Tendon Reflexes Research Articles

Barrier methods of prevention of epidural fibrosis at the lumbar level after microdiscectomy

The problem of cicatrical adhesion formation not only after microdiscectomies, but also after any spine surgery, remains unresolved to this day, being one of the main issues of spinal surgery. Several trigger mechanisms can be identified in the pathogenesis of epidural fibrosis formation: interaction of intervertebral cartilage components with surrounding tissues, disruption of vertebral canal integrity, dystrophy or complete absence of epidural fat, and presence of blood in the postoperative area. The pain syndrome associated with epidural fibrosis is persistent and increases after walking and prolonged being upright. There may be hyperaesthesia or hyperpathia in the innervation area of the affected roots and brisk tendon reflexes. Many authors are now trying to predict epidural fibrosis by analyzing immunological parameters and osteoprotegerin levels in blood serums, assessing anthropometric measures of patients, and examining the blood coagulation system. In modern neurosurgical society there is a clear view that epidural fibrosis should be prevented, but there are many prevention techniques. The following techniques have been identified: ligamentum flavum plasty and different variants of this operation, placement of an autograft from the inner flap of lumbar fascia into the intercostal space, use of autologous fat, use of fibrin glue, fibrous ring plasty, use of biodegradable membrane, application of anti-adhesion resorbable gel, insertion of wound drainage, use of amniotic sac, chitosan compounds in combination with L-glutamic acid, and many others.

A case report of peroneal muscle atrophy type 2A2 with central nervous system involvement as initial presentation

BackgroundCharcot-Marie-Tooth disease (CMT) is a group of single-gene hereditary diseases of peripheral nerve with high clinical variability and genetic heterogeneity. The typical clinical manifestations include progressive muscle weakness and muscle atrophy in the distal extremities, accompanied by disappearance of tendon reflexes and distal sensory disturbances. CMT2A2 (OMIM: 609260) is caused by the mutation of MFN2 (OMIM: 608507), is the most common type of axonal pattern. Although a small number of patients with X-linked CMT1 (CMT1X) present with central nervous system involvement, including reversible white matter lesions, it is rarely in CMT2A2.Case presentationA 3-year and 5-month-old girl had experienced motor lag, muscle tension, and abnormal gait for over a year. A reexamination of cranial MRI revealed an anterior enlargement of the abnormal signal range in the lateral ventricles and bilateral frontal lobes. And the whole exon sequencing showed that this girl carried a heterozygous missense mutation c.314C > T of MNF2 gene, inherited from her mother.ConclusionsIn this study, we retrospectively analyzed the clinical and molecular genetic findings of a child with Charcot-Marie-Tooth disease A2 with central nervous system involvement as the initial presentation, and explored its pathogenic mechanism.

Transcriptome analysis in a humanized mouse model of familial dysautonomia reveals tissue-specific gene expression disruption in the peripheral nervous system

Familial dysautonomia (FD) is a rare recessive neurodevelopmental disease caused by a splice mutation in the Elongator acetyltransferase complex subunit 1 (ELP1) gene. This mutation results in a tissue-specific reduction of ELP1 protein, with the lowest levels in the central and peripheral nervous systems (CNS and PNS, respectively). FD patients exhibit complex neurological phenotypes due to the loss of sensory and autonomic neurons. Disease symptoms include decreased pain and temperature perception, impaired or absent myotatic reflexes, proprioceptive ataxia, and progressive retinal degeneration. While the involvement of the PNS in FD pathogenesis has been clearly recognized, the underlying mechanisms responsible for the preferential neuronal loss remain unknown. In this study, we aimed to elucidate the molecular mechanisms underlying FD by conducting a comprehensive transcriptome analysis of neuronal tissues from the phenotypic mouse model TgFD9; Elp1Δ20/flox. This mouse recapitulates the same tissue-specific ELP1 mis-splicing observed in patients while modeling many of the disease manifestations. Comparison of FD and control transcriptomes from dorsal root ganglion (DRG), trigeminal ganglion (TG), medulla (MED), cortex, and spinal cord (SC) showed significantly more differentially expressed genes (DEGs) in the PNS than the CNS. We then identified genes that were tightly co-expressed and functionally dependent on the level of full-length ELP1 transcript. These genes, defined as ELP1 dose-responsive genes, were combined with the DEGs to generate tissue-specific dysregulated FD signature genes and networks. Within the PNS networks, we observed direct connections between Elp1 and genes involved in tRNA synthesis and genes related to amine metabolism and synaptic signaling. Importantly, transcriptomic dysregulation in PNS tissues exhibited enrichment for neuronal subtype markers associated with peptidergic nociceptors and myelinated sensory neurons, which are known to be affected in FD. In summary, this study has identified critical tissue-specific gene networks underlying the etiology of FD and provides new insights into the molecular basis of the disease.

