PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Parkinsonian Disorders”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1975

Ballistic and corrective movements on an aiming task. Intention tremor and parkinsonian movement disorders compared.

Six patients with Parkinson's disease, six patients with essential or intention tremor, and nine controls were tested on a step-tracking task using a joystick control and oscilloscope display. Tremor subjects resembled controls in making an initial ballistic movement followed by (defective) corrections, and took longer than the controls to reach the target with small amplitude jumps, but not with larger ones. The reverse was true for parkinsonian subjects, who acquired the target with slow corrective movements only. This suggests that two kinds of movement available to normal people are selectively impaired in these disorders; ballistic movements in Parkinson's disease and small amplitude corrective movements in the other disorders.

Aged↗
PubMedDate not supplied

Treatment of Parkinsonian syndrome with dexetimide.

In an open study, 60 Parkinson patients with varying aetiology were submitted to a treatment with the long-acting antiparkinsonian drug dexetimide and L-Dopa. Rigor, tremor and akinesia were favourably influenced. An advantage over other antiparkinsonian agents is its long duration of action and the possibility of a simple dosage. Further investigations concerning its long-term effect and elucidation of its interactions with different drugs commonly administered in parkinsonian disorders seem desirable.

Adult↗
PubMed1978

Abnormal epinephrine urinary excretion in Parkinsonians: correction of the disorder by levodopa administration.

Epinephrine (E) and norepinephrine (NE) as well as vanilmandelic acid (VMA) urinary excretion was investigated in 54 patient with Parkinsonism and 29 controls. In Parkinsonians the mean value of NE excretion was normal, while that of E was significantly higher than in controls (P less than 0.001). Analysis of results in terms of age showed that only the patients in the 5th and 6th decades displayed significant increases in E excretion when compared to age-matched controls. No age-group differences were found for NE excretion. VMA was significantly higher in Parkinsonians than in controls. Both in Parkinsonians and in controls VMA excretion correlated significantly with that of NE but not with the E excretion. Ten-day treatment with levodopa (1.5 g/day) of Parkinsonians below the age of 60 was followed by a constant decrease in the excretion of E and a less consistent, nonsignificant increase in the excretion of NE. The abnormality of E excretion noticed in younger Parkinsonians suggests involvement in the pathologic process, of adrenal medulla, the main site of E synthesis.

Adult↗
PubMed2026

Reversible exacerbation of parkinsonism during epirubicin-cyclophosphamide chemotherapy in a patient with PTEN hamartoma tumor syndrome and young-onset Parkinson's disease.

BACKGROUND: PTEN hamartoma tumor syndrome (PHTS), caused by germline loss-of-function variants in PTEN, typically manifests as macrocephaly, neurodevelopmental disorders, and cancer susceptibility. Parkinson's disease has not been recognized as part of its known neurological spectrum. METHODS: We describe the clinical course of a patient with a germline PTEN nonsense variant (p.Arg130Ter) who developed young-onset Parkinson's disease before being diagnosed with bilateral breast cancer. RESULTS: The patient developed asymmetric, levodopa-responsive parkinsonism at 35 years of age, with reduced bilateral striatal dopamine transporter uptake. During two cycles of epirubicin-cyclophosphamide chemotherapy, her previously well-controlled parkinsonism showed reproducible and severe exacerbations. Symptoms began several days after chemotherapy, reached their maximum severity approximately one week after treatment, and resolved completely within approximately two weeks without modification of her antiparkinsonian medications. No dehydration, electrolyte disturbance, infection, or exposure to dopamine-receptor antagonists was identified. The chemotherapy regimen was discontinued after the second episode because of the reproducible temporal association. CONCLUSIONS: This case demonstrates reproducible, fully reversible exacerbations of parkinsonism during epirubicin-cyclophosphamide chemotherapy in a patient with PHTS and young-onset Parkinson's disease. These episodes may reflect transient vulnerability of dopaminergic neurons to chemotherapy-related systemic stress, although the causal role of PTEN haploinsufficiency remains uncertain.

Humans↗
PubMed2026

Synaptic vesicle glycoprotein 2A PET imaging in parkinsonian α-synucleinopathies: a systematic review.

