Coma resulting from brain injury or illness usually is a transient state. Within a few weeks, patients in coma either recover awareness, die, or evolve to an eyes-open state of impaired responsiveness such as the vegetative or minimally conscious state. These disorders of consciousness can be transient stages during spontaneous recovery from coma or can become chronic, static conditions. Recent fMRI studies raise questions about the accuracy of accepted clinical diagnostic criteria and prognostic models of these disorders that have far-reaching medical practice and ethical implications (Full text).
A blog on biomedical research and clinical practice from selected open access articles.
Current controversies in states of chronic unconsciousness
Update: diagnosis, treatment, and prognosis of glioma
As the profession of neurology becomes increasingly subspecialized, it becomes more and more difficult for general neurologists to feel comfortable with every category of disease. At no time is this felt more keenly than when an imaging procedure has been performed on a patient for a seizure, headache, or focal neurologic complaint and a brain tumor is discovered. In contrast to consulting with a patient with a movement disorder or neuromuscular disease, there is no time to craft the discussion and discuss a differential diagnosis. As with demyelinating disease or stroke, the scan result dictates an immediate conversation with the patient, but in contrast to those disorders this takes place from the perspective of a provider who understands that the eventual outcome for the patient is likely to be guarded. How to give that message with tact, candor, and some optimism could be the sole topic of this article but, instead, we focus on 5 new ideas that are changing the management of brain tumor patients in the hopes that these points might prove useful during those times (Full text).
Update: Therapeutic options in multiple sclerosis
Care of the patient with multiple sclerosis (MS) is becoming increasingly complex, with new symptomatic therapies (e.g., dalfampridine), enhanced use of disease-modifying therapies that are potentially both more efficacious and more risky (e.g., natalizumab, rituximab) than “standard” immunomodulators, the advent of oral disease-modifying therapies (DMTs) (e.g., fingolimod, cladribine, teriflunomide, laquinimod), and the possibility of regenerative or reparative therapies (e.g., stem cells, neuroprogenitor cells, antibodies to leucine-rich repeat and immunoglobulin (Ig) domain containing NOGO receptor interacting protein-1, i.e., anti-LINGO therapies). All of this is happening in the context of a suggestion that MS may fundamentally result from aberrant venous flow, so-called chronic cerebrospinal venous insufficiency (CCSVI), and a similarly fundamental pathologic discussion of the relationship between inflammation and degeneration over time in patients with MS. Noting the difficulty of choosing among many options, we present discussions of 5 new topics relevant to patients with MS and their neurologists in 2010 (Full text).
Update in Stroke treatment and prevention
It has been almost 15 years since the publication of the landmark National Institute of Neurological Disorders and Stroke tissue plasminogen activator (NINDS-tPA) trial. The findings of the NINDS-tPA trial soon led to Food and Drug Administration (FDA) approval for IV alteplase (tPA) in the treatment of acute ischemic stroke (AIS) that transformed the way neurologists approach this devastating disease. Unfortunately, 15 years removed from the NINDS-tPA trial, IV tPA remains the only FDA-approved drug for the treatment of AIS. Although no major clinical breakthrough has occurred in the AIS treatment front, newer trials have increased the spectrum of patients who can be treated, but failed to find better lytic drugs or ways to identify treatable patients using advanced imaging. Major advancements have transpired in the arena of stroke prevention, especially in endovascular therapy and management of atrial fibrillation (AF). This article aims to summarize 5 new topics in stroke treatment, prevention, and poststroke care that have or will soon affect clinical treatment of stroke patients, and to offer critiques and commentary on how the results of the trials presented can be applied to the care of individual stroke patients (Full text).
Current understanding and management of Parkinson disease: Five new things
PubMed query for “Parkinson disease” yields more than 2,000 articles per year for each of the last 5 years. That is a daunting pile of bedside reading for even the most diligent neurologist. This review highlights 5 emerging topics that are changing our current understanding and management of Parkinson disease (PD). When using the term PD, we mean Lewy body parkinsonism as defined by the clinical criteria of the United Kingdom Parkinson's Disease Society Brain Bank. Other parkinsonian syndromes, such as progressive supranuclear palsy and multiple system atrophy, are beyond the scope of this review (Full text).
Approach to acute or subacute myelopathy
Improved understanding of the differential diagnosis and improved investigative techniques, particularly neuroimaging and serologic testing, have facilitated the diagnosis of patients with acute and subacute myelopathy and reduced the proportion of patients who are labeled as having “idiopathic transverse myelitis.” Additionally, these advances have identified subgroups of patients in whom progression of deficit or future relapses are anticipated, allowing intervention and prophylaxis as appropriate. However, early management remains empiric and consists of high-dose corticosteroids for most patients. In the event of an inadequate response to corticosteroids or a subsequent atypical course, further investigations to detect diagnoses other than “transverse myelitis” should be considered and additional treatments, such as plasmapheresis, may be appropriate. Individualized diagnosis and treatment is more feasible now than in the past (Full text).
Neurology November 1, 2010 vol. 75 no. 18 Supplement 1 S2-S8
Insular cortex
The insular taste cortex contributes to odor qualiting coding
Despite distinct peripheral and central pathways, stimulation of both the olfactory and the gustatory systems may give rise to the sensation of sweetness. Whether there is a common central mechanism producing sweet quality sensations or two discrete mechanisms associated independently with gustatory and olfactory stimuli is currently unknown. Here authors used fMRI to determine whether odor sweetness is represented in the piriform olfactory cortex, which is thought to code odor quality, or in the insular taste cortex, which is thought to code taste quality. Fifteen participants sampled two concentrations of a pure sweet taste (sucrose), two sweet food odors (chocolate and strawberry), and two sweet floral odors (lilac and rose). Replicating prior work we found that olfactory stimulation activated the piriform, orbitofrontal and insular cortices. Of these regions, only the insula also responded to sweet taste. More importantly, the magnitude of the response to the food odors, but not to the non-food odors, in this region of insula was positively correlated with odor sweetness rating. These findings demonstrate that insular taste cortex contributes to odor quality coding by representing the taste-like aspects of food odors. Since the effect was specific to the food odors, and only food odors are experienced with taste, authors suggest this common central mechanism develops as a function of experiencing flavors.
(A) Coronal and sagittal sections of the area of insula where neural response to the food odors shows a positive correlation with the sweetness ratings of those odors. The main images display the unmasked regression maps while the insets labeled 1 depict the masked regressions (i.e., using the “sweet odors and sweet taste overlap” inclusive mask). The insets labeled 2 depict the analysis with the pleasantness and familiarity ratings as covariates. (B) Shows neural response (in parameter estimate) in the insula (at the maximally responding voxel at −45 −3 9), plotted against sweetness ratings for the food (red squares) and floral odors (yellow diamonds). (C) Illustrates the magnitude of the correlation (averaged across all voxels ± standard deviation) in the insula for food odors (in red squares) and non-food odor (yellow diamonds) in comparison to the responses in other areas for food and non-food odors vs. odorless. Note that although there appears to be a significant difference between food and floral odors in the left OFC, this effect this effect does not survive authors' criterion for significance in SPM and is therefore not discussed.
Reference: Veldhuizen MG, Nachtigal D, Teulings L, Gitelman DR and Small DM (2010) The insular taste cortex contributes to odor quality coding. Front. Hum. Neurosci. 4:58. doi: 10.3389/fnhum.2010.00058
Etiquetas:
Insular Cortex,
Neuroimaging,
Neurology,
Neuropsychology
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