Neurorrehabilitación funcional de miembro superior tras ictus en lobulo parietal derecho. Revisión / Functional neurorehabilitation of the upper limb after stroke in the right parietal lobe. Review

Objetivos: profundizar en las diferentes técnicas de rehabilitación funcional de los miembros superiores afectados por una lesión neurológica en el lóbulo parietal tras un ictus, empleando métodos y/o abordajes que estén apoyados por diferentes marcos teóricos de referencia, dentro de la Neurorrehabilitación y la Terapia ocupacional. Métodos: en total han sido seleccionados 30 documentos para llevar a cabo la revisión bibliográfica, en inglés y español, utilizando buscadores como PubMed, Dialnet, Scielo, páginas web. Resultados: se muestran diferentes intervenciones terapéuticas que abordan de forma integral al paciente (función cognitiva, sensitiva y motora). Se diferencian terapias convencionales y modernas, existiendo dentro de estas últimas otras clasificaciones dependiendo de si utilizan dispositivos externos para lograr la reorganización cortical o métodos internos inherentes al paciente. Conclusiones: el inicio del tratamiento tras un daño parietal en hemisferio derecho debe ser lo más temprano posible y la mejor evidencia recae sobre el reaprendizaje orientado a tareas, que aumenta si a ésta se suman otras terapias, para abordar de forma integral las distintas áreas afectadas del paciente.(AU)

Objective: To delve into the different functional rehabilitation techniques of the upper limbs affected by a neurological lesion in the parietal lobe after a stroke, using methods and/or approaches that are supported by different theoretical frameworks of reference, within Neurorehabilitation and Therapy. occupational. Methods: A total of 30 documents have been selected to carry out the bibliographic review, in English and Spanish, using search engines such as PubMed, Dialnet, Scielo, web pages. Results: Different therapeutic interventions are shown that comprehensively address the patient (cognitive, sensory and motor function). Conventional and modern therapies are differentiated, existing within the latter other classifications depending on whether they use external devices to achieve cortical reorganization or internal methods inherent to the patient. Conclusions: The start of treatment after parietal damage in the right hemisphere should be as early as possible and the best evidence relies on task-oriented relearning, which increases if other therapies are added to it, to comprehensively address the different affected areas. of the patient.(AU)

The Roles of Dominance of the Nitric Oxide Fractions Nitrate and Nitrite in the Epilepsy-Prone EL Mouse Brain.

BACKGROUND: Oxidative stress is thought to be closely related to epileptogenesis. We have previously reported that nitric oxide (NO) levels are higher in epilepsy-prone EL mice between the ages of 3 and 8 weeks than in control mice. However, NO is divided into two fractions, nitrite (NO2) and nitrate (NO3), which appear to play different roles in epileptogenesis. METHODS: NO2 and NO3 levels were measured, in EL mice and the control mice, in the parietal cortex, which is thought to be the primary epileptogenetic center in EL mice, and measured in the hippocampus, which is thought to be the secondary center. RESULTS: NO3 levels in the hippocampus and parietal cortex of the immature EL mice (3 to 8 weeks of age) were significantly higher than those in the control mice; NO2 levels were significantly higher in the EL mice throughout the study period. The NO3 levels were significantly higher than the NO2 levels in the immature EL mice, but after the onset of ictogenesis at 10 weeks of age, the relative levels of the two fractions reversed. CONCLUSION: The reversal of the NO fraction distribution at the onset of seizures that we observed may be related to the developmental process of seizure susceptibility in the neural network of EL mice.

