An electroencephalographic study of psychiatric inpatients with antipsychotic-induced tardive dyskinesia

The awake EEGs of 48 psychiatric inpatients with tardive dyskinesia were compared with those of 29 matched controls without TD. EEGs of the TD patients were as follows: 22 (45.8%) were normal EEGs; 17 (35.4%), mildly abnormal EEGs; 8 (16.7%), moderately to severely abnormal EEGs. One record was excluded for severe artifacts. The control group showed a similar incidence of EEg abnormalities. EEGs with poor occipital alpha rhythm were significantly more frequent in the TD group than the control group. The TD patients tended to have an alpha rhythm of low voltage. Other characteristics of the alpha rhythm and amounts of theta, delta and beta activity showed no significant differences between the two groups. Severity of TD had no significant influence on EEG findings. The EEG similarities of TD and Huntington's chorea were discussed, and a suggestion was made that not only the basal ganglion, but also the cerebral cortex, could be involved in development of TD.     

Pallidal GABA and chorea in Huntington's disease

Summary Neurochemical correlates of chorea in Huntington's disease were studied using striatal and pallidal tissue taken post mortem from patients with mild and severe chorea. While GABA was decreased in all these areas in Huntington's disease, patients with mild chorea had significantly less GABA in the medial pallidum than did those with severe chorea. There was no relationship between the degree of chorea and concentrations of dopamine or its metabolite. Thus the chorea of Huntington's disease may relate to the balance of residual GABAergic innervation between specific areas of the basal ganglia, consistent with primate models of dyskinesias.     

Sydenham's chorea and seizures. Clinical and electroencephalographic studies

The hospital records of 28 children (mean age, 9.4 years) with typical Sydenham's chorea were reviewed. Nineteen of 28 patients had antistreptolysin O titers of greater than or equal to 200 Todd units. Other causes of chorea were excluded by appropriate laboratory and clinical follow-up studies. At the onset of the movement disorder, 17 of 28 patients had abnormal EEGs consisting of irregular posterior slowing in 15, sharp epileptic spikes in 5, and high-voltage sharp waves in 2. Two patients with spikes predominantly in the temporal lobe regions developed complex partial seizures. On follow-up evaluation, the EEGs returned to normal within one to four weeks. Seizures did not recur after therapy with anticonvulsants. Seizures have been reported only rarely in association with Sydenham's chorea. Our observation suggests that seizures may occur during chorea but may often be masked by frequent choreic movements and thus not recognized. The EEG changes and seizures were transient in our patients studied so far.     

Parasympathetic function in Huntington's disease

Parasympathetic function in 7 Huntington's chorea patients with a duration of the disease ranging from 1 to 20 years, was evaluated by studying R-R intervals during quiet and deep breathing and Valsalva manoeuvre. All 7 patients were free of neuropathy, orthostatic hypotension, heart or lung disease and had had no medication for at least 15 days prior to hospitalization. Seven normal subjects served as controls. On the whole, the responses of the Huntington's chorea patients were not significantly different from those of the controls. Abnormal responses to all the tests were received in only one patient and a low R-R variability during deep breathing in the youngest patients. Unlike other Central Nervous System degenerative disorders, in Huntington's disease parasympathetic autonomy seems to be sufficiently preserved.     

A blinded study of the suppressibility of involuntary movements in Huntington's chorea, tardive dyskinesia, and L-dopa-induced chorea

Videotapes of patients with Huntington's chorea, tardive dyskinesia (TD), and L-DOPA-induced chorea in Parkinson's disease were taken while the patients were seated with their legs dangling. The videotapes were scored in a blinded fashion for suppressibility of dyskinesias. Most patients with TD or L-DOPA-induced chorea substantially suppressed their involuntary movements, whereas most patients with Huntington's chorea did not. There was a small overlap between the TD and Huntington's chorea groups and suppressibility therefore could not absolutely distinguish between them. Suppressibility testing may nonetheless be a valuable clinical tool since a good, excellent, or complete suppressibility rating was highly suggestive of TD but not Huntington's chorea. TD and L-DOPA-induced chorea may be more pathophysiologically similar to each other than either is to Huntington's chorea.     

