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Abstract
Background
Clinicians generally agree on the association between depression and hypertension. Less clear is if the nature of the link is direct or indirect and if this should be considered confined only to syndromal forms or if it concerns also subsyndromal affective presentations. This study investigated the nature of the association between hypertension and subsyndromal depression in hospitalized hypertensive patients.
Methods
196 hypertensive and 96 non hypertensive inpatients underwent a SCID interview, to exclude patients positive for any Axis I or Axis II diagnosis. Symptomatic Subsyndromal Depression (SSD) was identified according to criteria proposed by Judd. Psychopathological assessment was performed with Anxiety Sensitivity Index (ASI) and Hopkins Symptom Checklist-90 (SCL-90). Clinical assessments included blood pressure measurement, evaluation of general health conditions and screening cardiovascular risk factors (smoke, alcohol, body weight, sedentary life style).
Results
Hypertensives met more frequently criteria for SSD. They also scored higher on ASI and SCL-90. However, those with more severe physical conditions, if compared with more healthy patients, did not show increased psychopathological severity. Similarly, psychopathological symptom severity did not differ among hypertensives positive for other cardiovascular risk factors, commonly more frequent among depressed subjects.
Limitations
Further analyses are needed to explore the potential advantage obtained on blood pressure control by treating SSD.
Conclusions
Hospitalized hypertensives, more frequently satisfied criteria for Symptomatic Subsyndromal Depression. These milder affective forms are probably directly linked to the presence of hypertension, rather than being indirectly associated to physical impairment or to higher prevalence of other cardiovascular risk factors.
Symptomatic subsyndromal depression in hospitalized hypertensive patients
Objective
Serum cholesterol was reported to be associated with depressed mood, but the studies conducted among household population are rare.
Methods
We used the data of 4115 men and 4275 women aged 18 or older, who completed a depression screening interview and had blood collected as a part of the National Health and Nutrition Examination Survey, 2005–2008. The serum concentrations of total cholesterol, high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were gender-specifically categorized into lower, intermediate, and upper quartiles. Depression was measured using the Patient Health Questionnaire, a 9-item screening instrument asking about the frequency of depression symptoms over the past 2
weeks.
Results
After adjustment for socio-demographics and behavioral risks, a U-shaped association was detected between severe depression and LDL-C among men. The odds ratios (ORs) of severe depression were 5.13 (95% CI=1.74–15.09), 1 (reference) and 2.28 (1.07–4.86) respectively for the men with lower (<169mg/dL), intermediate (169–221mg/dL), and upper quartile (≥222mg/dL) LDL-C. Among women, lower HDL-C was significantly associated with an elevated odds of severe depression [OR=2.96 (1.59–5.52)] compared with upper quartile of HDL-C, the association diminished after adjustment for covariates [OR=1.24 (0.66–2.32)]. No clear pattern of association between cholesterol and moderate depression was observed from either men or women.
Limitation
The inherent limitation of cross-sectional design prevented the authors from investigating causality.
Conclusions
A U-shaped association was identified between LDL-C and severe depression among men. Further studies are necessary to explore the biological mechanism and identify the clinical implication among populations vulnerable to psychiatric disorders.
Low cholesterol is associated with depression among US household population
Yes, this study says that having an MRI scan has a powerful antidepressant effect.
They took 51 depressed patients, and gave them all either an MRI scan or a placebo sham scan. The sham was a "scan" in a decommissioned scanner. The magnet was off but they played recorded scannerish sounds to make it believable. Patients were blinded to group.
They found that people in the scanner group improved much more than those in the sham group over two weeks. Actually there were two different kinds of scans, T1 structural MRI and EPI functional MRI, but they were the same
Does MRI Make You Happy?
On 8 November, Targacept, a drug company based in Winston-Salem, North Carolina, announced that TC-5214 had performed no better than placebo in one of four phase III trials. The results are a disappointment to clinicians eager for an innovative antidepressant.
TC-5214 is a form of mecamylamine, a blood-pressure drug introduced in the 1950s. It targets nicotinic α4β2 receptors (see ‘Mixed signals’), which normally receive chemical signals from the neurotransmitter acetylcholine. Because excess acetylcholine has been linked to major depression, blocking these signals might relieve the condition.
Depression drug disappoints
Background
Psychostimulants and non stimulants are effective in the treatment of ADHD. Efficacy of both methylphenidate and atomoxetine has been established in placebo controlled trials. Direct comparison of efficacy is now possible due to availability of results from several head-to-head trials of these two medications.
Methods
All published, randomized, open label or double blind trials, comparing efficacy of methylphenidate with atomoxetine, in treatment of ADHD in children, diagnosed using DSM-IVTM criteria were included. The outcome studied was ADHDRS-IVParent:Inv score. The standardized mean difference (SMD) was used as a measure of effect size.
