Effectiveness of User Controlled Peroneal Stimulator

for foot drop in patients with hemiplegia following

Cerebrovascular Accident in an Indian Rehabilitation

set up: A Randomized Control Trial, Pilot Phase

Dissertation submitted to the Tamil Nadu Dr. MGR Medical University,

Chennai, in the partial fulfillment of requirements for the

MD Branch XIX (Physical Medicine and Rehabilitation) examination in

March 2014

 

Certificate

This is to certify that “Effectiveness of User Controlled Peroneal

Stimulator for foot drop in patients with hemiplegia following

Cerebrovascular Accident in an Indian Rehabilitation set up: A

Randomized Control Trial, Pilot Phase” is the bona fide work of Dr Kriti

Mishra, Candidate number 20116502, in partial fulfilment of the

requirement of the Tamil Nadu Dr MGR Medical University, Chennai,

for the MD Branch XIX (Physical Medicine and Rehabilitation)

examination in March 2014.

Dr. Alfred Job Daniel

Principal

Christian Medical College

Vellore

 

Certificate

This is to certify that “Effectiveness of User Controlled Peroneal

Stimulator for foot drop in patients with hemiplegia following

Cerebrovascular Accident in an Indian Rehabilitation set up: A

Randomized Control Trial, Pilot Phase” is the bona fide work of Dr Kriti

Mishra, Candidate number 20116502, in partial fulfilment of the

requirement of the Tamil Nadu Dr MGR Medical University, Chennai,

for the MD Branch XIX (Physical Medicine and Rehabilitation)

examination in March 2014, under my supervision and guidance.

Dr. Raji Thomas

Professor

Department of Physical Medicine and Rehabilitation

Christian Medical College

Vellore

 

 

 

Acknowledgement

This study has been one of the most interesting and learning experience

of my PG curriculum.

My sincere gratitude to Dr. George Tharion who made me believe in the

feasibility of the study and encouraged me to take this topic as my

dissertation. I express my deep gratitude to Dr. Jacob George for his

constant guidance throughout and to Dr. Raji Thomas for helping me to

pen down the entire study.

A special thanks to Dr. Suresh Devasayam and Mr. Akhil Mohan for the

fabrication of the device and for the consistent technical inputs and

feedback regarding the study.

I thank Dr. Judy Ann John for her continuous motivation, Dr. V. Anand

and Dr.Rajdeep Ojha for their inputs regarding the data analysis, the

statistics and the dissertation presentation.

A heartfelt gratitude to Mr. Ramesh who was the primary physiotherapist

for the intervention group and the rest of the Rehabilitation Institute and

OPD physiotherapists without whose co-operation the study would not

have completed.

 

I would also like to thank all my colleagues who shared my clinical work

while I finalised the study; Ms. Joyce for being the neutral assessor of the

study outcome measures; Ms Grace for helping in the randomisation and

final statistical analysis.

Most of all, I am grateful to the patients and their relatives who readily

agreed to participate in the study and gave honest feedbacks regarding the

intervention and the study.

Kriti Mishra

 

Index

Chapter Page

Title 1

Aim and Objectives 2

1. Introduction 3-5

2. Justification for the study 6-8

3. Review of Literature 9-49

3.1. Epidemiology

3.2. Risk factors for CVA

3.3. Etiopathogenesis

3.4. Presentations of Stroke

3.5. Stroke Syndromes

3.6. Evaluation of a stroke patient

3.7. Initial Treatment

3.8. Admission to Hospital and Acute Management

(After Hospitalization)

3.9. Neurological Recovery

3.10. Motor Impairment

3.10.1. Normal Gait

3.10.2. Role of Ankle Muscles in Normal Gait

And Biomechanics

 

3.10.3. Biomechanics of the Ankle

3.10.4. Gait Impairments Seen in Stroke

3.11. Rehabilitation in Stroke

3.11.1. Principles of Stroke Rehabilitation

3.11.2. Rehabilitation Related to Motor

Impairments

3.12. FES System

3.12.1. FES System Components

3.12.2. Drop Foot Stimulator or Peroneal

Stimulator (PS)

3.12.3. Studies Related to the PS

4. Methodology 50-61

4.1. Study Design

4.2. Settings and Locations Where the Study was

Conducted

4.3. Participants

4.4. Sample Size

4.5. Randomization

4.6. Interventions

4.7. Outcome Measures

4.7.1. Primary Outcome

4.7.2. Secondary Outcomes

 

4.8. Statistical Analysis

4.9. Statistical Methods

5. Results 62-79

5.1. Recruitment, Screening and Randomization

5.2. Baseline Demographic and Clinical

Characteristics of Participants

5.3. Primary Outcomes

5.3.1. 6 minute walk test (Walking Endurance)

5.3.2. 10 meters test (Walking Speed)

5.4. Secondary Outcomes

5.4.1. Spatial Asymmetry

5.4.2. Stride Length

5.4.3. Stance Percentage (% of the total stride time)

5.4.4. Dynamic Ankle Range of Movement

5.5. Additional Analysis

5.5.1. Duration of the Stroke

5.5.2. MMSE

5.6. User Feedback

6. Discussion 70-91

7. Limitations 92

8. Recommendations for further Study 93

 

9. Conclusion 94-95

Bibliography

Annexure

1. Institutional Review Board Acceptance Letter

2. Patient Information Sheet and Consent Form

3. Case Sheet

4. Database for all Patients

1

Title of the study

“Effectiveness of User Controlled Peroneal Stimulator for foot

drop in patients with hemiplegia following Cerebrovascular

Accident in an Indian Rehabilitation set up: A Randomized

Control Trial, Pilot Phase”

Place of study

Department of Physical Medicine and Rehabilitation

Christian Medical College

Vellore

2

Aim

To evaluate the orthotic effectiveness of a peroneal stimulator [Functional

Electrical Stimulation (FES) based neuroprosthesis] controlled by a

switch placed on the user's assistive walking aid (quadripod) and compare

it with conventional rehabilitation method of using an Ankle Foot

Orthosis (AFO) in the treatment of foot drop in hemiplegic patients

following Cerebrovascular Accident (CVA).

Objectives

The study proposes to:

• Compare the orthotic effect of a user based PS to AFO in

hemiplegic foot drop rehabilitation.

• Compare the effectiveness of the manually controlled peroneal

nerve stimulator for gait training during sub-acute and chronic phases of

stroke rehabilitation and in patients with two different levels of cognitive

ability as measured by MMSE.

• Evaluate the subjective perception of patients regarding the

effectiveness of the manually operated hand switch in the Indian

rehabilitation setting.

3

1. Introduction

Over the past few decades, cerebrovascular accident (CVA) has become a

predominant global health care problem(1)and is one of the leading

causes of mortality as well as acquired disability worldwide. There has

been a change in the prevalence rate of CVA with the trend shifting from

developed countries to developing countries including India, where it has

become a silent epidemic(2). Lack of health care facilities at the primary

level for risk factor screening, non-accessibility to appropriate treatment

and common drugs, inadequate follow-up and secondary prevention

programmes and rehabilitation facilities have been attributed to higher

rates of death and disability in these low income countries, adding to the

disease burden(3). With these changing trends, a further increase in

prevalence of stroke related disease burden is anticipated over the next

two decades and hence, continuum of care post stroke and rehabilitation

has an essential role(4).

Stroke related impairment is multi-fold and include those related to

cognition, behaviour, language and speech, vision, swallowing, motor

and sensory functions. The motor impairment is the most widely

recognized impairment since it affects the mobility of patients and limits

the day to day functions(4). The hemiplegia leads to increase in muscle

4

tone in the lower limb. The weakness is more in distal muscles rather than

proximal. The weakness of ankle dorsiflexors results in inability to clear

the foot during the swing phase and inability to control foot falling after

the heel strike of stance phase (slap foot). The condition is called foot

drop(5). Ankle plantar -flexor spasticity or plantar flexor contracture can

further contribute to this impairment. A number of compensatory

movement patterns and limited functional mobility accompany the

condition(5).

In the conventional rehabilitation method, patients are trained to walk

with an ankle foot orthosis (AFO) to provide ankle stability, with or

without an appropriate walking aid.

An alternative tried over the past 6 decades is a drop-foot stimulator or

peroneal stimulator. The stimulator involves application of electric

current to the intact common peroneal nerve to generate muscle

contraction and enhance gait by improving foot clearance during the

swing phase and stability during initial stance phase(6). There have been

a number of studies to report a positive orthotic effect of Functional

Electrical Stimulation (FES) including recent studies comparing it with

AFO use(7–9). These studies have been done using automatic as well as

foot switches which have had their own limitations. Moreover, most of

5

these studies have evaluated FES in patients with hemiplegia of more

than 6 months duration.

The current study involved FES with a quadripod based switch gait

sensor making it a technically simpler and more adaptable device for use

in the Indian rehabilitation setting, with the sensor being a user controlled

system. Moreover, the stimulator, being an in-house development at our

Bioengineering department, was a low cost device. The study was

designed to investigate its use during the subacute and chronic phases of

stroke rehabilitation comparing its use with AFO and in patients with two

different levels of cognitive ability.

6

2. Justification for the study

Gait training with AFO and a walking aid (quadripod/ cane) is an

important goal of stroke rehabilitation. The AFO holds the foot in the

neutral position and prevents foot drop during the swing phase, thereby

helping in ground clearance. It also provides stability to the ankle during

the initial phase of stance(5). However, the AFO has its own

disadvantages in the form of limited ankle mobility, discomfort and

cosmetic issues(7,8).

The alternative option of providing electric stimulation to the common

peroneal nerve activates the ankle dorsiflexors and helps in ground

clearance. It has a two–fold effect: orthotic and therapeutic(7,8).

Immediate orthotic effect is that active dorsiflexion is more close to

physiologically normal gait biomechanics. Therapeutic effects include

improvement in muscle strength and joint range of motion and increased

voluntary control due to regular activation of the muscles.

Over the last six decades the PS (peroneal nerve stimulator) has

undergone constant innovations making it more user friendly with better

orthotic effect(6). Initial trials till the early 1990s involved stimulators

with surface electrodes activated by foot switches. However, foot

switches (either open/ close mechanical switch or force sensitive

7

resistors) tended to wear and tear on prolonged use, had inappropriate

firing of the switch due to poor contact or insufficient force during

hemiplegic gait (mainly because of gait asymmetry). The poor reliability

and size of the foot-switch, and the requirement for fitting of electrodes

and the foot-switch each day made these early devices unattractive(6).

In order to overcome these limitations came the advent of implantable PS

and automatic contactless artificial gait sensors in the form of

accelerometers and gyroscopes. The accelerometer with gyroscopes

detects the joint segment orientation and determines the timing for the

stimulus for dorsiflexion. However, being automatic sensors, they require

a more precise synchronization with the swing phase of gait cycle to

prevent inappropriate dorsiflexion. The gait asymmetry seen in

hemiplegic gait further contributes to this limitation.

Hence, in the present study, we chose to use a user controlled device.

Since the foot switch had its limitations as mentioned previously, a

manually operated hand switch was used to control stimulation. In low

resource settings as prevalent in India, where patients may prefer walking

bare-foot and are often given a walking stick/quadripod or similar aid for

safety purposes, a hand switch placed over the walking aid (quadripod)

was considered a reasonable option. It provided the patients with

8

voluntary control over the stimulation timing which is particularly useful

in avoiding small obstacles on the ground.

The evidence related to the effectiveness of hand switch based PS in the

literature is insufficient to approve or disprove its use clinically. A similar

device was fabricated in 1990’s (10). However, to our knowledge, its

effectiveness in clinical settings is unknown.

With these considerations, the study was designed to address the needs of

hemiplegic patients with foot drop admitted to our rehabilitation set-up

within 1 year of stroke. The study was also an attempt to make the PS

better adapted to the Indian settings mainly in terms of its low cost, small

size, technical simplicity and allowing option of bare-foot walking. In

view of better technical feedback, a wired switch was used for the study

with a plan to make a wireless device subsequently.

9

3. Review of Literature

Stroke or cerebrovascular accident as defined by WHO is “the rapid

development of clinical signs and symptoms of a focal neurological

disturbance lasting more than 24 hours or leading to death with no

apparent cause other than vascular origin”(11). It is caused by occlusion

or rupture of cerebral blood vessels resulting in sudden onset of

neurologic deficit characterized by loss of motor control, altered

sensation, cognitive or language impairment, disequilibrium, or coma

depending on the area in the brain affected. It excludes nonvascular

conditions of focal brain damage presenting with stroke-like symptoms,

such as seizure, hypoxemia, traumatic brain injury, demyelinating lesions

and brain tumour (12).

3.1 Epidemiology:

Incidence of stroke is 15 million per year worldwide and a prevalence

rate of 27–34/1,00,000 in the 35–44 age group to 822– 1116/100,000

in the 75+ age group has been noted in Indian studies(13). There has

been a recent trend change with stroke being more prevalent in

developing countries than in the high income countries. In fact, stroke in

younger age is more prevalent in India as compared to the global

prevalence of young stroke and hence, it has a significant economic

10

impact in developing nations like ours. This further adds to the disease

burden, in turn affecting the quality of life for these patients(13).

3.2 Risk factors for CVA:

This can be classified as modifiable and non-modifiable as shown

in figure 1 (12,14).

Figure 1: Risk factors

Table 1: Risk factors and Their Role

Risk factor Role in etiopathogenesis of CVA

Hypertension Increases risk of thrombotic, lacunar, and haemorrhagic stroke.

