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1.
Cornea ; 38(8): 1040-1042, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30950895

RESUMO

PURPOSE: To describe the development and resolution of corneal edema in 3 patients who were exposed to compounds that stimulate dopaminergic pathways. METHODS: We conducted a review of the literature on bilateral corneal edema secondary to amantadine use and report a case series of corneal edema seen in an outpatient ophthalmology specialty clinic, shortly after exposure to agents that enhance dopamine transmission. RESULTS: Cases 1 and 2 report a 25-year-old man with attention-deficit hyperactivity disorder and a 73-year-old man with Parkinson disease who were placed on dopaminergic medications to treat their conditions. The former was administered methylphenidate and the latter patient was administered ropinirole. Both patients developed corneal edema soon afterward. Case 3 is a 67-year-old man with a recent exposure to resin from Euphorbia resinifera, a cactus in his garden. After cessation of the offending medications and treatment for exposure to resiniferatoxin, the corneal edema progressively resolved and visual acuity returned to baseline in all 3 cases. CONCLUSIONS: Methylphenidate, ropinirole, and resiniferatoxin have different mechanisms of actions but have a common end point leading to increased dopamine. We believe that these agents are linked with the reversible corneal edema seen in our 3 patients. This strongly correlates with previous studies that have linked amantadine, a drug that blocks dopamine reuptake, to reversible corneal edema.


Assuntos
Edema da Córnea/induzido quimicamente , Dopaminérgicos/efeitos adversos , Adulto , Idoso , Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico , Transtorno do Deficit de Atenção com Hiperatividade/metabolismo , Edema da Córnea/diagnóstico , Edema da Córnea/fisiopatologia , Diterpenos/efeitos adversos , Dopamina/metabolismo , Humanos , Indóis/efeitos adversos , Masculino , Metilfenidato/efeitos adversos , Neurotoxinas/efeitos adversos , Doença de Parkinson/tratamento farmacológico , Doença de Parkinson/metabolismo
2.
Ann Otol Rhinol Laryngol ; 128(4): 316-322, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30614248

RESUMO

OBJECTIVES:: To determine the impact of socioeconomic status (SES) on voice outcomes for spasmodic dysphonia (SD) patients treated with botulinum toxin injections. METHODS:: This was a prospective cross-sectional study in a tertiary care, academic voice clinic in Canada. Adult SD patients returning to the voice clinic for their botulinum toxin injections were recruited from October 2017 to April 2018. Patients completed a questionnaire on demographic data, the Hollingshead Four-Factor Index for socioeconomic status (validated instrument based on education, occupation, gender, and marital status), and the Voice-Handicap Index 10 (VHI-10) (validated instrument on self-reported vocal handicap). Primary outcome was the association between VHI-10 and Hollingshead Index. Secondary variables were median household income by postal code, duration of disease, gender, age, and professional voice user. Descriptive statistics and multiple linear regression were conducted. RESULTS:: One hundred and one patients (age = 62.8 ± 13.7 years, 20.8% male) were recruited with VHI-10 of 22.1 ± 8.1 (out of 40) and Hollingshead Index of 46.3 ± 11.7 (range, 8-66). Median household income was $75 875 ± $16 393, which was above the Canadian average of $70 336. About 91.1% were Caucasian, 54.4% had university degree, 86.1% spoke English, and 43.5% were employed. In multiple linear regression, there was mild to moderate negative correlation (r = -.292, P = .004) between VHI-10 and Hollingshead Index when controlling for disease duration, age, gender, and professional voice use. CONCLUSION:: SD patients treated with botulinum toxin were mostly affluent, Caucasian, well educated, and English speakers. Lower self-perceived vocal handicap was associated with higher socioeconomic status.


Assuntos
Toxinas Botulínicas , Disfonia , Classe Social , Qualidade da Voz , Idoso , Atitude Frente a Saúde , Toxinas Botulínicas/administração & dosagem , Toxinas Botulínicas/efeitos adversos , Canadá/epidemiologia , Estudos Transversais , Avaliação da Deficiência , Disfonia/epidemiologia , Disfonia/fisiopatologia , Disfonia/psicologia , Disfonia/terapia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neurotoxinas/administração & dosagem , Neurotoxinas/efeitos adversos , Estudos Prospectivos , Autorrelato/estatística & dados numéricos
3.
Mar Drugs ; 17(1)2019 Jan 05.
Artigo em Inglês | MEDLINE | ID: mdl-30621279

