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Neuroanatomy and syndromes > Written Exam 2 > Flashcards

Written Exam 2 Flashcards

1
Q

What are the 3 major cerebral arteries?

From what arteries do they branch?

A
  1. Anterior cerebral artery (ACA) [from internal carotid artery]
  2. Middle cerebral artery (MCA) [from internal carotid artery]
  3. Posterior cerebral arteries (PCA) [branch of the basilar artery]
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2
Q

Which major cerebral artery/arteries supplies each of the following brain regions/structures:

Lateral frontal cortex
Medial frontal cortex

Lateral temporal cortex
Medial temporal cortex
Inferior temporal cortex

Lateral parietal cortex
Medial parietal cortex

Basal ganglia 
Hippocampal formation (medial temporal lobe)

Thalamus

Occipital cortex

A

Lateral frontal cortex – MCA
Medial frontal cortex – ACA

Lateral temporal cortex – MCA
Medial temporal cortex – MCA
Inferior temporal cortex - PCA

Lateral parietal cortex – MCA
Medial parietal cortex – PCA

Basal ganglia – MCA
Hippocampal formation (medial temporal lobe) – Anterior Choroidal Artery

Thalamus – PCA

Occipital cortex - PCA

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3
Q

What major regions do the subdivisions of the MCA supply?

A
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4
Q

What are the 3 major cerebellar arteries?

A
  1. Superior Cerebellar Artery (SCA)
  2. Anterior Inferior Cerebellar Artery (AICA)
  3. Posterior Inferior Cerebellar Artery (PICA)
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5
Q

Diagram and label the arteries of the circle of Willis:

A
  • ACA
  • ACom (connects ACA and MCA)
  • Internal carotid artery
  • MCA
  • PCom – connects anterior and posterior circulation systems
  • Anterior choroidal artery
  • PCA
  • Superior cerebellar artery
  • Basilar artery
  • Anterior inferior cerebellar arteries (AICA)
  • Posterior inferior cerebellar artery (PICA)
  • Vertebral artery
  • Anterior spinal artery
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6
Q

Cerebrovascular accident

A

Stroke is typically defined as the abrupt onset of a focal neurologic deficit that is consistent with a vascular distribution and lasts more than 24 hours with or without positive imaging results or less than 24 hours with a positive imaging result.

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7
Q

• Ischemia

A

Tissue ischemia occurs when there is insufficient oxygen supply to an organ, usually resulting from an occlusion of an artery that normally provides blood supply to that organ, frequently caused by atherosclerosis.

  • Ischemic = blockage (blood clot, plaque; dry; ~85%)
  • Ischemic stroke results in two zones of injury known as the core and the penumbra.
  • Ischemic stroke results from an obstruction of blood flow by thrombosis or embolism to an artery supplying the brain and can be classified by their underlying cause as: Large Artery Atherosclerotic, Lacunar, Cardioembolic, Cryptogenic or Other.
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8
Q

Infarction

A
  • Ischemia causes infarct (stroke)

* Area of necrotic tissue resulting from obstruction of local blood supply or ischemia (e.g., by thrombus or embolus)

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9
Q

Transient Ischemic Attack

A

A transient ischemic attack (TIA) is a brief episode of neurologic dysfunction caused by focal brain or retinal ischemia, with clinical symptoms typically lasting less than one hour but as long as 24 hours and without evidence of tissue death (negative neuroimaging).

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10
Q

Silent Stroke

A

Silent stroke refers to the presence of vascular-related brain injury seen on neuroimaging without associated clinical symptoms.

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11
Q

Atherosclerosis

A

Atherosclerosis is the progressive pathological process of buildup of plaque inside the blood vessels, resulting in blockage of blood flow through the vessels.

The plaque that causes atherosclerosis is com- prised of fatty substances, cholesterol, cells,
calcium, and fibrin, a stringy material found nor- mally in the blood to help clot the blood.

The plaque formation process stimulates the cells of the artery wall to produce substances that then accumulate in the vessel wall.

Fat builds up within these cells and around them, and they form con- nective tissue and calcium.

The artery wall thickens, the artery’s diameter is reduced, and blood flow and oxygen delivery are decreased.

Plaques can rupture or crack open, causing the sudden formation of a blood clot (thrombosis).

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12
Q

Thrombosis & thrombotic infarct

A

Thrombosis: Thrombosis is the process by which a blood clot, or thrombus, is formed.

Thrombotic infarct: ???

