The goal of this program is to improve the diagnosis of stroke. After hearing and assimilating this program, the clinician will be better able to:
Stroke: is a clinical-radiological diagnosis; results in neurologic dysfunction in patients because of focal brain ischemia typically caused by a single occluded artery, leading to specific neurologic deficits; focal weakness, facial droop, and speech/language dysfunction are often identifiable symptoms, especially when they occur together; generally, patients do not experience altered consciousness, at least not in acute cases, except in, eg, basilar occlusion; symptoms are abrupt and severe and tend to occur in patients with vascular risk factors
Stroke Mimics
Stroke vs stroke mimics: patients with stroke mimics present with a global level of impaired consciousness and confusion rather than focal signs, or they may show signs of systemic medical illness; patients with stroke can recall their symptoms and the timing of the incident, eg, being unable to hold a cup while eating breakfast; trouble recalling the onset of symptoms could be a sign of a noncerebrovascular cause
Metabolic or toxic disturbances and systemic infections: typically have global brain dysfunction causing nonlateralizing and nonlocalizing symptoms that usually do not appear suddenly; patients may have a history of recent medication changes, may feel worse over time, and may present with vital signs or laboratory results that indicate systemic inflammatory responses, eg, tachycardia or fever, but not elevated blood pressure (BP); an important metabolic derangement that can cause focal signs is disturbances in glucose, specifically low glucose (blood glucose levels should be checked in patients who present with hemiparesis)
Recrudescence: a patient with a previous central nervous system insult (eg, stroke, subdural traumatic brain injury, large meningioma causing brain compression) may recover with treatment as other areas of the brain compensate for the damaged tissue function; however, a subsequent toxic metabolic disturbance may result in remanifestation (recrudescence) of the focal neurologic symptoms that they had previously; sometimes referred to as anamnestic syndrome; computed tomography (CT) reveals volume loss in the area of the previous insult, suggesting the symptoms are not new
Functional neurologic disorders: are very common; some people refer to them as psychogenic nonepileptic seizures or functional seizures; they can manifest as functional tremors or paraparesis; common symptoms include no movement on one side of the body, facial droop, or acute speech disturbances; a physical examination is crucial, as the patient’s deficit pattern does not coincide with localization; check for inconsistency and incongruence between voluntary effort and findings elicited through compensatory motor responses; the Hoover sign is commonly used while patients lie down or sit; asking the patient to lift the opposite leg often reveals involuntary movement in the affected leg, indicating the corticospinal tracts are intact and no structural lesion is present; patients with upper motor neuron lesions exhibit pronator drift (the hand pronates and fingers curl) because of the weakness of the supinator; similarly, a sudden drop of an arm in a patient who initially held it up suggests a nonorganic issue rather than true weakness; in cases of functional facial weakness or dystonia, platysma muscle contraction pulls the lip down, distinguishing it from organic facial weakness
Migraine: the aura in migraines can cause focal neurologic symptoms, but they typically involve positive phenomena (eg, color distortions, scintillations, fortification spectrum), unlike stroke, which shows negative phenomena (eg, loss of vision); their somatosensory symptoms evolve, spread, and migrate slowly over several minutes; this phenomenon is sometimes referred to as “Chiro,” meaning hand, oral, and aura, ie, symptoms spread from the fingertips up the arm, to the wrist and elbow, and are accompanied by oral symptoms at the same time, suggesting a migraine rather than a cerebrovascular issue; specifically, the absence of headache does not rule out migrainous etiology, as older patients may experience aura-like episodes without a subsequent headache
