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Chapter 28 Catatonia, Neuroleptic Malignant Syndrome, and Serotonin Syndrome
Terms in this set (56)
When is catatonia thought to be the result of general medical condition
when the disturbance does not occur during the course of delirium, the disturbance is not better accounted for by another mental disorder, and there is evidence from history, physical examination, or laboratory findings that the disturbance is the direct physiological consequence of a general medical condition.
How is communication in catatonic patients
catatonic patients make little effort to communicate.
Differential Diagnosis of catatonia
What is Malignant hyperthermia
occurs post-operatively reaction to inhalation anesthetics
communicate via vertical eye movements and blinking,
Non-convulsive status epilepticus may mimic catatonia,
Parkinson's disease is typically less
acute than that of catatonia.
What is the next step once diagnosis of catatonia has been established
Once the diagnosis of catatonia has been established, the differential diagnosis remains broad in terms of etiology; a thorough work-up should be pursued even after a diagnosis has been made.
Pathophysiology of catatonia
Clinical features (such as rigidity) suggest involvement of the frontal lobe-basal ganglia circuitry.
Specific neurochemical aberrations commonly associated with catatonia include: hypo-dopaminergic states;
GABA-ergic withdrawal; and serotonergic excess.
Evaluation of catatonia
History will often reveal clues to the existence of a pre-morbid psychotic disorder or an underlying medication trial or medical condition
amobarbital in relation to catatonia tx
interview (although rarely used in clinical practice)
Explain the Bush Francis Catatonia scale
23-item Bush-Francis Catatonia Rating Scale is also used to rate the severity of illness
- severity is rated on a scale of 0 to 69
Patients must have 2 of the first 14 items (on this scale) to qualify for a diagnosis of catatonia;
Indications for Malignant catatonia or NMS
Autonomic instability or an increased basal body temperature may also indicate malignant catatonia or NMS.
Studies for catatonia
An EEG is a valuable tool in the detection of an underlying seizure disorder.
Laboratory tests can illuminate clues to both catatonia and the risk factors for the development of NMS
An elevated creatinine phosphokinase (CPK) typically occurs in both malignant catatonia and NMS preventing subsequent renal failure from rhabdomyolysis.
Iron studies are also useful as patients with low iron levels may be predisposed to developing catatonia and to suffering a switch to malignant catatonia.
How is a definitive diagnosis of catatonia determined
definitive diagnosis of catatonia is facilitated by a rapid and dramatic response to an IV benzodiazepine trial.
Treatment of catatonia
1) Discontinuation of potential offending pharmacologic agents, particularly dopamine-blockers (such as neuroleptics or metoclopramide) that can cause or worsen catatonia, should be considered.
2) Consideration should also be given to restarting any dopaminergic agents (such as stimulants or amantadine), that were recently discontinued.
3) Benzodiazepines are generally considered as the initial treatment of choice for catatonia regardless of its cause; response rates are thought to be 60%-80% over the course of hours to days.
Patients will sometimes respond dramatically to an IV benzodiazepine challenge, fully resolving the catatonic state after a single dose.
Close monitoring is imperative, most patients will gradually relapse over the ensuing hours; repeat dosing, typically three times daily for several days, is often needed. Benzodiazepines used to treat catatonia should generally be held only for respiratory depression (and not sedation), as signs of catatonia are often mistaken for over-sedation.
Other medications reported as efficacious in the treatment of catatonia
Other medications reported as efficacious in the treatment of catatonia include zolpidem, valproic acid, memantine, and amantadine.
Second-line treatment for catatonia? When should it be considered?
ECT continues to be a powerful and effective treatment of catatonia it should be considered in cases that fail to respond to IV benzodiazepines or when other treatments for catatonia are contraindicated.
Frequently two to three ECT treatments will suffice, although four to six treatments are usually given to prevent relapse.
If hyperthermia, autonomic instability, or malignant catatonia emerge, treatment in an intensive care unit (ICU) may be indicated.
