Myasthenic Crisis / Exacerbation

fatigable weakness · respiratory/bulbar failure · watch FVC · IVIG or PLEX · find the trigger · Super Compact

• Sx: worsening fatigable, fluctuating weakness — ptosis, diplopia, dysarthria, dysphagia, nasal speech, neck/proximal limb weakness; crisis = respiratory muscle weakness needing (or nearing) ventilation or severe bulbar weakness with aspiration; worse with activity/end of day, better with rest

• Neg: denies areflexia + ascending pattern (GBS) · denies fixed non-fatigable deficit (stroke) · denies pinpoint/dilated pupils + descending (botulism) · denies sensory loss (MG is pure motor) · denies muscarinic excess/miosis (cholinergic crisis)

• SHx: known MG + a trigger: infection (most common), surgery, pregnancy, tapering immunosuppression, or a new drug — aminoglycosides, fluoroquinolones, macrolides, beta-blockers, magnesium, neuromuscular blockers, iodinated contrast

• Etiology: autoantibodies (anti-AChR most common; anti-MuSK) block neuromuscular junction transmission; crisis = decompensation from trigger or undertreatment; thymoma/thymic hyperplasia association

• RF: modifiable — offending drugs, infection, undertreatment, fast steroid taper · non-mod — known MG, thymoma, MuSK antibody (more bulbar/crisis-prone)

• Data: serial FVC + NIF/MIP (key test — respiratory monitoring) · ABG (late) · anti-AChR/anti-MuSK Ab (if new dx) · infection workup (CXR, cultures, UA) · TFTs, CT chest (thymoma) · bedside swallow/single-breath count

• DDx: GBS (areflexia, sensory, ascending) · cholinergic crisis (overtreatment — SLUDGE, fasciculations, miosis) · Lambert-Eaton (improves with use, ↓reflexes, SCLC) · botulism (descending, pupils) · brainstem stroke (fixed) · thyroid eye disease

• Home Meds: continue/adjust pyridostigmine (may hold if secretions/intubated) · stop offending drugs · continue immunosuppression · avoid new triggering agents

Plan — ICU or step-down (crisis is ICU)

• Consults: neurology · ICU/pulmonary (airway) · ID if infection · thoracic surgery if thymoma

• Monitor FVC + NIF q2–4h. Intubate for FVC <15–20 mL/kg, NIF less negative than −25 to −30, or bulbar failure/aspiration — pre-emptively, before hypoxia/hypercapnia (late signs)

• Disease-modifying: IVIG 0.4 g/kg/day ×5 days OR plasma exchange (PLEX) — both rapid; PLEX may work faster in severe/bulbar crisis; do not combine

• Find & treat the trigger — culture/treat infection, review and stop offending drugs, address surgery/pregnancy/steroid taper

• Continue immunosuppression; start/continue corticosteroids — watch for transient steroid-induced worsening in first 1–2 weeks (begin under cover of IVIG/PLEX in crisis)

• Pyridostigmine (Mestinon): symptom relief only; often held while intubated (secretions); avoid overtreatment (cholinergic crisis)

• If intubated: avoid depolarizing/non-depolarizing blockers where possible (unpredictable response)

• Trend: FVC/NIF, bulbar function, strength, swallow, response to therapy

• → ICU if: FVC/NIF approaching thresholds, bulbar weakness with aspiration, rapid progression, or any respiratory distress — myasthenic crisis IS an ICU diagnosis

Myasthenic Crisis / Exacerbation

complete reference · fatigable weakness · FVC monitoring · IVIG/PLEX · trigger hunt · drug avoidance · Full Card

Symptoms / Associated Sx

• Fatigable, fluctuating weakness worsening with sustained activity and through the day, improving with rest — ocular (ptosis, diplopia), bulbar (dysarthria, dysphagia, nasal/"wet" voice, weak cough, jaw fatigue), neck, and proximal limb. Myasthenic crisis is the life-threatening extreme: respiratory muscle weakness requiring (or about to require) ventilation, and/or severe bulbar weakness causing aspiration. Sensation, reflexes, and pupils are normal — MG is a pure motor disorder of the neuromuscular junction.

Neg

• Reflexes preserved, no ascending pattern or sensory loss — argues against Guillain-Barré (GBS: areflexia, ascending weakness, albuminocytologic dissociation)

• Weakness fatigable and fluctuating, not fixed — argues against brainstem stroke (stroke gives fixed deficit, often crossed/long-tract signs)

• Pupils normal, no descending paralysis with autonomic features — argues against botulism (botulism: dilated/fixed pupils, descending)

• Strength worsens (not improves) with repeated effort, reflexes normal — argues against Lambert-Eaton (LEMS facilitates with use, ↓reflexes, SCLC association)

• No muscarinic excess (miosis, salivation, diarrhea, fasciculations) — argues against cholinergic crisis from pyridostigmine overdose (the key bedside fork in a weak treated MG patient)

Social History (SHx)

• Known MG, current pyridostigmine/immunosuppressive regimen and recent changes (taper), prior crises, thymectomy/thymoma history.

• Identify the precipitant: infection (most common), recent surgery, pregnancy/postpartum, physical/emotional stress, tapering of immunosuppression, and especially a newly started medication known to unmask or worsen MG.

Main Etiology

• Autoantibodies against the postsynaptic acetylcholine receptor (anti-AChR, most common) or muscle-specific kinase (anti-MuSK, more bulbar/respiratory and crisis-prone) impair neuromuscular junction transmission. Crisis = acute decompensation, typically from a trigger (infection, drug, surgery, pregnancy) or inadequate/withdrawn therapy. Strong association with thymic pathology (thymoma, hyperplasia).

RF

• Modifiable: offending medications, untreated infection, undertreatment or abrupt immunosuppression taper, perioperative stress.

• Non-modifiable: established MG (especially anti-MuSK), thymoma, prior crisis.

Data

• Serial FVC and NIF/MIP (decisive monitoring — track respiratory muscle strength, intubate pre-emptively; do not rely on oximetry)

• ABG (hypercapnia/hypoxia are LATE — a normal ABG does not reassure); bedside single-breath count and swallow assessment

• Anti-AChR and anti-MuSK antibodies (if new diagnosis); repetitive nerve stimulation/single-fiber EMG in unclear cases (decremental response)

• Trigger workup: CXR, blood/urine cultures, UA, viral studies (infection is leading precipitant); TSH; medication review

• CT chest (thymoma — relevant to thymectomy)

DDx

Guillain-Barré (areflexia, sensory, ascending) · cholinergic crisis (pyridostigmine excess — miosis, SLUDGE, fasciculations) · Lambert-Eaton (facilitation with use, ↓reflexes, SCLC) · botulism (descending, dilated pupils, autonomic) · brainstem stroke (fixed, crossed signs) · thyroid eye disease / thyrotoxic myopathy · organophosphate poisoning

Home Meds

• Stop drugs that worsen MG — aminoglycosides, fluoroquinolones, macrolides, beta-blockers, magnesium (IV and Mg-containing products), neuromuscular blockers, procainamide, iodinated contrast, immune checkpoint inhibitors.

• Continue immunosuppression (steroids, steroid-sparing agents); manage pyridostigmine carefully (hold if copious secretions or intubated; avoid overdosing).

Plan

Consults

• Neurology — confirm crisis vs cholinergic crisis, direct immunotherapy and chronic regimen.

• ICU / pulmonary — respiratory monitoring and airway management (crisis is ICU-level).

• Infectious disease — if a precipitating infection is identified.

• Thoracic surgery — for thymoma (thymectomy, after stabilization).

Respiratory monitoring (priority)

• Serial FVC and NIF every 2–4 hours. Intubate for FVC <15–20 mL/kg, NIF less negative than ~−25 to −30 cmH₂O, a falling trend, or bulbar failure with aspiration/inability to handle secretions. Intubate pre-emptively — hypoxia/hypercapnia are late. BiPAP can bridge selected early/cooperative patients without significant bulbar weakness, but keep a low threshold to intubate.

Disease-modifying therapy

• IVIG 0.4 g/kg/day for 5 days OR plasma exchange (PLEX) — both act within days; PLEX may improve severe bulbar/respiratory crisis faster, IVIG is easier and avoids central access. Do not combine. Start promptly.

Treat the trigger / immunosuppression

• Aggressively identify and treat the precipitant (especially infection); remove offending drugs. Continue or initiate corticosteroids for long-term control — but beware transient steroid-induced worsening in the first 1–2 weeks, so in crisis begin/escalate steroids under IVIG/PLEX cover with respiratory monitoring. Continue steroid-sparing agents (azathioprine/Imuran, mycophenolate/CellCept) per neurology.

Acetylcholinesterase inhibitor

• Pyridostigmine (Mestinon) gives symptomatic benefit but does not treat the crisis; frequently held during intubation (reduces airway secretions) and resumed in recovery. Avoid overdosing — cholinergic crisis mimics worsening weakness.

Always

• PT / OT / SLP eval and treat — swallow assessment before oral intake; graded reconditioning; aspiration precautions.

• Trend: FVC/NIF (key vital sign), bulbar function and secretions, limb strength, response to IVIG/PLEX, resolution of trigger.

• Escalation triggers: declining FVC/NIF or bulbar failure → intubation, ICU · aspiration → airway protection · inadequate response to first immunotherapy → switch IVIG↔PLEX, escalate immunosuppression · cholinergic features → hold pyridostigmine.

• Discharge checklist: optimized chronic immunosuppression with taper/maintenance plan · pyridostigmine dosing reviewed · written list of drugs to avoid given to patient · trigger addressed (infection treated, offending drug removed) · thymectomy planning if thymoma · neurology follow-up · MedicAlert and crisis-action education · return precautions (breathing/swallowing difficulty, rapidly worsening weakness → 911).

Red Flags — ICU

• Falling FVC/NIF (FVC <15–20 mL/kg, NIF > −25 to −30) → intubate pre-emptively; don't wait for hypoxia.
• Bulbar failure / aspiration (weak cough, pooling secretions, wet voice) → airway protection, ICU.
• Rapid progression of weakness → ICU monitoring.
• Cholinergic crisis (miosis, salivation, diarrhea, fasciculations from pyridostigmine excess) → hold the drug — it also causes weakness.
• New MG-worsening drug given (aminoglycoside, magnesium, fluoroquinolone) → stop immediately.

Senior IM Resident Pearls

• Watch the FVC, not the SpO₂. Like GBS, respiratory failure is neuromuscular — FVC and NIF fall well before oxygen drops. Trend them every few hours and intubate electively.
• A crisis is an ICU diagnosis. Respiratory or bulbar failure means continuous monitoring and a low threshold to secure the airway.
• Always hunt the trigger. Crisis rarely happens spontaneously — infection (most common), a new drug, surgery, pregnancy, or a steroid taper is usually behind it.
• Know the drug list cold. Aminoglycosides, fluoroquinolones, macrolides, beta-blockers, IV magnesium, neuromuscular blockers — magnesium for "eclampsia" or "repletion" is a classic iatrogenic crisis.
• IVIG or PLEX — not pyridostigmine — treats the crisis. The anticholinesterase relieves symptoms but doesn't fix decompensation, and it's often held while intubated to cut secretions.
• Steroids can transiently worsen MG. Starting/escalating high-dose steroids in crisis can deepen weakness for 1–2 weeks — do it under IVIG/PLEX cover with respiratory monitoring.
• Distinguish myasthenic from cholinergic crisis — look for muscarinic excess (miosis, SLUDGE, fasciculations) pointing to pyridostigmine overdose.
• Common mistake: giving magnesium or an aminoglycoside to a known myasthenic, or reassuring on a normal ABG while the FVC quietly falls.

Neurology — Neuromuscular

Acute Neuropathy Workup

pattern first · localize · rule out GBS/cord · find treatable causes · Super Compact

• Sx: weakness, numbness, paresthesias, or pain — characterize tempo (acute <4 wk vs subacute), pattern (symmetric length-dependent "stocking-glove" polyneuropathy vs asymmetric mononeuritis multiplex vs single nerve/root), motor vs sensory vs autonomic; areflexia suggests peripheral

• Neg: denies UMN signs/sensory level/sphincter loss (cord lesion — image) · denies fatigability/diurnal pattern (NMJ/MG) · denies proximal symmetric weakness w/o sensory (myopathy) · denies acute ascending areflexic (GBS — its own pathway) · denies cortical/aphasia signs (CNS)

• SHx: diabetes, alcohol, nutritional (B12, B1, B6 excess/deficiency, copper), toxins/heavy metals, chemo/drugs (vincristine, metronidazole, isoniazid, amiodarone), HIV, autoimmune, family history

• Etiology by pattern: symmetric — diabetic, alcoholic, nutritional, toxic, drug, CKD, paraproteinemia · asymmetric/mononeuritis multiplex — vasculitis, diabetes, sarcoid, infection (Lyme, HIV), cryoglobulinemia · acute demyelinating — GBS

• RF: modifiable — glycemic control, alcohol, neurotoxic drugs, B12/nutrition · non-mod — hereditary (CMT), age, autoimmune disease

• Data: glucose/A1c, B12 + MMA, TSH, CBC/CMP, ESR/CRP · SPEP/UPEP + free light chains (paraprotein) · HIV, Lyme, ANA/ANCA (vasculitis) · heavy metals if exposure · NCS/EMG (axonal vs demyelinating, localize) · MRI if cord/root suspected · LP if demyelinating/inflammatory

• DDx: GBS (acute, areflexic, monitor FVC) · cord compression/myelopathy (UMN, level) · radiculopathy (dermatomal) · MG (fatigable) · myopathy (proximal, CK) · functional

• Home Meds: review and stop neurotoxic drugs where feasible; correct deficiencies; optimize glycemic control

Plan — ward / often outpatient workup

• Consults: neurology (EMG, classification) · rheumatology if vasculitis · heme if paraprotein · ID if infectious

• First: exclude the emergencies — if acute, ascending, and areflexic, treat as GBS (FVC/NIF monitoring); if UMN signs or a sensory level, image the cord urgently

• Localize and characterize with exam + NCS/EMG: axonal vs demyelinating, length-dependent vs multifocal, motor vs sensory

• Targeted labs for treatable causes (glucose/A1c, B12/MMA, TSH, SPEP/free light chains, HIV, vasculitis serologies, heavy metals by history)

• Treat the cause: glycemic optimization, B12 repletion, stop offending drug/toxin, immunotherapy for vasculitic/inflammatory neuropathy (steroids ± agents, per specialty)

• Symptomatic: neuropathic pain — gabapentin (Neurontin) 300 mg TID titrate, pregabalin (Lyrica) 75 mg BID, or duloxetine (Cymbalta) 30–60 mg daily; foot care, fall precautions

• PT/OT for safety, bracing (foot drop), gait

• Trend: exam, strength, and — if any respiratory/ascending concern — FVC/NIF

• → ICU/urgent if: acute ascending weakness with falling FVC/NIF (GBS), autonomic instability, or a cord syndrome needing emergent decompression

Acute Neuropathy Workup

complete reference · localize by pattern · exclude GBS & cord · treatable causes · EMG-guided · Full Card

Symptoms / Associated Sx

• Numbness, paresthesias, neuropathic pain, and/or weakness. The whole workup hinges on three questions: tempo (hyperacute/acute <4 weeks vs subacute/chronic), pattern (symmetric distal "stocking-glove" polyneuropathy; asymmetric/stepwise mononeuritis multiplex; single nerve mononeuropathy; or dermatomal radiculopathy), and fiber type (motor, sensory, small-fiber/autonomic, or mixed). Peripheral lesions give lower-motor-neuron signs — hyporeflexia/areflexia, atrophy, fasciculations, distal sensory loss. Autonomic features (orthostasis, GI dysmotility) suggest small-fiber/autonomic involvement.

Neg

• No upper-motor-neuron signs, sensory level, or sphincter dysfunction — argues against a spinal cord lesion (a sensory level/UMN pattern mandates urgent cord MRI — the can't-miss surgical mimic)

• No fatigability or diurnal fluctuation and reflexes are reduced — argues against a neuromuscular-junction disorder (MG fatigues and spares reflexes/sensation)

• Sensory symptoms present and weakness is distal — argues against a pure myopathy (myopathy is proximal, symmetric, no sensory loss, elevated CK)

• Not acute, ascending, and areflexic — distinguishes from GBS (if it IS, divert to the GBS pathway with respiratory monitoring)

• No cortical signs, aphasia, or hemibody pattern — argues against a central process.

Social History (SHx)

• Diabetes and glycemic control (the most common cause); alcohol use; nutrition (B12, thiamine, folate, copper deficiency; B6 toxicity); occupational/environmental toxin and heavy-metal exposure (lead, arsenic, thallium).

• Neurotoxic drugs (vincristine, platinum agents, taxanes, metronidazole, isoniazid, amiodarone, nitrofurantoin, linezolid); HIV/infectious risk; autoimmune disease; family history (hereditary neuropathies — high arches, hammertoes, longstanding).

Main Etiology

• Symmetric length-dependent polyneuropathy: diabetes, alcohol, nutritional deficiency, chronic kidney disease, hypothyroidism, drugs/toxins, paraproteinemia.

