What Is Claw Hand?

Claw hand is a condition in which your fingers are

noticeably curved or bent. One or more of your

fingers on one or both hands may be affected.

The condition gets its name because the

curvature of the fingers makes the hands

resemble a bear’s claw.

Claw hand can be a congenital defect (a defect

present at birth) or it may be due to certain

disorders or injuries. Depending on the severity

of the condition, you may have difficulty using

your hands to pick up and grasp items.

Causes of Claw Hand

Common causes of claw hand include:

a congenital birth defect

damage to the nerves in the arm or hand from injuries or

diseases, such as diabetes

scarring of the skin on the arm or hand due to a burn injury

Many conditions can cause nerve damage. Some

of the common causes are:

cervical spondylosis: abnormal wear of the cartilage or

bone in your spine that can cause compression on your

nerves

carpal tunnel syndrome: damage to the nerves in your

wrist that results from repetitive activities involving your

wrists

alcoholic neuropathy: damage to the nerves caused by

excessive or long-term alcohol use

diabetic neuropathy: damage to the nerves caused by

uncontrolled blood sugar levels

Another cause of claw hand is the bacterial

disease leprosy, which affects the skin. Leprosy is

extremely rare in the United States. There are

currently an estimated 6,500 people in the

United States with leprosy, according to the U.S.

Department of Health and Human Services, and

only half of those cases cause enough symptoms

to require treatment (HRSA , 2012 ).How Is Claw Hand Diagnosed?

Doctors can make a diagnosis of claw hand

based on the appearance of your fingers.

However, your doctor may perform tests to

determine the cause and severity of the

condition. Tests your doctor may order include:

Medical History

Your doctor may ask you questions about your

medical history to determine if a past injury or

illness is causing your symptoms.

Physical Examination

Your doctor may ask you to bend your fingers

and grasp objects, in addition to other tests, to

see how much strength and flexibility you have in

your fingers and hand.

Electromyography

An electromyography (EMG) test is used to check

how well your nerves are working. To perform an

EMG, your doctor will insert thin needles through

your skin into the muscles of your hand. The

needles are connected to a machine that

measures electrical impulses from your nerves

when you move. You may feel a little bit of

discomfort from the small needles, but it is

usually mild. You may also have slight bruising or

experience minor soreness for a few days after

the test.

If the EMG test results show that you have

abnormal nerve activity, your doctor may run

more tests to determine the cause of your nerve

damage. The tests your doctor will perform are

dependent on your medical history and any other

symptoms you may be experiencing.

Are There Treatments for Claw Hand?

Claw hand is often treatable. With treatment,

your symptoms may improve or completely

disappear, depending on the cause and severity

of your condition. The type of treatment that is

best for you is dependent on what is causing your

symptoms.

Physical Therapy

Your doctor may recommend physical therapy to

help you gain more flexibility in your fingers and

hand. Physical therapy may consist of stretches

and strengthening exercises. Physical therapy

may be used as a sole treatment or in

combination with other treatments.

Home Treatment

If the curvature of your fingers is caused by

carpal tunnel syndrome or another similar injury,

resting your hand may be the only treatment you

need. Your doctor may also suggest that you

wear a brace to keep your wrist straight to

prevent further injury.

Surgery

You may need surgery to repair damaged nerves,

ligaments, or muscles that are causing your

symptoms. If your injury is due to tight skin—as

is seen in people who have burn injuries—skin

grafts and scar tissue removal surgery may be

necessary. Multiple surgeries may be required for

serious defects and for burn injuries.

Medications

Your doctor may prescribe medication to treat an

underlying disease that is causing your

symptoms. For example, leprosy is treated with

antibiotics.

When to See Your Doctor

Call your doctor if you notice that you are

developing claw hand or if you have claw hand

and your symptoms are getting worse or are not

responding to treatment.

What is Muscular Dystrophy?Muscular dystrophies are a group of diseases that are passed down genetically. These diseases cause damage and weakness to muscles over time. This damage and weakness is caused by the lack of a protein called dystrophin, which is necessary for normal muscle function. The absence of this protein can cause problems with walking, swallowing, and muscle coordination.

