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Chapter 11 Drugs for Parkinson’s disease and epilepsy

178

Calculations

1. A patient requires oral co-beneldopa which contains benserazide and levodopa, 100mg

3 times daily. The dose is expressed by the levodopa content. Your stock is benserazide

12.5mg/levodopa 50mg. How many tablets are required for a 7-day supply?

2. Sodium valproate suspension 200mg is prescribed for an individual. You only have 125mg in

5mL. How many mL would you give?

3. Orphenadrine 150mg is prescribed orally to be given in 3 divided doses over the day. Your

stock solution is 10mg/mL. How many mL would you give for each individual dose?

4. Your mentor asks you to check a dose of medication for oral administration. The patient

requires amantadine 100mg and the drug comes as 50mg in 5mL. How much should be

dispensed?

5. Sodium valproate suspension 50mg is prescribed for an individual. You only have 200mg in

5mL. How many mL would you give?

6. A child requires 50mg of phenobarbitone. If the stock ampoules contain 200mg in 2mL, how

much will you draw up?

7. A patient requires 1mg of cabergoline daily for 7 days, then 1.5mg daily for 7 days, and

finally 2mg daily for 14 days. You have none in stock and need to order 500mcg tablets from

the pharmacy. How many do you order for a 28-day period?

8. Carbamazipine 0.25g is needed and the suspension you have contains 100mg in 5mL. How

much would you administer?

9. Pramipexole dosing in the BNF is stated by amount of pramipexole base but there is an equiv-

alence by amount of pramipexole salt for immediate-release preparations. The equivalence is

88mcg of base to 125mcg of salt. The doctor has prescribed 88mcg 3 times per day. What

is the equivalent in salt of this for the whole day?

10. Sodium valproate suspension 90mg is approximately equivalent to 100mg capsules or tab-

lets. You have a patient with swallowing difficulties. How many mL of suspension (30mg in

5mL) should you give for a dose of 300mg capsules?

Multiple-choice questions

Try answering these multiple-choice questions to test what you have learned from reading this

chapter. You can check your answers at the end of the book.

1. Which of the following drugs is used in status epilepticus?

a) Lamotrigine

b) Diazepam

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Chapter 11 Drugs for Parkinson’s disease and epilepsy

179

c) Topiramate

d) Sodium valproate

2. Which of these drugs is a dopamine precursor?

a) Levodopa

b) Ropinirol

c) Procyclidine

d) Cabergoline

3. Which part of the brain shows dopamine neurone depletion in Parkinson’s disease?

a) The cortex

b) The mesencephalon

c) The substantia nigra

d) The cerebellum

4. Which of the following is a side-effect of increased dopamine in the treatment of

Parkinson’s disease?

a) Tremor

b) Muscle rigidity

c) Hallucinations

d) All of the above

5. Which of the following drugs inhibits MAO-B?

a) Selegiline

b) Levodopa

c) Pramipexole

d) Entacapone

6. Catechol-O-methyltransferase inhibitors stop the breakdown of levodopa where?

a) The blood–brain barrier

b) The periphery

c) The synapse

d) The receptors

7. Levodopa is often given with which other drug in the treatment of Parkinson’s

disease?

a) Pergolide

b) Carbidopa

c) Selegiline

d) All of the above

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Chapter 11 Drugs for Parkinson’s disease and epilepsy

180

8. Parkinson’s disease is caused by a lack of which substance?

a) Acetylcholine

b) Dopamine

c) Serotonin

d) Noradrenaline

9. The drug of choice in treating absence seizures is …

a) Ethosuximide

b) Gabapentin

c) Phenytoin

d) Sodium valproate

10. Which of the following neurotransmitters has an inhibitory function?

a) Noradrenaline

b) Acetylcholine

c) Gamma aminobutyric acid

d) Serotonin

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Recommended further reading

Drugs used in mental health

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Chapter 12 Drugs used in mental health

182

Introduction

The aim of this chapter is to introduce you to

drugs used in common mental health problems.

The chapter examines three key areas of mental

health intervention:

■ anxiety;

■ depression;

■ psychosis.

Mental health issues extend into all aspects of

nursing and an appreciation of the range of med-

ications and how they work is essential for all

nurses. One in four adults in the UK experience

at least one diagnosable mental health problem in

any one year, and one in six experience this at any

given time (Office for National Statistics 2001). It

is estimated that approximately 450 million people

worldwide have a mental health problem (World

Health Organization 2001).

