CNS Blood Supply, Stroke, & Head Trauma Flashcards

1
Q

Which two systems supply the brain?

A
  • the internal carotid (anterior system) (80%) and the vertebrobasilar (posterior system) (20%) systems
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2
Q

Which meninges are pierced by the major arteries supplying the CNS?

A
  • the dura mater and arachnoid mater; they lie in the subarachnoid space, floating in CSF
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3
Q

Follow the path of the vertebrobasilar system.

A
  • vertebral arteries ascend through the transverse foramina of the cervical vertebrae and then enter the cranial cavity through the foramen magnum
  • each vertebral artery gives off branches to form the anterior spinal artery, the two posterior inferior cerebellar arteries, and the two anterior inferior cerebellar arteries
  • the two vertebral arteries then converge at the ponto-medullary junction to form the basilar artery
  • the basilar artery gives off many small pontine branches, and then the two superior cerebellar arteries, before terminating into the two posterior cerebral arteries at the level of the midbrain
  • (basilar artery also gives of labyrinthine arterial branches)
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4
Q

Explain the blood supply to the spinal cord.

A
  • the spinal cord has 3 major arteries: 1 anterior spinal artery and 2 posterior spinal arteries
  • the anterior spinal artery is formed by branches arising from the vertebral arteries before they merge into the basilar artery
  • the 2 posterior spinal arteries arise from either the vertebral arteries themselves or from their posterior inferior cerebellar arterial branches
  • throughout the length of the spinal cord, these 3 vessels receive blood supply reinforcements via numerous segmental/radicular arteries (a major segmental/radicular artery is the artery of Adamkiewicz - which arises directly from the aorta)
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5
Q

What portions of the spinal cord does each spinal artery supply? Are there any major watershed areas of the spinal cord?

A
  • the anterior spinal artery supplies the anterior 2/3’s of the cord
  • the posterior spinal arteries supply the posterior 1/3
  • major watershed areas are those areas right before the next major segmental reinforcement: T4 and L1 (for anterior spinal cord), and T1-T3 (for posterior)
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6
Q

What portions of the brain are supplied by each branch of the vertebrobasilar system?

A
  • posterior inferior cerebellar arteries supply the inferior cerebellum and the lateral medulla
  • anterior inferior cerebellar arteries supply the inferior cerebellum and the lateral pons
  • labyrinthine arteries supply the labyrinths
  • pontine arteries supply the medial pons
  • posterior cerebral arteries supply the midbrain, inferior temporal lobes, and occipital lobe
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7
Q

Follow the path of the internal carotid system.

A
  • internal carotids enter the skull via the carotid canal and emerge into the middle cranial fossa via the foramen lacerum before ascending on each side of the pituitary gland
  • each internal carotid gives off an opthalamic arterial branch, which enters the optic canal
  • posteriorly, the internal carotids give off branches to form the posterior communicating arteries (these connect with the posterior cerebral arteries) and the anterior choroidal arteries
  • they then terminate into two branches: the middle cerebral arteries (running laterally) and the anterior cerebral arteries (running anteriorly)
  • an anterior communicating artery connects the two anterior cerebral arteries
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8
Q

What portions of the brain are supplied by each branch of the carotid system?

A
  • opthalamic arteries supply the retinas
  • middle cerebral arteries supply the deep structures (basal ganglia, thalamus, etc.), superior temporal lobes, and the inferior lateral regions of the frontal and parietal lobes
  • anterior cerebral arteries supply the medial and superior lateral regions of the frontal and parietal lobes
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9
Q

Which branches of the middle cerebral artery supply the deep structures (basal ganglia, internal capsule, thalamus, etc)?

A
  • the lenticulostriatal branches
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10
Q

Both the anterior and middle cerebral arteries supply parts of the frontal and parietal lobes - how does this affect the supply to the homunculus?

A
  • the ACA supplies the genitals, feet, and lower limbs
  • the MCA supplies the head, neck, hands, and upper limbs
  • note that the MCA supplies the internal capsule, where fibers projecting to every part of the body are condensed
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11
Q

What is a berry aneurysm? What is the most common site? What are some others? Which artery is most commonly occluded via embolism?

