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USMLE Step 2 CK High-Yield Neurology Topics
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Neurology
High Yield USMLE Step 2 CK Notes
Welcome to the Neurology High-Yield Notes for Step 2 CK.
These are the most commonly tested topics on the exam—ideal for quick review in your last 2 weeks before the exam, when you’re short on time, or when you’re just starting out and want to focus on what is high yield. Created and peer-reviewed by physicians who scored 260+ on Step 2 CK in a Q&A style to reinforce active learning.
How to use this file
- Read the question ➔ cover the answer ➔ self-quiz before revealing.
- Review the NOTES ➔ they include high-yield details you don’t want to miss.
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- Don’t forget to watch the video lessons that go with this file. Learn more here.
Table of Contents
Vascular Neurology
1. A 50-year-old man presents with confusion, vomiting, seizure, and severely elevated blood pressure. Fundoscopy shows retinal hemorrhages and cotton-wool spots. What is the diagnosis?
➔ Hypertensive encephalopathy (↑ BP + neurologic symptoms + signs of end-organ damage → think Hypertensive Encephalopathy)
- Note: Fundoscopy shows → Retinal hemorrhages, cotton-wool spots (hypertensive retinopathy)
- Treatment:
○ ↓ MAP by ≤25% in first hour
○ IV antihypertensives: Labetalol, Nicardipine, Esmolol, Nitroprusside
○ Avoid rapid BP drop → risk of ischemia
2. A 65-year-old man with poorly controlled hypertension suddenly develops vomiting, right-sided weakness, and confusion. Exam shows right-sided hemiparesis, hyperreflexia, and Babinski sign. What is the next step in diagnosis?
➔ Non-contrast CT scan of the head (to detect intracerebral hemorrhage) (sudden focal neuro deficit + vomiting + HTN → rule out Intracerebral Hemorrhage)
- Note: Most common site → Putamen
- Putaminal hemorrhage causes→ contralateral hemiparesis + gaze deviation toward the lesion
- Cerebellar hemorrhage causes → ataxia, vomiting, no hemiparesis, rapid deterioration → neurosurgical emergency
3. A 78-year-old man with a history of frequent falls and alcohol use presents with progressive headache and confusion. CT scan shows a crescent-shaped hyperdensity along the cerebral hemisphere, crossing suture lines. What is the diagnosis?
➔ Subdural Hematoma (SDH) (elderly + fall + slow neurologic decline + crescent-shaped bleed → think SDH)
- Note: It is caused by Rupture of bridging veins between cortex and dural sinuses
- Elderly (brain atrophy), alcohol use, Trauma, child abuse → are risk factors
- ↑ ICP (papilledema, herniation) → may cause herniation
- Management:
○ If Stable, small SDH → Monitor, supportive care
○ If Signs of mass effect/herniation → Do surgical evacuation (burr hole or craniotomy)
Subdural Hematoma
Unlike epidural hematoma (lens-shaped, lucid interval doesn’t cross suture line), SDH is crescent-shaped and slower in onset
4. A 45-year-old woman presents with a sudden, severe headache described as “the worst of her life.” She has photophobia, neck stiffness, and transient loss of consciousness. CT head is normal. What is the next step?
➔ Lumbar puncture to assess for xanthochromia (suspect subarachnoid hemorrhage ) (sudden thunderclap headache + normal CT → rule out Subarachnoid Hemorrhage via LP)
- Note: 1st step in diagnosis is CT head → If CT negative → Lumbar puncture→ shows xanthochromia
- Complications:
○ Rebleed (within 24 hrs)
○ Vasospasm (days 4–10) → prevent with nimodipine
○ Hydrocephalus
5. A 70-year-old man has transient right-sided weakness and aphasia that resolve within an hour. MRI brain shows no infarct. What is the most appropriate next step in management?
➔ Start aspirin and evaluate for embolic source (transient focal deficits + no infarct on MRI → think TIA and prevent future stroke)
- Note: TIA is caused by emboli (from carotid/aorta/heart) or small vessel disease
- Workup to know the cause includes → MRI brain, Carotid Doppler, ECG/Echo
- Treatment: Aspirin + statin ± anticoagulation if atrial fibrillation
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6. A 72-year-old woman is brought to the ER with left-sided weakness. Her family says she was last seen well 3 hours ago. CT shows no hemorrhage. What is the next step in management?
➔ Start IV alteplase (acute focal deficit + <4.5 hrs since last known well + no bleed → indicates a stroke in the window period → give tPA)
- Note: Stroke diagnosis:
○ Non-contrast CT → rule out hemorrhage
○ MRI brain (optional if diagnosis unclear) - Acute Management:
○ <4.5 hrs: IV alteplase (thrombolysis)
○ <24 hrs + large vessel occlusion on imaging: Consider thrombectomy
○ >4.5 hrs + no thrombectomy criteria: Start aspirin
○ Supportive care: BP control, DVT prophylaxis, statin - Always ask “When was the patient last seen normal?”
7. A 68-year-old man is hospitalized for acute ischemic stroke. He has a history of diabetes and long-standing hypertension. Which of the following is the most important modifiable risk factor for preventing future strokes?
➔ Hypertension (HTN is the strongest modifiable risk factor for both ischemic and hemorrhagic stroke)
- Note: Age is the strongest non-modifiable risk factor
8. A 64-year-old man with hypertension and diabetes presents with sudden right-hand clumsiness. He has no facial droop or speech changes. CT head is normal. What is the cause?
➔ Lacunar infarct (focal motor deficit + no cortical signs + HTN/DM → Think Lacunar Stroke from small vessel disease)
- Note: Lacunar stroke = small vessel occlusion due to lipohyalinosis
9. A 66-year-old man with poorly controlled hypertension presents with vertigo, nausea, ataxia, and left-sided facial numbness along with right arm and leg weakness. What is the cause of this presentation?
➔ Posterior circulation stroke (vertebral artery occlusion) (crossed findings + vestibular symptoms → think brainstem stroke from vertebral artery occlusion)
- Note: Posterior circulation stroke Presents with →
○ Vestibulocerebellar signs: Vertigo, vomiting, nystagmus, ataxia
○ Ipsilateral CN findings: Dysphagia, dysarthria, Horner syndrome
○ Contralateral findings:
■ Hemiparesis (corticospinal tract)
■ Pain/temp loss (spinothalamic tract)
■ Homonymous hemianopsia ± macular sparing (occipital lobe)
Differential Diagnosis: Posterior Stroke Syndromes
| Condition | Key Features |
|---|---|
| Vertebral artery occlusion | Vertigo, ataxia, ipsilateral CN signs, contralateral weakness/sensory loss |
| PICA infarct (Wallenberg) | Hoarseness, dysphagia, vertigo, ↓ pain/temp ipsilateral face + contralateral body |
| Basilar artery occlusion | Locked-in syndrome, preserved consciousness |
| Cerebellar infarct/hemorrhage | Ataxia, vertigo, nystagmus ± signs of ↑ICP |
10. A 68-year-old man with hypertension presents with sudden right-sided weakness and left eye ptosis with a “down and out” gaze. He also has a dilated left pupil. Where is the lesion located?