What is NMS
life-threatening, complication of neuroleptic therapy that confers high mortality if not treated in a prompt and skillful manner
What is malignant hyperthermia associated with
associated with general anesthesia during surgery
NMS as the development of severe muscle rigidity, an
elevated temperature in the setting of recent neuroleptic use, and two or more of the following:
diaphoresis, dysphagia, tremor, incontinence, changes in level of consciousness, mutism, tachycardia, elevated or labile blood pressure, leukocytosis, and laboratory evidence of muscle injury (an elevated CPK).
NMS Differential Diagnosis
Central nervous system (CNS) infections: prodromal viral illness and localizing neurological signs may help to distinguish NMS from a CNS infection
Cerebrospinal fluid (CSF) analysis and imaging studies may provide useful data as well.
Although muscle rigidity may lead to an elevation in CPK, EPS are not typically accompanied by fever, autonomic instability, elevation of the white blood
cell count, and other abnormal laboratory studies.
Malignant hyperthermia: administration of anesthesia and it is manifest by a characteristic histologic appearance of skeletal muscle fibers
Manifestations of anticholinergic excess lack diaphoresis. The diagnosis is further clarified by the administration of physostigmine, which will temporarily reverse signs and symptoms of anticholinergic excess.
Serotonin Syndrome Pathophysiology
mechanism thought responsible for NMS involves blockade of central dopamine receptors in the basal
ganglia, the hypothalamus, and peripherally in post-ganglionic sympathetic neurons and smooth muscle.
Which antipsychotics cause NMS?
How is NMS diagnosed?
All antipsychotics have been reported to induce NMS, although high-potency agents are thought to convey a greater risk than low-potency agents. Diagnosis of NMS is based on the clustering of signs and symptoms outlined above in the setting of a hypo-dopaminergic state
Findings that suggest NMS
In addition to leukocytosis and an elevated CPK, other findings suggestive of NMS include transaminitis, lactic acidosis, a low serum iron, and signs of myoglobinuric renal failure.
EEGs typical show diffuse slowing, while neuroimaging is non-specific.
What is the treatment for NMS
Any dopamine antagonists should be promptly discontinued and dopamine agonists resumed.
intensive hemodynamic monitoring and supportive care adequate IV hydration, active cooling, and close hemodynamic monitoring.
Electrolyte balance and renal function should be monitored closely, given the increased risk of renal failure associated with NMS.
Explain the use of Dantrolene and bromocriptine in NMS
Dantrolene may be helpful in reducing muscle rigidity, extreme temperature elevations, and hypermetabolism; however, it carries risks of
hepatotoxicity and respiratory failure. Bromocriptine is thought to be effective through its action as a central agonist at the D2 receptor, although it may potentially worsen any underlying psychosis.
Which treatments are beneficial for NMS
amantadine and benzodiazepines.
ECT has been used successfully in cases refractory to
pharmacologic treatment and it should be considered early in the course as a life-saving intervention. Six to 10 treatments are typically needed,
After NMS has resolved how should neuroleptic be re-instituted
Most investigators agree that re-institution of antipsychotics should be delayed at least two weeks after an episode of NMS has resolved, with lower potency neuroleptics preferentially used during a re-challenge.
What is the triad of serotonin syndrome
Serotonin syndrome is classically described as a triad of mental status changes, autonomic hyperactivity, and neuromuscular abnormalities that occurs in the setting of the use of serotonergic agents.
When does Serotonin syndrome most commonly occurs
Serotonin syndrome most commonly occurs in the setting of an interaction between a serotonergic agent and a monoamine oxidase inhibitor (MAOI).
What are symptoms of serotonin syndrome
Symptoms of serotonin syndrome include changes in mental status, restlessness, myoclonus, hyperreflexia, diaphoresis, shivering, and tremor.
