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Süleyman Öztürk 7 preguntas

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  1. 1Broca aphasia
    Damage: [blank_start]anterior/frontal left lesions[blank_end],
    Deficit: speech deficits (reduced vocabulary), unable to speak.

    Wernicke aphasia,
    Damage: [blank_start]left superior temporal gyrus[blank_end]
    Deficit: speech understanding, fluent but nonsensical speech

    [blank_start]Conduction aphasia[blank_end]
    Damage: arcuate fasciculus
    Deficit: fluent speech and good comprehension but [blank_start]impaired repetition[blank_end]

    [blank_start]Global aphasia[blank_end]
    Damage: Including both Broca's & Wernicke's areas
    Deficit: severe impairment in speech production and comprehension


    [blank_start]Anomic Aphasia[blank_end]
    Damage: [blank_start]Angular gyrus[blank_end] or other parietal/temporal areas
    Deficit: Difficulty finding words; fluent and grammatically correct speech; intact comprehension

    [blank_start]Transcortical Motor Aphasia[blank_end]
    Damage: Areas near Broca's area (frontal lobe)
    Deficit: Non-fluent speech; intact repetition; [blank_start]struggles to initiate speech[blank_end]

    [blank_start]Transcortical Sensory Aphasia[blank_end]
    Damage: Areas near Wernicke's area ([blank_start]parietal-temporal junction[blank_end])
    Deficit: Fluent speech; poor comprehension; intact repetition

    [blank_start]Mixed Transcortical Aphasia[blank_end]
    Damage: Widespread damage sparing the arcuate fasciculus
    Deficit: Severe impairment in speech and comprehension; intact repetition

    Subcortical Aphasia (Thalamic)
    Damage: Thalamus
    Deficit: Fluent speech with frequent pauses; [blank_start]impaired naming[blank_end]; variable comprehension

    Subcortical Aphasia (Non-thalamic)
    Damage: Basal ganglia (e.g., caudate nucleus, putamen)
    Deficit: [blank_start]Reduced speech output[blank_end]; mild comprehension deficits; articulation difficulties
    Imagen de la pregunta 1
    1. Aanterior/frontal left lesions
    2. Bleft superior temporal gyrus
    3. CConduction aphasia
    4. DGlobal aphasia
    5. EAnomic Aphasia
    6. FTranscortical Motor Aphasia
    7. GTranscortical Sensory Aphasia
    8. HMixed Transcortical Aphasia
    9. Iimpaired repetition
    10. Jimpaired naming
    11. KReduced speech output
    12. LAngular gyrus
    13. Mstruggles to initiate speech
    14. Nparietal-temporal junction
  2. 2[blank_start]Dehaene & Cohen’s[blank_end] model there are three systems:
    1) [blank_start]horizontal interparietal sulcus (HIPS)[blank_end], bilaterally
    2) left angular gyrus
    3) posterior superior parietal lobe


    The [blank_start]posterior superior parietal lobe[blank_end], bilaterally
    - [blank_start]explores the number line[blank_end]
    - is activated in number comparison, approximate calculation and counting

    HIPS, bilaterally is activated:
    -in [blank_start]quantity evaluation[blank_end]
    - in number processing (any code) and calculation
    - in approximate calculation > exact calculation (perhaps in different portions, Castelli et al. 2006)
    - [blank_start]subtraction and multiplication[blank_end]

    the [blank_start]left angular gyrus[blank_end] is activated:
    - in [blank_start]number fact retrieval[blank_end]
    - in [blank_start]verbal number processing[blank_end]
    - It is not involved in measuring quantities in operations like subtraction


    1. Aposterior superior parietal lobe
    2. Bhorizontal interparietal sulcus (HIPS)
    3. Cleft angular gyrus
    4. DDehaene & Cohen’s
    5. Eexplores the number line
    6. Fquantity evaluation
    7. Gnumber fact retrieval
    8. Hsubtraction and multiplication
    9. Iverbal number processing
  3. 3A “system for finger movements” localized in [blank_start]parietal and precentral[blank_end] areas would sustain quantity evaluation and finger counting. Active in development would keep in adult age and help in calculation (damaged in [blank_start]Gerstman syndrome[blank_end])
    1. Aparietal and precentral
    2. BGerstman syndrome
    3. CAmnesic syndrome
    4. DBroca
  4. 4[blank_start]Acalculia[blank_end], a disturbance in the ability to comprehend or write numbers properly, is common in patients with [blank_start]aphasia[blank_end]. The angular gyrus region in the left hemisphere appears to be important for numeracy.

    [blank_start]Anarithmetria,[blank_end] is characterized by the inability to perform number manipulations. Patients with this disorder correctly recognize and reproduce individual numbers and know their values, but cannot perform computations (addition, subtraction, etc.). This disorder is relatively common in patients with dementias, particularly Alzheimer’s disease.

