Selective T3-T4 sympathicotomy versus gray ramicotomy on outcome and quality of life in hyperhidrosis patients: a randomized clinical trial.

Compensatory hyperhidrosis is the leading cause of patients' dissatisfaction after thoracic sympathicotomy. The study aimed to reduce compensatory hyperhidrosis to increase patients' satisfaction. A prospective randomized study on palmar hyperhidrosis, May 2016-September 2019. Twenty-one patients T3-T4 sympathicotomy and 21 T3-T4 gray ramicotomy. Data prospectively collected. Analysis at study's end. Focus on the sweating, temperature, quality of life baseline and postoperatively, compensatory hyperhidrosis, hand dryness, patients' satisfaction, and if they would undergo the procedure again and recommend it. No baseline differences between groups. Hyperhidrosis was controlled postoperatively in all patients. No mortality, serious complications, or recurrences. Sympathicotomy worse postoperative quality of life (49.05 (SD: 15.66, IR: 35.50-63.00) versus ramicotomy 24.30 (SD: 6.02, IR: 19.75-27.25). After ramicotomy, some residual sweating on the face, hands, and axillae. Compensatory sweating worse with sympathicotomy. Satisfaction higher with ramicotomy. Better results with ramicotomy than sympathicotomy regarding hand dryness, how many times a day the patients had to shower or change clothes, intention to undergo the procedure again or recommend it to somebody else, and how bothersome compensatory hyperhidrosis was. T3-T4 gray ramicotomy had better results than T3-T4 sympathicotomy, with less compensatory sweating and higher patients' satisfaction.

Cell Proliferation in the Piriform Cortex of Rats with Motor Cortex Ablation Treated with Growth Hormone and Rehabilitation.

Traumatic brain injury represents one of the main health problems in developed countries. Growth hormone (GH) and rehabilitation have been claimed to significantly contribute to the recovery of lost motor function after acquired brain injury, but the mechanisms by which this occurs are not well understood. In this work, we have investigated cell proliferation in the piriform cortex (PC) of adult rats with ablation of the frontal motor cortex treated with GH and rehabilitation, in order to evaluate if this region of the brain, related to the sense of smell, could be involved in benefits of GH treatment. Male rats were either ablated the frontal motor cortex in the dominant hemisphere or sham-operated and treated with GH or vehicle at 35 days post-injury (dpi) for five days. At 36 dpi, all rats received daily injections of bromodeoxyuridine (BrdU) for four days. We assessed motor function through the paw-reaching-for-food task. GH treatment and rehabilitation at 35 dpi significantly improved the motor deficit caused by the injury and promoted an increase of cell proliferation in the PC ipsilateral to the injury, which could be involved in the improvement observed. Cortical ablation promoted a greater number of BrdU+ cells in the piriform cortex that was maintained long-term, which could be involved in the compensatory mechanisms of the brain after injury.

Selective block of grey communicantes in upper thoracic sympathectomy. A feasibility study on human cadaveric specimens.

Background: Sympathetic chain interruption is the gold standard treatment for essential hyperhidrosis. Postoperative compensatory hyperhidrosis, the main reason for patients' dissatisfaction, is reduced by selectively lesioning white and grey rami communicantes (ramicotomy).Objective: To develop an endoscopic surgical technique that interrupts only T3 and T4 grey rami communicantes to minimize compensatory hyperhidrosis.Material and Methods: T3 and T4 grey rami communicantes ramicotomy in fifteen cold-preserved cadavers through a uniportal axillary endoscopic approach. The sympathetic chain, its ganglia, and white rami communicantes were left intact. On opening the chest, the sympathetic chain, rami communicantes and ganglia were dissected, photographed, measured and excised for histological examination.Results: Dissecting the grey rami communicantes is feasible as they consistently lie between the intercostal nerve and the homonymous sympathetic ganglion. At some levels, Kuntz nerves, as well as more than one grey ramus communicans, can be found. White rami communicantes are more medial, therefore damaging them can be avoided. Intercostal veins can be obstructive, but these can be controlled via coagulation or clipping if necessary.Conclusion: Uniportal endoscopic selective excision of the T3 and T4 grey rami communicantes is feasible without damaging the white rami communicantes, the sympathetic chain or its ganglia. Clipping the grey rami communicantes is technically possible but not reliable due to their thin diameter. This study confirms that T3 and T4 grey rami sympathetic block is technically feasible. Its application might reduce compensatory hyperhidrosis, but clinical studies are needed.