➔ Left midbrain (Weber syndrome) (CN III palsy + contralateral hemiparesis → think midbrain stroke)
- Note: “Crossed signs” = CN findings + long tract signs on opposite sides → think brainstem lesion
- Localization rule: “Crossed signs” (CN deficit on one side + long tract signs on the other) → brainstem lesion
11. A 72-year-old man develops apathy, disinhibition, poor judgment, and impaired concentration following a recent hospitalization. Neurologic exam reveals no focal weakness. Which brain region is most likely affected?
➔ Frontal lobe dysfunction (behavioral/personality changes + poor executive function → think prefrontal cortex lesion)
- Note: Prefrontal cortex damage leads to → apathy, disinhibition, poor judgment, ↓ concentration
- Primary motor cortex leads to → contralateral weakness or psychomotor slowing
- Broca’s area (dominant frontal lobe) leads to → expressive aphasia (intact comprehension)
- Personality and executive function changes are classic for frontal lobe lesions
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Neurodegenerative Disorders
12. A 74-year-old man presents with occasional forgetfulness, decreased hearing, and slower movements. He has an absent Achilles reflex and arcus senilis. He lives independently and manages his finances. What is the explanation?
➔ Normal aging (mild sensory/cognitive changes + preserved independence → think normal aging)
- Note: Other Normal findings with aging: ↓ Achilles reflex, arcus senilis, presbycusis, psychomotor slowing
- No major functional impairment (e.g., finances, cooking)
- Differs from dementia → which involves functional decline
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Mild cognitive impairment | Subjective + objective memory loss, intact function |
| Dementia (e.g., Alzheimer’s) | Memory loss + impaired function (e.g., finances, cooking) |
| Depression in elderly | Pseudodementia, anhedonia, appetite/sleep changes |
| Hypothyroidism | Cognitive slowing + fatigue, cold intolerance, constipation |
13. A 74-year-old woman is brought by her daughter due to forgetting appointments and misplacing objects. She struggles to manage finances and recently got lost while walking in her neighborhood. What is the diagnosis?
➔ Alzheimer dementia (progressive memory loss + impaired activity of daily living → think Alzheimer’s disease)
- Note: Alzheimer Disease is the most common cause of dementia
- MRI shows → Diffuse cortical atrophy, especially hippocampus & temporal lobes
- The most significant risk factor is → advanced age
Differential diagnosis of Dementia
| Condition | Key Feature |
|---|---|
| Alzheimer | Gradual memory decline → executive/language |
| Vascular dementia | Stepwise decline + focal neuro signs |
| Lewy body dementia | Visual hallucinations + Parkinsonism + REM sleep behavior |
| Frontotemporal dementia | Early personality/language change, disinhibition |
| Huntington disease | Chorea + psychiatric symptoms + cognitive decline (early executive dysfunction) |
| Prion disease (CJD) | Rapidly progressive dementia + myoclonus + ataxia |
| Normal Pressure Hydrocephalus (NPH) | Gait disturbance + urinary incontinence + dementia (wet, wobbly, wacky) |
14. A 72-year-old woman is brought by her daughter for memory loss and apathy. She has poor concentration but no focal neurologic deficits. History includes diabetes and recent diphenhydramine use. What is the next step?
➔ Screen for reversible causes: TSH, B12, depression, medications (new cognitive decline → always rule out reversible causes before diagnosing dementia)
- Note: Anticholinergic meds (eg, diphenhydramine, TCA) → common reversible cause
15. A 72-year-old woman is diagnosed with mild Alzheimer dementia. She is independent in daily activities but has frequent forgetfulness. What is the best initial treatment?
➔ Start a cholinesterase inhibitor (eg, donepezil) (mild Alzheimer → start cholinesterase inhibitor to slow progression)
- Note: First-line treatment → Donepezil, rivastigmine, or galantamine
- Memantine is used in mild to moderate Alzheimer dementia
- Goal of treatment is to → slow cognitive decline, not curative
16. A 72-year-old man presents with progressive memory loss, visual hallucinations, and fluctuating alertness. His wife says he “acts out his dreams” during sleep. Exam shows bradykinesia and rigidity. What is the diagnosis?
➔ Lewy Body Dementia (LBD) (dementia + visual hallucinations + parkinsonism → think Lewy Body Dementia)
- Note: Other features include → REM sleep behavior disorder
- Caused by cortical deposition of α-synuclein (Lewy bodies)
USMLE Tip:
To differentiate from Parkinson Disease Dementia (PDD):
🡲 LBD: Dementia precedes or occurs within 1 year of motor symptoms
🡲 PDD: Dementia develops after ≥1 year of motor symptom onset
17. A 70-year-old man presents with slow movements, resting tremor, and muscle rigidity. His symptoms are progressively worsening and impairing daily activities. What is the initial treatment?
➔ Carbidopa-Levodopa (bradykinesia + resting tremor + functional decline → think Parkinson disease→ start levodopa)
- Note: Cardinal signs of Parkinson disease:
○ Bradykinesia (slowness of movement – required for diagnosis)
○ Resting tremor (“pill-rolling”)
○ Rigidity (cogwheel)
○ Postural instability (late finding) - Levodopa is converted to dopamine in CNS; carbidopa prevents peripheral breakdown
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Lewy body dementia | Dementia precedes or occurs within 1 year of motor symptoms |
| Drug-induced parkinsonism | Antipsychotics or antiemetics (reversible), symmetric symptoms |
18. A 35-year-old man presents with irritability, restlessness, and progressive memory loss. His mother had similar symptoms in her 40s. MRI shows caudate atrophy. What test is used to confirm the diagnosis?
➔ Genetic testing (behavioral + cognitive decline + chorea + family history → think Huntington disease)
- Note: Family history is often present; earlier onset in successive generations due to anticipation
- Confirm with → Genetic testing
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Parkinson disease | Bradykinesia, rigidity, resting tremor—no chorea or behavioral issues |
| Frontotemporal dementia | Personality changes, no chorea, typically older adults |
19. A 75-year-old man presents with progressive gait difficulty, urinary incontinence, and memory impairment. MRI shows enlarged ventricles. What is the most likely diagnosis?
➔ Normal-pressure hydrocephalus (NPH) (gait disturbance (magnetic gait) + urinary incontinence + dementia + ventriculomegaly → think NPH)
- Note: Imaging shows ventriculomegaly without cortical atrophy on MRI/CT
- Diagnosis is → Clinical + imaging
○ LP or high-volume tap → assess symptom improvement - Definite treatment is → Ventriculoperitoneal shunt
Hydrocephalus Differential diagnosis
| Type | Opening Pressure | Imaging Findings | Key Clinical Features |
|---|---|---|---|
| Normal Pressure Hydrocephalus (NPH) | Normal | Ventriculomegaly without sulcal atrophy | Triad: gait disturbance, dementia, incontinence (wet, wobbly, wacky) |
| Communicating Hydrocephalus (other than NPH) | ↑ or normal | Ventriculomegaly | Signs of ↑ ICP (headache, vomiting, papilledema) |
| Obstructive (Non-communicating) Hydrocephalus | ↑ | Enlarged ventricles proximal to obstruction | Signs of ↑ ICP |
| Idiopathic Intracranial Hypertension (Pseudotumor cerebri) | ↑↑ | Normal-sized ventricles ± empty sella | Obese woman, headache, papilledema, vision loss, CN VI palsy |
20. A 24-year-old obese woman presents with daily pulsatile headaches, transient vision loss when bending forward, and blurry vision. Fundoscopy shows papilledema. MRI is normal. What is the initial treatment?
