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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Visuospatial dysfunction is not generally considered a cardinal feature of the common neurodegenerative disorders of late life like Alzheimer's disease (AD), Parkinson's disease (PD), and Dementia with Lewy bodies (DLB). However, a large number of research studies have shown visually related disorders to be surprisingly pervasive among these disease states. Broader recognition of the problems is hindered by a complex literature, which suffers from a lack of uniform definitions of what constitutes "visuospatial" dysfunction and few commonly accepted theoretical models for interpreting results. The interface between visual-spatial function and other variably-defined constructs such as attention and executive function further complicates experimental approaches to this construct. Nonetheless, this review addresses both theoretical and practical issues regarding the presence, importance, and correlates of visual dysfunction associated with neurodegeneration. In addition, the functional impact of the deficits is addressed.
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PMID:Visuospatial dysfunction in the neurodegenerative diseases. 1295 79

Patients who have neurodegenerative disease frequently present to the ophthalmologist with visual complaints. The causes of the symptoms are varied and include visual sensory and ocular motor dysfunction. This article provides an overview of the neuroophthalmic manifestations of the most common neurodegenerative diseases presenting with visual dysfunction, including Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy, and others. Evaluation of visual function in patients who have neurodegenerative disorder can be challenging, but familiarity with the type of visual dysfunction most commonly associated with each disorder will allow for a focused assessment and treatment when possible.
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PMID:Neuro-ophthalmic manifestations of neurodegenerative disease. 1533 90

The retinal dopamine (DA) deficiency is an important feature of the pathogenesis in Parkinson's disease (PD) visual dysfunction. Systemic inhibition of complex I (rotenone) in rats has been proposed as a model of PD. In this study, we investigated whether systemic inhibition of complex I can induce impairment of DA-ergic cells in the retina, similar to the destruction of retinal cells found in PD patients. Rotenone (2.5mg/kg i.p., daily) was administered over 60 days. Neurochemically, rotenone treated rats showed a depletion of DA in the striatum and substantia nigra (SN). In addition, the number of retinal DA-ergic amacrine cells was significantly reduced in the rotenone treated animals. This study is the first one giving highlight towards a deeper understanding of systemic complex I inhibition (rotenone as an environmental toxin) and the connection between both, DA-ergic degeneration in the nigrostriatal pathway, and in the DA-ergic amacrine cells of the retina.
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PMID:A rat model of Parkinsonism shows depletion of dopamine in the retina. 1696 86

The authors review current literature on hallucinations in Parkinson's disease (PD). Recent neuropathological studies showed that hallucinations occur in synucleinopathies and are a significant predictor of Lewy Body depositions. Therefore, hallucinations are a hallmark of PD and of dementia with Lewy Bodies. Visual hallucinations are mostly complex and kinematic; preserved or disturbed insight on the nature of hallucinations is a major prognostic factor, although eventually all hallucinators will present with reduced insight. Current theories on the origin of hallucinations point to visual dysfunction, dream overflow and cognitive impairment, yet objection can be raised on each one of the putative models of hallucinations. Understanding of the origin of hallucinations is required in order to develop treatments: all treatment evaluations were focused in general on psychosis, and only clozapine obtained positive evidence-based ratings on efficacy. However, it is likely that cholinesterase inhibitors, antipsychotics and anti-5-hydroxytryptamine(3) agents and drugs acting on sleep regulation will have different and perhaps opposite effects on different types of hallucinations, whether they are accompanied by disturbed insight, sleep disorders or other psychotic features. Further studies will try to separate phenomenology and responses to treatment and will investigate the relevance of concomitant sleep disorders and abnormality of frontoparietal networks involved in the attention process.
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PMID:New approaches to understanding hallucinations in Parkinson's disease: phenomenology and possible origins. 1805 66

