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Clinical Management of Guillain Barre Syndrome across the

Continuum of Care

Laura Plummer PT, DPT, Neurologic Clinical Specialist

Lisa E. Brown PT, DPT, Neurologic Clinical Specialist

Erin Riley PT, DPT, Neurologic Clinical Specialist

Disclosures None to disclose

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Objectives

• Describe pathophysiology of GBS and typical course of disease process

• Discuss how you would proceed with examination of a patient with GBS at various points in the recovery process

• Develop a plan of care for a patient with GBS at various points in the recovery process

• Discuss principles of overwork and considerations for developing therapeutic exercise programs for patients with GBS

Guillain Barre Syndrome

Google images, 2019

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Guillain Barre Syndrome

• Acute immune mediated demyelinating disorder affecting Schwann cells in the peripheral nervous system

• Syndrome with multiple variant forms

• Acute demyelinating inflammatory polyneuropathy (AIDP) most common in US and Europe (85%-90%) of cases

• Several other variants classifies by fiber type, mode of injury and alterations in consciousness

• Incidence is approx .8-1.89 per 100,000 cases annually Van den berg, 2014

• Incidence rates increase with age, highest > 60 yrs

• More common in men than women (3:2)

• Most common type of acute paralytic neuropathy

Pathophysiology

Preceded by some event, typically respiratory or gastrointestinal,

in approximately 75% of cases 1-4 weeks prior to onset of symptoms

Most common virus’ linked to GBS:

Other triggers may include: • Surgery, trauma

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Epstein-Barr virus Varicella zoster virus

Cytomegalovirus (CMV) Human Immunodeficiency virus

Hepatitis A, B, and E Haemophilus influenzae

Zika virus Mycoplasms pneumoniae

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Diseasecourse

van den Berg et al, Nat Rev Neurol2014

Typical Clinical Presentation

• Motor weakness• Rapidly progressive, relatively symmetrical

• Usually distal to proximal progression

• Leg weakness before arm in 90% of cases

• Hypo-reflexia or Areflexia (esp. distally)

• Sensory symptoms (parathesias and hyperesthesias) distal > prox

• Cranial Nerve involvement (45-75%)• Primarily facial involvement

• May have oculomotor and oropharyngeal involvement

• Pain (neuropathic and/or musculoskeletal 54-89%)

• Absence of fever

• Progression of symptoms from 12 hrs to 28 days before plateau is reached

8Yuki, N. N Engl J Med 2012;366:2294-304.

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Additional Characteristics

• Autonomic dysfunction (up to 70% of cases, 20% can be severe)

• Low cardiac output

• Cardiac dysrhythmias

• Fluctuating BP

• Bladder/GI dysfunction 5%

• Respiratory difficulties (15-30%) require mechanical ventilation

• Impaired respiratory muscle strength

• Inability to clear secretions due to ineffective cough

• Decreases tidal volume, vital capacity and oxygen saturation

• (Anandan, 2017)

Medical Diagnosis

CSF examination:

• Increased protein levels without pleocytosis

• Protein elevation noted in 90% of cases by second week

Nerve Conduction studies:

• Reduced amplitude or absent distal motor action potential

• Decreased conduction velocity

• Increased temporal dispersion

• Latency prolongation of F wave

• Nerve conduction block (axonal GBS)

MRI:

• Enhancement and swelling/thickening of spinal nerve roots

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National Institute of Neurological Disorders and Stroke (NINDS) Criteria

• Required features

• Progressive weakness of the legs and arms (sometimes initially only in the legs), ranging from minimal weakness of the legs to total paralysis of all four limbs, the trunk, bulbar and facial muscles, and external ophthalmoplegia

• Areflexia or decreased reflexes in weak limbs

• Supportive features include:

• Progression of symptoms over days to 4 wks(80% reach nadir in 2 wks)

• Relative symmetry

• Mild sensory symptoms or signs

• Cranial nerve involvement, especially bilateral facial nerve weakness

• Recovery starting two to four weeks after progression halts

• Autonomic dysfunction

• Pain

• No fever at the onset

• Elevated protein in CSF with a cell count ≤50/mm3 (usually <5 cells/mm3)

