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Biomedical subjects

J L Ochoa

Publications and source records attributed to J L Ochoa.

At least 37 records · Page 2Linked to original sources
PubMed1998

An overview of the marine food poisoning in Mexico.

In the course of the last decade, huge events related to harmful algal blooms (HAB) have severely affected the environment in Mexico, even causing several human casualties. The tally of the toxins known up to date in Mexican waters includes: neurotoxin shellfish poisoning (NSP), paralytic shellfish poisoning (PSP), amnesic shellfish poisoning (ASP), tetrodotoxin (TTX) or puffer fish poisoning, ciguatera fish poisoning (CFP) and diarrhetic shellfish poisoning (DSP). Actual epidemiological figures profoundly modified the trends manifested on previous decades. Notwithstanding that the red tides are a long time known phenomena in Mexican coasts, no regular observation of the marine environment has been set up. Although there are monitoring activities for PSP toxins on the shellfish culturing facilities that are exploited for export to the U.S.A., these are only effectively applied on specific spots of the Mexican coasts, implying that the biggest part of the country coastal zones are not formerly surveyed. The misleads caused by the medical conception that food poisoning events are mainly due to microbial contamination, is among the factors why the marine food poisoning events are a neglected disease. In spite of the fact that no official statistics consider HAB related events as a subject of research or further monitoring by the health authorities, sporadic scientific documents related to poisoning events were produced in Mexico. An interesting picture is presented for most of the marine toxins mentioned. Trend and prognosis estimates made with such scarce information, provide a minimum measurement of the reality and urge the need for a permanent monitoring program on the Mexican coasts, a place with one of the greatest marine toxin diversity worldwide.

Animals↗
PubMed1998

Reversal of hypoaesthesia by nerve block, or placebo: a psychologically mediated sign in chronic pseudoneuropathic pain patients.

OBJECTIVES: To gain understanding of the mechanism and meaning of improvement of hypoaesthesia after a diagnostic intervention, and of the nature of the population that displays such a sign. METHODS: Patients with chronic "neuropathic" pain underwent rigorous clinical and laboratory investigations, including placebo controlled local anaesthetic block. Patients displaying profound regional cutaneous hypoaesthesia and pain entered the study through either of two criteria: (a) reversal of hypoaesthesia after diagnostic block, (b) nerve injury as the cause of hypoaesthesia and pain. The semeiology displayed by these patients together with the behaviour of their sensory phenomena in response to blocks were compared. Three groups were expected: (1) patients with "neuropathic" pain with profound hypoaesthesia reversed by block, but without neuropathy; (2) patients whose hypoaesthesia did not reverse and who had neuropathy as the cause of their sensory dysfunction; and (3) patients whose hypoaesthesia reversed, and had neuropathy. RESULTS: Two groups emerged: (1) patients with profound hypoaesthesia reversed by block, but without neuropathy (27 patients), and (2) patients whose hypoaesthesia did not reverse and who had a neuropathy (13 patients). No patient with neuropathy was found whose cutaneous hypoaesthesia improved with block. The first group displayed the sensory-motor characteristics of psychogenic pseudoneuropathy. The semeiology of the second group was in keeping with organic neuropathy and displayed no pseudoneurological features. Spontaneous pain was relieved by placebo in 66.6% of the patients in groupl and 53.8% in group 2. CONCLUSIONS: Such reversal of hypoaesthesia is due to a placebo effect, acting on a psychogenic symptom because: (a) 27 of 27 patients in which the sign occurred had absence of nerve disease behind the "neuropathic" symptoms, (b) In 26 of 27 patients the area of hypoaesthesia was non-anatomical, (c) 16 of 27 patients had other sensory-motor signs that could not be explained as a result of organic pathology (give way weakness and punctual denial of hypoaesthesia), and (d) the phenomenon was not found in patients with organic neuropathy.

Adult↗
PubMed1997

Sea bird mortality at Cabo San Lucas, Mexico: evidence that toxic diatom blooms are spreading.

