Neuropsychology

Research in neuropsychology is represented by the investigation of the neuropsychology of memory and learning, the study of the cerebellar contribution to cognition and the exploration of brain-behavior relationships in emotional processing. All investigations are carried out in close cooperation with the Department of Neurology and the Visual Science Section, University of Tⁿbingen. Further collaborative projects involve Prof. Larry Squire (University of San Diego, USA), Prof. Andrew Mayes (University of Sheffield, UK), and Prof. Kenneth Hugdahl (University of Bergen, Norway).

The research on memory is based on the multiple memory systems approach advanced by Larry Squire. With respect to long-term memory, a basic distinction is being drawn between declarative or explicit memory which refers to the ability to store and consciously recollect facts and events, and nondeclarative or implicit memory which involves instances of memory that are expressed through performance rather than by recollection. Implicit memory includes heterogenous abilities such as priming, skill acquisition, nonassociative memory and conditioning. While the hippocampus and related structures are known to be essential for explicit memory, the neuroanatomical correlates of implicit memory are less well established. The neuropsychological studies presented in the following abstracts aimed to assess the differential effect of normal aging and selective cortical and subcortical brain lesions on explicit and implicit memory.

The neuropsychology of amnesia

Amnesia or severe memory disorder is consistently seen after damage to the medial temporal lobes or medial diencephalic structures in humans. Whether the clinical patterns of memory dysfunction ocurring after lesions to both areas are comparable or even identical, has been a matter of controversy and empirical data are sparse. The issue is further complicated by the fact that animal models of amnesia are mainly based on hippocampal damage and spatial memory tasks whereas medial diencephalic lesions and non-spatial memory have been neglected in this regard.

In a series of studies, the specific pattern of memory breakdown is currently being investigated in patients with circumscribed medial temporal lobe and medial thalamic lesions and patients with additional brain damage outside the areas in question (e.g. patients with Korsakoff's syndrome).

Our recent studies indicate that in all types of severely amnesic patients, emotionally flavored memories are spared to a greater degree than neutral memories. Medial diencephalic, but not medial temporal lobe damage may be associated with frontal-type memory dysfunction such as deficits in working memory or memory for temporal order. Whether medial temporal lesions specifically impair memory functions that require the integration or "binding together" of different kinds of information, as hypothesized on the basis of animal research, is currently being evaluated.

Daum, I. & Ackermann, H. (1994). Frontal-type memory impairment associated with thalamic damage. International Journal of Neuroscience, 77, 187-198.

Daum, I., Flor, H., Brodbeck, S. & Birbaumer, N. (1996). Autobiographical memory for emotional events in amnesia. Behavioural Neurology, in press

Neuropsychology of implicit memory: Clinical studies

Animal studies have implicated the basal ganglia and the cerebellum in the mediation of implicit or nondeclarative memory. In order to explore the association of these subcortical brain systems with skill acquisition and priming tasks in humans, a series of experiments was carried out in subjects with damage to the basal ganglia (patients in the early stages of Parkinson's disease), subjects with damage to cerebellar circuitry (patients suffering from cerebellar atrophy or ischemic damage) and control groups of neurologically intact subjects and patients with selective frontal cortical lesions. The subjects completed tasks comprising perceptual (mirror reading), cognitive (complex puzzles) and motor skill acquisition (tracking), repetition priming (word stem and pattern completion) and a range of explicit recall and recognition tasks.

Damage to cerebellar circuitry was seen to disrupt performance on motor skill acquisition tasks, while performance on implicit and explicit non-motor tasks was spared. Patients with basal ganglia lesions were impaired at motor and cognitive skill acquisition. Apart from a motor learning deficit following damage to the supplementary motor area, there were no implicit learning deficits in the frontal group. In conclusion, the clinical results support the notion of an involvement of both cerebellum and basal ganglia in the mediation of motor skill acquisition; implicit cognitive learning may require the integrity of corticostriatal pathways.

Daum, I., Ackermann, H., Schugens, M.M., Reimold, C., Dichgans, J. & Birbaumer N. (1993). The cerebellum and cognitive functions in humans. Behavioral Neuroscience 107, 411-419.

Daum, I., Schugens, M.M., Spieker, S., Poser, U., Sch÷nle, P.W. & Birbaumer, N. (1995). Memory and skill acquisition in Parkinson's disease and frontal lobe dysfunction. Cortex, 31, 413-432.

Ackermann, H., Daum, I., Schugens, M.M. & Grodd, W. (1996). Impaired procedural learning following damage to the left supplementary motor area (SMA). Journal of Neurology, Neurosurgery and Psychiatry, 60, 94-97.

