How to determine an orthopedic or a neurologic cause of dysfunction

(See clickable video below.) Orthopedic and neurologic diseases are common in companion animals. In practice, it can sometimes be difficult to determine which system is abnormal in a given patient. There are important aspects of history acquisition, the examination, and recognizing specific conditions with pathognomonic findings that can help a practitioner distinguish between orthopedic and neurologic diseases. The purpose of this article is to aid the general practitioner in determining if a patient is experiencing an orthopedic or a neurologic cause of dysfunction. Specifically, there are notable orthopedic conditions that may be considered “neurologic imposters.” However, these orthopedic conditions lack key deficits consistent with neurologic dysfunction. These “neurologic imposters” are addressed below to aid the clinician in the evaluation of patients that are presented for gait dysfunction. Using the neurologic exam to identify neurologic versus orthopedic disease Figure 1 provides a summary chart of the segments of the spinal cord and expected neurologic findings. Figure 1: Neurolocalization chart for myelopathies. Courtesy Dr. Susan Arnold Gait evaluation Lameness: Lameness can occur from both musculoskeletal and neurologic dysfunction. The nerves of the peripheral nervous system are innervated with pain receptors, and bearing weight on a limb with nerves that are impinged due to disease or injury causes pain resulting in lameness. Lameness originating from neurologic dysfunction is called nerve root signature. In addition to overt lameness during ambulation, nerve root signatures can also lead to animals sitting with the affected thoracic limb lifted. Thus, lameness does not provide strong ability to distinguish between orthopedic and neurologic causes of a patient’s dysfunction. Paresis: Paresis is defined as decreased voluntary motor function and is a neurologic problem due to an issue either with the spinal cord or the nerves to the limb(s). Therefore, observing paresis provides the ability to determine that a patient’s dysfunction is neurologic, as orthopedic disease does not cause paresis. There are two types of paresis. Lower motor neuron paresis occurs due to a lesion in the spinal cord segment containing the lower motor neurons for the affected limb(s) or due to a lesion in the nerves that emerge from the spinal cord segment to travel to the effector muscles in the affected limb(s). Lower motor neuron paresis leads to weakness, difficulty bearing weight, and a short, choppy gait. In contrast, upper motor neuron paresis occurs due to a lesion in the spinal cord cranial to the affected limb(s). Upper motor neuron paresis leads to difficulty relaxing the limb, such that the gait looks stiff, with minimal limb flexion due to excessive tone in the extensor muscles. Ataxia: Ataxia is defined as impaired balance or coordination. Of the three forms of ataxia, general proprioceptive ataxia is the only one that can be observed in patients with a problem affecting either the sensory branches of nerves or the spinal cord. Therefore, observing general proprioceptive ataxia provides the ability to determine a patient’s dysfunction is neurologic, as orthopedic disease does not cause general proprioceptive ataxia. Patients with general proprioceptive ataxia knuckle the affected limb(s) and during ambulation, the affected limb(s) may cross midline or circumduct. Muscle mass: Both orthopedic and neurologic disease can lead to atrophy. Generally, though, neurologic disease affecting the peripheral nervous system leads to rapid, severe atrophy that can develop as soon as seven days after loss of innervation. This is called neurogenic atrophy. Orthopedic disease usually causes a slower, less severe atrophy, called disuse atrophy. Muscle tone: Increased muscle tone (making it difficult to flex the limb(s)) occurs with lesions in the spinal cord cranial to the affected limb(s). Thus, increased tone is a sign of neurologic dysfunction. Decreased muscle tone (making the limbs excessively easy to flex) occurs with lesions in the spinal cord segments containing the lower motor neuron cell bodies that innervate the affected limb(s) and in lesions affecting the nerves of the affected limb(s). Alternatively, patients with musculoskeletal pain may