Mild hypothermia reduces polymorphonuclear leukocytes infiltration in induced brain inflammation

Over the last 50 years deep hypothermia (23 degrees C) has demonstrated to be an excellent neuroprotective agent in cerebral ischemic injury. Mild hypothermia (31-33 degrees C) has proven to have the same neuroprotective properties without the detrimental effects of deep hypothermia. Mechanisms of injury that are exaggerated by moderate hyperthermia and ameliorated by hypothermia include, reduction of oxygen radical production, with peroxidase damage to lipids, proteins and DNA, microglial activation and ischemic depolarization, decrease in cerebral metabolic demand for oxygen and reduction of glycerin and excitatory amino acid (EAA) release. Studies have demonstrated that inflammation potentiates cerebral ischemic injury and that hypothermia can reduce neutrophil infiltration in ischemic regions. To further elucidate the mechanisms by which mild hypothermia produces neuroprotection in ischemia by attenuating the inflammatory response, we provoked inflammatory reaction, in brains of rats, dropping a substance that provokes a heavy inflammatory reaction. Two groups of ten animals underwent the same surgical procedure: the skull bone was partially removed, the duramater was opened and an inflammatory substance (5% carrageenin) was topically dropped. The scalp was sutured and, for the group that underwent neuroprotection, an ice bag was placed covering the entire skull surface, in order to maintain the brain temperature between 29.5-31 degrees C during 120 minutes. After three days the animals were sacrificed and their brains were examined. The group protected by hypothermia demonstrated a remarkable reduction of polymorphonuclear leukocytes (PMNL) infiltration, indicating that mild hypothermia can have neuroprotective effects by reducing the inflammatory reaction.

Nos últimos 50 anos, a hipotermia tem demonstrado ser um excelente agente neuroprotetor nas lesões isquêmicas encefálicas. A hipotermia moderada (310 C - 330 C) provou também apresentar as mesmas propriedades protetoras, sem os efeitos deletérios da hipotermia profunda. Dentre alguns mecanismos de lesão que são melhorados pela hipotermia e piorados pela hipertermia moderada, podemos citar a diminuição da demanda de oxigênio pelo encéfalo e a redução da glicina e aminoácidos excitatórios, evitando a produção de radicais de oxigênio, com aumento da peroxidase e conseqüente lesão aos lípides, proteínas e DNA, assim como pela ativação microglial e despolarização isquêmica. Alguns estudos demonstraram que a inflamação potencializa a lesão isquêmica e que a hipotermia pode reduzir a infiltração leucocitária nas áreas isquêmicas. Para melhor elucidar os mecanismos pelos quais a hipotermia apresenta efeito neuroprotetor através da redução da inflamação, no processo isquêmico, escolhemos o método utilizando a indução de uma reação inflamatória com a utilização de uma substância com capacidade promover intensa reação inflamatória em encéfalos de ratos. Dois grupos de dez animais foram submetidos a um mesmo procedimento cirúrgico: a calota craniana foi parcialmente removida, a duramáter aberta e uma substância com potente efeito inflamatório (carragenina a 5%) foi gotejada. A pele foi suturada e, para o grupo com neuroproteção, uma bolsa de gelo foi colocada, cobrindo toda a superfície craniana, de modo a manter a temperatura encefálica entre 29,50 C e 310 C durante 120 minutos. Três dias após, os animais foram sacrificados e os encéfalos examinados. O grupo protegido pela hipotermia apresentou considerável redução na infiltração leucocitária, demonstrando que a hipotermia pode apresentar função neuroprotetora por meio de uma redução no processo inflamatório.

Aggressive management of orbital meningeal melanocytoma.

OBJECTIVE: Meningeal melanocytoma generally occurs in the posterior fossa. Orbital manifestation is rarely encountered. METHODS: A thirty-five year-old man presented with progressive proptosis of his right eye. Computed tomography (CT) and Magnetic Resonance Imaging (MRI) of the brain showed an expansive intraconal mass lesion occupying the superior orbital compartment, the entire orbital apex, and the optic foramen. Histological analysis and Immunohistochemical staining for S-100 and HMB-45 monoclonal antibodies confirmed melanocytoma. FINDINGS: Microsurgical removal was accomplished through a fronto-orbital craniotomy. Chemotherapy and irradiation followed the initial intervention. The patient returned for follow up two years after surgery, complaining of headache and right visual loss. A subfrontal tumor with massive edema was found on follow up CT scan. INTERPRETATION: Meningeal melanocytomas are rare benign pigmented tumors of the central nervous system. They are predominant in the posterior fossa and spinal cord and frequently mistaken for melanomas, especially on frozen sections. Orbital presentation is rare. The natural history is poorly defined.

Actinomicose do sistema nervoso central: uma rara complicaçäo da actinomicose cervicofacial / Actinomycosis of the central nervous system: a rare complication of cervicofacial actinomycosis

A actinomicose do sistema nervoso central (SNC) é afecçäo rara, caracterizada pela formaçäo de absesso único e de evoluçäo crônica. Os autores descrevem o caso de um paciente jovem, imunocompetente, com actinomicose cerebral oriunda de foco primário cervicofacial, submetido a ressecçäo cirúrgica e antibioticoterapia. Ressalta-se a importância do conhecimento da entidade e de suas principais formas de acometimento, como a base do diagnóstico precoce dessa enfermedade potencialmente curável e de bom prognóstico

[Actinomycosis of the central nervous system: a rare complication of cervicofacial actinomycosis]. / Actinomicose do sistema nervoso central. Uma rara complicação da actinomicose cervicofacial.

Central nervous system actinomycosis is a rare but treatable chronic suppurative bacterial infection. The case of a young immunocompetent male with actinomycosis of the CNS is presented. The abscess originated from a primary cervico-facial infection and was located in the left parasellar region. After excision of the mass, that showed Actinomyces colonies, the patient was treated with intravenous Penicillin for 42 days followed by oral administration of the drug for 30 days. After surgery the patient was left with mild sequelae that had improved by the last follow-up, 7 months later. A new CT scan at that time revealed no residual disease or recurrence. The early diagnosis of cerebral actinomycosis relies essentially on a clinical suspicion. Hence it is imperative to be aware of the natural history of this infection and its various modes of presentation.