Intracranial pressure (ICP) is the pressure that exists within the cranium, including its compartments (e.g., the subarachnoid space and the ventricles). ICP varies as the position of the head changes relative to the body and is periodically influenced by normal physiological factors (e.g., cardiac contractions). Adults in the supine position typically have a physiological ICP of ≤ 15 mm Hg; an ICP of ≥ 20 mm Hg indicates pathological intracranial hypertension. ICP may be elevated in a variety of conditions (e.g., intracranial tumors) and can result in a decrease in cerebral perfusion pressure (CPP) and/or herniation of cerebral structures. Symptoms of elevated ICP are generally nonspecific (e.g., impaired consciousness, headache, vomiting); however, more specific symptoms may be present depending on the affected structures (e.g., Cushing triad if the brainstem is compressed). Findings from brain imaging (e.g., a midline shift) and physical examination (e.g., papilledema) can indicate ICP elevation, but may not be able to rule it out. Therefore, ICP monitoring and quantification are vital in at-risk patients. Management usually involves expedited surgery of resectable or drainable lesions, conservative measures (e.g., positioning, sedation, analgesia, and antipyretics), and medical therapy (e.g., hyperosmolar therapy such as mannitol or hypertonic saline, or glucocorticoids). Treatment options for refractory intracranial hypertension include temporary controlled hyperventilation, CSF drainage, and decompressive craniectomy (DC), as well as other advanced medical therapies (e.g., barbiturate coma, therapeutic hypothermia).
- CNS inflammation, infection, and/or abscess
- Space-occupying lesions
- Elevated venous pressure (e.g., as a result of heart failure)
- Increased CSF ()
- Metabolic disturbances; (e.g., , hepatic encephalopathy)
- seizures and
- Physiological ICP is ≤ 15 mm Hg in adults (in supine position), children generally have a lower ICP
- ICP varies with the relative position of the head towards the rest of the body and is influenced by certain physiological processes (e.g., cardiac contractions, sneezing, coughing, ).
- Expansion of either blood, CSF, or tissue within the skull → limited capacity for the intracranial volume to increase within the rigid skull → increase in intracranial pressure
Consequences of elevated ICP
Decreased cerebral perfusion pressure (CPP)
- CPP is the effective pressure that delivers blood to the cerebral tissue.
- CPP = mean arterial pressure - ICP
- Therefore, if the ICP rises, the CPP diminishes (as long as the arterial pressure remains constant).
Brain tissue herniation
- As a bony structure, the skull is rigid and can not expand to compensate elevated internal pressure.
- Increased pressure gradient within the skull in the presence of inflexible brain structures (e.g., tentorium cerebelli) → flexible brain tissue shifts → possible brain tissue herniation
- This may result in direct physical damage or in blocking of cerebral vessels and subsequent ischemia.
- ↑ Intracranial pressure → ↓ perfusion pressure within the brain → compensatory activation of the sympathetic nervous system to maintain cerebral perfusion → ↑ systolic blood pressure → stimulation of aortic arch baroreceptors → activation of the parasympathetic nervous system (vagus) → bradycardia
- ↑ Pressure on brainstem → dysfunction of respiratory center → irregular breathing
- Subfalcine herniation: cingulate gyrus of one hemisphere is compressed and herniates under the falx cerebri → compression of:
Uncal herniation: medial temporal lobe (the uncus) herniates at the tentorial incisure
- → Compression of:
- Ipsilateral oculomotor nerve palsy → fixed and dilated pupil
- Ipsilateral posterior cerebral artery → cortical blindness with contralateral homonymous hemianopia
- Contralateral cerebral peduncle → ipsilateral paralysis + Kernohan phenomenon: a paradoxical ipsilateral weakness (due to contralateral cerebral peduncle compression). This is unusual because commonly, an ipsilateral brain lesion results in contralateral motor symptoms. It occurs in patients with increased ICP caused by intracranial hemorrhage or cerebral edema.)
