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Subcortical dysrhythmia and catatonia
BIOL PSYCHIATRY 1986;21:1351-1355
1351
CORRESPONDENCE Letters of 600 words or less, with minimal allowance for tables, jigures, and references, will be considered for publication. Rules regarding prior publication, conflict of interest, etc.) are the same as for full manuscripts. All letters are subject to editing and condensation. Proofs will not be distributed.
Subcortical
Dysrhythmia
and Catatonia
To the Editor: Several authors have recently documented the striking response of catatonia, whether neurolepticinduced or grounded in a psychiatric disorder, to parenteral benzodiazepines (Fricchione et al. 1983; Lew and Tollefson 1983; McEvoy and Lohr 1984; WalterRyan 1985). Why benzodiazepines should so promptly dissolve catatonia remains unclear. Although Fricchione et al. (1983) have suggested that their anxiolytic or muscle relaxant properties might be responsible, more recently, Fricchione (1985) has focused on their possible effect on extrapyramidal dopamine-GABA feedback loops. I would like to supplement his neurochemical hypothesis with an electrophysiological one, namely, that benzodiazepines may be cataleptolytic by virtue of their anticonvulsant properties. Three kinds of evidence suggest that catatonia may be the behavioral expression of a cerebral dysrhythmia of a continuous, rather than ictal, nature. First, the three most efficient means of rapidly dissolving catatonic stupor [benzodiazepines, sodium amytal (Bleckwenn 1931), and electroconvulsive therapy (ECT)] share the common property of being anticonvulsants (for ECT as anticonvulsant, cf., Post et al. 1981). Second, anticonvulsants have acquired increasing prominence in the treatment of bipolar disorder-the illness now believed to provide the chief context for spontaneous catatonia (Ries 1985). Third, nonictal central discharges resonating continuously in a circuit, including internal globus pallidus, VM thalamus, and elsewhere, have been considered the driving agents of tremor and possibly rigidity in parkinsonism (e.g., Alberts 1972; Lamarre and Joffroy 1979), a syndrome with close affiliations to catatonia. On phenomenological grounds, several early clinicians argued for the close similarity between spontaneous catatonics and postencephalitic parkinsonians (e.g., Naville 1922), whereas more recently, on pathophysiological grounds, neuroleptic-induced catatonia, insofar as it results from massive dopamin-
ergic blockade in striatum and elsewhere (Caroff 1980), has been approximated to parkinsonism. As the akinetic-rigid syndrome termed catatonia thus resembles on phenomenological as well as pathophysiological grounds that termed parkinsonism, one wonders whether the central discharges documented in parkinsonism may also subserve catatonic states, and whether interruption of such subcortical discharges may explain the striking response of catatonic states to certain anticonvulsants. Note that the subcortical discharges documented in parkinsonism are emphatically not ictal, but rather are a species of self-perpetuating tonic oscillation, which does not imply a single abnormal focus (Lamarre and Joffroy 1979) and which requires computer enhancement to be detected on electroencephalograms (EEGs) (Alberts 1969) [EEG tracings in catatonia proper, while generally free of ictal features (e.g., Gjessing et al. 1967), have not been evaluated for nonictal waveforms in this manner]. Such polysynaptic hyperresonant states might lend themselves to interruption by agents which, like benzodiazepines, function as anticonvulsants, not by calming an irritable focus but rather by preventing its propagation (Browne and Penry 1973). It may be significant that the benzodiazepine-responsive members of the akinetic-rigid family may be distinguished from the nonresponsive ones not on the basis of an a priori distinction between psychiatric and organic states (as one might expect if benzodiazepines lysed catatonia simply by virtue of being anxiolytic), but rather according to acuteness of onset: those of acute onset [whether resulting from neuroleptics, carbon monoxide (Caruso and Barnaba 1968), or psychiatric disease] respond most dramatically, whereas idiopathic Parkinson’s disease does not [although it is ameliorated by ECT (e.g., Young et al. 1985), it may, in some cases, be worsened by oral benzodiazepines (Yosselson-Superstine and Lipman 1982)]. Other resemblances among the acute-onset akinetic-rigid states [which whether psychiatric or organic tend to occur in a young population (Kraepelin 1919; Stoudemire
t im-capondeni I
and Luther 198-k)and to fcaturc rigidity zmc trcmorcl. as opposed to the \low-onset condition of paralysi\ agitans (which generally occurx in an older population and features rigidity with tremor). huggeht that thih distinction may ultimately prove to he of greatct pathophysiological significance than that between psychiatric and organic illness. Although the relationships among different members of the akinetic-rigid family. including the syndromes termed catatonia and parkinsonism. remain unsettled. and although other anticonvulsants apart from those mentioned here have not heen tried in catatonia. the rationale for the dramatic response of some acute-onset catatonic--parkinsonian conditions to certain anticonvulsants would seem to merit further investigation.
