Dissociation of cerebrospinal fluid amyloid-β and tau levels in patients with prolonged posttraumatic disorders of consciousness.

Background: Traumatic brain injury (TBI) is a major risk factor for Alzheimer's disease (AD). Although the mechanisms that lead to AD after a TBI are unclear, we hypothesize that changes in amyloid-β (Aβ) metabolism and abnormal tau phosphorylation are reasonable candidates.

Objective: To investigate Aβ and tau dynamics in the chronic phase of TBI.

Risk Factors Associated With Peripheral Neuropathy in Heart Failure Patients Candidates for Transplantation.

Introduction: Peripheral neuropathy can affect patients with heart failure, though its prevalence is unknown. After heart transplantation, it can influence the postoperative course and quality of life, but screening for neuromuscular disease is not routinely performed.

Objective: The aim of this study was to identify the factors associated with neuropathy in a population of patients with heart failure who are candidates for heart transplantation.

Pain assessment with the revised nociception coma scale and outcomes of patients with unresponsive wakefulness syndrome: results from a pilot study.

The aim of this study was to evaluate whether standardized responses to nociceptive pain, assessed with the revised Nociception Coma Scale (NCS-R), were correlated with the outcomes of patients with unresponsive wakefulness syndrome (UWS) 6 months after admission to a rehabilitation department. We recruited 24 consecutive patients with UWS. Patients' consciousness levels were assessed with the revised Coma Recovery Scale (CRS-R) at admission and 6 months later, and their CRS-R scores were correlated with the NCS-R scores at admission.

Prolonged Cerebrospinal Fluid Neurofilament Light Chain Increase in Patients with Post-Traumatic Disorders of Consciousness.

The mechanisms involved in secondary brain injury after the acute phase of severe traumatic brain injury (TBI) are largely unknown. Ongoing axonal degeneration, consequent to the initial trauma, may lead to secondary brain injury. To test this hypothesis, we evaluated the cerebrospinal fluid (CSF) level of neurofilament light chain (NF-L), a proposed marker of axonal degeneration, in 10 patients who developed a severe disorder of consciousness after a TBI, including 7 in a minimally conscious state and 3 with unresponsive wakefulness syndrome (time since brain injury, 309 ± 169 days).

Longitudinal Assessment of Clinical Signs of Recovery in Patients with Unresponsive Wakefulness Syndrome after Traumatic or Nontraumatic Brain Injury.

Although clinical examination is the gold standard for differential diagnosis between unresponsive wakefulness syndrome (UWS) and minimally conscious state (MCS), clinical signs denoting the first occurrence of conscious behavior in patients with UWS have not been clarified. In this prospective single-center cohort study, 31 consecutive patients with UWS after traumatic brain injury (TBI) (17 patients) or non-TBI were assessed with the Coma Recovery Scale Revised (CRS-R) at admission to a rehabilitation department and after 1, 2, 3, 6, and 12 months. Of the 21 patients who recovered consciousness during the study, 90.

EEG epileptiform abnormalities at admission to a rehabilitation department predict the risk of seizures in disorders of consciousness following a coma.

Background: Seizures affect about a quarter of patients with disorders of consciousness (DOC) after a coma.

Aims: We investigated whether the presence of epileptiform abnormalities (EAs) in the electroencephalogram (EEG) of patients with DOC may predict the occurrence of seizures. Moreover, we evaluated whether EAs have a prognostic role in these patients.

Occurrence of neuropathies in patients with severe heart failure before and after heart transplantation.

Neuropathies may affect heart reinnervation and functional outcome after heart transplantation (HT). In this study, neurological evaluations, standard nerve conduction studies, and electromyography were performed in 32 HT candidates without a previous history of neuromuscular disorder. Ten patients underwent HT and were revaluated 3 months later.

Long-lasting coma.

In this report, we describe the case of a patient who has remained in a comatose state for more than one year after a traumatic and hypoxic brain injury. This state, which we refer to as long-lasting coma (LLC), may be a disorder of consciousness with significantly different features from those of conventional coma, the vegetative state, or brain death. On the basis of clinical, neurophysiological and neuroimaging data, we hypothesize that a multilevel involvement of the ascending reticular activating system is required in LLC.

EEG predictors of outcome in patients with disorders of consciousness admitted for intensive rehabilitation.

