Francis Catatonia Rating Scale Research Articles

Catatonia and neurocognitive disorder in the context of schizophrenia spectrum disorders

Background. Currently, researchers are aiming to establish the relationship between neurocognitive disorder and other clinical manifestations of endogenous diseases and functional indicators of the patient’s adaptation to social life. According to some data, the development of cognitive disorders is associated with the severity of catatonic disorders in the clinical picture of various diseases, in particular the presence of catatonic symptoms determines the worst indicators of cognitive functioning in the case of schizophrenia.The aim. To study the clinical and psychopathological features of catatonic syndrome in connection with schizophrenia spectrum disorders, as well as its connection with neurocognitive disorder manifestations among patients with endogenous disorders.Methods. From September 2022 to March 2024, we conducted a prospective, multicenter study of patients (n = 69) suffering from paroxysmal schizophrenia with primary catatonic symptoms in the structure of attacks. Mental status, the severity of catatonic symptoms using Bush – Francis Catatonia Rating Scale, neurocognitive profile using a number of validated scales (Montreal Cognitive Scale, Brief Assessment of Cognition in Schizophrenia, Frontal Assessment Battery) were assessed.Results. Neurocognitive disorder was revealed in all cases studied. It has been noted that, depending on the presence/absence of affective symptoms, various domains of the neurocognitive profile are affected. Thus, in patients without severe affective symptoms, auditory and verbal memory, attention, processing speed, and motor skills are impaired. In patients with pronounced affective disorders, processing speed, motor skills, and problem-solving behavior are affected.Conclusion. Based on the results of processing the material, it was revealed that the most pronounced neurocognitive disorders were found in case of the manifestation of paroxysmal paranoid schizophrenia in male patients with a relatively early onset of the disease and hypokinetic catatonic disorders. In the future, we are planning to compare these results with the results of control group of patients with endogenous diseases and without catatonia.

Associations of Genetic Polymorphisms and Neuroimmune Markers With Some Parameters of Frontal Lobe Dysfunction in Schizophrenia.

We investigated the associations of DRD3 rs6280, HTR1A rs6295, BDNF rs6265, SCL6A4 rs16965628, and 5HT2A rs7322347 with schizophrenia in a case–control study, and associations of these genetic variants with several clinical features. We also investigated markers of inflammatory response (C-reactive protein, IL-2, IL-6, IL-10), the activity of leukocytic elastase (LE) and α1-proteinase inhibitor (a1-PI), antibodies to S100B and myelin basic protein (MBP) in schizophrenia. Clinical symptoms were assessed on three scales: Positive and Negative Syndrome Scale, The Bush – Francis Catatonia Rating Scale and Frontal Assessment Battery. All SNPs were typed using predesigned TaqMan SNP genotyping assays. The biomarkers related to the immune system were routinely tested using ELISA kits. The association with schizophrenia was found for DRD3 rs6280 (p = 0.05) and HTR2A rs7322347 (p = 0.0013). We found differences between groups by parameters of LE and a1-PI and LE/a1-PI (p < 0.001). And IL-6 was evaluated in the schizophrenia group (p < 0.001). We showed that patients with the TT allele (BDNF rs6265) had more severe impairments in frontal lobe function. a1-PI can serve as a marker for assessing the severity of frontal lobe damage in patients with frontal dementia. We found some biological parameters reflecting the severity of frontal dysfunction in schizophrenia.

Acute onset mania with cycling between excitement and stupor.

