MKSAP: 49-year-old-man with right arm weakness

A 49-year-old man shows up with new right arm weakness. In MKSAP-land, that’s not a “huh, interesting” moment
it’s a “drop everything and localize” moment. Because right arm weakness can be anything from a pinched nerve to a
time-sensitive stroke, the trick is sorting “needs an ambulance now” from “needs a thoughtful workup soon” without
getting distracted by red herrings (which, sadly, do not show up on MRI).

This article walks through an MKSAP-style approach: triage first, then localization, then targeted testingplus the
common mimics that love to cosplay as stroke. It’s educational content, not personal medical advice. If someone has
sudden weaknessespecially with facial droop, speech trouble, severe headache, or confusiontreat it as an emergency
and call 911.

Why MKSAP loves this scenario

The “49-year-old with right arm weakness” vignette is classic because it tests the skills internal medicine actually uses:
(1) recognize time-critical neurologic deficits, (2) localize the lesion, and (3) choose the next best step that changes
management. It’s less “name the zebra” and more “don’t miss the stampede.”

Step 1: Assume stroke until proven otherwise (at least at the beginning)

Sudden focal weakness is stroke until proven otherwise, even in a relatively young patient. Yes, 49 is not “young-young,”
but it’s young enough that clinicians sometimes hesitate. Don’t. Stroke can happen at any age, and minutes matter.

Quick triage checklist

• Time last known well: When was the patient definitively normal?
• Symptom pattern: Sudden onset (seconds to minutes) vs. gradual progression (hours to weeks).
• Associated neurologic signs: face droop, speech difficulty, vision loss, gait issues, neglect.
• Immediate bedside test: check glucose (hypoglycemia can mimic stroke).

The point isn’t to declare “stroke!” dramatically. The point is to trigger a pathway that rapidly rules out hemorrhage,
evaluates for ischemia, and considers reperfusion therapies when appropriate.

Step 2: Localize the problemcentral vs peripheral

“Right arm weakness” is not a diagnosis. It’s a GPS coordinate. Your job is to figure out whether the problem is in the
brain/spinal cord (central nervous system) or in the nerve roots/plexus/peripheral nerves/muscle (peripheral nervous system).

Clues for a central cause (brain or spinal cord)

• Upper motor neuron signs: increased reflexes, spasticity, clonus, Babinski sign (upgoing toe).
• Pattern: weakness that doesn’t match a single nerve or root distribution.
• Cortical “extras”: aphasia (if dominant hemisphere), neglect (if non-dominant), visual field cuts.
• Face involvement: weakness of the lower face can point to a central lesion.
• Sudden onset: vascular events love surprise entrances.

Clues for a peripheral cause (root, plexus, nerve, muscle)

• Pain first, weakness second: radiculopathy or brachial neuritis can start with pain.
• Sensory distribution: numbness/tingling in a dermatomal or nerve territory.
• Lower motor neuron signs: decreased reflexes, atrophy, fasciculations, hypotonia.
• Highly focal deficits: wrist drop (radial nerve), thumb opposition weakness (median nerve), etc.

Translation: if the weakness respects neuroanatomy like it studied for boards, you can narrow the differential quickly.
If it doesn’t, you still canjust with more careful exam and fewer assumptions.

Step 3: A focused history that changes management

History is where you win time and avoid unnecessary tests. The goal is not “every symptom since kindergarten,” but
the details that separate stroke, mimic, and peripheral causes.

High-yield history questions

• Exact onset: sudden vs. gradual; woke up with symptoms; stepwise progression.
• Speech/vision symptoms: slurred speech, word-finding difficulty, double vision, field loss.
• Headache and neck pain: severe sudden headache (hemorrhage); neck pain after trauma (dissection).
• Recent seizure-like activity: confusion, tongue biting, incontinence, witnessed convulsions.
• Neck/shoulder pain: radiating pain suggests radiculopathy; severe shoulder pain suggests brachial neuritis.
• Vascular risk factors: hypertension, diabetes, smoking, hyperlipidemia, atrial fibrillation.
• Medication and toxins: sedatives, new meds, illicit substances; anticoagulants (bleed risk).
• Functional context: recent stressors don’t “cause” neurologic disease, but they can coexist with functional symptoms.

One particularly MKSAP-ish detail is the “last known well” time. It’s the key that unlocks (or closes) certain acute treatments.
If the onset was unclear, ask who last saw the patient normaland when.

Step 4: The exammake your reflex hammer earn its keep

In unilateral arm weakness, the neurologic exam is your fastest localization tool. The classic moves aren’t glamorous, but
they’re effectivelike a reliable old stethoscope that’s been through three hospital mergers.

