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neuropsych > lesson 11 > Flashcards

lesson 11 Flashcards

1
Q

the hemisphere specialized in the motor control is the dominant one

A

left

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2
Q

M1

A

controls actions (strict interaction with S1)

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3
Q

M1 lesion

A

Lesion leads to motor deficit

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4
Q

PMA, Area 5 and Area 7

A

selects action and timing based on environmental information (from parietal lobe) habits, associative rules

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5
Q

Prefrontal Cortex

A

control behavior depending on future plans, strategies, complex rules (ie social rules)

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6
Q

prefrontal cortex - lesion

A

Lesion does not lead to proper motor deficit

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7
Q

Cerebellum and basal ganglia

A

contributes to motor control

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8
Q

structures involved

A

cerebral motor cortex, thalamus, cerebellum, basal ganglia, brainstem, spinal cord

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9
Q

corticospinal tract pathway - efferent neurons

A

Primary motor cortex –>

internal capsule –>

medulla pyramid –>

cross over to opposite side –>

corticospinal tract of spinal cord –>

ventral horn of spinal cord –>

spinal nerve –> effector skeletal muscle

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10
Q

Somatotopic organization

A

the bigger the cortical region controlling a specific body part, the better control of the specific body part

Primary motor cortex, precentral sulcus (M1, BA 4)

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11
Q

M1 controls _____ which is active ____

A

M1 controls muscle contraction – active during movement executive

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12
Q

M1 receives input from

A

Thalamus

Premotor cortex and supplementary motor area – SMA (BA 6)

Primary somatosensory cortex, S1 (BA 1 – 2 – 3)

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13
Q

M1 primary output

A

Brainstem

Spinal cord (from the 5th layer, giant pyramidal Betz cells)

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14
Q

Hemiplegia

A

half of the body is paralyzed (half contralateral to lesion)

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15
Q

hemiplegia - lesion

A

due to lesion in M1, internal capsule, or corticospinal fasciculi

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16
Q

total hemiplegia

A

body and face paralysized

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17
Q

partial hemiplegia

A

face movements are spared (no lesion in ventral part of M1 and cranial nerve nuclei controlling facial muscles)

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18
Q

Hemiparesis

A

movements are still possible but reduced – the term indicates a partial loss of motor unction

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19
Q

damage of M1/efferent pathways

A

hemiplegia and hemiparesis

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20
Q

premotor areas

A

dorsal premotor cortex, supplementary motor area

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21
Q

dorsal premotor cortex (dPM)

A

involved in movement planning

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22
Q

dorsal premotor cortex is active

A

before and during movement execution

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23
Q

dorsal premotor cortex neurons

A

code for the desired (but not necessarily actual) direction

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24
Q

dorsal premotor cortex contributes to

A

action selection depending on environment information (i.e., perceptual rules), working together with the parietal regions

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25
Q

dorsal premotor lesion

A

deficit in movements guided by external stimuli

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26
Q

Supplementary motor area (SMA)

A

starting internally generated motor acts (intentional actions), or regulating go/no-go actions

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27
Q

SMA lesion

A

deficit in executing complex sequences + possible alien hand syndrome

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28
Q

visuo-motor networks

A

reaching - dorso-dorsal pathway

grasping - dorso-ventral pathway

ventral pathway

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29
Q

Reaching – Dorso-dorsal Pathway

A

control movements in space (peri-personal space)

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30
Q

Grasping – Dorso-ventral Pathway

A

controls visuo-motor transformation for interaction with the environment (object)

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31
Q

ventral pathway

A

object recognition

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32
Q

Affordances

A

indicate the action possibilities offered by objects, independent of the visual features that allow their recognition

Ex: an orange and a tennis ball look very different but they afford the same movements

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33
Q

Anosognosia

A

literally means “lack of awareness” for a disease/deficit - can be applied to any cognitive deficit (ex: memory loss in dementia)

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34
Q

anosognosia is

A

Normally very specific and selective (ex: the same patient anosognosia might regard the motor but not visual deficit or the motor deficit in hand but not leg, or aphasia but not hemiplegia)

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35
Q

anosognosia is independent of

A

memory or other cognitive deficits

They do not justify the delusion

Patients critical thinking is spared (in other domains)

