Recovery, Sparing, and Reorganization of Function

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Recovery of Function

  • Theoretical mech of recovery
    • 1st stage recovery: first few weeks/ days after onset of stroke is critical time of regrowth (recovery from acute effects of metabolic & membrane failure, ionic and NT imbalance, hemorrhage, cellular rxn & edema)
    • 2nd stage recovery: mech largely unknown; most likely see compensation with large lesions (see below)
  • Theories of cog recovery (note these aren’t exclusive/ independent of one another)
    • theory of equipotentiality & embryogenetic analogy
      • researchers like Lashley would argue that strict localization of fx not true b/c you see recovery of fx following BD (e.g., speech)
      • Lashley argued for the mass action theory that it was extent of damage (not damage to specific locale) which resulted in more impairment
        • only did work with animals, however would remove more and more layers of c.cortex to show greater impairment (general) with more removal did argue for basic fx location (i.e., cerebellum- coordination; medulla- vitals such as respiration & arousal)
        • compared the plasticity of cerebral cortex to embryogenetic capacity of organism to dev fully from fertilized ovum
    • redundancy via vicarious fx
      • there’s a bio protective mech built in an organism, anticipating injury; thus redundancy in structures that can substitute for damaged areas (notion of areas taking over for other areas)
      • Pavlov argued for this (many potential conditioned reflex paths that are never used by normal organism)
      • Lashley thought that preservation of a part of a system concerned with same fx is necessary for their to be recovery of fx
      • Bucy argued that although certain regions might take over during recovery of fx but normally might not be involved/ necessary for normal fx (e.g., RH take over of lang following aphasia)
    • H substitution
      • notion, particularly with speech/ lang, RH capable of assuming speech fx (comprehension- nouns better than verbs) & automatic nonpropositional speech
      • support from:
        • WADA studies in Ss who recovered from LH aphasia, RH injection produced aphasic speech;
        • rCBF studies showing RH hypometabolism in aphasic stroke pts, PET also shows this along with great deal of hypometabolism ipsilateral intact tissue surrounding the infarct (suggesting some ipsilateral reorganization/ contribution too)
    • Hierarchical representations
      • notion that fx represented at several levels & damage at higher levels releases lower ones from inhibition & leads to compensation
      • see this most frequently with multiplex cortical sensory and cortical/ subcortical visual systems (collicular, thalamic compensation for O damage)
    • Diaschisis
      • Manakow’s principle (est from 2nd stage of recovery)
      • acute damage to NS (stroke deprives surrounding fx connected tissues from innervation, become inactivated)
      • fx regained/ returned once innervation is restored or regained from somewhere else
    • Regeneration
      • both regeneration and collateral sprouting (axonal, dendritic) has been shown in mammalian NS; denervation hypersenstivity may explain why some central structures become more responsive
      • however, a neuron, once it dies, cannot be regenerated nor can you see new neuron growth in the human CNS
      • if neuronal cell body is injured & dies, rest of neuron parts disintegrate & degenerate; rarely see axonal regeneration in CNS, but do in PNS, abortive if seen b/c of env Fs (such as lack of trophic substances in adult CNS, glial scars, etc.) or intrinsic Fs (inappropriate metabolic responses of CNS cells to injury, lack of appropriate protein production to help CNS regrowth, etc.)
    • Fx compensation (see below)
    • Dennervation supersensitivity
      • after denervation in damaged area, remaining fibers/ postsynaptic processes may become overly sensitive to residual NTs
      • idea that small amnts of NTs lead from prelesion neurons in order to activate new postlesion pathway (growth)
      • however, most axonal regeneration has shown to be retractive and limited
  • Recovery from aphasia
    • Fs affecting recovery:
      • Etiology:
        • CHI show most rapid recovery whereas less rapid in stroke pts
      • aphasia type
        • anomic, conduction & transcortical aphasia have best prognosis
      • severity
      • age
      • greater plasticity/ transfer of fx in immature system (critical periods of dev)
      • sex & handedness
        • some claim L handers recover better
        • some say M more prone to posterior vs F anterior damage resulting in aphasia (strokes more likely to be seen with posterior, why more M seen as aphasic, perhaps appear more aphasic b/c greater % of M aphasics due to strokes whereas F might have more CHI)
      • anatomical & fx variations
        • anatomy of speech is variable and individual variations in intral and interhemispheric distribution of various fx components may contribute to extent mature brain is able to compensate after a single nonprogressive lesion
      • time course for recovery
        • see most recovery during 1st 3mos after onset; after 6 mos, rate of recovery significantly drops; for most, spontaneous recovery doesn’t seem to appear after 1 yr
      • linguistic features of recovery (various components show different recovery rates):
        • naming, oral imitation, Y/N responses, comprehension of nouns seem most resistant to BD and might be partially mediated by RH
        • studies have shown that highest recovery rates found in BA group (low-fluency, high-comprehension group); whereas WA pts showed recovery in Y/N comprehension & repetition tasks, BA recovered in all tasks except word fluency
      • lesion site & location in recovery
        • in WA, instrumental that areas that surround the superior T area are spared (for recovery of fx to be seen)
        • lesion size also effects extent of recovery (most important factor)
      • other Fs: premorbid intelligence, health & social milieu, age, ed, occupational status, etc.

