History
A focused medical history for patients with ischemic stroke aims to identify risk factors for atherosclerotic and cardiac disease, including the following (see Etiology):
-
Hypertension
-
Diabetes mellitus
-
Tobacco use
-
High cholesterol
-
History of coronary artery disease, coronary artery bypass, or atrial fibrillation
In younger patients, elicit a history of the following:
-
Recent trauma
-
Coagulopathies
-
Illicit drug use (especially cocaine)
-
Migraines
-
Oral contraceptive use
Stroke should be considered in any patient presenting with an acute neurologic deficit (focal or global) or altered level of consciousness. No historical feature distinguishes ischemic from hemorrhagic stroke, although nausea, vomiting, headache, and a sudden change in the patient’s level of consciousness are more common in hemorrhagic strokes.
Consider stroke in any patient presenting with acute neurologic deficit or any alteration in level of consciousness. Common signs and symptoms of stroke include the abrupt onset of any of the following:
-
Hemiparesis, monoparesis, or (rarely) quadriparesis
-
Hemisensory deficits
-
Monocular or binocular visual loss
-
Visual field deficits
-
Diplopia
-
Dysarthria
-
Facial droop
-
Ataxia
-
Vertigo (rarely in isolation)
-
Aphasia
-
Sudden decrease in the level of consciousness
Although such symptoms can occur alone, they are more likely to occur in combination.
Establishing the time at which the patient was last without stroke symptoms, or last known to be normal, is especially critical when fibrinolytic therapy is an option. Unfortunately, the median time from symptom onset to emergency department (ED) presentation ranges from 4-24 hours in the United States. [2]
Multiple factors contribute to delays in seeking care for symptoms of stroke. Many strokes occur while patients are sleeping and are not discovered until the patient wakes (this phenomenon is also known as "wake-up" stroke). Stroke can leave some patients too incapacitated to call for help. Occasionally, a stroke goes unrecognized by patients or their caregivers. [5, 58]
If the patient awakens with symptoms, then the time of onset is defined as the time at which the patient was last seen to be without symptoms or last known normal time. Input from family members, coworkers, and bystanders may be required to help establish the exact time of onset, especially in right hemispheric strokes accompanied by neglect or left hemispheric strokes with aphasia.
Physical Examination
The goals of the physical examination are as follows:
-
Detect extracranial causes of stroke symptoms
-
Distinguish stroke from stroke mimics
-
Determine and document for future comparison the degree of neurologic deficit (NIH Stroke Scale)
-
Localize the lesion
-
Identify comorbidities
-
Identify conditions that may influence treatment decisions (eg, recent surgery or trauma, active bleeding, active infection)
The physical examination always includes a careful head and neck examination for signs of trauma, infection, and meningeal irritation. A careful search for the cardiovascular causes of stroke requires examination of the following:
-
Ocular fundi (retinopathy, emboli, hemorrhage)
-
Heart (irregular rhythm, murmur, gallop)
-
Peripheral vasculature (palpation of carotid, radial, and femoral pulses; auscultation for carotid bruit)
The physical examination must encompass all of the major organ systems, starting with airway, breathing, and circulation (ABCs) and the vital signs. Patients with a decreased level of consciousness should be assessed to ensure that they are able to protect their airway. Patients with stroke, especially hemorrhagic stroke, can suffer quick clinical deterioration; therefore, constant reassessment is critical.
Ischemic strokes, unless large or involving the brainstem, do not tend to cause immediate problems with airway patency, breathing, or circulation compromise. On the other hand, patients with intracerebral or subarachnoid hemorrhage frequently require intervention for airway protection and ventilation.
Vital signs, while nonspecific, can point to impending clinical deterioration and may assist in narrowing the differential diagnosis. Many patients with stroke are hypertensive at baseline, and their blood pressure may become more elevated after stroke. While hypertension at presentation is common, blood pressure decreases spontaneously over time in most patients.
Head and neck, cardiac, and extremities examination
A careful examination of the head and neck is essential. Contusions, lacerations, and deformities may suggest trauma as the etiology for the patient's symptoms. Auscultation of the neck may elicit a bruit, suggesting carotid disease as the cause of the stroke.
Cardiac arrhythmias, such as atrial fibrillation, are found commonly in patients with stroke. Similarly, strokes may occur concurrently with other acute cardiac conditions, such as acute myocardial infarction and acute heart failure; thus, auscultation for murmurs and gallops is recommended.
Carotid or vertebrobasilar dissections and, less commonly, thoracic aortic dissections may cause ischemic stroke. Unequal pulses or blood pressures in the extremities may reflect the presence of aortic dissections.
