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Orthostatic tachycardia is a poorly understood syndrome in which patients develop dizziness, diaphoresis, or palpitations upon shifting from the supine to the upright posture. The present study was performed to determine whether autonomic neuropathy might be present in these patients, and whether the abnormal hemodynamic response to standing might be the result of failure of reflex vasoconstriction. We measured autonomic function in 9 patients with idiopathic orthostatic tachycardia and 2 patients with orthostatic tachycardia and insulin-dependent diabetes mellitus and compared them to 33 age-matched controls. Although most patients with orthostatic tachycardia had normal vasomotor reflexes and normal surface potential amplitudes, the latency of the autonomic response, a measure of sympathetic nerve conduction velocity, was prolonged in the soles (2.44 +/- 0.08 s in patients with idiopathic orthostatic tachycardia vs. 2.12 +/- 0.04 s in controls; P less than 0.005). In 6 of 9 patients, however, the latencies were within the normal range. Autonomic surface potentials were absent in 1 diabetic patient with orthostatic tachycardia; the latency of the response in the feet was greatly prolonged (2.95 s) in the second patient. We also assessed the response of orthostatic tachycardia patients to octreotide and dihydroergotamine, which are known to have a pressor effect in patients with recognized forms of autonomic neuropathy. These agents, in combination, suppressed orthostatic tachycardia (from 116 +/- 7 to 89 +/- 6 beats/min; P less than 0.001) in patients with this syndrome. In summary, our data indicate that evidence of autonomic dysfunction is present in only a minority of patients with orthostatic tachycardia. Nevertheless, administration of the vasoconstrictor drugs dihydroergotamine and octreotide can prevent the abnormal hemodynamic response to the upright posture shown by patients with this syndrome.
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PMID:The orthostatic tachycardia syndrome: evaluation of autonomic function and treatment with octreotide and ergot alkaloids. 204 64

Autonomic neuropathy is now well established as a relatively common and significant complication of diabetes mellitus. Its importance has been clarified in recent years during which the extent of autonomic control over all areas of body function has been defined. Using simple cardiovascular reflex tests, autonomic abnormalities can be demonstrated without any corresponding symptoms. The often stated concept of 'patchy' involvement in diabetic autonomic neuropathy should now be rejected as too should the view that autonomic neuropathy is either 'present' or 'absent' based on a single test result. When generalized and predominantly metabolic disturbances, as in diabetes, give rise to impaired nerve function, autonomic as well as somatic components of the nerve are affected. Where damage is severe this leads to the characteristic florid picture of symptomatic autonomic neuropathy with its particularly poor prognosis. For the physician in a busy clinic, much of the theoretical and experimental basis for autonomic neuropathy may not appear of direct relevance. However, he has now to be aware of the clinical implications of autonomic damage in the diabetic. This may have particular relevance in the care of the diabetic foot (see Chapter 10), the recognition of many of the vague symptoms associated with autonomic damage, the treatment of disabling features such as postural dizziness and nocturnal diarrhoea, and an awareness of the poor prognosis associated with symptomatic autonomic neuropathy. He will also need to be alert to the dangers of general anaesthesia in such patients, and the possibility of sudden unexpected deaths. Diabetic autonomic neuropathy causes widespread abnormalities, some of which are clinically apparent, some of which can be detected by sensitive tests, and others which have yet to be discovered. Inclusion of the neuropeptides and other hormones within the compass of autonomic control has opened up a whole new area of investigative interest, with many complex interrelationships which still need to be unravelled. This should lead to better understanding of the pathophysiological processes that cause damage to diabetic nerves. With so much research effort directed towards better glycaemic control and aldose reductase inhibitors (see Chapter 8), it may eventually be possible to reverse or prevent this potentially disabling and lethal complication of diabetes.
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PMID:Autonomic neuropathy: its diagnosis and prognosis. 353 3

