Ziprasidone in the treatment of delayed carbon monoxide encephalopathy

Delayed carbon monoxide (CO) encephalopathy is a serious complication of acute CO poisoning. We present a case of successful treatment of ziprasidone, a newer atypical antipsychotic, in delayed CO encephalopathy. A 52-year-old depressed woman suffered acute CO intoxication after an attempt of suicide by burning charcoal. She was initially treated with hyperbaric oxygen (HBO) therapy for the acute intoxication. One week later, the patient developed neuropsychiatric symptoms including parkinsonism, tardive dyskinesia (TD), cognitive deterioration, urinary incontinence, gait disturbance, mutism, disorientation to time, place and person, and disorganized as well as disturbing behavior. During her psychiatric hospitalization, the patient had been treated with daily HBO therapy, bromocriptine (2.5 mg/day), the conventional antipsychotic sulpiride (600 mg/day), and atypical antipsychotics such as risperidone (5 mg/day) and quetiapine (400 mg/day). However, her delayed neuropsychiatric sequelae of CO intoxication persisted despite of these treatments. It was until she had been treated with ziprasidone (80 mg/day) for 10 days that her mental condition was improved. With ziprasidone therapy, the patient obtained substantial improvement in her neuropsychiatric symptoms, cognitive function, and daily activities. Our case indicates that ziprasidone can be used effectively in the treatment of delayed CO encephalopathy.     

Electroconvulsive therapy in therapy-resistant mania. A case study

A 25-year-old woman was separated for 6 weeks on account of her suicidal and chaotic behaviour occurring within the framework of a first manic episode. Her response to medication (olanzapine 20 mg, clorazepate 50 mg and lithium (serum level 0.9 mmol/l)) was inadequate. After only one ect treatment her condition had improved to such an extent that she no longer needed to be isolated. After about 4 weeks her mental condition was reasonably good; her medication consisted only of 10 mg of olanzapine and she could be transferred to out-patient care. ect can bring about rapid improvement in patients with therapy-resistant manic symptoms.     

Delayed encephalopathy following acute fentanyl intoxicication]

We report an 84-year-old woman who suffered from acute fentanyl intoxication followed by delayed encephalopathy. She used fentanyl patch at her ached knee joint and stayed in the covered table with a heat source underneath. Serum concentration of fentanyl suddenly elevated and she developed coma due to acute fentanyl intoxication. She gradually recovered, however, she showed consciousness disturbance again at 15th day and developed neurological symptoms including mutism, pyramidal tract signs, frontal lobe signs and parkinsonism. These symptoms also steadily improved without specific treatment, and became able to talk with colleagues and walk with assistance at 90th day. We considered that delayed encephalopathy due to periodic anoxia caused by fentanyl intoxication occurred in the present patient; however, the neurological sequelae were relatively mild as compared with reported cases of carbon monoxide intoxication. Neuroprotective effect of fentanyl may have contributed to the better prognosis in the present patient.     

Generalized chorea due to delayed encephalopathy after acute carbon monoxide intoxication

Movement disorder due to delayed encephalopathy after carbon monoxide (CO) intoxication is uncommon. Generalized chorea, presenting as an initial symptom of delayed encephalopathy, is extremely rare. We describe a 60-year-old woman, who had completely recovered from acute CO poisoning, developed mental and behavioral changes, urinary incontinence and generalized chorea 2 weeks thereafter. T2-weighted brain magnetic resonance imaging showed extensive hyperintensity of the bilateral periventricular and subcortical white matter and the globus pallidus. Brain single-photon emission computed tomography (SPECT) with technetium-99 ethylene cysteine dimer showed inhomogeneous perfusion in the cerebral cortex, with decreased uptake in bilateral frontal regions. Delayed encephalopathy after acute CO intoxication was diagnosed, and the symptoms gradually improved after hyperbaric oxygen therapy (HBOT). This case report demonstrates that generalized chorea may be one of the initial presenting symptoms of delayed encephalopathy after acute CO intoxication. We hypothesize that the generalized chorea in our patient may have been caused by the subcortical white matter lesions, which most likely interrupted the basal ganglia-thalamocortical circuits and that HBOT may be the treatment of choice for such patients.     

