Sullivan, Katherine J. PhD, PT1; Hershberg, Julie DPT2; Howard, Robbin DPT1; Fisher, Beth E. PhD, PT2
Diagnosis is the process of determining the nature of a condition by way of examination. A medical diagnosis is characteristically based on the pathophysiology of a condition. The Guide to Physical Therapist Practice (2nd ed) and the American Physical Therapy Association's normative model of physical therapist professional education defines a physical therapy diagnosis as both a process and a label in which physical therapists perform an evaluation in order to provide a diagnosis that identifies the impact that a condition has on function.1,2 As the profession of physical therapy moves towards obligations inherent in autonomous practice, physical therapists will more frequently be required to perform examinations to determine if patients' conditions are within or outside of the scope of physical therapy practice.3
The diagnostic process for physical therapists includes the determination of the physical therapy diagnosis as well as recognition of clinical findings that would require referral to a medical care provider when the medical diagnosis (ie, diagnosis of the pathophysiologic condition) is in question.4 Both of these aspects of diagnosis are essential skills for physical therapists. Whether a client receives physical therapy with or without a physician prescription, physical therapists are responsible for the safety, appropriate treatment, and referral of individuals in their care.
The purpose of this article is to describe a clinical decision making framework for physical therapy clinical practice that can be used to determine appropriateness for physical therapy care for individuals with neurologic conditions. We will focus on the medical neurologic diagnosis in which the physical therapist uses the patient history and neurologic examination to identify patient problems that are within the scope of physical therapy practice or determine if signs and symptoms suggest that the expertise of a physician or other member of the health care team is warranted.
NEUROLOGIC DIFFERENTIAL DIAGNOSIS
Echternach and Rothstein5 first introduced a framework for clinical decision‐making in 1989 with the hypothesis‐oriented algorithm for clinicians (HOAC). More recently, a second, more comprehensive version of this algorithm has been presented that includes disablement terminology and incorporates prevention into the algorithm.6 While this algorithm is useful in providing a framework for clinical decision‐making in the realm of goal setting and treatment planning, it does not guide the physical therapist in the differential diagnosis process. This process requires the physical therapist to determine if the disease, with its concomitant movement dysfunction, is within the scope of physical therapy practice or requires medical referral. In the orthopedic physical therapy literature, there are several case studies or case study series where physical therapists have contributed to accurate medical diagnoses in patients with inaccurate musculoskeletal diagnoses.7‐11 In contrast, no published case studies have described the role of the physical therapist in accurate neurologic differential diagnosis in cases where the patient has a neuromuscular pathology. Furthermore, there are no clinical decisions making frameworks that describe an algorithm for determining the appropriateness for physical therapy or need for medical referral in individuals who present with neurologic conditions.
The neurologic examination is part of the systems and patient examination performed by physical therapists. The neurologic examination itself can provide important information that can contribute to an accurate neurologic differential diagnosis. One purpose of the physical therapist's neurologic examination is to establish the physical therapy diagnosis by identifying neurologic impairments that contribute to movement dysfunction in individuals with neurologic disease. Another important purpose of the neurologic examination is to determine if the neurologic presentation of the patient is within the scope of physical therapy practice or requires referral to another health care professional. Referral to a physician is particularly critical if the patient is presenting with emergent or evolving neurologic deterioration or in situations where the patient's condition is not consistent with the current medical diagnosis. In either case, immediate referral or consultation with the physician is required to insure optimal patient care.
Physical therapists engage in complex clinical decision making that involves interplay between both deductive (ie, knowledge‐base, diagnostic reasoning) and inductive (ie, patient‐centered, narrative reasoning) cognitive processes.12 Models of expert practice in physical therapy consistently show that both novice and expert practitioners draw upon a hypothetico‐deduction reasoning strategy to guide hypothesis formation, data gathering, and clinical decision making in situations where there is an unfamiliar problem or complex clinical presentation.12‐14 We propose that clinical decisions related to the appropriateness of physical therapy services or the identification of emergent medical or neurologic conditions are best resolved and taught using a hypothesis‐driven reasoning strategy. For this reason, we have adapted the method of neurologic differential diagnosis described by Victor and Ropper15 as the framework for our clinical decision making model.
