By Dr. Eugene Serafim
Dizziness is a nonspecific term that means various things to various people. It falls under a greater category of vertigo, but for our purposes we will concentrate on the subcategory of disequilibrium. This paper will review the origins, testing procedures as well as common disturbances of the physiologic and neurological systems that affect balance and contribute to disequilibrium. We will further concentrate on the familial link between structure and function of the cervical spine, and it’s pathogenesis of cervical disequilibrium in a mother and daughter case study.
Dizziness has a variety of meanings, but it is most often used as a means of describing unsteadiness. Notwithstanding layman’s terms; more specific identifiers are required, including: lightheadedness, pre-syncope, disequilibrium and vertigo. The diagnostic triage must include a thorough history, specialized testing, orthopedic and neurological workup to discern the specific symptom, correct diagnosis and optimal treatment. Allopathic medicine has traditionally addressed these symptoms pharmaceutically; however, a chiropractic/ rehab approach is successful in addressing the underlying structural root cause1. In this case study I cited; a mother/daughter case, both patients benefited from an approach using chiropractic and rehabilitation techniques. While this is not an exhaustive study, these cases provide an insight into the inherited structural or physiological etiology of disequilibrium.
In discussing balance and the loss of it (disequilibrium) we must start with reviewing the components that would affect it. Balance is accomplished through various systems that integrate in the cerebellum. Proprioception, vestibular, visual sensory input, and tactile sources combine to facilitate balance and coordination. Proprioception in the cervical spine provides sensory afferent input, which contributes to coordination of the eyes, head, and body.
Proprioception in the cervical spine is controlled by a variety of reflexes that include; the cervico-collic, the tonic neck reflex, and the cervico-occular reflex. Bolton states (Bolton, 1998); the first reflex stabilizes the head and integrates with the vestibulo-collic reflex (where the neck muscles are acted upon from the semi-circular canals). The tonic neck reflex is a asymmetrical reflex present in newborns, that controls the tonic activity of the limbs2. In discussing the tonic reflex, research by Hikosaka and Maeda (1973) documented the association of neck afferents originating at the dorsal roots and cervical facets at level C2/C3 and the vestibular nuclei3. These reflexes communicate with the vestibulo-ocular reflex.
When sensory input is interrupted, it causes a disparity in perceived information received from the vestibular, cervical proprioceptive or visual systems disequilibrium results.4 Research conducted by Dejong and Dejong further support this data.5
There are a number of differentials that should be excluded, before a diagnosis of cervicogenic disequilibrium can be assigned. Some diagnoses include; Benign Paroxysmal Positional Vertigo, Ménière’s disease, and Vertebrobasilar insufficiency.
Discerning between terminologies patients use to describe dizziness is another important aspect in evaluating a patient with unsteadiness. They include; presyncope, disequilibrium, vertigo, dystaxia, ataxia and light headedness. To further complicate matters, in its slang form, dizziness has been used to describe those that lack mentation.
Vertigo, cervical disequilibrium, lightheadedness, presyncope, dystaxia, ataxia, proprioception, cervico-collic, the tonic neck reflex and the cervical-ocular reflex
Dizziness—in general—is widely complained of and can have a component in virtually any medical condition. For our purposes we will only consider one symptom of dizziness; cervical disequilibrium. The diagnosis of cervicogenic disequilibrium is largely one of exclusion; thus, one should strive to rule out diseases of the inner ear(vestibule-cochlear apparatus), vertebral arteries and the spinal canal . Special attention must be paid to patients with a post traumatic onset. In those cases; vertebral artery compression and dissection, spinal stenosis, Cerebral Spinal Fluid leak, and of course whiplash should be ruled out, or referred to the appropriate provider before initiating a rehab protocol.
Evaluation of any disease begins with a thorough history; treating cervicogenic disequilibrium must include a detailed history. Special interest would include: the onset, duration, trauma, description, intensity, mechanism, previous treatment, cause, previous history, aggravating Factors(positional relation), relieving factors, environmental related triggers, previous episodes, effects on ADL’s, and functional deficits.
