Postural Reflexes Research Articles

Functional Neuroanatomy for Posture and Gait Control.

Here we argue functional neuroanatomy for posture-gait control. Multi-sensory information such as somatosensory, visual and vestibular sensation act on various areas of the brain so that adaptable posture-gait control can be achieved. Automatic process of gait, which is steady-state stepping movements associating with postural reflexes including headeye coordination accompanied by appropriate alignment of body segments and optimal level of postural muscle tone, is mediated by the descending pathways from the brainstem to the spinal cord. Particularly, reticulospinal pathways arising from the lateral part of the mesopontine tegmentum and spinal locomotor network contribute to this process. On the other hand, walking in unfamiliar circumstance requires cognitive process of postural control, which depends on knowledges of self-body, such as body schema and body motion in space. The cognitive information is produced at the temporoparietal association cortex, and is fundamental to sustention of vertical posture and construction of motor programs. The programs in the motor cortical areas run to execute anticipatory postural adjustment that is optimal for achievement of goal-directed movements. The basal ganglia and cerebellum may affect both the automatic and cognitive processes of posturegait control through reciprocal connections with the brainstem and cerebral cortex, respectively. Consequently, impairments in cognitive function by damages in the cerebral cortex, basal ganglia and cerebellum may disturb posture-gait control, resulting in falling.

Pyrazinamide Induced Parkinsonism

“Parkinsonism” refers to a syndrome characterized by the presence of tremor, rigidity and bradykinesia. In addition there is loss of postural reflexes as well as freezing. Drugs rank the second in the causes of parkinsonism. As it is reversible, drug-induced parkinsonism (Rabbit syndrome) should be borne in mind and suspected in any patient receiving drug treatment. We report a case of drug induced parkinsonism, evidently due to pyrazinamide. To the best of our knowledge, this is the first case to be reported in our country.J MEDICINE January 2017; 18 (1) : 42-43

Skin Hardness and Epidermal Thickness Affect the Vibration Sensitivity of the Foot Sole

Objective: The cutaneous mechanoreceptors of the foot sole detect the changes in the application of mechanical loads on the plantar surface during gait and standing, and contribute to controlling the standing balance and postural reflexes in healthy subjects. A local thickening of the foot sole skin occurs in response to repetitive load application. We hypothesized that an elevated skin hardness of the foot sole could reduce its mechano sensitivity. Methods: In healthy subjects, we quantified the sensation produced by different amplitudes of vibratory stimulations at two frequencies (25 and 150 Hz). The vibration threshold was determined on the 1st or 2nd, and 5th metatarsal heads, and the heel at each vibration frequency. The Stevens power function (Ψ=k.Φn) allowed to obtain regression equations between the estimate (Ψ) of the vibratory stimuli and their physical magnitude (Φ). Any increase in the absolute k value (all were negative) indicated a reduced sensitivity to the lowest loads. The n coefficient measured the global perception. The highest skin hardness (Shore) was measured on the 5th metatarsal head and the heel. In some subjects, superficial skin abrasion of the 5th metatarsal head was performed and the vibration sensitivity was tested again. Results: The vibration threshold was significantly higher at the level of the 5th metatarsal head and the heel. The k value was significantly higher at the 25 and 150 Hz frequencies for the 5th metatarsal head, and only at 25 Hz for the heel. At both vibration frequencies, negative correlations were obtained between the k values and skin hardness. After skin abrasion, the n coefficient was significantly higher at both vibration frequencies. Conclusion: Skin hardness affects the foot sole mechano sensitivity and could alter the control of posture during standing and walking. This indicates that foot care by podiatrist are relevant to improve posture control.

Neural substrates involved in the control of posture

This review argues neuronal mechanisms of postural control. Multi-sensory information such as somatosensory, visual, and vestibular sensation act on various areas of the brain so that adaptable postural control can be achieved. Automatic process of postural control, which is termed as postural reflexes including head–eye coordination accompanied by appropriate alignment of body segments, is mediated by the descending pathways from the brainstem. Cooperation of the vestibulospinal, reticulospinal, and tectospinal tracts contributes to this process. On the other hand, walking in unfamiliar circumstance requires cognitive process of postural control, which depends on knowledge of self-body, such as body schema, sense of postural verticality, and body motion in space. Such a bodily cognitive information is produced at the temporoparietal cortex. They are fundamental to sustention of vertical posture and construction of motor programs. The programs then run to execute anticipatory postural adjustment which is appropriate for achievement of goal-directed movements. The basal ganglia and cerebellum may affect both the automatic and cognitive processes of postural control through reciprocal connections with the brainstem and cerebral cortex, respectively. Consequently, impairments in cognitive function in addition to damages in the motor cortex, basal ganglia, and cerebellum may disturb appropriate postural control, resulting in falling.