• Electrodiagnostic abnormalities consistent with GBS

NINDS continued

• Following feature make diagnosis of GBS doubtful:

• Sensory level (decrement or loss of sensation below a spinal cord root level as determined by neurologic examination)

• Marked, persistent asymmetry of weakness

• Bowel and bladder dysfunction at onset

• Severe and persistent bowel and bladder dysfunction

• Severe pulmonary dysfunction with little or no limb weakness at onset

• Severe sensory signs with little or no weakness at onset

• Fever at onset

• CSF pleocytosis with a white cell count >50/mm3

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Brighton Criteria

• Level 3 of diagnostic certainty• Bilateral and flaccid weakness of the limbs; AND• Decreased or absent deep tendon reflexes in weak limbs; AND• Monophasic illness pattern; and interval between onset and nadir of weakness between 12

hours and 28 days; and subsequent clinical plateau; AND• Absence of identified alternative diagnosis for weakness

• Level 2• All of the above AND• CSF total white cell count <50 cells/microL (with or without CSF protein elevation above

laboratory normal value); OR electrophysiologic studies consistent with GBS if CSF not collected or results not available

• Level 1• All of the above AND• AND instead of OR• Electrophysiologic findings consistent with GBS

• Seivar, Kohl, Gidudu et al, 2011

Clinical Variants Vriesendorp, Uptodate, 2019

Clinical Variant Characteristics

AIDP Progressive symmetric muscle weakness; absent or depressed

deep tendon reflexes; often preceding illness

Miller-Fisher Syndrome Ophthalmoplegia, ataxia, areflexia, 25% develop extremity

weakness

AMAN Selective involvement of motor nerves presents with muscle

weakness, and electrophysiological pattern of axonal

involvement; Occasional preservation of deep tendon reflexes;

Sensory not affected; More prevalent in summer; preceded by C

jeuni infection

AMSAN Both sensory and motor marked axonal degeneration; delayed or

incomplete recovery

Bickerstaff encephalitis Encephalopathy and hyperreflexia and ophthalmoplegia and

ataxia

Pharyngeal-cervical-brachial Acute weakness of oropharyngeal, neck and shoulder muscles

with swallowing dysfunction. May have facial weakness, leg

strength and reflexes usually preserved. May overlap with MFS

and thought to represent localized axonal GBS

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Differentiation of GBS, A-CIDP, CIDP(van den Berg,2014)

GBS GBS-TRF A-CIDP CIDP

Time to nadir

<2 weeks-4 weeks

< 2 weeks-4 weeks

4-8 weeks, followed by progression with deteriorations

>8 weeks

Disease Course

Monophasic 1-2 deteriorations within 8 weeks

>2 deteriorations or deterioration after 8 weeks

Progressive, stepwise or fluctuating

Severity Highly variable Highly variable Mostly moderate Mostly moderate distal an proximal weakness

Treatment IVIg or plasma exchange

Repeat IVigOr plasma exchange

Ivig or PE on confirmed dx of CIDP consider switch to prednisolone maintenance treatment

IVIg, or PEprednisolone

Patient Case: Mrs. Granger

• 73-year-old female, retired nurse manager

• PMH: poorly controlled HTN, polymyalgia rheumatic, Essential tremor (BUE), depression, osteoporosis, DDD, LBP, L rotator cuff tear, breast cancer, retinal detachment, GERD

• Social/Living History: lives alone in 1 story house with 5 stairs to enter with rail, widowed, 2 supportive daughters, retired

• PLOF: I ambulator at home, used a SPC in the community, I in IADLS, drives. House cleaner once a week. Daughter lives nearby

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Video

Mrs. Granger – First ER visit

Symptom presentation:

• Gradual onset lower extremity weakness over the last couple of weeks, relatively symmetrical an distal > proximal

• Hypo-reflexive BLE’s but tells ER MD ”they always have a hard time getting them”

