专家谈如何鉴别TIA/卒中与症状相似疾病

檀香山——St. Mercy Saline医院卒中项目主任Susan L. Hickenbottom博士在美国心脏协会主办的国际卒中大会上指出，区分短暂性脑缺血发作(TIA)/卒中与症状类似的疾病(包括部分性发作和复杂性偏头痛)的关键在于临床病史。

Susan L. Hickenbottom博士

卒中和TIA通常具有特定临床表现，并且通常涉及血管通路，而随机症状模式不一定涉及血管通路。

症状发生时间提供的信息非常重要。TIA/卒中症状通常在几秒至几分钟内突然发生，并且无进一步进展。相比之下，复杂性偏头痛或部分性发作通常从身体的一部分开始，然后逐渐扩展，症状可能从手部开始，几分钟后向上扩展至手臂和面部，神经科医生称此类进展为“杰克逊发作”。

复杂性偏头痛是具有以下局灶性神经系统症状的偏头痛：身体一侧或另一侧无力、刺痛或麻木，这些症状可在头痛发生前、发生同时或发生后出现。复杂性偏头痛通常伴随典型偏头痛症状，包括恶心、畏光、视觉先兆现象，如闪光暗点或万花筒视觉。首次偏头痛发作很少为复杂性偏头痛。因此，发生疑似复杂性偏头痛但无偏头痛史的患者很可能发生的是TIA/卒中。

部分性发作可分为2类：复杂部分性发作和简单部分性发作。根据定义，复杂部分性发作与意识水平改变或意识丧失相关，但简单部分性发作与意识改变或丧失无关。发生复杂部分性发作的患者通常会往空旷处凝视。常见症状包括奇怪气味、发作恐惧、似曾相识或似不相识感、以及咂嘴或重复性手部动作等自动行为。需指出的是，这些症状为阳性现象。相比之下，TIA/卒中患者通常主要发生以下阴性现象：视力丧失(而非看见爆发式闪光)、言语丧失、运动功能丧失和/或感觉丧失。

Hickenbottom博士表示，目前对于TIA与卒中的区别，神经科医生已经转变了观念。过去人们根据症状持续时间来定义TIA，如果血管分布模式的症状持续不足1 h就认为是TIA。但现在观念已经改变。随着有效的组织型纤溶酶原激活剂被广泛用于治疗急性缺血性卒中，并且在再灌注这点上认识到“时间就是大脑”，目前卒中专科医生不愿再干等着记录症状持续时间。目前的趋势是摒弃任意的时间截点，从生理学上将TIA定义为无急性梗死或成像检查证据的由局灶性脑、脊髓或视网膜缺血引起的神经功能障碍发作。卒中则是具有此类证据的发作。

初级保健医生、心脏科医生和急诊科医生要想迅速鉴别TIA/卒中与症状相似的疾病，就需要学习像神经科医生那样思考。神经科医生考虑的第一个问题是症状是局灶性还是弥漫性，第二是发生的时间。接着，神经科医生会想要知道症状是否遵循典型血管通路，了解哪条脑动脉可能受累。

在前循环中，累及颈内动脉的血管症状以同侧单眼暂时失明(称为一过性黑朦)为特征，可伴随或不伴随对侧无力或感觉改变。

大脑前动脉闭塞可导致对侧无力、可能人格改变(如去抑制或缺乏动力)及感觉改变，腿部受累比面部或手臂受累更为常见。

大脑中动脉血管症状包括对侧无力和感觉改变，面部和手臂受累比腿部受累更为常见。在一些病例(并非所有病例)中，可伴随对侧视力缺陷。如果损伤位于优势半球，可导致失语(说话或理解语言困难)。如果非优势半球受累，患者的对侧身体可能发生视力/空间困难，有时可严重到他们不知道该侧身体存在。

在后循环中，累及椎基底动脉的血管症状可表现为同侧颅神经缺损和累及面部的共济失调及身体对侧或双侧感觉改变或无力。椎基底动脉受累的典型5D症状是复视、构音障碍、失衡、嗜睡和死亡。累及大脑后动脉的血管症状以对侧视力缺损为特征。

