Asunto(s)
Humanos , Masculino , Persona de Mediana Edad , Cauda Equina/diagnóstico por imagen , Síndromes de Compresión Nerviosa/diagnóstico , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Examen Físico , Imagen por Resonancia Magnética/métodos , Cauda Equina/fisiopatología , Dolor de la Región Lumbar/diagnóstico , Vértebras Lumbares , Antiinflamatorios/uso terapéuticoRESUMEN
Abdominal cutaneous nerve entrapment is a rarely diagnosed condition that leads to intense neuropathic pain in the anterolateral wall of the abdomen. Generally, it is triggered by some factor implied in the increase of the pressure on the nerve in its passage by the abdominal wall. Its most important differential diagnosis is pain of visceral origin. We present a case in which the clinical findings confirmed on ultrasound and other imaging tests established the diagnosis and in which the noninvasive treatment was effective.
Asunto(s)
Humanos , Masculino , Anciano , Pared Abdominal/anomalías , Nervios Intercostales/anomalías , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Síndromes de Compresión Nerviosa/diagnóstico por imagen , Dolor Abdominal/complicaciones , Dolor Crónico , NeuralgiaRESUMEN
Presentamos el caso de un paciente joven quien presenta 4 a 5 crisis diarias de vértigo espontáneo de segundos de duración, todos o casi todos los días desde hace 9 meses. Estas crisis no tienen gatillo posicional, y hay completa ausencia de sintomatologia entre crisis. Como discutimos en el artículo, este cuadro coíncide con los recientemente publicados criterios para una paroxismia vestibular, entidad supuestamente secundaria a la compresión neurovascular del nervio vestibular. El paciente respondió de forma inmediata y completa a carbamazepina a dosis bajas, el tratamiento de elección en la paroxismia vestibular.
We present the case of a young patient, with a 9-month long history of 4 to 5 daily spells of spontaneous vertigo, each lasting only seconds. There is no positional trigger, and there is a complete lack of symptoms between attacks. As is discussed in the article, this matches the recently published criteria for Vestibular Paroxysmia, an entity allegedly secondary to neurovascular compression of the vestibular nerve. The patient responded immediately and completely to carbamazepine at low dosage, the preferred treatment for vestibular paroxysmia.
Asunto(s)
Humanos , Masculino , Adulto , Enfermedades del Nervio Vestibulococlear/complicaciones , Vértigo/etiología , Síndromes de Compresión Nerviosa/complicaciones , Nervio Vestibular/patología , Enfermedades del Nervio Vestibulococlear/tratamiento farmacológico , Enfermedades del Nervio Vestibulococlear/diagnóstico por imagen , Carbamazepina/uso terapéutico , Vértigo/tratamiento farmacológico , Anticonvulsivantes/uso terapéutico , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Síndromes de Compresión Nerviosa/diagnóstico por imagenRESUMEN
BACKGROUND: The coexistence of hemifacial spasm and trigeminal neuralgia, a clinical entity known as painful tic convulsive, was first described in 1910. It is an uncommon condition that is worthy of interest in neurosurgical practice, because of its common pathophysiology mechanism: Neuro-vascular compression in most of the cases. OBJECTIVE: To present 2 cases of painful tic convulsive that received treatment at our institution, and to give a brief review of the existing literature related to this. The benefits of micro-surgical decompression and the most common medical therapy used (botulin toxin) are also presented. CLINICAL CASES: Two cases of typical painful tic convulsive are described, showing representative slices of magnetic resonance imaging corresponding to the aetiology of each case, as well as a description of the surgical technique employed in our institution. The immediate relief of symptomatology, and the clinical condition at one-year follow-up in each case is described. A brief review of the literature on this condition is presented. CONCLUSION: This very rare neurological entity represents less than 1% of rhizopathies and in a large proportion of cases it is caused by vascular compression, attributed to an aberrant dolichoectatic course of the vertebro-basilar complex. The standard modality of treatment is micro-vascular surgical decompression, which has shown greater effectiveness and control of symptoms in the long-term. However medical treatment, which includes percutaneous infiltration of botulinum toxin, has produced similar results at medium-term in the control of each individual clinical manifestation, but it must be considered as an alternative in the choice of treatment.
