Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monozygotic twin sisters developed Parkinson's disease and anosmia at the age of 39. The disease was kept under control and regressed with L. Dopa. Two families with the same association had been previously reported. An anomaly of the metabolism of dopamine, genetically determined, is probably responsible for these disorders.
 ...
PMID:[Parkinson's disease and anosmia in monozygotic twin sisters (author's transl)]. 98 58

Olfactory evoked potential (OEP) recordings were undertaken using amyl acetate stimulation in 20 patients with Parkinson's disease, nine patients with Alzheimer's disease, seven patients with olfactory dysfunction with no other neurological disorder, and 17 control subjects. In order to eliminate the somatosensory factor from the combined somatosensory and olfactory components produced by amyl acetate stimulation, we substracted the potentials using odorless air from those using amyl acetate. In normal subjects, three components were observed, the mean latencies of which were 309 +/- 46, 484 +/- 61 and 710 +/- 55 ms. In all subjects with anosmia (n = 7), no responses were observed. In the patients with Alzheimer's disease, the components were fewer despite having no olfactory dysfunction. In the 20 patients with Parkinson's disease, eight [corrected] patients showed no components, seven patients showed one component and four [corrected] patients showed two components. The components rarely were detected in spite of whether the patients had olfactory dysfunction or not. Olfactory evoked potentials are useful in detecting olfactory dysfunction and the early stages of Alzheimer's disease and Parkinson's disease.
 ...
PMID:Olfactory evoked potentials in Parkinson's disease, Alzheimer's disease and anosmic patients. 920 69

It has been known for over 30 years that olfactory function is disordered in idiopathic Parkinson's disease (IPD). The severity and partial specificity of anosmia was not realized until recently, with the advent of more detailed analysis and sophisticated measurement. The olfactory vector hypothesis suggests that the causative agent for IPD enters the brain via the nasal route, but the reason for olfactory dysfunction may be more subtle. Evidence for olfactory disturbance is reviewed from pathological, psychological, neurophysiological and genetic stand-points. It is proposed that the initial causative event in IPD may start in the rhinencephalon (olfactory brain) prior to damage in the basal ganglia.
 ...
PMID:Is Parkinson's disease a primary olfactory disorder? 1062 64

The amygdala exhibits significant pathological changes in Parkinson's disease, including atrophy and Lewy body (LB) formation. Amygdala pathology has been suggested to contribute to some clinical features of Parkinson's disease, including deficits of olfaction and facial expression. The degree of neuronal loss in amygdala subnuclei and the relationship with LB formation in non-demented Parkinson's disease cases have not been examined previously. Using stereological methods, the volume of neurones and the number of neurones in amygdala subdivisions were estimated in 18 prospectively studied, non-demented patients with Parkinson's disease and 16 age- and sex-matched controls. Careful exclusion (all cortical disease) and inclusion (non-demented, levodopa-responsive, idiopathic Parkinson's disease or controls) criteria were applied. Seven Parkinson's disease cases experienced well-formed visual hallucinations many years after disease onset, while nine Parkinson's disease cases and three controls were treated for depression. Anatomically, the amygdala was subdivided into the lateral nucleus, the basal (basolateral and basomedial) nuclei and the corticomedial (central, medial and cortical nuclei) complex. LB and Lewy neurites were identified by immunohistochemistry for alpha-synuclein and ubiquitin and were assessed semiquantitatively. LB were found throughout the amygdala in Parkinson's disease, being present in approximately 4% of neurones. Total amygdala volume was reduced by 20% in Parkinson's disease (P = 0.02) and LB concentrated in the cortical and basolateral nuclei. Lewy neurites were present in most cases but did not correlate with any structural or functional variable. Amygdala volume loss was largely due to a 30% reduction in volume (P = 0.01) and the total estimated number of neurones (P = 0.007) in the corticomedial complex. The degree of neurone loss and the proportion of LB-containing neurones in the cortical nucleus within this complex were constant across Parkinson's disease cases and neither variable was related to disease duration (R(2 )< 0.03; P > 0.5). The cortical nucleus has major olfactory connections and its degeneration is likely to contribute to the early selective anosmia common in Parkinson's disease. There was a small reduction in neuronal density in the basolateral nucleus in all Parkinson's disease cases, but no consistent volume or cell loss within this region. However, the proportion of LB-containing neurones in the basolateral nucleus was nearly doubled in cases that exhibited visual hallucinations, suggesting that neuronal dysfunction in this nucleus contributes to this late clinical feature. Detailed quantitation of the other amygdala subdivisions failed to reveal any other substantial anomalies or any associations with depression. Thus, the impact of Parkinson's disease on the amygdala is highly selective and correlates with both early and late clinical features.
 ...
PMID:Clinical correlates of selective pathology in the amygdala of patients with Parkinson's disease. 1239 Sep 70