There are more than 30 different kinds of muscular dystrophies, which vary in symptoms and severity.

Muscular dystrophy can occur at any age, but is usually diagnosed in childhood. Young boys are more likely to have this disease than girls.

The prognosis for muscular dystrophy depends on the type and the severity of

symptoms. However, most individuals with muscular dystrophy do lose the ability to walk and eventually require a wheelchair. There is no known cure for muscular dystrophies, but certain treatments may help.

Part 2 of 4: Types and Symptoms

Types of Muscular Dystrophy and Their SymptomsThere are over 30 different types of muscular dystrophy, which are divided into nine different categories used for diagnosis.

Duchenne

This type of muscular dystrophy is the most common among children. The majority of individuals affected are boys; it is rare for girls to develop Duchenne. Symptoms include:

trouble walking

loss of reflexes difficulty standing up poor posture bone thinning scoliosis, which is excessive curvature of the

spine mild mental impairment breathing difficulties swallowing problems lung and heart weakness

Individuals with Duchenne typically require a wheelchair before their teenage years. The life expectancy for those with this disease is late teens or twenties.

Becker

Becker muscular dystrophy is similar to Duchenne muscular dystrophy, but less severe. This type of muscular dystrophy also more commonly affects boys. Muscle weakness occurs mostly in the arms and legs, with symptoms appearing between age 11 and 25. Other symptoms of Becker muscular dystrophy include:

walking on the toes frequent falls muscle cramps trouble getting up from the floor

Many with this disease do not need a wheelchair until they are in their mid-thirties or older, while a small percentage never require one. Most individuals live until middle age or later.

Congenital

Congenital muscular dystrophies are often discovered between birth and age 2. This is when parents begin to notice that their child’s motor functions and muscle control are not developing as they should. Symptoms vary and may include:

muscle weakness poor motor control being unable to sit or stand without support scoliosis foot deformities trouble swallowing respiratory problems

vision problems speech problems intellectual impairment

While symptoms vary from mild to severe, the majority of those with congenital muscular dystrophy are unable to sit or stand without help. The lifespan of someone with this type also varies, depending on the symptoms. Some individuals die in infancy while others live until adulthood.

Mytonic Dystrophy

This form of muscular dystrophy, also called Steinert’s disease or dystrophia myotonica, causes an inability to relax muscles after they contract (myotonia). Myotonia is only found in this type of muscular dystrophy.

Myotonic dystrophy can affect the muscles in the face as well as the central nervous system, adrenal glands, heart, thyroid, eyes, and gastrointestinal (GI) tract. Symptoms most often appear first in the face and neck. Symptoms include:

drooping muscles of the face, producing a thin, haggard look

difficulty lifting the neck (weak neck muscles)

difficulty swallowing droopy eyelids (ptosis) early baldness in front area of the scalp poor vision, including cataracts weight loss increased sweating

This dystrophy type may also cause impotence and testicular atrophy in males; in women, it may cause irregular periods and infertility.

Mytonic dystrophy is typically diagnosed in adults in their twenties or thirties. While symptoms can affect quality of life, most are not life threatening, and sufferers often live a long life.

Facioscapulohumeral (FSHD)

FSHD is also known as Landouzy-Dejerine disease. This type of muscular dystrophy affects the muscles in the face, shoulders,

and upper arms. Individuals with FSHD may have difficulty chewing or swallowing; their mouths may take on a crooked appearance. Shoulders look slanted, and the shoulder blades appear wing like. A smaller number of individuals may develop hearing and respiratory problems.

FSHD tends to progress slowly; symptoms usually appear during an individual’s teenage years, but may lie dormant until his or her forties. Most individuals with this condition live a full lifespan.

Limb-Girdle

Limb-girdle muscular dystrophy causes weakening of the muscles and loss of muscle bulk. This type of muscular dystrophy usually begins in the shoulders and hips, and may also occur in the legs and neck. Individuals with limb-girdle muscular dystrophy may find it hard to get up out of a chair, walk up and down stairs, and carry heavy items. They may also stumble and fall more easily.

