Assessing the Patient With Suspected Stroke

The authors detail the phases of history-taking, observation and physical examination required to accurately characterize the cause of an acute focal neurologic deficit while the window of therapeutic opportunity remains open.

By David L. McDonagh, MD, and Larry B. Goldstein, MD

Dr. McDonagh is a resident in neurology at the Department of Veterans Affairs Medical Center in Durham, North Carolina. Dr. Goldstein is associate professor of medicine (neurology), director of the Duke Center for Cerebrovascular Disease, and head of the Stroke Policy Program in the Duke Center for Clinical Health Policy Research at Duke University. He is also attending neurologist at the Department of Veterans Affairs Medical Center in Durham.

The rapid and accurate clinical evaluation of the patient with an acute focal neurologic deficit is critical for selecting further diagnostic studies and arriving at a treatment plan. For selected patients with acute ischemic stroke, time is of the essence because the window of opportunity for thrombolytic therapy is so narrow. Accurate determination of the involved vascular territory is also critical in the emergency department setting as the symptoms and signs of focal cerebral ischemia may be transient with further management if a precisely correct anatomic diagnosis has been made.

Standardized, quantitative neurologic examinations for patients with stroke such as the Canadian neurologic Scale and the National Institutes of Health Stroke Scale have been developed and are useful both as research tools and therapeutic guides. The purpose of this article is to provide a brief overview of the clinical evaluation of patients with suspected stroke based on historic features and findings on routine general and neurologic examinations. Current guideline statements and other literature (see Suggested Reading) provide more detailed information concerning the clinical and laboratory evaluation of these patients as well as their management.

The physician confronting a patient with signs and symptoms that suggest possible stroke must address several key questions (see box below), which can usually be answered by obtaining a careful history and performing rapid general and neurologic examinations.

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Establishing the History

In addition to any history the patient is capable of providing, witness accounts of events surrounding the onset and progression of the patient's symptoms are important to obtain. Stroke generally has an acute onset. The physician must search for the time of onset, keeping in mind that it is defined as the last time the patient was known to be well. Thus the patient who awakens with a neurologic deficit is assumed to have suffered the injury when he was last known to be asymptomatic.

In the case of transient ischemic attacks (TIAs), which are generally quite brief, symptoms are often completely resolved by the time the patient reaches medical attention. It is critically important with these patients to establish the vascular distribution of symptoms in order to determine appropriate treatment.

Headache often accompanies stroke. The onset of an acute severe headache increases suspicion of a subarachnoid hemorrhage. Patients with carotid or vertebral artery dissection often have head or neck pain over the affected artery, or referred pain to the face or vertex. Migraine headache can be accompanied by a focal neurologic deficit, but to support that diagnosis, the patient should have a migraine history and other conditions must be excluded. Nausea and vomiting raise concern for posterior fossa (brain stem or cerebellar) events or increased intracranial pressure.

The nature of the neurologic deficit must be defined as a first step in determining which area of the brain is involved. Symptoms may be transient, and residual signs may be misleading. Pre-existing deficits that have not been identified as such may be misinterpreted as representing new abnormalities during the physical examination.

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Level of Consciousness is Crucial

The term "mental status change" can imply a wide array of conditions ranging from confusion to a language disturbance to depressed level of consciousness. For that reason, the term should be avoided and the actual deficits described. The patient's level of consciousness is of the utmost importance. The range of consciousness can be divided into alert, somnolent, stuporous, and comatose. Patients who are somnolent are sleepy, but easily arousable with mild stimulation. Patients who are stuporous are incompletely arousable, but still exhibit appropriate fending-off movements in response to noxious stimuli. Comatose patients are not arousable and do not respond to noxious stimuli.

A depressed level of consciousness implies multifocal or diffuse bihemispheric or brain stem dysfunction. In general, hemispheric strokes must either be multifocal or large and associated with mass effect to affect both cerebral hemispheres, or compress the brain stem and affect the reticular activating system, to depress level of consciousness. Brain stem strokes or cerebellar strokes with brain stem compression can also lead to depression of level of consciousness, as can intraventricular hemorrhage with or without secondary hydrocephalus.

