Hydrocephalus pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
* The pathophysiology of hydrocephalus is given below:.<ref>[http://www.ninds.nih.gov/disorders/hydrocephalus/detail_hydrocephalus.htm "Hydrocephalus Fact Sheet"], National Institute of Neurological Disorders and Stroke. (August 2005).</ref> | * The pathophysiology of hydrocephalus is given below:.<ref>[http://www.ninds.nih.gov/disorders/hydrocephalus/detail_hydrocephalus.htm "Hydrocephalus Fact Sheet"], National Institute of Neurological Disorders and Stroke. (August 2005).</ref> | ||
us]]. | |||
*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, and may be subatmospheric in newborns. | |||
*In adults, the intracranial compartment is protected by the skull which can hold internal volume of 1400 to 1700 mL. | |||
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ICP is normally lower in children than adults, and may be subatmospheric in newborns. | |||
In adults, the intracranial compartment is protected by the skull which can hold internal volume of 1400 to 1700 mL. | |||
Pathologic structures, including mass lesions, abscesses, and hematomas also may be present within the intracranial compartment. | Pathologic structures, including mass lesions, abscesses, and hematomas also may be present within the intracranial compartment. | ||
Since the overall volume of the cranial vault cannot change, an increase in the volume of one component, or the presence of pathologic components, necessitates the displacement of other structures, an increase in ICP, or both. | Since the overall volume of the cranial vault cannot change, an increase in the volume of one component, or the presence of pathologic components, necessitates the displacement of other structures, an increase in ICP, or both. | ||
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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] Cafer Zorkun M.D., PhD.,Kalsang Dolma, M.B.B.S.[3]
Overview
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).
Pathophysiology
- The pathophysiology of hydrocephalus is given below:.[1]
us]].
- 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, and may be subatmospheric in newborns.
- In adults, the intracranial compartment is protected by the skull which can hold internal volume of 1400 to 1700 mL.
Pathologic structures, including mass lesions, abscesses, and hematomas also may be present within the intracranial compartment. Since the overall volume of the cranial vault cannot change, an increase in the volume of one component, or the presence of pathologic components, necessitates the displacement of other structures, an increase in ICP, or both. Thus, ICP is a function of the volume and compliance of each component of the intracranial compartment, an interrelationship known as the Monro-Kellie doctrine.
- 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. Physiology and utility of an examination in disease states".)
Cerebral blood flow (CBF) determines the volume of blood in the intracranial space. CBF increases with hypercapnia and hypoxia. Other determinants of CBF are discussed below. Autoregulation of CBF may be impaired in the setting of neurologic injury, and may result in rapid and severe brain swelling, especially in children [7-9].
In summary, the major causes of increased intracranial pressure include:
●Intracranial mass lesions (eg, tumor, hematoma)
●Cerebral edema (such as in acute hypoxic ischemic encephalopathy, large cerebral infarction, severe traumatic brain injury)
●Increased cerebrospinal fluid (CSF) production, eg, choroid plexus papilloma
●Decreased CSF absorption, eg, arachnoid granulation adhesions after bacterial meningitis
●Obstructive hydrocephalus
●Obstruction of venous outflow, eg, venous sinus thrombosis, jugular vein compression, neck surgery
●Idiopathic intracranial hypertension (pseudotumor cerebri)
Intracranial compliance — The interrelationship between changes in the volume of intracranial contents and changes in ICP defines the compliance characteristics of the intracranial compartment. Intracranial compliance can be modeled mathematically (as in other physiologic and mechanical systems) as the change in volume over the change in pressure (dV/dP).
The compliance relationship is nonlinear, and compliance decreases as the combined volume of the intracranial contents increases. Initially, compensatory mechanisms allow volume to increase with minimal elevation in ICP. These mechanisms include:
●Displacement of CSF into the thecal sac
●Decrease in the volume of the cerebral venous blood via venoconstriction and extracranial drainage
However, when these compensatory mechanisms have been exhausted, significant increases in pressure develop with small increases in volume, leading to abnormally elevated ICP (figure 2).
Thus, the magnitude of the change in volume of an individual structure determines its effect on ICP. In addition, the rate of change in the volume of the intracranial contents influences ICP. Changes that occur slowly produce less of an effect than those that are rapid. This can be recognized clinically in some patients who present with large meningiomas and minimally elevated or normal ICP. Conversely, other patients may experience symptomatic elevations in ICP from small hematomas that develop acutely.
References
- ↑ "Hydrocephalus Fact Sheet", National Institute of Neurological Disorders and Stroke. (August 2005).