CNS Spectrums (2016), 21, 341–348. © Cambridge University Press 2016.

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doi:10.1017/S1092852916000274
REVIEW ARTICLE

Catatonia
Sebastian Walther* and Werner Strik

Translational Research Center, University Hospital of Psychiatry, University of Bern, Bern, Switzerland

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.

Received 17 September 2015; Accepted 6 February 2016; First published online 3 June 2016
Key words: Brain imaging, catatonia, DSM-5, motor symptoms, schizophrenia, treatment.

Introduction separated from schizophrenia in Diagnostic and

Statistical Manual of Mental Disorders, Fifth Edition
A complex syndrome of bizarre motor behavior, impaired (DSM-5).15 Here, we will summarize the literature of the
volition, and vegetative abnormalities was described by past decade focusing on prevalence rates and classification
Karl Kahlbaum in the 1870s and termed catatonia.1 issues. We will also discuss putative pathobiology and
Numerous inconsistent descriptions were to follow in the propose a new research strategy to approach catatonia.
psychiatric literature.2–5 The debate included the nosol-
ogy of the syndrome, its operationalization, and the
suspected pathology. Even its extinction by current
The Catatonic Syndrome
antipsychotic treatment has been suggested.6 Once
detected, catatonia may be effectively treated in many The rich clinical descriptions of catatonia are summar-
patients.7,8 Strikingly, most scientific articles on catato- ized elsewhere.3–5,7,16 Up to 40 different signs and
nia are merely case reports or case series, but original symptoms have been associated with catatonia.4,16 These
articles are much less available. Recently, progress has signs may be summarized in 4 groups5: pure motor signs
been achieved by studies reporting that catatonia is still (eg, posturing, rigor, immobility), disturbances of voli-
highly prevalent9–12 and not restricted to schizophrenia tion (eg, ambitendence, negativism, automatic obedi-
spectrum disorders.12–14 Finally, catatonia has been ence), inability to suppress complex motor activities
(eg, stereotypies, rituals, echophenomena), and auto-
nomic instability (eg, tachycardia, hyperthermia).
* Address for correspondence: Sebastian Walther, MD, Translational Symptoms usually wax and wane sometimes within
Research Center, University Hospital of Psychiatry Bern, Bolligenstrasse
1 hour. Even though some are more prevalent than
111, 3000 Bern 60, Switzerland. (Email: [email protected])
We thank Prof. Andrea Federspiel and Dr. Katharina Stegmayer for others, there is no single specific symptom to identify
preparing the figure. catatonia. Some authors, relying heavily on Kahlbaum’s

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342 S. WALTHER AND W. STRIK

TABLE 1. Diagnostic criteria of catatonia

DSM-5 ICD-10

Catatonia criteria Three or more of the following: Catatonic schizophrenia:

1. Catalepsy (ie, passive induction of a posture General criteria for schizophrenia are met. For at least two 2 weeks, the presence of 1 or more of
held against gravity) the following:
2. Waxy flexibility (ie, slight and even resistance 1. Stupor (marked decrease in reactivity to the environment and reduction of spontaneous
to positioning by examiner) movements and activity) or mutism
3. Stupor (no psychomotor activity; not actively 2. Excitement (apparently purposeless motor activity, not influenced by external stimuli)
relating to environment) 3. Posturing (voluntary assumption and maintenance of inappropriate or bizarre postures)
4. Agitation, not induced by external stimuli 4. Negativism (an apparently motiveless resistance to all instructions or attempts to be moved, or
5. Mutism (ie, no or very little verbal response) movement in the opposite direction)
6. Negativism (ie, opposing or not responding to 5. Rigidity (maintenance of a rigid posture against efforts to be moved)
instructions or external stimuli) 6. Waxy flexibility (maintenance of limbs and body in externally imposed positions)
7. Posturing (ie, spontaneous and active 7. Command automatism (automatic compliance with instructions).
maintenance of a posture against gravity)
8. Mannerisms (ie, odd caricature of normal Organic catatonic disorder:
actions) The general criteria for organic brain disorders must be met. One of the following must be present:
9. Stereotypies (ie, repetitive, abnormally 1. Stupor, ie, profound diminution or absence of voluntary movements and speech, and of normal
frequent, non-goal- directed movements) responsiveness to light, noise, and touch, but in the presence of maintenance of normal muscle
10. Grimacing tone, static posture, and breathing (with often limited coordinated eye movements)
11. Echolalia (ie, mimicking another’s speech) 2. Negativism (positive resistance to passive movement of limbs or body or rigid posturing)
12. Echopraxia (ie, mimicking another’s Further markers: Catatonic excitement (gross hypermotility of a chaotic quality with or without a
movements) tendency to assaultiveness). Rapid and unpredictable alternation of stupor and excitement

