How Acoustic Neuroma Or Vestibulocochlear Nerve Affect Hearing
Acoustic neuroma connects the inner ear with the brain. It also has two different parts. One part transmits sounds and the other part helps in sending balance information to the brain from the inner ear. The acoustic neuroma tumor usually arises from a balanced part of the vestibulocochlear nerve. The hearing part of the nerve can also be affected. In this tumor results, audiogram shows poor word recognization and high-frequency hearing loss. This tumor can also cause sudden hearing loss. It affects hearing either by directly affecting the auditory relay centers. It sometimes creates pressure or displaces a certain portion of the brain depending on the size of the brain. If that portion of the brain involves in hearing then the tumor patient may have hearing loss. Therefore hearing loss be a sign of a brain tumor.
Big Brains: An Autism Subtype
In the first study, published in Biological Psychiatry, the researchers used magnetic resonance imaging to track brain size in 294 children with autism and 135 children without autism between the ages of 3 and 12. In children with autism, they found evidence of larger brain size relative to height – or disproportionate megalencephaly – a subtype that has been linked to higher rates of intellectual disability and poorer overall prognosis.
Previous cross-sectional research had found that children with autism have larger brains at early ages, but no evidence of larger brains in later childhood. The widely accepted theory is that these brains normalized or shrank as the children grew up.
The MIND Institute study found that wasnt the case. The children who had bigger brains at age 3 still had bigger brains at age 12. Why? Unlike most research, which studies different individuals at different time points, this research studied the same children longitudinally, or over time.
Also, unlike most other studies, this one includes children with significant intellectual disabilities. These were the children who tended to have the big brain form of autism.
David Amaral, co-senior author on both studies, suggested that the difference between this and previous research was that children with intellectual disability were left out of previous cross-sectional studies focused on older children.
Proportion Of Total Fixation Duration
TD youth , youth with ASD , and PBTS spent comparable amounts of time viewing the screen in general with no significant group differences on percentage of total fixation duration across all the videos F = 1.49, p> .23, p2 = 0.03.
In the omnibus 3×2×2 repeated-measures ANOVA evaluating group differences in proportional total fixation duration by stimulus type and condition , there was a significant three-way interaction, F = 6.14, p< .01, p2 = 0.12 . Within the joint condition, there was a group difference in gaze duration towards faces, F = 6.12, p< .01, p2 = 0.12. Bonferroni post-hoc tests indicated that PBTS looked at faces less than TD youth, p< .01, with no differences between PBTS and youth with ASD, p> .88. There was not a group difference for gaze duration towards hands in the joint condition, F = 2.88, p = .06, p2 = 0.06. Within the parallel condition, there was a group difference in gaze duration towards faces, F = 4.85, p< .01, p2 = 0.10. Bonferroni post-hoc tests indicated that PBTS looked at faces less than TD youth, p< .01, with no differences between PBTS and youth with ASD, p = .28. There also was a group difference in fixation duration towards hands in the parallel condition, F = 3.40, p< .05, p2 = 0.07, with PBTS looking more at hands than youth with ASD, p< .05, with no differences between PBTS and TD youth, p = .42.
Proportional Gaze Fixation Duration: Faces and Hands by Group and Condition
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The Specificity Of Autism
Whereas synaptic changes presumably underlie all forms of learning, the synaptic view of autism does not provide an explanation for the preferential loss of linguistic and social functions in autism. Although there is little data on this point, several hypotheses seek to explain this specificity. In one view, specific neural circuits essential for social behavior are preferentially disrupted by mutations in either synaptic or other proteins. For example, vasopressin and oxytocin regulate social behavior in mammals , and hence synaptic defects in oxytocin and vasopressin pathways could cause defects in human social behavior . Such a social learning model may also relate to the observed male-female differences in autism prevalence . The basis for this male-female difference in autism prevalence is not understood, but one hypothesis is that the male brain may be built in such a way as to be particularly susceptible to abnormalities in pathways that control social behavior . In addition, some of the cognitive features of higher-functioning autistic patients or even the outstanding gifts of so-called autistic savants remain to be explained.