• Parasthesias in bilateral feet which she notes she’s had “for years” but in last week has started to travel up her leg

• No fever

• Urinalysis: no growth as yet

• Initial labs: WBC 4.0-11.3

K/uL

RBC4.2-5.4 m/uL

Hgb12.0-16.0 g/dl

Hct36-48%

ESR

10.9 3.18 10.0 29.3 68mm/h

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Video initial er visit

Video progression

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Mrs. Granger: Readmission

Symptom presentation:

• Continued progression of weakness now including bilateral UE’s as well as LE’s , relatively symmetrical an distal > proximal

• Areflexive

• Signs of autonomic dysfunction with Fluctuating BP.

• Progression of symptoms over last 1-2 weeks

• Parasthesias in bilateral feet progressing to entire leg

• Pain bilateral lower extremities

• No fever

Mrs. Granger: Differential

Diagnosis

• Spinal Imaging: L5 transverse process compression fracture

• Head/neck CT and CTA: mild microvascular white matter disease with no ICH, infarct or stenosis of arteries

• tachycardia

• normal WBC on day of entry into hospital

• EMG/NCV: polyradiculoneuropathy with no axonal changes (good prognosis)

• lumbar puncture: elevated total CSF protein

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Medical Management Of GBS

• Intravenous immunoglobulin (IVIG)

• hypothesized the block macrophage and antibody binding.

• Blood product administered to boost antigent production

• Plasma Exchange

• Removes antibodies and is associated with reduced nerve damage and faster clinical improvement.

• Typical treatment is 5 exchanges over a 2 week period.

• Recommended when patients not able to walk 10 meters w/o assistance

Clinical Medicine 2010, AAN 2016, Neuroanesthesial Crit Care 2019;6:160-166

* When started within 2 wks from the onset, IVIG has equivalent efficacy to PE in individuals with GBS who require aid to walk

Modulation of the immune response within the first 2-4 weeks

Multidisciplinary Supportive Care

• Monitor cardiac and pulmonary functioning• Monitoring for signs of autonomic

dysfunction, respiratory failure, bulbar dysfunction, aspiration

• DVT prophylaxis and prevention of pulmonary embolism• Heparin, calf compression

• Pain Management

• Anxiety/Depression

• Identify risks for secondary complications• Skin breakdown• Urinary tract infections• Pulmonary infections• Nutrition (continuous high caloric protein

diet)

• Clinical Medicine 2010, AAN 2016, Neuroanesthesial CritCare 2019;6:160-166

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Pulmonary Function tests

• Neuromuscular respiratory function becomes compromised in 17-30% of patients

• “20/30/40 Rule

• Early intubation in patients with autonomic dysfunction

• Vital capacity < 15-20 mL/kg

• Max expiratory pressure (Pe max) < 40cm H20

• Max inspiratory pressure (PI max) < 30 cm H20

• > 30% reduction in baseline VC, PE max, and PI max

Predictors of

Intubation and

Ventilatory Assistance

• Sign of respiratory failure

• Tachypnea

• Use of accessory muscles

• Paradoxical breathing with inadequate effort

• Unable to complete sentences

• Weak cough, difficulty clearing secretions

• Pulmonary infiltrates or atelectasis

• Abnormal ABC’s showing hypoxemia or hypercardia

• If PFTs do not improve over 2 weeks tracheostomy is usually indicated

• Neuroanesthesial Crit Care 2019;6:160-166

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Medical Pain Management

• Acetaminophen and NSAIDS

• Oral, parenteral and IV opioids

• Lidocaine

• Selective norepinephrine and seratonicreuptake inhibitors (SSRI)

• Tricyclic antidepressants

• Carbamazepine(tegretol) and gabapentin(neurontin)

• Evidence for acute pain management

• Often used in long term management

• Neuroanesthesial Crit Care 2019;6:160-166

Autonomic Dysfunction

• Important cause of morbidity

• Often includes:

• Paroxysmal fluctuations in BP (19-24%)

• Sustained hypertension (3%)

