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Anatomy and Phyisology > HLTH 2501: acute neurologic problems > Flashcards

HLTH 2501: acute neurologic problems Flashcards

1
Q

what can tumors be called in the brain?

A

space-occupying lesions

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2
Q

gliomas

A

are the largest category of primary malignant tumors and these arise from one of the glial cells (the parenchymal cells in the CNS); these can be further subdivided because of the cell of derivation

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3
Q

most common type of glioma

A

astrocytomas

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4
Q

types of brain tumors

A

gliomas, meningioma, or adenoma (pituitary gland)

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5
Q

what are secondary brain tumors often a result of?

A

breast or lung tumors

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6
Q

diagnosis for brain tumors

A

stereotactic biopsy or MRI

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7
Q

what do primary malignant brain tumors appear as?

A

not well-defined margins (project into adjacent tissue) and are surrounded by an area of inflammation

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8
Q

what brain tumors are common in young children?

A

brainstem and cerebellar tumors

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9
Q

where do brain tumors often develop in adults?

A

in the cerebral hemispheres

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10
Q

signs of brain tumors

A

morning headaches, vomiting, lethargy, irritability, personality changes, seizures, paralysis, visual problems, and adenomas will cause endocrinologic signs

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11
Q

why are there no systemic signs associated with brain tumors?

A

because they do not metastasize outside of the CNS and will cause death before this can occur

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12
Q

brain tumor treatment

A

surgery is often the treatment of choice, but chemo and radiation may also be used

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13
Q

2 origins of vascular disorders

A

hemorrhagic or ischemic

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14
Q

global cerebral ischemia

A

may develop secondary to severe shock or cardiac arrest and occurs when impaired perfusion of the entire brain results in loss of function and generalized cerebral edema

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15
Q

mild signs of global cerebral ischemia

A

will cause confusion and neurologic dysfunction but recovery will occur with no permanent damage

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16
Q

severe or prolonged global cerebral ischemia signs

A

significant diffuse necrosis or infarction will result in a deep doma

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17
Q

causes of a transient ischemic attack

A

results from temporary localized reduction of blood flow in the brain (partial occlusion of an artery, atherosclerosis, a small embolus, a vascular spasms, or local loss of autoregulation)

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18
Q

TIA

A

transient ischemic attack

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19
Q

what may a TIA predict?

A

a stroke

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20
Q

signs of a TIA

A

short episodes of impaired function (such as muscle weakness), visual disturbances, numbness, paresthesia, and transient aphasia

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21
Q

paresthesia

A

abnormal sensation of the skin or pins and needles

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22
Q

another name for a stroke

A

cerebrovascular accidents

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23
Q

stroke

A

is an infarction of brain tissue that results from lack of blood

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24
Q

two main causes of a stroke

A

2 ways; the brain tissue may become necrosis, leading to a total occlusion of a vessel by atheroma or embolus, which causes ischemia; it may also be the result of a ruptured vessel, causing a hemorrhage and increased ICP

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25
Q

how long of ischemia does it take to cause cell damage?

A

5 minutes

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26
Q

what is the result of ischemia in the brain?

A

a central area of necrosis develops, surrounded by inflammation, in which the tissue liquifies, leaving a cavity in the brain

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27
Q

three types of cerebrovascular accidents

A

thrombus, embolus, or hemorrhage

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28
Q

most common cause of a stroke

A

occlusion of an artery by an atheroma that often develop in large arteries

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29
Q

obstruction by an embolus leading to a stroke

A

may be lodged in a cerebral artery or in the heart, and may result from tumors, air, or infection

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30
Q

hemorrhage causing a stroke

A

usually is caused by the rupture of a cerebral artery is a patient with severe hypertension and cause increased ICP

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31
Q

most severe type of stroke

A

hemorrhage because they affect large portions of the brain

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32
Q

secondary effects of a hemorrhage stroke

A

the bleeding may result in vasospasms, electrolyte imbalances, acidosis, and cellular edema

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33
Q

what are strokes diagnosed with?

