A model for multisystem evaluation, interpretation, and treatment of individuals with neurologic dysfunction.

A Model for Multisystem Evaluation, Interpretation, and Treatment of Individuals with Neurologic Dysfunction In this article, we present a model for systematically analyzing dysfunction in patients who have sustained a neurologic insult. This model was motivated by the related model of orthopedic dysfunction developed by Dyrek et al. [1] Our model is intended to guide theclinician in identifying underlying causes of a patient's disability. The model facilities a problem-solving approach based on literature that interprets the interrelationship between pathology, impairments, and disabilities associated with neurologic insults. Many of the problems or disorders associated with neurologic insults, such as faulty balance, have multiple possible causes. The purpose of this model is to quide the clinician in a problem-solving approach to identify the underlying causes of observed deficits in neurologic dysfunction. The intentof this article is to demonstrate the conceptual use of this model so that clinicians can more effectively evaluate and treat these patients.

We use two neurologic disorders--stroke and Parkinson's disease--to illustrate the use of the model in two common neurologic disorders. We also focus on one impairment--faulty balance--to demonstrate how clinical strategies differ depending on the neuroanatomic pathology and the resulting impairments. We then demonstrate the use of the model when specific neuroanatomic pathology is unknown. A detailed description of specific kinesiological and motor control issues is beyond the scope of this article, although we must draw from some concepts of motor control to describe the model and its uses.

Definitions of Elements

of the Model

When treating individuals with peripheral or central nervous system disorders, we evaluate and treat both impairments and disabilities. Impairments refers to abnormalities of anatomic, physiologic, or psychologic origin; disabilities refers to restriction or inability to function within a range of normal. [2] A patient's goal is to overcome disabilities in daily life such as immobility, gait deviations, and inability to transfer and to perform housekeeping chores. We, the clinicians, should be advocates of goal setting that relates to a patient's inability to function. In addition, however, we recognize the necessity of evaluating and treating the impairments that lead to a particular disability such as sensory loss, abnormal muscle tone, and musculoskeletal limitations. To focus treatment on underlying problems rather than symptoms, it is useful to have a system for identifying how impairments relate to each other and to specific disabilities. Figure 1 represents an overview of the system we have developed for identifying interrelationships among pathology, impairments, and disabilities.

Insult and Neuroanatomic

Pathology

We use the term insult to refer to the neurologic occurrence that initiaties a patient's difficutlies. And insult might be vascular in origin, as in stroke. It might be traumatic, as in traumatic head injury. It might be degenerative, as in Parkinson's disease or amyotrophic lateral sclerosis. The type of insult frequently dictates constraints on a patient's potential for recovery.

We use the term neuroanatomical pathology to refer to the specific nervous system lesion that caused a patient's impairments and disability. For example, an insult such as a stroke might specifically result in a parietal lobe lesion or parietal lobe pathology. The degenerative process of Parkinson's disease results in pathology of the dopamine-producing cells of the substantia nigra in the midbrain. [3] This knowledge of specific pathology is of great value to the physical therapist. As we will demonstrate, just knowing the structures that have been damaged often leads the therapist to predictions regarding the impairmentsthat will ensue. This knowledge, in turn, leads the therapist to an understanidng of the causes underlying the patient's disability and ultimately to more effective intervention.

In this model, we use the term direct effects of pathology to refer to those impairments that result from the nervous system insult itself. Often one can predict from neuroanatomic and motor-control theory what impairments will occur directly as a result of specific insults. For example, a sensory neuropathy or a severed dorsal root of the sensory neuron results directly in a sensory loss. [4,5] Loss of anterior horn cells, as occurs in postpolio syndrome, results in a motor loss. [6] This impairment can likewise be considered a direct effect of the nervous system pathology. Certain cerebellar lesions produce abnormalities of integrative functions of the nervous system related to motor programs. [7,8] Certain basal ganglia lesions appear to result directly in abnormalities of integrative functions associated with motor planning. [9] These and other examples are given in Table 1.