Neurogenic orthostatic hypotension is a severely disabling condition due to deficient peripheral vasoconstrictor tone in response to the upright position and is characterized by a decrease in blood pressure upon standing associated with symptoms of lightheadedness, dizziness, visual "white-out", weakness, lack of energy, near syncope or even syncope. Previous pharmacologic treatment of neurogenic orthostatic hypotension has been problematic. Midodrine, a new specific alpha-1-agonist has been shown to produce arteriolar constriction and decrease in venous pooling via a constriction of venous capacitance vessels. Therefore, a recent multicenter study evaluated the safety and efficacy of midodrine therapy in 97 patients with neurogenic orthostatic hypotension due to various etiologies: Shy Drager syndrome (No. 18); Bradbury Eggleston syndrome (idiopathic orthostatic hypotension) (No. 20); diabetic autonomic neuropathy (No. 27); Parkinson's disease (No. 22); and miscellaneous (No. 10). Following one week of placebo therapy, the patients were randomized into 4 groups for a 4 week period of time; placebo, 2.5 mg, 5 mg, or 10 mg three times daily. The BE/SDS subgroup demonstrated a 27 +/- 8% (22 mmHg) increase in standing systolic blood pressure for the 10 mg dose. Diabetics achieved a significant increase at 5 mg. Similar increases were observed for the entire group on the 10 mg dose (p < 0.001). Symptoms or fainting, blurred vision, improved energy level, standing time, and depressed feelings were also significantly improved even at lower doses (p < 0.05 or less). Side effects were mild. Therefore, midodrine is an effective and safe agent for the treatment of neurogenic orthostatic hypotension.
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PMID:Midodrine in neurogenic orthostatic hypotension. A new treatment. 769 Mar 83

Postural hypotension is uncommon in diabetes but can occur secondary to autonomic neuropathy. Symptoms are rare and include dizziness, weakness, blurred vision, tiredness, and loss of consciousness. The pathophysiology of postural hypotension is not clear, but changes in intravascular volume, heart rate, cardiac output, and splanchnic vascular resistance are similar in patients and controls. The main factors producing hypotension are a blunted catecholamine response to standing, and failure of lower limb vascular resistance to increase adequately. Treatment for symptomatic postural hypotension includes avoidance of dehydration, adequate salt intake, and fludrocortisone. Other treatments are reviewed but are less helpful. Patients with postural hypotension have intermittent symptoms over the years but rarely become severely disabled. They have a poorer prognosis than patients with symptomatic autonomic neuropathy without postural hypotension.
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PMID:Postural hypotension in diabetic autonomic neuropathy: a review. 775 54

A 19-year-old woman with insulin-dependent diabetes mellitus (IDDM) of 3.5 years duration had been suffering from recurrent episodes of diabetic ketoacidosis (DKA), dizziness, and weight loss (16 kg, 29%) for 6 months. History and physical examination gave evidence of severe peripheral and autonomic neuropathy. Radionuclide retention on gastric emptying test at 60 min was greater than 90% (normal < 60%). On autonomic cardiovascular testing there was evidence of both parasympathetic and sympathetic damage. There was no evidence of nephropathy or retinopathy. Optimal diabetic control using 4 insulin injections (2 u/kg/day) and high-dose cisapride terminated the vomiting, and she regained the weight lost within 5 months. This case is unique in that severe diabetic neuropathy followed relatively soon after onset of disease, without other microvascular complications. The correct diagnosis of gastroparesis as the cause of the recurrent DKA and weight loss, and the specific prokinetic therapy and nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Specific prokinetic therapy and the nearly normoglycemic control of the diabetes led to dramatic clinical and functional improvement. Gastroparesis can cause recurrent DKA even in young patients with IDDM of short duration.
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PMID:[Severe neuropathy in a young diabetic]. 784 56