Speech and language should be explored next. Dysarthria (garbled speech) must be differentiated from aphasia (language disturbance related to a dominant hemisphere lesion). This can be difficult based on history alone. At times, patients with impaired speech may try to communicate by writing. Intact written language while symptomatic suggests a transient speech disturbance representing dysarthria rather than aphasia. In general, dysarthria is a non-localizing symptom, but in patients with unilateral limb weakness, its presence supports the presumption of a central rather than a peripheral cause.

Visual loss may be monocular, resulting from a thromboembolic event anterior to the optic chiasm, or binocular, typically due to a parietal or occipital lesion. The loss of half the visual field with a vertical meridian indicates unilateral damage to the retrochiasmal optic pathways. Diplopia suggests dysfunction of the oculomotor system related to cranial nerves (CN) 3 and 4 (midbrain), CN 6 (pons), or a combination. In stroke patients, diplopia typically occurs in association with other acute neurologic deficits. Isolated diplopia can occur after a brain stem injury, but is more likely to reflect intraocular injury or any type of injury to an oculomotor nerve, the neuromuscular junction, or the extraocular muscles. Patients with acute visual loss should always be asked if they alternately covered and uncovered each eye to determine whether both eyes were affected.

Facial weakness that spares the forehead affects the descending motor tracts above the level of the facial nucleus in the mid-pons (upper motor neuron facial weakness). In lower motor neuron facial weakness, the forehead as well as the lower face is weak. The facial nerve may be injured in a pontine lesion.

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Differentiating Dizziness

Patients often complain of dizziness, a term with many possible meanings that should be explored. For example, the word may be used to describe lightheadedness or presyncope, suggesting cardiovascular compromise. Sometimes it means disequilibrium (a vague sensation of imbalance) or vertigo (a sensation of turning, tilting, or rotation), either of which may reflect damage to the vestibular system in the inner ear, cerebellum, or brain stem.

Dysphagia is a non-localizing symptom seen at least transiently in a high proportion of stroke patients, regardless of the structures involved in the stroke.

Arm or leg weakness typically raises the initial suspicion of a stroke in most lay people. Weakness is usually unilateral in an acute stroke, except in the setting of bilateral cerebral infarcts, vertebrobasilar disease, or spinal cord infarction. Sensory loss or paresthesias may occur along with a motor deficit or in isolation. Gait disturbances, a common presenting symptom, may result from sensory dysfunction, vestibulopathy, or lower extremity weakness of any etiology.

The presence or absence of prolonged syncope should be determined by history. Isolated syncope is typically not a symptom of cerebrovascular disease. Transient loss of consciousness in the setting of a stroke should prompt the physician to look for a precipitating factor in addition to managing the acute stroke. Establishing the presence or absence of a preceding seizure is essential. The seizure may be the result of the stroke or may be the cause of a neurologic deficit, as in Todd's paralysis.

Finally, the patient's medical-surgical history is essential in determining candidacy for thrombolysis and potential causative factors for the stroke. Any history of intracranial hemorrhage is an absolute contraindication to thrombolysis. A medication review will identify patients on anticoagulation therapy. Certain over-the-counter cold medications, as well as illicit drugs (amphetamines and cocaine), can increase the risk for stroke or intracranial hemorrhage. Symptoms of acute myocardial infarction or a history of atrial fibrillation increase the likelihood of a cardiogenic etiology. The table below summarizes some important points to be addressed in the history.

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Keys to the Physical Examination

The assessment of airway, breathing, and circulation are the initial steps in evaluating any stroke patient. Most acute stroke patients will present with hypertension.

The general physical examination should include an assessment for head or neck trauma that may have preceded or followed the neurologic deficit. Pending appropriate radiographic studies, the neck should be immobilized if there is a possibility of neck trauma. The neck should otherwise be checked for meningismus (signifying meningitis or subarachnoid hemorrhage as the cause of the deficit). The presence of a fever would also suggest an infectious process.

Pulse irregularities may reflect atrial fibrillation or other cardiac arrhythmia. Cardiac murmur suggests valvular heart disease that can be the result of marantic or bacterial endocarditis. The presence of a gallop or elevated jugular venous pulse may indicate systolic dysfunction or congestive heart failure. Lower extremity edema or tenderness could be a sign of venous thrombophlebitis and possible paradoxical cerebral emboli (via a right to left intracardiac or pulmonary shunt). The skin examination may also reveal signs of stroke etiology or other conditions.

