Treatment of speech defects in a state school

Summary An attempt has been made to show that treatment of speech defects in a State school is worth while, inasmuch as a patient has a better chance for adjustment outside the institution if a speech defect has been corrected; and from the writers' results, it is shown that a suitable proportion of patients is benefited.The type of case most suitable for treatment has been described.The methods of treatment of the various types of speech defects have been touched upon.Read in part at the interhospital conference, Utica State Hospital, April 26, 1941.     

An investigation of the role played by oxygen and by cellular respiration in hypoglycemic coma

Summary It has been found that when oxygen is given to patients during insulin coma, the coma is intensified. It is suggested that, in hypoglycemia, the oxygen, that normally would combine with glucose, accumulates in the blood instead, increasing the pH and thereby inactivating the enzymes responsible for cellular respiration. Obviously if these views are correct, oxygen in excess must be regarded as a toxic substance and should never be administered in insulin coma emergencies. On the other hand, methylene blue, a substitute for the non-functioning enzymes, has been found to reestablish the normal processes quickly and safely when used in conjunction with the usual dextrose solution.Read at the Up-state Interhospital Conference of the New York State Department of Mnetal Hygiene at Syracuse Psychopathic Hospital, April 9, 1956.     

SECRETION OF HUMAN GROWTH HORMONE DURING INSULIN COMA AND ELECTROSHOCK THERAPIES

The responses of plasma HGH during psychiatric shock therapies were investigated, and the mechanisms of HGH secretion and of shock therapies were discussed. 1. The response following a sinall dose of i.v. insulin administrotion. a) The plasma HGH following 0.1 U/kg of i.v. insulin in schizophrenic patients showed marked elevation in six out of seven cases. It reached to the peak value of 30.4±9.2 mμg/ml between 60 and 90 minutes after i.v. insulin. b) This type of response was not affected by the various psychotropic drugs that were administered orally in controlling the mental symptoms of the patients. c) Intramuscular injection of chlorpromazine (30–50 mg) did not alter the pattern of the plasma HGH response. 2. Insulin coma therapy a) A marked elevation of plasma HGH level was observed in all cases of schizophrenia during insulin coma therapy. The peak value was 9–32 mμg/ml (average 22.6±8.1 mμg/ml). b) A tendency of delay in reaching the peak value was observed in the determination performed in the second week of coma days as compared to the initial determination in the early days of insulin coma. A tendency was observed that better therapeutic results were correlated with the absence of or decrease in the delay in reaching the peak value in the course of insulin coma therapy. c) The protracted insulin coma was associated with the marked decrease in the magnitude of the peak value of plasma HGH as compared to the initial determination, suggesting the presence of a fatigued state of the central mechanism regulating the secretion of HGH. 3. Electroshock therapy a) Elevation of the plasma HGH level was observed after electroshock therapy in five of six cases of schizophrenia. A non-responsive case was found to be moderately obese. A case of depression and a case of atypical psychosis lacked HGH response after EST in the absence of obesity. b) The peak value after the electroshock therapy was lower than the one during insulin coma therapy or after administration of a small dose of i.v. insulin. The average peak value after EST was 8.1±6.8 mμg/ml. c) The responsivity of plasma HGH was found to be unrelated to the various prernedications, such as i.v. thiopental and succinylcholine chloride. It was also concluded that the presence or absence of generalized convulsion was not related to the responses of HGH following EST. d) No correlation was found between the changes of blood sugar level and the type of plasma HGH responses following the EST. It was suggested that the elevation of HGH at the time of electroshock therapy was induced by the direct electric stimulation of the hypothalamic center, but the effect of stimulating the HGH secretion was much lower than that induced by the insulin coma or i.v. insulin administration.     

