Vascular Headache Epilepsy Immunology Movement Neuromuscular Dementia Other Topics Neurosurgery

Reversible & Secondary Dementias

What Do You Need to Know?

NPH classic triad — gait apraxia (first & most responsive to treatment), subcortical dementia, urinary incontinence; Evans index >0.3; lumbar tap test improves gait → VP shunt
B12 deficiency — subacute combined degeneration + cognitive decline; methylmalonic acid is the most sensitive marker (elevated even when B12 is borderline normal)
Hypothyroidism — most common endocrine cause of reversible dementia; always check TSH in every dementia workup
Hashimoto encephalopathy (SREAT) — high TPO antibodies, subacute cognitive decline ± seizures/myoclonus, dramatically steroid-responsive; diagnosis of exclusion
Neurosyphilis — CSF VDRL is specific but not sensitive; CSF FTA-ABS is sensitive; treat with IV penicillin G
Depression pseudodementia — patient complains of memory loss (vs. anosognosia in AD), gives “I don’t know” answers, mood symptoms precede cognition → treat depression and cognition improves
Medication-induced — anticholinergics are the biggest culprit; always review medication list before diagnosing neurodegenerative dementia

Normal Pressure Hydrocephalus (NPH)

Classic Triad

Feature	Details	Board Yield
Gait apraxia	Magnetic gait (feet stuck to floor), broad-based, short shuffling steps, difficulty initiating gait	First symptom to appear & most responsive to shunting
Dementia	Subcortical pattern — psychomotor slowing, executive dysfunction, apathy; memory less impaired than AD	Cortical features (aphasia, agnosia) argue against NPH
Urinary incontinence	Urinary urgency early; frank incontinence late; last to appear, least responsive to treatment	Full triad present in only ~50–60% of cases

Mnemonic: “Wet, Wacky, and Wobbly” — but gait (“wobbly”) is the dominant feature

Imaging & Diagnosis

Ventriculomegaly out of proportion to sulcal atrophy — distinguishes NPH from ex vacuo hydrocephalus (where sulci are widened proportionally)
Evans index = maximum width of frontal horns ÷ maximum internal diameter of skull at same level; >0.3 = ventriculomegaly
DESH sign (Disproportionately Enlarged Subarachnoid-space Hydrocephalus) — tight high-convexity sulci + dilated Sylvian fissures on MRI; strong predictor of shunt responsiveness
Periventricular T2/FLAIR hyperintensity — transependymal CSF flow (not always present)
Aqueductal flow void on MRI — hyperdynamic CSF flow through the aqueduct

Diagnostic Testing

Test	Method	Positive Result
Lumbar tap test (Miller Fisher test)	Remove 30–50 mL CSF via LP	Gait improvement within 30–60 min (video gait analysis before and after); sensitivity ~50–60%, specificity >90%
Extended lumbar drainage	Continuous CSF drainage via lumbar catheter over 72 hrs	Higher sensitivity (~80%) than single tap; used when tap test equivocal
CSF infusion test	Measure CSF outflow resistance	Resistance >18 mmHg/mL/min predicts shunt response

Treatment

VP shunt (ventriculoperitoneal) — definitive treatment; programmable valves preferred
Predictors of good shunt response: gait-predominant symptoms, known etiology (post-SAH, post-meningitic), short symptom duration, positive tap test, DESH on MRI
Complications: subdural hematoma/hygroma, infection, over-drainage, shunt malfunction
ETV (endoscopic third ventriculostomy) — alternative in selected cases (especially secondary/obstructive forms)

💎 Board Pearl

NPH vs. Parkinson disease: both have gait disturbance, but NPH gait is broad-based and “magnetic” (feet glued to floor) while PD gait is narrow-based with festination. NPH does NOT have resting tremor or rigidity.
The tap test has LOW sensitivity (~50%) but HIGH specificity (>90%). A negative tap test does NOT rule out NPH — proceed to extended lumbar drainage if clinical suspicion is high.
Opening pressure in NPH is typically NORMAL (<18 cmH₂O) — hence the name “normal pressure” hydrocephalus. The pathology is in impaired CSF absorption, not elevated ICP.

