Theoretical investigation on the electronic structure of pentacyano(L)ferrate(II) complexes with NO(+), NO, and NO(-) ligands. Redox interconversion, protonation, and cyanide-releasing reactions.

Reaction pathways for the one- and two-electron reductions of [Fe(CN)(5)NO](2)(-) have been investigated by means of a density functional theory (DFT) approach combined with the polarized continuum model (PCM) of solvation. In addition, UV-vis spectroscopic data were obtained using ZINDO/S calculations including a point-charge model simulation of solvent effects. DFT methodologies have been used to assess the thermodynamical feasibility of protonation and cyanide-release processes for the reduced species. We conclude that [Fe(CN)(5)NO](3)(-) is a stable species in aqueous solution but may release cyanide yielding [Fe(CN)(4)NO](2)(-), consistent with experimental results. On the other hand, the [Fe(CN)(5)NO](4)(-) complex turns out to be unstable in solution, yielding the product of cyanide release, [Fe(CN)(4)NO](3)(-), and/or the protonated HNO complex. All the structural and spectroscopic (IR, UV-vis) predictions for the [Fe(CN)(5)HNO](3)(-) ion are consistent with the scarce but significant experimental evidence of its presence as an intermediate in nitrogen redox interconversion chemistry. Our computed data support an Fe(II)(LS) + NO(+) assignment for [Fe(CN)(5)NO](2)(-), an Fe(II)(LS) + NO assignment for the one-electron reduction product, but an Fe(I)(LS) + NO(+) for the one-electron product after dissociation of an axial cianide, and an Fe(II) + singlet NO(-) for the two-electron reduction species.

[Intracranial hypertension syndrome due to giant frontoethmoidal osteoma]. / Síndrome de hipertensión endocraneal por osteoma frontoetmoidal gigante.

Osteomas are benign lesions that may cause life-threatening complications. Their radiological diagnosis usually is casual. Once diagnosed, periodic radiological follow-ups should be carried out and if growth occurs, surgical measures should be taken to prevent complications. The case of a 53-years-old white male admitted for injuries produced by a traffic accident is reported. He had a history of frontalization syndrome with episodes of disorientation and behavioral changes. Plain radiography, CAT, MRI and bicarotid angiography revealed a bone mass that occupied almost the entire anterior fossa. Intracranial hypertension syndrome caused by a giant ethmoidal osteoma was diagnosed. Surgery using a frontal approach was undertaken.

[Frontal sinus osteoma associated with intracranial porencephalic cavity]. / Osteoma de seno frontal asociado a cavidad porencefálica intracraneal.

A case of an eighteen-year-old student, complaining of frontal and periorbital headache is presented. Using conventional radiographies and CT Scan a frontal sinus osteoma is diagnosed, finding a hypodense image located in the left frontal cerebral lobe, without perilesional oedema or contrast uptake. During the surgical act, a destruction of the posterior wall of the left frontal sinus is found, penetrating the anterior cerebral fossa and connecting with the cerebral cavity in the left frontal cerebral lobe through a fistula of mucosal tissue that passes through the dura mater. Complete tumoral exeresis was undertaken as well as plastic reconstruction with excellent clinical and cosmetic results. We conclude that the early diagnosis and treatment of these benign lesions should be undertaken in order to avoid the potential complications they can provoke.

Recovery from locked-in syndrome after posttraumatic bilateral distal vertebral artery occlusion.

A 55-year-old man developed a delayed locked-in syndrome after a mild head injury. Angiography showed bilateral distal vertebral artery occlusion. Anticoagulant therapy and energetic medical management to promote collateral circulation to the structures in the posterior fossa led to a functional recovery. A review of the reported cases of posttraumatic locked-in syndrome has allowed the authors to differentiate between two types: the first is due to primary brainstem injury and the second is due to secondary brainstem ischemia. Both types have different modes of onset, mechanisms of production, angiographic findings, and prognosis. It is concluded that, with early diagnosis and vigorous medical management, expectations for a useful recovery are high, especially in those cases of posttraumatic locked-in syndrome due to secondary brainstem ischemia.