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The motor system is profoundly affected in schizophrenia, with a significant body of evidence confirming the presence of robust, observable movement disorders that are independent of antipsychotic medication or substance use. These abnormalities are not merely secondary features but represent core components of the illness, impacting various domains including posture, gait, balance, and fine motor control.

Prevalence and Clinical Manifestations of Intrinsic Motor Abnormalities

The clinical manifestations range from subtle deficits to overt syndromes like catatonia, and their prevalence varies significantly across different studies, reflecting differences in diagnostic criteria, assessment tools, and patient populations. A meta-analysis encompassing 74 studies found an overall mean prevalence of catatonia of 9.0% across all conditions, which narrowed to 8.1% when excluding enriched samples [1]. Specifically within schizophrenia, this prevalence was calculated at 9.8% (k=33, n=20,276) [1]. However, other sources report a wide spectrum of prevalence, from as low as 4% to as high as 67%, associated with the disorder [21]. This variability underscores the complexity of diagnosing and defining these phenomena.

Catatonia itself presents with a diverse array of symptoms that can be categorised into several clusters. These include negative symptoms such as stupor, mutism, and negativism; mannerisms and stereotypies, which are repetitive non-goal-directed movements; excited states involving purposeless motor activity; grimacing; posturing; rigidity; and echophenomena [20, 21, 22]. Factor analytic studies have identified distinct but overlapping symptom clusters, such as negative, stereotypy/mannerism, echo/ perseveration, excitement, and grimacing, suggesting that catatonia may be a syndrome composed of multiple underlying dimensions [20, 21]. The DSM-5 requires the presence of at least three out of twelve specific symptoms for a diagnosis, while the more sensitive Bush-Francis Catatonia Rating Scale (BFCRS) is widely used for screening and assessment [8, 20]. While historically linked to Kraepelin’s pre-neuroleptic era descriptions of “insane paralysis,” which included catalepsy and echopraxia, catatonia is now recognised as a transdiagnostic syndrome occurring across affective, autistic, neurological, and medical conditions [25, 32].

Beyond the discrete syndrome of catatonia, schizophrenia is characterised by a host of other intrinsic motor signs and syndromes. A comprehensive study of 200 antipsychotic-naïve patients with schizophrenia spectrum disorders using the Modified Rogers Scale found that 66% exhibited at least one motor sign and 40% met criteria for at least one motor syndrome [5]. These syndromes clustered into factors including abnormal involuntary movements, hypokinesia, both retarded and excited catatonia, catalepsy, and parkinsonism [5]. This highlights that motor dysfunction in schizophrenia is dimensional and multifaceted. Neurological soft signs (NSS), which are subtle impairments in motor sequencing, sensory integration, and coordination, are also highly prevalent. Studies show that schizophrenia patients and ultra-high-risk (UHR) individuals score significantly higher on NSS assessments than healthy controls and even first-degree relatives, suggesting a strong neurodevelopmental component to these deficits [18, 25]. These findings collectively confirm that motor disturbances are a central, intrinsic feature of schizophrenia, not an artefact of treatment.

Motor Abnormality	Prevalence in Antipsychotic-Naïve Schizophrenia	Key Associated Symptoms/Signs	Relevant Sources
Catatonia	9.8% – 20.0%	Mutism, stupor, negativism, posturing, mannerisms, stereotypies, waxy flexibility, excitement.	[1, 20, 21, 29]
Spontaneous Parkinsonism	14% – 19%	Bradykinesia, rigidity, tremor, stooped posture.	[5, 24, 32]
Spontaneous Dyskinesia	3% – 17%	Orofacial, limb, and truncal choreiform movements.	[14, 24, 32]
Psychomotor Slowing	Information not available in provided sources.	Reduced speed in fine/gross motor tasks, slow gait, reduced stride length.	[2, 6, 9]
Oculomotor Deficits	Present in >90% of cases	Impaired smooth pursuit tracking, antisaccade errors, abnormal saccadic latency, poor eye-head coordination.	[4, 7, 19]
Postural Instability	Increased sway area reported in multiple studies.	Hyperlordosis, forward head posture, increased postural sway, reliance on vestibular/ proprioceptive inputs.	[3, 6, 10, 17]

Oculomotor Dysfunction: A Core Biological Marker of Schizophrenia

Oculomotor abnormalities stand out as one of the most consistently replicated biological markers of schizophrenia, with extensive research demonstrating their presence in antipsychotic-naïve patients, thereby firmly establishing them as trait markers rather than medication-induced side effects [4, 19]. These deficits span multiple domains of eye movement control, including smooth pursuit eye movements (SPEM), saccades, and antisaccades, providing a rich source of information about the underlying pathophysiology of the disorder. The consistent finding of oculomotor impairment across untreated patient populations suggests a deep-seated dysfunction in the neural circuits governing visual tracking and rapid eye movements.