• Asymmetric / mononeuritis multiplex: vasculitis (systemic or non-systemic), diabetes, sarcoidosis, infection (Lyme, HIV, leprosy), cryoglobulinemia, amyloid — a multifocal pattern is a red flag for vasculitis and warrants prompt evaluation.

• Acute demyelinating: Guillain-Barré syndrome and its variants. Radiculopathy: disc/degenerative, infectious (CMV, zoster), or neoplastic root involvement.

RF

• Modifiable: hyperglycemia, alcohol, neurotoxic medications, nutritional deficiencies, treatable infections.

• Non-modifiable: hereditary neuropathy (Charcot-Marie-Tooth), advancing age, underlying autoimmune/inflammatory disease, malignancy.

Data

• Glucose and HbA1c, B12 with methylmalonic acid, folate, TSH, CBC, CMP, ESR/CRP (common, treatable metabolic/nutritional causes)

• SPEP/UPEP with immunofixation and serum free light chains (paraproteinemic neuropathy — easily missed; especially with demyelinating or painful sensory patterns)

• HIV, Lyme, hepatitis serologies; ANA, ANCA, rheumatoid factor, cryoglobulins, complement (vasculitic/inflammatory — particularly for mononeuritis multiplex); heavy-metal screen if exposure history

• Nerve conduction studies / EMG (the central test — axonal vs demyelinating, length-dependent vs multifocal, motor vs sensory, acute vs chronic; localizes radiculopathy vs plexopathy vs neuropathy)

• MRI spine/plexus if a root, plexus, or cord lesion is suspected; LP if an inflammatory/demyelinating process is likely (albuminocytologic dissociation in GBS/CIDP); nerve biopsy in selected vasculitis/amyloid cases.

DDx

Guillain-Barré syndrome (acute, ascending, areflexic — monitor FVC) · spinal cord compression/myelopathy (UMN signs, sensory level) · radiculopathy (dermatomal, often painful) · myasthenia gravis (fatigable, no sensory loss) · myopathy (proximal, ↑CK, no sensory) · motor neuron disease (mixed UMN/LMN, no sensory) · functional/somatic

Home Meds

• Review and stop neurotoxic medications where clinically feasible (in coordination with the prescribing service for chemotherapy).

• Correct deficiencies (B12, thiamine; stop excess B6) and optimize glycemic control.

Plan

Consults

• Neurology — EMG/NCS, classification, and directed workup.

• Rheumatology — suspected vasculitic neuropathy/mononeuritis multiplex.

• Hematology — paraproteinemia/amyloid.

• Infectious disease — HIV, Lyme, or other infectious neuropathy.

Exclude emergencies first

• If the picture is acute, ascending, and areflexic, manage as GBS with serial FVC/NIF and disease-modifying therapy. If there are UMN signs, a sensory level, or sphincter dysfunction, obtain an urgent spinal MRI to exclude cord compression.

Localize, then treat the cause

• Use the exam plus NCS/EMG to localize and characterize, then send targeted labs. Treat reversible causes — tighten glycemic control, replete B12/thiamine, remove the offending drug or toxin, and pursue immunotherapy (corticosteroids ± steroid-sparing/cytotoxic agents, IVIG) for vasculitic or inflammatory neuropathy under specialty guidance.

Symptomatic

• Neuropathic pain: gabapentin (Neurontin) 300 mg PO TID titrated to effect, pregabalin (Lyrica) 75 mg PO BID, or duloxetine (Cymbalta) 30–60 mg PO daily; tricyclics (nortriptyline) as alternatives. Foot care and protective footwear (insensate feet), fall-prevention.

Always

• PT / OT eval and treat — gait/safety, ankle-foot orthosis for foot drop, strengthening, ADL adaptation.

• Trend: serial neurologic exam and strength; if any ascending or respiratory concern, FVC/NIF; response to treatment of the underlying cause.

• Escalation triggers: acute ascending weakness with falling FVC/NIF → GBS pathway, ICU · autonomic instability → telemetry, ICU · evolving cord syndrome → emergent imaging and neurosurgery/neurology.

• Discharge checklist: documented cause or a defined outpatient workup plan with pending labs · neuropathic-pain regimen · deficiency repletion and glycemic optimization · neurotoxic-drug list addressed · neurology and relevant specialty follow-up (EMG results, biopsy if planned) · foot-care and fall-prevention education · return precautions (rapidly progressive or ascending weakness, breathing/swallowing difficulty).

Red Flags — Urgent

• Acute ascending areflexic weakness → treat as GBS; monitor FVC/NIF, ICU if declining.
• UMN signs / sensory level / sphincter loss → cord compression; emergent MRI.
• Mononeuritis multiplex (stepwise, multifocal) → vasculitis until proven otherwise; expedite workup and immunotherapy.
• Autonomic instability → telemetry, ICU.
• Rapidly progressive motor loss with weight loss/systemic illness → paraneoplastic/vasculitic; expedite.

Senior IM Resident Pearls

• Pattern before panel. Don't shotgun labs — first localize (tempo + distribution + fiber type). The pattern narrows the differential far more than a broad serology screen.
• Rule out the cord and GBS before calling it "just a neuropathy." A sensory level or acute areflexic ascending weakness changes everything and is time-sensitive.
• Mononeuritis multiplex = vasculitis until proven otherwise. An asymmetric, stepwise, multifocal neuropathy needs an expedited inflammatory workup — don't let it smolder.
• Send the SPEP and free light chains. Paraproteinemic neuropathy is a classic miss, and it's treatable — especially with painful or demyelinating sensory patterns.
• Diabetes and alcohol explain most, but don't anchor. A "diabetic neuropathy" that's asymmetric, rapidly progressive, or motor-predominant deserves a second look.
• Check B12 with MMA, not B12 alone. Low-normal B12 with a high MMA still causes neuropathy — and B6 toxicity (megadose supplements) causes a sensory neuropathy people forget.
• EMG/NCS is the anchor test — axonal vs demyelinating reorganizes the whole differential (demyelinating → GBS/CIDP/paraprotein; axonal → metabolic/toxic).
• Common mistake: starting gabapentin and stopping there. Symptomatic control is fine, but the workup for a treatable or dangerous cause still has to happen.

Neurology — Headache

Status Migrainosus

debilitating migraine >72h · exclude secondary causes · break the cycle · avoid opioids · Super Compact

• Sx: a debilitating migraine attack lasting >72 hours (with or despite treatment); typical migraine features — unilateral, pulsating, moderate-severe, photophobia/phonophobia, nausea/vomiting, worse with activity; ± aura; often with medication-overuse background

• Neg: denies thunderclap/worst-ever onset (SAH) · denies fever + neck stiffness (meningitis) · denies new focal deficit/papilledema (mass/↑ICP) · denies new headache >50 yo with jaw claudication (GCA) · denies positional/Valsalva pattern (CSF pressure) — i.e. no secondary red flags

• SHx: established migraine history, usual pattern, current/overused acute meds (triptans, NSAIDs, caffeine, opioids — medication-overuse headache), preventive regimen, triggers (sleep, stress, menses, dehydration)

• Etiology: prolonged neurovascular migraine attack with central sensitization; frequently perpetuated by medication overuse, dehydration, poor sleep, or an untreated trigger

• RF: modifiable — medication overuse, dehydration, sleep disruption, missed preventives · non-mod — established migraine, female, hormonal pattern

• Data: clinical diagnosis — primarily to exclude secondary causes if atypical/red flags: neuro exam, consider non-con CT/MRI, LP if SAH/meningitis suspected, ESR/CRP if >50 (GCA); electrolytes if vomiting; rule out CO/medication causes

• DDx: SAH (thunderclap) · meningitis (fever, stiff neck) · CVST (prothrombotic, papilledema) · mass/↑ICP (focal, positional) · GCA (>50, ESR↑, jaw) · medication-overuse headache · idiopathic intracranial hypertension

• Home Meds: stop overused acute meds (triptans/NSAIDs/caffeine/opioids — medication-overuse headache); continue/optimize preventive; avoid opioids/butalbital

Plan — ward / ED-obs (rarely needs admit)

• Consults: neurology (refractory cases, preventive optimization) · headache specialist if recurrent status

• First confirm it's primary — if any red flag, image/LP before attributing to migraine

• IV "migraine cocktail": IV fluids (NS) + antiemetic dopamine antagonist — metoclopramide (Reglan) 10 mg IV or prochlorperazine (Compazine) 10 mg IV (give with diphenhydramine 25 mg IV to prevent akathisia/dystonia) + ketorolac (Toradol) 15–30 mg IV

• Add: IV magnesium sulfate 1–2 g (esp. with aura); consider dihydroergotamine (DHE, Migranal) 0.5–1 mg IV if no vascular contraindication/recent triptan; dexamethasone (Decadron) 10 mg IV reduces early recurrence

• Avoid opioids and butalbital — worsen medication-overuse headache and chronify; not migraine-specific

• Break medication overuse if present (taper/stop the offending acute agent); treat dehydration, restore sleep

• Start/optimize a preventive (topiramate, propranolol, amitriptyline, or CGRP agent) on the way out

• Trend: pain score, hydration, nausea, response to cocktail

• → Escalate if: a red flag emerges (focal deficit, fever, thunderclap features) → urgent imaging/LP; or truly refractory → neurology, consider DHE protocol/admission

Status Migrainosus

complete reference · >72h migraine · exclude secondary · IV cocktail · break overuse · preventive · Full Card

Symptoms / Associated Sx

• A debilitating migraine attack persisting more than 72 hours despite usual treatment, in a patient with an established migraine history and the attack resembling their typical migraines — unilateral, pulsating, moderate-to-severe pain, aggravated by routine activity, with photophobia, phonophobia, and nausea/vomiting; aura may or may not be present. Persistent vomiting causes dehydration and electrolyte disturbance, which further perpetuate the attack. A background of escalating acute-medication use (medication-overuse headache) is common and important.

Neg

• No instantaneous thunderclap/"worst headache of life" — argues against SAH (any thunderclap onset demands CT ± LP regardless of migraine history)

• No fever, neck stiffness, or photophobia of meningitic quality — argues against meningitis (migraine photophobia is sensory sensitivity, not meningismus)

• No new focal deficit (beyond typical reversible aura), papilledema, or seizure — argues against a mass lesion or raised ICP (new or atypical neurologic signs → image)

• Not a new headache after age 50 with scalp tenderness/jaw claudication — argues against giant cell arteritis (check ESR/CRP and treat empirically if suspected)

• Not strictly positional or Valsalva/cough-triggered — argues against a CSF-pressure disorder (high or low) (different mechanism and workup)

Social History (SHx)

• Established migraine diagnosis and the patient's usual attack pattern (this attack should resemble it); current acute medications and frequency of use (triptans, NSAIDs, combination analgesics, caffeine, opioids, butalbital — medication-overuse headache); preventive regimen and adherence.

• Triggers — sleep disruption, stress, menstrual timing, dehydration, dietary; caffeine intake; pregnancy status (affects drug choice).

Main Etiology

• A prolonged primary migraine attack reflecting sustained neurovascular activation and central sensitization. It is frequently perpetuated by medication overuse, dehydration from vomiting, sleep deprivation, and an unresolved trigger — addressing these perpetuators is as important as aborting the pain.

RF

• Modifiable: acute-medication overuse, dehydration, sleep disruption, missed preventive therapy, ongoing triggers.

• Non-modifiable: established migraine disorder, female sex, hormonal/menstrual pattern.

Data

• Status migrainosus is a clinical diagnosis — investigations exist to exclude a secondary cause when features are atypical or red flags are present.

• Thorough neurologic exam and fundoscopy (focal deficit, papilledema → image)

• Non-contrast CT and/or MRI brain if new/atypical features, focal signs, or first severe headache; MR/CT venography if CVST is a concern (prothrombotic state, papilledema)

• LP if SAH (after negative CT) or meningitis is suspected; ESR/CRP if age >50 (giant cell arteritis); electrolytes/renal function if persistent vomiting (dehydration)

DDx

Subarachnoid hemorrhage (thunderclap) · meningitis (fever, stiff neck) · cerebral venous sinus thrombosis (prothrombotic, papilledema) · mass lesion / raised ICP (focal, positional, morning) · giant cell arteritis (>50, ESR↑, jaw claudication) · medication-overuse headache (frequent acute-drug use) · idiopathic intracranial hypertension (papilledema, young obese woman) · carbon monoxide

Home Meds

• Stop overused acute medications (triptans, NSAIDs, combination/caffeine analgesics, opioids, butalbital) when medication-overuse headache is contributing — this is central to breaking the cycle.

• Continue/optimize preventive therapy; avoid opioids and butalbital entirely.

Plan

Consults

• Neurology — for refractory status, preventive optimization, and DHE protocols.

• Headache specialist — recurrent status migrainosus or complex medication-overuse cases.

Confirm it's primary

• If any red flag is present, image (± LP) before attributing the headache to migraine. In a typical attack in a known migraineur with a normal exam, proceed to abortive treatment.

Abortive "cocktail"

• IV fluids (normal saline) for rehydration. Dopamine-antagonist antiemetic: metoclopramide (Reglan) 10 mg IV or prochlorperazine (Compazine) 10 mg IV — give with diphenhydramine (Benadryl) 25 mg IV to prevent akathisia/dystonia. NSAID: ketorolac (Toradol) 15–30 mg IV. Magnesium sulfate 1–2 g IV (particularly with aura). Dexamethasone (Decadron) 10 mg IV to reduce early headache recurrence.

• Dihydroergotamine (DHE/Migranal) 0.5–1 mg IV (with an antiemetic) for refractory cases — contraindicated in coronary/peripheral vascular disease, uncontrolled hypertension, pregnancy, or within 24h of a triptan/ergot. A repeated DHE protocol is an effective inpatient option for true status.

Break perpetuators / avoid harm

• Do not use opioids or butalbital — they are not migraine-specific, worsen medication-overuse headache, and promote chronification. Stop/taper the overused acute agent, correct dehydration and electrolytes, and restore sleep.

Prevention

• Initiate or optimize a preventive at discharge: topiramate (Topamax), propranolol (Inderal), amitriptyline (Elavil), or a CGRP-targeted agent (erenumab/Aimovig and others); discuss trigger management.

Always

• PT/OT rarely needed; address deconditioning if prolonged.

• Trend: pain score, nausea, hydration/electrolytes, and response to the cocktail; watch for akathisia from dopamine antagonists.

• Escalation triggers: emergence of any red flag (new focal deficit, fever, thunderclap quality, papilledema) → urgent imaging/LP · truly refractory pain → neurology, inpatient DHE protocol or admission.

• Discharge checklist: a defined acute regimen that is migraine-specific (triptan/NSAID with use limits to avoid overuse) · started/optimized preventive · explicit counseling to avoid opioids/butalbital and limit acute-medication days · medication-overuse plan if relevant · trigger and lifestyle counseling (sleep, hydration, regular meals) · neurology/headache follow-up · return precautions (new neurologic symptoms, worst-ever or thunderclap headache, fever).

Red Flags — Don't Miss (SNNOOP-type)

• Thunderclap onset → SAH; CT ± LP.
• Fever + neck stiffness → meningitis.
• New focal deficit, papilledema, or seizure → mass/raised ICP; image.
• New headache >50, jaw claudication, scalp tenderness → giant cell arteritis; ESR/CRP, empiric steroids.
• Prothrombotic/postpartum + headache → CVST.
• Progressive/positional pattern or change from usual → secondary cause; image.

Senior IM Resident Pearls

• Status migrainosus is >72 hours of a typical migraine — the diagnosis still requires confidence it isn't a secondary headache. Screen for red flags every time, even in a known migraineur.
• The cocktail beats opioids. IV fluids + a dopamine-antagonist antiemetic + ketorolac ± magnesium ± dexamethasone aborts most attacks. Opioids and butalbital don't help and make the next headache worse.
• Add dexamethasone to prevent the bounce-back. A single IV dose reduces early recurrence after the attack breaks.
• Give diphenhydramine with the dopamine antagonist — akathisia and dystonic reactions from metoclopramide/prochlorperazine are common and miserable.
• Think medication overuse. The patient stuck in status is often overusing triptans, caffeine, or analgesics — breaking the overuse is part of the cure, not an afterthought.
• DHE is potent but vascular. Great for refractory status, but not within 24h of a triptan and not with coronary/PVD, uncontrolled HTN, or pregnancy.
• Don't discharge without a preventive plan if attacks are frequent or this is recurrent status — the admission is a chance to fix the trajectory.
• Common mistake: reflexively giving opioids for "refractory headache" — it relieves pain briefly, chronifies the disorder, and obscures the diagnosis.

