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Group a β-hemolytic streptococcal meningitis associated with uncomplicated varicella
602
AMERICAN
JOURNAL
OF EMERGENCY
me 2B). CPR continued and the echocardiographic findings persisted. CPR was terminated 45 minutes later because there was no spontaneous circulation, and the patient was pronounced dead. The family refused an autopsy, and the cause of death remains unknown. Complications are common during our daily practice of CPR. Rib fracture is the leading type of complication encountered and is usually benign.‘s3 Morbid complications, such as cardiac rupture, rupture of the aorta, laceration of liver and spleen, and gastroesophageal laceration rarely occur during CPR and are hard to detect antemortem. Injury to the cardiovascular system during CPR, even very subtle, if not detected early and left untreated, may render the CPR futile.4 Aortic valve disruption with aortic regurgitation as a complication of external chest compression has not been described in the literature previously. Without the help of TEE during the procedure, it would have gone unnoticed throughout CPR. The mechanism of aortic valve prolapse after chest compression is not very clear because autopsy was not performed, but it may be related to the unusually large force applied to the ascending aorta of this patient because of different anatomy of the chest wall and the tortuosity of the ascending aorta. In this case, a marked collapse of the ascending aorta during the compression phase by TEE was observed, which is an unusual finding compared with other subjects receiving CPR and TEE. Although transthoracic echocardiography has become one of the most important noninvasive tools to study cardiovascular structures, it remains awkward to use during CPR. Chest compression and the use of ECG leads, defibrillation paddles, and ventilatory support preclude a good echocardiographic examination. On the other hand, TEE offers an excellent window to the heart and great vessels even with chest compression and artificial ventilation. The transesophageal probe can be inserted in the esophagus easily after successful and secured endotracheal intubation6 Manipulation of the transesophageal probe and images of good quality could be achieved without disturbing the practice of CPR.6 It seems that besides research purposes, TEE may play an important role in the clinical practice of CPR. It can be performed without additional difficulty during CPR by experienced hands, and its use should be considered to detect possible cause of cardiac arrest and unanticipated cardiovascular complications from CPR, when encountered. Cardiopulmonary resuscitation is not without danger, and cardiovascular complications from CPR may be catastrophic if left unattended. TEE easily may be performed in the ED and may be helpful in identifying the cause of cardiac arrest and detecting cardiovascular complications from CPR when suspected. MATTHEW HUEI-MING MA, MD &AN-TARN HUANG, MD SHIH-MING WANG, MD TONG-YUAN TAI, MD Department of Emergency Medicine
Kou-GI SHYU, MD JUEY-JENHWANG, MD YUNG-ZU TSENG, MD WEN-PIN LIEN, MD Department of Internal Medicine National Taiwan University Hospital Taipei, Taiwan
References 1. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closedchest cardiac massage. JAMA 1960;173: 1064-l 067 2. Himmelhoch SR, Dekker A, Lieutenant AB, et al: Closedchest cardiac resuscitation. A prospective clinical and pathological study. N Eng J Med 1964;270:118-122 3. Krischer JP, Fine EG, Davis JH, et al: Complications of cardiac resuscitation. Chest 1987;92:287-291 4. Nelson DA, Ashley PF: Rupture of the aorta during closedchest cardiac massage. JAMA 1965;193:681-683
MEDICINE
n Volume
12, Number
5 n September
1994
5. Werner JA, Greene HL, Janko CL, et al: Visualization of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Circulation 1981;64: 985991 6. Porter TR, Ornato JP, Guard CS, et al: Transesophageal echocardiography to assess mitral valve function and flow during cardiopulmonary resuscitation. Am J Cardiol 1992;70:10561060
GROUPA f3-HEMOLYTIC STREPTOCOCCALMENINGITIS ASSOCIATEDWITH UNCDMPLICATEDVARICELLA There has been an increase of complications caused by group A B-hemolytic streptococcus (GABHS) in recent years. GABHS, a rare cause of meningitis, accounts for less than 0.2% of all cases of meningitis. is2GABHS meningitis occurs most often in immunocompromised patients, but cases have occurred in previously healthy patients3 In the past 25 years, there have been only 23 case reports in the English language literature. 2.3-sThe second case in the literature of GABHS meningitis complicating varicella-zoster (VZV) infection is described here.
