Bilateral Globus Pallidus Lesions Research Articles

Dopaminergic denervation of the globus pallidus produces short-memory impairment in rats.

Rats with low-level globus pallidus (GP) dopaminergic denervation can develop anxiety without any motor alterations. The aim of this study was to evaluate the effect of low-level 6-OHDA-induced unilateral and bilateral GP lesions in male Wistar rats (n = 8/group) on recognition memory, motor activity, and the number of TH+ neurons in the SNc. For unilateral- and bilateral-lesioned animals, there was a significant decrease in the number of TH+ neurons (27% and 42%, respectively) and in the object, location, and temporal order discrimination indexes of recognition memory tests. Motor activity was unaffected. Thus, GP dopamine denervation was detrimental to short-memory.

Soroxchi after Traveling to South America: Cognitive and Neurobehavioral Changes in a Patient with Bilateral Globus Pallidus Lesions

Abstract Objective Soroxchi/Acute Mountain Sickness (AMS) is a condition that can result in cerebral and pulmonary hypoxia. Neuropsychological research on AMS is minimal and the long-term effects on cognition and behavior are unclear. AMS is associated with cognitive impairments in processing speed, attention, and executive functions as well as neurobehavioral symptoms. This case study delineates the neuropsychological and neurobehavioral changes secondary to bilateral globus pallidus (GP) lesions associated with AMS. Case Description Patient is a 51-year old, primarily Spanish-speaking, male of Mexican descent with 9 years of education, and who had traveled to La Paz, Bolivia (4,070 MASL) for work. Upon arrival, fatigue and dizziness led to hospitalization to treat acute pulmonary edema and hypoxia. Brain MRI revealed hyperintense bilateral GP lesions. Medical history was notable for hyperlipidemia. Psychiatric history was unremarkable. Neuropsychological assessment 4 months post-AMS revealed impairments in visuo-conceptual and speeded complex visuospatial abilities, executive functions, and confrontation naming. Cognitive improvements were noted in delayed recall of non-contextual verbal information and confrontation naming ten months post-AMS. Significant mood and personality changes were reported; patient endorsed anhedonia, fatigue, alexithymia, avolition, and sleep difficulties. Family described patient as depressed, apathetic, and socially withdrawn. Pharmacological and psychotherapy treatments were recommended and initiated. Diagnostic Impressions and Outcomes Findings were consistent with a diagnosis of Mild Neurocognitive Disorder. His family denied neurobehavioral improvements post interventions. Discussion This case study is the first to characterize the long-term neuropsychological and neurobehavioral changes following bilateral GP lesions secondary to AMS. Declines in visual-conceptual abilities reveal a new finding for this type of cerebral incident.

Memory deficits and frontal lobe syndrome associated with bilateral globus pallidus lesions in a patient with synthetic cannabinoid use (tur)

Memory deficits and frontal lobe syndrome associated with bilateral globus pallidus lesions in a patient with synthetic cannabinoid use (tur)

Correlation of computed tomography, magnetic resonance imaging and clinical outcome in acute carbon monoxide poisoning

Background and objectivesCarbon monoxide is a toxic gas for humans and is still a silent killer in both developed and developing countries. The aim of this case series was to evaluate early radiological images as a predictor of subsequent neuropsychological sequelae, following carbon monoxide poisoning. Case 1After carbon monoxide exposure, early computed tomography scans and magnetic resonance imaging findings of a 52-year-old woman showed bilateral lesions in the globus pallidus. This patient was discharged and followed for 90 days. The patient recovered without any neurological sequela. Case 2In a 58-year-old woman exposed to carbon monoxide, computed tomography showed lesions in bilateral globus pallidus and periventricular white matter. Early magnetic resonance imaging revealed changes similar to that like in early tomography images. The patient recovered and was discharged from hospital. On the 27th day of exposure, the patient developed disorientation and memory impairment. Late magnetic resonance imaging showed diffuse hyperintensity in the cerebral white matter. ConclusionWhite matter lesions which progress to demyelination and end up in neuropsychological sequelae cannot always be diagnosed by early computed tomography and magnetic resonance imaging in carbon monoxide poisoning.

