Anosagnosia

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Tardive Dyskinesia

  • Some suggest that over ½ TD pts unaware of their movement disorder (have been larger prevalence rates: 88%)
  • Some suggests that unawareness of TD might be due to primary illness (SZ>BP for unaware).
  • Some suggest they’re denying the disorder /hiding it (thumb in clenched fist; tongue against top/ bottom teeth)
  • Expect OF>LT (unaware) but research has found exact opposite
  • Research has also shown double-dissociation of awareness (e.g., can be aware of one but not other)
  • Hypotheses
    • TD patients that are unaware are more globally and cognitively impaired.
    • neuroleptics may damage mesolimbic/ mesocortical dopaminergic projections and thus may produce an iatrogenic “frontal lobe syndrome.”

Sensory-visual denial

Hemiplegia

  • minimize the extent of damage often in a jocular fashion (anosodiaphoria).
  • think limb does not belong to them or even attribute them to another person (somatoparphrenia); O. Sachs
  • overestimate the strength of an unaffected limb (anosognosic overestimation)
  • false belief that the limb is moving (kinesthetic hallucinations).
  • separate limb has appeared on another part of the body (phantom supernumerary limb).
  • These strange phenomena do not necessarily appear with hemiplegia.
    • studies have shown that anosognosia for hemiplegia associated with higher co-occurrence of confabulation
    • anosognosia more common for L side of body (RBD)

Hemianopia/ Anton’s Syndrome

  • great example (unaware of cortical blindness, & confabulatory)
  • can also see unawareness of visual field cuts (hemianopsia)
  • Hier et al. found that anososgnosia for hemianopsia & paresis associated with:
    • larger lesions
    • more severe hemiparesis
    • P lobes and surrounding tissue damage

Neglect

  • Unilateral neglect can occur from L or RBD (R>L)
  • damage to RH associated with:
    • greater impairment
    • longer lasting
    • anosognosia more likely
  • have demonstrated d.dissoc of neglect from other somato-sensory, motor, and visual field cuts (suggesting):
    • can’t infer causality of the existence of anosognosia of limb paralysis in relation to s-s disorders
    • anosog for L hemiplegia isn’t just a manifestation of inattn to the L side of egocentric space (b/c d.d)
    • unawareness of hemiplegia and neglect are functionally unrelated and if co-occurrence results, it is due to anatomical contiguity, not causality.
    • anosognosia is dissociable into function-specific forms. Anosognosia is not secured by some superordinate organ in the nervous system, but is decentralized into functional, specific blocks.

Amnesic Syndromes

MTL damage & thalamic damage not associated with anosognosia

  • H.M.
  • transient global amnesia
  • TLE (no difference btwn R/L- Seidenberg; aware of cogt impairments in relation to relatives reports)
  • A. (Squire’s pt)- thalamic damage: “My memory is like a filing cabinet…The problem is that I cannot find something when I want to” (p.385).

Diencephalic/ F lobe damage (do see anosognosi)

  • AD insight relatively intact early in disease course, but with greater F involvement, see poor insight
  • KD often present with anosognosia and confabulatory beh

Aphasia

  • BA (painfully aware of deficits)
  • WA often unaware of paraphasias/ receptive speech impairment. Lebrun stated this on grounds that:
    • many of these individuals are talkative- if aware, wouldn’t talk b/c of errors
    • often don’t refrain from speaking
  • dissoc of aphasic errors has been demonstrated:
    • WA (fluent), reading/ writing ok
    • self-corrected her phonemic paraphasic errors while ignoring her semantic errors.
    • different mechanisms might underlie the monitoring of these errors

THEORIES OF ANOSOGNOSIA

Neuroanatomically-based theories

Focal lesions

  • most agree that anosognosia results from R or bilateral damage
    • some WADA studies have suggested greater unawareness of hemiplegia following RH anethesia compared to LH; although Loring’s group didn’t find this (found that 82% unaware regardless of H)
  • Geschwind (1965) proposed a disconnection theory of anosognosia.
    • RHD>LHD to produce disturbed awareness; b/c RH normal poor linkage to speech areas assoc with LH is further weakened by RHD
    • confab is LH attempt to explain what pt can’t comprehend
    • pblms with theory (Bisiach et al.):
      • pts with telencephalic commissurotomies needn’t show misrepresentation of objects/ events in L side of personal/ xtrapersonal space which often happens following specific type of RBD
      • if info relative to the specific disorder is unable to be conveyed through the speech area, then nonverbal expression should be intact in these unaware patients, which it is not.
      • Often see cognitive disorders in nonverbal behavior but verbally acknowledge their illness. (e.g., pt admits their hemiplegia but still tries to walk or knit).
      • (mine)- see d.dissoc (theory can’t account for this)
    • Bisiach et al. : domain-specificity of anosognosia (not superordinate, monolithic monitoring system).
      • pts who are blind due to peripheral lesions are aware of their deficits and behave like a blind person.
      • pts with central lesions have an associated “visuo-specific cog impairment –> monitoring deficit.
      • model defines two breakdowns in the monitoring mechanism of cortical blindness.
        • failure of the “sensory transducer” which transmits impulses from the retina to the brain.
        • failure of the “sensory processor” which mediates the action between the transducer and the neural regions responsible for the cognitive processing of visual input

Diffuse damage

Little support for this (can see anosognosia but cog intact)

Motivation Theories

  • psych d. mech of denial (Weinstein & Kahn)
  • one’s premorbid personality (precursor for dev)
    • considerably insecure
    • strong drive for perfection and superiority.
    • Illness viewed as imperfection.
    • euphoric patients were once compulsive, meticulous and worrisome pre-insult.
    • “drive to self-actualization” & to be “well” is the motivating factor behind its dev
  • pblms with psychodynamic account:
    • dissoc (can’t account for)
    • anososog can dev after illness has been there for awhile (case study of paraplegic pt, suffered another stroke, became unaware of paralysis)
    • not lasting phenomenon (often subsides over time)- theory doesn’t account for this

Dissociable Interactions and Conscious Experience (DICE)

  • Schacter & McGlynn model conscious awareness system (CAS)
    • conscious experience of remembering, knowing, perceiving, comprehending…requires activation of specific/ distinct system which interacts with modular systems concerned with specific fx (receptive lang)
    • CAS input received from ouput of these cog fx
    • Low activation of normally highly active system would result in no input into CAS & thus anosog

Model allows for domain specificity, involves both P and F lobes (P= CAS, output link to F= ex system involved with initiating, organization, monitoring)