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Corpos Geniculados , Doenças Neuroinflamatórias , Humanos , Corpos Geniculados/patologia , Corpos Geniculados/diagnóstico por imagem , Doenças Neuroinflamatórias/diagnóstico por imagem , Doenças Neuroinflamatórias/patologia , Feminino , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , AdultoRESUMO
Mild traumatic brain injury (mTBI) affects millions of people in the U.S. Approximately 20-30% of those individuals develop adverse symptoms lasting at least 3 months. In a rat mTBI study, the closed-head impact model of engineered rotational acceleration (CHIMERA) produced significant axonal injury in the optic tract (OT), indicating white-matter damage. Because retinal ganglion cells project to the lateral geniculate nucleus (LGN) in the thalamus through the OT, we hypothesized that synaptic density may be reduced in the LGN of rats following CHIMERA injury. A modified SEQUIN (synaptic evaluation and quantification by imaging nanostructure) method, combined with immunofluorescent double-labeling of pre-synaptic (synapsin) and post-synaptic (PSD-95) markers, was used to quantify synaptic density in the LGN. Microglial activation at the CHIMERA injury site was determined using Iba-1 immunohistochemistry. Additionally, the effects of ketamine, a potential neuroprotective drug, were evaluated in CHIMERA-induced mTBI. A single-session repetitive (ssr-) CHIMERA (3 impacts, 1.5 joule/impact) produced mild effects on microglial activation at the injury site, which was significantly enhanced by post-injury intravenous ketamine (10 mg/kg) infusion. However, ssr-CHIMERA did not alter synaptic density in the LGN, although ketamine produced a trend of reduction in synaptic density at post-injury day 4. Further research is necessary to characterize the effects of ssr-CHIMERA and subanesthetic doses of intravenous ketamine on different brain regions and multiple time points post-injury. The current study demonstrates the utility of the ssr-CHIMERA as a rodent model of mTBI, which researchers can use to identify biological mechanisms of mTBI and to develop improved treatment strategies for individuals suffering from head trauma.
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Ketamina , Microglia , Ratos Sprague-Dawley , Sinapses , Animais , Ketamina/administração & dosagem , Ketamina/farmacologia , Microglia/efeitos dos fármacos , Microglia/metabolismo , Microglia/patologia , Ratos , Masculino , Sinapses/efeitos dos fármacos , Sinapses/metabolismo , Sinapses/patologia , Traumatismos Cranianos Fechados/patologia , Axônios/efeitos dos fármacos , Axônios/metabolismo , Axônios/patologia , Modelos Animais de Doenças , Corpos Geniculados/patologia , Corpos Geniculados/efeitos dos fármacos , Concussão Encefálica/patologia , Concussão Encefálica/metabolismo , Proteína 4 Homóloga a Disks-Large/metabolismo , Sinapsinas/metabolismo , Fármacos Neuroprotetores/farmacologia , Fármacos Neuroprotetores/administração & dosagemRESUMO
The pathobiology of tau is of great importance for understanding the mechanisms of neurodegeneration in aging and age-associated disorders such as Alzheimer disease (AD) and frontotemporal dementias. It is critical to identify neuronal populations and brain regions that are vulnerable or resistant to tau pathological changes. Pick disease (PiD) is a three-repeat (3R) tauopathy that belongs to the group of frontotemporal lobar degenerations. The neuropathologic changes of PiD are characterized by globular tau-positive neuronal intracytoplasmic inclusions, called Pick bodies, in the granule cells of the dentate gyrus and frontal and temporal neocortices, and ballooned neurons, named Pick neurons, in the neocortex. In the present study, we examined 13 autopsy-confirmed cases of PiD. Using immunohistochemistry for phospho-tau (AT8) and 3R tau isoform, all PiD cases demonstrated extensive lesions involving the hippocampus and neocortex. However, the lateral geniculate body (LGB) is spared of significant tau lesions in contrast to the neighboring hippocampus and other thalamic nuclei. Only 1 PiD case (7.7%) had tau-positive neurons, and 4 cases had tau-positive neurites (31%) in the LGB. By contrast, the LGB does consistently harbor tau lesions in other tauopathies including progressive supranuclear palsy, corticobasal degeneration, and AD.
