From one to many: Hypertonia in schizophrenia spectrum psychosis an integrative review and adversarial collaboration report.

Different types of resistance to passive movement, i.e. hypertonia, were described in schizophrenia spectrum disorders (SSD) long before the introduction of antipsychotics. While these have been rediscovered in antipsychotic-naïve patients and their non-affected relatives, the existence of intrinsic hypertonia vs drug-induced parkinsonism (DIP) in treated SSD remains controversial. This integrative review seeks to develop a commonly accepted framework to specify the putative clinical phenomena, highlight conflicting issues and discuss ways to challenge each hypothesis and model through adversarial collaboration. The authors agreed on a common framework inspired from systems neuroscience. Specification of DIP, locomotor paratonia (LMP) and psychomotor paratonia (PMP) identified points of disagreement. Some viewed parkinsonian rigidity to be sufficient for diagnosing DIP, while others viewed DIP as a syndrome that should include bradykinesia. Sensitivity of DIP to anticholinergic drugs and the nature of LPM and PMP were the most debated issues. It was agreed that treated SSD should be investigated first. Clinical features of the phenomena at issue could be confirmed by torque, EMG and joint angle measures that could help in challenging the selectivity of DIP to anticholinergics. LMP was modeled as the release of the reticular formation from the control of the supplementary motor area (SMA), which could be challenged by the tonic vibration reflex or acoustic startle. PMP was modeled as the release of primary motor cortex from the control of the SMA and may be informed by subclinical echopraxia. If these challenges are not met, this would put new constraints on the models and have clinical and therapeutic implications.

Parakinesia: A Delphi consensus report.

Abnormal movements are intrinsic to some forms of endogenous psychoses. Spontaneous dyskinesias are observed in drug-naïve first-episode patients and at-risk subjects. However, recent descriptions of spontaneous dyskinesias may actually represent the rediscovery of a more complex phenomenon, 'parakinesia' which was described and documented in extensive cinematographic recordings and long-term observations by German and French neuropsychiatrists decades before the introduction of antipsychotics. With the emergence of drug induced movement disorders, the description of parakinesia has been refined to emphasize the features enabling differential diagnosis with tardive dyskinesia. Unfortunately, parakinesia was largely neglected by mainstream psychiatry to the point of being almost absent from the English-language literature. With the renewed interest in motor phenomena intrinsic to SSD, it was timely not only to raise awareness of parakinesia, but also to propose a scientifically usable definition for this phenomenon. Therefore, we conducted a Delphi consensus exercise with clinicians familiar with the concept of parakinesia. The original concept was separated into hyperkinetic parakinesia (HPk) as dyskinetic-like expressive movements and parakinetic psychomotricity (PPM), i.e., patient's departing from the patient's normal motion style. HPk prevails on the upper part of the face and body, resembling expressive and reactive gestures that not only occur inappropriately but also appear distorted. Abnormal movements vary in intensity depending on the level of psychomotor arousal and are thus abated by antipsychotics. HPk frequently co-occurs with PPM, in which gestures and mimics lose their naturalness and become awkward, disharmonious, stiff, mannered, and bizarre. Patients are never spontaneously aware of HPk or PPM, and the movements are never experienced as self-dystonic or self-alien. HPk and PPM are highly specific to endogenous psychoses, in which they are acquired and progressive, giving them prognostic value. Their differential diagnoses and correspondences with current international concepts are discussed.

Paratonia, Gegenhalten and psychomotor hypertonia Back to the roots.

In the first half of the 20th century, well before the antipsychotic era, paratonia, Gegenhalten and psychomotor hypertonia were described as new forms of hypertonia intrinsic to particular psychoses and catatonic disorders. A series of astute clinical observations and experiments supported their independence from rigidity seen in Parkinson's disease. After World War II, motor disorders went out of fashion in psychiatry, with drug-induced parkinsonism becoming the prevailing explanation for all involuntary resistance to passive motion. With the 'forgetting' of paratonia and Gegenhalten, parkinsonism became the prevailing reading grid, such that the rediscovery of hypertonia in antipsychotic-naive patients at the turn of the 21st century is currently referred to as "spontaneous parkinsonism", implicitly suggesting intrinsic and drug-induced forms to be the same. Classical descriptive psychopathology gives a more nuanced view in suggesting two non-parkinsonian hypertonias: (i) locomotor hypertonia corresponds to Ernest Dupré's paratonia and Karl Kleist's reactive Gegenhalten; it is a dys-relaxation phenomenon that often needs to be activated. (ii) Psychomotor hypertonia is experienced as an admixture of assistance and resistance that partially overlaps with Kleist's spontaneous Gegenhalten, but was convincingly isolated by Henri Claude and Henri Baruk thanks to electromyogram recordings; psychomotor hypertonia is underpinned by "anticipatory contractions" of cortical origin, occurrence of which in phase or antiphase with the movement accounted for facilitation or opposition to passive motions. This century-old knowledge is not only of historical interest. Some results have recently been replicated in dementia and as now known to involve specific premotor systems.