Association between Parkinson's disease and diabetes: Data from NEDICES study.

BACKGROUND: Despite growing evidence showing an association between Parkinson's disease (PD) and diabetes, epidemiological studies have shown conflicting results. AIMS OF THE STUDY: To evaluate the association between PD and diabetes and the impact of diabetes duration in this association in an elderly (≥65 years) Spanish population. METHODS: Data for this cross-sectional population-based analysis were obtained from NEDICES study. Subjects were identified from census list. Diagnosis of PD was confirmed by neurological examination. Diabetes was defined by self-report, being on antidiabetic medication or diagnosis on medical records. Logistic regression analysis adjusted by potential confounders was performed to estimate the association between both conditions and also after dividing patients into short-duration (<10 years) and long-duration (≥10 years) diabetes. RESULTS: A total of 4998 subjects were included (79 PD and 4919 controls). Univariate analysis did not show any association between prevalence of PD and diabetes (OR 1.89, 95% CI 0.90-3.98, P=.09), although subgroup analysis showed a positive association in those with long-duration diabetes (3.27, 95% CI 1.21-8.85, P=.02). CONCLUSIONS: Diabetes duration might be an important factor in the association between PD and diabetes, and the risk might be limited to those with longer disease duration.

Clinical and imaging features of the room tilt illusion.

Room tilt illusion (RTI) is a transient disorder of the environmental visuo-spatial perception consisting of paroxysmal tilts of the visual scene. It is attributed to an erroneous cortical mismatch of the visual and vestibular three-dimensional coordinate maps. Thirteen subjects were included in this retrospective case series. Clinical presentation was 180º rotation of the visual scene following the coronal plane in seven patients. The most common cause for RTI in our series was posterior circulation ischaemia (five cases). Cases of endolymphatic sac tumour, critical illness neuropathy, acute traumatic myelopathy and multiple system atrophy causing RTI are reported for the first time. No case of supratentorial focal lesion was found. In order to describe the clinical and imaging features of RTI, 135 cases previously reported in the literature were reviewed along with our series. There was a male predominance (60.2 %). Mean age was 51.2 ± 20.3 years. The most common location of the injury was the central nervous system (CNS) (61.4 %). Supratentorial and infratentorial structures accounted for the same frequency of lesions. The most common aetiology was cerebral ischaemia (infarction or transient ischaemic episode; 27.7 %). These patients were significantly older and their lesions commonly involved posterior fossa structures when compared to patients with non-vascular disorders. In summary, RTI is a manifestation of several CNS and vestibular disorders, and rarely of peripheral nervous system disorders, triggered by disruption of vestibular and sensory perception or integration. Cerebral ischaemic disorders are the most common aetiology for this rare syndrome.

Hemifacial spasm, vertebrobasilar dolichoectasia and neurofibromatosis type 1.

Hemifacial spasm (HFS) is usually produced by compression of the facial nerve by tortuous blood vessels at the root exit zone, including vertebrobasilar dolichoectasia (VBD). Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder with a variety of symptoms, affecting mainly the skin and nervous system. Cerebrovascular abnormalities are becoming a recognized complication of the disease and the most constantly described lesions are stenosis and occlusions affecting the internal carotid artery. VBD has rarely been associated with NF1. We report a 38-year-old female patient with HFS produced by VBD with NF1 presenting with other cerebrovascular abnormalities associated with this disease. We discuss the possible association between these three entities, assuming that a causal relationship may be established and that VBD is part of the spectrum of vascular abnormalities caused by NF1 in this patient.

Mielitis longitudinal como forma de presentación de neurosarcoidosis / Longitudinal myelitis as the presenting symptom of neurosarcoidosis

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Hipoestesia del mentón secundaria a osteonecrosis mandibular inducida por bifosfonatos / Numb Chin syndorme caused by biphosphonates induced osteonecrosis of the Jaw