Non-fatal Bihemispheric Penetrating Brain Injury from a Crossbow Arrow with Good Clinical Outcome: Case Report

Crossbow injuries to the head have seldom been reported in the literature, and they represent a unique type of penetrating brain injury (PBI) in which a low-velocity arrow results in an intracranial fragment larger than most high-velocity projectiles, usually with a lethal outcome.We present the case of a 34-year-oldman who attempted suicide with a self-inflicted cranial injury from a crossbow arrow, with a right parietal point of entry and a palpable subcutaneous tip in the left parietal region. The emergency team reported a Glasgow coma scale (GCS) score of 15, and the patient was brought sedated and intubated. Computed tomography (CT) imaging scans showed that the arrow crossed both parietal lobes, with mild subarachnoid hemorrhage and small cerebral contusions adjacent to its intracranial path. Careful retrograde removal of the penetrating arrow was performed in the CT suite, followed by an immediate CT scan, which excluded procedure-related complications. The patient woke up easily and was discharged 3 days later withmild left hand apraxia and no other neurologic deficits. To the best of our knowledge, there are no similar case reports describing both good clinical outcome and rapid discharge after a bihemispheric PBI. Individualizing the management of each patient is therefore crucial to achieve the best possible outcome as PBI cases still represent a major challenge to practicing neurosurgeons worldwide.

Eyelid closing and opening disorders in patients with unilateral brain lesions: A case report with video neuroimage and a systematic review of the literature.

Eyelid closing or opening disorders have been only sporadically described in patients with focal brain lesions over the last decades. Furthermore, the restricted number of reports and the lack of uniform clinical assessment of affected individuals did not allow to define more in depth the clinical features and the underlying neural correlates of these uncommon clinical disorders. Here we report an 89-years old woman with a right hemispheric lesion who showed a contralesional defect of eyelid closure. We also include a video neuroimage of this case and a review of eyelid closing and opening disorders in patients with focal unilateral lesions. In this review we found a correlation between right hemisphere and eyelid motor control, particularly for apraxia of eyelid closure affecting only the contralesional eye. The right parietal lobe was most frequently affected in this unilateral form of eyelid closing disorders, whereas putamen and other subcortical structures were more involved in eyelid opening than in eyelid closing disorders. The relations between unilateral eyelid closing disorders and other forms of motor-intentional defects are shortly discussed.

Gait analysis in a rat model of traumatic brain injury.

Gait disruptions following traumatic brain injury (TBI) are noted in the clinical population. To date, thorough analysis of gait changes in animal models of TBI to allow for correlation of pathological alterations and utilization of this as a therapeutic outcome have been limited. We therefore assessed gait using the DigiGait analysis system as well as overall locomotion using the Beam Walk test in adult male Sprague-Dawley rats following a commonly used model of TBI, parietal lobe controlled cortical impact (CCI). Rats underwent DigiGait baseline analysis 24 h prior to injury, followed by a moderate CCI in the left parietal lobe. Performance on the DigiGait was then assessed at 1, 3, 7, and 14 days post-injury, followed by histological analysis of brain tissue. Beam walk analysis showed a transient but significant impairment acutely after injury. Despite observance of gait disturbance in the clinical population, TBI in the parietal lobe of rats resulted in limited alterations in hind or forelimb function. General hindlimb locomotion showed significant but transient impairment. Significant changes in gait were observed to last through the sub-acute period, including right hindpaw angle of rotation and left forelimb and right hindlimb swing phase duration. Slight changes that did not reach statistical significant but may reflect subtle impacts of TBI on gait were reflected in several other measures, such as stride duration, stance duration and stance width. These results demonstrate that moderate-severe injury to the parietal cortex and underlying structures including corpus callosum, hippocampus, thalamus and basal ganglia result in slight changes to gait that can be detected using the Digigait analysis system.

New-onset tic disorder following circumscribed brain injury.

Adult-onset tics represent either a secondary tic disorder ("tourettism") or a late presentation of childhood tics, which may have been previously unrecognised. Head trauma has been recognised as an infrequent cause of adult-onset tic disorder, which exhibits variable temporal relationship to the inciting injury and response to therapy. We present a patient who presented with late-onset tics seven years after a circumscribed brain injury, responding well to antidopaminergic treatment. A review of all the previously reported cases of post-traumatic tic disorder is provided. Our patient is unusual in that the injury presumed to be responsible for the development of tics was of a very focal nature, akin to previously described tic disorder following vascular insults. We discuss the rare occurrence of tourettism after such focal brain lesions and analyse the insights this provides into the anatomical substrates underlying tic disorders.

