How to tell TIA/stroke from mimics

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.

[email protected]

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.

[email protected]

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.

[email protected]