Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
71 Cards in this Set
- Front
- Back
|
how do you test biceps deep tendon reflexes? Which nerve root is tested?
|
: tap your thumb with reflex hammer while thumb is on pt's biceps tendon.Tests primarily C5 (with some C6) neurological level
|
|
|
How do you test brachioradialis reflex? Which nerve root is tested?
|
tap brachioradialis tendon at distal radius
Tests primarily C6 (with some C5) neurological level |
|
|
How do you test triceps reflex?Which nerve root is tested?
|
tap triceps tendon where it crosses ocecranon fossa. Tests primarily C7 (with some C8) neurological level
|
|
|
How are deep tendon reflexes documented?
|
on a scale of 0-4. 0= no response, 1-3 are all possibly normal. (1 is slight response, 3 is very brisk response)
4=a repeating/clonus reflex= always abnorma. |
|
|
What type of mechanics does the OA joint follow?
|
modified type I mechanics (atypical cervical vertebrae)
primary motions are flexion and extension |
|
|
Lateral translation test for OA joint
|
Pt lying supine. Dr sitting or standing at head of pt.
1. Grasp head with both hands, with tips of fingers 2 and 3 over occipital articulation 2.Translate head to right and left with head in neutral, noting any restriction of translation. (Restriction of trans to the R = SB R (hence rotated L), and vice versa) |
|
|
Rotational test of OA joint
|
palpate occipital ridge, note TART findings, compare side to side. hard end feel on one side indicates a rotation to that side.
Now to motion test for rotation and sidebending. PASSIVE test. Now flex head through occiput (not entire C-spine) and not any change in rotation. Increase in rotation during flextion indicates restrictive barrier to flexion=Extension dysfunction |
|
|
Chin nodding test for OA joint
|
1. Have patient nod head (flexion) THRU occiput.
2. Note any rotation of the mentum to right or left. 3. Rotation to the right during flexion indicates an OA rotated to the right with a restrictive barrier to flexion - OA E RrSBl 4. Then check in extension to determine any restrictive barriers. (i.e. rotation to one side during extension denotes OA rotated toward that side with a restrictive barrier to extension- OA F RRSBL |
|
|
What is the primary motion of the AA joint? (Axis-Atlas)
|
The atlas rotates in relation to the axis. It can become restricted in rotation. (Primary motion is rotation)
|
|
|
Atlas motion test
|
Pt supine, Dr sits or stands at head of patient.
1) Grash head with fingertips contacting lateral mass of the atlas 2) Flex the C-spine (this locks C2-7 isolating rotation to the atlas) 3) rotate head bilaterally, assessing ROM and freedom 4) Greater rotation to R implies restriction of L rotation. *Flexion and SB are not tested here |
|
|
What kind of mechanics do C2-C7 follow
|
Modified type II mechanices. typical cervical vertebrae
|
|
|
C2-C7 motion testing. Describe testing flexion and extension.
|
Difficult to asses flexion/extension at the segmental level, so done via lateral translation test.
|
|
|
C2-C7 motion testing. Describe testing sidebending/lateral translation test
|
1) support pts head with your hands while palpating lateral borders of the articular pillars
2) localize force to one segment, and test L and R lateral translation (note the end feel. if translates more freely to Left then it is SB right and rotated right) 4) now extend C-spine through the segment and repeat test. (hard end feel in extension=flexion dysfuntion/stuck in flexion) |
|
|
Rotation test of C2-C7.
|
1) test by rotating one segment at a time
2) rotational movement should follow the planes of the facets 3) testing force is directed up towards eye for upper cervical vertebrae and towards opposite ASIS for lower cervical vertebrae. NOT in a horizontal plane* unrestricted segment should rotate equal bilaterally. Test in flexion and in extension and in neutral. (worse in extension=flexion dysfunction) |
|
|
when testing rotation of C4 you find a restriction of right rotation....
|
the vertebrae is rotated left and side bent left (restriction of right rotation and right sidebending)
|
|
|
when testing lateral translation of C3 you find it translates more freely to the left...
|
this means the segment is SB right and rotated right. (type 2 goes same direction.)
|
|
|
how to decide which HVLA technique to use for treatment.
|
take segment with most significant dysfuntion in typical C spine. Figure out if SB component has harder end feel, if so use SB HVLA to correct. If the rotational componenent has a harder end feel use rotational HVLA.
|
|
|
Which Cervical vertebrae tend to have SB component dysfunction? Which have rotational component?
