New Hope for Nerve Injury Patients

Nerves are complicated structures, made of many axons (the actual connections or wires) some surrounded by a layer of myelin shealth (insulation), all bundled together with connective tissue into a giant cable.

Nerve injuries come in different varieties, depending on the mechanism and severity of the trauma:

The three categories of nerve injury Neurapraxia (top), Axonotomesis (middle) and Neurotmesis (bottom).

The mildest injury is neurapraxia, which is a short area of segmental demyelination.  Because the underlying axon is left intact, recovery can occur within days to week by simple remyelination.

The more severe injuries axonotomesis and neurotmesis involve axonal injury.  Once the axon is injured, the whole segment distal to the injury undergoes a pre-programmed process of degeneration called Wallerian degeneration:

Wallerian degeneration – the axon distal to (right of) the injury degenerates.

Even if the nerve injury is repaired, or gets better on it’s own, the axon has to grow back all the way from the injury site to the end of the nerve at the muscle before functional recovery can occur.

Even if a severed nerve is repaired (in this case by direct suturing), the axons have to regrow down the entire distal nerve segment before functional recovery can occur

Axonal regrowth is slow, occurring at a rate of no more than 1mm/d.

If we have a patient with a proximal nerve injury, for example a brachial plexus injury:

nevre injuryAxonal regrowth will have to occur over 600-800mm to restore function to the hand, and that will take more than 2 years, by which time the muscle may have deteriorated so much it can no longer receive a new nerve supply and recover.

However, new research in animals has led to a technique that reconnects the severed ends of a nerve, allowing it to begin carrying messages again very quickly, restoring conductivity before Wallerian degeneration has a chance to begin. This allows for almost immediate function recovery after nerve repair surgery.

In the experiments, the severed nerve are exposed and treated with chemical compounds to keep the axonal ends open, then the two nerve ends are sutured together, and are finally treated with more chemicals that cause the nerve ends to fuse.  Rats treated with his technique got better as soon as they began to recover from the surgery.

Researchers hopes to try the approach on people within a year.

Click here for a link to the full story.

Post-operative peripheral neuropathy


Post provided by Kevin Turezyn, Drexel University College of Medicine Class of 2013:


While the overall risks of undergoing a procedure involving general anesthesia have decreased dramatically over the last 25 years, there is one phenomenon that still puzzles both anesthesiologists and surgeons: post-operative peripheral neuropathies.

Why a patient undergoing an appendectomy would wake up with weakness in their arm is still in large part a mystery. Luckily most patients recover fully, but a small subset suffer from permanent damage.

While relatively infrequent, peripheral nerve injury after anesthesia is one of the largest sources of professional liability for anesthesiologists. Estimates of its frequency range from .03% to .11% of patients who undergo anesthesia.

Interestingly, despite numerous attempts to decrease its incidence, anesthesiologists have had little success.

While the exact cause is unknown, many believe that it relates to patient positioning. There are several points in the body where nerves run very close to the surface leaving them vulnerable to injury. For example, the most commonly injured nerve is the Ulnar nerve of the arm. When this nerve goes through the elbow, it is very close to the surface where it has little body tissue for protection. People commonly hit this nerve in daily life, giving them a painful sensation called hitting your “funny bone”. Other commonly injured nerves include the radial nerve (compression in the spiral groove against the humerus), brachial plexus from traction on the arm, sciatic nerve in the buttock and peroneal nerve against the fibula head.

The American Society of Anesthesiologists has published guidelines for prevention of perioperative peripheral neuropathies. The guidelines focus on pre-operative assessment for patients who are at higher risk ( diabetics, alcoholics, patients with peripheral vascular disease) as well as proper positioning of the extremities and adequate padding.

Click here for the full guidelines.


When peripheral nerve injury does occur, it frequently resolves on its own, although this can take take several months. During this time, there is little that can done to speed recovery. Physical therapy is often recommended to prevent muscle contractures and atrophy during this time period.

