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psychiatry shlav alef > neurology > Flashcards

neurology Flashcards

1
Q

Lisencephalies and heterotopia

A

disorders of incomplete neuron migration, the latter more focal. Underlie seizure disorders, autism and other.

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2
Q

Somatosensory pathway of pain, temperature, coarse touch, deep pressure

A

spinothalamic tract, VPL, VPI, intralaminar nuclei of thalamus, somatosensory cortex, prefrontal cortex, anterior cingulate gyrus, striatum S-11

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3
Q

Somatosensory pathway of 2 point discriminitaion, tactile , vibratory, kinesthetic, muscle tension, joint position

A

fasciuli gracillis and cuneatus, vpl of thalamus, somatosensory cortex

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4
Q

inferior temporal lobe

A

shape, form, and color of the object—the what questions

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5
Q

the posterior parietal lobe

A

location, motion, and distance—the where questions

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6
Q

responses to complex shapes

A

the right ITC.

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7
Q

prosopagnosia

A

disconnection of the left ITC from the visual association area in the left parietal lobe.

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8
Q

overall contour, perspective, gestalt

A

right hemisphere

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9
Q

adds internal detail and complexity

A

left hemisphere

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10
Q

Apperceptive visual agnosia

A

inability to identify and draw items using visual cues. bilateral lesions in the visual association areas.

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11
Q

Associative visual agnosia

A

inability to name or use objects despite the ability to draw them. bilateral medial occipitotemporal lesions

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12
Q

Color agnosia

A

the inability to recognize a color despite being able to match it.

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13
Q

Color anomia

A

is the inability to name a color despite being able to point to it.

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14
Q

Anton

A

bilateral occipital lobe lesions.

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15
Q

Etiologies for anton’s disorder

A

hypoxic injury, stroke, metabolic encephalopathy, migraine, herniation resulting from mass lesions, trauma, and leukodystrophy.

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16
Q

Balint’s syndrome

A

1 .optic ataxia (the inability to direct optically guided movements), 2. oculomotor apraxia (inability to direct gaze rapidly). 3. simultanagnosia (inability to integrate a visual scene to perceive it as a whole). bilateral parietooccipital lesions.

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17
Q

Gerstmann’s syndrome

A

agraphia, calculation difficulties (acalculia), right-left disorientation, and finger agnosia. dominant parietal lobe.

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18
Q

Color perception

A

lesions of the dominant occipital lobe that include the splenium of the corpus callosum.

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19
Q

Auditary system

A

brainstem cochlear nuclei, lateral lemniscus ,inferior colliculi, medial geniculate nucleus (MGN) of the thalamus. primary auditory cortex in the posterior temporal lobe.

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20
Q

auditory processing

A

left hemisphere tends to be dominant for it.

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21
Q

lexical processing

A

the extraction of vowels, consonants, and words from auditory input. occurs in higher language association areas, especially in the left temporal lobe

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22
Q

word deafnes

A

an inability to recognize speech, disconnection of the auditory cortex from Wernicke’s area- lesion in left parietal cortex.

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23
Q

auditory sound agnosia

A

inability to recognize nonverbal sounds, such as a horn or a cat’s meow. right hemisphere correlate of pure word deafness.

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24
Q

Olfactory system

A

1 or 2 of 3,000 processing units called glomeruli. Each neuron in the epithelium displays a unique odorant receptor- 10,000 different odors. Odorant binding- impulses to sensory nerves through the cribriform plate to the olfactory bulb.

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25
Q

Olfactory pathway

A

olfactory signals do not pass through the thalamus but project directly to the frontal lobe and the limbic system, especially the pyriform cortex. The connections to the limbic system (amygdala, hippocampus, and pyriform cortex) are significant. Olfactory cues stimulate strong emotional responses and can evoke powerful memories.

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26
Q

vomeronasal organ

A

is thought to detect pheromones

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27
Q

higher olfactory processing

A

in phylogenetically more primitive animals have evolved in humans into the limbic system.

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28
Q

Taste

A

gustatory nerves nucleus solitarius in the brainstem. only broad classes of stimuli: sweet, sour, bitter, and salty. Taste fibers activate the medial temporal lobe. higher cortical localization poorly understood.

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29
Q

Under a state of hypnosis

A

gross distortions of perception in any sensory modality and changes in the ANS can be achieved instantaneously. involves both sensory and association areas of the brain. shifts in attention in an environmental setting determine changes in the regions of the brain that are activated, on an instantaneous time scale. attention-mediated variations in synaptic utilization.

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30
Q

Activation of the rubrospinal tract

A

stimulates flexion of all limbs( primitive- newborns and anencephlic)

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31
Q

activation of the vestibulospinal tract

A

causes all limbs to extend.

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32
Q

corticospinal tract

A

controls fine movements, eventually dominates the brainstem system during the first years of life. in strokes- spasticity returns as the cortical influence is ablated and the actions of the brainstem motor systems are released from cortical modulation.