What To Ask Your Childs Doctor
To diagnose autism, a doctor will check your childâs development and behavior. The doctor may ask you questions, take a full health history, and observe your kid’s behavior.
If the doctor thinks they might have ASD, they may suggest an evaluation. Thatâs when a team of experts who specialize in autism — including a neurologist, psychologist, psychiatrist, speech therapist, or other professionals — do a series of tests and screenings to see if your child has autism or another issue, like a psychological or speech disorder.
If you think your child may have been misdiagnosed with autism or may have another health problem, ask your childâs doctor these questions:
Have you checked my childâs hearing?Hearing problems can cause speech development delays and other issues that can be mistaken for autism.
Are there other tests we should consider?For example, if you live in an old home, you may want to request a test to check for lead in your childâs blood.
Can I see a specialist or a team of specialists?If your doctor says your kid has autism, but your child hasnât also seen a neurologist, psychiatrist, or other professionals who specialize in ASD, ask for referrals so you can get more information.
Can we move forward with treatment even if weâre not sure what this is?If your child has a developmental delay that may or may not be autism, treatment such as occupational therapy, speech therapy, or social skills training may still help.
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One Gene Links Autism And Tumor Disorder
You are free to share this article under the Attribution 4.0 International license.
Scientists have linked mutations in a single gene to autism in people who have a rare tumor syndrome typically diagnosed in childhood.
The findings, in patients with neurofibromatosis type 1 , may lead to a better understanding of the genetic roots of autism in the wider population.
For a study published in JAMA Psychiatry, researchers looked at 531 patients at six clinical centers in the United States, Belgium, the United Kingdom, and Australia and found that mutations in the NF1 gene that cause the disease also contributed to autistic behaviors in almost half of the patients.
NF1 is caused by mutations in a single geneNF1, says first author Stephanie M. Morris, an instructor in neurology at Washington University in St. Louis.
Our research indicates that this single gene also is associated with autism spectrum disorders in these same patients. That may make it possible to look downstream from the gene to find common pathways that contribute to autism in the wider population.
In the 25-plus years that Ive taken care of kids with NF1, weve only recently started to recognize that these children also often have symptoms of autism, says senior investigator David H. Gutmann, professor of neurology and director of the Washington University NF Center.
Different Types Of Autism
Changes in epigenetic marks in three brain regions from patients with ASD-revealed shared molecular and cellular pathways. Graphic: Courtesy of Drs. Daniel Geschwind and Shyam Prabhakar
UCLA scientists and their colleagues have found evidence that an abnormal pattern of brain cells is common in people with different types of autism-spectrum disorders. The abnormal pattern discovered in the study concerns a certain type of epigenetic mark, a chemical modification that occurs frequently on chromosomes and helps regulate the activity of nearby genes.
The findings suggest that although autism-spectrum disorders have multiple causes, they mostly involve problems in a common set of biological pathways, which are actions among certain molecules within a cell that lead to specific changes such as turning genes on or off or assembling new molecules. The findings may lead to a better understanding of how autism-spectrum disorders arise and perhaps one day to the development of drugs that target some of these irregular pathways.
The uniformity of this abnormal pattern in the autism samples was surprising, given that these samples were from people whose autism was known to have different causes, says Daniel Geschwind, MD , PhD, Gordon and Virginia MacDonald Distinguished Chair in Human Genetics. It suggests the possibility that different factors can cause autism-spectrum disorders through a set of common pathways.
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White Matter: Connecting The Clinical Dots
The second study, also published in Biological Psychiatry, linked changes in the brains white matter growth with autism traits in some children.
The researchers used a type of MRI scan called diffusion-weighted imaging, which allowed them to look at white matter regions, or tracts, in the brain. White matter provides the structural connections in the brain, allowing different regions to communicate with each other.
