Tag: depression

Are cytokines associated with neuropsychiatric syndromes in humans?

Abstract:

Traditional aetiological models in neuropsychiatry have placed little emphasis on the abnormal behavioural responses (decreased psychomotor activity, anorexia, weight loss, decreased social exploration and sexual behaviour, impaired cognitive function and increased somnolence) that are common to both psychiatric syndromes, notably depression, and the illness behaviour of sick animals.

In recent years, the possible role of cytokines, as mediators of not only the immunological and metabolic responses to infection and inflammation but also a co-ordinated behavioural response, has been described. Further, a range of possible mechanisms for these effects has been postulated, notably involving corticotropin releasing factor (CRF) and prostaglandins of the E series (PgE) with the central nervous system (CNS).

Here we outline a series of human clinical conditions where neuropsychiatric syndromes co-occur with a host response to infection or inflammation. These may be characterized by cytokine production (e.g. acute, recurrent and chronic viral illness, systemic autoimmune diseases and chronic fatigue syndrome).

Other clinical situations characterized by exposure to or in vivo production of cytokines (e.g. treatment of chronic infections and malignancies, progression and/or recurrence of malignancies) are also discussed.

We postulate that the stereotyped behavioural repertoire observed is mediated by cytokine-dependent mechanisms within the CNS. Systematic studies of the behavioural responses of such patient groups are suggested, noting specifically correlations between the time course and severity of immune and neuroendocrine and behavioural responses and dose-response effects.

 

Source: Hickie I, Lloyd A. Are cytokines associated with neuropsychiatric syndromes in humans? Int J Immunopharmacol. 1995 Aug;17(8):677-83. http://www.ncbi.nlm.nih.gov/pubmed/8847162

 

Cognitive functioning and magnetic resonance imaging in chronic fatigue

Abstract:

BACKGROUND: This study examines whether cognitive dysfunction in chronic fatigue may be accounted for by depression and anxiety or is due to brain pathology evident on magnetic resonance imaging (MRI).

METHOD: Twenty-six subjects with chronic fatigue, with and without coexisting depression, and 18 age-matched normal controls were recruited from primary care following a presumed viral illness six months previously. Comparison was made with 13 psychiatric controls with depressive illness on standardised cognitive tests. MRI determined the presence of cerebral white-matter lesions.

RESULTS: No substantial differences in performance were shown between subjects with chronic fatigue, most of whom met the criteria for chronic fatigue syndrome, and controls. Subjective cognitive dysfunction increased with psychopathology. White-matter lesions were found in a minority from all groups. Improvement in fatigue and depression coincided with improved performance on cognitive measures.

CONCLUSIONS: Subjective complaints of cognitive impairment are a prominent feature of chronic fatigue, but objective cognitive and MRI abnormalities are not. Such complaints probably reflect psychopathology rather than a post-viral process.

 

Source: Cope H, Pernet A, Kendall B, David A. Cognitive functioning and magnetic resonance imaging in chronic fatigue. Br J Psychiatry. 1995 Jul;167(1):86-94. http://www.ncbi.nlm.nih.gov/pubmed/7551617

 

Chronic fatigue syndrome

Comment on: Chronic fatigue syndrome: a follow up study. [J Neurol Neurosurg Psychiatry. 1994]

 

Chronic fatigue syndrome: a follow up study by Bonner et al’ reported that 47 patients initially diagnosed with “chronic fatigue” were contacted for follow up four years later. The authors indicated that “These patients were initially assessed before the current criteria for chronic fatigue syndrome became available, but most would have satisfied the criteria retrospectively” (p 617). At the outset, all patients were offered cognitive behavioural treatment and some were offered antidepressant medications. Each patient then made a decision to either undergo or decline cognitive behavioural treatment. Four years later, those patients who reported functional improvement were more likely to have elected to receive the cognitive behavioural treatment. Additionally, patients in the group that did not report any functional improvement were more likely to score higher on measures of depression.

The US Centers for Disease Control and Prevention (CDC) case definition,2 the proposed revisions to the CDC case definition,3 and the guidelines for research set forth by Sharpe et al4 were cited, but the researchers did not make it clear as to which criteria were used to diagnose which patients. Thus it is unknown whether uniform criteria were applied to diagnose all patients at the outset. Moreover, the authors did not specify just how many of the initial 47 patients met any of the cited criteria for chronic fatigue syndrome, as opposed to chronic fatigue. In short, they did not differentiate the exact number of chronic fatigue syndrome v chronic fatigue cases.

