Mammals control the volume and osmolality of their body fluids from stimuli that arise from both the intracellular and extracellular fluid compartments. These stimuli are sensed by two kinds of receptors: osmoreceptor-Na+ receptors and volume or pressure receptors. This information is conveyed to specific areas of the central nervous system responsible for an integrated response, which depends on the integrity of the anteroventral region of the third ventricle, e.g., organum vasculosum of the lamina terminalis, median preoptic nucleus, and subfornical organ. The hypothalamo-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting vasopressin and oxytocin in response to osmotic and nonosmotic stimuli. Since the discovery of the atrial natriuretic peptide (ANP), a large number of publications have demonstrated that this peptide provides a potent defense mechanism against volume overload in mammals, including humans. ANP is mostly localized in the heart, but ANP and its receptor are also found in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation. Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors. Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP. This review emphasizes the role played by brain ANP and its interaction with neurohypophysial hormones in the control of body fluid homeostasis.

Objective To report radiological findings observed in computed tomography (CT) and magnetic resonance imaging (MRI) scans of the first cases of congenital infection and microcephaly presumably associated with the Zika virus in the current Brazilian epidemic.Design Retrospective study with a case series.Setting Association for Assistance of Disabled Children (AACD), Pernambuco state, Brazil.Participants 23 children with a diagnosis of congenital infection presumably associated with the Zika virus during the Brazilian microcephaly epidemic.Main outcome measures Types of abnormalities and the radiological pattern of lesions identified on CT and MRI brain scans.Results Six of the 23 children tested positive for IgM antibodies to Zika virus in cerebrospinal fluid. The other 17 children met the protocol criteria for congenital infection presumably associated with the Zika virus, even without being tested for IgM antibodies to the virus—the test was not yet available on a routine basis. Of the 23 children, 15 underwent CT, seven underwent both CT and MRI, and one underwent MRI. Of the 22 children who underwent CT, all had calcifications in the junction between cortical and subcortical white matter, 21 (95%) had malformations of cortical development, 20 (91%) had a decreased brain volume, 19 (86%) had ventriculomegaly, and 11 (50%) had hypoplasia of the cerebellum or brainstem. Of the eight children who underwent MRI, all had calcifications in the junction between cortical and subcortical white matter, malformations of cortical development occurring predominantly in the frontal lobes, and ventriculomegaly. Seven of the eight (88%) children had enlarged cisterna magna, seven (88%) delayed myelination, and six each (75%) a moderate to severe decrease in brain volume, simplified gyral pattern, and abnormalities of the corpus callosum (38% hypogenesis and 38% hypoplasia). Malformations were symmetrical in 75% of the cases.Conclusion Severe cerebral damage was found on imaging in most of the children in this case series with congenital infection presumably associated with the Zika virus. The features most commonly found were brain calcifications in the junction between cortical and subcortical white matter associated with malformations of cortical development, often with a simplified gyral pattern and predominance of pachygyria or polymicrogyria in the frontal lobes. Additional findings were enlarged cisterna magna, abnormalities of corpus callosum (hypoplasia or hypogenesis), ventriculomegaly, delayed myelination, and hypoplasia of the cerebellum and the brainstem.

Patients with coronavirus disease 2019 (COVID-19) may have symptoms of anosmia or partial loss of the sense of smell, often accompanied by changes in taste. We report 5 cases (3 with anosmia) of adult patients with COVID-19 in whom injury to the olfactory bulbs was interpreted as microbleeding or abnormal enhancement on MR imaging. The patients had persistent headache (n ¼ 4) or motor deficits (n ¼ 1). This olfactory bulb injury may be the mechanism by which the Severe Acute Respiratory Syndrome coronavirus 2 causes olfactory dysfunction. ABBREVIATIONS: COVID-19 ¼ coronavirus disease 2019; SARS-CoV-2 ¼ Severe Acute Respiratory Syndrome coronavirus 2 C oronavirus has the human respiratory system as its main target but also has neuroinvasive capabilities and can spread from the respiratory tract to the CNS. 1-3 Therefore, patients with coronavirus disease 19 (COVID-19) may present with neurologic symptomatology with repercussions on imaging examinations, 4-18 and these have been described in association with ischemic infarct, 8,9 hemorrhage, 11 acute hemorrhagic necrotizing encephalopathy, 10 cerebral venous thrombosis, 13 and diffuse leukoencephalopathy with microhemorrhage. 15 Transmission from person to person occurs mainly by direct contact or droplets spread by coughing or sneezing by an infected individual with Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2). 5,19 Symptoms of COVID-19 usually appear after an incubation period of about 5 days. The most common symptoms are fever, cough, fatigue, headache, and dyspnea. 5,19,20 In the most severe cases, patients may develop pneumonia, acute respiratory failure, distress syndrome, and acute heart problems. 5,19,20 Anosmia or partial loss of the sense of smell, usually accompanied by changes in taste, is a frequent symptom that helps in the diagnosis of COVID-19. 21-28 It is often a transitory

In conclusion, 14/48 patients (29%) suffered none of the above-mentioned symptoms, indicating that a significant number of patients may suffer from PDPH in the absence of any symptoms apart from the headache itself. This suggests that a further analyses of existing studies should be made to determine if a criteria change may need consideration.

