Block 13 Traum Brain Inj Raised Icp MCQ's

Compression of cranial nerve III is associated with the earliest manifestations of uncal herniation. This occurs when there is increased pressure in the brain, causing the uncus to herniate and compress the oculomotor nerve (cranial nerve III). This compression leads to a variety of symptoms, including pupillary dilation, ptosis (drooping of the eyelid), and impaired eye movement. These symptoms are often observed before other signs of uncal herniation, such as brainstem compression or infarctions.

Acute subdural hematomas are caused by tearing of bridging veins. These veins connect the surface of the brain to the dural sinuses, which are large veins located between the layers of the meninges. When a traumatic injury occurs, such as a blow to the head, these bridging veins can tear, leading to bleeding between the dura mater and the arachnoid membrane. This accumulation of blood can put pressure on the brain and cause symptoms such as headaches, confusion, and neurological deficits. Unlike epidural hematomas, which are commonly caused by tearing of middle meningeal arteries, acute subdural hematomas are typically associated with bridging vein injuries.

The fracture of the skull above and anterior to the external ear suggests a possible injury to the middle meningeal artery, which can result in an extradural hemorrhage. This hemorrhage can lead to an increase in intracranial pressure. If the pressure continues to rise, it can cause herniation of the uncus of the temporal lobe. This herniation can compress the oculomotor nerve, leading to a fixed and dilated pupil on the side of the lesion.

The most likely pathology in this patient is epidural hemorrhage/hematoma. This is suggested by the history of head trauma followed by a brief loss of consciousness, regaining consciousness, and then losing consciousness again after a period of time. The fixed and dilated right pupil on eye exam is indicative of increased intracranial pressure, which is commonly seen in epidural hematoma. A CT scan of the head would confirm the diagnosis by showing a collection of blood between the skull and dura mater.

Diffuse axonal injury is characterized by axonal swelling, which occurs due to the shearing forces applied to the brain during the injury. This swelling can disrupt the normal functioning of the axons and impair the transmission of nerve impulses. Other changes such as cerebral edema with herniation, widespread areas of cortical and subcortical hemorrhages, and neuronal swelling with dissolution of Nissl substance may be seen in different types of brain injuries, but they are not specifically characteristic for diffuse axonal injury.

Transtentorial herniation refers to the displacement of brain tissue through the tentorial notch, which can compress and damage structures in the brainstem. The clinical findings described in the question, including right ptosis and a dilated pupil non-reactive to light, are consistent with a third nerve palsy caused by compression of the oculomotor nerve. This is a classic sign of transtentorial herniation. Acute hydrocephalus, occipital lobe infarct, and lacerations of the pedunculi would not typically present with these specific findings.

Spinal tap, also known as a lumbar puncture, is a procedure used to collect and analyze cerebrospinal fluid (CSF) from the spinal canal. It is indicated in cases of acute meningitis and subarachnoid hemorrhage due to berry aneurysm rupture. Acute meningitis is an inflammation of the membranes surrounding the brain and spinal cord, while subarachnoid hemorrhage refers to bleeding in the space between these membranes. By performing a spinal tap, the CSF can be examined for signs of infection or bleeding, helping to diagnose and guide treatment for these conditions. The other options listed do not specifically indicate the need for a spinal tap.

Following a minor trauma to the brain, the activation of nociceptors in the muscles of the scalp and neck may help to explain the causation of post-traumatic headache. Nociceptors are sensory receptors that respond to pain stimuli, and the muscles of the scalp and neck can become tense and strained after a head injury, leading to the activation of these nociceptors and the subsequent sensation of headache. This mechanism is supported by the fact that many patients experience headache after trauma and that it can last for varying periods of time.