Two Pathwys of hearing

Air

Bone

Air conduction travels over the air filled external and middle ear through vibration of the typanic membrane and ossicles.

Sounds transmitted by bone conduction travel directly through bone to the inner ear, bypassing the typanic membrane and ossicles.

Air conduction is the more efficient pathway.

Single most improtant diagnostic instrument with hearing loss. are two kinds: pure tone and speech

Pure tone in which the sound stimulus consists of a pure or musical tone (the louder the tone before the patient perceived it, the greater the hearing loss.)

Speech audiometry in which the spoken word is used to determine the ability to hear and discriminate sounds and words.

When evaluating hearing three things are important: freguency, pitch, and intensity

When the stimulus is applied to the mastoid bone, bypassing the conductive mechanism ( the ossicles) , nerve conduction is tested.

When the tone is applied directly over the external auditory canal, air conduction is measured.

Frequency refers to the number of sound waves emanating from a source per second, measured as cycles per second or Hz. The normal human ear percieves sounds ranging in frequency from 20 to 20000 hz.

Pitch is the term used to describe frequency; a tone with 100 hz is considered of low pitch, and a tone of 10000 hz is considered high pitch.

The unit for measuring loudness is the decibel and is the intensity of sound. Hearing loss is measured in decibels. critical level of loudness is approx. 30 dB.

has been found to cause constriction of peripheral blood vessels, indcreased blood pressure and heart rate due to increased secretion of adrenalin, and increase GI activity.

noice induced hearing loss occures at about 4000 Hz.

aminoglycosides, aspirin, quinine

diabetes also is partially responsible for sensorineural hearing loss.

impaction occasionally occurs, causing otalgia, a sensation of fullness or pain in the ear, with or without hearing loss.

Cerumen can be removed by irrigation, suction, or instrumentation. UNLESS, ther person has a perforated eardrum or an inflamed external ear ( otitis externa). If the ear drum is perforated, water can enter the middle ear, producing acute vertigo and infection.

Instilling a few drops of warmed glycerin, mineral oil, or half-strength hydrogen peroxide into the ear canal for 30 min. can soften the cerumen before its removal

refers to an inflammation of the external auditory canal. Causes include water in the ear canal (swimmers ear), trauma to the skin of the ear canal, permitting entrance of organisms into the tissues; and systemic conditions, such as vitamin deficiency and endocrine disorders.

Clinical maifestations: patients report pain, dicharge from the external ausitory canal, aural tenderness (unually not present in middle ear infections), and occasionally fever, cellulitis, and lymphadenopathy. Also, may include puruitus and hearing loss or a feeling of fullness.

are small, hard, bony protrusions found in the lower posterior bony portion of the ear canal; they usuall occur bilaterally. The skin covering the exostosis is normal. It is believed that exostoses are caused by an exposure to cold water, as in scuba diving or surfing. The usual treatment, if any, is surgical excision.

Malignant turmors also may occur in the external ear. Most common are basal cell carcinomas on the pinna and squamous cell carcinomas in the ear canal. If untreated, the squamous cell carcinomas can spread through the temproal bone, causing facial nerve paralysis and hearing loss.

*Caused by infection or trauma. Sources of trauma include skull fracture, explosive injury, or a servere blow to the ear. Less common perforation is cause by foreign objects. During infection, the tympanic membrane can rupture if the pressure in the middle ear exceeds the atmospheric pressure in the external auditory canal.

The patien is observed for evidence of cerebrospinal fluid otorrhea or rhinorrhea- a clear, watery drainage fron the ear or nose.

*Perforation that do not heal on their owen may require surgery= Tympanoplasy= this is usually based on the need to prevent potentioal infection from water entering the ear or to improve patients hearing.

most commonly seen in children

AOM is an acute infection of the middle ear, usually lasting less than 6 weeks.

