scholarly journals Delayed Intraventricular Hemorrhage following a Ventriculoperitoneal Shunt Placement: Exploring the Surgical Anatomy of a Rare Complication

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Ioannis N. Mavridis ◽  
Athanassios Mitropoulos ◽  
Constantinos Mantas ◽  
Aikaterini Karagianni ◽  
Konstantinos Vlachos
Keyword(s):  
Ventriculoperitoneal Shunt ◽  
Intraventricular Hemorrhage ◽  
Vascular Malformations ◽  
Rare Complication ◽  
Normal Pressure ◽  
Brain Parenchyma ◽  
Surgical Anatomy ◽  
Neurosurgical Procedures ◽  
Potential Factors ◽  
The Brain

Ventriculoperitoneal shunt (VPS) placement is one of the commoner neurosurgical procedures worldwide. The purpose of this article is to report a case of delayed intraventricular hemorrhage (IVH) following a VPS and to review the literature regarding anatomic factors that could potentially explain this rare complication. A 78-year-old man with normal pressure hydrocephalus, who underwent an uneventful right VPS placement, suffered from a catastrophic isolated IVH five days later. The reported cases of delayed intracerebral hemorrhage (ICH) following VPS are rare and those with IVH are even rarer. Potential factors of surgical anatomy that could cause delayed ICH/IVH following a VPS procedure include erosion of vasculature by catheter cannulation, multiple attempts at perforation, puncture of the choroid plexus, improper placement of the tubing within the brain parenchyma, VPS system revision, venous infarction, vascular malformations, head trauma, and brain tumors. Other causes include generalized convulsion, VPS system malfunction, increased intracranial or blood pressure, sudden intracranial hypotension, and bleeding disorders. According to the current literature, our case is the first reported delayed isolated IVH after a VPS placement so far. Neurosurgeons should be aware of the delayed ICH/IVH as a rare, potentially fatal complication of VPS, as well as of its risk factors.

scholarly journals Death Resulting from Pneumocephalus Complicating Endoscopic Food Bolus Retrieval in a Patient with Eosinophilic Esophagitis

2016 ◽  
Vol 6 (4) ◽  
pp. 703-708 ◽  
Author(s):  
Amy K. Fuhs ◽  
Joseph A. Prahlow
Keyword(s):  
Eosinophilic Esophagitis ◽  
Rare Complication ◽  
Flexible Endoscopy ◽  
Brain Parenchyma ◽  
Esophageal Mucosa ◽  
Food Bolus ◽  
Patient Death ◽  
Injury Death ◽  
Computed Tomography Scanning ◽  
The Brain

Pneumocephalus is a rare complication of esophagogastroduodenoscopy (EGD), but existing literature does not discuss pneumocephalus surrounding endoscopic food bolus retrieval. We present a death involving pneumocephalus complicating endoscopic food removal from the esophagus. A 40-year-old man presented with dysphagia and suprasternal discomfort 12 hours following chicken ingestion. On flexible endoscopy, chicken was visualized in the distal esophagus. After successful retrieval, a mucosal laceration was noted where the chicken had been lodged. He was unarousable following the procedure and was emergently transported to a hospital, where computed tomography scanning showed pneumocephalus. He was later declared brain dead. The case was referred for medicolegal autopsy. The brain was examined first, revealing rare air bubbles within meningeal vessels and numerous, diffuse petechiae-like hemorrhages within the brain parenchyma. The esophageal mucosa had focal discoloration and a partial thickness laceration; microscopic examination revealed eosinophilic esophagitis. Eosinophilic esophagitis is a known risk factor for food bolus impaction and should be suspected in such patients. Pneumocephalus is a rare possible complication of EGD for food bolus retrieval. In patients unresponsive after endoscopy, radiographic detection of potential pneumocephalus should be encouraged to enable timely therapy and improved outcomes, or to supplement autopsy in the event of patient death. Forensic pathologists should understand that pneumocephalus is a potential mechanism of injury/death in patients experiencing esophageal trauma, including injury incurred during EGD.