If a patient feels that they suffered a nerve injury during surgery, it is important that they be evaluated right away by a trained neurologist. Testing such as an electromyogram (EMG) can be done to determine the location of the injury and prognosis for recovery.

cts emg

Feeling sunburnt in winter? It could be small fiber neuropathy.



Nerves are composed of bundles of individual fibers (axons)


Nerve fibers (axons) come in a variety of shapes and sizes.  Some are wrapped in insulation (myelinated) others are bare (unmyelinated).

Human nerve

You can see from the figure (above) that small unmyelinated fibers make up the majority of human sensory nerves.  These small unmyelinated fibers convey pain and temperature sensitivity.


Small fiber neuropathy

Some diseases, particularly diabetes, preferentially affect these small unmyelinated fibers, leaving the other fibers relatively unaffected, resulting in small fiber neuropathy.

Symptoms of small fiber neuropathy are usually a mixture of numbness (sensory loss) and neuropathic pain.

The pain can be superficial and burning, deep aching, pins-and-needles, electrical shocks, or knife-like stabbing.  Innocuous contact (such as with clothing or bedclothes) can become painful like a sunburn.

Small fiber symptoms often worsen at night (when there are fewer distractions) and in the cold.

The symptoms usually begin in the feet, often first affecting the toes and/or soles.  As the condition worsens, the symptoms usually spread proximally up on to the legs and ultimately on to the hands, leading to a “glove and stocking” pattern.

Peripheral Neuropathy, Length Dependent

In most neuropathies, the ends of longest nerves are affected first (left), leading to a glove and stocking distribution of pain and numbness (right).


Autonomic dysfunction from small fiber neuropathy can cause burning redness in the feet (“erythromelagia”):



Also, loss of innervation to the sweat glands can cause decreased sweating peripherally (where the neuropathy is worse), and lead to increased sweating on the head and trunk:

sweat test

Sweat test showing decreased sweating in t extremities (yellow) and increased sweating on the head and trunk (purple).


A Diagnostic Challenge!

It is the large myelinated fibers which sub-serve strength and deep tendon reflexes.  Furthermore, it it these same large myelinated fibers which are tested during a conventional nerve conduction study.

So the physical signs and electrophysiologic findings we typically rely on to diagnose neuropathy may be absent in small fiber neuropathy.

The most widely available diagnostic test is the punch skin biopsy to quantify epidermal innervation.

skin biopsy neuropathy

Skin biopsies, showing normal epidermal innervation (left) and epidermal denervation in small fiber neuropathy (right).


Managing Small Fiber Neuropathy

So, you know you have sunburn from small fiber neuropathy, now what?

The most important first step is to look for an underlying (treatable) cause, particularly occult diabetes, with blood work that includes a glucose tolerance test.  In the case of diabetes, monitoring and controlling the blood glucose, is the most important next step.

Otherwise, treatment is usually limited to symptomatic measures, using drugs like gabapentin, pregabalin and/or duloxetine.

Why the Brachial Plexus is like the London Underground

The brachial plexus is an interchange of nerve fibers that connects the cervical spinal cord to the major nerves in the arm.

This is analogous to the fuse box in your house, distributing electricity from the main electric cable to all of your individual appliances/outlets):

fuse box

Or a highway interchange which can route cars off an interstate to multiple local roads:



Brachial plexus injuries can be caused by trauma to the shoulder in accidents or during passage through the birth canal, and result in pain, numbness, weakness and muscle wasting in the affected arm.



This is a real human brachial plexus:

real anatomy plexus


However, in clinical practice, we are usually dealing with closed (traction) injuries to the plexus, so we are not too concerned about actual anatomy.

We are more interested in figuring out where the lesion lies within the plexus based on the patient’s clinical deficit.

We are therefore more likely to use diagrams of the plexus which distort anatomy, but emphasize branches and intersections, to localize these lesions:

post cord

For example, a patient with weakness of deltoid (axillary nerve) and triceps (radial nerve) but not biceps (musculocutaneous nerve) must have a lesion in the posterior cord (green in the figure above).


