低颅压综合征12例临床分析

目的 探讨低颅压综合征的临床特点、诊断、治疗及鉴别诊断。方法 回顾性分析12例低颅压综合征患者的临床资料。结果 所有患者均有体位性头痛，卧位时缓解，可伴有恶心、呕吐、耳鸣、眩晕、颈强直；CSF压力均低于60mm H2O，3例患者CSF中有轻中度白细胞增多和蛋白增高；1例患者为血性CSF；12例行头颅CT检查正常；2例头颅MRI示弥漫性硬脑膜增厚。治疗以大剂量补充生理盐水为主，2例腰穿时注入生理盐水治愈。结论 认识低颅压综合征的临床、CSF和MRI表现至关重要，因其极易与蛛网膜下腔出血等相混淆。     

原发性低颅压综合征26例临床分析

目的 探讨原发性低颅压综合征患者的临床特点、诊断、鉴别诊断、影像学改变及治疗.方法 回顾性分析26例原发性低颅压综合征患者的临床表现、脑脊液及影像学改变,对其进行分析.结果 26例患者均有为体位性头痛,侧卧位腰穿脑脊液压力均＜70mmH2O.其中7例为血性脑脊液(2例误穿),5例脑脊液蛋白定量增高.26例均行头部CT平扫,3例脑室、脑沟、脑池变小,其余均正常.9例行头部MRI检查,5例示硬脑膜增厚,3例硬脑膜窦扩张,1例硬脑膜下积液.结论 认识原发性低颅压综合征的临床特点、脑脊液和影像学改变,可提高临床诊断准确性,减少误诊.     

低颅压综合征13例临床分析

目的　探讨低颅压综合征的临床特点、诊断及治疗。方法　回顾性分析 13例低颅压综合征患者的临床资料。结果　本组患者均有体位性头痛、恶心、呕吐 ,伴有眩晕 4例、耳鸣 2例、颈项强直 2例。 9例行腰穿检查 ,脑脊液 (CSF)压力均 <70mmH2 O ,8例患者CSF中红细胞数有不同程度升高 ,1例患者为血性CSF。治疗以大剂量补充生理盐水为主 ,2例腰穿时行CSF置换 ,均痊愈。结论　体位性头痛是低颅压综合征的临床特征 ,腰穿CSF测压检查可确诊。本病一般预后较好。     

原发性低颅压综合征25例临床分析

目的研讨原发性低颅压综合征的临床及脑脊液特点。方法总结分析25例原发性低颅压综合征患者的临床资料。结果所有患者均有体位性头痛或伴有恶心、呕吐、头晕、目眩、颈强直等表现,脑脊液压力均低于70mmH2O,3例患者CSF红细胞增多,4例患者CSF蛋白增高,25例患者中23例头颅CT检查正常,2例双侧脑室系统均匀性缩小,给予大量补液,支持、对症治疗,症状严重者予以鞘内激素注入治疗,症状均消失。结论正确了解原发性低颅压综合征的临床表现,脑脊液特点,并鉴别继发性低颅压综合征。     

低颅压综合征合并颅内静脉血栓形成1例及文献回顾

目的 总结分析低颅压综合征合并颅内静脉系统血栓形成的临床特征、诊断方法及治疗原则.方法 报道1例低颅压综合征合并颅内静脉系统血栓形成病例,并复习相关文献.结果 患者以体位性头痛起病,经腰椎穿刺及影像学检查诊断为低颅压综合征,继发硬膜下积液及颅内静脉系统血栓形成.头颅CT、MRI均可提供低颅压综合征的表现,MRV及全脑血管造影术(DSA)是静脉系统血栓形成的重要诊断手段.结论 低颅压综合征是静脉系统血栓形成的危险因素之一,了解两者的临床特征有利于早期诊断及治疗.     

低颅压综合征50例临床分析

目的:探讨低颅压综合征的病因、临床特点、诊断、鉴别诊断及治疗。方法:总结分析50例低颅压综合征患者的临床资料。结果:所有患者均有体位性头痛,卧位时缓解,可伴恶心、呕吐、眩晕、颈强直、发热,CSF压力低于70mmH2O,15例患者CSF中有轻度一中度白细胞增多和蛋白增高,2例患者为血性CSF,10例患者脑电图异常;50例患者中有40例行头CT检查正常,10例头颅CT显示第三脑室及双侧脑室呈不同程度均匀一致缩小。治疗:以大量补充生理盐水为主,并给予激素治疗,其中5例鞘内注入生理盐水+氟美松治疗。结论:认识低颅压综合征的临床、病因、CSF及影象学表现至关重要,因其极易与蛛网膜下腔出血等相混淆。     

罕见影像表现低颅压综合征1例并文献回顾

目的通过报道及分析1例低颅压综合征的特殊影像表现及诊疗经过．合并相关文献分析．帮助避免临床误诊误治。方法回顾性分析1例影像学诊断为静脉窦血栓形成的低颅压综合征病例,并复习相关文献。结果患者最终被诊断为低颅压综合征,经保守治疗后病情痊愈。结论单纯的影像学表现不能用于临床诊断．必须紧密联系病史及实验室检查综合评估分析,才能降低误诊率。     

