Carpal Tunnel Syndrome

What is a Carpal Tunnel Syndrome?

Carpal Tunnel Syndrome

Carpal Tunnel Syndrome (CTS) is a condition that causes pain, numbness, and tingling in the hand and arm. It is caused by pressure on the median nerve, which runs through a narrow passageway called the carpal tunnel in the wrist. The median nerve provides sensation to the thumb, index finger, middle finger, and half of the ring finger. It also controls the movement of some of the muscles in the hand.

CTS can occur when the carpal tunnel becomes compressed or narrowed, which can happen due to a variety of reasons such as repetitive motions, injury, or medical conditions like rheumatoid arthritis, diabetes, or thyroid dysfunction. People who perform tasks that involve repetitive hand motions or forceful gripping, such as typing, sewing, playing an instrument, or using tools, are at a higher risk of developing CTS.

Symptoms of CTS may include pain, numbness, tingling, or a burning sensation in the hand, wrist, or forearm. Some people may also experience weakness in the hand and have difficulty gripping objects or performing fine motor tasks.

Treatment for CTS may include non-surgical options such as rest, splinting, physical therapy, and medication. In some cases, surgery may be necessary to relieve the pressure on the median nerve. It's important to seek medical attention if you suspect you have CTS, as early treatment can help prevent permanent nerve damage.

Related Anatomy

The carpal tunnel is a narrow passageway located in the wrist, formed by bones and ligaments that make up the wrist joint. The floor and sides of the tunnel are formed by bones called the carpal bones, while the roof of the tunnel is formed by a strong ligament called the transverse carpal ligament.

Inside the carpal tunnel runs several tendons, including the tendons that control the movement of the fingers and the median nerve. The median nerve originates from the brachial plexus, a network of nerves that emerge from the spinal cord in the neck region, and travels through the arm and forearm to reach the hand.

The median nerve provides sensation to the palm side of the thumb, index finger, middle finger, and half of the ring finger. It also controls the movement of some of the muscles in the hand, including the muscles that move the thumb and index finger.

Carpal Tunnel Syndrome occurs when the median nerve is compressed or irritated as it passes through the carpal tunnel, which can cause a range of symptoms in the hand and wrist.

Causes of Carpal Tunnel Syndrome

Carpal Tunnel Syndrome (CTS) can be caused by a variety of factors that lead to pressure on the median nerve as it passes through the carpal tunnel in the wrist. Some common causes of CTS include:

• Repetitive hand movements: Repeated and forceful use of the hands and wrists, such as typing, using a computer mouse, or using vibrating tools, can put pressure on the median nerve and cause CTS.
• Medical conditions: Certain medical conditions, such as rheumatoid arthritis, diabetes, and hypothyroidism, can cause swelling and inflammation that can compress the median nerve.
• Wrist injuries: Injuries to the wrist, such as fractures or sprains, can cause swelling and inflammation that can compress the median nerve.
• Pregnancy: Pregnant women may develop CTS due to hormonal changes that can cause swelling in the wrist and compress the median nerve.
• Genetics: Some people may have a genetic predisposition to developing CTS, such as having a smaller carpal tunnel or thicker ligaments that compress the median nerve.
• Obesity: Being overweight or obese can increase the risk of developing CTS due to increased pressure on the median nerve.
• Certain medications: Some medications, such as those used to treat breast cancer, can cause fluid retention and increase the risk of developing CTS.

Smoking: Smoking has been associated with an increased risk of CTS, although the exact mechanism is unclear.

Symptoms of Carpal Tunnel Syndrome

The symptoms of Carpal Tunnel Syndrome (CTS) can vary from person to person, and may range from mild to severe. Some common symptoms of CTS include:

• Numbness or tingling: People with CTS may experience numbness or tingling in the thumb, index finger, middle finger, and half of the ring finger. This may also be described as a "pins and needles" sensation.
• Pain: CTS can cause pain in the hand, wrist, forearm, and even the upper arm. The pain may be intermittent or constant, and may be worse at night.
• Weakness: CTS can cause weakness in the hand, making it difficult to grip objects or perform fine motor tasks like buttoning a shirt.
• Clumsiness: People with CTS may experience clumsiness or a tendency to drop objects due to weakness or numbness in the hand.
• Burning sensation: Some people with CTS may experience a burning sensation in the hand, wrist, or forearm.
• Swelling: In some cases, CTS can cause swelling in the fingers, hand, or wrist.

The symptoms of CTS can worsen over time if left untreated, and can eventually lead to permanent nerve damage. It's important to seek medical attention if you suspect you have CTS, especially if your symptoms are affecting your ability to perform daily activities.

