Ch. 11 Neural Function Flashcards Preview

Pathophysiology > Ch. 11 Neural Function > Flashcards

Flashcards in Ch. 11 Neural Function Deck (139):
1

what are the causes of neural disorders?

congenital defects, trauma, infections, tumors, chemical imbalances, and vascular changes

2

what are the functions that the nervous system manages?

structures such as muscles, glands, and organs; heart rate; blood flow; breathing; digestion; urination; and defecation

3

cranial nerves that carry only sensory fibers

I, II, and VIII

4

cranial nerves that carry only motor fibers

III, IV, VI, XI, and XII

5

cranial nerves that carry both sensory and nerve fibers

V, VII, IX, and X

6

facilitates volunatry motor activity and plays a role in personality traits

frontal lobe

7

receives and interprets sensory input, with the exception of smell, hearing, and vision stimuli

parietal lobe

8

processes visual information

occipital lobe

9

plays an essential role in hearing and memory

temporal lobe

10

includes the thalamus and hypothalamus

diencephalon

11

receives and relays most of the sensory input such as those of pain, termperature, and pressure; affects mood; and initiates body movments

thalamus

12

most inferior portion of the diencephalon; regulates many bodily functions such as temperature, respiratoins, and heart beat. directs hormone secretions of the pituitary

hypothalamus

13

crucial for many basic body functions such as maintaining heart rate, blood pressure, and respirations. collaborates with hypothalamus to regulate these vital activities. injury can easily result in death. origin of many cranial nerves. reflex center for movements of eyeballs, head, and trunk. plays a role in consciousness.

brain stem

14

part of the brainstem that contains nerves that regulate sleep and breathing

pons

15

smallest region of the brainstem, and brain in general. acts as a sort of relay station for auditory and visual information and controls the visual and auditory systems as well as eye movement

midbrain

16

part of the brainstem that is a conduction pathway for ascending and descending nerve tracts. coordinates heart rate, peripheral vascular resistance, breathing, swallowing, vomitine, coughing, and sneezing

medulla

17

acts like a gatekeeper, receiving all incoming and outgoing information. sends impulses to the cerebral cortex through specialized nerve fibers called reticular activation system

reticular formation

18

responsible for alertness during the day and can prevent sleeping at night

reticular formation and reticular activation system

19

communicates with other regions of the brain to coordinate the synergistic motion of muscle movement and balance as well as cognition. coordinates subconscious movements of skeletal muscles. contributes to muscle tone, posture, balance, and equilibrium

cerebellum

20

play a pivotal role in coordination, motor movement, and posture. slow, sustained movments. suppresses useless patterns of movement.

basal ganglia

21

works in conjunction with the hypothalamus to influence instinctive behavior, emotions, motivation, mood, pain, and pleasure

limbic system

22

large opening in the skull through which the spinal cord exits

foramen magnum

23

where does the spinal cord terminate

second lumbar vertebrae. here it splits into the cauda equana

24

how many pairs of spinal nerves are there?

31

25

permits sensation of light touch, pressure, tickling, and itching

anterior spinothalamic tracts

26

allow the sensatoins of pain and temperature

lateral spinothalamic tracts

27

establish the body's position in relation to the cerebellum

spinocerebellar tracts

28

coordinate movements, especially in the hands

corticospinal tracts

29

responsible for involuntary movements

vestibulospinal tracts and reticulospinal tracts

30

withdrawal reflex that occurs in response to touching an unpleasant stimulus

flexor reflex

31

of the 31 spinal nerves, how many are cervical, thoracic, lumbar, sacral, coccygeal?

8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal

32

spinal nerves arise from approximately 6-8 small nerves called

rootlets

33

what does each spinal nerve, with the exception of C1 have in common?

they each have a specific body surface area from which they obtain sensory information

34

what are the four plexuses and where are they located?

cervical - located from C1 to C4
brachial - from C5 to T1
lumbar - from L1 to L4
sacral - from L4-S4

35

controls smooth muscles and is responsible for the fight-or-flight response

autonomic nervous system

36

is the autonomic nervous system under conscious control?

no

37

what things does the ANS affect?

heart rate, blood pressure, and intestinal motility

38

what are the two divisions of the ANS?

the sympathetic nervous system (SNS) and the parasympathetic nervous system

39

responsible for fight-or-flight response; initiated when a person is startled or faced with danger and is augmented by secretions from the adrenal medulla

SNS

40

responsible for the rest and digest response

parasympathetic nervous system

41

how will the ANS initiate physiologic responses?

by stimulating or inhibiting neurotransmitters and receptors

42

which receptors does the SNS stimulate and which does the parasympathetic nervous system stimulate?

