Chapter 16--DO NOT STUDY Flashcards
1
Q
Traumatic brain injury (TBI)
A
a wound to the brain that results from a blow to the head, is the most common form of brain damage in people under age 40. TBI commonly results from the head making impact with other objects
2
Q
what do the brains of people with multiple concussions show?
A
extensive, diffuse loss of cerebral tissue.
3
Q
Brain damage from TBI
A
Trauma can disrupt the brain’s blood supply, induce bleeding (leading to increased intracranial pressure), cause swelling (leading to increased intracranial pressure), expose the brain to infection, and scar brain tissue (the scarred tissue becomes a focus for later epileptic seizures)
4
Q
Concussion,
A
the common term for mild traumatic brain injury (MTBI)
5
Q
what is chronic traumatic encephalopathy characterized by?
A
neurofibrillary tangles, plaques, and neuronal death. Cerebral atropy and expanded ventricles due to cell loss are typical in advanced cases.
6
Q
what commonly accompanies TBI?
A
a loss of consciousness that may be brief (minutes) or prolonged (coma
7
Q
what does the duration of unconsciousness during TBI tell you?
A
serves as a measure of the severity of damage, because it correlates directly with mortality, intellectual impairment, and deficits in social skills.
8
Q
two behavioral effects from TBI
A
(1) impairment of the specific func- tions mediated by the cortex at the coup (the site of impact) or countercoup (opposite side) lesion (2) more generalized impairments from widespread trauma throughout the brain.
9
Q
Movement of the hemispheres in relation to one another causes what?
A
tearing characterized by a loss of complex cognitive functions, including reductions in mental speed, concentration, and overall cognitive efficiency.
10
Q
Traumatic brain injuries that damage the frontal and temporal lobes also tend to significantly affect what?
A
personality and social behavior
11
Q
what is frustrating about TBI?
A
difficult to diagnose
12
Q
N-acetylaspartate (NAA),
A
the second most abundant amino acid in the human brain
13
Q
NAA &; TBI
A
People with traumatic brain injuries show a chronic decrease in NAA that correlates with the severity of the injury
14
Q
chronic traumatic encephalopathy (CTE)
A
Progressive degenerative disease caused by multiple concussions and other closed-head injuries, characterized by neurofibrillary tangles, plaques, and cerebral atrophy and expanded ventricles due to cell loss.
15
Q
magnetic resonance spectroscopy (MRS)
A
Modification of MRI to identify changes in specific markers of neuronal function; promising for accurate diagnosis of traumatic brain injuries.
16
Q
how long does recovery from head trauma last?
A
may continue for 2 to 3 years and longer, but most cognitive recovery occurs in the first 6 to 9 months
17
Q
recovery of memory symptoms in head trauma
A
Recovery of memory functions appears to be slower than recovery of general intelligence, and the final level of memory performance is lower than for other cognitive functions.
18
Q
People with brainstem damage,
A
as inferred from oculomotor disturbance, have a poorer cognitive outcome, and a poorer outcome is probably true of people with initial dysphasias or hemiparesis as well.
19
Q
what is significantly reduced after TBI?
A
quality of life—in social inter- actions, perceived stress levels, and enjoyment of leisure
20
Q
stroke
A
an interruption of blood flow from either the blockage of a vessel or bleeding from a vessel.
21
Q
ischemia
A
Lack of blood to the brain as a result of stroke.
22
Q
diaschisis
A
Neural shock that follows brain damage in which areas connected to the site of damage show a temporary arrest of function.
23
Q
neuroprotectant
A
Drug used to try to block the cascade of poststroke neural events.
24
Q
what happens in the first seconds to minutes after ischemia?
A
changes begin in the ionic balance of the affected regions, including changes in pH and in the properties of the cell membrane.
25
stroke & glutamate
Release of massive amounts of glutamate results in prolonged opening of calcium channels in cell membranes.
26
stroke & calcium channels
Open calcium channels in turn allow toxic levels of calcium to enter the cell, not only producing direct toxic effects but also instigating various second-messenger pathways that can harm neurons. In the ensuing minutes to hours, mRNA is stimulated, altering the production of proteins in the neurons and possibly proving toxic to the cells.
27
brain swelling & TBI
Brain tissues become inflamed and swollen, threatening the integrity of cells that may be far removed from the stroke site. As in TBI, an energy crisis ensues as mitochondria reduce their production of ATP to produce cerebral energy.
