The Efficacy of Cognitive Rehabilitation in Patients

specific deficits and specific remedia¬ strategies, as Glisky et al14 have demonstrated, may yield definitive conclusions. Specificity of deficit train¬ ing seems to be more effective than general intervention strategies. While computers may represent an impor¬ tant tool in the process, they are not synonymous with cognitive rehabilita¬ tion. There is, further, no convincing evidence that computer training gen¬ eralizes to activities of daily living when used as an independent modal¬ ity. The argument that cognitive reha¬ tion

bilitation is a "fad" has some merit. As with many therapeutic approaches, some programs deviated from the ba¬ sic principles in their application. However, well-documented evidence shows that appropriate patients who have sustained brain injury can be identified; that deficits responsive to cognitive intervention strategies can be identified; that hierarchical inter-

ventions

are more

effective than

non¬

specific therapies; and that functional abilities can be substantially increased as a

result.

References 1. Ryan EB, Short EJ, Weed KA. The role of cognitive strategy training in improving the academic performance of learning disabled children. J Learning Disabilities. 1986;19:521-529. 2. Luria AR, Naydin VL, Tsvetkova LS, Vinarskaya EN. Restoration of higher cortical function following local brain damage. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology. Amsterdam, the Netherlands: North-Holland Publishing Co; 1969;3:368-433. 3. Gummow L, Miller P, Dustman RE. Attention and brain injury: a case for cognitive rehabilitation of attentional deficits. Clin Psychol Rev.

1983;3:255-271.

4. Levin HS, Grossman RG, Rose JE, Teasdale G. Long term psychological outcome of closed head injury. J Neurosurg. 1979;50:412-422. 5. Luria AR. Restoration of Function After Brain Injury. Oxford, England: Pergamon Press

Ltd;

1963.

Oakley DA. The varieties of memory: a phylogenetic approach. In: Mayes A, ed. Memory in Animals and Humans. New York, NY: Van Nos6.

trand Reinhold Co; 1983;20:20-69. 7. Erickson KA, Chase WG, Falloon S. Acquisition of a memory skill. Science. 1980;208:1181\x=req-\ 1182. 8. Zihl J, von Cramon D. Restitution of visual field in patients with damage to geniculostriate visual pathways. Hum Neurobiol. 1982;1:5-8. 9. Weiskranz L. Varieties of residual visual experience. Q J Exp Psychol. 1980;32:365-386. 10. Weinberg J, Diller L, Gordon WA, et al. Training sensory awareness and spatial organization in people with right brain damage. Arch Phys Med Rehabil. 1979;60:491-496. 11. Ben-Yishay J, Silver SM, Piasetsky E, Rattock J. Relationship between employability and vocational outcome after intensive holistic cognitive rehabilitation. J Head Trauma Rehabil.

1987;2:45-48. 12. Prigatano GP,

et al. Neuropsychologic Rehabilitation After Brain Injury. Baltimore, Md: Johns Hopkins University Press; 1986. 13. Batchelor J, Shores EA, Marosszeky JE, Sandanam J, Lovarini M. Cognitive rehabilitation of severely closed-head-injured patients using computer-assisted and noncomputerized treatment techniques. J Head Trauma Rehabil. 1988; 3:78-85. 14. Glisky EL, Schacter DL, Tulving E. Computer learning by memory-impaired patients: acquisition and retention of complex knowledge.

Neuropsychologia. 1986;24:313-328.

The Efficacy of Cognitive Rehabilitation in Patients With Traumatic Brain Injury Bruce T.

