Quality of life in patients with mild Alzheimer disease: the mediator role of mindfulness and spirituality.

OBJECTIVES: This study examined the mediator role of mindfulness and spirituality in the relationship between psychological morbidity, awareness of the disease, functionality, social support, family satisfaction, and quality of life (QoL) in patients with mild AD. METHOD: The sample consisted of 128 patients who answered the Cognitive and Affective Mindfulness Scale-Revised (CAMS-R), the Assessment Scale of Psychosocial Impact of the Diagnosis of Dementia (ASPIDD), the Hospital Anxiety and Depression Scales (HADS), the Satisfaction with Social Support Scale (SSSS), the Family Satisfaction Scale (FSS), the Spiritual and Religious Attitudes in Dealing with Illness (SpREUK), the Index of Barthel, and the Quality of Life-Alzheimer's Disease (QoL-AD). RESULTS: Mindfulness and spirituality mediated the relationship between functionality, awareness of the disease, family satisfaction and QoL. Psychological morbidity had a direct negative impact on QoL and was negatively associated with awareness of the disease, family satisfaction and social support. Mindfulness was negatively associated with spirituality and the latter was negatively associated with QoL. More social support was associated with greater awareness of the disease and family satisfaction. More functionality, awareness of the disease and family satisfaction contributed to more QoL and this relationship was mediated by mindfulness and spirituality. CONCLUSION: Interventions directed at the promotion of the QoL of patients with mild AD should focus on the promotion of mindfulness skills in AD patients, in addition to the reduction of psychological morbidity and the promotion of functionality, awareness of the disease, family relationships and social support.

Huntington's Disease: Premotor Phase.

Huntington's disease (HD) is an incurable, neurodegenerative disease, which manifests via a triad of progressive symptoms: motor impairment, psychiatric disorders, and cognitive decline. Conventionally, the HD diagnosis is based on the presence of involuntary choreiform movements and a positive genetic test for the CAG-expanded allele gene. Although the diagnosis focuses on the motor part of the triad, there is increasing evidence that both cognitive and neuropsychiatric symptoms can, and often do, present decades before the onset of motor symptoms. In this paper, we review the evidence regarding the symptoms in the HD premotor phase and summarize the most relevant and robust studies in the last few years. Regarding neuropsychiatric symptoms, higher levels of depression, anxiety, apathy, irritability, psychosis, disinhibition, hostility, and sleeping problems were found. In terms of cognition, there was impairment in attention, working memory, episodic memory, language, recognition of facial emotions, empathy, and theory of mind. These early symptoms of HD can be very debilitating and are often disregarded by doctors. It is necessary to acknowledge them so that they can be treated or alleviated. Moreover, an earlier diagnosis can lead to the implementation of neurodegenerative prevention therapies, which may slow the progression of the disease and prolong overall functioning. This will improve the patient's independence and their quality of life.

Spectral-Domain Optical Coherence Tomography as a Potential Biomarker in Huntington's Disease.

BACKGROUND: Spectral-domain optical coherence tomography has been used in several neurological conditions, and peripapillary and macular measurements have been proposed as potential biomarkers in these disorders. The aim of this study was to investigate retinal and choroidal changes in Huntington's disease and to evaluate any potential correlation with the stage of the disease. METHODS: A cross-sectional observational study compared patients with Huntington's disease and controls. Patients were evaluated using the Unified Huntington's Disease Rating Scale. Spectral-domain optical coherence tomography with enhanced depth imaging was used, and peripapillary choroidal and retinal nerve fiber layer thickness and macular retinal and choroidal thickness were evaluated. RESULTS: Fifteen eyes of 8 patients and 16 eyes of 8 sex-, age-, and mean refractive error-matched healthy controls were included. Average (231.3 ± 52.8 vs 296.2 ± 57.1, P = 0.033), central (341.8 ± 70.5 vs 252.0 ± 57.9, P = 0.015), and inferior (225.3 ± 57.9 vs 313.8 ± 55.2, P = 0.007) macular choroidal thickness were significantly reduced in patients, in comparison with controls. No differences were observed in macular retina or peripapillary retinal and choroidal measurements. However, there was a negative correlation between Total Motor Score of the Unified Huntington's Disease Rating Scale and average (r(2) = 0.585, P = 0.027), superior (r(2) = 0.653, P = 0.015), nasal (r(2) = 0.642, P = 0.017), and inferior (r(2) = 0.574, P = 0.029) macular retinal thickness. CONCLUSIONS: Our results suggest that both the choroidal and retinal macula are altered in Huntington's disease and may become useful biomarkers for monitoring neurodegeneration in this disease. The involvement of the choroid may also support the recent findings of vascular involvement in Huntington's disease.

