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Chapter 3

Chapter 3.docx

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Zachariah Campbell

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Chapter 3 – Neurodegenerative Disorders Introduction Neurodegenerative disorders: disorders that involve progressive loss of function or destruction of neurons or various structures of the brain Acquired disorders: disorders caused by an accident, insult, or disease process coming from a source outside the cortex Degenerative Disorders Degenerative disorders: difficulties with destruction of neurons and/or specific areas within the central nervous system • In many cases, the loss of neurons/tissue is not reparable and the loss of ability is permanent Cortical Dementias Def.: damage within the cerebral cortex, which leads to symptoms of dementia. Dementia is usually described with behaviours falling into 3 stages 1. Behaviours that may deviate from the norm for the individual. The individual may not be aware of this a. Example: small changes in personality and memory lapses 2. Individual often notices memory problems and tries to conceal them from others. Confabulation (individual makes up a story to account for memory loss) may occur. a. As stage 2 progresses, the individual may become geographically lost b. May engage in activities that are dangerous to self or others c. Sundowning: worsening of symptoms as the day progresses d. Families begin to consider placement in treatment facilities 3. Serious cognitive deterioration along with problems with self-care a. Many find that individual requires care outside family environment People don’t usually die from dementia but from something else that takes advantage of a nonintact central nervous system. • May be unable to fight off viruses • Most frequent cause of death is pneumonia Affects 5-8% of people older than 65 and 25-50% of people older than 85. Alzheimer’s Type Dementia Def.: dementia characterized by neurofibrillary tangles and amyloid plaques; diagnosis cannot be made until autopsy but is termed Alzheimer’s type based on behavioural symptoms • Neurofibrillary tangles: composed of tau protein; tangles of dead tissue in the brain. Develop when microtubules become twisted. Volume of tangles obstructs living tissue and often strangle it. o Tau: protein that maintains microtubules structure but is altered, allowing tubules to twist. Believed to develop from abnormal phosphorylation • Amyloid plaques: deposits of aluminum silicate and amyloid peptides (beta- amyloid) believed to cause loss of neurons and vascular damage. Obstruct normal tissue. • These plaques/tangles normally appear in aging people but Alzheimer’s is diagnosed by the extent of these and the regions of the brain that they gravitate towards. Loss of neurons is a common feature, especially in the temporal area. • If neurons can’t communicate with major memory areas within cortex, significant memory loss may occur. Loss of neurons also leads to changes in anatomical structure, may point to enlargement of ventricles in Alzheimer’s disease. Present in 10% of people aged 65+ and 25% over 80. Also has inherited genetic component. • If a person has a first-degree relative with the disease, it doubles their chance of acquiring the disease. Three well-established risk factors for Alzheimer’s: • Age • The gene for the protein apolipoprotein E (Apo E) on chromosome 19. Is a naturally occurring protein, helps to carry phospholipids and cholesterol within the body. o The E4 allele (any one of a number of viable DNA codings that occupy a given position on a chromosome) has been linked to various disorders including Alzheimer’s. • Down syndrome. Almost all individuals with this show mental and physical deterioration characteristic of Alzheimer’s if they live longer than 30-40 years. Other factors: • Being female • Lower levels of education • Exposure to aluminum in drinking water • Traumatic brain injury – controversial. The more serious an injury, the more likely the person will develop the disease. • Low level of estrogen in postmenopausal women – controversial. May be confounded with educational level and socioeconomic status Most distinguishing cognitive feature of Alzheimer’s is severe verbal memory difficulties. • Difficulty is in all stages of memory • Other issues: o Orientation o Psychomotor performance o Language/speech fluency o Complex reasoning Treatment for Alzheimer’s: • Drinking red wine as preventative (antioxidants have protective effect) • Medications that stop the development of amyloid plaques • Cognitive deficits treatment is usually with anticholinesterase inhibitors that enhance cholinergic function o People either respond to this or they don’t • Antidepressants • May use typical or atypical antipsychotic medications Frontotemporal Dementias Degenerative disorders of the frontal and temporal lobes. The rest of the cortex remains mostly unharmed. • Slow onset and progression • Usually between 40-65 years of age Symptoms are very similar to Alzheimer’s and, in later stages, almost indistinguishable. Differentiation: • Changes in social behaviour and personality • Lack of insight • Stereotypic behaviours – repeating of a behavioural sequence • Eating a great deal of food • Speech and language changes • Extrapyrimidal symptoms • Primitive reflexes Etiology is unknown but 40-50% if cases are transmitted by autosomal dominate inheritance = dominant non-sex-linked gene • Greater than average incidence of brain trauma 4 years prior to occurrence of symptoms Before, was called Pick’s disease – that is now thought