This finding indicates that the relationship between dACC glutama

This finding indicates that the relationship between dACC glutamate concentrations and impulsive decision making can, at least partly, be attributed to connectivity of the left dACC with the midbrain. Preclinical literature has indicated a role for glutamate in impulsivity (for a review see Pattij and Vanderschuren 2008). For instance, selective and nonselective NMDA receptor antagonists have been shown to increase impulsive behavior in animal models (Higgins et al. 2003; Mirjana et al. 2004). Systemic pretreatment with an mGlu2/3 receptor agonist attenuates impulsive

behavior seen after serotonin receptor stimulation Inhibitors,research,lifescience,medical (Wischhof et al. 2011). In humans, a recent study of Hoerst et al. (2010) examined glutamate levels in the dACC in patients with borderline personality disorder and healthy controls. Irrespective of diagnosis, higher Glu/Cr was associated with higher self-reported (trait) impulsivity (Hoerst et al. 2010). Anterior cingulate Glu/Cr was also found Inhibitors,research,lifescience,medical to be increased in untreated children with ADHD, a disorder characterized by impaired impulse control (Hammerness et al. 2012). In keeping with these findings, Inhibitors,research,lifescience,medical the current study revealed that glutamate concentrations

in the dACC were associated with impulsive decision making. Interestingly, the current study revealed associations between dACC glutamate concentrations and resting state connectivity of the dACC with other brain regions (the midbrain and the left and right PCC). This is consistent with a previously described correlation between ¹H MRS glutamate concentrations and resting Inhibitors,research,lifescience,medical state functional connectivity (Horn et al. 2010), suggesting that the amount of glutamate, which is present in neuronal and glial metabolic and neurotransmitter pools as measured by ¹H MRS, underlies the observed synchronization Inhibitors,research,lifescience,medical among these brain regions as assessed with resting state functional connectivity measures. This is not very surprising, as it is thought that the intrinsic energy product info demands of neuron populations in different brain regions with a common functional purpose have wired together

through synaptic Cilengitide plasticity, and thereby form so-called resting state networks (e.g., Lewis et al. 2009). It is well known that glutamate plays a critical role in synaptic plasticity. Unfortunately, ¹H MRS does not allow distinguishing the specific contribution of different components of the glutamatergic system to spontaneous coherence of BOLD sellectchem signal fluctuations between brain regions. ¹H MRS glutamate measurements reflect primarily intracellular glutamate and does not directly measure synaptic glutamate transmission (Gruetter et al. 1998). Furthermore, quantification and separation of glutamate by use of ¹H MRS is technically difficult because glutamate overlaps in its chemical shift range with glutamine and γ-amino butyric acid (GABA).

Without tight regulatory mechanisms, this could dramatically alte

Without tight regulatory mechanisms, this could dramatically alter the neuronal membrane potential, leading to neuronal hyperexcitability and seriously compromising CNS

function.32 Such a scenario is prevented by the buffering of extracellular K+ by glial cells33,34 (Figure 2, orange box). Indeed, sellckchem astrocytes have a strongly negative resting potential and express a number of potassium channels, resulting Inhibitors,research,lifescience,medical in a high membrane permeability to K+.35 These features, in conjunction with the action of the Na+/K+ ATPase, enable astrocytes to accumulate the excess extracellular K+ 36, which can then travel in the astrocytic syncitium through gap junctions down its concentration gradient.34,35 Inhibitors,research,lifescience,medical This allows for the spatial dispersion of K+ from areas of high concentration to areas of lower concentration where it can be Dasatinib Sigma extruded either into the extracellular space or the circulation, thus

