The facial nerve is the seventh cranial nerve, or simply cranial nerve VII. It emerges from the pons of the brainstem, controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue. The nerves typically travels from the pons through the facial canal in the temporal bone and exits the skull at the stylomastoid foramen. It arises from the brainstem from an area posterior to the cranial nerve VI (abducens nerve) and anterior to cranial nerve VIII (vestibulocochlear nerve).

The facial nerve also supplies preganglionic parasympathetic fibers to several head and neck ganglia.

The facial and intermediate nerves can be collectively referred to as the nervus intermediofacialis.

The path of the facial nerve can be divided into six segments.

1. Iintracranial (cisternal) segment
2. Meatal segment (brainstem to internal auditory canal)
3. Labyrinthine segment (internal auditory canal to geniculate ganglion)
4. Tympanic segment (from geniculate ganglion to pyramidal eminence)
5. Mastoid segment (from pyramidal eminence to stylomastoid foramen)
6. Extratemporal segment (from stylomastoid foramen to post parotid branches)

1.The motor part of the facial nerve arises from the facial nerve nucleus in the pons while the sensory and parasympathetic parts of the facial nerve arise from the intermediate nerve.

2.From the brain stem, the motor and sensory parts of the facial nerve join together and traverse the posterior cranial fossa before entering the petrous temporal bone via the internal auditory meatus. Upon exiting the internal auditory meatus, the nerve then runs a tortuous course through the facial canal, which is divided into the labyrinthine, tympanic, and mastoid segments.

3.The labyrinthine segment is very short, and ends where the facial nerve forms a bend known as the geniculum of the facial nerve (“genu” meaning knee), which contains the geniculate ganglion for sensory nerve bodies. The first branch of the facial nerve, the greater superficial petrosal nerve, arises here from the geniculate ganglion. The greater petrosal nerve runs through the pterygoid canal and synapses at the pterygopalatine ganglion. Post synaptic fibers of the greater petrosal nerve innervate the lacrimal gland.

4.In the tympanic segment, the facial nerve runs through the tympanic cavity, medial to the incus.

5The pyramidal eminence is the second bend in the facial nerve, where the nerve runs downward as the mastoid segment. In the temporal part of the facial canal, the nerve gives rise to the stapedius and chorda tympani. The chorda tympani supplies taste fibers to the anterior two thirds of the tongue, and also synapses with the submandibular ganglion. Postsynaptic fibers from the submandibular ganglion supply the sublingual and submandibular glands.

6.Upon emerging from the stylomastoid foramen, the facial nerve gives rise to the posterior auricular branch. The facial nerve then passes through the parotid gland, which it does not innervate, to form the parotid plexus, which splits into five branches innervating the muscles of facial expression (temporal, zygomatic, buccal, marginal mandibular, cervical).

1.Greater petrosal nerve – It arises at the geniculate ganglion and provides parasympathetic innervation to several glands, including the nasal glands, the palatine glands, the lacrimal gland, and the pharyngeal gland. It also provides parasympathetic innervation to the sphenoid sinus, frontal sinus, maxillary sinus, ethmoid sinus and nasal cavity. This nerve also includes taste fibers for palate via lesser palatine nerve and greater palatine nerve.

2.Communicating branch to the otic ganglion – It arises at the geniculate ganglion and joins the lesser petrosal nerve to reach the otic ganglion.

3..Nerve to stapedius – provides motor innervation for stapedius muscle in middle ear

4.Chorda tympani
Parasympathetic innervation to submandibular gland
Parasympathetic innervation to sublingual gland
Special sensory taste fibers for the anterior 2/3 of the tongue.

