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54 Cards in this Set

  • Front
  • Back
Describe primary and secondary acalculia.
1. Primary acalculia - a disturbance in performing calculations specifically

2. Secondary acalculia - the more common of the two, refers to problems with calculations due to more general disturbances in memory, language, attention, etc.

Hans Berger (1926)
Acalculia associated with alexia and agraphia for numbers
a. Associated Features: aphasia (84%), verbal alexia (79%), ideational and ideomotor apraxia (36.5%), constructional deficits (68%), somatognosia (26%)
b. This type is most often associated with left hemisphere disease
c. McCloskey and Caramazza (1987) later subclassified “number processing skills” based on lexical and syntactic systems: Lexical processing involves the ability to read or write individual numbers and syntactic processing involves the ability to combine numbers into the correct form and quantity
Acalculia of the Spatial Type
Impaired spatial organization results in calculation problems due to misalignment of numbers, reversals of digits, inversions (e.g., 9 for 6) and reversal errors (e.g., 12 is 21). Actual calculation is largely preserved.

a. Generally associated with more general visual-constructive impairment
b. Right hemisphere is implicated: This type is ‘rare in patients with lesions confined to the left hemisphere’
Deficits in performing the calculation itself. This is consistent with Berger’s ‘Primary Acalculia’

a. Associated deficits: aphasia (62.5%), visuoconstructive deficits (61%), general cognitive deterioration (50%), verbal alexia (39%), directional confusion (37%), visual field defects (54.5%), oculomotor disturbance (33%), sensory impairment (37%)
b. Left sided and bilateral brain disease predominate these cases
Apperceptive Visual Agnosia
Difficulty recognizing objects because of failure to perceive them (differs from cortical blindness, because visual acuity is intact)

Lesion - bilateral damage to the lateral occipital lobes
Associative Visual Agnosia
In ability to recognize visual stimuli that are well perceived (difficulty arriving at meaning of stimuli)

Lesion - bilateral occipitotemporal lesions

Commonly associated with right homonymous hemianopia
Visual Optic Agnosia
Specific inability to recognize, name, or demonstrate use of object (don't know a face is a face or a car is a car)

Lesion - left unilateral or bilateral occipitotemporal area (lingual, fusiform, parahippocampal gyri); lesion to cortex or white matter of these will also create problem
Difficulty recognizing faces

Lesion - typically bilateral lesions of occipitotemporal cortex and underlying white matter

If a unilateral lesion exists, it will be on the right hemisphere
Color agnosia - 3 classes
1. Central Achromatopsia
2. Colof Anomia
3. Specific Color Aphasia
Central Achromatopsia
Loss of color vision due to CNS disease)

Things appear gray or washed out in affected area

Lesion - visual association cortex or subjacent white matter
Color Anomia
Cannot name colors

Associated features: right-homonymous hemianopia; intact color perception in left field; pure alexia

Lesion - left hemisphere, mesially, transition between occipital and temporal lobes
Specific Color Aphasia
In the context of aphasia, there is a disproportionate difficulty with naming colors

Lesion - left parietal
Failure to synthesize all elements of a picture or scene, even though components can be recognized in isolation

a) "Dorsal" - lesion - bilateral occipitoparietal) - patient can't see more than one object at a time

b) "Ventral" - lesion - left inferior occipital) - able to "see" more than one object at a time
Balint's Syndrome
Clinical triad:
1. Simultanagnosia
2. Ocular apraxia - inability to shift gaze voluntarily from a fixation point to objects of interest
3. Optic ataxia - deficit in reaching under visual guidance

Lesion - large bilateral parietal
Anton's Syndrome
aka - Cortical Blindness

Completely blind

** Quite adamant that they can see in spite of clear evidence of their blindness

Lesion - severe bilateral damage to visual cortices and to optic radiations
Auditory Agnosia
Impaired ability to recognize speech or nonverbal sounds in light of intact hearing

Lesion - temporal lobes

Severe lesion = cortical deafness
Pure Word Deafness (aka, Auditory Word Agnosia)
Impaired recognition of speech, while hearing and recognition of nonverbal sounds is intact

Spontaneous speech, reading, writing are all intact.

Word sounds are perceived normally, but they can't link sound to meaning.

