How Can PTNow Help You in Orthopedic Patient Care? Airelle Hunter-Giordano, PT, OCS, SCS 0

Benign Paroxysmal Positional Vertigo (BPPV) Most common cause of vertigo due to peripheral vestibular disorder Illusion of movement, spinning sensation –Episodic –Less than 1 minute –Occurs when head (labyrinth) is in certain positions –Characteristic nystagmus –Repeated provocation reduces signs and symptoms 1

BPPV Mechanical problem resulting from displacement of otoconia from the utricle to one of the semicircular canals (SCCs) Triggers –Lying down –Rolling over in bed –Bending over and looking up Diagnosis –Confirmed by observation of nystagmus when the patient is placed in a provoking position using: Dix Hallpike Test Sidelying Test Roll Test Bow and Lean Test –Rule out cervical and cervical-medullary disorders 2

BPPV Classification Primarily based on the SCC involved [*posterior (76-85%), anterior ( %), horizontal ( %)] Maneuver takes a few minutes to perform High rate of resolution Which canal is involved? –Based on the observation that nystagmus occurs when patient is in provoking position Canalithiasis Cupulolithiasis 3

Canalithiasis Delay in onset of vertigo of 1-40 sec after the patient has been placed in the provoking position Nystagmus that appears with the same latency as reports of vertigo Fluctuation in intensity of the vertigo and nystagmus, which increases and then decreases while the person is in a provoking position, disappearing in 60 sec 4

Cupulolithiasis Immediate onset of vertigo when patient is moved into provoking position Presence of nystagmus appearing with the same latency as reports of vertigo Persistence of vertigo and nystagmus as long as head is maintained in provoking position 5

Determining the SCC: Observed Patterns of Nystagmus* 6

Focus Areas for Examination* 7 Image from:

Differential Diagnosis: Central Positional Nystagmus and Vertigo Central positional nystagmus and vertigo Perilymphatic fistula Superior canal dehiscence Vestibular hypofunction Vertebrosbasilar artery insufficiency 8

Differential Diagnosis: Central Positional Nystagmus and Vertigo 9

Summary of Treatment Options Type of BPPVTreatment Posterior SCC CanalithiasisCanalith repositioning procedure or treatment (CRT) (Epley maneuver) Anterior SCC CupulolithiasisReverse Liberatory maneuver Anterior SCC CanalithiasisCanalith repositioning procedure on the affected side Horizontal SCC CanalithiasisRoll treatment, Forced prolonged position, Gufoni or Appiani maneuver Horizontal SCC CupulolithiasisNo treatment recommended 10

Prognosis Posterior SCC canalithiasis –Supported by systematic and Cochrane reviews with use of canalith repositioning (Epley maneuver) –Remission of symptoms usually occurs in 1-2 treatments If not remission in 4 treatments, reevaluate Horizontal and anterior SCCs –Equally effective treatment as posterior SCC; however, level of evidence is lacking Spontaneous recovery –In ~30% of patients with posterior SCC canalithiasis, remission is spontaneous Recurrence –More common if associated with head trauma (1/3) 11

Achilles Tendinopathy Tendinopathies are characterized by excessive loading and overuse resulting in tendon breakdown Often seen in middle-aged athletes (aged 30-50) but can also present in sedentary individuals Incidence: –Running: </ 9% in a given year –Competitive athletes lifetime incidence: 24% –Runners lifetime incidence: 40-50% –Acute or progressive rupture: 8% runners Pain: –Mid portion of the tendon –Tendon’s bony insertion 12

Achilles Tendon Largest and strongest tendon in the body connecting the gastroc and soleus to the calcaneous Tendon is 6 inches long –2-6 cm proximal to the tendon’s distal insertion is a zone of hypovascularity 13

