Clinical Evaluation
Pearls
The temporal relationship between headache and focal deficit is of major diagnostic importance in differentiating stroke from migraine and in determining the etiology of the stroke.
Careful observation during history constitutes an important part of the physical examination.
The presence of an enlarged pupil in a patient with altered consciousness suggests an imminent threat of irreversible brain injury or death and must prompt emergent measures to reduce cerebral edema, neuroimaging, and a neurosurgical consultation.
Acute stroke is a medical emergency requiring rapid recognition, etiologic diagnosis, and treatment. All of these steps must be performed simultaneously in an organized fashion, with clinicians keeping in mind two differential diagnoses. First, clinicians must consider the most likely diagnoses and work to rule them out. Second, and just as important, clinicians must construct a list of imminent, potentially reversible threats to the patient’s safety, and either treat them empirically or rule them out rapidly, even if they are unlikely. These two parallel differential diagnoses evolve as the results of history taking, examination, and laboratory and imaging studies are synthesized. The chapter discusses an organized approach to the evaluation of patients with acute-onset neurologic deficits that could be due to stroke. It promulgates an organized approach to obtaining the key clinical information needed to determine if stroke is the cause, and if it is, the type of stroke. The approach discussed here is geared toward providing the clinician with the information needed to choose among the treatments for acute stroke that are discussed in subsequent chapters.
♦ Acute Neurologic Syndromes: General Considerations
All acute neurologic complaints should be regarded as emergencies. The brain tolerates injury poorly, and the time window during which injury can be reversed is short. Because neurology is often viewed as complex by nonneurologists and may lead to a desire to call in a specialist before routine stabilization is accomplished, it is important to remember that all acutely ill patients, including those with neurologic complaints, require attention to the basics of medical care (Table 2.1). These include ensuring that the patient has an open and protected airway, and establishing an artificial airway if the patient’s respiratory function is compromised. The patient must have a stable, perfusing cardiac rhythm. Cardiac monitoring until the patient is stable is advised. A severe decline in blood pressure (BP) may cause central nervous system (CNS) dysfunction; determination of BP and correction of hypotension (generally defined as systolic BP <90 mm Hg with neurologic symptoms) must be accomplished. Finally, most acute neurologic syndromes including coma, stroke, and seizure, can be mimicked or caused by acute hypoglycemia. Therefore, if the blood glucose is not known at the time of first evaluation, it should be rapidly determined by bedside testing.1 Glucose should be given intravenously if the patient is hypoglycemic or if the glucose cannot be rapidly determined. Acute thiamine deficiency may cause altered consciousness (Wernicke encephalopathy) and may be precipitated in vulnerable patients by the administration of glucose; therefore, administration of 100 mg intravenous thiamine to all patients with acute CNS dysfunction is advisable prior to the administration of glucose. Because patients with acute CNS dysfunction may have fluctuating levels of consciousness, a policy of nothing by mouth (NPO) until the patient is stable may prevent aspiration. Any patient found on the floor must be presumed to have fallen and to have an unstable cervical spine injury until proven otherwise. Finally, if the overuse of sedatives or opiate analgesics is possible, a trial of naloxone should be considered
Is the Deficit Focal or Global, and Is It Likely to Be a Stroke?
The clinical hallmark of stroke is the sudden onset of a focal neurologic deficit. A focal deficit is one in which the neurologic problem can be ascribed to a lesion in a particular area of the CNS. The opposite, a global deficit, results from dysfunction of the entire cerebrum or the entire brain. The latter is less likely to be caused by acute stroke. After a patient is stabilized ( Table 2.1), the next step in evaluation is to determine if the patient has a focal or a global deficit, because they have different etiologies and treatments. Focal deficits may be elicited by both history and examination, and this determination can take place rapidly. Focal deficits that may be rapidly identified by history and examination include aphasia (inability to speak or understand in the setting of preserved consciousness); a visual field disturbance, unilateral weakness, or weakness affecting a single limb; unilateral numbness; unilateral incoordination; truncal or gait instability; hemispatial neglect; or inability to carry out learned motor tasks despite normal motor and sensory function. Because a decline in level of consciousness (LOC) requires bihemispheric or massive brainstem dysfunction, most patients with stroke have preserved consciousness, at least initially. Global deficits are usually characterized by a decline in level of consciousness out of proportion to any focal symptoms or signs. A patient who is lethargic but has intact motor and brainstem function is unlikely to have a stroke (with the exception of subarachnoid hemorrhage).