➔ Acetazolamide (Young obese woman + headache + papilledema + normal MRI → suggest idiopathic intracranial hypertension → treat with acetazolamide)
- Note: Triggers include → Vitamin A, isotretinoin
- Treat with
○ Acetazolamide is first-line → decreases CSF production
○ Weight loss, stop OCPS, avoid Vitamin A
○ Consider VP shunt or optic nerve sheath fenestration if vision threatened
21. A 68-year-old vegan presents with progressive gait instability, frequent falls, and numbness in her feet. Exam shows a wide-based gait, decreased vibration sense, and positive Romberg sign. What is the diagnosis?
➔ Subacute combined degeneration (due to vitamin B12 deficiency)
- Note: Subacute Combined Degeneration (B12 Deficiency) Affects:
○ Dorsal columns → ↓ vibration & proprioception
○ Lateral corticospinal tract → weakness, spasticity
○ Spinocerebellar tract → ataxia
Differential Diagnosis of Ataxia & Sensory Loss:
| Condition | Key Features | Distinction |
|---|---|---|
| Subacute combined degeneration | Ataxia + ↓ vibration/proprioception + anemia | B12 deficiency |
| Tabes dorsalis | Sensory ataxia, sharp pain | Hx of syphilis, Argyll Robertson pupils |
| Friedreich ataxia | Gait ataxia, scoliosis, cardiomyopathy | Onset <20 y/o, autosomal recessive |
| Peripheral neuropathy (DM) | Stocking-glove numbness | ↓ reflexes, preserved corticospinal |
22. A 60-year-old man presents with unsteady gait and sharp, shooting pains in his legs. He has a history of untreated syphilis. Neurologic exam shows wide-based gait, and pupils that constrict with accommodation but not with light. What is the diagnosis?
➔ Tabes dorsalis (sensory ataxia + lightning pains + Argyll Robertson pupils + syphilis history → think Tabes dorsalis)
- Note: Caused by tertiary syphilis affecting dorsal columns
- Features: Sensory ataxia, lightning-like leg pains, positive Romberg
- Positive Romberg = Patient sways/falls when eyes closed → impaired proprioception
- Pupils: Argyll Robertson pupils → they accommodate but don’t react to light
23. A 58-year-old man presents with progressive right hand weakness and occasional choking while eating. Exam shows muscle atrophy, fasciculations, spasticity, and brisk reflexes in the same limb. What is the diagnosis?
➔ Amyotrophic lateral sclerosis (ALS) (mixed UMN + LMN signs in same limb + bulbar symptoms → think ALS)
- Note: Diagnosis is clinical → Confirm with EMG
- Cause of death is → Respiratory failure
- No bowel/bladder or sensory symptoms (helps distinguish from MS or syrinx)
24. A 35-year-old man presents with progressive weakness and atrophy in both hands along with decreased pain and temperature sensation in his arms. Vibration and proprioception are intact. What is the diagnosis?
➔ Syringomyelia (cape-like pain/temp loss + hand atrophy + intact proprioception → think syringomyelia)
- Note: Affects spinothalamic tract (pain/temp) + anterior horn (LMNs)
- Spread may lead to → UMN signs in legs (spasticity, hyperreflexia, Babinski)
- Treat with → surgical decompression
Differentiate from: Peripheral neuropathy → Stocking-glove sensory loss, affects vibration/proprioception.
Syringomyelia
File:Syringomyelia.jpg: Cyborg Ninja at English Wikipedia (uploaded by User:ToNToNi Derivative work: User:SUM1, Syringomyelia (with arrow), CC BY 4.0
CNS Infections & Inflammatory Disorders
25. A 10-day-old infant has fever, poor feeding, and new-onset seizures. CSF shows lymphocytic pleocytosis, protein, low-normal glucose, and some RBCs. What is the most likely diagnosis?
➔ Neonatal herpes simplex virus (HSV) encephalitis (seizures + fever + CSF lymphocytes + RBCs in neonate → think HSV)
- Note: HSV encephalitis in neonates → leads to temporal lobe necrosis → RBCs in CSF
- Confirm with → PCR of CSF
- Start IV acyclovir immediately — don’t wait for PCR
Cerebrospinal fluid analysis results:
| Condition | WBC Type | Glucose | Protein |
|---|---|---|---|
| Bacterial Meningitis | ↑↑ Neutrophils | ↓ | ↑ |
| Viral Meningitis | ↑ Lymphocytes | Normal | Normal / ↑ |
| Fungal/TB Meningitis | ↑ Lymphocytes | ↓ | ↑ |
| Herpes Encephalitis | ↑ Lymphocytes + RBCs | Normal | ↑ |
| Guillain-Barré Syndrome | Normal cells | Normal | ↑ (albuminocytologic dissociation) |
26. A 3-week-old infant presents with fever, lethargy, and poor feeding. On exam, he is irritable with a bulging fontanelle. CSF shows neutrophilic pleocytosis, low glucose, and elevated protein. What is the empiric treatment?
➔ Ampicillin + cefotaxime ± gentamicin (suspected bacterial meningitis in neonate → start empiric broad-spectrum antibiotics targeting common pathogens)
- Note: Neonatal bacterial meningitis → most commonly caused by: Group B Strep, E. coli, Listeria monocytogenes
| Age Group | Empiric Treatment | Key Pathogens |
|---|---|---|
| <1 month | Ampicillin + cefotaxime ± gentamicin | GBS, E. coli, Listeria |
| 1 month – 50 yrs | Vancomycin + ceftriaxone | N. meningitidis, S. pneumo |
| >50 years | Vancomycin + ceftriaxone + ampicillin | S. pneumo, N. meningitidis, Listeria |
27. A 72-year-old man presents with fever, headache, neck stiffness.CSF shows neutrophilic pleocytosis, low glucose, and high protein. What is the empiric treatment?
➔ Vancomycin + ceftriaxone + ampicillin (elderly + classic meningitis signs → give empiric coverage including Listeria)
28. A 12-year-old boy presents with headache, fever, and vomiting for 4 days. He has a history of chronic otitis media. Neurologic exam shows papilledema and mild right-sided weakness. CT scan with contrast shows a ring-enhancing lesion in the left frontal lobe. What is the next step?
➔ Aspiration or surgical drainage with IV antibiotics (Focal neurologic signs + ring-enhancing lesion on imaging + history of otitis media → Indicates Brain Abscess → Requires drainage + empiric IV antibiotics)
- Note: Avoid LP due to risk of herniation from increased ICP
29. A 39-year-old HIV-positive man presents with headache, confusion, and blurry vision. MRI shows single ring-enhancing lesions in the periventricular region. CSF reveals EBV DNA. What is the diagnosis?