Focal seizure: after a focal seizure, patients often exhibit focal neurologic deficits in the same areas that are affected by the seizure, eg, twitching in the right hand can lead to paresis in that hand; seizures that start in language areas, typically in the left hemisphere, may result in aphasia as the cortex becomes overactive during the seizure and requires time to recover; if the symptoms persist, electroencephalography should be done to rule out ongoing nonconvulsive seizure activity that is causing protracted dysfunction; if it is still unclear, perform magnetic resonance imaging (MRI); rarely, a stroke can initially present as a seizure; in cases of first-time seizures followed by focal deficits, use MRI to ensure it is not a new stroke; patients with known epilepsy and repeated seizures may experience typical weakness after a seizure, which does not require further investigation and can be attributed to Todd paresis; space-occupying lesions, masses, neoplasms, and intracranial abscesses (rare) are typically thought to be slow-growing masses that lead to progressive neurologic dysfunction; brain masses rarely present acutely because seizures or edema reach a threshold that triggers dysfunction; CT can help with diagnosis in most cases, but some cases may require MRI for confirmation
Stroke Chameleons
Sudden coma: most patients presenting with sudden coma are considered acutely unresponsive because of drug overdose, metabolic derangements, or toxicity; if their level of consciousness is sufficiently depressed, they are often intubated quickly, leading to the discontinuation of most neurologic assessments; if such patients present acutely and are unclear about the onset of symptoms, suspect basilar occlusion; one notable exception to the typical presentation (normal awareness) of patients with stroke is when their ascending reticular activating system is compromised, often because of basilar occlusion; at bedside, such patients have signs of brainstem dysfunction, eg, skew deviation (vertical misalignment of the eyes) and ocular bobbing (rapid eye movement patterns), which are not seen with toxicity or metabolic causes; decerebrate posturing is likely caused by upper brain stem ischemia, not seizures; emergency physicians should assess the basilar artery by CT angiography, as brain CT during acute conditions may not reveal clots
Acute dizziness: identify whether it is a new problem, as opposed to long-standing dizziness; additional symptoms or neurologic signs unrelated to dizziness (eg, slurred speech, double vision, numbness, weakness) suggest a brainstem issue, and if it happened acutely, it is likely a stroke; non-neurologic symptoms accompanying the dizziness (eg, chest pain, shortness of breath, fever, tachycardia, hypotension) indicate a systemic issue rather than isolated dizziness; often, the dizziness may be secondary to the primary concern; isolated dizziness falls into 3 categories based on timing of symptoms and positional triggers; in many ways, dizziness acts like a chameleon or a mimic
Acute vestibular syndrome: patients present with acute dizziness with progressive symptoms but often improve over time; they may experience nausea, vomiting, nystagmus, struggle to stand, and may feel better without movement; if the dizziness persists and the patient shows nystagmus, a specific battery of tests named “HINTS+” helps to differentiate stroke from peripheral neuritis; if the patient does not have nystagmus and cannot stand or walk, it is likely a stroke; if the patient can walk, it is likely not a stroke
HINTS+: head impulse test — assesses the vestibulo-ocular reflex by having the patient focus on the clinician while their head is rapidly turned; eyes remaining fixed on the target indicate normal function; movement of the eyes with the head followed by a “catch-up saccade” back to the target suggests vestibulo-ocular dysfunction, specific to peripheral disorders; nystagmus — a sustained unidirectional type that intensifies toward the fast phase suggests a peripheral cause, while bidirectional nystagmus indicates a central cause; test of skew — eyes are misaligned on the vertical axis, almost always caused by a lesion in the brain stem; in subtle cases, an alternating cover test confirms the corrective eye movement in an uncovered eye when the clinician covers the eyes of a patient alternatively
Diagnostic criteria: unidirectional nystagmus, a normal head impulse test, no skew deviation, and lack of unilateral hearing loss suggest vestibular neuritis; if any criteria fail or nystagmus is absent, an MRI is necessary; presence of nystagmus and inability to stand indicates stroke; ability to stand does not rule out stroke; mild instability is not caused by stroke
