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1

The head and neck act as what type of lever?

A first-class lever.

2

What is a first class lever like and where is the fulcrum at?

Between the force point and the resistant point like a teeter-totter.

3

What is the most common cause of anterior head carriage?

Postural.

4

Will anterior head carriage be associated with shoulders rolled forward or backwards?

Forward.

5

What other syndrome is anterior head carriage associated with?

Upper crossed syndrome.

6

What is upper crossed syndrome?

Overactive tight neck extensors, inhibited or weak middle and lower traps, rhomboids, serratus anterior. This will produce elevation and protraction of the shoulders, winging of the scapula and protraction of the head.

7

Hyperplastic cervical articular pillars is what type of example of anterior head carriage?

Congenital.

8

Name 3 symptoms of anterior head carriage?

1. Neck pain. 2. Headaches. 3. Middle and/or upper thoracic pain.

9

Name 4 ypes of primary headaches?

Muscle tension, migraine, cluster, paroxysmal hemicrania.

10

Where will pain be at for muscle tension headaches?

Usually bilateral and is often suboccipital or supraorbital, pain is described as starting at the base of their skull then it creeps up and over the top of their head and settles in behind or above their eye.

11

When will muscle tension headaches be worse?

IN the afternoon or early evening.

12

How common are muscle tension headaches?

74% of people get them. 20-30% of these people get more than one a month.

13

What are the 2 types of muscle tension headaches?

episodic and chronic.

14

What makes a muscle tension headache chronic? How common are they?

more than 15 days per month. 3% of population will have chronic.

15

What is the female to male ratio for muscle tension headaches?

1.4:1 female:male

16

What is the most common of all headaches?

Episodic muscle tension headaches.

17

What are the diagnostic criteria needed to diagnose a headache as an episodic muscle tension headache?

at leaste 10 headaches with less than 15 a month, headaches last 30 minutes to 7 days. At leaste 2 of the following; bilateral, pressing/tightening(non-pulsating), mild or moderate, not aggravated by routing physical activity. Also no nausea or vomiting and no more than one of photophobia or phonophobia.

18

What are chronic muscle tension headaches like?

Generally continuous, seldom disabling and intensity flucuates.

19

A moderate or severe chronic muscle tension headache may have what type of features?

Mild migranious features like throbbing, nausea, mild hypersensitivity to light or noise.

20

What are the diagnostic criteria needed to diagnose a headache as a chronic muscle tension headache?

headaches that occur 15 or more days a month on average for more than 3 months. Headache may last hours or be continuous. At leaste 2 of the following; bilateral, pressing/tightening (non-throbbing), mild or moderate intensity, not aggravated by routine physical activity. No more than one of photophobia, phonophobia, or mild nausea. No severe nausea nor vomiting.

21

What are the intensities like for migraines?

No such thing as mild just severe and extra severe and I hate how bad this feels I want to die.

22

What is the female to male ratio for migraine headaches?

3:1 females:males.

23

Where will pain be at for migraine headaches?

Frontotemporal location commonly bilateral in young children and unilateral in adults.

24

Name the 4 possible phases of a migraine headache?

1. Premonitory. 2. Aura. 3. Headache. 4. resolution.

25

How consitent will migraines be to the 4 possible phases?

Not every migraine will have the phases and each migraine can be different for people.

26

What is another name for migarines with and without auras?

Without is aka common migraine. With Classic migraine.

27

What is more common with or without aura?

Without is twice as common.

28

Migraine attacks last how long?

4-72 hours unless you are me and then it is only 2 hours.

29

What will the migraine pain be described as?

Throbbing, moderate to severe, aggravated by routine activity, nasuea, photophobia, phonophobia.

30

What are the diagnostic criteria for a migraine without an aura?

At least 5 attacks that; last 4-72 hours and must have 2 of the following; unilateral location, pulsating quality, moderate to severe intensity, aggravated by or causing avoidance of routine physical activity. During the headache at least 1 of the following; nausea or vomiting, or photophobia and phonophobia.

31

What is an aura?

A complex of neurological symptoms that occurs just before or at the onset of the headache.

