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PubMed2005

Clinical management of oxaliplatin-associated neurotoxicity.

In recent years, oxaliplatin-based chemotherapy protocols, particularly oxaliplatin in combination with infusional 5-fluorouracil/leucovorin (FOLFOX or FUFOX), have emerged as the standard of care in first- and second-line therapy of advanced-stage colorectal cancer. Although oxaliplatin by itself has only mild hematologic and gastrointestinal side effects, its clinically dominating toxicity affects the peripheral sensory nervous system in the form of 2 distinct types of neurotoxicity: (1) a unique, frequent, acute sensory neuropathy that is triggered or aggravated by exposure to cold but at the same time is rapidly reversible without persistent impairment of sensory functions; (2) the dose-limiting toxicity of oxaliplatin, a cumulative, chronic sensory neurotoxicity that resembles that of cisplatin with the important difference of its being more rapidly and completely reversible. This chronic sensory neurotoxicity is highly predictable, being closely associated with the cumulative dose of oxaliplatin that is administered. Various strategies have been proposed to prevent or treat oxaliplatin-induced neurotoxicity. The stop-and-go concept uses the predictability and reversibility of neurologic symptoms to allow patients to stay on an oxaliplatin-containing first-line therapy for a prolonged period. Several neuromodulatory agents such as calcium-magnesium infusions; antiepileptic drugs like carbamazepine, gabapentin, and venlafaxine; amifostine; a-lipoic acid; and glutathione have demonstrated some activity in the prophylaxis and treatment of oxaliplatin-induced acute neuropathy. However, randomized trials demonstrating a prophylactic or therapeutic effect on oxaliplatin's cumulative neurotoxicity are still lacking. The predictability of neurotoxicity associated with oxaliplatin-based therapy should allow patients and doctors to develop strategies to manage this side effect in view of the individual patient's clinical situation. This is of increasing importance, because the addition of bevacizumab to FOLFOX will conceivably further prolong the progression-free survival achieved with FOLFOX so that neurotoxicity and not tumor progression could become the dominating treatment-limiting issue in the first-line therapy of advanced colorectal cancer.

Antineoplastic Agents↗

PubMed1999

Anatomical but not functional recovery from a sciatic nerve crush is enhanced by treatment with testosterone.

PURPOSE: Until recently, there has been a limited amount of research comparing functional and anatomical recovery following nerve injury. Previous studies emphasizing anatomical recovery (such as axonal number) have shown that testosterone promotes regeneration in crushed and transected nerves. The purpose of this study was to assess the effect of testosterone on the functional recovery of the sciatic nerve follow-ing a unilateral crush injury. METHODS: Young adult male Sprague-Dawley rats were injected daily with either 500 micro g testosterone proprionate or vehicle alone. The recovery course was followed for six weeks using functional and behavioral testing. Behavioral tests included a footprint gait analysis (as a measure of motor function), response to a skin pinch, and warm water withdrawal (measures of sensory function). RESULTS: Immediately following surgery, all tests indicated complete denervation to the leg distal to the crush site. Anatomical analysis revealed a 22 % increase in the number of axons in testosterone treated animals at 6 weeks post-crush, but no indication of differences in functional recovery. The results of behavioral testing indicated only minor differences in functional recovery as a result of testosterone treatment. CONCLUSION: The results indicate the need for a detailed comparison between anatomical regeneration and functional recovery. An increase in axon number alone may not be an accurate indicator of successful regeneration.

Journal Article↗

PubMed1985

[Reticular structures of the cat brain participating in startle reflexes in response to somatic stimuli of different modalities].

Characteristics and reticular mechanisms of two types of late reflex responses (equivalents of the startle reflex) evoked by weak (tactile stimuli) and strong (high-threshold peripheral nerve stimulation) stimulations were studied in chloralose-anesthetized cats; these responses were designated as "tactile" (T) and "spino-bulbo-spinal" (SBS) reflexes, respectively. Some differences in the peripheral and central (brainstem) organization of these reflexes were found. In particular, the existence of the rostro-caudal differentiation of reticular structures involved in these types of reflexes was revealed using differential lesions of the brainstem reticular formation as well as its pharmacologic blockades (by means of microinjections of sodium chloride or procaine); the T-reflex was found to relay mainly through the pontine RF level, while the SBS-reflex--predominantly through the bulbar RF. Possible functional significance of the revealed differentiation in organization of some motor and sensory functions of the brainstem are discussed.

