ABSTRACT
Akinetic mutism (AM) is a behavioral disorder characterized by impossibility to move or speak in awake patients. lt has been typically described as a transient disorder following posterior fossa tumour resection. Besides, AM may also appear after recurrent shunt failures in hydrocephalic patients, with no tendency towards improvement, either spontaneously or with shunt revisions. However successful treatment of this second type of AM has been achieved with bromocriptine. We present a patient who developed AM after a posterior fossa surgery complicated by ventriculitis and multiple hydrocephalic events. AM only improved with bromocriptine. We review AM pathophysiology. Although not well known, it appears to be quite different, depending on its cerebellar or hydrocephalic origin. Damage to dentate nucleus or its efferents (mainly of glutamate) should promote AM of cerebellar origin, while damage to paraventricular monoaminergic pathways could explain AM related to repeated shunt failures which has successful response to bromocriptine treatment. However, a more complete study of this disorder is required to ascertain its aetiology.
Subject(s)
Akinetic Mutism/drug therapy , Akinetic Mutism/etiology , Brain Neoplasms/pathology , Brain Neoplasms/surgery , Bromocriptine/therapeutic use , Central Nervous System Stimulants/therapeutic use , Cerebellum/pathology , Cerebellum/surgery , Dopamine Agonists/therapeutic use , Ephedrine/therapeutic use , Hemangioma, Cavernous, Central Nervous System/pathology , Hemangioma, Cavernous, Central Nervous System/surgery , Hydrocephalus/complications , Postoperative Complications , Akinetic Mutism/diagnosis , Brain Neoplasms/diagnostic imaging , Bromocriptine/administration & dosage , Central Nervous System Stimulants/administration & dosage , Dopamine Agonists/administration & dosage , Drug Administration Schedule , Ephedrine/administration & dosage , Female , Hemangioma, Cavernous, Central Nervous System/diagnostic imaging , Humans , Magnetic Resonance Imaging , Middle Aged , Neurosurgical Procedures/methods , Tomography, X-Ray ComputedABSTRACT
El mutismo acinético (MA) es un trastorno del comportamiento, caracterizado por la incapacidad para moverse o hablar en pacientes despiertos. Típicamente ha sido descrito como una complicación transitoria de la cirugía de tumores de fosa posterior. Sin embargo, el MA también puede aparecer tras múltiples fallos valvulares en pacientes hidrocefálicos. En estos casos, el MA no mejora espontáneamente, ni con revisiones valvulares, pero puede responder al tratamiento con bromocriptina. Presentamos una paciente con MA tras una cirugía de fosa posterior, complicada por una ventriculitis con dilataciones ventriculares repetidas, que sólo mejoró con bromocriptina. Revisamos la fisiopatología del MA. Aunque ésta no sea bien conocida, parece que la afectación del núcleo dentado y de sus eferencias (principalmente de glutamato) sería responsable del MA de origen cerebeloso, mientras que la afectación de las vías monoaminérgicas paraventriculares explicaría el MA relacionado con dilataciones ventriculares repetidas y que responde al tratamiento con bromocriptina. Aun así, se requiere un estudio más profundo de esta patología para aclarar su etiología
Akinetic mutism (AM) is a behavioral disorder characterized by impossibility to move or speak in awake patients. lt has been typically described as a transient disorder following posterior fossa tumour resection. Besides, AM may also appear after recurrent shunt failures in hydrocephalic patients, with no tendency towards improvement, either spontaneously or with shunt revisions. However successful treatment of this second type of AM has been achieved with bromocriptine. We present a patient who developed AM after a posterior fossa surgery complicated by ventriculitis and multiple hydrocephalic events. AM only improved with bromocriptine. We review AM pathophysiology. Although not well known, it appears to be quite different, depending on its cerebellar or hydrocephalic origin. Damage to dentate nucleus or its efferents (mainly of glutamate) should promote AM of cerebellar origin, while damage to paraventricular monoaminergic pathways could explain AM related to repeated shunt failures which has successful response to bromocriptine treatment. However, a more complete study of this disorder is required to ascertain its aetiology
Subject(s)
Male , Female , Humans , Akinetic Mutism/diagnosis , Akinetic Mutism/physiopathology , Akinetic Mutism/therapy , Bromocriptine/administration & dosage , Bromocriptine/therapeutic use , Hydrocephalus , Ephedrine/therapeutic use , Cerebellum/surgery , Cranial Fossa, Posterior/surgery , Brain NeoplasmsABSTRACT
