Cheiro-oral-pedal syndrome.

The cheiro-oral syndrome is a well-known peculiar sensory disturbance seen around the corner of the mouth and in the palm of the hand on the same side. However, sensory disturbance around the corner of the mouth, in the palm of the hand and in the foot on the same side (cheiro-oral-pedal syndrome) has not been reported until now. We examined 2 cases of cheiro-oral-pedal syndrome; the lesion responsible was confirmed by magnetic resonance imaging to be in the medial lemniscus and in the ventral ascending tract of the trigeminal nerve.     

Parasagittal hemangioma associates with unilateral cheiro-oral-pedal syndrome

Cortical lesion might elicit restricted acral sensory deficit but a disparity of topographies in cheiro-oral-pedal syndrome is very rare. We report the first case of cheiro-oral-pedal syndrome due to a contralateral parasagittal hemangioma involving the supplement sensory area in parietal lobe. This unusual link between neuroanatomy and neurological feature is discussed.     

Cheiro-oral-pedal syndrome due to brainstem hemorrhage

Cheiro-oral-pedal syndrome is characterized by specific sensory disturbance around the corner of the mouth, in the hand and in the foot on the same side. Lesions responsible for causing this syndrome vary. We report two cases of cheiro-oral-pedal syndrome due to midbrain and pontine hemorrhage, respectively. Pontine hemorrhage producing cheiro-oral-pedal syndrome has been reported in three cases, but this is the first case that midbrain hematoma exhibits this syndrome. Damage in the sensory pathway can cause cheiro-oral-pedal syndrome. Difference in the threshold may explain the specific sensory pattern in this syndrome. Cheiro-oral-pedal syndrome is caused by lacunar infarction in majority of the cases. However, it should be kept in mind that hematomas can cause cheiro-oral-pedal syndrome.     

Cheiro-oral syndrome following midbrain haemorrhage

Summary Cheiro-oral syndrome, a sensory disturbance of the corner of the mouth and the palm of the hand due to a lesion in the midbrain has never been reported previously. We describe a 67-year-old woman with cheiro-oral syndrome following midbrain haemorrhage confirmed by computed tomographic (CT) scan. A CT scan and neurological findings showed that the syndrome was due to a lesion in the medial lemniscus of left midbrain. Consequently, not only parietal lobe lesions and limited lesions in the inferior medial portion of the posterolateral ventral nucleus (VPL) and lateral part of the posteromedial ventral nucleus (VPM), but also damage to a restricted group of fibres reaching these nuclei, may cause cheiro-oral syndrome.     

Bilateral cheiro-oral syndrome following pontine haemorrhage

Summary Cheiro-oral syndrome is a peculiar sensory disturbance observed around the corner of the mouth and the palm of the hand on the same side, usually occurring unilaterally. A male patient with bilateral cheiro-oral syndrome following pontine haemorrhage is reported. CT, MRI and neurological findings showed that the syndrome was due to a lesion in the medial lemniscus and ventral secondary ascending tract of the trigeminal nerve on both sides. Although unilateral cheirooral syndrome has been reported with a lesion in the parietal lobe, thalamus or brain stem, a bilateral syndrome could be caused only by a lesion of the brain stem.     

Entopeduncular nucleus projections to the contralateral thalamic nuclei: an HRP study

Neurons of the entopeduncular nucleus projecting to the ventral anterior, ventral lateral and centromedian nuclei of the thalamus were identified on the contralateral, as well as the ipsilateral side, by the retrograde transport of horseradish peroxidase in the cat.     

Deep brain stimulation to treat hyperkinetic symptoms of Cockayne syndrome.

Cockayne syndrome manifests a spectrum of neurological dysfunction that includes medically intractable movement disorders. Deep brain stimulation has not been well studied in such rare neurodegenerative conditions. In this case, stimulation of the ventral intermediate nucleus of the thalamus was used to manage severe motor symptoms in a young man with Cockayne syndrome. There was a marked and progressive response to thalamic stimulation within weeks of surgery. These results suggest that patients with Cockayne syndrome should be considered for deep brain stimulation to treat refractory movement disorders.     

