Symptoms and Signs of Increased Intracranial Pressure (ICP)
The classic symptoms and signs of increased intracranial pressure include headache, nausea, vomiting, altered mental status, papilledema, and the late-appearing Cushing's triad (hypertension, bradycardia, and irregular respiration). 1
Early Clinical Manifestations
- Headache: Often worse in the morning or when lying flat, aggravated by Valsalva maneuvers
- Nausea and vomiting: Frequently projectile, may occur without nausea
- Visual disturbances:
- Blurred vision
- Diplopia (often from cranial nerve VI palsy)
- Visual field defects
- Transient visual obscurations (brief episodes of vision loss)
- Papilledema: Swelling of the optic disc due to increased pressure
- Altered mental status:
- Drowsiness
- Confusion
- Irritability
- Decreased level of consciousness
Late Clinical Manifestations
- Cushing's triad: A late sign indicating brainstem compression
- Hypertension with widened pulse pressure
- Bradycardia
- Irregular respiratory pattern
- Pupillary changes: Unequal, dilated, or poorly responsive pupils 2
- Abnormal posturing: Decorticate or decerebrate posturing
- Focal neurological deficits: Hemiparesis or quadriparesis
- Respiratory abnormalities: Cheyne-Stokes respiration, ataxic breathing
- Decreased consciousness: Progressing to stupor and coma 3
Signs of Herniation Syndromes
Uncal Herniation
- Unilateral pupillary dilation (ipsilateral to lesion)
- Hemiparesis (contralateral to lesion)
- Decreased level of consciousness
Central Herniation
- Bilateral small reactive pupils progressing to fixed midposition
- Bilateral motor deficits
- Cheyne-Stokes respiration progressing to ataxic breathing
- Rapid deterioration in consciousness
Tonsillar Herniation
- Neck stiffness and pain
- Lower cranial nerve dysfunction
- Respiratory and cardiac arrest
Specific Findings on Clinical Examination
- Vital signs: Monitor for Cushing's triad
- Neurological examination:
- Glasgow Coma Scale (GCS) assessment
- Pupillary size and reactivity
- Motor response and posturing
- Cranial nerve function (especially III and VI)
- Fundoscopic examination: Papilledema, loss of venous pulsations
- Transcranial Doppler findings: Decreased diastolic velocity and increased pulsatility index 2
Monitoring and Detection
- Clinical monitoring: Frequent neurological assessments are essential to detect early changes in mental status 1
- Invasive ICP monitoring: May be considered in patients with GCS <8 or clinical deterioration
- Normal ICP: 5-15 mmHg
- Elevated ICP: >20 mmHg (sustained)
- Imaging findings:
- CT/MRI: Mass effect, midline shift, effacement of basal cisterns, ventricular compression
- Loss of normal sulci and gyri pattern
- Periventricular lucency suggesting transependymal CSF flow in hydrocephalus
Subclinical Manifestations
- 25% of seizures in children with increased ICP may be subtle or subclinical, manifesting as:
- Eye deviation
- Irregular respiratory pattern
- Drooling 2
Risk Factors and Associations
- Increased ICP is more common in:
- Younger patients
- Supratentorial hemorrhage
- Presence of hydrocephalus (associated with worse outcomes) 2
- Large intracranial mass lesions
Pitfalls and Caveats
- Papilledema may be absent in acute, rapidly developing increased ICP
- Cushing's triad is a late finding and should not be relied upon for early detection
- Pupillary signs may be misleading in the peri-ictal state 2
- Focal neurological signs may be related to the underlying pathology rather than increased ICP itself
- Increased ICP can occur without obvious clinical manifestations, particularly in sedated or intubated patients
Early recognition of these signs and symptoms is crucial for timely intervention to prevent cerebral hypoperfusion and potential brain death. Monitoring should be tailored to the clinical context and underlying cause of increased ICP.