TO WHAT EXTENT IS BLOOD-INJURY PHOBIA DISTINCT FROM THE OTHER SPECIFIC PHOBIAS AND HOW DOES THIS INFLUENCE THE CLINICAL MANAGEMENT OF THE DISORDER?

University Degree Biological Sciences

STUDENT ESSAY No: 30

ABNORMAL PSYCHOLOGY

TERM 2

25 FEBRUARY 2008

TO WHAT EXTENT IS BLOOD-INJURY PHOBIA DISTINCT FROM THE OTHER SPECIFIC PHOBIAS AND HOW DOES THIS INFLUENCE THE CLINICAL MANAGEMENT OF THE DISORDER?

WORK COUNT: 2191

TO WHAT EXTENT IS BLOOD-INJURY PHOBIA DISTINCT FROM THE OTHER SPECIFIC PHOBIAS AND HOW DOES THIS INFLUENCE THE CLINICAL MANAGEMENT OF THE DISORDER?

Specific phobia is defined as an excessive or irrational fear of a place, object or situation, which is avoided at all cost or endured with intense distress and interferes significantly with a person’s normal daily routine (APA, 1994). The DSM-IV recognises four subtypes in specific phobias: situational type (e.g. flying by aeroplane), natural environment type (e.g. storms, height), animal type (e.g. spiders), blood-injury (BI) type (e.g. blood test, injury) and ‘other’ type (e.g. loud sounds). The category of BI phobia is characterised by a persistent fear that is excessive or unreasonable, this is triggered by direct or indirect exposure to blood, injuries and similar stimuli. The BI-related stimuli are either avoided or endured only with intense anxiety (APA, 1994). In addition, BI phobics are liable to faint in the presence of blood or injury (Page, 1994).

Factor analysis of specific phobia subtypes found evidence to suggest that situational and natural environment phobia types can be clustered together and possibly share a common underlying theme, whilst animal and BI phobias can be divided into distinct categories (Fredrikson et al, 1996). This essay will highlight the extent to which BI phobias are distinct from specific phobias in terms of its symptomalogy, aetiology, prevalence and biology, and as a result, what effect these differences have on the treatment phobics receive.

On exposure, patients with specific phobias exhibit somatic and autonomic changes to the phobic stimulus. This involves a marked global increase in sympathetic activity, known as the fight or flight response, which is common to all phobias, together with the subjective experience of heightened arousal. Physiological changes include tachycardia, increased respiration, increased blood pressure, increased adrenaline and noreadrenaline, and cephalic and peripheral vasoconstriction associated with increases in skeletal muscle blood flow (Sarlo et al, 2002; Hugdahl, 1989). Experiences of heightened arousal include high subjective tension and a tendency for avoidant and withdrawal behaviour. These changes are resolve when the subject has left the feared situation.

In addition to the sympathetic activation elicited in specific phobias, BI phobia involves a second autonomic nervous system response that entails activation of the parasympathetic nervous system resulting in the fainting (Ost et al, 1992). This is charaterised by a sudden onset of bradycardia and hypotension, increased blood glucose, cortisol, and human growth hormone and decreased noradrenaline (Vingerhoets, 1984).Eventually these physiological changes result in emotional fainting (vasovagal syncope) due to the considerable reduction in cerebral blood flow as blood is directed toward skeletal musculature (Ost et al, 1984a). Individuals report feelings of heat, dizziness, confusion, nausea, epigastric discomfort and yawning. Recovery is slow, leaving phobics in a state of suppressed heart rate and blood pressure (Page, 1994)

Even though many patients with other phobias may feel faint, actual fainting is rare. Connolly et al (1976) found that 100% of their sample of BI phobics reported fainting in the presence of feared stimuli, whereas only 0.02% of mixed phobics reported such fainting, thereby highlighting the fact that fainting is unique to BI phobia. Accurso et al (2001) found that 80% of BI phobia cases, were characterised by syncope, supporting Connolly’s findings. However, evidence from physiological studies is often limited its small sample size, making it difficult to generalise the findings, also these studies fail to explain what triggers the physiological response in the first place. Thus, BI phobia differs from other specific phobias in that it involves a diphasic autonomic nervous system response (Page, 2003).

In general, specific phobias have an early onset. Ost (1987a) reported mean onset ages of 7 and 9 years for animal and BI phobias respectively, thus suggesting that the fear has always been present. However such studies are criticised for its recall bias. The population prevalence of specific phobias is approximately 10%, with women being two to three times more likely to be affected than men (Mageeet et al, 1996). This is especially true for animal, situational and environmental phobias, however no gender differences have been found for BI phobias which has been found to be equally present in ...

