Clinical and magnetic resonance imaging patterns of extensive Chikungunya virus-associated myelitis.

Chikungunya fever is an arbovirus infection transmitted by the same mosquito vector of dengue and Zika virus. Besides high fever, common clinical symptoms include articular pain and general malaise. Neurological involvement is unusual, but some patients may develop peripheral and central nervous system involvement, including meningoencephalitis, myelitis, Guillain-Barré syndrome, and acute disseminated encephalomyelitis. We present three cases of Chikungunya fever complicated with extensive myelitis. The spinal cord magnetic resonance imaging (MRI) pattern is characterized by multiple dotted-like and longitudinal hyperintense lesions, with contrast enhancement, mostly distributed in the peripheral regions of the spinal cord. It seems that these lesions are mostly located in the perivascular spaces (PVS), related or not to virus attack. Involvement of brain PVS can also be demonstrated, as shown in two of the cases described. Considering the MRI pattern, extensive spinal cord lesion should include Chikungunya as a differential diagnosis, especially during an outbreak.

Imaging Aspects of Toxic and Metabolic Myelopathies.

Metabolic and toxic myelopathies usually occurs due to several different causes. Metabolic myelopathy usually occurs due to deficiency of a nutrient, such as vitamin B12. Toxic myelopathy occurs secondary to the exposure to an external toxic agent. Although they may have a difficult diagnosis, determination of the specific cause of myelopathy is of utmost importance, because many causes are amenable to treatment. Although they have many clinical, electrophysiologic, and neuropathologic similarities, imaging may aid in the suspicion of toxic or metabolic myelopathy. The aim of this article, is to review the imaging features of the main toxic and metabolic myelopathies.

The Hypoglossal Nerve.

The hypoglossal nerve is the 12th cranial nerve, exiting the brainstem in the preolivary sulcus, passing through the premedullary cistern, and exiting the skull through the hypoglossal canal. This is a purely motor nerve, responsible for the innervation of all the intrinsic tongue muscles (superior longitudinal muscle, inferior longitudinal muscle, transverse muscle, and vertical muscle), 3 extrinsic tongue muscles (styloglossus, hyoglossus, and genioglossus), and the geniohyoid muscle. Magnetic resonance imaging (MRI) is the best imaging exam to evaluate patients with clinical signs of hypoglossal nerve palsy, and computed tomography may have a complementary role in the evaluation of bone lesions affecting the hypoglossal canal. A heavily T2-weighted sequence, such as fast imaging employing steady-state acquisition (FIESTA) or constructive interference steady state (CISS) is important to evaluate this nerve on MRI. There are multiple causes of hypoglossal nerve palsy, being neoplasia the most common cause, but vascular lesions, inflammatory diseases, infections, and trauma can also affect this nerve. The purpose of this article is to review the hypoglossal nerve anatomy, discuss the best imaging techniques to evaluate this nerve and demonstrate the imaging aspect of the main diseases that affect it.

Intracranial vessel wall magnetic resonance imaging features of infectious vasculitis.

Vasculitis is a complication of several infectious diseases affecting the central nervous system, which may result in ischemic and/or hemorrhagic stroke, transient ischemic attack, and aneurysm formation. The infectious agent may directly infect the endothelium, causing vasculitis, or indirectly affect the vessel wall through an immunological mechanism. The clinical manifestations of these complications usually overlap with those of non-infectious vascular diseases, making diagnosis challenging. Intracranial vessel wall magnetic resonance imaging (VWI) enables the evaluation of the vessel wall and the diseases that affect it, providing diagnostic data beyond luminal changes and enabling the identification of inflammatory changes in cerebral vasculitis. This technique demonstrates concentric vessel wall thickening and gadolinium enhancement, associated or not with adjacent brain parenchymal enhancement, in patients with vasculitis of any origin. It permits the detection of early alterations, even before a stenosis occurs. In this article, we review the intracranial vessel wall imaging features of infectious vasculitis of bacterial, viral, and fungal etiologies.

The role of neuroimaging in the determination of brain death.

Brain death is the irreversible cessation of all brain function. Although protocols for its determination vary among countries, the concept of brain death is widely accepted, despite ethical and religious issues. The pathophysiology of brain death is related to hypoxia and ischemia in the setting of extensive brain injury. It is also related to the effects of brain edema, which increases intracranial pressure, leading to cerebral circulatory arrest. Although the diagnosis of brain death is based on clinical parameters, the use of neuroimaging to demonstrate diffuse brain injury as the cause of coma prior to definitive clinical examination is a prerequisite. Brain computed tomography (CT) and magnetic resonance imaging (MRI) demonstrate diffuse edema, as well as ventricular and sulcal effacement, together with brain herniation. Angiography (by CT or MRI) demonstrates the absence of intracranial arterial and venous flow. In some countries, electroencephalography, cerebral digital subtraction angiography, transcranial Doppler ultrasound, or scintigraphy/single-photon emission CT are currently used for the definitive diagnosis of brain death. Although the definition of brain death relies on clinical features, radiologists could play an important role in the early recognition of global hypoxic-ischemic injury and the absence of cerebral vascular perfusion.

