Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
43 Cards in this Set
- Front
- Back
|
Lateralization
|
The tendency for the right and left halves of a system to differ from one another. The left hemisphere corresponds with the right visual field and vice versa.
|
|
|
Roles of left and right hemisphere in language
|
Left hemisphere: Broca’s area in the anterior frontal region’s role is in speech production. Wernicke’s area in the temporoparietal cortex’s role is in language comprehension. Supramarginal gyrus’s role is in repetition of heard speech. In general: Left hemisphere dominance. Majority of language production and comprehension, sequences of movement, analysis of sequential stimuli. Right hemisphere: spatial relationships, emotion, communication about these functions, and emotional tone.
|
|
|
Role of posterior cortical area (association cortices!) in speech content
|
Cortical association areas - subject content of language. Current perception and memories of past experiences. Generate the subject matter to talk about. The parietal-temporal-occipital association area is responsible for language and includes Broca's area, Wernicke's area, angular gyrus, and supramarginal gyrus. There's a strip of the motor association cortex (inferior left motor association area) that is between the motor cortex and broca's area that is involved in language comprehension.
|
|
|
Speaking a heard word
|
1. Information about the sound is analyzed by PAC and transmitted to Wernicke’s area. 2. Wernicke’s area analyzes the sound info to determine the word that was said. 3. This info from Wernicke’s area is transmitted through the arcuate fasciculus to Broca’s area. 4. Broca’s area forms a motor plan to repeat the word and sends that info to motor cortex. 5. Motor cortex implements the plan, manipulating the larynx and related structures to say the word.
|
|
|
Speaking a written word
|
1. Visual cortex analyzes the image and transmits the info about the image to the angular gyrus. 2. The angular gyrus decodes the image info to recognize the word and associate this visual form with the spoken form in Wernicke’s area. 3. Info about the word is transmitted via the arcuate fasciculus to Broca’s area. 4. Broca’s area formulates a motor plan to say the appropriate word and transmits that plan to motor cortex for implementation.
|
|
|
Left anterior insular cortex
|
Active during speech production. Lesions result in apraxia- inability to execute learned movements.
|
|
|
Broca’s area- location, function, results of damage
|
Specialized area of the inferior left motor association cortex. This is the language production area. Damage results in Broca’s aphasia. Major disruptions of Broca’s aphasia are agrammatism- loss of function words (and, but, the), losing grammar, sentence structure. Reliance on content words. Anomia- loss of specific words, ability to find certain words, either omitted or replaced. Difficulty with articulation- labored and nonfluent language, very slow and frustrating. Deficits are seen in speech and writing. Language comprehension in Broca’s aphasia: Comprehension is better than the production of spoken/written language. Comprehension is disrupted by impaired grammatical abilities. Meaning may be deduced based on the words used. Meaning found in the grammatical construction of a sentence is lost.
|
|
|
Wernicke’s area – location, inputs to it, function, results of damage-
|
Left posterior superior temporal gyrus and surrounding region. Language comprehension area. Receives peripheral input from auditory and visual cortex. Uses memories of sounds to analyzed spoken language. Wernicke’s aphasia is damage to Wernicke’s area. This results in severely impaired language comprehension. There’s a failure to comprehend language (spoken/written/signed). Speech and writing are fluent but lack meaning. Sensitivity to tone of voice and conversation flow is preserved. No apparent awareness of these deficits. Major characteristics of Wernicke’s aphasia: Pure word deafness- inability to recognize spoken words. Damage to Wernicke’s area or the white matter connecting it with primary auditory cortex. Cannot analyze the sounds of words despite hearing them, not deafness.
|
|
|
Posterior language area – location, function, results of damage
|
Transcortical sensory aphasia- inability to comprehend the meaning of words or convert thoughts into meaningful language. This happens with damage to the posterior language area. Patients can repeat what they hear, but do not understand the words. This is due to a direct connection between Wernicke’s and Broca’s area. Posterior language area crucial for speech comprehension. Comprehension in the PLA --> Broca’s area --> speech production. Independent of the phonological loop.
|
|
|
Meaning of language – critical neural region, process of establishing meaning, how meaning is “stored”-
|
Comprehension of speech relies on activation of Wernicke’s area, the posterior language area and various regions of association cortex. Cortical association areas- subject content of language. Current perception and memories of past experiences. Generate the subject matter to talk about. Meaning is based on the memory associated with each word. Words defined by associated memories. Coactivation of neurons (Hebbian rule) results in a cell assembly. Cell assemblies connect: sound of a word, visual appearance of a word (written/signed), and the production of a word (written/signed). Cell assemblies exist throughout sensory and motor association cortex. Organized by categories of meaning. Loss of specific categories of meaning following localized damage suggests disconnection between memory and word recognition: Autotopagnosia – inability to name body parts - left parietal association cortex. Proper nouns - temporal pole. Common nouns - inferior temporal cortex.