Neurology — Headache

Secondary Headache Workup (Red Flags)

SNNOOP10 · find the dangerous cause · image and test by flag · Super Compact

• Sx / red flags (SNNOOP10): Systemic (fever, weight loss, cancer, HIV/immunocompromise) · Neurologic deficit or altered consciousness · Onset sudden/thunderclap · Older (new headache >50) · Pattern change/progressive · plus positional, precipitated by Valsalva, papilledema, pregnancy/postpartum, painful eye/autonomic, post-traumatic, painkiller overuse, prior cancer/immune

• Neg (reassuring/primary): denies sudden thunderclap · denies focal deficit/papilledema · denies fever/systemic illness · stable longstanding stereotyped pattern · normal neuro exam — favors primary headache (migraine/tension/cluster), reduces need for imaging

• SHx: age, cancer history, immunocompromise/HIV, anticoagulation, pregnancy/postpartum, trauma, prior headaches and their pattern, medication/analgesic use, toxin/CO exposure

• Etiology by flag: thunderclap → SAH/RCVS/dissection/CVST/apoplexy · fever+stiff neck → meningitis · focal/papilledema → mass/bleed/abscess/↑ICP · >50 + ESR↑ → GCA · postpartum/prothrombotic → CVST/PRES · positional → CSF pressure (high/low)

• RF: modifiable — anticoagulation, analgesic overuse, uncontrolled BP · non-mod — age, malignancy, immunocompromise, pregnancy state, prothrombophilia

• Data (flag-directed): non-con CT (acute bleed) → LP if SAH suspected & CT neg (xanthochromia) · MRI/MRV/MRA (mass, CVST, dissection, RCVS) · ESR/CRP (GCA) · LP opening pressure (↑ICP/IIH, low-pressure) · labs (CBC, infection), CO level, BP

• DDx (dangerous): SAH · meningitis/encephalitis · mass/tumor · CVST · GCA · dissection · RCVS · pituitary apoplexy · IIH · low-pressure (CSF leak) · hypertensive emergency/PRES · CO poisoning

• Home Meds: review anticoagulation/antiplatelet (bleed risk), analgesic overuse, vasoactive drugs (RCVS triggers)

Plan — ward / ED (depends on cause)

• Consults: neurology · neurosurgery if bleed/mass · IR/neuro-IR if vascular · rheumatology/ophtho if GCA · ID if infection

• Match the test to the flag — don't blanket-image every headache, but never miss a flagged one

• Thunderclap: non-con CT (near 100% <6h) → if neg & suspicious, LP for xanthochromia → CTA/MRA/MRV (aneurysm, dissection, RCVS, CVST)

• Fever + meningismus: blood cultures → empiric antibiotics ± acyclovir + dexamethasone → CT/LP (see meningitis card)

• Focal deficit / papilledema / new seizure: urgent neuroimaging (CT then MRI); no LP before imaging

• New headache >50 with jaw claudication / vision change: ESR + CRP, start high-dose steroids immediately (prednisone 40–60 mg, or IV methylprednisolone if vision threatened) BEFORE biopsy — don't wait for temporal artery biopsy

• Treat the identified cause on its specific pathway; if all negative and exam normal → primary headache management

• Trend: neuro exam, vitals, the specific abnormal finding

• → ICU/urgent if: SAH, depressed consciousness, status, hypertensive emergency, threatened vision (GCA), or any rapidly evolving deficit

Secondary Headache Workup (Red Flags)

complete reference · SNNOOP10 · flag-directed testing · the dangerous mimics · GCA & thunderclap · Full Card

Symptoms / Associated Sx (the red flags)

• The job is to separate a benign primary headache from a dangerous secondary one. The SNNOOP10 red flags: Systemic symptoms/signs (fever, weight loss); Neoplasm history; Neurologic deficit or altered consciousness; Onset sudden/thunderclap (peaks <1 min); Older age at onset (new headache >50); Pattern change or progressive headache; plus Positional, Precipitated by Valsalva/exertion, Papilledema, Pregnancy/puerperium, Painful eye with autonomic features, Post-traumatic onset, analgesic overuse (Painkiller), and Prior immunocompromise/HIV. Any one flag shifts the pre-test probability of a serious cause and dictates a specific investigation.

Neg (features favoring primary headache)

• No sudden thunderclap onset — argues against SAH/RCVS/dissection (gradual build favors primary)

• No focal deficit, papilledema, or altered consciousness — argues against mass, hemorrhage, or raised ICP (a normal neuro exam is reassuring but doesn't override a strong flag)

• No fever or systemic illness — argues against CNS infection/GCA.

• A longstanding, stereotyped, stable pattern matching prior episodes — favors an established primary headache and reduces (does not eliminate) the need for imaging.

Social History (SHx)

• Age and age at headache onset; cancer history (metastasis/leptomeningeal); immunocompromise/HIV (opportunistic infection, lymphoma); anticoagulant/antiplatelet use (hemorrhage); pregnancy/postpartum (CVST, PRES, pituitary apoplexy, preeclampsia).

• Recent head/neck trauma or manipulation (dissection, subdural); analgesic/triptan overuse; vasoactive drug or stimulant use (RCVS); carbon-monoxide exposure (faulty heating, multiple household members affected).

Main Etiology (the dangerous causes, by flag)

• Thunderclap: subarachnoid hemorrhage, reversible cerebral vasoconstriction syndrome, cervical artery dissection, cerebral venous thrombosis, pituitary apoplexy, third-ventricle colloid cyst.

• Fever + meningismus: meningitis/encephalitis. Focal/papilledema: tumor, abscess, hemorrhage, raised ICP. Age >50 + systemic/visual: giant cell arteritis. Postpartum/prothrombotic: CVST, PRES, pituitary apoplexy. Positional: high-pressure (IIH) or low-pressure (CSF leak) headache. Severe hypertension: hypertensive emergency/PRES. Toxic: carbon monoxide.

RF

• Modifiable: anticoagulation, analgesic overuse, uncontrolled hypertension, vasoactive drug use, CO exposure.

• Non-modifiable: advancing age, malignancy, immunocompromise, pregnancy/puerperium, thrombophilia.

Data (flag-directed, not blanket)

• Non-contrast CT head first for acute severe/thunderclap or focal presentations (hemorrhage; near 100% sensitive for SAH within 6h)

• Lumbar puncture if SAH suspected with a negative CT (xanthochromia, RBCs that don't clear), for meningitis, and to measure opening pressure (raised in IIH, low in CSF-leak headache)

• MRI brain with MRV/MRA (mass, CVST, dissection, RCVS — RCVS shows segmental "string-of-beads" vasoconstriction; dissection shows the flap/Horner)

• ESR and CRP for any new headache after 50 with systemic/visual features (giant cell arteritis — then temporal artery biopsy/ultrasound)

• CBC and infection workup; blood pressure; carboxyhemoglobin if CO suspected; pregnancy test in women of childbearing age.

DDx (dangerous secondary headaches)

SAH · meningitis/encephalitis · brain tumor/metastasis · cerebral venous sinus thrombosis · giant cell arteritis · cervical artery dissection · reversible cerebral vasoconstriction syndrome · pituitary apoplexy · idiopathic intracranial hypertension · spontaneous intracranial hypotension (CSF leak) · hypertensive emergency/PRES · carbon monoxide poisoning · acute angle-closure glaucoma

Home Meds

• Review anticoagulants/antiplatelets (hemorrhage risk and reversal), analgesic/triptan overuse, and vasoactive or serotonergic drugs and stimulants (RCVS triggers).

Plan

Consults

• Neurology — diagnosis and directed workup.

• Neurosurgery / neuro-IR — hemorrhage, mass, aneurysm, dissection.

• Rheumatology / ophthalmology — giant cell arteritis with visual symptoms.

• Infectious disease — CNS infection; OB if pregnant/postpartum.

Match test to flag

• Don't blanket-image every headache — but never let a flagged headache leave without the appropriate study. Use the flag to choose CT vs MRI vs vascular imaging vs LP vs ESR/CRP.

Thunderclap pathway

• Non-contrast CT (near 100% within 6h) → if negative and suspicion persists, LP for xanthochromia → CTA/MRA/MRV to evaluate aneurysm, dissection, RCVS, and venous thrombosis.

Infection pathway

• Fever + meningismus → blood cultures, then dexamethasone + empiric antibiotics (± acyclovir), then CT/LP per the meningitis protocol — never delay antimicrobials for the LP.

Giant cell arteritis pathway

• New headache >50 with jaw claudication, scalp tenderness, or visual symptoms → check ESR/CRP and start high-dose corticosteroids immediately (prednisone 40–60 mg PO daily, or IV methylprednisolone 500–1000 mg if vision is threatened) before the temporal artery biopsy/ultrasound — treatment prevents irreversible blindness and biopsy remains informative for ~1–2 weeks.

Always

• Treat the identified cause on its specific pathway. If the workup is negative and the exam is normal, manage as a primary headache and arrange follow-up. PT/OT as dictated by any deficits.

• Trend: the specific abnormal finding (neuro exam, BP, inflammatory markers, vision) and overall stability.

• Escalation triggers: SAH or other hemorrhage → ICU/neurosurgery · depressed consciousness/status → ICU · hypertensive emergency/PRES → controlled BP reduction, ICU · threatened vision (GCA) → emergent steroids, ophthalmology · rapidly evolving deficit → urgent re-imaging.

• Discharge checklist (if benign): documented reassuring workup, normal exam, and a clear primary-headache diagnosis · explicit written return precautions for each major red flag · primary-care/neurology follow-up · medication-overuse counseling if relevant · for treated secondary causes, the specific disease's discharge plan applies.

Red Flags — Act Now

• Thunderclap → SAH/RCVS/dissection/CVST; CT ± LP ± vascular imaging.
• Fever + neck stiffness/AMS → meningitis/encephalitis; antibiotics + acyclovir now.
• Focal deficit / papilledema / seizure → mass or raised ICP; image, don't LP first.
• New headache >50 + jaw claudication/visual loss → giant cell arteritis; steroids immediately, then biopsy.
• Postpartum/prothrombotic, or severe hypertension → CVST / PRES.
• Multiple household members ill + headache → carbon monoxide.

Senior IM Resident Pearls

• Let the red flag pick the test. SNNOOP10 isn't a checklist to recite — each flag points to a specific study. Thunderclap → CT/LP/vessels; fever → LP and antibiotics; >50 + visual → ESR and steroids.
• Thunderclap is SAH until excluded — CT within 6 hours is near-perfect, but after that you still need the LP. A normal CT later than 6h does not clear it.
• In suspected GCA, steroids come before the biopsy. Vision loss is preventable and irreversible once it happens — treat on clinical suspicion plus ESR/CRP; the biopsy stays positive for days.
• A normal neuro exam doesn't override a strong flag. Plenty of SAH, CVST, and early GCA patients look well — the history is doing the heavy lifting.
• Pregnancy/postpartum changes the differential — CVST, PRES, pituitary apoplexy, and preeclampsia all cluster here; image the venous system and check the BP and pregnancy status.
• Positional headaches split two ways: worse upright = low-pressure (CSF leak); worse lying down/with Valsalva = high-pressure (mass, IIH). The posture tells you which way to look.
• Don't forget carbon monoxide — a headache that improves away from home, or several household members affected, is the classic tell.
• Common mistake: either over-imaging every benign headache, or anchoring on "migraine" in a patient whose pattern just changed — the change from baseline is itself a flag.

Neurology — Demyelinating

Multiple Sclerosis Relapse

new deficit >24h, no fever · rule out pseudorelapse · steroids · MRI · Super Compact

• Sx: new or worsening neuro deficit lasting >24h developing over hours-days, attributable to CNS demyelination — optic neuritis (painful monocular vision loss, ↓color), partial myelitis (sensory level, weakness, bladder), brainstem/cerebellar (diplopia, INO, ataxia, vertigo); not explained by fever/infection

• Neg (rule out pseudorelapse): denies fever/infection (UTI, URI — pseudorelapse = old deficit unmasked by heat/infection — Uhthoff) · denies abrupt vascular onset (stroke) · denies complete cord syndrome (compression — image) · symptoms not purely fatigue/heat-triggered transient (not a true relapse)

• SHx: known MS (type, DMT, adherence), prior relapses/baseline disability, recent infection/illness/heat exposure, stressors, pregnancy/postpartum, vaccination

• Etiology: acute inflammatory demyelinating lesion in CNS white matter (new area of active inflammation/gadolinium enhancement); distinct from pseudorelapse (transient worsening from fever/heat/metabolic stress without new lesion)

• RF: modifiable — infection, missed DMT, heat, smoking, stress · non-mod — established MS, prior relapse rate, disease phenotype

• Data: rule out infection FIRST (UA/culture, CBC, CXR if symptomatic) · MRI brain ± spine with gadolinium (new T2/enhancing lesion = active) · exam vs baseline · consider LP/OCBs if new dx · evaluate for NMOSD/MOG if atypical (severe/bilateral optic neuritis, longitudinally extensive myelitis)

• DDx: pseudorelapse (infection/heat, no new lesion) · NMOSD/MOGAD (severe optic neuritis, LETM) · stroke (vascular onset) · cord compression (structural) · other inflammatory (sarcoid, vasculitis, ADEM) · functional

• Home Meds: continue disease-modifying therapy (DMT); treat any infection; do not start DMT acutely for the relapse itself

Plan — ward / often outpatient-manageable

• Consults: neurology (MS specialist) · ophthalmology if optic neuritis · PT/OT/urology as needed

• First exclude pseudorelapse and infection — treat the infection; a true relapse needs a NEW deficit >24h not explained by fever/metabolic stress

• Acute relapse treatment (if functionally significant): high-dose corticosteroids — methylprednisolone (Solu-Medrol) 1000 mg IV daily ×3–5 days (or bioequivalent oral) — speeds recovery, does not change long-term disability; mild sensory-only relapses may not need steroids

• If steroid-refractory or severe (esp. NMOSD): plasma exchange (PLEX)

• Symptomatic: spasticity (baclofen), neuropathic pain (gabapentin), bladder (anticholinergic/cath), fatigue; PPI + glucose monitoring with steroids

• Optimize/adjust DMT with neurology as outpatient (don't start acutely for the relapse)

• Trend: deficit vs baseline, recovery, steroid side effects (glucose, mood, BP)

• → Escalate if: severe myelitis with respiratory/bulbar involvement, rapidly progressive deficit, suspicion of NMOSD (consider PLEX early), or atypical features suggesting another diagnosis

Multiple Sclerosis Relapse

complete reference · >24h deficit · exclude pseudorelapse · steroids/PLEX · NMOSD caveat · Full Card

Symptoms / Associated Sx

• A new or worsening neurologic deficit lasting more than 24 hours, evolving over hours to days, in the absence of fever or infection, and attributable to CNS demyelination. Common presentations: optic neuritis (subacute painful monocular visual loss with reduced color/acuity and a relative afferent pupillary defect), partial myelitis (sensory level, limb weakness, bladder dysfunction, Lhermitte sign), and brainstem/cerebellar syndromes (diplopia, internuclear ophthalmoplegia, vertigo, ataxia, dysarthria). A relapse reflects a new area of active inflammation; transient worsening with heat or fatigue without a new lesion is a pseudorelapse.

Neg

• No fever or active infection driving the symptoms — argues against a pseudorelapse (infection/heat transiently unmask an old deficit via the Uhthoff phenomenon; treating the infection resolves it — no new lesion, no steroids needed)

• Onset over hours-days rather than seconds-minutes — argues against stroke (vascular events are abrupt and follow arterial territories)

• A partial cord syndrome rather than a complete one with a crisp structural level — argues against compressive myelopathy (image the cord if a complete or progressive level is present)

• Not severe bilateral optic neuritis or a longitudinally extensive cord lesion — argues against NMOSD/MOGAD (these atypical features should prompt aquaporin-4 and MOG antibody testing and change management)

Social History (SHx)

• Known MS — phenotype (relapsing-remitting vs progressive), current disease-modifying therapy and adherence, prior relapses and recovery, and baseline disability for comparison.

• Recent infection, illness, fever, or heat exposure (pseudorelapse triggers); psychological/physical stress; pregnancy/postpartum (postpartum relapse risk); recent vaccination; smoking (worsens course).

Main Etiology

• An acute inflammatory, demyelinating lesion in CNS white matter — a focus of active inflammation that typically enhances with gadolinium — producing a deficit referable to its location. This is mechanistically distinct from a pseudorelapse, where elevated body temperature or metabolic stress transiently impairs conduction in previously demyelinated pathways without new inflammation.

RF

• Modifiable: infection, missed disease-modifying therapy, heat exposure, smoking, stress, sleep deprivation.

• Non-modifiable: established MS, higher baseline relapse rate, disease phenotype, postpartum state.

Data

• Exclude infection/metabolic cause first — urinalysis and culture, CBC, and targeted workup (CXR if respiratory symptoms) (a UTI or other infection causing a pseudorelapse is common and treated differently)

• MRI brain and/or spinal cord with gadolinium (a new T2 lesion or a gadolinium-enhancing lesion confirms active disease and corresponds to the deficit; compare to prior imaging)

• Detailed neurologic exam compared to documented baseline; visual acuity/color and fundoscopy for optic neuritis.

• If new diagnosis: LP for oligoclonal bands/IgG index; aquaporin-4 (NMO) and MOG antibodies if atypical (severe or bilateral optic neuritis, longitudinally extensive transverse myelitis, area postrema syndrome) (NMOSD/MOGAD management differs and some MS therapies worsen NMOSD)

DDx

Pseudorelapse (infection/heat, no new lesion) · NMOSD / MOGAD (severe optic neuritis, longitudinally extensive myelitis, AQP4/MOG antibodies) · ischemic stroke (abrupt, vascular territory) · spinal cord compression (structural, complete level) · other inflammatory/ADEM/sarcoid/vasculitis · functional neurologic disorder · vitamin B12/metabolic myelopathy

Home Meds

• Continue the disease-modifying therapy (do not start a new DMT acutely to treat the relapse — DMTs prevent future relapses, they don't treat the current one).

