Quality of life of caregivers in Parkinson's disease.

OBJECTIVE: To assess the impact of PD on informal caregivers of patients and identify the main factors related to caregiver strain. PATIENTS AND METHODS: Pairs of PD patients and their caregivers. Evaluation by neurologists included the Hoehn and Yahr, Schwab and England, UPDRS (parts 1-3), ISAPD, and Pfeiffer's SPMSQ rating scales. Patients completed the Euro-QoL 5D, PDQ-8, and Hospital Anxiety and Depression Scale. The SQLC was used to assess caregivers' quality of life (QoL), with caregivers, in turn, applying the Euro-QoL and PDQ-8 to assess patients' health-related quality of life (HRQoL). Multiple linear regression models were fitted to ascertain factors linked to the SQLC. RESULTS: Significant correlations were in evidence between the following scores: SQLC and clinical rating scales and SQLC and patients' HRQoL. Based on multiple regression analysis, patients' functional state (ADL) proved to be the main predictor of caregivers' QoL. Self- and caregiver-assessed patients' HRQoL also proved to be a relevant factor. CONCLUSIONS: (1) Patients' functional state was significantly related to caregivers' psychosocial burden; (2) patients' HRQoL proved to be an additional factor linked to caregiver QoL; (3) improvement of patient disability and HRQoL might alleviate caregiver strain.

[Findings using magnetic resonance in a patient with non-traumatic anosmia]. / Hallazgos mediante resonancia magnética en un paciente con anosmia no postraumática.

INTRODUCTION: The presence of alterations in the neuroimaging in patients with anosmia without traumatic antecedents is not frequent. CASE REPORT: Male aged 38 who came to surgery after having suffered, 6 months earlier, for 1 week, a picture of intense, oppressive holocranial headache, accompanied by fever. Associated with this, an acute complete anosmia also began and persisted up to the moment the patient came for consultation. It was not associated with any infection of the respiratory tract, there was no history of cranial trauma, no ingestion of medicines nor toxins, nor had he been exposed to toxic products. The exploration to which he was submitted only showed an anosmia and was otherwise found to be normal. Cranial MRI showed signal alterations in both lower (orbitary) convolutions of the frontal lobes, in the anterior region of the right temporal lobe and in both olfactory nerves. Tests for HIV serology, parotiditis, hepatitis B and C virus, HSV, VZV, Mycoplasma pneumoniae and lues were negative. The acute onset of the anosmia in midst of a picture of febricula and headaches made us suspect the presence of an infectious aetiology, and the alterations found in the neuroimaging could be due to post encephalic lesions, with a special predilection for olfactory areas. CONCLUSIONS: 1. MRI plays a fundamental role in the topographic and aetiological evaluation of olfactory dysfunctions of a central origin; 2. Affectation of the central olfactory passages of an infectious aetiology in a non HIV patient and with neuroimaging findings is a rare complication.

Hallazgos mediante resonancia magnética en un paciente con anosmia no postraumática / Findings using magnetic resonance in a patient with non-traumatic anosmia

Introducción. La presencia de alteraciones en neuroimagen en pacientes con anosmia sin antecedente traumático es infrecuente. Caso clínico. Varón de 38 años que consulta por haber presentado seis meses antes, durante una semana, un cuadro de cefalea holocraneal intensa y opresiva acompañada de febrícula. Asociado al mismo comenzó de forma aguda una anosmia completa que persistía en el momento de la consulta. No refería asociación de infección del tracto respiratorio, ni antecedente de traumatismos craneales, ni ingesta medicamentosa o tóxica, ni exposición a productos tóxicos. En la exploración realizada sólo se constató una anosmia, siendo el resto normal. Una resonancia magnética (RM) craneal mostró alteraciones de señal en ambas circunvoluciones inferiores (orbitarias) de lóbulos frontales, en región anterior de lóbulo temporal derecho y en ambos nervios olfatorios. Las serologías de VIH, parotiditis, virus de las hepatitis B y C, VHS, VVZ, Mycoplasma pneumoniae y lúes fueron negativas. El inicio agudo de la anosmia, en el seno de un cuadro de febrícula y cefalea, hace sospechar una etiología infecciosa y las alteraciones encontradas en la neuroimagen podrían corresponder a lesiones postencefalíticas con especial predilección por áreas olfatorias. Conclusiones. 1. La RM desempeña un papel principal en la evaluación topográfica y etiológica de las disfunciones olfatorias de origen central. 2. La afectación de vías olfatorias centrales de etiología infecciosa en un paciente sin VIH y con hallazgos en neuroimagen es una complicación rara (AU)

Hyperhomocyst(e)inemia is a risk factor of secondary vascular events in stroke patients.

