A11. Clinical manifestation of increased intracranial pressure. Herniations. Flashcards
Causes of raised ICP
- Space-occupying lesions (eg. tumor, abscess, hemorrhage) - treat with surgery
- CSF disorders (occlusive hydrocephalus) - treat with CSF drainage
- Cerebral edema (vasogenic, cytotoxic, interstitial)
Space-occupying lesions - how to treat
(eg. tumor, abscess, hemorrhage) - treat with surgery
CSF disorders (occlusive hydrocephalus) - how to treat
treat with CSF drainage
Clinical manifestations of increased ICP
● Progressive headache (one of leading complaints)
● Vomiting
● Milder and atypical symptoms in elderly due to brain atrophy
● Papilloedema + blurred vision
● Always global cerebral dysfunction due to global cerebral ischemia.
* Cerebral cortex most sensitive → drowsiness, altered behaviour, slow thinking
* Focal symptoms if focal space occupying lesions
Treatment ICP
● Treat underlying etiology
● Osmodiuretics (mannitol, glycerol)
● Loop diuretics decrease CSF production
● ICU:
○Controlled hyperventilation
○Barbiturate narcosis
● Decompressive craniectomy
Treatment ICP in ICU
○Controlled hyperventilation
○Barbiturate narcosis
what diuretics are used to decrease ICP
● Osmodiuretics (mannitol, glycerol)
● Loop diuretics decrease CSF production
Monroe-Kellie principle- what is it about
-
3 main components of intracranial volume:
1. brain tissue
2. CSF
3. and blood.
These are in a state of equilibrium, and an increase in one must be compensated by a decrease in another.
- 3 main components of intracranial volume:
- brain tissue
- CSF
- and blood.
Monroe-Kellie principle
Cerebral blood flow is maintained by the difference of
arterial and venous pressure
which is called
cerebral perfusion pressure.
correlation between Intracranial pressure and cerebral venous pressure
Intracranial pressure and cerebral venous pressure are equal, thus the rise
of intracranial pressure always leads to the rise of cerebral venous pressure of equal degree
- how will the rise
of intracranial pressure (ICP) affect the cerebral venous pressure(CVP) - what will happen to cerebral perfusion pressure?
- how will body compensate?
- always leads to the rise of cerebral venous pressure of equal degree
- As a consequence, cerebral perfusion pressure is decreased.
- in order to maintain cerebral blood
flow, cerebral arterioles dilate causing the increase of intracerebral blood volume as well, which further
increases intracranial pressure. This positive feedback mechanism – called vasodilatory cascade –
eventually leads to global cerebral ischemia.
vasodilatory cascade - what is it
- positive feedback mechanism
- eventually leads to global cerebral ischemia
- if Cerebral perfusion pressure is decreased
- -> in order to maintain cerebral blood flow, cerebral arterioles dilate
- –> causing the increase of intracerebral blood volume as well,
- –> which further
increases intracranial pressure
Intracranial pressure (physiologic range)
10 mmHg
Intracranial pressure is regulated mainly by
- production
- and absorption
rate of the cerebrospinal fluid - slow mechanism.
fast mechanisms to compensate raised intracranial pressure
- The displacement of CSF
via the foramen magnum into the spinal canal is the principle compensatory mechanism under
physiological circumstances (e.g. Valsalva maneuver) -
decrease of cerebral blood volume . This mechanism
does NOT operate under physiological conditions, but it can be artificially activated by applying:
*controlled hyperventilation, *barbiturate narcosis and *hypothermia in intensive care units.
how does Hyperventilation affect
the partial pressure of blood CO2,
Hyperventilation decreases
the partial pressure of blood CO2,
* which results in:
*arteriolar constriction
*and the decrease of cerebral
blood volume.
How can Barbiturate narcosis and hypothermia decrease ICP
lead to a
* decrease of cerebral metabolism, which causes the
* further reduction of cerebral blood volume
Brain herniations
4 types of herniations may occur;
1. subfalcial,
2. central
3. uncal-transtentorial
4. foraminal
Subfalcial herniation
- (cingular herniation)
- Cingular gyrus in pressed under the falx.
- May compress circumferential branches of anterior cerebral artery (pericallosal, collosomarginal) if mass
effect is considerable
complication of subfacial herniation
- May compress:
1.circumferential branches of anterior cerebral artery (pericallosal, collosomarginal) if mass
effect is considerable
→ contralateral hemiparesis (predominantly lower limbs)
- Contralateral hemisphere → obstruction of the foramen of Monro → hydrocephalus
Subfalcial herniation Symptoms:
○ Progressive decrease in motivation (may lead to akinetic mutism)
○ Paraparesis
○ Urinary incontinence
○ Frontal release signs (primitive reflexes reappear - eg. sucking and grasping reflex)
Central herniation- what is it
- mass effect caused by bilateral or midline supratentorial lesions or severe brain edema → downward displacement of the diencephalon, midbrain, and pons
- Compression of diencephalon.
