Herpes zoster ophthalmicus-induced oculomotor nerve palsyHerpes zoster ophthalmicus HZO dht post cycle cause a variety of ocular conditions including: Cranial nerve palsies caused by herpes zoster HZ are relatively uncommon clinical findings. Previous case reports have looked at corticosteroides oftalmicos pdf relationship, but corticosteroides oftalmicos pdf overall case studies are few. Other causes of nerve palsies typically need to be ruled out first with neuro-imaging and corticosteroides oftalmicos pdf evaluations. HZO is a reactivation of the childhood chicken pox virus varicella zoster along the ophthalmic division of the 5th cranial nerve CN V 1 which typically reveals itself as a vesicular rash or dermatitis. The varicella zoster virus VZV typically lies latent in the dorsal root ganglion of corticosteroides oftalmicos pdf and, corticosteroides oftalmicos pdf reactivated, travels down the associated dermatome of the nerve involved. If it affects another nerve it is referred to as shingles or just generic HZ.
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Herpes zoster ophthalmicus HZO may cause a variety of ocular conditions including: Cranial nerve palsies caused by herpes zoster HZ are relatively uncommon clinical findings.
Previous case reports have looked at this relationship, but the overall case studies are few. Other causes of nerve palsies typically need to be ruled out first with neuro-imaging and blood evaluations.
HZO is a reactivation of the childhood chicken pox virus varicella zoster along the ophthalmic division of the 5th cranial nerve CN V 1 which typically reveals itself as a vesicular rash or dermatitis. The varicella zoster virus VZV typically lies latent in the dorsal root ganglion of nerves and, if reactivated, travels down the associated dermatome of the nerve involved. If it affects another nerve it is referred to as shingles or just generic HZ. Patients typically present with an acute onset of a unilateral vesicular dermatitis along the CN V 1 dermatome which respects the midline.
The patient had been released from a local hospital the previous day. She presented with a complaint of soreness around her upper left eyelid and concomitant blurry vision in her left eye OS. The patient denied diplopia and decrease in vision in her right eye OD. Her ocular history was positive for cataracts in both eyes OU , and she was scheduled for cataract extraction in 1—2 months.
The patient's medical history was positive for hypertension, kidney problems, and a history of breast cancer. She reported taking carvedilol, nifedipine, furosemide, and a potassium pill for her hypertension and kidney issues.
She reported compliance with medications. She was oriented to time, place, and person. The patient's pupils were equal, round, and reactive to light, with no sign of an afferent pupillary defect APD OU. Ocular motility showed full range of motion with no pain on eye movement OU. Confrontation visual fields were full-to-finger-count OD, with only a mild superior field defect OS secondary to her ptosis and mild edema of the upper eyelid.
Anterior segment examination revealed clear lids and lashes OD, but upper eyelid ptosis with mild edema and crusted-over vesicles were evident OS. The palpebral and bulbar conjunctivae were white and quiet OU. Corneal examination was clear OD, but pseudo-dendrites were noted superior temporally along the corneal limbus OS, which stained with sodium fluorescein NaFl but did not with lissamine green stain.
The patient was negative for Hutchinson's sign. All other findings were unremarkable. Fundus examination was also unremarkable. The patient presented one week later with complaints of fluctuating vision and tearing OS as well as an increased ptosis of the left eyelid. The patient felt her vision had decreased since the previous visit, and both she and her daughter reported excellent compliance with oral and topical medication therapy. Pupil examination revealed mild anisocoria with the left pupil being slightly larger than the right.
The left pupil had a remarkably minimal response to light compared to the right and also showed a positive APD when a binocular indirect ophthalmoscope BIO was used to test pupils.
The patient's ocular motility was normal OD, but was restricted in down gaze OS. Gross confrontation visual fields were full-to-finger-count OD, but the superior visual field defect was still present secondary to the increased lid ptosis OS.
Slit lamp biomicroscopy was unremarkable OD except for moderate nuclear sclerosis and anterior cortical changes of the lens.
Her dilated fundus examination was performed with a 90D lens, and with BIO in conjunction with a 20D lens. The fundus examination was unremarkable OD, OS. This condition is also referred to Herpes Zoster Ophthalmoplegia. Due to the cranial nerve and pupil involvement, she was referred her to her primary care physician for a magnetic resonance angiogram MRA and a magnetic resonance imaging MRI to rule out other etiologies of cranial nerve involvement such as an aneurysmal compression of the oculomotor nerve or space-occupying lesion.
The patient presented eleven days after her initial visit and reported undergoing the recommended imaging four days prior; however, the results were not scheduled to be discussed until she saw her primary care doctor the following day.
The patient complained of worsening of her left lid ptosis as well as diplopia when she manually lifted her left lid to see Fig. Her pupils were anisocoric OS larger and were minimally reactive to light when tested with a BIO light source. External examination revealed a complete left lid ptosis. Upon further questioning, the patient reported feeling slightly more ill than previously as well as having jaw pain and scalp tenderness along her left side.
Based on these new findings and complaints, she was sent for work-up for both aneurysmal compression of the third cranial nerve and giant cell arteritis GCA , which included erythrocyte sedimentation rate ESR and C-reactive protein CRP blood work, as well as treatment with intravenous steroids. Upon discharge from the hospital the patient returned to our clinic five days later for follow-up two and a half weeks after initial presentation.