Homovanilic acid in Huntington's disease and Sydenham's chorea.

Homovanilic acid (HVA) was determined in the lumbar CSF of 12 patients with Huntington's disease and 12 with Sydenham's chorea before and after probenecid administration. The means of HVA concentration (basal and after probenecid) were lower in those with Huntington's disease than in controls, and were even lower in a sub-group characterised by increased tone and slowness of voluntary movement. There was no correlation between CSF HVA values and the severity of abnormal movements, nor with length of the illness and age of the patients with Huntington's disease. The mean basal HVA concentration did not differ from controls in those with Sydenham's chorea but the accumulation with probenecid was significantly lower. These results suggest a decrease in cerebral dopamine release in both forms of chorea.     

EEG Changes 24 Hours after Myelography with Metrizamide

Abstract: A prospective study of EEG changes following metrizamide myelography was made on 34 patients aged 17–79 years. EEGs were recorded just before and 22–26 hours after myelography. Usually 8–10 ml of metrizamide was injected by either lumbar or lateral cervical puncture. The concentration of metrizamide was relatively high. EEGs were abnormal in 15 out of the 20 patients whose baseline EEGs were normal. EEGs deteriorated in 10 of the 14 patients whose control tracings were abnormal. High voltage delta activity and/or a great deal of theta activity were common abnormalities. Three patients showed triphasic waves. No relationships were found between the EEG changes and clinical variables. But central nervous system involvements by metrizamide tended to be accompanied by a severe EEG slowing.     

Correlations between EEG and CT in 79 cases of dementia

An EEG and CT study was carried out on 79 patients affected by dementia (24 SDAT and 55 MID). The EEG and CT patterns were compared with those of an age-matched control group. Statistical analysis of the CT findings between the demented and normal subjects showed significant differences only for severe atrophy. As far as EEG findings are concerned, no EEG pattern indicative of a specific type of dementia was observed even though a greater number of abnormal EEGs occurred in demented patients than in the control group. Finally, a poor EEG-CT correlation was found in demented patients.     

Habituation of the orbicularis oculi reflex in dementia and dyskinetic states.

The habituation index is a quantitative expression of the ability of the orbicularis oculi (blink reflex) to adapt to a series of electrical stimuli applied to the supraorbital region. This parameter has been studied in a group of normal control subjects, and the results compared with those in cases of idiopathic and drug-induced Parkinsonism, states of dementia, and dyskinesias such as Huntington's chorea and senile chorea. Patients with Huntington's chorea showed a tendency for the reflex to habituate readily in contrast to patients with dementia caused by cortical atrophy and those with Parkinson's disease. Younger patients with Huntington's chorea had indices within the normal range. It seems unlikely that this test will prove of value in the detection of clinically unaffected relatives. Where dementia was associated with a reversible intracranial lesion, the habituation index was studied before and after treatment. Failure of habituation in this condition appears to be due to the release of a primitive protective reflex.     

EEG changes in subcortical dementia: a study of 22 patients with Steele-Richardson-Olszewski (SRO) syndrome

To assess the value of EEG in distinguishing between cortical and subcortical dementia, we compared the EEGs of 22 patients with SRO syndrome with those of 22 patients who had a comparable degree of dementia due to cortical atrophy. EEG records from patients with SRO syndrome were of low voltage, but with preserved alpha rhythm at 8-10 Hz and were within normal limits in 12/22. In 8 there was an abnormal excess of theta activity and one had additional lateralizing asymmetries. One had frontal intermittent rhythmic slow wave activity. Comparison with records of 22 patients, with cortical atrophy due to Alzheimer's disease but with only mild to moderate dementia, showed a similar low frequency of non-specific abnormalities.     