• Treat any identified infection; add a PPI and monitor glucose during high-dose steroids.

Plan

Consults

• Neurology (MS specialist) — confirm relapse vs pseudorelapse, treatment, and DMT strategy.

• Ophthalmology — optic neuritis evaluation.

• PT / OT / urology — functional deficits, bladder management.

Exclude pseudorelapse / infection first

• Confirm a genuine new deficit >24h not explained by fever, infection, or heat. Treat any infection; a pseudorelapse improves once the trigger resolves and does not warrant steroids.

Acute relapse therapy

• High-dose corticosteroids for functionally significant relapses: methylprednisolone (Solu-Medrol) 1000 mg IV daily for 3–5 days (high-dose oral prednisone is bioequivalent and acceptable). Steroids speed recovery but do not alter long-term disability; a mild, sensory-only relapse may be observed without steroids.

• Plasma exchange (PLEX) for severe, steroid-refractory relapses — and considered early in suspected NMOSD.

Symptomatic / steroid care

• Spasticity — baclofen (Lioresal) or tizanidine; neuropathic pain — gabapentin (Neurontin)/pregabalin; bladder dysfunction — anticholinergic or intermittent catheterization; fatigue management. With steroids: gastroprotection, glucose monitoring, mood/sleep counseling, BP monitoring.

Always

• PT / OT eval and treat — rehabilitation of the relapse deficit; gait and ADL safety.

• Trend: the deficit against baseline, recovery trajectory, and steroid side effects (glucose, BP, mood, infection).

• Escalation triggers: severe cervical myelitis with respiratory/bulbar involvement → ICU · rapidly progressive deficit or steroid-refractory → PLEX, neurology · atypical/severe optic neuritis or longitudinally extensive myelitis → test/treat for NMOSD (PLEX early).

• Discharge checklist: steroid course completed with taper plan if used · DMT reviewed/optimized with neurology (escalate if breakthrough disease) · symptomatic regimens (spasticity, pain, bladder) · trigger mitigation (treat infection, smoking cessation, heat avoidance) · rehabilitation referral · MS-specialist follow-up with repeat MRI plan · vaccination/infection-prevention counseling · return precautions (new or worsening deficit, vision loss, breathing/swallowing difficulty).

Red Flags — Urgent

• Severe cervical myelitis (respiratory/bulbar compromise) → ICU.
• Rapidly progressive or steroid-refractory deficit → PLEX, neurology.
• Suspected NMOSD (severe/bilateral optic neuritis, longitudinally extensive myelitis) → AQP4/MOG testing, early PLEX; some MS DMTs worsen it.
• Complete cord syndrome with a structural level → image to exclude compression.
• Atypical features (encephalopathy, systemic illness) → reconsider ADEM/sarcoid/vasculitis/infection.

Senior IM Resident Pearls

• Rule out pseudorelapse before reaching for steroids. A UTI, fever, or hot weather can unmask an old deficit (Uhthoff) — treat the trigger and the "relapse" resolves. A true relapse is a NEW deficit >24h with a new lesion.
• Steroids speed recovery but don't change the destination. High-dose methylprednisolone shortens the relapse; long-term disability is unchanged — so mild sensory relapses can be observed.
• DMTs don't treat the relapse. They reduce future relapses — don't start or switch one acutely to "treat" the current attack; that's an outpatient decision with neurology.
• Think NMOSD when it's severe or bilateral. Severe optic neuritis, longitudinally extensive transverse myelitis, or intractable hiccups/vomiting should trigger AQP4/MOG testing — and several classic MS drugs make NMOSD worse.
• Optic neuritis is painful and monocular with reduced color vision and an afferent pupillary defect — get ophthalmology and an MRI of the orbits/brain.
• PLEX is the escalation for steroid-refractory or fulminant attacks — reach for it early in severe presentations rather than giving a second steroid course.
• Always check for infection — it's both a relapse mimic and a relapse trigger, and steroids on top of an untreated infection is the wrong move.
• Common mistake: steroid-treating a febrile MS patient whose old weakness flared from the fever — that's a pseudorelapse, and the real problem is the infection.

Neurology — Demyelinating

Transverse Myelitis

acute cord inflammation · sensory level + weakness + bladder · MRI/LP · exclude compression · Super Compact

• Sx: acute/subacute (hours-days) bilateral weakness + sensory level + bladder/bowel dysfunction below a spinal level; back pain/band-like sensation; ± ascending; reaches nadir 4h–21d; reflexes initially ↓ (spinal shock) then ↑ (UMN)

• Neg: denies compressive structural lesion on MRI (cord compression — surgical emergency, must exclude FIRST) · denies acute vascular onset (cord infarct) · denies areflexia + ascending peripheral pattern (GBS) · denies pure back pain w/o cord signs (mechanical)

• SHx: recent infection/vaccination (post-infectious), known MS/NMOSD/MOGAD, autoimmune disease (lupus, Sjögren, sarcoid), travel/exposures, malignancy (paraneoplastic)

• Etiology: idiopathic/post-infectious · demyelinating (MS — partial; NMOSD/MOGAD — longitudinally extensive) · autoimmune/systemic (SLE, Sjögren, sarcoid) · infectious (VZV, HSV, enterovirus, HIV, syphilis) · paraneoplastic; must distinguish from compressive & vascular

• RF: modifiable — treatable infection · non-mod — autoimmune disease, MS/NMOSD, recent viral illness

• Data: urgent MRI spine WITH and without contrast (+ brain) — first to EXCLUDE COMPRESSION, then shows cord T2/enhancement (count segments: <3 partial→MS; ≥3 longitudinally extensive→NMOSD/MOG) · LP (pleocytosis, ↑protein, OCBs, infectious studies) · AQP4/MOG Ab, autoimmune serologies, B12, HIV/syphilis

• DDx: compressive myelopathy (must exclude) · cord infarct (hyperacute, vascular) · MS/NMOSD/MOGAD · GBS (peripheral, areflexic) · B12/copper myelopathy · dural AV fistula · neoplastic

• Home Meds: treat identified infection; continue/adjust immunosuppression with specialty; steroids after compression excluded

Plan — ward (ICU if high cervical)

• Consults: neurology · neurosurgery (until compression excluded) · rheumatology/ID per cause · PT/OT/urology

• EXCLUDE compressive cord lesion first with urgent MRI — compression is a neurosurgical emergency and is treated entirely differently

• Once compression excluded — high-dose steroids: methylprednisolone (Solu-Medrol) 1000 mg IV daily ×3–5 days

• If severe or steroid-refractory (esp. NMOSD): plasma exchange (PLEX)

• Treat identified cause: antivirals (acyclovir for VZV/HSV), antimicrobials for infection, immunotherapy for autoimmune/NMOSD per specialty

• Supportive: bladder management (catheter/retention), bowel regimen, VTE/DVT prophylaxis, pressure-injury & aspiration precautions, neuropathic pain (gabapentin), spasticity (baclofen)

• Monitor respiratory status if cervical (FVC/NIF — diaphragm at C3–5)

• Trend: motor/sensory level, bladder, respiratory if cervical

• → ICU if: high cervical lesion with respiratory compromise, rapidly ascending deficit, or autonomic instability; → NEUROSURG emergently if MRI shows compression

Transverse Myelitis

complete reference · sensory level + weakness + bladder · exclude compression · steroids/PLEX · etiology hunt · Full Card

Symptoms / Associated Sx

• Acute or subacute (developing over hours to a few days, nadir between 4 hours and 21 days) bilateral motor, sensory, and autonomic dysfunction below a spinal cord level — limb weakness, a clearly demarcated sensory level, and bladder/bowel dysfunction (urinary retention is common), often with back pain or a band-like truncal sensation at the level. Reflexes are reduced early (spinal shock) and become hyperreflexic with up-going toes (upper-motor-neuron pattern) over time. The lesion level defines the deficit; a cervical lesion threatens respiration.

Neg

• No compressive structural lesion on MRI — this must be actively excluded (epidural abscess, metastasis, disc, or hematoma compressing the cord is a neurosurgical emergency and the single most important alternative to rule out before anything else)

• Not a hyperacute, vascular-onset, anterior-cord pattern — argues against cord infarction (spinal cord infarct is sudden/maximal at onset, often anterior spinal artery territory with preserved dorsal columns)

• Reflexes show a cord (UMN) pattern with a sensory level, not an ascending areflexic peripheral pattern — argues against GBS (GBS is peripheral, areflexic, without a sensory level)

• Cord signs are present, not isolated mechanical back pain — argues against a purely musculoskeletal process.

Social History (SHx)

• Recent infection or vaccination (post-infectious myelitis); known MS, NMOSD, or MOGAD; systemic autoimmune disease (SLE, Sjögren, sarcoidosis); travel and exposure history (infectious causes); malignancy (paraneoplastic); immune status (HIV).

Main Etiology

• Idiopathic/post-infectious (parainfectious immune response). Demyelinating: MS (typically a short, partial myelitis <3 vertebral segments) and NMOSD/MOGAD (typically longitudinally extensive, ≥3 segments). Systemic autoimmune: lupus, Sjögren, sarcoidosis, Behçet. Infectious: VZV, HSV, enteroviruses, HIV, syphilis, and others (direct or para-infectious). Paraneoplastic. Always separated from compressive and vascular myelopathy, which are managed completely differently.

RF

• Modifiable: treatable infection.

• Non-modifiable: autoimmune/connective-tissue disease, MS/NMOSD/MOGAD, recent viral illness, malignancy.

Data

• Urgent MRI of the spine with and without gadolinium (plus brain) (FIRST to exclude a compressive lesion; then characterizes the cord lesion — T2 hyperintensity and enhancement, and lesion length: a short segment suggests MS, a longitudinally extensive lesion ≥3 segments suggests NMOSD/MOGAD; brain MRI assesses dissemination)

• Lumbar puncture (pleocytosis and elevated protein support inflammation; oligoclonal bands favor MS; cytology, viral PCRs, and infectious studies as indicated)

• Aquaporin-4 (NMO) and MOG antibodies; autoimmune serologies (ANA, anti-Ro/La, ACE, ANCA); B12/copper; HIV, syphilis (RPR); paraneoplastic panel if suspected.

DDx

Compressive myelopathy (abscess, tumor, disc, hematoma — exclude first, surgical) · spinal cord infarction (hyperacute, anterior cord, vascular risk) · MS / NMOSD / MOGAD · Guillain-Barré (peripheral, areflexic, no level) · B12 or copper deficiency (subacute combined degeneration) · dural arteriovenous fistula (stepwise, lower cord) · neoplastic/paraneoplastic myelopathy · radiation myelopathy

Home Meds

• Treat any identified infection; continue or adjust immunosuppression in coordination with the relevant specialty.

• Defer steroids until a compressive lesion is excluded (and avoid steroids in undiagnosed infection without coverage).

Plan

Consults

• Neurology — diagnosis, etiologic workup, immunotherapy.

• Neurosurgery — engaged until a compressive lesion is excluded (and for decompression if found).

• Rheumatology / infectious disease — for systemic autoimmune or infectious causes.

• PT / OT / urology — rehabilitation and bladder management; ICU for high cervical lesions.

Exclude compression first

• Obtain urgent spinal MRI to rule out a compressive cord lesion before treating for inflammation — compression is a neurosurgical emergency with a completely different management pathway (decompression ± steroids).

Immunotherapy (after compression excluded)

• High-dose corticosteroids: methylprednisolone (Solu-Medrol) 1000 mg IV daily for 3–5 days.

• Plasma exchange (PLEX) for severe or steroid-refractory cases — used early in NMOSD-spectrum disease.

Treat the cause / supportive

• Antivirals (acyclovir for VZV/HSV) or antimicrobials for infectious myelitis; disease-specific immunotherapy for NMOSD/autoimmune causes. Bladder management (catheterization for retention), bowel regimen, VTE prophylaxis, meticulous skin/pressure-injury care, aspiration precautions, neuropathic pain control (gabapentin/Neurontin), and spasticity management (baclofen/Lioresal).

Always

• PT / OT eval and treat — early rehabilitation, mobility, ADLs, bladder retraining; rehab disposition planning.

• Trend: motor and sensory level, bladder function, and — for cervical lesions — respiratory status (serial FVC/NIF; the diaphragm is innervated C3–C5).

• Escalation triggers: MRI shows compression → emergent neurosurgery · high cervical lesion with respiratory compromise → ICU, possible intubation · rapidly ascending deficit or autonomic instability → ICU · steroid-refractory/severe → PLEX.

• Discharge checklist: etiology established or a clear pending-workup plan · immunotherapy course completed with maintenance plan (especially NMOSD/MOGAD — long-term immunosuppression) · bladder/bowel and spasticity regimens · inpatient or intensive outpatient rehabilitation referral · neurology (and rheum/ID as relevant) follow-up with repeat imaging · DVT and pressure-injury prevention education · return precautions (ascending weakness, breathing difficulty, worsening level).

Red Flags — Emergency

• Compressive lesion on MRI (abscess, tumor, hematoma, disc) → emergent neurosurgery — not steroids-alone.
• High cervical myelitis with respiratory compromise → ICU, monitor FVC/NIF, intubate as needed.
• Rapidly ascending deficit → ICU monitoring.
• Autonomic instability / neurogenic shock (high lesions) → ICU.
• Longitudinally extensive lesion / severe bilateral optic neuritis → NMOSD; test AQP4/MOG, PLEX early.

Senior IM Resident Pearls

• Image the cord before you call it inflammatory. The first and non-negotiable step is excluding a compressive lesion with an urgent MRI — compression is a surgical emergency and steroids alone would be the wrong treatment.
• Lesion length sorts the demyelinating causes. A short, partial lesion (<3 segments) leans MS; a longitudinally extensive lesion (≥3 segments) leans NMOSD/MOGAD — and that distinction changes both acute and long-term therapy.
• Always send AQP4 and MOG antibodies. NMOSD needs aggressive immunosuppression and early PLEX, and some MS drugs make it worse — don't lump it in with MS.
• Watch the diaphragm in cervical lesions. C3–C5 feeds the phrenic nerve — a high cervical myelitis can cause respiratory failure; trend FVC/NIF.
• Don't forget the treatable infections and deficiencies. VZV/HSV myelitis needs acyclovir; B12 and copper deficiency cause a myelopathy that mimics TM and is reversed by repletion.
• Manage the bladder early. Urinary retention is common and easily missed — check a post-void residual and catheterize to prevent injury.
• PLEX for the severe and refractory. Escalate beyond steroids quickly in fulminant or NMOSD-spectrum myelitis.
• Common mistake: giving high-dose steroids for a presumed inflammatory myelitis before the MRI — and missing an epidural abscess or compressive metastasis that needed the OR.

Neurology — Spinal Cord

Spinal Cord Compression (Cord Syndromes)

surgical emergency · sensory level + weakness + bladder · MRI NOW · steroids if malignant · Super Compact

• Sx: back/neck pain (often first, worse recumbent/at night in malignancy) + bilateral weakness + sensory level + bladder/bowel dysfunction (retention, then incontinence) + saddle anesthesia (cauda equina); UMN signs (hyperreflexia, Babinski) below level; gait difficulty

• Neg: denies areflexia + ascending peripheral pattern (GBS) · denies inflammatory cord lesion w/o structural cause (transverse myelitis — MRI distinguishes) · denies purely vascular hyperacute onset (cord infarct) · denies fatigable/fluctuating (NMJ)

• SHx: known cancer (breast/lung/prostate/myeloma/lymphoma — metastatic epidural), infection/IVDU/recent procedure (epidural abscess), anticoagulation (epidural hematoma), trauma, degenerative spine disease

• Etiology: malignant epidural metastasis (most common atraumatic — vertebral body → epidural) · epidural abscess (fever, IVDU, back pain triad) · epidural hematoma (anticoagulation, post-procedure) · disc herniation/spondylosis · trauma/burst fracture · cord syndromes: central, anterior, Brown-Séquard, cauda equina, conus

• RF: modifiable — anticoagulation, untreated infection · non-mod — malignancy, age, degenerative disease, immunocompromise

• Data: EMERGENT MRI of the WHOLE spine with and without contrast (level, cause, multiple levels) — do not delay · CBC/ESR/CRP/cultures (abscess) · coags (hematoma) · PSA/mammogram/CT C-A-P if malignancy source unknown · post-void residual (retention)

• DDx: transverse myelitis (inflammatory, no compression) · cord infarct (hyperacute) · GBS (peripheral) · B12/copper myelopathy · mechanical back pain (no cord signs) · functional

• Home Meds: reverse anticoagulation if hematoma · hold antithrombotics pre-op · reconcile; analgesia

Plan — surgical emergency (ward/ICU + OR)

• Consults: neurosurgery/spine surgery STAT · radiation oncology (malignant) · oncology · ID (abscess) · neurology · PT/OT/urology

• This is a time-critical emergency — neurologic recovery depends on how fast compression is relieved. MRI and surgical/RT decision NOW; ambulatory status at treatment is the strongest predictor of outcome

• Malignant cord compression: dexamethasone (Decadron) — 10 mg IV load then 4 mg IV/PO q6h (high-dose protocols up to 16 mg/day) — start immediately on suspicion · urgent surgical decompression + stabilization (if candidate) and/or radiation oncology; surgery+RT better than RT alone for selected patients

• Epidural abscess: blood cultures → empiric vancomycin (Vancocin) + ceftriaxone (Rocephin)/cefepime → emergent surgical drainage; do NOT give steroids reflexively

• Epidural hematoma: reverse anticoagulation + emergent decompression

• Supportive: bladder catheter (retention), VTE prophylaxis (mechanical pre-op), pressure care, pain control, spinal precautions if trauma/unstable

• Trend: motor/sensory level, ambulation, bladder, q-shift neuro checks

• → OR emergently for decompression; ICU if high cervical (respiratory) or unstable. Every hour of delay costs recovery

Spinal Cord Compression (Cord Syndromes)

complete reference · the surgical emergency · MRI whole spine · cause-specific Rx · cord syndromes · Full Card

Symptoms / Associated Sx

• Pain (back or neck, frequently the first symptom; in malignant compression it is often worse when recumbent and at night) followed by bilateral weakness, a sensory level, and bladder/bowel dysfunction (urinary retention with overflow, then incontinence; saddle anesthesia and areflexia in cauda equina). Upper-motor-neuron signs below the level (hyperreflexia, spasticity, extensor plantar responses) develop with cord (not cauda equina) lesions. Recognizable cord syndromes: central cord (arms > legs, after hyperextension), anterior cord (motor + spinothalamic loss, dorsal columns spared), Brown-Séquard (ipsilateral motor/proprioception, contralateral pain/temperature), conus medullaris, and cauda equina (LMN, saddle anesthesia, early bladder).

