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Vertigo, benign paroxysmal positional

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• 386.11 Benign paroxysmal positional vertigo
• H81.1 Benign paroxysmal (positional)
• H81.10 unspecified
• H81.11 right ear
• H81.12 left ear
• H81.13 bilateral
• Pattern 5A: Primary Prevention/Risk Reduction for Loss of Balance and Falling 1
• Pattern 5F: Impaired Peripheral Nerve Integrity and Muscle Performance Associated with Peripheral Nerve Injury 2

Description

• Disorder of the inner ear
• Vestibular part of inner ear has three semicircular canals and two otolith organs (utricle, saccule) that are interconnected and fluid-filled
• Calcium carbonate crystals (otoconia, otoliths, ear stones) break free from utricular macula and float into one or more of the semicircular canals, making hair cells sensitive to gravity
• Causes episodic feelings of rotary vertigo (illusion that the room or oneself is spinning) that occurs with head position changes and usually lasts less than one minute

Essentials of Diagnosis

• Physical exam, including neurotologic exam, typically normal
• Thorough and detailed history is essential to distinguish from other vestibular disorders and central pathology
• Positive positioning tests: Dix-Hallpike maneuver , roll test, or side-lying test
• Positioning maneuver results in particular pattern of nystagmus and simultaneous report of vertigo
• Must rule out central nervous system pathology, which may mimic BPPV, especially if symptoms associated with head trauma

General Considerations

• Patients feel like either they or the room is spinning
• Typically triggered by tilting the head backward, rolling over in bed, or bending over
• Can feel disoriented and off-balance between episodes of spinning

Demographics

• More common in women than men (2:1 ratio)
• Onset can range from 11 to 84 years of age; most common age of onset between 5 th and 7 th decades of life
• Uncommon in children
• Can run in families

Signs and Symptoms

• Patient reports spinning sensation triggered by specific head positions or head position changes
• Observe nystagmus and patient reports spinning during positioning test postures
• Reports of dizziness (disorientation, wooziness, lightheadedness) between episodes of vertigo
• Reports of loss of balance and falls
• May also have nausea and vomiting when spinning sensation is provoked
• No central signs (diplopia, dysarthria, dysphagia, dysmetria, numbness, or weakness)

Functional Implications

• Difficulty performing normal head movements (bed mobility, looking up, bending over) because symptoms are provoked
• Impedes balance and contributes to falls
• Reduced or lost ability to perform tasks in home, at work, driving

Possible Contributing Causes

• Primarily idiopathic
• Secondary etiology most commonly head trauma
• Other secondary causes are inner ear pathologies (Meniere’s, post-acute vestibulopathy, migraines)

Differential Diagnosis

• Necessary when BPPV suspected, but want to rule out other diagnoses because patient does not have classic signs and symptoms or patient does not respond to treatment
• Brainstem stroke or TIA
• Vertebrobasilar insufficiency
• Acoustic neuroma ...

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Vertigo Case Study

June 16, 2020 by Dr. Stefan Cohen

The patient is a female in her thirties. She presented to my office in acute distress with a recent onset of vertigo. Vertigo is defined as “a sensation of whirling and loss of balance, associated particularly with looking down from a great height, or caused by disease affecting the inner ear or the vestibular nerve; giddiness.” In her case, it had started abruptly a few days prior and the only thing she could do to alleviate it was lying down. She had seen her physician who prescribed medication that did not help.

On the first visit, I identified that her upper spine was misaligned in three key areas: C0, C1 & C2 (Occiput, Atlas & Axis). The brainstem exits the skull via the Foramen Magnum and occupies this region, below which it becomes the spinal cord. This region houses key autonomic functions such as heart rate and breathing. When there is stress in this region from misalignments, a lot of problems can occur in the nervous system and thus the body.

I released some tight suboccipital muscles using Active Release Technique (ART), a very specific soft tissue release technique, and then gently adjusted C0, C1 & C2. I also performed the Eply Maneuver, in case there was also inner ear involvement. The patient was able to lift her head for the first time since this started, and to also get up and walk out of the office without duress.

She returned a few days later. Only C1 was now out of alignment, and muscles on the other side of her upper cervical spine were still overly tight. Think of muscles like rubber bands – when tight, they pull whatever they’re attached to, which can pull a vertebra out of alignment. I again used ART and gently adjusted the Atlas.

