Materiały źródłowe

• #1 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  Ramsay Hunt syndrome, also known as herpes zoster oticus, is a late complication of varicella-zoster virus infection that results in inflammation of the geniculate ganglion of cranial nerve VII. […] Ramsay Hunt syndrome, also known as herpes zoster oticus or geniculate ganglion herpes zoster, is a late complication of varicella-zoster virus (VZV) infection, resulting in inflammation of the geniculate ganglion of cranial nerve VII. […] The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #2 Ramsay Hunt Syndrome: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1166804-overview

  Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves (CN) may also be involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy. […] Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome. Diminished level of VZV-specific cell-mediated immunity may lead to reactivation of this virus.

• #3 Ramsay Hunt syndrome | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/ramsay-hunt-syndrome?embed_domain=hackmd.io%2525252F%25252540yipuafecsl2jsu8smr5njq%2525252Fbnjhjgjghjghjghfavicon.icofavicon.ico&lang=us

  Ramsay Hunt syndrome, also known as herpes zoster oticus or Ramsay Hunt syndrome type 2, is shingles of the facial nerve. It is due to reactivation of the varicella zoster virus (VZV) in the geniculate ganglion. […] The syndrome is due to latent infection of the geniculate ganglion with varicella zoster virus (VZV) and subsequent reactivation.

• #4 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  Ramsay Hunt syndrome, also known as herpes zoster oticus, is a late complication of varicella-zoster virus infection that results in inflammation of the geniculate ganglion of cranial nerve VII. […] Ramsay Hunt syndrome, also known as herpes zoster oticus or geniculate ganglion herpes zoster, is a late complication of varicella-zoster virus (VZV) infection, resulting in inflammation of the geniculate ganglion of cranial nerve VII. […] The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #5 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  Ramsay Hunt syndrome, also known as herpes zoster oticus, is a late complication of varicella-zoster virus infection that results in inflammation of the geniculate ganglion of cranial nerve VII. […] Ramsay Hunt syndrome, also known as herpes zoster oticus or geniculate ganglion herpes zoster, is a late complication of varicella-zoster virus (VZV) infection, resulting in inflammation of the geniculate ganglion of cranial nerve VII. […] The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #6 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Once the clinical VZV infection, chickenpox, has cleared, the virus remains latent in cranial nerves or dorsal root ganglia and may subsequently reactivate in times of physiological stress or immunocompromise, leading to herpes zoster, known as „shingles” anywhere on the body or „Ramsay Hunt syndrome” when facial paralysis is involved. […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #7 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Once the clinical VZV infection, chickenpox, has cleared, the virus remains latent in cranial nerves or dorsal root ganglia and may subsequently reactivate in times of physiological stress or immunocompromise, leading to herpes zoster, known as „shingles” anywhere on the body or „Ramsay Hunt syndrome” when facial paralysis is involved. […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #8 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  Ramsay Hunt syndrome, also known as herpes zoster oticus, is a late complication of varicella-zoster virus infection that results in inflammation of the geniculate ganglion of cranial nerve VII. […] Ramsay Hunt syndrome, also known as herpes zoster oticus or geniculate ganglion herpes zoster, is a late complication of varicella-zoster virus (VZV) infection, resulting in inflammation of the geniculate ganglion of cranial nerve VII. […] The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #9 Ramsay Hunt Syndrome: An Introduction, Signs and Symptoms, and Treatment

  https://pmc.ncbi.nlm.nih.gov/articles/PMC9925029/

  Ramsay Hunt syndrome is the complication of the virus varicella-zoster and the infection caused by it, which shows apparent geniculate ganglion involvement. […] This article provides an overview of how the varicella-zoster virus causes facial paralysis and other neurological symptoms. […] Inflammation of the geniculate ganglion of eight cranial nerves is evident in Ramsay Hunt syndrome. […] Ramsay Hunt syndrome is a late consequence of an infection due to the VZV, which causes inflammation of the geniculate ganglion of the seventh cranial nerve. […] A characteristic feature of the Ramsay Hunt syndrome is the triad of ipsilateral facial paralysis, otalgia, and vesicular rash in the auricle or auditory canal. […] The virus is not cultured from ganglia, but by methods such as in situ hybridization, Southern blot analysis, or polymerase chain reaction (PCR), VZV may be detected.

• #10 Ramsay Hunt Syndrome – Rare Awareness Rare Education

  https://rareportal.org.au/rare-disease/ramsay-hunt-syndrome/

  Ramsay Hunt syndrome is a condition that arises as a complication of shingles specifically in the facial nerves. Shingles is caused by the varicella-zoster virus (VZV), the same virus responsible for chickenpox. The virus remains in the body of people who have had chicken pox but may be inactive (dormant) for a long period of time. When the virus becomes active again (reactivates), it causes shingles and can lead to Ramsay Hunt syndrome if the reactivation affects facial nerves. This causes a rash and paralysis on one side of the face, as well as other symptoms. If Ramsay Hunt syndrome is not treated quickly, it can lead to long-term complications. […] Ramsay Hunt syndrome is caused by reactivation of the varicella-zoster virus (VZV) in the facial nerves. Individuals that are infected with VZV will first develop chickenpox but even after they recover from chickenpox, the virus will remain inactive in their spinal cord. The virus can reactivate, usually later in life, resulting in shingles. In cases where the reactivation affects facial nerves it can cause Ramsay Hunt syndrome. […] Reactivation of varicella-zoster virus can be triggered by decreased immune system function. Immune function can decrease because of immunosuppressive medications, other diseases, stress and aging. Reactivation of the virus can occur more than once and individuals can get shingles multiple times.

• #11 Ramsay Hunt Syndrome – Facial Palsy UK

  https://www.facialpalsy.org.uk/causesanddiagnoses/ramsay-hunt-syndrome/

  Ramsay Hunt syndrome (RHS) is a complication of shingles. It is the name given to describe the symptoms of a shingles infection affecting the facial nerve. Shingles is caused by the same virus that causes chickenpox (varicella zoster virus, or VZV). As a result of this infection, the facial nerve becomes inflamed and irritated. […] If you develop RHS, you will have had chickenpox as a child but once the spots heal and you recover the virus continues to live in the nerves that it has infected by the virus. It is harmless unless it is reactivated and should this happen new symptoms will appear. This cluster of symptoms is called RHS. […] At times our immune system becomes depressed and is less able to fight off infection. The body then becomes vulnerable to reactivation of the chickenpox virus.

• #12 Ramsay Hunt Syndrome – Facial Palsy UK

  https://www.facialpalsy.org.uk/causesanddiagnoses/ramsay-hunt-syndrome/

  Stress is often a trigger. Many studies have shown that stress can weaken the immune system, and that people under significant stress are more likely to suffer from infections than those who are not. For this reason, it is believed that stress can be linked to outbreaks of shingles, and thus RHS could result.

• #13 Ramsay Hunt Syndrome: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1166804-overview

  Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves (CN) may also be involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy. […] Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome. Diminished level of VZV-specific cell-mediated immunity may lead to reactivation of this virus.

• #14 Ramsay Hunt Syndrome – Facial Palsy UK

  https://www.facialpalsy.org.uk/causesanddiagnoses/ramsay-hunt-syndrome/

  Stress is often a trigger. Many studies have shown that stress can weaken the immune system, and that people under significant stress are more likely to suffer from infections than those who are not. For this reason, it is believed that stress can be linked to outbreaks of shingles, and thus RHS could result.

