Patrón olfativo en lesiones cerebrales no psiquiátricas ni traumáticas / Olfactory Disorder Pattern In Patients With Neurological Diseases Excluding Psychiatric And Traumatic Aetiologies

INTRODUCCIÓN: Las etiologías más frecuente de las patologías olfativas dentro de la otorrinolaringología suelen ser las producidas por resfriados, inflamaciones nasosinusales, alergias y traumatismos craneo-faciales, fuera de estas etiologías tenemos, con menor frecuencia, las enfermedades neurológicas, psiquiátricas, metabólicas. Nuestro servicio ha podido atender a pacientes con alteraciones neurológicas que presentan patologías olfativas. OBJETIVO: Este trabajo tiene por finalidad verificar qué tipo de alteraciones olfativas se hallan en las personas que padecen lesiones del sistema nervioso central excluidos los traumatismos craneales, las enfermedades psiquiátricas, las epilepsias, las enfermedades de Parkinson y Alzheimer y las sinestesias. Material métodos: Se trata de un estudio descriptivo basado en un grupo de 61 pacientes diagnosticados de diversas lesiones neurológicas y de un grupo control. Ambos grupos fueron valorados por medio del olfatómetro BAST-24. Se comparan los resultados con un grupo control de 120 personas. RESULTADOS: Los resultados muestran que las personas con estos tipos de lesiones neurológicas tienen una capacidad de percibir olores que oscila entre el 60 y el 77% mientras que el grupo control se sitúa entre el 98 y el 100%. Respecto a la capacidad de reconocer correctamente los olores, los paciente neurológicos no superan el 32% de aciertos, mientras que el grupo control se sitúa entre el 59 y el 75% de aciertos, siendo las diferencias olor a olor presentado estadísticamente significativas (p < 0,05) tanto para la detección como para el acierto. CONCLUSIONES: a) Las alteraciones neurológicas no causadas por traumatismos craneales ni por alteraciones psiquiátricas pueden presentar una pérdida olfativa que oscila entre el 68 y el 89%. b) En este tipo de lesiones debe tenerse en cuenta la presencia de alteraciones olfativas. c) Hay alteraciones olfativas por afectación de otras áreas cerebrales distintas a las clásicas olfativas. d) Debe establecerse una colaboración entre los servicios de ORL y Neurología para poder atender dichas alteraciones

INTRODUCTION: The most common cause of olfactory ENT disorders are colds and flu, chronic sinusitis, allergies and traumatic brain injury. Rarer aetiologies include certain neurological, psychiatric and metabolic injuries. TARGET: The aim of this paper was to check the sort of olfactory disorders found in people who have suffered a brain injury, excluding: cranial traumas, psychiatric diseases, epilepsy, Parkinson's and Alzheimer's disease, and synaesthesia. MATERIAL AND METHODS: A descriptive study based on 61 patients with diagnoses of various neurological injuries, which were tested by BAST-24 olfactometer. The results were compared with those of a control group (n= 120). RESULTS: The results show major impairment in these patients' olfactory sense. The neurological injury patients were able to detect from 60-77% of the odours, while the control group were able to detect between 98-100%. The neurological patients were able, at best, to identify, 11-32% of the odours correctly, while the control group were able to correctly detect between 59 -75%. The differences between odour detection and correct identification were statistically significant (p<.05). CONCLUSIONS: We concluded: a) Neurological injury, not caused by traumatic brain injury, psychiatric disorders or ENT diseases, ranged from 68-89% of the olfactory failures. b) We must bear in mind that these sorts of injuries can cause olfactory disorders. c) ENT and Neurologists should collaborate in the treatment of these disorders

Olfactory Disorder Pattern In Patients With Neurological Diseases Excluding Psychiatric And Traumatic Aetiologies. / Patrón olfativo en lesiones cerebrales no psiquiátricas ni traumáticas.

INTRODUCTION: The most common cause of olfactory ENT disorders are colds and flu, chronic sinusitis, allergies and traumatic brain injury. Rarer aetiologies include certain neurological, psychiatric and metabolic injuries. TARGET: The aim of this paper was to check the sort of olfactory disorders found in people who have suffered a brain injury, excluding: cranial traumas, psychiatric diseases, epilepsy, Parkinson's and Alzheimer's disease, and synaesthesia. MATERIAL AND METHODS: A descriptive study based on 61 patients with diagnoses of various neurological injuries, which were tested by BAST-24 olfactometer. The results were compared with those of a control group (n= 120). RESULTS: The results show major impairment in these patients' olfactory sense. The neurological injury patients were able to detect from 60-77% of the odours, while the control group were able to detect between 98-100%. The neurological patients were able, at best, to identify, 11-32% of the odours correctly, while the control group were able to correctly detect between 59 -75%. The differences between odour detection and correct identification were statistically significant (p<.05). CONCLUSIONS: We concluded: a) Neurological injury, not caused by traumatic brain injury, psychiatric disorders or ENT diseases, ranged from 68-89% of the olfactory failures. b) We must bear in mind that these sorts of injuries can cause olfactory disorders. c) ENT and Neurologists should collaborate in the treatment of these disorders.

