Depressed Reflexes Research Articles

Motor point stimulation activates fewer Ia-sensory nerves than peripheral nerve stimulation in human soleus muscle.

Peripheral nerve stimulation (PNS) and motor point stimulation (MPS) are noninvasive techniques used to induce muscle contraction, aiding motor function restoration in individuals with neurological disorders. Understanding sensory inputs from PNS and MPS is crucial for facilitating neuroplasticity and restoring impaired motor function. Although previous studies suggest that MPS could induce Ia-sensory inputs less than PNS, experimental evidence supporting this claim is insufficient. Here, we implemented a conditioning paradigm combining transcutaneous spinal cord stimulation (tSCS) with PNS or MPS to investigate their Ia-sensory inputs. This paradigm induces postactivation depression of spinal reflexes associated with transient decreases in neurotransmitter release from Ia-afferent terminals, allowing us to examine the Ia-sensory input amount from PNS and MPS based on the depression degree. We hypothesized that MPS would induce less postactivation depression than PNS. Thirteen individuals underwent MPS and PNS on the soleus muscle as conditioning stimuli, with tSCS applied to the skin between the spinous processes (L1-L2) as test stimuli. PNS- and MPS-conditioned spinal reflexes were recorded at five interstimulus intervals (ISIs) and four intensities. Results revealed that all PNS conditioning showed significant decreases in spinal reflex amplitudes, indicating postactivation depression. Furthermore, PNS conditioning exhibited greater depression for shorter ISIs and higher conditioning intensities. In contrast, MPS conditioning demonstrated intensity-dependent depression, but without all-conditioning depression and clear ISI dependency as seen in PNS conditioning. In addition, PNS induced significantly greater depression than MPS across most conditions. Our findings provide experimental evidence supporting the conclusion that MPS activates Ia-sensory nerves less than PNS.NEW & NOTEWORTHY Peripheral nerve stimulation (PNS) and motor point stimulation (MPS) induce neuroplasticity, but differences in their effects on Ia-sensory inputs are unclear. We investigated their Ia-sensory inputs using a conditioning paradigm with spinal reflexes. Results showed that PNS conditioning significantly inhibited spinal reflexes than MPS conditioning, indicating greater postactivation depression due to Ia-sensory nerve activation. These findings provide experimental evidence that MPS activates Ia-sensory nerves to a lesser extent than PNS, enhancing our understanding of neuroplasticity.

Neonatal sepsis-a peek into our findings in Northwest Nigeria: a prospective study

BackgroundNeonatal sepsis is still a global health concern as it contributes to a high burden of neonatal morbidity and mortality especially in developing countries. The aim of the study is to give an insight into neonatal sepsis: risk factors, sepsis types, clinical features, pathogen burden with their antibiotic sensitivities, and outcome of admission in our facility. The study was a prospective hospital-based study conducted over 10 months, October 2018–July 2019.ResultOf the 248 term neonates with features of sepsis enrolled in the study 94 (37.9%) were confirmed to have sepsis. Late-onset sepsis LOS (68%) was found to be the most common, and most of the neonates were delivered elsewhere. Clinical features were non-specific for both early-onset (EOS) and LOS and include fever, jaundice, poor suck, and depressed primitive reflexes. Infections were mostly caused by gram-negative bacteria, and while Staphylococcus aureus was the single most common isolate for both EOS and LOS. Antibiotic sensitivity was highest with ciprofloxacin for both EOS and LOS. Mortality was high at 14.9% and was mostly contributed to by Staphylococcus aureus infection.ConclusionNeonatal sepsis is still a burden with mostly non-specific clinical features. The local prevalent organisms were Staphylococcus aureus, Enterobacter agglomerans and Klebsiella pneumonia with good antibiotic susceptibility to ciprofloxacin. Most presented with late-onset sepsis and therefore infection is likely to be community-acquired which to a great extent can be prevented with robust public health interventions.

Musculoskeletal mimics of lumbosacral radiculopathy.