• #15 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  Ramsay Hunt syndrome, also known as herpes zoster oticus, is a late complication of varicella-zoster virus infection that results in inflammation of the geniculate ganglion of cranial nerve VII. […] Ramsay Hunt syndrome, also known as herpes zoster oticus or geniculate ganglion herpes zoster, is a late complication of varicella-zoster virus (VZV) infection, resulting in inflammation of the geniculate ganglion of cranial nerve VII. […] The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #16 Ramsay Hunt Syndrome: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1166804-overview

  Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves (CN) may also be involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy. […] Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome. Diminished level of VZV-specific cell-mediated immunity may lead to reactivation of this virus.

• #17 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] When patients fail to recover premorbid function, synkinesis is a common sequela, in which aberrant reinnervation connects axons with neuromuscular junctions differently from the ones to which they were connected prior to the inflammation. Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve.

• #18 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] The neuritis associated with Ramsay Hunt syndrome appears to be more severe than that of Bell’s palsy, given that more than twice as many patients present with complete hemifacial paralysis with Ramsay Hunt syndrome as in Bell’s palsy. […] Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve. […] In synkinesis, newly regenerated axons will terminate at multiple neuromuscular junctions, which has the effect of further increasing dyscoordination as well as raising the resting tone of the muscles that now have more associated axons than they did before the injury. […] The proximity of the facial nerve to the vestibulocochlear nerve can result in hearing loss, tinnitus, and vertigo.

• #19 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] The neuritis associated with Ramsay Hunt syndrome appears to be more severe than that of Bell’s palsy, given that more than twice as many patients present with complete hemifacial paralysis with Ramsay Hunt syndrome as in Bell’s palsy. […] Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve. […] In synkinesis, newly regenerated axons will terminate at multiple neuromuscular junctions, which has the effect of further increasing dyscoordination as well as raising the resting tone of the muscles that now have more associated axons than they did before the injury. […] The proximity of the facial nerve to the vestibulocochlear nerve can result in hearing loss, tinnitus, and vertigo.

• #20 Ramsay Hunt Syndrome: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1166804-overview

  Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves (CN) may also be involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy. […] Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome. Diminished level of VZV-specific cell-mediated immunity may lead to reactivation of this virus.

• #21 Ramsay Hunt Syndrome: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1166804-overview

  Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves (CN) may also be involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy. […] Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome. Diminished level of VZV-specific cell-mediated immunity may lead to reactivation of this virus.

• #22 An unexpected case of Ramsay hunt syndrome: case report and literature review | BMC Research Notes | Full Text

  https://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-6-337

  Ramsay Hunt Syndrome (RHS) is a rare, severe complication of varicella zoster virus (VZV) reactivation in the geniculate ganglion. […] The risk of RHS in VZV reactivation has been quoted as little as 0.2% at day 60. […] In RHS, VZV reactivates in the geniculate ganglion, causing peripheral facial paralysis, otalgia and auricular vesicles. […] As RHS is a reactivation of VZV in the geniculate nucleus, the etiology of co-existent cervical dermatome involvement is not well understood. […] One such theory is that of cerebrospinal fluid (CSF)/hematogenous spread. […] Another theory is interneuronal communication. […] It is plausible that VZV and associated inflammation may spread from a primary site of reactivation, through these anastomoses. […] Finally, the simultaneous activation of multiple ganglia may occur and could account for this clinical picture.

• #23 A Case of Ramsay Hunt Syndrome with Cranial Polyneuropathy

  https://www.ejao.org/journal/view.php?doi=10.7874/kja.2012.16.2.80

  Ramsay Hunt syndrome is an infectious disease caused by the varicella zoster virus. It is characterized by the symptoms of facial paralysis, otalgia, and erythematous vesicular rash on the auricle and/or oral cavity. […] Ramsay Hunt syndrome (RHS), first described by J. Ramsay Hunt in 1907, refers to the association of unilateral peripheral facial nerve palsy (FNP) and reactivation of VZV along the sensory nerves innervating the ear (herpes zoster oticus). […] Hunt postulated that the syndrome is caused by a reactivation of VZV in the ganglion of cranial nerve VII, which was later confirmed by demonstration of presence of VZV DNA in the geniculate ganglion. […] Several mechanisms of multiple cranial nerve involvement due to a reactivation of VZV have been proposed. Hunt explained the mechanism of multiple cranial nerve palsy as an involvement of adjacent ganglia by contiguous anatomical contact from the original source of inflammation in a single ganglion. Another theory was that the spread of the virus through a common blood supply to cranial nerves might be the mechanism of multiple cranial nerve involvement.

• #24 Ramsay Hunt Syndrome Type 2 – EyeWiki

  https://eyewiki.org/Ramsay_Hunt_Syndrome_Type_2

  Ramsay Hunt syndrome type 2 is caused by reactivation of varicella zoster virus in the geniculate ganglion. […] The inflammatory response caused by reactivated virus can lead to lower motor neuron lesions of the facial nerve, leading to paralysis of facial muscles that can cause dry mouth, dry eyes, and hearing loss. […] Reactivation of varicella-zoster virus involving the geniculate ganglion is the main cause of Ramsay Hunt Syndrome Type 2. […] There are three theories on the pathophysiology of the polyneuropathy nature of Ramsay Hunt Syndrome. The hearing loss and vertigo are attributed to the close proximity of Vestibulocochlear nerve (CN VIII) to Facial nerve (CN VII) at the cerebellopontine angle. Alternatively, the virus could travel via vasa vasorum to nearby cranial nerves. Finally, varicella-zoster virus could spread anterograde through the intersynaptic transmission of the brainstem reflex pathway.

• #25 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] When patients fail to recover premorbid function, synkinesis is a common sequela, in which aberrant reinnervation connects axons with neuromuscular junctions differently from the ones to which they were connected prior to the inflammation. Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve.

• #26 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] The neuritis associated with Ramsay Hunt syndrome appears to be more severe than that of Bell’s palsy, given that more than twice as many patients present with complete hemifacial paralysis with Ramsay Hunt syndrome as in Bell’s palsy. […] Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve. […] In synkinesis, newly regenerated axons will terminate at multiple neuromuscular junctions, which has the effect of further increasing dyscoordination as well as raising the resting tone of the muscles that now have more associated axons than they did before the injury. […] The proximity of the facial nerve to the vestibulocochlear nerve can result in hearing loss, tinnitus, and vertigo.

• #27 Ramsay Hunt Syndrome – A Diagnostic Dilemma – MedCrave online

  https://medcraveonline.com/JOENTR/ramsay-hunt-syndrome-ndash-a-diagnostic-dilemma.html

  Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. Ramsay Hunt Syndrome (RHS) is a rare, severe complication of varicella zoster virus (VZV) reactivation in the geniculate ganglion. […] The VZV reactivation in the geniculate ganglia and subsequent neural inflammation, pressure, and possible destruction of the facial nerve in the temporal bone are suspected to cause facial palsy, while VZV migrates from the geniculate ganglia into the skin around the ear or into the oropharynx via the sensory fibers, where it replicates and produces zoster in RHS. […] The primary etiologic agent of RHS is VZV but Bell’s palsy, in contrast, has been attributed to herpes simplex virus type-1. […] Various associated complications include corneal abrasions and ulcers, if eye-lid closure is impaired, secondary infection with bacteria (cellulitis), Post herpetic neuralgia, as with other Varicella Zoster virus reactivations, permanent facial paralysis, and long term ipsilateral hearing loss and tinnitus.

• #28 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] When patients fail to recover premorbid function, synkinesis is a common sequela, in which aberrant reinnervation connects axons with neuromuscular junctions differently from the ones to which they were connected prior to the inflammation. Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve.

• #29 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] The neuritis associated with Ramsay Hunt syndrome appears to be more severe than that of Bell’s palsy, given that more than twice as many patients present with complete hemifacial paralysis with Ramsay Hunt syndrome as in Bell’s palsy. […] Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve. […] In synkinesis, newly regenerated axons will terminate at multiple neuromuscular junctions, which has the effect of further increasing dyscoordination as well as raising the resting tone of the muscles that now have more associated axons than they did before the injury. […] The proximity of the facial nerve to the vestibulocochlear nerve can result in hearing loss, tinnitus, and vertigo.