How common is serotonin syndrome
The syndrome is thought to occur in up to 16% of patients who overdose on a SSRI.
thorough medication history is essential for the diagnosis of serotonin syndrome
What are the most common culprits of serotonin syndrome?
What other medications have serotonergic effects
Among psychiatric medications, SSRIs, tricyclic
antidepressants (TCAs), and MAOIs are the most common culprits, though other agents (such as lithium, valproate, atypical antipsychotics, trazodone, and buspirone) also have serotonergic effects
Which commonly prescribed medications have serotonin activity
meperidine, fentanyl, tramadol, ondansetron, sumatriptan, dextromethorphan, tryptophan, and linezolid.
What are the symptoms of serotonin syndrome
initially experience tremor, mild confusion, and incoordination;
these are followed by systemic signs (such as hyperreflexia, diaphoresis, shivering, and agitation).
Mydriasis is frequently seen and patients may develop
fever, clonus (typically more pronounced in the lower extremities), and diarrhea
How long does it take for serotonin syndrome to develop
These clinical features can develop from hours to days
after the initiation of serotonergic agents and may persist as long as the offending agents are continued.
Differential Diagnosis of serotonin syndrome
- Anticholinergic toxicity: With anticholinergic excess, patients usually have normal reflexes and hypoactive, rather than hyperactive, bowel sounds.
- Malignant hyperthermia: malignant hyperthermia severe muscle rigidity, hyporeflexia, and exposure to anesthetic agents help to distinguish this syndrome from serotonin syndrome.
- NMS With NMS, the signs and symptoms tend to evolve over several days, rather than a few hours, and patients are generally hypokinetic.
presumed mechanism of serotonin syndrome involves multiple families of serotonin receptors, although 5-HT2A receptor agonism appears to contribute to many of the symptoms.
5-HT1A receptors, predominating in the caudal brain stem and spinal cord may be responsible for some of serotonin syndrome's motoric symptoms.
Other studies (as in NMS) have implicated both dopamine and serotonergic activation in the syndrome's pathogenesis, arguing that agents with a
greater ratio of serotonergic to dopaminergic properties are most likely to precipitate the syndrome.
initiation of psychotropic agents.
Serotonin syndrome Treatment
1) Discontinuation of the serotonergic agents and institution of supportive treatment are the primary treatments, although use of 5-HT receptor antagonists may also play a role.
2) Once treatment is initiated the syndrome usually resolves within 24 hours; associated confusion can last for days. cooling blankets (for the development of hyperthermia), anticonvulsants (if seizures arise), and antihypertensive agents, such as nifedipine (for severely elevated blood pressure).
3) Benzodiazepines are commonly used in serotonin syndrome to treat agitation, to control hyperthermia, to reduce myoclonus, and to blunt the adrenergic response
4) Serotonin antagonists (such as cyproheptadine) may
have a role in more severe cases or when offending agents have long half-lives. Although case reports have highlighted the use of propranolol and dantrolene, they are not routinely recommended.
What is the most important physical finding in establishing serotonin diagnosis. Which other test should be ordered
Clonus, particularly of the spontaneous and ocular varieties, is the most important physical finding in establishing the diagnosis.
Laboratory testing is useful to assess screen for elevated CPK (raising suspicion of NMS) investigate the presence of an underlying medical condition
Of note, certain monoamine secreting tumors (e.g., carcinoid tumors, oat cell lung malignancies) have been associated with the serotonin syndrome, and gastrointestinal and lung imaging may help during the initial investigation
Serotonin Syndrome prevention
Prevention of serotonin syndrome often involves a washout period when cross-titrating a serotonergic agent with an MAOI.
Current treatment practices include a two-week (or 5 half-lives) wash-out interval following the discontinuation of a MAOI.
In the case of fluoxetine, a minimum of five-week wash-out period is required before the initiation a MAOI due to its long half-life.
What are the parts of the Bush francis that is being tested
1) Observe patient while trying to engage in a conversation (Activity level. Abnormal movements. Abnormal speech.)