CaseReport A 12-year-old white girl with no history of previous illness broke out with a typical varicella rash beginning 1 week before admission. Four days later she complained of headache, fever, nausea, vomiting, and neck pain. She had mild neck discomfort at the time that was attributed to cervical lymphadenopathy. Her physician started her on acyclovir 200 mg orally every 4 hours. Three days later, she presented to the emergency department with a persistent and worsening headache, neck stiffness, back pain, and diffuse myalgas. The varicella lesions had crusted. Physical examination showed an afebrile patient with normal pulse, respirations, and blood pressure. She had mild conjunctivitis without photophobia. The tympanic membranes were normal. The pharynx showed mild tonsillar swelling without exudate or other lesions. Her mucous membranes were moderately dry, and her neck was stiff and painful with attempted flexion. Kemig’s and Brudzinski’s signs were positive. The lungs were clear to auscultation and percussion. The heart had a regular rate and rhythm without murmurs. She had a soft abdomen with normal bowel sounds. The varicella lesions over the face, extremities, and trunk crusted without signs of secondary infection. The extremities also showed mild diffuse erythema and some mottling around the knees and lower extremities. The lumbar puncture showed cloudy fluid. The cerebrospinal fluid showed a red blood cell count of 68 mL, a white blood cell count of 1,205 mL (65% polymorphonuclear cells and 35% mononuclear cells), a protein of 147 mg/dL, and glucose of 6 mg/dL. The cerebrospinal fluid grew GABHS and was sensitive to ampicillin, cephalothin, penicillin, and vancomycin. The cerebrospinal fluid bacterial antigen was negative for Haemophilis influenzae b, Streptococcus pneumonia, and three different subtypes of Neisseria meningitis. In addition, the Gram-stained smear, two blood cultures, and urine culture were all negative. On admission, the patient was given intravenously acyclovir 400 mg every 8 hours and ceftriaxone 1 g every 12 hours. After the antibiotic sensitivities returned, the patient was switched to 1.5 x lo6 units every 4 hours of intravenous penicillin. She was discharged with normal neurological examination results 10 days later. GABHS rarely causes meningitis. During the preantibiotic era, GABHS accounted for 10% to 20% of cases of nontuberculous purulent meningitis, with a fatality rate of more than 95%.6,9 Since the antibiotic era, the incidence of severe GABHS decreased until the mid 1980s when a resurgence of serious group A B-hemolytic strep-
CORRESPONDENCE
603
tococcal infections appeared.2,6 However, a recent increase in GABHS meningitis since the 1980s has not been described. GABHS often invades the central nervous system secondarily from another infected site. Postvaricella suppurative meningitis, GABHS septicemia associated with varicella, and GABHS endocarditis complicating varicella have been reported.6.‘@‘s However, only one other case of GABHS meningitis complicating varicella has been published.6 Previous cases of GABHS meningitis in nonimmunocompromised hosts have been described in patients with otitis media, septic arthritis, cavernous hemangiomas, acute hepatitis, pharyngitis, vaginitis, head injury, postmyelography, laceration with skull defect, surgery for epidural cyst, and sinusitis.‘.’ The emergency physician often treats the patient who has varicella presenting with cervical lymphadenopathy and neck pain. This case shows that meningitis should be considered in these patients. In addition, because of the recent increase in severe GABHS, one must be alert for the development of GABHS meningitis in children with varicella who show signs of meningeal irritation. This is the second case of GABHS meningitis complicating varicella infection described in the literature. Although there has been a recent increase in the severe complications related to GABHS infections, GABHS meningitis remains a rare disease. Patients with varicella who present with meningeal signs should be considered for bacterial meningitis. GABHS may cause meningitis in these patients. MARK WALSH, MD ROCHELLECHODOCK CHRISTOPHERQUINN, MD SHEREE PEGLOW, MD Department of Emergency Medicine Saint Joseph’s Medical Center South Bend, IN
References 1. Schlech WF Ill, Ward JI, Band JD, et al: Bacterial meningitis in the United States. 1978 through 1981: The National Bacterial Meninaitis Surveillance Studv. JAMA 1985:253:1749-1754 2. Chow>W, Muder RR: Group A streptococcal meningitis, Clin Infect Dis 1992;14:418-421 3. Murphy DJ: Group A streptococcal meningitis. Pediatrics 1983;71:1-5 4. Harnden A, Lennon D: Serious suppurative Group A streptococcal infections in previously well children. Pediatr Infect Dis J 1988;7:714-718 5. Chotmongkol V, Prathipanawatra T, Rojviroj S: Group A beta hemolytic streptococcal meningitis in adults. J Med Assoc Thai 1989;72:545-547 6. Gradon JD, Chapnick EK, Lutwick K, et al: Group A streptococcal meningitis complicating varicella. Pediatr Infect Dis J 1991;10:786-787 7. Peterson C, Smith P, Loomis G, et al: Group A streptococcal meningitis in an adult. Nebr Med J 1985;70:233-235 8. Damani NN, Chin AT: Streptococcus pyogenes meningitis after myelography. J Pak Med Assoc 1988;38:197-198 9. Finland M, Jones WF, Barnes MW: Occurrence of serious bacterial infection since introduction of antibacterial agents. JAMA 1959;170:2188-2197 10. Colman G, Tanna A, Efstratiou A, et al: The serotypes of Streptococcus pyogenes present in Britain during 1980-1990 and their associating with disease. J Med Microbial 1993;39:165178 11. Singer J: Post varicella suppurative meningitis. Am J Dis Child 1979;133:934-935 12. Karandanis D, Shulman JA: Recent survey of infectious meningitis in adults: Review of laboratory findings in bacterial, tuberculous, and aseptic meningitis. South Med J 1976;69:449457 13. Harnden A, Lennon D: Serious suppurative Group A strep-
tococcal infections J 1988;7:714-718
in previously
well children.
14. Smith EW, Garson A, Boyleston grenosa due to Group A betahaemolytic rics 1976;57:306-310
Pediatr
Infect Dis
JA et al: Varicella ganStreptococcus. Pediat-
15. Cowan MR, Primm PA, Scott SM, et al: Serious group A 8-hemolytic streptococcal infections complicating varicella. Ann Emerg Med 1994;23:818
BARBITURATE, ANALGESIC, AND CAFFEINE WITHDRAWAL To the Editor:-Drug abuse and dependence are not often included in the differential diagnosis of newly admitted patients. In particular, the abuse of barbiturates is unusual and, therefore, clinicians are unprepared for the special problem concerning the complications of withdrawal and coexistence of medical care for the life-threatening problems involved. ‘Z Treatment is effective in reducing patient morbidity; however, correct therapy could be delayed if the physician does not consider that the patient may be misusing a sedative hypnotic drug. We report one such case, describing acute withdrawal of butalbital, caffeine, and phenylbutazone, aggravated by the patient’s denial of drug abuse.