- Severity is proportional to lateral or axial shift of diencephalon.
Severity of Central herniation is proportional to
lateral or axial shift of diencephalon.
Central herniation Symptoms:
○ Early phase
■ Indifference, concentration and memory problems
■ Frequent yawning
Central herniation Symptoms in Later phase
■ Drowsiness → unconsciousness
■ Cheyne-Stokes respiratory pattern
■ Decorticate posture with bilateral Babinski reflex
* Oculomotor nerve compression → oculomotor nerve palsy with fixed and dilated pupils
* Brain stem dysfunction → decerebrate or decorticate posture, cardiac arrest, respiratory failure → vegetative state or death
* Stretching or tearing of basilar artery perforating branches → Duret hemorrhages
Central herniation General Symptoms:
■ Pupils are symmetric, constricted and reactive
■ Ciliospinal reflex is brisk (pinch skin over trapezius muscle evokes mydriasis)
■ Muscle tone is frequently increased (paratonia
Central herniation are symptoms reversible?
Symptoms are still reversible if treatment is applied,
but if not: transtentorial herniation occurs with irreversible symptoms
Transtentorial herniation- can be divided into
- Uncal herniation: mass effect caused by a supratentorial lesion → medial and downward displacement of the uncus at the tentorial incisure
- Central herniation: mass effect caused by bilateral or midline supratentorial lesions or severe brain edema → downward displacement of the diencephalon, midbrain, and pons
Compression of mesencephalon in tentorial incisure -
damaged blood supply of mesencephalon and secondary
intraparenchymal bleedings.
Transtentorial Uncal herniation early manifestation
Early manifestations
* Ipsilateral posterior cerebral artery compression→ cortical blindness with contralateral homonymous hemianopia
* Ipsilateral oculomotor nerve compression → Hutchinson pupil (ipsilateral fixed and dilated pupil)
* Ipsilateral cerebral peduncle compression → contralateral hemiparesis
* Midline shift → altered consciousness
Transtentorial Uncal herniation Late manifestation
- Contralateral cerebral peduncle compression against the tentorial notch → Kernohan phenomenon (a rare false localizing sign consisting of hemiparesis ipsilateral to the brain lesion)
- Downward shift of the brainstem → brainstem hemorrhages → focal deficits, impaired consciousness, death
abnormal Pupillary reactions in Uncal Transtentorial herniation
■ Axial: moderate dilation + react to light
■ Lateral: anisocoria + loss of light reflex (hippocampal uncus compress ipsilateral CN3)
in uncal Transtentorial herniation Unconsciousness is due to
damage to ARAS (ascending reticular activating system
uncal Transtentorial herniation - how is muscle tone
○ Increased extensor muscle tone
○ Increased bilateral Babinski sign
Kernohan’s notch phenomenon
Uncal Transtentorial herniation
- Contralateral cerebral peduncle compression against the tentorial notch → Kernohan phenomenon (a rare false localizing sign consisting of hemiparesis ipsilateral to the brain lesion)
Ipsilateral posterior cerebral artery compression→
Uncal Transtentorial herniation
cortical blindness with contralateral homonymous hemianopia
Ipsilateral oculomotor nerve compression
Uncal Transtentorial herniation
→ Hutchinson pupil (ipsilateral fixed and dilated pupil)
Ipsilateral cerebral peduncle compression
Uncal Transtentorial herniation
→ contralateral hemiparesis
Midline shift
Uncal Transtentorial herniation
→ altered consciousness
Transforaminal herniation/tonsillar herniation /Foramen magnum herniation
Structures of the posterior fossa (e.g., cerebellar tonsils, medulla) herniate through the foramen magnum
> compression of medulla
Transforaminal herniation/tonsillar herniation symptoms
- Impaired consciousness
- Decerebrate posturing
- Impaired circulation
- Death
- Upper extremities become flaccid, and lower extremities flexed
○ Neck stiffness and head tilt (tonsillar impaction on foramen magnum)
○ Respiration: Apnea → completely irregular → gasping
○ Vestibuloocular reflex is lost
○ Blood pressure drops
○ Death from respiratory and cardiac arrest
posture in Transforaminal herniation/tonsillar herniation
Decerebrate