2) Examiner scratches head in exaggerated manner (Echopraxia)
3) Examine arm for cogwheeling. Attempt to reposture, instructing patient to "keep your arm loose" - move arm with alternating lighter and heavier force.
(Negativism. Waxy flexibility. Gegenhalten. Rigidity.)
4) Ask patient to extend arm. Place one finger beneath hand and try to raise slowly after stating, "Do NOT let me raise your arm". (Mitgehen (passive obedience).)
5) Extend hand stating "Do NOT shake my hand". (Ambitendence)
6) Reach into pocket and state, "Stick out your tongue, I want to stick a pin in it". (Automatic obedience)
7) Check for grasp reflex. (Grasp reflex)
8) Check chart for reports of previous 24-hour period. In particular check for oral intake, vital signs, and any incidents.
9) Attempt to observe patient indirectly, at least for a brief period, each day.
What is catatonia
increased muscle tone at rest
what is waxy flexibility
sustatained abnormal position
What is the mechanism of action of Ambien (Zolpidem)
- GABA increases
- Works on GABA A receptor
- nonbenzo hypnotic
What is the mechanism of action of Depakote
- Blocks voltage gated Na channels and incr brain levels of GABA (antimanic effects)
- inhibit GABA degradative enzymes and inhibit re-uptake by neuronal cells
What does an organic work-up consist of
What is metoclopramide used for
Metoclopramide is a medication used mostly for stomach and esophageal problems. It is commonly used to treat nausea and vomiting, to help with emptying of the stomach in people with delayed stomach emptying due to either diabetes or following surgery, and to help with gastroesophageal reflux disease. It is also used to treat migraine headaches.
MOA of metoclopramide
It appears to bind to dopamine D2 receptors with nanomolar affinity (Ki 28.8 nM), where it is a receptor antagonist, and is also a mixed 5-HT3 receptor antagonist/5-HT4 receptor agonist.
The antiemetic action of metoclopramide is due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone in the central nervous system — this action prevents nausea and vomiting triggered by most stimuli. At higher doses, 5-HT3 antagonist activity may also contribute to the antiemetic effect.
The gastroprokinetic activity of metoclopramide is mediated by muscarinic activity, D2 receptor antagonist activity and 5-HT4 receptor agonist activity. The gastroprokinetic effect itself may also contribute to the antiemetic effect. Metoclopramide also increases the tone of the lower esophageal sphincter.
Diagnostic criteria for Catatonia
According to the DSM-V, "Catatonia Associated with Another Mental Disorder (Catatonia Specifier)" is diagnosed if the clinical picture is dominated by at least three of the following:
stupor (i.e., no psychomotor activity; not actively relating to environment)
catalepsy (i.e., passive induction of a posture held against gravity)
waxy flexibility (i.e., allow positioning by examiner and maintain position)
mutism (i.e., no, or very little, verbal response [exclude if known aphasia])
negativism (i.e., opposition or no response to instructions or external stimuli)
posturing (i.e., spontaneous and active maintenance of a posture against gravity)
mannerism (i.e., odd, circumstantial caricature of normal actions)
stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements)
agitation, not influenced by external stimuli
echolalia (i.e., mimicking another's speech)
echopraxia (i.e., mimicking another's movements)
Subtypes of catatonia
Stupor is a motionless, apathetic state in which one is oblivious or does not react to external stimuli. Motor activity is nearly non-existent. Individuals in this state make little or no eye contact with others and may be mute and rigid. One might remain in one position for a long period of time, and then go directly to another position immediately after the first position.
Catatonic excitement is a state of constant purposeless agitation and excitation. Individuals in this state are extremely hyperactive, although, as aforementioned, the activity seems to lack purpose. The individual may also experience delusions or hallucinations. It is commonly cited as one of the most dangerous mental states in psychiatry.
Malignant catatonia is an acute onset of excitement, fever, autonomic instability, delirium and may be fatal.
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