Catatonia diagnosis 1. Catatonic disorder due to a general medical 1. Organic catatonic disorder
condition 2. Catatonic schizophrenia
2. Catatonia specifier for
a. Schizophrenia
b. Schizoaffective disorder
c. Schizophreniform disorder
d. Brief psychotic disorder
e. Substance-induced psychotic disorder
3. Catatonia specifier for affective disorders
a. Major depressive disorder
b. Bipolar I disorder
c. Bipolar II disorder
4. Catatonic disorder NOS

initial descriptions,16,17 also consider affective distur- Classification Issues: DSM-5 vs. ICD-10
bances and behavioral problems (eg, nudism) as
part of the catatonic syndrome. Finally, the catatonic DSM-5 and the International Statistical Classification of
syndrome may become malignant with increased Diseases and Related Health Problems, Tenth Revision
mortality,2,16 particularly when autonomic instability is (ICD-10) differ substantially in their definitions and
included. classifications of catatonia (see Table 1). While DSM-5
The catatonia syndrome frequently occurs in schizo- conceptualized catatonia as a widely independent syn-
phrenia spectrum disorders and affective disorders, but drome, ICD-10 allows diagnosing catatonia only in the
also in autism, dementia, intoxications, and in general context of schizophrenia or as a syndrome due to an
medical conditions. The onset and duration of symptoms organic brain disorder. This might be due to the
vary considerably. Particularly among chronic schizo- perception of catatonia in the early 1990s when ICD-10
phrenia patients, cases with chronic catatonia course was proposed. DSM-IV, however, which was published a
have been reported.11 Some catatonia patients experi- few years before ICD-10, already offered the opportunity
ence complete remission within 24 hours.18 Acute and to code catatonia as a specifier of major mood
chronic forms of catatonia share the same symptoms, but disorders.15 In DSM-5, catatonia is now recognized in
some clinical differences in symptom endorsement all psychotic and major mood disorders as a syndrome
frequencies have been noted, and benzodiazepines are due to general medical conditions, or as a syndrome not
less effective in chronic catatonia.18–21 Catatonia may otherwise specified; this allows coding catatonia in the
occur in children. As in adults, insidious onset is context of other psychiatric disorders, such as autism or
associated with poorer outcome.22 obsessive compulsive disorder.