Impairments

We propose that those impairments that are direct effect of the insult and pathology are the basic underlying cause of a patient's disability. These impairments may have far-reaching sequelae, affecting both nervous system and non-nervous system processes. If the direct effects of a pathologic process are identified, the therapist and physicians can best direct treatment toward the underlying causes of disability.

In Figure 1, another group of impairments--the indirect effects of pathology--is also identified. We use the term "indirect" to indicate that those impairments occur in a system other than the neuromuscular system, such as the musculoskeletal, cardiopulmonary, integumentary, urogenital, and psychological systems. The term indirect is also used to emphasize that these impairments are not caused directly by a nervous system lesion but occur as sequelae to the direct impairments. For example, shoulder subluxation has been identified as a sequela of hypotonicity of the hemiplegic patient. [10-13] The shoulder subluxation might eventually lead to alterations of the musculoskeletal system, including chronic changes of the joint capsule and alteration of the length of muscles around the joint. These musculoskeletal impairments could become an additional source of disability for the patient, independent of the original insult. Once capsule alterations or muscle-length changes occur, they would not necessarily resolve spontaneously, even if the neurologic insult itself were to resolve. Furthermore, it has been suggested that shoulder subluxation need not occur if the hemiplegic patient's shoulder is adequately protected and supported. [11-13]

Another frequently seen indirect effect of neuroanatomical pathology is skin breakdown in patients with spinal cord injuries. The propensity for skin breakdown is due indirectly to the spinal cord injury and the patient's resulting immobility. [14] The skin breakdown itself represents an impairment in a system separate from the neurologic system. Like shoulder subluxation, skin breakdown is an indirect effect of neuroanatomical pathology, which could be prevented by appropriate positioning and turning. As with shoulder subluxation, once it occurs, it becomes a separate and very real contribution to the patient's disability.

Once impairments occur in these other systems, they may lead indirectly to additional pathology in systems other than the nervous system. We use the term indirect effects of nervous system pathology to indicate pathology that occurs in systems other than the nervous system as a sequela to the initial nervous system pathology. For example, skin breakdown can eventually lead to decubitus ulcers, which represent a pathology of the integumentary system. Pneumonia is an example of a pathology of the cardiopulmonary system that can indirectly result following nervous system lesions. Pneumonia is a frequent cause of death in individuals who have sustained a stroke [15] or who have Parkinson's disease. [16] We can postulate pneumonia to be a pathology that occurs indirectly through a sequence of events such as the following. Because of Parkinson's disease, an individual may lose a capacity for adequate chest expansion during breathing and for an adequate capacity for coughing. This patient may indirectly develop decreased vital capacity (VC). If the patient's cough becomes ineffective, secretions may accumulate in the lungs. Infections such as pneumonia may then result. The patient's impairments that predisposed him or her to pneumonia (a pathology that occurred indirectly) may also interfere with recovery from the pneumonia, which may be fatal. Pneumonia represents a pathology that could occur with or without CNS insult but that, in this case, occurred secondary to the insult. In this example, our model predicts that pneumonia will be treated most effective if both the pathology (pneumonia) and its underlying cause (decreased VC attributable to inadequate chest expansion, which is secondary to rigidity and kyphotic posture) are addressed.

Composite Effects of Pathology

Finally, certain impairments have multiple underlying causes, some direct and some indirect. We use the term composite effects of pathology to refer to these impairments. These composite effects of impairments are illustrated in Figure 1. The underlying causes of these impairments often include both direct and indirect effects of the original CNS insult and pathology. In addition, those pathologic processes that occurred indirectly may also contribute to these composite effects.

