Cerebrospinal fluid levels of 3‐methoxy4hydroxyphenylethylene glycol in Parkinsonism before and after treatment with L‐DOPA<sup>1</sup>

Wilk, Sherwin; Mones, Robert J.

doi:10.1111/j.1471-4159.1971.tb03753.x

Cited by 26 publications

(3 citation statements)

References 16 publications

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“…This finding corroborates earlier works [25]. Also in keeping with earlier studies, the drug treatment had no influence on the measured CSF NA and MHPG values [19,25].…”

Section: Discussionsupporting

confidence: 82%

Correlation of Autonomic Dysfunction to CSF Concentrations of Noradrenaline and 3-Methoxy-4-Hydroxyphenylglycol in Parkinson’s Disease

Turkka¹,

Juujärvi²,

Myllylä³

1987

Eur Neurol

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In order to study the role of the neurotransmitter noradrenaline (NA) and its main brain metabolite 3-methoxy-4-hydroxyphenylglycol (MHPG) in autonomic failure in Parkinson’s disease (PD), an analysis of the relation of cerebrospinal fluid (CSF) NA and MHPG levels and a rating of autonomic nervous system (ANS) impairment was carried out. The mean baseline NA level in CSF of PD patients was 220.0 ± 110.0 pg/ml, and the mean baseline MHPG level 9.9 ± 3.9 ng/ml. These levels did not differ from those of age-matched controls. Within the group of patients with PD neither the duration of the disease nor its medication influenced the results. No correlation could be found in patients with PD between the CSF NA levels and the severity of autonomic failure, but a clear correlation was found between the CSF MHPG concentrations and the severity of autonomic failure.

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“…This finding corroborates earlier works [25]. Also in keeping with earlier studies, the drug treatment had no influence on the measured CSF NA and MHPG values [19,25].…”

Section: Discussionsupporting

confidence: 82%

Correlation of Autonomic Dysfunction to CSF Concentrations of Noradrenaline and 3-Methoxy-4-Hydroxyphenylglycol in Parkinson’s Disease

Turkka¹,

Juujärvi²,

Myllylä³

1987

Eur Neurol

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“…CSF NE levels have been found normal (Turkka et al, 1987; Chia et al, 1993; Kuhn et al, 1996a; Engelborghs et al, 2003) or decreased (Martignoni et al, 1992; Eldrup et al, 1995) in PD patients. CSF levels of 3-methoxy-4-hydroxy-phenylethyleneglycol (MHPG), the main metabolite of NE, have been reported to be normal (Wilk and Mones, 1971; Davidson et al, 1977; Mann et al, 1983; Mena et al, 1984; Hartikainen et al, 1992; Martignoni et al, 1992; Chia et al, 1993; González-Quevedo et al, 1993; Mashige et al, 1994; Kuhn et al, 1996a; Engelborghs et al, 2003) or decreased (Granerus et al, 1974) in PD patients. CSF MHPG levels do not increase either after treatment with levodopa (Wilk and Mones, 1971; Davidson et al, 1977) or with the NE precursor L-Threo-3,4-dihydroxyphenylserine (L-threo-DOPS) (Yamamoto et al, 1986; Teelken et al, 1989), while L-threo-DOPS increases CSF NE levels (Tohgi et al, 1990, 1993d).…”

Section: Neurotransmitters Neuromodulators and Related Substancesmentioning

confidence: 99%

Cerebrospinal fluid biochemical studies in patients with Parkinson's disease: toward a potential search for biomarkers for this disease

Jiménez‐Jiménez¹,

Alonso‐Navarro

García‐Martín

et al. 2014

Front. Cell. Neurosci.

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The blood-brain barrier supplies brain tissues with nutrients and filters certain compounds from the brain back to the bloodstream. In several neurodegenerative diseases, including Parkinson's disease (PD), there are disruptions of the blood-brain barrier. Cerebrospinal fluid (CSF) has been widely investigated in PD and in other parkinsonian syndromes with the aim of establishing useful biomarkers for an accurate differential diagnosis among these syndromes. This review article summarizes the studies reported on CSF levels of many potential biomarkers of PD. The most consistent findings are: (a) the possible role of CSF urate on the progression of the disease; (b) the possible relations of CSF total tau and phosphotau protein with the progression of PD and with the preservation of cognitive function in PD patients; (c) the possible value of CSF beta-amyloid 1-42 as a useful marker of further cognitive decline in PD patients, and (d) the potential usefulness of CSF neurofilament (NFL) protein levels in the differential diagnosis between PD and other parkinsonian syndromes. Future multicentric, longitudinal, prospective studies with long-term follow-up and neuropathological confirmation would be useful in establishing appropriate biomarkers for PD.

