Vascular damage

Vascular damage
There may be stretching or compression of blood vessels, causing: haemorrhage when stretched blood vessels rupture ischaemia and infarction due to compression of blood vessels papilloedema (oedema round the optic disc) due to compression of the retinal vein in the optic nerve sheath where it crosses the subarachnoid space.
Neural damage The vital centres in the medulla oblongata may be damaged when the increased ICP causes ' coning' . Stretching may damage cranial nerves, especially the oculomotor (III) and the abducent (VI), causing disturbances of eye movement and accommodation.
Bone changes Prolonged increase of ICP causes bony changes, e.g erosion, especially of the sphenoid 
• stretching and thinning before ossification is complete.
Cerebral oedema There is movement of fluid from its normal compartment when oedema develops Cerebral oedema occurs when there is excess fluid in brain cells and/or in the interstitial spaces, causing increased intracranial pressure. It is associated with:
 • traumatic injury
 • haemorrhage
 • infections, abscesses
 • hypoxia, local ischaemia or infarcts
 • tumours inflammation of the brain or meninges
 • hypoglycaemia
Hydrocephalus 111 this condition the volume of CSF is abnormally high and is usually accompanied by increased ICP.
An obstruction to CSF flow  is the most common cause. It is described as communicating when there is free flow of CSF from the ventricular system to the subarachnoid space and non-communicating when there is not, i.e. there is obstruction in the system of ven-tricles, foramina or ducts. Enlargement of the head occurs in children when ossi-fication of the cranial bones is incomplete but, in spite of this, the ventricles dilate and cause stretching and thin-ning of the brain. After ossification is complete, hydro-cephalus leads to a marked increase in ICP and destruction of nervous tissue.
Primary hydrocephalus In this condition there is accumulation of CSF accompa-nied by dilation of the ventricles. It is usually caused by obstruction to the flow of CSF but is occasionally due to malabsorption of CSF by the arachnoid vi ii. It may be communicating or non-communicating. Without treatment, permanent brain damage occurs. Congenital primary hydrocephalus is due to malformation of the ventricles, foramina or ducts, usually at a narrow point. Acquired primary hydrocephalus is caused by lesions that obstruct the circulation of the CSF, usually expand-ing lesions, e.g. tumours, haematomas or adhesions between arachnoid and pia maters, following meningitis.
Secondary hydrocephalus Compensatory increases in the amount of CSF and ven-tricle capacity occur when there is atrophy of brain tis-sue, e.g. in dementia and following cerebral infarcts. There may not be a rise in ICP.
Head injuries Damage to the brain may be serious even when there is no outward sign of injury. At the site of injury there may be: 
• a scalp wound, with haemorrhage between scalp and skull bones 
• damage to the underlying meninges and/or brain with local haemorrhage inside the skull • a depressed skull fracture, causing local damage to the underlying meninges and brain tissue 
• temporal bone fracture, creating an opening between the middle ear and the meninges 
• fracture involving the air sinuses of the sphenoid, ethmoid or frontal bones, making an opening between the nose and the meninges.
Acceleration-deceleration injuries Because the brain floats relatively freely in 'a cushion' of CSF, sudden acceleration or deceleration has an inertia