maintaining the overall extracellular K+ concentration within the physiological range. In addition to spatial buffering, other mechanisms such as the transient storage of K+ ions appear to contribute to the potassium-buffering capacity of astrocytes.32 Supply of energy substrates Although the brain represents only 2% of the body weight, it is responsible for the consumption of an estimated 25% of all glucose in the body.37 This disproportionate energy need Inhibitors,research,lifescience,medical compared with other organs can be largely explained by the energetic cost of maintaining the steep ion gradients necessary for the transmission of action potentials.38 For this reason, neurons in particular have very high energy requirements, and are therefore highly dependent upon Inhibitors,research,lifescience,medical a tight regulation of energy substrate supply in order to sustain their normal function and cellular integrity. As mentioned previously, the morphological features of astrocytes ideally position them to sense neuronal activity at the synapse and respond with the appropriate metabolic supply via their astrocytic endfeet which almost entirely enwrap the intracerebral blood Inhibitors,research,lifescience,medical vessels (Figure 3). In line with this, an

increasing body of evidence suggests that astrocytes play a key role in the spatiotemporal coupling between neuronal activity and cerebral blood flow (known as functional hyperemia) in a process that involves transient neurotransmitterinduced increases of [Ca2+]i in astrocytes, the subsequent propagation GSK-3 of Ca2+ waves through the astrocytic syncitium and the release of vasoactive substances (such as arachidonic acid metabolites or ATP) by astrocytic endfeet.13 Importantly, the role of astrocytes in functional hyperemia does not preclude a concerted contribution of neurons via the release of vasoactive substances such as neurotransmitters, nitric oxide, H+, and K+ to name a few.39 Figure 3. Astrocytic endfeet in humans.

Taken together, diagnostic accuracy was better for P-tau181 (78%)

Taken together, diagnostic accuracy was better for P-tau181 (78%) than for T-tau (71%). In summary, P-tau181 may be a valuable biomarker, especially In the differential diagnosis between AD, LBD, and VD. CSF tau Wortmannin DNA-PK protein phosphorylated at serine 199 (P-tau199) In one study applying P-tau199, this meantime biomarker was shown to be superior to T-tau protein in separating AD from a patient group of non AD subjects.23 In a large multlcenter sample of 570 subjects,102 P-tau199 protein levels were elevated In the AD group, Independently of age, gender, cognitive status, and APOE e4 carrier status. In the AD

group versus the combined Inhibitors,research,lifescience,medical groups of demented and non- demented subjects In this study, ROC analysis showed a Inhibitors,research,lifescience,medical 85% sensitivity and 85% specificity for P-tau199.102 CSF tau protein phosphorylated at serine 396 and serine 404 (P-tau396/404) An ultrasensitive bienzyme-substrate-recycle ELISA for Ser 396 and Ser 404 has been developed, which Is slgnifIcantly more sensitive than conventional ELISA In determining the hyperphosphorylated tau protein and Inhibitors,research,lifescience,medical T-tau.96 In CSF of 52 AD patients, 56 normal controls, 46 VD patients, and 37 nonAD neurological patients, significantly elevated levels of P-tau396/404 were only found In AD. Using the ratio of hyperphosphorylated tau protein to T-tau of ≥0.33 as a cutoff for AD diagnosis, the

clinical diagnosis could be confirmed In 96% of the clinically Inhibitors,research,lifescience,medical diagnosed patients. The results of this study suggest that P-tau396/404 Is a promising marker, especially in the differential diagnosis between AD and VD. Measurement of P-tau epitopes

in the differential diagnosis of AD: a comparative CSF study A recent study directly compared the diagnostic performance of P-tau231, P-tau181, and P-tau199 In the same patient cohort, including a large series of patients with AD, LBD, FTD, VD, and other neurological disorders. Inhibitors,research,lifescience,medical The P-tau231 and P-tau181 assays performed nearly equally well In the discrimination of AD from nondemented controls, whereas the P-tau199 assay showed a weaker discriminatlon.103 Interestingly, the separation between AD and FTD was maximized using P-tau231. The separation between AD and DLB was maximized using P-tau181.103 Thus, differences In the phosphorylation Brefeldin_A of specific tau epitopes between dementia disorders may be reflected In the CSF level of the corresponding P-tau variant. Predictive value of CSF P-tau in MCI for AD In a longitudinal study, 77 MCI patients showed elevated levels for P-tau231 In comparison to HCs at baseline.104 High CSF P-tau231, but not T-tau levels at baseline, significantly correlated with subsequent cognitive decline. This study suggests that high P-tau231 may be a predictor for progressive cognitive decline In subjects with MCI.104 One study focused on P-tau231-235 In MCI subjects who converted to AD compared to individuals with subjective memory complaints without cognitive impairment.

