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A 62-year-old female acutely developed aphasia and right sided weakness while in the grocery
store. The store clerk immediately called 911, with the arrival of CFD paramedics within 9
minutes, at 6:43 PM. She arrived at the ED at 7:05 PM, completed her head CT at 7:25 PM, and
obtained a neuro consult at 7:35 PM, approximately one hour after the onset of her symptoms.
On exam, BP 116/63, P 90, RR 16, T 98, and pulse oximetry showed 99% saturation. The patient
appeared alert, and was able to slowly respond to simple commands. The patient had a patent
airway, no carotid bruits, clear lungs, and a regular cardiac rate and rhythm. The pupils were pin
point, and there was neglect of the R visual field. There was facial weakness of the R mouth, and
R upper and lower extremity motor paralysis. DTRs were 2/2 on the left and 0/2 on the right.
Planter reflex was up going on the right and down going on the left. The patient¶s estimated
weight was 50 kg. What are the next Rx steps?

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Emergency Physicians are on the front line in managing patients with cerebrovascular accidents
(CVAs) and many other acute neurologic disorders. Much has been written about conducting the
neurologic exam, both in general terms and in the Emergency Department setting. The goal of
the Emergency Physician is to accurately diagnose neurologic diseases and to provide effective
and timely therapies to maximize patient outcome. Given the time constraints placed upon the
Emergency Physician, every effort must be made to streamline this process, leading to the
concept of a ³focused neurologic exam´. What is meant by this term remains unclear to many,
even those physicians who have practiced for many years in the ED.

Considering the CVA patient as a model for discussing the focused neurologic exam is important
for many reasons. Patients commonly present to the Emergency Department with acute CVAs.
Over 700,000 patients will have a CVA each year, with a 20% one year mortality rate. The
annual costs of these CVAs are over $30 billion, including both direct medical costs and the
indirect costs associated with the long-term effects of this disease. At the same time, it is
important to note that tPA use for the ED CVA patient is being considered by many local and
national organizations that guide the healthcare of the public. The ACEP Clinical Policies
Committee is working with the ACEP board to develop a policy regarding tPA use in stroke, one
that will optimize patient outcome and the ability of the Emergency Physician to fulfill that
objective.
One cornerstone of tPA use is the ability to assess risk and benefit for each stroke patient, in
large part based on the patient¶s neurologic exam. In the clinical trials that led tPA to be deemed
efficacious, the NIH Stroke Scale (NIHSS) was used to quantify the severity of the CVA. Even
though it has been shown that it is essential to use tPA only in settings in which the clinical trial
protocol can be recreated, many Emergency Physicians do not know how to assess stroke
severity using the NIHSS. More importantly, even fewer understand the components of this
stroke scale, such that their neurologic exam can be focused to include those components that
predict outcome and guide ED tPA use.

The purpose of this article is to address the issue of the neurologic exam in ED patients who
present with an acute CVA. Upon review of this article, the reader should have a better
understanding of how the neurologic exam can be focused in ED stroke patients. Information
will be provided that will allow the ED physician to quickly identify important stroke syndromes
and allow their neurologic exam to support this tentative diagnosis. The neurologic exam will
also be focused so that the stroke etiology, need for further diagnostic testing, and ED therapy
can be consistently determined for each patient.

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In instances when there are confusing, non-persistent, or mild symptoms, a complete neurologic
exam is in order. It is only in detecting all of the specific neurologic findings that a provisional
diagnosis can be made. In the setting of an acute CVA, the fact that the patient has a stroke is
usually not hard to ascertain. As such, when a ³stroke´ patient presents to the ED, the same
neurologic exam that might be utilized for a TIA patient may not be necessary. The question is
raised; therefore, as to what ³focused neurologic exam´ must be completed.

Strokes can occur as a result of thrombotic and embolic vascular phenomena, as well as due to
acute hypoperfusion in the setting of cardiogenic shock. There are several stroke syndromes that
result from these events, including anterior and posterior circulation strokes, cerebellar and
lacunar infarcts, and carotid artery dissection strokes. In US Emergency Departments, where
access to CT scanning is readily available, one might ask why it is necessary to identify one of
these syndromes on physical exam. The answer to this question is yes, since the initial CT scan
will often be negative, especially in the setting of an ischemic stroke. The rationale for the
focused neurologic exam is to suggest a provisional stroke syndrome diagnosis, to identify the
likely precipitants of the stroke, to determine what further testing must be completed, and to
determine the appropriate ED therapies that will optimize patient outcome. Additionally, a
focused neurologic exam will allow for appropriate documentation to be completed.
In general, the neuro exam must identify whether the stroke is an anterior or posterior circulation
event, as well as to determine if the stroke is in the cerebellum, the brain stem, or whether the
findings are the result of a spinal cord lesion. The Emergency Physician is also attempting to
determine if the stroke is hemorrhagic, but the availability of CT makes this requirement a bit
less important. Determining this prior to obtaining the CT, however, will allow the Emergency
Physician to immediately begin required therapies such as intubation or to plan for subsequent
therapies such as tPA or nimodipine.

