ABSTRACT
BACKGROUND: Hypoxic-ischemic encephalopathy (HIE) appears in neurological conditions where some brain areas are likely to be injured, such as deep grey matter, basal ganglia area, and white matter subcortical periventricular áreas. Moreover, modeling these brain areas in a newborn is challenging due to significant variability in the intensities associated with HIE conditions. This paper aims to evaluate functional measurements and 3D machine learning models of a given HIE case by correlating the affected brain areas with the pathophysiology and clinical neurodevelopmental. CASE PRESENTATION: A comprehensive analysis of a term infant with perinatal asphyxia using longitudinal 3D brain information from Machine Learning Models is presented. The clinical analysis revealed the perinatal asphyxia diagnosis with APGAR <5 at 5 and 10 minutes, umbilical arterial pH of 7.0 BE of -21.2 mmol / L), neonatal seizures, and invasive ventilation mechanics. Therapeutic interventions: physical, occupational, and language neurodevelopmental therapies. Epilepsy treatment: vagus nerve stimulation, levetiracetam, and phenobarbital. Furthermore, the 3D analysis showed how the volume decreases due to age, exhibiting an increasing asymmetry between hemispheres. The results of the basal ganglia area showed that thalamus asymmetry, caudate, and putamen increase over time while globus pallidus decreases. CLINICAL OUTCOMES: spastic cerebral palsy, microcephaly, treatment-refractory epilepsy. CONCLUSIONS: Slight changes in the basal ganglia and cerebellum require 3D volumetry for detection, as standard MRI examinations cannot fully reveal their complex shape variations. Quantifying these subtle neurodevelopmental changes helps in understanding their clinical implications. Besides, neurophysiological evaluations can boost neuroplasticity in children with neurological sequelae by stimulating new neuronal connections.
Subject(s)
Asphyxia Neonatorum , Epilepsy , Hypoxia-Ischemia, Brain , Infant, Newborn , Infant , Pregnancy , Female , Child , Humans , Asphyxia/complications , Brain/diagnostic imaging , Hypoxia-Ischemia, Brain/diagnostic imaging , Hypoxia-Ischemia, Brain/therapy , Hypoxia-Ischemia, Brain/complications , Asphyxia Neonatorum/complications , Asphyxia Neonatorum/diagnostic imaging , Asphyxia Neonatorum/therapy , Seizures/complicationsABSTRACT
La enfermedad de Creutzfeldt-Jakob esporádica (ECJe) es un trastorno neurodegenerativo transmisible, extremadamente raro, caracterizado por demencia rápidamente progresiva. En la tomografía por emisión de positrones con 18F-fluoro-2-desoxi-D-glucosa (18F-FDG-PET/TC) de estos pacientes se ha descrito hipometabolismo cortical bilateral parietal, frontal y occipital, sin alteraciones en el cerebelo ni en los ganglios basales, lo que podría contribuir con el diagnóstico diferencial de demencia rápidamente progresiva. Se presenta el caso de un hombre de 75 años de edad, con antecedente de cáncer de próstata y trastorno afectivo bipolar, con cuadro de dos semanas de cambios comportamentales y anímicos, déficit cognitivo, alucinaciones visuales y auditivas y desorientación espacial con rápida progresión. Posteriormente, el paciente presenta marcha lenta, temblor en miembros inferiores y Babinski derecho. La resonancia magnética (RM) cerebral mostró restricción a la difusión en la corteza frontal y temporal bilateral y giro del cíngulo, con sospecha diagnóstica de síndrome paraneoplásico versus enfermedad por priones. La 18F-FDG-PET/TC demostró hipometabolismo en la corteza frontal bilateral y lóbulo temporal y parietal derechos. La medición de la proteína 14-3-3, proteína T-Tau y conversión de proteína priónica inducida por agitación en tiempo real (RT-QUIC) en líquido cefalorraquídeo confirmó el diagnóstico de enfermedad por priones.
Sporadic Creutzfeldt-Jakob disease (sCJD) is an extremely rare transmissible neurodegenerative disorder characterized by rapidly progressive dementia. 18F-fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG-PET/CT) in these patients has described bilateral parietal, frontal and occipital cortical hypometabolism, without alterations in the cerebellum or basal ganglia, which could contribute to the differential diagnosis of rapidly progressive dementia. We present the case of a 75-year-old man with a history of prostate cancer and bipolar affective disorder, with a two-week picture of behavioral and mood changes, cognitive deficit, visual and auditory hallucinations and spatial disorientation with rapid progression. Subsequently, the patient presented slow gait, tremor in lower limbs and right Babinski. Brain magnetic resonance imaging (MRI) showed diffusion restriction in the bilateral frontal and temporal cortex and cingulate gyrus, with diagnostic suspicion of paraneoplastic syndrome versus prion disease. 18F-FDG-PET/CT showed hypometabolism in the bilateral frontal cortex and right temporal and parietal lobe. Measurement of 14-3-3 protein, T-Tau protein and real-time shake-induced prion protein conversion (RT-QUIC) in cerebrospinal fluid confirmed the diagnosis of prion disease.
