吸食海洛因致海绵状白质脑病的CT及MRI诊断

目的评价海洛因中毒所致的海绵状白质脑病的CT、MRI表现及诊断价值.方法搜集6例海洛因海绵状白质脑病的CT及MRI资料,全部患者均进行MRI检查,检查序列包括T1WI、T2WI、FLAIR序列,其中2例同时行颅脑CT扫描. 结果全部患者MRI显示对称性双侧小脑半球、大脑半球后部、内囊后肢、胼胝体压部、脑干等皮质下白质为主的多发性大片状长T1、长T2信号,加强后病灶无强化;2例行头颅CT检查显示两大脑半球皮质下白质、基底节及两侧小脑呈对称性广泛低密度灶,无占位效应.结论海洛因中毒所致的海绵状白质脑病具有特征性的MRI表现,MRI对本病的诊断具有重要价值.     

Marchiafava-Bignami病的临床及影像学研究

目的 探讨Marchiafava-Bignami病(MBD)的临床及影像学改变.方法 回顾性分析了7例MBD患者的临床和CT、MRI资料,包括病灶形态、分布、信号或密度改变等影像学特征:4例同时行CT和MRI检查,2例仅行CT检查,1例仅行MRJ检查.结果 本组患者急性型5例,均表现为胼胝体肿胀及长T1、长T2信号改变,均有双侧脑室周围白质、额叶皮层下白质对称性累及:慢性型2例,胼胝体明显萎缩变薄,并呈长T1、长T2信号及FLAIR像点片状或线样低信号灶.5例患者DWI显示病灶区信号明显增高并有2例出现弥散受限改变.结论 MBD具有特征性MRJ表现,其影像学改变可能反映其临床及预后.     

儿童局灶性皮质发育不良的磁共振高分辨成像特征

目的探讨儿童局灶性皮质发育不良(Focal cortical dysplasia,FCD)的3D高分辨核磁共振(MRI特征。方法回顾性分析2015年4月-2018年6月山东大学齐鲁儿童医院收治的42例经病理证实为FCD的患儿MRI资料,观察下述征象:局灶性灰白质分界模糊、皮质结构异常(增厚或变薄)、T2WI/FLAIR白质信号增高,伴或不伴transmantle征(皮层下白质内向脑室方向延伸的异常信号),T2WI/FLAIR灰质信号增高,异常脑沟或脑回形态及节段性和/或脑叶发育不全/萎缩。结果 42例患儿中,37例(88.1%)可见MRI阳性征象,FCDⅠ型13例(35.1%),主要MRI特征为局灶性灰白质分界模糊、相应部位皮质结构异常及T2WI/FLAIR白质信号增高;FCDⅡ型17例(45.9%),表现为局灶性灰白质分界模糊及皮质结构异常、T2WI/FLAIR白质信号增高及transmantle征;FCDⅢ型共7例(18.9%),其中海马萎缩2例(28.6%)、胚胎发育不良性神经上皮瘤(Dysembryoplastic neuroepithelial tumor,DNET) 2例(28.6%)、节细胞瘤1例(14.3%)、软化灶并胶质增生2例(28.6%)。结论 FCD患儿的3D高分辨MRI特征具有特异性,可提高FCD病灶检出率。     

瘤样炎性脱髓鞘病MRI的临床意义

目的分析瘤样炎性脱髓鞘病(TIDD)临床、影像与病理特点,探讨磁共振(MRI)检查对TIDD的诊断价值。方法对39例TIDD患者进行头颅、脊髓CT和MRI扫描,并分析临床和影像学特点。结果病灶在头颅CT均为低密度,常规MRI扫描呈T1WI低信号、T2WI高信号,T1WI增强扫描44%可见"开环征",发病早期DWI可见高信号,FLAIR较T1WI及T2WI更清晰显示病灶及其范围。结论 DWI能发现TIDD早期病变,FLAIR较常规T1WI、T2WI敏感,"开环征"是磁共振诊断TIDD的重要辅助依据。     