Asunto(s)
Toxinas Botulínicas Tipo A/uso terapéutico , Espasmo Hemifacial/cirugía , Cirugía para Descompresión Microvascular/métodos , Síndromes de Compresión Nerviosa/complicaciones , Neuralgia del Trigémino/cirugía , Anciano , Arteria Basilar/diagnóstico por imagen , Arteria Basilar/patología , Arteria Basilar/cirugía , Toxinas Botulínicas Tipo A/administración & dosificación , Femenino , Estudios de Seguimiento , Espasmo Hemifacial/tratamiento farmacológico , Espasmo Hemifacial/etiología , Espasmo Hemifacial/fisiopatología , Humanos , Angiografía por Resonancia Magnética , Masculino , Persona de Mediana Edad , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Síndromes de Compresión Nerviosa/fisiopatología , Síndromes de Compresión Nerviosa/cirugía , Neuralgia del Trigémino/tratamiento farmacológico , Neuralgia del Trigémino/etiología , Neuralgia del Trigémino/fisiopatología , Arteria Vertebral/diagnóstico por imagen , Arteria Vertebral/patología , Arteria Vertebral/cirugíaRESUMEN
The susceptibility of changes in responsiveness to noxious cold stimulation of rats submitted to chronic constriction of the infraorbital nerve (CION) or carrageenan to drug inhibition was compared. Nocifensive responses were measured as total time rats engaged in bilateral facial grooming with both forepaws over the first 2 min following tetrafluoroethane spray application to the snout. Carrageenan (50 microg, s.c. into upper lip) caused short-lived ipsilateral cold hyperalgesia (peak at 3 h: vehicle 8.4+/-1.3, carrageenan 21.2+/-3.0 s) which was markedly suppressed by i.p. indomethacin (4 mg/kg), celecoxib (10mg/kg) or s.c. dexamethasone (0.5 mg/kg), endothelin ET(A) or ET(B) receptor antagonists (BQ-123 and BQ-788, respectively; 10 nmol/lip). CION caused ipsilateral cold hyperalgesia between Days 2 and 12, which peaked on Days 4 (sham 15.3+/-1.8, CION 32.4+/-5.3s) to 6. Established peak CION-induced cold hyperalgesia was unaffected by indomethacin and celecoxib, whereas dexamethasone, BQ-123, BQ-788, and i.v. injections of selective antagonists of ET(A) (atrasentan, 3-10 mg/kg) or ET(B) (A-192621, 5-20 mg/kg) receptors caused significant inhibitions lasting 1-2.5h (peaks approximately 65-90%). Bosentan (dual ET(A)/ET(B) receptor antagonist, 10 mg/kg, i.v.) abolished CION-induced cold hyperalgesia for up to 6h. Thus, once established, CION-induced orofacial hyperalgesia to cold stimuli appears to lack an inflammatory component, but is alleviated by endothelin ET(A) and/or ET(B) receptor antagonists. If this CION injury model bears predictive value to trigeminal neuralgia (i.e., paroxysmal orofacial pain triggered by various stimuli), endothelin receptors might constitute new targets for treatment of this disorder.
