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Chronic traumatic encephalopathy (CTE) is an acquired primary tauopathy with a variety of cognitive, behavioral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetitive traumatic brain injury (TBI). No definitive clinical diagnosis for this condition exists. In this work, we used [F-18]FDDNP PET to detect brain patterns of neuropathology distribution in retired professional American football players with suspected CTE (n = 14) and compared results with those of cognitively intact controls (n = 28) and patients with Alzheimer's dementia (AD) (n = 24), a disease that has been cognitively associated with CTE. [F-18]FDDNP PET imaging results in the retired players suggested the presence of neuropathological patterns consistent with models of concussion wherein brainstem white matter tracts undergo early axonal damage and cumulative axonal injuries along subcortical, limbic, and cortical brain circuitries supporting mood, emotions, and behavior. This deposition pattern is distinctively different from the progressive pattern of neuropathology [paired helical filament (PHF)-tau and amyloid-ß] in AD, which typically begins in the medial temporal lobe progressing along the cortical default mode network, with no or minimal involvement of subcortical structures. This particular [F-18]FDDNP PET imaging pattern in cases of suspected CTE also is primarily consistent with PHF-tau distribution observed at autopsy in subjects with a history of mild TBI and autopsy-confirmed diagnosis of CTE.

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Cerebral aspergillosis is a rare and highly fatal infection that mainly affects immunocompromised patients. We report on a case of a heart transplanted Caucasian man, who arrived at our hospital because of the onset of diplopy. We performed a broad diagnostic work-up: the brain MRI showed a single ring-enhancing thalamo-mesencephalic area suggestive of abscess lesion; cerebrospinal fluid (CSF) analysis disclosed galactomannan and beta-D-glucan antigens. Thus the antifungal therapy was immediately started. We decided to discontinue the therapy 16 months later because of severe hepatic toxicity, given that the patient was persistently asymptomatic, brain imaging showed a progressive resolution of the abscess area and CSF antigen analysis was persistently negative. The follow-up at three months was unchanged.

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We describe a case of brainstem infection by Listeria monocytogenes with right oculomotor palsy and lip drop, facial hypoesthesia, left arm paresthesia, positive blood culture, and sterile liquor in a 63-year-old man. Magnetic resonance imaging revealed an isolated mesencephalic lesion. Localization of this kind accounted for 3% of 111 cases reviewed.

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Parkinsonism has been associated with HIV/AIDS and cerebral cryptococcal disease, but to date there has been no report of histological cryptococcal lesions in the substantia nigra (SN) in a patient with parkinsonism. We report on a case of a 63-year-old man who presented with tremor, gait disturbance, and mask-like facies, and showed cryptococcal meningoencephalitis with cryptococcal abscesses in the SN at autopsy, without Lewy bodies or significant degeneration of the SN neurons. Parkinsonism also represented the first manifestation of AIDS in this previously undiagnosed patient. This case highlights the importance of considering infectious etiologies in patients presenting with parkinsonism, and underscores the need for autopsy in evaluation of patients with new or unexplained movement disorders. Movement disorders in association with AIDS and mesencephalic mass lesions are discussed.

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The label Holmes' tremor defines a rare symptomatic movement disorder frequently occurring with midbrain damage. It appears at rest and worsens adopting a posture and on attempting movements. We describe the case of a patient with Holmes' tremor due to a presumed Toxoplasma abscess of the midbrain. The positive response to a combined therapy with levodopa and isoniazid is also reported.

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The paper describes the most infrequent case of cryptococcal granuloma of the midbrain in a HIV-negative female patient aged 41 years. The patient with midbrain lesion without signs of meningitis was found to have a bulky midbrain opercular formation that was regarded as a nodal glioma. The diagnosis of cryptococcal granuloma was established after removal of the formation (via occipito-transtentorial access with dissection of the lamina tecti) and pathomorphological examination. Microbiological studies verified the diagnosis. Despite the initiation of specific treatment with amphotericin B, the patient died on day 12 following surgery for cryptococcal meningoencephalitis.