Risk Factor

There are several risk factors that can increase a person's likelihood of developing Carpal Tunnel Syndrome (CTS). Some common risk factors include:

• Repetitive hand movements: Performing tasks that involve repetitive hand motions or forceful gripping, such as typing, sewing, playing an instrument, or using tools, can increase the risk of CTS.
• Medical conditions: Certain medical conditions, such as rheumatoid arthritis, diabetes, and hypothyroidism, can increase the risk of developing CTS.
• Genetics: Some people may have a genetic predisposition to developing CTS, such as having a smaller carpal tunnel or thicker ligaments that compress the median nerve.
• Age and gender: CTS is more common in people over the age of 50, and women are more likely to develop CTS than men.
• Pregnancy: Pregnant women may develop CTS due to hormonal changes that can cause swelling in the wrist and compress the median nerve.
• Obesity: Being overweight or obese can increase the risk of developing CTS due to increased pressure on the median nerve.
• Smoking: Smoking has been associated with an increased risk of CTS, although the exact mechanism is unclear.

It's important to note that having one or more of these risk factors does not necessarily mean that a person will develop CTS, and some people may develop CTS without any known risk factors. However, being aware of these risk factors can help people take steps to prevent or manage CTS.

Differential Diagnosis

There are several conditions that can cause symptoms similar to Carpal Tunnel Syndrome (CTS), so it's important to get an accurate diagnosis from a healthcare provider. Some common conditions that can be mistaken for CTS include:

• Cervical radiculopathy: This is a condition in which a nerve in the neck is compressed, causing symptoms that can mimic CTS, such as pain, numbness, and tingling in the arm and hand.
• Tendinitis: Inflammation of the tendons in the wrist can cause pain and swelling that can be mistaken for CTS.
• Arthritis: Rheumatoid arthritis or osteoarthritis can cause swelling and stiffness in the joints of the hand and wrist, which can compress the median nerve and cause symptoms similar to CTS.
• Thoracic outlet syndrome: This is a condition in which the nerves and blood vessels that pass through a narrow space between the collarbone and the first rib are compressed, causing symptoms that can mimic CTS.
• Peripheral neuropathy: This is a condition in which the nerves that carry messages to and from the brain and spinal cord to the rest of the body are damaged or destroyed, causing symptoms such as pain, numbness, and tingling in the hands and feet.
• Ganglion cyst: This is a fluid-filled sac that can form on the wrist or hand, causing pain and discomfort that can be mistaken for CTS.
• Multiple sclerosis: This is a chronic autoimmune disease that affects the central nervous system, causing a range of symptoms that can include numbness, tingling, and weakness in the hands and arms.

Getting an accurate diagnosis is essential for effective treatment, so it's important to seek medical attention if you experience symptoms that may be related to CTS or any other condition.

Diagnosis

To diagnose Carpal Tunnel Syndrome (CTS), a healthcare provider will typically begin by taking a medical history and performing a physical exam. During the exam, the provider will check for signs of nerve damage, such as weakness or numbness in the hand, and may perform a few simple tests to check the sensation and strength in the fingers and thumb.

If CTS is suspected, the provider may order one or more diagnostic tests to confirm the diagnosis and rule out other conditions. These tests may include:

• Nerve conduction study (NCS): This test measures the speed at which electrical impulses travel through the nerves in the hand and wrist. People with CTS will typically have slower nerve conduction velocities than people without the condition.
• Electromyography (EMG): This test measures the electrical activity of the muscles and nerves in the hand and wrist. It can help determine if there is damage to the median nerve or other nerves in the area.
• X-rays or MRI: These imaging tests can help rule out other conditions, such as arthritis or a bone fracture, that can cause symptoms similar to CTS.

If CTS is diagnosed, treatment may include splinting or bracing of the wrist, physical therapy, pain management, or, in severe cases, surgery to relieve pressure on the median nerve. Early diagnosis and treatment are important for preventing long-term nerve damage and improving outcomes.

Treatment of Carpal Tunnel Syndrome

The treatment of Carpal Tunnel Syndrome (CTS) depends on the severity of symptoms and the underlying cause of the condition. Some common treatments for CTS include:

• Rest and activity modification: Avoiding activities that cause symptoms and taking frequent breaks can help reduce inflammation and pressure on the median nerve.
• Splinting or bracing: Wearing a splint or brace on the wrist can help keep the wrist in a neutral position and reduce pressure on the median nerve.
• Physical therapy: Exercises to stretch and strengthen the muscles and tendons in the hand and wrist can help improve symptoms and prevent further damage to the median nerve.
• Medications: Over-the-counter pain relievers, such as acetaminophen or nonsteroidal anti-inflammatory drugs (NSAIDs), can help relieve pain and reduce inflammation.
• Corticosteroid injections: Injections of a corticosteroid medication directly into the wrist can help reduce inflammation and relieve pain.
• Surgery: In severe cases of CTS that do not respond to other treatments, surgery may be necessary to relieve pressure on the median nerve. The most common surgical procedure for CTS is called carpal tunnel release, in which the ligament that is compressing the median nerve is cut to relieve pressure.

