RESUMEN
Spinal intramedullary cysticercosis is rare and usually afflicts adults. We report the case of a 5-year-old Mexican girl with back pain who had a complex thoracic spinal intramedullary mass on magnetic resonance imaging and a positive immunoblot for Taenia solium. Surgery revealed a cystic mass containing a cysticercus. Cysticercosis should be suspected as the cause of an intramedullary spinal mass in a patient from an endemic area.
Asunto(s)
Neurocisticercosis/diagnóstico , Neurocisticercosis/cirugía , Médula Espinal/parasitología , Antibacterianos , Antituberculosos/administración & dosificación , Preescolar , Quimioterapia Combinada/administración & dosificación , Femenino , Estudios de Seguimiento , Gadolinio , Humanos , Laminectomía , Imagen por Resonancia Magnética/métodos , Metronidazol/administración & dosificación , Neurocisticercosis/tratamiento farmacológico , Medición de Riesgo , Resultado del TratamientoRESUMEN
OBJECTIVE: To compare the features of intraoperative smears of hemangioblastomas with those of tumors with which it is most likely to be confused: meningiomas, anaplastic astrocytomas and renal cell carcinomas. STUDY DESIGN: Examples of hemangioblastomas with high-quality intraoperative smears were retrieved from the files of University Hospital, University of Southern California and Los Angeles County-University of Southern California. The characteristics of these smears were compared to those of meningiomas, anaplastic astrocytomas and renal cell carcinomas by two observes. RESULTS: Smears of hemangioblastomas were cellular but remarkably cohesive. Cytoplasmic borders were indistinct. The nuclei were hyperchromatic and mildly pleomorphic and had a relatively evenly dispersed chromatin pattern. Hemosiderin was invariably present. Smears of meningiomas, anaplastic astrocytomas and renal cell carcinomas were more discohesive than those of hemangioblastomas. Smears of hemangioblastomas lacked the cytoplasmic fibrillarity of those of astrocytic neoplasms and distinct cytoplasmic borders seen in smears of renal cell carcinoma. The nuclear features of the four neoplasms studied also differed. CONCLUSION: Smears of hemangioblastomas have characteristic features that differ reliably from those of meningiomas, anaplastic astrocytoma and renal cell carcinoma, neoplasms that commonly enter the differential with hemangioblastoma. Thus, a cytologic smear preparation made at the time of frozen section may be an invaluable aid in the intraoperative diagnosis of hemangioblastoma.
Asunto(s)
Carcinoma de Células Renales/patología , Glioblastoma/patología , Hemangioblastoma/patología , Meningioma/patología , Adulto , Anciano , Carcinoma de Células Renales/diagnóstico , Diagnóstico Diferencial , Femenino , Secciones por Congelación , Glioblastoma/diagnóstico , Hemangioblastoma/diagnóstico , Humanos , Masculino , Meningioma/diagnóstico , Persona de Mediana EdadRESUMEN
The objective of this study was to correlate cytomegalovirus (CMV) DNA levels in the cerebrospinal fluid (CSF) of subjects with AIDS with clinical and pathologic findings attributable to CMV infection of the central nervous system (CNS). CMV polymerase chain reaction (PCR) was done on serial dilutions of CSF samples from 24 AIDS patients with autopsy-proven CNS disorders. CMV DNA was detected in CSF from 12 of 13 subjects with evidence of CMV infection of the brain or spinal cord but in none of 11 subjects without autopsy evidence of CMV CNS infection. Subjects whose CSF contained > 10(3) CMV DNA molecules/8 microL of CSF had severe CMV CNS disease (e.g., ventriculoencephalitis). PCR appears to be more useful than clinical and neuroradiologic findings for documenting CMV infection of the CNS in patients with AIDS. Quantitation of CMV DNA in CSF shows promise for evaluation of the extent of involvement.