Smooth pursuit eye movements, which are responsible for keeping a moving object in focus, are profoundly impaired in schizophrenia. In unmedicated patients, SPEM deficits manifest as reduced gain (the ratio of eye velocity to target velocity), increased catch-up saccades (small corrective saccades needed to reacquire the target), and square-wave jerks (involuntary micro-saccades that move the eyes away from and back to the target) [4]. Research has shown that these impairments are present in both first-episode psychosis (FEP) and chronic schizophrenia, although they tend to be less severe in FEP, suggesting some degree of partial reversibility with long-term antipsychotic treatment [19]. Elevated root mean square error (RMSE), a measure of how closely the eyes follow the target, is also a key deficit and has been associated with general functional impairment [18, 19]. A 2016 meta-analysis confirmed that spontaneous parkinsonism, which includes tremor and rigidity, has a pooled prevalence of 15% in antipsychotic-naïve patients, further cementing the idea that these motor signs are inherent to the illness process [24].

Saccadic eye movements, the rapid jumps the eyes make to shift fixation, also exhibit characteristic abnormalities. Patients with schizophrenia often show impaired performance on antisaccade tasks, where they must look away from a suddenly appearing visual cue. This results in elevated error rates, increased latency for correct antisaccades, and more frequent incorrect pro-saccades (looking towards the cue) [18, 19]. Interestingly, findings on prosaccade latencies (reflexive looks towards a cue) are inconsistent, with some studies reporting no difference and others finding reduced latencies in drug-naïve FEP patients [19]. Another critical aspect of oculomotor control is the ability to adapt to task demands. A landmark study by Schwab et al. demonstrated that while healthy controls could modulate their saccadic latency based on task difficulty, patients with schizophrenia could not, indicating a fundamental deficit in attentional function and executive inhibition [7, 13]. Furthermore, patients showed more ‘uneconomic over-performance’ by making more compensatory head movements during simple tasks and exhibiting a greater delay between the onset of a saccade and a corresponding head movement, pointing to disrupted sensorimotor integration [7, 13]. Even in natural environments, mobile eye-tracking has revealed that patients make more fixations of shorter duration when focusing on stationary targets, suggesting a broader issue with gaze stability and maintenance [28]. These pervasive deficits in oculomotor control provide a powerful window into the dysfunction of fronto-striatal and cerebellar networks that are integral to planning and executing coordinated motor actions.

Gait, Posture, and Balance: Quantifiable Markers of Cerebellar and Cortical Dysfunction

Impairments in gait, posture, and balance are among the most quantifiable and clinically significant non-drug-induced motor disorders in schizophrenia. Unlike transient symptoms like catatonia, these deficits are typically persistent, affecting a patient’s daily functioning and contributing to poor outcomes. Advanced technologies such as motion capture (MoCap) systems and pressure-sensitive force plates have allowed researchers to move beyond subjective observation to identify precise, objective movement markers that differentiate patients with schizophrenia from healthy controls [11, 16]. These studies consistently implicate dysfunction within the cortico-cerebellar-thalamo-cortical circuit (CCTCC) as a core mechanism driving these motor abnormalities [6, 11, 25].

Gait analysis reveals a distinct pattern of motor dysfunction. Patients with schizophrenia walk at a slower pace compared to healthy individuals, and this slowness is primarily attributed to a shorter stride length rather than a reduced cadence (steps per minute) [3, 6, 16]. For example, one study found that unmedicated patients had a gait speed of 1.2 m/s compared to 1.4 m/s in controls [3], while another using MoCap technology identified reduced mean velocity driven by shorter strides [16]. Motion capture studies have uncovered a wealth of additional gait markers, including increased variation in gait patterns (indicating less regularity), a more rigid, “hanging” head posture, reduced arm swing in all planes, and impaired interlimb coordination, such as a disrupted integration between shoulder and hip movements [16]. Furthermore, patients exhibit stiffer arm movements, evidenced by a significantly lower range of motion in the elbow joint during walking [16]. These detailed observations paint a picture of a motor system struggling with regulation, timing, and fluidity.

Postural instability is another core feature, measured by increased postural sway during quiet standing [3, 6, 10]. One study found that unmedicated schizophrenia patients had a sway area nearly double that of healthy controls, particularly under challenging conditions with limited visual input (eyes closed) or conflicting vestibular signals (head rotation) [3, 11]. This suggests a profound impairment in integrating multisensory information for balance control. Patients appear to rely more heavily on vestibular and proprioceptive inputs, showing impaired use of visual information for stabilisation [6, 10]. Beyond sway, common postural abnormalities include hyperlordosis (exaggerated inward curvature of the lower back), a forward head posture, and scoliosis [6]. Critically, these deficits are observed in patients from the earliest stages of illness, with subgroup analyses suggesting that increased sway area and reduced gait speed are present in early-term disease (≤5 years) [3]. The consistent association of these motor impairments with negative symptoms and neurological soft signs further supports the hypothesis that they are part of a shared, intrinsic neurobiological process [9, 11]. The identification of these stable, quantifiable markers is crucial for developing a better understanding of the illness’s progression and for potentially identifying subtypes, such as a profile of early-onset versus adult-onset schizophrenia defined by specific motor characteristics [17].

