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The neurological complications of diabetes were first recognized in 1798, and until 1864, diabetes was considered an effect of neuropathy. y^ For discussion purposes, the neurological complications of diabetes can be divided into CNS, cranial nerve, and PNS disturbances, of which PNS disturbances predominate. These disorders involve different parts of the nervous system, and therefore, produce different clinical manifestations.

CENTRAL NERVOUS SYSTEM COMPLICATIONS OF DIABETES

The brain, although not frequently discussed as a target of the complications of chronic diabetes, is nonetheless affected by this disorder. In addition to the neurological complications of glycemic extremes previously discussed (see Hypoglycemia and Hyperglycemia), patients with diabetes have an increased stroke incidence, increased stroke severity, and possibly, a chronic encephalopathy. y] Regarding stroke, diabetes increases the risk of large, medium, and small vessel atheroma, as well as arteriolar and capillary microangiopathy, even after other concomitant risk factors (e.g., hypertension) are excluded. y^ In addition, studies have shown that the presence of hyperglycemia at the time of stroke results in more severe brain injury and, hence, a poorer stroke outcome (see Hyperglycemia). CNS abnormalities reported in patients with diabetes include increased P-300 latency, abnormal psychometric tests, and among children with diabetes, lower school achievement test scores.^ Potential causes for encephalopathy in patients with diabetes include vascular (e.g., stroke, altered BBB function, and cerebrovascular reactivity), metabolic (e.g., altered glycemia, ketosis, hypoxia, electrolyte changes, and neurotransmitter changes), and the co-existence of other disorders (e.g., hypertension, RF).^

Spinal cord abnormalities include infarction and pseudotabes diabetica. Pseudotabes diabetica reflects dorsal root ganglia disease, which, in turn, causes posterior column degeneration. Thus, this actually represents a disorder with a PNS onset resulting in secondary distal axon degeneration (i.e., the dying back phenomenon) causing posterior column degeneration.

CRANIAL NERVE COMPLICATIONS OF DIABETES

The cranial mononeuropathies complicating diabetes primarily involve the oculomotor nerves (i.e., oculomotor [cranial nerve (CN) III], trochlear [CN IV], and abducens [CN VI]). Facial neuropathy and anterior ischemic optic neuropathy are briefly discussed, because these items are reviewed elsewhere in this text. Although peripheral nerve infarction has been the presumed mechanism of cranial mononeuropathies among diabetic patients, microinfarction-induced fascicular disruption within the brain stem parenchyma has been identified in many of these patients. y] Diabetic oculomotor cranial mononeuropathies primarily involve CN III, followed by CN VI; CN IV is uncommonly affected alone. Clinically, patients notice the onset of eye pain or headache, followed by diplopia. The ophthalmoplegia reflects muscle weakness in the distribution of a single oculomotor nerve. Typically, in the setting of CN III involvement, pupillary sparing is noted. This likely reflects the peripheral location of the pupillomotor fibers, which are therefore supplied by external larger vessels, rather than internal small vessels. However, this is not always the case. Pupillary involvement is found in 10 to 20 percent of patients with vasculopathic (e.g., diabetes) cranial mononeuropathies and pupillary sparing is found in 8 to 15 percent of patients with aneurysms.^ , y^ Concerning the latter, pupillary involvement usually appears within 3 to 5 days. yj Even patients with complete paralysis tend to recover without residual weakness, usually within 3 months. y] Among patients with diabetes, facial mononeuropathies occur with increased frequency and a poor outcome may be observed.^ Thus, the facial mononeuropathy associated with diabetes may be secondary rather than idiopathic. Differences noted in diabetic patients with facial mononeuropathies support this statement and include (1) normal taste (argues for a different lesion site), (2) more frequent recurrent or bilateral facial nerve involvement, and (3) more frequent axon loss as the underlying pathophysiology rather than demyelinating conduction block, [1291 which explains the poorer outcome. Clinically, patients with CN II involvement and an anterior ischemic optic neuropathy suffer acute visual loss, visual field defects (usually inferior altitudinal), or both. Ophthalmologically, a pale and swollen optic disk (usually superiorly), accompanied by flame-shaped hemorrhages within the optic disk or

the peripapillary retina, is observed. In addition, most of these patients have a small optic disk, no central cup, and anomalous branching patterns of the optic disk vessels, a triad referred to as the disk at risk.^ Importantly, there is a 40-percent chance of a similar episode in the contralateral eye and a 2- to 4-percent chance of a recurrent episode in the same eye.W Among this patient population, the occurrence of diabetes mellitus is increased (20 percent). W However, this may reflect the increased prevalence of hypertension among the diabetic population.