Heart disease Coronary Artery Disease doubles stroke risk. Fivefold increase in stroke risk in chronic and stable atrial fibrillation and up to 17 times the normal in

Risk factors for CVA

Non‐modifiable: age, 

race/ethnicity, sex and family 

history 

Modifiable: hypertension, 

smoking, atrial fibrillation, diabetes, obesity, sedentary 

lifestyle 

11

atrial fibrillation related to rheumatic heart disease.

Diabetes mellitus Independent risk factor leading to two-fold increase in stroke risk

Smoking Directly proportional increase in stroke risk with greater amounts of smoking

Hyperlipidemia Indirect risk factor for stroke by its contribution to the development of coronary artery disease and atherosclerosis.

Metabolic Syndrome

Include high waist circumference, increased blood pressure, low HDL level, elevated serum triglyceride and elevated fasting glucose. A graded increase in stroke risk seen with an increased number of metabolic risk factors and hence, the presence of all five components led to a fivefold increase in stroke risk.

Homocysteine Elevated homocysteine levels have been associated with higher risk of ischemic stroke.

3.3 Etiopathogenesis:

Based on the etiopathogenesis, CVA can be broadly divided into

two categories(12,14)

A. Intracranial haemorrhage includes 15% of all strokes. It can

further be divided into:-

1. Intracerebral bleed (10%) caused by rupture within the brain

parenchyma of weakened vessels due to hypertension,

12

arteriovenous malformation (AVM), tumor or other risk factors

like trauma, vasculitis, and bleeding into a tumor, disorders of

bleeding diathesis (e.g.: thrombocytopenia or coagulation

disorders). Most common site for hypertensive bleed is putamen or

thalamus followed by cerebellum in 10 % of patients.

2. Subarachnoid haemorrhage (5%) resulting from aneurysmal

rupture of a cerebral artery into the subarachnoid space

surrounding the brain.

B. Ischemic injury is responsible for 85% of strokes resulting from:-

1. Thrombosis : large vessel (40%) or small vessel (20%) thrombosis

is commonly caused by atherosclerotic cerebrovascular disease.

Small vessel thrombosis is often associated with lipohyalinosis of

small, deep, perforating arteries found in chronic hypertension.

2. Cerebral embolism (20%): Emboli are often of cardiac origin,

formed due to valvular disease or atrial fibrillation or chronic

ischemic cardiovascular disease associated with secondary

ventricular wall hypokinesia and subsequent increased intra cardiac

thrombus formation. The deep vein thrombosis in pelvis or lower

limbs can embolize to the right side of the heart, through a patent

13

foramen ovale into the left atrium and then into the cerebral

circulation. This is known as paradoxical embolism

3. Other causes (5%) such as cerebral vasculitis or cerebral

hypoperfusion.

3.4 Presentations of stroke (12,14)

Transient Ischemic Attacks (TIA): American Stroke Association

defined TIA as “a brief episode of neurologic dysfunction caused

by focal brain or retinal ischemia, with clinical symptoms typically

lasting less than an hour, and without evidence of acute infarction”

as determined by cranial imaging. It is sudden in onset with

apparent full resolution of symptoms including no imaging

findings.

Cerebral thrombosis: Insidious onset, worsening of deficits over

hours or days followed by stabilisation and gradual improvement.

Cerebral Embolism: The presentation is sudden. The embolus may

break into smaller fragments and result in multiple small infarcts.

Hence the initial clinical deficits may change and eventually fade if

the embolus undergoes lysis and fragmentation.

14

Lacunar stroke: It arises due to small, circumscribed infarcts less

than 1.5 cm in diameter resulting from occlusions of the deep

penetrating branches of the large vessels perfusing the subcortical

structures. They are often associated with hypertension and can

cause major neurologic deficits if they occur in key regions, or

vice-versa.

Intracerebral Haemorrhage: Abrupt onset with severe headache,

rapidly progressive neurologic deficits and progressive impairment

of consciousness leading to coma. Brain displacement leading to

cerebral oedema and transtentorial herniation and death, is seen

within the first few days post-stroke.

Subarachnoid Haemorrhage: It presents as severe sudden

headache followed by vomiting and signs of meningeal irritation.

Focal signs may develop subsequently. Coma frequently occurs

and one third patients die acutely.

Higher mortality rate is seen in cerebral haemorrhage than

infarction. The neurological deficit from haemorrhage recovers

better than the initial deficit from an infarction. Urgent

decompression with hematoma evacuation can be lifesaving.

Nimodipine is routinely administered to reduce the severity of

arterial vasospasm seen with subarachnoid haemorrhage and early

15

surgical/ invasive radiological intervention in the form of clipping

the aneurysm neck or coiling to thrombose the aneurysm is done to

obliterate the aneurysm and prevent recurrent haemorrhage.

Hydrocephalus is common in SAH. It can develop immediately

due to obstruction of the ventricular system from intraventricular

haemorrhage or as a later complication due to arachnoiditis

(fibrosis of arachnoid granulations) from blood in the CSF causing

functional disruption of CSF resorption. It presents with the classic

symptoms of subcortical dementia, incontinence, and gait disorder

or decline in performance in a rehabilitation program.

3.5 Stroke Syndromes:

Based on the brain vascular anatomy, stroke involving certain

regional vascular supply leads to specific neurological deficits. This

produces ischemic stroke syndromes and thereby assist in localising the

stroke lesion and predicting functional outcome(12,14).

Internal Carotid Artery Syndrome: Depending on the collateral

circulation available, clinical consequences can vary from no

significant deficit to severe deficits. Massive infarction before the

ACA and MCA division can present with dense contralateral motor

and sensory deficits. Severe cerebral oedema can cause

16

transtentorial herniation and death. Decompression with

craniectomy can be lifesaving.

Middle Cerebral Artery Syndromes: It originates from internal

carotid artery. It passes through Sylvian fissure onto the lateral

surface and divides into upper and lower division. In the Sylvian

fissure, it gives rise to lenticulostriate arteries perfusing the basal

ganglia and internal capsule. Occlusion of MCA leads to different

symptoms as mentioned in Table 2

Table 2: MCA Occlusion Features

MCA1 occlusion site Features

Origin Depressed consciousness, deviation of eyes to

lesion side, contralateral hemiplegia, decreased

sensation, homonymous hemianopia

Dominant lobe: aphasia

Non-dominant lobe: dysphagia, contralateral

hemianopia, perceptual deficits and neglect

Superior Division Dense contralateral sensory-motor deficits,

initially global aphasia if dominant side

17

involved, later expressive aphasia

Inferior division Left side: aphasia, right side: severe left sided

neglect, attention deficits, constructional apraxia,

dressing apraxia, perceptual deficits, aprosodia,

Partial or complete contralateral homonymous

hemianopia

1MCA: Middle Cerebral Artery

Lacunar Stroke: The varied presentation of lacunar stroke

depends on the site of occlusion as specified in Table 3.

Table 3: Lacunar stroke

Site Features

Internal capsule Pure motor hemiplegia, associated dysarthria,

hand clumsiness in anterior lesion of the internal

capsule

Thalamus Contralateral sensory loss with or without

weakness

Anterior Cerebral Artery Syndromes: Anterior cerebral arteries

supply the median and paramedian regions of the frontal cortex

18

and the strip of the lateral surface of the hemisphere along its

superior border. The deep penetrating branches supply the head

of the caudate nucleus and the anterior limb of the internal

capsule. The deficits include contralateral hemiparesis (lower

limbs weaker than upper limbs), associated sensory loss of the

leg and foot, urinary incontinence , transcortical motor aphasia

with preserved repetition, behavioural issues like diminished

reasoning, lack of initiation, distractibility etc.

Vertebrobasilar Syndromes: The two vertebral arteries join to

form the basilar artery at the junction of the medulla and pons.

The basilar artery terminates into two posterior cerebral arteries

at the upper midbrain level. The posterior cerebral arteries are

connected to the middle cerebral arteries via the posterior

communicating arteries forming the circle of Willis. The

vertebral arteries and basilar artery supply the brainstem via

short circumferential and paramedian branches and through the

long circumferential branches supply the cerebellum. Lesions in

the vertebrobasilar system produces hemisensory deficits, visual

impairment, visual agnosia, prosopagnosia, dyschromatopsia,

alexia without agraphia, memory deficits, dysarthria, dysphagia,

disequilibrium and vertigo, and Horner’s syndrome.

19

3.6 Evaluation of a stroke patient

There are a number of guidelines for the management of patients

following stroke. In our hospital, the guidelines are broadly based on the

guidelines by the American Stroke Association(15). A few salient

features of the recent recommendations (March 2013) include the

following:

The goal of acute management is complete emergency evaluation

of patients with suspected stroke and initiate fibrinolytic treatment

within 60 minutes of arrival in emergency department. An

organized protocol is recommended for this evaluation (Class I;

Level of Evidence B).

Initial evaluation should include limited number of hematologic,

coagulation, and biochemistry tests with mandatory blood glucose

prior to the initiation of intravenous recombinant tissue

plasminogen activator  (rtPA). Baseline electrocardiogram and

cardiac enzymes (troponin) assessment to assess for associated

Coronary Artery Disease (CAD).

Non–contrast-enhanced CT or MRI to determine ischemia by

presence of CT hypodensity or MRI hyperintensity to exclude

20

intracerebral haemorrhage since it is an absolute contraindication

to rtPA

CT perfusion and MRI perfusion and diffusion imaging including

measures of infarct core and penumbra especially for patients

beyond time windows for intravenous fibrinolysis who are being

considered for rtPA

Noninvasive imaging of the cervical vessels for patients with

resolved cerebral ischemic symptoms and for those with suspected

TIAs

CT angiography or magnetic resonance angiography of the

intracranial vasculature to exclude the presence of proximal

intracranial stenosis and/or occlusion.

The imaging study should be interpreted within 45 minutes of

patient arrival in the emergency department by an expert physician

or radiologistto prevent any delay in administration of rtPA.

3.7 Initial treatment (15)

1. Airway support, including ventilatory assistance to maintain

oxygen saturation >94%.

21

2. Cardiac monitoring at least for the first 24 hours for atrial

fibrillation and cardiac arrhythmias.

3. Lowering of the blood pressure keeping systolic blood pressure <

185 mmHg and diastolic blood pressure <110 mmHg is important.

Many patients have spontaneous decline in blood pressure during

the first 24 hours after onset of stroke. Medications should be

withheld unless the systolic blood pressure is >220 mm Hg or the

diastolic blood pressure is >120 mm Hg. No data are available to

guide selection of medications for the lowering of blood pressure

in the setting of an acute ischemic stroke.

4. Correction of hypovolemia and correction of hypoglycemia (blood

glucose <60 mg/dL) or hyperglycemia should be done.

5. Intravenous Fibrinolysis rtPA (0.9 mg/kg, maximum dose 90 mg)

for eligible patients within 3 hours of onset of ischemic stroke. For

patients with time period of 3 to 4.5 hours after stroke onset, rtPA

can be considered following exclusion criteria: patients >80 years

old, those taking oral anticoagulants, baseline NIHSS score >25,

imaging showing ischemic injury involving more than one third of

the middle cerebral artery territory, or patients with a history of

both stroke and diabetes mellitus.

22

6. Endovascular Intervention: Intra-arterial fibrinolysis is useful in

patients with major ischemic strokes of less than 6 hours duration

caused by occlusion of the middle cerebral artery who are not

otherwise candidates for intravenous rtPA (Class I; Level of

Evidence B). The optimal dose of intra-arterial rtPA is not well

established.

Mechanical thrombectomy (Class I; Level of Evidence A):

Emergent angioplasty and/or stenting of the extracranial carotid or

vertebral arteries using stent retrievers such as Solitaire FR and

Trevo are generally preferred to coil retrievers such as Merci. It is

used in patients with contraindication to intravenous therapy or

those with large artery occlusion not responding to intravenous

fibrinolysis. It can be used alone or in combination with

pharmacological fibrinolysis (Class IIa; Level of Evidence B).

Additional randomized trial data are needed to prove its

effectiveness. (New recommendation)

7. Anticoagulants: Urgent anticoagulation not recommended for

treatment of patients with acute ischemic stroke (Class III; Level of

Evidence A).

8. Antiplatelet Agents: Oral Aspirin (initial dose is 325 mg) within 24

to 48 hours after stroke onset is recommended.(Class I; Level of

23

Evidence A). Other intravenous antiplatelet agents inhibiting the

glycoprotein IIb/IIIa receptor is not recommended (Class III; Level

of Evidence B).

9. Neuroprotective Agents are not recommended since no

pharmacological agents have demonstrated efficacy (Class III;

Level of Evidence A).

10. Surgical interventions: Emergent or urgent endarterectomy is not

recommended for a small infarct core with large territory at risk

(eg, penumbra), for patients with compromised inadequate flow

from a critical carotid stenosis or occlusion, or in patients with

unstable neurological status (either stroke in-evolution or

crescendo TIA), (Class IIb; Level of Evidence B).

3.8 Admission to the Hospital and Acute

Management (After Hospitalization)

The use of comprehensive specialized stroke care (stroke units)

including rehabilitation, as shown in Table 4, is recommended

(Class I; Level of Evidence A).

24

Table 4: Intervention post-acute phase with level of evidence

Intervention Level of evidence

Antibiotics : Suspected pneumonia or Urinary

tract infection

(Class I; Level of

Evidence A)

Anti-coagulants: to prevent deep vein

thrombosis

(Class I; Level of

Evidence A)

Nasogastric/ nasoduodenal/ PEG1 feeds: for

nutrition and adequate hydration especially in

patients with inadequate swallowing

(Class I; Level of

Evidence B).

Early mobilisation (Class I; Level of

Evidence C)

Early Interventions to prevent recurrent stroke (Class I; Level of

Evidence C)

Anticoagulants or aspirin: for DVT2

prophylaxis

(Class IIa; Level of

Evidence A).

