Our primary analysis was motivated by a specific hypoth- esis, based on previous research by our group, regarding re- duction in early visual sensory processing (ie, the P1 process- ing period) in clinically unaffected first-degree relatives. A measure of P1 amplitude was defined as the area under the curve (vs the 0-µV baseline) in the interval 87 to 97 millisec- onds, spanning the P1 component, chosen based on grand av- erage waveforms ( Figure 2 ). These area measures were then submitted to a repeated-measures multivariate analysis of variance (MANOVA) using SPSS software (SPSS Inc, Chicago, Il) with a between-subjects factor of group (relatives vs con- trols vs probands) and within-subjects factors of region (left, midline, or right) and electrode (O1/PO7/PO3/, Oz/POz/Pz, O2/PO4/PO8), covering the left lateral occipital, midline dor- sal, and right lateral occipital visual scalp regions, respec- tively. All tests were 2-tailed with a preset ␣ level of P ⬍ .05.
Conclusions: In patients with trigeminal neuralgia (TN), routine head imaging identifies structural causes in up to 15% of patients and may be considered useful (Level C). Trigeminal sensorydeficits, bilateral involvement of the trigeminal nerve, and abnormal trigeminal reflexes are associated with an increased risk of symptomatic TN (STN) and should be considered useful in distinguishing STN from classic trigeminal neuralgia (Level B). There is insufficient evidence to support or refute the usefulness of MRI to identify neurovascular compression of the trigeminal nerve (Level U). Carbamazepine (Level A) or oxcarbazepine (Level B) should be offered for pain control while baclofen and lamotrigine (Level C) may be considered useful. For patients with TN refractory to medical therapy, Gasserian ganglion percutaneous techniques, gamma knife, and microvascular decompression may be considered (Level C). The role of surgery vs pharmacotherapy in the management of TN in patients with MS remains uncertain. Neurology ® 2008;71:1183–1190
This report of the behavioral analysis on aging mice dis- rupted in the GAN gene evaluates for the first time the deterioration of motor and sensory functions, both of which are impaired in human GAN. Our analysis reveals a late onset but robust motor impairment over time, affecting preferentially the grip strength in the forelimbs from 60 weeks of age in a pure 129/SvJ background. The fact that a single mouse showed a persistent decrease in sensitivity to thermal stimulus might also suggest a possi- ble very low penetrance of sensory dysfunction. Sensorydeficits developed over time in the C57BL/6 GAN ani- mals that in turn displayed no motor deficits, which may indicate a modulation of the phenotype by the genetic background. Our results are in agreement with the absence of weakness in the hind limbs monitored over 15 months in another GAN model (GAN ex1 ) . In our
This study produced some novel findings. Compared to HCs, FM subjects have (1) consistent sensorydeficits on dynamic posturography despite a normal clinical neurological examination; (2) poorer scores on all bal- ance- and FM-related questionnaires, less strength, more pain areas and higher total myalgia scores but not anxiety and depression scores; (3) gastrocnemius and anterior tibialis MTPs were found in 76% to 84% of FM subjects, leading to the conjecture that active MTPs in these leg muscles may affect balance and falls as patients attempt to maintain postural stability through activation of the anterior and posterior leg muscles ; (4) pos- tural stability is best predicted by FM severity (FIQR), cognitive impairment (MASQ) and BMI; the use of opioids and/or benzodiazepines, the total number medi- cation tablets consumed per day, and muscle strength or pain scores did not predict objective measures of bal- ance; (5) motor tests, including limits of stability, were largely normal with the exception of longer latencies to backward perturbations and shorter end point excursion on limits of stability; and (6) these data confirm our ear- lier report of significantly more self-reported falls in FM patients compared to HCs.
