Histochemical and pharmacological analysis of catecholaminergic projections to the perifornical hypothalamus in relation to feeding inhibition

Three techniques, namely, midbrain lesions, fluorescence histochemistry, and brain cannulation, were used in combination to analyze noradrenergic projections to the paraventricular nucleus of the hypothalamus (PVN) and their function in stimulating feeding behavior. The convergence of evidence indicates that the dorsal component of the central tegmental tract (CTT), which ascends through the dorsal pons and then projects through the medial tegmental radiations (TR) into the ventral tegmentum just dorsal to the medial lemniscus, contains the crucial noradrenergic axons which innervate the PVN and mediate noradrenergic stimulation of feeding behavior. The primary evidence for this conclusion is that dorsal tegmental electrolytic or 6-OHDA lesions which damaged specifically these fibers invariably caused: (1) a reduction of catecholamine varicosities within the PVN (most notably, fine and moderate-size, rounded varicosities within the parvocellular area); (2) a strong reduction or loss of the feeding response elicited by PVN injection of the presynaptically-acting drugs tranylcypromine and desipramine; and (3) a potentiation of the same response produced by injected norepinephrine. These pharmacological and neurochemical changes in the PVN were reduced in magnitude if the dorsal CTT and medial TR fivers received only partial damage, and these changes did not occur at all if the lesion fell immediately dorsal to these fibers without damaging them. Specific lesions in the ventral tegmentum, which also failed to damage the dorsal CTT and TR axons but instead damaged the ventral component of the CTT, not only failed to disrupt the action of the antidepressant agents but actually potentiated their effectiveness in the PVN. Ventromedial lesions, however, which severed the rostroventral extension of the dorsal CTT and medial TR fibers, had the same behavioral consequences as had the dorsal lesions which damaged this projection at a more dorsocaudal level. Finally, damage to other catecholamine projections had little effect on PVN function in stimulating eating.     

Development of pyramidal cells in medial frontal cortex following neonatal lesions of anterior midline cortex

The anterior midline cortex of rats was removed on postnatal day 10. The development of layer II, III and V pyramidal cells in the tissue that subsequently formed the presumptive medial frontal cortex in these animals was studied in Golgi-Cox stained material on postnatal days 15, 25, 35, and 120. The results showed that the number of branch segments of both basilar and apical dendrites were significantly reduced relative to controls at the early developmental stages but by adulthood all regions analyzed were similar in operates and controls. Thus, the cells migrating into the lesion area were delayed in development but did eventually grow to resemble cells that were in the same region in normal controls. This anatomical development correlates with the functional recovery of animals with day 10 frontal lesions in other studies, and suggests that the growth of this tissue may play a role in functional recovery.     

Gait disturbances in patients with pontine medial tegmental lesions: clinical characteristics and gait analysis

OBJECTIVE: To determine the clinical characteristics of gait disorders in patients with pontine medial tegmental lesions. DESIGN: We compared features of gait disorders between patients with infarcts in the medial tegmentum and those with stroke in other areas of the pons (pathological control subjects) by measuring electromyographic results of lower limb muscles and several biomechanical parameters. PATIENTS: Two patients with infarcts in the rostral medial tegmentum and 4 control subjects. Two of the control patients had lesions in the pontine base, while the lesions in the other 2 were in the pontine tegmentum and base (combined lesions). RESULTS: Patients with rostral medial tegmental lesions and controls with pontine base lesions showed unstable walking characterized by irregular angular displacements and foot pressures. However, they differed by the following 3 features. (1) Rostral medial tegmental lesions elicited truncal ataxia without limb ataxia. In comparison, pontine base lesions elicited limb ataxia without truncal ataxia and caused hemiparesis. (2) Instability was more severe and persistent in patients with the former lesions than in those with the latter lesions. Slowness of walking speed and prolongation of the double-support period were clearly observed in the former group. (3) Electromyographic changes characteristic of cerebellar ataxia were clearly evident in patients with rostral medial tegmental lesions. The electromyographic amplitudes of the gastrocnemius and tibialis anterior muscles were almost constant throughout the gait cycle, resulting in the disappearance of the inherent periodic pattern of each muscle. CONCLUSION: Medial tegmental lesions in the rostral pons cause prolonged and severe unstable walking that resembles spinocerebellar ataxic pattern, and impairment of the spinocerebellar loop might be the pathomechanism underlying such a gait disturbance.     