Distal to stylomastoid foramen, the following nerves branch off the facial nerve:

Posterior auricular nerve – controls movements of some of the scalp muscles around the ear
Branch to Posterior belly of Digastric muscle as well as the Stylohyoid muscle
Five major facial branches (in parotid gland) – from top to bottom:



1.Temporal branch
2.Zygomatic branch
3.Buccal branch
4.Marginal mandibular branch
5.Cervical branch

Intra operatively the facial nerve is recognized at 3 constant landmarks:

1.At the tip of tragal cartilage where the nerve is 1cm deep and inferior
2.At the posterior belly of digastric by tracing this backwards to the tympanic plate the nerve can be found between these two structures
3.By locating the posterior facial vein at the inferior aspect of the gland where the marginal branch would be seen crossing it.
4.lateral semicircular canal
5.Foot of incus

The cell bodies for the facial nerve are grouped in anatomical areas called nuclei or ganglia. The cell bodies for the afferent nerves are found in

the geniculate ganglion for taste sensation. The cell bodies for muscular efferent nerves are found in the facial motor nucleus whereas the cell

bodies for the parasympathetic efferent nerves are found in the superior salivatory nucleus.

The facial nerve is developmentally derived from the second pharyngeal arch, or branchial arch. The second arch is called the hyoid arch because it contributes to the formation of the lesser horn and upper body of the hyoid bone (the rest of the hyoid is formed by the third arch). The facial nerve supplies motor and sensory innervation to the muscles formed by the second pharyngeal arch, including the muscles of facial expression, the posterior belly of the digastric, stylohyoid and stapedius. The motor division of the facial nerve is derived from the basal plate of the embryonic pons, while the sensory division originates from the cranial neural crest.

Although the anterior two thirds of the tongue are derived from the first pharyngeal arch, which gives rise to cranial nerve V, not all innervation of the tongue is supplied by CN V. The lingual branch of the mandibular division (V3) of CN V supplies non-taste sensation (pressure, heat, texture) from the anterior part of the tongue via general visceral afferent fibers. Nerve fibers for taste are supplied by the chorda tympani branch of cranial nerve VII via special visceral afferent fibers.

Facial expression
The main function of the facial nerve is motor control of all of the muscles of facial expression. It also innervates the posterior belly of the digastric muscle, the stylohyoid muscle, and the stapedius muscle of the middle ear. All of these muscles are striated muscles of branchiomeric origin developing from the 2nd pharyngeal arch.

In addition, the facial nerve receives taste sensations from the anterior two-thirds of the tongue via the chorda tympani. Taste sensation is sent to the gustatory portion (superior part) of the solitary nucleus. General sensation from the anterior two-thirds of tongue are supplied by afferent fibers of the third division of the fifth cranial nerve (V-3). These sensory (V-3) and taste (VII) fibers travel together as the lingual nerve briefly before the chorda tympani leaves the lingual nerve to enter the tympanic cavity (middle ear) via the petrotympanic fissure.

It joins the rest of the facial nerve via the canaliculus for chorda tympani. The facial nerve then forms the geniculate ganglion, which contains the cell bodies of the tastefibers of chorda tympani and other taste and sensory pathways. From the geniculate ganglion, the taste fibers continue as the intermediate nervewhich goes to the upper anterior quadrant of the fundus of the internal acoustic meatus along with the motor root of the facial nerve. The intermediate nerve reaches the posterior cranial fossa via the internal acoustic meatus before synapsing in the solitary nucleus.

The facial nerve also supplies a small amount of afferent innervation to the oropharynx below the palatine tonsil. There is also a small amount of cutaneous sensation carried by the nervus intermedius from the skin in and around the auricle (outer ear).

The facial nerve also supplies parasympathetic fibers to the submandibular gland and sublingual glands via chorda tympani. Parasympathetic innervation serves to increase the flow of saliva from these glands. It also supplies parasympathetic innervation to the nasal mucosa and the lacrimal gland via the pterygopalatine ganglion. The parasympathetic fibers that travel in the facial nerve originate in the superior salivatory nucleus.

The facial nerve also functions as the efferent limb of the corneal reflex.

The facial nerve carries axons of type GSA, general somatic afferent, to skin of the posterior ear.

The facial nerve also carries axons of type GVE, general visceral efferent, which innervate the sublingual, submandibular, and lacrimal glands, also mucosa of nasal cavity.

Axons of type SVE, special visceral efferent, innervate muscles of facial expression, stapedius, the posterior belly of digastric, and the stylohyoid.

The axons of type SVA, special visceral afferent, provide taste to the anterior two-thirds of tongue via chorda tympani.

