Neuropathology Cerebral Edema, Intracranial Shift, Herniation

Front 1

What is the falx cerebri?

Back 1

It acts as an incomplete partition separating the hemispheres in the sagittal plane, stopping just above the corpus callosum.

Front 2

What is the tentorium cerebelli?

Back 2

A horizontal reflection, which lies on the superior surface of the cerebellum, separates supra- form infra-tentorial spaces. The tentorium is open in the ventral midline to allow the midbrain to pass through (tentorial notch). Thus, each free edge of the tentorium lies adjacent to either side of the midbrain.

Front 3

Explain the consequences of volume changes in the brain

Back 3

Local expansion leads to local increase in pressure, and consequently to pressure gradients within the brain, These gradients result in shifts of tissue (deformation of brain substance). Thus structures at a distance from the main focus of a lesion can also be compromised.

Front 4

Define brain edema

Back 4

An increase in volume nad weight of the brain due to fluid accumulation. Edema is a common complication of many kinds of intracreanial lesions, and a serious one because it produces an additional increase in volume over and above that resulting from the lesion itself.

Front 5

What are the two categories of cerebral edema?

Back 5

Vasogenic
Cytotoxic

Front 6

What causes vasogenic edema?

Back 6

Increased vascular-permiability. This may be due to several alterations:
a) destruction of vessels (eg trauma, hemorrhage)
b) increased pinocytic activity
c) the growth of capillaries that do not have a competent BBB (eg: vessels in tumors, either in CNS or metastatic, or in granulation tissue

Front 7

What influences the extent of edema is vasogenic edema?

Back 7

-The mean systemic blood pressure
-The duration of incompetence of the BBB

Front 8

Describe the movement of fluid through the brain during edema

Back 8

-Edema arising foccaly can spread through the CNS
-Movement through white matter occurs more easily than through gray matter, since in the former, the extracellular space is irregular and wider (up to 800A).
-Fluid spread through gray matter is trestricted, because extracellular space is narrower (100-200A) and there are many synaptic junctions.

Front 9

What is the vasogenic edema fluid?

Back 9

A plasma filtrate, containing variable amounts of plasma protein

Front 10

What is Cytotoxic edema?

Back 10

-Refers to swelling of cellular elements in the presence of an intact BBB
-Two examples of tis are the consequences of triethyl tin and hexachlorophene toxicity (the former was used in cosmetic and the latter is a disinfectant).
-Both compounds cause an accumulation of fluid within the lamellae of myelin sheaths, inducing splits and blebs in the myelin

Front 11

What is the cytotoxic edema fluid?

Back 11

-An ultrafiltrate
-Does not contain plasma proteins

Front 12

Describe the edema that accompanies ischemic infarct

Back 12

-A characteristic pattern of edema formation has been observed in animal models of ischemic brain damage
-Early changes include an increase in water content, then swelling of astrocyte processes
-After several hours breakdown of the BBB occurs

-The early edema after ischemic injury is cytotoxic, whereas the later edema has a vasogenic component

Front 13

Describe hydrocephalus

Back 13

This term refers to enlargment of the ventricles, produced by
(1) Most commonly, an imbalance betweent eh production of CSF and its resoption
(2) Atrophy of the brain (hydrocephalus ex vacuo)

Front 14

Describe the normal balance of CSF

Back 14

-The production of CSF by the choroid plexus and the extrachoridal sites is balanced by resorption from the subarachnoid space through arachnoid villi into dural sinuses.

Front 15

What are the general causes of hydrocephalus?

Back 15

-Rarely, over production of CSF by choriod plexus papillomas
-Obstruction within the ventricular system leads to obstructive or non-communication hydrocephalus
-A block of CSF resoption is a communicating hydrocephalus

Front 16

Describe obstructive/non-communicating hydrocephalus

Back 16

-Many lesions can cause this
-Stenosis of the aqueduct of Sylvius is produced by infection or inflammation of the ependymal lining, by masses in the brain stem or posterior fossa that compress the aqueduct, or by hemorrhage and consequent scarring (as in intraventricular bleeds).
-Arnold-Chiari malformations are a common cause of childhood hydrocephalus
-Dandy-Walker syndrom is one in which the midline cerebellum does not form properly and the 4th ventricle enlarges to form a posterior fossa cyst.
-Occlusion of the 4th ventricle foramina leads to hydrocephalus

Front 17

Describe communicating hydrocephalus

Back 17

-There is free flow of CSF from the ventricles into the subarachnoid space
-Causes include meningitis, diffuse meningeal tumors (such as lymphomas), subarachnoid hemorrhage (leading to fibrosis), and dural sinus thrombosis.