Efferent connections of the lateral hypothalamic area of the rat: An autoradiographic investigation

The efferent projections of the lateral hypothalamic area (LHA) at mid-tuberal levels were examined with the autoradiographic tracing method. Connections were observed to widespread regions of the brain, from the telencephalon to the medulla. Ascending fibers course through LHA and the lateral preoptic area and lie lateral to the diagonal band of Broca. Fibers sweep dorsally into the lateral septal nucleus, cingulum bundle and medial cortex. Although sparse projections are found to the ventromedial hypothalamic nucleus, a prominent pathway courses to the dorsal and medial parvocellular subnuclei of the paraventricular nucleus. Labeled fibers in the stria medullaris project to the lateral habenular nucleus. The central nucleus of the amygdala is encapsulated by fibers from the stria terminalis and the ventral amygdalofugal pathway. The substantia innominate, nucleus paraventricularis of the thalamus, and bed nucleus of the stria terminalis also receive LHA fibers. Three descending pathways course to the brainstem: (1) periventricular system, (2) central tegmental tract (CTT), and (3) medial forebrain bundle (MFB). Periventricular fibers travel to the ventral and lateral parts of the midbrain central gray, dorsal raphe nucleus, and laterodorsal tegmental nucleus of the pens. Dorsally coursing fibers of CTT enter the central tegmental field and the lateral and medial parabrachial nuclei. The intermediate and deep layers of the superior colliculus receive some fibers. Fibers from CTT leave the parabranchial region by descending in the ventrolateral pontine and medullary reticular formation; some of these fibers sweep dorsomedially into the nucleus tractus solitarius, dorsal motor nucleus of the vagus, and nucleus commissuralis. From MFB, fibers descend into the ventral tegmental area and to the border of the median raphe and raphe magnus nuclei.     

Origin of brain stem and temporal cortical afferent fibers to the septal region in the squirrel monkey

The origins of the brain stem and temporal cortical projections to the septal region in the squirrel monkey were investigated with the horseradish peroxidase (HRP) retrograde axonal transport technique. After HRP injections placed into the septal region, labeled cells were observed in brain stem sites which generally correspond to regions which are associated with known monoamine cell groups previously identified in the primate. These structures include the nucleus locus ceruleus, dorsal tegmental nucleus of Gudden, nucleus reticularis tegmenti pontis, nucleus annularis, ventral tegmental region, and the medial aspect of the lateral hypothalamus. Temporal cortical efferent fibers to the septal region arise principally from layers II and III of the perirhinal region, suggesting the presence of a second-order olfactory innervation of this structure.     

Striatopallidonigral degeneration in Pick's disease: a clinicopathological study of 41 cases

Summary The frequency and degree of stiatopallidonigral (SPN) degeneration were examined in 41 autopsy cases of Pick's disease. Based on the degree of SPN degeneration, these cases were arranged into four groups: 1) group I (severely degenerate; 19.5%), 2) group II (moderately degenerate; 22.0%), 3) group III (mildly degenerate; 36.5%), and 4) group IV (non-degenerate; 22.0%). 17 of the 41 cases had a definite (moderate to severe) SPN degeneration. The striatum, especially the caudate nucleus, was most frequently and most severely affected, while the internal segment of the globus pallidus was least frequently and least severely affected. In general, the oral portions of the SPN nuclei were more severely involved. In addition, in the putamen and globus pallidus the dorsomedial portions adjacent to the internal capsule were apt to be affected more markedly than the other portions. In the substantia nigra the degeneration tended to be more predominant in the pars reticulata than in the pars compacta, although both were usually involved. In addition, the medial to central portions of the substantia nigra were more vulnerable. In comparing the severely and moderately degenerate groups (groups I and II) with the mildly and non degenerate groups (groups III and IV), the former had more female cases, longer duration of illness, and more third-stage cases. In addition, the former contained more cases with lower brain weight and (predominant) frontal atrophy type, and more atypical cases without Pick bodies, or with symmetrical pyramidal tract degeneration or with combined traumatic lesions. It is notable that in all cases with definite SPN degeneration no extrapyramidal involuntary movements had been detected.     

