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20th November 2023

Psychopathology of Neurosis

Classification

The classification of neurotic, stress-related and somatoform disorders cover ICD-10 codes F40-F48, and DSM-5 terminology has been included where appropriate. In ICD-11, anxiety or fear-related disorders (6B00-6B06), obsessive-compulsive related disorders (6B20-6B2Z), disorders specifically associated with stress (6B40-6B4Z) and dissociative disorders (6B60-6BZ) are separate categories.

References

  • International Statistical Classification of Diseases, tenth revision (ICD-10), Version:2016, https://icd.who.int/browse10/2016/en#/F40-F48
  • International Statistical Classification of Diseases, eleventh revision (ICD-11), Version 01/2023, https://icd.who.int/browse11/l-m/en

Panic Disorder

It would be difficult to talk about ‘neuroses’ without first looking at panic attacks and panic disorder. Although the term neurosis is not used commonly anymore, the breadth of the topics it refers to is vast and affects a considerable amount of the population. Panic attacks are characterised by a collection of physiological symptoms that happen spontaneously or occur in response to a situational stimulus. These include but are not limited to tachypnoea, tachycardia, palpitations, chest pain, nausea, vomiting, sweating, tremors, dizziness, derealisation and fear of death. When these attacks occur more frequently, you will start to consider if panic disorder (ICD-10 F41.0) is present. Understandably, patients may change the way they behave to avoid the symptoms they feel when they have panic attacks. For the rest of this section, we will look deeper into panic disorder.

Predisposition, onset and maintenance

There are two peaks in the age of onset of panic disorder; these are 15-24 and 45-54 years of age. The incidence is more common in females, who are 2-3 times more likely to be affected. Risk factors for developing panic disorder also include life events such as separation or divorce from a partner, death of a spouse or a parent at a young age, history of abuse, physical illness, low educational level, and even living in a city. Understanding some biological theories behind panic disorder can help to understand potential treatments.

Theory  Explanation Receptor
Serotonergic model Increased postsynaptic response to serotonin 5-HT
GABA model Decreased response to inhibitory neurotransmitter GABA (what a shock)
Noradrenergic model Increased activity and sensitivity of receptors α2

If treated, then 25-75% of patients recover in the first 1-2 years. However, this drops to 10-30% after 5 years. If left to go untreated, then the course is chronic. Good prognostic factors are mild symptoms at onset, absence of risk factors and other comorbidities, in particular personality disorders.

Focused history

Patients should be asked about any comorbid diagnoses or substance use, including alcohol, steroids, nicotine and caffeine. The time frame of onset of physiological symptoms should be elicited; commonly, peak intensity is reached within 10 minutes of onset and settles within half an hour. How long they have been experiencing symptoms, and how often they have been treated for something similar in the past. Most importantly, what impact this is having on the patient and their lifestyle.

Assessment of physical factors and investigations

Certainly, in the first presentation of panic attacks or disorder, it is important to rule out serious underlying pathology, but in the case of recurrent panic attacks with a clear history, this may not always be essential. Anyone who has spent time in an A&E setting will be able to think of a case where a patient presenting with chest pain, wholly convinced that they are having a heart attack, is actually in the throes of a panic attack. As there are no diagnostic investigations, the tests listed here are purely for purposes of exclusion:

  • Physical observations and examination.
  • Blood tests – FBC, U&E, TFTs, toxicology, calcium and glucose.
  • ECG – looking for other causes of palpitations and making sure the patient isn’t right about that MI!
  • ABG, urinary catecholamines, cortisol and drug screening may also be indicated.

Diagnosis

When panic attacks occur frequently for over at least one month, in the absence of other causes, a diagnosis of panic disorder can be considered. According to ICD-10 criteria, a diagnosis of panic disorder can be made when panic attacks occur when there is no real danger, in situations that cannot be predicted, with the absence of symptoms between attacks. Agoraphobia often comes hand in hand with panic disorder.

Treatment

Biological treatments – SSRIs (namely sertraline) are first-line treatment according to NICE guidance and should be started at half the recommended dose than for depression. If SSRIs are not appropriate, then tricyclic antidepressants such as imipramine can be considered. Although not recommended by NICE, in severe cases, benzodiazepines can be used only in the short term, and risks with concurrent substance use need to be considered.

Psychological treatments – Weekly CBT sessions lasting for up to 4 months or self-help programmes and groups. With waiting times for referrals being as they are, in practice, it is common to start medication first, which may also help the patient to get to a place where they are more able to engage with psychological therapies.

Social – Advice on alcohol and substance cessation and identifying social support networks.