Metabolic & Nutritional Causes

Deficiency	Neurological Syndrome	Key Lab	Board-Relevant Details
Vitamin B12	Subacute combined degeneration (dorsal columns + corticospinal tracts) + cognitive decline + megaloblastic anemia	Methylmalonic acid (MMA) — most sensitive; homocysteine also elevated	Serum B12 can be borderline normal → always check MMA. Nitrous oxide abuse causes acute B12 inactivation. Neurologic damage may be irreversible if treatment delayed
Thiamine (B1)	Wernicke encephalopathy (acute: confusion, ataxia, ophthalmoplegia) → Korsakoff syndrome (chronic: anterograde > retrograde amnesia, confabulation)	Erythrocyte transketolase (rarely measured); clinical diagnosis	Always give thiamine BEFORE glucose in malnourished patients — glucose metabolism consumes thiamine and can precipitate Wernicke. Mammillary body hemorrhage is pathognomonic
Folate	Cognitive decline + megaloblastic anemia (similar to B12 but NO subacute combined degeneration)	Serum folate, RBC folate	Folate supplementation can mask B12 deficiency by correcting anemia while neurologic damage progresses — always check B12 alongside folate
Niacin (B3)	Pellagra — the 3 D’s: Diarrhea, Dermatitis, Dementia (+ Death if untreated)	Urinary N-methylnicotinamide (low)	Associated with alcoholism, carcinoid syndrome (tryptophan diverted to serotonin), isoniazid use, Hartnup disease
Copper	Myelopathy mimicking B12 deficiency (dorsal column + corticospinal tract) + cognitive impairment	Serum copper & ceruloplasmin (both low)	Caused by excess zinc supplementation or gastric bypass surgery; zinc induces metallothionein in enterocytes which sequesters copper

💎 Board Pearl

B12 vs. folate deficiency: both cause megaloblastic anemia, but only B12 causes subacute combined degeneration (myelopathy). MMA is elevated in B12 deficiency only; homocysteine is elevated in both.
Copper deficiency mimics B12 deficiency on MRI (dorsal column T2 hyperintensity) — if a patient has a “B12-deficiency” picture but normal B12/MMA, check copper and zinc levels.
Wernicke encephalopathy is a clinical diagnosis. The classic triad (confusion, ophthalmoplegia, ataxia) is present in only ~10% of cases. Always treat empirically with high-dose IV thiamine when suspected.

Endocrine Causes

Condition	Mechanism	Key Features	Diagnosis
Hypothyroidism	Slowed neuronal metabolism, reduced cerebral perfusion	Most common endocrine cause of reversible dementia; psychomotor slowing, apathy, depression; may mimic AD in elderly	TSH (elevated), free T4 (low)
Addison disease	Cortisol deficiency → fatigue, confusion, delirium	Hypotension, hyperpigmentation, hyponatremia, hyperkalemia	Morning cortisol, ACTH stimulation test
Hyperparathyroidism / Hypercalcemia	Elevated Ca disrupts neuronal excitability and neurotransmission	“Stones, bones, groans, thrones, and psychiatric overtones” — cognitive decline, depression, psychosis	Serum calcium, PTH, ionized calcium
Hepatic encephalopathy	Ammonia → astrocyte swelling, glutamine accumulation, cerebral edema	Asterixis, confusion, sleep-wake reversal; chronic form → progressive cognitive impairment; T1 hyperintensity in globus pallidus (manganese deposition)	Ammonia (elevated but poorly correlates with severity), LFTs
Uremic encephalopathy	Accumulation of uremic toxins (urea, guanidine compounds)	Asterixis, myoclonus, seizures, cognitive decline; dialysis disequilibrium syndrome after rapid correction	BUN, creatinine, GFR

Clinical Pearl

TSH should be part of every dementia workup — hypothyroidism is common in the elderly and easily treatable. Even subclinical hypothyroidism can contribute to cognitive decline.
Hepatic encephalopathy can cause chronic subclinical cognitive impairment (minimal hepatic encephalopathy) detectable only on psychometric testing — suspect it in any patient with cirrhosis and subtle cognitive complaints.

