Post-herpetic neuralgia

Post-herpetic neuralgia (PHN) is defined as a chronic neuropathic pain that persists for three or more months following acute Herpes zoster (shingles) infection. It is a severe painful secondary phase, which may develop three to six months after the resolution of initial phase of Herpes zoster (HZ) infection. Pain has a dermatomal distribution and is confined to same dermatome as the rash. Herpes zoster infection results from activation of the varicella zoster virus (VZV) which remains latent in dorsal root ganglia since the first infection of chickenpox (varicella). Pain frequently precedes Herpes zoster infection (pre-herpetic neuralgia), and outlasts the herpetic rash by some weeks. It is more common in older individuals (develops in up to 75% of patients over 70 years of age) and is less common in individuals younger than fifty years of age.

Post-herpetic neuralgia subsides eventually on its own. However, it may make patients suffer for years and may leave a band of anaesthetic skin. It may lead to muscle weakness as well, if it affects major motor nerve.

Post-herpetic neuralgia is associated with persistent and, very often, refractory neuropathic pain. The neuralgia is excruciating with superimposed lancinating paresthesias. Pain may be constant or intermittent, aggravated by minor stimulus (allodynia) such as heat or touch, and is worse at night. The agony of pain leads to insomnia, anorexia, and changes in mood (severe depression).

Post-herpetic neuralgia may produce multiple types of pain in patient e.g.

  • Constant aching, deep, or burning pain
  • Paroxysmal lancinating pain
  • Hyperalgesia (increased sensitivity to pain)
  • Allodynia (pain associated with non-painful stimuli)


Post-herpetic neuralgia is a psychosocial condition with a significant impact on the psychological, social, and physical functioning of an individual.



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The crusts of Herpes zoster falls away on healing, and leave pink scars in the distribution of rashes. The scars gradually become hypo-pigmented and atrophic.

Symptoms of PHN are

  • Pain: Post-herpetic neuralgia may produce multiple types of pain in patients such as

1.     Constant aching, deep, or burning pain

2.     Paroxysmal lancinating pain

3.     Hyperalgesia (increased sensitivity to pain)

4.     Allodynia (pain associated with non-painful stimuli)

  • Sensory abnormalities in scarred skin: These may take the form of

1.     Hypo-aesthesia: There is hypo-aesthesia or decreased sensations in the scarred region in patients with PHN. Greater the degree of hypo-aesthesia, longer is the time nerve block treatment needs to be given.

2.     Allodynia and hyperaesthesia: Allodynia and hyper-aesthesia, are frequently noted in the scarred skin.

Chronic PHN is commonly shows psychiatric co-morbidity such as low mood and tendency to social isolation.

In most of the patients, pain and sensory abnormalities resolve as the skin lesions heal over time. In some, pain may persist in spite of healing.

Risk factors for developing PHN are

  • Old age
  • Severity of acute pain of HZ
  • Greater rash severity
  • Painful prodrome preceding acute symptoms
  • Sensory dysfunction in dermatome during HZ
  • Trigeminal distribution of infection
  • Fever
  • Psychosocial stress

PHN is a painful condition, which develops following acute Herpes zoster infection. Pain frequently precedes Herpes zoster (pre-herpetic neuralgia) and usually outlasts the rash of HZ by some weeks.

Acute Herpes zoster infection or shingles results from activation of the varicella zoster virus (VZV) infection, which is latent in the dorsal root ganglia since the initial infection (varicella). The virus replicates in the ganglionic neurones, and infects other neighbouring cells and then transmitted down the axon of nerve to infect the skin where it results in blister formation. To a limited extent, virus also travels centrally and causes inflammation of the meninges and spinal cord.

The diagnosis of PHN is by clinical examination in most of the patients.

AHZ is characterised by acute pain lasting for about two to four weeks and it precedes rash by about seven to ten days. The typical rash present as red maculopapular eruption that changes into vesicles, pustules, and finally crust formation. Normally the symptoms of AHZ resolves within two to four weeks, and only about ten percent of patients develop PHN. PHN is the frequent chronic complication of HZ and the most common neuropathic pain resulting from infection.

Testing is, generally done to identify coexisting treatable diseases such as vertebral compression or any underlying disease responsible for immunocompromised state of patient. Immunocompromised state predisposes to the infection with Herpes zoster infection.


Differential diagnosis:

  • Thoracic radiculopathy in cases with thoracic PHN
  • Peripheral neuropathy
  • Intrathoracic or intra-abdominal pathology may mimic pain of PHN affecting thoracic dermatome.
  • Intracranial pathology, diseases of Eye, and diseases of Ear, Nose and throat may mimic PHN in the distribution of trigeminal nerve.




