Symptoms In Normal Subjects Research Articles

Choosing Sides: Impact of Prismatic Adaptation on the Lateralization of the Attentional System.

Seminal studies revealed differences between the effect of adaptation to left- vs. right-deviating prisms (L-PA, R-PA) in normal subjects. Whereas L-PA leads to neglect-like shift in attention, demonstrated in numerous visuo-spatial and cognitive tasks, R-PA has only minor effects in specific aspects of a few tasks. The paucity of R-PA effects in normal subjects contrasts with the striking alleviation of neglect symptoms in patients with right hemispheric lesions. Current evidence from activation studies in normal subjects highlights the contribution of regions involved in visuo-motor control during prism exposure and a reorganization of spatial representations within the ventral attentional network (VAN) after the adaptation. The latter depends on the orientation of prisms used. R-PA leads to enhancement of the ipsilateral visual and auditory space within the left inferior parietal lobule (IPL), switching thus the dominance of VAN from the right to the left hemisphere. L-PA leads to enhancement of the ipsilateral space in right IPL, emphasizing thus the right hemispheric dominance of VAN. Similar reshaping has been demonstrated in patients. We propose here a model, which offers a parsimonious explanation of the effect of L-PA and R-PA both in normal subjects and in patients with hemispheric lesions. The model posits that prismatic adaptation induces instability in the synaptic organization of the visuo-motor system, which spreads to the VAN. The effect is lateralized, depending on the side of prism deviation. Successful pointing with prisms implies reaching into the space contralateral, and not ipsilateral, to the direction of prism deviation. Thus, in the hemisphere contralateral to prism deviation, reach-related neural activity decreases, leading to instability of the synaptic organization, which induces a reshuffling of spatial representations in IPL. Although reshuffled spatial representations in IPL may be functionally relevant, they are most likely less efficient than regular representations and may thus cause partial dysfunction. The former explains, e.g., the alleviation of neglect symptoms after R-PA in patients with right hemispheric lesions, the latter the occurrence of neglect-like symptoms in normal subjects after L-PA. Thus, opting for R- vs. L-PA means choosing the side of major IPL reshuffling, which leads to its partial dysfunction in normal subjects and to recruitment of alternative or enhanced spatial representations in patients with hemispheric lesions.

Depression and implicit emotion processing: An EEG study

Depression is one of the most prevalent mental illnesses and is associated with changes in emotion processing. The aim of this study was to determine the influence of depressive symptoms on EEG oscillatory dynamics accompanying implicit processing of angry and happy facial expressions in 46 healthy subjects. The Beck Depression Inventory was used to assess the presence of depressive symptoms in normal subjects. During the experiment, they were told to categorize the gender of angry, neutral, or happy faces presented to them, while high-resolution EEG was recorded. Analysis of the event-related spectral perturbations and the analysis of dipoles were carried out on EEG recordings using the EEGLAB toolbox. High depression (HD) and low depression (LD) groups did not differ on error rate and reaction time during categorization of gender. The perception of happy faces was accompanied by higher theta synchronization in the LD than the HD group. In contrast, theta synchronization was higher in the HD than the LD group during perception of angry faces. These findings imply that even at preclinical stages, HD scorers evidence increased emotional arousal to negative and decreased emotional arousal to positive stimuli during implicit emotion processing.

Metapoznanie nasila depresję poprzez cechę lęku: badania w populacji osób zdrowych psychicznie

Previous studies show that maladaptive metacognitive beliefs may constitute the psychopathological core of anxiety and depression. Recent findings also indicate that anxiety exacerbates the severity of depression. We investigated the hypothesis that anxiety mediates the relationship between faulty metacognitive beliefs and depressive symptoms in normal subjects. Two hundred and eight normal participants completed the Metacognitions Questionnaire (MCQ), the State-Trait Anxiety Inventory(STAI), and the Beck Depression Inventory (BDI). We performed mediation analysis to explore the relationships between metacognition, depression, and trait anxiety as a mediator. Our study showed that positive beliefs about worry, negative beliefs about uncontrollability and danger, low cognitive confidence, and negative beliefs about the need to control thoughts, and cognitive self-consciousness were mediated by the level of anxiety associated withthe severity of depression. Moreover, the mediation analysis indicated that only cognitive confidence beliefs directly influenced the intensity of depressive symptoms.