Finally, the facial nerve also carries axons of type GVA, general visceral afferent, which provide sensation to the soft palate and parts of the nasal



People may suffer from acute facial nerve paralysis, which is usually manifested by facial paralysis. Bell’s palsy is one type of idiopathic acute facial nerve paralysis, which is more accurately described as a multiple cranial nerve ganglionitis that involves the facial nerve, and most likely results from viral infection and also sometimes as a result of Lyme disease. Iatrogenic Bell’s Palsy may also be as a result of an incorrectly placed dental local-anesthetic (Inferior alveolar nerve block). Although giving the appearance of a hemi-plegic stroke, effects dissipate with the drug.

When the facial nerve is permanently damaged due to a birth defect, trauma, or other disorder, surgery including a cross facial nerve graft or masseteric facial nerve transfer may be performed to help regain facial movement.Facial nerve decompression surgery is also sometimes carried out in certain cases of facial nerve compression.



Voluntary facial movements, such as wrinkling the brow, showing teeth, frowning, closing the eyes tightly (inability to do so is called lagophthalmos) , pursing the lips and puffing out the cheeks, all test the facial nerve. There should be no noticeable asymmetry.

In an UMN lesion, called central seven, only the lower part of the face on the contralateral side will be affected, due to the bilateral control to the upper facial muscles (frontalis and orbicularis oculi).

LMN lesions can result in a CNVII palsy (Bell’s palsy is the idiopathic form of facial nerve palsy), manifested as both upper and lower facial weakness on the same side of the lesion.

Taste can be tested on the anterior 2/3 of the tongue. This can be tested with a swab dipped in a flavoured solution, or with electronic stimulation (similar to putting your tongue on a battery).

Corneal reflex. The afferent arc is mediated by the General Sensory afferents of the Trigeminal Nerve. The efferent arc occurs via the Facial Nerve.

The reflex involves consensual blinking of both eyes in response to stimulation of one eye. This is due to the Facial Nerve’s innervation of the muscles of facial expression, namely Orbicularis oculi, responsible for blinking. Thus, the corneal reflex effectively tests the proper functioning of both Cranial Nerves V and VII.

A facial palsy is weakness or paralysis of the muscles of the face.

Whilst the majority of cases are idiopathic, termed Bell’s Palsy, there are a wide range of potential causes of a facial palsy .

Bell’s palsy is a diagnosis of exclusion and hence all possible causes have to be excluded first prior to diagnosing Bell’s palsy. The majority of this article will discuss Bell’s Palsy and its associated clinical features and management.

Bell’s palsy remains a poorly understood condition. Many causative associations have been proposed, the most universally accepted theory suggests a viral origin, yet no conclusive evidence is available at present.

The main risk factor for developing Bell’s palsy is known concurrent viral infection, such as HSV-1(HERPES SIMPLEX  VIRUS 1), CMV (CYTOMEGALOVIRUS), and EBV (EBSTEIN VIRUS), whilst less common risk factors.

include diabetes mellitus and pregnancy.

Patients with a Bell’s Palsy will present with varying severity of painless unilateral lower motor neuron weakness of the facial muscles .

Depending on the severity and the ximity of the nerve affected, it can also result in:

Inability to close their eye (temporal and zygomatic branches)
Hyperacusis (nerve to stapedius)
Metallic taste (chorda tympani)
Reduced lacrimation (greater petrosal nerve)

To distinguish clinically between a LMN cause and UMN cause of the facial palsy, a patient with forehead sparing (i.e. no involvement to the occipitofrontalis muscle) will have a UMN origin to the palsy, due to the bilateral innervation of the forehead muscle).