Daum, I. & Ackermann, H. (1996). Non-deklaratives GedΣchtnis - Neuro-psychologische Befunde und neuroanatomische Grundlagen (Non-declarative memory - neuropsychological findings and neuroanatomical correlates). Fortschritte der Neurologie-Psychiatrie, in press.

The neuropsychology of classical conditioning

Classical eyelid conditioning has been frequently used to investigate the neuroanatomical correlates of memory and learning. Relatively little is, however, known about the effects of brain lesions on classical conditioning in humans, despite the clear similarities in experimental procedures and analyses in human and animal research. In a series of studies, classical eyelid conditioning has been investigated in patients with damage to hippocampal or cerebellar circuitry or basal ganglia dysfunction. Simple tone-airpuff conditioning or two-tone discrimination learning were found to be preserved in amnesic patients with temporal lobe/hippocampal lesions or bilateral thalamic damage. Performance on a conditional discrimination task, in which reinforcement of a CS tone was contingent upon the colour of a preceding light, however, was severely disrupted in this patient group. Patients with damage to cerebellar circuitry were impaired at acquiring conditional eyelid responses during tone-airpuff conditioning; electrodermal conditioning appeared intact. The severe conditioning deficit occurred in the presence of intact knowledge of stimulus contingencies and unimpaired slow negative cortical potentials normally seen between the CS and the UCS. There was no evidence of conditioning impairments after damage to the basal ganglia, which severely disrupted other forms of motor learning.

In summary, the present results based on human neuropsychological research support models derived from comparative research that relate (motor) CS-UCS associative learning to cerebellar circuitry and more complex forms of conditioning to the hippocampus and related structures.

Daum, I., Schugens, M.M., Ackermann, H., Lutzenberger, W., Dichgans, J. & Birbaumer, N. (1993). Classical conditioning after cerebellar lesions in humans. Behavioral Neuroscience 107, 748-756. Daum, I. & Schugens, M.M. (1995). Classical conditioning after brain lesions in humans: The contribution to neuropsychology. Journal of Psychophysiology, 9, 109-118.

Daum, I., Schugens, M.M., Breitenstein, C., Topka, H. & Spieker, S. (1996). Classical eyeblink conditioning in Parkinson's disease. Movement Disorders, in press.

The neuropsychology of aging

The idea of a general cognitive decline associated with non-disease aging has recently been challenged by studies suggesting that aging may selectively affect memory functions that are associated with the integrity of the hippocampus and the frontal cortex, i.e. those brain areas largely affected by age-related neurodegenerative changes.

In a series of investigations, tasks used to assess implicit memory (skill acquisition, word stem completion priming) and a range of explicit memory tasks involving different levels of effortful processing were administered to healthy subjects. In each study, five consecutive age groups (20-29 years, 30-39 years, 40-49 years, 50-59 years, 60-70 years) matched for sex, general intellectual abilities and mood variables were compared with respect to memory performance.

The results indicated that aging had no significant effect on skill acquisition, priming or recognition, while free recall of verbal or visuospatial material was consistently found to deteriorate with increasing age in all studies. Older subjects also performed poorly relative to younger subjects on clinical tasks of frontal-type memory problems such as impaired memory for temporal order or deficient prospective memory.

In summary, non-disease aging was found to selectively disrupt performance on memory tasks that required effortful processing, while implicit memory and less effort-demanding tasks such as recognition remained largely unaffected. The general pattern is consistent with cognitive impairment resulting from frontal lobe dysfunction in non-disease aging.

Breitenstein, C., Daum, I. & Schugens, M.M. (1996). Altersunterschiede beim motorischen Lernen (Age differences in motor learning). Zeitschrift fⁿr Geronto-psychologie und -psychiatrie, 9, 33-41.

Fahle, M. & Daum, I. (1996). Visual learning and memory as functions of age. Vision Research, in press.

Schugens, M.M., Daum, I., Spindler, M. & Birbaumer, N. (1996). Differential effects of aging on explicit and implicit memory. Aging, Neuropsychology and Cognition.

The cerebellar contribution to timing

Recent theories have emphasised that the cerebellum serves as an internal clock which is involved in the processing of temporal intervals in motor as well as perceptual tasks. Impaired timing has so far been demonstrated for intervals of 400 to 550 msec; the present research aimed to explore whether time reproduction deficits would extend to longer intervals that have wider implications in everyday life.

Patients with selective cerebellar damage and matched controls participated in a time reproduction task. Subjects were presented with visual stimuli lasting from 1 to 8 sec. They had to reproduce the respective target interval by switching off a second visual stimulus following each target. EEG was recorded throughout the experiment.

