Treatments  > Biological > Medication

To fully understand psychiatric medications, you first need to understand the relevant neurotransmitters involved and which drugs target these. 





  • Excitatory: Serotonin, noradrenaline, adrenaline, dopamine, glutamate

  • Inhibitory: Dopamine***,  GABA 

Medications aim to either increase or decrease the effect of the neurotransmitter involved.This can be achieved in several ways:

  • Precursor for the neurotransmitter

  • Stopping production

  • Stopping storage 

  • Increasing/reducing release

  • Mimicking/blocking at the receptor

  • Increasing/reducing reuptake or breakdown 

It is particularly important to familiarise yourself with DOPAMINE pathways (mesocorticl, mesolimbic, nigrostriatal, tuberoinfundibular). When particularly considering antipsychotic medications and their side effects, we consider all 4 pathways. Typically, antipsychotic block these pathways, thus treating positive psychotic symptoms, however they will also inevitably block the nigrostriatal pathway as well (leading to extra-pyramidal side effects) and tuberoinfundibular pathways (leading to hyperprolactinaemic). 


Click here to read more about antipsychotics:


Other medication resources:Leaflets from South West London and St George's Mental Health NHS Trust are available on their website (see what the patients see). The 'Handy Fact sheets' are particularly useful. You should be familiar with these concepts by the end of the placement:


For videos that teach about psychiatric medications, we suggest looking at the Speed Pharmacology YouTube channel:


Block dopamine and dampen symptoms.


Broadly 2 groups:

  • Typicals (Chlorpromazine,Thioridazine, Levomepromazine, Perphenazine, Trifluoperazine, Haloperidol, Fluphenazine, Zuclopenthixol (Clopixol), Flupentixol (Depixol), Prochlorperazine)

  • Atypicals (Amisulpride, Olanzapine, Paliperidone, Quetiapine, Risperidone, Sertindole, Sulpiride, Ziprasidone, Zotepine, Clozapine)


Mode of administration and monitoring

  • Standard tablets

  • Orodispersible preparations

  • IM injections – ‘depots’





Choice of Antipsychotic

Neuroleptic Malignant Syndrome (NMS)

Benzodiazepines (BZs)

Mechanism of action


  • BZs bind to specific sites (BZ binding sites) present on the GABAa receptor complex and potentiate the inhibitory action of GABA.

  • Flumazenil is a selective BZ antagonist, thus reverses the pharmacological actions of BZs. It is used to treat BZ overdosage.


Benzodiazepines are classified on their duration of action:


  • Short acting e.g. oxazepam, lorazepam, temazepam.

  • Long acting e.g. diazepam, chlordiazepoxide nitrazepam.


Extensive number of indications, in both physical and mental health. In mental health service, often used for agitation/behavioural disturbances/sedation, treatment of alcohol withdrawal.


Adverse effects:


  • Largely restricted to the CNS. Impairment of intellectual performance, motor performance (coordination, reaction time) and memory.


  • Paradoxical increase in hostility in some patients.


  • BZs potentiate the effects of other CNS depressant drugs, particular concern with other drugs of abuse including alcohol and opiates. These can lead to death due to respiratory depression.


  • Tolerance and dependence is a major problem.


  • BZs do not all have the same dependence potential. Those with the highest risk are those with high potency and short half life.

  • Propanolol

  • Extensive number of physical health indication, in mental health it is most commonly used to treat the peripheral symptoms of anxiety, such as sweating, tremor, tachycardia.

  • Tacrine, rivastigmine, galantamine and donepezil.

  • Inhibits the acetylcholinesterase enzyme from breaking down acetylcholine, thereby increasing both the level and duration of action of the neurotransmitter acetylcholine.

  • Decrease rate of cognitive decline in Alzheimer’s dementia.

The Z Drugs


  • Zopiclone, zolpidem and zalepon.

  • Licensed for the treatment of insomnia and have largely replaced BZs for this indication.

  • Like BZs they interact with BZ binding sites on the GABAa receptor.