• #30 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] The neuritis associated with Ramsay Hunt syndrome appears to be more severe than that of Bell’s palsy, given that more than twice as many patients present with complete hemifacial paralysis with Ramsay Hunt syndrome as in Bell’s palsy. […] Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve. […] In synkinesis, newly regenerated axons will terminate at multiple neuromuscular junctions, which has the effect of further increasing dyscoordination as well as raising the resting tone of the muscles that now have more associated axons than they did before the injury. […] The proximity of the facial nerve to the vestibulocochlear nerve can result in hearing loss, tinnitus, and vertigo.

• #31 Ramsay Hunt syndrome: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/001647.htm

  Complications of Ramsay Hunt syndrome may include: Changes in the appearance of the face (disfigurement) from loss of movement, Change in taste, Damage to the eye (corneal ulcers and infections), resulting in a loss of vision, Nerves that grow back to the wrong structures and cause abnormal reactions to a movement — for example, smiling causes the eye to close. […] There is no known way to prevent Ramsay Hunt syndrome, but treating it with medicine soon after symptoms develop can improve recovery.

• #32 Ramsay Hunt syndrome: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/001647.htm

  Complications of Ramsay Hunt syndrome may include: Changes in the appearance of the face (disfigurement) from loss of movement, Change in taste, Damage to the eye (corneal ulcers and infections), resulting in a loss of vision, Nerves that grow back to the wrong structures and cause abnormal reactions to a movement — for example, smiling causes the eye to close. […] There is no known way to prevent Ramsay Hunt syndrome, but treating it with medicine soon after symptoms develop can improve recovery.

• #33 Ramsay Hunt Syndrome | Treatment & Management | Point of Care

  https://www.statpearls.com/point-of-care/22843

  The facial paralysis resulting from Ramsay Hunt syndrome has a worse prognosis than that seen in Bell’s palsy, with only 70% regaining normal or near-normal facial function compared with over 90% in Bell’s palsy. […] The neuritis associated with Ramsay Hunt syndrome appears to be more severe than that of Bell’s palsy, given that more than twice as many patients present with complete hemifacial paralysis with Ramsay Hunt syndrome as in Bell’s palsy. […] Severe neuritis and resultant swelling of the facial nerve against the bony Fallopian canal that encases it within the temporal bone causes direct, physical neuronal injury. […] Consequently, Wallerian degeneration of facial nerve axons occurs along with varying degrees of damage to the internal architecture of the nerve. […] In synkinesis, newly regenerated axons will terminate at multiple neuromuscular junctions, which has the effect of further increasing dyscoordination as well as raising the resting tone of the muscles that now have more associated axons than they did before the injury. […] The proximity of the facial nerve to the vestibulocochlear nerve can result in hearing loss, tinnitus, and vertigo.

• #34 Early diagnosis and treatment of Ramsay Hunt syndrome: a case report | International Journal of Emergency Medicine | Full Text

  https://intjem.biomedcentral.com/articles/10.1186/s12245-024-00807-x

  Ramsay Hunt syndrome (RHS), a rare complication of varicella-zoster virus (VZV) reactivation, presents with ipsilateral facial paralysis, ear pain, and vesicular rash. Early recognition is crucial for prompt treatment and optimal outcomes. […] RHS is a significant otologic complication of VZV reactivation. The latent virus reactivates in the geniculate ganglion and may spread to the eighth cranial nerve, and in rare cases, it can involve multiple cranial nerves, particularly cranial nerves V, IX, and X. RHS typically presents with a triad of ipsilateral facial paralysis, ear pain, and vesicles in the auditory canal or on the auricle. Other symptoms, including altered taste perception, tongue lesions, hearing abnormalities (decreased hearing, tinnitus, hyperacusis), lacrimation, vertigo, and nystagmus, are frequently reported due to the involvement of the affected nerves.

• #35 Herpes Zoster Oticus (Ramsay Hunt Syndrome) | Doctor

  https://patient.info/doctor/herpes-zoster-oticus-ramsay-hunt-syndrome

  Ramsay Hunt syndrome (herpes zoster oticus or auricular herpes zoster) – described here. […] Herpes zoster oticus occurs when the varicella-zoster virus (chickenpox) becomes reactivated in the geniculate ganglion of the VIIth cranial nerve (facial nerve) causing facial paralysis, loss of taste, vestibulocochlear dysfunction and pain. […] As a general rule, shingles is a disease of sensory nerves but Ramsay Hunt syndrome is distinctive in that there is a motor component. J. Ramsay Hunt described the various clinical presentations of facial paralysis with a rash and also recognised other frequent symptoms and signs such as tinnitus, hearing loss, nausea, vomiting, vertigo and nystagmus. […] In Ramsay Hunt syndrome, these fibres are affected as they pass through the geniculate ganglion, impairing motor supply of the facial nerve.

• #36

  https://journals.lww.com/ijoo/fulltext/2021/27040/audiological_manifestations_of_ramsay_hunt.16.aspx

  Ramsay Hunt syndrome (RHS) Type II is characterized by facial paralysis, herpetic eruptions on the auricle/mouth, and otic pain due to reactivation of the latent varicella-zoster virus in the geniculate ganglion. […] Reactivation of latent varicella zoster in the geniculate ganglion is considered to be the pathogenesis of RHS. […] The clinical manifestation of RHS is vesicular rashes of the mouth or ear (around pinna or EAC); vesicular rashes might proceed with the onset of facial paresis, hearing loss, vertigo/dizziness, and tinnitus. […] As many as 90% of cases with RHS manifest vestibular disturbances, but auditory problems are rare. […] Sensorineural hearing loss is present in 10% of patients with RHS. […] In our case, the involvement of multicranial nerve (based on subjective assessment) might be the one reason for incomplete recovery. […] In addition, late diagnosis and treatment can also be the reason for poor recovery.

• #37

  https://journals.lww.com/ijoo/fulltext/2021/27040/audiological_manifestations_of_ramsay_hunt.16.aspx

  Ramsay Hunt syndrome (RHS) Type II is characterized by facial paralysis, herpetic eruptions on the auricle/mouth, and otic pain due to reactivation of the latent varicella-zoster virus in the geniculate ganglion. […] Reactivation of latent varicella zoster in the geniculate ganglion is considered to be the pathogenesis of RHS. […] The clinical manifestation of RHS is vesicular rashes of the mouth or ear (around pinna or EAC); vesicular rashes might proceed with the onset of facial paresis, hearing loss, vertigo/dizziness, and tinnitus. […] As many as 90% of cases with RHS manifest vestibular disturbances, but auditory problems are rare. […] Sensorineural hearing loss is present in 10% of patients with RHS. […] In our case, the involvement of multicranial nerve (based on subjective assessment) might be the one reason for incomplete recovery. […] In addition, late diagnosis and treatment can also be the reason for poor recovery.

• #38 Ramsay Hunt syndrome

  https://dermnetnz.org/topics/ramsay-hunt-syndrome

  Ramsay Hunt syndrome is a rare peripheral facial neuropathy. It is a type of shingles due to reactivation of the varicella zoster virus (VZV) in the geniculate ganglion of cranial nerve VII, which supplies the facial nerve. […] The reactivation of VZV in the geniculate ganglion of cranial nerve VII is what leads to the syndrome. VZV can also spread down the axons of other cranial nerves that share a blood supply with the geniculate ganglion. […] Reactivation of VZV is more likely for individuals with an immunodeficiency, such as infection with human immunodeficiency virus (HIV) or malignancy.

