Psoriasis and polyneuropathy. Three case histories.

Neurophysiological examination of 3 psoriasis patients with symptoms of polyneuropathy revealed varying degrees of both sensory and motor nerve affection and indicated nerve fibre loss as well as demyelination. Previous reports have suggested a connection between peripheral nerves and psoriasis.

Imipramine treatment in diabetic neuropathy: relief of subjective symptoms without changes in peripheral and autonomic nerve function.

The effect of imipramine on symptomatic peripheral diabetic neuropathy in 9 patients was examined in a double-blind cross-over study against placebo. The dose of imipramine was adjusted to yield optimal plasma levels of imipramine plus desipramine of 300-750 nM. Imipramine had a clear beneificial effect on the symptoms of the neuropathy, whereas no changes in a range of neurophysiological measurement was detected. Despite some adverse effects, especially of an anticholinergic nature, the patients generally preferred imipramine to placebo.

Peripheral nerve function during hyperglycemic clamping in healthy subjects.

The influence of hyperglycemia with physiological hyperinsulinemia on peripheral nerve function was studied in 10 non-diabetic subjects. Blood glucose concentration was raised from 3.8 +/- 0.2 mmol/l (mean +/- SEM) to 17.1 +/- 1.4 mmol/l (mean +/- SEM) within 15 min and kept at this level for 120 min by intravenous glucose infusion. Sensory and motor nerve conduction velocity, and distal motor latency in the ulnar nerve were determined before, immediately after induction of hyperglycemia, and again after 120 min of hyperglycemia. Mean sensory nerve conduction velocity increased from 57.7 m/s to 59.5 m/s (P less than 0.005) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia mean sensory nerve conduction velocity was 59.6 m/s (P less than 0.05). An insignificant increase was seen in motor nerve conduction velocity during hyperglycemia. Mean distal motor latency decreased from 3.1 ms to 3.0 ms (P less than 0.025) immediately after induction of hyperglycemia, and after 120 min of hyperglycemia distal motor latency was 2.9 ms (P less than 0.05). We conclude that short term hyperglycemia with physiological hyperinsulinemia seems to increase sensory nerve conduction velocity and decrease motor latency.

Facial clefts in sibs and children of epileptic patients.

The prevalence of facial clefts in sibs and children of 2,072 epileptics ascertained in a defined region was determined by record linkage with a national cleft register, which also provided expected figures. Observed/expected ratios were increased only for cleft lip with or without cleft palate if the mother had manifested epilepsy: it was 4.7 when anticonvulsants were given before and during pregnancy, 2.7 in cases with no treatment, and zero in children born prior to maternal epilepsy. Children of epileptic men and sibs of epileptics showed no increase. The prevalence of isolated cleft palate was not above expectation in any group.

Obstructive sleep apnea syndrome caused by oral cyst: a case report.

A 47-year-old man with a typical obstructive sleep apnea syndrome (OSAS) secondary to a large oral cyst is reported. Although the patient also had a nasal septum deviation with narrowed air passage, removal of the cyst resulted in complete and lasting relief from clinical symptoms despite persisting sleep apnea and unchanged arousal reaction in the EEG. The concurrent mechanisms of OSAS in the present case are discussed, and the importance of searching for a curable underlying disorder in clinical overt OSAS is emphasized.

Overdosage of antidepressants: clinical and pharmacokinetic aspects.

Twenty-nine cases of self-poisoning with antidepressants (amitriptyline, imipramine, clomipramine, maprotiline, doxepine, nortriptyline, opipramol) were examined by frequent observation of CNS effects, heart rate, blood pressure and standard ECG, 24h-ECG-monitoring, measurement of systolic time intervals, EEG recordings and frequent measurement of serum levels of antidepressants and primary metabolites. None of the patients died. Maximum total serum antidepressant level (parent compound + desmethyl metabolite) ranged from 20 to 2200 micrograms/l, with concentrations above 500 micrograms/l in 11 cases. The serum amitriptyline concentration remained high for 3-4 days in some of the severely intoxicated patients and the decay curves were compatible with partly saturated elimination. A degree of unconsciousness and the occurrence of excitation and hallucinations were generally seen in cases with total serum antidepressant levels above 500 micrograms/l. Grand mal seizures occurred more frequently at high antidepressant levels, but could not be predicted from the EEG recordings. Increased heart rate and prolonged QRS- and QTc-intervals were significantly correlated with the total serum antidepressant level. 24 h-ECG-monitoring revealed no serious arrhythmias or instances of heart block. Hypotension was only seen initially in few patients. Systolic time interval measurements showed changes suggesting impaired myocardial performance (elevated PEP/LVET ratio) at intermediate (60-500 micrograms/l) but not high (greater than 500 micrograms/l) total serum antidepressant levels. Measurement of serum concentration in antidepressant intoxication is important for identification of patients with high serum levels and the corresponding risk of developing toxic reactions, and to exclude patients with a low concentration who do not require intensive observation.

Facial clefts among epileptic patients.

Anticonvulsants have been suspected of teratogenicity, with facial clefts being the malformation most frequently associated with maternal anticonvulsant therapy. Paternal epilepsy has also been suggested as a factor in the genesis of birth defects, including facial clefts. An association between epilepsy per se and facial clefts would be reflected in a higher facial cleft prevalence among epileptics, and consequently result in an increase of such malformations among their children. The prevalence of facial clefts was determined in an unselected group of 3,203 epileptic probands: their personal data were cross-matched with a complete file of Danish facial cleft patients born between 1934 and 1977. Eleven epileptic probands had a facial cleft, which is twice the expected number. The increased prevalence of cleft defects among epileptics could partly explain why more of their children have facial clefts.