[Visual impairment following a suicide attempt with a crossbow]. / 'Ziende blind' na een suïcidepoging met kruisboog.

BACKGROUND: Bálint's syndrome is characterized by the triad of ocular apraxia, dorsal simultanagnosia and optic ataxia. It most commonly occurs following bilateral parieto-occipital brain injury, for which several aetiologies have been described. CASE DESCRIPTION: We present a case of a 39-year-old male with penetrating brain injury following a suicide attempt with a crossbow. A CT scan of the head revealed the intracranial position of the arrow, piercing the parietal and occipital cortex from the left-parietal direction with the tip on the right parietal bone. After surgical removal of the arrow, visuospatial symptoms persisted that were consistent with Bálint's syndrome. The characteristic symptoms, patho-anatomy and treatment of this syndrome are discussed in this article. CONCLUSION: The patient in this case had visual impairment following a suicide attempt with a crossbow. On the basis of neurological and neuropsychological assessments, the triad of ocular apraxia, dorsal simultanagnosia and optic ataxia was observed, characteristic of Bálint's syndrome.

Unilateral parietal brain injury increases risk-taking on a rat gambling task.

Traumatic brain injury (TBI) affects millions of individuals every year. Many of these injuries lead to lasting effects, particularly impairments in domains broadly classified as executive functions, such as impulse control and decision-making. While these impairments have been historically associated with frontal brain damage, other injuries such as concussion or parietal injury also contribute to similar dysfunction. However, it is unknown whether animal models of TBI would replicate these broad effects that are observed in human patients. In the current study, we delivered a unilateral parietal controlled cortical impact injury and assessed the performance of rats on a motoric task (rotarod) and a test of decision-making and impulsivity (rodent gambling task). TBI rats demonstrated significant motor impairments on the rotarod task; however, this did not extend to difficulties inhibiting motor actions (impulsivity). In addition, TBI caused chronic alterations to risk-based decision-making, extending out to 12 weeks post-injury. Specifically, rats with TBI preferred the riskiest, and most suboptimal option over all others. The current data suggest that models of unilateral TBI are sufficient for replicating some aspects of executive dysfunction (risky decision-making), while others are limited to frontal damage (impulsivity). These models may be used to develop therapeutics targeted at the chronic post-injury period when these symptoms often manifest in patients, a critically understudied area in preclinical TBI research.

NRG1-ErbB4 signaling promotes functional recovery in a murine model of traumatic brain injury via regulation of GABA release.

Traumatic brain injury (TBI) is a serious health problem in the world. However, little is known about the pathogenesis and molecular mechanisms of TBI. Here, we show that TBI activates neuregulin 1 (NRG1)-ErbB4 signaling, with an increased expression of NRG1 and ErbB4 in the traumatic region. Specifically knocking out ErbB4 in parvalbumin-positive (PV+) interneurons exacerbates motor function deficits in mice after TBI. Consistently, PV-ErbB4-/- mice showed larger necrotic area and more edema when compared with PV-ErbB4+/+ mice. Replenishment of NRG1 through intranasal application of the recombinant protein in PV-ErbB4+/+ mice enhanced neurological function. Moreover, using an in vitro neuronal culture system, we found that NRG1-ErbB4 signaling protects neurons from glutamate-induced death, and such protective effects could be diminished by GABA receptor antagonist. These results indicate that NRG-ErbB4 signaling protects cortical neurons from TBI-induced damage, and such effect is probably mediated by promoting GABA activity. Taken together, these findings unveil a previously unappreciated role for NRG1-ErB4 signaling in preventing neuronal cell death during functional recovery after TBI.