Important differential diagnosis for a facial palsy, other than Bell’s Palsy, include:

      UMN causes, such as a stroke, SDH, or tumour
Will present with forehead sparing

  • Infective such as acute otitis media, cholesteatoma, viral infection (including HSV-1, CMV, and EBV)
  • Neoplasm (parotid malignancy)
  • Trauma or iatrogenic
  • Neurological (Multiple sclerosis or Guillain-Barré syndrome)


symptoms of bells palsy
symptoms of bells palsy


The onset of facial paralysis is sudden with Bell’s palsy, and can worsen during the early stages. Symptoms will usually manifest and peak within 2-3 days, although it can take as long as 2 weeks. Common symptoms include, but are not limited to:

Muscle weakness or paralysis
Facial droop
Impossible or difficult to blink
Difficulty speaking
Difficulty eating and drinking
Nose runs
Nose is constantly stuffed
Difficulty breathing out of nostril on affected side
Nostril collapse on affected side
Forehead wrinkles disappear
Sensitivity to sound
Excess or reduced salivation
Facial swelling
Diminished or distorted taste
Pain behind ear
There are also some eye related symptoms, which may include but are not limited to:

Difficulty closing the eye
Sensitivity to light
Lower eyelid droop
Tears fail to coat cornea
Brow droop
Excessive tearing
Lack of tears

Most cases of Bell’s Palsy can be diagnosed clinically and no further investigations are required, unless any other clinical features are present that suggest another pathology.

Serology for HSV-1 and VZV can be performed, yet will unlikely alter future management if detected.

Patient reassurance is essential, as most cases return spontaneously to full function. Eye care is one of the most important aspect of the management, ensuring the patient uses lubricating drops hourly and potential for eye ointment at night and / or an eye patch.

All patients presenting within 72 hours of symptoms onset should be started oral steroids. Current NICE guidance recommends either:

Giving 25 mg twice daily for 10 days
Giving 60 mg daily for five days followed by a daily reduction in dose of 10 mg
Use of anti-viral agents is controversial.

A Cochrane Review found low level evidence that the combination of anti-virals and corticosteroids are more effective in Bell’s palsy treatment; many centers currently treat Bell’s palsy with both.

Referral to an ENT surgeon should be considered if there is any doubt over the diagnosis, recurrent or bilateral Bell’s palsy, or no sign of improvement after 1 month. There are surgical options available for patients who have persistent weakness or synkinesis. Synkinesis could be treated with botox injections whilst persistent weakness can be treated with anterior belly of diagastric transfer, fascia lata sling, or cross-facial nerve grafting.

A referral to ophthalmology should be made if the cornea remains exposed after attempting to close the eyelid (House Brackmann grade of IV or more).

85% of cases will recover from Bell’s palsy, the majority of which make a fully recovery with no evidence of residual symptoms. The factors that suggest a poor prognosis from a facial palsy include:

Complete palsy
No signs of recovery within 3 weeks
Age >60yrs
Associated pain
Ramsey Hunt syndrome
Associated HTN, DM, or pregnancy


In the first couple of days to a week after symptoms start,  physical therapist will evaluate your condition, including:

Review your medical history, and discuss any previous surgery or health conditions
Review when your current symptoms started and what makes them worse or better
Conduct a physical examination, focusing on identifying the patterns of weakness that are caused by Bell palsy

  • Facial movements of the eyebrow
  •  Eye closure
  • Ability to use the cheek in smiling
  • Ability to use the lips in a pucker
  • Ability to suck the cheeks between the teeth
  • Raising the upper lip
  • Raising or lowering the lower lip

Your physical therapist will immediately:

  • Educate you about how to protect your face and your eye
  • Show you how to manage your daily life functions while you have facial paralysis
  • Explain the expected path to recovery, so that you will know the signs and symptoms of recovery
  • Evaluate your progress, and determine whether you need to be referred to a specialist if progress is not being made The first priority is to protect your eye. The inability to completely and quickly
  • close your eye makes the eye vulnerable to injury from dryness and debris. Debris can scratch the cornea—the transparent front part of the eye that covers the iris, pupil, and front chamber of the eye—and couldpermanently harm your vision. physical therapist will immediately show you how to protect your eye, such as:
  • Using self-made and commercial patches
  • Setting a regular schedule for refreshing eye fluids
  • Carefully closing the eye with your fingers
  • If you have partial facial movement, your therapist will teach you a few general facial exercises to do at home. These exercises will help you learn to move the weak side of your face and help you use both sides of your face together. One of the exercises is a gentle blowing action through your lips.