Catatonia: An Integral Motor Syndrome of Schizophrenia

Catatonia represents a severe and complex motor dysregulation syndrome that is deeply intertwined with schizophrenia. It is characterised by a profound disturbance in the initiation, execution, and termination of voluntary movement, presenting along a spectrum from profound immobility to extreme psychomotor agitation [21, 22]. Despite historical associations and ongoing debate, it is now well-established that catatonic features are a significant part of the schizophrenia phenotype, occurring in approximately 10% of cases, with some estimates reaching as high as 20% depending on the population and diagnostic criteria used [1, 20, 29]. Its inclusion as a specifier for schizophrenia in the DSM-5 formally acknowledges its relevance to the disorder [8]. The symptoms are manifold, encompassing both positive and negative motor signs. Negative features include stupor (a state of unresponsiveness), mutism (inability or refusal to speak), negativism (resistance to instructions or external stimuli), and withdrawal [22, 23]. Positive features include excited or agitated states, stereotypies (repetitive, non-goal-directed movements), mannerisms (idiosyncratic, seemingly purposeful movements), posturing (holding a position against gravity), grimacing, echolalia (mimicking speech), and echopraxia (mimicking movements) [21, 22, 32].

The neurobiology of catatonia in schizophrenia points towards dysfunction in cortical-subcortical circuits, particularly those involving the supplementary motor area (SMA) and orbitofrontal cortex (OFC) [29]. Functional imaging studies have shown hyperperfusion of the SMA correlating with catatonia severity and hypofunction in the OFC and ventromedial prefrontal cortex [29]. This is strongly supported by evidence implicating GABAergic and glutamatergic neurotransmitter systems [8, 29]. Post-mortem and neuroimaging studies have revealed significantly lower GABA-A receptor binding in the right lateral orbitofrontal cortex of akinetic catatonic patients [23, 26]. Furthermore, genetic research has identified links between periodic catatonia—a rare heritable subtype—and mutations on chromosome 15q15, suggesting a genetic susceptibility locus [23, 26]. The cortico-cerebellar-thalamo-cortical circuit (CCTCC) is also implicated as a potential overarching network for the motor and cognitive disturbances seen in catatonia [25, 29].

Diagnosis and treatment present unique challenges. The Bush-Francis Catatonia Rating Scale (BFCRS) is the gold standard for assessment, capturing the full range of catatonic signs [8, 20]. Treatment is guided by the subtype and severity. Benzodiazepines, particularly lorazepam, are considered first-line therapy, with a lorazepam challenge test being a useful diagnostic tool due to its high sensitivity (~80%) [22, 23]. Electroconvulsive therapy (ECT) is highly effective, especially for malignant catatonia (characterised by autonomic instability and fever) or treatment-resistant cases, achieving response rates of around 90% [22]. It is critical to note that typical antipsychotics should be avoided as they can exacerbate or induce catatonia [22]. The prognosis for catatonia related to schizophrenia can be poor, with one study noting a poorer response to benzodiazepines and ECT compared to catatonia arising from mood disorders [8]. The subjective experience of catatonia is also important; patients may report feelings of intense anxiety, fear, or a sense of being dead or dying, and many suffer from “motor anosognosia”—a lack of awareness of their own profound motor disturbances [23]. Understanding catatonia as an intrinsic, treatable motor syndrome is therefore essential for comprehensive psychiatric care.

Pathophysiological Underpinnings: From Cortical Dysfunction to Neurotransmitter Imbalance

The diverse array of non-drug-induced motor disorders in schizophrenia is rooted in a complex and multifaceted pathophysiology involving widespread structural and functional brain abnormalities. Rather than being attributable to a single cause, these motor dysfunctions reflect a failure of distributed neural circuits responsible for planning, initiating, regulating, and executing movement. The evidence points towards a model where dysfunction in cortical-subcortical networks, particularly the cortico-cerebellar-thalamo-cortical circuit (CCTCC), basal ganglia, and premotor cortices, forms the anatomical substrate for these deficits [6, 25, 33]. This model is strongly supported by findings of altered structure, connectivity, and metabolism in these very regions in schizophrenia patients [6, 25].

