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PubMedDate not supplied

[Congenital analgesia].

The case of a 12 years old boy with a congenital anaesthesia covering all cutaneous and visceral districts is reported. There were no other neurological abnormalities apart a light mental retardation and loss of axon reflex after intradermal injection of hystamine. Notwithstanding this last finding a diagnosis of congenital indifference to pain was made. The differential diagnosis between indifference and insensitivity to pain is discussed.

Axons↗
PubMed1995

Mechanisms of syncope caused by transient bradycardia and the diagnostic value of electrophysiologic testing and cardiovascular reflexivity maneuvers.

Transient bradycardia may be intrinsic because of sinus node or atrioventricular (AV) conduction abnormalities, or extrinsic because of abnormal vagal reflex. Twenty-five consecutive patients, referred to us for study of unexplained syncope, who, during electrocardiographic monitoring, had a documented episode of intermittent bradycardia that caused syncope, underwent a full electrophysiologic study, carotid sinus massage, and the head-up tilt test. A prolonged ventricular asystole (5 to 20 seconds) was documented during syncope in all patients: sinus arrest in 13, AV block in 7, sinus arrest plus AV block in 3, and asystolic pause during atrial fibrillation in 2. Abnormal electrophysiologic findings suggested the correct diagnosis in 6 patients (24%): block within the bundle of His in 5 and sick sinus syndrome in 1. An abnormal response to carotid sinus massage or to the head-up tilt test suggested a neurally mediated mechanism in 17 patients (68%). Overall, electrophysiologic study and vasovagal maneuvers were able to identify the mechanism of spontaneous syncope in 23 patients (92%). Thus, in patients affected by syncope due to transient bradycardia, the most likely mechanism of syncope is neurogenic, whereas it is cardiogenic only in a few instances. Electrophysiologic testing, carotid sinus massage, and the head-up tilt test can identify most of these patients. Conversely, when all these tests are negative, it is unlikely that transient bradycardia is the cause of syncope. Because of the different mechanisms involved, electrophysiologic study and vasovagal maneuvers are complementary diagnostic tools.

Adult↗
PubMed2000

Mizuo phenomenon observed by scanning laser ophthalmoscopy in a patient with Oguchi disease.

PURPOSE: To elucidate the origin of the abnormal fundus reflex in Oguchi disease. METHODS: The ocular fundus of a 63-year-old woman who showed a homozygous arrestin 1147delA mutation was observed by scanning laser ophthalmoscopy with the use of an argon blue laser (wavelength, 488 nm), a helium-neon laser (633 nm), and an infrared laser (780 nm). RESULTS: Diffuse, fine, white particles, which do not exist in normal subjects, were clearly demonstrated only with the helium-neon laser. After 4-hour dark adaptation, the abnormal particles disappeared, but then they reappeared gradually during 30 minutes of light adaptation, in accordance with the golden metallic reflex. CONCLUSION: The white particles found by helium-neon laser could be the origin of the abnormal fundus reflex in Oguchi disease.

Arrestin↗
PubMed1998

Obstructive sleep apnoea and the autonomic nervous system.

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognized condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of few techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory manoeuvres. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalizing respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long-term cardiovascular morbidity is not established.

Journal Article↗
PubMed1999

[Autonomic nervous system and obstructive sleep apneas].

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognised condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with arterial hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of new techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory manoeuvres. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalising respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long term cardiovascular morbidity is not established.

Autonomic Nervous System↗
PubMed2000

[Autonomic nervous system and sleep apnea syndromes].

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognised condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with arterial hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of new techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory maneuvers. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalising respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long term cardiovascular morbidity is not established.

Acute Disease↗
PubMed1990

[Neurological and pathophysiological analyses of patients with absent auditory brainstem evoked response].

Seventeen patients with no auditory brainstem evoked response (ABR) who suffered from various neurological disorders were reported. We evaluated the possibilities of co-existent brainstem lesions in addition to the peripheral impairment in the auditory pathway, by assessing neurological findings and other laboratory examinations, including cranial CT and electrically elicited blink reflex. Patients who showed cranial nerve symptoms other than that of the acoustic nerve or abnormal postural reflexes were suspected to have brainstem dysfunction. It was difficult, however, to exclude the influence from the dysfunction in the more central level CNS. Definite brainstem atrophy was revealed radiologically only in one case who was at the end stage of the degenerative disease. Blink reflex was studied in eleven cases, four of whom revealed abnormal responses, also suggesting brainstem dysfunction. All the five cases, consistent with these abnormal laboratory findings, had shown severe delay in motor development. Other five patients who showed rather good auditory behavior were considered to have 'desynchronization' response to ABR in the auditory pathway at the peripheral level. Many pathophysiological conditions may be involved in the phenomenon of absent ABR, which should be carefully evaluated from the viewpoints of clinical neurology.