Methods: This study investigates the plasma levels of 8-isoprostane and Cysteinyl leukotrienes (CysLTs) in 44 autistic children and 40 healthy controls. The recruited autistic patients were assessed for behavior, cognitive and sensorydeficits by using different autism severity rating scales, including the Childhood Autism Rating Scales (CARS), Social responsiveness scale (SRS) and Short Sensory Profile (SSP). Receiver Operating Characteristics analysis (ROC) of the obtained data was performed to measure the predictive value of 8-isoprostane and Cysteinyl leukotrienes (CysLTs) as oxidative stress- related parameters. Pearson ’ s correlations between the measured parameters was also performed. Results: The concentrations of 8-isoprostane and CysLTs in autistic patients were significantly higher than those in controls. While cognitive and social impairments did not show any significant differences, the SSP results were strongly correlated with the levels of both of the biomarkers assessed. However, autistic children showed improvements in oxidative stress status (as determined by 8-isoprostane levels) at increasing ages.
history of upper respiratory tract illness 2 days to 4 weeks before presentation. An average of 10 days occurred between the upper respiratory tract illness and the appearance of neurologic symptoms. None of the patients had vaccinations in the 3 months before presentation. Details of the clinical presenta- tion are presented in Table 1. Nonspecific signs or symptoms of systemic illness, such as fever, head- ache, nausea, and vomiting, occurred in 74% of pa- tients (14 of 18). Motor deficits, the most common presenting signs/symptoms, included ataxia, para- paresis, hemiparesis, and monoparesis. Altered con- sciousness was the second most common neurologic sign/symptom. Five patients had urinary symptoms, which included retention of urine in 4 and inconti- nence in 1. Paraparesis, sensorydeficits, and urinary symptoms occurred predominantly in patients with spinal cord disease as seen on MRI images.
Figure 5 is the statistical cluster plot illustrating a posterior cluster in the time range of the P1, reflecting the group differences as reported in the ANOVA. Immediately following the P1 component, an in- creased positive activation was observed over frontal scalp in patients (see Fig. 1) The reader may note that an earlier difference at ~50 ms over fronto-central scalp sites also reaches significance in the statistical cluster plot. As this effect was unpredicted and not observed in any previous studies to our knowledge, it must be treated with some caution for now until such time as it is replicated 1 This may reflect increased recruitment of frontal brain regions similar to that found in recent studies [21, 26], albeit in an earlier time interval. ‘‘Hyperfrontality’’ in patients has been postulated to represent additional processing carried out in compensation for sensorydeficits . If this is indeed the case, then one might expect to find greater frontal activity in those patients exhibiting more deficient P1 amplitudes. To test whether the ampli- tude of the frontal positivity (here named ‘P1f’) in patients depends on the amplitude of the preceding posterior P1, a post-hoc correlation analysis was carried out. P1f was measured as the average ampli- tude in the interval 105–120 ms at fronto-central electrode site FCz where the increased activity relative to controls was maximal. As the full extent of these components may overlap both temporally and spa- tially, we controlled for biases arising from the choice of reference electrode by transforming the data to average-reference for this analysis. A significant neg- ative correlation was found for the patient group (r = )0.42; P = 0.002) (Fig. 6a). As the frontal posi- tivity is temporally coincident with the posterior N1 component, it might be argued that it reflects the same process, manifesting more faintly and with opposite polarity over frontal scalp. However, group differences are only observed for this frontal com- ponent, and not for the posterior N1, which is much larger and more robust and would therefore be ex- pected to produce stronger effects. Moreover, if the correlation could simply be explained by physical factors relating to dipolar sources and referencing,
The main inclusion criteria were age of 40–70 years, a diagnosis of unilateral subacute ischemic stroke, i.e., a left or right medial cerebral artery infarction with contralateral sensorimotor deficits of the upper limbs 3 to 4 weeks post-ictus. Also, patients should have low levels of spasticity, and stimulation perception thresh- olds of at least 20 mA. All patients were right-handed. Patients with mild transient ischemic stroke lasting fewer than 24 h, hemorrhagic stroke, and carotid artery dissection, history of cerebrovascular disease, wearing a pacemaker, aphasia, or cognitive impairment that prevented completion of the assessment were excluded. Patients were recruited with the help of physio- and occupational therapists at the rehabilitation clinic. The most relevant criteria patients did not meet were spasti- city and paresis. Because of difficulties with patient en- rollment, we widened the age criterion to patients aged 30 to 90 years.
