ABSTRACT
Achalasia is an esophageal motility disorder that is commonly misdiagnosed initially as gastroesophageal reflux disease. Patients with achalasia often complain of dysphagia with solids and liquids but may focus on regurgitation as the primary symptom, leading to initial misdiagnosis. Diagnostic tests for achalasia include esophageal motility testing, esophagogastroduodenoscopy and barium swallow. These tests play a complimentary role in establishing the diagnosis of suspected achalasia. High-resolution manometry has now identified three subtypes of achalasia, with therapeutic implications. Pneumatic dilation and surgical myotomy are the only definitive treatment options for patients with achalasia who can undergo surgery. Botulinum toxin injection into the lower esophageal sphincter should be reserved for those who cannot undergo definitive therapy. Close follow-up is paramount because many patients will have a recurrence of symptoms and require repeat treatment.
Subject(s)
Humans , Botulinum Toxins/administration & dosage , Deglutition Disorders/etiology , Diagnostic Errors , Endoscopy, Digestive System , Esophageal Achalasia/diagnosis , Esophageal Sphincter, Lower , Esophagus/physiopathology , Gastroesophageal Reflux/diagnosis , Injections, Subcutaneous , Manometry , Neurotransmitter Agents/administration & dosage , RecurrenceABSTRACT
La meningitis bacteriana continúa siendo una enfermedad potencialmente fatal, especialmente en países en vías de desarrollo. Los aminoácidos excitatorios están fuertemente implicados en la patogénesis del daño neuronal en meningitis bacteriana. El objetivo fue medir niveles de glutamato, GABA, glicina y taurina en liquido cefalorraquídeo y correlacionarlos con el grado de severidad, complicaciones y secuelas. Estudio prospectivo en 31 pacientes con meningitis bacteriana y 10 pacientes con líquido cefalorraquídeo normal (control), con edades de 1 mes - 13 años de edad. El análisis de aminoácidos se realizó al ingreso y al tercer día mediante cromatografía líquida de alta presión. De los 31 pacientes que ingresaron al estudio 64,5 % fueron de género femenino, 13 lactantes, 8 preescolares y 10 escolares. El promedio de aminoácidos en los niños con meningitis fue más alto que en el grupo control (P<0,01). El glutamato disminuyó significativamente en pacientes con hidrocefalia. El GABA está disminuido en pacientes con parálisis cerebral y la taurina está disminuida en higroma y aumentada en lesión de pares craneales, trastornos de la conducta e hipoacusia. Los cambios en los niveles de aminoácidos en líquido cefalorraquídeo refleja el estado patológico y severidad del daño cerebral. Este estudio provee información del eventual papel de la inmunomodulación y posible uso de antagonistas de aminoácidos excitatorios, con efecto neuroprotector, en el tratamiento de meninigitis bacteriana e indica que esta clase de molécula neurotóxica puede represetar un importante blanco en la terapia adyuvante para meningitis bacteriana.
Bacterial meningitis rmains a potentially fatal disease, especially in developing countries. Exitatory amino acids are strongly implicated in the pathogenesis of neuronal damage in bacterial meningitis. To measure levels of glutamate, GABA, glycine and taurine in cerebroespinal fluid and correlate with the degree of severity, complications and sequelae. Prospective study in 31 patients with bacterial meningitis and 10 patients with normal cerebrospinal fluid (control), aged 1 month - 13 years old. Amino acid analysis was performed on admission and on the third day using high pressure liquid chromatography. Of the 31 patients entering the study 64.5 % were females, 13 infants, 8 preschoolers and 10 elementary school students. The average number of amino acids in children with meningitis was higher than in the control group (P<0.01). Glutamate levels significantly decreased in patients with hydrocephalus. GABA levels decreased in patients with cerebral pasly, and taurine diminished in hygroma, and increased in cranial nerve injury, eating disorders and hearing loss. Changes in amino acid levels in cerebrospinal fluid reflect pathological state and severity of brain damage. This study provides information on the possible role of immunomudulation and possible use of excitatory amino acid antogonists with neuroprotective effects in the treatment of bacterial meningitis, indicating that this class of neurotoxic molecules may represent important target in adjuvant therapy for bacterial meningitis.