As mentioned above, the patient's level of consciousness can be described as alert, somnolent, stuporous, or comatose. If the patient is not alert, one should assess how easily he or she is aroused with verbal or noxious stimuli. The remainder of the examination may uncover a reason for the depressed level of consciousness (see table below).

Language function must be tested to avoid mislabeling an aphasic patient as "confused." The patient should be asked to name parts of an object such as a watch (band, crystal, clasp), repeat phrases, and follow verbal commands. The absence of a naming deficit suggests the speech disturbance is not due to aphasia. Aphasia can occur with either cortical or subcortical lesions affecting the dominant (usually left) hemisphere. Aphasia without hemiparesis does occur, classically (although not invariably) as the result of an embolism to a middle cerebral artery branch.

Spatial neglect suggests a contralateral parietal lesion. Evidence of spatial neglect may be found on visual field testing (the patient can identify fingers in the four visual quadrants of each eye individually, but not when both right and left visual fields are tested simultaneously), sensory examination with double simultaneous stimulation ("Did I touch your right or left hand or both?"), or motor testing (lack of use of an extremity out of proportion to the weakness). Patients may also be asked to bisect a line (crossing to the right or left of midline suggests a spatial neglect due to a contralateral parietal lesion), place numbers on a drawn clock face, or cross a series of random lines drawn on a blank page (see illustration below).

Spatial neglect testing. Upper panel, line bisection; middle panel, line cancellation; and bottom panel, clock drawing, consistent with left hemispatial neglect.

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CRANIAL NERVE ASSESSMENT

Visual field testing should be performed as the first part of the CN evaluation. Each eye should be tested separately. The examiner should instruct the patient to focus on the examiner's eye and then to detect finger movement presented in each quadrant (right and left inferior and superior). If the patient is encephalopathic or aphasic, the visual fields can be tested by visual threat. It is important not to fan air into the eye, which may provoke a corneal blink reflex. Strokes (excluding ocular or retinal infarcts) most commonly cause homonymous visual field deficits by damaging the optic radiations (usually middle cerebral or carotid artery distribution stroke) or occipital cortex (posterior cerebral artery distribution stroke).

The funduscopic examination may show evidence of chronic hypertension or diabetes. Papilledema suggests raised intracranial pressure. The vessels should be examined carefully for the presence of Hollenhorst plaques (see image below), indicating a proximal source of arterial or cardiac emboli.

Hollenhorst plaques (arrows) on funduscopic examination, indicating a proximal source of arterial or cardiac emboli.

Forced gaze deviation is a useful finding. Damage to a frontal eye field will cause the patient to gaze toward the side of the lesion. Pontine infarcts will cause the patient to gaze away from the side of the lesion (as will seizure activity in a frontal eye field). Therefore, the patient will look away from the hemiparesis with a frontal lobe stroke and toward the hemiparetic side when a pontine infarct or seizure has occurred. Another clue is that the eye deviation can often be overcome with ocular-vestibular maneuvers (see above) in the setting of hemispheric lesions, but cannot be overcome if there is damage to the parapontine reticular formation in the pons.

Pupillary size and reactivity should be assessed next. Anisocoria (unequal pupils), especially if the disparity is greater than 1 mm, can indicate a pathological process. A dilated, sluggishly reactive or nonreactive pupil in one eye can suggest transtentorial herniation or primary brain stem involvement in a patient with a depressed level of consciousness. The same finding in an awake patient may occur with a CN 3 injury (such as compression from an aneurysm) or midbrain stroke. A dilated pupil on the side of a ptosis or an eye with external deviation suggests injury to CN 3. Ptosis on the side of a small pupil suggests Horner's syndrome, which may occur in the setting of brain stem injury, carotid artery dissection, apical pulmonary lesion, and other conditions.

Extraocular movements (CN 3, 4, and 6) can be assessed by having the patient track the examiner's finger as it is moved in the pattern of an "H". Subjective diplopia or disconjugate eye movements suggest brain stem dysfunction if other signs of parenchymal injury are found. Likewise, the presence of nystagmus, especially vertical nystagmus concurrent with other cranial nerve abnormalities or limb sensorimotor abnormalities, suggests brain stem injury.

Facial sensation (CN 5) is probably most efficiently tested as part of the general sensory examination described below. In addition, the corneal response should be assessed.

