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These may appear several years before the first motor signs. Others suffer alterations with verbal fluency, decreased cognitive processing speed, visuospatial alterations, and impairment of executive functions. It also affects their attention and they have difficulties focusing and staying concentrated. There’s an alteration in the memory of procedures, which means that patients can forget how they perform learned and automated behaviors. Spatial and long-term memory disorders are common, although they don’t show severe gradual deterioration. The former is due to problems in information retrieval rather than consolidation problems. Cognitive disordersĭuring the first years of this disease, the most characteristic cognitive deficits affect memory and learning. There’s also dystonia and eye movement disorders. In addition, there are other alterations such as stiffness, slowness, and an inability to initiate voluntary movements, especially complex movements. In fact, the risk of suffocation due to swallowing increases. They end up causing significant limitations in a person’s life.įor instance, walking becomes increasingly unstable and people lose mobility entirely.Īlso, it affects their speech and communication becomes more difficult over time. It begins with small tics and progressively increases the choreic movements extending to the head, neck, and extremities.
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These are usually the best-known symptoms of this disease. The symptomatic triad of Huntington’s disease Motor disorders The alterations caused in these structures, or the result of their degeneration, are the causes of the characteristic symptomatic triad of HD. This one participates in motor and non-motor functions. The striatum lives in the anterior brain and is the main route of entry of information to the basal ganglia. Similarly, there’s an alteration in the neurotransmission systems, a lower density of dopamine receptors, and a loss of abundant glutamatergic afferents from the neocortex.
#Theine hundincton desease series
This mutation causes a series of changes in the structure of the striatum and in the cerebral cortex.Īs the disease progresses, there’s marked atrophy of the bilateral caudate nuclei and putamen, along with atrophy of the frontal and temporal lobes. The genetic alteration that causes Huntington’s disease happens in the short arm of chromosome number 4. The genetic cause of Huntington’s disease – an alteration of the brain structure A patient’s life expectancy is between 10 and 20 years. The deterioration is progressive after the appearance of the first symptoms. It brings about choreic symptoms mainly with little cognitive functioning alteration.
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This condition happens through maternal transmission and has a slower evolutionary course. Alterations after age 60 manifest in 10-15% cases. There’s a predominance of parental transition and a clinical picture characterized by slow movement, stiffness, important cognitive disorders, and even epilepsy. Symptoms appear before the age of 20 in 3-10% of cases. However, it’s normal for it to manifest halfway through life, between 35 and 50 years of age. The age of onset is wide, between the ages of 10 and 60. The prevalence of this disease is of about 5-10 people per 100,000 people.