Answer

Expressive Aphasia in Thrombotic Thrombocytopenic Purpura

Thrombotic thrombocytopenic purpura is an autoimmune condition that affects the coagulation system resulting in the formation of microscopic blood clots in any blood vessel such as cerebral arteries. It is a rare disorder caused by the failure in cleaving multimers of von Willebrand Factors due to inhibition or absence of the enzyme ADAMTS (Peyvandi et al., 2016). The clinical presentation in Thrombotic thrombocytopenic purpura occurs as a result of end-organ damage and reduced blood flow. Neurological manifestations such as expressive aphasia, altered mental status, visual disturbances, seizures, and paresthesia can often be experienced by these patients. This is due to the cerebral ischemia and associated neurological deficit caused by microscopic clots occurring in cerebral arteries.

Expressive aphasia is an example of neurological manifestation resulting from brain damage, particularly the areas concerned with language. Consequently, the patient’s speech production is severely damaged, even though his or her intellect might be intact. The usual causes of aphasia are brain injury or stroke that damages one or more areas of the brain dealing with language. In the majority of the cases, neurological symptoms including expressive aphasia occur in the course of thrombotic thrombocytopenic purpura (Sayani & Abrams, 2015)… This argument is based on the interaction between the circulating platelets and vascular endothelium that results in profound dysregulation of coagulation. Radiological Computed Tomography (CT) scan of these patients may demonstrate infarcts in specific sections of the brain that correlate with neurological findings including expressive aphasia (Sadler, 2015).

Research studies have demonstrated incidences of atypical thrombotic thrombocytopenic purpura in patients with strokes. A case involved a middle-aged woman with atypical thrombocytopenic purpura and presented with inability to speak, mild dysarthria and expressive aphasia (Idowu & Reddy, 2013).  The patient showed marked improvement in her neurological status upon receiving seven TPEs. Crum and O’Brien in their research article reported two TTP cases where initial findings majorly comprised of neurological deficits including expressive aphasia, hence causing delays in diagnosis. These neurological deficits were later followed by hematological manifestations (Idowu & Reddy, 2013). A research study has also shown that TTP is commonly associated with abnormal brain neuroimaging and therapeutic plasma exchange was useful in resolving the symptoms (Boattini & Procaccianti, 2013). A case report by Ahmad et al of a thirty-eight-year-old lady who presented with TTP, expressive aphasia and right-sided body weakness also show that these symptoms may commonly occur together(Azmi & Maizuliana, 2017). In conclusion, TTP is a hematologic condition that is described by a pentad of neurological and renal abnormalities, fever, anemia, and thrombocytopenia. Patients with TTP in most cases present with neurological deficits such as expressive aphasia hence requires further investigations to ensure effective management.