Electrodiagnostic evaluations are commonly requested for patients with suspected radiculopathy. Understanding lower extremity musculoskeletal conditions is essential for electrodiagnostic medicine specialists, as musculoskeletal disorders often mimic or coexist with radiculopathy. This review delineates radicular pain from other types originating from the lumbosacral spine and describes musculoskeletal conditions frequently mimicking radiculopathy, such as those that cause radiating pain and sensorimotor dysfunction. In clinical evaluation, a history of pain radiating along a specific dermatomal territory with associated sensory disturbance suggests radiculopathy. Physical examination findings consistent with radiculopathy include myotomal weakness, depressed or absent muscle stretch reflexes, focal atrophy along a discrete nerve root territory, and potentially positive dural tension maneuvers like the straight leg raise. However, electrodiagnostic medicine specialists must be knowledgeable of musculoskeletal mimics, which may manifest as incomplete radiation within or beyond a dermatomal territory, non-radiating pain, tenderness, and give-way weakness, in the context of a normal neurological examination. A systematic approach to musculoskeletal examination is vital, and this review focuses on high-yield physical examination maneuvers and diagnostic investigations to differentiate between musculoskeletal conditions and radiculopathy. This approach ensures accurate diagnoses, promotes resource stewardship, enhances patient satisfaction, and optimizes care delivery. Musculoskeletal conditions resembling L1 to S4 radiculopathy are reviewed, emphasizing their distinctive features in history, physical examination, and diagnostic investigation. Among the more than 30 musculoskeletal disorders reviewed are hip and knee osteoarthritis, lumbar facet syndrome, myofascial pain syndrome, greater trochanteric pain syndrome, and plantar fasciitis.

Exercise-induced neuroplasticity in autonomic nuclei restores the cardiac vagal tone and baroreflex dysfunction in aged hypertensive rats.

Aging is accompanied by considerable deterioration of homeostatic systems, such as autonomic imbalance characterized by heightened sympathetic activity, lower parasympathetic tone, and depressed heart rate (HR) variability, which are aggravated by hypertension. Here, we hypothesized that these age-related deficits in aged hypertensive rats can be ameliorated by exercise training, with benefits to the cardiovascular system. Therefore, male 22-mo-old spontaneously hypertensive rats (SHRs) and age-matched Wistar Kyoto (WKY) submitted to moderate-intensity exercise training (T) or kept sedentary (S) for 8 wk were evaluated for hemodynamic/autonomic parameters, baroreflex sensitivity, cardiac sympathetic/parasympathetic tone and analysis of dopamine β-hydroxylase (DBH+) and oxytocin (OT+) pathways of autonomic brain nuclei. Aged SHR-S versus WKY-S exhibited elevated mean arterial pressure (MAP: +51%) and HR (+20%), augmented pressure/HR variability, no cardiac vagal tone, and depressed reflex control of the heart (HR range, -28%; gain, -49%). SHR-T exhibited a lower resting HR, a partial reduction in the MAP (-14%), in the pressure/HR variabilities, and restored parasympathetic modulation, with improvement of baroreceptor reflex control when compared with SHR-S. Exercise training increased the ascending DBH+ projections conveying peripheral information to the paraventricular nucleus of hypothalamus (PVN), augmented the expression of OT+ neurons, and reduced the density of DBH+ neurons in the rostral ventrolateral medulla (RVLM) of SHR-T. Data indicate that exercise training induces beneficial neuroplasticity in brain autonomic circuitry, and it is highly effective to restore the parasympathetic tone, and attenuation of age-related autonomic imbalance and baroreflex dysfunction, thus conferring long-term benefits for cardiovascular control in aged hypertensive individuals.NEW & NOTEWORTHY Exercise training reduces high blood pressure and cardiovascular autonomic modulation in aged hypertensive rats. The dysfunction in the baroreflex sensitivity and impaired parasympathetic tone to the heart of aged hypertensive rats are restored by exercise training. Exercise induces beneficial neuroplasticity in the brain nuclei involved with autonomic control of cardiovascular function of aged hypertensive rats.

Muscle Spasms after Spinal Cord Injury Stem from Changes in Motoneuron Excitability and Synaptic Inhibition, Not Synaptic Excitation.