Animals↗

PubMed2000

Sensorimotor organization in patients who have undergone hemispherectomy: a study with (15)O-water PET and somatosensory evoked potentials.

To identify cortical structures that subserve residual motor and sensory function in patients with congenital hemiparesis due to a porencephalic cyst, we examined, using [(15)O]H2O, PET and somatosensory evoked potentials (SEPs) in three patients with left-sided hemiparesis who had undergone hemispherectomy. Motor stimulation of the affected hand produced ipsilateral activation in the premotor area in all patients, the SMA in two patients, and SII in two patients. Vibrotactile stimulation resulted in activation of the ipsilateral SII in all subjects. Median nerve stimulation of the affected hand produced ipsilateral long-latency SEPs in fronto-centro-parietal areas, whereas stimulation of the non-affected hand produced normal early cortical potentials in the contralateral hemisphere. Our results suggest that residual function in the paretic hand is warranted through non-primary motor and sensory areas, and higher order associative areas in the intact hemisphere.

Adult↗

PubMed2005

Sensory and motor function of the esophagus: lessons from ultrasound imaging.

Catheter-based high-frequency intraluminal ultrasound imaging is a powerful tool to study esophageal sensory and motor function and dysfunction in vivo in humans. It can be combined with manometry, pH, and impedance measurement techniques to determine the relationships between different physiologic parameters. High-frequency intraluminal ultrasound imaging has provided a number of important insights regarding the longitudinal muscle function of the esophagus. On the basis of the ultrasound images and intraluminal pressure recordings, it seems that there is synchrony in the timing and the amplitude of contraction between the circular and longitudinal muscle layers. A sustained contraction of the longitudinal muscle layer is temporally related to esophageal chest pain and heartburn. The biomechanics of the esophageal wall and its relationship to sensory and motor function can be studied in humans in vivo by using high-frequency intraluminal ultrasound much more precisely than has previously been possible. Achalasia, diffuse esophageal spasm, and nutcracker esophagus are associated with hypertrophy of circular and longitudinal muscle layers. Finally, high-frequency intraluminal ultrasound imaging is the only technique that can detect reflux-related distention of the esophagus and its role in esophageal symptoms. Future approaches to display and quantify ultrasound image data are discussed. The principles of high-frequency intraluminal ultrasound described here are also applicable to study of the motor and sensory function of the other regions of the gastrointestinal tract.

Esophageal Sphincter, Upper↗

PubMed2005

Different contributions of ASIC channels 1a, 2, and 3 in gastrointestinal mechanosensory function.

AIMS: Members of the acid sensing ion channel (ASIC) family are strong candidates as mechanical transducers in sensory function. The authors have shown that ASIC1a has no role in skin but a clear influence in gastrointestinal mechanotransduction. Here they investigate further ASIC1a in gut mechanoreceptors, and compare its influence with ASIC2 and ASIC3. METHODS AND RESULTS: Expression of ASIC1a, 2, and 3 mRNA was found in vagal (nodose) and dorsal root ganglia (DRG), and was lost in mice lacking the respective genes. Recordings of different classes of splanchnic colonic afferents and vagal gastro-oesophageal afferents revealed that disruption of ASIC1a increased the mechanical sensitivity of all afferents in both locations. Disruption of ASIC2 had varied effects: increased mechanosensitivity in gastro-oesophageal mucosal endings, decreases in gastro-oesophageal tension receptors, increases in colonic serosal endings, and no change in colonic mesenteric endings. In ASIC3-/- mice, all afferent classes had markedly reduced mechanosensitivity except gastro-oesophageal mucosal receptors. Observations of gastric emptying and faecal output confirmed that increases in mechanosensitivity translate to changes in digestive function in conscious animals. CONCLUSIONS: These data show that ASIC3 makes a critical positive contribution to mechanosensitivity in three out of four classes of visceral afferents. The presence of ASIC1a appears to provide an inhibitory contribution to the ion channel complex, whereas the role of ASIC2 differs widely across subclasses of afferents. These findings contrast sharply with the effects of ASIC1, 2, and 3 in skin, suggesting that targeting these subunits with pharmacological agents may have different and more pronounced effects on mechanosensitivity in the viscera.

