Diabetic, alcoholic, toxic and small fiber sensory neuropathy (SFSN)

Types of polyneuropathies (polyneuritis)

Diabetic polyneuropathy

Diabetic polyneuropathy is a type of nerve damage resulting from the intoxication of the body as a whole as a result of an impaired tissue metabolism in patients with diabetes mellitus. The leading factor in the onset of diabetic neuropathy (polyneuropathy) is angiopathy concomitant with diabetes, which leads to an impaired regional blood circulation.

Depending on the level of nerve damage in diabetic neuropathy (polyneuropathy) and alcoholic polyneuritis, sensitivity disorders (numbness, tingling, burning sensation), pain and muscle weakness in the patient will be at different levels.

Microvascular complications of diabetes mellitus:

Retinopathy	Neuropathy	Nephropathy
Cotton balls (cotton-like exudate) Retinal hemorrhage Retinal vascular microaneurysms Thickening of the macula (macular edema)	Peripheral neuropathy: Increase or decrease in pain sensations (hyper- and hypoesthesia) Painless injuries Decreased reflexes Autonomic neuropathy: Resting tachycardia Frequent urination Erectile dysfunction	Glomerulosclerosis Pyelonephritis

 

Macrovascular complications of diabetes mellitus:

Coronary complications	Cerebrovascular complications	Peripheral vascular disease
Chest pain Congestive (chronic) heart failure Dyspnoea	Intracerebral hemorrhage Cerebral infarction Memory impairment	Atherosclerosis Gangrene Trophic ulcers on the skin surface

 

Alcoholic polyneuropathy

Alcoholic polyneuropathy is a type of nerve damage that occurs in patients with long-term alcohol abuse.

 

Toxic polyneuropathy, chemotherapy-induced polyneuropathy

Most toxic polyneuropathies manifest as distal axonal degeneration, which develops gradually over time in the patient. The causes of toxic polyneuropathy are varied and include medications, heavy metals, production factors, and environmental substances. Newer anticancer drugs, antiretrovirals, or overuse of other medications (especially pyridoxine (vitamin B6)) can also cause toxic polyneuropathy. When assessing the patient's condition, a relationship is usually noted between the time of administration and the dosage of a toxic substance with the onset of clinical manifestations of toxic neuropathy. In general, the introduction of small doses of the drug over a long period is less toxic to the body than its large doses, administered over a short period, even if the total of these doses is equal.

The onset of the disease (after the introduction of a toxic agent) with subsequent recovery or at least a delay in the further development of the pathological process (after the termination of the administration of the toxin) is the best evidence of the presence of toxic polyneuropathy (along with other symptoms and signs typical of neuropathy caused by the putative toxic substrate). Neuropathy may initially appear and may continue to progress after the administration of the toxic substance is discontinued. This phenomenon of the development of a pathological process by inertia occurs when taking anticancer drugs platinum, benzene drugs, inhibitors of nucleoside reverse transcriptase, or pyridoxine (vitamin B6).

Clinical analysis of the history of the disease includes identifying the relationship between the moment the toxin enters the patient's body and the onset of the occurrence:

• motor and sensory symptoms of nerve damage
• another concomitant disease that can cause toxic neuropathy
• symptoms of general intoxication

A nerve biopsy sometimes reveals signs that are characteristic of this type of nerve injury:

• osmophilic inclusions in the Schwann cell during intoxication with amiodarone, perxylin, and chloroquinoline (a synthetic analogue of quinoline, used to treat malaria)
• perinodular axonal massive edema with benzene neuropathy

Certain toxins can be detected in certain types of body tissues:

• heavy metals can be detected in urine (arsenic, thallium), hair, and nails (arsenic)
• laboratory analysis of the level of the administered drugs in the blood plasma can also be useful in establishing the diagnosis of toxic neuropathy

 

Small fiber sensory neuropathy (SFSN)

Small fiber sensory neuropathy (SFSN) is a disorder in which only the small sensory cutaneous nerves are affected. The majority of patients experience sensory disturbances that start in the feet and progress upwards. These patients have what is called a length-dependent SFSN. This type of SFSN is often due to diabetes or impaired glucose metabolism (i.e., early or pre-diabetic state) and may progress to typical diabetic polyneuropathy. However, in a significant percentage of patients, no underlying etiology is found and the patients have idiopathic SFSN. A small percentage of patients with SFSN experience sub-acute onset sensory disturbances diffusely over the whole body, including the trunk and sometimes even the face. These patients have non-length-dependent SFSN and almost all cases are idiopathic.

 

Symptoms

The symptoms of small fiber sensory neuropathy are primarily sensory in nature and include unusual sensations such as pins-and-needles, pricks, tingling, and numbness. Some patients may experience burning pain or coldness and electric shock-like brief painful sensations. Since SFSN usually does not involve large sensory fibers that convey balance information to the brain or the motor nerve fibers that control muscles, these patients do not have balance problems or muscle weakness. In most patients, these symptoms start in the feet and progress upwards. In advanced cases, it may involve the hands.

 

Diagnosis

Diagnosis of SFSN is based on history, clinical examination, and supporting laboratory investigations. Electromyography and nerve conduction studies are done to eliminate the involvement of motor and large sensory nerve fibers. Skin biopsies are used to confirm the loss of cutaneous nerve innervation. Nerve and muscle biopsies are rarely needed.

 

Treatment

Treatment of SFSN depends on the underlying etiology. If it is due to diabetes or a pre-diabetic state, then optimum diabetic control and exercise, and weight loss to reduce insulin resistance are needed. Painful sensory paresthesias can be treated with anti-seizure medications, antidepressants, or analgesics including opiate drugs. In severe painful conditions, patients may be referred to the Blaustein Chronic Pain Clinic for a multidisciplinary approach to pain management.