Outcome assessments provide a qualitative baseline to allow for accurate case management. They also measure pain, disability, and psycho-social status. Questionnaires that measure pain would include; Visual analog scale, McGill, and Pain drawing. For disability; Neck disability index, The Dizziness Handicap Inventory, The Henry Ford Headache Disability Inventory (HDI ), Activities-specific Balance Confidence scale (Powell), Somatic Perception and PARQ. Psychosocial assessment would include Beck and SCL-90-R.
Orthopedic, Functional, and neurological testing must be combined to comprehensively evaluate a patient with cervicogenic disequilibrium. The orthopedic testing that would be appropriate would include:
- Jackson’s, Bakodys,
- Cervical distraction,
- Dix-Hallpike maneuver,
- Barany-caloric test,
- Hoffman’s sign,
- The Vertebral artery test,
- Rapid alternating movement (diadochokinesis),
- Saccadic and smooth pursuits eye movements
Functional testing would include;
- Berg balance scale
- The Clinical Test for Sensory Interaction in Balance
- Postural analysis and Gait analysis,
- Platform stabilometry7
- Cervical flexion test8
- Jull’s cervical cranial test(to quantify)9
- T4-T8 mobility test Wall Angel10
- Hautant’s test12
- Rotating stool test13
Neurologic testing would include cranial nerves (especially auditory), pathologic reflexes, deep tendon reflexes, sensory dermatomes as well as gait and station. Diseases of the brainstem (central lesion) affecting the vestibule-cochlear nerve will too affect adjacent cranial nerves (VII and IX).
Physical examination should focus on the vitals, with special attention being paid to the Vitals and Auscultation exam to rule out arrhythmias, stenosis, prolapsed, or congestive issues. Blood pressures should be assessed bilaterally as well, going from sitting to standing and laying down to standing.
Specialized testing for dizziness should rule out:
- Vetebrobasilar insufficiency
- Menierre’s disease
- Benign paroxysmal positional vertigo (BPPV)
Such specialized testing could include but not be limited to:
- Rotary chair testing
- Trans-cranial Doppler sonography
- MRI angiogram 14
- CSF leakage, hypoglycemia, as well as cardiovascular disorders. , ,
- Cervical and cranial MRI’s.
- Electrolyte Panel- disturbance of the acid base balance could lead to dizziness15
- Coagulation Profile and Lipids-to evaluate vertebra-basilar disorders16
- Serology-to rule out infectious diseases including syphilis and Lyme’s17
Case report 1
A 76 year old woman reported with a chief complaint of sub-occipital neck pain, head ache, and stiffness complicated by dizziness that is position aggravated. She notices it the most while flexing her head forward to putt during golf. It presents intermittently, and its duration can last anywhere from 3 days to 3 weeks. She reports suffering from the stiffness and dizziness for the better part of her adult life. Her sedentary computer occupation worsens her neck pain and stiffness. Movement of the head (especially ballistic) seems to increase her unsteadiness. She experiences feelings of movement from side to side and denies spinning (disequilibrium). She denies any tinnitus or obvious hearing deficit. These problems limit her daily living activities when the unsteadiness is at its worst (difficulty standing). She is also disabled from playing golf during these episodes. She had not sought treatment for this problem in the past. Disability indexes were assigned including:
- Neck disability index(46%[moderate}),
- Dizziness Handicap Inventory
- The Henry Ford Headache Disability Inventory (HDI )(10 on the emotional subscale and 25 on the functional subscale),
- Activities-specific Balance Confidence scale(Powel)rated at 75% episodically
- PARQ (cleared)
- Red Flags (yes to over 50 and 70 years old).
Psychosocial assessment included
- Beck(10 not depressed or mildly)
- Modified Somatic perception questionnaire(13high level of somatic complaint)
The patient could not relate, or report any family or social history that would apply to her complaint. The clinical impression was Ataxia, disequilibrium, and cervical spasm. Her working diagnosis was cervical disequilibrium related to functional disturbance.
Her evaluation was as follows; Vitals 5’9”, 128 lbs, 130/86 R, 128/80 L(B/L B.P.), (pulse)50 bpm, 99.0 F,(temp.), 15 breaths per min(resp.). No change in B.P. found in sit to stand or lye to stand.
