Aging and the rehabilitation of homonymous hemianopia: The efficacy of compensatory eye-movement training techniques and a five-year follow up.

The specificity and effectiveness of eye-movement training to remedy impaired visual exploration and reading with particular consideration of age and co-morbidity was tested in a group of 97 patients with unilateral homonymous hemianopia using a single subject /n-of-1 design. Two groups received either scanning training followed by reading training, or vice versa. The third group acted as a control group and received non-specific detailed advice, followed by training of scanning and reading. Scanning and reading performance was assessed before and after the waiting period, before and after scanning and reading training, and at short-term (11 weeks on average) and long-term follow-up (5 years on average). Improvements after training were practice-dependent and task-specific. Scanning performance improved by ∼40%, reading by ∼45%, and was paralleled by a reduction of subjective complaints. The advice (=control) condition was without effect. All improvements occurred selectively in the training period, not in treatment-free intervals, and persisted in the short- and long-term follow-up over several years. Age had only a minor, although significant effect on improvement in reading after training; co-morbidity had no significant impact on the outcome of training. In conclusion, visual impairments associated with homonymous hemianopia can be successfully and durably reduced by systematic and specific training of compensatory eye-movement strategies. The improvements in compensation strategies were independent of subjects' age and of co-morbidity.

[Disorders of visual perception]. / Störungen der visuellen Wahrnehmung.

Disorders of visual perception are frequent and disabling functional consequences of acquired brain injury (20-40%). They also have adverse effects on the assessment, diagnosis and treatment of other functional disorders. Most frequent are visual field disorders followed by disorders of visual acuity and contrast sensitivity, visual adaptation, color and visual space perception as well as of visual recognition. Multiple visual and/or additional cognitive disorders are most common. The differential diagnosis of cerebral visual disorders and an individually tailored and specific approach in the rehabilitation are therefore of great importance. Compensatory treatment methods are to be preferred because of their efficacy, ecological validity as well as a good cost-benefit ratio.

Cognitive function in acromegaly: description and brain volumetric correlates.

In acromegaly, we reported on increased rates of affective disorders such as dysthymia and depression, as well as structural brain changes. Objective of this study was to determine if cognitive impairments in patients with acromegaly exist and whether such impairments are associated with structural brain alterations defined by magnetic resonance imaging (MRI). In this cross-sectional study, 55 patients with biochemically confirmed acromegaly were enrolled. MRI data were compared with 87 control subjects. Main outcome measures were performance levels in 13 cognitive tests covering the domains of attention, memory and executive function, with performance below the cut-off level of the 16th percentile rated as impaired. In addition, individual global and hippocampal volume changes were defined for each patient in reference to a normative sample. We found that up to 33.3% of the patients were impaired in the attention, up to 24.1% in the memory, and up to 16.7% in the executive function domain. 67.3% of the patients failed to reach the cut-off level in at least one subtest. MRI demonstrated increased global, left and right hippocampal grey matter and white matter, particularly early in the disease course. Rather few positive than expected negative correlations could be established between the hippocampal grey matter gain and cognitive performance. Cognitive dysfunction, particularly attentional deficits, are common in acromegaly, rendering neuropsychological testing essential in the diagnostic work-up.

Cognitive impairment in unipolar depression is persistent and non-specific: further evidence for the final common pathway disorder hypothesis.

BACKGROUND: Cognitive performance is often impaired in depression, and these impairments can persist even after remission from psychopathological symptoms. However, it is still unclear whether cognitive dysfunction is associated with psychopathological symptoms or represents a genuine disorder. This study examined cognitive performance in acute depression, after remission, and 6 months after remission in order to determine the nature and specificity of cognitive dysfunction as well as its relevance for the further course of depression. METHOD: Assessments of cognitive function and psychopathology were carried out on admission and prior to discharge in 53 in-patients with unipolar depression. Twenty patients were retested 6 months after discharge. To correct for practice effects, 13 healthy subjects were included and assessed twice with the same cognitive tests. RESULTS: In acute depression, we found impairments of information processing/attention, memory, and executive functions. Cognitive impairments remained in a high proportion of patients, even after remission of psychopathological symptoms. After correcting for practice effects, a significant improvement was observed only for some tests of executive functioning. Severity of depression was only weakly correlated with one single cognitive measure, indicating that psychopathological and neuropsychological symptoms are dissociable. Furthermore, we found no evidence for specific cognitive dysfunction. CONCLUSIONS: Our results support the hypothesis that cognitive impairments in depression are neither selective nor specific; they have trait-like features and are, therefore, not merely an epiphenomenon of depression. Whether or not cognitive dysfunction is a prognostic marker for the course of depression remains still an open issue.

