Relationship between dysphagia and depressive states in patients with Parkinson's disease

Aspiration pneumonia related to dysphagia is known to be the leading cause of death in patients with Parkinson's disease (PD). We investigated the relationship between depressive states and dysphagia in patients with PD. A hundred and twenty-seven PD patients gave their informed consent and were enrolled in this study. We used the Beck Depression Inventory (BDI) questionnaire to determine the participants' depressive states, and also used a questionnaire to assess participants' state of dysphagia. Participants were divided into four groups according to their BDI score. We compared the PD patients with Swallowing Disturbances Questionnaire (SDQ) scores of more than or equal to 11 with the SDQ scores of less than 11 regarding depressive categories. A logistic regression analysis was conducted to calculate odds ratios (ORs) and their 95% confidence intervals (95%CI) adjusting for age, sex, disease duration, wearing-off phenomenon and severity of movement disorder. OR (95%CI) of depressive categories, in which the trivial class was set as a reference group, were 3.28 (0.93-11.55), 13.44 (3.10-58.16), 30.35 (5.65-162.97) in the mild class, the moderate class and the severe class, respectively. This study suggests that there may be a strong relationship between depressive states and dysphagia in patients with PD.     

Bickerstaff's brainstem encephalitis -- an analysis of clinical and MRI findings

BACKGROUND AND PURPOSE: Bickerstaff's brainstem encephalitis (BBE) is a very uncommon central nervous system disease. Its etiology remains unknown but it is postulated that BBE has an autoimmunologic origin. BBE is characterized by acute ophtalmoplegia, ataxia, pyramidal paresis and disturbance of consciousness. A special pattern of changes in magnetic resonance imaging (MRI) is characteristic of BBE. Lesions are located mainly in the brainstem. The aim of this paper is to analyze the clinical course and MRI changes in our own cases of BBE. MATERIAL AND METHODS: We have analyzed medical records, clinical findings and MRI images of the patients with BBE diagnosis established in our Department of Neurology in the years 1998-2004. RESULTS: During that period 4 cases of BBE were diagnosed with clinical sings of acute brainstem lesion and MRI imaging suggestive of BBE. In our patients we have observed ophtalmoplegia, ataxia, disturbances of consciousness and pyramidal signs. Two patients had a monophasic and 2 remitting-relapsing course of the disease. In all four cases we have seen on T2-weighted images large, irregular hyperintense lesions in the brainstem, especially in the pons, midbrain and medulla, but also in one case in the thalamus and vermis of the cerebellum. Patients were treated with steroids, plasmapheresis or acyclovir or a combination of these methods. We observed a complete recovery in two cases and significant improvement in the other two lasting more than two years confirming a relatively good prognosis in BBE. CONCLUSIONS: BBE despite severe initial presentation usually has a good prognosis. MRI plays critical role in the diagnosis of BBE.     

Plasma free cortisol in depressive illness--a review of findings and clinical implications

Measurements of a variety of parameters of biologically active cortisol indicate that a small number of patients with depressive illness have significantly elevated levels of unbound plasma cortisol. Abnormalities in corticosteroid binding globulin do not account for the hypercortisolemia, and elevated urinary levels of free cortisol confirm the data obtained for plasma free cortisol. Direct measurements of free cortisol suggest that the absence of physical effects of cortisol in patients with depression is related to the very mild elevation in plasma levels of free cortisol in these patients and that high levels are not sustained throughout the day as they are in patients with pathologic glucocorticoid excess. The apparent discrepancy between elevated total cortisol levels and the mild elevation of unbound plasma cortisol is best explained by the generous binding capacity of corticosteroid binding globulin. Total cortisol levels of greater than 25 micrograms/dl are necessary to saturate the binding sites of corticosteroid binding globulin. Only then can free cortisol be detected in plasma. Although these studies suggest that unbound plasma cortisol is elevated, whether these levels represent biologically active cortisol in other tissue sites as well, particularly the central nervous system, is still unclear. It is well accepted that discrete binding sites for cortisol and dexamethasone occur in hypothalamic and pituitary tissue, but the mechanism of glucocorticoid regulation of these binding sites has not been elucidated. Cortisol levels in cerebrospinal fluid correspond closely to plasma levels of unbound cortisol. Ruf and Steiner have shown that corticosteroid responsive neurons are present in the periventricular gray matter of the third ventricle, where other investigators have identified active ependymal transport mechanisms for cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)     

Echogenicity of the brainstem raphe in patients with major depression

A novel transcranial ultrasound technique was used to detect differences in the echogenicity and echotexture of the brainstem dorsal raphe nucleus in 20 patients with major depression compared with 20 age- and sex-matched healthy adults. Transcranial color-coded real-time sonography visualized the mesencephalic and pontine brainstem and its midline structure. The echogenicity of the raphe was classified in a four-point scale. Compared with healthy subjects, the depressed patients were characterized by a significant decrease in the echogenicity of the brainstem raphe. The echogenicity score was not correlated, however, with measures of psychopathology such as the Hamilton Rating Scale for Depression, the Clinical Global Impression Scale, the Global Assessment Scale, or the Depression Scale of von Zerssen. These preliminary findings suggest that the brainstem raphe may be involved in the etiopathogenesis of major depression. The echogenicity score should be further evaluated as a possible trait marker in different types of affective disorders.     

