Nerve Injury Positions of the Hand and Fingers

Written by Alec Bryson with Dr. Nabil Ebraheim

The presentation of a patient’s hand may provide insight to which nerve is damaged and the approximate location of the damage. When presenting with ulnar n. damage, a patient may show a claw hand, Wartenberg’s sign, or Froment’s sign. Claw hand will present with clawing of the fourth and fifth digits due to the inability to extend the fingers specifically at the interphalangeal joints. This presentation is due to the lack of innervation to the intrinsic muscles of the hands, and the unopposed action of the flexor digitorum profundus m. (Moore et al., 2018). This indicates damage near the distal end of the ulnar n., below the elbow, and potentially near the wrist. Wartenberg’s sign will be seen as the inability to adduct the fifth digit when extended as well as an inability to cross the second and third digit. This is due to ulnar n. injury leading to wasting of the fifth interosseous m. This causes the fifth digit to rest in a more abducted position due to the unbalanced action of the extensor digiti minimi m. (Ebraheim, 2021). There will also be loss of function of the lumbrical m. in the fourth and fifth digits. A Froment’s test will detect palsy of the ulnar n. resulting from compression in the cubital tunnel. When asking the patient to pinch a piece of paper between their thumb and second digit, a positive Froment’s Sign will show as the patient flexing their thumb’s interphalangeal joint to grip the paper as the paper is pulled away (Attum, 2021). This will result from a weak adductor pollicis m. due to ulnar n. palsy.

Depending on the location of a lesion to the median n., the patient will present with one of three signs. A positive Benedictine sign will be caused by proximal median n. damage. It will be seen as paralysis of the first and second digit, with weakness to the third digit. A proximal lesion would lead to paralysis of several muscles (FDS, FPL, FPB, and the radial half of FDP), leaving the ulnar half of the flexor digitorum profundus m. as the only remaining flexor (Ebraheim, 2021). When the patient is asked to make a fist, the hand will resemble the similar position taken during a blessing. A positive Benedict sign will also resemble the ulnar claw hand. However, the Benedict sign will present when the patient is flexing, not extending the fingers (Ebraheim, 2021). A median n. injury affecting the anterior interosseous n. branch will present as an inability to do the OK sign. This occurs due to paralysis of the flexor pollicus longus m. and the lateral part of the flexor digitorum m. (Moore et al., 2018). A positive Ape hand (Simian hand) is caused by paralysis of only the thenar m. from damage to the recurrent branch of the median n. to the thenar m. The thumb will be seen in the same plane as the other digits due the thumb being pulled more dorsal by the action of the adductor pollicis m., which is innervated by the ulnar n. (Moore et al., 2018).

Finally, proximal radial n. damage will be seen as wrist drop. This is usually caused by fractures of the distal third of the humeral shaft (Holstein-Lewis Fracture) and caused paralysis of the wrist and fingers extensors (Ebraheim, 2010). Lower radial n. injury will present in the patient as the ability to extend the wrist, but the loss of finger extension. There will be no wrist drop, but the patient would not be able to make a hitchhiking sign.

Reference List

Attum B. Physical exam of the hand [Internet]. Orthobullets. Lineage Medical, Inc.; 2021 [cited 2021Oct21]. Available from:

Ebraheim N. Anterior Interosseous Nerve Injury – Everything You Need To Know – Dr. Nabil Ebraheim [Internet]. YouTube. 2021 [cited 2021Oct21]. Available from:

Ebraheim N. Claw Hand, Ulnar Claw Hand – Everything You Need To Know – Dr. Nabil Ebraheim [Internet]. YouTube. 2017 [cited 2021Oct21]. Available from:

Ebraheim N. Nerve Injury Position of the Hand & Fingers – Everything You Need To Know – Dr. Nabil Ebraheim [Internet]. YouTube. 2021 [cited 2021Oct21]. Available from:

Ebraheim N. Radial Nerve Palsy, injury – WRIST DROP . Everything You Need To Know – Dr. Nabil Ebraheim [Internet]. YouTube. 2010 [cited 2021Oct21]. Available from:

Moore KL, Dalley AF, Agur A. Clinically Oriented Anatomy. 8th ed. Philadelphia, PA: Lippincott Williams and Wilkins; 2018.

Cubital Fossa

Cubital Fossa

Cubital FossaThis is about understanding the arrangement of the structures in the anterior elbow. This is an anatomy video, but this can also help surgeons in knowing how to approach the insertion of the distal biceps for repair or how to approach the proximal radius fracture anteriorly. If you look at the bony structures of the anterior elbow, you need to find out where the common flexor tendon origin is, where the brachialis muscle is inserted, and where the biceps is, supinator and the pronator teres located. These structures are definitely part of the anterior elbow. The cubital fossa is a triangular depression located in front of the anterior elbow. The medial border is formed by the pronator teres, which arises from the medial epicondyle of the humerus. The lateral border of the cubital fossa is formed by the brachioradialis muscle which arises from the lateral supracondylar ridge of the humerus. The meeting of these two muscles forms the apex of the cubital fossa. The brachioradialis muscle overlaps the pronator teres, so the lateral border overlaps the medial border. The base of the cubital fossa is superior and is represented by a horizontal line connecting the two epicondyles of the humerus, the lateral and medial epicondyles.