Pathogens= s.pneumoniae, H. influenzae, and M. catarrhalis, which enter the middle ear after eustachian tube dysfuntion caused by obstruction related to upper respiratory infections. inflammation suroouding structures, or allergic reactions (ex. allergic rhinitis).

(middle ear effusion) involves fluid, w/o evidence of active infection, in the middle ear. In theory, this fluid results from a negative pressure in the middle ear caused by eustachian tube obstruction. Frequently seen in patients afe radiation therapy or barotrauma an in patients with eustachian tube dyfunction from a concurrent URI or allergy. Barotrauma resuts from sudden pressure changes in the middle ear caused by changes in barometric pressure as in scuba diving or airplane descent.

Patients complain of hearing loss, fullness in the ear or a sensation of congestion

, or popping and cracking noises that occur as the eustachian tube attempts to open.

is the result of recurrent AOM causing irreversible tissue pathology and persistant perforation of the typmanic membrane. Chronic infection of the middle ear damage the typanic membrane, destroy the ossicles, and involve the mastoid.

symptoms may be minimal, with varying degrees of hearing loss and a persistant or intermittent , foul-smelling otorrhea. Pain is not usually experienced, except in cases of acute mastoiditis, when the postauricular area is tender and may be erythematous and edematous.

Cholesteatoma

common benign tumors of the inner ear.

is an ingrowth of the skin of the external layer of the eardrum into the middle ear. It is generally caused by a chronic retraction pocket of the tympanic membrane, creating a persistently high negative pressure of the middle ear.. The skin forms a sac that fills with degenerated skin and sebaceous materials. The sac can attach to the structures of the middle ear, mastoid, or both.

* Cholesteatomas may be asymptomatic or they may cause hearing loss, facial pain and paralysis, tinnitus, or vertigo.

involves the stapes and it thought to result from the formation of new, abnormal songy bone, especially around the oval window, with resulting fixation of the stapes.

The efficient transmission of sound is prevented because the stapes cannot vibrate and carry the sound as conducted from the malleus and incus to the inner ear.

* may involve one or both ears and manifests a a progressive conductive or mixed hearing loss. patient may or may not complain of tinnitus. Otoscopic examination reveals a normal typanic membrane.

* Dizziness is used freuently by patients and HCP to describe an altered sensation of orientation in space.

* Vertigo is defines as the misperception or illusion of motion of the person or the surroundings.Most people with vertigo describe a spinning sensation or say they feel as though objects are moving around them.

*Ataxia is a failure of muscular corrdination and may be present in patients with vestibular disease.

*Syncope, fainting, and loss of conciousness are not forms of vertigo and usually indicate disease in the cardiovascular system.

*Nystagmus is an involuntary rhythmic movement of the eyes. Pathologically it is an ocular disorder associated with vestibular dysfunction. Nystagmus can be horizontal, vertical, or rotary and can be caused by a disorder in the central or peripheral nervous system.

is a disturbance of equilibrium cased by constant motion.

The syndrome manifests itself in sweating, pallor, nausea, and vomiting caused by vestibular overstimulation.

is an abnormal inner ear fluid balance caused by malabsorption in the enolymphatic sac or a blockage in the endolyphatic duct. Endolymphatic hydrops, a dilation in the endolyphatic space, develops, and either increased pressure in the system or rupture of the inner ear membrane occurs, producing symptoms of Meniere's disease.

Symptoms include fluctuating, progressive sensorineural hearing loss; tinnitus or a roaring sound; a feeling of pressure or fullness in the ear; and episodic incapacitationg vertigo, often accompanied by nausea and vomiting.

disturbance in cranial nerve VIII

treated with diet and medication (low-sodium 1000-1500 mg/day or less)

Benign Paroxysmal Positional Vertigo

is a brief perios of incapacitation vertigo that occurs when the position of the patients head is changed with respect to gravity, typically by placing the head back with the affected ear turned down. It is thought to be due to the disruption of debris within the semicircular canal. This debris is formed from small crystals of calcium caronate for the inner ear structure, the utricle. this is frequently stimulated by head trauma, infection. Best rest is rocommended or repostioning.