Subject(s)
Humans , Male , Female , Infant , Child, Preschool , Child , Excitatory Amino Acid Antagonists/pharmacology , Meningitis, Bacterial/pathology , Neurotransmitter Agents/administration & dosage , Neurotransmitter Agents/antagonists & inhibitors , Glutamic Acid/administration & dosage , Glutamic Acid/therapeutic use , Excitatory Amino Acid AgonistsSubject(s)
Humans , Male , Adult , Cluster Headache/pathology , Cluster Headache/drug therapy , Cluster Headache , Cluster Headache/therapy , Facial Neuralgia , Facial Neuralgia/drug therapy , Facial Neuralgia , Facial Neuralgia/therapy , Catheter Ablation/methods , Electrocoagulation/methods , Transcutaneous Electric Nerve Stimulation/methods , Neurotransmitter Agents/administration & dosage , Neurotransmitter Agents/therapeutic useABSTRACT
We have demonstrated that central administration of zinc in minute amounts induces a significant antidipsogenic action in dehydrated rats as well as in rats under central cholinergic and angiotensinergic stimulation. Here we show that acute third ventricle injections of zinc also block water intake induced by central ß-adrenergic stimulation in Wistar rats (190-250 g). Central inhibition of opioid pathways by naloxone reverses the zinc-induced antidipsogenic effect in dehydrated rats. After 120 min, rats receiving third ventricle injections of isoproterenol (160 nmol/rat) exhibited a significant increase in water intake (5.78 ± 0.54 ml/100 g body weight) compared to saline-treated controls (0.15 ± 0.07 ml/100 g body weight). Pretreatment with zinc (3.0, 30.0 and 300.0 pmol/rat, 45 min before isoproterenol injection) blocked water intake in a dose-dependent way. At the highest dose employed a complete blockade was demonstrable (0.54 ± 0.2 ml/100 g body weight). After 120 min, control (NaAc-treated) dehydrated rats, as expected, exhibited a high water intake (7.36 ± 0.39 ml/100 g body weight). Central administration of zinc blocked this response (2.5 ± 0.77 ml/100 g body weight). Naloxone pretreatment (82.5 nmol/rat, 30 min before zinc administration) reverted the water intake to the high levels observed in zinc-free dehydrated animals (7.04 ± 0.56 ml/100 g body weight). These data indicate that zinc is able to block water intake induced by central ß-adrenergic stimulation and that zinc-induced blockade of water intake in dehydrated rats may be, at least in part, due to stimulation of central opioid peptides
Subject(s)
Animals , Male , Rats , Dehydration , Drinking/drug effects , Isoproterenol/pharmacology , Naloxone/pharmacology , Neurotransmitter Agents/administration & dosage , Receptors, Adrenergic, beta/drug effects , Thirst/drug effects , Zinc/administration & dosage , Analysis of Variance , Injections, Intraventricular , Neurotransmitter Agents/pharmacology , Opioid Peptides/drug effects , Rats, Wistar , Time Factors , Zinc/pharmacologyABSTRACT
The possible role of centrally administered tetrapeptide FMRFamide (Phe-Met-Arg-Phe-NH2) on gastric acid secretion in pylorus ligated rats was investigated. Intracerebroventricularly administered FMRFamide stimulated the gastric acid secretion in a dose-dependent manner. This stimulatory effect was abolished by vagotomy and atropine pretreatment. The presence of FMRFamide in rat brain and the ability of FMRFamide to stimulate gastric acid secretion suggest that FMRFamide plays a physiological role in brain modulation of gastric acid secretion.