Agnosias are disorders characterized by the inability to recognize and name objects despite intact sensory modalities, with diagnostic criteria including normal perception and the absence of dementia. The document outlines various types of agnosias, such as visual, auditory, and tactile agnosia, detailing specific conditions associated with each type and their underlying causes. Additionally, it discusses the implications of these disorders on sensory perception and the need for distinguishing them from other cognitive impairments.

1. AGNOSIAS

2. INTRODUCTION
 SIGMUND FREUD introduced the term
in 1891
 Agnosias (Gnosis- to know) are
disorders of recognition and naming of
object, in one sensory modality, in the
presence of intact primary sensation
 Normal percept stripped of its meaning.

3. CRITERIA FOR THE DIAGNOSIS
 Failure to recognize an object
 Normal perception of the object, excluding an
elementary sensory disorder
 Ability to name the object once it is recognized,
excluding anomia as the principal deficit
 Absence of a generalized dementia

4.  Agnosia results from lesions that disconnect and isolate
visual, auditory and somatosensory input from higher
level processing
 Defined as profound, modality-specific recognition
impairment in the presence of normal primary sensory
function that cannot be fully explained by:
 mental deterioration,
 attentional disturbances,
 unfamiliarity with the stimuli used to assess recognition
abilities

5. TYPES
 Visual
 Auditory
 Tactile
 Important : rule out primary sensory disorder- test
visual acuity/field, auditory function, aphasia,
cognition and somatosensory functions

6. VISUAL AGNOSIA

7. VISUAL AGNOSIA
 Cortical Visual Disturbances
 Cortical Visual Distortions
 Visual Object Agnosia
 Balint Syndrome and Simultanagnosia
 Optic Aphasia
 Prosopagnosia
 Klüver-Bucy Syndrome

8. CORTICAL VISUAL DISTURBANCES
 Cortical Blindness- Bilateral occipital lobe lesion
 Unaware that they cannot see, even confabulate
visual descriptions or blame their poor vision on dim
lighting or not having their glasses, describe objects
they “see” in the room but walk into wall - (Anton
syndrome)
 Perceptual deficit in which there is unawareness or
neglect of the sensory deficit

9. CORTICAL VISUAL DISTURBANCES
 Blindsight or inverse Anton syndrome- preserved ability to react
to visual stimuli, despite the lack of any conscious visual
perception
 Deny blindness despite objective evidence of visual loss
 May react to more elementary visual stimuli such as brightness,
size, and movement, whereas they cannot perceive finer
attributes such as shape, color, and depth
 Subjects sometimes look toward objects they cannot consciously
see

10. CORTICAL VISUAL DISTURBANCES
 Bonnet syndrome- Visual hallucinations in blindness
 Irritative lesions of occipital visual cortex produce
unformed hallucinations of lines or spots, & of the
temporal lobes produce formed visual images.
 Cortical blindness diagnosed by absence of ocular
pathology, preservation of pupillary light reflexes,
and associated neurological symptoms and signs

11. CORTICAL VISUAL DISTURBANCES
 B/L PCA territory stroke involves occipital lobes,
hippocampus, medial temporal lobe- confused,
agitated, short term memory loss
 HIE; PRES; Meningitis; SLE
 CJD- Heidenhain variant
 Posterior cortical atrophy syndrome in Alzheimer and
other dementia
 Transient phenomenon in:
 Traumatic brain injury
 Migraine
 Epileptic seizures
 Complication of iodinated contrast procedures

12. CORTICAL VISUAL DISTORTIONS
Positive visual phenomena- in migraine and visual field defects-
NOT AGNOSIA
 Metamorphopsia –
distortion shape
 Teichopsia - Scintillating
scotoma, irregular shapes
 Macropsia and micropsia
 Alice in wonderland
Syndrome- changes in
shape and size

13.  Achromatopsia – loss of
colour vision
 Akinetopsia -loss of
perception of motion
 Palinopsia -
Perseveration of visual
images

14.  Allesthesia –
spreadof visual
image from a normal
to a hemianopic field
 Polyopia –
duplication of
objects

15. COLOR VISION DEFICIT – OCCIPITAL LOBE
 Achromatopsia – complete loss of colour vision
occur either B/L or in one hemifield with lesions of
visual association cortex areas 18 and 19
 Color agnosia- confabulate an incorrect color name
when asked color of object; normally perceived
color cannot be properly recognized
 Difficulty naming or pointing to named colors
 Can match colors, normal color vision on Ishihara
charts
 Lesions of the left occipital

16. VISUAL OBJECT AGNOSIA
 Fails to recognize objects by
sight, with preserved ability to
recognize them through touch
or hearing, in the absence of
impaired primary visual
perception or dementia
 Appreciative visual object
agnosia
 Associative visual object
agnosia

17.  Visual object agnosia will be
unable to name or recognise a
picture of a kangaroo
 The same patient will have no
difficulty naming and describing
the characteristics of a kangaroo
if requested via the auditory
modality.
 Anomia- will be unable to name
the picture and may respond,
“it’s found in Australia, it jumps…
can’t think of its name,”
demonstrating intact
recognition.
 Semantic dementia have central
loss of knowledge and will be
unable to name the picture or
demonstrate any knowledge of
the object regardless of modality