Auscultation of the carotids and Inferior vena cava were normal. Observation showed a well formed, aware and alert 76 year old female. Percussion reveals tender paravertebral musculature at the occiput, cervico-thoracic junction, and the lumbo- sacral junction. Palpation reveals myo-facial trigger points at the occiput, levator scapulae, SCM’s, lumbar erector spinae, and gastrocs/soleus. All findings were B/L. Cervical spine X-ray examination confirmed a decreased cervical spine lordodic curve and generalized spondylosis C3-T1. Cervical ROM was found to be minimally limited in right lateral flexion, extension, and right rotation. Lumbar ROM was minimally limited in flexion and B/L lateral bending.
Postural analysis yielded; rounded shoulders, anterior lean, anterior head carriage, head tilt to the left, decreased cervical lordodic curve, dowagers hump, decreased lumbar lordotic curve, and posterior pelvic tilt. Chiropractic examination revealed shortened/facilitated SCM’s, levator Scapulae, scapular retractors, hamstrings, and gastroc/soleus complex. Lengthened/inhibited muscles included Cervical and lumbar erectors, longus coli, knee flexors, and pectoralis. Subluxation complexes were found at Occiput (inferior) C2 (right rot. restriction) T1 right lat flex restriction) L4 left rotation restriction and a right PI pelvis.
Examination began with a neurological exam including; cranial nerves (within normal), sensory dermatomes (within normal), pathological reflexes(absent) and deep tendon reflexes(+2/5 upper and lower B/L). Orthopedic examination consisted of Cervical compression(negative with pain), Jackson’s(negative with pain), Cervical distraction(negative), Berrie-Lou(negative), Deklines(negative), Maignes(negative), Dix-Hallpike maneuver(positive), Hoffman’s sign(absent), Rhombergs(positive), The Vertebral artery test(negative), Rapid alternating movement [(diadochokinesis)negative], Lhermitte’s(negative), saccadic and smooth pursuits eye movements(negative) and the swivel chair test(negative) . During Functional testing chin pointing was observed in the supine neck flexion test, disequilibrium with the sit to stand test worsening towards the 5th repetition, a medium fall risk (35/56) on the Berg standing18 , Clinical testing of sensory interaction for balance19 failing the 5th condition (eyes closed on unstable surface) within 5 seconds, gait analysis ataxia was noted with a wide stance being used. Functional analysis of respiration revealed paroxysmal breathing patterns. One legged standing (failed at 6 sec R 4 sec L). Other functional activity testing revealed scapular winging and altered scapular abduction. No specialized testing was performed at the time as no underlying pathology was suspected. The patient’s primary diagnosis was Layered syndrome, her secondary diagnosis was cervical disequilibrium and her tertiary diagnosis was cervalgia. Complicating factors included subluxation complex (full spine),cervical spondylosis, myofascial pain syndrome, altered gait, muscle weakness, muscle imbalance, and diminished proprioception.
Treatment consisted of passive care for the initial 2 weeks of care that included electro-therapies, soft tissue work, and manipulation 3 times a week. After the acute care thresholds were passed, transitional care was provided for an additional 6 weeks. It included facilitated stretching techniques, myofascial trigger point therapy, and non weight bearing short foot protocol on balance pads and pelvic stabilization protocols. Active care was initiated next, and included weight bearing Proprioceptive protocols, postural retraining (passive and active) as well as home exercises. The active care lasted 12 weeks at a frequency of 3 times a week.
Outcomes were measured at 2 week intervals and dictated the transition of care. Her Disability indexes improved consistently. Post 4 weeks [(neck disability index20 32%, The Henry Ford Headache Disability Inventory21 (HDI) (10 on the emotional subscale and 15 on the functional subscale), Activities-specific Balance Confidence scale222 (ABCl) rated at 50%. ABC assessment was most profoundly influenced by the active phase of rehab (25% at 6th week of active care). Other benchmarks for advancing stages of care included performance of orthopedic and functional testing.
|Initial||2 weeks||4 weeks||6 weeks||8 weeks||12 weeks|
|1 leg bal.||10 sec R 6 sec L||8 sec R 14 sec L||15 sec R 22 sec L||25sec R 33sec L||40 sec R 38sec L||40 sec R 46 sec L|
At the completion of her 12 week rehab protocol, the patient was able to perform Rhomberg’s with an acceptable level of sway, and their one legged balance had improved from 6 sec. to 72 sec. R, performance of functional activity improved in the neck flexion test, improved breathing patterns and the squat (improved forward lean). Postural analysis showed a marked decrease in the upper cross syndrome. She complied with her home exercise protocol as well as the sparing strategies issued for her work. At that point she was released from active care and was told to return PRN.
