明溪县总医院-膝关节粘连-专家在线问诊-京东健康互联网医院

简介:

明溪县总医院创建于1937年，原名县立卫生院，1963年2月随县名更名为“明溪县医院”，2017年7月因县域资源整合更名为“明溪县总医院”（在县医院现址设立明溪县总医院东区，在县中医院现址设立明溪县总医院西区并加挂明溪县中医院牌子），是一所政府举办的非营利性国家二级乙等综合医院，爱婴医院，医保、新农合定点医院机构，承担全县及周边地区人民群众的医疗、保健、救护等各项卫生工作任务。2017年9月，各乡镇卫生院（社区服务中心）作为明溪县总医院的分院一并纳入明溪县总医院实行一体化管理，建立县域内紧密型管理体制的医联体组织体系。医院目前占地面积28053.13㎡（东区22364.85㎡，西区5688.28㎡），总建筑面积28758.54㎡（东区23873.54㎡，西区4885㎡）。其中：业务用房2.8万平方米，编制床位控制数400张，现实际开放病床318张（东区：258张，西区：60张）。医院共设21个职能科室、19个临床科室、7个医技科室。截止2017年9月底，医院在职职工总数446人，其中：正式在编职工304人，非编聘用职工142人，返聘人员4人，借用人员5人，见习人员19人。职工总数中卫生专业技术人员339人，占76%，医师111人，护士172人，医技人员35人。医院拥有联影1.5T核磁共振、东芝16层螺旋CT机、奥林巴斯290电子胃肠镜系统、西门子DR机、日立7180型全自动生化分析仪、泰瑞MZ-08医用中心制氧系统、德国费森尤斯血液与血滤透析机、氧饱和度监测式体外反博装置等一批先进的医疗设备，及标准化的净化手术室、重症监护病房，为完善医院的功能和提升临床诊断治疗水平提供有力保障。明溪县总医院始终秉承“以病人为中心”的服务理念，倡导“崇德、尚医、拓新、和谐”的院训，以严谨的医疗作风、精湛的医疗技术和严格的科学管理，努力为广大人民群众提供优质、高效、便捷的医疗服务。在临床上引起膝关节粘连的常见原因有类风湿关节炎、骨质疏松、膝关节置换术后制动以及慢性劳损。治疗上,主要是加强关节康复锻炼,如果症状仍未缓解,可进行手术松解治疗。，类风湿关节炎、骨质疏松、膝关节置换术后制动以及慢性劳损。，膝关节，主要是加强关节康复锻炼,如果症状仍未缓解,可进行手术松解治疗。，无，无，X线检查、关节镜、CT及三维重建、磁共振、超声等。，。

true 卢淑华副主任医师

二级医院明溪县总医院

好评率：100% 接诊量：15 平均响应：-

小儿内科，呼吸，消化科，新生儿科，儿童保健及生长发育，矮小症及早发育

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二级医院明溪县总医院

好评率：100% 接诊量：1.6万平均响应：-

慢性胃炎、失眠、月经病等

接诊医生：

2024-10-31 07:23:37

科普文章

膝关节积液怎么消除？

膝关节是负重关节，膝关节积液很常见，病因很多，比如骨折、半月板、韧带等损伤引起的积液、关节炎引起的积液、感染引起的积液、滑膜炎、类风湿、风湿和免疫因素等引起的膝盖积液等。需要做抽血、X、彩超或者核磁共振检查查明原因和积液多少。治疗方法也是根据病因对症治疗，一般可以缓解症状。

积液早期一般处理：积液早期应该卧床休息，暂时避免负重，抬高患肢，冰敷，还可以用弹力绷带加压包扎等。这些基本处理可以缓肿胀，避免积液进一步加重，必要时予石膏、夹板等固定膝关节。

穿刺疗法：如果是关节炎、滑膜炎、感染引起积液较多、张力比较大时，可以行关节穿刺，将积液和积血抽净，抽液后向关节腔注射透明质酸钠后加压包扎，感染引起的还可以注射抗生素对症治疗。

手术治疗：对于骨折、半月板损伤严重、韧带断裂、滑膜增生严重和骨质增生严重的患者一般建议手术处理，手术处理后结合早期康复治疗可以消除膝盖积液。

康复治疗：比如行理疗，针灸、热敷泡脚、推拿治疗等可以缓解症状，减轻积液。

药物治疗：根据病因抗感染、活血消肿、利尿等方法消除积液。

综上所述，膝盖积液原因很多，要到医院专科检查，明确原因后，遵守医师医嘱，综合对症治疗，一般可以缓解症状，预后一般较好。

中老年人膝盖老化的直肠癌磨损，真的不能避免预防么？

既然中老年人的半月板损伤是慢性的老化磨损，那是不是移位着这种磨损是无法避免和预防的呢？

当然不能这么说！

我们是可以通过刻意的人为干预去避免和预防，或至少尽可能的向后推迟半月板退化损伤进程的。

今天咱们就来聊一聊中老年人如何在日常生活中刻意的去避免和预防半月板退化磨损。

在说如何预防之前，我们还是得先说一说半月板这个特殊的结构到底是怎样一个存在。

众所周知，我们每个膝盖里都有两个半月板，内侧和外侧各一个。这俩半月板就“垫”在大腿骨和小腿骨的中间。而且半月板这个垫子并不是一个长方体，而是如下图一样边缘厚中央薄的斜面结构。也正是因为半月板的这种特殊结构，才能更有效的缓冲撞击和摩擦力。

是的，半月板之所以存在，它的意义就是为了缓冲大腿骨和小腿骨之间的上下的冲击力和旋转的摩擦力。你不妨想象下：如果没有这个垫子，当我们从高处往下跳时，大腿骨会直接撞击小腿骨，那骨头，尤其是骨头表面的软骨就会很快的被磨损破坏。如果没有这个垫子，当我们快速旋转身体时，由于脚站在地上小腿不动，上半身旋转时大腿骨就会“研磨”小腿骨，这种酸爽感光想象下都觉得遭不住。

此外，正常的半月板表面是非常平整光滑的，因为它平时要持续遭受膝关节的反复冲击和研磨，只有光滑平整的表面才更安全。然而，只要半月板的表面出现一些破裂撕裂口，就像我们手指头上起了倒刺一样，随着冲击和研磨，这个本来很小的“倒刺”样撕裂口就会越来越大越来越深，以至于最终让半月板的一小块整个的破损脱落，这不仅会引起膝盖的疼痛肿胀，还会在膝盖弯曲到一定程度是阻挡关节的活动，引起膝关节的交锁卡住感。

