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neurology > NCC content > Flashcards

NCC content Flashcards

1
Q

what is caput succedaneum?

A

accumulation of serum above the periosteum

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2
Q

what can a caput be confused with?

A

subgaleal hemorrhage

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3
Q

what is a cephalohematoma?

A

accumulation beneath the periosteum

-not usually present right away at birth, but appears within 24 hours

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4
Q

how long can it take for a cephalohematoma to heal?

A

3 months

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5
Q

what other complications are associated with cephalohematoma?

A
  • skull fracture
  • hyperbili
  • mild anemia
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6
Q

what is a subgaleal hemorrhage?

A
  • extracranial bleed

- bleeding into the subaponeurotic space

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7
Q

what type of instrumentation is associated with a subgaleal hemorrhage?

A

vacuum-assisted delivery

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8
Q

what is a subarachnoid hemorrhage?

A

-intracranial hemorrhage (most common)
bleeding into the subarachnoid space from ruptured vessels
-relatively benign and often asymptomatic

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9
Q

presentation of subarachnoid hemorrhage

A
  • transient seizure activity on day 2-3

- abnormal neuro exam

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10
Q

prognosis for subarachnoid hemorrhage

A

generally good unless a massive hemorrhage develops

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11
Q

what is a subdural hemorrhage?

A
  • intracranial hemorrhage

- hemorrhage between the dura and the arachnoid

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12
Q

presentation of subdural hemorrhage?

A
  • presents within first 12 to 72 hours
  • severity ranges from asymptomatic lesions to massive hemorrhage
  • seizures and neurologic changes
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13
Q

prognosis with subdural hemorrhage

A
  • depends one extent and severity

- ranges from complete recovery to rapid deterioration and death

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14
Q

symptoms of facial nerve palsy

A
  • drooping mouth
  • perpetually open eye
  • ineffective suck and swallowing problems
  • persistant drooling
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15
Q

nerves effected in Erb’s palsy

A

C5 and C6

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16
Q

nerves effected in Klumpke’s palsy

A

C7 to T1

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17
Q

brachial plexus injury prognosis

A
  • full spontaneous recovery if some improvement within 2 weeks
  • partial recovery if initial improvement is delayed until 4 to 6 weeks
  • significant permanent deficit if no improvement by 3 months
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18
Q

what is scaphocephaly?

A

premature closer of the sagittal sutures

elongates in the occipitofrontal diameter

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19
Q

what is brachycephaly?

A

premature closure of the coronal sutures

overgrowth of the vertex and lateral aspects of the head

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20
Q

what is spina bifida occulta?

A
  • a defect in only the vertebral arch

- usually asymptomatic

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21
Q

what is a meningocele? (spina bifida cystica)

A
  • sac contains meninges
  • spinal cord is in normal position and doesn’t protrude
  • dermal covering is often present
22
Q

what is a myelomeningocele? (spina bifida cystica)

A
  • sac contains meninges and neural tissue

- functional abnormalities are dependent on the level of the defect

23
Q

what is an arnold-chiari malformation?

A
  • displacement of the medulla oblongata, the fourth ventricle and some of the cerebellum into the cervical canal
  • CSF flow is impaired
24
Q

what is rachischisis?

A
  • open spinal cord; failure of the neural folds to fuse

- often associated with anencephaly

25
Q

what is anencephaly?

A

failure of the rostral neuropore to close

  • missing forebrain, remainder of the brain is degenerative
  • spontaneous/pain induced movements; intact reflexes
26
Q

anencephaly pregnancy

A
  • increased alpha fetoprotein
  • polyhydramnios
  • postterm delivery
27
Q

what is hydranencephaly?

A
  • complete or nearly complete absence of the cerebral hemispheres
  • intact brain stem
28
Q

etiology of hydranencephaly

A
  • severe hydrocephaly
  • inutero infection
  • vascular occlusion
29
Q

clinical manifestations of hydranencephay

A

may appear normal at birth

  • irritability/hyper/hypotonia
  • intact reflexes
  • usually die early in infancy
30
Q

what causes holoprosencephaly?

A

failure of the prosencephalon (forebrain) to cleave to the telencephalon and diencephalon

31
Q

why is pachygyria?

A

-few broad gyro and shallow sulci

32
Q

define hydrocephaly

A

imbalance between CSF production and absorption from excess formation of CSF, decreased absorption of CSF or obstruction of flow

33
Q

define communicating hydrocephalus

A

obstruction occurs after CSF exits the ventricles

34
Q

define noncommunicating hydrocephalus

A

obstruction occurs along the passages connecting the ventricles

35
Q

when do most IVH occur?

A

50% by 24 hours
90% by 72 hours
almost 100% by 1 week

36
Q

describe the germinal matrix

A
  • beneath the ventricular wall
  • produces glial cells and neurons
  • primitive and highly vascular
  • most common area of origination for IVH
37
Q

what happens with bleeding into the germinal matrix?

A
  • hematoma forms

- blood is released into the ventricular system if the hematoma ruptures

38
Q

causes of IVH

A
  • fluctuating cerebral blood flow
  • arterial hypotension
  • increased venous pressure impedes cerebral venous return
  • excess fibrinolytic activity
  • platelet and coagulation disturbances
39
Q

describe posthemorrhagic hydrocephalus

A

usually with grade III/IV

  • blood clot obstruction
  • obstructive inflammation and scarring (inhibits absorption)
40
Q

treatment of posthemorrhagic hydrocephalus

A

-maintain normal ICP
-prevent compression of the periventricular white matter
-sustain cerebral perfusion
(serial LPs, VP shunts)
-50% resolve with no treatment

41
Q

about PVL

A
  • occurs only in premature infants
  • 27 to 30 weeks have the highest incidence
  • often associated with IVH
  • may be an infectious component
  • highest incidence PROM + chorio
42
Q

what is PVL

A
  • ischemic lesion
  • periventricular white matter necrosis
  • small cysts in white matter (where brain death has occurred)
43
Q

best way to diagnose PVL

A

-MRI

ultrasound only detects 40-60%

44
Q

prognosis for PVL

A
  • majority will have cerebral palsy, especially of the lower limbs
  • developmental delays
45
Q

effects of HIE

A
  • conversion to anaerobic metabolism
  • intracellular pump function failure: accumulation of Na, Ca, and H20 in brain cells, causing cellular death
  • accumulation of fatty acids and free radicals
  • excess release of neurotoxic excitatory neurotransmitters
  • cell apoptosis
46
Q

early phase of HIE

A

body is trying to compensate

  • decreased brain temperature
  • local release of GABA
  • temporarily decrease cerebral oxygen demand and limit impact
47
Q

latent phase of HIE

A

when intervention may be effective

48
Q

secondary phase of injury

A

-apoptosis: programmed cell death

49
Q

how does therapeutic hypothermia work?

A
  • decreases rate of cellular death
  • decreases cellular metabolism
  • conserves ATP stores
  • limits free radical release
50
Q

describe neonatal seizures

A

A symptom of neurologic dysfunction

-excessive simultaneous electrical discharge or depolarization

51
Q

pathophysiology of neonatal seizures

A
  • excessive excitatory amino acid release

- deficient inhibitory neurotransmitters (GABA)

neurology (1 decks)

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