Written by a CuraCore Veterinary Medical Acupuncture course graduate. Signed release obtained from client/author. 10D2018043
Abstract: An 11-year old male castrated Dalmatian presented for a chronic 6-month history of hindlimb weakness, with a presumptive diagnosis of degenerative lumbosacral stenosis. Medical therapy had failed to attain improvement and alternative therapies had not been attempted. Dry needling and massage therapy were performed weekly for one month to achieve neuroactivation and relieve compensatory strain patterns. Improvement in ambulation was observed post-treatment, in addition to slowed progression of neurological deficits.
History & Presentation: An 11-year old male castrated Dalmatian, presented for a progressive 6-month history of weakness and stumbling in the hind end. Examination by an orthopaedic specialist had determined the lameness to be of primary neurologic etiology. Further work-up with a neurologist determined that weakness was present in both hindlimbs, with the right more affected than the left (6 months prior to this presentation). No pain response was elicited during examination/manipulation. Based on examination findings, the most likely differential diagnosis was considered degenerative lumbosacral stenosis. Advanced imaging to confirm clinical suspicion was declined. Medical therapy was initiated with gabapentin with little to no improvement observed. Over the 6 months following presumptive diagnosis, a significant deterioration in condition had been observed. Progressive atrophy of the musculature bilaterally over the hind end, increasing difficulty walking and manoeuvring daily obstacles, and fecal incontinence had been noted. The left hindlimb was now considered equally affected as the right. At the time of presentation, daily medical therapy consisted of 200mg gabapentin PO BID and 0.6mg levothyroxine PO BID.
Physical Exam & Clinical Assessment: On presentation the dog was bright, alert, and responsive, with a body condition score of 6/9. Vital parameters were within normal limits. Marked muscle atrophy over the hind end was appreciated on palpation, with gluteal, quadriceps, and hamstring muscle groups affected, left side worse than right. On gait analysis bilateral hindlimb paresis was evident, with frequent hyperextension and foot dragging observed. Thorough neurologic exam revealed normal mentation and intact cranial nerves. Lower motor neuron deficits were appreciated in both hindlimbs, with reduced patellar reflexes bilaterally and paresis. Proprioceptive placement tests were delayed in both hindlimbs. Forelimbs were within normal limits, with no evidence of neurologic deficits identified. On myofascial exam, tight bands were palpable in the cervical and triceps regions bilaterally. Increased sensitivity to palpation was identified throughout thoracic and lumbar spine, with greatest sensitivity localised to lumbosacral region. Based on clinical assessment and physical exam, the main problems are bilateral hindlimb paresis with associated muscle atrophy and neurologic deficits, and fecal incontinence.
Differential Diagnoses: Differential diagnoses for bilateral hindlimb weakness with associated muscle atrophy and neurologic deficits include degenerative lumbosacral stenosis (cauda equina syndrome), neoplasia of the bone and/or nervous tissue, infectious/non-infectious inflammatory mass affecting the lumbosacral spinal canal, or congenital/acquired malformation of spinal vertebrae. Fecal incontinence differential diagnoses include degenerative lumbosacral stenosis, damage to superior rectal and/or hypogastric plexuses, neoplastic/infectious/non-infectious inflammatory mass causing neural tissue compression in the sacral region, or congenital/acquired malformation of spinal vertebrae.
Definitive Diagnoses: Degenerative lumbosacral stenosis (cauda equina syndrome) was considered as the most likely differential diagnosis in this case, based on the patient’s history, physical, myofascial and neurologic exam findings. This condition may occur due to numerous causes including chronic disc protrusion (Hansen type II), hypertrophied soft tissue (ligamentous and joint capsule structures), vertebral joint osteophytes, and lumbosacral instability. In most dogs, this is a multifactorial condition with more than one of these elements contributing to the development and progression of disease.
Medical Decision Making: A treatment plan to provide palliative therapy, promote neuroactivation in the hindlimbs, and alleviate strain patterns arising from abnormal ambulation was developed. Due to the sensitive nature of this dog, dry needling (without electrical stimulation) was elected in addition to massage therapy. Photobiomodulation was not available to supplement therapy in this case. All treatments were started with GV-14 for autonomic nervous system (ANS) stimulation and calming effects. Bai Hui was selected for further calming effects, and to treat lumbosacral pain locally. A selection of points on the Bladder channel were chosen for treatment of lumbosacral pain and local muscular pain, in addition to achieving neuroactivation through multiple spinal segments associated with back, hip, and pelvic nerve roots. With regards to targeted treatment of the hindlimbs, ST-36, BL 39-40, GB 31, KI 3, SP 6, LR 2, and Bafeng points, were selected to activate peripheral nerve branches. Dry needling treatment was performed weekly for one month, then reduced to every other week.
Medical Acupuncture and Related Techniques Used: The patient had never received acupuncture treatment prior to this presentation, and initially showed sensitivity to needling. As such, treatments were started with fewer needles to prevent hypersensitization, and gradually increased as tolerance improved. Seirin needles (0.16 x 30mm) were placed and gentle massage performed around the cervical region where tight bands were repeatedly palpable post-needling. First treatment acupuncture points included: GV 20, Bai Hui, BL 10, BL 13-15, SP 6, KI 3, BL 27, BL 28, and LR 2. ST 36 was placed in the right side. Trigger point needling was also performed in brachiocephalicus m., subclavius m., and descending pectoral m. bilaterally. Second treatment points included: GV 20, BL 10, SP 6, KI 3, BL 27-28, LR 2, and Bafeng. ST 36 and BL 39-40 were placed in only the left side, which was worse affected on this day of treatment. Trigger point needling was performed in brachiocephalicus m. and subclavius m. bilaterally. Third treatment points included: GV 20, BL 10, BL 11, SP 6, KI 3, BL 27-28, LR 2, and Bafeng. ST 36, BL 39-40, and GB 31 were placed in only the right side. Trigger point needling in brachiocephalicus m. and subclavius m. was also performed. For the fourth treatment, needling points were repeated from the third acupuncture treatment, with emphasis on left side for unilateral points.
Outcomes & Discussion: The patient did well with all treatments and showed no signs of adverse effects. The majority of needles remained static, however needles in the Bladder channel throughout the thoracic to mid-lumbar region were noted to intermittently experience de qi effect and be pulled into the skin, consistent with sensitivity on palpation in this area indicating myofascial tension. Following treatments, an improvement was noted in foot placement and strength in the hindlimbs which lasted for several days. Over the course of treatment, slowed progression of neurological deficits was observed by the owner. Unfortunately, treatment of this dog ceased due to financial constraints. From this case I learned how to treat lumbosacral disease in a dog, and the benefits that can be seen from these alternative therapies when medical therapy has been unrewarding. Had I been able to continue treatment, I would have aimed to reach a point at which electrical stimulation could be applied to enhance peripheral nerve stimulation. Ideally, photobiomodulation would have been used in the initial phases of treatment of sensitive areas which were primarily addressed with massage in this case. Improvement in hindlimb gait in this case was considered to be a result of neuromodulation in the hindlimbs and reduced inflammation.
References
1. Curacore Small Animal Point Manual
2. Curacore Clinical Intensive Notes
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