Intracranial Bleeding B&B Flashcards by casey kozak

what are 5 possible causes of raised intracranial pressure (ICP)?

mass lesions (tumors)
cerebral edema (large stroke, severe trauma)
hydrocephalus
obstruction of venous outflow (thrombosis)
idiopathic intracranial HTN (aka pseudotumor cerebri)

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what are the general symptoms of increased ICP (intracranial pressure)? (3)

headache (due to pain fibers of CN V in dura mater)
depressed consciousness (due to pressure on midbrain reticular formation)
vomiting

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what is the cause of papilledema? (2)

aka optic disc swelling - due to increased ICP (intracranial pressure)

also seen in severe HTN

usually bilateral, shows blurred margins of the optic disc on fundoscopy

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patients with very high intracranial pressure (ICP) can present with _____ triad:

Cushing’s Triad: HTN + bradycardia + irregular respiration

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unconscious patients with severely high intracranial pressure (ICP) may present with 1 of 2 “postures”… what are they, and what is the differentiating factor?

unconscious patients with severely high ICP may exhibit posturing, which comes in 2 varieties:

decorticate = arms flexed, due to cerebral hemisphere damage
decerebrate = arms extended (at sides), due to brainstem damage

it is believed the key difference is the red nucleus (controls a lot of flexors - if spared, pt exhibits decorticate; if lesion is below, pt exhibits decerebrate)

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Unconscious pt is brought to the ED and is found to have severely high ICP. They are lying with their arms flexed onto their abdomen. What kind of damage occurred?

unconscious patients with severely high ICP may exhibit posturing, which comes in 2 varieties:

decorticate = arms flexed, due to cerebral hemisphere damage
decerebrate = arms extended (at sides), due to brainstem damage

it is believed the key difference is the red nucleus (controls a lot of flexors - if spared, pt exhibits decorticate; if lesion is below, pt exhibits decerebrate)

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Unconscious pt is brought to the ED and is found to have severely high ICP. They are lying with their arms extended at their sides. What kind of damage occurred?

unconscious patients with severely high ICP may exhibit posturing, which comes in 2 varieties:

decorticate = arms flexed, due to cerebral hemisphere damage
decerebrate = arms extended (at sides), due to brainstem damage

it is believed the key difference is the red nucleus (controls a lot of flexors - if spared, pt exhibits decorticate; if lesion is below, pt exhibits decerebrate)

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how is the Glasgow Coma Scale scored?

GSC score is 3 (bad) to 15 (good)

eye (1-4 points): does not open, opens to painful stimuli, opens to voice, opens spontaneously
verbal (1-5 points): no sound, incomprehensible, inappropriate words, confused, oriented
motor (1-6 points): no movements, decerebrate posturing (arms extended), decorticate posturing (arms flexed), withdrawal to pain, localizes to pain, obeys commands

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what are the 4 types of brain herniation syndromes?

expanding volume (blood, tumor) forces brain through weakest points - most patients do not survive

subfalcine: side to side (cingulate gyrus under falx cerebri)
uncal: side to bottom, transtentorial (uncus into brainstem)
central: diencephalon downward towards midbrain
tonsillar: cerebellum through the “hole” (compress midbrain)

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what occurs in a subfalcine hernation?

cingulate gyrus (brain tissue right next to corpus collosum) herniates under the falx cerebri (dura mater separating hemispheres)

this drags the anterior cerebral artery (ACA) with it!! gets compressed —> contralateral leg paresis (supplies motor neurons of lower leg)

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which type of brain herniation presents with leg paresis due to compression of the ACA?

subfalcine herniation: cingulate gyrus (brain tissue right next to corpus collosum) herniates under the falx cerebri (dura mater separating hemispheres)

this drags the anterior cerebral artery (ACA) with it!! gets compressed —> contralateral leg paresis (supplies motor neurons of lower leg)

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what occurs in an uncal herniation?

uncal = medial temporal lobe

uncus herniates across the tentorium (dura mater above cerebellum) —> compresses midbrain

presents with dilated pupil (ipsilateral) + visual loss + hemiparesis or quadriparesis

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what are the symptoms of an uncal herniation? (4)

uncus (medial temporal lobe) herniates across the tentorium (dura mater above cerebellum), compressing midbrain

ipsilateral CNIII compression —> loss of PNS innervation causes dilated “blown” pupil
collapse of ipsilateral posterior cerebral artery (PCA) —> cortical blindness + homonymous hemianopsia
cerebral peduncle compression —> contralateral w/wo ipsilateral (Kernohan’s notch) paresis
duret hemorrhage of pons and midbrain (perforating branches of basilar artery draining veins)

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which type of brain herniation presents with blown (dilated) pupil + visual loss + hemiparesis OR quadriparesis?

uncus (medial temporal lobe) herniates across the tentorium (dura mater above cerebellum), compressing the midbrain

ipsilateral CNIII compression —> loss of PNS innervation causes dilated “blown” pupil
collapse of ipsilateral posterior cerebral artery (PCA) —> cortical blindness + homonymous hemianopsia
cerebral peduncle compression —> contralateral (hemi) w/wo ipsilateral (quad) (Kernohan’s notch) paresis
duret hemorrhage of pons and midbrain (perforating branches of basilar artery draining veins)