Neurologic examination
With the availability of fibrinolytic and endovascular therapies for acute ischemic stroke in selected patients, the physician must be able to perform a brief but accurate neurologic examination on patients with suspected stroke syndromes. The goals of the neurologic examination include the following:
-
Confirming the presence of a stroke syndrome
-
Distinguishing stroke from stroke mimics
-
Establishing a neurologic baseline (including documenting an NIH Stroke Scale) should the patient's condition improve or deteriorate
-
Establishing stroke severity to assist in prognosis and therapeutic selection (based on potential disability due to current neurologic deficits)
Essential components of the neurologic examination include the following evaluations:
-
Cranial nerves
-
Motor function
-
Sensory function
-
Cerebellar function
-
Gait
-
Language (expressive and receptive capabilities)
-
Mental status and level of consciousness
The skull and spine also should be examined, and signs of meningismus should be sought.
National Institutes of Health Stroke Scale
A useful tool in quantifying neurologic impairment is the National Institutes of Health Stroke Scale (NIHSS) (see Table 2, below). The NIHSS enables the healthcare provider to rapidly determine the severity and possible location of the stroke. NIHSS scores are strongly associated with outcome and can help to identify those patients who are likely to benefit from reperfusion therapies and those who are at higher risk of developing complications from the stroke itself and potential reperfusion strategies.
The NIHSS is easily performed; it focuses on the following 6 major areas of the neurologic examination:
-
Level of consciousness
-
Visual function
-
Motor function
-
Sensation and neglect
-
Cerebellar function
-
Language
The NIHSS is a 42-point scale. Patients with minor strokes usually have a score of less than 5. An NIHSS score of greater than 10 correlates with an 80% likelihood of proximal vessel occlusions (as identified on CT or standard angiograms). However, discretion must be used in assessing the magnitude of the clinical deficit and resulting disability; for instance, if a patient's only deficit is mutism or blindness, the NIHSS score will be 3. Additionally, the scale does not measure some deficits associated with posterior circulation strokes (ie, vertigo, ataxia). [59]
Table 2. National Institutes of Health Stroke Scale (Open Table in a new window)
|
Category |
Description |
Score |
1a |
level of consciousness (LOC) |
Alert Drowsy Stuporous Coma |
0 1 2 3 |
1b |
LOC questions (month, age) |
Answers both correctly Answers 1 correctly Incorrect on both |
0 1 2 |
1c |
LOC commands (open and close eyes, grip and release nonparetic hand) |
Obeys both correctly Obeys 1 correctly Incorrect on both |
0 1 2 |
2 |
Best gaze (follow finger) |
Normal Partial gaze palsy Forced deviation |
0 1 2 |
3 |
Best visual (visual fields) |
No visual loss Partial hemianopia Complete hemianopia Bilateral hemianopia |
0 1 2 3 |
4 |
Facial palsy (show teeth, raise brows, squeeze eyes shut) |
Normal Minor Partial Complete |
0 1 2 3 |
5 |
Motor arm left* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
6 |
Motor arm right* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
7 |
Motor leg left* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
8 |
Motor leg right* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
9 |
Limb ataxia (finger-nose, heel-shin) |
Absent Present in 1 limb Present in 2 limbs |
0 1 2 |
10 |
Sensory (pinprick to face, arm, leg) |
Normal Partial loss Severe loss |
0 1 2 |
11 |
Extinction/neglect (double simultaneous testing) |
No neglect Partial neglect Complete neglect |
0 1 2 |
12 |
Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty") |
Normal articulation Mild to moderate dysarthria Near to unintelligible or worse |
0 1 2 |
13 |
Best language** (name items, describe pictures) |
No aphasia Mild to moderate aphasia Severe aphasia Mute |
0 1 2 3 |
|
Total |
- |
0-42 |
* For limbs with amputation, joint fusion, etc, score 9 and explain ** For intubation or other physical barriers to speech, score 9 and explain. Do not add 9 to the total score. NIH Stroke Scale (PDF) |
|||
Middle cerebral artery stroke
Middle cerebral artery (MCA) occlusions commonly produce the following:
-
Contralateral hemiparesis
-
Contralateral hypesthesia
-
Ipsilateral hemianopsia
-
Gaze preference toward the side of the lesion
-
Agnosia
-
Receptive or expressive aphasia, if the lesion occurs in the dominant hemisphere
-
Neglect, inattention, and extinction of double simultaneous stimulation, with some nondominant hemisphere lesions
The MCA supplies the upper extremity motor strip. Consequently, weakness of the arm and face is usually worse than that of the lower limb.