Progesterone reduces wakefulness in sleep EEG and has no effect on cognition in healthy postmenopausal women.

Sleep is frequently impaired in postmenopausal women. Progesterone prompted benzodiazepine-like effects on sleep EEG in young normal male subjects. Aim of this study was to test if treatment with progesterone improves sleep after menopause. A randomised double blind crossover design study with 2 treatment intervals of 21 days duration separated by a 2 weeks washout was performed. An oral dose of 300 mg micronized progesterone was given each for 21 days. At the beginning and the end of the two intervals a sleep EEG was recorded and cognitive performance was assessed in 10 healthy postmenopausal women (age: 54-70 years). Progesterone treatment led to a decrease of intermittent time spent awake. During the first third of the night rapid eye movement (REM) sleep increased. The spectral analysis of the EEG resulted in no significant differences of the power spectra. Progesterone did not affect cognitive performance. In summary progesterone demonstrated a distinct sleep promoting effect by reduction of time of wake without impairing cognitive functions during daytime. As possible mechanisms of progesterone a GABA-agonistic effect and the regulation of gene expression via the progesterone receptor are discussed. Progesterone might be useful in the treatment of sleep disturbances of postmenopausal women.

The effect of growth hormone substitution on cognitive performance in adult patients with hypopituitarism.

OBJECTIVE: Adult hypopituitary patients with growth hormone deficiency, though on adequate adrenal, thyroid or sex hormone replacement therapy, complain of attention and memory disabilities. During the past years several studies have evidenced that growth hormone (GH) may exert distinctive effects on the central nervous system and induce beneficial effects on psychological capabilities. The aim of our study was to determine whether a long-term replacement therapy of recombinant human growth hormone (rhGH) affects cognitive performance in adults with GH deficiency. DESIGN: A double-blind, randomized placebo controlled trial over 6 months, followed by an open period of 6 months of rhGH treatment. MEASUREMENTS: The assessment of cognitive performance comprised attention, verbal memory and non-verbal intelligence and was examined at baseline (0), at 3, 6, 9, and 12 months. In addition, emotional well-being and energy were assessed using the Nottingham Health Profile self rating questionnaire. PATIENTS: Eighteen hypopituitary patients, mean age 41.6 (range 21-63) years with adult onset GH deficiency were evaluated. Patients were on adequate and stable adrenal, thyroid, gonadal and desmopressin replacement therapy where necessary, but not substituted for GH deficiency. RESULTS: After 3 and 6 months of rhGH treatment in the closed label phase a significant improvement of attentional performance was observed compared to baseline in the rhGH group but not in the placebo group. After 6 months scores of attention were significantly different between rhGH and placebo treatment for the digit cancellation test and marginally different for the trail-making test. In contrast, long-term verbal memory and non-verbal intelligence did not improve compared to baseline during therapy and short-term memory improved both in the GH and the placebo group after 3 and 6 months. This was considered as a placebo or practice effect. In the open-label phase a further improvement of attention was found in the GH group and subsequent treatment with rhGH for 3 and 6 months in the placebo group also significantly improved attentional performance supporting the results of the rhGH group in the first 6 months of the double-blind phase. CONCLUSION: RhGH treatment appears to have a beneficial effect on attentional performance in adult hypopituitary patients with GH deficiency when treated for at least 3 months. Our study does not support a role for GH in influencing verbal memory or non-verbal intelligence.

Impaired divided attention predicts delayed response and risk to relapse in subjects with depressive disorders.