The role of postural control in physical activity

Abstract Background: Postural control concerns control of body position in space in two aspects: 1. stability that is understood as ability to maintain projection of center of gravity on support surface 2. orientation understood as proper relation of individual body segments towards each other and towards surrounding In pediatric physiotherapy different term is used that constitute synonym of postural control - it is postural reflex mechanism of which the most important factor is postural tone Aim of study: To determine relation between postural control and moderate physical activity in children? Material/Methods: Method used in the study encompasses physiotherapeutic assessment of postural control before and after two weeks period of moderate physical activity. It included multi-sport activities (with prevalence of activities with use of water equipment), that stimulate postural control. 23 children (11 girls and 12 boys) aged 7-16 were examined. Their postural control was assessed with use of two parameters: size of postural tone (Postural Tone Coefficient) and body stabilization (Body Stabilization Test). Obtained results were processed statistically Results: After two weeks of moderate physical activity, parameters that concern postural control were improved. In the statistical analyze improvement appears to be statistically significant on the level of p < 0,05. Conclusions: Moderate physical activity influences postural control improvement.

Limb Remote Ischemic Postconditioning Reduces Ischemia-Reperfusion Injury by Inhibiting NADPH Oxidase Activation and MyD88-TRAF6-P38MAP-Kinase Pathway of Neutrophils.

Limb remote ischemic postconditioning (LRIP) has been confirmed to reduce the ischemia-reperfusion injury but its mechanisms are still not clear. This study clarified the mechanism of LRIP based on the nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase and Myeloid differentiation factor 88 (MyD88)-Tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6)-P38 pathway of neutrophils. Rat middle cerebral artery occlusion (MCAO) model was used in this study. Ischemia-reperfusion injury was carried out by MCAO 1.5 h followed by 24 h reperfusion. LRIP operation was performed to the left femoral artery at 0, 1 or 3 h after reperfusion. Behavioral testing, including postural reflex test, vibrissae-elicited forelimb placing test and tail hang test, showed that LRIP operated at 0 h of reperfusion could significantly ameliorate these behavioral scores. Pathological examinations, infarct size, Myeloperoxidase (MPO) activity showed that LRIP operated at 0 h of reperfusion could significantly ameliorate the pathological scores, reduce the infarct size and MPO activity in the brain and increase the MPO activity in the left leg. By using Neutrophil counting, immunofluorescence and real-time PCR techniques, we found that LRIP operated at 0 h of reperfusion could reduce neutrophil counts in the peripheral blood and downregulate the activation of neutrophil in the peripheral blood and rat brain. Western blots revealed that MyD88, TRAF6, p38 mitogen-activated protein kinase (p38-MAPK) in neutrophils and the phosphorylation of p47phox (Ser 304 and Ser 345) in neutrophil could be downregulated by LRIP. Our study suggests that LRIP inhibits the number and activation of neutrophils in the rat brain and peripheral blood linked to down-regulating the activation of NADPH oxidase in neutrophils by MyD88/TRAF6/p38-MAPK pathway.

Effect of acute lateral hemisection of the spinal cord on spinal neurons of postural networks

In quadrupeds, acute lateral hemisection of the spinal cord (LHS) severely impairs postural functions, which recover over time. Postural limb reflexes (PLRs) represent a substantial component of postural corrections in intact animals. The aim of the present study was to characterize the effects of acute LHS on two populations of spinal neurons (F and E) mediating PLRs. For this purpose, in decerebrate rabbits, responses of individual neurons from L5 to stimulation causing PLRs were recorded before and during reversible LHS (caused by temporal cold block of signal transmission in lateral spinal pathways at L1), as well as after acute surgical LHS at L1. Results obtained after Sur-LHS were compared to control data obtained in our previous study.We found that acute LHS caused disappearance of PLRs on the affected side. It also changed a proportion of different types of neurons on that side. A significant decrease and increase in the proportion of F- and non-modulated neurons, respectively, was found. LHS caused a significant decrease in most parameters of activity in F-neurons located in the ventral horn on the lesioned side and in E-neurons of the dorsal horn on both sides. These changes were caused by a significant decrease in the efficacy of posture-related sensory input from the ipsilateral limb to F-neurons, and from the contralateral limb to both F- and E-neurons. These distortions in operation of postural networks underlie the impairment of postural control after acute LHS, and represent a starting point for the subsequent recovery of postural functions.