It's important to work with a healthcare provider to develop a treatment plan that is tailored to your individual needs and circumstances. Early treatment can help prevent long-term nerve damage and improve outcomes.

Physiotherapy Treatment

Physical therapy can be an effective treatment option for Carpal Tunnel Syndrome (CTS). A physical therapist can work with you to develop a personalized treatment plan based on your individual needs and symptoms. Some common physical therapy treatments for CTS include:

• Stretching and strengthening exercises: Specific exercises can help stretch and strengthen the muscles and tendons in the hand and wrist, reducing pressure on the median nerve.
• Nerve gliding exercises: These exercises involve moving the median nerve back and forth within the carpal tunnel to help reduce pressure and improve blood flow to the affected area.
• Manual therapy: Hands-on techniques, such as massage or mobilization, can help reduce inflammation and improve mobility in the affected wrist and hand.
• Ultrasound therapy: This treatment uses high-frequency sound waves to create heat and promote healing in the affected area.
• Electrical stimulation: This treatment uses a small electrical current to stimulate the affected muscles and reduce pain.
• Education and ergonomic training: A physical therapist can teach you about proper posture and body mechanics to reduce strain on the wrist and prevent further damage to the median nerve.

Physical therapy is often used in combination with other treatments, such as splinting or medication, to provide a comprehensive approach to CTS management. It's important to work with a qualified physical therapist who has experience working with CTS to ensure the best possible outcomes.

Surgery

Surgery may be necessary to treat Carpal Tunnel Syndrome (CTS) in cases where symptoms are severe and/or have not responded to other treatments. The most common surgical procedure for CTS is called carpal tunnel release.

During this procedure, the surgeon cuts the transverse carpal ligament to relieve pressure on the median nerve. This can be done either through traditional open surgery, in which the ligament is cut through a small incision in the wrist, or endoscopic surgery, in which a small camera is used to guide the cutting instrument through a smaller incision.

Carpal tunnel release surgery is usually done on an outpatient basis, meaning you can go home the same day. Recovery time varies depending on the severity of the symptoms and the type of surgery performed, but most people are able to return to normal activities within a few weeks to a few months.

As with any surgery, there are risks associated with carpal tunnel release, including infection, bleeding, nerve damage, and stiffness or weakness in the wrist. It's important to discuss the potential risks and benefits of surgery with your healthcare provider to determine if it's the best treatment option for you.

Complication

As with any medical procedure, there are potential complications associated with carpal tunnel release surgery for Carpal Tunnel Syndrome (CTS). Some of these complications may include:

• Infection: Infection can occur at the incision site, which can lead to pain, swelling, redness, and fever.
• Bleeding: There may be some bleeding during or after surgery, which can lead to bruising, swelling, or nerve damage.
• Nerve damage: Although rare, nerve damage can occur during surgery, which can cause numbness, tingling, or weakness in the hand and fingers.
• Stiffness or weakness in the wrist: Following surgery, some people may experience stiffness or weakness in the wrist or hand, which can affect their ability to perform daily activities.
• Recurrence of symptoms: In some cases, symptoms may return after surgery, particularly if the underlying cause of CTS is not addressed.

It's important to discuss the potential risks and benefits of carpal tunnel release surgery with your healthcare provider before undergoing the procedure. Following surgery, it's important to follow all post-operative instructions carefully and attend any follow-up appointments to monitor healing and address any concerns or complications that may arise.

How to Prevent Carpal Tunnel Syndrome?

While Carpal Tunnel Syndrome (CTS) cannot always be prevented, there are several steps you can take to reduce your risk of developing the condition:

• Practice good posture: Maintaining proper posture can help reduce strain on the hands and wrists, reducing the risk of developing CTS.
• Take frequent breaks: If you perform repetitive tasks that involve your hands and wrists, take frequent breaks to stretch and rest your hands.
• Stretch regularly: Regular stretching of the hands, wrists, and forearms can help prevent CTS by reducing tension and pressure on the median nerve.
• Use proper ergonomics: Make sure your workstation is set up properly to reduce strain on the hands and wrists. Use ergonomic equipment, such as a keyboard and mouse that are designed to reduce strain on the hands and wrists.
• Avoid gripping objects too tightly: Avoid gripping objects too tightly, especially for extended periods of time, as this can put pressure on the median nerve.
• Manage underlying conditions: If you have an underlying condition such as diabetes, arthritis, or thyroid dysfunction, make sure it is properly managed to reduce your risk of developing CTS.

By taking these steps, you can help reduce your risk of developing Carpal Tunnel Syndrome and maintain good hand and wrist health.

