case study: peripheral polyneuropathy secondary to chronic ... · case study: peripheral...

Cascio 1

James Cascio April 18, 2016 Dr. Krasilovsky PT 840

Case Study: Peripheral

Polyneuropathy Secondary to Chronic Lyme Disease

Cascio 2

Lyme disease is a zoonosis, or infectious disease from animal origin that can naturally be

transmitted to humans, caused by the spirochete bacteria Borrelia (Barbour et al., 1993). The

bacteria are harbored in ticks of the genus Lxodes, more commonly known as deer ticks (Barbour

et al., 1993). In the Northeast, mid-Atlantic, and central United States, the Lxodes scapularis is

the most common culprit, while disease spread on the Pacific coast is usually from the lxodes

pacificus (CDC: “Transmission,” 2015) . The ticks are typically infected with the Borrelia

microbes in their nymphal stage, as they can go undetected due to their small size (Tilly et al.,

2008). They acquire the bacteria from feeding on infected small mammals and birds, although

deer are the preferred host of adult ticks, hence the nomenclature (CDC: “Transmission,” 2015).

Ticks find their host by ‘questing,’ or waiting on the tips of long grass or shrubs with their legs

outstretched, hoping to climb onto a passing organism (CDC: “Transmission,” 2015).

Transmission of the Borrielia microbes from an infected tick occurs during feeding, due

to regulation of certain surface proteins. During the feeding process, the tick cuts into the host’s

skin, and inserts a feeding tube. If the tick has previously fed on an organism infected with the

Borrielia microbes, it may pass the infection on to the new host (CDC: “Transmission,” 2015).

The bacteria moves to the tick’s salivary glands, where an immunosuppressive protein with

anesthetic properties prevents the host from sensing any pain or itch from the bite, allowing the

tick to remain unnoticed for the entirety of the feeding process (Hovius et al., 2007; Steere et al.,

2004). The tick typically must be attached to the host for 36 to 48 hours for the microbes to be

transmitted (Hovius et al., 2007). The ticks can attach to virtually any human body part, but are

most commonly found in discrete areas such as the groin, armpits and scalp (CDC:

Cascio 3

“Transmission,” 2015). Transmission cannot occur through person-to-person contact, or through

consumption of infected food.

Lyme disease was discovered in 1976, due to a geographic clustering of children being

diagnosed with early-onset Rheumatoid Arthritis in Lyme, Connecticut. The symptoms seemed

to be correlated with a characteristic skin rash, erythema migrans, which was known to be

associated with certain tick species (Barbour et al., 1993). Then, in 1981 Burgdorfer and

colleagues discovered the previously unidentified spirochetal bacteria in a nymphal tick. The

same bacterium was then cultured from patients who suffered from Lyme disease, and their

immune responses were linked, thus discovering the etiology of the infection (Steere et al.,

2004).

Lyme disease is the most common arthropod-borne illness in both the US and Europe,

and the numbers are steadily increasing (Barbour et al., 1993). According to the CDC, there are

approximately 30,000 new cases of Lyme disease reported in the US each year, an incidence of

roughly 7.9 cases per 100,000 persons (CDC, 2015). This number, however, is thought to be a

severe underestimation due to the nature of the disease. Researchers estimate that anywhere from

296,000-376,000 cases occur annually in the US (CDC, 2015). Most cases are concentrated to

the Northeast and Midwest, as 96% of all reported cases are from 14 states alone (CDC, 2015).

Reported cases are most common among boys aged 5-9, who are most likely infected in June,

July, or August resulting in an onset of symptoms in December through March (CDC, 2015).

According to Duray and Steele, the clinical pathologic process, as well as manifestation

of Lyme disease are highly variable, but commonly occur as followed: Stage one begins

immediately after the initial tick bite. Here, an ulceropapule consisting of hyperplastic epithelium

Cascio 4

covering an inflammatory infiltrate in the dermis of lymphocytes, plasma cells, macrophages,

and mast cells forms. This small red bump may appear like a mosquito bite, and can cause

irritation for one to two days. In this early stage, the bacteria itself is hard to see, but has already

infiltrated the host. Perivascular infiltrates of mostly lymphocytes, plasma cells, and mast cells

create the characteristic Erythema migrans lesion associated with acute local infection. These

lesions form a rash, which occurs in 70-80% of infected persons. The EM rash expands

gradually, reaching up to 12 inches in diameter, but may begin to clear up proximally as it

expands, resulting in a “bull’s eye” or target-like appearance. The rash is rarely painful or itchy,

but can be warm to the touch, and can appear anywhere on the body (CDC: “symptoms”, 2015).

