P21-5 Sural nerve excitability: Implications for the early identification of peripheral nerve dysfunction

OBJECTIVE One avenue of intense efforts to treat Parkinson's disease (PD) involves the delivery of neurotrophic factors to restore dopaminergic cell function. A source of neurotrophic factors that could be used is the Schwann cell from the peripheral nervous system. The authors have begun an open-label safety study to examine the safety and feasibility of implanting an autologous peripheral nerve graft into the substantia nigra of PD patients undergoing deep brain stimulation (DBS) surgery. METHODS Multistage DBS surgery targeting the subthalamic nucleus was performed using standard procedures in 8 study participants. After the DBS leads were implanted, a section of sural nerve containing Schwann cells was excised and unilaterally delivered into the area of the substantia nigra. Adverse events were continuously monitored. RESULTS Eight of 8 participants were implanted with DBS systems and grafts. Adverse event profiles were comparable to those of standard DBS surgery. Postoperative MR images did not reveal edema, hemorrhage, or significant signal changes in the graft target region. Three participants reported a patch of numbness on the outside of the foot below the sural nerve harvest site. CONCLUSIONS Based on the safety outcome of the procedure, targeted peripheral nerve graft delivery to the substantia nigra at the time of DBS surgery is feasible and may provide a means to deliver neurorestorative therapy. Clinical trial registration no.: NCT01833364 (clinicaltrials.gov)

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Sural nerve fibre pathology in diabetic patients with mild neuropathy: relationship to pain, quantitative sensory testing and peripheral nerve electrophysiology

Acta Neuropathologica ◽

10.1007/s004010000287 ◽

2001 ◽

Vol 101 (4) ◽

pp. 367-374 ◽

Cited By ~ 96

Author(s):

R. A. Malik ◽

A. Veves ◽

D. Walker ◽

I. Siddique ◽

R. H. Lye ◽

...

Keyword(s):

Peripheral Nerve ◽

Nerve Fibre ◽

Sural Nerve ◽

Quantitative Sensory Testing ◽

Diabetic Patients ◽

Sensory Testing

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Toxins and Environmental Neurologic Injury

10.1093/med/9780197512166.003.0128 ◽

2021 ◽

pp. 1170-1176

Author(s):

Sara E. Hocker ◽

Ali Daneshmand

Keyword(s):

Occupational Exposure ◽

Peripheral Nerve ◽

High Altitude ◽

Environmental Conditions ◽

Substance Misuse ◽

Environmental Exposures ◽

Neurologic Injury ◽

Clinical Syndromes ◽

Nerve Dysfunction ◽

Physical Effects

Toxins and environmental exposures may result in central or peripheral nerve dysfunction. Toxins may be purposely ingested (eg, substance misuse), or exposure may be accidental (eg, occupational exposure or terrorism). Certain environmental exposures (eg, lightning or high altitude) may also result in neurologic injury. This chapter reviews neurologic clinical syndromes associated with toxins and the physical effects of certain environmental conditions.

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Sensorimotor Perineuritis – An Autoimmune Disease?

Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques ◽

10.1017/s0317167100046837 ◽

1985 ◽

Vol 12 (2) ◽

pp. 129-133 ◽

Cited By ~ 20

Author(s):

Christopher N. Bourque ◽

Brian A. Anderson ◽

C. Martin del Campo ◽

Anders A. F. Sima

Keyword(s):

Peripheral Nerve ◽

Mononuclear Cells ◽

Sensory Neuropathy ◽

Nerve Biopsy ◽

Sural Nerve Biopsy ◽

Gradual Improvement ◽

Immune Mediated ◽

Nerve Dysfunction ◽

Inflammatory Infiltrates ◽

Perineurial Cells

ABSTRACT:The literature contains a single description of sensory perineuritis (Asbury et al 1972). These patients demonstrated a painful, distal, sensory neuropathy, and examination of peripheral nerve biopsies revealed focal thickening and inflammatory infiltrates of the perineurium. We report a patient with sensorimotor peripheral nerve dysfunction, accompanied by progressive slowing of nerve conduction velocity. Examination of a sural nerve biopsy demonstrated focal thickening of the perineurium, inflammatory infiltrates, and necrosis of perineurial cells. Immunohistology revealed a patchy precipitation of IgG and IgM on perineurial cells. Ultrastructurally, mononuclear cells were found adjacent to perineurial cells undergoing necrosis. The patient showed gradual improvement partially coinciding with a course of steroid therapy. We suggest that this neuropathy is caused by damage to the perineurial barrier possibly by an immune-mediated destruction of perineurial cells and subsequent compression of the endoneurial content by perineurial scarring.

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