Conclusion

Carpal Tunnel Syndrome (CTS) is a common condition that occurs when the median nerve, which runs through the wrist, becomes compressed or pinched, leading to symptoms such as pain, numbness, and tingling in the hand and fingers. It is often caused by repetitive motions or underlying health conditions, but can also be related to genetics or injury.

Treatment options for CTS include non-surgical approaches such as splinting, medications, and physiotherapy, as well as surgical options like carpal tunnel release. However, it is important to take steps to prevent CTS, such as practicing good posture, taking frequent breaks, stretching regularly, using proper ergonomics, and managing underlying health conditions.

If you are experiencing symptoms of CTS, it is important to consult with a healthcare professional for proper diagnosis and treatment. With proper management and prevention, it is possible to manage the symptoms of CTS and improve overall hand and wrist health.

FACIAL NERVE PALSY

 INTRODUCTION

ANATOMY:

 
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.

STRUCTURE:

 
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).

INTRACRANIAL BRANCH :

 
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.

EXTRACRANIAL BRANCHES
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:

                                                       
EXRACRANIAL BRANCH
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

NUCLEUS
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.

DEVELOPMENT
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.

FUNCTIONS
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.

FACIAL SENSATION
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).

OTHERS-
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.

FUNCTIONAL COMPONNENT-
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
cavity.

CLINICAL SIGNIFICANCE-

PALSY
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.

EXAMINATION-
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.

FACIAL NERVE PALSY-
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.

RISK FACTORS-
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.

CLINICAL FEATURE-
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)

DIFFERENCE BETWEEN THE UMN AND LMN LESION-
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).

DIFFERENTIAL DIAGNOSIS-

LMN AND UMN LESIONImportant 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

• LMN CAUSES
• 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
Drooling
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

INVESTIGATION
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.

MANAGEMENT-
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.

MEDICAL MANAGEMENT
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.

SURGICAL REFFERAL
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).

COMPLICATIONS
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

PHYSICAL THERAPY TREATMENT FOR FACIAL PARALYSIS :

 
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 could permanently 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.

DURING RECOVERY :

 
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.
AFTER RECOVERY-
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."

NEUROMUSCULAR RETRAINING (NMR)
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.

BENEFITS OF NMR
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.
VIABLE CANDIDATE FOR NMR
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
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.

 

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MULTIPLE SCLEROSIS AND TREATMENT

DEFINATION :

 
Multiple sclerosis (MS) is a autoimmune disease characterised by inflammation,selective demylination and gliosis.it can cause both acute and chronic symptoms and can results in a significant disability and impaired quality of life.MS affects approximately 400,000 persons in the united states ; worldwild MS affects approximately 2.1 millian people.
 

It was first defined by the Dr.jean charcot in 1868 by its clinical ans pathological characteristics : paralysis and the cardinal symptoms of intension tremor, scanning speech and nystagmus later termed ”CHARCOT’S TRIAD”.
using the autopsy studies he identifies the areas of hardened plaques and termed the dieses sclerosis in plaques.
 

Specific symptoms can include double vision, blindness in one eye, muscle weakness, trouble with sensation, or trouble with coordination. MS takes several forms, with new symptoms either occurring in isolated attacks (relapsing forms) or building up over time (progressive forms). Between attacks, symptoms may disappear completely; however, permanent neurological problems often remain, especially as the disease advances.
Multiple sclerosis is a chronic disease that attacks the central nervous systrem, it affects the spinal cord , brain,and optic nerve.
Multiple sclerosis affects the nerve cells.

WHAT IS MULTIPLE SCLEROSIS ?
 

In the CNS, nerve fibers are surrounded by a myelin sheath, which protects them. Myelin also helps the nerves conduct electrical signals quickly and efficiently. In MS, the myelin sheath disappears in multiple areas, leaving a scar, or sclerosis.
Multiple sclerosis means “scar tissue in multiple areas.”
The areas where there is no myelin or a lack of myelin are called plaques or lesions. As the lesions get worse, nerve fibers can break or become damaged. As a result, the electrical impulses from the brain do not flow smoothly to the target nerve.When there is no myelin, the fibers cannot conduct the electrical impulses at all. The messages from the brain to the muscles cannot be transmitted.