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CATATONIA 343

Besides the nosologic restrictions, the systems differ catatonia can occur irrespective of disease state
in the diagnostic criteria of catatonia (see Table 1). (first episode or chronic course) and treatment status
ICD-10 lists only 2 symptoms for organic catatonic (never medicated or medicated).5,9,11 Prevalence rates
disorder (stupor and negativism) and 7 symptoms for the increase when catatonia rating scales such as the Bush
catatonic subtype of schizophrenia. In contrast, DSM-5 Francis Catatonia Rating Scale (BFCRS)25 are applied.
lists 12 symptoms for catatonia independent of the DMS-5 or ICD-10 criteria are more conservative. In
underlying disorder. There is considerable overlap mixed inpatient populations of psychiatric institutions,
between the lists, as 5 out of 7 ICD-10 criteria are also catatonia appears to have a prevalence of 10–25%.23,26
found in the DSM-5 criteria (posturing, negativism, As noted by several authors, the use of clinical rating
stupor, waxy flexibility, and excitement/agitation). Yet, scales or experts is superior in detecting catatonia
rigor and automatic obedience are not included in the compared to registers of clinical diagnoses.6,9,10,23,27,28
DSM-5 criteria, while ICD-10 lacks relevant items such Reports agree that the presence of 3 or more catatonia
as the echophenomena, mutism, mannerisms, stereo- signs have optimal sensitivity and specificity to detect
typies, and grimacing. The diagnostic thresholds are catatonia among psychotic patients.9,26,29
different and affect the incidence of catatonia in Reported catatonia prevalence rates in mixed patient
schizophrenia.23,24 Three or more items without time groups were quite similar between affective disorders
limit are required in DSM-5, while only 1 lasting for and psychotic disorders.23,26 However, differences in
2 weeks is sufficient in ICD-10. onset, number of signs, and course were noted between
The ICD-10 catatonia concept has 2 major limita- catatonia due to schizophrenia and so-called idiopathic
tions: persistent catatonia will eventually be labeled as catatonia, ie, without any underlying axis-I disorder.30
schizophrenia, and catatonia observed in the context of Likewise, symptom presentation slightly differs
neurodevelopmental disorders or nonschizophrenic between catatonia due to schizophrenia and affective
psychoses cannot be coded. Instead, major advances of disorders.12,23,31
DSM-5 over DSM-IV are the introduction of a catatonia Even though a few studies on the prevalence of
specifier for psychotic disorders (see Table 1), the catatonia in mixed patient groups are available,10,23,24,26
change of the diagnostic criteria (3 or more of 12 signs), there is a lack of systematic investigations on the
the introduction of “catatonia not otherwise specified presentation of catatonia in different patient groups.
(NOS),” and the waiving of the catatonic subtype of While some studies in psychotic disorders assessed
schizophrenia.15 The DSM-5 catatonia specifier catatonia among other motor abnormalities,27,32–34 most
has been warmly greeted by catatonia experts, although reports fail to delineate catatonia from other movement
its impact on treatment is unclear: As Max Fink pointed disorders. Finally, studies that focus on the duration and
out, there might be problems when treating the course of catatonia are needed.
catatonia syndrome and the underlying disorder
concurrently.16 Still, many patients will have their
Factor structure
underlying condition when catatonia has already been
relieved.15 As catatonia includes a variety of symptoms, different forms
have been proposed. Many clinicians follow the classical
distinction between retarded and excited catatonia.16
Clinical Presentation Depending on the instruments used and the sample
investigated, studies reported 3,9,24 4,12,35 or 623 indepen-
Prevalence
dent factors. Consistently, studies disentangle excited
Prevalence rates of catatonia vary depending on catato- catatonia, retarded catatonia, and 1 factor describing
nia concepts and criteria (see Table 2). In schizophrenia, disturbances of volition. Besides the need to further

TABLE 2. Prevalence rates of catatonia

Study n Sample DSM-IV DSM-5 BFCRS ICD-10

Docx et al38 124 Chronic schizophrenia, in- and outpatients 35.5%

Grover et al26 201 Schizophrenia and mood disorders, inpatients 9.5%
Stuivenga and Morrens23 130 Mixed inpatient sample from acute psychiatric hospital 24.6% 16.9% 63.1%
Peralta et al9 200 Nonaffective, first episode, medication-naïve patients 12.0% 19.5%
Van der Heijden et al10 100 Schizophrenia and mood disorders, inpatients 18.0%
Ungvari et al11 225 Chronic schizophrenia 32.0%
Kleinhaus et al28 568 Population cohort of schizophrenia 7.6%