Isoforms of the Erythropoietin receptor in dopaminergic neurons of the Substantia Nigra.

Erythropoietin receptor (EpoR) regulates erythrocytes differentiation in blood. In the brain, EpoR has been shown to protect several neuronal cell types from cell death, including the A9 dopaminergic neurons (DA) of the Substantia Nigra (SN). These cells form the nigrostriatal pathway and are devoted to the control of postural reflexes and voluntary movements. Selective degeneration of A9 DA neurons leads to Parkinson's disease. By the use of nanoCAGE, a technology that allows the identification of Transcription Start Sites (TSSs) at a genome-wide level, we have described the promoter-level expression atlas of mouse A9 DA neurons purified with Laser Capture Microdissection (LCM). Here, we identify mRNA variants of the Erythropoietin Receptor (DA-EpoR) transcribed from alternative TSSs. Experimental validation and full-length cDNA cloning is integrated with gene expression analysis in the FANTOM5 database. In DA neurons, the EpoR gene encodes for a N-terminal truncated receptor. Based on STAT5 phosphorylation assays, we show that the new variant of N-terminally truncated EpoR acts as decoy when co-expressed with the full-length form. A similar isoform is also found in human. This work highlights new complexities in the regulation of Erythropoietin (EPO) signaling in the brain.

Effects of bicuculline application on the somatosensory responses of secondary vestibular neurons

Limb somatosensory signals modify the discharge of vestibular neurons and elicit postural reflexes, which stabilize the body position. The aim of this study was to investigate the contribution of the γ-amino-butyric-acid (GABA) to the responsiveness of vestibular neurons to somatosensory inputs. The activity of 128 vestibular units was recorded in anesthetized rats in resting conditions and during sinusoidal foreleg rotation around the elbow or shoulder joints (0.026–0.625Hz, 45° peak amplitude). None of the recorded units was influenced by elbow rotation, while 40% of them responded to shoulder rotation. The selective GABAA antagonist receptor, bicuculline methiodine (BIC), was applied by microiontophoresis on single vestibular neurons and the changes in their activity at rest and during somatosensory stimulation was studied. In about half of cells the resting activity increased after the BIC application: 75% of these neurons showed also an increased response to somatosensory inputs whereas 17% exhibited a decrease. Changes in responsiveness in both directions were detected also in the units whose resting activity was not influenced by BIC. These data suggest that the responses of vestibular neurons to somatosensory inputs are modulated by GABA through a tonic release, which modifies the membrane response to the synaptic current. It is also possible that a phasic release of GABA occurs during foreleg rotation, shaping the stimulus-elicited current passing through the membrane. If this is the case, the changes in the relative position of body segments would modify the GABA release inducing changes in the vestibular reflexes and in learning processes that modify their spatio-temporal development.

Studies on cerebral protection of digoxin against hypoxic-ischemic brain damage in neonatal rats.

Hypoxic-ischemic brain damage (HIBD) is a major cause of neonatal acute deaths and chronic nervous system damage. Our present study was designed to investigate the possible neuroprotective effect of digoxin-induced pharmacological preconditioning after hypoxia-ischemia and underlying mechanisms. Neonatal rats were assigned randomly to control, HIBD, or HIBD+digoxin groups. Pharmacological preconditioning was induced by administration of digoxin 72 h before inducing HIBD by carotid occlusion+hypoxia. Behavioral assays, and neuropathological and apoptotic assessments were performed to examine the effects; the expression of Na/K ATPase was also assessed. Rats in the HIBD group showed deficiencies on the T-maze, radial water maze, and postural reflex tests, whereas the HIBD+digoxin group showed significant improvements on all behavioral tests. The rats treated with digoxin showed recovery of pathological conditions, increased number of neural cells and proliferative cells, and decreased number of apoptotic cells. Meanwhile, an increased expression level of Na/K ATPase was observed after digoxin preconditioning treatment. The preconditioning treatment of digoxin contributed toward an improved functional recovery and exerted a marked neuroprotective effect including promotion of cell proliferation and reduction of apoptosis after HIBD, and the neuroprotective action was likely associated with increased expression of Na/K ATPase.