    [blank_start]Spatial dyscalculia[blank_end] is the difficulty in performing written calculations. Patients have difficulty aligning columns of figures and performing carrying tasks.

    [blank_start]Gerstmann’s syndrome[blank_end], also referred to as the angular gyrus syndrome, precentral areas and parietal: Agraphia, Acalculia, Right– left disorientation (hands), Finger agnosia.
    1. AGerstmann’s syndrome
    2. BSpatial dyscalculia
    3. CAnarithmetria,
    4. DAcalculia
    5. Eaphasia
    6. Fagnosia
  5. 5Apraxia is the inability to carry out complex motor acts [blank_start]despite[blank_end] intact motor and sensory systems and coordination, good comprehension, and full cooperation.

    The term ‘apraxia’ should be applied only to deficits with a [blank_start]motoric basis.[blank_end]

    [blank_start]Limb-kinetic apraxia[blank_end] (motor apraxia) Patients with this form of apraxia have a breakdown of [blank_start]fine motor organization[blank_end] and the coordination of finger movements necessary to perform fine motor tasks. They are particularly poor at copying meaningless hand positions and better when mimicking meaningful gestures (saluting, waving, etc.) and typically use real objects flawlessly. Patients with [blank_start]basal ganglia[blank_end] and supplementary motor area (SMA) pathology.

    [blank_start]Ideomotor apraxia[blank_end] => The idea or plan of action is not impaired but the implementation into a proper action is disturbed The patient [blank_start]does not know how to do[blank_end] it but it can perform the same act spontaneously. There is difficulty with the selection, sequencing, spatial orientation, and movements involved in meaningless and meaningful gestures (beckoning, etc.), and in pantomime particular actions (brushing teeth, use a comb, hammering a nail). The critical areas are the left inferior parietal and prefrontal areas and anterior callosal area.

    [blank_start]Ideational or conceptual apraxia[blank_end] => A patient [blank_start]does not know what to do[blank_end] because the idea or concept of the motor act is lacking. Patients may be able to make well-formed movements, which are nevertheless inappropriate and/or disorganised (unable to filling and lighting a pipe or making a cup of tea) although, in contrast to what happens in ideomotor apraxia, each separate component of the sequence can be successfully performed. Patients with Alzheimer disease, semantic dementia. [blank_start]Left temporal lobe.[blank_end]

    Orobuccal (oral) apraxia Patients with oral apraxia have difficulty performing [blank_start]learned, skilled movements of their face[blank_end], lips, tongue, cheeks, larynx, and pharynx such as whistling, winking, coughing etc on command. The inferior frontal region and the insula are affected. Thus oral apraxia commonly accompanies [blank_start]Broca’s aphasia[blank_end]. Frontotemporal dementia, progressive non-fluent aphasia, and cortico-basal degeneration

    [blank_start]Verbal Apraxia[blank_end] is a disorder where a child has great difficulty with the [blank_start]volitional production of speech[blank_end]. Other terms used for verbal apraxia are “Developmental Verbal Dyspraxia (DVD)”, “Developmental Apraxia of Speech (DAS)”, or “Childhood Apraxia of Speech (CAS)”. It can be also an acquired after a [blank_start]stroke[blank_end] for example.

    [blank_start]Dressing Apraxia[blank_end]: The term ‘apraxia’ is inappropriate, since it is not a motor disorder. Instead, the deficit is in the orientation of body parts in relation to garments because of faulty visuospatial mechanisms.
    1. AVerbal Apraxia
    2. BDressing Apraxia
    3. CIdeational or conceptual apraxia
    4. DIdeomotor apraxia
    5. ELimb-kinetic apraxia
    6. Fmotoric basis.
    7. Gdespite
    8. Hfine motor organization
    9. Ibasal ganglia
    10. Jlearned, skilled movements of their face
    11. KBroca’s aphasia
    12. Lstroke
    13. Mvolitional production of speech
    14. Ndoes not know how to do
    15. Odoes not know what to do
    16. PLeft temporal lobe.
  6. 6Right hemisphere in man is [blank_start]more important[blank_end] than the left for spatially directed attention. Patients with this lesion in right hemisphere behave as if one half— usually the left— of their body has ceased to exist.

    Whereas the [blank_start]left hemisphere[blank_end] contains mechanisms which maintain attention to the contralateral (right) half of the sensory world, [blank_start]the right hemisphere[blank_end] contains the neural apparatus for attending to both sides of space. Patients with right parietal damage are thought to have selective deficits in [blank_start]disengaging attention[blank_end] from stimuli to the right, resulting in an inability to shift and engage stimuli to the left.