Objective: This study examined the prognostic value of standard EEG in patients with unresponsive wakefulness syndrome (UWS) or in a minimally conscious state (MCS).

Methods: EEGs recorded at admission in 106 patients with UWS or in a MCS were analyzed retrospectively. EEG amplitude, dominant frequency, and reactivity to stimuli were correlated to patient outcomes according to the Coma Recovery Scale Revised (CRS-R).

Increased transcranial direct current stimulation after effects during concurrent peripheral electrical nerve stimulation.

In this study we tested the hypothesis whether a lasting change in the excitability of cortical output circuits can be obtained in healthy humans by combining a peripheral nerve stimulation during a concomitant depolarization and/or hyperpolarization of motor cortex. To reach this aim we combined two different neurophysiological techniques each of them able to induce a lasting increase of cortical excitability by them self: namely median nerve repetitive electrical stimulation (rEPNS) and transcranial direct current stimulation (tDCS). Ten normal young volunteers were enrolled in the present study.

Emerging from an unresponsive wakefulness syndrome: brain plasticity has to cross a threshold level.

Unresponsive wakefulness syndrome (UWS, previously known as vegetative state) occurs after patients survive a severe brain injury. Patients suffering from UWS have lost awareness of themselves and of the external environment and do not retain any trace of their subjective experience. Current data demonstrate that neuronal functions subtending consciousness are not completely reset in UWS; however, they are reduced below the threshold required to experience consciousness.

A range of antiepileptic drugs do not affect the recovery of consciousness in vegetative and minimally conscious states.

Since most antiepileptic drugs (AEDs) have cognitive effects, the aim of this study was to evaluate the influence of AED therapy on the recovery of consciousness in 103 consecutive patients in a vegetative or minimally conscious state (VS, MCS). The levels of cognitive functioning (LCF) score was retrospectively compared after a three-month period of rehabilitation between patients who were medicated (n=54) and patients who were not medicated (n=49) with AEDs. Mean LCF scores in AED-medicated and nonmedicated patients were 2.

Brain-derived neurotrophic factor (Val66Met) polymorphism does not influence recovery from a post-traumatic vegetative state: a blinded retrospective multi-centric study.

Brain-derived neurotrophic factor (BDNF) is a neurotrophin that influences neuronal plasticity throughout life. Emergence from a vegetative state (VS) after a traumatic brain injury (TBI) implies that the brain undergoes plastic changes. A common polymorphism in the BDNF gene--BDNF Val66Met (referred to herein as BDNF(Met))--impairs cognitive function in healthy subjects.

Patients in a vegetative state following traumatic brain injury display a reduced intracortical modulation.

Objective: Patients in coma who fail to wake develop a condition known as a vegetative state (VS). While we know that some cortical activities exist in patients in VS, it remains unclear whether interneuronal modulation can be abnormal in the cerebral cortex of these patients. The aim of the study was to evaluate the inhibitory and excitatory interneuronal circuits in patients in VS following a traumatic brain injury.

Impairment of sensory-motor plasticity in mild Alzheimer's disease.

Background: Primary motor cortex (M1) is relatively spared in the early stages of Alzheimer's disease (AD).

Objective: Aim of the present study was to investigate whether abnormal M1 synaptic plasticity is present at an early stage of AD. We employed an electrophysiological protocol, named rapid paired associative stimulation (rPAS), involving repetitive transcranial magnetic stimulation (rTMS) paired with electrical stimulation of the contralateral median nerve, that modifies corticospinal excitability and short latency afferent inhibition (SAI).

Neuromuscular involvement in vegetative and minimally conscious states following acute brain injury.

The aim of this study was to evaluate the presence of neuromuscular involvement in patients in vegetative and minimally conscious states (VS, MCS) following acute brain injury. Twenty-two patients (11 in VS, 11 in MCS) admitted to a rehabilitation department underwent nerve conduction, electromyography (EMG) for spontaneous activity and direct muscle stimulation (DMS). Twenty (90.

Usefulness of standard EEG in predicting the outcome of patients with disorders of consciousness after anoxic coma.