The history of brain retractors throughout the development of neurological surgery

2014 ◽  
Vol 36 (4) ◽  
pp. E8 ◽  
Author(s):  
Rachid Assina ◽  
Sebastian Rubino ◽  
Christina E. Sarris ◽  
Chirag D. Gandhi ◽  
Charles J. Prestigiacomo
Keyword(s):  
Degrees Of Freedom ◽  
Brain Parenchyma ◽  
Neurosurgical Procedures ◽  
Intracranial Surgery ◽  
Different Types ◽  
History Of ◽  
Brain Retraction ◽  
Neurological Surgery ◽  
The 19Th Century ◽  
The Brain

Early neurosurgical procedures dealt mainly with treatment of head trauma, especially skull fractures. Since the early medical writings by Hippocrates, a great deal of respect was given to the dura mater, and many other surgeons warned against violating the dura. It was not until the 19th century that neurosurgeons started venturing beneath the dura, deep into the brain parenchyma. With this advancement, brain retraction became an essential component of intracranial surgery. Over the years brain retractors have been created pragmatically to provide better visualization, increased articulations and degrees of freedom, greater stability, less brain retraction injury, and less user effort. Brain retractors have evolved from simple handheld retractors to intricate brain-retraction systems with hand-rest stabilizers. This paper will focus on the history of brain retractors, the different types of retractors, and the progression from one form to another.

Nonlinear poroplastic model of ventricular dilation in hydrocephalus

2008 ◽  
Vol 109 (1) ◽  
pp. 100-107 ◽  
Author(s):  
Shahan Momjian ◽  
Denis Bichsel
Keyword(s):  
Brain Tissue ◽  
Normal Pressure ◽  
Porous Matrix ◽  
Brain Parenchyma ◽  
Plastic Behavior ◽  
Fe Model ◽  
Mechanical Behaviors ◽  
Ventricular Dilation ◽  
Numerical Finite Element ◽  
The Brain

Object The mechanism of ventricular dilation in normal-pressure hydrocephalus remains unclear. Numerical finite-element (FE) models of hydrocephalus have been developed to investigate the biomechanics of ventricular enlargement. However, previous linear poroelastic models have failed to reproduce the relatively larger dilation of the horns of the lateral ventricles. In this paper the authors instead elaborated on a nonlinear poroplastic FE model of the brain parenchyma and studied the influence of the introduction of these potentially more realistic mechanical behaviors on the prediction of the ventricular shape. Methods In the proposed model the elasticity modulus varies as a function of the distension of the porous matrix, and the internal mechanical stresses are relaxed after each iteration, thereby simulating the probable plastic behavior of the brain tissue. The initial geometry used to build the model was extracted from CT scans of patients developing hydrocephalus, and the results of the simulations using this model were compared with the real evolution of the ventricular size and shape in the patients. Results The authors' model predicted correctly the magnitude and shape of the ventricular dilation in real cases of acute and chronic hydrocephalus. In particular, the dilation of the frontal and occipital horns was much more realistic. Conclusions This finding suggests that the nonlinear and plastic mechanical behaviors implemented in the present numerical model probably occur in reality. Moreover, the availability of such a valid FE model, whose mechanical parameters approach real mechanical properties of the brain tissue, might be useful in the further modeling of ventricular dilation at a normal pressure.