Case Study 2
A female 42 year old related family member (to the first patient) presents with a similar complaint of suboccipital neck pain, dizziness and headaches with a 14 year duration. Her complain has no vector of injury or known causative factor. She suffers from her pain and unsteadiness intermittently, and it persists for weeks at a time. She admits to an average of one attack per month, and relates her problem to work and emotional stress. Her work is a sedentary office position, she is an entrepreneur. She describes her dizziness as an unsteady feeling, a sensation of movement from side to side. This is exacerbated with rapid head movements and laying to sitting. It is an intense sensation which severely affects/limits her daily life. She denied any hearing difficulties or ringing in the ears. Outcome assessment in the form of Neck disability index [54%(moderate)], Pain disability questionnaire (60/180 ), The Henry Ford Headache Disability Inventory (HDI )(14 on the emotional subscale and 20 on the functional subscale), Activities-specific Balance Confidence scale(ABCl) 23rated at 36% and PARQ(all no’s) were performed during an episode. Family history was relevant due to the obvious similarities to her mother’s complaint. All other familial and social factors were denied. She had not seen any other provider for this problem. The clinical impression was postural overuse, psycho-somatic pain, dysmetria, and disequilibrium.
Her evaluation was as follows; Vitals 5’11”, 147 lbs, 146/72 R, 140/78 L(B/L B.P.), (pulse)72 bpm, 97.0 F,(temp.), 15 breaths per min(resp.). No change in B.P. found in sit to stand or lye to stand. Auscultation of the carotids and Inferior vena cava were normal. Observation revealed a well formed but distressed 42 y.o. woman. Percussion to the spine reveals tender musculature at the occiput, cervico-thoracic junction and the lumbo- sacral junction. Palpation showed active myo-facial trigger points at the occiput levator scapulae, SCM’s, rhomboids, lumbar erector spinae, psoas and plantar muscles. All findings were B/L with the exception of the L lateral head tilt. Cervical spine X-ray examination confirmed a “military spine” and mild spondylosis C5-C7. ; Cervical ROM was found to be minimally limited in right lateral flexion, extension and right rotation. Lumbar ROM was minimally limited in extension and mildly in flexion. Postural examination revealed forward head carriage with a left head tilt and rounded shoulders. Chiropractic exam showed shortened SCM’s, levator scapulae, upper trapezius, pectorals, anterior deltoids, psoas and hamstrings. Segmental dysfunction was noted as follows; Occiput (inferior) C2 (right rot. restriction) C6 and C7 right lat flex restriction) L5 left rotation restriction and a anterior sacrum.
During neurological examination she showed no pathologic reflexes, all deep tendon reflexes were +2/5 B/L, cranial nerve examination was within normal limits and sensory dermatomes were intact. Orthopedically she tested positive to Dix-Hallpike maneuver and Rhombergs. Previously mentioned testing was performed and found to be negative. Functional testing included ;chin pointing observed on curl up, disequilibrium with the sit to stand test worsening towards the 2nd repetition, a medium fall risk(35/56) on the Berg standing24, Clinical testing of sensory interaction for balance25 failing the 5th and 6th condition(eyes closed on unstable surface and under the dome ) within 5 seconds. Gait analysis showed toeing out. Functional analysis of respiration revealed paroxysmal breathing patterns. Scapular winging and altered scapular abduction were noted in the push up and shoulder abduction respectively.
Primary diagnosis was Upper Cross syndrome, Secondary diagnosis was Cervical disequilibrium and Tertiary diagnosis was Cervalgia. Her complicating factors included: psycho-somatic stress, myofascial pain syndrome, subluxation complex, muscle imbalance, muscle weakness, diminished proprioception and altered gait.