OBJECTIVE: Moderate hyperhomocyst(e)inemia is an independent risk factor for stroke, but it is unclear whether it also would be a risk factor for secondary vascular events after stroke. METHODS: Longitudinal study of 137 consecutive ischemic stroke patients (age 45-91 years) who were prospectively studied with a standard clinical protocol. Vascular events (stroke recurrence, ischemic heart disease, deep venous thrombosis or peripheral arterial disease) were identified during 2 years of follow-up. Serum homocyst(e)ine was determined 3 months after the stroke. The cumulative proportion of patients with homocyst(e)ine above or below the 75th percentile who survived free of vascular events was determined by Kaplan-Meier analysis. Cox models were used to estimate the relative risk of vascular events after controlling for other confounding factors. RESULTS: Serum homocyst(e)ine was significantly higher in patients with vascular events (26.2 versus 19.4 micromol/l; p = 0.016). The cumulative proportion of patients with vascular events was 46.5% in the group with homocyst(e)ine over the 75th percentile (>30 micromol/l) and 20.2% in the other group (log-rank test 7.5; p = 0.0062). After adjustment for age, sex, high blood pressure, diabetes, heart disease, previous cerebrovascular disease, smoking and serum cholesterol, the relative risk of vascular event for patients above compared with those below the 75th percentile of serum homocyst(e)ine was 2.8 (CI 95% 1.3-6; p = 0.01). CONCLUSION: Hyperhomocyst(e)inemia is a significant risk factor for vascular events after ischemic stroke. This finding is independent of other risk factors such as hypertension, and may have therapeutic relevance in the secondary prevention of vascular diseases in stroke patients.

Poststroke dementia : clinical features and risk factors.

BACKGROUND AND PURPOSE: The goal of the present study was to examine a series of putative risk factors of poststroke dementia (PSD), especially those factors usually associated with cerebrovascular disease and degenerative dementia, in a series of 251 consecutive unselected stroke patients. METHODS: A standard protocol was prospectively applied at admission and 3 months after stroke; this protocol included clinical, functional, and cognitive assessments, hemogram and serum biochemistry, ECG and CT exams, apolipoprotein E and angiotensin-converting enzyme genotype, and neuropsychological examination. After a neuropsychological examination and an interview with a relative, the following diagnostic criteria were used: the Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV for dementia after stroke, DSM-III-R for previous dementia and dementia stage, and Association Internationale pour la Recherche et l'Enseignement en Neurologie (NINDS-AIREN) for vascular dementia. RESULTS: Seventy-five cases (30%) demonstrated dementia at 3-month follow up; 25 of them (10%) had demonstrated dementia before the stroke. Dementia was unrelated to type (ischemic/hemorrhagic) or location of stroke, vascular factors (hypertension, diabetes, ischemic heart disease, or hypercholesterolemia), apolipoprotein E or angiotensin-converting enzyme genotype, and serum homocysteine. Age (odds ratio [OR] 1.1, 95% CI 1.03 to 1.2), previous nephropathy (OR 6.1, 95% CI 1.5 to 24.3), atrial fibrillation (OR 4.4, 95% CI 1. 4 to 13.9), low Canadian Neurological Scale score at discharge (OR 0. 5, 95% CI 0.4 to 0.6), and previous mental decline assessed by the shortened Spanish version of the Informant Questionnaire on Cognitive Decline in the Elderly (SS-IQCODE; OR 1.2, 95% CI 1.1 to 1. 4) were the correlates of dementia in logistic regression analyses. The same risks factors were found when cases with previous dementia and with hemorrhagic stroke were excluded. CONCLUSIONS: Dementia is frequent after ischemic or hemorrhagic stroke. Age, nephropathy, atrial fibrillation, previous mental decline, and stroke severity independently contribute to the risk.