Intraoperative MRI with integrated functional neuronavigation-guided resection of supratentorial cavernous malformations in eloquent brain areas

Between March 2009 and January 2010, 36 patients with 38 supratentorial cavernous malformations in eloquent brain areas underwent surgery with the aid of intraoperative MRI (iMRI), functional neuronavigation, and electrocorticography (ECoG). To optimize outcomes, the hemosiderin-stained tissue surrounding the lesion in addition to the cavernous malformation itself (lesion) was microsurgically removed, leaving behind only small areas adjacent to, or overlapping with, functional areas. According to the Zabramski classification, there were 13 type I lesions, which all underwent total resection. There were 25 type II or III lesions with a surrounding hypointense rim, and all of these lesions were completely removed; the surrounding hypointense rims were completely removed in 15 patients and partially removed in 10. No new neurologic disorders occurred postoperatively. Twenty patients had preoperative epileptic seizures, nine of whom were refractory to treatment. During follow-up, seizure outcome was assessed using the Engel classification, and 11 patients with non-refractory epilepsy had a class I outcome. Of the nine patients with refractory epilepsy, seven (77.8%) had a class I outcome, one (11.1%) had a class II outcome, and one (11.1%) had a class III outcome.     

Diagnostic difficulties in childhood bilateral thalamic astrocytomas

We report on two children with bilateral thalamic astrocytomas. The first patient developed psychomotor regression at the age of 20 months followed by rapidly progressive ataxia, intention tremor, slurred speech, and bouts of drowsiness. Magnetic resonance imaging (MRI) of the brain showed swelling and high signal intensity in both thalami accompanied by supratentorial hydrocephalus. The second patient presented with progressive cerebellar ataxia, headache, and vomiting at the age of 11 years. MRI of the brain revealed symmetrical, hyperintense and sharply delineated swelling of both thalami. Additional lesions were seen in the cerebellum and the right temporal lobe. In both cases proton magnetic resonance spectroscopy (MRS) of the lesions showed a striking decrease of the neuronal marker N-acetylaspartate, an increase of choline-containing compounds, and a minimal lactate peak. Stereotactic biopsies from the thalamus of the first patient and from a cerebellar lesion of the second patient finally revealed glial tumors, namely a diffuse astrocytoma of World Health Organization (WHO) grade II in the first patient and an anaplastic astrocytoma of WHO grade III in the second patient. We conclude that the clinical manifestations and MRI patterns of bilateral thalamic astrocytomas are very similar to those of encephalitis and neurometabolic disorders and should therefore be included in the differential diagnosis of these encephalopathies.     

Relation between the EEG image and the damaged area in cerebrovascular diseases

The author tried to establish the value of EEG investigations in the cases of cerebrovascular diseases of ischaemic type, mainly in relation to the site of damage. EEG investigations were carried out in 200 cases divided into 4 groups of 50 patients in each according to the location of the lesion. The sites of the lesions were in group I in the internal capsule, in group II in the cortex, in group III disseminated foci were situated in both cerebral hemispheres, in group IV in the brain stem. On the basis of EEG investigations certain tendencies were established differentiating these groups: in group I mostly episodic changes were found on the side of damage, in group II intensive focal changes prevailed, in group III changes of background activity were the most frequent finding, in group IV usually bilateral episodic changes were usually present. The obtained results point out that EEG may be of some use helping the clinician in recognizing the site of the lesion and in establishing the prognosis.     

GABAergic and non-GABAergic projections of accessory optic nuclei, including the visual tegmental relay zone, to the nucleus of the optic tract and dorsal terminal accessory optic nucleus in rat.

