10. Intracranial pressure

Question 1

What is the normal intracranial pressure?

Answer 1

5-15 mmHg

(Established by presence of neural tissue (brain + spinal cord), CSF and blood in intracranial cavity)

Question 2

How is ICP regulated in healthy individuals?

Answer 2

1. Blood flow regulation
   - autoregulation: vasoconstriction/vasodilation
   - chemoregulation: vasodilation in response to low cerebral pH (e.g. high pCO2)
2. CSF regulation - production/reabsorption

Question 3

Suggests 3 reasons why RICP causes neuronal damage.

Answer 3

1. Neuronal ischaemia:
   - RICP causes a decrease in cerebral perfusion pressure once it approaches level of mean systemic BP… neuronal ischaemia.
   - body response is to increase systemic BP and vasodilate cerebral BVs… increased cerebral blood volume… increase RICP - vicious cycle
   - neuronal ischaemia… Na/K ATPase halts… Na and water influx… cytotoxic cellular oedema… further swelling and compression - vicious cycle
2. Neuronal compression and damage
3. Midline shift can compress ventricles and lead to hydrocephalus

Question 4

Name 4 symptoms of RICP.

Answer 4

1. headache
2. nausea and vomiting (progressing to projectile vomiting)
3. visual disturbances (e.g. blurring, transient blindness)
4. depression of conscious level (confusion, delirium, LOC)

Question 5

Describe the characteristic headache of RICP. Name 2 factors that will worsen it.

Answer 5

Generalised ache of gradually progressive severity. Worse when:

1. waking in the morning - due to physiological hypoventilation and CO2 accumulation during sleep causing chemoregulation and vasodilation
2. coughing, straining, bending down - increase intra-abdominal and intra-thoracic pressure… decrease venous return of SVC

Question 6

Why can papilloedema be a sign of RICP?

Answer 6

Papilloedema = optic disc swelling caused by RICP

Compression of optic nerve… obstruction of axoplasmic flow within nerve… axon swelling… cellular content leaks into optic disc space.

Question 7

Why might Ps with RICP have decreased LOC and GCS?

Answer 7

Downward herniation of uncus through tentorial notch… midbrain compression… compression of reticular formation.

Question 8

Why might Ps with RICP have diplopia on horizontal gave?

Answer 8

Downward herniation of uncus through tentorial notch… compression of Pons… compression of CN6 (which exits posteriorly and loops around pons - can be compressed against petrous temporal bone).

Question 9

How might an infant with slowly increasing ICP present?

Answer 9

Gradually increasing head size.

Question 10

Describe the triad of signs seen in a severe RICP.

Answer 10

Cushing’s reflex (last effort to perfuse brain, poor prognostic sign):

1. high BP (activation of SNS in attempt to restore cerebral blood flow)
2. bradychardia (high BP causes activation of baroRs and PNS activation)
3. low resp. rate (altered breathing pattern due to ischaemia/compression or resp. centres at pons/medulla)

Question 11

Describe the symptoms associated with subfalcine herniation.

Answer 11

• may be asymptomatic
• headache and contralateral leg weakness if anterior cerebral artery is affected

Question 12

Describe the symptoms associated with uncal herniation.

Answer 12

Herniated uncus puts pressure on midbrain:

1. ipsilateral dilated pupil - compression of CN3 parasympathetics
2. contralateral leg weakness - compression of corticospinal tract in cerebral peduncle (have not yet decussated)

(above signs may be falsely localising if midbrain pushed against opposite side of tentorium)

3. decreased level of consciousness - compression of RF

Question 13

Describe the effects of tonsillar herniation.

Answer 13

Cerebellar tonsils herniate through foramen magnum - compression of medulla and upper spinal cord:

• cardiac and resp. dyfunction
• decreased level of consicousness

Question 14

What is the most common cause of RICP?

Answer 14

Traumatic brain injury, e.g. causing epidural, subdural or subarachnoid haemorrhages (remember to think of anticoagulant use)

Question 15

Describe the 2 main classifications of hydrocephalus.

Answer 15

1. Non-communicating/obstructive - CSF is obstructed within ventricles or between ventricles and subarachnoid space - most commonly due to aqueduct blockade: congenital or acquired - can involve tumours, e.g. meningioma 2. Communicating - there is communication between ventricles and subarachnoid space - due to reduced absorption or blockage of venous drainage system, e.g. subarachnoid haemorrhage, post-meningitis (debris block arachnoid vili), trauma and neoplastic infiltration of subarachnoid space - can also be due to increased CSF production (less common), e.g. choroid plexus papilloma

Question 16

What are the most common types of brain tumours in adults and children?

Answer 16

1. metastases (from lung, breast and kidneys)

Adults:

2. gliomas, meningiomas

Children:

3. astrocytomas, medulloblastomas (from neuroectoderm cells)

Question 17

What is idiopathic intracranial hypertension? In whom is it more common? How is it treated?

Answer 17

• raised intracranial pressure without evidence of hydrocephalus or mass lesion, with normal investigations
• usually obese young women after weight gain
• treatement options: weight loss, drugs (e.g. carbonic anhydrase inhibitors, CSF drainage - therapeutic LP - and shunts)

Question 18

How can RICP due to increased CSF be managed?

Answer 18

1. shunts, e.g. ventriculoperitoneal shunts
2. diuretics whilst awaiting intervention, e.g. furosemide, carbonic anhydrase inhibitors

Question 19

why might changing plasma osmolality help management of RICP?

Answer 19

CSF is hyperosmotic relative to plasma (more Na+).

So treatment with mannitol or hypertonic saline can increase plasma osmolality and reverse flow.