Atypical Presentations of Ischemic Cerebrovascular Disease: Part II
Atypical Presentations of Ischemic Cerebrovascular Disease: Part II
This is the second part of the article on atypical presentations of stroke and TIAs. We start with the same patient we introduced last time and discuss the differential diagnosis of his myriad complaints. This issue also deals with the diagnostic testing and initial management of these patients and concludes with a more thorough discussion of the outcome of this case.
Stroke and TIA are important, time-sensitive emergency conditions. All emergency providers need to understand the full spectrum of the disease. Many of our hospitals are seeking stroke certification from The Joint Commission and other certifying bodies. Such certification generally includes requirements for ongoing CME specific to stroke for emergency providers. This two-part series will provide CME toward that requirement.
Sandra M. Schneider, MD, FACEP, Editor
Case Presentation
A 62-year-old, right-handed, Caucasian male presents to the emergency department (ED) with a chief complaint of gait instability, slurred speech, and double vision. He is unable to recall when his symptoms began, but his son notes that he sounded normal on the telephone approximately 4 hours previously. On physical examination, the patient required repeated stimulation in order to cooperate with the exam. He was noted to have dysarthric speech, with pronounced involvement of palatal and lingual syllables. Cranial nerve evaluation revealed a dysconjugate gaze in primary position, with inability to look upward on command. Although motor strength was normal, the patient was unable to perform finger-to-nose testing or heel-knee-shin testing on the right side without considerable dysmetria. A noncontrast head CT was read by the radiologist as "normal."
What would be an appropriate lesion to explain this patient's symptoms, and what would be an appropriate disposition and management plan? The objective of this two-part article is to help arm the emergency physician to be able to answer these questions.
Diplopia
Acute changes in vision can be troubling both for the patient and the physician trying to diagnose the underlying cause. Diplopia occurs when single objects appear to be double. The first step in the evaluation of a patient with this complaint is to differentiate monocular versus binocular diplopia.1 If the patient covers one eye and the diplopia persists, then the diagnosis of monocular diplopia is made. Monocular diplopia usually is secondary to mechanical processes that involve ocular structures (eg, second opening in the iris, corneal distortion, subluxation of the lens, vitreous abnormalities, retinal conditions). This is not consistent with a central neurololgic cause.
If binocular diplopia is present, it can be helpful to determine if the diplopia is comitant or incomitant. Comitant diplopia occurs when there is no difference in separation of the images in all directions of gaze. However, if diplopic deviation changes (and possibly resolves in a given direction), then the deviation is incomitant. Most neurologic ocular misalignments are incomitant.2
In the absence of obvious other pathology (eg, trauma with extraocular muscle entrapment, orbital cellulitis, abscess, etc.), incomitant diplopia suggests a problem with innervation of an extraocular muscle. These extraocular muscles are controlled by cranial nerves, and disruption of the signal can result in ophthalmoparesis and diplopia. Following is a brief review of the cranial nerves responsible for extraocular motion and the clinical presentation of their dysfunctions.
Third Nerve (Oculomotor Nerve). The third cranial nerve originates in the dorsal midbrain, exits the brainstem ventrally, traverses the subarachnoid space, and enters the orbit via the superior orbital fissure. This nerve is responsible for elevation, depression, and adduction of the orbit. In a third nerve palsy, all third nerve muscles are impaired and there is ptosis.
Pupil involvement usually indicates a compressive lesion (PCOM aneurysm), while sparing of the pupil is more likely ischemia. Isolated ischemic lesions of the third-nerve nuclear complex are not rare, as small medial branches of the basilar artery selectively supply it.3
Fourth Nerve (Trochlear Nerve). The trochlear nerve originates in the dorsal midbrain. It enters the cavernous sinus then enters the superior orbital fissure and innervates the superior oblique muscle contralateral to its nucleus of origin. Injury to the trochlear nerve causes weakness of downward eye movement with consequent vertical diplopia (double vision). Weakness of intorsion (inward rotation of the eye toward the midline of the face) also results in torsional diplopia, in which two different visual fields, tilted with respect to each other, are seen at the same time. To compensate for this, patients with trochlear nerve palsies tilt their heads to the opposite side to fuse the two images into a single visual field. The characteristic appearance of patients with fourth nerve palsies (head tilted to one side, chin tucked in) suggests the diagnosis. Isolated involvement of the trochlear nucleus and nerve is very rare in vascular brainstem disease.