Core exam elements

• Motor testing: shoulder abduction, elbow flex/extend, wrist extension, finger abduction, grip.
• Pronator drift: subtle corticospinal weakness can show up here.
• Reflexes: biceps, brachioradialis, triceps; compare sides.
• Sensation: pinprick/light touch in dermatomal and peripheral nerve patterns.
• Cranial nerves and speech: facial asymmetry, dysarthria, aphasia.
• Coordination: finger-to-nose; cerebellar signs can masquerade as “weakness.”
• Gait (if safe): central processes often affect more than one “system.”

Upper motor neuron signs (like hyperreflexia or Babinski) push you toward brain/spinal cord. Lower motor neuron signs
(like diminished reflexes and atrophy) push you toward root/plexus/nerve. The pattern matters as much as the power grade.

Step 5: The differential diagnosiswhat’s most likely and most dangerous?

1) Ischemic stroke or transient ischemic attack (TIA)

Sudden unilateral arm weakness is a classic ischemic stroke symptom. If symptoms resolve quickly, think TIAbut still treat it
as a medical emergency, because it can be a warning shot for a larger stroke. Depending on the vascular territory, weakness may
be isolated (for example, small cortical or subcortical strokes) or accompanied by face/speech findings.

2) Intracerebral hemorrhage

Hemorrhagic stroke can also cause focal weakness, often with headache, vomiting, decreased level of consciousness, or very
high blood pressure. You can’t reliably distinguish ischemic vs hemorrhagic stroke by symptoms alonehence the urgent imaging.

3) Seizure with postictal (Todd) paresis

Todd paresis is temporary weakness after a seizure and can be strikingly focalsometimes a single limb. The history may reveal
convulsions or a period of confusion. This is a common stroke mimic. It still requires careful evaluation because seizures and
strokes can overlap (a stroke can provoke a seizure).

4) Cervical radiculopathy

Cervical radiculopathy (“pinched nerve”) can produce arm pain, numbness, and weakness in a dermatomal/myotomal pattern.
It tends to be associated with neck pain and symptoms that radiate down the arm, sometimes worsened by neck movement.
Reflex changes can help localize the affected root.

5) Brachial plexopathy (including Parsonage-Turner syndrome)

Brachial plexus conditions can cause weakness and sensory changes that don’t fit one root or nerve. Parsonage-Turner syndrome
(brachial neuritis) is a classic “pain first, weakness later” storyoften severe shoulder/upper arm pain followed by weakness.
It’s frequently misdiagnosed as radiculopathy.

6) Peripheral nerve palsies (radial, median, ulnar)

These usually produce very focal deficits: wrist drop (radial), “OK sign” weakness or thumb opposition issues (median),
finger abduction weakness (ulnar). Sensory changes often follow a nerve distribution. Compression injuries and repetitive
strain are common culprits.

7) Metabolic and systemic causes

Hypoglycemia is the headline mimic because it’s common, dangerous, and reversiblecheck glucose early. Electrolyte problems,
infections, and medication effects can contribute to generalized weakness, but truly isolated unilateral weakness is more often
neurologic.

8) Functional neurologic disorder (FND)

Functional weakness is real to the patient and can look dramatic, but it doesn’t follow typical neuroanatomy. Certain bedside
signs (used carefully and respectfully) may suggest functional weakness. Importantly, FND is a diagnosis made after appropriate
evaluationnot a shortcut when you’re tired.

Step 6: Testingwhat comes first and why

In MKSAP logic, the “next best step” depends on acuity and suspicion for stroke. For acute focal weakness, the early tests
are designed to rapidly identify conditions with immediate treatments.

Immediate and early tests (often in the ED)

• Point-of-care glucose: fast stroke mimic check.
• Non-contrast head CT: quickly evaluates for hemorrhage and major structural lesions.
• CT angiography (CTA) or MR angiography (MRA): evaluates for large vessel occlusion and vascular pathology in appropriate cases.
• ECG and cardiac monitoring: looks for atrial fibrillation and other arrhythmias.
• Basic labs: CBC, electrolytes, coagulation studiesespecially if reperfusion therapy is considered.

Follow-up tests based on localization

• MRI brain (diffusion-weighted imaging): sensitive for acute ischemia, helpful when CT is unrevealing but suspicion remains high.
• Carotid imaging: evaluates stenosis/dissection when clinically relevant.
• Cervical spine MRI: considered when myelopathy or radicular symptoms dominate.
• EMG/NCS: helps characterize peripheral nerve/plexus disorders (usually not the first-hour test).

The main exam-and-test principle: don’t order “everything.” Order what answers the life-or-function-threatening questions first,
then refine.