I-kxhonc
CiL. C’auem
NH. Hoobcrman
DH. et ;LI c‘t
1IW3): IV lorazcpam in ncurolcptic-induced tatonia. .I c‘li,~ /‘.s~c,ho~phtrrrncc(.o/
3:338-342,
GJebsmg LR. Harding GFA. Jcnner I$ ct al (lY671The EEG in three cases of pcnodic catatoniu. HV ./ Psvchitrf~\~ I 13: 137 I-- /7X2. Kraepelin t: ( 19lY): Dementia praecox and paraphrenia. Translated by KM Barclay. Facsimile I9 IO edition, Huntington, NY: Robert E. Kreiger. 1971. p 153. Lamarre Y. Joffroy AJ ( I Y7Y1: Experimental tremors m monkey: Activity of thalamic and precentral cortical neurons in the absence of peripheral feedback. In Poirier LJ, Sourkes TL. Bcdard PJ (cds). .-\tl~xmc~r.s irzNeurology. vol 24. New York: Raven Press. pp lO9--122.
Department of Psychiatry Dartmouth Medical School Hanover. NH 03756
Lew I-Y. ‘follefson G ( 1983): Chlorpromazine Induced neuroleptic malignant syndrome and its rcsponsc lo diazepam. Bid P.syhi+ IX: 1441-1446.
References
McEvoy JP, Lohr JB (1984): Diazepam for catatonia. .4rn .I Psychiatry I4 I :284-285.
Alberts WW (1969): Parkinsonian tremor and cerebral potentials. In Gillingham FJ, Donaldson IML (eds). Third Symposium on Purkinsvn’s Disease. Edinburgh: Livingstone, pp 146-149. Alberts WW (1972): A simple view of Parkinsonian tremor. Electrical stimulation of cortex adjacent to the rolandic fissure in awake man. Rrclin Res 441357-369.
Bleckwenn WJ ( I93 I ): The use of sodium amytal in catatonia. In Schizophrmiu (Research Publications of Association for Research in Nervous and Mental Disease. vol IO). Baltimore: Williams & Wilkins, pp 224-229. Brownc TR. Penry JK (1973): Benzodiazepines in the treatment of epilepsy: A review. Epilepsicr l4:237-3 IO. Caroff SN (1980): The neuroleptic malignant drome. J Clin P.~~c#ziat~ 41:79-83.
syn-
Caruso G. Barnaba A ( 1968): Treatment with diazepam and remission of the extrapyramidal symptoms in a case of parkinsonism caused by carbon monoxide poisoning. Actcr Neurd (Napoli) 23:103-l 10. Fricchione GL ( 1985): Neuroleptic catatonia and its relation to psychogenic catatonia. Bid Pswhiar~v 20: 304-3
I 3.
Navillc F (1’322): Etudes sur Its complications et ICS scqucllcs mcntales de I’encephalite epidemiquc Enwph& 171369-375. 323436. Post RM. Putnam FW. Contel NR (1981): Electroconvulsive shock inhibits amygdala kindling. Sot ~Yrur~osc~i A&r 7:587 Reiter PJ ( 1926): Extrapyramidal m dementia praccox. Acre I X7-3 IO.
motor disturbances Pswhiutr
Neuroi
Rica RK (19X5): DSM-III implications of the diagnose\ of catatonia and bipolar disorder. Am J PSI dzicrtry 142:1471-1474. Stoudcmire A. L,uther JS (1984): Ncuroleptic malignant syndrome and neuroleptic-induced catatonia. Differential diagnosis and treatment. ltzt J PSL drrtrtr Mrtl 14157-h3. Walter-Ryan WG (lY85): Treatment for catatomc symptoms with intramuscular lorazepam. J C/i/r I’s\‘c~hophartnuc.oi 5: 123-l 24. Yosselson-Superstine S. Lipman AG ( 1982): Chlordiazepoxide interaction with levodopa. Ann Inrertr Mrtl 96:259--260. Young KC. Alexopoulos GS. Shamoian CA (1985 ): Dissociation of motor response from mood and cognition in a parkinsonian patient treated with ECT Biol P.sychicrtn 20:566-569.