• #39 KoreaMed Synapse

  https://synapse.koreamed.org/articles/1110839

  Ramsay Hunt syndrome is a type of acute herpes zoster, which occurs by reactivation of the varicella-zoster virus at the geniculate ganglion. […] Additional variability of the clinical picture of Ramsay Hunt syndrome is produced by varying patterns of skin involvement explained by individual anastomoses between cranial and cervical nerves. […] Ramsay Hunt syndrome occurs by reactivation of the varicella-zoster virus in the geniculate or facial nerves. Due to anatomical associations with other cranial or cervical spinal nerves, various clinical features can present, such as tinnitus, hearing loss, nausea and vomiting, vertigo, and nystagmus. […] Combination treatment with anti-viral agents and steroids is recommended for the treatment of Ramsay Hunt syndrome. Additionally, early diagnosis of Ramsay Hunt syndrome is a crucial factor to improve damaged nerves in Ramsay Hunt syndrome, which initiates treatment as soon as possible.

• #40 Dysphagia in Ramsay Hunt’s Syndrome – A Case Report –

  https://www.e-arm.org/journal/view.php?number=64

  Ramsay-Hunt syndrome is caused by varicella zoster virus infection in the geniculate ganglion of the facial nerve. It is characterized by facial palsy, otic pain, and herpetic vesicles around the auricle and external auditory canal. Additionally, symptoms may develop related to other cranial nerve involvement, such as dizziness or hearing loss by the vestibulocochlear nerve being invaded. […] Ramsay-Hunt’s syndrome develops due to infection by herpes zoster virus in the geniculate ganglion of the facial nerve, and leads to facial palsy, otalgia, and skin lesions of the auricle and external auditory canal. In addition, symptoms such as dizziness and hearing loss may develop following involvement of the vestibulocochlear nerve. Rarely, there have been case reports describing simultaneous involvement of the glossopharyngeal nerve and vagus nerve.

• #41 KoreaMed Synapse

  https://synapse.koreamed.org/articles/1110839

  Ramsay Hunt syndrome is a type of acute herpes zoster, which occurs by reactivation of the varicella-zoster virus at the geniculate ganglion. […] Additional variability of the clinical picture of Ramsay Hunt syndrome is produced by varying patterns of skin involvement explained by individual anastomoses between cranial and cervical nerves. […] Ramsay Hunt syndrome occurs by reactivation of the varicella-zoster virus in the geniculate or facial nerves. Due to anatomical associations with other cranial or cervical spinal nerves, various clinical features can present, such as tinnitus, hearing loss, nausea and vomiting, vertigo, and nystagmus. […] Combination treatment with anti-viral agents and steroids is recommended for the treatment of Ramsay Hunt syndrome. Additionally, early diagnosis of Ramsay Hunt syndrome is a crucial factor to improve damaged nerves in Ramsay Hunt syndrome, which initiates treatment as soon as possible.

• #42 Herpes Zoster Oticus (Ramsay Hunt Syndrome) | Doctor

  https://patient.info/doctor/herpes-zoster-oticus-ramsay-hunt-syndrome

  The cell bodies of these special visceral afferent fibres are in the geniculate ganglion which is the site of virus reactivation when vesicles erupt on the tongue. […] The fibres reach the brainstem via the nervus intermedius and can be affected by local inflammation as they pass through the geniculate ganglion. […] Decreased lacrimation may result from involvement of these fibres as they branch at the level of the geniculate ganglion. […] Cell bodies of these neurons lie in the geniculate ganglia and are the site of viral reactivation in classic Ramsay Hunt syndrome, causing vesicular eruptions in geniculate zones.

• #43 Ramsay Hunt Syndrome – Rare Awareness Rare Education

  https://rareportal.org.au/rare-disease/ramsay-hunt-syndrome/

  Ramsay Hunt syndrome is a condition that arises as a complication of shingles specifically in the facial nerves. Shingles is caused by the varicella-zoster virus (VZV), the same virus responsible for chickenpox. The virus remains in the body of people who have had chicken pox but may be inactive (dormant) for a long period of time. When the virus becomes active again (reactivates), it causes shingles and can lead to Ramsay Hunt syndrome if the reactivation affects facial nerves. This causes a rash and paralysis on one side of the face, as well as other symptoms. If Ramsay Hunt syndrome is not treated quickly, it can lead to long-term complications. […] Ramsay Hunt syndrome is caused by reactivation of the varicella-zoster virus (VZV) in the facial nerves. Individuals that are infected with VZV will first develop chickenpox but even after they recover from chickenpox, the virus will remain inactive in their spinal cord. The virus can reactivate, usually later in life, resulting in shingles. In cases where the reactivation affects facial nerves it can cause Ramsay Hunt syndrome. […] Reactivation of varicella-zoster virus can be triggered by decreased immune system function. Immune function can decrease because of immunosuppressive medications, other diseases, stress and aging. Reactivation of the virus can occur more than once and individuals can get shingles multiple times.

• #44 Ramsay Hunt Syndrome in Asymptomatic COVID-19 Infection: A Case Report and a Literature Review

  https://www.mdpi.com/2077-0383/12/23/7407

  Ramsay Hunt Syndrome (RHS) is a rare syndrome described by James Ramsay Hunt in 1907. It occurs in 0.3–18% of patients and is characterized by a reactivation of VZV—an alpha herpes virus causing chickenpox and herpes zoster (shingles)—in the geniculate ganglion. This results in facial palsy along with an erythematous vesicular or maculopapular rash in the distribution of the facial nerve sensory supply. RHS sometimes involves the vestibulocochlear nerve (e.g., hearing loss, otalgia, tinnitus, vertigo) or even the vagus nerve. Some reports also evoke a plethora of other symptoms such as dysgeusia, dry eyes or mouth, dysarthria, hyperacusis, and tearing. […] The pathophysiology underlying RHS is based on the reactivation of VZV which resides chronically in the geniculate ganglion. From a mechanistic perspective, the immune alteration in COVID-19 patients could be the trigger of herpes virus reactivation. A few cases of such a reactivation have been described in the context of COVID-19 infection and might be associated with older age, psychological stress, mechanical trauma, immunosuppression, lymphopenia, and cell-mediated dysfunction. COVID-19 infection might constitute the stress factor for VZV reactivation. Some authors also reported common comorbidities in patients who had herpes virus reactivation and COVID-19, namely hypertension followed by diabetes mellitus.

• #45 Herpes Zoster Oticus – Ear, Nose, and Throat Disorders – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/ear-nose-and-throat-disorders/inner-ear-disorders/herpes-zoster-oticus

  Herpes zoster (shingles) is reactivation of varicella-zoster virus infection. Risk factors for reactivation include immunodeficiency secondary to cancer, chemotherapy, radiation therapy, and HIV infection. Typically, the virus remains latent in a dorsal root ganglion, and reactivation manifests as painful skin lesions in a dermatomal distribution. However, the virus rarely remains latent in the geniculate ganglion; when reactivated, the virus causes symptoms involving the 7th and 8th cranial nerves. […] Diagnosis of herpes zoster oticus is usually clinical. If there is any question about viral etiology, vesicular scrapings may be collected for direct immunofluorescence or for viral cultures, and MRI is done to exclude other diagnoses. […] Although there is no reliable evidence that corticosteroids, antivirals, or surgical decompression make a difference in herpes zoster oticus, they are the only possibly useful treatments. When used, corticosteroids are started with prednisone 60 mg orally once a day for 4 to 7 days, followed by gradual tapering of the dose over the next 2 weeks. Either acyclovir 800 mg orally 5 times a day or valacyclovir 1 g orally 2 times a day for 10 days may shorten the clinical course and is routinely prescribed for immunocompromised patients.