海洛因海绵状白质脑病的影像学特征

目的　探讨海洛因海绵状白质脑病 (HSL E)的 CT、MRI和 PET特点。方法　对 2 9例患者的CT、MRI以及 4例患者的 PET资料进行分析。结果　 (1) CT和 MRI显示病变位于双侧小脑、内囊后肢、枕顶叶深部等部位白质 ,病灶广泛且对称 ;(2 ) CT示界限清楚的低密度病灶 ,MRI呈长 T1 WI、长 T2 WI异常信号 ,无水肿 ,快速反转恢复序列 (FL AIR)和增强扫描提示血脑屏障无破坏 ,PET显示为低代谢或无代谢病灶 ;(3)未治疗患者内囊后肢、枕叶和小脑白质无代谢 ,康复期患者代谢明显减低 ;(4 )临床症状改善者和未治疗者小脑皮质代谢降低 ,临床症状明显改善者代谢正常。结论　 HSL E患者的 CT和 MRI改变多局限于白质 ,极为相似。 PET显示病变部位低代谢或无代谢 ,小脑皮质和白质代谢的恢复对 HSL E患者的临床转归非常重要 ,故判断 HSL E患者的转归 ,PET较之 MRI更有价值     

15例急性CO中毒伴发急性脑梗死的临床及MRI、MRA研究

目的评价MRI、MRA对急性CO中毒伴发急性脑梗死的诊断价值。方法回顾分析15例经临床确诊的急性CO中毒伴发急性脑梗死患者的头颅MRI、MRA资料。结果15例患者急性脑梗死病变部位:MRI为点状、片状异常信号;DWI表现为高信号;ADC为低信号;ADC值为(0.55±0.14)×10~(-3) mm~2/s;病灶直径(8.62±9.27)mm。病灶部位:10例脑叶,7例基底节及侧脑室旁,2例小脑,2例苍白球,1例脑干。12例侧脑室前后角白质周围片状、云雾状长T_1、长T_2异常信号病灶;11例双侧基底节及侧脑室旁点状长T_1、长T_2异常信号为陈旧性腔隙性梗死;7例脑萎缩。13例MRA表现:8例(61.53%)动脉狭窄,5例(38.46%)动脉管腔僵硬。结论应用头颅MRI、MRA对急性CO中毒伴发急性脑梗死的早期临床诊断、病情程度及预后的评估有一定的实用价值。     

妊娠相关性脑静脉及静脉窦血栓形成和可逆性后部白质脑病的磁共振鉴别

目的探讨MRI和MRV在妊娠相关性脑静脉及静脉窦血栓形成(CVST)和可逆性后部白质脑病综合征(RPLS)鉴别诊断中的价值。方法回顾性分析3例妊娠相关性CVST和6例重度子痫前期、子痫发生RPLS患者的影像学资料。所有患者均行MRI和DSA检查,其中7例患者行MRV检查。结果 3例CVST患者中,1例孤立性大脑上静脉前组血栓形成,MRI表现为相应部位T1WI低、等信号,T2WI、FLAIR等、稍高信号,DWI为等、高信号,ADC图为低、稍高信号;2例横窦血栓形成,表现为双侧枕叶皮质、皮质下白质片状T1WI低信号,T2WI、FLAIR高信号,DWI、ADC高信号,可不对称性地累及顶叶、小脑半球,MRV与DSA检查结果相符。6例RPLS患者MRI显示双侧顶、枕叶皮质、皮质下白质多发性、斑片状、对称性病变,部分严重患者大脑半球呈弥漫性、大片状受累,表现为T1WI低信号,T2WI、FLAIR高信号,DWI、ADC高信号;1例患者MRV检查示左侧横窦未显影,DSA检查示左侧横窦通畅。结论横窦血栓形成和RPLS患者MRI均显示血管源性脑水肿,两者脑水肿主要发生于双侧枕、顶叶,但前者范围较局限,后者范围更广泛,可累及基底节、额叶、颞叶。RPLS患者MRV检查可有假阳性,DSA是鉴别两者的重要检查方法。     

