RECOVERY IN APHASIA

Introduction
Most individuals with aphasia show some recovery of language function despite persisting
damage to left hemisphere language zones (Holland et al., 1996). Such recovery is a complex
process that is dependent on neurophysiological processes, environmental factors, and other
variables. Several mechanisms are presumed to be involved, such as recovery of penumbral
tissues, neural plasticity, resolution of diaschisis and behavioral compensation strategies.
Rehabilitation is believed to modulate this logistic pattern of recovery, probably by interacting
with these underlying processes.

Theories of Recovery
Considering recovery, it is necessary to include biological mechanisms and rehabilitation that
acts on plasticity of the brain and leads to restitution, substitution or compensation.
Theory of restitution of function assumes that behavioral improvement results from the
increasing integrity of the injured functional system. Restitution is relatively independent of
external factors such as physical or cognitive stimulation; This includes biochemical factors with
reduction of edema, absorption of blood or restoration of axonal transport.
Theory of substitution of function assumes that improvement results from system
reorganization. Substitution depends on external stimulation, i.e. practical activity of the paretic
arm or leg during rehabilitation. It involves functional adaptation to the deficit, through partially
restoring neural networks and compensation for the lost or broken connections after injury.
Substitution can be a process of partial reorganization of cortical representation for movement
and changes in activity in components of the motor network.
Theory of compensation aims to improve the mismatch between the patient's disability and
expectations, as well as demands of the patient's environment. Compensation in particular has an
impact on increasing the time, effort and amount of training of the damaged skill

Mechanisms Underlying Recovery

The mechanism of brain plasticity and its recovery depends on a dual mechanism: structural and
functional. Structural mechanism involves the creation of fibers of remaining neurons by
forming new functional synapses, whereas functional mechanism includes spread of the cortical
map by activating alternative neuronal networks (including damaged zone) of the previously
functionally inactive pathways.
Current evidence points to three kinds of changes in neural activity most relevant for aphasia
recovery:
1. Recruitment of lesioned and perilesional left hemisphere regions for language-related
tasks,
2. Acquisition, unmasking or refinement of language processing ability in the nondominant
right hemisphere, and
3. Dysfunctional activation of the nondominant hemisphere that may interfere with
language recovery
Researchers have emphasized that these mechanisms are not mutually exclusive, but rather
comprise a hierarchical framework of interacting language recovery mechanisms (Hamilton,
Chrysikou & Coslett, 2011).

Evidence from past researches support both left- and right-hemisphere models of aphasia
recovery, indicating that recovery is a dynamic process involving a variety of plastic changes in
both hemispheres. Hence, a hierarchical combination of changes is likely to occur in patients
recovering language function after stroke (Heiss & Thiel, 2006). The hierarchical model of
effective aphasia recovery can be summarized as follows:
(1) When lesions of the left hemisphere are very small or do not affect critical language
centers, complete or near-complete language recovery can often be achieved by
restoration of normal patterns of activation in left hemisphere language networks.

(2) When lesions of the left-hemisphere damage important language centers, perilesional
regions of the left hemisphere may be recruited to subserve language function, often
leading to good recovery (Karbe, Thiel, & Weber-Luxenburger, 1998).

(3) When left hemisphere language networks are more severely impaired, the right
hemisphere appears to be capable of assuming some language functions, by employing
homotopic regions in ways that may mirror some aspects of language processing in the
left hemisphere (Gold & Kertesz, 2000).

The beneficial role of the right hemisphere in aphasia recovery: This right hemisphere
recruitment for language may be facilitated by the release of interhemispheric inhibition from the
damaged left hemisphere (Barlow, 1877). Hence, right hemisphere recruitment for language
tasks may contribute to overall language recovery in severely affected patients.

The detrimental role of the right hemisphere in aphasia recovery: However, this remodeled
language network in aphasia patients is likely inefficient compared to premorbid intact left
hemisphere perisylvian regions.
This is in part because networks in the non-dominant right hemisphere may be intrinsically less
adept at language processing compared to their dominant left hemisphere counterparts due to
genetic predisposition, developmental factors, neuroplastic changes that occur during language
learning, or any combination thereof. Increased recruitment of right hemisphere networks may
also be inefficient because they may prevent activation of more efficient left hemisphere
language networks via transcallosal inhibition (Shimizu et al., 2002).

Differing accounts of plasticity in language systems in chronic aphasia

(a) After unilateral left hemisphere stroke (grey), some language functions may be subserved by
recovered lesional areas or recruited perilesional areas (light green). (b) Right perisylvian areas
(light green) may be recruited to subserve some language functions, a process facilitated by
decreased transcallosal inhibition of the right hemisphere by the damaged left hemisphere. (c) By
contrast, right hemisphere activity may be deleterious. Released from interhemispheric
inhibition, right hemisphere structures (red) may exert increased inhibitory influence on left
perisylvian areas, impeding functional recovery of lesional and perilesional areas in the left
hemisphere (dark green).