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36
Q

anosognosia usually manifests

A

soon after injury, with resolution in subsequent days or weeks, even related to a spontaneous recovery

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37
Q

Presence of anosognosia leads

A

to poorer outcomes

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38
Q

how does the presence of anosognosia leads to poorer outcomes

A

Patients show reduced compliance with rehabilitation since it’s difficult to motivate a patient unaware of a deficit

Patients refuse strategies to improve their Activities of Daily Living (ADL)

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39
Q

anosognosia assessment

A

Clinical observations of patient’s behavior

Self-evaluation compared to an evaluation provided by a caregiver/relative

(semi) structured interviews (except for aphasic patients

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40
Q

Some authors suggest that anosognosia evaluation should be divided between

A

(a) explicit aware of the deficit,

(b) implicit awareness of its functional consequences

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41
Q

Treatment of anosognosia proceeds

A

simultaneously to rehabilitation of the disorder the patient is unaware of

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42
Q

what might help anosognosia treatment

A

Awareness training may help, as well as observation of one’s past behavior (i.e. through video recordings)

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43
Q

examples of anosognosia

A

Anton syndrome, anosognosia for the aphasic disorder, anosognosia for amnesia, anosognosia for cognitive deficit, anosognosia for behavioral alterations

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44
Q

anton syndrome

A

the blind spot corresponds to the optic disk – optic nerve lacks photoreceptor cells (so its insensitive to light) ==> blind spot - represented in V1 but not in the visual associative cortices

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45
Q

blind spot

A

small portion of the visual field of each eye that cannot be seen

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46
Q

optic disk

A

where the optic nerve enters the retina

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47
Q

why are we unaware of the blind spot

A

perceptual completion

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48
Q

perceptual completion

A

cortical neurons receive signals from the adjacent visual field and complete the image

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49
Q

Bilateral cerebral lesions in V1 and visual associative cortices

A

= cortical blindness + anosognosia for the blindness

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50
Q

= cortical blindness + anosognosia for the blindness

A

Bilateral cerebral lesions in V1 and visual associative cortices

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51
Q

Anosognosia for the aphasic disorder

A

difficult to assess for the presence of aphasia that does not allow a clear communication between the patient and examiner

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52
Q

Believed that anosognosia for the aphasic disorder is more frequent for

A

the fluent dimension

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53
Q

anosognosia for the aphasic disorder could be for

A

whole disorder (global) or selective for a specific linguistic deficit (semantic versus syntactic)

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54
Q

Anosognosia for amnesia

A

patients are not aware that they don’t remember

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55
Q

Anosognosia for amnesia due to

A

subcortical lesions (diencephalic or fronto-basal lesions

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56
Q

Anosognosia for amnesia is NOT due to

A

temporal lesions

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57
Q

Anosognosia for amnesia - PLEASE NOTE

A

amnesia and anosognosia for amnesia could seem very similar but are 2 distinct and dissociable disorders

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58
Q

Anosognosia for cognitive deficit

A

(memory, space-time orientation, reasoning and planning, calculation, etc.)

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59
Q

anosognosia for behavioral alterations

A

(irritability, disinhibition, inappropriate emotional manifestation)

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60
Q

anosognosia for behavioral alterations and Anosognosia for cognitive deficit

A

Present in half of Alzheimer’s disease patients - when patients are self-evaluated, they could overestimate their cognitive abilities

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61
Q

anosognosia for hemiplegia

A

REGARDING THE MOTOR DEFICIT - refers to a condition in which the patient believe they are still able to move the superior and/or inferior limb in the paretic side of the body

Does not recognize nor refer to their disorder, firmly convinced that the motor function is spared

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62
Q

anosognosia for hemiplegia is more frequent in patients with

A

a right lesion

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63
Q

usual anosognosia for hemiplegia lesion

A

cerebrovascular lesion

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64
Q

when in timeline is anosognosia for hemiplegia most frequent and serious after the stroke

A

first weeks (acute or sub-acute phase)

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65
Q

anosognosia for hemiplegia usual co-occurrance

A

patients with neglect

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66
Q

anosognosia for hemiplegia lesion and neurolocation highlighted roles

A

discrete cortical lesions in right areas such as the lateral premotor cortex, the insula or fronto-parietal and parieto-occipital networks, supporting theories of motor and body awareness

