DISARTRIA ESPASTICA PDF

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PDF | El objetivo de este trabajo es conocer la repercusión que tiene en el habla la Atrofia Olivo-Ponto-Cerebral (AOPC). La medida de la inteligibilidad del. Antecedentes: Se desarrolló un estudio comparativo de modalidades de tratamiento para mejorar la articulación en un niño de 13 años con disartria espástica. de 13 an˜os con disartria espástica severa asociada a parálisis cerebral espástica que examinen los tratamientos en nin˜os con disartria leve y/o moderada.


Disartria Espastica Pdf

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y, dentro de ésta, entre apraxia del habla y disartria espástica basado en parámetros disartria espástica y 15 sin patología) realizaron tres tareas: repetir la. AFASIA, APRAXIA, ALEXIA, AGRAFIA, DISARTRIA Sergio Calleja .. DE LA PRIMERA MOTONEURONA• Disartria espástica: – Por ictus, TCE. Este diagnóstico se diferencia de los otros tipos en que, por ejemplo, aunque en la disartria espástica y en la disartria atáxica hay también.

Given the location of the causal gene, PMD is inherited in a X-linked recessive manner3. Although clinical manifestations are heterogeneous 5 , 6 , the most relevant neurological signs are nystagmus, developmental delay, spasticity, along with neuroimaging supporting aberrant myelination of the Central Nervous System CNS compromising primarily the periventricular white matter, with a tigroid striation pattern that responds to the conservation of myelinated islets, and also an alteration of the N-acetyl aspartate and choline profiles on the brain magnetic resonance spectroscopy 5 , 7.

Unlike other leukodystrophies in which there is a period of normal cortical myelination an then comes a disruption resulting in the lost of myelin sheaths demyelination , PMD has, from the beginning, an abnormal or low production of this very important protein hypomyelination , due to a damage on the PLP1 gene coding for the Protelipidic Protein type 1 that interferes with the oligodendrocyte synthesis of fully functional myelin sheaths and probably also affects the peripheral function of myelinated axons 3 , 8.

In general, PLP1 gene duplications result in a classical form of PMD, nonsense mutations in either form of SPG2 and connatal form of PMD, and other monoallelic mutations have been related to less circumscribed clinical phenotypes 6.

Patients suffering from a connatal form of PMD, the most severe phenotype, have histopathological studies revealing complete absence of myelination in the brain, explaining the rapid clinical deterioration and suggesting tan death of these patients may respond to nervous conduction alterations in brain control centers.

Frequently, the connatal form of PMD is expressed during the first weeks of life, through key findings in the clinical neurological examination, that include pendular nystagmus, hypotonia and laryngeal stridor; later in life, seizures and sever motor deficits appear, and hypotonia turns to weakening limb spasticity; affected patients may never walk Verbal language is limited, but patients understand simple orders and can follow them.

Affected individuals with the connatal form of PMD die in infancy, usually secondary to respiratory or deglutition complications, such as bronchoaspiration 9.

Classic PMD is characterized in the first stages of disease by nystagmus, hypotonia and tremor in male affected patients, joint progressively by ataxia and spastic quadriparesis in the school age. Motor impairment of the limbs is less severe tan that presented in the connatal form, and patients can frequently achieve walking even if requiring special aids, and have better control of voluntary movement of the upper limbs 9 , Classic PMD affected males also have improved cognitive development, with acceptable speech.

Survival rates in this patients have been described to be up to the seventh decade of life. In such situations careful selection of muscle of thumb were performed. After pre-oxygenating the the drug type and dose is required. Anesthesia is especially patient, anesthetic induction was carried out with fentanyl rare as in two patients with this disease in a very short space 1.

A central venous We describe two female siblings with FSP respectively catheter was inserted through the right internal jugular programmed for cholecystectomy and subtotal colectomy — vein, without incidents.

Maintenance was carried out with the two operations being spaced two months apart. The main a continuous infusion of propofol mg. Before at 23 years of age, with hypertension and dependent upon the end of the operation, intravenous ondansetron 4 mg, others for her basic activities.

The preoperative were administered.

Following administration of a dose of laboratory tests complete blood count, biochemistry and 2 mg. The patient was moved to serted and 2 mg of intravenous midazolam was administered.

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Serial laboratory tests and imaging pressure, bispectral index BIS and neuromuscular block studies were carried out and proved normal in all cases. After pre-oxygenating the patient, anesthetic of Surgery. A PubMed literature search with the key- ; relaxant use was not necessary during surgery. Extubation proved uneventful, fol- McTiernan et al 5 described the use of epidural anesthesia for lowing the administration of sugammadex 2 mg.

In block, until a TOF ratio of over 0. The patient turn, Mclve et al. The use of neuromuscular blockers is complicated in Case Report 2 patients with familial spastic paraplegia.

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Succinylcholine The second case corresponded to the younger 43 years of is contraindicated since it may induce hyperkalemia, and age female sibling of the above patient, who had been di- there should be caution in the use of non-depolarizing muscle agnosed with FSP at 16 years of age. In this case, the clinical relaxants due to the risk of exaggerated muscle relaxation.

However, repeated episodes of sigmoid volvulus and dolichomegaco- regional anesthesia is not always possible. Therefore general lon.

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Her usual treatment consisted of baclofen, tizanidine, anesthesia with non-depolarizing neuromuscular blockers clonazepam, and nicardipine. Kannan CR. Plenum Medica Liddle G. Enfermedades de la corteza suprarrenal.

Tratado de Medicina Interna. Interamericana Oelkers W. Adrenal insufficiency. N Engl J Med ; Burke C.

Enfermedades corticosuprarrenales. Oxford: Ed. Folium, ; 2: En: Farreras R. Medicina Interna.

Masa suprarrenal e insuficiencia suprarrenal. An Med Interna Madrid ; 3 2 : Tuberculous Addison's disease. Utility of CT in diagnosis and follow-up.

Eur J Radiol ; Clinical clues to the cause of Addison's disease. Am J Med ; Aron DC. Endocrine complications of the adquired inmunodeficiency syndrom. Arch Intern Med ; Recents advances in diagnosis and therapy of Addison's disease. Advances in Thomas Addison's Diseases.

London: Journal of Endocrinolgy. Primary adrenal insufficiency in patient with the adquired inmunodeficiency syndrome: a report of five cases. J Clin Endocrinol Metab ; Federmann D. IV Suprarrenales. En: Rubinstein y Federmann. Scientific American. Serden Wurm DJ.

Clinical and mutational spectrum of Colombian patients with Pelizaeus Merzbacher Disease

Metastases to the adrenal glands and the development of Addison's Disease. Cancer ; 54; Tucker WS Jr.

Reversible adrenal insufficiency induced by Ketoconazole. JAMA ; Clin Endocrinol ; Ann Otol Rhinol Laryngol. In the operating room ECG, pulse oxi- some patients 1,4. JAMA ; Copies of the written consents are available for review by the Editors of this journal and are kept within the clinical records of each patient. Frecuentemente por la toma de anticoagulantes 9, Hila A, Castell D.

Dysphagia screening: state of the art: invitational conference proceeding from the State-of-the-Art Nursing Symposium, International Stroke Conference

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