Assuntos
Doença de Alzheimer , Neocórtex , Doença de Pick , Tauopatias , Humanos , Doença de Pick/patologia , Proteínas tau/metabolismo , Corpos Geniculados/metabolismo , Corpos Geniculados/patologia , Tauopatias/patologia , Neocórtex/patologiaRESUMO
OBJECTIVE: The expression of early growth responsive gene-1 (Egr-1) in the lateral geniculate body in the normal kittens and those affected with amblyopia caused by monocular visual deprivation was compared to explore the potential significance of Egr-1 in the pathogenesis of amblyopia. METHODS: A total of 30 healthy kittens were equally and randomly divided into the control (n = 15) and the deprivation group (n = 15). The kittens were raised in natural light and the right eyes of the deprived kittens were covered with a black opaque covering. Pattern visual evoked potential (PVEP) was measured before and 1, 3, and 5 weeks after covering. Five kittens from each group were randomly selected and euthanized with 2% sodium pentobarbital (100â mg/kg) during the 1st, 3rd and 5th week after covering. The expression of Egr-1 in the lateral geniculate body in the two groups was compared by performing immunohistochemistry and in situ hybridization. RESULTS: After three weeks of covering, PVEP detection indicated that the P100 wave latency in the deprivation group was significantly higher than that in the control group (P < 0.05), whereas the amplitude decreased markedly (P < 0.05). The number of the positive cells (P < 0.05) and mean optical density (P < 0.05) of Egr-1 protein expression in the lateral geniculate body of the deprivation group were found to be substantially lower in comparison to the normal group, as well as the number (P < 0.05) and mean optical density of Egr-1 mRNA-positive cells (P < 0.05). However, with increase of age, positive expression of Egr-1 in the control group showed an upward trend (P < 0.05), but this trend was not noted in the deprivation group (P > 0.05). CONCLUSIONS: Monocular form deprivation can lead to substantially decreased expressions of Egr-1 protein and mRNA in the lateral geniculate body, which in turn can affect the normal expression of neuronal functions in the lateral geniculate body, thereby promoting the occurrence and development of amblyopia.
Assuntos
Ambliopia , Animais , Feminino , Gatos , Ambliopia/genética , Potenciais Evocados Visuais , Corpos Geniculados/metabolismo , Corpos Geniculados/patologia , Neurônios/metabolismo , RNA Mensageiro/genética , Privação Sensorial/fisiologiaRESUMO
BACKGROUND: Optic pathway is considered an ideal model to study the interaction between inflammation and neurodegeneration in multiple sclerosis (MS). METHODS: Optical Coherence Tomography (OCT) and 3.0 T magnetic resonance imaging (MRI) were acquired in 92 relapsing remitting (RR) MS at clinical onset. Peripapillary RNFL (pRNFL) and macular layers were measured. White matter (WM) and gray matter (GM) lesion volumes (LV), lateral geniculate nucleus (LGN) volume, optic radiations (OR) WM LV, thickness of pericalcarine cortex were evaluated. OCT and MRI control groups (healthy controls [HC]-OCT and HC-MRI) were included. RESULTS: A significant thinning of temporal pRNFL and papillo-macular bundle (PMB) was observed (p<0.001) in 16 (17%) patients presented with monocular optic neuritis (MSON+), compared to 76 MSON- and 30 HC (-15 µm). In MSON-, PMB was reduced (-3 µm) compared to HC OCT (p<0.05). INL total volume was increased both in MSON+ (p<0.001) and MSON- (p = 0.033). Inner retinal layers volumes (macular RNFL, GCL and IPL) were significantly decreased in MSON+ compared to HC (p<0.001) and MSON- (p<0.001). Reduced GCL volume in the parafoveal ring was observed in MSON- compared to HCOCT (p < 0.05). LGN volume was significantly reduced only in MSON+ patients compared to HC-MRI (p<0.001) and MSON- (p<0.007). GCL, IPL and GCIP volumes associated with ipsilateral LGN volume in MSON+ and MSON-. Finally, LGN volume associated with visual cortex thickness with no significant difference between MSON+ and MSON-. CONCLUSIONS: Anterograde trans-synaptic degeneration is early detectable in RRMS presenting with optic neuritis but does not involve LGN.
