PubMed Health⌕ Search

Biomedical subjects

R C van der Mast

Publications and source records attributed to R C van der Mast.

At least 19 recordsLinked to original sources
PubMed2006

[The relationship between atherosclerosis, cognitive impairment, and depression in old age].

It has been suggested in the literature that atherosclerosis is a common causal pathway of cognitive impairment and late-onset depression, which may explain their co-occurrence in old age. In both the 'Leiden 85-plus Study' and the literature, strong evidence is found for a causal relationship between atherosclerosis and cognitive impairment, but there is less evidence for a causal relationship between atherosclerosis and late-onset depression. In the 'Leiden 85-plus Study', cognitive impairment was a risk factor for the development of late-onset depression, but depression in old age did not predict cognitive decline. This means that the prevention of atherosclerosis might prevent cognitive impairment and hence late-onset depression in old age.

Aged↗
PubMed2006

[Unexplained physical symptoms: a widespread problem but still low-profile in training programs and guidelines].

Unexplained physical symptoms or functional somatic syndromes that cannot be explained in terms of a defined medical disease are common. If persistent, they can cause significant distress and disability, and lead to absenteeism and social isolation as well as major health-care costs. Unexplained physical symptoms form a spectrum from transient unexplained mild physical symptoms to chronic severe somatoform disorders. Various functional somatic syndromes overlap one another substantially in symptomatology and are often resistant to conventional medical therapy. The 'Vereniging Nederlands Tijdschrift voor Geneeskunde' (Dutch Journal of Medicine Association) recently held a special conference on unexplained physical symptoms. The conclusions were: (a) patients are reluctant to accept the diagnosis of unexplained physical symptoms, because physicians do not have sufficient knowledge, expertise, and skill to diagnose and treat them, (b) patients with unexplained physical symptoms do not necessarily need to be treated by a psychiatrist except in cases of chronic and serious somatoform disorder. Patients with unexplained physical symptoms, who often have multiple and complex problems, are best treated by a team of physicians and allied paramedical professionals; (c) patients with unexplained physical symptoms can be treated effectively by specialists using cognitive behaviour therapy. Different cognitive models are available; the 're-attribution model' focuses on the re-establishment of a liveable life, while 'the consequence model' is directed at reducing the consequences of the unexplained physical symptoms. Management using the attribution model may be followed up by the consequence model approach; (d) the development of a practice guideline for the diagnosis and treatment of patients with both acute and chronic unexplained physical symptoms would improve the quality of patient care, reduce disability, increase the possibility of reintegration, and stimulate scientific research; (e) both theoretical and practical training in the diagnosing and managing of unexplained physical symptoms is inadequate in both university curriculums and postgraduate training programmes for medical specialists. Scientific research for the development of an evidence-based practice guideline is urgently needed.

Cognitive Behavioral Therapy↗
PubMed2006

Progression of cerebral white matter lesions is not associated with development of depressive symptoms in elderly subjects at risk of cardiovascular disease: The PROSPER Study.

BACKGROUND: Cerebral white matter hyperintensities on magnetic resonance imaging (MRI) scans have been associated with vascular disease and late-life depression, both in the general population and in psychiatric patients. Therefore, a cerebrovascular etiology for late-onset depression has been hypothesized. However, longitudinal studies on the causal role of white matter hyperintensities in the development of depressive symptoms in elderly adults are lacking. OBJECTIVE: To investigate the relation between white matter hyperintensities and depressive symptoms in elderly subjects at risk of cardiovascular disease. METHODS: In the Dutch sample of the PROSPER (PROspective Study of Pravastatine in the Elderly at Risk of cardiovascular disease) cohort, 527 non-demented elderly, all aged 70 years or older, received a cranial MRI scan and the 15-item Geriatric Depression Scale, at baseline and 33 months (SD 1.6) later. RESULTS: Presence of white matter hyperintensities at baseline was not related to baseline depressive symptoms nor to the development of depressive symptoms during follow-up. Moreover, no association was found between progression of white matter lesion volume and progression of depressive symptoms. CONCLUSION: This longitudinal study does not confirm the involvement of cerebrovascular disease expressed as MRI white matter hyperintensities in the development of depressive symptoms in elderly subjects.

