Primitive (developmental) reflexes and diffuse cerebral dysfunction in schizophrenia and bipolar affective disorder: Overrepresentation in patients with tardive dyskinesia

Retained Primitive Reflexes and ADHD in Children

“…In the light of current findings these data are in agreement with neurological concept proposed by Jacksonian theory according to which persisting primitive reflexes may cause "dissolution" (Andermann, 1997;Franz & Gillett, 2011;Jacyna, 2011) that may result in ADHD patients into various symptomatic forms (Endo, Sugiyama, & Someya, 2006;Johnson et al, 2007). This process of dissolution related to retained primitive reflexes is based on disinhibition of neural functions or their release from control that leads to dysregulation of later developed adaptive functions (Franz & Gillett, 2011) and may be linked to various neuropsychiatric syndromes (Keshavan & Yeragani, 1987;Youssef & Waddington, 1988;Zafeiriou, 2004;Links et al, 2010;Nicolson et al, 2011;Sanders & Gillig, 2011).…”

“…Recent findings also indicate that persisting of the primitive reflexes may be linked to certain specific neuropsychiatric disorders (Keshavan & Yeragani, 1987;Youssef & Waddington, 1988;Zafeiriou, 2004;Links et al, 2010;Nicolson et al, 2011;Sanders & Gillig, 2011) although according to current scientific findings there is no evidence whether these persisting reflexes play a role in Attention Deficit and Hyperactivity Disorder (ADHD). With respect to these missing findings (or at least very rare) we have proposed and tested the hypothesis to which extent ADHD will be related to persisting Moro and Galant reflexes in children in the school age (8-11 years) compared to a control group of children of the same age.…”

The Pineal Gland and the Mechanisms of Tardive Dyskinesia

“…Klawans & Barr (1 982) have reported a 6.8% incidence of spontaneous lingual-facial-buccal dyskinesias in nonpsychiatric subjects in the sixth to seventh decade age group. These observations, together with recent reports suggesting an increased rate of "soft" neurological signs, cognitive deficits and primitive (release) reflexes in schizophrenic patients with T D compared to those without T D (Waddington & Youssef, 1986;Youssef & Waddington, 1988), strongly suggest that the emergence of abnormal involuntary movements may largely be the result of an underlying disease and/or aging processes. Neuroleptics may contribute secondary to the development of T D by accelerating or accentuating the effects of these primary cerebral processes.…”

“…It is therefore possible that the increased incidence of orofacial dyskinesias in elderly nonpsychiatric patients (Klawans & Barr, 1982) as well as in elderly schizophrenics and those with history of affective disorders may in part be associated with diminished secretory activity of pineal melatonin. Since the incidence of "soft" neurological signs, and the presence of primitive or release reflexes has been reported to be higher in T D compared to non-TD schizophrenic and bipolar patients (Wolf et al, 1983;Youssef & Waddington, 1988), the emergence of T D may reflect a pathological release phenomenon secondary to diffuse cerebral dysfunction. Alternatively, TD may be associated with diminished pineal melatonin-mediated physiological protection against the development of involuntary movements (Sandyk & Fisher, 1988).…”

“…Alternatively, TD may be associated with diminished pineal melatonin-mediated physiological protection against the development of involuntary movements (Sandyk & Fisher, 1988). Hence, neuroleptics may exacerbate the development of T D by potentiating the expression of the pathological release process (Kidger et al, 1980;Youssef & Waddington, 1988), or by attenuating the protective effect of melatonin by inhibiting melatonin synthesis (Hartley et al, 1972;Cremer-Bartels et al, 1983).…”