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Delirium, also known as acute confusional state, is a common reversible organic psychiatric syndrome. This paper focuses on toxic delirium associated with prominent paroxysmal electroencephalogram (EEG) dysfunction occurring in nonepileptic patients. Our data derive from observations in two conditions, viz., delirium induced by hypnosedative drug withdrawal and confusion activated by psychotropic drug overdosage. It is suggested that in these conditions, delirium represents a generalized symptomatic nonconvulsive epileptic state following a transient transmitter dysfunction. Dramatic relief of both clinical and EEG dysfunction by intravenous benzodiazepines is reported in detail. Finally, the informative value of the EEG in the differential diagnosis of acute confusional states is emphasized.

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Lead levels in the nervous system of rats intoxicated for 8 months by lead acetate (0.2% in drinking water) varied according to the region: the lowest levels were observed in sciatic nerve and the highest in hippocampus and cerebral neocortex, while intermediate levels were observed in pons medulla, cerebellum, midbrain, hypothalamus and striatum.

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During acute intoxications, the first EEG may show persistence or abolition of cerebral activity, but the possibility of recovery after isoelectric tracing in toxic comas must be emphasized. EEG patterns frequently suggest the probability of hypnotic tranquilizer poisoning; 4 types of EEG are encountered corresponding to different grades of toxic coma. Recurrent periods of electrical silence alternating with bursts of activity are habitually recorded in carus comas with hypothermia due to acute barbiturate intoxication, with good prognosis. The possibility of a neurological disturbance associated with drug overdose must be raised whenever an asymmetric tracing is encountered. Serial recordings may detect complications such as: a localized lesion, anoxia or, very rarely, typical paroxysmal abnormalities reappearing in comitial patients before emergence from a toxic coma. Paradoxical monomorphic delta activity corresponding to improvement must not be considered as an aggravation. Peculiar EEG findings occur after oral trichlorethylene poisoning, with temporary clinical deterioration and intermittent periods of electrical silence; recovery is possible. An alpha-like pattern after cardiac arrest of toxic origin has a poor prognosis. The appearance of alternating patterns suggests the development of irreversible brain damage.

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EEG, EMG and clinical correlates of myoclonus due to poisoning are reviewed. The authors propose a classification into two groups. I. Sporadic diffuse asynchronous asymmetrical myoclonic jerks, responding to treatment. These states are encountered essentially in acute intoxication by vegetal poisons (strychnine), rodenticide (chloralose) and various medications (isoniazide, tricyclic antidepressant agent, lithium). These transitory manifestations are functional and prognosis is favourable. II. Subintrant generalized synchronous symmetrical myoclonus, uncontrolled by therapeutics. These myoclonus states observed over weeks or months are frequently consecutive to organic injuries due to direct toxicity (methylbromide) or after anoxia (toxic cardiac arrest). EEG and EMG correlations are very inconstant in both groups. EEG abnormalities are a sign of cortical and/or subcortical dysfunction. Normal EEG suggests a disease of the lower central nervous structure (brain stem, medulla). Chronic bismuth and dialysis encephalopathies are also related. Withdrawal syndrome with myoclonus jerks after sudden cessation of barbiturate or benzodiazepine long-term treatment is mentioned.

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Withdrawal syndromes after discontinuation of benzodiazepine or meprobamate administration are rarely observed, in spite of the large number of prescriptions given. Similar manifestations are noted as after barbiturate withdrawal, and appear 1 to 10 days after sudden interruption of prolonged treatment at high doses. The 6 cases reported include 4 patients with withdrawal syndromes after benzodiazepines (diazepam, oxazepam, lorazepam) and 2 after meprobamate. No evidence of epilepsy was found in the patients, who were hospitalized for treatment after suicidal attempts, or medication overdosage (phenothiazine) in one case. Withdrawal symptoms appeared between the 2nd and 7th day with confusion and/or generalized convulsions and paroxystic changes with slow spike-wave type on EEG tracings. In such cases, precise information must be obtained about previous medication in order that it may be readministered and the diagnosis of epilepsy avoided in patients with withdrawal symptoms.

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The value of electroencephalographic recordings during eserine treatment for overdosage with anticholinergics is discussed, based on the results obtained in 6 cases. The results were spectacular in three cases, and a partial improvement was noted in one other case (suicide attempts with overdoses of atropine compounds), but only a slight effect was observed in two patients (with overdose of neuroleptics). Three points have to be underlined concerning the E.E.G. recordings: --eserine did not cause supplementary E.E.G. changes;--with eserine, the paroxystic abnormalities observed during overdoses of atropine compounds and amitriptyline rapidly disappear;--with mixed overdoses (atropine, barbiturates, or minor tranquillizers), eserine has no effect against non-anticholinergic products. Therapy with eserine, however, is still limited in its indications because of its short period of activity, its side-effects, and the possible risks of cardiac or convulsant complications.

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During last 7 years, 13 cases of acute ethylene glycol poisoning have been observed with 4 fatal outbreaks. All cases--except one--were accidental. Six patients had drunk a mixture of antifreeze in water as they were lost in a desert. A patient who had taken 970 ml of ethylene glycol survived. In one case, death was due to irreversible brain damage; two other fatalities occurred from cardiorespiratory distress. CNS involvement was noticed in 8 cases and acute renal failure-constantly controlled-occurred in 9 patients. Post mortem examination has shown bi-refringent calcium oxalate crystals in both kidney and brain. Specific treatment with ethanol has been performed in 3 cases with ingestion of large amounts of toxic who were seen before definitive renal lesions have occurred. Emphasis is placed in symptomatic treatment including gastric lavage, extrarenal epuration and conservative management.

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