May 30, 2024
Traumatic brain injury typically happens when the head or body is struck violently or suddenly. A gunshot or fractured piece of skull can likewise create worrying mind harm, as can an object that penetrates mind tissue.
Temporary effects on brain cells can also result from mild stressful brain injury. More severe stressful brain damage can include bleeding, bruises, torn tissues, and other physical mental injury. These wounds may result in permanent headaches or even death.
There are two types of serum markers for traumatic brain injury (TBI): Glial and neuronal-specific enolase, cleaved tau protein, neurofilament, and ubiquitin C-terminal hydroxylase-L1. For glial markers, an S100B value of more than 2 µg/ml is indicative of poor outcomes in patients with moderate to severe brain injury (more accurate than the GCS score).
Serum markers for traumatic brain injury (TBI) are presently only utilized in research; they may be helpful in detecting the course of the disease and tracking the effectiveness of treatment.
Also Read: Traumatic Brain Injury- Epidemiology And Pathology
Diabetes insipidus may result from a deficiency of antidiuretic hormone (ADH) in the early acute phase of the injury. Other pituitary hormone deficiencies may also occur subtly. If the pituitary location makes it vulnerable to injury in TBI, it causes pituitary hormone deficiencies leading to neuroendocrinal dysfunction.
The most prevalent endocrinopathy, growth hormone (GH) insufficiency, affects 10–30% of patients following traumatic brain injury (TBI).
A decrease in GH and thyroid-stimulating hormone (TSH) may result from the loss of cholinergic neurons caused by traumatic brain injury (TBI). A decrease in TSH and/or free T4 may indicate partial central hypothyroidism. Three to five percent of TBI patients exhibit multiple neuroendocrine abnormalities.
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CT and MRI scans are frequently utilized. A CT scan may be the initial test in the acute stage. CT is very good at detecting hematomas and quick changes in the neurological status brought on by bleeding. MRI is used to see white matter abnormalities and contusions. Small subdural collections and non-hemorrhagic lesions are more detectable on MRI.
Quantitative information on volumetric changes in the CSF, white matter, and grey matter is provided by structural volumetric magnetic resonance imaging (MRI). Diffusion tensor imaging (DTI) determines the direction of water diffusion in space.
White matter alterations, or the integrity of the myelin sheath following traumatic axonal injury, are studied using DTI. decreased anisotropy white matter alterations that manifest within the first 24 hours following traumatic brain injury Diffusion tensor tractography makes it possible to see and examine certain white matter pathways. It can effectively identify alterations in the corpus callosum following traumatic brain injury.
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Different types of functional imaging can be used to detect changes not seen in structural imaging. FMRI in task-based mode can be used to study working memory or tension, while the default mode network is used to study resting state. PET can be used to study 18F-FDG PET studies. SPECT (single photon emission CT) can be used to study blood flow and metabolic changes. MR Spectroscopy (MRS).
Using H1-MRS, MRS maps the metabolic distribution utilizing certain metabolite markers. The metabolic and neural density markers are indicated by N-acetyl aspartate (NAA). Compounds containing choline (CHO) indicate the metabolism of phospholipids. Compounds containing creatine (Cre) indicate the energy state of cells.
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The traditional electroencephalogram (EEG) is used to diagnose seizures and brain death as well as to monitor treatments like neurosurgery. Also utilized to identify the location of post-traumatic seizure focal and to diagnose epilepsy. If you have nasopharyngeal, anterior temporal, or sphenoidal leads, your chances of discovering an abnormality rise.
Other, less often utilized approaches that can distinguish any unclear irregularities are video EEG and 24-hour ambulatory recording. Quantitative EEG (QEEG) is employed as an auxiliary tool to assess the slow-wave abnormalities associated with brain injury. Additionally, it aids in the identification of temporal lobe epilepsy caused by trauma.
For atypical sleep problems linked to traumatic brain injury (TBI), such as sleep apnea, nocturnal myoclonus, atypical night terrors, and restless legs syndrome, polysomnography is utilized. Localizing the extent of CNS injury and detecting brain stem pathology are made easier by the use of visual, auditory, and somatosensory evoked potentials. P50 physiology: Given that patients with traumatic brain injury exhibit a deficiency in sensory gating, P50 may be a sign of hippocampal malfunction.
Hope you found this blog helpful for your Psychiatry residency Neurology and General Medicine preparation. For more informative and interesting posts like these, keep reading PrepLadder’s blogs.
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