Facial weakness (CN 7) can be assessed by first observing the patient at rest and looking for unilateral widening of the palpebral fissure or flattening of the nasolabial fold. The patient should then be asked to sequentially raise the eyebrows, close the eyes forcefully, smile, and puff out the cheeks. Unilateral weakness involving the forehead indicates lower motor neuron dysfunction. Keep in mind that this can occur in a pontine infarct as the facial nerve exits the pons. Unilateral weakness sparing the forehead suggests an upper motor neuron lesion in the contralateral brain stem above the level of the facial nucleus or cerebral hemisphere. Bilateral facial weakness suggests brain stem dysfunction (or a neuromuscular disorder).

Hearing (CN 8) can be tested at the bedside by whispering into each ear (acute hearing loss may occur in certain parietal, brain stem, and cochlear infarcts). In the patient with an altered level of consciousness, the vestibular aspect of CN 8 can be tested by evoking a vestibulo-ocular reflex (also called doll's-eyes maneuvers). This is performed only in a patient with no history of trauma or neck injury. The head is moved from side to side and up and down and the eye movements are observed. The eyes should move through their full range of motion. This indicates that the vestibulo-motor pathways between the inner ear, midbrain (CN 3, 4 nuclei) and pontine (CN 6, parapontine reticular formation) structures are intact.

Cranial nerves 9 and 10 (glossopharyngeal and vagal) are tested by assessing the symmetry of palatal elevation and the presence of the gag reflex. The patient may be hypophonic or dysarthric from injury to these nerves as well, but as previously indicated, dysarthria alone is non-localizing, occurring in a variety of stroke types and locations.

Testing shoulder shrug (trapezius) and head turning (sternocleidomastoid) strength assesses the spinal accessory nerve (CN 11).

The hypoglossal nerve (CN 12) is tested by protrusion of the tongue. The tongue will deviate toward the side of the weakness.

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Motor Examination

Individual muscle strength testing is of obvious importance. Brain or spinal cord injury produces an upper motor neuron pattern of weakness in the affected limbs. The extensors (deltoids, triceps, and wrist extensors) will be weakest in the upper extremities and the flexors (iliopsoas, hamstrings, and foot dorsiflexors) will be weakest in the lower extremities. Sequential testing of individual muscles should be performed with side-to-side comparisons. Muscle tone is usually decreased in the affected limb in an acute stroke, but may be normal. Increased tone suggests an older injury.

There are two techniques that will detect subtle weakness. The first is the pronator drift. The patient is asked to hold both arms straight out (or at 45 degrees to the horizontal if supine) with palms up (as if holding a tray) and eyes closed. In an upper motor neuron pattern of weakness, the affected forearm and hand will pronate due to weakness of the forearm supinators. More severe weakness will be accompanied by downward drift and wrist flexion. In the legs, subtle weakness is assessed with each leg held above the examining table while lying supine. Iliopsoas weakness will result in downward drift of the affected limb.

The motor examination is more limited in the encephalopathic or aphasic patient. Nonetheless, three techniques can be employed. The first is observation of spontaneous movement for any asymmetries. The weak lower extremity may be externally rotated. Next, the examiner can lift the patient's extremities and look for asymmetries in their rate of descent when released. Finally, the withdrawal reaction to pain can be tested. The painful stimulus should be applied to the trunk, as nail bed pressure can evoke a reflex withdrawal at a spinal level.

Coordination. The patient should be asked to perform finger-to-nose and heel-to-shin movements in order to elicit ataxia (inability to perform a smooth movement) or dysmetria (inability to hit a target). In the absence of a sensory deficit or weakness, these types of coordination deficit suggest an ipsilateral cerebellar or brain stem lesion. It should be remembered that ataxia must be disproportionate to any weakness in order to be considered significant; any weak limb will appear somewhat ataxic.

Reflexes. Deep tendon reflexes are usually hypoactive (in the weak limb) in acute brain or spinal cord injury. This rule is not absolute, however, and the examination should focus on reflex asymmetries. A patient with a prior stroke or spinal cord injury is expected to have increased reflexes on the affected side. Other pathologic reflexes can also be seen in the acute stroke setting. The most commonly used test is to lightly stroke the lateral aspect of the sole of the foot with a key or similar object and observe the first movement of the great toe. An extensor (upturning) response of the great toe (Babinski reflex) with flexion and fanning of the other toes is abnormal and indicates the presence of an upper motor neuron injury in the contralateral brain or ipsilateral spinal cord.

