Neuropathological Investigation of 28 Brains From Patients With Dyskinesia

Christensen, E. Hohwü; Møller, E M D Jørn; Faurbye, Arild

doi:10.1111/j.1600-0447.1970.tb02097.x

Cited by 167 publications

(30 citation statements)

References 11 publications

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“…Neuronal loss and infarction was also noted in the globus pallidum in 25% of cases. Similar findings were observed by other investigators (Nieto & Escobar, 1972;Christensen et al, 1970;Lesch & Bogerts, 1984). It is noteworthy that the distribution of the pathological lesions in schizophrenia overlap with those found in patients with postencephalitic Parkinsonism (Howard & Lees, 1987), which could explain the high incidence of schizophrenic symptoms in patients with postencephalitic Parkinsonism (Crow, 1983;Howard & Lees, 1987).…”

Section: Negative Schizophrenia Of Parkinsonismsupporting

confidence: 77%

Is negative schizophrenia a variant of parkinsonism?

Sandyk

Kay

1990

International Journal of Neuroscience

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Section: Negative Schizophrenia Of Parkinsonismsupporting

confidence: 77%

Is negative schizophrenia a variant of parkinsonism?

Sandyk

Kay

1990

International Journal of Neuroscience

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“…Simiexpression induced by haloperidol is not of uniform magnitude or occurrence throughout the brain. lar processes may contribute to the caudate enlargement [60][61][62] and striatal neuropathology 63,64 which are Synaptophysin expression is usually considered to reflect synaptic density, [8][9][10][11][12][13][14][15][16][17][18] and in this respect our data observed in patients treated long-term with these drugs.…”

Section: -57mentioning

confidence: 78%

Chronic haloperidol treatment differentially affects the expression of synaptic and neuronal plasticity-associated genes

1997

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Synaptophysin is a protein used as a marker of presynaptic terminals. We previously showed that, in dorsolateral striatum of the rat, 2 weeks' haloperidol treatment up-regulated synaptophysin mRNA. We have now investigated the effects of 16 weeks' treatment with haloperidol on synaptophysin expression in dorsolateral striatum, frontoparietal cortex and hippocampus, in order to see if the implied haloperidol-induced synaptic plasticity persists. For comparison, in both the 2-and 16-week treatment groups we determined the mRNA abundance of the neuronal plasticity-associated gene GAP-43, and the housekeeping gene cyclophilin. Sixteen weeks' haloperidol administration increased synaptophysin mRNA in striatum and frontoparietal cortex but not in hippocampus. The increase was demonstrable both regionally and per neuron. A similar trend was seen for synaptophysin protein using immunoautoradiography. GAP-43 mRNA was elevated in frontoparietal cortex by 2 weeks' haloperidol but was not significantly changed in any area in the 16-week treatment group. Cyclophilin mRNA, a marker of overall gene expression, was unaffected by haloperidol. The persistent increase in synaptophysin expression supports the evidence that chronic antipsychotic drug treatment induces synaptic reorganisation in some striatal and cortical neuron populations, whereas the GAP-43 mRNA data suggest that haloperidol does not produce a sustained alteration of neuronal plasticity. Further study of plasticity-associated gene expression may be valuable in clarifying the long-term neuronal and synaptic changes produced by antipsychotics, and how these are related to the neurochemical effects of the drugs.

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“…While some studies have noted an association between preexisting brain damage and TD, particularly in patients with aective disorders, perhaps the majority of studies have found no such correlation. Postmortem studies have been few and the positive ®ndings (nigral degeneration and increased iron deposition, midbrain gliosis, abnormal neurons in the cerebellar dentate nucleus) have yet to be replicated (Campbell et al, 1985;Arai et al, 1987;Christiansen et al, 1970). The ®ndings from in vivo neuroimaging studies have been mixed.…”

Section: Discussionmentioning

confidence: 93%