EEG changes 24 hours after myelography with metrizamide

A prospective study of EEG changes following metrizamide myelography was made on 34 patients aged 17-79 years. EEGs were recorded just before and 22-26 hours after myelography. Usually 8-10 ml of metrizamide was injected by either lumbar or lateral cervical puncture. The concentration of metrizamide was relatively high. EEGs were abnormal in 15 out of the 20 patients whose baseline EEGs were normal. EEGs deteriorated in 10 of the 14 patients whose control tracings were abnormal. High voltage delta activity and/or a great deal of theta activity were common abnormalities. Three patients showed triphasic waves. No relationships were found between the EEG changes and clinical variables. But central nervous system involvements by metrizamide tended to be accompanied by a severe EEG slowing.     

Reduced density of striatal somatostatin receptors in Huntington's chorea

A marked increase of the endogenous somatostatin has been reported in the striatum in Huntington's chorea by radioimmunoassay and immunohistochemistry. Using quantitative receptor autoradiography we examined the density and distribution of somatostatin receptors in the striatum of 6 patients dying from Huntington's chorea degree 3, in 12 control healthy patients dying without neurological diseases and 7 schizophrenic patients, using the stable somatostatin octapeptide analogue [¹²⁵I]204-090 as a radioligand. Marked reductions of the density of somatostatin binding sites were observed in the caudate and putamen of all patients with Huntington's chorea. However, these receptors were well preserved in the nucleus accumbens and in the ventral aspects of the anterior putamen. No alteration of somatostatin receptors was observed in other brain areas. These results suggest that somatostatin receptors in the human striatum are markedly down-regulated or localized on a population of neurons which is at risk in Huntington's chorea and questions the postulated role for the elevated somatostatin levels in choreiform movements.     

Cause and course in a series of patients with sporadic chorea

OBJECTIVE: To identify correlations between clinical and neuroimaging features in sporadic chorea and to explicate the evolution of choreas of differing aetiologies. METHODS: We analysed the clinical and neuroimaging data of 51 consecutive cases (17 males, 34 females; age 16-95 years) of sporadic chorea admitted to the neurology departments of two general hospitals from January 1994 to December 1999, and two neurological institutes from January 1997. Six months later the patients were reassessed clinically and those still with chorea (20 cases) were asked to undergo the genetic tests for Huntington's disease and dentatorubropallidoluysian atrophy. RESULTS: There were 9 cases of focal dyskinesias, 18 of hemichorea, and 24 of generalised chorea; onset was acute in 17, subacute in 27, and insidious in seven. Analysis permitted classification as follows: vascular-related (21 cases); vasculitis (1 case); hypoxia (2 cases); drug-induced (7 cases); AIDS-related (5 cases), borreliosis (1 case); Sydenham's chorea (1 case); hyperglycaemia (2 cases); hyponatraemia (2 cases); Huntington's disease (HD) (5 cases) and acanthocytosis (1 case). In 3 patients neither etiological factors nor neuroradiological alterations were found. CONCLUSIONS: Although a convincing concordance between choreic signs and neuroradiological findings was possible in 4 patients only, it was possible to assign an aetiology in most cases with vascular related causes the most frequent and metabolic factors often participating. Huntington's disease is not unusual as a cause of sporadic choreas. HIV infection is an emerging cause of chorea and AIDS-related disease should be considered in young patients presenting without a family history of movement disorders. We emphasize the importance of follow-up to identify persistent chorea for which genetic testing is mandatory.     

Surgery removes EEG abnormalities in patients with Chiari type I malformation and poor CSF flow.