原发性低颅压综合征18例临床、脑脊液和影像学特点分析

目的探讨原发性低颅压综合征的临床、脑脊液和影像学特点。方法回顾性分析18例原发性低颅压综合征的临床资料。结果原发性低颅压综合征以体位性头痛、恶心、呕吐、头晕、耳鸣为主要表现,部分伴有神经系统体征,腰穿脑脊液压力均低于70mmH2O,27%患者红细胞增多,33%脑脊液蛋白增高,影像学检查可见硬膜增厚、强化、硬膜下积液和硬膜下血肿等表现,给予大量补液治疗及对症支持治疗,效果良好。结论体位性头痛、腰穿脑脊液压力低为原发性低颅压综合征的主要临床特点,影像学可呈现硬膜增厚强化等特征性改变,治疗以大量补液为主。     

自发性低颅压综合征与肥厚性硬脑膜炎的临床及影像学对比分析

目的探讨自发性低颅压综合征(SIH)与肥厚性硬脑膜炎(HCP)的临床及影像学特点,以提高诊断及鉴别能力。方法回顾性分析20例SIH患者及6例HCP患者的临床及影像学资料并进行对比。结果两组患者均以头痛为主要临床表现,SIH患者的头痛多与体位改变有关,脑脊液压力明显低于正常,HCP患者除头痛之外,多组颅神经损害较SIH更为常见。影像学上两组均可表现为硬脑膜弥漫性增厚并异常强化,但HCP硬脑膜强化可为局限性,部分病例可见邻近部位感染灶,而SIH可出现硬膜下积液。结论自发性低颅压综合征与肥厚性硬脑膜炎有一定的相似之处,但在临床及影像学上均有各自的特点,应注意鉴别。     

低颅压综合征合并颅内静脉血栓2例并文献回顾分析

目的总结分析低颅压综合征(SIH)合并颅内静脉血栓形成(CVT)的临床表现,诊断和治疗方法。方法报道2例低颅压综合征合并颅内静脉血栓形成,并回顾文献报道15例同类病例,分析其临床特征、影像学表现、治疗和病理生理机制。结果17例患者均以亚急性起病,其中14例患者表现为体位性头痛。常见的伴随症状有恶心、呕吐、复视、耳鸣等。所有患者的影像学检查都存在SIH和CVT的表现,头部核磁共振(MRI)加静脉成像(MRV)是诊断颅内静脉血栓形成的主要手段。结论低颅压综合征是颅内静脉血栓形成的危险因素之一,了解两者内在的病理生理联系和临床特征有利于对该病的早期诊断和及时治疗。     

Munchausen syndrome, depression, and the dexamethasone suppression test

The authors describe two patients with Munchausen syndrome who met DSM-III criteria for major depression. Both patients exhibited evidence of nonsuppression of serum cortisol by dexamethasone. Although many patients with Munchausen syndrome have been reported to be depressed, only a few have received a diagnosis of major depression. Because the physical and psychiatric symptoms of the Munchausen patient are so complex, clinical assessment may stop at a diagnosis of Munchausen syndrome, and major depression may be overlooked. A diagnosis of major depression should be considered in the evaluation of these patients; the dexamethasone suppression test may enhance clinical assessment.     

Depressive symptom profile in Parkinson's disease: a comparison with depression in elderly patients without Parkinson's disease

OBJECTIVE: Depression is a common neuropsychiatric syndrome in Parkinson's disease (PD), and may be etiologically related to the neurochemical changes accompanying this disease. It is still unclear whether the disturbances of neurotransmitter activities lead to a specific profile of depressive symptoms, that is characteristic for PD and differs from that in depressed patients without PD. METHOD: We compared the individual depressive symptoms of 145 non-demented depressed patients with PD and 100 depressed patients without PD by comparing item scores on the Montgomery-Asberg Depression Rating Scale by way of MANCOVA. RESULTS: The severity of depression and the level of cognitive functioning in depressed PD patients were comparable with that of depressed control subjects. However, patients with PD showed significant less reported sadness, less anhedonia, less feelings of guilt and, slightly less loss of energy, but more concentration problems than depressed control subjects. CONCLUSION: The profile of depressive symptoms in PD differs from that in depressed subjects without PD. This finding is important for the conceptualisation and clinical diagnosis of depression in PD.     

Prevalence and correlates of parkinsonism in patients with primary depression

The authors examined the prevalence, clinical correlates, and longitudinal changes of parkinsonism in 94 patients with primary depression and 20 healthy control subjects. Parkinsonism was present in 20% of patients with primary depression. This syndrome was significantly associated with older age, more severe depression, and more severe cognitive impairment. In a subgroup of depressed patients, parkinsonism was reversible upon recovery from the mood disorder.     

Sadness as an integral part of depression

Sadness is considered by numerous authors to be a core symptom of depression. Currently, many arguments exist for its particular importance in depressed patients. Sadness makes up part of the various definitions of the depressive syndrome, even if its presence is not required for diagnosis. Furthermore, it is closely linked to the other depressive symptoms, and has prognostic value, in particular for remission. The recognition and measurement of sadness seem important for therapeutic evaluation, in clinical studies, and in depressed patients at an individual level. This paper presents a selective review of some of the various aspects of sadness as an integral part of depression, and an examination of its links with a disease which is a major health concern.     