Conflict of Interest None declared
Traditionally, both ast

Conflict of Interest None declared.
Traditionally, both astrocytes and microglia have been thought to act as supportive cells in the central nervous system (CNS). It is now widely appreciated that astrocytes and microglia are not only involved in virtually every aspects

of neural Belinostat HDAC function in the mature brain (Fields and molarity calculator Stevens-Graham 2002) but also play important roles during CNS development. For example, both astrocytes and microglia are involved in neuronal differentiation, migration, programmed cell death, neurite growth, axon guidance, as well as synaptic formation (Deverman and Patterson 2009). On the other hand, oligodendroglia or oligodendrocyte (OL) appears to resemble more closely to neuron rather Inhibitors,research,lifescience,medical than to astrocyte or microglia, in terms of developmental programs and susceptibility to injury. For instance, OL progenitor cells (OPCs) and neurons arise from similar regions of the neuroepithelium, and their fate determination is driven by similar transcription factors (Bradl and Lassmann 2010). Both OPCs and neurons are born in Inhibitors,research,lifescience,medical excess, but their numbers are reduced dramatically through programmed cell death (Barres et al.1992; Buss et al. 2006). As for cell survival, certain neurotrophic factors are critically involved Inhibitors,research,lifescience,medical for both types of cells, while most of those factors are known to be secreted by astrocytes and microglia (Althaus et al. 2008). In addition

to these similarities in developmental features, both neuron and Inhibitors,research,lifescience,medical OLs are susceptible to certain insults including glutamate excitotoxicity, inflammatory cytokines, and reactive oxidative stress (Leviton and Gressens 2007; Volpe et al. 2008; Volpe 2009). At present, OL lineage development is well characterized, especially in rodents (Miller 2002; Emery 2010a). Initially, OPCs proliferate in regions where they are generated from multipotent neural progenitor cells, and then migrate to their destination. To ensure that the number of OPCs matches with their corresponding axons, excessive Inhibitors,research,lifescience,medical OPCs are eliminated through apoptosis, and the survived cells then undergo terminal differentiation and start

to myelinate axons. One of the important features of OL development is that it is largely controlled by extracellular cytokines, most of which GSK-3 are known to be secreted by astrocytes and microglia. Although extensive studies have been conducted to understand the role of individual cytokine on OL development, it is most likely that OLs are exposed to multiple cytokines/growth factors in vivo, thus their biological responses depend on the types of the final signaling pathways activated. However, this is very difficult to assess in vivo. The conditioned medium from astrocytes or microglia offers some aspects of the in vivo environment and may provide information to better elucidate the roles of astrocytes and microglia during OL development.

Moreover, studies have shown that not only streptococci but also

Moreover, studies have shown that not only streptococci but also other infectious agents such as Borellia Burgdorferi or Mycoplasma Pneumoniae are associated with tics, ie, the association of tics and infectious agents is not restricted

