Disturbances Of Motor Activity Research Articles

Neuroprotective Effects of Selegiline Agent Methamphetamine-Prompted Mood-Related Behavior Disorder Mediated Via 5-HT2 and D2 Receptors.

Many previous studies demonstrated that methamphetamine (METH) abuses can cause mood-related behavioral changes. Previous studies indicated neuroprotective effects of Selegiline. Seventy male Wistar rats were randomly divided into eight groups (10 rats in each group). Group 1 and Group 2 received normal saline and methamphetamine (10 mg/kg) for 21 days, respectively. Groups 3, 4, and 5 were treated simultaneously with methamphetamine and Selegiline with doses of 10, 15, and 20 mg/kg for 21 days. Groups 6 and 7 are methamphetamine-dependent groups which received 15 mg/kg of Selegiline with haloperidol (as D2 receptor antagonist) and trazodone (as 5-HT2 receptor antagonist) for 21 days, respectively. In days 23 and 24, elevated plus maze (EPM) and open-field test (OFT) were conducted to assess motor activity and mood (anxiety and depression) levels. METH as 10 mg/kg causes reduction of rearing number, ambulation distances, time spent in central square and also number of central square entries in OFT. Also METH administration causes decreases of time spent in open arm and number of open arm entries and increases of time spent in closed arm and number of closed arm entries in EPM. In contrast, Selegiline (of 10, 15, and 20 mg/kg) inhibited behavioral effects of methamphetamine in both OFT and EPM. Also administration of haloperidol and trazodone inhibited these behavioral protective effects of Selegiline and caused decrease of OFT behaviors (rearing number, ambulation distances, time spent in central square, and also number of central square entries) and also caused decreases of spend times in open arm, number of open arm entries, and also increased closed arm time spending and number of entries in closed arm in EPM. Current research showed that Selegiline via mediation of D2 and 5-HT2 receptors inhibits METH-induced neurobehavioral changes, mood-related behavior, and motor activity disturbances.

ACTUAL DIRECTIONS OF THE OPTIMIZATION OF THE SURGICAL TREATMENT OF LOCOMOTOR DISORDERS IN SPASTIC FORMS OF INFANTILE CEREBRAL PALSY

The review of actual directions of optimization of surgical treatment of locomotor disorders in spastic forms of infantile cerebral palsy is presented. When choosing the tactics of the treatment for this category of patients, the following criteria should be taken into account: the degree of disturbances in motor activity associated with muscle tone disorders, the spasticity pattern, the presence of joint contractures, limb deformities, the level of intellectual development, the presence and severity of perceptual disorders. The implementation of simultaneous operations allows reducing the period of immobilization of the child and the period of temporary incapacity for work of parents and recommended for the treatment of patients with cerebral palsy at all levels of the Gross Motor Function Classification System (GMFCS). There are considered modern methods of surgical treatment of spastic instability of the hip when the choice of the method of correction of the acetabular component of instability depends on the degree of abnormalities of the anatomy of the acetabulum, mainly from the deficit of the bone covering of the head of the femur and the «slanting» of the roof of the acetabulum. In the treatment of contractures of knee joints in order to prevent сrush syndrome, the elongation of the medial group of tibial flexors is advisable to be used in conjunction with tonus-enhancing operations in the anterior group of femur muscles with their secondary weakness. When treating axial deformities of the knee joints and unequal length of the legs, it is important to observe the timeliness principle (during the active growth of the skeleton) with the use of minimally invasive surgical interventions - hemi and epiphysiodesis - to avoid the need for more traumatic interventions.

Virtual reality in multiple sclerosis rehabilitation: A review on cognitive and motor outcomes

Multiple sclerosis (MS) is a demyelinating neurodegenerative disease with lesions involving the central nervous system. Clinical symptoms consist of disturbances in motor activity (e.g., weakness, spasticity, and tremor), sensory functioning (e.g., pain), visual functions (e.g., diplopia and optic neuritis), besides different cognitive (attention deficit and executive dysfunction) and behavioral abnormalities. This review aims to evaluate the role of VR tools in cognitive and motor rehabilitation of MS patients. Studies performed between 2010 and 2017 and fulfilling the selected criteria were searched on PubMed, Scopus, Cochrane and Web of Sciences databases, by combining the terms “VR rehabilitation” and “MS”. Our findings showed that, following the use of VR training, MS patients presented a significant improvement in motor (especially gait and balance) and cognitive function (with regard to executive and visual-spatial abilities, attention and memory skills). This review supports the idea that rehabilitation through new VR tools could positively affect MS patients’ outcomes, by boosting motivation and participation with a better response to treatment.

