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P300 and executive function alterations: possible links in a case of Morgagni-Stewart-Morel syndrome.

To evaluate possible cause-effect relationships between hyperostosis frontalis interna and cognitive dysfunction, we performed a neurophysiological (event-related potentials, ERPs) and neuropsychological study in a case of Morgagni-Stewart-Morel (MSM) syndrome associated with frontal lobe compression. Neuropsychological evaluation evidenced selective impairment of executive function. Visual and auditory oddball ERPs revealed delayed P300 latency and reduced auditory P300 amplitude with multi-peaked morphology. ERP abnormalities and cognitive dysfunction could be due to the frontal bone-cortex conflict documented by neuroradiological investigations.

Cognition Disorders↗

NT-1, an active constituent extracted from Tiaoxin Recipe, enhances long-term potentiation of CA1 subfield in rat hippocampal slices.

Previous studies demonstrated that Tiaoxin Recipe (TXR), a traditional Chinese medicinal prescription, could alleviate cognitive dysfunction. NT-1, an active constituent isolated from this prescription under guidance of bioactive evaluation, was preliminarily proved to enhance the ability of spatial learning and memory in rats. In the present study, using hippocampal slice preparations, we investigated the mechanisms by which NT-1 improves cognitive dysfunction contributed to corticosterone (CORT). NT-1 ameliorated the inhibition of LTP by CORT more significantly than TXR did. These results suggested that enhancing LTP induction is one mechanism by which NT-1 improves spatial learning and memory impaired by CORT.

Animals↗

Awareness of involuntary movements in Huntington disease.

OBJECTIVE: To determine why patients with Huntington disease are apparently unaware of their involuntary movements. DESIGN: Correlative study using a subjective report questionnaire of physical symptoms and objective measures of neurologic and cognitive dysfunction. PATIENTS: Forty patients with Huntington disease attending a regional Huntington disease clinic. RESULTS: Patients were poor at reporting experiential symptoms of involuntary movements. There was no relationship between self-report of these symptoms and objective indices of motor dysfunction or severity of cognitive impairment. Patients could, however, report secondary consequences of their movement disorder, which correlated highly with nonchoreic indices of motor dysfunction. CONCLUSIONS: Patients with Huntington disease have impaired subjective experience of chorea. Denial of symptoms is likely to have a physiological basis and is not a secondary consequence of patients' cognitive impairment or a psychological defense against a debilitating disease.

Adaptation, Psychological↗

Operant-behavioural and cognitive-behavioural treatment for chronic low back pain.

Fifty-eight outpatients with chronic low back pain were randomly allocated to one of six experimental conditions. Four conditions were designated as treatment conditions and two as control conditions. The four treatment groups consisted of: cognitive treatment (either with or without relaxation training) and behavioural treatment (either with or without relaxation training). The cognitive and behavioural groups also received physiotherapy. The two control conditions consisted of: attention (physiotherapy plus discussion sessions) and no-attention (physiotherapy-only) conditions. All conditions, including the two controls, received the same physiotherapy back-education and exercise program. For the sample as a whole, improvements were obtained on measures of affective distress, functional impairment, medication use, pain-related dysfunctional cognitions and use of active coping strategies. These improvements were generally maintained at 6- and 12-month follow-ups. The combined psychological/physiotherapy treatment conditions improved significantly more than the physiotherapy-only conditions from pre to posttreatment on measures of pain intensity, self-rated functional impairment and pain-related dysfunctional cognitions. However, these differences were only weakly maintained at 6- and 12-month follow-ups. The behavioural conditions improved significantly more than the cognitive conditions from pre to posttreatment on the self-rated measure of functional impairment, but this difference was not maintained at 6- and 12-month follow-ups. Progressive relaxation training was found to make little contribution to either cognitive or behavioural treatments.

Adult↗

Cognitive and mood disturbance as causes and symptoms of fatigue in cancer patients.