to streptococci. A broader concept of this association, however, would more fulfill the needs for an infectious concept of TS. Conventional pharmacotherapeutic concepts of TS There is no doubt that dopaminergic neurotransmission is involved in the pathophysiology of TS. Dopamine (D2) receptor Inhibitors,research,lifescience,medical blocking agents such as haloperidol or pimozide have been shown to be effective in TS in several studies.79 Haloperidol showed an efficacy between 78% and 91% in 41 free overnight delivery reports over a 14-year period.4 Many patients, however, discontinue haloperidol due to extrapyramidal side effects, while pimozide showed a superior profile regarding side effects. Pimozide was effective in several doubleblind, placebo-controlled studies.80 There are also reports of effective treatment with Inhibitors,research,lifescience,medical drugs such as fluphenazine, penfluridol, trifluoperazine, and flupenthixol.81 In the meantime, atypical antipsychotics such as risperidone, which is not only a D2 receptor antagonist, but also a serotonin (5-HT)2 antagonist, has been shown to be effective in TS.82,83 Clozapine

was observed to be effective against tics,84 although there have also been negative results reported.81 A partial Inhibitors,research,lifescience,medical control of tics during therapy with olanzapine at a dose of 5 to 10 mg/day was reported, as well as a reduction in tics in a controlled study (n=4).85 Ziprasidone, at a dose of 5 to 40 mg/day, was shown to be significantly more effective than placebo in 28 patients (7 to 17 years old) in a double-blind, randomized study, and was well tolerated.86 It should be noted, however, that Inhibitors,research,lifescience,medical the sudden death of a TS patient under therapy with ziprasidone during a clinical trial was reported.87 Aripiprazole, a new atypical antipsychotic that acts as a dopaminergic modulator showing mixed

dopamine antagonistic Inhibitors,research,lifescience,medical and agonistic effects, may take a special position in the therapy of TS. Effective treatment of TS using aripiprazole was reported repeatedly, in contrast to those treated with other antipsychotics, a Batimastat number of patients showed complete recovery from tics without significant adverse effects.88-90 The drug of first choice, for therapy of tics, particularly for children in many European countries, is tiapride, a benzamide derivate, which selectively blocks dopamine in the basal ganglia. Although only double-blind, placebo-controlled studies show beneficial effects on movement disorders and tics,91,92 tiapride is widely used in countries such as Germany, France, and others. It is one of the few drugs which is prescribed not only in adults, but also in children. In contrast to several antipsychotics, however, no adverse effects on cognitive performance in children have been observed.

95 Finasteride reduces the formation of both 3α,5α-THP and 3α,5α-

95 Finasteride reduces the formation of both 3α,5α-THP and 3α,5α-THDOC by inhibiting the reduction of progesterone and DOC to intermediate precursors. Indeed, finasteride pretreatment blocked subjective effects of alcohol using three different scales to measure the activating, sedating, anesthetic, and peripheral dynamic aspects of alcohol actions. The Inhibitors,research,lifescience,medical ability of finasteride to reduce the subjective effects of alcohol was not observed in neverless individuals carrying the GABAA

α2 subunit polymorphism associated with alcoholism, suggesting that individuals carrying this polymorphism have reduced sensitivity to both alcohol and finasteride.95 Other studies show that 3α,5α-THP levels are decreased during the peak of alcohol withdrawal and return to normal levels upon recovery.96,97 Likewise, abstinent alcoholics exhibit diminished progesterone levels as well as a lowered ratio of progesterone to pregnenolone.98 In contrast, Inhibitors,research,lifescience,medical laboratory administration of low

or moderate doses of ethanol appears to have no effect on plasma 3α,5α-THP levels26 or to decrease 3α,5α-THP levels.27,99 The basis of these conflicting results is unknown, but may involve pharmacologically different ethanol doses, different analytic methods to measure neurosteroids, Inhibitors,research,lifescience,medical or environmental factors that influence neurosteroid synthesis in humans. Alternatively, different neuroactive steroids may be elevated in humans vs rodents, Inhibitors,research,lifescience,medical or the effects of ethanol on neuroactive steroid levels in humans may be restricted to brain. Table I summarizes