Only 29 of the original 47 patients (62%) agreed to be interviewed for the follow up. Thus 18 (38%) of the original patients were not included in the outcome data, where 10 subjects reported little or no improvement and 19 subjects reported improvement or recovery. The authors acknowledged that the small patient sample size constituted a methodological shortcoming, but nevertheless concluded “that there is a strong association between successful completion of [cognitive] treatment and the absence of functional disability at the four year follow up” (p 620). They further suggest that costs associated with long term disability could be reduced by the utilisation of cognitive therapy in the treatment of chronic fatigue syndrome. We would like to emphasise that the small patient sample size, together with the lack of availability of almost 40% of the initial patients for interview at follow up, make such conclusions highly inappropriate.

You can read the rest of this comment here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1073573/pdf/jnnpsyc00030-0116.pdf

 

Source: Lipkin DM, Robin R, Vasquez L, Plioplys AV, Plioplys S. Chronic fatigue syndrome. J Neurol Neurosurg Psychiatry. 1995 Jun;58(6):764-5. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1073573/

 

Neuroendocrine assessment of serotonin (5-HT) function in chronic fatigue syndrome

Abstract:

Prolactin and cortisol responses to dl-fenfluramine challenge were examined in 11 patients with chronic fatigue syndrome and in 11 healthy controls who were age and gender matched. After obtaining two baseline samples, each subject was given 60 mg of dl-fenfluramine orally and further blood samples were drawn hourly during the following five hours in order to measure prolactin and cortisol levels. There was no difference in either baseline or fenfluramine-induced hormonal responses between patients with chronic fatigue syndrome and controls. There was also no correlation between depression scores on HAM-D and hormonal responses in patients with chronic fatigue syndrome. The findings of this study do not support a role for 5-HT in chronic fatigue syndrome.

Comment in: Re: Endocrine responses to fenfluramine challenge in chronic fatigue syndrome. [Can J Psychiatry. 1996]

 

Source: Yatham LN, Morehouse RL, Chisholm BT, Haase DA, MacDonald DD, Marrie TJ. Neuroendocrine assessment of serotonin (5-HT) function in chronic fatigue syndrome. Can J Psychiatry. 1995 Mar;40(2):93-6. http://www.ncbi.nlm.nih.gov/pubmed/7788624

 

Frequency of deviant immunological test values in chronic fatigue syndrome patients

Abstract:

Of 11 immunological tests done on chronic fatigue syndrome patients and on fatigued controls, 3 tests (protein A binding, Raji cell, or C3 or C4 [deviant values in either complement component were counted as positive]) with deviant results discriminated best among the groups. Other tests, including immunoglobulin G subclasses, complement component CH50, interleukin-2, and anticardiolipin antibodies, did not discriminate well among the groups.

 

Source: Natelson BH, Ellis SP, Braonáin PJ, DeLuca J, Tapp WN. Frequency of deviant immunological test values in chronic fatigue syndrome patients. Clin Diagn Lab Immunol. 1995 Mar;2(2):238-40. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC170136/

You can read the full article here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC170136/pdf/020238.pdf

 

Neuropsychological impairments in chronic fatigue syndrome, multiple sclerosis, and depression

Abstract:

To examine the degree and nature of cognitive impairments in chronic fatigue syndrome, a comprehensive neuropsychological battery was given to patients with chronic fatigue syndrome, multiple sclerosis, depressed patients, and healthy controls. The battery included tests of attention and concentration, information processing speed, verbal and visual memory, intellectual ability, and concept formation. Measures of depression and anxiety were also obtained.

The chronic fatigue syndrome group did not differ from the depressed group in overall neuropsychological performance, but differed from the multiple sclerosis and control groups. The most significant impairment was in information processing speed in the chronic fatigue syndrome group. Depression and anxiety were not related to neuropsychological performance. The influence of reduced information processing on other areas of cognition is discussed.

 

Source: DeLuca J, Johnson SK, Beldowicz D, Natelson BH. Neuropsychological impairments in chronic fatigue syndrome, multiple sclerosis, and depression. J Neurol Neurosurg Psychiatry. 1995 Jan;58(1):38-43. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1073266/ (Full article)

 

Correlates of somatic causal attributions in primary care patients with fatigue

Abstract:

Researchers in the field of chronic fatigue in tertiary care found that patients’ somatic (e.g. viral) explanations for their condition may lead to chronicity of symptoms. We studied the influence of a somatic attributional bias on outcome and reported symptoms in primary care patients with fatigue.

We compared fatigue scores on a specific scale, and number of presented symptoms, in two groups of primary care patients with ‘functional’ fatigue: 75 with a high score on the somatic subscale of the Fatigue Attribution Scale (S-FAS), and 95 with a low score on the S-FAS. At the index visit, patients with low and high scores on the S-FAS were not different for age, sex, fatigue scores, and levels of depressive symptoms.

Patients with high scores on the S-FAS presented significantly more somatic and psychological symptoms-a total of 36 symptoms for 24 patients (25.3%) in the low-score group, and a total of 52 symptoms for 31 patients (41.3%) in the high-score group.