Treatment of acute neurological complications

Anti-oedema measures Class I; Level of

Evidence A

25

Close monitoring for signs of neurological

worsening

Class I; Level of Evidence

A

Decompressive surgical evacuation of a space-

occupying cerebellar infarction for treating

herniation and brain stem compression

(Class I; Level of

Evidence B).

Decompressive surgery for malignant oedema

of the cerebral hemisphere is effective and

potentially life saving

(Class I; Level of

Evidence B).

Ventricular drain for acute hydrocephalus ---

Anti-epileptics for recurrent seizures ---

1PEG: Percutaneous Entero Gastrostomy,

2DVT: Deep Vein Thrombosis

Rehabilitation is usually initiated during the acute phase. Subsequent to

the acute phase, rehabilitation depends on the deficits and disabilities in

an individual. The site and size of the initial stroke lesion and the extent

of subsequent recovery usually determines the long term effect of stroke.

26

3.9 Neurologic Recovery

Neurological recovery begins immediately after the stroke with initial

recovery in areas of the ischemic penumbra, mainly following resolution

of oedema and associated mass effect. Subsequently for several months,

cerebral plasticity and functional re-organization of the cerebral cortex

forms the basis for this recovery through spontaneous and learning-

dependent processes. This involves restitution (restoring the functionality

of damaged neural tissue), substitution (reorganisation of partly-spared

neural pathways to relearn lost functions), and compensation

(improvement of the disparity between the impaired skills of a patient and

the demands of their environment)(4). This learning dependent process is

observed with intensive training in stroke survivors and research is on-

going to determine the optimal training program to achieve maximal

motor recovery. Therefore approaches for rehabilitation have started

including interventions and therapy facilitating neuroplasticity, apart from

the compensatory techniques such as ambulating with a cane and AFO

for lower limb motor impairment.

Recovery from Impairments:

In the majority of hemiparetic patients, there is a classic pattern of

recovery. The functional motor recovery in the arm is less than in the leg,

27

reason being that ischemic strokes affecting the MCA territory are more

common than those affecting only the anterior cerebral artery territory.

This is due to higher flow through the MCA and the more direct path for

embolism. Other reason is the distinct functional demands placed on

the upper versus the lower limb. The lower limb can be functional with

some gross voluntary movements and its ability to maintain extended

position while the upper limb requires fine motor control for functional

tasks (12)

3.10 Motor Impairment

Motor impairment restricting mobility is the most easily

recognisable impairment. Motor impairment can include deficits in

muscle power (the speed with which force can be generated), motor

control and coordination, muscle tone, and balance(12).

Prior to specific motor problems related to CVA sequelae, a review

of the normal gait cycle and ankle biomechanics would enable better

understanding of the impairments following stroke.

3.10.1 Normal Gait:

Bipedal locomotion is unique to human beings with each person

having a characteristic gait pattern. It is a continuous movement with

repetition of the basic unit called the gait cycle. Each gait cycle starts

28

from the time a limb strikes the ground and continues till the whole

episode re-occurs on the same side. It has an alternate pattern of one

lower limb supporting the body weight and other limb advancing and

propelling the body further(14,16).

Hence, each gait cycle comprises of two phases: stance phase where

the foot is in contact with ground and swing phase when the foot is in the

air for limb advancement(14,16). Further functional subdivisions of the

swing and stance phase are as follows:

1. Stance phase:

Initial contact: Foot strikes the ground

Loading response: Foot in flat position on the ground till the

opposite foot is off the ground for swing at the end of double limb

support. It forms 11% of gait cycle

Midstance: body weight is directly over the supporting lower

extremity and involves lifting of the opposite foot until the

ipsilateral tibia is vertical. It starts at 11% of gait cycle and ends at

30 % of the gait cycle when the weight is directly over the

ipsilateral limb.

Terminal stance: It begins when weight is directly over the

supporting limb and continues until the opposite foot contacts the

29

ground (contralateral initial contact). It extends from 30 % of gait

cycle to 50% of the gait cycle.

Pre-swing: It begins with initial contact of the opposite foot and

ends with ipsilateral toe-off, i.e, toe of the ipsilateral foot leaves the

ground. It forms 10% of the stance phase.

2. Swing Phase:

Initial swing: involves the lift-off of the foot from the floor and

ends with alignment of the foot to the opposite foot until maximum

knee flexion occurs.

Midswing: begins with alignment of the ipsilateral foot to the

opposite foot and ends when the tibia is vertical.

Terminal swing: begins with vertical tibia and ends when the foot

contacts the ground (initial contact).

During the gait cycle, based on the foot-floor contact, the stance

phase can additionally be subdivided into two periods of double limb

support and one period of single limb support. Double limb support is the

period when both feet are on the ground for transferring the body weight

from one limb to the other. This period is seen during the beginning and

the end of the stance phase. When double support is absent completely,

the locomotion is running. Single limb support periods initiates when the

30

opposite foot is lifted off the ground for the swing phase. The gait cycle is

broadly divided into 60% of the stance phase and 40% of the swing phase

and approximately 10% overlap for each double support time. These

ratios changes with the variation in velocity of ambulation(14,16).

Gait cycle is further subdivided into different periods for better analysis.

The stride period is the time period involving an event of one foot till the

recurrence of the same event for the same foot, i.e., the initial contact to

the next initial contact of the same foot Stride length is the distance

covered between same events of the same foot in the direction of

progression during one stride. The step period is the time measured

from an event in one foot to the subsequent occurrence of the same event

in the other foot. Hence, each stride period of the gait cycle has two

step periods. Step length is the distance covered between the feet in the

direction of progression during one step. Cadence refers to the number

of steps in a period of time (commonly expressed as steps per minute).

The step length, step time and cadence are found to be symmetric for

both legs in normal individuals and is useful in identifying and

measuring asymmetry between the two sides of the body in pathologic

conditions and hence, are useful parameters when evaluating pathologic

gait(14,16).

31

3.10.2 Role of ankle muscles in normal gait and

biomechanics

Ankle dorsiflexors form the anterior compartment muscles of the

lower limb and include tibialis anterior, extensor hallucis longus,

extensor digitorum longus and peroneus tertius. They originate

from the tibia and fibula and adjoining interosseous membrane and

are inserted into the tarsal and meta-tarsal bones and phalanges of

the toes(16,17).

Ankle plantarflexors form the posterior compartment muscles of

leg and are classified as superficial and deep. The superficial

muscles include gastrocnemius, soleus and plantaris. Deep muscles

are popliteus, flexor digitorum longus, flexor hallucis longus and

tibialis posterior. Gastrocnemius originates from the femur and

capsule of knee joint and soleus from the tibia and fibular shaft.

Tendon of gastrocnemius and soleus fuses to form tendo-calcaneus

(achillis) and is inserted into the posterior surface of the

calcaneum. Rest of the muscles originate from tibia and fibular

shaft and adjoining interosseous membrane and are inserted into

tarsal bones and phalanges of the toes(16,17).

32

Nerve supply to these muscles is from the tibial and common

peroneal nerves, both of which are terminal divisions of the sciatic

nerve. The tibial part is formed by ventral divisions of anterior

primary rami of L4, L5, S1, S2, S3 and common peroneal nerve is

formed by dorsal divisions of anterior primary rami of L4, L5, S1,

S2. The common peroneal nerve is the smaller terminal branch and

extends from the superior angle of popliteal fossa to lateral angle,

along the medial border of biceps femoris. It continues and winds

around the posterolateral aspect of the neck of fibula, passes

through peroneus longus and divides into superficial and deep

peroneal nerves. The deep peroneal nerve supplies the anterior

compartment muscles. The tibial nerve is the larger terminal

branch of the sciatic nerve and extends from the superficial angle

to inferior angle of the popliteal fossa crossing popliteal vessels

from lateral to medial side. It gives muscular branches to posterior

compartment muscles(16,17).

3.10.3 Biomechanics of the ankle

Ankle joint is the articulation between the distal tibia and fibula

proximally and the body of the talus distally. It is a synovial hinge joint

and has single oblique axis with one degree of freedom around which the

motions of dorsiflexion/ plantarflexion occur. Muscles near ankle joint

33

produce movement across the sagittal, frontal, and transverse planes.

Dorsiflexion is the movement of the distal end of the foot towards the

tibia occurring in the saggital plane and in coronal axis and has a range of

10 – 20 degrees. Plantarflexion involves motion of the distal end of the

foot away from the tibia and has a range of 20 – 50 degrees(16).

The muscles function is dependent on where the muscle crosses in

relation to the joint axis. Hence, muscles passing anterior to ankle joint

act as dorsiflexors and posterior to the joint as plantarflexors. The

muscles on medial side of joint function as supinators and those on the

lateral side as pronators of the ankle. The muscles crossing the ankle joint

also cross the subtalar joint and hence, act at both joints resulting in a

combination of functions.

Any restriction or tension in the muscle property can affect the range of

joint. Gastrosoleus acts as plantarflexor when contracting concentrically

and on contracting eccentrically control dorsiflexion. Any limitation in its

length can result in limitation of dorsiflexion since it passes posterior to

ankle joint. This is especially evident when knees are extended as the

short gastrocnemius is lengthened over two joints (ankle and knee) in

knee extension. Since the Gastrosoleus tendon passes medial to the

subtalar joint and because of increased surface area, it becomes a

powerful supinator of the joint. Rest of the posterior compartment

34

muscles (tibialis posterior, flexor hallucis and flexor digitorum)

contribute to 5% of plantarflexion(16).

Anterior compartment muscles act as dorsiflexors as they pass anterior to

ankle joint and are activated in different phases of gait as discussed

subsequently. The extensor hallucis longus also extends MTP joint of

hallux and prevents dragging of the big toe. The extensor digitorum

longus and the peroneus tertius muscles insert anterior to ankle joint and

lateral to the subtalar joint axis and acts as dorsiflexors of the ankle and

pronators of the hindfoot. The extensor digitorum longus muscle also

keeps the lateral four toes up when foot is off the ground by extending the

metatarsophalangeal joints of toes. Tension in the anterior compartment

muscles can limit plantarflexion. Muscles are assisted in their function by

the ligaments which prevent excess dorsiflexion and plantarflexion,

minimize medio-lateral movement and/or rotation of ankle(16).

Ankle dorsiflexors during the stance phase of the gait cycle keeps foot in

neutral position at initial contact and contracts eccentrically in loading

response to make foot come in full contact with the ground. During the

swing phase, it contracts concentrically to keep the foot in neutral

position and clear the ground and help in limb advancement(16).

35

Ankle plantarflexors eccentrically contract during the midstance and

undergoes concentric contraction in the terminal stance and pre-swing, to

generate sufficient push-off for the limb advancement(16).

3.10.4 Gait impairments seen in stroke:

In stroke, there is residual weakness of the limbs with distal muscles

being weaker than the proximal. The weakness of the ankle dorsiflexors

leads to a condition called foot drop. The ankle plantarflexor spasticity or

contracture further contributes to the condition. Foot drop is seen in other

UMN conditions also like spinal cord injury, multiple sclerosis, cerebral

palsy, head injury and in LMN lesions as well. In the LMN lesions

(peripheral nerve injuries, neuropathies, drug toxities, diabetes), there is

direct damage to common peroneal nerve and cortical connections

(cortico-spinal tracts) are intact(12).

However, in UMN lesions, as in stroke, the foot drop is accompanied by a

number of other typical abnormal movement patterns like reduced knee

flexion during swing and stance phases (spastic paretic stiff-legged gait),

knee hyperextension (dynamic recurvatum) during stance, and excessive

ankle plantar flexion (equinus) during swing and/or stance(12).

36

Hence, in many stroke survivors, compensatory manoeuvres such as hip

circumduction, hip hiking, and contralateral vaulting with excessive

elevation of the pelvis to avoid toe drag is seen. In these patients, there is

asymmetry of stepping with reduced percentage of the gait cycle in

single-limb stance (SLS) on the affected side. There is a prolonged period

of weight release for the hemiparetic limb during double limb stance

(DLS) to correct foot drop. All these gait abnormalities lead to speed

reduction and associated increased energy cost and effort for

ambulation(12).

3.11 Rehabilitation in Stroke

Stroke rehabilitation broadly comprises of:

• Initial assessment to identify the patient's needs

• Goal setting to define realistic and attainable goals for

improvement

• Intervention to assist in the achievement of goals

• Reassessment to assess progress against agreed goals

Initial assessment done within few days post-stroke, should include a

complete neurological examination. This helps in prognostication,

entailing the rehabilitation plan, evaluation of long-term rehabilitation

37

needs and identifying the appropriate rehabilitation setting. Patients with

isolated disabilities such as a partial aphasia, visual loss, or monoparesis

can receive an out-patient rehabilitation(4)

3.11.1 Principles of Stroke rehabilitation include the following

as mentioned in table 5: - (4)

Table 5: Principles of stroke rehabilitation

Goal setting Specific, measurable and time-dependent to

guide management.

High-intensity practice Increased therapy or intervention.

Multidisciplinary team

care

Team of medical, nursing, therapy, and social-

work staff providing rehabilitation inputs and

coordinating their work

Task-specific training Rehabilitation approaches where specific

functional tasks are practised repeatedly.

3.11.2 Rehabilitation related to motor impairments

Motor impairments include weakness, incoordination and spasticity.

Spasticity can be managed conservatively with stretching, positioning,

oral antispasticity medications, use of injection therapy (principally

botulinum toxin, but previously more commonly phenol or alcohol

38

injection).Initial early poststroke phase should also include prevention of

contractures or nerve pressure palsies. Hence, proper positioning in bed

and wheelchair and range of motion exercises for all joints should be

done daily.

Numerous guidelines exist for stroke rehabilitation for motor impairment.