Protective role of metformin against methamphetamine induced anxiety, depression, cognition impairment and neurodegeneration in rat: The role of CREB/BDNF and Akt/GSK3 signaling pathways

BackgroundMethamphetamine is a neuro-stimulant with neurodegenerative effects, and ambiguous mechanism of action. Metformin is an antidiabetic agent with neuroprotective properties but not fully understood mechanisms. The present study investigated the molecular basis of metformin neuroprotection against methamphetamine-induced neurodegeneration. Brief methodSixty adult male rats were randomly divided into six groups: group 1 (received normal saline), group 2 (received 10 mg/kg of methamphetamine) and groups 3, 4, 5 and 6 [received methamphetamine (10 mg/kg) plus metformin (50, 75, 100 and 150 mg/kg) respectively]. Elevated Plus Maze (EPM), Open Field Test (OFT), Forced Swim Test (FST), Tail Suspension Test (TST) and Morris Water Maze (MWM) were used to assess the level of anxiety, depression and cognition in experimental animals. Also animals’ hippocampus were isolated and oxidative stress and inflammatory parameters and expression of total and phosphorylated forms of cAMP response element binding (CREB), brain-derived neurotrophic factor (BDNF), protein kinase B (Akt) and glycogen synthase kinase 3 (GSK3) proteins were evaluated by ELISA method. ResultsAccording to the data obtained, methamphetamine caused significant depression, anxiety, motor activity disturbances and cognition impairment in experimental animals. Metformin, in all used doses, decreased methamphetamine induced behavioral disturbances. Also chronic administration of methamphetamine could increase malondialdehyde (MDA), tumor necrosis factor-Alpha (TNF-α) and interleukine-1 beta (IL-1β) in rats, while caused reduction of superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione reductase (GR) activities. Metformin, especially in high doses, could prevent these malicious effects of methamphetamine. Also Metformin could activate CREB (both forms), BDNF and Akt (both forms) proteins’ expression and inhibited GSK3 (both forms) protein expression in methamphetamine treated rats. SignificanceAccording to obtained data, metformin could protect the brain against methamphetamine-induced neurodegeneration probably by mediation of CREB/BDNF or Akt/GSK3 signaling pathways. These data suggested that CREB/BDNF or Akt/GSK3 signaling pathways may have a critical role in methamphetamine induced neurotoxicity and/or neuroprotective effects of metformin.

Motor activity patterns in acute schizophrenia and other psychotic disorders can be differentiated from bipolar mania and unipolar depression

The purpose of this study was to compare 24-h motor activity patterns between and within three groups of acutely admitted inpatients with schizophrenia and psychotic disorders (n = 28), bipolar mania (n = 18) and motor-retarded unipolar depression (n = 25) and one group of non-hospitalized healthy individuals (n = 28). Motor activity was measured by wrist actigraphy, and analytical approaches using linear and non-linear variability and irregularity measures were undertaken. In between-group comparisons, the schizophrenia group showed more irregular activity patterns than depression cases and healthy individuals. The schizophrenia and mania cases were clinically similar with respect to high prevalence of psychotic symptoms. Although they could not be separated by a formal statistical test, the schizophrenia cases showed more normal amplitudes in morning to evening mean activity and activity variability. Schizophrenia constituted an independent entity in terms of motor activation that could be distinguished from the other diagnostic groups of psychotic and non-psychotic affective disorders. Despite limitations such as small subgroups, short recordings and confounding effects of medication/hospitalization, these results suggest that detailed temporal analysis of motor activity patterns can identify similarities and differences between prevalent functional psychiatric disorders. For this purpose, irregularity measures seem particularly useful to characterize psychotic symptoms and should be explored in larger samples with longer-term recordings, while searching for underlying mechanisms of motor activity disturbances.

Topiramate via NMDA, AMPA/kainate, GABAA and Alpha2 receptors and by modulation of CREB/BDNF and Akt/GSK3 signaling pathway exerts neuroprotective effects against methylphenidate-induced neurotoxicity in rats.

