Quantitative cytochemistry of RNA in axotomized feline rubral neurons

One-sided lateral funiculotomy at the C-2 segment induced axon reaction in the contralateral red nucleus of adult cats. Two to 60 days postoperatively the animals were sacrificed and the mesencephalon was fixed in ethanol-acetic acid, 3:1. Ten μm paraffin sections including both red nuclei were stained for RNA with azure B after incubation in DNAse. Cytophotometric measurements of RNA content of neurons from the caudal 600–1000 μm of each red nucleus were made with a Zeiss Cytoscan system using an automatic scanning stage. In contrast to the heightened RNA synthesis that has been reported for axotomized peripheral (extrinsic) neurons, the axotomized central (intrinsic) neurons of the red nucleus showed no evidence of accumulation of cytoplasmic or nucleolar RNA. Rather depletion of cellular RNA occurred. Further indication of the regressive nature of rubral axon reaction derived from morphometric measurements that showed cytoplasmic, nuclear and nucleolar atrophy of the neurons of the red nucleus contralateral to operation with the exception of a possible transient cytoplasmic enlargement 9 days postoperatively. From the cytophotometric and morphometric data here reported we are led to suggest that the frequenyly observed failure of axonal repair in mammalian CNS results from the innately regressive nature of the axon reaction of many mammalian central neurons.     

The electroencephalogram in neglect.

The extent of electroencephalographic (EEG) abnormalities in 23 consecutive patients with unilateral neglect was compared with the extent of EEG abnormalities in 20 matched aphasic controls. In the neglect group, 22 patients showed EEG slowing that extended over the entire hemisphere. In the control group only 8 patients showed similar hemispheric slowing. This study demonstrates that patients with unilateral neglect from discrete lesions may have EEG slowing in regions of the hemisphere that are remote from the lesion. This study also provides support for the hypothesis that neglect is a unilateral arousal defect.     

Perivascular hemosiderin deposition in muscle in Waldenström's macroglobulinemia

A 63-year-old woman with Waldenström's macroglobulinemia of 5 years' duration developed disabling pain in her extremities. The patient had required frequent plasmapheresis and transfusion for treatment of hyperviscosity. Muscle biopsy from 2 separate sites showed striking deposition of hemosiderin in macrophages surrounding small blood vessels and features of slight denervation. Immunofluorescence demonstrated IgM deposition in vessel walls. Perivascular hemosiderin deposition in muscle has not previously been described and may reflect transfusion-hemosiderosis in a patient with a dysglobulinemia.     

Bone marrow in the Batten-Vogt syndrome.

Six children with clinical and pathological features of Batten-Vogt syndrome showed autofluorescent material in bone marrow cells and in 5 of them sea-blue histiocytes were seen. It is suggested that bone marrow examination for sea-blue histiocytes and autofluorescenceis a useful screening test for ceroid-lipofuscinosis.     

Delayed,relapsing experimental allergic encephalomyelitis in mice: Role of adjuvants and pertussis vaccine

The effect was studied of varying the dosage of mycobacteria and pertussis vaccine in the immunization emulsion on the development of delayed, relapsing experimental allergic encephalomyelitis (DR-EAE) in SJL/J mice. DR-EAE could be induced with dosages of mycobacteria from 0.2 mg to 1.0 mg per mouse. Animals given pertussis vaccine from different batches and different sources all developed DR-EAE with similar percentages of animals sick, animals relapsing, and delay to onset. Mice immunized without pertussis vaccine also developed DR-EAE but had fewer relapses and a longer delay to onset. The role of antigens and adjuvants in relapsing EAE and analogies with multiple sclerosis are discussed.     

Lightning eye movements.

Physiologic studies were performed on a patient who demonstrated lightning eye movements, palatal myoclonus and myoclonic jerks of the left platysma and sternocleidomastoid muscles. The myoclonus and lightning eye movements were separate phenomena with no defined relationship to each other. Analysis of this ocular dyskinesia identified strictly horizontal saccadic oscillations, 2 to 5 Hz in frequency, with amplitudes varying greatly but often reaching 25 degrees. A brief stationary period between each saccadic oscillation was frequently observed. They were particularly induced by vertical or horizontal ocular pursuit as well as sustained upward or downward ocular deviation. Caloric nystagmus abolished the oscillations but they persisted, irregularly, during optokinetic nystagmus. Thus a faulty visual fixation mechanism is postulated to precipitate lightning eye movements. Constrast studies revealed a mass lesion arising from the right dorsolateral portion of the medulla. These results indicate that lightning eye movements occur with caudal as well as rostral brain-stem lesions. From the clinical findings cerebellar pathway involvement is likely.     