Mammalian reproduction is dependent upon intermittent delivery of luteinizing hormone-releasing hormone (LHRH) to the anterior pituitary. This mode of secretion is required to sensitize maximally the gonadotrophs to LHRH stimulation and to regulate gonadotropin gene expression. While LHRH secretion is pulsatile in nature, the origin of the pulse generator is unknown. In this report, we show that this oscillator could be located within the LHRH neuronal network. When immortalized LHRH neurons are placed into a perifusion system, LHRH is secreted into the medium in a pulsatile fashion under basal conditions. LHRH secretion and the number of LHRH pulses are reduced when calcium is removed from the medium. Perifusion also influences pro-LHRH processing, since the molar ratio of its processed products varies dramatically when the cells are transferred from a static system. Several different cellular mechanisms may underlie these changes in secretion and processing. Lucifer yellow experiments reveal that some cells are dye-coupled. Hence, these cells could be electrically coupled through gap junctions such that secretion from individual cells could be coordinated. Secretion could also be synchronized through the observed synapse-like contacts. These contacts could perform a negative-feedback role to regulate not only the amount of LHRH released but also the molecular forms secreted. The organization of LHRH neurons into interconnected clusters could serve to coordinate LHRH secretion from individual cells and, thereby, orchestrate functions in vivo as diverse as the onset of puberty, the timing of ovulation, and the duration of lactational infertility.Luteinizing hormone (LH)-releasing hormone (LHRH) is a major regulator of reproduction in mammals (1-3). While LHRH neuronal cell bodies are scattered throughout the anterior hypothalamic region, their nerve terminals converge on the median eminence. LHRH is secreted into the hypophysial portal circulation, where it is transported to the anterior pituitary to stimulate the release of LH and folliclestimulating hormone.In all mammalian species studied so far, secretion of LH into blood is episodic in nature (1,(4)(5)(6)(7)(8). Interestingly, LHRH is secreted into the hypophysial portal blood in a pulsatile manner (9-11), and LH pulses are preceded by LHRH release (1, 10, 11). In addition, LH pulsatile secretion is lost either after passive immunization with LHRH antiserum (12) or with administration of a LHRH antagonist (13). Lesions of either the medial basal hypothalamus or the arcuate nucleus also eradicate LH pulses (1). By comparison, continuous infusion of LHRH, which desensitizes the gonadotropes through down-regulation of the LHRH receptor (14), also abolishes episodic secretion of LH and reduces LH 03-and a-subunit mRNA levels (15, 16). While the relationship between LHRH and LH secretion is well established, it is unclear whether the generator for LHRH pulses is located within the LHRH neuronal network itself or within networks of other neighboring neuro...

Amorim JA, Remígio DSCA, Damázio Filho O, Barros MAG, Carvalho VN, Valença MM-Intracranial Subdural Hematoma Post-Spinal Anesthesia: Report of Two Cases and Review of 33 Cases in the Literature. Background and objectives: Intracranial subdural hematoma is a rare complication of spinal anesthesia. We report two cases of women who developed chronic subdural hematoma post-spinal anesthesia diagnosed after prolonged clinical evolution of post-dural puncture headache (PDPH) and we analyze other 33 cases found on literature review.

Odorants, isolated or in association, especially perfume, may trigger migraine attacks after a few minutes of exposure.

A detailed anatomic study was carried out on the lateral femoral cutaneous nerve to better understand the etiology and treatment of lateral femoral cutaneous neuralgia. As it passed from the pelvis into the thigh, the lateral femoral cutaneous nerve ran through an "aponeuroticofascial tunnel," beginning at the iliopubic tract and ending at the inguinal ligament; as it passed through the tunnel, an enlargement in its side-to-side diameter was observed, suggesting that the fascial structures proximal to the inguinal ligament may be implicated in the genesis of lateral femoral cutaneous neuralgia. The finding of pseudoneuromas at this location, distant from the inguinal ligament, supports this hypothesis. The anterior superior iliac spine is located approximately 0.7 cm from the lateral femoral cutaneous nerve and serves as the bony landmark for nerve localization. Within the first 3 cm of leaving the pelvis, the lateral femoral cutaneous nerve was observed deep to the fascia lata; therefore, surgical dissection within the subcutaneous fascia may be conducted with relative impunity near the anterior superior iliac spine just inferior to the inguinal ligament. In 36% of cases there was no posterior branch of the nerve, which is correlated to lateral femoral cutaneous neuralgia symptoms often being limited to the anterior branch region. An accessory nerve was found in 30% of cases.