Standardized evaluation of algorithms for computer-aided diagnosis of dementia based on structural MRI: the CADDementia challenge.

Algorithms for computer-aided diagnosis of dementia based on structural MRI have demonstrated high performance in the literature, but are difficult to compare as different data sets and methodology were used for evaluation. In addition, it is unclear how the algorithms would perform on previously unseen data, and thus, how they would perform in clinical practice when there is no real opportunity to adapt the algorithm to the data at hand. To address these comparability, generalizability and clinical applicability issues, we organized a grand challenge that aimed to objectively compare algorithms based on a clinically representative multi-center data set. Using clinical practice as the starting point, the goal was to reproduce the clinical diagnosis. Therefore, we evaluated algorithms for multi-class classification of three diagnostic groups: patients with probable Alzheimer's disease, patients with mild cognitive impairment and healthy controls. The diagnosis based on clinical criteria was used as reference standard, as it was the best available reference despite its known limitations. For evaluation, a previously unseen test set was used consisting of 354 T1-weighted MRI scans with the diagnoses blinded. Fifteen research teams participated with a total of 29 algorithms. The algorithms were trained on a small training set (n=30) and optionally on data from other sources (e.g., the Alzheimer's Disease Neuroimaging Initiative, the Australian Imaging Biomarkers and Lifestyle flagship study of aging). The best performing algorithm yielded an accuracy of 63.0% and an area under the receiver-operating-characteristic curve (AUC) of 78.8%. In general, the best performances were achieved using feature extraction based on voxel-based morphometry or a combination of features that included volume, cortical thickness, shape and intensity. The challenge is open for new submissions via the web-based framework: http://caddementia.grand-challenge.org.

Weight variation before and after surgery in Parkinson's disease: a noradrenergic modulation?

Changes in the nutritional profile of patients with Parkinson's disease have been reported before and after deep brain stimulation surgery. The major determinants of the weight variation in Parkinson's disease are not yet understood, and the mechanism seems complex. Based on the influence of the sympathetic nervous system in metabolic syndrome obesity, the intent of the present review is to consider the role of noradrenergic modulation on weight variations in Parkinson's disease. In this review the authors raise the following hypothesis: weight variation in Parkinson's disease before and after deep brain stimulation of the subthalamic nucleus could be influenced by noradrenergic interaction between the locus coeruleus, subthalamic nucleus, and hypothalamic nucleus.

Repeated Clinical Assessment Using Sensory Modality Assessment and Rehabilitation Technique for Diagnosis in Prolonged Disorders of Consciousness.

Purpose: The recommended way to assess consciousness in prolonged disorders of consciousness is to observe the patient's responses to sensory stimulation. Multiple assessment sessions have to be completed in order to reach a correct diagnosis. There is, however, a lack of data on how many sessions are sufficient for validity and reliability. The aim of this study was to identify the number of Sensory Modality Assessment and Rehabilitation Technique (SMART) assessment sessions needed to reach a reliable diagnosis. A secondary objective was to identify which sensory stimulation modalities are more useful to reach a diagnosis. Materials and Methods: A retrospective analysis of all the adult patients (who received a SMART assessment) admitted to a specialist brain injury unit over the course of 4 years was conducted (n = 35). An independent rater analyzed the SMART levels for each modality and session and provided a suggestive diagnosis based on the highest SMART level per session. Results: For the vast majority of patients between 5 and 6 sessions was sufficient to reach the final clinical diagnosis. The visual, auditory, tactile, and motor function modalities were found to be more associated with the final diagnosis than the olfactory and gustatory modalities. Conclusion: These findings provide for the first time a rationale for optimizing the time spent on assessing patients using SMART.

Lacsogram: A New EEG Tool to Diagnose Alzheimer's Disease.