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67
Q

white matter maps of disconnection - anosognia for hemiplegia

A

significant contribution of the cingulum, the third branch of the superior longitudinal fasciculus and connections to the pre-supplementary motor area

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68
Q

anosognosia for hemiplegia - tripartite disconnection syndrome

A

involving disruptions in tracts and structures belonging to three systems: the pre-motor loop, the limbic system and ventral attentional network

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69
Q

anosognosia for hemiplegia study CONCLUSION

A

motor awareness requires the integration of a number of cognitive processes, rather than being a purely motor monitoring function

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70
Q

Structured interview for the assessment of anosognosia for hemiplegia is

A

conducted separately for the superior and inferior limbs

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71
Q

anosognosia for hemiplegia - bimanual circle-line experiment

A

test of implicit awareness; draw lines with one hand and circle with the other

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72
Q

anosognosia for hemiplegia - bimanual circle-line experiment methods for patients

A

patients asked to simultaneously draw lines were their unaffected hand and circles with their paralyzed hand –> trajectories of the intact hand were influenced by the requested movement of the paralyzed hand with the intact hand tending to assume an oval trajectory

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73
Q

anosognosia for hemiplegia - bimanual circle-line experiment methods for healthy patients

A

planning a circle with one hand interferes with planning a line with the other hand (because of the inter-hemispheric communication through the corpus callosum –> lines become elliptical

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74
Q

anosognosia for hemiplegia - bimanual circle-line experiment authors suggest that

A

anosognosia patients may have intact motor intentionality and planning for plegic hand

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75
Q

Anosognosia for Hemiplegia – Hypothesis

Psychologically motivated denial (1955)

A

unconscious defense mechanism –> reduced distress of functional loss

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76
Q

Anosognosia for Hemiplegia – Hypothesis

Feedforward hypothesis

A

disorder of motor awareness due to a dissociation between the motor command and sensory feedback

Lack of awareness of the deficit is so strong that when faced with their deficits, patients contniue to confabulate (ex: when required to grasp a glass of water by the experimenter they may say that they are not thirsty

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77
Q

The intact intention hypothesis for anosognosia

A

if you cannot compare expectations/predictions with actual states, you cannot be aware of your errors

As in anosognosia for hemiplegia: movements are not performed, and patient does not realize it

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78
Q

Alien Hand Syndrome

A

a rare neurological disorder in which movements are performed without conscious will – it is not a praxix disorder

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79
Q

Alien Hand Syndrome - loss of

A

the sense of control (agency) over a specific body part (hand and leg)

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80
Q

alien hand syndrome - symptoms

A

Becomes hyper-reactive to environmental stimuli (affordances)

Performs stereotypes movements

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81
Q

Alien Hand Syndrome: What makes the alien hand alien?

A

3 factors

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82
Q

3 factors of alien hand syndrome

A

1: errant limb must be disinhibited and disproportionately reactive to the external environmental stimuli

2: limb is under less volitional control and produces perseverative movements in which motor stereotypes are concatenated –> disinhibited limb perseverates on external stimuli and appears purposeful, despite not being engaged in true goal-directed intentions

3: patient needs to have a relatively intact action-minotoring system to be aware of the abnormal movements as they are occurring

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83
Q

alien hand disorder is a

A

Rare disorder –> no complete concordance on lesion sites

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84
Q

alien hand disorder lesion sites

A

Corpus callosum, Medial frontal lobes, Parietal lobe

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85
Q

alien hand disorder lesion sites - corpus callosum

A

fibers that connect the 2 cerebral hemispheres

Damage may impair the ability of the left and right hemispheres to coordinate movements between limbs to inhibit unwanted movement

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86
Q

alien hand disorder lesion sites - medial frontal lobes

A

contains the supplementary motor area (involved in planning and initiation of movements)

Damage may impair the inhibition of unwanted movements

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87
Q

alien hand disorder lesion sites - Parietal lobe

A

important for processing sensory information

Damage may lead to a deficit in sensory input from the alien limb, contributing to problems in coordinate movement in alien limb and leading to perceiving the limb as foreign

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88
Q

The disconnection between motor planning and perception

A

plays a crucial role in the deficits of motor awareness and sense of agency as anosognosia for hemiplegia and alien hand syndrome

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89
Q

what network is mainly responsible for the disconnection between motor planning and perception