Neg

• Not an ascending areflexic peripheral pattern — argues against GBS (GBS lacks a sensory level and a structural lesion)

• A compressive structural lesion is present on MRI — distinguishes from transverse myelitis (TM is intrinsic cord inflammation without compression; the MRI is the arbiter and is why imaging comes first)

• Onset is not hyperacute/vascular with an anterior-cord pattern alone — argues against cord infarction (though anterior cord compression can mimic it)

• Deficits are fixed and structural, not fatigable — argues against a neuromuscular-junction disorder.

Social History (SHx)

• Known malignancy (breast, lung, prostate, multiple myeloma, lymphoma, renal — the cancers that metastasize to the spine); constitutional symptoms; prior spinal disease.

• Fever, injection drug use, recent spinal procedure/epidural, bacteremia, or immunocompromise (epidural abscess); anticoagulant/antiplatelet use or recent neuraxial procedure (epidural hematoma); trauma.

Main Etiology

• Malignant epidural spinal cord compression (most common non-traumatic cause — vertebral metastasis extending into the epidural space). Spinal epidural abscess (the classic triad of back pain, fever, and neurologic deficit; risk with IVDU, bacteremia, diabetes). Spinal epidural hematoma (anticoagulation, post-procedure). Degenerative (severe disc herniation, spondylotic stenosis). Trauma (fracture/dislocation). The cord syndrome reflects which tracts are compressed.

RF

• Modifiable: anticoagulation, untreated infection/bacteremia, injection drug use.

• Non-modifiable: malignancy, advancing age, degenerative spine disease, immunocompromise.

Data

• Emergent MRI of the entire spine with and without contrast (defines the level, the cause, and detects multiple/skip lesions common in metastatic disease — image the whole spine, not just the symptomatic level; do not delay for other tests)

• CBC, ESR, CRP, blood cultures (epidural abscess); coagulation studies (hematoma)

• If malignancy source unknown: PSA, mammography, CT chest/abdomen/pelvis, and biopsy planning; serum/urine protein electrophoresis for myeloma.

• Post-void residual/bladder scan (retention); CT for bony detail/instability in trauma.

DDx

Transverse myelitis (inflammatory, no compressive lesion) · spinal cord infarction (hyperacute, vascular) · Guillain-Barré (peripheral, areflexic, no level) · B12/copper deficiency myelopathy (subacute, dorsal columns) · mechanical/radicular back pain (no cord signs) · dural AV fistula · functional weakness

Home Meds

• Reverse anticoagulation emergently if an epidural hematoma is the cause; hold antithrombotics in anticipation of surgery.

• Reconcile and provide analgesia; manage the bladder.

Plan

Consults

• Neurosurgery / spine surgery — STAT (decompression and stabilization).

• Radiation oncology and medical oncology — malignant compression.

• Infectious disease — epidural abscess.

• Neurology, PT/OT, urology — co-management, rehab, bladder; ICU for high cervical/unstable.

Time is cord

• This is a neurologic emergency — recovery depends on the speed of decompression, and ambulatory/functional status at the time of treatment is the strongest predictor of outcome. Get the MRI and the surgical/radiation decision immediately; do not wait for morning.

Malignant epidural compression

• Dexamethasone (Decadron) immediately on suspicion — 10 mg IV load then 4 mg IV/PO every 6 hours (higher-dose protocols up to ~16 mg/day for severe deficits), to reduce edema while definitive treatment is arranged.

• Urgent surgical decompression with stabilization (for surgical candidates with a single level, instability, or unknown tissue) and/or radiation therapy; surgery followed by radiation outperforms radiation alone in selected patients (decompressive surgery trial data). Coordinate oncology for systemic therapy.

Epidural abscess

• Blood cultures, then empiric vancomycin (Vancocin) 15–20 mg/kg IV q8–12h + ceftriaxone (Rocephin) 2 g IV q12h or cefepime (cover MRSA and gram-negatives); emergent surgical drainage/decompression. Do not give steroids reflexively in infection.

Epidural hematoma

• Reverse the anticoagulant and proceed to emergent surgical decompression.

Supportive / Always

• Bladder catheterization for retention, bowel regimen, VTE prophylaxis (mechanical pre-operatively, pharmacologic when safe), meticulous pressure-injury prevention, analgesia, and spinal precautions/immobilization if traumatic or unstable.

• PT / OT eval and treat — early mobilization once stabilized, rehabilitation planning (often inpatient rehab).

• Trend: serial motor/sensory exam and level, ambulatory status, bladder function, and (for cervical lesions) respiratory status.

• Escalation triggers: emergent OR for decompression in all causes with progressive deficit · high cervical lesion with respiratory compromise → ICU/intubation · spinal instability → immobilization and urgent stabilization · neurogenic shock (high lesion) → ICU.

• Discharge checklist: cause-specific plan completed (oncologic — RT/systemic therapy and follow-up; infectious — prolonged IV antibiotics via OPAT with ID; surgical — wound and stability follow-up) · bladder/bowel program · VTE prophylaxis · inpatient-rehabilitation referral · spine surgery and relevant specialty follow-up · education on recurrent-compression warning signs · return precautions (new/worsening weakness, numbness, bladder change, fever).

Red Flags — Emergency / OR

• Progressive deficit (weakness, ascending level) → emergent decompression — every hour matters.
• New bladder/bowel dysfunction or saddle anesthesia → cauda equina; emergent MRI and surgery.
• Fever + back pain + neurologic deficit → epidural abscess; cultures, antibiotics, drainage.
• Anticoagulated + acute deficit → epidural hematoma; reverse and decompress.
• High cervical lesion → respiratory failure risk, ICU.
• Loss of ambulation → the prognostic window is closing; treat now.

Senior IM Resident Pearls

• Time is cord — and ambulation is prognosis. The best predictor of walking afterward is whether the patient is walking at treatment. A deficit that is hours old can recover; one that's been dense for a day often won't. Move fast.
• MRI the whole spine, not just the painful spot. Metastatic disease causes skip lesions at multiple levels — missing a second level changes the radiation/surgical plan.
• Steroids first in malignant compression, antibiotics first in abscess. Dexamethasone goes in the moment you suspect malignant cord compression; for an abscess, it's cultures and antibiotics, not reflexive steroids.
• Back pain that's worse lying down or wakes them at night is a malignancy flag — the opposite of mechanical pain, which eases with rest.
• Check a bladder scan. Painless urinary retention with overflow is an easily missed early sign of cord/cauda equina compromise.
• Surgery + radiation beats radiation alone for selected single-level malignant compression with a reasonable prognosis — get spine surgery and rad-onc to the bedside together.
• Reverse the anticoagulant immediately for a suspected epidural hematoma — it's both diagnostic reasoning and the first therapeutic step before the OR.
• Common mistake: admitting "mechanical back pain" with subtle weakness or new urinary symptoms and waiting until morning for the MRI — by then the window may have closed.

Neurology — Vestibular

Vertigo — Central vs Peripheral

the key fork · HINTS beats MRI early · don't miss posterior stroke · Super Compact

• Sx: illusion of movement/spinning; peripheral — intense, episodic, positional, with hearing/tinnitus, fatigable, horizontal nystagmus; central — often milder vertigo but worse gait/imbalance, may be constant, with brainstem/cerebellar signs (diplopia, dysarthria, dysphagia, focal weakness/numbness, ataxia)

• Neg (favor peripheral/benign): denies focal neuro deficit/diplopia/dysarthria · denies inability to stand/walk (severe truncal ataxia = central) · denies new severe headache/neck pain (dissection) · denies vascular risk + sudden constant vertigo · nystagmus not direction-changing/vertical/torsional

• SHx: vascular risk factors (HTN, DM, AF, smoking — central/stroke), prior episodes (BPPV, Ménière, migraine), recent viral illness (vestibular neuritis), hearing loss, head/neck trauma or manipulation (dissection), migraine history

• Etiology: peripheral — BPPV (brief, positional), vestibular neuritis/labyrinthitis (acute, viral, ± hearing), Ménière (recurrent + hearing/tinnitus/fullness) · central — posterior circulation (cerebellar/brainstem) stroke or TIA, vertebral artery dissection, MS, posterior fossa mass, vestibular migraine

• RF: modifiable — vascular risk factors · non-mod — age, AF, prior stroke, migraine

• Data: HINTS exam in AVS (acute continuous vertigo + nystagmus): Head Impulse, Nystagmus, Test of Skew — a central (dangerous) pattern = normal/negative head impulse, direction-changing nystagmus, or skew (HINTS more sensitive than early MRI for posterior stroke) · Dix-Hallpike for BPPV · finger-to-nose/gait/truncal ataxia · audiometry · MRI brain (DWI) + MRA if central suspected (early DWI can miss small posterior strokes)

• DDx: BPPV · vestibular neuritis/labyrinthitis · Ménière · vestibular migraine · posterior circulation stroke/TIA · vertebral dissection · cerebellar hemorrhage/mass · orthostatic/presyncope (not true vertigo)

• Home Meds: limit vestibular suppressants to <48–72h (meclizine — delays compensation); manage vascular risk; reconcile ototoxic drugs

Plan — ward / ED (admit if central suspected)

• Consults: neurology (if central/HINTS concerning) · ENT/audiology (peripheral, hearing loss) · stroke team if posterior stroke

• The whole task is central vs peripheral. In acute continuous vertigo, a properly performed HINTS exam outperforms early MRI for catching posterior stroke — a "benign" HINTS (abnormal head impulse, unidirectional nystagmus, no skew) is reassuring; any central feature → image and admit

• BPPV: Dix-Hallpike positive → Epley canalith repositioning maneuver (treatment); no long-term meds

• Vestibular neuritis/labyrinthitis: short course vestibular suppressant (meclizine/Antivert 25 mg q6h PRN ≤48–72h) + antiemetic; early vestibular rehab; steroids sometimes considered

• Ménière: low-salt diet, diuretic, ENT referral

• Central/posterior stroke: stroke pathway (MRI/MRA, admit, secondary prevention; cerebellar stroke can swell → herniation, neurosurgical watch)

• Vestibular migraine: migraine prevention/abortive

• Trend: nystagmus, gait, focal signs, hearing

• → ICU/NEUROSURG if: cerebellar stroke/hemorrhage with mass effect (posterior fossa swelling → brainstem compression/hydrocephalus), or declining consciousness

Vertigo — Central vs Peripheral

complete reference · the central/peripheral fork · HINTS · Dix-Hallpike/Epley · posterior stroke · Full Card

Symptoms / Associated Sx

• A false sensation of movement (spinning, tilting). Peripheral (inner ear/vestibular nerve): often intense, episodic, positionally triggered, fatigable, accompanied by hearing loss/tinnitus/aural fullness, with horizontal-torsional nystagmus that is unidirectional and suppressed by fixation; the patient can usually walk albeit unsteadily. Central (brainstem/cerebellum): vertigo may be milder but gait/truncal instability is disproportionately severe (unable to stand/walk), often constant, with accompanying brainstem/cerebellar signs — diplopia, dysarthria, dysphagia, facial numbness, limb ataxia, focal weakness — and nystagmus that may be vertical, torsional, or direction-changing and not suppressed by fixation. The dangerous central cause is posterior-circulation stroke; isolated vertigo can occasionally be its only manifestation.

Neg

• No focal neurologic deficit (diplopia, dysarthria, dysphagia, hemisensory/motor signs) — favors a peripheral cause (any such sign points central and mandates imaging)

• The patient can stand and walk (only mild unsteadiness) — favors peripheral (inability to stand/walk unaided is a central red flag — severe truncal ataxia suggests cerebellar pathology)

• No new severe headache or neck pain — argues against vertebral artery dissection or cerebellar hemorrhage (these can present with vertigo plus head/neck pain)

• Nystagmus is unidirectional, horizontal-torsional, and fixation-suppressed (not vertical/direction-changing) — favors peripheral (direction-changing, vertical, or non-suppressible nystagmus is central)

Social History (SHx)

• Vascular risk factors (hypertension, diabetes, atrial fibrillation, smoking, prior stroke — raise concern for central/stroke); migraine history (vestibular migraine).

• Prior similar episodes (BPPV, Ménière), recent viral illness (vestibular neuritis/labyrinthitis), hearing loss/tinnitus, and recent head or neck trauma/chiropractic manipulation (arterial dissection).

Main Etiology

• Peripheral: benign paroxysmal positional vertigo (brief, positional, recurrent — displaced otoconia), vestibular neuritis (acute sustained vertigo after a viral illness, no hearing loss) or labyrinthitis (with hearing loss), and Ménière disease (recurrent vertigo with fluctuating hearing loss, tinnitus, and aural fullness).

• Central: posterior-circulation ischemic stroke or TIA (cerebellar/brainstem), vertebral or basilar artery dissection, cerebellar hemorrhage or mass, multiple sclerosis, and vestibular migraine.

RF

• Modifiable: hypertension, diabetes, atrial fibrillation, smoking, hyperlipidemia (central/vascular).

• Non-modifiable: advancing age, prior stroke, migraine, structural inner-ear disease.

Data

• HINTS exam — in the acute vestibular syndrome (acute, continuous vertigo with nystagmus and gait instability): Head Impulse test, Nystagmus character, Test of Skew. The reassuring (peripheral) pattern is an abnormal (corrective saccade) head impulse, unidirectional nystagmus, and no skew deviation. A central pattern — a normal/negative head impulse, direction-changing nystagmus, or skew deviation — is more sensitive than early MRI-DWI for posterior-circulation stroke. (HINTS is validated for continuous vertigo with nystagmus, not for episodic/positional vertigo.)

• Dix-Hallpike maneuver for BPPV (positional torsional-upbeat nystagmus with latency and fatigability); bedside gait and truncal stability, finger-to-nose for cerebellar signs; audiometry for hearing loss.

• MRI brain with diffusion + MRA when central cause is suspected (note early DWI can miss small posterior-fossa strokes in the first 24–48h — a concerning HINTS or focal sign warrants admission and repeat imaging even if initial MRI is negative)

DDx

BPPV (brief, positional, Dix-Hallpike positive) · vestibular neuritis/labyrinthitis (acute sustained, post-viral, ± hearing loss) · Ménière disease (recurrent + hearing/tinnitus/fullness) · vestibular migraine (migraine history, recurrent) · posterior-circulation stroke/TIA (vascular risk, central HINTS, focal signs) · vertebral artery dissection (neck pain, trauma) · cerebellar hemorrhage/mass (headache, ataxia, mass effect) · presyncope/orthostasis (lightheadedness, not true spinning)

Home Meds

• Limit vestibular suppressants (meclizine, benzodiazepines) to <48–72 hours — prolonged use delays central compensation and recovery.

• Optimize vascular risk-factor medications when a central cause is found; reconcile ototoxic drugs (aminoglycosides, loop diuretics, cisplatin).

Plan

Consults

• Neurology / stroke team — central pattern, concerning HINTS, or focal signs.

• ENT / audiology — peripheral causes, hearing loss, recurrent Ménière.

• Neurosurgery — cerebellar stroke/hemorrhage with mass effect.

Decide central vs peripheral

• The entire task is this fork. In the acute vestibular syndrome, a correctly performed HINTS exam outperforms early MRI for catching posterior stroke. A benign HINTS plus a reassuring exam supports a peripheral cause; any central HINTS feature, focal sign, severe truncal ataxia, or inability to walk → image (MRI/MRA) and admit to a stroke pathway.