Growing up with Bilateral parieto-occipital injury: over ten years of clinical observation and neuropsychological follow-up.

This paper presents a follow-up of a child with Balint's syndrome over more than a decade. The patient experienced traumatic brain injury before age 12, resulting in bilateral occipito-parietal infarctions and a clinical presentation of Balint's syndrome. Neuropsychological assessments at three time points showed average verbal abilities alongside persistent difficulties in visual orientation, mirrored in the patient's daily life. Her outstanding compensatory abilities in the face of these impairments are discussed with respect to the recruitment of the ventral visual stream and the role of top-down processing. This profile may help to determine interventions for younger patients with similar lesions.

Subacute to chronic Alzheimer-like alterations after controlled cortical impact in human tau transgenic mice.

Repetitive traumatic brain injury (TBI) has been linked to late life development of chronic traumatic encephalopathy (CTE), a neurodegenerative disorder histopathologically characterized by perivascular tangles of hyperphosphorylated tau at the depth of sulci to later widespread neurofibrillary pathology. Although tau hyperphosphorylation and neurofibrillary-like pathology have been observed in the brain of transgenic mice overexpressing human tau with aggregation-prone mutation after TBI, they have not been consistently recapitulated in rodents expressing wild-type tau only. Here, we characterized Alzheimer-like alterations behaviorally, biochemically and immunohistochemically 6 weeks and 7 months after unilateral mild-to-moderate controlled cortical impact (CCI) in 5-7-month-old Tg/htau mice, which express all six isoforms of non-mutated human tau in a mouse tau null background. We detected hyperphosphorylation of tau at multiple sites in ipsilateral hippocampus 6 weeks but not 7 months after CCI. However, neuronal accumulation of AT8 positive phospho-tau was sustained in the chronic phase, in parallel to prolonged astrogliosis, and decreased neural and synaptic markers. The mice with CCI also exhibited cognitive and locomotor impairment. These results indicate subacute to chronic Alzheimer-like alterations after CCI in Tg/htau mice. This is the first known study providing insight into the role of CCI in Alzheimer-like brain alterations in young adult mice expressing only non-mutated human tau.

Damage to the right temporoparietal junction, but not lateral prefrontal or insular cortex, amplifies the role of goal-directed attention.

Whether an object captures attention depends on the interplay between its saliency and current behavioral predispositions of the observer. Neuroimaging work has implied a ventral attention network, comprising the temporoparietal junction (TPJ), lateral prefrontal cortex (lPFC) and the insula, in attentional orienting toward salient events. Activity of the TPJ is driven by novel and unexpected objects, while the lateral prefrontal cortex is involved in stimulus-driven as well as goal-directed processing. The insula in turn, is part of a saliency network, which has been implicated in detecting biologically salient signals. These roles predict that damage to the TPJ, lPFC, or insula should affect performance in tasks measuring the capture of attention by salient and behaviorally relevant events. Here, we show that patients with lesions to the right TPJ have a characteristic increase of attentional capture by relevant distracters. In contrast, damage to the lPFC or insular cortex only increases reaction times, irrespective of the task-relevant properties of distracters. These findings show that acquired damage to the TPJ pathologically amplifies the capture of attention by task-relevant information, and thus indicate that the TPJ has a decisive role in goal-directed orienting.

What bilateral damage of the superior parietal lobes tells us about visual attention disorders in developmental dyslexia.