Cost comparison of adding pregabalin or gabapentin for the first time to the therapy of patients with painful axial radiculopathy treated in Spain.

OBJECTIVES: This paper aims to compare the costs of initiating pregabalin or gabapentin in the therapeutic management of patients with painful axial radiculopathy in routine medical practice. METHODS: A retrospective claim database analysis was carried-out using medical records of patients of both gender aged >18 years with axial painful radiculopathy (ICD-9-CM codes: 353.0 [cervical], 353.3 [thoracic] or 353.1 [lumbar]) who initiated pregabalin or gabapentin therapy between 2006 and 2008. The economic evaluation included healthcare resource utilisation and corresponding costs from a third-payer perspective during 12 months post index date. Estimates of indirect costs due to sick leave were also computed. RESULTS: A total of 571 records were eligible for analysis: 375 (66%) treated with pregabalin and 193 (34%) gabapentin. Time since diagnosis, duration of treatment, prevalence of most co-morbidities and previous use of analgesics were comparable. However, concomitant use of analgesics was higher in the gabapentin cohort; 3.1 (1.7) vs. 2.8 (1.8); p<0.05, mainly due to greater use of opioids (31.1% vs. 21.2%; p<0.05) and non-narcotic drugs (63.7% vs. 52.1%; p<0.01). Adjusted total costs per patient were significantly lower in the pregabalin group; €2.472 (2.101-2.836) vs. €3.346 (2.866-3.825); p=0.005, due to lower absenteeism costs; €1.012 (658-1.365) vs. €1.595 (1.129-2.062); p=0.042, and lower adjusted healthcare costs; €1.460 (1.360-1.560) vs. €1.750 (1.618-1.882); p=0.001. CONCLUSIONS: In a population setting, pregabalin-treated patients with painful radiculopathies were considerably less costly for the healthcare payer than those treated with gabapentin in routine clinical practice. Patients treated with pregabalin had significantly fewer days of sick leave than gabapentin-treated patients.

Cost analysis of adding pregabalin or gabapentin to the management of community-treated patients with peripheral neuropathic pain.

OBJECTIVE: To compare the cost of adding either pregabalin or gabapentin to the management of community-treated patients with peripheral neuropathic pain (PNP). METHODS: A retrospective observational study was conducted using medical records from a Spanish health care provider claims database. Patients receiving health care for PNP, above 18 years and for which either pregabalin or gabapentin was initiated between 2006 and 2008 were included. Economic evaluation included health care resource utilization costs and costs due to sick leave. RESULTS: A total of 1163 patients with PNP were eligible for analysis: 764 were prescribed pregabalin and 399 gabapentin in addition to current pain therapy. Mean age was 59.2 years and 62.2% were female. Concomitant use of analgesics was higher in the gabapentin cohort (3.2 vs. 2.7; P = 0.003), mainly due to non-steroidal anti-inflammatory drugs (74.9% vs. 69.5%; P = 0.018) and opioids (27.7% vs. 17.9%; P = 0.031). Adjusted total costs per patient was lower in pregabalin-treated patients (€2514 vs. €3241; P = 0.003), due to less sick leave (€1067 vs. €1633; P = 0.018) and lower health care costs (€1447 vs. €1609; P = 0.004). The higher acquisition cost of pregabalin (€351 vs. €191; P < 0.001) was largely compensated with lower costs in medical visits, physiotherapy, hospital stays and concomitant analgesics. CONCLUSIONS: In community-treated patients with PNP, total costs were considerably less for those patients initiated with pregabalin therapy than for those patients starting gabapentin add-on therapy. The relatively higher treatment acquisition cost of pregabalin was largely compensated by the overall lower costs for the other components of health care resources and sick leave, thus reducing the economic impact on the health care provider's budget and society.

Efficacy of long-term continuous subcutaneous apomorphine infusion in advanced Parkinson's disease with motor fluctuations: a multicenter study.

Continuous subcutaneous apomorphine infusion (CSAI) is, at present, an alternative option for advanced Parkinson's disease (PD) with motor fluctuations. We studied the evolution of patients with PD and severe motor fluctuations long-term treated with CSAI. We reviewed data from 82 patients with PD (mean age, 67 +/- 11.07; disease duration, 14.39 +/- 5.7 years) and severe motor fluctuations referred to 35 tertiary hospitals in Spain. These patients were long-term treated (for at least 3 months) with CSAI and tolerated the procedure without serious side effects. We compared the baseline data of these 82 patients (before CSAI) with those obtained from the last follow-up visit of each patient. The mean follow-up of CSAI was 19.93 +/- 16.3 months. Mean daily dose of CSAI was 72.00 +/- 21.38 mg run over 14.05 +/- 1.81 hours. We found a statistically significant reduction in off-hours, according to self-scoring diaries (6.64 +/- 3.09 vs. 1.36 +/- 1.42 hours/day, P < 0.0001), total and motor UPDRS scores (P < 0.0001), dyskinesia severity (P < 0.0006), and equivalent dose of antiparkinsonian therapy (1,405 +/- 536.7 vs. 800.1 +/- 472.9 mg of levodopa equivalent units P < 0.0001). CSAI is an effective option for patients with PD and severe fluctuations, poorly controlled by conventional oral drug treatment.