A Case of Nonfluent Aphasia Treated Successfully With Speech Therapy and Adjunctive Mixed Amphetamine Salts

Our patient is a right-hand-dominant 39-year-old man who was presenting with dysarthria and right sided weakness for 1 hour. MRI of the brain revealed diffuse enhancement of cortical structures within the left middle cerebral artery distribution with territorial ischemia.

After being medically treated, the patient started physical/occupational and speech therapy. On physical examination, he had right-sided hemiparesis. On psychiatric evaluation, he was noted to be apathetic (but denied depression) with nonfluent aphasia. On language evaluation, the latter was manifested by an inability to repeat sentences, unable to name any of three objects, being only able to name three words beginning with the letter “F” in 1 minute, although he correctly answered eight “yes-no” questions correctly. His speech was telegraphic (without articles or conjunctions). We started treating him with amphetamine/dextroamphetamine, 2.5 mg daily, which was increased gradually, and after 2 weeks of treatment, was increased to 10 mg/day.

Within 3 weeks, his language abilities improved to include speech that contained articles and prepositions. The patient's apathy had resolved. He was able to name two-thirds of objects, could name 10 “F” words in 1 minute, was more accurate (although not completely) with repeating phrases and was able to draw intersecting pentagons and copy a clock drawing. Notably, his blood pressure remained normotensive throughout the medication trial.

Aphasic patients may lose the ability to produce speech, to comprehend speech, to repeat, and to hear and read words. Our patient presented with nonfluent aphasia where repetition, naming, fluency, reading, and writing were impaired, although his comprehension seemed intact.² With treatment with amphetamine/dextroamphetamine and speech therapy, his language functioning demonstrated improvement.

Amphetamines are indirect sympathomimetics exerting their action by stimulating the release of endogenous norepinephrine and dopamine from storage sites in central nerve terminals.³

Based on data from animal models and subsequent human studies, it was found that the concentration of catecholamines in human CSF is decreased after cerebral cortical infarction fluid; this is the rationale for augmenting these transmitters in the brains of patients after stroke. Amphetamines (and other dopamine agonists) share evidence that suggest these medications can enhance recovery from stroke-induced motor and language deficits.⁴ Dextroamphetamine has been reported to result in neural plasticity, such as enhancement of neural sprouting and synaptogenesis after experimental infarctions.⁵ Increased levels of central noradrenergic activity are thought to mediate the beneficial effects of dexamphetamine in recovery after brain injury.⁵

Our results should be viewed cautiously as our patient's apathy also improved, which could have helped his performance. Additionally, psychostimulants can treat symptoms of depression, which could also aid in treatment outcomes, although our patient denied dysphoria. His blood pressure remained normotensive; however, elevated BP can occur with psychostimulants. On the basis of our case report, we suggest further controlled studies combining speech therapy with adjunctive psychostimulant usage for the treatment of nonfluent aphasia.