Idiopathic Intracranial Hypertension

Pseudotumor cerebri (PTC), also called benign intracranial hypertension (BIH), is characterized by elevated intracranial pressure that is unrelated to hydrocephalus, tumor, brain edema, or any other structural entities associated with normal CSF analysis (12). Usually, PTC presents with headache, and, often, there are changes in the vision of obese women of childbearing age (13). Almost all patients with PTC have headaches, i.e., 90-94%. Their headaches are associat5ed with a feeling of pressure and throbbing. The headaches usually are continual and occur with retro-ocular pain, and the patient may become nauseated (13, 14) Vision loss is the most-feared result of PTC, but it is usually temporary. Approximately 68-85% of such patients experience vision loss (13-16). There usually are impairments in the visual field, the most common of which is tunnel vision (13). The vision changes are usually explained as transient ischemia of the optic nerve due to pressure (16). Photopsia (54%) and eye pain (44%) are other common symptoms (16). More severe symptoms occur infrequently, but diplopia (38%) and vision

The typical eye indication of inflicted head injury is retinal haemorrhage and thus the severity of the head trauma correlates with the degree of the eye haemorrhage. Most haemorrhages tend to be concentrated near the posterior pole, and can involve one or more layers of the retina. Diffuse fundi bleeds, vitreous haemorrhage or even large subhyaloid haemorrhages are usually associated with worse visual outcomes and even blindness. The cause of retinal haemorrhaging is not entirely clear, but there is a supporting theory as to why retinal haemorrhages do occur. The theory suggests that it is caused by haemorrhages which arise from the back pressure on the central retinal vein, which is caused by elevated intracranial or intrathoracic pressure (Blumenthal, 2002).

Colton et al. (2014) research looked at 117 clients who experienced increase intracranial pressure as a result of severe traumatic brain injury. Their research looked at client’s respond to pharmacological interventions and these pharmacological interventions include hypertonic saline, mannitol, propofol, fentanyl, and barbiturate. In their research Colton et al., (2014) found “all treatment resulted in significant intracranial pressure changes after 1 hour or 2 hours except for mannitol and barbiturate administration” (Colton at el., 2014). This finding is significant given that mannitol is used as a first line treatment for management of increased intracranial pressure. The chart below demonstrates how each of these pharmacological interventions decreased intracranial pressure and it allows us to compare each pharmacological intervention to each other. (Colton et al., 2014)

The clinical manifestations include; bulging fontanels, high pitched cry, head circumference is larger than chest circumference, sac like projection on lumber spine, cry when your stroke is fingers and toes, sensory impairment, delay in developmental growth, eyes depressed and rotated downward, sluggish pupils, and structural malformations cause by intracranial pressure (Perry, Hockenberry, Lowdermilk, & Wilson, 2014, p. 1455).

Cerebral edema is swelling (edema) in your child’s brain. Cerebral edema is caused by a buildup of fluid in brain tissue in response to a brain injury or condition.

in such cases the cause may be a ruptured aneurysm which may be lead to bleeding , then this may cause a coma for person . in such cases the both pupil will be dilated and they are not responding to fixation light so this may be indicates deep coma or possibly brain death .

Vascular blockage or hemodynamic disturbances from intracranial or the extra cranial vascular injury (stenosis, splitting, vasculitis)

Acute occlusion of the intracranial artery causes reduced blood flow to the brain region it supplies.

First, inspect the head and heck when obtaining the objective data. The scalp, hair, and cranium should are reviewed for any deformities, lumps, or tenderness. Secondly, review the face for any changes to facial expression, symmetry, or involuntary movements. Any changes in the face may be a reflection of problem to Cranial Nerve 7. Next is the assessment of the temporal artery and the mandibular joint. The patient will open and close their mouth at least twice to ensure there are no deficiencies in this area. Lastly, is the observation of the maxillary and frontal sinuses and inspect for any swelling or tenderness.

. Overview of processes involved ischemic stroke and high potential therapeutic microRNAs. Cerebral ischemia includes several injurious mechanisms (excitotoxicity, oxidative stress, inflammation and apoptosis) to confer neuronal injury. Potential therapeutic areas to compensate these pathogenic process include promoting angiogenesis, neurogenesis and neuroprotection which they are as recovery and repair

Cerebral arteriovenous malformations are presumably congenital vascular malformations that may present clinically with a variety of symptoms, including hemorrhage, seizures, headaches, progressive neurologic deficits, and intellectual deterioration. Hemodynamic alterations caused by the complex Angioarchitecture of CAVMs play a role in seizure manifestation [43]. Large CAVM size and high flow through the arterial feeding vessels of the CAVMs were related to seizure susceptibility on the basis of the assumption that the large Nidus creates a low-resistance vascular bed redirecting blood away from the surrounding brain tissue, thus creating local hypoxemia in the adjacent brain tissue, which, in turn, may trigger gliosis and seizure activity. This pathomechanism was referred to as “arterial steal.” Cerebral arteriovenous malformations (CAVM) are a common form of cerebral vascular malformation and are composed of a NIDUS of vessels through which arteriovenous shunting occur [44].

Because of the misdiagnosis of LP shunt-induced cerebellar tonsillar ptosis, she was conservatively treated with medications, such as Promethazine and Trifluoperazine. Her nausea and headache were exacerbated, and she was readmitted. Her computed tomography (CT) scan of the brain indicated left frontotemporoparietal subacute subdural hematoma with subfalcine herniation (Figure 3). In her second surgery, the left parietal Burr-Hole was performed, and the subdural hematoma was evacuated. The post-operative period was uneventful, and her symptoms disappeared. Her delay brain CT showed relief of hematoma and herniation (Figure

Symptoms of an intracerebral hemorrhage normally begin with sudden headache, often during increased amounts of activity. Loss of consciousness is also a common symptom, often within a few minutes or even seconds. Nausea, vomiting, delirium, and focal or generalized seizures are also common. Neurologic deterioration is usually sudden and progressive. Large hemorrhages, when located in the hemispheres, cause hemiparesis, which is the weakening of an entire side of the body; when located in the posterior fossa of the brain, they cause cerebellar or brain stem deficits such as pinpoint pupils, stertorous breathing, conjugate eye deviation or ophthalmoplegia, and even a coma. Large hemorrhages have proven to be fatal within only a few days in the

The authors stated that the atlas subluxation hindered with the movement of cerebrospinal fluid affecting midbrain function and producing extreme stress in the brain.

No history of head trauma of any kind was reported in this patient. Contrary to hydrocephalic patients, the literature did not provide any previous report of subacute or chronic subdural hematoma subsequent to placement of LP shunt in patients with BIH. Persistent symptoms, such as a headache, nausea, and vomiting, after placement of a lumboperitoneal shunt, should be taken seriously, and CT imaging of the brain should be done to rule out a subdural hematoma.