The spinal cord facilitates cerebellar upper limb motor learning and control; inputs from neuromusculoskeletal simulation.

Complex interactions between brain regions and the spinal cord (SC) govern body motion, which is ultimately driven by muscle activation. Motor planning or learning are mainly conducted at higher brain regions, whilst the SC acts as a brain-muscle gateway and as a motor control centre providing fast reflexes and muscle activity regulation. Thus, higher brain areas need to cope with the SC as an inherent and evolutionary older part of the body dynamics. Here, we address the question of how SC dynamics affects motor learning within the cerebellum; in particular, does the SC facilitate cerebellar motor learning or constitute a biological constraint? We provide an exploratory framework by integrating biologically plausible cerebellar and SC computational models in a musculoskeletal upper limb control loop. The cerebellar model, equipped with the main form of cerebellar plasticity, provides motor adaptation; whilst the SC model implements stretch reflex and reciprocal inhibition between antagonist muscles. The resulting spino-cerebellar model is tested performing a set of upper limb motor tasks, including external perturbation studies. A cerebellar model, lacking the implemented SC model and directly controlling the simulated muscles, was also tested in the same. The performances of the spino-cerebellar and cerebellar models were then compared, thus allowing directly addressing the SC influence on cerebellar motor adaptation and learning, and on handling external motor perturbations. Performance was assessed in both joint and muscle space, and compared with kinematic and EMG recordings from healthy participants. The differences in cerebellar synaptic adaptation between both models were also studied. We conclude that the SC facilitates cerebellar motor learning; when the SC circuits are in the loop, faster convergence in motor learning is achieved with simpler cerebellar synaptic weight distributions. The SC is also found to improve robustness against external perturbations, by better reproducing and modulating muscle cocontraction patterns.

Wu Type GRIA3 Mutation Associated X-Linked Syndromic Intellectual Developmental Disorder: A Case Report

Background: A Wu type X-linked syndromic intellectual developmental disorder is caused by mutations in the GRIA3 gene This disorder is characterised by autistic features, hyporeflexia, intellectual disability and facial dysmorphism. Case report: The patient, a 4 year old male child, came with chief complaints of runny nose and tooth ache for 5 days. There was a past history of frequent falls, myoclonic jerks, tongue fibrillation, shudder attacks and delayed developmental milestones. The child at presention did not have myoclonic jerks or frequent falls. Family history is significant for maternal aunt presenting with similar complaints. On examination, protruding tongue, depressed nasal bridge, high arched palate, short fingers, right eye divergent squint, cafe-au-lait spot on the right knee, deep tendon reflexes- sluggish on both upper and lower limbs, power of 3/5 and hypotonia was observed in all four limbs with plantar- extensor bilaterally. Conclusion: On DNA testing, a missense mutation of GRIA 3 gene was noted. He was treated on a multidisciplinary approach and was admitted in a special school where occupational therapy, speech therapy, behavioural therapy and physiotherapy was given.

Peripheral neuropathy associated with severe glial fibrillary acidic protein (GFAP) astrocytopathy: a case report

A 44-year-old man was admitted due to a fever. He developed unconsciousness and respiratory failure, necessitating mechanical ventilation. After the administration of methylprednisolone and intravenous immunoglobulin for suspected autoimmune encephalitis, his consciousness and respiratory state improved. However, he exhibited pronounced tetraparalysis and impaired sensation below the neck. A spinal MRI revealed swelling of the entire spinal cord, indicating myelitis. Deep tendon reflexes were diminished in all extremities, and a nerve conduction study confirmed motor-dominant axonal polyneuropathy. Subsequently, he developed a fever and headache. Brain MRI demonstrated FLAIR hyperintensities in the basal ganglia and brain stem. CSF analysis for anti-glial fibrillary acidic protein (GFAP) antibody turned out positive, leading to the diagnosis of GFAP astrocytopathy. Although the steroid re-administration improved muscle strength in his upper limbs and reduced the range of diminished sensation, severe hemiparalysis remained. Severe GFAP astrocytopathy can be involved with polyneuropathy. Early detection and therapeutic intervention for this condition may lead to a better prognosis.