Chronic abuse of methylphenidate (MPH) often causes neuronal cell death. Topiramate (TPM) carries neuroprotective effects, but its exact mechanism of action remains unclear. In the present study, the role of various doses of TPM and its possible mechanisms, receptors and signaling pathways involved against MPH-induced hippocampal neurodegeneration were evaluated in vivo. Thus, domoic acid (DOM) was used as AMPA/kainate receptor agonist, bicuculline (BIC) as GABAA receptor antagonist, ketamine (KET) as NMDA receptor antagonist, yohimbine (YOH) as α2 adrenergic receptor antagonist and haloperidol (HAL) was used as dopamine D2 receptor antagonist. Open field test (OFT) was used to investigate the disturbances in motor activity. Hippocampal neurodegenerative parameters were evaluated. Protein expressions of CREB/BDNF and Akt/GSK3 signaling pathways were also evaluated. Cresyl violet staining was performed to show and confirm the changes in the shape of the cells. TPM (70 and 100mg/kg) reduced MPH-induced rise in lipid peroxidation, oxidized form of glutathione (GSSG), IL-1β and TNF-α levels, Bax expression and motor activity disturbances. In addition, TPM treatment increased Bcl-2 expression, the level of reduced form of glutathione (GSH) and the levels and activities of superoxide dismutase, glutathione peroxidase and glutathione reductase enzymes. TPM also inhibited MPH-induced hippocampal degeneration. Pretreatment of animals with DOM, BIC, KET and YOH inhibited TPM-induced neuroprotection and increased oxidative stress, neuroinflammation, neuroapoptosis and neurodegeneration while reducing CREB, BDNF and Akt protein expressions. Also pretreatment with DOM, BIC, KET and YOH inhibited TPM-induced decreases in GSK3. It can be concluded that the mentioned receptors by modulation of CREB/BDNF and Akt/GSK3 pathways, are involved in neuroprotection of TPM against MPH-induced neurodegeneration.

The Neuroprotective Effect of Curcumin Against Nicotine-Induced Neurotoxicity is Mediated by CREB–BDNF Signaling Pathway

Nicotine abuse adversely affects brain and causes apoptotic neurodegeneration. Curcumin- a bright yellow chemical compound found in turmeric is associated with neuroprotective properties. The current study was designed to evaluate the role of CREB-BDNF signaling in mediating the neuroprotective effects of curcumin against nicotine-induced apoptosis, oxidative stress and inflammation in rats. Sixty adult male rats were divided randomly into six groups. Group 1 received 0.7ml/rat normal saline, group 2 received 6mg/kg nicotine. Groups 3, 4, 5 and 6 were treated concurrently with nicotine (6mg/kg) and curcumin (10, 20, 40 and 60mg/kg i.p. respectively) for 21 days. Open Field Test (OFT) was used to evaluate the motor activity. Hippocampal oxidative, anti-oxidant, inflammatory and apoptotic factors were evaluated. Furthermore, phosphorylated brain cyclic adenosine monophosphate (cAMP) response element binding protein (P-CREB) and brain derived neurotrophic factor (BDNF) levels were studied at gene and protein levels. We found that nicotine disturbed the motor activity in OFT and simultaneous treatment with curcumin (40 and 60mg/kg) reduced the nicotine-induced motor activity disturbances. In addition, nicotine treatment increased lipid peroxidation and the levels of GSH, IL-1β, TNF-α and Bax, while reducing Bcl-2, P-CREB and BDNF levels in the hippocampus. Nicotine also reduced the activity of superoxide dismutase, glutathione peroxidase and glutathione reductase in hippocampus. In contrast, various doses of curcumin attenuated nicotine-induced apoptosis, oxidative stress and inflammation; while elevating P-CREB and BDNF levels. Thus, curcumin via activation of P-CREB/BDNF signaling pathway, confers neuroprotection against nicotine-induced inflammation, apoptosis and oxidative stress.

