Catatonia


Catatonia

Description, Causes and Risk Factors:

A syndrome of psychomotor disturbances characterized by periods of physical rigidity, negativism, or stupor; may occur in schizophrenia, mood disorders, or organic mental disorders.

Catatonia

The exact cause of catatonia has not been elucidated, but a number of hypotheses have been offered. Catatonia may result by neurochemical abnormalities including low gamma-aminobutyric acid (GABA) activity in the frontal cortex, low dopamine (D2) activity in the basal ganglia, high glutamate—N-methyl-D-aspartate (NMDA) — activity in the parietal cortex, or a combination of these. Catatonic signs occur when these neurochemical changes cause aberrant signals and trigger a neural circuit affecting the medial gyrus of the orbital frontal lobe, the lateral gyrus, caudate nucleus, globus pallidus, and thalamus.

According to Northoff, a `top-down modulation' of basal ganglia due to deficiency of cortical gamma-aminobutyric acid (GABA), the primary inhibitory neurotransmitter of the brain, may explain the motor symptoms of catatonia. Similarly, hyperactivity of glutamate, the primary excitatory neurotransmitter, has also been suggested as an underlying neurochemical dysfunction.

Researchers also suggested that catatonia is caused by a sudden and massive blockade of dopamine. This may explain why dopamine-blocking antipsychotics are not generally beneficial in catatonia. Indeed, by exacerbating dopamine deficiency, antipsychotics may actually precipitate a worsening of the condition.

Medications that can induce catatonia include antipsychotics, corticosteroids at therapeutic doses. Drug abuse and withdrawal of benzodiazepine may also lead to catatonia in some cases.

In chronic catatonia with prominent speech abnormalities, positron emission tomography (PET) has identified abnormalities in metabolism bilaterally in the thalamus and frontal lobes.

A very interesting hypothesis proposed by Moskowitz suggests that catatonia may be understood as an evolutionary fear response, originating in ancestral encounters with carnivores whose predatory instincts were triggered by movement. This response, of remaining still, is now expressed in a range of major psychiatric or medical conditions, where catatonic stupor may represent a common `end-state' response to feelings of imminent doom.

Symptoms:

Patients suffering from this disorder either experience an extreme loss of motor skills or they exhibit hyper motor activity. Resistance to movement is observed in such patients. Symptoms also involve repetition of nonsensical phrases and imitating another person.

A few other symptoms are neglect of personal hygiene, lack of emotions, angry outbursts, trouble functioning at school or work, social isolation and clumsy, uncoordinated movements. This also includes a posture called waxy flexibility, which means that the person when placed by others in a specific position maintains that posture for a long time.

A particular condition is experienced by these patients, which is called the catatonic excitement. It pertains to persistent useless agitation. The individuals in this state become hyperactive, although the activity does not yield anything constructive.

Diagnosis:

A careful history and thoroughphysical examination and mental status examare essential for making anaccurate diagnosis and ruling out medical conditions that could present with or mimic catatonia.

Investigations for a patient presenting with catatonia may include:

First-line:

    Full blood count.

  • Renal function tests.

  • Liver function tests.

  • Thyroid function tests.

  • Blood glucose measurement.

  • Creatine phosphokinase (CPK) measurement.

  • Drug screen of urine.

Further investigations (depending on findings on physical examination):

    Magnetic resonance imaging.

  • Electroencephalography.

  • Electrocardiography.

  • Computed tomography.

  • Urine culture.

  • Blood culture.

  • Heavy-metal screen.

  • Auto-antibody screen.

  • Lumbar puncture.

  • Test for HIV.

Treatment:

Catatonia related to medical and psychiatric causes has been shown to respond to lorazepam and to ECT (electroconvulsive therapy). Lorazepam is preferred because of its specificity for the GABAa receptor and ease of administration. Other agents that act on GABA—including amobarbital and zolpidem—have also been used. Catatonia's hallmark features such as mutism and immobility have been shown to respond to lorazepam.

Antipsychotics have been investigated as a possible treatment for catatonia. The literature suggests that conventional antipsychotics may cause catatonia and atypical antipsychotics may improve it.

ECT is a first-line treatment for catatonia with life-threatening conditions and should be considered for refractory cases. Medical catatonias and neuroleptic malignant syndrome (NMS) have responded favorably to ECT.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.

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