Limb-girdle muscular dystrophy affects both males and females. Most people with this form of muscular dystrophy are disabled by age 20; however, most individuals have a normal life expectancy.Oculopharyngeal (OPMD)

OPMD causes weakness in the facial, neck, and shoulder muscles. Other symptoms include:

drooping eyelids trouble swallowing voice changes vision problems heart problems difficulty walking

OPMD occurs in both men and women and is usually diagnosed when individuals are in their forties or fifties.

Distal

This type, also called Distal myopathy, affects the muscles in the forearms, hands, calves, and feet. It may also affect the respiratory system and heart muscles.

Symptoms, which include the loss of fine motor skills and difficulty walking, tend to progress slowly. Most individuals, both male and female, are diagnosed between 40 and 60 years of age.

Emery-Dreifuss

Emery-Dreifuss muscular dystrophy tends to affect more boys than girls. This type of muscular dystrophy usually begins in childhood. Symptoms include:

weakness in upper arm and lower leg muscles

breathing problems heart problems shortening of the muscles in the spine, neck,

ankles, knees, and elbowsMost individuals with Emery-Dreifuss muscular dystrophy die in mid-adulthood from heart or lung failure.

Part 3 of 4: Tests

How Is Muscular Dystrophy Diagnosed?There are a number of different tests used to diagnose muscular dystrophies. These tests include:

enzyme tests—blood is tested for enzymes released by damaged muscles

genetic testing—blood is tested for genetic markers for muscular dystrophy

electromyography—an electrode needle is inserted into a muscle to test the muscle’s electrical activity

muscle biopsy—a sample of the muscle is tested for muscular dystrophyPart 4 of 4: Treatment Options

How Are Muscular Dystrophies Treated?There is currently no cure for muscular dystrophy, but treatments can help to manage symptoms and slow the progression

of the disease. Treatments depend on the symptoms experienced.

Treatment options include:

corticosteroid drugs, which help strengthen muscles and slow the progression of muscle deterioration

physical therapy, which helps to strengthen muscles and maintain their range of motion

occupational therapy, which helps the individual to become more independent. This therapy addresses coping skills, social skills, and how to access helpful community services.

assisted ventilation medication for heart problems surgery to help correct shortening of

muscles, treat scoliosis, repair cataracts, or treat cardiac problems

What Is Leprosy?Leprosy is a chronic, progressive bacterial infection. It primarily affects the nerves of

the extremities, the lining of the nose, and the upper respiratory tract. It is caused by the bacteria Mycobacterium leprae. Leprosy produces skin sores, nerve damage, and muscle weakness if left untreated. It can cause severe disfigurement and significant disability.Leprosy is one of the oldest diseases in recorded history. According to the World Health Organization (WHO), the first known written reference to leprosy is from 600 B.C. (WHO, 2010).Leprosy is common in many countries, especially those with tropical or subtropical climates. However, it is not as commonin the United States. The National Institutes of Health (NIH) reports that only about 100 new cases are diagnosed in the United States each year (NIH, 2011).More than half of leprosy cases reported in the United Statesin 2006 were found in California, Florida, Louisiana, Massachusetts, New York, and Texas. The majority of cases

involved people emigrating from developing countries(Merck, 2009).Part 2 of 9: Types

Types of LeprosyThere are three systems for classifying leprosy.The first system recognizes two types of leprosy—tuberculoid and lepromatous. These are based on a person’s immune response to the disease.

The immune response is good and the disease is limited to a few lesions (sores on the skin) in tuberculoid leprosy. The disease is mild and only slightly contagious. The immune response is poor in lepromatous leprosy and affects the skin, nerves, and other organs. Lesions andnodules (large lumps and bumps) are widespread. The disease is more contagious.WHO categorizes the disease based on the type and number of skin areas affected. They are:

paucibacillary—five or fewer lesions with no bacteria detected in the skin smear (sample taken from the area)

multibacillary—more than five lesions or bacteria is detected in the skin smear, or bothThe Ridley-Jopling system is used globally in clinical studies. It has six classifications based on severity of symptoms. They are:

intermediate leprosy—a few flat lesions that sometimes heal by themselves and can progress to a more severe type

tuberculoid leprosy—a few flat lesions, some large and numb; some nerve involvement; can heal on its own, persist, or may progress to a more severe form

borderline tuberculoid leprosy—lesions like tuberculoid but small and more numerous; less nerve enlargement; may persist, revert to tuberculoid, or advance to another form

mid-borderline leprosy—reddish plaques, moderate numbness, swollen lymph glands;

may regress, persist, or progress to other forms

borderline lepromatous leprosy—many lesions with flat lesions, raised bumps, plaques, and nodules, sometimes numb; may persist, regress, or progress

lepromatous leprosy—many lesions with bacteria; hair loss; nerve involvement; limb weakness; disfigurement; does not regressPart 3 of 9: Transmission

How Is Leprosy Spread?Leprosy is spread through contact with mucous of infected person, usually when he or she sneezes or coughs. The disease is not highly contagious. Close, frequent contact with an untreated person is required to contract leprosy.

The bacteria responsible for leprosy multiply very slowly. Therefore,the disease has an incubation period (the time between infection and the appearance of the first symptoms) of up to five years. Symptoms

may not appear for as long as 20 years (WHO, 2010).According to the New England Journal of Medicine, a certain type of armadillo native to the southern United States can also carry and transmit the disease to humans (NEJM, 2011).Part 4 of 9: Symptoms

What Are the Symptoms of Leprosy?The main symptoms of leprosy include:

muscle weakness numbness in the hands, arms, feet, and legs skin lesions that: have decreased sensation to touch,

temperature, or pain do not heal after several weeks or month are lighter than your normal skin tone

Part 5 of 9: Diagnosis

How Is Leprosy Diagnosed?

Your doctor will conduct a physical exam to look for telltale signs and symptoms of the disease.He or she will also perform a skin biopsy or scraping. Your doctor will remove a small piece of skin and send it to a laboratory for testing.In addition, your doctor may perform a lepromin skin test to determine which form of leprosy you have.A small amount of leprosy-causing bacteria is injected into the skin, typically on the upper forearm. People who have tuberculoid or borderline tuberculoid leprosy will experience irritation at the injection site.Part 6 of 9: Treatment

How Is Leprosy Treated?WHO developed a multidrug therapy in 1995 to cure all types of leprosy. It is available free of charge worldwide (WHO, 2010). Additionally, several antibiotics are used to treat leprosy by killing the bacteria that causes it, including:

dapsone rifampin

minocycline ofloxacin

Your doctor may prescribe more than one antibiotic at the same time. He or she also may want you to take an anti-inflammatory medication such as aspirin, prednisone, orthalidomide. However, never take thalidomide if you are or may become pregnant. It can produce severe birth defects.

Part 7 of 9: Complications

What Are the Potential Complications of Leprosy?Serious complications may occur when diagnosis and treatment are delayed. Complicationsinclude:

disfigurement hair loss, particularly on the eyebrows and

eyelashes muscle weakness

permanent nerve damage in the arms and legs

inability to use the hands and feet chronic nasal congestion, nosebleeds, and

collapse of the nasal septum iritis (inflammation of the iris of the eye),

glaucoma (an eye disease that causes damage to the optic nerve), and blindness

erectile dysfunction and infertility kidney failure

Part 8 of 9: Outlook

What Is the Outlook for Leprosy?The overall outlook is good if leprosy is diagnosed promptly. Early treatment prevents tissue damage, stops the spread of the disease, and prevents serious health complications.

The outlook is worse when the disease is diagnosed at a more advanced stage, after it has caused significant disfigurementor disability. It may be impossible to lead a normal life despite treatment in these cases.

Part 9 of 9: Prevention

How Can I Avoid Contracting Leprosy?The best means of preventing leprosy is to avoid long-term, close contact with an untreated, infected person.

Background

Anatomy of the muscles of the hand

Normal positioning and movement of the digits depends on the functional integrity of extrinsic and intrinsic muscles. The extrinsic muscles originate in the forearm, and the intrinsic muscles originate distal to the wrist. The intrinsic muscles are traditionally divided into 5 groups: thenar, hypothenar, palmar interossei,[1] dorsal interossei, and lumbricals.