A

Fronto-parietal networks

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90
Q

Apraxia

A

literally means - without action: defines a condition in which the patiens fails to voluntary perform skilled, purposeful movements/gestures

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91
Q

what does the patient with apraxia have to have an absence of

A

Primary motor loss and other motor deficit (hemiplegia or hemiparesis, weakness, seizures, sensory loss, seizures, sensory loss, dystonia, tremor chorea, athetosis, ballism)

Sensory pathways deficits

Impairment of perceptive abilities

Comprehension disorders

Severe mental deterioration

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92
Q

what may the apraxia deficit also include

A

inability to correctly code others’ actions

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93
Q

apraxia frequently follows a stroke lesion in the

A

left hemisphere but also common in patients with Alzheimer’s disease and sometimes related to Parkinson’s Disease

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94
Q

apraxia refers to

A

a disorder of motor cognition (aka higher-level steps of movement planning and motor control) in which movements are selected to best adapt to the environmental situation

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95
Q

what kind of patients are not apraxic

A

PATIENTS WITH LESION IN M1 (HEMIPLEGIA/HEIPARESIS) ARE NOT APRAXIC

96
Q

apraxia - Automatic-voluntary dissociation

A

the execution of a movement/gesture can be impaired when the patient is explicitly asked to perform it but not when it occurs automatically or must be imitated

97
Q

apraxia - Automatic-voluntary dissociation frequency

A

30 – 50% of left-brain injured people

98
Q

apraxia - Automatic-voluntary dissociation - study

A

German psychiatrist described an aphasic woman who had been raised a devout Catholic but now failed to make the sign of the cross after grace

Couldn’t do it on her own (tried but did it incorrectly) when asked but could imitate it exactly

99
Q

apraxia - Automatic-voluntary dissociation does not

A

depend on the kinematic features of the movement (velocity, direction, amplitude, etc) BECAUSE it is NOT a disorder of movement execution

100
Q

Both apraxia and aphasia typically depend on a lesion in the

A

left hemisphere (dorsal part, fronto-parietal or parieto-occipital areas)

101
Q

apraxia and aphasia deficits often

A

co-occur in the same patient but can also be dissociated: 45% of patients with aphasia without apraxia, rarer are cases of apraxia without aphasia

102
Q

Left hemisphere is dominant for

A

both language and motor planning

103
Q

Historically, both aphasia and apraxia were attributed to

A

a disorder of the symbolic function

104
Q

both aphasia and apraxia were

A

Interpreted as an inability to recognize signals, both written/heard or conveyed through pantomime = deficit in abstraction and conceptualization

105
Q

More recently, suggested aphasia and apraxia

A

may both represent deficits in the ability to generate hierarchical representations, which are crucial for both motor control and language (especially syntax)

106
Q

Language and praxis can be seen as

A

two complex, independent, and distributed functions, whose co-occurrence may simply depend on the contiguity of their neurofunctional correlates in the dorsal regions of the left hemisphere (fronto-parietal areas where the middle cerebral artery is responsible for blood supply), although the hypothesis of a common core cognitive deficit is still being explored

107
Q

apraxia classifications

A

based on level of processing process, the affected effector systems, on the type of activity disrupted

108
Q

based on level of processing process

A

ideomotor apracia and ideational apraxia

109
Q

ideomotor apraxia

A

inability to translate the known motor sequence into corresponding motor program —- the patient doesn’t know HOW to do it

110
Q

ideational apraxia

A

inability to mentally represent the gesture or sequence of movements to be performed —- the patient does not know WHAT to do

The Liepmann’s model, the Geschwind model, the Renzi and Faglioni model, the Rothi model

111
Q

based on the affected effector systems

A

Limb apraxia

Oral or buccofacial apraxia

Trunk apraxia

Other forms: constructive apraxia, gaze apraxia, gait apraxia, clothing apraxia

112
Q

based on the type of activity disrupted

A

Examples: use of objects, production of complex motor sequences, production of symbolic gestures, imitation of gestures, etc.