The use of reduced doses of Ritonavir (RIT) and Saquinavir (SQV) is considered a potent alternative in treating patients infected by HIV-1. We tested a combination of 300mg of RIT plus 600mg of SQV, twice daily, in association with two reverse transcriptase inhibitors to treat AIDS patients for a period of 6 monts. Evaluation of HIV-1 RNA plasma levels, CD4+/CD8+ cell count and biochemical/hematological parameters (liver enzymes, serum electrolytes, creatinin, blood glucose, uric acid, white blood cell count, platelet count, and hemoglobin level) were performed after 30, 90 and 180 days of therapy. Clinical failure and adverse reactions were also recorded in order to assess safety and efficacy of the treatment. A total of 30 AIDS patients (25 male; 5 female) were enrolled in the study. Eight patients discontinuede the therapy due to intolerance, 2 patients presented clinical failure (onset of AIDS defining events during the study period), 2 patients were excluded due to protocol violation. Five patients tolerated only a lower dose of RIT (400mg/day). Patients who completed 6 months of therapy had a drop in viral load from 4.8ñ.7log10median4.9log) to 3.4ñ1.0log10(median 2.6log), and an increase in CD4+ count from 109ñ86 cells/ml(median 84 cells/ml) to 249ñ114 cells/ml(median 265cells/ml), compared to baseline values. However, patients who used a lower dose of RIT (400mg/day) had a less impressive drop in viral load values(mean0.6log10RNA copies/ml) when compared with those using the 600mg/day of the drug(mean 2.4log10). The percentage of patients presenting undetectable levels of HIV-1 RNA in plasma was quite different for the 2 groups: 92 percent of patients with a viral load <400 RNA copies/ml were using 600mg of RIT. The combination of reduced doses of RIT and SQV reduced viral load >1.0log10 after 6 months in 83 percent of study patients. The dose of 600mg/day of RIT was more effective in reducing viral load than 400mg/day, but was less well-tolerated. CD4+ cell counts increased in all patients regardless of the RIT dose used.
Subject(s)
Humans , Male , Female , Adult , Acquired Immunodeficiency Syndrome , HIV-1/drug effects , Ritonavir/adverse effects , Ritonavir/pharmacology , Saquinavir/adverse effects , Saquinavir/pharmacology , Drug Evaluation , HIV Protease Inhibitors/metabolism , Viral LoadABSTRACT
The use of reduced doses of Ritonavir (RIT) and Saquinavir (SQV) is considered a potent alternative in treating patients infected by HIV-1. We tested a combination of 300mg of RIT plus 600mg of SQV, twice daily, in association with two reverse transcriptase inhibitors to treat AIDS patients for a period of 6 months. Evaluation of HIV-1 RNA plasma levels, CD4+/CD8+ cell count and biochemical/hematological parameters (liver enzymes, serum electrolytes, creatinin, blood glucose, uric acid, white blood cell count, platelet count, and hemoglobin level) were performed after 30, 90 and 180 days of therapy. Clinical failure and adverse reactions were also recorded in order to assess safety and efficacy of the treatment. A total of 30 AIDS patients (25 male; 5 female) were enrolled in the study. Eight patients discontinued the therapy due to intolerance, 2 patients presented clinical failure (onset of AIDS-defining events during the study period), 2 patients werc excluded due to protocol violation. Five patients tolerated only a lower dose of RIT (400mg/day). Patients who completed 6 months of therapy had a drop in viral load from 4.8+/-.7 log(10) median 4.9 log) to 3.4 +/- 1.0 log(10) (median 2.6 log), and an increase in CD4+ count from 109 +/- 86cells/ml (median 84cells/ml) to 249+/- 114 cells/ml (median 265 cells/ml), compared to baseline values. However, patients who used a lower dose of RIT (400mg/day) had a less impressive drop in viral load values (mean 0.6 log(10) NA copies/ml) when compared with those using the 600mg/day of the drug (mean 2.4 log(10)). The percentage of patients presenting undetectable levels of HIV-1 RNA in plasma was quite different for the 2 groups: 92% of patients with a viral load <400 RNA copies/ ml were using 600mg of RIT. The combination of reduced doses of RIT and SQV reduced viral load >1.0 log(10) after 6 months in 83% of study patients. The dose of 600mg/day of RIT was morc effective in reducing viral load than 400mg/day, but was less well-tolerated. CD4+ cell counts increased in all patients regardless of the RIT dose used.
ABSTRACT
The spontaneous perforation of the esophagus is an entity with a difficult diagnosis due to the absence of predisposing pathological antecedents and the variability of symptoms. Although the diagnosis may be clinically suspected, only the imaging techniques, mainly thoracic radiography, esophagogram and, most recently, axial computerized tomography and nuclear magnetic resonance, allow a reliable diagnosis. We present the case of a spontaneous perforation of the esophagus in which the image obtained with computerized tomography allowed its diagnosis and surgical treatment within a short period of time.