Psychoses occurring in a father and his two daughters

Summary Elmira was subjected to the dominance of her grandmother who allowed her very little liberty and restricted her social life. A very strong mutual attachment developed between Elmira and her father. The mental illness of her sister, Dorothy, apparently precipitated Elmira's mental upset. She had a residence in Kings Park State Hospital, admitted there her attachment for her father and dramatized her conflict regarding it by means of his photograph which she carried with her and shich she could not decide whether to keep or to destroy. She recovered from her upset, was discharged and then married very suddenly, because as she stated herself her home life was unsatisfactory. Apparently marriage to her, as to her sister, Dorothy, was the means of escape. The presence of typical manic symptoms, elation, flight of ideas, distractibility, overactivity with recovery and the history of a previous attack with recovery of a manic episode indicate the diagnosis of manic-depressive psychosis; manic type. Nevertheless some schizophrenic features were present in addition as evidenced in the ideation. The prognosis seems more uncertain than in the case of Dorothy.     

Delirium syndrome as a side-effect of lithium in normal lithium levels

Lithium is used with great success in the treatment of manic patients and for prophylaxis of bipolar disorders. There are only few reports about neuropsychiatric side effects at therapeutic serum levels. We report on a 38 year old woman with bipolar disorder who was treated with lithium for 20 years without side-effects. Subsequent to a manic episode, she became disoriented at night and showed marked memory deficits. The patient did not show any neurological or gastrointestinal signs of intoxication. Lithium serum-levels were in therapeutic range. The psychiatric symptoms disappeared when lithium was stopped. We interpret these symptoms as delirant syndrome with pseudo-dementia at therapeutic lithium serum levels. This side-effect must be taken into account even in patients on successful longtime lithium therapy.     

A case of phenytoin intoxication induced by hypothyroidism

A 42-year-old woman who presented phenytoin intoxication induced by acute hypothyroidism was reported. She had a 29-year history of hypothyroidism and a 18-year history of epilepsy. She was treated with phenytoin (PHT) 100 mg, mephobarbital (MPB) 200 mg, valproic acid (VPA) 400 mg and thyroid powder 100 mg daily for 2 years. She had no medical problem until she noticed gait disturbance and diplopia which appeared 1 month after sudden withdrawal of thyroid powder. On admission, she was somnolent and somewhat disoriented. She had nystagmus in horizontal direction of gaze. Her speech was slurred and she could not sit nor stand due to trunkal ataxia. There was prominent intentional tremor in finger-nose test and heel-shin test showed severe ataxia. Blood cell count and blood chemistry examinations were normal. Serum PHT, phenobarbital (PB) levels were elevated as to 26.4, 36.4 micrograms/ml, respectively. VPA level was low. The endocrinological examinations revealed primary hypothyroidism. EEG showed generalized slow background, but cranial MRI, EMG, SEP and ECG were normal. Thyroxine (T4) administration was started soon, and in the course of thyroid hormone replacement, her cerebellar symptoms gradually improved and serum PHT level decreased even to the subtherapeutical level with the same amount of antiepileptic drugs treatment. By the 40th day of admission, thyroid function became normal and cerebellar signs disappeared, however, she needed 200 mg PHT daily to obtain good control of epilepsy. Cerebellar symptoms of this patient were thought to be PHT intoxication rather than ataxia caused by hypothyroidism itself from the viewpoint of clinical manifestations.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reversible choreoathetosis associated with lithium intoxication]

Several reports have been published in the literature of choreoathetosis associated with lithium intoxication, but little is known about choreoathetosis without concurrent antipsychotic treatment. We report a 65-year-old woman with lithium intoxication whose choreoathetosis completely recovered without sequela following decrease of her serum lithium level. She had been treated elsewhere for bipolar II disorder and also for hypertension, chronic hepatitis type C and diabetes mellitus. As she became hypomanic, lithium carbonate at 600 mg/day was commenced, which was increased to 1200 mg/day due to unfavorable therapeutic response. She began to manifest disorientation and abnormal involuntary movement and was therefore referred to our Department of Psychiatry. Her clinical symptoms at admission included consciousness disturbance with marked bilateral symmetrical slow-wave activity in her EEG and choreoathetosis was observed in her face and upper and lower extremities. Cerebellar symptoms were minimal with only mild ataxic gait and finger-to-nose test did not show dysmetria or intention tremor. Her serum lithium level was 3.52 mEq/L, which was clearly in the toxic range. She demonstrated no metabolic abnormalities including hyperglycemia, and was diagnosed with lithium intoxication and treated with water loading and mannitol for forced diuresis. On the 14th day after admission her consciousness disturbance and choreoathetosis resolved, but EEG abnormalities still persisted. On the 23rd day after admission, she was discharged with clinical remission and normal EEG background activity. Although she developed mild renal dysfunction, hemodialysis was not indicated. Hypersensitivity of dopamine receptor in the nigrostriatal pathways may contribute to choreoathetosis in association with the patient's vulnerability. Choreoathetosis can be a sign of lithium intoxication and prompt treatment is required following careful differential diagnosis.     

