Mark Kritchevsky

Cognitive Impairment Following Frontal Lobe Damage and Its Relevance to Human Amnesia

Whether frontal lobe pathology can account for some of the cognitive impairment observed in amnesic patients with Korsakoffs syndrome was investigated. Various cognitive and memory tests were given to patients with circumscribed frontal lobe lesions, patients with Korsakoffs syndrome, non-Korsakoff amnesic patients, and control Ss. Patients with frontal lobe lesions were not amnesic. Nevertheless they exhibited 2 deficits that were also exhibited by patients with Korsakoffs syndrome but not by other amnesic patients: (a) impairment on the Wisconsin Card Sorting Test and (b) impairment on the Initiation and Preservation subscale of the Dementia Rating Scale. Thus, frontal lobe pathology can explain some of the cognitive deficits observed in patients with Korsakoffs syndrome.

Description of brain injury in the amnesic patient N.A. based on magnetic resonance imaging.

N.A. has been amnesic since 1960 when at the age of 22 years he sustained a penetrating brain injury with a miniature fencing foil. The amnesia primarily affects verbal material and occurs in the absence of other detectable cognitive deficits. Previous CT scans demonstrated a lucency in the region of the left mediodorsal thalamic nucleus, but no additional damage was revealed. Beginning in 1986 when he was 48 years old, N.A. was evaluated with a series of magnetic resonance imaging (MR) studies. Three major areas of damage were identified. In the left thalamus there is a prominent 3- to 4-mm-wide linear lesion that approximates the position and orientation of the internal medullary lamina. The defect extends for approximately 20 mm anteroposteriorly and likely involves the rostral group of intralaminar nuclei (central medial, paracentral, central lateral, rhomboid, and reuniens nuclei), the caudal group of intralaminar nuclei (centrum medianum and parafascicular nuclei), the ventral aspect of the mediodorsal nucleus, and the ventral lateral and ventral anterior nuclei. It also likely interrupts the trajectories of the mammillothalamic tract and postcommissural fornix. The posterior hypothalamus is markedly disrupted and the mammillary nuclei appear to be missing bilaterally. Finally, the right anterior temporal lobe is damaged for a distance of about 3.5 cm from the pole to midway through the amygdaloid complex. This damage probably occurred during exploratory neurosurgery done at the time of N.A.s injury. The hippocampal formation appears intact on both sides. A comparison of these findings with those from other patients with diencephalic amnesia suggests that amnesia can result when several diencephalic structures are damaged conjointly, including the internal medullary lamina, the intralaminar nuclei, the mediodorsal nucleus, and the mammillothalamic tract. Whether amnesia as severe as N.A.s would result from selective damage to any one of these structures remains to be determined.

Production of complex syntax in normal ageing and alzheimer's disease

Abstract Word-finding difficulties are among the earliest symptoms of Alzheimers disease (AD), but most AD patients retain the ability to produce well-formed sentences until the late stages of their disease. This dissociation has been used to argue for a modular distinction between grammar and the lexicon. In this paper, we offer an alternative view. First, we show that grammatical production is impaired in AD patients when grammar is assessed under highly constrained conditions in a film description task. Furthermore, these grammatical deficits are comparable in some respects to the patterns of lexical impairment observed in this and other studies of AD; specifically, patients do not produce frank lexical or grammatical errors, but they do find it difficult to access the “best fit” between meaning and form. We propose that differences in the onset time for lexical and grammatical symptoms in AD are due not to a disconnection between modules, but to fundamental differences in the automaticity and/or acce...

Transient global amnesia Characterization of anterograde and retrograde amnesia

Five patients with transient global amnesia (TGA) were given neuropsychological tests during and after their episode. During TGA, all patients were impaired on tests of new learning ability for both verbal and nonverbal material. Retrograde amnesia was patchy and covered a variable period of time before the onset of the episode: from about 36 hours in one case to 4 years in two cases. Some cognitive impairment in addition to amnesia was present during the episode. For example, patients copied a complex figure more poorly during the episode than afterwards. All patients had normal memory at follow-up testing. These data are consistent with the idea that the amnesic symptoms of TGA are caused by transient bilateral dysfunction of medial temporal brain structures important for memory.