Asunto(s)
Infecciones Oportunistas Relacionadas con el SIDA/virología , Síndrome de Inmunodeficiencia Adquirida/complicaciones , Infecciones por Citomegalovirus/virología , Citomegalovirus/genética , ADN Viral/líquido cefalorraquídeo , Infecciones Oportunistas Relacionadas con el SIDA/líquido cefalorraquídeo , Infecciones Oportunistas Relacionadas con el SIDA/complicaciones , Síndrome de Inmunodeficiencia Adquirida/líquido cefalorraquídeo , Síndrome de Inmunodeficiencia Adquirida/virología , Estudios de Casos y Controles , Citomegalovirus/aislamiento & purificación , Infecciones por Citomegalovirus/líquido cefalorraquídeo , Infecciones por Citomegalovirus/complicaciones , Humanos , Reacción en Cadena de la Polimerasa/métodos , Tasa de SupervivenciaRESUMEN
Depletion of brain dopamine (DA) by pretreatment with the tyrosine hydroxylase inhibitor alpha-methyl-p-tyrosine (AMT) has been shown to prevent the long-term neurotoxic effects of methamphetamine (MA). In addition, it has recently been reported that the neurotoxins 6-hydroxydopamine (6-OHDA) and 5,6-dihydroxytryptamine (5,6-DHT) are formed endogenously in neostriatum and hippocampus, respectively, following a single neurotoxic dose of MA. We, therefore, have examined the ability of AMT pretreatment to prevent the MA-induced formation of 6-OHDA and 5,6-DHT. We report that AMT pretreatment significantly decreases the frequency with which 6-OHDA and 5,6-DHT are detected following MA administration. Neurotoxin formation is compared with brain levels of DA and 5-hydroxytryptamine (5-HT) 2 weeks after MA administration. It is concluded that the ability of AMT to attenuate both 6-OHDA formation and long-term depletions of DA is due to a decrease in the MA-releasable pool of DA. The effect of AMT on MA-induced depletions of 5-HT is less clear and may involve additional factors.
Asunto(s)
5,6-Dihidroxitriptamina/metabolismo , Encéfalo/metabolismo , Dopamina/metabolismo , Hidroxidopaminas/metabolismo , Metanfetamina/farmacología , Metiltirosinas/farmacología , Neurotoxinas/metabolismo , Animales , Encéfalo/efectos de los fármacos , Masculino , Neurotoxinas/farmacología , Oxidopamina , Ratas , Ratas Endogámicas , alfa-MetiltirosinaRESUMEN
6-Hydroxydopamine (6-OHDA; 200 micrograms, 150 micrograms or 110 micrograms) or vehicle was infused stereotaxically into the lateral ventricles of rats, usually following pretreatment with desmethylimipramine (DMI). Various brain regions were then assayed for dopamine (DA), serotonin (5-HT) and norepinephrine (NE). As expected, 6-OHDA depleted DA in all brain regions examined. Unexpectedly, however, the two highest doses of 6-OHDA significantly decreased 5-HT levels in the hippocampus and increased 5-HT levels in the striatum. In addition, despite pretreatment with doses of DMI commonly considered adequate to block 6-OHDA-induced depletion of NE, all doses of 6-OHDA tested significantly reduced NE levels in the hippocampus, hypothalamus and septum. We interpret our data as suggesting that some brain regions are susceptible to nonspecific toxic effects of 6-OHDA at doses commonly employed. Furthermore, these nonspecific effects may or may not occur, depending on seemingly minor variations in experimental technique.
Asunto(s)
Encéfalo/efectos de los fármacos , Hidroxidopaminas/toxicidad , Simpatectomía Química , Animales , Aminas Biogénicas/metabolismo , Cuerpo Estriado , Desipramina/farmacología , Dopamina/metabolismo , Inyecciones , Inyecciones Intraventriculares , Masculino , Norepinefrina/metabolismo , Oxidopamina , Ratas , Ratas Endogámicas , Serotonina/metabolismoRESUMEN
In summary, we have shown that MA is toxic to both 5-HT and DA cells and we have proposed a mechanism that would account for this response, namely, the conversion of the transmitters to neurotoxins. In addition, brain depletions of DA seem regionally specific with larger depletions occurring in some areas than in others. The depletions, however, do not seem to depend entirely on the nuclei of origin, that is, substantia nigra versus VTA. 5-HT was depleted by different amounts in the various regions examined and the 5-HT depletions, although proportional to the DA depletions, were consistently greater. The reasons for this differential sensitivity of the 5-HT and DA systems to the toxic effect of MA is speculative, but may be related to the differential formation of toxins due to the differing availability of oxygen and superoxides at serotonergic and dopaminergic synapses.
