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Radiation therapy targeting the central nervous system is widely utilized for the management of various brain tumors, significantly prolonging patient survival. Presently, investigations are assessing both clinical and preclinical applications of low-dose radiation (LDR) for the treatment of neuropathological conditions beyond tumor therapy. Special focus is given to refractory neurodegenerative diseases linked to neuroinflammation, such as Alzheimer's and Parkinson's diseases, where LDR has shown promising results. This comprehensive review examines the existing experimental data regarding the utilization of LDR in neurological disorders. It covers potential advantages in reducing neurodegenerative alterations and inflammation, as well as possible adverse effects, including neurological impairments. The review underscores the importance of the exposure protocol and the age at which LDR is administered in the context of the nervous system's pathological and physiological states, as these elements are crucial in determining LDR's therapeutic and toxic outcomes. The article concludes with a discussion on the future directions and challenges in optimizing LDR use, aiming to reduce toxicity while effectively managing neurological disorders.

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Rosette-forming glioneuronal tumor is a rare World Health Organization grade I neoplasm, primarily involving the posterior fossa. Most cases have been reported in young adults. Although maximal surgical resection is advocated, a precise treatment modality is yet to be established. We describe an unusual presentation of rosette-forming glioneuronal tumor occurring in the optic pathway in a child. As the site of the tumor was not amenable to resection, he underwent radiotherapy and is currently well on follow-up.

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Far-infrared ray (FIR) is an electromagnetic wave that produces various health benefits against pathophysiological conditions, such as diabetes mellitus, renocardiovascular disorders, stress, and depression etc. However, the therapeutic application on the FIR-mediated protective potentials remains to be further extended. To achieve better understanding on FIR-mediated therapeutic potentials, we summarized additional findings in the present study that exposure to FIR ameliorates stressful condition, memory impairments, drug dependence, and mitochondrial dysfunction in the central nervous system. In this review, we underlined that FIR requires modulations of janus kinase 2 / signal transducer and activator of transcription 3 (JAK2/STAT3), nuclear factor E2- related factor 2 (Nrf-2), muscarinic M1 acetylcholine receptor (M1 mAChR), dopamine D1 receptor, protein kinase C δ gene, and glutathione peroxidase-1 gene for exerting the protective potentials in response to neuropsychotoxic conditions.

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OBJECTIVE: To understand the frequency of electrographic and clinical seizures in patients with stroke-like migraine attacks after radiation therapy (SMART), and determine whether SMART warrants comprehensive electroencephalographic (EEG) monitoring and aggressive seizure management. METHODS: We searched our magnetic resonance brain imaging report database for all patients between January 2013 and December 2015 for suspected SMART syndrome. Clinical inclusion criteria were further applied as follows: inpatient adults (>18 years of age) with history of cranial radiation presenting with acute neurologic deficits as primary admission reason who lacked evidence of recurrent or new brain malignancy, stroke, or infectious agents in cerebrospinal fluid. Six patients were identified. All 6 patients underwent prolonged video EEG monitoring as part of our standard protocol. RESULTS: All patients but 1 were found to have multiple or prolonged electrographic seizures consistent with status epilepticus during video EEG monitoring. Their neurological deficit and/or mental status change improved in parallel with resolution of the seizure activity. SIGNIFICANCE: SMART is likely a misnomer that underestimates the significance of seizures and status epilepticus in the pathophysiology and clinical presentation of the syndrome. Systematic continuous EEG monitoring and appropriate seizure management is warranted to reduce symptom duration and optimize clinical outcome.

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PURPOSE OF REVIEW: Acute and chronic leukemias are heterogeneous diseases and can affect any part of the body upon initial discovery. Understanding the sequela of systemic involvement is key for proper diagnosis and treatment. RECENT FINDINGS: Over the decades, new research has emerged regarding neurological complications of the myeloid or lymphoid leukemias. Central nervous system involvement usually confers a poor prognosis and requires emergent treatment. Standard of care still involves systemic therapy, intrathecal administration of chemotherapeutic agents, and cranial radiation. Treatment-related side effects can occur and need to be recognized by any practitioner involved with patient care. It is imperative to understand neurologic complications from leukemia to prevent delays and initiate necessary treatment to maintain neurologic and cognitive function.