A subset of thalamocortical projections to the retrosplenial cortex possesses two vesicular glutamate transporter isoforms,VGluT1 and VGluT2, in axon terminals and somata

Vesicular glutamate transporter isoforms, VGluT1–VGluT3, accumulate glutamate into synaptic vesicles and are considered to be important molecules in glutamatergic transmission. Among them, VGluT2 mRNA is expressed predominantly throughout the dorsal thalamus, whereas VGluT1 mRNA is expressed in a few thalamic nuclei. In the thalamic nuclei that project to the retrosplenial cortex (RSC), VGluT1 mRNA is expressed strongly in the anterodorsal thalamic nucleus (AD), is expressed moderately in the anteroventral and laterodorsal thalamic nuclei, and is not expressed in the anteromedial thalamic nucleus. Thus, it has been strongly suggested that a subset of thalamocortical projections to RSC possesses both VGluT1 and VGluT2. In this study, double‐labeled neuronal somata showing both VGluT1 and VGluT2 immunolabelings were found exclusively in the ventral region of AD (vAD). Many double‐labeled axon terminals were also found in two major targets of vAD, the rostral part of the reticular thalamic nucleus and layers Ia and III–IV of the retrosplenial granular b cortex (RSGb). Some were also found in layer Ia of the retrosplenial granular a cortex (RSGa). These axon terminals contain significant amounts of both VGluTs. Because the subset of thalamocortical projections to RSC has a unique molecular basis in the glutamatergic transmission system, it might play an important role in the higher cognitive functions processed in the RSC. Furthermore, double‐labeled axon terminals of a different type were distributed in RSGb and RSGa. Because they are small and the immunoreactivity of VGluT2 is significantly weaker than that of VGluT1, they seemed to be a subset of corticocortical terminals. J. Comp. Neurol. 522:2089–2106, 2014. © 2013 Wiley Periodicals, Inc.     

Monosynaptic and disynaptic projections from the substantia nigra pars reticulata to the parafascicular thalamic nucleus in the rat

We examined a direct pathway and an indirect pathway via the reticular thalamic nucleus (RT) from the substantia nigra pars reticulata (SNr) to the parafascicular thalamic nucleus (PF) by using anterograde and retrograde tract tracing methods. After biotinylated dextranamine (BDA) injection into the dorsolateral part of the SNr, many labeled fibers and axon terminals were distributed in the ventral part of the RT, as well as in the ventrolateral part of the PF, bilaterally with an ipsilateral dominance. After BDA injection into the ventral part of the RT, a plexus of labeled axons was found bilaterally with an ipsilateral dominance in the ventrolateral part of the PF. After combined injections of BDA into the dorsolateral part of the SNr and cholera toxin B subunit (CTb) into the ventrolateral part of the PF on the same side, overlapping distribution of BDA-labeled fibers and CTb-labeled neurons was observed in the ventral part of the RT ipsilateral to the injection sites, where the BDA-labeled axon terminals made symmetrical synaptic contacts with soma and dendrites of the CTb-labeled neurons.     

Modulatory role of catecholamines in the transsynaptic expression of c-fos in the rat medial prefrontal cortex induced by disinhibition of the mediodorsal thalamus: a study employing microdialysis and immunohistochemistry

We studied the interaction of catecholaminergic and thalamic afferents of the medial prefrontal cortex (PFC) by analyzing the effects of catecholamine depletion on thalamus-induced c-fos expression in the PFC of freely moving rats. Thalamic projections to the PFC were pharmacologically activated by perfusing the GABA-A receptor antagonist bicuculline (0.03 mM or 0.1 mM) through a dialysis probe implanted into the mediodorsal thalamic nucleus. Bicuculline perfusion induced Fos-like immunoreactivity in the thalamic projection areas, including the PFC, and in the thalamic nuclei surrounding the dialysis probe. 6-Hydroxydopamine lesions of the ventral tegmental area causing a 70–80% depletion of catecholamines in the PFC did not influence the increase in the number of Fos-like immunoreactive nuclei in the prefrontal cortex in response to thalamic stimulation. However, densitometric image analysis revealed that the intensity of Fos-like immunoreactivity in the PFC of lesioned rats perfused with 0.1 mM bicuculline was higher than in correspondingly treated controls. The behavioral activity to bicuculline perfusion, an increase of non-ambulatory activity (0.03 mM) followed by locomotion and rearing (0.1 mM), was not changed in 6-hydroxydopamine-lesioned rats. It is suggested that the thalamically induced c-fos response is directly mediated by excitatory, presumably glutamatergic, transmission and not indirectly by an activation of catecholaminergic afferents of the PFC. The increase in the intensity of Fos-like immunostaining in strongly stimulated, catecholamine-depleted rats suggests that catecholamines modulate the degree to which thalamic activity can activate the PFC of awake animals.     