Infusion treatments and deep brain stimulation in Parkinson's Disease: The role of nursing

Parkinson's Disease (PD) represents one of the most common neurodegenerative disorders in the elderly. PD is caused by a loss of dopaminergic cells in the substantia nigra pars compacta. The motor cardinal signs include a resting tremor, bradykinesia, rigidity and postural reflex impairment. Although levodopa represents the gold standard also in the advanced stage of the disease, over the years most patients develop disabling motor fluctuations, dyskinesias, and non-motor complications, which are difficult to manage. At this stage, more complex treatment approaches, such as infusion therapies (subcutaneous apomorphine and intraduodenal levodopa) and deep brain stimulation of the subthalamic nucleus or the globus pallidus internus should be considered. All three procedures require careful selection and good compliance of candidate patients. In particular, infusional therapies need adequate training both of caregivers and nursing staff in order to assist clinicians in the management of patients in the complicated stages of disease.

Parkinson Disease: Treatment

Parkinson disease (PD) is a chronic neurodegenerative disorder affecting more than 4 million people worldwide. It is expected that this number will potentially double by 2030 due to the aging population, thus transforming PD into an even bigger worldwide health concern. As PD knowledge has expanded over the past three decades, it is now recognized that multiple brain neurotransmitters and circuits are altered and collectively contribute to a constellation of motor and nonmotor symptoms. The classic symptoms required for the clinical diagnosis of PD are bradykinesia, resting tremor, rigidity, and/or loss of postural reflexes. Due to the multiple brain circuits affected as the disease advances, the nonmotor manifestations become equally, or even potentially, more troublesome for patients and caregivers. This review covers general considerations and aspects of treatment of PD. Figures show expected phases of PD, how to start therapy, and the approach to levodopa-induced complications. Tables list suggested dosages of available medications for the treatment of motor symptoms in PD, classification of levodopa-induced complications, suggested dosages of available medications for the treatment of neuropsychiatric symptoms, and suggested dosages of available medications for the treatment of autonomic symptoms and sleep disorders. Key words: levodopa, levodopa-induced complications, movement disorders, neurodegenerative disorders, Parkinson disease This review contains 3 highly rendered figures, 4 tables, and 226 references.

Autonomic Testing in Women with Chronic Pelvic Pain

We determined whether abnormal autonomic nervous system innervation of the bladder underlies IC (interstitial cystitis)/BPS (bladder pain syndrome) differently than other chronic pelvic pain. In this institutional review board approved protocol 39 healthy controls and 134 subjects were enrolled, including 36 with IC/BPS, 14 with myofascial pelvic pain and 42 with IC/BPS plus myofascial pelvic pain. Three subjects were excluded from study. Autonomic nervous system evaluations included deep breathing, the Valsalva maneuver, and the tilt table and sudomotor tests. The latter evaluates autonomic neuropathy. A modified validated composite autonomic laboratory score was applied. Median age in the IC/BPS group was 47.5 years (range 21 to 78), greater than in healthy controls (34 years, range 20 to 75, p = 0.006), the myofascial pelvic pain group (33 years, range 22 to 56, p = 0.004) and the IC/BPS plus myofascial pelvic pain group (38 years, range 18 to 64, p = 0.03). Body mass index did not significantly differ but the myofascial pelvic pain and IC/BPS plus myofascial pelvic pain groups had a higher body mass index than healthy controls (p = 0.05 and 0.03, respectively). Cardiovascular and adrenergic indexes did not differ. The tilt table test showed more orthostatic intolerance in all chronic pelvic pain groups. Tilt table test diagnoses (orthostatic hypotension, postural tachycardia syndrome and reflex syncope) were rare. Baseline heart rate was higher in all chronic pelvic pain groups (p = 0.004). Compared to healthy controls all myofascial pelvic pain groups showed significantly more clear-cut autonomic neuropathy, defined as a sweat score of 3 or greater (vs IC/BPS plus myofascial pelvic pain p = 0.007 and vs myofascial pelvic pain p = 0.03). Some chronic pelvic pain types show autonomic neuropathy and some show vagal withdrawal. In all types orthostatic intolerance likely reflects central sensitization and perhaps catastrophizing. Some of these findings suggest novel therapeutic targets.