This study examines the non-gamma-amino butyric acid (GABA)ergic (group I neurons) and GABAergic neurons (group II neurons) of the accessory optic system projecting to the nucleus of the optic tract (NOT)/dorsal terminal nucleus (DTN) of the accessory optic system in rat. These nuclei include the dorsal (MTNd) and ventral (MTNv) divisions of the medial terminal nucleus, the lateral terminal nucleus, the interstitial nucleus of the superior fasciculus, the posterior fibers, and the visual tegmental relay zone. GABAergic neurons of these nuclei that do not target the NOT/DTN (group III neurons) have also been observed. The fluorescent retrograde tracer fluoro-gold was injected into the pretectum, targeting the NOT/DTN and the tissue prepared immunocytochemically to reveal neurons containing the neurotransmitter GABA. Three groups of neurons (groups I, II, and III neurons) were examined in terms of their distribution, density, and percentage present. Group I neurons are single-labeled with fluoro-gold and represent non-GABAergic neurons projecting to the NOT/DTN. These neurons are of the highest density in the lateral terminal nucleus (204 neurons/mm2). Their densities are also substantial in the MTNv (120 neurons/mm2), interstitial nucleus of the superior fasciculus, posterior fibers (96 neurons/mm2), and visual tegmental relay zone (93 neurons/mm2). Group II neurons are double-labeled with fluoro-gold and GABA. They form a system of GABAergic neurons projecting to the NOT/DTN, which are exceedingly dense in the MTNd (78 neurons/mm2) but are also dense in both the visual tegmental relay zone (49 neurons/mm2) and MTNv (33 neurons/mm2). Group III neurons are GABAergic neurons that do not target the NOT/DTN but must project to other brain nuclei and/or be interneurons. These are of extremely high concentration in the visual tegmental relay zone (316 neurons/mm2) and are also of substantial densities in the MTNd (77 neurons/mm2), lateral terminal nucleus (72 neurons/mm2), and MTNv (44 neurons/mm2). The MTNd has the highest percentage of GABAergic neurons projecting to the NOT/DTN (72%). GABAergic neurons also form significant percentages of the projections to the NOT/DTN from the visual tegmental relay zone (34%) and MTNv (21%). The percentage of the total GABAergic neurons that project to the NOT/DTN is the highest in the MTNd (50%) and MTNv (42%). The described GABAergic afferents to the NOT/DTN may function to process information concerned with the compensation for retinal slip.     

Postnatal development of preproenkephalin mRNA containing neurons in the rat lower brainstem

Postnatal developmental changes of preproenkephalin (PPE) gene expression in rat brainstem neurons were studied by in situ hybridization histochemistry. On the basis of PPE mRNA expression, brainstem neurons were categorized into three types: 1) type I neurons were characterized by constant or increasing expression of PPE mRNA during postnatal development; 2) type II neurons started to express PPE mRNA several days after birth and continued to do so thereafter; and 3) type III neurons showed transient expression of PPE mRNA or stopped expressing the mRNA during early postnatal development. Type I PPE neurons were observed in diverse brainstem structures including the mesencephalic and pontine central gray matter, various reticular and raphe nuclei, the ventral tegmental area of Tsai, the interpeduncular nucleus, the nucleus of the brachium of the inferior colliculus, the ventral and dorsal tegmental nuclei of Gudden, the sphenoid nucleus, the laterodorsal tegmental nucleus, Barrington's nucleus, the parabrachial region, the lateral lemniscus and its related nuclei, the trapezoid nucleus, the rostral and ventromedial periolivary nuclei, the mesencephalic trigeminal and principal sensory trigeminal nuclei, the locus coeruleus, the subcoeruleus nucleus, the medial and spinal vestibular nuclei, the dorsal and ventral cochlear nuclei, the medial and lateral cerebellar nuclei, the Roller nucleus, and the intermedius nucleus of the medulla. Type II PPE neurons were found in the superior colliculus, the inferior colliculus, the central part of the dorsal tegmental nucleus, and as Golgi neurons in the granular layer of the cerebellum. Type III PPE neurons were located in the substantia nigra, the red nucleus, the superior olive, the motor trigeminal nucleus, the facial nucleus, the inferior olive, the dorsal motor nucleus of the vagus, and the hypoglossal nucleus. Such region-specific expression of the PPE gene during postnatal ontogeny suggests that rat brainstem PPE neurons may be involved in a variety of developmental events, such as cell proliferation, differentiation, and migration.     