28
neuronal shock & TBI
A form of neural shock occurs. During this diaschisis, areas distant from the damage are functionally depressed. Thus, not only are localized neural tissue and its function lost but areas related to the damaged region also suffer a sudden withdrawal of excitation or inhibition.
29
stroke & metabolism
Stroke may also be followed by changes in the metabolism of the injured hemi- sphere, its glucose utilization, or both, which may persist for days. Like diaschisis, these metabolic changes can have severe effects on the functioning of otherwise normal tissue. For example, after a cortical stroke, metabolic rate has been shown to decrease about 25 percent throughout the rest of the hemisphere.
30
tissue plasminogen activator (t-PA)
clot-busting drug; must be administered within 3 to 5 hours to be effective; ideal treatment is to restore blood flow in blocked vessels before the cascade of nasty events begins.
31
constraint-induced therapy,
confronts a problem in poststroke recovery related to learned nonuse. For example, stroke patients with motor deficits in a limb often compensate by overusing the intact limb, which in turn leads to increased loss of use in the impaired limb.
32
what is done in constraint-induced therapy?
the intact limb is held in a sling for several hours per day, forcing the patient to use the impaired limb
33
what can help augment speech therapy after a left-hemisphere stroke?
music and singing
34
epilepsy
a person suffers recurrent seizures that register on an electroencephalogram (EEG) associated with disturbances of consciousness; 1 person in 20 experiences at least one seizure in his or her lifetime
35
what three symptoms are found within the variety of epileptic episodes?
aura, loss of consciousness, seixures
36
aura
or warning, of impending seizure may take the form of a sensation—an odor or a noise—or may simply be a “feeling” that the seizure is going to occur.
37
loss of consciousness
ranges from complete collapse in some people to simply staring off into space in others. The period of lost consciousness is often accompanied by amnesia, including forgetting the seizure itself.
38
seizures
commonly have a motor component, but as noted, the movement characteris- tics vary considerably. Some people shake; others exhibit automatic movements, such as rubbing the hands or chewing.
39
Jacksonian focal seizures
for example, the at- tack begins with jerking movements in one part of the body—a finger, a toe, or the mouth—and then spreads to adjacent parts
40
Complex partial seizures
originate most commonly in the tem- poral lobe and somewhat less frequently in the frontal lobe
41
three common manifestations of Complex partial seizures
Subjective experiences, Automatisms, Postural changes,
42
subjective experiences in complex partial seizures
for example, forced, repetitive thoughts, alterations in mood, feelings of déjà vu, or hallucinations—before the attack
43
automatisms in complex partial seizures
repetitive, stereotyped movements such as lip smacking or chewing or activities such as undoing buttons during the attack
44
postural changes in complex partial seizures
such as when the person assumes a catatonic (frozen) posture, during the attack
45
symptomatic seizure
Identified with a specific cause, such as infection, trauma, tumor, vascular malformation, toxic chemicals, very high fever, or other neurological disorders.
46
idiopathic seizure
Appears spontaneously and in the absence of other diseases of the central nervous system.
47
focal seizure
Seizure that begins locally (at a focus) and then spreads out to adjacent areas.
48
automatism
Unconscious, repetitive, stereo- typed movement characteristic of seizure.
49
catatonic posture
Rigid or frozen pose resulting from a psychomotor disturbance.
50
grand mal seizure
Seizure characterized by loss of consciousness and stereotyped motor activity.
51
postictal depression
Postseizure state of confusion and reduced affect.
52
petit mal seizure
Seizure of brief duration, characterized by loss of awareness with no motor activity except for blinking, turning the head, or rolling the eyes.
53
4 stages of grand mal seizures
1. tonic stage (body stiffens and breathing stops) 2. clonic stage (rhythmic shaking) 3. postseizure postictal depression 4. a period of coma after the seizure ends
54
how long to petit mal seizures last?
typically less than 10 seconds
55
The treatment of choice for epilepsy
anticonvulsant drugs, including diphenylhy- dantoin (DPH, Dilantin), phenobarbital, or one of about twenty other approved drugs; mainly sedative and anesthetic agents when given in low doses
56
A major site of action in epilepsy medications
the inhibitory GABAA receptor, which acts on a wide variety of neurons.