Topographical organization of the projections from the reticular thalamic nucleus to the intralaminar and medial thalamic nuclei in the cat

The topography of the projections from the reticular nucleus of the thalamus (RT) to the intralaminar and medial thalamic nuclei were studied in the cat by the method of retrograde transport of horseradish peroxidase (HRP). Single small injections of the enzyme were made in the different intralaminar nuclei--mediodorsal, ventromedial, midline, and habenular--and in anterior group nuclei. The location and density of the neuronal labeling in the different parts of the RT were studied in each case. Our results show that 1) after injections located in all the nuclei here studied, a consistent number of labeled neurons were found in the RT, except for the injections in the lateral habenula and the anterior thalamic nuclear complex, both of which did not label neurons in the RT. 2) Among the other thalamic nuclei here studied, the most medially situated receive less numerous RT projections than those most laterally located. 3) Injections in all the nuclei studied gave rise to a cellular labeling in the anterior sectors of the RT, except for the anterior nuclear group and the lateral habenula. The projections from the rostral pole of the RT were topographically mediolaterally organized. 4) The anterodorsal part of the pregeniculate sector of the RT projects upon the large-celled part of the lateral central nucleus and to a lesser extent upon the paracentral, centromedian, and ventromedial nuclei, the anterior part of the lateral central nucleus, and the lateral band of the mediodorsal nucleus. The posterodorsal part of the RT pregeniculate sector only projects to the large-celled part of the lateral central nucleus. The dorsal portion of the posteroventral part of the RT pregeniculate sector also projects upon the large-celled part of the lateral central nucleus; its ventral portion projects to the ventromedial nucleus, the posterior part of the paracentral nucleus, the lateral band of the mediodorsal nucleus, and the centromedian nucleus. 5) The infrageniculate sector of the RT projects to the posterior part of the ventromedial nucleus. A weaker projection to the large-celled part of the lateral central nucleus, the centromedian nucleus, and the lateral band of the mediodorsal nucleus was also observed. 6) The ventral lateral geniculate nucleus projects upon the large-celled part of the lateral central nucleus, the lateral band of the mediodorsal nucleus, and the ventromedial nucleus. All these findings suggest an important modulatory action of the RT on the activity of the thalamic nuclei considered here.     