BACKGROUND: This study addresses the complex relationship between cognitive function and the course of depression. METHOD: A sample of patients (n=73) in a depressive episode (major depression or bipolar disorder) was tested with a comprehensive battery of attention and executive tasks at both admission and discharge. In addition, response to pharmacological treatment and remission was assessed with standardized rating scales. Nineteen patients, recovered from depression, were re-investigated 6 months after discharge to determine whether specific cognitive parameters were related to subsequent relapse. RESULTS: On admission, patients were impaired in almost all cognitive tasks. At discharge, we found a significant reduction in psychopathology, but only marginal cognitive improvements. Non-responders after 4 weeks of antidepressive medication and subjects who did not achieve remission prior to discharge were specifically impaired in divided attention on admission (p < 0.05). In addition, a trend was found for the association between impaired divided attention at discharge and an elevated risk to relapse (p < 0.10). CONCLUSIONS: We observed generalized cognitive impairment in most cognitive domains in acute depression. Cognitive impairments were still within abnormal ranges at discharge but less distinct. Divided attention performance predicted response to treatment, remission of symptoms, and risk to relapse. Impaired divided attention capacity can be explained either by reduced attentional resources or impaired activation and/or top-down control of attentional resources by the central executive.

A neurodynamical model of visual attention: feedback enhancement of spatial resolution in a hierarchical system.

Human beings have the capacity to recognize objects in natural visual scenes with high efficiency despite the complexity of such scenes, which usually contain multiple objects. One possible mechanism for dealing with this problem is selective attention. Psychophysical evidence strongly suggests that selective attention can enhance the spatial resolution in the input region corresponding to the focus of attention. In this work we adopt a computational neuroscience perspective to analyze the attentional enhancement of spatial resolution in the area containing the objects of interest. We extend and apply the computational model of Deco and Schürmann (2000), which consists of several modules with feedforward and feedback interconnections describing the mutual links between different areas of the visual cortex. Each module analyses the visual input with different spatial resolution and can be thought of as a hierarchical predictor at a given level of resolution. Moreover, each hierarchical predictor has a submodule that consists of a group of neurons performing a biologically based 2D Gabor wavelet transformation at a given resolution level. The attention control decides in which local regions the spatial resolution should be enhanced in a serial fashion. In this sense, the scene is first analyzed at a coarse resolution level, and the focus of attention enhances iteratively the resolution at the location of an object until the object is identified. We propose and simulate new psychophysical experiments where the effect of the attentional enhancement of spatial resolution can be demonstrated by predicting different reaction time profiles in visual search experiments where the target and distractors are defined at different levels of resolution.

Can a motion-blind patient reach for moving objects?

It has been claimed that the visual brain is organized in two separate processing streams for spatial vision: one for perception and one for action. To determine whether motion vision is also divided into vision for action and for perception we examined the interceptive behaviour of the motion-blind patient LM. The task for LM and three age-matched control subjects was to reach-and-grasp for an object that moved away. Three experiments were conducted to examine the effects on perfomance of target speed (Expt 1), observation time (Expt 2) and visual feedback (Expt 3). As LM is only able to reach for objects which move at 0.5 m/s or less, her performance is inferior to that of controls who can reach for objects moving at 1.0 m/s, but it is better than would be expected from her performance in psychophysical experiments on her motion vision. Kinematic analysis of LM's reaching movements showed that she adapted the speed of her moving hand to the speed of the target but only when full vision was available. In contrast to normal subjects, LM required long observation times and vision of her moving hand to produce successful reaching responses. Thus, the impairment of both perception and action in LM suggests that the motion area MT/V5 is located at an early stage of the extrastriate hierarchy and provides input to both the perception and the action processing streams.

Neuropsychological assessments before and after treatment in patients with anorexia nervosa and bulimia nervosa.