Anterior cerebral artery stroke
Anterior cerebral artery (ACA) occlusions primarily affect frontal lobe function. Findings in ACA stroke may include the following:
-
Disinhibition and speech perseveration
-
Primitive reflexes (eg, grasping, sucking reflexes)
-
Altered mental status
-
Impaired judgment
-
Contralateral weakness (greater in legs than arms)
-
Contralateral cortical sensory deficits
-
Gait apraxia
-
Urinary incontinence
Posterior cerebral artery stroke
Posterior cerebral artery (PCA) occlusions affect vision and thought. Manifestations include the following:
-
Contralateral homonymous hemianopsia
-
Cortical blindness
-
Visual agnosia
-
Altered mental status
-
Impaired memory
Vertebrobasilar artery occlusions are particularly difficult to localize because they may cause a wide variety of cranial nerve, cerebellar, and brainstem deficits, and may be vague in nature. These include the following:
-
Vertigo
-
Nystagmus
-
Diplopia
-
Visual field deficits
-
Dysphagia
-
Dysarthria
-
Facial hypesthesia
-
Syncope
-
Ataxia
A hallmark of posterior circulation stroke is the presence of crossed findings: ipsilateral cranial nerve deficits and contralateral motor deficits. This contrasts with anterior stroke, which produces only unilateral findings.
Lacunar stroke
Lacunar strokes result from occlusion of the small, perforating arteries of the deep subcortical areas of the brain. The infarcts are generally from 2-20 mm in diameter. The most common lacunar syndromes include pure motor, pure sensory, and ataxic hemiparetic strokes. By virtue of their small size and well-defined subcortical location, lacunar infarcts do not lead to impairments in cognition, memory, speech, or level of consciousness.
-
Maximum intensity projection (MIP) image from a computed tomography angiogram (CTA) demonstrates a filling defect or high-grade stenosis at the branching point of the right middle cerebral artery (MCA) trunk (red circle), suspicious for thrombus or embolus. CTA is highly accurate in detecting large- vessel stenosis and occlusions, which account for approximately one third of ischemic strokes.
-
Axial noncontrast computed tomography (NCCT) scan demonstrates diffuse hypodensity in the right lentiform nucleus with mass effect upon the frontal horn of the right lateral ventricle in a 70-year-old woman with a history of left-sided weakness for several hours.
-
Magnetic resonance imaging (MRI) scan in a 70-year-old woman with a history of left-sided weakness for several hours. An axial T2 fluid-attenuated inversion recovery (FLAIR) image (left) demonstrates high signal in the lentiform nucleus with mass effect. The axial diffusion-weighted image (middle) demonstrates high signal in the same area, with corresponding low signal on the apparent diffusion coefficient (ADC) maps, consistent with true restricted diffusion and an acute infarction. Maximum intensity projection from a 3-dimensional (3-D) time-of-flight magnetic resonance angiogram (MRA, right) demonstrates occlusion of the distal middle cerebral artery (MCA) trunk (red circle).
-
Cardioembolic stroke: Axial diffusion-weighted images demonstrate scattered foci of high signal in the subcortical and deep white matter bilaterally in a patient with a known cardiac source for embolization. An area of low signal in the left gangliocapsular region may be secondary to prior hemorrhage or subacute to chronic lacunar infarct. Recurrent strokes are most commonly secondary to cardioembolic phenomenon.
-
Axial noncontrast computed tomography (CT) scan demonstrates a focal area of hypodensity in the left posterior limb of the internal capsule in a 60-year-old man with acute onset of right-sided weakness. The lesion demonstrates high signal on the fluid-attenuated inversion recovery (FLAIR) sequence (middle image) and diffusion-weighted magnetic resonance imaging (MRI) scan (right image), with low signal on the apparent diffusion coefficient (ADC) maps indicating an acute lacunar infarction. Lacunar infarcts are typically no more than 1.5 cm in size and can occur in the deep gray matter structures, corona radiata, brainstem, and cerebellum.
-
Magnetic resonance imaging (MRI) scan was obtained in a 62-year-old man with hypertension and diabetes and a history of transient episodes of right-sided weakness and aphasia. The fluid-attenuated inversion recovery (FLAIR) image (left) demonstrates patchy areas of high signal arranged in a linear fashion in the deep white matter, bilaterally. This configuration is typical for deep border-zone, or watershed, infarction, in this case the anterior and posterior middle cerebral artery (MCA) watershed areas. The left-sided infarcts have corresponding low signal on the apparent diffusion coefficient (ADC) map (right), signifying acuity. An old left posterior parietal infarct is noted as well.
