. Incidence and prognosis of transient neurological attacks. JAMA. 2007 Dec 26;298(24):2877-85. PubMed.

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  1. In this paper, the Rotterdam group confirmed that persons with focal transient neurologic attacks (TNAs or TIAs) were at higher risk for stroke than people without TNA, although both groups appeared to have the potential for developing ischemic heart disease and dementia. The kicker in this study is that individuals with non-focal (or global) TNA symptoms showed not only a higher risk for stroke when compared to a control group without TNA but also revealed a higher risk for dementia.

    Even worse were patients identified with mixed TNA showing focal and non-focal symptoms who apparently had a higher risk for stroke, ischemic heart disease, dementia, and vascular-related death when compared to control subjects without TNA.

    This study by Breteler and her colleagues points to an important gap in management that physicians need to bridge when evaluating people who present with focal, non-focal, or mixed signs associated with TNA. Because TNAs are almost always accompanied by a brief interruption of local cerebral blood flow in the absence of neurologic injury, conventional neuroimaging in patients experiencing TNAs is advisable. This should be done in a hospital setting where the patient can be monitored and observed. Swift neuroimaging, echocardiography, and risk factor assessment may identify the presence of brain hypoperfusion, a silent stroke, or cardiac pathology that can be managed to prevent escalation to irreversible cognitive dysfunction. Rapid treatment to control the cause or recurrence of focal or non-focal TNAs may provide an excellent opportunity to prevent permanent neuronal damage from continuous brain hypoperfusion or incomplete infarction (1).

    TIAs are similar to angina pectoris, since both are signals of temporary ischemia and both can lead to serious infarcts. Although several studies have reported that cognitive impairment can follow a TNA attack, the report by Breteler and her group indicates that non-focal and mixed TNA can also lead to the development of vascular dementia. We should point out, no conclusive study has yet shown TNAs can lead to an increased risk of Alzheimer disease, though we have predicted (1) this is only a matter of time due to the brain hypoperfusion that accompanies each attack.

    References:

    . How do heart disease and stroke become risk factors for Alzheimer's disease?. Neurol Res. 2006 Sep;28(6):637-44. PubMed.

  2. This is a very carefully performed prospective study discriminating two types of transient neurological events, either focal attacks or more diffuse disturbance in neurological dysfunction in which loss of consciousness is the most prominent symptom. It is difficult for me as a basic scientist to evaluate how readily classifiable these events are, or how likely it might be for individuals to simply not report such events. Nonetheless, the results imply that focal events (TIAs) are linked to increased risk of stroke, and more diffuse events (TNAs) are more closely associated with risk of dementia, both Alzheimer and vascular variants, and to a lesser extent increased risk of stroke. Perhaps the most surprising outcome was the absence of increased risk for vascular dementia with TIAs, but the small number of incident cases (one for the entire study) probably indicates statistical power was inadequate.

    The primary conclusion of the authors is that transient neurological attacks, those without focal symptoms, are not benign as had been previously argued and led to increased risk for stroke and dementia. The more focal symptoms associated with TIAs, evidently, did not lead to increased risk of dementia, and a slightly greater risk of stroke than patients with TNAs. One potential explanation is that the neurological dysfunctions underlying these two disorders may be different. For TIAs, there appears to be stenosis or occlusion of a specific artery leading to ischemia in a restricted portion of the brain, and this results in focal symptoms. It seems logical to predict these would be harbingers of similar events from which recovery was less than complete, in which case it would be called a stroke. The TNAs, on the other hand, might be associated with more general declines in blood flow, but also may reflect underlying deterioration of neurological functions due to Alzheimer-type pathology. This pathology may be subthreshold for traditional symptoms of dementia, but when combined with loss of blood flow, may predispose towards more diffuse symptoms, such as loss of consciousness, due to the localization of Alzheimer pathology outside the sensorimotor areas most clearly involved in the focal symptoms of stroke. Obviously, further work leading to greater understanding of the triggers for TNAs will be needed to address the specific mechanisms involved in these events.