113
Q

Limb Apraxia: Liepmann’s model

A

Liepmann’s model is based on the level of processing process - classical classification distinguishes between 3 types of apraxia

limb-kinetic apraxia (LKA)

ideomotor apraxia (IMA)

ideational apraxia (IA)

114
Q

Limb-kinetic apraxia (LKA)

A

inability to perform complex and skilled movements (i.e. rotate a coin with the fingers), without automatic-voluntary dissociation

115
Q

Limb-kinetic apraxia (LKA) - lesion

A

Unilateral lesion in M1-S1 –> loss of dexterity and hemiparesis

116
Q

Limb-kinetic apraxia (LKA) - special fact

A

Nowadays is not considered a proper form of apraxia

117
Q

Ideomotor apraxia (IMA)

A

inability to translate the known motor sequence into the corresponding motor program –> difficulty correctly imitate hand gestures and/or voluntarily mime took use

118
Q

ideomotor apraxia - explanation

A

Spatial and temporal errors due to the inability to correctly represent, plan and perform the action, independently of the hand used; the patient doesn’t know HOW to perform the specific actions – ability to spontaneously use tools (brush one’s hair in the morning) may remain intact

119
Q

ideomotor apraxia - errors

A

Patient cannot imitate nor imagine how to do specific actions

Make typical errors, as body-part-as-object errors

Make spatial errors, perseverations, hesitations, conduit d’approaches, inserts unrelated movements in the action sequence, and makes body-part-as-object errors

120
Q

ideomotor apraxia - lesion

A

left posterior parietal and premotor areas (visuo-motor networks)

57% of cases after left lesion, 34% after right lesion – still evident after 1 year from stroke 45%

121
Q

Ideational apraxia (IA)

A

‘amnesia of usage’; inability to mentally represent the gesture or sequence of movement to be performed –> difficulty to retrieve the use of objects (i.e. candle and matchsticks), independently of the hand used; complex and skilled sequence of actions

122
Q

Ideational apraxia (IA) - explanation

A

Disorder of conceptual knowledge or recall from semantic memory of the object use –> patient doesn’t know WHAT to do with specific objects

123
Q

Ideational apraxia (IA) - symptoms

A

Can not select the correct sequence of actions (i.e. prepareing coffee)

124
Q

Ideational apraxia (IA) - lesion

A

left occipito-temporo-parietal junction (–> tool use)

28% of cases after left lesion, 13% after right lesion

125
Q

Limb Apraxia: the Geschwind Model

A

apraxia as a disconnection syndrome

gesture-to-command tasks and imitation-to-command tasks

126
Q

Geschwind model - lesion

A

lesion of the arcuate fasciculus, dominant for visuo-motor connections

127
Q

Gesture-to-command tasks

A

disconnection between Wernicke area (comprehension) and premotor areas that plan the target movement

128
Q

Imitation-to-command tasks

A

disconnection between dorsal pathways (posterior parietal cortex, where the kinesthetic-motor engrams are stored) and premotor areas that plan the target movement

129
Q

Limb Apraxia: the Rothi model

A

Observed dissociations between:
Action discrimination and action production
Selective deficits by modality
Understanding versus imitation of gestures

130
Q

Action discrimination and action production

A

= hypothesis of 2 mechanisms

131
Q

Action discrimination and action production - lesions

A

Lesion of memory traces in parietal lobe

Lesion of anterior areas

132
Q

Lesion of memory traces in parietal lobe –>

A

discrimination and production deficit on verbal command

133
Q

discrimination and production deficit on verbal command =

A

Lesion of memory traces in parietal lobe

134
Q

Lesion of anterior areas –>

A

production deficit but not discrimination one

135
Q

production deficit but not discrimination one =

A

Lesion of anterior areas

136
Q

Selective deficits by modality

A

(visual versus verbal); some patients perform verbally commanded gestures but are unable to understand/discriminate visually presented gestures

137
Q

Selective deficits by modality - lesion

A

Occipito-temporal lesion

138
Q

Understanding versus imitation of gestures

A

some patients imitate gestures well but are unable to understand/discriminate between them

Imitates can occur through a “non-lexical” way of gestural imitation

139
Q

Understanding versus imitation of gestures - lesion

A

may be mediated by a direct pathway between the visual system and the premotor cortex

140
Q

Non-lexical conversion

A

visuo-motor conversion –> imitation without comprehension of the meaning or imitation of meaningless gestures

141
Q

Transitive actions

A

object-related actions

142
Q

Intransitive actions

A

typically convey communicative content (without use of objects)