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In following a formerly successful protocol designed to produce antibodies to A. fumigatus (Fres) we observed a disseminated, lethal fungal infection in healthy, specific pathogen-free (SPF) rabbits. The pathomorphological findings included multiple miliary to avenaceous whitish nodules in the livers and kidneys, mycotic mesencephalitis, nephritis, hepatitis, myocarditis, hemorrhagic enteritis, and splenitis. The hyphae were surrounded by necrosis, which also occurred in the liver without the hyphae. Comparative gas chromatographic and metabolic investigations on this strain and some environmental A. fumigatus strains showed significant differences. The findings are discussed with particular reference to the pathogenicity of A. fumigatus.

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Several viruses, including mouse hepatitis virus strain JHM (MHV-JHM), enter the brain after intranasal inoculation and spread transneuronally to other parts of the central nervous system (CNS). Both the olfactory and trigeminal nerves innervate the nasal cavity and are potential portals of virus entry into the CNS. To evaluate the relative importance of each nerve for MHV infection, mice were infected under conditions that discriminated between trigeminal and olfactory nerve entry. When olfactory nerve entry was selectively eliminated by surgical removal of both olfactory bulbs or by chemical destruction of the olfactory epithelium, MHV-JHM spread into the CNS was completely prevented. On the other hand, direct inoculation into the olfactory bulb, which eliminates all entry via the trigeminal nerve, had no effect on the pattern of virus infection. Thus MHV-JHM enters the CNS via the olfactory nerve after intranasal inoculation while entry via the trigeminal nerve is an insignificant part of this process.

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The attachment to and penetration of endothelial cells in the pons and midbrain (especially the substantia nigra) regions of the brains of BALB/c mice by log-phase Nocardia asteroides GUH-2 cells were determined by both scanning and transmission electron microscopic analysis. Within 15 min after exposure, the nocardiae attached to the surface of the endothelial cell membrane. This attachment occurred primarily at the growing tip of the nocardial filament, and the outermost layer of the nocardial cell wall had regions (electron-dense areas) that bound firmly to the cytoplasmic membrane of the host cell. There appeared to be specificity for this binding localized within the capillaries and arterioles because some regions had large numbers of bacteria bound, whereas adjacent areas had no bacterial cells. Nocardial filaments that attached by the apex induced a cuplike deformation of the endothelial cell membrane. This was followed by a rapid penetration of the endothelial cell so that within 25 min many of the bacteria were internalized within the host cell. These internalized bacteria remained within vesicles, and there was no ultrastructural evidence of damage to the nocardial cell during this process. Heat-killed GUH-2 cells still attached to endothelial surfaces (at a reduced frequency), but they did not penetrate into the endothelial cell. These data suggest that brain-invasive nocardiae possess both an adhesin for attachment to the membrane of endothelial cells and an invasion factor that promotes nocardial penetration of these cells.

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Herpes simplex virus (HSV) infection induces numerous electrophysiological and microscopic changes in neurons in vitro. To investigate the effect of HSV infection on in vivo neuronal activity, we induced an acute, latent and reactivated HSV infection of the trigeminal ganglia of guinea pigs through orofacial HSV inoculation and studied its effect on the trigeminal jaw-opening reflex of anesthetized guinea pigs. During the acute viral infection period both the threshold for elicitation of the reflex, and the latency to the onset of the reflex response were increased. During the latent viral infection in the trigeminal ganglia, the jaw-opening reflexes in the viral infected animals were not different from those of non-infected control animals. However, reactivation of the latent viral infection in these animals resulted in increases in both the threshold and latency of the jaw-opening reflex. These changes were similar to those found in animals with the acute viral infection. These results indicate that acute or reactivated latent HSV infection of the nervous system results in functional changes in the reflex pathways involving the trigeminal gasserian ganglia and brainstem neurons harboring infectious HSV-1.

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