32

What is the diagnostic criteria for a migrain with an aura?

at least 2 attacks, presence of an aura, identified by typical migraine features.

33

Name 4 different types of auras?

Visual, Sensory, speech, Motor.

34

What type of aura is most common?

Visual.

35

What are sensory auras like?

Parestheisas, numbness, hypersensitivity to touch, auditory or olfactory hallucinations, vertigo, confusion.

36

What is the most uncommon type of aura?

Motor.

37

What is migraine aura status?

Rare condition which a visual aura persists for weeks, months, or longer.

38

What are some of the common symptoms of the premonitory phase?

food cravings, constipation or diarrhea, depression, irritability, difficulty concentrating, muscle stiffness, fatigue, increased frequency of urination, light or sound sensitivity, nausea, blurred vision, yawning, pallor.

39

Resolution phase of a migraine is aka?

Postheadache.

40

What are some common triggers of migraines?

Stress, pregnancy, birth control, menstruation, lack of sleep, foods, eye strain, perfumes, smoke, cervical problems, physical exertion, fatigue, head injury, change in weather and temperature, glare or dazzle.

41

What types of foods can trigger migraines?

Alcohol (red wine), chocolate, red meat.

42

What are some less common triggers of migraines?

Too much sleep, flicker phenomena, allergies, drugs, high humidity, cold foods, high altidues, reading or refractive errors, pungent odors.

43

What type of chiropractive manipulative therapy is most effective for migraine headaches?

Upper cervicals.

44

When will soft tissue therapy be most effective for migraines?

During the prodrome or aura stage.

45

Besides eliminating triggers what nutritional items can help with migraines?

Magnesium, riboflavin, vitamin E, Fish oil concentrate, cod liver oil, antioxidants, feverfew, 5-hydroxytryptophan, calcium and vitamin D.

46

Who is most likely to get a basilar-type migraine?

Young adults.

47

What will not be present with basilar-type migraines?

No motor weakness will be present.

48

What are the criteria to diagnose someone with a basilar-type migraine?

An aura with at leaste 2 of the following; dysarthria, vertigo, tinnitus (ear buzzing), hypacusia (impaired hearing), diplopia, visual symptoms in both eyes, ataxia, decreased level of consciousness, simultaneously bilateral peraesthesias.

49

Basilar-type migraines have in general what type of characteristics?

Stroke like.

50

Who will most commonly get cluster headaches and what are they like?

Very rare, 80% male and usually 20-50 years old. The headaches are excruciating and attacks occur in groups or clusters and laste for weeks or months separated by remissions lasting for months or years.

51

What will patients do during cluster headaches?

Move around, pacing the floor, shifting and rocking the head.

52

Cluster headaches frequently occur when?

At night.

53

What are some triggers of cluster headaches?

Alcohol, smoking, stress, glare, or specific foods.

54

Are cluster headaches considered episodic or chronic?

Both.

55

What are the diagnostic criteria for cluster headaches?

at leaste 5 attacks that are severe or very severe and are unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes if untreated. Also they must include one of the following; ipsilateral conjuctival injection and or lacrimation, ipsilateral nasal congestion and or rhinorrhea, ipsilateral eyelid edema, ipsilateral forehead and facial sweating, ipsilateral miosis and or ptosis, sense of restlessness or agitation.

56

To be considered a cluster headache attacks must be how frequent?

1 every other day to 8/day.

57

What are some treatments for cluster headaches?

Chiropractic maniplative treatment, soft tissue manipulation, ice on the back of the neck or face, melatonin, capsaicin (stuff that makes peppers hot), avoid triggers, oxygen inhalation, meds.

58

What anscillary test should be done with cluster headaches and why?

MRI of head to exlude rare tumors which may cause cluster-like headaches.

59

What are paroxysmal hemicranias?

Headaches that are same location, intensity as cluster headaches, but are shorter-lasting and more frequent.

60

What is more rare cluster headaches or paroxysmal hemicranias?

Paroxysmal hemicranias.

61

Who is more likely to get paroxysmal hemicranias?

70% are female.