Meaningful versus meaningless

143
Q

Motor cognition

A

refers to the higher-level steps of motor planning adn control and deals with the concept of motor representations

144
Q

action

A

= movement(s) with a specific goal and intention, e.g., grasping a glass for drinking

145
Q

Cognitive systems store

A

(motor) representations of actions

146
Q

Same motor representations are used for

A

(i) planning actions, (ii) imaging actions, (iii) coding (and predicting the unfolding) actions observed in others)

147
Q

motor representations depends on

A

the activity of fronto-parietal networks (partly lateralized on the left)

148
Q

actions are represented as

A

a bidirectional link between movements and their effects (goals)

149
Q

experimental evidence shows that motor imagery and action observation

A

evokes brain activity in (nearly) the same brain regions involved in action planning and (partly) execution

150
Q

note about motor representations experiments

A

only if imagery is performed in first-person perspective and while trying to evoke the same kinesthetic feedbacks of action execution (motor imagery)

151
Q

Motor imagery (fMRI)

A

the somatotopy found during motor imagery mirrors the one of action execution

152
Q

Motor imagery (fMRI) - crucial role of what

A

SMA

153
Q

Motor imagery (fMRI) - minimal activation of what

A

Minimal activation of M1 during imagery because no movement is performed

154
Q

Motor imagery (fMRI) - observation

A

The observation of actions performed with different effectors produces activations that respect the classic motor homunculus at the level of the premotor and parietal cortecies (somatotopic activations)

155
Q

Mirror system

A

during the OBSERVATION of an ACTION, the same neural population (F5) that controls the execution of a specific action becomes active in the observer’s motor areas

156
Q

Mirror system TMS studies showed

A

that observing actions produced an increase in excitability of the cortico-spinal system specific to the muscles involved in the observed movement

157
Q

Mirror system - The observers motor system

A

behaves as if the same action were actually performed –> the vision of action implies their internal simulation

158
Q

ideational (conceptual) apraxia - knowledge of the sequence of motor events

A

impaired

159
Q

ideational (conceptual) apraxia - imitation/pantomimes

A

spared

160
Q

ideomotor apraxia - knowledge of the sequence of motor events

A

spared

161
Q

ideomotor apraxia - imitation/pantomimes

A

impaired

162
Q

Assessment – Ideational Apraxia

A

Object use test (verbal, visual and tactile modalities)

purposeful use testing of multiple objects

Most frequent errors

163
Q

most frequent errors

A

perplexity
clumsy
omissions
localization errors
misuse of objects
sequence errors

164
Q

perplexity

A

the patient gives the impression of not knowing what to do

165
Q

clumsy

A

the action is conceptually appropriate, but performed in a rough and ineffective way

166
Q

omissions

A

the action sequence is missing some parts (e.g. the patient pours the water into the glass without having removed the cap from the bottle

167
Q

localizations errors

A

e.g. the patient lights the match but places it close to the candlestick and not the candle

168
Q

Misuse of objects

A

e.g. the candle is rubbed on the table

169
Q

Sequence errors

A

e.g. the patient puts the coffee powder in the filter before putting the water

170
Q

Assessment – Ideomotor Apraxia

A

Imitation of proximal-distal actions, symbolic-non-symbolic gestures

Most frequent errors

171
Q

Most frequent errors:

A

Spatial distortion, gesture orientation, poor coordination between different joints, incorrect timing of the gesture

Body-part-as-object errors

Perseveration

The gesture contains extraneous elements or lacks key features, is replaced by another, is preceded by abortive movement that were never completed, is made awkwardly, with hesitation and uncertainty

The action, the more complex it is, is not implemented by arranging the individual gestures in correct succession

172
Q

Body-part-as-object errors

A

the hand/finger is used as an object

173
Q

Perseveration

A

the subject repeats, in whole or in part, the gesture just performed

174
Q

Comprehensive assessment of gesture production

A

a new test of upper limb apraxia (TULIA)

175
Q

TULIA

A

comprehensive, short to administer and standardized; consists of 48 items including imitation and pantomime domain of non-symbolic (meaningless), intransitive (communicative) and transitive (tool related) gestures corresponding to 6 subtests

176
Q

TULIA 6 subtests

A

Construct validity was demonstrated by a high correlation (r = 0.82) with the De Renzi-test