Neuroimaging studies have identified the superior parietal lobules bilaterally as the neural substrates of reduced visual attention (VA) span in developmental dyslexia. It remains however unclear whether the VA span deficit and the deficits in temporal and spatial attention shifting also reported in dyslexic children reflect a unitary spatio-temporal deficit of attention - probably linked to general posterior parietal dysfunction- or the dysfunction of distinct attentional systems that relate to different neural substrates. We explored this issue by testing an adult patient, IG, with a specific damage of the bilateral superior parietal lobules after stroke, on tasks assessing the VA span as well as temporal and spatial attention shifting. IG demonstrated a very severe VA span deficit, but preserved temporal attention shifting. Exogenous spatial orientation shifting was spared but her performance was impaired in endogenous attention. The overall findings show that distinct sub-systems of visual attention can be dissociated within the parietal lobe, suggesting that different attentional systems associated with specific neural networks can be selectively impaired in developmental dyslexia.

The different association of allocentric and egocentric neglect with dorsal and ventral pathways: A case report.

RATIONALE: Egocentric neglect is characterized by responses missing on the contralateral side with respect to the viewer, while allocentric neglect is characterized in responses missing on the contralateral side with respect to the object . However, little has been reported about the neural tracts associated with egocentric and allocentric neglect. We investigated which neural tracts were involved in two types of neglect (egocentric and allocentric) in a stroke patient who showed allocentric neglect by using the Apple Cancellation test, a specialized test to distinguish between egocentric and allocentric neglect. PATIENT CONCERNS: He showed good cognitive function but presented with severe neglect on the left side (A 42-year-old, right-handed male patient). He was unable to undergo even the pencil and paper test for evaluation of the severity of neglect. DIAGNOSES: He was diagnosed as spontaneous intracerebral hemorrhage at the right basal ganglia and underwent conservative management at the neurosurgery department of a university hospital. INTERVENTIONS: Two weeks after onset, he began rehabilitation at the rehabilitation department of the same university hospital. During a seven month rehabilitation, the patient showed significant improvement of his severe left neglect. OUTCOMES: We used the Apple Cancellation test to distinguish between egocentric and allocentric neglect; the results failed to reveal egocentric neglect, however, they did reveal severe allocentric neglect. In addition, on diffusion tensor tractography (DTT) at 2 weeks after onset, the right superior longitudinal fasciculus (SLF) showed partial injury and narrowing in the parietal lobe compared to that of the left SLF. In addition, the right inferior fronto-occipital fasciculus (IFOF) was not reconstructed. By contrast, on 7-month post-onset DTT, the right SLF revealed elongation and thickening in the parietal lobe that approached similarity to that for the left SLF. However, the right IFOF was still not reconstructed. LESSONS: The associations of egocentric neglect with the dorsal pathway (SLF) and the association of allocentric neglect with the ventral pathway (IFOF) in the right hemisphere were demonstrated in a stroke patient. It appears that DTT can be helpful in demonstrating both the affected pathway and the neglect type in patients with neglect.

Differential roles of polar orbital prefrontal cortex and parietal lobes in logical reasoning with neutral and negative emotional content.

To answer the question of how brain pathology affects reasoning about negative emotional content, we administered a disjunctive logical reasoning task involving arguments with neutral content (e.g. Either there are tigers or women in NYC, but not both; There are no tigers in NYC; There are women in NYC) and emotionally laden content (e.g. Either there are pedophiles or politicians in Texas, but not both; There are politicians in Texas; There are no pedophiles in Texas) to 92 neurological patients with focal lesions to various parts of the brain. A Voxel Lesion Symptom Mapping (VLSM) analysis identified 16 patients, all with lesions to the orbital polar prefrontal cortex (BA 10 & 11), as being selectively impaired in the emotional reasoning condition. Another 17 patients, all with lesions to the parietal cortex, were identified as being impaired in the neutral content condition. The reasoning scores of these two patient groups, along with 23 matched normal controls, underwent additional analysis to explore the effect of belief bias. This analysis revealed that the differences identified above were largely driven by trials where there was an incongruency between the believability of the conclusion and the validity of the argument (i.e. valid argument/false conclusion or invalid argument/true conclusion). Patients with lesions to polar orbital prefrontal cortex underperformed in incongruent emotional content trials and over performed in incongruent neutral content trials (compared to both normal controls and patients with parietal lobe lesions). Patients with lesions to parietal lobes underperformed normal controls (at a trend level) in neutral trials where there was a congruency between the believability of the conclusion and the validity of the argument (i.e. valid argument/true conclusion or invalid argument/false conclusion). We conclude that lesions to the polar orbital prefrontal cortex (i) prevent these patients from enjoying any emotionally induced cognitive boost, and (ii) block the belief bias processing route in the neutral condition. Lesions to parietal lobes result in a generalized impairment in logical reasoning with neutral content.

