2.3: 14. Neuropathology 2: Pathophysiologic Complications

Front 1

Swelling of the brain leads to....

Back 1

1) narrowed sulci and flattened gyri
2) blood flow to brain becomes impaired

Symptoms include: headache, nausea and vomiting (if the chemoreceptors in the medulla are compressed and activated), papilledema (water from swollen brain tracts down the optic nerve to the eye, which you can see on an eye exam), or even focal signs and seizures

Front 2

If the edema/swelling of the brain is not alleviated, this can lead to ______ syndromes. Name three varieties of this type of syndrome.

Back 2

1) Herniation syndromes

2) a. subfalcine herniation
b. transtentorial herniation = uncal herniation
c. cerebellar tonsillar herniation

Front 3

1) What is a subfalcine herniation?

2) The subfalcine herniation leads to the compression of _____ which causes an infarction in the _________.

Back 3

1) occurs when swelling pushes brain parenchyma UNDERNEATH FALX CEREBRI at the midline of the cerebrum

2) anterior cerebral artery; medial frontal cortex

Front 4

1) What is a transtentorial herniation or an uncal herniation?

2) What nerve does a transtentorial herniation compress and what results?

3) What vessel does a transtentorial herniation compress and what results?

Back 4

1) portion of the brain parenchyma is pushed BENEATH THE TENTORIUM CEREBELLI that lies atop the cerebellum

2) compression of oculomotor nerve; pupillary dilation

3) compression of posterior cerebral artery; occipital lobe infarction

Front 5

What is Kernohan's notch?

Back 5

Kernohan's notch - when the a lesion pushes the brainstem over and the cerebral peduncle on the opposite side is compressed, which results in a deficit on the ipsilateral side to the lesion (because opposite spinal-thalamic tracts are compressed.)

Front 6

What occurs when the brainstem is compressed?

Back 6

Compression of brainstem → necrosis of contralateral cerebral peduncle → hemiplegia ipsilateral to the mass lesion and rupture of small blood vessels in the midbrain and pons → DURET HEMORRHAGE → brain-dead

Front 7

1) What is cerebellar tonsillar herniation?

2) T/F Cerebellar tonsillar herniation is not an immediate medical emergency you can wait a few days before you can go to the doctor. Hell you should go to ihop before you go....

3) How would you treat this? Should you resect the tonsils?

Back 7

1) Cerebellar Tonsillar Herniation - severely elevated intracranial pressure leads to pushing of brain downward into foramen magnum → impact the medulla → compress respiratory centers → DEATH

2) FALSE FALSE FALSE
Tonsillar herniations are NEUROSURGICAL EMERGENCY

3) REMOVE THE PRESSURE by drilling a Burr hole into the skull (anywhere is fine, JUST GET THE PRESSURE OUT ); do NOT resect the tonsils

DO NOT RESECT THE TONSILS

Front 8

What are the several layers beneath the skull and what are their associated potential spaces where blood can accumulate?

Back 8

Dura Mater
-epidural space is above the dura mater periosteum; below the skull
- subdural space btw dura and arachnoid

Arachnoid Mater
-subarachnoid space is between arachnoid and pia (where CSF flows)

Pia Mater
- single cell layer on surface of brain itself

Front 9

The Blood-Brain Barrier: created by tight-junctions between the endothelial cells in the blood vessels and epithelial cells in the choroid plexus

1) What does disruption of the blood brain barrier lead to?

2) What are the two kinds of edema?

Back 9

1) Disruption of this barrier leads to leaking of fluid into interstitial fluid space → can lead to EDEMA

2)
a) vasogenic edema
b) cytotoxic edema

Front 10

Explain what vasogenic edema is.

Back 10

Vasogenic Edema - result of injury to blood-brain barrier such that its structural integrity is damaged

Front 11

Explain what cytotoxic edema is.

Back 11

Cytotoxic Edema - edema associated with individual cell injury - classic cloudy swelling that is expected to occur with any type of cellular injury (ie. when there is damage so that the Na+/K+ pump is compromised)

Front 12

1) What is hydrocephalus?

2) What are the two forms of hydrocephalus?

