Catatonic Stupor Syndrome - An Overview

Introduction

Catatonic stupor refers to a certain symptom of catatonia where all sorts of interaction with the surroundings are significantly diminished with the abolition of interpersonal communication and illustrated as an ‘end-state’ response to feelings of imminent destruction. “Neurological” stupor is a syndrome of neuromuscular abnormalities, one of the most theatrical presentations of catatonia, where an individual lies mute, immobile, and unwilling to contemplate meaningful interaction with the environment and adopt odd and graceless postures, their bodies such as bizarre posture, rigidity, and waxy flexibility, which is considered as a serious medical problem. A catatonic stupor is a non-specific syndrome common to various systemic and neuropsychiatric diseases and an aggressive form of negativism, which encircles the host symptoms that reflect an active or passive denial to interact with individuals and the environment. Neurologists believed that catatonia might be the brain disease's chief or sole manifestation, reflecting the progression of the degenerative process in the brain part.

What Is the Mechanism of the Catatonia Stupor?

The actual cause of catatonia has not been enlightened, but several hypotheses have been proposed.

• A ‘top-down modulation’ refers to basal ganglia due to a deficiency of cortical gamma-aminobutyric acid (GABA), the brain's primary inhibitory neurotransmitter (Chemical messengers that carry chemical signals from one neuron to another), which may justify the motor symptoms of catatonia, which is highlighted after by the therapeutic effect of benzodiazepines that cause an upsurge in GABA activity. Similarly, glutamate hyperactivity (primary excitatory neurotransmitter) has a role in underlying neurochemical dysfunction.

• Sudden and massive blockades of dopamine can lead to catatonia. Evidence-based studies show that dopamine-blocking antipsychotic medications are not typically beneficial in catatonia. Despite it heightening dopamine deficiency, antipsychotics may precipitate a worsening condition.

• Clozapine withdrawal catatonia is hypothesized due to cholinergic and serotonergic rebound hyperactivity. The cholinergic and serotonergic are the receptors for chemical signals that perform a specific function in the brain.

• In chronic catatonia with major speech oddities, positron emission tomography (PET), a medical procedure to measure the metabolic activity of the body cell, tissue, or organ, has recognized abnormalities in metabolism bilaterally in the thalamus and frontal lobes.

What Are the Complications of Catatonia Stupor Syndrome?

Middle- and old-age females generally exhibit catatonia and rapidly progress to subsequent death; this condition is termed “late catatonia” or “lethal catatonia.” The medical complications resulting from catatonia are as follows:

• Rhabdomyolysis: Muscular tissue breakdown results in the release of a protein called myoglobin into the blood.

• Renal Failure: Myoglobin protein, normally present in muscles due to rhabdomyolysis, is released into the blood that can not be filtrated by the kidney and thus results in kidney failure.

• Disseminated Intravascular Coagulation (DIC): In which blood clotting elements become overactive, forming clots in the body.

• Tachycardia: Increase in heart rate.

• Bradycardia: Decrease in heart rate.

• Cardiovascular Collapse: Abrupt loss of heart function due to disruptions in blood flow of the heart.

• Myocardial Infarction: A blood clot in the heart's arteries that blocks blood flow to the heart and other tissues.

• Acute Respiratory Distress Syndrome: Fluid collection in the air sac of the lungs cause, depriving the oxygen supply to the tissue.

• Upper Gastrointestinal Tract Bleeding: The main cause is peptic ulceration on the stomach lining.

• Sepsis: Generalized state of infection or widespread systemic inflammation.

• Seizures: Altered or abnormal electrical activity in the brain that leads to convulsion.

• Hypoglycemia: Extreme low blood sugar level leads to unconsciousness.

• Hepatocellular Damage: Accomplished by inflammatory infiltration, where the liver cell is replaced by scar tissue.

• Intestinal Pseudo-Obstruction: Impairment of the intestinal muscle contraction that moves food through the digestive tract.

• Deep Venous Thrombosis: Blood clot formation in deep veins, mainly in the lower legs and thigh.

• Pulmonary Embolism: More than one arteriole of the lungs is blocked by blood clots and reduces the flow of blood and oxygen to the tissue.

What Is the Relationship Between Catatonia and Neuroleptic Malignant Syndrome?

The syndrome's progression starts with signs of catatonia, followed by bodily disturbances, and ends in death as the condition overlaps with the neuroleptic malignant syndrome. Philbrick and Rummans 1994 suggested the term “malignant catatonia,” which involves both neuroleptic- and non-neuroleptic-induced severe catatonia. In severe catatonia, patients flaunt autonomic instability or hyperthermia (high temperature).

The neuroleptic malignant syndrome may be conceptualized as an antipsychotic-induced form of lethal catatonia and has emphasized a significant clinical difference between lethal catatonia and neuroleptic malignant syndrome, that the former commonly initiates with extreme psychotic excitement. In contrast, the latter triggers severe extrapyramidal muscular rigidity.

Catatonia depicts a highly substantial risk factor for following neuroleptic malignant syndrome.

What Are the Clinical Signs and Symptoms Of Catatonia Stupor Syndrome?

• Ambitendency: Patients alternate between resistance and cooperation and mimic the examiner's movements.

• Automatic Obedience: The patient demonstrates exaggerated cooperation, obeying every examiner's instruction.

• Aversion: Patients move away from the examiner when addressed.

• Catalepsy: An extreme version of holding a posture.

• Echolalia: Imitates the words of the examiner.

• Echopraxia: Imitates the action of the examiner.

• Excitement: Hyperactive or aggressive behaviors.

• Mannerisms: Repetitive, goal-directed movements (e.g., saluting).

• Negativism: The patient opposes the examiner's attempts to move parts of their body, and the resistance is equal to the strength applied.

• Posturing: The patient can hold the exact posture for prolonged periods. e.g., ‘crucifix.’

• Stupor: A combination of immobility and mutism that occur independently.

• Waxy Flexibility: Highly uncomfortable postures for a considerable time.

• Withdrawal and forced grasping.

• Mutism, immobility, and rigidity.

• Staring look.

What Are the Treatment Options for Catatonia Stupor Syndrome?

Treatments with robust evidence-based results are

• Benzodiazepines: The drug of choice for catatonic stupor syndrome help by acting on gamma-aminobutyric acid (GABA).

• Electroconvulsive Therapy: Therapy that delivers an electrical impulse to the brain by holding the electrodes across the head of the patient.

• Mood Stabilizers: Like Carbamazepine.

• Antipsychotics.

• N-methyl-D-aspartate (NMDA) Antagonists: Amantadine and Memantine. N-methyl-D-aspartate (NMDA) receptor hypofunction within the brain is associated with memory and learning impairments, psychosis, and, ultimately, excitotoxic brain injury.

• Dopamine Agonists Therapy: A dopamine agonist is a compound that activates dopamine receptors. E.g., Bromocriptine.

• Skeletal Muscle Relaxants: Dantrolene, especially in neuroleptic malignant syndrome.

Conclusion

Catatonia appears in both functional and organic disorders. The therapy of the catatonic phase is practically exact and reacts well to benzodiazepines or ECT. Catatonia is more typically associated with mood disorders than schizophrenia, and its occurrence phenomenon is crucial in psychiatry and general medicine, but still, its underlying mechanism needs to be clarified.