Term
| Case Presentation: History |
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Definition
• An80yearoldright-handedgentlemanwith atrial fibrillation (on Coumadin), HTN, dyslipidemia, and prior TIA presents to the ED for evaluation of acute right sided weakness.
• HewasinUSOHuntil90minpriorto presentation when he was at home with his wife. His wife states he had just gotten up from bed that morning and was brushing his teeth when she heard a loud “thump.”
• Shewentovertothebathroomandfoundthe patient on the floor. She said he was alert, conscious, and lying on his right side, but unable to communicate with her.
• Hewastryingtosaysomethingtoherbut unable to articulate words; he became increasingly more frustrated. She asked him if he hit his head during the fall, but he was unable to answer her.
• Shetriedtomovehimofftheground,buthewas unable to move his right side.
- Past Medical History:
• Atrial fibrillation
• Hypertension
• Hyperlipidemia
• TIA 2 months ago (word-finding difficulties)
- Past Surgical History:
• AAA repair 3 years ago
• Inguinal hernia repair 40 years ago
- SocialHistory:
• Quit smoking 30 years ago • Glass of wine every evening • No IVDA/marijuana use
- FamilyHistory:
• Non-contributory
- Homemedications:
• Coumadin 5 mg qdaily
• HCTZ 25 mg qdaily
• Metoprolol 25 mg qdaily • Atorvastatin 40 mg qdaily |
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Term
| Case Presentation: General Physical Examination |
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Definition
• Vitals = T 99.1 HR 114, BP 240/120, RR 24
• General: slightly obese man, anxious appearing
• HEENT/Neck:NC/AT,MMM; no bruising
• CV: an irregularly irregular heartrate
• Lungs:CTAB/L,NoW/R/R
• Abdomen: no abdominal bruits
• Extremities:2+LE pulses; trace peripheral edema |
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Term
| Case Presentation: Neurological Examination |
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Definition
• Mental status: awake, alert, responsive to commands but unable to produce spontaneous speech or repeat
• CNs: R lower facial droop, PERRLA with no evidence of Horner’s syndrome; possible R hemianopia to confrontation
• Motor exam: RUE/RLE weakness and flaccid tone noted; 0/5 RUE, 3/5 RLE
• Sensory exam: difficult to assess; double simultaneous extinction on right
• Cerebellar: intact F à N à F on left, unable to move right
• DTR’s: decreased on R with R sided upgoing toe
• Gait: deferred
• NIHSS=15 |
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Term
Case Presentation: Update
• Initial Laboratory Data |
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Definition
• Platelets = 210 • FS: 88
• BUN/Cr = wnl • INR = 1.6 |
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Term
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Definition
So if you were to imagine that you're accompanying this patient into the CAT scanner, this would be the left side of the patient. This would be the right side of the patient. And typically, on CAT scan, things are dense. So the denser or more hyper-dense it is, the whiter it is.
One way to think about it is that things that have a divalent charge, like calcium and iron, tend to be denser. So that's why we see the calvarium-- the bone is denser. That's why, also, if someone were to have a hemorrhagic stroke because of the iron in the blood, that would appear white as well.
So, so much of the neurologic examination, we're comparing one side to the other. We're doing the same thing for the CAT scan. This is a non-contrast head CT, meaning that this patient, for example, did not get contrast in the vein. When we give contrast, it will light up. It will go throughout the arteries of the brain, and we will be able to see all the blood vessels.
So this is a non-contrast head CT, but what we see here is something that's hyper-dense, and it's in the very proximal or the M1 component of the MCA-- Middle Cerebral Artery. When we see this, this is considered a dense MCA sign. And this is what a clot looks like, causing ischemic stroke on a non-contract head CT. |
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Term
| Differential Diagnosis for our case study |
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Definition
- Vascular Etiologies:
• Ischemic stroke
• ICH
• Carotid or vertebral dissection
• Subarachnoid hemorrhage
• Subdural hematoma
• Epidural hematoma
• Hypertensive crisis
• Tumor with secondary hemorrhage
- Electrical
• Seizure with postictal Todd’s paralysis
• Complicated migraine
• Hemiplegic migraine
- Infectious:
• Encephalitis
• Cerebral abscess
• Empyema
- Immunologic:
• Multiple sclerosis
- Toxic/Metabolic/Systemic:
• Electrolyte abnormalities (in patient with prior stroke) • Exception: hypoglycemia or hyperglycemia
• UTI/PNA (inpatientwithpriorstroke) |
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Term
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Definition
So in thinking about the case that we went over, what we'll try to do next is think about where the lesion may be. I find it helpful in thinking about where a lesion may be, especially if I think that it may be in the brain, is superimposing these two pictures on one another. So here we think about the different vascular distributions, in blue the anterior cerebral artery, in salmon, the posterior cerebral artery, in green, less common, the anterior caudal, and in mustard, seeing the middle cerebral artery.
