Isquemia Cerebral

Síndrome de Fahr Secundario a Hiperparatiroidismo Primario e Isquemia Cerebral: A Propósito de un Caso. Fahr Syndrome Secondary To Primary Hyperparathyroidism And Cerebral Ischemia: A Case Report.

Fahr’s syndrome (FS) is a rare neurodegenerative condition, characterized by cerebral calcifications mainly in the basal ganglia. Although its most common presentation are the disorders of movement, cognition, behavior and epilepsy, in recent years cases of cerebrovascular disease (CVD) related to this entity have been appearing.

We report a 59-year-old male patient who presented 2 transitory ischemic attacks (TIAs), the 1st of 5 minutes, of speech alteration what happened unnoticed, and the second of 45 minutes, 2 weeks later, of speech alteration, loss of muscle strength and tingling sensation in the left side of the body. Brain computed tomography and magnetic resonance imaging revealed calcifications suggestive of FS and a treatable cause was found (primary hyperparathyroidism with hypovitaminosis D). The patient was treated with aspirin, atorvastatin and colecalciferol without vascular recurrence and the levels of vitamin D and PTH normalized. Although the association between CVD in young people and SF has not yet been determined, the occurrence of these cases leads us to suspect that ischemic CVD could be part of the natural history of this entity. Being the prevalence of FS unknown, we alert clinicians to keep CVD in mind as a form of presentation of this condition. We review the association between FS and ischemic CVD (without in clusion of aneurysmal disease).

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Palabras clave: Hiperparatiroidismo primario, Isquemia Cerebral, Síndrome de Fahr,

Keywords: Cerebral ischemia, Fahr's syndrome, Primary hyperparathyroidism,

Neuroprotección en la Isquemia Cerebral. Experiencias con la Eritropoyetina Humana Recombinante.

The current therapeutic strategies are oriented to reestablish the cerebral blood flow and to protect the nervous cells during cerebrovascular disease. Searching neuroprotective agents has been guided to block some of the molecular events that nervous cells suffer as a consequence of ischemia. Human recombinant erythropoietin constitutes a recent proposal, demonstrating to have neuroprotective mechanisms of action at more than one level, appearing to be a short term promising option. Its erythropoietic action can represent an convenience for chronic treatments or in secondary prevention. The use of an erythropoietin with low content of sialic acids –with neuroprotective activity but not erythropoietic– may be a good option. This molecule should be administered by a non systemic route as is the intranasal in order to prevent the hepatic degradation. Intranasal administration of human recombinant erythropoietin has shown to be quick and safe in accessing the brain, it does not stimulate erythropoiesis in acute treatments and it shows therapeutic effectiveness in several models of cerebral ischemia in rodents. This proposal can become a therapeutic option in cerebrovascular diseases.

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Palabras clave: Eritropoyetina, Intranasal, Isquemia Cerebral, Neuroprotección,

Keywords: Cerebral ischaemia, Erythropoietin, Intranasal route, Neuroprotection,

Comparison of hemorheology and plasma contents of TXB2, 6-Keto-PGF1 alpha in model rats with three kinds of cerebral ischemia.

Objective: To compare changing features of hemorheological, TXB2 and 6-keto-PGF1 alpha in plasma in three kinds of model rats with cerebral ischemia.

Materials and Methods: 128 adult male Sprague-Dawley rats were randomly divided into four groups: a middle cerebral artery occlusion with intraluminal thread group (MCAO-group), a bilateral common carotid artery ligation group (BCCA-group), a unilateral common carotid artery ligation group (UCCA-group) and a normal control group (NC-group). Blood for hemorheological testing of all rats was taken from abdominal aorta 24h following cerebral ischemia and hemorheological index was determined. Plasma contents of TXB2 and 6-keto-PGF1 alpha were detected by radio-immunity.

Results: The whole blood viscosity value, plasma viscosity value, and hematocrit were higher in MCAO-group among three model groups, followed by BCCA-group and UCCA-group. The deformity index of RBC in MCAO-group was significantly lower than that in normal-group. There were significant differences for plasma contents of TXB2 and 6-keto-PGF1 alpha among the three model groups and the normal group. There were significant differences for plasma level of 6-Keto-PGF1a, TXB2 between MCAO-group and the normal group, but no difference among the three model groups(p>0.05).

Conclusion: MCAO was the greatest in contribute to changes of hemorheology and plasma contents of TXB2, 6-keto-PGF1 alpha among three rat models with cerebral ischemia.

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Palabras clave: 6 –keto-PGF1 alfa, Hemorreología, Isquemia Cerebral, Ligadura bilateral de la arteria carótida común, Obstrucción de la arteria cerebral media, Tromboxano B2,

Keywords: 6-keto-PGF1 alpha, Bilateral common carotid artery ligation, Cerebral ischemia, Hemorheology, Middle cerebral artery occlusion, Thromboxane B2,

Neuroprotección en isquemia cerebral aguda. Estado actual e importancia clínica de la cascada isquémica.

Knowledge of physiophatological mechanisms of cerebral ischemia permits understanding the mechanisms of action on which many aspects of treatment are based and the clinical and neuro-radiological changes. The only treatment with clinically demonstrated success is the use of thrombolytic to restore the cerebral circulation. A cellular and molecular mechanisms such as free radical production, lipid peroxidation, excitotoxicity and calcium ion overload constitute the important therapeutic targets of neuroprotection and it is now known that interventions such a delivering neuroprotective agents can participate to salvage a portentially reversible ischaemic region known as the ischaemic penumbra. We review the vascular and biochemistry that produce necrosis of neurons after a cerebrovascular occlusion and actual evidence of neuroprotective drugs.