Volpe, MD, Fletcher H. McDowell, MD

therapy for patients Doeswithspecific cognitive disorders that oc-

after traumatic brain injury (TBI) a specific and obvious improvement in quality of life? The medical literature on this question is voluminous but this review is limited to 20 relevant publications.1-19 First there are chapters, reviews, and editorials that sound a clarion call for action. There can be no disagreement that the loss of intellect and subsequent personality changes in patients with TBI are catastrophic. Unlike other neurologic disease, TBI compounds the basic neurologic infirmity with the prospect of 30 to 40 more years of disabled life. The burden for families and in many cases the eventual burden to society has received attention from medical economists and cur

produce

Accepted for publication April 12, 1989. From the Department of Neurology, Cornell University Medical School, the Burke Rehabilitation Center, White Plains, NY. Reprint requests to Cornell University Medical School, the Burke Rehabilitation Center, 785 Mamaroneck Ave, White Plains, NY 10605 (Dr Volpe).

head injury foundation lobbyists. There is no reprieve in sight from the essential "accidental" pathophysiology that causes TBI. Seat belts have had some effect on the incidence of TBI and gun control should have an addi¬ tional preventative effect, but the cur¬ rent epidemiologie findings, if true, are staggering.20·21 Modern medicine can save lives of patients with brain injury who formerly would have died, but it cannot restore damaged brain to nor¬ mal function. Investigators have surveyed current programs from the prospective of neu¬ rologists and physicians,17 psycholo¬ gists and neuropsychologists,3·6'8'14·1517'19 educational experts,214 and medical economists.612 There is general agreement that the long-term problems of patients with TBI are complex because of the variability of location and se¬ verity of brain injury. Factors that in¬ fluence outcome include age, depth and duration of coma as measured by Glas¬ gow Coma Scale,22 and also computed tomographic abnormality, evoked po¬ tentials, and serum catecholamine levels.23'27 Thus, there should be gen-

Downloaded From: http://archneur.jamanetwork.com/ by a Cornell University User on 12/06/2013

eral agreement among investigators who study groups of patients with TBI that there must be a concerted effort to be certain of the extent of brain dam¬ age following head injury. A study of a group of patients makes the strong as¬ sumption that there is a set of common characteristics for all members. The feat of achieving a homogeneous group in any study of behavior is even more complex in head injury. Current meth¬ ods, notably magnetic resonance im¬ aging to determine extent of brain in¬ jury, are improving and most imaging methods often indicate multiple sites of damage of varying severity that may be quantitated. Magnetic reso¬ nance imaging will be an important addition to the clinical and psycholog¬ ical scales now in use, although one type of injury, called diffuse axonal injury, can only be seen micro¬ scopically.28 Imaging data, electrical data, and serum catecholamine levels may permit a more definitive stratifi¬ cation of patients based on the sever¬ ity and extent of brain damage. Strat¬ ification by psychologic testing results and by clinical scales is helpful; they

are

important predictors but now they

must be combined with more advanced methods to determine degree of injury.

fact, several careful studies have already demonstrated the usefulness of these techniques.23·29 It is disquieting then to discover In

that there is more attention to devel¬ oping additional methods for clinical and psychological assessment rather than seeking a biological correlate. It is possible that a combination of clin¬ ical, psychological, and biological in¬ formation will lead to new treatment techniques or at least to a comparison of the effectiveness of current treat¬ ment techniques. Perhaps an approach to the questions raised by this first group of references is to develop gener¬ al protocols to use in multicenter tri¬

als. This model of multicenter research appears to have had some success in other studies of neurologic disease.30 The alternative to group studies is the single case method that raises for analysis the second group of target ar¬ ticles in which investigators have doc¬ umented change in behavior after spe¬ cific treatments.118 The foremost criti¬ cism of such studies is the lack of control. Patients were tested at some time after TBI, in these studies 2 months, then were exposed to a pro¬ gram, and retested; and improvement was reported. Other studies have dem¬ onstrated improvement in cognitive ability after TBI without specific tar¬ get-directed therapy months after injury.31 Thus, it is impossible to con¬ clude from the above reports'·18 that the program was critical for the im¬ provement, nor is it possible to con¬ clude the improvement in test mea¬ sures was

significant statistically

or

permanent. Finally and most impor¬ tantly, in none of these studies did pa¬

tients resume vocational or avocational activities that were equal or close to preaccident levels. Single case methodology has several convincing proponents but the method works best when a specific hypothesis about cognitive processes is being tested.32 Other, perhaps more difficult, problems with single case studies re¬ volve around replicating the improve¬ ment in other patients, testing alter¬ native interpretations of the behav¬ ioral symptom complex and, therefore, alternative mechanisms by which a particular therapy is effective. Repli¬ cation necessarily involves detailed de¬ scription of the next studied patient and it may be that no two patients with head trama are similar, a possibility that can be subjected to an empirical test. Testing alternative interpreta¬ tions involves gathering converging

evidence

ply (to

on our

been done.