Domoic acid was found to be responsible for an isolated event involving the massive death of brown pelicans (Pelecanus occidentalis) in January 1996, at the tip of the Baja California peninsula. The death of these sea birds was the result of feeding on mackerel (Scomber japonicus) contaminated by domoic acid-producing diatoms (Pseudonitzschia sp.). The number of dead birds (150 animals) found during a period of 5 days caused alarm and called for a governmental task force that would help to implement emergency measurements to protect other species of bird. Also, local canneries were inspected to verify the safety of their recent production and prevent the toxin entering the human market. Fortunately, the timing, response and coordination of this task force enabled identification of the origin and nature of the toxin that provoked such a phenomenon. Future monitoring is recommended to avoid a larger impact of domoic acid spreading and the occurrence of similar toxic events.

Animals↗
PubMed1996

C-polymodal nociceptors activated by noxious low temperature in human skin.

1. Fifty-five C-polymodal nociceptors innervating hairy skin in human volunteers were tested for discrete stimulus-response properties through microneurography. 2. All fifty-five units were responsive to mechanical and heat stimuli. Twenty-two (40%) of these exhibited an additional response to noxious low temperature. The twenty-two mechano-heat-cold nociceptors displayed similar receptor responses to heat and mechanical stimuli, and conduction velocity, as those of the pure mechano-heat C-polymodal nociceptors. 3. Low temperature stimuli between 19 and 0 degree C evoked responses at low discharge frequency (0.4 +/- 0.22 impulses s-1, mean +/- S.E.M.) in the twenty-two units sensitive to such energy. These units displayed a tendency to decrease their discharge after a few seconds of steady stimulation. 4. Three units tested with a freezing stimulus responded with relatively vigorous discharge, which never exceeded the maximal discharge frequency elicited by either mechanical or heat stimuli. One of these units became sensitized to heat after the freezing challenge. 5. It is concluded that a subpopulation of C-polymodal nociceptors is sensitive to noxious low temperature and may thus contribute to the determination of cold pain. The same type of primary afferent is probably one mediator of the symptom cold hyperalgesia in peripheral nerve disease.

Action Potentials↗
PubMed1996

Pain from excitation of identified muscle nociceptors in humans.

The technique of intraneural microstimulation (INMS) combined with microneurography was used to excite and to record impulse activity in identified afferent peroneal nerve fibers from skeletal muscle of human volunteers. Microelectrode position was minutely adjusted within the impaled nerve fascicle until a reproducible sensation of deep pain projected to the limb was obtained during INMS. During INMS trains of 5-10 s in duration and at threshold for sensation, volunteers perceived a well defined area of deep pain projected to muscle. Psychophysical judgements of the magnitude of pain increased with increasing rates of INMS between 5 and 25 Hz. Also, the area of the painful projected field (PF) evoked during trains of INMS of various duration but constant intensity and rate typically expanded with duration of INMS. The intraneural microelectrode was alternatively used to record neural activity originating from primary muscle afferents. Eight slowly adapting units with moderate to high mechanical threshold were identified by applying pressure within or adjacent to the painful PF. Conduction velocities ranged from 0.9 to 6.0 m/s, and fibers were classed as Group III or Group IV. Capsaicin (0.01%) injected into the RF of two slowly conducting muscle afferents (one Group III and one Group IV) produced spontaneous discharge of each fiber and caused intense cramping pain, suggesting that the units recorded were nociceptive. Our results endorse the concept that the primary sensory apparatus that encodes the sensation of cramping muscle pain in humans is served by mechanical nociceptors with slowly conducting nerve fibers. Results also reveal that muscle pain can be precisely localized, although the human cortical function of locognosia for muscle pain becomes blunted as a function of duration of the stimulus.

Adult↗
PubMed1996

Biochemical method for chlorine dioxide determination.

Chlorine dioxide is a disinfectant used worldwide. In this article, a new enzymatic method for the determination of chlorine dioxide has been developed. This rapid spectophotometric assay is able to detect from 0.2 to 4 mg/liter of chlorine dioxide. The method is based on the capacity of horseradish peroxidase to decolorize reactive yellow 17 in the presence of chlorine dioxide. The effects of several compounds on the assay have been determined. Except sodium hypochlorite, no interference was detected with 18 compounds including chlorides, sulfates, carbohydrates, amino acids, proteins, and organics. The biochemical method is faster and easier than the previous volumetric, amperometric, and colorimetric methods which are laborious and time-consuming.

Chemistry Techniques, Analytical↗
PubMed1995

Reflex sympathetic dystrophy. A common clinical avenue for somatoform expression.