Memory deficits.

In this chapter, the neuropsychologic literature concerning memory deficits following parietal lesions is reviewed. Left inferior parietal lobule lesions definitely cause verbal short-term memory impairments, while right parietal lesions disrupt visuospatial short-term memory. Episodic memory, as well as autobiographic memory, does not seem to be impaired after both unilateral and bilateral parietal lesions, in contrast with neuroimaging studies reporting activation of the lateral parietal cortex during memory tasks. The most substantiated hypothesis is that the parietal lobe is involved in the subjective experience of recollection. Indeed, patients with parietal lesions produce fewer false memories and show lower confidence in their source recollections, possibly due to a limited number of details that they are able to report. Finally, the parietal lobes contribute to semantic memory as far as abstract concepts are concerned; in addition some sparse evidence on traumatic brain injury suggests that the parietal lobe is part of the distributed network involved in prospective memory.

Management of Penetrating Brain Injury Caused by a Nail Gun: Three Case Reports and Literature Review.

BACKGROUND: Penetrating brain injury (PBI) caused by a nail gun is an extremely rare neurosurgical emergency that poses a challenge for neurosurgeons because of its rarity and complexity. CASE DESCRIPTION: Here we present 3 cases of PBI caused by a nail gun. In the first case, the nail entered through the right parietal bone and lodged in the right parietal lobe and basal ganglia. In the second case, the nail entered through the right occipital bone and lodged in the right occipital lobe. In the third case, the nail entered through the right parietal bone and lodged in the right frontal and parietal lobes. All patients underwent surgical removal of the nail. The first patient presented with reduced left-side strength, whereas the second and third patients were neurologically intact on presentation. CONCLUSIONS: PBI caused by a nail gun can present with differing clinical manifestations, and most cases require immediate surgery. A rational management strategy should provide a good postoperative prognosis with minimal neurologic deficits in these patients.

Lateral medullary syndrome following injury of the vestibular pathway to the core vestibular cortex: Diffusion tensor imaging study.

OBJECTIVE: The parieto-insular vestibular cortex (PIVC) is a core region of vestibular input into regions of the cortex. The vestibular nuclei have reciprocal connections with the PIVC. However, little is known about injury of the core vestibular pathway to the PIVC in patients with dorsolateral medullary infarctions. In this study, using diffusion tensor tractography (DTT), we investigated injury of the neural connections between the vestibular nuclei and the PIVC in patients with typical central vestibular disorder. METHODS: Eight consecutive patients with lateral medullary syndrome and 10 control subjects were recruited for this study. To reconstruct the core vestibular pathway to the PIVC, we defined the seed region of interest (ROI) as the vestibular nuclei of the pons and the target ROI as the PIVC. Fractional anisotropy (FA), mean diffusivity (MD), and tract volume were measured. RESULT: The core vestibular pathway to the PIVC showed significantly lower tract volume in patients compared with the control group (p<0.05). By contrast, other DTI parameters did not show significant differences between the patient and control groups (p>0.05). CONCLUSION: In conclusion, injury of the core vestibular pathway to the PIVC was demonstrated in patients with lateral vestibular syndrome following dorsolateral medullary infarcts. We believe that analysis of the core vestibular pathway to the PIVC using DTT would be helpful in evaluating patients with lateral medullary syndrome.