Intracranial Mass Lesions
Signs and symptoms: The symptom most often associated with intracranial mass lesions is headache, although it has little localizing value. The typical headache from mass lesion has a boring pain, and may awaken the patient during sleep. Projectile vomiting without nausea is a common feature. More commonly, the headache is dull, moderate in intensity and chronic. Often, coughing, bending over and exertion will exacerbate the headache.
Other signs associated with intracranial mass lesions include transiently obscured vision, seizures, loss of consciousness, changes in mental status and drop attacks. In the hydrocephalic state--which may occur when the mass blocks cerebrospinal fluid flow and expands the cerebral ventricles--there may be loss of memory, gait ataxia, balance disturbance and urinary incontinence.
The clinical finding most associated with an intracranial mass lesion is papilledema. Other findings may include horizontal diplopia from unilateral or bilateral CN VI palsy.
Pathophysiology: The disorder begins with a space-occupying lesion within the cranial vault. The lesion can be a primary intracranial tumor such as meningioma, a metastatic lesion such as adenocarcinoma, or a non-neoplastic lesion such as a colloidal cyst or arteriovenous malformation.
The lesion may exert effects two ways. It can grow so large that it occupies intracranial space at the expense of brain tissue, causing dysfunction of structures governed by compressed brain tissue. As it compresses pain-sensitive structures, patients report head pain. This may also cause nausea.
If the lesion blocks the flow of cerebrospinal fluid through the aqueducts, the cerebral ventricles will expand and compress brain tissue in this hydrocephalic state. As the ventricles expand, the brain parenchyma will be compressed and the myelinated tracts of the internal capsule will be stretched. This governs the muscles of the legs and voluntary muscles of the bladder. This will manifest as a slowly progressive gait disturbance with unsteadiness and difficulty navigating curbs and steps, as well as increased urinary urgency. Urinary incontinence follows.
Compression of the frontal lobe by the expanding ventricle leads to changes in mental status, especially loss of short-term memory--often making the patient unconcerned about incontinence. The projectile vomiting that occurs has never been adequately explained. Perhaps it may be a reflex mechanism to dehydrate the body and thus reduce intracranial volume.
Papilledema results from increased intracranial subarachnoid pressure, which is continuous with the subarachnoid space surrounding the optic nerve. The resultant increase in tissue pressure blocks axoplasmic flow and compresses vascular channels and capillaries, with subsequent swelling of nerve fibers and capillary leakage. This results in the disc edema seen in papilledema. Interrupted axoplasmic flow and compressed fibers may manifest as transient visual obscurations with a graying out of vision.
As intracranial pressure increases, the CN VI can be compressed against the petrous apex of the temporal bone. The increased intracranial pressure may herniate the brainstem down through the foramen magnum. This stretches the CN VI across the petrous apex of the temporal bone as it arises from the pontomedulary junction and ascends the clivus. The result is unilateral or bilateral CN VI palsy with ophthalmoplegia and diplopia.
Management: Whenever you suspect an intracranial mass lesion, neuroimaging is mandatory within 48 hours. MRI is typically superior to CT-scan. Contrast enhancement is preferable.
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