Reflex sympathetic dystrophy (RSD) and causalgia appear to reflect identical pictures even though the latter is related to nerve injury and the former is not. Overriding past and present skepticism about a role for the sympathetic system in their cause and treatment, the International Association for the Study of Pain still recommends sympathetic blocks and sympathectomy for both causalgia and RSD. Such fallacy is traceable to fragmentary clinical observations, to ad-hoc experiments, and to traditional neglect of the placebo phenomenon in chronic "neuropathic" pain patients.

Causalgia↗
PubMed1994

The triple cold syndrome. Cold hyperalgesia, cold hypoaesthesia and cold skin in peripheral nerve disease.

A syndrome of cold hyperalgesia associated with cold hypoaesthesia is described in 28 patients with peripheral polyneuropathy or mononeuropathy of various aetiologies. A mechanism of sensory disinhibition, where diminished cold-specific A delta input releases cold pain input carried by C nociceptors, is proposed to explain the hyperalgesia. In most patients, the symptomatic skin is abnormally cold. This is a likely consequence of vasospasm, due to sympathetic denervation supersensitivity, caused by dropout of sympathetic efferents as part of the small caliber nerve fibre insult. The term 'triple cold syndrome' is coined to describe this specific pathophysiological condition. Descriptively it is a mirror image of erythralgia, as described by Sir Thomas Lewis (1936) and updated by one of the present authors, a human condition also centred around anomalous primary nociceptor input, in which there is heat hyperalgesia and hot symptomatic skin due to C nociceptor sensitization and vasodilatation from antidromic discharge. Thus, like the latter condition, the triple cold syndrome emerges as an independent clinical entity with definable abnormal mechanisms which should be retrieved out of the all-embracing, descriptive, diagnostic category 'reflex sympathetic dystrophy--causalgia'.

Adult↗
PubMed1994

Pain mechanisms in neuropathy.

Current opinion on "neuropathic" pain is chaotic and divided. This review is a summary attempt at describing the principal hypotheses that are currently entertained and at interpreting the basic underlying mechanisms of these pains. Rather than relying preferentially on rigorous data generated from neurophysiological animal experimentation, reasonable priority is given to evidence derived from rigorous neurophysiological and psychophysical studies in human volunteers and patients. Issues such as the concept of "centralization" of neuropathic pain mechanisms, which dwell excessively upon extrapolation from animal experiment to human clinical reality, are highlighted as questionable. Psychogenic pseudoneuropathy, an entity of high clinical prevalence and low appreciation by basic scientists and the reflex sympathetic dystrophy establishment, is also given the emphasis it deserves.

Afferent Pathways↗
PubMed1994

Identification of muscle afferents subserving sensation of deep pain in humans.

1. Intraneural microstimulation (INMS) and microneurography were used in combination to stimulate and record from muscle nociceptor primary afferent fibers of the common peroneal nerve of healthy volunteers. When pain evoked by INMS was projected to muscle, afferent activity could be evoked by innocuous and noxious pressure applied within the projected painful area. Conduction velocity of single fibers was determined by stimulating the receptive fields (RFs) electrically via needle electrodes inserted into the RF and measuring conduction latency and distance between the RF and recording electrode. 2. Pain projected to muscle during INMS trains 5-10 s in duration at threshold intensity for pain sensation was typically described as cramping and was well localized. Subjects mapped the area of the painful projected field (PF) over the skin using a pointer. 3. Fourteen slowly adaping mechanoreceptors with RF in muscle and with moderate to high receptor threshold were identified within or near the painful PF. Conduction velocities were in the range of Group III (n = 8) and Group IV (n = 6) fibers. Mean RF areas of Group III and Group IV afferents, determined by applying pressure percutaneously, were 2.71 +/- 1.14 (SE) cm2 and 3.40 +/- 1.08 (SE) cm2, respectively. Only one Group III afferent unit exhibited spontaneous activity (< 1 Hz). 4. One additional high-threshold mechanoreceptor was identified, with its RF located in the extensor tendon at the base of the big toe. This fiber had a conduction velocity of 32 m/s. During INMS, a well-localized sharp pain was projected to the tendon.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

'Sympathetically maintained pain.' I. Phentolamine block questions the concept.