MODULATION OF THE MONOSYNAPTIC REFLEX POTENTIALSIN THE DECEREBRATED RATS UNDER THE INFLUENCE OF HYDROXYTRYPTOPHAN.

We studied the serotonin effect on monosynaptic reflex potentials (MSR) of spinal motorneurons in the decerebrated rats in control and after intraperitoneal administration of serotonin precursor – 5-Hydroxytryptophan (5-HTP). MSR of motorneurons in the lumbar spinal cord were registered using electrical stimulation of dorsal root of the 5th lumbar section. During stimulation physiological saline or 5-hydroxytryptophan was injected intraperitoneally. In comparison with average amplitude of the control MSR there were registered significant increase in amplitudes of the MSR (169% and +172%, P <0,001) in animals with injection 5-HTP. These data suggest that serotonin release after 5-HTP administration leads to activation of motorneurons in the lumbar spinal cord. The mechanism of this activation may be related to the weakening of the inhibitory control of interneurons in the transmission pathways of the excitatory influences from muscle afferent to motorneurons and to the postural (antigravity) reflex reactions which necessary for the initiation of locomotion.

About existence of overmedication in patients with depressive symptoms and the appearance of un-induced movement disorder

Overmedication and the combined use of various antidepressants while increasingly seen in daily clinical practice. The drug-induced Parkinsonism, often presented as tremor, rigidity, bradykinesia and impaired postural reflexes. The syndrome is caused by multiple drug drugs can be classified into high risk, intermediate and low. This case is a 75-year-old woman diagnosed with recurrent depressive disorder, which after several adjustments in medication for depressive symptoms with poor response to treatment. It is referred by her family doctor to the neurologist at the onset of tremors in limbs, dyskinesia orolinguales, rigidity and bradykinesia. After studies to rule out organic neurology disease, is derived psychiatry for changing inducing drugs parkinsonism. The last scheduled treatment was: Mirtazapine 15 mg/day, quetiapine 25 mg/day, Clonazepam 2 mg/day, paroxetine 40 mg/day, Sulpiride 50–150 mg daily. After confirming parkinsonism signs, psychiatry proceeds to changing pharmacology, with slow decline until suspension of antipsychotics, paroxetine by venlafexina change, and also change of antihypertensive (captopril). After review at 2 months it is seen signs of improvement parkinsonism, appreciating the mental patient improvement with decreased physical discomfort and keeping the improvement in the last review (4 month) with venlafaxine 150 mg/day, Lorazepam 1 mg casual. The prevalence of drug-induced Parkinson's can go from 15 to 32% of the population. Risk factors identified are: advanced age, family predisposition, doses and drug power inductor, female gender and the presence of brain atrophy. The main objective should be to prevent the onset of Parkinson drug, to monitor patients that may be at higher risk of developing it.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Temporal, but not Directional, Prior Knowledge Shortens Muscle Reflex Latency in Response to Sudden Transition of Support Surface During Walking.

The central nervous system takes advantage of prior knowledge about potential upcoming perturbations for modulating postural reflexes. There are two distinct aspects of prior knowledge: spatial and temporal. This study investigated how each of spatial and temporal prior knowledge contributes to the shortening of muscle response latency. Eleven participants walked on a split-belt treadmill and perturbed by sudden acceleration or deceleration of the right belt at right foot contact. Spatial prior knowledge was given by instruction of possible direction (e.g., only acceleration) of upcoming perturbation at the beginning of an experimental session. Temporal prior knowledge was given to subjects by warning tones at foot contact during three consecutive strides before the perturbation. In response to acceleration perturbation, reflexive muscle activity was observed in soleus (SOL) and gastrocnemius (GAS) muscles. Onset latency of the GAS response was shorter (72 ms vs. 58 ms) when subjects knew the timing of the upcoming perturbation, whereas the latency was independent of directional prior knowledge. SOL onset latency (44 ms) was not influenced by directional nor temporal prior knowledge. Although spinal neural circuit that mediates short-latency reflex was not influenced by the prior knowledge, excitability in supra-spinal neural circuit that mediates medium- and long-latency reflex might be enhanced by knowing the timing of the upcoming perturbation.

