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Neuroplasticity Ch10
Physiological psychology exam #6
| Question | Answer |
|---|---|
| Seizures | -Primary symptoms of epileptics -Generated by brain dysfunction - Caused by brain damage, genes - Preceded by aura -Can be convulsions or minor changes in thought, mood, behavior |
| Epilepsy: Partial | -Simple: symptoms sensory, motor, both symptoms spread as epileptic discharge spreads -Complex: temporal lobes; patient engages in compulsive and repetitive behaviors (automatisms) |
| Epilepsy: Generalized | -Entire brain -Grand mal: loss of consciousness, equilib; tonic-clonic convulsions Resulting hypoxia may cause brain damage -Petit mal: no convulsions; disruption of consciousness assoc. w/ cessation of ongoing behavior (petit mal absence) |
| Parkinson's Disease - Symptoms | -Tremor during inactivity, but not voluntary movement or sleep -Muscular rigidity -Difficulty initiating movement -Mask-like face -Pain, depression develop before motor symptoms |
| Parkinson's Disease - Neurotransmitters involved | -DA: little found in SN and striatum of patients -Autopsy reveals Lewy bodies -Substantia nigra (nigrostriatal pathway to striatum of basal ganglia) -Symptoms can be alleviated by L-dopa, DA agonists |
| Huntington's Disease - Different from Parkinson's | -Rare -Strong genetic basis -Associated w/ severe dementia |
| Huntington's Disease - Symptoms | -Increased fidgetiness -Rapid, complex, jerky movements of entire limbs -Dementia -Eventually incapable of: feeding self, controlling bowels, recognizing children -No cure; death occurs about 15 yrs after onset |
| Multiple Sclerosis - Myelin disorder | -Autoimmune disorder: myelin is the focus (oligodendrocytes, schwann cells) -Areas of degeneration on myelin sheaths -Axons become dysfunctional -Hard scar tissue |
| Multiple Sclerosis - Symptoms | -Visual disturbances -Muscular weakness -Numbness -Tremor -Ataxia (loss of motor coordination) -Dx hard b/c of remission (up to 5 yrs) |
| Multiple Sclerosis - Treatments | -No cure -Some drugs can slow the progression of clinical MS |
| Alzheimer's Disease - Characteristics | -Progressive dementia; selective decline in memory -Intermediate stages marked by: confusion, irritability, anxiety, deterioration of speech -Terminal, no cure -Neurofibrillary tangles, amyloid plaques -Entorhinal cortex, amygdala, hippocampus |
| Alzheimer's Disease - Characteristics (con't) | -NF tangles, amyloid plaques, & neuronal loss also in inf. temporal cortex, post. parietal cortex, PFC -Major genetic component -Definitive Dx only at autopsy |
| Alzheimer's Disease - Amyloid hypothesis | -Amyloid plaques are primary symptom of the disorder, cause all other symptoms -Support: studies ID'd 3 gene mutations causing early-onset of AD & all 3 influence synthesis of amyloid |
| Alzheimer's Disease - Treatments | -Early Tx focus on decline in ACh; low ACh levels were earliest apparent neurochemical changes -Cholinergic agonists -Immunotherapeutic approach: amyloid vaccine |
| Animal models - Kindling model of Epilepsy | -Series of periodic brain stimulations eventually elicit convulsions -Neural changes permanent -Produced by stim. distributed over time -Convulsions similar to those of human epileptics -Comparable to epileptogenesis |
| Animal models - Transgenic mouse model of Alzheimer's Disease | -Genes that accelerate synth. of human amyloid injected into mouse eggs Mice brains contain amyloid plaques like humans, distribution comparable (high concentration in med. temporal lobes) -Mice with amyloid = neural loss, memory disturbances |
| Animal models - MPTP model of Parkinson's Disease | -MPTP found in synthetic heroin -MPTP causes cell loss in subst. nigra similar to that of PD -Level of DA reduced -Deprenyl (monoamine agonist) blocks effects of MPTP; slows progression |
Created by:
rebelis
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