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Anatomy and Phyisology > HLTH 2501: congenital neurological disorders and seizures > Flashcards

HLTH 2501: congenital neurological disorders and seizures Flashcards

1
Q

hydrocephalus

A

is a condition mostly in infants is which excess CSF accumulates within the skull, compressing the brain tissues and blood vessels; this can occur because the sutures of the skull have no yet closed

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2
Q

why does excess CSF form in hydrocephalus?

A

because there is usually an obstruction in some area, causing more to be produced than is absorbed

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3
Q

two types of hydrocephalus

A

noncommunicating (obstructive) or communicating

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4
Q

noncommunicating hydrocephalus

A

occurs in babies when the flow of CSF through the ventricular system is blocked, usually at the aqueduct of Sylvius or the foramen magnu,

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5
Q

what does noncommunicating hydrocephalus result from?

A

a fetal developmental abnormality like stenosis, a neural tube defect or Arnold-Chiari malformation; the obstruction will lead to increased back pressure of fluid in the ventricles, which gradually enlarge

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6
Q

communicating hydrocephalus

A

occurs when the absorption of CSF through the subarachnoid villi is impaired, resulting in increased pressure of CSF in the system

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7
Q

atresia

A

is the absence of a canal or opening at the connecting channels between the ventricles

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8
Q

most common causes of hydrocephalus

A

stenosis, an atreisa, or a thickened arachnoid membrane

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9
Q

signs of hydrocephalus

A

enlarges head, scalp veins appear dilated, enlarged eyes (sunset sign), pupil response is slow, lethargy, and high-pitched dry

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10
Q

sunset sign

A

is when the white sclera of the eyes is visible above the coloured pupil; is a sign of hydrocephalus in infants

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11
Q

hydrocephalus signs in adults

A

decreased memory, difficulty in coordination, impaired balance, and urinary incontinence

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12
Q

when may hydrocephalus develop in adults?

A

from obstruction due to tumors, infection, or scar tissue, as well as meningitis

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13
Q

diagnosis for hydrocephalus

A

a CT or MRI

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14
Q

treatment for hydrocephalus

A

surgery to remove an obstruction or provide a shunt for CSF from the ventricle

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15
Q

spina bifida

A

refers to a group of neural tube defects that are congenital anomalies of varying severity

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16
Q

how do spina bifida disorders develop?

A

is failure of the posterior spinous processes on the vertebrae to fuse, which may permit the meninges and spinal cord to herniate, resulting in neurologic impairment

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17
Q

where does spina bifida most commonly develop?

A

the lumbar region

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18
Q

three types of spina bifida

A

spina bifida occulta, meningocele, and myelomeningocele

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19
Q

spina bifida occulta

A

develops when the spinous processes do not fuse, but when herniation of the spinal cord and meninges does not occur, leaving a small gap in the bones of the spine

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20
Q

how is spina bifida occulta diagnosed?

A

by a dimple or a tuft on hair present on the skin over the site

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21
Q

meningocele

A

spinous processes do not fuse but herniation of the meninges occurs through the defect and the meninges and CSF form a sac on the surface; neurological impairment is usually not present

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22
Q

myelomeningocele

A

the most serious form of spina bifida and occurs when there is herniation of the spinal cord and nerves along with the meninges and CSF, resulting in considerable neurological damage

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23
Q

what spina bifida is often seen in conjunction with hydrocephalus?

A

myelomeningocele

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24
Q

how is spina bifida generally diagnosed?

A

by alpha-fetoprotein that has leaked from the defect into the amniotic fluid surrounding the fetus and ultrasounds

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25
Q

spina bifida causes

A

is multifactorial; genetic conditions like anencephaly or environmental conditions like exposure to radiation, gestational diabetes, and deficits of vitamin A or folic acid

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26
Q

anencephaly

A

is the absence of cerebral hemispheres and superior cranial vault

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27
Q

what spina bifida disorders appear as a protruding sac over the spine?

A

meningocele and myelomeningocele

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28
Q

myelomeningocele neurological impairments

A

may be lost sensory and motor function at and below the level of the herniation, muscle weakness or paralysis, and bladder and bowel control may be lost

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29
Q

spina bifida treatment

A

surgical repair may be done in utero before birth and PT and OT after birth to manage neurological deficits

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30
Q

potential complications of surgery with spina bifida

A

rupture and infection

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31
Q

cerebral palsy

A

is a group of disorders marked by some degree of motor impairment, caused by genetic mutations, abnormal fetal formation, infection, or brain damage in the perinatal period

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32
Q

what may impact the brain in a child with cerebral palsy?

A

mechanical trauma, hypoxia, hemorrhage, hypoglycemia, hyperbilirubinemia, or infection

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33
Q

major causes of cerebral palsy

A

hypoxia or ischemia which can occur prenatally, perinatally, or postnatally

34
Q

what can hypoxia be caused by?

A

placental complications, a difficult delivery, hemorrhage, aspiration, or respiratory impairment

35
Q

kernicterus

A

occurs when bilirubin crosses the blood-brain barrier and damaged the neurons

36
Q

what is cerebral palsy classified on?