A

an MRI

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34
Q

what are neurons replaced with after a stroke?

A

residual scar tissue and cysts

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35
Q

secondary complications of strokes

A

recurrent strokes, contractures as a result of paralysis, and secondary problems related to immobility like pneumonia, aspiration, and constipation

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36
Q

contracture meaning

A

A permanent tightening of the muscles, tendons, skin, and nearby tissues that causes the joints to shorten and become very stiff

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37
Q

risk factors for a stroke

A

diabetes, hypertension, lupus, elevated cholesterol, hyperlipidemia, atherosclerosis, a history of TIA, increasing age, obstructive sleep apnea, oral contraceptives, cigarette smoking, and heart disease

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38
Q

warning signs of a stroke

A

sudden weakness, numbness or tingling in the face, arm or leg, or on one side of the body, loss of speech, confusion, sudden loss of vision, severe headache, and unusual dizziness or unsteadiness

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39
Q

stroke scale

A

created by the national institute of health and includes commands to determine capacity for speech, level of consciousness, motor abilities, and assessment of eye movement

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40
Q

small infarctions and strokes

A

small infractions may make a ‘silent stroke’ in which there are not obvious signs until several small infarctions have occured

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41
Q

evolving stroke

A

is a stroke that develops slowly over a period of hours

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42
Q

paralysis for a stroke

A

flaccid paralysis will first occur, and spastic paralysis will develop weeks later

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43
Q

what are the signs of a hemorrhagic stroke

A

severe headache and increasingly severe neurologic defects

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44
Q

signs of a stroke resulting from occlusion of an anterior cerebral artery

A

this affects the frontal lobe so signs are contralateral muscle weakness or paralysis, sensory loss in the leg, confusion, loss of problem-solving skills, and personality changes

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45
Q

signs of a stroke resulting from occlusion of an middle cerebral artery

A

affects the central hemisphere so contralateral paralysis and sensory loss of the upper body and arm occur; as well, aphasia when the dominant hemisphere of the brain is affected, or spatial relationships are impacted if it is the right lobe

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46
Q

signs of a stroke resulting from occlusion of the posterior cerebral artery

A

vision loss as the occipital lobe is affected

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47
Q

clot-busting agents

A

are tissue-plasminogen activator which reduces the effects of the stroke

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48
Q

function of glucocorticoids for a stroke

A

reduce cerebral edema

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49
Q

treatment for stroke

A

can be clot-busting agents, surgery to relieve obstruction, glucocorticoids, O2 supply, getting the patient to stand up to maintain muscle tone, PT, OT, speech therapy, and treating the underlying problem ex. hypertension

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50
Q

what is an aneurysm?

A

a localized dilation in an artery caused by the force of blood (hypertension) leading to a bulging in the wall

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51
Q

where do cerebral aneurysms occur?

A

at the points of bifurcation on the circle of Willis, specifically at points of weakness in the wall, often where branching occurs

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52
Q

development of an aneurysm

A

initially they are asymptomatic and develop very gradually until they compress a nearby structure or until rupture occurs

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53
Q

what does an aneurysm rupture result from?

A

a sudden increase in BP during exertion, causing bleeding to occur into the subarachnoid space and the CSF

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54
Q

blood in the meninges

A

is irritating and will cause an inflammatory response and an irritation of the nerve roots passing through here; it can also cause a vasospasm in the cerebral arteries, as well as a hemorrhage which will cause increased ICP

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55
Q

signs of an aneurysm that is creating pressure

A

pressure on the surrounding structures such as the optic chiasm or the cranial nerves can lead to the loss of the visual fields and it can also result in a headache

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56
Q

signs of small leak aneurysm

A

headache, photophobia, and intermittent periods of dysfunction such as confusion, slurred speech, or weakness, and a stiff neck (nuchal rigidity)

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57
Q

phototopia

A

increased sensitivity of the eyes to light

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58
Q

nuchal rigidity

A

is a stiff neck that develops as a response to escaped blood that irritates the spinal nerve roots and causes contractions in the neck

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59
Q

signs of a massive rupture aneurysm

A

immediate and severe blinding headache, vomiting, photopia, and sometimes seizures of a loss of consciousness; death may also occur

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60
Q

treatment for an aneurysm

A

is often treated with surgery through clipping or tying it off, while also focusing on reducing increased ICP and cerebral vasospasm

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61
Q

how do microorganisms arrive at the brain through the blood?