Muscle spasms are common in chronic spinal cord injury (SCI), posing challenges to rehabilitation and daily activities. Pharmacological management of spasms mostly targets suppression of excitatory inputs, an approach known to hinder motor recovery. To identify better targets, we investigated changes in inhibitory and excitatory synaptic inputs to motoneurons as well as motoneuron excitability in chronic SCI. We induced either a complete or incomplete SCI in adult mice of either sex and divided those with incomplete injury into low or high functional recovery groups. Their sacrocaudal spinal cords were then extracted and used to study plasticity below injury, with tissue from naive animals as a control. Electrical stimulation of the dorsal roots elicited spasm-like activity in preparations of chronic severe SCI but not in the control. To evaluate overall synaptic inhibition activated by sensory stimulation, we measured the rate-dependent depression of spinal root reflexes. We found inhibitory inputs to be impaired in chronic injury models. When synaptic inhibition was blocked pharmacologically, all preparations became clearly spastic, even the control. However, preparations with chronic injuries generated longer spasms than control. We then measured excitatory postsynaptic currents (EPSCs) in motoneurons during sensory-evoked spasms. The data showed no difference in the amplitude of EPSCs or their conductance among animal groups. Nonetheless, we found that motoneuron persistent inward currents activated by the EPSCs were increased in chronic SCI. These findings suggest that changes in motoneuron excitability and synaptic inhibition, rather than excitation, contribute to spasms and are better suited for more effective therapeutic interventions.Significance Statement Neural plasticity following spinal cord injury is crucial for recovery of motor function. Unfortunately, this process is blemished by maladaptive changes that can cause muscle spasms. Pharmacological alleviation of spasms without compromising the recovery of motor function has proven to be challenging. Here, we investigated changes in fundamental spinal mechanisms that can cause spasms post-injury. Our data suggest that the current management strategy for spasms is misdirected toward suppressing excitatory inputs, a mechanism that we found unaltered after injury, which can lead to further motor weakness. Instead, this study shows that more promising approaches might involve restoring synaptic inhibition or modulating motoneuron excitability.

Blood-brain barrier lesion - a novel determinant of autonomic imbalance in heart failure and the effects of exercise training.

Heart failure (HF) is characterized by reduced ventricular function, compensatory activation of neurohormonal mechanisms and marked autonomic imbalance. Exercise training (T) is effective to reduce neurohormonal activation but the mechanism underlying the autonomic dysfunction remains elusive. Knowing that blood-brain barrier (BBB) lesion contributes to autonomic imbalance, we sought now to investigate its involvement in HF- and exercise-induced changes of autonomic control. Wistar rats submitted to coronary artery ligation or SHAM surgery were assigned to T or sedentary (S) protocol for 8 weeks. After hemodynamic/autonomic recordings and evaluation of BBB permeability, brains were harvesting for ultrastructural analysis of BBB constituents, measurement of vesicles trafficking and tight junction's (TJ) tightness across the BBB (transmission electron microscopy) and caveolin-1 and claudin-5 immunofluorescence within autonomic brain areas. HF-S rats vs. SHAM-S exhibited reduced blood pressure, augmented vasomotor sympathetic activity, increased pressure and reduced heart rate variability, and, depressed reflex sensitivity. HF-S also presented increased caveolin-1 expression, augmented vesicle trafficking and a weak TJ (reduced TJ extension/capillary border), which determined increased BBB permeability. In contrast, exercise restored BBB permeability, reduced caveolin-1 content, normalized vesicles counting/capillary, augmented claudin-5 expression, increased TJ tightness and selectivity simultaneously with the normalization of both blood pressure and autonomic balance. Data indicate that BBB dysfunction within autonomic nuclei (increased transcytosis and weak TJ allowing entrance of plasma constituents into the brain parenchyma) underlies the autonomic imbalance in HF. Data also disclose that exercise training corrects both transcytosis and paracellular transport and improves autonomic control even in the persistence of cardiac dysfunction.

Differential central integration of left versus right baroreceptor afferent input in spontaneously hypertensive rats.

