672
Correspondence
BIOLPSYCHIATRY 1990;27:671-685
Merck Sharp & Dohme Laboratories 10 Sentry Parkway Blue Bell, PA 1~422
References AdlerL0AngristB, Peselow(1985):Efficacyof propranolol in neuroleptic-inducedakau~sia../Ciin P~chopt~rmaco/osy 5:164-166. Adler L, AngristB, Peselow El) (1986): A controlledassessmentof propranololin the treatmentof neurolepticinduced akathisia. Br J Psychiatry 149:~t2-45.
Panic Attacks and Multiple Sclerosis To the Editor: In addition to the familiar motor, sensory, and autonomic symptoms of multiple sclerosis (MS), psychiatric symptoms have often been found to be present in MS patients, even prior to the typical neurological manifestations of the disease (Skegg et al. 1988). Patients with MS have an increased incidence of depression, psychosis, and atypical bipolar disorders (Stenager and Jensen 1988). However, to our knowledge, because recurrent panic attacks associated with MS have apparently not been reported in the literature, we wish to describe such a case. Mrs. M, a 27-year-oldwhite woman, had a 9-month history of recurrent panic attacks characterized by unexpected and rapid onset of anxiety, fearfulness, palpitations, feelings of choking, flushes, and fear of losing consciousness. The panic attacks would occur at an average frequency of two per day, had a mean duration of 30 rain, and were unrelated to any particular situation. No avoidance pattern of behavior was noted, but the patient suffered so much anticipatory anxiety that she refused lactate infusion. No family history of neurological or psychiatric disorder was noted, except for her father, who had suffered a majordepression. There was no history of drag or alcohol abuse. Because Mrs. M was a graduate in psychology, ~"was easy for her to identify her symptoms as panic attacks. When she first experienced these panic attacks, she hypervcn~ated and had secondary feelings of diT~!nessand faintness. She reported that she could
BernickC (1982):Methysergide-inducedakathisia. Clinical Neuropsychopharmacology 11:87-89. KramerMS, GorkinRA, DiJohnsonC (1988): Propranolol in the treatmentof neuroleptic-inducedakathisia(NIA) in schizophrenics: a double-blind, placebo-controlled study. Biol Psychiatry 24:823-827. SandykR, ConsroePF, laconoRP (1986): L-tryptophanin drag-inducedmovement¢fisorders with insouu~. N Engl J Med 314:1257. Simpson GW, Angus JWS (1970): A rating scale for extmpyramidal symptoms. Acta Psychiatr $cand 212(suppl):11-19. Young SN, Sourkes TL (1974): Antidepressant"action of ~ . . - - , ^ , k , , , . ~ n c e f i b. . 80"/_RQR ..Vp,vt,.,tu. ......
ameliorate these panic attacks by reducing respiratory frequency. Mrs. M had two previous episodes of acute motor and sensory symptoms; the last episode required hospitalization. A magnetic resonance imaging test (MRD revealed several high intensity areas (plaques) in the white matter of both cerebral hemispheres, mostly affecting the left side, with no cervical spinal involvement. Cerebmspinal fluid examination was normal, but with oligoclonal bandy positive, and 0.038 g/L of IgG, establishing a diagnosis of MS. While hospitalized she continued to have sudden similar panic attacks for several months while her MS symptoms improved. Several EEOs during hospitalization and afterwards when off medication were normS, including visual- and somatosensoryevoked potentials. Mrs. M was treated with clonazepam, with an initial dose of 0.5 roB/day, later increased to 2 rag/day. This dose led to complete control of her panic attacks. She continued taking this dose of cionazepam and no panic attacks took place for the following 8 months. AIdmugh this may be the first reported case of a patient with recurrent panic attacks associated with MS, we recently reported an increased incidence of neuroanatomical abnormalities revealed by MRI in panic disorder patients. These were mostly temporal lobe changes, focal lesions of the white matter (5-10 mm in diameter), and/or atrophy (Fontaine et al., in press). Moreover these abnormalities were found to correlate with the severity of the panic disorder (Ontiveros et al., in press). Thus, some
Correspondence
BIOL PSYCHIATRY 1990;27:671-685
common pathophysiological mechanism for the MS and recurrent panic attacks could be hypothesized in the present case. Furthermore, the remarkable response to an antipanic drag, clonazepam, is interesting and suggests that a kindling phenomenon may be involved (Post and Uhde 1986). The incidence of rec,wrent panic attacks in MS patients and its underlying pathophysiological mechanism deserve further attention. Alfonso Ontiveros Rdjean Fontaine
Louis H. ~ou~aine Hospital 7401 Hochelaga Street Montreal, Ou.ebec HIN 3M5 Canada
Metoprolol Versus Propranolol To the Editor: Beta-blockers, particularly propr~olol, can effectively treat neuroleptic-induced akathisia (NIA) (Lipinski et al. 1983; Adler et al. 1985, 1986, 1989a; Kramer et el. 1988). Propranolol nonselectively blocks both Beta-I and Beta-2 receptors; the relative contribution of Beta-1 versus Beta-2 receptor blockade to the therapeutic effect is unresolved. Two prior studies have evaluated metoprolol, which is Be~-I selective in doses ~). One iavestigator (LAA) presc~bed the Betablocker, whereas another (BA) rat~l akathisia and was blind to order of treatment. Ratings were done prior to drag administration and approximately 4 hr after receiving the second dose of metoprolol or propranolol. This timing of ratings was chosen to allow absorption of both doses. Akathisia was rated by the Barnes akathisia scale mo,,,~ !988). This study was
Correspondence
BIOLPSYCHIATRY 1990;27:671-685
Merck Sharp & Dohme Laboratories 10 Sentry Parkway Blue Bell, PA 1~422
References AdlerL0AngristB, Peselow(1985):Efficacyof propranolol in neuroleptic-inducedakau~sia../Ciin P~chopt~rmaco/osy 5:164-166. Adler L, AngristB, Peselow El) (1986): A controlledassessmentof propranololin the treatmentof neurolepticinduced akathisia. Br J Psychiatry 149:~t2-45.