RESUMO

Tetrodotoxin (TTX) is a potent marine neurotoxin with bacterial origin. To date, around 28 analogs of TTX are known, but only 12 were detected in marine organisms, namely TTX, 11-oxoTTX, 11-deoxyTTX, 11-norTTX-6(R)-ol, 11-norTTX-6(S)-ol, 4-epiTTX, 4,9-anhydroTTX, 5,6,11-trideoxyTTX, 4-CysTTX, 5-deoxyTTX, 5,11-dideoxyTTX, and 6,11-dideoxyTTX. TTX and its derivatives are involved in many cases of seafood poisoning in many parts of the world due to their occurrence in different marine species of human consumption such as fish, gastropods, and bivalves. Currently, this neurotoxin group is not monitored in many parts of the world including in the Indian Ocean area, even with reported outbreaks of seafood poisoning involving puffer fish, which is one of the principal TTX vectors know since Egyptian times. Thus, the main objective of this review was to assess the incidence of TTXs in seafood and associated seafood poisonings in the Indian Ocean and the Red Sea. Most reported data in this geographical area are associated with seafood poisoning caused by different species of puffer fish through the recognition of TTX poisoning symptoms and not by TTX detection techniques. This scenario shows the need of data regarding TTX prevalence, geographical distribution, and its vectors in this area to better assess human health risk and build effective monitoring programs to protect the health of consumers in Indian Ocean area.


Assuntos
Doenças Transmitidas por Alimentos/epidemiologia , Doenças Transmitidas por Alimentos/etiologia , Neurotoxinas/efeitos adversos , Alimentos Marinhos/efeitos adversos , Tetrodotoxina/efeitos adversos , Animais , Humanos , Incidência , Oceano Índico
4.
Neuropharmacology ; 144: 219-232, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30366005

RESUMO

Methoxetamine (MXE) is a novel psychoactive substance that can induce several short-term effects on emotional states and behavior. However, little is known about the persistent emotional and behavioral effects of MXE. Moreover, neurotoxic effects of MXE have been hypothesized, but never demonstrated in vivo. To clarify these issues, rats received repeated treatment with MXE every other day (0.1-0.5 mg/kg, i.p., × 5), and 7 days later they were challenged with MXE (0.1-0.5 mg/kg, i.p.). Behavioral effects of MXE were first evaluated by measuring emission of ultrasonic vocalizations and locomotor activity after each administration. Thereafter, persistent behavioral effects of MXE were evaluated, starting 8 days after challenge, through elevated plus maze, spontaneous alternation, novel object recognition, and marble burying tests. After completion of behavioral analysis, neurotoxic effects of MXE were evaluated by measuring densities of dopamine transporter, tyrosine hydroxylase, and serotonin transporter in various brain regions. Repeated treatment and challenge with MXE affected neither calling behavior nor locomotor activity of rats. Conversely, rats previously treated with MXE exhibited behavioral alterations in the elevated plus maze, marble burying and novel object recognition tests, suggestive of increased anxiety and impaired non-spatial memory. Noteworthy, the same rats displayed dopaminergic damage in the medial prefrontal cortex, nucleus accumbens, caudate-putamen, substantia nigra pars compacta, and ventral tegmental area, along with accumbal serotonergic damage. Our findings show for the first time that repeated administration of MXE induces persistent behavioral abnormalities and neurotoxicity in rats, which can help elucidating the risks associated with human MXE consumption.


Assuntos
Comportamento Animal/efeitos dos fármacos , Cicloexanonas/efeitos adversos , Cicloexilaminas/efeitos adversos , Síndromes Neurotóxicas , Neurotoxinas/efeitos adversos , Psicotrópicos/efeitos adversos , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/patologia , Proteínas da Membrana Plasmática de Transporte de Dopamina/metabolismo , Relação Dose-Resposta a Droga , Emoções/efeitos dos fármacos , Masculino , Memória/efeitos dos fármacos , Atividade Motora/efeitos dos fármacos , Síndromes Neurotóxicas/metabolismo , Síndromes Neurotóxicas/patologia , Síndromes Neurotóxicas/psicologia , Proteínas de Ligação a RNA/metabolismo , Ratos Sprague-Dawley , Tirosina 3-Mono-Oxigenase/metabolismo
5.
Chemosphere ; 214: 623-632, 2019 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-30290362

RESUMO

The non-proteinogenic amino acid ß-N-methylamino-l-alanine (BMAA) is associated with the development of neurodegenerative diseases such as Alzheimer's disease, amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS-PDC) and amyotrophic lateral sclerosis. BMAA is known to induce neurotoxic effects leading to neurodegeneration via multiple mechanisms including misfolded protein accumulation, glutamate induced excitotoxicity, calcium dyshomeostasis, endoplasmic reticulum stress and oxidative stress. In the present study, for the first time, genotoxic activity of BMAA (2.5, 5, 10 and 20 µg/mL) was studied in human peripheral blood cells (HPBCs) using the comet and cytokinesis-block micronucleus cytome assays. In addition, the influence of BMAA on the oxidative stress was assessed. At non-cytotoxic concentrations BMAA did not induce formation of DNA strand breaks in HPBCs after 4 and 24 h exposure; however, it significantly increased the number of micronuclei after 24 and 48 h at 20 µg/mL and nucleoplasmic bridges after 48 h at 20 µg/mL. The frequency of nuclear buds was slightly though non-significantly increased after 48 h. Altogether, this indicates that in HPBCs BMAA is clastogenic and induces complex genomic alterations including structural chromosomal rearrangements and gene amplification. No influence on oxidative stress markers was noticed. These findings provide new evidence that environmental neurotoxin BMAA, in addition to targeting common pathways involved in neurodegeneration, can also induce genomic instability in non-target HPBCs suggesting that it might be involved in cancer development. Therefore, these data are important in advancing our current knowledge and opening new questions in the understanding of the mechanisms of BMAA toxicity, particularly in the context of genotoxicity.