- → Downward shift of the brainstem → brainstem hemorrhages → focal deficits, impaired consciousness, death
- → Compression of:
- Foramen magnum herniation: structures of the posterior fossa (e.g., cerebellar tonsils, medulla) herniate at the foramen magnum → impaired consciousness, decerebrate posturing, apnea, impaired circulation, death
Neuroimaging (CT head/MRI head) 
Neuroimaging findings of intracranial hypertension: indirect indicators of elevated ICP and cerebral edema
- Midline shift
- Mass lesions
- Effacement of the basilar cisterns
- Effacement of cerebral sulci
- Evidence of brain herniation (e.g., uncal herniation or tonsillar herniation)
- Changes in ventricular size (e.g., enlarged with hydrocephalus, reduced with diffuse cerebral edema)
Invasive ICP monitoring
- Invasive monitoring is typically required for confirmation and accurate measurement of ICP.
- ICP should be evaluated in combination with CPP to guide therapeutic interventions and help prevent secondary brain injury and brain herniation. 
- There are no absolute contraindications for invasive ICP monitoring.
- Consider the risks versus the benefits in consultation with a specialist.
- Traumatic brain injury: ICP monitoring in severe TBI reduces in-hospital and two-week postinjury mortality. 
- Mass lesions: e.g., brain tumors, ICH, SAH, SDH, EDH
- Diffuse brain injury due to:
- Other: nonsurgical intracranial hemorrhages in patients who cannot undergo full clinical evaluation
Methods to monitor ICP 
Intraventricular catheters; with an external ventricular drain (EVD) and intraparenchymal catheters; (IPC) are most commonly used to monitor ICP, as they have the highest accuracy compared with other monitoring methods.
Intraventricular catheter: a monitoring device placed into the ventricles of the brain along with a CSF drainage system (i.e., an EVD) 
- Allows for continuous ICP monitoring and evaluation of intracranial compliance
- Useful in conditions in which CSF drainage is required for both diagnostic and therapeutic purposes
- The preferred monitoring method for intracranial lesions associated with hydrocephalus 
- Hemorrhage attributable to the placement of the device
- Malpositioning and/or accidental removal
- Blockage with blood or debris
Intraparenchymal catheter: a fiberoptic device placed into the brain parenchyma without an accompanying CSF drainage system 
- Allows for continuous ICP monitoring
- Accuracy and effect on patient outcomes are considered equivalent to intraventricular catheters
- Lower risk of infection and hemorrhage compared with intraventricular catheters
- Technical complications: e.g., dislodgement, breakage
- Generally, ICP > 20 mm Hg indicates intracranial hypertension, which requires treatment. 
- ICP varies in a complex cyclical manner and is influenced by hemodynamic and metabolic factors.
- Monitor ICP along with CPP = MAP − ICP. to calculate using the formula
Do not use the ICP value in isolation as a prognostic marker or to inform therapeutic decisions. 
- Indications for ICP management
- Goals: Maintain (CBF) and prevent .
- Acute resuscitation and stabilization: Follow the .
- Consultation: Early involvement of neurosurgery and a neurocritical care specialist is essential.
|Stepwise ICP management (based on a multifactorial response) |
|Subsequent step|| |
|Elective temporizing step|
General therapeutic targets: Base treatment decisions on trends identified using repeat assessments of ICP, CPP, and clinical status. 
- Target ICP: < 20 mm Hg
- Target CPP range: 60–70 mm Hg
Conservative therapy 
See also “Neuroprotective measures.”
- Patient positioning ;:
Sedation and analgesia 
- Prevents unnecessary spikes in ICP due to pain, agitation, and patient-ventilator dyssynchrony
- Combinations of benzodiazepines, opioid analgesics, and dexmedetomidine are generally used.
- Ketamine was previously contraindicated, but recent evidence suggests that it may be suitable for use.
- Propofol may be used but caution should be taken when using high doses because of the risk of hypotension. 
- Minimize waking patients up for neurological assessments.
- See “ ” for dosages and further information.
- Temperature management: : Maintain normothermia; fever should be treated with antipyretics.
- Fluid management: Target euvolemia and avoid serum hypoosmolarity.
- Seizure control
Medical therapy 
- Hyperosmolar therapy
|Overview of hyperosmolar therapies in ICP management |
|Pharmacology || |
|Therapeutic targets to consider |
|Adverse effects |
|Considerations || || |
Although hyperosmolar therapies can lower ICP, they have not been shown to improve neurological outcomes in patients with underlying TBI, acute ischemic stroke, ICH, SAH, or hepatic encephalopathy. 