The study included 125 children with autism and 69 typically developing children who served as controls, between the ages of 2.5 and 7.
The researchers found that the development of the white matter tracts in the brain was linked to changes in autism symptom severity. They observed slower development in children whose symptom severity increased over time, and faster development in those with decreased severity over time.
From a biological standpoint, this emphasizes the role of white matter development in autism and autism symptoms, said Derek Sayre Andrews, postdoctoral scholar at the MIND Institute and lead author on the paper. We hope that in the future, measurements like this can identify children who would benefit from more intensive intervention and serve as a marker to determine the effectiveness of an intervention for a particular child, he said.
Aphasia From Brain Tumor
Although aphasia typically results from a stroke or brain injury, brain tumors can also cause aphasia. A brain tumor is a mass of cells that grows in the brain. Brain tumors can either be benign or malignant . A tumor can cause aphasia if it impacts the brains language centers. Aphasia due to cancer is called neoplastic aphasia.
Although brain tumors are not as common as strokes, about 30-50% of people with brain tumors experience aphasia. This is higher than the rate of people who experience aphasia following a stroke.
As with aphasia from other causes, the specific impairments will vary from one person to another. Impairments are impacted by the location, size, and grade of the tumor as well as the age of person. Aphasia due to brain tumor appears to be similar to aphasia due to stroke. However, there is not a lot of research on aphasia due to brain tumor and the similarities and differences to aphasia from other causes.
The most common type of aphasia due to brain tumor is anomic aphasia. Aphasia due to brain tumors is more likely to be short-term and more mild than post-stroke aphasia. The outcome and prognosis for cancer-related aphasia is also dependent on the success of the medical treatment. If the tumor is treated successfully, the aphasia is likely to resolve.
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An Accumulation Of T Cells And Astrocytes In Postmortem Brain Tissue Hints At Possible Autoimmune Origins For Many Cases Of Autism
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About four years ago, pathologist Matthew Anderson was examining slices of postmortem brain tissue from an individual with autism under a microscope when he noticed something extremely odd: T cells swarming around a narrow space between blood vessels and neural tissue. The cells were somehow getting through the blood-brain barrier, a wall of cells that separates circulating blood from extracellular fluid, neurons, and other cell types in the central nervous system, explains Anderson, who works at Beth Israel Deaconess Medical Center in Boston. I just have seen so many brains that I know that this is not normal.
He soon identified more T-cell swarms, called lymphocytic cuffs, in a few other postmortem brains of people who had been diagnosed with autism. Not long after that, he started to detect another oddity in the brain tissuetiny bubbles, or blebs. Id never seen them in any other brain tissue that Ive looked at for many, many different diseases, he says. Anderson began to wonder whether the neurological features he was observing were specific to autism.
Ashley Yeager is an associate editor at The Scientist. Email her at .Follow her on Twitter .
What Causes Brain And Spinal Cord Tumors In Adults
Many different types of tumors can start in the brain or spinal cord. These different tumors are unlikely to all have the same causes, but they might share some things in common.
The cause of most brain and spinal cord tumors is not fully understood, and there are very few well-established risk factors. But researchers have found some of the changes that occur in normal brain cells that may lead them to form brain tumors.
Normal human cells grow and function based mainly on the information in each cells DNA. Brain and spinal cord tumors, like other tumors, are caused by changes in the DNA inside cells. DNA is the chemical that makes up our genes, which control how our cells function. We usually look like our parents because they are the source of our DNA. But DNA affects more than how we look.
Some genes control when our cells grow, divide into new cells, and die:
- Certain genes that help cells grow, divide, and stay alive are called oncogenes.
- Genes that help keep cell division under control, repair mistakes in DNA, or make cells die at the right time are called tumor suppressor genes.
