Catatonia Fast Facts
Catatonia is a condition in which a person’s ability to react to the world around them is impaired.
Catatonia is referred to as a psychomotor disorder, meaning it involves disruption between the brain’s mental processes and the ability to move or act.
The disorder affects an estimated 10% of people hospitalized for a psychiatric illness.
Catatonia was once believed to be associated solely with schizophrenia, but it is now considered a disorder that affects a much larger population.
The disorder affects an estimated 10% of people hospitalized for a psychiatric illness.
What is Catatonia?
Catatonia is a brain-related disorder in which a person’s ability to move, communicate, or otherwise respond to the world around them is impaired. The symptoms of catatonia vary, and the condition may be associated with many different mental health-related issues, neurological disorders, and medical illnesses.
In the past, catatonia was thought to be a symptom of schizophrenia. However, a more up-to-date understanding of the disorder acknowledges that it can be associated with many other underlying conditions. Some researchers also believe that catatonia may sometimes occur on its own without the presence of an underlying trigger. There is still some controversy over defining and diagnosing catatonia, but it is generally considered more common than once believed.
Symptoms of catatonia can include:
- Unresponsiveness
- Repetitive, purposeless movements
- Unusual or exaggerated movements
- Agitation
- Inability to speak
- Holding an unusual posture or facial expression
- Mimicking sounds or movements made by others
- Holding a position that someone else moves them into (catalepsy)
Types of Catatonia
Catatonia is categorized into different types depending on its primary symptoms.
- Hypoactive catatonia is characterized by general unresponsiveness. People with this type of catatonia may not move or speak and may be unresponsive to stimuli around them. This type may also be called withdrawn or akinetic catatonia
- Hyperactive catatonia is characterized by restlessness, agitation, or aggression, not in response to any situation in the person’s environment. This type may also be called excited catatonia.
- Mixed catatonia involves shifts between the other two types.
Malignant Catatonia
This type of catatonia is potentially life-threatening. In this type of the disorder, nervous system impairment extends to autonomic functions, the automatic neurological processes that keep the person alive. Without quick medical treatment, this type of catatonia can be fatal.
Symptoms of malignant catatonia include:
- High body temperature
- Rapid heart rate
- Sweating
- Highly variable blood pressure
- Blue color in the skin, lips, and fingernails (cyanosis) caused by lack of oxygen in the blood
What Causes Catatonia?
Catatonia can be associated with many different psychiatric illnesses, medical conditions, or neurological conditions.
Some mental health-related conditions sometimes associated with catatonia include:
Neurological and medical disorders that may be associated with catatonia include:
- Autism
- Down syndrome
- Epilepsy
- Stroke
- Hydrocephalus
- Encephalitis
- Dementia
- Parkinson’s disease
- Tourette syndrome
- Electrolyte imbalances
- Lupus
- Multiple sclerosis
- Side effects of medications or drugs
Is Catatonia Hereditary?
Catatonia usually results from an identifiable underlying condition and is not inherited. However, some of the conditions that can cause catatonia do have a genetic component; genetics may play some role in increased catatonia risk. Schizophrenia, a disorder commonly linked to catatonia, is thought to have an inherited component in some cases, for example. In addition, one study has suggested that genetic factors may increase the risk of catatonic schizophrenia.
How Is Catatonia Detected?
The early stages of catatonia can vary widely from case to case. The condition may come on suddenly, or it may develop gradually over an extended period. Doctors can generally diagnose catatonia if a patient exhibits three or more of the condition’s symptoms.
How Is Catatonia Diagnosed?
There is no definitive test or exam to diagnose catatonia. To make a diagnosis, a doctor will look for signs of impairment in movement, communication, responsiveness, and other areas usually affected by the conditions. Exams and tests will determine the severity of the impairment and rule out other potential causes for the symptoms.
Diagnostic steps may include:
- Taking a medical history
- A physical exam
- Neurological exams
- Blood and/or urine laboratory tests
- Lumbar puncture (spinal tap) to examine the cerebrospinal fluid
- Imaging exams to look for signs of neurological problems in the brain
- Electroencephalogram (EEG) to look for abnormalities in electrical brain activity
The official diagnostic criteria for catatonia laid out in the Diagnostic and Statistical Manual of Mental Disorders (DSM) include twelve symptoms of the condition:
- Stupor (lack of responsiveness to the environment)
- Catalepsy (holding unusual postures)
- Waxy flexibility (maintaining a position that another person moves the patient into)
- Mutism (little or no verbal communication)
- Negativism (little or no response to instructions or stimuli)
- Posturing (holding a posture actively against gravity)
- Mannerism (unusual or exaggerated actions)
- Stereotypy (repetitive, purposeless actions)
- Agitation (agitated actions not in response to any stimulus)
- Grimacing (holding a stiff facial expression)
- Echolalia (mimicking another person’s speech)
- Echopraxia (mimicking another person’s movements)
For diagnosis, the patient must exhibit at least three of these symptoms.
A doctor might also use one of several assessment scales to determine a patient’s level of catatonia. The most commonly used of these scales is the Bush-Francis Catatonia Rating Scale (BFCRS).
PLEASE CONSULT A PHYSICIAN FOR MORE INFORMATION.
How Is Catatonia Treated?
An important step in treating catatonia is to focus on the underlying cause, and the proper course of treatment will vary depending on what’s causing the catatonia.
Treatment of catatonia itself usually involves medications. The most commonly used medications include:
- Benzodiazepines such as lorazepam, clonazepam, or diazepam
- Amobarbital
- Bromocriptine
- Carbamazepine
- Lithium carbonate
- Thyroid hormone
- Zolpidem
Electroconvulsive therapy (ECT)
This therapy involves inducing a seizure by administering an electrical current to the brain. ECT is effective at treating catatonia in many cases, and it is commonly used as an emergency treatment of malignant catatonia.