Working with the body is like peeling away of an onion skin in that the next layer of dysfunction present itself once the preceding one is cleared up. With this in mind,  I then determined that there was a stressor in the fascial system which was triggering the muscles in the first place. And this time, this trigger was in the emotional body.

We store our emotions in the connective tissue, Aka Fascia. Complex polypeptides of emotion find receptor sites in the fascia and can trigger physical consequences as we’ve seen above (see Candice Pert, Molecules of Emotion, The Science Beind Mind-Body Medicine, Touchstone, 1999). I used Neuroemotional Tehnique (NET) to deprogram this fascial memory, and  only then did the muscle spasm fully release. The patient left the office feeling almost back to normal. And by the third visit, she had no complaints!

In this case study, I adressed two sides of the Triad of Health: Physical & Emotional stressors. There may also be a chemical trigger which we didn’t identify in this case.

Vertigo can be tricky because there can be various triggers & causes. In this case, I believe it was emotional physiology leading to muscle contraction and eventually cervical misalignments, which further lowered the neurological threshold leading to vertigo by some unidentified pathway.

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Characteristics of assessment and treatment in Benign Paroxysmal Positional Vertigo (BPPV)

Laura power.

a Balance Disorders and Ataxia Service, Royal Victorian Eye and Ear Hospital, East Melbourne, VIC, Australia

b Dizzy Day Clinics, Burnley, VIC, Australia

Katherine Murray

David j. szmulewicz.

c Cerebellar Ataxia Clinic, Neuroscience Department, Alfred Health/Monash University, Melbourne, VIC, Australia

Benign Paroxysmal Positional Vertigo (BPPV) is the most common cause of dizziness presenting to specialist vestibular centres and accounts for approximately 20–30% of referrals to these clinics. In spite of the amount of clinical knowledge surrounding its diagnosis and management, the treatment of BPPV remains challenging for even the most experienced clinicians. This study outlines the incidence of BPPV in a specialised vestibular physiotherapy clinics and discusses the various nuances encountered during assessment and treatment of BPPV.

Observational Study

PARTICIPANTS:

314 patients with various forms of Benign Paroxysmal Positional Vertigo (BPPV)

INTERVENTION:

Canalith repositioning manoeuvres (CRP) for posterior canal (PC) or horizontal canal (HC) BPPV depending on the canal and variant of BPPV.

OUTCOME MEASURES:

Negative Dix-Hallpike (DHP) or Supine roll test (SRT) examination.

In 91% of cases, PC BPPV was effectively treated in 2 manoeuvres or less. Similarly, 88% of HC BPPV presentations were effectively managed with 2 treatments. Bilateral PC, multiple canal or canal conversions required a greater number of treatments. There was no noticeable difference in treatment outcomes for patients who had nystagmus and symptoms during the Epley manoeuvre (EM) versus those who did not have nystagmus and symptoms throughout the EM. Nineteen percent of patients experienced post treatment down-beating nystagmus (DBN) and vertigo or “otolithic crisis” after the first or even the second consecutive EM.

CONCLUSION:

Based on the data collected, we make several clinical recommendations for assessment and treatment of BPPV. Firstly, repeated testing and treatment of BPPV within the same session is promoted as a safe and effective approach to the management of BPPV with a low risk of canal conversion. Secondly, vertigo and nystagmus throughout the EM is not indicative of treatment success. Thirdly, clinicians must remain vigilant and mindful of the possibility of post treatment otolithic crisis following the treatment of BPPV. This is to ensure patient safety and to prevent possible injurious falls. Our results challenge several clinical assumptions about the assessment and treatment of BPPV including the utility of certain markers of treatment success; hence influencing the current clinical guidelines and clinical practice and paving the way for future studies of the assessment and management of patients with BPPV.

1. Introduction

Benign Paroxysmal Positional Vertigo (BPPV) accounts for approximately 20–30% of referrals to specialised vestibular clinics [ 51 ] with an incidence of BPPV as high as 64 per 100,000 [ 2, 15 ]. The cumulative lifetime incidence is approximately 10% at 80 years [ 51 ], with the peak incidence of BPPV between 50 and 70 years of age [ 54 ] and a predilection towards women at 2.2 : 1 when compared to men [ 33 ].