18. APPERCEPTIVE VISUAL AGNOSIA
 Intact vision:
 Acuity, brightness discrimination, color vision, & other
elementary visual capabilities
 Deficits:
 Abnormal Perception (pictures, letters, simple shapes)
 unable to access the structure or spatial properties of
a visual stimuli and the object is not seen as a whole or
in a meaningful way
 Cannot recognize, copy or match objects
 Useful tests- Incomplete letters and object decision
from silhouettes

20. ASSOCIATIVE VISUAL AGNOSIA
 Failure of recognition, assign meaning to appropriately
perceived objects
 Patients can copy or match pictures but they cannot name
what they have drawn, excludes primary defect of visual
perception
 Can recognize objects by tactile or auditor stimulus and
have intact knowledge of objects
 Visual perception better than in apperceptive agnosia
 Lesion: bilateral inferior temporo-occipital junction and
subjacent white matter

22. APPERCEPTIVE ASSOCIATIVE

23. SIMULTANAGNOSIA
 Partial Balint syndrome deficit; described by Wolpert
in 1924
 Loss of ability to perceive more than one item at a
time
 Sees details of pictures, but not the whole
 Seen in bilateral parieto-occipital strokes; posterior
cortical atrophy and related neurodegenerative
involving posterior parts of both hemispheres

24. BALINT SYNDROME
 Bilateral hemisphere lesions, often involving the
parietal and frontal lobes.
 Triad of deficits:
(1) Ocular motor apraxia- inability to voluntarily shift
gaze despite the intact function of extra-ocular
muscles- psychic gaze palsy.
(2) Optic ataxia- lack of coordination between visual
inputs and and hand movements
(3) Simultagnosia- Inability to identify different items
in a visual scene simultaneously
 These deficits result in the perception of only small
details of a visual scene, with loss of the ability to
scan and perceive the “big picture.”

26. OPTIC APHASIA/OPTIC ANOMIA
 Intermediate between agnosias and aphasias
 Cannot name objects presented visually but can
demonstrate recognition of objects by pantomiming or
describing their use
 Preserved recognition of the objects distinguishes it from
associative visual agnosia
 Information about the object reach parts of the cortex
involved in recognition in the right hemisphere, but the
information is not available to the language cortex for
naming

27. PROSOPAGNOSIA
 Inability to recognize faces
 Apperceptive prosopagnosia – inability to even perceive and
process the face
 Associative prosopagnosia- inability to recognize or apply
any meaning to face despite perceiving it.

28. KLÜVER-BUCY SYNDROME
 Visual agnosia
 Prosopagnosia
 Memory loss
 Language deficits
 Changes in behaviour, altered sexual orientation ,
placidity and excessive eating
 Bitemporal damage: Herpes simplex and surgical
ablation.
 Connections appear to be disrupted between vision and
memory and limbic structures, so visual percepts do not
arouse their ordinary associations

29. AUDITORY AGNOSIA

30. CORTICAL DEAFNESS
 Acquired bilateral lesions in
 Primary auditory cortex- Broadman area 41 and 42 ( HESCHL
gyri)
 Auditory radiations projecting to HESCHL gyri
 Can hear noises but cannot appreciate their meaning
 Cannot understand speech or music
 Unilateral lesions- little effect on hearing

31. AUDITORY AGNOSIA
 Hear noises but not appreciate their meanings
(1) Pure word deafness
(2) Pure auditory nonverbal agnosia
(3) Phonagnosia
(4) Pure amusia

32. PURE WORD DEAFNESS/ AUDITORY VERBAL AGNOSIA
 Inability to comprehend spoken
words, with preserved ability to
hear and recognize nonverbal
sounds
 Disconnection of both primary
auditory cortices from the left
hemisphere Wernicke area
 Deaf hearing
 Cannot repeat words or write
from dictation
 Spontaneous reading, writing
speaking preserved
 Non speech auditory information
processing - normal
Comprehensi
on of spokne
words
Impaired
Non verbal
sounds
Can recognize
Reading,
writing, spoken
speech
Inatact

33. AUDITORY NONVERBAL AGNOSIA
 Inability to identify meaningful nonverbal sounds but
have preserved
 Pure tone hearing and
 Language comprehension
 Bilateral temporal lobe lesions chiefly right

34. PHONAGNOSIA
 Failure to recognize familiar people by their voices
( analogous – prosopagnsoia)
 Lesion: Right parietal lobe
 Difficulty in matching of unfamiliar voices
 Lesion: Unilateral or bilateral temporal lobe

35. AMUSIA
 Loss of musical abilities
 Recognition of melodies and musical tones
 Right temporal lobe
 Analysis of pitch, rhythm, and tempo
 Left temporal lobe
 Can sing from memory

36. TACTILE AGNOSIA

37. TACTILE AGNOSIAS
 Fail to recognise numbers or letters written on hand and
contralateral he not able to recognise - parietal lobe
 Astereognosis – inability to identify object by touch
 Agraphesthesia- inability to recognise a written number
or letter traced on the skin

38. TACTILE APHASIA
 Inability to name a palpated object despite intact recognition
of the object and intact naming when presented in other
sensory modality

39. SUMMARY
 Disorders of sensory perception and recognition.
 It may be due to primary sensory cortical defects or
its connections.
 Recognition not only requires primary sensations but
also association of perceived items and previous
sensory experience and associated memories

40. THANK YOU