Asunto(s)
Antiinflamatorios no Esteroideos/uso terapéutico , Carragenina/toxicidad , Frío/efectos adversos , Aseo Animal/efectos de los fármacos , Hiperalgesia/tratamiento farmacológico , Nervio Maxilar/fisiopatología , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Receptor de Endotelina A/efectos de los fármacos , Receptor de Endotelina B/efectos de los fármacos , Neuralgia del Trigémino/tratamiento farmacológico , Animales , Atrasentán , Bosentán , Celecoxib , Dexametasona/uso terapéutico , Modelos Animales de Enfermedad , Evaluación Preclínica de Medicamentos , Endotelina-1/farmacología , Endotelinas/farmacología , Hiperalgesia/fisiopatología , Indometacina/uso terapéutico , Masculino , Síndromes de Compresión Nerviosa/fisiopatología , Oligopéptidos/farmacología , Oligopéptidos/uso terapéutico , Fragmentos de Péptidos/farmacología , Péptidos Cíclicos/farmacología , Péptidos Cíclicos/uso terapéutico , Piperidinas/farmacología , Piperidinas/uso terapéutico , Pirazoles/uso terapéutico , Pirrolidinas/farmacología , Pirrolidinas/uso terapéutico , Ratas , Ratas Wistar , Receptor de Endotelina A/fisiología , Receptor de Endotelina B/fisiología , Sulfonamidas/farmacología , Sulfonamidas/uso terapéutico , Neuralgia del Trigémino/fisiopatologíaRESUMEN
Vestibular paroxysmia is a syndrome of cross-compression of the VIII cranial nerve and was first described by Jannetta who used the term "disabling positional vertigo". This syndrome is characterized by brief attacks of vertigo, tinnitus, vestibular and auditory deficits. MRI may show the VIII nerve compression from vessels in the posterior fossa, such as the basilar, vertebral, anterior-inferior cerebellar or the posterior-inferior cerebellar arteries. Vestibular paroxysmia may be treated either with medical therapy, such as carbamazepine, phenytoin or gabapentin or with the microvascular decompression of the VIII nerve. This study describes eight patients with vestibular paroxysmia. Four of them showed also clinical signs suggesting cross-compression of the V and/or VII nerve. Seven patients treated with carbamazepine had significant improvement of vertigo and tinnitus.
Asunto(s)
Pérdida Auditiva Sensorineural/diagnóstico , Síndromes de Compresión Nerviosa/diagnóstico , Acúfeno/diagnóstico , Vértigo/diagnóstico , Nervio Vestibulococlear , Anciano , Aminas/uso terapéutico , Anticonvulsivantes/uso terapéutico , Carbamazepina/uso terapéutico , Ácidos Ciclohexanocarboxílicos/uso terapéutico , Femenino , Gabapentina , Pérdida Auditiva Sensorineural/tratamiento farmacológico , Humanos , Imagen por Resonancia Magnética , Masculino , Persona de Mediana Edad , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Estudios Retrospectivos , Acúfeno/tratamiento farmacológico , Vértigo/tratamiento farmacológico , Ácido gamma-Aminobutírico/uso terapéuticoRESUMEN
A paroxismia vestibular é uma síndrome de compressão do VIII nervo craniano e foi denominada inicialmente por Janetta "vertigem posicional incapacitante". Esta síndrome é caracterizada por episódios curtos de vertigem, zumbido, déficit vestibular e auditivo. A RM pode mostrar compressão do VIII nervo por vasos da fossa posterior, como a artéria basilar, artéria vertebral, artéria cerebelar inferior anterior, artéria cerebelar inferior posterior. A paroxismia vestibular pode ser tratada com terapia medicamentosa tais como carbamazepina, fenitoína ou gabapentina, ou com descompressão microvascular do VIII nervo. Este estudo descreve oito pacientes com paroxismia vestibular. Quatro deles mostraram também sinais clínicos sugerindo compressão do V e/ou VII nervos. Sete pacientes tratados com carbamazepina tiveram melhora significativa da vertigem e zumbido.