Aphasia: patients, particularly those with receptive or fluent aphasia, may be misidentified as confused, encephalopathic, or psychotic because of their speech patterns; they are not characterized by a lack of verbal output but are often fluent or sometimes hyperfluent and deliver nonsensical speech filled with paraphasic errors that are semantic (meaning-related) or phonemic (sound-related); they are also often isolated; patients with nonfluent (Broca) aphasia exhibit facial droop and some hemiparesis, while those with fluent (Wernicke) aphasia do not display these signs because the Wernicke area is located further away from the motor cortex; level of consciousness is normal, whereas patients with delirium have elevated or diminished consciousness; test the patient’s understanding with simple or complex commands (eg, make a fist, show 2 fingers), as patients may rely on social cues rather than truly comprehending the instructions
Delirium: the right hemisphere correlates to left temporal and parietal dysfunction; patients present as agitated, disoriented, and confused, typically because of metabolic toxicities, but it can mimic right cerebral dysfunction (rare); bedside testing of neglect, extinction, visual field difficulties on the left hemisphere, or checking for subtle signs of right brain dysfunction can help differentiate; the abrupt onset of symptoms suggests an acute ischemic cause rather than a metabolic issue
Mononeuropathies: often mimic acute strokes where patients may present with sudden onset, lack of pain, and no preceding trauma; rule out cerebrovascular etiology; isolated hand or arm weakness may indicate a small middle cerebral artery stroke, while isolated legs, particularly the distal leg, suggest anterior cerebral artery involvement; the most common mimic is radial nerve palsy, sometimes “Saturday night palsy” where a patient wakes up with wrist drop after resting their arm in an uncomfortable position; another mimic is toilet bowl neuropathy, where patients with sciatic nerve pain fall asleep on the toilet and experience foot drop upon standing
Hypertensive urgency: focal neurologic signs, eg, unilateral weakness or numbness, or speech impairment with high BP, indicates a stroke rather than hypertensive urgency; patients with hypertensive urgency (posterior reversible encephalopathy syndrome) exhibit headache, seizures, encephalopathy, and often visual signs and symptoms (sometimes blindness and visual association issues) because there is disproportionate posterior edema; if there is any confusion, an MRI can confirm the condition
Visual disturbances: sudden, nontraumatic, painless, unilateral vision loss implies a central retinal artery occlusion; ensure that there is no blood behind the eye before thrombolysis, as it is done in cerebral infarction cases; some individuals exhibit hemianopia, but the patient may be unaware they have lost vision in one field bilaterally; visual field tests are often required to detect this; homonymous visual field deficits suggest stroke
Transient ischemic attacks (TIA): minor strokes that require emergency treatment; patients with transient focal brain ischemia have ≤20% increased risk for stroke ≤3 mo, with half the risk within the first few days; patients with TIA are at higher risk for complete infarction than patients with unstable angina; patients with symptoms in the first few days should go to the emergency department for confirmation and to plan a secondary prevention strategy; the ABCD2 score helps evaluate risk based on age, diabetes mellitus history, BP, clinical features, and symptom duration; score ≥4 indicates the need for admission for expedited workup
Ansari FH, Juergens AL. Compressive radial mononeuropathy. StatPearls Publishing. 2023 Apr 24. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557520/; H Buck B, Akhtar N, Alrohimi A, et al. Stroke mimics: incidence, aetiology, clinical features and treatment. Ann Med. 2021;53(1):420-436. doi:10.1080/07853890.2021.1890205; Huff JS, Tadi P. Coma. StatPearls Publishing; 2023 Jul 3. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430722/; Lu WZ, Lin HA, Hou SK, et al. ABCD2-I Score Predicts Unplanned Emergency Department Revisits within 72 Hours Due to Recurrent Acute Ischemic Stroke. Diagnostics. 2024; 14(11):1118. https://doi.org/10.3390/diagnostics14111118; Shankar Kikkeri N, Nagalli S. Migraine with aura. StatPearls Publishing. 2024 Feb 29. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554611/; Tarnutzer AA, Berkowitz AL, Robinson KA, et al. Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ. 2011;183(9):E571-E592. doi:10.1503/cmaj.100174.
For this program, members of the faculty and planning committee reported nothing relevant to disclose.
Dr. Switzer was recorded at Seizures, Spells and Shakes: Neurology for the Non-Neurologist, held July 11-13, 2024, on Kiawah Island, SC, and presented by Medical College of Georgia, Augusta University. For information about upcoming CME activities from this presenter, please visit https://mcg.cloud-cme.com. Audio Digest thanks speakers and presenters for their cooperation in the production of this program.
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