A

they can bind to nasopharyngeal cells, cross the mucosal barrier, attach to the choroid plexus, and enter the CSF

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62
Q

what does the brain look like when infected by meningitis?

A

inflamed and swollen (there is increased ICP as a result), blood vessels appear dilated, and purulent exudate covers the surface, filling in the sulci causing them to appear flat

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63
Q

meningococcus other name

A

neisseria meningitidis

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64
Q

meningococcus

A

is the classic meningitis pathogen and enters in the nasopharynx of carriers; it is spread by respiratory droplets and occurs more often in the late winter and early spring

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65
Q

treatment for meningococcus organism

A

prophylactic treatment

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66
Q

E coli and meningitis

A

commonly affects neonates and is common is those with a neural tube defect, premature rupture of the amniotic membranes, or a difficult delivery

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67
Q

haemophilus influenzae and meningitis

A

commonly occurs in the autumn or winter and often affects young children

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68
Q

meningitis in elderly people

A

is often caused by streptococcus pneumoniae

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69
Q

common organisms causing meningitis

A

streptococcus pneumoniae, haemophilus influenzae, E coli, and meningococcus (neisseria meningitidis)

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70
Q

other causes of meningitis

A

can be secondary to other infections like sinusitis or otitis, may result from an abscess that spreads, or can be a result of viral infections like mumps or measles

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71
Q

signs of meningitis (specifically meningeal irritation)

A

severe headache, back pain, photophobia, nuchal rigidity, kernig sign, and brudzinski sign

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72
Q

kernig sign

A

resistance to leg extension when lying with the hip flexed

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73
Q

brudzinski sign

A

neck flexion cause flexion of hip and knee

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74
Q

signs of meningitis (specifically for increased ICP)

A

vomiting, irritability, lethargy, and seizures

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75
Q

signs of meningitis (specifically for infection)

A

fever, chills, leukocytosis, and a rose-colored petechial rash over the body

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76
Q

signs of meningitis in a newborn

A

feeding problems, irritability, lethargy, a high-pitched cry, and bulging fontanelles (soft spots on head)

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77
Q

potential complications of meningitis

A

hydrocephalus, cranial nerve damage, mental retardation, seizures, or motor impairment

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78
Q

fulminant meaning

A

rapidly progressive and severe

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79
Q

fulminant meningitis

A

is caused by highly virulent organisms, causing intravascular coagulation or hemorrhage of the adrenal glands, resulting in vascular collapse or shock and death

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80
Q

diagnosis for meningitis

A

lumbar puncture; CSF is cloudy and contains an increased number of WBCs if infection is present

81
Q

treatment for meningitis

A

aggressive antimicrobial therapy (ex. ampicillin) along with treatment of ICP and seizures if needed, and glucocorticoids for inflammation

82
Q

vaccines available for meningitis

A

are available for S. pneumoniae and H. influenzae

83
Q

brain abscess

A

is a localized infection frequently occuring in the frontal or temporal lobes; necrosis of brain tissue and edema are usually also present

84
Q

where do brain abscesses usually result from?