PERIPHERAL NERVOUS SYSTEM COMPLICATIONS OF DIABETES

A great variety of PNS disorders are observed among patients with diabetes, and these disorders can be divided into focal, segmental, and generalized.

Focal Peripheral Nervous System Disorders. The focal PNS disorders include focal myopathies and mononeuropathies. The etiologies of focal myopathies include traumatic (associated with insulin injection injury) and vascular (related to thigh muscle infarction). Mononeuropathies may be divided into those affecting the cranial nerves (discussed earlier) and those affecting the somatic nerves. Somatic mononeuropathies result from entrapment or compression and nerve infarction. Entrapment and compression tend to occur in the same nerves and at the same sites as among the nondiabetic population-median mononeuropathies at the wrist (i.e., CTS), ulnar mononeuropathies at the elbow, and common peroneal mononeuropathies at the fibular head. The prevalence of CTS among diabetics, as among the nondiabetic population, increases in the presence of polyneuropathy. [130] An increased incidence of ulnar neuropathy also exists, whereas the occurrence of a common peroneal mononeuropathy at the fibular head is likely coincident. W Concerning the lower extremity, although femoral mononeuropathies are the most frequently reported lower extremity mononeuropathies among diabetic patients, they are extremely rare. The initial publications on diabetic femoral neuropathies likely represent mislabeled diabetic amyotrophy (discussed later), and in subsequent publications, these authors noted that the lesions were located more proximally. W Thus, common peroneal mononeuropathies are the most common lower extremity mononeuropathy. These lesions occur unilaterally or bilaterally and can be caused by either compression or nerve infarction. '129] Regarding patients with nerve infarction, the onset is acute and painful, the pathophysiology reflects axon loss, and recovery is often slow and suboptimal. The poor outcome reflects several features, including (1) the lesions tend to be complete, and robust collateral sprouting cannot occur; (2) the lesions tend to involve the nerve trunks proximally or in their midportion, and the distance required for proximodistal regeneration is greater; and (3) the lesions tend to occur in elderly patients. W Unlike nerve infarction, which produces solely axon loss, compressive lesions may produce demyelinating conduction block, axon loss, or a combination of the two, and therefore, it is not unexpected that, in general, patients with compressive lesions tend to have a better outcome. Except for an attempt to control the serum glucose concentration better, the mononeuropathies occurring among diabetic patients are treated in the same manner as those occurring among nondiabetic patients.

Segmental Peripheral Nervous System Disorders.The diabetic polyradiculopathy syndromes belong to this category. The term diabetic myelopathy was introduced by Bruns in 1890 and was displaced by Garland in 1955 when it became clinically and pathologically apparent that the disease process was not a myelopathy. [123] Garland suggested the intentionally nonlocalizing term diabetic amyotrophy. Several years later, Sullivan suggested the term asymmetrical (motor) proximal neuropathy, variations of which appear in most current discussions. [131] Historically, at least 20 synonyms for this entity have been used, which is a reflection of its varied presentations.^ The term diabetic thoracoabdominal neuropathy (discussed later) has at least 10 synonyms. W In 1981, Bastron and Thomas proposed the more general term diabetic polyradiculopathy for all of the diabetic neuropathies other than distal symmetrical polyneuropathy, W thereby incorporating several of the various diabetic polyradiculopathy syndromes into a single entity (e.g., diabetic amyotrophy and diabetic thoracoabdominal neuropathy). In addition, they coined the term territorial extension to describe the cephalad, caudal, or contralateral progression of this process from the root region to another. Based on this framework, Wilbourn drew several important conclusions, including (1) the root level is primarily attacked; (2) single or contiguous roots are attacked most severely; (3) territorial extension occurs in approximately two thirds of patients; (4) some root regions are more likely to be affected than others; (5) when uncommon root regions are involved, they generally follow involvement of the more typical root region; (6) the predominant pathophysiology is axon loss; and (7) the majority of patients have co-existing diabetic distal symmetrical polyneuropathy (DdSPN). W Thus, the commonly observed diabetic amyotrophy reflects isolated root involvement of the L2-L4 root levels, whereas diabetic thoracoabdominal neuropathy reflects isolated root involvement of the mid- to lower thoracic root levels. Also, when patients with diabetic amyotrophy develop foot drop, it most likely reflects territorial extension into the L5 level, and should it progress more caudally, global leg muscle involvement will develop. Bilateral shoulder girdle weakness is occasionally observed. [129]

