FSD Secondary to Clitoral Neuropathy
601
fall caused transient total leg numbness and paralysis and marked bruising
of her lower back and upper buttocks. Although she recovered her strength
completely, she had worsening genital pain, numbness, and fibromyalgia.
She was able to have sexual intercourse and orgasm in spite of the persis-
tence of the pain, but had recently noted decreased orgasmic sensation and
increased latency. She also had a generalized burning, numbness, and itch-
ing dysesthesia of her genitalia and hypersensitivity to any stimulation. Topi-
cal treatment with salves and ointments had been ineffective. Low-dose
doxepin had reduced some of the itching and improved her sleep. On ex-
amination, she has a hyperpathia and hyperesthesia to repetitive stimuli to,
in, and around her clitoris, throughout the vulva and extending into her
saddle area. The sensory changes were in S2–S4 dermatomes. Her deep
tendon reflexes were normal, as was her anal sphincter tone. The bulbocav-
ernosus reflex was diminished. The patient had decreased clitoral blood
flow by Doppler measures and excellent response to sildenafil. The patient
had llumbosacral (LS) and pelvic MRI, EMG and NCS, including the puden-
dal nerve and GCERs. Oral sildenafil when given after the initial studies,
worsened the dysesthesia and resulted in extreme pain on urination. The
discomfort associated with sildenfil abated after 36 hours. Baclofen was given
to reduce the neuralgic component of the pain.
DISCUSSION
At the time of the Civil War, S. Weir Mitchell recognized that peripheral nerve
injuries could lead to persistent burning pain, which he called causalgia,
which at times was progressive and associated with trophic changes in the
affected area. These changes indicated hyperactivity of the sympathetic ner-
vous system, and have been called mimocausalgia, posttraumatic pain syn-
drome, and sympathalgia. These conditions are considered a form of reflex
sympathetic dystrophy, a syndrome that characteristically includes not only
pain, but also hyperpathia, dysesthesia, and pseudo and vasomotor changes.
It can follow trauma, surgery, infection, degenerative joint disease, or cere-
bral or myocardial infarction. The signs vary from minimal or no tissue change
to marked atrophy and profound bony and soft tissue change, as seen in
Sudek’s atrophy.
The LS roots originate at bony level Ti 2-Li, the beginning of the
caudaequina, and are considered part of the peripheral nervous system once
these nerves pass the pia and enter the subarachnoid space. The pudendal
nerve, which originates from S2 to S4 sacral roots, passes between the coc-
cygeus muscles and the piriformis. It exits from the pelvis through the distal
part of the greater sciatic foramen and reenters through the lesser sciatic
foramen, where it lies along the wall of the ischiorectal fossa. The nerve then
exits from the pudendal (Alcock’s) canal and branches to form the inferior
rectal nerve, which innervates the skin around the anus and the external