57
multiple sclerosis
the myelin that encases axons is damaged and the functions of the neurons disrupted. MS is characterized by the loss of myelin in both motor and sensory tracts and nerves. The myelin sheath and in some cases the axons are destroyed in both brain and spinal cord
58
autoimmune disease
Illness resulting from the loss of the immune system’s ability to discriminate between foreign pathogens in the body and the body itself.
59
dementia
Acquired and persistent syndrome of intellectual impairment characterized by memory and other cognitive deficits and impairment in social and occupational functioning.
60
prevalence of dementias
affect from 1 to 6 percent of the population older than age 65 and from 10 to 20 percent older than age 80.
61
Nondegenerative dementias,
a heterogeneous group of disorders with diverse eti- ologies, including diseases of the vascular or endocrine systems, inflammation, nutri- tional deficiency, and toxic conditions
62
Degenerative dementias
presumably have a degree of genetic transmission; Parkinson’s disease and Alzeimer’s disease
63
what is implicated in Parkinson's?
seems related to degeneration of the substantia nigra and to the loss of the neurotransmitter dopamine produced there and released in the striatum.
64
onset of Parkinson's
The symptoms of Parkinson’s disease begin insidiously, often with a tremor in one hand and slight stiffness in the distal parts of the limbs. Movements may then become slower, the face becoming masklike with loss of eye blinking and poverty of emotional expression.
65
The four major symptoms of Parkinson’s disease
are tremor, rigidity, loss of spontaneous movement (akinesia), and disturbances of posture.
66
positive symptoms of Parkinson's disease
tremor at rest, muscular rigidity, involuntary movements
67
tremor at rest
Alternating movements of the limbs occur when they are at rest and stop during voluntary movements or sleep.
68
Muscular rigidity
Rigidity,or increased muscle tone simultaneously in both extensor and flexor muscles, is particularly evident when the limbs are moved passively at a joint. Movement is resisted, but with sufficient force, the muscles yield for a short distance and then resist movement again. Thus, complete passive flexion or exten- sion of a joint occurs in a series of steps, giving rise to the term cogwheel rigidity.
69
Involuntary movements.
Small movements or changes in posture, sometimes referred to as akathesia or “cruel restlessness,” may be concurrent with general inactivity to relieve tremor and sometimes to relieve stiffness but often occur for no apparent reason. Other involuntary movements are distortions of posture, such as occur dur- ing oculogyric crisis (involuntary turns of the head and eyes to one side), which last for periods of minutes to hours.
70
negative symptoms of Parkinson's disease
disorders of posture, disorders of righting, disorders of locomotion, speech disturbance, akinesia
71
Disorders of posture
A disorder of fixation; Disorders of equilibrium
72
Disorders of righting
A person has difficulty in achieving a standing position from a supine position. Many advanced patients have difficulty even in rolling over.
73
Disorders of locomotion
Normal locomotion requires support of the body against gravity, stepping, balancing while the weight of the body is transferred from one leg to the other, and pushing forward. Parkinson patients have difficulty initiating stepping. When they do walk, they shuffle with short footsteps on a fairly wide base of sup- port because they have trouble maintaining equilibrium when shifting weight from one leg to the other. On beginning to walk, Parkinson patients often demonstrate festination: they take faster and faster steps and end up running forward.
74
Speech disturbances
One symptom most noticeable to relatives is the almost complete absence of prosody (rhythm and pitch) in the speaker’s voice.
75
Akinesia
Poverty or slowness of movement may also manifest itself in a blankness of facial expression, a lack of blinking or swinging the arms when walking, a lack of spontaneous speech, or an absence of normal fidgeting. Akinesia is also manifested in difficulty making repetitive movements, such as tapping, even in the absence of rigidity. People who sit motionless for hours show akinesia in its most striking manifestation.
76
disorder of fixation
presents as an inability or difficulty in main- taining a part of the body in its normal position in relation to other parts. A person’s head may droop forward or a standing person may gradually bend forward, ending up on the knees
77
Disorders of equilibrium
create difficulties in standing or even sitting unsupported. In less severe cases, people may have difficulty standing on one leg, or if pushed lightly on the shoulders, they may fall passively without taking corrective steps or attempting to catch themselves.
78
cognitive symptoms of parkinson's
impoverishment of feeling, libido, motive, and attention; people may sit for hours, apparently lacking the will to begin or con- tinue any activity.
