The following is a description of a patient that was presented in the Journal of the American Medical Association, 2009, volume 302, number 1.
I noticed pain in my left foot—it was always the left foot first—and that's when I had just started nursing, back in ’88. I spoke to a friend who was a podiatrist and he started wrapping it and giving me cortisone shots. As time went by, it started developing in my right foot as well....
About 9 years ago I was diagnosed with diabetes... and I notice a correlation between the control of the diabetes and the pain, the neuropathy symptoms. If I lapse into a sugar binge, I will feel heat and pain in my feet...
My symptoms have gotten much worse since it was first diagnosed. There are cramps that have recently kicked in. My pain has become bilateral, and the numbness seems to be crawling up my legs as well as the swelling in my ankles and my legs.
Ms Q is a 52-year-old registered nurse with lower extremity neuropathy diagnosed 6 years ago. She lives in the greater Boston area and has managed care health insurance.
Ms Q's symptoms began about 8 years ago with pain at the base of her left foot. She was seen by a podiatrist, initially diagnosed with plantar fasciitis, and underwent serial cortisone injections. The injections minimized symptoms initially, but her pain persisted. Her pain spread to her right foot....
Ms Q says that her neuropathic symptoms, which include numbness, tingling, pain, and burning bilaterally, have worsened over the years. Her symptoms seem to worsen when her diabetes is less well controlled.
QUESTION: Is there anything suspicious about the neuropathy symptoms appearing about the same time as diabetes is diagnosed?
QUESTION: Do you notice anything here that suggests something is present besides ordinary type 2 diabetes?
As Ms Q symptoms worsened, the pain spread to her right foot, and, given the lack of improvement, she was referred for nerve conduction studies and electromyography (EMG). The studies showed mild reduction in the sural sensory response amplitudes bilaterally with normal conduction velocities; these findings were consistent with a mild distal axonal neuropathy...
In a nerve conduction study, the nerve is shocked at one place to start action potentials in all the axons at that point of the nerve. Then, at a specific distance, the voltage change due to the arrival of all the action potentials is recorded. With diabetic neuropathy, you would expect the calculated conduction velocity to be normal, since the problem is axonal rather than with the myelin. Degeneration of axons, by contrast, should make the amplitude of the summed response smaller, which was observed. In an EMG test, action potentials in muscle cells are recorded, either with or without nerve stimulation.
Her hemoglobin A1C was 7.6% at the time of the diagnosis of diabetes.... She has had difficulty keeping her diabetes under tight control, however, and her hemoglobin A1C is currently 8.8%.
Her vitamin B12 and thyrotropin (TSH) levels were normal. On examination, her blood pressure was 146/74 mm Hg; pulse, 68/min; weight, 237 lb (106.6 kg); and height, 5 ft, 4 in (162.5 cm). Distal strength in the legs and feet was normal. Reflexes were 2+ at the knees and trace at both ankles; no Babinski signs were present. There was a graded reduction in sensation to pinprick and cold in both feet, normalizing at the midshins bilaterally. Vibration was reduced to 2 to 3 seconds in the great toes but was normal proximally. Joint position sense was intact in both feet. Gait was narrow-based, and a Romberg sign was absent.
Due to the diabetes, the final diagnosis was diabetic neuropathy.
Optional notes: The sural nerve is a cutaneous nerve in the lower leg and foot. The tough fascia covering the bottom of the foot is called the plantar fascia. Plantar fasciitis is inflammation of this fascia at the point where it attaches to the calcaneus. It is a common problem in athletes, the obese, and others who put extra stress on their plantar fascia during walking and running. This is unrelated to the diabetic neuropathy.
Optional notes: The Romberg sign occurs when a patient, standing with feet together, becomes unsteady with eyes closed. If the patient becomes unsteady with eyes closed, it is a sign of proprioception loss.
