[Memory symptom exaggeration in a patient with progressive multiple sclerosis outside any medico-legal context]. / Exagération de symptômes mnésiques hors contexte médicolégal chez un patient atteint de sclérose en plaques.

INTRODUCTION: Memory symptom exaggeration or malingering in the forensic neuropsychological evaluation of well-documented brain pathology is seldom described. For some, documented neuropathology and malingering are considered to be mutually exclusive. CASE REPORT: We report an original clinical observation of an amnesic factitious disorder in a patient with progressive multiple sclerosis. This patient, who was seen for a routine comprehensive neuropsychological evaluation, demonstrated a severe memory encoding deficit in a classical standard episodic memory test. This amnesic syndrome was not in agreement with the neurological condition where deficits in retrieval memory processes are essentially observed. Moreover, his performance at two symptom validity tests fell below the admitted cut-off scores. In fact, the patient obtained an accuracy score of 3 (cut-score<10) in the Rey's 15-Items Test, a well known malingered amnesia measure. His performance in the 21-Items Test French adaptation was well below the proposed cut-off score of 15/21 and inferior to the results obtained by an Alzheimer patients group (n=30). A clinical approach of memory symptom exaggeration is described. We discuss the diagnosis of this false disorder. CONCLUSION: This case report demonstrates unequivocally that memory symptom exaggeration or malingering can and does occur in patients seen without litigious contexts and who have a well-documented neurological pathology. Failure to address malingering may compromise neuropsychological clinical findings. Nevertheless, there is a lack of up-to-date standard French-language documentation in this topic.

[Lack of sensitivity to per-anesthetic malignant hyperthermia in 32 patients who developed neuroleptic malignant syndrome]. / Absence de sensibilité à l'hyperthermie maligne peranesthésique chez 32 patients ayant développé un syndrome malin des neuroleptiques.

The aim of this study was to verify whether a relationship exists between neuroleptic malignant syndrome (NMS) and anaesthetic-induced malignant hyperthermia (MH) or not. The in vitro halothane-caffeine tests were performed on muscle tissue obtained from 32 patients with documented NMS episodes. The diagnosis of NMS relied on Levenson's criteria. The results, expressed in accordance with the criteria of the European MH Group, defined 29 subjects as MH non-susceptible. Three patients were classified as MH equivocal. These findings demonstrate the lack of any link between NMS and MH. Therefore, patients with a history of NMS are not likely to be at risk of developing MH and special measures against MH are not required for anaesthesia in these patients.

[Cerebellar syndrome after carbon monoxide poisoning. Magnetic resonance imaging and single photon emission tomography]. / Syndrome cérébelleux après intoxication oxycarbonée. Imagerie par résonance magnétique et tomographie d'émission monophotonique.

A 19-year-old woman presented with severe carbon monoxide poisoning resulting in coma, brain stem signs, cerebellar syndrome, anterograde memory disorder and some frontal signs. Nine years later, generalized seizures appeared. At the age of 31, the cerebellar syndrome and memory disorders persisted. MRI showed cerebellar and internal temporal atrophy with high-intensity signals, and hippocampal and callosal atrophy. SPECT (Xe133) showed a low cerebellar blood flow.

Sodium lactate reversal of electrophysiological effects of imipramine in guinea-pig ventricular myocardium.

Overdose cardiac effects of imipramine are due to fast Na channel blockade and are clinically reversed by administration of sodium lactate which induces alkalosis (about pH 7.50) and hypernatremia (about 8 mM). The mechanisms of this beneficial effect of Na lactate were explored in vitro on guinea-pig ventricular myocardium using the microelectrode technique. The time-course effects of the clinically relevant concentration of 10 microM imipramine on action potential characteristics were examined at pH 7.20 and pH 7.50. To test whether alkalinisation per se is important or whether an increase in Na concentration plays a major role in the reversal effect, preparations were exposed to increasing concentrations (1, 3, 10, 30, 100 mM) of either Na lactate, bicarbonate or chloride in the absence or in the presence of 10 microM imipramine at pH 7.50. The influence of elevating osmolality was evaluated with equivalent concentrations of sucrose. Imipramine alone significantly depressed Vmax and shortened action potential duration at all phases of repolarisation. All three high sodium solutions reversed imipramine effects. However the reversal effect was already obvious with 10 mM Na lactate and 10 mM NaHCO3 but not 10 mM NaCl. Osmolality did not reverse the imipramine-induced Vmax depression. The results suggest that at the clinically relevant 10 mM concentration, sodium lactate and bicarbonate may displace imipramine from its receptor site on the Na channel by causing alkalosis at the membrane level without profoundly affecting the driving force of the Na current, whereas at the upper concentrations, the increase in Na ion concentrations is predominantly involved in the reversal of imipramine effects.

Lone atrial fibrillation and stroke.

We studied 21 consecutive patients from the Lausanne Stroke Registry, who had first-ever ischemic stroke and lone atrial fibrillation, with a standard protocol of investigations including brain CT, and non-invasive cardiac and arterial tests. Rarity of associated risk factors and extracranial; arterial disease, presence of distal intracerebral occlusions on early angiography, and topography of cerebral infarct suggested that cardioembolism was the cause of stroke, though echocardiographic evidence for an atrial thrombus was uncommon. There was no recurrence during a post-stroke 14-day phase, during which anticoagulant and antiaggregant therapies were systematically avoided. Though low, the main risk of stroke recurrence was 0.99 per 100 patient-years during a mean follow-up period of 4.8 years, including a mean duration of anticoagulant therapy of 2.3 years in 18 patients. On the other hand, no death, severe cardiac events, or disabling anticoagulation-related hemorrhages occurred.

The association between the neuroleptic malignant syndrome and malignant hyperthermia.

The neuroleptic malignant syndrome (NMS) is an uncommon but dangerous complication of treatment with neuroleptic drugs. A primary defect in skeletal muscle has been suggested in view of similarities in the clinical presentations of NMS and anaesthetic-induced malignant hyperthermia (MH). The in vitro halothane-caffeine contracture tests are the most reliable method of identifying individuals susceptible to MH. The aim of this study was to define if a relationship exists between NMS and MH susceptibility. Hence, the in vitro halothane and caffeine contracture tests were performed on muscle tissue obtained from eight NMS, ten MH-susceptible and ten control patients. The results, which are expressed in accordance with the criteria of the European MH Group, defined the eight NMS subjects as MH non-susceptible. The response to halothane and caffeine exposure of skeletal muscle from NMS and control subjects was the same and significantly different from that of muscle from patients susceptible to MH. Furthermore, muscle from subjects in NMS and control group responded similarly to increasing concentrations of chlorpromazine. These results do not point towards an association between NMS and MH.