    The Visual Object and Space Perception Battery ([blank_start]VOSP[blank_end]) consists of eight tests each designed to assess a particular aspect of [blank_start]object or space perception[blank_end], while minimising the involvement of other cognitive skills (incomplete letters, position discrimination etc.)

    [blank_start]Sensory[blank_end] neglect: the selective defect of a deficit in awareness, which may apply to all stimuli on the affected side of space or may be confined to stimuli impinging on the patient’s body (personal neglect). Subtypes of sensory neglect exist for the visual, auditory, and tactile modalities. If the lack of awareness and attentional bias are present only when there is a [blank_start]competing stimulus[blank_end] at the ipsilesional location, the disorder is known as [blank_start]extinction.[blank_end]

    Motor neglect involves a [blank_start]response failure[blank_end] that cannot be explained by weakness, sensory loss, or inattention.Patients with motor neglect may also have [blank_start]intentional biases[blank_end] such that there is a tendency to move towards the ipsilesional space.

    [blank_start]Extrapersonal neglect[blank_end]: This is usually tested by asking patients to divide lines of varying length, to perform cancellation tasks, or to draw and copy pictures.

    Neglect dyslexia: Neglect dyslexia is a reading impairment in which people [blank_start]misread letters[blank_end] presented on one side of individual words

    Hemi-spatial neglect => [blank_start]Inferior parietal lobule lesion[blank_end], course of where pathway

    [blank_start]Benton Line Orientation Text[blank_end] => The patient is insructed to look at the two lines of the stimulus card and to find which of the lines below are in exactly the same position and point in the same direction. Patients with [blank_start]right hemisphere lesion[blank_end] struggle with this test.
    1. ASensory
    2. Bleft hemisphere
    3. Cthe right hemisphere
    4. Dmore important
    5. EExtrapersonal neglect
    6. FInferior parietal lobule lesion
    7. GBenton Line Orientation Text
    8. Hdisengaging attention
    9. Iengaging attention
    10. Jright hemisphere lesion
    11. Kleft hemisphere lesion
    12. Lcompeting stimulus
    13. Mobject or space perception
    14. NVOSP
    15. Oresponse failure
    16. Pintentional biases
    17. Qextinction.
    18. Rmisread letters
  7. 7Visual/tactile/uditory/body scheme agnosia implies a disorder of recognition that cannot be attributed to general intellectual impairment, aphasia, or basic sensory dysfunction. A patient with visual object agnosia sees objects but [blank_start]fails to recognize[blank_end] what they are.

    There are two principal types of object recognition disorder: [blank_start]“Apperceptive agnosia”[blank_end]: involves the earlier perceptual stage of object analysis : failing on more complex tasks involving object identification and naming however, patients retain full knowledge about the unidentified items, and can name them by palpation or if given a verbal description. (parietal lesion) [blank_start]“Associative agnosia”[blank_end]: there is a breakdown in the processes by which meaning is ascribed to visual percepts. The defect in object recognition is not limited to visual presentation but also to identify objects in any modality (touch, or verbal description), as well as a loss of verbal knowledge. (temporal lesion)

    Optic aphasia is a disorder when naming or verbally describing visually presented items. In contrast to what is found in visual agnosia, patients with optic aphasia can recognize items visually, as demonstrated by their accurate pantomiming of their use, even though they cannot access their names (left medial occipital region).

    [blank_start]Prosopagnosia[blank_end]: This term describes the inability to recognize familiar faces. While patients state that all faces are unfamiliar or unrecognizable, they are able to use cues such as voice, gait, or distinctive clothing to identify familiar people ([blank_start]bilateral inferior occipitotemporal[blank_end] lesions)

    Balint’s syndrome (i) [blank_start]psychic paralysis of gaze[blank_end], that is to say an inability to direct voluntary eye movements to visual targets; (ii) [blank_start]optic ataxia[blank_end], the inability to reach for, or point to, visual targets, also referred to as visual disorientation; (iii) a visual attentional deficit in which only one stimulus at a time is apparently perceived, and even the attended stimulus may spontaneously slip from attention; this last feature is termed [blank_start]‘simultanagnosia[blank_end]’. The brain damage responsible is always bilateral, and includes the superior parieto- occipital region most common in posterior cortical atrophy, a variant of Alzheimer’s disease.
    1. Apsychic paralysis of gaze
    2. Boptic ataxia
    3. C‘simultanagnosia
    4. Dfails to recognize
    5. E“Apperceptive agnosia”
    6. F“Associative agnosia”
    7. Gbilateral inferior occipitotemporal
    8. HProsopagnosia

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Descripción
Test sobre Second Slide, creado por Süleyman Öztürk el 18/01/2025.
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