In psychiatric patients the identification of cognitive deficits which predict a poor clinical outcome is important for the development of specific treatment strategies aimed at the amelioration of these impaired cognitive functions to increase the likelihood of full clinical remission. However, such attempts are absent in bulimia nervosa (BU), are scarce in anorexia nervosa (AN) and, furthermore, provide conflicting results. In the present prospective study we investigated the neuropsychological demands in 12 patients with AN and in 14 patients with BU before, during, and after a treatment period. At the initial testing session, both patients samples showed similar and impaired performance levels on tasks measuring attentional demands and problem solving abilities, while their mnemonic functions were preserved. At the final testing session, which took place 7 months thereafter, the impaired cognitive functions had improved to a similar degree in the AN and the BU subgroups. However, although the eating disorder symptomatology had ameliorated in parallel, no direct associations could be established with the initial neuropsychological demands and their rectification, respectively. On an individual level, 11 patients initially showed obvious cognitive deficits. However, the clinical characteristics of this subgroup differed not from that found in the 15 'good performers'. These findings indicate that the cognitive functions in the acute AN and BU are similarly impaired, but also ameliorate in a similar manner with clinical remission. Because no associations were obvious between cognitive and clinical rectifications, significant contributions of mediating factors (e.g., changes in metabolic brain turnover and in steroid hormones) are suggested.

Cognitive deficits in schizophrenia and affective disorders: evidence for a final common pathway disorder.

This study was designed to determine whether patients with schizophrenia and those with affective disorders display a common pattern of cognitive deficits. Cognitive performance was assessed with a neuropsychological test battery in consecutively admitted in-patients with schizophrenia (n=100) and affective disorders (n=100). The two groups of patients showed a similar pattern of cognitive deficits, especially in tests focusing on attentional capacities. The groups only differed significantly in their performance on the Wisconsin Card Sorting Test (WCST), with the schizophrenic patients performing less well. These results suggest that, with the exception of the deficit as measured by the WCST, similar cognitive impairments exist in schizophrenia and affective disorders, even at very early stages of the illness. Therefore, patients with schizophrenia and those with affective disorders cannot be qualitatively distinguished with sufficient reliability. We postulate that the cognitive deficit pattern represents a final common pathway disorder in the two groups of patients.

Comparing the visual deficits of a motion blind patient with the visual deficits of monkeys with area MT removed.

The performance of a 'motion blind' patient on a series of tasks in which the perception of motion played an essential or no role was compared with that of a human subject with normal vision and with that of macaque monkeys in which cortical visual area MT had been removed and adjacent areas damaged. The patient experienced difficulties on those tasks in which the perception of motion was essential, but was unimpaired on those tasks that did not require it. Similarly, the tasks which the 'motion blind' patient found impossible or difficult were precisely those tasks on which monkeys lacking area MT performed poorly. Similarly, the tasks on which the patient performed well also presented no difficulties for the animals lacking cortical area MT. The close correlation between the pattern of visual perceptual impairments in the patient and monkeys indicates that the patient's inability to perceive most forms of visual movement is attributable to total loss of, or extensive damage to, a cortical visual area that is the human equivalent of area MT and perhaps its adjacent areas.

Visual motion perception after brain damage: I. Deficits in global motion perception.

We report on the test results of a group of 32 mostly unilaterally brain-damaged patients examined for global visual motion perception. Three of these patients had severely impaired visual motion perception in their contralateral visual half-field, a deficit remarkably similar to the perceptual defects found in V5-lesioned monkeys. Two of these three patients had a right-hemisphere lesion; the remaining one had a left-hemisphere lesion. We conclude that both hemispheres of the human brain contain an area, functionally equivalent to V5, which subserves visual motion perception in the contralateral visual half-field. Lesion analysis revealed that this area is located in the posterior medial temporal gyrus.

Visual motion perception after brain damage: II. Deficits in form-from-motion perception.

We investigated form-from-motion perception (FFM perception) in a sample of 39 patients with acquired brain damage. Pronounced FFM deficits were found in two patients (FM1 and FM2) with biparietal lesions. Both patients were able to identify the relevant figure, when it was not embedded in obstructive texture. Moreover, they could localize the figures in the FFM condition, although they could not reliably identify them. The two patients had normal motion coherence thresholds. Their performance in a static figure-ground task did not differ from that of other patients. These findings imply that the FFM deficits are not caused by impairment of basic visual motion or form perception but are the consequence of damage to a parietal brain structure involved in the combined analysis of visual motion and form information. The nature and functional role of this brain structure as well as the implications of our results for models of FFM perception are discussed.