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In general, specific phobias have an early onset. Ost (1987a) reported mean onset ages of 7 and 9 years for animal and BI phobias respectively, thus suggesting that the fear has always been present. However such studies are criticised for its recall bias. The population prevalence of specific phobias is approximately 10%, with women being two to three times more likely to be affected than men (Mageeet et al, 1996). This is especially true for animal, situational and environmental phobias, however no gender differences have been found for BI phobias which has been found to be equally present in men and women (2.7% , 3.2% respectively) (Fredrikson et al, 1996). Data collected on gender difference in phobia is not supported by the assumption that it is more socially acceptable for women to report fear than for men as response bias would affect reporting of all phobia types alike, and therefore be unable to explain the balanced sex distribution of BI phobia. Possibly, other predisposing factors also play a role in the skewed sex distribution of some specific phobias.

Several large scale twin studies have explored to what extent genetic factors predispose phobic to their fears; the studies indicate that a genetic factor is common to all phobias, thereby strongly predisposing a person to a specific phobia (Kendler et al, 1992). The genetic factors underlying specific fears appear to be of a general nature, suggesting that phobics are predisposed to neurotic complaints rather than an inheritance of a specific fear, thus making vulnerable individuals more prone to developing an anxiety disorders (Andrews et al, 1990). However, BI phobia may represent an exception to this pattern. There is some evidence suggesting that in BI phobia, the genetic contribution is fairly specific. Stevenson et al (1992) found in their study of common fears in twins aged 8 - 18, a substantial heritability for fear of injury and small animals. Unfortunately, these two heritability factors were not assessed separately (Page, 1994). The findings in this study were limited as they were based on a single lifetime assessment and not followed up. Additionally it is difficult to distinguish whether the effect were due to genetic or environmental factors in the study. Therefore suggesting BI phobia is not distinct from other specific phobias in its aetiology.

A different approach to the acquisition of phobia is the behavioural approach which suggests that phobias can be elicited through the conditioning process (Rachman, 1991). Accordingly, painful experiences can condition fear of specific stimuli. However this is disputable for BI phobia, for example, if a child faints after receiving an injection this can’t be due to conditioning as there is no apparent unconditioned stimulus. Injections do not unconditionally lead to fainting. It is more likely that the fainting itself is a manifestation of a pre-existing problem.

Furthermore, it has also been suggested that BI phobics do not fear blood (Rachman, 1990). Fainting may cause injury or embarrassment, which may result in the person fearing stimuli that appear to trigger these events. Instead, BI phobics fear the consequences of fainting when confronted with blood. This fear of body sensation suggests a connection between BI phobia and panic disorder, however, the DSM-IV treats BI phobia as a specific phobia.

Additional evidence suggests that BI phobia is qualitatively different from other specific phobias in the sense that phobic distress takes the form of disgust rather than (threat-induced) fear (De Jong et al, 2007). Although phobia is traditionally associated with fear, descriptive studies have shown that BI phobics report greater disgust towards stimuli related to blood, mutilation, and surgeries, as well as a disgust reactions towards a broader range of stimuli unrelated to phobic concerns (Sawchuk et al, 2000). Moreover, Sawchuk et al (2000) also found that BI phobic participants were more likely to complete general disgust-related word stems than were non-phobic participants, suggesting an implicit memory bias towards disgust. However, such evidence is correlational and does not prove causation. As most studies on disgust and phobia relied on a correlational approach, they do not rule out the possibility that fear enhances disgust or rather than vice versa.

Using fMRI technology to address this elevated level of disgust found in BI phobics, Hermann at al (2007) observed diminished medial prefrontal cortex (MPFC) activity in BI phobic patients compared to controls. The MPFC has been shown to be involved in the automatic and effortful cognitive regulation of emotions, reflecting the reduced cognitive control of emotions seen in BI phobia during the experience of phobic symptoms. However, Hermann’s finds are limited as they are based on a small sample of female participants therefore lacking ecological validity, additionally there is a need for more supporting evidence there are only 2 published fMRI studies.