Anterior circulation stroke is the stroke syndrome that most of people think of when considering
the use of tPA. Commonly as the result of middle cerebral artery occlusion, the patient will
present with unilateral paralysis speech and sensory abnormalities, and visual and gaze findings
of sudden onset. Posterior strokes present with a more insidious onset, often with minimal motor
findings, marked sensory findings, and ataxia.

Cerebellar hemorrhage is a diagnosis that should be suspected clinically because the diagnosis of
this requires CT scanning utilizing thin cuts of the posterior fossa and because there is a specific
therapy for this stroke: operative evacuation of the clot. Also, determining that the hemorrhage
is actually in the posterior fossa can be difficult, even when this diagnosis is suspected. The
neurologic findings of a cerebellar hemorrhage include headache, nausea, vomiting, ataxia, and
altered mental status (when brain stem compression occurs due to the cerebellar hemorrhage).

Significant brain stem lesions usually present a picture of critical illness, with prominent
alteration in mental status. Vital signs often will be abnormal, as will respirations, suggesting the
need for immediate intubation. Spinal cord lesions present either in the setting of acute injury or
with findings that are so specific that a cerebrovasuclar accident is not part of the differential
diagnosis. For example, a patient with an epidural abcess may have sensory or motor findings in
one lower extremity in conjunction with back pain, with no other associated prodromal or
neurologic findings.

Besides attempting to identify the likely stroke syndrome, the neurologic exam is being
completed in order to identify the etiology of the stroke: embotic, thrombolic, hemorrhagic or
subarachnoid. Embolic CVAs are most often sudden in onset and involve the anterior
circulation. They are suggested by a carotid bruit, atrial fibrillation, or heart murmur, all as
sources of embolism. Thrombotic strokes are suggested by gradual symptom onset, posterior
circulation symptoms, and findings suggesting atherosclerosis, such as a carotid bruit, ventricular
heave suggesting LVH, an abdominal aortic aneurysm, and poor extremity pulses. Hemorrhagic
CVAs present with impaired consciousness as a key element, with symptoms of abrupt onset and
maximal severity at symptom onset. Hypertension and bradycardia are found with large ICH, as
well as papilledema and retinal hemorrhages. Subarachnoid hemorrhage patients may have
varied symptom onset and severity, but most often present with noted headache, neck
meningismus, and possibly retinal hemorrhage.

The neurologic exam should also direct the need for further diagnostic tests and therapies. An
EKG and CXR are reasonable baseline screening tests to rule out cardiac ischemia or infaract, as
well as CHF and a pulmonary source of a metastatic CNS lesion. A contrast CT is useful when
the plain brain CT shows a suspected lesion with mass effect or midline shift. Angiography is
useful to detect a aneurysm in the setting of SAH. CT or ultrasound testing will detect an AAA,
and echocardiography will detect suspected cardiac lesions. Other testing, such as MRI, is not
at this time indicated in the acute evaluation of the stroke patient. Emergency therapies for
ischemic stroke are limited to aspirin, heparin, and tPA. Hemorrhagic stroke patient therapy is
limited to mannitol, decadron, phenytoins, and operative intervention. Nimodipine and operative
intervention are the only therapies that should be considered by the Emergency Physician for
subarchnoid hemorrhage.

The focused neurologic exam also allows for proper documentation of the stroke patient¶s
clinical status when emergency care was provided. The documentation allows other healthcare
providers to determine stroke severity at the time of presentation as well as to establish if the ED
therapies were consistent with the patient¶s stroke severity. A well documented exam will also
allow for the NIHSS to be determined in retrospect, especially when CQI audits are examining
the efficacy of tPA use in each institution.

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There are three components of the focused neurologic exam in the ED: the history, the general
physical exam, and the neurologic part of the physical exam. Each of these components are used
to develop a provisional stroke syndrome diagnosis, to determine the etiology of the stroke, and
to direct emergent diagnostic testing and therapy.

The history catalogues the symptoms that will usually lead to a provisional stroke syndrome
diagnosis even before the physical exam is initiated. The time of symptom onset is also critical
when tPA use is contemplated in anterior circulation strokes. Associated symptoms or medical
history may assist in determining the etiology of the stroke.
The most important components of the general physical exam are the appearance of the patient,
the vital signs, and the patient¶s mental status. These elements answer for the Emergency
Physician the most important clinical question: is this patient stable enough to get a CT scan, or
must something be done to treat the ABCs or prevent a stroke complication? Once determined,
the general physical exam will detect important findings such as carotid bruits, atrial fibrillation,
CHF, meningismus, and the presence of an AAA.