Infectious Causes

Infection	Cognitive Syndrome	Key Diagnostic Findings	Treatment
HIV-associated neurocognitive disorder (HAND)	Subcortical dementia — psychomotor slowing, executive dysfunction, apathy; ranges from asymptomatic neurocognitive impairment → mild → HIV-associated dementia (HAD)	CD4 typically <200 in HAD; MRI: periventricular/subcortical white matter changes, atrophy; CSF: HIV viral load	cART with CNS-penetrating agents; HAND has decreased markedly since cART era
Neurosyphilis	General paresis (dementia, personality change, psychosis) — occurs 10–25 years after primary infection; tabes dorsalis (dorsal column degeneration)	CSF VDRL — specific (~100%) but not sensitive (~50%); CSF FTA-ABS — sensitive but less specific; CSF pleocytosis, elevated protein	IV penicillin G × 10–14 days; follow CSF VDRL q6 months to confirm response
Whipple disease	Cognitive decline + GI symptoms (diarrhea, weight loss, arthralgias); CNS involvement in 10–40%	PAS-positive macrophages on small bowel biopsy; oculomasticatory myorhythmia (pathognomonic); CSF Tropheryma whipplei PCR	IV ceftriaxone × 2 weeks → TMP-SMX × 1 year; relapses common
Chronic meningitis (TB, fungal)	Subacute cognitive decline + headache + cranial neuropathies; basilar meningitis pattern	TB: CSF lymphocytic pleocytosis, low glucose, high protein, AFB smear/culture, adenosine deaminase. Fungal: CSF cryptococcal antigen, India ink, culture	TB: RIPE × 12 months + steroids. Crypto: amphotericin B + flucytosine → fluconazole
PML (Progressive Multifocal Leukoencephalopathy)	Rapidly progressive multifocal white matter disease → cognitive decline, hemiparesis, visual field cuts, ataxia	JC virus (CSF PCR); MRI: multifocal, asymmetric, non-enhancing white matter lesions (NO mass effect); immunosuppression (HIV, natalizumab, rituximab)	Restore immune function (stop immunosuppressant, start cART); no specific antiviral therapy

💎 Board Pearl

Oculomasticatory myorhythmia is pathognomonic for Whipple disease — pendular convergent nystagmus synchronous with jaw contractions. If you see this description on a board question, the answer is Whipple.
CSF VDRL vs. FTA-ABS: VDRL is the confirmatory test (highly specific but only ~50% sensitive). FTA-ABS is a screening test (highly sensitive but may be false positive from serum contamination). A positive CSF VDRL essentially confirms neurosyphilis.
PML does NOT enhance with gadolinium (unless immune reconstitution is occurring — IRIS). Non-enhancing, asymmetric, multifocal white matter lesions in an immunosuppressed patient = PML until proven otherwise.

Autoimmune & Inflammatory Causes

Condition	Key Features	Diagnostic Markers	Treatment
Hashimoto encephalopathy / SREAT	Subacute cognitive decline, seizures, myoclonus, stroke-like episodes, tremor; relapsing-remitting or progressive; often in women with known thyroid disease	Markedly elevated anti-TPO antibodies (anti-thyroglobulin less specific); thyroid function may be normal, hypo, or hyper; EEG: diffuse slowing; MRI often normal	Dramatically steroid-responsive (hence “SREAT” = Steroid-Responsive Encephalopathy Associated with autoimmune Thyroiditis); IVIg/PLEX for refractory cases
Neurosarcoidosis	Cranial neuropathies (facial nerve most common), hypothalamic dysfunction, cognitive impairment, seizures; leptomeningeal enhancement	Elevated ACE (low sensitivity), chest CT (bilateral hilar lymphadenopathy), biopsy: non-caseating granulomas; CSF: lymphocytic pleocytosis, elevated protein	Corticosteroids; steroid-sparing agents (methotrexate, azathioprine, infliximab)
CNS vasculitis (PACNS)	Headache + multifocal neurologic deficits + cognitive decline; progressive or relapsing	Angiography: beading pattern (alternating stenosis/dilation); brain & leptomeningeal biopsy (gold standard); ESR/CRP may be normal	Cyclophosphamide + steroids; distinguish from reversible cerebral vasoconstriction syndrome (RCVS)
Autoimmune encephalitis	Subacute cognitive decline + psychiatric symptoms + seizures; varies by antibody type	Anti-NMDAR (young women, ovarian teratoma), anti-LGI1 (faciobrachial dystonic seizures, hyponatremia), anti-CASPR2, anti-AMPAR, anti-GABA_B	Immunotherapy (steroids, IVIg, PLEX) + tumor removal if paraneoplastic

