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Transmitter Actions and Interactions on Pallidal Neuronal function
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Pallidal brain structures include three major divisions: the external globus pallidus of the primate is represented in non-primate mammals by the dorsal or supracommissural pallidum (globus pallidus; GP), the internal or medial pallidum finds its rodent homolog in the entopeduncular nucleus; and the ventral, mostly infracommissural, extension of the pallidum, including the rostral end of the substantia innominata, is designated as the ventral pallidum (VP).
Neuronal Networks in Convulsant Drug-Induced Seizures
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Thalamic nuclei are implicated as being important in the neuronal network subserving pilocarpine-induced limbic/forebrain seizures. Direct unilateral injections of bicuculline or picrotoxin into the amygdala produce recurrent seizures. Bilateral injections of GABA antagonists lead to status epilepticus, which are accompanied by histological damage in the thalamus, amygdala, olfactory cortex, SN, hippocampus, and neocortex.82 During seizures induced by a combination of lithium and pilocarpine labeling of 2-DG is increased in different brain regions, including the thalamus.83 Bilateral injections of small doses of AP7 and muscimol into the mediodorsal thalamus blocks pilocarpine-induced seizures.84 The same effect is observed with the injections of these agents in the lateral habenula.84 Systemic administration of paraoxon, an irreversible acetylcholinesterase inhibitor resulted in increased 2-DG labeling in ventral anterior nucleus of thalamus as well as external globus pallidus, entopeduncular nucleus, and SNR.85
Cyanides: Toxicology, Clinical Presentation, and Medical Management
Published in Brian J. Lukey, James A. Romano, Salem Harry, Chemical Warfare Agents, 2019
Gary A. Rockwood, Gennady E. Platoff Jr., Harry Salem
Several human case reports have described the neurological and neuropathological sequelae of acute CN poisoning. Some representative examples of acute and delayed effects are as follows. Finelli (1981) described a 30-year-old male who attempted suicide with CN, and 14 months later developed choreiform movements and dysdiadochokinesis of the left hand. Sixteen years after the incident, mental status was normal, but he was mildly dysarthric and had decreased limb muscle tone and mild athetoid movements in the upper limbs. Computerized axial tomography (CAT) showed bilateral infarction of the globus pallidus and left cerebellar hemisphere. Utti et al. (1985) described an 18-year-old male who swallowed KCN and after 4 months, developed generalized rigidity and bradykinesia with intermittent resting and postural tremor in the arms. Autopsy (after an overdose of imipramine and alcohol) at 18 months after the original poisoning incident revealed lesions in the globus pallidus and widespread lacunae in the striatum. Varnell et al. (1987) described two cases of lethal CN poisoning due to ingestion of adulterated Excedrin capsules. A CAT scan carried out within 3 h showed diffuse cerebral edema with diffuse loss of white–gray discrimination. Borgohain et al. (1955) described a 27-year-old female who attempted suicide with KCN and subsequently developed persistent generalized dystonia. Cranial CAT demonstrated bilateral putaminal lucencies, and magnetic resonance imaging (MRI) showed sharply delineated lesions corresponding to the two putamina. Grandas et al. (1989) described a man who became comatose after ingesting NaCN, and after regaining consciousness, he had reduced speech and loss of balance. During the subsequent years, dystonia and Parkinsonism developed, and CAT revealed lucencies in the putamen and external globus pallidus. Feldman and Feldman (1990) described a 28-year-old man who swallowed KCN and subsequently developed Parkinsonian signs, including micrographia and hypersalivation. Lovecchio et al. (2006) described cranial CAT scan findings in a 43-year-old man who swallowed CN in a suicide attempt. He collapsed, had a grand mal seizure, became apneic, and died within 24 h despite sodium nitrite–thiosulfate treatment; blood CN was 167 mg dL−1. The CAT scan showed diffuse hypodensity involving the brain and cerebellum with a small fourth ventricle, cisternal space effacement, and abnormal density of the basal ganglia. The authors regarded the findings as consistent with diffuse cerebral and cerebellar edema with impending brainstem herniation. Further details and additional case reports have been given by Ballantyne and Salem (2005), Hantson and Duprez (2006), and Isom and Borowitz (2015).