Transient global amnesia: Evidence for extensive, temporally graded retrograde amnesia

We gave six patients with transient global amnesia (TGA) neuropsychological tests during and after their episodes. During TGA, all patients had severe anterograde amnesia for verbal and nonverbal material and a patchy but temporally graded retrograde amnesia for personal and public events dating back to at least 1960. In addition, they were unusually passive during TGA, had impaired ability to copy a complex figure, and possibly had mild impairment of confrontation naming. All exhibited complete recovery of memory and other cognitive abilities after the episode. There are similarities between the transient amnesia of patients with TGA and the chronic amnesia of patients with presumed bilateral damage to the medial temporal region or the diencephalic midline.

Discourse Deficits Following Right Hemisphere Damage in Deaf Signers

Previous findings have demonstrated that hemispheric organization in deaf users of American Sign Language (ASL) parallels that of the hearing population, with the left hemisphere showing dominance for grammatical linguistic functions and the right hemisphere showing specialization for non-linguistic spatial functions. The present study addresses two further questions: first, do extra-grammatical discourse functions in deaf signers show the same right-hemisphere dominance observed for discourse functions in hearing subjects; and second, do discourse functions in ASL that employ spatial relations depend upon more general intact spatial cognitive abilities? We report findings from two right-hemisphere damaged deaf signers, both of whom show disruption of discourse functions in absence of any disruption of grammatical functions. The exact nature of the disruption differs for the two subjects, however. Subject AR shows difficulty in maintaining topical coherence, while SJ shows difficulty in employing spatial discourse devices. Further, the two subjects are equally impaired on non-linguistic spatial tasks, indicating that spared spatial discourse functions can occur even when more general spatial cognition is disrupted. We conclude that, as in the hearing population, discourse functions involve the right hemisphere; that distinct discourse functions can be dissociated from one another in ASL; and that brain organization for linguistic spatial devices is driven by its functional role in language processing, rather than by its surface, spatial characteristics.

Permanent global amnesia with unknown etiology.

Three patients developed severe and selective memory impairment with no known cause, one during a period of a few days and two others during a period of 1 to 2 years. In two of these patients, the amnesia has been stable and circumscribed for 5 to 6 years. The third patient appears to have declined in cognitive functions during the past year, at the age of 78, after 6 years of stable, circumscribed amnesia. Neuropsychological testing reveals severe impairment in the ability to learn verbal and nonverbal material as well as retrograde amnesia covering at least 20 years. CT and routine brain MRIs were uninformative. Subsequently, a high-resolution protocol for imaging human hippocampus with MR revealed that the hippocampal formation was markedly reduced in size in all three patients. The pattern of cognitive impairment and the MR findings are similar to the findings in other patients with chronic amnesia due to a known anoxic or ischemic episode, and differ from the findings in amnesic patients with alcoholic Korsakoff s syndrome. We suggest that the amnesia may be due to ischemic damage to medial temporal lobe brain structures important for memory.

The role of the left frontal operculum in sign language aphasia

Abstract Brocas area has long been implicated in aspects of speech production. But does this region play a role in the production of signed language in prelingually deaf individuals? In this report, we describe our findings in a patient, congenitally deaf and a native user of American Sign Language, who suffered an ischemic infarct involving the left frontal operculum. Our patient presented with an acute expressive aphasia that subsequently resolved, and a chronic deficit predominantly characterized by frequent phonemic-like paraphaslas. We conclude that the left frontal operculum does, in fact, play a role in the production of signed language.

Exacerbation of Charcot‐Marie‐Tooth disease in pregnancy

A severe exacerbation of subclinical Charcot-Marie-Tooth disease commenced in the third trimester of an otherwise normal pregnancy. Following cesarean section there was immediate improvement and twelve weeks later the patient was asymptomatic. It is concluded that Charcot-Marie-Tooth disease, like other forms of chronic demyelinating neuropathy, may be rarely exacerbated in pregnancy. Pathogenetic mechanisms leading to exacerbation of neuropathy in pregnancy may be related to nerve edema.

Transient global amnesia: a complication of incremental exercise testing.

Incremental exercise testing is routinely used for diagnosis, rehabilitation, health screening, and research. We report the case of a 71-yr-old patient with chronic obstructive pulmonary disease (COPD) who suffered an episode of transient global amnesia (TGA) several minutes after successfully completing an incremental exercise test on a cycle ergometer. TGA, which is known to be precipitated by physical or emotional stress in about one-third of cases, is a transient neurological disorder in which memory impairment is the prominent deficit. TGA has a benign course and requires no treatment although 24-h observation is recommended. Recognition of TGA as a potential complication of incremental graded exercise testing is important to both aid diagnosis of the amnesia and to spare a patient unnecessary evaluation.