So what I try to do is to think about this as if I'm facing the patient. And what we see here are coronal sections, again, as if you're facing someone, and then superimposed on that, the homunculus. So for example, with the ACA distribution, this is typically where the foot lies. Then, as we sort of carry over, that hand and the face for the middle cerebral artery. And then for the PCA, typically this is where we'll have patients with visual field deficits.
So to the point earlier, when patients have face and upper extremity weakness which will localize here more than leg weakness, we would think that the possibility of a lesion in the MCA distribution is higher. As all the corticospinal tracks come through here, they start funneling downward such that if you were to have a lesion sort of deeper in the brain in the subcortical region, that's when a lot of these fibers get closer together, meaning that's also when you'll have patterns of weakness that the face, arm, and leg weakness approximate one another. |
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Term
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Definition
I also think it's useful to think of how the arteries come off the aorta. So typically we have the aorta, the brachiocephalic trunk, and then this would be the right common carotid, and then it splits off into the external carotid, which supplies the face. And then the internal carotid continues along into the brain. Here's the extracranial part of it, and this is where it dives into the brain, and it does a bit of a turn, and then becomes the middle and anterior cerebral arteries.
Back here we see that the vertebral artery will dive through into the cervical region, so at approximately the C6 level. So as you can imagine, older persons that have a lot of osteoarthritis there may damage the vertebral artery as it goes through this part of the spinal column. |
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Term
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Definition
So we started to talk a little bit in terms of differences between ischemic stroke and hemorrhagic stroke. When you look at the numbers, about 80% of all strokes are ischemic. And what happens is that you have a clot that gets lodged in one of the blood vessels of the brain, and everything downstream of that is deprived of oxygen, nutrients, and there's a decreased capacity to remove waste.
So this, on CAT scan, is what it looks like if someone had a stroke of their entire middle cerebral artery. So this area preserved would be the anterior cerebral territory. This area preserved would be the posterior cerebral artery. And everywhere we see a darker area is ischemic stroke. Typically, and depending on when patients present, the sooner that they present, the less likely you are to see imaging findings on CAT scan. The reason for this is that there's a delay in terms of seeing ischemic changes on CT scan.
What happens as time goes on, the tissue that's either dead or at risk of dying becomes hypodense. Depending on the amount of territory that's involved, this stroke could push the good part of the brain in this hemisphere to the other side. So here we see the right lateral ventricle, which should be typically here, pushing to the other side. Also, if we look at the healthier side of the brain, we follow the general pattern. But here we don't see it as well. What happens is that the brain is being pressed up against the inside of the calvarium.
Now going to hemorrhagic stroke, where a blood vessel will leak or burst into the brain parenchyma, we see that as hyperdense and a little less hyperdense, or a little less bright compared to the bone. We see some hypodensity around it, which is some edema from it. And then similar to what we see here with ischemic stroke, where it's pushing the brain to one side, we also see that the hemorrhagic stroke is doing something similar. |
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Term
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Definition
Frontal pole and mesial frontal lobe. Contralateral: leg > face and arm weakness
Frontal signs such as abulia |
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Term
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Definition
Posterior frontal, temporal, parietal lobe.
Contralateral: face and arm > leg weakness, sensory loss to all modalities, visual field cut, visual-spatial neglect Ipsilateral: gaze preference
Dominant hemisphere affected: aphasia, alexia, agraphia, acalculia |
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Term
| Posterior cerebral artery |
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Definition
| Occipital lobe. Contralateral: homonymous hemianopia With thalamic involvement: Sensory loss to all modalities or pain |
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Term
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Definition
Pons (locked-in syndrome).