|
|
|
Repetition of language – neural structures involved, role in rehearsal
|
Impaired repetition of words due to damage to the arcuate fasciculus, but comprehension is present. Words can be spoken if understood. Comprehension in the posterior language area goes to Broca’s area goes to speech production. If foreign/non-sense words are used, patient is unable to repeat word. Direct connection between Wernicke’s and Broca’s areas. Conveys the sound of a word from Wernicke’s to Broca’s area. Meaning is conveyed by indirect connections from the posterior language area Reading out loud is similarly affected- comprehension needed.
|
|
|
Memory of words – neural regions involved, order of activation of neural regions when a) understanding speech and b) producing speech
|
Anomic aphasia: Focal cortical damage --> partial amnesia for words. Anomia (loss of words) - characteristic of all aphasias; pure anomic aphasia is the loss of specific words alone. Anomia for nouns - damage to the left temporal or parietal lobe. Anomia for verbs - damage to the frontal cortex around Broca’s area
|
|
|
Prosody
|
The musical and emotional quality of speech. Rhythm, emphasis, melody, intonation, and cadence. Conveys meaning beyond word definition. Patterns of stress and inflection convey the importance of specific words; indicate the presence of a statement vs. a question. Prosody is controlled in the RIGHT hemisphere. Right hemisphere- expression and recognition of emotion, musical skills. Prosody unaffected in people with aphasias
|
|
|
Aphasia
|
Deficits in Broca’s aphasia are agrammatism- loss of function words (and, but, the), losing grammar, sentence structure. Reliance on content words.
|
|
|
Anomia
|
loss of specific words, ability to find certain words, either omitted or replaced.
|
|
|
Difficulty with articulation
|
labored and nonfluent language, very slow and frustrating. Deficits are seen in speech and writing.
|
|
|
Wernicke’s aphasia
|
occurs in the left posterior superior temporal gyrus and surrounding region. Wernicke’s area which is in the temporoparietal cortex. In Wernicke’s aphasia there is severe lack of language comprehension along with pure word deafness- inability to recognize spoken words. Damage to Wernicke’s area or the white matter connecting it with primary auditory cortex. Cannot analyze the sounds of words despite hearing them, not deafness. Also called fluent aphasia.
|
|
|
Autotopagnosia
|
inability to name body parts - left parietal association cortex. Proper nouns - temporal pole. Common nouns - inferior temporal cortex
|
|
|
Conduction aphasia
|
impaired repetition of words due to damage to the arcuate fasciculus, but comprehension is present.
|
|
|
Anomic aphasia
|
The inability to name persons or objects readily.
|
|
|
Pure alexia- pure word blindness
|
the inability to recognize written words. Lesions prevent visual info about written words from reaching the left extrastriate cortex involved in the visual recognition of words.
|
|
|
Dyslexia (surface, phonological, direct, developmental)
|
Dyslexia is a reading disorder attributed to brain impairment. Acquired dyslexia is dyslexia that occurs as a result of injury or disease. Surface dyslexia is an acquired dyslexia in which the patient seems to attend only to the fine details of reading. Surface dyslexia- impairment in whole-word reading. Damage to the left lateral lobe. Phonetic reading remains- difficulty with words with irregular spelling (vague, knickers). Comprehension of identified words remains intact. Phonological (deep) dyslexia- impairment in phonetic reading. Damage to the left frontal lobe, near Broca’s area. Recognition of known whole words. Comprehension of identified words remaining intact. Deep dyslexia is an acquired dyslexia in which the patient reads a word as another word that is semantically related. Direct dyslexia- inability to comprehend written words. Written words can be read out loud, but there is no comprehension. Similar to transcortical sensory aphasia. Seen in some patients with Wernicke’s aphasia. Developmental dyslexia- written information is processed differently. Deficits in both phonetic and whole-word reading.
|
|
|
Parkinson’s disease
|
Major degenerative disease resulting from degeneration of dopamine producing neurons in the substantia nigra that project to the striatum. There are also lewy bodies prevalent in PD.
|
|
|
Damage to the nigrostriatal system/dopamine neurons
|
Progressive degeneration of dopamine-containing cells in the substantia nigra. The loss of cells in this area is continual, but symptoms appear only after a major loss.
|
|
|
Cause of damage – Lewy bodies (characteristics)
|
Lewy bodies are abnormal accumulation of clumps of a-synuclein in the dopaminergic cells.
