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T Ayuso Blanco

Publications and source records attributed to T Ayuso Blanco.

12 recordsLinked to original sources
PubMed2006

[Fatal familiar insomnia: clinical, neurophysiological and histopathological study of two cases].

INTRODUCTION: Family prion diseases are caused by mutations in the gene coding the prion protein (PrP), originating an altered isoform called prion. One of the most uncommon is the fatal familial insomnia (FFI), an entity characterized by sleep disorders and that is associated to a mutation in codon 178. METHODS: We have studied two male patients, aged 43 and 49 years respectively, from the same family. RESULTS: The most significant symptoms were sleep disorders with agitation, fractionated sleep, snoring and daytime sleepiness. The evolution was brief, the patient dying at a few months of the clinical debut. Sleep registries showed destructuration with total loss of the normal cycle of the phases and great decrease of the sleep spindles and K complexes in both cases. The polygraphy showed tachycardia and apnea pauses. In the molecular study, a mutation in the codon 178 was detected, both being methionine/methionine homozygotes at position 129. The most outstanding neuropathological abnormalities were located in the thalamus with gliosis and neuronal loss of anterior and dorsomedial ventral nuclei and also intense neuronal loss in olive of the first case. CONCLUSIONS: This study describes two new cases of FFI with genotype D178N-129M and short course classical phenotype. The polysomnography is essential in the diagnostic strategy of this disease whose neuropathological substrate is the thalamic alterations and of the inferior olive. Molecular biology permits an exact diagnosis of FFI although there is still controversy on the phenotypal variability and physiopathogenic mechanisms.

Adult↗
PubMed1995

[Wernicke encephalopathy in patients given parenteral nutrition].

Wernicke's encephalopathy is caused by thiamin deficiency and can be recognized by severe neurological symptoms that are occasionally accompanied by systemic signs. The syndrome is often found in alcoholics, although other causes have also been identified, such as intravenous feeding, in which the main pathogenic mechanisms are the administration of carbohydrates and the low standard dose of vitamin B1--in relation to the increase in metabolic load--delivered in a medium of substances that favor inactivation of the vitamin. We present 3 intravenously fed patients who developed the syndrome, even though in 2 cases they were given thiamin. Only the third patient's history included chronic alcoholism, and this patient also suffered severe cardiac symptoms and amaurosis. We believe that the amount of thiamin provided through parenteral nutrition, as well as the medium in which it is delivered, must be reviewed.

Adult↗
PubMed1995

[Neurobrucellosis. A report of 13 cases].

Thirteen patients with nervous system brucellosis are described. The clinical signs were heterogeneous: meningoencephalitis in 5 cases, meningoradiculitis in another 5, meningomyelitis with cranial neuropathy in 1 and of a vascular nature in 2 others. Neurologic signs appeared during the active phase in 5 patients and later in 8. Diagnosis was based on clinical manifestations, serum and cerebrospinal fluid (CSF) serology, quantitative changes in CSF and favorable response to treatment. Therapy consisted of a combination of 2 or 3 of the following drugs: rifampin, doxycycline, streptomycin and trimethoprim sulfamethoxazole. In spite of favorable evolution, 5 patients suffered sequelae. We suggest that brucellosis be investigated when neurologic deficit ensues with no known etiology, especially in endemic countries.

Adolescent↗
PubMed1994

[Involvement of cranial pairs as manifestation of prostatic cancer].

Two cases of prostate cancer (PC) which presented clinically with affectation of the cranial pairs due to skull base metastasis. In both cases, existence of intraparenchimatous brain metastasis was excluded. Initial improvement with hormonal therapy was followed by clinical, analytical and radiological relapse due to spread of process until death, at 11 and 36 months from diagnosis. Although PC's bone metastasis are frequent, their location at the skull base is uncommon. Even more rare are the cases which present with changes in the cranial pairs in the absence of signs and symptoms of prostatism.

Adenocarcinoma↗
PubMed1994

[A iatrogenic pathology study in an internal medicine service].