Persistent but reversible coma in encephalitis

Introduction: Nontraumatic coma in adults has a poor prognosis, and late recovery of consciousness is unlikely. Functional recovery is usually extremely poor. However, a few nontraumatic comatose patients have shown late recovery of both awareness and function. Methods: A retrospective survey was conducted by reviewing the medical records of all inpatients to our department during the 1990s. Patients with persistent but reversible nontraumatic coma were identified according to the following criteria: (a) deep coma with a Glasgow Coma Scale (GCS) score of 7 or less on admission; (b) nontraumatic cause; (c) persistence of unconsciousness for longer than 1 month; and (d) subsequent recovery of GCS (total) to normal. The clinical spectrum of patients meeting these criteria was evaluated. Results: Six patients (ages 16–75 years) met the criteria. Viral encephalitis was diagnosed in five (two with herpes simplex virus, two with cytomegalovirus, and one with Epstein-Barr virus or cytomegalovirus). Two young female patients with encephalitis manifested extremely protracted coma persisting for 3 and 18 months, respectively. Complications included nonconvulsive status epilepticus in two patients and relative overdose of clonazepam in one patient. Conclusion: Recognition of the clinical spectrum of persistent but reversible nontraumatic coma is important.     

Memory and socioemotional behavior in monkeys after hippocampal damage incurred in infancy or in adulthood.

The present study reviews the long-term effects of neonatal hippocampal damage in monkeys on the development of memory functions and socioemotional behavior. The results showed that neonatal damage to the hippocampal formation impairs specific memory processes, such as those subserving automatic (as opposed to effortful) recognition memory and relational learning, while sparing the abilities to acquire skills, such as object discriminations. Furthermore, the neonatal hippocampectomy led to a progressive loss of social affiliation and a protracted emergence of locomotor stereotypies. While the memory losses following neonatal hippocampal lesions resemble those found after similar lesions acquired in adulthood, only the neonatal lesions resulted in a protracted emergence of abnormal behaviors. These later findings suggested that, presumably, the neonatal lesions impacted on neural systems remote from the site of damage. This was confirmed by our more recent neurobiological studies, demonstrating that neonatal, but not late, lesions of the medial temporal lobe region, disrupt the normal behavioral and cognitive processes subserved by the prefrontal cortex and the caudate nucleus. All together the data support the neurodevelopmental hypothesis viewing early insult to the medial temporal region as the origin of developmental psychosis in humans, such as schizophrenia.     

Electric stimulation and insulin coma

Summary Observations with nonconvulsive stimulation during insulin coma have been presented. The method is useful in arousing patients from coma, provided that they have not entered a deep phase. Adrenalin and blood sugar responses suggest that activation of the diencephalic pituitary-adrenal axis occurs. The theory that during insulin coma a successive inactivation of phylogenetic layers within the brain takes place is supported by the observations reported here. Therapeutic results suggest a favorable comparison with deep insulin coma, provided a differential and dynamic approach is followed. Complications, such as delayed and protracted coma, have not been encountered. Treatment time is shortened to about two hours, and the average number of treatments is about 40.Read at the 109th annual meeting of the American Psychiatric Association at Los Angeles, May 1953.     

Prognosis in prolonged coma patients with diffuse axonal injury assessed by somatosensory evoked potential

A total of 43 prolonged coma patients with diffuse axonal injury received the somatosensory evoked potential examination one month after injury in the First Affiliated Hospital, School of Medicine, Zhejiang University in China. Somatosensory evoked potentials were graded as normal, abnormal or absent (grades Ⅰ-Ⅲ) according to N20 amplitude and central conduction time. The outcome in patients with grade Ⅲ somatosensory evoked potential was in each case unfavorable. The prognostic accuracy of grade Ⅲ somatosensory evoked potential for unfavorable and non-awakening outcome was 100% and 80%, respectively. The prognostic accuracy of grade Ⅰ somatosensory evoked potential for favorable and wakening outcome was 86% and 100%, respectively. These results suggest that somatosensory evoked potential grade is closely correlated with coma severity and degree of recovery. Somatosensory evoked potential is a valuable diagnostic tool to assess prognosis in prolonged coma patients with diffuse axonal injury.     