the different effects of ethanol on neuroactive steroid levels in rodents, monkeys, and humans. Humans, but not rodents, synthesize multiple 5β-reduced neuroactive steroids including 3α,5β-THP and 3α,5β-THDOC. 3α,5β-THP levels are comparable to those of 3α,5α-THP in human Inhibitors,research,lifescience,medical plasma and cerebrospinal fluid.15,16 These neuroactive steroids also modulate GABAergic transmission,8,13,14 but have not been measured in humans after ethanol administration. Dacomitinib Additionally, the primary stress steroids in humans are Cortisol and 11-deoxy Cortisol, while progesterone and corticosterone are the primary stress steroids in rodents. 3α,5β-reduced Cortisol is a negative modulator of GABAA receptors,17 and could contribute to the subjective effects of ethanol in humans. Thus, the combined effects of 3α,5α- and 3α,5β-reduced neuroactive steroids may contribute to the effects of ethanol in humans and nonhuman primates. These steroids have never been measured following ethanol, stress, or HPA axis activation in humans or nonhuman primates. Comprehensive studies of neuroactive steroid levels in humans are needed. While 3α,5α-THP and 3α,5α-THDOC are the primary neuroactive steroids in rodents, other neuroactive steroids may be more relevant in humans.

Specific objectives – Describe the average profile of healthcare

Specific objectives – Describe the average profile of healthcare resource consumption of a retrospective cohort (patients who died from malignant neoplasm) in the last 30 days of life by diagnosis and age group. – Quantify and compare the costs of the use of healthcare resources in the cohorts of patients with and without SAIATU intervention. – Compare quality of life in Inhibitors,research,lifescience,medical the cohorts of patients with and without SAIATU intervention. Methods/design Hypothesis

The intervention of SAIATU (a resource for the social support of end-of-life patients) improves efficiency in the use of healthcare resources in end-of-life patients, decreasing the consumption of hospital resources and increasing the home-based activities conducted by Primary Care in the last 30 days of life. Location and date of study The study will be conducted in the provinces of Guipúzcoa. Period of study: Inhibitors,research,lifescience,medical September 2012 – October 2013. Study design The study was designed in two phases. Phase 1: RETROSPECTIVE study to register a control cohort of patients who died from malignant neoplasm The objective of this study is to determine the baseline risk of the principal variable, consumption of resources in the population of patients Inhibitors,research,lifescience,medical who die from malignant neoplasm. Thus, the study characterises, by primary diagnosis (criteria

and rules established by the International Statistical Classification of Diseases 10 [ICD-10] [26]) and age, the behaviour of different malignant Inhibitors,research,lifescience,medical neoplasms, with regard to resource consumption: number of visits to or consultations with Primary Care, number of external consultations, number of visits to hospital emergency departments, number of hospital admissions, average length of stay, and days in home hospitalisation. Time of study: time series of 4 years, to be determined based on Osakidetza records and the mortality register. Based on the results of this

study and on the hypothesis of the decrease in, and improved efficiency of, resource consumption through the intervention of support programs, formulated as a result of the retrospective observational study carried out, the sample size of cohorts and Inhibitors,research,lifescience,medical subgroups will be defined for Phase 2: PROSPECTIVE cohort study. For this analysis, the error will be established at α=5% with a statistical significance of 80% (error β=20%). The sample size of each subgroup n will be the maximum of the sample sizes obtained for the comparison of means or proportions of Cilengitide the main variables in each subgroup. For the comparison of two means: n=2Zα/2+Zβ∧2*S∧2/d∧2 (1) where: Zα/2=1.960Zβ=0.842 (2) S2=variance in the quantitative variable of the control group d=Minimum value of the difference to be detected (quantitative values) For the comparison of two proportions: n=2p*q∧2Zα/2+Zβ∧2/pA−pB∧2 (3) where: Zα/2=1.960Zβ=0.842 (4) p=Mean of the two proportions pA y pB The parameters will be analysed with the statistical software SPSS 15.0 for Windows.

