Biomedical subjects

H Ackermann

Publications and source records attributed to H Ackermann.

At least 73 records · Page 4Linked to original sources

PubMed1996

Impaired procedural learning after damage to the left supplementary motor area (SMA).

Two paradigms of procedural learning, serial reaction time and tracking tasks, were given to a patient with damage to the supplementary motor area (SMA) of the left mesiofrontal cortex. This patient exhibited impaired procedural learning during the serial reaction time test and mirror reversed tracking. Unreversed tracking performance was normal. Therefore the SMA--as well as the cerebellum and the striatum--participate in the development of skills requiring internal elaboration of motor behaviour.

Adult↗

PubMed1995

Pain-related cerebral potentials in patients with frontal or parietal lobe lesions.

The present study investigated the processing of painful electrical stimuli in patients with unilateral frontal or parietal lobe damage and matched control subjects. Patients with frontal lesions showed increased pain thresholds when the stimuli were administered contralateral to the lesion. While the peak-to-peak amplitudes of the N150/P250 components of the somatosensory potentials increased linearly with stimulus intensity in the control subjects, the responses in the frontal group did not change significantly between stimulation at pain and tolerance threshold. There was no evidence for altered pain processing in patients with parietal lobe lesions. The findings of the present study support the hypothesis of an involvement of the frontal cortex in pain perception in humans.

Adult↗

PubMed1995

Cerebellar contributions to cognition.

This review summarises the present evidence for the contribution of the cerebellum to cognition. While a data base from both animal and human clinical research supports the hypothesis of an important cerebellar role in motor adaptation, motor learning and timing, the evidence for the implication of the cerebellum in psychopathology and non-motor cognitive functions is incomplete and does not allow unequivocal conclusions. Methodological shortcomings and the lack of theoretical models on the nature of the cerebellar contribution to cognition limit the interpretation of the empirical studies available so far.

Animals↗

PubMed1995

Kinematic analysis of lower lip movements in ataxic dysarthria.

The present study investigates the influence of cerebellar disorders on articulatory performance. A linear trend between peak velocity and movement amplitude seems to represent a basic organizational principle both of upper limb and speech motor control. This relationship is preserved in arm movements of patients with cerebellar dysfunction. However, these subjects show a decreased slope of the respective regression lines under the instruction to perform movements as fast as possible. In order to find out whether these findings also hold for speech motor control, peak velocity, range, and duration both of the opening and closing gestures during production of /pap/- as well as /pa:p/-sequences-embedded into a carrier phrase each-were measured using an optoelectric system. In addition, vowel length (/a/, /a:/) was determined at the acoustic speech signal: (a) The cerebellar patients showed a prolongation of both vowel targets. Most of them, nevertheless, presented with discernible durational contrasts; (b) The articulatory gestures were characterized by a highly linear relationship between peak velocity and movement range in the cerebellar as well as in the control group; (c) As a rule, the cerebellar subjects had decreased velocity-displacement ratios as compared to the normals; (d) The discrepancy in slope of the computed regression lines between the controls and the patients varied according to the type of movement (opening vs. closing gesture) and-to a lesser decree-linguistic demands (short vs. long vowel). These data indicate an impaired ability of cerebellar patients to increase muscular forces in order to produce adequately scaled articulatory gestures of short duration.

Adult↗

PubMed1995

[The cerebellum and cognition--psychopathological, neuropsychological and neuroradiological findings].