This work proposes the application of a new electroencephalogram (EEG) signal processing tool - the lacsogram - to characterize the Alzheimer's disease (AD) activity and to assist on its diagnosis at different stages: Mild Cognitive Impairment (MCI), Mild and Moderate AD (ADM) and Advanced AD (ADA). Statistical analyzes are performed to lacstral distances between conventional EEG subbands to find measures capable of discriminating AD in all stages and characterizing the AD activity in each electrode. Cepstral distances are used for comparison. Comparing all AD stages and Controls (C), the most important significances are the lacstral distances between subbands θ and α ( p = 0.0014 0.05). The topographic maps show significant differences in parietal, temporal and frontal regions as AD progresses. Machine learning models with a leave-one-out cross-validation process are applied to lacstral/cepstral distances to develop an automatic method for diagnosing AD. The following classification accuracies are obtained with an artificial neural network: 95.55% for All vs All, 98.06% for C vs MCI, 95.99% for C vs ADM, 93.85% for MCI vs ADM-ADA. In C vs MCI, C vs ADM and MCI vs ADM-ADA, the proposed method outperforms the state-of-art methods by 5%, 1%, and 2%, respectively. In All vs All, it outperforms the state-of-art EEG and non-EEG methods by 6% and 2%, respectively. These results indicate that the proposed method represents an improvement in diagnosing AD.

Suicide attempts after subthalamic nucleus stimulation for Parkinson's disease.

A higher risk of suicidal attempt after subthalamic nucleus deep brain stimulation (STN-DBS) for Parkinson's disease (PD) has been consistently reported. We retrospectively analyzed 3 PD patients with suicide attempts after STN-DBS. All patients had normal pre- and immediate postoperative psychopathological and cognitive evaluations, with STN-DBS yielding a good motor benefit. Levodopa medication was markedly reduced. Albeit there was a significant reduction in dopaminergic medication, there was also a considerable time lag to suicide attempt. Impulsive behavior could have played a higher role, going unnoticed in punctual psychopathological examinations. STN-DBS patients need a closer postoperative psychiatric and behavioral follow-up.

[Genetic Study of Primary Dystonias: Recommendations from the Centro Hospitalar São João Neurogenetics Group]. / Estudo Genético nas Distonias Primárias: Recomendações do Grupo de Neurogenética do Centro Hospitalar São João.

The primary dystonias are a particular group of dystonias of presumed genetic origin, with a wide age of onset and variable progression. The diagnosis is, therefore, a challenge and the issue of the genetic investigation presents frequently in clinical practice. In the past few years several gene mutations have been identified as causative of primary dystonias. The choice of molecular testing is complex, given the clinical specificities and low frequency of these entities and the cost of genetic testing. It must follow observation by specialized clinicians highly differentiated in this area and be supported by a rational plan of investigation. The Centro Hospitalar São João Neurogenetics Group, a multidisciplinary team of Neurologists and Geneticists with special interest in neurogenetic disorders, devised consensus recommendations for the investigation of the genetic etiology of the primary dystonias, based on international consensus documents and recent published scientific evidence. This manuscript adopts the new classification system for genetic movement disorders, allowing for its systematic and standardized use in clinical practice.

As distonias primárias são um grupo particular de distonias, de etiologia presumivelmente genética e com sintomas que podem surgir em diversas idades e progredir durante um período variável de tempo. O seu diagnóstico constitui, por isso, um desafio, colocando-se frequentemente na prática clínica a questão da realização do estudo genético. Nos últimos anos foram identificadas várias mutações genéticas causadoras de distonia primária. A escolha do teste molecular é complexa, quer pela especificidade clínica e baixa frequência, quer pelo custo associado ao estudo genético. Esta escolha deve ser feita mediante observação especializada por médicos com elevada diferenciação nesta área, apoiada num plano racional de investigação. O Grupo de Neurogenética do Centro Hospitalar São João (grupo multidisciplinar de Neurologistas e Geneticistas com interesse especial na área das doenças neurogenéticas) delineou recomendações de consenso para a investigação da etiologia genética das distonias primárias, tendo por base documentos de consenso internacionais e a evidência científica entretanto publicada. Este documento adota o novo sistema de nomenclatura para as formas genéticas de doenças do movimento, permitindo a sua utilização padronizada e sistemática na prática clínica.

[Investigation of Genetic Etiology in Neurodegenerative Dementias: Recommendations from the Centro Hospitalar São João Neurogenetics Group]. / Investigação de Etiologia Genética nas Demências Neurodegenerativas: Recomendações do Grupo de Neurogenética do Centro Hospitalar São João.