Metapoznanie nasila depresję poprzez cechę lęku: badania w populacji osób zdrowych psychicznie

Previous studies show that maladaptive metacognitive beliefs may constitute the psychopathological core of anxiety and depression. Recent findings also indicate that anxiety exacerbates the severity of depression. We investigated the hypothesis that anxiety mediates the relationship between faulty metacognitive beliefs and depressive symptoms in normal subjects. Two hundred and eight normal participants completed the Metacognitions Questionnaire (MCQ), the State-Trait Anxiety Inventory(STAI), and the Beck Depression Inventory (BDI). We performed mediation analysis to explore the relationships between metacognition, depression, and trait anxiety as a mediator. Our study showed that positive beliefs about worry, negative beliefs about uncontrollability and danger, low cognitive confidence, and negative beliefs about the need to control thoughts, and cognitive self-consciousness were mediated by the level of anxiety associated withthe severity of depression. Moreover, the mediation analysis indicated that only cognitive confidence beliefs directly influenced the intensity of depressive symptoms.

Esophageal Submucosal Injection of Capsaicin but Not Acid Induces Symptoms in Normal Subjects.

Background/AimsTransient receptor potential vanilloid-1 (TRPV1) is a candidate for mediating acid-induced symptoms in the esophagus. We conducted studies to determine if the presence of acid in the mucosa/submucosa and direct activation of TRPV1 by capsaicin elicited symptoms in normal healthy subjects. We also studied the presence of TRPV1 receptors in the esophagus.MethodsUnsedated endoscopy was performed on healthy subjects with no symptoms. Using a sclerotherapy needle, normal saline (pH 2.0–7.5) was injected into the mucosa/submucosa, 5 cm above the Z line. In a separate group of healthy subjects, injection of capsaicin and vehicle was also studied. Quality of symptoms was reported using the McGill Pain Questionnaire, and symptom intensity using the visual analogue scale (VAS). Immunohistochemistry was performed on 8 surgical esophagus specimens using TRPV1 antibody.ResultsAcid injection either did not elicit or elicited mild symptoms in subjects at all pH solutions. Capsaicin but not the vehicle elicited severe heartburn/chest pain in all subjects. Mean VAS for capsaicin was 91 ± 3 and symptoms lasted for 25 ± 1 minutes. Immunohistochemistry revealed a linear TRPV1 staining pattern between the epithelial layer and the submucosa that extended into the papillae. Eighty-five percent of papillae stained positive for TRPV1 with a mean 1.1 positive papillae per high-powered field.ConclusionsThe mechanism of acid-induced heartburn and chest pain is not the simple interaction of hydrogen ions with afferents located in the esophageal mucosa and submucosa. TRPV1 receptors are present in the lamina propria and their activation induces heartburn and chest pain.

The role of cannabinoids in the neurobiology of sensory gating: A firing rate model study

Gating of sensory (e.g. auditory) information has been demonstrated as a reduction in the auditory-evoked potential responses recorded in the brain of both normal animals and human subjects. Auditory gating is perturbed in schizophrenic patients and pharmacologically by drugs such as amphetamine, phencyclidine or ketamine, which precipitate schizophrenic-like symptoms in normal subjects. The neurobiological basis underlying this sensory gating can be investigated using local field potential recordings from single electrodes. In this paper we use such technology to investigate the role of cannabinoids in sensory gating. Cannabinoids represent a fundamentally new class of retrograde messengers which are released postsynaptically and bind to presynaptic receptors. In this way they allow fine-tuning of neuronal response, and in particular can lead to so-called depolarisation-induced suppression of inhibition (DSI). Our experimental results show that application of the exogenous cannabinoid WIN55, 212-2 can abolish sensory gating as measured by the amplitude of local field responses in rat hippocampal region CA3. Importantly we develop a simple firing rate population model of CA3 and show that gating is heavily dependent upon the presence of a slow inhibitory ( GABA B ) pathway. Moreover, a simple phenomenological model of cannabinoid dynamics underlying DSI is shown to abolish gating in a manner consistent with our experimental findings.