A
  • these are aneurysms that occur at arterial branch points; these areas lack a media (due to the turning/branching) and are therefore at risk (also increases risk of rupture)
  • most common: at the branch points of the anterior communicating artery and anterior cerebral artery (40% of brain aneurysms occur here)
  • other common areas: junction of the internal carotid and posterior communicating artery, bifurcation of the middle cerebral artery
  • the middle cerebral artery is the most common site of embolic occlusion (the embolus is usually from the left heart due to atrial fibrillation)
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12
Q

Circle of Willis

A
  • connections between the 2 anterior carotid systems as well as connections between the carotid systems with the posterior vertebrobasilar system
  • (anterior communicating artery –> anterior cerebral artery + middle cerebral artery –> posterior communicating artery –> posterior cerebral arteries –> posterior communicating artery –> middle cerebral artery + anterior cerebral artery –> back to anterior communicating artery)
  • provides a high degree of collateral flow
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13
Q

Give a generalized explanation of which parts of the cerebral hemispheres are supplied by each cerebral artery.

A
  • anterior cerebral artery: supplies the medial hemisphere
  • middle cerebral artery: supplies the lateral hemisphere
  • posterior cerebral artery: supplies the occipital lobe
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14
Q

The thoracic region of the spinal cord is most vulnerable to receiving insufficient blood supply, especially anteriorly - occlusion of the anterior spinal artery will result in what signs and symptoms?

A
  • (this leads to acute thoracic cord syndrome)
  • paraplegia and incontinence
  • the spinothalamic tracts are mainly lost, with preservation of the dorsal columns
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15
Q

Explain the venous drainage of the spinal cord.

A
  • there are 6 longitdunal interconnecting venous channels (an anterior spinal vein, a posterior spinal vein, 2 anterolateral veins, and 2 posterolateral veins)
  • these drain via the anterior and posterior radicular veins into the internal vertebral venous plexus (between dura mater and vertebral periosteum), which eventually drains into the main venous system
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16
Q

Which cerebral artery is the largest?

A
  • the middle cerebral artery
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17
Q

What is a stroke? What are the two main types?

A
  • blockage (ischemia) or rupture (hemorrhage) of vessels in the cerebral circulation, resulting in a focal neurological syndrome
  • 85% are ischemic, 15% are hemorrhagic
  • if it involves the anterior/carotid system: focal epilepsy, contralateral sensory/motor deficit, psychological deficit (ex: aphasia)
  • if it involves the posterior/vertebrobasilar system: vision loss, focal brainstem lesion
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18
Q

Explain the venous drainage of the brain.

A
  • (note that these veins are valve-less)
  • deep veins, superficial veins, and dural venous sinuses are involved
  • the deep veins drain the internal structures of the forebrain; they merge within each hemisphere to form the 2 internal cerebral veins, which then merge in the midline to form the great cerebral vein
  • venous blood then flows into the internal jugular vein
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19
Q

Explain the difference between a transient ischemic attack (TIA) and an ischemic stroke.

A
  • TIA: a transient, fully reversible neurological event that lasts less than 24 hours (typically they last less than 1 hour)
  • ischemic stroke: the sudden onset of neurological deficits as a result of an ischemic event (deficit lasts more than 24 hours); more commonly due to embolism than to thrombosis
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20
Q

What percentage of patients with a stroke will suffer a second one within twelve months? What percentage with a TIA will suffer a stroke within one WEEK?

A
  • about 10% of patients with a stroke will suffer a 2nd one within a year
  • 5-7% of patients with a TIA will suffer a stroke within the next week!
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21
Q

What are the major risk factors for TIAs and ischemic strokes?

A
  • diabetes, hypertension, and dyslipidemia
  • since embolism is the most common mechanism for ischemic stroke (vs. thrombosis), myocardial dysfunctions are also major risk factors (cardiac mural emboli are the most common source of cerebral embolism)
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22
Q

What clinical signs indicate a patient has suffered a hemorrhagic stroke?

A
  • rapid onset of neurological deficits
  • neck stiffness, coma, seizures, vomiting, headache, diastolic BP greater than 110 mmHg
  • the only way to be sure, however, is with neuroimaging
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23
Q

Which neuroimaging is recommended for detecting strokes?