The Nursing and Midwifery Council’s Standards

for Pre-Registration Nursing Programmes pub-

lished in May 2018 state that education must:

ensure that field-specific content in relation to

the law, safeguarding, consent, pharmacology

and medicines administration and optimisa-

tion is included for entry to the register in one

or more fields of nursing practice

Although this could be interpreted as only relating

to mental health students, Platform 3 of the Profi-

ciencies from the NMC also states:

3.3 demonstrate and apply knowledge of all

commonly encountered mental, physical,

behavioural and cognitive health conditions,

medication usage and treatments when

undertaking full and accurate assessments of

nursing care needs and when developing, pri-

oritising and reviewing person-centred care

plans

The main mental health conditions encountered

are as follows.

Anxiety

Anxiety is a common, normal and usually self-

limiting emotion, with which we are all familiar. For

some people, however, feelings of anxiety can be

intolerable and can become disabling. This level of

anxiety is pathological and requires prompt diagno-

sis and active treatment to help the sufferer regain

and maintain their previously normal lifestyle. At

this level, anxiety can manifest with wide and var-

ied symptoms, both physical and psychological.

Anxiety is not simply one illness, but a group

of disorders characterized by psychological

symptoms such as diffuse, unpleasant and vague

feelings of apprehension, often accompanied by

physical symptoms of autonomic arousal such as

palpitations, light-headedness, perspiration, ‘but-

terflies’ and, in some patients, restlessness.

According to the International Statistical

Classification of Diseases and Related Health

Problems (ICD-10; WHO 2016), there are six main

classifications of anxiety disorders:

panic disorder;

social phobia;

generalized anxiety disorder;

■ Outline the mode of action of selective serotonin re-uptake inhibitors (SSRIs).

■ Name two drugs used in bipolar depressive illness.

■ Explain simply the biological basis of schizophrenia.

■ List the positive and negative symptoms of schizophrenia.

■ Give reasons why there are differences between typical and atypical antipsychotics.

■ Give examples of typical and atypical antipsychotic drugs.

■ Give reasons for the difference in side-effects between typical and atypical antipsychotics.

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Chapter 12 Drugs used in mental health

183

obsessive-compulsive disorder (OCD);

post-traumatic stress disorder (PTSD);

mixed anxiety and depressive disorder.

An understanding of the physiological mecha-

nisms thought to be involved in the development

of pathological anxiety is vital to ensure appro-

priate treatment of anxiety disorders. First, it is

important to understand that two brain systems

appear to be involved in the generation of anxiety.

The defence system

The defence system controls our responses to dan-

ger. It receives stimuli related to the threat of danger

and the brain interprets these stimuli and responds

as required. The defence system is responsible

for the so-called ‘fear, fight or flight’ responses. It

can be a protective mechanism, whereby we can

respond to threats or perceived threats and prepare

the body to defend itself or to flee from the danger.

It can also be activated by things which are not real

threats but are perceived to be real by the anxiety

sufferer and can become pathological.

The behavioural inhibition system

This system prevents a person from getting into

danger and is responsible for avoidance behav-

iour. It is also involved in learning not to do dan-

gerous things, thereby allowing future avoidance

of anxiety-provoking situations. This can lead to

anxiety sufferers withdrawing from real-life situa-

tions because of the fear of being placed in danger,

leading to agoraphobia, claustrophobia and social

isolation.

Neurotransmitters in anxiety

The brain is a complex organ and with respect

to anxiety many different neurotransmitters are

involved. These include the following monoamines:

■ noradrenaline (NA);

■ 5-hydroxytryptamine (5-HT) or serotonin;

■ gamma-aminobutyric acid (GABA).

The exact role these neurotransmitters play in

anxiety is not fully elucidated but using drugs that

act on these systems can be beneficial in the man-

agement of anxiety.

Medicine management of anxiety

Although the various anxiety disorders share

some characteristics, they each need to be eval-

uated and treated in their own way. Anxiety man-

agement can be broken down into the following

categories:

■ non-pharmacological: psychological;

■ pharmacological: single and combined psy-

chotropic and non-psychotropic treatments;

■ combinations of pharmacological and

non-pharmacological treatments.