The blood pressure (BP) regulatory impact of the arterial baroreflex has been well established in health and disease. Under normotensive conditions, we have previously demonstrated functional differences in the central processing of the left versus right aortic baroreceptor afferent input. However, it is unknown if lateralization in aortic baroreflex function remains evident during hypertension. We therefore, investigated the effects of laterality on the expression of baroreflex-driven cardiovascular reflexes in a genetic model of essential hypertension, the spontaneously hypertensive rat (SHR). Anesthetized male SHRs (total n = 9) were instrumented for left, right, and bilateral aortic depressor nerve (ADN) stimulation (1-40 Hz, 0.2 ms, and 0.4 mA for 20 s) and measurement of mean arterial pressure (MAP), heart rate (HR), mesenteric vascular resistance (MVR), and femoral vascular resistance (FVR). Left right, and bilateral ADN stimulation evoked frequency-dependent decreases in MAP, HR, MVR, and FVR. Left and bilateral ADN stimulation evoked greater reflex reductions in MAP, HR, MVR, and FVR compared with right-sided stimulation. Reflex bradycardia to bilateral stimulation was larger relative to both left-sided and right-sided stimulation. Reflex depressor and vascular resistance responses to bilateral stimulation mimicked those of the left-sided stimulation. These data indicate a left-side dominance in the central integration of aortic baroreceptor afferent input. Furthermore, reflex summation due to bilateral stimulation is only evident on the reflex bradycardic response, and does not drive further reductions in BP, suggesting that reflex depressor responses in the SHRs are primarily driven by changes in vascular resistance. Together, these results indicate that lateralization in aortic baroreflex function is not only evident under normotensive conditions but also extends to hypertensive conditions.

Phenotypic characterization of autosomal dominant progressive cone dystrophies associated with a heterozygous variant c.2512C>T of GUCY2D gene in a large kindred.

In this study, we described a large family presenting different manifestations of cone dystrophy at different ages associated with GUCY2D gene mutation. Sixty-three individuals of a single kindred, including 23 affected with cone dystrophies, were recruited and received ocular examinations, including best corrected visual acuity, intraocular pressure, slit-lamp biomicroscopy, color fundus photograph (CFP), fundus autofluorescence, optical coherence tomography, fluorescence fundus angiography, color vision testing, full-field electroretinography, and electro-oculogram. Whole exome sequencing (WES) and Sanger sequencing were performed for underlying mutations associated with cone dystrophy. There were 23 affected family members. Clinical analysis showed that the proband and other patients had impaired visual acuity ranging from 20/800 to 20/50 with impaired color vision. Fundus photograph showed retinal pigment epithelium (RPE) granular abnormalities with depressed macular reflex in young patients and macular or retinochoriodal atrophy in older patients. OCT examination confirmed the reduced outer retinal thickness or inner retinal thickness, absence of the ellipsoid zone (EZ) and retinal atrophy to varying degrees. Electroretinography revealed a reduced cone response combined with a relatively maintained rod response. WES and Sanger sequencing revealed a heterozygous variant c.2512C>T in the GUCY2D gene of the affected family members. We reported cone dystrophy in 23 affected individuals in a five-generation family and demonstrated different macular abnormalities in OCT scans and CFP at different ages. The multimodal ocular records in our study provide physicians and ophthalmologists with a better understanding of cone dystrophy associated with GUCY2D mutation.

Clinical profile and outcome of Guillain Barre syndrome in a tertiary care hospital

Background: Guillain Barre syndrome (GBS) is a progressive symmetric muscular weakness with absent or depressed deep tendon reflexes. Wide spectrum of disease severity can be seen ranging from a mild disease to quadriparesis, cranial nerve involvement and autonomic instability. Methods: Hospital based observational study is planned for GBS patients admitted to Cheluvamba hospital, a tertiary care hospital in South India, for a period of 2.5 years from Jan 2020 to August 2022.Results: 30 patients (12 males; 18 females; mean age of 7.7 years) were enrolled in this study. Among which 11 were in age group of 0-5 (36%), 10 were in the age group of 6-10 (33%), 7 were in age group of 10-15 (23%), 2 were in age group 16 and above (6.6%). Type of paralysis was paraparesis in 14 (46%) children quadriparesis in 15 (50%) children and one child had no limb involvement. In associated dysfunctions, autonomic dysfunction was seen in 1 (4.5%), bulbar palsy in 3 (13.6%). One child presented with features of Miller Fischer variant of GBS which are ophthalmoplegia and ataxia. Among 30 children 22 were recovered and discharged, 3 children died, and 5 children left against medical advice.Conclusions: The clinical characteristics, subtype of GBS, and outcome vary according to geographic area. This study is directed to find the clinical pattern and outcome of the same in tertiary care hospital in south India.

