Muscular rigidity, unusual posturing, negativism, mutism, echolalia, echopraxia, and stereotyped mannerisms—the signs of catatonia—can appear suddenly and immobilize the patient. When the disorder is transient, it may be disregarded, but when it persists, it dominates the patient's mental state and behaviour, threatening his or her life. The patient undergoes forced feeding and develops bedsores, muscular atrophy, and limitations in limb movement caused by prolonged immobility.
Infections occur subsequent to repeated bladder catheterization, and embolization follows from blood clots in immobilized limbs.
Catatonia is recognized in patients with affective illnesses, both depression and mania, in patients with systemic disorders, and in those with toxic brain states caused by hallucinogenic drugs. One present North American view is that catatonia is a syndrome with multiple causes and not a specific psychopathological disorder. (31) This view contrasts with the traditional European view of catatonia as a specific subtype of dementia praecox described by Kraepelin. This view was adopted by Bleuler, Gjessing, Kleist, and Leonhard, and is represented today in the writings of Beckmann. For decades, the prevailing belief in psychiatry was that each instance of catatonia represented a subtype of schizophrenia. The major classification systems in psychiatry (DSM-III, DSM-IIIR, ICD-9 and ICD-10) assigned to all patients with catatonia the diagnosis of schizophrenia, catatonic type. As a consequence, few of these patients were treated with sedatives or ECT, despite their efficacy, because neither was recommended for schizophrenia/32) This short-sighted view was somewhat corrected in the 1994 classification system of the American Psychiatric Association (DSM-IV), which recognized catatonia as secondary to systemic illness in the class of 'Catatonic disorder due to (indicate the general medical condition) [293.89]'.
Catatonia, defined by two or more characteristic motor signs in a patient with a mental disorder, appears in many guises. (33) Prominent examples are pernicious catatonia or malignant catatonia, with a high risk of death, and the neuroleptic malignant syndrome, which may follow the administration of neuroleptic drugs. (34> The disorder may be transitory or may persist for months or years. It responds to sedation with barbiturates or benzodiazepines, and amobarbital was frequently called on until the merits of diazepam and lorazepam became known. If these medications fail, catatonia can be quickly relieved by ECT, which remarkably can almost always cure within three treatments.
This toxic response to neuroleptic drugs, evinced by fever, motor rigidity, negativism, mutism, and cardiovascular and respiratory instability, is indistinguishable from catatonia, except that a specific precipitant is defined. Cases have been observed in association with almost all neuroleptics, most commonly with the high-potency types such as haloperidol, fluphenazine, and thiothixene, but it is also caused by atypical ones. Like catatonia, neuroleptic malignant syndrome is responsive to ECT.
Whether neuroleptic malignant syndrome is the consequence of an excessive reduction in the amount of brain dopamine or whether it is a type of catatonia is still undetermined. Those who believe it to be a specific disorder in dopamine activity try to increase brain dopamine by prescribing bromocriptine or L-dopa and to relieve muscular rigidity and fever by using the muscle relaxant dantrolene.(35) Neither of these treatments has proved effective.
The motor rigidity and tremors associated with Parkinson's disease are symptoms of other conditions as well, such as the cerebrovascular changes in the elderly, the effects of infections, and following the extended use of neuroleptic drugs. Depressed patients are often slow and hesitant in movement, rigid in posture, and tremulous. When they are treated for depression with ECT, both their motor irregularities and depressed mood are relieved. (36) To distinguish ECT's effects on rigidity from its effects on mood, Swedish scientists studied hospitalized patients suffering from a severe form of parkinsonism who were not depressed. Using real and sham ECT, they found that real ECT relieved the rigidity but not the tremor.(37,3 and 39) ECT is now an accepted treatment for parkinsonism marked by severe rigidity, whether or not a mood disorder is also evident.(40)
threshold despite repeated seizures, and the failure of the usual biochemical inhibitory mechanisms to terminate an isolated seizure. (43) The administration of ever larger doses of anticonvulsant medications, proceeding from lorazepam to phenytoin, phenobarbitone (phenobarbital), and to general anaesthesia with midazolam or barbiturates, can help. But ECT is an alternative.(44)
The seizures in status epilepticus are not robust; they do not stimulate the inhibitory mechanisms required to terminate seizures. An example of the strength of a seizure can be judged by the immediate rise in serum prolactin after a sustained epileptic seizure. Within an hour after a seizure, the level of serum prolactin will indicate whether the seizure is epilepsy or a pseudoseizure. In status epilepticus, as in pseudoseizures, prolactin levels do not rise; indeed, they remain normal. This suggests that the seizures are partial or incomplete; i.e. they have failed to stimulate an inhibitory termination process. But even in patients in status epilepticus, ECT elicits maximal seizures, making it a reasonable alternative to general anaesthesia as a treatment for intractable seizures.
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