Repositioning (the canalith procedure is commonly used. This noninvasive procedure, which involves quick movements of the body, rearranges the debris in the canal.

is a symptom of an underlying disorder of the ear that is associated with hearing loss. a roaring, buzzin, or hissing sound in one or both ears.

Factors that contribute to tinnitus: ototoxic substances, thyroid disease, hyperlipidemia, vitamin b12 deficiency, phycological disorders (depression, anxiety), fibromyalgia, otologic disorders (menieres disease, acoustic neuroma, and neurologic disorders (head injury, multiple sclerosis.)

an inflammation of the inner ear, can be bacterial or viral in origin. affects hearing and balance.

most common viruses: mumps, rubella, rubeola, and influenza. Also, viral illnesses of the URT and herpetiform disorders. Labyrinthitis is characterized by a sudden onset of incapacitation vertigo, usually with N/V, various degrees of hearing loss, and pissibly tinnitis.

The infundibulum of the hypothatamus connects it to the posterior pituitary gland. The hypothalamus plays an improtant tole in the endocrine system because it regulates the pituitary secretion of hormones that influence metabolism, reproduction, stress response, and urine production. It works with the pituitary to maintain fluid balance through hormonal release and maintains temperature regulation by promoting vasoconstriction or vasodilation. site of hunger, and involved in appetitie control. It contains centers that regulate the sleep-wake cycle, blood pressure, aggressive and sexual behavior , and emotional response (blushing, rage, depression, panic, and fear)

Note: The hypothalamus also controls and regulates the autonomic nervous system. The optic chiasm (the boint at which the tow optic tracts cross) and the mamillary bodies (involved in olfactory reflexes and emotion response to odors) are also found in this ares.

consists of the midbrain, pons, and medulla oblongata.

The midbrain connects the pons and the cerbellum with the cerebral hemispheres; it contains sensory and motor pathways and serves as the center for auditory and visual reflexes. Cranial nerves III and IV originate in the midbrain. The pons is a bridge between the two halves of the cerbellus, and between the medulla and midbrain. The pons also contains motor and sensory pathways. Portions of the pons help regulate respiration.

Motor fibers from the brain to the spinal cord and seonsory fibors from the spinal cord to the brain are located in the medulla. Most of these fibers cross, or decussate, at this level. Reflex centers for respiration, BP, heart rate, coughing, vomiting, swallowing, and sneezing are located in the medulla as well.

I (olfactory)-sensory- sense of smell

II (Optic)- sensory- visual acuity and visual fields.

III (Oculomotor)- motor- muscles that move the eye and lid, pupillary constriction, lens accommodation.

IV (Trochlear)-motor- muscles that move the eye

V (Trigeminal)- mixed- facial sensation, corneal reflex, mastication.

VI (Abducens)-motor- muscles that move the eye.

VII (Facial)-mixed- facial expression and muscle movement, slaivation, tearing, taste, sensation in the ear.

VIII (Acoustic)-sensory- hearing and equlibrium

IX (Glossopharyngeal)- mixed- taste, sensation in pharynx and tongue, paryngeal muscles, swallowing.

X (vagus)-mixed- muscles of pharynx, larynx, and soft palate; sensation in external ear, pharynx, larynx, thoracic and abdominal viscera; parasypathetic innervation of thoracic and abdominal organs.

XI (spinal accessory)-motor- sternocleidomastoid and trapezius muscles.

XII (hypoglossal)-motor- movement of the tongue

Spinal Nerves

Dorsal / Vental

Dorsal roots are sensory and transmit sensory impulses from specific areas of the body known as dermatomes to the dorsal horn ganglia. The sensory fiber may be somatic, carrying information about pain, temperature, touch, and position sense from the tendons, joints, and body surfaces; or visceral, carrying info from the internal organs.

