Module 1 Disorders Flashcards

(43 cards)

1
Q

What is visual agnosia

A

failure to recognize objects from sight

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2
Q

Subtypes of visual agnosia

A

Apperceptive
Associative

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3
Q

What is apperceptive visual agnosia
Where is the damage

A

Patient can process elements of what the person is looking at, but is unable to comprehend a fully formed percept of what the object is

Bilateral occipital/occipital parietal type lesions - extensive damage

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4
Q

What is associative visual agnosia

A

The percept of the object is fully formed, but the person cannot connect the visual representation with semantic meaning - disconnect between the visual representation and semantic meaning

Damage more anterior

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5
Q

What is prosopagnosia
Where is the damage

A

Deficit in identifying familiar faces
Can usually describe discrete aspects (nose, mouth etc)
Sometimes use other sensory cues to identify the person (voice, posture, key feature)

Damage in the ventral processing stream, in the fusiform face area

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6
Q

What is simultanagnosia

A

Another type of agnosia where there is impairment in the ability to see more than one object in a scene at a time or appreciate the multiple aspects of a single object

Difficulties reading - have to process each letter individually

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7
Q

What is cortical blindness and what is is caused by

A

Loss of vision caused bilateral damage in the visual pathway posterior to the LGN (very early in the visual processing pathway) - entire occipital lobe or major components of the pathway

Patient cannot see however, this is not typical blindness due to eyes (their eyes are healthy)

Interestingly, they can avoid obstacles - another visual pathways that bypasses the LGN - used for reflexes information and operates outside consciousness

Most common cause is anoxia

Have normal pupillary reflexes

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8
Q

What is hemispatial neglect

A

Failure to report, respond or orient to stimuli on one side

Patients may behave like one side of space does not exist

Different from visual field deficit patients, who would think to turn their heads, hemispatial neglect patients don’t think to turn their heads - nothing exists on that side to them

Almost like an attention deficit

Not attributed to sensory or motor impairment

Neglect is perceptual and representational

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9
Q

What form of hemispatial neglect is most common

A

Left side hemispatial neglect, resulting from a lesion on the right side

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10
Q

Diseases that impact visuospatial abilities

A

Stroke (right MCA or PCA)
Anoxia
Alz
Lewy Body
Posterior cortical atrophy

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11
Q

Symptoms of corticospinal tact lesions

A
  1. Weakness
  2. Increased muscle tone / hypertonia
  3. Increased reflexes / hyperreflexia
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12
Q

Stroke - Upper or lower

A

Upper motor neuron damage
Contralateral lower portion of the face is affected, but NOT the upper part - can raise their eyebrows. This is because there is bilateral innervation of the upper part of the face

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13
Q

Bell’s palsy - upper or lower

A

Lower motor neurone damage of cranial nerve 7 (not brain injury)
Complete weakness on the contralateral side - cannot raise eyebrow

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14
Q

Term: -paresis (hemi)

A

Weakness (partial paralysis) - partial weakness

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15
Q

Term: -plegia (hemi)

A

Complete paralysis

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16
Q

Term: Plasy

A

Weakness (partial) or complete paralysis due to lower motor neuron lesion

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17
Q

Basal ganglion damage

A

contralateral movement disorders
weakness +/- involuntary movements
(also cognitive and behavioural changes)

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18
Q

Lesions in the cerebellum

A

Ipsilateral deficits
Ataxic gait
Intention Tremor
Nystagmus
Scanning speech

19
Q

3 types of disorders involving muscle tone

A
  1. Spasticity
  2. Rigidity
  3. Dystonia
20
Q

Symptoms of hyperkinetic movement disorders

A

Tremor
Tics
Myoclonus
Chorea
Hemi/ballismus

21
Q

Three types of tremors

A

Essential
Resting
Intention/Action

22
Q

Types of gait disorders

A

Spastic/hemiplegic
Ataxic
Parkinsonian

23
Q

What is a spastic/hemiplegic gait disorder

A

Stiff-legged, decreased arm swing on same side

One leg is tight (hypertonic), doesn’t bend at the knee, stays stiff and swings + upper extremity weakness and spasticity on the same side

MCA stroke, cerebral palsy

Typically CST lesion

24
Q

What is an ataxic gait disorder

A

Wide-based, unsteady, staggering
Cerebellar stroke or tumour, alcohol intoxication

25
What is a parkinsonian gait disorder
Shuffling, narrow based Short shuffling gate, associated with extrapyramidal lesion Parkinson’s disease, Progressive Supranuclear Palsy, neuroleptic drugs
26
What is apraxia
Inability to perform previously learned sequential motor movements Not explained by weakness or motor incoordination
27
Lesions causing apraxia
Left inferior parietal lobe Fibers crossing the CC (unilateral apraxia) Parietal association cortex Association motor cortex
28
What is aphasia
Impairment in language processing Deficits with expressive and/or receptive communication Also affects reading and writing (usually)
29
What is aphasia not
Vocabulary loss Slurry (dysarthria) Vocal cord damage Hearing problem
30
What is Borca's aphasia
Non-fluent Effortful, halting Compensatory behaviours Comprehension preserved Aware of deficits A-grammatical speech
31
What is Wernicke's Aphasia
Fluent, but non sensical Comprehension impaired Poor awareness of deficit (anoagnosia) Writing is also nonsensical Stereotyped phrases
32
Speech errors in aphasia
Anomic errors Phonemic paraphasia Semantic paraphasia Neologisms
33
What is global aphasia
combination of wernicke's and Broca's
34
Apraxia of speech Lesion location
Disruption in the phasing of movements involved in speech Slow speech rate Segmentation of syllables Sound distortion Trial and error articulatory movements Increased difficulty with increased length and complexity of utterances Often accompanies confluent aphasia Premotor area and motor strip
35
Aprosodia Lesion location
Inability to express and/or understand the emotive content of spoken language Difficulty with sarcasm and humour Associated with frontoparietal (expression) and temporoparietal (comprehension) Aprosodia more associated with right side damage (aphasia more left) Monotone, emotionless = "Broca's" on the right Expressive deficits = "Wernicke's" on the right
36
Alexia
Aquired dyslexia Difficulty reading Usually accompanied with agraphia (difficulty writing) Types of reading/writing errors differ by lesion location
37
Surface dyslexia (what, where)
Disruption to the visual word recognition pathway Difficulty reading and spelling irregular words Left temporoparietal (angular gyrus)
38
Phonological dyslexia (what, where)
Disruption in the grapheme-phoneme pathway Difficulty sounding out words Left temporoparietal (angular gyrus)
39
Pure Alexia (Alexia w/o agraphia), what where
Information from the visual cortex not reaching the other language processing areas Slow letter by letter reading, no difficulties writing Left primary visual cortex and the splenium of the of the CC
40
Deep Alexia, what where
Semantically related words said when reading Semantic paraplegia errors when reading Large left hemisphere lesions
41
Medial temporal damage - disease, mem compr
Alz Mesial temporal lobe epi Anoxia Limbic encephalitis Korsakoff's disease Episodic memory impaired (encoding and consolidation)
42
Frontal-subcortical system - disease, mem compr
TBI MS AIDS Vascular MCI Parkinson's HTT Retrieval Working memory
43
Retrograde amnesia
Episodic and autobiographic and semantic memories Inability to consciously re-activate information that was consolidated long ago Can occur with TBI, Korsakoff’s, advanced dementia, and with ECT Co-occurs with anterograde amnesia