Cases reported "Syndrome"

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11/41. Irukandji-like syndrome in South florida divers.

    Irukandji syndrome is a constellation of delayed severe local and systemic symptoms occurring after a Carukia barnesi box jellyfish sting involving any exposed skin. These cases are limited to australia, the habitat of that animal. Numerous other cases of an Irukandji-like syndrome after other small Carybdeid genus envenomations have been reported elsewhere in the world. There have yet been no reports of Irukandji-like syndrome occurring in continental US coastal waters. We describe 3 cases of marine envenomation causing such a symptom complex in US military combat divers off Key West, FL. It is unclear what species caused the injuries, but a member of the Carybdeid genus seems most likely.
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12/41. acute coronary syndrome and crystal methamphetamine use: a case series.

    "Ice" is a form of methamphetamine commonly used as a recreational drug in hawaii and the philippines, but seldom encountered in the continental united states. It differs in appearance from methamphetamine tablets, but otherwise has exactly the same molecules, only arranged in a crystalline structure. A sizeable body of in vitro, animal, and autopsy data suggest a linkage between methamphetamine use and myocardial pathology. In this report, we describe a series of eight patients who developed unstable angina or acute myocardial infarction in association with smoking crystal methamphetamine. The findings, to a large extent, resemble those with cocaine-associated acute coronary syndromes. Given the widespread abuse of methamphetamine among young age groups, the recognition and primary prevention of cardiovascular toxic effects is of mounting socioeconomic importance.
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13/41. The space of senses: impaired crossmodal interactions in a patient with Balint syndrome after bilateral parietal damage.

    Balint syndrome after bilateral parietal damage involves a severe disturbance of space representation including impaired oculomotor behaviour, optic ataxia, and simultanagnosia. Binding of object features into a unique spatial representation can also be impaired. We report a patient with bilateral parietal lesions and Balint syndrome, showing severe spatial deficits in several visual tasks predominantly affecting the left hemispace. In particular, we tested whether a loss of spatial representation would affect crossmodal interactions between simultaneous visual and tactile events occurring at the same versus different locations. A tactile discrimination task, where spatially congruent or incongruent visual cues were delivered near the patient's hands, was used. Following stimulation of the left hand in the left side of space, we observed visuo-tactile interactions that were not modulated by spatially congruent conditions. In contrast, performance following stimulation of the right hand in the right side of space was affected in a spatially selective manner--facilitated for congruent stimuli and slowed for incongruent stimuli. To dissociate effects on somatotopic and spatiotopic coordinates, we crossed the patient's hands during unimodal tactile discriminations. Tactile performance of the left hand improved when it was positioned in the right hemispace, whereas placing the right hand in left space produced no significant changes, suggesting that left-sided tactile inputs are coded with respect to a combination of limb- and trunk-centred coordinates. These data converge with recent findings in animals and healthy humans to indicate a critical role of the posterior parietal cortex in multimodal spatial integration, and in the fusion of different coordinates into a unified representation of space.
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14/41. Athymhormia and disorders of motivation in basal ganglia disease.

    The author proposes a general model of human motivation as a separate function at the interface between emotion and action, which can be ascribed to subcortical circuits that are mainly centered on a subset of the basal ganglia and on their limbic connections. It is argued that the long-standing historical understatement of the notion of motivation in neurology is not only due to the complexity of the issue, which has proven hard to disentangle from other domains of dysfunction, but also to the persistence of some misleading conceptual orientations in the way neurologists have considered the brain mechanisms of goal-directed action, torn between a nonspecific "activation" view and an exclusively cognitive conception of motivation. How combining early clinical intuitions of some psychiatrists, careful clinical observations of neurological patients, and data derived from experimental studies in animals provide the basis for a coherent model of human motivation and its specific impairment in clinical neurology is explained. Clinical implications that can be drawn from such a model for some neuropsychiatric conditions are proposed.
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15/41. tremor syndrome associated with a fungal toxin: sequelae of food contamination.

    We report on an elderly couple who presented with a syndrome that included severe generalised tremor and incoordination after eating soup from a damaged can. Black mould contaminating the can was subcultured and the fungus penicillium crustosum was identified. This fungus usually produces a potent neurotoxin called penitrem A. The couple displayed symptoms consistent with penitrem A ingestion, all of which resolved fully. Penitrem A intoxication has been well documented in animals, but not in humans.
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16/41. Human parvovirus B-19: not just a pediatric problem.