Synaptic dysfunction is increasingly recognized as an early and biologically relevant component of α-synucleinopathies. However, conventional imaging biomarkers mainly assess dopaminergic dysfunction, glucose metabolism, or structural damage rather than presynaptic density itself. Synaptic vesicle glycoprotein 2A (SV2A) PET enables in vivo assessment of presynaptic terminal integrity and may provide complementary information in Parkinson's disease (PD), Parkinson's disease dementia/dementia with Lewy bodies (PDD/DLB), and multiple system atrophy (MSA). This systematic review synthesized the available evidence on SV2A-targeted PET in parkinsonian α-synucleinopathies, focusing on regional imaging patterns, clinical associations, longitudinal findings, and methodological determinants of interpretation. Seventeen reports were included. In PD, the most recurrent finding was reduced SV2A binding in the substantia nigra, although additional involvement of brainstem, caudate, striatal, thalamic, raphe, or cortical regions was reported in selected cohorts. In PDD/DLB, abnormalities appeared broader and more cortical, with evidence of association between cortical SV2A binding and cognitive performance. In MSA, one study suggested a distinct infratentorial and cerebellar pattern with potential relevance for phenotypic stratification. SV2A PET is a promising research biomarker for biological characterization of synucleinopathies. However, the field remains limited by small cohorts, methodological heterogeneity, variable quantification strategies, limited longitudinal evidence, and potential cohort overlap. Multicentre validation and harmonized protocols are required before clinical translation.

Humans↗
PubMed2026

ACE2 and Parkinsonism‑related bone metabolic alterations: signaling pathways and hub gene analysis.

Clinical co-occurrence of Parkinson's disease (PD) and age-related bone loss in elderly patients has garnered increasing attention, yet its molecular mechanisms remain incompletely elucidated. This study used an 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD model in Ace2-/y mice to investigate the regulatory mechanisms of bone-brain axis-related genes and signaling pathways. Behavioral tests assessed motor and non-motor symptoms. Immunohistochemistry, Western blot, and histopathological staining analyzed dopaminergic neuron activity, microglial activation, and bone metabolic abnormalities. GEO dataset transcriptomics and weighted gene co-expression network analysis (WGCNA) identified key hub genes, with receiver operating characteristic (ROC) curves evaluating their diagnostic value in public single-disease transcriptome data. MPTP significantly exacerbated motor dysfunction and depression-like behaviors; Ace2 deletion lowered total Wnt, β-catenin, BMP and IGF-1 protein abundance alongside reduced phosphorylation ratios of their downstream kinases in brain and bone, while upregulating RANKL/RANK/OPG-associated inflammatory mediators, accompanied by elevated total α-synuclein, Casp3 and Bax protein levels. The parallel reduction of these signaling proteins only suggests potential perturbation of related cascades; WGCNA identified 10 hub genes (e.g., DNM1, OCRL, OPA1), whose dysregulation was linked to synaptic dysfunction and inflammation. ROC analysis based on single-disease datasets showed high diagnostic accuracy for PD and `osteoporosis (OP) (AUC: 0.683-0.981), with core genes influencing synaptic, MAPK, Rap1, and Ras pathways. These preclinical findings indicate that Ace2 deficiency is associated with concurrent pathological abnormalities in the brain and transient bone metabolic disturbance under short-term MPTP treatment in growing young male mice; coordinated dysregulation of shared signaling pathways was observed in the two tissues, consistent with a potential bone-brain axis pathological phenotype, though causal bidirectional tissue cross-talk cannot be confirmed in the current experimental design, providing candidate targets that warrant further validation.

Animals↗
PubMed2025

Parabacteroides goldsteinii mitigates parkinsonism in LRRK2 mutant mice by reducing neuroinflammation through Gut-Brain axis.

INTRODUCTION: Alterations in the gut microbiota accompanied by intestinal inflammation are early features of Parkinson's disease (PD). Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene represent a common genetic risk factor for PD and inflammatory bowel disease. Parabacteroides goldsteinii has been reported to alleviate intestinal and systemic inflammation. However, whether modulation of the gut microenvironment at early disease stage can attenuate PD progression remains unclear. OBJECTIVE: To investigate the impact of P. goldsteinii colonization prior to the onset of motor dysfunction on PD progression. METHODS: We established a germ-free PD mouse model carrying the LRRK2 G2019S mutation and administered P. goldsteinii orally at the pre-symptomatic stage to evaluate its effects on motor performance and PD-related neuropathology. Spatial and bulk RNA transcriptomic analyses of brain tissue, together with cytokine profiling, were conducted to assess central changes. To investigate gut immunomodulatory mechanisms, we performed intestinal bulk and single-cell RNA sequencing, spectral flow cytometry as well as cellular bioenergetic analyses. RESULTS: Germ-free conditions partially alleviated PD-like phenotypes in LRRK2 G2019S mice. Colonization with P. goldsteinii at 5-months of age, prior to motor symptom onset, further improved locomotor performance, reduced neuronal α-synuclein aggregations, and mitigated microglial activation and dopaminergic neurodegeneration. Neuroprotection was mediated through enhanced noncanonical neuronal IL-12 receptor-dependent neurotrophic support without activating the canonical STAT4 phosphorylation pathway, along with suppression of microglial activation and downregulation of LRRK2 kinase activity. At the intestinal level, P. goldsteinii suppressed TLR4-driven inflammation, expanded anti-inflammatory intraepithelial CD4+CD8αα+ T cells, promoted dendritic cell and macrophage differentiation, upregulated epithelial tight-junction genes, and improved mitochondrial bioenergetics in intestinal cells. CONCLUSION: P. goldsteinii colonization attenuates the progression of LRRK2-associated parkinsonism by restoring intestinal homeostasis and reducing neuroinflammation. These findings underscore the therapeutic potential of modulating the gut-immune-brain axis during the prodromal stage of PD.