Acute care included management of myofascial pain through electrotherapies, trigger point compression, spray and stretch techniques, PIR stretching diversified CMT as well as contrast treatment. Transitional care focused on patient reactivation, and included gait training, PNF stretching, pelvic stabilization, scapular stabilization, postural retraining, and sparing strategies at home and work. Active care included isometric to isotonic strengthening and closed chain kinematics (from supine to prone, to quadruped then seated to standing). We also provided Ergonomic analysis, coping strategies (to address the bio-psycho-social aspect and limit chronicity) and a home stretching and strengthening routine.
Treatment was initiated at a 3x a week frequency; passive care lasted 3 weeks. Transitional care was rendered at 2x’s per week (2 weeks) and active rehab was 2x’s per week (6 weeks). Outcome measures were given every 2 weeks, and were compared to clinical benchmarks to progress the patient through the phases of care. Her pain and disability showed improvement subjectively, and on the Neck disability index they improved on the 4th week assessment (35%). Her disequilibrium and headaches, did not respond until the 4th week of active rehab. At the end of her treatment protocol her outcome assessments were: Neck disability index[20%(moderate)], Pain disability questionnaire (30/180 ), The Henry Ford Headache Disability Inventory (HDI )4 on the emotional subscale and 10 on the functional subscale), and the Activities-specific Balance Confidence scale(ABCl)26rated at 65%(administered during an episode). Repeated Functional testing confirmed her improvement with a low fall risk(45/56) on the Berg standing27, Clinical testing of sensory interaction for balance28 failing the 5th and 6th condition(eyes closed on unstable surface and under the dome )after 35 seconds, and improved posture and gait( improved head and shoulder carriage and no toeing out on gait. She was released to PRN care, and was instructed to return if her symptoms reappear.
|Initial||2 weeks||4 weeks||6 weeks||8 weeks||12 weeks|
|1 leg bal.||6 sec R 4 sec L||8 sec R 7 sec L||33 sec R 22 sec L||59 sec R 55 sec L||40 sec R 56 sec L||72 sec R 66 sec L|
Treatment protocols and benchmarks
The patients’ short term goals included: stretching shortened facilitated muscles and activating inhibited muscles (PIR), decreasing myofascial trigger points, improving subluxation complex, instruct positions of comfort, and decreasing pain.
The Intermediate goals centered around early reactivation include: postural re-education, stretching shortened facilitated muscles, activating inhibited muscles (PNF, Flex building), improve proprioception (non weight bearing), improve core stabilization (via breathing techniques), monitor and track progress via outcome assessment, and rule out vestibular dysfunction. Considering the patient’s complicating factors, we initiated sparing strategies according to the patients A.D.L.’s.
Long term goals would include home/self care activities, and Stage 1 active rehab-Core and postural stabilization; They enhance disequilibrium through improving faulty mechanics/postural imbalances, propriosensory retraining, a system of exercises that utilize balance boards, balance beams, rocker boards, wobble boards, and balance shoes29. Increased Proprioceptive input (weight bearing), improved coordination/integration of the vestibular, ocular and tactile sources of balance (via closed chain kinematics, unstable surfaces). Stage 2 active rehab-Endurance training, improves aerobic potential (brisk walk, HIIT30). Stage 3 active rehab-Strength training includes isometric protocols to improve functional reserve of strength in the postural muscles. Hettinger-Mueller protocols are instituted to create static strength at 2/3 maximum contraction, then they are graduated to multiple angles; Isotonic strength is the next progression31, D.A.P.R.E. protocol is used. The adaptation in the D.A.P.R.E. protocol makes it ideal for the rehab setting32. Stage 4 active rehab-home protocol includes self care, which is administered in the form of a home exercise routine that includes stabilization exercise, postural training, and applicable muscle lengthening procedures.