1351
CORRESPONDENCE Letters of 600 words or less, with minimal allowance for tables, jigures, and references, will be considered for publication. Rules regarding prior publication, conflict of interest, etc.) are the same as for full manuscripts. All letters are subject to editing and condensation. Proofs will not be distributed.
Subcortical
Dysrhythmia
and Catatonia
To the Editor: Several authors have recently documented the striking response of catatonia, whether neurolepticinduced or grounded in a psychiatric disorder, to parenteral benzodiazepines (Fricchione et al. 1983; Lew and Tollefson 1983; McEvoy and Lohr 1984; WalterRyan 1985). Why benzodiazepines should so promptly dissolve catatonia remains unclear. Although Fricchione et al. (1983) have suggested that their anxiolytic or muscle relaxant properties might be responsible, more recently, Fricchione (1985) has focused on their possible effect on extrapyramidal dopamine-GABA feedback loops. I would like to supplement his neurochemical hypothesis with an electrophysiological one, namely, that benzodiazepines may be cataleptolytic by virtue of their anticonvulsant properties. Three kinds of evidence suggest that catatonia may be the behavioral expression of a cerebral dysrhythmia of a continuous, rather than ictal, nature. First, the three most efficient means of rapidly dissolving catatonic stupor [benzodiazepines, sodium amytal (Bleckwenn 1931), and electroconvulsive therapy (ECT)] share the common property of being anticonvulsants (for ECT as anticonvulsant, cf., Post et al. 1981). Second, anticonvulsants have acquired increasing prominence in the treatment of bipolar disorder-the illness now believed to provide the chief context for spontaneous catatonia (Ries 1985). Third, nonictal central discharges resonating continuously in a circuit, including internal globus pallidus, VM thalamus, and elsewhere, have been considered the driving agents of tremor and possibly rigidity in parkinsonism (e.g., Alberts 1972; Lamarre and Joffroy 1979), a syndrome with close affiliations to catatonia. On phenomenological grounds, several early clinicians argued for the close similarity between spontaneous catatonics and postencephalitic parkinsonians (e.g., Naville 1922), whereas more recently, on pathophysiological grounds, neuroleptic-induced catatonia, insofar as it results from massive dopamin-
ergic blockade in striatum and elsewhere (Caroff 1980), has been approximated to parkinsonism. As the akinetic-rigid syndrome termed catatonia thus resembles on phenomenological as well as pathophysiological grounds that termed parkinsonism, one wonders whether the central discharges documented in parkinsonism may also subserve catatonic states, and whether interruption of such subcortical discharges may explain the striking response of catatonic states to certain anticonvulsants. Note that the subcortical discharges documented in parkinsonism are emphatically not ictal, but rather are a species of self-perpetuating tonic oscillation, which does not imply a single abnormal focus (Lamarre and Joffroy 1979) and which requires computer enhancement to be detected on electroencephalograms (EEGs) (Alberts 1969) [EEG tracings in catatonia proper, while generally free of ictal features (e.g., Gjessing et al. 1967), have not been evaluated for nonictal waveforms in this manner]. Such polysynaptic hyperresonant states might lend themselves to interruption by agents which, like benzodiazepines, function as anticonvulsants, not by calming an irritable focus but rather by preventing its propagation (Browne and Penry 1973). It may be significant that the benzodiazepine-responsive members of the akinetic-rigid family may be distinguished from the nonresponsive ones not on the basis of an a priori distinction between psychiatric and organic states (as one might expect if benzodiazepines lysed catatonia simply by virtue of being anxiolytic), but rather according to acuteness of onset: those of acute onset [whether resulting from neuroleptics, carbon monoxide (Caruso and Barnaba 1968), or psychiatric disease] respond most dramatically, whereas idiopathic Parkinson’s disease does not [although it is ameliorated by ECT (e.g., Young et al. 1985), it may, in some cases, be worsened by oral benzodiazepines (Yosselson-Superstine and Lipman 1982)]. Other resemblances among the acute-onset akinetic-rigid states [which whether psychiatric or organic tend to occur in a young population (Kraepelin 1919; Stoudemire
t im-capondeni I
and Luther 198-k)and to fcaturc rigidity zmc trcmorcl. as opposed to the \low-onset condition of paralysi\ agitans (which generally occurx in an older population and features rigidity with tremor). huggeht that thih distinction may ultimately prove to he of greatct pathophysiological significance than that between psychiatric and organic illness. Although the relationships among different members of the akinetic-rigid family. including the syndromes termed catatonia and parkinsonism. remain unsettled. and although other anticonvulsants apart from those mentioned here have not heen tried in catatonia. the rationale for the dramatic response of some acute-onset catatonic--parkinsonian conditions to certain anticonvulsants would seem to merit further investigation.