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what occurs in a transtentorial herniation?

transtentorium = dura matter separating cerebrum from cerebellum

thalamus/ hypothalamus/ medial parts of both temporal lobes are forced through tentorium cerebellum (downwards)

—> somnolence, LOC, small/reactive pupils (early) to non-reactive (late), posturing, death

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how does a transtentorial herniation present?

transtentorium = dura matter separating cerebrum from cerebellum

thalamus/ hypothalamus/ medial parts of both temporal lobes are forced through tentorium cerebellum (downwards)

—> somnolence, LOC, small/reactive pupils (early) to non-reactive (late), posturing, death

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An unconscious pt is brought to the ED. Upon initial assessment, the pupils are small and reactive. However, within a few hours they become non-reactive, and the patient exhibits posturing. What has likely occurred?

transtentorium = dura matter separating cerebrum from cerebellum

thalamus/ hypothalamus/ medial parts of both temporal lobes are forced through tentorium cerebellum (downwards)

—> somnolence, LOC, small/reactive pupils (early) to non-reactive (late), posturing, death

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what occurs in a tonsillar herniation?

cerebellar tonsils (bottom portions) herniate downward through foramen magnum

most commonly caused by posterior fossa mass lesion

compression of medulla —> depressed respiratory/cardiac centers —> cardio-respiratory failure

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what is the cause of death from a tonsillar herniation?

cerebellar tonsils (bottom portions) herniate downward through foramen magnum

most commonly caused by posterior fossa mass lesion

compression of medulla —> depressed respiratory/cardiac centers —> cardio-respiratory failure

which type of brain herniation causes depression of the respiratory and cardiac rhythm centers in the medulla?

tonsillar herniation: cerebellar tonsils (bottom portions) herniate downward through foramen magnum

most commonly caused by posterior fossa mass lesion

compression of medulla —> depressed respiratory/cardiac centers —> cardio-respiratory failure

what are the 4 types of intracranial bleeds?

epidural hematoma
subdural hematoma
subarachnoid hemorrhage
hemorrhagic stroke

what is the cause of epidural hematoma, and how does it appear on imaging?

rupture of middle meningeal artery (branch of maxillary artery), usually via trauma (temporal bone fracture)

CT shows convex/lens shape because the lesion CANNOT cross suture lines (dura are attached to sutures of the skull)

what are the symptoms of epidural hematoma? (3 general, 1 specific)

rupture of middle meningeal artery (branch of maxillary artery), usually via trauma (temporal bone fracture) —> convex shape on CT (cannot cross sutures)

general: headache, drowsiness, LOC

specific: lucid interval - pt initially loses consciousness, then regains consciousness and appears fine, then 20-30mins later they pass out from the intracranial bleeding

A very smart football coach brings their player in for evaluation after a serious blow to the head knocked the player unconscious. The athlete is complaining about being there - they claim they regained consciousness quickly and now only have a headache. Why is it so important that they are continuously monitored for the next few hours?

epidural hematoma: rupture of middle meningeal artery (branch of maxillary artery), usually via trauma (temporal bone fracture) —> convex shape on CT (cannot cross sutures)

general: headache, drowsiness, LOC

specific: lucid interval - pt initially loses consciousness, then regains consciousness and appears fine, then 20-30mins later they pass out from the intracranial bleeding

what is the cause of subdural hematoma, and how does it appear on imaging?

traumatic rupture of the *bridging veins*, allowing blood to accumulate between the dura mater and arachnoid space —> SLOW bleeding due to low pressure of venous system CT shows *crescent shaped* bleed because it CAN cross suture lines, but limited by dural reflections (falx cerebri, tentorium, falx cerebelli)

why is an epidural hematoma considered more dangerous than a subdural hematoma?

epidural hematoma = rupture of middle meningeal *artery* (HIGH pressure system) —> quicker bleed subdural hematoma = rupture of bridging *veins* (LOW pressure system) —> slower bleed

what are the risk factors of subdural hematoma? (4)

traumatic rupture of the *bridging veins*, bleed between dura mater and arachnoid space —> *crescent shaped* CT 1. old age (cortex shrinks, bridging veins have to travel farther) 2. alcoholics 3. blood thinners (warfarin, anti-platelets) 4. shaken baby syndrome

Pt is a 88yo M brought to a neurologist by their partner. The partner reports that a few weeks ago, the pt had a traumatic head injury and now is beginning to show signs of confusion. What should you be concerned of? What might you find on CT?

*subdural hematoma*: traumatic rupture of the *bridging veins*, allowing blood to accumulate between the dura mater and arachnoid space —> SLOW bleeding due to low pressure of venous system CT shows *crescent shaped* bleed because it CAN cross suture lines, but limited by dural reflections (falx cerebri, tentorium, falx cerebelli)

What type of brain bleed are you concerned of in a child with suspected shaken baby syndrome?

What type of brain bleed is seen on CT to track in between the lobes of the brain?