Lesion - disconnection of primary auditory area on both sides from Wernicke's area. May be bilateral or unilateral Left temporal
Auditory Sound Agnosia
Nonverbal counterpart of word deafness - involves deficits in recognizing environmental sounds (bell ringing)

Lesion - right hemisphere analog to pure word deafness
Inability to recognize familiar voices
Cortical Deafness
An extreme lack of awareness of auditory stimuli of any kind.

Lesion - bilateral destruction of auditory radiations or primary auditory cortex
Receptive Amusia
Inability to appreciate various characteristics of heard music.

Found in all cases of auditory sound agnosia and in majority of pure word deafness.
Auditory Affective Agnosia
Impaired comprehension of prosody.

Lesion - Right temporoparietal lesions and neglect
Tactile Agnosia
Impaired ability to recognize objects by touch.

Lesion - two views:
a) Contralateral primary somatosensory area in postcentral gyrus
b) Diffuse areas of cortex (posterior parietal lobe) involved in perception
Apperceptive Variety of Tactile Agnosia (aka, Astereognosis)
Impaired ability to identify objects by touch (i.e., deficit in tactile recognition in basic somatosensory perception).

** Usually unilateral
** Often seen with agraphesthesia (impaired recognition of characters drawn on palm)

Lesion - contralateral primary sensory cortex
Associative Variety of Tactile Agnosia
Inability to recognize objects by touch in the absence of primary somatosensory dysfuntion.

**Can't recognize object in hand, but can draw the object even when palpations fail to elicit recognition

Lesion - inferior parietal cortex, where high-level tactile processing occurs
Lissauer's 2-stage model of Perception/Recognition
Elementary sensation = awareness of stimulus quality and intensity => Object perception (apperception) = conscious perception of a form, object, "thing" => Object recognition (association) = recognition of category or identity of this "thing" => Naming = retrieval of the name or category
Disconnection model - Geschwind
Agnosia results from disconnection between visual and verbal processes

**This theory can't, by itself, account for the fact that most agnosics show abnormal verbal and nonveral processing of viewed objects
An acquired deficit - inability to produce written language
Aphasic Agraphias
1. Fluent agraphias - associated with Wernicke's = writing of normal quantity, but full of paraphasic errors and lack of substantive words

2. Nonfluent agraphias - associated with Broca's = effortful, sparse production; writing large and messy; prefer printing vs. writing; spelling errors due to letter omission

3. Alexia with agraphia = lesion of inferior parietal lobe

4. Gerstmann Syndrome w/ agraphia

5. Confusional state agraphia

6. Pure agraphia - writing deficit in absence of other aphasic symptoms
Nonaphasic Agraphias
1. Apraxic agraphias
Acquired inability to interpret written language
3 Major types of Alexia
1. Central Alexia (Alexia with Agraphia)

2. Posterior Alexia (Alexia without Agraphia)

3. Anterior Alexia (Frontal Alexia)
Central Alexia (Alexia with Agraphia)
a) Severe disturbance of both reading and writing
b) Loss of ability to name letters, comprehend spelled words, or read out loud

Associated features: aphasia; Gerstmann Syndrome components; hemisensory loss and/or right homonymous visual field deficit

Lesion - Inferior parietal lobe of language dominant hemisphere, centering on angular gyrus; typically damage to both cortex and white matter
Posterior Alexia (Alexia without Agraphia)
Individuals cannot comprehend written material.

They readily understand words spelled aloud or written on the palm of their hand.

Can write, but will not be able to read own writing.

With practice, can learn to read most letters out loud, which then can be recognized auditorily.

Associated findings:
a) Right homonymous hemianopia
b) Color naming deficit

Lesion - Left posterior artery territory including the splenium of the corpus callosum, which disconnects visual information from language cortex.
Anterior Alexia (Frontal Alexia)
Great difficulty naming individual letters of the alphabet, but can recognize some written words

Severe agraphia, can't copy written language

The most striking feature of this alexia is an impaired ability to understand function words, such as conjunctions, and word endings.Patients with anterior alexia understand single, semantically significant words but cannot handle sequences of these words.