Modelling Normal Pressure Hydrocephalus as a ‘Two-Hit’ Disease Using Multiple-Network Poroelastic Theory

2010 ◽  
Author(s):  
Brett Tully ◽  
Yiannis Ventikos
Keyword(s):  
Normal Pressure Hydrocephalus ◽  
Normal Pressure ◽  
Brain Parenchyma ◽  
Strongly Correlated ◽  
Clinical Markers ◽  
Cerebral Diseases ◽  
Spatio Temporal ◽  
Multiple Network ◽  
Poroelastic Theory ◽  
The Brain

The evolution of many cerebral diseases such as Alzheimer’s and Parkinson’s Disease, Hydrocephalus, Cerebral Oedema, Stroke, and Tumour are strongly correlated to a change in the transport properties of fluid in the brain. This research proposes a novel application of Multiple-Network Poroelastic Theory (MPET) to investigate cerebral hydrodynamics through a detailed investigation of multiscalar, spatio-temporal transport of fluid between the cerebral blood, cerebrospinal fluid (CSF) and brain parenchyma. Specifically, MPET is used to interrogate the clinical markers of Normal Pressure Hydrocephalus (NPH).

Progressive Expanding Congenital Porencephalies: A Treatable Cause of Progressive Encephalopathy

PEDIATRICS ◽  
1981 ◽  
Vol 68 (2) ◽  
pp. 198-202
Author(s):  
Marc Tardieu ◽  
Philippe Evrard ◽  
Gilles Lyon
Keyword(s):  
Brain Lesion ◽  
Normal Pressure ◽  
Brain Parenchyma ◽  
Motor Deficits ◽  
Ventriculoperitoneal Shunting ◽  
Progressive Encephalopathy ◽  
Computed Tomography Scans ◽  
Gradual Expansion ◽  
Normal Thickness ◽  
The Brain

In congenital porencephalies, diverticulation of the lateral ventricle is a dynamic process producing compression and stretching of the brain tissue bordering the diverticulum, bulging of the overlying skull, macrocephaly, and occasionally progressive neurologic signs (hemiplegia, raised intracranial pressure), even when the rest of the ventricular system is not dilated and the CSF pressure is normal. Ventriculoperitoneal shunting can result in remarkable improvement of focal motor deficits and may apparently also play a beneficial role on further mental development. Successive computed tomography scans demonstrate that the brain parenchyma, which had been stretched by the porencephalic pouch, is capable of regaining near normal thickness. Congenital porencephalies are initiated by a limited destructive brain lesion, but the gradual expansion of the ventricular herniation may imply a mechanism identical to that which has been postulated in normal pressure hydrocephalus. Nine cases of unilateral "expanding" congenital porencephalies are presented and the treatment of this condition is discussed.

scholarly journals Iatrogenic cortical pseudoaneurysm following ventriculoperitoneal shunt insertion presenting with intraventricular hemorrhage

2019 ◽  
Vol 10 ◽  
pp. 179
Author(s):  
Leonard H. Verhey ◽  
Theresa A. Elder ◽  
Joseph G. Adel
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Ventriculoperitoneal Shunt ◽  
Intraventricular Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Rare Complication ◽  
Definitive Treatment ◽  
Ventricular Catheter ◽  
Shunt Insertion ◽  
Independent State ◽  
Pseudoaneurysm Formation

Background: Cerebral pseudoaneurysm formation associated with ventricular catheterization is an exceedingly rare complication that results from direct catheter-induced injury to a vessel. We report a case of intracerebral pseudoaneurysm formation associated with ventricular catheterization in a patient with hydrocephalus following aneurysmal subarachnoid hemorrhage. Case Description: The patient presented with aneurysmal subarachnoid hemorrhage and underwent partial endovascular embolization of the offending wide-necked basilar tip aneurysm with the plan for a Stage 2 stent-assisted coiling after initial recovery. Before discharge, a ventriculoperitoneal shunt (VPS) was placed for postaneurysmal hydrocephalus. Three weeks later, she presented with intraparenchymal and intraventricular hemorrhage. Angiography revealed a cortical aneurysm contiguous to the ventricular catheter of the VPS. She underwent microsurgical excision of the aneurysm, and a new VPS was placed after resolution of the intraventricular hemorrhage. She later underwent the second stage of the treatment and had an excellent neurological recovery to an independent state. Conclusion: Iatrogenic intracerebral pseudoaneurysm formation is an exceedingly rare complication of ventricular catheterization but is associated with significant mortality. Identifying a pseudoaneurysm in this context warrants prompt and definitive treatment with microsurgical or endovascular treatment.