Results
Nine randomized trials comparing methylphenidate and atomoxetine, with a total of 2762 participants were included. Meta-analysis did not find a significant difference in efficacy between methylphenidate and atomoxetine (SMD= 0.09, 95% CI -0.08-0.26) (Z=1.06, p=0.29). Synthesis of data from eight trials found no significant difference in response rates (RR=0.93 95% CI 0.76-1.14, p=0.49). Sub group analysis showed a significant standardized mean difference favouring OROS methylphenidate (SMD=0.32, 95% CI 0.12-0.53 (Z=3.05, p<0.002). Immediate release methylphenidate was not superior to atomoxetine (SMD= -0.04, 95% CI -0.19-0.12) (Z=0.46, p=0.64). Excluding open label trials did not significantly alter the effect size (SMD=0.08, 95% CI -0.04-0.21) (Z=1.27, p=0.20). All-cause discontinuation was used as a measure of acceptability. There was no significant difference in all cause discontinuation between atomoxetine and methylphenidate (RR 1.22, 95% CI 0.87-1.71). There was significant heterogeneity among the studies (p=0.002, I2=67%). Subgroup analysis demonstrated the heterogeneity to be due to the open label trials (p=0.001, I2=81%).
Conclusions
In general atomoxetine and methylphenidate have comparable efficacy and equal acceptability in treatment of ADHD in children and adolescents. However OROS methylphenidate is more effective than atomoxetine and may be considered as first line treatment in treatment of ADHD in children and adolescents.
Comparative efficacy and acceptability of methylphenidate and atomoxetine in treatment of attention deficit hyperactivity disorder in children and adolescents: a meta-analysis
The randomized, double-blind, placebo-controlled study compared two doses of Serdaxin, 0.5 mg and 5 mg, to placebo over an 8-week treatment period. Results from the study did not demonstrate Serdaxin's efficacy compared to placebo measured by the Montgomery-Asberg Depression Rating Scale (MADRS).
Many patients with Alzheimer's disease are simultaneously prescribed cholinesterase inhibitors (ChIs) and anticholinergics (AChs), 2 drug classes that have the potential to cancel each other out.
Physical activity produces many positive physiological changes. Some of these physiological changes, however, can adversely affect the absorption, distribution, metabolism, and/or excretion of certain medications when taken concurrently. Blood flow distribution is fundamental to the study of pharmacokinetics and can vary dramatically during rest compared with exercise. The liver and the kidney play significant roles in calculating the pharmacokinetic parameters of medications. Blood flow to these organs is significant at rest but decreases during exercise. These changes in blood flow, as well as other physiological changes during exercise, have shown to alter the pharmacokinetics of some drugs. Medications that require extra therapeutic monitoring may be affected by this drug-exercise interaction. Health care professionals and patients should be aware of these potential drug-exercise interactions.
Pharmacokinetic Drug Interactions with Physical Activity
Of great interest are findings that microglial cells—the macrophages of the brain—are activated during psychosis.6 Cells visualized with a positron emission tomography tracer (PK11195) that binds to peripheral benzodiazepine receptors, an indicator of microglia activation, were found to have greater receptor expression in patients with recent-onset schizophrenia.7 Activated microg-lia stimulate astrocytes to produce S100B, a marker of inflammation that is considered to be the equivalent of C-reactive protein in the brain.8 Serum S100B levels are elevated in patients with schizophrenia, and antipsychotics such as haloperidol (Drug information on haloperidol) and clozapine (Drug information on clozapine) have been shown to decrease S100B release from glial cells.
The Link Between Immune System Dysregulation and Schizophrenia
The investigators administered methylene blue to 37 subjects meeting criteria for bipolar disorder, while maintaining lamotrigine(Drug information on lamotrigine) as their primary mood stabilizer. Patients were randomized to receive 13 weeks treatment with either 195 mg methylene blue daily, or 15 mg as a putative subtherapeutic dose in lieu of a placebo that mimics the color in urine; with groups switching the regimen for an additional 13 weeks.
Alda reported that the active dose was associated with statistically significantly improved mood symptom scores from baseline on multiple measures, including the Montgomery-Asberg Depression Rating Scale (MADRS). There was no therapeutic effect apparent on cognitive performance, but no decrement observed with its use.
Methylene Blue Studied for Bipolar as FDA Issues Warning
A 52-year-old Chinese man was admitted to the inpatient psychiatric unit of an academic teaching hospital with an admitting diagnosis of major depressive disorder (MDD) with psychotic features. His chief complaint was "I do not feel happy." The patient endorsed insomnia, hopelessness, passive suicidal ideation, and increased anxiety, especially at bedtime. He was disheveled, guarded, demonstrated poor eye contact, slurred and decreased speech output, psychomotor retardation, poor cognition, flat affect, and vague auditory and visual hallucinations of seeing and hearing people. The patient had a past psychiatric history of MDD with psychotic features diagnosed when he was in his early 30s, and suicidal gestures. He had two previous inpatient admissions while in China in 2008, for psychotic features described then as robotic speech, flat affect, and minimal verbal responsiveness. At the time of his current admission, he was being followed in the psychiatry outpatient clinic. He denied past or current substance abuse. The patient's past medical history was significant for one observed tonic–clonic seizure in December 2009, which was managed with phenytoin 300 mg daily. At that time, neurologic evaluation was unrevealing, and no etiology of the seizure was identified.