A
  • non-contrast CT imaging is used MAINLY for detecting hemorrhagic strokes (ischemic strokes are hard to detect with imaging)
  • the sensitivity of the imaging for hemorrhagic stroke is 95-100% during the first 12 hours, but severely decreases as the blood is cleared - after 1 week, it is 50% sensitive; by week 2 or 3, it will no longer be detectable
24
Q

Other than the neuroimaging, what other investigations should be performed in a patient with a stroke?

A
  • CT angiography and Duplex Doppler scan of the carotid arteries should be done ASAP - to check for stenosis of these major vessels
  • blood tests and ECG should be done to rule out coronary artery disease (CAD)
25
Q

How do we treat ischemic strokes? What do we give to prevent ischemic strokes?

A
  • treatment: IV tissue plasminogen activator (tPA) to dissolve the clots (thrombolysis) causing the ischemia (must be given within the 1st 4 and a half hours to be effective)
  • prevention with antiplatelets: aspirin (the mainstay), dipyridamole (side effects decrease compliance), clopidogrel (PPIs interfere with clopidogrel!), warfarin
  • in patients who received thrombolysis, wait 24 hours before giving prophylactic aspirin
26
Q

Patients suffering a stroke recover via two mechanisms - what are they?

A
  • 1st recovery: due to resolution of the harmful local features (edema, loss of circulation, toxins, etc.)
  • 2nd recovery: due to neural plasticity (new connections are made)
27
Q

What is a subarachnoid hemorrhage? How do patients commonly present? What are the most common causes?

A
  • SAH is bleeding into the subarachnoid space, resulting in raised ICP (blood is also toxic to the brain parenchyma; the CSF and brain ECF are in full communication) - it is a medical emergency
  • patients present with “the worst headache of my life,” nausea, vomiting, and photophobia; 50% also have a loss of consciousness
  • most common causes: ruptured intracranial aneurysm (ruptured berry aneurysm, usually of the anterior communicating artery branch points) and trauma
28
Q

What investigations do we use when a subarachnoid hemorrhage is suspected? How do we treat them?

A
  • investigations: CT followed by a LP if unrevealing; if ruptured aneurysm is the cause, we can confirm with a cerebral angiography; FBC, clotting profile, electrolytes (hyponatremia may result), troponin I; ECG (50% have abnormal ECGs)
  • the LP will have increased RBC count and a yellow-ish tinge (called xanthochromia) due to the presence of bilirubin
  • treatment: stabilize (cardio-pulmonary support) + surgical clipping or endovascular coil embolization
  • give these patients Ca2+ channel blockers, stool softeners, and antitussives (cough suppressant) to prevent future vasospasms/re-bleeding during the recovery period; also give anticonvulsants to decrease risk of seizure (which would most likely cause re-bleeding)
29
Q

What are the major risk factors for subarachnoid hemorrhage?

A
  • older age (greater than 50), female, black
  • smoking, HTN, ADPKD (adult polycystic kidney disease), Marfan’s syndrome, Ehlers-Danlos syndrome
  • family history of SAH
30
Q

A patient presents with “the worst headache of his life” and one eye is unresponsive to light and points down and out - what should you suspect?

A
  • a ruptured aneurysm at the junction of the internal carotid and posterior communicating arteries (compression of the 3rd CN), resulting in SAH
31
Q

Subdural and Epidural Hematomas

A
  • subdural (SDH): between the dura and arachnoid; can be due to whiplash forces, tearing the veins (much more common) separating the dura and arachnoid does not require much pressure - venous pressure is enough to do so; slow
  • epidural (EDH): between the skull and dura; nearly always due to skull fracture with laceration of meningeal arteries (less than 1% of head injuries) to separate the dura mater and the skull, you need arterial pressure, which requires a skull fracture to rupture an artery; rapid (can result in herniation, CN III compression)
  • patients present with loss of consciousness/drowsiness, unilateral headache, and unilaterally slightly enlarged pupil
  • in acutely deteriorating patients, emergency drainage holes (burr holes) or craniotomy is needed
32
Q

What is a concussion? How are these diagnosed? What is a contusion?

A
  • a concussion is a function (not structural) brain injury resulting in rapid onset of symptoms (headache, nausea, confusion, memory disturbances, loss of consciousness) and eventual spontaneous resolution (10-14 days later)
  • it is clinical diagnosis without any reliable tests/markers
  • a contusion is a surface bruise of the brain resulting from the brain hitting the skull
33
Q

What are some complications of a concussion?