BPPV is a mechanical disorder of the peripheral vestibular system, characterised by repeated brief (less than 1 minute) episodes of positional vertigo caused by crystals of calcium carbonate (otoconia) which are (1) dislodged from the utricle and travel into the semicircular canals (canalithasis) [ 50 ], or (2) less commonly, adhering to the cupula and rendering it sensitive to gravity (cupulolithasis) [ 2 ]. Posterior canal BPPV (PC BPPV) is the most common canal affected, accounting for 80 to 90% of cases, followed by horizontal canal BPPV (HC BPPV), (5 to 15%) and anterior canal BPPV (AC BPPV) being the least common (1 to 2%) [ 5, 7, 25 ]. Diagnosis of this condition is based on the characteristics of the nystagmus elicited by performing the Dix-Hallpike manoeuvre (DHP)[ 10, 12 ] or Supine roll test (SRT) [ 31 ] which elicits characteristic nystagmus that follows head movement in the plane of the involved semicircular canal, with features of latency and fatigability [ 50 ]. The patient’s symptoms of vertigo are commonly reproduced during positioning [ 10 ], and BPPV is typically responsive to Canalith repositioning procedures (CRP) [ 47 ]. However, it is important to note that the latter is not adequate for diagnosis because other conditions may mimic the symptoms of BPPV [ 4, 11, 38, 52 ].

The term ‘benign’ generally implies that a disease or condition is not harmful in its effect, but despite this label in BPPV, the burden of disease experienced by those suffering from BPPV suggests otherwise. Greater than 60% of patients with BPPV require leave from work [ 3 ], and 86% experience interruption to activities of daily living [ 51 ]. Significant economic and health care costs are associated with hospital admissions, secondary to vertiginous episodes, at approximately two billion dollars annually in the USA for the diagnosis of BPPV alone [ 27 ]. Falls and falls-related injuries are significantly higher in BPPV patients, than those without BPPV, with up to 38% experiencing falls as a direct consequence of BPPV, with the incidence of both BPPV and falls increasing with increasing age [ 26 ]. The treatment of positional vertigo has been demonstrated to reduce the incidence of falls by 64% [ 20 ]. Although BPPV may resolve spontaneously, without treatment, up to 50% of cases may take longer than three months to resolve, hence the CRP is the preferred treatment option [ 22, 29 ]. Clinicians must also be wary, that structural cerebellar pathology, (including tumours of the cerebellum [ 38, 39 ]), along with more benign vestibular conditions such as vestibular migraine (VM) [ 24, 43 ] may mimic BPPV, and accounts for up to 20% of cases of positional vertigo [ 4 ].

Despite a comprehensive understanding of the pathophysiology of BPPV, the assessment and treatment of this condition may be challenging for even the most experienced clinicians. There is a multitude of reasons for the difficulties experienced. They include difficulties in positioning patients due to medical comorbidities (e.g. limited cervical range of motion or lower back pain), challenges interpreting the patterns of nystagmus, BPPV affecting the horizontal, anterior, bilateral or multiple canals and refractory or recurrent BPPV [ 25, 40 ]. This study outlines the incidence of BPPV in a specialised vestibular physiotherapy clinic and discusses the various nuances encountered during assessment and treatment of BPPV.

A prospective study of 314 patients who presented with a history suggestive of BPPV were assessed by physiotherapists specialising in vestibular disorders in a speciality vestibular physiotherapy clinic in Melbourne, Australia. A comprehensive assessment determined the diagnosis of definite BPPV according to the Barany Society diagnostic criteria for BPPV using the DHP or SRT [ 5, 12 ]. These patients were included in the study. Patients whose nystagmus did not concur with the diagnostic characteristics of BPPV, including those with vestibular migraine (VM) or central positioning nystagmus (CPN) were excluded from the study. Diagnosis was based on visual observation of the nystagmus (Frenzel goggles or video-oculography were not employed). A successful treatment was defined by the presence of a negative DHP or SRT (i.e. the absence of nystagmus which represents active BPPV) on retesting within the same clinical session.