➔ Primary central nervous system lymphoma (HIV + solitary ring-enhancing lesion + CSF EBV DNA → think CNS lymphoma)
- Note: Occurs in AIDS (CD4 <100), strongly EBV-associated
Ring-enhancing lesions in HIV
| Diagnosis | Clue |
|---|---|
| Toxoplasmosis | Multiple lesions, basal ganglia, IgG+ |
| CNS lymphoma | Periventricular, EBV+, fewer lesions |
| Neurocysticercosis | Multiple cystic/calcified lesions, exposure to pigs, seizures, Latin America endemic |
30. A 35-year-old HIV-positive man with a CD4 count of 45 presents with headache, fever, and confusion. MRI reveals multiple ring-enhancing lesions in the basal ganglia and cortex. What is the diagnosis?
➔ Cerebral toxoplasmosis (AIDS + multiple ring-enhancing lesions + CD4 <100 → think toxoplasmosis)
- Note: Common in CD4 <100, especially without prophylaxis
- MRI shows → Multiple ring-enhancing lesions
- Treatment
○ Prophylaxis: TMP-SMX if CD4 <100
○ Empiric: Pyrimethamine + sulfadiazine + leucovorin
○ Add ART after stabilization
31. A 28-year-old woman has had two episodes of neurologic symptoms (weakness, paresthesia, and diplopia) over the past 6 months. MRI shows periventricular white matter lesions. What is the next step in management?
➔ Start interferon beta or glatiramer acetate (relapsing neurologic symptoms + periventricular lesions → think Multiple sclerosis → start disease-modifying therapy)
- Note: Neurologic symptoms may be motor, sensory, urinary, or optic.
- MRI shows → periventricular white matter hyperintensities (dissemination in space)
- Most patients experience transient symptom exacerbation in → high environmental temperatures
- Treat acute flare with IV corticosteroids
○ Start interferon beta or glatiramer for long-term control
Headache & Cranial Neuropathies
32. A 27-year-old woman presents with recurrent unilateral, pulsatile headaches associated with nausea, photophobia, and visual aura. What is the next step in management?
➔ Administer NSAIDs (classic migraine features + mild-to-moderate severity → start with NSAIDs)
- Note: Migraine triggered by stress, menstruation; relieved by rest or darkness
- Acute treatment: NSAIDs or triptans (based on severity)
- Prophylaxis if ≥4/month or disabling: Beta blockers, amitriptyline, venlafaxine
Differential Diagnosis
| Condition | Key Features |
|---|---|
| Migraine | Unilateral, pulsatile, aura, nausea, photophobia |
| Cluster Headache | Severe periorbital pain, lacrimation, nasal congestion, occurs in clusters |
| Tension Headache | Bilateral, band-like pressure, no nausea or aura, not worsened by activity |
| Medication Overuse | Chronic daily headache, worsened by abortive meds (e.g., triptans, NSAIDs) |
| Pseudotumor cerebri | Obese woman, vision changes, papilledema, ↑ICP symptoms |
| SAH | Sudden thunderclap headache, worst ever |
33. A 30-year-old pregnant woman in her second trimester presents with a severe pulsatile headache associated with photophobia and nausea. She has a history of migraines. What is the safest acute treatment?
➔ Acetaminophen (migraine in pregnancy → avoid NSAIDs and triptans → use acetaminophen first)
34. A 12-year-old boy presents with recurrent, throbbing headaches associated with photophobia and nausea. He prefers to lie in a dark room during episodes. What is the next best step in management?
➔ Administer acetaminophen or NSAIDs (classic migraine symptoms in a child → start with simple analgesics)
- Note: Triptans (e.g., sumatriptan) can be used in older children/adolescents if severe
35. A 35-year-old woman with chronic migraines presents with daily morning headaches that are dull and unrelenting. She has been using sumatriptan and ibuprofen almost daily. What is the most likely cause of her current symptoms?
➔ Medication overuse headache (daily dull headache in a patient overusing acute migraine meds → think rebound headache)
- Note: Caused by frequent use of abortive meds (eg, NSAIDs, triptans, opioids) ≥10–15 days/month
- Treatment → Stop overused meds gradually, may worsen before improvement
36. A 34-year-old man presents with a sudden-onset right-sided facial droop. He is unable to close his right eye or raise his right eyebrow. He recently recovered from a cold sore. What is the next step in management?
➔ Start oral glucocorticoids (± antivirals in severe cases) (unilateral facial weakness including forehead + recent HSV → think Bell palsy → treat with steroids)
- Note: Bell palsy → often post-viral (HSV, VZ) (other causes include sarcoidosis and lyme disease)
- Treat with oral steroids ± antivirals, add eye care to prevent corneal injury
- If left untreated → most patients improve gradually over several months
VS UMN lesion (e.g., stroke) → Spares forehead
37. A 34-year-old man develops fever, severe headache, and diplopia 4 days after popping a pimple on his nose. Exam shows periorbital edema, ptosis, and impaired eye movements. What is the diagnosis?
➔ Cavernous sinus thrombosis (facial infection + fever + cranial nerve palsies + periorbital edema → think cavernous sinus thrombosis)
- Note: Caused by septic thrombus from facial skin infection (danger triangle)
- Involves CNs III, IV, V1/V2, VI → ophthalmoplegia, ↓ corneal reflex, diplopia
- Confirm diagnosis with → CT/MR venography
- Treat with IV antibiotics ± anticoagulation to limit thrombus spread
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Orbital cellulitis | Pain with eye movement, proptosis, fever—but no multiple CN deficits |
| Mucormycosis | Diabetic/immunocompromised, black eschar, rapid tissue necrosis |
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Tumors & Neurocutaneous Disorders
38. A 64-year-old man presents with progressive headache, focal weakness, and new-onset seizures. Brain MRI reveals a large mass with surrounding vasogenic edema and midline shift. What is the next step in management?
➔ Administer corticosteroids (e.g., dexamethasone) (mass lesion + vasogenic edema + mass effect → give steroids to stabilize)
- Note: Brain mass with vasogenic edema → ↑ ICP, herniation risk
- IV dexamethasone reduces edema and stabilizes symptoms
○ Add anticonvulsants if seizures present
39. A 60-year-old man with a history of lung cancer presents with new-onset headache. MRI brain shows multiple ring-enhancing lesions at the gray-white junction with surrounding vasogenic edema. What is the next step in management?
➔ Start corticosteroids (e.g., dexamethasone) (multiple brain lesions + vasogenic edema → think brain metastases → give steroids to reduce edema)
- Note: Common primaries: lung, breast, melanoma, renal, colorectal
40. A 52-year-old woman undergoes brain imaging for unrelated reasons and is found to have a well-circumscribed, dural-based mass. She has no neurological symptoms.
What is the next step in management?