79
causes of Parkinson's
loss of cells in the substantia nigra—may be due to disease, such as encephalitis or syphilis, to drugs such as MPTP, or to unknown causes. Idiopathic causes—those related to the individual—may include environmental pollutants, insecticides, and herbicides;
80
MPTP
(1-methyl-4-phenylpyridinium), a modi- fied form of heroin that causes Parkinson’s disease.
81
treatments for Parkinson's
physical therapy, psychological treatment, music and exercise therapy, drugs
82
objectives of pharmacological treatments for Parkinson's
1. To increase the activity in whatever dopamine synapses remain 2. Tosuppresstheactivityinstructuresthatshowheightenedactivityintheabsenceof adequate dopamine action
83
how L-dopa works
l-Dopa is converted into dopamine in the brain and enhances effective dopamine transmission; Naturally occurring anticholinergic drugs, block the cholinergic systems of the brain that seem to show heightened activity in the absence of adequate dopamine activity.
84
newer treatment for Parkinson's
A newer course of treatment proposes to increase the number of dopamine cells either by transplanting stem cells that could then be induced to take a dopaminergic phenotype or by stimulating the production of endogenous stem cells and their migration to the basal ganglia
85
risk factors for alzheimers
include the presence of the Apoe4 gene, below-average IQ, poor education, and TBI.
86
anatomical changes in alzheimers
emergence of amyloid plaques (clumps of protein from dead neurons and astrocytes), chiefly in the limbic cortex and neocortex. Increased plaque concentration in the cortex has been cor- related with the magnitude of cognitive deterioration; neurofibrillary tangles (accu- mulations of microtubules from dead cells) found in both the neocortex and the limbic cortex, where the posterior half of the hippocampus is affected more severely than the anterior half
87
brain changes in alzheimers
the cortex atrophies (shrinks) and can lose as much as one-third of its volume as the disease progresses
88
what is spared in alzheimers?
the primary sensory and motor areas, especially the visual cortex and the sensory–motor cortex, are relatively spared.
89
what is most affected in alzheimers?
The entorhinal cortex is affected earliest and most severely. The entorhinal cortex is the major relay for information from the neocortex traveling to the hippocampus and related structures, then back to the neocortex. Entorhinal damage is associated with memory loss.
90
what causes widespread atrophy in alzheimers?
loss of dendritic arborization
91
drugs that treat alzheimers
Exelon, the trade name for rivastigmine, a cholinergic agonist that appears to provide temporary relief from disease progression.
92
age related loss
Aging is associated with declines in perceptual functions, especially vision, hearing, and olfaction, and declining motor, cognitive, and executive (planning) functions as well.
93
are related brain changes
aging is correlated with a decrease in white-matter volume probably related to myelin loss; reduction in neurogenesis in the hippocampus.
94
performance on what is reduced in old age?
on tests of working memory as well as attentional and executive tasks.
95
what may dementia reflect?
a chronic cerebrovascular condition, marginal high blood pressure. Marginal elevations in blood pressure can lead to cerebral microbleeds, especially in white matter.
96
Lewy body
Circular fibrous structure found in several neurodegenerative disorders; forms within the cytoplasm of neurons and is thought to result from abnormal neurofilament metabolism.
97
type I schizophrenia
Disorder characterized predominantly by positive symptoms (e.g., behavioral excesses such as hallucinations and agitated movements) likely due to a dopaminergic dysfunction and associated with acute onset, good prognosis, and a favorable response to neuroleptics.
98
type II schizophrenia
Disorder characterized by negative symptoms (behavioral deficits) and associated with chronic affliction, poor prognosis, poor response to neuroleptics, cognitive impairments, enlarged ventricles, and cortical atrophy, particularly in the frontal cortex.
99
concordance of schizophrenia
70% in identical twins
100
Development of schizophrenia
Typically, schizophrenia is diagnosed in young adulthood, but a body of evidence suggests that its origins occur much earlier in development, even prenatally. Its expression in adulthood must therefore await the conclusion of a host of developmental processes that ultimately shape the adult human brain.