A modification of eye-head coordination by CNS disease

When a subject, seated and facing ahead, was asked to look toward one side, the result was a combined movement of the eyes and head. Normal subjects began the eye movement just before the onset of head movement; 4 neurologic patients who showed abnormalities in eye movements (saccades that tended to be smaller in amplitude and lower in velocity than those of the control subjects) regularly began eye movement after the onset of head movement. Thus the initiation of head rotation was not as much retarded in these patients as that of eye movement. Amplitudes of the movements were reduced in the patients, but this change too was less for the head than for the eyes.Because the amplitude and velocity of the head movement were less affected in the patient group, the relative contribution of the head to the total gaze shift was increased.It appears as if, when the oculomotor system is affected, the head can assume a leading role in the initiation and execution of gaze shifts.     

Diagnosis of schizophrenia by computer and clinicians: A pilot study

Investigations show significant disagreement among mental health professionals in diagnosing schizophrenia.^1–11 Recently, computer-based systems have been used in attempts to improve diagnostic consistency. Spitzer and Endicott, among others, have devised a computer program using the Mental Status Examination Report (MSER) as input data.^12–19 The MSER is a systematic, relatively objective inventory of observed behaviors used to obtain a mental status. The MSER was used at the Hillside Division during 1973 and 1974. It was filled out 1 week after admission by therapists who were specially trained for this task. It was noted that a nonschizophrenic computer diagnosis was given to a number of patients diagnosed schizophrenic by clinicians, but the reverse rarely occurred. Was this due to the computer program, the MSER, clinicians, or other factors? These questions have heightened relevance in light of the imminence of Professional Standards Review Organization (PSRO).²⁰ Hospitals may be required to establish definitive operational diagnostic criteria and correlated treatments in order to maintain accreditation and be reimbursed by third-party payers. This study investigated these diagnostic discrepancies in order to ascertain what specific criteria could be used in making a schizophrenic diagnosis in hospitalized patients. Secondarily, the study sought to shed further light on whether such a computer system could be useful as an adjunctive diagnostic modality to pinpoint difficult cases.     

Amnestic disturbance following infarction of the left dorsomedial nucleus of the thalamus

A patient with a discrete lesion in the region of the left dorsomedial nucleus of thalamus had anterograde memory impairment for verbal material.     

Membranous neuronal and neuroglial inclusions produced by intracerebral injection of suramin

A single intracerebral injection of 5 μg of the trypanocidal drug Suramin, into the left hemisphere of young rats, resulted in the formation of membranous inclusion bodies within the perikarya and processes of neurones and neuroglia. These inclusion bodies were round or oval in shape and 0.5–3.0 μm in their longest diameter. They were bounded by a single trilaminar membrane and contained closely packed membranes in concentric, curved or parallel arrays. The inclusions were distributed throughout the cerebral cortex and underlying hippocampus at the injection site, and in reduced numbers up to 1 mm anteriorly and posteriorly from it. They formed within 22 hr of the injection and had increased in numbers and in the complexity of their arrays 3 days after injection. Within 14 days, the inclusions were markedly reduced in number. As Suramin is known to inhibit lysosomal hydrolases required for the degradation of proteins, glycolipids and mucopolysaccharides, the membranous inclusions could form as a result of the accumulation of these substances within lysosomes. These experiments indicate a possible experimental model for storage diseases. It is hoped that the extension of this paradigm to other enzyme inhibitors will provide a new means of identifying some of the unusual inclusions that can be found in neurones and neuroglia (Rees 1975).     

Facilitation of the lordosis reflex in female rats by electrical stimulation of the lateral vestibular nucleus.

(1) Electrical stimulation of the lateral vestibular nucleus (LVN) facilitated lordosis reflex responses to somatosensory stimulation, in estrogen-primed female rats. (2) Unilateral LVN stimulation was sufficient for this effect. Currents as low as 10muA could be used. (3) With the stimulus parameters used, the effect develops within 5 min of LVN stimulation and decays within 10 min following cessation of stimulation. (4) Together with previous evidence that LVN lesions disrupt lordosis, these results suggest LVN facilitation of spinal reflex mechanisms for lordosis.     

Familial concordance in schizophrenia: a comparative study of pairs of sibs.

Intrafamilial resemblance in psychiatric clinical features may provide a powerful tool to the search for an explanation of the distheis-stress duality. Family studies of schizophrenia have emphasized the role of familial concordance for subtype diagnosis,^1,2 symptomatology,^2,3,5 mode,² and age of onset,^2,5,7 outcome,⁸ and sex^9–14 in psychiatric research. Most of these studies have failed, however, to apply uniform criteria for the selection of patients and were based on retrospective and non-blind evaluation of family members.An attempt has been made in this study to apply updated research criteria for the diagnosis of schizophrenia and to evaluate probands in a blind fashion as regards their relatives. Combined variables have been analyzed in order to further elucidate the issue of familial homogeneity in schizophrenia. Efforts to correlate between the results of this study and certain biologic derangements are currently being made (Baron, et al.: Tissue-Serum Affinity in Schizophrenia: Clinical and Familial Determinants, in preparation), aimed at achieving a better understanding of the “nature-nurture” duality.     