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Esclerose Múltipla Recidivante-Remitente , Esclerose Múltipla , Neurite Óptica , Humanos , Esclerose Múltipla Recidivante-Remitente/complicações , Esclerose Múltipla Recidivante-Remitente/diagnóstico por imagem , Esclerose Múltipla Recidivante-Remitente/patologia , Esclerose Múltipla/complicações , Esclerose Múltipla/diagnóstico por imagem , Esclerose Múltipla/patologia , Degeneração Retrógrada/patologia , Corpos Geniculados/diagnóstico por imagem , Corpos Geniculados/patologia , Retina/diagnóstico por imagem , Retina/patologia , Neurite Óptica/diagnóstico por imagem , Neurite Óptica/patologia , Tomografia de Coerência ÓpticaRESUMO
Traumatic brain injury (TBI)-induced axonal degeneration leads to acute and chronic neuropsychiatric impairment, neuronal death, and accelerated neurodegenerative diseases of aging, including Alzheimer's and Parkinson's diseases. In laboratory models, axonal degeneration is traditionally studied through comprehensive postmortem histological evaluation of axonal integrity at multiple time points. This requires large numbers of animals to power for statistical significance. Here, we developed a method to longitudinally monitor axonal functional activity before and after injury in vivo in the same animal over an extended period. Specifically, after expressing an axonal-targeting genetically encoded calcium indicator in the mouse dorsolateral geniculate nucleus, we recorded axonal activity patterns in the visual cortex in response to visual stimulation. In vivo aberrant axonal activity patterns after TBI were detectable from 3 days after injury and persisted chronically. This method generates longitudinal same-animal data that substantially reduces the number of required animals for preclinical studies of axonal degeneration.
Assuntos
Lesões Encefálicas Traumáticas , Lesões Encefálicas , Doenças Neurodegenerativas , Camundongos , Animais , Lesões Encefálicas/patologia , Axônios/patologia , Lesões Encefálicas Traumáticas/patologia , Doenças Neurodegenerativas/patologia , Corpos Geniculados/patologiaRESUMO
BACKGROUND: Case presentation of acute onset bilateral painless vision loss caused by bilateral infarction of the lateral geniculate bodies (LGB) and a systematic review of the literature. METHODS: A descriptive case report is presented on a 17-year-old female diagnosed with acute pancreatitis who developed acute onset bilateral painless vision loss. A systematic literature review of cases with bilateral LGB lesions was conducted across three electronic databases (PubMed/PubMed Central/MEDLINE, Scopus, and ScienceDirect). The review was conducted in concordance with PRISMA guidelines and prospectively registered on PROSPERO (CRD42022362491). RESULTS: The reported 17-year-old female was found to have MRI findings consistent with bilateral hemorrhagic infarction of the LGB and Purtscher-like retinopathy. A systematic literature review of bilateral LGB infarction yielded 23 records for analysis. 19/23 (82.6%) of reported cases occurred in women. Bilateral vision loss was noted in all cases. The average reported age was 27 years old with a range from 2-50. Gastrointestinal pathology (e.g., pancreatitis, gastroenteritis) was present in 8/23 (34.7%) of cases. 8/23 (34.7%) cases had neuroimaging or pathological evidence of hemorrhagic transformation of the infarct. Most cases experienced partial recovery of visual loss; only one case (4.7%) had complete visual recovery. 9/23 (39.1%) cases were reported from the United States and 4/23 (17.3%) from India. CONCLUSIONS: Bilateral LGB lesion is a rare cause of vision loss, typically caused by systemic diseases and with female preponderance. Purported pathophysiology relates to increased vulnerability of the LGB to ischemic and metabolic stress.