Speechreading in the akinetopsic patient, L.M.

Patient L.M. has a well-documented, long-standing and profound deficit in the perception of visual movement, following bilateral lesions of area V5 (visual movement cortex). Speechreading was explored in this patient in order to clarify the extent to which the extraction of dynamic information from facial actions is necessary for speechreading. Since L.M. is able to identify biological motion from point-light displays to whole-body forms and has some limited visual motion capabilities, we expected that some speechreading of faces in action would be possible in this patient. L.M.'s reading of natural speech was severely impaired, despite unimpaired ability to recognize speech-patterns from face photographs and reasonable identification of monosyllables produced in isolation. She was unable to track multisyllabic utterances reliably and was insensitive to vision when incongruent audiovisual speech syllables were shown. Point-light displays of speech were as poorly read as whole face displays. Rate of presentation was critical to her performance. With speech, as with other visual events, including tracking the direction of gaze and of hand-movement sequences, she could report actions that unfolded slowly (approximately one event per 2 s). In line with this, she was poor at reporting whether seen speech rate was normal, fast (double-speed) or slow (half-speed). L.M.'s debility is the converse of that reported for a patient with lesions primarily to V4 (H.J.A.), who is unable to speechread photographs of faces but can speechread moving faces. The visual analysis of both form and motion is required for speechreading; the neural systems that support these analyses are discussed.

Illumination perception in photophobic patients suffering from panic disorder with agoraphobia.

Ten (6.9%) of a sample of 144 patients with panic disorder and agoraphobia developed photophobic behaviour in the course of their anxiety disorder. Their illumination ratings were characterized before and after cognitive behaviour therapy and compared to 10 age- and sex-matched normal control subjects. The illumination of a sheet of printed paper by a continuously adjustable reading lamp was rated by the subjects as 'too dark', 'comfortable' or 'too bright'. The ratings for comfortable luminance were significantly lower in the photophobic patients than in the controls, and renormalized after cognitive behavioural therapy. No differences were observed in the ratings for 'too dark' and 'too bright'. Photophobia in a subsample of patients with panic disorder is a state-dependent phenomenon that can be influenced by cognitive behavioural therapy. The role of neurotransmitters, conditioning processes and a concomitant neurasthenic syndrome requires further characterization.

Patterns of oculomotor scanning in patients with unilateral posterior parietal or frontal lobe damage.

Eye movements were recorded during the inspection of dot patterns in control subjects and in patients with acquired unilateral brain damage involving posterior parietal or frontal cortical regions. Normal subjects adapted their oculomotor scanning pattern effectively to the stimulus configuration. Patients' oculomotor scanning patterns were characterized by a rather rigid sequence of fixations and saccades, with no evidence for a systematic and flexible spatio-temporal organization. In a stimulus condition where dots were grouped, patients with frontal damage accurately shifted their gaze between the dot groups, but had difficulties with dot sampling. These observations suggest that the posterior parietal damage mainly affected the visuo-spatial guidance of the scanpath, whereas the frontal damage impaired its planning. It is concluded that both, posterior parietal and frontal brain structures, and their reciprocal connections, are part of a distributed neural network subserving visually-guided oculomotor scanning, and that the spatio-temporal organization of the scanpath depends critically on both structures and their close co-operation.

[The contribution of neuropsychology to psychiatry]. / Der Beitrag der Neuropsychologie zur Psychiatrie.

Human neuropsychology is the study of brain-behavior relationships based on the analysis of functional disturbances after brain damage. The assessment and analysis of pathological states and processes in the brain on cognition, speech and language, praxis, motivation and affectivity, represent the main topics of neuropsychological research. Patients with psychiatric disorders very often exhibit cognitive impairments which should also be assessed by means of specific neuropsychological diagnostic tools. The advantage of such tools is their validity and reliability which allow accurate qualitative and quantitative analysis and characterization of the various cognitive impairments. Neuropsychological methods of assessment can also be used for follow-up measurements, for example, in studies on the effect of medication. Finally, the outcome of a comprehensive neuropsychological assessment can provide a useful basis for the treatment of cognitive impairments in psychiatric patients using means that have proved successful in brain-damaged patients.