In the past few years several gene mutations have been identified as causative of the most frequent neurodegenerative dementias (Alzheimer disease and frontotemporal dementia). These advances, along with the complex phenotype-genotype relationships and the costs associated with genetic testing, have often made it difficult for clinicians to decide with regard to a rational plan for the investigation of the genetic etiology of the degenerative dementias. The Centro Hospitalar São João Neurogenetics Group, a multidisciplinary team of Neurologists and Geneticists with special interest in neurogenetic disorders, devised consensus recommendations for the investigation of the genetic etiology of Alzheimer disease and frontotemporal dementia in clinical practice, based on international consensus documents (currently containing partly outdated information) and published scientific evidence on this topic. Alzheimer disease may be caused by mutations in PSEN1, PSEN2 and APP. APOE genotyping is not recommended for the diagnostic or genetic counseling purposes in Alzheimer disease. Frontotemporal dementia may be caused by mutations in several genes such as c9orf72, PGRN, MAPT, TBK1, VCP, SQSTM1, and UBQLN2. This paper pragmatically approaches the process of genetic diagnosis in Alzheimer disease and frontotemporal dementia, with specific recommendations for both disorders.

Nos últimos anos foram identificadas várias mutações genéticas causadoras das demências neurodegenerativas mais frequentes (doença de Alzheimer e demência fronto-temporal). Estes avanços, em conjunto com a complexidade das relações entre genótipo e fenótipo, e os próprios custos associados ao processo de diagnóstico genético, tornaram por vezes difícil aos clínicos a escolha de um plano racional para a investigação da etiologia genética das demências neurodegenerativas. O Grupo de Neurogenética do Centro Hospitalar, grupo multidisciplinar de Neurologistas e Geneticistas com interesse especial na área das doenças neurogenéticas, delineou recomendações de consenso para a investigação da etiologia genética da doença de Alzheimer e demência fronto-temporal na prática clínica, tendo por base documentos de consenso internacionais (contendo atualmente informação parcialmente desatualizada) e a evidência científica publicada sobre este tópico. A doença de Alzheimer pode ser causada por mutações nos genes PSEN1,PSEN2 e APP. Não é recomendada a genotipagem da APOE para o diagnóstico ou aconselhamento genético na doença de Alzheimer. A demência fronto-temporal pode ser causada por mutações em vários genes como c9orf72, PGRN, MAPT, TBK1, VCP, SQSTM1 e UBQLN2. Este documento aborda de forma pragmática o processo utilizado para o diagnóstico genético da doença de Alzheimer e demência fronto-temporal, com recomendações específicas para ambas as situações.

Medication adherence in Alzheimer's disease: The mediator role of mindfulness.

BACKGROUND: Medication adherence is often assessed based on compliance to the dosage and frequency of physician's prescription. Cognitive impairment is one of the biggest barriers in elderly patients with Alzheimer's disease (AD), who are usually polymedicated with different oral drugs. Transdermal drug delivery, also requires mobility abilities, reinforcing the role of patients' caregivers. OBJECTIVE: To evaluate the relationship between psychological variables such as social support, family satisfaction, psychological morbidity, awareness of the disease, coping, mindfulness and medication adherence, in patients with AD, taking in consideration the patient's perspective. DESIGN: Cross-sectional and quantitative study including 128 patients with mild AD. RESULTS: Medication adherence showed a positive relationship with social support, mindfulness, family satisfaction and awareness of the disease. Mindfulness was a mediator in the relationship between awareness of the disease and medication adherence. CONCLUSIONS: This study reinforces the importance of psychological assessment in medication adherence in mild AD patients, specially the role of mindfulness. Intervention programs to promote mindfulness may have a potential dual benefit, preserving cognitive skills and promoting medication adherence.

Predictors and Moderators of Quality of Life in Alzheimer's Disease Patients.

BACKGROUND: Alzheimer's disease (AD) is a chronic degenerative disease leading to global cognitive and functional decline. Quality of Life (QOL) is an important variable in the effectiveness of intervention programs in dementia. OBJECTIVE: This study analyzed the relationships between gender, psychological variables and QOL, the predictors of QOL, and the role of spirituality as a moderator between functionality and QOL. METHOD: A cross-sectional study was conducted with 128 patients with mild AD. RESULTS: Being a male, good social support, and high functionality were significant predictors of better QOL. Spirituality was a moderator in the relationship between functionality and QOL. CONCLUSION: These results reinforce the importance of gender, psychological morbidity, social support, and functionality, with special emphasis on the role of spirituality, regarding intervention programs that promote QOL, in patients with mild AD.

Molecular diagnosis of Huntington disease in Portugal: implications for genetic counselling and clinical practice.