Assuntos
Corpos Geniculados , Pancreatite , Humanos , Feminino , Adulto , Adolescente , Corpos Geniculados/patologia , Doença Aguda , Pancreatite/complicações , Pancreatite/patologia , Transtornos da Visão/etiologia , Infarto/complicações , Fatores de Risco , Cegueira/complicaçõesRESUMO
PURPOSE: The present study compared the expression of activity-regulated cytoskeleton-associated protein (ARC/Arg3.1) in the lateral geniculate body between form deprivation amblyopia kittens and normal kittens to examine the significance of ARC/Arg3.1 in the lateral geniculate body in the pathogenesis of amblyopia. METHODS: Twenty kittens were randomly divided into an experimental group (n = 10) and a control group (n = 10). Black opaque covering cloth was used to cover the right eye of kittens in the experimental group. Pattern visual evoked potentials (PVEP) were detected weekly in all kittens. The expression of the ARC/Arg3.1 gene was detected by immunohistochemistry and in situ hybridization, and apoptosis of lateral geniculate body cells was detected by TUNEL. RESULTS: PVEP detection showed that at the age of 5 and 7 weeks, the latency of P100 in the right eye of the experimental group was higher than that of the other three groups (P < 0.05), and the amplitude of P100 was lower than that of the other three groups (P < 0.05). The expression of ARC/Arg3.1 protein (P < 0.05) and mRNA (P < 0.05) in the lateral geniculate body of the experimental group was significantly lower than that of the control group. The level of neuronal apoptosis in the experimental group was higher than that in the control group (P < 0.05). The expression of the ARC/Arg3.1 gene was negatively correlated with the apoptosis level of lateral geniculate body neurons. CONCLUSIONS: The expression of ARC/Arg3.1 is associated with monocular form deprivation amblyopia and apoptosis of lateral geniculate body cells.
Assuntos
Ambliopia , Animais , Gatos , Ambliopia/genética , Potenciais Evocados Visuais , Olho , Corpos Geniculados/metabolismo , Corpos Geniculados/patologia , Imuno-HistoquímicaRESUMO
Sudden bilateral visual loss because of bilateral lateral geniculate body (LGB) necrosis is a very rare entity. The mechanisms causing these isolated lesions have still not been fully understood. We report a case of sudden loss of vision in a 22-year-old female following an attack of acute pancreatitis, just after starting the paleo diet. Neuroimaging revealed bilateral LGB necrosis. Multidisciplinary approach was sought and she was subsequently managed successfully. On follow-up, her visual acuity showed improvement, and neuroimaging revealed resolution of hyperintensities in bilateral LGB with residual blooming suggestive of old hemorrhagic gliosis. The possible reasons for isolated lesions of the LGB are hemorrhagic infarction and osmotic demyelination. In the present case, we postulate a vascular pathology, possibly hypo-perfusion because of shock following acute pancreatitis.
Assuntos
Corpos Geniculados , Pancreatite , Humanos , Feminino , Adulto Jovem , Adulto , Doença Aguda , Corpos Geniculados/irrigação sanguínea , Corpos Geniculados/patologia , Pancreatite/complicações , Pancreatite/diagnóstico por imagem , Transtornos da Visão/etiologia , Transtornos da Visão/patologia , Cegueira , Necrose/patologiaRESUMO
This study assessed the role of caffeine (adenosine receptor antagonist) in the Lateral geniculate body as well as the primary visual cortex of hyaluronic acid model of glaucomatous rats. Twenty (20) male Long evans rats were randomly divided into four groups with five animals each. This research confirmed that hyaluronic acid (HA) significantly induces elevated intraocular pressure from 18 to 35 mmHg and caffeine had no effect on its reduction to palliate visual impairment; There were a significant increase in the lipid peroxidation and conversely decrease in superoxide level with HA which were attenuated by caffeine. Although, caffeine showed a capability of ameliorating the histopathological changes induced by HA in terms of maintenance of a viable neuronal cell count and significant reduction of tumour necrosis factor-α immune positive cells in the LGB and visual cortex. These findings suggest that caffeine was unable to lower the intraocular pressure after hyaluronic acid exposure but has the ability to restore the antioxidant imbalance via mitigating pro-oxidant mediators and abrogate neurodegeneration.