Generalized Peripheral Nervous System Disorders. Disorders included in this category are DDSPN and diabetic autonomic neuropathy. DDSPN is the most common form of diabetic neuropathy and resembles the polyneuropathies caused by numerous other disorders. Different diagnostic criteria and methods of detection, applied to patients with diabetes of varying duration (i.e., patient selection bias), have lead to a wide variation in its reported incidence and prevalence. Typically, paresthesias and numbness begin in the toes and ascend proximally in a stocking-like distribution. When the ascent reaches the upper tibia, the hands begin to become involved. Once involved, the upper extremity disturbance also progresses proximally, in a glovelike distribution. This distribution pattern, in which the longest nerves are first affected, is often referred to as a dying-back neuropathy. At this time, diminished or absent ankle reflexes and foot intrinsic muscle weakness are evident. Even anhidrosis follows this pattern, which typically begins in the foot and predisposes patients to foot ulcers.

The electrodiagnostic abnormalities also show a distal to proximal gradient. The most sensitive NCS are the plantar mixed NCS, followed by the superficial peroneal and sural sensory NCS, followed by the upper extremity sensory NCS. The motor NCS abnormalities and needle electrode examination abnormalities follow this same pattern. When one considers that a nerve is made of sensory, motor, and autonomic axons ranging in size from small to large, it is easy to envision the range of clinical symptoms this disorder produces. Small fiber sensory disruption causes loss of pain and temperature perception, as well as more prevalent features of dysautonomia. Large fiber sensory involvement impairs proprioception, vibratory perception, gait (sensory ataxia), and reflexes. Motor axon dysfunction produces weakness, and autonomic axon involvement produces various dysautonomic features. Occasionally, patients present with disproportionate small fiber or large fiber sensory involvement or autonomic involvement. As pointed out by Dyck and colleagues, a continuum of fiber involvement is most common, with the disproportionate cases representing the extremes of a normal distribution. '123] , W Thus, diabetic autonomic neuropathy can present in isolation, although uncommonly; and the symptoms reflect the wide distribution of autonomic fibers: pupillary (miotic pupils with sluggish light reflex), cardiovascular (resting tachycardia, orthostatic hypotension), GI (constipation), genitourinary (impotence, reduced vaginal lubrication), and sudomotor (distal anhidrosis) systems. [125] The symptoms, evaluation, and management of diabetic autonomic neuropathy have been reviewed.'^ Hyperglycemic polyneuropathy refers to transient, distal paresthesias or dysesthesias occurring just before the diagnosis of diabetes or following ketoacidotic coma. The treatment of painful diabetic neuropathy is often the major management problem and can be challenging. For mild cases, simple analgesics may suffice, as may cold water soaks and the use of support stockings for evening pain. The potential for nephrotoxicity limits the usefulness of chronic nonsteroidal anti-inflammatory drugs, and the potential for addiction (as well as the occurrence of tolerance) limits the utility of narcotics. Tricyclic antidepressants, such as amitriptyline and nortriptyline, desipramine, carbamazepine (perhaps the drug of choice if the pain is lancinating or paroxysmal), and mexiletine have been shown to be of value. The anticholinergic side effects associated with the tricyclic antidepressants limit their utility for patients with accompanying autonomic dysfunction. These agents, as well as others, have been reviewed. '125]

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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