Hypouricemia in chronic schizophrenic patients with polydipsia and hyponatremia.

BACKGROUND: Polydipsia is a common disorder among chronic psychiatric patients. Impaired water excretion due to enhanced action and secretion of antidiuretic hormone has been reported in hyponatremic patients with polydipsia. Hypouricemia coexisting with hyponatremia is a hallmark of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The transitory coexistence of hyponatremia and hypouricemia in patients with polydipsia-hyponatremia syndrome is presented. METHOD: We examined the course of hypouricemia and hyponatremia in three schizophrenic patients with a long-standing history of polydipsia resulting in the presence of these conditions. In addition, we investigated the renal clearance of uric acid in five polydipsic patients without a previous history of water intoxication or hyponatremia (simple polydipsia). RESULTS: Both hyponatremia and hypouricemia were demonstrated in the presence of SIADH in one patient, during an episode of acute water intoxication in another, and in association with chronic hyponatremia in a patient who was following the target weight procedure. Elevated fractional excretion of uric acid percentage (FEUA%) was detected in two patients. These states appeared to be episodic or transitory. In the five patients with simple polydipsia, serum uric acid concentrations and FEUA% were maintained within the normal range. CONCLUSION: Altered uric acid regulation that resembles SIADH is present in patients with polydipsia-hyponatremia syndrome. Monitoring the uric acid concentration and FEUA% in polydipsic patients may be useful in identifying those patients with transiently impaired water excretion.

[Three patients from two families with familial Creutzfeldt-Jakob disease having a point mutation in the prion protein gene at codon 200 (Glu-->Lys)].

We present three patients with Creutzfeldt-Jakob disease (CJD). They lived in Fuji city and its neighboring towns in the eastern part of Shizuoka prefecture. Patient 1 and patient 2 were cousins. Patient 1 developed the illness at the age of 50 in 1987 and died 13 months later. Patient 2 became ill at the age of 73 in 1989 and died seven months later. Patient 3 was related to a familial CJD cases in Yamanashi prefecture, known as Akai's "H" family (Akai et al in 1979, Yamamoto et al in 1986). She became ill at the age of 78 in 1990 and died four months later. Their clinical features were common; rapidly progressive dementia, generalized myoclonus, and periodic synchronous discharges on electroencephalographies. They were autopsied and neuropathologically diagnosed as typical CJD. Molecular genetic analysis of the prion protein (PrP) gene was performed on patient 2 and patient 3 using their frozen brain sections. The results showed a point mutation in the PrP gene at codon 200; GAG to AAG (Glu-->Lys). The eastern part of Shizuoka prefecture is adjacent to Yamanashi prefecture where a large number of patients with CJD including familial cases has been found during the recent 15 years. This study suggests that the patients with CJD in both Yamanashi and Shizuoka prefecture should be re-evaluated by analysis of the PrP gene.

Quantitative EEG in patients with presenile and senile dementia of the Alzheimer type.

EEG data obtained from 27 patients with presenile Alzheimer's disease (AD) and 28 patients with senile dementia of the Alzheimer type (SDAT) were compared with data from 30 age- and sex-matched controls. Both patient groups exhibited more pronounced delta and theta activity and less prominent alpha and beta activity than the controls. AD, however, was accompanied by more severe slowing than SDAT. The slowing was distributed in the left temporal and frontal regions in AD, and bilaterally in the frontal regions in SDAT. As the severity of the dementia increased, delta activity alone increased in AD, whereas, there were significantly greater increases in both delta and theta activity and decreases in alpha and beta activity in SDAT. These EEG differences appear to be related to the degree of brain damage and the speed of progression of the disease process.

Computerized EEG and brain imaging studies in untreated schizophrenic patients: a report of seven cases.

We undertook routine EEG, Z-map, CT and PET scans in seven acute untreated schizophrenics. Routine EEGs showed slower activity in only one case. However, the Z-map showed slower activity in all the cases. CT demonstrated brain atrophy in three of the cases, and PET revealed hypofrontality in two, right hypoparietality in four, and both conditions in one case. There was no relation between CT and PET or the Z-map. However, a significant increase in alpha 1 activity was demonstrated on the Z-map in cases who were found to be the parietal type on PET; this was not conspicuous in the frontal type on PET. Moreover, in three of the patients, the Z-map findings were similar to the lesion indicated on PET.

Computerized analysis of EEG background activity in epileptic patients.