Peripheral management

• BPPV: Dix-Hallpike positive → treat with the Epley canalith-repositioning maneuver (definitive); avoid chronic medication.

• Vestibular neuritis/labyrinthitis: short-course vestibular suppressant — meclizine (Antivert) 25 mg PO q6h PRN for ≤48–72h — plus an antiemetic (ondansetron/Zofran); begin vestibular rehabilitation therapy early; corticosteroids are sometimes used.

• Ménière disease: low-sodium diet, a diuretic (e.g. hydrochlorothiazide), and ENT referral; betahistine where available.

Central management

• Posterior-circulation stroke/TIA: enter the stroke pathway (MRI/MRA, admit, antithrombotic and secondary prevention, risk-factor management). Cerebellar infarct or hemorrhage can swell and compress the brainstem or obstruct CSF — monitor closely with neurosurgery on board. Vestibular migraine: migraine abortive/preventive therapy.

Always

• PT / OT eval and treat — vestibular rehabilitation (peripheral) and fall-prevention; gait safety.

• Trend: nystagmus character, gait/truncal stability, any evolving focal signs, hearing; level of consciousness if cerebellar lesion.

• Escalation triggers: cerebellar stroke/hemorrhage with mass effect (worsening headache, vomiting, declining consciousness, new brainstem signs) → ICU, emergent neurosurgery for decompression/EVD · basilar/dissection concern → urgent vascular imaging and stroke intervention.

• Discharge checklist (peripheral): Epley taught/performed and home exercises · vestibular rehab referral · suppressant limited and tapered · ENT/audiology follow-up if hearing loss/recurrent · counseling on benign course and recurrence · return precautions for central features (new focal deficit, severe headache, inability to walk). (Central): stroke secondary-prevention plan and neurology follow-up.

Red Flags — Central / Emergency

• Central HINTS (normal head impulse, direction-changing nystagmus, or skew) → posterior stroke; image and admit.
• Any focal neurologic sign (diplopia, dysarthria, dysphagia, weakness/numbness, limb ataxia) → central.
• Cannot stand or walk unaided (severe truncal ataxia) → cerebellar lesion.
• New severe headache or neck pain → cerebellar hemorrhage or vertebral dissection.
• Cerebellar stroke with swelling (declining consciousness, vomiting) → posterior-fossa herniation/hydrocephalus — neurosurgical emergency.

Senior IM Resident Pearls

• The whole game is central vs peripheral. Everything — history, nystagmus, gait, HINTS — is aimed at not missing a posterior-circulation stroke dressed up as "just vertigo."
• HINTS beats MRI early — but only in the right patient. It's validated for the acute vestibular syndrome (continuous vertigo with nystagmus), where a central pattern is more sensitive than early DWI. Don't apply it to brief positional or episodic vertigo.
• A "benign" head impulse is the scary one. Counterintuitively, a NORMAL head-impulse test in acute continuous vertigo suggests a central cause — the abnormal corrective saccade is the reassuring peripheral finding.
• Watch the gait. If they truly cannot stand or walk, think cerebellum — peripheral vertigo lets you walk, however miserably.
• Early MRI can lie. Small posterior-fossa strokes are missed on DWI in the first 24–48h — a concerning exam trumps a negative scan; admit and re-image.
• Treat BPPV with the Epley, not with meclizine. The repositioning maneuver is curative; suppressants just prolong recovery and don't fix the otoconia.
• Limit the meclizine to a couple of days. Vestibular suppressants delay central compensation — early vestibular rehab works better.
• Common mistake: discharging an "inner ear" patient with vascular risk factors, a normal head impulse, and an inability to walk — that's a cerebellar stroke until proven otherwise.

Neurology — Geriatric / Cognitive

Dementia with Acute Decompensation

baseline dementia + acute change = superimposed delirium · find the cause · protect function · Super Compact

• Sx: a patient with known/probable dementia who acutely worsens — increased confusion, agitation or withdrawal, hallucinations, functional decline, sleep-wake disruption over hours-days; the acute fluctuating change on top of a chronic baseline = delirium superimposed on dementia until proven otherwise

• Neg: denies a purely chronic gradual decline w/o acute change (dementia progression alone) · denies focal deficit/aphasia of sudden onset (stroke) · denies isolated low mood w/ intact attention (depression) · denies seizure activity (ictal/postictal)

• SHx: baseline cognition & function from collateral (essential), dementia type, meds (anticholinergics, benzos, opioids), recent infection/falls, hydration, sensory aids, caregiver/placement

• Etiology (the decompensation is almost always reversible/multifactorial): infection (UTI, pneumonia), drugs (anticholinergic, sedative, opioid, polypharmacy), metabolic (Na, glucose, Ca, uremia), pain, urinary/stool retention, dehydration, hypoxia, new stroke/bleed (esp. subdural after falls), environment change

• RF: modifiable — deliriogenic meds, tethers/restraints, sleep disruption, sensory deprivation, infection · non-mod — underlying dementia (the dominant predisposing factor), age, frailty

• Data: CBC, CMP, glucose, Ca/Mg/Phos, UA/culture, CXR · med review · O2 sat · TSH/B12 (if not done) · ECG · CT head if focal/anticoag/trauma/no cause (subdural after falls) · EEG if ?NCSE · avoid over-testing if a clear cause is found

• DDx: delirium superimposed on dementia (most common) · new stroke/subdural · NCSE · depression (pseudodementia) · medication effect · sundowning (a description, not a cause)

• Home Meds: deprescribe anticholinergics/benzos/sedatives/opioids; continue cholinesterase inhibitor/memantine unless contributing; do NOT abruptly stop chronic benzo/alcohol

Plan — ward

• Consults: geriatrics · neurology if focal/seizure/dx unclear · psychiatry for severe behavioral · PT/OT · social work/case management (disposition)

• Treat it as delirium: find and fix the cause(s) — the acute change is not "just the dementia"

• Non-pharm bundle (first-line): reorient, glasses/hearing aids, day-night lighting, sleep protocol, mobilize, remove tethers (Foley/lines/restraints), family/familiar objects at bedside, hydration/nutrition, bowel/bladder care

• Treat reversibles: antibiotics for infection, correct electrolytes/glucose, O2, relieve retention, control pain (non-opioid first)

• Meds only for dangerous agitation (threat to self/others): low-dose haloperidol (Haldol) 0.25–0.5 mg or quetiapine (Seroquel) 12.5–25 mg, shortest course; avoid benzodiazepines (worsen delirium) except in withdrawal; antipsychotics carry ↑mortality in dementia — use sparingly, document, reassess daily

• Trend: attention/CAM vs baseline, sleep-wake, med list, resolution of cause

• → Escalate if: new focal deficit/declining LOC (image for stroke/subdural), suspected NCSE, sepsis/hemodynamic instability, or agitation uncontrollable and unsafe

Dementia with Acute Decompensation

complete reference · delirium-on-dementia · cause hunt · non-pharm first · antipsychotic caution · Full Card

Symptoms / Associated Sx

• A person with established (or clinically probable) dementia who develops an acute, fluctuating worsening — heightened confusion, new or increased agitation or, just as often, hypoactive withdrawal and somnolence, visual hallucinations, a step-down in function (no longer feeding/toileting as before), and disrupted sleep-wake cycles, over hours to days. This acute change layered on a chronic baseline is delirium superimposed on dementia until proven otherwise — and it signals an underlying medical precipitant, not simply "the dementia getting worse." Dementia is the single strongest risk factor for delirium, so these patients decompensate easily and are often under-recognized (especially the hypoactive form).

Neg

• The change is acute and fluctuating, not a purely chronic gradual slide — argues against attributing it to dementia progression alone (progression is slow and steady over months; an abrupt change demands a search for a cause)

• No sudden focal deficit or aphasia — argues against a new stroke as the explanation (though a strategic stroke or subdural can present as confusion — image if focal, anticoagulated, or post-fall)

• Attention is impaired (not intact with low mood) — argues against depression/pseudodementia (depression preserves attention)

• No witnessed convulsive activity, but failure to return toward baseline → consider non-convulsive status (EEG)

Social History (SHx)

• Baseline cognition and function from collateral (family, facility, prior notes) is essential — you cannot grade an acute change without the baseline. Type of dementia (Alzheimer, vascular, Lewy body — the last is exquisitely antipsychotic-sensitive).

• Medication list (anticholinergics, benzodiazepines, opioids, polypharmacy), recent infections or falls, hydration and intake, sensory aids (glasses/hearing aids), alcohol use, and caregiver/placement situation for disposition planning.

Main Etiology

• The decompensation is almost always a reversible, often multifactorial precipitant: infection (urinary tract, pneumonia — frequently presenting only as confusion in elders), medications (anticholinergics, sedative-hypnotics, opioids, recent additions), metabolic derangement (hyponatremia, hypo-/hyperglycemia, hypercalcemia, uremia), uncontrolled pain, urinary or stool retention, dehydration, hypoxia/hypercapnia, a new intracranial event (ischemic stroke or — after a fall — subdural hematoma), and environmental change (hospitalization itself, sleep disruption, restraints).

RF

• Modifiable: deliriogenic medications, physical tethers/restraints, sleep deprivation, sensory deprivation, untreated pain/infection, dehydration, immobility.

• Non-modifiable: underlying dementia (dominant predisposing factor), advanced age, frailty, multiple comorbidities, prior delirium.

Data

• CBC, CMP (electrolytes, renal, glucose, LFTs), calcium, magnesium, phosphate, urinalysis + culture, chest X-ray (infection and metabolic causes — the highest yield)

• Thorough medication reconciliation (the most common reversible contributor); pulse oximetry/ABG; TSH and B12 if not recently checked; ECG/troponin if cardiac suspicion.

• Non-contrast head CT if focal deficit, anticoagulation, head trauma/recent fall, depressed consciousness, or no cause found (subdural hematoma is a classic post-fall miss in the elderly on antiplatelets/anticoagulants)

• EEG if non-convulsive status is suspected (not returning to baseline); avoid over-investigation once a sufficient precipitant is identified.

DDx

Delirium superimposed on dementia (most common — find the precipitant) · new ischemic stroke or subdural hematoma (focal signs, post-fall, anticoagulated) · non-convulsive status epilepticus (EEG) · depression/pseudodementia (attention intact) · medication toxicity (anticholinergic burden) · rapid dementia progression or a new dementia subtype (diagnosis of exclusion)

Home Meds

• Deprescribe anticholinergics (diphenhydramine, oxybutynin), benzodiazepines, sedative-hypnotics, opioids where feasible, and other high-anticholinergic-burden drugs.

• Continue cholinesterase inhibitors (donepezil/Aricept) and memantine (Namenda) unless implicated; do not abruptly withdraw chronic benzodiazepines or alcohol (precipitates withdrawal).

Plan

Consults

• Geriatrics — delirium management, deprescribing, goals of care.

• Neurology — focal signs, suspected seizure, or diagnostic uncertainty.

• Psychiatry — severe or refractory behavioral disturbance.

• PT / OT and social work/case management — function, safety, and disposition.

Find and treat the cause

• Treat this as delirium — the acute change is a symptom of an underlying precipitant. Systematically address each contributor (infection, drugs, metabolic, pain, retention, hypoxia, intracranial event). The workup is the treatment.

Non-pharmacologic bundle (first-line)

• Reorientation, restore glasses/hearing aids, day-night lighting and sleep promotion (cluster care, minimize nocturnal disturbances), early mobilization, remove tethers (Foley, lines, telemetry, restraints) as soon as possible, family presence and familiar objects, ensure hydration/nutrition, regular bowel/bladder routines. These reduce delirium severity and duration; medications do not.

Pharmacologic — only for dangerous agitation

• Reserve antipsychotics for agitation threatening safety or essential care that cannot be redirected. Low-dose haloperidol (Haldol) 0.25–0.5 mg PO/IM (watch QTc, extrapyramidal effects) or quetiapine (Seroquel) 12.5–25 mg PO (preferred in Lewy body/Parkinson's). Lowest dose, shortest duration, reassess daily. Antipsychotics carry an increased mortality risk in dementia (black-box warning) — document the indication and discuss with family. Avoid benzodiazepines (worsen delirium) except for alcohol/benzodiazepine withdrawal.

Always

• PT / OT eval and treat — mobilize, prevent deconditioning and falls, assess function for disposition.

• Trend: attention/CAM against the documented baseline, sleep-wake pattern, medication list, and resolution of the precipitant.

• Escalation triggers: new focal deficit or declining consciousness → CT for stroke/subdural · failure to improve/return toward baseline → EEG for NCSE, broaden workup · sepsis or hemodynamic instability → ICU · agitation uncontrollable and unsafe despite measures → closer monitoring.

• Discharge checklist: deprescribed medication list with deliriogenic drugs removed/flagged · precipitant treated and documented · baseline vs current cognition recorded (delirium can take weeks to resolve and may not fully return in dementia) · caregiver education on delirium, recurrence risk, and sensory aids · goals-of-care/advance-directive discussion where appropriate · geriatrics/PCP follow-up · safe disposition (home with support vs facility) · return precautions.

Red Flags — Don't Miss

• Subdural hematoma after a fall in an anticoagulated/antiplatelet elder presenting as worsening confusion → CT head.
• Occult infection/sepsis presenting only as delirium → full septic workup.
• Hypoactive delirium — the quiet, withdrawn patient is missed and does worse.
• Non-convulsive status epilepticus if not returning to baseline → EEG.
• Lewy body dementia — severe antipsychotic sensitivity; avoid/minimize, use quetiapine if needed.
• Withdrawal (alcohol/benzo) — treat with benzodiazepines, not antipsychotics.

Senior IM Resident Pearls

• "It's just their dementia" is the trap. An acute change in a demented patient is delirium with a cause until proven otherwise — look for the infection, drug, or metabolic trigger every time.
• Get the baseline from collateral. Without knowing prior cognition and function you can't recognize the acute delta or set realistic goals.
• Check the bladder and the med list before reaching for sedation. Urinary retention, constipation, and anticholinergic burden are common, fixable, and frequently overlooked.
• Image after a fall. A subdural can simmer for days — a confused, anticoagulated elder who fell needs a head CT.
• Antipsychotics are a last resort with a mortality warning. Use the smallest dose for the shortest time, only for dangerous agitation, and document the discussion — they don't treat delirium.
• Benzodiazepines worsen it — except in withdrawal. Don't reach for lorazepam to "settle" a confused demented patient.
• Mind Lewy body disease. Visual hallucinations, fluctuations, and parkinsonism plus antipsychotic sensitivity — haloperidol can be dangerous; favor quetiapine.
• Common mistake: discharging before the delirium clears and without a deprescribing plan — recurrence and readmission are high, and the new sedating med you started is often the culprit.

Neurology — Geriatric / General

Falls with Neuro Evaluation

syncope vs mechanical vs neuro · find why · screen for injury (subdural/C-spine) · prevent the next · Super Compact

• Sx: a fall — characterize it: preceding symptoms (lightheaded, palpitations, aura, vertigo), loss of consciousness (syncope vs mechanical trip), post-event confusion (seizure), witnessed account; screen for injury (head strike, neck pain, hip); recurrent falls; gait/balance on exam

• Neg: denies LOC + rapid recovery (favors mechanical over syncope/seizure) · denies post-ictal confusion/tongue-bite/incontinence (seizure) · denies focal deficit/aphasia (stroke) · denies true spinning vertigo (vestibular) · denies exertional/cardiac prodrome (cardiac syncope)

• SHx: prior falls, meds (antihypertensives, sedatives, hypoglycemics, anticoagulants, polypharmacy), alcohol, vision/hearing, footwear/home hazards, cognition, frailty, devices used

• Etiology (usually multifactorial): mechanical/environmental (trip, weakness, gait/balance) · syncope (orthostatic, cardiac/arrhythmia, vasovagal) · neuro (stroke/TIA, seizure, parkinsonism, peripheral neuropathy, vestibular/vertigo, normal-pressure hydrocephalus, myelopathy) · meds/polypharmacy · deconditioning

• RF: modifiable — psychoactive/BP meds, orthostasis, vision, vitamin D, home hazards, footwear · non-mod — age, prior falls, cognitive impairment, parkinsonism, neuropathy

• Data: orthostatic vitals, ECG, glucose, CBC/CMP, vit D · medication review · gait & balance exam (Timed Up-and-Go), neuro exam · CT head if head strike/anticoag/LOC/focal/confusion (subdural) · C-spine imaging if neck pain/LOC/high-risk · echo/telemetry if cardiac syncope · MRI brain/spine if focal/myelopathy/NPH

• DDx: mechanical/multifactorial fall (most) · syncope (cardiac/orthostatic/vasovagal) · seizure · stroke/TIA · parkinsonism · neuropathy/myelopathy · vestibular/vertigo · NPH (gait + cognition + incontinence)

• Home Meds: reduce fall-risk-increasing drugs (FRIDs) — sedatives, benzos, antipsychotics, opioids, antihypertensives causing orthostasis, hypoglycemics; review anticoagulation risk/benefit

Plan — ward or observation

• Consults: PT/OT (gait, balance, home safety) · neurology if focal/seizure/parkinsonism/myelopathy · cardiology if cardiac syncope · geriatrics · pharmacy (deprescribing)

• Two jobs: (1) screen for and treat injury, (2) determine WHY they fell — don't stop at "mechanical fall"

• Injury screen: CT head if head trauma/anticoag/LOC/confusion (subdural), C-spine imaging if neck pain/distracting injury, hip/long-bone films as indicated

• Determine mechanism: orthostatic vitals, ECG/telemetry (arrhythmia), neuro and gait exam; target imaging/echo by clues

• Treat reversible contributors: deprescribe FRIDs, correct orthostasis (fluids, med adjustment), treat arrhythmia, optimize vision, replace vitamin D, treat neuropathy/parkinsonism

• Prevent the next fall: PT for strength/balance/gait aids, OT home-hazard assessment, footwear, bone health (DEXA, calcium/vit D, osteoporosis Rx)

• Trend: orthostatics, gait, neuro exam, telemetry

• → Escalate if: focal deficit/declining LOC (stroke/expanding subdural → CT, neurosurgery), high-risk cardiac syncope (admit/telemetry), C-spine injury, or unexplained recurrent syncope

Falls with Neuro Evaluation

complete reference · syncope vs mechanical vs neuro · injury screen · multifactorial prevention · Full Card

Symptoms / Associated Sx

• The history is the diagnosis: characterize the fall — what was the patient doing, were there preceding symptoms (lightheadedness or palpitations → cardiac/orthostatic; aura, then post-event confusion/tongue-biting/incontinence → seizure; spinning → vestibular; none, with a clear trip → mechanical), was there loss of consciousness, and what does a witness describe. Then screen for the consequences — head strike, neck pain, hip/limb injury — and examine gait, balance, strength, and the neurologic exam. Recurrent falls and fear of falling are themselves important. The cause is usually multifactorial, especially in older adults.

