Third Cranial Nerve Palsy in the Setting of Chikungunya Virus Infection.

We report the case of a 62-year-old patient who developed an acute painless isolated left third cranial nerve palsy sparing the pupil in the setting of an acute chikungunya infection. The patient had no significant medical history. Specifically, he had no vascular risk factors. Ocular involvement in chikungunya fever is uncommon. The potential virus- and infection-related mechanisms of this third cranial nerve palsy are discussed.

Painful ophthalmoplegia with simultaneous orbital myositis, optic and oculomotor nerve inflammation and trigeminal nucleus involvement in a patient with herpes zoster ophthalmicus.

Viral infection is a rare cause of painful ophthalmoplegia. We report on a 67-year-old patient who developed painful double vision after a vesicular skin rash on the left forehead. MRI disclosed simultaneous inflammatory lesions in all extraocular muscles, the second and third cranial nerve, as well as pathological signal intensity along the spinal trigeminal tract and nucleus within the medulla oblongata and the pons. Cerebrospinal fluid and serum tests for varicella zoster were positive. The patient was treated effectively with intravenous acyclovir and methylprednisolone. Simultaneous lesions in various neighbouring neural structures may be characteristic for the highly neurotropic behaviour of the herpesviridae and should be considered as a cause of painful ophthalmoplegia that can be depicted by appropriate imaging.

Prevalence and distribution of HSV-1, VZV, and HHV-6 in human cranial nerve nuclei III, IV, VI, VII, and XII.

The etiology of idiopathic cranial nerve palsies often remains unresolved. It has been hypothesised that viral reactivation of herpesviruses in the corresponding nuclei in the brainstem is the cause. We investigated the distribution of herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) in nuclei that are associated with peripheral sensory ganglia [oculomotor (nIII), facial (nVII) nuclei] and in nuclei that are not associated with peripheral sensory ganglia [trochlear (nIV), abducens (nVI), and hypoglossal (nXII) nuclei] of five human brainstems. Samples of the cranial nerve nuclei and adjacent control tissue were taken from histological sections after precise identification of every single nucleus and control tissue. DNA and RNA amplification methods were used to determine the prevalence and distribution of HSV-1 and VZV. The distribution of human herpes virus type 6 (HHV-6) was also determined and served as a control, since HHV-6 infection has never been associated with idiopathic cranial nerve palsies. HSV-1 was distributed at random in all cranial nerve nuclei and control tissue, whereas VZV DNA was not detected in any of the samples examined. Surprisingly, HHV-6 was present in almost all samples where HSV-1 was also present, however, the latency associated transcript (LAT) of HSV-1 was not found in any of the samples positive for HSV-1 DNA. The absence of LAT in the samples positive for HSV-1 and the distribution of HSV-1 and HHV-6 do not support the hypothesis that idiopathic cranial nerve palsies result from viral reactivation in the brainstem nuclei.

Rapid spread of a neurovirulent strain of HSV-1 through the CNS of BALB/c mice following anterior chamber inoculation.

Following uniocular anterior chamber (AC) inoculation of BALB/c mice with the KOS strain of herpes simplex virus type 1 (HSV-1), virus spreads from the injected eye to the ipsilateral suprachiasmatic nucleus (SCN) in the central nervous system (CNS) to infect the optic nerve and retina of the contralateral eye, and mice develop retinitis in that eye only. In contrast, after AC inoculation of BALB/c mice with the H129 strain of HSV-1, mice develop bilateral retinitis. The pathway(s) by which H129 spreads to cause bilateral retinitis is not known. To determine the route and timing of H129 spread after AC inoculation, BALB/c mice were injected in the AC of the right eye with 5 x 10(3) PFU of H129. Brains from 30 mice were sectioned on a brain matrix and the amount of virus in the brain and eyes was determined by plaque assay. Frozen sections were prepared from the eyes, brain, and trigeminal ganglia of an additional 30 mice, and HSV-1 antigen was detected by immunohistochemistry. After AC inoculation, H129 follows a pathway similar to KOS in the CNS, but H129 appears to spread more rapidly than KOS within the CNS. Unlike KOS, H129 is able to infect brain stem nuclei and H129-infected mice developed neurological impairments in addition to bilateral retinitis. The results of these studies suggest that the ability of H129 to spread rapidly in the CNS allows early virus infection of retino-recipient nuclei proximal to the contralateral and ipsilateral optic nerves. Early infection of retino-recipient nuclei, such as the SCN may allow virus to spread into the retinas before a virus-specific immune response can be induced.