reversible medical causes of catatonia. vital signs should be frequently monitored as catatonia can progress to malignant catatonia which is life-threatening. malignant catatonia is characterized by fever, hypertension, tachycardia, and tachypnea. rating scale various rating scales for catatonia have been developed, however, their utility for clinical care has not been well established. the most commonly used scale is the bush-francis catatonia rating scale (bfcrs) (external link is provided below). the scale is composed of 23 items with the first 14 items being used as the screening tool. if 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items. a diagnosis can be supported by the lorazepam challenge or the zolpidem challenge. while proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ect. differential diagnosis the differential diagnosis of catatonia is extensive as signs and symptoms of catatonia may overlap significantly with those of other conditions. therefore, a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. furthermore, some of these conditions can themselves lead to catatonia. the differential diagnosis is as follows: neuroleptic malignant syndrome (nms) and catatonia are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium. lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders further complicating the diagnosis. there are features of malignant catatonia (posturing, impulsivity, etc.) that are absent from nms and the lab results are not as consistent in malignant catatonia as they are in nms. some experts consider nms to be a drug-induced condition associated with antipsychotics, particularly, first generation antipsychotics, but it has not been established as a subtype. therefore, discontinuing antipsychotics and starting benzodiazepines is a treatment for this condition, and similarly it is helpful in catatonia as well. anti-nmda receptor encephalitis is an autoimmune disorder characterized by neuropsychiatric features and the presence of igg antibodies. the presentation of anti-nmdar encephalitis has been categorized into 5 phases: prodromal phase, psychotic phase, unresponsive phase, hyperkinetic phase, and recovery phase. the psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia. both serotonin syndrome and malignant catatonia may present with signs and symptoms of delirium, autonomic instability, hyperthermia, and rigidity. again, similar to the presentation in nsm. however, patients with serotonin syndrome have a history of ingestion of serotonergic drugs (ex: ssri). these patients will also present with hyperreflexia, myoclonus, nausea, vomiting, and diarrhea. malignant hyperthermia and malignant catatonia share features of autonomic instability, hyperthermia, and rigidity. however, malignant hyperthermia is a hereditary disorder of skeletal muscle that makes these patients susceptible to exposure to halogenated anesthetics and/or depolarizing muscle relaxants like succinylcholine. malignant hyperthermia most commonly occurs in the intraoperative or postoperative periods. other signs and symptoms of malignant hyperthermia include metabolic and respiratory acidosis, hyperkalemia, and cardiac arrhythmias. akinetic mutism is a neurological disorder characterized by a decrease in goal-directed behavior and motivation; however, the patient has an intact level of consciousness. patients may present with apathy, and may seem indifferent to pain, hunger, or thirst. akinetic mutism has been associated with structural damage in a variety of brain areas. akinetic mutism and catatonia may both manifest with immobility, mutism, and waxy flexibility. differentiating both disorders is the fact that akinetic mutism does not present with echolalia, echopraxia, or posturing. furthermore, it is not responsive to benzodiazepines as is the case for catatonia. elective mutism has an anxious etiology but has also been associated with personality disorders. patients with this disorder fail to speak with some individuals but will speak with others. likewise, they may refuse to speak in certain situations; for example, a child who refuses to speak at school but is conversational at home. this disorder is distinguished from catatonia by the absence of any other signs/symptoms. nonconvulsive status epilepticus is seizure activity with no accompanying tonic-clonic movements. it can present with stupor, similar to catatonia, and they both respond to benzodiazepines. nonconvulsive status epilepticus is diagnosed by the presence of seizure activity seen on electroencephalogram (eeg). catatonia on the other hand, is associated with normal eeg or diffuse slowing. delirium is characterized by fluctuating disturbed perception and consciousness in the ill individual. it has hypoactive and hyperactive or mixed forms. people with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation, and aggression. those with hypoactive delirium present with similarly to retarded catatonia, withdrawn and quiet. however, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines. patients with locked-in syndrome present with immobility and mutism; however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking. furthermore, locked-in syndrome is caused by damage to the