Animals↗
PubMed2026

Combining neuromelanin-sensitive MRI and quantitative susceptibility mapping for enhanced diagnosis and differentiation of parkinson's disease: A systematic review.

BACKGROUND: Loss of dopaminergic neurones and iron deposition in the substantia nigra pars compacta (SNpc) are two major pathological hallmarks of Parkinson's disease (PD). Such changes can be visualised by advanced techniques including neuromelanin-sensitive MRI (NM-MRI) and quantitative susceptibility mapping (QSM). This systematic review investigates the diagnostic performance and methodological development of the integrated use of NM-MRI and QSM in PD. METHODS: The systematic search was performed in four databases (Scopus, PubMed, ScienceDirect, and Web of Science) according to the PRISMA 2020 guidelines until July 2026. Bias was assessed using QUADAS-2 and certainty of evidence was assessed using GRADE. RESULTS: Seventeen studies with 2228 participants were included. Combined NM-MRI and QSM consistently showed reduced neuromelanin volume/contrast and increased iron deposition in the SNpc of PD patients compared to healthy controls. Multimodal integration yielded a significant improvement in diagnostic accuracy (AUC values 0.86-0.99), and was able to successfully differentiate PD. Recent methodological advances included simultaneous acquisition sequences (e.g. MTC-GRE, STAGE, setMag) and AI-driven automated segmentation, which led to significantly reduced scan times and improved reproducibility. CONCLUSION: The combination of NM-MRI and QSM has a synergistic effect and provides powerful complementary biomarkers for the diagnosis and differential diagnosis of PD.

Humans↗
PubMed1978

[Tachylalia: clinical and acoustic study of 149 subjects (author's transl)].

Speech was studied subjectively (listening to recordings) and objectively (measurement of durations) in 67 Parkinsonians, 10 subjects with neurological disorders and 72 psychiatric patients. Acceleration of speech was greatest in the Parkinsonians (8.5 syllables per second). The total duration of a sentence read by several of tachylalic Parkinsonians was the same as that of normal control subjects reading as fast as they could. The duration of the pauses between words varied greatly in all categories of subjects. Almost half of the tachylalic Parkinsonians (10 out of 23) had a speaking time (excluding pauses) shorter than the shortest duration recorded among same-age normal controls. The authors attach particular significance to the cases in which tachylalia is observed in the absence of lesions in the central gray nuclei. These cases suggest that speech automatisms are regulated at several levels.

Adolescent↗
PubMed1975

Why transcortical reflexes?

Experiments in humans and in monkeys have indicated that load perturbations, occurring during voluntary movements and postural activity, may be automatically compensated for. Overall muscle stiffness opposing load changes is determined by the visco-elastic properties of the muscle, by segmental reflex actions and finally by long-loop reflexes. Under certain circumstances, for instance when the subject or the experimental monkey is "prepared" to counteract perturbations which are unpredictable in time, the long-loop "reflexes" appear to be responsible for most of the corrective muscle tension. Experiments in anaesthetized monkeys revealed that signals from stretch afferents reach neurons of the motor cortex, possibly via a relay in the cortical area 3a. The latencies of these responses to well controlled muscle stretches were in the same range as motor cortical cell discharges recorded in alert monkeys subjected to load perturbations. Furthermore, these responses of cells in the motor cortex also had the appropriate timing to indicate a causal relationship with the long-latency electromyographic responses to load changes referred to above. These experimental results therefore strongly support the hypothesis, first proposed by Phillips (1969), of a transcortical servo-loop adjusting motor cortical output according to the load conditions in which movements are performed. The major advantage of transcortical regulations as opposed to segmental regulations, seems to be a powerful gain control acting at the cortical level; it was repeatedly shown that the long-loop reflexes are strongly modifiable and under voluntary control. It is suggested that an adaptive gain control at the cortical level is a prerequisite to preserve the complex capabilities of the motor cortex as the chief "executive" for skilled, preprogrammed movements. A loss of this adaptive gain control may be, at least partly, the cause of motor disorders such as rigidity in Parkinsonian patients, as reported by Tatton and Lee (1975). It is suggested that further investigations of the control of transcortical reflexes may aid in the understanding of the pathophysiology of motor disabilities.