ODP526 Thyrotoxic Periodic Paralysis in Graves’ Disease: A rare presentation in an African American male

Abstract INTRODUCTION: Thyrotoxic Periodic Paralysis is a rare but life-threatening manifestation of hyperthyroidism characterized by hypokalemia, acute flaccid paralysis, and signs of hyperthyroidism. Despite being commonly seen in East Asian males, TPP has been increasingly reported in other parts of the world including western countries. Early recognition and prompt treatment of TPP is essential in preventing its grave and potentially life-threatening consequences. CASE PRESENTATIONA 21-year-old African American male patient with past medical history significant for hypertension and untreated hyperthyroidism presented to the emergency department with sudden onset bilateral lower extremity weakness and difficulty walking for one day. Upon arrival to the emergency department, vitals were unremarkable. On examination, patient had a decreased muscle tone in bilateral lower extremities with depressed deep tendon reflexes. The thyroid gland was diffusely enlarged. The remainder of physical exam was normal. Electrolyte abnormalities were also present with decreased serum potassium level of 1.2 mEq/L (3.6-5.1 mEq/L) and magnesium of 1.7 mg/dL (1.8-2.5 mg/dL). A low TSH level of <0. 010 mIU/mL (0.350-4.940 mIU/mL) with elevated free T4 levels of 4.30 ng/dL (0.70-1.48 ng/dL) were noted. CT Head/ Brain without contrast and Chest X ray were unremarkable. Potassium replacement was initiated with oral and intravenous potassium chloride. He was also started on oral atenolol (25 mg daily) and methimazole (10 mg daily). The patient's symptoms resolved in few hours after the treatment was started. An ultrasound of the thyroid gland showed diffuse heterogeneity of the gland most consistent with thyroiditis or similar abnormality. No definite focal abnormalities were noted. TSH receptor antibodies were also elevated with levels at 10.70 IU/L (≤1.75 IU/L) making Graves’ disease the most likely diagnosis. The patient's condition significantly improved along his hospitalization with complete resolution of symptoms and electrolyte abnormalities. He was subsequently discharged on atenolol and methimazole with outpatient follow up at the endocrinology clinic. DISCUSSION TPP is an underreported yet possibly fatal medical complication of hyperthyroidism. Prevalence is higher in Asia, however, incidence in Western countries has been increasing. While the underlying pathophysiology is poorly understood, h ypokalemia in TPP results from an intracellular shift of potassium induced by an increased adrenergic sensitization of Na + /K + –ATPase pump. Genetic and environmental factors may possibly play a role. Treatment of TPP entails beta-blockade to prevent intracellular shift of potassium, replenishing potassium stores, as well as correcting the underlying hyperthyroid state. Immediate diagnosis and initiation of treatment prevents serious cardiopulmonary complications and increases the probability of full recovery of muscle weakness. Presentation: No date and time listed

Ophthalmic manifestation of Hereditary Sensory and Autonomic Neuropathy – Five-year follow up

Hereditary Sensory and Autonomic Neuropathy (HSAN) is a rare genetic disorder that usually begins in childhood. It is associated with sensory dysfunction (depressed reflexes, altered pain and temperature perception). We report a case of an orphan and adopted girl child with HSAN type IV masquerading as keratomalacia with normal developmental milestones, absent sensation to pain and temperature, bilateral absent corneal reflexes, corneal xerosis, anhidrosis, and trophic ulcers in both hands and feet.