Abstract TP97: Experimental Stroke During Aging: Docosahexaenoic Acid Therapy Provides Robust Neuroprotection

Introduction: Recently we have shown that docosahexaenoic acid (DHA) is neuroprotective after experimental stroke in young rats. The purpose of this study was to determine whether treatment with DHA would be protective in aged rats after focal cerebral ischemia. Methods: Isoflurane/nitrous oxide-anesthetized normothermic (brain temperature 36-36.5 o C) male Sprague-Dawley aged rats (16-months old) received 2h middle cerebral artery occlusion (MCAo) by poly-L-lysine-coated intraluminal suture. The behavioral function was evaluated during occlusion (60 min), and on days 1, 3 and 7 after MCAo; a grading scale of 0-12 was employed (0=normal and 12=maximal deficit). The agent (DHA, 5 mg/kg; n=6) or vehicle (saline; n=7) was administered i.v. at 3h after MCAo onset. The composite neuroscore comprises two different neurological tests, the postural reflex test and the forelimb placing test, to measure visual, tactile and proprioceptive stimuli, which were evaluated on days 1, 2, 3 and 7. High resolution ex vivo MRI using an 11.7T Bruker was performed on day 7. The core and penumbra were automatically identified using the Hierarchical Region Splitting method for penumbra identification. Histopathology and immunostaining were conducted after completion of MRI on day 7. Results: DHA treatment improved neurological scores on days 1 (by 18%), 2 (by 25%), 3 (by 22%) and 7 (by 36%). Total, cortical and subcortical lesion volumes computed from T2WI were significantly reduced by DHA treatment (by 62-75%). DHA treatment also reduced cortical, subcortical and total brain infarction (by 65- 80%). In addition, DHA therapy decreased ED-1 positive microglia/microphages (by 62%), GFAP-positive astrocytes (by 21%), and NeuN-positive neurons (by34%), and it increased SMI-71-positive vessels (by 46%) in the ischemic penumbra. Conclusion: DHA therapy is highly neuroprotective in aged rats following focal cerebral ischemia and has potential for the effective treatment of ischemic stroke in aged individuals.

Carnosine Reduces Oxidative Stress and Reverses Attenuation of Righting and Postural Reflexes in Rats with Thioacetamide-Induced Liver Failure.

Cerebral oxidative stress (OS) contributes to the pathogenesis of hepatic encephalopathy (HE). Existing evidence suggests that systemic administration of l-histidine (His) attenuates OS in brain of HE animal models, but the underlying mechanism is complex and not sufficiently understood. Here we tested the hypothesis that dipeptide carnosine (β-alanyl-l-histidine, Car) may be neuroprotective in thioacetamide (TAA)-induced liver failure in rats and that, being His metabolite, may mediate the well documented anti-OS activity of His. Amino acids [His or Car (100 mg/kg)] were administrated 2 h before TAA (i.p., 300 mg/kg 3× in 24 h intervals) injection into Sprague–Dawley rats. The animals were thus tested for: (i) brain prefrontal cortex and blood contents of Car and His, (ii) amount of reactive oxygen species (ROS), total antioxidant capacity (TAC), GSSG/GSH ratio and thioredoxin reductase (TRx) activity, and (iii) behavioral changes (several models were used, i.e. tests for reflexes, open field, grip test, Rotarod). Brain level of Car was reduced in TAA rats, and His administration significantly elevated Car levels in control and TAA rats. Car partly attenuated TAA-induced ROS production and reduced GSH/GSSG ratio, whereas the increase of TRx activity in TAA brain was not significantly modulated by Car. Further, Car improved TAA-affected behavioral functions in rats, as was shown by the tests of righting and postural reflexes. Collectively, the results support the hypothesis that (i) Car may be added to the list of neuroprotective compounds of therapeutic potential on HE and that (ii) Car mediates at least a portion of the OS-attenuating activity of His in the setting of TAA-induced liver failure.