The latest guidelines by NICE released in June 2013 recommends initial

physiotherapy for at least 45 minutes of each relevant rehabilitation

therapy for a minimum of 5 days per week for people who have the

ability to participate, and where functional goals can be achieved. Later

the rehabilitation therapy is modified according to the person's needs at

that time. Treatment is recommended to be continued until the person is

able to maintain or progress function either independently or with

assistance from others(18).

Progressive strengthening exercises include increasing repetitions of body

weight activities (for example, sit-to-stand repetitions), weights (for

example, progressive resistance exercise), or resistance exercise on

machines such as stationary cycles. Approaches to facilitate and enhance

motor recovery, including traditional approaches by Rood, the

neurodevelopmental technique advocated by Bobath, Brunnstrom

technique, proprioceptive neuromuscular facilitation, rehabilitation

approaches where specific functional tasks are practised repeatedly,

39

functionally oriented exercise training (such as practising transfers and

early ambulation), and a recent focus on repetitive task-oriented practice

has been tried. Walking therapies like treadmill with or without body

weight support helps in mobility training for stroke patients.

Electromechanical gait training is still in the research/ experimental

stages(18).

The conventional ambulation training is mainly with use of Ankle–foot

orthoses (AFO). Ankle foot orthosis is a device applied externally over

the ankle and foot of the lower limb which can be fabricated from

metal/leather, thermoplastics, carbon, graphite, or a hybrid design

assembly incorporating some or all the mentioned materials . It can be a

solid ankle or articulated type or a leaf spring type. It helps in providing

foot clearance in the swing phase of the gait cycle thereby prevent

tripping and falling. It also provides stance-phase control by preventing

knee and ankle collapse or by preventing knee hyper-extension that in

turn, affects walking. Effectiveness of AFO is determined in terms of

speed, ease of walking and comfort (5,14).

The alternative is the Functional Electrical Stimulation (FES) system. As

per NICE guidelines, 2013, there is adequate evidence on the safety and

efficacy ( in terms of improving gait) of FES for drop foot of central

neurological origin to support its use (18).

40

3.12 FES system

Electrical stimulation can be used in a number ways in rehabilitation. It

can be used for therapeutic or functional purposes. Therapeutic

stimulation induces physiological changes that are persistent even after

stimulation and thereby improve the voluntary contraction. It therefore

decreases or prevents further impairment as a consequence of

immobilisation or disuse atrophy(19).

Functional Electrical Stimulation (FES) is the application of electric

current to stimulate nerve or muscle to generate muscle contraction and

incorporation of multiple co-ordinated muscle contractions to bring about

functional activity. The effect lasts till the time the FES application

system is giving the stimulation and hence, these systems have to be

donned by the user to bring about the functional activity and act as

replacement for the lost function. Hence, they are called neuroprosthesis.

They bring about specific, active repetitive movements to facilitate motor

relearning by reducing the intracortical inhibition as evidenced in

functional MRI (fMRI) studies. Hence, it facilitates probably motor

neuroplasticity via cortical mechanisms(19).

In the neuroprosthesis, electrical current is delivered via a pair of

electrodes which generates a localised electric field causing

41

depolarisation of motor axonal membranes. When the depolarisation

reaches the critical threshold, the sodium ions move from the

extracellular compartment to the intracellular space leading to an action

potential. This action potential propagates from the site of stimulation and

reaches the axon terminals, releasing the neurotransmitter and causing the

contraction of muscle fibres.

The advantage is easier stimulation of nerve than muscle. The lowest

level of current is able to stimulate neural tissue since the stimulation

threshold for neural tissue is lesser than that of the muscle fibre. Hence,

for the application of neuroprosthesis, the peripheral nerve should be

intact, i.e., lower motor neurons must be preserved from the anterior

horns of the spinal cord to the neuromuscular junctions of the target

muscles(19).

On application of neuroprosthesis to nerves, the large diameter axons get

excited as they have a lower stimulus threshold and preferably, recruit the

type 2 muscle fibres (fast fatiguing). With disuse that occurs in any

chronic disease, the type 1 muscle fibres (fatigue resistant) get converted

to the type 2 muscle fibres (fast fatiguing). However, fatigue resistant

fibres are required for the application of neuroprosthesis and hence, over

a period of time, use of neuroprosthesis converts these fast fatiguing

fibres to fatigue resistant fibres. Also, application of neuroprosthesis

42

should be accompanied by muscle conditioning regimen to maintain

fatigue resistant muscle. Electrodes for the neuroprosthesis delivering the

stimulation should be placed in close proximity to the target nerve as the

trans membrane potentials generated in axons near the electrode are

largest and the electric field generated is maximum(19).

The stimulation parameters determining the waves of current pulses and

therefore strength of a muscle contraction include the pulse frequency,

amplitude, and duration. The ideal stimulation frequency is the lowest

frequency producing a fused contraction. This in turn depends on the type

of muscle fibre and manner of stimulation delivery (surface vs. implanted

electrode). A too low pulse frequency produces a series of twitches and

increase in frequency causes overlapping of twitches to produce a fused

contraction (temporal summation). However, if the frequency is too high,

the muscle fatigues more rapidly. Hence, exact pulse frequency is needed.

Increase in the pulse amplitude and pulse duration also increases the

strength of muscle contraction since it increases the electric charge per

pulse, generates a larger electric field and activates a broader region and

thus recruits more axons and more motor units (spatial summation). In

most neuroprostheses, pulse frequency is kept constant and modulation of

the pulse amplitude and pulse duration controls the strength of the muscle

43

contraction. The pulse frequency is not only constant but also as low as

possible to prevent premature muscle fatigue(19).

3.12.1 FES system components:

Functional ES systems comprises of electrodes, a multichannel

stimulator, and a controller. The stimulator produces the current

waveforms for multiple cathodes and this current is delivered to the

excitable tissue via the electrodes. The controller regulates the

stimulation according to the user. The controller can be a simple switch

modulated by the patient on and off, or may include sensors recording

patient-elicited bio potentials (e.g., EMG or EEG) and using these signals

to regulate the stimulation(19).

Electrodes used include an active electrode or cathode placed near the

nerve or muscle motor point to be stimulated and the return electrode or

anode over less excitable tissue (tendon or fascia). In multichannel

NMES systems, additional electrodes are required to bring about

simultaneous activation of multiple muscles in a co-ordinated manner.

They use either a bipolar (1 anode for each cathode) or monopolar (1

anode for multiple cathode) arrangement of electrodes. Bipolar

multichannel systems allow greater selective activation but require more

electrodes and leads. Monopolar electrode systems addresses this issue by

reducing the number of electrodes(19).

44

Based on arrangement of the electrodes, multichannel stimulator and the

controller, the neuroprosthesis can be categorized as surface,

percutaneous, or implanted. In surface systems, all the three components

are external to the body. The advantages include the easier application of

the electrodes, reversible and non-invasive stimulation mode and being

relatively inexpensive. These systems also have disadvantages like

inability to produce isolated muscle contractions, change in electrode

position with movement of the target muscle causing inconsistent muscle

contraction and force production, varying position of electrodes due to

daily donning and doffing of the device and intolerance to increased

sensation of stimulation application site mainly due to stimulation of

cutaneous pain receptors. In order to overcome these disadvantages,

implanted electrodes were designed(19).

In percutaneous systems, stimulator is external and connected through

leads to the electrodes implanted near a muscle or nerve. This activates

deep muscles and hence provides isolated and repeatable muscle

contractions. Since it does not stimulate the sensory afferents in the skin,

the chances of pain during stimulation are minimal. The electrodes are

made of multifilament lead within a single insulator with a helical

configuration to produce maximum flexibility. The electrodes are inserted

using a hypodermic needle with withdrawing of the needle leaving the

45

electrode in place and lead exiting the skin. The exit sites on the skin are

cleaned and maintained to reduce the risk of complications. The return

electrode is a large surface electrode. Since they are minimally invasive,

they investigate the feasibility of functional muscle contractions prior to

implantable system surgery and hence, have served as precursors to fully

implanted systems. The longevity of percutaneous electrodes and failure

of the system depends on type of percutaneous lead, lead-routing

technique, and the muscles implanted. Potential complications include

infection due to electrodes and granuloma formation due to retained

electrode fragments(19).

In implanted systems, both electrodes and stimulator are implanted and

the controller components are either external or partly implanted and

partly external. It is mainly designed for long term use. The connection

between the controller and stimulator is through radio-frequency (RF)

transmission. The stimulator receives radio-frequency impulses, generates

stimuli and directly sends to the implanted electrodes connected directly

to the implanted stimulator with inline connectors. The RF link eliminates

the need for an active battery and the need for replacements. The

controller receives inputs from the user via switches, sensors, an

implanted joint angle sensor, or bio potential electrodes to determine

stimulation accordingly. Implanted systems have advantages mainly in

46

terms of improved convenience, cosmesis, reliability and repeatability.

Electrodes used for implanted NMES systems include epimysial

electrodes (sutured directly to the epimysium on the muscle surface),

intramuscular electrodes (inserted directly into a muscle belly), epineural

electrodes(sutured to the connective tissue surrounding a motor nerve and

nerve helix) or cuff electrodes (implanted around a nerve)(19).

Numerous neuroprosthesis have been tried to facilitate functional activity

in paralysed lower limbs affected by UMN lesions (like traumatic brain

injury, stroke) as the peripheral nervous system is still intact in these

patients. One of the commonest used and experimented is drop foot

stimulator. Drop foot stimulator or peroneal stimulator involves

application of electric current to stimulate intact peroneal nerve to

generate muscle contraction and enhance gait by improving foot

clearance during swing phase and stability during initial stance phase(19).

3.12.2 Drop foot stimulator or peroneal stimulator(PS)

The concept of foot drop stimulator was first proposed by Liberson in

1961 where he synchronized the electrical stimulation to swing phase of

gait cycle using a foot-switch and achieved the orthotic effect of

stimulation. Thereafter, a number of modifications have been made over

the past 6 decades ranging from hard wired single channel surface

stimulator to hard wired multichannel surface stimulator to single channel

47

implanted system followed by microprocessor based surface and

implantable single/ multichannel DFS systems(6).

There has been an evolution in the footswitches being replaced by sensors

initially artificial and currently natural sensors. The artificial sensors

include a tilt sensor (an accelerometer which detects the joint segment

orientation and determines the stimulus for dorsiflexion). Natural sensors

like the sural nerve, a purely sensory nerve, have also been tried where

inputs are the touch sensors on the lateral part of the foot and detects if

the affected foot was supporting weight. This information was used to

control the application of stimulus in the DFS. There are DFS systems

incorporating real-time control of FES. There also have been

development and trial of completely implanted DFS systems(6).

3.12.3 Studies related to the PS

There have been a number of studies to report positive orthotic effect of

FES. Evidence based review for stroke rehabilitation done in Canada in

2007 by commissioned group states that there is strong (Level 1a)

evidence that FES and gait retraining results in improvements in

hemiplegic gait(20). East midlands specialized commissioning group in

April 2011 evaluated orthotic effect of the drop foot FES system and

found that there are nearly 15 studies including 2 systematic reviews that

reported positive effect. It also mentions that 3 high quality and two low

48

quality systematic reviews show inconclusive evidence for effectiveness

of stimulator in treatment of drop foot(21).

NICE guidelines, 2013 have recommended the use of FES system based

on the current evidence on its safety and efficacy(18). Recent studies

have shown that the stimulator has significant orthotic effect in

comparison to no orthosis(13). There have been small scale and also

multicentre trial studies that have directly compared the system with

conventional AFO(7–9). These trials still have not proven which of the

two is better since patients in both the groups were found to improve

significantly. Studies have also shown that there is near normal gait

pattern with the stimulator group(22).

In most of the trials, the peroneal stimulator has been tried in the chronic

phase of the stroke. Few studies have investigated its use in the acute and

sub-acute phases (23,24).

Currently, FES systems are being tried outside the clinical settings, on a

daily use basis. However, the evidence that the drop foot system is more

beneficial than AFO is lacking.

This study is designed for trial of drop foot system in Indian rehabilitation

settings. It involved the use of a stimulator with a user controlled hand

switch making it technically simpler and more adaptable device for use,

49

the sensor being the user controlled switch. The stimulator was adapted to

Indian settings mainly in terms of its low cost, small size, no requirement

for foot switch, allowing bare-foot walking. The study proposed to

compare its use in the rehabilitation of patients in the sub-acute and

chronic phases of stroke (which largely is the stroke population admitted

in our rehabilitation set-up) and its comparison with AFO.

50

4. Methodology

4.1. Study Design: Randomized Control Trial, pilot phase, parallel

groups

4.2. Settings and locations where the study was conducted:

Department of Physical Medicine and Rehabilitation, Christian Medical

College, Vellore.

4.3. Participants: Persons with hemiplegia secondary to

cerebrovascular accident

I Inclusion Criteria:

Age 18 to 70 years

Adequate cognition and communication abilities (> 18/30 on

MMSE)

History of independent function prior to stroke, including walking

with assistive device

2 weeks to 1 year post stroke

Inability to dorsiflex ankle to clear foot during swing phase of gait

51

Ankle dorsiflexion range of motion coming to at least neutral in

affected lower limb with application of peroneal FES stimulation

Ability to walk 5 meters using AFO and quadripod inside parallel

bar.