Glucocorticoids: e.g., dexamethasone
- Recommended only if elevated ICP is caused by vasogenic edema secondary to: 
- Avoid in patients with ICH. 
- Not recommended in large hemispheric stroke 
- Contraindicated in TBI (associated with increased mortality) 
- Emergency surgery (if possible): e.g., resection of brain tumor, hematoma evacuation 
- Indications 
- Risks: hemorrhage, infection (e.g., ventriculitis, encephalitis, meningitis)
Decompressive craniectomy (DC): removal of a portion of the skull, which allows the brain to expand in volume, thereby reducing ICP 
- Primary DC: removal of a skull flap following evacuation or resection of an intracranial lesion (e.g., brain tumor)
- Secondary DC: removal of a skull flap without additional surgical procedures to treat refractory elevated ICP
- Recommended for (controversial): 
- Late refractory elevated ICP: reduced mortality, improved outcomes
- Early or late refractory elevated ICP: improved control of ICP, reduced neuro-ICU length of stay
- Large hemispheric stroke (e.g., malignant MCA infarction) in patients with an infarct > 12 cm and within 24–48 hours of symptom onset 
- Not recommended for patients with early refractory elevated ICP
- Recommended for (controversial): 
- Multiple approaches have been described in the literature (suboccipital, subtemporal, frontotemporoparietal, etc.) depending on the type and location of the brain lesion. 
- Lowers mortality in TBI without improving neurological or functional outcomes 
Nonsurgical therapy for refractory intracranial hypertension 
- Indications 
- Therapeutic targets
Controlled hyperventilation should only be used short-term and is not recommended routinely or for prophylaxis. Avoid excessive hyperventilation (PaCO2 < 30 mm Hg), prolonged hyperventilation, and hypoventilation of any kind, as CBF and perfusion may become compromised.
These are primarily reserved for patients with persistently refractory intracranial hypertension.
- Barbiturate coma: e.g., pentobarbital (off-label, not routinely recommended) 
Therapeutic hypothermia: highly controversial 
- No benefit has been observed when used prophylactically 
- Not recommended in TBI 
Irreversible loss of brain function (brain death)
- Definition: irreversible, complete loss of function of the entire brain (including the brainstem), even if cardiopulmonary functions can be upheld by artificial life support.
- Practical steps for determination of brain death: The American Academy of Neurology has published a practical guide that consists of four steps. It cites specific measures and interpretations (e.g., limits of body temperature) that can be used to determine brain death, although not all of them are evidence-based
Requirements for the diagnosis of brain death
- Loss of brain function must be attributable to a specific cause (e.g., clinical or radiologic evidence of acute, severe damage to the CNS that is consistent with brain death).
- Irreversible loss of brain function
- Factors that may impede proper clinical judgment must be absent.
- Coma (with a known cause)
Absence of brainstem reflexes
- eye normally causes pupils to constrict in adaptation to bright light) (shining of light into the
Vestibuloocular reflex (VOR): eye movement that is ellicited by activating the semicircular canals of the vestibular system and mediated by the afferent sensory pathway of CN VIII and the efferent motor pathway of the contralateral CN VI and the ipsilateral CN III
- Oculocephalic maneuver: used to test VOR by observing the patient's eye movement while stimulating the vestibular system
- Caloric test: used to test VOR by stimulating the vestibular system
- Corneal reflex (touching of the cornea, e.g., with a sterile cotton swab, normally triggers blinking)
- Gag reflex (touching of either side of the pharynx, e.g., with a sterile tongue depressor, normally triggers gagging)
- Cough reflex (stimulation of the larynx or the respiratory epithelium normally provokes coughing)
- No reaction to irritation of trigeminal nerve branches (normally painful)
- Deep tendon reflexes are occasionally seen in brain-dead patients who have intact spinal cords
- Apnea (absence of breathing drive)
- Ancillary brain death tests: only to be performed if clinical examination and/or apnea testing are inconclusive, or if patient is < 1 year
- Definition: excess accumulation of fluid within the brain parenchyma as a result of damage to the blood-brain barrier and/or the blood-CSF barrier 
- Management: treatment of raised ICP
We list the most important complications. The selection is not exhaustive.