Back 12

1) Accumulation of CSF within the brain

2)
a) noncommunicating
b) communicating

Front 13

1) What is a noncommunicating hydrocephalus?

2) How would you treat this?

Back 13

1) Noncommunicating - result of obstruction of the normal CSF outflow, foramina are blocked

2) treat with insertion of shunt

Front 14

1) What is communicating hydrocephalus?

2) What disease does this occur in?

Back 14

1) Communicating - impaired resorption (or excessive production) of CSF

2) Alzheimer's Disease

Front 15

1) What are the two kinds of skull fractures and describe them?

2) Which one typically requires surgical intervention?

3) Which one can lead to seizures?

4) Which one does not typically need surgical intervention?

Back 15

1) Linear Fractures - bones of the calvaria are broken but still held in place by dura → do not usually require surgical intervention

Depressed Fractures - bone fragments are splintered and push into the brain parenchyma (this will require surgery) → can lead to seizures (need to be surgically removed)

2) Depressed fractures

3) Depressed fractures

4) linear fracture

Front 16

1) What occurs in diffuse axonal injury?

2) T/F This has a great prognosis.

Back 16

Occurs as consequence of disease or trauma: white matter tracts are sheared or cut

Usually see in motor accidents → causes coma immediately, which is a very bad sign (may never regain consciousness and are usually in vegetative state)

2) FALSE FALSE FALSE

Front 17

What are the two kinds of dural hemorrhages?

Back 17

Epidural and Subdural hemorrhage

Front 18

1) What artery is most commonly ruptured in a epidural hemorrhage?

2) What happens when the artery is injured?

3) Why does an epidural hematoma develop more quickly than a subdural hematoma?

Back 18

1) middle meningeal artery (due to skull fracture)

2) When an artery is injured, the blood tends to accumulate above the dura very quickly and displaces the brain → rapid increase in intracranial pressure

3) Epidural hematoma develops much more quickly than with subdural hematoma because this involves arteries rather than veins

Front 19

1) What causes a subdural hemorrhage?

2) Describe the loss of blood in a subdural hemorrhage. Does it lead to immediate herniation?

3) Why do subdural hemorrhages occur more frequently in the elderly than in younger populations?

Back 19

1) Subdural hemorrhage - most commonly caused by damage to bridging veins beneath the dura mater

2) Tearing leads to slow blood loss and venous blood accumulates slowly; herniation takes much longer to occur

3 ) Occurs more often in elderly vs. younger population because brain becomes smaller in older people and bridging veins are stretched

Front 20

1) What is a concussion?

2) What is a contusion?

3) What is the difference between the two?

Explain the difference between a concussion and a contusion.

Back 20

1) Concussion: transient loss of consciousness/mental capabilities without damage to brain (functional injury)

2) Contusion: anatomical damage to brain, which leads to necrosis of brain tissue and possible hemorrhage → plaque jaune = depressed yellow patches which can result in seizures

3) A contusion produces actual anatomical damage to the brain whereas a concussion does not.

Front 21

What is a plaque Jaune?

Back 21

signature mark of contusion on brain parenchyma

appear as depressed yellow patches that involve the crests of the affected gyri

plaque jaune can become epileptogenic

Front 22

1) What is a coup contusion?

2) What is a countrecoup contusion?

3) What is the primary difference between the two? (EXAM QUESTION)

Back 22

1) Coup Contusion - bruising of tissue immediately beneath the point of injury

2) Contrecoup Contusion - bruising of tissue that is immediately opposite that affected by the coup contusion; this results from the hitting of the brain into the opposite side of the skull after the blow

3) A contrecoup contusion is usually larger than the coup contusion because it results from the brain “rubbing up” against bony protuberances in the skull, exaggerated by a pressure wave (CLASSIC EXAM QUESTION)

Front 23

1) What is a thrombotic infarct?

2) What artery does this typically occur in?

3) What are transient ischemic attacks?

Back 23

1) Thrombotic - result of progressive, slow narrowing of cerebral vessels by atherosclerosis → can still lead to liquefactive necrosis (pictured below)

2) carotid artery

3) Transient ischemic attacks: focal stroke-like symptoms that last a few hours and then resolve. Harbinger that a major thrombotic event is coming

Front 24

1) What happens in an embolic infarct?

