Differentials

Stroke

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Sudden-onset, focal neurologic deficit that cannot be explained by another condition such as hypoglycemia.[43] An ischemic brain lesion on brain imaging, even if a patient's episode of focal neurologic dysfunction rapidly resolves, signifies an ischemic stroke.[3]

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Clinical diagnosis: CT may be normal, or may show signs of infarction or hemorrhage.

Hypoglycemia

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Most commonly seen in a patient who takes hypoglycemic medications.

Can cause syncope, generalized weakness, or confusion, but also reported to cause focal deficits, especially if old cerebral insults are present.

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Blood glucose <60 mg/dL.

Seizure with post-seizure (Todd's) paralysis

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One of the most frequent mimics of cerebral ischemia.

Patients will frequently have pre-existing epilepsy.[50]

Witnesses will report positive motor symptoms (such as tonic-clonic activity) prior to onset of weakness.

Symptoms may have "Jacksonian march" across the affected area.

Incontinence, tongue biting, and post-event altered mental status suggest seizure rather than TIA.

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The distinction is frequently made based on the clinical history.[50]

Electroencephalogram can be done to evaluate for seizures or for postictal slowing.

Elevated prolactin level has a secondary role to suggest seizure. However, prolactin testing is associated with low diagnostic sensitivity.[72]

Complex migraine

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Usually occurs in patients with prior history of migraine headaches.[50]

Aura or scotomata may precede onset of weakness.[50]

Presence of headache and nausea along with neurologic symptoms suggest complex migraine.[50]

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Clinical diagnosis: no differentiating tests.

Space-occupying lesion (intracranial hemorrhage, abscess, or mass)

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Preceding trauma or anticoagulation predisposes to hemorrhage.

Fever or leukocytosis would suggest central nervous system (CNS) infection rather than ischemia.

Headache and vomiting may occur with increased intracranial pressure.

May have a relatively gradual onset compared with ischemic neurologic deficits.

Rapid complete resolution of symptoms would be atypical of an irreversible structural lesion.

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Noncontrast head CT rules out presence of acute hemorrhage.

CT with contrast or MRI can be done if continued suspicion for CNS abscess or mass.

Elevated WBC count in an infection.

Functional neurologic and somatic symptom disorders

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Deficits may not fit a single vascular territory.

Physical exam may demonstrate inconsistencies such as demonstrating "breakpoint" weakness.

Some patients will have had adverse live events, but these are neither necessary nor sufficient for the diagnosis.[73] Psychological comorbidities - especially anxiety, panic, and depression - are common, affecting over 50% of patients.[74]

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Clinical diagnosis: no differentiating tests.

Labyrinthine disorders

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Benign positional vertigo may be mistaken for posterior circulation infarct.

Hearing loss and tinnitus suggest Meniere disease.

Labyrinthitis can cause vertigo and disequilibrium but motor function and other cranial nerves should be normal.

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Clinical diagnosis: no differentiating tests.

Multiple sclerosis (MS)

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New MS lesions or a pseudoexacerbation might be mistaken for TIA, but MS will tend to cause reversible neurologic deficits lasting longer than those of TIA.

History of symptoms (vision loss, in particular) suggestive of MS is very helpful.

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MRI can reveal MS plaques.

Lumbar puncture in MS may demonstrate slightly elevated cerebrospinal fluid (CSF) cell count but never above 50/microliter; glucose and protein should be normal; oligoclonal bands and elevated CSF IgG and IgG synthesis rates are present in 80% of MS cases.

Peripheral neuropathy

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Bell palsy may be mistaken for ischemic insult. Unlike central ischemia, Bell palsy does not spare the forehead.

Visualizing the tympanic membrane and surrounding skin can be helpful to rule out a similar condition, Ramsay Hunt syndrome, which is a herpes infection of the geniculate ganglion. Vesicles are present in the canal or as the canal meets the pinna.

Peripheral neuropathies with the exception of transient compression neuropathy tend to last longer than 24 hours.

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For peripheral neuropathy with transient symptoms, no testing is generally needed.

Global hypoperfusion/syncope

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Syncope caused by basilar TIA is almost always associated with focal neurologic signs/symptoms in addition to the syncope itself.

Systemic illness is suspected based on fever, tachycardia, or hypotension.

Systemic illness, especially with hypotension, may mimic TIA by causing preexisting central nervous system injuries such as multiple sclerosis plaques or old strokes to have more pronounced symptoms.

BP may be low, or orthostatic vital signs may be positive, in the patient with hypotension as cause of syncope/weakness.

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If underlying infection, may have an elevated WBC count.

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