A

the spread of infections from the ear, throat, lung, or sinus infections, as well as endocarditis

85
Q

common causative organisms for brain abscesses

A

staphylococci, streptococci, and pneumococci

86
Q

signs of brain abscess

A

neurologic deficits and increasing ICP

87
Q

treatment for brain abscess

A

antimicrobial therapy and surgical drainage

88
Q

encephalitis

A

is an infection of the parenchymal or CT in the brain and spinal cord, particularly of the basal ganglia; inflammation and necrosis develop in the brain tissue

89
Q

early signs of encephalitis

A

severe headache, stiff neck, lethargy, vomiting, seizures, and fever

90
Q

western equine encephalitis

A

is an arboviral infection spread by mosquitoes and is common in children and summer

91
Q

St Louis encephalitis

A

is found throughout the US and affects older persons more seriously

92
Q

West Nile fever

A

is a form of encephalitis that is caused by a flavivirus and is spread by mosquitoes and uses birds as an intermediate host

93
Q

signs of west nile fever

A

low-grade fever, headache, confusion, and tremors

94
Q

another name for lyme

A

neuroborreliosis

95
Q

what causes lyme

A

a spirochete called borrelia burgdorferi that is transmitted by tick bites

96
Q

what does a tick bite look like?

A

red with a pale centre that gradually increases in size to form the unique marker lesion the ‘bull’s eye’

97
Q

signs of lyme

A

first sore throat, dry cough fever, and headache; this is followed by cardiac arrhythmias, neurological abnormalities, and pain and swelling in large joints that may persist to chronic arthritis

98
Q

treatment for lyme

A

prolonged therapy with antimicrobials like doxycycline

99
Q

herpes simplex encephalitis

A

arises from the spread of herpes simplex virus type 1 from the trigeminal nerve ganglion; causes extensive necrosis and hemorrhage in the brain

100
Q

treatment for herpes simplex encephalitis

A

acyclovir antiviral drugs

101
Q

amoebic meningoencephalitis causative organism

A

the amoeba Naegleria fowleri which thrives in warm water and is found in southern US

102
Q

amoebic meningoencephalitis

A

rare infection that results in inflammation and swelling of the brain or spinal cord; is almost always fatal

103
Q

types of encephalitis

A

western equine encephalitis, St louis encephalitis, west nile fever, lyme, herpes simplex encephalitis, and amoebic meningoencephalitis

104
Q

other infections that can target the CNS or PNS

A

rabies, tetanus, poliomyelitis, candida albicans or toxoplasma gondii

105
Q

rabies other name

A

hydrophobia

106
Q

rabies

A

is a virus that is transmitted by the bite or a rapid animal; the virus travels along the peripheral nerves to the NS, where is causing severe inflammation and necrosis, particularly in the brainstem and basal ganglia

107
Q

signs of rabies

A

headache, fever nervous hyperirritability (including sensitivity to touch and seizures), difficulty swallowing, foaming at the mouth, and respiratory failure

108
Q

treatment for rabies

A

immediate cleansing of the bite area and prophylactic immunization

109
Q

another name for tetanus

A

lockjaw

110
Q

what is tetanus caused by?

A

clostridium tetani which is a spore-forming bacillus

111
Q

signs of tetanus

A

the exotoxin enters the nervous system, causing tonic muscle spasms causing jaw stiffness, difficulty swallowing, stiff neck, headache, skeletal muscle spasm, and even respiratory failure

112
Q

treatment for tetanus

A

an antitoxin, mechanical respiration, and immunization

113
Q

poliomyelitis other name

A

infantile paralysis

114
Q

poliomyelitis

A

the virus reproduces in the lymphoid tissue in the oropharynx and digestive tract, then enters the blood and the CNS and targets the motor neurons of the spinal cord and medulla

115
Q

signs of poliomyelitis

A

fever, headache, vomiting, stiff neck, flaccid paralysis and sometimes respiratory failure

116
Q

what may cause infections in the brain of immune-suppressed people

A

candida albicans or toxoplasma gondii

117
Q

herpes zoster other name

A

shingles

118
Q

what is herpes zoster caused by?

A

varicella-zoster virus (chickenpox) and it occurs years after this primary infection

119
Q

what does herpes zoster affect?

