scholarly journals Secondary Myelitis in Dermal Sinus Causing Paraplegia in a Child with Previously Normal Neurological Function

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Sakina Rashid ◽  
Grace Kinabo ◽  
Marissa Kellogg ◽  
William P. Howlett ◽  
Marieke C. J. Dekker
Keyword(s):  
Congenital Anomaly ◽  
Spina Bifida ◽  
Neural Tube ◽  
Clinical Course ◽  
Acute Infection ◽  
Early Embryogenesis ◽  
The Other ◽  
Neurological Deficits ◽  
Dermal Sinus ◽  
Neurological Development

Neural tube defects result from failure of neural tube fusion during early embryogenesis, the fourth week after conception. The spectrum of severity is not uniform across the various forms of this congenital anomaly as certain presentations are not compatible with extrauterine life (anencephaly) while, on the other hand, other defects may remain undiagnosed as they are entirely asymptomatic (occult spina bifida). We report a child with previously normal neurological development, a devastating clinical course following superinfection of a subtle spina bifida defect which resulted in a flaccid paralysis below the level of the lesion and permanent neurological deficits following resolution of the acute infection and a back closure surgery.

Features of the course and treatment of glaucoma during pregnancy

2020 ◽  
Vol 98 (3) ◽  
pp. 178-184
Author(s):  
T. V. Chernyakova ◽  
A. Yu. Brezhnev ◽  
I. R. Gazizova ◽  
A. V. Kuroyedov ◽  
A. V. Seleznev
Keyword(s):  
Pregnant Women ◽  
Laser Treatment ◽  
Progressive Disease ◽  
Clinical Course ◽  
The Other ◽  
Third Trimester ◽  
The Third ◽  
Chronic Progressive Disease ◽  
Hypotensive Therapy ◽  
Eye Pressure

In the review we have integrated all up-to-date knowledge concerning clinical course and treatment of glaucoma among pregnant women to help specialists choose a proper policy of treatment for such a complicated group of patients. Glaucoma is a chronic progressive disease. It rarely occurs among childbearing aged women. Nevertheless the probability to manage pregnant patients having glaucoma has been recently increasing. The situation is complicated by the fact that there are no recommendations on how to treat glaucoma among pregnant women. As we know, eye pressure is progressively going down from the first to the third trimester, so we often have to correct hypotensive therapy. Besides, it is necessary to take into account the effect of applied medicines on mother health and evaluate possible teratogenic complications for a fetus. The only medicine against glaucoma which belongs to category B according to FDA classification is brimonidine. Medicines of the other groups should be prescribed with care. Laser treatment or surgery may also be a relevant decision when monitoring patients who are planning pregnancy or just bearing a child. Such treatment should be also accompanied by medicines.

Detection of spina bifida in the first trimester of gestation in association with triploidy

2017 ◽  
Author(s):  
K.K. Otaryan , C.G. Gagaev
Keyword(s):  
Spina Bifida ◽  
Early Detection ◽  
Neural Tube ◽  
Neural Tube Defects ◽  
First Trimester ◽  
Termination Of Pregnancy ◽  
Diagnostic Tools ◽  
Prenatal Detection ◽  
Post Abortion

The case of prenatal detection of spina bifida at 12+3 weeks of gestation is described. Termination of pregnancy was performed at 13+3 weeks. Post-abortion karyotyping revealed triploidy (69XXX). Diagnostic tools for early detection of neural tube defects in the 1st trimester of gestation and subsequent appropriate management of pregnancy are discussed.

scholarly journals Gasperini Syndrome: A Case Report and Systematic Review and Proposing a New Definition

2020 ◽  
Vol 12 (3) ◽  
pp. 433-439
Author(s):  
Riwaj Bhagat ◽  
Siddharth Narayanan ◽  
Marwa Elnazeir ◽  
Thong Diep Pham ◽  
Robert Paul Friedland ◽  
...  
Keyword(s):  
Systematic Review ◽  
Brain Mri ◽  
Cranial Nerves ◽  
Clinical Manifestations ◽  
The Other ◽  
Neurological Deficits ◽  
Brainstem Stroke ◽  
Neurological Features ◽  
The Right ◽  
Core Features

Gasperini syndrome (GS), a rare brainstem syndrome, is featured by ipsilateral cranial nerves (CN) V–VIII dysfunction with contralateral hemibody hypoesthesia. While there have been 18 reported cases, the GS definition remains ambiguous. We report a new case and reviewed the clinical features of this syndrome from all published reports to propose a new definition. A 57-year-old man with acute brainstem stroke had right CN V–VIII and XII palsies, left body hypoesthesia and ataxia. Brain MRI showed an acute stroke in the right caudal pons and bilateral cerebellum. After a systematic review, we classified the clinical manifestations into core and associate features based on the frequencies of occurring neurological deficits. We propose that a definitive GS requires the presence of ipsilateral CN VI and VII palsies, plus one or more of the other three core features (ipsilateral CN V, VIII palsies and contralateral hemibody hemihypalgesia). Additionally, GS, similar to Wallenberg’s syndrome, represents a spectrum that can have other associated neurological features. The revised definition presented in this study may enlighten physicians with the immediate recognition of the syndrome and help improve clinical localization of the lesions and its management.