The similarities in these cases are by no means a quantitative measure of the effects of functional disturbances on the balance and stabilization systems of the body. They do however, provide a basis for further testing and a qualitative example of structure as it relates to function. The link between these two cases—while not genetic—still shared many of the postural and altered movement patterns. The shared link in these cases is the upper cervical dysfunction. Hulse has shown the relationship between upper cervical joint dysfunction and disequilibrium, and recommends an integrated approach.33 The aforementioned etiologies can prompt disturbances in the cerebellar integration of sensory afferents of cervical proprioception, as nociception can contribute to dysafferentation from the zygapophyseal joints.34
Chiropractic care and the rehab mindset in treating cervicogenic disequilibrium, is custom tailored to identify and address the root causes of this issue, and equally suited to alleviate the contributing factors. The advantage over other types of providers would be in the ability to treat, diagnose, and monitor simultaneously. The last of which is pivotal, as the complaint can constantly change when the treatment is implemented. The practitioner must be ready for an immediate unexpected reaction, therefore it is imperative that the practitioner rule out more sinister etiologies before instituting a conservative care program. In addition, one must be equipped with the diagnostic triage required in a working diagnosis. The distinction between central and peripheral lesions causing vertigo/dizziness must be accurately deduced and is a major differential in case management, that would determine conservative care vs. further investigation and outside referral.
Dizziness, and more specifically cervicogenic disequilibrium, is a complex and multifaceted issue with a very high prevalence. It is concluded that 23-30% of adults have experienced at least one episode of dizziness, and 3.5% of adults experience a chronic recurrent episode greater than a one-year duration by age 6535. Familial similarities (body-type, psycho-somatic stress and postural stress) can sometimes predispose a patient to functional disturbances. Disequilibrium can commonly be related to cervical dysfunction36, and manipulation is a safe37 and effective3839 way of restoring cervical function. The correct diagnosis along with a diversified approach that concentrates on addressing joint dysfunction, soft tissue changes, and functional disturbances can correct such issues. The rehab mindset including outcome assessment tools are essential in monitoring progress, establishing benchmarks, and justifying changes in the clinical protocols. Self care and stress management are other valuable tools in maintaining positive results.
Powell LE, Myers AM. The activities-specific balance confidence
(ABC) scale. / Gerontol. 1995;50A:M23-M34.
1 Hulse M, Holzl M. [The efficiency of spinal manipulation in otorhinolaryngology. A retrospective long-term study.]
2 Bolton, P, (1998). The somatosensory system of the neck and its effects on the central nervous system. J. Manip. & Physiol. Therapy., 21 (8): 553-563.
3 Hikosaka O & Maeda M, (1973). Cervical effects on abducens motor neurons and their interaction with vestibulo-ocular reflex. Exp. Brain Res.,18: 512-539
4 D. Boyling, G. Grieve & G. Jull, (2004). Grieve’s modern manual therapy: the vertebral column. Elsevier, 463pp.
5 De Jong P, De Jong M, Cohen B, Jongkees L. Ataxia and nystagmus induced by injection of local anesthetics in the neck. Ann Neurol, 1, 240-246, 1977
6 Shumway-Cook A, Horak FB. Assessing the influence of sensory interaction on balance: Suggestions from the field. Phys Ther. 1986; 1584-1550.
7 A.Bastos Evaluation of patients with dizziness and normal electronystagmography using Stabilometry. Rev Bras Otorhinolaryngology. V.71, n.3, 305-10, may/jun. 2005
8 C. Liebenson (Ed), Rehabilitation of the Spine. A Practitioner’s Manual. Lippincott Williams & Wilkins Philadelphia, Pennsylvania: 2007, 870 pp.
9 C. Liebenson (Ed), Rehabilitation of the Spine. A Practitioner’s Manual. Lippincott Williams & Wilkins Philadelphia, Pennsylvania: 2007, 872 pp.
10 C. Liebenson (Ed), Rehabilitation of the Spine. A Practitioner’s Manual. Lippincott Williams & Wilkins Philadelphia, Pennsylvania: 2007, 864 pp.
11 C. Liebenson (Ed), Rehabilitation of the Spine. A Practitioner’s Manual. Lippincott Williams & Wilkins Philadelphia, Pennsylvania: 2007, 862pp.