Organization of thalamic projections to the ventral striatum in the primate

Although thalamic projections to the dorsal striatum are well described in primates and other species, little is known about thalamic projections to the ventral or “limbic” striatum in the primate. This study explores the organization of the thalamic projections to the ventral striatum in the primate brain by means of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) and Lucifer yellow (LY) retrograde tracer techniques. In addition, because functional and connective differences have been described for the core and shell components of the nucleus accumbens in the rat and are thought to be similar in the primate, this study also explores whether these regions of the nucleus accumbens can be distinguished by their thalamic input. Tracer injections are placed in different portions of the ventral striatum, including the medial and lateral regions of the ventral striatum; the central region of the ventral striatum, including the dorsal part of the core of the nucleus accumbens; and the shell region of the nucleus accumbens. Retrogradely labeled neurons are located mainly in the midline nuclear group (anterior and posterior paraventricular, paratenial, rhomboid, and reuniens thalamic nuclei) and in the parafascicular thalamic nucleus. Additional labeled cells are found in other portions of the intralaminar nuclear group as well as in other thalamic nuclei in the ventral, anterior, medial, lateral, and posterior thalamic nuclear groups. The distribution of labeled cells varies depending on the area of the ventral striatum injected. All regions of the ventral striatum receive strong projections from the midline thalamic nuclei and from the parafascicular nucleus. In addition, the medial region of the ventral striatum receives numerous projections from the central superior lateral nucleus, the magnocellular subdivision of the ventral anterior nucleus, and parts of the mediodorsal nucleus. After injection into the lateral region of the ventral striatum, few labeled neurons are seen scattered in nuclei of the intralaminar and ventral thalamic groups and occasional labeled cells in the mediodorsal nucleus. The central region of the ventral striatum, including the dorsal part of the core of the nucleus accumbens, receives a limited projection from the midline thqlamic, predominantly from the rhomboid nucleus. It receives much smaller projections from the central medial nucleus and the ventral, anterior, and medial thalamic groups. The shell of the nucleus accumbens receives the most limited projection from the thalamus and is innervated almost exclusively by the midline thalamic nuclei and the central medial and parafascicular nuclei. The shell is distinguished from the rest of the ventral striatum in that it receives the fewest projections from the ventral, anterior, medial, and lateral thalamic nuclei. © 1995 Wiley-Liss, Inc.     

Combination targeting of subthalamic nucleus and ventral intermediate thalamic nucleus with a single trajectory in deep brain stimulation for tremor-dominant Parkinson’s disease

Deep brain stimulation (DBS) has traditionally been used to target the subthalamic nucleus (STN) or globus pallidus internus (GPi) to treat Parkinson’s disease (PD) and the ventral intermediate thalamic nucleus (VIM) to treat essential tremor (ET). Recent case reports have described targeting both the STN and VIM with a single trajectory and electrode to treat patients with tremor-dominant PD, yet outcome data for this procedure remains sparse. Our objective is to determine the safety and efficacy of combination STN-VIM DBS. We conducted a single-center retrospective case series of all patients who underwent combined STN-VIM DBS. Demographic, perioperative, and outcome data, including Unified Parkinson Disease Rating Scale-III (UPDRS) and tremor scores (OFF-medication), and levodopa equivalent daily dose (LEDD), were collected and analyzed. Nineteen patients underwent this procedure. Patients were 89% male and 11% female, with a mean age of 63.6 years. Mean preoperative UPDRS was 24.1, and LEDD was 811.8. At a mean follow-up of 33.8 months, UPDRS and LEDD decreased by an average of 9.2 (38.2%) and 326.3 (40.2%), respectively. Tremor scores decreased by 4.9 (59.0%), and 58% were able to decrease total medication burden. One patient developed transient left-sided weakness, yielding a complication rate of 5.3%. Combined targeting of STN and VIM thalamus via a single frontal trajectory for tremor-dominant Parkinson’s Disease results in similar UPDRS outcomes to STN DBS and improved control of tremor symptoms. Larger multicenter studies are necessary to validate this as the optimal DBS target for tremor-dominant PD.     

Odor abnormalities caused by bilateral thalamic infarction

Odor is the only sensation thought to be unrelated to the thalamus. However, accumulating evidence suggests that the dorsomedial nucleus (DM) of the thalamus is associated with odor. Although the thalamus is prone to ischemia, only a single patient with bilateral DM infarctions was reported to have odor abnormalities. We describe a second such patient with infarctions involving the left DM and the right ventral posterior nucleus and ventral lateral nucleus, nuclei adjacent to the DM, associated with transient edema. In contrast to the previous case, our patient had transient odor abnormality. These observations suggested that direct and/or indirect bilateral involvement of the DM might be associated with odor abnormalities in patients with thalamic infarction.     