Assuntos
Diamino Aminoácidos/efeitos adversos , Biomarcadores/metabolismo , Células Sanguíneas/patologia , Neurotoxinas/efeitos adversos , Estresse Oxidativo/efeitos dos fármacos , Adulto , Células Sanguíneas/efeitos dos fármacos , Células Sanguíneas/metabolismo , Dano ao DNA , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Agonistas de Aminoácidos Excitatórios/efeitos adversos , Feminino , Humanos
6.
J Toxicol Sci ; 43(11): 671-684, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30405000

RESUMO

Thalidomide was originally developed to treat primary neurological and psychiatric diseases. There are reports of anticonvulsant effects of thalidomide in rats and antiepileptic effects in patients. Hence, thalidomide (100, 200 and 400 mg/kg) was herein administered to mice to evaluate possible protection against seizures induced by the systemic administration of neurotoxins: 10 mg/kg of 4-aminopyridine (4-AP), 90 mg/kg of pentylenetetrazol (PTZ), or 380 mg/kg of pilocarpine. The effect of an NO and COX inhibitor (7-NI and ibuprofen, respectively) was also examined. The results show that thalidomide (1) induces the typical sedative effects, (2) has no anticonvulsant effect in mice treated with 4-AP, and (3) has anticonvulsant effect (400 mg/kg) in mice treated with PTZ and pilocarpine. It was found that 7-NI has an anticonvulsant effect in the pilocarpine model and that thalidomide's effect is not enhanced by its presence. However, thalidomide (200 mg/kg) plus 7-NI or ibuprofen tend to have a toxic effect in PTZ model. On the other hand, the combination of thalidomide and 7-NI or ibuprofen protects against pilocarpine-induced seizures. In conclusion, thalidomide did not exert an anticonvulsant effect for clonic-tonic type convulsions (4-AP), but it did so for seizures induced by PTZ and pilocarpine (representing absence seizures and status epilepticus, respectively). NO and prostaglandins were involved in the convulsive process elicited by pilocarpine.


Assuntos
Anticonvulsivantes , Neurotoxinas/efeitos adversos , Pentilenotetrazol/efeitos adversos , Pilocarpina/efeitos adversos , Convulsões/prevenção & controle , Talidomida/administração & dosagem , Talidomida/farmacologia , 4-Aminopiridina/efeitos adversos , Doença Aguda , Animais , Modelos Animais de Doenças , Quimioterapia Combinada , Ibuprofeno/administração & dosagem , Indazóis/administração & dosagem , Masculino , Camundongos Endogâmicos , Óxido Nítrico , Convulsões/induzido quimicamente
8.
Metas enferm ; 21(3): 67-73, abr. 2018. tab, graf
Artigo em Espanhol | IBECS | ID: ibc-172676

RESUMO

Objetivo: determinar la incidencia y evolución de la neuropatía periférica inducida por taxanos (NPIT) en pacientes con cáncer de mama y valorar la influencia de la NPIT en la calidad de vida global (CV). Método: estudio descriptivo longitudinal prospectivo realizado en el Servicio de Oncología del Hospital Clínic de Barcelona (julio 2015-abril 2016). Se incluyeron mujeres diagnosticadas de cáncer de mama en su primera línea de tratamiento con quimioterapia (paclitaxel o docetaxel) en quienes se evaluó la neurotoxicidad y la calidad de vida mediante tres cuestionarios autoinformados validados al inicio, a las 6 y 12 semanas y un mes tras finalizar el tratamiento. Resultados: participaron 33 pacientes de las cuales el 84,4% había desarrollado algún grado de NP al final del seguimiento. La neurotoxicidad empeoró de manera estadísticamente significativa con la acumulación de dosis hasta el final del tratamiento y se mantuvo estable un mes tras la última administración (p< 0,001). La neuropatía sensitiva aumentó de manera estadísticamente significativa a lo largo del seguimiento (p< 0,001). La afectación de la sensibilidad motora también, salvo en la última medición (p< 0,005). Se observó una correlación positiva entre la neurotoxicidad y deterioro de la CV (r= 0,609 (p< 0,0001)) Conclusiones: la NPIT es un efecto secundario con una alta incidencia en la población de mujeres con cáncer de mama estudiada y provoca un efecto negativo en la CV percibida de las pacientes. Las enfermeras oncológicas son profesionales clave en la prevención y el manejo de este efecto secundario