Sixth Nerve (Abducens Nerve). The abducens nerve originates in the caudal pons, exits the brainstem ventrally, and travels in the subarachnoid space. It pierces the dura and ultimately enters the superior orbital fissure to innervate the lateral rectus. Abducens dysfunction results in ipsilateral abduction paresis and esotropia (the eye looks toward the nose). Microvascular ischemia may cause an acute onset, isolated sixth nerve palsy.
There are many syndromes that involve brainstem ischemia that will involve these cranial nerve nuclei and can result in ophthalmoplegias. Larger areas of ischemic compromise, however, result not just in isolated oculomotor palsies, but also in severe neurologic sequelae that include ataxia, altered levels of consciousness, paralysis, and sensory deficits. The diplopia may be the least of the patient's concerns. This also holds true for most conjugate gaze deviations that are caused by ischemia supratentorially. These tend to be severe cerebral infarctions and are rarely present without associated concomitant paralysis.4
Summary Points
With the complaint of diplopia, the clinician should differentiate between monocular vs. binocular diplopia.
When diplopia has been established, incomitant vs. comitant diplopia should be established.
Acute incomitant diplopia is suggestive of an ischemic brain attack.
Acute Loss of Vision
Sudden monocular blindness is the major symptom of an ocular stroke causing permanent vision loss. Transient or persistent loss of vision in one eye is a common and distinctive manifestation of occlusive vascular disease. Amaurosis fugax (transient monocular visual loss) is a form of acute vision loss caused by reduced blood flow to the eye and has been described as an "ocular TIA."
Ocular strokes are most commonly either central retinal artery occlusion (CRAO), branch retinal artery occlusion (BRAO), and anterior ischemic optic neuropathy (AION - optic nerve infarction). These are all distal branches supplied by the internal carotid artery.
In addition to the usual suspects when it comes to cerebrovascular disease (embolic arterial obstruction and occlusion in situ due to plaque rupture), giant cell arteritis also should be considered, as well as arterial occlusion that can occur with high hydrostatic pressure associated with glaucoma. However, this clinical scenario also can be caused by migraine or retinal vein occlusion.
Clinical signs include a pupil that does not constrict with direct illumination but that has an intact consensual light response (afferent pupillary defect). Intraocular pressure tends to be low. Pain is rare, but if present, could imply involvement of the ophthalmic artery.
Unilateral complete loss of vision secondary to vascular occlusion should be considered a subset of ischemic brain attack even though no other neurologic sequelae may be evident. The treatment of CRAO will not be discussed here, but in addition to treatment to save the function of the eye, this event must be viewed as a brain attack in terms of management and disposition, which will be discussed in depth later.
A brief mention must be given to cortical blindness. Cortical blindness is the total or partial loss of vision in a normal-appearing eye caused by damage to the visual area in the visual cortex located in the occipital area of the brain. Lesions in the occipital lobes, which typically result from occlusion of the posterior cerebral artery, result in visual field cuts. The most typical pattern is a homonymous hemianopia with macular sparing. However, in the case of bilateral occipital lobe injury, cortical blindness may result. In this case, patients are unable to see but will have preserved pupillary response to light and normal fundoscopic examinations. Patients may have some sparing of vision that allows them to avoid objects in the setting of this blindness and may be able to perceive motion but not still objects. Anton-Babinski syndrome is an interesting presentation of cortical blindness in which patients deny that they have vision deficits and may try to convince health care workers and family members of their falsely intact vision.
Summary Points
Sudden atraumatic vision loss should be considered a neurologic emergency.
Optical nerve ischemia yields a pupil that does not constrict to direct illumination, while in a visual cortex lesion, the pupillary light reflex is preserved.
Dysarthria and Aphasia
When presented with a chief complaint of unintelligible speech, it is important to distinguish between dysarthria and aphasia. Patients with dysarthria present with slurring, poor enunciation, and/or alteration in the quality and tone of voice. These symptoms may result from motor or mechanical impediments to speech production or from systemic conditions such as sepsis, hypoglycemia, and drug effects that result in generalized alterations in level of consciousness.