A
  • impaired performance
  • cerebral edema (called “2nd impact syndrome”)
  • prolonged symptoms
  • depression
  • CTE (chronic traumatic encephalopathy: cumulative cognitive deficits due to repeated concussions)
34
Q

What is the most prevalent cause of neurological morbidity?

A
  • cerebrovascular disease! (via embolism, thrombosis, or rupture)
35
Q

What percentage of the cardiac output does the brain receive? What percentage of the body’s oxygen consumption is due to the brain?

A
  • brain receives 15% of cardiac output and is responsible for 20% of the body’s O2 consumption
36
Q

What is the leading cause of death in patients younger than 45 years of age?

A
  • trauma

- 50% of these cases involve the head

37
Q

When does cerebral vasodilation occur? What about vasoconstriction?

A
  • cerebral vasodilation (along with systemic constriction) results in increased blood flow to the brain and occurs in: acidosis, hypotension, and hypoxia
  • cerebral vasoconstriction occurs in: alkalosis and hypertension
38
Q

What drives the autoregulation of cerebral blood flow? Between what range of cerebral perfusion pressure (CPP) does autoregulation occur?

A
  • autoregulation is primarily driven by the pressure of CO2 (pO2 drives it in cases of severe hypoxia) this is why therapeutic hyperventilation helps lower ICP! the decrease in pCO2 decreases cerebral perfusion by vasoconstriction
  • CPP will increase as pCO2 increases until pCO2 exceeds 90 mmHg (normal is 40 mmHg) and then CPP plateaus off at this point
  • when CPP is between 50-150 mmHg, autoregulation occurs; outside of this range, this regulation is lost
  • (CPP = MAP - ICP) normal ICP = 0-10 mmHg
39
Q

Which clinical signs suggest a skull fracture has occurred?

A
  • subconjunctival bleeding, hemotympanum, CSF rhinorrhea, CSF otorrhea, Battle’s sign (bruising around the post-auricular surface), and raccoon eyes
40
Q

The Glasgow-Coma Scale scores range from 3 to 15 - which score classifies as a severe traumatic brain injury?

A
  • any score less than 9 suggests the trauma was very severe (these make up 10% of head injuries presenting to the ED)
  • a score between 9 and 13 suggests a moderate injury
  • a score of 14-15 suggests a mild injury (these make up 70-80% of head injuries presenting to the ED)
41
Q

Even if a patient has a GCS of 15, under what conditions should you still perform a CT scan?

A
  • if you suspect a skull fracture, if the patient is on anticoagulation therapy, if the patient is drunk, if the patient is elderly, and/or if the patient has any of the following: abnormal neurology, any L.O.C., vomiting twice or more, seizure, ongoing headaches, amnesia
42
Q

How can you tell the difference between an epidural hematoma, subdural hematoma, subarachnoid hemorrhage, and intracerebral hemorrhage?

A
  • EDH: the blood will NOT cross suture lines (b/c dura mater and bone are very tightly attached here); classic lens shaped lesion
  • SDH: the blood WILL cross suture lines, but will NOT enter the sulci (b/c arachnoid is blocking); classic crescent-shaped lesion
  • SAH: the blood WILL enter the sulci
  • intracerebral hemorrhage: blood will be past the meninges
43
Q

What is global central ischemia? What can cause this condition? How do patients present based on severity?

A
  • global central ischemia is a global version of ischemic stroke
  • it can be due to: global decreased perfusion (diffuse atherosclerosis), acute decrease in blood flow (shock), chronic hypoxia (anemia), or repeated episodes of hypoglycemia (as occurs with insulinomas)
  • mild: transient confusion; complete recovery
  • moderate: infarction of watershed areas and cortical necrosis
  • severe: diffuse necrosis; survival unlikely/vegetative stae
44
Q

Ischemic stroke can be due to thrombosis or embolism - what is a third potential cause? How can we tell all these apart (on autopsy)?

