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3P: Neuro > Infarct Syndromes > Flashcards

Infarct Syndromes Flashcards

1
Q

Atrial fibrillation

A
  • clot formation risk due to combination of 1) brief stationary pool of blood in atrium 2) tissue damage in atrium can activate clotting cascade
  • newly formed volt travels via common carotid, up internal carotid, most likely up MCA. Other common scenarios: in ophthalmic artery, ACA
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2
Q

Vascular disease assocaited wtih stroke

A
  • stenosis: reduced cerebral blood flow to suboptimal levels
  • atherosclerosis: plaque breaks off, forms embolism, or emboli shower
  • artery dissection: incision in lumen wall, creates flap that can occlude
  • arteries: inflamamtory damage within artery wall, triggers clot formation
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3
Q

ACA supplies

A

Rostral parts of corpus callosum

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4
Q

PCA supplies

A

Ipsilateral part of splenium, branches from circle of Willis supply diencephalon

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5
Q

MCA supplies

A

Part of the basal ganglia and internal capsule
Inferior division supplies the optic radiations
Superior division supplies the corona radiata, optic radiations

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6
Q

ACA territory defects

A
  • Visual system: full VF, potential deficits in spatial/motion/depth perception
  • oculomotor system: FEF spared, visual system guidance of potentially impaired
  • somatosensory: loss of sensation in lower extremity
  • motor strength: weakness in lower extremity, deep tendon reflexes
  • incontinence: possible, but unilateral damage spares some functional control
  • executive function: cognitive deficits, possible emotional/behavioral disturbances
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7
Q

MCA

A

Has superior and inferior divisions

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8
Q

ACA territory of cortical regions

A 
Primary visual cortex (medial aspect)
Visual association cortex 
Primary somatosensory cortex 
Primary motor cortex 
Cortical micturition center 
Supplementary motor area 
Prefrontal cortex
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9
Q

Visual system problems if there is a ACA lesion

A

Full visual fields, potential deficits in spatial/motion/depth perception

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10
Q

Deficits in oculomotor system with an ACA infarct

A

FEF spared, visual system guidance of potentially impaired

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11
Q

Somatosensory deficits with an ACA infarct

A

Loss of sensation in lower extremity

-homunculus shows that the lower extremities are in the medial aspect of the gyri

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12
Q

Motor strength deficits with an ACA infarct

A

Weakness in lower extremity, reflexes still in tact

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13
Q

Incontinence with an ACA infarct

A

Possible, but usually unilateral damage spares from functional control

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14
Q

Executive function and ACA infarct

A

Cognitive deficits, possible emotional/behavioral disturbance

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15
Q

MCA superior cortical territory

A 
Brocca
Somatosensory cortex 
Motor cortex 
FEF
Premotor cortex 
Supplemental motor cortex 
Prefrontal cortex
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16
Q

Visual system deficits in a MCA superior division infarct

A

FEF: cannot track to the opposite side of the lesion. (Left FEF will not allow tracking to the right). VOR will work still because it is a reflex and does not need the UMN that are being affected.

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17
Q

Motor strength and MCA superior division infarct

A

FATL (face, arms, trunk, limbs)

In descending order, the above will be weak

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18
Q

Language problems and MCA superior divion infarct

A

Will affect brocca.
-problem with language output, can comprehend language, you just cannot get out what you are saying. Cannot write words eithr

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19
Q

Executive function and MCA superior division

A

Problem due to prefrontal cortex

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20
Q

MCA inferior division cortical territory

A

Wernickes
Auditory
Object visual pathway (ventral)
Small lateral part of visual cortex

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21
Q

Visual system deficits in a MCA inferior infarct

A

Damage visual association cortex. Object and spatial system. Should not have VF loss because the PCA is the main blood supply to the visual cortex

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22
Q

Somatosensory and motor deficits in an MCA inferior infarct

A

None really, they are mainly by the superior division and the ACA

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23
Q

Language deficits in an inferior MCA infarct

A

Lack of comprehension of language, any form of language. Output will be intact

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24
Q

PCA cortical territory

A

Object visual system
Visual cortex
Hippocampus (memory)

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25
Q

Damage to the PCA: visual system

A

Left PCA damage

  • right hemifield visual loss in the periphery. Lateral surface is saved by MCA and could save the central vision
  • hemionopia with mac sparing
26
Q

Damage to PCA: hippocampus

A

Memory loss

27
Q

Blood supply to the neuro-ophthalmic pathway

A

Course of ICA entry into the middle cranial fossa, giving rise to the ophthalmic artery, central retinal artery, and ciliary arteries

28
Q

What is the blood supply to the optic tract

A

Anterior choroidal artery

29
Q

Artery that supplies the LGN

A

Thalamogeniculate arteries
-branch of the PCA

PCA damage can take out the LGN potentially and it could take out central vision
-hemionopia without macular sparing

30
Q

Anteiror ischemic optic neuropathy (AION)

A

-ischemia of anteiror optic nerve (portion in the orbit) is a common cause of sudden vision loss, especially >50 years old. (Intracranial portion of optic nerve, chiasm, and optic tract are much less vulnerable to ischemia due to rich arterial supply from the circle of Willis

31
Q

Blood supply to the anterior optic nerve (part in the orbit)

A

Short ciliary arteries, derived from the ophthalmic artery

32
Q

Arteritis AION

A

In temporal arteritis, inflammatory process occluder arteries, treatable with glucocorticoids

