Rehabilitation Of The Older A... Health Article

Recovery After Stroke

Early recovery after a stroke is caused by spontaneous mechanisms related to resolution of harmful local factors (ie, local edema, resorption of local toxins, improved local circulation, and resolution of arterial spasm). Motor recovery has been well-described and the most studied of all stroke impairments. The classic paper by Twitchell [35] in 1951 first described the pattern of motor recovery following stroke from a flaccid state to progressive increase in tone. The phases of recovery described by Twitchell [35] were later formalized into stages by Brunnstrom in 1970 [36]. The general pattern of recovery in a classic middle cerebral artery infarction is as follows: (1) proximal recovery occurs before distal; (2) the lower extremity recovers earliest and most completely; and (3) synergy patterns, stereotyped mass movements, occur before isolated, voluntary movements.

Neural plasticity is the potential of the central nervous system to reorganize its structure and function based on the idea that the brain is responsive, flexible, and dynamic. There is modification of neural networks that are use-dependent. After early, spontaneous recovery after stroke, several mechanisms are thought to occur. Bach-Y-Rita [37] described several theories on recovery and neuroplasticity, including collateral sprouting, unmasking, and diaschisis. Regeneration or collateral sprouting describes when a neighboring axon branches to assume the territory of a denervated region or injured axon. Unmasking of pathways is the activation of previously latent pathways when the dominant system fails. There may exist redundant pathways in which there is unmasking of the uninjured parallel pathway. The concept of diaschisis, coined by Constantin Von Monakow in 1914, describes how a site away from the primary injury may be affected when there is loss of neural input from the injured part of brain. Reversal of this process may contribute to neurologic and functional recovery after a stroke [38].

There is a clinical perception that these restorative processes are age-dependent. The question remains whether brain plasticity still exists and to what extent in the aging human brain because most studies have reported on young animals. Animal studies by Popa-Wagner and coworkers [39] report quantitative changes in the hippocampus and qualitative changes in the cortex with increased age. There seems to be a regenerative potential of the aged brain that is competent but attenuated after a stroke. Human studies further evaluate the ability of the aging motor cortex to reorganize. It is now well-known that cortical reorganization underlies functional recovery after a stroke and is elicited by motor training that uses practiced movements. The influence of age on this form of plasticity has been specifically studied by Sawaki and coworkers [40] who found a significant decrease in training-dependent plasticity as a function of age. Further studies are needed to delve into the mechanism and to quantify these changes in the aged brain.

Pharmacologic Agents And Recovery

An important goal during rehabilitation is to identify and minimize the use of pharmacologic agents that may impede recovery after stroke. Many drugs commonly used to treat new or chronic conditions have central nervous system side effects. Studies in laboratory animals indicate that certain centrally acting drugs (ie, clonidine, prazosin, neuroleptics, and other dopamine receptor antagonists; benzodiazepines; phenytoin; and phenobarbital) impair behavioral recovery after focal brain injury. Even single doses may have long-term harmful effects [41]. Consistent with previous reports, haloperidol retards motor recovery after sensory motor cortex injury in rats. The use of low doses of atypical antipsychotics provides a safer alternative to haloperidol in the treatment of agitated stroke patients [42]. The Stroke Council of the American Heart Association endorses the clinical practice guidelines for the pharmacologic management of stroke rehabilitation [43].

The practice of neurorehabilitation is unique in that it provides an opportunity to enhance intensive rehabilitation with pharmacologic interventions that facilitate the recovery of damaged neurons and plastic responses in underused and unused brain tissue. Animal studies reveal that norepinephrine, amphetamine, and other α-adrenergic stimulating drugs can enhance motor performance after unilateral ablation of the sensory motor cortex. Although widely used, there are limited data to support the use of neurostimulants in stroke recovery. The most studied in clinical trials is dextroamphetamine, which has been shown both to expedite motor recovery and improve aphasia [44–46]. Other agents commonly used and studied in small controlled trials or case series to treat motor, language, and cognitive-behavioral syndromes include methylphenidate, amantadine, levodopa, selective serotonin reuptake inhibitors, and modafinil [47–53].