➔ Observation with serial imaging (MRI monitoring) (dural-based, asymptomatic mass on imaging → think meningioma → observe if small)
- Note: Meningioma is more common in women; associated with NF 2 mutations
- It has Mass effect without invasion
- If symptomatic or growing → treat with surgical resection
41. A 48-year-old man presents with right-sided hearing loss, tinnitus, light-headedness, and numbness over the right cheek. Weber test lateralizes to the left, and Rinne test is normal bilaterally. What is the diagnosis?
➔ Vestibular Schwannoma (Acoustic Neuroma) (progressive unilateral hearing loss + imbalance + facial numbness → think vestibular schwannoma)
- Note: VIII affection causes:
○ Unilateral sensorineural hearing loss, tinnitus
○ Vestibular symptoms: imbalance, light-headedness - Trigeminal nerve compression → facial numbness or paresthesia
- Diagnose with → MRI with gadolinium
Differentiate from → Meniere disease causes episodic vertigo and fluctuating hearing loss, VS vestibular schwannoma causes progressive, unilateral hearing loss with persistent imbalance and facial numbness.
42. A 58-year-old man presents with new-onset seizures and worsening headaches. MRI of the brain reveals a large, irregular, rim-enhancing mass with central necrosis crossing the corpus callosum. What is the next step in management?
➔ Surgical resection (ring-enhancing mass with necrosis crossing corpus callosum → think Glioblastoma Multiforme → resect if possible)
- Note: Glioblastoma Multiforme is the most common primary malignant brain tumor in adults
- Initial step: Attempted surgical resection → for decompression and histologic confirmation
- Poor prognosis → median survival ~15–18 months
43. A 12-year-old boy presents with vision changes, poor growth, and increased thirst and urination. Physical exam shows bitemporal hemianopsia. MRI reveals a suprasellar mass with calcifications. What is the diagnosis?
➔ Craniopharyngioma (child + vision loss + pituitary symptoms + calcified suprasellar mass → think craniopharyngioma)
- Note: Benign tumor from Rathke pouch remnants (ectoderm origin)
- Common in children; suprasellar location compresses optic chiasm and pituitary
- MRI shows → Calcified suprasellar mass (vs. pituitary adenoma = non-calcified)
Craniopharyngioma
Differentiate from Pituitary Adenoma:
🡲 Craniopharyngioma: Seen in children, calcifications
🡲 Pituitary adenoma: Adults, no calcifications
44. A 12-year-old boy with a family history of bilateral hearing loss and intracranial tumors is diagnosed with neurofibromatosis type 2. What is the most appropriate annual screening test for this patient?
➔ Brain MRI (NF2 = risk of vestibular schwannomas and CNS tumors → screen annually with brain MRI)
- Note: NF2: Mutation in NF2 tumor suppressor gene (autosomal dominant)
- Classic presentation → Bilateral vestibular schwannomas, ± meningiomas, ependymomas
- Surveillance:
○ Annual brain MRI (start age ~10)
○ Annual audiometry
Differential Diagnosis
| Condition | Key Features |
|---|---|
| NF1 | Café-au-lait spots, axillary freckling, Lisch nodules, neurofibromas, optic gliomas |
| NF2 | Bilateral vestibular schwannomas, meningiomas, juvenile cataracts, subcutaneous schwannomas |
| Tuberous sclerosis | Seizures, ash-leaf spots, angiofibromas, cortical tubers, renal angiomyolipomas |
| Von Hippel-Lindau | Hemangioblastomas, renal cell carcinoma, pheochromocytomas, pancreatic cysts |
45. A 2-year-old child presents with seizures and developmental delay. Exam shows ash leaf spots and a rough plaque on the lower back. Brain MRI reveals subependymal nodules. What is the diagnosis?
➔ Tuberous sclerosis complex (TSC) (seizures + skin lesions + brain findings → classic triad for TSC)
- Note: Skin findings:
○ Ash leaf spots (hypopigmented, Wood lamp)
○ Shagreen patch (leathery plaque, lower back)
○ ± Facial angiofibromas - Brain findings: Subependymal nodules
- Cardiac rhabdomyoma, renal angiomyolipoma → are common
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Back Pain & Spinal Cord Syndromes
46. A 38-year-old man presents with acute low back pain after lifting a heavy box. He has no fever, trauma, weight loss, or neurologic symptoms. Exam shows paraspinal tenderness and full strength and sensation in the lower limbs. What is the next step in management?
➔ Conservative treatment (NSAIDs, physical therapy) (localized mechanical back pain without red flags → treat conservatively, no imaging needed)
- Note: Likely muscle strain or ligament injury
- Treat with: NSAIDs, physical therapy, activity as tolerated
VS If Red Flags are present → Consider Imaging (MRI) & Workup:
- Age >50
- History of cancer
- Fever or infection risk (IVDU, immunosuppression)
- Trauma
- Neurologic deficits (eg, saddle anesthesia, bowel/bladder issues)
- Unintentional weight loss
- Night pain
Differential Diagnosis of Low Back Pain
| Condition | Key Features |
|---|---|
| Mechanical (muscle strain) | Localized pain, no neuro signs, triggered by movement/lifting |
| Disc herniation | Radiculopathy, positive straight leg raise, dermatomal pain |
| Spinal stenosis | Pain worse with walking/standing, relieved by sitting/flexion |
| Vertebral osteomyelitis | Fever, IVDU, back tenderness, ↑ESR/CRP |
| Metastatic cancer | Constant pain, night pain, weight loss, history of malignancy |
| Epidural abscess | Triad: Fever + back pain + neurologic deficit |
| Cauda equina syndrome | Urinary retention, saddle anesthesia, decreased rectal tone (surgical emergency) |
47. A 67-year-old woman has bilateral buttock, posterior thigh, and calf pain after walking or standing for 10 minutes. The pain is relieved by sitting or bending forward. Neurologic exam is normal. What is the most appropriate next step in diagnosis?
➔ MRI of the lumbar spine (to evaluate for spinal stenosis) (neurogenic claudication relieved by flexion + normal exam → suspect spinal stenosis → MRI)
- Note: Spinal canal narrowing compresses nerve roots → causes neurogenic claudication
- Best initial test is → MRI lumbar spine
- Treatment:
○ Conservative: PT, NSAIDs, ± steroid injections
○ Surgery: Laminectomy if disabling
48. A 60-year-old man with diabetes and recent IV drug use presents with fever, severe back pain, and new-onset lower extremity weakness. Exam shows tenderness over the lumbar spine. What is the diagnosis?
➔ Spinal epidural abscess (fever + severe back pain + neuro deficits + IVDU → think epidural abscess)
- Note: May present without fever → just high WBC/ESR
- IVDU, immunosuppression → increase the risk
- Confirm diagnosis with → MRI spine with contrast
- Treat with → IV vancomycin + ceftriaxone/cefepime ± surgical drainage if deficits
49. A 59-year-old man presents with bilateral leg weakness, urinary retention, and numbness in the inner thighs and buttocks. Exam shows decreased rectal tone and saddle anesthesia. MRI confirms the diagnosis. What is the next step in management?