Case Report At 8 AM a 36-year-old woman was urgently taken to the emergency department for two episodes of lipotimia that had been preceded by nausea and vomiting. On first clinical examination, she was aware and compliant. Pulse, blood pressure, and respiration were 86 beatsimin, 140/70 mm Hg, and 20 breaths/min, respectively. Pulmonary, cardiac, and abdominal examinations were normal. She had a graze to the scalp that was immediately sutured and dressed. No fractures were shown with a radiography of the cranium. Therefore, because of the persistence of nausea, she was admitted to the emergency medical section. Her medical history was negative until 6 years ago when a migraine syndrome appeared. The episodes of severe frontotemporal bilateral headache recurred with almost daily frequency. She admitted to using, “when needed,” an analgesic combination: Optalidon (Sandoz Prodotti Farmaceutici S.p.a., Milan, Italy) suppositories (propylphenazone 375 mg, butalbital 150 mg, and caffeine 75 mg). Two weeks before hospitalization a treatment with trifluoperazine (2 mg/day) and alprazolam (0.5 mg/day), suggested by a neurologist for anxiety and depression problems, was started. She complained that in the days before hospitalization the headache had worsened, and that she had begun to vomit the day before. She denied the abuse of alcohol, smoking. and, in particular, drugs. The first day after admission to the hospital, she showed mild drowsiness, and neurological examination showed horizontal nystagmus to the right and diffuse hyperreflexia. The presence of headache and sensation of nausea, raised by any movement of the head, prevented the evaluation of upright position and gait. A brain computed tomographic (CT) scan was normal. Hematochemical examinations showed a moderate normocytic anemia (hemoglobin 102 g/L and hematocrit 0.32 fraction of l.OO), and an increase of creatinine phosphokinase (CPK) (835 u/L) and y-glutamyl transferase (205 u/L). Intravenous fluids and symptomatic drugs (metoclopramide lO/mg day) stopped the vomiting. On the morning of the second day she seemed lucid and perfectly orientated. Nystagmus and hyperreflexia persisted. An electroencephalogram (EEG) showed a diffused slow rhythm with bilateral epileptic discharges in synchronous sequences. In the afternoon of that day (approximately 36 hours after admission), she presented restlessness, confusion, tremors, and visual hallucinations. A dose of 20 mg of chlorhydrate promazine was given without any result.
AMERICAN
JOURNAL
OF EMERGENCY
me 2B). CPR continued and the echocardiographic findings persisted. CPR was terminated 45 minutes later because there was no spontaneous circulation, and the patient was pronounced dead. The family refused an autopsy, and the cause of death remains unknown. Complications are common during our daily practice of CPR. Rib fracture is the leading type of complication encountered and is usually benign.‘s3 Morbid complications, such as cardiac rupture, rupture of the aorta, laceration of liver and spleen, and gastroesophageal laceration rarely occur during CPR and are hard to detect antemortem. Injury to the cardiovascular system during CPR, even very subtle, if not detected early and left untreated, may render the CPR futile.4 Aortic valve disruption with aortic regurgitation as a complication of external chest compression has not been described in the literature previously. Without the help of TEE during the procedure, it would have gone unnoticed throughout CPR. The mechanism of aortic valve prolapse after chest compression is not very clear because autopsy was not performed, but it may be related to the unusually large force applied to the ascending aorta of this patient because of different anatomy of the chest wall and the tortuosity of the ascending aorta. In this case, a marked collapse of the ascending aorta during the compression phase by TEE was observed, which is an unusual finding compared with other subjects receiving CPR and TEE. Although transthoracic echocardiography has become one of the most important noninvasive tools to study cardiovascular structures, it remains awkward to use during CPR. Chest compression and the use of ECG leads, defibrillation paddles, and ventilatory support preclude a good echocardiographic examination. On the other hand, TEE offers an excellent window to the heart and great vessels