CAUSES OF MULTIPLE SCLEROSIS:

 
The cause of multiple sclerosis is unknown. It’s considered an autoimmune disease in which the body’s immune system attacks its own tissues. In the case of MS, this immune system malfunction destroys myelin (the fatty substance that coats and protects nerve fibers in the brain and spinal cord).
Myelin can be compared to the insulation coating on electrical wires. When the protective myelin is damaged and nerve fiber is exposed, the messages that travel along that nerve may be slowed or blocked. The nerve may also become damaged itself.
It isn’t clear why MS develops in some people and not others. A combination of genetics and environmental factors appears to be responsible.
PATHOPHYSIOLOGY:
1 .In patients with MS the immune response triggers activation of immune cells that cross the blood brain barries. these cells activates the autoantigens, producing’‘ AUTO- IMMUNE CYTOTOXIC EFFECTS’‘ within the central nervous system. demylination slows neural transmission and cause nerve to fatigue rapidly.
2.demylinated areas eventually become filled with fibrous astrocytes and undergo a process called ”GLIOSIS”.
DISEASE COURSE:
Most people with MS have a relapsing-remitting disease course. They experience periods of new symptoms or relapses that develop over days or weeks and usually improve partially or completely. These relapses are followed by quiet periods of disease remission that can last months or even years.
Small increases in body temperature can temporarily worsen signs and symptoms of MS, but these aren’t considered disease relapses.
About 60 to 70 percent of people with relapsing-remitting MS eventually develop a steady progression of symptoms, with or without periods of remission, known as secondary-progressive MS.
The worsening of symptoms usually includes problems with mobility and gait. The rate of disease progression varies greatly among people with secondary-progressive MS.
Some people with MS experience a gradual onset and steady progression of signs and symptoms without any relapses. This is known as primary-progressive MS.
TYPES OF MS
There are four types of MS:
1.Clinically isolated syndrome (CIS): This is a single, first episode, with symptoms lasting at least 24 hours.
2.Relapse-remitting MS (RRMS): This is the most common form, affecting around 85 percent of people with MS and involving attacks of new or increasing symptoms.
3.Primary progressive MS (PPMS): Symptoms worsen progressively, without early relapses or remissions. Around 15 percent of cases are PPMS.
4.Secondary progressive MS (SPMS): After initial episodes or relapse and remission, the disease progresses steadily.
RISK FACTORS:
These factors may increase your risk of developing multiple sclerosis:
Age. MS can occur at any age, but most commonly affects people between the ages of 15 and 60.
Sex. Women are about twice as likely as men are to develop MS.
Family history. If one of your parents or siblings has had MS, you are at higher risk of developing the disease.
Certain infections. A variety of viruses have been linked to MS, including Epstein-Barr, the virus that causes infectious mononucleosis.
Race. White people, particularly those of Northern European descent, are at highest risk of developing MS. People of Asian, African or Native American descent have the lowest risk.
Climate. MS is far more common in countries with temperate climates, including Canada, the northern United States, New Zealand, southeastern Australia and Europe.
Certain autoimmune diseases. You have a slightly higher risk of developing MS if you have thyroid disease, type 1 diabetes or inflammatory bowel disease.
Smoking. Smokers who experience an initial event of symptoms that may signal MS are more likely than nonsmokers to develop a second event that confirms relapsing-remitting MS.
SYMPTOMS:
 


Symptoms of MS vary considerably, depending on the location of the lesion.Early symptoms typically include minor visual disturbance, and paresthesias, progressing to numbness, weakness and fatigability.
Multiple sclerosis signs and symptoms may differ greatly from person to person and over the course of the disease depending on the location of affected nerve fibers.
They may include:
1.SENSORY- Altered sensations are far more common and can including paresthesias, numbness of face , body and extremities.
Numbness or weakness in one or more limbs that typically occurs on one side of your body at a time, or the legs and trunk
2.VISION -Partial or complete loss of vision, usually in one eye at a time, often with pain during eye movement
Prolonged double vision
”MARCUS GUNN PUPIL”
Scotoma
Optic neuritis
Nystagmus
INO-interneuclear ophthelmoplegia , produce lateral gaze palsy
Tingling or pain in parts of your body
Electric-shock sensations that occur with certain neck movements, especially bending the neck forward (Lhermitte sign)
Tremor, lack of coordination or unsteady gait
Slurred speech
Fatigue
Dizziness
Headache.
trigeminal neuralgia
Paroxysmal limb pain
hyperpathia
chronic neuropathic pain
Musculoskeletal pain
Problems with bowel and bladder function
3.PAIN – Approximately 80% patients with MS experience pain.almost half experience pain.Anxiety and fear woersen the pain symptoms.
4.MOTOR-
Weakness
Spasticity
5.FATIGUE.
6.COORDINATION AND BALANCE-Ataxia
7.GAIT AND MOBILITY-Ataxic gait
8.SPEECH AND SWALLOWING-Dysarthria
9. COGNITIVE-In MS short term memory , attension and concentration ,information processing, executive functions, visuospatial functions affected.
10.DEPRESSION
11.EMOTIONAL-Pseudobulbar affect.
12.SEXUAL DYSFUNCTION.
13.UTTHOF’S SYMPTOMS
DIAGNOSIS:
Tests for MS include:
1.Neurological examination
2.MRI scanning
3.Evoked potentials
4.Lumbar puncture
5.Other tests
The neurologist will use specific criteria to diagnose MS, known as the McDonald criteria.
1-Neurological examination
Your neurologist will ask you lots of questions about your ‘history’, meaning your health problems and symptoms, now and in the past. This helps the neurologist get a better picture of you and can help identify any other problems that may explain current symptoms.
A physical examination checks for changes or weaknesses in your eye movements, leg or hand coordination, balance, sensation, speech or reflexes. Whilst a neurologist may strongly suspect MS at this stage, a diagnosis won’t be given until other test results confirm MS.
2-Magnetic Resonance Imaging (MRI)
 