Asunto(s)
Encéfalo/metabolismo , Dopamina/metabolismo , Metanfetamina/toxicidad , Serotonina/metabolismo , Anfetamina/farmacología , Animales , Encéfalo/efectos de los fármacos , Cuerpo Estriado/efectos de los fármacos , Cuerpo Estriado/metabolismo , Sistema Límbico/efectos de los fármacos , Sistema Límbico/metabolismo , Mesencéfalo/efectos de los fármacos , Mesencéfalo/metabolismo , Metanfetamina/farmacología , Vías Nerviosas/efectos de los fármacos , Vías Nerviosas/metabolismo , Especificidad de la Especie , Sustancia Negra/efectos de los fármacos , Sustancia Negra/metabolismoRESUMEN
Para-chloroamphetamine (PCA) has been used to deplete brain serotonin (5-HT) in numerous studies of serotonergic involvement in various behaviors and physiological functions. PCA is believed to cause long-lasting depletions of 5-HT by causing the selective degeneration of serotonergic nerve terminals, but the mechanism by which it exerts this neurotoxic effect is not understood. In this experiment, 5,6-dihydroxytryptamine (5,6-DHT), a serotonergic neurotoxin, was detected by high performance liquid chromatography in the rat hippocampus 0.5-4 h after a single 15 mg/kg i.p. injection of PCA. 5,6-DHT was also detected in the somatosensory cortex following PCA administration, but much less frequently than in the hippocampus. Degenerating nerve terminals were observed in the striatum and somatosensory cortex in silver-stained brain sections from rats injected with PCA 1 or 2 days prior to sacrifice. Laminae III and IV of the somatosensory cortex also contained degenerating neuronal perikarya. The neurochemical and histological effects of PCA are very similar to those produced by a large dose of methylamphetamine (MA) in that both drugs are toxic to serotonergic nerve terminals and neuronal perikarya in the somatosensory cortex. We hypothesize that the formation of 5,6-DHT, perhaps from endogenous 5-HT, may mediate the toxic effects of PCA, MA and other amphetamine-related drugs on serotonergic neurons and on a subpopulation of cortical neurons.
Asunto(s)
5,6-Dihidroxitriptamina/metabolismo , Anfetaminas/farmacología , Química Encefálica/efectos de los fármacos , Degeneración Nerviosa/efectos de los fármacos , Neurotoxinas/farmacología , p-Cloroanfetamina/farmacología , 5,6-Dihidroxitriptamina/fisiología , Animales , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Hipocampo/patología , Ácido Hidroxiindolacético/metabolismo , Inyecciones Intraperitoneales , Masculino , Neurotoxinas/metabolismo , Ratas , Ratas Endogámicas , Serotonina/metabolismo , Corteza Somatosensorial/efectos de los fármacos , Corteza Somatosensorial/metabolismo , Corteza Somatosensorial/patología , p-Cloroanfetamina/metabolismoRESUMEN
(+/-)-3,4-Methylenedioxymethylamphetamine (MDMA) was administered s.c. to rats (10, 20 or 40 mg/kg b. wt.) and guinea pigs (20 mg/kg) twice a day for 4 days, 2 weeks before decapitation. Norepinephrine, dopamine and serotonin (5-HT) levels were assayed in the hippocampus, hypothalamus, striatum and neocortex. In rats, MDMA produced dose-dependent reductions in 5-HT in all brain regions examined. The highest dose also reduced norepinephrine and/or dopamine in some regions. The 20-mg/kg dose of MDMA depleted 5-HT in all regions of the guinea pig brain assayed. In both species, repeated administration of 20 mg/kg of MDMA reduced the Vmax but not the Km of 5-HT uptake 2 weeks after administration. A single 40-mg/kg injection of MDMA depleted 5-HT 2 and 8 weeks after administration to rats in all regions of the brain examined except the hypothalamus. Administration of 80 mg/kg of MDMA twice a day for 2 days to rats depleted striatal 5-HT and dopamine. Brain sections from rats injected with MDMA according to this dosage regimen were stained by the Fink-Heimer method. Degenerating axon terminals and cell bodies were observed in the striatum and somatosensory cortex, respectively. These findings suggest that MDMA is toxic to serotonergic and, to a lesser extent, catecholaminergic neurons. Some neurons that do not contain these transmitters (neocortical neurons) are also affected.