尽管部分性发作和复杂性偏头痛是TIA/卒中最常见和重要的类似症状，但有时惊恐发作、转换障碍、眩晕和晕厥也会与TIA相混淆。

惊恐发作有时涉及局灶性神经系统症状，但症状通常较为模糊和随机。患者主诉可能为全身麻刺而非一半身体麻刺。患者一般具有惊恐障碍或焦虑障碍史，提示神经系统疾病的症状伴有其他惊恐症状，包括气短、头晕、心悸、腹痛或恐惧死亡。

具有与转换障碍相关的似乎为神经系统症状的患者通常具有其他一些类型的精神疾病史。仔细检查可发现他们看似是神经系统的症状不遵循生理模式。留意检查发现的不一致：非生理性的感觉丧失或无力，或通过任务转移患者注意力时未见震颤。差别可能较为细微；在怀疑转换障碍时，寻求神经科会诊会非常有帮助。

无其他伴随性神经系统症状的孤立性眩晕很少为血管性。

晕厥是一个弥漫性/急性过程，而非定义TIA/卒中的局灶性/急性过程。神经科医生经常参与对晕厥患者的会诊，但事实上晕厥很少由神经系统疾病引起。然而，如果患者在晕厥发作醒来后出现几分钟以上的精神错乱，则需加以注意，因为晕厥患者通常在醒来后即可恢复正常精神状态，而长时间的精神错乱表明存在癫痫伴发作后精神错乱的可能性增加。

Hickenbottom博士声明无经济利益冲突。

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By: BRUCE JANCIN, Internal Medicine News Digital Network

HONOLULU – The key to differentiating transient ischemic attacks and strokes from their main mimics – including partial seizures and complicated migraine – lies in the clinical history, Dr. Susan L. Hickenbottom said at the International Stroke Conference sponsored by the American Heart Association.

"The idea is that there are specific clinical presentations that go along with stroke and TIA. Almost always the vascular pathways are respected, as opposed to random patterns of symptoms that don’t really respect a vascular pathway," explained Dr. Hickenbottom, a neurologist who is director of the stroke program at St. Mercy Saline (Mich.) Hospital and a consortium of other community hospitals.

The timing of symptom onset provides important information. TIA/stroke symptoms typically start suddenly within seconds to minutes and don’t progress further. In contrast, the symptoms of complicated migraine or partial seizures often evolve in what neurologists call ‘the Jacksonian march,’ starting in one part of the body and then gradually spreading.

"The symptoms might start in, say, the hand, then over several minutes move up the arm and then to the face. Whereas typically with TIA or stroke, ‘boom,’ the patient has symptoms," she continued.

Complicated migraine is migraine with focal neurologic symptoms: weakness, tingling, or numbness on one side of the body or the other that can precede, accompany, or follow the actual headache. Complicated migraine is often accompanied by classic migraine symptoms, including nausea, photophobia, and visual aura phenomena such as scintillating scotoma or kaleidoscope vision.

It’s rare for a patient’s first-ever migraine episode to involve complicated migraine. Thus, a patient who presents with what looks like complicated migraine but no history of migraine is much more likely to have TIA/stroke.

Partial seizures can be divided into two types: complex partial seizures, which by definition are associated with an altered level or loss of consciousness; and simple partial seizures, which are not.

A patient experiencing a complex partial seizure will often stare off into space. Strange odors, ictal fear, the sensation of déjà vu or jamais vu, and automatic behaviors such as lip smacking or repetitive hand movements are common.

Notably, these symptoms are positive phenomena. In contrast, patients with TIA/stroke usually experience predominantly negative phenomena: loss of vision rather than seeing bursts of flashing lights, loss of speech, loss of motor function, and/or loss of sensation.