|
Usually C2-C3 have rotational component predominating and C4-7, SB comp. pred
|
|
|
Which vertebra is C1
|
atlas (TOP)
|
|
|
which vertebra is C2
|
axis
|
|
|
what plane do the cervical facets lie?
|
the upper ones are in a plane that points towards eye, lower facets plane points towards the opposite ASIS
|
|
|
what are the major motions of the OA joint
|
flexion and extension. (SB and rotation are minor)
|
|
|
what is the primary motion of the atlantoaxial joint?
|
rotation. Atlas rotates around the dens. almost no SB or flexion/extension
|
|
|
describe the coupled motion of typical cervical segments (C2-C7)
|
rotation and SB to same side. Modified type II mechanics. (some have found clinically SB and rotation to same side, which would be type I)
|
|
|
HVLA for AA
|
rotate opposite
|
|
|
HVLA for OA
|
thrust toward eyes
|
|
|
HVLA for typical C-spine (C2-C7)
|
SB focus= towards T1 spinous process
rotational focus= use Rays of sun |
|
|
HVLA contraindications
|
RA and Down syndrome (weak odontoid ligament susceptible to rupture)
Known PVD or risks, known osteoporosis or risks, PTs on anticoagulants (shear stress=intracranial bleed) |
|
|
most frequent serious complications results from HVLA to C-spine. list a few
|
occipitobasilar strokes (Wallenberg syndrome)
Vertebral artery compression with thrombosis arterial dissections cerebellar infarcts |
|
|
what is the primary cause of HVLA complications?
|
rotation of c-spine when already extended. Right rotation occules left vertebral artery. (commonly age 35-40)can also have problems if you flex and rotate pt with buldging disc
|
|
|
What brings more risk of vertebral artery dissection than HVLA?
|
daily activities, spontaneous vertebral artery dissection with normal motion such as looking over the shoulder.
|
|
|
Whiplash
|
generic term used for hyperflexion-hyperextension injuries of c-spine. usually due to MVA (7mph speeds can cause tissue damage)
|
|
|
evaluation of whiplash patients include
|
MOI, predisposing factors, neuro deficits, structural deviations, somatic dysfunctions, syhmpathetic hyperactivity
|
|
|
MOI from whiplash
|
Impact that produces the injuries propels
body in a linear horizontal direction – Head momentarily remains stationary – Then abruptly moves in opposite direction of impact force vector – Cessation of impact, combined with an acute stretch reflex, causes recoil in same direction as initial force vector |
|
|
which movement causes greater injuries? Hyperextension or hyperflexion?
|
hyperextension. Flexion is limited by chin on chest, nothing except back of seat restricts extension
|
|
|
why are there no immediate signs/symptoms of a whiplash injury
|
the injuries are microscopic and no major nervous structures initially injured so no immediate S/S.
|
|
|
what is the first muscle to become injured in a whiplash injury
|
Sternocleidomastoid. can develop head tilt and painful torticollis. (deeper muscles next, scalenes and longissimus colli. Lastly pharynx, esophagus and prevertebral fascia are injured)
|
|
|
what are the posterior muscles that can be injured in whiplash injury?
|
suboccipital muscles=rectus capitis major and minor, semispinalsis capitis, splenius capitus.
intrinsic muscles=multifidus and rotator muscles shoulder girdle muslces=levator scapulae, rhomboid, trapezius |
|
|
hyperextension
|
• Strain/tearing of anterior longitudinal ligament
• Vertebral body or spinous process fracture • Facet encroachment due to posterior glide |
|
|
hyperflexion
|
• Sprain/tearing of supraspinal, intraspinal, or posterior
longitudinal ligaments • Capsular tears +/- facet subluxation or dislocation • Rarely, posterior disc herniation |
|
|
what causes much of the cephalgia and neck pain associated with whiplash?
|
chronic irritation as perineural scar tissue forms. Greater and lesser occipital nerve and suboccipital nerve (C1-C2) irritation.
|
|
|
sympathetic nerves in whiplash
|
cervical nerves connected to sympathetic system via preganglionic fibers in lateral horn cells from T1-T6
|
|
|
what symptoms appear from sympathetic nerve injury in whiplash?
|
aural symptoms (tinnitus, deafness, postural dizziness)
ocular symptoms (blurred vision, retrolobular pain, pupil dilation with turning of head) vestibular (vertigo) |
|
|
vascular system injury with whiplash. at which specific level usually?