Fatigue, cognitive dysfunction, and depression are very common in cancer patients. A relationship among the three entities is recognized but poorly understood. Factors that contribute to this poor understanding are the subjective nature of the symptoms, multiple potential causes, and a lack of reliable assessment tools. An understanding of fatigue in cancer patients may benefit from studies of chronic fatigue syndrome (CFS) and other nonmalignant diseases indicating that cognitive impairment varies with physical and mental fatigue, and that symptoms of depression experienced by patients with physical illnesses and primary mood disorders are qualitatively different. The multidimensional nature of fatigue suggests that interventions should be patient-specific. They could be related to lifestyle or involve the use of specific behavioral or pharmacologic therapies. As is the case with depression and cognitive disorders, targeted interventions against cancer-related fatigue will benefit from a better understanding of its potential biologic causes. Consideration of cognitive dysfunction and depression complicates the understanding of cancer-related fatigue; however, it provides opportunities to assist patients who must deal with this serious problem.

Cognition Disorders↗

[Event related potentials and neuropsychological studies in sleep apnea patients].

Patients with obstructive sleep apnoea syndrome (OSAS) commonly complain about daytime sleepiness and a decline of cognitive functions. Several diagnostic tools have been established to judge objectively vigilance and cognitive impairment. Forty OSAS patients aged between 34 and 74 years were examined via several neuropsychological tests (e.g. vigilance test of the Wiener Testsystem, number connection test ("Zahlenverbindungstest-ZVT") to assess working velocity and information processing, d2-test to rate concentration on exertion) before starting continuous positive airway pressure (CPAP) therapy. In addition, visual evoked event-related potentials (ERPs) were recorded; the P3-component was evaluated. All patients subjectively stated daytime sleepiness and cognitive dysfunctions to variable degrees. Each patient showed at least one pathological result in the neuropsychological tests; vigilance impairment could be revealed only in 7 patients. P3-latencies were increased in OSAS patients when compared to age-matched controls (408.1 +/- 44.4 ms versus 373.4 +/- 32.5 ms; p < 0.03). P3-latencies and concentration on exertion showed a significant correlation with respect to the relative part of the total sleep time in which the patient's oxygen saturation was below 90% (p < 0.05). Thus it could be demonstrated that cognitive deficits in OSAS patients are a result of chronic intermittent oxyhaemoglobin desaturation rather than of a decline in daytime vigilance. ERPs represent an objective neurophysiological tool in neuropsychological examination. As they are also generated in subcortical cerebral structures they may indicate cognitive dysfunctions which cannot be evaluated by neuropsychological tests. If lead of ERPs is possible in special sleep centres they should be additionally used in the assessment of cognitive functions in OSAS patients.

Adult↗

Cognitive impairment, dementia and psychosocial functioning in human immunodeficiency virus infection. A prospective study based on DSM-III-R and ICD-10.

Progressive cognitive impairment in human immunodeficiency virus (HIV) infection, called acquired immunodeficiency syndrome (AIDS) dementia complex (ADC), significantly influences the social prognosis of afflicted patients. The frequency and character in different stages of the infection are controversially discussed. In previous studies, differences in the selection of patients and methods of testing led to widely differing results. For these reasons, in the present prospective study on 45 HIV-infected patients, a structured psychiatric interview (SIDAM) was conducted based on the algorithm of diagnosing dementia in DSM-III-R and the ICD-10 guidelines. The psychopathological findings are expressed in syndrome scores; the results are summarized in a total score (SISCO). The interview contains the Mini-Mental State Examination. The degree of psychosocial functioning was estimated on the global assessment of functioning, Axis V of DSM-III-R. In stages preceding AIDS, only slight cognitive dysfunction was found compared with age- and education-matched normal controls, and this caused no relevant disturbance of psychosocial functioning. In 9 patients with manifest AIDS, dementia was diagnosed with DSM-III-R criteria and ICD-10 guidelines (30% of the AIDS patients). They showed marked impairment of intellectual ability, memory, verbal ability and calculation and constructional ability and fewer cortical focal symptoms (aphasia and apraxia). Corresponding to previous studies, major cognitive dysfunction in HIV infection can be characterized as subcortical dementia.