Sensation.< Sensory loss may accompany a motor deficit or occur in isolation. The patient's ability to detect pain (accomplished with a safety pin), light touch, and proprioception can be assessed quickly. If these modalities are intact, cortical sensory modalities and neglect (described above) can be tested as well, primarily to evaluate for parietal lobe injury. Stereognosis is tested by asking the patient to identify an object placed in his hand while his eyes are closed. Graphesthesia is assessed by identification of numbers written on the patient's fingertips with a blunt object.

Gait. This should be deferred in the assessment of a patient with an acute stroke pending the above examinations, primarily to avoid a drop in blood pressure and cerebral hypoperfusion. However, examination of the gait is critical when the anatomic localization of the stroke is uncertain. The stability of the gait may be affected by limb weakness, sensory loss, disequilibrium, vertigo, postural instability, or ataxia due to cerebellar disease.

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Interpreting the Findings

The table below provides a summary of the clinical evaluation of suspected stroke. Interpretation of findings on neurologic examination requires knowledge of basic neurologic and vascular anatomy. For example, a stroke in the dominant hemisphere with middle cerebral artery distribution can cause aphasia with a contralateral motor and sensory deficit affecting the face and arm to a greater degree than the leg. Anterior cerebral artery distribution deficits cause predominant leg weakness with lesser sensory involvement. Contralateral brain stem lesions can produce crossed signs affecting cranial nerve functions on the side of the lesion but producing weakness or numbness on the opposite side of the body.

Which cranial nerve or nerves are involved depends on the level of the brain stem affected. For example, midbrain lesions can cause an ipsilateral CN 3 palsy and contralateral limb weakness. Pontine lesions can cause an ipsilateral lower motor neuron facial paresis with eyes deviated away from the lesion and contralateral weakness.

Cerebellar hemispheric lesions may produce ataxia in the ipsilateral limbs or truncal ataxia with an unstable gait if the lesion is midline. Small subcortical lesions, or "lacunar infarcts," are characterized by symptoms and signs equally affecting the face, arm, and leg and may produce any of several characteristic deficit patterns such as pure motor, pure sensory, ataxic hemiparesis, or clumsy-hand dysarthria.

Primary intracerebral hemorrhage due to hypertension can often be ascribed to lesions in particular areas (thalamus, basal ganglia, pons, and cerebellum), but hemorrhage cannot be distinguished from an ischemic or other lesion on clinical grounds alone. Neuroimaging is required in addition to a careful history and a competent physical examination.

Undoubtedly, the neurologic examination requires practice. However, with experience, a basic screening examination can be performed in minutes. The examination can be further tailored to the individual patient. A logical approach will allow the examiner to analyze most clinical presentations, though they may at first seem daunting.

Suggested Reading Adams HP Jr, et al: Guidelines for the management of patients with acute ischemic stroke. Stroke 25:1901, 1994. Adams HP Jr, et al: Guidelines for thrombolytic therapy for acute stroke: A supplement to the guidelines for the management of patients with acute ischemic stroke. Stroke 27:1711, 1996. Albers GW, et al: Antithrombotic and thrombolytic therapy for ischemic stroke. Chest 119:300S, 2001. Brott T, et al: Measurements of acute cerebral infarction: a clinical examination scale. Stroke 20:864, 1989. Cote R, et al: The Canadian Neurological Scale: A preliminary study in acute stroke. Stroke 17:731, 1986. Cote R, et al: The Canadian Neurological Scale: Validation and reliability assessment. Neurology 39:638, 1989. Culebras A, et al: Practice guidelines for the use of imaging in transient ischemic attacks and acute stroke. A report of the Stroke Council, American Heart Association. Stroke 28:1480, 1997. Feinberg WM, et al: Guidelines for the management of transient ischemic attacks. Stroke 25:1320, 1994. Goldstein LB and Matchar DB: Clinical assessment of stroke. JAMA 271:1114, 1994. Goldstein LB, et al: Interrater reliability of the NIH stroke scale. Arch Neurol 46:660, 1989. Quality Standards Subcommittee of AAN: Thrombolytic therapy for acute ischemic stroke-summary statement. Neurology 47:835, 1996.

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