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PubMed2005

Cognitive findings after transient global amnesia: role of prefrontal cortex.

The aim of this study is to verify, after recovery, the presence of specific patterns of cognitive dysfunctions in Transient Global Amnesia (TGA). Fourteen patients with the diagnosis of TGA were submitted to a battery of neuropsychological tests and compared to a matched control group. We found significant qualitative and quantitative differences between TGA patients and controls in the California Verbal Learning Test (CLVT) and Rey-Osterrieth Complex Figure Test. Our data support the presence of selective cognitive dysfunctions after the clinical recovery. Moreover, for Verbal Fluency, Digit Span Backward, and Number of Clusters in the CVLT short-term memory test, the relation resulted as positively related with the temporal interval from the TGA episode. Reduction of categorical learning, attention, and qualitative alterations of spatial strategy seem to postulate a planning defect due to a prefrontal impairment.

Aged↗

PubMed2004

Detection of delayed focal MR changes in the lateral hippocampus in transient global amnesia.

BACKGROUND: There is still limited knowledge on the location and etiology of transient global amnesia (TGA). MR studies including diffusion-weighted imaging (DWI) have been unable to demonstrate consistently the location and underlying pathology of TGA. OBJECTIVE: To investigate patients with TGA using serial DWI performed from the day of symptom onset through days 1 and 2. METHODS: After reporting negative DWI results in a previous study, the authors used a modified study design to investigate patients with TGA using serial DWI performed from the day of symptom onset through days 1 and 2. RESULTS: Of 31 consecutive patients studied, 26 developed a small, punctate DWI lesion in the lateral aspect of the hippocampal formation (pes and fimbria hippocampi) on either side (left, n = 15; right, n = 6) or bilaterally (n = 5). Lesions were rarely noted in the hyperacute phase (n = 2), but all became visible regularly at 48 hours. CONCLUSIONS: The study confirms the involvement of hippocampal parenchyma in the pathophysiology of TGA. The delayed detectability of the lesions may explain the incongruence of previous MR DWI studies in TGA patients.

Adult↗

PubMed2004

Activated platelets in transient global amnesia and TIA.

To assess whether platelets are activated in transient global amnesia (TGA) and TIA, blood samples were analyzed by fluorescence-activated cytoscan using antibodies specific for platelet fibrinogen receptor (PAC1) and P-selectin (CD62P). Samples from TIA contained high levels of CD62P compared with age-matched control subjects, whereas those from TGA did not. The authors suggest that activated platelets are involved in brain ischemia, whereas ischemia appears not to be associated with most TGA.

Aged↗

PubMed1979

Transient global amnesia: clinical and electroencephalographic findings in 10 cases.

We studied 10 patients with transient global amnesia (TGA). Routine electroencephalograms (EEGs) were normal in six; two showed mild temporal lobe abnormalities, one had bitemporal delta activity with rare sharp waves, and one showed bioccipital rhythmic theta activity. Nasopharyngeal (NP) recordings were obtained in seven patients; five showed independent mesial temporal spike discharges during drug-induced sleep. The discharges are probably due to transient ischemia in deep temporal structures.

Aged↗

PubMed1980

Transient global amnesia due to glioma in the dominant hemisphere.

A patient with transient global amnesia (TGA) had a glioma in the dominant hippocampus. Neuroradiologic studies showed local mass effect on the posterior choroidal artery on that side. This finding suggests that unilateral involvement is sufficient to cause the syndrome despite the widely held view that bilateral lesions are essential.

Amnesia↗

PubMed1981

Transient global amnesia and migraine.

Twelve patients with transient global amnesia (TGA) had prior migraines (six classical and six common). In three patients, classic migrainous phenomena accompanied TGA, and in nine patients severe headache accompanied the amnestic attack. Migrainous vascular dysfunction in the dominant posterior cerebral artery territory could explain TGA: (1) The pathophysiology and transient nature of TGA have led many to postulate posterior circulation vascular disease; migraine is a vascular disorder with a posterior circulation bias. (2) TGA and migraine share common precipitants. (3) Migraine differs from arteriosclerotic ischemia; the repetitive queries of TGA are absent in amnestic stroke. (4) TGA and migraine are usually benign.

