CaseLD

At the age of 49 years, this individual suffered a cerebral stroke in the distribution of the left middle cerebral artery. His right leg and arm were partially paralyzed and his speech was moderately disturbed. The right-sided weakness resolved within several days but the speech deficits slowly resolved over the next year, at which time his naming and ability to understand spoken and written words were normal and he returned to work. About 6 months later, he suffered a second stroke, this time in the right cerebral hemisphere. This stroke evolved over the next 48 hr. Initially, he was globally aphasic and could neither understand commands nor repeat simple sentences. Spontaneous speech was occasionally clear but interspersed with jargon. The motor system appeared to be relatively unaffected apart from an extensor left plantar response, but over the next 24 hr a dense left-sided hemiparesis developed, which resolved by 48 hr. His language disturbances persisted. A computerized tomography scan 3 months later indicated that the infarction had been in the right posterior temporal region. When examined 6 months after the second stroke, the only remaining physical abnormalities were a mild left lower facial weakness, mild left hyperre-flexia, and extinction of pin prick in the right face, arm, and leg with bilateral simultaneous stimulation. Neuropsychological testing at this time demonstrated that his IQ was in the average range. His spoken language was generally correct in content but had a loud, explosive quality. Despite a relatively normal audiogram, he was severely deficient in understanding spoken language and environmental sounds. In fact, in the absence of contextual cues he was never observed to understand a single spoken word. He was also unable to repeat words, letters, numbers, phonemes, or nonsense sounds. He did only slightly better than chance at determining whether two letters spoken successively were the same or different. In contrast, he was able to point correctly to a picture in an array when a word for one of the pictures was spoken. If he heard the name of the object, he pointed correctly to its picture and said the word. If he heard an associated word (e.g., "gambling" when confronted with an array of three objects including a picture of dice), he said the word of the picture while pointing to it ("dice") but never uttered the semantically related word.

The patient gave no indication that his hearing was defective, consistent with the audiogram, and he claimed that he could hear all the sounds presented to him. However, several subtle lower level abnormalities emerged during testing that could account for his auditory agnosia. First, reaction times to brief (30msec) suprathreshold tones were very slow (averaging about 380 msec), whereas reaction times to longer (100-msec) tones were within the normal range for his age group (averaging about 250 msec). Reaction times to visual stimuli were also in the 250-msec range for both 30- and 100-msec stimulus durations (Fig. 1). Since consonants in speech have durations in the 30- to 40-msec range, slow processing of such sounds could clearly lead to problems understanding speech. Second, the patient required almost a quarter of a second of silence between two brief (30-msec) tones in order to be hear them as separate (Fig. 2). This suggests that the sound of the first tone persisted in his auditory system long after its offset. If so, the resulting "avalanching" of sounds while listening to someone speak would clearly interfere with comprehension.

The previous case is an example of auditory agnosia in which the loss of comprehension may have had an apperceptive rather than associative origin. In this patient the disorder was probably the consequence, at least in part, of a very slow analysis of brief sounds and an independent or derivative slow decay of sounds in the auditory system. Because only supplementary tests demonstrated the possible apperceptive nature of his deficit, it is possible that many other cases of auditory

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