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344 S. WALTHER AND W. STRIK

develop appropriate clinical instruments to cover Suspected Pathophysiology

the catatonia syndrome among various underlying
Neurotransmitter systems
conditions, the precise structure of catatonia has yet to
be discovered.24 Several neurotransmitter disturbances have been dis-
cussed as putative causes for catatonia, including
dopamine, glutamate, and gamma-aminobutyric acid
Special forms
(GABA). Dopamine has been put forward as dopamine
As acknowledged by DSM-5, catatonia may occur in antagonism may produce rigor and immobility, and
various conditions across the lifespan. In childhood dopamine-D2 antagonists may worsen catatonia in some
onset schizophrenia with catatonic features, comorbid cases.8 However other signs of catatonia cannot be
medical conditions are found in 22% and developmental explained by dopamine antagonist action. One syndrome
disorders in 31% of cases.36 Childhood catatonia often closely related to catatonia—the neuroleptic malignant
presents as excited catatonia including aggression.37 syndrome—is probably caused by antidopaminergic
Even though, in many cases, catatonia is associated with drugs.16 Dopamine agonists, however, fail to alleviate
another psychiatric disorder or general medical condi- the neuroleptic malignant syndrome8 as well as chronic
tion, in some cases catatonia is the only detectable catatonia.41 The few studies on dopamine metabolism or
syndrome. Based on their impressive clinical data, receptor occupancy in catatonia remain inconclu-
Peralta et al32 proposed to separate idiopathic catatonia sive.42,43 Glutamate dysfunction may contribute to some
from catatonia secondary to a psychiatric disorder or of the catatonia phenotypes. The N-methyl-D-aspartate
medical condition. (NMDA)-receptor antagonist ketamine elicited
In non-affective psychoses, catatonia frequently co- catatonia-like signs when administered in healthy sub-
occurs with other motor abnormalities, particularly jects.44 In line with this, a mouse model of reduced
abnormal involuntary movements and parkinson- NMDA-receptor expression indicated abnormal motor
ism.27,32,34,38 Besides the co-existence of various motor and social behavior with face validity when compared to
abnormalities, there is conceptual overlap, as some catatonia.45 Furthermore, the clinical presentation of
symptoms such as rigor are classified either as a sign of many subjects with anti-NMDA-receptor encephalitis
parkinsonism or of catatonia.5 In schizophrenia, catato- mimics acute catatonia with stereotypies, mutism,
nia symptoms interfere with correct performance of hand echophenomena, rigidity, and abnormal involuntary
gestures and even with nonverbal social perception.39,40 facial movements.46 In fact, some acute catatonia cases
Thus, catatonia may strongly hamper nonverbal commu- may even resemble misdiagnosed anti-NMDA-receptor
nication and contribute to poor social functioning in encephalitis.47 In contrast, anecdotal reports suggest
schizophrenia. some efficacy of the NMDA-antagonist amantadine in
treating catatonia.8,43 GABAergic drugs are most effec-
tive in treating acute catatonia, as evidenced by
Treatment
numerous case reports and clinical trials.8,43 Moreover,
Evidence from numerous case reports and a few decreased GABAA-receptor density was detected in the
controlled clinical studies advocates the use of benzodia- left sensorimotor cortex of catatonia patients, which
zepines in adults8,16 and in children.22 Diazepam, correlated with the severity of catatonia.48 Very recently,
clonazepam, or oxazepam are also effective.8 In chronic antibodies against GABAA-receptor subunits were
schizophrenia, the situation is less clear.20 In subjects detected in patients with neuropsychiatric syndromes,
with insufficient response to benzodiazepines or in including 2 subjects with catatonia-like behaviors; 1 of
life-threatening conditions, electroconvulsive therapy the 2 improved rapidly following plasma exchange.49
(ECT) is the method of choice to treat catatonia. Patients Still, a controlled clinical trial of GABA agonist
with chronic catatonia seem to benefit from a combina- lorazepam indicated no effect on chronic catatonia.20
tion of ECT and clozapine.8 Taken together, alterations in GABAergic and glutama-
In order to treat the underlying condition, patients tergic neural activity may contribute to some but not all
with catatonia often receive antipsychotic drugs when phenotypes of catatonia, while the case is much less clear
catatonia accompanies schizophrenia. The use of for dopamine.
antipsychotic agents in catatonia is intensely debated.8,16
An excellent study investigated the effect of a 4-week Brain circuitry
trial of antipsychotics on motor syndromes in 100
medication-naïve, first-episode psychosis patients.33 The neuroimaging literature on catatonia still is slowly
Catatonia was treatment responsive in 15/18 (83%) evolving.50 To many patients with catatonia, the scan-
cases, remained unchanged in 3 subjects, and appeared ning procedure would be intolerable, while others are
with treatment in 2 patients. incapable of providing informed consent. The current