Neurophysiologic evaluation of cyclosporine toxicity associated with bone marrow transplantation

Introduction – Cortical blindness, a rare form of cyclosporine (CSA) neurotoxicity, has previously been described in only nine bone marrow transplant (BMT) recipients. Methods - Our institution averages 35 allogeneic BMT's per year. In the past year we have seen two women with reversible cortical blindness secondary to CSA toxicity. Results - Age (years) (Case 1; Case 2): 32; 22. Day post-BMT: 41; 50. Peak CSA level (ng/ml): 1159; 632. Both had a history of renal toxicity requiring adjustment of CSA dosage. MRI - both with diffuse white matter changes. EEG-both with moderate to severe generalized slowing. Visual evoked potentials were markedly prolonged in both. Auditory evoked potentials: minimally abnormal; normal. Somatosensory evoked potentials - both normal. Prompt improvement occurred with discontinuation of CSA. Followup neurophysiologic evaluations were normal, however structural changes remained on MRI. Conclusion - As neurophysiologic studies closely follow the clinical status they should be included in the evaluation and followup of CSA neurotoxicity.     

The interaction of delirium and seizures

The induction of a delirium by medical illness, somatic treatments, or experimental drugs occasionally relieves psychotic, excited, and manic states. An induced delirium is a feature of modern electroconvulsive therapy (ECT), and was a feature of insulin coma therapy and psychosurgery. Case material explores the relationship between psychosis, mania, seizures, and electroencephalogram. From our understanding of the mechanism of ECT in relieving intractable status epilepticus, we suggest a hypothesis for the beneficial interaction between delirium and ECT.     

Cerebral mitochondrial respiration in diabetic and chronically hypoglycemic rats

The respiratory function of cerebral mitochondria harvested from genetically diabetic (BB/W) and streptozotocin-diabetic rats deprived of insulin for 3-4 weeks was found to be unchanged from control values. Furthermore, insulin-deprived BB/W rats subjected to 30 min of insulin-induced hypoglycemic coma demonstrated a normal mitochondrial respiration following a 60 min period of glucose restitution, a finding consistent with earlier results in non-diabetic rats. However, in rats exposed to 1 week of moderate hypoglycemia (plasma glucose = 3.0 mumol.ml-1), both state 3 respiration and the respiratory control ratio (RCR) were reduced from control. In fact, when the chronic hypoglycemia was imposed following a 3-4 week period of diabetic hyperglycemia, the state 3 rate and RCR were found to be reduced to a greater degree than in chronically hypoglycemic, non-diabetic, previously normoglycemic rats. Finally, when 1 week of moderate hypoglycemia preceded a 30 min period of insulin-induced hypoglycemic coma, a disturbed pattern of mitochondrial respiration (i.e. increased state 4, decreased RCR) was found at 60 min of recovery following coma. These results indicate that chronic increases in glucose (and insulin deprivation) have no effect on cerebral mitochondrial respiratory function, whereas prolonged, albeit moderate, reductions in cerebral glucose supply result in perturbations in mitochondrial respiration. These results demonstrate the importance of an adequate glucose supply for normal mitochondrial activity.     

Neurophysiologic evaluation of cyclosporine toxicity associated with bone marrow transplantation

Introduction —Cortical blindness, a rare form of cyclosporine (CSA) neurotoxicity, has previously been described in only nine bone marrow transplant (BMT) recipients. Methods —Our institution averages 35 allogeneic BMT's per year. In the past year we have seen two women with reversible cortical blindness secondary to CSA toxicity. Results —Age (years) (Case 1; Case 2): 32; 22. Day post-BMT: 41; 50. Peak CSA level (ng/ml): 1159; 632. Both had a history of renal toxicity requiring adjustment of CSA dosage. MRI - both with diffuse white matter changes. EEG - both with moderate to severe generalized slowing. Visual evoked potentials were markedly prolonged in both. Auditory evoked potentials: minimally abnormal; normal. Somatosensory evoked potentials - both normal. Prompt improvement occurred with discontinuation of CSA. Followup neurophysiologic evaluations were normal, however structural changes remained on MRI. Conclusion —As neurophysiologic studies closely follow the clinical status they should be included in the evaluation and followup of CSA neurotoxicity.     