Patients who were diagnosed with PC BPPV canalithasis were treated with the Epley manoeuvre (EM) [ 13, 26 ], or in the case of cupulolithasis, the Semont manoeuvre[ 44 ]. Patients with HC BPPV canalithasis were treated with either the Barbeque roll (BBQ)[ 41 ] or Appiani manoeuvre [ 1, 29 ], or in the case of HC cupulolithasis, the modified Brandt Daroff (mBD) or the Casani manoeuvre [ 9, 30 ] which was then followed by the appropriate canalithasis manoeuvre. In one case of anterior arm HC BPPV, the Gufoni manoeuvre was applied [ 46 ]. A combination of treatments was required if the otoconia resided in more than one canal, i.e. bilateral or multiple canal BPPV. If otoconia resided in more than one canal simultaneously, treatment occurred across more than one treatment session, i.e. one canal treated per day. The combinations included 2 cases of ipsilateral PC and HC BPPV, 1 case of PC and contralateral HC BPPV, and one case of bilateral PC plus left sided AC BPPV. In the case of AC BPPV, the EM was also carried out. Where an initial treatment selection was unsuccessful (i.e. the DHP or SRT remained positive), an alternate CRP could be selected by the clinician. In the case of canal conversion [ 18 ], an alternate CRP was selected to treat the affected canal. Patients were treated with a maximum of 3 manoeuvres within 1 session, or until a negative DHP or SRT was obtained, unless contraindicated (treatment selection was based on clinician preference). In line with the clinical practice guidelines for BPPV, no post treatment precautions were provided to patients post management for their BPPV [ 5 ].

Data regarding age, gender, aetiology, associated symptoms, duration of symptoms, positional testing characteristics, canal distribution, nystagmus features, treatment outcomes and incidence of nausea and vomiting during repositioning were recorded at the time of the consultation. All patients provided informed consent. This study was approved by the Royal Victorian Eye and Ear Hospital (RVEEH) Human Research Ethics committee (HREC) (HREC Reference Number: 11/994H/16).

Three hundred and fourteen patients were diagnosed with BPPV. Subject demographic data is presented in Table 1 .

Patient demographic data

At the time of symptom onset, 100% (314) of patients reported associated symptoms of vertigo, 75% (235) experienced gait unsteadiness or balance impairment, 55% (175) experienced nausea, with 10% (31) also vomiting. Nineteen percent (59) reported a sensation of head “fogginess” and 6% (18) experienced falls as a direct consequence of a vertiginous episode. Seventy percent (219) of patients presented within the first 30 days of symptom onset ( Fig. 1 ) with a median of 42 days.

Time from BPPV symptom onset.

In some subjects, repeated performance of the DHP was required in order to obtain a positive result. DHP was repeated when the patient history was strongly suggestive of BPPV, and symptoms were relatively close to the time of presentation (e.g. the morning of the assessment). The average number of DHP manoeuvres required to obtain a positive result was 1.15 with a range of 1 to 3. Thirty patients (10%) required 2, whilst 10 patients (3%) required 3 DHP manoeuvres before a positive result was obtained. In PC BPPV, DBN during the DHP on the contralateral side occurred in 6% (15) of patients.

The distribution of BPPV by affected canal is shown in Table 3 . Multiple canal BPPV was found in 4 patients (1%), bilateral PC BPPV in 14 patients (5%) and cupulolithasis in 8 patients (3%). BPPV affected the right ear in 163 patients (52%), the left side in 133 patients (42%). Bilateral PC BPPV was found in in 14 patients (5%) and multiple canal BPPV in 4 patients (1%). The incidence of multiple canal (4 patients, 11%) and bilateral posterior canal (2 patients, 6%) was higher in the post-traumatic BPPV group (36), with an incidence of 17%, compared to 6% in the sample of this study.

Distribution of BPPV by canal(s) affected

In PC BPPV, 79% (197) resolved following one CRP manoeuvre and 91% (227) after two manoeuvres. The EM was selected as the CRP in 98% (246) of PC BPPV presentations. If the EM was unsuccessful, or in the case of cupulolithasis, the Semont manoeuvere was performed. In HC BPPV 69% (31) were resolved after 1 treatment and 88% (40) with two manoeuvres. In HC canalithasis, the BBQ roll was performed in 41% (19) of patients, and in 45% of patients (21) the Appiani manoeuvre. There were four instances (4/19, 21%) in which the BBQ roll failed to clear the otoconia, and the Appiani manoeuvre was performed resolving the BPPV. In 1 case (5%) the Appiani failed, and the BBQ roll was then used and resolved the BPPV. Five patients with HC cupulolithasis underwent several treatments with a median of 2 (range 1–4) treatments being required to obtain symptom resolution.

