Microbiota dysbiosis caused by dietetic patterns as a promoter of Alzheimer's disease through metabolic syndrome mechanisms.

Microbiota dysbiosis and metabolic syndrome, consequences of a non-adequate diet, generate a feedback pathogenic state implicated in Alzheimer's disease development. The lower production of short chain fatty acids (SCFAs) under dysbiosis status leads to lipid homeostasis deregulation and decreases Angptl4 release and AMPK activation in the adipose tissue, promoting higher lipid storage (adipocyte hypertrophy) and cholesterol levels. Also, low SCFA generation reduces GPR41 and GPR43 receptor activation at the adipose tissue (increasing leptin release and leptin receptor resistance) and intestinal levels, reducing the release of GLP-1 and YPP. Therefore, lower satiety sensation and energy expenditure occur, promoting a weight gaining environment mediated by higher food intake and lipid storage, developing dyslipemia. In this context, higher glucose levels, together with higher free fatty acids in the bloodstream, promote glycolipotoxicity, provoking a reduction in insulin released, insulin receptor resistance, advanced glycation products (AGEs) and type 2 diabetes. Intestinal dysbiosis and low SCFAs reduce bacterial biodiversity, increasing lipopolysaccharide (LPS)-producing bacteria and intestinal barrier permeability. Higher amounts of LPS pass to the bloodstream (endotoxemia), causing a low-grade chronic inflammatory state characterized by higher levels of leptin, IL-1ß, IL-6 and TNF-α, together with a reduced release of adiponectin and IL-10. At the brain and neuronal levels, the generated insulin resistance, low-grade chronic inflammation, leptin resistance, AGE production and LPS increase directly impact the secretase enzymes and tau hyperphosphorylation, creating an enabling environment for ß-amyloid senile plaque and tau tangled formations and, as a consequence, Alzheimer's initiation, development and maintenance.

Ataxia and focal dystonia in Kallmann syndrome.

A case of Kallmann syndrome (KS) associated with rare neurological manifestations is presented. Cerebellar ataxia probably caused by a small posterior fossa and a focal dystonia affecting the left lower limb expand the spectrum of neurological manifestations occurring in KS. Further studies are needed to better understand these manifestations.

¿El abuso de fármacos en pacientes con migraña crónica influye en la efectividad del tratamiento preventivo con topiramato? / Does medication abuse in patients with chronic migraine influence the effectiveness of preventive treatment with topiramate?

Introducción. Los pacientes con migraña crónica (MC) y abuso de medicación son difíciles de tratar y tienen peor calidad de vida que otros pacientes con migrañas. Objetivo. Valorar si la presencia de abuso de fármacos disminuye la efectividad del topiramato. Pacientes y métodos. Una serie de pacientes con MC fueron agrupados según presentasen criterios de abuso o no abuso de fármacos. Se les aconsejo la supresión del fármaco del cual abusaban. Se ajustó el tratamiento de sus crisis y se inició tratamiento preventivo desde el principio con topiramato. Se valoró el número días con cefalea y migrañas intensas en el mes previo y al cuarto mes de tratamiento. Resultados. Fueron seleccionados 262 pacientes con criterios de MC, y de ellos 167 (63,7%) cumplieron criterios de abuso. En ambos grupos hubo una reducción significativa del número de días con cefalea/mes y numero de crisis de migraña/mes al cuarto mes de tratamiento con topiramato. Porcentaje de reducción de días con cefalea/mes en MC sin abuso, 59,3} 36,1%; y con abuso, 48,7} 41,7% (p = 0,0574). Porcentaje de reducción de migrañas intensas/mes en MC sin abuso, 61,2%; y con abuso, 50% (p = 0,0224). Tasa de respondedores según numero de días con cefalea/mes en MC sin abuso, 69%; y con abuso, 57%. Tasa de respondedores según numero de migrañas intensas/mes en MC sin abuso, 76,8%; y en MC con abuso, 61% (p = 0,0097). Conclusiones. El topiramato fue efectivo en pacientes con MC sin y con abuso de fármacos, aunque con menor efectividad en estos últimos (AU)

