relation between these changes and the presence of side effects. Thalamic lesions produced local and distant alterations along the trajectory of the DRTT, and each correlated with clinical improvement. Regarding side effects, gait imbalance after thalamotomy was associated with greater impact on the DRTT, whereas the presence of paresthesias was significantly related to a higher overlap between the lesion and the medial lemniscus. This work represents the largest series describing the microstructural changes following transcranial MR‐guided focused ultrasound thalamotomy in essential tremor. These results suggest that clinical benefits are specific for the impact on the cerebello‐thalamo‐cortical pathway, thus reaffirming the potential of tractography to aid thalamotomy targeting. [ABSTRACT FROM AUTHOR]

Background: Multiple sclerosis (MS) is an autoimmune disorder of the CNS in which inflammation, demyelination, and axonal damage of the central nervous system coexist. Fatigue is one of the most disabling symptoms in MS and little is known about the neurophysiological mechanisms involved. Methods: To give more mechanistic insight of fatigue in MS, we studied a cohort of 17 MS patients and a group of 16 age-matched healthy controls. Baseline Fatigue Severity Scales and Fatigue Rating were obtained from both groups to check the level of fatigue and to perform statistical correlations with fatigue-induced neurophysiologic changes. To induce fatigue we used a handgrip task. During the fatiguing task, we evaluated fatigue state (using a dynamometer) and after the task we evaluated the Borg Rating of Perceived Exertion Scale. Transcranial magnetic stimulation and peripheral electric stimulation were used to assess corticospinal tract and peripheral system functions before and after the task. Results: Clinically significant fatigue and central motor conduction time were greater in patients than in controls, while motor cortex excitability was decreased and maximal handgrip strength reduced in patients. Interestingly, fatigue state was positively correlated to perceived fatigue in controls but not in patients. Furthermore, in the presence of similar fatigue state over time, controls showed a significant fatigue-related reduction in motor evoked potential (a putative marker of central fatigue) whereas this effect was not seen in patients. Conclusions: in MS patients the pathogenesis of fatigue seems not driven by the mechanisms directly related to corticospinal function (that characterize fatigue in controls) but seems probably due to other "central abnormalities" upstream to primary motor cortex. [ABSTRACT FROM AUTHOR]

Spinal plasticity is thought to contribute to sensorimotor recovery of limb function in several neurological disorders and can be experimentally induced in animals and humans using different stimulation protocols. In healthy individuals, electrical continuous Theta Burst Stimulation (TBS) of the median nerve has been shown to change spinal motoneuron excitability in the cervical spinal cord as indexed by a change in mean H-reflex amplitude in the flexor carpi radialis muscle. It is unknown whether continuous TBS of a peripheral nerve can also shift motoneuron excitability in the lower limb. In 26 healthy subjects, we examined the effects of electrical TBS given to the tibial nerve in the popliteal fossa on the excitability of lumbar spinal motoneurons as measured by H-reflex amplitude of the soleus muscle evoked by tibial nerve stimulation. Continuous TBS was given at 110% of H-reflex threshold intensity and compared to non-patterned regular electrical stimulation at 15 Hz. To disclose any pain-induced effects, we also tested the effects of TBS at individual sensory threshold. Moreover, in a subgroup of subjects we evaluated paired-pulse inhibition of H-reflex. Continuous TBS at 110% of H-reflex threshold intensity induced a short-term reduction of H-reflex amplitude. The other stimulation conditions produced no after effects. Paired-pulse H-reflex inhibition was not modulated by continuous TBS or non-patterned repetitive stimulation at 15 Hz. An effect of pain on the results obtained was discarded, since non-patterned 15 Hz stimulation at 110% HT led to pain scores similar to those induced by EcTBS at 110% HT, but was not able to induce any modulation of the H reflex amplitude. Together, the results provide first time evidence that peripheral continuous TBS induces a short-lasting change in the excitability of spinal motoneurons in lower limb circuitries. Future studies need to investigate how the TBS protocol can be optimized to produce a larger and longer effect on spinal cord physiology and whether this might be a useful intervention in patients with excessive excitability of the spinal motorneurons. [ABSTRACT FROM AUTHOR]