Ventral roots are motor and transmit impulses from the spinal cord to the body; and these fibers are also eithe somatic or visceral. The visceral fibers nclude autonomic fibers that control the cardia muscles and glaular secretions.

regulates the activities of internal organs such as the heart, lungs, blood vessels, digestive organs, and glonds.

Maintenance and restoration of homeostais is largely the responsibility of the ANS.

Two divisions (sympathetic and parasypathetic)

Sympathetic- predominantly excitatory

Parasympathetic- which controls mostly visceral functions.

Sympathetic Syndromes

Diseases of the sypathetic nerve trunks

Can occur in the motor cortex, internal capsule, the spinal cord gray matter, and other structures of the brain through with the corticospinal tract descends.

If the upper motor neurons are damaged or destroyes, as frequently occurs with stroke or spinal cord injury, paralysis (loss of voluntary movement) results. However, because the inhibitory influences of intact upper mortor neurons are imapired, reflex (involuntary) movements are uninhibites, and hence hyperactive deep tendon reflexes, diminished or absend superficial reflexes, and pathological reflexes sucha s babinski response occur.

damage of a motor neuron between the spinal cord and muscle. The result of lower motor neuron damage is muscle paralysis. Reflexes are lost, and the muscle become faccid (limp) and atrophied from disuse. If the patient had injured the spinal trunk and it can heal, use of the muscles connected to that section of the spinal cord may be regained. However, if the anterior horn motor cells are destryoed, the nerves cannot regernate and the muscles are never useful again.

Flaccid paralysis and atrophy of the affected muscles are the principal signs of lower motor neuron disease.

Pain is multidimensonal and entirely subjective.

In deurologic disease, acute pain may be associated with brain hemorrhage, spinal disk disease, or tigeminal neuralgia

Chronic pain can occur with many degenerative and chronic neurologic conditions (ex. multiple sclerosis)

seizures are the result of abnormal paroxysmal discharges in the cerbral cortex, which then manifest as an alteration in sensation, behvior, movement, perception, or consciousness.

The alteration may be short, as in a blank stare that lasts only a second, or of longer duration, such as tonic-clonic grand mal seizure that can last several minutes.

a pathologic reflex seen in neurologic disease. normally indicative of CNS disease affecting the corticospinal tract.

Babinski's reflex occurs when the big toe moves toward the top of the foot and the other toes fan out after the sole of the foot has been firmly stroked.

is apparent in the patien who is not oriented, does not floow commands, or needs persistent stimuli to achieve a state of alertness.

Coma- clinical state of unarousable unresposiveness in which there is no puposeful responses to internal or external stimuli.

Akinetic mutism is a state of unresponsiveness to the environment in which the patien make no voluntary movement.

Persistent vegetative state- is a condition in which the unresponsive patient resumes sleep-wake cycles after coma but is devoid of cognitive or affective mental function.

Locked-in sydrome results from a lesion affecting the pons and results in paralysis and the inability to speak, but veritcal eye movements and lid elevation remain intact and are used to indicate responsiveness.

evaluates eye opening ,verbal resonse, and motor response.

3-15 scale

a score of 3 indicates severe impairment of neurologic function, brain death, or pharmacologic inhibition of the neurologic response.

A score of 15 indicates that the client is fully responsive.

The cranial vault contains brain tissue (1400 g), blood (75 mL), and CSF (75mL). The volume and pressure of these three compnents are usually in a state of equilibrium and produce the ICP. ICP is usuall measred in the lateral ventricles, with th normal pressure being 0-10 mmHg, and 15 mm Hg bein the upper limit of normal.

the Monro-Kellie hypothesis states that, because of limited space for expansion within the skull, and increase in any one of the components causes a change in the volume of the others. Because brain tissue has limited space to expand, compensation typicall s accomplished by dislacing or shifting CSF, increasing absorption or diminishing the production of CSF, or decreasing cerebral blood volume. W/O such changes ICP begins to rise. Under normal cercumstances, minor changes in blood voume of CSF volume occur constantly as a result of alteration in intrathoracic pressure (coughing, sneezing, straining), posture, BP, and systemic oxygen and CO2 levels.