Introduction: Patients with chronic migraine (CM) and medication abuse are difficult to treat, and have a greater tendency towards chronification and a poorer quality of life than those with other types of headache. Aim: To evaluate whether the presence of medication abuse lowers the effectiveness of topiramate. Patients and methods: A series of patients with CM were grouped according to whether they met abuse criteria or not. They were advised to stop taking the drug that they were abusing. Treatment was adjusted to match their crises and preventive treatment with topiramate was established from the beginning. The number of days with headache and intense migraine in the previous month and at four months of treatment was evaluated. Results. In all, 262 patients with CM criteria were selected and 167 (63.7%) of them fulfilled abuse criteria. In both groups there was a significant reduction in the number of days with headache/month and number of migraine attacks/month at the fourth month of treatment with topiramate. The percentage of reduction in the number of days with headache/ month in CM without abuse was 59.3} 36.1%, and with abuse, 48.7} 41.7% (p = 0.0574). The percentage of reduction in the number of days with intense migraine/month in CM without abuse was 61.2%, and with abuse, 50% (p = 0.0224). Response rate according to the number of days with headache/month in CM without abuse was 69%, and with abuse, 57%. Response rate according to the number of intense migraines/month in CM without abuse was 76.8%, and in CM with abuse, 61% (p = 0.0097). Conclusions. Topiramate was effective in patients with CM with and without medication abuse, although effectiveness is lower in the latter case (AU)

Diferencias clínicas y terapéuticas de la afectación neurooftalmológica secundaria a sífilis / Clinical and therapeutic differences in neuro-ophthalmological involvement secondary to syphilis

Introducción. Existen múltiples formas de afectación neurooftalmológica secundaria a sífilis, no siempre bien conocidas. Nuestro objetivo es conocer las diferencias clínicas y de tratamiento en estos pacientes. Casos clínicos. Se incluyeron ocho pacientes diagnosticados de afectación ocular y neurooftalmológica por sífilis durante los años 2012 y 2013. Cinco presentaron uveítis, siendo la panuveítis la forma más frecuente, con tres casos. Dos casos presentaron papiledema, y otro, neuropatía óptica retrobulbar. Un 62,5% fue diagnosticado de neurosífilis, cuya presencia se relacionó con la afectación del nervio óptico (p = 0,035). Ninguno de ellos presentó positividad para VDRL en el líquido cefalorraquídeo, y se diagnosticaron por la presencia de anticuerpos FTA junto con hiperproteinorraquia, pleocitosis linfocitaria o síntesis intratecal de anticuerpos. En ausencia de uveítis, se produjo un retraso diagnóstico medio de 2,6 meses (p = 0,047). Todos los pacientes, salvo uno que precisó vitrectomía, evolucionaron favorablemente con antibioterapia intravenosa. Conclusiones. En casos de afectación neurooftalmológica, inflamatoria y no inflamatoria, el clínico debe tener en cuenta la sífilis como potencial etiología para evitar un retraso diagnóstico, puesto que un adecuado tratamiento precoz puede evitar una pérdida de visión permanente (AU)

Introduction. There are many forms of neuro-ophthalmological involvement secondary to syphilis, and not all of them are well known. Our aim is to determine the clinical and therapeutic differences in these patients. Case reports. Our sample included eight patients diagnosed with an ocular and neuro-ophthalmological disorder due to syphilis over the years 2012 and 2013. Five of them presented uveitis, pan-eveitis being the most frequent, with three cases. Two cases presented papilloedema and another displayed retrobulbar optic neuropathy. A total of 62.5% were diagnosed with neurosyphilis, the presence of which was related with compromise of the optic nerve (p = 0.035). None of them gave positive for VDRL in cerebrospinal fluid and they were diagnosed by the presence of FTA antibodies together with high protein levels in cerebrospinal fluid, lymphocytic pleocytosis or intrathecal synthesis of antibodies. In the absence of uveitis, diagnosis was delayed by a mean time of 2.6 months (p = 0.047). All the patients, except one who required a vitrectomy, progressed favourably with intravenous antibiotic therapy. Conclusions. In cases of neuro-ophthalmological compromise, whether inflammatory or non-inflammatory, the physician must bear syphilis in mind as a potential causation in order to avoid delays in the diagnosis, since early well-tailored treatment can prevent permanent loss of sight(AU)

Síndrome de ataxia cerebelosa, arreflexia vestibular y neuropatía: diagnóstico mediante estimulación vestibular calórica / Syndrome of cerebellar ataxia, neuropathy and vestibular areflexia: diagnosis by caloric vestibular stimulation

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