Intracranial hypertension

– In a person at rest and supine intracranial pressure is normally 10 mmHg (10 cm H2O). It is equal to the hydrostatic pressure of the CSF.

– Intracranial pressure (intracranial hypertension) is defined by numbers greater than 15 mmHg.

Cerebral edema of various types: vasogenic (by increasing capillary permeability); cytotoxic (ballooning injury and glial cell by hypoxia, hypo-osmolality, ischemia or toxic products); interstitial (crossing of cerebrospinal fluid in excess periventricular during obstructive hydrocephalus).

The Cushing reflex: is the elevation of systemic blood pressure during the HIC for brain perfusion pressure can overcome intracerebral pressure.

– Installation The speed of HIC depends on the location of the injury, its nature and its growth rate. The tumors in the posterior fossa quickly cause HIC; some smaller tumors cause significant peritumoral edema (glioblastoma, metastases). In contrast some slow-growing tumors (meningioma) can reach a significant volume before driving a HIC.

Intracranial hypertension

1- Positive diagnosis:

– Headache intermittent at first and then rapidly permanent; diffuse or localized to a hemicranium or occipital. It may not manifest until an advanced stage.

– Vomiting: Easy Jet, independent of meals. They may be absent or replaced by abdominal pain (child).

– Visual disturbances: horizontal diplopia by unilateral or bilateral nerve damage VI (oculomotor nerve external), which has no localizing value; visual blurring can be replaced diplopia. Visual eclipses or decreased visual acuity occur in severe or advanced HIC and precede blindness by optic atrophy, and final major complication of HIC. The study of the visual field shows an enlargement of the blind spot of moriotte (early sign).

– Security disorders: attention deficit disorder, slowness of ideation, apathy and indifference (remote patient). Then increasing confusion, confusion, drowsiness before installing a coma.

– Attention: behavioral disorders and psychiatric manifestations are possible.

– None of these signs is constant.

– The fundus: search a bilateral papilledema. Loss of normal concavity of the papilla. protruding disc to blurry edges, hyperaemic; the veins are tortuous and dilated. At a more advanced stage, flame-shaped haemorrhages and exudates peripapillary. Her

– Normality FO does not eliminate the diagnosis (infant, elderly, acute ICH).

– Other clinical signs: signs of localizations (seizures, neurological deficits); autonomic disorders (hiccup, yawn, bradycardia or tachycardia)

– In infants: increased head circumference, eyes “sunset”; disjunction of sutures; digestive symptoms, normal FO.

– In children: the risk of optic atrophy (blindness) is important; frequency of behavioral disorders, digestive disorders and learning difficulties.

Foster-Kennedy Syndrome: combines unilateral optic atrophy (direct compression) and contralateral papilledema. It evokes a tumor in the vicinity of the optical channel (meningioma of the small wing of the sphenoid, fronto-orbital tumors).

2- Cerebral Commitments:

A- Hernias transtentorielles (through the foramen ovale):

– From top to bottom, commitment hippocampal uncus in case of expansive processes, especially temporal

– These hernias compress three formations: the III, the cerebral peduncle and the posterior cerebral artery.

– Clinical expression: mydriasis (by reaching the III); hemiplegia contralateral or ipsilateral rarely; new or worsening impaired consciousness; decerebrate rigidity and contralateral homonymous hemianopia (compression of the posterior temporal artery).

B- Herniated cerebellar tonsils:

– Is done through the foramen magnum (foramen magnum); mainly seen with tumors of the posterior fossa.

– Grave by compression of the bulb: respiratory disorders with risk of sudden death.

– Clinic: stiff neck; or lateral tilt of the head (head stilted) hypertension with painful neck muscle by irritation of the spinal (XI). Sometimes subsequent tonic seizures; consciousness disorders are late.

C- hernia cingulate under the falx:

frontal tumors; own semiotics years with increase in clinical signs and disorders of consciousness. Can compress the contralateral hemisphere and anterior cerebral artery responsible for crural hemiplegia.

D- central Commitment:

With rostrocaudal deterioration. For overall lowering of central nervous system through the tensor hole. Caused by supratentorial process paramedian to slow development or bilateral cerebral edema. progressive deterioration of descending brainstem structures.

3- Appendix:

– X-ray of the skull in children (HIC chronic): finger-printing; platybasia; enlargement of the sella; quatrilatère erosion of the blade and clinoid processes.

– The cerebral thrombophlebitis: HIC associates, seizures; neurological deficit (hemiplegia rocking when the superior sagittal sinus thrombosis).

– The malformation Chiari associated hydrocephalus + downward displacement of the cerebellar tonsils and the medulla through the foramen magnum. Often associated with syringomyelia, a bone abnormality of the cervical-occipital hinge (occipitalisation atlas + atlantoaxial dislocation) and spina bifida.

– The Dandy-Walker malformation associated hydrocephalus imperforation holes Magendie and Luschka associated with agenesis of the cerebellar vermis.

– A tumor at the ponytail can cause hydrocephalus by HIC.

4- Treatment:

– Avoid hypoxia and hypercapnia that aggravate cerebral edema.

– Maintain proper hemodynamics: G + 5% 500 cm3 multivitamins

– Semi-upright position

– Fluid restriction

antiœdémateux treatment

– Osmotic Products: Mannitol 20% by IV then relay Glycerol orally (to avoid the rebound effect).

– Corticosteroids: mainly active on the HIC tumor cause; no interest in stroke

HIC called benign (pseudo-tumor cerebri):

Chart HIC with risk of blindness from optic atrophy stasis without tumor or hydrocephalus, or vigilance disorders. The ventricles are small; sulci inconspicuous. Caused by an arachnoid barrier to the absorption of CSF or venous obstruction. The main causes are: cerebral venous thrombosis; intracellular hydration (hyponatremia); endocrine causes (Addison, hypoparathyroidism); lead poisoning; medication (cold turkey corticosteroids, tetracycline, nalidixic acid derivatives of vitamin A). Treatment: acetazolamide (Diamox®), carbonic anhydrase inhibitor, reduces the secretion of CSF by the choroid plexus. PL evacuative