THE CLINICAL SYNDROME

• The varicellazoster virus is the causative agent of herpes zoster, which is an infectious disease (VZV).

  • The clinical manifestation of a primary infection with VZV in a host that is not immune is the childhood disease known as chickenpox (varicella).

    • It has been hypothesized by researchers that during the course of this original infection, the virus moves to the cranial ganglia or the dorsal root, where it remains latent and does not generate any clinically visible pathology.

  • In some people, the virus becomes active again and travels down the sensory pathways of the first division of the trigeminal nerve. There, it causes the pain and skin blisters that are typical of herpes zoster, also known as shingles.

• After the thoracic dermatomes, the first division of the trigeminal nerve is the second most common site for the development of acute herpes zoster.

  • This occurs most frequently in adults. In extremely rare cases, the virus will infect the geniculate ganglion, which will cause discomfort, vesicles within the ear, and loss of hearing.

  • The Ramsay Hunt syndrome is a collection of symptoms that must be differentiated from acute herpes zoster that affects the first division of the trigeminal nerve. This illness bears the name of its namesake.

SIGNS AND SYMPTOMS

• Ganglionitis and peripheral neuritis are two painful conditions that can arise in conjunction with flu-like symptoms when viral reactivation takes place.

  • In most cases, the dull, aching feeling that initially characterizes the pain gives way, in the distribution of the first division of the trigeminal nerve, to dysesthetic or neuritic pain.

  • The discomfort associated with acute herpes zoster typically begins three to seven days before the appearance of the rash; unfortunately, this delay frequently results in a diagnosis that is incorrect.

• On the other hand, a clinical diagnosis of shingles may be made with relative ease in the majority of patients after the distinctive rash appears.

  • Herpes zoster causes a rash that is similar to that caused by chickenpox. It begins as a crop of macular lesions that quickly transform into papules and subsequently into vesicles. At some point, the vesicles will begin to consolidate, which will be followed by crusting.

• The affected region can be exceedingly painful, and the pain has a tendency to become worse whenever there is any movement or contact with the area (e.g., with clothing or sheets).

  • The crust that covered the lesions eventually peels off as the lesions heal, leaving behind pink scars that over time become hypopigmented and atrophic.

• The majority of patients get a relief from their hyperesthesia and discomfort when their skin lesions heal. However, for some people, the discomfort continues even after the lesion has healed.

  • Postherpetic neuralgia is a common and dreaded sequel of acute herpes zoster, and the elderly are more likely to be impacted by it than the general population that is afflicted with acute herpes zoster.

• The symptoms of postherpetic neuralgia can range from a slight disease that resolves on its own to a devastating, persistent pain that is made worse by light touch, movement, anxiety, or changes in temperature.

TESTING

• Even while it is possible to make a diagnosis based just on clinical evidence in the vast majority of cases, further testing may be necessary on occasion.

• In patients who also have other skin lesions that confound the clinical image, such as patients with acquired immunodeficiency syndrome who are suffering from Kaposi sarcoma, such testing may be desired.

  • Patients with other skin lesions that confuse the clinical picture include: In patients like these, testing with immunofluorescent antibodies and polymerase chain reaction can quickly identify herpes zoster virus and differentiate it from herpes simplex infections.

• Obtaining a Tzanck smear from the base of a fresh vesicle might help improve the diagnosis of acute herpes zoster in instances that are not problematic.

  • This smear displays multinucleated large cells and eosinophilic inclusions. This easy and inexpensive test performed at the bedside, on the other hand, is unable to differentiate between lesions brought on by herpes simplex infections and those brought on by the varicella-zoster virus.

DIFFERENTIAL DIAGNOSIS

• All patients who are experiencing acute herpes zoster of the trigeminal nerve should have a meticulous first evaluation that includes an in-depth medical history as well as a comprehensive physical examination.

  • The aim of this process is to determine whether or not the immunocompromised status of the patient is the result of an undiagnosed malignant or systemic condition.

• A quick diagnosis allows for the early observation of changes in clinical status that may precede the development of problems, such as myelitis or the propagation of the disease.

  • Trigeminal neuralgia, sinus disease, glaucoma, retro-orbital tumor, inflammatory disease (such as Tolosa-Hunt syndrome), and intracranial disease, including tumor, are some other conditions that can cause pain in the region served by the first division of the trigeminal nerve.

TREATMENT

Nerve Block

• To treat acute trigeminal nerve herpes zoster and avoid postherpetic neuralgia, stellate ganglion block with local anesthesia and steroid is the best treatment. Vesicular crusting reduces neuronal scarring.

• Sympathetic nerve block is expected to achieve these goals by preventing viral nerve and gasserian ganglion inflammation-induced significant sympathetic activation.

• Intraneural capillary bed ischemia can result from sympathetic hyperactivity if left untreated. If this ischemia persists, endoneural edema increases pressure and reduces blood supply, causing irreparable nerve injury.

Opioid Analgesics

• While sympathetic nerve blocks are used, opioid analgesics can reduce the agonizing pain of acute herpes zoster. Common neuritic pain is less relieved by opioids.

• A time-contingent dose of powerful, long-acting opioid analgesics like oral morphine elixir or methadone may enhance sympathetic neural blockade's pain relief.

Adjuvant Analgesics

• Gabapentin is the first-line treatment for acute trigeminal herpes zoster neuritic pain.

• Gabapentin may prevent postherpetic neuralgia.

  • Early gabapentin treatment may be utilized with neural blockade, opioid analgesics, and other adjuvant analgesics, including antidepressants, to reduce central nervous system side effects.

  • Gabapentin is started at 300 mg at bedtime and titrated up in 300-mg increments to 3600 mg in separate doses when side effects allow. Pregabalin may be better tolerated than gabapentin.

  • As side effects allow, pregabalin is started at 50 mg three times a day and increased to 100 mg.

  • Patients with renal impairment should reduce pregabalin dosage because the kidneys eliminate it.

Antiviral Agents

• There are a few antiviral medicines, such as valacyclovir, famciclovir, and acyclovir, that have the ability to shorten the course of acute herpes zoster and may even help prevent postherpetic neuralgia from occurring.

  • They could be helpful in reducing the severity of the disease in patients whose immune systems are compromised.

  • These antiviral medicines may be utilized in combination with the therapy techniques that have been discussed previously.

  • It is required that careful monitoring for adverse effects take place.