Soon after this occurrence, the spirochetes enter the bloodstream and randomly disperse

throughout the body, which commands an immune response from the host, of which usually

involves all of the organs and structures of the reticuloendothelial system. Clinical pain and

discomfort are associated with hyperplasia of lymph nodes, spleen, and bone marrow in this

acute phase, and symptomatology mimics that of mononucleosis and other viral syndromes.

Symptoms may include fever, headache, muscle and joint aches, fatigue, conjunctivitis,

pharyngitis, pneumonitis with a dry cough, hepato-splenic tenderness, and lymph node swelling

in the neck and groin (Barbour et al., 1993; CDC: “symptoms”, 2015). There is also a transient

hepatitis secondary to elevated liver cell enzymes seen at this stage, which can have varying

levels of severity. Soon after, an interstitial pneumonitis may occur, causing the irregularity of

alveolar spaces.

A few weeks to several months following the initial infection, stage two begins. This

progression is mainly characterized by the involvement of cardiovascular and central nervous

Cascio 5

system structures. At this point, the acute reactive phase has ended. Cardiovascular symptoms

manifest as benign transient arrhythmias, such as complete or incomplete AV blocks, which are

usually unnoticed by the patient (Lyme carditis). A transient infiltrate consisting of lymphocytes,

plasma cells, and macrophages can be found in all three layers of the myocardium. Clinical signs

and symptoms of meningioencephalitis are developed in this stage as well; the patient will suffer

from headaches, stick neck, and photophobia. Here, patients can have either severe

encephalopathy, varying forms of psychoneurosis such as depression, sleep disturbances, mood

changes, and memory loss, or may have entirely absent encephalopathic changes. Bilateral Bell’s

palsy is also a clinical manifestation of this stage. Aggregates of lymphocytes infiltrate

autonomic ganglia, as well as afferent and efferent rootles, leading to a common triad of cranial

neuritis, meningitis, and rediculoneuritis.

Stage three, also known as the chronic stage of Lyme disease, begins several months after

the acute phage, and can last many years. This stage is characterized by varying levels of

involvement of joints, peripheral nervous system, and skin. ‘Lyme Arthritis’ causes swelling and

pain secondary to hypertrophic changes, synovitis, fibrosis, and lymphocytes within the

subsynovium. This type of arthritis is found to be intermittent, and usually affecting the knee

wrist and shoulder. Involvement of the peripheral nervous system in this stage is indicated by the

onset of various peripheral sensorimotor neuropathies. Infiltration of lymphocytes and plasma

cells occurs along the perineurium, as well as internal segments of nerves, leading to possible

nerve fiber loss, demyelination, and Wallerian-like degenerative changes. This can lead to

permanent impairment of sensory and motor function of the extremities, and shooting pains to

Cascio 6

the hands or feet. Stage three can also cause acrodermatitis or a bilateral, symmetrical, reddish

discoloration of acral skin (such as feet, ankles, hands, and wrists) (Barbour et al., 1993).

Diagnosis of Lyme disease if based on a multifaceted approach; current symptoms,

objective physical findings, potential exposure to ticks, and exposure to endemic areas all lead

to a clinical hypothesis, which is then proven through a testing regime. Due to the varying and

unpredictable nature of the disease, it is necessary to rule out other potential causes for any

present symptoms. Most patients who present with Erythema migrans can be diagnosed along

with a careful history and physical examination (Meyerhoff et al., 2016). However, in the many

cases that don’t present with this symptom, Lyme disease is often overlooked as a possible

cause, as it can mimic the presentations of other disorders, such as Bell’s palsy, chronic fatigue

syndrome, contact dermatitis, fibromyalgia, insect bites, juvenile idiopathic arthritis, ankylosing

spondylitis, RA, myocarditis, SLE, third-degree AV blocks, and other tick-borne illness

(Meyerhoff et al., 2016) . The pathogens Babesiosis and Ehrilichiosis share the same tick as

Lyme disease, which may lead to false positives during immune testing, however neither of these

infections causes chronic problems.

