scholarly journals Area postrema: fetal maturation, tumours, vomiting centre, somatic growth and role in neuromyelitis optica

Author(s):  
HB Sarnat ◽  
L Flores-Sarnat ◽  
E Boltshauser

The area postrema (AP) in the caudal 4th ventricular floor is unique, highly vascular without blood/brain or /CSF barrier. In addition to its function as the vomiting centre, several other important functions are: part of the circumventricular organs for vasomotor and angiotensin II regulation; a role in neuromyelitis optica related to aquaporin-4; contributor to fetal and postnatal somatic growth. Functions are immature at birth.The purpose of this study was to demonstrate AP neuronal/synaptic/glial maturation in normal fetuses and 3 AP tumours. Transverse sections of the caudal 4th ventricle of 18 normal human fetal brains at autopsy, 6 to 40 weeks were examined; also 3 infants 3-18mos; 2 children. A battery of immunocytochemical neuronal and glial markers: MAP2; calretinin; synaptophysin; vimentin; nestin; GFAP; S-100β protein; were applied to paraffin sections. Two children with AP tumours and one with neurocutaneous melanocytosis, all with pernicious vomiting, were studied. In normal fetuses, AP neurons exhibited cytological maturity and well-formed synaptic circuitry by 14wk gestation. Size/volume increase was disproportionately greater than brainstem growth in 2nd and 3rd trimesters and postnatally. Astrocytes co-expressed vimentin/GFAP but glia were best demonstrated by S-100β protein. Ependyma over the AP in fetuses is simple cuboidal, adjacent to pseudostratified columnar of the 4th ventricular floor. Melanocytes infiltrated AP in the toddler with pernicious vomiting; 2 children had primary AP pilocytic astrocytomas. Though AP is cytologically mature by 14wk, growth increases and functions mature into the postnatal months. We recommend that AP neuropathology include synaptophysin and S-100β at autopsy if AP dysfunction suspected.LEARNING OBJECTIVESThis presentation will enable the learner to:1.Explain the maturation of neurons, synaptic circuits and glial elements of the AP2.List and recognize tumours that can affect the area postrema3.Describe functions of the area postrema

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chenyang Zhang ◽  
Kang Zhang ◽  
Bing Chen ◽  
Jiao Yin ◽  
Miaomiao Dong ◽  
...  

Abstract Background Neuromyelitis optica spectrum disorders (NMOSD), a group of autoimmune neurological diseases, involve the optic nerve, spinal cord, and brain. Meningitis is rarely reported as the primary clinical manifestation of both anti-aquaporin-4 (AQP4)/ anti-myelin oligodendrocyte glycoprotein (MOG) antibody-negative NMOSD (NMOSDneg). Case presentation A 30-year-old man initially presented with fever, headache, and neck stiffness. Lumbar puncture revealed mixed cell reaction and decreased glucose levels. As a result, tuberculous meningitis was suspected. After 1 month, the patient developed longitudinally extensive transverse myelitis and area postrema syndrome. This was followed by the presentation of meningitis-like symptoms once again in the third attack, but his condition eventually improved after corticosteroid treatment without relapse for 2 years. However, he was readmitted to our hospital owing to symptoms of diplopia, hiccup, and numbness in the right hand. Brain magnetic resonance imaging (MRI) revealed that the area postrema still contained lesions. Spinal MRI revealed several segmental enhancements at the C4–C5, T1, and T5 levels. Anti-AQP4 and anti-MOG antibodies were persistently absent in the serum and cerebrospinal fluid (CSF). The patient was finally diagnosed with NMOSDneg. Conclusions Meningitis could be a recurrent manifestation of NMOSDneg and requires more careful evaluation.


