Early endovascular management of oculomotor nerve palsy associated with posterior communicating artery aneurysms.

Palsy of the third cranial nerve (oculomotor nerve, CNIII) is a well-known clinical presentation of posterior communicating artery (P-com) aneurysm. We report a series of 11 patients with partial or complete third nerve palsy secondary to P-com aneurysm. All were treated with endovascular embolization within seven days of symptom onset. Third nerve palsy symptoms resolved in 7/11 (64%), improved in 2/11 (18%) and did not change in 2/11 (18%) patients.

Novel microcatheters for selective intra-arterial injection of fluid in the rat brain.

BACKGROUND AND PURPOSE: The internal carotid artery (ICA) in the rat has a single extracranial branch, which supplies the muscles of mastication. The rat ICA also has multiple intracranial branches including (from proximal to distal): multiple small perforating arteries which supply the hypothalamus and the anterior choroidal artery which supplies the choroid plexus and part of the basal ganglia. At the ICA terminus, the vessel bifurcates into the anterior and middle cerebral arteries. The purpose of this study was to demonstrate selective injection of ICA branches in the rat. MATERIALS AND METHODS: Microcatheters (mucath1 and mucath2) were fabricated by plugging the tip of 169-mum outer diameter polyimide tubing and perforating the sidewalls. A 450-mum polydimethyl-siloxane cylinder was affixed to the distal tip of mucath2 but not mucath1. We evaluated the territory of mucath1 injection ex vivo using magnetization-prepared rapid acquisition of gradient echo MR imaging of brain specimens injected at necropsy. Territories of mucath1 and mucath2 injection were evaluated in vivo with dynamic susceptibility-weighted contrast-enhanced MR imaging. The territory of mucath2 also was evaluated in vivo with fused static microPET/T1 MR images performed after [(18)F] fluorodeoxyglucose ((18)FDG) injection. We evaluated additional catheterized and injected animals at 48 hours using physical examination, T2 MR images, and postmortem brain histologic specimens. RESULTS: Gadolinium-diethylene-triamine pentaacetic acid (Gd-DTPA) and (18)FDG injected through mucath1 selectively opacified the ipsilateral cerebral hemisphere, with no contralateral opacification. Gd-DTPA injected through mucath2 selectively opacified the territories of the hypothalamic perforating arteries, and anterior choroidal artery. There was no iatrogenic complication 48 hours after 20- to 25-minute injections performed with mucath1 or mucath2. CONCLUSIONS: We have developed 2 microcatheters which can be placed in the ICA for selective injection of its branches. One microcatheter selectively injects the ipsilateral cerebral hemisphere. The other selectively injects only the hypothalamus and lateral thalamus.

Hippocampal synaptic dysfunction in a murine model of human immunodeficiency virus type 1 encephalitis.

Alterations in hippocampal physiology affect cognition in human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD). The mechanism for how this occurs is not well understood. To address this, we investigated how changes in synaptic transmission and plasticity are affected by viral infection and macrophage activation using a severe combined immunodeficiency mouse model of human HIV-1 encephalitis (HIVE). HIVE was induced in mice by stereotactic injection of HIV-1-infected human monocyte-derived macrophages (MDM) into the striatum. Animals were sacrificed after 3, 7 and 15 days. Hippocampal slices were prepared from HIV-1, MDM- and sham-injected animals. Electrically evoked field excitatory postsynaptic potentials were recorded in the CA1 region of the hippocampus. Neuronal physiology was assessed by input-output and by long-term potentiation (LTP) assays. We observed that a higher stimulation intensity (mA) was required to induce a 1-mV response in the HIVE mice (0.32+/-0.06) compared with shams (0.17+/-0.01) at day 7. The stimulation intensities at day 15 were 0.44+/-0.07 and 0.23+/-0.05 in the HIVE and shams, respectively. An impairment of synaptic function was detected through measuring synaptic responses induced by stimuli with different intensities. Paired-pulse facilitation (PPF) showed deficits in HIVE mice at days 3, 7, and 15. At day 3, PPF ratios were 1.13+/-0.02 and 1.24+/-0.04 in HIVE and sham. The induction and maintenance of LTP was also impaired in HIVE mice. The average magnitude of LTP was 131.23+/-15.26% of basal in HIVE as compared with sham animals of 232.63+/-24.18%. MDM-injected mice showed an intermediate response. Taken together, the results show a range of neuronal synaptic transmission and plasticity changes in HIVE mice that may reflect the mechanisms of cognitive dysfunction in human HAD.

Model systems for assessing cognitive function: implications for HIV-1 infection and drugs of abuse.

Memory deficits are common among drug abusers and in those with chronic neurodegenerative disorders. Currently, the mechanisms through which diverse neurophysiologic processes alter memory are not known. This review describes the current systems and rationale for studying memory formation, consolidation, and recall. Special attention is given to physiologic (hippocampal long-term potentiation) and behavioral animal models. The principles and methods described can be applied to studies of diverse clinical disorders.

The neuropathogenesis of HIV-1 infection.

HIV encephalitis is the common pathologic correlate of HIV-dementia (HAD). HIV-infected brain mononuclear phagocytes (MP) (macrophages and microglia) are reservoirs for persistent viral infection. When activated, MP contribute to neuronal damage. Such activated and virus-infected macrophages secrete cellular and viral factors, triggering neural destructive immune responses. Our Center's laboratories have begun to decipher the molecular and biochemical pathways for MP-mediated neuronal damage in HAD. This review will discuss the salient clinical and pathological features of HAD and highlight the recent advances made, by our scientists and elsewhere, in unraveling disease mechanisms, including the role of chemokines and their receptors in the neuropathogenesis of HIV-1 encephalitis.