• Arrythmias

• Sinus tachycardia most common (25-38%)

• Brady arrythmias also common

• Life threatening cardiac arrythmias can occur and require intervention

• Monitoring instituted at time of admission and continued until recovery underway and/or no longer need for ventilatory support

• Intravascular volume should be maintained

• Medications with hypotensive side effects should be avoided

• Monitoring of BP and HR and rhythm with position changes and suctioning

• Vriesendrop, 2019

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Mrs. Granger – Medical

Management

Admitted to ICU for close monitoring of symptom progression

Medical Management:

• Treatment 5 days of plasmaphoresis

Pain Management: • Gabopentin

Pulmonary Function: • Max Inspiratory pressure -40 cm H2O

Autonomic Function:• Orthostatic with position change

Supportive Care

• Compression stockings

• High protein diet and hydration

Clinical Course

Acute Phase

• Rapid progression of symptoms

• Symptoms peak (nadir) between 2-4 weeks

• 50% reach nadir within 1 week, 70% by 2 weeks, 80% by 3 weeks, and 98% by four weeks

Plateau Phase

• Characterized by stability of symptoms

• May last only days, but can last months

Recovery Phase

• Gradual improvement in symptoms. Individual time frame.

• Most patients show gradual recovery of muscle strength 2-4 weeks after plateau

• Sensory disturbance and fatigue can persist for years

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Prognostic Indicators

• Indicators of poorer prognosis

• Older age at onset (>60)

• Need for ventilatory support

• Rapid onset (less than 7 days) prior to admission

• An average distal motor response amplitude reduction to <20% of normal

• History of GI illness (presence of diarrhea)

• Prognostic scoring system can be used at 1 and 2 weeks after admission to estimate ability to walk at 6 months

• IGOS GBS Prognostic Tool

• 1 week (patient age, presence of preceding diarrhea and strength measure by medical research council sum score

• 2 weeks, GBS disability score replaces MRC sum score

• Ropper AH 1993, Khan F 2010, Walgaard, 2011, van Koningsveld, 2007

Outcomes

• 80% recover ambulation within 6 months

• 50% may continue to experience minor neurological deficits• Paresthesias, distal muscle weakness (foot drop), Moderate

to severe pain and extreme fatigue

• 5-10% have prolonged course with months of ventilatory support and incomplete recovery

• 3-7% die from pulmonary or cardiac complications or organ failure

• Relapses occur in 10% of patients• 2% end up being CIDP

• Bernsen et al reported 32% had changed their work and 52% had altered leisure activities at one year after onset

Total recovery time can take up to 2 years

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Van den Berg B. Nature Reviews. Neurology 2014

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Mrs. Granger: Acute

Hospital Course

Day 1-7: Intensive Care Unit

• Nadir reached.

• Autonomic responses stable with improved BP regulation

• Improvement of UE and facial weakness

• No mechanical ventilation required.

Day 7-10: Moved to acute care floor.

• No bulbar signs

• LE weakness beginning to improve

• decrease in light touch and vibration of UE and RLE vibration

• Autonomic responses stable

Mrs. Granger: ICU and acute

care considerations

PT Intervention

• Prevention of loss of ROM

• Positioning

• Resting foot splints

• PROM AAROM

• Pain Management

• Gentle pain free ROM

• Bed tent

• Modalities

• Coordination with team

• Pulmonary Function and airway clearance

• Positioning

• Deep breathing and assisted cough

• Maintenance of skin integrity

• Education of caregivers regarding frequent re positioning

• Specialty mattress or wheelchair cushions

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ICU/Acute Intervention

• Early Mobilization with cardiac monitoring (after nadir)

• Increase tolerance to upright

• Chair position of bed lift to cardiac chair

• Functional task practice

• Bed mobility, sitting balance, transfers

• Literature on immobility and early mobilization

• Immobility hastens physical deconditioning and muscle weakness

• Immobility is associated with increased risk for falls, delirium, skin breakdown, and venous thromboembolic disease