Acid Sensing Ion Channels↗

PubMed1991

The effects of 2,4-dithiobiuret on sensory and motor function.

2,4-Dithiobiuret (DTB) exposure causes a delayed onset muscle weakness in rats that has been attributed to depressed neuromuscular transmission. The present study compares the effects of DTB on both sensory and motor function in rats. Adult male Long-Evans hooded rats were exposed to saline, 0.25, 0.5, or 1.0 mg/kg/day DTB, ip, for 5 consecutive days (Days 1-5). Body weights were monitored throughout the experiment. Motor activity was measured for 1 hr in figure-eight mazes on Days 0, 6, 13, and 27. Forelimb and hindlimb grip strength were assessed on Days 6, 13, and 27. Auditory thresholds were determined for 5- and 40-kHz tones using reflex modification of the startle response on Days 0, 7, 14, and 28. Visual function was examined on Day 6 in animals exposed at 0.5 mg/kg/day using flash- and pattern-elicited visual evoked potentials (FEPs and PEPs, respectively). Thermal sensitivity was measured using the hot plate procedure. All motor endpoints were decreased in a dosage- and time-dependent manner; the higher the dosage the longer the effects lasted. There were no effects on any measure of sensory function with the exception of peak N2 of the FEP. Both the amplitude and latency of FEP N2 were altered by DTB exposure. Decreases in body weight were maximal on Day 9 at 1.0 mg/kg/day (20% from control), but recovered by Day 22. Motor activity was suppressed on Day 6 only, whereas grip strength measures were decreased on both Days 6 and 13. Auditory thresholds were not significantly altered; however, baseline startle amplitude was decreased at the highest dosage on Days 7 and 14, but recovered by Day 28. Hot plate latencies were not altered by DTB treatment. These data demonstrate that DTB produces a reversible impairment of motor function, without altering auditory, thermal, or pattern visual function. FEP N2, which is thought to arise from activity generated in the superficial layers of visual cortex, was diminished by DTB treatment, indicating that DTB can alter the function of the CNS, although effects on the motor system are more pronounced.

Animals↗

PubMed2004

Gastrointestinal pain in functional bowel disorders: sensory neurons as novel drug targets.

Functional bowel disorders (FBDs) are defined by symptoms of gastrointestinal (GI) dysfunction, discomfort and pain in the absence of a demonstrable organic cause. Since the prevalence of FBDs, particularly functional dyspepsia and irritable bowel syndrome, can be as high as 20%, FBDs represent a significant burden in terms of direct healthcare and productivity costs. There is emerging evidence that the discomfort and pain experienced by many FBD patients is due to persistent hypersensitivity of primary afferent neurons, which may develop in response to infection, inflammation or other insults. This concept identifies vagal and spinal sensory neurons as important targets for novel therapies of GI hyperalgesia. Sensory neuron-specific targets can be grouped into three categories: receptors and sensors at the peripheral nerve terminals, ion channels relevant to nerve excitability and conduction and transmitter receptors. Particular therapeutic potential is attributed to targets that are selectively expressed by afferent neurons, such as the transient receptor potential channel TRPV1, acid-sensing ion channels and tetrodotoxin-resistant Na + channels.

Analgesics↗

PubMed2000

Differences in gastric mechanosensory function after repeated ramp distensions in non-consulters with dyspepsia and healthy controls.

BACKGROUND: Abnormal visceral mechano-sensory function has been reported in 50% of non-ulcer (functional) dyspepsia patients. However, only a minority of subjects with functional dyspepsia ever seek medical attention. Whether factors promoting health care seeking behaviour explain visceral hypersensitivity is unknown. Decreased rectal thresholds following sigmoid mechanical stimulation have been observed in irritable bowel but this mechanism has not been evaluated in functional dyspepsia. AIMS: To compare visceral mechanosensory function in healthy asymptomatic subjects and non-consulters with chronic unexplained dyspepsia. METHODS: Forty two volunteers were recruited: 10 had a history of chronic or recurrent upper abdominal pain or discomfort as assessed by a standardised questionnaire, and Helicobacter pylori status was determined (ELISA and (13)C urea breath test). Eight H pylori negative, currently asymptomatic dyspeptic subjects who were non-consulters and eight asymptomatic age and sex matched H pylori negative controls were enrolled. With a barostat bag in the proximal part of the stomach, visceral perception thresholds were determined by random tracking. Thereafter, standardised ramp distensions were performed (2 mm Hg increments, duration of each pressure step 30 seconds, maximum pressure 35 mm Hg (or occurrence of pain)) and tracking of sensory thresholds and ramp distension repeated every 30 minutes for a total of two hours. RESULTS: Overall, thresholds for first perception were significantly lower in dyspeptic subjects compared with asymptomatic controls (12.5 (0.6) mm Hg v 17.5 (1.0) mm Hg; p<0.02). After repeated ramp distensions, thresholds for first perception significantly increased by 3.6 (0.7) mm Hg in healthy subjects compared with 0.1 (1.4) mm Hg in subjects with dyspepsia (p<0.05 dyspeptics v controls). CONCLUSIONS: (1) Repeated mechanical stimulation increases visceral sensory thresholds in asymptomatic subjects while thresholds remain unchanged in dyspeptics. (2) Visceral hyperalgesia occurs in dyspeptic subjects who are not health care seekers.