62

What are the diagnostic criteria for a paroxysmal hemicrania?

at leaste 20 attacks of severe unilateral orbital, supraorbital or temporal lasting 2-30 minutes and are accompanied by at leaste 1 of the following; ipsilateral conjunctival injection, ipsilateral nasal congestion and or rhinorrhea, ipsilateral eyelid edema, ipsilateral forehead and facial sweating, ipsilateral miosis and or ptosis.

63

What is the frequency of paroxysmal hemicranias?

above 5 per day for more than half of the time.

64

How are paroxysmal hemicranias treated and how effective is the treatment?

Attacks are prevented completely by therapeutic doses of the indomethacin.

65

Name 5 types of secondary headaches?

1. Cervicogenic headaches. 2. Posttraumatic headaches. 3. Giant cell arteritis. 4. Medication-overuse. 5. Headaches due to other neurologicla causes.

66

What are cervicogenic headaches?

headaches cuased by referral from a primary source in the cervial spine.

67

Cervicogenic headaches are aka?

CEH.

68

What type of cervicogenic headaches respond well to conservative treatment?

those related to joint dysfunction, or soft tissue abnormality.

69

What is the prevelance of CEH in adults?

18% from one study, but it is unknown the % of headaches are this type.

70

What are some possible pathophysiology of CEH?

convergence between trigeminal afferents and afferents from the upper three cervical spinal nerves. The possible source of cervicogenic headaches lie in the structures innervated by the C1 to C3 spinal nerves.

71

What are the diagnostic criteria for a CEH?

Clinical laboratory and/or imaging evidence of a disorder or lesion within the cervical spine or soft tissue of the neck known to be or accepted as a valid cause of a headache (not inculding cervical spnodylosis and osteochondritis and cant be myofascial tender spots) and evidence that the pain can be attributed to the neck disorder or lesion based on at least one of the following; Demonstration of clinical signs that implicate a source of pain in the neck or abolition of headache following a diagnostic blockade of a cervial structure.

72

For a CEH to be diagnosed as a CEH how long after treatment can the headaches remain?

Pain must resolve within 3 months after successful treatment of the cause.

73

What will CEH pain be like?

Usually dominates on one side, but may be bilateral.

74

Can there be a cervicogenic component to other types of headaches?

no not according to the IHS.

75

How are CEH treated?

Chiropractic manipulative treatment, soft tissue manipulation, posture fixes, workplace modifications, excersice.

76

What are the major causes of posttraumatic headaches?

CAD trauma (whiplash).

77

How common are headaches after a CAD trauma?

70-90% of whiplash patients develop a headache and headaches are the 2nd most common complaint following CAD trauma.

78

What are giant cell arteritis headaches?

Headaches caused by systemic panarteritis affecting medium sized and large vessels.

79

Giant cell arteritis usually affects who?

those over 50.

80

Giant cell arteritis causes what commonly?

Blindness and it is usually permanent.

81

What are the diagnostic criteria for giant cell arteritis?

at leaste one of the following; swollen tender scalp artery with elevated erythrocyte sedimentation rate and or C-reactive protein, or temporal artery biopsy demonstrating giant cell arteritis.

82

How is giant cell arteritis treated?

Headaches usually resolves or improves within 3 days of a high-dose of steroid treatment.

83

What makes a headache a medication-overuse headache?

headaches greater than or equal to 15 days a month that result from frequent use of medications taken to alleviate headaches, and they resolve to normal headache pattern within 2 months after discontinuation of meds.

84

Medication-overuse headaches are the most common cause of what?

Migraine-like and mixed migraine-like and tension-type-like headaches occuring 15 days or more per month.

85

Name the things that are potential neurologic causes of headaches?

intracranial mass lesion, cerebrovascular disease, subarachnoid hemorrhage, meningeal infections, lumbar puncture (spinal tap).

86

What is the most commonly proposed and reported serious side effect of cervical manipulation?

Vertebrobasilar complications.

87

What is CVA, VBA, VBI, VBS, CAD?