Facial Paralysis Secondary to Hypothyroidism in a Dog

Background: Secondary neurological disorders hypothyroidism is unusual in dogs, especially when compared with other clinical signs, such as lethargy, weight gain and dermatological alterations. When manifested, these signals refer to the peripheral or central nervous system and the most common include: vestibular disease, seizures, laryngeal paralysis, poly­neuropathy and paralysis of the facial nerve. Several reports of neurological disorders associated with hypothyroidism are found in literature, basically international. In the national literature, however, there are few reports on the subject. Thus, the aim of this study was to report a case of facial paralysis associated with hypothyroidism in a dog.Case: A male canine, the boxer race, with 7-year-old were referred to the Veterinary Medical Teaching Hospital of the UFSM with a history of difficult water and food intake and asymmetry of the face for seven days. On neurological ex­amination, the animal found itself alert and locomotion, postural reactions and segmental reflexes without changes. In the evaluation of the cranial nerves, there was a menace response absent the right side, however with preserved vision, palpebral and lip ptosis of the right side and reflection palpebral absent on the same side. Opposite the historical, clinical, neurological and laboratory test findings, the diagnosis was facial paralysis secondary to hypothyroidism. As differential diagnoses were listed, inner otitis neoplasm in inner ear, trauma and idiopathic facial paralysis. After the diagnosis, clini­cal treatment was instituted with levothyroxine sodium, at a dose of 0.02 mg kg orally every 12 h, being observed total improvement of clinical signs (no changes for water intake and food, menace response and reflection palpebral normal and symmetry of the face) in 32 days.Discussion: The diagnosis of facial paralysis associated with hypothyroidism was based on the history, clinical and neurological examination findings, laboratory assessment of thyroid function by observing low serum free T4 and high concentrations of TSH, the therapeutic response after supplementation levothyroxine sodium, and exclusion of other pos­sible causes, such as otitis interna and traumatic. The pathogenesis of this change associated with hypothyroidism is not completely understood, although it is believed that cranial nerve paralysis (trigeminal, facial and vestibulocochlear) may result from the resulting compression of myxedema deposit nerve or in the tissues of the head and neck, demyelination caused by disordered metabolism of Schwann cells, decreased blood perfusion of the inner ear secondary to hyperlipidemia and increased blood viscosity or metabolic defects ranging from change in axonal transport to severe axonal loss. Treatment consists of supplementation of levothyroxine and most dogs with neurological disorders associated with hypothyroidism will present partial or total improvement of clinical signs between two and four months, generally being observed improve­ment within the first week of treatment. In the dog this report, after the beginning of treatment, improvement was observed partial and total clinical signs in 15 and 32 days, respectively. Therefore, with appropriate treatment, hypothyroidism is a disease with an excellent prognosis. The report brings to clinical relevance, the importance of hypothyroidism in the dif­ferential diagnosis of facial paralysis in dogs with face asymmetry history, the laboratory evaluation of thyroid function and response to therapy with levothyroxine sodium supplementation essential for definitive diagnosis. Keywords: neurology, facial nerve, peripheral neuropathy, dogs.

The relationship between intermittent limit cycles and postural instability associated with Parkinson's disease

BackgroundMany disease-specific factors such as muscular weakness, increased muscle stiffness, varying postural strategies, and changes in postural reflexes have been shown to lead to postural instability and fall risk in people with Parkinson's disease (PD). Recently, analytical techniques, inspired by the dynamical systems perspective on movement control and coordination, have been used to examine the mechanisms underlying the dynamics of postural declines and the emergence of postural instabilities in people with PD. MethodsA wavelet-based technique was used to identify limit cycle oscillations (LCOs) in the anterior–posterior (AP) postural sway of people with mild PD (n = 10) compared to age-matched controls (n = 10). Participants stood on a foam and on a rigid surface while completing a dual task (speaking). ResultsThere was no significant difference in the root mean square of center of pressure between groups. Three out of 10 participants with PD demonstrated LCOs on the foam surface, while none in the control group demonstrated LCOs. An inverted pendulum model of bipedal stance was used to demonstrate that LCOs occur due to disease-specific changes associated with PD: time-delay and neuromuscular feedback gain. ConclusionOverall, the LCO analysis and mathematical model appear to capture the subtle postural instabilities associated with mild PD. In addition, these findings provide insights into the mechanisms that lead to the emergence of unstable posture in patients with PD.