Adult↗

PubMed2005

Dopaminergic influence on disturbed spatial discrimination in Parkinson's disease.

Various sensory symptoms and disturbed sensory perception are often observed in patients with idiopathic Parkinson's disease (PD). The basis of sensory disturbance in PD is unknown but possibly reflects a role for the basal ganglia in sensory processing. To investigate the relationship between the sensory dysfunction and dopaminergic deficiency in PD, we measured spatial discrimination using the Grating Orientation Task in 21 drug-naive patients with PD, before and after long-term antiparkinson therapy, and 25 age-matched healthy controls. The grating orientation threshold was significantly higher in patients (3.03 +/- 0.84) than controls (2.03 +/- 0.79). After 3 to 10 months of antiparkinson therapy, the grating orientation threshold was significantly lowered (2.66 +/- 0.84), although it was still higher than that in controls. Improvement in the patients' sensory function was significantly correlated with motor improvement (r = 0.44). These results suggest that sensory dysfunction in Parkinson's disease is related at least in part to the dopaminergic deficit.

Antiparkinson Agents↗

PubMed2001

Neuroprostheses for the upper extremity.

Functional electrical stimulation (FES) neuroprostheses can be used to replace lost motor and sensory function in persons with neurological disorders. FES technology has subsequently been shown effective and safe in restoring hand function in adults with spinal cord injury. The freehand system consists of an implanted receiver-stimulator, an external shoulder position sensor, and an external control unit. Commands are originated by voluntary movement of the contralateral shoulder and are measured by the sensor. There are several types of electrodes: epimysial, intramuscular, nerve cuff, and intraneural. Neuroprostheses are recommended within the context of all available reconstructive options for the upper limbs. Voluntary tendon transfers are the first choice. The clinical outcomes as measured by improvement on scales of impairment, activities of daily living, and satisfaction are rewarding. The next step in improvement of the motor function of person with spinal cord injury will be the addition of a controllable second upper extremity and the elimination of additional external hardware.

Animals↗

PubMed2007

Perceived control is a concurrent predictor of activity limitations in patients with chronic idiopathic axonal polyneuropathy.

OBJECTIVES: To investigate (1) whether control perceptions (person's perception of ease or difficulty of performing behavior) and emotions contribute to activity limitations and if so (2) whether these variables mediate the relation between impairment and activity limitations in patients with chronic idiopathic axonal polyneuropathy (CIAP). DESIGN: Cross-sectional study. SETTING: Outpatient clinics of a university medical center. PARTICIPANTS: Fifty-six patients diagnosed with CIAP. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Control perceptions about performing activities (questionnaire based on the theory of planned behavior), emotions (Hospital Anxiety and Depression Scale), activity limitations (performance: Shuttle Walk Test [SWT]; self-report: Medical Outcomes Study 36-Item Short-Form Health Survey [SF-36] physical functioning subscale, self-reported ability to walk), and physical impairments (muscle strength, sensory function). RESULTS: Control perceptions significantly (P<.01) correlated with all measures of activity limitations (r range, .58-.69). Hierarchical multiple regression analyses showed that perceived control explained 9% of the variance in the SWT (beta=.34, P<.01), 12% in the SF-36 (beta=.40, P<.01), and 24% in ability to walk (beta=.54, P<.01). In all measures of activity limitations, perceived control significantly mediated the effect of impairment. CONCLUSIONS: Perceived control explained and mediated variance in activity limitations, whereas emotions did not. This suggests that increasing patients' perceptions of control might enhance performance of activities, even without changes in impairment.

