Ch 10 Brain Damage & Neuroplasticity (pt2)

March 20, 2013 Ch 10 Brain Damage & Neuroplasticity (pt2)

Causes of Brain Damage • Brain Tumors • Cerebrovascular Disorders (Strokes) • Cerebral Hemorrhage & Ischemia • Closed-Head Injuries • Infections • Bacterial & Viral • Neurotoxins • Genetic Factors • Programmed Cell Death

Genetic Factors • 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

Programmed Cell Death • 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

Neuropsychological Diseases • Epilepsy • Parkinson’s Disease • Huntington’s Disease • Multiple Sclerosis • Alzheimer’s Disease

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

Epilepsy • 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

Epilepsy • 2 types • Partial • Partial seizure does not involve the whole brain • Caused by synchronous burst of neuron firing • Generalized • Entire brain is involved • Grand mal (“classic” seizure) • Petit mal (no convulsions)

Parkinson’s Disease • Symptoms of a resting tremor, muscular rigidity, difficulty initiating movement, slow movement, masklike face • Associated with degeneration of the substantianigra in the midbrain • Primarily of dopaminergic neurons • So symptoms can be alleviated by L-Dopa injections (but not permanently) • Other treatments include dopamine agonists

Huntington’s Disease • Another progressive motor disorder • Late stages involve severe cognitive decline • Onset around age 40 • No cure & usually death within 15 years • Rare • Has a strong genetic basis • If a parent has it, 50/50 chance child will have it

Multiple Sclerosis • 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

Alzheimer’s Disease • 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 • Neuroplastic responses to brain damage • Degeneration • Regeneration • Reorganization • Recovery of function

Neural Degeneration • aka neural deterioration • 2 types • 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 • 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

Neural Regeneration • 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

Neural Reorganization • 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

Neuroplasticity & the Treatment of Nervous System Damage • 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

Neuroplasticity & the Treatment of Nervous System Damage • 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

Ch 10 Brain Damage & Neuroplasticity (pt2)