不幸的是，半月板并不是都有血液循环供应。如上图所示，半月板的边缘是有血液循环供应养分的，所以称之为“红区”，而半月板的中央是没有血液循环的，被称之为“白区”。有没有血液循环供应意义重大，因为不仅仅是营养问题，当半月板损伤后损伤部位能不能恢复好“长”好，很大程度上就取决于受伤区有没有血液循环供应，因为人体想修复损伤组织，必须先往损伤区域“运输”足够多的的修复“原材料”才行。而如果没有血液循环，那就好像是边远山区不通公路，连修补的选材料都没法运输过来，哪还谈修复。所以，这也是为什么很多半月板损伤别说无法自我修复了，就算是手术修补术后都很难长好而选择切除的原因。

量力而行，不逞强，是首先需要注意的。网络上有一些不服老的中老年人依旧从事着如年轻人一样的高强度运动，不仅没有损伤还获得了非常多的荣誉。这些除了有个体差异的存在外，这些高强度运动没有损伤的中老年人他们也是长时间循序渐进运动的结果。然而生活中我见过很多平时不运动，甚至身体条件比较差的中老年人，因为看了一篇“鸡汤文”或者“鸡汤视频”就心血来潮的也去猛运动，最终导致了不可逆的损伤。所以，对于中老年人来说，体育运动是必须坚持的，但是要选择符合自己年龄和能力的运动，而且在运动量和运动时间上都要适时适度且循序渐进。

客观说，对于半月板来说，有一些运动动作是非常危险的。比如健身房高强度的负重深蹲，再比如球类竞技运动中的“疾跑急停急转身”等动作，再比如平时训练中的蹲在行走或过度的弯曲膝关节等，再比如登山爬楼。这些都是膝盖，尤其是半月板不喜欢的高危动作，中老年人应该尽可能的避免。

膝关节自身稳定性增强，会大大减少半月板损伤以及关节磨损的风险。所以中老年人选择合适的动作（比如靠墙深蹲等）来锻炼膝盖周围的肌肉，尤其是大腿前方股四头肌，可以有效增强膝关节的稳定性，减少半月板的磨损。

半月板术后练习

术后早期练习，以避免粘连和肌肉萎缩为主要目标，不得过多行走，不应以行走作为练习的方法，否则极易引起关节肿胀和关节积液，影响功能恢复及组织愈合。

手术当天，待麻醉消退以后，可开始活动足趾和踝关节，即认真做好踝泵运动，具体方法为用力缓慢，全范围伸曲踝关节，每组 5 分钟。同时，也可进行股四头肌练习。

术后第一天，进行直抬腿练习及各方向的抬腿练习。直抬腿练习方法是伸直后，直腿抬高至足跟离床 15 厘米处，保持 5 秒，每组 30 次，每日 3 到 4 组。同时，也可以下床活动并进行负重的平衡练习。但要求患者在医护人员的保护下进行活动。

半月板修整术后的功能锻炼：除了踝泵和直抬腿练习，术后第一天可下床活动外，3 天可拆除辅料，并且要求膝关节功能弯曲达到 90°，在术后一周拆线，术后一个月可恢复正常生活，运动员术后 3 个月可恢复训练。

半月板切除术后功能锻炼：术后一周主动屈曲达到 90°，2 周主动屈曲达到 120°～130°，6～8 周可上下楼和骑自行车，2～3 个月可恢复训练和正常生活。

半月板缝合的功能锻炼：术后一周被动屈曲达 90°，2～4 周被动屈曲增加 10°，4 周开始部分负重，负荷大约为体重的 1/3 或 1/2，6 周可完全负重，8 周后可做固定自行车练习。

半月板手术 3 天以后即可出院，手术后一周到门诊进行复查拆线。如果出院以后有明显的关节肿胀、体温升高需随时到医院就诊。按计划进行功能练习，术后 3 个月可恢复正常的生活。

半月板损伤的磁共振分型

正常半月板MRI表现为三角形或菱形形态信号。在所有扫描序列中均为低密度、均质且较软骨密度弱的低信号。半月板撕裂表现为T1像和T2像正常密度条件下的线性高密度信号。与黏液样变性相关的退行性变为T1像局部高密度信号，在T2像更为明显。半月板病变信号分为以下三级：

1级：半月板内圆形或椭圆形大小不同的高密度信号，信号未延伸至半月板表面。

2级：大体呈线性高密度信号，信号常呈水平走行且大小各不相同。信号未及半月板表面，但可达半月板关节囊连接部位。

3级：为延伸至半月板表面并可见游离缘的高密度信号，该信号的出现说明存在半月板撕裂。

外伤性半月板损伤及分型

创伤性半月板损伤的分型主要是根据形态学分型，既ISAKOS分型。是2006年国际关节镜、膝关节外科和骨科运动医学学会（the Internationgal Society of Arthroscopy,Knee Surgery and Orthopaedic Sports Medicine,ISAKOS）提出的国际化标准半月板损伤分型系统，其分型依据是撕裂在关节镜下的形态学特点。