Front 18

Describe chronic hydrocephalus

Back 18

-Usually progressive, leading to developmental failure in children
-Treatment is either to remove the obstruction (if that can be done) or to place a shunt from the ventricles into some other body site where absorption of the extra fluid is relatively efficient
-This site is often the pleural or peritoneal cavity
-If the elevation in pressure is not releved, CSF may breach the ependyma and extend into the extracellular space of the periventricular white matter (interstitial edema)

Front 19

Describe normal intracranial pressure

Back 19

-Normally maintained by maintaining intracranial volume through cerebral blood flow regulation and by a balance of cerebrospinal fluid production and resorption.
-Normal ICP limit falls below 15mmHg

Front 20

What causes an increase in intracranial pressure?

Back 20

-Mass lesions
-Edema
-Vascular changes
-Cerebrospinal fluid
-Serum osmolality

Front 21

Describe the effect of mass lesions on intracranial pressure

Back 21

-Increased ICP is a major, serious complication of a variety of mass lesions - tumors, hematomas, abscesses, or granulomas.
-Brain edema due to incompetence of the BBB in these lesions may further increase ICP

Front 22

Describe edema

Back 22

-Most commonly, edema is focal, occuring about lesions where there is BBB breakdown
-Generalized cerebral edema, although rare, is observed in several settings

Front 23

Where is generalized cerebral edema seen?

Back 23

-Pseudotumor cerebri
-Reye's syndrome
-Viral encephalitis
-Diabetic ketoacidosis (rarely)

Front 24

Describe Pseudotumor cerebri

Back 24

-A cause of general edema
-A condition seen largely in young woman, associated with obesity and endocrine dysfunction, produces headache and papilledema
-The latter, if untreated, may result in visual field defects and even blindness.

Front 25

What is the result of compression of the jugular veins? of the abdominal veins?

Back 25

-Compression of jugular veins leads to increased intracranial blood volume and increased ICP
-Compression of abdominal veins by Valsalva maneuver increased intraspinal pressure
-This can be used in testing patency of the subarachnoid space, since, with a cervical or thoracic mass lesion, Valsalva produces a quick rise in lumbar pressure measures at lumbar puncture, but jugular compression will not.
-If the block is partial, a slow rise after jugular compression may be seen

Front 26

Describe hypercapnea

Back 26

-Too much CO2 in the blood
-Causes intracranial vasodilation
-The increased ICP seen in some patients with pulmonary disease may be due in part to vasodilation from CO2 retention

Front 27

Describe how head trauma can cause increased intracranial pressure

Back 27

-Head trauma is sometimes accompanied by a loss of the normal vasoregulation of the intracranial circulation, leading to uncontrolled vasodilation.
-This complication, whiach appears to be more prevalent in children, leads to increased ICP
-The loss of vasoregulation is usually transient, but requires treatment to prevent irreversible brain damage

Front 28

Describe the relationship between CSF and intracranial pressure

Back 28

-Blockage of CSF pathways can lead to increased ICP
-Removal of CSF by lumbar puncture will transiently decrease ICP

Front 29

Describe the relationship between serum hypo-osmolality and intracranial pressure

Back 29

The brain, like other tissues, is in osmotic equilibrium with blood. Hypo-osmolal states, such as water intoxication, will lead to an increase in brain water and brain volume
-Symptoms of headache, seizures, and eventually coma can occur with a fall from the normal 310 milliosmoles of serum to 260 mosm.

Front 30

Describe the relationship between serum hyper-osmolality and intracranial pressure

Back 30

-Hyper-osmolal states produce CNS dehydration
-When serum osmolality rises to about 380 mosm, dehydration and brain shrinkage may produce mechanical distortion, with tearing of blood vessels.
-This complication is more important in dehydrated infants, or those fed inadvertently with too much salt in the formula
-In adults, in whom it is rare, it is seen only in severe dehydration or uremia

Front 31

Describe plateau waves

Back 31

-In patients with increased ICP, continupus pressure measurements have demonstrated that the ICP does not remain constant
-THere are episodic increases reaching over 50 mmHg and lasting 5 to 20 minutes
-These waves reflect hyperemia
-An increase in cerebral blood volume accompanies plateau waves
-Plateau waves may be associated with transient worsening of neurologic deterioration

Front 32

Describe volume changes and the brain

Back 32

-Brain is intolerant of rapid volume changes but can adjust to slow changes
-Slowly growing lesions (eg meningiomas), may reach substantial size without producing an increased ICP
-Brain adjacent to such a lesion will be compressed and gliotic, however

Front 33

Describe the pathologic consequences of a generalized increase in intracranial volume leading to increased ICP

Back 33

-Signs and symptoms include headache, nausea, vomiting, papilledema, and, rarely, a sixth nerve palsy (false localizing sign).
-In pseudomotor cerebri, there is no obstruction to CSF flow nor is regulation of cerebral blood flow disturbed.
-Brain volume is increased diffusely
-Shifts in brain substance usually do not occur

Front 34

When do shifts in brain matter occur? When is it clinically significant?