SNS stimulates the adrenergic receptors while the parasympathetic nervous system stimulates the cholinergic receptors

43

cranial nerve I

olfactory

44

CN II

optic

45

CN III

occulomotor

46

CN IV

trochlear

47

CN V

trigeminal

48

CN VI

abducens

49

CN VII

facial

50

CN VIII

vestibulocohlear

51

CN IX

glosopharyngeal

52

CN X

vagus

53

CN XI

spinal accessory

54

CN XII

hypoglossal

55

condition in which excess CSF accumulates within the skull, which dilates the ventricles and compresses the brain and blood vessels

hydrocephalus

56

what occurs during hydrocephalus?

the pressure from the excess CSF thins the cortex, causing severe brain damage.

57

when does CSF accumulate?

when the flow is disrupted (referred to as noncommunicating or an obstructive hydrocephalus) or when too much CSF is made or not properly absorbed by the blood stream (referred to as communicating hydrocephalus)

58

is hydrocephalus a common condition?

yes

59

when does hydrocephalus occur?

it may be present at birth or develop later in life

60

what are risk factors for the development of hydrocephalus at any age?

prematurity, pregnancy complications, other congenital defects especially nervous system defects such as spina bifida, nervous system tumors, CNS infections, cerebral hemorrhage, and severe head injuries

61

what do clinical manifestations of hydrocephalus vary depending on?

the age group, underlying etiology and disease progression

62

what are the clinical manifestations of hydrocephalus in infants?

an unusually large head, a rapid increase in the head size, a bulging fontanelle or soft spot on top of the head, vomiting which is often projectile, lethargy, irritability, high-pitched cry, feeding difficulties, seizures, eyes that gaze downward, developmental delays

63

what are the clinical manifestations of hydrocephalus in older children and adults?

headache followed by vomiting, nausea, blurred vision or diplopia, sluggish pupil response to light, eyes that gaze downward, problems with balance, coordination or gait, extreme fatigue, slowing or regression of development, memory loss, confusion, urinary incontinence, irritability, personaility, memory or cognition changes, impaired performance in school or work

64

when does the neural tube usually close?

by the fourth week of gestation

65

what occurs with spina bifida?

the posterior spinous processes on the vertebrae fail to fuse and this opening permits the meninges and spinal cord to herniate, resulting in neurologic impairment

66

what is the most common site of spina bifida?

the lumbar area of the vertebrae

67

what is the cause of spina bifida?

the exact cause is unknown but it is thought to be a result of genetic and environmental influences

68

who is spina bifida most common in?

caucasians and hispanics

69

what are maternal risk factors for the development of spina bifida?

family history of neural defects, folate deficiency, certain medications, diabetes mellitus, prepregnancy obesity, and increased body temperature (from fevers, hot tubs, saunas, and tanning beds)

70

what complications can arise because of spina bifida?

physical and neurologic impairments as well as hydrocephalus and meningitis

71

do children with spina bifida usually have deficits in intelligence?

no they are usually of normal intelligence but may have learning problems because of the chronic nature of the condition

72

mildest and most common form of spina bifida. results from a small gap in one or more of the vertebrae. the spinal nerves and meninges do not usually protrude through the opening so children with this usually do not have any manifestations and experience no neurological deficits

spina bifida occulta

73

what may be a sign of spina bifida occulta?

the child may have a dimple, birthmark, or tuft of hair over the site

74

rare form of spina bifida where the meninges and CSF protrude through the vertebral opening and form a sac on the surface of the infants back. there is no nerve tissue in the sac.

meningocele

75

is neurologic impairment common with meningocele?

no, it is usually not present and these membranes can be removed by surgery with little or no damage to nerve pathways. neurologic impairment can develop if there is infection or rupture of the sac.

76

most severe form of spina bifida. the spinal canal remains open along several vertebrae in the lower and middle back and the meninges, spinal cord, spinal nerves, and CSF protrude through this large opening to form a sac on the infants back

myelomeningocele

77

why is the infant so vulnerable to life-threatening infections when they have myelomeningocele?

because the tissues and nerves are exposed if the sac is not covered by skin

78

what are some complications that can arise with myelomeningocele?

neurologic impairment, bowel and bladder problems, seizures

79

group of non-progressive disorders that appear in infancy or early childhood and permanently affect motor movement, muscle coordination, and other cerebral functioning

cerebral palsy (CP)

80

when does CP usually develop?

damage to the cerebellum during the prenatal period, but it can occur any time during the first three years of life when the brain is developing

81

is CP curable?