The iconic London Underground map, first designed by Harry Beck in 1931, is based on a similar principle.

Earlier maps were geographically correct, but as more lines and stations were added these maps became more cumbersome and confusing.

geographical underground map1

Beck realized that because the railways were underground, the physical locations of the stations were irrelevant to the traveller wanting to know how to get to one station from another, so he devised a simplified map showing only stations, straight line segments connecting them, and the river.  All lines ran only vertically, horizontally, or on 45 degree diagonals, ignoring the actual geography:


You can easily use this kind of map to find the best way to get from Park Royal to Oxford Circus, with the least number of stops and line changes.


Do you see the similarity?



Other examples of medical uses of Beck’s London Underground map:



Sciatic Neuropathy

The terms lumbar radiculopathy and sciatica are used interchangeably to indicate radiating pain, numbness and weakness in a leg from a pinched nerve root in the back.

However, it is important to recognize that similar symptoms and signs can be caused by injury or compression of the sciatic nerve outside the spine, either in the buttock or thigh.

The sciatic nerve is the longest and widest nerve in the body, extending from the spine all the way to the foot, and contributes most of the nerve supply to the leg:

Sciatic nerve injury presents with:

1. Numbness affecting the entire leg, aside from the front of the thigh.

2. Weakness of the hamstrings, and all movement at the ankle.

3. Absent ankle jerk.

Sciatic Nerve Injury in the Buttock:

The nerve can be injured by misplaced buttock injections, gunshot wounds and knife injury. Buttock injections should be given in the upper outer quadrant to avoid the sciatic nerve

Buttock injections should be given in the upper outer quadrant to avoid the sciatic nerve

The sciatic nerve injury can also be injured by prolonged sitting on a toilet seat, either from direct nerve compression or hemorrhage and compartment syndrome into the gluteal muscles.  This has been reported in cases of  severe prolonged diarrhea, or drug induced coma on the toilet, so called toilet seat neuropathy.


Sciatic Nerve Injury at the Hip:

The sciatic nerve runs behind the hip joint as it travels through the buttock.
The sciatic nerve is frequently injured by a posterior dislocation of the hip:

Sciatic nerve injury occurs in as many as 1%–3% of patients who undergo total hip replacement surgery, usually from a stretch injury to the nerves, but occasionally from a misplaced crew, broken piece of wire, fragment of bone or cement pressing on the nerve:

Sciatic nerve injury after hip arthroplasty. (a) The skin incision for the transgluteal approach is in a continuous line. The cross on the left shows the ischium and the one on the right shows the trochanter. Between them, the skin projection of the sciatic nerve is seen. (b) The sciatic nerve was freed from all attachments. The arrows identify acrylic material from the hip arthroplasty, which was damaging the nerve

Sciatic nerve injury after hip arthroplasty. (a) The skin incision for the transgluteal approach is in a continuous line. The cross on the left shows the ischium and the one on the right shows the trochanter. Between them, the skin projection of the sciatic nerve is seen. (b) The sciatic nerve was freed from all attachments. The arrows identify acrylic material from the hip arthroplasty, which was damaging the nerve

Piriformis Syndrome:

However, symptoms of sciatic neuropathy most often result from nerve compression by the piriformis muscle at the level of the sciatic notch, so-called piriformis syndrome.


This presents with buttock tenderness and pain, radiate down the posterior thigh.  Symptoms are made worse by prolonged sitting, bending at the waist, and activities involving hip adduction and internal rotation.  The pain can be reproduced by deep palpation over the sciatic notch.

Diagnostic modalities such as CT, MRI, ultrasound, and EMG may all be normal in piriformis syndrome, but are still useful for excluding other conditions.

Magnetic resonance neurography is a specialized imaging technique which can confirm the presence of sciatic nerve irritation or injury of the sciatic nerve in the piriformis muscle.