Panic Attacks and Multiple Sclerosis To the Editor: In addition to the familiar motor, sensory, and autonomic symptoms of multiple sclerosis (MS), psychiatric symptoms have often been found to be present in MS patients, even prior to the typical neurological manifestations of the disease (Skegg et al. 1988). Patients with MS have an increased incidence of depression, psychosis, and atypical bipolar disorders (Stenager and Jensen 1988). However, to our knowledge, because recurrent panic attacks associated with MS have apparently not been reported in the literature, we wish to describe such a case. Mrs. M, a 27-year-oldwhite woman, had a 9-month history of recurrent panic attacks characterized by unexpected and rapid onset of anxiety, fearfulness, palpitations, feelings of choking, flushes, and fear of losing consciousness. The panic attacks would occur at an average frequency of two per day, had a mean duration of 30 rain, and were unrelated to any particular situation. No avoidance pattern of behavior was noted, but the patient suffered so much anticipatory anxiety that she refused lactate infusion. No family history of neurological or psychiatric disorder was noted, except for her father, who had suffered a majordepression. There was no history of drag or alcohol abuse. Because Mrs. M was a graduate in psychology, ~"was easy for her to identify her symptoms as panic attacks. When she first experienced these panic attacks, she hypervcn~ated and had secondary feelings of diT~!nessand faintness. She reported that she could
BernickC (1982):Methysergide-inducedakathisia. Clinical Neuropsychopharmacology 11:87-89. KramerMS, GorkinRA, DiJohnsonC (1988): Propranolol in the treatmentof neuroleptic-inducedakathisia(NIA) in schizophrenics: a double-blind, placebo-controlled study. Biol Psychiatry 24:823-827. SandykR, ConsroePF, laconoRP (1986): L-tryptophanin drag-inducedmovement¢fisorders with insouu~. N Engl J Med 314:1257. Simpson GW, Angus JWS (1970): A rating scale for extmpyramidal symptoms. Acta Psychiatr $cand 212(suppl):11-19. Young SN, Sourkes TL (1974): Antidepressant"action of ~ . . - - , ^ , k , , , . ~ n c e f i b. . 80"/_RQR ..Vp,vt,.,tu. ......
ameliorate these panic attacks by reducing respiratory frequency. Mrs. M had two previous episodes of acute motor and sensory symptoms; the last episode required hospitalization. A magnetic resonance imaging test (MRD revealed several high intensity areas (plaques) in the white matter of both cerebral hemispheres, mostly affecting the left side, with no cervical spinal involvement. Cerebmspinal fluid examination was normal, but with oligoclonal bandy positive, and 0.038 g/L of IgG, establishing a diagnosis of MS. While hospitalized she continued to have sudden similar panic attacks for several months while her MS symptoms improved. Several EEOs during hospitalization and afterwards when off medication were normS, including visual- and somatosensoryevoked potentials. Mrs. M was treated with clonazepam, with an initial dose of 0.5 roB/day, later increased to 2 rag/day. This dose led to complete control of her panic attacks. She continued taking this dose of cionazepam and no panic attacks took place for the following 8 months. AIdmugh this may be the first reported case of a patient with recurrent panic attacks associated with MS, we recently reported an increased incidence of neuroanatomical abnormalities revealed by MRI in panic disorder patients. These were mostly temporal lobe changes, focal lesions of the white matter (5-10 mm in diameter), and/or atrophy (Fontaine et al., in press). Moreover these abnormalities were found to correlate with the severity of the panic disorder (Ontiveros et al., in press). Thus, some
Correspondence
BIOL PSYCHIATRY 1990;27:671-685
common pathophysiological mechanism for the MS and recurrent panic attacks could be hypothesized in the present case. Furthermore, the remarkable response to an antipanic drag, clonazepam, is interesting and suggests that a kindling phenomenon may be involved (Post and Uhde 1986). The incidence of rec,wrent panic attacks in MS patients and its underlying pathophysiological mechanism deserve further attention. Alfonso Ontiveros Rdjean Fontaine
Louis H. ~ou~aine Hospital 7401 Hochelaga Street Montreal, Ou.ebec HIN 3M5 Canada
Metoprolol Versus Propranolol To the Editor: Beta-blockers, particularly propr~olol, can effectively treat neuroleptic-induced akathisia (NIA) (Lipinski et al. 1983; Adler et al. 1985, 1986, 1989a; Kramer et el. 1988). Propranolol nonselectively blocks both Beta-I and Beta-2 receptors; the relative contribution of Beta-1 versus Beta-2 receptor blockade to the therapeutic effect is unresolved. Two prior studies have evaluated metoprolol, which is Be~-I selective in doses ~). One iavestigator (LAA) presc~bed the Betablocker, whereas another (BA) rat~l akathisia and was blind to order of treatment. Ratings were done prior to drag administration and approximately 4 hr after receiving the second dose of metoprolol or propranolol. This timing of ratings was chosen to allow absorption of both doses. Akathisia was rated by the Barnes akathisia scale mo,,,~ !988). This study was
