After some discussion that goes around in circles, you decide to call an ambulance and ask Maria's mother and your receptionist to supervise Maria. She is taken to hospital where the staff advise you of her progress. She continues to express the belief that she is dead, rotting inside. She refuses to eat, drink, wash or bathe. She is seen by two psychiatrists and she is treated as an involuntary patient under the mental health act. The plan is for her to receive ECT. You then are met by Maria's father who is very angry that you sent her to hospital. He is very worried Maria will receive ECT and wants to know more about it. He states her mother was never the same after receiving ECT and he remembers her often having bruising from being held during the treatment. Q 10. What information can you provide to the father about ECT? Uptodate patient information – key points: The mechanism of ECT is not fully understood. More than 70 percent of depressed people who receive it respond favorably. Anaesthesia and muscle relaxants are administered. There is very limited movement due to the electrical stimulus: “toes wiggling or other parts of your body moving a little”. Anterograde and retrograde memory loss occurs but should recover within several weeks of the treatment. However, some memories before, during, and after treatment may never be recovered. “To speed and improve recovery of your memory, use your brain. Read, ask questions, and watch continuing stories on TV. This is the best way for you to help your memory return.” Risks: rarely, ECT can cause arrhythmia or other serious complications. On sustained loss of memory: CURRENT Diagnosis & Treatment: Psychiatry "A small group of patients report that their memory never returned to normal after ECT. The etiology for this phenomenon is unclear, and objective memory testing generally does not substantiate the subjective complaint. Possible explanations for this phenomenon may include (1) patients incorrectly attribute memory problems associated with depression to prior ECT, (2) anesthetic misadventure (e.g., hypoxia), or (3) other, occult memory impairment (e.g., evolving dementia)." "The long-term memory problems associated with ECT are more troubling to patients than are the short-term ones. ECT creates a persistent storage deficit that results in accelerated forgetting. Capacity for new learning recovers substantially by several months after ECT, but accelerated forgetting can be documented for up to 6 months post- ECT." Q 11. How has the treatment changed from 40 years ago? ECT facts: True/False 1. It's over 400 years old! Sort of. There are records of convulsions being induced (chemically) to cure psychiatric problems from the 16th century. 2. It's really only 73 years old. Sort of. Electric charges were first used to induce seizure to treat delusions in 1938. 3. It's been totally revolutionised in the last 40 years. I'm going to get off the fence and say this is False. From quite early on muscle relaxants have been used (sorry, lost the reference). Starting from the late 1950s unilateral electrodes have been used, reducing short-and-long-term cognitive deficits. Since 1976 the electrical current waveform has changed from sinusoidal to “brief pulse” or even “ultrabrief pulse”, which has been shown to reduce or even eliminate memory impairment. The specific protocol (stimulus waveform, electrode placement, stimulus intensity, dosage relative to threshold, and number and spacing of treatments) makes a difference. Shop around. Patient factors are significant: stupid old women do badly. NANCY A. PAYNE and JOAN PRUDIC, 2009. Electroconvulsive Therapy: Part I: A Perspective on the Evolution and Current Practice of ECT. Journal of Psychiatric Practice Vol. 15, No. 5. Maria returns to see you one month later having been diagnosed with Major Depressive Disorder with Psychotic Features. Her current medication is venlafaxine XR 225mg Mane and risperidone 2mg Nocte. She is euthymic and has little recollection of the events that lead to her hospitalisation. She wants to know how long she needs to remain on the medication and the possible side effects it might cause her. Q 12.What advice will you give Maria regarding side effects of the antidepressant and the atypical antipsychotics such as risperidone? Venlafaxine patient information: • Feeling lightheaded, sleepy, having blurred vision, or a change in thinking clearly. • Nervous and excitable. • Nausea or vomiting. • Constipation. • Dry mouth. • Change in sexual ability or desire. This is usually reversible. • Inability to sleep. Risperidone patient information: • Feeling lightheaded, sleepy, having blurred vision, or a change in thinking clearly. • Feeling dizzy. Rise slowly over several minutes from sitting or lying position. • High blood sugar. Usually reverses when stopped. • Weight gain. • Change in sexual ability or desire. This is usually reversible. • Drooling, especially when sleeping. • Inability to sleep. Akathisia and dystonia are also relatively common, and beware neuroleptic malignant Q 13. What physical examination and investigations will you do at base line and follow up for a patient on atypical antipsychotics? General: Weight! Weight gain is the most common side effect of atypical antipsychotics. Fasting BSL, BP, fasting lipids – associated with hyperglycaemia, hypertension, dyslipidaemia Neurological: Extrapyramidal symptoms, such as acute dystonia, parkinsonism, akathisia, and tardive dyskinesia (less frequent than with typical antipsychotics). Prefrontal D2 blockade: neurocognitive impairment and negative symptoms (less frequent than with typical antipsychotics). Anticholinergic toxicity, including confusion (from muscarinic blockade – not so much for risperidone) Lethargy and sedation (from histamine blockade) Miosis (from alpha adrenergic blockade) Cardiovascular: tachycardia, and orthostatic hypotension (from alpha adrenergic blockade) ECG – QT prolongation and effects on repolarisation. Risk of sudden death. Q 14. How long will Maria need to stay on these medications? There's little data, but at least until remission occurs for the antipsychotic, and six to nine months of the anti-depressant, as for uncomplicated major depression. "For patients successfully treated with the combination of an antipsychotic plus an antidepressant, there are few data that address how long patients should continue to take the antipsychotic. An open label study of 30 patients with unipolar psychotic depression, treated with fluoxetine plus perphenazine, found that after the perphenazine was discontinued, 22 (73 percent) remained free of relapse over 11 months of follow-up . The methods of the study were such that the 30 patients had initially responded to four months of treatment with fluoxetine 20 to 40 mg/day given in the morning and perphenazine 8 to 32 mg per day given at bedtime (response defined as 50 percent reduction in symptoms measured on both the Hamilton Rating Scale for Depression and the Brief Psychiatric Rating Scale). The perphenazine was then tapered each week by 25 percent of the total dose and discontinued after four weeks. Fluoxetine monotherapy continued for eight months and then was tapered and discontinued, followed by three additional months of assessment.” Q 15. During one of her appointments, Maria asks if the abuse she experienced in childhood is the cause of her psychotic depression? What is the association between the childhood trauma that Maria experienced and her psychotic depression? It may well have contributed. "Early life adversity — Early life stress such as childhood trauma influences vulnerability to psychopathology throughout life and may predispose individuals to major depression by altering sensitivity to stress and response to negative stimuli. Preclinical studies suggest early life stress causes long-lived hyperactivity of corticotropin-releasing factor cells in the hypothalamus, which leads to increased stress responses."
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