The 4 thenar muscles are the abductor pollicis brevis, flexor pollicis brevis, opponens pollicis, and adductor pollicis. The abductor pollicis brevis abducts the thumb away from the palm. The flexor pollicis brevis flexes the thumb metacarpophalangeal (MCP) joint. The opponens pollicis abducts, flexes, and pronates the first metacarpal. With these muscles, the thumb is

brought from lateral to medial position across the palm in opposition to the 4 ulnar digits. The adductor pollicis adducts the thumb toward the palm.

The hypothenar muscles are the abductor digiti minimi, the flexor digiti minimi brevis, and the opponens digiti minimi. The abductor digiti minimi abducts the little finger away from the fourth finger. The flexor digiti minimi brevis flexes the little finger at the MCP joint. The opponens digiti minimi abducts, flexes, and supinates the fifth metacarpal. With these muscles, the little finger is brought into opposition to the thumb.

Most anatomists describe 3 palmar interossei and 4 dorsal interossei muscles. The dorsal interosseous muscles flex the MCP joints and extend the interphalangeal (IP) joints. The dorsal interossei also abduct the 4 ulnar digits from one another; the volar interosseous muscles adduct the 4 ulnar digits together toward the third finger. There are 4 lumbrical muscles. They function as a connection between the flexor digitorum profundus (FDP) and the extensor mechanism. Their main function is to facilitate extension of the IP joints. The lumbricals can extend the IP joints in any position of the MCP joints.

An image depicting the Froment sign can be seen below.

Image in a patient with ulnar neuropathy demonstrates the Froment sign during pinching. Loss of the ulnar-innervated adductor pollicis results in reliance on the flexor pollicis longus and exaggerated interphalangeal (IP) joint flexion. Loss of the metacarpophalangeal (MCP) joint flexor leads to MCP hyperextension over time.Anatomy of the nerves of the hand

The ulnar nerve innervates most of the intrinsic muscles in the hand: all the interossei, the 3 hypothenar muscles, the adductor pollicis, the deep head of flexor pollicis brevis, and the 2 ulnar lumbricals. All remaining intrinsic muscles—that is, the 2 radial lumbricals, the abductor pollicis brevis, the opponens pollicis, and the superficial head of the flexor pollicis brevis—are thus innervated by the median nerve.[2]

Table. Muscles of the Forearm (Open Table in a new window)

Muscles of anterior fascial compartment

Name of Muscle Nerve Supply

Pronator teres Median nerve

Flexor carpi radialis Median nerve

Palmaris longus Median nerve

Flexor carpi ulnaris Ulnar nerve

Flexor digitorum superficialis Median nerve

Flexor pollicis longus Anterior interosseous

branch of median nerve

Flexor digitorum profundus Ulnar and median nerves

Median nerve supplies index and middle fingers in 75% of patients. Ulnar nerve supplies middle, ring, and little fingers in 75% of patients (therefore, the middle finger has dual innervation in 75% of patients)

Pronator quadratus Anterior interosseous branch of median nerve

Muscles of lateral fascial compartment

Brachioradialis Radial nerve

Extensor carpi radialis longus Radial nerve

Muscles of posterior fascial compartment

Extensor carpi radialis brevis Deep branch of radial nerve

Extensor digitorum Deep branch of radial Nerve

Extensor digiti minimi Deep branch of radial Nerve

Extensor carpi ulnaris Deep branch of radial Nerve

Anconeus Radial nerve

Supinator Deep branch of radial Nerve

Abductor pollicis longus Deep branch of radial Nerve

Extensor pollicis brevis Deep branch of radial Nerve

Extensor pollicis longus Deep branch of radial Nerve

Extensor indicis Deep branch of radial Nerve

Muscles of the hand lumbricals

Two radial lumbricals Median nerve

Two ulnar lumbricals Ulnar nerve

Interossei Ulnar nerve

Abductor pollicis brevis Median nerve

Flexor pollicis brevis Median nerve

Opponens pollicis Median nerve

Adductor pollicis Ulnar nerve

Abductor digiti minimi Ulnar nerve

Flexor digiti minimi Ulnar nerve

Opponens digiti minimi Ulnar nerve

Median nerve injury

Median nerve injuries are commonly referred to as high (ie, at or above the elbow) or low (ie, distal to mid forearm). While a high injury affects both intrinsic and intrinsic motor function, a low injury affects only intrinsic motor function.