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33
Q

The basal ganglia

A

a subcortical group of gray matter nuclei. mediate postural tone. striatum, the pallidum, the substantia nigra, and the subthalamic nucleus

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34
Q

bradykinesia

A

Overactivity of the striatum owing to lack of dopaminergic inhibition (e.g., in parkinsonian conditions) results in, an inability to initiate movements.

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35
Q

corpus striatum

A

the caudate and putamen and globus alllidus: harbor components of both motor and association systems. caudate nucleus plays an important role in the modulation of motor acts. The caudate is also thought to influence associative, or cognitive, processes.

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36
Q

Huntington

A

caudate shrinks dramatically in Huntington’s disease. This disorder is characterized by rigidity, on which is gradually superimposed choreiform, or “dancing,” movements.

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37
Q

The globus pallidus

A

receives input from the corpus striatum and projects fibers to the thalamus. This structure may be severely damaged in Wilson’s disease and in carbon monoxide poisoning, which are characterized by dystonic posturing and flapping movements of the arms and legs.

38
Q

The substantia nigra

A

has two parts, one of which is functionally equivalent to the globus pallidus interna(pars reticulata- output from basal ganglia to ther areas in the brain). The pars compatcta (inhibitory dopamine input to striatum) degenerates in Parkinson’s.

39
Q

depression in Parkinson

A

more than 30 percent of cases.

40
Q

subthalamic nucleus

A

lesions yield ballistic movements, sudden limb jerks of such velocity that they are compared to projectile movement.

41
Q

proprioceptive feedback

A

also Basal ganglia

42
Q

cerebellum

A

activated several milliseconds before a planned movement. modulates the tone of agonistic and antagonistic muscles by predicting the relative contraction needed for smooth motion. lesion renders intentional movements coarse and tremulous.

43
Q

motor homunculus

A

in the precentral gyrus, Brodmann’s area 4 .

44
Q

supplementary motor area

A

The brain region immediately anterior to the motor strip is called the, Brodmann’s area 6. This region contains cells that when individually stimulated can trigger more complex movements.

45
Q

Praxis

A

The skillful use of the hands

46
Q

Limb-kinetic apraxia

A

inability to use the contralateral hand in the presence of preserved strength- results from isolated lesions in the supplementary motor area.

47
Q

Ideomotor apraxia

A

the inability to perform an isolated motor act on command, despite preserved comprehension, strength, and spontaneous performance of the same action. Ideomotor apraxia simultaneously affects both limbs and involves functions so specialized that they are localized to only one hemisphere.

48
Q

Causes of ideomotor apraxia

A

-Disconnection of the language comprehension area, Wernicke’s area, from the motor regions causes an inability to follow spoken commands

49
Q

Ideational apraxia

A

sequence of skilled acts can be performed in isolation, but the entire series cannot be organized and executed as a whole. Caused by lesion to the left parietal cortex, but it likely also relies on the sequencing and executive functions of the prefrontal cortex. typical finding of diffuse cortical degeneration, such as Alzheimer’s disease.

50
Q

autonomic motor system

A

hypothalamus- houses a set of paired nuclei that appear to control appetite, rage, temperature, blood pressure, perspiration, and sexual drive.

51
Q

ventromedial nucleus

A

the satiety center, lesions produce a voracious appetite and rage.

52
Q

the hunger center

A

upper region of the lateral nucleus . lesion produce a profound loss of appetite

53
Q

Brodmann

A

defined 47 areas on the basis of cytoarchitectonic distinctions.

54
Q

provide arousal and set up attention

A

brainstem and the thalamic reticular activating system.

55
Q

posterior cortex

A

integrates perceptions and generates language.

56
Q

the frontal cortex

A

the highest level generates programs and executes plans

57
Q

unilaterality and bilaterallity

A

representation The primary sensory cortices and first level of abstraction for sensory modalities: usually represented bilaterally. The highest levels of feature extraction is unilateral.

58
Q

cortical processing of olfaction

A

occurs in the right frontal lobe.

59
Q

Prosody

A

the emotional and affective components of language, or “body language,” appears to be localized in a mirror set of brain units in the right hemisphere. Patients with right hemisphere lesions, who have impaired comprehension or expression of prosody, may find it difficult to function in society despite their intact language skills.

60
Q

Broca’s

A

1865 description of a loss of fluent speech caused by a lesion in the left inferior frontal lobe.

61
Q

.Wernicke’s

A

1874 localization of language comprehension to the left superior temporal lobe(In planum temorale).

62
Q

Semantic processing

A

connects words to meaning. middle and superior gyri of the left temporal lobe. isolated defect in semantic processing may retain the ability to repeat words in the absence of an ability to understand or spontaneously generate speech.

63
Q

Phonological processing

A

inferior frontal gyrus. Men- left unilateral, women- bilateral.

64
Q

phonems

A

there are 44 basic phonemes of sounds. Phoneme develops at about the age of 4 to 6 years and appears to be prerequisite to acquisition of reading. Inability to recognize distinct phonemes is the best predictor of a reading disability.