Dopamine reward circuitry: two projection systems from the ventral midbrain to the nucleus accumbens-olfactory tubercle complex

Anatomical and functional refinements of the meso-limbic dopamine system of the rat are discussed. Present experiments suggest that dopaminergic neurons localized in the posteromedial ventral tegmental area (VTA) and central linear nucleus raphe selectively project to the ventromedial striatum (medial olfactory tubercle and medial nucleus accumbens shell), whereas the anteromedial VTA has few if any projections to the ventral striatum, and the lateral VTA largely projects to the ventrolateral striatum (accumbens core, lateral shell and lateral tubercle). These findings complement the recent behavioral findings that cocaine and amphetamine are more rewarding when administered into the ventromedial striatum than into the ventrolateral striatum. Drugs such as nicotine and opiates are more rewarding when administered into the posterior VTA or the central linear nucleus than into the anterior VTA. A review of the literature suggests that (1) the midbrain has corresponding zones for the accumbens core and medial shell; (2) the striatal portion of the olfactory tubercle is a ventral extension of the nucleus accumbens shell; and (3) a model of two dopamine projection systems from the ventral midbrain to the ventral striatum is useful for understanding reward function. The medial projection system is important in the regulation of arousal characterized by affect and drive and plays a different role in goal-directed learning than the lateral projection system, as described in the variation-selection hypothesis of striatal functional organization.     

Leucotomized schizophrenics lose neurons in the mediodorsal thalamic nucleus

It has previously been shown that chronic schizophrenic patients have a 40–50% reduction in the total number of nerve and glia cells in the mediodorsal thalamic nucleus and the nucleus accumbens compared with controls, while the total neuron and glia number is the same in the two groups in the ventral pallidum. Using new stereological cell counting methods, neuron and glia cell numbers were estimated in the mediodorsal thalamic nucleus, the ventro-medial part of nucleus accumbens and the ventral pallidum in nine brains from leucotomized schizophrenics. This number was compared with counts from control cases and chronic schizophrenics without leucotomy. The results showed that the total number of nerve cells in the mediodorsal thalamic nucleus was statistically significantly reduced from 1.08 × 10⁶ in chronic schizophrenics to 0.88 × 10⁶ in leucotomized schizophrenics. Total neuron number was statistically significantly reduced in the ventro-medial part of the nucleus accumbens in schizophrenics without further reduction in leucotomized schizophrenics. The total neuron number in ventral pallidum was normal. With frontal leucotomy it is possible to investigate the consequences of disconnection of the prefrontal cortex to central regions in the human brain. The mediodorsal nucleus of thalamus represents a major efferent projection to the prefrontal cortex. The dorsal prefrontal cortex projects to nucleus caudatus and the orbital prefrontal cortex to the nucleus accumbens, a prominent region in the limbic system. It was expected that a lesion to the prefrontal region by anterograde, retrograde degeneration may affect the mediodorsal nucleus of thalamus.     

Absence of spindle oscillations in the cat anterior thalamic nuclei

Intracellular recordings were performed in cat anterior thalamic nuclei (anterior ventral, medial and dorsal) which, according to a recent anatomical study, do not receive afferents from the reticularis thalami nucleus. Neurons of anterior nuclei did not display spontaneous membrane potential oscillations of the spindle type and such oscillations could neither be evoked in these cells by cortical stimulation. The absence of spontaneous and evoked spindling activity was observed despite that anterior thalamic cells displayed intrinsic membrane properties similar to those of thalamocortical cells in other nuclei. Electrographic recordings from cortical areas connected to anterior thalamic nuclei were also free of spindle activity. Taken together with the evidence that thalamic relay neurons deprived from their reticularis input by sections or kainic acid lesions lose their spindling activity, our results point to the essential role of the reticularis complex in the genesis of thalamic spindle waves.     

Evidence for GABAergic projections from the tegmental nuclei of Gudden to the mammillary body in the rat

Immunochemical studies have demonstrated the presence of large numbers of cells immunoreactive for glutamic acid decarboxylase (GAD) within the dorsal and ventral tegmental nuclei of gudden. Following injections of Fluoro-Gold into the medial mammillary nucleus, a substantial proportion of the retrogradely labeled neurons within the ventral tegmental nucleus displayed GAD-like immunoreactivity. Conversely, electrolytic or excitotoxic lesions of the ventral tegmental nucleus produced a large decrease in the number of fibers and terminals immunoreactive for GAD within the medial mammillary nucleus. In contrast, electrolytic lesions of the dorsal tegmental nucleus were found to produced a large decrease in GAD-like immunoreactivity which was restricted to the lateral mammillary nucleus. Control lesions placed caudal to the dorsal tegmental nucleus were without effect. These findings suggest that the dorsal and ventral nuclei send a substantial, topographically organized, GABAergic input to the mammillary body.     