Transitive and intransitive actions/meaningful

This and the Florida Apraxia Screening and Battery are both based on the Rothi model

177
Q

Treatment of apraxia arouses little interest since…

A

The spontaneous recovery

Lack of recognition

apparent small impact on daily life

178
Q

The spontaneous recovery of praxis disorders is

A

good (50% recovered 3 – 5 months after stroke)

179
Q

Lack of recognition

A

because it can be ‘hidden’ by other disorders (hemiplegia, aphasia) and patients often are anosognosia

180
Q

apparent small impact on daily life

A

due to Automatic/voluntary dissociation

181
Q

Apraxia through imitation or verbal command is associated with

A

a notable reduction in patient’s autonomy in various aspects of daily life

182
Q

why are movements more awkward with apraxia?

A

the neuromotor rehabilitation is interfered with

183
Q

what do apraxia patients have difficulty with

A

Difficulty in problem solving, emerging in carrying out non-habitual actions or using objects in an unusual way

Difficulty recalling the use of a certain object in usual activities –> patients are less organized, use fewer objects and perform fewer actions with objects

184
Q

in case of hemiparesis…

A

difficulties caused using the non-dominant hand and the impossibility of carrying out some usual actions bimanually

185
Q

Compared to other deficits, the presence of apraxia is strongly correlated with

A

the request for assistance in daily situations

186
Q

ADL

A

a set of everyday tasks required for personal care and independent living, executed through a complex interaction between sensorimotor integration and motor learning

187
Q

Deficit management

A

adaption of environmental conditions functional to the patient’s difficulties – remove tools that may be dangerous, limit the number of objects needed for certain purposes (e.g. shaving)

188
Q

Deficit treatment

A

any direct intervention on the deficient behavior, which may consist of:

Restorative approach and compensatory approach

189
Q

Restorative approach

A

(in the acute phase) aimed at restoring lost function to promote and accelerate spontaneous recovery

Direct intervention to eliminate strategies that are no longer efficient

Intervention aimed at establishing more efficient behaviors

190
Q

Compensatory approach

A

(in chronic cases), boosting residual functions

External compensatory strategies and internal compensatory strategies

191
Q

External compensatory strategies

A

when using external aids to overcome the obstacle (e.g. the patient has difficulty in sequencing the actions –> photographs are used to show the different phases or steps of that action)

192
Q

Internal compensatory strategies

A

use of other cognitive functions to compensate for the deficient one (e.g. patient learns to visualize and/or to verbalize the exact sequence of actions while performing them)

193
Q

Treatment of Apraxia – Intervention Methods

A

Gesture training, Strategy training,

194
Q

what approach does gesture training use

A

restorative

195
Q

gesture training

A

consisting of transitive gestures (e.g. using a spoon), intransitive-symbolic gestures (e.g. greetings0, and intransitive-nonsymbolic gestures (e.g. raising only the second finder)

Three levels which increase in complexity

196
Q

first level of gesture training

A

the real tool is shown to the patient

197
Q

second level of gesture training

A

a picture of the tool in use is shown

198
Q

third level of gesture training

A

patient is shown a picture (drawing) of the tool and asked to use pantomime to express it

199
Q

Strategy training

A

uses compensatory approach that provides internal and external assistance to minimize problems caused by apraxia while performing ADL

200
Q

what kind of approach does strategy training use

A

compensatory

201
Q

what exactly does strategy training entail

A

While patient performs ADL, the therapist provides assistance by classifying the activity participation stages into initiation, execution, and control for the therapy strategy

202
Q

three stages of strategy training

A

initiation stage, execution, and control stage

203
Q

initiation stage

A

therapist provides instructions (e.g. further explanation using pictures)

204
Q

Execution stage

A

therapist provides assistance (e.g. verbal cues or physical guidance)

205
Q

Control stage

A

feedback on performed contents through video recording is provided to help teh patients successfully participate in the activities

206
Q

Treatment of Apraxia – Advanced Technologies

In stroke patients,

A

anodal tDCS over the Left Inferior Parietal Lobe may improve limb apraxia

207
Q

Treatment of Apraxia – Advanced Technologies

56 year old man with

A

right frontal, parietal and corpus callosal infraction –> efficacy of immersive VR training for ideomotor apraxia