A high median nerve division paralyzes the extrinsic muscles: pronator teres, flexor carpi radialis, palmaris longus, flexor digitorum superficialis (FDS), flexor pollicis longus, radial half of the FDP, and pronator quadratus. As a result, the forearm tends to rest in supination with the wrist in ulnar deviation. The median-innervated intrinsic muscles are also paralyzed. The lumbricals to the index and long fingers are paralyzed. Therefore, only weak flexion of the MCP joints is possible with the ulnar-innervated interosseous muscles.[3, 4, 5]

The IP joints of the thumb and the index and middle fingers cannot flex as a result of paralysis of the FDP and FDS motor units. If the ulnar nerve supplies the FDP to the ring finger, the ring finger IP joints can then flex. The ulnar nerve supplies the FDP motor units to the ring and little fingers, so the fourth and fifth fingers can flex. The abductor pollicis brevis, and opponens pollicis muscles are paralyzed. The thumb rests in the plane of the palm and cannot be positioned for a pulp-to-pulp pinch between the thumb and fingers. The thumb IP joint is extended due to paralysis of the flexor pollicis longus.

Median nerve injury at the wrist preserves extrinsic muscle function. The pronator teres, FDS, FDP, and flexor pollicis longus motor units are intact. The first 2 lumbricals, the abductor pollicis brevis, and the opponens pollicis are paralyzed. When the patient slowly makes a fist, the index and middle fingers clearly lag behind the fourth and fifth fingers because of a lack of initiation of flexion at the MCP joints by the lumbricals. The thumb rests in the plane of the palm and cannot oppose the fingers (see image below). The patient can flex the thumb terminal phalanx because the flexor pollicis longus is not paralyzed.

The intrinsic muscles innervated by the median nerve (abductor pollicis brevis and opponens pollicis) are checked by resisting palmar abduction of the thumb.Ulnar nerve injury

Ulnar nerve lacerations are commonly referred to as high or low to reflect whether the injury affects extrinsic and intrinsic muscles.[4, 6, 7, 8]

High ulnar nerve injury results in paralysis of the flexor carpi ulnaris and the ulnar half of the flexor FDP muscles, generally FDP III-V. The distal phalanges of the fourth and fifth fingers cannot flex. Because the FDP motor units have a common origin, some weak flexion of the fourth and fifth fingers may be possible, even if the ulnar half is supplied by the ulnar nerve. An attempt to flex the wrist results in radial deviation due to paralysis of the flexor carpi ulnaris.

All 7 interosseous muscles, the third and fourth lumbrical muscles, the adductor pollicis muscle, generally also one head of FPB, and all 3 hypothenar muscles (flexor digiti minimi brevis, abductor digiti minimi, and opponens digiti minimi) are paralyzed. The patient cannot adduct or abduct

the fingers. If the examiner places a piece of paper between the patient's fingers he or she cannot hold it when the examiner pulls the paper away.

The MCP joints are hyperextended, and the IP joints are flexed. These changes are more obvious at the ring and little fingers, because the first and second lumbrical muscles are not paralyzed. This condition is called a claw-hand deformity. The thumb can weakly adduct through the extensor pollicis longus. The patient can pinch and hold a paper between the thumb and index finger by strongly flexing the IP joint with the flexor pollicis longus. The combination of strong IP and weak MCP flexion called the Froment sign.

Ulnar nerve injury at the wrist spares the flexor carpi ulnaris and the medial half of the FDP muscles. The patient can flex the wrist and all the distal IP (DIP) joints. However, all intrinsic muscles innervated by the ulnar nerve are paralyzed, and both the clawhand deformity and the Froment sign are prominent (see image below).

