Catatonia | Why Do Some Individuals Freeze and Become Unresponsive?

Catatonia is a complex neuropsychiatric syndrome characterized by a collection of motor, behavioral, and vocal abnormalities. It is not simply "freezing" but a state of profound disruption in the brain's ability to regulate movement and behavior. The core feature is a marked decrease in reactivity to the environment, which can manifest in various ways. One of the most recognized symptoms is immobility or stupor, where an individual remains motionless and appears unresponsive for long periods. Another is mutism, a complete lack of verbal response. Conversely, some individuals may display excessive and purposeless motor activity, known as catatonic excitement. Other specific motor signs are central to its definition. These include posturing, which is the spontaneous and active maintenance of a posture against gravity, and catalepsy, a more passive state where a light pressure is sufficient to maintain an induced posture. Waxy flexibility is a classic sign where an individual's limbs can be moved into new positions and will remain there, similar to bending a wax figure. Negativism, another key symptom, is an apparently motiveless resistance to all instructions or attempts to be moved. These signs are not voluntary acts of defiance but are direct results of underlying brain circuit dysfunction that disconnects intention from motor execution.

Catatonia is not classified as an independent disorder in current diagnostic systems like the DSM-5. Instead, it is considered a syndrome or a clinical specifier that occurs in the context of another underlying medical or psychiatric condition. This is a critical distinction for treatment, as addressing the root cause is paramount. While historically linked almost exclusively with schizophrenia, it is now understood that catatonia is more frequently associated with mood disorders, particularly bipolar disorder and major depressive disorder. Furthermore, catatonia can be a manifestation of various general medical conditions. These include neurological diseases (such as encephalitis, stroke, or Parkinson's disease), metabolic disorders (like diabetic ketoacidosis), and autoimmune conditions (such as lupus). The presence of catatonia signals a severe state of brain dysfunction that requires immediate medical investigation to identify and treat the primary illness causing the catatonic state.

The precise neurobiology of catatonia is an area of active research, but current evidence points to a significant dysregulation in key neurotransmitter systems and brain circuits. A primary hypothesis involves dysfunction in the gamma-aminobutyric acid (GABA) system, the brain's main inhibitory or "calming" neurotransmitter. Reduced GABAergic activity, particularly in the frontal cortex, is thought to lead to a state of motor system over-inhibition or dysregulation, resulting in the characteristic symptoms. The dopamine system is also implicated, with both excessively high and low dopamine levels being associated with catatonic states, depending on the underlying cause. Brain circuits connecting the cortex (especially the prefrontal and motor areas), thalamus, and basal ganglia—which are all crucial for planning and executing movement—are believed to be disrupted. This circuit failure effectively disconnects the will to move from the physical ability to do so.

The diagnosis of catatonia is made through careful clinical observation and the systematic assessment of its characteristic signs. There is no single blood test or brain scan that can definitively diagnose catatonia itself. Clinicians rely on standardized instruments, with the Bush-Francis Catatonia Rating Scale (BFCRS) being the most widely used tool. This scale lists specific symptoms, such as immobility, mutism, posturing, and waxy flexibility. A diagnosis is typically confirmed if a patient exhibits a certain number of these signs. The diagnostic process also involves a thorough medical workup to identify the underlying cause. This includes a physical and neurological examination, blood tests to check for metabolic or infectious issues, and often brain imaging like an MRI or CT scan to rule out structural brain problems like tumors or strokes. An electroencephalogram (EEG) may also be used to check for seizure activity that can sometimes mimic catatonia.

The treatment for catatonia is highly effective and often leads to a rapid and dramatic resolution of symptoms when initiated promptly. The first-line treatment is a class of medications known as benzodiazepines, with lorazepam being the most commonly used. These drugs work by enhancing the effect of GABA, the brain's primary inhibitory neurotransmitter. By boosting this "braking" system in the brain, benzodiazepines can quickly alleviate the motor abnormalities of catatonia, often within minutes to hours of the first dose. A positive response to a "lorazepam challenge" is also considered a supportive diagnostic sign. If an individual does not respond to benzodiazepines, or in cases of a particularly severe and life-threatening form called malignant catatonia, the second-line treatment is Electroconvulsive Therapy (ECT). ECT is a safe and extremely effective procedure where a brief, controlled electrical current is passed through the brain, inducing a seizure. This process is thought to act as a "reset" for brain circuits, rapidly restoring normal neurotransmitter function and resolving the catatonic state. Simultaneously, treatment must address the underlying psychiatric or medical condition that triggered the catatonia.