Psychotic and Depressive Symptoms in Parkinson's Disease a Study of the Growth Hormone Response to Apomorphine

1995 ◽  
Vol 167 (4) ◽  
pp. 522-526 ◽  
Author(s):  
John D. C. Mellers ◽  
Niall P. Quinn ◽  
Maria A. Ron

BackgroundThe growth hormone (GH) response to apomorphine, thought to reflect central dopaminergic receptor sensitivity, has been reported as enhanced in acute schizophrenia. We investigated this response in relation to the psychotic episodes associated with Parkinson's disease (PD).MethodThe GH response to apomorphine was measured in three groups of patients with Parkinson's disease: those currently psychotic (n = 9), those with a past history of psychosis (n = 7) and those who had never been psychotic (n = 8).ResultsApomorphine-induced GH response was not related to psychosis but was unexpectedly associated with measures of depression.ConclusionsVisual hallucinations were a prominent feature in the psychotic patients and the atypical nature of these psychoses might explain why we found no evidence of dopaminergic sensitivity. Serotonergic dysfunction would be in keeping with this. Dopaminergic mechanisms may contribute to the minor depressive symptomatology seen in PD.

1974 ◽  
Vol 77 (4) ◽  
pp. 686-690 ◽  
Author(s):  
S. E. Johnson ◽  
N. Norman ◽  
O. Sjaastad

ABSTRACT A study has been carried out in 8 patients with Parkinson's disease in order to measure the growth hormone response to arginine before treatment with L-DOPA and during such treatment. A significant lowering of the HGH response was found during treatment.


The Lancet ◽  
1976 ◽  
Vol 307 (7957) ◽  
pp. 483-484 ◽  
Author(s):  
J.D. Parkes ◽  
A.G. Debono ◽  
C.D. Marsden

Genes ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 430
Author(s):  
Steven R. Bentley ◽  
Ilaria Guella ◽  
Holly E. Sherman ◽  
Hannah M. Neuendorf ◽  
Alex M. Sykes ◽  
...  

Parkinson’s disease (PD) is typically sporadic; however, multi-incident families provide a powerful platform to discover novel genetic forms of disease. Their identification supports deciphering molecular processes leading to disease and may inform of new therapeutic targets. The LRRK2 p.G2019S mutation causes PD in 42.5–68% of carriers by the age of 80 years. We hypothesise similarly intermediately penetrant mutations may present in multi-incident families with a generally strong family history of disease. We have analysed six multiplex families for missense variants using whole exome sequencing to find 32 rare heterozygous mutations shared amongst affected members. Included in these mutations was the KCNJ15 p.R28C variant, identified in five affected members of the same family, two elderly unaffected members of the same family, and two unrelated PD cases. Additionally, the SIPA1L1 p.R236Q variant was identified in three related affected members and an unrelated familial case. While the evidence presented here is not sufficient to assign causality to these rare variants, it does provide novel candidates for hypothesis testing in other modestly sized families with a strong family history. Future analysis will include characterisation of functional consequences and assessment of carriers in other familial cases.


2021 ◽  
Vol 182 ◽  
pp. 106396
Author(s):  
David A. Kaminsky ◽  
Donald G. Grosset ◽  
Deena M. Kegler-Ebo ◽  
Salvador Cangiamilla ◽  
Michael Klingler ◽  
...  

2006 ◽  
Vol 21 (11) ◽  
pp. 1899-1907 ◽  
Author(s):  
David Burn ◽  
Murat Emre ◽  
Ian McKeith ◽  
Peter Paul De Deyn ◽  
Dag Aarsland ◽  
...  

Author(s):  
Yasmin C Aquino ◽  
Lais M Cabral ◽  
Nicole C Miranda ◽  
Monique C Naccarato ◽  
Barbara Falquetto ◽  
...  

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, mainly affecting people over 60 years of age. Patients develop both classic symptoms (tremors, muscle rigidity, bradykinesia and postural instability) and nonclassical symptoms (orthostatic hypotension, neuropsychiatric deficiency, sleep disturbances and respiratory disorders). Thus, patients with PD can have a significantly impaired quality of life, especially when they do not have multi-modality therapeutic follow-up. The respiratory alterations associated with this syndrome are the main cause of mortality in PD. They can be classified as peripheral when caused by disorders of the upper airways or muscles involved in breathing and as central when triggered by functional deficits of important neurons located in the brainstem and involved in respiratory control. Currently, there is little research describing these disorders, and therefore, there is no well-established knowledge about the subject, making the treatment of patients with respiratory symptoms difficult. In this review, the history of the pathology and data about the respiratory changes in PD obtained thus far will be addressed.


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