References

Generalised Anxiety Disorder

Generalised anxiety disorder (GAD, ICD10 F41.1)) is characterised by symptoms of anxiety that are present (unsurprisingly) in general day-to-day life rather than being related to particular circumstances. It is natural to have worries and anxieties, but in GAD, they are hard to control and disproportionate to the context.

Predisposition, onset and maintenance

In the UK, 1 in 25 people will be affected by GAD, and it is more common in females than males. The lowest incidence is in 18-29 years and 60+ years (4.1% and 3.7% respectively), and the highest is in 45-59 years (7.7%). Let’s talk about the triple vulnerability model for developing GAD:

Generalised biological vulnerability  Genetic – Common inheritance with depression.

Neurobiological – Linked with many systems, including HPA axis, autonomic nervous system, amygdala and stria terminalis, septohippocampal system, benzodiazepine-GABA system and other neurotransmitter dysregulation.
Generalised psychological vulnerability  Diminished sense of control – Relates to insecure attachment types and past trauma.

Parenting – Stems from styles that are either too protective or unaffectionate.
Specific psychological vulnerability  Life events – Traumas and unstable relationships.

Generally poor prognosis with a chronic course of illness. After 3 years, around 30% of treated patients will be in remission; after 6 years, 68% will continue to have mild symptoms, and in 9% the symptoms will still be severe.

Focused history

Make sure to elicit any underlying comorbidities and identify any medications that could be inducing symptoms. When asking about the symptoms, make sure to inquire about how much this affects their functioning socially, in daily activities and at work or school. Address possible causes as they may help to guide future treatments.

Assessment of physical factors and investigations

Similarly to panic disorder, there are no specific tests for GAD, and investigations should be undertaken to rule out other physical causes.

Diagnosis

A diagnosis can be made when patients describe a 6-month history of anxiety that is present on most days and not related to a specific situation. ICD-10 suggests that at least 4 of the following should be present: autonomic stimulation, impairments in concentration, muscular tension or aches, physical symptoms such as chest, GI and breathing difficulties, mental symptoms such as dizziness, light-headedness, derealisation, nervousness and fears someone close to them may come to harm and finally overreaction to mild stimulus. DSM-5 takes into consideration irritability, restlessness, feelings of fatigue and sleep problems.

Treatment

Biological treatments – SSRIs are first-line according to NICE; if ineffective, then a second SSRI can be tried before moving on to SNRIs or pregabalin if antidepressants are contraindicated or as an adjuvant. Like panic disorder, benzodiazepines should only be offered in crises.

Psychological treatments – In mild-moderate cases, 5-14 week independent self-help courses can be offered, or courses with others would last 6 weeks. Applied relaxation or CBT focused on behavioural and cognitive methods may be useful for moderate-severe cases; these are offered as weekly sessions for 3-4 months.

Social – Advice on alcohol cessation and identifying social support networks.

References

Obsessive-Compulsive Disorder 

OCD (ICD-10 F42) is characterised by either obsessions or compulsions, or both, is usually accompanied by anxiety and negatively impacts functioning. Let’s have a look at the definitions of obsessions and compulsions.

Obsessions – Frequent intrusive and distressing thoughts, images or impulses that the patient recognises as being their own. For example, the thought that a partner may be unfaithful.

Compulsions – Compulsive acts or rituals can be mental or behavioural. These repeated behaviours are used to counteract obsessions and not to provide enjoyment or complete beneficial tasks. For example, excessive cleaning or reciting a phrase in their head. These can take up a considerable portion of the patient’s day.

Predisposition, onset and maintenance

OCD is usually sudden onset and affects males and females equally. The age of onset is 20, with 70% of cases starting before the age of 25. It affects as much as 0.5-3% of the population. There is evidence from family and twin studies that patients may be genetically predisposed to developing OCD; however, no specific genes have been identified. It is possible that compulsions are learned responses to try and reduce the anxiety induced by obsessions, which leads us to psychoanalytical aetiology and Freud’s ‘obsessional neurosis’, where aggressive or sexual impulses lead to regression to previous psychosexual developmental stages. Following on from this, neurotic defence mechanisms commonly associated with OCD are undoing, isolation and reaction formation. Other explanations include dysregulation of serotonin and autoimmune response against the basal ganglia (see investigations below).

Improvement in symptoms is seen significantly in 20-30%, moderately in 40-50%, but chronically or even worsening in 20-40% of cases. Patients with worse prognoses often obey compulsions, have had OCD for a long time, were younger when it started or have psychiatric comorbidities. The rates of suicide are high, especially with concurrent depression.