Magnetic resonance neurography findings in piriformis syndrome. A: Axial T1-weighted image of piriformis muscle size asymmetry (arrows indicate piriformis muscles). The left muscle is enlarged. B and C: Coronal and axial images of the pelvis (arrows indicate sciatic nerves). The left nerve exhibited hyperintensity. D: Curved reformatted neurography image demonstrating left sciatic nerve hyperintensity and loss of fascicular detail at the sciatic notch (arrows). Filler AG, Haynes J, Jordan SE, et al, "Sciatica of nondisc origin and piriformis syndrome: Diagnosis by magnetic resonance neurography and interventional magnetic resonance imaging with outcome study of resulting treatment," J Neurosurg Spine 2: 99-

MRN findings in piriformis syndrome. A: Axial T1-weighted image of piriformis muscle size asymmetry (arrows indicate piriformis muscles). The left muscle is enlarged. B and C: Coronal and axial images of the pelvis (arrows indicate sciatic nerves). The left nerve exhibited hyperintensity. D: Curved reformatted neurography image demonstrating left sciatic nerve hyperintensity and loss of fascicular detail at the sciatic notch (arrows).

Conservative treatment can include medications, physical therapy and stretching, or injection of a paralysing agent such as botulinum toxin into the piriformis muscle under ultrasound or CT control. Surgery may be necessary for recalcitrant cases.

Phantom Limb Pain

This post is provided by Ilya Shnaydman, Drexel University College of Medicine Class of 2013:

Phantom Limb is the sensation that an amputated limb is still attached to the body. It may occur after removal of other organs such as breast, eye, teeth, etc. It can even occur after a hysterectomy, where patients may suffer “phantom menstrual cramps.”  Approximately half of patients with phantom limb feel that they can move the missing body part, and the other half feel that the phantom limb is there, but “paralyzed” and frozen in space. These patients feel that if they could only relax the body part they would feel a great deal of relief. This is especially common if the body part is in a contracted, or fixed state prior to the amputation.

In the case of a paralyzed leg for example, the patient’s brain is sending signals telling the (paralyzed) limb to move, but since the leg can not move, the patient does not get the visual feedback of a moving limb. This leads to a “learned” pattern of paralysis. After an amputation, often this learned paralysis can remain with the patient feeling a clenched spasm of the missing extremity. The limb often feels as if it is burning, aching, in a painful position, or having electric-type pain. Phantom Limb Pain can occur anywhere from just after the amputation to even years later.

Our brains are hardwired from birth with sensations reaching the brain through predefined pathways. When you touch an object with your finger, those sensations reach the brain through complex pathways ending in a specialized area of the brain responsible for perceiving sensation. If that finger tip was amputated, and the remaining finger were to touch an object, the brain may perceive it as being the fingertip due to the similarity in the sensory pathways.

There are several theories for why phantom limb pain occurs. One theory is that the pain is caused by irritation of the severed nerve endings. The nerve endings can form a neuroma, or an abnormal growth of nerves. Some believe that the brain perceives these ‘nonsense’ stimulations as pain. This theory led to many patients undergoing revisional surgeries hoping to remove the inflamed nerve endings. Unfortunately in most cases it rarely helped.

Research at the National Institutes for Health (NIH) showed that the area of the brain responsible for interpreting sensation (primary somatosensory cortex) underwent reorganization after the loss of sensory input, as occurs after an amputation.  Phantom Limb Pain results when a conflict between signals received from the limb and a lack of visual input from the missing limb.

Stump Pain can result from other causes such as ischemia (lack of blood flow to the stump), infection, or pressure points over bony spurs. Phantom limb can only be diagnosed if all other causes of stump pain are ruled out.

The incidence of phantom limb pain varies from 50-85% depending on the diagnostic criteria used to define the syndrome. A minority of patients have such severe pain that it interferes with work, sleep and daily social life. The pain can be worsened by stress, anxiety and even weather changes. Phantom limb pain can be quite severe, leading to depression and even suicide.