Much treatment for anxiety involves a phar-

macological component. Anxiolytic treatment

should ideally be effective and rapid for the relief

of disabling symptoms. The treatment should not

be too sedative, as this can be as detrimental as

the anxiety itself. This is achievable in the current

pharmacological climate but can often come at a

price. The following drugs have all been used to

treat the symptoms of anxiety, many of which are

still in use today:

■ barbiturates;

■ benzodiazepines;

■ beta-adrenergic blockers;

■ azaspirodecanediones;

■ antipsychotics;

■ antidepressants.

Barbiturates

Barbiturates are potentiators of the GABA

recep-

tor, which has a pentameric structure. It consists

of five sub-units that surround an ion channel

which conducts chloride (Cl

) ions (see Figure 12.1).

It is the major inhibitory neurotransmitter in the

brain and central nervous system. Therefore,

potentiation of an inhibitory transmitter channel

leads to increased inhibition, or reduced activity at

the receptors the chloride ion acts on. This causes

a ‘dampening down’ of neuronal activity. When

the chloride ion channel is opened up by GABA,

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Chapter 12 Drugs used in mental health

184

the barbiturate drug molecule enters the channel

and causes it to remain open for longer than GABA

on its own can. This allows for more chloride from

outside the neurone to enter, so reducing the like-

lihood of an action potential being generated. This

means that the barbiturate drug causes a poten-

tiation of GABA transmission and a reduction in

neuronal activity.

There are downsides to using barbiturate

drugs such as amobarbital (formerly amylobar-

bitone) because they have a narrow therapeutic

index, which means that the dose of the drug

needed for a beneficial effect is very close to

that considered toxic. Thus it is easy to take too

little and have no effect, or too much and result

in an overdose. They also have addictive proper-

ties and patients can easily become dependent

on them. The effects of barbiturates can also be

magnified when taken with alcohol. For these

reasons, they are rarely used in the management

of anxiety today.

Benzodiazepines

For many years, the most common first-line phar-

macological treatment for anxiety disorders was

a benzodiazepine drug. More recently, however,

benzodiazepines such as diazepam and temaze-

pam have become associated with problems of

addiction and dependence, and the potential for

abuse. And because the use of benzodiazepines

has been related to significant long-term problems,

they should be used in the short term only for the

management of anxiety-related conditions. NICE

clinical guideline CG113 (2011) on the manage-

ment of generalized anxiety disorder and panic

disorder in adults suggests:

1 – Benzodiazepines should not be offered except

as a short-term measure during crisis. This

applies to primary and secondary care settings.

2 – The use of benzodiazepines is associated

with a less good outcome long term and should

not be prescribed in panic disorder.

Despite the above, benzodiazepines are still

an effective treatment for acute, transient anxi-

ety. Like barbiturates, these drugs potentiate the

effects of GABA but do so by a different mech-

anism. They bind to a specific benzodiazepine

binding site (or receptor) situated on one of the

sub-units of the GABA

receptor. Their mechanism

of action is to increase the affinity of GABA, which

increases the ability of and frequency with which

GABA can open the chloride ion channel. Unlike

barbiturates, benzodiazepines need GABA to be

present all the time the channel is open, not just

at activation, for them to have their effect. This

makes them safer than barbiturates because they

have a wider therapeutic index, so there is less

chance of toxicity and accidental overdose.

For use in anxiety, the dose tends to be low, with

higher doses being reserved for use with insom-

niacs. This means that the side-effect of sedation

should occur less often, although for some people

drowsiness is a problem.

Another major side-effect of benzodiazepines is

respiratory depression, and this should be moni-

tored on initiation of therapy.

Figure 12.1 Barbiturate binding

–

Represents barbiturate binding

Represents benzodiazepine binding to the

receptor and increasing its affinity for GABA

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Chapter 12 Drugs used in mental health

185

Beta-adrenergic blockers

These drugs are used not to treat the central nerv-

ous system transmitters thought to be involved in

anxiety, but to treat the physical symptoms that

are manifest in anxiety such as palpitations, trem-

ors, sweating and shortness of breath. They do

not have an effect on the psychological aspects of

anxiety, so the patient will still feel anxious.

There are many beta-blocking drugs, but only

propranolol and oxprenolol are licensed for use in

the management of anxiety. These drugs may help

people with mild anxiety to function in everyday

situations where before their symptoms would

have proved problematic.

weeks. This can be problematic in the treatment

of anxiety, as patients often cannot tolerate the

delayed onset of action.