Deep brain stimulation and stereotactic-assisted brain graft injection targeting fronto-striatal circuits for Huntington’s disease: an update
Published in Expert Review of Neurotherapeutics, 2022
Thomas Kinfe, Alessandro Del Vecchio, Martin Nüssel, Yining Zhao, Andreas Stadlbauer, Michael Buchfelder
We aimed to evaluate the safety and efficacy of stereotactic-guided invasive therapies for HD defined as deep brain stimulation and stereotactic-guided brain graft injection. Noninvasive brain stimulation (transcranial magnet stimulation, transcranial direct current stimulation) and ablative procedures were excluded. A literature search was performed based on the following terms – ”Huntington’s disease”, ‘chorea,’ ‘movement disorders,’ ‘dystonia,’ ‘parkinsonism,’ ‘involuntary movements,’ ‘internal/external globus pallidus,’ ‘GPi/GPe,’ ‘striatum,’ ‘basal ganglia,’ ‘UHDRS,’ ‘deep brain stimulation,’ ‘brain grafts,’ ‘stem cell’ and ‘DNA/RNA-therapies’ – using the databases PubMed, Embase, and Cochrane Library and a manual library search covering 2000–2022. In particular, studies assessing the impact of intrathecal applications (cerebrospinal fluid) were not considered in this review. In view of the limited quantity and the premature characteristics of the literature available, the findings assessed herein will be discussed via a comprehensive review. Due to the higher numbers of uncontrolled case series and case reports, DBS in-human studies including ≥5 participants are summarized and referenced in Table 1, while describing the responsiveness of stereotactic-guided restorative therapies in a comprehensive manner.
A case study of foliglurax, the first clinical mGluR4 PAM for symptomatic treatment of Parkinson’s disease: translational gaps or a failing industry innovation model?
Published in Expert Opinion on Investigational Drugs, 2020
Dario Doller, Anton Bespalov, Rob Miller, Malgorzata Pietraszek, Mikhail Kalinichev
It is currently well accepted that a balance between the inhibitory and excitatory neurotransmission within the basal ganglia is critical for motor control, as disruptions in this balance have been implicated in a range of movement disorders, including PD[21]. For example, recordings made from patients with PD reveal abnormal firing patterns, that correlate with symptom severity [22–24]. In accord with these findings, recordings from Parkinsonian nonhuman primates also show marked increases in rhythmic oscillatory spike discharge in the globus pallidus [25–27]. It has been hypothesized that there is an increased GABAergic input from the striatal medium spiny neurons to the GABAergic neurons of the external globus pallidus in the Parkinsonian basal ganglia, which in turn, reduces its inhibitory input into the subthalamic nucleus, leading to its hyperactivity. These disruptions in the inhibitory/excitatory balance in the so-called indirect pathway are believed to underly some of the key features of Parkinsonian symptomatology. Therefore, decreasing GABAergic neurotransmission in the striato-pallidal pathway through the activation of presynaptic mGluR4, can normalize the inhibitory input into the globus pallidus, restore the inhibitory/excitatory balance in the basal ganglia and reduce Parkinsonian symptomatology.
Subthalamic nucleus deep brain stimulation for Parkinson’s disease: current trends and future directions
Published in Expert Review of Medical Devices, 2020
Antonella Macerollo, Ludvic Zrinzo, Harith Akram, Thomas Foltynie, Patricia Limousin
The role of the STN in PD was explored in mainly non-human primate models treated with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Overactivity of the STN was identified in comparison to control animals [17]. Lesions [17,18] or high-frequency stimulation of the STN [19] resulted in improvement in hemibody bradykinesia and rigidity. Interest in the STN was incited by the strategic position of this nucleus within the basal ganglia circuitry (Figure 1). It receives input from the cerebral cortex and external globus pallidus and sends output to the globus pallidus (internal as well as external part) [20]. The development of STN DBS was also facilitated by progress in MRI allowing direct visualization of the nucleus [21] and, thus, precise localization with imaging.