no, but the right treatment can make an impact on the child's prognosis

82

what are factors that contribute to the development of CP?

prematurity, breech births, multiple fetuses, hypoxia, hypoglycemia, cerebral hemorrhage, neurologic infections, head injury, maternal infection during pregnancy, maternal exposure of toxins during pregnancy, severe jaundice

83

what is CP classified based on? what are the three classifications?

based upon the movement disorder involved, which reflects the area of the brain affected. spasticity (stiff muscles, most common), dyskinesia (uncontrolled movement), ataxia (poor balance and coordination)

84

what parts of the body might CP affect?

may affect the entire body or just one area, may affect one side or both sides of the body

85

what are clinical manifestations of CP?

persistence of early reflexes, developmental delays, ataxia, spasticity, flaccidity, hyperreflexia, asymmetrical walking gait with one foot or leg dragging, unusual positioning of limbs when resting or when held up, excessive drooling, difficulties swallowing, sucking, or speaking, facial grimaces, tremors, difficulty with precise motion

86

what are complications that can develop because of CP?

balance and coordination issues, contractures, scoliosis, malnutrition, communication issues, learning or cognitive difficulties, seizures, vision and hearing loss, urinary incontinence, constipation, osteoporosis, chronic pain, injury

87

an inflammation of the meninges, usually resulting from an infection. the CSF may also become affected.

meningitis

88

what things can cause meningitis?

any number of bacterial or viral agents, chemical irritants, tumors, fungi, parasites, and allergens

89

how do the infectious agents invade the meninges in meningitis?

through the blood or nearby structures, or through direct access

90

what are risk factors for the development of meningitis?

being younger than 25, living in a community setting, pregnancy, working with animals, and immunodeficiency

91

is meningitis life-threatening?

it can be self limiting or life threatening

92

what are some complications that can occur because of meningitis?

permanent neurologic damage, seizures, hearing loss, blindness, speech difficulties, learning disabilities, behavior problems, paralysis, acute renal failure, adrenal gland failure, cerebral edema, shock, and death

93

what are the clinical manifestations of meningitis?

initially mimic influenza infections. fever and chills, mental status changes, nausea and vomiting, photobia, severe headache, stiff neck, agitation, bulging fontanelle, decreased consciousness, opisthotonos, poor feeding or irritability in children, tachypnea, tachycardia, rash

94

when the brain collides with the skull or any penetrating object this is called

a traumatic brain injury

95

what things usually cause a TBI

a sudden and violent blow or jolt to the head, penetrating head wound that disrupts the brains normal function

96

what are the main sources of TBIs?

falls, motor vehicle accidents, penetration of an object, and assaults

97

what people are at higher risk for experiencing a TBI?

males are twice as likely as females, young children and 15-19 year olds, adults 75+, certain military personnel, African Americans

98

many TBIs will result in a wide range of long-term and potentially life-altering complications such as...

changes in thinking, sensation, language or emotions

99

what can TBIs increase the risk for?

seizures, migraine headaches, Alzheimer's disease, and Parkinson's disease

100

true or false: neurologic dysfunction will not result from multiple small TBIs

false, multiple mild TBIs can have an accumulative effect and result in neurologic dysfunction, cognitive deficits, and death

101

momentary interruption in brain function that usually results from a mild blow to the head that causes sudden movement of the brain, disrupting neurologic function

concussion

102

what things may follow a concussion for weeks or months?

amnesia, confusion, sleep disturbances, and headaches

103

bruising of the brain accompanied by rupture of small blood vessels and edema

cerebral contussion

104

what do most contussions result from?

a blunt blow to the head that causes the brain to make sudden impact with the skull

105

the initial area where the brain impacts the skull

coup

106

the area where the brain impacts the opposite side of the skull after it has rebounded

countercoup

107

type of fracture located at the base of the skull and is usually accompanied by CSF leakage

basilar skull fracture

108

how may clinical manifestations of a TBI develop?

they may develop slowly or they may be sudden and severe. symptoms may improve and then suddenly worsen

109

what should the individual be asked when a TBI is suspected?

to give an account of the accident. not being able to recall details is an indication of a TBI

110

what are clinical manifestations of TBIs?

indications of a concussion, changes in or unequal size of pupils, seizures, asymmetrical facial features, fluid drainage from the nose, mouth, and ears, fracture in the skull or face, bruising of the face, swelling at the site of injury, scalp wound, impaired senses and speech, inability to move one or more limbs, irritability, personality changes, or unusual behavior, loss of consciousness, bradypnea, hyptension, restlessness, lack of coordination, lethargy, stiff neck, vomiting