Byline: Mohapatra. Debadatta, Sahoo. Ashrumochan, Chittaranjan. Andrade Sir, Mania is commonly characterized by motor activation that can sometimes peak in extreme excitement and depression by retardation that can sometimes peak in a state of stupor. Paradoxically, stupor may (rarely) complicate mania; although this was recognized by Kraepelin over a century ago,[sup][1] down the decades, cases of manic stupor have seldom been described in literature.[sup][2],[3] We present herein two patients who experienced stupor associated with mania; our cases are interesting in that the onset of excitement and the switch to stupor was abrupt in both cases; one patient, additionally, showed cycling between excitement and stupor. Case Reports Case 1 A, 22-year-old farmer, had a 6-day history of irritable mood, loud and excessive talk, excessive and unnecessary spending, excessive working in the fields without experiencing fatigue, increase in appetite, and decrease in sleep. He boasted of divine powers and the ability to change the future. Aggressiveness developed, abruptly followed by reduced communication. By the 5[sup]th day, he stopped talking, stared mutely, refused food, and even neglected bowel and bladder needs. There was no history of head injury, fever, or any other past or present feature to suggest a medical origin of these symptoms. General medical examination and laboratory investigations, including hemogram, serum electrolytes, and hepatic and renal function tests, were all within normal limits. The patient was mute and immobile. He maintained eye contact without blinking. Other catatonic signs at different points in time included negativism, posturing, grimacing, verbigeration, rigidity, automatic obedience, and stereotypy. He required nasogastric feeding and urinary catheterization. The Bush–Francis (BF) Catatonia Rating Scale score was 22. The dominant clinical picture was one of stupor. Parenteral lorazepam at 8 mg/day for 3 days elicited no improvement. Thrice weekly, bilateral electroconvulsive therapy (ECT) was initiated. There was progressive improvement from the first ECT with resolution of catatonia by the third treatment; manic symptoms, however, reemerged. On inquiry, he reported that during the period of stupor, he was blissful, disinterested in worldly matters, and in close contact with God. He described experiences related to Hindu mythology. His Young Mania Rating Scale (YMRS) score was 31. Valproate and quetiapine were initiated, and ECT was continued to a total of six treatments. He was discharged in almost complete remission after a hospital stay of 16 days. Case 2 B, a 31-year-old peon, had a 5-day history of grandiosity with claims such as that he could become the Prime Minister and change the world. He was irritable, talked excessively, participated intensely in activities, and slept little. After 3 days of such behavior, there was an 18–20 h period of mutism, laughing without reason, and food refusal; manic symptoms subsequently reemerged in greater force. …

Catatonia in Patients with Frontotemporal Dementia

Introduction Catatonia is a neuropsychiatric syndrome described in a variety of medical and psychiatric conditions. Its association with frontotemporal dementia (FTD) has been sparsely described. Objetives We reported two patients with FTD that present a catatonic state. Aim Case reports Method Literature review through Pubmed and report of a clinical cases. Results Case 1: Frontotemporal dementia, behavioral variant. 65 year old female who was hospitalized after losing weight due to his active refusal to eat and subsequently was undergone a gastrostomy. Once stabilized physically was derived to psychogeriatric ward where the patient was stuporous, mute, with mannerisms and rigidity. Continued with refusal to take food. On examination she had staring, posturing, echophenomena, automatic obedience, Gegenhalten, ambitendency and perseveration. It featured 12 of 23 symptoms of Bush and Francis Catatonia Rating Scale (BFCRS), scoring 32. She improved completely her catatonic state within one week with lorazepam 2.5 mg /day and zolpidem 10mg/day. Perseverative behavior and mannerisms was maintained. Case 2: Frontotemporal dementia, primary progressive aphasia 67 years old male who was admitted to psychogeriatric ward because had aggressivity and negativism. On examination immobility, mutism, staring, echolalia, rigidity, negativism, withdrawal, perseveration, Gegenhalten, impulsiveness and combativeness were observed. It featured 11 of 23 symptoms of BFCRS, scoring 22. He was treated with lorazepam 10mg/day and valproic acid 900 mg/day. Catatonic symptoms disappeared a month later. Negativism and impulsiveness persisted slightly. Conclusions The catatonic syndrome may occur in patients with FTD. In both conditions symptoms overlap. The response to GABAergic drugs was optimal.