Neurosurgery ◽  
2013 ◽  
Vol 72 (5) ◽  
pp. 855-860 ◽  
Author(s):  
Pierluigi Longatti ◽  
Luca Basaldella ◽  
Francesco Sammartino ◽  
Alessandro Boaro ◽  
Alessandro Fiorindi

Abstract BACKGROUND: Fluorescein enhancement to detect retinal disorder or differentiate cancer tissue in situ is a well-defined diagnostic procedure. It is a visible marker of where the blood-brain barrier is absent or disrupted. Little is reported in the contemporary literature on endoscopic fluorescein-enhanced visualization of the circumventricular organs, and the relevance of these structures as additional markers for safe ventricular endoscopic navigation remains an unexplored field. OBJECTIVE: To describe fluorescein sodium–enhanced visualization of circumventricular organs as additional anatomic landmarks during endoscopic ventricular surgery procedures. METHODS: We prospectively administered intravenously 500 mg fluorescein sodium in 12 consecutive endoscopic surgery patients. A flexible endoscope equipped with dual observation modes for both white light and fluorescence was used. During navigation from the lateral to the fourth ventricle, the endoscopic anatomic landmarks were first inspected under white light and then under the fluorescent mode. RESULTS: After a mean of 20 seconds in the fluorescent mode, the fluorescein enhanced visualization of the choroid plexus of the lateral ventricle, median eminence–tuber cinereum complex, organum vasculosum of the lamina terminalis, choroid plexus of the third and fourth ventricles, and area postrema. CONCLUSION: Fluorescein-enhanced visualization is a useful tool for helping neuroendoscopists recognize endoscopic anatomic landmarks. It could be adopted to guide orientation when the surgeon deems an endoscopic procedure unsafe or contraindicated because of unclear or subverted anatomic landmarks. Visualization of the circumventricular organs could add new insight into the functional anatomy of these structures, with possible implications for the site and safety of third ventriculostomy.


2014 ◽  
Vol 306 (3) ◽  
pp. R175-R184 ◽  
Author(s):  
Florencia M. Dadam ◽  
Ximena E. Caeiro ◽  
Carla D. Cisternas ◽  
Ana F. Macchione ◽  
María J. Cambiasso ◽  
...  

Previous studies indicate a sex chromosome complement (SCC) effect on the angiotensin II-sexually dimorphic hypertensive and bradycardic baroreflex responses. We sought to evaluate whether SCC may differentially modulate sexually dimorphic-induced sodium appetite and specific brain activity due to physiological stimulation of the rennin angiotensin system. For this purpose, we used the “four core genotype” mouse model, in which the effect of gonadal sex and SCC is dissociated, allowing comparisons of sexually dimorphic traits between XX and XY females as well as in XX and XY males. Gonadectomized mice were sodium depleted by furosemide (50 mg/kg) and low-sodium diet treatment; control groups were administered with vehicle and maintained on normal sodium diet. Twenty-one hours later, the mice were divided into two groups: one group was submitted to the water-2% NaCl choice intake test, while the other group was perfused and their brains subjected to the Fos-immunoreactivity (FOS-ir) procedure. Sodium depletion, regardless of SCC (XX or XY), induced a significantly lower sodium and water intake in females than in males, confirming the existence in mice of sexual dimorphism in sodium appetite and the organizational involvement of gonadal steroids. Moreover, our results demonstrate a SCC effect on induced brain FOS-ir, showing increased brain activity in XX-SCC mice at the paraventricular nucleus, nucleus of the solitary tract, and lateral parabrachial nucleus, as well as an XX-SCC augmented effect on sodium depletion-induced brain activity at two circumventricular organs, the subfornical organ and area postrema, nuclei closely involved in fluid and blood pressure homeostasis.


