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Guillain-Barré Syndrome (GBS) : Prepared by Dr. Madiha Anees PT Asst. Prof/VP RCRS MS-PT, BS-PT

Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy of the peripheral nervous system that occurs when the immune system attacks the nerves. There are several subtypes of GBS that can affect motor or sensory nerves. GBS is usually preceded by a bacterial or viral infection and causes progressive muscle weakness and paralysis. Treatment involves hospitalization, monitoring of respiratory function, intravenous immunoglobulin or plasma exchange to treat symptoms, and long-term rehabilitation to regain motor function and strength.
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0% found this document useful (0 votes)
358 views26 pages

Guillain-Barré Syndrome (GBS) : Prepared by Dr. Madiha Anees PT Asst. Prof/VP RCRS MS-PT, BS-PT

Guillain-Barré syndrome (GBS) is an acute inflammatory demyelinating polyneuropathy of the peripheral nervous system that occurs when the immune system attacks the nerves. There are several subtypes of GBS that can affect motor or sensory nerves. GBS is usually preceded by a bacterial or viral infection and causes progressive muscle weakness and paralysis. Treatment involves hospitalization, monitoring of respiratory function, intravenous immunoglobulin or plasma exchange to treat symptoms, and long-term rehabilitation to regain motor function and strength.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
  • Introduction: Provides an overview of Guillain-Barré syndrome and its significance as an autoimmune disorder affecting the peripheral nervous system.
  • Incidence: Describes the frequency and demographic information about individuals affected by Guillain-Barré syndrome.
  • Classification: Outlines the different subtypes of Guillain-Barré syndrome, including AIDP, MFS, and others, with brief characteristics.
  • Pathophysiology: Explores the underlying autoimmune mechanisms and pathophysiological aspects of Guillain-Barré syndrome.
  • Causes: Discusses potential triggers for Guillain-Barré syndrome, including infections and immune responses.
  • Risk Factors: Lists factors that increase susceptibility to Guillain-Barré syndrome, such as age and recent infections.
  • Signs and Symptoms: Outlines the clinical signs and symptoms associated with Guillain-Barré syndrome.
  • Diagnostic Evaluation: Details the diagnostic process and tests used to confirm Guillain-Barré syndrome.
  • Medical Management: Explains treatment strategies and management approaches for patients with Guillain-Barré syndrome.
  • Physiotherapeutic Problems: Identifies physical therapy concerns and goals for treating Guillain-Barré syndrome symptoms.
  • Associated Problems: Describes additional health issues linked with Guillain-Barré syndrome, such as mobility and circulation challenges.
  • Short Term Goals: Focuses on immediate therapeutic objectives for mitigating Guillain-Barré syndrome's effects.
  • Long Term Goals: Outlines prolonged recovery objectives to enhance functionality and independence post-Guillain-Barré syndrome.

Guillain-Barré syndrome

(GBS)
Prepared by
Dr. Madiha Anees PT
Asst. Prof/VP RCRS
MS-PT, BS-PT
Content

 Introduction
 Incidence
 Classification
 Pathophysiology
 Causes
 Risk factors
 Symptoms
 Diagnosis
 Managment
Introduction

 Guillain Barre Syndrome (GBS) or Landry's paralysis is a serious disorder that occurs
when the body’s defense (immune) system mistakenly attacks part of the peripheral
nervous system.
 It is an acute, progressive, autoimmune, inflammatory demyelination of polyneuropathy of
the peripheral sensory and motor nerves and nerve roots.
 The syndrome is named after the French physicians Georges Guillain and Jean Alexandre
Barré and strohl. who described it in 1916.
INCIDENCE

 1–2 cases per 100,000 people annually


 Men are one and a half times more likely to be affected than women
 It is the most common cause of acute non- trauma-related paralysis in the world.
Classification

 There are 6 different subtypes of GBS and they are:


 Acute Inflammatory demyelinating polyneuropathy
 Miller Fisher syndrome
 Acute motor axonal neuropathy
 Acute motor sensory axonal neuropathy
 Acute panautonomic neuropathy
 Bickerstaff’s brainstem encephalitis
1) Acute Inflammatory Demyelinating
Polyneuropathy (AIDP)
 Most common
 Auto immune response against schwann
cell.
2) Miller Fisher Syndrome (MFS)

 Rare variant
 Manifest as a descending paralysis.
 Usually affects the eye muscles first and
presents with the triad of ophthalmoplegia,
ataxia, and areflexia.
3) Acute Motor Axonal Neuropathy (AMAN)

 Also known as Chinese paralytic


syndrome.
 Attacks motor nodes of Ranvier and is
prevalent in China and Mexico.
4) Acute Motor Sensory Axonal Neuropathy
(AMSAN)
 Similar to AMAN
 Affect the sensory with several axonal damage.
5) Acute Panautonomic Neuropathy

 Is the most rare variant of GBS, sometimes accompanied by encephalopathy.


 Frequently occurring symptoms include
 Impaired sweating
 Lack of tear formation
 Photophobia
 Dryness of nasal and oral mucosa
 Itching and peeling of skin
 Nausea
 Dysphagia
 Constipation unrelieved by laxatives or alternating with diarrhea.
Contt.

  Initial nonspecific symptoms of


 Lethargy
 Fatigue
 Headache
 decreased initiative
 followed by autonomic symptoms including
 Orthostatic lightheadedness
 Blurring of vision
 Abdominal pain
 Diarrhea
 Dryness of eyes
 Disturbed micturition.
6) Bickerstaff's brainstem encephalitis (BBE)

 It is characterized by acute onset of


 Ophthalmoplegia
 Ataxia
 Disturbance of consciousness
 Hyperreflexia.
 Large, irregular hyper intense lesions located mainly in the brainstem, especially in the
pons, midbrain and medulla, are described in the literature.
Pathophysiology

 GBS is a rare and severe disease.


 It occurs after an acute infectious procedure.
 Normally it is acute form of paralysis in lower body area that moves towards upper limb
and face.
 Gradually patient loses all his/her reflexes and goes through a complete body paralysis.
 GBS is a life threatening disorder and needs timely treatment and supportive care.
Contt..

 GBS is considered to be an autoimmune disease triggered by a preceding bacterial or viral


infection.
 Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus and Mycoplasma pneumoniae are
commonly identified antecedent pathogens.
 They have specific antigens in their capsule that they share with nerves.
 The immune system usually then response to these components in the capsule by producing
antibodies that cross-react wit the myelin in the peripheral nervous system, causing
demyelination and then damage to the peripheral nervous system.
 In GBS there is infiltration of the spinal roots and peripheral nerves via the lymphatic system,
causing stripping of the myelin.
 This will lead to a defect in the transmission of electrical nerve impulses which will then lead to
flaccid paralysis.
Causes

 Nobody knows precisely what the exact cause is.


 It is due to an immune response to foreign antigens, such as infectious agents (bacteria,
etc.) that the body's immune system mistargets - attacks good tissue by mistake.
 Experts believe our immune system mistakenly attacks gangliosides - compounds which
are naturally present in nerve tissues.
 The most common infection which precedes the development of GBS is Campylobacter
jejuni - one of the most widespread causes of human gastroenteritis.
 Even so, in over half of all cases no previous infection was present; in other words, there
was nothing to which the doctor could link the syndrome.
 It is believed that influenza virus may also trigger an autoimmune response which causes
the syndrome.
Contt…

 Experts believe the foreign agent (bacterium/virus) causes the body's immune system to
attack the myelin sheath of the peripheral nerves.
 The sheath becomes damaged, causing nerve damage, resulting in faulty sending of signals
between nerves and muscles.
 This faulty wiring causes muscle weakness, numbness and tingling, and eventually
paralysis.
Risk factors

 Age (15-35) and (60-75)