the test

subject, and, sim¬ knowledge), this has not

Perhaps most dangerously, this type of anecdotal reporting causes a ripple of unrealistic expectations. Unsophis¬ ticated readers of these reports are quick to assume that replication of the putative treatment effects are likely. The ethics of avoiding false hope should not be transgressed, as genera¬ tions of responsible print journalists, now often joined by scientists, have strictly observed. This type of case re¬ porting should be restricted to the theater. The final studies deal with groups of patients with TBI exposed to treat¬ ment programs.4·5·7·9""13·16 These studies are of two types. The first rely on psy¬ chometric principles7·91113 and are not strongly driven by a theory of cogni¬ tive functioning. For example, cogni¬ tive psychology relies, in part, on the assumption that a complex behavior can be studied in basic components or modules.33 The further assumption, and optimism, is that the tested per¬ formance of the brain-damaged indi¬ vidual will permit an investigator to discern which component or module is disrupted. In contrast the target experiments457·9111316 depend on the fact that after recovery from TBI and coma almost everyone improves to some degree, and these studies char¬ acterize that change. Such studies are not making a specific prediction about behavior or testing a specific hypothe¬ sis of abnormal or normal behavior. For the most part they are attempting to quantify overall behavioral change using a variety of standard neuropsy¬ chological batteries and some specially designed tests. In the most primitive studies,911 there are no controls, ie, pa¬ tients with TBI are exposed to the same rehabilitation environment but they are not exposed to the specific training technique. At times there is no effort to classify the variability of the TBI group. In the better studies7·13 there is attention to experimental de¬ sign. Patients are stratified or other¬ wise matched for obvious variables such as age, education, time from in¬ jury, and severity of injury that may be important in outcome. There are matched control groups. In these reports713 the differences between pa¬ tients with TBI treated with a specific program and control patients with TBI

positive, significant (statisti¬ cally), yet "modest."7 Experimental groups demonstrate improved test were

scores, but whether these skills can be translated into increased independent activities remains moot. One of the


studies7 reported that 50% of the ex¬ perimental group returned to work (9 of 18 patients) while the control group had a return to work rate of 36% (6 of 17 patients). Generally a 30% to 40% return to work rate has been reported without specific treatment. However,

these few studies must be taken

as en¬

couraging.

Another group of studies tests whether patients with amnesia follow¬ ing TBI can learn new information about a specific domain of knowledge and further explores the psychological mechanisms that might underlie new learning.4-516 There is attention to ex¬

perimental design, ie, adequate psy¬ chological classification, nearly appro¬ priate controls, and a well-designed training program. The results show that amnesic patients with TBI of varying severity can learn, albeit slower than controls, to executive sim¬ ple computer skills. Interestingly, among the patients with TBI, new knowledge was characterized differ¬ ently from that of the controls. It was "hyperspecific,... inflexible, rigidly organized and only narrowly acces¬ sible."4 Another study, however, indi¬ cates that improvements in tested memory generalized to other activi¬ ties.34 New possibilities for inter¬ vention arise out of both studies for

using the microcomputer as a pros¬ thetic device, but such patient treat¬ ment strategies are possible for a lim¬ ited number of patients. These studies too are encouraging in opening new approaches to non-medicine-based therapeutic intervention. They pre¬ dict, at least with other similar TBI groups with a relatively high level of performance, little ability of the pa¬ tient to generalize task specific infor¬ mation to other aspects of cognitive

life. Before making some conclusions, there are two other sets of data worth mentioning. First, just as there is some recovery of cognitive function after TBI, there is also some recovery of motor function. Recent reports of suc¬ cessful approaches to specific gait training for well-characterized and se¬ lected ataxic patients have indicated significant and permanent improve¬ ment.3536 While some forms of gait ataxia will improve spontaneously,37 patients in the study by Balliet et al35 were well beyond the stage of sponta¬ neous recovery. The training was sim¬ ple and relied on repetitive practice, balance, posture, and sequencing exer¬ cises over a 3-month to 2-year period. The mechanism for these training ef¬ fects is unknown. Whether there is a fundamental change in the neural ba-