Adult↗

PubMed1982

Whiplash amnesia.

A 67-year-old woman was in the front seat of a stopped car that was struck from the rear by a truck. She was wearing a seat belt, and it was observed that her head did not strike the windshield. She immediately became amnesic and recovered in 72 hours. It is postulated that the transient amnesia was the result of a whiplash insult to the brain.

Accidents, Traffic↗

PubMed1984

Failure of preference formation in amnesia.

Information about the frequency of a stimulus influences the formation of preference judgments in normal subjects. In contrast, results show that patients who have amnesic syndromes have difficulty generating preferences on the basis of frequency information. It is unlikely that difficulty in forming preferences is caused merely by poor mnemonic capacity. Patients with amnesia may lack the affective response to stimuli that may be important for remembering events.

Adult↗

PubMed1984

Amnesia with hippocampal lesions after cardiopulmonary arrest.

A patient developed an amnesic syndrome after cardiopulmonary arrest. Neuropathologic examination revealed pronounced anoxic injury to both hippocampi with little damage to other hemisphere structures. The clinical and pathologic findings suggest that lesions limited to the hippocampus can cause profound amnesia.

Amnesia↗

PubMed1986

Consciousness and amnesia after penetrating head injury: neurology and anatomy.

Among 342 men who survived severe penetrating brain wounds, only 15% had prolonged unconsciousness and 53% had no or momentary unconsciousness after injury, emphasizing the focal nature of these wounds. The left (or language-dominant) hemisphere was dominant for the "wakefulness" component of consciousness. The areas most associated with unconsciousness included the posterior limb of the left internal capsule, left basal forebrain, midbrain, and hypothalamus. Left dominance was not seen for posttraumatic amnesia after elimination of the wakefulness variable, suggesting that wakefulness may be linked to the role of the left hemisphere in verbal memory.

Amnesia↗

PubMed1986

Further characterization of patients with amnesia after cardiac arrest: preserved recognition memory.

We observed that patients with amnesia after cardiac arrest had preserved recognition memory despite profound loss of recall memory. In the present study, rate of forgetting was measured in six amnesic subjects for both recall and recognition memory of verbal material. The data show that recall decayed significantly faster for the amnesic subjects than for controls, whereas the rate of forgetting for recognition memory was comparable in both groups. Dissociation between recall and recognition performance is a feature of the amnesic syndrome after cardiac arrest.

Adult↗

PubMed1987

Transient global amnesia: clinical characteristics and prognosis.

We studied the clinical characteristics of transient global amnesia (TGA) in 277 patients with an average follow-up of 80 months. The syndrome occurred most frequently after age 50. There was a history of migraine in 14.1% and cerebrovascular diseases in 11.2% of patients, but these conditions were usually not temporally linked to TGA. Characteristic antecedent events and activity such as exertion existed in 33.4%. The incidence of TGA was 5.2 per 100,000 per year in Rochester, MN. Although 23.8% of the patients had recurrent episodes, they were not at increased risk for subsequent stroke.

Aged↗

PubMed1991

Thalamic ischemia in transient global amnesia: a SPECT study.

We performed 99mTc-HMPAO SPECT in a patient during transient global amnesia and twice thereafter. SPECT during the attack showed a significant diminution of regional blood flow in the left thalamus and a less marked diminution in the right thalamus. Quantitative evaluation of global 99mTc-HMPAO uptake indicated a diffuse depression of cerebral blood flow. At follow-up to 40 days after the attack, global uptake and thalamic flow indices normalized, but there was a persistent reduction of left frontal flow values.

Amnesia↗

PubMed1993

Selective dorsolateral frontal lobe dysfunction associated with diencephalic amnesia.