II. Exclusion Criteria:

Excessive pain in affected leg (>5 on a 10 point visual analog

scale)

Participating in any other studies

Implants such as cardiac pacemaker or vagal nerve stimulator or

implants generating electrical signals or implants in lower limb

having metal parts

Lower motor neuron disease or injury resulting in inadequate

response to stimulation

Significant swelling in affected leg extending up to knee

Disease limiting wearing of orthosis such as venous stasis or

history of lower extremity ulcer, chronic skin condition or

peripheral neuropathy

Pregnancy

52

Pre-existing orthopedic condition or history of pain that could limit

ambulatory progress (eg: total hip or knee replacement, limited

ROM, arthritis)

Contracture of ankle

4.4. Sample size: 20 (10 in experimental group and 10 in control

group). Since the study was testing the feasibility of the user controlled

hand switch based peroneal stimulator in a clinical setting, it was done as

a pilot study and both intervention and control participants were kept at

equal numbers.

Approval was obtained from the Institutional Review Board and Ethics

committee.

4.5 Randomisation:

Method of allocation concealment: Serially labelled opaque envelopes

concealed random allocation

Method of randomization: Block randomisation (block size=5); (uniform

distribution random numbers generated by computer)

Blinding and masking was not possible as the stimulator and AFO are

externally applied. However, the outcome assessor was not directly

involved with the study.

53

Implementation: The random allocation sequence was computer

generated and was concealed in opaque envelopes. After the recruitment

of the participants by the principal investigator based on the inclusion/

exclusion criteria, an informed written consent was obtained and a pre-

analysis of the outcome measures was done. The group to which the

particular patient was assigned to was disclosed by the statistician to the

principal investigator. The participants were accordingly assigned to the

respective therapists for the intervention and control group for 3 weeks.

4.6. Interventions: Both the groups initially received physiotherapy

for 3-4 weeks as per the requirement to ambulate for 5 meters within

parallel bars. Following this, they were randomly allocated into PS group

and AFO group.

Peroneal Nerve Stimulator(PS): The device as shown in figure 2

included 3 components: (i) a pair of surface electrodes (square shaped

and re-usable), (ii) an electrical stimulator with in-built microprocessor

based controller and (iii) a hand switch mounted on the quadripod. The

stimulator is an in-house development of the Department of

Bioengineering of our institution. It has the following specifications:

frequency= 20 Hertz, pulse amplitude=70 milli Amperes, pulse width=

250 microseconds. It was operated using a small mobile phone battery.

54

The stimulator was controlled by a push-button switch, and was normally

off.

The cathode electrode was placed over the common peroneal nerve (as

identified 2 cm below the head of fibula where the nerve winds around

the fibular neck) and the anode electrode was placed over the anterior

compartment muscles. The electrode locations were adjusted so that

maximum ankle dorsiflexion was noticed. The inter-electrode distance

was usually around 4 cm.

The electrodes were connected through wires to the portable stimulator,

often kept in the trouser pocket of the participant. The stimulator was

further connected through wires to the switch placed on the quadripod,

which the participant held on the unaffected side.

Figure 2: In-built User Controlled Peroneal Stimulator

55

On pressing the switch by the subject during the pre-swing phase of gait

of the affected limb, the electric stimuli generated, are transmitted via the

electrodes to the common peroneal nerve. This activates the dorsiflexors

of the ankle and toes causing ankle lift resulting in ground clearance

during the swing phase for the affected limb. As the limb progressed

towards initial contact of the stance, the participant would release the

switch and stimulation would stop. Since the switch release was done at

the initial contact, the stimulation was continued till initial loading

response and helped in smooth foot contact thereby, preventing the foot

slap. Hence, the switch press was co-ordinated with different gait phases

and required the patient to voluntarily control the movement.

The patient received gait training with the peroneal stimulator and

quadripod for 1 hour during the therapy time. Initial 4 days were given as

the familiarisation time to get used to the stimulator and understanding

the mechanism of operating and co-ordination of the switch. Remaining

hours of the therapy training was continued with AFO and walking aid

since the patient had to be discharged from the hospital with an AFO.

Control group: The control group received gait training using AFO and

walking aid all throughout the therapy hours.

56

At the end of 3 weeks, post-intervention analysis was performed for both

groups and a feedback form was used for the intervention group to assess

the patients’ satisfaction with the device.

4.7. Outcome measures:

4.7.1. Primary Outcome:

The effectiveness of peroneal stimulator was measured in terms of

walking speed and endurance.

1. Walking speed was assessed by the 10 meters walk test in meters

per second(25). This test involves the individual to walk a distance

of 10 meters with or without assistive device at self-selected

“comfortable speed” and at “as-fast-as-possible” speed. The time

taken for initial and last 2 meters is not used for measurement to

accommodate for the acceleration and deceleration. The starting

time is when foot crosses 2 meters mark and stop time is when the

foot crosses 8 meters and this intermediate time duration for the

intermediate 6 meters is considered. A total of 3 trials is done and

an average of the three time durations is taken. The speed is

obtained by dividing the 6 meters with the calculated average time.

2. Walking endurance is measured by the 6 minute walk test(26). It

measures the distance walked in the time period of 6 minutes over

57

an even surface kept constant for all the participants. Each patient

is asked to perform at the preferred speed possible.

4.7.2. Secondary Outcomes:

Kinematic Gait parameters:

1. Step length ( distance covered during an event of one foot till the

recurrence of the same event for the other foot ,i.e., the initial

contact of the one foot to the initial contact of the alternate foot)

Spatial Asymmetry: derived from the step length of the each

patient using the formula:

Step length (unaffected limb) – Step length (affected limb)/ Step

length (unaffected limb)

2. Stride length (distance from heel strike of one leg to heel strike of

the same leg in meters)

3. Stance percentage: Duration of swing phase and stance phase is

measured. Stance percentage is computed as percentage of stance

duration for each stride.

All these parameters were assessed in the Gait lab of the Department of

PMR The patient had infra-red LEDs placed on specific points on their

limbs and ankles and their movements were recorded on infra-red

58

sensors. A computerized system computes the position of limbs and the

information hence obtained, gives the above data.

4. Dynamic range of motion of the ankle (during ambulation):

The ankle angle change in the PS group is calculated for the period

when the stimulator was switched on up to its switch off period.

This is done from the video analysis of the gait cycle of each

participant (as explained subsequently). The change in ankle is also

timed according to different phases of gait cycle. The difference

between the maximum plantarflexion during the pre-swing and

maximum dorsiflexion during the midswing is taken as the ankle

angle change and is attributed as the orthotic function of the PS.

The ankle angle in control group using AFO was taken as neutral

(0 degrees).

Statistical analysis:

Data collection and outcome assessment: The primary and secondary

outcomes for all the 20 patients were measured by a neutral assessor (gait

lab co-ordinator) both for pre and post-intervention analysis. The derived

calculations were done by the principal investigator.

It is should be noted that during the study period, there was technical

difficulty in the force plate system of the gait lab and hence, computer

59

generated values from patient no. 7 till patient no. 14 could not be

obtained. Hence, a manual calculation of each of the kinematic

parameters from the video was done as follows:

A gait cycle perpendicular to the camera is selected from the chosen

video. The frames sorting each phase of the gait cycle was obtained and

using the software GIMP and individual’s shank length, the step length

and stride length were calculated. The number of frames corresponding to

the stance phase was calculated as percentage of the total gait cycle.

The same frame is used to assess the ankle angle range. Each frame is

labelled according to the gait phase and ankle angle is calculated in each

frame and the difference of the maximum plantarflexion and maximum

dorsiflexion is calculated. This difference was accepted as the ankle angle

change.

60

Figure 3: Video frame with Maximum Plantarflexion

Figure 4: Video frame with Maximum Dorsiflexion

4.8. Statistical methods:

Continuous variables were assessed using t-test (paired t test) (to check

pre-post effect) for within the groups.

61

For inter group comparison, Student t-test (two sample, unequal

variance) was used. Fischer exact test was used for inter group

comparison regarding the improved and not-improved categories.

Methods for additional analyses for subgroup analysis:-

Spearman's rank correlation coefficient (Spearman's rho) was used for the

subgroup analyses, i.e., MMSE score and the duration from the stroke

and their correlation with the outcome measures.

62

5. RESULTS

5.1. Recruitment, screening and randomization

More than 200 patients post stroke admitted as in-patients as well as

attending the outpatient clinics including the Stroke clinic were screened

for eligibility to participate in the study based on the inclusion criteria. 45

patients were found to match the inclusion criteria. Among them, 13

patients were excluded based on the exclusion criteria and 9 patients

refused to give consent for the study. 3 other patients were noted to have

significant behavioural issues hindering their participation in the

rehabilitation programme. Hence, 20 patients were enrolled and

randomised into intervention and control groups.

Both PS and AFO groups had 10 participants each and all 20 participants

received the treatment for 3 weeks. They were analysed for primary and

secondary outcomes both pre training and 3 weeks post training. There

were no drop-outs after recruitment throughout the study. The study was

conducted from 1st July 2012 to 3rd August 2013.

63

CONSORT(27)

Excluded (n= 25 )    Not meeting inclusion criteria

(n=13 ) More than 1 year (n=3) Cardiac Implants (n=2) Arthritic pain/ OA (n=2) Multiple co-morbidities

(n=4) Improved (n =1) Too much assistance (

n=1)    Declined to participate (n=9 )    Other reasons (n= 3 )

Analysed (n=10)

 Excluded from analysis (n=0) 

Lost to follow-up (n= 0)

Discontinued intervention (n=0)

Allocated to Intervention PS (n=10)

 Received allocated intervention (n=10) 

 Did not receive allocated intervention

(n=0 ) 

Lost to follow-up (n=0)

Discontinued intervention (n= 0)

Allocated to Control AFO (n=10)

 Received allocated intervention

(n=10 ) 

 Did not receive allocated intervention

(n= 0 )

Analysed (n=10)

 Excluded from analysis (n= 0) 

Allocation 

Analysis 

Follow‐Up 

Randomized (n= 20)

Enrolment 

64

5.2. Baseline demographic and clinical characteristics of

the participants

Baseline parameters among the subjects differed mainly in terms of

treatment of acute event and duration following the acute event. About 60

% of the participants in the intervention group were within 3 months of

the acute episode, 10% had stroke for 3-6 months and 30% had onset of

stroke more than 6 months ago. On the other hand, the control group had

a more uniform distribution of patients with 40 % within 3 months, 30%

within 3- 6 months and 30% had the stroke more than 6 months ago.

Among the intervention group, 60 % were managed conservatively

(non-surgically and no thrombolysis) while 60% of the control group

patients were treated with decompressive surgeries. Rest of the

parameters were uniform between the two groups.

65

Table 6: Demographic details in the AFO and PS group

Characteristics PS AFO

Age (mean+/- S.D) 45.8 +/- 13.73 56.3 +/- 8.95

Gender (Male /

Female)

10 / 0 9 / 1

CVA TYPE

Haemorrhage (H) 2 2

Ischemic ( I ) 8 8

Affected side (right/ left)

Right / Left 5/5 5/5

MMSE score

18 - 23 5 5

24 - 30 5 5

Treatment group

T1 (rt-PA) 1 2

T2 (conservative) 6 2

66

T3 (surgical

decompression)

2 6

T4 (rt-PA &

decompression)

1 0

Duration

< 3 months 6 4

3 – 6 months 1 3

> 6 months 3 3

5.3. Primary outcomes:

5.3.1. 6 minute walk test (Walking endurance):

At the end of 3 weeks, there was improvement in the mean walking

endurance for both the groups, but this was not statistically significant (p

value of 0.95 in control and 0.78 in PS). The difference between the two

groups at the end of 3 weeks was not statistically significant. (t-test for

intergroup comparison: p value: 0.423 and Fischer exact test p value: 1)

as shown in table 7.

67

Table 7: Primary Outcome- 6 minute walk test for AFO and PS

(meters)

Statistical tests AFO STIMULATOR

Pre Mean ±

S.D1

54.39 ± 37.72 59.56 ± 16.19

Post Mean ± S.D 73.8 ± 41.71 77.89 ± 46.89

Post-pre Mean ± S.D 19.41 ± 29.14 18.32 ± 42.75

Within group p-value 0.95 0.78

Inter-group t-

test

p-value Pre: 0.503 Post: 0.423

Fischer exact

test

p-value 1

1S.D: Standard deviation

68

5.3.2. 10 meters test (Walking speed):

There was improvement in the mean speed for both the groups. However,

it was not statistically significant (p value for AFO: 0.97 and PS: 0.794).

For intergroup, post analysis values calculated did not show any

statistically significant difference. (t-test for intergroup comparison: p

value: 0.456 and Fischer exact test p value: 1) as shown in table 8.

Table 8: Primary Outcome- 10 meter walk test for AFO and PS,

(time in minutes)

Statistical tests AFO STIMULATOR

Pre Mean ± S.D 9.84 ± 7.77 10.3 ± 2.79

Post Mean ± S.D 14.43 ± 8.65 13.3 ± 9.06

Post-pre Mean ± S.D 4.58 ± 5.77 3 ± 7.18

Within group p-value 0.97 0.794

Inter-group t-

test

p-value Pre: 0.41 Post: 0.456

Fischer exact

test

p-value 1

69

5.4. Secondary outcomes:

All the kinematic gait outcome measures had similar pattern with no

significant difference between the groups as well as within the groups.

5.4.1. Spatial Asymmetry: There was no significant change in the spatial

asymmetry in the PS (p-value: 0.713) or the AFO group (p value: 0.62).

The difference between the two groups was not significant (Fischer exact

test: p value: 1 and t-test for intergroup: p value: 0.718) as mentioned in

table 9.