OBJECTIVE: To study the outcome of EEG from patients with Chiari I malformations and nonspecific EEG abnormalities, after posterior fossa decompression and CSF flow normalization. METHODS: Three 'apparently asymptomatic' children who had been diagnosed with Arnold-Chiari type 1 EEG abnormalities and who exhibited (a) a wide range of abnormalities according to common anatomical Chiari MRI classifications (Elster AD, Chen MY. Chiari I malformations: clinical and radiologic reappraisal. Radiology 1992;183:347-53), (b) a lack of specific, clinical signs of increased intracranial pressure, and (c) apparently unrelated, EEG-nonspecific abnormalities (focal intermittent rhythmic delta activity (IRDA)--solely in patients 1 and 3, and with focal IRDA plus spikes and spike waves of high voltage in patient 2). Standard EEGs were recorded before surgery and within one month of surgery, which was performed in conjunction with intraoperative echo-Doppler ultrasonography to control CSF flow. Subsequent EEGs and clinical follow-ups were performed within 6-12 months of surgery. RESULTS: In all patients, intraoperative echo-Doppler ultrasonographic control demonstrated poor CSF flow, which was completely restored by posterior fossa decompression. In all patients, the EEG abnormalities disappeared within one month of surgery and the EEGs were normal at follow-up. CONCLUSIONS: A new CNS symptom, identified as focal IRDA alone or focal IRDA plus spikes and spike waves of high voltage in the EEG, seems to be associated with poor CSF flow in 'apparently asymptomatic' patients with Chiari type I malformations. SIGNIFICANCE: The identified, paroxysmal EEG abnormalities should be interpreted as an indirect sign of subtle CNS distress.     

Electroencephalogram and seizures in chronic alcoholism.

CNS complications of chronic alcoholism are frequently difficult to assess due to the variety of direct and secondary conditions which can result from alcoholic drinking and lifestyles. The influence of alcoholism and alcohol-related factors on the EEG of patients with chronic alcoholism was studied in 213 patients (15.4% of all adults who had EEGs) using visual analysis. The influence of a variety of alcohol-related factors - drinking history, clinical complications, traumatic head injuries, head CT findings and laboratory results - on the EEG and alcohol-related seizures was studied. The effect of EEG results on the decision to treat alcohol-related seizures was also assessed. 152 of the patients had seizures, mostly (90% of those with defined seizure types) generalized tonic-clonic seizures. 53% of all seizures occurred in the early withdrawal period (8 h to 7 days abstinence). A history of partial seizures was significantly associated with findings of focal EEG abnormalities, a history of head injuries and structural lesions on CT. The clinical significance of these findings was unclear, however, as the majority of patients who had focal EEG abnormalities or structural brain lesions still appeared to have generalized withdrawal seizures. The EEG and CT appeared to be complementary tests: for most patients, focal abnormalities were demonstrated on only one of the two tests. The majority of patients (56%) with normal EEGs had predominantly low voltage recordings (less than 25 muV), compared with 13.9% of 1167 patients without a history of alcoholism (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Intracortical inhibition of the motor cortex is normal in chorea

Intracortical inhibition of the motor cortex was investigated using a paired pulse magnetic stimulation method in 14 patients with chorea caused by various aetiologies (six patients with Huntington's disease, one with chorea acanthocytosis, a patient with systemic lupus erythematosus with a vascular lesion in the caudate, three with senile chorea and three with chorea of unknown aetiology). The time course and amount of inhibition was the same in the patients as in normal subjects, suggesting that the inhibitory mechanisms of the motor cortex studied with this method are intact in chorea. This is in striking contrast with the abnormal inhibition seen in patients with Parkinson's disease or focal hand dystonia, or those with a lesion in the putamen or globus pallidus. It is concluded that the pathophysiological mechanisms responsible for chorea are different from those producing other involuntary movements.     

Electroencephalography in tetanus

ABSTRACT To assess the brain involvement caused by tetanus, we examined the EEGs of 39 patients recovered from tetanus and those of 39 sex- and age-matched controls. The patients had significantly more frequent and more severe EEG abnormalities than their controls. The most marked difference was in the occurrence of diffuse EEG abnormalities (P < 0.05). Twenty patients had normal EEGs. EEGs of 14 patients (5 of whom in this follow-up) during acute tetanus showed abnormalities in 10 patients, marked in degree in 3 of those. EEG abnormalities started to improve after the acute phase of tetanus. It is concluded that EEGs of patients with tetanus are often abnormal and that EEG is helpful in revealing brain involvement in patients after tetanus.     