-
A 48-year-old man presented with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference. Angiogram with selective injection of the right internal carotid artery demonstrates occlusion of the M1 segment of the right middle cerebral artery (MCA) and A2 segment of the right anterior cerebral artery (ACA; images courtesy of Concentric Medical).
-
Follow-up imaging after mechanical embolectomy in 48-year-old man with acute left-sided hemiplegia, facial palsy, and right-sided gaze preference demonstrates complete recanalization of the right middle cerebral artery (MCA) and partial recanalization of the right A2 segment (images courtesy of Concentric Medical).
-
Cerebral angiogram performed approximately 4.5 hours after symptom onset in a 31-year-old man demonstrates an occlusion of the distal basilar artery (images courtesy of Concentric Medical).
-
Image on the left demonstrates deployment of a clot retrieval device (older generation device) in a 31-year-old man. Followup angiogram after embolectomy demonstrates recanalization of the distal basilar artery with filling of the superior cerebellar arteries and posterior cerebral arteries. The patient had complete resolution of symptoms following embolectomy (images courtesy of Concentric Medical).
-
Noncontrast computed tomography (CT) scan in a 52-year-old man with a history of worsening right-sided weakness and aphasia demonstrates diffuse hypodensity and sulcal effacement with mass effect involving the left anterior and middle cerebral artery territories consistent with acute infarction. There are scattered curvilinear areas of hyperdensity noted suggestive of developing petechial hemorrhage in this large area of infarction.
-
Magnetic resonance angiogram (MRA) in a 52-year-old man demonstrates occlusion of the left precavernous supraclinoid internal carotid artery (ICA, red circle), occlusion or high-grade stenosis of the distal middle cerebral artery (MCA) trunk and attenuation of multiple M2 branches. The diffusion-weighted image (right) demonstrates high signal confirmed to be true restricted diffusion on the apparent diffusion coefficient (ADC) map consistent with acute infarction.
-
Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery (MCA), with the apex representing the Sylvian point.
-
Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICAs) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICAs) arise from the proximal basilar artery. The superior cerebellar arteries (SCAs) arise distally from the basilar artery prior to its bifurcation into the posterior cerebral arteries (PCAs).
-
Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery (ICA) illustrates the anterior circulation. The anterior cerebral artery (ACA) consists of the A1 segment proximal to the anterior communicating artery, with the A2 segment distal to it. The middle cerebral artery (MCA) can be divided into 4 segments: the M1 (horizontal segment) extends to the anterior basal portion of the insular cortex (the limen insulae) and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities).
-
Regions of interest are selected for arterial and venous input (image on left) for dynamic susceptibility-weighted perfusion magnetic resonance imaging (MRI). Signal-time curves (image on right) obtained from these regions of interest demonstrate transient signal drop following the administration of intravenous contrast. The information obtained from the dynamic parenchymal signal changes postcontrast is used to generate maps of different perfusion parameters.
-
Vascular distributions: Middle cerebral artery (MCA) infarction. Noncontrast computed tomography (CT) scanning demonstrates a large acute infarction in the MCA territory involving the lateral surfaces of the left frontal, parietal, and temporal lobes, as well as the left insular and subinsular regions, with mass effect and rightward midline shift. There is sparing of the caudate head and at least part of the lentiform nucleus and internal capsule, which receive blood supply from the lateral lenticulostriate branches of the M1 segment of the MCA. Note the lack of involvement of the medial frontal lobe (anterior cerebral artery [ACA] territory), thalami, and paramedian occipital lobe (posterior cerebral artery [PCA] territory).
-
Vascular distributions: Anterior choroidal artery infarction. The diffusion-weighted image (left) demonstrates high signal with associated signal dropout on the apparent diffusion coefficient (ADC) map involving the posterior limb of the internal capsule. This is the typical distribution of the anterior choroidal artery, the last branch of the internal carotid artery (ICA) before bifurcating into the anterior and middle cerebral arteries. The anterior choroidal artery may also arise from the middle cerebral artery (MCA).
-
Vascular distributions: Anterior cerebral artery (ACA) infarction. Diffusion-weighted image on the left demonstrates high signal in the paramedian frontal and high parietal regions. The opposite diffusion-weighted image in a different patient demonstrates restricted diffusion in a larger ACA infarction involving the left paramedian frontal and posterior parietal regions. There is also infarction of the lateral temporoparietal regions bilaterally (both middle cerebral artery [MCA] distributions), greater on the left indicating multivessel involvement and suggesting emboli.