Physical therapist will help you regain the healthy pattern of movements that you need for facial expressions and function. Recovery can be challenging because:

Normally, the ability to make facial expressions and many facial movements is “automatic”;—that is, you’re born with this ability and never had to think about it before Unlike other muscles in your body, the facial muscles do not have sensors that tell your brain all of the necessary “details” about how to move Physical therapist will be your coach throughout this challenging time, guiding you through special exercises that are designed to help you relearn facial movements based on your particular movement problems. Your exercises may change over the course of recovery:

“Initiation” exercises. In the early stages, when you might have difficulty producing any facial movement at all, your therapist will teach you exercises that cause (“initiate”) facial movement. Your therapist will show you how to position your face to make it easier to move (called “assisted range of motion”) or how to “trigger” the facial muscles to do what you want them to do.

“Facilitation” exercises. Once you’re able to initiate movement of the facial muscles, your therapist will design exercises to increase the activity of the muscles, strengthen the muscles, and improve your ability to use the muscles for longer periods of time (“facilitate” muscle activity).

Movement control exercises. therapist will design exercises to:

  • Improve the coordination of your facial muscles
  • Refine your facial movements for specific functions, such as speaking or closing your eye
  • Refine movements for facial expressions, such as smiling
  • Correct abnormal patterns of facial movement that can occur during recovery
  • To work on coordinating your facial muscles, you’ll need to have a sufficient level of activation of facial muscles first.

RELAXATION- During recovery, you might have facial spasms or twitches. Your physical therapist will design exercises to reduce this unwanted muscle activity. The therapist will teach you how to recognize when you are activating the facial muscle and when the muscle is at rest. By learning to contract the facial muscle forcefully and then stop, you will be able to relax your facial muscles at will and decrease twitches and spasms.

Some people might have greater difficulty moving their face after a period of improvement in facial movement, which can make them worry that the facial paralysis is returning. However, actual recurrence of facial paralysis of the Bell Palsy type is uncommon.

New difficulty in moving the face is more likely the result of increasing the strength of the facial muscles without improving the ability to coordinate and control the movement. To keep this from happening, physical therapist will show you what facial movements you should avoid during recovery. For instance, the following might lead to abnormal patterns of facial muscle use:

Trying to make the biggest facial movement or muscle contraction that you can, such as smiling as much as you can

  • Chewing gum with great force
  • Blowing up a balloon with all of your effort to work the facial muscles
    Therapist will coach you to use your face as naturally as possible, without trying to restrict facial expressions because they look “different.”

NMR involves the use of subtle but critically important exercises to teach and retrain the brain to coordinate the facial muscles more effectively and efficiently.

NMR re-teaches facial paralysis patients which muscles are required to move different parts of the face. This type of physical therapy enables a patient’s brain to reconnect facial muscles and corresponding facial movements. It teaches patients how to isolate facial muscles, use only the correct muscles to make their desired facial movements and suppress muscles that otherwise cause unwanted facial movements.

Patients dealing with Bell’s palsy or other viral infections of the facial nerve often recover on their own completely and spontaneously within about three months of an initial diagnosis. For those who do not fully recover, it is possible that the facial nerve will heal improperly, which causes spontaneous, unwanted facial movements (or synkinesis). For example, when a Bell’s palsy patient tries to smile, his or her eye may twitch at the same time. In this scenario, the patient does not require additional strength in the facial muscles. Instead, he or she needs to improve facial muscle coordination to prevent facial muscles from flexing out of sequence – something that causes distorted facial movements.

Manual massage involves a series of different massage techniques. The goal of manual massage is to decrease facial muscle tightness and improve flexibility and range of motion. Initially, manual massage techniques may be performed by physical therapists, but the therapist ultimately will teach a patient the techniques so he or she can perform them regularly at home.


Emphysema And Physiotherapy :

DEFINATION-”Emphysema is a condition of the lung characterised by  Permanent dilation of the air spaces distal to thr terminal bronchioles with destruction of the walls of these airways”.It is always associated with chronic bronchitis and is difficult to distinguish the two  Conditions during life.

causes and predisposing factors-
1-CONGENITAL OR PRIMARY EMPHYSEMA –May be caused by the alfa1-antitrypsin deficiency.This is a rare in-herited condition, which affect one person in 4000 and results in the complete absence of one of the key antiprotease systems in the lung.This consequence is the early development of COPD, especially if the patient is already smoker.Although alpha1-antitrypsin deficiency is responsible for less than 1 per cent of cases of COPD, Its hereditary nature means that is worth diagnosing.It should, therefore, be consideres in any young COPD patient.