Blinking↗
PubMed1992

Mechanisms of obstructive sleep apnea.

This article has reviewed the anatomic, compliance, reflex, and respiratory muscle variables that affect upper airway caliber and abnormalities which may precipitate upper airway collapse during sleep. One or more of these variables may be important in the mechanism of OSA in any given patient. First, anyone with anatomic narrowing of the upper airway is susceptible to OSA. However, we do know if anatomic narrowing of the upper airway is necessary for the development of OSA. Surely, heavy snoring produces pharyngeal trauma and possibly edema or inflammation, which in turn may narrow the upper airway. Submucosal adipose tissue or cervical adipose tissue may compress the airway when the tonic electrical activity of the pharyngeal muscles decreases with sleep onset. Data reviewed support the idea that the upper airway of OSA patients may be more collapsible than the upper airway of nonapneic subjects. Intrinsic tissue abnormalities have not been demonstrated that might be responsible for this collapsibility. Changes in collapsibility found are consistent with, and may be due to, changes in tonic and phasic contraction of upper airway muscles. Abnormalities in reflexes affecting upper airway size surely might exist in OSA. Edema or inflammation of pharyngeal tissues might not only narrow the upper airway but might also impair normal function of the receptors responsible for initiating protective reflexes. We propose the fluctuation between a low- and a high-drive state contributes to upper airway collapse in OSA. With this fluctuation the balance of forces and critical pressure concepts discussed above come into play (Fig 6). By stimulating upper airway inspiratory muscles, CO2 eliminates the hypoapneic, low-drive, high-resistance periods and thereby reduces the number of apneas. In addition, preferential stimulation of upper airway muscle activity dilates the upper airway per se. If the relative value of each of these factors can be determined diagnostically, perhaps therapy can be made more specific. By being more specific, therapy should be more successful than the present practice of prescribing a particular therapy, regardless of the specific mechanism responsible for the OSA in a given patient.

Humans↗
PubMed1994

[Idiopathic pure sudomotor failure].

We describe three cases of acquired generalized anhidrosis without other autonomic and somatic nervous dysfunctions (idiopathic pure sudomotor failure; IPSF) and a review of the literature was made in regard to the clinical features of this disease. Patient 1. A 17-year-old man was found to be severely anhidrotic and intolerant to heart loading, which produced an immediate sharp pain over the entire body surface in April, 1989. Sudden and spontaneous remission occurred in July, 1990, but relapsed six months later. He was admitted to our hospital seeking for therapy in April, 1991. There were no abnormal findings on physical and neurological examinations except for anhidrosis. Patient 2. A 14-year-old boy was admitted to our hospital in March 1991 with complaints of intolerance to heart loading and sharp pain, which had begun ten months before admission. Physical and neurological examinations revealed no abnormal findings except for anhidrosis. Patient 3. A 21-year-old woman suddenly experienced a burning sensation in the whole body in 19th, February, 1991, which was followed by severe pain. She was admitted to our hospital in the next day. Apart from sensory impairment of glove and stocking type, neurological examination revealed no abnormal findings. Reflex sweating to pilocarpine was absent in all three cases, suggesting abnormality in the postganglionic sudomotor nerves or cholinergic receptors. Skin biopsy was performed in one patient (patient 1), and revealed no abnormalities of the sweat glands and ducts.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis.

The aetiology of exercise-associated muscle cramps (EAMC), defined as 'painful, spasmodic, involuntary contractions of skeletal muscle during or immediately after physical exercise', has not been well investigated and is therefore not well understood. This review focuses on the physiological basis for skeletal muscle relaxation, a historical perspective and analysis of the commonly postulated causes of EAMC, and known facts about EAMC from recent clinical studies. Historically, the causes of EAMC have been proposed as (1) inherited abnormalities of substrate metabolism ('metabolic theory') (2) abnormalities of fluid balance ('dehydration theory'), (3) abnormalities of serum electrolyte concentrations ('electrolyte theory') and (4) extreme environmental conditions of heat or cold ('environmental theory'). Detailed analyses of the available scientific literature including data from recent studies do not support these hypothesis for the causes of EAMC. In a recent study, electromyographic (EMG) data obtained from runners during EAMC revealed that baseline activity is increased (between spasms of cramping) and that a reduction in the baseline EMG activity correlates well with clinical recovery. Furthermore, during acute EAMC the EMG activity is high, and passive stretching is effective in reducing EMG activity. This relieves the cramp probably by invoking the inverse stretch reflex. In two animal studies, abnormal reflex activity of the muscle spindle (increased activity) and the Golgi tendon organ (decreased activity) has been observed in fatigued muscle. We hypothesize that EAMC is caused by sustained abnormal spinal reflex activity which appears to be secondary to muscle fatigue. Local muscle fatigue is therefore responsible for increased muscle spindle afferent and decreased Golgi tendon organ afferent activity. Muscles which cross two joints can more easily be placed in shortened positions during exercise and would therefore decrease the Golgi tendon organ afferent activity. In addition, sustained abnormal reflex activity would explain increased baseline EMG activity between acute bouts of cramping. Finally, passive stretching invokes afferent activity from the Golgi tendon organ, thereby relieving the cramp and decreasing EMG activity.