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We aimed to reappraise whether post-stereotactic radiosurgery (SRS) results for brain metastases differ between patients with and without neurological symptoms. This was an institutional review board-approved, retrospective cohort study using our prospectively accumulated database including 2825 consecutive BM patients undergoing gamma knife SRS alone during the 15-year period since July 1998. The 2825 patients were divided into two groups; neurologically asymptomatic [group A, 1374 patients (48.6 %)] and neurologically symptomatic [group B, 1451 (51.4 %)]. Because there was considerable bias in pre-SRS clinical factors between groups A and B, a case-matched study was conducted. Ultimately, 1644 patients (822 in each group) were selected. The standard Kaplan-Meier method was used to determine post-SRS survival. Competing risk analysis was applied to estimate cumulative incidences of neurological death, neurological deterioration, local recurrence, re-SRS for new lesions and SRS-induced complications. Post-SRS median survival times (MSTs) did not differ between the two groups; 7.8 months in group A versus 7.4 months in group B patients (HR 1.064, 95 % CI 0.963-1.177, p = 0.22). However, cumulative incidences of neurological death (HR 1.637, 95 % CI 1.174-2.281, p = 0.0036) and neurological deterioration (HR 1.425, 95 % CI 1.073-1.894, p = 0.014) were significantly lower in the group A than in the group B patients. Neurologically asymptomatic patients undergoing SRS for BM had better results than symptomatic patients in terms of both maintenance of good neurological state and prolonged neurological survival. Thus, we conclude that screening computed tomography/magnetic resonance imaging is highly beneficial for managing cancer patients.

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Neuropathic pain (NP) is one of the most suffered conditions in medical disciplines. The role of reactive oxygen species (ROS) and oxidative stress in the induction of NP was studied by many researchers. Neuropathies lead to medical, social, and economic isolation of the patient, so various therapies were used to treat or reduce it. During the recent years, low-level laser therapy (LLLT) has been used in certain areas of medicine and rehabilitation. Chronic constriction injury (CCI) is a well-known model for neuropathic pain studies. In order to find the effects of different wavelengths of LLLT on the injured sciatic nerve, the present research was done. Thirty Wistar adult male rats (230-320 g) were used in this study. The animals were randomly divided into three groups (n = 10). To induce neuropathic pain for the sciatic nerve, the CCI technique was used. Low-level laser of 660 and 980 nm was used for two consecutive weeks. Thermal and mechanical hyperalgesia was done before and after surgery on days 7 and 14, respectively. Paw withdrawal thresholds were also evaluated. CCI decreased the pain threshold, whereas both wavelengths of LLLT for 2 weeks increased mechanical and thermal threshold significantly. A comparison of the mechanical and thermal threshold showed a significant difference between the therapeutic effects of the two groups that received LLLT. Based on our findings, the laser with a 660-nm wavelength had better therapeutic effects than the laser with a 980-nm wavelength, so the former one may be used for clinical application in neuropathic cases; however, it needs more future studies.

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Radiotherapy is a primary mode of treatment of many of the disease entities seen by the neurologist. Therefore knowledge of how ionizing radiation works and when it is indicated is a crucial part of the field of Neurology. The neurologist may also be confronted with some of the side effects and complications or radiotherapy treatment. This chapter attempts to serve as a review of the current day process of radiotherapy, a brief review of biology and physics of radiation, and how it is used in the treatment diseases which are common to the Neurologist. In addition we review the more commonly seen side effects and complications of treatment which may be seen by the neurologist.

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Transcranial brain stimulation with low-level light/laser therapy (LLLT) is the use of directional low-power and high-fluency monochromatic or quasimonochromatic light from lasers or LEDs in the red-to-near-infrared wavelengths to modulate a neurobiological function or induce a neurotherapeutic effect in a nondestructive and non-thermal manner. The mechanism of action of LLLT is based on photon energy absorption by cytochrome oxidase, the terminal enzyme in the mitochondrial respiratory chain. Cytochrome oxidase has a key role in neuronal physiology, as it serves as an interface between oxidative energy metabolism and cell survival signaling pathways. Cytochrome oxidase is an ideal target for cognitive enhancement, as its expression reflects the changes in metabolic capacity underlying higher-order brain functions. This review provides an update on new findings on the neurotherapeutic applications of LLLT. The photochemical mechanisms supporting its cognitive-enhancing and brain-stimulatory effects in animal models and humans are discussed. LLLT is a potential non-invasive treatment for cognitive impairment and other deficits associated with chronic neurological conditions, such as large vessel and lacunar hypoperfusion or neurodegeneration. Brain photobiomodulation with LLLT is paralleled by pharmacological effects of low-dose USP methylene blue, a non-photic electron donor with the ability to stimulate cytochrome oxidase activity, redox and free radical processes. Both interventions provide neuroprotection and cognitive enhancement by facilitating mitochondrial respiration, with hormetic dose-response effects and brain region activational specificity. This evidence supports enhancement of mitochondrial respiratory function as a generalizable therapeutic principle relevant to highly adaptable systems that are exquisitely sensitive to energy availability such as the nervous system.