• Improved mobility during hospitalization has been linked to decreased risk of death at two years

• Mattison, 2019

ICU/Acute Intervention

• Ventilation/Gas Exchange

• Diaphragmatic breathing

• Incentive spirometer

• Pain

• Low grade moist heat to low back and posterior thighs while in bed

• Patient Education

• Monitoring of overwork symptoms

• Energy conservation

• Anxiety management

• Consult with team regarding sleep hygiene, timing of interventions-schedule

• Coping strategies

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Video 2 slides exam in acute

PT Intervention

Acute- Subacute Phase –

• Progressive Functional Training

• Core functional tasks (bed mobility, transfers, gait, stairs)

• Balance Training

• Adaptive Equipment

• Wheelchair, assistive device for mobility

• Improve ROM/Strength

• Progression from AAROM AROM

• Self stretching of key muscle groups

• Hip flexors, hamstrings, gastroc

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PT Intervention-Ventilation Gas

Exchange/Airway Clearance

Acute to subacute phase:

• Optimize gas exchange and prevent pulmonary complications

• Airway clearance interventions: postural drainage, positive expiratory pressure (PEP) devices, assisted cough, suctioning

• Ventilatory pump or respiratory muscle training, incentive spirometry, resistive breathing devices, diaphragmatic breathing

• Early functional mobilization

Screening to prevent or

manage common

secondary complications

• Dysautonomia (present in 70%, severe in 20% of cases)

• Integumentary systems review

• Facial weakness

• Dysphagia

• Visual or hearing impairment (rare)

• Fall risk assessment

• Depression/anxiety

• Pain assessment (change throughout course of disease process)

• Fatigue

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GBS specific Tests and Measures

• 7 point scale rating level of global disability between 0 (healthy), 3 able to walk with a stick, appliance or support (5 m across an open space) and 6 (death)

GBS Disability Scale

• Includes UE and LE functional tasks scored on range of 0 (no signs of disability) to 12(severe disability)

• Can be score through interview or by individual

• Reliable, valid and responsive to change across spectrum of care

• Significant association with patient’s own perception of clinical condition

Overall Disability Sum Score (ODSS)

GBS Disability ScaleHughes, 2002

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ODSS

Merkies, et al, 2002

Mrs. Granger: Acute

Discharge

Day 10: Discharge to Acute Rehab

• Function:

• Mod assist bed mobility

• Mod assist sit to stand

• Min assist amb with RW 5-10’

• Autonomic response to position change normal

• Cough strong. Does not require any ventilatory support

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Examination of patients

with GBS

• History:

• Patterns and sequence of symptom onset

• Medications, medical diagnostic tests

• Activity Limitations and Participation restrictions

• ADLs/IADLs

• Hobbies, activities, interests

• Contextual Factors

• Social support

• Environmental barriers

GBS specific history questions

• What were your specific symptoms?

• When did they start?

• Did you have a respiratory or diarrheal illness prior to symptoms?

• How long did you have symptoms prior to being hospitalized/seeking medical attention?

• How long until your symptoms stopped getting worse?

• Did you receive IVIG or plasmaphoresis?

• Any readmission/exacerbations of symptoms

• Did you require ventilatory support?

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Movement Analysis

• Understand important core tasks

• Helps guide exam as to priorities

Video 2 slides functional exam and motor exam sub acute rehab

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Core Outcome

Measures for Adults with Neurologic Conditions

• Berg Balance Scale

• FGA

• 10 MWT

• ABC

• 6 minute walk test

• 5 time sit to stand

Examination:Body

Structure and Function

• Body Structure and Function• Muscle Performance

• MMT• Dynamometry

• ROM• Goniometry

• Fatigue• Fatigue Severity Scale

• Sensory Integrity• Various modalities (light touch, vibration and

proprioception)