A

one cranial nerve or one dermatome on one side of the body

120
Q

dermatone

A

a cutaneous area innervated by a spinal nerve

121
Q

signs of herpes zoster

A

pain, paresthesia (pins and needles), and a vesicular rash develop in a line, unilaterally usually on the face or hip

122
Q

prognosis of herpes zoster

A

the lesions usually clear up in a few weeks but some older individuals experience pain after these disappear and sometimes they spread for autoimmune individuals

123
Q

treatment for herpes zoster

A

antiviral medications like acyclovir or the vaccine zostavax

124
Q

postpolio syndrome

A

occurs 10 to 40 years after the original infection recovery and is progressive fatigue, weakness, pain and muscle atrophy

125
Q

what percentage of those with polio develop postpolio syndrome?

A

25-50%

126
Q

why does postpolio syndrome develop?

A

because the surviving motor neurons developed new additional axon branches to serve muscle cells as a compensation but could not maintain them, and end up dying

127
Q

what causes reye syndrome?

A

is not fully understood but is linked to a viral infection like influenza in young children who have been treated with aspirin

128
Q

what happens in reye syndrome?

A

a noninflammatory cerebral edema develops, leading to increased ICP; the liver also enlarges, developing fatty changes and progress to acute failure; kidneys may also be affected

129
Q

serum levels in Reye syndrome

A

high ammonia, high serum liver enzymes (jaundice not present), low glycogen, and high lactic acid

130
Q

signs of Reye syndrome

A

lethargy, headache, vomiting, disoreration, hyperreflexia, hyperventilation, seizures, stupor, or coma

131
Q

treatment for Reye syndrome

A

no cure so treatment focuses on metabolic imbalances and cerebral edema

132
Q

other names for Guillain Barre syndrome

A

postinfectious polyneuritis, acute idiopathic polyneuropathy, and acute infectious polyradiculoneuritis

133
Q

guillian-barre syndrome

A

is an inflammatory condition of the PNS

134
Q

cause of guillian-barre syndorme

A

unknown but it may be an abnormal immune response precipitated by a preceding viral infection or immunization

135
Q

what occurs during guillian-barre syndrome

A

local inflammation, accumulated lymphocytes, demyelination, and axon destruction; this causes impaired nerve conduction, mostly motor but also sensory

136
Q

what body parts does guillain-barre syndrome affect?

A

initially the legs, then the spinal nerves involving the trunk and neck, and then the cranial nerves; critical period develops when the diaphragm and respiratory muscles are affected

137
Q

recovery for guillian-barre syndrome

A

occurs spontaneously and in the reverse order, so the motor function is regained first

138
Q

signs of guillian-bare syndrome

A

progressive muscle weakness and areflexia, which leads to flaccid paralysis, accompanied by paresthesia (pins and needles) and general muscle aching; vision, speech, swallowing, and respiration may be affected

139
Q

treatment for guillian-bare syndrome

A

ventilator, immunoglobulin therapy, PT, OT, and respiratory therapy

140
Q

immunoglobulin therpay

A

is when the immunoglobulin G (IgG) is separated and removed from the patients blood

141
Q

types of brain injuries

A

may be skull fractures, hemorrhage, edema, or direct injury to brain tissue

142
Q

another name for concussion

A

mild traumatic brain injury

143
Q

concussion

A

is a reversible interference with brain function, in which neurologic dysfunction and a loss of consciousness may be experienced; memory loss and headaches may also temporarily occur

144
Q

amnesia

A

memory loss

145
Q

contusion

A

is bruising of brain tissue with rupture of small blood vessels and edema that usually result from a blunt blow to the head

146
Q

closed head injury

A

occur when the skull is not fractured in the injury, but the brain tissue is injured and blood vessels may be ruptured

147
Q

open head injuries

A

are those involving fractures or penetration of the brain by missiles or sharp objects

