Utilizing Cerebral Perfusion Scan and Diffusion-tensor MR Imaging to Evaluate the Effect of Hyperbaric Oxygen Therapy in Carbon Monoxide-induced Delayed Neuropsychiatric Seqeulae- A Case Report and Literature Review.

PURPOSE: Detection of regional cerebral blood flow (rCBF) and/or brain magnetic resonance imaging (MRI) has been used to investigate functional defect of brain caused by carbon monoxide (CO) poisoning. In this report, we attempted to demonstrate the correlation of changes in brain singlephoton emission computed tomography (SPECT) and diffusion-tensor MR image (DTI) with functional improvement of severe delayed neuropsychiatric sequelae (DNS) after CO intoxication during the treatment of hyperbaric oxygen therapy (HBOT). CASE REPORT: The patient had normal activities of daily life after he recovered from acute CO poisoning. One month later, he presented symptoms of declined cognitive functioning, aphasia, apraxia, dysphagia, muscle rigidity, urine and fecal incontinence. After one course of HBOT, these symptoms improved significantly and the patient could regain most of his previous functioning. The patient's improvement was evidenced by increased rCBF in Brodmann areas 7, 8, 11 and 40, as well as higher mean fractional anisotropy (FA) value of DTI. CONCLUSION: Although the efficacy of HBOT in DNS patients is still needed to be evaluated in large clinical study, these data suggest that HBOT may be the choice to improve DNS efficiently and shorten the duration of suffering with favorable outcome.

[A 78-year-old female patient with dizziness, apraxia and seizure under proton pump inhibitor therapy]. / 78-jährige Patientin mit Unwohlsein, Schwindel, Apraxie und Krampfanfall unter Protonenpumpeninhibitortherapie.

We report about a female patient with severe hypomagnesemia under therapy with proton pump inhibitors (PPI) who presented with a cerebral seizure. Chronic use of PPIs can cause hypomagnesemia. Because of mostly unspecific symptoms which become symptomatic only with severe deficiency, the disease pattern is underdiagnosed. Hypomagnesemia is currently coming increasingly more to the forefront of medical literature.

[Acute lithium intoxication. Apropos of a case]. / Intoxication au lithium. A propos d'une observation.

Lithium salts are used in psychiatry for the treatment of bipolar depression. An overdose is potentially serious, sometimes fatal, and the clinical signs are variable. The authors report the case of a 70 year old man. He had a recent history of a transient ischaemic attack and was admitted to the coronary care unit for bradycardia at 35-40 BPM and episodes of sino-atrial block with a clinical presentation suggestive of a stroke. The diagnosis of lithium intoxication was made accounting for the present hospital admission and for the previous neurological event which had been diagnosed as a transient ischaemic attack. The difficulty of diagnosis of this condition is discussed.

Meige syndrome with apraxia of lid opening after the discontinuation of sulpiride treatment.

We report a case of Meige syndrome with apraxia of lid opening that lasted for about seven months after discontinuation of sulpiride treatment. To our knowledge, this is the first report demonstrating that Meige syndrome with apraxia of lid opening is induced by sulpiride, and that the condition persists.

"Apraxia of eyelid opening" induced by levodopa therapy and apomorphine in atypical parkinsonism (possible progressive supranuclear palsy): a case report.

We report a female patient in whom so-called apraxia of eyelid opening (AEO) developed after the onset of possible progressive supranuclear palsy (National Institute of Neurological Disorders and Stroke criteria) and the introduction of antiparkinsonian medications including levodopa. Although parkinsonian symptoms responded poorly to levodopa, AEO worsened after increasing levodopa dosage and disappeared when levodopa was discontinued. Later, a dose of apomorphine widely accepted for acute tests had no significant effect on limb motor activity but induced AEO. Overall, these observations are grounds for thinking that AEO developing in the course of parkinsonism may be either disease- or drug-related. The possibility of manipulating dopaminergic treatment should always be considered when dealing with AEO associated with parkinsonism.

Blepharospasm and apraxia of eyelid opening in lithium intoxication.

We present the case of a 72-year-old woman with a history of a bipolar mood disorder chronically treated with lithium. Upon having the dose increased, she developed an acute confusional state accompanied by blepharospasm (BS) and apraxia of eyelid opening. Gait instability with frequent falls, pyramid tract signs, and postural tremor in both hands were also evident. On withdrawing lithium, symptoms remitted within 2 weeks. This patient illustrates that BS and apraxia of eyelid opening may be triggered by lithium overdose. Our case warrants the inclusion of lithium in the list of drugs liable to induce such movement disorders.

