Are pharmacotherapeutics effective for treating aphasia?

Introduction: Aphasia is a communication disorder resulting from stroke and/or neurodegenerative conditions which involve the left cerebral hemisphere. It is a debilitating disorder affecting a person's ability to speak, understand, read, and write. Its impact on daily life necessitates therapeutic strategies to aid patients with aphasia.

Turning the Spotlight to Cholinergic Pharmacotherapy of the Human Language System.

Even though language is essential in human communication, research on pharmacological therapies for language deficits in highly prevalent neurodegenerative and vascular brain diseases has received little attention. Emerging scientific evidence suggests that disruption of the cholinergic system may play an essential role in language deficits associated with Alzheimer's disease and vascular cognitive impairment, including post-stroke aphasia. Therefore, current models of cognitive processing are beginning to appraise the implications of the brain modulator acetylcholine in human language functions.

Pharmacotherapy for post-stroke aphasia: what are the options?

Introduction: Aphasia is a common, long-lasting aftermath of stroke lesions. There is an increased integration of pharmacotherapy as an adjunctive strategy to speech and language therapy (SLT) for post-stroke aphasia (PSA). Nevertheless, more research in pharmacotherapy for acute and chronic PSA is necessary, including the election of drugs that target different neurotransmitter systems and deficits in specific language domains.

Brain structural and functional correlates of the heterogenous progression of mixed transcortical aphasia.

Mixed transcortical aphasia (MTCA) is characterized by non-fluent speech and comprehension deficits coexisting with preserved repetition. MTCA may evolve to less severe variants of aphasias or even to full language recovery. Mechanistically, MCTA has traditionally been attributed to a disconnection between the spared left perisylvian language network (PSLN) responsible for preserved verbal repetition, and damaged left extrasylvian networks, which are responsible for language production and comprehension impairments.