148
Q

compound brain fracture

A

involve trauma in which the brain tissue is exposed to the environment and is likely to be severely damaged because bone fragments may penetrate the tissue, thus the risk of infection is high

149
Q

basilar fracture

A

occurs at the base of the skull and are often accompanied by leaking of CSF through the ears or nose; often occur when a forehead hits a car windshield; cranial nerve damage and dark discoloration around the eyes are common

150
Q

contrecoup injury

A

occurs when an area of the brain contralateral to the site of damage in injured as the brain bounces off the skull, so are secondary injuries; damage is usually minor

151
Q

primary brain injuries

A

are direct injuries such as lacerations or crushing of the neurons, glial cells, and vessels resulting from a piece of bone or foreign object, as well as ruptures of vessels

152
Q

shearing injury

A

is when the lobes of the brain move against eachother

153
Q

how does a primary brain injury heal?

A

after the bleeding and inflammation subside, some recovering of the neurons may occur and the central area of damage undergoes necrosis and is replaced by scar tissue or a cyst

154
Q

secondary brain injuries

A

result from the additional effects of cerebral edema, hemorrhage, hematoma, cerebral vasospasm, infection, and ischemia related to systemic factors

155
Q

hematoma

A

is a collection of blood in the tissue that develops from ruptured blood vessels

156
Q

4 types of hematomas

A

epidural, subdural, subarachnoid, and intracerebral

157
Q

epidural hematoma

A

results from bleeding between the dura and the skull, usually caused by tearing of the middle meningeal artery in the temporal region

158
Q

subdural hematoma

A

develops between the dura and the arachnoid; frequently these are caused by a small tear in a vein, in which blood slowly accumulates; can be acute or subacute

159
Q

hygroma

A

is a tear in the arachnoid that can allow CSF to leak into the subdural space and this creates pressure

160
Q

subarachnoid hemorrhage

A

is between the arachnoid and pia and is associated with traumatic bleeding from the blood vessels at the base of the brain; because blood mixes with circulating CSF, a hematoma cannot form

161
Q

intracerebral hematoma

A

results from contusions or shearing injuries

162
Q

what may arise secondary to a hematoma?

A

local pressure on adjacent tissues and a general increase in ICP; this is due to blood accumulating, then undergoing hemolysis which draws in water due to osmosis and thus creating pressure; this may also cause vasospasm, leading to ischemia and further dmage

163
Q

alcohol and brain injuries

A

alcohol is a common factor leading to injuries and tends to delay the onset of cerebral edema and elevation of ICP, but this leads to a greater increase at a later time

164
Q

signs in someone with a head injury

A

seizures, cranial nerve impairment, otorrhea and rhinorrhea, fever, or stress ulcers

165
Q

rhinorrhea

A

is the leaking of CSF from the ear or nose

166
Q

otorrhagia

A

is the leaking of blood through the ear through a fracture site with torn vessels and meninges

167
Q

how are brain injuries diagnosed?

A

CT and MRI

168
Q

treatment for brain injuries

A

glucocorticoid agents and antibiotics for infection, surgery for ICP, O2 to protect the remaining tissue, head injury assessments by family and friends, PT and OT

169
Q

simplified head injury test

A

is done by a family or friend and involves checking for reactive pupils, watching for vomiting, change in movement, sensation, or behaviour

170
Q

what do spinal cord injuries usually result from?

A

fracture or dislocation of the vertebrae which compresses, stretches or tears the spinal cord; supporting ligaments and the discs may also be damaged

171
Q

where do most spinal cord injuries occur?