1、撕裂长度

撕裂长度是指达半月板表面的撕裂长度，此类分型不包括未达表面的半月板内部撕裂（MRI Ⅱ级撕裂）。

2、撕裂深度

既MRI分型0～3级损伤。完全撕裂是指达半月板上、下表面的撕裂，部分撕裂仅累及单个表面。

3、撕裂部位

1区撕裂是指半月板-关节囊连接部位撕裂，撕裂缘宽度小于一3毫米。2区撕裂缘宽度为3～5毫米。3区撕裂缘宽度大于5毫米。

以上分区与解剖学上局部血供相关的红-红区、红-白区、白-白区相对应，因关节镜无法评估损伤部位血供情况，此分型系统更适用于对术前半月板损伤的分型评估。

半月板也可根据前后部位分为2个区，即前角、后角，有时候也有中1/3部的描述。

图1.半月板的分区示意图

4、撕裂模式

（1）纵向-垂直撕裂：可位于半月板内任何部位，此类撕裂延伸可导致桶柄样撕裂。

（2）水平裂：自半月板内缘延伸至关节囊。也叫层裂。

（3）辐射状裂：自半月板内侧缘延伸至关节囊，此类型撕裂通常位于外侧半月板中互殴1/3连接处，可贯穿整个半月板，使半月板横裂。

（4）瓣状裂：可为垂直或水平状。垂直瓣状裂可累及半月板上、下表面。水平瓣状裂为水平裂的延伸。发生水平瓣状裂的半月板上、下表面可保持完整。

（5）复杂裂：是指多个平面存在撕裂。多见于半月板退行性变，但并非独有表现。

图2.半月板撕裂模式类型示意图

（6）盘状观半月板

盘状半月板为一类遗传变异病变，通常见于外侧半月板，Watanabe将盘状半月板病变分为3型：

①不完全型。病变半月板较正常半月板形状大且存在正常半月板的附属结构；

②完全型。盘状的病变半月板覆盖整个胫骨平台；

③第三种类型盘状半月板病变无后侧关节囊连接，较其他两型更易出现临床症状。

图3.Watanabe盘状半月板分型

罹患双癌，依然有办法治疗！“海外二诊”为客户快速链接全球权威专家资源！

病症：胃癌恶性黑色素瘤

患者：李女士

年龄：70岁

罹患癌症，毫无疑问对每个人都是重大打击。而如果一位患者不幸同时罹患两种癌症，我们可以想象得出他的心情会是怎样的沉重。

但时至今日，癌症早已不再是什么“不治之症”，很多良好的治疗方法，可帮助患者迈过重重困境，预后得到极大提升。

不仅如此，在医疗全球化的今天，中国患者也能通过“海外二诊”服务，快速触达到国际权威专家资源，为自己的治疗保驾护航！

今天的案例主人公李女士，正是一位“海外二诊”的受益者。我们来一起看看她的故事。*为保护隐私，文中患者个人信息均已经脱敏处理。

70岁的李女士在去年年底，因脚底疼痛去医院看病，结果发现脚后跟有一个1厘米的黑色肿物。医生判断是冻疮，于是开了点外用药，李女士也就没有再放在心上。

大概4个月后，真正的噩梦降临：李女士通过影像检查，被诊断为胃癌，而且有了淋巴结转移。她还出现了多次呕血，病情非常危急。很快,医生为她实施了全胃切除。令人意想不到的是，几天后通过检查，医生发现李女士后脚跟的肿物竟然也是癌症——恶性黑色素瘤。于是大概2个月后，医生又切除了她的足底肿瘤。

为了降低复发风险，李女士开始了3个周期的化疗联合免疫治疗（替吉奥联合纳武单抗）。

虽然该做的都已做完，但对于李女士来说，恐惧感还远未被消除。因为癌症最令人恐惧的，是其具有“复发转移”的能力。一旦癌症再次袭来，李女士不知道自己该如何应对。另外，两种癌症的治疗以及术后辅助药物治疗，也让李女士遭遇了一些副作用。比如腹泻、味觉障碍还有体重明显下降的问题。这些对于已经70岁的李女士来说，都很影响生活质量，所以迫切需要解决。

在本次的国际专家“海外二诊”服务中，李女士预约的是来自日本某知名综合性医院肿瘤中心的外科部长医生，他的专长领域既包括肿瘤外科，又包括各类癌症药物疗法、姑息治疗，是一位“内外兼修”的权威专家。在充分了解了李女士既往的病情和治疗经过后，医生很快通过远程会诊的方式，为患者详细解答了当前她的所有问题。

1、未来如果转移或复发了该怎么办？

医生：假如您未来不幸出现转移或复发，那么化疗是核心治疗手段。对于单发的孤立转移灶，可以选择手术、放疗来进行局部治疗。

具体化疗方案选择，我按使用的先后顺序列出了3类，当前面的方案失效后，可更换为后面的方案。

一类方案：化疗联合/不联合免疫方案

CAPOX (卡培他滨+奥沙利铂)±O药（即免疫药物纳武单抗）

SOX (替吉奥+奥沙利铂)±O药

FOLFOX (5-FU+奥沙利铂)±O药

二类方案：化疗联合/不联合抗血管药物方案

Taxane (紫杉醇/白蛋白结合型紫杉醇/多西紫杉醇)±雷莫芦单抗

三类方案：化疗方案

曲氟尿苷/盐酸替吡嘧啶

伊立替康

2、N K细胞疗法是否对我有帮助？副作用是否可控？ X医生：目前尚没有证据表明NK细胞疗法对癌症有效，因此不予推荐。

3、口服替吉奥会腹泻，是否需要调整方案？ II/III期胃癌患者术后采用辅助治疗方案，分别为：

替吉奥口服 1 年（口服 4 周，停药 2 周，共 8 个疗程或口服 2 周，停药 1 周，共 16个疗程）

CAPOX (卡培他滨+奥沙利铂) 共半年（每 3 周一次，共 8 个疗程）

SOX (替吉奥+奥沙利铂) 共半年（每 3 周一次，共 8 个疗程）

这三种方案中，替吉奥方案和CAPOX方案等效，但SOX要优于替吉奥。另外，胃癌术后直接使用纳武单抗免疫治疗无意义。

替吉奥确实会出现腹泻等代表性不良反应，患者可以考虑对症治疗，比如调节肠道的药物、止泻药等缓解副作用。如果副作用太严重，那么可以考虑减少药物剂量。

替吉奥的标准用药剂量为120mg，但用量低于80mg无法达到预期效果。如果当前患者用药为100mg，那么为了降低副作用，可以减少剂量到80mg；但如果目前剂量已经是80mg，则无法进一步降低剂量，此时考虑更换方案为CAPOX方案替代。如果不良反应严重到干扰日常生活，则患者可以选择停药，持续观察病情变化。

对于无淋巴结转移的II期B和II其C的患者，可选择使用1年帕博丽珠单抗免疫治疗。

4 、术后患者很瘦，味觉障碍，如何调理改善？通常，手术后患者体重会减轻20%左右。这是患者消化吸收能力低下、促食欲的胃肠激素减少引起的。大约6个月到1年时间，患者可以恢复正常。

味觉障碍可能是抗癌药的副作用引起的，也可能是饮食减少导致缺乏锌等微量元素引起的。建议患者采用少食多餐的方式饮食，每天分5-6次吃饭。在日本，我们有时也会给患者用一些营养补充剂。

另外，也可以考虑采用中草药的对症治疗，改善症状，比如十全大补汤、六君子汤。会诊结束后，李女士的心情得到了极大的平复。她对自己未来要走的路更清晰了，也对日本专家的细致指导和会诊的快速响应非常满意。