The PDQ-39 Spanish version: reliability and correlation with the short-form health survey (SF-36).

BACKGROUND AND METHODS: The Parkinson's Disease Questionnaire (PDQ-39) was the first specific instrument for evaluation of the "health-related quality of life" (QoL) in Parkinson's disease patients. The PDQ-39 has been subjected to adaptation to Spanish language and culture (PDQ-39 Spanish version, PDQ-39SV) and this version has been validated in aspects of internal consistency and construct validity. The present study assess the test-retest reliability and the convergent validity of the PDQ-39SV with a generic QoL instrument (SF-36). RESULTS: Most of the PDQ-39 dimensions showed an adequate consistency-Cronbach's alpha > 0.7 for six dimensions. As a whole, test-retest reliability resulted satisfactory. Two dimensions-activities of daily living and emotional well-being- showed a low grade significant difference (paired Student t-test, p < 0.05) due to improvement in the second survey (at 10 to 14 days from the first one) perhaps related to adjustments of the treatment at the first visit. A strong association (Spearman r, p < 0.001), indicative of convergent validity, was obtained for the PDQ-39 dimensions and the relevant SF-36 scales, as well as for the physical and mental component summary scores of the SF-36. CONCLUSIONS: Taking into account these results and previous studies, it is concluded that the PDQ-39 SV is a reliable measure that has construct validity.

Anticholinergic therapy and dementia in patients with Parkinson's disease.

In a cross-sectional study performed in 1980 on 70 consecutive Parkinson's disease (PD) outpatients, we investigated the factors associated with dementia, especially anticholinergic drugs. All cases fulfilled three major clinical criteria of PD, and underwent extensive clinical and laboratory examinations, including brain CT and neuropsychological assessment. Cases with mental deterioration at the onset of the illness or confusional status were excluded. In 15 patients the diagnosis of dementia was made according to DSM-III criteria; 15 other non-demented patients scoring 4 on the Reisberg's Global Deterioration Scale were labelled as "mentally deteriorated", and the remaining 40 cases were considered cognitively normal. In a logistic multiple regression analysis only age, female sex and time of anticholinergic intake were significantly associated with dementia. We conclude that anticholinergic drugs must be avoided in PD patients with some cognitive decline.

[Intracranial hypotension and sixth cranial nerve palsy]. / Hipotensión intracraneal espontánea y parálisis del sexto nervio craneal.

The sixth cranial nerves may be involved in rare cases of post-puncture syndrome after lumbar anesthesia as well as in cases of spontaneous intracranial hypotension. We present 3 cases of spontaneous intracranial hypotension with unilateral or bilateral sixth nerve palsy.

Changes induced by zinc on thyroxine deiodination by rat liver in vivo and in vitro.

The effects of in vivo administration or in vitro addition of zinc on 5'-deiodination of thyroxine (T4) and the concentration of nonprotein sulfhydryl groups (NPSH) in rat liver were studied in 200-240 g body weight male Wistar rats. Twelve rats were injected i.p. with zinc sulphate 2 mg/kg body weight 24 h before the experiments were started. Animals were killed by cervical dislocation and the liver was immediately removed and homogenized. Dithiothreitol (DTT) (0, 2.5, 5 or 10 mM, final concentration) and 1 microCi 125I-T4 were added to homogenates. For the in vitro studies, animals were killed by cervical dislocation and the liver removed and added zinc or cadmium (2.5 or 5 mM) plus DTT and labelled T4. Homogenates were incubated for 90 min at 37 degrees C and thereafter chromatographed in Whatman 1 paper. Zinc-injected rats had a significant (P < 0.01) decrease in T4 deiodination and in the generation of iodine (P < 0.02) and T3 (P < 0.05). In the in vitro studies, both zinc and cadmium reduced (P < 0.02) the deiodination of T4, and the generation of iodine (P < 0.02) for zinc and P < 0.05 for cadmium) as well as the generation of T3 (p < 0.05). The NPSH in zinc-injected rats were within normal levels. Serum T4 and T3 in zinc-treated rats were normal, whereas in cadmium-treated rats were both significantly decreased (P < 0.01 for T4 and P < 0.02 for T3). The data indicate that zinc blocks the activity of liver 5'-deiodinase through a mechanism probably related to its binding to the sulfhydryl groups of the enzyme.

