Late Onset Involuntary Movements in Chronic Schizophrenia: Relationship of ‘Tardive’ Dyskinesia to Intellectual Impairment and Negative Symptoms

1986 ◽  
Vol 149 (5) ◽  
pp. 616-620 ◽  
Author(s):  
J. L. Waddington ◽  
H. A. Youssef

Intellectual impairment, negative symptoms, and medication history were assessed in chronic schizophrenic patients with and without abnormal involuntary movements (tardive dyskinesia). Patients with involuntary movements had received neither longer nor more intensive treatment with neuroleptics or anticholinergics. However, the presence or absence of involuntary movements was prominently associated with the presence or absence of intellectual impairment/negative symptoms; these features are characteristic of the defect state/type II syndrome of schizophrenia, in which structural abnormalities of the brain may be over-represented. The role of subtle organic changes in conferring vulnerability to the emergence of such involuntary movements should be re-evaluated.

1992 ◽  
Vol 22 (4) ◽  
pp. 923-927 ◽  
Author(s):  
K. W. Brown ◽  
T. White

SynopsisSyndromes of dyskinetic movements in subjects (N = 70) with chronic schizophrenia were investigated, using principal components analysis of AIMS ratings. Consonant with previous research, three discrete groupings were found, namely dyskinetic movements of lips-jaw-tongue, limb-truncal and facial movements. These were then related to demographic, psychological and movement disorder variables. The limb-truncal, but neither the lips-jaw-tongue nor facial movements components, were associated with negative symptoms and cognitive impairment.


1990 ◽  
Vol 157 (3) ◽  
pp. 430-433 ◽  
Author(s):  
Nicholas Argyle

Of 20 patients attending a clinic for maintenance therapy of schizophrenia, seven had regular panic attacks, and these were often associated with agoraphobia and social phobia. Similar fears and avoidance in other cases were associated with paranoid ideas and negative symptoms. The relationship of panic to psychotic symptoms varied greatly. In two patients neuroleptics were associated with an increase in panic attacks.


1978 ◽  
Vol 16 (14) ◽  
pp. 55-56

Neuroleptic drugs cause many forms of extra-pyramidal syndromes. One of these, tardive dyskinesia,1 occurs only after the patient has been taking the drug for some time (‘tardive’ refers to the late onset). The movements are involuntary and repetitive usually involving the face and tongue, but they may also affect the limbs and trunk. Tongue protrusion, licking and smacking of the lips, sucking and chewing movements, grimacing, grunting, blinking and furrowing of the forehead have all been described and attributed to long-continued medication with neuroleptic drugs of the phenothiazine, butyrophenone and thioxanthene groups. The patient can inhibit the movements, but anxiety makes them worse. Many of these symptoms were noticed in schizophrenic patients before neuroleptic drugs were introduced2 and they can occur in otherwise normal untreated elderly people. Nevertheless it is generally accepted that in most cases tardive dyskinesia is an unwanted effect of neuroleptic medication. Despite suggestions to the contrary, the abnormal movements are not necessarily associated with high dosage of neuroleptic drugs or with pre-existing brain damage.3 4 Tardive dyskinesia has been reported in 3–6% of a mixed population of psychiatric patients5 and over half of a group of chronic schizophrenics on long-term treatment.4 The more careful the neurological examination, the greater the apparent incidence.


1994 ◽  
Vol 164 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Simon M. Halstead ◽  
Thomas R. E. Barnes ◽  
Jeremy C. Speller

In a sample of 120 long-stay in-patients who fulfilled DSM–III–R criteria for schizophrenia, chronic akathisia and pseudoakathisia were relatively common, with prevalence figures of 24% and 18%, respectively. Compared with patients without evidence of chronic akathisia, those patients with the condition were significantly younger, were receiving significantly higher doses of antipsychotic medication, and were more likely to be receiving a depot antipsychotic. Patients who experienced the characteristic inner restlessness and compulsion to move of akathisia also reported marked symptoms of dysphoria, namely tension, panic, irritability and impatience. The findings support the suggestion that dysphoric mood is an important feature of akathisia. Male patients appeared to be at an increased risk of pseudoakathisia. No significant relation was found between chronic akathisia and tardive dyskinesia, although there was a trend for trunk and limb dyskinesia to be commonest in patients with chronic akathisia while orofacial dyskinesia was most frequently observed in those with pseudoakathisia. Akathisia may mask the movements of tardive dyskinesia in the lower limb. There was no evidence that akathisia was associated with positive or negative symptoms of schizophrenia nor with depression.


1992 ◽  
Vol 160 (1) ◽  
pp. 110-112 ◽  
Author(s):  
Robertson Macpherson ◽  
Rachel Collis

Of 113 patients in long-stay wards of a psychiatric hospital, 43 had TD. Twenty-six of the 39 patients who consented to take part in the study were unaware of abnormal involuntary movements. These patients scored significantly lower on a short test of cognitive function than patients who were aware of such movements. The diagnosis of schizophrenia, perticularly the ‘defect’ state with cognitive deficit and negative symptoms, was found to be associated with lack of awareness of TD.