Neuroimaging studies focusing on other anxiety disorders besides BI phobia have often found increased activity in regions involved in the automatic processing of fear stimuli such as the amygdala, the hippocampus and the anterior cingulate cortex (ACC) (Schienle et al, 2005), with a decrease in activity being frequently noted in the prefrontal cortex region (Kim and Gorman, 2005). This decrease in activity might reflect a deficit in cognitive control during excessive states of anxiety and could possibly lead to reduced inhibitory regulation of limbic regions, which are assumed to have specific functions in emotional modulation and cognitive processing (Phan et al, 2004). Taking this into account, it is likely that abnormal activity in MPFC areas might be an important characteristic of anxiety disorders (LeDoux, 2002). Again, these studies are criticised for having small single sex participant foundations, therefore we cannot infer that these findings are applicable to the whole population.

To summarise, it appears that an inherited vulnerability and conditioning episodes may be involved in the aetiology of BI phobia in the same way they are found in other phobias. However BI phobia additionally displays vasovagal syncope and disgust, thereby distinguishing it from other phobias which cannot be explained by conditioning and genetic vulnerability alone.

Until recently, BI phobia was regarded and treated in a similar way to other specific phobias. Whilst specific phobia appears to be a highly common disorder in the general population, treatment seeking is relatively rare. Treatment for BI phobia is compulsory when it endangers the patient’s life through avoiding medical procedures. In specific phobia, behavioural therapy is the treatments of choice (Ost et al., 1984b). The important component of therapy is to challenge the beliefs phobic individuals hold as they rarely encounter situations where they can disconfirm their phobic beliefs. Treatment involves the patient being exposed to situations that induce fear and faintness for a prolonged amount of time. The patient is asked to carry out exposure homework to those situations between sessions and to record details and reactions in a diary. These principles can be applied to patients with BI phobia; such as looking at a vial of blood or handling needles. Research has shown this technique to be effective in BI phobia, (Ost et al, 1984b; Curtis and Thyer, 1983). However, these studies are limited as due to unrealistic nature and small sample size. Furthermore, fainting hinders the exposure exercises; thereby reducing the treatment success as fear is not reduced (Page, 1994).

As a result, modifications have been made to reduce the likelihood of fainting. Patients with BI phobia begin exposure while reclining, with gradual progression until they are able to stand and face their phobic objects (Marks, 1988). Treatment for BI phobia is more successful when used in combination with relaxation techniques; such as deliberately try to feel angry (Cohn et al, 1976) or by tensing muscles (Ost et al, 1984b). This is based on the assumption that any activity incompatible with syncope would prevent fainting. For example, being angry involves increases in heart rate and blood pressure which increase venous return and cardiac output, thereby prevents or reverses syncope. This technique is known as ‘applied tension’ (Kozak and Montgomery, 1981). There are many investigations reporting success of patients with BI phobia even after several months follow up (Cohn et al, 1976; Wardle & Jarvis, 1981)

A new treatment procedure has recently been proposed for individuals suffering from specific phobias called Eye Movement Desensitisation and Reprocessing (EMDR). EMDR assumes that phobias are both derived from and driven by earlier life experiences. The treatment aims to reduce anxiety using saccadic eye movements (De Jongh et al, 1999). Studies have found that improvement can be achieved in a limited number of sessions and reports similar levels of susses in treating BI phobia. However, support for these findings is limited and there is potential for re-sensitization (Willemsen et al., 2002). However, an atypical phobia such as BI which is without a known traumatic component in its aetiology generally tend to respond less strongly to EMDR than those who do. This notion is supported by the finding that the severity of BI phobia is highly associated with disgust (Page, 1994). Therefore one should remain cautious in regards to the application of EMDR with specific phobias.

Overall, BI phobia is a distinctive specific phobia in that it shares some characteristic with specific phobia and has distinct characteristics of its own. In line with specific phobia, sufferers have a strong family history and most manifest their problem in childhood. However, on seeing their phobic cues some patients experience nausea and disgust rather than fear. Additionally, BI phobics have a diphasic autonomic response, often faint in bradycardic syncope, whereas patients with other phobias get persistent tachycardia. BI phobia can be successfully treated by systematic exposure however treatment may differ in comparison to specific phobics, including additional techniques to reduce fainting. Despite these differences BI phobia is still treated as a specific phobia in the DSM-IV and may need to be reviewed in light of these findings from research.

REFERENCES

Accurso V, Winnicki M, Shamsuzzaman ASM, Wenzel A, Johnson AK & Somers VK. (2001) Predisposition to Vasovagal Syncope in Subjects with Blood/Injury Phobia. Circulation, 104, 903-907.

APA (1994). Diagnostic and statistical manual of mental disorders (4th ed.) Washington, DC: American Psychiatric Association.