Functional mapping of the effects of lesions of the habenular nuclei and their afferents in the rat

Through the use of the quantitative autoradiographic 2-[14C]deoxyglucose technique, we have investigated the functional significance of the habenular nuclei by the measurement of local cerebral glucose utilization (LCGU) in discrete brain areas of conscious rats following 3 kinds of lesioning. Bilateral electrolytic lesions of the habenular nuclei decreased LCGU in a limited number of well-defined brain areas (the interpeduncular nucleus, median and dorsal raphe, mammillary body and dorsal tegmental nucleus) at 7 and 14 days after lesions. These changes were also observed 180 days following lesioning except that of the dorsal tegmental nucleus. At 14 days after bilateral ibotenic acid-induced lesions of the lateral habenula, LCGU was significantly decreased in the median and dorsal raphe, mammillary body and interpeduncular nucleus. In further studies, bilateral electrolytic lesions of the stria medullaris (which conveys the major afferents to the habenula) decreased glucose use in the interpeduncular nucleus less than that observed after bilateral electrolytic lesions of the habenular nuclei. A highly significant positive correlation was observed between LCGU and choline acetyltransferase activity in the interpeduncular nucleus after all types of lesion. These results further support the view that the medial and the lateral habenula exert a major influence upon functional activity in the interpeduncular nucleus and the mesencephalic raphe nuclei, respectively.     

Neuroanatomy of pseudobulbar affect

Pseudobulbar affect (PBA) is defined as episodes of involuntary crying, laughing, or both in the absence of a matching subjective mood state. This neuropsychiatric syndrome can be found in a number of neurological disorders including multiple sclerosis (MS). The aim of this study was to identify neuroanatomical correlates of PBA in multiple sclerosis (MS) using a case-control 1.5T MRI study. MS patients with (n = 14) and without (n = 14) PBA were matched on demographic, disease course, and disability variables. Comorbid psychiatric disorders including depressive and anxiety disorders were absent. Hypo- and hyperintense lesion volumes plus measurements of atrophy were obtained and localized anatomically according to parcellated brain regions. Between-group statistical comparisons were undertaken with alpha set at 0.01 for the primary analysis. Discrete differences in lesion volume were noted in six regions: Brainstem hypointense lesions, bilateral inferior parietal and medial inferior frontal hyperintense lesions, and right medial superior frontal hyperintense lesions were all significantly higher in the PBA group. A logistic regression model identified four of these variables (brainstem hypointense, left inferior parietal hyperintense, and left and right medial inferior frontal hyperintense lesion volumes) that accounted for 70% of the variance when it came to explaining the presence of PBA. In conclusion, MS patients with PBA have a distinct distribution of brain lesions when compared to a matched MS sample without PBA. The lesion data support a widely-dispersed neural network involving frontal, parietal, and brainstem regions in the pathophysiology of PBA.     

Comparison of subgroups based on hemorrhagic lesions between SWI and FLAIR in pediatric traumatic brain injury

Purpose

The purpose of this study was to investigate efficient ways to diagnose and predict clinical outcomes for childhood traumatic brain injury.

Methods

Hemorrhagic signal intensities in nine brain regions were observed using axial fluid-attenuated inversion recovery (FLAIR) and susceptibility-weighted imaging (SWI). After having divided the subjects into mild presentation (GCS 14–15) and moderate-to-severe presentation groups (GCS ≤13), we divided the patients into three subgroups: Subgroup I, hemorrhagic foci observed only on SWI and not on FLAIR; Subgroup II, hemorrhagic foci observed on both SWI and FLAIR in the same brain regions; and Subgroup III, any cases with additional foci on SWI in other brain regions. We investigated the clinical course and compared lesion numbers and distributions of hemorrhagic lesions on SWI among the subgroups.