As a more complete picture of the clinical phenotype of Parkinson's disease emerges, non-motor symptoms have become increasingly studied. Prominent among these non-motor phenomena are mood disturbance, cognitive decline and dementia, sleep disorders, hyposmia and autonomic failure. In addition, visual symptoms are common, ranging from complaints of dry eyes and reading difficulties, through to perceptual disturbances (feelings of presence and passage) and complex visual hallucinations. Such visual symptoms are a considerable cause of morbidity in Parkinson's disease and, with respect to visual hallucinations, are an important predictor of cognitive decline as well as institutional care and mortality. Evidence exists of visual dysfunction at several levels of the visual pathway in Parkinson's disease. This includes psychophysical, electrophysiological and morphological evidence of disruption of retinal structure and function, in addition to disorders of 'higher' (cortical) visual processing. In this review, we will draw together work from animal and human studies in an attempt to provide an insight into how Parkinson's disease affects the retina and how these changes might contribute to the visual symptoms experienced by patients.
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PMID:The retina in Parkinson's disease. 1933 64

Visual complaints in patients with dementia are varied and attributable to both visual sensory (afferent) and ocular motor (efferent) dysfunction. This review focuses exclusively on the efferent visual dysfunction associated with dementia and aging. It provides a brief overview of the most common ocular motility disturbances associated with dementia, including Alzheimer's disease, Parkinson's disease, diffuse Lewy body disease, corticobasal syndrome, progressive supranuclear palsy, frontotemporal lobar degeneration, Creutzfeldt-Jakob disease, and others. An introduction to the six eye movement systems and the terminology associated with the evaluation of each system are reviewed. Assessment of efferent visual function in patients with dementia may be challenging, but familiarity with the potential pathologic eye movement findings in patients with dementia will allow for a focused assessment, diagnosis, and treatment when possible.
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PMID:Ocular motility of aging and dementia. 2069 81

Among the various visuospatial dysfunctions, deficits of stereopsis could be associated with Parkinson's disease. We examined differences in regional gray matter volume between Parkinson's disease patients with normal stereopsis and with abnormal stereopsis to delineate the possible anatomical correlate of stereopsis. Stereopsis was assessed using the Titmus test in 35 drug-naive patients with Parkinson's disease. Voxel-based morphometry was utilized to assess regionally specific differences in gray matter volume between 16 patients with normal stereopsis and 19 patients with abnormal stereopsis. Patients with abnormal stereopsis had a significant gray matter volume reduction in the right extrastriate visual cortex compared with patients with normal stereopsis (P<0.05, corrected for multiple comparisons). Voxel values extracted from the significant cluster in group comparison were negatively correlated with log seconds of arc of the Titmus test (Spearman correlation, P<0.001). Our results suggest that deficits of stereopsis are associated with nondominant extrastriate cortical atrophy and that abnormal stereopsis implicates the cortical visual dysfunction as part of the nonmotor symptoms in Parkinson's disease.
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PMID:Stereopsis and extrastriate cortical atrophy in Parkinson's disease: a voxel-based morphometric study. 2337 33

Visual hallucinations (VHs) can be associated with a variety of clinical conditions, and are also experienced by healthy people due to visual impairment. The condition is known as Charles Bonnet Syndrome (CBS). The circumstances favoring VHs support the hypothesis that sensory deprivation enhances the ongoing activity of the visual system after sensory loss. Clinician should be aware that a significant proportion of visually impaired patients experience complex VHs, which are sometimes distressing. Herein, we report two cases of CBS. Case 1 is a 60-year-old man with visual impairment due to orbit pseudotumor in autoimmune hypothyroidism. Case 2 is an 87-year-old woman with Parkinson's disease and a 15-year history of intermittent complex VHs due to age-related macular degeneration in both eyes. In both cases investigations for alternative pathological causes of VHs were negative and, therefore, the aetiology of hallucinations was attributed to CBS. The course and treatment of CBS patients vary according to the nature of the visual dysfunction. Drug treatments remain partially satisfactory, with individual cases successfully treated with atypical antipsychotics. Nonpharmacological interventions aimed to reduce the visual pathway deprivation. Reassurance of the benign nature of CBS is essential to support patients and reduce caregiver's burden.
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PMID:Charles Bonnet syndrome: two case reports and review of the literature. 2338 16

