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Intracranial lesions

  • Consequences of space-occupying lesions (e.g. haemorrhage)
    • Raised intracranial pressure
      • Intracranial shift and herniations
    • Epilepsy (due to abnormal neuronal discharge)
    • Focal neurological deficits
      • Eg: paralysis, vision problems; due to disruption of axonal tracts
      • Headache - worse at night/early in morning, worse on coughing

Raised intracranial pressure

  • Cerebral perfusion pressure = systemic blood pressure – intracranial pressure
    • As ICP increases towards systemic BP, cerebral perfusion decreases
      • Thus there is a reflex increase in systemic blood pressure (Cushing reflex)
      • If ICP is too high, the Cushing reflex fails and this can lead to systemic generalised ischaemia due to cerebral perfusion being too low and the brain not getting enough blood (lactic acid build up, detected, resulting in sympathetic outflow to increase systemic blood pressure, also vagal-mediated bradycardia)
  • Clinical features
    • Headache – stretching of the dura, BVs, nerves, many causes
    • Nausea, vomiting
    • Papilloedema – difference in visual fields; look at the optic fundus with an opthalmoscope
    • Hypertension and bradycardia (due to Cushing reflex)
    • Herniation symptoms
  • Eg: if pressure in the CSF increases (due to ICP), the optic nerve can become occluded and thus cause the optic disk to swell up
    • papilloedema - loss of optic cup, loss of pulsation in retinal vessels, swollen optic disk, blurred outlines of optic disk
      • due to reduced axoplasmic flow down optic nerve, causing edema of optic nerve axons

Intracranial herniations

  • Subfalcine
    • Cingular guyrus herniates under falx cerebri, obstructing the anterior cerebral artery, resulting in weakness of contralateral limb
  • Transtentorial (‘uncal’)
    • Parts of the brain near the tentorium cerebelli herniate into the space and cause compression of BVs, peduncles
      • Thus cause paralysis, unconsciousness (compression of the midbrain esp reticular activating system important for consciousness. Cerebral peduncle compression results in weakness. Occasionally you get a false localising sign because of compression of the other cerebral peduncle - ipsilateral weakness)
    • CN3 (occulomotor nerve) is compressed - dilation of pupil on side of lesion; later on there is complete loss of occulomotor function
  • Cerebellar tonsillar (‘coning’)
    • Cerebellar tonsil is forced through the foramen magnum
    • Causes compression of the medulla and blood vessels
    • can be fatal as this is where vital centres are located
  • Pathologically, may cause grooving and may lead to haemorrhages
  • Another complication = haemorrhages into the midbrain (duret haemorrhages) - causing disruption of reticular activating system

Intracranial haemorrhage

  • Can be traumatic/spontaneous and occur in various locations
    • Traumatic are commonly: epidural or subdural
  • Types:
    • Epidural (between skull and dura)
    • Subdural (between dura and arachnoid)
    • Subarachnoid (between arachnoid and pia)
    • Intracerebral (within the brain itself)

Epidural (extradural) haemorrhage

Common in younger people; almost always due to a high-impact trauma e.g. hit with cricket ball

  • Traumatic, often associated with a fractured skull
  • Shearing of artery, usually middle meningeal artery as it runs under the squamous part of the temporal bone. Correlated with fractures of that part of the temporal bone
  • May have a lucid interval (unconsciousness due to initial trauma, then regain consciousness, then fall unconscious due to the bleed, resulting in herniation of cerebellar tonsils)
    • Ie: trauma
      • unconscious
      • wake up
      • fall unconscious again due to increasing ICP
    • May cause a rapid increase in ICP
  • Results in all those herniation syndromes listed above
  • CT: typically has biconcave appearance, appears denser than brain tissue. Hypodense regions are areas of rapid bleeding (unclotted blood)
    • Here, the lateral ventricles have been pressed and pushed across the midline
  • Young people at risk due to: trauma risk higher (go skiing etc); and with age, fibrous adhesions to the skull prevent haemorrhage.

Subdural haemorrhage

  • Traumatic, with shearing of bridging veins between cortex and sinus
  • Acute or chronic
  • Acute:
    • After severe head injury
    • Leads to acute neurological deterioration due to raised ICP
      • Similar
      • Dural sinuses are fixed in position, whereas movement of the brain in trauma is possible.

  • Chronic:
    • If the brain shrinks, worse effects – eg: age, chronic alcoholism, Alzheimer’s disease
    • Easily injured – minimal head trauma only required
    • Thus, common in elderly or alcoholics
    • May present subtley. Subdural haematoma is a reversible cause of dementia
    • Rebleeding and osmotic effects can lead to increased ICP
    • Gradual development of symptoms
    • Confusion, personality change, memory loss, headache, weakness on contralateral side or bilaterally (due to compression of cerebral cortex)
    • Body can try to organise the blood that collects in the subdural space and thus scar/granulation tissue can form
    • Granulation tissue grows new BVs which can rupture and cause rebleeding
    • Can be treated surgically

Clinical aspects

  • Neurological assessment
    • level of consciousness (Glasgow Coma Scale – GCS); do this whenever someone presents with head injury; universal scale, correlates well with likely outcome
    • pupillary response to light (assessing CN3 function; CN3 may be compressed in herniation syndromes)
    • spinal cord function
  • Depressed level of consciousness is usually caused by intracranial pathology
  • However, 30% with depressed level of consciousness are intoxicated (so it's not indicative of their pathology)
  • GCS <8 requires definitive airway protection