exhibit decreased muscle tone due to reluctance to move the limb. However, extremely reduced tone indicates neurologic dysfunction over musculoskeletal dysfunction. Proprioceptive testing: Postural reaction deficits (paw replacement, hopping, wheelbarrowing) occur due to neurologic dysfunction. Patients with musculoskeletal dysfunction remain able to successfully replace their paws or hop when supported. Thus, observing proprioceptive deficits confirms a neurologic issue rather than an orthopedic issue. Spinal reflex testing: Reflex arcs consist of sensory input, carried toward the spinal cord in a sensory nerve, a synapse between the sensory neuron and the motor neuron (in the spinal cord), and motor output, carried away from the spinal cord in a motor nerve to the effector muscle(s). The withdrawal reflex of the thoracic limb thus tests all nerves of the thoracic limb (musculocutaneous, axillary, median, ulnar, radial) and the C6-T2 region of the spinal cord. The withdrawal reflex of the pelvic limb tests the sciatic nerve and the L6-S1 region of the spinal cord. The patellar reflex tests the femoral nerve and the L4-L6 region of the spinal cord. The perineal reflex tests the pudendal nerve and the S1-S3 region of the spinal cord. A reflex deficit indicates an issue with either the nerve(s) or the spinal cord region involved in the given reflex. Patellar and perineal reflex deficits are the most reliable in indicating a neurologic issue. Withdrawal reflex deficits can sometimes be more difficult to interpret, and animals with orthopedic pain may be reluctant to withdraw their limbs because doing so elicits discomfort. In these cases, using a pair of hemostats to generate a sufficient stimulus to override their reluctance is sometimes necessary to determine if withdrawal is or is not possible. The absence of spinal reflex deficits does not rule out neurologic dysfunction. Rather, it rules out that the spinal cord segments involved in each reflex are not affected. Recall that patients with C1-C5 myelopathies will have normal reflexes in all limbs, patients with C6-T2 myelopathies will have thoracic limb reflex deficits and normal pelvic limb reflexes, patients with T3-L3 myelopathies will have normal reflexes in all limbs, and patients with L4-S3 myelopathies will have normal reflexes in the thoracic limbs and pelvic limb/perineal reflex deficits. Patients with C6-T2 and T3-L3 myelopathies may also have cutaneous trunci deficits. Palpation: Localized pain along the vertebral column occurs with neurologic diseases that involve vertebrae, or meningeal/nerve root compression, as all these regions have pain receptors. Not all neurologic diseases lead to localized pain. Further, pain with manipulation of the hips does not exclusively indicate an orthopedic abnormality affecting the hips. Animals with lumbosacral stenosis and other conditions affecting this region of the vertebral column may also react to hip manipulation. Neurologic and orthopedic diseases: by limb(s) affected Single limb abnormalities Thoracic limb: Neurologically, unilateral thoracic limb abnormalities can occur secondary to a lesion in the peripheral nervous system involving the nerves that innervate the thoracic limb. Theoretically, they can also occur secondary to a lesion in either the ipsilateral C1-C5 or C6-T2 regions of the spinal cord. Almost always, for a lesion affecting the spinal cord, deficits will not be limited to a single limb, and upper motor neuron deficits are likely to be observed in at least the ipsilateral pelvic limb for a truly unilateral lesion, and often in all four limbs. This is because even small lesions in the spinal cord tend to impact the projections traveling to and from all limbs. However, with small spinal cord lesions or early in the disease phase, signs might be most prominent in a single thoracic limb, but careful evaluation of the remaining limbs may show they are also affected. For this reason, lesions in the C1-C5 and C6-T2 regions of the spinal cord are included in this section. Overall, though, a neurologic cause of unilateral thoracic limb gait dysfunction remains much more likely to be due to a lesion in the peripheral nervous system rather than the central nervous system. Neurologic causes of unilateral thoracic limb dysfunction Intervertebral disc extrusion, lateralized Neoplasm (most often