Pharmacology: ECT Flashcards

1
Q

What is the definition of ECT?

A

ECT is defined as “passage of a small electric current through the brain with a view to inducing a generalised fit which is therapeutic”.

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2
Q

What depressive symptoms can get worse on antidepressants and why?

A

Suicidal ideation - probably because motivation increases but maybe not yet mood. So you need to check in on patients often.

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3
Q

What is the history of ECT?

A

Hippocrates noted that malarial febrile seizures ‘cured the insane’

Cholera outbreaks later in history also caused febrile seizures and did the same

Later in the 1940s/50s it was used therapeutically

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4
Q

What are the indications of ECT?

A

Indications for ECT According to NICE there are three main indications for ECT.

  1. Severe depressive illness: only if there is a life threatening situation i.e. poor oral intake, acutely suicidal or if the depressive illness is treatment resistant.
  2. Uncontrolled mania
  3. Catatonia: this is a motor symptom of schizophrenia, in which there is increased resting muscle tone which is not present on active or passive movement.
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5
Q

Can the patient refuse ECT?

A

Informal patients with capacity- need to complete a written consent form.

Patient might lack capacity to consent but not objecting to treatment- Mental capacity Act

Those under MHA ‘section’ and have capacity- they need to complete a specific consent form.

Those refusing treatment- emergency sections of the MHA. (after first 2 treatments need to be authorised by a SOAD)

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6
Q

How do you describe ECT? (e.g. in PACES station) What does the patient need to do before the procedure?

A

Inducing a seizure but modified as using anaesthetic and muscle relaxant. This anaesthetic is at high dose but very short lasting. Muscle anaesthetic means that it won’t be a full convulsive seizure.

Electrodes will be placed on the forehead and behind ears

Not food or drink 8 hours prior to the procedure.

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7
Q

What investigations are done before ECT?

A

Routine physical examination for all patients

Investigations:

  • Bloods (FBC, U&E’s, LFTs, Sickle test for specific ethnic groups)
  • ECG - for all pts >50 yrs of age; 55 yrs of age, <55 only if medical history indicates

Medication review:

  • Medications increase seizure threshold: Benzodiazepines, Mood stabilisers (Anticonvulsants)
  • Medications reduce seizure threshold: antipsychotics, TCAs, Lithium
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8
Q

How are outcomes of ECT measured?

A

Outcomes:

  • Rating scales e.g. MADRS
  • Cognitive tests e.g. MMSE
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9
Q

How many courses of ECT are usually used for treatment?

A

6-12 courses

usually 2 sessions a week

Can be delivered to both inpatients and outpatients

ECT is ‘prescribed’ by a psychiatrist and is reviewed after each session

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10
Q

What are the risks of ECT? What are the complications?

A

Risks of anaesthetic (similar to getting a tooth out) - MI, arrhythmis, aspiration, prolonged apnoea, malignant hyperthermia, broken teeth, death (1 in 50,000)

Risks from ECT:

Common complaints (80%) confusion, muscle pain, headache, nausea

Effect on cognition (10%) - usually retrograde and enterograde memory so events immediatedly before and after ECT and most patients recover fully after 6 months

Very rare to have long term complications

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11
Q

How long does the induced ECT seizure last?

A

15-45 seconds

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12
Q

What are the advantages and disadvantages of unilateral vs bilateral ECT?

A
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13
Q

How effective is ECT?

A

Yes - 8/10 patients will respond to ECT treatment

Equal or better than antidepressants. Likely best in combination. Often fewer s/e cf antidepressants and quicker acting

RCT show that the seizure should be between 15-25 seconds to be effective

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14
Q

Are there any contraindications to ECT?

A

Technically no absolute contraindications

Caution in higher risk patients

  • Heart disease/stroke
  • Raised ICP
  • Risk of cerebral bleeding (hypertension, stroke etc)
  • Pacemaker, Pregnant women, Epilepsy
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15
Q

What is the MOA of ECT?

A

Specific MOA is unknown:

  • The seizure releases a large number of signalling chemicals that, in turn, produce changes on the surface and then within nerve and glial cells in target areas of the brain such as the hippocampus, amygdala, and prefrontal cortex.
  • Genes in these cells are activated or suppressed, which in turn leads to increase or decrease in the number, activity, and connectivity of these cells.
  • Increased number and connectivity of cells in the hippocampus and prefrontal cortex probably improve thinking and coping abilities, whereas decreased number and connectivity of cells in the amygdala reduce negative emotions attached to unpleasant memories; both effects can be expected to be therapeutic in depressed patients.
  • The time course of recovery from depression seems to parallel the time course of occurrence of these cellular changes.
  • Wide range of effects on neurotransmitters (facilitates monoaminergic transmissionNA, 5HT,DA): in animals 1 seizure can increase functional measures of dopamine*
  • Andrade C. A primer for the conceptualization of the mechanism of action of electroconvulsive therapy, 2: Organising the Information. The Journal of Clinical Psychiatry 2014; 75(6): 548-551*
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16
Q

What are the uses of TMS?

A

(Electromagnets placed on the scalp in order to induce an electrical current in the cortex)

Has been included into NICE guidelines since 2015 but not widely used. NICE concluded ‘no major safety concerns’

Evidence suggests might be effective in short term and there is variable clinical response. But research is ongoing.

17
Q
A

B

18
Q
A

B

19
Q
A

C

20
Q
A

D