Relationship of substantia nigra echogenicity and motor function in elderly subjects

BACKGROUND: Patients with Parkinson's disease (PD) exhibit an increased echogenicity of the substantia nigra (SN) on transcranial sonography. Some healthy adults with the same echo characteristics showed a reduced 18fluorodopa uptake on PET, indicating a subclinical alteration of the nigrostriatal system. OBJECTIVES: To determine whether the sonographic phenotype of hyperechogenic SN has any relevance for motor function in elderly subjects and whether an increased echogenicity of the SN is associated with an impaired motor function. METHOD: In a population-based, cross-sectional study, 93 subjects older then 60 years without history of extrapyramidal disorder underwent sonographic and neurologic examinations, with a quantitative motor assessment. RESULTS: Elderly healthy subjects without prediagnosed extrapyramidal disorder but with SN hyperechogenicity had more frequent and more severe parkinsonian symptoms and a slower finger tapping than those with a regular echogenicity of the SN (p < 0.05, U test). CONCLUSION: With increasing age, subjects with SN hyperechogenicity develop a more substantial slowing of movements than subjects without this echo pattern, stressing the functional relevance of this sonographic finding. The authors speculate that hyperechogenicity of the SN may be detected by transcranial sonography early in life and may serve as a risk marker for nigral injury, although only a minority of these subjects will develop the full clinical picture of PD.     

貌似大脑半球病变的脑干梗死临床和影像分析

目的　分析貌似大脑半球病变的脑干梗死的临床和影像学特点及临床定位错误的原因。方法　连续1年观察发病 6h内收治的首发脑梗死 118例 ,先行OCSP(theOxfordshirecommunitystrokeproject)分型、NIHSS评分 (thenationalinstitutesofhealthstrokescale)和超早期头颅CT平扫 ,再结合 72h内的头颅MR筛出貌似大脑半球病变的脑干梗死。结果　 118例中首诊分型 5 0例为腔隙梗死 ,其中 4 4例行MR复查并证实貌似大脑半球病变的脑干梗死 12例。头颅CT均未检出脑干病灶 ,MR准确检出了脑干责任灶。病灶多在脑桥的三叉神经根平面、脑桥旁正中动脉的血供分布区。 11例病灶小于 2 0mm ,呈纵向条状、片状。结论　早期行MR有助于明确诊断貌似大脑半球病变的脑干梗死。对有糖尿病病史、起病有头晕、临床呈单纯运动性轻偏瘫或单纯性偏瘫的LACI,要注意其病灶有可能在脑干。     

More tryptophan hydroxylase in the brainstem dorsal raphe nucleus in depressed suicides

Deficient serotonin neurotransmission in suicide is indicated by reduced brainstem serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA), fewer 5-HT(1A) autoreceptors and reduced cortical serotonin transporter binding in suicide victims. Tryptophan hydroxylase (TPH) is the rate-limiting enzyme in the synthesis of 5-HT, and alterations in TPH could explain some of these findings. We sought to determine the amount of TPH immunoreactivity (TPH-IR) in the dorsal (DRN) and median (MRN) raphe nuclei in suicides and controls. Brainstems of suicide victims and controls (n = 11 pairs) were collected at autopsy, matched for age, sex and postmortem interval, frozen and sectioned (20 microm). Immunoautoradiography, using an antibody to label TPH, was performed, slides exposed to film and autoradiograms quantified by a computer-based image analysis system. We examined sections every 1000 microm throughout the whole length of the nucleus, performing statistical analysis only on those subjects for whom the raphe was complete (n = 8 pairs). TPH-IR (microCi/g) was higher in suicides than controls (S: 300.8 +/- 70.8 vs. C: 259.6 +/- 40.7, t = 2.57, df = 7, P = 0.04) in the dorsal raphe nucleus (DRN), and not different between suicides and controls (S: 251.3 +/- 44.2 vs. C: 235.9 +/- 27.4, t = 1.49, df = 7, P = 0.18) in the MRN. DRN TPH-IR was higher in male suicide victims (MS) compared to male controls (MC; MS: 318.4 +/- 54.4 vs. MC: 271.9 +/- 22.5, t = 2.66, df = 6, P = 0.03). The analysis of TPH-IR area and density at each DRN rostrocaudal levels showed higher area and density in suicides compared to controls in the rostral DRN and lower area and density in the caudal DRN. TPH-IR, an index of the amount of TPH enzyme, in the DRN is higher in depressed suicides. More TPH may be an upregulatory homeostatic response to impaired serotonin release or less autoreceptor activation. Alternatively, the serotonin impairment in suicide may be due to hypofunctional serotonin-synthesizing enzyme.