➔ IV steroids (Signs of Cauda Equina Syndrome → urgent imaging + steroids + surgery)
- Note: Compression of cauda equina nerve roots (L2 and below) → leads to Cauda Equina Syndrome
○ Compression causes include Herniated disc, tumor, trauma, abscess - 1st step is → Emergent MRI of lumbosacral spine
- Treat with IV dexamethasone → urgent surgical decompression
Always rule out spinal epidural abscess if fever + back pain + neuro deficits
| Feature | Cauda Equina | Conus Medullaris |
|---|---|---|
| Onset | Gradual | Sudden |
| Weakness | Asymmetric, LMN | Symmetric (UMN + LMN) |
| Reflexes | Hyporeflexia | Mixed (↓ or ↑) |
| Sensory loss | Saddle anesthesia (variable) | Perianal more symmetric |
| Bowel/bladder | Late (overflow) | Early (retention/incontinence) |
50. A 45-year-old man presents with back pain radiating to the medial leg and medial foot. Exam shows reduced knee extension strength and diminished patellar reflex. What is the diagnosis?
➔ L4 Radiculopathy (radiating pain + ↓ knee extension + ↓ patellar reflex → L4 nerve root involvement)
- Note: Motor: Weak knee extension (quadriceps), hip adduction
- Reflex: ↓ patellar reflex
- Sensory: Medial leg + foot (L4 dermatome)
- Management: Conservative (NSAIDs, PT)
○ if severe/persistent → Do MRI
Radiculopathy: L4 vs L5 vs S1
| Nerve Root | Motor Deficit | Reflex Affected | Sensory Loss |
|---|---|---|---|
| L4 | Knee extension (quads), hip adduction | ↓ Patellar | Medial leg, medial foot, hallux |
| L5 | Dorsiflexion (foot drop), toe extension | None | Lateral leg, dorsum of foot, big toe |
| S1 | Plantarflexion, hip extension | ↓ Achilles | Posterior leg, lateral foot, sole |
51. A 6-year-old boy with Down syndrome presents for preoperative evaluation before a tonsillectomy. He has no symptoms, but a physical exam reveals hyperreflexia and a positive Babinski sign. What is the next step?
➔ Cervical spine X-rays (flexion/extension views) (Down syndrome + upper motor neuron signs → evaluate for atlantoaxial instability)
- Note: Atlantoaxial instability (AAI) = excessive mobility between C1 and C2 → risk of spinal cord compression
- Seen in → Down syndrome & Rheumatoid arthritis
Peripheral Neuropathies & Neuromuscular Junction Disorders
52. A 62-year-old man presents with progressive bilateral hand tremor that worsens with activity and improves after drinking alcohol. He has no rigidity or bradykinesia. What is the next step in management?
➔ Start propranolol (bilateral action tremor + improvement with alcohol → think essential tremor)
- Note: It is an Action tremor → worse with movement, better with rest
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Parkinson disease | Resting tremor, bradykinesia, rigidity, unilateral onset |
| Cerebellar tremor | Intention tremor, ataxia, dysmetria |
| Physiologic tremor | Fine, high-frequency; triggered by anxiety, meds, hyperthyroidism |
| Dystonic tremor | Irregular tremor with abnormal posturing, younger onset |
53. A 26-year-old medical intern notices fine hand tremors when holding instruments during surgery. He recently started drinking more coffee and reports trouble sleeping. What is the most likely diagnosis?
➔ Enhanced physiologic tremor (fine, symmetric, high-frequency tremor + stress/caffeine → think physiologic tremor)
- Note: Triggers include → Anxiety, caffeine, sleep deprivation, medications (e.g., albuterol, SSRIs)
- Management: Remove triggers; reassurance
54. A 45-year-old woman presents with nocturnal hand numbness and tingling in the thumb, index, and middle fingers. Shaking her hand provides relief. What is the initial step in management?
➔ Wrist splinting at night (median nerve compression symptoms → start with conservative management)
- Note: Associated with: Pregnancy, hypothyroidism, RA, amyloidosis, acromegaly, obesity, trauma
- Classic signs: + Tinel’s (percussion) and Phalen’s (wrist flexion) tests
- Treatment:
○ Mild: Wrist splinting (esp. at night), glucocorticoid injection
○ Severe/persistent: surgical decompression
Differentiate from: Ulnar nerve entrapment → causes paresthesia in medial 1½ digits, hypothenar atrophy
55. A 58-year-old man with poorly controlled type 2 diabetes presents with numbness and burning pain in both feet for the past few months. Examination reveals decreased vibration and pinprick sensation in a stocking-glove distribution.. What is the cause?
➔ Diabetic peripheral neuropathy (Bilateral stocking-glove sensory loss + reduced reflexes + diabetes history → Indicates symmetric peripheral neuropathy → Most commonly due to diabetic neuropathy)
- Note: Complications → Ulcers, Charcot joint, infections
- Treatment with → Optimize glycemic control; symptomatic relief with pregabalin, gabapentine, duloxetine, or TCAs
56. A 32-year-old man presents with progressive bilateral leg weakness and areflexia following a diarrheal illness 2 weeks ago. Vitals show labile blood pressure. What is the next step in management?
➔ Assess pulmonary function with spirometry (Post infection ascending weakness + autonomic signs → suspect GBS; check FVC to monitor for respiratory failure)
- Note: A key feature is → albuminocytologic dissociation (↑ protein, normal WBCs)
- Triggers include: Campylobacter jejuni (most common), EBV, HIV, Vaccinations
- Treatment: IVIG or plasmapheresis
○ Monitor FVC (respiratory failure = major cause of mortality)
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Botulism | Descending paralysis, pupillary involvement |
| Tick paralysis | Rapid ascending paralysis (can be unilateral unlike GBS), no autonomic features, linked to tick exposure |
57. A 28-year-old woman presents with intermittent diplopia, ptosis, and proximal muscle weakness that worsens in the evening. Neurologic exam shows normal reflexes. Ice pack test improves her ptosis. What is the diagnosis?
➔ Myasthenia Gravis (MG) (fluctuating weakness + ocular symptoms + ice pack test improvement → Think MG)
- Note: Ice pack test: ↓ ACh breakdown → improves ptosis (supports MG)
- Diagnosed with Anti-AChR antibodies + repetitive nerve stimulation
- Treat with Pyridostigmine
○ in severe cases → steroids/immunosuppressants;
○ In case of crisis → IVIG/plasmapheresis
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Lambert-Eaton Myasthenic Syndrome (LEMS) | Improves with use, absent reflexes, autonomic symptoms, associated with small cell lung cancer, ↓ ACh release |
| Botulism | Descending paralysis, pupil involvement, toxin blocks ACh release |
| ALS | Both UMN + LMN signs, no fluctuation, no improvement with rest |
| Multiple Sclerosis | Young woman, optic neuritis, sensory symptoms, MRI brain with periventricular plaques |
58. A 65-year-old man with a history of smoking presents with progressive proximal muscle weakness, erectile dysfunction, and dry mouth. Reflexes are decreased but improve after brief exercise. What is the next step in management?