Image in a patient with ulnar neuropathy demonstrates the Froment sign during pinching. Loss of the ulnar-innervated adductor pollicis results in reliance on the flexor pollicis longus and exaggerated interphalangeal (IP) joint flexion. Loss of the metacarpophalangeal (MCP) joint flexor leads to MCP hyperextension over time.

Epidemiology

Frequency

Open or closed trauma is the most frequent cause of intrinsic hand deformities. Although sensory loss contributes to the overall impairment, it does not contribute to the deformity. Ulnar nerve compression can occur at the elbow (the cubital tunnel) or at the wrist (in the Guyon canal). Median nerve compression associated with intrinsic loss can occur with pronator syndrome or carpal tunnel syndrome. Anterior interosseous nerve compression does not result in intrinsic loss because this nerve innervates only the extrinsic motor units.

One third of all patients with rheumatoid disease develop some degree of intrinsic contracture during the course of their disease. Peripheral nerve

palsy, most commonly afflicting the ulnar nerve at the elbow, occurs in 20-25% of patients with leprosy. Claw hand due to ulnar nerve paresis is therefore the most common presentation in this group of patients.

EtiologyIntrinsic muscle contracture can be caused by trauma,[9] inflammation, tumor, central nervous system disease, joint destruction, leprosy (Hansen disease), compartment syndrome, or rheumatoid disease.

PathophysiologyFixed contractures of the intrinsic muscles may severely impair the function of the hand. A mild contracture may inhibit certain hand functions without any gross deformity. The patient may complain of a weak grip when using, for example, a screwdriver or a hammer. Severe contractures cause MCP joint flexion and IP joint extension, resulting in an intrinsic-plus deformity. The patient experiences difficulty in grasping, pinching, and abducting the fingers. In combination with sensory loss, the hand is severely disabled.

Individual involvement of intrinsic muscles results in characteristic deformities. Lumbrical contracture causes finger extension while the patient is trying to flex the finger. The origin of the lumbrical is pulled proximally with extrinsic flexion, and the IP joints are extended.

Contraction of the abductor digiti minimi presents as small-finger abduction and causes MCP joint flexion and IP joint extension. Thenar intrinsic muscle contracture can cause thumb adduction, MCP joint flexion, and IP joint hyperextension. The patient loses effective pinch, large-volume grip, and hand dexterity.

Presentation

History

The patient may present with a history of trauma, inflammation, tumor, leprosy disease, compartment syndrome, or rheumatoid disease.

Physical examination

The first dorsal interosseous muscle is tested by having the patient place the ulnar side of the hand on the examination table. The radial side of the index finger is facing up. The patient is asked to raise the index finger toward the ceiling. The examiner applies resistance and observes the patient's strength. Muscle strength testing is likely to be more sensitive if

the right and left sides are tested simultaneously rather than one after the other.[10]

The second, third, and fourth dorsal interosseous muscles are tested by having the patient place the palm on the examination table. The patient spreads all of the fingers against resistance (see image below). The volar interosseous muscles are examined by placing a piece of paper between the digits and by having the patient hold his or her fingers tightly together as the examiner tries to withdraw the paper. The test is repeated between each of the adjacent fingers.

The ulnar-innervated intrinsic muscles can be checked by resisting abduction of the index (first dorsal interosseous muscle) and small fingers (abductor digiti quinti muscle).Adhesions and contractures of the intrinsic and extrinsic extensor muscles can limit flexion of the digits. The intrinsic tightness test can be used to differentiate extrinsic pathology from intrinsic pathology. During a test for intrinsic tightness, the examiner usually attempts to fully flex the proximal interphalangeal (PIP) joint of an examined finger while the MCP joint is kept in full extension and flexion, respectively. In the case of intrinsic tightness, (passive) flexion of the IP joint is more restricted when the MCP joint is in extension than when the MCP joint is in flexion (see image below).