65
Q

identification of letters

A

occipital lobe adjacent to the primary visual cortex.

66
Q

developmental nonverbal learning disorder

A

right hemisphere dysfunction. poor fine-motor control in the left hand, deficits in visuoperceptual organization, problems with mathematics, and incomplete or disturbed socialization.

67
Q

ascending reticular activating system (ARAS)

A

set the level of consciousness. a diffuse set of neurons that projects to the intralaminar nuclei of the thalamus, and these nuclei in turn project widely throughout the cortex.

68
Q

Wakefulness and sleep

A

the thalamus and the cortex fire rhythmical bursts of neuronal activity at rates of 20 to 40 cycles per second. During sleep, these bursts are not synchronized. During wakefulness, the ARAS stimulates the thalamic intralaminar nuclei, which in turn coordinate the oscillations of different cortical regions. The greater the synchronization, the higher the level of wakefulness.

69
Q

persistent vegetative state

A

bilateral cortical dysfunction. Sleep-wake cycles may be preserved, and the eyes may appear to gaze; but the external world does not register and no evidence of conscious thought exists. This condition represents the expression of the isolated actions of the ARAS and the thalamus.

70
Q

maintenance of attention

A

requires an intact right frontal lobe. the more generally adaptive skill of maintaining a coherent line of thought is diffusely distributed throughout the cortex.

71
Q

ADHD

A

frontal lobe or right hemisphere hypometabolism

72
Q

immediate memory

A

functions over a period of seconds. Immediate memory is implicit in the concept of attention and the ability to follow a train of thought.

73
Q

recent memory

A

minutes to days

74
Q

remote memory

A

months to years.

75
Q

working memory

A

incorporating immediate and recent memory- which is the ability to store information for several seconds, whereas other, related cognitive operations take place on this information. Mostly left frontal cortex, but Clinically- bilateral prefrontal cortex lesions are required for severe impairment of working memory

76
Q

dorsolateral prefrontal cortex - memory

A

working memory, and the certainty with which the information is known and the degree of expectation assigned to the permanence of a particular environmental feature.

77
Q

goal-directed behavior

A

depends also on the emotional value of an item contained in the working memory

78
Q

Three brain structures critical to the formation of memories

A

the medial temporal lobe, certain diencephalic nuclei, and the basal forebrain.

79
Q

déjà vu

A

Although no data yet support the notion, it is conceivable that the hippocampal cognitive map is inappropriately reactivated during a déjà vu experience.

80
Q

immediate and recent memories

A

hippocampus. NMDA) glutamate receptors and the calcium-calmodulin kinase II (CaMKII)

81
Q

Memorized motor acts

A

initially require activation of the medial temporal lobe. With practice, however, the performance of an act necessary to achieve a goal become encoded within premotor and parietal cortices, particularly the left parietal cortex, and the medial temporal lobe is bypassed. corticalization of motor commands.

82
Q

Memory formation in diencephalon

A

dorsal medial nucleus of the thalamus and the mammillary bodies These two structures are damaged in thiamine deficiency states

83
Q

The regulation of drives

A

requires an intact frontal cortex.

84
Q

The right hemisphere dominance

A

for affect, socialization, and body image

85
Q

Damage to the left hemisphere

A

produces intellectual disorder and loss of the narrative aspect of dreams.

86
Q

Damage to the right hemisphere

A

produces affective disorders, loss of the visual aspects of dreams, and a failure to respond to humor, shadings of metaphor, and connotations.

87
Q

TLE personality

A

hyposexuality, emotional intensity, and a perseverative approach to interactions, termed viscosity. left TLE- may generate references to personal destiny and philosophical themes and display a humorless approach to life. patients with right TLE may display excessive emotionality, ranging from elation to sadness.

88
Q

Kluver Bucy

A

an experimental model of temporal lobe ablation in monkeys. hypersexuality, placidity, a tendency to explore the environment with the mouth, inability to recognize the emotional significance of visual stimuli, and constantly shifting attention, called hypermetamorphosis . after head trauma, cardiac arrest, herpes simplex encephalitis, or Pick’s disease.

89
Q

Mood elevation

A

left prefrontal cortex., A lesion to the left prefrontal area, at either the cortical or the subcortical level, produces depression and uncontrollable crying. seizure - gelastic seizures. It has been shown that during depressive states there is left prefrontal hypoperfusion which normalized after the depression was treated successfully

90
Q

Depression

A

right prefrontal cortex . lesions may produce laughter, euphoria, and witzelsucht.seizures: Dacrystic seizures.

91
Q

The Papez circuit

A

hippocampus, the fornix, the mammillary bodies, the anterior nucleus of the thalamus, and the cingulate gyrus. The HIPPOpotAMUS and the Phoenix are not single mammals.

92
Q

Additional limbic structures not in papez circuit

A

amygdala, septum, basal forebrain, nucleus accumbens, and orbitofrontal cortex.

psychiatry shlav alef (22 decks)

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