Aphasia, on the other hand, presents with inability to comprehend speech or with inability to produce coherent language. Impaired comprehension is consistent with a Wernicke's aphasia, otherwise known as sensory aphasia, fluent aphasia, or receptive aphasia. In this condition, patients typically are able to speak fluently and with normal enunciation but produce completely nonsensical sentences. This type of speech is sometimes referred to as "word salad." In Broca's aphasia, also known as motor aphasia, dysfluent aphasia, or expressive aphasia, patients generally retain speech comprehension but have impaired oral expression. Some patients may be completely mute on presentation; others demonstrate slow, hesitant speech with frequent pauses that is sometimes described as "word finding difficulty." Patients may demonstrate grammatical inaccuracies as well as difficulty with repetition and naming objects. The ability to write may be impaired as well. Patients often demonstrate preservation of automatic speech: that is, rote phrases that are overlearned and can be spoken unconsciously. For instance, a patient with a motor aphasia and pronounced verbal dysfluency may retain the ability to recite the alphabet.
The physical examination of a patient with speech complaints should focus on mental status and level of consciousness, cranial nerve function, language, and comprehension. The patient's level of arousal and attention can be assessed by routine interaction at the bedside. In a person who is alert and acutely responsive to the examiner, systemic problems such as sepsis, hypoglycemia, and drug intoxication are unlikely. The cranial nerves should be examined to evaluate for evidence of brainstem pathology. In particular, tongue movements, palatal elevation, facial symmetry, facial sensation, and extraocular movements are important. Inspection of the oral mucosa may reveal evidence of local pathology, such as an abscess, which may be contributing.
Some assessment of language function may be possible simply from the normal course of interacting with the patient. For instance, a patient with a dense receptive aphasiathat is, inability to comprehend speechwill not be able to follow verbal commands but likely can be encouraged to mimic the examiner's movements.
Dysarthria without aphasia can be present in a variety of situations. Broadly speaking, the differential diagnosis includes trauma; tumors, either of the head and neck or of the posterior fossa of the skull; infectious processes; degenerative neurological syndromes; congenital malformations; and toxic-metabolic causes. It may be a prominent symptom in vertebrobasilar strokes involving the cranial nerves VII, IX, or XII; or it can be secondary to facial weakness associated with strokes in the MCA territory.
Aphasia, as opposed to dysarthria, is the result of damage to the cerebral cortex or underlying fiber tracts in the dominant hemisphere. The left hemisphere is dominant in most right-handed individuals and roughly two-thirds of left-handed people.12 Lesions of the temporal lobe, specifically in the superior temporal gyrus, affect speech comprehension and result in Wernicke's aphasia. It is not uncommon for Wernicke's aphasia to present in the absence of a motor deficit. If the lesion also involves adjacent portions of the parietal lobe, reading may be compromised as well. Broca's aphasia classically results from dysfunction to the inferior frontal lobe. Depending on the extent of the injury, patients may have features of both Wernicke's and Broca's aphasias. This syndrome, called a global aphasia, usually is accompanied by hemiplegia and is almost always due to large infarcts in the MCA distribution.5 Damage to the areas of the brain involved in speech processing also can occur with trauma, some neurodegenerative conditions, herpes encephalitis, tumors, and cerebral abscesses, but stroke should be considered in any patient presenting acutely with aphasia.
Summary Points
Aphasia is always the result of a central nervous system lesion.
Dysarthria can occur as part of a stroke syndrome, but it rarely is the sole finding.
Miscellaneous Complaints and Syndromes
A few additional stroke syndromes deserve special mention. Lesions in the parietal lobes can present with a variety of cognitive complaints that may or may not be accompanied by focal motor abnormalities. The term apraxia applies to an inability to execute skilled movements, which can occur in the absence of sensory or motor abnormalities. Patients have difficulty miming actions such as brushing their teeth or combing their hair but may perform much better when prompted with the appropriate tool. This deficit typically results from lesions in the inferior portion of the dominant parietal lobe. Apraxias result in considerable disability secondary to inability to perform complex tasks associated with activities of daily living. Lesions in the more dorsal portion of the dominant parietal lobe can produce Gerstmann's syndrome, a constellation of right-left confusion, acalculia (loss of mathematical skills), finger agnosia (inability to recognize fingers), and agraphia (inability to write). These deficits result from loss of association areas in the parietal lobes responsible for integrating sensory data from various other cortical regions.
Lesions in the nondominant parietal lobe can result in hemi-neglect, in which the patient is unable to attend to the contralateral side of the body. In a mild form, this can present as extinction with double simultaneous stimulation. Patients can be presented with a stimulus, such as a moving finger in a particular visual field or a light touch on the hand. They can identify the stimulus when it is present on the right and on the left individually, but when presented with bilateral, simultaneous stimulation they are aware only of the stimulus on the unaffected side. In severe cases, patients may be unable to recognize the affected side of their body or notice objects and people on a particular side of the room.
