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mise à jour du
5 février 2006
Arch Gen Psychiatry
1993; 50; 4; 306-317
False suffocation alarms, spontaneous panics,
and related conditions.
An integrative hypothesis.
Klein DF
Department of Psychiatry, Columbia University, New York


Abstract : A carbon dioxide hypersensitivity theory of panic has been posited. We hypothesize more broadly that a physiologic misinterpretation by a suffocation monitor misfires an evolved suffocation alarm system. This produces sudden respiratory distress followed swiftly by a brief hyperventilation, panic, and the urge to flee. Carbon dioxide hypersensitivity is seen as due to the deranged suffocation alarm monitor. If other indicators of potential suffocation provoke panic this theoretical extension is supported. We broadly pursue this theory by examining Ondine's curse as the physiologic and pharmacologic converse of panic disorder, splitting panic in terms of symptomatology and challenge studies, reevaluating the role of hyperventilation, and reinterpreting the contagiousness of sighing and yawning, as well as mass hysteria. Further, the phenomena of panic during relaxation and sleep, late luteal phase dysphoric disorder, pregnancy, childbirth, pulmonary disease, separation anxiety, and treatment are used to test and illuminate the suffocation false alarm theory.
Chronic hyperventilation causes both low PCO2 and bicarbonate levels. These normalize during panic remission ,76 suggesting that chronic hyperventilation does not cause panic, but rather it adaptively compensates for a lowered suffocation alarm threshold by keeping PCO2 below the triggering range.
Chronic hyperventilation might entail a vicious circle if hypocapnia produced a deafferentation hypersensitivity, thus further decreasing the alarm threshold. However, chronic hyperventilation effects on carbon dioxide sensitivity are markedly variable, so this remains an interesting possibility.'
Chronic hyperventilation as an adaptive hypocapnia inducing mechanism is consonant with frequent sighing, a venerable feature of neurosis. A feeling of respiratory oppression precedes sighing. The deep inspiration that initiates a sigh, triple the normal tidal volume, abruptly lowers PCO2 and relieves respiratory distress. Therefore, chronic hyperventilation and sighing may adaptively keep PCO2 below a depressed suffocation alarm threshold. (It is arresting that frequent extreme yawning inspirations often accompany increased sighing, indicating a common function.) A sigh or yawn may serve as a bioanalytical test for high ambient carbon dioxide. If, on deep inhalation, the PCO2 failed to fall sufficiently, an asphyxiai cue would be detected.
That suffocation serves as a particularly traumatic unconditional stimulus was made plain by Sanderson et al and Campbell et al. These investigators gave alcoholic volunteers an injection of succinyicholine, producing a "harrowing" period of 90 to 130 seconds in which they were unable to move or breathe while remaining conscious. A tone, to which they had previously been habituated, was played during the apnea.
After the paralysis, many took occasional deep breaths that led to an immediate suppression of respiration for 12 to 15 seconds. Curiously this re-creation of the traumatic stimulus was not aversive. This becomes comprehensible if the sighs served as ambient carbon dioxide bioassays. Since the sigh-induced apneas diagnosed a safe low carbon dioxide environment they were safety signals, although they should be anxiogenic by conditioning theory. The potency and specificity of the suffocation stimulus is indicated by the marked resistance to extinction of these subjects sighing.
The mysterious contagious effects of yawns and sighs are well known. Observed acute inspirations may be interpreted as tests of increased ambient carbon dioxide or efforts to overcome breathlessness. Thus, observing another's yawn incites ones' own yawning test without any relevant cognition, thus resembling an ethologic fixed action pattern.
Panics occur during relaxation' and deepening nonrapid eye movement s1eep despite lack of danger cues or cognitions. However, both states cause sharply increasing PCO2, especially in those with chronic hyperventilation.
If sensitivity to increasing PCO2 incites panics during relaxation and sleep, then those who panic during deepening sleep should also be likely to panic during relaxation. Mellman and Uhdde have shown this.
Ley suggests that patients who panic during sleep are chronic hyperventilators with diminished buffer. Therefore, minor nocturnal ventilatory reductions cause hypercapnic respiratory acidosis, which incites hyperventilation, swinging into hypocapnia that triggers panic.
However, even given that nocturnal panickers chronically hyperventilate, carbon dioxide increase due to nocturnal ventilatory reduction might lead only to a compensatory tidal volume increase, producing eucapnia rather than hypocapnia. Ley's model does not account for overshoot. Further, even given overshoot, it does not follow that acute hypocapnia produces panic since controlled studies indicate hypocapnic hyperventilation is insufficient.
In our model, hyperpnea, hypocapnia, and alkalosis are consequences of panic rather than causal antecedents. If nocturnal carbon dioxide challenges were panicogenic prior to respiratory alkalosis onset, this would resolve this disagreement.
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Observation personnelle
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mise à jour le
28 septembre 2008
ECG Clin Neurophysiol
Lafleur J, Reiher J
Sheerbrook, Quebec
Hyperventilation-induced alterations in the level of consciousness with electroencephalographic slowing have been documented repeatedly. Over the past 5 years, three children presented with hyperventilation-stereotyped attacks that impressed us as being extremely unusual, both clinically and electroencephalographically. These attacks we have termed 'pseudoabsences.'
In contrast to the striking ictal discharges of typical or atypical absences, the concomitants of pseudoabsences resemble but a mere accentuation of the hyperventilation buildup.
It should be stressed, however, that:
(1) electroencephalographically, the sinusoidal slow waves of pseudo-absences are of higher voltage, more widely distributed, and distinctly slower than those encountered with the usual hyperventilation buildup.
(2) clinically, concomitantly with the appearance of these slower waves, the child stops breathing, stares, fails to obey simple commands, and may exhibit automatic movements such as yawning, swallowing, and smiling.
Seconds after cessation of overbreathing, the electroencephalogram reverts gradually to a more normal appearance. The child then begins spontaneously to hyperventilate again, as if resuming activity where he had left off. The same sequence of events recurs repeatedly, the second and subsequent attacks being precipitated by much shorter bouts of hyperventilation than the initial one.