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Anatomy and Phyisology > HLTH 2501: general effects of neurological dysfunction > Flashcards

HLTH 2501: general effects of neurological dysfunction Flashcards

1
Q

why is diagnosing neurologic damage difficult?

A

because different causes have many similarities on how they affect the brain

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2
Q

local (focal) effects

A

are signs related to the specific area of the CNS in which the lesion or trauma is located

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3
Q

example of a local effect

A

damage to the left frontal lobe results in paralysis of the right arm

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4
Q

supratentorial lesions

A

occurs in the cerebral hemispheres above the tentorium cerebelli; leads to specific dysfunctions

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5
Q

infratentorial lesion

A

is located in the brainstem or below the tentorium; leads to widespread impairment because nerves are bundled together in the brainstem when passing through, ex. respiration and circulatory function

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6
Q

left hemisphere damage

A

may lead to a loss of logical thinking, analytic skills, and communication

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7
Q

right hemisphere damage

A

impairs the appreciation of music and art and causes behavioural problems

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8
Q

what in the brain determine an individual’s level of consciousness?

A

the cerebral cortex and the RAS

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9
Q

early change noted in those with acute brain disorders

A

decreasing level of consciousness or responsiveness

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10
Q

what may cause decreased consciousness levels?

A

a large supratentorial lesion or a small infratentorial lesion which can affect the RAS

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11
Q

what systemic disorders may interfere with consciousness?

A

acidosis or hypoglycemia

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12
Q

signs of reduced consciousness

A

lethargy, confusion, disorientation, memory loss, unresponsive to stimuli, or difficulty is arousal

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13
Q

standard tool in medical assessment for consciousness

A

the Glasgow Coma Scale

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14
Q

most serious level of loss of consciousness

A

is a coma when the affected person does not respond to painful or verbal stimuli, the body is motionless, although some reflexes are still present

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15
Q

deep coma

A

the terminal stage when there is a loss of all reflexes, fixed and dilated pupils, an slow and irregular pulse and respirations

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16
Q

vegetative state

A

is a loss of awareness and mental capabilities, resulting from diffuse brain damage, although brain stem functions continue (respiration, cardiovascular, and ANS)

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17
Q

in what state is there a sleep-wake cycle?

A

the vegetative state

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18
Q

locked in syndrome

A

refers to a condition in which an individual with brain damage is aware and capable of thinking but is paralysed and cannot communicate

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19
Q

criteria for brain dead

A

cessation of brain function (flat or inactive EEG), absence of brain stem reflexes, absence of spontaneous respirations, and establishment of the certainty of irreversible brain damage

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20
Q

what can temporarily cause loss of brain activity?

A

drug overdose or hypothermia

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21
Q

what does motor dysfunction result from?

A

damage to the UMNs in the posterior zone of the frontal lobe, to the corticospinal tracts, or to the LMNs in the anterior horn

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22
Q

what does UMN dysfunction cause?

A

weakness or paralysis on the opposite side of the body

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23
Q

hyperreflexia

A

reflexes may be increased due to CNS damage because the spinal cord continues to conduct impulses with no moderating or inhibiting influences from the brain

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24
Q

spastic paralysis

A

muscle tone may be increased due to CNS damage because the spinal cord continues to conduct impulses with no moderating or inhibiting influences from the brain

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25
Q

what does LMN damage cause?

A

weakness or paralysis on the same side of the below, at and below the level of damage

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26
Q

what does lower motor dysfunction make muscles appear as>

A

flaccid (absence of tone)

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27
Q

flaccid paralysis

A

absence of reflexes

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28
Q

damage to cranial nerves

A

may result in ipsilateral weakness or flaccid paralysis

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29
Q

two involuntary motor responses that occur in persons with brain damage

A

decorticate and decerebrate posturing

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30
Q

decorticate responses

A

rigid flexion in the upper limbs, with adducted arms and internal rotation of the hands; the lower limbs are extended

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31
Q

what individuals often display decroticate responses

A

those with severe damage in the cerebral hemispheres

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32
Q

decerebrate responses

A

both the upper and lower limbs are extended, as is the head, and the body is arched

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33
Q

who does decerebrate responses often occur in?

A

those with brain stem lesions and CNS depression caused by systemic effects

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34
Q

sensory deficits

A

results from damage to the somatosensory cortex in the parietal lobe (may result in touch, pain, temperature, position, vision, hearing, taste, and smell loss); may also result from damage to the cranial nerves or their nuclei

35
Q

when is vision lost in both eyes?

A

when the optic chiasm is totally destroyed

36
Q

fibres from the medial half of each retina (nasal side)

A

these crossover

37
Q

fibres from the lateral half of each retina (temporal side)

A

do not crossover

38
Q

homonymous hemianopia

A

occurs when the optic tract or occipital lobe is damaged and vision is lost from the medial half of one eye and the lateral half of the other eye; it results in loss of the visual field on the opposite side to that of the damage

39
Q

diplopia

A

double vision that results in loss of depth perception and hand-eye coordination; may result from partial loss of vision that leads to an inability to coordinate input from right and left visual fields

40
Q

aphasia

A

refers to an inability to comprehend or to express language; 3 types and 2 subtypes

41
Q

main types of aphasia

A

expressive, receptive, and global; subtypes are fluent and nonfluent

42
Q

dysphasia

A

refers to partial impairment and is more common; aphasia is still used often to refer to partial loss though

43
Q

expressive aphasia

A

aka motor aphasia; damage to the Broca’s area or left frontal lobe results in an impaired ability to speak or write fluently or appropriately

44
Q

receptive aphasia

A

aka sensory aphasia; this results from damage to the Wernicke area and the left temporal lobe results in not being able to understand written or spoken language (does not include hearing)

