Resolution of Catatonia after Treatment with Stimulant Medication in a Patient with Bipolar Disorder

Lorazepam-Resistant Catatonia in an Antipsychotic-Naïve 24-Year-Old with Psychotic Symptoms

“…The exact pathophysiological mechanisms remain to be defined; however, several neurobiological hypotheses have been proposed. Based on the pharmacologic properties of the currently indicated treatments, it is believed that catatonia is caused by a pathway dysregulation which implicates GABA-A, glutamate, and dopamine systems [8,[22][23][24][25][26]. More precisely, Neuhut et al propose three pathophysiological hypotheses for the development of a catatonic state: lower binding of GABA-A in the right lateral orbitofrontal and parietal frontex, glutamate hyperactivity in the striatum, and dopamine hypoactivity in the prefrontal cortex [26,27].…”

“…Methylphenidate has been recently studied as a potential therapeutic agent of catatonia, with a few case reports where it is successfully used to treat the syndrome, in the context of various underlying diseases [27,39,40]. The rationale for stimulant treatment in catatonia is provided by the "diminished dopamine hypothesis," which proposed pathophysiological mechanism of the syndrome, according to which catatonia is caused by decreased dopamine activity in the mesostriatum [26,27]. However, there are cases where we can observe catatonia-like symptoms after cocaine use [45], thus indicating a more complex etiological link.…”

Some patients with advanced malignancies also have reversible catatonia or limbic encephalitis

“…Other medications reported to reverse catatonia include zolpidem, methylphenidate, topiramate, valproic acid, memantine and atypical anti-psychotic agents. [3][4][5][6][7][8][9][10] Zolpidem is a common hypnotic that also stimulates GABA receptors; methylphenidate acts as a general central nervous system stimulant, elevating dopamine, serotonin and norepinpehrine, and memantine is a noncompetive antagonist of NMDA type glutamate receptors. The other agents produce "awakenings" either through indirect potentiation of the GABAergic spiny interneurons or through some other mechanism.…”

“…2 Score on the Bush-Francis scale before and after treatment could then be measured. 5. All patients should be tested for serology with a comprehensive panel of autoantibodies, using as a model the work of Endres et al: anti-NMDA receptor antibodies, antibodies against other neutroansmitter receptors (AMPA-1/2-R, GABA-B-R,VGKC-complex), antibodies against intracellular synaptic antigens (GAD, amphiphysin), and intracellular onconeuralantigens (Yo,Hu,Ri, Cv2/CRMP5, Ma1,Ma2,SOX1), and anti-thyroid antibodies (anti-thyroidperoxidase antibodies, antithyroglobulin antibodies and thyroid-stimulating hormone receptor antibodies).…”

Special Medical Conditions Associated with Catatonia in the Internal Medicine Setting: Hyponatremia-Inducing Psychosis and Subsequent Catatonia

“…However, second-generation antipsychotic medication on several occasions did treat the symptoms of catatonia. 12 In addition, there are many reports that strongly suggest that stimulant medication can treat catatonia symptoms in patients with bipolar disorder 13 or depression. 14 Imaging results are different in various stages of catatonia.…”