碳酸锂结合氟哌啶醇致恶性综合征(英文)

一名39岁的女性双相障碍患者因再次出现伴精神病性症状的躁狂发作而住院,总病程20年。用常规剂量的碳酸锂和氯氮平治疗。入院3天后,患者出现攻击行为,并拒绝服药,因而停用氯氮平口服,予氟哌啶醇肌注。3天后,患者出现高热以及其他恶性综合征的表现,如大量出汗,肢体肌肉痉挛、震颤,肌强直以及意识障碍。立刻停用氟哌啶醇和锂盐,对症支持治疗,同时用多巴胺激动剂溴隐亭治疗。恶性综合征的症状在3天内缓解,但精神病性症状依然很严重。继而使用丙戊酸钠和奥氮平治疗,未再出现恶性综合征。又治疗1个月后,患者康复出院。过去有若干个病例也与此类似,这些病例提示抗精神病药物合并锂盐治疗引起恶性综合征的风险可能比单用一种抗精神病药物要高。当然病例报告本身无法证实这一点。     

Lithium treatment of a patient with Addison's disease and affective psychosis

A female patient born in 1941, who suffers from affective psychosis and Addison's disease, first received lithium carbonate in 1983 during a severe, therapy-resistent depression. With lithium treatment she showed a considerable improvement. In the following months, with a daily dosage of 24.4 mmol, the blood lithium levels were between 0.8 and 0.9 mmol/l. One year later she suffered a severe lithium intoxication after a virus infection. Shortly afterwards, she had a manic and then a depressive phase. She was now put on a regimen of with 12.2 mmol lithium carbonate per day, which produced blood levels between 0.3 and 0.4 mmol/l. In the following years, values of about 0.9 mmol/l were observed several times, therapy and clinical condition remaining unchanged. These spontaneous fluctuations of the blood lithium level, a hitherto unreported phenomenon are discussed as a possible cause of the lithium intoxication. The consequences for clinical practice are outlined.     

Lithium intoxication in a patient with severe motor and intellectual disabilities

A severaly retarded 30-year-old woman developed acute lithium intoxication. Since the age of 22, she had been treated with neuroleptics for her aggressive behavior. At 30 years of age, lithium carbonate was added to arrest self-injurious behavior, at an initial dosage of 300 mg/day and a maintenance dosage of 900 mg/day. She subsequently developed anorexia and weight loss, and was admitted to our hospital. After 7 months of lithium therapy, she suddenly had a high fever (38.3 degrees C), diabetes inspidus, severe hypernatremia, and became akinetic and mute. Under the suspicion of lithium intoxication, all medication was discontinued, and mannitol to increase renal lithium clearance. She was given gradually improved over a month, but remained hypothyroid. This case shows the importance of interaction of lithium carbonate and other drugs which may cause lithium intoxication. In patients with severe intellectual disabilities who are unable to complain their symptoms, lithium therapy requires particularly close attention to signs of early toxicity.     

Topiramate monotherapy in the maintenance treatment of bipolar I disorder: effects on mood, weight and serum lipids

Topiramate is a newly developed anticonvulsant agent with possible mood-stabilizing properties. Little is known about the short- and long-term effects of topiramate monotherapy in bipolar disorder. We here present the case of a 60-year-old female bipolar patient who received topiramate alone as maintenance treatment after recovering from euphoric mania. During 7 months, she was free from new manic symptomatology and she was able to reduce her overweight by 16.5 kg. The patient who is known to have a strongly hyperthymic temperament described symptoms of fatigue and sedation and eventually discontinued topiramate monotherapy. When she presented again in our bipolar clinic, severe euphoric mania had developed. After hospitalization, she slowly responded to oral sodium valproate loading plus zotepine. Her weight increased again and so did her triglyceride serum levels. Topiramate treatment and discontinuation did not seem to affect cholesterol serum levels.     