A prospective comparative study of efficacy of intravenous magnesium sulfate infusion versus placebo, as an adjuvant to nebulized salbutamol in the management of acute exacerbations of chronic obstructive pulmonary disease

Background: Acute exacerbations of chronic obstructive pulmonary diseases (AECOPD) are a frequent cause of hospitalization, morbidity, and mortality and require serious medical attention. Much research has demonstrated the beneficial effects of intravenous and nebulized magnesium sulfate (MgSO4) as a bronchodilator, in the management of acute severe asthma. Nevertheless, the extent of the benefits of intravenous MgSO4 as an adjuvant to bronchodilators in AECOPD remains uncertain. Therefore, the current study aims to address this gap in knowledge. Aims and Objectives: The study aimed to compare the effectiveness of intravenous magnesium sulfate (MgSO4) versus placebo when used as an adjuvant to nebulized salbutamol in managing AECOPD. Materials and Methods: In this comparative prospective interventional, parallel-group, placebo-controlled study, a total of 60 subjects were assigned to two groups consisting of 30 individuals each. The allocation was non-randomized and open-label, with one group receiving intravenous MgSO4 as an adjuvant to nebulized salbutamol, while the other group received a placebo in the same manner. The evaluation of MgSO4 efficacy involved measuring the peak expiratory flow rate (PEFR), which served as the primary outcome parameter. PEFR measurements were taken at 0, 15, 30, and 45 min to assess the effectiveness of MgSO4. Safety and tolerability of MgSO4 were assessed based on changes in heart rate, blood pressure, deep tendon reflexes, and respiratory rate. Results: At 45 min, the mean change in PEFR was significantly higher (P = 0.061) in the MgSO4 group (178.33 ± 49.18) compared to the placebo group (155.43 ± 41.86). Moreover, the mean difference in PEFR between the two groups was consistently higher in the MgSO4 group at every observation. MgSO4 showed considerable safety and tolerability in subjects based on the postmedication monitoring of hypermagnesemia symptoms. Conclusion: Administering intravenous magnesium sulfate (MgSO4) as an adjuvant to bronchodilators in AECOPD led to the improvement of both clinical condition and PEFR. In AECOPD, MgSO4 exhibits enhanced early bronchodilator response when combined with other drugs, demonstrating significant efficacy, good safety, and tolerability at the prescribed dosage.

MAGNETIC RESONANCE IMAGING FINDINGS IN SEIZURE PATIENTS WITH NORMAL NEUROLOGICAL EXAMINATION

Background: Imaging plays a critical role in the treatment and diagnosis of individuals experiencing seizures, particularly those whose seizures cannot be explained. In various circumstances, CT scans and MRIs (Magnetic Resonance Imaging) are utilized in tandem. Objective: The purpose of this research was to evaluate the MRI findings of patients referred to Alavi Hospital with seizures and a normal neurological examination. Methods: This case-series study examined one hundred patients with epilepsy who underwent normal neurological examinations. All patients' imaging reports were meticulously examined, and any changes were documented in pre-established checklists that comprised of the following: age, gender, family history, EEG (electroencephalogram) results, neurological assessments (including motor, plantar, and tendon reflexes), and MRI findings derived from the patients' files and clinical histories. Result: In the range of 11 to 58 years, the mean age of patients was 7.46 + 32.62 years. Males comprised forty-six (46%) of the patients. In45% of the cases, a familial history of seizures was documented (n=45). Normal EEG results were obtained in 62 cases (62%). Twenty cases (20%) of abnormalities were detected on MRI, seven of which were tumor lesions, as reported by the radiologist. The imaging of the patient's brain revealed no significant correlation between the pathological findings and variables such as age, gender, or family history. No significant correlation was observed between electroencephalogram results and pathological findings on brain imaging in patients with epilepsy. Conclusion: brain imaging partially compensates for the false negatives that occur during electroencephalograms, and concurrently employing both modalities enhances the ability to diagnose underlying issues in patients experiencing seizures.

Advancing Intraoperative Neurophysiological Monitoring With Human Reflexes.