EMPHYSEMA may be SECONDARY to other factors, such as:

1.Obsructive airways disease -e.g. asthma , cystic fibrosis and chronic bronchitis.
2.Occupational lung disease-e. g. pneumoconiosis.
3.Compensatory to contraction of one secton of the lung-e.g. fibrous collapse or removal , when the remaining lung expands to fill the space.

Emphysema is usually of the panacinar (panlobular) types.

In centrilobular emphysema the upper zones of the lung are usually affected.This causes gross disturbance of the ventilation /perfussion relationship since there is a relatively well-preserved blood supply to the alveoli, but the amount of oxygen reaching the capillary is decreased owing to the damage to airways proximal to the alveoli.

2.PANACINAR EMPHYSEMA-Predominantly affects the lower lobes and lower lobe involvement is more common in individuals with alfa1-antitrypsin deficiency. This has a less drastic effect on the ventilation/perfussion relationship, since the blood supply in the damaged areas is decreased in proportion to the decreased ventilation in those areas.


emphysema (1)
The alveoli and the small distal airways are primarily affected by the disease, followed by effects in the larger airways . Elastic recoil is usually responsible for splinting the bronchioles open. However, with emphysema, the bronchioles lose their stabilizing function and therefore causing a collapse in the airways resulting in gas to be trapped distally.

There is an erosion in the alveolar septa causing there to be an enlargement of the available air space in the alveoli.

There is sometimes a formation of bullae with their thin walls of diminished lung tissue.

Smoking contributes to the development of the condition initially by activating the inflammatory process . The inhaled irritants cause inflammatory cells to be released from polymorphonuclear leukocytes and alveolar macrophages to move into the lungs. Inflammatory cells are known as proteolytic enzymes, which the lungs are usually protected against due to the action of antiproteases such as the alpha1-antitrypsin . However, the irritants from smoking will have an effect on the alpha1-antitrypsin, reducing its activity. Therefore emphysema develops in this situation when the production and activity of antiprotease are not sufficient to counter the harmful effects of excess protease production . A result of this is the destruction of the alveolar walls and the breakdown of elastic tissue and collagen. The loss of alveolar tissue leads to a reduction in the surface area for gas exchange, which increases the rate of blood flow through the pulmonary capillary system .

1. PROGRESSIVE DYSPNEA-Shortness of breath occurs initially on exertion , but as the disease progresses it will gradually occure after less and less activity and finally at rest .

2. RESPIRATORY PATTERN –The patient has a ‘fishlike’ inspiratory gasp, which is followed by prolonged, forced expiration usually against ‘pursed lips’.A ‘flick’ or bounce of the abdominal muscles may be seen on expiration as the outward flow of air is suddenly checked by obstruction of the airways.

3.COUGH WITH SPUTUM-This will be present if the disease is associated with chronic bronchitis or if there is infection.

4.CHEST SHAPE-The chest becomes barrel-shaped and fixed in inspiration, with widening of the intercostal spaces.There may also be indrawing of the lower intercostal spaces and supraclavicular fossa on inspiration .This is also associated with the difficulty of ventilating stiff lungs through narrowed airways.The ribs are elevated by the accesory muscles of respiration and there is loss of thoracic mobility.

5. POOR POSTURES-There may be a thoracic kyphosis plus elevated and protracted shoulder girdle.

6. POLYCYTHEMIA-This may develop in response to prolonge decrease in pao2 owing to the ventilation/perfusion imbalance.

7. CORE PULMONALE-This occurs in advanced stages of thje disease.

8.LUNG FUNCTION-The FEV1/FVC ratio is usually below 70per cent. RV is increased and lung volume may exceed the predicted total lung capacity(TLC).

EXAMINATION-The percussion note will be normal or hyper-resonant due to air trapping. Auscultation will reveal decreased breath sounds and prolonged expiration.