A

in the areas that provide more mobility and less support; C1-C7 and T12-L2

172
Q

4 types of spinal cord injuries

A

hyperextension or hyperflexion of the neck, dislocation of any vertebrae, compression fractures, and penetration injuries

173
Q

hypertension/hyperextension spinal cord injuries

A

occur in the cervical spine and sometimes include fracture; usually there is damage to the disc and ligaments, which leads to dislocation, loss of alignment and compression or stretching of the spinal cord

174
Q

dislocation of the vertebrae

A

may crush or compress the spinal cord and compromise the blood supply

175
Q

compression fractures to the spinal cord

A

cause injuries when great force is applied to the top of the skull or to the feet, and is transmitted to the spine; this results in shattered bone that exerts horizontal pressure against the cord and sharp edges may tear nerves or vessels

176
Q

spinal cord penetration injuries

A

may result form a bullet wound

177
Q

4 types of vertebrae fractures

A

simple, compression, wedge, or dislocation

178
Q

wedge fracture

A

a displaced angular section of bone

179
Q

nerve damage from spinal cord injuries

A

may be temporary or permanent as nerves cannot undergo mitosis, only axonal regrowth; nerves are affected at or below the level of injury (except for C3-C5 that projects up)

180
Q

secondary effects of spinal cord injuries

A

bruising, edema, minor bleeding, and ischemia; released enzymes also cause vasoconstriction, leading to more ischemia and inflammation, and possibly necrosis; longer effects may cause contractures, decubitus ulcers, and urinary infections

181
Q

when may respiration be impaired from a spinal cord injury?

A

if it occurs in the cervical region, inflammation may extend up to C3-C5, interfering with phrenic nerve innervation to the diaphragm

182
Q

spinal shock

A

occurs initially and is when conduction of impulses ceases in the nerve tracts and grey matter; reflexes are also absent

183
Q

how do spinal cord injuries heal?

A

inflammation subsides, phagocytes remove damaged tissue, and scar tissue begins to form

184
Q

two stages in the posttraumatic period of spinal cord injuries

A

spinal shock and recovery

185
Q

spinal shock signs

A

flaccid paralysis, hyperreflexia, sensory loss, absence of reflexes, and loss of motor control; if injury is in the cervical area, loss of motor control includes blood pressure, diaphoresis, body temperature, and emptying; urinary retention and paralytic ileus and present

186
Q

how is spinal cord injury recovery tested?

A

via a check of the dermatone response

187
Q

what is damaged in a cervical spine injury?

A

motor and sensory function in the arms, trunk, and legs, respiratory function, SNS function, and sacral parasympathetic fibres

188
Q

quadriplegia

A

paralysis of all four extremities

189
Q

paraplegia

A

refers to paralysis of the lower part of the trunk and legs

190
Q

autonomic dysreflexia

A

occurs in a cervical spine injury and is the triggering of a massive SNS reflex that cannot be controlled by the brain; causes distention of bladder, vasoconstriction, severe headache, and visual impairment; prolonged period of this can result in stroke or heart failure

191
Q

sex and spinal cord injuries

A

sexual and reproductive function is often impaired; men may have neurogenic reflex erections and may also be infertile is the injury is higher

192
Q

international standards for neurological classification of spinal cord injury

A

developed by the american spinal injury association and includes criteria A-E

193
Q

‘A’ spinal damage criteria

A

complete, no motor or sensory function is preserved in the sacral segments S4-S5

194
Q

‘B’ spinal damage criteria

A

incomplete; sensory, but not motor function is preserved below the neurologic level, and includes the sacral segments S4-S5

195
Q

‘C’ spinal damage criteria

A

incomplete; motor function is preserved below the neurologic level and more than half of the key muscles below that level have a muscle grade less than 3

196
Q

‘D’ spinal damage criteria

A

incomplete; motor function is preserved below the neurologic level and at least half of the key muscles below the level have a muscle grade of 3 or more

197
Q

‘E’ spinal damage criteria

A

normal, motor and sensory function are normal

198
Q

treatment for spinal cord injuries

A

immobilizing the spin, maintaining breathing and preventing shock; more specifically, can be traction, surgery, glucocorticoids (methylprednisolone), OT, PT, respiratory therapists, psychotherapists, and myriad assistive devices

199
Q

leading cause of spinal cord injury death

A

pneumonia, followed by renal failure

Anatomy and Phyisology (71 decks)

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