Within the profession, it is well recognized that physical therapists do not determine the pathology or etiology of disease.14 The medical diagnosis is the pathologic or etiologic diagnosis that is determined by the physician as a result of the medical differential diagnosis process (ie, history, physical examination, lab, radiological, other medical diagnostic tests). Victor and Ropper15 describe a method of neurologic differential diagnosis commonly used by neurologists. This method entails a series of clinical steps that assists the physician in determining the most salient features in the complex presentation of an individual with a neurologic disorder (Figure 1). These steps have been modified to make it more clearly a hypothetico‐deductive clinical reasoning model that can be used by physical therapist for neurologic differential diagnosis.
Step one in the process involves the elicitation of clinical facts derived from the patient's history and neurologic examination. This step is an iterative process in which the signs and symptoms are interpreted in the context of the relevant anatomy and physiology. The goal of this step is to generate a list of hypothesized lesion localizations that in turn directs the evaluation process and test selection. History and neurologic evaluation results are interpreted and signs and symptoms are clustered into recognizable syndromes. For example, a clustering of signs such as weakness, exaggerated deep tendon reflexes, and a positive Babinski sign would be indicative of an upper motor neuron syndrome. The next step is the localization of the lesion in order to determine the anatomic diagnosis. The anatomic diagnosis identifies the part or parts of the nervous system that could most likely account for the complete presentation of the patient. Finally, the anatomic diagnosis is combined with the temporal features of the disease (ie, mode of onset, course of illness, relevant past and family histories) and the laboratory findings to determine the pathologic and etiologic diagnosis. In a hypothetico‐deductive reasoning strategy, generation and verification of hypotheses are confirmed or negated as ongoing analysis of patient information and data collection are interpreted.16
An accurate neurologic diagnosis is the essential end product of the differential diagnosis process and leads to determination of the appropriate treatment and prognosis. The examination performed by the physical therapist can provide valuable information to the physician in the determination of an accurate neurologic diagnosis. Accuracy in the neurologic differential diagnosis process is critical since the consequences of misdiagnosis can be dire. For example, an undetected spinal abscess or spinal arteriovenous malformation can cause permanent and irreversible damage to the spinal cord and leave the affected individual with complete paralysis and sensory loss. Often patients with these serious medical conditions complain of symptoms that are commonly seen by physical therapists such as severe localized acute back pain, weakness, or incontinence. Additionally, autoimmune or systemic inflammatory processes can result in complaints of musculoskeletal pain, fatigue, and weakness, which are frequently encountered by physical therapists.10 An accurate diagnosis is critical for determining the most effective treatment to prevent further neurologic deterioration and to provide therapeutic interventions that may reverse pathophysiologic processes. Furthermore, genetic or family counseling are necessary for diseases that are progressive‐degenerative in nature. Understanding the long‐term outcomes associated with these diseases is a critical component of the therapeutic process for an individual and his or her family.
Physical therapists have an important role in the neurologic differential diagnosis process in every setting in which they work. One might assume that physical therapists may play a greater role in the neurologic differential diagnosis process or be more frequently involved in that process in an acute hospital setting compared with an outpatient or rehabilitation setting. In the acute hospital setting, patients are often medically unstable and so a physical therapist might encounter patients with changing neurological status with greater frequency. However, in an outpatient or rehabilitation setting, the physical therapist may spend considerably more time with the patient than the physician, and as such, have more opportunity to observe alterations in physical or cognitive status.
In a rehabilitation or outpatient setting, the physical therapist is a key practitioner for differentiating changes in a patient's condition that may need medical attention. It is not unusual for the physical therapist to identify neurologic signs such as hyper‐reflexia or radiating paresthesias in an outpatient orthopedic setting after a ‘whip lash’ injury or provide important differential neurologic clinical findings for conditions that are given a symptom‐level diagnosis such as dizziness.17 A recent case study series by Walsworth, Mills, and Michener11 provides excellent examples of how physical therapists have contributed to accurate neurologic diagnoses of individuals with suprascapular neuropathy initially diagnosed with subacromial impingement syndrome. The selection and performance of neurologic tests, identification of neurologic signs, as well as the ability to communicate evaluation findings to the physician and request appropriate diagnostic tests during referral are the types of skills physical therapists must have in order to responsibly practice under direct access.