In those with bilateral PC BPPV 71% (10) resolved with 2 treatments over 2 treatment sessions. In multiple canal BPPV, 75% (3) resolved after 3 manoeuvres (over 2 or more treatment sessions). Thirteen of the 314 patients experienced canal conversions (posterior canal to horizontal canal BPPV) and 81% of those patients resolved in 2 treatments or less. The incidence of canal conversion was 5% (16). In the post-traumatic group, 83% (30) of patients were treated in 2 treatments. In the migraine group 94% (103) resolved in 2 treatments or less. ( Fig. 2 )

Comparison of type of BPPV and number of treatments required.

There was minimal difference in treatment outcomes for patients who had nystagmus and vertigo during the EM, versus those that did not ( Table 4 ). A post treatment otolithic crisis (thought to represent mass movement of otoconia or an otolithic crisis or catastrophe) occurred in 19% (48) [ 30, 45 ] of patients and describes the presence of DBN and vertigo occurring on sitting up after either the first or even the second consecutive EM. Ten of these patients (4%) experienced simultaneous trunk retropulsion consistent with the otolithic crisis [ 30, 45 ].

Vertigo and nystagmus during the Epley manoeuvre (EM)

The incidence of nausea and vomiting was also recorded. Ninety-five patients (30%) experienced nausea, whilst 22 (7%) vomited during repositioning. In the PC BPPV group, 24% (60) experienced nausea, whilst 4% (9) vomited. The incidence of vomiting was higher if the otoconia resided in the HC (11 patients, 25%), if there were a past history of migraine (11 patients, 10%) or if there was a canal conversion, with half of this latter group experiencing nausea, and 2 patients (12%) vomiting.

4. Discussion

In the sample examined, age and gender predilections were consistent with those reported in the literature [ 32, 51, 54 ]. Similarly, a greater incidence of isolated PC BPPV (79%) when compared to HC BPPV (15%), and AC BPPV (0%) reflects what has previously been reported, and so too, the aetiologies ( Table 2 ) [ 7, 19, 25 ]. The incidence of bilateral and multiple canal BPPV was higher in the post-traumatic BPPV group (17%, 6/36), consistent with previous studies [ 36, 42 ]. Unlike some previous studies, the subjects in our study presented acutely [ 21, 24 ]. This discordance may be due to the more lengthy referral processes and waiting times for hospital based tertiary referral centres. The initial assessment undertaken in our study was 43 days from symptom onset (on average) with almost half presenting in the first 10 days of onset. These findings may in part be due to the increased profile of physiotherapy in the assessment and management of BPPV and that patients in the Australian health care system may self-refer to private specialist physiotherapy clinics [ 53 ].

Aetiology of BPPV

Previous studies have suggested that when the patient history is strongly suggestive of BPPV, repeated examination across multiple sessions is required to confirm the diagnosis of BPPV [ 37 ]. In our study 13% of patients (40) required up to three DHP tests to elicit the characteristic nystagmus and confirm a diagnosis of BPPV, highlighting the importance of repeated clinical testing for BPPV within the same session to avoid a false negative DHP or SRT. In an earlier study, Viirre and Baloh described the importance of repeated DHP within the same session [ 49 ]. This practice is more efficient than repeat testing over multiple sessions because it decreases the risks of BPPV such as falls and their sequelae, as well as the cost to the patient and public purse.

Additionally, the findings of our study support retesting for BPPV within the same session following the CRP, to determine the efficacy of the treatment [ 23, 35 ][ 23, 35, 44, 45 ]. Many clinicians fear retesting a patient with the DHP in the same session because of the risks of canal conversion or re-entry. This was not the case in our study, where only 5% (16) underwent a ‘canal switch’[ 28, 49 ] compared to previous studies which reported canal conversion ranging from 6% [ 18 ] to 16% [ 14, 47 ]. The incidence of vomiting was relatively low in PC BPPV (4%) but is significantly higher in HC BPPV (25%), following canal conversions (12%), and when there was a past history of migraine (14%), a finding that has not been reported previously.