高龄+多基础病，该手术还是姑息治疗？日本专家为7旬胃癌患者一锤定音！

中国是消化道癌症发病数量较多的国家，根据国家癌症中心发布的《2022年中国恶性肿瘤疾病负担情况》数据，2022年我国胃癌新发病例约为35.87万例，死亡人数26.04万人。

总体来说，胃癌属于严重威胁我国国民生命健康的蕞常见癌症之一。胃癌如能在早、中期发现，还是有很大机会通过手术实现根治的，患者仍有一定机会得到临床治愈（术后5年不复发即为临床治愈）。

但在胃癌患者中，一部分人会因为【年龄较高】、伴有诸多【基础病】等问题，对手术存有疑虑，担心“下不来手术台”，甚至会放弃手术机会，选择吃药等姑息治疗。这样的选择真的正确吗？现如今的技术能否支持这类老年患者安全手术呢？接下来，我们一起看一个真实案例。

01七旬老人遭遇中期胃癌

一位七十多岁的“老胃病”项女士，因短时间体重骤降（8斤）前往就医。血液检测显示，她有一项指标异常升高。进一步检查发现，她的食道和胃连接的地方（贲门）以及胃的“外墙”（胃壁）都变得异常的厚，而且形状不均匀——这正是胃癌常见的表现。

医生随后通过胃镜检查和病例活检（取一小块组织观察上面的细胞），确诊了老人患有胃癌。由于还没有出现胃以外的远处其他器官的转移，也没有附近淋巴结转移，因此项女士的胃癌分期为中期。虽不是早期，但中期胃癌通常是可以手术的。为项女士提供诊疗的医生也表示，可以通过全胃切除手术实现根治。

但一来项女士已经七十多岁，二来她有20多年的糖尿病（手术伤口会更慢愈合、感染风险高、术后并发症风险高）、右肺还有一枚1.2厘米的肺结节。种种问题让老人和家人们都比较犹豫，担心扛不住治疗，最终“越治越糟”。在这样的背景下，项女士决定找一位足够权威的外科专家，来为自己进行全面评估，看看能不能兼顾好肿瘤根治以及手术的安全性。

不久后，项女士预约了来自日本癌研有明医院消化中心胃外科部长布部创也医生为自己提供指导。

02日本专家咨询内容分享

在充分了解了项女士的病情信息和全部资料后，布部创也医生给出了如下指导建议：首先，患者此前接受的是普通CT而非增强CT，胃镜也没有清晰展示食道上肿瘤具体侵犯的程度，因此很难得出精准的分期判断。

后面患者来癌研有明医院就医时，医疗团队会在治疗前为她做一套非常精细、全面的检查，此后就可以明确肿瘤情况了。届时如果发现患者的分期、肿瘤侵犯的范围确实和现在的结果相同，那么可以通过一个腹腔镜微创手术实现根治，损伤会非常小；如果届时发现肿瘤侵犯食道过多，则需要消化道联合食道外科共同进行胸腔镜手术治疗。

但无论是哪一种情况，患者都可以耐受手术，并且保留一部分胃。癌研有明医院是一家极为擅长肿瘤微创手术的知名癌症专科医院。在胃癌方面，2005年，医院开始导入腹腔镜，2019年又引入了达芬奇手术机器人，患者术后并发症更少了。如今，癌研有明医院98%的外科手术都采用微创。

受益于此，很多在别的医院需要胃全切的胃癌患者，到癌研有明后可以保留一部分胃，还能兼顾临床治愈。这对于术后患者的长期营养摄入和体重维持都很有帮助。布部创也医生所在科室的主要目标之一，正是在做到根治性切除的前提之下，将原本的胃全切术式变为次全胃切除术，尽可能为患者保留一些胃，让他们未来的生活质量得到提升。

那么项女士的糖尿病问题，会不会影响到手术呢？对此，布部创也医生认为完全不必担心，因为对于这类患者，癌研有明医院会进行详细的术前评估，并且有专业团队介入，从生活方式调整和专业治疗入手，帮助患者控制好血糖，让血糖水平达到符合手术的标准，从而降低术后愈合不良风险。

关于肺部的1.2厘米结节，布部医生认为可以暂不处理，无论它到底是良性还是恶性。因为这枚结节属于纯磨玻璃结节，即便是恶性，进展也非常缓慢，并不会快速出现转移扩散。而胃癌根治手术虽然会采用微创方式，但依然会给患者带来一定的负担，如果同时处理肺结节，会导致负担过重、患者难以承受。所以当前蕞好的处理办法，是先集中精力解决胃癌肿瘤，术后安排呼吸科专家为患者进行肺结节诊断，给出随访或手术或根治性放疗的建议。

03项女士术后，是否需要化疗来降低复发风险、争取更大治愈希望？

对此，布部创也医生表示，是否化疗现在还不能判断。因为术后患者能获得蕞精准的分期判断，有可能患者术前被认为是2期，但实际上术后成了1期（无需化疗）；有时也可能患者术前是1期，但术后成了2-3期。假如是2-3期，则患者术后需要坚持1年的辅助化疗，大概可以降低10%的复发风险。

有效减少不良反应，AD新药改良给药方案来了

当地时间10月29日礼来宣布了Ⅲb期临床试验（TRAILBLAZER-ALZ 6）的积极结果，对于早期症状性阿尔茨海默病成人患者，用改良滴定方案接受donanemab治疗的患者在24周主要终点时，伴水肿/积液的淀粉样蛋白相关影像学异常（ARIA-E）有所减少。

donanemab这个新药在今年7月获批于美国，又在之后获日本厚生劳动省、英国药品和医疗产品监管局批准，用于轻度阿尔茨海默病、轻度认知功能障碍的治疗。donanemab在国内2023年取得突破性治疗药物认定，并纳入优先审评审批程序，目前还在审评审批过程中。

CDE官网截图

但在FDA说明书中有黑框警告，大意是应用该药时应注意淀粉样蛋白相关影像学异常（ARIA），表现为ARIA-E和ARIA伴含铁血黄素沉积（ARIA-H），通常发生在治疗早期，且无症状，很少发生严重和危及生命的事件。本次试验的积极结果和这个黑框警告相关。一起来看详情。

FDA说明书截图

给药方式有哪些改变？会不会影响效果？

TRAILBLAZER-ALZ 6是一项多中心随机双盲Ⅲb期研究，主要研究donanemab的不同给药方案对早期症状性AD患者ARIA-E和淀粉样蛋白清除率的影响，这里的早期AD指的是轻度认知障碍（MCI）和轻度痴呆疾病阶段。