Factors Involved in the Functional Motor Recovery of Rats with Cortical Ablation after GH and Rehabilitation Treatment: Cortical Cell Proliferation and Nestin and Actin Expression in the Striatum and Thalamus.

Previously we demonstrated, in rats, that treatment with growth hormone (GH) and rehabilitation, carried out immediately after a motor cortical ablation, significantly improved the motor affectation produced by the lesion and induced the re-expression of nestin in the contralateral motor cortex. Here we analyze cortical proliferation after ablation of the frontal motor cortex and investigate the re-expression of nestin in the contralateral motor cortex and the role of the striatum and thalamus in motor recovery. The rats were subjected to ablation of the frontal motor cortex in the dominant hemisphere or sham-operated and immediately treated with GH or the vehicle (V), for five days. At 1 dpi (days post-injury), all rats received daily injections (for four days) of bromodeoxyuridine and five rats were sacrificed at 5 dpi. The other 15 rats (n = 5/group) underwent rehabilitation and were sacrificed at 25 dpi. GH induced the greatest number of proliferating cells in the perilesional cortex. GH and rehabilitation produced the functional recovery of the motor lesion and increased the expression of nestin in the striatum. In the thalamic ventral nucleus ipsilateral to the lesion, cells positive for nestin and actin were detected, but this was independent on GH. Our data suggest that GH-induced striatal nestin is involved in motor recovery.

S1 Pedicle Subtraction Osteotomy in Sagittal Balance Correction. A Feasibility Study on Human Cadaveric Specimens.

BACKGROUND: A cadaveric feasibility study was carried out. Osteotomies to correct fixed sagittal imbalance are usually performed at L3/ L4. OBJECTIVE: To investigate the feasibility of S1 pedicle subtraction osteotomy to correct spinal deformity and spinopelvic parameters, achieving better results with more limited exposure. The data obtained will allow a fixation construct specific for this osteotomy to be designed. METHODS: S1 pedicle subtraction osteotomy was performed on 12 cadaveric specimens. Baseline and postprocedural computed tomography and biomechanical studies were performed. Data were analyzed with a fixation system SolidWorks model, and the redesigned fixation construct was described and analyzed with an ANSYS model. RESULTS: S1 pedicle subtraction osteotomy is technically feasible. The fixation can be achieved with L4, L5, and iliac screws connected with bars. The system can be reinforced with a polyetheretherketone cage placed anteriorly in the S1 body osteotomy site, a cross-connecting bar, a double iliac screw, or an anterior interbody cage placed at the L5-S1 disc. The fixation strength is improved by angulating the iliac rod channel 10°, adding a semi-sphere to the locking screw contact surface and 2 fins to its saddle. The redesigned construct showed suitable stress and deformation levels, achieving the expected biomechanical requirements. DISCUSSION: Compared with surgery on higher levels, S1 pedicle subtraction osteotomy allows greater correction with shorter fixation, because the osteotomy is performed at a more caudal level, modifying the spinopelvic parameters. CONCLUSIONS: S1 pedicle subtraction osteotomy is technically feasible. Finite element analysis results indicate that it has appropriate biomechanical properties.

Overexpression of kynurenic acid and 3-hydroxyanthranilic acid after rat traumatic brain injury.