AIDS Dementia Complex↗

Enhanced emotion-induced amnesia in borderline personality disorder.

BACKGROUND: Current biological concepts of borderline personality disorder (BPD) emphasize the interference of emotional hyperarousal and cognitive functions. A prototypical example is episodic memory. Pre-clinical investigations of emotion-episodic memory interactions have shown specific retrograde and anterograde episodic memory changes in response to emotional stimuli. These changes are amygdala dependent and vary as a function of emotional arousal and valence. METHOD: To determine whether there is amygdala hyper-responsiveness to emotional stimuli as the underlying pathological substrate of cognitive dysfunction in BPD, 16 unmedicated female patients with BPD were tested on the behavioural indices of emotion-induced amnesia and hypermnesia established in 16 healthy controls. RESULTS: BPD patients displayed enhanced retrograde and anterograde amnesia in response to presentation of negative stimuli, while positive stimuli elicited no episodic memory-modulating effects. CONCLUSION: These findings suggest that an amygdala hyper-responsiveness to negative stimuli may serve as a crucial aetiological contributor to emotion-induced cognitive dysfunction in BPD.

Adult↗

Long-lasting impairment of associative learning is correlated with a dysfunction of N-methyl-D-aspartate-extracellular signaling-regulated kinase signaling in mice after withdrawal from repeated administration of phencyclidine.

In humans, the administration of phencyclidine causes schizophrenic-like symptoms that persist for several weeks after withdrawal from phencyclidine use. We demonstrated here that mice pretreated with phencyclidine (10 mg/kg/day s.c. for 14 days) showed an enduring impairment of associative in a Pavlovian fear conditioning 8 days after cessation of phencyclidine treatment. Extracellular signaling-regulated kinase (ERK) was transiently activated in the amygdalae and hippocampi of saline-treated mice after conditioning. In the phencyclidine-treated mice, the basal level of ERK activation was elevated in the hippocampus, whereas the activation was impaired in the amygdala and hippocampus after conditioning. Exogenous N-methyl-D-aspartate (NMDA), glycine, and spermidine-induced ERK activation was not observed in slices of hippocampus and amygdala prepared from phencyclidine-treated mice. Repeated olanzapine (3 mg/kg/day p.o. for 7 days), but not haloperidol (1 mg/kg/day p.o. for 7 days), treatment reversed the impairment of associative learning and of fear conditioning-induced ERK activation in repeated phencyclidine-treated mice. Our findings suggest an involvement of abnormal ERK signaling via NMDA receptors in repeated phencyclidine treatment-induced cognitive dysfunction. Furthermore, our phencyclidine-treated mice would be a useful model for studying the effect of antipsychotics on cognitive dysfunction in schizophrenia.

Amygdala↗

Sleep disordered breathing and cognitive function in a retirement village population.

Sleep disordered breathing (SDB) may be associated with cognitive dysfunction in non-demented elderly people. A random sample of 96 retirement village residents were given both neuropsychological assessment and overnight sleep monitoring with a portable microprocessor based system (Vitalog PMS-8). Respiratory disturbance index (RDI) was calculated as the number of apnoeas and hypopnoeas per hour of sleep. RDI was not associated with 'memory', 'verbal', and 'motor' factors identified from the analysis of cognitive tests, but was associated with the 'cerebral efficiency' factor (R2 = 0.21, p less than 0.0001). Seventy-three subjects had repeat neuropsychological tests, median time to follow-up being 17 months. Baseline RDI did not predict changes in scores on the two factors identified from the second analysis. We conclude that mild to moderate disturbance of breathing during sleep is not associated with cognitive dysfunction in non-demented subjects.

Activities of Daily Living↗

Cognitive findings after transient global amnesia: role of prefrontal cortex.