Asunto(s)
Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Pérdida Auditiva Sensorineural/diagnóstico , Síndromes de Compresión Nerviosa/diagnóstico , Acúfeno/diagnóstico , Nervio Vestibulococlear , Vértigo/diagnóstico , Aminas/uso terapéutico , Anticonvulsivantes/uso terapéutico , Carbamazepina/uso terapéutico , Ácidos Ciclohexanocarboxílicos/uso terapéutico , Pérdida Auditiva Sensorineural/tratamiento farmacológico , Imagen por Resonancia Magnética , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Estudios Retrospectivos , Acúfeno/tratamiento farmacológico , Vértigo/tratamiento farmacológico , Ácido gamma-Aminobutírico/uso terapéuticoRESUMEN
Low intrathecal (i.t.) doses of the nitric oxide (NO)-donor 3-morpholinosydnonimine (SIN-1) (0.1-2.0 microg/10 microl) reduced, while higher doses had no effect (5 or 100 microg/10 microl) or increased (10 and 20 microg/10 microl) the mechanical allodynia induced by chronic ligature of the sciatic nerve in rats. SIN-1 (0.1-100 microg/10 microl; i.t.) produced only antinociceptive effect in the rat tail flick test. The inhibitor of guanylate cyclase, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (4 microg/10 microl; i.t.), abolished the antinociceptive effects of SIN-1 in both tests and reduced the effect of high doses of SIN-1 in neuropathic rats. Hemoglobin (100 microg/10 microl; i.t.), a NO scavenger, inhibited the effect of low dose of SIN-1 and reduced the effect of high dose of SIN-1 in neuropathic rats. 8-Bromo-cGMP (125-500 microg/10 microl; i.t.), reduced the mechanical allodynia in neuropathic rats. The NO-synthase inhibitors, NG-nitro-L-arginine (L-NOARG) and NG-monomethyl-L-arginine (L-NMMA) (75-300 microg/10 microl; i.t.) reduced the mechanical allodynia evoked by nerve injury and increased the tail-flick latency, respectively. These effects were reduced and inhibited, respectively, by previous i.t. ODQ. The effect of L-NOARG was enhanced in a non-significant manner by hemoglobin. These results indicate that SIN-1 and NO-synthase inhibitors reduce pain through a spinal mechanism that involves activation of guanylate cyclase. The effects of SIN-1 vary depending on the dose and pain model utilized, but its most sensitive effect seems to be antinociception. However, high doses of the NO-donor can intensify ongoing pain.
Asunto(s)
GMP Cíclico/análogos & derivados , Molsidomina/farmacología , Neuralgia/tratamiento farmacológico , Donantes de Óxido Nítrico/farmacología , Nociceptores/efectos de los fármacos , Animales , Enfermedad Crónica , GMP Cíclico/farmacología , Relación Dosis-Respuesta a Droga , Inhibidores Enzimáticos/farmacología , Hemoglobinas/farmacología , Inyecciones Espinales , Ligadura , Masculino , Molsidomina/análogos & derivados , Síndromes de Compresión Nerviosa/tratamiento farmacológico , Síndromes de Compresión Nerviosa/fisiopatología , Neuralgia/fisiopatología , Óxido Nítrico/metabolismo , Nitroarginina/farmacología , Nociceptores/metabolismo , Oxadiazoles/farmacología , Dimensión del Dolor , Quinoxalinas/farmacología , Ratas , Ratas Wistar , Nervio Ciático/fisiopatología , omega-N-Metilarginina/farmacologíaRESUMEN
A 38-year-old woman from Antigua had compressive optic neuropathy of the right eye caused by orbital involvement with sinus histiocytosis. There was also nasal sinus involvement and massive cervical lymphadenopathy resulting in radiographic compression of the airway and carotid sheath. Because of the compressive optic neuropathy and threat to the airway and carotid perfusion, the patient underwent a 6-month chemotherapeutic regimen of cyclophosphamide, vincristine, and prednisone. After chemotherapy, the visual dysfunction resolved in correlation with diminution of the orbital mass, and marked regression of the cervical lymphadenopathy. This case demonstrates the potential efficacy of chemotherapy in the treatment of compressive optic neuropathy in cases of orbital sinus histiocytosis with massive lymphadenopathy (Au)