even with chest compression and artificial ventilation. The transesophageal probe can be inserted in the esophagus easily after successful and secured endotracheal intubation6 Manipulation of the transesophageal probe and images of good quality could be achieved without disturbing the practice of CPR.6 It seems that besides research purposes, TEE may play an important role in the clinical practice of CPR. It can be performed without additional difficulty during CPR by experienced hands, and its use should be considered to detect possible cause of cardiac arrest and unanticipated cardiovascular complications from CPR, when encountered. Cardiopulmonary resuscitation is not without danger, and cardiovascular complications from CPR may be catastrophic if left unattended. TEE easily may be performed in the ED and may be helpful in identifying the cause of cardiac arrest and detecting cardiovascular complications from CPR when suspected. MATTHEW HUEI-MING MA, MD &AN-TARN HUANG, MD SHIH-MING WANG, MD TONG-YUAN TAI, MD Department of Emergency Medicine
Kou-GI SHYU, MD JUEY-JENHWANG, MD YUNG-ZU TSENG, MD WEN-PIN LIEN, MD Department of Internal Medicine National Taiwan University Hospital Taipei, Taiwan
References 1. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closedchest cardiac massage. JAMA 1960;173: 1064-l 067 2. Himmelhoch SR, Dekker A, Lieutenant AB, et al: Closedchest cardiac resuscitation. A prospective clinical and pathological study. N Eng J Med 1964;270:118-122 3. Krischer JP, Fine EG, Davis JH, et al: Complications of cardiac resuscitation. Chest 1987;92:287-291 4. Nelson DA, Ashley PF: Rupture of the aorta during closedchest cardiac massage. JAMA 1965;193:681-683
MEDICINE
n Volume
12, Number
5 n September
1994
5. Werner JA, Greene HL, Janko CL, et al: Visualization of cardiac valve motion in man during external chest compression using two-dimensional echocardiography. Circulation 1981;64: 985991 6. Porter TR, Ornato JP, Guard CS, et al: Transesophageal echocardiography to assess mitral valve function and flow during cardiopulmonary resuscitation. Am J Cardiol 1992;70:10561060
GROUPA f3-HEMOLYTIC STREPTOCOCCALMENINGITIS ASSOCIATEDWITH UNCDMPLICATEDVARICELLA There has been an increase of complications caused by group A B-hemolytic streptococcus (GABHS) in recent years. GABHS, a rare cause of meningitis, accounts for less than 0.2% of all cases of meningitis. is2GABHS meningitis occurs most often in immunocompromised patients, but cases have occurred in previously healthy patients3 In the past 25 years, there have been only 23 case reports in the English language literature. 2.3-sThe second case in the literature of GABHS meningitis complicating varicella-zoster (VZV) infection is described here.
CaseReport A 12-year-old white girl with no history of previous illness broke out with a typical varicella rash beginning 1 week before admission. Four days later she complained of headache, fever, nausea, vomiting, and neck pain. She had mild neck discomfort at the time that was attributed to cervical lymphadenopathy. Her physician started her on acyclovir 200 mg orally every 4 hours. Three days later, she presented to the emergency department with a persistent and worsening headache, neck stiffness, back pain, and diffuse myalgas. The varicella lesions had crusted. Physical examination showed an afebrile patient with normal pulse, respirations, and blood pressure. She had mild conjunctivitis without photophobia. The tympanic membranes were normal. The pharynx showed mild tonsillar swelling without exudate or other lesions. Her mucous membranes were moderately dry, and her neck was stiff and painful with attempted flexion. Kemig’s and Brudzinski’s signs were positive. The lungs were clear to auscultation and percussion. The heart had a regular rate and rhythm without murmurs. She had a soft abdomen with normal bowel sounds. The varicella lesions over the face, extremities, and trunk crusted without signs of secondary infection. The extremities also showed mild diffuse erythema and some mottling around the knees and lower extremities. The lumbar puncture showed cloudy fluid. The cerebrospinal fluid showed a red blood cell count of 68 mL, a white blood cell count of 1,205 mL (65% polymorphonuclear cells and 35% mononuclear cells), a protein of 147 mg/dL, and glucose of 6 mg/dL. The cerebrospinal fluid grew GABHS and was