Asunto(s)
3,4-Metilenodioxianfetamina/toxicidad , Anfetaminas/toxicidad , Encéfalo/citología , Neuronas/efectos de los fármacos , 3,4-Metilenodioxianfetamina/análogos & derivados , Animales , Encéfalo/efectos de los fármacos , Cuerpo Estriado/efectos de los fármacos , Dopamina/metabolismo , Cinética , Masculino , N-Metil-3,4-metilenodioxianfetamina , Norepinefrina/metabolismo , Ratas , Ratas Endogámicas , Serotonina/metabolismo , Corteza Somatosensorial/efectos de los fármacos , Sinaptosomas/efectos de los fármacos , Sinaptosomas/metabolismo , Distribución TisularRESUMEN
Methamphetamine (MA) in high doses produces long-term toxic effects on the serotonergic system in the rat brain, including depletions of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid and reductions in 5-HT reuptake and tryptophan hydroxylase activity. In this study, the formation of 5,6-dihydroxytryptamine (5,6-DHT), a serotonergic neurotoxin, was observed in the rat hippocampus after a single 100 mg/kg injection of MA. The 5,6-DHT was detected by reverse-phase high-performance liquid chromatography with electrochemical detection in tissue samples taken 0.5-4 h after MA administration; the highest levels of 5,6-DHT (0.032 ng/mg wet tissue) were detected at 1 h. Following administration of MA, 5-HT was also depleted in the neocortex, but 5,6-DHT was not detected as frequently in this brain region as in the hippocampus. Comparisons were made between the long-term hippocampal 5-HT depletions seen either after an injection of MA or after intraventricular 5,6-DHT infusions and the levels of 5,6-DHT measured in the hippocampus shortly after each treatment. The amount of 5,6-DHT produced after MA administration appears to be adequate to cause the observed long-term 5-HT depletions. We suggest that 5,6-DHT formed from 5-HT may mediate the neurotoxic effects of MA on serotonergic nerve terminals.
Asunto(s)
5,6-Dihidroxitriptamina/biosíntesis , Encéfalo/metabolismo , 5,6-Dihidroxitriptamina/administración & dosificación , Animales , Corteza Cerebral/efectos de los fármacos , Corteza Cerebral/metabolismo , Hipocampo/efectos de los fármacos , Hipocampo/metabolismo , Ácido Hidroxiindolacético/metabolismo , Inyecciones Subcutáneas , Masculino , Metanfetamina/farmacología , Ratas , Ratas Endogámicas , Serotonina/metabolismo , Factores de TiempoRESUMEN
Neurochemical and histological studies suggest that methylamphetamine (MA) administered continuously or in high doses is toxic to dopaminergic and serotonergic nerve terminals. Degeneration of the dopaminergic or serotonergic cell bodies themselves has not been reported, however. In the present study, administration of a single 100 mg/kg dose of MA was toxic to a subpopulation of neurons in the somatosensory cortex, an area of the brain which does not contain catecholaminergic or serotonergic cell bodies. This dose of MA also produced a long-lasting depletion of serotonin (5-HT) but not norepinephrine in the somatosensory cortex. Dopamine levels in the somatosensory cortices of control animals were virtually undetectable and therefore were not studied further. Administration of alpha-methyltyrosine (alpha-MT), a catecholamine synthesis inhibitor, prior to the injection of MA blocked both the depletion of 5-HT and the degeneration of cortical perikarya produced by MA alone. Since the MA-induced depletion of 5-HT and the MA-induced degeneration of cortical perikarya are correlated, we suggest that the serotonergic system may be involved in the toxic effects of MA on the cortical neurons.