Rapid resolution of akinetic mutism in delayed post-hypoxic leukoencephalopathy with intravenous magnesium sulfate

Delayed post-hypoxic leukoencephalopathy is a rare condition marked by the development of neuropsychiatric symptoms, parkinsonism and akinetic mutism days to weeks after an individual has recovered from a prolonged cerebral hypoxic event. This syndrome can cause significant long-term neurologic dysfunction. At present there are no acute treatment strategies that have been identified that have been shown to alter the natural course of this disorder. In most instances all that can be offered to patients is early supportive care and then subsequent rehabilitation services. Case Report. A patient is presented who developed new onset encephalopathy, extrapyramidal symptoms and akinetic mutism three weeks after being discharged for a respiratory arrest from a drug overdose. MRI showed the development of extensive white matter and bilateral globus pallidus lesions. She had rapid resolution of akinetic mutism with intravenous magnesium sulfate as well as improvement in her other associated neurologic symptoms. The case report suggests the use of intravenous magnesium sulfate as an acute treatment for the akinetic mutism associated with delayed post-hypoxic leukoencephalopathy. In addition it also may improve the extrapyramidal and neuropsychiatric symptoms associated with this syndrome. This may be the first potential acute treatment for this rare neurologic condition.

Magnetic resonance imaging findings in chronic carbon monoxide intoxication

To define the cranial magnetic resonance imaging (MRI) features of the chronic stage of carbon monoxide (CO) poisoning in patients with and without neuropsychiatric sequelae. Eight patients who had neither symptoms nor neurological sequelae and eight patients with neuropsychiatric sequelae were included in the study. Patients aged between 9 to 57 (mean 32.2 years). All patients had been comatose at initial admittance and awoke after normobaric 100% oxygen therapy within 1-7 days. In this study, the patients were being examined with routine cranial MRI between 1 and 10 years (mean 3.4 years) after exposure to CO. The most common finding was bilateral symmetric hyperintensity of the white matter, which was more significant in the centrum semiovale, with relative sparing of the temporal lobes and anterior parts of the frontal lobes on T2-weighted and FLAIR images in all patients. Cerebral cortical atrophy was seen in 10 patients; mild atrophy of cerebellar hemispheres in 8; and vermian atrophy in 11. Corpus callosum was atrophic in one patient. Bilateral globus pallidus lesions were seen in three patients. The lesions were hypointense on T1-weighted images and hyperintense on T2-weighted and FLAIR images. Patients with severe CO intoxication may develop persistent cerebral changes independently of their neuropsychiatric findings in the chronic stage. They may present with characteristic MRI findings as described here, even if asymptomatic. The history of CO exposure is therefore helpful for recognizing and interpreting the MRI findings of chronic stage CO intoxication.

Definition of the Clinical Spectrum of Kernicterus and Bilirubin-Induced Neurologic Dysfunction (BIND)

Kernicterus, currently used to describe both the neuropathology of bilirubin-induced brain injury and its associated clinical findings, is a complex syndrome. The neurobiology of kernicterus, including the determinants and mechanisms of neuronal injury, is discussed along with traditional and evolving definitions ranging from classical kernicterus with athetoid cerebral palsy, impaired upward gaze and deafness, to isolated conditions, for example, auditory neuropathy or dys-synchrony (AN/AD), and subtle bilirubin-induced neurological dysfunction (BIND). The clinical expression of BIND varies with location, severity, and time of assessment, influenced by the amount, duration and developmental age of exposure to excessive free bilirubin. Although total serum bilirubin (TSB) is important, kernicterus cannot be defined based solely on TSB. For study purposes kernicterus may be defined in term and near-term infants with TSB > or = 20 mg/dl using abnormal muscle tone on examination, auditory testing diagnostic of AN/AD, and magnetic resonance imaging showing bilateral lesions of globus pallidus+/-subthalamic nucleus.

Bilateral globus pallidus lesions in a patient with Tourette syndrome and related disorders

Background: The neuroanatomic and pathologic basis of Tourette’s syndrome or related disorders such as obsessive-compulsive disorder and attention deficit-hyperactivity disorder remains unknown. Although a substantial body of neuroimaging and other data implicate basal ganglia and some point out specifically the globus pallidus in the etiopathogenesis of these three related disorders, no clear or pathologically significant isolated lesions restricted to this region have yet been demonstrated, with the exception of obsessive-compulsive disorder. Methods: A seventeen-year-old male case of Tourette syndrome with comorbid obsessive-compulsive disorder, attention deficit-hyperactivity disorder, stuttering and gait disturbance, who had negative family history is presented. Results: The patient has failed to respond to drug treatment and his MRI scan revealed bilateral and symmetrical globus pallidus lesions with specific “tiger’s eye” appearance of unknown etiology. Conclusions: Well-localized lesions in the globus pallidus support growing data suggesting the involvement of this brain region in Tourette syndrome and related disorders.