Objective: to determine the incidence and evolution of taxane-induced peripheral neuropathy (TIPN) in breast cancer patients, and to assess the influence of TIPN on overall quality of life (QoL). Method: a prospective longitudinal descriptive study conducted at the Oncology Unit of the Hospital Clínic de Barcelona (July, 2015- April, 2016). The study included women with diagnosis of breast cancer, on their first line of treatment with chemotherapy (paclitaxel or docetaxel); neurotoxicity and quality of life were evaluated through three self-reported questionnaires validated at baseline, at 6 and 12 weeks, and one month after completing treatment. Results: the study included 33 patients; 84.4% of them had developed some degree of PN at the end of follow-up. There was a statistically significant worsening in neurotoxicity with dose accumulation until the end of the treatment, and it remained stable one month after the last administration (p< 0.001). There was a statistically significant increase in sensitive neuropathy throughout follow-up (p< 0.001); also in terms of involvement in motor sensitivity, except in the final measurement (p< 0-005). A positive correlation was observed between neurotoxicity and QoL deterioration (r= 0.609 (p<0.0001)). Conclusions: TIPN is a side effect with high incidence among the population studied of women with breast cancer, and it causes a negative impact on patient-perceived QoL. Oncology nurses are the key professionals for the prevention and management of this side effect


Assuntos
Humanos , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Neoplasias da Mama/tratamento farmacológico , Antineoplásicos/efeitos adversos , Taxoides/toxicidade , Estudos Prospectivos , Neoplasias da Mama/complicações , Neurotoxinas/efeitos adversos , Qualidade de Vida , Paclitaxel/toxicidade , Resultado do Tratamento , Autorrelato
9.
Molecules ; 23(2)2018 Feb 07.
Artigo em Inglês | MEDLINE | ID: mdl-29414872

RESUMO

Suramin is a trypan blue analogon originally developed to treat protozoan infections, which was found to have diverse antitumor effects. One of the most severe side effects in clinical trials was the development of a peripheral sensory-motor polyneuropathy. In this study, we aimed to investigate suramin-induced neuropathy with a focus on calcium (Ca2+) homeostasis as a potential pathomechanism. Adult C57Bl/6 mice treated with a single injection of 250 mg/kg bodyweight suramin developed locomotor and sensory deficits, which were confirmed by electrophysiological measurements showing a predominantly sensory axonal-demyelinating polyneuropathy. In a next step, we used cultured dorsal root ganglia neurons (DRGN) as an in vitro cell model to further investigate underlying pathomechanisms. Cell viability of DRGN was significantly decreased after 24-hour suramin treatment with a calculated IC50 of 283 µM. We detected a suramin-induced Ca2+ influx into DRGN from the extracellular space, which could be reduced with the voltage-gated calcium channel (VGCC) inhibitor nimodipine. Co-incubation of suramin and nimodipine partially improved cell viability of DRGN after suramin exposure. In summary, we describe suramin-induced neurotoxic effects on DRGN as well as potentially neuroprotective agents targeting intracellular Ca2+ dyshomeostasis.


Assuntos
Neuroproteção/efeitos dos fármacos , Fármacos Neuroprotetores/farmacologia , Neurotoxinas/efeitos adversos , Suramina/efeitos adversos , Animais , Cálcio/metabolismo , Canais de Cálcio/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Modelos Animais de Doenças , Relação Dose-Resposta a Droga , Avaliação Pré-Clínica de Medicamentos , Gânglios Espinais/citologia , Camundongos , Modelos Animais , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Polineuropatias/tratamento farmacológico , Polineuropatias/etiologia , Polineuropatias/fisiopatologia
10.
Indian J Ophthalmol ; 66(2): 306-308, 2018 02.
Artigo em Inglês | MEDLINE | ID: mdl-29380788

RESUMO

We describe a case of 55-year-old male farmer presented with recurrent corneal abrasions with a spastic entropion in the left eye. Superior cornea showed typical nummular opacities suggestive resolved herpetic eye diseases. On further enquiry, he had similar episodes in the past. Contralateral eye was essentially normal. Following the botulinum toxin injection for the management of spastic entropion, subject developed reactivation of herpetic necrotizing stromal keratitis. Diagnostic corneal scrapings were negative for herpes simplex virus-1 antigen by immunofluorescence assay and for DNA by molecular techniques. The case was successfully managed with topical steroids and antiviral medications.