-
Vascular distributions: Posterior cerebral artery (PCA) infarction. The noncontrast computed tomography (CT) images demonstrate PCA distribution infarction involving the right occipital and inferomedial temporal lobes. The image on the right demonstrates additional involvement of the thalamus, also part of the PCA territory.
-
The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (MCA; red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes; insula; and basal ganglia. The anterior cerebral artery (ACA; blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (PCA; green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
Tables
VASCULAR TERRITORY |
Structures Supplied |
Anterior Circulation (Carotid) |
|
Anterior Cerebral Artery |
Cortical branches: medial frontal and parietal lobe Medial lenticulostriate branches: caudate head, globus pallidus, anterior limb of internal capsule |
Middle Cerebral Artery |
Cortical branches: lateral frontal and parietal lobes, lateral and anterior temporal lobe Lateral lenticulostriate branches: globus pallidus and putamen, internal capsule |
Anterior Choroidal Artery |
Optic tracts, medial temporal lobe, ventrolateral thalamus, corona radiata, posterior limb of the internal capsule |
Posterior Circulation (Vertebrobasilar) |
|
Posterior Cerebral Artery |
Cortical branches: occipital lobes, medial and posterior temporal and parietal lobes Perforating branches: brainstem, posterior thalamus and midbrain |
Posterior Inferior Cerebellar Artery |
Inferior vermis; posterior and inferior cerebellar hemispheres |
Anterior Inferior Cerebellar Artery |
Anterolateral cerebellum |
Superior Cerebellar Artery |
Superior vermis; superior cerebellum |
|
Category |
Description |
Score |
1a |
level of consciousness (LOC) |
Alert Drowsy Stuporous Coma |
0 1 2 3 |
1b |
LOC questions (month, age) |
Answers both correctly Answers 1 correctly Incorrect on both |
0 1 2 |
1c |
LOC commands (open and close eyes, grip and release nonparetic hand) |
Obeys both correctly Obeys 1 correctly Incorrect on both |
0 1 2 |
2 |
Best gaze (follow finger) |
Normal Partial gaze palsy Forced deviation |
0 1 2 |
3 |
Best visual (visual fields) |
No visual loss Partial hemianopia Complete hemianopia Bilateral hemianopia |
0 1 2 3 |
4 |
Facial palsy (show teeth, raise brows, squeeze eyes shut) |
Normal Minor Partial Complete |
0 1 2 3 |
5 |
Motor arm left* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
6 |
Motor arm right* (raise 90°, hold 10 seconds) (preferably with the palm facing up) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
7 |
Motor leg left* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
8 |
Motor leg right* (raise 30°, hold 5 seconds) |
No drift Drift Cannot resist gravity No effort against gravity No movement |
0 1 2 3 4 |
9 |
Limb ataxia (finger-nose, heel-shin) |
Absent Present in 1 limb Present in 2 limbs |
0 1 2 |
10 |
Sensory (pinprick to face, arm, leg) |
Normal Partial loss Severe loss |
0 1 2 |
11 |
Extinction/neglect (double simultaneous testing) |
No neglect Partial neglect Complete neglect |
0 1 2 |
12 |
Dysarthria (speech clarity to "mama, baseball, huckleberry, tip-top, fifty-fifty") |
Normal articulation Mild to moderate dysarthria Near to unintelligible or worse |
0 1 2 |
13 |
Best language** (name items, describe pictures) |
No aphasia Mild to moderate aphasia Severe aphasia Mute |
0 1 2 3 |
|
Total |
- |
0-42 |
* For limbs with amputation, joint fusion, etc, score 9 and explain ** For intubation or other physical barriers to speech, score 9 and explain. Do not add 9 to the total score. NIH Stroke Scale (PDF) |
|||
What would you like to print?
- Overview
- Presentation
- DDx
- Workup
- Treatment
- Approach Considerations
- Emergency Response and Transport
- Acute Management of Stroke
- Fibrinolytic Therapy
- Intra-arterial Reperfusion
- Antiplatelet Agents
- Blood Pressure Control
- Mechanical Thrombectomy
- Fever Control
- Cerebral Edema Control
- Seizure Control
- Acute Decompensation
- Anticoagulation and Prophylaxis
- Neuroprotective Agents
- Stroke Prevention
- Specialized Stroke Centers
- Consultations
- Diet
- Show All
- Guidelines
- Medication
- Questions & Answers
- Media Gallery
- Tables
- References