Rapid-onset focal neurologic deficits should be considered to be a stroke until proven otherwise, but there are other causes of these deficits that must be considered.1 These include the entities listed in Table 2.2 . It is important to note that it may not be possible to adequately rule out stroke acutely in patients with acute focal deficits purely based on clinical evaluation, even if they have features of the other conditions listed in the table. Several validated prehospital screening tools to differentiate stroke from other causes of acute brain dysfunction are available and have been shown to improve ambulance recognition of stroke.2 , 3
♦ Early Clinical Evaluation of Acute Stroke
History
Once it is determined that stroke is a likely or possible diagnosis, a focused history and physical neurologic examination may both clarify the diagnosis, guide further testing, and determine the patient’s eligibility for acute treatment. It is essential to accurately determine the time of onset of the neurologic symptoms. If the patient or reliable witnesses cannot report the time of onset, the time the patient was last confirmed to be normal must be determined. In patients who are aphasic, the patient must have been heard to speak normally to establish that the deficit was not present; normal motor function without a witnessed attempt to speak does not establish the absence of a deficit, even if a motor deficit is present at the time of medical evaluation. Patients with large nondominant hemispheric lesions may not be aware of their deficit and therefore may not be able to accurately report symptom onset. Every effort must be made to contact witnesses in the home, workplace, or wherever the patient was found to determine as unambiguously as possible the time the patient was last normal.
The mode of onset of the deficit should be determined by history. Ischemic strokes often have a maximum deficit at onset, whereas deficits from intracerebral hemorrhage (ICH) may worsen over seconds to minutes due to expansion of the hematoma. Deficits that spread over contiguous parts of the body over 10 to 30 minutes suggest migraine. Deficits preceded by positive symptoms (shaking) may be due to seizure, although rarely brain ischemia may cause limb shaking. Additionally, between 2% and 10% of strokes are accompanied by a seizure at or near the time of onset.4 Therefore, the occurrence of a seizure does not rule out the presence of a coexisting stroke.
The history should elicit the patient’s handedness. The presence of stroke risk factors, such as prior stroke, prior myocardial infarction, hypertension, diabetes mellitus, smoking, atrial fibrillation, or peripheral vascular disease should be determined. A complete medication list should be obtained if possible; if not, the use of antithrombotic medications, anticoagulants, and insulin or oral hypoglycemics must be specifically queried. The use of illicit drugs should also be determined, especially sympathomimetics (cocaine, amphetamine) and herbal supplements. The presence of headache should be queried. A headache that occurred prior to or with the onset of the deficit is consistent with either ischemic or hemorrhagic stroke (including subarachnoid hemorrhage [SAH]), or may indicate arterial thrombosis or injury (dissection) or intracranial venous occlusion. A headache that comes on after a focal deficit has resolved may indicate migraine.
Finally, it is crucially important to determine if the focal complaint has resolved. If it has completely resolved and the patient feels entirely back to normal, this must be clearly documented. In some circumstances, recurrence of the deficit may then be treatable with thrombolysis even many hours later. Dramatic but incomplete improvement is also important to document. Some interventions might not be needed if the patient improves dramatically without treatment. It is usually best to describe something the patient could not do that he or she can now do (e.g., lift an arm, tie one’s shoelaces, speak).
A particularly difficult situation is the recognition and evaluation of patients with in-hospital strokes.5 These patients often have complex underlying acute medical problems and have undergone multiple medical and surgical treatments and diagnostic procedures. In this setting, the history must include an analysis of the reason for hospitalization; all medications that have been used, with a focus on antithrombotic therapies and sedatives; any recent invasive procedures, including central line placement, biopsies, surgeries, and endoscopies; and the presence of underlying infection or immune deficiencies. In addition, the occurrence of any episode of hypotension, hypoxia, hypoglycemia, or cardiac arrest or dysfunction must be determined.
Physical Examination
The importance of determining the vital signs has been discussed above. The remainder of the physical examination may be divided into a general (nonneurologic) examination, and the neurologic examination. However, it is important to note that talking with the patient while taking the history affords an invaluable chance to make observations that can focus the neurologic examination. A patient who can relate a cogent, accurate history and carry on a normal conversation is unlikely to have a clinically significant aphasia. A patient who is aware of, concerned about, and frustrated by a motor deficit likely does not have significant anosognosia. A patient who has no recollection of a transient focal deficit that was clearly witnessed by others, and that was not accompanied by a loss of consciousness, may have had a seizure. Patients who appear to move their arms and legs normally while changing position or gesturing, despite complaints of focal weakness, may have a functional (conversion) disorder.
General Physical Examination
Cardiac examination should focus on the regularity of the pulse, looking for signs of atrial fibrillation; the presence of cardiac murmurs that could suggest endocarditis; and the presence of peripheral edema, suggesting congestive heart failure that predisposes to embolism. Pulmonary examination should search for the presence of pulmonary edema that requires treatment in its own right and suggests the presence of left ventricular dysfunction (see above). The skin should be carefully examined for stigmata of endocarditis (Osler nodes, Janeway lesions, splinter hemorrhages), and for rashes that may suggest the presence of an autoimmune disease or hypercoagulable state (e.g., livedo reticularis). Finally, signs of trauma or seizure should be sought, such as lacerations; bruises; hip, knee, or elbow pain; or a bitten tongue. The general physical examination of a stroke patient in the acute setting should take no more than 2 to 3 minutes.
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