Persistent DBN during the DHP test on the contralateral side to the ear affected with PC BPPV has previously been reported to occur in 6–13% of patients [ 48 ], with our study finding 6% (15) of patients exhibiting this sign. Certain authors have proposed this to be an apogeotropic variant of PC BPPV [ 8, 48 ]. Another alternative theory is the co-planar push-pull mechanism of the AC of one side and PC of the other side, resulting in a compensatory DBN on the unaffected side [ 48 ]. This DBN typically resolves with treatment of the affected PC, as it did in our experience. This is relevant to the need for any investigation aimed at excluding a structural posterior fossa aetiology [ 38 ].

Previous studies have suggested that vertigo and nystagmus during the EM, in particular, in the second position, is required for successful treatment and that absence of this is indicative of treatment failure [ 17, 22, 34 ]. Our study found that the incidence of vertigo and nystagmus throughout the EM was not particularly high (19–35%, Table 5) nor predictive of a successful treatment outcome. A negative repeat DHP or SRT remains the only highly predictive indicator of treatment success [ 35, 45 ].

In the current study, 90% of patients were treated effectively with two or less treatment manoeuvres. Bilateral PC BPPV, multiple canal BPPV, cupulolithasis required a greater number of treatment manoeuvres to obtain symptom resolution, which is consistent with past studies [ 36, 40 ]. If a patient fails to respond to a modest number of repositioning manoeuvres, further investigation is recommended in order to exclude central causes for the presentation, such as cerebellar structural pathology [ 39, 38 ]. The number of treatments manoeuvres required in the post-traumatic group was not significantly higher than those in the idiopathic group (unless the otoconia resided in multiple canals simultaneously). In our study 83% of patients in the post-traumatic BPPV group responded to repositioning in less than 2 treatments compared to 61% in the literature [ 16 ]. Our findings concur with a previous study which showed performing more than one treatment in a single session to obtain a negative outcome, rather than repeated EM over concurrent sessions is effective [ 23, 44 ].

When performing repeated EMs within the same session, clinicians must be mindful of the possibility of a second post treatment otolithic crisis [ 30, 33 ]. When patients sit up from the second consecutive Epley manoeuvre, irrespective of whether the DHP is negative, 19% of patients may experience intense but brief vertigo, often perceived as a falling sensation, along with DBN, previously described as similar to the crisis of Turmarkin [ 30, 33 ]. A smaller percentage of patients (4% experienced trunk retropulsion, as described previously [ 6 ]. We strongly recommend that clinicians be vigilant and support the patient’s trunk during the sitting up phase of the EM in the event that they experience truncal retropulsion and/or anteropulsion.

The limitations of this study were: Firstly, the relatively short duration of data collection (10 months) which prevented a comprehensive analysis of BPPV recurrence rates. Secondly, this was a descriptive and observational study of BPPV management in the “real world” of clinical practice at a tertiary centre. We acknowledge controlled trials are required to compare the efficacy of different treatments to determine whether early intervention enhances patient outcomes in patients with BPPV.

5. Conclusion

This study offers insight into the ‘real world’ of BPPV management. Hitherto, similar studies have been performed in tertiary referral centres where access limitations have precluded the data collection of acute BPPV assessment and management.

Based on our data, we recommend when if the patient history is suggestive of BPPV, repeated positional testing within the same session be conducted to confirm or refute the diagnosis of BPPV. Repeated testing and treatment within the same session is a safe and more efficient approach to treatment, with a low risk of canal conversion. In PC BPPV, vertigo and nystagmus during the EM are not indicative of treatment success. Performing the DHP and SRT (as relevant) remain the only indicators of treatment outcome. We strongly recommend, if patients do not respond promptly to CRP, further investigation is mandatory to exclude cerebellar or brainstem structural pathology.

Ethics approval

This study was approved by the Royal Victorian Eye and Ear Hospital (RVEEH) Human Research Ethics committee (HREC) (HREC Reference Number: 11/994H/16).

Acknowledgments

We wish to acknowledge the team members at Dizzy Day Clinics for their efforts in data collection on this project: Arimbi Winoto, Belinda Reid, Amy Gillon, Mandy Lenwood and Marianna Harrison

Emery Evans

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