Table 9: Spatial Asymmetry for AFO and PS, pre and post

intervention

Statistical Analysis AFO STIMULATOR

Pre Mean ± S.D 0.023 ± 0.313 0.0802 ± 0.39

Post Mean ± S.D 0.0913 ± 0.336 0.226 ± 0.326

Post-pre Mean ± S.D 0.068 ± 0.310 0.146 ± 0.49

Within group p-value 0.626 0.713

Inter-group t-

test

p-value Pre: 0.487 Post: 0.718

Fischer exact

test

p-value 1

70

5.4.2. Stride length:

The post intervention stride length improved in the AFO group and

reduced in PS group; but this was not statistically significant with

AFO group p value 0.668 and PS group p-value 0.417. The difference

was not statistically significant between the two groups (Fischer exact

test: p value: 1 and T-test for intergroup: p value: 0.373) as mentioned

in table 10.

Table 10: Stride length for AFO and PS (meters)

Statistical Analysis AFO STIMULATOR

Pre Mean ± S.D 45.1 ± 11.81 54.8 ± 12.99

Post Mean ± S.D 51.3 ± 17.44 50.5 ± 26.65

Post-pre Mean ± S.D 6.2 ± 24.4 -4.3 ± 29.16

Within group p-value 0.668 0.417

Inter-group t-

test

p-value Pre: 0.924 Post: 0.373

Fischer exact

test

p-value 1

71

5.4.3. Stance percentage (% of the total stride time):

No significant changes seen in the pre and post stance percentages in both

the groups [AFO (p value: (0.917) and PS (p-value: 0.565)] The

difference between the two groups was not significant [Fischer exact test

: p value: 1 and T-test for intergroup: p value: 0.486] as specified in table

11.

Table 11: Stance % for AFO and PS, pre and post intervention

Statistical Analysis AFO STIMULATOR

Pre Mean ± S.D 82.6 ± 8.07 77.9 ± 3.48

Post Mean ± S.D 78.2 ± 11.25 76.5 ± 10.12

Post-pre Mean ± S.D -4.4 ± 7.75 -1.4 ± 11.69

Within group p-value 0.917 0.565

Inter-group t-

test

p-value Pre: 0.91 Post: 0.486

Fischer exact

test

p-value 1

72

5.4.4. Dynamic ankle range of movement showed a mean ankle angle

change of 11.31 ± 3.56 degrees (between pre-swing to mid-swing phase)

as shown in table 12. This was nearly two-third of the normal ankle angle

change of 18 ± 2 (as determined in our gait lab for the normal subjects.)

Table 12: Ankle angle change before and during the stimulation

(degrees)

Sl.no. Maximum Drop Maximum Lift Difference

1 -30.08 -15.95 14.13

2 -23.2 -12.03 11.17

3 -26.08 -14.27 11.81

4 -7.88 2.74 10.62

5 -16.49 -2.29 14.2

6 -20.61 -16.41 4.2

7 -19.66 -12 7.66

8 -18.19 -7.62 10.52

9 -26.33 -9.3 17.03

10 -25.02 -13.24 11.78

Mean 11.312

S.D 3.56663801

73

IC  LR MST PSW ISW MSW

Angle Chan

ge

GAIT PHASES

ANKLE ANGLE

Graph 1: Trend of ankle angle change in PS group patient

The graph above illustrates the trend of the ankle angle change seen in

one of the patients in the PS group. The graph nearly matches the

trajectory of the ankle angle change during gait cycle of a normal

individual.

Graph 2: Ankle angle change during normal gait cycle

74

5.5. Additional analysis:

Additional analysis was done to correlate the duration of stroke and

MMSE with the outcome measures.

5.5.1. Duration of the stroke:

The 6 minute walk test was found to have a statistically significant

inverse co-relation with duration of the stroke for the stimulator group

and no statistically significant difference for the AFO group (Graph 3).

The 10 meter walk test (Graph 4) and the spatial asymmetry (Graph 5)

was found to be non- significant for both stimulator and AFO group.

The ankle angle change (Graph 6) had a statistically significant

correlation with duration of the stroke in the PS group; i.e., in patients

with longer duration from the event of stroke, there was more increase in

the dynamic ankle angle change observed during the application of PS.

5.5.2. MMSE:

Change in the speed as noted with 10 meter walk test (Graph 8) was

better in patients with MMSE > 21 in the PS group as compared to the

patients with MMSE < 21. This was statistically significant. Similar

changes were not seen with AFO group.

75

The 6 minute walk test (Graph 7) and the spatial asymmetry (Graph 9)

was found to be non- significant for both stimulator and AFO group.

The ankle angle change (Graph 10) had a statistically significant

correlation with MMSE. Patients with MMSE > 23 had changes in the

ankle angle significantly better than patients with MMSE < 23 in PS

group.

5.6. User feedback:

Of the 10 patients in the stimulator group, 5 patients preferred PS over

AFO, 3 patients liked AFO and 2 patients could not decide which of the

two is better.

No adverse effects or harms were seen throughout the study.

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

6 MIN PRE 6 MIN POST

Graph 3: Correlation of duration of stroke with 6 minute walk test pre

and post intervention

76

0

0.2

0.4

0.6

0.8

1

1.2

10 M PRE 10 M POST

AFO

PS

Graph 4: Correlation of duration of stroke with 10 meter walk test pre

and post intervention

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

SPAs Pre SPAs Post

AFO

PS

Graph 5: Correlation of duration of stroke with spatial asymmetry test

pre and post intervention

77

0

0.01

0.02

0.03

0.04

0.05

ANGLE

CHANGE

AFO

PS

AFO

PS

Graph 6: Correlation of duration of stroke with ankle angle changet pre

and post intervention

0

5

10

15

20

25

30

35

40

45

6 MIN PRE 6 MIN POST

AFO

PS

Graph 7: Correlation of MMSE with 6 minute walk test pre and post

intervention

78

‐0.8

‐0.6

‐0.4

‐0.2

0

0.2

0.4

0.6

0.8

10 M PRE 10 M POST

AFO

PS

Graph 8: Correlation of MMSE with 10 meter walk test pre and post

intervention

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

SPAs Pre SPAs Post

AFO

PS

 

Graph 9: Correlation of MMSE with spatial asymmetry pre and post

intervention

79

0

0.005

0.01

0.015

0.02

0.025

ANGLE

CHANGE

AFO

AFO

PS

Graph 10: Correlation of MMSE with ankle angle change pre and post

intervention

80

6. Discussion

This study aimed to study the orthotic effect of a user controlled hand

switch based peroneal nerve stimulator and compare it with the ankle foot

orthosis in patients with stroke having foot drop. After three weeks of

training with either PS or AFO, no statistically significant difference was

observed ‘between the two groups’ in terms of walking speed, walking

endurance and gait parameters including spatial asymmetry, stride length

and stance percentage. The results for ‘within group’ comparison also did

not reveal any statistically significant difference for the above parameters.

A number of factors could be attributed to the ‘no difference’ seen for

‘between the groups’ analysis. Firstly, patients in PS group received only

1 hour of training with PS and the remaining 6-7 hours of gait training

was with AFO. This was mainly due to the fact that patient was planned

to be discharged with AFO since the PS was still in the pilot phase and

also due to the technical constraints of a single PS device. Hence, the

training with AFO had to be continued for the intervention group as well.

Besides, the control group also received electrical stimulation for muscle

strengthening during the routine physiotherapy sessions. A small sample

size of 10 patients in each arm could also possibly contribute to the lack

of difference ‘between the two groups’.

81

A number of recent trials support similar findings. P. Kluding et al

conducted a 30 week multicentre randomised controlled single blinded

trial comparing the in-shoe pressure sensor based PS and AFO for stroke

patients more than 3 months duration with foot drop and found no

significant difference in the gait speed ‘between the two groups’ at the

end of 30 weeks(8). Similar findings were replicated by Richard B. Stein

et al in their initial 6 week phase 1 trial with AFO and foot drop

stimulator in terms of the gain in walking speed. After this, in the phase

2, cross over trial of 6 weeks duration was done and the orthotic effect of

AFO was found to be better than the PS though values were not

statistically significant(7). Sheffler et al too demonstrated absence of

significant difference in walking speed ‘between the two groups’.

However, the study used quantitative gait analysis for assessment of

speed instead of the 10 meters walk test, as used in our study(9).

In a within-subject study of 26 community dwellers with stroke using

AFO, the PS for 8 weeks did not show any difference in walking speed in

comparison to the AFO(28). A randomised control trial by Kottink et al

using an implantable PS indicated comparable results for 6 minutes walk

test between the two groups at 12 weeks, but showed a significant

difference at 26 weeks. For 10 meters walk test, an improvement of 10 %

was observed at the end of 26 weeks for FES group and no change in

82

control group. However, this study included a mixed ‘control’ population

wherein the patients were allowed to use an AFO, walking aid and even,

no device(29). Both the randomised control studies done by Kottnik et al

and Kluding et al have a shown a within group improvement in terms of

walking speed and other gait parameters at 30 weeks and 26 weeks.

Among the limited Indian trials, Sabut et al performed an uncontrolled

trial of FES application as an orthosis and revealed an improved walking

velocity and endurance after 12 weeks of FES based rehabilitation(23).

This ‘within group’ improvement was not demonstrated in our study.

This may be because the follow-up evaluation was a short time period of

3 weeks.

It has been observed in our rehab set-up that the patients with stroke

usually require a stipulated time of 3-4 weeks to complete gait training

with AFO with or without the walking aid once they have started

ambulating 5 meters within the parallel bar. Hence a follow up period

was kept in accordance with this protocol of finishing training within the

3 week time frame. Besides, the accommodation phase of getting

accustomed to the device was also a short period of 4 days. The previous

studies have had a follow-up of minimum 8 to 12 weeks to demonstrate a

change or improvement in either of the arms with an accommodation

time of 2 weeks or more.

83

Prior clinical studies have shown that PS has advantages over the AFO in

terms of gait pattern and other kinematic and kinetic parameters. A single

case report by van Swigchem in a chronic stroke patient with an

implantable system showed normalised knee and hip movements with

increased knee and hip flexion angles, increased movement symmetry,

increased ankle push-off and ability to avoid sudden obstacles(22).

Kottink et al randomised 23 chronic stroke patients to receive either

implantable PS or conventional treatment (AFO, no device, shoes) and

found the stance period and double limb support to be normalised for the

paretic side and single limb support normalised for the non-paretic side.

The rest of the gait parameters of stride length, step length, stride time

and walking speed did not show any significant changes ‘within the

group’ as well as ‘between the groups’(30).

Sheffler et al observed improved stride length with both AFO and the PS

group compared to no device in a case series of 12 patients. There was no

difference in other gait parameters of cadence, double limb support

within and between the groups(9). The data in our study does not show

any ‘within group’ or ‘between the group’ differences for stance

percentage, stride length and spatial asymmetry. The probable reasons for

the same have been mentioned earlier.

84

A significant finding of the study is the dynamic ankle angle change in

the PS group. The database for the normal subjects in our gait lab have

shown a mean ankle ROM of 13 ± 2 in the pre-swing phase to the mean

ROM of 5 ± 2 in the mid-swing phase making the total ankle angle

change from the pre-swing to mid-swing is noted to be 18 ± 2 degrees.

This gait phase corresponds to the application of PS device. The PS group

was able to achieve ankle angle change of 11 ± 3 degrees during this

phase of gait cycle. This finding is essential for proving the feasibility of

the PS as an orthotic device and for its immediate orthotic effect. The

above values were deduced from the video gait analysis where all the 10

participants were observed to obtain a sufficient foot lift and achieve

ground clearance preventing any foot/ toe drag.

Most of the studies have measured the ankle active and passive ROM

using a goniometer and only few kinematic and kinetic studies so far have

studied the dynamic ankle dorsiflexion in the swing phase and plantar

flexion in the stance phase. The case series by Sheffler et al did not find

any device effect on the peak dorsiflexion in swing with statistically

insignificant values for the transcutaneous PS, AFO and no device

group(9). Kottink et al noted a significant change in the minimum ankle

dorsiflexion angle achieved in the swing phase and thereby, a

significantly reduced ankle plantar flexion during swing in the PS group.

85

Hence, they concluded that implantable PS is an effective option in

providing the ankle dorsiflexion during the swing phase of gait cycle(30).

These findings are similar to those found in our study.

This study brings forth a noteworthy perspective regarding the AFO as

well. Inspite of the AFO being considered the conventional therapy mode

for stroke rehabilitation, the AFO group did not reveal any ‘within the

group’ improvement at the end of 3 weeks of training in terms of walking

speed, endurance and gait asymmetry. A quasi-experimental study of 16

hemiplegic stroke patients demonstrated that the walking speed was

unaffected by the use of AFO and there was no significant difference

‘between the control group’ with no AFO and the three arms using the

different AFOs. The study also revealed that the AFO use decreased the

plantar flexion at the initial contact and the mid swing phase(31). These

results were comparable to those obtained by S. J. Mulroy et al in a study

assessing the effect of AFO design on ambulation in 30 stroke patients.

Walking with or without AFO had a minimal impact on gait speed. On

the contrary, rigid AFO reduced the speed in some of the patients with

neutral or some ankle dorsiflexion. Irrespective of the different AFO

designs used in the study, all AFOs prevented the excess plantar flexion

during the swing phase and increased dorsiflexion at initial contact(32).

These are consistent with the findings in our study. However, there are

86

numerous studies which are at odds with these results including a recent

systemic review which showed that the AFO improved the balance and

walking in patients with stroke. Studies have also shown that step length

and stride length are also enhanced with use of AFO for the paretic limb.

However, the results in our study did not show any ‘within group’

improvements for the kinematic assessment.

A notable feature is the therapeutic affects related to PS. PS has been

found to bring about changes in the properties of stimulated muscle as

observed by alteration in the electromyographical activity. It has been

speculated that electrical stimulation enhances the cortical excitability

and facilitates neuromuscular activity(33,34). These properties are not

seen with an AFO. Nevertheless, the study did not involve investigating

the therapeutic effects of PS since the PS is still in the preliminary stages

of trial.