COURSE OF ACTION
If the physical therapist decides that the patient's neurologic presentation is not within the scope of physical therapy practice, then appropriate action must be taken. A clinical decision making algorithm to determine whether a patient presenting with neurologic findings is within the scope of physical therapy care or requires referral to a physician is presented in Figure 2. Of particular concern are emergent neurologic conditions that require immediate medical attention. Table 1 describes neurologic signs and symptoms that require immediate action. For example, severe headache with no previous history may be an early warning sign of hemorrhagic leakage from an intracerebral aneurysm.18 A flu‐like illness with fever and neurologic signs such as nuchal rigidity (resistance to active or passive neck flexion accompanied by severe pain) may indicate bacterial meningitis.19 A rapid onset of focal neurologic signs such as unilateral weakness, visual changes, or inability to speak can indicate a stroke in progress.18 The physical therapist must have knowledge of the range of neurologic signs and symptoms that underlie serious neurologic conditions that are in process. Clearly, immediate medical referral is essential to ensure optimal patient management.
Trained to provide thorough musculoskeletal and neuromuscular evaluations, physical therapists are key practitioners for identifying changes in neurologic status or inconsistencies in patient presentation in relation to the working medical diagnosis. For example, the diagnosis of shoulder weakness due to rotator cuff tear may be called into question if the physical therapist notes severe atrophy and fasciculation during the examination. These neurologic signs are associated with lower motor neuron disease and would warrant further diagnostic investigation to rule out a more serious neurologic condition. An individual referred for deconditioning or unsteady gait could possibly be in the early stages of a progressive degenerative condition if other neurologic signs such as abnormalities in postural control, muscle tone, or strength are present. Examples of signs and symptoms that may reflect a progressive neurologic process or compromise of a neurologic structure are listed in Table 1. While this grouping of signs and symptoms may not require emergency medical attention, referral to a physician would be warranted.
Determining the medical differential diagnosis has traditionally been considered the sole responsibility of the physician. However, physical therapists are equipped to make important contributions to this process as a result of their education and training. The case studies presented below are actual clinical cases in which the neurologic examination performed by physical therapists provided critical information leading to a timely and accurate neurologic diagnosis.These cases illustrate the application of the neurologic differential diagnosis framework and clinical decision‐making algorithm presented in this paper. The essential role that physical therapists can play in the neurologic differential diagnosis process that leads towards an. accurate diagnosis and optimal treatment is illustrated.
Case # 1 Description
JG, a 53‐year‐old Hispanic male, presented to the inpatient rehabilitation facility for a physical therapy evaluation following a left temporal parietal craniotomy with evacuation of an intracerebral hematoma. A head computed tomography scan (CT scan) revealed a large intracerebral hemorrhage (ICH) in the left temporal and parietal lobes and an old lacunar infarct in the right basal ganglia. According to the patient's wife, he appeared unable to recognize family members and had occasional bouts of agitation and combative behavior that required the use of soft restraints.
During the initial physical therapy examination, JG was lethargic, disoriented, and agitated. He inconsistently followed one‐step commands and demonstrated global aphasia. During functional activities, he required moderate assistance secondary to decreased safety awareness, lack of insight into balance deficits, delayed balance reactions, right‐sided weakness and neglect, ataxia, and agitation. Additionally, the evaluation revealed the following: resting blood pressure (BP) was 138/78, heart rate (HR) was 64 beats per minute (bpm), and cranial nerves II‐XII were intact. He was taking the following medications: Vasotec®, Labetalol®, Zantac®, Dilantin®, Haldol®, and Tylenol®.