|
|
|
Symptoms – motor and cognitive of Parkinson's
|
Symptoms are primarily motor deficits: muscular rigidity- muscle tone increased to point of rigidity; slowness of movement- motor output is slow and labored; resting tremor- hands/arms shake at rest, stops with purposeful movement; postural instability- balance is compromised, patients fall often and can’t catch their fall. Cognitive deficits appear in late stages of PD. Speech is impaired by a combination of motor deficits and memory loss. Dementia is seen in late stages of PD in 25% of patients.
|
|
|
Causes of Parkinson’s disease (genetic, toxins, head trauma)-
|
In the noninherited cases of PD, other factors such as toxins or brain injury may accelerate the formation of Lewy bodies that kill the dopaminergic cells. Mutations result in misfolding a-synuclein and/or failure to destroy damaged proteins. Misfolded proteins accumulate as Lewy bodies. Some specific toxins have been linked in PD such as MPTP, which is found is synthetic heroin. Rotenone, paraquat, and PCBs, and other agricultural/manufacturing chemicals. Head trauma is linked to later development of PD-like symptoms. Pugilistic Parkinson’s syndrome results from repeated head trauma and concussions.
|
|
|
Treatment (L-DOPA, stem cell transplants, pallidotomy, deep brain stimulation)
|
L-dopa is the immediate precursor of the transmitter dopamine which markedly reduces symptoms in patients with PD, notably, it decreases tremors and increases the speed of movements. Although it reverses some symptoms of PD, nerve cell degeneration in the substantia nigra is relentless. Eventually, too few dopamine-containing neurons remain in the substantia nigra, and L-dopa stops being effective. Stem cell transplants- dopamine cells taken from fetal substantia nigra or cultured from omnipotent stem cells. Inserted into substantia nigra of PD patients. Most cells die upon transplantation, a few graft into the host and make dopamine. Research is still in the early stages, looking into umbilical cords. Pallidotomy is the removal of inhibitory region of globus pallidus. The internal globus pallidus sends inhibitory output to the motor cortex. In PD patients, this provides too much inhibition, due to lack of dopamine.
|
|
|
Alzheimer’s disease
|
A form of dementia that may appear in middle age but is more frequent among the aged. Dementia is a drastic failure of cognitive ability, including memory failure and loss of orientation. Alzheimer’s is a type of senile dementia which is a neurological disorder of the aged that is characterized by progressive behavioral deterioration, including personality change and profound intellectual decline. It includes, but isn’t limited to, Alzheimer’s disease.
|
|
|
5 stages of cognitive loss
|
Stage 1: Characterized by absentmindedness. Stage 2: Confusion becomes more profound, noticeable losses in memory and concentration. Language deficits, Memory loss, and Personality changes. Stage 3: Memory is severely diminished. Visual recognition of people and objects is severely impaired. Stage 4: Memory and personality are mostly gone. Stage 5: All language, emotion and most motor abilities are gone.
|
|
|
Neural damage of Alzheimer's– location, protein accumulation (neuritic plaques, neurofibrillary tangles – characteristics and source of each)
|
Neural damage is seen throughout the cortex, limbic system, and brainstem. Deficits are seen in most systems and functions. Correlated with presence of two abnormal protein accumulations: neuritic plaques and neurofibrillary tangles. Neurofibrillary tangles are twisted filaments of tau proteins in degenerating neurons. Tau proteins make up microtubules which are important for intracellular transport. Neuritic plaques aka senile plaques appear in frontal and temporoparietal cortex, the hippocampus, and limbic system. They’re formed by the buildup of B-amyloid.
|
|
|
Causes of Alzheimer’s disease (genetic, other possibilities)
|
All damage seen in AD patients comes from abnormally high amounts of neuritic plaques which consist of extracellular deposits consisting of a dense core of B-amyloid protein surrounded by degenerating neurons. Mutations in some genes result in excess production of long form B-amyloid and/or inability to clear it from the brain. Most cases aren’t hereditary. They’re believed to be linked to injury, infection, drug/alcohol abuse and exposure to toxins.
|
|
|
Treatment for AD (NSAIDs, vaccine)
|
All Ad treatments are in preliminary stages of development. NSAID (Nonsteroidal anti-inflammatory drugs) reduce the progression of cognitive loss. NSAIDs may reduce the production of B-amyloid. Vaccine against B-amyloid being developed. In AD mice, the vaccine suppresses development of B-amyloid plaques. Reverses the buildup of plaques in mice already showing AD symptoms. In humans, trial found that patients generated antibodies against B-amyloid and showed reduced cognitive decline. Antibodies cleared B-amyloid from the brain.