A case of severe parkinsonism associated with short-term treatment with milnacipran

A 51-year-old woman became depressed following the death of her father-in-law. She was given 50 mg of milnacipran a day. One week after starting milnacipran, she developed parkinsonism. The milnacipran was increased to 100 mg/d, resulting in a situation where her symptoms of parkinsonism and depression worsened, which was associated with the reduction of 125I-meta-iodobenzylguanidine (MIBG) uptake. Three hundred milligrams of levodopa plus 30 mg of carbidopa was subsequently added to her medications. However, her symptoms still continued for 2 more weeks. Then the milnacipran was tapered, and she was given fluvoxamine with levodopa plus carbidopa. The parkinsonism and the depression gradually improved within 1 month after starting the regimen of fluvoxamine. The MIBG uptake also recovered (Heart to Lung ratio, 2.1) within 2 months. To our knowledge, this is the second reported case of parkinsonism associated with the use of serotonin noradrenaline reuptake inhibitor. This case showed a transient reduction of MIBG uptake associated with the parkinsonism and depression. Clinicians should be aware that serotonin noradrenaline reuptake inhibitors as well as selective serotonin reuptake inhibitors can cause parkinsonism.     

Partial Recovery from Cortical Blindness Following Monoxide Intoxication

Patients with carbon monoxide (CO) intoxication may show neurological signs such as headache, seizures, extrapyramidal findings, and coma. However, cortical blindness is rare in these cases. This study describes a woman exhibiting confusion and axial rigidity after CO intoxication. Ten days after intoxication, her pupils were isonormocoric and reactive to light. A fundoscopic examination was normal, but visual acuity was light-perception in both eyes. There were diffuse EEG slow waves. Magnetic resonance imaging (MRI) demonstrated bilateral hyperintensity in the basal ganglia. The P100 latencies of visual evoked potentials (VEP) were increased and dispersed. One year later, the patient's visual acuity was almost normal and VEPs showed mild dispersion in P100 latencies. The authors found this case of interest because cortical blindness due to CO intoxication is only rarely seen with a relatively good outcome.     

Partial recovery from cortical blindness following carbon monoxide intoxication

Patients with carbon monoxide (CO) intoxication may show neurological signs such as headache, seizures, extrapyramidal findings, and coma. However, cortical blindness is rare in these cases. This study describes a woman exhibiting confusion and axial rigidity after CO intoxication. Ten days after intoxication, her pupils were isonormocoric and reactive to light. A fundoscopic examination was normal, but visual acuity was light-perception in both eyes. There were diffuse EEG slow waves. Magnetic resonance imaging (MRI) demonstrated bilateral hyperintensity in the basal ganglia. The P100 latencies of visual evoked potentials (VEP) were increased and dispersed. One year later, the patient's visual acuity was almost normal and VEPs showed mild dispersion in P100 latencies. The authors found this case of interest because cortical blindness due to CO intoxication is only rarely seen with a relatively good outcome.     

Susceptibility-weighted imaging findings of subacute delayed carbon monoxide intoxication: a report of five cases

Brain injury from carbon monoxide (CO) poisoning occurs due to tissue hypoxia and direct CO-mediated histotoxicity. Recently developed susceptibility-weighted imaging (SWI) is sensitive for the detection of accumulated hemosiderin and iron secondary to cerebral hemorrhage. Therefore, we hypothesized that SWI may be helpful for identifying petechial hemorrhagic transformation secondary to acute hypoxic damage during subacute CO intoxication. Our case series with subacute CO intoxication revealed that the SWIs of all patients showed low signal intensities in the globus pallidus, representing the accumulation of iron or calcium secondary to hypoxic damage from acute CO intoxication. These results suggest that SWI may be a useful MR technique for illustrating brain damage in subacute delayed CO intoxication.     

A case of Brown-Vialetto-van Laere (BVVL) syndrome in Japan]

Here we report a sixty-year-old woman of Brown-Vialetto-van Laere (BVVL) syndrome in Japan. She had sensorineural deafness, weakness and atrophy of her extremities from 15 years of age. Her neurological symptoms slowly progressed. She first visited our hospital in 1993 when she was 49 years old. At that time, she had distal muscle weakness and atrophy of the four extremities and bulbar palsy. Deep tendon reflexes were absent and the plantar toe reflex was flexor. EMG revealed neurogenic changes and the nerve conduction studied were normal. The vital capacity was marked decreased. On August 10, 2003, she was admitted to our hospital because of CO2 narcosis. She had III, VII, X, XI, XII cranial nerve palsy, distal muscle weakness and atrophy of the four extremities. From her neurological symptoms and signs, we made a diagnosis of BVVL syndrome. MRI revealed no high signal in pyramidal tract by FLAIR image. ABR showed no response, and VEP demonstrated delay of the P100. She was intubated, and was attached to a respirator to improve her CO2 narcosis. After treatment she improved and did not need to be assisted by a respirator during daytime. During night time, she had apnea, and her blood gas showed the retention of CO2, and she still required the respiratory assistance during her sleep. This is the first report of BVVL syndrome in Japanese literature.     