The neurologic exam in stroke patients should focus on seven elements: level of consciousness
(LOC), cranial nerve (CN) exam, visual exam (including neglect), motor, sensory, cerebellar,
and language. LOC should be measured using the AVPU or GCS systems for documentation,
since all health care providers can consistently use them. The CN exam should focus on facial
motor function and the presence of a gag reflex. The eye exam will detect nystagmus, CN
palsies, and papillary findings that may suggest the etiology of the stroke symptoms. Neglect of
one part of the visual field confirms the presence of an anterior circulation stroke.

The motor exam includes the exam for pronator drift of the upper extremities and dorsi- and
plantarflexion of the ankle. In the presence of hemiparesis, neither of these is indicated. The
sensory exam only requires the detection of sensory light touch abnormalities in order to confirm
the motor findings in a suspected anterior circulation stroke. In posterior circulation stroke,
when the prominent symptom may be marked sensory dysfunction with minimal motor paralysis,
a more complete sensory exam is indicated.

Only rarely is it indicated to detect cerebellar findings are rarely indicated in the presence of
clear anterior circulation stroke symptoms. Having the patient attempt to sit on the cart can test
truncal ataxia. Otherwise, no cerebellar tests need to be performed. The presence of pathologic
reflexes such as clonus and a positive Babinski¶s sign suggest the loss of upper motor neuron
control of lower motor neuron function. This is evident in the presence of anterior circulation
stroke flaccid paralysis, and, as such, does not necessarily add to the Emergency Physician¶s
ability to confirm a stroke syndrome. Language testing is useful in establishing the location of
the stroke syndrome vascular event. Aphasia, sign of abnormal language processing, is more
commonly seen in anterior circulation stroke, and dysarthria, a motor dysfunction, is more
commonly seen with symptoms such as dysphagia and dizziness in posterior circulation stroke.

The NIHSS utilized seven general parts of the neurologic exam to determine stroke severity.
These include LOC, CN, motor, sensory, cerebellar, visual, and language. In the NINDS stroke
trial, the median NIHSS score in tPA-treated patients was 14, a score that suggests moderate
stroke severity. To put this in perspective, the authors of that clinical trial manuscript state in the
methods, under outcome measures, ³the NIHSS, a serial measure of neurologic deficit, is a 42-
point scale that quantifies neurologic deficits in 11 categories. For example, a mild facial
paralysis is given a score of 1, and a complete right hemiplegia with aphasia, gaze deviation,
visual field deficit, dysarthria, and sensory loss is given a score of 25.´

Both the neurologic exam and the use of the NIHSS can be facilitated through the use of the
internet. Using the Google search engine, the term ³neurologic exam´ will suggest sites that
facilitate the general neurologic exam, some of which specifically address calculation of the
NIHSS.

     
     

The neurologic exam should be described in terms of what was done, not the conclusion of the
testing. For example, do not state ³CN II-XII intact´. Instead, document that ³cheek, eye,
shoulder shrug, and tongue function were tested to be normal´. Also, in documenting the exam
of the stroke patient, state clearly the provisional stroke syndrome diagnosis as the neurologic
exam is described. For example, state ³the L sided weakness and dysphagia are consistent with
an anterior circulation stroke´. The neurologic findings should be also framed in terms of the
seven areas of the NIHSS. Even if a formal NIHSS cannot be completed, a card that outlines
how each of the components is scored will allow for an estimated score to be calculated. This
score, if estimated, should be stated to be an estimate only.

Finally, all of the general physical findings that support an etiology should be listed as pertinent
positives and negatives in the documented patient physical exam.

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When treating the ED stroke patient, the Emergency Physician should develop a provisional
stroke syndrome diagnosis, use the focused neurologic exam to support this diagnosis, and
attempt to establish the suspected etiology of the stroke. In addition, the exam should direct
further diagnostic testing and required ED therapies. Finally, the ED documentation must
support the diagnosis and therapies provided in the ED, as well as allow for CQI audits to
retrospectively determine stroke severity using the NIHSS, especially when tPA use is
considered.

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The patient¶s CT scan of the head showed no low-density areas or ICH. There were no clear
contraindications for the use of tPA. The NIHSS was approximately 20. Consultation with a
neurologist cleared the use of tPA. No family was present to defer the use of tPA and tPA was
administered without complication. The administration of tPA occurred at approximately 8:20
PM, about 1 hour and 45 minutes after the onset of the stroke symptoms. An initial bolus of 5
mg was given slow IV push over two minutes, followed by an infusion of 40 mg over 1 hour.

Upon re-exam at 90 minutes, the patient had some increased speech and the use of her right arm,
and the amount of mouth droop and visual neglect was decreased. The repeat NIHSS score at
that time was approximately 14-16. In the hospital, the patient had no ICH and had improved
neurologic function. At the time of hospital discharge, the patient had near complete use of her
right upper extremities, speech and vision were improved and there was some residual gait
difficulties based on right lower extremity weakness. At disposition from the hospital, the
patient went to a rehabilitation hospital.

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