to be a subtype of FTD. Set apart from other FTDs by Pick bodies: composed of tau protein and shaped differently than neurofibrillary tangles Dementia with Lewy Bodies About 20% of patients with dementia. Symptoms include progressive dementia, extrapyramidal signs similar to Parkinson’s, visual hallucinations, delusions, and possibly severe cognitive fluctuations. More rapid decline than other dementias. Presence of Lewy bodies: protein deposits throughout the cortex, paralimbic area, and in the substantia nigra. Improvement has been shown with using cholinesterase inhibitors Subcortical Dementias Affect subcortical brain structures. The behavioural changes that differentiate from cortical dementias: 1. Cognitive slowing with problems in attention and concentration, executive disturbances including impaired concept manipulation, visuospatial abnormalities, and memory difficulties that affect retrieval 2. Absence of aphasia (loss of expressive or receptive language), apraxia (inability to perform purposeful movements), and agnosia (inability to recognize sensory input) 3. Emotional features including apathy, depression, and personality changes. Have movement difficulties – extrapyramidal motor system: modulates movement and maintains muscle tone and posture. Parkinson’s Disease/Parkinsonism Def.: Movement disorder with attendant symptoms. Involuntary tremulous motion with lessened muscle power. May include difficulties moving from resting to walking (vice versa), tendency to bend forward while walking, and cognitive/emotional sequelae. • Not all patients exhibit these • Almost always present is ‘resting tremor’ which disappears during movement and in sleep • Another classic symptom is ‘masked faces’, a lack of facial expressions • Depression is one of most common symptoms but severity appears unrelated to severity of motor symptoms The disease is associated with the depletion of the neurotransmitter dopamine in the basal ganglia, subthalamic nucleus, substantia nigra, and the connections between them all. Etiology is unknown. Typically affects individuals in their fifties. • There may be genetic inheritance • May be related to viral encephalitis, drugs with dopamine antagonistic properties, toxic substances, and vascular disease. PD does have an incidence of dementia that ranges from 2-93%. Treatment: • Medical focuses on the alleviation of symptoms or slowing disease progression o L-Dopa is used to replace dopamine depletion in the subtantia nigra • Surgical treatments include lesions or placing a deep brain stimulator in the regions of the globus pallidus, subthalamic nuclei, or ventral intermediate thalamic nuclei Huntington’s Disease Anatomically caused by atrophy of the GABAergic neurons fo the caudate nucleus and putamen in the corpus striatrum. • Gamma-aminobutyric acid (GABA) is the most common inhibitory neurotransmitter. • Atrophy may also affect the cerebellum, thalamic nucleu, and other subcortical tissue. Reported effects on the basal ganglia as well. Steadily progressive disease, tends to affect individual between 10-20 years of age. • First symptoms are mild and often ignored • As motor symptoms are involved, the disease becomes visible to the individual and others • Pneumonia is most common cause of death Hereditary condition – passes from generation to generation • Caused by an excess number of trinucleotide CAG repeats (cystosine, adenine, and guanine) on chromosome 4 • Is an autosomal dominant disease – half of all offspring of a carrier parent will acquire the disease if they live long enough • Affects more Caucasians Treatment is usually palliatative. Neuroleptic medications are often used to deal with spasmodic movements Progressive Supranuclear Palsy Also known as Steele-Richardson-Olszewski disorder. Classic feature is an inability to look downward. • Similar motor/cognitive/emotional disturbances as with other dementias • Progression of cognitive decline appears to be greater and is consistent with degeneration of both cortical and subcortical regions • Sites of lesions are in the upper brain stem to the basal ganglia and may include the limbic structures and basal ganglia • Degeneration appears to disconnect ascending pathways from these structures to the prefrontal cortex Nonfamilial condition, tends to develop in 60s. May have connection to environmental toxins. Has limited response to dopaminergic or anticholonergic drugs. Progressive Disorders of the Central Nervous System Multiple Sclerosis Def.: Disease caused by destruction of the myelin sheath that covers the axons. At the demyelinated sites, multiple discrete plaques are formed by astrocytes. Classic symptoms: • Weakness • Stiffness • Lack of coordination • Gait disturbances • Bladder and bowel difficulties • Sexual dysfunction • Sensory changes • Heat sensitivity • Fatigue Cognitive impairment is evident in 40-60% of patients. Memory is one of most commonly affected areas. The extent of cognitive deficits is related to location and extent of damage. Tends to follow one of several courses: • Relapsing-remitting: most common. Characterized by clearly defined diseases relapses. Recovery can be full or with residual deficit. No progression of disease between relapses • Secondary-progressive: second most common. First characterized by relapsing- remitting course then progression. Relapses and remissions may or may not occur • Primary-progressive: third most common. Unremitting disease progression from onset for most patients but occasional stabilization and improvement in others. No clear relapse. •
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