Structures Located In and Around The Cubital Fossa

The base of the cubital fossa is seen as an imaginary line drawn between the medial epicondyle and the lateral epicondyle of the distal humerus. The pronator teres is the medial border, and the brachioradialis muscle forms the lateral border. The contents of the cubital fossa from medial to lateral are median nerve, brachial artery, biceps tendon, and radial nerve. The floor of the cubital fossa is made up of the lower part of the brachialis muscle medially and the supinator muscle laterally. The roof of the cubital fossa is made up of skin, fascia, and the bicipital aponeurosis. CFS

The median nerve disappears by entering the forearm between the two heads of the pronator teres muscle. The brachial artery bifurcates into the ulnar artery and the radial artery. The brachial artery is over the brachialis muscle. The ulnar artery leaves the fossa by going under the deep head of the pronator teres muscle. The deep head of the pronator teres muscle separates the median nerve, which goes between two heads of the pronator teres muscle from the ulnar artery, which goes deep to the deep head of the pronator teres muscle. Another branch that is in the cubital fossa is the radial artery. The radial artery descends laterally and is overlapped by the brachioradialis muscle. The biceps tendon is lateral to the brachial artery within the cubital fossa. The biceps tendon has one main insertion laterally to the radial tuberosity and another insertion going medially to the bicipital aponeurosis. The bicipital aponeurosis covers and protects the vital structures medially to the biceps tendon (brachial artery and median nerve). The biceps tendon passes backwards (twisted) towards its insertion into the radial tuberosity. Lateral to the biceps tendon is the radial nerve and its major branch, the posterior interosseous nerve. Other important nerves in the vicinity of the cubital fossa include the superficial radial nerve which is below the brachioradialis and the lateral cutaneous nerve of the forearm which is a branch of the musculocutaneous nerve and lies below the biceps proximally and then finally lies laterally.


Concussion in Athletes

A concussion is a transient impairment of the brain function occurring due to a violent shake of the brain. A concussion is a function impairment, not a structural brain injury, therefore a CT scan will be normal. In the United States alone, sports injuries lead to 1.6-3.8 million concussions annually. In head to head collisions in football, a player’s head may experience G forces ranging from 100-190Gs. These forces and rapid deceleration speeds exerted on the brain are similar to being hit on the head with a sledge hammer. A sudden blow to the head leads to bouncing of the brain back and forth in the skull cavity. The shaking motion of the brain within the skull cavity may lead to a concussion.


Only 10% of concussions are associated with loss of consciousness (LOC). Therefore, LOC is not necessary to diagnose a concussion. Symptoms of concussions include: headache and dizziness (most common), confusion, imbalance LOC, vomiting, and convulsions or seizures. Other symptoms include:

  • Amnesia
  • Slurred speech
  • Feeling sluggish or foggy
  • Double/blurry vision
  • Light sensitivity
  • Sensitivity to noise
  • Decreased playing ability

When managing a concussion, one must first assess airway, breathing, and circulation. The cervical spine should also be assessed in case of an injury. Assessment of sensory and motor functions. Diagnosing a concussion depends on careful clinical examination and asking questions to assess the patient’s attention, memory, orientation, concentration, balance, and reaction time. When a concussion is diagnosed, the player must NOT return to play.

Concussion assessment tools such as the Standard Assessment of Concussion Test (SAC) or Immediate Post-Concussion Assessment and Cognitive Test (impact) may be used on the sidelines and at later follow-ups to assess the patient’s brain function and compare the pre-injury scores. It is worth noting that the SAC test does not include a neurologic exam and does NOT measure reaction time, coordination or balance. When concussion assessment tools are not available on the sidelines, the following questions can be used to quickly assess orientation, anterograde and retrograde amnesia, concentration, and the patient’s ability to recall word lists (adopted from the CDC with minor modifications):

  1. Concentration
    1. Ask the patient to repeat days of the week backwards
  2. Orientation
    1. What stadium are we in?
    2. Who scored last?
    3. What is the name of the opposing team?
  3. Retrograde Amnesia
    1. Do you remember the hit?
    2. What was the score prior to the hit?
  4. Anterograde Amnesia
    1. Choose any three words and ask the patient to repeat them
  5. Ability to recall word list
    1. Ask patient to recall the three words you asked earlier


It is worth noting that remote memory loss is more worrisome than recent memory loss. Patients who demonstrate any of the following signs and symptoms should be taken to the emergency room immediately: worsening headaches, repeated vomiting, seizures or convulsions, prolonged LOC, focal neurological sign, disorientation to time, place, and person, neck pain, increasing irritability and confusion, and upper or lower limb weakness or numbness. Red flags that may indicate the need to acquire head imaging such as CT scans include: A prolonged LOC, post-traumatic amnesia, persistently altered mental status, focal neurological deficits, and continued deterioration of clinical signs.

