scholarly journals Relations of Serum Soluble E-Selectin and Adiponectin with Enlarged Perivascular Spaces in Patients with Recent Lacunar Infarction

2014 ◽  
Vol 20 (4) ◽  
pp. 382-384
Author(s):  
Wen Sun ◽  
Zhi-Xin Huang ◽  
Zuo-Wei Duan ◽  
Lu-Lu Xiao ◽  
Xin-Feng Liu
Keyword(s):  
Lacunar Infarction ◽  
Perivascular Spaces ◽  
Soluble E Selectin

Normal perivascular spaces mimicking lacunar infarction: MR imaging.

Radiology ◽  
1988 ◽  
Vol 169 (1) ◽  
pp. 101-104 ◽  
Author(s):  
C A Jungreis ◽  
E Kanal ◽  
W L Hirsch ◽  
A J Martinez ◽  
J Moossy
Keyword(s):  
Mr Imaging ◽  
Lacunar Infarction ◽  
Perivascular Spaces

scholarly journals 041Enlarged Perivascular Spaces of Subjects with Silent Lacunar Infarction from A National Longitudinal Study on Ageing

2017 ◽  
Vol 46 (Suppl_3) ◽  
pp. iii1-iii12
Author(s):  
Anne Buckley ◽  
James Meaney ◽  
Rose Anne Kenny ◽  
Joseph Harbison
Keyword(s):  
Longitudinal Study ◽  
Lacunar Infarction ◽  
Perivascular Spaces ◽  
National Longitudinal Study

Ultrastructural Aspects of Golgi Complex Function in Parathyroid Cells of Winter Frogs

1973 ◽  
Vol 31 ◽  
pp. 680-681
Author(s):  
William J. Dougherty
Keyword(s):  
Golgi Complex ◽  
Secretory Granules ◽  
Complex Function ◽  
Secretory Activity ◽  
Secretory Proteins ◽  
Perivascular Spaces ◽  
Pituitary Cells ◽  
Electron Microscopic ◽  
Ca Ions ◽  
Regulation Of Secretion

The regulation of secretion in exocrine and endocrine cells has long been of interest. Electron microscopic and other studies have demonstrated that secretory proteins synthesized on ribosomes are transported by the rough ER to the Golgi complex where they are concentrated into secretory granules. During active secretion, secretory granules fuse with the cell membrane, liberating and discharging their contents into the perivascular spaces. When secretory activity is suppressed in anterior pituitary cells, undischarged secretory granules may be degraded by lysosomes. In the parathyroid gland, evidence indicates that the level of blood Ca ions regulates both the production and release of parathormone. Thus, when serum Ca is low, synthesis and release of parathormone are both stimulated; when serum Ca is elevated, these processes are inhibited.

scholarly journals An autopsy-proven case of Corticobasal degeneration heralded by Pontine infarction

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dallah Yoo ◽  
Sung-Hye Park ◽  
Sungwook Yu ◽  
Tae-Beom Ahn
Keyword(s):  
Neurodegenerative Disorders ◽  
Clinical Manifestations ◽  
Neuronal Loss ◽  
Corticobasal Degeneration ◽  
Executive Dysfunction ◽  
Lacunar Infarction ◽  
Cortical Atrophy ◽  
Dystonic Posturing ◽  
Proven Case ◽  
The Right

Abstract Background Neurodegenerative disorders are characterized by insidious progression with poorly-delineated long latent period. Antecedent clinical insult could rarely unmask latent neurodegenerative disorders. Here, we report an autopsy-proven case of corticobasal degeneration which was preceded by a lacunar infarction. Case presentation A 58-year-old man presented with acute ataxia associated with a lacunar infarction in the right paramedian pons. His ataxia persisted with additional progressive gait difficulty and left arm clumsiness. Six months later, a follow-up neurological examination showed asymmetrical bradykinesia, apraxia, dystonic posturing, postural instability, and mild ataxia of the left limbs. Cognitive examination revealed frontal executive dysfunction and visuospatial difficulties. Dopamine transporter imaging scan demonstrated bilateral reduced uptakes in mid-to-posterior putamen, more prominent on the right side. Levodopa-unresponsive parkinsonism, asymmetric limb dystonia, and ideomotor apraxia became more conspicuous, while limb ataxia gradually vanished. The patient became unable to walk without assistance after 1 year, and died 4 years after the symptom onset. Autopsy findings showed frontoparietal cortical atrophy, ballooned neurons, and phosphorylated tau-positive astrocytic plaques and neuropil threads with gliosis and neuronal loss, confirming the corticobasal degeneration. Conclusions The case illustrates that precedent clinical events such as stroke might tip a patient with subclinical CBS into overt clinical manifestations.

scholarly journals Perivascular spaces and brain waste clearance systems: relevance for neurodegenerative and cerebrovascular pathology

2021 ◽  
Author(s):  
Kaylene Gouveia-Freitas ◽  
António J. Bastos-Leite
Keyword(s):  
Basal Ganglia ◽  
Lymphatic Vessels ◽  
Vascular Wall ◽  
Lymphatic Drainage ◽  
Basement Membranes ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Functional Abnormality ◽  
Ischaemic Injury ◽  
Cerebrovascular Pathology

AbstractPerivascular spaces (PVS) of the brain, often called Virchow-Robin spaces, comprise fluid, cells and connective tissue, and are externally limited by astrocytic endfeet. PVS are involved in clearing brain waste and belong to the “glymphatic” system and/or the “intramural periarterial drainage” pathway through the basement membranes of the arteries. Related brain waste clearance systems include the blood–brain barrier, scavenger cells, cerebrospinal fluid, perineural lymphatic drainage pathways and the newly characterised meningeal lymphatic vessels. Any functional abnormality of PVS or related clearance systems might lead to accumulation of brain waste. It has been postulated that PVS enlargement can be secondary to accumulation of β-amyloid. Lack of integrity of the vascular wall, microbleeds, cerebral amyloid angiopathy (CAA) and enlarged PVS often occur in the preclinical stages of Alzheimer’s disease, preceding substantial brain atrophy. PVS enlargement in the form of état criblé at the basal ganglia has also been considered to reflect focal atrophy, most probably secondary to ischaemic injury, based upon both pathological and imaging arguments. In addition, distinct topographic patterns of enlarged PVS are related to different types of microangiopathy: CAA is linked to enlarged juxtacortical PVS, whereas subjects with vascular risk factors tend to have enlarged PVS in the basal ganglia. Therefore, enlarged PVS are progressively being regarded as a marker of neurodegenerative and cerebrovascular pathology. The present review addresses the evolving concept of PVS and brain waste clearance systems, the potential relevance of their dysfunction to neurodegenerative and cerebrovascular pathology, and potential therapeutic approaches of interest.

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