Lower Extremity Sensory Loss Research Articles

Back Pain and Lower Extremity Sensory Loss in an ESKD Patient.

A 33-year-old man on maintenance hemodialysis for 6 years for ESKD secondary to IgA nephropathy presented with acute back pain and loss of sensation in his feet, in the absence of recent trauma. His past medical history included severe hyperparathyroidism, with intact parathyroid hormone levels (iPTH) more than ten times the upper limit of the normal range (80 pg/ml) for 4 years, despite the prescription of phosphate binders, calcitriol, cinacalcet, and—lately—etelcalcetide. Clinical examination was marked by symmetric sensory loss and weakness in the lower extremities, together with deep-tendon hyperreflexia and Babinski signs. Plasma levels of electrolytes were normal. iPTH (855 pg/ml) and alkaline phosphatase (500 IU/L; normal range, 40–130 IU/L) levels were unchanged. Magnetic resonance imaging …

Sensory retraining of the lower extremity post-stroke

Sensory deficits are demonstrated in 50–85% of individuals post-stroke and lead to slower motor recovery and to poorer prognosis. Yet, sensory rehabilitation is often not set as a therapeutic target within the therapeutic setting. Sensory Retraining (SR) has been found effective for the upper extremity post-stroke. To study the effectiveness of Sensory Retraining (SR), an explicit perceptual learning approach focusing on sensation to the lower extremity post-stroke, and to compare it with Repeated Exposure (RE) to sensory stimuli, an implicit perceptual learning approach. An RCT was conducted comparing the two sensory rehabilitation approaches in subjects with chronic hemiparesis (> 6 months post-stroke) and lower extremity sensory loss. Sixty-four recruited volunteers (SR-34, RE-30) were assessed by a physical therapist blind to treatment allocation for sensory capabilities, activity performance and participation. Two pre-intervention assessments were conducted a week apart, followed by 10 treatment sessions of 45 minutes each, and two post-intervention assessments (immediately after treatment and following 3 months). ANOVA and post-hoc tests were used to determine treatment effects over time. Significance was set at P ≤ 0.05. The study demonstrated significant clinically meaningful differences for most sensory variables of the involved foot, and for all activity and participation variables. For example: A significant time effect ( P < 0.0001) for barefoot Timed Up and Go test demonstrated clinically significant decrease in time for both SR and RE groups (from 43.7 to 30.1 seconds and from 45.3 to 31.1 seconds respectively). A trend interaction effect ( P = 0.08) for tactile threshold was found, with post-hoc analysis demonstrating improvement only for the SR group. Sensory rehabilitation treatment by either SR or RE can make clinically significant changes in performance and participation in subjects with sensory loss post-stroke.

Spinal arteriovenous malformation associated with spinal metameric syndrome: a treatable cause of long-term paraplegia?

Cutaneomeningospinal angiomatosis, or Cobb syndrome, is a rare metameric developmental disorder presenting as an extradural-intradural vascular malformation that involves bone, muscle, skin, spinal cord, and nerve roots. A 14-year-old girl with a red nevus involving the T6-9 dermatomes on the left side of her back presented with a 5-year history of bowel and bladder incontinence, paraplegia, and lower-extremity sensory loss. Magnetic resonance imaging demonstrated a hemangioma in the T-8 and T-9 vertebral bodies and a spinal cord AVM nidus extending from T-6 to T-9. The AVM was successfully embolized and the patient regained lower-extremity strength, ambulation, and normal sphincter functions after 5 years of having been wheelchair bound. The authors report the restoration of ambulation after endovascular embolization of a large spinal AVM in a patient with long-standing paraplegia due to Cobb syndrome.

Glioneuronal tumor with neuropil-like islands of the spinal cord with diffuse leptomeningeal neuraxis dissemination

A 54-year-old Caucasian female presented with a 1year history of intermittent numbness of the left leg progressing to bilateral, lower extremity sensory loss that advanced to include impaired vibration and proprioception. The subsequent thoracic spine magnetic resonance imaging (MRI) scan revealed a heterogeneous, avidly enhancing, centrally situated spinal cord mass involving T7 through T10 in association with thick linear enhancement of the anterior and posterior cord surfaces extending both superiorly and inferiorly. Both the cervical and lumbar spine MRI demonstrated diffuse leptomeningeal disease as well. A brain MRI revealed focal leptomeningeal enhancement in the left and right sylvian fissures, the suprasellar cistern, and the posterior fossa; a pattern consistent with metastatic disease. The patient underwent a T6-T10 laminectomy for tumor biopsy and debulking. Histology revealed a WHO grade III glioneuronal tumor with rosetted neuropil-like islands. Synaptophysin and neurofilament (NF) positive staining was noted within the neural appearing component, whereas, glial fibrillary acidic protein (GFAP) immunopositivity was evident in the fibrillary astrocytoma component of the tumor. The Ki-67 labeling index was 7%. This tumor pattern, now included in the 2007 World Health Organization (WHO) classification of central nervous system tumours as a pattern variation of anaplastic astrocytoma (Kleihues et al. In: Louis et al. (eds) WHO classification of tumours of the central nervous system, 2007), was first described in a four-case series by Teo et al. in 1999. The majority of subsequently reported cases described them as primary tumors of the cerebrum. Herein, we report a unique example of a spinal glioneuronal tumor with neuropil-like islands with associated leptomeningeal dissemination involving the entire craniospinal axis.