Cranial MRI changes may precede symptoms in Hallervorden-Spatz syndrome

Two families are presented in which siblings of children affected with Hallervorden-Spatz syndrome exhibited characteristic cranial magnetic resonance imaging changes before developing clinical features of the disease. Linkage to a major locus on chromosome 20p supported the diagnosis of Hallervorden-Spatz syndrome. In some patients with Hallervorden-Spatz syndrome, iron is radiographically evident before the onset of clinical symptoms.     

Catatonia in depression: prevalence, clinical correlates, and validation of a scale.

OBJECTIVES--To examine the clinical correlates of catatonia in depression, to validate a scale for catatonia, and to assess the validity of the DSM-IV criteria of the catatonic features specifier for mood disorders. METHODS--A series of 79 consecutive patients with depression and 41 patients with Parkinson's disease without depression were examined using the modified Rogers scale (MRS), the unified Parkinson's disease rating scale (UPDRS), and the structured clinical interview for DSM-III-R (SCID). RESULTS--Sixteen of the 79 depressed patients (20%) had catatonia. Depressed patients with catatonia had significantly higher scores on the MRS than non-catatonic depressed patients matched for severity of depression, or non-depressed patients with Parkinson's disease matched for severity of motor impairment. Depressed patients with catatonia were older, had a significantly higher frequency of major depression, more severe cognitive impairments, and more severe deficits in activities of daily living than depressed non-catatonic patients. The DSM-IV criteria of catatonia separated depressed catatonic patients from patients with Parkinson's disease matched for motor impairment, with a specificity of 100%. Catatonic signs did not improve after apomorphine. CONCLUSIONS--catatonia is most prevalent among elderly patients with severe depression. The study showed the validity of the MRS for the diagnosis of catatonia in depressed patients, as well as the specificity of the DSM-IV criteria of the catatonic features specifier.     

Objective assessment of personality disorder in chronic fatigue syndrome

OBJECTIVES: This study aims to objectively assess the prevalence and nature of personality disorders in depressed and nondepressed chronic fatigue syndrome (CFS) patients and compare this to depressed and healthy control groups. METHODS: Sixty-one patients attending a tertiary referral clinic with chronic fatigue syndrome, 40 psychiatric inpatients with depressive disorder and 45 healthy medical students completed the Structured Clinical Interview for DSM-III-R Diagnoses (SCID-II) in addition to providing routine clinical and demographic information. RESULTS: Thirty-nine percent of the CFS group, 73% of the depressed group and 4% of the healthy group were diagnosed with personality disorders. Cluster C disorders were the most common in both the CFS and depressed group. The depressed CFS patients had more Cluster B personality disorders than nondepressed CFS patients. Overall for CFS patients there was no association between mood state and personality disorder. CONCLUSIONS: High levels of personality disorder are found on objective assessment of CFS patients attending a teaching hospital clinic. This cannot be accounted for by comorbid depression.     

POEMS综合征20例临床分析

目的探讨POEMS综合片的临床特征,提高对POEMS综合征的诊疗认识。方法回顾性分析20例POEMS综合征患者的临床表现、辅助检查、治疗及预后。结果20例患者均有多发性神经病、水肿及皮肤色素沉着,淋巴结肿大者18例,内分泌改变者18例,异常球蛋白血症者16例。16例患者给予激素治疗,其中7例合用人血免疫球蛋白静滴。18例患者有不同程度的好转。结论POEMS综合征临床表现复杂多样,各主要症状出现顺序不一,涉及多系统,临床应注意鉴别诊断。     

Can drugs cause depression? A review of the evidence.

Drug-induced depressive disorders are classified in the DSM-III-R as organic mood syndrome, depressed type. The ability of certain drugs to cause depression is of clinical relevance because organic mood syndrome is a component of the differential diagnosis of depressive symptoms. Consequently, psychiatric textbooks often provide different lists of drugs thought to be capable of causing depression. Strong evidence supporting the existence of causal associations is often lacking. There is no specific drug for which there is definitive evidence of a causal association with depressive symptoms or depressive disorders. Nevertheless, for a number of drugs, the evidence is suggestive, although not conclusively, of a causal association. Despite this, rational decisions about the continuation or discontinuation of drugs can often be made. In this paper, the literature is reviewed and guidelines are suggested for the management of patients with depressive symptoms which may be related to drugs.     

Course-related depressive syndromes in schizophrenia

The authors evaluated 20 patients, diagnosed by Research Diagnostic Criteria after 1 week of hospitalization as having schizophrenia, weekly throughout their hospitalization. Four patients developed syndromes of depression after resolution of their psychoses: three manifesting a "minor" and one a "major" postpsychotic depressive syndrome. Four other patients went on to develop syndromes equivalent to major depression at a time when they were still actively psychotic, and their cross-sectional diagnoses were therefore changed to schizoaffective disorder, depressed type. The authors discuss the implications of these findings for diagnosis.