24例原发性中枢神经系统血管炎患者的MRI表现

目的观察24例原发性中枢神经系统血管炎(PACNS)的磁共振成像(MRI)表现,探讨PACNS的MRI诊断价值。方法对急性期进行了MRI检查的24例经病理证实的PACNS的MRI特点进行了回顾性分析。结果 24例患者中,病灶以幕上多见[19例(79.2%)],最常累及颞叶、额叶、顶叶及基底节区(包括丘脑),分别为13例(54.2%)、10例(41.7%)、8例(33.3%)、8例(33.3%);大部分病灶累及双侧大脑半球[15例(72.5%)],灰质和白质均受累[21例(87.5%)]。MRI上病灶可多发或单发,均为12例(50%)。病灶形态大致可分为四种类型:斑片状、肿块样、脑回状和混合性,分别为12例(50%)、8例(33.3%)、2例(8.3%)和2例(8.3%)。MRI上所有病灶均呈长(稍长)T1WI、长(稍长)T2WI异常信号,增强扫描可见病灶均有强化,FLAIR上均呈高或稍高信号,9例(37.5%)病灶中心呈散点状短T1WI、短T2WI混杂信号。17例行DWI和ADC序列检查者中,9例(52.9%)在DWI上呈高(稍高)信号,ADC上呈等信号或混杂信号影,8例(47.1%)在DWI及ADC上呈等信号。11例行GRE序列检查者,8例(72.7%)可见病灶局部有点状低信号影或病灶周围血管影增粗,余3例未见异常。8例行MRA序列检查者,仅1例发现异常,可见病灶供血区相应血管局部有狭窄。结论本组24例PACNS患者急性期头MRI均有异常,表现多样,病灶以幕上多见,可累及各个脑区,病灶可多发或单发,多数灰白质均受累。其形态可表现为斑片状、肿块样、脑回状或混合性,增强扫描均可见强化,以斑片状或脑回样强化多见。头MRI上病灶多变、灰白质受累、斑片状或脑回样强化等表现对PACNS诊断有一定提示性。     

桥本氏脑病的临床特点

目的探讨桥本氏脑病(HE)的临床特点。方法对本院收治的11例和文献报道的17例HE患者的临床资料进行回顾性分析。结果本组男5例,女23例;年龄21～81岁;伴有甲状腺功能亢进3例,亚临床甲状腺功能亢进4例,亚临床甲状腺功能减低1例。首发症状为智能下降、癫痫、精神症状、头痛、卒中样发作、行走不稳、行动迟缓、构音和吞咽障碍。主要临床症状依次为智能下降23例(82.1%),癫痫发作14例(50.0%),精神症状14例(50.0%),意识障碍7例(25.0%),头痛7例(25.0%),行动迟缓4例(14.3%),发热3例(10.7%),卒中样发作3例(10.7%),构音/吞咽障碍2例(7.1%),复视1例,伴有心脏受累2例,多发大动脉炎及雷诺病各1例。26例患者查血甲状腺球蛋白抗体及27例查血甲状腺过氧化物酶抗体均显著升高。21例患者行脑电图检查,17例异常,均为全脑的广泛慢波。26例头颅MRI检查17例异常,主要累及皮质和皮质下白质,大多呈边界模糊的斑片状长T1、长T2;T2Flair呈高信号,部分为混杂信号。糖皮质激素治疗均有明显的疗效,1例死亡,其余预后良好。结论 HE多见于中年以上的女性,首发及主要症状以双侧脑皮质或皮质下白质损害症状为主,甲状腺相关抗体指标显著升高;MRI可见分布广泛的斑片状长T1、长T2信号病灶。早期糖皮质激素治疗预后较好。     

磁共振梯度回波T2*加权成像诊断家族性多发性脑海绵状血管畸形的价值

目的 探讨磁共振梯度回波T2*加权成像(GRE T2*-WI)诊断家族性多发性脑海绵状血管畸形(FCCM)的价值.方法 对FCCM患者的2个家系26名成员进行颅脑CT、常规MRI(T1WI、T2WI、T2FLAIR、DWI及SE)及GRE T2*-WI检查.结果 GRE T2*-WI检查发现FCCM患者12例,均为多发病灶,平均检出病灶23个,病灶主要位于基底节区,其次为皮质-皮质下、丘脑、小脑和脑干.病灶呈特异的高低混杂信号,周边围有一圈黑色低信号环,极具特征性.常规MRI检出脑内病灶数目(平均病灶数5～17个)、疑诊或确诊为FCCM患者的例数(平均例数3～9例),由多至少依次为SE、DWI、T2FLAIR、T1WI和T2WI,均较GRE T2*-WI少.而颅脑CT仅对病灶较大、合并有钙化或出血的3例患者疑诊为脑海绵状血管畸形.结论与CT和常规MRI相比,GRE T2*-WI可以更清楚地显示脑海绵状血管畸形病灶,为诊断提供更可靠的依据.     

Altered mental status in thrombotic thrombocytopenic purpura is secondary to nonconvulsive status epilepticus

Thrombotic thrombocytopenic purpura (TTP) is a syndrome with numerous neurological manifestations including altered mental status and seizures. At least 10% of the patients with TTP seen at our institution had non-convulsive status epilepticus as a cause of or associated with their altered mental status. We propose that altered mental status secondary to nonconvulsive status epilepticus requiring electroencephalographic diagnosis and antiepileptic medication occurs in a substantial proportion of patients with TTP.     