The chest X-RAY shows low flat diaphrams and hyperinflation.


PROGNOSIS OF EMPHYSEMA-The patients become progressively more disabled, with death ultimately occuring from respiratory failure.Complications of the emphysema is pneumothorax due to the rupture of the emphysematous bulla, and congestive cardiac failure.


1-Decrease the bronchial irritation to a minimum stop smoking , avoid dusty, smoky , damp or foggy atmosphere.
2- Control infections-The should have a supply of antibiotics at home and receive a vaccination against influenza each winter.
3-Control bronchospasm
4-Control/decrease the amount of sputum
5-Oxygen therapy
6-Long-term oxygen therapy (LTOT)

1- Beta2 agonists-(salbutamol and turbutalin) ,and long acting beta agonist (salmeterol and formoterol) the 2-Anticholinergics-(Ipratropium bromoide and Oxitropium bromide)
3-Xanthen derivatives -(Theophyllin and Aminophyllin)

1- Corticosteroids-(Beclometason, Budesonide)

Goals of treatment for COPD include:

  • Relieving symptoms
  • Slowing progress of the disease
  • Improving exercise tolerance (ability to stay active)
  • Preventing and treating complications
  • Improving overall health
  • COPD is not a reversible condition and has no cure yet, but conservative treatment for COPD can slow its progression (smoking cessation being the most important).

Aims of COPD Therapy

  • To remove excess bronchial secretion and reduce the airflow obstruction.
  • To establish the coordinated pattern of breathing
  • To promote relaxation and improve posture
  • To improve the mobility of thorax, shoulder girdle and neck
  • To increase the exercise tolerance
  • To encourage a full and active life style.

Means of COPD Treatment

1.POSTURAL DRAINAGE (P.D) is necessary for all patients. In chronic bronchitis regular postural drainage should be given. In case of acute emphysema, postural drainage is not necessary but in an infection episode,  where sputum may be present PD may be needed. The optimum position must be established with individual and advice for postural drainage at home.

Clapping and Shaking are effective over the affected lung segments and help to loosen and move the secretions to central airways during expiration. Then ask the patient to take 2-3 coughs to remove the secretions out. If the patient is unable to clear the secretions which are accumulated in lungs, then increased ventilation and humidification by IPPB conjoint with P.D are provided. This is very effective for patient. But in presence of emphysematous bullae, it is contraindicated because of risk of causing pneumothorax.


ACBTThe Active Cycle of Breathing Techniques (ACBT) is an active breathing technique performed by the patient to help clear their sputum the lungs. The ACBT is a group of techniques which use breathing exercises to improve the effectiveness of a cough, loosen and clear secretions and improve ventilation.

ACBT consists of three main phases:

1.Breathing Control
2.Deep Breathing Exercises or thoracic expansion exercises
3.Huffing OR Forced Expiratory Technique (F.E.T)

Additionally, a manual technique (MT) or positive pressure can be added if and when indicated, to create a more complex cycle to help improve removal of secretions on the lungs.

1.Breathing Control
Breathing control is used to relax the airways and relieve the symptoms of wheezing and tightness which normally occur after coughing or breathlesness. Breathing should be performed gently through the nose using as little effort as possible. If this is not possible then breathing should be done by mouth. If it is necessary to breathe out through the mouth this should be done with ‘pursed lips breathing’. While performing this technique it is important to encourage the patient use it as an opportunity to reduce any tension they may have, Encouraging the patient to close their eyes while performing Breath Control can also be beneficial in helping to promote relaxation. It is very important to use Breathing Control in between the more active exercises of ACBT as it allows for relaxation of the airways. Breathing Control can also help you when you are short of breath or feeling fearful, anxious or in a panic. The length of time spent performing Breathing Control will vary depending on how breathless patient feels.

When using this technique with a patient as part of the ACBT the patient should be instructed to usually 6 breaths. Instructions to patient: Rest one hand on your stomach and keep your shoulders relaxed to drop down. Feel your stomach rise as you breathe in and fall when you breathe out.