Quantitative and cytometric analysis of the ventral cochlear nucleus in man

A systematic quantitative and cytometric study of the ventral cochlear nucleus has been performed on 3 groups of histologically normal brains, ranging in age from 20 weeks of gestation to adult life. Serial sections, 20 μm in thickness, through the length of the nucleus were obtained from paraffin-embedded blocks of the ponto-medullary junction. Every 10th section was analyzed with a Cambridge Imanco quantimet 720 Image Analyzing system. The surface area of the nucleus was determined on each slide. Cells showing neuronal characteristics were individually counted and classified into 18 pre-determined cell size classes. The raw total number of cells was then corrected for periodicity and split cell error. The total volume of the nucleus and cell packing density were estimated. The mean total number of neurons was 26,098 in premature, 31,802 in full term and 30,440 in adult cases. There was no significant difference among these values. The mean volume of the nucleus was 1.32 mm³ in premature, 3.84 in full term and 5.43 in adult cases. Positive correlation coefficients were found comparing volume versus age. A negative correlation coefficient was detected comparing cell packing density versus age from the full term period to adult life. A significant increase in the number of cells in the largest cell classes was also found with increasing age. The mean neuronal diameter did not change significantly between premature and full term cases but was significantly different between full term and adult cases. These findings are discussed and compared to already reported quantitative studies of the ventral cochlear nucleus in man, which involved manual counting techniques.     

Material specific hemispherical arousal.

It has been previously demonstrated that warning stimuli (WS) reduce reaction time (RT) by causing cortical activation. The purpose of this study was to use verbal and non-verbal WS to see if these stimuli asymmetrically activate the cerebral hemispheres.Sixteen right-handed Ss were given a manual RT task using a light as the RT stimulus and either verbal or non-verbal sounds as WS. RTs by the right hand were significantly faster with verbal WS than with non-verbal WS. There were no significant differences for the left hand between the verbal and non-verbal WS. These results give partial support to the asymmetrical activation hypothesis.     

Hydrocephalus and dementia in Paget's disease of the skull

Three patients with Paget's disease of the skull are reported. These individuals developed basilar impression associated with impairment of gait, sphincter incontinence and mental deterioration. The memory loss of the early stages was followed later by progressive psychomotor retardation, apathy and inattention eventually leading to stupor and akinetic mute states.The underlying pathologic disturbance is progressive communicating hydrocephalus that develops as a consequence of obstruction of the posterior fossa cisterns and anatomical distortion of the Sylvian aqueduct, in turn the result of basilar impression. In the final stages the advancing basilar impression pushes the brain stem against the expanding floor of the third ventricle occluding the cisterna interpeduncularis and probably compromising the blood flow through the vessels therein contained, namely arteriae thalamo-perforantes and choroidea posterior mediales, with resulting chronic anoxia of thalamic nuclei.The establishment of a ventriculo-jugular shunt in case 3 resulted in remarkable temporary restitution of mental faculties. A similar operation in case 1 was unsuccessful possibly because of permanent thalamic lesions. In case 2 a suboccipital craniectomy was followed a week later by the establishment of a ventriculo-jugular shunt. The patient developed progressive stupor and died, presumably as a consequence of the severe hydrodynamic alteration surgically created.The pathogenetic postulates hereby presented offer a rationale for the palliative treatment of progressive dementia occurring in association with acquired basilar impression in Paget's disease.     

Experimental ischemic myopathy: Effects of aortic ligation and serotonin

Support for the hypothesis that biogenic amines are involved in the production of muscle diseases comes from a report that rat muscle is damaged by combining distal aortic ligation with serotonin injection. Our studies explore the role of serotonin in the production of the myopathic changes in the aortic ligation-serotonin model. Twenty-six young Sprague-Dawley rats were subjected either to aortic ligation alone, aortic ligation followed by injection of serotonin (40 mg/kg, i.p.), or injection of serotonin alone. Following sacrifice 7–14 days later, 10 μm frozen sections of the soleus muscle were stained by trichrome, NADH-TR, and ATPase methods. Focal necrosis and phagocytosis or focal regeneration were seen after aortic ligation with, or without, subsequent serotonin injection. Serotonin alone produced only occasional mild changes in muscle. Therefore, we conclude that the significant damage to muscle in the ligation-serotonin model is provided by the aortic ligation, not the serotonin injection.