Three-word recall as a measure of memory

Abstract

Clinical examination of memory functions often includes the administration of simple free recall tasks, such as the recall of several words following a few minutes. Little is known, however, about the normative parameters or psychometric properties of such procedures, and such techniques have rarely been compared with more comprehensive, well-standardized memory indices. To address these issues, two three-word recall tasks were administered to a large group of carefully selected healthy subjects over the age of 50 years. The Mini-Mental State Examination (MMSE) was obtained as an index of global cognitive status, and the California Verbal Learning Test (CVLT) was used to exclude subjects with abnormal memory abilities. Significant but modest relationships were found between two three-word recall tasks and CVLT results. Substantial variability was seen on three-word recall, with a significant proportion of normal subjects recalling zero or one word. Results suggest using caution in interpreting simple recall performance as an index of memory, as great variability in results is seen among healthy (particularly older) individuals.     

Dermatoglyphics in female schizophrenia

Summary Dermatoglyphic analysis was performed on the prints obtained from 82 schizophrenic female patients at Utica State Hospital. These were compared with those of a control population of 295 healthy white women. Discriminant analysis revealed that separation of the two groups on the basis of the dermatoglyphic features was possible with a level of discrimination of 82%. The individual features of the prints which appeared to contribute most importantly to this discrimination were: the occurrence of abnormal creases in 24% of the schizophrenic group as compared to 2.7% of the controls; an increased frequency in the number of arches on the fingers—10.4% of all schizophrenic fingerprints, versus 4.9% of controls; an increased number of individuals with one or more arches among the schizophrenics—32% against 18% among the controls; deficiency of the main line C of some degree among the schizophrenics; and a decreased frequency of radial loops on the index finger among the schizophrenics. Numerous other differences of lesser frequency were also noted.Luke's Memorial Hospital Center, Utica, N. Y.; Computer Symbolic, Rome, N. Y.; and Rome Air Development Center, U.S.A.F., Griffiss A.F.B., Rome, N.Y.     

Evaluation of renal parathyroid hormone receptor function in myotonic dystrophy

Endocrine abnormalities in myotonic dystrophy (MyD) reflect some of the multisystemic involvement resulting from this disorder. One of these, abnormal insulin secretion, is considered to be caused by receptor dysfunction. Bone abnormalities, cataract and calcium transport defect suggest the abnormal calcium metabolism in MyD. The calcium metabolism is chiefly regulated by parathyroid hormone (PTH). An interest in the similarity between MyD and pseudohypoparathyroidism, which is a disorder of PTH receptor dysfunction, encouraged the authors to evaluate renal PTH receptor function from the responses of urinary adenosine 3′,5′-monophosphate (cAMP) and phosphate excretion after administration of human PTH(1–34). The responses of cAMP were high in 3 cases, low in one case, but normal in the 4 other cases. The phosphaturic responses were elevated in 3 cases, reduced in 3 cases, and normal in 2 other cases. Since these abnormal responses closely mimic those in hypoparathyroidism, there may also be renal PTH receptor dysfunction in some cases of MyD. The results of the present study suggest another peptide hormone receptor defect, similar to insulin, which supports the hypothesis of generalised receptor dysfunction in MyD.     

Seizure-induced memory impairment is reduced by choline supplementation before or after status epilepticus

Prenatal choline supplementation can protect rats against cognitive deficits induced by status epilepticus induced by the cholinergic agent pilocarpine [J. Neurosci. 20 (2000) 1]. In the present day, we have extended this novel finding by investigating the effects of pre- and postnatal choline supplementation in memory deficits associated with status epilepticus induced with kainic acid (KA). In the first experiment pregnant rats received a normal, choline-supplemented, or choline deficient diet starting on the 11th day of gestation and continuing until postnatal (P) 7. At P42, rats were given a convulsant dosage of KA. Two weeks following the KA-induced status epilepticus rats underwent testing of visual-spatial memory using the Morris water maze test. Rats receiving supplemental choline performed better in the water maze than the deficient and control groups. Moreover, the activity of hippocampal choline acetyltransferase was 18% lower in the choline deficient animals as compared with the other two groups. In the second experiment we administered KA to P35 rats that had been given a normal diet. Following the status epilepticus the rats were given a choline-supplemented or control diet for 4 weeks and then tested in the water maze. Rats receiving choline supplementation performed far better than rats receiving a regular diet. This study demonstrates that choline supplementation prior to or following KA-induced status epilepticus can protect rats from memory deficits induced by status epilepticus.     

