Management of catatonia in Parkinson’s disease with comorbid bipolar disorder: A case report and review of literature

Table 1 Differentiating depression from parkinsonian symptoms

Clinical profile of depressive disorders in PD	Shared symptoms of depressive disorders and PD	Discriminating symptoms of depressive disorders and PD	Diagnosing depressive disorder in PD
Persistent and pervasive low mood, sadness, and tearfulness	Lowered mood	Motor features	Low mood, anhedonia, and apathy are the most sensitive indicators of depressive disorders in PD
Dysphoria, irritability	Anhedonia	Downcast look, low mood, reduced or preserved mood reactivity, and agitation in depressive disorder	Neurovegetative symptoms are less effective in distinguishing patients with PD with or without depressive disorders
Preserved mood reactivity	Apathy	Bradykinesia, rigidity, tremor, stooped posture, shuffling gait, and masked facies in PD[18]	The presence of typical melancholic symptoms may help differentiate patients with PD with or without depressive disorders
Anxiety and panic attacks	Diminished emotional expression - lack of facial expressions, flat mood	Psychomotor slowing	A focus on mood and cognitive symptoms rather than neurovegetative symptoms helps in the diagnosis of depressive disorder in PD[18,19]
Anhedonia - diminished enjoyment	Anxiety	Similarities between parkinsonian motor symptoms, psychomotor slowing, negative symptoms and depressive symptoms in major schizophrenia, depressive, and bipolar disorder are evident	An inclusive approach that takes into account neurovegetative symptoms regardless of their possible aetiology is recommended for the diagnosis of depressive disorder in PD[10,30]
Apathy - reduced interest, loss of initiative	Autonomic symptoms	Despite these similarities, motor symptoms of parkinsonism are not correlated with negative and depressive symptoms in schizophrenia and mood disorders	-
Pessimism	Loss of energy, fatigue, tiredness	Motor symptoms of PD are not strongly associated with psychomotor slowing in schizophrenia and mood disorders	The motoric state, wearing on or off, s should be considered while diagnosing depressive disorders in PD[15,31]
Hopelessness	Slowing and retardation	A total score of ≥ 4 on the Simpson-Angus Scale is a clinically meaningful and reliable method for distinguishing parkinsonian from depressive symptoms[35]	The presence of coexisting cognitive impairment should be noted[30]
Mental slowing	Loss of appetite, weight loss	-	-
Diminished concentration	Insomnia, hypersomnia	-	-
Memory impairment	Mental slowing	-	-
Loss of energy, fatigue, tiredness	Diminished concentration	-	-
Slowing and retardation	Memory impairment[7,9,10,19,30]	-	-
Mild symptom severity	-	-	-
Present during wearing-off periods	-	-	-
Relative absence of self-blame, guilt, reproach, and low self-esteem	-	-	-
Frequent suicidal ideations but very few suicide attempts	-	-	-
Relative lack of psychotic symptoms[3,18,19,36,37]	-	-	-

PD: Parkinson’s disease.

Table 2 Differentiating drug-induced and idiopathic Parkinson’s disease

Clinical features and other characteristics	DIP	IPD
Cause	Blockade of dopamine D2 receptors. Temporal association with offending medications	Degeneration of nigrostriatal dopaminergic neurons
Sex distribution	More common in women	Slightly more common in men
Symmetry	Usually bilateral and symmetric features, but asymmetric features may be present in up to half of the patients	Unilateral and/or asymmetric features
Bradykinesia	More prominent	Present
Rigidity	More prominent	Present
Resting tremors	Relatively absent	Present
Coexistence of tardive dyskinesia	More common	Less common
Freezing gait	Relatively absent	Present
Olfactory dysfunction	Absent	Present in about 90% of the patients at any stage of IPD
Other non-motor symptoms	Absent	Sleep disturbance and urinary dysfunction may be present
Response to levodopa	Lack of response or a diminished response	Usually, a good response that is diagnostically useful
Dopamine transporter imaging by SPECT or PET	Medications causing parkinsonism, including antipsychotics, have negligible affinity for the transporter, so scans may demonstrate normal uptake even with significant DIP	Transporter uptake in the striatum is significantly decreased in patients with IPD, even in early stages of the disease
Resolution of symptoms	DIP usually resolves within months of stopping the offending drug, but unmasked PD may persist or progress in 10%-50% patients	Symptoms increase with time

PD: Parkinson’s disease; DIP: Drug-induced parkinsonism; IPD: Idiopathic Parkinson’s disease; SPECT: Single-photon emission computed tomography; PET: Positron emission tomography.

