Motor function, non-verbal communication & the motor system
One of the most exciting psychiatric conditions is the bizarre psychomotor syndrome called catatonia, which may present with a large number of different motor signs and even vegetative instability. Catatonia is potentially life threatening. The use of benzodiazepines and electroconvulsive therapy (ECT) has been efficient in the majority of patients. The rich clinical literature of the past has attempted to capture the nature of catatonia. But the lack of diagnostic clarity and operationalization has hampered research on catatonia for a long time. Within the last decades, it became clear that catatonia had to be separated from schizophrenia, which was finally accomplished in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). In DSM-5, catatonia syndrome may be diagnosed as a specifier to major mood disorders, psychotic disorders, general medical conditions, and as catatonia not otherwise specified. This allows diagnosing the syndrome in a large variety of psychiatric disorders. Currently, the pathobiology remains widely unknown. Suspected neurotransmitter systems include gamma-aminobutyric acid (GABA) and glutamate. Neuroimaging reports pointed to reduced resting state activity and reduced task activation in motor areas of the frontal and parietal cortex. The new classification of catatonia will foster more clinical research and neuroscientific approaches by testing catatonia in various populations and applying stringent criteria. The scarce number of prospective trials will hopefully increase, as more trials will be encouraged within a more precise concept of catatonia.
Classical schizophrenia literature reports motor symptoms as characteristic of the disorder. After the introduction of neuroleptic drugs, the existence of genuine motor disorders was challenged. Renewed interest arose as symptoms were found in never-medicated patients. Reports focused on abnormal involuntary movements, parkinsonism, neurological soft signs, catatonia, negative symptoms, or psychomotor slowing. Since these syndromes refer to different concepts, however, the definitions are not congruent and the symptoms overlap. The prevalence rates of motor symptoms in schizophrenia are surprisingly high, and recent studies indicate a possible pathobiology. In particular, the development and maturation of the human motor system appears to be closely linked to the emergence of motor symptoms observed in schizophrenia. Post-mortem and neuroimaging results demonstrated aberrant structure and function of premotor and motor cortices, basal ganglia, thalamus, and the connecting white matter tracts. Animal models have focused on aberrant neurotransmission and genetic contributions. Findings of localized abnormal oligodendrocyte function and myelination point to the special role of the white matter in schizophrenia, and recent studies specifically found an association between motor abnormalities and white matter structure in schizophrenia. This review of the literature supports the idea that motor symptoms are closely related to the neurodevelopmental disturbances of schizophrenia and a distinct syndromal dimension with its own pathophysiology.
Schizophrenia is a devastating disorder thought to result mainly from cerebral pathology. Neuroimaging studies have provided a wealth of findings of brain dysfunction in schizophrenia. However, we are still far from understanding how particular symptoms can result from aberrant brain function. In this context, the high prevalence of motor symptoms in schizophrenia such as catatonia, neurological soft signs, parkinsonism, and abnormal involuntary movements is of particular interest. Here, the neuroimaging correlates of these motor symptoms are reviewed. For all investigated motor symptoms, neural correlates were found within the cerebral motor system. However, only a limited set of results exists for hypokinesia and neurological soft signs, while catatonia, abnormal involuntary movements and parkinsonian signs still remain understudied with neuroimaging methods. Soft signs have been associated with altered brain structure and function in cortical premotor and motor areas as well as cerebellum and thalamus. Hypokinesia is suggested to result from insufficient interaction of thalamocortical loops within the motor system. Future studies are needed to address the neural correlates of motor abnormalities in prodromal states, changes during the course of the illness, and the specific pathophysiology of catatonia, dyskinesia and parkinsonism in schizophrenia.
Motor symptoms are frequent in schizophrenia and relevant to diagnosis. They are usually assessed by clinical observation and ratings based on psychometric scales. However, investigations with quantitative measurements are rare. To understand the relationship between the objective parameters of a quantitative motor activity measurement and the items related to motor symptoms of the Positive and Negative Syndrome Scale (PANSS), 55 schizophrenia patients were studied with 24-h continuous wrist actigraphy. We conclude that the objectively measured quantity of movement is related to the clinically assessed negative syndrome in schizophrenia. In contrast, PANSS items related to psychomotor behavior imprecisely reflect real quantitative motor activity.
Comparison of objectively measured motor behavior with ratings of the motor behavior domain of the Bern Psychopathology Scale (BPS) in schizophrenia
Motor symptoms in schizophrenia occur frequently and are relevant to diagnosis and antipsychotic therapy. To date motor symptoms are difficult to assess and their pathobiology is a widely unresolved issue. The Bern Psychopathology Scale for the assessment of system-specific psychotic symptoms (BPS) was designed to identify homogenous patient groups by focusing on three domains: language, affectivity and motor behavior. The present study aimed to validate the motor behavior domain of the BPS using wrist actigraphy. In conclusion, we provided substantial external validity for global, quantitative and subjective ratings of the BPS motor behavior domain. Thus, the BPS is suitable to assess the dimension of quantitative motor behavior in the schizophrenia spectrum.
