Chronic Traumatic Encephalopathy (CTE) is a neurodegenerative disease found in people with a history of repetitive brain trauma, including athletes, veterans, and victims of domestic abuse. Symptoms of CTE lead to changes in mood and behavior and progress over time. The symptoms occur in three clusters: cognitive, behavioral, and mood. Cognitive changes involve difficulty with learning and executive function. Behavioral changes entail decreased impulse control and aggressive or violent behaviors. Mood changes include irritability, lack of motivation, depression, and suicidal thoughts.
Symptoms in all three clusters become more severe over time, and progression of the disease typically leads to dementia. CTE results from years of repetitive brain trauma, which leads to the accumulation of Tau protein in the brain. Research indicates the largest casual factor is sub-concussive impacts sustained frequently over extended periods of time. The repetitive trauma results in formation of clumps of Tau proteins, which spread throughout the brain, causing widespread neurodegeneration.
The limitations of CTE diagnoses complicate treating the disease. Currently, postmortem neuropathological examination is the only way to diagnose CTE. Consequently, treatment of CTE focuses solely on alleviating symptoms via targeted therapies, such as cognitive behavioral therapy and memory training exercises.
Kleine-Levin Syndrome (KLS), a rare neurological disorder, affects approximately one in a million people. About seventy percent of KLS patients are male, and most of them are adolescents or teenagers. KLS symptoms occur in episodes, which typically last from a few days to a few weeks. Episode onset is abrupt but sometimes preceded by flu-like symptoms. The primary symptom of KLS is hypersomnia, but episodes often include a variety of other symptoms such as excessive food intake, irritability, and uninhibited sex drive. After eight to twelve years, episodes typically decrease in both frequency and intensity.
The cause and basis of KLS are unknown, but researchers speculate symptoms may result from malfunction in or damage to the hypothalamus, possibly due to head injury or infectious disease affecting the region. Researchers also suggest some individuals may have a genetic predisposition to develop KLS. According to Stanford Health Care, KLS diagnoses occur by exclusion. To receive the diagnosis, patients experiencing hypersomnia undergo laboratory tests to rule out all other conditions that cause similar symptoms.
Treatment for KLS is minimal. No definitive treatment exists, so patients typically practice watchful waiting for episodes at home. Some individuals with KLS use stimulants to reduce sleepiness, but the medication can simultaneously increase symptoms of irritability.
Tourette’s Syndrome (TS), a neurological disorder named for Dr. Tourette who first described the condition, manifests primarily through symptoms called tics. It occurs across all ethnic groups and affects males about three times more often than females.While the symptoms of TS vary among patients, all individuals with TS exhibit tics. Tics are repetitive, involuntary movements and vocalizations and can be simple or complex. Simple tics occur in a limited number of muscle groups; examples include eye movements and grunting. Complex tics incorporate several muscle groups and involve coordinated movement, such as jumping or exclaiming phrases. Tics tend to improve after the early teen years, and TS patients have a normal life expectancy.
The anatomical basis and cause of TS remain unknown, but research continues to build theories on both. Research indicates TS may result from abnormalities in specific brain regions and neurotransmitters, especially the reduced size of the basal ganglia. The cause of the abnormality is unknown, but may be due to a dopamine imbalance or sensitivity. Twin and family studies suggest TS may be inherited, but researchers remain open to the possibility of environmental and developmental factors, as well.
Tay-Sachs disease is a rare neurodegenerative disorder. It is notably more common in people of Ashkenazi Jewish or French-Canadian descent. Tay-Sachs results from inherited mutations in the HEXA gene, which lead to deficiency of the enzyme hexosaminidase A. The mutations cause failure to produce functional hexosaminidase A; without this enzyme, lipids called gangliosides accumulate in the brain and spinal cord, leading to progressive dysfunction in the central nervous system.
Symptoms and prognosis of Tay-Sachs vary depending on the level of deficiency of hexosaminidase A; the less of the enzyme present, the more severe the symptoms and the earlier the onset. There are three forms of Tay-Sachs: infantile, juvenile, and late onset. Infantile and juvenile forms involve muscle weakness that leads to paralysis, loss of mental function that leads to unresponsiveness, progressive blindness, and seizures; the late onset form includes limited mobility and difficulty speaking and swallowing. While infantile and juvenile Tay-Sachs entail rapid deterioration and early death, late onset Tay-Sachs usually does not lead to shortened lifespan. Although physicians can easily diagnose Tay-Sachs via a blood test to detect levels of hexosaminidase A activity, there is no cure or treatment to slow its progression. Individuals with Tay-Sachs manage the disease with treatments that alleviate symptoms, such as anti-seizure medication to reduce seizures.
Attention Deficit Hyperactivity Disorder (ADHD) is a brain disorder that affects approximately six percent of children and three percent of adults worldwide. The Americans with Disabilities Act recognizes ADHD as a disability. The primary symptoms of ADHD are inattention and/or hyperactivity-impulsivity; these symptoms persist, although sometimes with change, throughout adulthood. Patients may exhibit one or both symptoms; the symptoms must prove chronic and long-lasting, and they must interfere with typical functioning and/or development. Over time, hyperactivity tends to decrease, but inattention and impulsivity continue throughout the life span.
The cause of ADHD is unknown, but research supports several theories that assert it results from chemical, structural, and connectivity abnormalities in the brain. ADHD patients tend to show poor dopamine and norepinephrine function, atypical volume in various brain structures, and differences in brain metabolism. Research suggests these differences may result from interactions between genetic and non-genetic factors. While various genes correlate with ADHD, environmental factors such as maternal prenatal drug use and postnatal exposure to environmental toxins correlate as well. An ADHD diagnosis involves a comprehensive evaluation completed by a licensed clinician or psychiatrist. The evaluation includes interviews, behavior and symptoms rating skills, and review of patient history. While there is no cure for ADHD, treatment options can reduce symptoms and improve functioning. Many patients use a combination of treatments, such as stimulants to improve attention and cognitive behavioral therapy to help monitor behavior.
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