Kinaesthetic ipsilateral and crossed extensor plantar response: A new way to elicit upgoing toe sign (Babinski response)?

Abstract

We describe a phenomenon of “kinaesthetic extensor plantar response” in advanced pyramidal dysfunction, an interesting observation noted in a patient with dorsal myelopathy. A 44-year-old woman presented with one-year history of gradually progressive weakness and stiffness of both lower limbs along with urge incontinence of urine. Examination showed spontaneous elicitation of extensor plantar response while assessing the tone by rolling method as well as on noxious stimulation of the thigh. Magnetic resonance imaging (MRI) of the dorsal spine and digital subtraction angiography showed the presence of spinal dural arteriovenous fistula causing myelopathy. This case exemplifies the fact that in advanced pyramidal dysfunction, not only the receptive field of Babinski reflex may extend to the leg or thigh, but may also integrate with other modalities of stimulation, such as the rolling movement. The possible underlying pathophysiology of such a phenomenon is discussed.

Introduction

Of all the signs described in the field of clinical neurology, probably the most famous and illustrious sign is the plantar response described by Joseph Babinski.[1] Babinski sign refers to the dorsiflexion of the great toe, with or without fanning of the other toes, on plantar stimulation, and its presence signifies an upper motor neuron dysfunction. After the description by Babinski, many authors have described various methods of eliciting the “upgoing toe” response. Indeed, Babinski himself used various methods of stimulation to obtain the response. In his more detailed and important communication, he wrote about the effects of stimulating the internal and external parts of the plantar surface.[2] Later he referred to “stroking” of the sole rather than pricking as the adequate stimulus. Eventually, he summarised his findings that the reflex movement that follows stimulation of the plantar surface of the foot from an organic lesion of the central nervous system can vary not only in its intensity but also in its character.[2] We describe such a phenomenon of variability, in our case, especially in longstanding pyramidal dysfunction.

Patient

A 44-year-old woman presented with insidious onset, gradually progressive weakness and stiffness of both lower limbs along with decreased sensations below the waist and urge incontinence of urine of one year duration. Examination revealed severe spastic paraparesis with a sensory level at D-11 segment. Spasticity on the right side was significantly more as compared to that on the left. An interesting finding was noted while assessing the tone in the lower limbs by the rolling method: There was spontaneous elicitation of extensor plantar response with all the components described by Babinski,[1,2] and this finding was consistent with every attempt [Video1-part 1: A and B]. A similar response was noted on noxious stimulation of the anterior thigh on both sides (Video1-part 2: A and B). In addition, “crossed upgoing toe” was noted on the right side upon stimulation on the left, by either method. Magnetic resonance imaging (MRI) showed a long segment, ill-defined T₂ hyperintense signal within the cord, with mild swelling extending from D-7 to conus medullaris indicative of cord edema. Additionally, there were multiple tortuous flow voids surrounding the cord, consistent with spinal dural arteriovenous fistula (AVF) [Figure 1a]. Subsequently, the patient underwent digital subtraction angiography (DSA), which confirmed the presence of spinal dural AVF [Figures 1b–d].

Figure 1.

Sagittal T₂-weighted magnetic resonance imaging, dorsal spine (a) showing multiple fl ow voids (white thin arrow), suggesting spinal dural arteriovenous fistula (DAVF). Digital subtraction angiogram (b-d) with selective catheterisation shows DAVF arising from radicular branch of the right D-6 intercostal artery with venous drainage into radicular vein and perimedullary venous plexus draining both superiorly and inferiorly (black thick arrows)

Discussion

Similar to the abdominal and cremasteric reflexes, the normal plantar response to cutaneous stimuli of the sole is a superficial reflex. These superficial reflexes are abolished in patients with an upper motor neuron lesion, wherein normal plantar response is replaced by the Babinski response.[1,2] Anatomically, the upgoing toe, an important component of the Babinski sign, is an extension of the great toe.[3] Physiologically, it is part of a flexor reflex synergy of the lower limb as described by Sherrington.[4] The main function of the flexor reflex synergy is to contract flexor muscles of the lower limb and shorten the limb as a protective reflex. As the central nervous system matures, this flexor reflex synergy is inhibited to facilitate ambulation. However, with upper motor neuron dysfunction, it is disinhibited, thereby resulting in reflex flexion withdrawal, the Babinski sign being only a part of this reflex. It has been suggested that dysfunction of pyramidal tract fibers, which project on interneurons that subserve the flexor reflex synergy, leads to the phenomenon of disinhibition and the appearance of Babinski sign.[5] On the other hand, weakness in the same area that is representing dorsiflexors of the great toe occurs due to impaired function of the fibers that project directly onto the motoneurons of the effector muscles.[5] It is well known that following an acute lesion in the cerebral hemispheres, there is initially a profound inhibition of the monosynaptic stretch reflexes and, after a variable period of time, the myotatic reflexes become hyperactive. Similarly, as the time progresses, with chronic pyramidal dysfunction, the threshold of the Babinski reflex gradually decreases, while its receptive field (the area from which the reflex can be elicited) gradually increases. In some instances, this field may extend to the leg or thigh.[6] This led to the description of many “reflexes” such as Chaddock's, Oppenheim's, and Gordon's signs, which were simply different ways of eliciting the Babinski sign.[7–9] Estanol in his study demonstrated that most of the patients with acute cerebrovascular occlusion show a gradual decline in the threshold and, at the same time, increase in the receptive field, for elicitation of the Babinski sign.[6] Our case also exemplifies this phenomenon. We further postulate that the phenomenon of “kinaesthetic extensor plantar response” suggests that in advanced pyramidal dysfunction, the receptive field may not remain confined to the cutaneous modality of stimulation alone and, it may integrate with other modalities such as kinaesthetic stimulation associated with the rolling movement, as seen in our case.