Buspirone is not associated with addiction or

dependence. Although usually licensed for short-

term use only, it can be used for several months

under specialist supervision. In practice, this drug

is not used alone but in combination with other

medication and can be a useful adjunct.

Antipsychotics

There is evidence that certain antipsychotic drugs

have a positive effect in the treatment and man-

agement of anxiety. The method by which they

relieve anxiety is not known, but these drugs are

associated with emotional changes and the relief

of symptoms such as agitation. In the management

of anxiety, they are used in doses much lower than

would be required to induce their antipsychotic

effects. Drugs such as haloperidol, flupentixol and

tri-fluoperazine can be used as anxiolytics and

have a rapid onset. They are especially useful if

the patient has a diagnosis of psychosis, as their

anxiety may be related to this.

Like barbiturates and benzodiazepines, some of

the side-effects of antipsychotic drugs can be com-

pounded by alcohol. This makes the prescription

of these drugs less likely.

Antidepressants

The tricyclic antidepressants (TCAs) have a pos-

itive effect in generalized anxiety disorder and

panic disorder, although many of these drugs are

not licensed for such indications. The TCAs were

used in the past for mixed anxiety/depressive dis-

orders but they do not appear to have any specific

anxiolytic activity. It may be that their anxiolytic

effect is related to their sedative properties. It

takes 2–3 weeks for the anxiolytic and antidepres-

sant effects to develop, suggesting that the mech-

anisms for these effects may be related.

Another type of antidepressant, the selective

serotonin re-uptake inhibitors (SSRIs), can appro-

priately be used in chronic anxiety of more than

4 weeks’ duration. Their mechanism of action is

fully explained in the section on depression. Their

Clinical tip

When a patient starts taking a benzo-

diazepine, it is very important that you warn

them of the possible sedative effects and

discuss the dangers of driving or operating

heavy machinery. This is a requirement of

legislation amending the Road Traffic Act

to incorporate ‘The Drug Driving (Specified

Limits) (England & Wales) (Amendment)

Regulations 2015’.

Clinical tip

If a patient also suffers from diabetes,

do not forget to warn them that taking a beta

blocker may inhibit the normal signs and

symptoms of a hypoglycaemic attack.

Azaspirodecanediones

Buspirone is the only member of this class of drugs

available for the treatment and management of

anxiety symptoms. Its mechanism of action is

not fully elucidated but it is known to affect the

serotonergic receptors, inhibiting serotonergic

transmission. This effect develops quickly but the

anxiolytic effect does not typically occur for 2–3

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Chapter 12 Drugs used in mental health

186

anxiolytic action takes 2–3 weeks to develop,

which is consistent with the onset of their antide-

pressant effect, again suggesting that the mecha-

nisms are related. Some SSRIs are associated with

increased anxiety until the antidepressant effect

kicks in, and for this reason concomitant use of

a benzodiazepine for the first 2–3 weeks is often

recommended, with a low starting dose that can

be increased as tolerated.

Treatment is usually long term and often the

doses prescribed are at the higher end of the scale

for full effect. The SSRIs commonly use for anxi-

ety include:

■ fluoxetine and sertraline, licensed to treat anx-

iety symptoms with depression and for OCD

and PTSD;

■ fluvoxamine, licensed for the treatment of

OCD;

■ citalopram, licensed for the treatment of panic

disorder;

■ paroxetine, licensed for the treatment of social

phobia, panic disorder, OCD and mixed anxi-

ety and depression.

Depression

Depression is a common serious psychiatric

illness. Depressive or affective disorders involve

disturbances of mood or affect (cognitive and

emotional symptoms), which are frequently asso-

ciated with changes in behaviour, energy levels,

appetite and sleep patterns (biological and phys-

iological symptoms). People who suffer from

depression report a poor quality of life. This often

extends to their carers, and can be detrimental to

their close relationships. Depression is associated

with a high incidence of suicidal tendency and

thus mortality. Depression can be either:

■ Unipolar – where the mood or affect is always

low. This is characterized by misery, malaise,

despair, guilt, apathy, indecisiveness, low

energy and fatigue, changes in sleep patterns,

loss of appetite and thoughts of suicide. It can

be either reactive or endogenous. Reactive

depression implies that the cause of the illness

is brought about by severe stress. Endogenous

depression, on the other hand, occurs when no

obvious external causative factor can be iden-

tified; or

■ Bipolar – where the mood or affect and behav-

iour swing between depression and mania.