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“…Dopamine may not have access to dopamine beta-hydroxylase or only a fixed amount may be converted to norepinephrine. Clinically, chronic levodopa administration fails to alter MHPG levels in CSF of treated patients (63)(64)(65).…”

Section: Neurobiology Of Dementia and Cognitive Impairmentmentioning

confidence: 99%

A current analysis of behavioral problems in patients with idiopathic Parkinson's disease

Mayeux

1989

Mov Disord.

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Parkinson's disease (PD) is a progressive disabling neurological disorder resulting from degeneration of dopamine-containing cells in the substantia nigra (1). Tremor, rigidity, bradykinesia, diminished hand and foot dexterity, and postural instability are the characteristic motor manifestations. Dementia, various forms of cognitive impairment, and depressive disorders are also present in PD (2). Although postmortem studies indicate that motor signs develop when 80% of the cells in the substantia nigra are lost, the pathophysiology of the nonmotor features, in particular, dementia and depression, is only partially understood. For example, the course of the motor disability parallels the degenerative process in the nigra, and biochemical and pharmacological studies implicate that this results from the loss of dopamine (1). Behavioral manifestations of PD, on the other hand, are linked to degenerative changes in other neurotransmitter systems. Although levodopa and related agents alleviate most of the motor manifestations, they are ineffective or of limited value in patients with nonmotor behavioral manifestations. Because behavioral problems have a significant impact on the management of PD, the purpose of this review is to highlight current understanding of these manifestations of the idiopathic form of PD. EPIDEMIOLOGY OF IDIOPATHIC PDBecause the age of onset of the motor manifestations may increase the risk of developing a behavioral change, it is important to first consider the epidemiology of this degenerative disorder. The prevalence of PD in the general population varies from -100 to 200 per 100,000 (3,4). Idiopathic PD (IPD) is the most common form, accounting for >85% of patients with PD (5). Age-specific prevalence of IPD dramatically increases in each decade; after age 65 the prevalence is twice that for all lower age ranges and the prevalence again doubles after age 75. At age 65 and older the prevalence of IPD is approximately 1,000 per 100,000 (3,4). S48 BEHAVIOR PROBLEMS IN IDIOPATHIC PD s49Recent investigations indicate that prevalence for blacks and women is similar to those for whites and men (4).The incidence of IPD is -20 per 100,000 in the general population, but the incidence also rises dramatically with age (5). Rajput and associates ( 5 ) found the rate to be 113.4 per 100,000 person-years between the ages of 65 and 74 and 254.4 per 100,000 person-years at ages 75-84. Sex and race differences in incidence were not apparent. Survival after diagnosis of PD is similar to that in healthy aged adults when levodopa is used (5). However, the mortality rates for untreated or partially treated patients with PD, as might be expected with dementia, is higher. EPIDEMIOLOGY OF DEPRESSION IN IPDDepression is probably the most common mental disturbance in IPD (2). In a review of 14 recent studies that included >1,500 patients, Gotham et al. (6) estimated the mean prevalence to be 46%. Prevalence ranged from 20% to as high as 90% in these studies. In our own investigations (7,8), depression was present in...

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Cerebrospinal fluid levels of 3‐methoxy4hydroxyphenylethylene glycol in Parkinsonism before and after treatment with L‐DOPA¹

Cited by 26 publications

References 16 publications

Correlation of Autonomic Dysfunction to CSF Concentrations of Noradrenaline and 3-Methoxy-4-Hydroxyphenylglycol in Parkinson’s Disease

Correlation of Autonomic Dysfunction to CSF Concentrations of Noradrenaline and 3-Methoxy-4-Hydroxyphenylglycol in Parkinson’s Disease

Cerebrospinal fluid biochemical studies in patients with Parkinson's disease: toward a potential search for biomarkers for this disease

A current analysis of behavioral problems in patients with idiopathic Parkinson's disease

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Cerebrospinal fluid levels of 3‐methoxy4hydroxyphenylethylene glycol in Parkinsonism before and after treatment with L‐DOPA1

Cited by 26 publications

References 16 publications

Correlation of Autonomic Dysfunction to CSF Concentrations of Noradrenaline and 3-Methoxy-4-Hydroxyphenylglycol in Parkinson’s Disease

Correlation of Autonomic Dysfunction to CSF Concentrations of Noradrenaline and 3-Methoxy-4-Hydroxyphenylglycol in Parkinson’s Disease

Cerebrospinal fluid biochemical studies in patients with Parkinson's disease: toward a potential search for biomarkers for this disease

A current analysis of behavioral problems in patients with idiopathic Parkinson's disease

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Cerebrospinal fluid levels of 3‐methoxy4hydroxyphenylethylene glycol in Parkinsonism before and after treatment with L‐DOPA¹