A morte encefálica é a cessação irreversível de todas as funções cerebrais. Embora os protocolos para sua determinação variem entre os países, o conceito de morte encefálica é amplamente aceito, apesar de questões éticas e religiosas. A fisiopatologia da morte encefálica está relacionada a hipóxia e isquemia no cenário de uma lesão cerebral difusa. Também está relacionada aos efeitos do edema cerebral, que aumenta a pressão intracraniana, levando à parada da circulação cerebral. Embora o diagnóstico de morte encefálica seja baseado em parâmetros clínicos, o uso de neuroimagem para demonstrar lesão cerebral difusa como causa do coma antes do exame clínico definitivo é um pré-requisito. A tomografia computadorizada (TC) e a ressonância magnética (RM) de crânio demonstram edema difuso e apagamento de ventrículos e sulcos, associados a herniações transcompartimentais. A angio-TC e a angio-RM demonstram a ausência de fluxo arterial e venoso intracraniano. Em alguns países, a eletroencefalografia, a angiografia por subtração digital cerebral, a ultrassonografia transcraniana com Doppler ou a cintilografia/TC por emissão de fóton único são atualmente usadas para o diagnóstico definitivo de morte encefálica. Embora a definição de morte encefálica dependa de características clínicas, os radiologistas podem desempenhar papel importante no reconhecimento precoce da lesão hipóxico-isquêmica global e da ausência de perfusão vascular cerebral.

Neurological symptoms and neuroimaging alterations related with COVID-19 vaccine: Cause or coincidence?

Although vaccination against Coronavirus disease-2019 (COVID-19) is still occurring, several adverse effects temporally related to these vaccines are already being reported, even if through isolated case reports. In the present study, we describe the lesions seen on magnetic resonance imaging (MRI) of three patients who developed neurological symptoms after receiving the ChAdOX1 nCoV-19 vaccine (Oxford/AstraZeneca). The first patient presented with an ischemic stroke in the posterior limb of the left internal capsule, two days after vaccination. The second patient presented with a left facial nerve palsy, seven days after vaccination. The third patient presented with myelitis, eight days after receiving the vaccine. All patients presented the symptoms after the first dose of the vaccine and did not have a history of previous COVID-19. The real incidence of these types of complications is not known yet, but it is important to consider the possibility of COVID-19 vaccine complications, in patients with a recent history of vaccination and recent development of neurological symptoms, even though this association is only casual. Longitudinal studies are necessary to further analyze the incidence of the adverse effects of each vaccine against SARS-CoV-2.

Potential role of diffusion tensor MRI in the differential diagnosis of mild cognitive impairment and Alzheimer's disease.

OBJECTIVE: The purpose of this study was to evaluate the fractional anisotropy values of several white matter tracts with the aim of differentiating a healthy population from persons with mild cognitive impairment or Alzheimer's disease. SUBJECTS AND METHODS: Seventy-nine patients with memory impairment and 16 volunteer controls participated in the study. MRI was performed with a 1.5-T system. Conventional MR images and diffusion tensor images were obtained for all participants. The diffusion tensor imaging data were postprocessed, and low b-value, fractional anisotropy, and fractional anisotropy color-coded maps were calculated. With the three maps as an anatomic reference, fractional anisotropy was measured for hippocampal formations, superior longitudinal fascicles, posterior cingulate gyri, and the splenium of the corpus callosum. Kruskal-Wallis and Steel-type multiple-comparison nonparametric tests were performed for the statistical analysis. RESULTS: The fractional anisotropy values for the splenium of the corpus callosum, bilateral posterior cingulate gyri, and bilateral superior longitudinal fascicles of patients with mild cognitive impairment and those with probable Alzheimer's disease were significantly lower than the values of controls. No differences were found in hippocampal formations in any group. No significant difference was found in fractional anisotropy values in comparisons of mild cognitive impairment versus possible Alzheimer's disease and probable Alzheimer's disease or comparisons of probable Alzheimer's disease and possible Alzheimer's disease. CONCLUSION: Diffusion tensor imaging is a promising technique for the evaluation of patients with probable mild cognitive impairment. Early detection of the disease expands the treatment options, increasing the likelihood of a good clinical response and enhancing the quality of life of patients and their relatives. Further studies with larger populations are needed to confirm the role of diffusion tensor imaging in the evaluation of memory impairment.

Proton magnetic resonance spectroscopy in school-aged autistic children.

PURPOSE: This study aims to assess cerebral metabolites in school-aged autistic patients through proton magnetic resonance spectroscopy. METHODS: This case-control study included 10 right-handed male children (median age, 9.53 years +/- 1.80) with autism according to DSM-IV criteria, and 10 healthy age- and sex-matched healthy controls (median age, 8.52 years +/- 1.42). Imaging was performed on a 1.5-T scanner utilizing a single voxel point-resolved spectroscopy (PRESS) technique (TR = 1,500 ms, TE = 30 ms). Four cerebral areas were evaluated: bilateral anterior cingulate, left striatum, left cerebellar hemisphere, and left frontal lobe. Peak areas and ratios to creatine (Cr) of N-acetylaspartate (NAA), choline (Cho), and myo-inositol (mI) were analyzed. RESULTS: Compared with controls, autistic children showed a significant increase in mI (P= .021) and Cho (P= .042) peak areas in anterior cingulate and in mI/Cr ratio in anterior cingulate (P= .037) and left striatum (P= .035). The remaining metabolites and ratios were not significantly different between the 2 groups. CONCLUSIONS: This study found a statistically significant increase in myo-inositol and choline in anterior cingulate and left striatum of autistic children compared with controls. In contrast to previous studies, NAA peak area and NAA/Cr and NAA/Cho ratios had no statistically significant decrease in any of the 4 brain regions.