CVA- cerebrovascular accident. VBA- vertebrobasilar accident, VBI- vertebrobasilar ischemia, VBS- Vertebrobasilar stroke, CAD- Cervical artery dissection.

88

What are the proposed effects of pathophysicology of vertebrobasilar complications?

Trauma to arterial wall ---> vasospasm or frank damage ----> flood flow changes -----> cascade mechanism ----> dislodged thrombus which becomes an embolus ----> brain stem or cerebellar infarct.

89

What part of the vertebral artery is most susceptible?

C1-C2 segment due to movement/position.

90

If there is a vasomotor response and arterial vasospams to the vertebral artery what can happen?

1. May last for only a short period with temoprary symptoms. 2. may produce a persistent constriction reduction in blood supply producing ischemia this could also lead to stagnation of blood flow producing a clot.

91

What are the 2 outcomes of injury to the arterial wall?

1. Normal repair with no further problems. 2. Thrombus formation, possible embolus, infarct at the endpoint of the blood vessel.

92

What is wallenburg's syndrome?

Infarct in the distribution of the PICA (posteroinferior cerebellar artery). The findings are assoicated with structures innervated by the crainial nerves.

93

What is locked-in syndrome?

basilar artery occlusion that leaves patient with only vertical ocular mobility and blinking. AKA the corpse with the living eyes.

94

The vertebral artery is compromised on the ______ _______ the neck rotation.

side opposite.

95

What type of people are more susecptible to flow reduction due to head rotation?

Persons who have had a prior vascular injury.

96

What happened to most people who experienced decreased vertebral artery blood flow?

They did not exhibit signs or symptoms of neurologic compromise.

97

What are the 4 possible scenarios whereby vascular injury and CSMT may be related?

The four C's; Catastrophic, Congenital, Cumulative, Coincidental.

98

Can forces produced by CSMT physically injure the artery?

yes.

99

Symons and herzog's study showed that it was not possible to produce mechanical failure of the vertebral artery, but what were some of the limitations to the study?

Most common VA dissection site not measured, ipsilateral rotation adjustments were used not contralateral, they used old cadavers with decreased ROM, Arteries are different in cadavers (not pressurized and other stuff).

100

One study showed that loads on the neck during normla CSMT were similar to what?

A low velocity rear end accident and these are not associated with VA dissections.

101

Of the 198 cases studied where patients had a VA disection after chiropractic treatment when did the VA dissection occur?

63%- immediately during SMT, the rest of the % are spread out between 6%-9% and happened within minutes- up to 24 hours or more after.

102

An ontario study (case-control) found people under age 45 were _____ times more likely to have seen a chiropractor within one week prior to the stroke.

five.

103

There is a lot of temporal relationship seen with CSMT and stroke what is the problem with this relationship?

Temporal relationship alone is inadequate to establish causality.

104

Explaine congenital development of a VA dissection?

Genetic predisopsition is necessary and needs to be triggered by risk factors, environmental exposure, with or without trauma for CAD to occur.

105

Is there any evidence to show a cumulative effect from CSMT on VA dissections?

No, but there is no evidence to show it is not associated.

106

What is the prevelance of postmanipulation dissection and occlusion, and what is the prevelence of spontaneous cases?

Postmanipulation- 31%. Spontaneous- 44%.

107

Why might it seem like CSMT is associated with VA dissections?

Initail symptoms of a VA dissection may be neck pain and headaches and the person may seek chiropractic care.

108

What is the strongest evidence that CSMT will not cause VA dissections?

There is an increased association of chiropractic visits and VA dissections, but there is also an increased association of Primary care providers and VA dissections. So if chiropractic visits cause VA dissections then with this association so would seeing a PCP.

109

What is associated with more adverse reactions with VA dissections low or high velocity procedures?

Low .

110

According to the research is any adjustive technique more risky for VA dissection?

no.

111

Why may it appear that rotation is most likely to cause VA dissection?

It is the most common manipulation of the cervical spine.

112

Forces to the Vertebral artery were the greatest with what manipulation?

Contralateral rotation.

113

What significant forces were measured during manipulation of C6-7?

Vertebral artery forces at C0-1.