• #46 Ramsay Hunt Syndrome in Asymptomatic COVID-19 Infection: A Case Report and a Literature Review

  https://www.mdpi.com/2077-0383/12/23/7407

  Ramsay Hunt Syndrome (RHS) is a rare syndrome described by James Ramsay Hunt in 1907. It occurs in 0.3–18% of patients and is characterized by a reactivation of VZV—an alpha herpes virus causing chickenpox and herpes zoster (shingles)—in the geniculate ganglion. This results in facial palsy along with an erythematous vesicular or maculopapular rash in the distribution of the facial nerve sensory supply. RHS sometimes involves the vestibulocochlear nerve (e.g., hearing loss, otalgia, tinnitus, vertigo) or even the vagus nerve. Some reports also evoke a plethora of other symptoms such as dysgeusia, dry eyes or mouth, dysarthria, hyperacusis, and tearing. […] The pathophysiology underlying RHS is based on the reactivation of VZV which resides chronically in the geniculate ganglion. From a mechanistic perspective, the immune alteration in COVID-19 patients could be the trigger of herpes virus reactivation. A few cases of such a reactivation have been described in the context of COVID-19 infection and might be associated with older age, psychological stress, mechanical trauma, immunosuppression, lymphopenia, and cell-mediated dysfunction. COVID-19 infection might constitute the stress factor for VZV reactivation. Some authors also reported common comorbidities in patients who had herpes virus reactivation and COVID-19, namely hypertension followed by diabetes mellitus.

• #47 Ramsay Hunt Syndrome and the Pharmacist

  https://www.uspharmacist.com/article/ramsay-hunt-syndrome-and-the-pharmacist

  Ramsay Hunt syndrome (RHS) begins with an attack of herpes zoster (i.e., shingles) inside the ear canal. RHS primarily affects the facial nerve, but it can also affect cranial nerves that communicate with the facial nerve. Damage to cranial nerves causes otic pain, otic rash, hemifacial paralysis, and several other complications. […] The etiology of RHS is varicella zoster virus (VZV), the causal agent of chickenpox, a disease that the vast majority of adults had in childhood. VZV lies dormant in cranial-nerve (CN) neurons and dorsal root ganglia. Stress or natural or medically induced immunosuppression (e.g., azathioprine therapy) may cause the dormant virus to reactivate. The reactivation of VZV causes HZ. […] RHS primarily affects the facial nerve (CN VII), but it can also affect CNs that communicate with the facial nerve, such as III, V, VIII, IX, X, XI, and XII. The prognosis of RHS differs radically from that of idiopathic Bells palsy in that fewer than 50% of persons with RHS experience full recovery.

• #48 Epidemiology, clinical manifestations, and diagnosis of herpes zoster – UpToDate

  https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster

  PATHOGENESIS […] During the initial phase of varicella, varicella-zoster virus (VZV) infects the nasopharyngeal lymphoid tissue of a susceptible person. This results in a viremia consisting of VZV-infected T cells that travel throughout the body. […] […] VZV enhances infection by inhibiting multiple host defenses, such as downregulation of major histocompatibility complex class I expression and inhibition of interferon response genes. This enables the virus to partially evade the immune response. The prolonged incubation period prior to the onset of skin lesions in varicella reflects the time required for VZV to overcome local innate defenses, such as alpha interferon production by epidermal cells. […] […] Once the rash develops, cell-free virus, which is present only in skin vesicles, is postulated to infect nerve endings in skin and move retrograde along sensory axons to establish life-long latency in neurons within the regional ganglia. VZV may also reach and infect neurons as a consequence of the viremia. VZV-specific cell-mediated immune responses that develop during varicella are required to end the infection. These responses also play a critical role in controlling VZV latency and limiting the potential for reactivation to cause herpes zoster.

• #49 Epidemiology, clinical manifestations, and diagnosis of herpes zoster – UpToDate

  https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster

  PATHOGENESIS […] During the initial phase of varicella, varicella-zoster virus (VZV) infects the nasopharyngeal lymphoid tissue of a susceptible person. This results in a viremia consisting of VZV-infected T cells that travel throughout the body. […] […] VZV enhances infection by inhibiting multiple host defenses, such as downregulation of major histocompatibility complex class I expression and inhibition of interferon response genes. This enables the virus to partially evade the immune response. The prolonged incubation period prior to the onset of skin lesions in varicella reflects the time required for VZV to overcome local innate defenses, such as alpha interferon production by epidermal cells. […] […] Once the rash develops, cell-free virus, which is present only in skin vesicles, is postulated to infect nerve endings in skin and move retrograde along sensory axons to establish life-long latency in neurons within the regional ganglia. VZV may also reach and infect neurons as a consequence of the viremia. VZV-specific cell-mediated immune responses that develop during varicella are required to end the infection. These responses also play a critical role in controlling VZV latency and limiting the potential for reactivation to cause herpes zoster.

• #50 Epidemiology, clinical manifestations, and diagnosis of herpes zoster – UpToDate

  https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster

  PATHOGENESIS […] During the initial phase of varicella, varicella-zoster virus (VZV) infects the nasopharyngeal lymphoid tissue of a susceptible person. This results in a viremia consisting of VZV-infected T cells that travel throughout the body. […] […] VZV enhances infection by inhibiting multiple host defenses, such as downregulation of major histocompatibility complex class I expression and inhibition of interferon response genes. This enables the virus to partially evade the immune response. The prolonged incubation period prior to the onset of skin lesions in varicella reflects the time required for VZV to overcome local innate defenses, such as alpha interferon production by epidermal cells. […] […] Once the rash develops, cell-free virus, which is present only in skin vesicles, is postulated to infect nerve endings in skin and move retrograde along sensory axons to establish life-long latency in neurons within the regional ganglia. VZV may also reach and infect neurons as a consequence of the viremia. VZV-specific cell-mediated immune responses that develop during varicella are required to end the infection. These responses also play a critical role in controlling VZV latency and limiting the potential for reactivation to cause herpes zoster.

• #51 Epidemiology, clinical manifestations, and diagnosis of herpes zoster – UpToDate

  https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster

  PATHOGENESIS […] During the initial phase of varicella, varicella-zoster virus (VZV) infects the nasopharyngeal lymphoid tissue of a susceptible person. This results in a viremia consisting of VZV-infected T cells that travel throughout the body. […] […] VZV enhances infection by inhibiting multiple host defenses, such as downregulation of major histocompatibility complex class I expression and inhibition of interferon response genes. This enables the virus to partially evade the immune response. The prolonged incubation period prior to the onset of skin lesions in varicella reflects the time required for VZV to overcome local innate defenses, such as alpha interferon production by epidermal cells. […] […] Once the rash develops, cell-free virus, which is present only in skin vesicles, is postulated to infect nerve endings in skin and move retrograde along sensory axons to establish life-long latency in neurons within the regional ganglia. VZV may also reach and infect neurons as a consequence of the viremia. VZV-specific cell-mediated immune responses that develop during varicella are required to end the infection. These responses also play a critical role in controlling VZV latency and limiting the potential for reactivation to cause herpes zoster.

• #52 Ramsay Hunt Syndrome in Asymptomatic COVID-19 Infection: A Case Report and a Literature Review

  https://www.mdpi.com/2077-0383/12/23/7407

  The reactivation of VZV could serve as an indicator of the individual’s declining immune response. In this context, additional investigations become necessary to assess the immune status. The causes of immunosuppression can be diverse and complex. In the evaluation process, only a few possibilities have been ruled out based on medical history, clinical evaluation, and initial workup. A comprehensive assessment might have allowed formal conclusions to be drawn on the immune status, as well as providing further understanding of the pathophysiological mechanisms behind this manifestation.

