“…A cyst had distended the third ventricle of the brain, and relief followed the removal of its fluid; permanent relief followed its excision (211). Similar descriptions dot the medical literature in patients with tumors and blood vessel abnormalities in and around the brain's third ventricle and the basilar artery (212)(213)(214)(215)(216)(217)(218). The stuporous state is thought to result from the direct structural involvement of the base of the brain (209).…”
Section: Akinetic Mutismmentioning
confidence: 93%
“…'In those catatonic schizophrenic states that simulate akinetic mutism, there is awareness, as these patients do have memory of the events happening during the catatonic state' (213). The author of a detailed 1962 review of akinetic mutism and its symptoms from New York State Psychiatric Institute writes that these 'simulate, in many respects, catatonic schizophrenia' (214). In each description, the signs of catatonia are among the physical signs noted in the examination, but because the accompanying behaviors, thoughts, or course are not those of schizophrenia, catatonia is not identified.…”
Section: Akinetic Mutismmentioning
confidence: 99%
“…In each description, the signs of catatonia are among the physical signs noted in the examination, but because the accompanying behaviors, thoughts, or course are not those of schizophrenia, catatonia is not identified. The author of a detailed 1962 review of akinetic mutism and its symptoms from New York State Psychiatric Institute writes that these 'simulate, in many respects, catatonic schizophrenia' (214).…”
Applying the treatments for catatonia to patients with these syndromes offers opportunities for clinical relief. Catatonia is a recognizable and effectively treatable neuropsychiatric syndrome. It has many faces. It warrants recognition outside schizophrenia in the psychiatric disease classification.
“…A cyst had distended the third ventricle of the brain, and relief followed the removal of its fluid; permanent relief followed its excision (211). Similar descriptions dot the medical literature in patients with tumors and blood vessel abnormalities in and around the brain's third ventricle and the basilar artery (212)(213)(214)(215)(216)(217)(218). The stuporous state is thought to result from the direct structural involvement of the base of the brain (209).…”
Section: Akinetic Mutismmentioning
confidence: 93%
“…'In those catatonic schizophrenic states that simulate akinetic mutism, there is awareness, as these patients do have memory of the events happening during the catatonic state' (213). The author of a detailed 1962 review of akinetic mutism and its symptoms from New York State Psychiatric Institute writes that these 'simulate, in many respects, catatonic schizophrenia' (214). In each description, the signs of catatonia are among the physical signs noted in the examination, but because the accompanying behaviors, thoughts, or course are not those of schizophrenia, catatonia is not identified.…”
Section: Akinetic Mutismmentioning
confidence: 99%
“…In each description, the signs of catatonia are among the physical signs noted in the examination, but because the accompanying behaviors, thoughts, or course are not those of schizophrenia, catatonia is not identified. The author of a detailed 1962 review of akinetic mutism and its symptoms from New York State Psychiatric Institute writes that these 'simulate, in many respects, catatonic schizophrenia' (214).…”
Applying the treatments for catatonia to patients with these syndromes offers opportunities for clinical relief. Catatonia is a recognizable and effectively treatable neuropsychiatric syndrome. It has many faces. It warrants recognition outside schizophrenia in the psychiatric disease classification.
“…14 There is also significant overlap between catatonia and other motor disorders commonly associated with DNS and DPHL such as parkinsonism and akinetic mutism, a problem alluded to in the German literature nearly 100 years ago. 37,45 The neurologist C. Miller Fisher, in his treatise on catatonia, grappled with the similarities between akinetic mutism and catatonia but ultimately failed to parse them into distinct disorders with distinct etiologies. 46 Akinetic mute patients, who display little to no volitional movement or speech but manifest alertness and engagement with their eyes, easily qualify for caseness on the Bush-Francis Catatonia Rating Scale by having 2 of the 14 cardinal symptoms; 47,48 utilizing these criteria the number of DNS and DPHL cases with catatonia would reach into the hundreds.…”
Introduction
Neurologic deterioration occurring days to weeks after a cerebral hypoxic event accompanied by diffuse white matter demyelination is called delayed post-hypoxic leukoencephalopathy (DPHL). Manifestations of DPHL are diverse, and include dementia, gait disturbance, incontinence, pyramidal tract signs, parkinsonism, chorea, mood and thought disorders, akinetic mutism, and rarely catatonia.
Methods
The authors report a case of malignant catatonia in a patient diagnosed with DPHL that was refractory to electroconvulsive therapy (ECT), and review the literature on catatonia in DHPL.
Results
The patient was a 56 year-old female with schizoaffective disorder who was admitted with catatonia two weeks after hospitalization for drug overdose and respiratory failure. Her catatonic symptoms did not respond to lorazepam, amantadine, methylphenidate, or ten sessions of bilateral ECT at maximum energy. Repeat magnetic resonance imaging revealed extensive periventricular white matter lesions not present on admission scans, and she was diagnosed with DPHL.
Discussion
No treatment for DPHL has been proven to be widely effective. Hyperbaric oxygen treatments may reduce the rate of development, and symptom improvement has been reported with stimulants and other psychotropic agents. Review of the literature reveals rare success with GABAergic agents for catatonia after cerebral hypoxia, and no cases successfully treated with ECT. There are seven case reports of neurologic decompensation during ECT treatment after a cerebral hypoxic event.
Conclusion
Caution is advised when considering ECT for catatonia when delayed sequelae of cerebral hypoxia are on the differential diagnosis, as there is a dearth of evidence to support this treatment approach.
“…Metabolic conditions include: diabetic ketoacidosis [40]; parathyroid adenoma [41]; pellagra [42]; and homocystinuria [43]. Neurological disorders can result in catatonia; akinetic mutism [44] is an excellent example.…”
Catatonia is a psychomotor syndrome which has historically been associated with schizophrenia. Many clinicians have thought that the prevalence of this condition has been decreasing over the past few decades. This review reminds clinicians that catatonia is not exclusively associated with schizophrenia, and is still common in clinical practice. Many cases are related to affective disorders or are of an idiopathic nature. The illusion of reduced prevalence has been due to evolving diagnostic systems that failed to capture catatonic syndromes. This systemic error has remained unchallenged, and potentiated by the failure to perform adequate neurological evaluations and catatonia screening exams on psychiatric patients. We find that current data supports catatonic syndromes are still common, often severe and of modern clinical importance. Effective treatment is relatively easy and can greatly reduce organ failure associated with prolonged psychomotor symptoms. Prompt identification and treatment can produce a robust improvement in most cases. The ongoing prevalence of this syndrome requires that psychiatrists recognize catatonia and its presentations, the range of associated etiologies, and the import of timely treatment.
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