Peripheral nerve involvement in diabetes is common and may be
characterized by polyneuropathy, which is of mixed (sensory, motor, and
autonomic) character in approximately 70% of cases and predominantly sensory in
about 30%; mononeuropathy multiplex; or mononeuropathy simplex (Table 6–5).
Such clinical manifestations can occur in isolation or in any combination. The
incidence of peripheral nerve involvement may be influenced by the adequacy of
diabetes control, which should, in any event, be optimal.
Table
6–5. Neuropathies Associated with Diabetes.
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The most common manifestation is a distal sensory or mixed polyneuropathy,
which is sometimes diagnosed, before it becomes symptomatic, from the presence
of depressed tendon reflexes and impaired appreciation of vibration in the
legs. Symptoms are generally more common in the legs than in the arms and
consist of numbness, pain, or paresthesias. In severe cases, there is distal
sensory loss in all limbs and some accompanying motor disturbance. Diabetic
dysautonomia leads to many symptoms, including postural hypotension,
disturbances of cardiac rhythm, impaired thermoregulatory sweating, and
disturbances of bladder, bowel, gastric, and sexual function. Diabetic mononeuropathy
multiplex is usually characterized by pain and weakness and often has a
vascular basis. The clinical deficit will depend on the nerves that are
affected. Diabetic amyotrophy is due to radiculoplexopathy,
polyradiculopathy, or polyradiculoneuropathy. Pain, weakness, and atrophy of
pelvic girdle and thigh muscles are typical, with absent quadriceps reflexes
and little sensory loss. Diabetic mononeuropathy simplex is typically
abrupt in onset and often painful. CSF protein is typically increased in
diabetic polyneuropathy and mononeuropathy multiplex.
No specific treatment exists for the peripheral nerve complications of
diabetes except when the patient has an entrapment neuropathy and may benefit
from a decompressive procedure. The role of growth factors in treatment is
currently under study. Pain is troublesome in some patients and responds to the
measures outlined earlier (Idiopathic Inflammatory Neuropathies).
Postural hypotension may respond to treatment with salt supplementation;
sleeping in an upright position; wearing waist-high elastic hosiery; fludrocortisone, 0.1–1 mg/d; and midodrine (an 
-agonist), 10 mg three times daily.
Treatment is otherwise symptomatic. Diabetic amyotrophy and mononeuropathy
simplex usually improve or resolve spontaneously.
-agonist), 10 mg three times daily.
Treatment is otherwise symptomatic. Diabetic amyotrophy and mononeuropathy
simplex usually improve or resolve spontaneously.
Hypothyroidism
is a rare cause of polyneuropathy. More commonly, hypothyroidism is associated
with entrapment neuropathy, especially carpal tunnel syndrome. Polyneuropathy
may be mistakenly diagnosed in patients with proximal limb weakness caused by
hypothyroid myopathy or in patients with delayed relaxation of tendon reflexes,
a classic manifestation of hypothyroidism that is independent of neuropathy.
Other neurologic manifestations of hypothyroidism such as acute confusional
state , dementia , and cerebellar degeneration are discussed elsewhere.
Acromegaly
also frequently produces carpal tunnel syndrome and, less often,
polyneuropathy. Because many acromegalic patients are also diabetic, it may be
difficult to determine which disorder is primarily responsible for
polyneuropathy in a given patient.
A symmetric sensorimotor polyneuropathy, predominantly axonal in type,
may occur in uremia. It tends to affect the legs more than the arms and is more
marked distally than proximally. Restless legs, muscle cramps, and burning feet
have been associated with it. The extent of any disturbance in peripheral nerve
function appears to relate to the severity of impaired renal function. The
neuropathy itself may improve markedly with renal transplantation. Carpal
tunnel syndrome (see later) has also been described in patients with renal
disease and may develop distal to the arteriovenous fistulas placed in the
forearm for access during hemodialysis. In patients on chronic hemodialysis, it
often relates to amyloidosis and the accumulation of 
2-microglobulin.
2-microglobulin.
Primary biliary cirrhosis may lead to a sensory neuropathy that is
probably of the axonal type. A predominantly demyelinative polyneuropathy can
occur in patients with chronic liver disease. There does not appear to be any
correlation between the neurologic findings and the severity of the hepatic
dysfunction.
Vitamin B12 deficiency is associated with many features that
are characteristic of polyneuropathy, including symmetric distal sensory and
mild motor impairment and loss of tendon reflexes. Because controversy exists
about the relative importance of polyneuropathy and myelopathy in producing
this syndrome, vitamin B12 deficiency is considered in more detail
below in the section on myelopathies. It should be noted, however, that nolyradiculoneuropathy,
polyneuropathy, and myelopathy may follow bariatric surgery and relate to
nutritional deficiencies, including but not limited to vitamin B12.