|
|
|
Constraint-induced movement
|
A therapy for recovery of movement after stroke or injury, in which the person’s unaffected limb is constrained while he is required to perform tasks with the affected limb.
|
|
|
Autism
|
A disorder arising during childhood, characterized by social withdrawal and perseverative behavior (such as continually nodding the head or making stereotyped finger movements.)
|
|
|
Symptoms of Autism
|
Affective abnormalities: Lack of Bonding and Social relationships starting at a young age. Behavioral abnormalities: Preoccupations. Perseverative behaviors (nodding the head). Routines. Cognitive abnormalities. Retardation. Savant syndrome
|
|
|
Brain pathology of Autism
|
Abnormal brain volumes such as reduction in size of corpus callosum. Increased grey matter. Their frontal cortex is less activated than control subjects when they are making “copycat” movements of the fingers or body. This region is also underactivated when people with autism try to mimic emotional facial expressions of others.There are fewer neurons in the amygdala but they show greater activation of the amygdala when they’re gazing at faces, implying they’re more afraid of making eye contact with people. Hippocampal complex. Decreased grey matter. Cerebellar cortex. Decreased white matter connecting distal brain regions. Impaired activation of the fusiform gyrus. Facial recognition area. Active when looking at human faces. No activation seen in autistic brains. Brainstem nuclei small or missing. Facial nucleus of the brainstem. Motor neurons decreased by 90%. Superior olivary complex.
|
|
|
Possible causes of Autism
|
Genetic heritability. 70% of monozygotic twins are concordant. 2-3% of siblings are concordant. Numerous genes have been implicated. Prenatal infection. Rubella. Herpes encephalitis. Tuberous sclerosis. Early brainstem injury. Brainstem nuclei fail to develop. Result of assault during day 20-24 of development, as neural tube is closing. Thalidomide. Other teratogens. Prenatal infection or genetic abnormalities may cause these injuries. No evidence of childhood immunizations causing/influencing autism!!
|
|
|
Schizophrenia
|
Serious mental disorder characterized by distinct symptoms. A severe psychopathology characterized by negative symptoms such as emotional withdrawal and impoverished thought, and by positive symptoms such as hallucinations and delusions.
|
|
|
Positive/negative symptoms
|
Positive symptoms, in psychiatry, an abnormal state. Examples include hallucinations, delusions, and excited motor behavior. Basically it’s the addition of abnormal things. Negative symptoms, in psychiatry, are symptoms that reflect insufficient functioning. Examples include emotional and social withdrawal, blunted affect, and slowness and impoverishment of thought and speech. It’s the taking away of normal traits
|
|
|
Brain abnormalities of schizophrenia
|
Patients with schizophrenia have consistently shown that they have an enlargement of cerebral ventricles, especially the lateral ventricles. The amygdala and the hippocampus are smaller in the twin with schizophrenia. Because the hippocampus and amygdala help form some of the walls of the lateral ventricles, this observation suggests that the ventricular enlargement in patients with schizophrenia arises from atrophy or destruction of adjacent neural tissue.
|
|
|
Possible causes of schizophrenia (2 hypotheses)
|
Dopamine hypothesis: the hypothesis that schizophrenia results from either excessive levels of synaptic dopamine or excessive postsynaptic sensitivity to dopamine. Positive symptoms may result from an excess of dopamine activity in the mesolimbic system.
However studies of dopamine metabolites in blood, cerebrospinal fluid, and urine provide inconsistent results. Another problem is the lack of correspondence between the speed with which drugs block dopamine receptors (within hours) and how long it takes for symptoms to diminish (weeks). Another weakness is that some patients show no changes when treated with dopamine antagonists. Atypical neuroleptics which are a class of antischizophrenic drugs that have actions other than the dopamine D2 receptor antagonism that characterizes the typical neuroleptics.These drugs are just as effective as the older generation of drugs for relieving the symptoms of schizophrenia, so that’s another weakness for the dopamine hypothesis. The glutamate hypothesis is the hypothesis that schizophrenia may be caused in part, by understimulation of glutamate receptors. Blocked or reduced activity of NMDA receptors is part of the cause of schizophrenia. These symptoms vary from memory disturbances to a clinical syndrome very similar to acute schizophrenia. |
|
|
Treatments of schizophrenia
|
Antipsychotic drugs. Typical antipsychotics. Dopamine antagonists. Chlorpromazine (Thorazine). Haloperidol (Haldol). Pimozide. Atypical antipsychotics. Work at a variety of post-synaptic receptors. Clozapine. Aripiprazole (Abilify). Psychotherapy. Cognitive-behavioral therapy
|