Results

Three clinical variables (hospitalization period in intensive care unit, total days of hospitalization, and outcome based on Pediatric Cerebral Performance Category Scale score) showed significant relevance to the three subgroups. Subgroup I showed the fewest lesions followed by Subgroups II and III, respectively. In all three subgroups, lesions were most abundant in cortical regions. Lesion in the thalamus, basal ganglia, corpus callosum, and brainstem was least in Subgroup I and gradually increased in Subgroups II and III. Such distinction was more significant in the moderate-to-severe group when compared with the mild group.

Conclusions

In cases of pediatric traumatic brain injury, categorizing patients into one of the above three subgroups based on hemorrhagic lesions on SWI and FLAIR is a promising method for predicting patient’s clinical outcome.     

Streptokinase treatment versus calcium overload blockade in experimental thromboembolic stroke

Thromboembolic brain ischemia was produced in dogs using an autologous blood clot model. The effect of postembolic treatment with flunarizine and streptokinase on hemispheric cerebral metabolic rate for oxygen (CMRO2), oxygen extraction ratio (OER), and cerebral blood flow (CBF) was studied by positron emission tomography (oxygen-15 technique) 24 hours after the insult. We studied five groups of experimental dogs and compared them with a control group of nonembolized dogs. Group I received no treatment, Group II was treated locally with 500,000 IU streptokinase starting 30 minutes after the insult, Group III received streptokinase locally 30 minutes after the insult and 0.1 mg/kg i.v. flunarizine immediately after the insult and 2 hours later, Group IV received flunarizine as Group III, and Group V was orally pretreated with 0.5 mg/kg/day flunarizine during 2 weeks preceding embolization. Compared with the contralateral hemisphere, in the embolized hemisphere a significant reduction of CMRO2 (-25% to -40%) and CBF in normocapnia (-35%) and hypercapnia (-50%) was observed in Groups I, II, and V. In Groups III and IV, CMRO2, OER, and CBF of the embolized hemisphere were within the normal range during normocapnia and hypercapnia; the extent of the ischemic lesions was markedly less than in the other groups of experimental dogs. We conclude that flunarizine treatment after experimental thromboembolic stroke had a favorable influence on brain tissue. Chronic preventive flunarizine treatment failed to have a beneficial effect.     

Psychiatric co-morbidity in 75 patients undergoing epilepsy surgery: lack of correlation with pathological findings

BACKGROUND: Psychiatric disorders may occur in patients with intractable partial epilepsy after surgical treatment. Previous reports attributed the presence of psychological adverse events to specific pathological entities such as dysembryoplastic neuroepithelial tumors (DNETs) and gangliogliomas. The rationale for the present study is to evaluate the importance of the surgical pathology in individuals undergoing epilepsy surgery. METHODS: The patients were separated into three groups based on the surgical pathology: group I ganglioglioma (N=25), group II DNETs (N=25), and group III mesial temporal sclerosis (N=25). Thirteen of the 75 patients (17.3%) had a preexisting psychiatric disorder. The most common preoperative psychiatric diagnosis was depression (N=4). Sixty-three of the lesions (84%) were restricted to the temporal lobe. The operative strategy included resection of the lesion and epileptogenic cortex. Sixty-two of the 75 patients (83%) were rendered seizure-free. RESULTS: Eight of the 75 patients (10.7%) had an acquired psychiatric illness following surgical treatment. A mood disorder developed in three patients after surgery. No statistical difference emerged in preoperative psychiatric co-morbidity (no group difference; p=1.0) or in newly diagnosed postoperative psychiatric disease (group I vs. II, p=0.67; group I vs. III, p=1.0; and group II vs. III, p=0.67) within the three surgical pathology groups. CONCLUSION: This study indicates that the presence of psychiatric disease before and after surgery for intractable partial epilepsy, predominantly of temporal lobe origin, was independent of the pathological findings.     

Hemispheric lateralization of spatial contrast sensitivity

Visuospatial contrast sensitivity was determined by the Arden grating chart in 23 patients with cerebral infarctions involving the primary visual cortex or visual association cortex. Subjects were classified into three groups according to their lesions: I, 6 patients with unilateral medial occipital or occipitotemporal lesions; II, 6 patients with left lateral parieto-occipital lesions; and III, 11 patients with right lateral parieto-occipital lesions. Contrast sensitivity was markedly reduced in Group III, especially in patients having hemispatial agnosia. Group I patients with hemispatial agnosia showed almost normal contrast sensitivity. Spatial contrast sensitivity appears to be more affected when the lesion has an influence on the nondominant lateral parieto-occipital cortex.     