A
  • (embolism is most common cause)
  • lacunar stroke via hyaline arteriosclerosis (secondary to HTN, diabetes, etc.) of the small branches (most commonly affected are the lenticulostriate vessels); these result in small circular infarcts
  • a thrombotic stroke (usually at branch points) will result in pale infarcts
  • an embolic stroke (usually in MCA via thrombi from left heart) will result in hemorrhagic infarcts (because the embolus will get lysed and reperfusion injury will occur)
45
Q

What is an intracerebral hemorrhage? What do they result from? What is the most common site of an intracerebral hemorrhage?

A
  • bleeding into the brain parenchyma (AKA intraparenchymal hemorrhage or hypertensive hemorrhage)
  • results from ruptured Charcot-Bouchard microaneurysms (these form from unmanaged HTN)
  • most common site is in the basal ganglia (due to ruptured aneurysms in the lenticulostriate vessels)
46
Q

What is a major potential complication of hematomas and hemorrhages? What are the areas where this most commonly occurs?

A
  • herniation! (displacement of brain tissue due to a mass effect or raised ICP)
  • most common: subfalcine hernation (frontal lobe’s cingulate gyrus herniates into the falx cerebri and compresses the anterior cerebral artery)
  • tonsillar herniation (cerebellar tonsils herniate through the foramen magnum and compress the brainstem)
  • uncal herniation (uncus of temporal lobe herniates into the tentorium and compresses CN III, posterior cerebral artery, and brainstem’s vascular supply)
47
Q

How will a patient suffering from a stroke involving the middle cerebral artery present?

A
  • motor and sensory cortexes affected involve upper limb and face: contralateral paralysis of upper limb and face; contralateral loss of sensation in face, upper AND lower limbs
  • temporal lobe and frontal lobe affected: aphasia if in left (dominant) hemisphere
48
Q

How will a patient suffering from a stroke involving the anterior cerebral artery present?

A
  • motor and sensory cortexes affected involve lower limb: contralateral paralysis and contralateral loss of sensation of lower limb
49
Q

How will a patient suffering from a stroke involving the lenticulostriate artery?

A
  • striatum and internal capsule affected: contralateral hemiparesis/hemiplegia
  • (due to lacunar strokes, secondary to unmanaged HTN)
50
Q

How will a patient suffering from a stroke involving the anterior spinal artery present?

A
  • lateral corticospinal tract affected: contralateral hemiparesis
  • medial lemnisucs affected: contralateral loss of proprioception
  • (note that these strokes are usually bilateral)
51
Q

How will a patient suffering from a stroke involving the posterior inferior cerebellar artery present?

A
  • lateral medulla affected (nucleus ambiggus, vestibular nuclei, sympathetic fibers, etc.): dysphagia and hoarseness, vomiting, vertigo, nystagmus, decreased gag reflex, ipsilateral Horner’s syndrome
  • inferior cerebellar peduncle affected: ataxia
  • lateral spinothalamic tract affected: ipsilateral loss of pain and temperature of face
52
Q

How will a patient suffering from a stroke involving the anterior inferior cerebellar artery present?

A
  • lateral pons affected (facial nucleus, CN nuclei, vestibular nuclei, cochlear nuclei, sympathetic fibers, etc.): facial paralysis, vomiting, vertigo, nystagmus, loss of lacrimation and salivation and taste, ipsialteral Horner’s syndrome, ipsilateral loss of hearing, loss of pain and temp in face
  • middle and inferior cerebellar peduncles affected: ataxia
53
Q

How will a patient suffering from a stroke involving the posterior cerebral artery present?

A
  • occipital cortex/visual cortex affected: contralateral hemianopia w/ macular sparing
54
Q

How will a patient suffering from a stroke involving the basilar artery present?

A
  • pons, medulla, lower midbrain, corticospinal and corticobulbar tracts, etc. affected: “locked-in syndrome” (conscious and able to blink/some eye movement w/ quadriplegia and loss of facial, mouth, and tongue movements)
55
Q

How will a patient suffering from a stroke involving the anterior communicating artery present?

A
  • most common lesion here is an aneurysm, not a stroke

- cranial nerves impinged by aneurysm: visual field defects

56
Q

How will a patient suffering from a stroke involving the posterior communicating artery present?

A
  • most common lesion here is an aneurysm, not a stroke

- cranial nerve III palsy: pupil is dilated, eye is “down and out”, ptosis