A cross-sectional study was designed to identify a relationship between the presence of symptoms usually related to nervous system involvement as well as other chronic complications of diabetes with three objectively defined degrees of autonomic neuropathy (AN). Symptoms usually related to peripheral sensitive neuropathy and AN were assessed using a questionnaire applied to 132 diabetics (38 IDDM and 94 NIDDM), 65 without and 67 with AN. AN was classified as follows according to 5 cardiovascular autonomic tests described by Ewing: 1) early involvement-1 abnormal test (N = 27); 2) definite involvement-2 or 3 abnormal tests (N = 26); 3) severe involvement-4 or 5 abnormal tests (N = 14). A statistically significant association was observed between degree of autonomic involvement and the presence of the following symptoms: dizziness on standing, dysphagia, vomiting, diarrhea, fecal incontinence, gustatory sweating, urinary retention, numbness and hyperesthesia of the feet or legs. Constipation and cystitis were not significantly related to cardiovascular AN. Only 3% of the patients without neuropathy and with early involvement had four or more than four of the symptoms. The prevalence of proliferative retinopathy and nephropathy was increased among patients with more severe degrees of AN. For IDDM patients there was a positive correlation between the degree of cardiovascular AN and the duration of diabetes. We conclude that: 1) severe cardiovascular AN is usually related to 4 or more of the evaluated symptoms and those patients usually have the other complications of diabetes; 2) severe AN could be a risk factor or an indicator of the same underlying process that determines the beginning of proliferative retinopathy and/or nephropathy.
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PMID:Relationship between the degree of cardiovascular autonomic dysfunction and symptoms of neuropathy and other complications of diabetes mellitus. 858 Aug 65

Orthostatic tachycardia is common but its specificity remains uncertain. Our preliminary work suggested that using autonomic function testing in conjunction with time-frequency mapping (TFM), it might be possible to characterize a subset of the postural tachycardia syndrome (POTS), that is due to a restricted autonomic neuropathy. We describe 20 patients (17 women and 3 men, aged 14-43 years) with florid POTS and 20 controls (14 women and 6 men, aged 20-41 years). Autonomic failure was quantified by its distribution (cardiovagal, adrenergic and sudomotor) and severity, a symptom profile was generated, and spectral indices, based on modified Wigner distribution during rest and head-up tilt (80 degrees) were evaluated. During tilt-up POTS patients differed from controls by an excessive heart rate (> 130 bpm) (P < 0.001), and higher diastolic pressure (P < 0.01). During rest, cardiovagal oscillations (at respiratory frequencies [RF]) and slow rhythms at nonrespiratory frequencies (NONRF) (from 0.01 to 0.07 Hz) in R-R intervals (RRI) (P < 0.01) were reduced. Both RF and NONRF rhythms in RRI were further blunted with tilt-up (P < 0.001). Slow adrenergic vasomotor rhythms in blood pressure (BP) (approximately 0.07 Hz) surged with tilt-up and returned to normal levels afterwards. The index of sympatho-vagal balance (NONRF-Systolic BP (SBP)/RF-RRI) was dramatically increased in POTS (P < 0.001). Distal postganglionic sudomotor failure was observed, and impairment of the BP responses to the Valsalva maneuver (phase II) suggested peripheral adrenergic dysfunction. Persistent orthostatic dizziness, tiredness, gastrointestinal symptoms and palpitations were common in POTS patients. It is possible to identify a subset of POTS patients who have a length-dependent autonomic neuropathy, affecting the peripheral adrenergic and cardiovagal fibers, with relative preservation of cardiac adrenergic fibers.
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PMID:Postural tachycardia syndrome: time frequency mapping. 898 90

