This material was presented in the 25th European Congress of Psychiatry which was organised by the European Psychiatry Association in Florence, Italy from 1-4th April 2017. I had access to the material as I attended the full Congress. Please note that this material remains the intellectual property of the European Psychiatry Association and its authors and any citation should include a full reference to it. For more information on the EPA and how to become a member, please visit: http://www.europsy.net/

1. MEDICAL BACKGROUND
1
Complex Assistencial Salut Mental CASM, Benito Menni. Hospitalització Aguts i Unitat de TEC. Granollers, Spain.
Electroconvulsive Therapy in Major Recurrent Depressive Syndrome
with Parkinsonism Syndrome. A Case Report.
Gómez-Alemany T1
, Alcoverro O1
, Soler J,1
Targa I1
Suarez D1
, Oscoz M1
, Centeno, M1
DISCLOSURE OF INTEREST: All authors report no potential conflicts of interest.
INTRODUCTION
DISCUSSION
REFERENCES
(1) Borisovskaya, A. Electroconvulsive therapy for depression in Parkinson’s disease: systematic review of evidence and recomendations; Neurodegenrative Disease Managemen 2016
(2) Pla director de salut mental i addiccions. Guia de bona pràctica clínica sobre la teràpia electroconvulsiva. Barcelona: Direcció General de Planificació i Recerca en Salut, Generalitat de Catalunya; 2014.
(3) Cheng-Che Shen, Shih-Jen Tsai, Chin-Li Perng, Benjamin Ing-Tiau Kuo, Albert C. Yang. Risk of Parkinson disease after depression. A nationwide population-based study. Neurology 2013; 81: 1538-1544
(4) S. Pridmore, C Polland. Electroconvulsive therapy in Parkinson’s disease: 30 month follow up. J Neurol Neurosurg Psychiatry 1996; 60: 993
(5) R. Kennedy, D.Mittal, J. O’Jile. Electroconvulsive therapy in movement disorders: an update. J Neuropsychiatry Clin Neurosci 2003; 15:407-421.
(6) M. Fink. Rediscovering catatonia: the biography of a treatable syndrome. Acta Psychiatr Scand 2013: 127 (suppl. 441): 1-47
(7) M. Fink, A. Taylor. Cap. 7: Tratamiento actual de la catatonía, pag. 169- 203. En: Catatonía. Guía clínica para el diagnóstico y el tratamiento. Ed.Masson . 2005. Barcelona. España.
(8) Pia Baldinger, Amit Lotan, Richard Frey, Siegfried Kasper, Bernard Lerer, Rupert Lanzenberger. Neurotransmitters and electroconvulsive therapy. J ECT 2014, 30: 113-121.
(9) Samantha K. Cumper, Gabriella M. Ahle, Lauren S. Liebman, Charles H. Kellner. J ECT 2014, 30: 122-124.
(10) Borisovskaya, A. Electroconvulsive therapy for depression in Parkinson’s disease: systematic review of evidence and recomendations; Neurodegenrative Disease Managemen 2016
CURRENT EPISODE AND PSYCHOPATHOLOGY
The previous month before the admission, the patients’ sadness worsens, and starts
to experience asthenia, clinofilia, suicidal thoughts, increased levels of anxiety, low
food intake and swallowing difficulties severe enough as to reduce food intake down to
milkshakes due to choke fearness, hence she had a weight loss of up to 10 kg within
two months. She experiences mood improvements in the evenings.
Nevertheless, she does not carry out any diurnal activity nor does she speak unless
she is spoken to. She is oriented in person, space and partially in time and needs
supervision for personal hygiene. Depressive facial expression, anxious, tense, with
an uncontrollable and spontaneous cry. Ongoing demands towards the medical staff
claiming for treatment. No speech disturbances. Hopelessness and hypochondriacal
thoughts under delusional boundaries. Denial of sensoperception alterations. Passive
thoughts of death.
DIAGNOSIS
● ECT is an effective treatment for most patients with Parkinson Disease (PD) and
concomitant Depression (1).
● As psychiatrists, in our daily clinical practice we sometimes find it difficult to separate
psychiatric symptoms overlapped by similar ones from other disorders.
● Depression symptoms are sometimes presented in PD. Patients with Depression
Disorder can also present Parkinsonism-like symptomatology.
● For this reason, it is interesting to establish which therapeutical approach is better in
this cases.