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13
Q

embolism & embolic infarct

A

A cerebral embolism is a blood clot (thrombus) that starts from the heart or blood vessel where the clot
originates and stops in an artery that leads to or rests within the brain. The result is occlusion of the vessel and obstruction of the flow of oxygen and blood to the brain tissue supplied by that artery.

cerebral embolism = cerebral infarct

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14
Q

What are 3 demographic factors that increase the risk for stroke?

A
  • Race/ethnicity
  • Age – relative risk doubles every decade after 55
  • Geography
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15
Q

What are 5 medical factors increase the risk for stroke?

A
  1. hypertension
  2. diabetes
  3. atherosclerosis
  4. heart disease
  5. smoking
    (6. OSA)
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16
Q

What is the most important risk factor for ischemic stroke?

A

hypertension

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17
Q

What is the most important risk factor for hemorrhagic stroke?

A

hypertension

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18
Q

What medical/vascular conditions can cause intracerebral hemorrhages? Be able to describe what these conditions are.

A

Chronic Hypertension

Vascular malformation

Arterial aneurysm

Cerebral Amyloid Angiopathy

Cavernous malformations

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19
Q

What are the types of ischemic strokes?

Ischemic stroke is the most common type of stroke, accounting for about 80% of all events. It is caused by a blockage, usually as a consequence of atherosclerosis, of a blood vessel that normally provides blood supply to the brain.

A
  1. Embolic strokes
    a. Clot forms somewhere else in body and travels through the blood vessel to your brain
  2. Thrombotic strokes
    a. Caused by blood clot that forms in an artery that supplies blood to the brain

The lack of oxygen in the brain tissue that results from the blockage causes either reversible injury (ischemia), if it is not prolonged or severe, or death or irreversible damage of the tissue (infarction) if the interruption of blood supply is prolonged and severe.

The arterial blockage may derive primarily at the site of occlusion, in which case it is called a “thrombus.” Alternatively, it may arise elsewhere in the vascular system, usually in the heart, and leave that primary site, flow through the vessels until it encounters a narrow lumen, thereby closing off that area; in this case, it is called an “embolism.”

About 60% of all strokes are thrombotic and 15–20% are embolic in origin. Both cause neurological deficits, which tend to be localizing. However, there are some differences; symptoms of thrombotic strokes tend to be slower to develop, while the presentation of embolic strokes tends to be more sudden and dramatic, including seizure, headache, syncope, and
presentations with multiple simultaneous dispa- rate neurological findings. Embolic strokes tend to occur in the context of known cardiac disease. Treatment depends on the specific cause, but gen- erally relies on reducing the vascular obstruction and preventing future events. Rehabilitation and long-term care of the deficits are identical for each type of stroke.

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20
Q

Describe the motor, cognitive, and sensory impairments that commonly result from strokes involving each of the major cerebral arteries.

ACA

A

Left ACA
a. Right leg weakness of the upper motor neuron type and right leg cortical-type sensory loss. Grasp reflex, executive function deficits, and transcortical motor aphasia can also be seen. Larger infarcts may cause right hemiplegia.

Right ACA
a. Left leg weakness of the upper motor neuron type and left leg cortical-type sensory loss. Grasp reflex, executive function deficits, and left hemineglect can also be seen. Larger infarcts may cause left hemiplegia.

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21
Q

Describe the motor, cognitive, and sensory impairments that commonly result from strokes involving each of the major cerebral arteries.

MCA

A
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22
Q

Describe the motor, cognitive, and sensory impairments that commonly result from strokes involving each of the major cerebral arteries.

PCA

A

PCA

  • contralateral homonymous hemianopia
  • contralateral hemisensory loss
  • contralateral hemiparesis
  • LEFT: alexia without agraphia (extension to the splenium of the corpus callosum)
  • LEFT: transcortical sensory aphasia
  • LEFT: Memory deficits (especially verbal) if lesion extends to left medial temporal lobe, esp. hippocampus.
  • RIGHT: Memory deficits (especially spatial) if lesion extends to right medial temporal lobe, esp. the hippocampus.
23
Q

What is the most common psychiatric consequence of stroke?

A

depression

24
Q

What type(s) of neuroimaging (including types of sequences) is/are best for detecting ischemic stroke in the acute stage?

After the acute stage?

A
25
Q

What type(s) of neuroimaging is/are best for detecting acute hemorrhagic stroke?

A
26
Q

What type(s) of neuroimaging is/are best for detecting abnormal vascular formations?

A
27
Q

What is the medical treatment for acute ischemic stroke?

When must this treatment be administered in order to be effective?

A
28
Q

What is a treatment for acute hemorrhagic stroke?

A
29
Q

What are the diagnostic criteria for mild/major vascular neurocognitive disorder?

What cognitive domains are most commonly impaired?