Autoimmune Encephalitis — Key Antibodies

Antibody	Typical Patient	Distinguishing Features	Tumor Association
Anti-NMDAR	Young women	Psychiatric symptoms → seizures → movement disorders (orofacial dyskinesias) → autonomic instability → decreased consciousness	Ovarian teratoma (~40%)
Anti-LGI1	Older men	Faciobrachial dystonic seizures (pathognomonic), hyponatremia, mesial temporal T2 signal	Rare
Anti-CASPR2	Older men	Morvan syndrome (encephalopathy + neuromyotonia + dysautonomia + insomnia), neuropathic pain	Thymoma
Anti-AMPAR	Older women	Limbic encephalitis, prominent psychiatric features, relapses common	Lung, breast, thymus
Anti-GABA_B	Older adults	Limbic encephalitis with prominent seizures	SCLC (~50%)

💎 Board Pearl

Hashimoto encephalopathy is a diagnosis of exclusion. Anti-TPO antibodies are common in the general population (~10%) — their presence alone does not confirm the diagnosis. The key is: subacute encephalopathy + high TPO + exclusion of other causes + dramatic steroid response.
Faciobrachial dystonic seizures (FBDS) are pathognomonic for anti-LGI1 encephalitis. Brief (<3 sec) unilateral arm/face contractions, often refractory to AEDs but responsive to immunotherapy. They frequently precede full limbic encephalitis — early immunotherapy may prevent cognitive decline.
PACNS vs. RCVS: PACNS is progressive/relapsing with inflammatory CSF; RCVS presents with thunderclap headache, has normal CSF, and resolves within 3 months. Beading on angiography can be seen in both.

Medication-Induced Cognitive Impairment

Drug Class	Examples	Mechanism / Notes
Anticholinergics	Diphenhydramine, oxybutynin, tricyclic antidepressants, benztropine, first-generation antipsychotics	Biggest culprit — block muscarinic receptors in hippocampus and cortex; cumulative anticholinergic burden correlates with dementia risk; Beers criteria flag these in elderly
Benzodiazepines	Lorazepam, diazepam, clonazepam, alprazolam	GABA_A enhancement → sedation, anterograde amnesia; long-acting agents worse in elderly; controversial association with long-term dementia risk
Opioids	Morphine, oxycodone, fentanyl, tramadol	Central sedation, executive dysfunction; elderly especially susceptible; delirium risk
Anticonvulsants	Topiramate (“dopamax”), phenobarbital, valproate	Topiramate causes word-finding difficulty, psychomotor slowing; phenobarbital causes sedation; valproate → reversible parkinsonism and cognitive slowing in elderly
Chemotherapy	Methotrexate, cisplatin, 5-FU, cytarabine	“Chemo brain” — cognitive dysfunction during/after chemotherapy; may persist months to years; methotrexate leukoencephalopathy (especially intrathecal)
Others	Lithium, digoxin, beta-blockers (lipophilic), corticosteroids, H2 blockers (cimetidine)	Often overlooked; polypharmacy in elderly amplifies risk

Clinical Pearl

Always perform a medication reconciliation before diagnosing a neurodegenerative dementia. Use the Anticholinergic Cognitive Burden (ACB) Scale to quantify anticholinergic load — a total score ≥3 significantly increases cognitive impairment risk.
Topiramate is the anticonvulsant most likely to cause cognitive side effects — word-finding difficulty is so common it earned the nickname “dopamax.” Consider switching to an alternative if cognitive complaints develop.

Depression Pseudodementia

Pseudodementia vs. True Dementia

Feature	Depression Pseudodementia	Alzheimer Disease
Onset	Acute/subacute, dateable onset	Insidious, gradual (family may not recall exact onset)
Awareness of deficits	Patient complains of memory loss, exaggerates disability	Anosognosia — patient unaware of or minimizes deficits
Typical answers	“I don’t know” answers; doesn’t try	Near-miss confabulatory answers; tries but fails
Mood vs. cognition	Mood symptoms precede cognitive symptoms	Cognitive symptoms precede mood changes
Effort on testing	Effort-dependent poor performance; inconsistent deficits	Genuine effort with consistent deficit pattern
Progression	Rapid decline	Slow, progressive decline over years
Response to treatment	Cognition improves with antidepressant therapy	No improvement with antidepressants
History	Prior psychiatric history common	No prior psychiatric history (typically)

💎 Board Pearl

The single most distinguishing feature: In pseudodementia, the patient complains of memory loss (insight preserved); in AD, the patient denies or is unaware of deficits (anosognosia). If the patient is the one bringing up memory concerns, think depression first.
Pseudodementia is a risk factor for true dementia — patients who present with depressive pseudodementia have a higher rate of developing AD in subsequent years. Follow these patients longitudinally.