Neuroimaging studies provide compelling evidence for this distributed dysfunction. Structural abnormalities, such as reduced volume in the cerebellum and atrophy of the cerebellar vermis, are frequently reported in schizophrenia and are directly linked to postural instability and gait deficits [3, 10, 11]. Functional imaging reveals altered activation in the supplementary motor area (SMA) and basal ganglia, which correlates with the severity of psychomotor slowing and catatonic symptoms [2, 29]. Disrupted connectivity, particularly between the motor cortex and the cerebellum, is implicated in gait impairment [6]. Post-mortem and neurochemical studies further refine our understanding by pointing to specific neurotransmitter imbalances. The strongest evidence implicates the GABAergic system, with decreased GABA-A receptor density and binding reported in the orbitofrontal cortex of akinetic catatonic patients and hypothesised to play a role in psychosis and motor disturbances [8, 26, 29]. Similarly, dysfunction in the glutamatergic system, particularly involving NMDA receptors, is a leading hypothesis for the pathophysiology of schizophrenia, and agents like memantine have shown efficacy in treatment-resistant catatonia [23].

Beyond these large-scale circuit and neurotransmitter issues, research has delved into more granular biological mechanisms. There is growing evidence for abnormal oligodendrocyte function and myelination, which would impact the integrity of white matter tracts connecting motor centres [33]. Microglial activation and subsequent neuroinflammation have also been proposed as contributing factors, potentially linking immune dysfunction to the development of motor symptoms [29]. Genetic studies are beginning to uncover susceptibility genes. For instance, abnormalities in the CNP gene, which is involved in oligodendrocyte function, have been linked to catatonic signs in preclinical models [29]. The convergence of these findings—from macroscopic circuit-level changes to microscopic cellular and molecular processes—paints a coherent picture of schizophrenia as a disorder of neural network integrity and communication. This integrated perspective explains why motor symptoms are so closely intertwined with cognitive and negative symptoms, as these different domains are governed by overlapping and interconnected brain networks. The consistent demonstration of these abnormalities in antipsychotic-naïve patients solidifies the conclusion that this pathophysiology is intrinsic to the illness itself, not an epiphenomenon of treatment [12, 33].

Clinical Implications and Future Directions in UK Psychiatry

The recognition of non-drug-induced movement disorders as core features of schizophrenia carries profound implications for clinical practice, research, and service delivery within the UK healthcare system. Acknowledging that these motor abnormalities are intrinsic, not just iatrogenic side effects, shifts the paradigm from viewing them as a treatment complication to considering them as integral components of the illness that require targeted assessment and management. This has direct consequences for diagnosis, treatment planning, and patient outcome monitoring. In the UK, where mental health services are increasingly focused on recovery-oriented models and holistic care, a deeper understanding of these motor deficits is essential.

From a clinical standpoint, routine screening for motor symptoms should become standard practice. Given the high prevalence of catatonia and the strong link between motor signs and negative symptoms, utilising validated tools like the Bush-Francis Catatonia Rating Scale (BFCRS) can aid in early detection [1, 20]. Early identification of catatonia is critical, as prompt treatment with benzodiazepines or ECT can lead to dramatic improvements and prevent life-threatening complications like malignant catatonia [22]. Similarly, the quantifiable nature of gait and balance deficits offers opportunities for objective measurement. Integrating simple balance tests or gait assessments into routine evaluations could help stratify risk for falls and inform interventions aimed at improving mobility and functional independence. The link between motor impairment and poor functional outcomes, such as vocational functioning and quality of life, underscores the need for rehabilitation strategies targeting these areas [2].

Future research directions are vast and promising. The use of advanced technologies like motion capture and portable eye-tracking devices allows for the identification of “movement markers” that could serve as endophenotypes for schizophrenia [16, 28]. These markers could be invaluable in longitudinal studies aimed at identifying ultra-high-risk individuals and predicting the transition to psychosis. They could also serve as biomarkers to track illness progression or response to novel treatments. For example, investigating whether emerging therapies targeting glutamatergic or anti-inflammatory pathways also improve motor symptoms could provide new insights into their mechanism of action and efficacy [23, 29]. Furthermore, exploring the relationship between motor dysfunction and self-disturbances, as suggested by recent studies linking postural patterns to anomalous self-experience, opens up exciting avenues for integrating phenomenological and neurobiological approaches to understanding psychosis [17].

In summary, the field is moving towards a more integrated, multi-system view of schizophrenia. The motor system is no longer seen as a peripheral concern but as a critical window into the core pathophysiology of the disorder. For UK psychiatry, this means embracing a more holistic approach that values the assessment of physical signs alongside cognitive and emotional symptoms. By doing so, clinicians and researchers can develop more comprehensive treatment plans that address the full spectrum of the illness, ultimately leading to improved functional outcomes and a better quality of life for people living with schizophrenia.

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