nerve sheath tumor, meningioma) Ganglioneuritis or brachial plexus neuritis Brachial plexus root injury/avulsion Neurologic imposters of unilateral thoracic limb dysfunction Infraspinatus contracture: Infraspinatus contracture occurs secondary to either acute or chronic injury of the infraspinatus muscle. It is most often seen in active, generally large-breed dogs. Following the initial injury, fibrosis develops, leading to a characteristic carriage of the limb. Dogs with infraspinatus contracture have medial rotation of the elbow and lateral paw positioning as a result of the fibrotic infraspinatus muscle. This abnormal limb carriage is most evident during gait evaluation. During ambulation, a carpal flip is often observed. This condition can be confused for thoracic limb neurologic dysfunction because of the abnormal limb carriage. However, patients with infraspinatus contracture have normal postural reactions, normal muscle tone, and normal thoracic limb withdrawal reflexes. Infraspinatus contracture of the right thoracic limb in a dog, showing the classic limb carriage associated with this condition. Photo IVIS.org Superficial digital flexor contracture: Flexor tendon contractures (and laxities) occur in actively growing dogs for poorly understood reasons. The superficial digital flexor tendons course along the palmar aspect of the manus and function to flex the phalanges. Contracture of these tendons results in a curled appearance to the manus, which can be mistaken for knuckling. However, patients with superficial digital flexor contracture have fixed flexion of their digits, and have no evidence of paresis or ataxia, with normal postural reactions. Pelvic limb: Neurologically, unilateral pelvic limb abnormalities can occur secondary to a lesion in the peripheral nervous system involving the nerves that innervate the pelvic limb, and can also occur secondary to a lesion in either the ipsilateral T3-L3 or L4-S1 regions of the spinal cord. Almost always, for a lesion affecting the spinal cord, deficits will not be limited to a single limb, although there can be marked differences in the severity of signs in one pelvic limb versus the other. Neurologic causes of unilateral pelvic limb dysfunction Intervertebral disc extrusion or protrusion, lateralized Lumbosacral stenosis or L7-S1 foraminal stenosis Neoplasm (most often nerve sheath tumor, meningioma, or bony tumors impinging on sciatic nerve) Ganglioneuritis Sciatic nerve trauma Fibrocartilaginous embolic myelopathy Neurologic imposters of unilateral pelvic limb dysfunction Fibrosis of caudomedial thigh muscles: This is a relatively common condition observed most often in German shepherds and similar breeds. It is usually unilateral, but can occur bilaterally, as well. A fibrous band of tissue develops in association with the caudomedial thigh muscles (semimembranosus, semitendinosus, and gracilis muscles). This fibrous band limits and alters the normal range of motion of the limb during protraction, terminating protraction prematurely such that it appears the limb is unable to advance fully forward during the swing phase of the gait. Since the fibrous band is on the medial aspect of the limb, it also pulls the stifle medially while the tarsus rotates laterally. This band can often be palpated when the limb is held in extension. The condition is often confused for a neurologic issue because there is no overt evidence of lameness or identifiable orthopedic abnormalities in these dogs, yet their gait appears abnormal. However, dogs with this condition have normal postural reactions and spinal reflexes, ruling out a neurologic cause. German shepherd with fibrosis of the left caudomedial thigh muscles. Gastrocnemius tendon rupture: The common calcanean tendon is composed of the tendons of the biceps femoris, semitendinosus, gracilis, gastrocnemius, and superficial digital flexor muscles. If the gastrocnemius and superficial digital flexor tendons are ruptured simultaneously, the patient develops a plantigrade stance. However, if the gastrocnemius tendon ruptures, but the superficial digital flexor tendon is spared, this results in a plantigrade stance with flexed digits, sometimes to the extent of causing the foot to appear curled. This curling is confused for knuckling. Palpation of the common calcanean tendon in affected patients may reveal swelling