Innervation of sweat glands in the forehead. A study in patients with Horner's syndrome

The amount of sweating in lateral and medial sites in the forehead was investigated with quantitative evaporimetry in 18 patients with Horner's syndrome: eight cases with a central (1st), five with a preganglionic (2nd), and five with a postganglionic (3rd) neurone lesion. The amount of sweating was measured after body heating, and, at another occasion, after intracutaneous injection of the cholinergic drug pilocarpine. The two sites were at the root of the nose (medial position) and at the lateral angle of the eye (lateral position). Generally, there was a reduced level of sweating on the symptomatic versus the non-symptomatic side in both positions during body heating, except in the lateral part of the forehead in the 3rd neurone lesions, where sweating was greater on the symptomatic than on the non-symptomatic side. There was a nearly symmetrical sweating response after pilocarpine injection at all sites. There was one exception to this rule; the lateral position in the preganglionic neurone lesion group where pilocarpine induced more sweating on the non-symptomatic side. Thus, the results suggest a relative supersensitivity to pilocarpine in the medial position for all patients and in the lateral position for the central neurone lesion group. The findings suggest that the innervation of sweat glands in the medial and lateral parts of the forehead is different, the medial part being supplied by nerve fibres from the sympathetic plexus of the internal carotid artery, while the sweat glands in the lateral part is furnished from the plexus surrounding the external carotid artery.     

The prognostic value of somatosensory evoked potentials in traumatic primary and secondary brain stem lesions

To estimate the prognostic value of somatosensory evoked potentials elicited via stimulation of the median nerve (M-SSEP) in cases of primary and secondary brainstem lesions 126 patients with traumatic brainstem lesions (GCS < or = 6) were investigated on admission to our hospital. Various parameters of the patients' M-SSEP were compared with the corresponding data of 40 healthy persons. Latency and amplitude of the cervical (N14) and cortical (N20) derived potentials and the central conduction time (CCT) were taken into account. Changes or a loss of the N20 signal and of the CCT were related to clinical outcome for up to two years. All patients had a normal N14 bilaterally. Most patients with a primary brainstem lesion (n = 25) showed symmetrical N20 changes bilaterally. However, the majority of patients with a secondary brainstem lesion (n = 62) showed asymmetric N20 changes in M-SSEP which became more symmetrical in cases with marked progressive brainstem compression. Irrespective of a primary or secondary traumatic brainstem lesion, marked changes of N20 represented an unfavourable clinical prognosis. A loss of N20 was closely correlated with a very poor outcome (GOS 1-2) if the N20 potential had not recovered within 48 hours. The recovery of this potential, however, was not necessarily correlated to a recovery of the brain function.     

Frontal torticollis (head tilt) induced by electrolytic lesion and kainic acid injection in monkeys and cats

Unilateral electrolytic lesions (11 monkeys, 7 cats), kainic acid (KA) injections (3 cats), or 5,7-dihydroxytriptamine (5,7-DHT) injections (5 cats) were made in the dorsomedial mesencephalic tegmentum. Electrolytic and KA lesions, but not 5,7-DHT lesions, produced some degree of frontal torticollis (16 animals). The frontal torticollis, characterized by a lateral flexion of the head (tilt) to the shoulder opposite the side of the lesion, was associated with intermittent contractions of the neck muscles resulting in spasmodic head movements. Histological analysis of the electrolytic lesions indicated that the medial mesencephalic reticular formation and fibers from the superior cerebellar peduncle and the central tegmental tract were involved whether frontal torticollis was present or not. Conversely, among several cell groups that were sometimes affected, the interstitial nucleus of Cajal (INC) was always damaged in animals displaying frontal torticollis, whereas it was spared in animals not displaying head tilt. These results suggest that lesion of the INC is critical for the production of frontal torticollis.