This type of depression has a greater tendency

to include an inherited component.

For a diagnosis of depression to be applied, the

patient must display certain key symptoms and

also exhibit some ancillary symptoms. This assists

the diagnosis and categorization of the depression.

Key symptoms

■ depressed mood;

■ an inability to experience pleasure from normally

pleasurable life events such as sex (anhedonia);

■ a lack of energy.

Ancillary symptoms

■ changes in weight and appetite;

■ sleep disturbance;

■ low self-esteem;

■ psychomotor agitation or retardation;

■ guilt or self-reproach;

■ difficulty concentrating;

■ suicidal thoughts.

The National Institute for Health and Care Excel-

lence (NICE) base their definition of the severity of

depression on the Diagnostic and Statistical Man-

ual of Mental Disorders IV (DSM-IV; APA 1994) and

ICD-10 (WHO 2016). This gives the following classi-

fications of depression for treatment and manage-

ment purposes:

■ Sub-threshold depressive symptoms, where the

patient has fewer than five of the above symp-

toms of depression (can be called reactive sad-

ness and may be in response to a life event).

■ Mild depression, where the patient has more

than five of the symptoms of depression but

displays only a mild functional impairment.

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Chapter 12 Drugs used in mental health

187

■ Moderate depression, or the stage between

mild and severe depression where more than

five symptoms are displayed.

■ Severe depression, where the patient has most

of the symptoms of depression and also shows

a marked functional impairment. Although

psychotic features will always indicate severe

depression, they are not necessary for a diag-

nosis of severe depression to be made.

The aetiology of depression is still unclear. The

biological theories relating to the disease would

suggest that there are many factors in the devel-

opment of depressive disorders, including psycho-

logical, genetic, biological and neurochemical.

Psychological factors

These are known to play a part in the development

of many types of depression and can be catego-

rized as follows:

■ Childhood and developmental experiences that

are seen as negative, such as abuse, whether it

be physical, mental or sexual; separation from

one or both parents, with maternal separation

being particularly traumatic; breakdown of

the relationship between parents and/or prob-

lems with the parent-child relationship.

■ An unusually high number of what are termed

‘significant life events’. These are often

ranked according to their perceived impact,

with bereavement, especially of a spouse, at

the top of the list. Surprisingly, ‘positive’ life

events such as getting married or the birth of

a baby can also have a significant negative

impact. This may be due to a major change in

lifestyle.

■ Stress that can be deemed unusual or contin-

ual, such as stress at work or in a relation-

ship.

■ The absence of a secure or confiding relation-

ship. This can be particularly relevant to the

elderly and those who have lost a loved one,

and may also explain why those who live alone

have a higher tendency to become clinically

depressed.

Genetic factors

Genetic factors are implicated in many areas of men-

tal and physical health. Although no individual gene

has been identified in depressive disease, there is a

strong suggestion from family and twin studies that

there is a genetic basis for vulnerability to depression.

A number of genes may be related to the function of

known neurotransmitters and receptors, suggesting

a biological effect. Other genes may be involved in

influencing how a person perceives and responds to

a certain kind of event or stressor, which may lead to

depression in certain people but not in others.

Biological factors

Biological factors are a major focus for research

into depression and antidepressant drugs. Much of

this research has concentrated on:

■ hormonal influences; or

■ the monoamine hypothesis.

Hormonal influences

Cortisol, a corticosteroid, is known as the ‘stress

hormone’ and has been linked to depression. Many

people go on to develop depression if they are sub-

jected to repeated and prolonged stress. Ongoing

research is linking corticosteroids with monoam-

ines to try to complete the picture.

The monoamine hypothesis

Many monoamines have been implicated in depres-

sion. Monoamines are, as their name suggests,

organic compounds with a single (mono) amine

group. They have the biological function of being

neurotransmitters and neuromodulators and exert

their effects at receptors located predominantly

on neurones. They were first implicated as having

a role in depression in the 1960s. This was because

the main antidepressant drugs used at that time

(the TCAs and monoamine oxidase inhibitors,

MAOIs) both have chemical actions on monoam-

ines. It was suggested that reduced levels of mon-

oamines could be a causative factor in depressive

illness, although a case can be made both for and

against this claim. Hence the monoamine hypothe-

sis could explain why:

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