 In men more likely than woman
 Recent gastrointestinal or respiratory infection by viruses or bacteria
 Recent vaccination (especially influenza and meningococcal)
 Recent surgery
 History of lymphoma, Systemic lupus erythromatosus, or HIV and AIDS
Signs and Symptoms

 Pain
 Progressive Muscle weakness
 Numbness
 Loss of reflexes in arms and legs
 Low blood pressure
 Uncoordinated movement
 Facial weakness
 Clumsiness and falling
 Severe pain in the lower back
 Sensation changes
 Tenderness or muscle pain
 Blurred vision
 Respiratory problems
DIAGNOSTIC EVALUATION

 Medical history
 Physical examination
 Tests -
 Nerve conduction studies (NCS)
 CSF examination
 Electromyography (EMG)
 Electrocardiogram (ECG)
 Pulmonary Function Test (PFT)
Medical management

 Treatment is non specific and symptomatic.


 Observe continuously for adequacy of respiratory effort. 
 Patients with GBS will be hospitalized initially (medical emergency).
 It is important to monitor the individual's respiration carefully.
 If breathing problems are severe he/she may be placed in an ICU and put on a ventilator.
 According to the National Health Service, the two main initial treatment options for GBS
are intravenous immunoglobulin, which is safer and easier to give, or plasmapheres
(plasma exchange).
 After the acute phase of the syndrome, the patient may need rehabilitation to regain
functions that were lost.
 Treatment concentrates on improving activities for daily living, such as brushing teeth,
washing, getting dressed and performing some other everyday tasks.
Physiotherapeutic problems

 Acute Respiratory failure due to paralysis of diaphram and secretions


 Decreased A/E due to paralysis of diaphram and secretions
 Decreased chest expansion due to decreased A/E
 Increased secretions due to pneumonia, poor cough attempt and weakness of respiratory
muscles
 Post acute Decreased Fx w.r.t. ADL due to muscle weakness
 Poor proximal and distal control due to weakness
 Decreased Fx due to immobility
Associated problems

 Muscle atrophy due to weakness and inactivity


 Poor sensation due to nerve damage
 Contractures due to immobility
 Decreased exercise tolerance due to inactivity
 Decreased circulation due to inactivity
 Secondary lung infection due to secretions
 Pressure sores and DVT due to immobility
 Weakness due to inactivity
Short term Goals

 Improve/maintain respiratory function


 Prevention of pressure sores and DVT
 Prevention of muscle atrophy
 Improve/maintain muscle strength
 Improve/maintain function
Long term Goals

 Maintain exercise tolerance


 Maintain function
Wheelchair handling
 Support groups
 Retrain proximal control
 Maintain muscle strength
 Retraining of gait
That’s All Folks…..

Guillain-Barré syndrome 
(GBS)
Prepared by
Dr. Madiha Anees PT
Asst. Prof/VP RCRS
MS-PT, BS-PT
Content

Introduction

Incidence

Classification

Pathophysiology

Causes

Risk factors

Symptoms

Diagnosis

Managm
Introduction

Guillain Barre Syndrome (GBS) or Landry's paralysis is a serious disorder that occurs 
when the body’s defense
INCIDENCE

1–2 cases per 100,000 people annually

Men are one and a half times more likely to be affected than women

It i
Classification

There are 6 different subtypes of GBS and they are:

Acute Inflammatory demyelinating polyneuropathy

Mill
1) Acute Inflammatory Demyelinating 
Polyneuropathy (AIDP)

Most common

Auto immune response against schwann 
cell.
2) Miller Fisher Syndrome (MFS)

Rare variant 

Manifest as a descending paralysis. 

Usually affects the eye muscles firs
3) Acute Motor Axonal Neuropathy (AMAN)

Also known as Chinese paralytic 
syndrome.

Attacks motor nodes of Ranvier and is
4) Acute Motor Sensory Axonal Neuropathy 
(AMSAN)

Similar to AMAN 

Affect the sensory with several axonal damage.
5) Acute Panautonomic Neuropathy

Is the most rare variant of GBS, sometimes accompanied by encephalopathy. 

Frequently oc

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