Assuntos
Cafeína/farmacologia , Corpos Geniculados/efeitos dos fármacos , Ácido Hialurônico/toxicidade , Estresse Oxidativo/efeitos dos fármacos , Córtex Visual Primário/efeitos dos fármacos , Adjuvantes Imunológicos/toxicidade , Animais , Antioxidantes/farmacologia , Corpos Geniculados/metabolismo , Corpos Geniculados/patologia , Peroxidação de Lipídeos/efeitos dos fármacos , Peroxidação de Lipídeos/fisiologia , Masculino , Estresse Oxidativo/fisiologia , Córtex Visual Primário/metabolismo , Córtex Visual Primário/patologia , Antagonistas de Receptores Purinérgicos P1/farmacologia , Ratos , Ratos Long-Evans , Fator de Necrose Tumoral alfa/metabolismoRESUMO
The age-related loss of GABA in the inferior colliculus (IC) likely plays a role in the development of age-related hearing loss. Perineuronal nets (PNs), specialized aggregates of extracellular matrix, increase with age in the IC. PNs, associated with GABAergic neurotransmission, can stabilize synapses and inhibit structural plasticity. We sought to determine whether PN expression increased on GABAergic and non-GABAergic IC cells that project to the medial geniculate body (MG). We used retrograde tract-tracing in combination with immunohistochemistry for glutamic acid decarboxylase and Wisteria floribunda agglutinin across three age groups of Fischer Brown Norway rats. Results demonstrate that PNs increase with age on lemniscal and non-lemniscal IC-MG cells, however two key differences exist. First, PNs increased on non-lemniscal IC-MG cells during middle-age, but not until old age on lemniscal IC-MG cells. Second, increases of PNs on lemniscal IC-MG cells occurred on non-GABAergic cells rather than on GABAergic cells. These results suggest that synaptic stabilization and reduced plasticity likely occur at different ages on a subset of the IC-MG pathway.
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Envelhecimento/patologia , Neurônios GABAérgicos/patologia , Neurônios GABAérgicos/fisiologia , Colículos Inferiores/citologia , Colículos Inferiores/patologia , Rede Nervosa/patologia , Rede Nervosa/fisiopatologia , Tálamo/citologia , Tálamo/patologia , Animais , Vias Auditivas/fisiologia , Corpos Geniculados/citologia , Corpos Geniculados/patologia , Glutamato Descarboxilase/metabolismo , Perda Auditiva/etiologia , Perda Auditiva/patologia , Masculino , Lectinas de Plantas , Ratos , Receptores de N-AcetilglucosaminaRESUMO
ABSTRACT: A 58-year-old man presented with a complaint of subjective visual field loss on the right side and hypertensive emergency. Examination revealed a right homonymous hemianopia. Computed tomography imaging revealed an acute stroke of the left lateral geniculate body. A few months later, automated perimetry revealed characteristic visual field changes associated with this lesion. In this report, the anatomy, pathophysiology, clinical findings, and previously reported etiologies of lateral geniculate body lesions are reviewed.
Assuntos
Acidente Vascular Cerebral , Testes de Campo Visual , Corpos Geniculados/patologia , Hemianopsia/diagnóstico , Hemianopsia/etiologia , Humanos , Imageamento por Ressonância Magnética/métodos , Masculino , Pessoa de Meia-Idade , Acidente Vascular Cerebral/complicações , Acidente Vascular Cerebral/diagnóstico , Testes de Campo Visual/métodos , Campos VisuaisRESUMO
Age-related hearing loss is the most prevalent sensory impairment in the older adult population and is related to noise-induced damage or age-related deterioration of the peripheral auditory system. Hearing loss may affect the central auditory pathway in the brain, which is a continuation of the peripheral auditory system located in the ear. A debilitating symptom that frequently co-occurs with hearing loss is tinnitus. Strikingly, investigations into the impact of acquired hearing loss, with and without tinnitus, on the human central auditory pathway are sparse. This study used diffusion-weighted imaging (DWI) to investigate changes in the largest central auditory tract, the acoustic radiation, related to hearing loss and tinnitus. Participants with hearing loss, with and without tinnitus, and a control group were included. Both conventional diffusion tensor analysis and higher-order fixel-based analysis were applied. The fixel-based analysis was used as a novel framework providing insight into the axonal density and macrostructural morphologic changes of the acoustic radiation in hearing loss and tinnitus. The results show tinnitus-related atrophy of the left acoustic radiation near the medial geniculate body. This finding may reflect a decrease in myelination of the auditory pathway, instigated by more profound peripheral deafferentation or reflecting a preexisting marker of tinnitus vulnerability. Furthermore, age was negatively correlated with the axonal density in the bilateral acoustic radiation. This loss of fiber density with age may contribute to poorer speech understanding observed in older adults.SIGNIFICANCE STATEMENT Age-related hearing loss is the most prevalent sensory impairment in the older adult population. Older individuals are subject to the cumulative effects of aging and noise exposure on the auditory system. A debilitating symptom that frequently co-occurs with hearing loss is tinnitus: the perception of a phantom sound. In this large DWI-study, we provide evidence that in hearing loss, the additional presence of tinnitus is related to degradation of the acoustic radiation. Additionally, older age was related to axonal loss in the acoustic radiation. It appears that older adults have the aggravating circumstances of age, hearing loss, and tinnitus on central auditory processing, which may partly be because of the observed deterioration of the acoustic radiation with age.