33
Q

Other etiologies of AION

A

Typical risk factors for occlusion: atherosclerosis, HTN, Diabetes, smoking. Can also result from nocturnal hypotension with patient noticing vision loss on waking

34
Q

Presentation of AION

A

Painless, visual field loss may be total, sector, or scotoma

35
Q

Ophthalmic exam for AION

A

Reduced CD ratio

36
Q

Ischemic damage to the optic tract or LGN/thalamus

A
  • ischemic damage to optic tracts is rare, due to many branches from the anterior chorooidal artery
  • thalamus, and thus LGN, more vulnerable to ischemic damage
37
Q

Sensory effects of unilateral thalamic damage

A

Left VPL and VPM damage=right face and right body deficit

38
Q

Visual deficits of unilateral thalamic damage

A

Left LGN damage=right homonymous hemianopsia

39
Q

Motor deficits and unilateral thalamic damage

A

Left VA/VL damage-impairments in motor coordination and fine tuning
-disruption to the left side of the body

40
Q

Vessles that can damage the internal capsule if they are damaged

A

Lenticulostriate arteries and anterior choroidal artery

41
Q

Internal capsule infarcts

A
  • lesion: right internal capsule or complete unilateral damage to right corticospinal tracts in brainstem, i.e. right cerebral peduncle, right basically pons, right pyramid, left lateral corticospinal tract
  • hemiplegic gait: pateitn compensates for weakness in leg by using trunk postural movements to passively swing the affected leg around to a forward postion
  • additional signs: lower face weakness ipsilateral to the side showing hemiplegia, slight head deviation due to sternocleidomastoid weakness
42
Q

Midbrain vasculature

A

Supply by branches of PCA and quadrigeminal

43
Q

Pons blood supply

A

Basically artery ascends along midline. Branches that curve around pons and then penetrate pons: medial vs lateral terrritoies

44
Q

Medulla blood supply

A

ASA, vertebral artery, and PICA. Supply medial;. Intermediate, and lateral territories

45
Q

Medial zone blood supply of medulla

A

anterior spinal artery

46
Q

Middle zone of medial blood supply

A

Vertebral artery

47
Q

Lateral zone of medulla supplied by

A

Posterior inferior cerebellar artery

48
Q

Anterior spinal artery infarct of the medulla

A

-corticopsinal damage: right pyramid damage. Contralateral sided weakness
-medial lemniscus damage: fine touch from the body on the contralateral side
Right hypoglossal nucleus/nerve damage: tongue protrusion toward the side of the damage
-MLF damage: vestibular information to control posture

49
Q

Wallenberg syndrome

A

PICA infarct in the medulla

  • hypothalamic projections affected: miosis
  • vestibular nuclei damage: slow eye movement to the side of the damage and a fast phase to the opposite side of the damage.
  • anterolateral/spinothalamic tract damage: pain and temp lost on contralateral side
  • spinal trigmeinal tract/nucleus damage:pain and temp on the ipsilateral face, have not crossed yet
  • peduncle damage: vestibular and prorioceptive information getting into the cerebellum. Motor coordination problems ipsilateral
50
Q

Medial pontine syndrome

A

Pretty much the same as the medulla

Abducens VI nerve

  • not nucleus damage, just a nerve, so its a palsy
  • looking left: right eye can look left, but the left eye cannot look left

Weakness and somatosensory problems

51
Q

If rostral pons has lateral infarct

A

Right anteiror/ventral trigeminothalamic tract: loss of somatosensation from the contralateral face

52
Q

If mid-level pons has lateral infarct

A
  • right trigeminal main sensory nucleus (V): loss of fine touch on right face
  • right trigmeminal motor nucleus (V): right paresis/paralysis of mastication muscles
53
Q

Ventral zone of the migraine blood supply

A

Medial branches of PCA

54
Q

Lateral zone blood supply of the midbrain

A

Quadrigeminal artery (Off PCA)

55
Q

Dorsal zone blood supply to the midbrain

A

Branches from SCA

56
Q

Webers syndrome

A

midbrain infarct:If occurred on paetitns left

  • left CNIII nerve: ipsilateral CN3 palsy, ptosis, failure of direct/consensual pupillary constriction in left eye. Sometimes parasympathetic fibers are spared (more medial in midbrain than CN3 fibers)
  • left crus cerebri (Cerebral peduncle): right hemifield paralysis/paresis of extremities and UMN signs for CN 4/6/7/9/10/12 (for CN 11: unilateral weakness, side os variabile)
57
Q

Claude’s syndrome

A

Midbrain infarct: if on patients left

  • left CN3: ipsilateral CN3 palsy, ptosis, failure of direct/consensual pupillary constriction in left eye. Sometimes parasympathetic fibers are spared (more medial in midbrain than CN3 fibers)
  • left red nucleus: possibly ataxia for right limbs: as if damage to right lateral cerebellar cortex, which projects on to left thalamus and left motor neocortex, controlling right limbs

No weakness

58
Q

Superior cerebellar artery

A

Superior surface

Superior cerebellar peduncle

59
Q

Anterior inferior cerebellar artery

A

Lateral (anteiror) aspect of inferior surface, middle cerebellar peduncle

60
Q

Posterior inferior cerebellar artery

A

Medial (posterior) aspects of inferior surface, inferior cerebellar peduncle

61
Q

Oculomotor system deficits in cerebellar infarct syndromes

A

Smoothness of smooth pursuits disrupted, accuracy of saccades impaired, nystagmus

3P: Neuro (11 decks)

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