JG participated in the physical therapy program for over 2 weeks. As anticipated, his status improved. He became alert and oriented to self, required minimal assistance during functional activities for balance and safety, and exhibited episodes of agitation and combative behavior only when his wife was unavailable during treatment sessions. However, on day 18, JG demonstrated a significant functional decline compared to the previous day. He was somewhat lethargic, required assistance to sit on the edge of his bed, and required maximal assistance of 2 people for standing and gait. The sudden change in JG's functional level prompted a re‐examination of his vitals and neurologic status that revealed a BP of 160/94, HR of 86 bpm, gaze‐evoked nystagmus, ataxia, altered mental status, and possible right LE sensory changes indicated by the patient's spontaneous one word response of “weird” when asked about his extremities.
The sudden onset of nystagmus, altered mental status, ataxia, and new sensory deficits, as well as a decline in functional ability are clinical features indicative of a changing neurologic status that could indicate an evolving neurologic pathology such as a recurrent ICH. These signs and symptoms are an example of an emergency medical situation as described in Table 1.
It was critical that the physical therapist immediately report the neurologic and functional changes to the attending physician in order to determine if the noted changes represented an emergent event. The prompt referral with a report of the above mentioned clinical findings allowed the physician to expeditiously order the most appropriate diagnostic testing. The physician immediately ordered a CT scan to rule in or rule out an acute hemorrhage.20 In addition to imaging, the physician ordered a comprehensive metabolic panel, complete blood count with differential, and a dilantin screen secondary to his suspicion of possible toxicity.
The head CT identified no change from the patient's baseline imaging. The dilantin screen, however, revealed a toxic level of 50.5 mcg/mL. The therapeutic level of dilantin ranges from 10‐20 mcg/mL with anything greater than 20 mcg/mL considered toxic.21 The most frequent clinical findings associated with dilantin toxicity are nystagmus, ataxia, and lethargy.21‐23 JG demonstrated these signs over the course of his decline.
JG's decline in medical and functional status was attributed to dilantin toxicity. Over the course of the following week, JG's dilantin level decreased to the therapeutic level. In addition to improved functional mobility, he was no longer agitated or combative and was discharged to home from the rehabilitation hospital 10 days later.
In retrospect, the agitation and combative behavior reported by the wife in the acute hospital and observed by the interdisciplinary team in the rehabilitation setting were possible early indicators of toxicity. Additionally, ataxia is not usually associated with ICH to parietal‐temporal areas. However, the patient's case was complicated by difficulty with communication (secondary to global aphasia) and the concurrence of his agitation/combative behavior with his family's absence.
Case #2 Description
RP, a 50‐year‐old male with a recent onset of neurosyphilis, was transferred to a rehabilitation center due to deconditioning, weakness, and functional decline after a month long hospitalization. Two months prior to his acute hospital admission, RP began to experience difficulty walking and progressive weakness and numbness in his legs. One week prior to admission he had several falls because of his instability while walking. During his stay in the hospital, RP underwent multiple tests including laboratory studies, a lumbar puncture, an electromyography/nerve conduction study (EMG/NCS), and brain magnetic resonance imaging (MRI), which resulted in the diagnosis of neurosyphilis.
On the day of transfer to the rehabilitation hospital, RP's initial physical therapy examination was consistent with the clinical picture of tabes dorsalis, a type of neurosyphyilis, with absent proprioception, impaired sensation, and diminished reflexes distally in bilateral lower extremities.15 However, he also had weakness in all 4 limbs that exceeded what might be anticipated from deconditioning. This finding was discussed with the physician, who agreed that this did not fit the clinical picture of neurosyphilis. However, it was possible to rule out alternative diagnoses that could account for the weakness such as paraneoplasm, multiple sclerosis, polyneuropathy, and toxicity, based on the results of the extensive testing that had previously been done.15,24,25 A possible variant of neurosyphilis was considered and further diagnostic work‐up commenced.26,27
While RP again underwent multiple tests, he began his rehab program consisting of functional training and therapeutic exercise during physical therapy. One week into his stay, he began to complain of fatigue, nausea, nasal congestion, and headache. In addition, he had difficulty swallowing, problems with urinary output, and early satiety. These symptoms were again discussed with the physician. Because of RP's multiple symptoms and change in status, the physician ordered a repeat brain MRI. The findings of this MRI were consistent with a diagnosis of multiple sclerosis (MS).28 RP was given the working diagnosis of possible MS and the recent changes in his status were attributed to an acute exacerbation. He immediately began treatment with high‐dose intravenous steroids29 and started therapy for MS with Avonex.30 RP's symptoms improved during the first day of treatment, but were then followed by further functional decline over 3 days. He changed from requiring minimal assistance to get out of bed to needing nearly total assistance. In addition, he needed help to sit at the side of his bed and was unable to walk after previously being able to sit independently and ambulate with minimal assistance approximately 10 to 20 ft with a walker. RP's main complaint was that he “felt much weaker.”