A
30
Q

Alcohol Toxicity in Chronic Heavy Alcohol Use

A
31
Q

Chronic heavy alcohol use = 4 or more drinks every day. When determining whether someone has been drinking heavily, keep in mind that people typically under-report the amount consumed.

A
32
Q

• Brain changes associated with chronic heavy alcohol use include:

A
  1. Atrophy of cerebral cortex
  2. Reduced white matter volume
  3. Enlarged ventricles
  4. Atrophy of subcortical structures (e.g, hypothalamus, cerebellum)
33
Q

Risk factors that contribute to cognitive dysfunction in alcoholics:

  1. Aging
  2. Race (being Native American)
  3. Sex differences
  4. Family history
  5. Diet (malnutrition)
A
  1. Aging
  2. Race (being Native American)
  3. Sex differences
  4. Family history
  5. Diet (malnutrition)
34
Q

• Neuro-Pathophysiology in chronic heavy alcohol consumers

A

o Both the cerebrum and the cerebellum are vulnerable to damage and dysfunction associated with chronic heavy alcohol use.
o White matter atrophy is more prominent than gray matter atrophy.
o Gray matter atrophy especially involves the dorsolateral prefrontal cortex.
o Alcohol impacts hippocampal functioning.

35
Q

Sudden withdrawal in long-term very heavy drinkers can lead to xxx and xxx

A

Sudden withdrawal in long-term very heavy drinkers can lead to seizures and delirium tremens.

36
Q

Delirium tremens – an acute disorder in which the most prominent symptoms are xxx, xxx, and xxx that can lead to death from exhaustion.

A

nausea
tremulousness
insomnia

37
Q

Sensory and motor function impacts in chronic heavy alcohol consumers

A

o Abnormal smooth pursuit eye movements and impaired visual scanning
o Ataxic gait
o Intention tremor

38
Q

Cognitive impacts in chronic heavy alcohol consumers

o Research findings of xxx impairment are inconsistent in the literature. Some found impaired xxx (specifically, the use of xxx strategies), others found impaired xxx, and some chronic alcoholics had xxx memory impairment at all.

o When xxx is impaired it can be seen in both xxx and xxx memory tasks.

o xxx memory impairments

o xxx is the most xxx and most xxx cognitive impairment in chronic heavy alcohol consumers.

o xxx age predicts xxx cognitive improvement with sustained abstinence.

o Alcoholic dementia (i.e., major alcohol-induced NCD) features widespread cognitive deterioration xxx the profound amnesia of Korsakoff’s syndrome .

A

Cognitive impacts in chronic heavy alcohol consumers
o Research findings of memory impairment are inconsistent in the literature. Some found impaired encoding (specifically, the use of encoding strategies), others found impaired retrieval, and some chronic alcoholics had no memory impairment at all.
o When memory is impaired it can be seen in both verbal and visuospatial memory tasks.
o Prospective memory impairments
o Executive dysfunction is the most common and most severe cognitive impairment in chronic heavy alcohol consumers.
o Younger age predicts more cognitive improvement with sustained abstinence.
o Alcoholic dementia (i.e., major alcohol-induced NCD) features widespread cognitive deterioration without the profound amnesia of Korsakoff’s syndrome .

39
Q

Wernicke’s encephalopathy is the result of

A

thiamine deficiency

40
Q 
Wernicke’s encephalopathy involves:
o	Involuntary rapid eye movements (nystagmus)
o	Gaze paresis 
o	Ataxia 
o	Confusion 
o	Amnesia
A 
o	Involuntary rapid eye movements (nystagmus)
o	Gaze paresis 
o	Ataxia 
o	Confusion 
o	Amnesia
41
Q

xxx is the (potential) long term outcome of an episode of Wernicke’s encephalopathy.

A

Korsakoff’s syndrome

42
Q

Neuro-Pathophysiology in Korsakoff’s syndrome
o xxx lesions in specific xxx nuclei and in the xxx .
o Loss of xxx matter in the xxx cortex and in the xxx lobes.
o xxx are likely associated with xxx within the xxx frontal lobes and possibly dysfunction in the xxx. Of note, confabulation occurs in other conditions that damage these regions, such as an xxx xxx

A

o Hemorrhagic lesions in specific thalamic nuclei and in the mammillary bodies .
o Loss of gray matter in the orbitofrontal cortex and in the temporal lobes.
o Confabulations are likely associated with hypometabolism within the orbital-medial frontal lobes and possibly dysfunction in the basal forebrain. Of note, confabulation occurs in other conditions that damage these regions, such as an anterior communicating artery hemorrhage.