Mir-181c acts via targeting mitochondrial COX1 (cytochrome c oxid

Mir-181c acts via targeting mitochondrial COX1 (cytochrome c oxidase subunit 1), and miR-181c treatment selectively affected the expression of mitochondrial complex IV genes in the heart. Importantly, following miR-181c administration several mitochondrial Receptor Tyrosine Kinase Signaling functions were impaired, such as O2 consumption, ROS production, matrix calcium levels as well as mitochondrial membrane potential. 181 Another group sought to investigate the role of miR-30c in the

heart, due to the implication of miR-30 family in several aspects of CMC function and heart pathophysiology. To this aim they generated transgenic mice specifically overexpressing miR-30c in CMCs. They observed that these animals develop severe DCM after 6 weeks of age, and expression analysis of the transgenic hearts prior to phenotype onset revealed changes indicating mitochondrial function impairment. In addition to these findings, mitochondrial oxidative phosphorylation (OXPHOS) complexes III and IV were downregulated at the protein level. These observations indicate that miR-30c triggered mitochondrial dysfunction may account for the DCM phenotype of the miR-30c transgenic mice, thus uncovering a specific role of miR-30c in cardiac physiology. 182 Overall, these findings indicate a role of miRNAs in mitochondrial expression modifications that may underlie cardiac dysfunction. MiRNAs in the diagnosis and prognosis

of HF Since HF is a highly heterogeneous disease, both in terms of etiology, clinical manifestation and outcome, early diagnostic and/or prognostic markers could considerably contribute towards the

timely detection and more effective management of the disease. 128 Towards this direction, significant ongoing efforts are aiming to depict miRNAs that could fulfill this role. A plethora of studies refer to observed changes in miRNA expression as potentially relevant in the diagnostic or prognostic setting. However, a very limited number of studies have been designed to address the per se diagnostic classification and/or prognostic value of miRNA markers. These studies have assessed cardiac tissue biopsies derived during surgery and peripheral blood. Diagnosis Cardiac tissue miRNAs A recent study by Leptidis et al performed next generation sequencing in human failing left ventricles of end-stage HF patients of HCM and DCM etiology and reported over 250 significantly Anacetrapib changed miRNAs in HF. 33 Interestingly, the miRNA signatures differed significantly based on the pathology preceding HF (DCM or HCM), 33 a finding consistent with other studies of distinct miRNA profiles in different HF diagnostic groups (e.g. DCM, ICM, AS). Importantly, the differences reported by the latter study appear to suffice for accurate patient classification. 69 In specific, Ikeda et al used 67 microRNA signatures of control, ICM, DCM and AS heart tissue in order to develop a microRNA-based classifier.

As phantom limb and phantom body (ie, one’s own double) are conce

As phantom limb and phantom body (ie, one’s own double) are conceptually related phenomena,25 antagonistic behavior displayed by a single limb should perhaps not be regarded as principally different from that of a reduplicated figure of one’s entire body. An understanding

of the complexity of interactions between a person and his or her double will barely be possible without the preceding understanding of the Enzastaurin price mechanisms allowing a single hand to live a life of its own. Although there is no direct clinical or neuroanatomic evidence for a primary callosal pathology in cases of heautoscopy or its nonvisual precursors, it is not entirely implausible to assume an interhemispheric disconnection at the basis Inhibitors,research,lifescience,medical of heautoscopic aggression. One thing is certain: more than anything else, it is the careful observation of neuropsychiatrie disorders from which we can learn about the relations between body Inhibitors,research,lifescience,medical and self. In the words of the French