The aim of this study is to verify, after recovery, the presence of specific patterns of cognitive dysfunctions in Transient Global Amnesia (TGA). Fourteen patients with the diagnosis of TGA were submitted to a battery of neuropsychological tests and compared to a matched control group. We found significant qualitative and quantitative differences between TGA patients and controls in the California Verbal Learning Test (CLVT) and Rey-Osterrieth Complex Figure Test. Our data support the presence of selective cognitive dysfunctions after the clinical recovery. Moreover, for Verbal Fluency, Digit Span Backward, and Number of Clusters in the CVLT short-term memory test, the relation resulted as positively related with the temporal interval from the TGA episode. Reduction of categorical learning, attention, and qualitative alterations of spatial strategy seem to postulate a planning defect due to a prefrontal impairment.

Aged↗

Depressive symptomatology and vital exhaustion are differentially related to behavioral risk factors for coronary artery disease.

OBJECTIVE: This study proposes to assess the differences of two psychosocial risk indicators for coronary artery disease (CAD), ie, depressive symptoms and vital exhaustion. METHOD: In a representative, stratified, nation-wide sample of the population of Hungary over the age of 16 years (N = 12,640), analyses were made of whether those risk indicators were differentially related to several illness behaviors (including history of cardiovascular treatment and cardiovascular sick days), cognitions, mood states, and socioeconomic characteristics that may generally be associated with increased CAD risk. The sample was stratified by age, sex, and composition of the population of all counties in Hungary. RESULTS: Although depressive symptoms and vital exhaustion correlated strongly, there were clear and significant differences in strength of association between depressive symptoms, vital exhaustion and several variables under study. Dysfunctional cognitions, hostility, lack of purpose in life, low perceived self-efficacy, illegal drug use, alcohol and drug abuse, several forms of subjective disability complaints and history of treatment because of congenital disorders, and chronic skin and hematological disorders were more often associated with depressive symptoms, whereas loss of energy, use of stimulants, chest-pain-related disabilities, history of treatment because of cardiovascular disorders, and self-reported cardiovascular sick days were significantly more often associated with vital exhaustion. CONCLUSIONS: Vital exhaustion and depressive symptomatology are differentially associated with relevant external criteria. Vital exhaustion is associated with perceived cardiovascular complaints and history of cardiovascular treatment, whereas depressive symptomatology seems to be more closely connected to disabilities and complaints related to alcohol, drug, and congenital-disorder, and to dysfunctional cognitions and hostility.

Adolescent↗

Psychopathology in medical inpatients and its relationship to length of hospital stay: a pilot study.

A composite screening instrument measuring depression, anxiety, cognitive dysfunction, and pain identified 40 percent of a sample of general medical inpatients (30% of total patients before exclusions) as having significant psychopathology or pain, a reasonable number based on clinical incidence literature. These identified patients' hospital length of stay did not differ from the length of stay for other patients. The screen identified 21 percent as very depressed, 19 percent as very anxious, 15 percent as having cognitive dysfunction, and 11 percent with high pain levels. Depression, anxiety, and pain frequently occurred together. Further study is required to refine the instrument and assess its effectiveness at targeting patients for psychiatric intervention.

Anxiety Disorders↗

Dementia of frontal lobe type in Kennedy's disease.

The pathomorphological correlate of Kennedy's disease (KD) is a degeneration of spinal and bulbar alpha-motor neurons. The disease is caused by a CAG repeat expansion in the first exon of the X-chromosomal androgene receptor gene. Contrary to the common belief that cognitive disorders in motor neuron diseases (MND) are either rare or only mild, there is now an increasing number of case reports on dementia in amyotrophic lateral sclerosis (ALS). In ALS, dementia of the frontal lobe type (frontotemporal dementia, FTD) seems to be the characteristic pattern. However, in KD cognitive dysfunction has not been studied systematically. Here we present a case with clinical characteristics of FTD in a patient with genetically confirmed KD. It remains speculative whether there is an association between KD and FTD comparable to a genetic linkage between ALS and FTD, which has been proposed in recent years. However, we suggest that cognitive dysfunction may be more common in KD than reported until today.

Adult↗

Cognitive and motor dysfunction in Parkinson's disease. Clinical, performance, and computed tomographic correlations.