Analysis of shoulder dysfunction in a patient with a parietal lobe lesion illustrates this concept. The impairment of reduced endurance in upper extremity activity could arise from a composite effect created by three different components: 1) impairments that are direct effects of the patient's parietal lobe damage, 2) impairments of the musculoskeletal system that are indirect effects of the lesion, and 3) pathology of the musculoskeletal system that occurs as an indirect effect of the lesion. This composite effect is outlined conceptually in Figure 2 and could occur as follows. Sensory loss and hypotonia may both occur as impairments directly resulting from the parietal lobe lesion. [4] Glenohumeral subluxation is an impairment of the musculoskeletal system that may occur indirectly as a result of hypotonicity. [10,13] Sensory loss, hypotonicity, and glenohumeral subluxation may all contribute to the composite effect, which leads to impairments of upper extremely undurance. With hypotonicity, there is inadequate automatic muscle contraction to sustain a voluntary contraction. [17] With sensory loss, there is inadequate sensory awareness and feedback to sustain the contraction, [18] and with malalignment, muscles must act in a situation of unfavorable length-tension relationship, which we assume would contribute to the losof ability to sustain the contraction. Thus, decreased upper extremity endurance for activity can be considered a composite effect of multiple underlying causes. Some of these underlying impairments are direct effects of the lesion, and some occur indirectly. Furthermore, malalignment and subluxation could potentially lead to musculoskeletal pathological conditions such as bursitis, tendinitis, or rotator-cuff tears. These indirect pathologies are also illustrated in Figure 2 and, as indicated, could themselves contribute to the composite effects on upper extremity endurance. Furthermore, the musculoskeletal pathology could contribute indirectly to additional nervous system impairments such as reflex sympathetic dystrophy. [19] Reflex sympathetic dystrophy (or shoulder-hand syndrome) then becomes yet another contributing source to the impairment of loss of endurance for upper extremity activity. This example serves to illustrate the multiple underlying causes that can contribute to impairments that are composite in nature.

Clinical Problem Solving when

Neuroanatomic Pathology

Is Known

The knowledge of the neuroanatomic basis of movement is very useful in predicting the consequences of impairments in the patient with CNS pathology. [7] From work on motor control over the past century, we can predict many of the expected effects of specific impairments. For example, from the work of Critchley, [4] Twitchell, [5] and Sanes and Evarts, [18] we can predict that sensory loss, whether peripheral or cortical, will result in hypotonia and in decreased endurance. From the work of Critchley [4] and Holmes, [17] we can predict that an individual with a parietal lobe lesion may have apparent paralysis of the upper extremity as a result of the loss of sensory awareness of the limb rather than as a result of a true motor loss.

The knowledge of the neuroanatomic basis of movement also leads us to postulate a relationship between parietal lobe lesions and balance. We can hypothesize that impaired balance responses may be a composite effect of multiple impairments, some of which are direct effects of the lesion and some of which are indirect. Two contributing causes that are direct effects of the lesion are incorrect perception of body position and hypoteonia. Furthermore, we can predict that the indirect impairment of malalignment may occur, resulting in a pronated foot or subluxated shoulder. We propose that these musculoskeletal impairments further compound the patient's difficulties with balance. In Tables 2 and 3, a few examples are given of possible effects of some impairments that arise directly and indirectly, respectively.

Each patient's impairments should be analyzed to identify their relative contribution to the patient's disability. This analysis is essential because those impairments that have the same effect for the patient may have a multiplicity of causes. For example, faulty balance may result directly from a nervous system lesion. [7] Several areas such as the basal ganglia and the vestibular brain stem system have been implicated as directly responsible for the integration mechanism of balance responses. [7,8] With lesions in these areas, we can predict that faulty balance will be a direct effect of the pathology. There are, however, a number of other potential causes of faulty balance. Figure 3 illustrates the use of the model to identify the variety of pathologies and impairments that could lead to faulty balance. As previously discussed, faulty balance may be a consequence of sensory loss secondary to a parietal lobe lesion. Faulty balance has been identified as an effect to incoordination following cerebellar disease and could be considered an impairment of motor programming. [7] Faulty balance also occurs in the apraxic patient and can be considered an effect of motor-planning deficits. [20] Faulty balance might also be associated with spasticity secondary to certain strokes. Furthermore, one can predict from clinical experience that faulty balance could result from an indirect musculoskeeletal impairment such as limitation in lumbo-pelvo-femoral mobility or malalignment of the foot.

