Further study is needed to determine the safest mode of delivery and anesthetic management for parturients with ventriculoperitoneal shunts (VP). Prior recommendation for delivery in women with ventriculoperitoneal shunts was cesarean delivery. However, both vaginal delivery and neuraxial anesthesia have been shown to be safe in women with appropriately functioning VP shunts. We present a case series of parturients with VP shunt. Parturients with VP shunts were identified and VP shunt placement indications, neurologic symptoms during pregnancy, delivery mode, anesthetic type, and postpartum complications were reviewed. Forty patients were identified, and fifteen women with twenty deliveries were included. Two women experienced neurological symptoms during pregnancy and one required postpartum shunt revision for blurry vision and ataxia. There were ten cesarean deliveries and ten vaginal deliveries (eight normal spontaneous, one vacuum assisted, and one forceps assisted). Assisted vaginal deliveries were performed to decrease Valsalva including the patient with neurological symptoms related to shunt malfunction. Of the vaginal deliveries, six (60%) had epidural analgesia. Anesthesia for cesarean delivery included neuraxial anesthesia (n = 5) and general anesthesia (n = 5). In our cohort, women with VP shunt received neuraxial blockade without complication. Neuraxial techniques should be offered to women with appropriately functioning VP shunt.

UNASSIGNED: Bare lymphocyte syndrome type II (BLS II) is a rare form of severe combined immunodeficiency caused by mutations in the CIITA gene, which regulates major histocompatibility complex class II (MHC II) expression.
UNASSIGNED: We report the case of a Saudi boy with a novel mutation in the CIITA gene who presented with acute and late meningoencephalomyelitis, resulting in severe neurodevelopmental regression.
UNASSIGNED: We reviewed the patient\'s clinical and laboratory data obtained from medical records and performed a literature search on BLS II.
UNASSIGNED: The patient presented with acute meningoencephalomyelitis confirmed by MRI findings and was later found to carry a homozygous pathogenic variant in the CIITA gene p.(Leu473Hisfs*15). The patient had no MCH II expression, confirming the genetic diagnosis of autosomal recessive BLS II. Surprisingly, the patient\'s prior clinical history was unremarkable for significant infections or autoimmunity.
UNASSIGNED: We report a case with a novel CIITA gene mutation presenting atypically with a late and isolated severe infection. Isolated severe meningoencephalomyelitis may be a manifestation of primary immunodeficiency.

Lafora disease is a rare inherited neurodegenerative disease with onset in adolescence. Patients present with progressive myoclonic seizures and cognitive decline. The disease is linked to mutations in either of the two genes encoding malin and laforin, and it is associated with the accumulation of polyglucosan inclusions (Lafora bodies [LBs]) in various tissues, such as brain, liver, muscle, and skin, with the skin being particularly accessible for biopsy. Histopathologic examination of affected tissue with demonstration of LBs, together with the presence of pathologic mutation in EPM2A or NHLRC1 genes, is sufficient for diagnosis of this neurologic disorder when clinically suspected. Here, we report the case of a 16-year-old female with progressive neurologic symptoms and homozygous mutation in the NHLRC1 gene encoding malin. The skin biopsy was instrumental in reaching the final diagnosis by showing LBs in sweat glands by histopathologic and electron microscopic examination.

OBJECTIVE: To describe the clinical presentation, treatment, and clinical outcome of horses with ocular disease and evidence of systemic or ocular Lyme disease.
METHODS: Five horses met the inclusion criteria of ocular disease with evidence of B burgdorferi present in ocular or CNS tissues.
METHODS: The goal of this study was to describe the clinical presentation and progression of ocular disease when associated with ocular or CNS B burgdorferi infection in horses. A retrospective review of medical records was performed on horses admitted for ocular disease with evidence of B burgdorferi infection between 1998 and 2015. The diagnosis of B burgdorferi-associated uveitis was based on histopathologic lesions of lymphohistiocytic and suppurative uveitis/endophthalmitis and intralesional argyrophilic spirochetes in either ocular or CNS tissue consistent with Borrelia. Leptospiral uveitis was ruled out by PCR.
RESULTS: All five horses in the current study had intraocular inflammation at the time of presentation. Medical management with anti-inflammatories was successful in controlling uveitis in the two horses in which treatment of uveitis was attempted. Systemic treatment with oral tetracyclines was unsuccessful in a single case in which treatment of Borrelia was attempted. Four horses were euthanized due to progression of neurologic disease. The surviving horse had an enucleation performed and did not show systemic signs.
CONCLUSIONS: Infection with Borrelia burgdorferi should be considered in endemic areas as a differential for horses with ocular disease, in particular, uveitis. The prognosis for uveitis and neurologic disease associated with Lyme disease was poor in the current study.

BACKGROUND: Intracranial abscess formation is an extremely rare and sporadically documented disease in South American Camelids (SACs). Herein we report the first case of otogenic brain abscess formation in this species.
METHODS: A 4 years old female alpaca was presented to our veterinary hospital with a 6 month history of neurologic disorder symptoms, mainly head tilt to the right and emaciation. A comprehensive workup (ultrasound and computed tomography) revealed irreversible cranial nerve abnormalities, extensive lesions in the region of external, middle and internal right ear including destruction of bony structures (tympanic bulla, parts of temporal bone) and severe brain deformation caused by an intracranial abscess. The lesion was up to 6x7x4 cm and occupying almost 40% of the cranial cavity. No pathological findings were evident in other organs or structures. The late referral of the alpaca at this advanced stage of destructive disease precluded surgical intervention.
CONCLUSIONS: This case report describes the clinical signs, diagnostic procedures and pathological findings in an adult female alpaca suffering from cranial nerve abnormalities caused by a massive otogenic brain abscess. Camelids suffering from otitis may not present with clinical signs until the pathology is severe. The importance of considering intracranial abscess formation as differential diagnosis in SACs showing the merest hint of nerve deficits cannot be emphasized enough in order to diagnose such pathological processes at an early and treatable stage.