Back 34

-When pressure gradients develop within the CNS. Local increases increases in pressure, due to the increase in volume of mass lesions, cause shifts away from the lesion.
-Areas remote from the lesion as well as areas adjacent to the lesion may therefore suffer distortion. If the distortion is severe enough to interfere with blood flow, tear vessels, or compress CNS fiver pathways or CN, then clinically significant effects occur

Front 35

Describe cingulate herniation

Back 35

A lateral hemispheric lesion will shift the hemisphere medially, pushing the ipsilateral cingulate gyrus under the free edge of the falx cerebri. This may compress the internal cerebral vein and the ipsilateral anterior cerebral artery.

Front 36

What occurs with supratentorial lesions?

Back 36

With supratentorial lesions, particularly those in the temporal and lateral parietal lobes, the increased pressure is directed medially and downward, forcing the most medial part of the temporal lobe - the uncus and hippocampal gyrus - over the free edge of the tentorium cerbelli. Several importan consequences ensure

Front 37

Describe uncal herniation compressing the ipsilateral IIIrd nerve

Back 37

The ipsilateran IIIrd nerve is compressed by the uncus agains the tentorial edge or, anteriorly, against the supraclinoid ligament, leading to ipsilateral pupillary dilation, one os the earliest signs of uncla herniation, and eventually ipsilateral oculomotor palsy

Front 38

Describe uncal herniation compressing the midbrain

Back 38

The herniating uncus will push against the midbrain, compressing the ipsilateral cerebral peduncle or forcing the contralateral cerebral peduncle against hte contralateral free edge of the tentorium and resulting in hemorrhage and pressure necrosis of the peduncle

Front 39

What is the result of peduncular compression by the uncus?

Back 39

Ipsilateral peduncular compression leads to hemoparesis or hemiplegia on the side oppsoite the lesion, while contralateral peduncular compression leads to hemiparesis or hemiplegia ipsilateral to the lesion (contralateral compression is known as Waltman-Kernohan's notch).

Front 40

What is the result of the uncus compressing the ipsilateral posterior cerebral artery?

Back 40

This leads to ischemic necrosis in its arterial supply: infarcts of the calcarine cortex prioduced hemoanopsia; infartcts of posterior thalamus may also occur

Front 41

What occurs with increasing ICP and uncal herniation?

Back 41

With increasing ICP and further herniation, pressure is transmitted to middle and lower brain stem levels, causing the stem to buckle. Pathophysiology of stem dysfunction includes ischemic changes, due to vascular compression, and hemorrhages (Duret hemorrhage). The latter are often multiple, appear in the lower midbrain and pons, and predominate in the midsagittal region. Duret hemorrhages are arterial resulting from stretching or perforating vessels of the stem.

Front 42

Describe the clincial signs of brain stem compromise during uncal herniation

Back 42

Clinical signs referable to brain stem compromise during herniation progress in a rostral to caudal fashion.
-Ipsilateral pupillary dilatation usually occurs first (midbrain)
-Disappearance of oculocephalic and oculovestibular reflexes indicates pontine dysfunction
-Coma develops as midbrain and pontine reticular formaiton is compromised
-In late stages, the eye signs and pryamidal tract signs become bilateral

Front 43

Describe central herniation

Back 43

Supratentorial lesions produce a downward shift of the hemisphere, first compressing the diencephalon, then forcing the midbrain down through the tentorial notch, and eventually distorting pons and medulla.

Front 44

Describe the result of mass lesions in the frontal, parietal , or occipital lobes

Back 44

May produce a downward shift of the hemisphere, first compressing the diencephalon, then forcing the midbrain down through the tentorial notch, and eventually distorting the pons and medulla

Front 45

Describe the result of extracerebral lesions at the vertex

Back 45

May produce a downward shift of the hemisphere, first compressing the diencephalon, then forcing the midbrain down through the tentorial notch, and eventually distorting the pons and medulla

Front 46

What are the central herniation related consequences of Reye's syndrome or trauma with loss of vagoregulation

Back 46

The hemispheric white matter may swell diffusely, faster than the brain step, producing a downward pressure gradient. Progression of signs reflects a rostra-to-caudal progression of the herniation.