101
brain correlates of schizophrenia
especially in the temporal and frontal lobes; 1. Suggesting cell loss in these areas, the schizophrenic brain generally has large ven- (B) tricles and thinner cortex in the medial temporal regions and frontal cortex. 2. Some aspects of the composition of neurons and fibers of the temporal lobes and the frontal lobes are changed. 3. Show abnormal dendritic fields in cells in the dorsal prefrontal regions; in the hippocampus and in the entorhinal cortex
102
neurochemical correlates of schizophrenia
in particular, abnormalities in dopamine and dopamine recep- tors and in GABA and GABA-binding sites. Recent evidence also suggests changes in glutamate receptors in schizophrenia,
103
dopamine hypothesis
Dopamine abnormalities were the first to be linked to schizophrenia. First, that most neuroleptic drugs act on the dopamine synapse was taken as evidence that schizophrenia is a disease of heightened activity in the ventral tegmental dopamine system. Second, drugs that enhance dopaminergic activity, such as amphetamine, can produce psychotic symptoms reminiscent of schizophrenia.
104
how does antidepressant medication work?
antidepressants act, at least in part, on signaling pathways, such as on cAMP, in the postsynaptic cell. Neurotrophic factors appear to affect the action of antidepressants and furthermore may underlie the neurobiology of depression. Investigators know, for example, that brain- derived neurotrophic factor (BDNF) is down-regulated by stress and up-regulated by antidepressant medication; Antidepressant medication may increase the release of BDNF through its actions on cAMP.
105
Mood and reactivity to stress in depression
When we are stressed, the HPA axis is stimulated to secrete corticotropin-releasing hormone, which stimulates the pitu- itary to produce adrenocorticotropic hormone (ACTH). ACTH circulates through the blood and stimulates the adrenal medulla to produce cortisol. Normally, cortisol helps us deal with stress. If we cannot cope, or if stress is intense, excessive cortisol can wield a negative influence on the brain, damaging the feedback loops the brain uses to turn off the stress response.
106
monoamines
the noradrenergic and serotoninergic activating systems modulate hormone secretion by the hypothalamic-pituitary-adrenal system—the HPA axis
107
detrimental effects of stress
Excessive stress in early life may be especially detrimental; can perma- nently disrupt the reactivity of the HPA axis so that it is constantly overactive
108
HPA Axis
Hypothalamic-pituitary-adrenal circuit that controls the production and release of hormones related to stress.
109
CBT
Problem-focused, action-oriented, structured, treatment for eliminating dysfunctional thoughts and maladaptive behaviors.
110
brain activity in anxiety disorders
Imaging studies of people with anxiety disorders record increased baseline activity in the cingulate cortex and parahippocampal gyrus and an enhanced response to anxiety- provoking stimuli in the amygdala and prefrontal cortex.
111
cognitive enhancement
Brain-function enhancement by pharmacological, physiological, or surgical manipulation.
112
acquired savant syndrome.
The phenomenon in which an individual acquires a new skill after an injury
113
newer treatment for Parkinson's
A newer course of treatment proposes to increase the number of dopamine cells either by transplanting stem cells that could then be induced to take a dopaminergic phenotype or by stimulating the production of endogenous stem cells and their migration to the basal ganglia
114
risk factors for alzheimers
include the presence of the Apoe4 gene, below-average IQ, poor education, and TBI.
115
anatomical changes in alzheimers
emergence of amyloid plaques (clumps of protein from dead neurons and astrocytes), chiefly in the limbic cortex and neocortex. Increased plaque concentration in the cortex has been cor- related with the magnitude of cognitive deterioration; neurofibrillary tangles (accu- mulations of microtubules from dead cells) found in both the neocortex and the limbic cortex, where the posterior half of the hippocampus is affected more severely than the anterior half
116
brain changes in alzheimers
the cortex atrophies (shrinks) and can lose as much as one-third of its volume as the disease progresses
117
what is spared in alzheimers?
the primary sensory and motor areas, especially the visual cortex and the sensory–motor cortex, are relatively spared.
118
what is most affected in alzheimers?
The entorhinal cortex is affected earliest and most severely. The entorhinal cortex is the major relay for information from the neocortex traveling to the hippocampus and related structures, then back to the neocortex. Entorhinal damage is associated with memory loss.
119
what causes widespread atrophy in alzheimers?
loss of dendritic arborization
120
drugs that treat alzheimers
Exelon, the trade name for rivastigmine, a cholinergic agonist that appears to provide temporary relief from disease progression.
121
age related loss
Aging is associated with declines in perceptual functions, especially vision, hearing, and olfaction, and declining motor, cognitive, and executive (planning) functions as well.