Additional analysis of the data suggested a significant inverse correlation

of the 6 minute walk test with the duration of the stroke within the PS

group. This implied that the PS group patients who were within 3 months

of stroke (subacute phase) had better improvement in walking endurance

than those who used the PS in the chronic phase (more than 6 months).

However, there was an unequal distribution of the patients in the PS

group for the three time durations taken (within 3 months, 3-6 months

87

and more than 6 months). As per the random allocation, the subgroup of

within 3 months duration had 6 patients, 1 patient for 3-6 months duration

and 3 patients were in more than 6 months category. This could have

possibly influenced the result. The control group had a more uniform

distribution in terms of duration with 4, 3, 3 patients in the respective

three time periods. The study by Sabut et al who compared various gait

parameters between the subacute and chronic period found that ‘within

each group’, significant improvements in walking parameters was seen.

However, no statistically significant difference was noted for ‘between

the group’ comparison(23). The authors interpreted the results as

facilitation of recovery and functional gains with early intervention with

FES in rehabilitation for stroke patients on the basis of a previous study

by K Dunning et al(24).

Another finding is the significant association between the MMSE score

and 10 meter walk test in PS group. This proved that the patients with

better cognitive ability (as determined by MMSE in our study) were able

to perform better with the device in terms of ambulation speed. This is

unsurprising because the device requires voluntary co-ordination of the

stimulation with the appropriate gait phase.

An essential aspect of the study was to the patient’s perception about the

device. This was done through a questionnaire assessing the difficulties

88

with the device and their preference for the device. Of the 10 patients, 6

did not feel any difficulty in using the device. 3 patients felt the co-

ordination of the switch with the ambulation as a difficult feature and the

remaining 1 patient found it difficult to re-learn a new walking pattern

after having been trained with the AFO. These 4 patients also felt that the

accommodation time of 4 days was too short to adjust to the device.

Overall, 5 patients preferred the device over the AFO, 3 participants

preferred the AFO and 2 patients could not decide their preference.

The feedback from the patients included several other noteworthy points.

Though there were no adverse effects of the surface stimulation seen or

any untoward events throughout the study, one patient experienced ankle

pain with stimulation throughout walking for initial 2 weeks which later

subsided spontaneously. There were two patients who were gradually

weaned off the walking aid in the therapy and hence, the switch had to be

hand held for rest of the therapy. Another patient had significant

spasticity of the dorsiflexors and hence, the stimulation was effective in

causing sufficient ankle lift only after few initial steps. Repeated training

and instructions had to be given to the patients including visual and

verbal feedback and a step-wise task analysis to teach the co-ordination

to these patients.

89

One of the patients brought forth the point that the device made walking a

conscious effort since every step had to be synchronised with stimulation.

However, this point was considered prior to the designing of the device

and it was believed that the co-ordination would be a learnt motor task as

any other learnt motor behaviour in our day to day activities and this

would improve with greater duration of training and use of the device.

Another feature was muscle fatigability experienced by one patient on

continuous use of the stimulator. A possible explanation for that could be

the presence of more of the type 2 fibres (fast fatiguing) in the ankle

dorsiflexors probably as a result of disuse atrophy. However, further

evaluation of the muscle changes and the therapeutic effects of the device

were beyond the scope of the current pilot study.

One patient had greater fear of falling with the device than with the AFO.

This could be due to the ability of the AFO to provide mediolateral

stability during the stance and also prevention of hyperextension. AFO

prevents posterior tibial rotation in relation to the foot and reduces the

large internal flexor moment generated at the hyperextended knee during

the first half of stance phase, thereby limiting the hyperextension of the

knee.

During the study, the device enabled the patients to walk bare foot or

choose a foot wear according to their convenience. This is the more

90

socially and culturally acceptable option in an Indian scenario. The study

did not explore the functional independence in terms of ADL and

advanced gait training and community use as these were beyond the

scope of this study at present.

The device had certain technical drawbacks. The stimulation used a

simple ON/OFF of 20Hz stimulation, and hence transition of movement

was abrupt. This was noted as a jerking movement of the foot with

stimulated foot lift. Also since the device was wired, there was frequent

detachment and breakage of wires, requiring re attachment, an average of

2 times per patient during the 3 week usage. The device also did not have

an indicator to show the discharging and recharging status of the battery.

Thus, the insufficient generation of ankle lift and gradual decrease in

dorsiflexion was taken as an indication for discharging of the battery.

In spite of these flaws, the novelty of the study lies in an attempt to

explore a user controlled hand switch based peroneal stimulator for

which, to our knowledge, no randomised control trials in the clinical

settings have been done. Literature mentions experiments with a similar

device designed in 1990’s by E. Ott et al(10). However, application of

this device under clinical set-up has not been mentioned. In view of the

lack of evidence, the results obtained in our study have been compared to

other studies using different sensors (either foot switches or automatic

91

sensors) and using different electrodes (either transcutaneous or

implantable). Therefore, results of the current preliminary design of PS

may not be expected to yield the same results as for the previous devices

which have undergone recurrent technical improvements.

It is notable that even with the limited training for a short duration and

time; the stimulator did not show worse results as compared to the

standard therapy of AFO in terms of its walking ability. It also had the

advantage of a more physiological form of ground clearance due to the

ankle angle change achieved. The mixed acceptability of the device

among the patients was anticipated in such a pilot study. In view of these

results, the manually controlled Peroneal Nerve Stimulator can be offered

as an alternative option for a selected group of hemiplegic population

with good cognitive abilities and in their initial phase of training,

following the acute event. The device definitely requires further

modifications in terms of the technical designing to obtain smooth

movements and also training of longer duration to prove or disprove its

efficacy.

92

7. Limitations

• Small sample size of 20 participants with 10 in each arm.

• Absence of blinding in the study.

• Non uniform distribution of patients in PS group in terms of

duration of the stroke.

• Influence of gender difference could not be detected since there

was only 1 female participant.

• Continued use of the AFO in the intervention group.

• Short duration of follow-up of 3 weeks.

• Manual calculations of the kinematic parameters from patient 7 to

patient 14 with a probable error of ± 5.

• Technical drawbacks of the device (wired device, battery charging

status, graded current generation).

• Device suitability to selected hemiplegic patients with a certain

level of cognitive ability for learning the co-ordination and

synchronization with gait cycle and cannot be used by patients with

more cognitive deficits.

• Non validated questionnaire used for patient feed-back.

93

8. Recommendations for further study

• Trial of a radiofrequency wireless hand switch for making the

device less cumbersome

• Comparison of the user based hand switch PS to an automatic PS

incorporating automatic stimulation control using accelerometers

and gyroscopes to determine the swing phase of gait.

• Trial of the PS for longer duration of therapy allowing the

intervention group patients to use the device for equivalent number

of hours as the control group using the AFO

• Trial involving longer accommodation phase with PS and longer

follow-up period (minimum 12 weeks)

• Trial with increased sample size and blinding

• Trials exploring the therapeutic effects of the PS

• Trials exploring the feasibility of PS in community and studying

the functional independence in ADL and other vocational tasks

while using the device.

• Usage of a validated questionnaire for patient’s feedback for

further studies

94

9. Conclusion

1. The study suggests some orthotic effect of a user controlled PS but

in comparison to an AFO, it was inconclusive. The assessments

were made after rehabilitation training of one hour daily for 3

weeks. The orthotic effect was measured in terms of walking

speed, endurance and kinematic gait parameters.

2. The orthotic effect of the PS when measured in terms of dynamic

ankle angle change achieved during the ambulation showed a

significant change with nearly two-third of normal angle change

during the swing phase of the gait phase.

3. The stimulator had a better orthotic effect in patients in the

subacute phase of rehabilitation as compared to those in the

chronic phase.

4. The stimulator proves a useful option for hemiplegic patients with

good cognitive abilities.

5. The stimulator received a mixed response from the patients

regarding its effectiveness as an orthosis with 50 % patients

preferring the device over the AFO and 60% claiming no difficulty

in use of the device.

95

6. The study has demonstrated a user operated hand switch PS as an

alternative to an AFO for foot drop correction, in the Indian

rehabilitation setting. This needs to be further technically

improved and its efficacy investigated on a larger scale.

Bibliography

1. Mukherjee D, Patil CG. Epidemiology and the global burden of

stroke. World Neurosurg. 2011 Dec;76(6 Suppl):S85–90.

2. Mishra NK, Khadilkar SV. Stroke program for India. Ann Indian

Acad Neurol. 2010;13(1):28–32.

3. Norrving B, Kissela B. The global burden of stroke and need for a

continuum of care. Neurology. 2013 Jan 15;80(3 Suppl 2):S5–12.

4. Langhorne P, Bernhardt J, Kwakkel G. Stroke rehabilitation.

Lancet. 2011 May 14; 377(9778):1693–702.

5. Walter R. Frontera, JAD. D E L I S A’ S Physical Medicine &

Rehabilitation PRINCIPLES AND PRACTICE. Fifth Edition.

LIPPINCOTT WILLIAMS & WILKINS;

6. Lyons GM, Sinkjaer T, Burridge JH, Wilcox DJ. A review of

portable FES-based neural orthoses for the correction of drop foot.

IEEE Trans Neural Syst Rehabil Eng Publ IEEE Eng Med Biol Soc.

2002 Dec;10(4):260–79.

7. Everaert DG, Stein RB, Abrams GM, Dromerick AW, Francisco

GE, Hafner BJ, et al. Effect of a foot-drop stimulator and ankle-foot

orthosis on walking performance after stroke: a multicenter

randomized controlled trial. Neurorehabil Neural Repair. 2013

Sep;27(7):579–91.

8. Kluding PM, Dunning K, O’Dell MW, Wu SS, Ginosian J, Feld J,

et al. Foot drop stimulation versus ankle foot orthosis after stroke:

30-week outcomes. Stroke J Cereb Circ. 2013 Jun;44(6):1660–9.

9. Sheffler LR, Bailey SN, Wilson RD, Chae J. Spatiotemporal,

kinematic, and kinetic effects of a peroneal nerve stimulator versus

an ankle foot orthosis in hemiparetic gait. Neurorehabil Neural

Repair. 2013 Jun;27(5):403–10.

10. Ott E, Munih M, Kralj A. Voluntary controlled peroneal stimulator.

Eng Med Biol 1999 21st Annu Conf 1999 Annu Fall Meetring

Biomed Eng Soc BMESEMBS Conf 1999 Proc First Jt. 1999. p.

661 vol.1–.

11. Microsoft Word - Stroke.doc -

bod_cerebrovasculardiseasestroke.pdf [Internet]. [cited 2013 Oct

13]. Available from:

http://www.who.int/healthinfo/statistics/bod_cerebrovasculardisease

stroke.pdf

12. Walter R. Frontera JAD. D E L I S A ’ S Physical Medicine &

Rehabilitation PRINCIPLES AND PRACTICE. Fifth.

LIPPINCOTT WILLIAMS & WILKINS;

13. Khattar B, Banerjee A, Reddi R, Dutta A. Feasibility of Functional

Electrical Stimulation-Assisted Neurorehabilitation following

Stroke in India: A Case Series. Case Reports Neurol Med.

2012;2012:830873.

14. RANDALL L. BRADDOM. Physical Medicine and Rehabilitation.

Fourth. Elsevier Saunders;

15. Jauch EC, Saver JL, Adams HP, Bruno A, Connors JJ (Buddy),

Demaerschalk BM, et al. Guidelines for the Early Management of

Patients With Acute Ischemic Stroke A Guideline for Healthcare

Professionals From the American Heart Association/American

Stroke Association. Stroke. 2013 Jan 31;STR.0b013e318284056a.

16. Cynthia C. Norkin PKLN. Joint Structure and Function: A

Comprehensive Analysis. Fourth Edition. F. A. Davis Company;

17. B.D. Chaurasia. Human Anatomy, Regional and Applied. CBS;

18. Stroke rehabilitation: Long term rehabilitation measures, NICE

guidelines [Internet]. [cited 2013 Oct 14]. Available from:

http://www.nice.org.uk/nicemedia/live/14182/64098/64098.pdf

19. Walter R. Frontera JAD. D E L I S A ’ S Physical Medicine &

Rehabilitation PRINCIPLES AND PRACTICE. Fifth.

LIPPINCOTT WILLIAMS & WILKINS;

20. 9. Mobility and the Lower Extremity [Internet]. [cited 2013 Oct 14].

Available from: http://www.ebrsr.com/uploads/Module-

9_mobility.pdf

21. Elizabeth Orton, Linda Ward. Orthotic Functional Electrical

Stimulation (FES) for “drop foot” of neurological origin. East

Midlands Specialised Commissioning Group; 2010.

22. Van Swigchem R, Weerdesteyn V, van Duijnhoven HJ, den Boer J,

Beems T, Geurts AC. Near-normal gait pattern with peroneal

electrical stimulation as a neuroprosthesis in the chronic phase of

stroke: a case report. Arch Phys Med Rehabil. 2011 Feb;92(2):320–

4.

23. Sabut SK, Sikdar C, Kumar R, Mahadevappa M. CLINICAL USE

OF FUNCTIONAL ELECTRICAL STIMULATION FOR

CORRECTION OF FOOT DROP: A COMPARISON BETWEEN

SUBACUTE AND CHRONIC STROKE PATIENTS. J Mech Med

Biol. 2011 Dec;11(05):1165–77.

24. Dunning K, Black K, Harrison A, McBride K, Israel S.

Neuroprosthesis peroneal functional electrical stimulation in the

acute inpatient rehabilitation setting: a case series. Phys Ther. 2009

May;89(5):499–506.

