Following surgery, a large bulky cotton wrapping immobilizes the ankle joint without plaster. The dressing may be removed at the one-week point and sutures at about three weeks. Complications may include bleeding, infection, and unpredictable healing. The incision may open from swelling. There may be considerable pain and cramping. Regenerating nerve fibers may create shooting pains. Patients may have hot or cold sensations and may feel worse than before surgery. Crutches are usually recommended for the first two weeks, as well as elevation to minimize swelling. The nerve will grow at about one inch per month. One can expect to continue the healing process over the course of about one year. Many patients report good results. Some, however, experience no improvement or a worsening of symptoms. In the Pfeiffer article (Los Angeles, 1996), fewer than 50% of the patients reported improvement, and there was a 13% complication rate. Tarsal tunnel can greatly impact patients quality of life. Depending on the severity, the ability to walk distances people normally take for granted (such as grocery shopping) may become compromised. Proper pain management and counseling is often required. Results of surgery can be maximized if all four of the medial ankle tunnels are released and you walk with a walker the day after surgery. Success can be improved to 80%. Incidence
Though TTS is rare, its cause can be determined in 70% of reported cases.
In rare cases, the patient might also experience muscle weakness, tremor, or paralysis if the nerves involved also control muscle movement. Pathophysiology
Postherpetic neuralgia is thought to be due to nerve damage caused by herpes zoster. The damage causes nerves in the affected dermatomic area of the skin to send abnormal electrical signals to the brain. These signals may convey excruciating pain, and may persist or recur for months, years, or for life.A key factor in the neural plasticity underlying neuropathic pain is altered gene expression in sensory dorsal root ganglia neurons. Injury to sensory nerves induces neurochemical, physiological, and anatomical modifications to afferent and central neurons, such as afferent terminal sprouting and inhibitory interneuron loss. Following nerve damage, NaCl channel accumulation causes hyperexcitability, and downregulation of the TTX-resistant Nav1.8 (sensory neuron specific, SNS1) channel and upregulation of TTX-sensitive Nav1.3 (brain type III) and TRPV1 channels. These changes contribute to increased NMDA glutamate receptor-dependent excitability of spinal dorsal horn neurons and are restricted to the ipsilateral (injured) side. A combination of these factors could contribute to the neuropathic pain state of postherpetic neuralgia. Diagnosis
Lab Studies:
No laboratory work is usually necessary. Results of cerebrospinal fluid evaluation are abnormal in 61%. Pleocytosis is observed in 46%, elevated protein in 26%, and VZV DNA in 22%. These findings are not predictive of the clinical course of postherpetic neuralgia. Viral culture or immunofluorescence staining may be used to differentiate herpes simplex from herpes zoster in cases that are difficult to distinguish clinically. Antibodies to herpes zoster can be measured.