Neg

• No loss of consciousness with a clear environmental trigger and rapid recovery — favors a mechanical/multifactorial fall (LOC redirects toward syncope or seizure)

• No post-event confusion, tongue-biting, or incontinence — argues against seizure (a true post-ictal state and lateral tongue-bite point to seizure)

• No focal deficit or aphasia — argues against stroke/TIA as the cause (focal signs mandate stroke workup and imaging)

• No exertional onset or cardiac prodrome (palpitations, chest pain) — lowers concern for dangerous cardiac syncope (exertional or sudden LOC without warning is a red flag for arrhythmia/structural heart disease)

Social History (SHx)

• Prior falls (the strongest predictor of future falls), medications (antihypertensives, sedatives/benzodiazepines, antipsychotics, opioids, hypoglycemics, anticoagulants, polypharmacy), alcohol use.

• Vision and hearing, footwear, home hazards (rugs, lighting, stairs, bathroom), assistive-device use, cognitive status, frailty, and continence.

Main Etiology

• Usually multifactorial. Mechanical/environmental (trips, lower-extremity weakness, gait/balance impairment). Syncope — orthostatic hypotension (volume depletion, autonomic failure, medications), cardiac (arrhythmia, structural — the dangerous kind), or reflex/vasovagal. Neurologic — stroke/TIA, seizure, parkinsonism and other movement disorders, peripheral neuropathy (proprioceptive loss), vestibular disease/vertigo, cervical myelopathy, normal-pressure hydrocephalus (gait apraxia + cognitive decline + incontinence). Medication side effects and deconditioning compound all of these.

RF

• Modifiable: fall-risk-increasing drugs (sedatives, antihypertensives causing orthostasis, hypoglycemics), orthostatic hypotension, visual impairment, vitamin D deficiency, environmental hazards, poor footwear, deconditioning.

• Non-modifiable: advanced age, prior falls, cognitive impairment, parkinsonism, peripheral neuropathy, frailty.

Data

• Orthostatic vital signs, 12-lead ECG, point-of-care glucose, CBC, CMP, vitamin D (orthostasis, arrhythmia/conduction disease, hypoglycemia, anemia, electrolyte and renal contributors)

• Full medication review; bedside gait and balance assessment (Timed Up-and-Go, gait observation) and a focused neurologic exam.

• Non-contrast head CT if head strike, anticoagulation/antiplatelet, loss of consciousness, focal deficit, or new confusion (traumatic/subdural hemorrhage); cervical-spine imaging if neck pain, LOC, a distracting injury, or high-risk criteria.

• Telemetry/echocardiography if cardiac syncope is suspected; MRI brain/spine if focal signs, suspected myelopathy, or NPH; consider EEG if seizure suspected.

DDx

Mechanical/multifactorial fall (most common; gait, weakness, environment) · syncope (cardiac/arrhythmic — dangerous; orthostatic; vasovagal) · seizure (aura, post-ictal, tongue-bite) · stroke/TIA (focal deficit) · parkinsonism (rigidity, bradykinesia, postural instability) · peripheral neuropathy/myelopathy (sensory ataxia, UMN signs) · vestibular/vertigo · normal-pressure hydrocephalus (gait + cognition + incontinence)

Home Meds

• Reduce fall-risk-increasing drugs (FRIDs): taper/stop benzodiazepines, sedative-hypnotics, antipsychotics, and opioids; adjust antihypertensives causing orthostasis; review hypoglycemic regimens.

• Reassess anticoagulation — balance fall-related bleeding risk against the indication (falls alone rarely outweigh a strong anticoagulation indication, but the head-injury risk must be weighed and discussed).

Plan

Consults

• PT / OT — gait and balance training, assistive devices, home-safety/hazard assessment.

• Neurology — focal deficit, suspected seizure, parkinsonism, myelopathy, or NPH.

• Cardiology — suspected cardiac/arrhythmic syncope.

• Geriatrics and pharmacy — multifactorial assessment and deprescribing.

Two parallel jobs

• (1) Screen for and treat injury — head CT for trauma/anticoagulation/LOC/confusion (subdural), C-spine imaging for neck pain or high-risk mechanism, fracture evaluation (hip, wrist, ribs). (2) Determine why they fell — do not stop at "mechanical fall"; orthostatic vitals, ECG/telemetry, neuro and gait exam, with targeted imaging/echo driven by the clues.

Treat reversible contributors

• Deprescribe FRIDs; correct orthostatic hypotension (hydration, medication adjustment, compression, and—if needed—midodrine/fludrocortisone for autonomic failure); treat arrhythmia (cardiology, possible pacing); optimize vision; replace vitamin D; manage neuropathy, parkinsonism, or vestibular disease; treat NPH (neurosurgical shunt evaluation if the triad and imaging fit).

Prevent the next fall

• Structured PT for strength, balance, and gait with appropriate aids; OT home-hazard modification (lighting, grab bars, remove rugs); proper footwear; and bone-health optimization — DEXA, calcium and vitamin D, and osteoporosis pharmacotherapy (e.g. bisphosphonate) to reduce future fracture, since the fracture is often what changes the trajectory.

Always

• PT / OT eval and treat — central to both diagnosis and prevention; arrange the right level of rehab/disposition.

• Trend: orthostatic vitals, telemetry, gait/balance, and the neurologic exam; response to deprescribing and to treating the identified mechanism.

• Escalation triggers: focal deficit or declining consciousness → CT for stroke/expanding subdural, neurosurgery · high-risk cardiac syncope (exertional, structural heart disease, abnormal ECG) → admit, telemetry, cardiology · cervical-spine injury → immobilize, spine service · unexplained recurrent syncope → extended monitoring.

• Discharge checklist: documented fall mechanism and contributors · deprescribed FRID list · orthostatic/cardiac causes addressed · PT/OT and home-safety plan in place · bone-health workup and treatment initiated · vision and footwear addressed · caregiver education and a personal-emergency-response plan · PCP/geriatrics follow-up · return precautions (head injury symptoms, recurrent falls, syncope).

Red Flags — Urgent

• Head strike on anticoagulation/antiplatelet or new confusion/focal deficit → CT head for subdural/traumatic hemorrhage; expanding bleed → neurosurgery.
• Syncope with exertional onset, no prodrome, abnormal ECG, or structural heart disease → dangerous cardiac cause; admit and monitor.
• Neck pain or high-risk mechanism → C-spine injury; immobilize and image.
• Focal neurologic deficit → stroke workup.
• Recurrent unexplained falls/syncope → extended cardiac monitoring; don't discharge as "mechanical."

Senior IM Resident Pearls

• "Mechanical fall" is a description, not a diagnosis. Always ask why — orthostasis, an arrhythmia, a new med, a stroke, or a neuropathy is often hiding behind it.
• The history sorts it out: prodrome and LOC point to syncope; post-ictal confusion and tongue-bite to seizure; a clear trip with no LOC to mechanical. Get the witness account.
• Two jobs every time: screen for injury (head, C-spine, hip) and find the mechanism. Missing the subdural in an anticoagulated elder who hit their head is the classic error.
• Check orthostatics and an ECG on essentially everyone. They're cheap and catch the two most actionable causes — orthostatic hypotension and arrhythmia.
• Deprescribing is the highest-yield intervention. Sedatives, antihypertensives causing orthostasis, and hypoglycemics drive falls — cutting them prevents the next one.
• Don't forget the bones. The fracture, not the fall, often ends independence — start vitamin D, calcium, a DEXA, and osteoporosis treatment.
• Think NPH when gait disturbance, cognitive decline, and incontinence cluster — it's a treatable cause of falls.
• Common mistake: discharging after treating the laceration without ever establishing why the patient fell or doing anything to prevent the next one — recurrence and injury are high.

Neurology — General Neuro

Acute Weakness Workup

localize before you label · UMN vs LMN vs NMJ vs muscle · don't miss stroke/cord/GBS · Super Compact

• Sx: new weakness — define distribution (one limb, one side, both legs, all four, proximal vs distal, face involved?), tempo (sudden = vascular; hours-days = inflammatory/compressive; subacute), and associated signs (sensory level, reflexes, tone, fatigability, pain, sphincter, bulbar/respiratory)

• Neg: denies true power loss (vs fatigue/pain-limited/give-way) · denies fluctuating fatigable pattern (NMJ) · denies sensory level + sphincter loss when not cord · denies areflexic ascending pattern when not GBS · inconsistent/non-anatomic exam (functional)

• SHx: vascular risk (stroke), trauma/cancer/anticoag (cord), recent infection (GBS), known MG, statins/alcohol/thyroid (myopathy), family history, toxins/meds

• Localize (the core step): UMN (cortex/cord — spastic, hyperreflexia, ↑tone, Babinski) · LMN (anterior horn/root/nerve — flaccid, areflexia, atrophy, fasciculations) · NMJ (fatigable, normal sensation/reflexes) · muscle (proximal, symmetric, ↑CK, normal sensation)

• RF: modifiable — vascular risk, statins, alcohol, thyroid, electrolytes · non-mod — age, hereditary, malignancy, autoimmune

• Data (guided by localization): glucose, electrolytes (K, Ca, Mg, Phos), CK, TSH, CBC/CMP · stroke → urgent CT/CTA + MRI · cord signs → urgent spine MRI · GBS → LP + NCS/EMG, FVC/NIF · NMJ → AChR/MuSK Ab, EMG · myopathy → CK, EMG, ± biopsy

• DDx by localization: stroke/TIA (UMN, sudden, one side) · cord compression/myelitis (UMN, level, sphincter) · GBS (LMN, ascending, areflexic) · MG (NMJ, fatigable) · myopathy/periodic paralysis (proximal, K+) · radiculopathy/plexopathy · functional

• Home Meds: review statins/steroids/diuretics (↓K), MG-worsening drugs; correct electrolytes; hold contributors

Plan — depends on localization & tempo

• Consults: neurology · stroke team if acute focal · neurosurgery if cord · ICU if respiratory/bulbar (GBS/MG)

• First triage the time-critical localizations: sudden focal/one-sided → stroke pathway (NIHSS, urgent CT/CTA, tPA/thrombectomy window); sensory level + sphincter → urgent spine MRI for cord compression; ascending areflexic → GBS (FVC/NIF, IVIG/PLEX)

• Localize with a structured exam (tone, power, reflexes, sensation, fatigability, distribution) before broad testing

• Check the immediate reversibles: glucose, potassium (periodic paralysis), calcium/magnesium, sodium

• Then targeted workup & treat by cause: stroke (reperfusion/secondary prevention), cord (steroids/decompression per cause), GBS (IVIG/PLEX, no steroids), MG (IVIG/PLEX), myopathy (treat cause, stop offending drug, steroids if inflammatory)

• Trend: serial strength/reflexes, sensory level, FVC/NIF if neuromuscular, electrolytes

• → ICU/urgent if: acute stroke in treatment window, cord compression (decompress), falling FVC/NIF (GBS/MG), or bulbar weakness/aspiration

Acute Weakness Workup

complete reference · localize (UMN/LMN/NMJ/muscle) · triage emergencies · targeted testing · Full Card

Symptoms / Associated Sx

• "Weakness" must first be confirmed as true loss of power (versus fatigue, pain-limited effort, or give-way), then characterized on three axes: distribution (monoparesis, hemiparesis, paraparesis, quadriparesis; proximal vs distal; facial/bulbar involvement), tempo (sudden/seconds-minutes suggests vascular; hours-to-days suggests inflammatory, compressive, or metabolic; subacute-chronic suggests degenerative/neoplastic), and accompanying signs (sensory level, reflex changes, tone, fatigability, pain, sphincter dysfunction, respiratory or bulbar compromise). These three axes, plus the exam, localize the lesion — which is the entire game.

Neg

• There is genuine reduced power, not fatigue or pain-limited/give-way effort — confirms true weakness (give-way or inconsistent effort with a non-anatomic distribution suggests a functional or pain-limited process)

• Weakness is not fatigable/fluctuating with normal sensation and reflexes — argues against a neuromuscular-junction disorder (MG fatigues, spares sensation/reflexes)

• No sensory level or sphincter dysfunction (when the picture isn't cord) — argues against myelopathy (a level/sphincter loss is the cord until imaged)

• Exam findings are internally consistent and anatomically coherent — argues against a functional neurologic disorder (Hoover sign and distractibility help, but functional is a diagnosis made on positive signs, not by exclusion alone)

Social History (SHx)

• Vascular risk factors (stroke), trauma/malignancy/anticoagulation (cord compression/hemorrhage), recent infection (GBS), known myasthenia gravis, statin/alcohol/thyroid disease (myopathy).

• Family history (hereditary myopathy/neuropathy, periodic paralysis), toxin/medication exposures, and the functional baseline.

Main Etiology — organized by localization

• Upper motor neuron (brain or spinal cord): ischemic/hemorrhagic stroke, cord compression, transverse myelitis, MS, mass. Signs: spasticity, hyperreflexia, increased tone, upgoing toes; a sensory level localizes to the cord.

• Lower motor neuron (anterior horn cell, root, plexus, peripheral nerve): GBS, radiculopathy, plexopathy, motor neuron disease, neuropathy. Signs: flaccidity, hyporeflexia/areflexia, atrophy, fasciculations.

• Neuromuscular junction: myasthenia gravis (fatigable), Lambert-Eaton, botulism. Normal sensation, fatigability the hallmark.

• Muscle: inflammatory myopathy, statin/toxic myopathy, metabolic/electrolyte (hypokalemic periodic paralysis), endocrine (thyroid). Proximal, symmetric, often elevated CK, normal sensation and reflexes.

RF

• Modifiable: vascular risk factors, statins and other myotoxic drugs, alcohol, thyroid disease, electrolyte derangements.

• Non-modifiable: age, hereditary neuromuscular disease, malignancy, autoimmune disease.

Data

• Immediate, broadly useful: point-of-care glucose, electrolytes (potassium, calcium, magnesium, phosphate, sodium), CK, TSH, CBC, CMP (catch reversible metabolic causes — hypokalemic paralysis, hypoglycemia, severe electrolyte shifts — fast)

• Localization-driven imaging/tests: sudden focal/hemiparesis → urgent non-contrast CT + CTA (then MRI) on the stroke pathway; UMN signs with a sensory level/sphincter loss → urgent spine MRI for cord compression; ascending areflexic weakness → LP (albuminocytologic dissociation) + NCS/EMG and serial FVC/NIF for GBS.

• NMJ: anti-AChR/anti-MuSK antibodies, repetitive nerve stimulation/EMG. Muscle: CK, EMG, inflammatory markers, ± muscle biopsy and myositis antibodies. Brain MRI for central lesions.

DDx (by localization)

Stroke/TIA (UMN, sudden, often hemibody) · cord compression/transverse myelitis (UMN, sensory level, sphincter) · Guillain-Barré (LMN, ascending, areflexic) · myasthenia gravis (NMJ, fatigable) · myopathy / hypokalemic periodic paralysis (proximal, ↑CK or K shift) · radiculopathy/plexopathy (root/limb pattern) · functional weakness (positive signs, non-anatomic)

Home Meds

• Review statins and other myotoxic agents (myopathy), diuretics/laxatives and other causes of hypokalemia, and MG-worsening drugs.

• Correct electrolyte derangements and hold contributors; reconcile anticoagulation in the context of possible hemorrhage.

Plan

Consults

• Neurology — localization and directing the targeted workup.

• Stroke team — acute focal/hemibody weakness within a treatment window.

• Neurosurgery — cord compression.

• ICU / pulmonary — respiratory or bulbar involvement (GBS, myasthenic crisis).