Mediatory role of NMDA, AMPA/kainate, GABAA and Alpha2 receptors in topiramate neuroprotective effects against methylphenidate induced neurotoxicity in rat

Prolonged abuse of methylphenidate (MPH) often causes neuronal damage. Topiramate (TPM) has neuroprotective properties, but its mechanism of action remains unclear. The current study evaluates in vivo role of various doses of TPM (10, 30, 50, 70 and 100mg/kg) and its possible mechanisms against MPH-induced hippocampal oxidative stress, inflammation and apoptosis, in absence and presence of different receptor agonists and antagonists. Domoic acid (DOM) as AMPA/kainate receptor agonist, bicuculline (BIC) as GABAA receptor antagonist, ketamine (KET) as NMDA receptor antagonist, yohimbine (YOH) as ɑ2 adrenergic receptor antagonist and haloperidole (HAL) as D2 dopamine receptor antagonist was used. Open Field Test (OFT) was used to investigate the disturbances in motor activity. Hippocampal oxidative, anti-oxidant and inflammatory parameters and apoptotic factors were studied. Expressions of BDNF at gene and protein levels were also evaluated. Crystal violet staining was performed to determine neuronal cell density. TPM (70 and 100mg/kg) reduced MPH-induced rise in lipid peroxidation, oxidized form of glutathione (GSSG), IL-1β and TNF-α levels, Bax expression and motor activity disturbances. In addition, TPM treatment increased BDNF gene and protein expressions, Bcl-2 expression, the level of reduced form of glutathione (GSH) and activities of enzymes superoxide dismutase, glutathione peroxidase and glutathione reductase.TPM also inhibited MPH-induced hippocampal degeneration. Pretreatment of animals with DOM, BIC, KET and YOH inhibited TPM-induced neuroprotection and increased oxidative stress, neuroinflammation, neuroapoptosis and neurodegeneration while reducing BDNF expressions. Thus, TPM by interacting with AMPA/kainate, GABAA, NMDA and ɑ2-adrenergic receptors improves BDNF expression and acts as a neuroprotective agent against MPH-induced neurodegeneration.

Possible involvements of glutamate and adrenergic receptors on acute toxicity of methylphenidate in isolated hippocampus and cerebral cortex of adult rats.

Neurodegeneration induced by methylphenidate (MPH), as a central stimulant with unknown long-term consequences, in adult rats' brain and the possible mechanisms involved were studied. Rats were acutely treated with MPH in the presence and absence of some receptor antagonists such as ketamine, topiramate, yohimbine, and haloperidol. Motor activity and anxiety level in rats were monitored. Antioxidant and inflammatory parameters were also measured in isolated hippocampus and cerebral cortex. MPH-treated groups (10 and 20 mg/kg) demonstrated anxiety-like behavior and increased motor activity. MPH significantly increased lipid peroxidation, GSSG content, IL-1β and TNF-α levels in isolated tissues, and also significantly reduced GSH content, superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GR) activities in hippocampus and cerebral cortex. Pretreatment of animals by receptor antagonists caused inhibition of MPH-induced motor activity disturbances and anxiety-like behavior. Pretreatment of animals by ketamine, topiramate, and yohimbine inhibited the MPH-induced oxidative stress and inflammation; it significantly decreased lipid peroxidation, GSSG level, IL-1β and TNF-α levels and increased GSH content, SOD, GPx, and GR activities in hippocampus and cerebral cortex of acutely MPH-treated rats. Pretreatment with haloperidol did not cause any change in MPH-induced oxidative stress and inflammation. In conclusion, acute administration of high doses of MPH can cause oxidative and inflammatory changes in brain cells and induce neurodegeneration in hippocampus and cerebral cortex of adult rats and these changes might probably be mediated by glutamate (NMDA or AMPA) and/or α2 -adrenergic receptors.

Neuroprotective effects of various doses of topiramate against methylphenidate-induced oxidative stress and inflammation in isolated rat amygdala: the possible role of CREB/BDNF signaling pathway.

Methylphenidate (MPH) abuse damages brain cells. The neuroprotective effects of topiramate (TPM) have been reported previously, but its exact mechanism of action still remains unclear. This study investigated the in vivo role of various doses of TPM in the protection of rat amygdala cells against methylphenidate-induced oxidative stress and inflammation. Seventy adult male rats were divided into seven groups. Groups 1 and 2 received normal saline (0.7ml/rat) and MPH (10mg/kg), respectively, for 21days. Groups 3, 4, 5, 6, and 7 were concurrently treated with MPH (10mg/kg) and TPM (10, 30, 50, 70, and 100mg/kg), respectively, for 21days. elevated plus maze (EPM) was used to assess motor activity disturbances. In addition, oxidative, antioxidantand inflammatory factors and CREB, Ak1, CAMK4, MAPK3, PKA, BDNF, and c FOS gene levels were measured by RT-PCR, and also, CREB and BDNF protein levels were measured by WB in isolated amygdalae. MPH significantly disturbed motor activity and TPM (70 and 100mg/kg) neutralized its effects. MPH significantly increased lipid peroxidation, mitochondrial GSSG levels and IL-1β and TNF-α level and CAMK4 gene expression in isolated amygdala cells. In contrast, superoxide dismutase, glutathione peroxidase, and glutathione reductase activities and CREB, BDNF Ak1, MAPK3, PKA, BDNF, and c FOS expression significantly decreased. The various doses of TPM attenuated these effects of MPH. It seems that TPM can be used as a neuroprotective agent and is a good candidate against MPH-induced neurodegeneration.