43
Q

Cognitive impacts in Korsakoff’s syndrome

A

o Slow perceptual processing speed
o Dysexecutive syndrome
o Apathetic syndrome / inertia / emotionally bland
o Both anterograde and retrograde memory impairments
- Anterograde memory impairment results from impaired encoding.

  • Retrograde memory impairment results from poorly organized retrieval of remote information.
  • Frequent intrusion errors, particularly involving erroneous retrieval of information from the wrong stimulus set (i.e., poor source memory).
  • Poor retrieval memory for the order in which events took place in time.
  • Confabulation involves disorganized retrieval of recent and remote autobiographical memories combined with an inability to monitor for errors in what they’re saying. Essentially, confabulation encompasses the previous two points (i.e., retrieval from the wrong set and from the wrong time).
44
Q

HYPOXIA OF THE CENTRAL NERVOUSSYSTEM

A
45
Q

Identify the conditions mentioned in the Introduction that can cause hypoxic/anoxic injury to the brain:

A
  1. asthma
  2. cardiac or respiratory arrest
  3. cardiac disease or surgery
  4. carbon monoxide poisoning
  5. attempted hanging
  6. complications of anesthesia
  7. near downing
  8. obstructive sleep apnea (OSA)
  9. chronic obstructive pulmonary disease (COPD)
  10. acute respiratory distress syndrome
46
Q

Know the difference between ischemia and anoxia

A
  • Ischemia =insufficient blood supply to the brain or other organs (i.e., cardiac arrest) due to interruption or reduction of blood delivery
  • Anoxia = the absence or near complete absence of oxygen in the arterial blood supply to an organ or tissue
  • Hypoxia involves less oxygen reduction than anoxia and may go on for a longer duration before damage is done.
47
Q

Brain structures most vulnerable to anoxic/hypoxic injury:

A 
Brain structures most vulnerable to anoxic/hypoxic injury - NHB CPF T
•	Neocortex
•	Hippocampus
•	Basal ganglia
•	Cerebellar Purkinje cells
•	Primary visual cortex
•	Frontal regions
•	Thalamus

The above regions are vulnerable due to their relatively high dependence on oxygen.

48
Q

Watershed zones are vulnerable to anoxic injury due to the relatively limited arterial supply.

A
49
Q

Chronic Hypertension

A

Hypertension is the single most important risk factor for both hemorrhagic and ischemic stroke, with approximately 77% of individuals presenting with first stroke having blood pressures higher than 140/90 and about 50% having a history of hypertension.

Blood pressure ordinarily increases with age.

Elevation of blood pressure above standard norms for age occurs in approximately a third of the general adult population and prevalence increases with age.

High blood pressure places stress on blood vessel walls and subsequent morphologic changes result in cerebrovascular remodeling, impaired vasodilation and autoregulation, amyloid angiopathy, the accumulation of atherosclerotic plaque, white matter changes, and cognitive changes ranging from mild cognitive impairment to dementia.

50
Q

Vascular malformation

A

An arteriovenous malformation (AVM) is a tangle of blood vessels that form an abnormal connection between arter- ies and veins without an intervening capillary network

51
Q

Arterial aneurysm

A

The most common cause of nontraumatic subarachnoid hemorrhage (SAH) is aneurysmal rupture.

An aneurysm is a saccular outpouching of a blood vessel at a site of local weakness in the elastic membrane.

There are three major types of aneurysm, the most common of which is round in shape and known as a berry aneurysm.

Saccular aneurysms tend to form at the bifurcation or branching of a vessel, and the majority develop within the anterior circulation at the ACom (30%) though other common sites include the PCom (25%), MCA (20%), and the vertebrobasilar apex (15%).

52
Q

Cerebral Amyloid Angiopathy

A

Cerebral amyloid angiopathy (CAA) refers to the deposition of the protein beta amyloid in small and midsized blood vessels of the brain and leptomenginges, weakening the vessel walls and making them vulnerable to rupture.

CAA is an important cause of both large hemorrhages and microbleeds, typically in the cortex.

The inci- dence of CAA increases with age and is relatively uncommon before 60 years of age.

53
Q

Cavernous malformations

A

Cavernous malformations consist of a large vascular lumen with collagenous walls lined with a layer of endothelial cells and may vary in size from 2 mm to several centimeters.

These vascular anomalies are typically sporadic though there are familial occurrences, particularly among indi- viduals of Mexican descent.

In contrast to AVMs, cavernous malformations affect veins with trivial arterial connections.

The majority of cavernous malformations are located in the supratentorial white matter.

About a quarter of cases occur infratentorially, most often in the pons, followed by cerebellum, midbrain, and medulla.

Neuroanatomy and syndromes (2 decks)

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