Glasgow Coma Scale

  • The GCS is scored between 3 and 15. (Because a score of 0 will distress relatives). It is composed of three parameters : Best Eye Response, Best Verbal Response, Best Motor Response
  • Best Eye Response. (4)
    • 1.No eye opening.
    • 2.Eye opening to pain.
    • 3.Eye opening to verbal command.
    • 4.Eyes open spontaneously.
  • Best Verbal Response. (5)
    • 1.No verbal response
    • 2.Incomprehensible sounds.
    • 3.Inappropriate words.
    • 4.Confused
    • 5.Orientated
  • Best Motor Response. (6)
    • 1.No motor response.
    • 2.Extension to pain.
    • 3.Flexion to pain.
    • 4.Withdrawal from pain.
    • 5.Localising pain.
    • 6.Obeys Commands.
  • A Coma Score of 13 or higher correlates with a mild brain injury, 9 to 12 is a moderate injury and 8 or less a severe brain injury (protect airway with intubation and ventilation).
  • Can use consecutive measurements to identify a lucid interval and the need of urgent intervention.

Subarachnoid haemorrhage

  • Trauma, or aneurysms from circle of Willis (saccular, "berry" aneurysms). These are common - present in 2% of population


  • rupture of berry aneurysm; these start small, but, once they're large, they produce a 50% chance of rupture per year
  • trauma
  • extension of intracerebral haemorrhage
  • rupture of AV malformations

Berry aneurysms

  • Occurs in 1-2% of the population, may have multiple
    • More often in females than males
  • Congenital weakness (defect in the muscle layer) at branch points on the Circle of Willis can predispose to aneurysms
  • Often associated with hypertension – can rupture during acute elevations of BP, eg: sex/constipation
    • Chronic hypertension, aneurysms increase in size more rapidly and happen earlier in life
  • See diagram indicating frequency
  • Mostly they are asymptomatic, so we don't know about them until they rupture. Sometimes they get large enough to compress surrounding structures, so they may be seen in imaging (esp angiography). Treatment: Coils or lasering can be used to try to induce a thrombus, or clip them

Rupture of berry aneurysms

  • Sudden severe headache and meningism – into arachnoid/pia; due to blood rushing into the subarachnoid space
    • Also: photophobia and neck stiffness
  • May be rapidly fatal due to increased ICP, significant mortality due to rebleeding
    • The whole brain is bathed in blood, increased ICP causing global ischaemia (therefore 25-50% are fatal). High risk of re-bleeding
  • Patients surviving 2-3 days may experience vasospasm of cerebral arteries (due to release of vasoactive substances e.g. endothelin)
    • This may lead to ischaemia and infarction causing further damage
      • Therefore surgically or other means - need to prevent the aneurysm rebleeding
  • Long term survivors:
    • Organisation of the haemorrhage, lining with granulation tissue
      • Arachnoid villi absorb CSF, if granulation tissue lines these reabsorption of CSF is impaired
    • This causes hydrocephalus – water in the brain, CSF compresses the underlying brain
  • Can tell a haemorrhage is in the subarachnoid space because the blood follows the contours of the sulci and hyri
  • If someone has had a surgical clip, they must NEVER have an MRI

Intracerebral haemorrhage

  • Often occurs in/around the basal ganglia, brainstem or cerebellum. Often calamatous - rapid fatality. Example shows blood filling ventricular system as well
  • Spontaneous in hypertensive patients
    • High risk in chronic hypertension (which causes hyaline arteriolar sclerosis in the blood vessels off the circle of Willis). Can cause tortuosities or microaneurysms, resulting in Charcot-Bouchard aneurysms
  • Other causes:
    • Trauma (coup, and contre-coup cortical contusions)
    • Arteriovenous malformation, neoplasm, haemorrhagic infarcts
    • Bleeding disorders, anticoagulants (eg. warfarin)
    • Extension of subarachnoid haemorrhages
      • Eg a berry haemorrhage buried in underlying brain
  • Majority start in the brain itself and can rip through the brain and enter the lateral ventricles
    • Especially as arterial blood pressure increases

Hypertensive intracerebral haemorrhage

  • Commonest site is the basal ganglia-thalamus-internal capsule region
    • Also occurs in the pons and cerebellum
    • Disrupts axonal tracts, and causes rapid increase in ICP
  • Chronic hypertension causes hyaline arteriolosclerosis of small perforating vessels
    • This can lead to lacunar infarcts and weakening of vessel walls (Charcot-Bouchard aneurysms)
  • Weakening of the vessel walls can cause rupture and intracerebral haemorrhage
    • Cause a rapid development of increased ICP (mins to hours)
    • Often can extend into the ventricular system
    • Depending on location/size of haemorrhage, can survive
  • Dementia patients: risk of spontaneous haemorrhage into the cerebral hemispheres, due to deposition of beta-amyloid in cerebral arteries (same beta-amyloid thought to be important in Alzheimer's disease)


  • A contusion is a traumatic intracerebral haemorrhage.
  • If someone hits their face straight into the ground, they'll get bleeding in the frontal lobe or anterior part of the temporal lobe. This is a coup contusion
  • If you fall backwards, the bouncing of the brain can cause a contre-coup contusion on the opposite side of the brain to where the impact was (because of the design of the skull).
  • Coup – on the same side as the blow
    • Susceptible areas: under surfaces of the frontal lobe, anterior poles of the temporal lobe
  • Due to the rough surfaces of the petrous temporal bone
  • Contre-coup – on the opposite side of the blow due to rubbing of the brain against rough areas of skull

  • Note ICP due to:
    • Mass of blood
    • Oedema in the brain
    • Ventricles:
      • CSF drainage blocked causing internal hydrocephalus