Changes induced by zinc on thyroxine deiodination by rat liver in vivo and in vitro

Se estudió el efecto de la administración in vivo o del agregado in vitro de zinc sobre la deiodinación 5'de la tiroxina (T4) por el hígado de rata y sobre la concentración hepática de grupos sulfhidrilos libres (NPSH). Se usaron ratas Wistar macho de 200-240g de peso corporal. A un grupo de 12 ratas se les inyectó i.p. sulfato de zinc 2mg/Kg de peso, 24h antes de iniciar el estudio. Se sacrificaron los animales por dislocación cervical y el hígado fue inmediatamente homogeneizado. Se agregó a los homogenatos dithithreitol (DTT) (0,2.5,5 o 10mM concentración final) y 1µCi de 125I-T4. Para los estudios in vitro en animales sin tratar, se agregó al homogenato de hígado sulfato de zinc o cloruro de cadmio (2.5 o 5mM) más DTT y T4 marcada. Todos los homogenatos fueron incubados durante 90 min a 37ºC y luego cromatografiados en papel Whatman 1. Las ratas inyectadas con zinc tuvieron una disminución significativa (p<0.01) de la deiodinación de T4, de la producción de 125 iodo (P<0.02) y de triiodotironina (T3) (P<0.05). En los estudios in vitro, el agregado de zinc o cadmio disminuyó significativamente la degradación de T4 (P<0.02) y la producción de iodo (P<0.02 para el zinc y P<0.05 para el cadmio) y de T3 (P<0.05). La concentración hepática de NPSH en los animales inyectados con zinc fue normal. La concentración sérica de T4 y T3 en los animales inyectados con zinc fue normal pero en los inyectados con cadmio se redujo significativamente (P<0.01 para T4 y P<0.02 para T3). Los resultados indican que el zinc inhibe la actividad de la 5'-deioidnasa hepática, por um mecanismo probablemente relacionado con la unión del metal a los grupos sulfhidrilos de la enzima

Changes induced by zinc on thyroxine deiodination by rat liver in vivo and in vitro.

The effects of in vivo administration or in vitro addition of zinc on 5-deiodination of thyroxine (T4) and the concentration of nonprotein sulfhydryl groups (NPSH) in rat liver were studied in 200-240 g body weight male Wistar rats. Twelve rats were injected i.p. with zinc sulphate 2 mg/kg body weight 24 h before the experiments were started. Animals were killed by cervical dislocation and the liver was immediately removed and homogenized. Dithiothreitol (DTT) (0, 2.5, 5 or 10 mM, final concentration) and 1 microCi 125I-T4 were added to homogenates. For the in vitro studies, animals were killed by cervical dislocation and the liver removed and added zinc or cadmium (2.5 or 5 mM) plus DTT and labelled T4. Homogenates were incubated for 90 min at 37 degrees C and thereafter chromatographed in Whatman 1 paper. Zinc-injected rats had a significant (P < 0.01) decrease in T4 deiodination and in the generation of iodine (P < 0.02) and T3 (P < 0.05). In the in vitro studies, both zinc and cadmium reduced (P < 0.02) the deiodination of T4, and the generation of iodine (P < 0.02) for zinc and P < 0.05 for cadmium) as well as the generation of T3 (p < 0.05). The NPSH in zinc-injected rats were within normal levels. Serum T4 and T3 in zinc-treated rats were normal, whereas in cadmium-treated rats were both significantly decreased (P < 0.01 for T4 and P < 0.02 for T3). The data indicate that zinc blocks the activity of liver 5-deiodinase through a mechanism probably related to its binding to the sulfhydryl groups of the enzyme.

