Study design, materials and methods
Seventy-eight patients underwent TTNS therapy for overactive bladder symptoms (OAB). To identify the right place to stick TTNS stickers, tibial nerve was stimulated at the ankle using EMG machine ( Cadwell Sierra Summit -UK). Tibial nerve response was recorded from Abductor Hallucis (AH) muscle using surface EMG electrodes after stimulating the tibial nerve below the medial Malleolus. Since routine TTNS machines can deliver up to a maximum of 50 mA current at 0.2 duration, the absence of AH response at these settings was considered abnormal. An additional sural nerve sensory study was done when tibial nerve response was absent. The absence of sural nerve response was regarded as sensory neuropathy in the lower limbs(1).
Patients were trained to use an electrical stimulator (Neurotrac continence – de smit medical -UK) to stimulate their posterior tibial nerve at the ankle using 5 cm x 5 cm square neurostimulation electrodes (Pals 5x5 cm – Axekgaard Stimulation electrodes – Digitimer -UK)
The electrical pulse’s duration and frequency were fixed at 0.2 ms and 10 Hz, respectively. The amplitude of the electric pulses was selected based on the patient’s toe twitch and satisfactory sensory responses in any medial plantar, lateral plantar or calcaneal nerve distributions. In case of no consistent sensory feedback from the patient in the plantar distribution of the foot, toe twitch alone was considered to decide the required current strength.
Patients were asked to use the TTNS machine for 20 minutes daily for six months. A follow-up study was done after six months. Three days of bladder diaries were filled before and after TTNS therapy.
Results
Seventy-eight patients, 54 women and 24 men, mean age of 57.9 years (Range: 26-78 years), had completed TTNS therapy for six months. Most patients with OAB symptoms referred to TTNS therapy were with an underlying cause of either Multiple Sclerosis (43.5%) or Parkinson’s disease (27.6%). The rest of the patients reported having a variety of underlying causes, such as Cauda equina syndrome or Spinocerebellar and other neurological conditions. None of these patients was investigated for sensory or motor neuropathy before coming to the department.
Absent motor and sensory responses were noted in 13 (16.6 %) patients due to severe oedema in the feet or underlying neuropathy. Sural nerve sensory response was absent, but a good motor response, including toe twitch, was seen in 3 (3.8%) patients.
A total of 12 patients (15.3%) were removed from the analysis due to missing pre- or post-TTNS bladder diaries.
Daytime voidings and night-time voidings were listed in Table 1 for all three groups
Interpretation of results
The primary aim of the TTNS treatment is to inhibit detrusor contraction by inhibiting the pelvic nerve within the spinal cord(2). This can be achieved by inhibiting the second-order neurons in the lumbosacral spinal cord by a frequency-dependent gating mechanism activated by afferent Aδ- and C-fibers in the dorsal root ganglia(3) after stimulating the tibial nerve. However, swollen ankles or peripheral neuropathy can defeat the purpose of stimulating afferent fibres in the tibial nerve.
Fifty patients showed improvement in nocturia with the TTNS. Some of these patients also noticed an improvement in controlling their bladder until they could reach a toilet. TTNS outcome in this observational study is in line with published data(4,5).
Thirteen patients with no motor and sensory responses showed no significant improvement with the TTNS. The poor TTNS outcome in this group could be due to insufficient stimulation of afferent fibres in the tibial nerve. Insufficient tibial nerve stimulation could be for several reasons, such as local oedema at the ankle, underlying peripheral neuropathy, or both.
Three patients with pure sensory neuropathy (1-Friedreich ataxia, 1-Cerebellar ataxia with neuropathy and 1- Hereditary spastic paraplegia with sensory neuropathy) showed a good motor response at AH and good toe twitch approximately between 25 to 30mA current stimulations. However, TTNS did not improve void frequency in this group. This observation further strengthens the hypothesis that stimulating afferent fibres in the tibial nerve is essential for a better TTNS outcome.
Further studies are required to assess motor and sensory neuropathies in patients with OAB symptoms to test this hypothesis. Further studies are also needed in peripheral neuropathy or severe oedema patients to stimulate the tibial nerve at a proximal site, such as the popliteal fossa, to assess the TTNS outcome. In the interim, it is prudent to rely on sensory feedback from the patient than toe twitch alone while setting up the TTNS equipment.