Animals↗
PubMed1979

Factors related to tardive dyskinesia.

The authors found a 31% incidence of tardive dyskinesia among 261 schizophrenic outpatients treated with neuroleptics. Multiple linear logistic regression analysis revealed a higher incidence of tardive dyskinesia among elderly patients, those with longer records of hospitalization, those for whom neuroleptic medication had little therapeutic effect, and those treated with fluphenazine. Patients manifesting tardive dyskinesia tended to have fewer parkinsonian symptoms than those without the disorder, especially when tremors and akathisia were excluded from consideration. Multiple linear regression analysis indicated that brain-damaged patients and male patients were more susceptible to severe forms of the disorder, even though these factors were not implicated in its initial appearance.

Adult↗
PubMed1976

Amino acid abnormalities in cerebrospinal fluid of patients with parkinsonism and extrapyramidal disorders.

Free amino acid determinations in the cerebrospinal fluid of patients with Parkinson's disease or other extrapyramidal disorders showed that in both groups most amino acids were increased. Significantly increased amino acids were neutral and basic amino acids. Amino acid clusters were present and corresponded with the grouping of amino acids in accordance with amino acid transport systems. The amino acids within the clusters showed a remarkable degree of correlation, and there was a notable correlation between the clusters both in the parkinsonian group and in the group of extrapyramidal disorders, but not in a control group. Our data suggest that in a number of extrapyramidal disorders, Parkinson's disease included, a more generalized abnormality exists than neuronal loss only and, in addition, that patients with these neurologic conditions have a common biochemical defect in their amino acid transport systems.

Adult↗
PubMed1976

[Memory disorders in parkinsonism patients].

The experience of memory and retention weaknesses in Parkinsonian patients led us to question if these are only due to age-specific deteriorations, and if these weaknesses change during the L-Dopa therapy of the underlying disease. For this reason 30 Parkinsonian patients and 30 normal subjects of a matched control group took part in five different tests of retention and memory: digit span (Wechsler), visual retention test (Benton), Wechsler Memory Scale (subtests 4 and 7), delayed recall (Williams). The results (including some further samples of the test literature) gave some evidence of test-material-specific weaknesses in Parkinsonian patients: especially such memory decay as is dependent on the interval of retention. An organic deterioration of the intermediate term memory is suggested. This result could not be fully explained by known psychological or neurological characteristics of the underlying disease.

Age Factors↗
PubMed1979

Management of palilalia with a pacing board.

Palilalia is a speaking disorder that has been likened to the festinating gait of Parkinsonian patients. This report describes a pacing device developed as a means of controlling the severely palilalic output of one patient. The device is a modeled after Luria's suggestion that a treatment program for such patients can be developed successfully by transferring automatic motor acts to a conscious, reactive level.

Humans↗
PubMedDate not supplied

[Physiopathological and clinical aspects of Parkinson disease. Current problems].

Some interpretative hypotheses of the most important symptoms of Parkinson's disease are formulated, on the ground of acquired neurohistopathologic elements and in the light of new observations of experimental neuro-physiology. The possible role of the inferior olivary body in the genesis of parkinsonian tremor is pointed out. The psycho-behavioural disorders and among these the severe weakness of pulsional control and the scanty elaboration of the affective-emotional motivation would be in relation, according to the Authors, to the involvement of the pallido-habenular pathways and the habenuloreticular midbrain outflow (limbic midbrain area).

Animals↗
PubMed1978

Possible involvement of central pacemakers in clinical disorders of movement.

This review considers the evidence for possible involvement of central nervous system pacemaker neurons in several clinical disorders of movement. Two basic types of tremor are discussed from this point of view, i.e., 4--7/sec parkinsonian tremor, of possible thalamocortical origin, and 7--11/sec essential tremor of possible olivo-cerebellar origin. The importance of motor programs and abnormalities in their utilization are considered with reference to the loss of motor function in parkinsonism (? loss of motor programs), and the inappropriate release of such programs as a possible basis for the involuntary movements seen in other movement disorders, such as chorea, athetosis, dystonia, and hemiballismus. The possible role of pacemaker neurons controlling such programs is considered. Finally, the subject of locomotion and the pacemaker model of the spinal locomotor pattern generator for stepping are considered in relation to clinical disorders of gait. While critical evidence is lacking for pacemaker inovlvement in any of these disorders, their possible role is emphasized.

Feedback↗