I-kxhonc
CiL. C’auem
NH. Hoobcrman
DH. et ;LI c‘t
1IW3): IV lorazcpam in ncurolcptic-induced tatonia. .I c‘li,~ /‘.s~c,ho~phtrrrncc(.o/
3:338-342,
GJebsmg LR. Harding GFA. Jcnner I$ ct al (lY671The EEG in three cases of pcnodic catatoniu. HV ./ Psvchitrf~\~ I 13: 137 I-- /7X2. Kraepelin t: ( 19lY): Dementia praecox and paraphrenia. Translated by KM Barclay. Facsimile I9 IO edition, Huntington, NY: Robert E. Kreiger. 1971. p 153. Lamarre Y. Joffroy AJ ( I Y7Y1: Experimental tremors m monkey: Activity of thalamic and precentral cortical neurons in the absence of peripheral feedback. In Poirier LJ, Sourkes TL. Bcdard PJ (cds). .-\tl~xmc~r.s irzNeurology. vol 24. New York: Raven Press. pp lO9--122.
Department of Psychiatry Dartmouth Medical School Hanover. NH 03756
Lew I-Y. ‘follefson G ( 1983): Chlorpromazine Induced neuroleptic malignant syndrome and its rcsponsc lo diazepam. Bid P.syhi+ IX: 1441-1446.
References
McEvoy JP, Lohr JB (1984): Diazepam for catatonia. .4rn .I Psychiatry I4 I :284-285.
Alberts WW (1969): Parkinsonian tremor and cerebral potentials. In Gillingham FJ, Donaldson IML (eds). Third Symposium on Purkinsvn’s Disease. Edinburgh: Livingstone, pp 146-149. Alberts WW (1972): A simple view of Parkinsonian tremor. Electrical stimulation of cortex adjacent to the rolandic fissure in awake man. Rrclin Res 441357-369.
Bleckwenn WJ ( I93 I ): The use of sodium amytal in catatonia. In Schizophrmiu (Research Publications of Association for Research in Nervous and Mental Disease. vol IO). Baltimore: Williams & Wilkins, pp 224-229. Brownc TR. Penry JK (1973): Benzodiazepines in the treatment of epilepsy: A review. Epilepsicr l4:237-3 IO. Caroff SN (1980): The neuroleptic malignant drome. J Clin P.~~c#ziat~ 41:79-83.
syn-
Caruso G. Barnaba A ( 1968): Treatment with diazepam and remission of the extrapyramidal symptoms in a case of parkinsonism caused by carbon monoxide poisoning. Actcr Neurd (Napoli) 23:103-l 10. Fricchione GL ( 1985): Neuroleptic catatonia and its relation to psychogenic catatonia. Bid Pswhiar~v 20: 304-3
I 3.
Navillc F (1’322): Etudes sur Its complications et ICS scqucllcs mcntales de I’encephalite epidemiquc Enwph& 171369-375. 323436. Post RM. Putnam FW. Contel NR (1981): Electroconvulsive shock inhibits amygdala kindling. Sot ~Yrur~osc~i A&r 7:587 Reiter PJ ( 1926): Extrapyramidal m dementia praccox. Acre I X7-3 IO.
motor disturbances Pswhiutr
Neuroi
Rica RK (19X5): DSM-III implications of the diagnose\ of catatonia and bipolar disorder. Am J PSI dzicrtry 142:1471-1474. Stoudcmire A. L,uther JS (1984): Ncuroleptic malignant syndrome and neuroleptic-induced catatonia. Differential diagnosis and treatment. ltzt J PSL drrtrtr Mrtl 14157-h3. Walter-Ryan WG (lY85): Treatment for catatomc symptoms with intramuscular lorazepam. J C/i/r I’s\‘c~hophartnuc.oi 5: 123-l 24. Yosselson-Superstine S. Lipman AG ( 1982): Chlordiazepoxide interaction with levodopa. Ann Inrertr Mrtl 96:259--260. Young KC. Alexopoulos GS. Shamoian CA (1985 ): Dissociation of motor response from mood and cognition in a parkinsonian patient treated with ECT Biol P.sychicrtn 20:566-569.