➔ Chest CT to evaluate for small cell lung cancer (proximal weakness + autonomic signs + reflexes improve with use → Think Lambert-Eaton Myasthenic Syndrome)
- Note: EMG shows → ↑ response on repetitive stimulation
- Treat underlying small cell lung cancer ± IVIG/steroids for symptom relief
Other neurologic disorders
59. A 17-year-old boy is brought to the ED after a football collision. He briefly loses consciousness and appears confused. He vomited once. On exam, he has no focal neurologic deficits. What is the diagnosis?
➔ Mild traumatic brain injury (concussion) (LOC + confusion + vomiting + normal neuro exam → think concussion)
- Note: Concussion presents with normal exam → so observe only → CT only if red flags
- Managed with Graded return of activity:
○ cognitive rest → school → sports (only after clearance)
○ if not, he will have persistent headache and amnesia - CT Indications (Red flags): GCS <15, focal deficits, persistent vomiting, seizure, anticoagulants, >65 y/o, skull fracture signs
Differentiate from
Epidural hematoma which causes Brief loss of consciousness → causing lucid interval → leading to deterioration
60. A 35-year-old woman experiences recurrent episodes of right arm tingling and numbness that gradually spread to her face. She remains fully alert during these episodes. What is the diagnosis?
➔ Simple partial somatosensory seizure (focal onset + preserved awareness → think simple partial seizure)
- Note: No LOC → distinguishes from complex (focal impaired) seizures
- Confirm clinical diagnosis with → EEG
- Consider MRI brain to rule out structural cause (tumor, stroke, AVM)
- Treat with → Anti-seizure meds (e.g., carbamazepine, levetiracetam)
- If consciousness is impaired consider → focal impaired awareness (complex partial)
61. A 6-year-old girl is brought by her teacher due to frequent brief episodes of staring lasting about 10 seconds. She is unresponsive during these episodes but returns to baseline immediately afterward with no confusion. EEG shows 3-Hz spike-and-wave discharges. What is the treatment?
➔ Ethosuximide (Sudden brief staring spells + no postictal confusion + 3-Hz spike-and-wave on EEG → Indicates absence seizure → Treat with Ethosuximide)
- Note: Often remits in adolescence
62. A 27-year-old man is brought to the ED after experiencing continuous generalized tonic-clonic seizures for the past 7 minutes. He has not regained consciousness between episodes. What is the next step?
➔ IV lorazepam (Seizure lasting >5 minutes without return to baseline → Indicates Status Epilepticus → Treat immediately with benzodiazepine)
- Note: First-line treatment → IV benzodiazepines (e.g., lorazepam)
63. A 46-year-old man is comatose after a severe intracranial hemorrhage. Neurologic examination shows absent brainstem reflexes and no response to painful stimuli. What is the next step to confirm the diagnosis?
➔ Perform an apnea test (no brainstem reflexes → assess spontaneous breathing to confirm brain death)
- Note: Absent brainstem reflexes include:
○ Pupillary light reflexCorneal reflex
○ Oculocephalic reflex (doll’s eyes)
○ Oculovestibular reflex (cold calorics
○ Gag and cough reflex - Confirm with clinical exam + apnea test (no respiratory effort when ↑PaCO₂)
- Brain death = legal death so → no consent needed to withdraw life support
- Spinal reflexes (e.g. triple flexion) may persist and do not rule out brain death
64. A 28-year-old woman receives epidural anesthesia during labor. Two days later, she complains of a severe headache that worsens when standing and improves when lying down..What is the diagnosis?
➔ Post-dural puncture headache (Headache following epidural → Indicates CSF leak from accidental dural puncture → Classic for post-dural puncture headache)
- Note: Improves when supine, worsens upright
- Treat with → Epidural blood patch if persistent
- Another common complication is hypotension (due to sympathetic blockade)
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Ophthalmology
65. A 28-year-old woman presents with acute unilateral vision loss and pain with eye movement. Exam shows decreased visual acuity and a relative afferent pupillary defect. MRI shows optic nerve hyperintensity. What is the diagnosis?
➔ Optic neuritis (Sudden, painful monocular vision loss in young woman → classic for optic neuritis)
- Note: Common presenting symptom of multiple sclerosis
- Treat with IV methylprednisolone → shortens symptom duration → no impact on long-term vision
Differential diagnosis of acute vision loss
| Condition | Key Features |
|---|---|
| Optic Neuritis | Unilateral vision loss, pain with eye movement |
| Amaurosis Fugax | Transient monocular vision loss (<10 min), embolic |
| Temporal (Giant Cell) Arteritis | Elderly, headache, jaw claudication, scalp tenderness |
| Retinal Detachment | Flashes, floaters, curtain-like shadow |
| Vitreous Hemorrhage | Sudden vision loss, floaters, seen in diabetic retinopathy |
| Acute Angle-Closure Glaucoma | Painful red eye, mid-dilated pupil, halos, ↑IOP, nausea/vomiting |
66. A 66-year-old man presents with sudden, painless, transient vision loss in his right eye lasting 5 minutes. He has a history of hypertension and smoking. Fundus exam is normal. What is the next step?
➔ Carotid duplex ultrasound (sudden transient monocular vision loss → Amaurosis Fugax → think embolic TIA from carotid artery)
- Note: Amaurosis Fugax can also be caused by → Giant cell arteritis (temporal arteritis)
- Order → ESR/CRP, platelets if GCA suspected (e.g., headache, jaw claudication)
67. A 72-year-old man with hypertension and a carotid bruit presents with sudden, painless vision loss in the right eye. Fundoscopy shows a pale retina with a cherry-red spot at the fovea. What is the next step in the workup?
➔ Carotid Doppler ultrasound (Symptoms suggestive of central retinal artery occlusion → Carotid doppler ultrasound to look for embolic source)
- Note: Workup includes:
○ Carotid Doppler & Echocardiogram (embolic source)
○ ESR/CRP/platelets if GCA suspected (especially >50 with headache/jaw pain)
Differential Diagnosis of Painless Vision Loss:
| Condition | Clues | Distinction |
|---|---|---|
| CRAO | Sudden, painless, cherry-red spot | Afferent pupillary defect |
| CRVO | “Blood and thunder” retina (retinal hemorrhage) | Wrinkled retina, visual field loss |
| Retinal Detachment | Flashes/floaters → curtain over vision | Wrinkled retina, visual field loss |
68. A 64-year-old woman presents with sudden, severe eye pain, blurred vision, and nausea. Eye exam reveals a red eye, a hazy cornea, and a fixed mid-dilated pupil. What is the diagnosis?
➔ Acute angle-closure glaucoma (Sudden unilateral red, painful eye + mid-dilated fixed pupil + blurred vision → think Acute angle-closure glaucoma)
- Note: Triggered by Mydriasis (e.g. dark rooms), topiramate, anticholinergics, anatomy (shallow anterior chamber)
- Diagnosis: Clinical + tonometry (↑IOP) ± gonioscopy
- Treatment:
○ Initial: Timolol, acetazolamide, pilocarpine
○ Definitive: Laser peripheral iridotomy (both eyes)
69. A 17-year-old boy presents after blunt trauma to the eye with pain and decreased vision. Slit-lamp exam shows blood layering in the anterior chamber. What is the diagnosis?