Introducción. El síndrome de hipoestesia del mentón (numb chin syndrome) se produce por una mononeuropatía del nervio mentoniano o del nervio alveolar inferior. Las causas más frecuentes del síndrome son la traumática y la infecciosa, y siempre que no se encuentre un antecedente relevante debe investigarse la posibilidad de que la etiología sea neoplásica. Otras causas del síndrome son excepcionales. Caso clínico. Mujer de 73 años de edad con cáncer de mama en estadio diseminado y en tratamiento crónico con ácido zoledrónico, que consultó por hipoestesia y disestesias en el territorio de inervación del nervio mentoniano. Se realizó una tomografía computarizada mandibular que demostró una lesión osteolítica con secuestro óseo compatible con osteonecrosis inducida por bifosfonatos. Tras la suspensión del tratamiento, las alteraciones sensitivas y la lesión radiológica permanecieron estables. Conclusiones. La osteonecrosis mandibular por bifosfonatos es una patología relativamente reciente que ha sido descrita de forma excepcional como causa de un síndrome de hipoestesia mentoniana. En el futuro próximo, debe ser tenida en cuenta como parte del diagnóstico diferencial de este síndrome en pacientes oncológicos en tratamiento con bifosfonatos (AU)

Introduction. Numb chin syndrome is caused by a mental or inferior alveolar nerve neuropathy. Traumatic and infectious injuries are the most frequent causes of the syndrome but, if an evident cause does not exist, a neoplastic etiology must be investigated. Other causes of the numb chin syndrome are rare. Case report. A 73-year-old woman had had a diagnosis of metastatic breast cancer and was been treated with zoledronic acid. She attended because of hypoesthesia and dysesthesia of the chin congruent with mental nerve distribution. A computed tomography of the jaw showed an osteolytic lesion with central bone sequestration, so biphosphonate-induced osteonecrosis of the jaw was diagnosed. After zoledronic acid was withdrawn, clinical neuropathy and imaging findings remained stable. Conclusions. Biphosphonates-induced osteonecrosis of the jaw is a recently described condition. It has been rarely reported as a cause for numb chin syndrome. In the future, osteonecrosis of the jaw must be considered in the differential diagnosis of this syndrome in cancer patients treated with biphosphonates (AU)

[Numb chin syndrome caused by biphosphonates-induced osteonecrosis of the jaw]. / Hipoestesia del mentón secundaria a osteonecrosis mandibular inducida por bifosfonatos.

INTRODUCTION: Numb chin syndrome is caused by a mental or inferior alveolar nerve neuropathy. Traumatic and infectious injuries are the most frequent causes of the syndrome but, if an evident cause does not exist, a neoplastic etiology must be investigated. Other causes of the numb chin syndrome are rare. CASE REPORT: A 73-year-old woman had had a diagnosis of metastatic breast cancer and was been treated with zoledronic acid. She attended because of hypoesthesia and dysesthesia of the chin congruent with mental nerve distribution. A computed tomography of the jaw showed an osteolytic lesion with central bone sequestration, so biphosphonate-induced osteonecrosis of the jaw was diagnosed. After zoledronic acid was withdrawn, clinical neuropathy and imaging findings remained stable. CONCLUSIONS: Biphosphonates-induced osteonecrosis of the jaw is a recently described condition. It has been rarely reported as a cause for numb chin syndrome. In the future, osteonecrosis of the jaw must be considered in the differential diagnosis of this syndrome in cancer patients treated with biphosphonates.

[Reversal of vision metamorphopsia as a manifestation of cerebellar infarct]. / Metamorfopsia invertida como manifestación de un infarto cerebeloso.

INTRODUCTION: Reversal of vision metamorphopsia is a disorder affecting the visuospatial perception of objects, without any changes in their shape, size or colour. It generally involves a full 180 degrees rotation of the visual field in the coronal plane. Its chief causation is vertebrobasilar ischaemia, although the phenomenon has also been linked to many other conditions, such as multiple sclerosis, epilepsy, migraine or traumatic head and neck injuries. Some notable features of reversal of vision metamorphopsia are the wide topographic variety of the lesions responsible for the condition, the transient nature of the symptom and its improvement or resolution in the presence of certain stimuli. CASE REPORT: A 35-year-old male with a sudden episode of instability that prevented him from walking, together with vomiting and reversal of vision metamorphopsia that lasted for an hour. A magnetic resonance scan enabled us to identify an acute ischaemic cerebellar lesion as the cause of the condition. CONCLUSIONS: The variety of locations of the lesions that give rise to reversal of vision metamorphopsia would be mainly due to the multisensory nature of the neurons in the posterior parietal cortex, the area of the brain where the visuospatial integration of images is performed. These neurons receive visual, proprioceptive and vestibular afferences, which means that any lesions that occur in these three systems or in the central integrator itself could cause the phenomenon of reversal of vision metamorphopsia.