DIAGNOSIS OF MS- ”BRIGHT SPOT”

An MRI scanner uses a strong magnetic field to create a detailed image of inside your brain and spinal cord. It is very accurate and can pinpoint the exact location and size of any inflammation, damage or scarring (lesions). MRI scans confirm a diagnosis in over 90 per cent of people with MS.
To get the image of a person’s brain and spinal cord they must lie down and enter a small tunnel in the centre of the MRI scanner. The process can take between 10 and 60 minutes and is painless, though some people can feel a little claustrophobic in the scanner. The Newcastle Upon Tyne Hospitals NHS Foundation Trust has produced a video which explains what to expect when you have an MRI
3-Evoked potentials tests
This painless test involves measuring the time it takes for your brain to receive messages from your eyes, ears and skin. Small electrodes are placed on your head. These check how your brain reacts to sounds you hear in headphones, patterns you see on a screen or sensations you feel on your skin. Messages to and from your brain will be slower if MS has damaged the myelin covering around some of your nerves.
4-Lumbar puncture
This is sometimes called a spinal tap. A needle is inserted in your lower back, into the space around your spinal cord. You have a local anaesthetic for this. A small sample of the fluid around your spinal cord is taken and tested for signs of MS. People with MS often have antibodies in this fluid. Antibodies show your immune system is active in your brain and spinal cord. This is something that isn’t seen in people who don’t have MS.
People often get headaches following a lumbar puncture. The medical staff should advise you on how to manage this. Lumbar punctures are used less now that MRI scans are more common.
5-Other tests
To rule out conditions that are similar to MS, other tests may also be done. These may include blood tests to reveal certain antibodies, and inner ear tests to check your balance.
The McDonald Criteria is distinguished by incorporating clinical evaluation with magnetic resonance imaging (MRI) scans in establishing MS. But, like an earlier approach, it too requires:
Evidence of damage to the central nervous system (CNS; the brain, spinal cord and optic nerves) that is “disseminated in time,” meaning damage that occurs on different dates;
Evidence of damage “disseminated in space,” or found on two or more parts of the CNS.
TREATMENT:
There is no cure for multiple sclerosis. Treatment typically focuses on speeding recovery from attacks, slowing the progression of the disease and managing MS symptoms. Some people have such mild symptoms that no treatment is necessary.
Treatments for MS attacks
1-Corticosteroids, such as oral prednisone and intravenous methylprednisolone, are prescribed to reduce nerve inflammation. Side effects may include insomnia, increased blood pressure, mood swings and fluid retention.
2-Plasma exchange (plasmapheresis). The liquid portion of part of your blood (plasma) is removed and separated from your blood cells. The blood cells are then mixed with a protein solution (albumin) and put back into your body. Plasma exchange may be used if your symptoms are new, severe and haven’t responded to steroids.
Symptom: Sensory symptoms (parasthesias)
Numbness, tingling, pins and needles
Treatment
No treatment required unless interfering with function; medication if necessary; referral to PT/OT if necessary
Symptom: Primary pain
*Central neuropathic pain – continuous (dysesthesias)
Medications:
Tricyclic antidepressant medications (amitriptyline, nortriptyline, desipramine); antiepileptic medications (pregabalin, gabapentin)
Other:
topical appliation of capsaic acid cream;behavioral self-management (mindfulness,meditation)
hypnosis,cognitive behavior therapy
*Central neuropathic pain – intermittent (trigeminal neuralgia)
Treatment
Medications
First-line: carbamazepine
Alternate options: oxcarbazepine, lamotrigine, baclofen
Additional options with lower levels of evidence: phenytoin, clonazepam, valproic acid, intranasal lidocaine
Surgery:
radiofrequency rhizotomy; radiofrequency electrocoagulation; glycerol rhizotomy
Psychosocial Implications for each pain symptom
Clumsiness, balance problems, and loss of dexterity from sensory loss
Discomfort that is sometimes excruciating
Increase in fatigue caused by medications and interrupted sleep
NOTE: Many people are still told by doctors that MS does not cause pain, yet pain is a common symptom of MS that is distracting, depressing, and debilitating.
*Symptom: Secondary pain (musculoskeletal)
Resulting from poor posture/balance in ambulatory individuals or improper use/fitting of wheelchair
Treatment
Interventions:Referral to PT: gait and balance training; assessment of all seating (home, automobile, work, and wheelchair/scooter);
Medications:analgesics
PHYSICAL THERAPY MANAGEMENT:
Physical therapy can play an essential role in keeping a patient with MS active and functional within the community.While there is no cure for multiple sclerosis, exercise appears to be beneficial at multiple levels and it may have an important role to play in delaying negative symptoms of the disease. Exercises should be chosen according to one’s strengths and weaknesses . It is suggested that exercise therapy does have efficacy in MS.It is to state the best ’dose’ (intensity, frequency and duration) of treatment to achieve optimal beneficial effects of exercise therapy in terms of activities and participation for patients suffering from MS. There was no evidence describing harmful effects of exercise therapy for MS patients. .Exercise is consider as a safe effective means of rehabilitation.
The PT assessment should focus on posture, movement and function, carefully considering how a patient’s performance may be limited by fatigue, pain or other factors. Analyzing these results together with the proper opinion and interest of the person with MS will enable the physiotherapist to set up an individualized program. This program needs to be set up so that it can easily be performed at home.Education is also important to assist patients in managing their programs as independently as possible. A multidisciplinary treatment for MS patients may lead to positive effects.