Huntington disease (HD) is a neurodegenerative, autosomal dominant disorder of late-onset, caused by the expansion of a CAG repeat in the coding region of the gene. Ours is the reference laboratory for genetic testing in HD, in Portugal, since 1998; 90.1% of all 158 families known were identified for the first time, including patients with unusual presentation or without family history. A total of 338 genetic tests were performed: 234 for diagnosis, 96 for presymptomatic and four for prenatal testing (four were done for family studies). Most referring physicians were neurologists (90.6%); 82.8% of all clinical diagnosis were confirmed, while 83.1% of those sent for exclusion were in fact excluded. In presymptomatic testing, an excess of female subjects (59.4%) was again verified; 37.5% of the consultands were found to be carriers. None of the foetuses, in four prenatal tests, were mutation carriers. One juvenile case was inherited from her mother. Our patient population is very similar to others described so far, namely in terms of mean age at onset and (CAG)(n) distribution, except perhaps for a higher frequency of large normal (class 2) alleles (3.7%). We also identify cases posing particular problems for genetic counselling, such as, 'homozygosity' that can pose a serious ethical dilemma, carriers of large normal alleles, and 'homoallelism' for a normal gene, which will demand further procedures and may delay results in presymptomatic and prenatal testing.

[Imaging in Parkinson disease surgery]. / A imagem na cirurgia da doença de Parkinson.

Parkinson's disease is a progressive degenerative disease of the central nervous system frequently becoming motor disabling. Deep brain stimulation is one more therapeutic option. The authors describe the different steps of this therapeutic procedure with detail on imaging protocol to the precise and exact targeting of subthalamic nucleus. MR and CT imaging on stereotactic conditions are the imaging support to the determination of the anatomic target allowing also the choose of trajectory for the surgical procedure. Neurophysiologic exploration and clinical evaluation during the surgery give us the functional target. Deep brain stimulation has been revealing as a safe and effective therapy on some cases of Parkinson's disease with a significant improvement on quality of life of those patients. The brain imaging is a fundamental tool on target determination.

Deep brain stimulation of the subthalamic nucleus in advanced Parkinson's disease: five year follow-up at a Portuguese center.

INTRODUCTION: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) in Parkinson's disease (PD) is safe and effective. Most series report stable long-term motor responses. AIM: To report the long-term outcome of STN-DBS in advanced stage PD patients at a Portuguese center. PATIENTS AND METHODS: Motor status was evaluated before surgery ('off' medication and best 'on'), post-operatively, and at five years ('on' medication and stimulation) using UPDRS part III. Axial symptoms subscores were quantified. Disability was assessed with the modified Rankin Scale (mRS). Development of dementia was assessed at 6 months and five years post-DBS. RESULTS: Of the 183 patients submitted to STN-DBS, 71 had completed 5 years of follow-up. Ten patients were not included: two died (cancer, myocardial infarction), five were lost to follow-up and three had their stimulation systems removed. Motor function improved by 78% and 66% postoperatively and at five years, respectively. There was improvement of axial symptoms postoperatively, with significant worsening at five years (p<0.001). mRS scores improved postoperatively, but declined at five years, although most patients (88.5%) remained ambulatory (mRS<4). One patient (1.6%) and 19 patients (31,2%) were demented at 6 months and 5 years, respectively. Patients who developed dementia were significantly older than non-demented patients (56.5±7.8 vs 63.7±5.9 years-old; p<0.001). CONCLUSIONS: In this series STN-DBS proved its efficacy regarding motor symptom improvement even five years after the procedure. Deterioration of axial symptoms and disability, as well as new onset dementia were observed in this period, but the possible role of STN-DBS as a causative factor is yet to be defined.