scholarly journals Analysis for Stroke Etiology in Duplicated/Accessory MCA-Related Cerebral Infarction: Two Case Report and Brief Literature Review

Diagnostics ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 205
Author(s):  
Kou Tsuyama ◽  
Nobukazu Miyamoto ◽  
Atsuhiko Shindo ◽  
Kenichiro Hira ◽  
Yuji Ueno ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Clinical Course ◽  
The Other ◽  
Shearing Stress ◽  
Common Site ◽  
Arterial Diameter ◽  
Stroke Etiology ◽  
Proximal Site ◽  
The Media ◽  
Intracranial Arteries

Duplication and accessory of the middle cerebral artery (MCA) constitute a rare congenital variation. MCA anomalies are found at a lesser frequency than the vascular anomalies of the other major intracranial arteries. Duplicated/accessory MCA was usually noted incidentally with subarachnoid hemorrhage, due to resulted aneurysmal formation. However, duplicated/accessory MCA-related cerebral infarction is rarer. We report two cases of cerebral infarction due to dissection at the entry of the duplicate/accessory MCA. Both cases were similar in dissected site and clinical course, without headache or injury. In 20 previously reported cases and our two cases of duplicated/accessory MCA-related infarction, mean age (55.8 ± 21.2 years) was slightly younger for cerebral infarction, and stroke etiology was mainly embolism. The main etiologies of stroke were embolism and dissection. Considering embolism etiology, proximal site of arterial diameter changing lesion was a common site for embolism, as duplicated/accessory MCA was usually smaller than normal M1 segment. In cerebral dissection cases, the dissected site was similar to our cases. Numerous mechanisms of dissection were considered, but they mainly included dysfunction of the media and endothelium or shearing stress at the entry of duplication. As the detailed mechanisms of cerebral dissection remain unknown, clinicians should include a differential diagnosis for MCA dissection.

scholarly journals Parenchymal Guidewire Perforation during ERCP: An Unappreciated Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
M. Ezzedien Rabie ◽  
Saad Al Faris ◽  
Ali Nasser ◽  
Abdul Aziz Shahir ◽  
Yasser Al Mahdi ◽  
...  
Keyword(s):  
Conservative Treatment ◽  
Emergency Surgery ◽  
Clinical Course ◽  
The Other ◽  
Clinical Deterioration ◽  
Medical Community ◽  
Successful Outcome ◽  
Hepatic Parenchyma ◽  
Pancreatic Parenchyma ◽  
Intraperitoneal Drainage

ERCP is attended with certain complications, the majority of which are well known to the medical community. Other less-known complications also exist. Guidewire injury to the hepatic or pancreatic parenchyma represents one of the much less appreciated, albeit preventable, complications. In this report, we present the clinical course of three patients who sustained guidewire perforation of the pancreatic or hepatic parenchyma. In one patient, the clinical deterioration was confidently attributed to guidewire perforation of the pancreatic parenchyma. Conservative treatment was successful and unnecessary emergency surgery was thus avoided. In the other two, in whom the cause of the clinical deterioration was unclear, an emergency surgery was performed. Guidewire injury to the hepatic parenchyma was then confirmed which needed only intraperitoneal drainage, with successful outcome.

Discontinuity of primary and secondary neural tube in spina bifida induced by retinoic acid in mice

Teratology ◽  
1990 ◽  
Vol 41 (3) ◽  
pp. 257-274 ◽  
Author(s):  
Yoshiko Yasuda ◽  
Hiroyoshi Konishi ◽  
Takahide Kihara ◽  
Takashi Tanimura
Keyword(s):  
Retinoic Acid ◽  
Spina Bifida ◽  
Neural Tube

CONGENITAL PTERIONAL DERMAL SINUS IN AN 18-MONTH-OLD CHILD

Neurosurgery ◽  
2007 ◽  
Vol 61 (3) ◽  
pp. E661-E661 ◽  
Author(s):  
William J. Mack ◽  
Saadi Ghatan
Keyword(s):  
Clinical Features ◽  
Neural Tube ◽  
Clinical Presentation ◽  
Sinus Tract ◽  
Dermal Sinus ◽  
Operating Microscope ◽  
First Case ◽  
Dermal Sinus Tract ◽  
Cranial Fossa ◽  
Congenital Dermal Sinus