Triage the time-critical localizations first

• Sudden focal/one-sided weakness → stroke pathway (NIHSS, urgent non-contrast CT/CTA, assess tPA/thrombectomy eligibility). UMN signs with a sensory level or sphincter loss → urgent spine MRI for cord compression (a surgical emergency). Ascending areflexic weakness → GBS (serial FVC/NIF, IVIG or PLEX). These three cannot wait for a leisurely workup.

Localize, then test

• Perform a structured exam (tone, power, reflexes, sensation, fatigability, distribution, sphincter, bulbar/respiratory) to place the lesion (UMN / LMN / NMJ / muscle) before ordering broad tests — localization dictates which imaging and labs are actually useful.

Reversibles and cause-directed treatment

• Check and correct the immediate metabolic causes (glucose, potassium — including hypokalemic periodic paralysis, calcium, magnesium, sodium). Then treat by cause: stroke (reperfusion and secondary prevention), cord compression (high-dose steroids for cord/neoplastic edema and urgent decompression/RT per etiology), GBS (IVIG or PLEX, no steroids), myasthenic crisis (IVIG or PLEX), inflammatory myopathy (corticosteroids), statin/toxic myopathy (stop the drug).

Always

• PT / OT eval and treat — strengthening, mobility aids, safety; intensive rehab as appropriate to the cause.

• Trend: serial strength and reflexes, sensory level (if cord), FVC/NIF (if neuromuscular), and electrolytes; response to cause-directed therapy.

• Escalation triggers: acute stroke within the treatment window → reperfusion, stroke unit · cord compression → emergent neurosurgery/RT · falling FVC/NIF (GBS/MG) → ICU, airway · bulbar weakness/aspiration → airway protection.

• Discharge checklist: established localization and diagnosis · cause-specific treatment in place · electrolyte/medication contributors corrected · rehabilitation referral appropriate to deficit · relevant specialty follow-up (neurology, stroke, neuromuscular) · pending studies (EMG, antibodies, MRI) followed up · return precautions (worsening or spreading weakness, breathing/swallowing difficulty, new focal deficit).

Red Flags — Urgent

• Sudden focal/hemibody weakness → acute stroke; CT/CTA now, assess reperfusion window.
• Sensory level + sphincter dysfunction → cord compression; urgent spine MRI, neurosurgery, steroids if neoplastic.
• Ascending areflexic weakness with falling FVC/NIF → GBS; ICU, IVIG/PLEX.
• Fatigable weakness with bulbar/respiratory involvement → myasthenic crisis; ICU.
• Profound weakness with abnormal potassium → periodic paralysis or severe electrolyte derangement; correct and monitor cardiac rhythm.

Senior IM Resident Pearls

• Localize before you label. "Weakness" is not a diagnosis — UMN vs LMN vs NMJ vs muscle is the decision that drives every subsequent test. Tone, reflexes, distribution, fatigability, and a sensory level do most of the work.
• Three emergencies live in this complaint: stroke, cord compression, and GBS. Triage for them first — each has a time-critical intervention.
• A sensory level means the cord. It is an MRI-now, surgical-emergency finding — don't let it sit in a general "weakness" workup.
• Check a potassium. Hypo- and hyperkalemic periodic paralysis and severe electrolyte shifts cause dramatic, reversible weakness — and the potassium is also a cardiac issue.
• Tempo is a clue: seconds-to-minutes is vascular; hours-to-days is inflammatory/compressive; weeks-plus is degenerative/neoplastic.
• Fatigability points to the NMJ. Weakness that worsens with repetition and spares sensation/reflexes is myasthenia until proven otherwise — and check the FVC.
• Proximal + high CK + normal sensation = muscle. Think statin/toxic, inflammatory, or endocrine myopathy; stop the offending drug.
• Common mistake: ordering a brain MRI for everything before localizing — a low potassium, a cord lesion, or a neuromuscular cause gets missed while waiting for the wrong scan.

Neurology — General Neuro

Acute Vision Changes / Diplopia

monocular vs binocular · localize the lesion · don't miss GCA, stroke, ICP, aneurysm · Super Compact

• Sx: vision loss (transient vs persistent, monocular vs hemifield) or diplopia — first ask monocular (resolves covering affected eye = ocular/refractive) vs binocular (resolves covering either eye = ocular misalignment, neuro); characterize CN III/IV/VI palsy, pain, pupil involvement, associated neuro signs

• Neg: diplopia resolves with one eye covered → binocular (neuro) vs persists monocular (lens/cornea/retina) · denies eye pain + ↓color/APD (optic neuritis) · denies jaw claudication/scalp tenderness/age >50 (GCA) · denies headache + transient visual obscurations (↑ICP) · denies thunderclap/painful CN III (aneurysm)

• SHx: vascular risk, age >50 + GCA symptoms, MS history, diabetes (microvascular palsy), thyroid eye disease, trauma, anticoagulation, prior similar episodes

• Etiology: monocular vision loss — GCA, central/branch retinal artery or vein occlusion, optic neuritis, retinal detachment, amaurosis fugax (carotid) · binocular field loss — stroke (PCA/occipital), chiasmal/retrochiasmal lesion · diplopia — CN III/IV/VI palsy (microvascular, aneurysm, ↑ICP), MG, thyroid eye, brainstem stroke, INO (MS)

• RF: modifiable — vascular risk, diabetes · non-mod — age (GCA), MS, aneurysm, thyroid disease

• Data: visual acuity, fields, pupils (APD), fundoscopy, EOM · ESR/CRP urgently if GCA suspected (+ temporal artery biopsy) · MRI brain/orbits (optic neuritis, stroke, lesion) · CTA/MRA if pupil-involving CN III (posterior communicating aneurysm) · glucose/A1c, AChR Ab if fatigable, TFTs, carotid imaging if amaurosis

• DDx: GCA (age >50, can't-miss) · retinal artery/vein occlusion · optic neuritis (MS) · pituitary/chiasm lesion (bitemporal) · occipital stroke (homonymous) · CN palsy (microvascular vs aneurysm vs ICP) · MG (fatigable, pupil-sparing) · INO

• Home Meds: review anticoagulation; if GCA suspected do NOT delay steroids for biopsy; reconcile diabetes meds

Plan — depends on cause; some are emergencies

• Consults: ophthalmology (urgent) · neurology · neurosurgery/neuro-IR if aneurysm · rheumatology if GCA · stroke team if retrochiasmal/stroke

• Triage the emergencies: GCA → start high-dose steroids NOW (before biopsy) to save the other eye; retinal artery occlusion → emergent ophtho (stroke equivalent, vascular workup); pupil-involving CN III → urgent CTA/MRA for aneurysm; acute field loss → stroke pathway

• Monocular vs binocular first (cover test) — directs the entire workup

• GCA: prednisone 40–60 mg PO daily (or IV methylprednisolone if vision loss) immediately; ESR/CRP; temporal artery biopsy within ~1–2 weeks (steroids won't quickly change histology)

• Optic neuritis: MRI brain/orbits; IV methylprednisolone 1 g/day ×3–5 days (speeds recovery; assess MS risk — ONTT)

• Microvascular CN palsy (pupil-sparing III, or IV/VI, vascular risk): usually self-limited — control vascular risk, observe, image if not resolving or atypical

• Trend: acuity, fields, diplopia, pupil, response to therapy

• → Urgent/ICU if: GCA with vision loss (sight-threatening), pupil-involving CN III (aneurysm — rupture risk), acute stroke in window, or ↑ICP with papilledema

Acute Vision Changes / Diplopia

complete reference · monocular vs binocular · localize · GCA/stroke/aneurysm/ICP · Full Card

Symptoms / Associated Sx

• Two broad complaints: vision loss (clarify transient vs persistent, monocular vs a hemifield defect, painful vs painless) and diplopia. The single most useful question for diplopia is monocular vs binocular: cover one eye — if double vision resolves with either eye covered, it is binocular (ocular misalignment — a cranial-nerve palsy, neuromuscular-junction, or restrictive cause, i.e. the neurologic territory); if it persists with the affected eye open and the other covered, it is monocular (a lens, cornea, or retinal/refractive problem — ophthalmologic). Characterize any cranial nerve III/IV/VI pattern, pupil involvement, pain, ptosis, fatigability, and associated neurologic signs.

Neg

• Diplopia resolves when one eye is covered (binocular) rather than persisting monocularly — localizes to ocular misalignment/neurologic causes rather than a lens/cornea/retina problem (monocular diplopia is almost always ophthalmologic — refractive, cataract, corneal)

• No eye pain with movement, reduced color vision, or afferent pupillary defect — argues against optic neuritis (those point to optic-nerve inflammation, often MS-associated)

• No jaw claudication, scalp tenderness, headache, or age >50 — lowers concern for giant cell arteritis (but a low threshold: GCA can present with isolated visual loss, and missing it costs the other eye)

• No headache with transient visual obscurations or pulsatile tinnitus and no papilledema — argues against raised intracranial pressure (papilledema + a sixth-nerve palsy is a classic ICP picture)

• No thunderclap headache and the CN III is pupil-sparing — lowers (but does not eliminate) concern for an aneurysm (a pupil-involving third-nerve palsy is a compressive/aneurysmal emergency)

Social History (SHx)

• Vascular risk factors (retinal/occipital stroke, microvascular cranial palsy), age >50 with GCA symptoms (jaw claudication, scalp tenderness, polymyalgia, weight loss), known MS (optic neuritis, internuclear ophthalmoplegia).

• Diabetes (microvascular palsy), thyroid disease (thyroid eye disease/restrictive), trauma, anticoagulation, and prior similar transient episodes (amaurosis fugax → carotid).

Main Etiology

• Monocular vision loss: giant cell arteritis (arteritic anterior ischemic optic neuropathy), central/branch retinal artery occlusion (a stroke equivalent), retinal vein occlusion, optic neuritis, retinal detachment, vitreous hemorrhage, amaurosis fugax (carotid embolic source).

• Binocular field loss: retrochiasmal stroke (posterior cerebral/occipital → homonymous hemianopia), chiasmal lesion (pituitary tumor/apoplexy → bitemporal hemianopia).

• Diplopia: cranial nerve III, IV, or VI palsy — microvascular (diabetes/hypertension, usually pupil-sparing III), posterior communicating artery aneurysm (pupil-involving III — emergency), raised ICP (VI palsy, false-localizing), brainstem stroke; neuromuscular — myasthenia gravis (fatigable, pupil-sparing, variable); restrictive — thyroid eye disease; internuclear ophthalmoplegia (MS, brainstem).

RF

• Modifiable: vascular risk factors, diabetes/hypertension, carotid disease, thyroid dysfunction.

• Non-modifiable: age >50 (GCA), multiple sclerosis, intracranial aneurysm, autoimmune/thyroid disease.

Data

• Bedside exam: visual acuity, visual fields (confrontation), pupils (afferent pupillary defect), fundoscopy (disc edema/pallor, retinal findings), and extraocular movements/cover testing to define the pattern.

• ESR and CRP urgently if GCA is suspected (markedly elevated; arrange temporal artery biopsy) (do not delay steroids for the biopsy)

• MRI brain and orbits (optic neuritis, demyelination, mass, brainstem/occipital stroke); CTA/MRA if a pupil-involving third-nerve palsy (posterior communicating artery aneurysm)

• Glucose/HbA1c (microvascular palsy), anti-AChR antibodies and consider EMG if fatigable/variable (myasthenia), TFTs and thyroid antibodies (thyroid eye disease), carotid imaging for amaurosis fugax/retinal embolism.

DDx

Giant cell arteritis (age >50, ↑ESR/CRP — sight-threatening, can't-miss) · retinal artery/vein occlusion (painless monocular loss; CRAO = stroke equivalent) · optic neuritis (painful, ↓color, APD, MS) · pituitary/chiasmal lesion (bitemporal hemianopia) · occipital/PCA stroke (homonymous hemianopia) · cranial nerve palsy (microvascular vs aneurysm vs ICP) · myasthenia gravis (fatigable, pupil-sparing) · internuclear ophthalmoplegia (MS/brainstem)

Home Meds

• If GCA is suspected, do not delay corticosteroids waiting for the biopsy — vision loss can become bilateral and permanent within days.

• Review anticoagulation (hemorrhagic causes, vitreous hemorrhage); reconcile diabetes medications and optimize vascular risk factors.

Plan

Consults

• Ophthalmology — urgent for monocular vision loss, retinal occlusion, optic neuritis, or any acute visual loss.

• Neurology — diplopia, field defects, optic neuritis/MS, internuclear ophthalmoplegia.

• Neurosurgery / neuro-interventional — pupil-involving third-nerve palsy (aneurysm).

• Rheumatology — GCA management and biopsy; stroke team for retrochiasmal field loss or retinal artery occlusion.

Triage the emergencies

• Giant cell arteritis → start high-dose corticosteroids immediately (before the biopsy) to protect the fellow eye. Central retinal artery occlusion → emergent ophthalmology; treat as a stroke equivalent with an urgent embolic-source/vascular workup. Pupil-involving third-nerve palsy → urgent CTA/MRA for a posterior communicating artery aneurysm (rupture risk). Acute homonymous field loss → stroke pathway/imaging.

Monocular vs binocular first

• The cover test answer (monocular = ocular/ophthalmologic; binocular = misalignment/neurologic) directs the entire subsequent workup and which service leads.

Cause-directed treatment

• GCA: prednisone 40–60 mg PO daily, or IV methylprednisolone 0.5–1 g/day for established visual loss; ESR/CRP; temporal artery biopsy within ~1–2 weeks (histology persists despite steroids).

• Optic neuritis: MRI brain/orbits to stratify MS risk; IV methylprednisolone 1 g/day ×3–5 days speeds recovery (does not change final acuity) — per the Optic Neuritis Treatment Trial; avoid low-dose oral prednisone alone (ONTT showed higher recurrence).

• Microvascular cranial nerve palsy (pupil-sparing III, or IV/VI with vascular risk): typically self-limited over weeks — optimize vascular risk factors, observe, and image if atypical, progressive, or not resolving. Myasthenia: treat per MG pathway. Thyroid eye disease: endocrine/ophthalmology co-management.

Always

• PT / OT eval as needed for functional/visual rehabilitation; low-vision services for persistent deficits; fall precautions with field loss.

• Trend: visual acuity, fields, the diplopia pattern, and pupil status; response to steroids (GCA, optic neuritis) and resolution of microvascular palsies.

• Escalation triggers: GCA with vision loss → emergent IV steroids (sight-threatening, fellow eye at risk) · pupil-involving CN III → urgent vascular imaging, neurosurgery (aneurysm) · acute stroke within window → reperfusion · papilledema with raised ICP → urgent neuro evaluation/imaging.

• Discharge checklist: diagnosis and localization documented · GCA steroid taper plan with rheumatology and biopsy arranged · optic neuritis MS-risk counseling and neurology follow-up · vascular risk-factor optimization and carotid workup where relevant · ophthalmology follow-up for all visual-loss cases · low-vision resources if needed · return precautions (worsening or new vision loss, new neurologic symptoms, severe headache).

Red Flags — Urgent

• Suspected giant cell arteritis (age >50, ↑ESR/CRP, jaw claudication, vision loss) → high-dose steroids NOW, before biopsy — the fellow eye is at risk within days.
• Central retinal artery occlusion → stroke equivalent; emergent ophthalmology and vascular workup.
• Pupil-involving third-nerve palsy → posterior communicating artery aneurysm until excluded; urgent CTA/MRA, neurosurgery.
• Acute homonymous hemianopia → occipital/PCA stroke; stroke pathway.
• Papilledema → raised ICP; urgent imaging and workup.
• Pituitary apoplexy (sudden headache + bitemporal loss + ophthalmoplegia) → endocrine emergency.

Senior IM Resident Pearls

• Monocular or binocular? Ask first. The cover test splits the entire differential — monocular diplopia is the eye (ophthalmology), binocular is misalignment (neurology). It saves a misdirected workup.
• GCA is the can't-miss. In anyone over 50 with visual loss, headache, or jaw claudication, send an ESR/CRP and start steroids immediately — don't wait for the biopsy. The biopsy can be done within a week or two; the fellow eye can't wait.
• A pupil-involving third-nerve palsy is an aneurysm until proven otherwise. The pupil fibers run on the outside of CN III — compression (PCom aneurysm) takes them out; ischemia (microvascular diabetes) usually spares them. Pupil-involving → urgent CTA/MRA.
• CRAO is a stroke. Painless monocular vision loss with a cherry-red spot is a retinal stroke — emergent ophthalmology and the same embolic-source workup you'd do for a brain stroke.
• Optic neuritis: pulse IV steroids, not oral alone. ONTT showed IV methylprednisolone speeds recovery and low-dose oral prednisone alone increases recurrence — and the MRI stratifies MS risk.
• Sixth-nerve palsy can be false-localizing. A long intracranial course makes CN VI vulnerable to raised ICP — look for papilledema before assuming a benign microvascular palsy.
• Fatigable, variable, pupil-sparing diplopia/ptosis is myasthenia — it can mimic any pupil-sparing ocular motor palsy.
• Common mistake: sending a "routine" outpatient referral for acute monocular vision loss in an older patient and missing GCA or a retinal artery occlusion — both are same-day emergencies.