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This year marks the 50th anniversary of the discovery of the laser. The development of lasers for medical use, which became known as low-level laser therapy (LLLT) or photobiomodulation, followed in 1967. In recent years, LLLT has become an increasingly mainstream modality, especially in the areas of physical medicine and rehabilitation. At first used mainly for wound healing and pain relief, the medical applications of LLLT have broadened to include diseases such as stroke, myocardial infarction, and degenerative or traumatic brain disorders. This review will cover the mechanisms of LLLT that operate both on a cellular and a tissue level. Mitochondria are thought to be the principal photoreceptors, and increased adenosine triphosphate, reactive oxygen species, intracellular calcium, and release of nitric oxide are the initial events. Activation of transcription factors then leads to expression of many protective, anti-apoptotic, anti-oxidant, and pro-proliferation gene products. Animal studies and human clinical trials of LLLT for indications with relevance to neurology, such as stroke, traumatic brain injury, degenerative brain disease, spinal cord injury, and peripheral nerve regeneration, will be covered.

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Radiation therapy is commonly used to prevent heterotopic ossification, and the dose-dependent effects of this treatment have been well documented in patients after total hip arthroplasty (THA). However, the efficacy and dose requirement of radiation therapy to prevent heterotopic ossification of nonsurgical origin have not been studied. The purpose of this retrospective case-control study was to determine the effects of prophylactic radiation therapy on severe heterotopic ossification recurrence, postoperative range of motion (ROM), and wound healing in patients with heterotopic ossification secondary to neurologic deficits. Selection was not blinded, and higher risk patients were generally assigned to the treatment group. Standard doses of radiation therapy did not adequately lower recurrence rates; in fact, there was a higher incidence of heterotopic ossification formation necessitating revision in the treatment group (15.0%) compared to the control group (5.1%). Moreover, patients who received radiation therapy were not more successful at maintaining intraoperative ROM over time. There was a similar incidence of delayed wound healing between groups (12.8% in the control group and 12.5% in the treatment group), and no other negative side effects or complications were observed. These results suggest that the 700 cGy dose of radiation therapy typically used for the prophylaxis of heterotopic ossification associated with THA does not effectively prevent the recurrence of neurogenic heterotopic ossification in high-risk patients. Further studies are needed to determine whether higher doses of radiation therapy will provide more effective prophylaxis for heterotopic ossification.

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Radiosurgery has a long history dating back to the 1950s. Only in the last decade or so have advances in radiation delivery and visualization allowed export of this paradigm to extracranial sites. This review evaluates the efficacy and safety of such ablative radiation courses using dose per fraction schedules of 10 Gy or above. Retrospective published experience in functional and benign tumor radiosurgery is reviewed. Prospective controlled clinical trials in ablative cancer therapy of early-stage lung cancer and metastatic disease in the brain, liver, and spine are reviewed.

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PURPOSE: Sevoflurane and propofol are both suitable for neuroanesthesia but have not previously been compared as maintenance agents for long duration (one to five hours) procedures. METHODS: Using a multicentre international study protocol, 103 patients were randomized to receive either sevoflurane or propofol for maintenance of anesthesia during interventional neuroradiology procedures. After a standardized induction of anesthesia with propofol, 53 patients received sevoflurane 1 to 3% with 60% nitrous oxide (N(2)O) in oxygen (O(2)), and 50 patients received propofol 4 to 10 mg x kg(-1) x hr(-1) with 60% N(2)O in O(2). Maintenance agents were titrated against systemic arterial blood pressure (baseline mean arterial pressure +/- 20%). Recovery times, changes in sedation, pain, nausea and vomiting and psychomotor function during recovery and use of rescue medication were recorded. RESULTS: The group receiving sevoflurane had a more rapid recovery to spontaneous ventilation, extubation, eye opening and orientation compared to the group receiving propofol (3 vs 4 min, P = 0.01; 5 vs 6 min, P = 0.015; 7 vs 10 min, P < 0.001; 13 vs 17 min, P = 0.028; respectively). Sedation, pain, nausea and vomiting, and psychomotor function scores were similar in the two groups. Use of opioid boluses and vasopressors were similar. CONCLUSION: The use of sevoflurane for maintenance of anesthesia for prolonged neuroradiological procedures is associated with more rapid early recovery than propofol and is associated with similar side effects. Sevoflurane and propofol can both be recommended for these procedures. The clinical benefit of the more rapid recovery with sevoflurane is unknown.