Assuntos
Perda Auditiva/patologia , Zumbido/patologia , Estimulação Acústica , Adolescente , Adulto , Idoso , Envelhecimento/patologia , Atrofia , Vias Auditivas/patologia , Axônios/patologia , Imagem de Tensor de Difusão , Feminino , Corpos Geniculados/patologia , Perda Auditiva/complicações , Testes Auditivos , Humanos , Masculino , Pessoa de Meia-Idade , Bainha de Mielina/patologia , Percepção da Fala , Zumbido/complicações , Adulto JovemRESUMO
Following lesions of the primary visual cortex (V1), the lateral geniculate nucleus (LGN) undergoes substantial cell loss due to retrograde degeneration. However, visually responsive neurons remain in the degenerated sector of LGN, and these have been implicated in mediation of residual visual capacities that remain within the affected sectors of the visual field. Using immunohistochemistry, we compared the neurochemical characteristics of LGN neurons in V1-lesioned marmoset monkeys (Callithrix jacchus) with those of non-lesioned control animals. We found that GABAergic neurons form approximately 6.5% of the neuronal population in the normal LGN, where most of these cells express the calcium-binding protein parvalbumin. Following long-term V1 lesions in adult monkeys, we observed a marked increase (~ sevenfold) in the proportion of GABA-expressing neurons in the degenerated sector of the LGN, indicating that GABAergic cells are less affected by retrograde degeneration in comparison with magno- and parvocellular projection neurons. In addition, following early postnatal V1 lesions and survival into adulthood, we found widespread expression of GABA in putative projection neurons, even outside the degenerated sectors (lesion projection zones). Our findings show that changes in the ratio of GABAergic neurons in LGN need to be taken into account in the interpretation of the mechanisms of visual abilities that survive V1 lesions in primates.
Assuntos
Corpos Geniculados , Degeneração Retrógrada , Córtex Visual , Animais , Callithrix , Corpos Geniculados/patologia , Degeneração Retrógrada/patologia , Córtex Visual/patologia , Vias Visuais/patologia , Ácido gama-AminobutíricoRESUMO
BACKGROUNDS: Optic radiation protection is crucial in the basal temporal approach to the mesial temporal lobe. Clear description of the optic radiation in the basal brain surface is lacking. Our aim is to describe the anatomy of optic radiation in the basal cerebral surface and define safety zone of basal temporal approach avoiding of optic radiation injury. METHODS: Five brain specimens (10 hemispheres) were dissected using Klingler method to observe the course of the optic radiation. Diffusion tensor imaging data of 25 volunteers were used to verify the fiber dissection results. The relationship of the optic radiation to nearby structures were illustrated and measured. RESULTS: The optic radiation bends from the lateral wall of the lateral ventricle to its bottom at a basal turning point of optic radiation (bTPOR). The bTPOR is at the plane crossing the center point of the splenium of corpus callosum. MRI measurements showed no significant difference in the distance from the center of the splenium of corpus callosum and the bTPOR to the occipital pole (59.46 ± 4.338 mm vs 59.54 ± 3.805 mm, p = 0.95). Anterior to bTPOR, no optic radiation fibers were found at the basal brain surface. CONCLUSIONS: The bTPOR was found as a landmark of the optic radiation in the cerebral basal surface. With neuronavigation, the splenium of corpus callosum can be a landmark of the bTPOR. By approaching mesial temporal lesions using the basal temporal approach anterior to bTPOR, optic radiation injury can be prevented.