Human reflexes are simple motor responses that are automatically elicited by various sensory inputs. These reflexes can provide valuable insights into the functioning of the nervous system, particularly the brainstem and spinal cord. Reflexes involving the brainstem, such as the blink reflex, laryngeal adductor reflex, trigeminal hypoglossal reflex, and masseter H reflex, offer immediate information about the cranial-nerve functionality and the overall state of the brainstem. Similarly, spinal reflexes such as the H reflex of the soleus muscle, posterior root muscle reflexes, and sacral reflexes provide crucial information about the functionality of the spinal cord and peripheral nerves. One of the critical benefits of reflex monitoring is that it can provide continuous feedback without disrupting the surgical process due to no movement being induced in the surgical field. These reflexes can be monitored in real time during surgical procedures to assess the integrity of the nervous system and detect potential neurological damage. It is particularly noteworthy that the reflexes provide motor and sensory information on the functional integrity of nerve fibers and nuclei. This article describes the current techniques used for monitoring various human reflexes and their clinical significance in surgery. We also address important methodological considerations and their impact on surgical safety and patient outcomes. Utilizing these methodologies has the potential to advance or even revolutionize the field of intraoperative continuous monitoring, ultimately leading to improved surgical outcomes and enhanced patient care.

Parkinson’s New Advancements in Diagnosis and Treatment: A Review

Parkinsonism Disease (PD) is a progressive neurological disorder. Although PD is associated with a variety of Non-motor symptoms (NMS) in virtually all patients including hyposmia, constipation, pain and sleep disturbances. It is age related disorder and affects more than 6 million population every year. It is associated with neuronal degeneration in substantia nigra and to lesser extent, in the globus pallidus, putamen and caudate nucleus. The degeneration of the neurons of the substantia nigra that send their axons to the corpus striatum results in reduction in the release of neurotransmitter dopamine with in corpus striatum. This leads to hypersensitivity of the dopamine receptors in the post synaptic neurons in the striatum. Individuals have characteristics signs and symptoms tremors, bradykinesia, postural instabilities, rigidity. Neither loss of sense nor muscle power is usually seen in such cases. Deep tendon, Superficial and Abdominal reflexes are well retained on evaluation. There has been various types of classification in Parkinsonism which are described later. Together with aging, genetics, environment and the role of biological sex as important factor in development of PD has been widely discussed in the past decade. Investigations in PD remains a challenge, recent studies included 7 Tesla MRI, PET and SPECT have proved to be confirmatory in diagnosis of PD. Parkinsonism disease treatment includes increasing the levels of dopamine in brain by giving its immediate precursor L-dopa which can easily cross blood brain barrier unlike dopamine. Evidence of slowing the process of degeneration has been seen with drug selegiline. Other than drugs surgical options include pallidotomy

Successful Management of Guillain-Barre Syndrome Management through Ayurveda: A Case Report

Abstract Outcome of Ayurveda management in Guillain–Barre syndrome (GBS) is studied. A 43-year-old female patient diagnosed with GBS for 10 days approached our hospital. History revealed that the patient was immediately managed in an intensive care unit of a tertiary care hospital for 9 days and was intervened with antibiotics, glucocorticoids, and intravenous immunoglobulins, but the patient’s attenders were not satisfied with the clinical improvements. The patient has a sensory deficit in the whole body below the neck level, loss of power in all extremities, and hypotonia with loss of deep tendon reflexes in all limbs and was diagnosed as Sarvāṅga vāta. Treatment was with panchakarma procedures such as Sarvāṅga alēpa (medicated paste applied to the whole body), Pariṣēka (medicated liquid poured over the whole body), abhyaṅga (therapeutic whole-body massage), Ṣaṣṭika śālī piṇḍa svēda (sudation massage using bolus of boiled rice with balā mūla decoction and milk), Nirūha basti (type of enema therapy), Anuvāsana basti (enema therapy), Grīvā Basti (oil pooling at cervical region of spine), Śirōtalam (medicated paste applied over the scalp), and oral medications. Usually, clinical worsening is observed in the first 2 weeks and then reaches a plateau and recovery might begin. The patient got total relief from the symptoms on the 80th day of the treatment. The patient was observed for the next 175 days. Assessments through the Barthel index, modified Rankin Scale, NIH Stroke Scale, and nerve conduction study showed complete recovery. Ayurveda treatment was effective in total recovery of GBS.