Testing for Lyme disease is typically a two-tier process, meaning two tests are used to

determine if a person has the disease. The first test is used as a screening tool, to detect anyone

who could possibly have the disease. The second test then seeks to make sure that only those

who actually have Lyme disease are diagnosed. The second test has a very high specificity, and

thus yields a low amount of false positives. The first test, however, has a very low sensitivity and

thus fails to effectively identify patient’s with the disease. Because of this, the system only

identifies roughly 46% of patients with the disease (lymedisease.org, 2016).

Cascio 7

The first test, known as the Enzyme-Linked Immunosorbent Assay (ELISA), measures

the person’s immune response to the bacteria that causes Lyme disease (lymedisease.org, 2016).

It is very common for a patient who does not have Lyme disease to test positive on this test, so

the CDC recommends that doctors then use a second test to confirm the diagnosis. Common

causes of false positives on the ELISA include syphilis, SLE, bacterial endocarditis, Epstein

Barr, Anaplasmosis, and other autoimmune disorders (CDC: “Understanding the EIA Test,”

2015). The second test, used to specifically indicate those with the disease, is the Western Blot

test. This test utilizes electric currents to separate antigens into bands, forming a pattern. The

pattern associated with the patient’s blood is then compared to a template pattern representing

known cases of Lyme disease (lymedisease.org, 2016). If the two patterns match, it can be

concluded that they do in fact have the disease. The CDC requires that at lead 5 out of the 10

bands must match, however since some bands are more highly associated with the diseases and

thus more heavily weighted, a doctor can still determine that the patient suffers from Lyme

disease even though the CDC guidelines have not been met (lymedisease.org, 2016). These tests

are unreliable for the first four to six weeks following infection, as most individuals have not

developed an immune reaction yet at that point (lymedisease.org, 2016).

Other common tests used to help diagnose Lyme disease include, polymerase chain

reaction, antigen detection, and culture testing; all of which are direct tests, indicating that they

seek to determine the level of bacterial infection, rather than the body’s response to it

(lymedisease.org, 2016).

The clinical manifestation of the disease, as well as the progression, determines the

appropriate treatment for a patient. Selection of antibiotic, administration route, and the duration

Cascio 8

of therapy, are based on a patient’s individual case, as well as the presence of any allergies or

associated medical conditions (Meyerhoff et al., 2016). The acute stage of Lyme disease is

managed through oral Amoxicillin, Doxycycline, or Cefuroxime axetil for 14-21 days

(Meyerhoff et al., 2016). Middle and late stage Lyme disease is managed similarly, however

more progressive manifestations can indicate the use of IV antibiotics such as Ceftriaxone,

Cefotaxime, and Penicillin G for up to 28 days (Meyerhoff et al., 2016). Symptoms may persist

for up to two weeks following treatment, and a second round of antibiotics may be indicated if

there is a worsening of symptoms (Meyerhoff et al., 2016). Persistent arthritis following

treatment is managed with NSAIDs, or in extreme cases, a synovectomy can eliminate chronic

inflammation (Meyerhoff et al., 2016). For patients with Lyme carditis, a temporary pacemaker

may be required, but will be discontinued once the heart block has reversed (Meyerhoff et al.,

2016).

Patients should be educated on management of exposure to potential tick bites, especially

if they reside endemic locations. Prevention of tick encounters through personal hygiene

methods, as well as environmental awareness should be implemented. Patients who notice an

attached tick should immediately remove it with tweezers, making sure to remove the entire

body and mouth. The patient should then wash the bite area with soap and water to remove any

remnant microorganisms (Meyerhoff et al., 2016). Antibiotic prophylaxis for individuals with

suspected tick bites in endemic areas are often indicated, however not routinely recommended,

as early antibiotic regimen upon appearance of symptoms will be very effective (Meyerhoff et

al., 2016) . Environmental exposure can be managed through landscape management, keeping

shrubbery and grass well-kempt, as well as routine acaricide spraying, preventing ticks from

Cascio 9

infiltrating their yard (Meyerhoff et al., 2016). Protection of skin by clothing, such as hats, long

sleeved shirts, long pants, and boots can also decrease the probability of a tick attachment.