*subarachnoid hemorrhage*: bleeding into space between arachnoid and pia mater (recall pia matter is directly on surface of brain lobes) usually from ruptured berry aneurysms (Circle of Willis)

what type of brain bleed does this describe: SUDDEN onset of SEVERE headache + fever + nuchal rigidity + xanthochromia on spinal tap

*subarachnoid hemorrhage*: bleeding into space between arachnoid and pia mater usually from ruptured berry aneurysms (Circle of Willis) xanthochromia = yellow-colored CSF presents with NO focal deficits!!

what is the most common site of subarachnoid hemorrhage?

ruptured berry aneurysms most commonly located in *anterior Circle of Willis* at the branch points of the *anterior communicating artery*

what are 4 risk factors for subarachnoid hemorrhage?

1. AVMs (anterior venous malformations) 2. Marfan syndrome 3. ADPKD 4. Ehlers-Danlos (this is due to risk of berry aneurysm!)

what are the possible causes of hemorrhagic stroke? (4)

aka *intraparenchymal bleed* - occur in small arteries/arterioles, caused by: 1. HTN 2. anti-coagulation 3. CNS malignancy 4. ischemic stroke followed by reperfusion

what occurs in intraparenchymal bleeds of the brain?

aka *hemorrhagic stroke*: rupture of small arteries or arterioles caused by HTN, anti-coagulation, CNS malignancy, ischemic stroke followed by reperfusion

where are the most common sites of hemorrhagic strokes? (5) why does this make sense?

rupture of small arteries or arterioles caused by HTN, anti-coagulation, CNS malignancy, ischemic stroke followed by reperfusion 1. *putamen* (35%) 2. *subcortex* (30%) 3. cerebellum (16%) 4. thalamus (15%) 5. pons (5-12%) these are all structures supplied by tiny arteries!

how do hemorrhagic strokes (intraparenchymal bleeds) present? (3)

most commonly affect *putamen* and surrounding structures (supplied by small arteries) —> 1. *contralateral hemiparesis* (internal capsule) 2. *hemisensory loss* (thalamus) 3. *gaze deviation towards bleed* (frontal eye field lesion) usually present in a patient with HTN

Pt is a 45yo M with PMH of uncontrolled HTN presenting to the ED with L paralysis and sensory loss. PE is notable for eye deviation towards the R. What are you most concerned about? What side is the injury on?

*hemorrhagic stroke*: aka intraparenchymal bleed, rupture of small arteries or arterioles caused by HTN, anti-coagulation, CNS malignancy, ischemic stroke followed by reperfusion 1. *contralateral hemiparesis* (internal capsule) 2. *hemisensory loss* (thalamus) 3. *gaze deviation towards bleed* (frontal eye field lesion) [so stroke is on RIGHT side of this patient - follow the eyes]

Pt presents with a hypertensive hemorrhagic stroke (ICH, intracranial hemorrhage). What is the most likely mechanism?

*Charcot-Bouchard aneurysm*: micro-aneurysm of small branches of lenticulo-striate arteries supplies basal ganglia and thalamus believed to be the origin of HTN ICH

what is the cause and presentation of cerebral amyloid angiopathy?

*recurrent hemorrhagic strokes* due to *beta-amyloid* deposits in artery walls (weak, prone to rupture) causes *smaller* strokes of *lobar hemorrhages* (frontal, parietal, occipital) will present in an elderly person

elderly person with recurrent hemorrhagic strokes =

*cerebral amyloid angiopathy*: recurrent hemorrhagic strokes due to *beta-amyloid* deposits in artery walls (weak, prone to rupture) causes *smaller* strokes of *lobar hemorrhages* (frontal, parietal, occipital) will present in an elderly person

how do strokes caused by cerebral amyloid angiopathy differ from those caused by hypertension?

hemorrhagic strokes due to HTN are big and affect *basal ganglia* hemorrhagic strokes due to cerebral amyloid angiopathy are small and affect *lobes (frontal, parietal, occipital)*, due to beta-amyloid deposits in artery walls

intraventricular hemorrhages are a complication of…

… *premature birth* hemorrhage into lateral ventricle within first ~5 days of life (premature babies have poor auto regulation of blood flow near ventricles) can be asymptomatic or cause LOC/hypotonia/loss of spontaneous movements, massive bleed can cause seizure/coma

4 day old premature baby presents with LOC, hypotonia, and loss of spontaneous movements - what is your primary concern?

*intraventricular hemorrhage*: complication of premature birth, hemorrhage into lateral ventricle within first ~5 days of life due to poor autoregulation of blood flow near ventricles can be asymptomatic or cause LOC/hypotonia/loss of spontaneous movements, massive bleed can cause seizure/coma

a premature baby presenting with intraventricular hemorrhage may have obstruction of… how should this be treated?

… *foramen of Monro* (between lateral and 3rd ventricles) —> enlargement of lateral ventricles with normal 3rd/4th ventricles due to germinal matrix problem - highly vascular around ventricles, premature babies do not have sufficient auto-regulation of blood flow (full-term infants have less vascularity in this area) tx: *ventriculoperitoneal (VP) shunt*