Focused history

It can be useful to ask about specific compulsions; excessive cleaning, checking, counting, list making, arranging things specifically, touching them repeatedly or carrying out actions a specific amount of times are commonly reported. Or about specific obsessions: cleanliness, needing symmetry or order, violent or sexual thoughts, fear of doing the wrong thing or things that are against the law or their religion, that they have forgotten something or have left their property in an unsafe state. The patient would feel like the thoughts came from themselves, in contrast to thought insertion seen in schizophrenia. Again, it is important to know how much of their day is taken up by these thoughts or acts and how much harm or distress it is causing them. Patients may not recognise these undertakings as being separate from their daily routine.

Assessment of physical factors and investigations

You guessed it, just like panic disorder and GAD, there are no specific investigations for OCD, and imaging is not usually offered. Despite this, CT and MRI head imaging may reveal a bilateral reduction in caudate nucleus size. PET / SPECT scans show increased metabolism in the basal ganglia, orbitofrontal gyrus and cingulum.

Diagnosis

Presence of obsessions, compulsions or both that impact functioning or activities on most days for at least 2 weeks.

Treatment

Referral to specialist services should be completed to give access to clinicians who can undertake assessments and offer both psychological and biological treatments.

Biological treatment – SSRIs are equally as effective as intensive CBT in moderate impairment. These interventions can be offered in combination if monotherapy is inadequate. Second line pharmacological treatment is with clomipramine. Next, treatment with SSRI and antipsychotics such as aripiprazole or risperidone should be considered; following this treatment with a combination of clomipramine and citalopram is recommended by NICE.

Psychological treatment – In mild impairment, then up to 10 hours of individual or group CBT or exposure and response prevention therapy should be offered first. If this is unsuccessful, then biological treatment or more intensive therapy should be suggested.

Social treatment – Educating families and carers to build an understanding of the symptoms and support. OCD symptoms may be linked to religious beliefs; support and advice can be sought from appropriate religious leaders.

References

Post-Traumatic Stress Disorder

This is another disorder where the clue is in the name. Post-traumatic stress disorder (PTSD, ICD-10 F43.1) occurs in response to a particularly traumatic life event or even multiple life events. Patients describe reliving the experience, understandably avoiding events that remind them of it and heightened reactions to stimulus or hypervigilance.

Predisposition, onset and maintenance

It is more common in patients of lower social or educational status, from Afro-Caribbean or Hispanic backgrounds, previous psychiatric comorbidities or traumas and low self-esteem. More common in females with a ratio of 1:2, men have an 8-13% chance of developing PTSD following an event compared with 20-30% for females. There may be psychological and biological roles in developing PTSD. Psychologically, reliving the experience, keeping the experience as an active memory until it has been dealt with or dissociating from it play a role. There are neurophysical changes in response to stress caused, which may lead to neuronal changes. Stress hormones like glucocorticoids and catecholamines, alongside serotonin, GABA and opioids, are associated.

Focused history

Firstly, it would be critical to identify the stressful event and then move on to assessing the impact. The patient may experience flashbacks in day-to-day life or nightmares; this can be coupled with strong sensations and intense emotions. They may be actively avoiding thinking about the event, which would cause setbacks in coming to terms with what has happened or avoiding places, situations or people that were there. The patient may perceive that they are constantly under threat.

Assessment of physical factors and investigations

Similarly to OCD, imaging is not used in the diagnosis, but there may be changes seen, for example, reduced volume of the hippocampus. The fear response may be heightened due to irregular functioning of the amygdala, hippocampus, prefrontal cortex and septum. Whereas the anterior cingulate, medial prefrontal cortex and thalamus may play a role in hyperarousal. The occipital, parietal and temporal cortices mediate dissociative phenomena.

Diagnosis

Symptoms are seen within 6 months of the initial traumatic stressor, present for 1 month, with a negative impact on functioning. Symptoms should not be present before the event, and patients must experience two or more of the following: flashbacks, remembering, reliving, hypervigilance, exaggerated response to stimulus, irritability or anger, sleep disturbance, reckless behaviour, avoidance of the stressor, inability to recall all or parts of the event.

Treatment

Biological – Again, SSRIs are most effective, namely paroxetine, sertraline or fluoxetine. Next, venlafaxine can be trialled. Second line treatments include antipsychotics, MAOIs and tricyclic antidepressants, even IV ketamine.

Psychological – Recommended as first line by NICE are trauma focussed CBT and EMDR. These should be used before moving on to pharmacological treatments.

Social – Education of family and carers (it is possible they were also exposed to the same traumatic event and may require support themselves). Awareness of maintaining environments the patient feels safe in. Continuity of care by professionals.

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