Abstract OBJECTIVE Congenital dermal sinus tracts most frequently occur in the midline and are often associated with dermoid or epidermoid inclusion cysts. A lateral cranial origin is extremely rare and anatomically inconsistent with an etiology involving closure of the rostral neural tube during embryogenesis. CLINICAL PRESENTATION We describe the first case of a pterional cranial dermal sinus tract associated with a small epidermoid, with extension to the dura of the anterior cranial fossa. INTERVENTION The extra- and intracranial portions of the tract were visualized and resected with the use of an operating microscope. Pathological diagnosis confirmed dermal sinus tract. CONCLUSION We review the existing literature and address the developmental and clinical features pertinent to the management of cranial dermal sinus tracts, emphasizing the need for exploration of these potentially harmful lesions.

scholarly journals Evaluation of an in vivo model for ventricular shunt infection: a pilot study using a novel antimicrobial-loaded polymer

2019 ◽  
Vol 131 (2) ◽  
pp. 587-595 ◽  
Author(s):  
Rajiv R. Iyer ◽  
Noah Gorelick ◽  
Karen Carroll ◽  
Ari M. Blitz ◽  
Sarah Beck ◽  
...  
Keyword(s):  
Animal Model ◽  
Experimental Animal ◽  
Control Animal ◽  
Shunt Infection ◽  
The Other ◽  
Neurological Deficits ◽  
In Vivo Model ◽  
Ventricular Catheter ◽  
Catheter Implantation

OBJECTIVEVentricular shunt infection remains an issue leading to high patient morbidity and cost, warranting further investigation. The authors sought to create an animal model of shunt infection that could be used to evaluate possible catheter modifications and innovations.METHODSThree dogs underwent bilateral ventricular catheter implantation and inoculation with methicillin-sensitive Staphylococcus aureus (S. aureus). In 2 experimental animals, the catheters were modified with a polymer containing chemical “pockets” loaded with vancomycin. In 1 control animal, the catheters were polymer coated but without antibiotics. Animals were monitored for 9 to 11 days, after which the shunts were explanted. MRI was performed after shunt implantation and prior to catheter harvest. The catheters were sonicated prior to microbiological culture and also evaluated by electron microscopy. The animals’ brains were evaluated for histopathology.RESULTSAll animals underwent successful catheter implantation. The animals developed superficial wound infections, but no neurological deficits. Imaging demonstrated ventriculitis and cerebral edema. Harvested catheters from the control animal demonstrated > 104 colony-forming units (CFUs) of S. aureus. In the first experimental animal, one shunt demonstrated > 104 CFUs of S. aureus, but the other demonstrated no growth. In the second experimental animal, one catheter demonstrated no growth, and the other grew trace S. aureus. Brain histopathology revealed acute inflammation and ventriculitis in all animals, which was more severe in the control.CONCLUSIONSThe authors evaluated an animal model of ventricular shunting and reliably induced features of shunt infection that could be microbiologically quantified. With this model, investigation of pathophysiological and imaging correlates of infection and potentially beneficial shunt catheter modifications is possible.

scholarly journals CIC missense variants contribute to susceptibility for spina bifida

2021 ◽  
Author(s):  
Xiao Han ◽  
Xuanye Cao ◽  
Vanessa Aguiar-Pulido ◽  
Wei Yang ◽  
Menuka Karki ◽  
...  
Keyword(s):  
Spina Bifida ◽  
Cell Line ◽  
Neural Tube ◽  
Folate Receptor ◽  
Spinocerebellar Ataxia Type ◽  
Loss Of Function ◽  
Missense Variants ◽  
Increased Risk ◽  
Cell Line Hela

Neural Tube Defects (NTDs) are congenital malformations resulting from abnormal embryonic development of the brain, spine, or spinal column. The genetic etiology of human NTDs remains poorly understood despite intensive investigation. CIC, homolog of the Capicua transcription repressor, has been reported to interact with ataxin-1 (ATXN1) and participate in the pathogenesis of spinocerebellar ataxia type 1. Our previous study demonstrated that CIC loss of function (LoF) variants contributed to cerebral folate deficiency by downregulating folate receptor 1 (FOLR1) expression. Given the importance of folate transport in neural tube formation, we hypothesized that CIC variants could contribute to increased risk for NTDs by depressing embryonic folate concentrations. In this study, we examined CIC variants from whole genome sequencing (WGS) data of 140 isolated spina bifida cases and identified 8 missense variants of CIC gene. We tested the pathogenicity of the observed variants through multiple in vitro experiments. We determined that CIC variants decreased FOLR1 protein level and planar cell polarity (PCP) pathway signaling in a human cell line (HeLa). In a murine cell line (NIH3T3), CIC loss of function variants down regulated PCP signaling. Taken together, this study provides evidence supporting CIC as a risk gene for human NTD.

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