Haloperidol Decreases Hyperkinetic Paw Treading Induced by Globus Pallidus Lesions in the Rat

Systemic haloperidol injections decrease the severity of several hyperkinetic syndromes caused by damage to the basal ganglia in humans. A model of hyperkinesia in the rat, exaggerated paw treading triggered by oral sensory stimulation, has been reported previously to result from lesions of the globus pallidus or ventral pallidum/substantia innominata. This hyperkinesia appears as forepaw and forelimb extension and retraction, which can be emitted vigorously and repeatedly for up to minutes at a time. The present study aimed to discover whether this experimental hyperkinesia is pharmacologically similar to human hyperkinetic syndromes: can it be suppressed by neuroleptic administration? Systemic injections of haloperidol (2 mg/kg), diazepam (5 mg/kg, as a sedative comparison), or vehicle were given to rats that expressed the paw treading syndrome after pallidal lesions. Effects on hyperkinetic treading and on tests of sensorimotor function were compared. Results indicated that haloperidol was effective in ameliorating the hyperkinesia in rats with bilateral globus pallidus lesions but not in rats with ventral pallidum/substantia innominata lesions. By contrast, diazepam, which produced sedation and sensorimotor impairment, did not decrease the hyperkinesia induced by either lesion. Although only haloperidol decreased hyperkinetic treading after globus pallidus lesions, haloperidol produced less of a sensorimotor impairment than diazepam on climbing, hanging, and righting reflex tests. These results implicate a specific role for dopamine neurotransmission in the expression of triggered hyperkinetic treading induced by globus pallidus lesions.

Frontal lobe syndrome from bilateral globus pallidus lesions a complication of Wernicke's encephalopathy

A 38 year-old man developed the classical clinical picture of Wernicke's encephalopathy as a consequence of prolonged total parenteral nutrition. As a late complication he developed a frontal lobe syndrome. Bilateral globus pallidus lesions were observed in the CT-scan examination. Some aspects related to the cortical syndromes caused by subcortical lesions are discussed.

Behaviorally specific limb use deficits following globus pallidus lesions in rats

The effects of bilateral globus pallidus lesions were observed in rats trained to perform a somatosensory/proprioceptive guided forelimb reaching task. Postlesion reaching became very inaccurate, characterized by gross abnormalities in limb and body posture. Postural abnormalities and paw use deficits were not observed in other situations. These results suggest that pallidal damage does not result in a simple motor deficit but interferes with motor performance when movements depend upon somesthetic and proprioceptive feedback.

Experimental studies to develop local prophylactic agents against syphilis.

<h3>Objective:</h3> Broadening the differential for bilateral globus pallidus MRI T2 hyperintense lesions beyond carbon monoxide poisoning. <h3>Background:</h3> Bilateral symmetric lesions of areas of the brain supplied by a perforating arterial branches (internal capsule, basal ganglia and thalamus) are rare and specifically bilateral globus pallidus lesions are even rarer. They have been associated with various conditions, but most commonly its a pathognomonic sign of carbon monoxide poisoning. There is not much evidence in the literature for the combination of drug abuse resulting in similar imaging presentation. <h3>Design/Methods:</h3> Case series of 5 patients seen in one academic hospital presenting with acute bilateral globus pallidus lesions over six months. <h3>Results:</h3> All five patients were found unresponsive after illicit drug use and had abused cocaine, with other substances, and found to have bilateral globus pallidus lesions T2 intense on MRI. Most commonly, it was cocaine with opiates (3 patients), one with cocaine and levamisole, and one with cocaine only (though limited toxicology screen). Clinical presentations early in the course ranged from myoclonus to additional ischemic lesions causing cortical blindness, but all had some degree of cognitive impairment. <h3>Conclusions:</h3> We found that use of cocaine, typically with other illicit drugs, can present a similar imaging presentation as would be seen in carbon monoxide poisoning. Mechanism may be from hypo ventilation and additional vasospasm selectively impacting the metabolically high demand basal ganglia and in particular globus pallidus, though etiology remains uncertain. <b>Disclosure:</b> Dr. Azeem has nothing to disclose. Dr. Cheraghi has nothing to disclose. Dr. Nagy has nothing to disclose. Dr. Vu has nothing to disclose. Dr. Maliakal has nothing to disclose. Dr. Henninger has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Omniox, Inc. Dr. Daniello has nothing to disclose.