122
are related brain changes
aging is correlated with a decrease in white-matter volume probably related to myelin loss; reduction in neurogenesis in the hippocampus.
123
performance on what is reduced in old age?
on tests of working memory as well as attentional and executive tasks.
124
what may dementia reflect?
a chronic cerebrovascular condition, marginal high blood pressure. Marginal elevations in blood pressure can lead to cerebral microbleeds, especially in white matter.
125
Lewy body
Circular fibrous structure found in several neurodegenerative disorders; forms within the cytoplasm of neurons and is thought to result from abnormal neurofilament metabolism.
126
type I schizophrenia
Disorder characterized predominantly by positive symptoms (e.g., behavioral excesses such as hallucinations and agitated movements) likely due to a dopaminergic dysfunction and associated with acute onset, good prognosis, and a favorable response to neuroleptics.
127
type II schizophrenia
Disorder characterized by negative symptoms (behavioral deficits) and associated with chronic affliction, poor prognosis, poor response to neuroleptics, cognitive impairments, enlarged ventricles, and cortical atrophy, particularly in the frontal cortex.
128
concordance of schizophrenia
70% in identical twins
129
Development of schizophrenia
Typically, schizophrenia is diagnosed in young adulthood, but a body of evidence suggests that its origins occur much earlier in development, even prenatally. Its expression in adulthood must therefore await the conclusion of a host of developmental processes that ultimately shape the adult human brain.
130
brain correlates of schizophrenia
especially in the temporal and frontal lobes; 1. Suggesting cell loss in these areas, the schizophrenic brain generally has large ven- (B) tricles and thinner cortex in the medial temporal regions and frontal cortex. 2. Some aspects of the composition of neurons and fibers of the temporal lobes and the frontal lobes are changed. 3. Show abnormal dendritic fields in cells in the dorsal prefrontal regions; in the hippocampus and in the entorhinal cortex
131
neurochemical correlates of schizophrenia
in particular, abnormalities in dopamine and dopamine recep- tors and in GABA and GABA-binding sites. Recent evidence also suggests changes in glutamate receptors in schizophrenia,
132
dopamine hypothesis
Dopamine abnormalities were the first to be linked to schizophrenia. First, that most neuroleptic drugs act on the dopamine synapse was taken as evidence that schizophrenia is a disease of heightened activity in the ventral tegmental dopamine system. Second, drugs that enhance dopaminergic activity, such as amphetamine, can produce psychotic symptoms reminiscent of schizophrenia.
133
how does antidepressant medication work?
antidepressants act, at least in part, on signaling pathways, such as on cAMP, in the postsynaptic cell. Neurotrophic factors appear to affect the action of antidepressants and furthermore may underlie the neurobiology of depression. Investigators know, for example, that brain- derived neurotrophic factor (BDNF) is down-regulated by stress and up-regulated by antidepressant medication; Antidepressant medication may increase the release of BDNF through its actions on cAMP.
134
Mood and reactivity to stress in depression
When we are stressed, the HPA axis is stimulated to secrete corticotropin-releasing hormone, which stimulates the pitu- itary to produce adrenocorticotropic hormone (ACTH). ACTH circulates through the blood and stimulates the adrenal medulla to produce cortisol. Normally, cortisol helps us deal with stress. If we cannot cope, or if stress is intense, excessive cortisol can wield a negative influence on the brain, damaging the feedback loops the brain uses to turn off the stress response.
135
monoamines
the noradrenergic and serotoninergic activating systems modulate hormone secretion by the hypothalamic-pituitary-adrenal system—the HPA axis
136
detrimental effects of stress
Excessive stress in early life may be especially detrimental; can perma- nently disrupt the reactivity of the HPA axis so that it is constantly overactive
137
HPA Axis
Hypothalamic-pituitary-adrenal circuit that controls the production and release of hormones related to stress.
138
CBT
Problem-focused, action-oriented, structured, treatment for eliminating dysfunctional thoughts and maladaptive behaviors.
139
brain activity in anxiety disorders
Imaging studies of people with anxiety disorders record increased baseline activity in the cingulate cortex and parahippocampal gyrus and an enhanced response to anxiety- provoking stimuli in the amygdala and prefrontal cortex.
140
cognitive enhancement
Brain-function enhancement by pharmacological, physiological, or surgical manipulation.
141
acquired savant syndrome.
The phenomenon in which an individual acquires a new skill after an injury