Spontaneous Recovery
The course of recovery of aphasia after stroke is highly variable. The neurological mechanisms
underlying functional recovery are still largely unknown. Two mechanisms generally associated
with spontaneous recovery include regression of diaschisis or reperfusion of ischemic tissue
surrounding the stroke and rapid functional reorganization.
Spontaneous recovery of language in patients with aphasia occurs between 4 and 34 weeks after
stroke. Studies of spontaneous recovery from aphasia indicate that only a limited set of variables
(severity, lesion size, time post-onset) have proven to be reliable prognostic factors, while others,
such as age, gender, or handedness, have a less predictable relationship with clinical outcome.
Factors Affecting Recovery
Patient related variables:
 Age: Increasing age is associated with inferior recovery. Age associated medical and
neurological diseases (comorbidity), such as hypertension, diabetes, and dementing
conditions, can affect the brain, and thus interfere with the neurological modifications
associated with functional recovery.
In the case of childhood aphasia: a fast and relatively complete recovery can be expected
in children with acquired aphasia (Martins, Castro-Caldas, Van Dongen, & Van Hout,
1991). Within this population there is a trend for a better prognosis being associated with
earlier lesion onset (Martins & Ferro, 1992).

 Linguistic Background: No clear-cut pattern emerges from the literature. It hass been
reported that multilingual aphasics have better recover patterns as compared to their
monolingual counterparts (Paradis, 1993).

 Although researchers suggest that left-handed individuals have better prognosis, factors
like gender and handedness and have not been found to be robust predictors of
recovery.

 Studies have suggested that patients with higher literacy levels, higher pre-morbid
intelligence and those with higher motivation levels, respond better to therapy and hence
have a better prognosis. However, limited evidence is available about the possible role of
other potentially relevant patients’ characteristics (education, motivational and
intellectual level).

Disease-Related Variables
 Etiology: Negative prognostic factor for aphasia is a nonstatic etiology, that is, its
association with a progressive disease of the nervous system, such as a malignant tumor
or a degenerative condition. Evidence shows that aphasia due to traumatic brain injury
recovers better than aphasia due to cerebrovascular lesion (Basso & Scarpa, 1990).
Concerning aphasia due to vascular lesions, hemorrhagic strokes tend to be associated
with a more severe clinical picture, but with better outcome in comparison with ischemic
strokes (Basso, 1992; Nicholas et al., 1993); this may be related to the less destructive
effects of a hematoma on brain tissue, and/or to the less frequent presence of diffuse
ischemic changes in the brain of patients with hemorrhagic stroke.

 Lesion Size: Many studies performed after the introduction of CT scan have assessed the
size of vascular lesions in aphasic patients. The size of the cerebral lesion, together with
the closely associated variable of aphasia severity, seems to be the strongest negative
predictor of recovery in all studies (for examples, see Goldenberg & Spatt, 1994).
  Lesion Site: Knauff and her colleagues have reported that improved recovery is
associated with lesions that are less extensive and limited to the cerebral cortex.
Information related to site and size of lesion has been reported in a number of studies.
Studies report persistent deficits in speech fluency when lesions extend into underlying
white matter. Imaging studies suggest that functional recovery of the left superior
temporal cortex is associated with more positive long-term prognosis for receptive
language. Strategically placed lesions in the left temporal lobe appear critical to recovery
of comprehension abilities.

Rehabilitation and Recovery

Studies have reported contradictory findings with respect to rehabilitation and spontaneous
recovery. Some have revealed no significant difference in spontaneous recovery with and
without rehabilitation (Kertesz & McCabe, 1977), while others have reported a better recovery
with rehabilitation (Hamilton, Chrysikou & Coslett, 2011). Literature however predominantly
points to better long-term recovery and prognosis with rehabilitation therapy. Smaller the
time window between onset of stroke and onset of rehabilitation, the better the recovery.
Significant improvement can be observed in severely aphasic patients up to 2 years post-onset
(Hanson, Metter, & Riege, 1989).

Recovery Across Aphasia Types

The greatest spontaneous recovery was seen in "Broca's" aphasics, followed by the "conduction"
group. Anomic aphasia appeared to be a common end-stage of evolution. Long-term follow-up
(twelve months or more) demonstrated that global aphasics have a poor prognosis, while Broca's
and Wernicke's have an intermediate one. Complete recovery occurred frequently among
anomic, conduction and transcortical aphasics (Kertsz & McCabe, 1977).
Levita (1979), found that in the first 6 months fluent aphasics improved more than non-fluent,
who improved more than global aphasics, whereas in the second 6 months after stroke, fluent
aphasics improved least and global aphasics the most.

Recovery in Bilingual Aphasics

Paradis (1977) described 6 basic patterns in which a bilingual aphasic could recover their
language abilities: parallel – both languages are impaired to a similar degree and recover at the
same rate, differential – recovery rates differ relative to pre-morbid levels, selective – not all
languages are fully restored, antagonistic – one language regresses as the other recovers,
successive – one language may only begin to recover once the other is fully restored, and
mixed/blended – languages are inappropriately mixed and interfere in the recovery process.
(Covered in the topic: Aphasia in multilinguals)
References:
Culton, G. L. (1968). Spontaneous recovery from aphasia.
Rothi, L. J., & Horner, J. (1983). Restitution and substitution: Two theories of recovery with
application to neurobehavioral treatment. Journal of Clinical Neuropsychology,5(1), 73-81.
doi:10.1080/01688638308401152
Kertesz, A., & McCabe, P. (1977). Recovery patterns and prognosis in aphasia. Brain, 1(1), 848-
849. doi:10.1136/bmj.2.6091.848-a.
Hamilton, R. H., Chrysikou, E. G., & Coslett, B. (2011). Mechanisms of aphasia recovery after
stroke and the role of noninvasive brain stimulation. Brain and Language,118(1-2), 40-50.
Fridriksson, J., & Smith, K. (2016). Neuroplasticity Associated with Treated Aphasia
Recovery. Neurobiology of Language,1007-1013. doi:10.1016/b978-0-12-407794-2.00080-8