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organ systems > First aid neuro - lesions/strokes/hemorrhage > Flashcards

First aid neuro - lesions/strokes/hemorrhage Flashcards

1
Q

Amygdala lesion

A

Kluver-Bucy Syndrome

  • hyperorality
  • hypersexuality
  • disinhibited behavior

assoc. HSV-1

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2
Q

Frontal lobe lesion

A

-disinhibition and deficits in concentration, orientation and judgement; may have reemergence of primitive reflexes

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3
Q

Right parietal-temporal cortex lesion

A
  • non dominant hemisphere normally

- spatial neglect syndrome (agnosia of contralateral side of the world)

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4
Q

Left parietal-temporal cortex lesion

A

-dominant hemisphere normally

Gerstmann syndrome:
agraphia
acaculia
finger agnosia
left right disorientation
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5
Q

Reticular activating system (midbrain)

A

Reduced levels of arousal and wakefullness - coma

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6
Q

Mammillary bodies lesion (bilateral)

A

Wernicke-Korsakoff syndrome:

  • confusion
  • opthalmoplegia, nystagmus
  • ataxia
  • memory loss
  • anterograde and retrograde amnesia
  • confabulation
  • personality changes

assoc. with thiamine B1 defiency excessive ETOH use, can be precipitatwd by giving glucose without B1

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7
Q

Cerebral hemisphere lesion

A
  • intention tremor, limb ataxia, and loss of balance
  • damage to the cerebellum results in ipsilateral deficits; fall toward side of lesion
  • hemispheres are lateraly located and afted lateral limbs
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8
Q

Cerebral vermis lesion

A

Truncal ataxia, dysarthia

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9
Q

STN lesion

A

contralateral hemibalismus

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10
Q

Bilateral hipocampus lesion

A

anterograde amnesia

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11
Q

PPRF lesion

A

eyes look away from the lesion

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12
Q

Front eye field lesion

A

Eyes look toward lesion

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13
Q

Central pontine myelenosis

A

-osmotic demyelination syndrome
massive axonal demyelnation in pontine white matter tracts secondary to osmotic forces and edema. Commonyl iatrogenicm caused by overly rapid correction of hyponatremia

can cause:
-acute paralysis, dysarthia, dysphagia, diplopia, loss of consciousness
“locked in syndrome”

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14
Q

Dysphagia

A

Difficulty with swallowing is the sensation that food is stuck in the throat

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15
Q

Dysarthia

A

motor inability to speak

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16
Q

aphasia

A

higher order inability to speak (language deficit)

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17
Q

Broca Aphasia

A
  • nonfluent aphasia with intact comprehension

- broca area inferior frontal gyrus of frontal love

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18
Q

Wernicke aphasia

A

Fluet aphasia with impaired comprehension and repetition.

-superiror temporal gyrus of temporal love

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19
Q

Global aphasia

A

nonfluet aphasia and impaired comprehesions, both broca and wernicke areas affected

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20
Q

Conduction aphasia

A
  • poor repetition but fluent speech
  • intact comprehension
  • can be caused by damage to left superior temporal love and or left supramarginal gyrus
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21
Q

Transcortical motor aphasia

A

-nonfluent aphasia with good comprehension and repetition

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22
Q

Transcortical sensory aphasia

A

poor comprehension with fluent speech and repetition

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23
Q

mixed transcortical -

A

nonfluent speech, poor comprehesion but good repetition

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24
Q

Medial medullary syndrome artery?

A

ASA

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25
Q

Lateral medullary syndrome (wallenberg) artery?

A

PICA

26
Q

Lateral pontine syndrome artery?

A

AICA

27
Q

Middle cerebral artery MCA stroke

A

lesion:
motor cortex: upper limb and face
-contralateral paralysis upper limb and face

Sensory cortex:upper limb and face
contralateral loss of sensation- upper and lower limbs and face

Temporal lobe wernickes
frontal lobe: broca
aphasia if dominant or hemineglect if lesions affects nondominant side

28
Q

Anterior cerebral artery ACA stroke

A

Lesion
motor cortex- lower limb
-contralateral paralysis of lower limb

sensory cortex: lower limb
contralateral loss of sensation in lower limb

29
Q

Lenticulostriate artery stroke

A

Lesion: striatum and internal capsule
symptoms: hemiparesis/hemipegia

common location of lacunar infacrts secondary to HTN

30
Q

Anterior spinal artery ASA stroke

A

areas affected:

  • lateral corticospinal tract
  • medial leminiscus
  • caudal medulla - hypoglossal nerve
  • contralateral hemiparesis-upper and lower limbs
  • decreased contralateral proprioception (ML)
  • ipsilateral hypoglossal dysfunction (lick your wounds)

Medial medullary syndrome - cause by infarct of paramedian branches of ASA and venrtebral arteries

31
Q

PICA stroke

A

area affected:
lateral medulla-vesitbular nuclei, lateral spinothalamic tract, spinal trigeminal nucleus, nucleus ambiguous, sympathetic fibers, inferior cerebellar peduncle

Vomiting, vertigo, nystagmus; decreased pain and temperature sensation from ipsilateral face and contralateral body, dysphagia, hoarseness, decreased GAG reflex, ipsilateral horner syndrome; ataxia, dysmetria

LATERAL MEDULLARY SYNDROME
-nucleus ambiguous effects are specific to PICA lesions

32
Q

AICA

A

areas affected:
lateral pons,-cranial nerve nuclei; vestibular nuclei, facial nucleus, spinal trigeminal nucleus, chclear nuclei, sympatheitc fibers

middle and infereior cerebral peduncles –> ataxia and dysmetra

vomiting, vertigo, nystagmus, paralysis of face, decreased lacrimination, salivation, decreased taste from 2/3 anterior tongue, decreased corneal reflex (facial nerve), Decreased pain and temperature on face, ipsilateral decreased in hearing and ipsilateral horner syndrome

Lateral Pontine syndrome

33
Q

Facial nucleus effets are specific to what lesions?