Hyponatremia Related To Pericardial Tamponade Caused By Renal Cell Carcinoma: A Rare Cause of Cardiac Tamponade

Hyponatremia is defined as serum concentration of sodium below 135 mEq/L. It is the most common electrolyte disturbance in daily clinical practice and is associated with high morbidity and mortality [1]. It is most commonly asymptomatic but can be associated with symptoms such as headaches, nausea, vomiting, muscle cramps, seizures, convulsions, lethargy, disorientation, depressed reflexes and death due to cerebral edema [2].

Effect of Long-Term Classical Ballet Dance Training on Postactivation Depression of the Soleus Hoffmann-Reflex.

Classical ballet dancing is a good model for studying the long-term activity-dependent plasticity of the central nervous system in humans, as it requires unique ankle movements to maintain ballet postures. The purpose of this study was to investigate whether postactivation depression is changed through long-term specific motor training. Eight ballet dancers and eight sedentary subjects participated in this study. The soleus Hoffmann reflexes were elicited at after the completion of a slow, passive dorsiflexion of the ankle. The results demonstrated that the depression of the soleus Hoffmannreflex (i.e.,postactivation depression) was larger in classical ballet dancers than in sedentary subjects at two poststretch intervals. This suggests that the plastic change through long-term specific motor training is also expressed in postactivation depression of the soleus Hoffmann reflex. Increased postactivation depression would strengthen the supraspinal control of the plantarflexors and may contribute to fine ankle movements in classical ballet dancers.

The underlying mechanisms of improved balance after one and ten sessions of balance training in older adults.

Training improves balance control in older adults, but the time course and neural mechanisms underlying these improvements are unclear. We studied balance robustness and performance, H-reflex gains, paired reflex depression, and co-contraction duration in ankle muscles after one and ten training sessions in 22 older adults (+65yrs). Mediolateral balance robustness, time to balance loss in unipedal standing on a platform with decreasing rotational stiffness, improved (33%) after one session, with no further improvement after ten sessions. Balance performance, absolute mediolateral center of mass velocity, improved (18.75%) after one session in perturbed unipedal standing and (18.18%) after ten sessions in unperturbed unipedal standing. Co-contraction duration of soleus/tibialis anterior increased (16%) after ten sessions. H-reflex gain and paired reflex depression excitability did not change. H-reflex gains were lower, and soleus/tibialis anterior co-contraction duration was higher in participants with more robust balance after ten sessions, and co-contraction duration was higher in participants with better balance performance at several time-points. Changes in robustness and performance were uncorrelated with changes in co-contraction duration, H-reflex gain, or paired reflex depression. In older adults, balance robustness improved over a single session, while performance improved gradually over multiple sessions. Changes in co-contraction and excitability of ankle muscles were not exclusive causes of improved balance.

Transient increase in recurrent inhibition in amyotrophic lateral sclerosis as a putative protection from neurodegeneration.

Adaptive mechanisms in spinal circuits are likely involved in homeostatic responses to maintain motor output in amyotrophic lateral sclerosis. Given the role of Renshaw cells in regulating the motoneuron input/output gain, we investigated the modulation of heteronymous recurrent inhibition. Electrical stimulations were used to activate recurrent collaterals resulting in the Hoffmann reflex depression. Inhibitions from soleus motor axons to quadriceps motoneurons, and vice versa, were tested in 38 patients and matched group of 42 controls. Compared with controls, the mean depression of quadriceps reflex was larger in patients, while that of soleus was smaller, suggesting that heteronymous recurrent inhibition was enhanced in quadriceps but reduced in soleus. The modulation of recurrent inhibition was linked to the size of maximal direct motor response and lower limb dysfunctions, suggesting a significant relationship with the integrity of the target motoneuron pool and functional abilities. No significant link was found between the integrity of motor axons activating Renshaw cells and the level of inhibition. Enhanced inhibition was particularly observed in patients within the first year after symptom onset and with slow progression of lower limb dysfunctions. Normal or reduced inhibitions were mainly observed in patients with motor weakness first in lower limbs and greater dysfunctions in lower limbs. We provide the first evidence for enhanced recurrent inhibition and speculate that Renshaw cells might have transient protective role on motoneuron by counteracting hyperexcitability at early stages. Several mechanisms likely participate including cortical influence on Renshaw cell and reinnervation by slow motoneurons.