A comprehensive neurological perspective on tick-borne flaviviruses, with emphasis on Powassan virus.

Powassan virus (POWV), a tick-borne flavivirus transmitted primarily by Ixodes ticks, poses a significant threat as it can lead to severe neuroinvasive illness. This review delves into the nuanced clinical presentation of Powassan infection, a challenge in diagnosis exacerbated by the absence of an available vaccine. Over the past decade, the prevalence of POWV has surged in North America, necessitating a thorough examination of its neurological manifestations alongside tick-borne encephalitis virus (TBEV). A comprehensive literature search conducted up to January 2024 revealed 135 cases of neurological symptoms associated with either Powassan or TBEV infection. Notably, severe occipital headache emerged as the most prevalent symptom (22.75%), followed by meningoencephalitis (10.34%), seizures (8.27%), and flaccid paresis (6.8%). Additional manifestations included poor balance, wide gait, dysarthria, facial nerve palsy, seizure, slurred speech, and absent deep tendon reflexes. Tragically, nine cases resulted in fatal outcomes attributed to POWV infection. This analysis highlights the intricate spectrum of neurological symptoms associated with Powassan infection and underscores the necessity for heightened awareness among medical practitioners, particularly in regions with a higher prevalence of the virus. The complexity of symptoms emphasizes the need for further research to unravel the factors contributing to this diversity. Additionally, exploring potential treatment avenues and vaccine development is crucial in addressing the rising threat posed by POWV, ultimately enhancing our ability to manage and prevent severe neurological outcomes.

Tactile stimulation restores inhibited stretch reflex attributable to attenuation of Ia afferents during surprise landing

AbstractArthrogenic muscle inhibition (AMI) is induced by pathological knee conditions. The present study aimed to investigate the effect of tactile stimulation on reflex changes induced by simulated AMI during unpredictable landing performances. Twenty participants performed six unilateral landing tasks: 15 cm normal landing (15NL), 30 cm normal landing (30NL), surprise landing (SL), 30 cm normal landing following vibration (30NLV), SL following vibration (SLV), and SL following vibration with Kinesiology tape (SLK). For SL, the solid landing platform (15 cm) was removed and replaced by a false floor. Since the false floor dislodged easily under load, participants unpredictably fell through the platform to the actual landing surface 15 cm below. After completing 15NL, 30NL, and SL, vibration was applied to participants' knees to induce neurological changes similar to AMI. After vibration, participants performed 30NLV, SLV, and SLK in a random order. EMG signals in the post‐landing short latency (31–60 ms) and medium latency (61–90 ms) periods were examined. EMG signals from the vastus lateralis (VL), vastus medialis (VM), and biceps femoris (BF) were recorded and compared between tasks. EMG signals of all muscles in SL were significantly enhanced in the medium latency period as compared with 30NL. Enhanced EMG signals in SL were suppressed by vibration stimulation in the VL, but the suppressed EMG signals were restored after cutaneous stimulation with Kinesiology tape (p < 0.01). Our findings suggest that AMI could alter motor control patterns during unpredictable landing and that tactile stimulation could restore the altered motor control to a normal state.

¿Guillain Barre syndrome and inadequate secretion of antidiuretic hormone, is their relationship possible?

Guillain-Barré syndrome (GBS) is a polyradiculoneuropathy of acute onset and the most common cause of acute flaccid paralysis. It is characterized by the appearance of sensory and/or motor symptoms, accompanied by a decrease or absence of muscle stretch reflexes and other symptoms such as facial paralysis, altered eye movements, bulbar symptoms, altered wakefulness, dysautonomia and ataxia. On the other hand, hydroelectrolyte disorders are associated with serious neurological diseases as a poor prognostic factor; the most affected electrolyte is sodium; in fact, hyponatremia is the most common disorder in hospitalized patients, regardless of the cause; in GBS, it is a frequent finding on admission. It is important to recognize hyponatremia, due to its high morbidity and mortality; it is also a marker of an underlying disease. Syndrome of inappropriate secretion of antidiuretic hormone (SSIADH) is the most common cause of hyponatremia and has been associated with Guillain Barre syndrome; in this way, its diagnosis is a challenge for the doctor; finally, below we describe details of a 70-year-old male patient who was admitted to the intensive care unit, with hyponatremia with a SSIHAD, with good subsequent evolution.