Assuntos
Lobo Occipital/patologia , Lobo Temporal/patologia , Vias Visuais/patologia , Cadáver , Imagem de Tensor de Difusão , Dissecação , Corpos Geniculados/diagnóstico por imagem , Corpos Geniculados/patologia , Humanos , Ventrículos Laterais/diagnóstico por imagem , Ventrículos Laterais/patologia , Lobo Occipital/diagnóstico por imagem , Lobo Temporal/diagnóstico por imagem , Vias Visuais/diagnóstico por imagemRESUMO
The 22q11.2 deletion syndrome (22q11.2 DS), one of the highest genetic risk for the development of schizophrenia, offers a unique opportunity to understand neurobiological and functional changes preceding the onset of the psychotic illness. Reduced auditory mismatch negativity response (MMN) has been proposed as a promising index of abnormal sensory processing and brain pathology in schizophrenia. However, the link between the MMN response and its underlying cerebral mechanisms in 22q11.2 DS remains unexamined. We measured auditory-evoked potentials to frequency deviant stimuli with high-density electroencephalogram and volumetric estimates of cortical and thalamic auditory areas with structural T1-weighted magnetic resonance imaging in a sample of 130 individuals, 70 with 22q11.2 DS and 60 age-matched typically developing (TD) individuals. Compared to TD group, the 22q11.2 deletion carriers reveal reduced MMN response and significant changes in topographical maps and decreased gray matter volumes of cortical and subcortical auditory areas, however, without any correlations between MMN alteration and structural changes. Furthermore, exploratory research on the presence of hallucinations (H+\H-) reveals no change in MMN response in 22q11.2DS (H+ and H-) as compared to TD individuals. Nonetheless, we observe bilateral volume reduction of the superior temporal gyrus and left medial geniculate in 22q11.2DSH+ as compared to 22q11.2DSH- and TD participants. These results suggest that the mismatch response might be a promising neurophysiological marker of functional changes within the auditory pathways that might underlie elevated risk for the development of psychotic symptoms.
Assuntos
Córtex Auditivo , Percepção Auditiva/fisiologia , Síndrome de DiGeorge , Potenciais Evocados Auditivos/fisiologia , Corpos Geniculados , Alucinações , Adolescente , Adulto , Córtex Auditivo/diagnóstico por imagem , Córtex Auditivo/patologia , Córtex Auditivo/fisiopatologia , Criança , Síndrome de DiGeorge/diagnóstico por imagem , Síndrome de DiGeorge/patologia , Síndrome de DiGeorge/fisiopatologia , Eletroencefalografia , Feminino , Corpos Geniculados/diagnóstico por imagem , Corpos Geniculados/patologia , Corpos Geniculados/fisiopatologia , Alucinações/diagnóstico por imagem , Alucinações/patologia , Alucinações/fisiopatologia , Humanos , Imageamento por Ressonância Magnética , Masculino , Adulto JovemRESUMO
BACKGROUND AND PURPOSE: Idiopathic sudden sensorineural hearing loss is an acute unexplained onset of hearing loss. We examined the central auditory pathway abnormalities in patients with unilateral idiopathic sudden sensorineural hearing loss using diffusion spectrum imaging and the relationships between hearing recovery and diffusion spectrum imaging parameters. MATERIALS AND METHODS: Forty-eight patients with unilateral idiopathic sudden sensorineural hearing loss with a duration of ≤2 weeks (range, 8.9 ± 4.3 days) and 20 healthy subjects underwent diffusion spectrum imaging tractography. Hearing levels were evaluated using a pure-tone average at initial presentation and 3-month follow-up. Clinical characteristics and MR imaging findings were assessed. RESULTS: Compared with healthy control subjects, the generalized fractional anisotropy values of patients decreased significantly in the bilateral posterior limbs of the internal capsule, with no differences between the ipsilateral and contralateral sides. The quantitative anisotropy values decreased in the Brodmann area 41, contralateral medial geniculate body, bilateral lateral lemniscus, anterior limb of internal capsule, middle temporal gyrus, and anterior corona radiata. Furthermore, at 3-month follow-up, 14 patients had <15 dB of hearing gain. Receiver operating characteristic curve analysis demonstrated that generalized fractional anisotropy in the ipsilateral medial geniculate body was related to prognosis (sensitivity = 64.7%; specificity = 85.7%; area under the curve = 0.796, 95% CI, 0.661-0.931; P < .01). CONCLUSIONS: Diffusion spectrum imaging can detect abnormalities of white matter microstructure along the central auditory pathway in patients with unilateral idiopathic sudden sensorineural hearing loss. The generalized fractional anisotropy value of the ipsilateral medial geniculate body may help to predict recovery outcomes.