sensitive to ampicillin, cephalothin, penicillin, and vancomycin. The cerebrospinal fluid bacterial antigen was negative for Haemophilis influenzae b, Streptococcus pneumonia, and three different subtypes of Neisseria meningitis. In addition, the Gram-stained smear, two blood cultures, and urine culture were all negative. On admission, the patient was given intravenously acyclovir 400 mg every 8 hours and ceftriaxone 1 g every 12 hours. After the antibiotic sensitivities returned, the patient was switched to 1.5 x lo6 units every 4 hours of intravenous penicillin. She was discharged with normal neurological examination results 10 days later. GABHS rarely causes meningitis. During the preantibiotic era, GABHS accounted for 10% to 20% of cases of nontuberculous purulent meningitis, with a fatality rate of more than 95%.6,9 Since the antibiotic era, the incidence of severe GABHS decreased until the mid 1980s when a resurgence of serious group A B-hemolytic strep-
CORRESPONDENCE
603
tococcal infections appeared.2,6 However, a recent increase in GABHS meningitis since the 1980s has not been described. GABHS often invades the central nervous system secondarily from another infected site. Postvaricella suppurative meningitis, GABHS septicemia associated with varicella, and GABHS endocarditis complicating varicella have been reported.6.‘@‘s However, only one other case of GABHS meningitis complicating varicella has been published.6 Previous cases of GABHS meningitis in nonimmunocompromised hosts have been described in patients with otitis media, septic arthritis, cavernous hemangiomas, acute hepatitis, pharyngitis, vaginitis, head injury, postmyelography, laceration with skull defect, surgery for epidural cyst, and sinusitis.‘.’ The emergency physician often treats the patient who has varicella presenting with cervical lymphadenopathy and neck pain. This case shows that meningitis should be considered in these patients. In addition, because of the recent increase in severe GABHS, one must be alert for the development of GABHS meningitis in children with varicella who show signs of meningeal irritation. This is the second case of GABHS meningitis complicating varicella infection described in the literature. Although there has been a recent increase in the severe complications related to GABHS infections, GABHS meningitis remains a rare disease. Patients with varicella who present with meningeal signs should be considered for bacterial meningitis. GABHS may cause meningitis in these patients. MARK WALSH, MD ROCHELLECHODOCK CHRISTOPHERQUINN, MD SHEREE PEGLOW, MD Department of Emergency Medicine Saint Joseph’s Medical Center South Bend, IN
References 1. Schlech WF Ill, Ward JI, Band JD, et al: Bacterial meningitis in the United States. 1978 through 1981: The National Bacterial Meninaitis Surveillance Studv. JAMA 1985:253:1749-1754 2. Chow>W, Muder RR: Group A streptococcal meningitis, Clin Infect Dis 1992;14:418-421 3. Murphy DJ: Group A streptococcal meningitis. Pediatrics 1983;71:1-5 4. Harnden A, Lennon D: Serious suppurative Group A streptococcal infections in previously well children. Pediatr Infect Dis J 1988;7:714-718 5. Chotmongkol V, Prathipanawatra T, Rojviroj S: Group A beta hemolytic streptococcal meningitis in adults. J Med Assoc Thai 1989;72:545-547 6. Gradon JD, Chapnick EK, Lutwick K, et al: Group A streptococcal meningitis complicating varicella. Pediatr Infect Dis J 1991;10:786-787 7. Peterson C, Smith P, Loomis G, et al: Group A streptococcal meningitis in an adult. Nebr Med J 1985;70:233-235 8. Damani NN, Chin AT: Streptococcus pyogenes meningitis after myelography. J Pak Med Assoc 1988;38:197-198 9. Finland M, Jones WF, Barnes MW: Occurrence of serious bacterial infection since introduction of antibacterial agents. JAMA 1959;170:2188-2197 10. Colman G, Tanna A, Efstratiou A, et al: The serotypes of Streptococcus pyogenes present in Britain during 1980-1990 and their associating with disease. J Med Microbial 1993;39:165178 11. Singer J: Post varicella suppurative meningitis. Am J Dis Child 1979;133:934-935 12. Karandanis D, Shulman JA: Recent survey of infectious meningitis in adults: Review of laboratory findings in bacterial, tuberculous, and aseptic meningitis. South Med J 1976;69:449457 13. Harnden A, Lennon D: Serious suppurative Group A strep-
tococcal infections J 1988;7:714-718
in previously
well children.