As with other forms of neuropathic pain, the treatment of Phantom Limb Pain has included pain medication, antidepressants, anticonvulsants, spinal cord stimulation, vibration therapy, acupuncture, hypnosis and biofeedback under the guidance of an experienced neurologist.

Biofeedback helps teach amputees with burning/tingling pain to unconsciously keep their phantom limb as warm as the intact limb. For cramping pain, the goal is to teach patients to prevent the onset of muscle tension leading to pain. Patients are hooked up to a biofeedback machine which consists of electrodes places on the body. The patient is then shown the relationship between temperature or muscular activity and the onset of phantom pain. Once they are convinced of this relationship, they undergo various exercises to increase their temperature/muscle tension awareness. After some time patients are able to sense these changes and control them effectively.

Some studies have shown that calcitonin (a hormone naturally occurring in the body that regulated calcium metabolism) and ketamine (an anesthetic drug) are effective in treating Phantom Limb Pain. If all other methods have failed, surgical intervention may be indicated.

Mirror Box Therapy

A novel way of relieving the clenched pain that patients with phantom limb face was created by  Vilayanur S. Ramachandran. He proposed placing a mirror between the patient’s two limbs, tricking the eyes into seeing that the amputated limb is actually still there.

The ‘phantom limb’ is placed behind the mirror, and the normal limb on the other side. The patient then makes the same clenched position with their normal limb. This brings the visual impression that the phantom limb is still there. By relaxing their normal limb, patients can trick their brain into relieving the pain of the phantom limb. This shows how the theory of  ‘learned paralysis’ applies to phantom limb and how it can be overcome with a simple visual aid.

If you have any questions about this condition, please comment below!

Do you have a pinched nerve?

Radiculopathy (often referred to as a “pinched nerve” in the neck or back) is usually caused by compression of a nerve root as it exits the spine either by a herniated disc or arthritic changes.

Disc herniation copy

Compression of the affected nerve root results in pain (radicular pain), weakness, numbness, and/or loss of deep tendon reflexes.

In cervical radiculopathy (“pinched nerve in the neck”), the radicular pain is referred from the the neck down the arm on the affected side:


The pain and numbness are usually felt most strongly in the area of the arm innervated by the affected nerve root (dermatome). For example, pain from a herniated C67 disc compressing the C7 nerve root will radiate down the arm into the back of the hand and middle finger:

UE derm

In lumbar radiculopathy (“pinched nerve in the back”), the radicular pain will usually radiate from the low back or buttock down the leg (“sciatica”):


A herniated L5S1 disc will usually compress the S1 nerve root, the sciatica will radiate down the back of the leg into the little toe, and the ankle jerk will be absent:

LE derm

In most cases, the diagnosis of radiculopathy, as well as the spinal level involved, can be deduced from a careful review the history and examination findings.

An electrodiagnostic study (electromyogram, or EMG) can be useful for confirming the diagnosis of radiculopathy and quantifying the degree of nerve damage in selected cases.

Spinal imaging studies, including plain X-rays, computed tomography (CT) or magnetic resonance (MR) imaging studies are usually needed to identify the cause of the radiculopathy, such as herniated disc, osteoarthritis, tumor or infection.

Disc herniationMRI copy

Most cases of radiculopathy are treated conservatively with pain medicines, activity modification and physical therapy, and ultimately recover spontaneously.

The SPORT study found that while lumbar radiculopathy patients treated surgically with discectomy improved more rapidly that those treated conservatively, both groups improved to about the same degree by 2 years.

Epidural steroid injections are frequently advocated as a treatment modality for recalcitrant cases, despite a paucity of well-designed trials of their efficacy. In fact a recent randomized controlled study published in Evidence Based Medicine showed no benefit of epidural steroids over saline or sham injections, click here for more details.

Surgery is usually reserved for patients with intractable pain despite an adequate trail of conservative measures, or those with severe and progressive motor deficits or cauda equina syndrome (with bowel and bladder dysfunction).

Surgical interventions can include a simple discectomy, discectomy with fusion, percutaneous discectomy, or microdiscectomy.