2019 ◽  
Vol 10 (4) ◽  
pp. 222 ◽  
Author(s):  
GauravKumar Mittal ◽  
Shilpa Sekhar ◽  
JohnJacob Mathew ◽  
Jennifer Singhdev

2019 ◽  
Vol 7 (5) ◽  
pp. 301-302
Author(s):  
Irene Treviño‐Frenk ◽  
Rogelio Dominguez‐Moreno ◽  
Dioselina Panama Tristan‐Samaniego ◽  
David Davila‐Sosa ◽  
Gladys Vanessa Barriga‐Maldonado

Biomedicines ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 42 ◽  
Author(s):  
Marco A. Lana-Peixoto ◽  
Natália Talim

Neuromyelitis optica spectrum disorder (NMOSD) and anti-myelin oligodendrocyte glycoprotein (anti-MOG) syndromes are immune-mediated inflammatory conditions of the central nervous system that frequently involve the optic nerves and the spinal cord. Because of their similar clinical manifestations and habitual relapsing course they are frequently confounded with multiple sclerosis (MS). Early and accurate diagnosis of these distinct conditions is relevant as they have different treatments. Some agents used for MS treatment may be deleterious to NMOSD. NMOSD is frequently associated with antibodies which target aquaporin-4 (AQP4), the most abundant water channel in the CNS, located in the astrocytic processes at the blood-brain barrier (BBB). On the other hand, anti-MOG syndromes result from damage to myelin oligodendrocyte glycoprotein (MOG), expressed on surfaces of oligodendrocytes and myelin sheaths. Acute transverse myelitis with longitudinally extensive lesion on spinal MRI is the most frequent inaugural manifestation of NMOSD, usually followed by optic neuritis. Other core clinical characteristics include area postrema syndrome, brainstem, diencephalic and cerebral symptoms that may be associated with typical MRI abnormalities. Acute disseminated encephalomyelitis and bilateral or recurrent optic neuritis are the most frequent anti-MOG syndromes in children and adults, respectively. Attacks are usually treated with steroids, and relapses prevention with immunosuppressive drugs. Promising emerging therapies for NMOSD include monoclonal antibodies and tolerization.


2019 ◽  
Vol 26 (2) ◽  
pp. 253-255 ◽  
Author(s):  
Jonathan Ciron ◽  
Fanny Sourdrille ◽  
Damien Biotti ◽  
Thierry Tchoumi ◽  
Anne Ruiz ◽  
...  

Anti–Glial fibrillary acidic protein (GFAP) encephalomyelitis is a recently described entity and while the spectrum of this disease has been explored, further research is needed to fully describe its phenotype. Area postrema syndrome (APS) is usually associated with neuromyelitis optica spectrum disorders (NMOSDs), whereas no case of APS has been previously reported with anti-GFAP encephalomyelitis. In this article, we report a case of APS in a 41-year-old woman in the context of anti-GFAP encephalomyelitis. This case was not associated with additional anti-AQP4 IgG and therefore extends the clinico-radiological spectrum of anti-GFAP encephalomyelitis.


2007 ◽  
Vol 293 (3) ◽  
pp. C1181-C1185 ◽  
Author(s):  
Sandra B. Ross ◽  
Catherine M. Fuller ◽  
James K. Bubien ◽  
Dale J. Benos

Despite intensive research, brain tumors remain among the most difficult type of malignancies to treat, due largely to their diffusely invasive nature and the associated difficulty of adequate surgical resection. To migrate through the brain parenchyma and to proliferate, glioma cells must be capable of significant changes in shape and volume. We have previously reported that glioma cells express an amiloride- and psalmotoxin-sensitive cation conductance that is not found in normal human astrocytes. In the present study, we investigated the potential role of this ion channel to mediate regulatory volume increase in glioma cells. We found that the ability of the cells to volume regulate subsequent to cell shrinkage by hyperosmolar solutions was abolished by both amiloride and psalmotoxin 1. This toxin is thought to be a specific peptide inhibitor of acid-sensing ion channel (ASIC1), a member of the Deg/ENaC superfamily of cation channels. We have previously shown this toxin to be an effective blocker of the glioma cation conductance. Our data suggest that one potential role for this conductance may be to restore cell volume during the cell's progression thorough the cell cycle and while the tumor cell migrates within the interstices of the brain.


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