Parkinson's disease is a common movement disorder associated with considerable disability. The clinical syndrome of parkinsonism is based on the presence of core clinical features of rest tremor, bradykinesia, rigidity and impaired postural reflexes or gait. Parkinsonism is most often caused by Parkinson's disease, but can also be caused by other disorders, including cerebrovascular disease, multiple-system atrophy, progressive supranuclear palsy and other disorders. Parkinsonism can be identified by questionnaires and confirmed in person or by videotaped clinical examinations. The identification of presymptomatic cases remains problematic but is motivated by the hope for treatment before symptoms appear. Quantitative approaches to the diagnosis of parkinsonism based on the measurement of the cardinal features are available. Clinical approaches should include identification of features atypical for Parkinson's disease, which exclude the diagnosis, and documentation of a response to dopaminergic medications, which support a diagnosis of Parkinson's disease. Loss of smell and visual dysfunction are found in early patients and may be useful in screening protocols. In addition, behavioral changes, including depressive symptoms, may be detected in presymptomatic cases. Cognitive changes, such as impaired set shifting, have been observed in early Parkinson's disease, but can be seen with other causes of parkinsonism. Neuroimaging techniques, including positron emission tomography or single-photon emission computed tomography, are available to quantify dopaminergic neurons, while magnetic resonance imaging may be helpful in differentiating other forms of parkinsonism from Parkinson's disease. There are numerous approaches available to the identification of parkinsonism and Parkinson's disease. The gold standard remains a clinical diagnosis, confirmed by autopsy.
 ...
PMID:Identification of parkinsonism and Parkinson's disease. 1258 53

There has been an increase of interest in olfactory dysfunction since it was realised that anosmia was a common feature of idiopathic Parkinson's disease (PD) and Alzheimer-type dementia (AD). It is an intriguing possibility that the first sign of a disorder hitherto regarded as one of movement or cognition may be that of disturbed smell sense. In this review of PD, parkinsonian syndromes, essential tremor, AD, motor neurone disease (MND) and Huntington's chorea (HC) the following observations are made: 1). olfactory dysfunction is frequent and often severe in PD and AD; 2). normal smell identification in PD is rare and should prompt review of diagnosis unless the patient is female with tremor-dominant disease; 3). anosmia in suspected progressive supranuclear palsy and corticobasal degeneration is atypical and should likewise provoke diagnostic review; 4). hyposmia is an early feature of PD and AD and may precede motor and cognitive signs respectively; 5). subjects with anosmia and one ApoE-4 allele have an approximate 5-fold increased risk of later AD; 6). impaired smell sense is seen in some patients at 50% risk of parkinsonism; 7). smell testing in HC and MND where abnormality may be found, is not likely to be of clinical value; and 8). biopsy of olfactory nasal neurons shows non-specific changes in PD and AD and at present will not aid diagnosis.
 ...
PMID:Olfaction in neurodegenerative disorder. 1267 41

