Intracranial pressure (ICP) is the pressure exerted by cerebrospinal fluid and/or masses on brain tissue.
ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally 7–15 mmHg for a supine adult.
The body has various mechanisms by which it keeps the ICP stable, with CSF pressures varying by about 1 mmHg in normal adults through shifts in production and absorption of CSF.
Changes in ICP are attributed to volume changes in one or more of the constituents contained in the cranium.
CSF pressure has been shown to be influenced by abrupt changes in intrathoracic pressure during coughing (intra-abdominal pressure), the valsalva maneuver, and communication with the vasculature (venous and arterial systems).
Intracranial hypertension is elevation of the pressure in the cranium.
ICP is normally 7–15 mm Hg; at 20–25 mm Hg, the upper limit of normal.
Changes in intracranial pressure (ICP) are clinically significant because they directly affect brain perfusion, brain tissue integrity, and overall neurologic function. Understanding the significance of ICP changes helps guide emergency and critical care management.
Below is a clear, structured explanation:
The skull is a closed, rigid compartment. It contains:
Brain tissue (~80%)
Cerebrospinal fluid (CSF) (~10%)
Blood (arterial + venous) (~10%)
These components are governed by the Monro–Kellie doctrine, which states that if one component increases, one or both of the others must decrease to maintain a normal ICP (typically 5–15 mm Hg in adults). When compensation fails, ICP rises.
Cerebral perfusion pressure = Mean arterial pressure (MAP) – ICP.
If ICP increases, CPP decreases.
Low CPP (<60–70 mm Hg) leads to cerebral ischemia.
Symptoms: reduced consciousness, focal neurological deficits, eventually herniation.
Thus, even a moderate increase in ICP can severely compromise brain oxygenation.
When ICP becomes markedly elevated, pressure forces brain tissue to shift across rigid intracranial structures.
Common herniation syndromes:
Uncal herniation: dilated pupil (CN III), hemiparesis.
Central herniation: progressive decline in consciousness, abnormal posturing.
Tonsillar herniation: compression of medulla → respiratory arrest → death.
Rapidly rising ICP is a neurosurgical emergency.
Increased ICP can impair CSF absorption at the arachnoid villi, worsening hydrocephalus.
This creates a vicious cycle of rising pressure.
The brain normally autoregulates blood flow.
When ICP rises significantly:
Autoregulation fails.
Cerebral vessels may constrict or dilate inappropriately.
Leads to further ischemia, edema, and ↑ICP.
This self-amplifying loop is called the intracranial hypertension spiral.
Even minor increases in ICP can produce early warning signs:
Headache
Nausea/vomiting (often projectile)
Papilledema
Restlessness/changes in mental status
Subtle cranial nerve abnormalities
Cushing’s triad (bradycardia, hypertension, irregular respirations)
Decline in LOC
Posturing (decorticate/decerebrate)
Pupillary changes
Late signs indicate very high ICP and impending herniation.
Increased ICP suggests a dangerous process:
Traumatic brain injury
Intracranial hemorrhage
Stroke with edema
Brain tumor
Abscess
Hepatic encephalopathy
Hydrocephalus
Thus, changes in ICP often reflect disease progression or treatment failure/success.
ICP trends influence management:
When to hyperventilate (temporarily reduce CO₂ to lower ICP)
When to give mannitol or hypertonic saline
When to drain CSF
When to perform decompressive craniectomy
Safe transfer decisions for critically ill neurologic patients
Changes in intracranial pressure are significant because they:
Directly influence cerebral perfusion
Predict risk of brain herniation
Indicate worsening or improving brain pathology
Guide life-saving interventions
Rapidly rising ICP is a medical emergency requiring immediate evaluation and management.
Clinical Senario
Here is a clear, realistic clinical scenario showing how changes in intracranial pressure (ICP) develop, how they manifest, and why they matter.
A 32-year-old man is brought to the emergency department after a motorcycle accident. He was initially awake but confused at the scene.
GCS: 14 (confused)
Vital signs: BP 134/82, HR 98, RR 20
Findings: Right temporal scalp hematoma
CT scan: Small right temporal epidural hematoma, minimal midline shift
ICP (if monitored): ~18 mm Hg (elevated but still compensating)
The skull can compensate somewhat by reducing venous blood and displacing CSF.
Patient has mild ICP elevation → subtle symptoms.
Headache
Confusion
Nausea
These are early signs of increasing ICP.
Patient becomes more somnolent; arousable only to voice
Vital signs: BP 150/88, HR 85
Repeat CT: Hematoma has enlarged
ICP: ~25–28 mm Hg
Compensatory mechanisms are failing.
CPP is beginning to fall.
CPP = MAP – ICP
If MAP ≈ 108 mm Hg and ICP ≈ 28 → CPP ≈ 80 mm Hg (borderline but decreasing)
Worsening headache
Persistent vomiting
Slowing responsiveness
This stage shows declining cerebral perfusion.
Nurse notes:
Patient difficult to awaken
Left pupil slightly larger and slower to react
Vital signs: BP 165/90, HR 68 (starting Cushing response)
This indicates marked intracranial hypertension with early transtentorial (uncal) herniation.
Ipsilateral (right-sided) uncal herniation → compression of CN III on right
Right pupil dilated ("blown") and non-reactive
Left arm weakness
Changes in breathing pattern (irregular)
This is a neurosurgical emergency.
Mannitol or hypertonic saline administered
Patient is intubated and mildly hyperventilated (temporary ICP reduction)
Neurosurgeon performs emergent craniotomy and evacuation of epidural hematoma
Post-op ICP drops to 12 mm Hg
Mental status gradually improves
After surgical decompression and ICU management:
Patient regains full consciousness by day 3
Discharged with mild short-term memory issues but no major deficits
Compensation → Decompensation → Intracranial hypertension → Herniation
Early: headache, confusion
Intermediate: vomiting, somnolence
Late: pupillary changes, Cushing triad, posturing
Even if blood pressure increases, rising ICP can critically reduce brain perfusion.
Often indicate impending herniation.
Mannitol, CSF drainage, hypertonic saline, hyperventilation (short-term), and surgery.
If you’d like, I can provide:
A pediatric version of this scenario
A medical student “exam-style” question with answer
A diagram illustrating the ICP progression
A scenario involving stroke, brain tumor, or hepatic encephalopathy