Catatonia and neuroleptic malignant syndrome

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Catatonia and neuroleptic malignant syndrome

  1. 1. D R S A L M A N K A R E E M J U N I O R R E S I D E N T D E P A R T M E N T O F P S Y C H I A T R Y Catatonia and Neuroleptic Malignant Syndrome
  2. 2.  Catatonia is a state of apparent unresponsiveness to external stimuli in a person who is apparently awake, manifested by stupor.  First described by Kahlbaum (1874).
  3. 3. Diagnostic Criteria  The ICD–10 diagnosis of catatonic schizophrenia (category F20.2) requires that the patient prominently exhibits at least one of the following catatonic features, for at least 2 weeks: stupor, excitement, posturing, negativism, rigidity, waxy flexibility and command automatism (automatic obedience).  If a patient with severe depression is in a stupor, a diagnosis of ‘severe depressive episode with psychotic symptoms’ (F32.3) is made, even if there are no delusions or hallucinations.  Similarly, a patient with manic stupor will be diagnosed as having ‘mania with psychotic symptoms’ (F30.2).  Catatonia due to physical causes is diagnosed as ‘organic catatonic disorder.
  4. 4.  In DSM–IV a diagnosis of ‘schizophrenia, catatonic type’ (code 295.20) is made if the clinical picture is dominated by at least two of the following: motor immobility, excessive motor activity, extreme negativism, peculiarities of voluntary movements, and echolalia/echopraxia.  If a physical cause is identified the diagnosis is ‘catatonic disorder due to a medical condition’ (code 293.89).
  5. 5. Mechanism of Action  Deficits in fetal cortical development  Developmental disorders  Dopaminergic blockade - catatonia is caused by a sudden and massive blockade of dopamine. Antipsychotics may actually precipitate a worsening of the condition.  Glutamatergic dysfunction - hyperactivity of glutamate, the primary excitatory neurotransmitter, has also been suggested as an underlying neurochemical dysfunction.  Clozapine-withdrawal catatonia is postulated to be due to cholinergic and serotonergic rebound hyperactivity.
  6. 6. Psychiatric condition  Acute stress disorder  Anorexia nervosa  Autistic disorder  Brief reactive psychosis with catatonia  Conversion disorder  Hysteria  Major depression, single episode with catatonic features  Mood disorders  Neuroleptic malignant syndrome  Posttraumatic stress disorder  Schizophrenia  Substance intoxication (3,4-methylenedioxymethamphetamine [ie, "ecstasy"], alcohol, amphetamine, phencyclidine, substance withdrawal, hypnotic-sedative, lorazepam
  7. 7. Neurologic conditons  Administration of agents that block postsynaptic dopamine receptors  Administration of sibutramine.  Akinetic-rigid syndrome  Arachnoid cyst in right parietal region  Astrocytoma  Atrophy of left amygdala  Autistic disorder  Basilar artery thrombosis  Bilateral hemorrhagic lesions of temporal lobes  Cerebellar catalepsy  Cerebral hemorrhage  Cerebral infarct  Cerebrovascular disease  Cortical venous thrombosis  Central pontine myelinolysis  Cortical basal ganglionic degeneration  Dystonia  Encephalitis (herpes, Trypanosoma
  8. 8.  Encephalopathy (Borrelia burgdorferi, human immunodeficiency virus [HIV] infection, Wernicke encephalopathy)  Familial fatal insomnia  Fibromuscular dysplasia with dissection of basilar artery  Frontal lobotomy  Head injury  Huntington disease  Hydrocephalus  Hypopituitarism secondary to postpartum hemorrhage  Idiopathic recurring stupor  Inherited neurometabolic disorders  Locked-in syndrome  Meningitis, tuberculous  Meningoencephalitis  Multiple sclerosis  Neurosyphilis  Nonconvulsive status epilepticus  Pervasive developmental disorders  Pallidoluysian atrophy  Paraneoplastic encephalitis  Parkinsonism  Postencephalitic parkinsonism
  9. 9.  Progressive multifocal leukoencephalopathy  Progressive supranuclear palsy  Schizencephaly  Seizures (complex with partial symptomatology)  Stiff-man syndrome  Stroke  Stupor  Subarachnoid hemorrhage  Subdural hematoma  Substance intoxication (alcohol, disulfiram, organic fluorides, phencyclidine)  Subthalamic mesencephalic tumor  Surgical removal of cerebellar tumor  Tay-Sachs disease  Temporal lobe epilepsy  Tuberous sclerosis  Tumors  Vegetative state  Wilson disease
  10. 10. Clinical presentation  typically episodic, with periods of remission  presence of a variety of behavioral and motoric traits – almost 2 dozen.  Mutism  Negativism  Echopraxia  Echolalia  Waxy flexibility  Withdrawal
  11. 11.  Excited state –  people with catatonia may injure themselves and assault others.  autonomic instability manifested by hyperthermia, tachycardia, and hypertension  Exhaustion  Immobile state  Akinesia and stupor  patient may appear unresponsive to external stimuli.  unable to eat  may exhibit catalepsy, the persistent maintenance of spontaneous or imposed postures.
  12. 12.  Posturing  The patient is able to maintain the same posture for long periods. An extreme version of posturing is catalepsy.  Waxy flexibility (cerea flexibilitas)  The examiner is able to position the patient in what would be highly uncomfortable postures, which are maintained for a considerable period of time.
  13. 13. Negativistic Phenomena  Gegenhalten  Rigidity  demonstrate increasing resistance to passive movement of the limbs  Automatic obedience (Mitgehen)  patient moving in the direction of a slight push from the examiner in spite of the command to remain still  Motor persistence  The patient persists with a particular movement that has lost its initial relevance.  withdrawal from all usual activities and refusal to eat.