Aged↗
PubMed2006

[Diagnosing frontotemporal dementia, a chameleon in psychiatry].

BACKGROUND: Frontotemporal dementia (FTD) generally has a presenile onset, behavioural problems dominate the clinical picture and cognitive functions are still relatively intact. Therefore particularly in the early stages of FTD it is difficult to differentiate this type of dementia from other types of dementia and psychiatric disorders. AIM: To review the options currently available for diagnosing FTD and to evaluate their significance for clinical practice. METHOD: A literature search via PubMed, Embase and the Cochrane Library (1999-2005) using the key words 'frontotemporal dementia' and 'diagnosis' or 'differential diagnosis'. Genetic and post-mortem studies were excluded. RESULTS: The selected literature concerned differential clinical symptoms, neuropsychological research and questionnaires, neuroimaging and fluid abnormalities and dealt mainly with the difference between FTD and other types of dementia but not with differences between FTD and psychiatric disorders. CONCLUSION: Measuring instruments that are helpful for diagnosing FTD are the Manchester Behavioural Questionnaire, the Frontal Behaviour Inventory and the Frontal Assessment Battery. Even better indicators of FTD are asymmetrical frontotemporal structural abnormalities in a CT- or MRI-scan and a decrease infrontal metabolism and perfusion in a PET- or SPECT-scan, although not all detected abnormalities are specific for FTD. Whatever the method used, early diagnosis is difficult; the sensitivity of nearly all diagnostic methods increases as the illness progresses. On the basis of this review of the literature some diagnostic techniques are recommended that can be applied if FTD is suspected.

Decision Making↗
PubMed2005

[Electroconvulsive therapy in patients with Huntington's disease and depression].

Two patients, a 50-year-old man and a 51-year-old woman, with genetically confirmed Huntington's disease (HD) were admitted to a psychiatric department because of therapy-resistant major depression. Both patients were successfully treated with electroconvulsive therapy (ECT). The lifetime prevalence of depression in HD patients is high and, together with movement and cognitive disturbances, causes a heavy disease burden for patients and their families. ECT is an effective and relatively fast antidepressive treatment. Although ECT use has been reported in only 11 depressive HD patients in the literature, in our opinion it is an adequate antidepressive treatment that should be considered before further drug treatment for patients who are substantially limited in their daily functioning.

Depressive Disorder↗
PubMed2005

Generalized atherosclerosis, cognitive decline, and depressive symptoms in old age.

BACKGROUND: Atherosclerosis may be linked to cognitive decline and depression in old age. METHODS: The Leiden 85-Plus Study is a prospective population-based study of 599 subjects from age 85 onward. The generalized atherosclerotic burden was rated by the number of cardiovascular pathologies at baseline, as assessed by history taking from treating physicians and EKG. Cardiovascular pathologies included myocardial infarction, angina pectoris or myocardial ischemia, claudicatio intermittens, and arterial surgery. Global cognitive function (Mini-Mental State Examination), attention (Stroop Test), processing speed (Letter Digit Coding Test), immediate recall memory (Word Learning Test-Immediate Recall), delayed recall memory (Word Learning Test-Delayed Recall), and depressive symptoms (15-item Geriatric Depression Scale) were assessed each year from ages 85 through 90. The prospective associations between both the generalized atherosclerosis rating and stroke with cognitive function and depressive symptoms were analyzed by linear mixed models adjusted for sex and level of education. RESULTS: During follow-up, there was a significant cognitive decline and a significant increase of depressive symptoms. At baseline, a history of stroke was correlated with lower global cognitive function, slower processing speed, impaired immediate and delayed recall memory, and more depressive symptoms. In addition, a higher generalized atherosclerosis rating was correlated with impaired global cognitive function, lower attention, and a slower processing speed at baseline. During follow-up, a higher generalized atherosclerosis rating was associated with an accelerated decline of immediate recall memory and delayed recall memory. In contrast, there was no relation between the generalized atherosclerosis rating and depressive symptoms, either in the cross-sectional analysis or in the prospective analysis. CONCLUSION: In the population at large, generalized atherosclerosis contributes to cognitive decline in old age but not to depression.

