Beruflich Dokumente
Kultur Dokumente
Huang H. Structure of the Fetal Brain: What We Are Learning from Diffusion
Tensor Imaging. Neuroscientist 2010 16: 634
GWAS
TAYLOR MJ. fMRI and MEG in the study of typical and atypical cognitive
development. Neurophysiologie Clinique/Clinical Neurophysiology (2011) 42,
TAYLOR MJ. fMRI and MEG in the study of typical and atypical cognitive
development. Neurophysiologie Clinique/Clinical Neurophysiology (2011) 42,
TAYLOR MJ. fMRI and MEG in the study of typical and atypical cognitive
development. Neurophysiologie Clinique/Clinical Neurophysiology (2011) 42,
TAYLOR MJ. fMRI and MEG in the study of typical and atypical cognitive
development. Neurophysiologie Clinique/Clinical Neurophysiology (2011) 42,
NEUROBIOLOGA TND
SISTEM
A
LMBIC
O
CORTEZA
CEREBRA
L
AUTISMO
TDAH
TALLO
CEREBRA
L
NCLE
OS DE
LA
BASE
CEREBEL
O
anisotropy in autism, particularly in the frontal lobe and corpus callosum (Ben
Bashat et al., 2007), consistent with evidence presented above for early
overgrowth of white matter. By five years of age, however, fractional anisotropy
is found to be reduced in children with autism for tracts that interconnect cortical
regions within the frontal lobes (Sundaram et al., 2008) although it is equivalent
to that found in typically developing children for tracts connecting the frontal
lobes to more posterior cortical regions. In older children and adolescents (1018year-olds) analyses of specific frontal-posterior tracts indicate reduced fractional
anisotropy in autism (Sahyoun et al., 2010) and autism-related differences in
hemispheric lateralization of fractional anisotropy in the arcuate fasciculus
connecting frontal, parietal, and temporal cortices (Fletcher et al., 2010; Knaus et
al., 2010).
Wan CY et al. From music making to speaking: Engaging the mirror neuron
system in autism.
We propose that ASD begins with a failure in the emergence of the specialized functions of
one or more of the set of neuroanatomical structures involved in social information
processing. This failure happens early in ontogeny, within the first nine months to one year
of life, if not earlier. In turn, because the affected regions do not generate the normal stream
of both intrinsic and stimulus driven signals, the normal developmental pattern of
connections among these brain regions is greatly altered. Abnormal brain development is
canalized because the individual with an ASD must develop in a highly social world without
the specialized neural systems that would ordinarily allow him or her to partake in the fabric
of social life, which is woven from opportunities for social reciprocity. These opportunities
provide the basis for normal cognitive development in typically developing children, but are
greatly decreased in ASD.
We are
aware of cases where a child has received a diagnosis of
SLI
from a speech and language therapist, dyslexia from an
educational
psychologist, ADHD from a pediatrician, ASD from
a child psychiatrist and developmental dyspraxia from an
occupational therapist!
ADHD symptoms,
in association with cognitive and learning disorders are
frequent in posttraumatic and postinfectious encephalopathy;
fetal alcohol syndrome and effects; chronic lead poisoning;
cerebral palsy; prematurity; neuromuscular disorders (especially
myotonic dystrophy); neurofibromatosis; fragile X,
Turner, Klinefelter, and Williams syndromes; seizure disorders;
congenital brain anomalies; metabolic disorders; as well
as in a host of less prevalent neurogenetic syndromes (94).
Chronic
hypoxia, as in congenital heart
disease (CHD) and sleep disordered
breathing have actually been shown
to be causal for
ADHD (95).
Castellanos FX, Giedd JN, Marsh WL, Hamburger SD, et al. Quantitative brain magnetic resonance
imaging in attention dficit hiperactivitydisorder.ArchivesGeneral Psychiatry 1996; 607-16
TDAH
ALTERACIONES NEUROANATMICAS:
Kaplan & Sadock's Concise Textbook of Child and Adolescent Psychiatry. Sadock BJ and Sadock VL.
2009. Lippincott Williams & Wilkins.
TDAH
NEUROFISIOLOGA
:
EEG:
Descargas
Actividad Irritativa
epileptiformes
TDAH
NEUROFISIOLOGA:
Hallazgos EEG:
TDAH
TDAH
Atencin
Fronto estriatal
Funcin
ejecutiva
Fronto cerebelar
Recompensa
Booth et al., 2005; Durston et al., 2003, 2006; Epstein et al.,2007; Pliszka et
al., 2006; Rubia et al., 1999, 2005; Schulz et al., 2004, 2005; Smith et al.,
Booth et al., 2005; Durston et al., 2003, 2006; Epstein et al.,2007; Pliszka et
al., 2006; Rubia et al., 1999, 2005; Schulz et al., 2004, 2005; Smith et al.,
Booth et al., 2005; Durston et al., 2003, 2006; Epstein et al.,2007; Pliszka et
al., 2006; Rubia et al., 1999, 2005; Schulz et al., 2004, 2005; Smith et al.,