PHN is an exceptionally complex drug resistant neuropathic pain. It results from changes in central and peripheral nervous system somatosensory processing.

Aim is to treat patient with Post-herpetic neuralgia within first 72 hours of the rash, in order to reduce both acute neuralgia (AN) and PHN.

PHN is one of the most difficult pain syndromes to treat. The reason why PHN occurs in some patients and not in others, is not known. The condition occurs more frequently in older patients, and also following acute Herpes zoster infection of the trigeminal cranial nerve, as compared to acute Herpes zoster involving thoracic region. It is said that aggressive treatment of acute Herpes zoster infection helps in avoiding PHN.


Preventive vaccination:

A live attenuated vaccine to boost immunity to VZV and reducing the risk of HZ, is recommended for adults older than 60 years of age. It significantly reduces both HZ and PHN.


Medical therapy:

  • Antiviral drugs: Antiviral drugs such as acyclovir, valacyclovir, and famciclovir may reduce both acute neuralgia (AN) and PHN. These drugs reduce viral shedding and help in resolution of symptoms.
  • Anticonvulsant gabapentin: Gabapentin is effective in management of PHN. The mechanism of action of gabapentin is unknown.
  • Anticonvulsant Pregabalin: Pregabalin reduces release of excitatory neurotransmitters. Treatment with pregabalin results in significant improvement, as is seen in controlled study.
  • Tricyclic anti-depressants (TCAs): Tricyclic anti-depressants block certain receptors and inhibit serotonin and norepinephrine reuptake, and thus block the painful stimulus. Examples are amitriptyline, nortriptyline, desipramine and imipramine. Serotonin noradrenaline reuptake inhibitors (SNRIs) such as venlafaxine and duloxetine have given promising results in the treatment of PHN. Recent studies have shown that venlafaxine may be of some benefit in patients who cannot tolerate other anti-depressants. Due to incomplete efficacy and side effects of monotherapy, many trials have been conducted to have a combined drug therapy. For example, combination of nortriptyline and gabapentin have been tried.
  • Opioids: Opioids such as morphine and tramadol are shown to relieve pain of PHN. Earlier evidence favoured TCAs but latest controlled trials support opioids over TCAs.


Topical therapy:

Due to the associated side effects of systemic therapy, the focus has shifted to topical therapy. It is a convenient and pain-free self-administration by the patient. There is reduced frequency of administration, reduced systemic exposure due to limited absorption from the skin surface, and enhancement of patient compliance.

Local topical therapy includes

  • Lidocaine: 5% Lidocaine patch is a safe and efficient option of local therapy in case of localised neuropathic pain (LNP). Lidocaine patch is a targeted peripheral analgesic. It has high safety, efficacy, and tolerability and is a chosen treatment in case of local neuropathic pain.
  • Capsaicin: 8% Capsaicin patch may be used in the treatment of peripheral neuropathic pain either alone or in combination of other medicines. However, capsaicin may cause transient adverse effects such as erythema and pain.
  • Topical and intranasal analgesic pharmacotherapy: Topical and intranasal analgesic pharmacotherapy may be used in place of systemic therapy. Intranasal 10% ketamine may be combined with topical 6% gabapentin, 10% ketoprofen, 5% lidocaine, or 10% ketamine cream.
  • Gabapentin: 6% Gabapentin gel patches have been tried. It is a recent advance in the treatment of PHN. Topical gabapentin provided rapid improvement of symptoms.
  • Transcutaneous Electrical Nerve Stimulation (TENS): Transcutaneous Electrical Nerve Stimulation is a recent advance in the management of PHN. Patients refractory to medical therapy may be treated with TENS. Patients with TENS report a significant decrease in pain. It is seen that whether use of TENS or antivirals, either alone or in combination, cannot completely prevent PHN. However, TENS is found to be most successful in reducing the incidence of subacute herpetic neuralgia.
  • Ultrasound-guided musculocutaneous peripheral nerve block: A patient with excruciating pain and not responding to any treatment was selected. Ultrasound-guided musculocutaneous peripheral nerve block helped in control of symptoms due to PHN.


Surgical therapy:

Surgical approaches such as stereotaxic trigeminal tractotomy and dorsal root entry zone (DREZ) treatment procedures have been described in the treatment of PHN.

  • PUBLISHED DATE : Mar 18, 2019
  • CREATED / VALIDATED BY : Dr. S. C. Gupta
  • LAST UPDATED ON : Mar 18, 2019


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