Severe hypoplasia of medullary arcuate nucleus: quantitative analysis in sudden infant death syndrome

The human arcuate nucleus (ARCn) is postulated to be homologous to ventral medullary cells involved in chemoreception, and respiratory and blood pressure responses. Abnormalities in central respiratory control may result from dysfunction of this anatomic ventral area. We evaluated the changes of the neuronal population of the medullary ARCn in infants victims of the sudden infant death syndrome (SIDS). In this study we tested the hypothesis that anatomical deficiency of the ARCn is associated with SIDS. The volume and neuronal density of the ARCn were morphometrically quantified with an image analyzer in 36 cases of SIDS and 12 age-matched controls. We found a marked hypoplasia in the SIDS ARCn compared to controls and, particularly, in 11 SIDS cases (30%) in which the ARCn exhibited a severe hypoplasia, being almost totally absent. Three-dimensional reconstructions and morphometric measurements of ARCn confirmed this marked hypoplasia in all the serial sections examined (P = 0.0001) and the reduced neuronal density (P = 0.0025) in relation to control cases. In conclusion these abnormalities observed in the ARCn are consistent with the idea that ARCn dysfunction plays an important role among the causative factors of sudden infant death. The hypoplasia of the ARCn represents the most frequent congenital abnormality in our experience, and can be a plausible morphological substrate for a subset of SIDS. Received: 11 May 1999 / Accepted: 6 August 1999     

Synaptic organization of GABAergic projections from the substantia nigra pars reticulata and the reticular thalamic nucleus to the parafascicular thalamic nucleus in the rat

The ventrolateral part of the parafascicular thalamic nucleus (PF), which is considered to take part in the control mechanism of orofacial motor functions, receives projection fibers not only from the dorsolateral part of the substantia nigra pars reticulata (SNr) but also from the ventral part of the reticular thalamic nucleus (RT) [Tsumori et al., Brain Res. 858 (2000) 429]. In order to better understand the influence of these fibers upon the PF projection neurons, the morphology, synaptology and chemical nature of them were examined in the present study. After ipsilateral injections of Phaseolus vulgaris-leucoagglutinin (PHA-L) into the dorsolateral part of the SNr and biotinylated dextran amine (BDA) into the ventral part of the RT, overlapping distributions of PHA-L-labeled SNr fibers and BDA-labeled RT fibers were seen in the ventrolateral part of the PF. At the electron microscopic level, the SNr terminals made synapses predominantly with the medium to small dendrites and far less frequently with the somata and large dendrites, whereas approximately half of the RT terminals made synapses with the somata and large dendrites and the rest did with the medium to small dendrites of PF neurons. Some of single dendritic as well as single somatic profiles received convergent synaptic inputs from both sets of terminals. These terminals were packed with pleomorphic synaptic vesicles and formed symmetrical synapses. After combined injections of PHA-L into the dorsolateral part of the SNr, BDA into the ventral part of the RT and wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the ventrolateral part of the striatum or into the rostroventral part of the lateral agranular cortex, WGA-HRP-labeled neurons were embedded in the plexus of PHA-L- and BDA-labeled axon terminals within the ventrolateral part of the PF, where the PHA-L- and/or BDA-labeled terminals were in synaptic contact with single somatic and dendritic profiles of the WGA-HRP-labeled neurons. Furthermore, the SNr and RT axon terminals were revealed to be immunoreactive for gamma-aminobutyric acid (GABA), by using the anterograde BDA tracing technique combined with immunohistochemistry for GABA. The present data suggest that GABAergic SNr and RT fibers may exert different inhibitory influences on the PF neurons for regulating the thalamic outflow from the PF to the cerebral cortex and/or striatum in the control of orofacial movements.