A

AICA

34
Q

Nucleus ambigous effects are specific to what lesions?

A

PICA

35
Q

PCA stroke

A

affect
occipital cortex and visual cortex

contralateral hemianopia with macular sparing

36
Q

Basilar artery stroke

A

affect the pons, medulla, lower midbrain, corticospinal and corticobulbur tracts, ocular cranial nerve nuclei, PPRF

-preserved consciousness and blinking, quadriplegia, loss of voluntary facial, mouth and tongue imovements

Locked in syndrome

37
Q

Acom aneurism

A
  • most common lesion in aneurysm
  • can lead to stroke
  • saccular (berry) aneurysm can impinge on CN

-lead to visual field defects

38
Q

Pcom aneurism

A

-common site of berry aneurysm
-can lead to CNIII palsy
down and out with ptosis and pupil dilation

39
Q

CNIII palsy

A

down and out with ptosis and pupil dilation

40
Q

Berry aneurism risk factors

A 
ADPKD
Ehlers danlos
marfans
advanced age
HTN
smoking
black race
41
Q

Berry aneurism rupture

A
  • most common site is junction of the AComm and ACA
  • rupture leads to subarachnoid hemorrhage (worst headache of life) or hemorrhagic stroke.
  • can cause bitemporal hemianopia via compression of optic chasm
42
Q

Charcot bouchard micoaneurysm

A

assoc with chronic HTN, affects small vessels (basal ganglia and thalamus)

43
Q

central post-stroke syndrom

A

neuropathic pain due to thalamic lesions
-intial sensation of numbness and tingling followed in weeks to months by allodynia (ordinary painless stimuli cayse pain) and dysaesthesia.
occurs in 10% of stroke patients

44
Q

Epidural hematoma

A
  • rupture of middle menigeal artery (branch of the maxilarry artery)
  • often secondary to fracture of temporal bone
  • lucid interval
  • rapid expansion under systempic arterial pressure can cause atranstentorial herniation –> CN III palsy

CT - Lens (biconvex)
hyperdense blood collection
Can cross the flax, tentorium

45
Q

the middle mengeal arter is a branch of what artery?

A

maxillary

46
Q

Subdural hematoma

A
  • Rupture of bridging veins
  • slow venous bleeding (less pressure = hematoma develops over time)
  • elderly, alcoholids, blunt trauma, SHAKEN BABY

CT: Crescent shaped hemorrhace that cross suture lines, may also see midline shift. CANNOT cross the falx , tentorium

47
Q

Subarachnoid hemorrhage

A

Rupture of an aneurysm (such as berry aneurism)

  • Rapid time course
  • WORST HEADACHE OF MY LIFE)
  • Bloody or yellow (xanthocromic) spinal tap
  • 2-3 days afterward risk of vasospasm due to blood breakdown (not visible on CT, treat with nimodipine) and rebleed
48
Q

Intraparenchymal hemorrhage (HTN)

A

most commonly caused by sytemic HTN
also seen with:
amyloid angiopathy, vasculitis, and neoplasm

typically occurs in basal ganglia and internal capsule (charcot-bouchard aneurysm of lenticulstirate vessels)

49
Q

Most vulneralbe areas to ischemia?

A

after 5 minutes of hypoxia irreversible damage hippocampus>neocortex>cerebellum>watershed areas

50
Q

stroke imaging

A

Bright on diffusioon weighted MRI in 3- 30 mins

dark abnormality on noncontrast CT within 12-24 hours

51
Q

hemorrhage imaging

A

CT

remember dont use tPA if you suspect a hemorrhage

52
Q

Stoke histo 12-48 hours

A

red neurons

53
Q

Stoke histo 24-72 hours

A

necrosis and neutrophils

54
Q

Stoke histo 3-5 days

A

macrophages

55
Q

Stoke histo 1-2 weeks

A

reactive gliosis (astrocytes) + vascular proliferation

56
Q

Stoke histo > 2 weeks

A

glial scar

57
Q

Ventricular system

A

lateral ventricle –> 3rd ventricle via the right and left interventricular foramina of monro
3rd ventricle to 4th ventricle via cerebral aqueduct of sylvius then 4th to subarachnoid space via foramine of luschka = lateral and foramen of magendie = medial

58
Q

Communication (non-obstructive)hydrocephalus

A

-decrease in CSF absorption by arachnoid granulations, which can lead to increased intracranial pressure, pappiladema and herniation

59
Q

Normal pressure hydrocephalus

a type of communicating

A

-does not result in increased subarchnoid space volume.
expansion of ventricles distort fibers of the corona radiate and leads to clinical triad of wet wobbly and wacky
urinary incontinence, ataxia and cognitive dysfunction

60
Q

Hydrocephalus ex vacu

a type of non communicating

A
  • appearence of increase CSF in atrophy (alzheimers, advanced HIV, Pick)
  • intracranial pressure normal, triad not seen
61
Q

Non-communicating hydrocephalus

A

-caused by structural blockage of CSF circulation within the ventricular system (stenosis of the aqueduct of sylvius)

organ systems (25 decks)

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