45
Q

global aphasia

A

is a combination of expressive and receptive aphasia from results from major damage to the brain, including the Broca and Wernicke areas; therefore the individual cannot express self or comprehend others language

46
Q

fluent aphasia

A

the pace of speech is relatively normal, but the speech itself contains made-up words and sentences that do not make sense; this is associated with damage to the Wernicke area

47
Q

nonfluent aphasia

A

is slow and labored speech with short phrases, often small words are omitted; it is associated with damage to the Broca’s area

48
Q

dysarthria

A

occurs when words cannot be articulated clearly; it is a motor dysfunction that usually results from cranial nerve damage or muscle impairment

49
Q

agraphia

A

is impaired writing ability

50
Q

alexia

A

is impaired reading ability

51
Q

agnosia

A

is the loss of recognition or association; ex. visual agnosia indicates an inability to recognize objects

52
Q

another name for seizures

A

convulsions

53
Q

what are seizures caused by?

A

spontaneous excessive discharge of neurons in the brain

54
Q

precipitating cause of seizures

A

inflammation, hypoxia, or bleeding in the brain

55
Q

symptoms of seizures

A

temporary confusion, a staring spell, uncontrollable jerking of the arms and legs, loss of consciousness or awareness, and cognitive, emotional symptoms like fear and anxiety

56
Q

tardive dyskinesia

A

is a neurological disorder caused by longtime use of neuroleptic drugs or antipsychotic drugs

57
Q

what are neuroleptic drugs used for?

A

psychiatric disorders as well as some GI disorders

58
Q

characteristics of tardive dyskinesia

A

repetitive, involuntary movements such as grimacing, tongue protrusion, lip smacking, puckering, pursuing, and rapid eye blinking

59
Q

treatment for tardive dyskinesia

A

minimizing the use of neuroleptic or antipsychotic drugs; the drugs may also be replaced with. options like valbenazine or tetrabenazine

60
Q

increased intracranial pressure

A

occurs when any increase in fluid volume (inflammatory exudate or blood) or a mass (tumor) causes an increase in pressure in the brain

61
Q

result of increased intracranial pressure

A

less arterial blood can enter the high pressure area and eventually the brain tissue is compressed, and this decreases the functions of the neurons both locally and generally; eventually brain tissue can die

62
Q

how can changes in intracranial pressure be measured?

A

by instruments placed in ventricles, by radiologic examinations, and by assessment of consciousness

63
Q

what neurologic problems are increased intracranial pressure associated with?

A

brain hemorrhage, trauma, cerebral edema, infection, tumors, or accumulation of excessive amounts of CSF

64
Q

early signs of increased intracranial pressure

A

decreasing level of consciousness, headache, vomiting, and papilledema

65
Q

papilledema

A

increased pressure of CSF causes swelling around the optic disc

66
Q

how does the body compensate for increased intracranial pressure?

A

by shifting more CSF into the spinal cavity, increasing venous return from the brain, and causing arterial vasodilation in the brain

67
Q

why does headache occur with increased intracranial pressure?

A

stretching of the dura and walls of large blood vessels

68
Q

vital signs of increased intracranial pressure

A

cerebral ischemia, systemic vasoconstriction, slowed heart rate, reduced respiratory rate, and fixed and dilated pupils, or ptosis

69
Q

cushing reflex

A

is a response of cerebral ischemia due to the vasomotor centres attempting to increase arterial blood supply to the brain

70
Q

what can occur if increased intracranial pressure is not relived?

A

neuronal death will prevent circulatory and respiratory control and BP drops

71
Q

Cheyne-Stoke respirations

A

may occur with increased intracranial pressure and are alternating apnea and periods of increasing and decreasing respirations

72
Q

why do fixed and dilated pupils occur with increased intracranial pressure?

A

because the pressure on the oculomotor nerve affects the size and response of the pupils; usually one pupil is fixed and dilated and the other is nonfunctional, but can be both is pressure continues to increase

73
Q

ptosis

A

droopy eyelid that may occur due to pressure on the oculomotor nerve that may occur with increased intracranial pressure

74
Q

ngstagmus

A

excessive eye movements that may occur with increased intracranial pressure

75
Q

lumbar puncture

A

can test the CSF by inserting a fine needle between L3 and L4

76
Q

what is elevated intracranial pressure

A

> 20 mm Hg

77
Q

what will CSF from a spinal puncture look like if there is a hemorrhage?

A

pinkish

78
Q

what will CSF from a spinal puncture look like if there is an infection?

A

cloudy and yellowish

79
Q

what will levels of CSF be from a spinal puncture if there is a neoplasm?

A

abnormal levels of protein

80
Q

herniation

A

occurs when a mass, such as a blood clot or tumor becomes large enough that it may displace brain tissue

81
Q

transtentorial (central) herniation

A

occurs when the cerebral hemispheres, diencephalon, and midbrain and displaced downward; the resulting pressure affects the flow of blood and CSF, as well as the RAS and respirations

82
Q

uncal (uncinate) herniation

A

occurs when he uncus of the temporal lobe is displaced downward past the tentorium cerebelli, creating pressure on the third cranial nerve, the posterior cerebral artery, and the RAS

83
Q

cerebellar or tonsillar (infratentorial) herniation

A

occurs when the cerebellar tonsils are pushed downward through the foramen magnum, which compresses the brain stem and vital centres, causing death

84
Q

diagnostic tests for brain damage

A

CT, MRIs, cerebral angiography, doppler ultrasound, EEG, lumbar puncture, and the Glasgow Coma Scale

Anatomy and Phyisology (94 decks)

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