Assuntos
Toxinas Botulínicas/efeitos adversos , Substância Própria/patologia , Herpesvirus Humano 1/genética , Ceratite Herpética/diagnóstico , Antivirais/administração & dosagem , Toxinas Botulínicas/administração & dosagem , Substância Própria/virologia , DNA Viral/análise , Diagnóstico Diferencial , Entrópio/tratamento farmacológico , Epitélio Anterior/patologia , Epitélio Anterior/virologia , Humanos , Ceratite Herpética/tratamento farmacológico , Ceratite Herpética/virologia , Masculino , Pessoa de Meia-Idade , Neurotoxinas/administração & dosagem , Neurotoxinas/efeitos adversos , Soluções Oftálmicas/administração & dosagem , Microscopia com Lâmpada de Fenda
11.
Eur J Oncol Nurs ; 32: 1-11, 2018 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-29353626

RESUMO

PURPOSE: The purpose of this study was to evaluate for differences in demographic, clinical, and pain characteristics, as well as measures of sensation, balance, perceived stress, symptom burden, and quality of life (QOL) among survivors who received neurotoxic chemotherapy (CTX) and who reported only chemotherapy-induced neuropathy (CIN, n = 217), CIN and hearing loss (CIN/HL, n = 69), or CIN, hearing loss, and tinnitus (CIN/HL/TIN, n = 85). We hypothesized that as the number of neurotoxicities increased, survivors would have worse outcomes. METHODS: Survivors were recruited from throughout the San Francisco Bay area. Survivors completed self-report questionnaires for pain and other symptoms, stress and QOL. Objective measures were assessed at an in person visit. RESULTS: Compared to survivors with only CIN, survivors with all three neurotoxicities were less likely to be female and less likely to report child care responsibilities. In addition, survivors with all three neurtoxicities had higher worst pain scores, greater loss of protective sensation, and worse timed get up and go scores. These survivors reported higher state anxiety and depression and poorer QOL. For some outcomes (e.g., longer duration of CIN, self-reported balance problems), significantly worse outcomes were found for the survivors with CIN/HL and CIN/HL/TIN compared to those with only CIN. CONCLUSIONS: Our findings suggest that compared to survivors with only CIN, survivors with CIN/HL/TIN are at increased risk for the most severe symptom burden, significant problems associated with sensory loss and changes in balance, as well as significant decrements in all aspects of QOL.


Assuntos
Antineoplásicos/efeitos adversos , Sobreviventes de Câncer/psicologia , Transtorno Depressivo/induzido quimicamente , Perda Auditiva/induzido quimicamente , Neoplasias/tratamento farmacológico , Neurotoxinas/efeitos adversos , Doenças do Sistema Nervoso Periférico/induzido quimicamente , Zumbido/induzido quimicamente , Adulto , Idoso , Idoso de 80 Anos ou mais , Antineoplásicos/uso terapêutico , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Neurotoxinas/uso terapêutico , Qualidade de Vida/psicologia , São Francisco , Autorrelato , Inquéritos e Questionários
12.
Dermatol Surg ; 44(5): 721-725, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-29315143

RESUMO

BACKGROUND: Botulinum-derived neurotoxins have become a substantial tool in dermatologists' armamentarium for facial/neck rejuvenation. Current literature discusses anatomical "danger zones" to avoid during neurotoxin injection to prevent brow ptosis, blepharoptosis, and lower facial ptosis. OBJECTIVE: The aim of this study was to determine whether lidocaine 1% local anesthetic can be used to predict botulinum toxin treatment outcomes and prevent adverse effects of unwanted paralysis. MATERIALS AND METHODS: One percent lidocaine was drawn up using BD ultra-fine 31 G (5/16″), 0.5-mL insulin syringes in the same quantity that would be drawn up for neurotoxin placement. The patient's face was cleansed and mapped; 0.1 mL of 1% lidocaine was injected × 5 sites in the glabella; and 3 sites were injected with 0.05 mL in the frontalis. The patient was assessed after 10 minutes. RESULTS: Improvement in frontalis and glabellar rhytides was appreciated, with noted "spocking" of the lateral brows. This technique allowed the authors to visualize the need for placement of toxin more laterally with eventual successful predictive placement for neurotoxin. CONCLUSION: This technique of using local 1% lidocaine allows the practitioner to devise a neurotoxin distribution map tailored for each patient to limit unwanted paralysis from improper neurotoxin placement.


Assuntos
Toxinas Botulínicas Tipo A/administração & dosagem , Neurotoxinas/administração & dosagem , Rejuvenescimento , Envelhecimento da Pele/efeitos dos fármacos , Adulto , Anestésicos Locais/administração & dosagem , Toxinas Botulínicas Tipo A/efeitos adversos , Técnicas Cosméticas , Face , Humanos , Injeções Intradérmicas , Lidocaína/administração & dosagem , Masculino , Pescoço , Neurotoxinas/efeitos adversos , Valor Preditivo dos Testes , Medição de Risco , Fatores de Risco , Resultado do Tratamento
13.
Artigo em Inglês | MEDLINE | ID: mdl-29267198

RESUMO

In the United States, regulations are in place to ensure the quality of drinking water. Such precautions are intended to safeguard the health of the population. However, regulatory guidelines may at times fail to achieve their purpose. This may be due to lack of sufficient data regarding the health hazards of chronic low dose exposure to contaminants or the introduction of new substances that pose a health hazard risk that has yet to be identified. In this review, examples of different sources of contaminants in drinking water will be discussed, followed by an evaluation of some select individual toxicants with known adverse neurological impact. The ability of mixtures to potentially cause additive, synergistic, or antagonistic neurotoxic responses will be briefly addressed. The last section of the review will provide examples of select mechanisms by which different classes of contaminants may lead to neurological impairments. The main objective of this review is to bring to light the importance of considering trace amounts of chemicals in the drinking water and potential brain abnormalities. There is continued need for toxicology studies to better understand negative consequences of trace amounts of toxins and although it is beyond the scope of this brief overview it is hoped that the review will underscore the paucity of studies focused on determining how long-term exposure to minute levels of contaminants in drinking water may pose a significant health hazard.