• #53 Ramsay Hunt Syndrome in Asymptomatic COVID-19 Infection: A Case Report and a Literature Review

  https://www.mdpi.com/2077-0383/12/23/7407

  While herpes virus reactivation post-COVID-19 vaccine might be related to inflammation, autoimmunity, vaccine-induced hyperviscosity, vaccine-mediated hampering of the innate immunity targeting VZV, and the unavailability of VZV-specific CD8 cells due to the shift in naive CD8+ cells to target the vaccine, the underlying mechanisms action in the context of COVID-19 infection could involve various COVID-19-related T cell immune dysfunctions. Here, it is worth noting that our patient had a low or inverted CD4/CD8 ratio which could reflect a suppression of the CD4+ T cells and/or an activation of the cytotoxic CD8+ T cells. Such a finding has been previously documented in the context of COVID-19 infection, but also in association with other conditions such as aging, chronic inflammation, metabolic or cardiovascular diseases, immune dysfunction, or immune senescence.

• #54 Ramsay Hunt Syndrome in Asymptomatic COVID-19 Infection: A Case Report and a Literature Review

  https://www.mdpi.com/2077-0383/12/23/7407

  While herpes virus reactivation post-COVID-19 vaccine might be related to inflammation, autoimmunity, vaccine-induced hyperviscosity, vaccine-mediated hampering of the innate immunity targeting VZV, and the unavailability of VZV-specific CD8 cells due to the shift in naive CD8+ cells to target the vaccine, the underlying mechanisms action in the context of COVID-19 infection could involve various COVID-19-related T cell immune dysfunctions. Here, it is worth noting that our patient had a low or inverted CD4/CD8 ratio which could reflect a suppression of the CD4+ T cells and/or an activation of the cytotoxic CD8+ T cells. Such a finding has been previously documented in the context of COVID-19 infection, but also in association with other conditions such as aging, chronic inflammation, metabolic or cardiovascular diseases, immune dysfunction, or immune senescence.

• #55 Ramsay Hunt syndrome: Symptoms, causes, and treatments

  https://www.medicalnewstoday.com/articles/191575

  Ramsay Hunt syndrome, also known as herpes zoster oticus, is an infection of a facial nerve. It is a neurological disorder in which the Varicella zoster virus infects specific nerves in the head. […] The Varicella zoster virus can also cause chicken pox. People who have had chicken pox carry the dormant virus in their nerves. Some years later it may become active again, infecting the facial nerve, causing Ramsay Hunt syndrome. […] The damage caused by Ramsay Hunt syndrome is reversible. […] Complications are rare if treatment starts within a few days of the onset of symptoms. A small percentage of patients may, however, experience permanent hearing loss and facial weakness even if their treatment was applied quickly and effectively. […] If treatment is delayed, there is a risk of losing facial movement permanently, as well as uncontrolled movements, such as blinking. Some people may find it hard to close one eye, which can eventually damage the cornea, leading to eye pain and vision problems. […] A doctor will probably make a diagnosis if the hallmark signs of facial weakness and a blister-like rash are detected. A nerve conduction study may be performed to determine the extent of damage to the facial nerve, as well as defining the likelihood of recovery.

• #56 Ramsay Hunt Syndrome – A Diagnostic Dilemma – MedCrave online

  https://medcraveonline.com/JOENTR/ramsay-hunt-syndrome-ndash-a-diagnostic-dilemma.html

  Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. Ramsay Hunt Syndrome (RHS) is a rare, severe complication of varicella zoster virus (VZV) reactivation in the geniculate ganglion. […] The VZV reactivation in the geniculate ganglia and subsequent neural inflammation, pressure, and possible destruction of the facial nerve in the temporal bone are suspected to cause facial palsy, while VZV migrates from the geniculate ganglia into the skin around the ear or into the oropharynx via the sensory fibers, where it replicates and produces zoster in RHS. […] The primary etiologic agent of RHS is VZV but Bell’s palsy, in contrast, has been attributed to herpes simplex virus type-1. […] Various associated complications include corneal abrasions and ulcers, if eye-lid closure is impaired, secondary infection with bacteria (cellulitis), Post herpetic neuralgia, as with other Varicella Zoster virus reactivations, permanent facial paralysis, and long term ipsilateral hearing loss and tinnitus.

• #57 Ramsay Hunt syndrome: MedlinePlus Medical EncyclopediaLock

  https://medlineplus.gov/ency/article/001647.htm

  Complications of Ramsay Hunt syndrome may include: Changes in the appearance of the face (disfigurement) from loss of movement, Change in taste, Damage to the eye (corneal ulcers and infections), resulting in a loss of vision, Nerves that grow back to the wrong structures and cause abnormal reactions to a movement — for example, smiling causes the eye to close. […] There is no known way to prevent Ramsay Hunt syndrome, but treating it with medicine soon after symptoms develop can improve recovery.

• #58 Ramsay Hunt Syndrome and the Pharmacist

  https://www.uspharmacist.com/article/ramsay-hunt-syndrome-and-the-pharmacist

  The cause of PHN is VZV-induced damage to the nerve fibers. PHN affects about 50% of persons older than age 60 years, and it may occur years after the patient had shingles. […] Recommended pharmacologic therapy for RHS includes a combination of antiviral and corticosteroid medications. Prompt initiation within 72 hours of symptom onset has been associated with significant improvement versus delayed treatment, so rapid diagnosis and management are critical.

• #59 Ramsay Hunt Syndrome and the Pharmacist

  https://www.uspharmacist.com/article/ramsay-hunt-syndrome-and-the-pharmacist

  The cause of PHN is VZV-induced damage to the nerve fibers. PHN affects about 50% of persons older than age 60 years, and it may occur years after the patient had shingles. […] Recommended pharmacologic therapy for RHS includes a combination of antiviral and corticosteroid medications. Prompt initiation within 72 hours of symptom onset has been associated with significant improvement versus delayed treatment, so rapid diagnosis and management are critical.

• #60 An unexpected case of Ramsay hunt syndrome: case report and literature review | BMC Research Notes | Full Text

  https://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-6-337

  Despite the absence of RCTs on RHS management, when considering the possibility of lifelong facial paralysis and hearing loss, experts recommend combination antiviral and corticosteroid therapy within the first 72 h of symptoms. […] Early intervention with antivirals and corticosteroids has shown to significantly improve outcomes in these patients.

• #61 Ramsay hunt syndrome- expect the unexpected: A case report – JOOO

  https://www.joooo.org/html-article/14915

  Ramsay Hunt syndrome is considered as an emergency condition and requires early diagnosis followed by management for a good prognosis and less long term adverse effects. Despite of diagnostic challenge, unilateral pattern of facial involvement and vesicular eruption helps in early diagnosis and differentiate the syndrome with diseases that mimicks other severe neurological diseases. The treatment should be initiated within 72 hours of the disease onset to prevent further morbidity. Antiviral therapy along with steroids should be initiated to prevent the disease progression, which lead to permanent neuronal damage.

• #62 An unexpected case of Ramsay hunt syndrome: case report and literature review | BMC Research Notes | Full Text

  https://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-6-337

  Despite the absence of RCTs on RHS management, when considering the possibility of lifelong facial paralysis and hearing loss, experts recommend combination antiviral and corticosteroid therapy within the first 72 h of symptoms. […] Early intervention with antivirals and corticosteroids has shown to significantly improve outcomes in these patients.

