DNA Fragmentation in Central Nervous System Vascular Malformations

2000 ◽  
Vol 142 (9) ◽  
pp. 987-994 ◽  
Author(s):  
Y. Takagi ◽  
I. Hattori ◽  
K. Nozaki ◽  
M. Ishikawa ◽  
N. Hashimoto
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Dna Fragmentation ◽  
Vascular Malformations

Central Nervous System Malformations in a Perinatal/Neonatal Autopsy Series

1998 ◽  
Vol 1 (1) ◽  
pp. 42-48 ◽  
Author(s):  
H. Pinar ◽  
N. Tatevosyants ◽  
D.B. Singer
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vascular Malformations ◽  
The Body ◽  
Growth Disorders ◽  
Agenesis Of Corpus Callosum ◽  
Arterial Perfusion ◽  
Neuronal Migration Disorders ◽  
Cerebellar Malformations ◽  
Cns Malformations

Congenital malformations of the central nervous system (CNS) are among the most common anomalies, but data on the incidence of CNS malformations in autopsy populations are scant. We examined 4122 autopsies between the years 1958 and 1995. There were 363 cases (8.8%) with CNS malformations; 235 were neonates and 128 stillborns. The overall gender ratio was 1:1, although more male neonates and more female stillborns had malformations. The body weights ranged from 24 to 6440 g. Neural tube defects were the most common types of malformations (45.5%) and included anencephaly, meningoencephalocele, meningocele/meningomyelocele, craniospinal rachischisis, and spina bifida occulta. The incidences of other malformations were: congenital hydrocephalus (12.4%), neuronal/glial proliferation disorders such as micro- and macrocephaly (8.8%), neuronal migration disorders (8.8%), prosencephalon growth disorders such as holoprosencephaly and arhinencephaly (8.5%), abnormalities of the midline structures such as agenesis of corpus callosum (4.1%), developmental cysts (3.3%), cerebellar malformations (3%), and vascular malformations (2%). Miscellaneous malformations (3%) consisted of acephalia in four cases with twin reversed arterial perfusion (TRAP), two cases of hydranencephaly, and four cases of rare degenerative and metabolic encephalopathies.

Expression of Angiogenic Factors and Structural Proteins in Central Nervous System Vascular Malformations

Neurosurgery ◽  
1996 ◽  
Vol 38 (5) ◽  
pp. 915-925 ◽  
Author(s):  
David Rothbart ◽  
Issam A. Awad ◽  
Jiyon Lee ◽  
Jung Kim ◽  
Robert Harbaugh ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vascular Malformations ◽  
Angiogenic Factors ◽  
Structural Proteins

scholarly journals Vascular malformations of central nervous system: A series from tertiary care hospital in South India

2016 ◽  
Vol 07 (02) ◽  
pp. 262-268
Author(s):  
Sudhir Babu Karri ◽  
Megha S. Uppin ◽  
A. Rajesh ◽  
K. Ashish ◽  
Suchanda Bhattacharjee ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vascular Malformations ◽  
Demographic Data ◽  
Periodic Acid ◽  
Tertiary Care ◽  
Care Hospital ◽  
Periodic Acid Schiff ◽  
Radiological Features ◽  
Risk Of Hemorrhage

ABSTRACT Aims and Objectives: To describe clinicopathological features of surgically resected vascular malformations (VMs) of central nervous system (CNS). Materials and Methods: Histologically diagnosed cases of VMs of CNS during April 2010–April 2014 were included. Demographic data, clinical and radiological features were obtained. Hematoxylin and eosin slides were reviewed along with Verhoeff-Van Gieson (VVG), Masson’s trichrome, periodic acid-Schiff, and Perls’ stains. Morphologically, cavernomas and arteriovenous malformations (AVMs) were distinguished on the basis of vessel wall features on VVG and intervening glial parenchyma. Results: Fifty cases were diagnosed as VMs of CNS with an age range of 14–62 years. These included 36 cavernomas, 12 AVMs, 2 mixed capillary-cavernous angiomas. Most of the cavernoma patients (15/36) presented with seizures, whereas AVM patients (8/12) had a headache as the dominant symptom. Twenty-nine patients were reliably diagnosed on radiological features. Microscopic evidence of hemorrhage was seen in 24/36 cavernomas and 6/12 AVMs, as opposed to radiologic evidence of 10 and 4, respectively. Reactive gliosis was seen in 16 cavernomas. Conclusions: Histological features are important for classifying the VMs of CNS as there are no specific clinical and radiological features. Type of VM has a bearing on management, prognosis, and risk of hemorrhage.

scholarly journals Poliovirus Induces Apoptosis in the Mouse Central Nervous System

1999 ◽  
Vol 73 (7) ◽  
pp. 6066-6072 ◽  
Author(s):  
Sophie Girard ◽  
Thérèse Couderc ◽  
Josette Destombes ◽  
Danièle Thiesson ◽  
Francis Delpeyroux ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Dna Fragmentation ◽  
Morphological Changes ◽  
Paralytic Poliomyelitis ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cns Injury ◽  
Viral Antigens ◽  
Mouse Central Nervous System

ABSTRACT Poliovirus (PV) is the etiological agent of human paralytic poliomyelitis. Paralysis results from the destruction of motoneurons, a consequence of PV replication. However, the PV-induced process leading to the death of motoneurons is not well known. We investigated whether PV-induced central nervous system (CNS) injury is associated with apoptosis by using mice as animal models. Transgenic mice expressing the human PV receptor were infected intracerebrally with either the neurovirulent PV-1 Mahoney strain or a paralytogenic dose of the attenuated PV-1 Sabin strain. Nontransgenic mice were infected with a mouse-adapted PV-1 Mahoney mutant. DNA fragmentation was demonstrated in CNS tissue from paralyzed mice by visualization of DNA oligonucleosomal laddering and by enzyme-linked immunosorbent assay. Viral antigens and DNA fragmentation detected by the in situ terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling technique were colocalized in neurons of spinal cords from paralyzed mice. In addition, morphological changes characteristic of cells undergoing apoptosis were observed in motoneurons by electron microscopy. Thus, we show that PV multiplication and CNS injury during paralytic poliomyelitis are associated with apoptosis.

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