Assuntos
Encéfalo/fisiopatologia , Substâncias Perigosas/efeitos adversos , Neurotoxinas/efeitos adversos , Poluentes Químicos da Água/efeitos adversos , Qualidade da Água/normas , Abastecimento de Água/normas , Humanos , Estados Unidos
14.
BMC Ophthalmol ; 17(1): 249, 2017 Dec 13.
Artigo em Inglês | MEDLINE | ID: mdl-29237498

RESUMO

BACKGROUND: The authors report a case of a rare complication that occurred after botulinum toxin injection to the extraocular muscle, which was easily overlooked and successfully corrected by surgery. CASE PRESENTATION: A 34-year-old female patient visited our clinic for diplopia and ocular motility disorder after removal of an epidermoid tumor of the brain. At her initial visit, her best-corrected visual acuity (BCVA) was 20/20 for both eyes. An alternate cover test showed 45 prism-diopter esotropia and 3 prism-diopter hypertropia in the right eye. Following 6 months of observation, the deviation of the strabismus did not improve, and botulinum toxin was injected into the right medial rectus (RMR). After 6 days, she visited our clinic with decreased visual acuity of her right eye. The BCVA was found to be 20/50 for her right eye. Funduscopic examination presented a retinal tear inferonasal to the optic disc with preretinal hemorrhage. Subretinal fluid nasal to the fovea was seen on optical coherence tomography (OCT). Barrier laser photocoagulation was done around the retinal tear; however, her visual acuity continued to decrease, and vitreous hemorrhage and subretinal fluid at the lesion did not improve. In addition, a newly developed epiretinal membrane was seen on OCT. An alternate cover test presented 30 prism-diopter right esotropia. 19 weeks after RMR botulinum toxin injection, she received pars plana vitrectomy, membranectomy, endolaser barrier photocoagulation, and intravitreal bevacizumab (Avastin®) injection. After 4 months, her visual acuity improved to 20/20, and only 4 prism-diopter of right hypertropia and 3 prism-diopter of exotropia were noted. Vitreous opacity and the epiretinal membrane were completely removed, as confirmed by funduscopic and examination. CONCLUSIONS: Sudden loss of vision after injection of botulinum toxin into the extraocular muscle may suggest a serious complication, and a prompt, thorough ophthalmic examination should be performed. If improvements are not observed, rapid surgical intervention is recommended to prevent additional complications.


Assuntos
Toxinas Botulínicas/efeitos adversos , Neurotoxinas/efeitos adversos , Descolamento Retiniano/induzido quimicamente , Hemorragia Vítrea/induzido quimicamente , Adulto , Feminino , Humanos , Injeções Intramusculares/efeitos adversos , Injeções Intraoculares/efeitos adversos
15.
Ann Work Expo Health ; 61(9): 1118-1131, 2017 Nov 10.
Artigo em Inglês | MEDLINE | ID: mdl-29136419

RESUMO

Objectives: Exposure to manganese (Mn) may cause movement disorders, but less is known whether the effects persist after the termination of exposure. This study investigated the association between former exposure to Mn and fine motor deficits in elderly men from an industrial area with steel production. Methods: Data on the occupational history and fine motor tests were obtained from the second follow-up of the prospective Heinz Nixdorf Recall Study (2011-2014). The study population included 1232 men (median age 68 years). Mn in blood (MnB) was determined in archived samples (2000-2003). The association between Mn exposure (working as welder or in other at-risk occupations, cumulative exposure to inhalable Mn, MnB) with various motor functions (errors in line tracing, steadiness, or aiming and tapping hits) was investigated with Poisson and logistic regression, adjusted for iron status and other covariates. Odds ratios (ORs) with 95% confidence intervals (CIs) were estimated for substantially impaired dexterity (errors >90th percentile, tapping hits <10th percentile). Results: The median of cumulative exposure to inhalable Mn was 58 µg m-3 years in 322 men who ever worked in at-risk occupations. Although we observed a partly better motor performance of exposed workers at group level, we found fewer tapping hits in men with cumulative Mn exposure >184.8 µg m-3 years (OR 2.15, 95% CI 1.17-3.94). MnB ≥ 15 µg l-1, serum ferritin ≥ 400 µg l-1, and gamma-glutamyl transferase ≥74 U l-1 were associated with a greater number of errors in line tracing. Conclusions: We found evidence that exposure to inhalable Mn may carry a risk for dexterity deficits. Whether these deficits can be exclusively attributed to Mn remains to be elucidated, as airborne Mn is strongly correlated with iron in metal fumes, and high ferritin was also associated with errors in line tracing. Furthermore, hand training effects must be taken into account when testing for fine motor skills.