114

What type of manipulation cause most force on the vertebral artery?

Rotational.

115

How can rotation adjustments be done to limit force on the vertebral artery?

Combine contralateral lateral flexion in the setup to minimize the rotational forces.

116

Amoung all the different types of strokes how common is CVA?

1.3 out of every 1000.

117

1 in how many chiropractors will encounter a serious post-cervical manipulation neurologic complication?

1 in 33.

118

What did the AAFP say about NSAIDS VS. adjustments?

They found insufficient evidence on the effects of analgesics NSAIDS, antidepressants or muscle relaxants for neck pain although they are widely used. Several drugs used to treat neck pain are associated with well-documented adverse effects. RCT's have found limited evidence that manipulations or mobilizations improved symptoms compared with other or no treatment in people with neck pain.

119

How helpful are provacative tests at screening for vertebrobasilar ischemia?

They have been determined to be ineffective means of risk assessment, and should be abandoned.

120

What is a pre-SMT test?

Hold the premanipulative postion for 5-10 seconds and look for patient dizziness.

121

What happens if the patient gets dizzy with a pre-SMT test?

Don?t adjust, consider soft tissue therapy. However, it doesn?t mean that the dizziness is a result of vertebrobasilar artery compromise or that it will not respond to SMT.

122

Name 5 doubtfull risk factors for a CVA?

advanced age, smoking, oral contraceptives, carotid arterial bruits, oestoarthritis.

123

Name 7 Important risk factors for a CVA?

dizziness/unsteadyness/vertigo, sudden severe pain in the side of the head or neck, migraine, under 45 years of age, Connective tissue disease, recent infection, particularly upper respiratory, Hypertension.

124

What is the prominent early symptom in CAD?

Headache in 67-81% of cases.

125

Name 4 connective tissue diseases mentioned in the notes?

autosomal dominant polycystic kidney disease, ehlers-danlos syndrome type IV, mafrans syndrome, fibromuscular dystrophy.

126

What is ehlers-danlos syndrome type IV like?

weakened linings of blood vessels, easy brusing, thin translucent skin, minimal joint hyperextensibility.

127

Name 2 theoretical risk factors of CAD?

elevated homocysteine levels, A1-antitrypsin deficiency.

128

What will happen with elevated homocysteine levels?

Linked to disruption of the collagen and elastin in the arterial wall which increases wall fragility.

129

What is the job of A1-antitrypsin?

TO maintain integrity of connective tissue.

130

What are the signs and symptoms of a vertebrobailar ishcemia?

5 D's And 3 N's. Diplopia (doulbe vision), Dizziness (vertigo, light-headedness), drop attacks (collapse suddenly), dysarthria (speaking problems), Dysphagia (cant swallow), Ataxia of gait (unstable gait), Nausea, numbness, nystagmus (jerky movemnts).

131

What are the signs and symptoms of carotid artery ischemia?

Confusion, dysphasia, headache anterior neck and or facial pain, hemianesthesia, hemiparesis or monoparesis, visual field distrubances.

132

Is it possible to determine through physical examination or testing those rare patients who are at risk of vertebral arery injury?

No.

133

If a patient has responeded well to cerivical manipulation will this decrease the risk of Cerebral artery complications?

no.

134

What tests can be done to determine if a patient is having a stroke?

have the patients; smile, raise both arms, stand steady on both feet with their eyes closed, speak simple senetences with several vowels that run together like simple simon says, stick out their tounge.

135

What should you do if you suspect the patient is having a stroke?

Place the patient on a flat surface lying on their side and call 911 and tell them you have a patient with a suspected stroke, their age, time of onset, and any known medical history. Do not give them anything to eat or drink, DO NOT allow any patients that improve spontaneously to go home.

136

The cervical region of the spine is important in what things?

Vision, balance, hearing.

137

Why is the cervical spine a common site of compenstation?

The end of the kinetic chain.

138

What is the normal curve of the cervical spine like (degrees)?

Lordotic at 30-40 degrees. Can be up to 47 in males and down to 32 for females.

139

What will help determine the cervical lordotic curve?

Facet angle and pillar height.