Basilar artery thromboses represent a particularly important clinical situation due to their variable presentation and high mortality rate. Most patients will have a history or physical symptoms consistent with brainstem ischemia as discussed in prior sections, but occasionally the complaints can be quite nebulous. For instance, patients may complain of hemiplegia that alternates sides. Top of the basilar syndrome results from occlusion of the distal basilar artery, usually secondary to embolic phenomena. Symptoms can include depressed level of consciousness, oculomotor abnormalities, memory difficulties, diplopia, and/or visual field cuts.
Balint's syndrome, described in Table 1, results from damage to the bilateral parietotemporal regions and can occur with top of the basilar syndrome. If untreated, basilar artery thrombosis can result in locked-in syndrome or even death. Locked-in syndrome results from lesions to the bilateral ventral pons, with sparing of the dorsal brainstem. The patient develops quadriplegia, bilateral facial weakness, and loss of motor control to the lower cranial nerves. Occasionally, lateral gaze is lost as well due to cranial nerve VI involvement. The reticular activating system, located in the dorsal pons, is preserved in this syndrome; this means that the patient remains fully awake. Often the only indication of this is the ability to look up and down upon command.
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Diagnostic Evaluation
Strictly speaking, stroke and TIA are clinical diagnoses. Generally, ischemic cerebrovascular disease presents with the sudden onset of neurological deficits that are classically described as being maximal at onset. The National Institutes of Health Stroke Score (NIHSS) is useful both as a rapid evaluation tool for patients with stroke symptoms and as a means for scoring stroke severity. (See Table 2.) Because it not always possible to distinguish intracerebral hemorrhage (ICH) and ischemic stroke on clinical grounds alone, a non-contrast head CT should be performed on any patient suspected of having had a stroke. This examination is highly sensitive for the detection of ICH and is about 90-95% sensitive for the detection of subarachnoid hemorrhage. Unfortunately, a non-contrast CT is usually negative in acute ischemic events; radiographic changes typically will not appear until several hours after the event.6
The laboratory evaluation of patients with suspected stroke is geared toward excluding stroke mimics and identifying potentially serious comorbidities. All patients should undergo a serum blood glucose, electrolytes and renal function testing, complete blood count with platelet count, oxygen saturation, and coagulation panel. The results of these findings may identify conditions such as hypoglycemia that can present with focal neurological findings and may impact patient treatment with respect to blood pressure management and eligibility for thrombolysis. In addition, patients should be screened for myocardial infarction with an electrocardiogram and markers of cardiac ischemia because arrhythmias and cardiac ischemia often are found in patients with stroke and may require acute intervention.7
Contrasted CT studies increasingly are being used instead of the standard, noncontrast study in the evaluation of acute cerebral ischemia. CT angiography can provide an excellent view of the intracranial vasculature. It is useful to exclude the presence of vascular malformations and to evaluate for carotid stenosis or intracranial atherosclerotic disease. Most importantly, CT angiography may demonstrate an arterial occlusion that may be amenable to endovascular therapy. CT perfusion imaging is an evolving modality available at some institutions that can provide a measure of cerebral blood flow, blood volume, and mean transit time in given regions of tissue. The latter is a measure for the amount of time it takes contrast to travel from the injection site to the region in question; it is prolonged in ischemic parenchyma.6,8 Analysis of this data can give the clinician information regarding the extent of the injury and the viability of the affected tissue; some centers use this information to assess suitability for endovascular treatment.
MRI is also a powerful tool in acute stroke. Diffusion-weighted MRI (DWI) detects increased cellular water content and is 95% sensitive for stroke. Ischemic lesions will become diffusion-positive within minutes of symptom onset; the diffusion sequence will then gradually normalize over 5-10 days.9 Although MRI is not usually necessary in the acute setting, it is much more sensitive than noncontrasted CT for cerebral ischemia and is very useful in cases where the diagnosis cannot be made on clinical grounds alone. However, it is important to recall that MRI may be negative in the setting of transient ischemic attack, especially if the patient is imaged after symptoms have resolved. MR perfusion, similar to CT perfusion, can be used to provide information about tissue blood flow and blood volume, among other measures. When combined with diffusion-weighted MRI, this can help distinguish the infarct core, infarct penumbra, and oligemic regions. A combination of these modalities is being used in some centers to extend the window for IV thrombolysis and endovascular therapies as described below.10,11
Summary Points
Patients suspected of having had a stroke should have a CT to rule out hemorrhage.