Optimizing assessment of low frequency H-reflex depression in persons with spinal cord injury.

Considering the growing interest in clinical applications of neuromodulation, assessing effects of various modulatory approaches is increasingly important. Monosynaptic spinal reflexes undergo depression following repeated activation, offering a means to quantify neuromodulatory influences. Following spinal cord injury (SCI), changes in reflex modulation are associated with spasticity and impaired motor control. To assess disrupted reflex modulation, low-frequency depression (LFD) of Hoffman (H)-reflex excitability is examined, wherein the amplitudes of conditioned reflexes are compared to an unconditioned control reflex. Alternatively, some studies utilize paired-pulse depression (PPD) in place of the extended LFD train. While both protocols induce similar amounts of H-reflex depression in neurologically intact individuals, this may not be the case for persons with neuropathology. We compared the H-reflex depression elicited by PPD and by trains of 3-10 pulses to an 11-pulse LFD protocol in persons with incomplete SCI. The amount of depression produced by PPD was less than an 11-pulse train (mean difference = 0.137). When compared to the 11-pulse train, the 5-pulse train had a Pearson's correlation coefficient (R) of 0.905 and a coefficient of determination (R2) of 0.818. Therefore, a 5-pulse train for assessing LFD elicits modulation similar to the 11-pulse train and thus we recommend its use in lieu of longer trains.

Functional organization of vestibulospinal inputs responsible for tail postural control in larval Xenopus.

In all vertebrates, maintaining trunk posture primarily depends on descending commands originating from brainstem vestibulospinal nuclei. Despite being broadly outlined across species, the detailed anatomical and operational structure of these vestibulospinal networks remains poorly understood. Xenopus frogs have previously served as an excellent model for exploring such anatomical and functional aspects in relation to the animal's behavioral requirements. In this study, we examined the reflex motor reactions induced by vestibular stimulation in pre-metamorphic tadpoles. Our findings indicate that natural vestibular stimulation in the horizontal plane yields greater efficacy compared to stimulation in other planes, a phenomenon replicated in a frequency-dependent manner through specific galvanic stimulation (GVS) of the horizontal semicircular canals. With the exception of a very rostral cluster of neurons that receive vestibular inputs and project to the spinal cord, the overall anatomical segregation of vestibulospinal nuclei in the brainstem mirrors that observed in juvenile frogs. However, our results suggest closer similarities to mammalian organization than previously acknowledged. Moreover, we demonstrated that vestibulospinal cells project not only to spinal motoneurons in rostral segments but also to more distal segments that undergo regression during metamorphosis. Lastly, we illustrated how vestibular-induced spinal reflexes change during larval development, transitioning from tail swim-based activity to rostral trunk bursting responses, likely anticipating postural control in post-metamorphic frogs.

Occult Pheochromocytoma and Acute Ischaemic Stroke in Young Adult: Cause or Association

Pheochromocytoma is a rare catecholamine-secreting tumours of chromaffin tissues that cause a constellation of symptoms. It is closely associated with endocrine hypertension that can be masked, sustained or paroxysmal leading to hypertensive crisis, resulting in vascular and non-vascular complications and rarely cerebral ischaemia and stroke. A healthy 22 year old male reported with acute Right upper limb(RUL) monoplegia and Motor aphasia for five days with raised blood pressure levels. hypertonia was present, deep tendon reflexes were exaggerated in RUL and Right Plantar was extensor. General and systemic findings were nonsignificant . Routine investigations showed thrombocytosis and M.R.I. Brain was suggestive of acute infarction of Left Parieto-Temporal region. Renal doppler, Carotid Intima Media Thickness, Cerebral Angiogram, 2D-E.C.H.O. and Fundoscopy were normal. AntinuclearAntibody was negative. Contrast CT of abdomen revealed right adrenal mass suggestive of isolated Pheochromocytoma. Vanyl-Mandelic Acid was positive. Patient was stabilised and managed conservatively for 4 weeks followed by adrenalectomy and appropriate medical therapy. Patient is on regular followup and does not seem to require any antihypertensives or any other intervention. Pheochromocytoma is a notorious tumor and a great masquerader specially in young adults. A keen eye, routine checkups and evaluation is the key to detecting and preventing its associated morbidity and mortality.