Treatment Strategies when

Neuroanatomic Pathology

Is Known

The treatment strategy for these various types of patients should differ depending on the underlying cause. If faulty balance is due to a sensory loss, resulting in an inaccurate interpretation of position in space, it then makes sense to focus intervention toward the patient's knowledge of body position in space. Immobility of the lumbo-pelvo-femoral area may prevent a patient from being able to produce a balance response. In this case, it is important to direct intervention toward reestablishing mobility in that area so that the patient has the structural capability for a balance response. If apraxia is the cause of faulty balance, remediation may be difficult because apraxia has been notoriously difficult to correct. If the integrative mechanism of the balance response is directly altered by a neurologic insult, it may be very difficult or impossible to remediate the faulty balance with physical therapy intervention. We use these examples to illustrate the importance of identifying probable causes and effects. This knowledge can help to determine prognosis for improvement and strategies for intervention. Furthermore, once patients can be categorized with some confidence regarding the underlying causes of their balance impairments, it may be possible to devise treatments that specifically reflect the underlying cause of the impairment and to test whether specificity of treatment is more effective than nonspecific treatments.

Parietal lobe injury secondary to stroke and Parkinson's disease can be used to illustrate this point. When a patient has a parietal lobe lesion, knowledge of the underlying pathology suggests the need for an especially careful sensory evaluation. From knowledge of neuroanatomy, we can predict potential losses of sensory perception and loss of ability to interpret sensory phenomena. From knowledge of motor control, we can predict that even an apparently subtle loss of sensory interpretation or of attention may potentially be detrimental to both voluntary movement and automatic balance. If our careful sensory examination has indicated potential sensory causes of voluntary and automatic motor loss, we propose retraining of correct sensory perception and interpretation when treating that patient's loss of voluntary movement or impairment of balance control.

Parkinson's disease provides another example in which pathology and its consequences can easily be predicted. Parkinson's disease has long been known to result in cardinal signs and symptoms incluidng rigidity, tremor, bradykinesia, and postural instability. [21] Postural instability (or faulty balance) can be considered one of the direct effects of the pathology for Parkinson's disease. A variety of other impairments, however, may also contribute to the composite effect of faulty balance, as illustrated in Figure 4. Rigidity and impairments of alerting mechanisms (leading to bradykinesia) and motor planning-programming can be identified as direct effects of the pathology. [21] We can hypotehsize that all of these impairments may contribute indirectly to fault balance, which is a composite effect of the insult. In addition we postulate that rigidity and bradykinesia, two direct effects of the pathology of Parkinsonhs disease, lead to musculoskeletal impairments incluidng a flexed posture with loss of cervico-thoraco-lumbo-pelvic mobility. These musculoskeletal impairments could also contribute to balance impairment in patients with Parkinson's disease (fig. 4). It is useful, therefore, to evaluate the patient's extent of rigidity, loss of ability to combine motor programs, and impairment of trunk and pelvic mobility. The therapist can then make clinical iterpretations or hypotheses regarding the extent to which each of these other impairments contributes to the composite effect of faulty balance. Physical therapy may not be very effective in remediating the direct effects of pathology of Parkinson's disease on the integrative mechanisms for balance. Physical therapy, however, could be effective in reducing contributions of other impairments, such as loss of trunk and pelvic mobility, in remediating balance impairments. The clinician, therefore, might focus treatment on the patient's ability to self-relax rigidity to regain trunk and pelvic mobility if these impairments appear to contribute to the faulty balance. Rehabilitation for balance impairment in patients with Parkinson's disease might also be directed toward their awareness and conscious use of correct mechanisms for balance responses. These two examples illustrate that the cause of the patient's faulty balance should determine the strategy for remediating the impairment.

Problem Solving when

Neuroanatomic Pathology

Is Not Known

So far, we have presented examples in which we have been able to analyze the causes of impairments because we know the pathology. We can also use this model, however, to structure evaluation, clinical interpretations, and treatment when we do not know the underlying pathology for a patient. interpretation of a patient's difficulty with transfers (a physical disability) serves as a good example (Fig. 5). In this instance, we start from the disability and work upward in the model toward impairments. By using this analysis technique, we can consider all of the possible contributing impairments that lead to transfer disability. A few exmaples are impaired balance, loss of trunk mobility, apraxia, and presence of a positive support reaction. Each of these cause should be either ruled in or ruled out by evaluation of the patient.