Background activity was studied in 128 idiopathic epilepsy patients and 30 normal controls using EEG topography and t-statistic significance probability mapping (t-SPM). In epileptic patients, EEG background activity showed a marked increase in delta, theta, alpha 1, and beta 1, and a decrease in alpha 2 activity as compared with controls. Untreated epileptic patients had a significant increase in delta, theta, and alpha 1 as compared with controls. For epileptic patients treated with antiepileptic drugs (AEDs), the most marked slowing was observed in the polytherapy group, followed by the monotherapy group and then the untreated group. Among seizure types, patients with partial seizures (PS) tended to exhibit more slowing than patients with only generalized tonic-clonic seizures (GTC). Moreover, PS had a right-left asymmetry in alpha 2 and beta 1 activities. In a comparison of AEDs, patients receiving carbamazepine (CBZ) and phenobarbital (PB) showed no significant difference as compared with the untreated group. In contrast, patients receiving valproate (VPA) showed a decrease in slow and fast activities. EEG changes associated with each AED were different in GTC and PS. Patients receiving VPA for GTC showed a decrease in theta and beta 1 activities, but those with PS showed a decrease only in delta activity.

[Computerized analysis of EEG background activity in mono-therapeutic patients with epilepsy--relationships between antiepileptic drugs and types of seizures].

EEG background activity influenced by antiepileptic drugs (AED) was studied in 109 monotherapy and drug-free epileptic patients using t-Statistical Significance Probability Mappings (t-SPMs). Patients taking phenobarbital (PB) had an increase in alpha 1 and a decrease in alpha 2 activity in comparison with drug-free epileptics. Patients taking PB for generalized seizures with tonic-clonic convulsion only (GTC) also had a significant increase in alpha 1 and a decrease in alpha 2, whereas those with partial seizures (PS) had an increase in theta and beta 1 and a decrease in alpha 2 activity. Patients taking valproic acid (VPA) had a decrease in only beta 1 activity. Patients taking VPA for GTC showed an increase in delta activity, but those with PS did not show any changes. Patients taking carbamazepine (CBZ) for PS exhibited marked slowing with an increase in theta and alpha 1 and a decrease in alpha 2 activity. These results mean that changes in EEG due to AEDs differ depending on the type of seizures. More interestingly, discrepancy between EEG background activity and effects of AEDs was found: In PS type of seizures, the most effective CBZ exhibited striking slowing, PB was next, and VPA was last. In GTC, VPA resulted in greater slowing than PB.

Computerized EEG in schizophrenic patients.

We undertook a study of electroencephalograms (EEGs) in 30 right-handed, untreated patients (27.3 +/- 10.0 years; hebephrenic, 16; paranoid, 12; residual, 2) who fulfilled ICD-9 criteria for schizophrenia and compared them with sex- and age-matched controls by using the percentage of power in six EEG frequency bands calculated as a fraction of total power. T-statistic significance probability mapping (t-SPM) showed that, compared with normal controls, schizophrenics had more slow activity (delta, theta, and alpha 1) in the parieto-occipital regions, and more fast activity (beta 1) in the occipital regions. In contrast, alpha 2 activity decreased strikingly in the occipital regions and this decreased activity extended over much of the head. These findings were thought to indicate both cerebral hypofunction and excitability in acute untreated schizophrenia.

[EEG background activity in patients with dementia of the Alzheimer type--with special reference to analysis by t-statistic significance probability mapping (SPM) in Alzheimer's disease and senile dementia].

EEG power amplitude and power ratio data obtained from 15 (3 men and 12 women) patients with Alzheimer's disease (AD) and 8 (2 men and 6 women) with senile dementia of Alzheimer type (SDAT) were compared with similar data from 40 age- and sex-matched normal controls. Compared with the healthy controls, both patient groups demonstrated increased EEG background slowing, and it indicated more slower in AD than in SDAT. Moreover, both groups showed characteristic findings respectively on EEG topography and t-statistic significance probability mapping (SPM). The differences between AD and their controls indicated high slowing with reductions in alpha 2, beta 1 and beta 2 activity. The SPMs of power ratio in theta and alpha 2 bands showed most prominent significance in the right posterior-temporal region and delta and beta bands did in the frontal region. Severe AD indicated only frontal delta slowing compared to mild AD. The differences between SDAT and their controls indicated only mild slowing in delta and theta bands. The SPM of power amplitude showed occipital slowing, whereas the SPM of power ratio showed the slowing in the frontal region. Judging from both topographic findings, these were considered to denote diffuse slow tendency. In summary, these results presumed that in AD, cortical damages followed by EEG slowing with reductions of alpha 2 and beta bands originated rapidly and thereafter developed subcortical (non-specific area in thalamus) changes with frontal delta activity on SPM. On the other hand, in SDAT, diffuse cortico-subcortical damages with diffuse slowing on EEG topography were caused gradually.