Simulation of Spinal Cord Reflexes

The importance of spinal reflexes is connected to the rehabilitation processes in neural prostheses and to the neuromuscular junction. In order to model neuron networks as electronic circuits, a simulation environment like LTSpice XVII or PSpice can be used to create a complete electronic description. There are four types of neurons employed in spinal reflexes: α-motoneurons, sensitive neurons, excitatory interneurons, and inhibitory interneurons. Many proposals have been made regarding methods that can be used for assimilating neurons using electronic circuits. In this paper, only a single internal model of a neuron is considered enough to simulate all four types of neurons implicated in the control loops. The main contribution of this paper is to propose the modeling of neurons using some electronic circuits designed either with a bipolar transistor or with CMOS transistors for the input and output of circuits stages. In this way, it is possible to mimic the neural pulses’ circulation along the loops of the spinal reflexes and to prove the accuracy of the simulation results with respect to the biological signals collected from the bibliographic materials.

ENHANCE proof-of-concept three-arm randomized trial: effects of reaching training of the hemiparetic upper limb restricted to the spasticity-free elbow range

Post-stroke motor recovery processes remain unknown. Timescales and patterns of upper-limb (UL) recovery suggest a major impact of biological factors, with modest contributions from rehabilitation. We assessed a novel impairment-based training motivated by motor control theory where reaching occurs within the spasticity-free elbow range. Patients with subacute stroke (≤ 6 month; n = 46) and elbow flexor spasticity were randomly allocated to a 10-day UL training protocol, either personalized by restricting reaching to the spasticity-free elbow range defined by the tonic stretch reflex threshold (TSRT) or non-personalized (non-restricted) and with/without anodal transcranial direct current stimulation. Outcomes assessed before, after, and 1 month post-intervention were elbow flexor TSRT angle and reach-to-grasp arm kinematics (primary) and stretch reflex velocity sensitivity, clinical impairment, and activity (secondary). Results were analyzed for 3 groups as well as those of the effects of impairment-based training. Clinical measures improved in both groups. Spasticity-free range training resulted in faster and smoother reaches, smaller (i.e., better) arm-plane path length, and closer-to-normal shoulder/elbow movement patterns. Non-personalized training improved clinical scores without improving arm kinematics, suggesting that clinical measures do not account for movement quality. Impairment-based training within a spasticity-free elbow range is promising since it may improve clinical scores together with arm movement quality.Clinical Trial Registration: URL: http://www.clinicaltrials.gov. Unique Identifier: NCT02725853; Initial registration date: 01/04/2016.

A Velocity Stretch Reflex Threshold Based on Muscle-Tendon Unit Peak Acceleration to Detect Possible Occurrences of Spasticity during Gait in Children with Cerebral Palsy.

Spasticity might affect gait in children with cerebral palsy. Quantifying its occurrence during locomotion is challenging. One approach is to determine kinematic stretch reflex thresholds, usually on the velocity, during passive assessment and to search for their exceedance during gait. These thresholds are determined through EMG-Onset detection algorithms, which are variable in performance and sensitive to noisy data, and can therefore lack consistency. This study aimed to evaluate the feasibility of determining the velocity stretch reflex threshold from maximal musculotendon acceleration. Eighteen children with CP were recruited and underwent clinical gait analysis and a full instrumented assessment of their soleus, gastrocnemius lateralis, semitendinosus, and rectus femoris spasticity, with EMG, kinematics, and applied forces being measured simultaneously. Using a subject-scaled musculoskeletal model, the acceleration-based stretch reflex velocity thresholds were determined and compared to those based on EMG-Onset determination. Their consistencies according to physiological criteria, i.e., if the timing of the threshold was between the beginning of the stretch and the spastic catch, were evaluated. Finally, two parameters designed to evaluate the occurrence of spasticity during gait, i.e., the proportion of the gait trial time with a gait velocity above the velocity threshold and the number of times the threshold was exceeded, were compared. The proposed method produces velocity stretch reflex thresholds close to the EMG-based ones. For all muscles, no statistical difference was found between the two parameters designed to evaluate the occurrence of spasticity during gait. Contrarily to the EMG-based methods, the proposed method always provides physiologically consistent values, with median electromechanical delays of between 50 and 130 ms. For all subjects, the semitendinosus velocity during gait usually exceeded its stretch reflex threshold, while it was less frequent for the three other muscles. We conclude that a velocity stretch reflex threshold, based on musculotendon acceleration, is a reliable substitute for EMG-based ones.