Opening the Nasal Valve with External Dilators Reduces Congestive Symptoms in Normal Subjects

We examined whether the use of two different external nasal dilator devices influenced the size of the nasal valve area and symptoms of nasal congestion. This was a randomized blind-allocation, open three-way crossover study of Breathe Right, Side Strip Nasal Dilators, and placebo. We studied 12 healthy subjects (10 female, 2 male; age range 26-56 years). Measures of total volume and total minimum cross-sectional area were collected. Subjective symptoms were collected using a visual analog scale and an ordinal scale. With both products, there was significant increase in the size of the minimum cross-sectional area compared to placebo, p = 0.004. This is supported by the decrease in the subjective reports of congestion; on the visual analog scale, compared to placebo p = 0.012 and the ordinal scale, compared to placebo, p = 0.004. Both devices significantly increase the size of the nasal valve area and reduce congestion in normal subjects.

Effect of Aging on Gene Expression of Metabotropic Glutamate Receptor 5 and Glutamate Transporter‐1 in the Prefrontal Cortex of Schizophrenics

Background: The involvement of the glutamatergic system in the patho‐physiology of schizophrenia is attracting interest because an antagonist of N‐methyl‐D‐aspartate (NMDA) glutamate receptor has been demonstrated to induce schizophrenic‐like symptoms in normal subjects. The results of previous studies have also suggested that glutamatergic function is reduced in the prefrontal cortex (PFC) of diagnosed schizophrenics. In order to provide additional evidence for this, we investigated whether expression of metabotropic glutamate receptor 5 (mGluR5) and glutamate transporter‐1 (GLT‐1) in the PFC is altered in schizophrenia. Methods: We compared the expression of mGluRS and GLT‐1 by in situ hybridization in Brodmann area 9 (B9) and 10 (B10) of the prefrontal cortex in 5 normal individuals and 5 schizophrenics that were younger than in previous studies, and examined the relationship between age and mRNA expression. Results: There were no significant differences in either mGluR5 or GLT‐1 mRNA expression between the schizophrenics and controls, however, there was a significant correlation to increase mGluR5 mRNA levels in the schizophrenics in both layer III and layer V of B9 with age, a finding not observed in the controls. Conclusion: The results suggest that the brains of schizophrenics may be vulnerable to aging and that the glutamatergic dysfunctions previously reported in schizophrenics may be partly explained by the aging process.

424. Executive function deficits in adults with attention deficit hyperactivity disorder (ADHD)

that S-ketamine and psilocybin produce overlapping psychotic symptoms in normal subjects that were associated with a common metabolic activation of prefrontal, limbic, striatal, and thalamic structures similarly as seen in some acute schizophrenic patients (Vollenweider 1998). In animals, behavioral effects of NMDA antagonists can be attenuated with the atypical 5-HT2A/D1,2,4 antagonist olanzapine or the 5-HT2A antagonist MDL 100907. This finding suggest that 1) 5-HT2 receptor antagonism may ameliorate ketamine-induced psychosis and 2) that serotonin via 5-HT2A receptors may modulate the glutamate system. To further explore the role of fronto-limbic pathways in acute psychotic states, the pretreatment effects of clozapine on S-ketamine and of ketanserin on psilocybin-induced metabolic hyperfrontality and associated symptoms were investigated in healthy volunteers in placebocontrolled studies using FDG-PET and statistical parametric mapping (SPM96). Drug-induced psychopathology was assessed after PET scanning using the Altered State of Consciousness Questionnaire. Pretreatment with the 5-HT2A/D2 antagonist clozapine (35 mg po) and the 5-HT2A antagonist ketanserin (50 mg), respectively, significantly reduced S-ketamineand psilocybin-induced metabolic hyperfrontality and associated psychotic symptoms. The present results strongly suggest that fronto-striato-thalamic pathways may be a common and critical substrate involved in both Sketamineand psilocybin-induced psychotic symptom formation. The finding that clozapine and ketanserin, respectively, significantly reduced S-ketamineand psilocybin-induced effects suggests that 5-HT2 receptor stimulation may be a common denominator in drug-induced and possibly also naturally occurring psychoses.