Activities of Daily Living↗

PubMed2006

Laryngeal inflammation assessed using the reflux finding score in obstructive sleep apnea.

OBJECTIVES: To evaluate the relationships between laryngeal inflammation assessed using the Reflux Finding Score (RFS), laryngeal sensory function, and apnea severity in patients with obstructive sleep apnea (OSA). METHODS: Endoscopic sensory testing (EST) was performed with subsequent blinded scoring from video of RFS. An RFS>7 was indicative of increased inflammatory change. RESULTS: Of 34 patients evaluated, 29 had OSA (apnea-hypopnea index [AHI]>or=15 events/h) at polysomnography. Increased inflammation was present in 26/29 (90%), with changes suggestive of laryngopharyngeal reflux. There were significant correlations between: inflammation and OSA severity (eg, RFS vs AHI, r=0.57, P<0.001); inflammation and laryngeal sensory impairment (EST detection threshold and pressure required to elicit the laryngeal adductor reflex, LAR); and the degree of sensory impairment and OSA severity. CONCLUSIONS: Laryngeal inflammation is prevalent among OSA patients and correlates with laryngeal sensory dysfunction, attenuation of the LAR, and apnea severity. EBM RATING: C-4.

Adult↗

PubMed2003

[Diagnosis and conservative therapy of anal fecal incontinence].

The main diagnostic tool for patients with anal incontinence is the anorectal physiology. The anorectal sphincter can be reliably tested. Due to the fact that an obstetric damage is the most common cause of anal incontinence, the transanal endosonography is the imaging method of choice for detecting a muscle defect. With high frequency ultrasound probes (preferable 10 Mhz) the pathomorphology of the sphincter can be studied in details. If conservative treatment is failing, the neurophysiology testing is helpful in deciding which surgical method (sphincter repair in case of an intact nervus pudendus, artificial sphincter or sacral stimulation in case of neuropathy). The conservative treatment includes increasing the internal sphincter muscle tonus by applying Phenylephrine locally or Loperamid per os. The biofeedback is basically a physical muscle training of the external sphincter with a visual or acoustic feedback of the muscle function to the patient. However, newer studies show that by this method the sensory function and the coordination of the anal sphincter are improving as well. With these conservative treatment options most of the patients suffering from anal incontinence can be treated satisfactorily.

Anal Canal↗

PubMed2002

Refractory skin injury in complex knock-out mice expressing only the GM3 ganglioside.

We generated double knock-out mice lacking the GM2/GD2 and the GD3 synthase gene by mating single gene mutants, and we analyzed the abnormal phenotypes of the mutant mice expressing only the GM3 ganglioside. We observed a refractory skin lesion that appeared primarily on the face of the mutant mice at 25 weeks after birth or later. Frequent scratching of the wound sites was observed in mutant mice with the skin injury, suggesting that it is a triggering factor that exacerbates the injury. This was confirmed by isolating mice in special cages for metabolic study in which the skin injury developed more rapidly. Characteristic proliferation of nerve fibers was found in the epidermis and subepidermis at the injured sites of the mutants, probably a result of continuous skin injury. Peripheral nerve degeneration was observed in young mutant mice, suggesting that reduced sensory function induced over-scratching and the resulting skin lesion. The fact that sensory response to mechanical stimuli decreased while that to hot stimuli increased in the mutant mice supports this interpretation. Thus, only GM3-expressing mice displayed the important role of gangliosides in maintaining skin integrity via regulation of the peripheral nerves.

Animals↗

PubMed2006

Polycystin-2 cation channel function is under the control of microtubular structures in primary cilia of renal epithelial cells.