核磁共振脑灌注成像及DWI联合应用在诊断早期脑梗死缺血半暗带中的临床价值

目的 探讨核磁共振脑部灌注加权成像(PWI)及脑部弥散加权成像(DWI)联合应用在诊断早期脑梗死缺血半暗带中的临床价值。方法 本研究中的受试对象均来自2016年1月-2017年4月来本院就诊的脑梗死患者,选出符合纳入标准的100例作为研究对象,并根据脑梗死发生时间分成超急性期、急性期、亚急性期和慢性期,分别观察PWI和DWI表现,以表观弥散系数(ADC)为DWI的检测评价指标,以局部脑血容量(rCBV)、局部脑血流量(rCBF)、平均通过时间(MTT)和达峰时间(TTP)为PWI的检测评价指标,并比较不同时期脑梗死的PWI和DWI表现。结果 随着脑梗死患者发病时间的延长,T₂WI显示信号随之增高,DWI信号随之降低,ADC信号随之增高。随着梗死时间延长,梗死区ADC值随之增加,健侧对应区随着梗死时间的变化,ADC值无明显变化; 在每个不同分期中健侧对应区的ADC值均高于梗死区(P均<0.05); 超急性期rCBV和rCBF值均为降低信号,MTT和TTP均为升高信号; 急性期rCBV、rCBF、MTT和TTP值在三种信号上均有表现,但rCBV和rCBF值均以降低信号为主,MTT和TTP均以升高信号为主; 亚急性期中rCBV和rCBF为正常和降低信号,其中以正常信号为主,MTT和TTP均为降低和升高信号,并以升高信号为主; 慢性期rCBV和rCBF均表现为降低信号,MTT和TTP均为降低和升高信号,并以降低信号为主; 超急性期DWIPWI均有表现,并以DWIPWI均有表现,并以DWIPWI为主; 亚急性期DWI=PWI和DWI>PWI均有表现,并以DWI=PWI为主; 慢性期均为DWI=PWI。结论 PWI联合DWI对脑梗死早期的诊断价值较高,PWI对缺血半暗带有较好的诊断,其与DWI相结合可更准确地判定缺血半暗带。     

血栓性血小板减少性紫癜临床分析

目的:探讨血栓性血小板减少性紫癜(TTP)的临床特点、诊断要点及治疗方法。方法:分析7例患者的临床特点、血液学特征性改变、影像学特征及实验室检查结果。结果:急性发病,临床表现为贫血、皮肤淤斑、鼻出血、黑便等血液学的异常;头痛、头晕、意识障碍、神经功能缺损或癫痫发作;黄疸、血尿及发热等,实验室检查为溶血性贫血、血小板减少和肾功能异常,神经影像学表现为脑梗死灶或伴出血。在明确诊断后应用激素、血浆置换治疗及对症治疗,7例中2例基本痊愈,2例放弃治疗,3例死亡。结论:对临床急性起病的表现为贫血、出血、头痛、神经功能缺损或癫痫发作的患者,结合血小板减少应高度怀疑TTP,及时进行骨髓像等血液学检查,一旦确诊,及早给予激素、血浆置换治疗及相应对症治疗具有挽救生命的重要意义。     

Acute intermittent porphyria presenting as acute pancreatitis and posterior reversible encephalopathy syndrome

Acute intermittent porphyria (AIP) is an inherited metabolic disease that can affect the autonomic, peripheral and central nervous systems. Pancreatic diseases assocated with AIP is rarely reported. We report here a 60-year-old non-alcoholic male who had typical manifestations of AIP, including abdominal pain, constipation, tachycardia, hypertension, mental disturbances, psychiatric manifestations, seizures, peripheral neuropathy, and excessive excretion of porphyrin precursors in urine. Increases of serum amylase and lipase, as well as mild pancreatic edema on ultrasonography, were noted during the acute attack of AIP, suggesting concomitant acute pancreatitis. In this patient, brain magnetic resonance imaging revealed reversible multifocal cerebral lesions resembling a posterior reversible encephalopathy syndrome (PRES) during the acute attack of AIP. Because the clinical manifestations of acute pancreatitis could be present with an acute attack of AIP, early confirmation of diagnosis is mandatory to effectively manage the attack and avoid inappropriate treatment.     