scholarly journals Finite Element Analysis of Normal Pressure Hydrocephalus: Influence of CSF Content and Anisotropy in Permeability

2010 ◽  
Vol 7 (3) ◽  
pp. 187-197 ◽  
Author(s):  
K. Shahim ◽  
J.-M. Drezet ◽  
J.-F. Molinari ◽  
R. Sinkus ◽  
S. Momjian
Keyword(s):  
Finite Element ◽  
Normal Pressure Hydrocephalus ◽  
Diffusion Tensor ◽  
Great Influence ◽  
Normal Pressure ◽  
Element Model ◽  
Brain Parenchyma ◽  
Element Analysis ◽  
Cerebral Disease ◽  
The Brain

Hydrocephalus is a cerebral disease where brain ventricles enlarge and compress the brain parenchyma towards the skull leading to symptoms like dementia, walking disorder and incontinence. The origin of normal pressure hydrocephalus is still obscure. In order to study this disease, a finite element model is built using the geometries of the ventricles and the skull measured by magnetic resonance imaging. The brain parenchyma is modelled as a porous medium fully saturated with cerebrospinal fluid (CSF) using Biot's theory of consolidation (1941). Owing to the existence of bundles of axons, the brain parenchyma shows locally anisotropic behaviour. Indeed, permeability is higher along the fibre tracts in the white matter region. In contrast, grey matter is isotropic. Diffusion tensor imaging is used to establish the local CSF content and the fibre tracts direction together with the associated local frame where the permeability coefficients are given by dedicated formulas. The present study shows that both inhomogeneous CSF content and anisotropy in permeability have a great influence on the CSF flow pattern through the parenchyma under an imposed pressure gradient between the ventricles and the subarachnoid spaces.

Intracerebral infusion of thrombin as a cause of brain edema

1995 ◽  
Vol 83 (6) ◽  
pp. 1045-1050 ◽  
Author(s):  
Kevin R. Lee ◽  
A. Lorris Betz ◽  
Richard F. Keep ◽  
Thomas L. Chenevert ◽  
Seoung Kim ◽  
...  
Keyword(s):  
Brain Edema ◽  
Brain Parenchyma ◽  
Thrombin Inhibitor ◽  
Neurosurgical Procedures ◽  
Edema Formation ◽  
Content Type ◽  
The Right ◽  
The Brain ◽  
Brain Water ◽  
Fine Print

✓ Purified thrombin from an exogenous source is a hemostatic agent commonly used in neurosurgical procedures. The toxicity of thrombin in the brain, however, has not been examined. This study was performed to assess the effect of thrombin on brain parenchyma, using the formation of brain edema as an indicator of injury. Ten µl of test solution was infused stereotactically into the right basal ganglia of rats. The animals were sacrificed 24 hours later, and the extent of brain edema and ion content were measured. Concentrations of human thrombin as low as 1 U/µl resulted in a significant increase in brain water content. Rats receiving 10 U/µl had a mortality rate of 33% compared to no mortality in the groups receiving smaller doses. Thrombin-induced brain edema was inhibited by a specific and potent thrombin inhibitor, hirudin. A medical grade of bovine thrombin commonly used in surgery also caused brain edema when injected at a concentration of 2 U/µl. Edema formation was prevented by another highly specific thrombin inhibitor, Nα-(2-Naphthalenesulfonylglycyl)-4-dl-phenylalaninepiperidide (α-NAPAP). Thrombininduced brain edema was accompanied by increases in brain sodium and chloride contents and a decrease in brain potassium content. Changes in brain ions were inhibited by both hirudin and α-NAPAP, corresponding to the inhibition of brain water accumulation. This study shows that thrombin causes brain edema when infused into the brain at concentrations as low as 1 U/µl, an amount within the range of concentrations used for topical hemostasis in neurosurgery.