The etiology of sympathotonic orthostatic hypotension (SOH) is still unknown. We reported a 50-year-old male case of SOH associated with herpes simplex encephalitis. Eight days before admission to our hospital, he noticed fever, which was followed by intractable hiccup. He was admitted to a local hospital, where nuchal rigidity and mononuclear CSF pleocytosis were noted. On the 9th hospital day, he suddenly developed respiratory arrest, and his consciousness state deteriorated to coma. He was transferred to our hospital with artificial ventilation on the same day. The second CSF examination revealed pleocytosis and positive herpes-simplex-virus antibody. CAT scan showed diffuse high density areas in the bilateral temporal lobes. Intensive anti-herpetic therapy was started. On the 14th hospital day, spontaneous respiration came back and consciousness state was improved from coma to stupor. He gradually recovered to alert state and became ambulatory by the 30th hospital day. Seven weeks after the onset of his illness, he noticed orthostatic dizziness for the first time during his rehabilitation exercises. Blood pressure was 116/78mmHg at supine position and 82/62mmHg at standing position, and the heart rate was 83bpm, and 141bpm, respectively. Plasma noradrenaline concentration was 0.09 ng/ml (within normal range) at supine position, but increased to 0.29ng/ml upon standing. Catecholamine infusion tests revealed hyposensitivity in beta 2-receptors; decrease in blood pressure in response to isoprenaline was blunted, while increase of blood pressure to noradrenaline was not impaired. Nerve conduction studies and sweating tests were normal. When he was discharged from our hospital on the 87th hospital day, he still had orthostatic symptoms. His complete recovery took full one year. Some authors claimed that SOH is an abortive form of acute autonomic neuropathy, while others postulated that it was due to unbalanced cardiovascular alpha- and beta-adrenoceptor functions. SOH of the present case seems to be caused by the central nervous lesions; especially, the brain stem involvement due to herpes simplex encephalitis may well be causing SOH.
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PMID:[A case of sympathotonic orthostatic hypotension following herpes simplex encephalitis]. 899 41

Arrhythmias are frequent among the dialysis population and can cause symptoms of palpitations or dizziness. Since autonomic disturbances are known to cause an increased arrhythmogenic stimulus, we questioned whether the presence of central autonomic neuropathy increased the frequency of arrhythmias as identified by 24-hour electrocardiographic monitoring in dialysis patients. Seventy-one patients were randomly chosen from patients established on dialysis in two centers. The mean age of the patients was 71.3 years (median age, 67 years) and median duration on dialysis was 17.0 months (range, 1 to 175 months). Four patients had diabetes. Each patient was tested for autonomic control of blood pressure and heart rate, and underwent Holter electrocardiographic monitoring, commencing 30 minutes before dialysis, for a 24-hour period. The tapes were then analyzed for ventricular and atrial rhythm changes. There was a significantly increased incidence of arrhythmias in individuals with abnormal blood pressure responses (P = 0.005), heart rate responses (P = 0.01), and combined blood pressure and heart rate responses (P = 0.004). We conclude that patients with autonomic dysfunction had an increased frequency of arrhythmias during dialysis.
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PMID:Autonomic neuropathy predisposing to arrhythmias in hemodialysis patients. 926 Oct 32

Stimulated by the widespread use of head-up tilt testing, transient episodes of neurocardiogenically mediated hypotension and bradycardia have become a well recognized cause of recurrent syncope and near syncope (generally referred to as neurally mediated syncope). On the other hand, a large subgroup of patients was identified, who appeared to have a less severe hypotension and orthostatic intolerance that is characterized by postural tachycardia, exercise intolerance, disabling fatigue, lightheadedness and dizziness. This form of disability has been recognized as postural orthostatic tachycardia syndrome (POTS). While the etiology of POTS is still unclear, a mild form of idiopathic peripheral autonomic neuropathy (partial dysautonomia) or beta-receptor hypersensitivity has been suggested for the pathophysiology of this disorder. A detailed history and physical examination that includes a careful neurologic examination are essential for diagnosis. Head-up tilt testing is often useful as a standardized measure of response to postural change. This review summarizes the history, current knowledge of clinical features, diagnosis and therapeutic strategies.
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PMID:[Idiopathic postural orthostatic tachycardia syndrome] 1101 90


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