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Radiolabelled peptides are an emerging class of radiopharmaceuticals that share chemical and biological properties. From the chemical point of view they have a poly-amino acid structure varying from 3 to more that 200 amino acids, and they are labelled with different isotopes directly or by a linker. Biologically, they bind to specific cell membrane receptors, thus providing in vivo histopathological information for diagnostic purposes, therapy follow-up or targeted radiotherapy. This paper reviews most of the radiolabelled peptides that have been tested in animals and humans in the fields of oncology, neurology, cardiology, inflammation/infection, atherosclerosis and thrombosis. A new classification is also proposed for peptides targeting tumour cells based on the biological function of target receptors. These tailored radiopharmaceuticals are the basis of the new era of "molecular nuclear medicine".

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A new millimeter-wave therapeutic technique, which combines pulsed electromagnetic radiation with noise, was developed. This technique produces analgesic and trophic effects, and it also produces an effect on the functional activity of electrically excitable regions of nerve fibers. It can therefore be employed for treating affected nerves and muscles. Hence, it may broaden the range of optimal combinations of biotropic parameters of millimeter-wave methods used in neurological practice.

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OBJECTIVE: To assess the effectiveness of alternative treatments for patients with refractory neurosarcoidosis. DESIGN: Nonrandomized, retrospective patient survey. SETTING: Multicenter, involving patients cared for by their primary physicians and neurologists, and referred for management advice to a neurology consultant. INTERVENTIONS: Patients were treated with corticosteroids and alternative treatments, including azathioprine, cyclosporine, cyclophosphamide, chlorambucil, methotrexate, and radiation therapy. RESULTS: Prednisone dosage was successfully tapered to 10 to 20 mg/d without worsening symptoms in 10 (38%) of the 26 patients studied. Six (23%) patients had improved conditions while receiving alternative medication and nine (35%) patients' conditions remained stable with no further progression of their symptoms. Radiotherapy was beneficial for one of three patients. Four (15%) patients did not respond to alternative treatment and died of worsening symptoms or infection. Adverse effects of the alternate medications resolved on discontinuing treatment with the offending agent. CONCLUSION: Alternative treatment is an effective adjunct to corticosteroid therapy for some patients with refractory neurosarcoidosis. Clinical deterioration may occur despite combined therapy. Choice of alternative therapy should be determined, in part, by its potential adverse effects.

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The neurological diseases with definite or putative immune pathogenesis include myasthenia gravis; Lambert-Eaton myasthenic syndrome; IgM monoclonal anti-myelin-associated glycoprotein-associated demyelinating polyneuropathy; Guillain-Barré syndrome; chronic inflammatory demyelinating polyneuropathy; multifocal motor neuropathy with or without GM1 antibodies; multiple sclerosis; inflammatory myopathies; stiff-man syndrome; autoimmune neuromyotonia; paraneoplastic neuronopathies and cerebellar degeneration; and neurological diseases associated with systemic autoimmune conditions, vasculitis, or viral infections. The events that lead to these autoimmune diseases are not clear but the following sequential steps are critical: (a) the breaking of tolerance, a process in which cytokines, molecular mimicry, or superantigens may play a role in rendering previously anergic T cells to recognize neural autoantigens; (b) antigen recognition by the T-cell receptor complex and processing of the antigen via the major histocompatibility complex class I or II; (c) costimulatory factors especially B7 and B7-binding proteins (CD28, CTLA-4) and intercellular adhesion molecule (ICAM)-1 and its leukocyte function-associated (LFA)-1 ligand; (d) traffic of the activated T cells across the blood-brain or blood-nerve barrier via a series of adhesion molecules that include selectins, leukocyte integrins (LFA-1, Mac-1, very late activating antigen [VLA]-4) and their counterreceptors (ICAM-1, vascular cell adhesion molecule [VCAM]) on the endothelial cells; and (e) tissue injury when the activated T cells, macrophages, or specific autoantibodies find their antigenic targets on glial cells, myelin, axon, calcium channels, or muscle. In designing specific immunotherapy, the main players involved in every step of the immune response need to be considered. Targets for specific therapy in neurological diseases include agents that (a) interfere or compete with antigen recognition or stimulation, (b) inhibit costimulatory signals or cytokines, (c) inhibit the traffic of the activated cells to tissues, and (d) intervene at the antigen recognition sites in the targeted organ. The various immunomodulating procedures and immunosuppressive drugs currently used for nonselective neuroimmunotherapy are discussed in the context of their interference with the above-described immune mediators.

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