给药方式和既往不同，既往标准给药方案是在前三次输注时接受2瓶（700mg）donanemab，然后再接受4瓶（1400mg）；改良滴定方式是患者第一次输注1瓶（350mg），第二次输注2瓶（700mg），第三次输注3瓶（1050mg），此后每次输注4瓶（1400mg）。

研究的主要终点是第24周时患者出现ARIA-E占总参与者的比例，结果显示接受改良滴定方式的患者ARIA-E发生率为14%，而标准给药方案为24%，相对风险降低41%。载脂蛋白E（APOE）是已知的阿尔茨海默病遗传风险因素的携带者，在这些患者中，19%患者在改良滴定时患有ARIA-E，而标准给药方案中为57%，相对风险降低67%。

看到这里你或许也有疑问，虽然ARIA-E的发生风险降低了，但改良滴定方案会不会影响疗效？答案是不会。

与接受标准给药方案的患者相比，改良滴定患者淀粉样斑块和p-tau217减少。改良滴定的患者的淀粉样斑块水平较基线平均降低 67%，而标准给药组患者为69%。

参考来源

1.Modified Titration of Donanemab Demonstrated Reduction of ARIA-E in Early Symptomatic Alzheimer's Disease Patients in Phase Ⅲb study.

2.CED官网.

3.A Study of Different Donanemab (LY3002813) Dosing Regimens in Adults With Early Alzheimer's Disease (TRAILBLAZER-ALZ 6).

重磅！白血病一线新药获FDA加速批准

当地时间10月29日，阿西米尼（asciminib）获美国食品药品管理局（FDA）加速批准^[1] ，用于慢性期新诊断的费城染色体阳性慢性粒细胞白血病（Ph+CML）成年患者。CML是一种骨髓和血细胞癌症，通常由费城染色体的异常染色体引起。在一线治疗中，约1/3的患者会出现下列问题：由于不良反应或者治疗无效而停止酪氨酸激酶抑制剂（TKI）治疗。

为了解决这一问题，需要开发新的药物，asciminib就是解决这一困境的新药。早在2022年8月，加拿大药物和卫生技术局（CADTH）建议^[2] ：“若满足条件，可通过公共药物计划报销asciminib用于治疗费城染色体阳性慢性粒细胞白血病。”

asciminib为何得到FDA的青睐？

本次获批基于一项III期多中心随机研究，研究目的是比较每日80mg的asciminib与TKI治疗的疗效。TKI治疗是接受伊马替尼、尼洛替尼、达沙替尼或博舒替尼任意一种治疗。

共有405名患者被随机分配（1:1）进两组治疗。主要疗效结局指标是48周时的主要分子反应（MMR）率。这个指标是慢性髓性白血病的关键指标，这个比例越高，说明该治疗在基因水平上对疾病的控制效果越好，能够更有效地抑制疾病相关基因的表达，进而有望更好地控制疾病的进展、改善患者的症状和预后。

研究结果显示，48周时MMR率方面，asciminib组中为68%（95% CI: 61, 74)，TKI组为49%（95% CI: 42, 56），二者相差19%。细看具体的TKI，入组伊马替尼和其他TKI药物入组比例为1:1；asciminib组的MMR率为69%（95% CI: 59, 78），而伊马替尼组为40%（95% CI: 31, 50），相差近30%（95% CI: 17, 42）。

这个新药安全吗？每周需要打几次药？

根据FDA数据显示，在新诊断和既往接受过治疗的患者，应用新药最常见的不良反应（≥20%）是肌肉骨骼疼痛、皮疹、疲劳、上呼吸道感染、头痛、腹痛和腹泻。若只看新诊断的患者，最常见的实验室异常（≥40%）是淋巴细胞计数降低、白细胞计数降低、血小板计数降低、中性粒细胞计数降低等。

根据FDA已批准的asciminib说明书，用药期间还需要注意一下事项：

1.骨髓抑制：用药期间可能因出现骨髓抑制，发生血小板减少症、中性粒细胞减少症和贫血。用药应在治疗的前3个月，需要每两周进行一次全血细胞计数，此后每月进行一次检测，从而判断患者有无骨髓抑制症状。根据严重程度，咨询医生是否需要停药。

2.胰腺毒性：患者可能出现血清脂肪酶和淀粉酶无症状升高，每月需评估血清脂肪酶和淀粉酶水平，如果您有胰腺炎，则注意主动告知医生，需要进行频率更高的检测。

3.高血压风险：可能出现3级或4级高血压风险，应注意检测血压。

4.超敏反应：可能出现3级或4级超敏反应，包括皮疹、水肿和支气管痉挛。如果出现这些症状，需及时反馈医生，医生会根据超敏反应的体征和症状，开始适当的治疗。

5.心血管毒性：如果您有心血管病史，需要告知医生；对于3级或更高级别的心血管毒性，医生会考虑暂停用药、减少剂量或永久停药。

6.胚胎/胎儿毒性：若您在怀孕期间用药或在服用药物期间怀孕，可能对孩子有潜在风险。这个新药是口服药，需要根据不同的给药剂量（80mg或40mg）每天/或每两天用药。

近些年来，还有哪些白血病药物获批FDA？

根据FDA肿瘤学/血液系统恶性肿瘤批准通知，白血病相关新药整理如下表。

另外可以看出21年时asciminib已获批白血病治疗，但限定既往接受过两种或更多TKIs治疗，本次获批属于扩大适应证。

参考来源：

1.FDA grants accelerated approval to asciminib for newly diagnosed chronic myeloid leukemia. 2.Asciminib(Scemblix):CADTHReimbursementRecommendation:Indication:ForthetreatmentofadultpatientswithPhiladelphiachromosome-positivechronicmyeloidleukemia(Ph+CML)inchronicphase(CP)previouslytreatedwith2ormoretyrosinekinaseinhibitors.Ottawa(ON):CanadianAgencyforDrugsandTechnologiesinHealth;2022Aug.PMID:38713779. 3.AStudyofOralAsciminibVersusOtherTKIsinAdultPatientsWithNewlyDiagnosedPh+CML-CP. 4.Product information：SCEMBLIX-asciminibtablet,filmcoated.UpdatedAugust7,2024. 5.Oncology(Cancer)/HematologicMalignanciesApprovalNotifications.