'alpha pattern coma' following cerebral anoxia.

In 30 patients, who were all comatose as a result of cerebral anoxia after cardiac arrest, at least one EEG with activity in the alpha frequency range was recorded. Regionally the activity of the above mentioned characteristic was often diffusely distributed or most pronounced occipitally, whereas a tendency to affect other regions was rarely observed. In 50% of the patients, where more than one EEG was recorded, the 'alpha' rhythm was still present in the following record. Only one of the patients survived, and even so, with considerable mental defects. In 4 patients the level of consciousness improved, but 3 of them never reached a definite level of cortical function and died as a result of cerebral anoxia.

Psychomotor epilepsy and psychosis. III. Social and psychological correlates.

In a controlled investigation of paranoid hallucinatory chronic or episodic epileptic psychoses, the social data, psychopathological symptoms and the psychological test findings (WAIS, Rorschach, object-sorting, proverb-interpretation and the Stroop test) were analyzed in order to delineate the characteristics of the psychotic syndrome and to evaluate the significance of organic etiological factors. The study comprised 45 patients with complex partial epilepsy followed by psychosis after median 23 years, and 34 control patients with the same type of epilepsy of median 30 years' duration. Among the psychotic symptoms, simple, mostly empathizable persecutory delusions and auditory hallucinations predominated. The affect tended to remain appropiate, and autistic traits were uncommon. In accordance with this finding of a relatively circumscribed psychotic personality disturbance, psychotic test indicators were infrequent in the psychological tests, the Rorschach test 28%, and the object-sorting test 18% of the cases. The poorer test performances in the WAIS and the Stroop tests, and the preponderance of organic Rorschach test signs in the psychotic group indicate that organic cerebral damage is of etiological significance in paranoid epileptic psychosis.

Sphenoidal electrodes: their use and value in the electroencephalographic investigation of complex partial epilepsy.

The diagnostic value of sphenoidal electrode EEG recordings in patients with seizures characteristic for epilepsy with complex partial symptomatology was assessed in a study comprising 404 patients; 71.3% of the patients had seizures with automatisms and amnesia, and 28.7% had psychic seizures with subjective phenomena such as hallucinations and illusions. A total of 59.6% of the patients had diagnostic EEG changes in routine waking or sleep EEG. In sphenoidal EEG recording including thiopenthone activation, diagnostic changes were found in 40.5% of the patients without specific changes in waking or sleep EEG, the chance of a positive finding being more than five times higher in patients with automatisms than patients with psychic seizures. Apart from cases where surgical treatment of temporal lobe epilepsy is considered, sphenoidal electrode EEG recording, including intravenous thiopenthone activation, should be performed in patients with seizure phenomena raising suspicion of epilepsy with complex partial symptomatology but where waking and sleep EEGs fail to demonstrate specific abnormalities.

Psychomotor epilepsy and psychosis. I. Physical aspects.

In a controlled investigation the clinical findings in 96 patients with paranoid/hallucinatory psychosis and partial epileptic seizures with complex symptoms, were compared with the findings in 96 control patients with the same type of epilepsy without psychosis of median 24 years' duration. The median age at onset of psychosis was 34 years, after epilepsy of median 21 years' duration. The seizure frequency of complex, partial seizures was significantly lower in the psychotic group, while the frequency of generalized seizures did not differ. A significant preponderance in the psychotic group of left-handed patients, etiological factors and neurological signs reflecting organic damage, and seizures of automatic behaviour indicates that epileptic psychoses are caused by structural lesions affecting the deep parts of the temporal lobe.

Psychomotor epilepsy and psychosis. II. Electroencephalographic findings (sphenoidal electrode recordings).

The EEG findings in waking, sleep, and sphenoidal electrode recordings in 96 patients with partial epileptic seizures with complex symptoms, who, after a median interval of 18 years developed paranoid/hallucinatory psychosis, were compared with the findings from a group of patients without psychosis, who had had the same type of epilepsy in median 24 years. There were no significant differences between the two groups with regard to median age at onset of epilepsy or complex partial seizures, age, or duration of epilepsy at time of examination. The psychotic patients had a significant preponderance of temporal medio-basal spike foci, recorded on the sphenoidal electrode, indicating deep temporal lobe dysfunction as an important factor in the pathogenesis of psychosis. A significant higher frequency of bilateral and multiple spike foci, together with a significant frequency of slow-wave admixture to the waking background EEG activity, indicated more extensive and severe epileptogenic lesions in the psychotic patients. There was no correlation between psychosis and unilateral EEG-foci in either temporal lobe.

Electroencephalographic prediction of anoxic brain damage after resuscitation from cardiac arrest in patients with acute myocardial infarction.

The short-term prognostic value of routine electroencephalography (EEG), carried out on the days after cardiac arrest, was evaluated in a consecutive study of 185 patients with acute myocardial infarction together with an episode of clinical cardiac arrest. The individual EEGs were classified on a 5-grade scale. Of the 89 patients who survived, 18 had signs of anoxic brain damage; 96 patients died, 76 as a result of cerebral anoxia. Only 2 patients survived out of the total of 72 for whom the first EEG was classified as grades III--V. The EEGs of both these patients were recorded within a few hours after the cardiac arrest. None of the patients with an EEG of grade I died of cerebral anoxia, while all degrees of brain damage were otherwise observed in connection with EEGs of both grades I and II. It is concluded that an EEG of grades III--V indicates a fatal outcome, provided it has been recorded more than 24 hours after the cardiac arrest. A grade III--V EEG that is recorded within 24 hours after a cardiac arrest should be repeated some days later. It is not possible, on the basis of a single EEG, to predict the extent of the anoxic brain damage.