140

What is more common the hyper- or hypo- lordotic cervical curve?

Hypolordotic is most common.

141

A hyperlordotic cervical curve can occur from what things?

Osteoporosis, hyperkypotic thoracis.

142

What will happen with a hyperlordotic cervical curve?

Posterior disc compression, tensile stress anteriorly, shortening of posterior musculature, predisposition to facet syndrome.

143

What are 4 things that can lead to a hypolordotic cervical curve?

1. Congenital (hyperplatic pillars). 2. Compensational (for flat back posture). 3. Post-traumatic (CAD). 4. Antalgic (CAD, facet syndrome).

144

What will happen with a hypolodrotic cervical curve?

Anterior disc compression, tensile stress on posterior ligaments and stuff, increased work load on paravertebral muscles leading to anterior head carriage, shortening of anterior cervical muscles, decreased shock absorption, protective muscle splinting.

145

How many degrees are in normal cervical flexion?

60 degrees.

146

How many degrees are in normal cervical extension?

75 degrees.

147

How many degrees are in normal cervical lateral flexion?

45 degrees.

148

How many degrees are in normal cervical rotation?

80 degrees.

149

How much rotation of the 80 degrees of cervical area comes from C1-2?

40 degrees.

150

What will non-segmental muscles do vs. segmental muscles in the cervical area?

Non-segmental- Global movement as a result of the head's moving in relation to the trunk. Segmental- coordinates and integrates segmental motion acting as involuntary integrators of overall movement.

151

What muscles will be more likely to cause static listings the non-segmental or segmental?

Segmental.

152

What is the most complex and unique and specialized area of the spine?

Upper cervicals (C0-2).

153

What is the dichotomous function of the upper cervicals?

Mobility and stability.

154

Name 3 reasons the upper cervicals are often an area of complaint?

site of compenstation (end of kinetic chain), commonly associated with cervicogenic headaches, common site of injury.

155

What is the neurological significance of the upper cervicals?

ligamentous injury- brain stem location. Reflex and proprioception- cervicogenic vertigo.

156

What are the occipital condyles like?

convex, face laterally, wider posterior narrower anteriorly, converge anteriorly.

157

What are the atlas facets like?

Concave, face medially, slightly wider posterior, converge anteriorly.

158

What is flexion/extension like at C0-1?

Greatest range in cervicals with a combined 25 degrees (much more extension than flexion).

159

Where is the IAR of flexion/extension of C0-1?

Just behind the odontoid.

160

What is the pattern of movement for flexion/extension of C0-1?

sagittal plane, paradoxical movement of the occiput.

161

What is paradoxical movement of the occiput? What causes it?

During cervical flexion a large % of the population will extend at C0-1 at the end range of cervical flexion. Results from tension in the posterior cervical muscles and possibly of the nuchal ligament.

162

How will the joints move for flexion/extension of C0-1?

Flexion- Posterior joint surface of C0 glides up the articular surface of C1 as the anterior surface glides down and the gap widens between the occiput and the posterior arch of the atlas while the occiput rolls anteriorly and slides posteriorly. Extension- the opposite happens.

163

What is lateral flexion of C0-1 like (degrees)?

5 degrees to each side. Limited by the alar ligament.

164

What is the IAR for lateral flexion of C0-1?

midway between odontoid tip and EOP.

165

Where will motion of lateral flexion of C0-1 happen at?

Coronal plane, coupled with contralateral rotation.

166

What happens at the joints with lateral flexion of C0-1?

Lateral-flexion side- articular surface of C0 is gliding down the articular surface of C1 as the side opposite the lateral flexion is gliding up. The occiput is rolling toward the side of lateral flexion and sliding to the opposite side. Side opposite lateral flexion- opposite movements are happening.

167

What is rotation like (degrees) for C0-1?

average 5 degrees to each side, and is limited by articular anatomy and connections to the alar ligaments.

168

What is the IAR for rotation of C0-1?

Undetermined.

169

Where will rotion of C0-1 rotation happen at?

At the end of cervical rotation.

170

What is happening at the joints of C0-1 with rotation?