Sparing/ Plasticity of Fx (early BD)

Theories

  • critical periods of development: Hubel & Weisel’s work
    • lesions before 1 (greatest impairment & reduced IQ)
  • lesions btwn ages 1-5 (allows relative reorganization and sparing of lang fx)
    • lesions from age 5 up (shows little/no sparing)
    • Kennard’s principle: generalization that sparing of fx follows infant lesions;
    • now know it’s not always true, and sometimes early BD associated with worse fx outcome
    • speech survives early BD, but some elements may not survive (i.e., syntax, nonlang fx) and general IQ declines
  • effects of BD on language
    • lang ds in childhood following BD usually short-lived and recovery is nearly complete
    • transient lang disordered following RBD more common in kids than adults (suggests lateralization not complete)
    • Woods & Teuber looked at lang with prenatal or early postnatal BD
      • lang survived after early LBD
      • much of survival due to occupation of potential lang zones in RH
      • shift of lang not without a price (v-s usually impaired)
      • early lesions to RH produce deficits similar to those in adulthood
      • LHD (depressed V and PIQ) & RHD (depressed PIQ only)
  • reorganization of lang
    • series of studies by Rasmussen & Milner (WADA, dichotic listening task):
    • lesions of both anterior & posterior speech zones for lang (see shift to RH for lang) found also bilateral representation of speech in TLEs
    • also found rare to see recovery of speech after age 5 and if seen, due to interhemispheric organization (ipsi)
    • several TLE studies have also shown that bilateral and RH lang more likely to be seen after an early age of onset

Compensation/ Reorganization of Fx

  • following large lesions, most likely see compensation of focal cog or lang loss most likely involving:
    • ipsi cortical structures physiologically & antomically connected to damaged structures (e.g., LTLE could have some sparing of verbal memory due to good tissue beyond the extent of the sclerotic hippocampus, such as parahippocampus, entorhinal cortex, etc.)
    • contralteral homologous areas (this is the notion of reorganization; e.g., speech which is often bilateral or RH in TLE with early seizure LTLE onset)
  • explains recovery with a behavioral rather than neural mech; notion that BD organism dev new slns to pblms using residual structures
  • Studies
    • Animals
      • early studies by Kennard showed that there is greater plasticity in infants; found that unilateral lesions to precentral motor cortex of newborn monkeys have minimal effects compared to same lesion in adult monkeys
      • Hubel & Weisel showed that there are critical periods of dev (depth perception, complex cells of visual system- respond to bars of light) and that kittens with eyes sewn shut during these critical periods never learn to dev these
      • G-R removed DLPF in monkeys (infant & adult) finding that learning of delayed responses unaffected in prenatal or infants but adult monkeys failed to learn this; argued that DLPF not innate in solving delayed response tasks, but dev this fx later
    • Human
      • despite good recovery in children, unilateral BD still results in overall decrement in IQ, with PIQ more affected
      • Miner found that children, after CHI, did better in comparison to adults on cog measures
      • Fletcher argues that even though you might see recovery of fx in child, still disrupts normal dev of cognitive growth and will see more deviant patterns of dev (i.e., more likely to dev LD later)
      • Kolb pointed out that FBD during 1st year of life inevitably results in lowered IQ & poor performance on tests sensitive to F fx
      • Finger argued that although an injury may trigger neuronal growth, the ensuing changes may not always be beneficial for individual (inappropriate, fast-growing connections, exaggerated growth, misconnections) & that recovery may be an epiphenomenon