Rate and correlates of weight change in Huntington's disease

OBJECTIVE: To determine the rate and correlates of weight change in a large, well characterised sample of patients with Huntington's disease followed at 44 sites by the Huntington Study Group. Participants and methods: Weight change was assessed in 927 adults with a definite diagnosis of Huntington's disease who were followed prospectively for (mean (SD)) 3.4 (1.4) years. The unified Huntington's disease rating scale was used to assess weight, motor dysfunction (including chorea and dystonia), depressive symptoms, and functional decline. RESULTS: Random effects modelling determined that patients gained an average of 0.11 (1.7) kg/year and their chorea scores increased by 0.36 (0.78) points/year. There were significant but weak relations between weight loss and increasingly severe chorea (r = -0.13), worse baseline motor performance (r = -0.12), less severe baseline depressed mood (r = 0.14), and poorer baseline independence ratings (r = 0.07). Patients who were within 0 to 2 years of symptom onset at the time of the baseline visit gained more weight than those with longer disease duration. CONCLUSIONS: Weight loss following symptom onset is not a consistent feature of Huntington's disease. The mechanisms contributing to weight change in this condition are unclear and probably multifactorial. Future studies examining asymptomatic carriers of the mutation could be helpful in identifying incipience of low body weight and may be better suited for identifying clinical correlates of weight loss than studies in symptomatic patients.     

Predictive value of electroencephalography for electroconvulsive therapy

The EEG has been a widely-used screening procedure before ECT. Previous studies have correlated seizures and post-ECT slowing with ECT efficacy. We investigated the utility of pre-ECT EEG in predicting therapeutic response and post-ECT confusion. EEGs were normal in 54 of 100 patients undergoing first courses of ECT for refractory depression. Patterns within the normal range, were present in 26/100 while 2/100 had paroxysmal discharges without clinical evidence of epilepsy. Focal and generalized EEG slowing were each present in 9/100 records. Full recovery occurred after ECT in 66.6 per cent of those with normal pre-ECT records, 61.5 per cent with borderline EEGs, 55.5 per cent of patients with diffuse EEG slowing, and 22.2 of cases with focal slow waves. Of those with EEG slowing 22.2 percent had little or no response to ECT as compared to 19.2 per cent with EEGs within normal limits and 9.3 per cent with normal EEGs. Four of 6 patients with prolonged confusion had normal EEGs, while 1 each had focal and generalized slowing. EEG slowing was related to incomplete ECT response, but not to therapeutic failure or post-ECT confusion. The limited predictive power of pre-ECT EEG may reflect the prevalence of normal or nonspecifically abnormal EEGs in psychiatric patients and the general efficacy of ECT. Other neurophysiologic methods may yield more definitive information about the mechanism and use of ECT.     

Positron emission tomography in cases of chorea with different underlying diseases.

Local cerebral metabolic rate for glucose (LCMRglc) was measured with positron emission tomography using the 18F-fluorodeoxy-glucose method in five patients with chorea due to different underlying diseases. Hypometabolism was observed in the striatum bilaterally in patients with Huntington's disease, choreoacanthocytosis, sporadic progressive chorea and dementia, and pseudo-Huntington form of dentato-rubro-pallido-luysian atrophy (DRPLA). The patient with hemichorea showed hypometabolism in the striatum on the contralateral side to the chorea. The patient with pseudo-Huntington form of DRPLA showed a diffusely decreased LCMRglc in other structures including the cerebral cortex, thalamus and cerebellum. These findings indicated that dysfunction of the striatum is relevant to the genesis of chorea in all these patients, even though the extent of dysfunction in other structures is different in each case.