• Skin Integrity• Inspect skin and identify areas for potential pressure sores

• Postural Control

• Motor Control• Quality of movement

PainUse a body chartQuality and intensityRelieving and exacerbating conditions

Aerobic Capacity/EnduranceHR, RR, BP rest and with activity

PulmonaryBreathing pattern, auscultationCough

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Mrs. Granger: PT Exam

summary

• Cognition

• Alert and orientated to person, place, time and situation

• Requires simple commands due to decreased attention from fatigue

• Pain: aching

• 4/10 in low back and thighs during day

• 6/10 at night

• Fatigue:

• Fatigue Severity Scale: 7

Rehab PT examination

continued

• Functional Mobility: limited by fatigue

• Rolling: mod assist * 1 with rail

• Supine sit: mod assist *1 with rail

• Sit supine: max A *1 with rail

• Transfer: max A *1 squat pivot, mod A*1 stand step transfer with rolling walker (RW)

• Sitting static: Supervised (S) with LE support

• Sitting dynamic: With reaching 1-2 inches outside base of support required min A

• BERG: 9/56

• 5 x STS: 47s

• GBS disability scale score: 4

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Muscle Strength Right Left

Hip flexion 3-/5 3-/5

Hip abduction 2+/5 2+/5

Hip extension 2-/5 2-/5

Knee Extension 3+/5 3+/5

Knee flexion >=2+/5 >=2+/5

DF 3-/5 3/5

PF >=2+/5 >=2+/5

Shoulder flexion 3-/5 2-/5

Shoulder abduction 3-/5 2-/5

Elbow flex 3/5 3/5

Elbow extension 3/5 3/5

Grasp (finger flexion) 4/5 4/5

PT Examination

Body Structure and Function:Muscle Performance

PT Exam-Body Structure and

Function

• Sensory Integrity:

• Tingling in lower legs, feet and fingertips

• Impaired light touch distal verses proximal LE

• Impaired proprioception B great toes 7/10; intact ankle and B index fingers

• Cranial Nerve Exam:

• Intact

• Ventilation/Gas Exchange

• Pattern: decreased lateral costal expansion

• Cough: spontaneous, effective but fatigues

• 02 sat >95% rest on room air

• Aerobic Capacity/Endurance

• Rest BP 124/80, HR 92, RR 16, 02 sat 95% room air

• After transfer: BP 144/90, HR 112, RR 28, O2s sat 96% room air

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Prognosis

Positive Factors

• Slow disease progression <4 weeks

• No axonal damage

• No mechanical ventilation

• Lack of significant cardiac and pulmonary complications

• No preceding diarrheal illness

Negative Factors

• 73 years of age

• Multiple comorbidities

• Higher GBS Disability Score

• Previous level of function requiring cane and history of fall

• Social support- daughter local

Goals- rehab

Long term goals (LTGs) 2-4 weeks

• Mod I for all bed mobility

• Mod I transfers with RW

• Mod I ambulation 50 feet with RW level surfaces

• Min A up and down 5 stairs with B rails, step to pattern

• Mod I wheelchair mobility on level surfaces 50 feet

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PT Interventions

• Functional Training

• Balance Training

• Aerobic Conditioning

• Ventilation/Gas Exchange/Airway Clearance

• Strengthening

• Pain Management

• Positioning/ROM

• Orthotic/Adaptive Equipment

• Individual/Family/Caregiver Education

PT Intervention – Functional Training

Sub Acute:

• Transfers to varied height surfaces, car transfers

• Gait training varied surfaces/environments

• Stair training

• Balance Training: Steady state, anticipatory, reactive

Chronic:

• Community Mobility

• Recreational Activities

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Plan of care

Functional retraining

• avoid stress to muscles without anti gravity strength (use of assistive devices-rail, RW)

Strengthening

• AAROM to muscles with 3/5 muscle strength, non fatiguing

• AROM and functional task training to muscles >3/5, non fatiguing

• Avoid eccentric exercise to muscle without antigravity strength

• Monitor for signs of over work

Aerobic Conditioning

• Early

• Low intensity aerobic conditioning, 40-60% heart rate max

• Careful monitoring of resting and exertional vital signs

• Energy conservation

• Chronic

• Sub max (70-85%) beneficial

• Monitoring of physiological responses

• Gradual increase of continuous exercise time

Considerations for Exercise Prescription in Patients with GBS

• Progressive functional exercise improves physical outcomes

• Appears sub-maximal strength training is appropriate as recovery begins (increase in muscle strength and nerve conduction)• Sub maximal non fatiguing training with rest periods has not

shown adverse effects• Sub acute (>=3/5 but fatigues): <1 set 10-15 rep at 60-70% of 1