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CATATONIA 345

literature is limited to case series on cerebral metabolism his perfusion MRI indicated abnormal hyperperfusion
or regional cerebral blood flow obtained during the at rest within the supplementary motor area (see the
resting state. Very few studies have managed to test Case Report in the Appendix and Figure 1). We have
neural activation during tasks. Therefore, neuroimaging introduced a rating scale for 3 psychopathological
studies in catatonia are particularly affected by selection dimensions of psychoses, the Bern Psychopathology
bias, strongly limiting the generalizability of results. Scale,64 including a motor dimension that separates
Alterations of brain function or structure due to motor inhibition from excitement. In schizophrenia,
catatonia are found within the cerebral motor circuit.50 inhibition in this motor domain was associated
The majority of studies reported hypoactivity in cortical with increased volume of the supplementary motor
motor areas of the frontal and parietal cortex. Early work area.65
on regional cerebral blood flow (rCBF) indicated frontal While some progress was made in unraveling the
and parietal hypoperfusion in mixed groups of predomi- pathobiology of catatonia in the 1990s and 2000s, we are
nantly akinetic catatonia.51–53 Furthermore, some currently facing a deadlock of research on this topic. In
reports noted an increase of frontal motor and parietal our view, there are 2 main reasons for this dilemma: the
rCBF during the improvement of catatonia by ECT.52,54 clinical description of the syndrome and the lack of
Moreover, akinetic catatonia patients had delayed onset sufficient neuroscientific methods. While DSM-5 has
of movement-related potentials and readiness potentials now offered a way to detect and classify catatonia, in
in motor areas, which correlated with catatonia sever- many instances providing a clear general set of criteria, a
ity.55 Likewise, few studies consistently found reduced number of problems remain: the heterogeneity of signs in
neural activation in cortical motor and premotor areas, the clinical presentation, the overlap of signs with other
as well as in the parietal cortex in catatonia during syndromes such as parkinsonism, the association with
finger-tapping or finger-opposition tasks.56–58 Finally, 2 different underlying disorders, and the heterogeneous
studies suggested impaired orbitofrontal function during course. To date, it is unclear whether the catatonia
processing of negative emotions in catatonia.59,60 syndrome resembles a general clinical phenotype with
In contrast to the above mentioned studies, there have different underlying pathomechanisms or whether cata-
been reports of chronic catatonia patients in whom tonia has a common phenotype and pathobiology.
cerebral correlates of catatonia symptoms revealed Currently, the first assumption seems more likely.
different patterns. Three cases of chronic catatonia Several psychiatric and medical conditions may produce
presented with separate patterns of brain metabolism transient catatonia and a few chronic forms of catatonia.
according to symptoms: One patient experienced frontal The majority responds well to rather unspecific treat-
hypermetabolism and thalamic hypometabolism while ments, such as benzodiazepines and ECT.8 The associa-
presenting with speech prompt symptoms, ie, immediate tion with a broad variety of underlying conditions that
verbal response. In contrast, 2 subjects with speech have not very much in common argues against a common
sluggish catatonia presented the opposite pattern: left cause for catatonia. Given this magnitude of hetero-
frontal hypometabolism and thalamic hyperactivity.42 geneity in symptom presentation, course, and underlying
Likewise, a case of very late onset catatonia was reported condition, we may not be able to find a substrate when
to have retarded catatonia and cerebral hypoperfusion applying neuroimaging, endocrine markers, or immuno-
within striatum and thalamus, but hyperperfusion in the logical assays in a group of catatonia patients.
left lateral frontal cortex; both localized perfusion
changes were ameliorated by effective therapy.61 The
Proposed research strategy
identical pattern of cerebral metabolism was reported in
a case of a young girl with catatonia with stereotypies The changes in DSM-5 will hopefully increase catatonia
and mutism/immobility.62 Near Infrared spectroscopy awareness. Progress in catatonia research may be
revealed phasic hyperactivity in the left anterior pre- achieved at a basic clinical level and at a neuroscientific
frontal cortex during episodes of staring, mutism, and level. The basic clinical level would include data on
catalepsy in a patient with treatment-resistant catato- frequencies and enhanced catatonia instruments.
nia.63 Thus, patterns of altered cerebral metabolism or With the new DSM-5 criteria, there is clearly a need for
neural activity are not necessarily driven by the presence more prevalence data, which must also take into account
or absence of catatonia, but may correspond to specific the heterogeneous course of catatonia. In addition,
symptoms. For further illustration, please also see our as pointed out by several groups, the current rating
Case Report (in the Appendix) of a young patient with scales require well-considered improvements, as the
chronic catatonia who experiences mainly volitional structure of catatonia has not yet been fully discovered.24
problems, eg, during movement initiation while the On the neuroscientific level, which must rely on clear
movements are executed rapidly and correctly once clinical descriptions and delineations, there is a need
started. In contrast to the findings in akinetic catatonia, for further neuroimaging studies. In fact, most