Metabolic mapping of the rat brain after subanesthetic doses of ketamine: potential relevance to schizophrenia

Subanesthetic doses of ketamine have been shown to exacerbate symptoms in schizophrenia and to induce positive, negative, and cognitive schizophrenic-like symptoms in normal subjects. The present investigation sought to define brain regions affected by subanesthetic doses of ketamine, using high resolution autoradiographic analysis of 14C-2-deoxyglucose (2-DG) uptake and immunocytochemical staining for Fos-like immunoreactivity (Fos-LI). Both functional mapping approaches were used because distinct and complementary information is often obtained with these two mapping methods. Ketamine, at a subanesthetic dose of 35 mg/kg, substantially increased 2-DG uptake in certain limbic cortical regions, including medial prefrontal, ventrolateral orbital, cingulate, and retrosplenial cortices. In the hippocampal formation, the subanesthetic dose of ketamine induced prominent increases in 2-DG uptake in the dentate gyrus, CA-3 stratum radiatum, stratum lacunosum moleculare, and presubiculum. Increased 2-DG uptake in response to 35 mg/kg ketamine was also observed in select thalamic nuclei and basolateral amygdala. Ketamine induced Fos-LI in the same limbic cortical regions that exhibited increased 2-DG uptake in response to the subanesthetic dose of the drug. However, no Fos was induced in some brain regions that showed increased 2-DG uptake, such as the hippocampal formation, anterioventral thalamic nucleus, and basolateral amygdala. Conversely, ketamine induced Fos in the paraventricular nucleus of the hypothalamus and central amygdala, although no effect of the drug on 2-DG uptake was apparent in these regions. In contrast to the increase in 2-DG uptake observed in select brain regions after the subanesthetic dose, an anesthetic dose of ketamine (100 mg/kg) produced a global suppression of 2-DG uptake. By contrast, a robust induction of Fos-LI was observed after the anesthetic dose of ketamine that was neuroanatomically identical to that produced by the subanesthetic dose. Results of the present investigation show that anesthetic and subanesthetic doses of ketamine have pronounced effects on regional brain 2-DG uptake and induction of Fos-LI. The alterations in regional brain metabolism induced by the subanesthetic dose may be relevant to effects of ketamine to induce schizophrenic-like symptoms.

Caffeine withdrawal: a contrast of withdrawal symptoms in normal subjects who have abstained from caffeine for 24 hours and for 7 days

Two groups of normal subjects were withdrawn from caffeine for either 24 h (n = 9) or 7 days (n = 12). Following a pre-drug test sequence, subjects were given either 250 mg or 500 mg of anhydrous caffeine or a placebo. Tests were repeated 1, 3 and 5 h later. Tiredness, as measured by a visual analogue scale, was the most sensitive indicator of caffeine withdrawal. Headache was only apparent for subjects off caffeine for 24 h and given placebo, confirming this as a specific withdrawal effect, coming on 24-30 h after stopping caffeine. Alertness was increased by caffeine only in the group abstinent for 24 h. After longer term abstention, caffeine had no effects, confirming that drowsiness and lethargy are transient caffeine withdrawal symptoms.

Simulating amnesic symptoms in normal subjects.

Patients with organic brain damage resulting in anterograde amnesia cannot recall a list of words, but when given the first three letters of each word, they complete these word stems with words from the list. We simulated this phenomenon in normal subjects who examined the list words for vowels while ignoring their semantic component. The subjects produced the list words when completing the word stems although they could not recall the words.

Suggestibility and Neurotic Symptoms in Normal Subjects

(1938). Suggestibility and Neurotic Symptoms in Normal Subjects. The Journal of General Psychology: Vol. 19, No. 2, pp. 391-399.