Chronic Subdural Hematoma

Key Features

Epidemiology: elderly patients, often on anticoagulants/antiplatelets; minor or forgotten head trauma
Pathophysiology: bridging vein tear → slow accumulation of blood in subdural space → membrane formation with neo-vascularization → recurrent micro-hemorrhages
Presentation: gradual cognitive decline, personality change, headache, gait instability, focal deficits (hemiparesis); can mimic neurodegenerative dementia or NPH
CT appearance: crescent-shaped collection conforming to brain surface; hyperdense (acute), isodense (subacute — easily missed), hypodense (chronic); mixed density suggests re-bleeding
MRI: more sensitive than CT, especially for isodense collections and bilateral thin subdurals

Treatment

Surgical evacuation — burr hole drainage is standard; craniotomy for organized/septated collections
Reverse anticoagulation — correct INR, hold anticoagulants
Middle meningeal artery (MMA) embolization — emerging treatment option to reduce recurrence
Small, asymptomatic collections — may be observed with serial imaging

Clinical Pearl

An elderly patient on anticoagulation with subacute cognitive decline over weeks should always prompt neuroimaging to rule out chronic subdural hematoma. Isodense subdurals on CT can be easy to miss — look for sulcal effacement, midline shift, or “white matter buckling sign.” When in doubt, get an MRI.

Sleep Disorders & Cognitive Impairment

Obstructive Sleep Apnea (OSA)

Mechanism: intermittent hypoxia + sleep fragmentation → hippocampal atrophy, white matter changes, impaired attention/executive function/memory
Prevalence: up to 50% of elderly patients with dementia have comorbid OSA
Cognitive domains affected: attention, vigilance, executive function, working memory; can mimic or exacerbate neurodegenerative dementia
Diagnosis: polysomnography (AHI ≥5 events/hr with symptoms); screening: STOP-BANG questionnaire, Epworth Sleepiness Scale
Treatment: CPAP improves attention, executive function, and psychomotor speed; may slow cognitive decline in mild cognitive impairment (MCI)
Alzheimer link: OSA increases amyloid-beta deposition (impaired glymphatic clearance during disrupted sleep) → possible modifiable risk factor for AD

💎 Board Pearl

OSA is a treatable contributor to cognitive decline — always screen for sleep disorders in the dementia workup. An obese, snoring patient with daytime somnolence and executive dysfunction may have “reversible dementia” from untreated OSA.
The glymphatic system clears cerebral metabolic waste (including amyloid-beta) during deep sleep. Sleep disruption from OSA impairs this clearance → increased amyloid deposition. This is why OSA is now considered a modifiable risk factor for Alzheimer disease.

Screening Workup for Reversible Dementias

Must-Order Labs for Every Dementia Evaluation

Category	Test	What It Rules Out
Metabolic	CBC with differential	Megaloblastic anemia (B12/folate), infection
	CMP (BUN, creatinine, electrolytes, glucose, calcium, LFTs)	Uremia, hepatic encephalopathy, hypercalcemia, hyponatremia, hypoglycemia
	Ammonia	Hepatic encephalopathy (if liver disease suspected)
Endocrine	TSH	Hypothyroidism (most important single screening test for reversible dementia)
Endocrine	Free T4	Confirms hypothyroidism if TSH elevated
Nutritional	Vitamin B12	B12 deficiency
	Methylmalonic acid (MMA)	B12 deficiency (order if B12 borderline 200–400 pg/mL)
	Folate	Folate deficiency
	Thiamine (B1)	Wernicke-Korsakoff (if alcoholism or malnutrition suspected)
Infectious	RPR/VDRL	Syphilis (if positive → CSF VDRL/FTA-ABS)
Infectious	HIV testing	HIV-associated neurocognitive disorder
Inflammatory	ESR, CRP	Vasculitis, chronic infection, inflammatory conditions
Inflammatory	Anti-TPO antibodies	Hashimoto encephalopathy / SREAT (if subacute presentation)
Imaging	Brain MRI (or CT if MRI contraindicated)	NPH, chronic subdural hematoma, mass lesion, vascular disease, white matter disease
Other	Urinalysis	UTI (common delirium trigger in elderly, can worsen baseline dementia)
Other	Medication review	Drug-induced cognitive impairment (anticholinergics, benzodiazepines, opioids)

