Pain in the brain
List three categories of secondary headaches that present with neurologic symptoms.
Vascular (SAH, CVST, ICH), Infectious (meningitis/encephalitis), Structural (mass, IIH)
Which cranial nerve finding best indicates increased ICP and why?
CN VI palsy — long intracranial course vulnerable to downward pressure shifts.
Why is glucose decreased in bacterial meningitis but not viral?
Bacteria consume glucose and impair transporter function; viruses rely on host metabolism only.
Explain why encephalitis produces seizures while meningitis usually does not.
Parenchymal involvement disrupts cortical neurons and synapses → hyperexcitability and seizure generation.
Explain why primary maternal HSV near delivery increases neonatal risk.
No maternal IgG antibodies → fetus lacks passive protection; high viral shedding.
Explain the mechanism of thunderclap headache in subarachnoid hemorrhage.
Rapid rupture of berry aneurysm → meningeal irritation by blood → trigeminal nociceptor activation → sudden pain.
Describe the Monro–Kellie doctrine and its clinical relevance.
Cranial volume fixed = brain + CSF + blood; increase in one → compensatory decrease in others; decompensation = rapid ICP rise → herniation.
Explain the protein elevation in bacterial meningitis.
BBB permeability increases → serum proteins leak into CSF + bacterial lysis products.
Trace HSV entry from oral mucosa to temporal lobe.
HSV-1 infects epithelial cells → retrograde axonal transport via trigeminal/olfactory nerve → latency in ganglia → reactivation → CNS invasion.
Mechanism by which HSV crosses from mucosa to CNS in a neonate.
Viral replication at entry → retrograde axonal spread to sensory ganglia → CNS via trigeminal or sacral nerves.
Differentiate between headache from increased ICP vs meningeal irritation using history and exam.
↑ICP: morning-worse, vomiting, papilledema
meningeal: photophobia, nuchal rigidity, positive Kernig/Brudzinski.
Explain why LP can cause herniation in patients with mass effect.
Pressure gradient from rapid CSF removal → cerebellar/uncal herniation through tentorium or foramen magnum.
A CSF sample shows 500 lymphocytes, high protein, normal glucose — what are two viral causes and their mechanisms?
HSV (latent trigeminal infection → reactivation → necrosis) and enterovirus (fecal-oral spread → hematogenous).
Pathologic hallmark of HSV encephalitis on histology and its cause.
Hemorrhagic necrosis due to viral replication, endothelial injury, and immune-mediated destruction in limbic cortex.
Compare immune responses in neonatal HSV vs adult HSV encephalitis.
Neonates: immature innate/interferon response → disseminated spread; adults: localized necrotizing inflammation.
A 40-year-old with thunderclap headache and normal CT — what is the next diagnostic step and why?
LP for xanthochromia — bilirubin from RBC breakdown confirms SAH missed on early CT.
Mechanistic link: how does inflammation in meningitis increase ICP?
Cytokine-driven BBB permeability → vasogenic edema + impaired CSF reabsorption → raised ICP and papilledema.
Differentiate fungal/TB from bacterial CSF using immunologic mechanisms.
Fungal/TB → Th1 immune response → lymphocytic inflammation, granuloma formation → ↓ glucose, ↑ protein.
Bacterial meningitis: extracellular pathogens → activate innate immune system → neutrophils flood CSF quickly.
Fungal/TB meningitis: intracellular or slow-growing organisms → activate a delayed-type hypersensitivity (Type IV) response dominated by Th1 lymphocytes.
Explain the clinical triad of HSV encephalitis (AMS, fever, focal deficits) using neuroanatomy.
Altered Mental Status (AMS) & Behavioral Changes
Involvement of the limbic system—particularly the amygdala and orbitofrontal cortex—disrupts emotional regulation and judgment.
Extension to the hippocampus impairs short-term memory and orientation, contributing to confusion and personality change.
Fever
Reflects systemic and central cytokine release from viral replication and necrotizing inflammation within these richly vascularized cortical areas.
Focal Neurologic Deficits & Seizures
Temporal cortex irritation produces focal seizures, often with olfactory or gustatory auras.
In the dominant temporal lobe, involvement of Wernicke’s area causes receptive aphasia or paraphasic speech errors.
Spread to adjacent insular or frontal regions can yield hemiparesis or other focal findings.
Predict lab abnormalities in disseminated neonatal HSV and explain why.
Elevated AST/ALT, DIC, thrombocytopenia — hepatic necrosis and systemic endothelial injury from viremia
Integrate pathophysiology: how does infection, mass, and hemorrhage each produce headache via the same neural mechanism?
All cause distention/inflammation of pain-sensitive meninges and blood vessels, activating CN V and C2 afferents → referred pain to head/scalp.
Distinguish cytotoxic vs vasogenic edema and identify which predominates in HSV encephalitis.
Cytotoxic = intracellular Na⁺/water accumulation (ischemia); Vasogenic = BBB disruption (infection/tumor). HSV → both, but vasogenic dominates due to necrotizing inflammation.
Compare the underlying mechanisms of elevated opening pressure across bacterial, fungal, and viral infections.
Bacterial: exudate blocks CSF flow; fungal/TB: granulomatous obstruction; viral: inflammation-induced CSF overproduction and decreased reabsorption.
Why does early IV acyclovir improve outcomes, and why is timing critical?
Acyclovir inhibits viral DNA polymerase; early use limits replication before irreversible necrosis; delay allows viral-induced apoptosis and vasculitis.
Explain why suppressive acyclovir is continued after neonatal CNS HSV treatment.
Reduces relapse by suppressing residual latent virus in ganglia until immune system matures.