1997 ◽  
Vol 9 (2) ◽  
pp. 64-67
Author(s):  
R.S. Kahn

The dopamine (DA) hypothesis of schizophrenia, postulating that schizophrenia is characterized by increased dopamine function, has been the most influential theory on the pathogenesis of schizophrenia. It has recently been revised based on the appreciation that the core symptoms of schizophrenia may not be the positive (psychotic) symptoms, but rather the negative symptoms and the cognitive deficits found in schizophrenic patients. This revision has prompted the hypothesis that schizophrenia is characterized by both decreased prefrontal dopamine activity (causing deficit symptoms) and increased dopamine activity in mesolimbic dopamine neurons (causing positive symptoms).Notwithstanding this revision of a role for dopamine in schizophrenia, it has become increasingly evident that dysfunction of other monoaminergic systems may be as important in contributing to the pathophysiology of schizophrenia. Specifically, the putative role of serotonin (5-hydroxytryptamine, 5-HT) in schizophrenia is gaining considerable attention. Several observations, such as the ability of the 5-HT antagonist, ritanserin, to alleviate schizophrenic symptoms and, when added to haloperidol (Haldol®), to decrease its extrapyramidal side-effects (EPS), have stimulated studies into a role of 5-HT in schizophrenia. The finding that clozapine (Leponex®), clinically superior to conventional neuroleptics, is a weak DA2 antagonist but a potent 5-HT1c and 5-HT2 antagonist has further stimulated 5-HT-related research in schizophrenia.


1989 ◽  
Vol 155 (S5) ◽  
pp. 112-116 ◽  
Author(s):  
Kurt Hahlweg ◽  
Eli Feinstein ◽  
Ursula Müller ◽  
Matthias Dose

Hypotheses on the relationship of schizophrenia and family variables have changed considerably over the last 15 years: whereas speculations on the causal role of familial interaction for the onset of schizophrenic psychosis previously dominated the field of psychological theorising and psychotherapy (Bateson et al, 1956), it was not possible to confirm these theories empirically. In accordance with the research on Expressed Emotion (EE), a shift in emphasis to the influence of family variables on the further course of the illness has taken place. As a consequence, promising new techniques have been developed for the prevention or postponement of relapse.


1989 ◽  
Vol 155 (S7) ◽  
pp. 119-122 ◽  
Author(s):  
P.F. Liddle ◽  
Thomas R.E. Barnes ◽  
D. Morris ◽  
S. Haque

In recent years, exploration of the distinction between positive and negative symptoms of schizophrenia has provided a fruitful basis for attempts to relate the clinical features of schizophrenia to the accumulating evidence of brain abnormalities in schizophrenic patients. By 1982, there was an extensive body of evidence supporting the hypothesis that negative schizophrenic symptoms, such as poverty of speech and flatness of affect, were associated with substantial brain abnormalities, such as increased ventricular to brain ratio, and extensive cognitive impairment (Crow, 1980; Andreasen & Olsen, 1982). However, at that stage there were several fundamental unanswered questions about the nature of negative symptoms, and their relationship to indices of brain abnormality. This paper presents some findings of a series of studies initiated in 1982 to seek answers to some of these questions.


2003 ◽  
Vol 33 (3) ◽  
pp. 541-547 ◽  
Author(s):  
D. C. STEFFENS ◽  
M. C. NORTON ◽  
A. D. HART ◽  
I. SKOOG ◽  
C. CORCORAN ◽  
...  

Background. The role of allelic variation in APOE, the genetic locus for apolipoprotein E, in geriatric depression is poorly understood. There are conflicting reports as to an association between the ε4 allele and depression in late life.Method. Using a community based study of non-demented elders in Cache County, Utah, that included many very old individuals, we examined the relationship between APOE and late-onset (age >60) depression, with particular attention to possible age effects.Results. There was no overall association between APOE and depression. However, there was a significant interaction effect of APOE and age such that the relationship of late-onset depression with respect to presence of the ε4 allele was larger among those 80 and older compared with those below age 80. Consistent with previous studies, women were more likely to experience late-onset depression than men.Conclusions. Because we excluded prevalent cases of dementia, this pattern of relative risk with age may reflect the appearance of depressive symptoms as a prodrome of Alzheimer's disease or vascular dementia. Longitudinal studies should help to confirm or refute this explanation of the data.


2001 ◽  
Vol 35 (2) ◽  
pp. 217-223 ◽  
Author(s):  
Ross M. G. Norman ◽  
Ashok K. Malla

Objective: It has been hypothesized that patients with a diagnosis of schizophrenia who have a positive family history for schizophrenia will show greater reactivity of their symptoms to increasing levels of stress or negative affect than will patients without such a family history. In the past this hypothesis has only been tested through manipulations of negative affect in laboratory settings. In this paper we test this hypothesis using longitudinal clinical data. Method: Data were derived from an earlier longitudinal study using monthly assessments of daily stressors (Hassles Scale) and symptom measures (the Scale for the Assessment of Positive Symptoms and the Scale for the Assessment of Negative Symptoms). We compared longitudinal stress to symptom relations in 12 patients with schizophrenia for whom a positive family history of schizophrenia could be identified with 12 matched schizophrenic patients without any known family history of psychiatric illness. Results: There was evidence that patients with a family history of schizophrenia demonstrated a stronger relation between stress and total score on the Scale for the Assessment of Positive Symptoms. This difference appears to have primarily reflected a greater reactivity to stress of reality distortion symptoms in the positive family history group. The two groups did not differ in apparent reactivity to stress of the disorganization and psychomotor poverty dimensions of symptomatology. Conclusions: The results of this study provide support from a naturalistic, longitudinal clinical study for the hypothesis that reactivity to stress of some symptoms of schizophrenia may vary as a function of family history of the disorder.


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