Combined chemoreflexes of the vertebral arteries zone on the systemic arterial pressure, cerebral and infra-aural blood circulation in the experiment

To study reflexes coming from the chemoreceptors in the humoral-isolated vertebral artery zone on systemic arterial pressure, cerebral and intra-ear hemodynamics in separate stimulation with angioprotectors. A more pronounced reflex depression of the above-described effectors was caused by Nicergoline, it was less pronounced when using Vinpocetine and Pentoxifylline. Correlation analysis in doing so of the dynamics of arterio-venular coefficient of bulbar conjunctiva vessels and the membrane of the ears labyrinth round window revealed a direct relationship. These studies objectivize the therapy of ear labyrinth discirculation with angioprotectives.

The Role of Mutations on HLA Genes in Lambert-Eaton Myasthenic Syndrome

Lambert-Eaton myasthenic syndrome (LEMS) is a rare presynaptic disorder of neuromuscular transmission in which quantal release of acetylcholine (ACh) is impaired, causing a unique set of clinical characteristics, which include proximal muscle weakness, depressed tendon reflexes, posttetanic potentiation, and autonomic changes. [1] The initial presentation can be similar to that of myasthenia gravis (MG), but the progressions of the 2 diseases have some important differences. LEMS disrupts the normally reliable neurotransmission at the neuromuscular junction (NMJ). This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca2+ channels involved with neurotransmitter release.

Цереброспінальний та комісуральний діашиз у пацієнтів iз гострим інсультом: аналіз клінічних випадків

Актуальність. Інсульт залишається другою основною причиною інвалідності та смертності з найвищими показниками захворюваності та летальності в країнах Східної Європі порівняно з Західною Європою та США. Раннє відновлення неврологічних функцій після інсульту пов’язане з реорганізацією в моторних і премоторних ділянках кори головного мозку та пояснюється феноменом діашизу. Проте на сьогодні опубліковано недостатньо проспективних досліджень щодо клінічного аналізу та порівняння різних варіантів церебрального діашизу, особливо в пацієнтів iз гострим ішемічним інсультом. Мета дослідження: динамічний аналіз клінічних проявів цереброспінального та коміссурального варіантів церебрального діашизу в пацієнтів iз гострим ішемічним інсультом на основі презентації клінічних випадків. Матеріали та методи. Ми провели проспективне госпітальне когортне дослідження хворих на гострий інсульт (n = 124), якi надійшли до відділення цереброваскулярних захворювань Університетської лікарні (Олександрівська клінічна лікарня, м. Київ, Україна) протягом перших 24 годин після розвитку інсульту. Під час госпіталізації всі пацієнти пройшли комплексне клініко­неврологічне, лабораторне, ультразвукове та нейровізуалізаційне обстеження. Результати. Серед 124 обстежених iз гострим інсультом церебральний діашиз було діагностовано в 26 пацієнтів (цереброспінальний (n = 22) та комісуральний (n = 4)). Ми провели детальний клінічний аналіз проявів мозкового діашизу. Описано специфічні неврологічні зміни за територіальних інфарктів мозку та дзеркальних інсультів, викликаних діашизом. Висновки. Семіотика гострого церебрального інсульту визначається не тільки первинним інфарктом мозку, але й діашизом, що обумовлює більш серйозний неврологічний дефіцит. Церебральний діашиз пов’язаний з розвитком дзеркальних інфарктів мозку, пригніченням сухожилкових та періостальних рефлексів, атонією м’язів кінцівок.