Front 47

Describe signs of diencephalic dysfunction

Back 47

-Decreasing alertness progressing to stupor or coma (upper reticular formation)
-Small pupils
-Babinski reflexes
-Cheyne-Stokes breathing
-Decorticate posturing

Front 48

Describe signs of midbrain dysfunction

Back 48

-Moderate pupillary dilatation
-Dysconjugate eye movements
-Hyperventilation
-Decerebration

Front 49

Describe signs of pontine and upper medullary dysfunction

Back 49

-Loss of oculocephalic and oculovestibular reflexes
-Shallow, irregular breathing
-Flaccidity of limbs
-Pupils are at midposition and unresponsive
Medullary involvmet produces:
-Irregular respiration
-Apneic periods
-Tachy- or bradycardia
-Hypotension
*This is terminal stage*

Front 50

Where are the cerebellar tonsils displaced in cerebellar tonsillar herniation?

Back 50

Cerebellar tonsils are displaced downward through the foramen magnum

Front 51

When does cerebellar tonsillar herniation occur?

Back 51

It can be seen as a late stage of uncal or central herniation, or may result from rapidly expanding cerebellar lesions

Front 52

Describe the consequences of cerebellar tonsillar herniation

Back 52

The tonsils are compressed against the margins of the foramen magnus, causing tonsillar necrosis. More importrantly, the herniating tonsils squeeze the medulla, producing medullary paralysis and death. This involves
-Loss of conssciousness
-Bradycardia
-Irregular respirations or apneic periods
-Hypotension

Front 53

What may be the consequences of cerebellar masses?

Back 53

They may produce signs of lower midbrain and of pontine compression

Front 54

What is the most appropriate treatment for brain herniations?

Back 54

Removal of the mass lesion, but there are many instances when, because of the location of lesions, the rapidity with which brain swelling occurs or because of the presence of hemorrhages such intervention is not feasible.

Front 55

Describe the role of osmotically active substance in treatment of brain edema

Back 55

-Osmotically active substances are often life saving
-Brain capillaries are impermiable to most substances, the exceptions being gases (O2, CO2, N2O, anesthetics), glucose, H2O, and lipid soluble substrances (such as many drugs)
-Osmotic gradients are easily established between brain and plasma water
-Osmotic agents dehydrate the brain
-Areas of cerebral edema are less easily dehydrated than normal brain tissue, but the net effect in reducing intracranial pressure is beneficial

Front 56

What are the osmotic agents used in the treatment of brain herniations?

Back 56

Urea, mannitol, glycerol

Front 57

Describe the use of diuretic furosemide

Back 57

-Useful in reducing cerebral edema
-Increases serum osmolality
-Acts specifically on the choroid plexus to reduce the rate of formation of CSF, thereby lowering intracranial pressure

Front 58

What drugs are most important for treating cerebral edema?

Back 58

Corticosteroids, especially the synthetic steroids prednisolone and dexamethasone

Front 59

Describe the use of steroids for cerebral edema

Back 59

-Beneficial effects of steroid therapy in patients with cerebral edema secondary to tumors and in pseudotumor cerebriare well established
-There is controversty as tho whether steroids are effective in ischemic edema assocaited with strokes, but their use in patietns with stroke is widespread
-Very effect in reducing edema secondary to abscesses or TB meningitis, but must be used with caution since they may drpess host's resistance to primary infecctions

Front 60

How long does it take for steroids to act?

Back 60

Improvements are evident within 24 hours after initiation of treatment and can be maintained for prolonged periods of time

Front 61

How do steroids act on brain edema?

Back 61

-They may extert their beneficial effects by more than one mechanism
-May also affect cerebral function directly
-May decrease the size of the primary lesion, such as a tumor
-Mechanism of action on cerebral edema not fully understood
-Suppresses activation of lysosomal hydrolyzing enzymes
-May reduce disruption of brain capillaries in areas adjacent to lesions and restrict the spread of cerebral edema from a site of injury

Front 62

Describe direct measurement of ICP

Back 62

-Performed by insertion of a catheter into a lateral ventricle or into the subdural or epidural space
-Catheter is then attached to a pressure transducer
-Advocated for children with Reye's syndrome and head trauma patietns with severe neurological deficits
-ICP monitoring allows ofr the detection of increases in pressure before clinical manifestations occur

Front 63

Describe inducing coma for ICP

Back 63

-Done with phenobarbital
-It is accompanied by a decrease in ICP
-For patients with Reye's syndrome when ICP remains too high even after other treatments
-Patient must receive artificial ventilation and close monitoring