Involvement of AMPA/kainate and GABAA receptors in topiramate neuroprotective effects against methylphenidate abuse sequels involving oxidative stress and inflammation in rat isolated hippocampus

Abuses of methylphenidate (MPH) as psychostimulant cause neural damage of brain cells. Neuroprotective properties of topiramate (TPM) have been indicated in several studies but its exact mechanism of action remains unclear. The current study evaluates protective role of various doses of TPM and its mechanism of action in MPH induced oxidative stress and inflammation. The neuroprotective effects of various doses of TPM against MPH induced oxidative stress and inflammation were evaluated and then the action of TPM was studied in presence of domoic acid (DOM), as AMPA/kainate receptor agonist and bicuculline (BIC) as GABAA receptor antagonist, in isolated rat hippocampus. Open Field Test (OFT) was used to investigate motor activity changes. Oxidative, antioxidant and inflammatory factors were measured in isolated hippocampus. TPM (70 and 100mg/kg) decreased MPH induced motor activity disturbances and inhibit MPH induced oxidative stress and inflammation. On the other hand pretreatment of animals with DOM or BIC, inhibit this effect of TPM and potentiate MPH induced motor activity disturbances and increased lipid peroxidation, mitochondrial oxidized form of glutathione (GSSG) level, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in isolated hippocampal cells and decreased reduced form of glutathione (GSH) level, superoxide dismutase, glutathione peroxidase and glutathione reductase activity. It seems that TPM can protect cells of hippocampus from oxidative stress and neuroinflammation and it could be partly by activation of GABAA receptor and inhibition of AMPA/kainite receptor.

The quality of nighttime sleep in patients with multiple sclerosis

to study the quality of nighttime sleep in multiple sclerosis (MS) using the PSQI. The quality of nighttime sleep was compared in 48 patients with relapsing MS. Patients were divided into 2 groups according to the PSQI scores. Sleep disturbances were more frequent in patients with MS. Women had higher risk of sleep disturbances. In the group with a poor quality of nighttime sleep, complaints about the increase in latency and low quality of sleep and daily activities were more common. The global severity of neurological deficit and disturbance of motor activity affected the quality of nighttime sleep.

Development of an abbreviated version of the Delirium Motor Subtyping Scale (DMSS-4)

Delirium is a common neuropsychiatric syndrome with considerable heterogeneity in clinical profile. Identification of clinical subtypes can allow for more targeted clinical and research efforts. We sought to develop a brief method for clinical subtyping in clinical and research settings. A multi-site database, including motor symptom assessments conducted in 487 patients from palliative care, adult and old age consultation-liaison psychiatry services was used to document motor activity disturbances as per the Delirium Motor Checklist (DMC). Latent class analysis (LCA) was used to identify the class structure underpinning DMC data and also items for a brief subtyping scale. The concordance of the abbreviated scale was then compared with the original Delirium Motor Subtype Scale (DMSS) in 375 patients having delirium as per the American Psychiatric Association's Diagnostic and Statistical Manual (4th edition) criteria. Latent class analysis identified four classes that corresponded closely with the four recognized motor subtypes of delirium. Further, LCA of items (n = 15) that loaded >60% to the model identified four features that reliably identified the classes/subtypes, and these were combined as a brief motor subtyping scale (DMSS-4). There was good concordance for subtype attribution between the original DMSS and the DMSS-4 (κ = 0.63). The DMSS-4 allows for rapid assessment of clinical subtypes in delirium and has high concordance with the longer and well-validated DMSS. More consistent clinical subtyping in delirium can facilitate better delirium management and more focused research effort.