After initial evaluation in the hospital, the patient was started on escitalopram 15 mg daily and paliperidone 3 mg daily, and his phenytoin 300 mg daily was continued. ECT had been considered while he was being followed as an outpatient. Upon admission, he was started on a course of ECT. Despite numerous medication trials including paliperidone, olanzapine, and clozapine, as well as a series of 12 ECT treatments, the patient's condition did not improve, and he began to show signs of cognitive decline. A neurology consult was requested for continued agitated and bizarre behavior. An EEG showed diffuse slowing, and a magnetic resonance (MRI) scan showed only small-vessel ischemic microvascular disease.
After 2 months, while still on the psychiatry inpatient unit, he developed symptoms of extreme agitation, aggressiveness, and unusual behavior, and was verbally unresponsive. His agitation was treated with lorazepam. Vital signs at that time revealed tachycardia to a heart rate of 120 bpm, a blood pressure of 90/50 mmHg, and O2 saturation of 90% at room air. His temperature was 102.3°F. The patient was transferred to the medical intensive care unit (MICU) and intubated for airway protection. Laboratory data at transfer revealed a white cell count of 11.2 K/µl, BUN 32 mg/dl, Cr 1.2 mg/dl, and creatine kinase 2,361 u. Neuroleptic malignant syndrome was suspected but ruled out, as the patient's temperature and creatine kinase trended down in the subsequent days without any active intervention. After 11 days, he was extubated. He displayed echopraxia, but no focal findings were documented.
Because of his unusual course, failure to respond to standard treatments for depression and psychosis, and the presence of a documented seizure 1 month before admission, a work-up for possible anti-NMDA receptor antibody encephalitis was started. Lumbar puncture yielded clear, colorless fluid which was acellular, with a glucose of 76 mg/dl and protein of 21 mg/dl. VDRL and oligoclonal bands were negative. CSF and serum sample was also sent for anti-NMDA receptor antibody testing. The patient had an EEG performed, which revealed bilateral independent temporal lobe discharges more prominent in the left hemisphere than the right, but no active seizures were seen. CSF and serum results confirmed the patient's diagnosis of anti-NMDA antibody encephalitis by the presence of antibodies against NRI-NR2 heteromers of the NMDA receptor. The patient was transferred to another hospital and lost to follow-up.
An Unusual Case of Anti-NMDA-Receptor Encephalitis in the Psychiatry Inpatient Unit
Extracts of sage (Salvia officinalis/lavandulaefolia) with terpenoid constituents have previously been shown to inhibit cholinesterase and improve cognitive function. The current study combined an in vitro investigation of the cholinesterase inhibitory properties and phytochemical constituents of a S. lavandulaefolia essential oil, with a double-blind, placebo-controlled, balanced crossover study assessing the effects of a single dose on cognitive performance and mood. In this latter investigation 36 healthy participants received capsules containing either 50 µL of the essential oil or placebo on separate occasions, 7 days apart. Cognitive function was assessed using a selection of computerized memory and attention tasks and the Cognitive Demand Battery before the treatment and 1-h and 4-h post-dose. The essential oil was a potent inhibitor of human acetylcholinesterase (AChE) and consisted almost exclusively of monoterpenoids. Oral consumption lead to improved performance of secondary memory and attention tasks, most notably at the 1-h post-dose testing session, and reduced mental fatigue and increased alertness which were more pronounced 4-h post-dose. These results extend previous observations of improved cognitive performance and mood following AChE inhibitory sage extracts and suggest that the ability of well-tolerated terpenoid-containing extracts to beneficially modulate cholinergic function and cognitive performance deserves further attention.
Monoterpenoid extract of sage (Salvia lavandulaefolia) with cholinesterase inhibiting properties improves cognitive performance and mood in healthy adults
They collected the sweat from 14 white male patients with schizophrenia and 14 comparable patients with ‘organic brain syndromes’ and found they could train rats to reliably distinguish the odours while a human panel of sweat sniffers seemed to be able to do the same.
Seemingly backed up by the nasal ninja skills of two different species, science attempted to determine the source of the ‘schizophrenic odour’.
Two years later researchers from Washington suggested the smell might be triggered by the bacteria Pseudomonas aeruginosa but an investigation found it was no more common in people with schizophrenia than those without the diagnosis.
But just before the end of the 60s, the original research team dropped a scientific bombshell. They claimed to have identified the schizophrenia specific scent and got their results published in glittery headline journalScience.
Using gas chromotography they identified the ‘odorous substance’ as trans-3-methyl-2-hexenoic acid, now known as TMHA.
Looking back, we now know that TMHA is genuinely an important component in sweat odour. Curiously, it turns out it is largely restricted to Caucasian populations but no link to mental illness or psychiatric disorder has ever been confirmed.
The theory seems like an curious anomaly in the history of psychiatry but it occasionally makes a reappearance. In 2005 study claimed that the odour exists but is “complex and cannot be limited to a single compound, but rather to a global variation of the body odor” but no replications or further investigations followed.
A whiff of madness