Lesion - Left frontal area, same for Broca's area

Associated findings:
a) Right hemiplegia
b) Nonfluent aphasia
c) Unilateral sensory and/or visual-field neglect
Phonological Alexia
1. Inability to make spelling-to-sound correspondence rules
2. Real words are misread as visually similar words ("cat" for "car")
3. Better reading for high frequency words or words with which they have familiarity

Lesion - quite variable, within the distribution of the left middle cerebral artery. Superior temporal lobe is frequently involved.
Surface Alexia
1. Rely upon the pronunciations of written words in order to ascertain their meanings
2. Can't read words with irregular orthograpy (e.g., "tough" read as "tug")

Lesion - Left temporoparietal region
Deep Alexia
1. Primary feature - smenatnic paralexia => a type of reading error in which the word produced is related in meaning to the written target word. The semantic relationship may take many forms: synonyms (lawyer--attorney); antonyms (hot--cold); subordinates (bird--robin); superordinates (celery--vegetable); attributes (grass--green); associates (house--garden).
2. Syntactic (functional) words are almost totally omitted
3. Pseudowords can not be produced

Lesion - typically quite extensive, including much of the left frontal lobe, and extending posteriorly.
Central alexia
A total loss of the ability to understand written or printed language
Can read adequately in one visual field but not in the other

Often seen when posterior corpus callosum is severed but both visual sensory areas remain intact
Hemi-Spatial Alexia
A reading disorder where only half of the word is read
Literal Alexia
Inability to recognize letters of the alphabet

Significant feature of Anterior Alexia
Verbal Alexia
Can read individual letters but can't read full word

Associated with Posterior Alexia
Substitutions made when reading aloud

Types: literal, semantic, phonemic, etc.
Spatial Alexia
Difficulty perceiving location (place holding) of letters or words or maintaining the correct sequence of lines of print

Generally seen in the context fo right hemisphere dysfunction
Attentional Dyslexia
A reading disorder characterized by gross disturbance in reading mutiple words or text, secondary to distubrance in visual attention

Single word reading is relatively preserved
Central Dyslexias
Disorder that affects processed by which word forms activate meaning or speech production mechanism
Peripheral Dyslexias
Disorder caused by visual processing deficits in which visual inputs can't be associated with stored representations of written words

Includes attentional and neglect dyslexias and alexia without agraphia
An acquired disorder of skilled, purposeful movement.

The term purposeful is important here, because these individuals may exhibit automatic behaviors (e.g., wiping crumbs off lap) that they can not do to command.
3 Main Subtypes of Apraxia
1. Limb-Kinetic Apraxia (aka, melokinetic or innervatory apraxia)

2. Ideomotor Apraxia

3. Ideational Apraxia
Limb-Kinetic Apraxia
The loss of kinetic memories for a single limb.

Movements are appropriate for intended action, but are clumsy, unskilled, or imprecise. Affects fine motor movement, especially fingers. It is more obvious when testing distal movements, especially for rapid movments. It is unilateral.

Testing: Decreased simple manual acts (buttoning shirt); problems on grooved pegboard, finger tapping speed, etc.

Lesions: Contralateral premotor area or subjacent white matter.
Literally - "lack of order"

Disordered contractions of agonist and antagonist muscles, and the lack of normal coordination between movements at different joints that is seen in patients with cerebellar dysfunction.
Lateral medullary syndrome (a.k.a., Wallenberg's syndrome)
A relatively common brainstem infarct.

Usually caused by vertebral thrombosis.

The most disabling features are ipsilateral ataxia caused by infarction of the infereior cerebellar peduncle, and vertigo caused by infarction of the vestibular nuclei.

Unsteady gait, horizontal or rotatory nystagmus, nausea, and vomiting are common associated features.

Decreased pain and temperature sensation of teh ipsilateral face (spinal trigeminal nucleus and tract) and of the contralateral body (spinothalamic tract)
Progressive supranuclear palsy (PSP)
A neurodegenerative condition in which parkinsonism is prominent.

There is degeneration of multiple structures around the midbrain-diencephalic junction, inlcluding the superior colliculus, red nucleus, dentate nucleus, subthalamic nucleus, and globus pallidus.

Vertical eye movement is usually markedly limited

Waxy rigidity, bradykinesia, falls, and wide-eyed stares are associated features.