How Does Catatonia Progress?
Catatonia is usually temporary, but in some cases, symptoms may last for weeks or months. In cases where benzodiazepines or ECT are effective, improvement may begin within minutes.
Responsiveness to treatment may vary depending on the underlying disorder. Catatonia associated with mood disorders such as depression or bipolar disorder tends to be more responsive than catatonia associated with schizophrenia.
Catatonia itself does not have life-threatening effects, but people who experience long-term akinetic catatonia may be vulnerable to potentially life-threatening complications such as respiratory infections.
How Is Catatonia Prevented?
There is no known way to prevent catatonia.
Catatonia Caregiver Tips
The most important thing you can do for a loved one with catatonia is to show love and support. Many people who have experienced catatonia say that they were at least somewhat aware of their surroundings despite being unresponsiveness while catatonic. Ways to help include:
- Keep things simple and calm.
- Let your loved one know that they are safe.
- Be alert for signs that a person with catatonia may pose a danger to themselves or others, and get emergency help when necessary.
Catatonia Brain Science
Scientists don’t know precisely what causes catatonia. Most suspect that the problem lies with the action neurotransmitters, chemicals that allow nerve cells to communicate with one another. Some neurotransmitters, called excitatory neurotransmitters, increase the transmission of signals between nerve cells. Others, called inhibitory neurotransmitters, decrease signaling. A disruption in the normal production or activity of neurotransmitters, such as the excessive activity of inhibitory chemicals or decreased activity of excitatory ones, may underlie the symptoms of catatonia.
Catatonia Research
Title: Blood Concentration in Lorazepam and Treatment in Adult Catatonia (PHARMAPREDICAT)
Stage: Recruiting
Principal investigator: Ali Amad, MD
University Hospital
Lille, France
Catatonia is a severe form of psychomotor disturbance with a heterogenous presentation. It affects approximately 10% of acute psychiatric inpatients. According to the fifth edition of DSM-5, the diagnosis of catatonia can be made when three or more symptoms from the twelve following are present: catalepsy, waxy flexibility, stupor, agitation, mutism, negativism, posturing, mannerisms, stereotypies, grimacing, echolalia, echopraxia. It can occur in various psychiatric diseases, including mood disorders or schizophrenia, but also in various non-psychiatric disorders [metabolic disturbances, viral infections (including HIV), typhoid fever, heat stroke, and autoimmune disease].
Benzodiazepines, especially lorazepam, are the most common initial treatment, with a remission rate of approximately 70-80 %, regardless of the cause or the clinical manifestations. This first-line treatment is titrated gradually according to the therapeutic response over a few days up to 20-25 mg daily. Electroconvulsive therapy (ECT) is initiated on patients with catatonia who do not respond to benzodiazepines.
Interestingly, pharmacogenetic variants can alter the metabolism of lorazepam (e.g., the UGT2B15 * 2 allele slows it down).
The main objective of this study is to assess the link between clinical response to lorazepam, residual plasma concentrations of lorazepam after 72 hours of fixed dosage, and the existence of genetic polymorphisms modifying the metabolism of lorazepam. We hypothesize that non-responding patients have lowered blood concentrations of lorazepam associated with a genetic profile of rapid metabolism. Evaluating the predictive factors of the response to treatment would allow early and precise identification of non-responder patients to adapt their first-line treatment.
Title: Clonidine to Prevent Delirium After Electroconvulsive Therapy. (ECaTa)
Stage: Recruiting
Principal investigator: Patrick Y. Wüthrich, Prof, MD
Bern University Hospital
Bern, Switzerland
Electroconvulsive therapy (ECT) is a highly effective treatment for some psychiatric disorders like major depression or bipolar disorder but may lead to agitation and delirium after the procedure in up to 65% of patients. This can have negative side effects and be dangerous for patients and attending staff. Clonidine, a central-acting alpha2-receptor agonist, is an approved antihypertensive medication with known sedative side effects. Clonidine’s newer but more expensive successor, dexmedetomidine, has recently shown its potential to reduce this kind of delirium. The investigators, therefore, hypothesize that pre-treatment with 2 mcg/kg clonidine before electroconvulsive therapy will significantly reduce the incidence of postictal delirium. This potentially makes a highly efficient treatment for patients with otherwise refractory psychiatric illnesses safer and more accessible.
Title: Personalized Non-invasive Neuromodulation by rTMS for Chronic and Treatment Resistant Catatonia (RETONIC)
Stage: Recruiting
Principal investigator: Jack Foucher, MD
University Hospital
Strasbourg, France
Investigators hypothesize that personalizing rTMS targets using functional MRI will allow for improved symptoms of patients suffering from chronic catatonia.
Two dysfunctional networks or regions will be chosen (verum 1 and 2) based on their abnormal rCBF. In line with the symptoms, dorso-lateral prefrontal and premotor regions are expected to be chiefly concerned. A normal region regarding its rCBF will be used as a placebo. Targets will be stimulated using intermittent or continuous theta-burst according to the rCBF anomaly as an attempt to “normalize” their activity. The coil will be positioned using a robotic device under the control of a neuronavigation system to deliver a homogeneous stimulation. Using a balanced blinded randomized cross-over design, patients will be stimulated on 5 consecutive days (4 sessions per day) and evaluated pre-, post-stimulation, and 1 month after. In this pilot study, the primary outcome measures will be the clinical global impression scale, whereas MRI will ensure that stimulations achieve the correction of the rCBF anomalies. Secondary outcome measures will include personalized target symptom scales, and scales for catatonic, apathetic, and obsessive-compulsive symptoms.
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