  14. 14.  Stereotypies - patient repetitively performs apparently meaningless activities. Common motor stereotypes include the following:  Nose wrinkling  Repetitive movements of the mouth and the jaw  Repetitive eye movements  Repetitive tapping of the foot, the finger, or the hand  Repetitive abdomen patting, shoulder shrugging, or body rockin
  15. 15.  Preservation  Ambitendency  The patient alternates between resistance to and cooperation with the examiner’s instructions; for example, when asked to shake hands, the patient repeatedly extends and withdraws the hand.  Echophenomena  Echolalia - Echolalia refers to the repetition of the examiner’s words.  Echopraxia - The patient imitates the actions of the interviewer.
  16. 16.  comprehensive physical examination  specific emphasis on neurological signs, and a thorough mental state examination, with special emphasis on identifying catatonic signs  history of similar episodes of catatonia is important to elicit. Determine whether the precipitating events of the earlier episode are present in the current episode
  17. 17.  emergency physician must quickly consider the presence of neuroleptic malignant syndrome,encephalitis, nonconvulsive status epilepticus, and acute psychosis.  must identify comorbid disorders, including schizophrenia, mood disorders, psychological stressors, medical conditions.  Catatonia and the related condition, neuroleptic malignant syndrome, may follow the administration of neuroleptic medications
  18. 18. Work up  Complete blood counts (CBC)s, electrolytes, and chemical analyses of blood.  Fibrin D-dimer greater than 500 ng/mL.  serum creatine kinase level and WBC count and perform liver function tests, to rule out neuroleptic malignant syndrome.  Serum ceruloplasmin.  magnetic resonance imaging (MRI) or computed tomography (CT) scanning is indicated to rule out treatable mass lesion.  EEG is indicated to rule out a seizure disorder.
  19. 19. Further investigations (depending on findings on physical examination)  Electroencephalography  Urine culture  Blood culture  Test for syphilis  Test for HIV  Heavy-metal screen  Auto-antibody screen  Lumbar puncture
  20. 20. Differential diagnoses of catatonia  Schizophrenia  Depression  Mania  Organic disorders: e.g. infections, epilepsy, metabolic disorders  Drugs: prescribed or recreational  Hysteria (psychogenic catatonia)  Idiopathic
  21. 21. Treatment and management  Due to risk of serious complications of catatonia, admission to an intensive care unit is the treatment of choice for a patient with catatonia.  Benzodiazepines are the drugs of choice for catatonia.  unresponsive or in-sufficiently responsive to benzodiazepines need electroconvulsive therapy (ECT) - functional psychiatric disorders (including schizophrenia) or organic causes.  Antipsychotics are generally not recommended during a catatonic phase even if there is an underlying psychotic illness such as schizophrenia, as the risk of precipitating neuroleptic malignant syndrome is considerably increased.
  22. 22.  carbamazepine is effective in both the acute and maintenance phases of catatonia.  Combination of lithium and an antipsychotic may be an option in treatment-resistant catatonic stupor  NMDA antagonists: amantadine and memantine  Dopamine agonists (e.g. bromocriptine) and skeletal muscle relaxants (e.g. dantrolene), especially if neuroleptic malignant syndrome is suspected
  23. 23. other treatment  refusal to eat requires parenteral nutrition.  Vitamin K deficiency must be identified and treated in people with catatonia.  Autonomic instability requires intravenous fluids and monitoring of vital signs.
  24. 24.  life-threatening neurological disorder .  mortality rate is 10-20%  adverse reaction to neuroleptic or antipsychotic drugs.  haloperidol or chlorpromazine have the greatest risk.
  25. 25. Clinical presentation  Hyperthermia  Diaphoresis , tachycardia , elevated or labile blood pressure  Dysphagia , incontinence  Tremor  Changes in the level of consciousness , ranging from confusion to coma  Mutism  Leukocytosis  Lab evidence of muscle injury  Liver enzyme elevation
  26. 26. pathophysiology Mechanism of action  Dopamine receptor blockade  Genetically reduced function of dopamine receptor D2.  Release of calcium is increased from the sarcoplasmic reticulum with antipsychotic usage. This can result in increased muscle contractility, which can play a role in breakdown of muscle, muscle rigidity, and hyperthermia.  sympatho-adrenal hyperactivity (results from removing tonic inhibition from the sympathetic nervous system)
  27. 27. treatment options and implications  Aggressive use of supportive measures as well as specific interventions.  discontinue all antipsychotics  Patients should receive circulatory and ventilatory support as needed.  Cooling blankets and antipyretics can be used to control temperature  Aggressive fluid resuscitation and alkalization of urine can help prevent acute renal failure and enhance excretion of muscle breakdown products
  28. 28. Lab findings Increased LDH Increased CK Increased AST Increased ALT Increased alkaline phosphatase Hyperuricemia Hyperphosphatemia Myoglobinemia Leukocytosis Thrombocytosis Proteinuria Decreased serum iron Increased cerebrospinal fluid (CSF) protein Hypocalcemia Myoglobinuria
  29. 29. medications  Dantrolene has been used when needed to reduce muscle rigidity  dopamine pathway medications such as bromocriptine.  Benzodiazepines may be used to control agitation.  Amantadine  Levodopa/ carbidopa  ECT.
  30. 30. complications  potential complications of neuroleptic malignant syndrome includes the following:  Rhabdomyolysis  Renal failure  Cardiac arrest  Infection  Aspiration  Respiratory failure  Seizure  Pulmonary embolism  Hepatic failure  Uncontrolled psychoses

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