    Parvoviruses have long been associated with disabling and even fatal illnesses in animals. The discovery of the human parvovirus B-19 in 1975 (1) and subsequent studies of its effects in humans identified this virus as the causative agent of erythema infectiosum ("fifth disease") in children. (2). erythema infectiosum (EI) is a common, self-limited infectious disorder in children, easily recognized by the classic "slapped cheek" facial erythema and fine reticular rash. Only in the 1980s have further investigations linked HPV B-19 infection with more significant clinical syndromes, among which is an adult polyarthropathy. This presentation in adults is more common than is currently understood and is easily confused with other symmetric polyarthropathies. Recognition and conservative treatment of this disorder are important for the emergency physician, to whom these patients may present.
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17/41. role of HOXA7 to HOXA13 and PBX1 genes in various forms of MRKH syndrome (congenital absence of uterus and vagina).

    The Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome refers to the congenital absence or severe hypoplasia of the female genital tract, often described as uterovaginal aplasia which is the prime feature of the syndrome. It is the second cause of primary amenorrhea after gonadal dysgenesis and occurs in approximately 1 in 4500 women. Aetiology of this syndrome remains poorly understood. Frequent association of other malformations with the MRKH syndrome, involving kidneys, skeleton and ears, suggests the involvement of major developmental genes such as those of the HOX family. Indeed mammalian HOX genes are well known for their crucial role during embryogenesis, particularly in axial skeleton, hindbrain and limb development. More recently, their involvement in organogenesis has been demonstrated notably during urogenital differentiation. Although null mutations of HOX genes in animal models do not lead to MRKH-like phenotypes, dominant mutations in their coding sequences or aberrant expression due to mutated regulatory regions could well account for it. sequence analysis of coding regions of HOX candidate genes and of PBX1, a likely HOX cofactor during Mullerian duct differentiation and kidney morphogenesis, did not reveal any mutation in patients showing various forms of MRKH syndrome. This tends to show that HOX genes are not involved in MRKH syndrome. However it does not exclude that other mechanisms leading to HOX dysfunction may account for the syndrome.
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18/41. Asplenia syndrome in a pair of monozygotic twins.

    Asplenia syndrome is one of the heterotaxy syndromes, which many familial and animal studies suggest are caused by the loss of adequate genetic control of normal left-right asymmetry development. Moreover, there has not been any environmental factor documented to cause these syndromes. Asplenia syndrome occurring in a pair of monozygotic twins is reported. In view of the negative family history, a new germline mutant gene might be the aetiology of our patients. Both twins are associated with some degree of discordant complex heart defects within the context of a high degree of "mirror-image" of the unpaired thoracoabdominal organs. CONCLUSION: This report implies that sporadic asplenia syndrome might associate with new mutations and further genetic study may be indicated. These monozygotic twins' discordant phenotypes imply that some unidentified factors play an important role in their ultimate development of the same genetically determined abnormalities.
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19/41. mortality and pathological findings in C (Opitz trigonocephaly) syndrome.

    Even as a rare multiple congenital anomalies/mental retardation syndrome, the C-syndrome (CS, or Opitz C-trigonoecephaly syndrome) is, at long last, beginning to attract attention because of its developmental and causal complexity. Also, the possibility that the apparently balanced translocation recently described in an affected Japanese boy may soon provide a molecular/causal insight into this disorder. The manifestations recorded in the previously published patients, those autopsied within recent years, and the unpublished instances in our files suggest that the CS is a heterogeneous genetic disorder, predominantly sporadic but with sufficient familial cases (at times with consanguinity) to allow postulation of an entity due to autosomal dominant mutations with a high rate of germinal mosaicism, or due to both autosomal dominant mutations and an autosomal recessive genocopy. In any event, elucidation of cause and pathogenesis of CS will, in due time, shed light on its developmental pleiotropy, rarity in liveborn infants, prevalence in stillborn fetuses, recurrence risk in humans, and occurrence in other animals (e.g., mice) to further understanding of pathogenesis.
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20/41. Hypothalamic-midbrain dysregulation syndrome: hypertension, hyperthermia, hyperventilation, and decerebration.

    Certain decerebrate lesions of brain stem or hypothalamus induce pharmacologically reversible hypertension and hyperthermia in animals. We observed three young patients with episodic decerebration, hyperthermia, hypertension, and hyperventilation during recovery from comas of different etiologies. The shared pathology on neurologic examinations and computed tomographic scans was hypothalamic-mesencephalic dysfunction, suggesting a diencephalic-brain-stem disconnection syndrome or brain-stem release mechanism. propranolol was the most effective drug tested, but only two patients responded, one dramatically. This novel clinical syndrome may have localizing and therapeutic significance in pediatric coma that needs to be further defined in future studies.
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