111

increased volume in the limited space of the cranial cavity

increased intracranial pressure

112

what is the Monro-Kellie hypothesis

hypothesis that states that the cranial cavity cannot be compressed, and that the volume inside the cavity is fixed. the skull and its components create a state of volume equilibrium, such that any incres in the volume of one component must be compensated by a decrease in the volume of another component

113

how does the brain usually compensate for increased ICP?

by shifts in the CSF and to a lesser extent, blood volume. these fluids respond to increases in the volume of remaining components

114

what do transient increases in ICP routinely occur with?

position changes, coughing, or sneezing

115

what are two compensatory mechanisms to maintain tissue perfusion?

autoregulation and Cushing's syndrome

116

when the blood vessels dilate to increase blod flow and constrict if the ICP is increased

autoregulation

117

complex cascade of events that results in increased blood pressure. when the mean arterial pressure drops below the ICP, the hypothalamus increases sympathetic stimulation causing vasoconstriction, increased cardiac contractility, and increased cardiac output

Cushing's reflex

118

if unresolved, increased ICP leads to a trio of effects known as

Cushing's triad - increased blood pressure, bradycardia, and changes in respiratory pattern

119

what causes bradycardia with increased ICP?

it can be caused because the baroreceptors in the carotid arteries detect the increase in blood pressure and trigger the parasympathetic response through vagal stimulation or it could be because the increased ICP impinges on the vagal nerve, causing a parasympathetic response

120

as pressure increases inside the skull and space becomes limited, what happens?

brain tissue shifts downward

121

what respiratory changes usually occur with increased ICP on the brainstem

Cheyne-Stokes respirations and bradypnea

122

what are the clinical manifestations of increased ICP?

decreasing level of consciousness, vomiting which is often projectile, increasing blood pressure with increasing pulse pressure, bradycardia, papilledema, fixed and dilated pupils, posturing, behavior changes, severe headache, lethargy, neurologic deficits, seizures. two manifestations unique to infants are separated sutures and bulging fontanelles

123

flexion of the arms, wrists, and fingers with adduction in upper extremities, extension, internal rotation, and flantar flexion in lower extremities

decorticate response

124

all four extremities in rigid extension with hyperpronation of forearms and plantar extension of the feet

decerbate response

125

left side of the body and decerebrate response on the right side of the body

decorticate response

126

collection of blood in the tissues that develops from ruptured blood vessels

hematoma

127

result from bleeding between the dura and skull, usually caused by an arterial tear

epidural hematoma

128

what are the clinical manifestations of a hematoma?

marked neurologic dysfunction that usually develops within a few hours of injury. brief loss of consciousness, followed by a short period of alertness, then loss of consciousness again

129

hematoma that develops between dura and the arachnoid and are frequently caused by a small venous tear

subdural hematomas

130

type of subdural hematoma in which manifestations of neurologic deficits are present within 24 hours of injury. this type progresses rapidly and has a high mortality. ICP increases over a period of about a week after the injury

acute subdural hematoma

131

type of subdural hematoma in which the manifestations develop several weeks after an injury because of a slow leak. more common in elderly adults because of the brain atrophy that occurs with age, which give the hematoma more space to develop

chronic subdural hematoma

132

result from bleeding in the brain tissue itself. usually caused by contusion or shearing injuries, but can also result from hypertension, cerebral vascular acidents, aneurysms, or vascular abnormalities

intracerebral hematomas

133

results from bleeding in the space between the arachnoid and pia. its primary clinical presentation is a severe headache that has a sudden onset and is worse near the back of the head

subarachnoid hemorrhage

134

in all types of hematomas, what does the bleeding lead to?

localized pressure on nearby tissue and increases intracranial pressure

135

how can a hematoma increase ICP?

the hematoma becomes encapsulated by fibroblasts and blood cells within the capsule lyse. the fluid from the hemolysis exerts osmotic pressure drawing more fluid into the capsule. the edema increases the size of the mass, applying pressure on surrounding tissue and increasing ICP. bleeding can trigger vasospasms, worsening ischemia.

136

result from direct injury to the spinal cord or indirectly from damage to surrounding bones, tissues, or blood vessels

spinal cord injuries

137

what are the main causes of spinal cord injuries?

falls, motor vehicle accidents, violence, ans sports injuries. mild injuries can occur because of weakening of vertebral structures. direct damage can occur if the spinal cord is pulled, pressed sideways, or compressed

138

temporary suppression of neurologic function because of spinal cord compression. neurologic function gradually returns.

spinal shock

139

who is spinal cord injuries most common in?

caucasians and males between the ages of 15 and 35 years