Abstract: Sensory gating disturbances in schizophrenia are often described as an inability to filter redundant sensory stimuli that typically manifest as inability to gate neuronal responses related to the P50 wave, characterizing a decreased ability of the brain to inhibit various responses to insignificant stimuli. It implicates various deficits of perceptual and attentional functions, and this inability to inhibit, or “gate”, irrelevant sensory inputs leads to sensory and information overload that also may result in neuronal hyperexcitability related to disturbances of habitu- ation mechanisms. These findings seem to be particularly important in the context of modern electrophysiological and neuroimaging data suggesting that the filtering deficits in schizophrenia are likely related to deficits in the integrity of connections between various brain areas. As a consequence, this brain disintegration produces disconnection of information, disrupted binding, and disintegration of consciousness that in terms of modern neuroscience could connect original Bleuler’s concept of “split mind” with research of neural information integration.
The aim of this article is to explore the validity of the twin deficits hypothesis in nine OECD countries using panel cointegration tests with structural breaks from 1990 to 2007. This article differs from existing related studies in three ways. First, although some studies have used trade deficits in the twin deficits hypothesis, this paper includes the current account of the balance of payments. The current account deficit, more comprehensive than the trade deficit, is the sum of the balance of trade (the export of goods and services minus the import goods and services) and net current transfers (interests, dividends, and foreign aid). Second, although there is now significant evidence to support the twin deficits hypothesis (Piersanti, 2000; Normandin, 1999; Chinn and Ito, 2005), none of these previous studies is based on panel cointegration with structural breaks. Most studies use time series data (Holmes, 2009; Grier and Ye, 2009) or classical panel data in their modeling (Saleh et al., 2005; Baharumshah et al., 2006); there are not structural breaks in either the unit root tests or the cointegration analysis. Third, some researchers have focused their attention on the relationship between the two deficits in one country, such as the United States, Egypt, Korea or Greece. A study of one country certainly cannot lead to an empirical generalization. To fill these gaps in the literature and to capitalize on the attention paid to the impact of the current economic crisis on budget deficits and current account deficits, this article examines the relationship between budget deficits and current account deficits in nine OECD countries using panel cointegration with structural breaks tests developed by Banerjee and Carrion-i-Silvestre (2006).
Schizophrenia, as known, is a remarkably disabling illness. Functional decline persisting for six months is one of the criteria for diagnosis of schizophrenia. In developed countries, it ranks near the top among other causes of disability in both gender and among young adult population. Functional deficits, similar to cognitive deficits are seen at the onset of illness. The disability results from neuro-cognitive compromise and the disability is mainly seen in aspects of decrease in social competence, decrease in capacity of individual living and decrease in vocational success. About 20-30 % of people recover fully but a smaller proportion of this group however develop functional deterioration before oldage.
Current management criteria for feline pelvic fractures appears to work well, with excellent long term outcomes. Surgical complications are infrequent but are most commonly varying degrees of sciatic impairment. Positively, neurological deficits from the trauma or surgery resolve in most and improve in the remainder. No cats developed megacolon however a few did have intermittent issues with constipation, although the relationship to pelvic injuries is unclear. On balance it appears that narrowing of up to 45-50% is not a direct risk factor for development of constipation and megacolon, however narrowing of greater than 50% could potentially still be a risk and therefore should remain as an indication for surgical intervention.