Dopamine (DA) functions as an essential neuromodulator in the brain and retina such that disruptions in the dopaminergic system are associated with common neurologic disorders such as Parkinson's disease. Although a reduction in DA content has been observed in diabetes, its effects in the development of diabetes-induced neuropathy remains unknown. Because the retina is rich in DA and has a well known diabetes-induced pathology (diabetic retinopathy or DR), this study was designed to examine the role of retinal DA deficiency in early visual defects in DR. Using rodent models of type 1 diabetes mellitus, we investigated whether diabetes caused a reduction in retinal DA content in both rats and mice and determined whether restoring DA levels or activating specific DA receptor pathways could improve visual function (evaluated with optokinetic tracking response) of diabetic mice, potentially via improvement of retinal function (assessed with electroretinography). We found that diabetes significantly reduced DA levels by 4 weeks in rats and by 5 weeks in mice, coincident with the initial detection of visual deficits. Treatment with l-DOPA, a DA precursor, improved overall retinal and visual functions in diabetic mice and acute treatment with DA D1 or D4 receptor agonists improved spatial frequency threshold or contrast sensitivity, respectively. Together, our results indicate that retinal DA deficiency is an underlying mechanism for early, diabetes-induced visual dysfunction and suggest that therapies targeting the retinal dopaminergic system may be beneficial in early-stage DR.
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PMID:Dopamine deficiency contributes to early visual dysfunction in a rodent model of type 1 diabetes. 2443 31

In Parkinson's disease, visual dysfunction is prominent. Visual hallucinations can be a major hallmark of late stage disease, but numerous visual deficits also occur in early stage Parkinson's disease. Specific retinopathy, deficits in the primary visual pathway and the secondary ventral and dorsal pathways, as well as dysfunction of the attention pathways have all been posited as causes of hallucinations in Parkinson's disease. We present data from patients with Parkinson's disease that contrast with a known neuro-ophthalmological syndrome, termed 'blindsight'. In this syndrome, there is an absence of conscious object identification, but preserved 'guess' of the location of a stimulus, preserved reflexive saccades and motion perception and preserved autonomical and expressive reactions to negative emotional facial expressions. We propose that patients with Parkinson's disease have the converse of blindsight, being 'blind to blindsight'. As such they preserve conscious vision, but show erroneous 'guess' localization of visual stimuli, poor saccades and motion perception, and poor emotional face perception with blunted autonomic reaction. Although a large data set on these deficits in Parkinson's disease has been accumulated, consolidation into one specific syndrome has not been proposed. Focusing on neuropathological and physiological data from two phylogenetically old and subconscious pathways, the retino-colliculo-thalamo-amygdala and the retino-geniculo-extrastriate pathways, we propose that aberrant function of these systems, including pathologically inhibited superior colliculus activity, deficient corollary discharges to the frontal eye fields, dysfunctional pulvinar, claustrum and amygdaloid subnuclei of the amygdala, the latter progressively burdened with Lewy bodies, underlie this syndrome. These network impairments are further corroborated by the concept of the 'silent amygdala'. Functionally being 'blind to blindsight' may facilitate the highly distinctive 'presence' or 'passage' hallucinations of Parkinson's disease and can help to explain handicaps in driving capacities and dysfunctional 'theory of mind'. We propose this synthesis to prompt refined neuropathological and neuroimaging studies on the pivotal nuclei in these pathways in order to better understand the networks underpinning this newly conceptualized syndrome in Parkinson's disease.
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PMID:Are patients with Parkinson's disease blind to blindsight? 2476 73


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