Your response must include a description of the current treatment options, both pharmaceutical (including mechanism of action for any drug therapies) and behavioral (based on the functional deficits associated with the disorder) that are available for the disorder your peer described.
You must use a minimum of two peer-reviewed sources in your response.
Pure Word Deafness (Auditory verbal agnosia)
Explain the symptoms of the disorder
Pure word deafness is the ability to hear, to speak, and (usually) to read and write without being able to comprehend the meaning of speech (Carlson, 2013). The primary symptom of pure word deafness is the inability to comprehend spoken words. A person with pure word deafness can hear, but cannot understand speech.
Describe how the diagnosis is made (e.g., findings on brain imaging, laboratory testing, etc.).
A diagnosis is made by a physical examination, neurological examination, and routine laboratory tests. Detailed neuropsychological assessments are also performed (Lizuka et al., 2007). MRI scans can show damage to the superior temporal lobe of a patient with pure word deafness. PET scans indicate the regions of the superior temporal lobe that respond to speech sounds.
Discuss the neurobiological basis for the disorder (e.g., CNS structures involved and neurotransmitters).
The Wernicke’s area is a region of auditory association cortex on the left temporal lobe of humans. It is important in the comprehension of words and the production of meaningful speech. Damage restricted to Wernicke’s area causes pure word deafness. There are two types of brain injuries that can cause pure word deafness: disruption of auditory input to the superior temporal cortex or damage to the superior temporal cortex itself. Either type of damage disturbs the analysis of the sounds of words and prevents people from recognizing other people’s speech (Carlson, p. 485 &487).
Describe the functional deficits associated with the disorder including how these may impact the patient’s ability to carry out activities of daily living (e.g., occupational, social, recreational).
A person with pure word deafness can still write, hear, talk, and still have reading comprehension, but they cannot understand speech (Jacobs & Schneider, 2003). This would result in difficulties in everyday conversations with others. A new way of communicating would have to be developed. This functional deficit would make it hard to work or socialize unless measures are put into place to assist with the communication challenges.
Carlson, N. R. (2013). Physiology of behavior (11th ed.). Boston, MA: Pearson
Jacobs, B. J., & Schneider, S. L. (2003). Analysis of lexical-semantic processing and extensive neurological, electrophysiological, speech perception, and language evaluation following a unilateral left hemisphere lesion: Pure word deafness?. Aphasiology, 17(2), 123
Lizuka, O., Suzuki, K., Endo, K., Fujii, T., & Mori, E. (2007). Pure word deafness and pure anarthria in a patient with frontotemporal dementia.European Journal Of Neurology, 14(4), 473-475. doi:10.1111/j.1468-1331.2007.01671.x
Prosopagnosia, also called face blindness, is a neuropsychological condition that refers to impairment in the recognition of faces. Although, patients with prosopagnosic suffer from other types of recognition impairments (place recognition, car recognition, facial expression of emotion, est.), they experience face recognition problems above or over other types impairments. prosopagnosia occurs without intellectual, sensory or cognitive impairments; in other words, people with prosopagnosia can still recognize people from non-facial cues. They cannot recognize familiar people by their faces alone, and often use alternative routes to alleviate the effects of this impairment. These routes include using voice, gait, clothing, hairstyle, and other information rather than faces. Not surprisingly, prosopagnosia can be socially crippling. In absence of these non-facial cues failures of recognizing familiar faces reveal; in fact, patients are unable to recognize famous people, close friends, family members, and even their images in the mirror.
Bodamer, a German neurologist, coined the term prosopagnosia in 1947 (Suscillo, Wright, Tree & Duchaine, 2015). “The word prosopagnosia is a combination of Greek word for face (prosopon) and the medical term for recognition impairment (agnosia). Bodamer also stated prosopagnosia was related to brain injury (head trauma, stroke, and degenerative disease), which refers to acquired prosopagnosia” (Suscillo, Wright, Tree & Duchaine, p.15, 2015).
People with acquired prosopagnosia had normal face recognition ability and then that was impaired. In contrast, prosopagnosia can occur from birth with no medical record of brain damage, which refers to pure developmental or congenital prosopagnosia.
Prosopagnosia is classified as face recognition impairment and differentiated from other types of impairments that can compromise face recognition (Bennetts, Butcher, Lander, Udale & Bate, 2015). People with prosopagnosia can achieve recognition using non-facial cues. Prosopagnosia is not a unitary syndrome, and different patients may show different types of recognition impairments.
Bennetts, R. J., Butcher, N., Lander, K., Udale, R., & Bate, S. (2015). Movement cues aid face recognition in developmental prosopagnosia. Neuropsychology, 29(6), 855-860. doi:10.1037/neu0000187
Susilo, T., Wright, V., Tree, J. J., & Duchaine, B. (2015). Acquired prosopagnosia without word recognition deficits. Cognitive Neuropsychology, 32(6), 321-339. doi:10.1080/02643294.2015.1081882