14. Smith EW, Garson A, Boyleston grenosa due to Group A betahaemolytic rics 1976;57:306-310
Pediatr
Infect Dis
JA et al: Varicella ganStreptococcus. Pediat-
15. Cowan MR, Primm PA, Scott SM, et al: Serious group A 8-hemolytic streptococcal infections complicating varicella. Ann Emerg Med 1994;23:818
BARBITURATE, ANALGESIC, AND CAFFEINE WITHDRAWAL To the Editor:-Drug abuse and dependence are not often included in the differential diagnosis of newly admitted patients. In particular, the abuse of barbiturates is unusual and, therefore, clinicians are unprepared for the special problem concerning the complications of withdrawal and coexistence of medical care for the life-threatening problems involved. ‘Z Treatment is effective in reducing patient morbidity; however, correct therapy could be delayed if the physician does not consider that the patient may be misusing a sedative hypnotic drug. We report one such case, describing acute withdrawal of butalbital, caffeine, and phenylbutazone, aggravated by the patient’s denial of drug abuse.
Case Report At 8 AM a 36-year-old woman was urgently taken to the emergency department for two episodes of lipotimia that had been preceded by nausea and vomiting. On first clinical examination, she was aware and compliant. Pulse, blood pressure, and respiration were 86 beatsimin, 140/70 mm Hg, and 20 breaths/min, respectively. Pulmonary, cardiac, and abdominal examinations were normal. She had a graze to the scalp that was immediately sutured and dressed. No fractures were shown with a radiography of the cranium. Therefore, because of the persistence of nausea, she was admitted to the emergency medical section. Her medical history was negative until 6 years ago when a migraine syndrome appeared. The episodes of severe frontotemporal bilateral headache recurred with almost daily frequency. She admitted to using, “when needed,” an analgesic combination: Optalidon (Sandoz Prodotti Farmaceutici S.p.a., Milan, Italy) suppositories (propylphenazone 375 mg, butalbital 150 mg, and caffeine 75 mg). Two weeks before hospitalization a treatment with trifluoperazine (2 mg/day) and alprazolam (0.5 mg/day), suggested by a neurologist for anxiety and depression problems, was started. She complained that in the days before hospitalization the headache had worsened, and that she had begun to vomit the day before. She denied the abuse of alcohol, smoking. and, in particular, drugs. The first day after admission to the hospital, she showed mild drowsiness, and neurological examination showed horizontal nystagmus to the right and diffuse hyperreflexia. The presence of headache and sensation of nausea, raised by any movement of the head, prevented the evaluation of upright position and gait. A brain computed tomographic (CT) scan was normal. Hematochemical examinations showed a moderate normocytic anemia (hemoglobin 102 g/L and hematocrit 0.32 fraction of l.OO), and an increase of creatinine phosphokinase (CPK) (835 u/L) and y-glutamyl transferase (205 u/L). Intravenous fluids and symptomatic drugs (metoclopramide lO/mg day) stopped the vomiting. On the morning of the second day she seemed lucid and perfectly orientated. Nystagmus and hyperreflexia persisted. An electroencephalogram (EEG) showed a diffused slow rhythm with bilateral epileptic discharges in synchronous sequences. In the afternoon of that day (approximately 36 hours after admission), she presented restlessness, confusion, tremors, and visual hallucinations. A dose of 20 mg of chlorhydrate promazine was given without any result.