Hydrocephalus pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Ahsan Hussain, M.D.[2]


Hydrocephalus mostly results due to CSF flow obstruction, hindering the free passage of cerebrospinal fluid through the ventricular system and it can also be caused by overproduction of cerebrospinal fluid (relative obstruction).


  • The pathophysiology of hydrocephalus is given below:.[1][2][3][4][5]
  • Intracranial pressure is normally ≤15 mmHg in adults, and pathologic intracranial hypertension (ICH) is present at pressures ≥20 mmHg.
  • ICP is normally lower in children than adults.
  • In adults, the intracranial compartment is protected by the skull which can hold internal volume of 1400 to 1700 mL.
  • Mass lesions, abscesses, and hematomas also causes the intracranial compartment pressure.
  • ICP is a function of the volume and compliance of each component of the intracranial compartment.
  • The volume of brain parenchyma is relatively constant in adults which constitutes 80% of total volume.
  • The volumes of CSF and blood in the intracranial space vary to a greater degree.
  • Abnormal increases in the volume due to mass lession or cerebral edema which lead to ICP elevation.
  • The volume of brain parenchyma is constant, with the exception of any abnormality like mass lesions or cerebral edema.
  • The volumes of CSF and blood in the intracranial space vary to a greater degree.
  • CSF is produced by the choroid plexus and elsewhere in the central nervous system (CNS) at a rate of approximately 20 mL/h (500 mL/day).
  • CSF is resorbed by arachnoid granulations into the venous system.
  • CSF abnormal flow generally result from impaired outflow due to ventricular obstruction or venous congestion.
  • The Venous sinus thrombosis can be pathologically increase which can be seen in the setting of choroid plexus papilloma.
  • The other causes of increased ICP are given below:
    • Intracranial mass lesions (eg, tumor, hematoma).
    • Cerebral edema.
    • Acute hypoxic ischemic encephalopathy.
    • Large cerebral infarction.
    • Severe traumatic brain injury.
    • Choroid plexus papilloma (increased ICP).
    • Arachnoid granulation adhesions after bacterial meningitis (decreased ICP).
    • Venous sinus thrombosis.
    • Idiopathic intracranial hypertension (pseudotumor cerebri).


  1. "Hydrocephalus Fact Sheet", National Institute of Neurological Disorders and Stroke. (August 2005).
  2. Strandgaard S, Paulson OB (June 1989). "Cerebral blood flow and its pathophysiology in hypertension". Am. J. Hypertens. 2 (6 Pt 1): 486–92. PMID 2757806.
  3. Strandgaard S, Andersen GS, Ahlgreen P, Nielsen PE (1984). "Visual disturbances and occipital brain infarct following acute, transient hypotension in hypertensive patients". Acta Med Scand. 216 (4): 417–22. PMID 6516910.
  4. Enevoldsen EM, Jensen FT (May 1978). "Autoregulation and CO2 responses of cerebral blood flow in patients with acute severe head injury". J. Neurosurg. 48 (5): 689–703. doi:10.3171/jns.1978.48.5.0689. PMID 641549.
  5. Bruce DA, Alavi A, Bilaniuk L, Dolinskas C, Obrist W, Uzzell B (February 1981). "Diffuse cerebral swelling following head injuries in children: the syndrome of "malignant brain edema"". J. Neurosurg. 54 (2): 170–8. doi:10.3171/jns.1981.54.2.0170. PMID 7452330.