It is a classical topic of clinical neurology that cerebellar dysfunctions give rise to motor deficits but spare the sensory and mental domains. Since the last century, however, cognitive decline occasionally has been attributed to diseases and lesions of the cerebellum. In recent years this assumption has gained in importance. The recent literature puts forward four arguments in favour of this suggestion: a) The neocerebellum has large reciprocal fibre connections with the association areas of the cerebral cortex. b) Functional imaging studies revealed activation of circumscript cerebellar regions during cognitive tasks. c) Patients with cerebellar malformations and diseases, respectively, may present with psychopathological signs and neuropsychological deficits. d) Atrophy of the cerebellum has been reported in schizophrenic and autistic syndromes. The present review aims at a critical evaluation of the relevant clinical and neuropsychological literature. So far there is no convincing evidence that lesions and diseases restricted to the cerebellum give rise to dementia or to impaired verbal and visual memory functions. With respect to specific perceptual tasks such as the discrimination of time intervals, problem solving, and visuospatial functions, no definite conclusion is possible so far. Some studies revealed cerebellar atrophy in schizophrenic and autistic patients. However, the functional relevance of these findings must be questioned since cytoarchitectonic alterations in extracerebellar areas, e.g. the basal forebrain, are present in these disorders as well.

Brain Damage, Chronic↗

PubMed1995

[Akinetic mutism--a review of the literature].

Cairns and coworkers (1941) introduced the term "akinetic mutism" to denote a syndrome characterised by lack of responsiveness in the presence of apparently preserved vigilance. The present paper reviews clinical data as well as results of animal experimentation to outline the functional-neuroanatomic basis of this constellation. The clinical literature following the original publication of Cairns et al. (1941) reported syndromes of "akinetic mutism" in bilateral mesodiencephalic or frontal lesions of various aetiology. At least two pathomechanisms of akinetic mutism can be differentiated: (a) reduced "arousal" of cortical functions due to lesions at or rostral to the mesodiencephalic junction; (b) impaired activation of the motor system following bilateral damage to the frontal lobes. Since perceptual and cognitive functions are disturbed as well in mesodiencephalic akinetic mutism, the latter notion does not seem to be adequate. The terms "apallic syndrome" or "vegetative state" are rather more appropriate in these instances. The label "akinetic mutism" can then be restricted to a pathophysiologically distinct syndrome, i.e. reduced motor activation following bilateral frontal damage.

Akinetic Mutism↗

PubMed1995

Oral diadochokinesis in neurological dysarthrias.

Rapid syllable repetitions require alternating articulatory movements and, thus, provide a test for oral diadochokinesis. The present study performed an acoustic analysis of rapid syllable repetitions in patients suffering from idiopathic Parkinson's disease (n = 17), Huntington's chorea (n = 14), Friedreich's ataxia (n = 9), or from a purely cerebellar syndrome (n = 13). Four parameters were considered: the mean number of syllables per train, the median syllable duration with its variation coefficient, and articulatory imprecision in terms of the percentage of incomplete closures. Apart from a few subjects with minor motor deficits only, in all patients at least one of the four measures of diadochokinesis exceeded the normal range. Accordingly, discriminant analysis revealed a highly significant difference between controls and patients with respect to the considered parameters. Thus, oral diadochokinesis tasks represent a sensitive measure of orofacial motor impairment. Moreover, multivariate analysis showed that Parkinson's disease and Friedreich's ataxia are characterized by a highly specific profile of diadochokinesis performance.

Adult↗

PubMed1995

Gender-specific vocal dysfunctions in Parkinson's disease: electroglottographic and acoustic analyses.

Electroglottographic (EGG) and acoustic recordings were obtained during sustained vowel production in men and women suffering from Parkinson's disease (PD). The computed EGG spectrograms allowed us to differentiate various kinds of phonatory disturbances: intervals with subharmonic energy ("low-frequency segments"), "noise-like regions," and abrupt shifts of fundamental frequency (F0). Female PD subjects presented with a significantly increased portion of subharmonic segments and with significantly more abrupt F0 shifts as compared to both controls and male PD subjects. Presumably, these alterations in spectral energy distribution reflect different oscillatory modes of the glottal source. Thus, PD seems to have a differential impact on phonation in men and women. Conceivably, these gender-specific vocal dysfunctions are determined by the well-known sexual dimorphism of laryngeal size.

Acoustics↗

PubMed1994

Acoustic analysis of speech timing in Huntington's disease.

