Intracranial pressure (ICP) is the pressure that exists within the skull and all of its compartments (e.g., the subarachnoid space and the ventricles). ICP varies with the relative position of the head towards the rest of the body and is periodically influenced by normal physiological factors (e.g., cardiac contractions). Adults in supine position have a physiological ICP of 15 mm Hg or less while a pressure of 20 mm Hg or more indicates pathological intracranial hypertension.
Elevation of ICP may occur 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 raised 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). Brain imaging (e.g., showing a midline shift) and physical examination (e.g., papilledema) can detect ICP elevation, but not necessarily rule it out. Therefore, ICP monitoring and quantification is vital in at-risk patients. Management usually involves osmotic diuretics such as mannitol or hypertonic saline. Further therapeutic options include controlled hyperventilation, removal of CSF, and decompressive craniectomy.
- 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
- CT/MRI: may indicate mass lesions, midline shift, or effacement of the basilar cisterns
- Ultrasound (e.g., ocular sonography): measures the optic nerve sheath diameter
Clinical examination and imaging may indicate elevated ICP, but cannot rule it out! Additionally, these tests do not allow quantification of intracranial pressure, which is necessary to determine CPP!
Invasive ICP monitoring
- Placement of monitors
- Analysis: > 20 mmHg indicates elevated intracranial pressure that requires treatment
Acute stabilization and treatment
- Resuscitation and emergency measures (head elevation, controlled hyperventilation and IV mannitol)
- Cardiopulmonary support
- Sedation, analgesia, antipyretic therapy, antiseizure medication
- General approach
- Goal of ICP management is generally to keep ICP < 20 mm Hg.
- Positioning : e.g., head elevation (about 30 degrees), avoiding neck flexion/rotation or circumstances that may provoke Valsalva responses
- Fluid management: patients should be euvolemic, blood hypoosmolarity should be avoided
- Hyperventilation: up to a pCO2 of 26–30 mm Hg
- Causal treatment (e.g., removal of brain tumor) if possible
- Medical therapy
- Removal of CSF via an intraventricular monitor with drainage system (e.g., external ventricular drain or lumbar drain) or a (e.g., in patients)
- Decompressive craniectomy: removal of part of the skull, allowing the brain to expand and reduces ICP.
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.