● We present a case of and old woman admitted to the psychiatric ward due to
depressive symptomatology non-responsive to the psychopharmacological treatment,
that after being treated with ECT
● 17 month before admission: Vasovagal syncope with clinical weakness of the left
hemibody. Diagnosed as Ischaemic Stroke with correct treatment afterwards (Aspirin
300mg/d, Atorvastatine 40mg/d.
● Nevertheless, she started a progressive cognitive impairment to the extent of requiring a
wheelchair.
● 9 months before admission: Incipient shake with predominance of the upper right extremity
after being treated with fluvoxamine 200 mg a day and aripiprazol 10 mg a day as a
antidepressant enhancer.
● 1 month before the admission: Assessed by the Specialist in Neurology, who observed
static tremor on the right hand together with parkinsonism syndrome two months after the
withdrawal of the dopaminergic drug. The Neurologist diagnosed Akinetic-rigid Syndrome
with right predominance. Suggested to initiate levodopa/carbidopa 100mg/25mg up to
1-1-1.
PSYCHIATRIC BACKGROUND
Toxic habits were declined. Cluster C traits. History of three depressive episodes (38
years old; after her father died; and at the age of 50) treated with clomipramine.
Stable until her mother died 5 years before the current admission. During these
time, she suffers from residual depressive symptomatology even though treated with
clomipramina, fluvoxamina and escitalopram.
Major recurrent depressive syndrome resistant to treatment
Parkinsonism syndrome
THERAPEUTICAL APPROACH
● 1st-5th ECT Sessions: Bifrontotemporal stimulation was placed with 0.5 mseg pulse
width and a total energy between 35-50%
● 6th ECT session: Etomidate was administered during the anesthetic procedure instead
of propofol, together with atropine and succinylcholine.
● Since the 7th ECT Session: Mianserine 30 mg/day was added to the pharmacological
treatment due to still undercontrolled anxiety.
● After the hospital discharge she was treated with mianserine 40 mg/day, lorazepam 5
mg/day and levodopa/carbidopa 150/37,5 mg/day and ECT.
● Another 20 sessions were applied with etomidate as the main anesthetic, atropine and
succinylcholine, LART position was carried out (due to anterograde amnesic complaints)
with a 0.5 mseg pulse width, and a decreasing energy from 50 to 30% at the same time
the ECT sessions were spaced in time.
● The levodopa/carbidopa treatment was reduced down to 100/25 mg/day from the 9th
months of its first administration due to buccolingual dyskinesias.
● After a year of follow-up, the patient shows euthimia without extrapyramidal symptoms
and has retaken the social and familial activities. The neurological evaluation after 6
weeks once ECT was finished, redirects the symptomatology towards a pharmacological
parkinsonism and decides to withdraw the levodopa.
ECT is indicated in both depressive syndromes and parkinsonism syndromes (2), and it is
already known that the first increases the risk of suffering the second (3). The ECT effectiveness
has also been brought to light in relation with the pharmacological parkinsonisms (4,5). It should
not surprise us if we take into account authors such as Fink (6), who proposes these side effects
as another face of catatonia, widely known to be highly responsive with ECT (7).
Nevertheless, although it is not yet known the specific mechanisms in which these improvements
occur, there are sufficient evidences showing that the ECT has an effect in the dopaminergic
system at different levels: dopamine release, dopamine neurotransmission and linkage with its
receptor 8), and these effects differ between an acute stimulation and when repeated stimulation
are carried out. (9).
This case illustrates the successful response with ECT towards a depressive syndrome
associated with a pharmacological parkinsonism maintained over the long-term (one year with
ECT), and the fact that the potential elevation of dopaminergic neurotransmission could have
played an important role in the appearance of dyskinesia when treated together with l-dopa.
Finally, it must be taken into consideration the fact that the concomitant existence of depression
and parkinsonism could represent another indication for ECT, since the pharmacological
management of these patients is highly complex and could even more if we bear in mind that one
of the therapeutical options towards the antidepressant potentiation (atypical antipsychotics) can
worsen the symptomatology.
RESULTS
As shown on the following image, the progression of the patient is outstanding.
There was high improvement of the mood, remission of the parkinsonism
symptomatology and the dysphagia, enabling her to gain 4,7 kg in one month.
METHODOLOGY
To asses the evolution of our patient we used the following Evaluation Scales since the
first day in the Psychiatry ward, and on the next months, until completing a year:
● Yesevage Depression scale to assess the Depression symptomatology.
● HAMD-17 to rate the severity of Depression
● SCOPA-motor for assessment of Parkison’s disease
In all the evaluations in the it was always the same Psychiatry expert who interviewed the
patient, so there is no possible variability in the interviewer.
Hospital
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