Facts, fallacies, fears, and frustrations with human pheromones

Among primates in general, pheromones are of variable importance to social communication. Data on humans have generated the greatest controversy regarding the existence of pheromonal communication. In this review, the likelihood of pheromonal communication in humans is assessed with a discussion of chemical compounds produced by the axilla that may function as pheromones; the likelihood that the vomeronasal organ (VNO), a putative pheromone receptor organ in many other mammals, is functional in humans; and the possible ways pheromones operate in humans. In the human axilla, the interactions between the cutaneous microflora and axillary secretions render this region analogous to scent glands found in other primates. Both the chemistry of axillary secretions and their effects on conspecifics in humans appear to be analogous to other mammalian pheromone systems. Whichever chemical compounds serve a pheromonal function in humans, another unknown is the receptor. Although the VNO has been implicated in the reception of pheromones in many vertebrates, it is not the only pathway through which such information has access to the central nervous system; there is ample evidence to support the view that the olfactory epithelium can respond to pheromones. Furthermore, if a chemical activates receptors within the VNO, this does not necessarily mean that the compound is a pheromone. An important caveat for humans is that critical components typically found within the functioning VNO of other, nonprimate, mammals are lacking, suggesting that the human VNO does not function in the way that has been described for other mammals. In a broader perspective, pheromones can be classified as primers, signalers, modulators, and releasers. There is good evidence to support the presence of the former three in humans. Examples include affects on the menstrual cycle (primer effects); olfactory recognition of newborn by its mother (signaler); individuals may exude different odors based on mood (suggestive of modulator effects). However, there is no good evidence for releaser effects in adult humans. It is emphasized that no bioassay-guided study has led to the isolation of true human pheromones, a step that will elucidate specific functions to human chemical signals.     

Depersonalization,adversity, emotionality,and coping with stressful situations

Depersonalization is defined as persistent or recurrent episodes of feeling detached or estranged from a sense of self and the world. This study addressed the primary question: Do nonclinical individuals who endorse high symptomatic depersonalization have inherently more intense emotional responses, along with more childhood adversity and past trauma? In this IRB approved study, participants who met clinical levels of depersonalization (n = 43, 16.3%) were compared to a group without clinical levels of depersonalization (n = 221, 83.7%). Adverse childhood experiences, adult traumatic events, emotional overexcitability, coping strategies under stress, and anxiety were examined in both groups. The variables to assess depersonalization severity included the Dissociative Experience Scale-II, Cambridge Depersonalization Scale, and Multiscale Dissociation Inventory. The results indicated that clinical levels of depersonalization were identified in 16.3% of the sample. The high depersonalization group had significantly more adverse childhood experiences, in particular, emotional abuse and neglect. They also experienced more adult traumatic events, higher levels of anxiety, more emotional overexcitability, and they employed a less adaptive emotion-oriented coping strategy under stress. It is recommended that treating depersonalization symptoms should include examining childhood adversity, especially emotional abuse and neglect. Based on study findings, emotion regulation skills should be promoted to help individuals with elevated depersonalization manage their emotion-oriented coping strategies, anxiety, and emotional overexcitability.     

Life-threatening overdose with lamotrigine, citalopram, and chlorpheniramine

Lamotrigine is a commonly used agent for seizure control in epilepsy. There are limited data on the adverse effects of lamotrigine in overdose. We report a number of serious side-effects associated with a large overdose of lamotrigine. A 23-year-old female presented to the emergency department after taking an intentional overdose of 9.2 g of lamotrigine, 56 mg of chlorpheniramine, and 220 mg of citalopram. On admission, she had a reduced level of consciousness and electrocardiographic abnormalities; a widened QRS and a prolonged corrected QT (QTc) interval. Prompt treatment with early intubation, along with the use of magnesium for cardioprotection and administration of sodium bicarbonate may have aided in a quick recovery with a short intensive care stay and good outcome.     

Osteochondrodysplasia with rhizomelia, platyspondyly, callosal agenesis, thrombocytopenia, hydrocephalus, and hypertension

A female infant born at term to phenotypically normal nonconsanguinous parents had hypertension, thrombocytopenia, hydrocephalus, callosal agenesis, and nonlethal rhizomelic osteochondrodysplasia. Her osteochondrodysplasia was characterized roentgenographically by shortening and metaphyseal broadening of long bones, without bowing, and by platyspondyly, with deficient ossification of dorsal and central portions of vertebral bodies. By light microscopy, the iliac crest growth plate showed expansion of the zone of chondrocyte hypertrophy and degeneration, with faulty columnar alignment, sparse vascular ingrowth, and irregular mineralization at the zone of chondroosseous transformation. These findings appear to define a novel osteochondrodysplasia, which in association with hypertension, thrombocytopenia, hydrocephalus, and callosal agenesis may constitute a new syndrome.     

Comparison of CLA with BPT, SPT, and RAST in children with asthma

Bronchial provocation tests (BPT) with allergen extracts were performed in 82 children with asthma, and the results were compared with the chemiluminescent assay (CLA), the radio-allergo-sorbent-test (RAST) and skin prick test (SPT). It was found that CLA matched BPT with a concordance of 87% (77-93%), RAST with a concordance of 74% (64-83%) and SPT with 80% (70-88%). Most often, CLA and RAST gave similar results, although their classes did not match precisely.     

Sibs with growth deficiency, delayed bone age, congenital hip dislocation, and iridocorneal abnormalities with glaucoma

We report on a brother and sister with short stature, delayed bone age, developmental delay, congenital hip dislocation, and iridocorneal abnormalities with onset of glaucoma at or soon after birth. Results of endocrine evaluation were normal. To our knowledge, no similar pattern of defects has been reported previously.     

RAST with animal dander, urine, saliva and serum

Binding of specific IgE antibodies from the sera of patients allergic to animals was investigated by direct RAST, using the animal's dander, urine, saliva or blood serum as insolubilized allergens. In allergy to rat, mouse, guinea pig, dog, cat or horse, the RAST results with the excretions of a particular animal were mutually well correlated. RAST with the animal blood serum was positive less often, and only in cases of a positive dander RAST. It is concluded that a RAST with animal dander precludes the use of other animal products.     

Parkinsonian symptoms with lithium, lithium-neuroleptic, and lithium-antidepressant treatment

Eighty-one patients treated for a least 3 months with lithium were examined for the presence of parkinsonian symptoms. Twenty-four patients were receiving treatment with lithium alone, 30 with lithium and 1 or more neuroleptics, and 27 with lithium and antidepressant. Twenty-four of the patients were found to be free from parkinsonian symptoms. Severe rigidity was not found. Two patients receiving neuroleptic with lithium and 6 on lithium-antidepressant combinations exhibited severe tremor. Neuroleptics administered concomitantly with lithium did not aggravate parkinsonian symptoms. The combination of lithium and an antidepressant significantly increased tremor in comparison to lithium alone.