Cardiac arrhythmias and myocardial infarction occur not uncommonly in patients presenting with ischemic stroke.
Techniques like CT perfusion and MRI can be used to give information about the functional state of the brain tissue.
Management and Disposition
The treatment of acute stroke is a rapidly evolving field. Thrombolytic therapy with tissue plasminogen activator (tPA) received FDA approval in 1996. Intravenous tPA is approved for use up to 3 hours after symptom onset. Although administration of tPA does not alter mortality, treated patients have a significantly greater chance of recovering to normal or near-normal function (30% relative risk reduction of significant disability).4 The benefit is most pronounced in patients treated early, i.e. within 90 minutes of symptom onset. tPA does carry a risk of hemorrhagic complications, including intracranial hemorrhage. The risk of symptomatic intracranial hemorrhage has been estimated at 3-6% when administered according to standard guidelines.7,12,13 Consequently, any patient being considered for tPA must have a clearly defined time of onset, a head CT without evidence of hemorrhage, and a careful screening for contraindications such as recent surgery, gastrointestinal or genitourinary bleeding, history of prior ICH, or previous stroke within the last 3 months.
In general, tPA is indicated for any patient with an ischemic stroke who can be treated within 3 hours of symptom onset. The presence of "minor" or rapidly improving deficits has been suggested as a relative contraindication to thrombolysis; however, excluding patients from treatment on this basis can be controversial. Pitfalls arise when a patient who initially was denied treatment due to his or her minor or improving symptoms later suffers a significant decline after the treatment window has closed. In one large, community-based series, 32% of patients excluded from treatment for these reasons either remained dependent or died during hospital admission.14 A reasonable approach is to consider tPA in any patient with potentially disabling symptoms. For instance, isolated aphasia may warrant treatment, whereas a pure sensory deficit may not. Patients with particularly severe strokes, usually defined as an NIHSS > 22, are at an increased risk of symptomatic ICH, as are those with early radiographic involvement of more than two-thirds of the MCA territory. These patients have a poor prognosis, although some benefit of tPA treatment has been documented.15 The decisions regarding whether to offer thrombolysis in this group must be made with caution.
Since its initial approval, the safety and efficacy of IV thrombolysis for acute ischemic stroke has been reaffirmed in a number of clinical trials.13,16-20 The recently-published ECASS III trial investigated the use of tPA in ischemic stroke patients presenting between 3-4.5 hours after symptom onset. Patients were randomized to tPA versus placebo on the basis of history and a non-contrast head CT. The investigators reported a significant improvement in outcome in the tPA group, with a 2.4% rate of symptomatic intracranial hemorrhage.21
Endovascular therapy for ischemic stroke is increasingly being utilized for those patients with significant deficits who are not candidates for tPA, or in whom IV thrombolysis fails to result in prompt recanalization of the occluded vessel. These interventions may be appropriate for patients with large-vessel occlusions. Intra-arterial thrombolytics can be administered by catheter directly to the site of the thrombus. Although initial trials were performed using pro-urokinase,22 that agent is no longer available within the United States and, consequently, interventionalists have turned to using low-dose tPA in an off-label fashion.15 Intra-arterial tPA generally is considered for patients within 6 hours of symptom onset, or those in whom perfusion imaging suggests that a significant volume of ischemic tissue remains viable. This therapy has been successfully used in patients at high risk of systemic bleeding and in those who present after 3 hours; it is also being investigated as a potential adjunct to intravenous thrombolysis.23,24 Additionally, a number of mechanical devices have been designed to physically remove clot material from large cerebral blood vessels.25-28 The safety and efficacy of mechanical thrombolysis using a variety of techniques has been evaluated up to 8 hours after symptom onset. While these techniques appear safe, data from randomized controlled trials are lacking.