As an example, evaluation of the patient who has difficulty with transfers might indicate that the patient does have a balance impairment. Further evaluation might rule out apraxia or a positive support reaction as causes of the difficulty with transfers. We, therefore, might begin with a clinical hypothesis that there is a causal relationship between the balance impairement and the transfer disability. Once this causal relationship has been postulateD, it would also be necessary to further evaluate the patient to identify the impairements underlying the faulty balance. Evaluation findings are used to predict whether faulty balance is a direct effect or a composite effect of some other impairments. For example, is altered perception a potential cause? Is weakness a cause? Do musculoskeletal limitations contribute? Figure 5 illustrates the decision-making process in which the clinician works from difficulty with transfers to identify the probable causes of that disability in terms of possible impairements that occured as direct and indirect effects of the lesion.

Interpretation and Clinical

Decision Making when

Neuroanatomic Pathology

Is Not Known

When problem solving is carried out without the benefit of a clearly defined pathology, it is not possible to determine absolutely which impairments are direct effects of the pathology, which are indirect effects, and which are composite effects. It is possible, however, for the clinician to make very sound clinical judgments, or clinical hypotheses, about causes and effects. If these interpretations are founded on concepts of neuroanatomy, kinesiology, and motor control, they should have potential validity. Treatment strategies can then be designed around these educated hypotheses. By choosing treatment strategies based on clinical hypotheses, the clinician can easily integrate techniques from a variety of schools of thought, including techniques of joint mobilization and the techniques of Bobath, [11] Johnstone, [12] Feldenkrais, [22] and Rood. [23] Furthermore, the therapist can devise new techniques based on an understanding of probable causes and effects. Success of a particular strategy helps to support the interpretation the clinician has made. If the treatment is not successful, or if improvement has reached a plateau, evaluation findings should be reexamined to determine whether there are alternative explanations for the disability. The model should serve as a guide to potential alternative explanations for disability and serve as a guide to potential limitations for recovery. We make clinical judgments or hypotheses every time we treat a patient. This model is offered as one way to harness motor control literature into a clinical context so that these judgments can be made within the context of current physiology, anatomy, and kinesiology.

Summary

We have presented a model that can be used to organize current concepts of neuroanatomy, neurophysiology, and motor control theory into a clinically relevant context. This model can be used to postulate the causal relationship among pathology, impairments, and disabilities. Knowledge of the insult often provides predictive information regarding stability of the disability, progression of the disease, and possibly recovery. Knowledge of neuropathology should guide the clinician regarding the types of impairments that are expected. Thus, by knowing the type and location of the lesion, the clinician already has a perspective regarding which evaluative tests should be emphasized and what treatment strategies will be most effective. In the absence of known pathology, knowledged of motor control theory, neuroanatomy, and neuropathology can still help the clinician make educated judgments regarding the interrelationship of the patient's impairments.

In this model, we separate impairments that result directly from neuropathology and those that arise indirectly to help the clinician keep the total patient in perspective and to focus intervention. This separation emphasizes the applicability and limitations of motor control theories in the treatment of neurologically impaired individuals. Motor control theory helps to identify the relationship between direct impairments and their likely consequences; motor control theory does not address the very real issue of impairments that arise indirectly in systems such as the muscoloskeletal and cardiopulmonary systems. Impairments that occur as a composite effect of multiple causes are identified as a separate category. Some of the causes of these impairments can often be addressed by physical therapy intervention, and some cannot. We suggest that those contributions that are indirect effects of a lesion are likely to be most amenable to physical therapy intervention. This suggestion can be tested experimentally. In focusing treatment, it is important to have a working hypothesis regarding what we can achieve and what we cannot achieve. Treatment is likely to be most effective when the underlying cause is addressed along with the sympton.

This model is intended to guide the clinician in making clinical hypotheses regarding causal relationships between all contributors to the disability. We have provided a few examples of how the model can be used to analyze balance disorders, both when a specific pathology is understood and when it is unknown. The clinician can extrapolate from these examples to interpret any patient's impairments and to understand the patient's total disability. This model is intended to help the clinician make decisions regarding evaluation and treatment of patients, to teach current concepts of motor control in a clinical context, and to identify clinically relevant research questions that will further our knowledge and treatment of the neurologically impaired individual.