Re‐examination revealed significant motor and sensory deterioration compared to the initial exam. The changes in manual muscle testing were approximately 1 to 2 grades below the initial findings in all muscles with distal muscles being more affected than proximal. Proprioception and light touch of the limbs were both greatly diminished and had progressed proximally. In addition, upper and lower extremities were areflexic bilaterally with negative Babinski signs. RP also had complete facial weakness (forehead and lower face) and increased difficulty swallowing.
This patient presented with progressive weakness in all 4 extremities with no UMN signs, therefore, the most likely localization included peripheral neuromuscular structures. The differential diagnosis process included the determination of weakness due to neuromuscular junction, peripheral nerve, nerve root, or anterior horn cell involvement. The LMN weakness syndrome, in combination with the stocking‐glove progressive sensory loss, is consistent with peripheral nerve involvement.15,25 LMN involvement of cranial nerves was indicated by the presence of bilateral upper and lower face weakness (CN VII) and difficulty swallowing (CN IX, X, XII).19 Peripheral involvement of autonomic nerves may explain the early satiety and urinary retention. The combination of signs and symptoms, patient history, and temporal progression were consistent with a progressive polyneuropathy.
The progressive nature of RP's symptoms along with the MRI findings had initially led to a diagnosis of a MS exacerbation. However, the accuracy of the MS diagnosis was in question since the patient did not present with UMN signs, which are expected with a progressive central nervous system demyelinating disease such as MS, and the patient did not respond to steroid treatment.29,30 The decline in functional status and progression of neurologic signs and symptoms were clearly red flags that necessitated further investigation and discussion with the physician.
The primary physician was immediately consulted to discuss examination findings. The next day an electromyographic (EMG) and nerve conduction study was completed. Results were consistent with a progressive demyelinating polyneuropathy.31 RP was diagnosed with chronic inflammatory demyelinating polyneuropathy (CIDP) and treated with intravenous immunoglobulin.32‐34 During treatment, RP's symptoms minimally improved and he maintained his functional status. Discharge goals were changed to reflect RP's current status and progressive nature of his diagnosis and his length of stay was extended for family training, patient and family education, equipment evaluation and ordering, home evaluation, and discharge planning.
This case is an example of a non‐emergent situation requiring medical referral. Despite a neurologic diagnosis (ie, MS), which may have accounted for the decrement in motor and sensory status, this patient demonstrated signs and symptoms inconsistent with this diagnosis. The physical therapy examination revealed the change in neurologic and functional status that lead to further investigation by the physician and, ultimately, resulted in an accurate diagnosis and treatment.
These 2 cases illustrate the critical role that physical therapists have in the neurologic differential diagnosis process. The prompt referral to the physician which reflected the change in physical, cognitive, and functional status in Case 1, as well as the inconsistency between a LMN presentation with an UMN diagnosis in Case 2, led to determination of the correct diagnoses and implementation of appropriate treatment.
These cases reflect the neurologic knowledge base and clinical decision making process that are required of physical therapists. We have proposed a hypothetico‐deductive clinical reasoning model to guide physical therapists in the neurologic differential diagnosis process. In addition, a clinical decision making algorithm is presented to illustrate the process involved in determining whether a patient presenting with neurologic findings is within the scope of physical therapy practice. As the profession makes the transition to autonomous practice, entry‐level or transitional physical therapy doctorate programs should incorporate educational objectives and content that will prepare doctors of physical therapy for this level of practice.
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