Dr. Hickenbottom said neurologists have changed their thinking about the distinction between TIA and stroke. It used to be that TIA was defined based upon duration: if symptoms in a vascular distribution pattern lasted less than 1 hour, it was a TIA. No longer. With the widespread availability of effective tissue plasminogen activator therapy for acute ischemic stroke, and the recognition that "time is brain" when it comes to reperfusion, stroke specialists are loath to stand around clocking symptom duration.

"The trend now is to move away from an arbitrary time cutoff and define TIA physiologically as an episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without evidence of acute infarction on imaging studies. And stroke is an episode with such evidence," she explained.

For primary care physicians, cardiologists, and emergency physicians to quickly distinguish TIA/stroke from its mimics, it’s important to learn to think like a neurologist, according to Dr. Hickenbottom. The first issue neurologists consider, she said, is whether the symptoms are focal or diffuse. The second is the temporal onset. And then neurologists want to see if the symptoms follow a characteristic vascular pathway informative of which brain artery is likely involved.

In the anterior circulation, vascular syndromes involving the internal carotid artery are characterized by the ipsilateral monocular temporary vision loss known as amaurosis fugax, which may or may not be accompanied by contralateral weakness or sensory changes.

Occlusion of the anterior cerebral artery brings contralateral weakness, possibly personality changes such as disinhibition or lack of motivation, and sensory changes, with the leg being more often affected than the face or arm.

Middle cerebral artery vascular syndromes entail contralateral weakness and sensory changes, with the face and arm more commonly involved than the leg. In some but not all cases, this is accompanied by a contralateral visual deficit. If the injury is in the dominant hemisphere it can result in aphasia: difficulty in speaking or understanding language. If the nondominant hemisphere is affected, people may experience visual/spatial difficulties on the opposite side of the body, even to the extent that they’re no longer aware of the existence of that side of the body.

In the posterior circulation, vascular syndromes involving the vertebrobasilar artery may manifest as ipsilateral cranial nerve deficits and ataxia involving the face along with contralateral or bilateral sensory changes or weakness on the body. The classic ‘5Ds’ of vertebrobasilar artery involvement, Dr. Hickenbottom observed, are diplopia, dysarthria, disequilibrium, drowsiness, and death. Vascular syndromes involving the posterior cerebral artery characteristically involve a contralateral visual field deficit.

While partial seizures and complicated migraine are the most common and important TIA/stroke mimics, on occasion panic attacks, conversion disorder, vertigo, and syncope can also be confused with TIA.

Panic attacks occasionally involve focal neurologic symptoms, but more typically the symptoms are vague and random. "It’s ‘I got numb and tingly all over,’ rather than ‘I got numb and tingly on one-half of my body,’ " the neurologist said.

Affected patients generally have a history of panic disorder or an anxiety disorder, and symptoms suggestive of a neurologic condition are accompanied by other panic symptoms, including shortness of breath, dizziness, palpitation, abdominal pain, or fear of dying.

Patients with conversion disorder–related symptoms that appear to be neurologic most often have a history of psychiatric disease of some other kind. On careful examination their seemingly neurologic symptoms don’t adhere to a physiologic pattern. Look for inconsistencies on examination: nonphysiologic sensory loss or weakness, or absence of tremor when the patient is distracted by a task. The distinctions can be subtle; a neurologic consultation can be very helpful when conversion disorder is suspected, according to Dr. Hickenbottom.

Isolated vertigo with no other accompanying neurologic symptoms is seldom vascular in nature.

"The brain stem is so small that to have a vascular episode that just affects the vestibular nuclei without getting double vision, or slurred speech, or a droopy face, or something else is pretty unlikely," she said.

Syncope is a diffuse/acute process rather than the focal/acute process which defines TIA/stroke. Neurologists get lots of consultations for patients with syncope, but the fact is syncope rarely has a neurologic cause. However, that possibility is heightened when a patient experiences more than a few minutes of confusion after waking up from a syncopal episode. Patients typically return to their normal mental status almost as soon as they wake up. Prolonged confusion raises the possibility of a seizure disorder with post-ictal confusion, according to Dr. Hickenbottom.

She reported having no financial conflicts.