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Dopaminergic Dysfunction (dopaminergic + dysfunction)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Neuroradiologic Evidence of Pre-Synaptic and Post-Synaptic Nigrostriatal Dopaminergic Dysfunction in Idiopathic Basal Ganglia Calcification: A Case Report

JOURNAL OF NEUROIMAGING, Issue 2 2010
Takahiro Saito MD
ABSTRACT Idiopathic basal ganglia calcification (IBGC) is a neuropathological condition known to manifest as motor disturbance, cognitive impairment, and psychiatric symptoms. The pathophysiology of the psychiatric symptoms of IBGC, however, remains controversial. A previous biochemical study suggested that dopaminergic impairment is involved in IBGC. We thus hypothesized that dopaminergic dysfunction might be related with the psychiatric manifestations of IBGC. We used positron emission tomography to measure glucose metabolism and dopaminergic function in the basal ganglia of an IBGC patient with psychiatric symptoms. The results showed that widespread hypometabolism was evident in the frontal, temporal, and parietal cortices while the decline in dopaminergic function was severe in the bilateral striatum. The functional decline of the dopamine system in the calcified area of the bilateral striatum and the disruption of cortico-subcortical circuits may contribute to clinical manifestations of IBGC in our patient. [source]

Clinical and imaging characterization of a patient with idiopathic progressive ataxia and palatal tremor

EUROPEAN JOURNAL OF NEUROLOGY, Issue 8 2007
R. Cilia
We describe clinical and imaging features of a patient with sporadic progressive ataxia and palatal tremor (PAPT) of unknown etiology. There was hypertrophy of bilateral inferior olivary nuclei with hyperintense T2-weighted signal and mild cerebellar atrophy at brain magnetic resonance imaging. 18F-fluoro-2-desoxy- d -glucose positron emission tomography scanning (FDG-PET) showed hypometabolism in the red nucleus, external globus pallidus and precuneus while FP-CIT-SPECT imaging revealed mild and progressive loss of striatal dopaminergic terminals. Our findings suggest that in idiopathic PAPT involvement of the dentato-rubro-olivary pathway occurs along with some dopaminergic dysfunction. [source]

Neuroradiologic Evidence of Pre-Synaptic and Post-Synaptic Nigrostriatal Dopaminergic Dysfunction in Idiopathic Basal Ganglia Calcification: A Case Report

Recognition, diagnosis, and treatment of restless legs syndrome

JOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS, Issue 8 2008
ARNP (Adult Nurse Practitioner, Jennifer E. Smith MSN, Manager of an Anticoagulation Clinic)
Abstract Purpose: To review the symptoms, diagnosis, and treatment of restless legs syndrome (RLS) and its relevance to nurse practitioners (NPs). Data sources: Comprehensive review of the scientific literature on the diagnosis and treatment of RLS in adults. Conclusions: RLS is a chronic neurological disorder that, with varying degrees of severity, affects 5%,10% of the general population. Because of the circadian pattern of onset, the symptoms of RLS may be associated with significant sleep disturbance and may have a negative impact on quality of life. RLS is characterized by a compelling urge to move the legs and usually accompanied or caused by uncomfortable sensations in the legs. Symptoms begin or worsen during periods of rest or inactivity and are worse in the evening or at night. Other features supportive of a diagnosis include a family history, the presence of periodic leg movements in sleep, and the relief of symptoms after treatment with a dopaminergic therapy. Although the etiology of RLS is unknown, it is thought that symptoms result from a central dopaminergic dysfunction and dopamine agonists are considered first-line treatment for moderate-to-severe primary RLS. Nondopaminergic therapies and nonpharmacologic interventions may also be appropriate in the management of less severe cases of RLS. Implications for practice: NPs are often the first healthcare providers to see patients with RLS and therefore need to be able to accurately recognize and diagnose the disorder; this, in turn, will enable them to successfully manage the treatment of RLS. [source]

[123I] FP-CIT spect study in vascular parkinsonism and Parkinson's disease

MOVEMENT DISORDERS, Issue 9 2007
Jan Zijlmans MD
Abstract There is substantial evidence to support a role for small vessel disease (SVD) as a cause for vascular parkinsonism (VP). Using [123I] FP-CIT SPECT (single photon emission computed tomography), we have tried to determine whether VP patients have pre-synaptic dopaminergic function similar to PD patients, and whether the severity of parkinsonian symptoms as well as the levodopa response in VP patients are correlated with pre-synaptic dopaminergic dysfunction. Thirteen patients fulfilling operational clinical criteria for VP had [123I] FP-CIT scans. Mean [123I] FP-CIT uptake in the basal ganglia was significantly lower in VP patients than in healthy controls, and the asymmetry index was not significantly different between these groups. In contrast, compared with the PD group, only the mean asymmetry index was significantly lower in VP patients. None of the parameters measured was significantly different between VP patients who had an insidious onset of parkinsonism (VPi) and those who had an acute onset (VPa). There was a significant correlation between the bilateral basal ganglia FP-CIT uptake reduction in the VP patients and UPDRS motor scores, but not with the mean % reduction in motor UPDRS after levodopa. We suggest that in the majority of VP patients, pre-synaptic dopaminergic function is reduced. The presence of a rather symmetrical FP-CIT uptake in the basal ganglia may help to distinguish VP from PD and could therefore be used as a criterion for the clinical diagnosis of VP. © 2007 Movement Disorder Society [source]

Extrastriatal dopaminergic dysfunction in tourette syndrome

ANNALS OF NEUROLOGY, Issue 2 2010
Thomas D. L. Steeves MD
Objective Tourette syndrome (TS) is a neuropsychiatric disorder presenting with tics and a constellation of nonmotor symptoms that includes attention deficit hyperactivity disorder, obsessive,compulsive disorder, and impulse control disorders. Accumulated evidence from pharmacological trials and postmortem analyses suggests that abnormalities of dopaminergic neurotransmission play a key role in the pathogenesis of TS. A substantial body of evidence has also accrued to implicate regions outside the striatum in the generation of tics. Methods We initiated an [11C]FLB 457 positron emission tomography study in conjunction with an amphetamine challenge to evaluate extrastriatal dopamine (DA) D2/D3 receptor binding and DA release in a group of treatment-naive, adult TS patients compared with a group of age- and sex-matched controls. Results At baseline, TS patients showed decreased [11C]FLB 457 binding potentials bilaterally in cortical and subcortical regions outside the striatum, including the cingulate gyrus, middle and superior temporal gyrus, occipital cortex, insula, and thalamus. Amphetamine challenge induced DA release in both control and TS subjects bilaterally in many cortical regions; however, in TS patients, regions of increased DA release were significantly more widespread and extended more anteriorly to involve anterior cingulate and medial frontal gyri. Conversely, and in contrast to healthy controls, no significant DA release was noted in the thalami of TS patients. Interpretation These abnormalities of dopaminergic function localize to brain regions previously implicated in TS and suggest a mechanism for the hyperexcitability of thalamocortical circuits that has been documented in the disorder. ANN NEUROL 2010;67:170,181 [source]