Duration measurements at the acoustic speech signal of sentence utterances including syllable lengths, vowel durations, and voice-onset-time (VOT) were performed in 13 subjects with Huntington's disease (HD) and in 12 control speakers. First, all 13 HD subjects presented with increased variability of utterance duration and/or VOT. Second, a subgroup had reduced speech tempo concomitant with overproportional lengthening of short vowels. Presumably, these deviations result from slowed movement execution (bradykinesia) and delayed between-movement transitions. Third, durational parameters of phonetic timing, e.g. stress contrast, were largely unimpaired. In a further patient (HD14) severely reduced articulatory accuracy did not allow acoustic measurements. He presented with truncated, barely intelligible, diphthongized sentence utterances. A slight tendency for these deviations could be noted in two of the HD subjects who underwent acoustic analysis. Since all three subjects had a rather long disease duration, this constellation might represent an advanced stage of HD dysarthria into which the other syndromes ultimately will develop.

Adult↗

PubMed1994

[Mutism in central motor disorders--a review of the literature].

Mutism can be defined as "a condition in which there is no, or very little, oral-verbal expression, whereas comprehension of speech ... is normal or at least at a considerably higher level" (Lebrun, 1990). Benson (1979) enumerates five neuroanatomical correlates of mutism: (a) damage to the Broca region, (b) lesion of the supplementary motor area of the dominant hemisphere, (c) dysfunction of the mesencephalic reticular system, (d) thalamotomy, and (e) bilateral pathology of cortical and subcortical motor structures. The last item refers to syndromes of mutism resulting from central motor disorders. Depending on location and size of the lesion this pathophysiological interpretation should hold true for the fourth point as well. In mutism due to central motor disturbances lacking verbal expression represents the most severe degree of dysarthria, i.e. anarthria. The present review provides a detailed description of mutism following corticobulbar, striatal, and cerebellar dysfunctions.

Brain↗

PubMed1994

[Mutism and aphasia--a review of the literature].

Mutism in the sense of a complete inability to produce oral language is a rare symptom in aphasic disorders and most often occurs as a transient initial sign. Among the pathomechanisms causing muteness in aphasia, disturbances of speech initiation and of limbic aspects of speech production on the one hand and speech motor programming impairments on the other are considered. This article reviews clinical reports of extremely reduced speech or complete muteness in the context of aphasia, discussing the observed symptom patterns as well as their neuroanatomic correlates and aspects of their recovery.

Aphasia↗

PubMed1994

Speech rate and rhythm in cerebellar dysarthria: an acoustic analysis of syllabic timing.

Auditory-perceptual studies reported inconsistent data with respect to syllabic timing in cerebellar dysarthria, i.e. both reduced and increased variability of syllable durations. The present study performed a comprehensive analysis of syllabic timing during sentence utterances in 14 subjects with a pure cerebellar syndrome (CA). First, the CA patients presented with reduced speech tempo in terms of syllable and utterance durations. Second, a tendency for intrautterance syllabic isochrony, being an aspect of the percept of 'scanning speech', characterized a subgroup of patients with cerebellar dysarthria. Third, increased interutterance durational variability was found in three out of the five syllables considered. Thus, both reduced intrautterance and increased interutterance variability of syllable durations may pertain to cerebellar dysarthria. The latter dimension, however, seems to be more prominent.

Adult↗

PubMed1994

Acoustic analysis of vocal instability in cerebellar dysfunctions.

Acoustic analysis of vocal instability during the production of isolated vowels, including computation of mean fundamental frequency (F0), period-to-period variability (jitter), pitch fluctuations, and between-trial variation of F0, was performed in 20 patients with cerebellar cortical dysfunction. Eleven subjects suffered from purely cerebellar atrophy (CA). In the remaining 9 patients olivopontocerebellar atrophy (OPCA) had been diagnosed. A subgroup of both the CA and OPCA subjects presented with enlarged pitch fluctuations and/or increased jitter values. It is conceivable that asymmetrically distributed motor deficits at the laryngeal level and altered gain settings of laryngeal and/or respiratory reflexes account for the observed phonatory instability. Moreover, 5 of the 20 cerebellar patients had a pitch level exceeding the upper limit of the normal range. Presumably, this deviation reflects increased vocal effort.

