migraineDiagnosis of Ischemic Stroke
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Diagnosis of Stroke
Classification of Ischemic Stroke
PATHOGENESIS, ETIOLOGY, EVIDENCE AND DIAGNOSIS
Stroke is a clinical diagnosis, i.e. based on the history and physical examination. CT scans and other tests are ordered to confirm, classify and typify the diagnosis. There are several situations that can mimic a stroke. The differential diagnosis includes almost any disease that can produce a neurologic deficit of sudden onset like:
migraine
postictal paralysis of some forms of epilepsy (Todd's paralysis)
tumors (especially malignant ones with necrosis or hemorrhage)
In the history the clinician must elicit the risk factors for cerebrovascular disease and, being so closely associated, of cardiac disease. These include:
hypertension
diabetes mellitus
hyperlipidemia
previous stroke
coronary artery disease
atrial fibrillation
male sex
smoking
age over 55 (men) or 65 (women)
Although these are the most common ones, other factors may increase an individual's risk for a stroke. Hypertension is the most common risk factor for stroke across all ages. In young patients, however, other etiologies have to be considered, including trauma, autoimmune diseases (eg. lupus), hypercoagulable states, collagenopathies, vasculitides and congenital heart disease, among others.
The history must also seek for associated symptoms like:
palpitations
chest pain
dizziness
headache
reported audible bruits
signs of heart failure (dyspnea, orthopnea, paroxysmal nocturnal dyspnea, leg swelling)
leg pain or swelling
other
A search for precipitant factors or surrounding circumstances is also necessary. Some of these include:
1. trauma
2. dehydration (eg. as in sickle cell disease, venous strokes, etc)
3. positional changes (eg. suggesting hemodynamic mechanism)
4. drug intake (both legal and illegal drugs)
5. onset at rest, during sleep (usual for thrombotic mechanism)
6. onset during physical activity (usual for embolism)
7. onset during defecation, micturition or heavy lifting (suggesting a right-to-left shunt or very low cardiac output), etc.
Finally, the temporal profile of the deficit is of importance. Did it start....
1...suddenly? (suggesting embolism)
2...in a smooth, gradual fashion? (suggesting hemorrhage or thrombosis)
3... in a waxing-and-waning or stuttering fashion over several hours?
(suggesting thrombosis)
In our times, TIME OF ONSET is extremely important. Most of the events that lead to brain tissue loss happen in the first few hours after a stroke (particularly the first 60 minutes). This is the famous "therapeutic window" or "window of opportunity". Thus, therapy should generally be instituted early. Tissue plasminogen activator, tPA, was approved by the FDA for use in patients with an acute ischemic stroke of less than 3 hours duration and fulfilling certain safety and efficacy criteria. The criteria have already been published by the American Heart Association and the American Academy of Neurology). . .
How is that for medical progress, huh?! Additionally, most research drugs for stroke, including neuroprotective agents must be administered within less than 6-8 hours, in most cases.
The physical examination should include a general examination with emphasis on the cardiovascular system and a complete neurologic exam.
The cardiovascular examination should include observing for signs of congestive heart failure (pallor, edema, jugular venous distention, etc.), Raynaud's phenomenon, livedo reticularis, vasculitic skin changes, cyanosis, clubbing, peripheral vascular disease, venous insufficiency of the legs, trophic changes due to neuropathies, etc. Cardiac auscultation for murmurs (especially mitral stenosis), extra sounds and the regularity of rhythm is important. The temples, eyes, carotids, mastoids and subclavicular areas (and if you will, the epigastrium and renal artery areas) should be auscultated in search for arterial bruits. Then, palpate the pulses; check for symmetry and volume. Feel the position of the apex of the heart for enlargement.
The neurologic examination is extensive and detailed. An abbreviated neurologic exam that gives the physician an idea of the size and severity of the ischemic lesion is more appropriate in the acute setting. The basic elements are: mental status, cranial nerves, motor, sensory, brainstem and cerebellar functions. The use of neurologic scales (e.g. NIH Stroke Scale) has greatly facilitated the evaluation of patients to document severity in an objective scoring system. The scales not only measure the size/severity of the lesion but also allow for an assessment of outcome in populations of patients.
It may sound burdensome and long examination. However, with experience, you will learn what are the essential elements that you should seek for before making a decision. Some of the details of the examination can be completed after basic emergency decisions are made.
The diagnosis of stroke has three parts:
anatomic...where is the lesion?
pathogenetic...why did the lesion occur?
etiologic....what caused it?
The diagnosis and proposed mechanisms are confirmed by a paraclinical evaluation that includes ultrasound, computed tomography (CT scan) and magnetic resonance studies. While it was 15% permissible in yesteryear to miss the diagnosis of hemorrhage vs. infact, or to mistake a subdural hematoma for a stroke or vice versa, the wide availability of CT scan has improved the rate of correct diagnosis leaving very little chances of error between these diagnoses.
Thus, for those of you who tend to think in computer terms, the format of the diagnosis of stroke should be:
"This patient had a {anatomic diagnosis}{pathogenetic diagnosis}{etiologic diagnosis} ischemic stroke.
For example: "This patient had a left frontal ischemic stroke, caused by occlusion of the proximal anterior division of the MCA. The mechanism of the stroke is embolic, more specifically, cardioembolic, from atrial fibrillation."
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