Cytokines involved in CNS manifestations caused by Mycoplasma pneumoniae

Mycoplasma pneumoniae sometimes causes central nervous system manifestations, which may involve the host immune response, as the organism does not directly damage neural cells, or release toxins. Therefore we measured the levels of interleukin-6, interleukin-8, interleukin-18, interferon-gamma, tumor necrosis factor-alpha, and transforming growth factor-beta1 in serum and cerebrospinal fluid samples from patients who manifested central nervous system manifestations during acute M. pneumoniae infection. The subjects were nine patients with early-onset encephalitis (central nervous system disease onset within 7 days from the onset of fever), four with late-onset encephalitis (onset at 8 days or later), three with encephalitis but without fever, and three with aseptic meningitis. Intrathecal elevations of interleukin-6 and interleukin-8 in all four types of central nervous system manifestations, and of interleukin-18 in late-onset encephalitis were observed. None of the cerebrospinal fluid samples contained detectable levels of interferon-gamma, tumor necrosis factor-alpha, or transforming growth factor-beta1. In conclusion, interleukin-6, interleukin-8, and interleukin-18 might be involved in the inflammatory process leading to the central nervous system manifestations caused by M. pneumoniae.     

Neurologic presentations of mitochondrial disorders

This article describes the neurologic presentations of children with mitochondrial disorders. The charts of 42 children with highly suspect mitochondrial disorders were reviewed. Thirty-seven children were diagnosed as having definite mitochondrial disorders based on a suggestive clinical presentation and at least one accepted criteria, while in five patients the diagnosis remained probable. All patients had nervous system involvement, but it was the presenting symptom in 28 of 42. Eighteen children had normal intelligence and 24 had mental retardation or developmental delay at the onset of their disease. Twenty-five patients had either an acute regression or a progressive encephalopathy. The most frequent neurologic manifestations were abnormal tone, seizures, extrapyramidal movements, and autonomic dysfunction. The eyes were involved in 11 children. Nerve deafness was found in seven patients. Myopathy was found in only six patients. In conclusion, a complex neurologic picture, especially with other organ involvement, warrants a full mitochondrial evaluation.     

Diffusion- and perfusion-weighted MRI. The DWI/PWI mismatch region in acute stroke.

BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) are relatively new MR techniques increasingly used in acute stroke. During the first hours of stroke evolution, the regions with abnormal perfusion are typically larger than the DWI lesions, and this mismatch region has been suggested to be "tissue at risk." The aim of this study was to evaluate the PWI/DWI mismatch region in acute stroke patients and find parameters indicative of both infarct progression and functional impairment. METHODS: Twenty patients with nonlacunar ischemic stroke were imaged with DWI, PWI, and conventional MRI within 24 hours of symptom onset and after 1 week; in addition, the European Stroke Scale (ESS) score was recorded. With PWI, the volumes of regions with "time-to-peak" (TTP) delays of >/=2, 4, 6, 8, and 10 seconds were measured; these volumes were compared with the acute DWI lesion volumes, final infarct size, and ESS score. RESULTS: In 80% of patients the acute DWI lesion was surrounded by regions with abnormal TTP delays (PWI>DWI lesion). A TTP delay of >/=6 s in the mismatch region was found to be associated with lesion enlargement between the initial and follow-up MRI scans. Lesions increased in 9 of 12 patients (75%) in whom the area with TTP delay >/=6 s was larger than the DWI lesion, but they increased in only 1 of 8 (12.5%) of the remaining patients, in whom the area with a TTP delay >/=6 s was smaller than the DWI lesion. The volume of the regions with TTP delays of >/=4 s correlated better with ESS (r=-0.88, P<0.001) than other PWI (or DWI) volumes, which indicated that a TTP delay of approximately 4 s might be the threshold for functional impairment of brain tissue. CONCLUSIONS: Only patients with severe perfusion deficits in the PWI/DWI mismatch (TTP delays of >/=6 s) are at high risk of lesion enlargement. Functionally, more moderate perfusion deficits (TTP delays >/=4 and <6 s) appear to also contribute to the acute clinical deficit.     

Elevated plasma neutrophil elastase concentration is associated with disease activity in patients with thrombotic thrombocytopenic purpura

Introduction

Genetic and autoimmune risk factors contribute to the development of thrombotic thrombocytopenic purpura (TTP) but triggers are needed to bring about acute disease.The aim of the study was to investigate the association of neutrophil activation with acute TTP, to assess whether neutrophil activation changes during plasma exchange therapy and to show if complement- and neutrophil activation are parallel, characteristic processes in acute TTP.