A

the area affected (ex. quadriplegia or diplegia) or on the basis of the motor disability

37
Q

4 types of cerebral palsy

A

spastic, dyskinetic, ataxic, and mixed

38
Q

largest group of cerebral palsy

A

spastic paralysis

39
Q

spastic paralysis

A

results from damage to the pyramidal tracts, the motor cortex, or from general cortical damage; is characterized by hyperreflexia, increased muscle tone, and the scissors gait

40
Q

scissors gait

A

on the toes and with crossed legs

41
Q

dyskinetic cerebral palsy

A

results from damage to the extrapyramidal tract, basal nuclei, and cranial nerves; characterized by athetoid, choreiform involuntary movements, and loss of coordination with fine movements

42
Q

athetoid

A

slow, involuntary writhing

43
Q

choreiform

A

rapid and jerky movements

44
Q

ataxic cerebral palsy

A

commonly develops from damage to the cerebellum and manifests as loss of balance and coordination

45
Q

why do spasms occur in cerebral palsy?

A

increased muscle tone

46
Q

general signs of cerebral palsy

A

spasticity, unilateral use of hands and feet, writhing movements, unusual positions, impaired intellectual function, impaired communication and speech, seizures, and visual problems

47
Q

why is communication hard for cerebral palsy individuals?

A

because of motor disability, possible impaired mentation, and visual or hearing defects

48
Q

learning disabilities in those with cerebral palsy

A

ADD, spatial disorientation, and hyperactivity

49
Q

what type of seizure is common for cerebral palsy individuals?

A

tonic-clonic

50
Q

visual problems in those with cerebral palsy

A

astigmatism and strabismus

51
Q

treatment for those with cerebral palsy

A

speech therapy, PT (Medak program), regular exercise, OT, seizure medication, and hearing devices

52
Q

what do seizures result from?

A

uncontrolled, excessive discharge of neurons in the brain, which cause abnormal motor or sensory activity, and possibly loss of consciousness

53
Q

what are recurrent seizures called?

A

convulsions or epilepsy

54
Q

what are seizure disorders classified on?

A

their location in the brain and their clinical features (including EEG patterns during and between)

55
Q

generalized seizures

A

have multiple foci or origins in the deep structures of both cerebral hemispheres and the brain them, and cause loss of consciousness

56
Q

partial seizures

A

have a single or focal origin, often in the cerebral cortex, and may or may no involve altered consciousness; may progress to generalized seizures

57
Q

primary seizures

A

are idiopathic

58
Q

secondary seizures

A

are acquired with an identified cause such as PTSD

59
Q

what systemic causes may cause seizures?

A

hypoglycemia or withdrawl from drugs

60
Q

neurons causing seizures

A

are hyperexcitable and have a lowered threshold for stimulation; they can be stimulated by physiologic changes like alkalosis or flashing lights

61
Q

how are seizures analyzed?

A

EEG’s and MRI’s

62
Q

status epilepticus

A

is recurrent or continuous seizures without recovery of consciousness; can lead to hypoxia, hypoglycemia, acidosis, and decreased BP

63
Q

causes of seizures

A

varies and is idiopathic but are associated with 4 genes, CP, head injuries, tumor, infections, hemorrhage in the brain, renal failure, and substance withdrawal

64
Q

precipitating factors

A

are seizure triggers like physical stimuli, loud noises, bright lights, or biochemical stimuli like stress, excessive premenstrual retention, hypoglycemia, change in medication or hyperventilation (alkalosis)

65
Q

another name for absence seizures

A

petit mal

66
Q

absence seizures

A

common in children, last about 5-10 seconds, and may occur many times in a day; there is a brief loss of awareness, sometimes facial movements, and no memory of the episode

67
Q

another name for tonic-clonic seizures

A

grand mal

68
Q

tonic-clonic seizures

A

may occur spontaneously or after simple seizures; includes prodromal signs, an aura, loss of consciousness, strong muscle contraction, followed by a clonic stage and consciousness returning; the person is fatigued, with aching muscles after

69
Q

prodromal signs of a tonic-clonic seizure

A

nausea, irritability, depression, or muscle twitching

70
Q

aura

A

is a peculiar visual or auditory sensation, immediately preceding the loss of consciousness

71
Q

tonic muscle contraction

A

is flexion, followed by extension of the limbs and rigidity in the trunk

72
Q

clonic stage

A

is when the muscles alternately contract and relax, resulting in a series of forceful jerky movement; may involve foaming at the mouth and bowel and bladder incontinence

73
Q

why may hypoxia occur with a seizure?

A

the individual may have airway obstruction due to excess saliva and tongue position, while contracting muscles have a higher need for O2

74
Q

types of general seizures

A

tonic-clonic and absence

75
Q

another name for partial seizures

A

focal seizures

76
Q

partial seizures

A

arise from an epileptogenic focus, often related to a single area of damage in the cortex

77
Q

signs of a partial seizure

A

repeated motor activity causing jerking or turning the head or eye aside, sensation such as tingling that beings in the one area and spreads, auditory or visual experiences, and memory and consciousness remain, although awareness is reduced

78
Q

jacksonian seizure

A

is a focal motor seizure in which the clonic contraction begins in a simple area and spreads progressively

79
Q

temporal lobe seizures

A

aka psychomotor seizures; these are complex, partial seizures that originate in the temporal lobes, but may also involve the frontal lobe and limbic system

80
Q

signs of a temporal lobe seizure

A

an aura like the perception of a odd odor, bizarre behaviour like waving and clapping the hands, visual or auditory hallucinations or feeling of deja vu, and the person is unresponsiveness during the episode

81
Q

treatment for seizures

A

anticonvulsant drugs like phenytoin raise the threshold for neuronal stimulation which are often combined with sedatives like phenobarbital

82
Q

adverse effects for seizure medication

A

they may affect dosage of other medications, cause gingival hyperplasia, reduce WBC count, and reduce blood-clotting capability

Anatomy and Phyisology (71 decks)

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