Cognitive disorders, such as Parkinson’s disease (PD), multiple sclerosis (MS), various dementias, epilepsy, vascular disorders and traumatic brain injuries (TBI), exert a heavy burden on sufferers, their families, and on society. The possibility of neuropharmacologic rehabilitation of patients with such deficits is a challenge for clinicians and scientists. In a special issue of Behavioural Neurology, six articles survey the latest developments in pharmacologic treatment of selected clinical disorders.
Special issue editors Reva Klein, Patrick McNamara and Martin L. Albert (Harold Goodglass Aphasia Research Center, Department of Neurology, Boston University Medical School and the Medical Research Service, VA Boston Healthcare System), writing in an introductory article, describe their selection of contributions that covered not only treatments of existing disease, but also approaches to prevention and rehabilitation.
The National Institutes of Health has defined a Roadmap Initiative for Translational Research: “To improve human health, scientific discoveries must be translated into practical applications. Such discoveries typically begin at ‘the bench’ with basic research-in which scientists study disease at a molecular or cellular level-then progress to the clinical level…Translational research has proven to be a powerful process that drives the clinical research engine. However, a stronger research infrastructure could strengthen and accelerate this critical part of the clinical research enterprise.” According to the editors, clinicians and scientists, for the most part, have yet to accept the challenge.
The first three papers discuss disorders (dementias, vascular disorders and TBI) that share a long tradition of research into cognitive deficits. Studies of pharmacologic management of cognitive disturbances in these disorders are considerably more advanced than those for disorders discussed in the last three papers (PD, MS and epilepsy).
In their review of the dementias, Ringman and Cummings discuss how cholinesterase inhibitors such as donepezil, rivastigmine and galantamine have demonstrated efficacy in improving cognition and global status in mild to moderate Alzheimer’s disease. The benefits from these drugs, however, are limited and their long-term effectiveness has not been well-studied. Unfortunately, there is no currently proven therapy for the prevention of dementia.
In their paper on cerebrovascular disorders, Romero and his colleagues review recent research on basic mechanisms of neuronal injury. They focus on new opportunities to promote recovery after injury or to protect against cellular damage in the first place.
For the treatment of cognitive disorders after brain injury, Arciniegas and Silver note that impairments in the areas of arousal, speed of processing, and attention can be improved with agents that enhance catecholaminergic transmission. When the predominant posttraumatic impairment is in the domain of memory, cholinergic agents are recommended. The authors do point out that pharmacotherapy is only one of several possible interventions for posttraumatic cognitive impairments, and is at present best regarded as an adjunct to nonpharmacologic therapies for such problems.
In their paper on treatment of cognitive deficits in Parkinson’s disease, McNamara and Durso note that many patients with PD experience significant cognitive impairment in the realm of executive function, which can often be as disabling as the motor impairment. These mental impairments are only partially responsive to levodopa treatment. They note that there have been only a handful of properly controlled clinical trials of intervention targeted at improving mental function in PD.
Discussing MS, Pierson and Griffith note that cognitive impairments in multiple sclerosis are centered in executive function and speed of processing. Although emotional well-being and pharmacologic stabilization of associated affective disorders can have a positive influence on cognitive performance in MS, significant deficits may remain even after treatment of depression.
In their paper on epilepsy Mula and Trimble note that such patients frequently have disorders of attention and memory. Sources of these cognitive deficits likely involve some combination of the underlying pathology and antiepileptic drugs themselves. The authors highlight the need and promise of focusing on neuroprotection in future studies of epilepsy, and they note that a number of psychotropic agents enhance synaptogenesis and neurogenesis while improving cognition.
The editors urge “the establishment of a national database on drugs potentially effective in treating cognitive processes or symptoms in neurologic disor¬ders. Currently the neuropharmacologic literature is organized along traditional medical lines according to disorder. While such an approach to classification is certainly valuable, an alternative approach that targets selected subsystems or subprocesses within a larger cognitive processing module might be useful as well. Such a database could be clinically useful in helping to identify promising new treatments across disorder types. For example, episodic memory lapses are common features of many neurologic conditions and perusal of the reviews in this Special Issue suggests that a small class of cholinesterase inhibitors may be effec¬tive in treating these memory lapses regardless of the neurologic diagnostic label.”
02 Jun 2006
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