sis of movement or the motor systems less damaged or have a greater ability to mend after TBI remains for future inquiry. Important to this dis¬ cussion, however, these data suggest that careful studies to examine a spe¬ cific effect of a treatment program can be accomplished and may even cause are

significant, permanent improvements. The second set of data, also impor¬

tant,

is

the

work

on

neuronal

plasticity.38 Whether new growth or sprouting of axons to re-form synapses has functional significance and whether neosynaptogenesis may be a physiologic basis for recovery of func¬ tion after TBI are questions of enor¬ mous import. Investigations in many

laboratories are in progress with as yet no clear answers to these questions. This report focused on whether there are experimental data to show that specific therapy for cognitive dis¬ orders that occur in patients with TBI leads to specific and permanent im¬ provement. The target data demon¬ strate that patients with TBI have major problems in cognition, in adap¬ tation to civilized norms, and in re¬ suming productive involvement in so¬ ciety. Evidence suggests that the fol¬

lowing therapeutic make

maneuvers

may

difference in outcome: treatment of seizures, social interac¬ tion with a peer group, encouragement from health professions of many va¬ rieties, relief of depression, education about adaptation, and understanding on the part of the family and signifi¬ cant others about the degree of im¬ pairment suffered by individuals with TBI and how to deal with it. If there are specific improvements in addition to the above brought about by focused treatment programs rather than non¬ specific intervention, they have not as yet been demonstrated by careful stud¬ ies that account for the severity of head injury, the sites of brain damage, use of matched control groups, and that measure the degree and character of cognitive impairment. Patients should be matched as closely as possi¬ ble into treated and control groups, omitting the specific treatment for one group and applying it in the other. Both groups should be exposed to other types of environmental pressure and stimuli that are likely to bring about change. Most importantly, changes or improvements may start with mea¬ sured neuropsychological changes but investigators should have as an ulti¬ mate goal some "real world" effect.39 While there are a few encouraging studies now, it is difficult to support the notion that specific programs will offer more than general rehabilitation some

efforts. In a world of shrinking re¬ sources it is not unimportant to note that the specific programs are expen¬ sive. If they are to be applied, they must be shown to produce something worth the cost. If it is the nonspecific pressures and stimuli that produce change, these could be widely applied, perhaps at less cost, to patients in dis¬ tant parts of the country where spe¬ cific expertise in cognitive training does not exist. There is not enough ev¬ idence to reject the null hypothesis al¬ though preliminary work is encourag¬ ing. It may be that for such a complex problem the solution will necessarily come from more central and organized planning and the execution of a wider range of multicenter trials. References

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ory

1986;67:366-374. 11. Corrigan JD, Arnett JA, Houck LJ, Jackson

RD. Reality orientation for brain injured patients. Arch Phys Med Rehabil. 1985;66:626-630. 12. Cole JR, Cope DN, Cervelli L. Rehabilitation of the severely brain-injured patient. Arch Phys Med Rehabil. 1985;66:38-40. 13. Weinberg J, Diller L, Gordon WA, et al. Training sensory awareness and spatial organization in people with right brain damage. Arch Phys Med Rehabil. 1979;60:491-496. 14. Willis SL. Cognitive training in everyday competence. Ann Rev Gerontol Geriatr. 1987; 7:159-188. 15. Abreu BC, Toglia JP. Cognitive rehabilitation: a model for occupational therapy. Am J Occup Ther. 1987;41:439-448. 16. Kirn TF. Tapping into 'procedural' memory helps patients with amnesia to acquire new occupational skills. JAMA. 1987;257:3187. 17. Report of research aspects of rehabilitation after acute brain damage in adults. Lancet. 1982; 2:1034-1036.


18. Malec J,

Questad K. Rehabilitation of mem-

ory after craniocerebral trauma:

case

report.

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