Electromyography↗
PubMed2003

Magnetic resonance imaging in reflex sympathetic dystrophy syndrome of the foot.

OBJECTIVE: The purpose was to analyze magnetic resonance imaging (MRI) abnormalities in reflex sympathetic dystrophy syndrome (RSDS) of the foot, with the goal of helping to meet the difficult diagnostic challenges raised by this condition. METHODS: Retrospective study of 20 patients with RSDS of the foot, 15 at the warm phase and five at the dystrophic phase. RESULTS: Of the 15 patients at the warm phase, seven had evidence of bone edema (low signal on T1-weighted images and high signal on T2, T2 STIR, and fat saturation images) and five had occult fractures (linear band of low signal on T1 and T2 weighted images with no enhancement after contrast injection). Other abnormalities included soft tissue changes in three patients, joint effusion in five, and synovial hypertrophy in one. Of the five patients at the dystrophic phase, one had a fracture with a joint effusion, one had isolated joint edema, and three had normal MRI findings. CONCLUSION: Bone marrow edema is inconsistent at the warm phase of RSDS and is never present at the dystrophic phase. Thus, absence of bone edema does not rule out RSDS. Fractures may be visible by MRI in one-third of patients with RSDS and no clinical or plain radiography evidence of fracturing.

Adult↗
PubMed1994

Abnormal thermoregulatory responses in patients with reflex sympathetic dystrophy syndrome.

OBJECTIVE: To look for asymptomatic thermoregulatory abnormalities in the noninvolved limbs in patients with well established reflex sympathetic dystrophy syndrome (RSDS). The study was prompted by the observation of development of severe upper limb Raynaud's phenomenon in a young woman with a history of RSDS affecting both lower limbs. METHODS: Eleven patients and 11 age and sex matched control subjects underwent a standard thermal stress test: cold water immersion of a hand unaffected by RSDS in water at 15 degrees C for one min. All controls had had injuries uncomplicated by RSDS. RESULTS: Lag time (the lag phase between the end of the cold challenge and the onset of rewarming) was significantly increased (p < 0.01) in the patient group (median 5.67 min, range 0.50 to > 15) compared to the control group (median 0.50 min, range 0.50 to 12.92). The median maximum temperature recovery was lower in the patient group (81.6%, range 0 to 170.4) than in the control group (119.3%, range 49.1 to 153.1). CONCLUSION: Our findings support an association between RSDS and a generalized abnormal response to cold challenge. Further studies are required to examine the temporal relationship underlying this. Early screening for thermoregulatory dysfunction of patients after fractures might allow identification of patients at risk of developing RSDS.

Adolescent↗
PubMed1999

Auditory deprivation of the central auditory system resulting from selective inner hair cell loss: animal model of auditory neuropathy.

Auditory neuropathy is often characterized by normal thresholds, present otoacoustic emissions, poor speech discrimination, absent acoustic reflexes, absent or abnormal auditory brainstem response waveform, but normal late cortical potential. This paper describes an animal model that has many characteristics of auditory neuropathy. Chinchillas can be deprived of a significant portion of the neural inputs to the central auditory system by administering carboplatin, an antineoplastic agent that selectively destroys inner hair cells (IHCs) and type I auditory nerve fibers. Selective IHC loss has no effect on distortion product otoacoustic emissions or the cochlear microphonic potential, implying normal outer hair cell function. However, selective IHC loss causes the amplitude of the compound action potential to decrease in proportion to the degree of IHC loss. However, the threshold of the CAP shows little increase with mild to moderate IHC loss. Acoustically responsive auditory nerve fibers in ears with mild to moderate IHC loss have normal thresholds and tuning curves with narrowly tuned tips. Although the central auditory pathway is deprived of much of its sensory inputs, the amplitude of the local field potential in the auditory cortex was normal or enhanced, while those from the inferior colliculus were slightly reduced. The results are related to those of a patient with auditory neuropathy.

Animals↗