Intrinsic Abnormal DF motion Abnormal subtalar motion PF strength Abnormal pronation Abnormal foot/tendon structure Lateral ankle instability Age Male sex Obesity Hypertension Diabetes Cholesterol Adverse drug events Extrinsic Training errors (change in intensity, duration, level) Environmental factors (surfaces, temperature) Faulty equipment (shoe wear) 14 Risk Factors

Classification Tendinitis –Acute trauma or muscle fatigue and characterized by edema and hyperemia of the involved tendon –Pain and tenderness –Crepitus Tendinosis –Chronic condition, gradual onset and lacking inflammatory cells –Tender nodules around tendon –Diffuse thickening of surrounding soft tissue –More prone to injury Tendinopathy –Term suggested to avoid confusion 2 locations –Mid portion (2-6 cm proximal to tendon insertion) –Insertion to calcaneus (insertional tendinopathy) 15

Screening Differential Diagnosis –Achilles tendon rupture –Partial tear of Achilles tendon –Calf strain –Retrocalcaneal bursitis –Posterior ankle impingement –Sural nerve irritation and/or neuroma –Tarsal tunnel syndrome –Peroneal tenosynovitis and/or dislocation –Os trigonum syndrome –Accessory soleus muscle –Ossification of Achilles tendon –Systemic inflammatory disease –Lumbar radiculopathy 16

Examination & Diagnosis Moderate evidence supports use of a group of signs –Achilles tendon palpation test –Decreased PF strength and endurance –Arc sign –Royal London Hospital test Strong evidence to incorporate validated functional outcome measures before and after intervention –Victorian Institute of Sport Assessment (VISA-A) –The Foot and Ankle Ability Measure (FAAM) Moderate evidence to analyze walking ability, stair decent, unilateral heel raise, single limb hop, and participation in recreational activities 17

Diagnostic Imaging May be needed when examination findings are ambiguous Ultrasound and magnetic resonance imaging (MRI) were found to be most helpful Ultrasound slightly less sensitive than MRI MRI is preferred due to 3-dimensional abilities and soft tissue visulaization MRI sensitivity=94 or 95%; specificity=50% to 81%. Increased risk of false negatives because symptomatic tendons may appear normal upon imaging. Acute tendinitis diagnosis: presence of fluid surrounding the tendon Tendinosis: hypoechoic areas with poorly defined structural borders Tendon degradation and disease progression graded: (1=normal tendon, 2=enlarged tendon, 3=tendon containing a hypoechoic area) 18

Intervention 19

Intervention 20

Prognosis Conservative care 6 to12 weeks’ duration: significant decreases in pain with the maintenance of long-term function without reinjury. Prognosis in the more sedentary population is not as encouraging. Conservative management may be unsuccessful in as much as 24% to 49% of patients. Surgery (eg, excision of fibrotic adhesions, removal of degenerated nodules, longitudinal incisions to restore vascularity) is a favorable option after 4 to 6 months of failed conservative measures. 21

Medical Management Extracorporeal Shockwave Therapy (ESWT): A series of 2 or 3 high-energy pulses per second to promote healing through neovascularization. Research on effectiveness limited and conflicting. ESWT is not FDA-approved for this purpose. Local Corticosteroid Injection: Used to decrease acute inflammation, pain, and promote function and activity. May decrease tensile strength. Sclerosing Injection (Polidocanol): Used to manage the more chronic, mid- substance form of Achilles tendinopathy, especially when less invasive strategies have failed; decreases pain via the analgesic effects of the medication and reducing high-flow areas within the tendon. Oral Nonsteroidal Anti-inflammatory Drugs (NSAIDs): Used as an adjunct to other treatments to control pain and inflammation. Side effects are common. Should be used with consideration of comorbidities, especially in the older population. Surgical Intervention: Percutaneous tenotomy and open removal of the tendon pathology. Used when conservative management fails and functional decline continues. Prognosis based on the extent of remaining tendon structure. If condition progresses to the point of tendon rupture, primary Achilles tendon repair is performed. 22