TITLE: Estimulacion cerebral profunda del nucleo subtalamico en la enfermedad de Parkinson avanzada: seguimiento de cinco años en un centro portugues.Introduccion. La estimulacion cerebral profunda (ECP) del nucleo subtalamico (NST) en la enfermedad de Parkinson (EP) es segura y eficaz: en la mayoria de series se describen respuestas motoras duraderas y estables. Objetivo. Informar sobre el desenlace a largo plazo de la ECP del NST en pacientes con EP avanzada atendidos en un centro hospitalario portugues. Pacientes y metodos. El estado motor se valoro con la escala unificada de valoracion de la enfermedad de Parkinson, parte III, antes de la intervencion quirurgica ­en dos situaciones: sin efecto de la medicacion (off) y bajo el mejor efecto (on)­, en el postoperatorio y al cabo de cinco años (medicacion y estimulacion en on). Se cuantificaron las puntuaciones de cada sintoma axial. La incapacidad se evaluo con la escala de Rankin modificada (mRS). La aparicion de demencia se valoro seis meses y cinco años despues de la ECP. Resultados. Setenta y uno de los 183 pacientes sometidos a la ECP del NST concluyeron los cinco años de seguimiento. Diez de ellos quedaron excluidos: dos por fallecimiento (cancer e infarto de miocardio), cinco por perdida de seguimiento y tres por la retirada del sistema de estimulacion. La funcion motora manifesto una mejora del 78% en el postoperatorio y del 66% a los cinco años. En el postoperatorio se aprecio mejoria de los sintomas axiales, pero al cabo de los cinco años habian empeorado de manera significativa (p < 0,001). Las puntuaciones de la mRS tambien mejoraron en el postoperatorio, pero a los cinco años tambien habian disminuido, pese a que la mayoria (88,5%) conservaba la capacidad ambulatoria (mRS < 4). Un paciente (1,6%) manifesto demencia a los seis meses, mientras que otros 19 (31,2%) la manifestaron al cabo de los cinco años. La edad de los pacientes dementes era notablemente mayor (56,5 ± 7,8 frente a 63,7 ± 5,9 años; p < 0,001). Conclusiones. En esta serie de casos, la ECP del NST demostro su eficacia en la mejora de los sintomas motores, aunque habian transcurrido cinco años desde la implantacion. En ese periodo hubo un deterioro de los sintomas axiales y de la incapacidad, y surgieron casos de demencia, pero el posible papel de la ECP del NST como factor causal resta pendiente de concretar.

Not all sounds sound the same: Parkinson's disease affects differently emotion processing in music and in speech prosody.

Does emotion processing in music and speech prosody recruit common neurocognitive mechanisms? To examine this question, we implemented a cross-domain comparative design in Parkinson's disease (PD). Twenty-four patients and 25 controls performed emotion recognition tasks for music and spoken sentences. In music, patients had impaired recognition of happiness and peacefulness, and intact recognition of sadness and fear; this pattern was independent of general cognitive and perceptual abilities. In speech, patients had a small global impairment, which was significantly mediated by executive dysfunction. Hence, PD affected differently musical and prosodic emotions. This dissociation indicates that the mechanisms underlying the two domains are partly independent.

Locus coeruleus is involved in weight loss in a rat model of Parkinson's disease: an effect reversed by deep brain stimulation.

INTRODUCTION: In Parkinson's disease (PD) weight loss is a secondary phenomenon to the progressive neurodegeneration that changes after deep brain stimulation of the subthalamic nucleus (DBS-STN) leading to increased weight gain. The mechanism responsible for this profile in weight variation may be secondary to a central metabolic control influenced by the noradrenergic system. In this study authors evaluate the effect of additional noradrenergic neuronal degeneration, namely of the locus coeruleus (LC), on weight variation in the 6-hydroxydopamine (6-OHDA) rat model of PD. MATERIAL AND METHODS: An experimental group of parkinsonian animals with additional 6-OHDA lesion of the LC was developed to analyze the effect of this lesion on the metabolic state of rats before and after DBS-STN. Rats were placed in metabolic cages for evaluation of weight, food and liquid intake and urine and fecal volume, before and after DBS-STN. The effects of 6-OHDA lesions and DBS-STN on motor behavior were also monitored. Tissue levels of monoamines in the striatum of 6-OHDA-lesioned animals and catecholamine levels in urine and plasma were evaluated. RESULTS: In the experimental group of Parkinsonian animals with 6-OHDA degeneration of the striatum alone, no effects on weight gain, food intake and other metabolic parameters were observed before or after DBS-STN. Additional lesion of the LC produced a significant decrease in weight gain with a trend toward a decrease in solid intake. Chronic DBS-STN in rats with LC and striatum degeneration abolished the weight loss without producing changes to food intake and other metabolic parameters. Additional degeneration of the LC was not accompanied by significant changes in motor behavior but produced an additional decrease in striate monoamines levels namely a decrease in the DA/l-DOPA ratio. CONCLUSIONS: In PD degeneration of noradrenergic neurons, in particular of the LC, may be required to observe side effects unrelated to motor symptoms such as body weight deregulation. Our results support the notion that the LC may be important in maintaining the activity of the nigrostriatal dopamine pathways, and thus play a crucial role in weight variation in a PD.