Olfactory dysfunction is a characteristic clinical sign in Parkinson's disease (PD); it is also present in multiple system atrophy (MSA). The pathological basis of hyposmia or anosmia in PD is well known: the olfactory bulb (OB) contains numerous Lewy bodies and severe neuronal loss is present in the anterior olfactory nucleus (AON). We established that glial cytoplasmic inclusions (GCIs) are present in all the OBs from MSA cases. Their presence in the OB is diagnostic for MSA. Additionally, neuronal loss is present in the AON in MSA. These pathological changes might be responsible for the olfactory dysfunction seen in MSA.
 ...
PMID:Olfactory bulb in multiple system atrophy. 1288 86

There has been gradual increase of interest in olfactory dysfunction since it was realised that anosmia was a common feature of idiopathic Parkinson's disease (IPD) and Alzheimer-type dementia. It is an intriguing observation that a premonitory sign of a disorder hitherto regarded as one of movement or cognition may be that of disturbed sense of smell. In this review of aging, IPD, parkinsonian syndromes, tremor, Alzheimer's disease (AD), motor neuron disease (MND), Huntington's chorea (HC) and inherited ataxia, the following observations are made: (1) olfactory senescence starts at about the age of 36 years in both sexes and accelerates with advancing years, involving pleasant odours preferentially; (2) olfactory dysfunction is near-universal, early and often severe in IPD and AD developing before any movement or cognitive disorder; (3) normal smell identification in IPD is rare and should prompt review of diagnosis unless the patient is female with tremor-dominant disease; (4) anosmia in suspected progressive supranuclear palsy and corticobasal degeneration is atypical and should likewise provoke diagnostic review; (5) subjects with hyposmia and one ApoE4 allele have an approximate 5-fold increased risk of later AD; (6) impaired sense of smell may be seen in some patients at 50% risk of parkinsonism, and possibly in patients with unexplained hyposmia; (7) smell testing in HC and MND where abnormality may be found is not likely to be of clinical value, and (8) biopsy of olfactory nasal neurons reveals non-specific changes in IPD and AD and at present will not aid diagnosis.
 ...
PMID:Olfaction in neurodegenerative disorder. 1673 38

Lewy-type pathology is a characteristic of a number of neurodegenerative disorders, including Parkinson's disease and dementia with Lewy bodies. Thus far, the definitive diagnosis of these dementias can only be confirmed at post-mortem. However, it is known that the loss of smell (anosmia) is an early symptom in patients who develop dementia, and the use of the smell test has been proposed as an early diagnostic procedure. The aim of this study was to understand further the extent of Lewy pathology in the olfactory system of patients with neurodegenerative disorders. Post-mortem tissue from 250 subjects was obtained from the OPTIMA brain bank. Five areas of the olfactory pathway were examined by immunolabelling for alpha-synuclein - a major component of Lewy pathology: the olfactory tract/bulb (n = 79), the anterior olfactory nucleus in the lateral olfactory gyrus (n = 193), the region of olfactory projection to the orbito-frontal cortex (n = 225), the hippocampus (n = 236) and the amygdala (n = 201). Results show that Lewy pathology affects different parts of the olfactory pathways differentially, suggesting a specific pattern of development of pathology. Clinical Parkinson's disease is most likely to be identified if the orbito-frontal cortex is affected, while the diagnosis is less likely if the pathology is restricted to the olfactory bulb or tract. These results suggest that pathology in the olfactory bulb and tract occurs prior to clinical signs of Parkinson's disease. Furthermore, the results presented here provide further evidence supporting the possible value of a smell test to aid the clinical diagnosis of neurodegenerative diseases.
 ...
PMID:Alpha-synuclein pathology in the olfactory pathways of dementia patients. 1755 2

There is growing evidence that a variety of symptoms can precede the classical motor features of Parkinson's disease (PD). The period when these symptoms arise can be referred to as the premotor phase of the disease. Well-documented premotor symptoms in PD include constipation, loss of smell, sleep disturbances such as REM sleep behavior disorder (RBD), and mood disturbances like depression. Diagnostic and therapeutic implications linked to improved identification of these premotor features are discussed.
 ...
PMID:The premotor phase of Parkinson's disease. 1768 39


1 2 3 4 5 6 Next >>