2) What is the time frame of an embolic infarct?

3) What is the source of the embolic infarct?

4) In terms of reperfusion, what distinguishes embolic infarcts from thrombotic infarcts?

Back 24

1) Cardiac mural thrombus is usually the source of embolus; can lodge in cerebral circulation
(Similar to dropping piece of soap bar into drainage and getting it stuck there immediately)

2) Embolic - usually have much more acute onset

3) cardiac mural thrombus

4) Reperfusion leads to hemorrhage in embolic infarcts (but NOT in thrombotic infarcts)

Front 25

In patients with hypertension, small arterioles can also become thickened produce in the characteristic onion skinned histological appearance.

1) What can this potentially lead to?

2) Where is this most common?

Back 25

1) This can lead to LACUNAR INFARCTS

2) most common places in basal ganglia and pons

Front 26

1) With regards to intracerebral hemorrhage, patients who have hypertension are prone to hemorrhage in which arteries? ( HINT BRANCH OFF MCA)

2) What area of the brain does it affect?

Back 26

1) Lenticulostriate arteries (small, penetrating blood vessels that branch off the MCA) in basal ganglia are most prone to rupture and hemorrhage, secondary to hypertension

2) basal ganglia

Front 27

1) What is congophilic angiopathy?

2) What protein is significant to this condition?

3) What does the deposition of this protein lead to?

Back 27

1) Hemorrhage in some elderly patients might result from deposition beta-amyloid protein = congophilic angiopathy = amyloid angiopathy (usually in midsized arteries)

2) Beta amyloid protein

3) deposition of beta amyloid protein leads to structural damage of the vessels which leads to hemorrhage

congophilic angiopathy is most common cause of spontaneous, lobar intracerebral hemorrhage in elderly

Front 28

1) What are the most common cerebral aneurysms and where do they occur?

2) a) 90% occur in _____
b) 10% occur in _____

Back 28

1) Berry aneurysms at proximal bifurcations of cerebral blood vessels = most common cerebral aneurysms

2) a) anterior circulation
b) 10% in posterior circulation

Front 29

1) T/F Aneurysms aren't really a big deal, people get them all the time, they go untreated and resolve on their own.

2) What happens to the prognosis of patients suffering from an aneurysm upon re-rupture?

3) Histologically the ruptured aneurysm lacks what? Why is that lack significant?

Back 29

1) FALSE FALSE FALSE
25-50% mortalitiy

2) prognosis gets progressively worse

3) ruptured aneurysm lacks internal elastic lamina
which leads decreased structural integrity lead to its rupture (this can spread to the subarachnoid space produce a massive and acute bleed)

Front 30

1) T/F venous angiomas are extremely dangerous. Like insanely dangerous so dangerous Bruce Li wouldn't mess with them.

2) Are venous angiomas a common occurrence?

Back 30

1) FALSE
venous angiomas are clinically silent and require no therapy

2) venous angiomas are the most common vascular formations

Front 31

1) What are cavernous angiomas?

2) What can these cause?

Back 31

1) cavernous angiomas appear as back-to-back proliferative vessels without intervening parenchyma; these are persistent and can cause hemorrhage or be epileptic focus

2) hemorrhage or be epileptic focus

Front 32

What is capillary telangiecstasias?

Back 32

another vascular malformation that is frequently ASYMPTOMATIC

Front 33

1) What are ateriovenous malformations AVM?

2) When do they present?

3) Why do vessels show arteriolization of veins?

4) How would you diagnose it?

5) What is the risk of hemorrhage?

6) How is it treated?

Back 33

1) Arteriovenous Malformations (AVM) - most common vascular malformation requiring clinical intervention

2) Most commonly present after intracerebral hemorrhage

3) Vessels show arteriolization of the veins because of arterial blood pressure communicating directly with veins caused by abnormal anastomoses

4) Usually diagnose with an angiogram

5) 10% one-year risk of hemorrhage after a primary bleed

6) Treatments: embolization, gamma knife, surgical resection