There were few differences in performance between the DCD and hemiplegia groups, suggesting that MI ability may be similarly impaired in both groups. If this is the case, and the suggestion of Mutsaarts and colleagues that there is a link between deficits in MI ability and motor planning deficits (Mutsaarts et al., 2007) is correct, then this supports the likelihood of motor planning deficits in children with DCD, similar to that observed in hemiplegia. It remains unclear whether this impairment is one of the underlying causes of motor skill impairment in children with DCD. Instead, their motor skill impairment may prevent them from accurately forming internal models, which is then reflected in MI impairments. Future research needs to explore this issue as it will have a significant impact on approaches taken to
In the present study, we quantified inflammation, pain, and locomotor deficits in untreated and MTX-treated CIA mice and controls to objectively grade functional deficits over the disease course and in response to treat- ment. We found that sensory and motor deficits were correlated with the severity of arthritis and propose a new tool, the ArthriSM scale, to predict functional defi- cits based on the clinical score. To our knowledge, this is the first detailed correlation between clinical score and functional deficits in the CIA mouse model. Hayer et al.  already showed a relationship between gait pa- rameters and the extent of cartilage and bone erosion during arthritis course, but no exhaustive study has been performed so far to correlate functional deficits with the clinical score.
Since motor deficits are a characteristic of the PEA and the treatment of this pathology should consider interventions to improve these deficits, including motor performance along with motor coordination (gait, balance, arm functions and movement planning) (Fournier et al., 2010). Thus, the use of physical exer- cise as an instrument for the development of children with autism has been in- creasingly used, requiring theoretical research that supports this use, giving it greater scientific robustness.
A feature of SSD is difficulty with goal-directed behaviors, which can impact ADLs (APA, 2013). Like the finding of those with schizophrenia in residential and outreach programs needing at least a minimal level of assistance (Fossey et al., 2006), it was found in this study that the participants showed deficits in ADL skills and similarly needed assistance in the community. The relationship between motor and process skills; the relationship of sensory avoidance with both motor and process skills; and the link between sensory sensitivity, sensory avoidance, ADL skill deficits, and depression and anxiety may provide insight into the mechanism behind functional difficulties and impaired quality of life among people with SSD. For instance, it may be reasonable to assume that increased sensory sensitivity in this population results in avoidance of tasks that are rich in sensory input and/or a deficient task performance. This, in turn, may lead to decreased energy and low motivation to participate in daily activities, increased social isolation, and increased feelings of depression and anxiety. Further research is merited.
In the current study, emotion recognition accuracy was associated with scores on the drive for thinness subscale of the EDI. It is notable that previous work in subclinical samples has identified body dissatisfaction (Ridout et al., 2010; 2012) and bulimia (Sharpe et al., 2016) as the critical factor accounting for emotion recognition deficits. This suggests that, although the presence of facial emotion recognition deficits in subclinical disordered eating appears to be a robust phenomenon, its relationship to specific eating disorder symptoms is not reliable. As noted above, the scores for body dissatisfaction exhibited by the high EDI scorers in the current study did not differ significantly from norms for healthy controls. In contrast, the samples reported in our previous work (Ridout et al., 2010; 2012) exhibited elevated scores on this measure. This might account for the variations in the findings across the different studies.
• they reduce the demand for imports when much of the remittances are in kind. On this reasoning the adjustment mechanisms that balance trade ensure that free trade is beneficial for all. The essential benefit is that losers (countries with trade deficits) become winners as trade surplus countries become losers, through any of the adjustment mechanisms that balance trade. An equilibrium is thereby established. But this story is built on the assumptions of Say’s Law and no money flow reversals, both of which are relaxed below. Finally, high price elasticity of demand for exports/imports and high-income elasticity of demand for exports/imports are necessary conditions for the price and income adjustment mechanisms to balance trade. When these do not hold, trade imbalances are entrenched and the argument for free trade is severely weakened. The price adjustment mechanism implicitly assumes full employment: otherwise, an income adjustment mechanism would balance trade. This is why Say’s Law is an important foundation of free trade theory, explaining that any excess supply of goods will automatically readjust with price changes. Popularly known as ‘supply creates its own demand’, Say’s Law ensures that aggregate demand (AD) equals aggregate supply (AS) at a unique equilibrium of full employment (Keynes 1936:26). The latter is a necessary condition that ensures the price adjustment mechanism is feasible. When Say’s Law is relaxed, however, this paves the way for an income adjustment mechanism to balance trade.