• #63 (PDF) Ramsay Hunt Syndrome: An Introduction, Signs and Symptoms, and Treatment

  https://www.academia.edu/105130298/Ramsay_Hunt_Syndrome_An_Introduction_Signs_and_Symptoms_and_Treatment

  Ramsay Hunt syndrome is the complication of the virus varicella-zoster and the infection caused by it, which shows apparent geniculate ganglion involvement. […] This article provides an overview of how the varicella-zoster virus causes facial paralysis and other neurological symptoms. […] Ramsay Hunt syndrome is characterized by herpetic lesions combined with peripheral facial nerve palsy. The disease is caused by a reactivation of the varicella zoster virus and can be deceiving since the herpetic lesions are not always present (zoster sine herpete) and might mimic other severe neurological illnesses. […] The main prognostic factor is the severity of the initial symptoms. […] Ramsay Hunt Syndrome (RHS), also called as Herpes Zoster Oticus, as well as, Shingles of the geniculate ganglion, is caused by reactivation of Varicella Zoster Virus (VZV) in the geniculate ganglia.

• #64 Ramsay Hunt Syndrome – A Diagnostic Dilemma – MedCrave online

  https://medcraveonline.com/JOENTR/ramsay-hunt-syndrome-ndash-a-diagnostic-dilemma.html

  The most recommended therapy for RHS is the combination of acyclovir and prednisone. Acyclovir is an effective antimicrobial agent against actively replicating herpes zoster viruses. […] Adjunctive steroid therapy can be helpful in the management of the facial paralysis of RHS. […] Advanced age, initial House-Brackmann grades V or more, time before commencement of treatment, associated metabolic diseases, impairment of the cochleovestibular, or other cranial nerves, oropharynx lesions, dry eye, and lagophthalmus must be assessed at the initial physical examination, since they suggest worse prognosis of the facial palsy secondary to Ramsay Hunt syndrome. […] To conclude, although patients with Ramsay Hunt syndrome have poorer prognosis than do those with Bells palsy, early combination therapy of steroids with antivirals within 3days of the onset of facial palsy is beneficial.

• #65 Ramsay Hunt Syndrome – A Diagnostic Dilemma – MedCrave online

  https://medcraveonline.com/JOENTR/ramsay-hunt-syndrome-ndash-a-diagnostic-dilemma.html

  The most recommended therapy for RHS is the combination of acyclovir and prednisone. Acyclovir is an effective antimicrobial agent against actively replicating herpes zoster viruses. […] Adjunctive steroid therapy can be helpful in the management of the facial paralysis of RHS. […] Advanced age, initial House-Brackmann grades V or more, time before commencement of treatment, associated metabolic diseases, impairment of the cochleovestibular, or other cranial nerves, oropharynx lesions, dry eye, and lagophthalmus must be assessed at the initial physical examination, since they suggest worse prognosis of the facial palsy secondary to Ramsay Hunt syndrome. […] To conclude, although patients with Ramsay Hunt syndrome have poorer prognosis than do those with Bells palsy, early combination therapy of steroids with antivirals within 3days of the onset of facial palsy is beneficial.

• #66 SciELO Brazil – Treatment and Prognosis of Facial Palsy on Ramsay Hunt Syndrome: Results Based on a Review of the Literature Treatment and Prognosis of Facial Palsy on Ramsay Hunt Syndrome: Results Based on a Review of the Literature

  https://www.scielo.br/j/iao/a/t886ttpTDLRTnJY7WC6QdrN/?lang=en

  Ramsay Hunt syndrome (RHS) is an infectious disease caused by the varicella zoster virus (VZV). The physiopathological mechanism is the reactivation of the VZV in the geniculate ganglion, with subsequent inflammation, edema, and compression of the VII cranial nerve. Viral demyelination may also contribute to further damage of the nerve. […] Treatment of RHS involves high doses of steroids and virostatic agents, especially acyclovir. […] The combination of steroids and acyclovir reached better recovery rates than steroids in monotherapy. […] Clinical data such as age, associated metabolic diseases, impairment of the cochleovestibular, or other cranial nerves, oropharynx lesions, dry eye, and lagophthalmus must be assessed at the initial physical examination, since they suggest worse prognosis of the facial palsy secondary to Ramsay Hunt syndrome.

• #67

  https://journals.lww.com/ijoo/fulltext/2021/27040/audiological_manifestations_of_ramsay_hunt.16.aspx

  Ramsay Hunt syndrome (RHS) Type II is characterized by facial paralysis, herpetic eruptions on the auricle/mouth, and otic pain due to reactivation of the latent varicella-zoster virus in the geniculate ganglion. […] Reactivation of latent varicella zoster in the geniculate ganglion is considered to be the pathogenesis of RHS. […] The clinical manifestation of RHS is vesicular rashes of the mouth or ear (around pinna or EAC); vesicular rashes might proceed with the onset of facial paresis, hearing loss, vertigo/dizziness, and tinnitus. […] As many as 90% of cases with RHS manifest vestibular disturbances, but auditory problems are rare. […] Sensorineural hearing loss is present in 10% of patients with RHS. […] In our case, the involvement of multicranial nerve (based on subjective assessment) might be the one reason for incomplete recovery. […] In addition, late diagnosis and treatment can also be the reason for poor recovery.

• #68 A Case of Ramsay Hunt Syndrome with Cranial Polyneuropathy

  https://www.ejao.org/journal/view.php?doi=10.7874/kja.2012.16.2.80

  The associated complications of cranial polyneuropathy might lead to life-threatening conditions such as a serious acute respiratory distress. Moreover, in case of widespread involvement of unilateral cranial nerves, the possibility of malignant infiltration or sarcoidosis should be considered. […] Although the beneficial evidence of antiviral therapy in RHS still remains controversial, more aggressive managements including systemic administration of antiviral agents might be required in cases of RHS with CP.

• #69 A Case of Ramsay Hunt Syndrome with Cranial Polyneuropathy

  https://www.ejao.org/journal/view.php?doi=10.7874/kja.2012.16.2.80

  The associated complications of cranial polyneuropathy might lead to life-threatening conditions such as a serious acute respiratory distress. Moreover, in case of widespread involvement of unilateral cranial nerves, the possibility of malignant infiltration or sarcoidosis should be considered. […] Although the beneficial evidence of antiviral therapy in RHS still remains controversial, more aggressive managements including systemic administration of antiviral agents might be required in cases of RHS with CP.

• #70 Ramsay hunt syndrome- expect the unexpected: A case report – JOOO

  https://www.joooo.org/html-article/14915

  Ramsay Hunt syndrome is considered as an emergency condition and requires early diagnosis followed by management for a good prognosis and less long term adverse effects. Despite of diagnostic challenge, unilateral pattern of facial involvement and vesicular eruption helps in early diagnosis and differentiate the syndrome with diseases that mimicks other severe neurological diseases. The treatment should be initiated within 72 hours of the disease onset to prevent further morbidity. Antiviral therapy along with steroids should be initiated to prevent the disease progression, which lead to permanent neuronal damage.

• #71 Ramsay hunt syndrome- expect the unexpected: A case report – JOOO

  https://www.joooo.org/html-article/14915

  Ramsay Hunt syndrome is considered as an emergency condition and requires early diagnosis followed by management for a good prognosis and less long term adverse effects. Despite of diagnostic challenge, unilateral pattern of facial involvement and vesicular eruption helps in early diagnosis and differentiate the syndrome with diseases that mimicks other severe neurological diseases. The treatment should be initiated within 72 hours of the disease onset to prevent further morbidity. Antiviral therapy along with steroids should be initiated to prevent the disease progression, which lead to permanent neuronal damage.