病例31-2023：一名79岁男性，身体不自主运动，一过性反应迟钝

以下内容来源于新英格兰医学杂志。

Presentation of Case

Dr. Carrie Chui (Neurology): A 79-year-old man was admitted to this hospital because of involuntary movements on the left side and transient unresponsiveness.

The patient had been in his usual state of health until 9 months before admission, when involuntary movements of the left shoulder and left side of the face developed. The movements were described by the patient as twitching, were not associated with a change in the level of consciousness, and resolved after 1 to 2 minutes. During the next 6 months, the patient had similar episodes approximately once per month, but the episodes increased in duration, lasting 5 to 6 minutes.

Three months before admission, the episodes of involuntary movements increased in frequency, and the patient was evaluated by his primary care physician. The physical examination was normal. Results of kidney-function tests were normal, as were blood levels of glucose and electrolytes, except for the sodium level, which was 129 mmol per liter (reference range, 135 to 145). There was a history of inappropriate antidiuretic hormone secretion, and the sodium level was similar to levels obtained during the past 4 years. Magnetic resonance imaging (MRI) of the head (Figure 1A), performed before and after the administration of intravenous contrast material, revealed a focus of enhancement in the right middle frontal gyrus that was thought to be a small vascular anomaly. Electroencephalography (EEG), performed with the patient in awake and drowsy states, revealed rare, brief, focal slowing in the left temporal lobe during drowsiness; no epileptiform abnormalities were present.

Figure 1

MRI of the Head and CT Angiogram of the Head and Neck.

Two months before admission, the patient was evaluated in the epilepsy clinic affiliated with this hospital. He reported that the episodes of involuntary movements had increased in both frequency and duration, occurring once or twice per day and lasting approximately 10 minutes. Episodes began with tingling and numbness in the left leg that prompted the patient to voluntarily stomp the left foot to relieve the uncomfortable sensation. Then, the patient had involuntary movements that he described as an uncontrollable invisible force moving the left leg and arm, with hyperextension of the arm backward and pronation of the wrist. There was associated numbness in the distal portions of the left third, fourth, and fifth fingers and involuntary movement of the left cheek. No prodromal symptoms occurred. The patient had awareness during the episodes, and after the episodes, he felt fatigued but had a normal level of consciousness, without confusion. The examination in the epilepsy clinic was normal. A diagnosis of seizure disorder was considered, and treatment with levetiracetam was started.

Three weeks before admission, the patient was again evaluated in the epilepsy clinic. He reported that the episodes of involuntary movements still occurred on a daily basis but had decreased in duration and involved only the left leg, without abnormal movements of the arm or face. Dizziness, headache, and weakness had developed and were attributed to the use of levetiracetam. The patient’s family had recorded a video of one of the episodes of involuntary movements. After reviewing the video, the patient’s neurologist thought that the episodes were less likely to be caused by seizures and more consistent with choreoathetoid movements. Cross-tapering of medications — with the simultaneous administration of levetiracetam in decreasing doses and clobazam in increasing doses — was initiated, and the patient was referred to the movement disorders clinic affiliated with this hospital.

On the morning of admission, an episode of involuntary movements of the left leg and left shoulder occurred and persisted for 1 hour. Several hours after the symptoms abated, the patient’s wife found the patient to be unresponsive; he was sitting in a chair. Emergency medical services were called, and when they arrived, the patient was responsive. The fingerstick blood glucose level was 180 mg per deciliter (10.0 mmol per liter) and the blood pressure 110/80 mm Hg. The patient was transported to the emergency department of this hospital for further evaluation.

In the emergency department, the patient reported dysuria and increased urinary frequency. The patient’s daughter noted that he had been more anxious during the past 3 years and occasionally had trouble with memory. Other medical history included Barrett’s esophagus, benign prostatic hypertrophy, chronic hepatitis B virus infection, eczema, gastroesophageal reflux disease, hypertension, nonischemic cardiomyopathy, and osteoporosis. There was no history of head trauma or extended loss of consciousness. Medications included aspirin, atorvastatin, doxazosin, finasteride, omeprazole, metoprolol, sacubitril, and valsartan. There were no known drug allergies. The patient was a lifelong nonsmoker and drank alcohol rarely; he did not use illicit drugs. His mother had had gastric cancer, and his sister had had esophageal cancer; there was no family history of seizures.

On examination, the temporal temperature was 36.8°C, the blood pressure 152/97 mm Hg, the pulse 65 beats per minute, the respiratory rate 16 breaths per minute, and the oxygen saturation 96% while the patient was breathing ambient air. The body-mass index (the weight in kilograms divided by the square of the height in meters) was 21.7. The blood pressure decreased to 130/63 mm Hg with standing. The patient was alert and interactive. The lower jaw was held to the left, but the nasolabial folds and smile were symmetric with activation. There were nonrhythmic, nonstereotyped, writhing movements of the left arm. Tone was normal, and strength was assessed as 5 out of 5 in the arms and legs. Results of liver-function and kidney-function tests were normal, as were blood levels of glucose and electrolytes, except for the sodium level, which was 125 mmol per liter. The lactate level was 2.1 mmol per liter (19 mg per deciliter; reference range, 0.5 to 2.0 mmol per liter [5 to 18 mg per deciliter]). The urinalysis was normal. Intravenous fluids were administered. Imaging studies were obtained.

Dr. Rajiv Gupta: Computed tomographic (CT) angiography of the head and neck (Figure 1B) revealed extensively calcified plaque with severe stenosis of the distal right common carotid artery (CCA), extending into the proximal right internal carotid artery (ICA), as well as stenosis of the right and left paraclinoid ICAs and the left vertebral artery at its origin. There was no vascular abnormality on the CT angiogram that corresponded to the abnormality in the right middle frontal gyrus seen on the previous MRI.

Dr. Chui: The patient was admitted to the hospital. On the second hospital day, the sodium level had increased to 130 mmol per liter, and the lactate level was normal. Additional imaging studies were obtained.

Dr. Gupta: MRI of the head showed no evidence of acute infarction. The focus of enhancement in the right frontal lobe that had been noted previously was not seen on the current MRI.

Dr. Chui: Blood levels of thyrotropin, cobalamin, and glycated hemoglobin and results of coagulation tests were normal. Screening tests for Lyme disease, tuberculosis, and syphilis were negative, as were tests for antibodies to cardiolipin and β₂-glycoprotein. A test for antinuclear antibodies was positive, at a titer of 1:160 in a homogeneous pattern. During a physical therapy session, the patient had abnormal movements of the left leg, left arm, and left side of the face. The abnormal movements diminished when the patient used distraction techniques, such as thigh tapping, finger snapping, and walking while holding a glass of water.