Cancers can be caused by DNAchanges that turn on oncogenes or turn off tumor suppressor genes. These gene changes can be inherited from a parent, but more often they happen during a persons lifetime.
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When To See A Gp
See a GP if you have these types of symptoms, particularly if you have a headache that feels different from the type of headache you usually get, or if headaches are getting worse.
You may not have a brain tumour, but these types of symptoms should be checked.
If the GP cannot identify a more likely cause of your symptoms, they may refer you to a doctor who specialises in the brain and nervous system for further assessment and tests, such as a brain scan.
Apparent Reversal Of Neurobiological Defects In The Adult
A remarkable finding in some recently studied animal models of autistic symptoms has been the surprising degree to which autistic symptoms have been apparently reversed or ameliorated by replacing or modulating gene function after birth or even in the adult. The first example of this came with a Drosophila model of Fragile × syndrome . Normally, the mutant flies have a defect in social/courtship learning and also have defects in the axons of neurons clustered in a brain region known as the mushroom body. The Fragile × disease pathway was modulated by administration of several drugs including metabotropic glutamate antagonists that can decrease the excessive protein translation caused by mutations in FMR or even using lithium carbonate, which modulates downstream signaling of the Fragile × pathway through the kinase GSK-3. Remarkably, in flies born with fixed defects in social behavior the phenotype could be rescued almost completely in adulthood by administration of metabotropic glutamate antagonists or even lithium .
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Research Shows Gene Reactivation Can Be Used To Treat Fragile X Syndrome
- University of California – Riverside
- Researchers report they were able to ameliorate Fragile X syndrome symptoms after inserting the Fmr1 gene into the brains of very young transgenic mice that had been genetically engineered to lack this gene. When the researchers measured brain activity for signs of anxiety and hyperactivity in response to stimuli such as stresses and sounds, they found that the reactivation of the gene in these mice had led them to no longer show Fragile X syndrome symptoms.
Fragile X syndrome, or FXS, a leading genetic cause of autism, affects around one in 4,000 males and one in 6,000 females. Its symptoms include increased anxiety, intellectual disability, repetitive behaviors, social communication deficits, and abnormal sensory processing. People living with FXS generally lack the fragile X mental retardation 1 gene, or Fmr1, in their brain cells. If their cells have this gene, it is silent and not producing a protein called FMRP.
Researchers at the University of California, Riverside, report in the journal Neurobiology of Disease they were able to ameliorate FXS symptoms after inserting Fmr1 into the brains of very young transgenic mice that had been genetically engineered to lack this gene. When the researchers measured brain activity for signs of anxiety and hyperactivity in response to stimuli such as stresses and sounds, they found that the reactivation of the Fmr1 gene in these mice had led them to no longer show FXS symptoms.
More Evidence That Autism Is A Brain ‘connectivity’ Disorder
- Children’s Hospital Boston
- Studying a rare disorder that also causes autism in 25-50 percent of affected patients, new research supports the emerging idea that autism results from disrupted brain “connectivity” causing improper information flow. These abnormalities might be reversible with rapamycin or rapamycin-like drugs, which the studies researchers will be bringing to clinical trial later this year.
Studying a rare disorder known as tuberous sclerosis complex , researchers at Children’s Hospital Boston add to a growing body of evidence suggesting that autism spectrum disorders, which affect 25 to 50 percent of TSC patients, result from a miswiring of connections in the developing brain, leading to improper information flow. The finding may also help explain why many people with TSC have seizures and intellectual disabilities.
Findings were published online in Nature Neuroscience on January 10.
TSC causes benign tumors throughout the body, including the brain. But patients with TSC may have autism, epilepsy or intellectual disabilities even in the absence of these growths. Now, researchers led by Mustafa Sahin, MD, PhD, of Children’s Department of Neurology, provide evidence that mutations in one of the TSC’s causative genes, known as TSC2, prevent growing nerve fibers from finding their proper destinations in the developing brain.
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