RM with careful monitoring• Mode: functional task practice, light free weight, low resist t-

band, aquatic therapy• Chronic (>=3/5 no complaints of overwork): ACSM guidelines: 60-

80% 1 RM, 2-3 times per week, major ms groups• Mode free weights or machines (consider motor control)

• Evaluate for symptoms of overwork

60Arsenault NS 2016

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Overwork Weakness

“ a prolonged weakness in the absolute strength and endurance of a muscle due to excessive activity.”

• Delayed onset muscle soreness

• Peaking 1-5 days post activity

• Reduction in maximum isometric force production that gradually recovers

Central and Peripheral Fatigue

Google images

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PT Interventions: Fatigue

• Low to moderate intensity exercise

• Energy Conservation

• Sleep Hygiene

• Home modifications/ Adaptive equipment

• Cognitive Behavioral Therapy

Central Fatigue

• LE Orthotic for foot dropPeripheral

Fatigue

Eur Neurol 2016;75:199–206Cell Mol Life Sci. 2010 Mar; 67(5): 701–713.

Orthotic Prescription

More stability Less stability

Non-articulating/Solid AFO Articulating AFO PLS or FRO

• poor balance/unstable in

stance

•Unable to transfer weight onto

LE

•Requires med/lat support at

ankle

• quad weakness with genu

recurvatum or > mod knee

instability

• DF weakness is primary

with full PROM

• w/ DF stop (limited DF/free

PF) to control for mild knee

flexion instability

•w/ PF stop (limited PF/free

DF) to control for genu

recurvatum

•Isolated DF weakness with

full PROM

•Normal or near normal

muscle activation with fatigue

•Normal medial-lateral ankle

stability

•No assist needed for knee or

hip control

Patient GoalsGait SpeedGait endurance/efficiencyBalance

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PT Intervention

• Later Phase – Restoration of Function

• Functional Task Practice!

• Fatigue Management

• Strengthening

• Aerobic conditioning

Mrs. Granger:

• 3 weeks in sub-acute rehab before D/C home

• Home PT 2x/wk for 6-8 weeks.

• Long term goals 6-8 weeks

• I in house hold without device

• Mod I st cane 1000 feet in community

• Mod I up and down 5 steps with B rail alternating

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Plan of Care

Gait training with and without cane of various surfaces household and community

Incorporate activities relevant to life roles (grocery shopping, hobbies)

Functional training

walking while carrying light objects, standing static and dynamic activities on various surfaces with and without vision

Balance training:

60-80% of 1 RM for muscle groups greater than 3, 2 times per week for major muscle groups

•Monitor for overwork

Strengthening

Interval walking or stationary bike, 60-80% max heart rate working up to 20-30 minutes, 3 times per week, RPE 12-13

Monitoring RPE, vitals and symptoms of fatigue

Energy conservation

Aerobic Training

Safety with gradual resumption of activities

•Not overstressing weakened muscles/ self monitoring for overwork

Self monitoring of vitals during exercise

Patient Education

4 video slides of exam and function at home

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Follow-up

Functional Status

Bed mobility and transfers Independent

Ambulates with st. cane mod I household,

S community

Negotiates stair with B rail and S

Continues to be fatigued, average

FSS=4.5

7 months after initial symptoms, 6 months after nadir, After 4 months acute and subacute rehab

Take Aways

GBS is a heterogenous polyneuropathy

Supportive care is important early for a favorable outcome

Progressive exercise improves physical outcomes but requires careful monitoring for overwork

Recovery is prolonged >=2 years

Persistent fatigue and sensory disturbance are common complaints even later out

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