Catatonia: Clinical Overview of the Diagnosis, Treatment, and Clinical Challenges

Abstract

Catatonia is a syndrome that has been associated with several mental illness disorders but that has also presented as a result of other medical conditions. Schizophrenia and other psychiatric disorders such as mania and depression are known to be associated with catatonia; however, several case reports have been published of certain medical conditions inducing catatonia, including hyponatremia, cerebral venous sinus thrombosis, and liver transplantation. Neuroleptic Malignant Syndrome and anti-NMDA receptor encephalitis are also prominent causes of catatonia. Patients taking benzodiazepines or clozapine are also at risk of developing catatonia following the withdrawal of these medications—it is speculated that the prolonged use of these medications increases gamma-aminobutyric acid (GABA) activity and that discontinuation may increase excitatory neurotransmission, leading to catatonia. The treatment of catatonia often involves the use of benzodiazepines, such as lorazepam, that can be used in combination therapy with antipsychotics. Definitive treatment may be found with electroconvulsive therapy (ECT). Aberrant neuronal activity in different motor pathways, defective neurotransmitter regulation, and impaired oligodendrocyte function have all been proposed as the pathophysiology behind catatonia. There are many clinical challenges that come with catatonia and, as early treatment is associated with better outcomes, it becomes imperative to understand these challenges. The purpose of this manuscript is to provide an overview of these challenges and to look at clinical studies regarding the pathophysiology, diagnosis, and treatment of as well as the complications and risk factors associated with catatonia.

Molecular and cellular mechanisms leading to catatonia: an integrative approach from clinical and preclinical evidence

“…Congruently, BDZ efficacy is directly related to GABAergic enhancement (Walther et al, 2019 ). Some authors attribute the success of BDZ to an induced decreased activation of mPFC and OFC (Edinoff et al, 2021 ). We support this hypothesis and suggest that a GABAergic potentiation would decrease preSMA-SMA hyperactivation and, moreover, that BDZ could generate diffuse brain circuitry hyperpolarization.…”

Novel Designer Benzodiazepines: Comprehensive Review of Evolving Clinical and Adverse Effects

“…The potential use of alprazolam in treating post-traumatic stress disorder (PTSD) is also being explored; however, it seems that its effects are on the secondary symptom of anxiety, not the primary symptoms of the condition [ 33 , 34 ]. Another use of benzodiazepines in the treatment of catatonia is a neurological condition comprised of psychomotor disturbances thought to stem from a disturbance in GABA transmission [ 33 , 35 ].…”

Maintenance Electroconvulsive Therapy, Developmental Regression, Depression and Catatonia in an Adolescent With Down Syndrome: A Case Report

“…In the setting of severe, treatment-refractory mood disorders, catatonia can also arise. Catatonia is a complex neuropsychiatric syndrome typically manifesting with a combination of motor and behavioral abnormalities characterized by marked hypoactivity [ 3 ]. Catatonia manifests as a subtype of a distinct general medical or psychiatric syndrome or, in the setting of a particular disorder-not as a discrete, isolated medical condition [ 4 ].…”

“…Catatonia is very responsive to first-line treatment with benzodiazepines (such as lorazepam) or ECT for refractory cases [ 3 ]. A positive Lorazepam Challenge Test (administration of one to two mg of Lorazepam by mouth, intravenously, or intramuscularly resulting in rapid but temporary resolution of all symptoms) supports a diagnosis of catatonia.…”

“…ECT is a well-established and highly effective treatment for catatonia [ 3 ]. In ECT, patients are placed under anesthesia and exposed to brief electrical pulses to the brain.…”