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neuro > A11. Clinical manifestation of increased intracranial pressure. Herniations. > Flashcards

A11. Clinical manifestation of increased intracranial pressure. Herniations. Flashcards

1
Q

Causes of raised ICP

A
  1. Space-occupying lesions (eg. tumor, abscess, hemorrhage) - treat with surgery
  2. CSF disorders (occlusive hydrocephalus) - treat with CSF drainage
  3. Cerebral edema (vasogenic, cytotoxic, interstitial)
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2
Q

Space-occupying lesions - how to treat

A

(eg. tumor, abscess, hemorrhage) - treat with surgery

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3
Q

CSF disorders (occlusive hydrocephalus) - how to treat

A

treat with CSF drainage

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4
Q

Clinical manifestations of increased ICP

A

● 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

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5
Q

Treatment ICP

A

● Treat underlying etiology
● Osmodiuretics (mannitol, glycerol)
● Loop diuretics decrease CSF production
● ICU:
○Controlled hyperventilation
○Barbiturate narcosis
● Decompressive craniectomy

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6
Q

Treatment ICP in ICU

A

○Controlled hyperventilation
○Barbiturate narcosis

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7
Q

what diuretics are used to decrease ICP

A

● Osmodiuretics (mannitol, glycerol)
● Loop diuretics decrease CSF production

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8
Q

Monroe-Kellie principle- what is it about

A
  • 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.
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9
Q
  • 3 main components of intracranial volume:
A
  1. brain tissue
  2. CSF
  3. and blood.

Monroe-Kellie principle

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10
Q

Cerebral blood flow is maintained by the difference of

A

arterial and venous pressure

which is called
cerebral perfusion pressure.

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11
Q

correlation between Intracranial pressure and cerebral venous pressure

A

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

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12
Q
  • 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?
A
  • 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.
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13
Q

vasodilatory cascade - what is it

A
  • 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
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14
Q

Intracranial pressure (physiologic range)

A

10 mmHg

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15
Q

Intracranial pressure is regulated mainly by

A
  • production
  • and absorption
    rate of the cerebrospinal fluid - slow mechanism.
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16
Q

fast mechanisms to compensate raised intracranial pressure

A
  • 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.
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17
Q

how does Hyperventilation affect
the partial pressure of blood CO2,

A

Hyperventilation decreases
the partial pressure of blood CO2,
* which results in:
*arteriolar constriction
*and the decrease of cerebral
blood volume.

18
Q

How can Barbiturate narcosis and hypothermia decrease ICP

A

lead to a
* decrease of cerebral metabolism, which causes the
* further reduction of cerebral blood volume

19
Q

Brain herniations

A

4 types of herniations may occur;
1. subfalcial,
2. central
3. uncal-transtentorial
4. foraminal

20
Q

Subfalcial herniation

A
  • (cingular herniation)
  • Cingular gyrus in pressed under the falx.
  • May compress circumferential branches of anterior cerebral artery (pericallosal, collosomarginal) if mass
    effect is considerable
21
Q

complication of subfacial herniation

A
  • May compress:
    1.circumferential branches of anterior cerebral artery (pericallosal, collosomarginal) if mass
    effect is considerable
    → contralateral hemiparesis (predominantly lower limbs)
  1. Contralateral hemisphere → obstruction of the foramen of Monro → hydrocephalus
22
Q

Subfalcial herniation Symptoms:

A

○ Progressive decrease in motivation (may lead to akinetic mutism)
○ Paraparesis
○ Urinary incontinence
○ Frontal release signs (primitive reflexes reappear - eg. sucking and grasping reflex)

23
Q

Central herniation- what is it

A
  • 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.
24
Q

Severity of Central herniation is proportional to

A

lateral or axial shift of diencephalon.

25
Q

Central herniation Symptoms:
○ Early phase

A

■ Indifference, concentration and memory problems
■ Frequent yawning

26
Q

Central herniation Symptoms in Later phase

A

■ 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

27
Q

Central herniation General Symptoms:

A

■ Pupils are symmetric, constricted and reactive
■ Ciliospinal reflex is brisk (pinch skin over trapezius muscle evokes mydriasis)
■ Muscle tone is frequently increased (paratonia

28
Q

Central herniation are symptoms reversible?

A

Symptoms are still reversible if treatment is applied,
but if not: transtentorial herniation occurs with irreversible symptoms

29
Q

Transtentorial herniation- can be divided into

A
  • 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.

30
Q

Transtentorial Uncal herniation early manifestation

A

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

31
Q

Transtentorial Uncal herniation Late manifestation

A
  • 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
32
Q

abnormal Pupillary reactions in Uncal Transtentorial herniation

A

■ Axial: moderate dilation + react to light
■ Lateral: anisocoria + loss of light reflex (hippocampal uncus compress ipsilateral CN3)

33
Q

in uncal Transtentorial herniation Unconsciousness is due to

A

damage to ARAS (ascending reticular activating system

34
Q

uncal Transtentorial herniation - how is muscle tone

A

○ Increased extensor muscle tone
○ Increased bilateral Babinski sign

35
Q

Kernohan’s notch phenomenon

Uncal Transtentorial herniation

A
  • Contralateral cerebral peduncle compression against the tentorial notch → Kernohan phenomenon (a rare false localizing sign consisting of hemiparesis ipsilateral to the brain lesion)
36
Q

Ipsilateral posterior cerebral artery compression→

Uncal Transtentorial herniation

A

cortical blindness with contralateral homonymous hemianopia

37
Q

Ipsilateral oculomotor nerve compression

Uncal Transtentorial herniation

A

→ Hutchinson pupil (ipsilateral fixed and dilated pupil)

38
Q

Ipsilateral cerebral peduncle compression

Uncal Transtentorial herniation

A

→ contralateral hemiparesis

39
Q

Midline shift

Uncal Transtentorial herniation

A

→ altered consciousness

40
Q

Transforaminal herniation/tonsillar herniation /Foramen magnum herniation

A

Structures of the posterior fossa (e.g., cerebellar tonsils, medulla) herniate through the foramen magnum

> compression of medulla

41
Q

Transforaminal herniation/tonsillar herniation symptoms

A
  • 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
42
Q

posture in Transforaminal herniation/tonsillar herniation

A

Decerebrate

neuro (32 decks)

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