of the calcaneus secondary to rupture of the gastrocnemius tendon. This condition is most often observed in Dobermans and Labradors. It usually starts with one limb and progresses to affect the contralateral limb. These patients have normal postural reactions and spinal reflexes, ruling out a neurologic cause. Figure 3: Doberman with left gastrocnemius rupture. Note the plantigrade stance and the curling of the digits, often confused with knuckling due to proprioceptive dysfunction. Courtesy Dr. Susan Arnold Doberman with left gastrocnemius rupture. Both pelvic limbs affected: Neurologically, conditions causing both pelvic limbs to be abnormal occur secondary either to a lesion in the spinal cord or in the peripheral nervous system. Regarding lesions in the spinal cord, issues with both the T3-L3 and L4-S1 regions of the spinal cord, will result in abnormalities in the pelvic limbs without concurrent abnormalities in the thoracic limbs. These two localizations produce nearly opposing neurologic deficits. Patients with T3-L3 myelopathies have upper motor neuron paraparesis, characterized by stiffness and limited limb flexion, and general proprioceptive ataxia. Patients with L4-S1 myelopathies have lower motor neuron paraparesis, characterized by weakness and difficulty bearing weight, with or without observable general proprioceptive ataxia. T3-L3 myelopathies result in increased pelvic limb tone and mild atrophy with time, whereas L4-S1 myelopathies result in decreased pelvic tone and often moderate to marked atrophy over a short period of time. Both can lead to postural reaction deficits. Patients with T3-L3 myelopathies have normal patellar and pelvic limb withdrawal reflexes, whereas patients with L4-S1 myelopathies have decreased patellar and pelvic limb withdrawal reflexes. Patients with lesions that span beyond L4-S1 to also include the S1-caudal regions of the spinal cord may also have absent perineal reflexes and lower motor neuron fecal and urinary incontinence. Neurologic causes: Intervertebral disc extrusion or protrusion Lumbosacral stenosis or bilateral foraminal stenosis Degenerative myelopathy Severe kyphosis or other severe malformations Neoplasia (extradural masses affecting the vertebrae, intradural-extramedullary masses affecting the meninges, intramedullary masses) Discospondylitis with secondary empyema or vertebral column instability Meningomyelitis of unknown etiology Vertebral column trauma (fracture, subluxation, luxation) Fibrocartilaginous embolic myelopathy Geriatric onset laryngeal paralysis polyneuropathy (causing sciatic nerve dysfunction) Neurologic imposters of bilateral pelvic limb dysfunction Bilateral cranial cruciate ligament rupture: Cranial cruciate ligament rupture is the most common orthopedic condition managed in small animal practice, and generally only affects one limb at a time. In these typical cases, diagnosis is usually straightforward. However, cranial cruciate ligament rupture can affect both limbs simultaneously. In these cases, clinicians may struggle to determine if the underlying cause of a patient’s bilateral pelvic limb gait abnormality is orthopedic or neurologic. Patients with bilateral cranial cruciate ligament ruptures present with bilateral pelvic limb lameness. Careful observation will reveal dogs with bilateral cranial cruciate ligament rupture collapse on the stifle while weight-bearing. Performing drawer testing and cranial tibial thrust and observing stifle instability confirms the diagnosis. Bilateral cranial cruciate ligament ruptures are sometimes confused for myelopathies because their bilateral instability can make them alter their gait to reduce their discomfort. However, patients with bilateral cranial cruciate ligament ruptures have no overt stiffness or weakness, no general proprioceptive ataxia, appropriate muscle tone, normal postural reactions, and normal spinal reflexes. Dog with bilateral cranial cruciate ligament rupture. Distal aortic thromboembolism: Most clinicians are able to identify distal aortic thromboembolic disease (saddle thrombus) in cats, which develop such emboli more frequently than dogs and with more consistent clinical signs. Distal aortic thromboemboli can cause more vague heterogeneous presentations in dogs. Most affected dogs have a chronic or insidious onset of signs over a period of weeks to months (Winter et al. 2012). Some dogs experience dramatic alterations in their pelvic limb dysfunction, oscillating from mild deficits to severe dysfunction in short periods of time. Patients with distal aortic thromboemboli may mistakenly be considered to have neurologic dysfunction because loss of blood supply to their limbs results in weakness that appears very similar to lower motor neuron paraparesis. In severe cases, they may be paraplegic and also have reduced tone and spinal reflexes due to lack of arterial supply to their limbs. However, a critical observation in dogs with distal aortic thromboemboli is weak or absent femoral pulses. Therefore, any patient with pelvic limb dysfunction, especially if they have signs consistent with lower motor neuron dysfunction, should have femoral pulse quality assessed. Dog with distal aortic thromboembolism. All four limbs affected: Neurologically, in patients with all four limbs affected, there are three possible localizations provided they have normal mentation and a normal cranial nerve exam: C1-C5 myelopathy, C6-T2 myelopathy, and diffuse neuromuscular. Refer to Figure 1 for examination findings for patients with C1-C5 and C6-T2 myelopathies. Patients with diffuse neuromuscular disease have lower motor neuron tetraparesis, meaning they look weak, and either have exercise intolerance or take short, choppy steps when they walk. They also have difficulty bearing weight. They do not have general proprioceptive ataxia and also have normal postural reactions, and can have normal to absent limb reflexes, depending on the underlying etiology. Neurologic causes: C1-C5 and C6-T2 myelopathies: Intervertebral disc extrusion or protrusion Cervical spondylomyelopathy Atlantoaxial subluxation or luxation Neoplasia (extradural masses affecting the vertebrae, intradural-extramedullary masses affecting the meninges, intramedullary masses) Meningomyelitis of unknown etiology Steroid-responsive meningitis arteritis (neck pain only, no deficits) Vertebral column trauma (fracture, subluxation, luxation) Fibrocartilaginous embolic myelopathy Diffuse neuromuscular disease: Polyradiculoneuritis Myasthenia gravis Tick paralysis Botulism Polymyositis Neurologic imposter of dysfunction in all limbs Immune-mediated polyarthritis: Immune-mediated polyarthritis is characterized by noninfectious inflammation of multiple joints. Dogs with this condition are reluctant to walk and exhibit a stiff, stilted and short, choppy gait in all limbs secondary to their discomfort. Some dogs also have accompanying neck pain. Their abnormal gait can sometimes be confused for either C1-C5 myelopathy or diffuse neuromuscular disease. However, unlike patients with C1-C5 myelopathy, patients with immune-mediated polyarthritis have no general proprioceptive ataxia, and have normal postural reactions. Unlike patients with diffuse neuromuscular disease, patients with immune-mediated polyarthritis have normal spinal reflexes. Patients with immune-mediated polyarthritis often have an elevated core body temperature, palpable joint effusion, and evidence of pain with joint manipulation. Conclusion Neurologic dysfunction relative to a specific region of the nervous system results in consistent deficits across patients. Thus, recognizing the pattern of abnormalities expected with each localization is important in confirming that a patient presented for gait abnormality is truly neurologically abnormal. Conversely, there are many musculoskeletal/orthopedic conditions that are rarely encountered and, therefore, may be challenging to recognize. Awareness of these uncommon conditions can aid the practitioner in diagnosis and treatment of patients with “neurologic imposter” conditions. Susan A. Arnold, DVM, DACVIM (Neurology) is an assistant professor of neurology and neurosurgery at the University of Minnesota College of Veterinary Medicine. She is boarded within the American College of Veterinary Internal Medicine (Neurology). In her role, Dr. Arnold practices neurology and neurosurgery, trains interns and residents, and teaches veterinary medical students in both didactic and clinical settings.

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How to determine an orthopedic or a neurologic cause of dysfunction

An overview for general practitioners to boost diagnoses

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