Extended Workup (When Indicated)

Test	When to Order	What It Rules Out
Copper, ceruloplasmin, zinc	Myelopathy with cognitive decline; gastric bypass history	Copper deficiency, Wilson disease
Heavy metals (lead, mercury, arsenic)	Occupational exposure, environmental concerns	Heavy metal toxicity
CSF analysis (cells, protein, glucose, cytology, 14-3-3, RT-QuIC)	Rapidly progressive dementia, suspicion for CJD, autoimmune, infectious, or neoplastic etiology	CJD, autoimmune encephalitis, chronic meningitis, leptomeningeal carcinomatosis
Autoimmune encephalitis panel (serum + CSF)	Subacute onset, seizures, psychiatric symptoms, movement disorder	Anti-NMDAR, anti-LGI1, anti-CASPR2, anti-AMPAR, anti-GABA_B
Paraneoplastic antibodies	Cancer history, subacute cerebellar degeneration, limbic encephalitis	Anti-Hu, anti-CV2, anti-Ma2, anti-amphiphysin
EEG	Fluctuating cognition, seizures, rapidly progressive dementia	Non-convulsive status epilepticus, CJD (periodic sharp wave complexes), autoimmune encephalitis
Polysomnography	Daytime somnolence, snoring, obesity, witnessed apneas	Obstructive sleep apnea
PTH, ionized calcium	Elevated serum calcium	Hyperparathyroidism
Morning cortisol, ACTH stimulation test	Hypotension, hyperpigmentation, electrolyte abnormalities	Addison disease
ACE level, chest CT	Multi-system disease, cranial neuropathy, leptomeningeal enhancement	Neurosarcoidosis

💎 Board Pearl

The “minimum” dementia workup per AAN guidelines: CBC, CMP, TSH, B12, RPR/VDRL, brain imaging (MRI preferred). HIV testing and additional labs are ordered based on clinical suspicion.
Reversible causes account for <5% of all dementias in most studies — but they must always be screened for because treatment can dramatically change outcomes. The yield is highest in younger patients (<65) and those with subacute or atypical presentations.
A “rapidly progressive dementia” (weeks to months rather than years) demands an aggressive workup including CSF studies, EEG, and autoimmune panels — the differential shifts from neurodegenerative to potentially treatable etiologies (autoimmune encephalitis, CJD, infection, malignancy).

High-Yield Summary Table

Reversible Cause	Classic Clue	Key Test	Treatment
NPH	Magnetic gait + dementia + incontinence; ventriculomegaly without proportional atrophy	Lumbar tap test; Evans index >0.3	VP shunt
B12 deficiency	Subacute combined degeneration + megaloblastic anemia	MMA (most sensitive)	B12 supplementation (IM or high-dose oral)
Hypothyroidism	Psychomotor slowing, weight gain, cold intolerance in elderly	TSH	Levothyroxine
Neurosyphilis	Personality change + Argyll Robertson pupils + CSF pleocytosis	CSF VDRL (specific); CSF FTA-ABS (sensitive)	IV penicillin G
Hashimoto encephalopathy	Subacute encephalopathy + high TPO + thyroid disease	Anti-TPO antibodies	Corticosteroids (dramatic response)
Chronic SDH	Elderly, anticoagulated, subacute cognitive decline	CT head (crescent-shaped collection)	Surgical evacuation
Depression pseudodementia	Patient complains of memory loss; “I don’t know” answers; mood precedes cognition	Clinical assessment; neuropsychological testing	Antidepressants → cognition improves
Medication-induced	Temporal correlation with offending drug; anticholinergic burden	Medication reconciliation; ACB scale	Discontinue/substitute offending agent
Wernicke-Korsakoff	Alcoholism + confusion + ataxia + ophthalmoplegia	Clinical diagnosis; MRI: mammillary body changes	High-dose IV thiamine (before glucose!)
OSA	Obesity, snoring, daytime somnolence, executive dysfunction	Polysomnography (AHI ≥5)	CPAP
Autoimmune encephalitis	Subacute onset, seizures, psychiatric symptoms, young patient	Autoimmune encephalitis panel (serum + CSF)	Immunotherapy + tumor removal
Hepatic encephalopathy	Cirrhosis + asterixis + sleep-wake reversal; T1 bright globus pallidus	Ammonia (but poor correlation); clinical diagnosis	Lactulose + rifaximin

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