Physical therapy management is fairly limited amongst patients who suffer from Lyme

disease. Early Lyme disease is treated through a strict regimen of antibiotics as well as pain

medication, however as the disease progresses through its various stages, the role of physical

therapy expands. Chronic symptoms of Lyme disease that do not respond to traditional

medication can be effectively treated by a physical therapist. De-conditioning secondary to Lyme

disease can also be treated by a physical therapist, through exercise education and

implementation. Treatment by a physical therapist usually aims to create an exercise protocol

that maximizes the benefits of activity, without exacerbating the symptoms associated with

Lyme disease (Beale, 2016). Patient education on proper exercise technique, frequency, and

duration of a protocol that involves whole-body workouts, stretching, light calisthenics, and light

resistance training with an emphasis on endurance can be effective in pain reduction, as well as

increasing overall mobility and quality of life (Beale, 2016). Other physical therapy interventions

that may be implemented include massage, myofascial release, and various modalities such as

ultrasound, paraffin baths, and heat (Beale, 2016).

Patients who suffer from chronic Bell’s palsy symptoms secondary to Lyme disease are

also great candidates to benefit from physical therapy intervention. Anti-gravity massage

techniques can limit the adverse effects of gravity on the de-innervated facial muscles. Isolated

low effort motor re-education, as the patient begins to regain function in those muscles, will

increase the selective control that’s desired. EMG biofeedback has also been shown to be

effective in neuromuscular reeducation of the facial muscles.

Cascio 10

Lyme arthritis is another unfortunate symptom of the disease that can be managed with

physical therapy. These patients can develop arthralgia due to wasting of the quadriceps muscles,

with secondary development of patellofemoral dysfunction, or chondromalacia patella (Sigal,

1999). Physically therapy along with short term use of anti-inflammatory drugs is the most

appropriate method to treating this condition (Sigal, 1999).

The research regarding physical therapy as appropriate treatment for Lyme disease is

scarce as best, however the benefits of exercise are immeasurable physically, psychologically,

and socially. A case study published in the Journal of the American Physical Therapy

Association in 2011 outlined the experience of a 14-year-old girl with Lyme disease, who was

treated using therapeutic exercise and gait training. The researchers sought out to present an

example of effective physical therapy intervention, on a pediatric patient who suffered from

musculoskeletal dysfunction secondary to late stage Lyme disease. Due to impairments in

strength and endurance, coupled with chronic pain, fatigue and constant tremor, this patient

presented with impaired functional mobility in both ADLs and IADLs. Because of this, the

patient was unable to participate in many school, Church, and sporting events with other children

her age, contributing to her overall low quality of life. A home exercise plan, as well as a

therapeutic exercise regimen was designed with the patient’s specific goals in mind. Due to her

initial debilitation, the protocol was designed in a stepwise fashion, allowing for controlled,

consistent progression in her ROM and strength deficits. The patient recorded her levels of pain,

fatigue, and tremor both before and after each exercise session. The patient also engaged in gait

training focused on normalizing cadence, increasing speed and coordination of movements, and

increasing aerobic capacity. Upon conclusion of the 18 week exercise program, the patient

Cascio 11

achieved her goal of playing soccer, a high-intensity sport, for up to two hours. The patient was

able to score 96.9% of her age-predicted six minute walk test, with improved gait mechanics, as

well as score of 4/5 on all major muscle groups; a marked improvement. She reported

diminishing pain and tremors, and was able to resume her previous level of function regarding

both school and church functions. Due to the nature of a case study, is it difficult to come to any

concrete conclusions regarding this scenario; however it reinforces the multifaceted benefits of

exercise within this patient population (Moser, 2011).

Dr. Joseph Burrascano writes in ‘Advanced Topics in Lyme Disease; Diagnostic Hints

and Treatment Guidelines for Lyme and other Tick Borne Illnesses,’ that it is theorized that

Lyme spirochete will die when exposed to both oxygen and high temperatures. Thus, an exercise

protocol that seeks to improve tissue perfusion and oxygen levels, as well as elevate body

temperature may play a role in the resolution of this illness (Burrascano, 2005). The exercise

may weaken the bacteria, enhancing the effect of both antibiotic treatments, and the body’s

immune response (Burrascano, 2005).