The transient unresponsiveness that led to the patient’s admission was attributed to a combination of sedation from clobazam and hypovolemia. Treatment with clobazam was stopped, and hydration was encouraged. A diagnosis of functional neurologic disorder was considered; outpatient physical therapy with continued use of distraction techniques was recommended. The patient was discharged home on the third hospital day.

Episodes of involuntary movements continued to occur on a daily basis at home. Two weeks after discharge, when the patient was doing exercises while sitting in a chair and having a conversation with his wife, he suddenly stopped talking. She found him slumped in the chair with his eyes closed, no longer exercising. When she asked him questions, he repeatedly said “yes.” Emergency medical services were called, and when they arrived, the patient was alert, diaphoretic, and nonverbal. He had a facial droop on the left side and a right gaze preference. The fingerstick blood glucose level was 130 mg per deciliter (7.2 mmol per liter) and the blood pressure 120/60 mm Hg. The patient was transported to the emergency department of this hospital for further evaluation.

In the emergency department, the temporal temperature was 36.6°C, the blood pressure 143/63 mm Hg, the pulse 66 beats per minute, the respiratory rate 18 breaths per minute, and the oxygen saturation 98% while the patient was breathing ambient air. He was alert and interactive. There was a facial droop on the left side. There was no effort against gravity in the left arm. The patient was able to lift the left leg off the bed for 1 to 2 seconds. He had a right gaze deviation that could not be overcome and mild dysarthria. The remainder of the examination was normal. A diagnosis of stroke was considered, and emergency CT angiography was performed.

Dr. Gupta: CT angiography showed no evidence of acute territorial infarction and no changes in cerebrovascular disease.

Dr. Chui: On repeat physical examination performed after CT angiography, the gaze deviation and dysarthria had resolved, and strength was normal. Mild facial paralysis was present.

A diagnosis was made.

Differential Diagnosis

Dr. Albert Y. Hung: This 79-year-old man initially presented with involuntary movements of the left shoulder and face without associated loss of consciousness. Diagnosis of an unusual movement disorder, especially one that is present episodically, can be challenging. Videos brought in by the patient can be very useful.¹ Most movement disorders result from abnormal functioning of extrapyramidal circuits involving the basal ganglia, rather than a specific neuroanatomical lesion, and the first step toward diagnosis is to identify the type of abnormal movements.²

Four salient aspects of this patient’s involuntary movements can help in characterizing the movement disorder before generating a differential diagnosis. First, the movements were paroxysmal, lasting for short periods of time with resolution between episodes. Second, the movements were nonstereotyped, appearing randomly and variably. Third, the movements were restricted to the left side of his body throughout the course, localizing the disease process to the right cerebral hemisphere. Finally, the symptoms were progressive, increasing in both duration and frequency.

Movement Disorders

This patient had abnormal involuntary movements, symptoms indicative of a hyperkinetic movement disorder. Tremor, the most common hyperkinetic disorder, is unlikely because the patient did not have rhythmic movements. Dystonia is also unlikely, because he did not have sustained muscle contractions that were causing twisting or abnormal postures of the legs, arms, head, neck, or face. Although the patient initially described the movements as twitching, his later descriptions are not suggestive of myoclonus or tics, which manifest as sudden, rapid, recurrent movements.

This patient’s neurologist described the involuntary movements as “choreoathetoid” after reviewing a video of an episode. Chorea, athetosis, and ballism make up a spectrum of involuntary movements that often occur in combination. Chorea refers to involuntary movements that are “dancelike” — irregular, random, unintended, and flowing from one body part to another. When these movements are slow and writhing (with a lower amplitude) and involve the distal limbs, the term athetosis is used. The presence of both chorea and athetosis in the same patient is referred to as choreoathetosis. When the movements are fast and flinging (with a higher amplitude) and involve the proximal limbs, the term ballism is used. Although the description of this patient’s movements was not clearly suggestive of ballism, hemichorea and hemiballismus often occur together.

The term dyskinesia can refer to any abnormal movements and is often used to describe hyperkinetic disorders that are induced by specific drugs, such as tardive dyskinesia induced by dopamine antagonists or dyskinesia induced by levodopa in patients with Parkinson’s disease. Often, dyskinesia manifests as chorea or choreoathetoid movements, but chorea and dyskinesia are not synonymous. This patient appears to have involuntary dyskinesia with choreoathetosis as the primary phenomenology. Before constructing a differential diagnosis for dyskinesia in this patient, I will consider two conditions that mimic dyskinesia: seizures and functional movement disorder.

Seizures

Various movement disorders may be mistaken for seizures, although these movement disorders are not associated with EEG abnormalities during the episode. Patients with some forms of epilepsy may present with abnormal movements without other features that are typically associated with seizures, such as aura, change in responsiveness, incontinence, or a postictal state.^3,4 Seizures were initially suspected in this patient, and he was referred to the epilepsy clinic. Recurrent focal seizures were probably suspected because of the transient nature of the episodes. Initial MRI had shown a small abnormality in the right middle frontal gyrus, but this finding was not seen on follow-up imaging, which makes it unlikely to be related to the overall presentation. Baseline EEG had shown only brief left temporal slowing, without epileptiform abnormalities. The EEG was an interictal study, so the findings do not rule out seizures. However, the slowing was ipsilateral to the abnormal movements, so it is unlikely to be related to the episodes. In addition, the patient’s involuntary movements were nonstereotyped and nonrhythmic, which makes his presentation unlikely to be due to a seizure disorder.

Functional Movement Disorder

Because this patient’s movements diminished with the use of distraction techniques, a diagnosis of functional movement disorder was considered. Most cases of functional movement disorder begin abruptly after a trigger, such as a mild physical injury or illness; a psychological stressor can be present but is not required for diagnosis. Symptoms are typically most severe around the time of onset and may wax and wane over time. Although distractibility is a finding associated with functional disorders, abnormal movements that occur with nonfunctional syndromes can sometimes be suppressed by action or incorporated into voluntary movements in a manner that may appear distractible. Several clinical features in this patient make a diagnosis of functional disorder unlikely. Functional movement disorder is more common in women than in men, and the average age at onset is 40 years.⁵ In addition, tremor is the most common clinical phenotype seen in patients with functional movement disorder; chorea or choreoathetosis, which was seen in this patient, is very unusual in patients with functional movement disorder. Overall, functional movement disorder is unlikely to explain this patient’s presentation.