Changes induced by zinc on thyroxine deiodination by rat liver in vivo and in vitro

Se estudió el efecto de la administración in vivo o del agregado in vitro de zinc sobre la deiodinación 5de la tiroxina (T4) por el hígado de rata y sobre la concentración hepática de grupos sulfhidrilos libres (NPSH). Se usaron ratas Wistar macho de 200-240g de peso corporal. A un grupo de 12 ratas se les inyectó i.p. sulfato de zinc 2mg/Kg de peso, 24h antes de iniciar el estudio. Se sacrificaron los animales por dislocación cervical y el hígado fue inmediatamente homogeneizado. Se agregó a los homogenatos dithithreitol (DTT) (0,2.5,5 o 10mM concentración final) y 1ACi de 125I-T4. Para los estudios in vitro en animales sin tratar, se agregó al homogenato de hígado sulfato de zinc o cloruro de cadmio (2.5 o 5mM) más DTT y T4 marcada. Todos los homogenatos fueron incubados durante 90 min a 37ºC y luego cromatografiados en papel Whatman 1. Las ratas inyectadas con zinc tuvieron una disminución significativa (p<0.01) de la deiodinación de T4, de la producción de 125 iodo (P<0.02) y de triiodotironina (T3) (P<0.05). En los estudios in vitro, el agregado de zinc o cadmio disminuyó significativamente la degradación de T4 (P<0.02) y la producción de iodo (P<0.02 para el zinc y P<0.05 para el cadmio) y de T3 (P<0.05). La concentración hepática de NPSH en los animales inyectados con zinc fue normal. La concentración sérica de T4 y T3 en los animales inyectados con zinc fue normal pero en los inyectados con cadmio se redujo significativamente (P<0.01 para T4 y P<0.02 para T3). Los resultados indican que el zinc inhibe la actividad de la 5-deioidnasa hepática, por um mecanismo probablemente relacionado con la unión del metal a los grupos sulfhidrilos de la enzima (AU)

Changes induced by cadmium administration on thyroxine deiodination and sulfhydryl groups in rat liver.

The effects of cadmium on 5'-deiodination of thyroxine (T4) by rat liver and on the hepatic concentration of non-protein sulfhydryl groups (NPSH) were studied in Wistar rats of 200-250 g body weight. A group of ten rats was injected with cadmium chloride (300 micrograms/100 g body weight i.p.) daily for 4 days. Another group of six rats received, in addition, dithiothreitol (DTT; 1 mg/100 g body weight i.p.) daily for the same period. A group of eight normal untreated rats served as control. T4 deiodination was also determined in aliquots of liver from untreated rats, with cadmium (2 or 5 mmol/l) and with or without DTT (0, 2.5, 5 or 10 mmol/l) plus 1 microCi 125I-labelled T4. Hepatic NPSH were measured by a colorimetric method employing dithioldinitrobenzoic acid. Homogenates were incubated for 90 min at 37 degrees C and chromatographed in a tertiary amyl alcohol:hexane:ammonia (2 mol/l) (10:1:12) system. Cadmium-injected rats showed a significant (P < 0.01) decrease in T4 deiodination and in the generation of 125I (P < 0.01) and tri-iodothyronine (T3) (P < 0.02). NPSH were also decreased (P < 0.02). Administration of DTT restored T4 deiodination and NPSH to normal. In-vitro addition of cadmium or DTT to normal rat liver homogenates induced similar effects on the degradation of T4. Serum concentrations of T4 (P < 0.01) and T3 (P < 0.01) declined significantly in cadmium-injected rats, whereas DTT administration failed to normalize serum hormone levels. The data suggest that cadmium may have decreased 5'-deiodinating activity through binding to sulfhydryl groups of 5'-deiodinase as it does in other enzymes.(ABSTRACT TRUNCATED AT 250 WORDS)

Serum levels of vitamin A in Parkinson's disease.