The gloved examiner checks for intrinsic tightness. With the metacarpophalangeal (MCP) joint hyperextended, the proximal interphalangeal (PIP) joint is passively flexed. The intrinsic muscles are volar to the axis of rotation of the MCP joint and dorsal to the axis of the PIP joint. MCP joint hyperextension tightens the intrinsics. Results of this test are compared with those in the contralateral, normal hand. Note intrinsic atrophy in the first dorsal web space.If the intrinsic muscles are scarred, passive MCP joint extension increases PIP joint extension and makes passive PIP joint flexion more difficult (see images below).

Image in a patient with a partial ulnar nerve paralysis is asked to extend the digits. Hyperextension of the metacarpophalangeal (MCP) joints of the ring and small fingers occurs with the loss of intrinsic ulnar-innervated MCP flexors. The index and middle fingers have median innervated intrinsics (lumbricals) that allow the extrinsics to extend the interphalangeal (IP) joints.

When the examiner prevents metacarpophalangeal hyperextension of the ring and fifth fingers, the patient can completely extend the interphalangeal joints with the extrinsic tendons.The abductor pollicis brevis is tested as the patient pushes against resistance while the thumb is in the abducted position. The opponens pollicis is similarly tested with the thumb more circumducted. The adductor pollicis is evaluated as the patient pinches a piece of paper between the thumb and index finger while the examiner pulls on the paper. The flexor pollicis brevis is assessed with the thumb MCP joint in flexion and with resistance applied volarly.

The abductor digiti minimi is tested by having the patient place the back of the hand on the examining table while the little finger is abducted against resistance. The flexor digiti quinti is examined by flexing the MCP joint while the finger is adducted. The IP joints must be kept in extension. To test the opponens digiti minimi, the patient performs a pulp-to-pulp pinch by moving the little finger to the thumb.

Intrinsic tightness can result in a swan-neck deformity, which is characterized by PIP joint hyperextension and DIP joint flexion. The tight intrinsic muscles pull the PIP joints into extension, which allows passive DIP joint flexion. Over time, the PIP joint volar plate stretches as the extensor mechanism pulls the proximal phalanx into hyperextension. As PIP joint hyperextension increases, DIP joint flexion increases.

Intrinsic contracture disturbs fine hand-muscle balance. The fingers become stiff, function deteriorates, and the hand becomes disabled.

Boutonniere deformity

The boutonniere deformity involves PIP joint flexion and hyperextension of DIP and MP joints. Attenuation of the central slip with separation from the transverse retinacular ligaments cause migration of the lateral bands volar to the PIP joint rotational axis. Thus the lateral bands act as flexors of the PIP joint. As a result, the FDS meets less resistance and flexes the PIP joint. Contraction of the lateral bands and oblique retinacular ligaments prevents extension of the PIP joint. The lateral bands extend the DIP joint. The MCP joint hyperextends as the sagittal band applies traction on the extensor tendon.[11, 12, 13]

Physical examination involves evaluation of the range of motion, both active and passive, of both DIP and PIP joints. The examiner tries to passively flex the DIP joint while passively extending the PIP joint. In the presence of boutonniere deformity, both lateral bands and oblique retinacular ligaments are contracted and the DIP joint will not flex. The examiner flexes the PIP joint, and the DIP joint can then actively and passively flex because both the lateral bands and the oblique retinacular ligaments are now relaxed.

IndicationsIntrinsic and extrinsic tightness may coexist in the same patient. Intrinsic contracture may not be clinically apparent until associated extrinsic changes are corrected.

In cases of extrinsic tightness, PIP joint flexion increases when the MCP joint is extended and decreases when the MCP joint is flexed.

What to Expect at Your Office Visit

Your doctor or nurse will examine you, and closely look at your hands

and feet. You will be asked questions about your medical history and

symptoms.

The following tests may be done to check for nerve damage:

Electromyography (EMG)

Nerve conduction studies

TREATMENT

Treatment depends on the cause. It may include:

Splinting

Surgery to fix problems that may be contributing to the claw hand,

such as nerve problems, tendon abnormalities, or scar tissue

Therapy to straighten the fingers

http://www.nlm.nih.gov/medlineplus/ency/article/003169.htmhttp://emedicine.medscape.com/article/1243669-overview#a0104