Central Nervous System Physiology

Also written as Brain‑Spinal Axis.

The brain and spinal cord operate within a rigid, non‑expansile compartment, relying on cerebrospinal fluid dynamics and vascular autoregulation. Disruption of these mechanisms produces focal neurological signs, raised intracranial pressure, and systemic complications.

Overview

The brain and spinal cord are protected by the skull, vertebral column, meninges and cerebrospinal fluid (CSF). They depend on tightly regulated blood flow, CSF production/absorption, and neuronal signaling to maintain consciousness, motor control and autonomic function.

• Rigid compartment limits volume expansion → small increases in content raise pressure.
• CSF is produced mainly by choroid plexus (≈500 mL/day) and absorbed via arachnoid villi.

How it works

Neuronal activity generates metabolic demand met by cerebral autoregulation (maintains flow 50‑150 mL/100 g/min). CSF cushions the CNS and removes waste; its pressure (ICP) normally 5‑15 mm Hg.

• Autoregulation: vessels dilate when MAP falls <70 mm Hg, constrict when MAP >150 mm Hg.
• Blood‑brain barrier restricts entry of large molecules, protecting neural tissue.

Regulation

ICP is balanced by the Monro‑Kellie doctrine: the sum of brain tissue, blood, and CSF volumes is constant. Venous outflow, CSF absorption and respiratory CO₂ drive are key modulators.

• Fundoscopic examination: Detects papilledema, indicating chronic ICP elevation; a normal exam suggests ICP <20 mm Hg.
• Bedside optic nerve sheath diameter (ultrasound): Estimates ICP when CT unavailable; diameter >5 mm suggests ICP >20 mm Hg.

• Hypercapnia → cerebral vasodilation → ↑ ICP.
• Hypocapnia → vasoconstriction → ↓ ICP.

What goes wrong

Common pathologies in low‑resource settings include meningitis, tuberculous meningitis, cerebral malaria, HIV‑related opportunistic infections, and spinal epidural abscesses. All raise ICP or produce focal deficits.

• Lumbar puncture (LP) – opening pressure: Answers if ICP is elevated; opening pressure >250 mm H₂O indicates raised ICP. If unavailable, rely on clinical signs.
• CSF analysis: Distinguishes bacterial vs. TB vs. viral meningitis; low glucose <40 mg/dL and high protein >100 mg/dL suggest bacterial.
• Rapid malaria test: Detects Plasmodium falciparum; a positive test in a comatose patient points to cerebral malaria.

• Meningitis: fever, neck stiffness, photophobia, altered mental status; CSF pleocytosis >100 cells/µL.
• TB meningitis: subacute headache, cranial nerve palsies, basal meningeal enhancement on imaging.
• Cerebral malaria: seizures, coma, retinal hemorrhages; parasitemia >5 %.
• Spinal epidural abscess: back pain, fever, motor weakness; MRI gold standard.

Clinical relevance

Bedside assessment focuses on level of consciousness (GCS), focal deficits, and signs of raised ICP. Early recognition of treatable infections and prompt ICP control are lifesaving.

• Glasgow Coma Scale: Quantifies consciousness; score ≤8 mandates airway protection.
• Kernig’s sign: Positive when leg cannot be extended with hip flexed 45°; suggests meningeal irritation.

• GCS ≤8 → airway protection, consider intubation.
• New focal weakness → urgent imaging if available; otherwise, treat presumptive infection.

Exam pearls

Examiners test integration of physiology with clinical decision‑making: interpreting ICP changes, choosing empiric therapy, and recognizing red‑flag signs.

• Distinguish raised ICP from metabolic encephalopathy by checking papilledema and CSF pressure.
• Know first‑line empiric antibiotics for bacterial meningitis in East Africa (ceftriaxone + vancomycin).
• Identify when steroids are indicated (TB meningitis, bacterial meningitis with high inflammation).

Questions an examiner may ask

• A 4‑year‑old with fever, neck stiffness, and GCS 13 – what is your next diagnostic step and why? — Perform LP after ruling out raised ICP; CSF analysis will differentiate bacterial from TB meningitis.
• A patient with HIV presents with headache and cranial nerve VI palsy – which condition is most likely and how would you confirm it? — Tuberculous meningitis; confirm with CSF analysis (high protein, low glucose) and, if possible, MRI showing basal meningeal enhancement.
• In a comatose malaria patient, papilledema is absent – can you exclude raised ICP? — No; papilledema may be delayed; assess ICP with optic nerve sheath ultrasound or LP if safe.
• You suspect spinal epidural abscess but MRI is unavailable – what management should you start? — Begin empiric IV ceftriaxone + metronidazole covering Staph aureus and anaerobes, monitor neuro status, arrange transfer for imaging.
• Why is hyperventilation used temporarily in acute raised ICP? — It lowers PaCO₂, causing cerebral vasoconstriction and transient ICP reduction; only a bridge to definitive therapy.
• Explain the Monro‑Kellie doctrine and its clinical implication in traumatic brain injury. — The rigid skull contains fixed volume; any increase in brain, blood, or CSF raises ICP, necessitating rapid decompression.
• When is dexamethasone contraindicated in meningitis? — In viral meningitis and when the causative organism is unknown and bacterial coverage is not started, because steroids may worsen outcomes.
• A patient on antiretroviral therapy develops seizures and CSF shows 150 cells/µL with lymphocytic predominance – what is the likely diagnosis? — HIV‑associated cryptococcal meningitis; confirm with India ink stain or cryptococcal antigen test.

When to seek help

• Rapidly decreasing GCS
• New onset seizures
• Signs of brain herniation (fixed dilated pupils, posturing)
• Severe neck stiffness with fever

Quick questions

Why is CSF pressure measured before removing fluid?

Opening pressure reflects true ICP; removing fluid can artificially lower pressure and mask pathology.

Can malaria cause raised ICP?

Yes, cerebral malaria leads to sequestration of infected erythrocytes, causing cerebral edema and raised ICP.

When are steroids useful in meningitis?

Adjunctive dexamethasone reduces inflammation in bacterial meningitis (especially pneumococcal) and is essential in TB meningitis.