• #72 Early diagnosis and treatment of Ramsay Hunt syndrome: a case report | International Journal of Emergency Medicine | Full Text

  https://intjem.biomedcentral.com/articles/10.1186/s12245-024-00807-x

  RHS is relatively uncommon, with less than 1% of zoster cases involving the facial nerve and resulting in RHS. RHS is typically characterized by facial paralysis and a rash affecting the ear, predominantly in Hunts Zone, which includes the tympanic membrane, middle ear, and cavum conchae. Additional symptoms frequently reported include ipsilateral altered taste perception and tongue lesions, hearing abnormalities (such as decreased hearing, tinnitus, and hyperacusis), vestibular disturbances (such as vertigo), and lacrimation, though these symptoms do not necessarily coincide. […] Treatment for RHS includes symptom control, antiviral agents, and glucocorticoids. Elderly and immunocompromised patients are at increased risk for varicella-zoster virus reactivation and its complications. RHS has a high rate of complete recovery, with up to 70.4% of patients regaining facial nerve function, particularly with early medical treatment. Therefore, early identification and treatment of RHS are essential.

• #73 Early diagnosis and treatment of Ramsay Hunt syndrome: a case report | International Journal of Emergency Medicine | Full Text

  https://intjem.biomedcentral.com/articles/10.1186/s12245-024-00807-x

  RHS is relatively uncommon, with less than 1% of zoster cases involving the facial nerve and resulting in RHS. RHS is typically characterized by facial paralysis and a rash affecting the ear, predominantly in Hunts Zone, which includes the tympanic membrane, middle ear, and cavum conchae. Additional symptoms frequently reported include ipsilateral altered taste perception and tongue lesions, hearing abnormalities (such as decreased hearing, tinnitus, and hyperacusis), vestibular disturbances (such as vertigo), and lacrimation, though these symptoms do not necessarily coincide. […] Treatment for RHS includes symptom control, antiviral agents, and glucocorticoids. Elderly and immunocompromised patients are at increased risk for varicella-zoster virus reactivation and its complications. RHS has a high rate of complete recovery, with up to 70.4% of patients regaining facial nerve function, particularly with early medical treatment. Therefore, early identification and treatment of RHS are essential.

• #74 Ramsay Hunt Syndrome – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK557409/

  Ramsay Hunt syndrome, also known as herpes zoster oticus, is a late complication of varicella-zoster virus infection that results in inflammation of the geniculate ganglion of cranial nerve VII. […] Ramsay Hunt syndrome, also known as herpes zoster oticus or geniculate ganglion herpes zoster, is a late complication of varicella-zoster virus (VZV) infection, resulting in inflammation of the geniculate ganglion of cranial nerve VII. […] The causative agent in Ramsay Hunt syndrome is the varicella-zoster virus, a member of the human herpesvirus family. More specifically, it is part of the alphaherpesvirinae subfamily, along with herpes simplex viruses 1 and 2 (HHV-1 and HHV-2). VZV is a double-stranded DNA virus, more technically known as human alphaherpesvirus 3 (HHV-3). […] Initial infection with the varicella-zoster virus causes a disseminated vesicular rash with fever, known as chickenpox. During the acute phase of this infection, the virus is spread by respiratory droplets. After the viremia and exanthem have resolved, the virus can remain dormant in cranial nerves and dorsal root ganglia. During times of physiological stress or immunocompromise, reactivation of the virus within the distribution of the nerve in which it has been dormant can occur. In Ramsay Hunt syndrome, the virus lays dormant within the geniculate ganglion and primarily reactivates along the facial nerve, although other cranial nerves may be involved.

• #75 Ramsay Hunt syndrome | Radiology Reference Article | Radiopaedia.org

  https://radiopaedia.org/articles/ramsay-hunt-syndrome?embed_domain=hackmd.io%2525252F%25252540yipuafecsl2jsu8smr5njq%2525252Fbnjhjgjghjghjghfavicon.icofavicon.ico&lang=us

  Ramsay Hunt syndrome, also known as herpes zoster oticus or Ramsay Hunt syndrome type 2, is shingles of the facial nerve. It is due to reactivation of the varicella zoster virus (VZV) in the geniculate ganglion. […] The syndrome is due to latent infection of the geniculate ganglion with varicella zoster virus (VZV) and subsequent reactivation.

• #76 Ramsay Hunt Syndrome, Explained by Dr. Amit Kochhar – Pacific Neuroscience Institute

  https://www.pacificneuroscienceinstitute.org/blog/facial-pain/ramsay-hunt-syndrome-explained-by-dr-amit-kochhar/

  Ramsay Hunt syndrome is a form of virally-induced facial paralysis caused by reactivation of the herpes zoster virus, which is more commonly known as varicella zoster, the chickenpox virus. […] When this happens, the nerve can become inflamed within the bone that is supposed to protect it. When the nerve expands, the nerve can get crushed by bone, causing the nerve to stop functioning and leading to sudden onset facial paralysis. […] Ramsay Hunt syndrome is believed to occur during periods of high stress that can cause ones immune system to be suppressed. This can also occur if someone is taking immunosuppressive medications to artificially suppress the immune system as well.

• #77 Ramsay Hunt Syndrome: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/1166804-overview

  Ramsay Hunt syndrome is defined as VZV infection of the head and neck that involves the facial nerve, often the seventh cranial nerve (CN VII). Other cranial nerves (CN) may also be involved, including CN VIII, IX, V, and VI (in order of frequency). This infection gives rise to vesiculation and ulceration of the external ear and ipsilateral anterior two thirds of the tongue and soft palate, as well as ipsilateral facial neuropathy (in CN VII), radiculoneuropathy, or geniculate ganglionopathy. […] Subsequent reactivation of latent VZV can result in localized vesicular rash, known as herpes zoster. VZV infection or reactivation involving the geniculate ganglion of CN VII within the temporal bone is the main pathophysiological mechanism of Ramsay Hunt syndrome. Diminished level of VZV-specific cell-mediated immunity may lead to reactivation of this virus.

• #78 Ramsay Hunt Syndrome – A Diagnostic Dilemma – MedCrave online

  https://medcraveonline.com/JOENTR/ramsay-hunt-syndrome-ndash-a-diagnostic-dilemma.html

  Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth. Ramsay Hunt Syndrome (RHS) is a rare, severe complication of varicella zoster virus (VZV) reactivation in the geniculate ganglion. […] The VZV reactivation in the geniculate ganglia and subsequent neural inflammation, pressure, and possible destruction of the facial nerve in the temporal bone are suspected to cause facial palsy, while VZV migrates from the geniculate ganglia into the skin around the ear or into the oropharynx via the sensory fibers, where it replicates and produces zoster in RHS. […] The primary etiologic agent of RHS is VZV but Bell’s palsy, in contrast, has been attributed to herpes simplex virus type-1. […] Various associated complications include corneal abrasions and ulcers, if eye-lid closure is impaired, secondary infection with bacteria (cellulitis), Post herpetic neuralgia, as with other Varicella Zoster virus reactivations, permanent facial paralysis, and long term ipsilateral hearing loss and tinnitus.

• #79 Ramsay hunt syndrome- expect the unexpected: A case report – JOOO

  https://www.joooo.org/html-article/14915

  Ramsay Hunt syndrome is considered as an emergency condition and requires early diagnosis followed by management for a good prognosis and less long term adverse effects. Despite of diagnostic challenge, unilateral pattern of facial involvement and vesicular eruption helps in early diagnosis and differentiate the syndrome with diseases that mimicks other severe neurological diseases. The treatment should be initiated within 72 hours of the disease onset to prevent further morbidity. Antiviral therapy along with steroids should be initiated to prevent the disease progression, which lead to permanent neuronal damage.

• #80 An unexpected case of Ramsay hunt syndrome: case report and literature review | BMC Research Notes | Full Text

  https://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-6-337

  Despite the absence of RCTs on RHS management, when considering the possibility of lifelong facial paralysis and hearing loss, experts recommend combination antiviral and corticosteroid therapy within the first 72 h of symptoms. […] Early intervention with antivirals and corticosteroids has shown to significantly improve outcomes in these patients.

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