Initially I was put on small dose of amitriptyline at bed time and that caused terrible dryness of my mouth. I would wake up and not even be able to open my mouth. So that stopped. Then I started on Neurontin [gabapentin], and I think dry mouth was still a problem.
Notes: Amitriptyline is a tricyclic antidepressant, which has various cellular actions, including inhibition of serotonin-norepinephrine re-uptake into presynaptic terminals. While tricyclic antidepressants are, of course, used for depression, certain drugs in this class are also used for pain. Gabapentin is an anticonvulsant drug originally used to control seizures, but is also used for a variety of purposes, as illustrated here. Its exact mechanism of action is unknown. Its structure is similar to GABA, although it is more likely to act by binding to voltage gated Ca++ channels.
My diabetic doctor started me on [lidocaine] patches, and prior to that, he started me on [duloxetine], 60 mg at bedtime. The [duloxetine] really helped initially, a whole lot. It was like a wonder drug for me.
Optional notes: Duloxetine is also a serotonin-norepinephrine re-uptake inhibitor at presynaptic terminals and is used for both depresssion and painful peripheral neuropathy. It is substantially more expensive than amitriptyline or gabapentin.
Other things that help are sometimes a massage or arnica rubbed into it to create a little bit of heat. Also ice massages help quite a bit, but I’m hesitant to use that because of vascular complications from the diabetes. Acupuncture helped, but the price of the acupuncture is a deterrent.
My understanding of the treatment of neuropathy is that ultimately, there is very little to do for it. Treat the symptoms is what I’ve been doing. It is not something that is going to go away. It may, with better control of the diabetes, become less uncomfortable. I was planning to have a gastric bypass to help reduce my intake, but that's a little too scary for me. So now I’m reconsidering having a band done.
I’d like to know if it ever gets better, instead of progressively worse. There are new medications on the market that are supposed to help it—I don't know why I’m not on them, or if those medications could be helpful for me, or if there is anything else that I could do.
She has tried a range of medications with only moderate relief. Amitriptyline caused intolerable mouth dryness. Topiramate and gabapentin were ineffective. To treat her pain, she currently uses lidocaine patches, takes 60 mg of duloxetine daily, and uses alternative treatments including arnica cream.
Optional notes: Her other medications include atenolol, 100 mg once a day; atorvastatin, 80 mg once a day; fluticasone, 50 µg spray, 1 to 2 sprays daily; glyburide, 10 mg twice daily; hydrochlorothiazide, 25 mg once a day; lisinopril, 40 mg 4 times a day; metformin, 1000 mg twice daily; oxycodone/acetaminophen (5 mg/325 mg), 1 to 2 tablets every 4 hours as needed for pain; trazodone, 100 mg before bed; and ranitidine, 150 mg twice daily.
Lidocaine you know about. Topiramate, like gabapentin, in an anticonvulsant used in epilepsy. It mode of action is not clear, and it has a number of cellular actions. It also is used in mood and various other disorders. Atenolol, hydrochlorothiazide and isinopril are medications for high blood pressure. Atorvastatin is a "statin" drug, which you know about. Fluticasone inhaled is a glucocorticoid used to suppress inflammation in asthma and atopic rhinoconjunctivitis. Metformin you know about. Oxycodone is a powerful opiate drug used to relieve pain. Ranitidine inhibits stomach acid secretion. Trazodone is another inhibitor of serotonin-norepinephrine re-uptake used in depression.
Ms Q's other medical problems include obesity, hypercholesterolemia, depression, hypertension, and back pain which persists after a left L5 to S1 hemilaminectomy, medial facetectomy, and microdiskectomy for disk disease in 2000.
QUESTION: In the nerve conduction study, why would you expect to see the normal conduction velocity?
QUESTION: What is the action of lidocaine?
QUESTION: Would receptor potentials also be blocked with the lidocaine?
QUESTION: Is the absence of a Babinski sign consistent with peripheral neuropathy? (see lab)
QUESTION: What does the somewhat reduced vibration sense seem to imply?