Observations on organic brain damage and clinical improvement following protracted insulin coma

Summary A study of eight cases of chronic schizophrenics who developed protracted coma during insulin shock therapy is reported. Five of the eight patients showed a marked improvement after protracted coma, and three remained unimproved. The improvement consisted of loss of tension and hostility. Patients became friendly, affable, relaxed and interested in the environment. In spite of the return of delusional systems, the improved patients were able to function on a higher level than previously. In four of the five improved patients, improvement was preceded by severe organic brain deficit of varied duration. The organic deficit was demonstration through clinical observation, a battery of psychological tests and electro-encephalograms. Improvement is attributed to the organic brain damage which results in disruption of associative pathways not unlike the disruption in lobotomy.Published with permission of the chief medical director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions expressed or conclusions drawn by the author.     

Ocular Dipping in Creutzfeldt-Jakob Disease

Background

Ocular dipping (OD), or inverse ocular bobbing, consists of slow, spontaneous downward eye movements with rapid return to the primary position. It has been mainly reported following hypoxic-ischemic encephalopathy, but has also been described in association with other types of diffuse or multifocal encephalopathies and structural brainstem damage.

Case Report

We report the case of a previously asymptomatic 66-year-old woman who presented with confusion, recent memory disturbances, and abnormal involuntary movements, followed by a coma. Abnormal spontaneous vertical eye movements consistent with OD developed from the fourth day after admission, and the patient died 20 days later. The pathological examination of the brain confirmed the diagnosis of Creutzfeldt-Jakob disease.

Conclusions

The precise location of damage causing OD is unknown. In contrast to ocular bobbing, OD has no localizing value itself, but structural brainstem damage is likely when it appears combined with other spontaneous vertical eye movements.     

Neuromuscular transmission defect caused by carbamazepine.

The clinical effect of carbamazepine (CBZ) on neuromuscular transmission is described in two children who presented in coma with diffuse hypotonia and areflexia following CBZ overdose. Repetitive nerve stimulation (RNS) showed a decremental response only at high-frequency stimulation. With supportive care, the patients made an uneventful recovery. Follow-up RNS was normal. This is the first report of a clinically evident neuromuscular transmission defect produced by CBZ. We postulate that CBZ's known effect on decreasing sodium channel depolarization produced a defect in neuromuscular transmission. The report emphasizes the contribution of RNS in the evaluation of coma of uncertain etiology, particularly in cases of possible intoxication, and the potential for CBZ to compromise neuromuscular transmission in normal individuals or in patients with a decreased neuromuscular transmission safety factor.     

Paradoxical alpha waves seen in the course of subacute sclerosing panencephalitis

Serial EEG findings of two cases with subacute sclerosing panencephalitis were compared with concurrent clinical status and CT findings. Case 1, a 16-year-old boy, showed transient abnormal diffuse alpha waves during sleep record. That had been seen for six months after the disappearance of periodic synchronous discharges. Clinically this abnormal EEG finding was observed at the transitional phase from stage II to III, when CT showed severe brain atrophy. Case 2, an 11-year-old boy, showed similar abnormal alpha waves for three months in the same phase as case 1. There have been many reports regarding the EEG findings of SSPE. However, these abnormal EEG findings were not reported. These abnormal alpha waves during sleep are considered to develop at the transitional phase from stage II to III, when pathologically SSPE goes from inflammation to destruction.     

Valproate-induced coma with ketosis and carnitine insufficiency

We observed two patients who developed coma following administration of valproate in dosages of 32 to 40 mg/kg per day. Valproate levels were within the therapeutic range, and results of liver function studies were normal. Both patients had ketosis and adipic aciduria. Plasma free carnitine levels were decreased during coma and after recovery. One patient excreted ethylmalonic acid, butyrylcarnitine, and glutarylcarnitine during and after resolution of coma, suggesting a multiple acyl coenzyme A dehydrogenation defect. Low serum carnitine levels may predispose patients to development of altered consciousness when treated with valproate.