During EARLY STAGEof MS patients may present with minimal impairments. At this time, the PT can focus on educating the patient and family members or caregivers on disease progression and compensatory strategies to conserve energy. Physiotherapy emphasize movement outdoors especially in sunlight in order to avail the direct benefits of sunlight in MS.The recent study suggests life time sun exposure appears to reduce the risk of Multiple Sclerosis regardless of race/ethnicity. Study indicates the protective effect of sun exposure in MS is most likely mediated throgh immunomodulatory mechanisms.

Due to the progressive nature of the disease, those in the MODERATE STAGE might notice impairments at varying degrees and activities of daily living (ADL) may require assistance. At this middle stage,therapy should focus more on improving or maintaining motor functions through strength, endurance, flexibility, balance, respiratory training and assistive device training as well as suggesting environment modifications to the home or assessing mobility aids required to move about in the community to sustain quality of life. Informing the carers about correct postures will prevent further complications. A close collaboration between professional community carers and non-professional caregivers at home is a key factor for the successful management of the rehabilitation.
Advanced stages of MS often present with multiple impairments at incresing severity compared to earlier stages. The primary goals of the PT in late stages is to maximize independence through postural and ADL training, respiratory function, safety and prevention strategies for contracture development or pressure wounds, equipment suggestions, and proper transfer techniques.

PHYSIOTHERAPY TREATMENT : active/passive/active assisted exercises(carried with partner or with help of equipment like elastic bands);techniques like Bobath,Vojtas,Proprioceptive Neuromuscular Techniques; carried out regularly and with sufficient intensity, have evidence of improvement in patients with MS.
Use of therapeutic corticosteriods and inactivity due to fatigue and weakness,may lead to osteoporosis and pathological fractures.Weight bearing exercises can slow down the loss of bone and muscle mass. Resistance training program is recommended for maintaining bone and muscle mass,According to Döring et al. aerobic training seems to have a positive effect on fatigue.Aerobic exercise training with low to moderate intensity can result in the improvement of aerobic fitness and reduction of fatigue in MS patients,affected with mild or moderate disability.

BALANCE EXERCISE can improve balance.Poor postural control increases risk of falls.MS patients have increased sway in quiet stance,delayed postural perturbations and reduced ability to move towards limits of stability.These impairments are likely causes of falls.Reduced gait speed,decreased stride length, cadence,and joint movement are observed in most studies of gait in MS. The therapist must identify several factors that may be amenable to intervention to prevent falls in people with MS.Comprehensive exercise interventions can facilitate improvements in balance impairments.Functional balance exercises can extensitively impact balance, physical activity and quality of life in adults with multiple sclerosis.

MOTOR IMAGERY is increasingly used in neuro-rehabilitation in-order to facilitate motor performance.Motor imagery and rhythmic auditory stimulation can be used for walking rehabilitation in MS patients..Randomized control trial studying the effects of motor imagery showed significant improvement in walking speed,walking distance,perception and quality of living.

HIPPOTHERAPY has a positive effect on balance of persons with multiple sclerosis and has an added benefit of enhancing quality of life. A systematic review and meta-analysis of therapeutic effect of Horseback riding intervention shows positive physical and emotional effects of horse riding in individuals with neuromotor development and physical disabilities. Therapeutic horseback riding improved balance and gait of ambulatory patients with MS. Hippotherapy helps the rider,by providing effective sensory stimulation and rhythmic anterior and posterior swinging motion.It encourages the rider to achieve proper posture and balance.