Step 7: Managementwhat happens once you suspect stroke?

If stroke is on the table, management becomes protocol-driven (and blessedly less philosophical). The overarching goals:
stabilize, image, determine eligibility for reperfusion therapy, and prevent complications.

Reperfusion therapy (high-level overview)

• IV thrombolysis: For selected patients with acute ischemic stroke within a limited time window from symptom onset,
  after appropriate screening and imaging.
• Mechanical thrombectomy: For selected patients with large vessel occlusion, sometimes within extended windows when imaging
  supports salvageable brain tissue.

If symptoms are due to TIA or minor stroke, clinicians often pivot quickly to secondary prevention: antiplatelet therapy when appropriate,
risk factor control (blood pressure, lipids, diabetes), smoking cessation, and evaluation for cardioembolic sources such as atrial fibrillation.

Board-style pearls (a.k.a. how to keep your future self from yelling at you)

• Sudden focal weakness = emergency evaluation. Don’t “watch it overnight” at home.
• Localize before you memorize. Neuroanatomy beats random test ordering every time.
• UMN vs LMN signs matter. Reflexes and tone are not decorative features.
• Check glucose early. It’s the fastest “fix it now” mimic to rule out.
• Seizure can mimic stroke. Postictal weakness existsand it can be very convincing.
• Pain patterns are clues. Neck/arm pain suggests radiculopathy; severe shoulder pain then weakness suggests brachial neuritis.

Conclusion

A 49-year-old man with right arm weakness is exactly the kind of case that rewards calm urgency: treat acute focal deficits like stroke
until proven otherwise, localize central vs peripheral, and order tests that change immediate decisions. The “right answer” in an MKSAP-style
approach is rarely a fancy diagnosisit’s usually the correct next step that protects brain function, prevents complications, or both.

And if you remember only one thing: sudden weakness is not a “wait and see” symptom. Brains are not fans of delays. They don’t send polite reminder emails.

Experiences related to “49-year-old man with right arm weakness” (about )

In real clinical settings, the experience of right arm weakness often begins with confusion rather than certainty. Many patients describe a moment that feels
strangely ordinary: a coffee mug slips, a shirt button suddenly becomes “impossible,” or the hand won’t do what it has done flawlessly for decades. Because
the symptom can be painless, people sometimes bargain with it“Maybe I slept on it wrong,” or “It’ll pass after lunch.” That hesitation is one reason public
health messaging leans so hard on simple recognition tools like FAST: when your brain is improvising excuses, a memorized checklist can cut through the fog.

In emergency departments, clinicians often experience a different kind of uncertainty: not whether the symptom is serious, but what it represents. Stroke
teams are trained to move fast, yet they also know that stroke mimics are common. It’s a balancing actactivate the pathway aggressively enough to avoid
missing treatable stroke, while staying careful enough not to overlook alternatives like hypoglycemia, seizure, or a peripheral nerve problem. The practical
reality is that “over-triage” is sometimes the safer choice, because the cost of delay can be permanent disability.

Patients who ultimately learn the cause was a peripheral issuelike cervical radiculopathyoften report a different emotional arc. There’s relief that it
wasn’t a stroke, followed quickly by frustration: pain that radiates, weakness that interferes with work, sleep, and hobbies, and a recovery timeline that
isn’t instant. People are often surprised by how much daily life depends on subtle arm function: typing, driving, cooking, carrying a child, or even holding
a phone without discomfort. When the diagnosis is brachial neuritis (Parsonage-Turner), the “pain-then-weakness” pattern can be particularly unsettling,
because it feels like the body changed its rules overnight.

For those with stroke or TIA, the experience is frequently described as two overlapping events: the acute medical emergency and the longer recovery journey.
Even mild weakness can trigger a major identity shake-upespecially for someone in their 40s who didn’t expect a “stroke conversation” until much later in
life. Rehabilitation is often framed as regaining strength, but many patients also work on coordination, endurance, and confidence. Occupational therapy can
feel like “learning your own arm again,” practicing real-life tasks (grip, reach, fine motor control) instead of just lifting weights. Small milestonesopening
a jar, writing legibly, returning to a hobbybecome meaningful in a way that outsiders may not fully appreciate.

Clinicians, meanwhile, often emphasize a lesson that fits both stroke and its mimics: symptoms are information, not moral judgments. A stroke doesn’t mean
someone “failed” at health. A functional neurologic diagnosis doesn’t mean someone is “faking.” And a pinched nerve doesn’t mean someone is “overreacting.”
The shared goal is clarity, safety, and functiongetting the right workup, the right treatment, and the right follow-up so that a single symptom doesn’t
quietly become a lifelong limitation.