Aged, 80 and over↗
PubMed2005

[Guideline 'Delirium'].

The Dutch Association of Psychiatry, together with the Dutch Association of Clinical Geriatrics and with methodological support from the Dutch Institute for Healthcare Improvement (CBO) has developed a guideline for the optimal diagnosis, treatment and prevention of delirium. Delirium is caused by somatic illness or the use of medication, drugs or alcohol. Delirium is common among the somatically ill admitted to a general hospital and is associated with increased morbidity and mortality. Important predisposing factors for delirium are: age > or =70 years, cognitive disturbances, sensory impairments, problems in daily activities, and the use of alcohol and opiates. Precipitating factors that may provoke delirium are: infection, fever, dehydration, serum electrolyte imbalance, polypharmacy, and the use of psychotropic medication, particularly anticholinergic drugs. Detection, diagnosis, and assessment of the severity of delirium are based on clinical examination, case history, observation, mental status examination including tests of cognitive function, and diagnosis of underlying somatic diseases. For daily practice, measurement tools are not necessary, nor are laboratory or imaging tests, such as electroencephalography. Haloperidol is the treatment of first choice for delirium due to somatic illness, except in patients with delirium due to drug use or medication, Parkinson's disease or Lewy body dementia. In cases of concurrent alcohol withdrawal syndrome, delirium may be treated with haloperidol and a benzodiazepine and B-vitamins. Medical and environmental interventions have been shown to reduce the incidence and duration of delirium.

Aged↗
PubMed2005

Clinical subtypes of delirium and their relevance for daily clinical practice: a systematic review.

BACKGROUND: Delirium is a disorder that besides four essential features consists of different combinations of symptoms. We reviewed the clinical classification of clusters of symptoms in two or three delirium subtypes. The possible implications of this subtype classification may be several. The investigation and exploration of clinical subtypes of delirium may provide information concerning the etiology, the pathogenesis, and the prognosis of delirium, but also may have therapeutic consequences. METHODS: We searched several database for English-language articles. Selected articles were cross-checked for other relevant publications. DATA SYNTHESIS AND CONCLUSION: We conducted a systematic review and retrieved ten clinical studies. The studies described in this review show different results, partly due to methodological problems and possibly by lack of a standard classification for delirium subtypes. According to the present literature a useful and reproducible method to classify (patterns of) symptoms in delirium subtypes seems to be the general rating of and division in to psychomotor subtypes. The Memorial Delirium Assessment Scale (MDAS) and the Dublin Delirium Assessment Scale (DAS) appear to be reliable methods, together with the new version of the Delirium Rating Scale (DRS-R-98).

Aged↗
PubMed2003

[The Dutch College of General Practitioners' practice guideline 'Delirium in elderly people'; response from psychiatry].

Delirium is a common psychiatric illness among the medically ill and is associated with significant morbidity and mortality. Although delirium may develop at any age, the elderly are particularly vulnerable. Since the number of elderly with chronic diseases, dementia, sensory handicaps and the use of several (anticholinergic) medications--all predisposing factors for delirium--is rising, it is essential that general practitioners can recognise, adequately diagnose and treat delirium. This guideline may aid the general practitioner in diagnosing and treating this generally underestimated psychiatric disturbance in somatically ill elderly patients. Evidence on clinical features, differential diagnosis, prevalence, course, aetiology, and risk factors for delirium in primary care is lacking. In general hospitals, the prevalence of delirium in the elderly is about 10-40%; it is probably much less in primary care. This guideline does not provide an adequate description of the clinical presentations of delirium, and does not sufficiently stress the importance of recognising any new behavioural problem in an elderly patient as an indication of possible delirium.

Aged↗
PubMed2002

[Depressive patients who don't recover].

Three patients, two men aged 43 and 53 years, respectively, and one woman aged 40 years, remained depressed despite years of medicinal therapy and counselling, although some improvement was eventually achieved in the woman. Although in general, depression can be treated successfully, in clinical practice many patients experience only limited improvement. It is important to follow through all the steps of the guidelines for treatment of depression and to continue psychiatric management and care in these kind of situations.

Adult↗
PubMed2001

ECT in mental retardation: a review.

