These are transient neuropathic syndromes characterized by an acute onset of pain in the lower limbs. Acute neuropathies present in a symmetrical fashion are relatively uncommon. Pain is invariably present and is usually distressing to the patient, and can sometimes be incapacitating. There are two distinct syndromes, the first of which occurs within the context of poor glycemic control, and the second with rapid improvements in metabolic control (43).
This may occur in the context of type 1 or type 2 diabetic subjects with poor glycemic control. There is no relationship to the presence of other chronic diabetic complications. There is often an associated severe weight loss (44). Ellenberg coined the description of this condition as "neuropathic cachexia" (45). Patients typically develop persistent burning pain associated with allodynia (contact pain). The pain is most marked in the feet, but often affects the whole of the lower extremities. As in chronic distal symmetrical neuropathy, the pain is typically worse at night although persistent pain during day time is also common. The pain is likened to "walking on burning sand" and there may be a subjective feeling of the feet being "swollen." Patients also describe intermittent bouts of stabbing pain that shoot up the legs from the feet (peak pain), superimposed on the background of burning pain (background pain). Not surprisingly therefore, these disabling symptoms often lead to depression (21,43).
On examination, sensory loss is usually surprisingly mild or even absent. There are usually no motor signs, although ankle jerks may be absent. Nerve conduction studies are also usually normal or mildly abnormal. However, temperature discrimination threshold (small-fibre function) is affected more commonly than vibration perception threshold (large-fibre function) (46). There is usually complete resolution of symptoms within 12 months, and weight gain is usual with continued improvement in glycemic control with the use of insulin. The lack of objective signs should not raise the doubt that these painful symptoms are not real. Many patients feel that people including health care professionals do not fully appreciate their predicament.
Acute Painful Neuropathy of Rapid Glycemic Control (Insulin Neuritis)
The term "insulin neuritis" was coined by Caravati (47) who first described the syndrome of acute painful neuropathy of rapid glycemic control. The term is a misnomer as the condition can follow rapid improvement in glycemic control with oral hypo-glycemic agents, and "neuritis" implies a neural inflammatory process for which there is no evidence. The author has therefore recommended that the term "acute painful neuropathy of rapid glycemic control" be used to describe this condition (48).
The natural history of acute painful neuropathies is an almost guaranteed improvement (49) in contrast to chronic distal symmetrical neuropathy (36). The patient presents with burning pain, paraesthesiae, allodynia, often with a nocturnal exacerbation of symptoms; and depression may be a feature. There is no associated weight loss, unlike acute painful neuropathy of poor glycemic control. Sensory loss is often mild or absent, and there are no motor signs. There is little or no abnormality on nerve conduction studies, but there is impaired exercise induced conduction velocity increment (48,50). There is usually complete resolution of symptoms within 12 months.
On sural nerve biopsy, typical morphometric changes of chronic distal symmetrical neuropathy but with active regeneration, were observed (49). In contrast, degeneration of both myelinated and unmyelinated fibres was found in acute painful neuropathy of poor glycemic control (44). A recent study looking into the epineurial vessels of sural nerves in patients with acute painful neuropathy of rapid glycemic control demonstrated marked arterio/venous abnormality including the presence of proliferating new vessels, similar to those found in the retina (48). The study suggested that the presence of this fine network of epineural vessels may lead to a "steal" effect rendering the endoneurium ischaemic, and the authors also suggested that this process may be important in the genesis of neuropathic pain (48). These findings were also supported by studies in experimental diabetes, which demonstrated that insulin administration led to acute endoneurial hypoxia, by increasing nerve arterio-venous flow, and reducing the nutritive flow of normal nerves (51). Further work needs to address whether these observed sural nerve vessel changes resolve with the resolution of painful symptoms.
Was this article helpful?