novelist Marcel Proust (Le côté de Guermantes): “It is in moments of illness that we are compelled to recognize that we live not alone but chained to a creature of a different kingdom, whole worlds apart, who has no knowledge of us and by whom it is impossible to make ourselves understood: our body
Neurophysiologists used to view the basal ganglia mainly as structures for regulating voluntary movement. The recent neuroanatomical, neuropsychological, and functional Imaging literature, however, has Inhibitors,research,lifescience,medical made It Increasingly clear that these subcortical structures are also Intimately Involved In regulating higher cerebral processes that control cognition, decision-making, the planning of complex behavioral strategies, and neuropsychiatrie symptoms.1,2 The frontal-subcortical circuitry provides a unifying framework Inhibitors,research,lifescience,medical for understanding the behavioral changes that accompany neurodegenerative disorders.3 In the past three decades, a

number of significant CHIR99021 clinical advances have been made in our understanding, not Inhibitors,research,lifescience,medical only of the neuroanatomy, but also of the neurophysiology and chemoarchitecture, of the frontal-subcortical circuits.4 Parallelling this new understanding, an increasingly broad spectrum of neuropsychiatrie phenomenology is recognized as being interprétable in the context of frontal-subcortical circuit dysfunction. A series of parallel segregated frontal-subcortical circuits are now known to link specific regions of the frontal cortex to the striatum, the globus pallidus (GP) and substantia nigra (SN), and the thalamus, constituting an important effector AV-951 mechanism that allows the organism to interact adaptively with its environment.5 Impaired executive functions, apathy, and impulsivity are hallmarks of frontal-subcortical circuit dysfunction. In a recent event-related functional MRI (fMRI) study, for instance, the authors concluded that the caudate nucleus and the putamen are particularly important, respectively, in the planning and the execution of a self-generated novel action.

have proposed a technique to identify FOG episodes based on the f

have proposed a technique to identify FOG episodes based on the frequency properties of leg vertical accelerations. The approach is based on the hypothesis that FOG occurrences are associated to trembling motion, which affect limb acceleration signal. They have introduced the so-called freeze index (FI): the ratio between the sellekchem signal (limb acceleration) power in the ��freeze�� band and the signal power in the ��locomotor�� band. The FI method was validated using one to seven accelerometers mounted on patients with satisfactory detection results [19]. In the present paper we propose a complementary index in order to take into account both trembling and festination situations. Our objective is to anticipate the occurrence of FOG episodes in order to propose a robust solution for real-time control of assisted devices. We believe, festination is one of the FOG expressions and precedes most of gait interruptions and is an interesting marker of gait modification. Furthermore we intend to propose a solution based on a minimal number of embedded sensors and detection algorithms for future real-time applications.In Section 2 we recall the definition of FI and introduce our FOG criterion (FOGC). In Section 3 we present the inertial sensor on which our solution is based and we describe the experimental setup. In Section 4 the results are described and discussed.2.?Freezing of Gait DetectionMoore et al. introduced the freeze index (FI) as the power of the considered body segment acceleration signal in the ��freeze�� band (3�C8 Hz) divided by the power of the signal in the ��locomotor�� band (0.5�C3 Hz) [18�C20]. For each instant t, FI(t) is defined as the square of the area under the power spectra of a 6 s window of data (centered at time t) in the ��freeze�� band, divided by the square of the area under the power spectra in the ��locomotor�� band. The width of the sliding window is based on FOG duration. It has been determined that the optimal window width has to approximately be twice the duration of the shortest FOG event to be detected. Increasing the window size reduces the sensitivity of the FI, acting as a low-pass filter by not identifying the short-duration freeze events. A FI threshold is chosen such that FI values above this limit are designated as FOG. In their article, Moore et al. have chosen the threshold as the mean plus one S.D. of the peak FI from nine epochs of volitional standing.Here, we introduce a new approach for the observation of gait changes and the detection of FOG events, the so-called FOG criterion (FOGC). FOGC is based on the continuous evaluation of two gait parameters: cadence and stride length. Cadence during festination in PD patients reported values less than 3 Hz (2.8 Hz [S.D.0.2]) [5]. Our hypothesis is that, before a FOG event occurs, the cadence should increase whereas the stride length decreases (festination).