Table 3 Clinical profile of patients with Parkinson’s disease presenting with catatonia

Patient reports
Ref.	Patient	Primary diagnosis	Catatonic features	Treatment	Outcome
Suzuki et al[49], 2006	62-year-old woman	PD with psychosis	Acute onset of catatonic excitement followed by stupor, features of neuroleptic malignant syndrome, probably induced by quetiapine	Quetiapine stopped, dantrolene for neuroleptic malignant syndrome, reinstatement of levodopa, and 12 ECT sessions	Marked improvement: Near-complete resolution of catatonia and psychiatric symptoms with ECT
Kamigaichi et al[50], 2009	75-year-old woman	PD with psychosis	Acute onset of catatonic stupor following withdrawal of some dopaminergic medications. Associated psychotic symptoms, but no features of neuroleptic malignant syndrome. No cognitive impairment	Increase in the dose of levodopa. Did not respond to benzodiazepines. Two ECT sessions	Complete resolution of catatonia with ECT
Poyraz et al[51], 2016	80-year-old woman	PD with psychosis	Past history of catatonic stupor. Acute onset of catatonic stupor associated with psychotic symptoms. Features of delirium	Partial response to benzodiazepines. Optimisation of anti-parkinsonian treatment and increase in the dose of levodopa. Six sessions of ECT once the patient was clinically stable	Improvement in catatonic symptoms with ECT, but residual catatonia and mild cognitive impairment persisted
Ramesh et al[52], 2019	55-year-old man	PD with psychosis	Acute onset of catatonic stupor following institution of quetiapine	Treatment with levodopa. Partial response to lorazepam. Six sessions of ECT	Complete resolution of catatonia and marked improvement in psychotic symptoms with ECT
Elefante et al[36], 2022	56 and 58-year-old women	PD with BD, type I and type II. Comorbid anxiety	Acute onset of catatonic stupor during depressive episodes with psychotic symptoms. No cognitive impairment	Antiparkinsonian medication. Poor response to lorazepam. Eight to fifteen ECT sessions	Complete resolution of catatonia with ECT
Longitudinal cohort study
Study	Patient sample	Prevalence of catatonia	Other features
Onofrj et al[29], 2021	Clinical cohort of 250 patients with BD and PD. Followed up at 3 and 6 years. BD preceded the onset of PD by several years	Seven per cent of the patients (n = 14) with BD and PD had catatonia. Prevalence was significantly greater than in patients with only PD (1%)	The prevalence of catatonia was considerably lower than that of depression, psychosis, and dementia. Two patients were carriers of GBA gene mutations

PD: Parkinson’s disease; BD: Bipolar disorder; ECT: Electroconvulsive therapy.

Table 4 Electroconvulsive therapy in Parkinson’s disease: Reviews and meta-analysis

Acute ECT
Ref.	Study type	Key findings
Faber and Trimble[53], 1991	Narrative review of 27 studies, mostly case reports and uncontrolled studies with small samples; only one randomised-controlled trial; 20 studies included patients with comorbid depression	Approximately 50% of patients receiving ECT, irrespective of the presence or absence of psychiatric comorbidity, showed improvement in parkinsonian symptoms
Kennedy et al[54], 2003	Systematic review of 51 studies evaluating ECT in movement disorder	Significant improvement in both psychiatric and motor symptoms of Parkinson’s disease with ECT; however, significant side effects, particularly delirium (44%-85%), were reported
Borisovskaya et al[55], 2016	Systematic review of 43 studies of ECT in Parkinson’s disease with comorbid depression	Depression improved in 93% of patients; motor symptoms improved in 83%; up to 56% developed delirium, but no long-term cognitive impairment was observed in 94% of patients
Takamiya et al[56], 2021	Meta-analysis of 14 studies (including 1 randomised-controlled trial1) evaluating ECT in PD	ECT significantly improved motor manifestations of Parkinson’s disease; improvement was significant in patients without psychiatric symptoms; ECT also significantly improved depression and psychosis, relieved the wearing-off phenomenon, and did not worsen cognitive functioning
Maintenance ECT
Kramer et al[57], 1999	Major depressive disorder (n = 24)	Major depressive disorder with PD (n = 10)
	Much improved 75%	Much improved 50%
	Partially improved 12.5%	Partially improved 40%

¹The only randomised-controlled trial of active vs sham electroconvulsive therapy was conducted by Andersen et al[58]. In 11 patients with Parkinson’s disease, electroconvulsive therapy improved motor symptoms and the wearing-off phenomenon, but the effects were short-lasting.

PD: Parkinson’s disease; ECT: Electroconvulsive therapy.