Physical Therapy may also be an effective method for management of neurological

manifestations of chronic Lyme disease. Typically, when Borrelia burgdorferi infects the

nervous system, it results in a cranial neuropathy or asymmetric painful radiculopathy (Mygland

et al., 2006). Numerous other phenomena have been observed, encompassing a large spectrum of

possibilities, including; brachial and lumbar plexopathies, nerve root involvement,

mononeuropathy multiplex, as well as a chronic peripheral polyneuropathy with a skin disorder

known as acrodermatitis chronica atrophicans, which can be clinically suggestive of Guillain-

Barre syndrome (Mygland et al., 2006; Halperin, 2003). This peripheral polyneuropathy is

Cascio 12

symmetrical, mostly sensory, tends to affect the lower extremity first, and follows the ACA skin

lesions or presents in stocking-glove fashion (Mygland et al., 2006; Rizvi, Diamond, 2008).

Damage to large, myelinated fibers impairs vibratory, proprioceptive, and discriminatory

sensations in the affected areas. Other symptoms associated with this condition include

hypoesthesia, dysesthesia, parasthesia, and sensory ataxia in the affected areas. These deficits

can lead to much functional impairment including decreased postural stability, impaired gait, and

impaired static and dynamic balance. Physical therapy seeks to limit these deficits through

endurance training, progressive strengthening and flexibility regimens, balance and coordination

exercises, skin care and management, patient education, gait training, and the use of various

modalities. The use of EMG biofeedback methods have been shown to help regrow the damaged

peripheral nerves.

Case Study: Peripheral Polyneuropathy Secondary to Chronic Lyme Disease

A 45 year old left handed male has been referred to physical therapy for the evaluation

and treatment of neurological involvement secondary to chronic Lyme disease. The patient has

recently been diagnosed with Lyme disease by a neurologist, who suspected that the disease was

contracted several months ago, and is now in the late disseminated phase of infection. The

diagnosis was made after the patient presented with chronic fatigue, stiff neck, severe headaches,

and a non-specific burning, tingling sensation in the arms and legs. The patient never noticed a

tick bite, and did not present with the classic Erythemia migrans, which led to the disease going

undiagnosed for an extended period of time. Due to the presentation of the patient, as well as the

fact that he resides in rural Connecticut, an endemic area, and spends a large amount of time

outside for recreational activities, the doctor ran both an ELSIA, and a Western Blot Test, both

of which came back positive. The infection was treated with 100mg of oral Doxycycline twice a

Cascio 13

day for 14-28 days, until the symptoms dissipated. Upon conclusion of the antibiotic treatment,

however, the sensory impairments lingered.

The patient works a desk job, but enjoys outdoor activities such as Golf, running, and

hiking. He lives with his wife and two young children, who like to participate in these

recreational activities with him. Ever since the onset of his Lyme symptoms, the patient has not

been able to engage in much of the hobbies that he enjoys, leading to mild depression and

decreased performance at work. He has stated that he wishes to return to his previous level of

function, and resume his normal life.

The patient complains of bilateral hypoesthesia, dysesthesia, and parasthesia in both the

feet and hands in a stocking-glove distribution pattern, as well as slight weakness in the feet. He

rates the pain on a Visual Analog Scale as 5/10, and describes the symptoms as insidious in

nature, building steadily over the past several months. Other than these complaints, the patient

describes himself as in good health, and is not currently taking any medication other than

occasional Ibuprofen for pain. Medical, surgical, and family history of the patient revealed no

relevant information. The patient had not received any other treatment for the Lyme disease

other than the initial bout of antibiotics.

Upon a systems review of the patient, there is no apparent cardiovascular, integumentary,

circulatory, cognitive, or gastrointestinal impairment. Sensation testing yields diminished

vibration sense as tested with a tuning fork, diminished light touch sensation as tested with

Symmes-weinstein mono-filaments, diminished temperature sensation, and diminished sharp-

dull discrimination, all in bilateral feet greater than bilateral hands, with decreasingly severe

involvement proximally. Proprioception and kinesthetic testing through awareness of passive toe

movements were also noted to be diminished. Two-pint discrimination, graphesthesia, and

stereognosis were intact.

Neuromuscular testing revealed normal muscle strength (4+-5/5) throughout, with

minimal muscular weakness (3+/5) in bilateral ankle plantarflexors, dorsiflexors, and foot

intrinsics. Deep tendon reflexes were normal, except noted to be depressed bilaterally (1+) in the

Achilles tendon. AROM and tone were both WNL throughout, and pathological reflexes (Clonus

and Babinski) were negative.