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346 S. WALTHER AND W. STRIK

FIGURE 1. Cerebral resting state perfusion in healthy controls (upper row left), schizophrenia patients (upper row middle), and a single catatonia patient with
predominantly impaired volition and motor initiation (upper row right). Numbers below the slices indicate the z coordinate of the axial slice. Perfusion values of
4 motor regions are given at the bottom (controls in blue, patients in red, catatonia case indicated by black triangle).

neuroimaging studies would not meet the current educational speaker, speaker’s fee; Sandoz, educational
standards of image processing and data reporting. speaker, speaker’s fee; Lundbeck and Otsuka, advisory
Advances in structural neuroimaging and new methods board member, honoraria. Werner Strik does not have
of assessing the brain’s resting state could contribute anything to disclose.
to the understanding of the catatonia neurobiology.
Maybe these techniques could disentangle different types
R E F E R E NC E S :
of disturbances within the motor circuitry. Finally, we
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Sebastian Walther has the following disclosures: Janssen psychometric validity and response to antipsychotic medication.
Cilag, educational speaker, speaker’s fee; Eli Lilly, Schizophr Res. 2010; 118(1–3): 168–175.

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Appendix: Case Report when triggered by external stimuli. Thus, the main clinical
problem is volition and movement initiation. Perfusion
An 18-year-old patient had been suffering from chronic MRI with arterial spin labeling (ASL) indicated increased
catatonia with predominant negativism, blocking, staring, resting state cerebral blood flow predominantly in
posturing, rituals, and stereotypy for more than 2 years. premotor areas of the brain (see Figure 1, top panel).
He experienced an insidious onset that first included In comparison to healthy controls and a cohort of
generalized slowing. For most of this period, severity schizophrenia patients, he had maximum perfusion in the
remained basically the same, but symptom intensity waxed supplementary motor area and high perfusion in the
and waned. Little benefit was achieved by administering cingulate motor area, but average values in the bilateral
clozapine 200 mg/d. On the Bush Francis Catatonia striatum (see Figure 1, bottom panel). Thus, the problem
Rating Scale, he had a score of 19. Interestingly, he may with this patient appears to be one of ineffective motor
exhibit good performance and endurance in physical planning, which seems to be related to hyperperfused
exercise once the movements are started, particularly premotor areas.

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