Assuntos
Poluentes Ocupacionais do Ar/efeitos adversos , Manganês/efeitos adversos , Destreza Motora/fisiologia , Transtornos dos Movimentos/etiologia , Neurotoxinas/efeitos adversos , Exposição Ocupacional/efeitos adversos , Idoso , Humanos , Íons , Masculino , Manganês/sangue , Pessoa de Meia-Idade , Fenômenos Fisiológicos Musculoesqueléticos , Neurotoxinas/sangue , Ocupações/estatística & dados numéricos , Razão de Chances , Estudos Prospectivos , Análise de Regressão
16.
Rev. neurol. (Ed. impr.) ; 65(5): 223-225, 1 sept., 2017. ilus
Artigo em Espanhol | IBECS | ID: ibc-166958

RESUMO

Introducción. El tratamiento con litio puede ocasionar diversos efectos adversos neurológicos, incluso con niveles terapéuticos. Caso clínico. Mujer de 49 años, con trastorno bipolar y depresión, en tratamiento con litio, antidepresivos y antipsicóticos, que ingresó por un cuadro de alucinaciones visuales con una litemia elevada de 2,1 mEq/L (rango terapéutico: 0,6-1,2 mEq/L). Progresó a una encefalopatía grave que requirió asistencia respiratoria en la unidad de cuidados intensivos. La resonancia magnética cerebral inicial mostró una hiperintensidad simétrica bilateral reversible en los núcleos dentados en las secuencias T2 y T2-FLAIR. A lo largo de los meses posteriores desarrolló de forma progresiva un síndrome pancerebeloso con evidencia de una marcada pérdida de volumen bilateral en el cerebelo, sobre todo a expensas del vermis, que se acompañó clínicamente de un síndrome cerebeloso permanente e invalidante. Conclusiones. Aunque el tratamiento con litio ocasiona efectos adversos neurológicos variados, éstos suelen ser reversibles. Puede dar lugar a secuelas permanentes e incapacitantes, como la paciente descrita, con una atrofia cerebelosa marcada y progresiva, acompañada de secuelas permanentes en forma de síndrome cerebeloso invalidante. La neurotoxicidad cerebelosa del litio debe considerarse en el amplio diagnóstico diferencial que representa la ataxia cerebelosa del adulto (AU)


Introduction. Treatment with lithium can cause several neurological side effects, even at therapeutic levels. Case report. We report the case of a 49-year-old woman, with bipolar disorder and depression, undergoing treatment with lithium, antidepressants and antipsychotics, who was admitted to hospital due to a clinical picture of visual hallucinations with an elevated lithaemia of 2.1 mEq/L (therapeutic range: 0.6-1.2 mEq/L). The patient developed a severe encephalopathy that required the use of assisted ventilation in the intensive care unit. Initial magnetic resonance imaging showed a reversible bilateral symmetrical hyperintensity in the dentate nuclei in T2 and T2-FLAIR sequences. Over the following months she gradually developed a pancerebellar syndrome with evidence of a marked loss of bilateral volume in the cerebellum, above all at the expense of the vermis, which was accompanied by a permanent and disabling cerebellar syndrome. Conclusions. Although treatment with lithium can cause a variety of neurological side effects, they are usually reversible. However, they occasionally give rise to permanent and disabling sequelae, as in the case of the patient reported here, with a marked and progressive cerebellar atrophy, accompanied by permanent sequelae in the form of a disabling cerebellar syndrome. The cerebellar neurotoxicity of lithium must be taken into account in the broad differential diagnosis of cerebellar ataxia in adults (AU)


Assuntos
Humanos , Feminino , Pessoa de Meia-Idade , Lítio/efeitos adversos , Dissinergia Cerebelar Mioclônica/induzido quimicamente , Transtorno Bipolar/tratamento farmacológico , Neurotoxinas/efeitos adversos , Espectroscopia de Ressonância Magnética/métodos , Neuroimagem Funcional
17.
Mayo Clin Proc ; 92(9): 1359-1367, 2017 09.
Artigo em Inglês | MEDLINE | ID: mdl-28789780

RESUMO

BACKGROUND: In essential tremor and Parkinson disease (PD) tremor, administration of onabotulinumtoxinA via a fixed injection approach improves the tremor, but many patients (30%-70%) develop moderate to severe hand weakness, limiting the use of onabotulinumtoxinA in clinical practice. OBJECTIVE: To evaluate the safety and efficacy of incobotulinumtoxinA (IncoA) injection for the treatment of tremor in PD. PATIENTS AND METHODS: In this double-blind, placebo-controlled, crossover trial, 30 patients each received 7 to 12 (mean, 9) IncoA injections into hand and forearm muscles using a customized approach. The study was performed from June 1, 2012, through June 30, 2015, and participants were followed for 24 weeks. Treatment efficacy was evaluated by the tremor subsets of the Unified Parkinson's Disease Rating Scale and the Patient Global Impression of Change 4 and 8 weeks after each of the 2 sets of treatments. Hand strength was assessed using an ergometer. RESULTS: There was a statistically significant improvement in clinical rating scores of rest tremor and tremor severity 4 and 8 weeks after the IncoA injection and of action/postural tremor at 8 weeks. There was a significant improvement in patient perception of improvement at 4 and 8 weeks in the IncoA group. There was no statistically significant difference in grip strength at 4 weeks between the 2 groups. CONCLUSION: Injection of IncoA via a customized approach improved PD tremor on a clinical scale and patient perception, with a low occurrence of significant hand weakness. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT02419313.