Cascio 14

An evaluation of the patent's gait indicates slight impairment as evidenced by diminished

foot clearance in swing with a slight foot drop, compensated with minimal contralateral vaulting,

and circumduction. Balance evaluation though use of the Mini BESTest scored 20/28, indicating

some slight impairment with dynamic balance. There were no apparent difficulties or complaints

of difficulty with ADLs.

Based on the evaluation, it can be concluded that the physical therapy diagnosis is an

apparent peripheral polyneuropathy characterized by mostly sensory involvement, and slight

motor involvement secondary to chronic Lyme disease, with impairments in functional mobility

as a result. Goals of treatment will include strengthening of weak muscles, normalization of gait

and balance impairments, restoration of previous function, and reduction of pain and sensory

symptoms.

Due to the varying nature of this condition, the treatment protocol will be highly

dependent on the patients’ progression of symptoms, and exercise tolerance. Similarly, it is

difficult to present a timeline, as these conditions tend to be unpredictable, and rarely the same.

Despite this, the prognosis for this patient is good, and I would anticipate a steady reversal of

symptoms over the span of several months.

Physical Therapy treatment sessions with this patient will often start with a brief bout of

aerobic exercise, in order to provide a warming effect. This will also hopefully work to improve

tissue perfusion and oxygen levels, which may have a positive effect on destroying any lingering

bacteria. It will also be highly encouraged that the patient engages in a self-directed long term

aerobic exercise regimen, in order to maximize the benefits associated with doing so.

Exercise Sets and Reps

Aerobic exercise Stationary bike Low resistance 10-‐15 minute warm up

Jogging (optional )

On own, as tolerated 30 mins/day 3-‐5x per week

Walking (optional)


Swimming (optional)


Cascio 15

Despite the patients normal ROM upon evaluation, it is important to maintain that, and

prevent deterioration via stretching of the effected body parts. This will also have a positive

effect on the gait deviations seen in this patient. Focusing on the muscles of the lower leg and

foot will play the biggest role in achieving this goal.

Exercise Sets and Reps ROM Calf stretch 30 seconds X 5 sets Soleus stretch 30 seconds X 5 sets Plantar fascia stretch 30 seconds X 5 sets

Calf and Soleus stretch will both be performed on a slant board, or against a wall. The

calf stretch will be performed with straight legs, while the Soleus stretch is done with bent knees.

Plantar fascia stretch will be performed by placing the heel as close to the wall as possible, the

slowly shifting the body weight forward, allowing the heel to slide backwards as the toes extend

up against the wall. The stretch will be felt at the bottom of the foot.

Due to the bilateral weakness in the patient’s lower leg and foot, a strengthening program

designed to target those areas will have an impact on decreasing any gait deviations associated

with that weakness, such as the patient’s foot drop and associated decreased clearance during

swing. Similarly, improving strength in the lower leg will work to improve deficits in dynamic

balance. Targeting of the intrinsic foot muscles will help improve stabilization, static and

dynamic balance, and reinforce the structural integrity and mechanical abilities of the foot. These

muscles will be worked by having the patient, who is seated in a chair, lift rubber bands off the

floor with their toes, and carefully placing them back into their receptacle. In addition to the

specific targeting of these muscles, we will work to integrate functional activities to promote

crossover to ADLs and leisure activities such as golf and hiking, in turn improving quality of

life.

Cascio 16

Exercise Sets and Reps Progression

Strengthening Heel raises 3 sets X 10-‐15 reps -‐ Flat on floor -‐ Off edge of stool -‐ 2 up, 1 down -‐ Single leg

Theraband dorsiflexion 3 sets X 10 reps -‐ Yellow -‐ Red -‐ Green -‐ Blue -‐ Black

Theraband eversion 3 sets X 10 reps -‐ As above Theraband Inversion 3 sets X 10 reps -‐ As above Intrinsic strengthening