The use of electroconvulsive therapy (ECT) in patients with mental retardation and a psychiatric disorder seems to be infrequent, and controlled studies are not available. We reviewed the literature on the use of ECT in mental retardation, using Medline, Embase, and the Cochrane Library. References were checked and ECT experts consulted. The reported case studies were examined on patients' characteristics and illness, treatment, and outcome variables. Forty-four patients, mostly with a diagnosis of psychotic depression, were found. In 84% (n = 37) of them, ECT was effective and without important side effects. However, relapse occurred frequently, in 48% (n = 21) of the patients. In 16% (n = 7), side effects and/or no improvement were noted. The reported case studies suggest that ECT may be of value in treating severe psychiatric disorders in mentally retarded patients, with similar indications as in general psychiatry. However, the lack of strong scientific evidence, besides complicated psychiatric assessment as well as ethical and legal issues, probably cause an unnecessarily limited use of ECT in these patients. Further controlled trails are needed to firmly establish the efficacy and safety of ECT in mental retardation.

Adolescent↗
PubMed2000

[Delirium? Admission to the general hospital, rather than a psychiatric hospital].

Delirium is often not recognized either by psychiatrists or by other physicians. In two men, aged 78 and 70 years, a diagnosis of delirium was not recognized at admission. The first patient had Alzheimer's disease with superimposed delirium caused by pulmonary embolism, which led to cardiopulmonary arrest during his stay in a psychiatric hospital. The other patient had a delirium due to multiple somatic causes (carbon monoxide poisoning with cerebral damage, pulmonary infection, heart attack) which was not recognized leading to an early discharge from the general hospital. The first patient died later on because of complications of a pneumonia and the other patient was transferred to a nursing home on a maintenance dose of haloperidol. Since delirium is a symptom of a medical disorder, delirious patients should be referred primarily to a general hospital.

Aged↗
PubMed2000

Is delirium after cardiac surgery related to plasma amino acids and physical condition?

The authors studied interrelationships between plasma levels of amino acids, physical condition (as apparent from cortisol, albumin, and thyroid hormone concentrations), and postoperative delirium in 296 patients undergoing elective cardiac surgery. Both plasma tryptophan (Trp) and ratio of Trp to the other large neutral amino acids (oLNAA) were reduced in delirious patients compared with control patients. The lower availability of Trp for the brain in delirious patients may lead to decreased serotonergic function. Besides, the ratio of phenylalanine (Phe) to the oLNAA was increased in delirium, which may result in a higher synthesis of cerebral dopamine and norepinephrine. Delirious patients were also in poorer physical condition than nondelirious patients, having decreased albumin level and increased ratio of inactive reverse triiodothyronine (T3) to active T3. Decreased Trp and increased Phe availability may give rise to an imbalance in cerebral neurotransmitters and thus contribute to delirium.

Adult↗
PubMed2000

Serotonin and amino acids: partners in delirium pathophysiology?

Delirium may be the result of dysfunction of multiple interacting neurotransmitter systems. Changes in the levels of various amino acids being precursors of cerebral neurotransmitters may affect their function and, thus, contribute to the development of delirium. Serotonin is one of the neurotransmitters that may play an important role in medical and surgical delirium. Normal serotonin synthesis and release in the human brain is, among others, dependent on the availability of its precursor tryptophan (Trp) from blood. The essential amino acid Trp competes with the other large neutral amino acids (LNAA) tyrosine, phenylalanine, valine, leucine, and isoleucine for transport across the blood-brain barrier. This competition determines its uptake into the brain, represented by the ratio of the plasma level of Trp to the sum of the other LNAA. The plasma ratio of Trp/LNAA, plasma level of Trp, and serotonin in plasma and platelets have been used as indirect peripheral measures for central serotonergic functioning. Both increased and decreased serotonergic activity have been associated with delirium. Serotonin agonists can induce psychosis, both elevated Trp availability and increased cerebral serotonin have been associated with hepatic encephalopathy, and excess serotonergic brain activity has been related to the development of the serotonin syndrome of which delirium is a main symptom. On the other hand, alcohol withdrawal delirium, delirium in levodopa-treated Parkinson patients, and postoperative delirium have been related to reduce cerebral Trp availability from plasma suggesting diminished serotonergic function. Rick factors for delirium such as severe illness, surgery, and trauma can induce immune activation and a physical stress response comprising increased activity of the limbic-hypothalamic-pituitary-adrenocortical axis, the occurrence of a low T3 syndrome, and, possibly, changes in the permeability of the blood-brain barrier. There are indications that these changes have their effect on plasma amino acid concentrations, e.g., Trp, and multiple cerebral neurotransmitters, including serotonin. This stress response may be different depending on the stage of illness being acute or chronic. It will require further study to determine the complex influence of the stress response and immune activation on plasma amino acids, neurotransmitter function and the development of delirium, especially in the more vulnerable older patients.