Materials and Methods

Altogether 49 EDTA-plasma samples of 21 TTP patients with acute disease and 17 in remission were investigated along with 20 healthy controls.A stable complex of PMNE-proteinase-inhibitor was measured by ELISA (Calbiochem, Merck-Millipore, Darmstadt, Germany).

Results

Acute disease was associated with significantly increased PMNE levels, the group medians were similarly low in TTP patients in remission and in healthy controls. Increased PMNE levels were characteristic for hematologically active and ADAMTS13 deficient form of TTP. PMNE concentration inversely correlated to disease activity markers platelet count (r = − 0.349, p = 0.032) and hemoglobin levels (p = − 0.382 p = 0.018). Achievement of remission was associated with significant reduction of plasma PMNE levels (p = 0.031, Wilcoxon test). There was positive correlation between PMNE levels and complement activation markers C3a and Bb.

Conclusions

We report increased PMNE levels in acute TTP and showed its association to activity markers of acute TTP and complement activation. Effective treatment of an acute TTP episode resulted in marked decrease in PMNE levels. Our data support and extend previous observations that neutrophil extracellular traps may be released in acute TTP and potentially contribute to the pathophysiology of this disease.     

Clinical features of encephalopathy in children with cancer requiring cranial magnetic resonance imaging

We analyzed acute neurotoxic problems attributable to chemotherapy or immunosuppression in the context of childhood neoplastic diseases, based on clinical and neuroradiologic findings. This retrospective single-center study reviewed the acute neurologic complications of 62 children receiving conventional chemotherapy or hematopoietic stem cell transplantation from July 2005-July 2008. We excluded patients with central nervous system metastasis and various neurotoxic manifestations not usually requiring cranial magnetic resonance imaging. Of 62 patients, 12 (19.3%) developed acute neurologic complications. The most common complications included posterior reversible encephalopathy syndrome in six of 12 (50%) patients, and Wernicke's encephalopathy in three of 12 (25%) patients. Other complications included chemical arachnoiditis, grey matter injury induced by postchemotherapeutic angiopathy, and leukoencephalopathy. Posterior reversible encephalopathy syndrome was accompanied by hypertensive episodes in most patients (5/6), and Wernicke's encephalopathy was evident with altered mental status in malnourished children. These data indicate that posterior reversible encephalopathy syndrome and Wernicke's encephalopathy are the predominant complications in children undergoing chemotherapy or hematopoietic stem cell transplantation. Early radiologic and clinical evaluation and prompt treatment for these complications are necessary to prevent their progression to irreversible brain damage.     

Neuropsychiatric evaluation of patients with brucellosis

Brucellosis is a multisystem disease that may present with a broad spectrum of clinical manifestations. Neurobrucellosis is one of the complications. The objective of this study was to determine neuropsychiatric manifestations among patients with brucellosis. Twenty-seven consecutive patients with brucellosis (14 patients with manifest neurological manifestation and 13 patients without apparent neurological manifestation) were recruited from Assiut University hospital and compared with 50 healthy controls matched with respect to age, sex, and social economic and educational levels. They were subjected to systemic, meticulous neuropsychiatric evaluations, laboratory, radiological, neurophysiology, and psychometric assessment with Mini-Mental State Examination, Wechsler Memory Scale—Revised. and Hamilton Depression Rating. Overt or apparent neurological manifestation was recorded in 14 patients (51.85%) and 13 patients (48.15%) with brucellosis without apparent neuropsychiatric involvement. Central nervous system (CNS) involvement (vascular stroke, meningeoencephalitis, and dementia) was recorded in 9 patients (33.3%) and 6 patients (22.2%) had peripheral nervous sytem (PNS) involvement (polyneuropathy, radiculoapathy, and polyradiculoneuropathy). Depression was recorded in 7 (29.2%) patients; 3 patients (21.4%) of the neurobrucellosis group and 4 patients (30.8%) with brucellosis without neurological manifestations. Patients with brucellosis (neurobrucellosis and patients without neurological manifestations) reported highly significant impairment in some cognitive function measures (mental control, logical memory, visual reproduction) and higher scores on depressive symptoms compared with controls. Patients with a Brucella infection usually manifest central nervous system involvement. Clinicians, especially serving in endemic areas or serving patients coming from endemic areas, should consider the likelihood of neurobrucellosis in patients with unexplained neurological and psychiatric symptoms, and should perform the necessary tests, including cognitive function and depression tests.