During time estimation, CNV-like negative brain potentials developed during the presentation of target stimuli and during the reproduction of all intervals. During time reproduction, patients with cerebellar dysfunction as a group showed larger deviations from targets (i.e. increased underestimation) compared to controls, with deficits being more pronounced at longer intervals. Patients with mild clinical symptoms displayed larger CNV-like potentials relative to controls, which coincided with a smaller impairment in time reproduction. The clinically more impaired subgroup of cerebellar lesion patients, on the other hand, showed negative potentials of very small amplitude and a severe deficit in time estimation.

The findings extend timing deficits in patients with cerebellar dysfunction to time intervals up to 8 sec. Several studies are currently in progress, aiming to explore the cerebellar contribution to time perception and to motor speech processes that depend on accurate timing.

Daum, I., Ackermann, H. (1995). Cerebellar contributions to cognition. Behavioural Brain Research, 67, 201-210.

Daum, I. & Schugens, M.M. (1996). On the cerebellum and classical conditioning. Current Directions in Psychological Science, in press.

Ackermann, H., GrΣber, S., Hertrich, I. & Daum, I. (1996). Categorical speech perception in cerebellar disorders. Brain and Language, in press.

Memory dysfunction in Alzheimer's disease

Alzheimer's disease (AD) constitutes the only amnesic disorder that shows a clear association with semantic memory impairment. A number of single case and group studies were carried out to investigate the nature of the semantic disorder in AD in more detail.

The semantic memory test battery administered in the present studies comprised naming and defining common concepts as well as decisions about perceptual and functional attributes of animate and inanimate objects. Our studies indicated a severe impairment of AD patients in all semantic knowledge tasks, with knowledge of animate objects being significantly more impaired than knowledge of inanimate objects which was relatively intact. When knowledge was assessed implicitly, i.e. by preference ratings, performance was significantly better compared to conditions that required explicit decisions in real-unreal judgement tasks. A similar pattern of deficit and preservation of function emerged in the study of a patient with selective bilateral temporal lobe damage.

The findings in AD patients suggest the presence of a category-specific semantic memory disorder, with knowledge of concepts mainly defined in terms of perceptual attributes (animate objects) being more affected than knowledge of objects defined in terms of functional attributes (inanimate objects). These results are consistent with the pronounced damage to the temporal lobes in AD, which is believed to impaired storage of perceptual information. The relative preservation of semantic memory as seen in implicit tasks supports the hypothesis of a retrieval deficit rather than a complete loss of knowledge.

Mauri, A., Daum, I., Sartori, G., Riesch, G. & Birbaumer, N. (1994). Category-specific semantic impairment in Alzheimer's disease and temporal lobe dysfunction: a comparative study. Journal of Clinical and Experimental Neuropsychology 16, 689 - 701.

Daum, I., Riesch, G., Sartori, G. & Birbaumer, N. (1996). Semantic memory impairment in Alzheimer's disease. Journal of Clinical and Experimental Neuropsychology, in press.

Processing of affective prosody after cortical and subcortical brain damage

A well-documented neuropsychological model of affect processing is based on the hypothesis that distinct subtypes of affect processing disturbances are related to dysfunction of neural systems in the right or left hemisphere. Recent studies propose the existence of specific neural networks of nonverbal affect signals ("nonverbal affect lexicon") in the right hemisphere, comprising independent lexicons for faces and prosody. With respect to the neuroanatomical correlates of the lexicons, earlier studies have implicated the anterior right hemisphere in expressive affective prosody and the posterior right hemisphere in receptive processing; more recent views, however, emphasise the involvement of subcortical structures, i.e. the basal ganglia and the thalamus, in emotional processing.

The ongoing project aims to develop a standardized procedure for the investigation of perception and processing of affective prosodic stimuli (German standardization of the "Florida Affect Battery"). A further purpose is to explore differential patterns in different groups of patients with cortical and subcortical brain lesions.

Studies carried out so far have confirmed the applicability of our German version of the Florida Affect Battery ("Tⁿbingen Affect Battery") in a sample of 100 healthy controls. In further investigations, tests of receptive and expressive affective prosody will be administered to different clinical samples with selective brain lesions in order to establish a standard clinical assessment tool for neurological patient groups with prosodic deficits.

Breitenstein, C., Daum, I., Ackermann, H., Lⁿtgehetman, R. & Mⁿller, E. (1996). Erfassung der Emotionswahrnehmung bei zentralnerv÷sen LΣsionen und Erkrankungen: Psychometrische Kriterien der "Tⁿbinger Affekt Batterie" (Assessment of the perception of emotions following brain damage: Psychometric properties of the "Tⁿbingen Affect Battery"). Neurologie und Rehabilitation, in press.


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Hubert Preißl
Maintainer: hubert.preissl@uni-tuebingen.de(hubert.preissl@uni-tuebingen.de)