Validation and psychometric properties of the Delirium Motor Subtype Scale in elderly hip fracture patients (Dutch version)

The Delirium Motor Subtype Scale (DMSS) was developed to capture all the previous different approaches to delirium motor subtyping into one new instrument and emphasize disturbances of motor activity rather than associated psychomotoric symptoms. We investigated reliability and validity of the DMSS Dutch version. Elderly patients who had undergone hip fracture surgery received the DMSS and the Delirium Rating Scale Revised-98 (DRS-R-98). A diagnosis of delirium was defined according to the Confusion Assessment Method (CAM). Among 146 patients, 46 (32%) patients were diagnosed with delirium (mean age 86.3 years; SD 5.2). The internal consistency of the DMSS was acceptable (Cronbach's alpha=0.72). If an item was removed at random the internal consistency of the scale remained the same. Similarly the concurrent validity of DMSS was good (Cohen's kappa=0.73) while for each motor subtype the Cohen's kappa ranged from 0.58 to 0.85. The sensitivity and specificity of DMSS to detect each subtype ranged from 0.56 to 1 and from 0.88 to 0.98, respectively. This study suggests that the Dutch version of the DMSS is a reliable and valid instrument. The DMSS has scientific validity that could allow for greater precision in further research on motor subtypes.

Replication analysis for composition of the Delirium Motor Subtype Scale (DMSS) in a referral cohort from Northern India

The Delirium Motor Subtype Scale (DMSS) was developed by discerning the best differentiating motor activity symptoms from the Delirium Motor Checklist (DMC), a compilation of psychomotor symptoms from other subjective scales. To broaden its validation we replicated the original work done in a palliative care population in a psychiatric referral population. 100 consecutive C/L Psychiatry referrals with DSM-IV delirium in an Indian general hospital were assessed with the Delirium Rating Scale-Revised-98 (DRS-R98) and DMC and compared to 60 nondelirious hospitalized controls. Disturbances of motor activity were almost invariably present in patients with delirium and at a much higher frequency than in nondelirious control subjects. Principal components analysis identified 5-factors for the DMC where Factor 1 explained 37.3% of the variance and correlated significantly with DRS-R98 motor items. Items loading at >0.65 were selected for the replication scale if they also either correlated significantly with DRS-R98 motor items or were significantly more frequent in delirious patients vs. controls. The resultant scale comprised 12 items (five hyperactive and seven hypoactive) and was similar to the original DMSS. Combining motor items from the original DMSS and replicated version produced a 13-item amended DMSS that may have broader generalizability than the original DMSS.

Neuropsychiatric and cognitive profile of patients with DSM-IV delirium referred to an old age psychiatry consultation-liaison service

The phenomenology of delirium is understudied, including how the symptom profile varies across populations. The aim of this study was to explore phenomenology occurring in patients with delirium referred to an old age psychiatry consultation-liaison setting and compare with delirium occurring in palliative care patients. Consecutive cases of DSM-IV delirium were assessed with the Delirium Rating scale Revised-98 (DRS-R98) and Cognitive Test for Delirium (CTD). Eighty patients (mean age 79.3 ± 7.7 years; mean DRS-R98 total score 21.7 ± 4.9 and total CTD score 10.2 ± 6.3) were included. Forty patients (50%) with comorbid dementia were older, had a longer duration of symptoms at referral, and more severe delirium due to greater cognitive impairments. Inattention (100%) was the most prominent cognitive disturbance, while sleep-wake cycle disturbance (98%), altered motor activity (97%), and thought process abnormality (96%) were the most frequent DRS-R98 non-cognitive features. Inattention was associated with severity of other cognitive disturbances on both the DRS-R98 and CTD, but not with DRS-R98 non-cognitive items. The phenomenological profile was similar to palliative care but with more severe delirium due to greater cognitive and non-cognitive disturbance. Delirium is a complex neuropsychiatric syndrome with generalized cognitive impairment and disproportionate inattention. Sleep-wake cycle and motor-activity disturbances are also common. Comorbid dementia results in a similar phenomenological pattern but with greater cognitive impairment and later referral.