Adult↗

PubMed1994

Frontal-type memory impairment associated with thalamic damage.

The present case report adds further evidence to the hypothesis that material-specific memory problems arise from unilateral thalamic damage and that frontal cortical dysfunction may affect the nature of the memory disorder. A 64-year old patient who had suffered an ischemic lesion limited to the right anterior thalamus showed marked deficits in immediate and delayed recall of visuospatial material and face recognition. In addition, there was evidence of frontal-type memory problems including impaired spatial working memory, increased forgetting rates, poor prospective memory and inadequate elaborative encoding. Concomitant behavioral changes characterized by increased irritability and disinhibition also supported the hypothesis of frontal lobe dysfunction after thalamic damage.

Brain Diseases↗

PubMed1994

Dissociation of declarative and nondeclarative memory after bilateral thalamic lesions: a case report.

The case of a 63-year-old woman who suffered bilateral ischemic damage in the region of blood supply of the paramedian thalamic arteries is reported. She displayed severe deficits on immediate and delayed recall of both verbal and visuospatial material in the presence of intact IQ and attentional abilities. Performance on tests of all major components of nondeclarative memory (skill acquisition, perceptual priming, classical conditioning) was also preserved. The present report, thus, provides a further example for dissociations of declarative and nondeclarative memory functions following bilateral thalamic damage.

Conditioning, Classical↗

PubMed1993

Dysarthria in bilateral thalamic infarction. A case study.

A patient suffering from bilateral thalamic infarction in the region supplied by the paramedian arteries sparing the internal capsules underwent acoustic analysis of sentence utterances. The results were compared with the findings obtained in parkinsonian subjects, in patients with upper motor neuron lesions, and in normal subjects. Acoustic measurements revealed increased pitch, monotonous speech, rough voice quality, and normal speech tempo concomitant with articulatory impreciseness in terms of incomplete closure productions. This constellation resembled parkinsonian dysarthria. Damage to the thalamic projection area of the pallidal efferents, therefore, seems to be the most probable cause of the patient's speech disorders. In parkinsonian subjects stereotactical lesions of this structure ameliorate rigor, but not akinesia. Thus, our patient's speech deficits, and by analogy the corresponding parkinsonian dysarthric disturbances, may be considered akinetic signs.

Adult↗

PubMed1993

The cerebellum and cognitive functions in humans.

Recent neuropsychological studies have given rise to the hypothesis that the cerebellum is involved in nonmotor cognitive functions. The interpretation of these findings is, however, restricted by methodological problems, such as heterogenous patient samples. The present study compared patients with pathology confined to the cerebellum and patients with combined cerebellar and brainstem lesions to matched normal controls on a range of memory and learning tasks. Two procedural learning tasks were also conducted, involving perceptual (mirror reading) and conceptual skill acquisition (the Tower of Hanoi task). Patients with damage to both cerebellum and brainstem, but not patients with cerebellar pathology alone, showed impairments on memory and visuoconstructive tasks and evidence of frontal lobe dysfunction. Cerebellar damage had no effect on skill acquisition. These results do not support the hypothesis of cerebellar involvement in procedural learning per se.

Adult↗

PubMed1993

Classical conditioning after cerebellar lesions in humans.

We explored classical conditioning in human subjects who had lesions in their cerebellar circuitry. Seven patients with damage to cerebellar structures and matched control subjects underwent simple delay tone-airpuff conditioning. Eyelid conditioned response (CR) acquisition was severely disrupted in the patient group, whereas autonomic CRs and slow cortical potentials developing between conditioned stimulus (CS) and the unconditioned stimulus (UCS) were unaffected. Results are consistent with animal studies and earlier case reports indicating that intact cerebellar structures are necessary for the acquisition of classically conditioned motor responses.

Adult↗