Transcranial magnetic stimulation (TMS) gives rise to muscle responses, known as motor evoked potentials (MEP), through activation of the motor pathways. Voluntary contraction causes facilitation of MEPs, which consists of shortening MEP latency, increasing MEP amplitude and widening MEP duration. While an increase in excitability of alpha motorneurons and the corticospinal tract can easily explain latency shortening and amplitude increase, other mechanisms have to be accounted for to explain the increase in duration.We measured the increase in duration of the MEP during contraction with respect to rest in a group of healthy volunteers and retrospectively assessed this parameter in patients who were examined in a standardized fashion during the past 5 years. We included 25 healthy subjects, 21 patients with multiple sclerosis, 33 patients with acute stroke, 5 patients with hereditary spastic paraparesis, and 5 patients with signs suggesting psychogenic paresis. We found already significant differences among groups in the MEP duration at rest, patients with MS had a significantly longer duration, and patients with stroke had significantly shorter duration, than the other two groups. The increase in MEP duration during voluntary contraction was different in patients and in healthy subjects. It was significantly shorter in MS and significantly longer in stroke patients. It was absent in the five patients with suspected psychogenic weakness. In patients with HSP, an abnormally increase in duration occurred only in leg muscles. Our results suggest that the increase in duration of the MEP during contraction may reveal the contribution of propriospinal interneurons to the activation of alpha motorneurons. This mechanism may be altered in some diseases and, therefore, the assessment proposed in this work may have clinical applicability for the differential diagnosis of weakness. [ABSTRACT FROM AUTHOR]

The article presents a reprint of the article "Transcranial direct current stimulation effects on I-wave activity in humans" by M.A. Nitsche and colleagues that was published in the March 23, 2011 issue of the periodical. The authors investigated the physiological mechanisms and effects of anodal transcranial direct current stimulation (tDCS) of the human cerebral cortex. They concluded that anodal tDCS develops its facilitatory effects on motor evoked potential amplitudes.

We describe a patient with a familial form of amyotrophic lateral sclerosis (ALS) in which a heterozygous G > A exchange at position 1087 in the SOD1 gene was detected. This mutation results in an amino acid substitution of aspartate for glycine at position 93 (G93D). The patient had a five-year history of fasciculations in all four limbs, with no clear evidence of muscular atrophy or weakness at last follow-up. However, electrophysiological examination revealed lower and upper motor neuron involvement. His mother and a cousin had died of ALS after prolonged disease. This report shows that G93D may cause a form of ALS with slow progression, long-lasting paucisymptomatic phase and both lower and upper motor neuron involvement. [ABSTRACT FROM AUTHOR]

Abstract: Repetitive transcranial magnetic stimulation (rTMS) of brain can modulate cortical neurotransmission, a novel paradigm of repetitive stimulation termed continuous theta-burst stimulation (cTBS) produces a pronounced and prolonged suppression of motor cortex excitability. The aim of this preliminary study was to investigate whether cTBS of motor cortex could have any beneficial effect in patients with amyotrophic lateral sclerosis (ALS). We performed a double-blind, placebo-controlled trial. Twenty patients with definite ALS were randomly allocated to blinded active or placebo stimulation. Repetitive stimulation of the motor cortex was performed for five consecutive days every month for six consecutive months. The primary outcome was the rate of decline as evaluated with the ALS functional rating scale. The treatment was well tolerated by the patients. Fifteen patients (seven active and eight sham) completed the study and were included in the 6-months analysis. Both active and sham patients deteriorated during treatment, however, active patients showed a modest but significant slowing of the deterioration rate. Though we cannot be sure whether the effects observed can be attributed to cTBS, because of the restricted number of patients studied, further investigation on a larger group of ALS patients is warranted. The results of the pilot study might open up a new therapeutic perspective in ALS based on neuromodulation. [Copyright &y& Elsevier]

Inhibition is of fundamental importance to regulate activity in cortical circuits. Inhibition is mediated through a diversity of different interneurones and γ-aminobutyric acid A receptor (GABAAR) subtypes. Here we employed paired-pulse transcranial magnetic stimulation (TMS) to measure short interval intracortical inhibition (SICI), a GABAAR-mediated inhibition in human motor cortex, to address the question of which GABAAR subtype is responsible for this form of inhibition. It has been shown that classical benzodiazepines (diazepam and lorazepam) have a non-selective affinity profile at different α-subunit-bearing subtypes of the GABAAR while zolpidem has a 10-fold greater affinity to the α1-subunit-bearing GABAAR compared with those bearing the α2- or α3-subunit. We found that, in seven healthy subjects, a single oral dose of 20 mg of diazepam or 2.5 mg of lorazepam significantly increased SICI, whereas 10 mg of zolpidem did not change SICI. This dissociation occurred despite equal sedation by all three drugs, an α1-subunit GABAAR-mediated effect. The findings strongly suggest that SICI is not mediated by the α1-subunit-bearing subtype of the GABAAR but by those bearing either the α2- or α3-subunit. This study represents an attempt by means of TMS to identify GABAAR subtype-specific action at the systems level of human cortex, a highly relevant issue because the different α-subunit-bearing subtypes of the GABAAR are differently involved in benzodiazepine-mediated effects such as sedation, amnesia or anxiolysis, in developmental cortical plasticity, and in neurological disorders such as epilepsy. [ABSTRACT FROM AUTHOR]