Assuntos
Vias Auditivas/diagnóstico por imagem , Corpos Geniculados/diagnóstico por imagem , Perda Auditiva Neurossensorial/etiologia , Perda Auditiva Súbita/etiologia , Neuroimagem/métodos , Adulto , Idoso , Vias Auditivas/patologia , Imagem de Tensor de Difusão/métodos , Feminino , Corpos Geniculados/patologia , Humanos , Interpretação de Imagem Assistida por Computador , Masculino , Pessoa de Meia-Idade , Prognóstico , Substância Branca/diagnóstico por imagem , Substância Branca/patologiaRESUMO
PURPOSE: Periventricular leukomalacia (PVL) is a structural loss of white matter pathways that carry visual information from the lateral geniculate bodies to the visual cortex. It is observed radiologically in patients with a history of prematurity and is associated with visual field (VF) defects and optic disc cupping. Advances in perinatal care have improved survival for premature babies, so many now present as adolescents and adults to comprehensive eye doctors who are unaware of the relationship of cupping, field defects, and prematurity and who may diagnose manifest or suspected normal tension glaucoma. We describe 2 such patients to raise awareness of this entity. DESIGN: Case series. METHODS: Review of clinical information of 2 patients identified during clinical practice. Charts were reviewed for gestational age, optic nerve appearance, intraocular pressure (IOP), and sequelae of prematurity. Magnetic resonance imaging (MRI), optical coherence tomography (OCT), VF, and optic disc photographs were reviewed. RESULTS: Two young patients with a history of prematurity presented with enlarged cup-to-disc ratio and normal IOP. OCT thinning was most prominent superiorly, with VF defects more notable inferior and homonymous. No progression on VF or OCT was noted in the index case over almost 4 years. CONCLUSIONS: Periventricular leukomalacia should be added to the differential diagnosis of normal tension glaucoma (NTG) when there is a history of prematurity. Careful examination of the optic nerve will assist in differentiating from NTG. Specifically, horizontal cupping with minimal or no nasal displacement of vessels, and superior optic nerve thinning with inferior VF defects, suggest PVL.
Assuntos
Leucomalácia Periventricular/diagnóstico , Glaucoma de Baixa Tensão/diagnóstico , Retinopatia da Prematuridade/diagnóstico , Adolescente , Diagnóstico Diferencial , Corpos Geniculados/patologia , Idade Gestacional , Humanos , Pressão Intraocular , Imageamento por Ressonância Magnética , Masculino , Disco Óptico/patologia , Doenças do Nervo Óptico/diagnóstico , Tomografia de Coerência Óptica , Tonometria Ocular , Transtornos da Visão/diagnóstico , Córtex Visual/patologia , Testes de Campo Visual , Campos Visuais , Adulto JovemRESUMO
Traditionally, the dorsal lateral geniculate nucleus (LGN) and the inferior pulvinar (IPul) nucleus are considered as anatomically and functionally distinct thalamic nuclei. However, in several primate species it has also been established that the koniocellular (K) layers of LGN and parts of the IPul have a shared pattern of immunoreactivity for the calcium-binding protein calbindin. These calbindin-rich cells constitute a thalamic matrix system which is implicated in thalamocortical synchronisation. Further, the K layers and IPul are both involved in visual processing and have similar connections with retina and superior colliculus. Here, we confirmed the continuity between calbindin-rich cells in LGN K layers and the central lateral division of IPul (IPulCL) in marmoset monkeys. By employing a high-throughput neuronal tracing method, we found that both the K layers and IPulCL form comparable patterns of connections with striate and extrastriate cortices; these connections are largely different to those of the parvocellular and magnocellular laminae of LGN. Retrograde tracer-labelled cells and anterograde tracer-labelled axon terminals merged seamlessly from IPulCL into LGN K layers. These results support continuity between LGN K layers and IPulCL, providing an anatomical basis for functional congruity of this region of the dorsal thalamic matrix and calling into question the traditional segregation between LGN and the inferior pulvinar nucleus.