To elucidate a possible role of vitamin A in the pathogenesis of Parkinson's disease (PD) we compared serum levels of retinol (vitamin A), measured by HPLC, and the vitamin A/retinol binding protein (RBP) ratio of 42 PD patients (22 males and 20 females, mean age 67.3 +/- 1.34 years) and their respective spouses as control group (20 males and 22 females, mean age 66.2 +/- 1.42). The serum levels of vitamin A did not differ significantly between the 2 groups (0.59 +/- 0.03 microgram/dl for PD patients and 0.57 +/- 0.03 microgram/dl for controls), nor did the vitamin A/RBP ratio (0.87 +/- 0.04 and 0.82 +/- 0.03, respectively). There was no influence of antiparkinsonian therapy on vitamin A or vitamin A/RBP ratio. Serum levels of vitamin A, and vitamin A/RBP ratio did not correlate with age, age at onset, scores of the Unified Parkinson's Disease Rating Scale or the Hoehn and Yahr staging in the PD group. These results suggest that serum concentrations of vitamin A, do not play a role in the pathogenesis of PD.

Serum levels of alpha-tocopherol (vitamin E) in Parkinson's disease.

To elucidate the possible role of vitamin E in the pathogenesis of Parkinson's disease (PD), we compared serum levels of alpha-tocopherol (vitamin E), measured by high-performance liquid chromatography, and the vitamin E/cholesterol ratio of 42 Parkinson's disease (PD) patients using their spouses as the control group. The serum levels of vitamin E did not differ significantly between the groups (13.84 +/- 0.56 micrograms/ml for PD and 14.80 +/- 0.57 micrograms/ml for controls), nor did the vitamin E/cholesterol ratio (0.64 +/- 0.03 for both groups). There was no influence of antiparkinsonian therapy on vitamin E or the vitamin E/cholesterol ratio. Serum levels of the vitamin E and vitamin E/cholesterol ratio did not correlate with age, age at onset, scores of the Unified Parkinson's Disease Rating Scale or the Hoehn and Yahr staging in the PD group. These results suggest that serum vitamin E concentrations do not play a role in the pathogenesis of PD.

Serum lipid peroxides in patients with Parkinson's disease.

To elucidate whether high serum lipid peroxidation rates may increase the risk of developing Parkinson's disease (PD), we assessed serum levels of malondialdehyde (MDA), an intermediate in lipid peroxidation processes, in 37 PD patients, with their spouses as the control group. Serum MDA levels did not differ significantly between these two groups (8.7 +/- 0.51 and 8.8 +/- 0.48 nmol/ml, resp.), and were not influenced by antiparkinsonian therapy in the PD patients. Serum MDA levels were inversely correlated with age and age at onset (P less than 0.01) in the PD group, but they were not correlated with disease duration, Unified Parkinson's Disease Rating Scale scores or Hoehn and Yahr staging. In the control group there was no correlation between serum MDA and age. These results suggest that, although serum levels of lipid peroxides were similar in both the PD and control groups, high serum lipid peroxidation rates might constitute a risk factor for younger onset of PD in predisposed individuals.

[Neuro-psychological disorders in hypothyroid dementia. Description of case]. / Trastornos neuropsicológicos de la demencia hipotiroidea. Descripción de un caso.

Hypothyroidism is one of the most frequent causes of treatable symptomatic dementia. However a detailed description of its neuropsychologic characteristics in the medical literature is lacking. We have studied a 70 year old patient suffering severe mental deterioration, cerebellopathy, myopathy and hypothyroidism with a complete set of neuropsychologic and psychometric tests: mental mini-examination, Blessed's scale, neuropsychologic examination, WAIS, Bento visual retention test, Rey's picture, words learning, delayed recall of words, verbal fluency, reaction times and maintained attention. This type of dementia is characterized by a low score in all tests which improves progressively with the treatment and it is also accompanied by a lack of language defects, nonconstructive apraxia or agnosia. The recovery involves the attentional field and the memory as well as the two intelligence indices. However this improvement is more apparent in the tests related to attention and visuospatial information processing. It is concluded that hypothyroid dementia in this patient had characteristics "subcortical dementia" and a neuropsychologic deterioration pattern rather nonspecific with a slight predominance of the attentional and visuospatial defects.