It is important to remember that the following are contraindications to return to play:

  • Symptoms lasting more than 15 minutes
  • Prior concussion within the same season
  • Loss of consciousness
  • Amnesia
  • Development of complications such as post-concussion syndrome
  • Recurrence of symptoms on exertion

Complications include conditions such as second impact syndrome. Second impact syndrome occurs after sustaining a second head impact, even if minor, before achieving recovery from the first concussion may be potentially fatal. The mortality rate associated with second impact syndrome is approximately 50%. It occurs due to loss of autoregulation of the brain’s blood supply leading to vascular engorgement and herniation of the lower brain. Treatment usually consists of close observation, intubation, hyperventilating the patient and administration of IV osmotic diuretics.

Post-concussion syndrome occurs when persistent symptoms such as headaches, dizziness, and confusion lasting for weeks or even months after a concussion. Treatment is symptomatic and the patient will return to play is contraindicated. Epidural bleeding is associated with a lucid interval during which the patient feels find, followed by sever neurological decline. Seizure prophylaxis and surgical decompression are usually indicated. Cumulative effects may occur whether or not repetitive concussions have a cumulative effect remains a controversial topic.

Even though players may be eager to return to the game quickly, they must be advised to follow a stepwise strategy in order to achieve complete recovery and avoid potentially life threatening complications. The recovery strategy should include the following steps: a period of complete physical and mental rest until the symptoms subside. This should be followed by a return to light aerobic activities. Sports-specific training (still no contact). The recovery strategy should include non-contact drills and full-contact drills.

MRSA Screening & Decolonization

The best way to prevent surgical site infection, is optimizing the patient prior to surgery. The physician will want to make sure that the patient is nutritionally fit. Specific protocols will need to be followed for patients with conditions such as diabetes, are overweight, or who smoke. It is also important to improve the skin and soft tissue condition (area where the incision will be). The physician should try to reduce the bacterial burden that the patient is carrying. Immediately before surgery, the patient should be given prophylactic preoperative antibiotics and try to decrease the contamination in the operating room. The patient may bring organisms on themselves into the operating room (about 80% of these organisms are brought in by the patient). A screening for Methicillin-Sensitive Staphylococcus Aureus (MSSA) or Methicillin Resistant Staphylococcus Aureus (MRSA) and decolonization. Identifying the patients carrying diseases and treating the condition prior to going into the hospital will reduce the infection rate. Once patients are in the hospital, it is possible for them to spread bacteria to other patients. The best way to prevent the spread of bacteria is with PROPER HAND WASHING PRACTICES!

How can we decrease the bacterial burden of the patient bringing these organisms to the operating room? What are the tests that we should do? How can we help the situation when the patient is in the clinic or in the office?

areasThe patient should be screened for MSSA or MRSA and then a decolonization should be done. Some patients have large reservoirs of bacteria (carriers) and these are the patients who will have an increased risk of surgical site infection. These reservoirs are located in the nose, axilla, groin, and perianal area. These patients will need to be identified so the bacteria can be eradicated and the risk of surgical site infection can decrease. Being a MRSA carrier will increase the chances of infection (about 10x more risk for surgical site infection). You wouldn’t know that the patient is a MRSA carrier unless you test them. It is important to identify these MRSA carriers so that proper antibiotics can be given. A MRSA “carrier” is an individual who can carry the bacteria without necessarily becoming ill. About 2% of the population are MRSA carriers.

MRSA is a contagious bacteria that is difficult to treat because it is resistant to most commonly used antibiotics. In the bacteria cell wall, there is a penicillin binding protein. When penicillin is able to bind to the binding protein of the cell wall, disruption of the cell wall and destruction of the bacteria is possible. However, if the staph aureus acquires the mecA gene, then it can alter the penicillin binding protein, making the bacteria resistant to all penicillin. The primary way of transmitting MRSA is through direct contact from another person, an object that has it, or from sneeze droplets of an infected person. 30% of staph bacteria lives in the nose. About 25-30% of the population is colonized with S. aureus.


This means that the bacteria is present; however, it is not causing an infection with S. aureus. Ironically, if you are a carrier, you are only 6 times as likely to receive an infection, while non-carriers are 10 times as likely. MRSA carriers are diagnosed by examining a swab or culture of the nose. The physician will want to identify these patients before bringing them to the hospital, and eradicate or decolonize the organisms by using a 2-4% chlorhexidine bath for 5 days. The patient should leave the chlorhexidine on the surface of the skin (it works better if kept on for a longer time), so it is better not to wash it off. A 2% nasal mupirocin for five days may also be used. By the screening and eradication program, you can drop the infection rate by about 40-60% or more depending on the compliance of the patient. Our institution showed that empiric treatment is less costly than S. aureus screening and decolonization in total joint arthroplasty patients. They find that the cost is much less than the cost of the standard screening and decolonization of the S. aureus. They found that the empiric treatment allows for more efficient workflow without compromising the patient.