An Appraisal-Driven Componential Approach to the Emotional Brain

This article suggests that methodological and conceptual advancements in affective sciences militate in favor of adopting an appraisal-driven componential approach to further investigate the emotional brain. Here we propose to operationalize this approach by distinguishing five functional networks of the emotional brain: (a) the elicitation network, (b) the expression network, (c) the autonomic reaction network, (d) the action tendency network, and (e) the feeling network, and discuss these networks in the context of the affective neuroscience literature. We also propose that further investigating the “appraising brain” is the royal road to better understand the elicitation network, and may be key to revealing the neural causal mechanisms underlying the emotion process as a whole.

Autonomic reaction to vestibular damage

The vestibular system provides inputs to many neurons in the brain stem that participate in autonomic control. This multiplicity of vestibular-autonomic connections plays a variety of roles. Whereas it has been known for decades that unilateral vestibular lesions can result in motion sickness, recent data suggest that the vestibular system participates in making adjustments in blood pressure and respiration that are necessary to maintain homeostasis during movement and changes in posture. Animals with bilateral vestibular lesions are more susceptible to posturally related hypotension than vestibularly intact animals, and it is also possible that orthostatic hypotension after space flight is caused in part by microgravity-related changes in otolith function. Patients with vestibular lesions could also be more vulnerable to respiratory disturbances related to posture, such as obstructive apnea. Vestibular dysfunction has additionally been linked with anxiety disorders, such as agoraphobia, which may result from alteration of vestibular inputs to brain stem monoaminergic neurons (which are known to process these signals). Even sleep disturbances might be connected with vestibular disorders because neurons in the pontine reticular formation that are critical in switching between sleep states may be influenced by labyrinthine inputs. Thus it is likely that vestibular damage will result in a number of parallel disturbances in autonomic function. (Otolaryngol Head Neck Surg 1998;119:106-12.)

Changes in the Anterior Chamber of the Eye during Acute Hypoglycaemia in Humans

1. The changes in the volume and depth of the anterior chamber of the eye during acute insulin-induced hypoglycaemia were examined in nine healthy non-diabetic subjects (aged 23–31 years). The dimensions of the anterior chamber of the eye were measured by a photogrammetric technique, with Polaroid photographs taken of the lower half of the mid-sagittal plane of the eye at an angle of 55° at a magnification of × 16. Photographs were taken before and at regular intervals after the induction of acute hypoglycaemia using an infusion of unmodified (soluble) insulin at 2.5 m-units min−1 kg−1. Plasma adrenaline was measured regularly throughout the study. 2. Plasma glucose fell from 4.5 ± 0.2 mmol/l (mean ± SEM) to a nadir of 1.0 ± 0.1 mmol/l (P <0.01), which coincided with the onset of the acute autonomic reaction. Plasma adrenaline rose from 0.3 ± 0.1 nmol/l to a peak of 3.2 ± 0.6 nmol/l (P <0.01) at 15 min after the autonomic reaction. 3. The volume of the anterior chamber decreased by 8.2% from 284.7 ± 21.5 μl at baseline to 264.5 ± 17.0 μl (P <0.01) at the onset of the autonomic reaction. No significant alteration in axial anterior chamber depth was evident, but peripheral anterior depth decreased from 2.25 ± 0.20 mm at baseline to 2.07 ± 0.14 mm (P <0.05) at the onset of the autonomic response. Pupillary constriction was demonstrated in all subjects, which was most marked at 10 min after the autonomic reaction (baseline 5.0 ± 0.2 mm versus 10 min after reaction 3.7 ± 0.2 mm, P < 0.001). 4. This study has demonstrated an alteration in the dimensions and a reduction in volume of the anterior chamber of the eye in humans during acute insulin-induced hypoglycaemia. These changes in the anterior segment of the eye are probably mediated by autonomic mechanisms which are stimulated by hypoglycaemia.

Autonomic mechanisms underlying intraocular pressure changes during insulin-induced hypoglycaemia in normal human subjects: effects of pharmacological blockade

1. A fall in intraocular pressure is induced by acute hypoglycaemia in humans. The role of the autonomic nervous system in mediating this response was investigated in 24 normal volunteers in whom hypoglycaemia was induced with intravenous soluble insulin, under four experimental conditions: (1) control (n = 6), (2) nonselective α-adrenoceptor blockade (phentolamine) (n = 6), (3) non-selective β-adrenoceptor blockade (propranolol) (n = 6) and (4) cholinergic blockade (atropine) (n = 6). Intraocular pressure was measured by using an applanation tonometer. In 12 subjects intraocular pressure was measured during each type of pharmacological blockade of similar duration without induction of hypoglycaemia, to assess the effects of individual antagonists. 2. In the control study intraocular pressure fell during hypoglycaemia from 15 ± 1.0 to 10 ± 1.3 mmHg (P <0.01) 10 min after the autonomic reaction. β-Adrenoceptor blockade caused a reduction in intraocular pressure from 15 ± 1.1 to 9 ± 1.0 mmHg (P <0.001) before the administration of insulin, and when hypoglycaemia was induced intraocular pressure decreased further to 7 ± 1.0 mmHg (P <0.05, compared with immediately before insulin). A decrease in intraocular pressure of similar magnitude was observed with propranolol alone (16 ± 1.0 to 10 ± 1.0 mmHg, P <0.05). 3. Cholinergic blockade had no immediate effect on intraocular pressure, and the reduction in intraocular pressure during hypoglycaemia was of similar magnitude to that observed during the control study. α-Adrenoceptor blockade did not affect basal intraocular pressure, but the small reduction induced by hypoglycaemia (from 14 ± 1.4 to 12 ± 1.1 mmHg; P = not significant) was less than the decrement observed in the control experiment. The administration of atropine or phentolamine in the absence of hypoglycaemia had no significant effect on intraocular pressure. 4. In humans the reduction of intraocular pressure induced by acute hypoglycaemia appears to be mediated principally via an α-adrenoceptor-mediated mechanism.

A Psychophysiological Interpretation of Voodoo Illness and Voodoo Death

Voodoo illness is a form of psychosomatic illness. When sufficiently intense and prolonged, the extreme physiological arousal pattern to stimulation that comprises emotional behavior produces pathological changes in physiological functioning and anatomic structure, which are psychophysiological and psychosomatic disorders. New stimuli may become associated with established autonomic reaction patterns that are emotional behavior; also particular autonomic reactions may be strengthened through differential reinforcement. Thus, emotional stimuli and emotional response patterns may be learned. When the emotional reaction patterns are sufficiently frequent or prolonged and sufficiently intense in the person socially prepared to react and physically predisposed (i.e., vulnerable via genetically determined or later acquired biological weakness), changes of such magnitude may occur in physiological functioning or anatomical structure as to be incompatible with continued life. Voodoo death corresponds to that formulation of psychosomatic death.

Cholinergic Manifestations of the Acute Autonomic Reaction to Hypoglycaemia in Man

1. The effects of insulin-induced hypoglycaemia on pupil size, parotid salivary secretion and sweating were studied in seven normal volunteers. 2. Hypoglycaemia was associated with an acute stimulation of parotid salivary secretion and of sweating, synchronous in onset with the rise in heart rate. There was no clear evidence of concurrent pupillary constriction.