Actigraphic registration of motor activity reveals a more structured behavioural pattern in schizophrenia than in major depression

BackgroundDisturbances in motor activity pattern are seen in both schizophrenia and depression. However, this activity has rarely been studied objectively. The purpose of the present study has been to study the complexity of motor activity patterns in these patients by using actigraphy.FindingsMotor activity was recorded using wrist-worn actigraphs for periods of 2 weeks in patients with schizophrenia and major depression and compare them to healthy controls. Average motor activity was recorded and three non-parametric variables, interdaily stability (IS), intradaily variability (IV), and relative amplitude (RA) were calculated on the basis of these data. The motor activity was significantly lower both in patients with schizophrenia (153 ± 61, mean ± SD, p < 0.001) and depression (187 ± 84, p < 0.001), compared to controls (286 ± 80). The schizophrenic patients had higher IS and lower IV than the controls reflecting a more structured behavioural pattern. This pattern was particularly obvious in schizophrenic patients treated with clozapine and was not found in depressed patients.ConclusionsMotor activity was significantly reduced in both schizophrenic and depressed patients. However, schizophrenic patients differed from both depressed patients and controls, demonstrating motor activity patterns marked by less complexity and more structured behaviour. These findings may indicate that disturbances in motor activity reflect different pathophysiological mechanisms in schizophrenia compared to major depression.

Specific Loss of Brain ABCA1 Increases Brain Cholesterol Uptake and Influences Neuronal Structure and Function

The expression of the cholesterol transporter ATP-binding cassette transporter A1 (ABCA1) in the brain and its role in the lipidation of apolipoproteins indicate that ABCA1 may play a critical role in brain cholesterol metabolism. To investigate the role of ABCA1 in brain cholesterol homeostasis and trafficking, we characterized mice that specifically lacked ABCA1 in the CNS, generated using the Cre/loxP recombination system. These mice showed reduced plasma high-density lipoprotein (HDL) cholesterol levels associated with decreased brain cholesterol content and enhanced brain uptake of esterified cholesterol from plasma HDL. Increased levels of HDL receptor SR-BI in brain capillaries and apolipoprotein A-I in brain and CSF of mutant mice were evident. Cholesterol homeostasis changes were mirrored by disturbances in motor activity and sensorimotor function. Changes in synaptic ultrastructure including reduced synapse and synaptic vesicle numbers were observed. These data show that ABCA1 is a key regulator of brain cholesterol metabolism and that disturbances in cholesterol transport in the CNS are associated with structural and functional deficits in neurons. Moreover, our findings also demonstrate that specific changes in brain cholesterol metabolism can lead to alterations in cholesterol uptake from plasma to brain.

Screening methods for delirium: early diagnosis by means of objective quantification of motor activity patterns using wrist-actigraphy

Delirium after cardiac surgery is a risk factor for adverse outcome and even death. Disturbance of motor activity is a core feature of delirium, but hypoactive delirium often remains unrecognized. We explored wrist-actigraphy as a tool to objectively quantify postoperative recovery of 24-h rest-activity patterns to improve the early recognition of delirium after surgery. Motor activity was recorded by wrist-actigraphy after cardiac surgery in 88 patients over 65 years of age. Patients were assessed daily by using the CAM-ICU. Our final analyses were based on 32 non-delirious patients and 38 patients who were delirious on the first day after surgery. The delirious patients showed lower mean activity levels during the first postoperative night (P<0.05), reduced restlessness during the first day (P<0.05), and a lower mean activity of the 5 h with lowest activity within the first 24 h (P=0.01), as compared to the non-delirious patients. Already at a very early stage after cardiac surgery, a difference in motor activity was observed between patients with and without a delirium. As an unobtrusive method, actigraphy has the potential to be a screening method that may lead to early diagnosis and treatment of delirium.

Pentylenetetrazole-induced status epilepticus following training does not impair expression of morphine-induced conditioned place preference

Learning and memory play an important role in morphine addiction. Status epilepticus (SE) can impair the spatial and emotional learning and memory. However, little is known about the effects of SE on morphine-induced conditioned place preference (CPP). The present study was designed to investigate the effects of SE on morphine CPP, with food CPP being used as a control. The effects of SE on spatial memory in the Morris water maze (MWM) and Y-maze were investigated. SE was induced in adult mice using intraperitoneal injection of pentylenetetrazole; control mice received saline. The data indicated that SE had no effects on the formation of morphine CPP; however, the formation of food CPP was blocked by SE. Meanwhile, spatial memory assayed in the MWM and Y-maze was impaired by SE. In addition, the data demonstrated that SE did not cause a lasting disturbance of motor activity nor a change in the mice's appetite. These results suggested that although SE had no effects on morphine CPP, there was impaired food CPP and spatial memory in both the MWM and the Y-maze. The mechanisms underlying memory process of morphine CPP may be different from other types of memory.