Dyskinesia

Primary paroxysmal dyskinesia refers to a group of heterogeneous syndromes characterized by recurrent involuntary movements that occur episodically and abruptly, without loss of consciousness.⁶ These disorders usually begin in childhood or young adulthood. Both the age of this patient and the described phenomenology make a diagnosis of primary paroxysmal dyskinesia unlikely.

The differential diagnosis in this case is therefore focused on causes of secondary dyskinesia, of which there are many.⁷ MRI ruled out the presence of a mass lesion suggestive of cancer. The patient had no history of acute illness suggestive of a viral or other infectious encephalitis, and there was no history of trauma or exposure to drugs or other toxins. Although his daughter mentioned trouble with memory, there was no compelling history suggestive of a neurodegenerative disease.

A common metabolic cause of secondary dyskinesia is diabetic striatopathy, a syndrome involving the acute-to-subacute onset of chorea and ballism in the context of hyperglycemia.⁸ This syndrome can occur as the initial manifestation of type 2 diabetes mellitus or as a complication of poorly controlled diabetes. Diabetic striatopathy is more likely to develop in women than in men, and the average age at onset is 70 years. Most patients present with hemichorea and hemiballismus, rather than bilateral symptoms. CT shows hyperdensity, and T1-weighted MRI shows hyperintensity, in the contralateral basal ganglia. However, this patient had no history of diabetes and had a normal blood glycated hemoglobin level, features that rule out a diagnosis of diabetic striatopathy.

Choreiform movements can also be a manifestation of autoimmune conditions.⁹ This patient’s initial presentation with unilateral shoulder and face movements would have suggested the possibility of faciobrachial dystonic seizures associated with anti–leucine-rich, glioma-inactivated 1 (anti-LGI1) encephalitis.¹⁰ This condition is often associated with hyponatremia, which was present in this patient. However, as the case evolved, leg involvement and sensory changes developed that would be atypical for anti-LGI1 encephalitis.

One key clue in this case is that the patient did not have an isolated movement disorder. In addition to motor symptoms, he had a variety of sensory symptoms involving both the left arm and the left leg. His first hospital admission was precipitated by an episode of unresponsiveness. The clinical event that led to his second presentation to the emergency department was distinctly different: an acute onset of speech difficulty accompanied by left hemiparesis and right gaze deviation that was worrisome for an acute right middle cerebral artery (MCA) syndrome. The symptoms resolved without intervention, which indicates that he may have had an acute transient ischemic attack (TIA). The most relevant imaging finding was severe cerebrovascular disease, including severe stenosis of the distal right CCA and proximal right ICA. Could this patient’s movement disorder be explained by a vascular lesion?

Limb-Shaking TIAs

Limb-shaking TIAs were first described by C. Miller Fisher in 1962.¹¹ In most case reports, these episodes are associated with high-grade stenosis of the ICA, which was seen in this patient.^12,13 The mechanism is thought to be cerebral hypoperfusion, and changes in posture or head position that decrease cerebral blood flow can precipitate these episodes. In this patient, the first episode of unresponsiveness that led to hospital admission occurred when he was sitting. He then had an acute episode involving right gaze preference that was provoked by exercise and was very suggestive of a TIA in the right MCA territory. These findings are highly suggestive of a diagnosis of limb-shaking TIAs, and I would refer this patient for emergency carotid endarterectomy.

Clinical Impression and Initial Management

Dr. Scott B. Silverman: When I evaluated this patient, his transient right gaze preference and left hemiparesis were consistent with a right MCA syndrome due to a TIA from symptomatic severe stenosis of the right ICA. The mechanism of this event was either artery-to-artery embolism or hypoperfusion. His previous, recurrent episodes of transient choreoathetosis on the left side that had occurred mainly while he was sitting, standing, or exercising were consistent with limb-shaking TIAs from hypoperfusion or low flow.

The pathogenesis of a low-flow state related to severe carotid stenosis resulting in limb-shaking TIAs is described in a small case series.¹⁴ In six out of eight patients, the transient, stereotyped, involuntary movements were eliminated with carotid artery revascularization. Positional cerebral ischemia in patients without orthostatic hypotension has been described.¹⁵

Treatment with atorvastatin was continued, the dose of aspirin was increased to 325 mg per day, and an intravenous heparin infusion was started. The strategy of permissive hypertension was used, with high blood pressure allowed to a maximum systolic blood pressure of 180 mm Hg. The patient was admitted to the stroke service, and carotid artery duplex ultrasonography was performed.

Dr. Gupta: Doppler ultrasonography of the carotid arteries (Figure 2) revealed markedly elevated Doppler flow velocities within the proximal right ICA. There was a parvus et tardus waveform in the distal right ICA, a finding indicative of low flow related to the more proximal high-grade stenosis. The Doppler waveform contours had poststenotic turbulence.

Figure 2

Doppler Ultrasound Image.

Dr. Silverman: The vascular surgery service was consulted, and the patient underwent right carotid endarterectomy.

Clinical Diagnosis

Limb-shaking transient ischemic attacks.

Dr. Albert Y. Hung’s Diagnosis

Limb-shaking transient ischemic attacks due to severe carotid stenosis, with secondary paroxysmal dyskinesia.

Pathological Discussion

Dr. Caroline F. Hilburn: The endarterectomy specimen included the carotid bifurcation and was notable for firm arterial walls, a finding consistent with calcification. On gross examination (Figure 3A), a large plaque was centered at the carotid bifurcation and protruded into the lumen, resulting in a maximal luminal stenosis of 80%. The plaque had an irregular and focally friable surface. On microscopic examination (Figure 3B), the plaque was characterized by extensive calcification. Some regions of the plaque had a smooth, healed fibrous cap, whereas other regions had an irregular surface suggestive of ulceration, which indicated potential sites of plaque rupture. Multiple smaller calcified plaques were present, affecting both branches of the artery.

Figure 3

Endarterectomy Specimen.

Pathological Diagnosis

Complex atherosclerotic plaque with portions of attached media.

Additional Management

Dr. Silverman: After the procedure, the patient had an uneventful recovery and was discharged home on the fifth hospital day. He was seen 1 month after discharge in the stroke prevention clinic. There had been no further episodes of involuntary movements or choreoathetosis and no stroke or TIA. The patient continues to take aspirin, atorvastatin, and antihypertensive medications.