25. Rehab Measures - 10 Meter Walk Test [Internet]. Rehabil. Meas.

Database. [cited 2013 Oct 13]. Available from:

http://www.rehabmeasures.org/Lists/RehabMeasures/PrintView.asp

x?ID=901

26. Rehab Measures - 6 Minute Walk Test [Internet]. Rehabil. Meas.

Database. [cited 2013 Oct 13]. Available from:

http://www.rehabmeasures.org/Lists/RehabMeasures/DispForm.asp

x?ID=895

27. The CONSORT Group > CONSORT Statement > Flow Diagram

[Internet]. [cited 2013 Oct 14]. Available from: http://www.consort-

statement.org/consort-statement/flow-diagram0/

28. Van Swigchem R, Vloothuis J, den Boer J, Weerdesteyn V, Geurts

ACH. Is transcutaneous peroneal stimulation beneficial to patients

with chronic stroke using an ankle-foot orthosis? A within-subjects

study of patients’ satisfaction, walking speed and physical activity

level. J Rehabil Med Off J UEMS Eur Board Phys Rehabil Med.

2010 Feb;42(2):117–21.

29. Kottink AI, Hermens HJ, Nene AV, Tenniglo MJ, van der Aa HE,

Buschman HP, et al. A randomized controlled trial of an

implantable 2-channel peroneal nerve stimulator on walking speed

and activity in poststroke hemiplegia. Arch Phys Med Rehabil. 2007

Aug;88(8):971–8.

30. Kottink A, Tenniglo M, de Vries W, Hermens H, Buurke J. Effects

of an implantable two-channel peroneal nerve stimulator versus

conventional walking device on spatiotemporal parameters and

kinematics of hemiparetic gait. J Rehabil Med. 2012;44(1):51–7.

31. Fatone S, Gard SA, Malas BS. Effect of ankle-foot orthosis

alignment and foot-plate length on the gait of adults with poststroke

hemiplegia. Arch Phys Med Rehabil. 2009 May;90(5):810–8.

32. Mulroy SJ, Eberly VJ, Gronely JK, Weiss W, Newsam CJ. Effect of

AFO design on walking after stroke: impact of ankle plantar flexion

contracture. Prosthet Orthot Int. 2010 Sep;34(3):277–92.

33. Israel S, Kotowski S, Talbott N, Fisher K, Dunning K. The

therapeutic effect of outpatient use of a peroneal nerve functional

electrical stimulation neuroprosthesis in people with stroke: a case

series. Top Stroke Rehabil. 2011 Dec;18(6):738–45.

34. Kottink AI, Hermens HJ, Nene AV, Tenniglo MJ, Groothuis-

Oudshoorn CG, IJzerman MJ. Therapeutic Effect of an Implantable

Peroneal Nerve Stimulator in Subjects With Chronic Stroke and

Footdrop: A Randomized Controlled Trial. Phys Ther. 2008 Apr

1;88(4):437–48.

Annexure

1. Institutional Review Board Acceptance letter.

2. Patient Information Sheet and Consent Form

3. Case Sheet

4. Database for all patients

Institutional Review Board Acceptance letter

PATIENT INFORMATION SHEET

Title of the study: Effectiveness of peroneal stimulator for foot drop in

hemiplegic patients during subacute phase of rehabilitation

Principal Investigator: Dr. Kriti Mishra

Department: Physical Medicine and Rehabilitation (PMR), CMC, Vellore

There are certain diseases which affect normal walking patterns. Foot

drop is a condition where a patient is unable to clear the foot off the

ground mainly due to weakness of some ankle muscles and overactivity

of certain muscles. This is seen in patients with stroke wherein there is

also some minimal weakness of hip muscles and tightness in knee

muscles. The conventional rehabilitation method used has been AFO

along with physiotherapy. AFO is used to keep foot straight and helps in

ground clearance during walking. There is another alternative where the

patient wears a device just below the knee and this device stimulates the

nerve directly and causes muscle to contract and hence helps in lifting the

foot off ground. Since usage of this device permits ankle to be free during

rest of walking phase, it is more physiological. However, this needs co-

ordination between different components and is more user dependent

unlike the AFO. Besides, patient may also experience some unpleasant

sensations due to stimulation.

The PMR department of CMC is conducting a study to compare between

AFO and this device in stroke patients in sub acute phase, mainly in terms

of walking speed and distance patient can walk without stopping

(endurance). The stimulator being used involves a cane based switch gait

sensor making it a simpler and more adaptable device for use, the sensor

being first of its type.

The study will recruit hemiplegic patients with foot drop and suitable

physical and cognitive abilities. If you are willing to be part of study, you

will be randomly allocated into any of the two groups, first group using

device and other group receiving standard treatment of AFO.

Initially both groups will receive training in parallel bar with AFO, and

later will be randomly allocated into two groups. Each group will receive

therapy with respective mode for 3 weeks and will be assessed in terms of

walking speed, endurance, ankle ROM, other walking parameters

(cadence, step length, stride length) and also difficulties in usage and

satisfaction level. Post interventional analysis for both groups will be

done to see for statistically significant results in above parameters.

Participation in this study is not likely to cause harm to your health in any

foreseeable manner. If there is any skin changes or abnormal intolerable

sensory changes as experienced by patient, it will medically sorted out

cost being borne by the department.

All your personal information obtained by us from you will be kept

completely confidential. If you do not want to participate in this study,

you are free to say so. You can also choose to withdraw from the study at

any time without being obliged to provide an explanation. This will not

affect the treatment to be received by you in this hospital in any way.

If you need additional information, you are welcome to contact us.

Contact information is available below. Additional information on

peroneal stimulator and the assessment tests that will be used in this study

will be provided on request.

Dr. Kriti Mishra

Department of Physical Medicine and Rehabilitation

Christian Medical College,

Vellore, Tamil Nadu – 632002, INDIA

Phone: +91 –7639831201 (mobile)

E-mail: kritimishra1@yahoo.co.in

INFORMED CONSENT

Title of the study: Effectiveness of peroneal stimulator for foot drop in

hemiplegic patients during subacute phase of rehabilitation

Principal Investigator: Dr. Kriti Mishra

Department: Physical Medicine and Rehabilitation (PMR), CMC, Vellore

I, ________________ have been explained the details of the proposed

study to me. I have understood what has been said including the

following:

1. If I give consent to participate in this study, I may be randomly

allocated into any of the two groups, first group using peroneal

stimulator device and other group receiving standard treatment of

AFO . I am willing to take part in study irrespective of the group I

am allocated to.

2. Usage of stimulator is not likely to adversely affect my health in

any foreseeable manner.

3. I can choose not to give consent to be part of this study. I can also

choose to withdraw myself from the study at any time without

being obliged to provide an explanation. In any case, my decision

will not affect the treatment given to me in this hospital.

I am willing to give consent to be part of this study voluntarily and

without any coercion from the investigators of this project.

Signature of patient

Signature of investigator

Signature of witness

Date:

CASE SHEET

Sl. No.

Name Hospital No.:

Sex: M / F Age: Date of Onset:

Type of CVA: Haemorrhage

Ischemic : Thrombic / embolic

Vessel involved: Right / Left , MCA / ACA

Management: _____________________________________

__________________________________________________

Deficits: __________________________________________

______________________________________________________

______________________________________________________

__________________________________________

Examination:

CNS:

HMF: MMSE:

Cranial Nerves:

Motor system: Right Left

Tone : UL

LL

Voluntary Control:

Shoulder

Elbow

Wrist

Hand

Hip

Knee

Ankle

Sensory system: ____________________________________

Cortical sensation:

Reflexes:

Superficial:

Plantars:

Deep tendon reflexes: BJ TJ SJ KJ AJ

Right

Left

Cerebellar signs:___________________________________

Skull & spine:

Other systems:

CVS/RS/PA:

Musculoskeletal: _________________________________

ROM:

MMSE: Procedure Maximum

Score

Orientation

What are the day, date, month, season, and year? ___/5

Where are we? Country, state, city, hospital, floor? ____/5

Registration

Name three objects: 1 second to say each. Then ask patient to

repeat all three. Give 1 point for each correct answer. Then repeat

until all three are registered.

_____/3

Attention and calculation

Serial 7s.( one point for each correct) Stop after five answers.

Alternatively, spell world backward.

______/5

Recall

Ask for the three objects repeated above. Give 1 point for each

correct. ______/3

Language

Name a pencil and a watch. (2 points)

______/2

Repeat the following: “No ifs, ands, or buts.” (1 point)

______/1

Follow a three-stage command: “Take a piece of paper in your

right hand, fold it in half, and put it on the floor.” (3 points)

_______/3

Read and obey the following: “Close your eyes.” (1 point)

______/1

Write a sentence. (1 point)

_______/1

Copy design. (1 point)

_______/1

From: Folstein MF, Folstein S, McHugh P. “Mini-mental state”: a

practical method for grading the cognitive state of patients for the

clinician. J Psychiatr Res 1975;12:189-198.

6 min walk(meters)

Sl. No AFO Stimulator

Pre Post Post-Pre Pre Post Post-Pre

1 52 95 43 20.5 47.35 26.85 2 150.8 142 -8.8 72 85.2 13.2 3 26 59 33 70.75 66 -4.75 4 61 138 77 54.8 50 -4.8 5 27 55 28 45 46 1 6 23 32 9 66 192 126 7 70 53 -17 74 121.3 47.3 8 36.4 43 6.6 66 59 -7 9 61 95 34 62.6 38 -24.6 10 36.7 26 -10.7 64 74 10

Mean 54.39 73.8 19.41 59.56 77.88

5 18.32 SD 37.72 41.71 29.14 16.19 46.89 42.75

Within t-test 0.064 0.28 group

p-value 0.95 0.784

Inter t-test pre 0.69 t-test post 0.84

group

p-value

pre 0.503 p-value post 0.423

AFO Stim Total

Fisher Exact Test Bette

r 7 6 13 Wors

e 3 4 7 Total 10 10 20

p-

value 1

10 m walk(meters/seconds))

Sl. no AFO Stimulator

Pre Post Post-Pre Pre Post Post-Pre

1 11 22 11 5 8 3 2 30 28 -2 11 14 3 3 5 11 6 12 12 0 4 12 28 16 10 9 -1 5 5 11 6 8 7 -1 6 4 6 2 15 36 21 7 11 9 -2 13 21 8 8 3.45 7 3.55 9 9 0 9 10 16 6 11 6 -5 10 7 6.3 -0.7 9 11 2

Mean 9.845 14.43 4.585 10.3 13.3 3

SD 7.77 8.65 5.77 2.79 9.06

8 7.18

within t-test 0.033 t-test 0.27

p-value 0.97 p-value 0.79

4

Inter t-test pre 0.86 t-test post 0.78 p-value

pre 0.41 p-value post 0.45

6

AFO Stim Fisher Exact

Test Better 7 7 14 Worse 3 3 6

10 10 20 p-

value 1

Spatial Asymmetry AFO Stimulator

Pre Post Post-Pre Pre Post

Post-Pre

1 0 0 0 0 0 0 2 0 0 0 0 0 0 3 0 0 0 0 0 0 4 0 0.048 0.048 -0.85 0.65 1.5 5 -0.4 -0.46 -0.06 0.51 0.725 0.215 6 0.83 0.6 -0.23 0.19 -0.068 -0.258 7 0 0 0 0.512 0.31 -0.202 8 0 0 0 0.44 0.65 0.21 9 0 0 0 0 0 0 10 -0.2 0.725 0.925 0 0 0

Mean 0.023 0.0913 0.0683 0.0802 0.226 0.146 SD 0.313 0.336 0.310 0.395 0.326 0.49

within t-test 0.504 t-test 0.38

p-value 0.626 p-value 0.713

Inter t-test pre 0.724 t-test post 0.372

p-value pre 0.487

p-value post 0.718

AFO Stim total Fisher Exact Test Better 2 2 4

Worse 8 8 16 Total 10 10 20

p-value 1

Stride Length(meters) Sl.no AFO Stimulator

Pre Post Post-Pre Pre Post Post-Pre

1 44 64 20 77 20 -57 2 66 48 -18 68 49 -19 3 37 61 24 43 22 -21 4 32 84 52 34 43 9 5 33 57 24 61 51 -10 6 33 46 13 54 101 47 7 46 18 -28 61 93 32 8 47 38 -9 57 39 -18 9 53 44 -9 52 45 -7 10 60 53 -7 41 42 1

Mean 45.1 51.3 6.2 54.8 50.5 -4.3 SD 11.81 17.44 24.40 12.99 26.65 29.16

within t-test 0.44 t-test 0.85

p-value 0.668 p-value 0.417

Inter t-test pre 0.098 t-test post 0.94

p-value pre 0.924

p-value post 0.373

AFO Stim Total Fisher Exact Test Better 5 4 4

Worse 5 6 6 Total 10 10 10

p-value 1

Stance % Sl.no AFO Stimulator

Pre Post Post-Pre Pre Post

Post-Pre

1 93 80 -13 80 86 6 2 71 62 -9 77 79 2 3 91 95 4 76 72 -4 4 77 59 -18 72 87 15 5 74 75 1 79 77 -2 6 85 86 1 78 55 -23 7 77 82 5 85 66 -19 8 94 88 -6 77 76 -1 9 82 82 0 80 87 7 10 82 73 -9 75 80 5

Mean 82.6 78.2 -4.4 77.9 76.5 -1.4

SD 8.071 11.25 7.75 3.48 10.1

2 11.69

within t-test 0.106 t-test 0.59

6

p-value 0.917 p-value 0.56

5

Inter t-test pre 0.116 t-test post 0.72

6 p-value

pre 0.91 p-value

post 0.48

6

AFO Stim Total

Fisher Exact Test Better 5 5 5 Worse 5 5 5 Total 10 10 10

p-

value 1