Acknowledgments

We gratefully acknowledge the invaluable comments and critiques of Alan M Jette, PhD, PT, Bette Ann Harris, MS, PT, Emmanuel Lo Monaca, and our other colleagues at the MGH Institute of Health Professions.

M Schenkman, PhD, PT, is Assistant Professor, MGH Institute of Health Professions, 15 River St, Boston, MA 02108-3402 (USA).

RB Butler, MD, is Chief of Neurology, Emerson Hospital, Old Road to Nine Acre Corner, Concord, MA 01742, and assistant Professor, Department of Neurology, Boston university, Boston, MA.

References

[1] Dyrek DA, Harris BA, Riegger CA: A model of orthopaedic dysfunction: Implications in examination and treatment. Abstract. Phys Ther 67:740, 1987

[2] Wood PHN: The language of disablement: A glossary relating to disease and its consequences. Int Rehabil Med 2:86-92, 1980

[3] Williams A, Calne DB: Treatment of parkinsonism. In Barbeau A (ed): Disorders of Movement. Philadelphia, PA, JB Lippincott Co, 1981, pp 171-190

[4] Critchley J MacD: Discussion on volitional movement. Proceedings of the Royal Society of Medicine 47:593-599, 1954

[5] Twitchell T: Sensory factors in purposive movement. J Neurophysiol 17:339-352, 1954

[6] Dalakas MC, Haleit M: The post-polio Syndrome. In Plum F (ed): Advances in Contemporary Neurology. Philadelphia, PA, F A Davis Co, 1988, pp 57-88

[7] Brooks V: The Neural Basis of Motor Control. Oxford, England, Oxford University Press, 1986

[8] Gilman S, Bloedel J, Lechtenberg R: Disorders of the Cerebellum. Philadelphia, PA, F A Davis Co, 1981

[9] Marsden CD: The mysterious motor function of the basal ganglia: The Robert Wartenberg Lecture. Neurology 32:514-539, 1982

[10] Griffin J, Reddin G: Shoulder pain in patients with hemiplegia: A literature review. Phys Ther 61:1041-1045, 1981

[11] Bobath B: Adult Hemiplegia: Evaluation and Treatment, rev ed 2. London, England, William Heinemann Medical Books Ltd, 1978

[12] Johnstone M: Restoration of Motor Function in the Stroke Patient, ed 2. Edinburgh, Scotland, Churchill Livingstone, 1983

[13] Ryerson S, Levit K: The shoulder in hemiplegia. In Donatelli R (ed): Physical Therapy of the Shoulder. New York, NY, Churchill Livingstone Inc, 1987, pp 105-131

[14] Schneider F: Traumatic spinal cord injury. In: Umpheld D (ed): Neurological Rehabilitation. St Louis, MO, CV Mosby Co, 1985, pp 314-374

[15] Schmidt EV, Smirnov EV, Ryabova VS: Results of the sevey-year prospective study of stroke patients. Stroke 19:942-949, 1988

[16] Hoehn M, Yahr M: Parkinsonism: Onset, progression, and mortality. Neurology 17:427-442, 1967

[17] Holmes G: The cerebellum of man. Brain 62:1-30, 1939

[18] Sanes JN, Evarts EV: Motor psychosis. Human Neurology 2:217-225, 1988

[19] Appenzeller O: The Autonomic Nervous System, ed 3. Philadelphia, PA, F A Davis Co, 1982

[20] Poeck K, Lehmkuhl G, Willmes K: Axial movements in ideomotor apraxia. J Neurol Neurosurg Psychiatry 45:1125-1129, 1982

[21] Ilson J, Bressman S, Fahn S: Current concepts in Parkinson's disease. Hosp Med 1933-58, 1983

[22] Feldenkrais M: Awareness Through Movement: Health Exercises for Personal Growth. New York, NY, Harper & Row, Publishers Inc, 1972

[23] Stockmeyer S: An interpretation of the approach of Rood to the treatment of neuromuscular dysfunction. Am J Phys Med 46:900-954, 1967