Bilateral: progressive quadriplegia, facial weakness
Lateral gaze weakness with sparing of vertical gaze |
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Term
| Ischemic stroke modifiable vs nonmodifiable factors |
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Definition
modifiable:
Hypertension Diabetes
Atrial fibrillation Smoking Hyperlipidemia Carotid stenosis
nonmodifiable:
Age >55
Male gender
Black race
Family history of stroke Personal history of stroke |
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Term
| Intraparenchymal hemorrhage modifiable vs nonmodifiable factors |
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Definition
modifiable:
Hypertension Amyloid angiopathy Anticoagulant use Thrombolytic use
nonmodifiable:
Vascular malformation Neoplasm
Trauma
Acute ischemic stroke |
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Term
| Large-Artery Atherosclerosis (ischemic stoke) |
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Definition
| High-grade stenosis or occlusion of the major intra- and extracranial arteries, which include the internal carotid artery, the vertebral artery, the basilar artery, and other major branches of the circle of Willis, occur due to deposition of plaque and often leads to a flow-dependent state of perfusion |
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Term
| Cardioembolism (ischemic stroke) |
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Definition
| Turbulent or stagnant flow states in the heart can result in formation of thrombi. These thrombi can dislodge and occlude blood vessels in the intracranial circulation farther downstream. The most common cause of cardioembolic stroke is atrial fibrillation. Other causes include severe left ventricular dysfunction resulting in a low ejection fraction, paradoxical embolus from the venous system due to a shunt through a septal defect such as an aneurysm or patent foramen ovale, or vessel-to-vessel atheroembolism due to atherosclerotic disease in the vertebral arteries, carotid arteries, and aortic arch. |
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Term
| Small-Vessel Disease (ischemic stroke) |
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Definition
| Changes in the arterial vasculature of small perforating arteries can result in narrowing of the vessel lumen and eventual occlusion. Chronic hypertension is one state that leads to vessel damage secondary to lipohyalinosis and endothelial damage. Hyperlipidemia, smoking, and diabetes also lead to changes in the vessel wall that result in decreased compliance and intraluminal stenosis. These changes often result in lacunar infarcts, which are small infarcts defined by their size (<15 mm3) and are typically located in deep structures such as the internal capsule, basal ganglia, thalamus, and brainstem. |
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Term
| Stroke of Other Determined Etiology (ischemic stroke) |
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Definition
| The majority of ischemic strokes are classified in one of the previous categories. Rarely, other causes must be investigated, particularly in patients who are young and have no risk factors for stroke. Among these causes are coagulopathies, vasculopathies, genetic disorders, and metabolic disorders. |
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Term
| Stroke of Undetermined Etiology (ischemic) |
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Definition
| In a significant number of cases (≤40%), no clear explanation can be found for an ischemic stroke despite an extensive diagnostic evaluation. These strokes are classified as strokes of undetermined etiology, or cryptogenic strokes. This is a diagnosis of exclusion, however, and should only be made once a thorough search for both common and uncommon causes of stroke has been completed. |
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Term
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Definition
| And similar to what we looked at before, did someone have thromboembolic disease from carotid artery disease where clot build up caused-- cholesterol buildup caused a clot that went to the brain, or did someone develop or have a left atrial appendage? Did they develop atrial fibrillation that caused the blood to get sticky momentarily and then when the person went into sinus rhythm threw the clot throughout the body? Could someone have had a right to left shunt, such as a PFO? And that's commonly but more specifically for ascending aortic atherosclerosis. This would cause clots that could go to the brain as well. |
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Term
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Definition
Intracerebral hemorrhage occurs when a blood vessel within the brain parenchyma ruptures and causes accumulation of blood within the brain tissue. Weakening of the blood vessel wall is often a result of chronic uncontrolled hypertension or a problem intrinsic to the blood vessel such as amyloid angiopathy or other vascular malformation. In hypertension, microaneurysms in perforating vessels, known as Charcot-Bouchard aneurysms, can rupture and cause bleeding.
The thalamus, basal ganglia, pons, and cerebellum are the most common sites for these hypertensive bleeds. Lobar hemorrhages more commonly result from amyloid angiopathy, which is typically seen in older patients. |
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Term
| So this is the paper from the JAMA Clinical Rationale Exam series. And what it did was that it did a meta analysis to get a sense of, can we identify neurologics-- focal neurologic deficits and what-- if patients have this, how likely are they to have a stroke? |
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Definition
And typically, we won't make a diagnosis with a stroke with an isolated deficit. Again, going back to some of the things we talked about-- that a lot of what we do in neurology is pattern recognition. So, in this case, what they found is if you have more than two of the following-- two or more of the following-- that you're more and more likely to have an ischemic stroke.