(rubber band pickup) 3 minutes 5 minutes

Functional exercises Wall-‐sits 30 seconds X 3-‐5 sets

-‐ Mini squats -‐ Sit-‐stand exercises

-‐ Full squats -‐ Leg press

-‐ add weight R -‐ sport specific

-‐ golf -‐ Hiking

Gait retraining will play a large role in the rehabilitation program designed for

this patient. Due to the diminished foot clearance in swing, slight foot drop, and subsequent

compensation; it will be crucial that his gait pattern be normalized to both restore effective

functionality, and prevent any future complications of chronic gait disturbances. Gait retraining

will consist of specific strengthening programs of important ambulatory muscles, as well as the

specific weak muscles (see above). This protocol will be slow and progressive, focusing on

correct form and safe progression, with constant re-evaluation. Dorsiflexor strengthening

coupled with Plantarlexor flexibility will eliminate the foot drop, and allow for adequate

clearance. This should lead to a decrease in the impulse to compensate with contralateral

vaulting, and circumduction. Steps up and step down exercises from varying heights will help to

develop concentric and eccentric control of the weak lower leg musculature in a dynamic

fashion. Treadmill training, as well as visual feedback via mirrors and videotaping will help

reinforce the corrected gait pattern.

Cascio 17

The results of the miniBEST test indicate some difficulties with dynamic balance, which

is an issue that should be addressed during Physical Therapy sessions. Improving balance plays a

key role in patient safety, by decreasing falls risk, and thus decreasing risk of any future injury.

Balance impairments are diagnostic in nature; meaning that treatment is based entirely on the

specific difficulties observed. We will build from the basics, progressing through a series of

static balance progressions, culminating in the initiation of a dynamic balance regimen that

includes exercises which focus on reactive postural control.

Exercise Sets and Reps Progression

Static Balance Single leg balance 30 seconds X 3 sets -‐ 30 seconds X 5 sets -‐ 1 minute X 3 sets

-‐ Flat on floor -‐ Eyes closed -‐ Airex pad

-‐ Narrow BOS -‐ Tandem stance

Balance board 30 seconds X 3 sets -‐ 30 seconds X 5 sets -‐ 1 minute X 3 sets

-‐ Eyes clsoed Reactive postural

control Playing catch while

balancing 3 sets X 20 reps -‐ increasing weight of ball

-‐ varying throwing angle -‐ varying balancing

surface Dynamic balance Forward Right and Left

Step 5 reps with each

leading leg -‐ Increase volume -‐ Increase speed

Creek Crossing 5 times with each leading leg

-‐ Increase volume -‐ Increase speed

Ball Rolls 10 clockwise 10 counter clockwise

(each leg)

-‐ Increase volume -‐ Increase speed

Walk through cones (“s” shaped)

3-‐5 laps -‐ increase volume -‐ Increase speed

Obstacle negotiation 3-‐5 laps -‐ Increase volume -‐Increase speed

Grapevine 2-‐5 laps X 20ft -‐Increase distance -‐ Increase speed

Cascio 18

Reduction of pain will also play a huge role in the Physical Therapy management of this

condition. Various modalities can be used to decrease symptoms of pain, as well as help improve

some of the sensory issues associated with this disorder. Neuromuscular electrical stimulation

(E-stim) activates muscles by stimulating the partially intact peripheral nerve. This can have

numerous physiological effects including prevention of atrophy in partially denervated muscles,

reduction of pain, and improved regeneration of the damaged nerve. A more specific type of E-

stim, known as Transcutaneous Electrical Nerve Stimulation (TENS) will help block

transmission of pain signals to the brain, thus decreasing any painful sensation. The release of

endogenous opioids as a result of the stimulation will have a similar effect in masking the pain.

EMG biofeedback is another useful tool in pain reduction, as well as stimulation of nerve

growth. Here, electrodes are placed on specific muscles and the electrical output from those

muscles is broadcasted on a visual display. The patient can then regulate the tension in those

muscles, as they learn to selectively control them by manipulating the reading on the display.

This can be used to either target a partially denervated muscle, stimulating a contraction, and

thus promoting nerve regeneration, or to relax a chronically tense muscle. In this case, both

TENS and EMG biofeedback can be utilized in the distal LE to promote nerve regeneration, and

help relieve the chronic neuropathic pain.

TENS protocol frequency Intensity Pulse

duration

Nerve Time

Conventional 100hz

(high)

Low 50-‐80 μ

(short)

Group II (Aß

afferent)

30 mins/day

(at home)

Finally, one of the most important aspects of this rehabilitation process will be

patient education. It is crucial that the patient adopt these lifestyle changes in order to have a

successful, safe recovery. Management and care of the areas, such as the feet, which present with

altered sensation will prevent any wounds or skin breakdown from developing. A regular

Cascio 19

inspection of skin integrity on the bottom of the feet, proper fitting shoes, and avoidance of

barefoot walking will reinforce this. It is also prudent to manage the expectations of the patient,

informing him that this process can take time, and that nothing is guaranteed. The program will

stress slow, safe progression, with constant re-evaluation, and adjustments based on the specific

needs of the patient.