Patients with "reflex sympathetic dystrophy" or "causalgia" underwent sympathetic blocks. In protocol A (77 patients), we infused placebo (saline) for 30 minutes followed by phentolamine (35 mg). In protocol B (23 patients), the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 micrograms), a second phase of saline, and then the other active drug. We assessed magnitudes of pain and mechanical hyperalgesias on a 0-to-10 pain scale and monitored sensory and sympathetic effects. With protocol A, pain diminished significantly (> or = 50%) during placebo in 22 patients (28.9%) and during phentolamine in seven (9.2%). With protocol B, four patients (17.3%) had relief of pain during placebo, four (17.3%) during phenylephrine, and two (8.7%) during phentolamine. All "phentolamine responders" had progressive pain relief from placebo. Two patients expressed relief during phenylephrine and worsening during phentolamine. Most patients did not respond significantly to saline or drugs. Thus, pharmacologic manipulation of the alpha-1 adrenergic receptor by either agonist or antagonist drug does not influence neuropathic pains. These results raise questions about the existence of "sympathetically maintained pain," as diagnosed by sympathetic blocks improperly controlled for placebo.

Adult↗
PubMed1994

Phentolamine sympathetic block in painful polyneuropathies. II. Further questioning of the concept of 'sympathetically maintained pain'.

To test for the presence of "sympathetically maintained pain" (SMP), we administered placebo-controlled phentolamine sympathetic blocks to 14 patients with painful polyneuropathies. Six received i.v. infusion of saline for 30 minutes, followed by phentolamine (35 mg). In eight patients, the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 micrograms), a second saline phase, and then the other active drug. We measured magnitudes of spontaneous pain and mechanical hyperalgesias on a 0-to-10 pain scale every 5 minutes and monitored sensory and sympathetic effects clinically and through quantitative thermotest and thermography. Five patients reported significant diminution of pain (> 50%), all in response to placebo. Neither phentolamine nor phenylephrine provided relief, although all patients had signs of physiologic abnormalities reputed to be determinants or predictors of SMP. These results complement previous studies demonstrating the nonexistence of SMP among "reflex sympathetic dystrophy" patients and further question the concept of SMP.

Adult↗
PubMed1993

Mechanical hyperalgesias in neuropathic pain patients: dynamic and static subtypes.

Two behavioral kinds of mechanical hyperalgesia can be clearly discerned by clinical criteria in patients with neuropathic syndromes, i.e., a dynamic type, elicitable by lightly stroking the symptomatic skin, and a static type, elicitable by steadily applying gentle pressure on it. Of 28 patients studied, 19 had dynamic and 18 had static type mechanical hyperalgesia (9 expressed both types). Experimental compression-ischemia nerve block totally abolished the dynamic hyperalgesia in all patients except in 2, in whom it was markedly diminished. Disappearance of dynamic hyperalgesia occurred contemporaneously with block of myelinated A fibers, as expressed by abolition of the sensations of touch and cold, monitored quantitatively. Static hyperalgesia, however, outlasted A-fiber block in 15 of 18 patients; the phenomenon persisted during the stage when only unmyelinated fibers were available for impulse conduction. It is thus concluded that, at the primary afferent level, dynamic hyperalgesia is mediated by myelinated fibers, whereas static hyperalgesia depends on unmyelinated afferents. These two kinds of hyperalgesia represent discrete pathophysiological entities with distinct clinical connotations.

Adult↗
PubMed1993

Use and misuse of conventional electrodiagnosis, quantitative sensory testing, thermography, and nerve blocks in the evaluation of painful neuropathic syndromes.

A number of laboratory tests are critically important in the quest to diagnose presence or absence of organic neuropathic dysfunction and to establish the relevance of such to the subjective pain complaints. However, none of these tests has absolute diagnostic value and their results must be interpreted in the light of the clinical picture. Conventional electrophysiology evaluates function of large caliber afferent and motor fibers leaving the function of small caliber afferent fibers unexplored, and cannot explore the basis for positive sensory phenomena. The quantitative somatosensory thermotest is the best test available to explore function of small caliber afferents. It allows documentation of positive sensory phenomena in the form of thermal hyperalgesia. Because it is a psychophysical test, it lacks localizing value. Thermography sensitively detects and precisely delineates areas of cutaneous thermal change of neural origin. Three types of diagnostic neurologic blocks are used in the clinic: compression-ischemia, local anesthetic and sympathetic blocks. Although they may provide important information about the pathophysiology of pain and hyperalgesias, adequate placebo control is of the essence because chronic neuropathic pain patients may express a high incidence of placebo response.

Electrodiagnosis↗