12 Lewit K. Manipulative Therapy in the Rehabilitation of the Motor System. Boston: Butterworths, 1985.
13 Fitz-Ritson D. Assessment of cervicogenic vertigo. J Manipulative Physiol Ther 1991; 14(3):193-198.
14 Rigmor M, et al. Magnetic Resonance Imaging Assessment of the Alar Ligaments in Whiplash Injuries A Case-Control Study. SPINE Volume 33, Number 18, pp 2012–2016, 2008
15 Labtestsonline. American Association for Clinical Chemistry. October 13, 2011
16 Merkmanuals online. E.A. Giraldo, MD. The Merk Manual for Professionals. April, 2007
17 Merkmanuals online. D.L. Tucci, MD. The Merk Manual for Professionals. January 2009
18 Berg KO, Wood-Dauphinée S, Williams JI & Maki B (1992). Measuring balance in the elderly: validation of an instrument. Canadian Journal of Public Health, 83 (Suppl 2): S7-S11.
19 Shumway-Cook A, Horak FB. Assessing the influence of sensory interaction on balance: Suggestions from the field. Phys Ther. 1986; 1584-1550.
20 Vernon H, Mior S. The Neck Disability Index: A study of reliability and validity. J Manipulative Physiol Ther 1991;14:409-415, Copyright Vernon H and Hagino C, 1990.
21 Jacobson GP, Ramadan NM, et al. The Henry Ford Hospital headache disability inventory (HDI). Neurology 1994; 44:837-842.
22 Powell, LE & Myers AM. The Activities-specific Balance Confidence (ABC) Scale. J Gerontol Med Sci 1995; 50(1): M28-34
23 Powell, LE & Myers AM. The Activities-specific Balance Confidence (ABC) Scale. J Gerontol
Med Sci 1995; 50(1): M28-34
24 Berg KO, Wood-Dauphinée S, Williams JI & Maki B (1992). Measuring balance in the elderly: validation of an instrument. Canadian Journal of Public Health, 83 (Suppl 2): S7-S11.
25 Shumway-Cook A, Horak FB. Assessing the influence of sensory interaction on balance: Suggestions from the field. Phys Ther. 1986; 1584-1550.
26 Powell, LE & Myers AM. The Activities-specific Balance Confidence (ABC) Scale. J Gerontol
Med Sci 1995; 50(1): M28-34
27 Berg KO, Maki BE, Williams JI, Holliday PJ, Wood-Dauphinee SL. Clinical and laboratory measures of postural balance in an elderly population. Arch Phys Med Rehab.1992; 73: lO73-lO8O.
28 Shumway-Cook A, Horak FB. Assessing the influence of sensory interaction on balance: suggestion from the field. Phys Ther. 1986;66: 1548-1550
29 Murphy, Donald, and Craig Liebenson. “Chiropractic Rehabilitation in the Treatment of Dizziness.” Dynamic Chiropractic. 1983. Web. 17 Nov. 2011.
30 Tabata I, Nishimura K, Kouzaki M, et al. (1996). “Effects of moderate-intensity endurance and high-intensity intermittent training on anaerobic capacity and VO2max”. Med Sci Sports Exerc 28 (10): 1327–30
31 Hettinger, T., and E.A. Muller 1953. Muscle strength and training. 15:111-26
32 T.Beacham & R. Earle. Essentials of Strength and Conditioning. Champaign: Human Kinetics. 2008. 536pp
33 Hulse M. Disequilibrium, caused by a functional disturbance of the upper cervical spine. Clinical aspects and differential diagnosis. Man Med 1983; 1:18-23.
34 Biemond A, De Jong JMBV. On cervical nystagmus and related disorders. Brain 1969; 92:437-458.
35 Ojala, M (1989). Etiology of dizziness: a neurological and neuro-otological study. Helsinki, University of Helsinki, Academic Dissertation.
36 Hulse M. Disequilibrium, caused by a functional disturbance of the upper cervical spine. Clinical aspects and differential diagnosis. Man Med 1983; 1:18-23.
37 Haldeman S, Kohlbeck FJ, McGregor M (1999) Risk factors and precipitating neck movements causing vertebrobasilar artery dissection after cervical trauma and spinal manipulation. Spine 24(8):785-94.
38 Spitzer WO, Skovron ML, et al. (1995) Scientific Monograph of the Quebec Task Force on Whiplash-associated Disorders: redefining Whiplash and its Management. Spine 1995; 20:8S.
39 Coulter ID, Hurwitz EL et al. (1996) the Appropriateness of Manipulation and Mobilization of the Cervical Spine. Santa Monica, California: RAND, Document NO. MR-781-CR.