Cascio 20

References

Barbour, A. G., & Fish, D. (1993). The Biological and Social Phenomenon of Lyme Disease. Science, 260(5114), 1610-‐1616. Retrieved April 1, 2016, from https://www.wc4eb.org/wp-‐ content/documents/BarbourFish.pdf.

Beale, K. (n.d.). Lyme Disease. Retrieved April 05, 2016, from http://www.physio-‐ pedia.com/Lyme_Disease#Physical_Therapy_Management_.28current_best_evidence.29

Burrascano, J. J., MD. (2005). DIAGNOSTIC HINTS AND TREATMENT GUIDELINES FOR LYME AND OTHER TICK BORNE ILLNESSES. ADVANCED TOPICS IN LYME DISEASE, 15. Retrieved April 1, 2016, from http://www.gimnazjum.jadowniki.pl/borelioza/materialy_lyme/diagnositc_hints_and_treatmen t_guidelines_by_dr_burrascano_2005.pdf

Halperin, J. J. (2003). Lyme disease and the peripheral nervous system. Muscle & Nerve, 28(2), 133-‐ 143. Retrieved from http://onlinelibrary.wiley.com/doi/10.1002/mus.10337/epdf

Hovius JW, van Dam AP, Fikrig E (September 2007). "Tick-‐host-‐pathogen interactions in Lyme borreliosis". Trends Parasitol. 23(9): 434–8. doi:10.1016/j.pt.2007.07.001. PMID 17656156.

“How many people get Lyme disease?” (2015). Retrieved April 05, 2016, from http://www.cdc.gov/lyme/stats/humancases.html\

Lyme disease is a clinical diagnosis, based on your medical history, symptoms and exposure to ticks. (n.d.). Retrieved April 05, 2016, from https://www.lymedisease.org/lyme-‐basics/lyme-‐ disease/diagnosis/

Meyerhoff, J. O., MD, & Diamond, H. S., MD. (n.d.). Lyme Disease Differential Diagnoses. Retrieved April 05, 2016, from http://emedicine.medscape.com/article/330178-‐differential

Moser, M. M. (2011). Treatment for a 14-‐Year-‐Old Girl With Lyme Disease Using Therapeutic Exercise and Gait Training. Physical Therapy, 91(9), 1412-‐1423. Accessed March 31, 2016. http://dx.doi.org/10.2522/ptj.20110020.

Mygland, A., Skarpaas, T., & Ljøstad, U. (2006). Chronic polyneuropathy and Lyme disease. European Journal of Neurology, 13(11), 1213-‐1215. Retrieved April 1, 2016, from http://onlinelibrary.wiley.com/doi/10.1111/j.1468-‐1331.2006.01395.x/epdf

Rizvi, S., MD, & Diamond, A., MD. (2008). Neurological Complications of Lyme Disease. Medicine & Health, 91(7), 216-‐218. Retrieved April 1, 2016, from http://med.brown.edu/neurology/articles/sr21608.pdf

Sigal LH. Management of Lyme arthritis. Comprehensive Therapy 1999; 25(4): 228–38. http://link.springer.com/article/10.1007/BF02889624#page-‐1

Cascio 21

Steere AC, Coburn J, Glickstein L (April 2004). "The emergence of Lyme disease". J. Clin. Invest. 113 (8): 1093–101.doi:10.1172/JCI21681. PMC 385417. PMID 15085185.

Symptoms. (2015). Retrieved April 01, 2016, from http://www.cdc.gov/lyme/signs_symptoms/index.htm

Tilly, K., Rosa, P. A., & Stewart, P. E. (2008). Biology of Infection with Borrelia burgdorferi. Infectious Disease Clinics of North America, 22(2), 217–234. http://doi.org/10.1016/j.idc.2007.12.013

Transmission. (2015). Retrieved April 05, 2016, from http://www.cdc.gov/lyme/transmission/index.html

Understanding the EIA Test. (2015). Retrieved April 05, 2016, from http://www.cdc.gov/lyme/diagnosistesting/labtest/twostep/eia/index.html

case study: peripheral polyneuropathy secondary to chronic ... · case study: peripheral...

Documents