AQUATIC EXERCISE program could have a positive effect for persons with progressive multiple sclerosis. Interventions that promote general health, improve energy levels and mental health, and faster social interaction in the presence of physical disability are beneficial for individuals with progressive multiple sclerosis. Because of reduced impact of gravity, aquatic training allows patients with even severe paresis of the lower extremities to perform standing and moving exercises.
In MS patients, beneficial effects of regular physical activity and exercise on mood and quality of life have been repeatedly reported.Valid data on the effect on cognitive function are hardly available.


Cognitive Behavioral Therapy (CBT) ] :

CBT have amoderately positive effect on fatigue in MS. However,this effect declines after cessation of treatment. Since the short-term effect of CBT on MS-related fatigue is positive, there is a need for more research, to develop interventions that, maintain these short-term effects in the long term.To have good results, it is best that the patient should be referred to a CBT specialist. CBT can also be an effective intervention for reducing moderate depression, over a short-term, in MS patients,which may also improve patient quality of life.
Throughout all stages of MS,PT can offer psychological support to the patient and family/caregiver.
PT Interventions for Common Symptoms of Patients with MS:
PAIN- Patients with MS often experience pain directly from the disease, secondary to medication or other symptoms, or from something completely separate. PT helps relieve pain through exercise, stretching, massage, ultrasound, postural training, or hydrotherapy.

SENSORY DEFICITS-Tapping and verbal cues during exercise and resistance training can help improve proprioception losses. Vision issues, such as blurred or double vision, often occur in patients with MS. PT can offer education on how to be safe at home and offer strategies to improve balance and coordination in dimly lit settings. PT treatment interventions for decreased sensation to light touch include education on awareness, protection, and personal care to desensitized body parts. Pressure-relieving devices are a primary prevention strategy along with proper transfer techniques and daily skin inspections for maintaining skin integrity.

FATIGUE– One of the most debilitating symptoms of MS is experienced by an overwhelming majority of patients: fatigue. PT strategies to help patients combat feelings of excessive tiredness include aerobic exercise, energy conservation, and activity pacing. Aerobic exercise activities is closely monitored by a PT to ensure a patient does not overheat, but is able to work on increasing their endurance capacity which will help them be more functional throughout the day. PT’s can also teach energy conservation strategies and activity pacing to help someone sustain their daily activities by minimizing fatigue.

SPASTICITY- The physical and functional limitations spasticity leads to include include a variety of impariments which can present as contractures, postural deformities, decubitus ulcers, and more. PT interventions range from cryotherapy and hydrotherapy to therapeutic exercise, stretching, range of motion activities, postural training, and electrical stimulation. A combination of therapeutic interventions is often the route taken.
Balance, Coordination, & Postural Deficits. Ataxia, postural instability, muscle spasms, and generalized muscle weakness al contribute to balance and coordination deficits. PT techniques to address these issues include postural exercise, core strengthening, rhythmic stabilization, static/dynamic balance training, aquatic therapy, proprioceptive loading, and resistance training.
Mobility Issues. Weakness, particularly in the lower extremity, balance deficits, fatigue, posture, contractures, sensation deficits, heat intolerance, among other deficits, can impede an individual’s ability to be mobile. In combination of the treatment previously described, PT’s work to help patient’s overcome their mobility limitations through locomotor and functional training.
Locomotor training focuses on increasing thigh and hip strength along with posture and balance training through walking activities. Orthotics and assistive devices are added as necessary. Functional training involves bed mobility, transfers, and developing strategies with the patient on how to be able to safely navigate around the home and out in the community.
 
DIETARY MODIFICATION:
Diet plays a huge role in health.Research suggests adding inflammatory fighting foods to diet can help in chronic inflammation.

Number of factors may be thought to play role in triggering inflammation- gluten and dairy products,vitamin D deficiency.Diet rich in whole fresh foods and eliminating dairy,sugar,high salt and processed food is highly recommended.

Many researchers are exploring dietary intervention approaches in MS to improve lifestyle. Probiotics may improve the health of people with MS by reducing disability and improving inflammatory and metabolic parameters according to an Iranian study.

Vitamin D supplementation helps prevention and treatment of MS. Various research studies are studying the effectiveness of vitamin D therapy in MS.

Fish oil supplementation given together with vitamins and dietary advice can improve clinical outcome in patients with newly diagnosed MS.More research is required to assess the effectiveness of dietary interventions of omega 3 in MS and it’s interaction with medications used for treating MS.

Dysfunction of mitochondria is thought to play an important role in mechanism of progression of demyelinating disorders.Observations in animal and histopathological studies,suggest that,dysfunctional mitochondria are important contributors to damage and loss of both axons and neurons.The relationship between mitochondrial dysfunction and neurodegeneration in MS is explored.The Ketogenic diet has the potential to treat the neurodegenerative component of progressive MS,though more research is required in this field.

 

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