Mononeuropathies of the lower extremities are commonly encountered in clinical practice. A mononeuropathy may result from pathology located anywhere along the course of the peripheral nerve, from the dorsal root ganglion through to the lumbosacral plexus and the terminal individual named nerves. Dysfunction can lead to weakness, pain, or sensory deficits. These entities are a major source of neurological referral.
Mononeuropathies can be thought of as compressive or non-compressive. Compressive neuropathies produce symptoms in the distribution of the affected nerve root, plexus, or individual nerve. Non-compressive mononeuropathies may be sequelae of underlying systemic disease (e.g., diabetes, malignancy, infection, and inflammatory conditions). Viral infections such as herpes zoster virus, herpes simplex virus (HSV), Epstein-Barr virus (EBV), and cytomegalovirus (CMV) can involve nerve roots, leading to a painful radiculitis, or may trigger a Guillain-Barre syndrome 1 to 3 weeks after infection. This is more commonly seen in people with altered immune function: for example, older people or those with HIV. Vasculitic neuropathy usually occurs suddenly and is painful. The typical vasculitic picture is stepwise involvement of multiple individual nerves (mononeuritis multiplex) rather than an isolated mononeuropathy. Because individual nerves are affected, one does not see the distal and symmetrical (e.g., stocking-glove) distribution of deficits typical of a generalised polyneuropathy, at least early on. In advanced cases, however, a confluent pattern can emerge that mimics that of a length-dependent polyneuropathy. Mononeuritis multiplex may also be seen with infection. Cancer can produce nerve dysfunction secondary to compression by solid tumours, infiltration by malignant cells, or paraneoplastic immune-mediated attack.
Neuropathy involving the lumbosacral plexus. It can be caused by compressive, infectious, malignant, and inflammatory aetiologies.
Neuropathy involving the nerve root. It can also be caused by compressive, infectious, malignant, and inflammatory aetiologies.
- Diabetic amyotrophy
- Lumbosacral radiculopathy
- Meralgia paraesthetica
- Peroneal neuropathy
- Morton's neuroma
- Lumbosacral plexopathy (non-neoplastic compressive)
- Obturator neuropathy
- Sciatic neuropathy
- Tarsal tunnel syndrome
- Tibial neuropathy
- Femoral mononeuropathy
- Hereditary neuropathy with liability to pressure palsies (HNPP)
- Herpes zoster
- Herpes simplex
- Epstein-Barr virus
- Lyme disease
- Peripheral nerve vasculitis
- Sjogren's syndrome
- Rheumatoid arthritis
- Acquired demyelinating sensorimotor polyneuropathy
- Lumbosacral plexopathy (inflammatory)
- Lumbosacral plexopathy (neoplastic compressive)
- Radiation-induced plexopathy
- Paraneoplastic immune-mediated attacks
- Nerve sheath tumours
Kevin R. Scott, MD
Colorado Springs Neurological Associates
KRS declares that he has no competing interests.
Dr Kevin R Scott would like to gratefully acknowledge Dr Milind J. Kothari, a previous contributor to this topic.
MJK declares that he has no competing interests.
Nizar Souayah, MD
Assistant Professor of Neurology
Director of EMG Laboratory & Peripheral Neuropathy Center
Department of Neurology & Neurosciences
New Jersey Medical School
NS declares that he has no competing interests.
Giuseppe Lauria, MD
Neuromuscular Diseases Unit
IRCCS Foundation "Carlo Besta" Neurological Institute
GL declares that he has no competing interests.
- Guidelines on neuropathic pain assessment: revised 2009
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