Cohn CF, Kron RE, Brady JP. (1976) A case of blood-illness-injury phobia treated behaviourally. . 162, 65-68

Connolly JC, Hallam RS, Marks IM. (1976). Selective association of fainting with blood-injury-illness fear. Behaviour Therapy, 7, 8-13

Craske, MG, Barlow, DH, Clark, D, Curtis, G, Hill, EM, Himle, J. (1996). Specific (simple) phobia. In T. A. Widiger, A. Frances, H. Pincus, R. Ross, M. First, & W. Davis (Eds.), DSM-IV sourcebook, Vol. 2 (pp. 473–506). Washington, DC: American Psychiatric Association.

Curtis GC. & Thyer B. (1983) Fainting on exposure to phobic stimuli. American Journal of Psychiatry 140 (6), 771-774.

De Jongh A, Broeke ET, Renssen MR. (1999) Treatment of Specific Phobias with Eye Movement Desensitization and Reprocessing (EMDR): Protocol, Empirical Status, and Conceptual Issues. Journal of Anxiety Disorders, 13, 69–85.

Fredrikson M, Annas P, Fischer H, & Wik G. (1996). Gender and age differences in the prevalence of specific fears and phobias. Behaviour Research and Therapy, 34, 33-39.

Hermann A, Schäfer A, Walter B, Stark R, Vaitl D, Schienle A. (2007) Diminished medial prefrontal cortex activity in blood-injection-injury phobia. Biological Psychology, 75, 124–130

Hugdahl, K. (1989). Simple phobias. In G. Turpin (Ed.), Handbook of clinical psychophysiology. Chichester: Wiley.

Kim J, Gorman J. (2005). The psychobiology of anxiety. Clinical Neuroscience Research, 4, 335–347.

Kozak MJ, Montgomery GK. (1981). Multimodal behavioral treatment of recurrent injury scene-elicited fainting (vasodepressor syncope). Behavioural Psychotherapy, 9, 316-321.

LeDoux JE. (2002). Synaptic Self: How Our Brains Become Who We Are. Penguin Books, New York.

Marks IM. (1988). Blood-injury phobia: A review. American Journal of Psychiatry, 145, 1207-1213.

Ost LG. (1992). Blood and injection phobia: background and cognitive, physiological, and behavioural variables. Journal of Abnormal Psychology, 101, 68-74.

Ost LG, Sterner U, Lindahl IL, (1984a). Physiological responses in blood phobics. Behaviour Research and Therapy, 22, 109-117.

Ost LG, Lindahl LL, Sterner U. (1984b) Exposure in vivo vs applied relaxation for blood phobia. Behaviour Research and Therapy, 22, 205-216

Page AC. (2003). The role of disgust in faintness elicited by blood and injection stimuli. Journal of Anxiety Disorders, 17, 45–58.

Page AC. (1994). Blood-injury phobia. Clinical Psychology Review, 14, 443-461

Phan KL, Wager TD, Taylor SF, Liberzon I. (2004). Functional neuroimaging studies of human emotions. CNS Spectrums, 9, 258–266.

Mageet WJ, Eaton WW, Wittchen HU, McGonagle KA, Kessler RC (1996). Agoraphobia, simple phobia, and social phobia in the National Comorbidity Survey. Archives of General Psychiatry, 53, 159 –168.

Schienle A, Schafer A, Walter B, Stark R, Vaitl D. (2005). Brain activation of spider phobics towards disorder-relevant, generally disgust- and fear inducing pictures. Neuroscience Letters, 388, 1–6.

Sarlo M, Palomba D, Angrilli A & Stegagno L. (2002) Blood phobia and spider phobia: two specific phobias with different autonomic cardiac modulations, Biological Psychology, 60, 91-108.

Stevenson J, Batten N, Chemer M. (1992). Fears and fearfulness in children and adolescents: A genetic analysis of twin data. Journal of Child Psychology and Psychiatry, 33, 977-985.

Vingerhoets AJJM. (1984). Biochemical changes in two subjects succumbing to syncope. Psychosomatic Medicine, 46, 95-103.

Wardle J, Jarvis M. (1981) The paradoxical fear response to blood, injury and illness: a treatment report. Behavioural Psychotherapy, 9, 13-24

Willsemsen H, Chowdhury U & Briscall L. (2002). Needle Phobia in Children: A Discussion of Aetiology and Treatment Options. Clinical Child Psychology and Psychiatry, 7(4), 609-619.