She reported feeling better and noticed slight reduction in the degree of her left ptosis. The patient brought her emergency visit records with her for us to review as well. The complete blood count CBC with differential proved virtually normal as well. However, her CD3 and CD4 white blood cell counts were low indicating a certain degree of immunosuppression. Thus, the hospital physicians scheduled her for consultation with a neurologist secondary to her history of breast cancer.
Gross confrontation visual fields were full-to-finger-count in the OD, while the superior visual field defect remained secondary to the lid ptosis OS. Her ocular motility was still full OD, but reduced in nasal, inferior, and superior gazes OS.
Her slit lamp examination revealed fully resolved corneal issues in the OS and otherwise normal anterior segments OU. Four weeks after her initial presentation, our patient reported improvement in her signs and symptoms. Her confrontation visual fields were unchanged from previous visits. Her ocular motility was still full OD and restricted OS, but definitely improving from previous visits. Adnexal examination revealed the on-going ptosis OS, but the remaining components of the slit lamp examination were normal OU with the exception of the lenticular changes previously noted.
The patient was released and asked to return for follow-up after her neurology consult in 2 weeks. The patient returned 2 weeks after her consultation with the neurologist seven weeks after her initial presentation. The neurologist agreed with our diagnosis of oculomotor nerve palsy most likely induced by the HZO outbreak.
Her ocular motility had dramatically improved, yet a residual ptosis was still noted OS, though it had improved from previous visits Fig. Again, her slit lamp examination was within normal limits except for the on-going lenticular changes OU. The patient was told to keep her follow-up appointment with her neurologist and to follow up with us in 4—6 weeks to monitor for anticipated continuing improvement in ocular motilities.
Six months after the patient's initial presentation, her ptosis OS had resolved and she regained full ocular motilities. She is currently being followed every six months and denies ocular problems other than persistent irritation and tingling around her left eye.
Nine diagnostic action fields of gaze demonstrating improvement in EOMS of the left eye. A cranial nerve III palsy results in adduction and vertical ocular motility deficits when the entire nerve is implicated and the pupil can be involved as the pupillary fibers course through cranial nerve III. Causes are varied and can include space-occupying lesions, microvascular infarctions, aneurysmal compressions, inflammation, infections, and trauma.
Our patient initially showed anisocoria, ptosis, and restricted down gaze, which was suggestive of a partial cranial nerve III palsy. Two weeks after her initial presentation, she showed a positive APD, increased ptosis, and restricted extraocular motilities suggestive of a complete CN III palsy.
The patient's ophthalmoplegia and ptosis continued after the resolution of her cutaneous lesions and keratitis. Secondary to the ophthalmoplegia, the patient was treated with intravenous and oral steroids. Over the course of six months, the patient's signs and symptoms improved markedly.
Six months after the onset of HZO, she had fully recovered from the ophthalmoplegia. There are various ocular sequelae with HZO, some more common than others. On an average, HZO-induced ophthalmoplegia occurs 9. Ophthalmoplegia has been reported to occur concurrently with the HZO outbreak, although this is not the normal presentation.
Treatment of HZO has historically been with oral antiviral agents and consists of: One study by Theil et al. This finding suggests that the triggering of the nerve palsies is in the cranial nerve nuclei and most likely occurs further downstream in the nerve conduction pathway. In general, the pathophysiology of HZO is believed to be derived from different components: The patient's blood sugar was monitored regularly as elevated blood sugar is a known side effect of systemic steroids and has been reported to be a common cause of drug-induced diabetes mellitus.
However, for our patient, it was not needed due to the ptosis preventing diplopia. One of the most common complications of any herpes zoster outbreak is PHN and treatment success remains moderate at best. Topical agents such as lidocaine patches or capsaicin creams have been shown to have some efficacy. We will continue to monitor our patient for PHN, along with her neurologist, and if any lingering pain occurs we plan to refer her to either the neurologist or a pain specialist for PHN therapy.
A newer treatment to reduce the risk of HZ is via vaccination with a drug known as Zostavax. Due to the success of this vaccination, medical professionals may recommend Zostavax for patients older than 50 years of age. Vaccination is not necessary for those individuals who have already experienced a HZ outbreak as that event parallels exactly what the vaccine would do by boosting the immune system.
Re-activation of a second HZ event is very unlikely for this same reason. As with any condition that can have many causes, timely referral, imaging, and blood work are important when a cranial nerve palsy is diagnosed, to rule out possible life-threatening conditions. Once these conditions were ruled out then we could be more confident that our patient's signs and symptoms were secondary to HZO-induced ophthalmoplegia, for which our patient fits the typical timeline, signs, and symptoms.
The jaw pain and scalp tenderness that our patient complained of often associated with GCA , was most likely related to PHN. PHN can affect the branches of the trigeminal nerve that are sensory to the same areas CN V1, V2, V3 and is the most common complication for individuals who have experienced HZO attacks. Blood work revealed lowered CD3 and CD4 counts in our patient signaling a certain degree of immunosuppression, which was most likely the inciting event of the original HZO outbreak.
Immunosuppression is also a very common finding in individuals suffering from HZ outbreak. This case demonstrates the relatively uncommon ophthalmoplegia induced by HZO, and the importance of co-management between health care practitioners.
National Center for Biotechnology Information , U. Journal List J Optom v. Published online Sep Received Jul 10; Accepted Aug