[Reversible neuropsychiatric side effects of lithium with normal serum levels. A case report]. / Reversible neuropsychiatrische Nebenwirkungen von Lithium bei normalen Serumspiegeln. Eine Fallbeschreibung.

Lithium therapy in patients with manic depressive disorder occasionally causes neuropsychiatric side effects even at therapeutic serum levels. Those lithium-induced symptoms can be polymorphous and may be hard to differentiate from other disorders and from other drugs' side effects. We report the case of a 56-year-old woman with manic-depressive illness, who developed neuropsychiatric side effects from lithium prophylaxis at therapeutic serum levels. The symptoms included disorientation, aphasia, ideatoric apraxia, parkinsonism, restlessness and severe sleep disorder. In contrast to previous reports, the casual role lithium was underscored by symptom increase after lithium re-exposure at therapeutic serum levels. The patient recovered completely after cessation of the lithium prophylaxis.

[Gesture apraxia disclosing carbon monoxide poisoning]. / Apraxie gestuelle révélant une intoxication oxycarbonée.

A seventy year old right handed woman presented progressive limb apraxia and headache due to carbon monoxide poisoning. Thereafter, when in hospital for one week, she developed akinetic mutism, coma and died. Limb apraxia has been rather uncommonly reported in carbon monoxide poisoning. The akinetic mutism observed after the patient had been removed from intoxication could be analysed as a delayed encephalopathy related to a chronic carbon monoxide poisoning.

Dysarthria and apraxia of speech associated with FK-506 (tacrolimus).

The immunosuppressive agent FK-506 (tacrolimus) is one of the agents most commonly used to prevent rejection after liver transplantation. Neurologic toxicity related to FK-506 has been reported, including speech disorders; however, a detailed analysis of the speech disorder associated with use of FK-506 has not been presented. Herein we describe a patient who exhibited mutism, then severe apraxia of speech with a concomitant hypokinetic, spastic, and ataxic dysarthria after administration of FK-506. His residual mixed dysarthria, without radiographic evidence of a structural lesion, suggests dysfunction of one or more neurochemical systems. The pathophysiologic mechanisms underlying this intriguing entity remain obscure.

Intranasal butorphanol-induced apraxia reversed by naloxone.

Intranasal butorphanol is an opioid agonist-antagonist that is effective for the treatment of acute pain. Common adverse effects associated with the agent are somnolence, dizziness, nausea, and vomiting; they are readily reversed with naloxone. A patient developed signs and symptoms consistent with apraxia after a single dose of intranasal butorphanol. She was mentally alert, but she was unable to move or speak despite normal muscle tone and reflex movements. When she attempted to speak she had no voluntary control. At the emergency room she was administered naloxone 2 mg intramuscularly, which resulted in complete reversal of the symptoms in a short time. No other published cases describe these findings with butorphanol. Health care professionals should be aware that patients who are prescribed intranasal butorphanol, even in typical doses, may be at risk for such a reaction. This is important because, unlike the injectable formulation, the intranasal product is primarily used in the outpatient setting.

[Speech apraxia in dialysis-associated aluminum encephalopathy]. / Sprechapraxie bei dialyseassoziierter Aluminiumenzephalopathie.

A 57-year-old man on long-term renal dialysis presented with speech dyspraxia, a symptom characteristic of early aluminium encephalopathy. Once fully developed, this condition has a poor prognosis despite deferoxamine (DFO) treatment.

Aphasia, apraxia and neurogenic stuttering as complications of metrizamide myelography (speech deficits following myelography).

Aphasia following metrizamide myelography has been reported infrequently. During a seven-month period, we examined two patients who developed Broca's aphasia, apraxia of speech, oral-buccal-facial apraxia and neurogenic stuttering after intrathecal metrizamide administration. In each case, focal neurologic deficits were accompanied by clinical, electroencephalographic and radiologic signs of generalized neurologic disease. Serial speech and language evaluations initially revealed severe deficits that were largely resolved by the third day post-myelography. Out-patient follow-up examinations demonstrated persistence of mild speech and language abnormalities in each case. Our findings suggest that metrizamide may cause longlasting neurologic dysfunction.

[Various rarely encountered adverse effects and complications of psychopharmacotherapy]. / O nekotorykh redko vstrechaiushchikhsia pobochnykh éffektakh i oslozhneniiakh psikhofarmakoterapii.

Nine patients are described in whom psychopharmacotherapy was associated with the development of rare complications in the form of the syndrome of cortical disturbances, psychosensory disorders and toxic polyneuropathy. All patients presented residual organic insufficiency of the CNS, with some of them exhibiting endocrine-metabolic disorders as well.