The issue of blood pressure management in acute stroke is an important one but is not without controversy. In general, it is thought that a precipitous drop in blood pressure should be avoided due to the fact that it may compromise blood flow to the penumbra and thereby extend the cerebral infarction. However, significant hypertension (greater than 185/110) increases the risk of intracranial hemorrhage in patients receiving thrombolytics. Consequently, judicious use of antihypertensive agents is indicated in patients who may be candidates for IV thrombolytics or endovascular therapy. In this scenario, a target blood pressure of < 180/90 is desirable. For patients in whom no acute intervention is planned, permissive hypertension is appropriate. In the absence of complicating factors such as myocardial infarction, acute renal failure, or hypertensive encephalopathy, systolic pressures as high as 220 may be tolerated.29
For patients with stroke or TIA who are not candidates for acute intervention, the evaluation is geared toward determining the cause of the stroke and identifying risk factors that may increase the likelihood of recurrence. Patients with symptoms arising from the carotid territories should be screened for carotid stenosis. Carotid stenosis can be evaluated either by vascular ultrasound, CT angiography of the neck, or catheter angiogram. A patient with 70-99% stenosis ipsilateral to the affected brain region is at high risk of recurrent stroke or TIA and should be referred for urgent carotid endarterectomy. Ideally, the procedure should be completed within 2 weeks to provide maximal benefit. Patients with 50-70% stenosis on the ipsilateral side also may be candidates for surgery, depending upon their age, comorbidities, and the severity of the presenting symptoms.30 Any patient with stroke or TIA should receive an ECG to screen for atrial fibrillation and coronary ischemia. Further, cardiac monitoring, such as inpatient telemetry, outpatient Holter monitoring, or a 30-day event monitor, may be necessary to rule out paroxysmal atrial fibrillation.29 A transthoracic or transesophageal echocardiogram may be indicated to evaluate for segmental wall motion abnormalities, cardiomyopathy, atrial septal aneurysm, valvular heart disease, and other factors that may predispose patients to intracardiac thrombus formation.
In general, decisions about patient disposition must be made on a case-by-case basis. Studies have established the fact that patient outcomes after stroke are improved when care is handled by multidisciplinary stroke teams.31-34 This observation has resulted in a movement to designate facilities with certain featuresincluding stoke units, presence of neurology coverage, written protocols, and 24-hour access to neuroimagingas primary stroke centers.34 Recommendations for comprehensive stroke centers also exist,35,36 although no formal pathway for the designation of comprehensive centers is yet available. Acute stroke patients, especially those presenting within the window for thrombolysis or endovascular therapies, should be considered for transfer to stroke centers with these capabilities. Patients with large hemispheric strokes, fluctuating symptoms, or posterior circulation strokes should also be considered for transfer.
Most patients presenting with ischemic cerebrovascular events will require hospital admission to facilitate a diagnostic work-up, rehabilitation assessment, and risk factor modification. However, a subset of patients with minor, completed stokes, or low-risk patients with TIA, conceivably may be managed as outpatients in certain communities.37 Factors to be considered include patient reliability, availability of prompt follow-up, social support, and need for rehabilitation services.
Summary Points
Patients suspected of suffering an ischemic stroke within the past 3 hours should be evaluated for tPA candidacy. This window may soon be extended to 4.5 hours.
Relative hypotension should be avoided in the acute phase following stroke.
The majority of patients with ischemic stroke will require inpatient admission. Admission to a stroke center is associated with improved outcomes.
Case Outcome and Discussion
In the case of the 62-year-old male who presents with slurred speech, ataxia, and diplopia, despite the initial head CT that was read as "normal," it was presumed likely that the patient was experiencing brainstem ischemia based on the clinical presentation. The patient was emergently transferred to a primary stroke center. En route, his level of consciousness declined and he was intubated for airway protection. Upon arrival at the stroke center, a repeat head CT was notable for a hyperdense basilar artery (see Figure 1A); an emergent angiogram confirmed the presence of a basilar artery occlusion (Figure 1B). Intra-arterial thrombolysis was performed with excellent effect (see Figure 1C), and following the procedure the patient demonstrated an improvement in his level of consciousness. He sustained infarctions to the right cerebellum and portions of the midbrain and thalamus, resulting in residual right-sided hemiataxia, paresis of up-gaze, and hemisensory loss, but ultimately had a good recovery and was discharged to an inpatient rehabilitation facility.
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In today's medical and medicolegal environment, ischemic brain attacks are a serious and, in recent years, have become a time-sensitive disease. Early recognition and treatment of cerebral ischemia can increase the chances of survival and return to independent living. While the classic presentation of stroke with speech difficulties and paralysis is readily recognized, many syndromes exist that present diagnostic challenges to the emergency clinician.
The syndromes of cerebrovascular disease can be highly variable and can present with vague and seemingly benign complaints. The challenge for today's emergency provider is to develop an appropriate level of suspicion for acute ischemic brain attack in patients who present with non-paretic or dysarthric neurologic symptoms.
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This is the second part of the article on atypical presentations of stroke and TIAs. We start with the same patient we introduced last time and discuss the differential diagnosis of his myriad complaints.Subscribe Now for Access
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