Using an immunohistochemical technique, we have studied the distribution of kynuneric acid (KYNA) and 3-hydroxyanthranilic acid (3-HAA) in a rat brain injury model (trauma). The study was carried out inducing a cerebral ablation of the frontal motor cortex. Two mouse monoclonal specific antibodies previously developed by our group directed against KYNA and 3-HAA were used. In control animals (sham-operated), the expression of both KYNA and 3-HAA was not observed. In animals in which the ablation was performed, the highest number of immunoreactive cells containing KYNA or 3-HAA was observed in the region surrounding the lesion and the number of these cells decreased moving away from the lesion. KYNA and 3-HAA were also observed in the white matter (ipsilateral side) located close to the injured region and in some cells placed in the white matter of the contralateral side. The distribution of KYNA and 3-HAA perfectly matched with the peripheral injured regions. The results found were identical independently of the perfusion date of animals (17, 30 or 54 days after brain injury). For the first time, the presence of KYNA and 3-HAA has been described in a rat trauma model. Moreover, by using a double immunocytochemistry protocol, it has been demonstrated that both metabolites were located in astrocytes. The findings observed suggest that, in cerebral trauma, KYNA and 3-HAA are involved in tissue damage and that these compounds could act, respectively, as a neuroprotector and a neurotoxic. This means that, in trauma, a counterbalance occurs and that a regulation of the indoleamine 2,3 dioxygenase (IDO) pathway could be required after a brain injury in order to decrease the deleterious effects of ending metabolites (the neurotoxic picolinic acid). Moreover, the localization of KYNA and 3-HAA in the contralateral side of the lesion suggests that the IDO pathway is also involved in the sprouting and pathfinding that follows a traumatic brain injury.

Motor Improvement of Skilled Forelimb Use Induced by Treatment with Growth Hormone and Rehabilitation Is Dependent on the Onset of the Treatment after Cortical Ablation.

We previously demonstrated that the administration of GH immediately after severe motor cortex injury, in rats, followed by rehabilitation, improved the functionality of the affected limb and reexpressed nestin in the contralateral motor cortex. Here, we analyze whether these GH effects depend on a time window after the injury and on the reexpression of nestin and actin. Injured animals were treated with GH (0.15 mg/kg/day) or vehicle, at days 7, 14, and 35 after cortical ablation. Rehabilitation was applied at short and long term (LTR) after the lesion and then sacrificed. Nestin and actin were analyzed by immunoblotting in the contralateral motor cortex. Giving GH at days 7 or 35 after the lesion, but not 14 days after it, led to a remarkable improvement in the functionality of the affected paw. Contralateral nestin and actin reexpression was clearly higher in GH-treated animals, probably because compensatory brain plasticity was established. GH and immediate rehabilitation are key for repairing brain injuries, with the exception of a critical time period: GH treatment starting 14 days after the lesion. Our data also indicate that there is not a clear plateau in the recovery from a brain injury in agreement with our data in human patients.

Can we safely monitor posterior fossa intracranial pressure? A cadaveric study.

BACKGROUND: measuring intracranial pressure (ICP) is considered the gold standard of care for brain injury. While supratentorial ICP monitoring has been adopted everywhere, posterior fossa ICP monitoring is rarely performed. In this study, we aimed to evaluate the feasibility of inserting ICP sensors into the posterior fossa of cadavers, to measure ICP in the posterior fossa. METHODS: An ICP sensor was transcranially implanted into the posterior fossa of fifteen fresh adult cadavers. An extracranial point was defined in the retroauricular area 2 cm behind the tip of the mastoid process and 2 cm below the transverse sinus, in order to implant an ICP probe. The cranial cavity was opened and measures were taken of the distance that the ICP sensor had penetrated inside the posterior fossa, as well as the distance to nearby venous sinuses (lateral, transverse, sigmoid, inferior petrosal sinus, and jugular bulb). The cerebellar hemisphere was searched for any possible damage. RESULTS: the selected extracranial point (2 cm behind the tip of the mastoid process and 2 cm below the transverse sinus) was a safe location. Intracranial structures such as the brainstem and the cerebellar hemisphere were not damaged. The implanted ICP probe was at least 2 cm away from the venous sinuses, which were not damaged. CONCLUSION: ICP monitoring is safe and reliable at the described ICP probe placement site of the posterior fossa.

Electromyographic biofeedback training for reducing muscle pain and tension on masseter and temporal muscles: A pilot study.