BASIS: It's obvious that the current medicine practice generates iatrogenesis . However, we are unaware about its magnitude and severity, specially in Spain, where this item has been scarcely studied. METHODS: All the patients admitted to the Department of Internal Medicine were prospectively studied during a 13 months period, selecting among the patients those fulfilling criteria for an iatrogenic problem both of pharmacological origin and not pharmacological. The kind of iatrogenesis, its severity, related mortality, gravity of the basic illness, affected organ and avoidability of the iatrogenesis were evaluated. Infusion phlebitis were recorded only during 6 months. RESULTS: Iatrogenic pathology was found in 228 cases over 1.549 patients admissions, accounting for 14.7% of incidence. Iatrogenic pathology was the reason for admission in 65 cases. The average stay was significantly increased in patients with iatrogenic pathology (p < 0.01). Adverse reactions to drugs accounted for 62% of the total account with 141 cases. The non-steroids antiinflammatory (NSA) drugs were the most frequently troublesome pharmacological agents. The GI tract was the more affected system (84 cases). Infusion phlebitis are not included in the total account of cases. CONCLUSIONS: a) iatrogenic pathology is an illness of very high incidence in our surroundings; b) NSA is a group of drugs generating frequently adverse reactions in off-hospital environment; c) GI hemorrhage is an iatrogenic illness accounting for high percentage of cases; d) many of the iatrogenic events can be catalogued as avoidable and with more accurate attention to some factors the more of them could be prevented.

Age Distribution↗
PubMed1994

[Brain stem encephalitis due to herpes simplex].

Brainstem encephalitis is an unusual infection caused by a variety of agents, among them the herpes simplex (HS) virus. The difficulty of establishing a diagnosis by neurophysiological and radiological examination is greater in this type of encephalitis than in the usual form produced by HS. We describe a fatal case of brainstem encephalitis. Inflammatory and necrotic lesions in the pous and medulla confirmed the clinical diagnosis, while the etiology was determined by immuno-histo-chemical techniques and viral culture of the cerebral parenchyma. Early diagnosis of this form of encephalitis, based on new virological techniques, allows more effective antiviral treatment.

Acyclovir↗
PubMed1993

[Neurological disease due to the varicella-zoster virus without a skin lesion].

We studied three cases of inflammatory neurological disease and serological evidence of varicella-zoster viral (VZV) infection without cutaneous manifestation. They corresponded to a case of cranial multi-neuritis, a case of aseptic meningitis, and another case of meningoencephalitis. Despite the infrequency of any such association, the spectrum of the neurological diseases associated with VZV without skin lesions is quite wide. We are motivated to present our experience by the belief that it is important to think about this possible etiology based on inflammatory areas at different levels of the Nervous System in patients who are still immunocompetent.

Abducens Nerve↗
PubMed1991

[Neck-tongue syndrome secondary to abrupt head movements. Clinical study and conservative treatment].

The neck-tongue syndrome is an extremely rare entity consisting of the compression of the second cervical root in the atloaxoid space in relation to certain brusque movements of the neck. Given the infrequency of this syndrome, the authors present a diagnosed and controlled case of the same in the Reina Sofia Hospital in Tudela. A 25 year old patient was consulted who, for some time, had presented paresthesia in the right half of the tongue and contraction of the cervical musculature related to certain neck postures made during sports activities. Clinical examination was completely normal. Radiography only demonstrated a defect in the segmentation between the posterior C2, C3 arches. Herewith, the authors have revised the literature concerning the topic, discuss the physiopathological theories made in other studies and analyze the therapeutic possibilities of the disease inclinning towards conservative treatment.

Adult↗
PubMedDate not supplied

[Chronic polyneuropathy due to vitamin E deficiency].

Vitamin E deficiency has been implicated as a causal factor in neurological disease for some time. Nevertheless, only in the last 10 years have we begun to understand the role this vitamin plays in the normal functioning and structure of the nervous system. Chronic fat malabsorption syndromes are the most common causes of low levels of this highly fat-soluble vitamin. We present a case of chronic polyneuropathy due to vitamin E deficiency caused by malabsorption in which a biliary-cholonic fistula was present. Plasma tocopherol levels were normalized by parenteral substitution, leading to substantial clinical improvement. We suggest that vitamin E levels be determined in cases of digestive disorders involving malabsorption of fats and in chronic neurological diseases, particularly spinal-cerebral degenerative and polyneuropathic diseases that are mainly sensory or motor-sensory in nature, given the potential reversibility of these disorders when caused by vitamin E deficiency.

Female↗