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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