Forty-two days later, at the follow-up visit, the fatigue scores were similar in both groups. In primary care patients with fatigue not due to somatic illness or major depression, the tendency to attribute fatigue to somatic causes is not associated with a worse outcome, but with a higher number of reported symptoms.

 

Source: Cathébras P, Jacquin L, le Gal M, Fayol C, Bouchou K, Rousset H. Correlates of somatic causal attributions in primary care patients with fatigue. Psychother Psychosom. 1995;63(3-4):174-80. http://www.ncbi.nlm.nih.gov/pubmed/7624463

 

Psychobehavioral and immunological characteristics of adult people with chronic fatigue and patients with chronic fatigue syndrome

Abstract:

The psychobehavioral responses and cellular immune function were investigated in healthy people (control, N = 21), adult people with chronic fatigue (fatigue-non-CFS group, N = 24), and patients with chronic fatigue syndrome (CFS, N = 10).

Based on psychobehavioral responses, the fatigue-non-CFS group had low general activity levels (p < .05) and slightly depressive tendencies (p < .01) compared with the control. They had many life event stresses (p < .05) and sleep disturbances (p < .01), and they could not cope appropriately with stresses.

The fatigue-non-CFS group also showed significantly lower natural killer (NK) cell activity (p < .01) and decreased numbers of CD16+ and CD56+ cells (p < .05). Compared with the fatigue-non-CFS group, patients with CFS had higher degrees of physical fatigue (p < .01) and more life event stresses (p < .05).

They had lower general activity levels and social introversion. They were also in a depressive state. NK cell activity and the numbers of CD16+ and CD56+ cells were significantly reduced in patients with CFS (p < .01).

These findings suggest that adult people with chronic fatigue may be in an intermediate state between the healthy control and patients with CFS in terms of psychobehavioral responses and low NK cell activity. We observed three cases in such an intermediate state in whom CFS subsequently developed.

 

Source: Masuda A, Nozoe SI, Matsuyama T, Tanaka H. Psychobehavioral and immunological characteristics of adult people with chronic fatigue and patients with chronic fatigue syndrome. Psychosom Med. 1994 Nov-Dec;56(6):512-8. http://www.ncbi.nlm.nih.gov/pubmed/7871106

 

Epidemiologic study of chronic fatigue in primary care (general practice)

Abstract:

The results of a cross sectional study of fatigue in two large samples of patients attending primary care physicians are reported. The level of complaint of fatigue was higher in the prospective sample, which consisted of patients who had been diagnosed as suffering from a viral infection six months earlier. Duration and frequency of experience of fatigue correlated with severity in both samples. Severity, duration and frequency were continuously distributed in these populations.

Attribution of fatigue in these two samples was mixed: social stresses, current physical illness and psychological problems all being offered as explanations. 11% of the cross sectional sample and 17% of the prospective sample met study operational criteria for a possible chronic fatigue state. These patients were assessed in greater detail. The majority had a diagnosable psychiatric disorder, predominantly depression. Physical illnesses were not adequate to explain these fatigue states.

These studies in primary care do not support a clinical entity of a “chronic fatigue syndrome”. Some patients in primary care settings have complaints of fatigue that are both disabling and long lasting, but they do not form a distinct group although the majority are likely however to be suffering from a concurrent psychiatric disorder. In contrast to similar patients with chronic fatigue syndromes attending hospital clinics, primary care patients with complaints of fatigue are much more varied in their ideas of causation with considerable less evidence of disease conviction.

 

Source: Mann AH, Mc Donald E, Cope H, Pelosi A, David A. Epidemiologic study of chronic fatigue in primary care (general practice). Encephale. 1994 Nov;20 Spec No 3:575-9. [Article in French] http://www.ncbi.nlm.nih.gov/pubmed/7843054

 

Stealth viruses as neuropathogens

Abstract:

Neuropsychiatric diseases viewed as multifaceted expression of a dysfunctional brain in which atypical responses are evoked by various sensory inputs. Disease entities have traditionally been classified according to the predominant manifestation ( ) without regard to the overlapping features of many of the diseases (+/-). Thus, mild to moderate pain, mood, cognitive, and neurosomatic symptoms are frequently present in chronic fatigue syndrome (CFS) patients. Fibromyalgia syndrome (FMS) is listed as an example of a predominantly chronic pain syndrome. Affect (mood) disorders include depression (Depress.), anxiety, panic reactions, blunted affect, mania, etc. Schizophrenia (Schizo.) is listed as an example of a major cognitive psychosis. Autism as well as various forms of dementia would be included in this category. Irritable bowel syndrome (IBS) is an example of a neurosomatic disease.

 

Source: Martin WJ. Stealth viruses as neuropathogens. CAP Today. 1994 Oct;8(10):67-70. http://www.ncbi.nlm.nih.gov/pubmed/10150189