Ischemic Stroke Clinical Presentation

Updated: May 27, 2020
  • Author: Edward C Jauch, MD, MS, FAHA, FACEP; Chief Editor: Helmi L Lutsep, MD  more...
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Presentation

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. [1]

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. [4, 57]

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.

Next:

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). [58]

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.

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