MRI findings of brain-stem tuberculoma in a case of tuberculous meningitis]

A 54-year-old woman developed headache and slight fever. When she consulted a physician, she could not move either of her eyes to the right. Cranial CT scan revealed no significant findings. Lumbar puncture was performed and CSF examination showed the cell count of 10,304/mm3, glucose level of 10 mg/dl, and total protein value of 270 mg/dl. Her symptoms and laboratory findings suggested meningitis and she was admitted to our hospital. Neurological examination revealed bilateral dilated pupils with sluggish light reflex, right gaze palsy, and hypesthesia of the left side of her face. A diagnosis of tuberculous meningitis was established by a positive test for acid-fast bacillus in CSF, and anti-tuberculous therapy was started at once. One month after the onset of symptoms, her main complaints were double vision and cerebellar ataxia. Both CT and MRI revealed a right brain-stem lesion. Pre-contrast CT could not clearly visualize the lesion but with contrast medium a homogeneously-enhanced circular lesion was shown. MRI on T2WI demonstrated the right brain-stem lesion to have a central bright core with hypointense periphery, which in turn was surrounded by hyperintensity. The lesion appeared isointense with cerebral white matter and the "central bright core" area was demonstrated to be slightly hypointense on T1WI. On post-contrast T1WI (with Gd-DTPA), the lesion showed strong homogeneous enhancement. The CT and MRI findings indicated a brain-stem tuberculoma, which was regarded as the cause of the ocular movement paralysis and cerebellar ataxia. As the clinical symptoms gradually resolved with anti-tuberculous treatment, the MRI appearance of the lesion also improved.(ABSTRACT TRUNCATED AT 250 WORDS)     

Safety of fluoxetine treatment in a case of acute intermittent porphyria

Acute intermittent porphyria (AIP) is a metabolic disease characterized by recurrent attacks of neurological and psychiatric dysfunction. It is a rare disorder of heme metabolism that usually presents with abdominal pain, gastrointestinal symptoms and autonomic nervous system disturbances. Exposure to certain drugs, dieting, starvation and infection during pregnancy may precipitate AIP attacks. Psychiatric manifestations of AIP include mood changes, organic brain syndrome and psychosis. Here, we present a 21-year-old female patient with AIP and major depression. She had a caesarean section under general anesthesia with pentothal and her recovery time from anesthesia took longer than usual. She had a blood transfusion because of severe anemia following the operation. Three days after her discharge she was readmitted to the hospital with confusion and seizure. It was her first AIP attack and it started 6 days after caesarean section. Two months after her first attack, we saw her for anxiety and depressive symptoms. She was in severe anxiety and depression and she was put on fluoxetine (20 mg/day liquid form). Following the treatment she did not develop any other porphyria attack. Her symptoms vanished and she improved functionally. She stayed on fluoxetine for 6 months without any new AIP attack. Despite limited data regarding fluoxetine therapy in porphyria patients, it seems to be safe for the treatment of depressive and anxiety symptoms in these patients.     

Videofluorographic evaluation of dysphagia in a patient with myasthenia gravis]

A 64-year-old woman with myasthenia gravis (MG) presented with isolated bulbar symptoms. Two years earlier, she had developed neck weakness, diplopia, and ptosis and was diagnosed with MG. Extensive thymectomy was performed, and she was treated with predonisolone (PSL). The neck weakness, diplopia, and ptosis improved over a 2-year period. However, dysphagia developed, and her voice took on a nasal tone that did not improve subjectively even after administration of 10 mg of edrophonium chloride (EC). We then performed videofluorography (VF). After consumption of 10 ml of liquid barium and 8 g of corned beef hash, she attempted to swallow, but the residue remained in the valleculae and the piriform fossa. After the EC injection, her dysphagia on ingestion of corned beef hash improved; however, there was slight subjective improvement in swallowing. Drinking of liquid barium resulted in some residue with slight improvement of dysphagia. After treatment with 70 mg of PSL for 4 weeks, VF showed improvement of dysphagia. Thus, VF, particularly during consumption of solid food, with EC administration is helpful in evaluating bulbar symptoms in patients with MG.