Aged↗
PubMed1999

Incidence of and preoperative predictors for delirium after cardiac surgery.

Incidence of and preoperative predictors for postoperative delirium were studied in 296 patients (age 26-83 years, mean age 63 years) undergoing elective cardiac surgery. Delirium occurred in 40 (13.5%) patients. Predictors included old age, low level of albumin, poor physical condition, use of nifedipine, and a high ratio of the amino acids phenylalanine to the sum of isoleucine, leucine, valine, tyrosine, and tryptophan. These findings suggest that preoperative physical condition and amino acid disturbances may be related to delirium after cardiac surgery in the elderly.

Adult↗
PubMed1998

Mood correlates with blood serotonin, but not with glucose measures in patients with recurrent suicidal behavior.

Depressive mood and impulsive-aggressive behavior are relevant to suicidal behavior and have been associated with decreased central serotonergic function. Impulsive behavior and aggression have also been related to abnormal glucose metabolism. To investigate these relationships further, blood serotonin (5-HT), blood glucose measures (glycated hemoglobin (HbA1C) and fructosamine) and self-reported depressive symptoms and anger were repeatedly measured, during a 1-year follow-up, in 106 patients who had recently attempted suicide for at least a second time. A major DSM-III-R Axis I diagnosis or use of antidepressants were reasons for exclusion. Intra-individual variations in blood 5-HT were inversely correlated with variations in depressive mood, self-depreciation, and anger, and positively with variations in fructosamine. Intra-individual variations of HbA1c or fructosamine were not correlated with mood. Mean blood 5-HT levels per patient were positively correlated with mean scores of depression and self-depreciation. The contrast between the intra-individual and the inter-individual correlations may reflect a difference between short- vs. long-term effects. The results do support an association between serotonergic function and mood, but not between glucose metabolism and mood, in recurrent suicide attempters.

Adolescent↗
PubMed1998

Pathophysiology of delirium.

Hypotheses about the pathophysiology of delirium are speculative and largely based on animal research. According to the neurotransmitter hypothesis, decreased oxidative metabolism in the brain causes cerebral dysfunction due to abnormalities of various neurotransmitter systems. Reduced cholinergic function, excess release of dopamine, norepinephrine, and glutamate, and both decreased and increased serotonergic and gamma-aminobutyric acid activity may underlie the different symptoms and clinical presentations of delirium. According to the inflammatory hypothesis, increased cerebral secretion of cytokines due to a wide range of physically stressful events plays an important role in the occurrence of delirium. Since cytokines can influence the activity of various neurotransmitter systems, these mechanisms may interact. Also, more fundamental processes like intraneuronal signal transduction, second messenger systems that at the same time use neurotransmitters as first messengers and play an important role in their synthesis and release, may be disturbed. Furthermore, severe illness and physiologic stress may give rise to modification of blood-brain barrier permeability, the sick euthyroid syndrome with abnormalities of thyroid hormone concentrations, and increased activity of the hypothalamic-pituitary-adrenal axis. These circumstances possibly also contribute to changes in neurotransmitter synthesis and release of cytokines in the brain, and consequently to the occurrence of delirium. Elderly patients are more at risk for developing delirium,very likely due to age-related cerebral changes in stress-regulating neurotransmitter and intracellular signal transduction systems. This paper will expand upon these current theories and discuss their applicability to research and clinical work with elderly patients suffering from delirium.

Aged↗