Although standard EEG is performed routinely in patients with disorders of consciousness after coma, its prognostic value is still debated. The aim of the present study was to evaluate the role of standard EEG in predicting the recovery of cognitive functioning in patients affected by severe disturbances of consciousness after coma caused by cerebral anoxia. A standard EEG was recorded at admission to our Rehabilitation Department in 15 patients experiencing impaired consciousness because of cerebral anoxia.

Motor cortex abnormalities in amyotrophic lateral sclerosis with transcranial direct-current stimulation.

The aim of this study was to identify a neurophysiological marker of upper motoneuron involvement in patients with sporadic amyotrophic lateral sclerosis (ALS). For this purpose we evaluated the after-effects of transcranial direct-current stimulation (tDCS) on excitability of the motor cortex of eight ALS patients and eight healthy controls. Healthy controls showed a transient polarity-specific change in corticospinal excitability of about +/-45%, with anodal tDCS inducing facilitation and cathodal tDCS leading to inhibition, whereas no change could be induced in ALS patients after either type of tDCS.

Rapid-rate paired associative stimulation of the median nerve and motor cortex can produce long-lasting changes in motor cortical excitability in humans.

Repetitive transcranial magnetic stimulation (rTMS) or repetitive electrical peripheral nerve stimulation (rENS) can induce changes in the excitability of the human motor cortex (M1) that is often short-lasting and variable, and occurs only after prolonged periods of stimulation. In 10 healthy volunteers, we used a new repetitive paired associative stimulation (rPAS) protocol to facilitate and prolong the effects of rENS and rTMS on cortical excitability. Sub-motor threshold 5 Hz rENS of the right median nerve was synchronized with submotor threshold 5 Hz rTMS of the left M1 at a constant interval for 2 min.

Enhanced long-term potentiation-like plasticity of the trigeminal blink reflex circuit in blepharospasm.

Benign essential blepharospasm (BEB) is a focal cranial dystonia affecting eye closure. Here, we tested the hypothesis that BEB is associated with abnormal plasticity of the neuronal circuits mediating reflex blinks. In patients with BEB and healthy age-matched controls, we used the conditioning protocol introduced by Mao and Evinger (2001) to induce long-term potentiation (LTP)-like plasticity in trigeminal wide dynamic range neurons of the blink reflex circuit.

Corticospinal excitability during motor imagery of a simple tonic finger movement in patients with writer's cramp.

Motor imagery (MI) is the mental rehearsal of a motor act without overt movement. Using transcranial magnetic stimulation (TMS), we tested the effect of MI on corticospinal excitability in patients with writer's cramp. In 10 patients with writer's cramp and 10 healthy controls, we applied focal TMS over each primary motor area and recorded motor evoked potentials (MEPs) from contralateral hand and arm muscles while participants imagined a tonic abduction of the index finger contralateral to the stimulated hemisphere.

Homeostatic-like plasticity of the primary motor hand area is impaired in focal hand dystonia.

The excitability of inhibitory circuits in patients with writer's cramp is reduced at multiple levels within the sensorimotor system, including the primary motor hand area (M1). Although this may play a major role in the pathophysiology of writer's cramp, it is still unclear what factors may cause the imbalance between inhibition and excitation to arise. One possibility is that homeostatic mechanisms that keep cortical excitability within a normal physiological range are impaired.

Long lasting effects of transcranial direct current stimulation on motor imagery.

Transcranial magnetic stimulation (TMS) was employed to probe the modulatory effects of transcranial direct current stimulation of motor cortex on motor evoked responses (MEPs) produced during motor imagery. MEP amplitudes at rest and during motor imagery were assessed before and for a period of 60 min after transcranial direct current stimulation (tDCS) applied over the primary motor cortex at 1 mA for 5 min. Cathodal stimulation induced a decrease of about 30% of MEP amplitude at rest and a 50% reduction of MEP size during imagery.

Usefulness of behavioral and electrophysiological studies in transgenic models of Alzheimer's disease.

Over the past several years researchers have engineered many transgenic models of Alzheimer's disease. Since loss of memory is one of the major hallmarks of the disorder, the phenotypic characterization of these animals has included both behavioral tests which aim to evaluate learning abilities, and electrophysiological studies to analyze synaptic transmission and long-term potentiation, a widely studied cellular model of learning and memory. These studies are fundamental for the design of novel therapies for the treatment and/or prevention of Alzheimer's disease.