Altered cortico-basal ganglia motor pathways reflect reduced volitional motor activity in schizophrenia
Little is known about the neurobiology of hypokinesia in schizophrenia. Therefore, the aim of this study was to investigate alterations of white matter motor pathways in schizophrenia and to relate our findings to objectively measured motor activity. Our results point to reduced volitional motor activity and altered motor pathway organisation in schizophrenia. The identified associations between the amount of movement and structural connectivity of motor pathways suggest dysfunction of cortico-basal ganglia pathways in the pathophysiology of hypokinesia in schizophrenia. Schizophrenia patients may use cortical pathways involving the supplementary motor area to compensate for basal ganglia dysfunction.
Gesture is an integral feature of nonverbal communication that serves as an outward manifestation of several interacting fundamental processes including motor behavior, language, and sensory integration. Likewise, gesturing has been linked to semantic retrieval, learning, and communicative ability. Indeed, processing of gesture performance and perception involves cerebral networks of multimodal integration, action planning and semantic association. Despite the fact that gesture has been a central topic in areas of cognitive-developmental psychology, and that psychoses are characterized by deficits in several of these fundamental processes, the scientific community’s interest in gesture in schizophrenia spectrum disorders is only just evolving.
Schizophrenia patients are severely impaired in nonverbal communication, including social perception and gesture production. However, the impact of nonverbal social perception on gestural behavior remains unknown, as is the contribution of negative symptoms, working memory, and abnormal motor behavior. The study confirmed a generalized nonverbal communication deficit in schizophrenia. Specifically, the findings suggested that nonverbal social perception in schizophrenia has a relevant impact on gestural impairment beyond the negative influence of motor/frontal abnormalities.
Gestures are important for nonverbal communication and were shown to be impaired in schizophrenia. Two categories of gestures can be differentiated: pantomime on verbal command and imitation of seen gestures. There is evidence that the neural basis of these domains may be distinct, pantomime being critically dependent on prefrontal cortex function. The aim of the study was to investigate gestural deficits in schizophrenia and their association with frontal lobe function and motor performance. Conclusion: Pantomime is frequently impaired in chronic schizophrenia and may critically depend on motor planning, reflecting a further example of brain disconnectivity in schizophrenia.
Schizophrenia patients frequently present with subtle motor impairments, including higher order motor function such as hand gesture performance. Using cut off scores from a standardized gesture test, we previously reported gesture deficits in 40% of schizophrenia patients irrespective of the gesture content. However, these findings were based on normative data from an older control group. Hence, we now aimed at determining cut-off scores in an age and gender matched control group. Furthermore, we wanted to explore whether gesture categories are differentially affected in Schizophrenia. In conclusion, gestural deficits in schizophrenia are even more frequent than previously reported. Gesture categories that pose higher demands on planning and selection such as pantomime of meaningless gestures are predominantly affected and associated with the well-known frontal lobe dysfunction.
Gesturing plays an important role in social behavior and social learning. Deficits are frequent in schizophrenia and may contribute to impaired social functioning. Information about deficits during the course of the disease and presence of severity and patterns of impairment in first-episode patients is missing. Hence, we aimed to investigate gesturing in first- compared to multiple-episode schizophrenia patients and healthy controls. Conclusions: Subjects with multiple psychotic episodes have severe deficits in gesturing, while only mild impairments were found in first-episode patients independent of age, gender, education and negative symptoms. The results indicate that gesturing is impaired at the onset of disease and likely to further deteriorate during its course.
We aimed to investigate whether aberrant motor behavior in schizophrenia was associated with structural alterations in the motor system. Whole brain voxel based morphometry of patients with different severity of motor symptoms identified altered gray matter volume in the supplementary motor area (SMA), a key region of the motor system
The neural correlates of impaired performance of gestures are currently unclear. Lesion studies showed variable involvement of the ventro-dorsal stream particularly left inferior frontal gyrus (IFG) in gesture performance on command. However, findings cannot be easily generalized as lesions may be biased by the architecture of vascular supply and involve brain areas beyond the critical region. The neuropsychiatric syndrome of schizophrenia shares apraxic-like errors and altered brain structure without macroanatomic lesions. Schizophrenia may therefore qualify as a model disorder to test neural correlates of gesture impairments. Impaired performance of meaningful gestures on command was linked to volume loss predominantly in the praxis network in schizophrenia. Thus, the behavioral similarities between apraxia and schizophrenia are paralleled by structural alterations. However, few associations between behavioral impairment and structural brain alterations appear specific to schizophrenia.
Altered structural connectivity is a key finding in schizophrenia, but the meaning of white matter alterations for behavior is rarely studied. In healthy subjects, motor activity correlated with white matter integrity in motor tracts. Conclusion: Structural disconnectivity could lead to disturbed motor behavior in schizophrenia.