2.Deep Breathing Exercises
Deep breathing is used to get air behind the sputum stuck in small airways:
Relax your upper chest.
Breathe in slowly and deeply.
Breathe out gently until your lungs are empty – don’t force the air out.
Repeat 3 – 4 times, if the patient feels light headed then it is important that they revert back to the Breathing Control portion of the cycle.
At the end of the breath in, hold the air in your lungs for 3 seconds (this is known as an inspiratory hold).
Deep breathing/thoracic expansion exercises recruit the collateral ventilatory system assisting, the movement of air distal to mucus plugs in the peripheral airways.
Deep breaths to utilise collateral channels and get air behind sputum to mobilise it towards larger airways and towards the mouth. Instructions to patient:

  • Relax your shoulders.
  • Place both hands on either side of ribs.
  • Breathe in deeply feeling as your ribs expand.
  • Breathe out gently as far as you can until your lungs feel empty.
  • Deep breathing/thoracic expansion is usually repeated 4 times.

The FET is an integral part of the ACBT described by Pryor and Webber .

  • A huff is exhaling through an open mouth and throat instead of coughing.Huffing moves sputum from the small airways to the larger airways, from where they are removed by coughing. Coughing alone does not remove sputum from small airways.

1.Take a small-medium sized breath in

  • Squeeze the breath out by contracting your tummy muscles and keep your mouth and throat open to perform a huff. This small-medium sized huff helps with the removal of sputum in the lower reaches of the lungs.
  • To remove sputum in the higher portions of the lungs take a large breath in.
  • Squeeze the air out as before to perform a huff.
  • Cough and expectorate any sputum. If no sputum is produced with 1 or 2 coughs, try to stop coughing by encouraging the patient to use Breathing Control, the main technique used in between the more active stages of the as ACBT.
  • Allow your breathing to settle with breathing control and then repeat the cycle until your chest feels clear.
    Small long huffs move sputum from low down into chest whereas big short huffs moves sputum from higher up into chest, so use this huff when it feels ready to come out, but not before; huffs work via dynamic compression.
    Instructions to patient:ACBT

2.Take a medium sized breath in.
Squeeze the breath out fairly hard and fast keeping mouth and throat open. Imagine trying to steam up a mirror or blow a tissue held out in front of you.
Attempt to clear sputum 2-3 times then return to breathing control (Phase one) to relax airways.
Repeat as above except for a larger breath in to remove secretions/sputum in other areas of the lungs.

In case of acute exacerbation of chronic bronchitis the physiotherapy must be given vigorously. IPPB has great value in this case. It is given with mask to improve ventilation. It is important to observe the chest wall movement and level of consciousness. The patient should be observed for any signs of drowsiness after taking the treatment. Assisted ventilation with vigorous chest shacking and postural drainage are more effective. A ventilatory mask providing controlled oxygen therapy is usually required.

3.BREATHING EXERCISE- should be given in a correct way in treatment for COPD. The main emphasis is given on diaphragmatic breathing with relaxed expiration. The diaphragmatic breathing with decreased upper chest movements and relaxed shoulder girdle is preferred. Expansion of basal lung segments are taught to ventilate these areas.

Pursed lip breathing with prolonged expiration is given as treatment for COPD especially in presence of emphysematous bullae.

3. POSTURE CORERECTION Patient should be taught to attain maximal relaxation of the upper chest as well as movements of lower chest. The main emphasis is on relaxed and controlled diaphragmatic breathing. For maintaining posture the patient should not be kept with forward head and rounded shoulder.

4. THORACIC MOBILITY EXERCISE are given along with shoulder girdle movements. Free active exercises for whole spine to prevent kyphosis and fixed inspiration.

Important COPD exercise in sitting is trunk turning with loose arm swinging in rotation for relaxation. It is also essential to emphesise postural awareness so that the patient practices shoulder girdle retraction and lateral rotation of arm.

5. These patients should be as mobile and active as possible. Their exercise tolerance may be increased by gradually increasing the distances walked both on the flat and upstairs or slopes while practising breathing control. A graduated exercise programme can also be given to these patients during the later part of their stay in hospital and should be continued at home.

6. In daily life style patient should avoid smoking and encouraged to keep fit and eat sensibly. For gaining relaxation, swimming helps very much. Jerky and quick movements should be strictly avoided.