Linda Sternau

Ischemia-Induced Neurotransmitter Release: Effects of Mild Intraischemic Hyperthermia

Small differences in intraischemic brain temperature can significantly affect the neuropathological and functional outcome following transient global forebrain ischemia. Lowering intraischemic brain temperature by 2–3°C in the rat prevents the delayed neuronal damage that typically occurs in zones of selective vulnerability following 20 minutes of ischemia (Busto et al, 1987), and improves the behavioral outcome following a 10 min insult (vanDijk et al, 1991). Conversely, raising the intraischemic brain temperature to 39°C significantly worsen ischemic outcome and increased the vulnerability of resistant brain areas (Dietrich et al, 1990a). The protective effect of intraischemic hypothermia was not associated with the reduction in the degree of ischemia as reflected by the magnitude of energy metabolites depletion or cerebral blood flow recluction (Busto et al, 1987; Busto et al, 1989), suggesting that Some other mechanism prevails.

Temperature Modulation of Neuronal Injury

The concept of altering the body temperature to achieve a therapeutic result in an injured brain is not new. Much has been written, both in the experimental and clinical literature, on therapeutic hypo- and hyperthermia. The protective effect of profound hypothermia (30°C or less) has been well established during cardiac and intracranial surgical procedures necessitating interruption of blood flow to the brain. Hypothermia has also been and continues to be used in the head-injured patient for the control of increased intracranial pressure that is refractory to hyperventilation, ventricular drainage, osmotherapy, and barbiturates. Conversely, the adjunctive chemotherapeutic effect of selective brain tumor hyperthermia remains under intense investigation.

Neuro-ophthalmic manifestations of fungal disease associated with posthurricane environment.

Background: Allergic fungal sinusitis (AFS) is thought to represent an immunologic response to exposure to dematiaceous fungi. These fungi are known to cause disease more frequently in hot and humid climates and seasons. Methods: Three patients presented with unusual manifestations of fungal disease after exposure to environments recently affected by hurricanes. Results: Two patients had AFS, 1 with gradual painless visual loss from an AFS mass extending into the suprasellar region and 1 with orbital apex syndrome. Another patient had invasive fungal disease and developed orbital apex syndrome. Conclusions: These cases underscore the importance of clinical recognition of fungal disease in patients with sinus, orbital, or skull base involvement as well as its potential for causing permanent visual loss. This report suggests a potential association between fungal disease and tropical storm exposure.

Primary dural lymphoma masquerading as a meningioma.

A 39-year-old woman noted progressive blurred vision in the right eye for 1 year. The right eye had visual acuity of 20/25, an afferent pupillary defect, pale optic nerve, and cecocentral scotoma. Magnetic resonance imaging findings were consistent with en plaque meningioma of the planum sphenoidale, which encircled the right optic nerve at the optic canal. The tumor was internally debulked to preserve the optic nerve. Histopathologic and molecular analysis revealed a low-grade B-cell lymphoma. Further evaluation showed no evidence of systemic disease. Primary dural lymphomas are a distinct entity that may mimic meningioma and cause vision loss.

A 44-year-old Man With Bilateral Optic Neuropathy, Optic Nerve Sheath Enhancement, and Cardiac Dysfunction

A 44-year-old man presented to the emergency department with progressive painless vision loss in the right eye for 3 months. Visual acuity was 4/200, right eye and 20/ 20, left eye with a right relative afferent pupillary defect. Automated perimetry revealed a central scotoma in the right eye and was normal in the left eye. The remainder of the examination was normal with the exception of slight elevation of the right optic disc (Fig. 1). Brain and orbital magnetic resonance imaging (MRI) was performed.

TB or Not TB? That is the Question.

A 36-year-old man was evaluated in the emergency department with severe headaches, bilateral leg numbness, and bilateral decreased vision. Headaches, neck stiffness, and intermittent blurry vision had begun 6 months earlier, at which time brain magnetic resonance imaging (MRI) with contrast was unremarkable. Symptoms slowly progressed and 1 month before presentation, while on vacation in Ecuador, the patient had a prolonged generalized seizure requiring intubation, after which he was discharged without antiepileptic medication. The patient’s medical history was significant for a Bacillus Calmette–Guérin (BCG) vaccination as a child in Ecuador. He emigrated to the United States at age 19 years. In 2005, he had a positive purified protein derivative test for tuberculosis (TB) but a negative chest x-ray. In 2011, he developed pleuritic chest pain and chest radiography showed a 3-cm cavitary lung lesion in the right upper lobe. He was diagnosed with active pulmonary TB and completed treatment in 2013, 4 months before the onset of initial neurological symptoms. On examination, the patient was drowsy but arousable to verbal stimuli and oriented to person, place, and time. Visual acuity was light perception in each eye and pupils reacted sluggishly to light. Ocular versions were full, with an exotropia of 30 prism diopters. Ophthalmoscopy showed bilateral optic disc edema. Strength was reduced in all limbs. There was less response to painful stimuli in the lower extremities than in the upper extremities. Reflexes were 2+ and symmetric with absent Hoffman and Babinski signs. Differential diagnosis included an intracranial mass lesion, vasculitis involving the central nervous system (CNS), encephalopathy of toxic, nutritional, infectious, or inflammatory etiology, or a meningeal process of infectious, inflammatory, or neoplastic etiology. A repeat brain MRI was performed with and without contrast. A lumbar spine MRI also was performed. Dr. Schatz:

Optic Nerve Involvement From Pseudomonas aeruginosa –Associated Skull Base Osteomyelitis

prevalence of infection in children and young adults (up to 40% in children), and reports of outbreaks are common in closed populations such as those of military recruits and college students. All 3 patients in our series presented to our service within a 2-month period, and 2 of the patients were college students. Although permanent vision loss from optic papillitis has been previously reported, all 3 of our patients recovered their baseline visual acuity within 1 month of treatment. M pneumoniae contains both glycolipid and protein antigens that elicit antibody responses in infected individuals. Circulating immune complexes have been found in the serum of patients with M pneumoniae–associated pneumonia, and this type III hypersensitivity reaction is believed to cause microvasculitis from immune complexes depositing along vessel walls in the eye. Another mechanism by which Mycoplasma infection is thought to cause uveitis is through direct invasion of the bacteria in the anterior chamber. The most common method for diagnosing Mycoplasma infect ion is through serology testing for IgM and IgG antibodies. Direct polymerase chain reaction analysis is still not widely available, and a culture of M pneumoniae takes up to several weeks. The enzyme-linked immunosorbent assay test used at our institution has a sensitivity and specificity of 94.5% and 87.5%, respectively. There have been only 5 reported cases in the literature of anterior uveitis secondary to M pneumoniae (Table). In 3 of the 5 cases, concomitant findings of bilateral optic disc edema and anterior uveitis were reported, but those patients had normal retinal findings. Case 2 in our series is, to our knowledge, the first case of uveitis from M pneumoniae associated with bilateral macular and peripapillary serous detachments, but perhaps this is a more severe presentation along the same clinical spectrum of inflammatory disease. Of our 3 patients, only the 20-yearold man who presented with a 1-month history of blurry vision (case 1) had pneumonia secondary to his infection, which underscores the fact that extrapulmonary involvement can occur even in the absence of clinically overt respiratory tract disease. We hope that our case series will help highlight this common human pathogen as a cause of uveitis and papillitis, and we believe that M pneumoniae should be included in the differential diagnosis when a young and otherwise healthy person presents with uveitis or optic disc edema preceded by a febrile illness.