A Clinicopathologic Study of 100 Cases of Parkinson's Disease

Hughes, Andrew; Daniel, Susan E.; Blankson, Siobhan; Lees, Andrew J.

doi:10.1001/archneur.1993.00540020018011

Cited by 852 publications

(597 citation statements)

References 41 publications

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“…Infarctions of the basal ganglia and deep white matter occur very frequently in the elderly who do not have parkinsonism, and patients with pathologically confirmed PD may present with vascular lesions as incidental findings. Hence, a large proportion of patients with late-onset PD have some white matter changes on brain scans that may prompt physicians to incorrectly diagnose VP 9,36 . The association bet we en comorbid white matter disease and PD most consisten tly manifests as an impairment of axial motor symptoms and executive functions; therefore a subtype of a more rapidly evol ving and aggressive PD could misdirect physicians to a diag nosis of VP 37 .…”

Section: Discussionmentioning

confidence: 99%

Vascular parkinsonism: a case series of 17 patients

Vale

Caramelli

Cardoso

2013

Arq. Neuro-Psiquiatr.

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Objective To report the clinical and neuroimaging findings in a case series of vascular parkinsonism (VP). Methods Seventeen patients with VP were evaluated with motor, cognitive, and neuroimaging standardized tests and scales. Results All patients had arterial hypertension. Ten patients were male and the mean age of the whole sample was 75.8±10.1 years. The mean age of parkinsonism onset was 72.2±10.0 years. Common clinical features were urinary incontinence (88.2%), lower limb parkinsonism with freezing of gait and falls (82.3%), and pyramidal signs (76.4%). The mean Unified Parkinson’s Disease Rating Scale (UPDRS) and Hoehn-Yahr scores were 72.5±21.6 points and 3.3±0.9 points, respectively. Sixteen (94.1%) patients had freezing of gait and executive dysfunction. Twelve (70.5%) patients had probable vascular dementia. The mean dose of levodopa was 530.9 mg/day. Unresponsiveness to the drug was confirmed by a 6.9 mean point reduction in the UPDRS score after the “practically defined off” test. Conclusion This series provides a profile of VP with predominant lower-limb involvement, freezing of gait and falls, pyramidal signs, executive dysfunction, concomitant vascular dementia, and poor levodopa response.

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Section: Discussionmentioning

confidence: 99%

Vascular parkinsonism: a case series of 17 patients

Vale

Caramelli

Cardoso

2013

Arq. Neuro-Psiquiatr.

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“…4 Clinical features of PD include tremor at rest, bradykinesia, rigidity and flexed posture. 48 Pathologically, the key deficit in PD has been considered to be the loss of dopaminergic neurons in the substantia nigra, which causes consequent reduction of dopamine level. 98 Cell loss and Lewy body formation (abnormal intraneuronal aggregates of protein, predominantly a-synuclein) occur in the locus coeruleus, dorsal motor nucleus, and substantia innominata.…”

Section: Parkinson Diseasementioning

confidence: 99%

Nanoparticle transport across the blood brain barrier

et al. 2016

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While the role of the blood-brain barrier (BBB) is increasingly recognized in the (development of treatments targeting neurodegenerative disorders, to date, few strategies exist that enable drug delivery of non-BBB crossing molecules directly to their site of action, the brain. However, the recent advent of Nanomedicines may provide a potent tool to implement CNS targeted delivery of active compounds. Approaches for BBB crossing are deeply investigated in relation to the pathology: among the main important diseases of the CNS, this review focuses on the application of nanomedicines to neurodegenerative disorders (Alzheimer, Parkinson and Huntington's Disease) and to other brain pathologies as epilepsy, infectious diseases, multiple sclerosis, lysosomal storage disorders, strokes.

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“…Neuronal loss is usually greatest in the ventrolateral tier of the substantia nigra, as in PD [44], but there is often more extensive neuronal loss throughout all regions of the substantia nigra [50]. Neuronal cell loss is accompanied by fibrillary gliosis and globose-shaped NFT.…”

Section: Neuropathology Of Pspmentioning

confidence: 99%

Neuropathologic differentiation of progressive supranuclear palsy and corticobasal degeneration

1999

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Neuropathologic differentiation of progressive supranuclear palsy and corticobasal degeneration atypical cases are described that have overlapping clinical and pathologic features. Both PSP and CBD have similar biochemical alterations in the tau protein, with the abnormal tau protein containing predominantly four-repeat tau. While there is overlap in the pathology in PSP and CBD, there are sufficient differences to continue the present day trend to consider these separate disorders. Several important pathologic features differentiate PSP from CBD. Ballooned neurons are frequent and nearly a sine qua non for CBD, but they are found in PSP at a frequency similar to that of other neurodegenerative diseases, such as Alzheimer's disease. Astrocytic lesions are different, with tufted astrocytes found in motor cortex and striatum in PSP and astrocytic plaques in focal atrophic cortices in CBD. The most characteristic neuronal tau pathology in CBD is wispy, fine filamentous inclusions within neuronal cell bodies, while affected neurons in PSP have compact, dense filamentous aggregates characteristic of globose neurofibrillary tangles. Thread-like processes in gray and white matter are much more numerous and widespread in CBD than in PSP. The brunt of the pathology in CBD is in the cerebrum, while the basal ganglia, diencephalon and brainstem are the targets of PSP. Further clinicopathologic studies will refine our understanding of these disorders and open the possibility that common etiologic factors may be identified for these unusual sporadic tauopathies. Abstract Progressive supranuclear palsy (PSP) and corticobasal degeneration (CBD) are usually sporadic multisystem degenerations associated with filamentous tau inclusions in neurons and glia. As such they can be considered sporadic tauopathies in contrast to familial tauopathies linked to mutations in the tau gene. Mutations have not been found in the tau gene in either PSP or CBD. The clinical syndromes and neuroimaging of typical cases of PSP and CBD are distinct; however, Key words

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A Clinicopathologic Study of 100 Cases of Parkinson's Disease

Cited by 852 publications

References 41 publications

Vascular parkinsonism: a case series of 17 patients

Vascular parkinsonism: a case series of 17 patients

Nanoparticle transport across the blood brain barrier

Neuropathologic differentiation of progressive supranuclear palsy and corticobasal degeneration

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