Ch 10 Brain Damage & Neuroplasticity (pt2)

January 23, 2018 | Author: Anonymous | Category: Science, Health Science, Neurology
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March 20, 2013

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Brain Tumors Cerebrovascular Disorders (Strokes)  Cerebral Hemorrhage & Ischemia

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Closed-Head Injuries Infections  Bacterial & Viral

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Neurotoxins Genetic Factors Programmed Cell Death

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Normal human cells have 23 pairs of chromosomes An extra chromosome 21 results in Down syndrome  Occurs in 0.15% of births ▪ Likelihood increases with maternal age

 Flattened skull & nose, inner eye folds of skin,

short fingers, intellectual impairment & medical complications

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Apoptosis: genetic self-destruct program for neurons (cell suicide) Functions in early development by eliminating extra, unnecessary neurons Also involved in brain damage Passive cell death (necrosis) occurs only when neurons are damaged severely The majority is due to apoptosis  Neurons slowly shrivel, die & break down without

inflammation or causing damage to nearby cells

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Epilepsy Parkinson’s Disease Huntington’s Disease Multiple Sclerosis Alzheimer’s Disease

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Main symptom is repeated seizures, caused by chronic brain dysfunction Different types of seizures  Convulsions ▪ Motor seizures; involve tremors (clonus), rigidity (tonus) & loss of balance and consciousness

 Others happen with seemingly no change in behavior

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All of the previously discussed causes of brain damage can cause epilepsy Often associated with problems at inhibitory synapses

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Diagnosed with scalp electroencephalography (EEG) People often experience a weird psychological change before a convulsion (epileptic aura)  Ex: bad smell, déjà vu, hallucination  Can give a hint of brain area causing

seizures

2 types 1. Partial 

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Partial seizure does not involve the whole brain Caused by synchronous burst of neuron firing

Generalized

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Entire brain is involved Grand mal (“classic” seizure) Petit mal (no convulsions)





Symptoms of a resting tremor, muscular rigidity, difficulty initiating movement, slow movement, masklike face Associated with degeneration of the substantia nigra in the midbrain  Primarily of dopaminergic neurons  So symptoms can be alleviated by L-Dopa

injections (but not permanently)  Other treatments include dopamine agonists



Another progressive motor disorder  Late stages involve severe cognitive decline



Onset around age 40  No cure & usually death within 15 years

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Rare Has a strong genetic basis  If a parent has it, 50/50 chance child will have it

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MS is a progressive disease that attacks the myelin of axons in the CNS Eventually causes dysfunction in the axons & scar tissue develops (sclerosis) An autoimmune disorder Symptoms include visual disturbances, muscular weakness, numbness, tremor & ataxia (loss of motor coordination) Genetic & environmental influences

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The most common cause of dementia Likelihood of having it increases with age  10% of age 65+; 35% of age 85+



Progressive disease

 Early stage: memory decline, attention problems &

personality changes  Mid stage: confusion, irritability, anxiety, problems with speech, swallowing & bladder control  Ultimately terminal



Can only be certain of diagnosis during autopsy

 Presence of neurofibrillary tangles &

amyloid plaques

Neuroplastic responses to brain damage 1. Degeneration 2. Regeneration 3. Reorganization 4. Recovery of function 

 aka neural deterioration  2 types 1. Anterograde degeneration  Degeneration of distal segment ▪ ▪

(Section of axon between the cut & the synaptic terminal) Segment no longer gets energy from the cell body

Retrograde degeneration

2. 

Degeneration of proximal segment ▪ ▪

(Section of axon between the cut & the soma) If the axon cannot reestablish contact with a target, the neuron eventually dies

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Regrowth of damaged neurons Not as successful in mammals as in lower vertebrates & inverts  Almost nonexistant in CNS of adult mammals





Regrowth from proximal stump 2-3 days after axonal damage Does not necessarily mean that function will be returned



The brain can effectively reorganize itself in response to damage  Other areas can compensate for the damaged

area’s function 



Ex: blind individuals have little use for visual cotex, so the auditory & somatosensory cortex expands into this region, giving them heightened sensitivity to hearing & touch Works by strengthening existing connections & making new ones



May be possible to reduce brain damage by blocking neural degeneration  Apoptosis inhibitor proteins  Nerve growth factor  Estrogren ▪ Potentially explains why several brain disorders are less common in women



Molecules that limit degeneration also promote regeneration

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Regeneration in mammalian CNS doesn’t normally happen, but in the lab it can be induced Potential treatment with transplantation of fetal tissue into the brain or injection of embryonic stem cells Rehabilitation training can help by encouraging brain reorganization  Ex: treadmill for spinal cord injuries



Physically & mentally active individuals are less likely to contract neurological disorders & if they do, their symptoms are more mild & they have fuller recovery

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