Cognitive Neuropsychology and Functional Brain Imaging: Implications for functional and anatomical models of cognition

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The document discusses how cognitive neuropsychology uses functional brain imaging techniques and data from patients with brain lesions to inform models of normal cognition and its neural underpinnings. Functional imaging allows more precise localization of brain areas involved in cognitive tasks compared to other neuropsychological methods. While early models linked specific cognitive functions to brain regions based on patient data, modern approaches recognize interactive and distributed neural systems and acknowledge limitations of making inferences from single cases or accidental brain lesions.

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Cognitive Neuropsychology and Functional Brain Imaging: Implications for functional and anatomical models of cognition Humphreys & Price, 2001

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Problems for Cognitive-Anatomical Models Damaging Representations, Disconnections and Sampling Bias 1 2 Some brain regions more vulnerable to damage than others. 3 Some cognitive precesses are represented bilaterally, making their disturbances rare.

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#36421 Topic: Discussion 7 Number of Pages: 1 (Double Spaced) Number of sources: 1 Writing Style: APA Type of document: Essay Academic Level:Master Category: Psychology Language Style: English (U.S.) Order Instructions: ATTACHED I will upload the instruction Module Chapter 5 wk6 p630 chapter 5 Methods and Strategies of Research Outline · ■ Experimental Ablation Evaluating the Behavioral Effects of Brain Damage Producing Brain Lesions Stereotaxic Surgery Histological Methods Tracing Neural Connections Studying the Structure of the Living Human Brain Section Summary · ■ Recording and Stimulating Neural Activity Recording Neural Activity Recording the Brain’s Metabolic and Synaptic Activity Stimulating Neural Activity Section Summary · ■ Neurochemical Methods Finding Neurons That Produce Particular Neurochemicals Localizing Particular Receptors Measuring Chemicals Secreted in the Brain Section Summary · ■ Genetic Methods Twin Studies Adoption Studies Genomic Studies Targeted Mutations Antisense Oligonucleotides Section Summary In July 1982, several young people began showing up at neurology clinics in northern California displaying dramatic, severe symptoms (Langston et al., 1983). The most severely affected patients were almost totally paralyzed. They were unable to speak intelligibly, they drooled constantly, and their eyes were open with a fixed stare. Others, less severely affected, walked with a slow, shuffling gait and moved slowly and with great difficulty. The symptoms looked like those of Parkinson’s disease, but that disorder has a very gradual onset. In addition, it rarely strikes people before late middle age, and the patients were all in their twenties or early thirties. The common factor linking these patients was intravenous drug use; all of them had been taking a “new heroin,” a synthetic opiate related to meperidine (Demerol). Some detective work revealed that the illicit drug was contaminated with MPTP, a toxic chemical that damaged dopaminergic neurons and caused the neurological symptoms. Because the symptoms looked like those of Parkinson’s disease, the patients were given L-DOPA, the drug that is used to treat this disease, and they all showed significant improvement in their symptoms. Unfortunately, the improvement was temporary; the drug lost its effectiveness. Fetal transplantation, an experimental neurosurgical method of treating parkinsonism, has shown some promise. The rationale for the procedure is this: The symptoms of parkinsonism, whether from Parkinson’s disease or the toxic effects of MPTP, are caused by the lack of dopamine in the caudate nucleus and putamen. There is at present no way to induce the brain to grow new dopaminergic neurons. However, if dopamine-secreting neurons can be introduced into the caudate nucleus and putamen and if they survive and secrete dopamine, then perhaps the parkinsonian symptoms will diminish. Because the implanted neurons must be healthy and vigorous and not t.

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#36420 Topic: Discussion 6 Number of Pages: 1 (Double Spaced) Number of sources: 1 Writing Style: APA Type of document: Essay Academic Level:Master Category: Psychology Language Style: English (U.S.) Order Instructions: I will upload the instruction Module Chapter 5 wk6 p630 chapter 5 Methods and Strategies of Research Outline · ■ Experimental Ablation Evaluating the Behavioral Effects of Brain Damage Producing Brain Lesions Stereotaxic Surgery Histological Methods Tracing Neural Connections Studying the Structure of the Living Human Brain Section Summary · ■ Recording and Stimulating Neural Activity Recording Neural Activity Recording the Brain’s Metabolic and Synaptic Activity Stimulating Neural Activity Section Summary · ■ Neurochemical Methods Finding Neurons That Produce Particular Neurochemicals Localizing Particular Receptors Measuring Chemicals Secreted in the Brain Section Summary · ■ Genetic Methods Twin Studies Adoption Studies Genomic Studies Targeted Mutations Antisense Oligonucleotides Section Summary In July 1982, several young people began showing up at neurology clinics in northern California displaying dramatic, severe symptoms (Langston et al., 1983). The most severely affected patients were almost totally paralyzed. They were unable to speak intelligibly, they drooled constantly, and their eyes were open with a fixed stare. Others, less severely affected, walked with a slow, shuffling gait and moved slowly and with great difficulty. The symptoms looked like those of Parkinson’s disease, but that disorder has a very gradual onset. In addition, it rarely strikes people before late middle age, and the patients were all in their twenties or early thirties. The common factor linking these patients was intravenous drug use; all of them had been taking a “new heroin,” a synthetic opiate related to meperidine (Demerol). Some detective work revealed that the illicit drug was contaminated with MPTP, a toxic chemical that damaged dopaminergic neurons and caused the neurological symptoms. Because the symptoms looked like those of Parkinson’s disease, the patients were given L-DOPA, the drug that is used to treat this disease, and they all showed significant improvement in their symptoms. Unfortunately, the improvement was temporary; the drug lost its effectiveness. Fetal transplantation, an experimental neurosurgical method of treating parkinsonism, has shown some promise. The rationale for the procedure is this: The symptoms of parkinsonism, whether from Parkinson’s disease or the toxic effects of MPTP, are caused by the lack of dopamine in the caudate nucleus and putamen. There is at present no way to induce the brain to grow new dopaminergic neurons. However, if dopamine-secreting neurons can be introduced into the caudate nucleus and putamen and if they survive and secrete dopamine, then perhaps the parkinsonian symptoms will diminish. Because the implanted neurons must be healthy and vigorous and not trigger the .

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