scholarly journals Glymphatic System as a Gateway to Connect Neurodegeneration From Periphery to CNS

2021 ◽  
Vol 15 ◽  
Author(s):  
Gianfranco Natale ◽  
Fiona Limanaqi ◽  
Carla L. Busceti ◽  
Federica Mastroiacovo ◽  
Ferdinando Nicoletti ◽  
...  
Keyword(s):  
Interstitial Fluid ◽  
Lymphatic Vessels ◽  
Normal Pressure ◽  
Lymphatic Drainage ◽  
Brain Parenchyma ◽  
Waste Products ◽  
Pathological Conditions ◽  
The Central Nervous System ◽  
Glymphatic Pathway ◽  
The Brain

The classic concept of the absence of lymphatic vessels in the central nervous system (CNS), suggesting the immune privilege of the brain in spite of its high metabolic rate, was predominant until recent times. On the other hand, this idea left questioned how cerebral interstitial fluid is cleared of waste products. It was generally thought that clearance depends on cerebrospinal fluid (CSF). Not long ago, an anatomically and functionally discrete paravascular space was revised to provide a pathway for the clearance of molecules drained within the interstitial space. According to this model, CSF enters the brain parenchyma along arterial paravascular spaces. Once mixed with interstitial fluid and solutes in a process mediated by aquaporin-4, CSF exits through the extracellular space along venous paravascular spaces, thus being removed from the brain. This process includes the participation of perivascular glial cells due to a sieving effect of their end-feet. Such draining space resembles the peripheral lymphatic system, therefore, the term “glymphatic” (glial-lymphatic) pathway has been coined. Specific studies focused on the potential role of the glymphatic pathway in healthy and pathological conditions, including neurodegenerative diseases. This mainly concerns Alzheimer’s disease (AD), as well as hemorrhagic and ischemic neurovascular disorders; other acute degenerative processes, such as normal pressure hydrocephalus or traumatic brain injury are involved as well. Novel morphological and functional investigations also suggested alternative models to drain molecules through perivascular pathways, which enriched our insight of homeostatic processes within neural microenvironment. Under the light of these considerations, the present article aims to discuss recent findings and concepts on nervous lymphatic drainage and blood–brain barrier (BBB) in an attempt to understand how peripheral pathological conditions may be detrimental to the CNS, paving the way to neurodegeneration.

scholarly journals Transient Cerebral Vasculopathy: A Rare Complication Associated with Cerebral Gnathostomiasis

2018 ◽  
Vol 08 (01) ◽  
pp. e27-e30
Author(s):  
Vitchayaporn Saengow ◽  
Oragarn Wongfukiat
Keyword(s):  
Intraventricular Hemorrhage ◽  
White Matter Lesion ◽  
Rare Complication ◽  
Parasitic Infection ◽  
Imaging Study ◽  
Enzyme Linked Immunosorbent Assay ◽  
Serological Testing ◽  
Mortality And Morbidity ◽  
Elisa Technique ◽  
The Brain

AbstractGnathostomiasis is a common parasitic infection in Southeast Asia, involving many organs in infected human hosts. Common neurological manifestations of Gnathostoma infection include radiculomyelitis, eosinophilic meningitis, and nontraumatic subarachnoid hemorrhage, leading to a high mortality and morbidity. This study first reported transient cerebral vasculopathy, an atypical neurological manifestation, in an 11-year-old Thai girl. The patient was diagnosed with intracerebral and intraventricular hemorrhage, and meningitis with atypical cerebrospinal fluid (CSF) profile. The imaging study of the brain revealed the abnormal white matter lesion and transient cerebral vasculopathy with the cerebral hemorrhage showing a track-like appearance (at the level of the corpus callosum). The serological testing in CSF and serum using the enzyme-linked immunosorbent assay (ELISA) technique was positive for Gnathostoma spinigerum. The patient spontaneously recovered within 3 months without albendazole or corticosteroid treatments.

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