Mutations in the gene encoding polycystin-2 (PC2) result in autosomal dominant polycystic kidney disease and defects in left-right asymmetry during embryogenesis. PC2 is a TRP-type Ca(2+)-permeable non-selective cation channel, which is expressed in kidney and other organs. PC2 is present and functional in microtubule-containing primary cilia of renal epithelial cells. However, no information is yet available as to whether PC2 interacts with microtubules. Here, we assessed the role of microtubular dynamics in regulating PC2 channel function in primary cilia. Isolated ciliary membranes from LLC-PK1 epithelial cells were reconstituted in a lipid bilayer system. The acute addition of the microtubular disrupter colchicine (15 mum) rapidly abolished, whereas the addition of the microtubular stabilizer paclitaxel (taxol, 15 mum) increased ciliary PC2 channel activity. The further addition of alpha-tubulin plus GTP also stimulated PC2 channel activity in ciliary membranes. However, alpha-tubulin and GTP had no effect on in vitro translated PC2. Using the yeast two-hybrid assay, we found that PC2 interacts with the microtubule-dependent motor kinesin-2 subunit KIF3A, a protein involved in polycystic kidney disease. The interaction occurred through the carboxyl termini domain of both proteins, which was further confirmed by in vitro glutathione S-transferase pull-down and dot blot overlay assays. Co-immunoprecipitation experiments showed that PC2 and KIF3A are in the same complex in native HEK293, Madin-Darby canine kidney cells (MDCK), and LLC-PK1 cells. Immunofluorescent staining also showed substantial PC2 and KIF3A co-localization in primary cilia of renal epithelial cells. The data indicate that microtubular organization regulates PC2 function, which may explain, among others, the regulatory role of PC2 in the sensory function of primary cilia.

Animals↗

PubMed2002

Treatment of delayed-onset neurological deficit after aortic surgery with lumbar cerebrospinal fluid drainage.

OBJECTIVE: The phenomenon of delayed neurological deficit after thoracoabdominal aortic aneurysm repair was first reported in the late 1980s. The mechanism may be reduced collateral circulation during periods of hypotension, cord edema, or reperfusion injury. Few patients with delayed-onset neurological deficit have recovered from this devastating complication. The experience with six patients treated with lumbar cerebrospinal fluid (CSF) drainage is reported. METHODS: Five patients underwent thoracoabdominal aortic aneurysm repair. Before and immediately after the operation, the patients exhibited no abnormalities in motor or sensory function. Patients presented between 12 and 40 hours postoperatively with rapid motor and sensory loss in their lower extremities. Hypotensive events immediately preceded the onset of deficit in five patients. The sixth patient experienced an acute onset of back pain and was found to have thrombus without evidence of dissection in the descending aorta. RESULTS: Patients were treated with volume expansion and vasoactive drugs to achieve a mean arterial pressure of more than 70 mm Hg. Lumbar CSF drainage was instituted promptly in four patients; all displayed marked neurological improvement. Two patients underwent CSF drainage several hours after the onset of symptoms and did not improve. The duration of CSF drainage ranged from 15 to 72 hours, with a goal of maintaining the lumbar CSF pressure at less than 10 mm Hg. CONCLUSION: The efficacy of CSF drainage may relate to reducing CSF pressure, which may increase spinal cord perfusion. Rapid initiation of CSF drainage with aggressive support of blood pressure may result in neurological improvement in some patients.

Aged↗

PubMed1989

[Acute pandysautonomia and acute autonomic and sensory neuropathy].

Acute pandysautonomia and acute autonomic and sensory neuropathy were reviewed with special reference to their clinical entity, pathogenesis and clinical course. Since acute pandysautonomia was primarily described as an entity by Young et al. in 1969, a number of similar cases have been described. The disorder is characterized by severe sympathetic and parasympathetic impairment with relative or complete preservation of somatic motor and sensory functions. Some cases have only shown a cholinergic dysautonomia, while others have displayed a loss of autonomic function together with other impairments of nervous function. In 1980, Colan et al. reported a patient with acute autonomic and sensory neuropathy, manifesting severe sensory impairment and dysautonomia with marked loss of myelinated and unmyelinated fibers. Several other similar cases have appeared in the literature. Four years prior to the Colan et al. report, the author described a case which showed almost the same symptoms. At the present time, it is not clear whether this disorder is a new syndrome that is different from acute pandysautonomia or merely a subtype of it. The causes of the above two syndromes are unknown; however, an immunological disorder similar to the Guillain-Barré syndrome has been suggested. The clinical course is often protracted with slow improvement. However, from the author's experience, a relatively rapid improvement occurs after a single systemic administration of either parasympathomimetic or sympathomimetic agonists. Acute pandysautonomia which includes acute autonomic and sensory neuropathy has recently become more common: A number of similar cases have been reported worldwide, including many areas in Japan.

Acute Disease↗