We report three cases with unilateral thalamic ischemic lesions that resulted in lasting material-specific memory impairments and concomitant selective frontal lobe-related cognitive deficits. In two cases the lesions were limited to the left thalamus, and in the third the right thalamus was involved. These deficits were associated with ipsilateral diencephalic, striatal, and dorsolateral prefrontal hypoperfusion. The damage implicated the ventral anterior nucleus, the mamillothalamic tract, and the rostroventral internal medullary lamina. These findings suggest that medial thalamic damage involving the ventral and rostral sector of the dorsal thalamus will concurrently affect functionally and neurally distinct limbodiencephalic pathways and diencephalic connections with the frontal cortex. A review of the neuropsychological and neuroimaging findings from previously reported cases with vascular lesions of the thalamus further supports this contention. The presence of frontal lobe-related cognitive deficits, though not obligatorily related to the memory problems, may contribute to some aspects of the memory deficits and affect the nature of the memory disorder observed in some cases with diencephalic amnesia.

Aged↗

PubMed1995

Amnesia of the epileptic aura.

In a prospective study lasting 6 months, we recorded on video 108 seizures with aura of 23 patients in an attempt to evaluate the mechanisms involved in the encoding of memories. In 88 of those seizures, we also recorded an EEG. The percentage of auras remembered decreased significantly with increasing severity of the seizures. The recollection of auras was also significantly dependent on the ictal EEG changes during the aura. Ninety-seven percent of the auras without EEG changes, 94% of the auras with unilateral EEG changes, and 73% of the auras with bilateral EEG changes during the aura were remembered. The spread of the ictal EEG pattern during the aura also showed a significant correlation with the severity of the ensuing seizure. Three patients with bitemporal epilepsy made up a considerable proportion of those who never remembered their aura before secondary generalized tonic-clonic seizures (2 of 3) and of those who had a transient postictal amnesia of their aura (2 of 3). The only patient who failed to remember a previously documented isolated aura also suffered from bitemporal epilepsy. During the second part of the study, we questioned whether information provided during the history could be helpful in defining the type of epilepsy syndrome or localizing the EEG seizure pattern of the 80 patients who had been admitted for presurgical epilepsy diagnosis. Localized (regional, unilateral, and independent left and right lateral) EEG seizure patterns occurred in 82% of the 51 patients with auras in their history as compared with 24% of the 17 patients who did not have auras in their history (p < 0.01).

Amnesia↗

PubMed1998

Impaired recall and preserved encoding in prominent amnesic syndrome: a case of basal forebrain amnesia.

We describe a patient who developed amnesia following extensive basal forebrain infarct. He completely recovered from the infarct 32 days postonset. He had poor spontaneous recall and preserved recognition of recent as well as more remote events. Surprisingly, he could recall events in sequence during the postictal amnesic period after recovery. We speculate that encoding and recall may employ different neural systems.

Aged↗

PubMed1998

Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia.

We present a patient with transient global amnesia (TGA) whose diffusion-weighted MRI (DWI) showed increased signal in the splenium of the corpus callosum and in the left parahippocampal gyrus. The absence of high signal on the corresponding apparent diffusion coefficient (ADC) images supports the diagnosis of an acute infarction. This finding provides a temporal relation between cerebral ischemia and infarction in the territory of posterior cerebral artery and in certain cases of TGA. An early means of detecting ischemia in TGA by DWI may influence clinical decisions made in patient evaluation and management.

Amnesia↗

PubMed2002

Functional changes in temporal lobe activity during transient global amnesia.

The integrity of temporal lobe activity during and after recovery from transient global amnesia (TGA) was assessed in a case study using functional MRI. TGA was associated with scene-encoding deficits in a temporolimbic circuit that recovered over time. Frontoparietal areas recruited during the amnesic state may signify a compensatory reliance on visuospatial or working memory strategies. Reduction of extrastriate cortex responses over repeated testing sessions possibly indicates intact visual priming in TGA.

Adult↗