➔ Hyphema (blood in the anterior chamber due to trauma)
- Note: Blunt trauma → tears in iris root or ciliary body vessels
- Can lead to:
○ Corneal blood staining → may impair vision permanently
○ Retinal ischemia in sickle cell patients due to sickling & blockage - Manage with → eye shield, bed rest, head elevation
→ surgical treatment for SCD
70. A 6-year-old boy presents with red, watery eyes and a recent history of fever and rhinorrhea. Exam shows preauricular lymphadenopathy. What is the next step in management?
➔ Cool compresses, artificial tears (Symptoms suggestive of Viral Conjunctivitis)
Conjunctivitis Types Summary
| Type | Key Features | Management |
|---|---|---|
| Viral (Adenoviral) | Follicular pattern, watery discharge, preauricular lymphadenopathy | Supportive care (cool compresses, artificial tears) |
| Allergic | Papillary pattern, intense itching | Antihistamines ± mast cell stabilizers |
| Bacterial | Purulent discharge, no URI symptoms | Topical antibiotics (e.g., erythromycin, polymyxin) |
71. A 62-year-old man with poorly controlled diabetes presents for routine eye screening. He has no visual complaints. Fundoscopy shows microaneurysms, hard exudates, and cotton-wool spots. What is the diagnosis?
➔ Nonproliferative diabetic retinopathy (Asymptomatic + microaneurysms, hemorrhages, exudates → nonproliferative stage)
- Note: Early stages are asymptomatic → screen annually with dilated fundus exam
- Progresses to Proliferative: Neovascularization → risk of vitreous hemorrhage, retinal detachment
72. A 70-year-old man with longstanding hypertension presents for routine evaluation. Fundoscopy shows arteriovenous nicking, cotton-wool spots, flame hemorrhages, and a pale optic disc. What is the next step in management ?
➔ Strict BP control (chronic HTN → AV nicking + hemorrhages + cotton-wool spots → Hypertensive retinopathy → retinal microvascular damage)
73. A 35-year-old woman presents with eye pain, photophobia, and blurred vision in one eye. On examination, there is ciliary injection, a constricted pupil, and cells in the anterior chamber. What is the next best step in management?
➔ Initiate topical glucocorticoids and cycloplegics (Findings suggest anterior uveitis → start steroids + dilating drops to prevent complications)
- Note: Slit lamp confirms diagnosis
- Associated with: autoimmune diseases (e.g., HLA-B27 spondyloarthropathies, sarcoidosis, IBD)
74. A 2-year-old boy presents with leukocoria noted by his parents in photos. Exam shows an absent red reflex in the left eye. What is the next step in management?
➔ Urgent ophthalmology referral for MRI of brain/orbits (Leukocoria in a child → suspect retinoblastoma → rule out bilateral/multifocal disease)
- Note: Associated with RB1 gene mutation (autosomal dominant) → screen siblings if familial
- Increased osteosarcoma risk.
EAR
75. A 42-year-old woman presents with recurrent episodes of vertigo lasting several hours, unilateral hearing loss, and a ringing sensation in her left ear. Weber test lateralizes to the right, and Rinne is positive bilaterally. What is the diagnosis?
➔ Meniere disease (Episodic vertigo + sensorineural hearing loss Tinnitus ± ear fullness → think Meniere disease)
- Note: Treated with
○ Lifestyle: ↓ Salt, caffeine, alcohol, stress
○ Vertigo relief: Meclizine, promethazine
○ Refractory cases: Diuretics or surgical intervention
76. A 5-year-old boy presents with ear pain, fever, and purulent discharge from the right ear. Exam shows a red, bulging tympanic membrane with signs of rupture. What is the diagnosis?
➔ Acute Otitis Media with Tympanic Membrane Perforation (Ear pain + fever + purulent otorrhea → think acute otitis media with TM rupture)
- Note: Most common organisms: Streptococcus pneumoniae, H. influenzae, Moraxella
- Sudden pain relief + otorrhea → indicates TM rupture
- Treat with amoxicillin-clavulanate or fluoroquinolone ear drops if perforated
- Most TM perforations heal spontaneously without intervention
77. A 32-year-old swimmer presents with right ear pain, itching, and mild hearing loss. On exam, the external ear canal is erythematous, swollen, and tender to manipulation. What is the diagnosis?
➔ Otitis externa (Pain with pinna movement + canal edema/erythema → think otitis externa)
- Note: Treat with → Topical fluoroquinolone ± corticosteroid drops
78. A 72-year-old diabetic man presents with severe ear pain, headache, and purulent ear discharge for several days. Exam shows granulation tissue in the external auditory canal and cranial nerve VII palsy. What is the diagnosis?
➔ Malignant otitis externa (Severe otalgia + granulation tissue in diabetic/elderly → think malignant otitis externa)
- Note: Seen in elderly diabetics or immunocompromised
- Caused by → Pseudomonas aeruginosa
- Treat with → IV antipseudomonal antibiotics (e.g., ciprofloxacin), possible surgical debridement
- Differentiate from cholesteatoma → Chronic ear discharge + pearly mass + hearing loss → treat with surgery
79. A 40-year-old man presents with sudden-onset vertigo, nausea, and difficulty walking. He has no hearing loss or tinnitus. Symptoms started after a recent upper respiratory illness. Neurologic exam shows horizontal nystagmus but no focal deficits. What is the diagnosis?
➔ Vestibular neuritis (Post-viral persistent vertigo vertigo + no hearing loss → think vestibular neuritis)
- Note: Post-viral Inflammation of the vestibular branch of CN VIII (no cochlear involvement)
- No hearing loss → unlike labyrinthitis
- Treatment: Supportive — meclizine, antiemetics, vestibular rehab if prolonged
Differentials & Key Clinical Correlation
| Condition | Key Differentiator |
|---|---|
| Vestibular neuritis | Similar to labyrinthitis but no hearing loss |
| Ménière disease | Recurrent episodes, tinnitus, aural fullness, low-frequency hearing loss |
| BPPV | Brief vertigo episodes triggered by head position, positive Dix-Hallpike maneuver |
| Cerebellar stroke | Risk factors (HTN, AF), persistent vertigo with neurological signs |
| Acoustic neuroma | Chronic progressive hearing loss ± imbalance, MRI confirms diagnosis |
80. A 50-year-old woman reports brief episodes of dizziness lasting less than a minute, triggered by rolling over in bed or looking up. Neurologic exam is normal. What is the next best step in diagnosis?
➔ Dix-Hallpike maneuver (Positional vertigo + brief episodes (seconds) + normal exam → think benign paroxysmal positional vertigo (BPPV) → Do Positive Dix-Hallpike test for diagnosis)
- Note: Caused by Displaced otoliths in the semicircular canals
- Triggered by → head position changes (e.g., turning in bed, looking up)
- Treat with → Epley maneuver (canalith repositioning)
🏁 Final Thoughts
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Disclaimer
Version 1.0 August 2025. No part of this document may be reproduced or distributed without written permission. For personal study only. Medical information herein is for educational purposes and does not constitute clinical advice. Always confirm with current guidelines and your institution’s policies.
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