brainstem. stiff-person syndrome and catatonia are similar in that they may both present with rigidity, autonomic instability and a positive response to benzodiazepines. however, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-gad) antibodies and other catatonic signs such as mutism and posturing are not part of the syndrome. untreated late-stage parkinson's disease may present similarly to retarded catatonia with symptoms of immobility, rigidity, and difficulty speaking. further complicating the diagnosis is the fact that many patients with parkinson's disease will have major depressive disorder, which may be the underlying cause of catatonia. parkinson's disease can be distinguished from catatonia by a positive response to levodopa. catatonia on the other hand will show a positive response to benzodiazepines. extrapyramidal side effects of antipsychotic medication, especially dystonia and akathisia, can be difficult to distinguish from catatonic symptoms, or may confound them in the psychiatric setting. extrapyramidal motor disorders usually do not involve social symptoms like negativism, while individuals with catatonic excitement typically do not have the physically painful compulsion to move that is seen in akathisia. certain stimming behaviors and stress responses in individuals with autism spectrum disorders can present similarly to catatonia. in autism spectrum disorders, chronic catatonia is distinguished by a lasting deterioration of adaptive skills from the background of pre-existing autistic symptomatology that cannot be easily explained. acute catatonia is usually clearly distinguishable from autistic symptoms. the diagnostic entities of obsessional slowness and psychogenic parkinsonism show overlapping features with catatonia, such as motor slowness, gegenhalten (oppositional paratonia), mannerisms, and reduced or absent speech. however, psychogenic parkinsonism involves tremor which is unusual in catatonia. obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of obsessive compulsive disorder to catatonia. treatment the initial treatment of catatonia is to stop medication that could be potentially leading to the syndrome. these may include steroids, stimulants, anticonvulsants, neuroleptics, dopamine blockers, etc. the next step is to provide a "lorazepam challenge," in which patients are given 2 mg of iv lorazepam (or another benzodiazepine). most patients with catatonia will respond significantly to this within the first 15–30 minutes. if no change is observed during the first dose, then a second dose is given and the patient is re-examined. if the patient responds to the lorazepam challenge, then lorazepam can be scheduled at interval doses until the catatonia resolves. the lorazepam must be tapered slowly, otherwise, the catatonia symptoms may return. the underlying cause of the catatonia should also be treated during this time. if within a week the catatonia is not resolved, then ect can be used to reverse the symptoms. ect in combination with benzodiazepines is used to treat malignant catatonia. in france, zolpidem has also been used in diagnosis, and response may occur within the same time period. ultimately the underlying cause needs to be treated. electroconvulsive therapy (ect) is an effective treatment for catatonia that is well acknowledged. ect has also shown favorable outcomes in patients with chronic catatonia. however, it has been pointed out that further high quality randomized controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ect in catatonia. antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic. there is evidence clozapine works better than other antipsychotics to treat catatonia, following a recent systematic review. excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, nmda antagonists such as amantadine or memantine may be used. amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of ampa receptors. prognosis patients who experience an episode of catatonia are more likely to recur. treatment response for patients with catatonia is 50–70% and these patients have a good prognosis. however, failure to respond to medication is a very poor prognosis. many of these patients will require long-term and continuous mental health care. for patients with catatonia with underlying schizophrenia, the prognosis is much poorer. epidemiology catatonia has been mostly studied in acutely ill psychiatric patients. catatonia frequently goes unrecognized, leading to the belief that the syndrome is rare; however, this is not true and prevalence has been reported to be as high as 10% in patients with acute psychiatric illnesses. one large population estimate has suggested that the incidence of catatonia is 10.6 episodes per 100 000 person-years. it occurs in males and females in approximately equal numbers. 21-46% of all catatonia cases can be attributed to a general medical condition. history reports of stupor-like and catatonia-like states abound in the history of psychiatry. after the middle of the 19th century there was an increase of interest in the motor disorders accompanying madness, culminating in the publication by karl ludwig kahlbaum in 1874 of die katatonie oder das spannungsirresein (catatonia or tension insanity).