Abstract 1122‐000193: Intracranial Bleeding in a Juvenile Nasopharyngeal Angiofibroma Stage IVb

Introduction : The trigeminocardiac reflex has been reported in craniofacial, neurosurgery, ophthalmological surgeries, and recently at endovascular procedures. Therefore, it has been called by other names also as trigeminal depressor reflex, reflex vagal trigeminal, or oculocardiac reflex. It is provoked by the stimulation of branches of the trigeminal nerve and presents cardiovascular alterations such as hypotension, bradycardia, cardiac arrhythmias, which can lead to asystole. This reflex originates at the brainstem and occurs as a rare autonomic dysfunction triggered by the stimulation of baroreceptors. Some factors predispose the appearance of this type of reflex, such as hypercapnia, hypoxemia, superficial anesthetic depth, and acidosis, among others. During these procedures is recommended continuous monitoring of the ECG and PAM. It is always essential to know the patient and modify the risk factors, or even stop the stimulus notifying the surgeon, if there is no adequate response, anticholinergic therapy, such as atropine, and the use of vasopressors should be applied. Methods : We report a clinical case of an 18‐year‐old male with a history of 3 years of recurrent epistaxis diagnosed with a Juvenilenasopharyngeal angiofibroma stage IVB, who underwent diagnostic cerebral angiography for surgical planning. Results : Angiography was performed under conscious sedation. When we placed the JB2 diagnostic catheter in the external carotid artery, the patient presented bradycardia of 40bpm. The catheter was removed, and the heart rate improved; we made a second attempt again with bradycardia, for which atropine was administered, and continued with the procedure without incident. We evaluated the vascular supply to the tumor and ruled out the involvement of the ipsilateral internal carotid artery. An occlusion test was also performed, which was positive. No aneurysms were found during angiography. At the end of the angiography, the patient presented anisocoria and left hemiparesis, so due to the suspicion of a thromboembolic event, a new femoral approach was performed to assess the intracranial circulation we found adequate patency. A non‐contrast head CT was performed, a subarachnoid hemorrhage in the prepontine and the interpeduncular cistern was observed. Medications used for sedation were discontinued to assess his neurological status at that time with GCS of 12. 48 hrs later, the patient was neurologically intact and without sequelae. In the literature review, we did not find reports of intracranial hemorrhage as complications in nasopharyngeal angiofibroma with intracranial extension or secondary to the presentation of the trigeminocardiac reflex. However, we suspected that it could result from a transient elevation of arterial hypertension due to the administration of anticholinergic therapy. Conclusions : Neuroanesthesiologists and endovascular surgeons must be aware of its manifestations and management to avoid complications due to the presentation of this reflex.

Persephin as a diagnostic marker of acute brain injury in critically ill newborns: a clinical trial

Aim. To study the correlation of serum persephin with clinical, instrumental and biochemical indicators of brain damage and with an adverse outcome in critically ill newborns.Materials and Methods. The study included 44 critically ill newborns. Blood samples were collected on the 1stand 7thday of life. Brain injury was assessed by recording Apgar score, depression of consciousness and brainstem reflexes in unsedated patients over 7 days of life, convulsions, neurosonographic signs of cerebral edema, serum protein S100B on the 1stand 7thday of life, and using indicators of adverse neurological outcome. The correlation of serum persephin on the 1stand 7thday of life with signs of brain damage was evaluated using the Spearman's rank correlation coefficient and Mann-Whitney U-test.Results. No statistically significant correlation was found between the concentrations of serum persephin on the 1stand 7thday of life and Apgar score (p = 0.721 and 0.222, respectively), depression of consciousness and stem reflexes (p < 0.05), convulsions (p = 0.673 and 0.432, respectively), cerebral edema (p = 0.737 and 0.558, respectively), and serum protein S100B both on the 1stday (p = 0.095 and 0.475, respectively) and 7thday of life (p = 0.988 and p = 0.775, respectively). Further, there was no statistically significant association of the serum persephin on the 1stday of line with an unfavorable outcome (p = 0.294). Yet, we revealed an association of serum persephin on the 7thday of life with an unfavorable outcome (p = 0.013), with a cut-off point of 828 ng/mL, a sensitivity of 39%, and a specificity of 100%.Conclusion. Persephin has poor diagnostic and prognostic significance for assessing the severity of brain damage in critically ill newborns. The obtained data on the correlation of the concentration of persephin for 7 days with an unfavorable outcome are doubtful due to the lack of data on its correlation with signs of severe brain damage.