208
Q

Treatment of Apraxia – Advanced Technologies

53 secondary progressive MS patients with apraxia –>

A

VR training significantly improved constructive and ideomotor apraxia

209
Q

what are apraxic classifications based on

A

the affected effector system

210
Q

based on the affected effector system

A

limb apraxia, oral or buccofacial apraxia, trunk apraxia

211
Q

limb apraxia

A

ideomotor or ideational forms previously described

212
Q

oral or buccofacial apraxia

A

difficulty in performing non-verbal, purposefully learned movements with the face and its parts (e.g. blow a kiss)

Both after verbal request or during imitation

213
Q

oral or buccofacial apraxia - lesion

A

Usually associated with a lesion in the left frontal operculum/inferior frontal gyrus –> may co-occur with apraxia of speech and Broca’s aphasia (contiguity of neural bases)

214
Q

trunk apraxia

A

disturbance of the control of axial muscles

215
Q

trunk apraxia - association with

A

gait apraxia

216
Q

trunk apraxia - lesion

A

Usually associated with a bilateral frontal lesion

217
Q

other praxic deficits

A

Callosal apraxia, gait, dressing, gaze

218
Q

callosal apraxia - lesion

A

following a lesion in the corpus callosum, the dominance hemisphere (specialized in motor control) cannot properly send information to the other hemisphere –> right-handed patients may show apraxia when required to perform actions with the left hand

219
Q

gait apraxia

A

disturbances in the voluntary control of gait patterns

Have a hard time getting started with walking and may have a “magnetic” or shuffling gait –> different from ataxia – loss of movement coordination

Common in dementia and Parkinson’s disease

220
Q

dressing apraxia

A

difficulties in dressing up, inability to match pieces of clothes with the correct body part (e.g. tuck the trousers on the arms)

Common in dementia

221
Q

gaze apraxia

A

inability to voluntarily control eye movement

222
Q

constructional apraxia type of disorder

A

visuo-motor disorder

223
Q

constructional apraxia

A

visuo-constructive disorder leading to the inability to accurately reproduce two-dimensional or three-dimensional spatially-organized visual models –> representation loses spatial features

224
Q

constructional apraxia - the drawing/building disability does not depend on _____ and why

A

purely motor control deficit –> visuo-motor disorder

225
Q

what else does constructional apraxia include because it is a complex disorder

A

Visuo-spatial perception and attention (neglect), memory (semantic and short-term memory), executive functions, online visuo-motor control (visual feedback monitoring

226
Q

what kind of “lesion” does constructional apraxia depend on

A

Depends on the disconnection between (or dysfunction of) perceptual and motor centers

227
Q

how do you usually test constructional apraxia

A

Usually tests by asking the patient to draw/copy simple or complex figures

228
Q

when lesion on left - constructional apraxia

A

patient usually omits crucial details

simplification, distortion, omission of crucial details but with relatively spared spatial relationships

229
Q

when lesion on the right - constructional apraxia

A

the figure loses the spatial relationships (disorganized)

left-sided omissions and frequent visuospatial defects, the figure loses the spatial relations

230
Q

left brain damage constructional apraxia –> deficit

A

–> motor planning and execution deficit

231
Q

right brain damage constructional apraxia –> deficit

A

–> visuo-spatial deficit

232
Q

Developmental disorder of motor planning and motor coordination skills

A

delay of the acquisition of motor skills, coordination difficulties, which prevent the child from carrying out daily tasks effectively, in the absence of a medical/neurological cause

Used to be called “clumsy children”

233
Q

Developmental disorder of motor planning and motor coordination skills - high incidence in…

A

school-aged population, more frequent in males

234
Q

Developmental disorder of motor planning and motor coordination skills - diagnostic criteria

A

Learning adn execution of coordinated motor skills is below expected level for age, given oppportunity for skill learning

Motor skill difficulties significantly interfere with activities of daily living and impact academic/school productivity, prevocational and vocational activities, leisure and play

Onset is in the early developmental period

Motor skills difficulties are not better explained by intellectual delay, visual impairment or other neurological conditions that affect movement

235
Q

what is Developmental Coordination Disorder often associated with

A

other developmental disorders (e.g. learning disabilities like dyslexia, or ADHD) generated impairment not only in motor skill but also in emotional and social development (importance of treatment)

neuropsych (25 decks)

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