|
vertebral artery compression and spasm. usually at C1-C2 level where it makes acute turn to enter skull. (vertigo, syncope, near syncope, nystagmus with head rotation)
|
|
|
cerebral concussion
|
impact of brain against vault. head trauma is not necessary for concussion. pts often describe bliding or exploding sensation in head at time of injury. immediate HA, resllessness, insomnia, mood changes
|
|
|
bracing hands on steering wheel
|
reduces anterior translation of body
|
|
|
awareness of impact
|
tension of muscles reduces excess motion of head and reduces degree of injury
|
|
|
often the head is somewhat turned to one side on impact
|
rotation narrows foramen on side which head is turned, reduces physiologic range of extension. some believe increases risk of fracture
|
|
|
Sacral injury in whiplash injury
|
during injury sacrum is lifted and moved from its postition then rebounds and lodges at verying degrees.
|
|
|
pelvic injury in whiplash injury
|
ilial rotations and pubic shears frequently occur. due to fact that usually only one foot is planted. (braking)
|
|
|
thoracic and lumbar injuries in whiplash injury
|
interconnection of musculature and ligamentous structures. forces acting upon the areas with anterior translation of the body upon impact
|
|
|
cranial injury with whiplash injury
|
as a rule, occiput and sacrum exibit same restriction. (flex or ext, Right of Left)
asymmetric contraction of attaching muscles results in torsions and sidebending or rotatory dysfunction |
|
|
upper extremity injury in whiplash injury
|
usually from bracing against steering wheel. soft tissues of shoulder, local dysfunction in hands, wrists and elbows.
|
|
|
lower extremity injury in whiplash injury
|
pain and decreased ROM due to sacral or iliac dysfunctions as well as iliopsoas strains. inj to foot, knee, ankle, pelvic fracture can occur if foot was firmly planted.
|
|
|
symptoms of whiplash
|
pain next day due to progression of swelling.
HA usually occipital and may radiate to the frontal region. some symptoms come in 2-3 weeks. sympatheic NS involvement... |
|
|
treatment for whiplash injury patient
|
individualized to pt and b y stage of recovery from injury. avoid treating just thoracic and cervical regions and overtreating injured tissues.
|
|
|
acute stage treatment for whiplash
|
OMT should be instituted ASAP after pt has stabilized.
minimize edema development and tissue reaction.. lympathic drainage, treat sacrum and cranium to restore motion |
|
|
adjunct treatments for acute stage whiplash
|
NSAIDS, Ice packs, ultrasound, immobilization if acute inflammatino and only in early stages, traction
|
|
|
physical activity in acute whiplash injury
|
severe injuries often requre 1-3 days bedrset, passive exercise in bed to prevent atrophy.
mod-mild injury=begin limited activities immediately as tolerated, passive ROM daily. avoid rapid movements of head |
|
|
treatment in early chronic stage (1wk-1mo) whiplash injury
|
acute inflammation has subsided, but increased muscle tension remains. OMT can be more aggressive now. ME and HVLA in thoracic and lumbar areas. ME to C-spine and vigorous lymphatic drainage. Also=moist heat, ultrasound, Estim, NSAIDs
|
|
|
at what point can you do HVLA on the C-spine for whiplash injuries?
|
late chronic stage. (1-3 months or longer)
|
|
|
predictors of pain in whiplash injury
|
pain at time of rear-end collision, presence of a compensation clain. (when compensation for pain is removed, pts improved)
|
|
|
what is the single best outcome predictor in whiplash injury
|
ROM of C-spine.
a study of 141 pts w acute whiplash, reduction in c-spine ROM was best predictor of long term handicap |
|
|
torticollis
|
torus=twisted
collum=neck cervical dystonia, wryneck |
|
|
torticollis, vs laterocollis, anterocollis and retrocollis
|
Torticollis=rotational twisting
lateral=lateral tilt anterocollis=flexion retrocollis=extension |
|
|
injury or malformation to sternocleidomastoid muscle which does not lengthen with childs growing neck
|
rare, congenital torticollis
|
|
|
causes of adult torticollis
|
very common, usually idiopathic but may be secondary to anything=sleeping wrong, strain at work...
|
|
|
what is klippel-fell syndrome?
|
fusion of 2 or more cervical vertebrae
|
|
|
treatment for congenital torticollis
|
stretching the SCM muscle. (if no response in 1-2 months refer to ortho)
1 hand stabilizes chest/shoulders, and other tilts head away from contracted ms and rotates chin towards contracted side, holding for 10 seconds, with 15 reps |
|
|
what meds can be used to treat torticollis
|
botox, anticholinergics, benzodiazepines, muscle relaxants
|
|
|
surgical treatment for torticollis
|
muscle resection, nerve ablation
|