So, if someone were to have unilateral facial weakness, if someone were to have arm weakness, where their arm were to drift down, or if they have speech difficulties, the more of those that someone has, the more likely it is that someone's had an ischemic stroke.
In large part from this meta analysis, we have the acronym FAST-- F-A-S-T-- facial weakness, arm weakness, speech deficits, and T for time.
Several years ago, the American Heart Association, American Stroke Association, started a nationwide campaign to increase stroke awareness. And this acronym was part of it-- the idea that if someone has facial weakness, arm weakness, speech difficulties, T-- time is of the essence, please call 911.
One of the other reasons why I like this paper is because it also looked to see if there are neurologic deficits that when present in the emergency room or in the hospital, predict poor prognosis.
As you can imagine, the weaker that someone is or the more complete the weakness is, the more the brain may be involved. And that's a poor prognostic sign. So if someone is completely weak on one side versus having some weakness, being completely weak has a higher prognosis-- has a higher likelihood of worse prognosis, more specifically, high rates of mortality in the hospital.
If someone has a decreased level of consciousness, that typically implies a larger stroke with increased intracranial pressure. That too is a poor prognostic sign.
Also, if someone has a gaze deviation to the other side, then that typically implies a larger stroke as well.
So, not only do we have the FAST acronym, but there's also some neurologic signs when present that make it such that we should be more cautious, or that we should maybe keep a closer eye on a patient that may portend a worse prognosis. |
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Term
| Case Presentation: General Physical Examination |
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Definition
• Vitals = T 99.1 HR 114, BP 240/120, RR 24
• NeuroExam:ConsistentwithLeftMCAinfarct
• HeadCT:DenseMCAsign;noacuteintracranial hemorrhage
• Labs:INR1.6
So, the gentleman has an elevated heart rate, grossly elevated blood pressure. The fact that with his examination it sounds as if he has a Broca's aphasia, so he's not able to produce spontaneous speech for the most part, but does understand. He has face and arm weakness, greater than leg weakness, and now that initial head CT that we saw has a dense MCA sign with no intracranial hemorrhage. This is someone that has a history of atrial fibrillation, and the INR is low, meaning, that Coumadin wasn't providing him as much protection as if the INR was higher.
So, typically, when we're seeing someone in the clinic-- oh, excuse me-- when we're seeing someone in the hospital, in this case, we make determinations about whether or not someone may be a candidate for a clot busting medication. In this scenario, he was a candidate. He received clot busting medication, and his weakness had improved over a couple of days into the hospital stay. He would be later discharged to receive rehabilitation to help to maximize his recovery.
In 1995, the FDA approved intravenous TPA for the management of acute ischemic stroke. The primary outcome of that study was something called the Modified Rankin Scale.
So 90 days after someone were to have a stroke, are they more ambulatory? Are they more independent-- if they got TPA as opposed to if they didn't?
The results of this trial show that getting TPA in the hospital stay improves rehab recovery, improved the Modified Rankin Scale. And hence, that's how TPA came to be as one of the mainstays of treatment.
Within the last several years, an additional mainstay has been the addition of endovascular therapies. So for example, when we see someone and they have that dense MCA sign, that typically means that the clot there, that could be retrieved. We'll do cerebral angiography and do things such as mechanical stent removal, as well as the local administration in the clot to TPA, to try to remove the clot, and thereby improve the chances to reperfuse the brain, and ultimately to improve patient outcomes.
So that tended to be some of the hyper acute and acute treatments for ischemic stroke, but we do all these to help to improve perfusion to the part of the brain that the stroke has effected. But the story doesn't stop there.
So, we had mentioned the risk factors in large part, because it's important to understand what puts someone at risk for having a stroke, but then identify, what are the thing that we need to treat longitudinally to provide for a healthier person, but also decrease the chances of someone having another stroke? |
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Term
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Definition
• Centerpiece of the stroke recovery process
• Goal is to restore as much independence as possible
• Rehabilitation team may differ based on the location of the stroke and residual deficits
- Rehabilitation providers
• Physical therapy: gross motor skills
• Occupational therapy: fine motor skills • Speech therapy
• Health counselor
• Psychologist/therapist |
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