Side of rotation- C0 articular surface slides posterior and superior on the articular surface of C1. Side opposite rotation- it slides anterior and superior.

171

What is the articular surfaces of C1-2 like?

two facet joints plus the atlas odontoid joint.

172

What are the planes of the C1-2 facets like?

Mostly horizontal.

173

What will the C1-2 facets often be like?

Asymmetrical.

174

What are the inferior facet of C1 and the superior facet of C2 like?

C1- circualr shape, slightly convex, directly below the superior facets, face inferior and medially. C2- Oval shaped, slightly convex, face superior and laterally.

175

What are the articular surfaces of the atlas odontoid joint like?

anterior arch is a synovial joint. Gutter- is the posterior joint and it is fibrocartilage and made up of the transverse ligament.

176

What will surround the dens?

anterior- anterior arch (anterior joint), Laterally- lateral masses. Posteriorly- transverse ligament.

177

What is the gutter joint of the dens like?

Imbedded in fibroadipose and tissue and lacks a capsule.

178

What is flexion/extension like at C1-2?

combined 20 degrees.

179

What is the IAR for flexion/extension of C1-2?

Middle thrid of the dens.

180

Where will the flexion/extension of C1-2 happen at?

angular sagittal plane coupled with saggital plane translation. Checked by dens and transverse ligament.

181

What happens at the joints with flexion/extension of C1-2?

Flexion- posterior joint surfaces and posterior arches separate as the atlas articular surfaces slide posteriorly. Extension- approximation of posterior joint surfaces and posterior arches as the atlas articular surfaces glide anteriorly.

182

What is lateral flexion of C1-2 like (degrees)?

Limited active range, but averages 5 degrees to each side.

183

What is the IAR of lateral flexion of C1-2?

Undetermined.

184

Where will lateral flexion of C1-2 happen at?

Coronal plane angular movement with translation in the coronal plane towards the side of lateral flexion.

185

What is happening at the joints of C1-2 with lateral flexion?

C1 articular surfaces translate on the C2 articular surface toward the side of lateral flexion. There may be some very slight tilting between the joint surfaces.

186

What is rotation like (degrees) for C1-2?

Very mobile. 40 degrees each side.

187

The first ____ degrees of cervical rotation occur exclusivley at C1-2.

25 degrees.

188

Where is the IAR of C1-2 rotation?

vertical axis of the dens.

189

_______ movements of the upper cervical spine are unusual.

Isolated.

190

How is flexion and extension done for the cervicals?

Flexion- initiated by anterior concentric activity and guided by posterior eccentric activity. Extension- initiated by concentric activity and guided by eccentric activity.

191

The capsular ligaments of the cervical spine allow for what and limit what?

Allow for rotation and limit lateral flexion.

192

How is rotation done in the neck?

combination of concentric and eccentric activity.

193

What angle are the articular facets like in the lower cervicals (C3-7)?

45 degrees with the horizontal plane.

194

What is the disc to body ratio for cervicals, lumbar and thoracics?

Cervical- 2:5. Lumbar- 1:3. Thoracic- 1:5.

195

In general what is flexion and extension like in the lower cervicals (degrees)?

about 15 degrees per segment, but kind of like a bell curve being largest in the middle with 20 degrees.

196

What is the motion of flexion/extension like in the lower cervicals?

coupled translation is greater in the upper cervical spine than it is in the lower leading to a steeper arch of movement in the lower as compared to the upper.

197

During lower cervical extension what is compression like?

Anterior disc distraction, posterior compression. Facets approximated leading to maximal compression is at the inferior margins with some distraction at the superior margins.

198

What is lateral flexion like in the lower cervicals?

lateral bending coupled with ipsilateral axial rotation. The degree of coupled rotation decreases in a cephalic to caudal direction.

199

What is rotation like (in degrees) in the lower cervicals?

About 5 degrees to each side.

200

Name the muscles that can do contralateral rotation of the cervicals?

Semispinalis, SCM, Multifidus.

201

Name the 3 ligaments that limit flexion in the neck?

Nuchal, PLL, Flaval.