Assuntos
Toxinas Botulínicas Tipo A/administração & dosagem , Doença de Parkinson/tratamento farmacológico , Tremor/tratamento farmacológico , Idoso , Idoso de 80 Anos ou mais , Toxinas Botulínicas Tipo A/efeitos adversos , Toxinas Botulínicas Tipo A/uso terapêutico , Connecticut , Estudos Cross-Over , Método Duplo-Cego , Feminino , Humanos , Injeções Intramusculares , Masculino , Pessoa de Meia-Idade , Neurotoxinas/administração & dosagem , Neurotoxinas/efeitos adversos , Neurotoxinas/uso terapêutico , Avaliação de Resultados (Cuidados de Saúde)/estatística & dados numéricos , Doença de Parkinson/fisiopatologia , Índice de Gravidade de Doença , Perfil de Impacto da Doença , Tremor/etiologia
18.
J Am Acad Dermatol ; 76(6): 1027-1042, 2017 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28522039

RESUMO

The use of neuromodulators for therapeutic and cosmetic indications has proven to be remarkably safe. While aesthetic and functional adverse events are uncommon, each anatomic region has its own set of risks of which the physician and patient must be aware before treatment. The therapeutic usages of botulinum toxins now include multiple specialties and multiple indications. New aesthetic indications have also developed, and there has been an increased utilization of combination therapies to combat the effects of global aging. In the second article in this continuing medical education series, we review the prevention and treatment of adverse events, therapeutic and novel aesthetic indications, controversies, and a brief overview of combination therapies.


Assuntos
Toxinas Botulínicas/administração & dosagem , Neurotoxinas/administração & dosagem , Administração Tópica , Toxinas Botulínicas/efeitos adversos , Toxinas Botulínicas/uso terapêutico , Técnicas Cosméticas , Dermatologia/métodos , Humanos , Injeções , Neurotoxinas/efeitos adversos , Neurotoxinas/uso terapêutico
19.
Sci Rep ; 7: 43642, 2017 03 09.
Artigo em Inglês | MEDLINE | ID: mdl-28276430

RESUMO

Quinolinic acid, a macrophage/microglia-derived excitotoxin fulfills a plethora of functions such as neurotoxin, gliotoxin, and proinflammatory mediator, and it alters the integrity and cohesion of the blood-brain barrier in several pathophysiological states. Beta-trace protein (BTP), a monomeric glycoprotein, is known to indicate cerebrospinal fluid leakage. Thus, the prior aim of this study was to investigate whether BTP might non-invasively indicate quinolinic acid-induced impaired blood-brain barrier integrity. The research hypotheses were tested in three subsamples with different states of immune activation (patients with HCV-infection and interferon-α, patients with major depression, and healthy controls). BTP has also been described as a sensitive marker in detecting impaired renal function. Thus, the renal function has been considered. Our study results revealed highest quinolinic acid and highest BTP- levels in the subsample of patients with HCV in comparison with the other subsamples with lower or no immune activation (quinolinic acid: F = 21.027, p < 0.001 [ANOVA]; BTP: F = 6.792, p < 0.01 [ANOVA]). In addition, a two-step hierarchical linear regression model showed that significant predictors of BTP levels are quinolinic acid, glomerular filtration rate and age. The neurotoxin quinolinic acid may impair blood-brain barrier integrity. BTP might be a new non-invasive biomarker to indicate quinolinic acid-induced impaired blood-brain barrier integrity.


Assuntos
Barreira Hematoencefálica/efeitos dos fármacos , Barreira Hematoencefálica/metabolismo , Oxirredutases Intramoleculares/metabolismo , Lipocalinas/metabolismo , Ácido Quinolínico/efeitos adversos , Adulto , Biomarcadores , Barreira Hematoencefálica/imunologia , Feminino , Taxa de Filtração Glomerular , Humanos , Oxirredutases Intramoleculares/sangue , Oxirredutases Intramoleculares/imunologia , Lipocalinas/sangue , Lipocalinas/imunologia , Masculino , Pessoa de Meia-Idade , Neurotoxinas/efeitos adversos , Insuficiência Renal Crônica/complicações , Insuficiência Renal Crônica/tratamento farmacológico , Insuficiência Renal Crônica/etiologia , Insuficiência Renal Crônica/metabolismo
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