The neuropathologic and pathophysiological relationship of specific to more generalized cognitive dysfunction in Parkinson's disease (PD) remains incompletely understood. This issue was examined in a study of 39 patients with PD, utilizing standardized clinical measures, computerized neuropsychological tests, and quantitative computed tomography. Disorders of visuospatial discrimination and perceptual-motor function closely paralleled motor scores, suggesting a common neuropathologic basis. Caudate nuclear and mesocortical dopamine depletion play a role in this context. More generalized cognitive dysfunction occurred in older patients with a somewhat longer disease duration, more advanced parkinsonism, and computed tomographic evidence of subcortical and frontal cortical atrophy but without significant cerebral atrophy when compared with age-matched controls. Further prospective clinicopathologic studies will be required to clarify the relative contribution of the primary dopaminergic dysfunction, age-related changes, Alzheimer-type pathologic condition, and other coexisting neurotransmitter deficits to the dementia seen in PD.

Cognition Disorders↗

Cancer as a risk factor for long-term cognitive deficits and dementia.

Previous studies have shown that cancer survivors frequently experience short-term cognitive deficits, but it is unknown how long these deficits last or whether they worsen over time. Using a co-twin control design, the cognitive function of 702 cancer survivors aged 65 years and older was compared with that of their cancer-free twins. Dementia rates were also compared in 486 of the twin pairs discordant for cancer. Cancer survivors overall, as well as individuals who had survived cancer for 5 or more years before cognitive testing, were more likely than their co-twins to have cognitive dysfunction (odds ratio [OR] = 2.10, 95% confidence interval [CI] = 1.36 to 3.24; P<.001; and OR = 2.71, 95% CI = 1.47 to 5.01; P<.001, respectively). Cancer survivors were also twice as likely to be diagnosed with dementia as their co-twins, but this odds ratio did not reach statistical significance (OR = 2.0, 95% CI = 0.86 to 4.67; P = .10). These results suggest that cancer patients are at increased risk for long-term cognitive dysfunction compared with individuals who have never had cancer, even after controlling for the influence of genetic factors and rearing environment.

Aged↗

Relationship of the factor structure of psychopathology in schizophrenia to the timing of initial intervention with antipsychotics.

Timing of intervention with antipsychotic medication may influence long-term outcome in schizophrenia in a manner that is poorly understood. This study evaluated psychopathology, its factor structure, and cognitive dysfunction in older patients with chronic schizophrenia in relation to the intervals from onset of psychosis to initiation of treatment with antipsychotics, and from initiation of antipsychotic treatment to current assessments. The subjects were 129 patients with schizophrenia, many of whom became ill in the preneuroleptic era. Their current psychopathology was assessed using the Positive and Negative Syndrome Scale, and its factor structure examined using principal component analysis. Current general and executive cognitive function was evaluated using the Mini-Mental State Examination and the Executive Interview, respectively. Using multiple regression modelling, increasing duration of initially unmedicated psychosis, but not the much longer duration of subsequently treated illness, was the primary predictor of psychomotor poverty (negative symptoms) but not of reality distortion or disorganisation over the three domains of psychopathology resolved; duration of initially unmedicated psychosis marginally predicted the severity of general, but not of executive, cognitive dysfunction. Delayed intervention with antipsychotics appears associated with poorer long-term course in terms of increased severity of psychopathology in the psychomotor poverty domain.

Aged↗

Behavior problems in geriatric pets.

Aging pets often suffer a decline in cognitive function (eg, memory,learning, perception, awareness) likely associated with age-dependent brain alterations. Clinically, cognitive dysfunction may result in various behavioral signs, including disorientation; forgetting of previously learned behaviors, such as house training; alterations in the manner in which the pet interacts with people or other pets;onset of new fears and anxiety; decreased recognition of people, places, or pets; and other signs of deteriorating memory and learning ability. Many medical problems, including other forms of brain pathologic conditions, can contribute to these signs. The practitioner must first determine the cause of the behavioral signs and then determine an appropriate course of treatment, bearing in mind the constraints of the aging process. A diagnosis of cognitive dysfunction syndrome is made once other medical and behavioral causes are ruled out.

Aging↗