BACKGROUND: Due to the absence of agreement about an effective unified treatment for temporomandibular disorders, non-invasive therapies such as EMG-biofeedback generate a greater interest. Furthermore, most studies to the present show methodological deficiencies that must be solved in the future, which makes important to emphasize this line of studies. MATERIAL AND METHODS: Fourteen patients were selected for this case series study, and replied to a questionnaire concerning awareness of bruxism, painful muscles, and muscle tension. They also practiced an intraoral exploration (occlusal analysis and mandibular dynamics), and an extraoral exploration of the head and neck muscles and the temporomandibular joint. Before each session, patients responded to a questionnaire about the subjective perceived improvement. In each session, a period of three minutes of pre-biofeedback EMG activity of right masseter and temporal muscles was registered, then patients performed 30 iterations of visual EMG-biofeedback training and finally, a period of three minutes of post-EMG activity was also registered for those muscles. Patients performed four sessions. RESULTS: A decrease in painful symptoms was found for all patients since the first session. EMG activity decreases (p<0,05) in both muscles during the biofeedback training stage, in the four sessions. It is also observed a decrease (p<0,05) in EMG activity in the masseter muscle at the post-biofeedback stage, in the second and third sessions. There is likewise a decrease in EMG post-biofeedback activity of the temporal muscle (p<0,05) in sessions two, three, and four. CONCLUSIONS: EMG-biofeedback training produces a decrease in EMG activity in both masseter and temporal muscles during the session. This decrease persists during the post-biofeedback period since the second session. Also there is a decrease in painful symptoms for all patients. Key words:Muscle tension, muscle pain, EMG-biofeedback, masseter muscle, temporal muscle.

Embryonic amygdalar transplants in adult rats with motor cortex lesions: a molecular and electrophysiological analysis.

Transplants of embryonic nervous tissue ameliorate motor deficits induced by motor cortex lesions in adult animals. Restoration of lost brain functions has been recently shown in grafts of homotopic cortical origin, to be associated with a functional integration of the transplant after development of reciprocal host-graft connections. Nevertheless little is known about physiological properties or gene expression profiles of cortical implants with functional restorative capacity but no cortical origin. In this study, we show molecular and electrophysiological evidence supporting the functional development and integration of heterotopic transplants of embryonic amygdalar tissue placed into pre-lesioned motor cortex of adult rats. Grafts were analyzed 3 months post-transplantation. Using reverse transcriptase quantitative polymerase chain reaction, we found that key glutamatergic, GABAergic, and muscarinic receptors transcripts were expressed at different quantitative levels both in grafted and host tissues, but were all continuously present in the graft. Parallel sharp electrode recordings of grafted neurons in brain slices showed a regular firing pattern of transplanted neurons similar to host amygdalar pyramidal neurons. Synaptic connections from the adjacent host cortex on grafted neurons were electrophysiologically investigated and confirmed our molecular results. Taken together, our findings indicate that grafted neurons from a non-cortical, non-motor-related, but ontogenetical similar source, not only received functionally effective contacts from the adjacent motor cortex, but also developed electrophysiological and gene expression patterns comparable to host pyramidal neurons; suggesting an interesting tool for the field of neural repair and donor tissue in adults.

Glutamatergic synaptic depression by synthetic amyloid beta-peptide in the medial septum.

The medial septum/diagonal band region, which participates in learning and memory processes via its cholinergic and GABAergic projection to the hippocampus, is one of the structures affected by beta amyloid (betaA) deposition in Alzheimer's disease (AD). The acute effects of betaA (25-35 and 1-40) on action potential generation and glutamatergic synaptic transmission in slices of the medial septal area of the rat brain were studied using current and patch-clamp techniques. The betaA mechanism of action through M1 muscarinic receptors and voltage-dependent calcium channels was also addressed. Excitatory evoked responses decreased (30-60%) in amplitude after betaA (2 microM) perfusion in 70% of recorded cells. However, the firing properties were unaltered at the same concentration. This depression was irreversible in most cases, and was not prevented or reversed by nicotine (5 microM). In addition, the results obtained using a paired-pulse protocol support pre- and postsynaptic actions of the peptide. The betaA effect was blocked by calcicludine (50 nM), a selective antagonist of L-type calcium channels, and also by blocking muscarinic receptors with atropine (5 muM) or pirenzepine (1 microM), a more specific M1-receptor blocker. We show that in the medial septal area this oligomeric peptide acts through calcium channels and muscarinic receptors. As blocking any of these pathways blocks the betaA effects, we propose a joint action through both mechanisms. These results may contribute to a better understanding of the pathophysiology at the onset of AD. This understanding will be required for the development of new therapeutic agents.