Increased ICP affects many patiens with acute neurologic conditions because pathologic conditions alter the relationship between intrcranial volume and ICP. Although elevated ICP is normally due to head injury, it also may be seen as a secondary effect of such things as brain tumors, subarachnoid hemorrhage, toxic and viral encephalopathies. Increased ICP from any cause decreases cerebral perfusion, stimulates further swelling (cerebral edema), and may shift brain tissue, resulting in herniation, a dire and frequently fatal event.

Increased ICP may reduce cerebral blood flow, resulting in ischemia and cell death. The early stages of cerebral ischemia, the vasomotor centers are stimulated and the systemic pressure rises to maintain cerebral blood flow. Usually accompanied by a slow, bounding pulse and respiratory irregularities.

As ICP rises, compensatory mechanisms in the brain work to maintain blood flow and prevent tissue damage. The brain can maintain a stready perfusion pressure if the arterial systolic pressure is 50-150 mm Hg and the ICP is less than 40 mm Hg. Changes in the ICP are closely linked with cerebral perfusion pressure or CPP. The CPP is calculated by subtracting the ICP from the mean arterial pressure (MAP). Example. MAP is 100 mm Hg and the ICP is 15 mm Hg.  Therefore the CPP is 85 mm HG.

The normal CPP is 70-100 mm Hg. As ICP rises the autoregulatory mechanism of the brain is overwhelmed, the CPP can increase to greater than 100 mm Hg or decrease to less than 50 mm Hg.

NOTE: Patients with a CPP of less than 50 mm Hg experience irreversible neurologic damage, so it is improtatnt to maintaine the CPP at 70-80 mm Hg to ensure adequate blood flow to the brain.

If ICP is equal to MAP, cerbral circulation ceases!!!!!

At a certain point , the brains ability to autoregulate becomes ineffective and decompensation (inchemia and infarction begins. When this occures the patien exhibits significant changes in mental status and vital signs.

Bradycardia, hypertension and brdypnea is associated with this deterioration.

At this point, herniation of the brain stem and occlusion of cerebral blood flow occur if therapeutic intervention in not initiated. Herniated tissue exerts pressure on the brain area as it shifts from and area of high pressure to an area of low pressure. This shift interfers with blood flow resulting in ichemia, infarction, and brain death.

SIADH

Seizures are episodes of abnormal motor, sensory, autonomic, or psychic activity ( sometime a combination of these) that results from sudden excessive discharge from cerebral neurons.

Two types

partial- begin in one part of the brain

generalized- involve electric discharges in the whole brain.

seizures can be categorized as idiopathic (genetic or developmental defects) or acquired that include: CVD, hypoxia, fever, head injury, hypertension CNS infections, metabolic and toxic conditions, brain tumor, or alergies.

Prondrome- is experienced by 60% of patients, with syptoms that occur hours to days before a migraine, symptoms include depression, irritability, feeling cold, food cravings, anorexia, change i level of activity, increased urination, diarrhea, or constipation. Patients usually experience the same prodrome with each migraine headache.

Aura- usually lasts less than an hour, and my provide enough time for the patient to take meds to prevent migraine. This period is characterized by focal neuologic symptoms. visual disturbances (light flashes/bright spots), numbness/tingling in lips, face, or hands, mild confusion, slight weakness of an exremity, drowsiness and dizziness. this period corresponds to the phenomenon of cortical spreading depression that is associated with reduced metabolic demand in abnormally functioning neurons.

Headache phase- As vasodilation and a decline in serotonin levels occur, a throbbing headache (unilaterial in 60% of patients) intensifies over several hours. This headache is severe and incapacitating and is often associated with photophobia nausea, and vomiting.

Recovery- (termination and postdrome) pain gradually subsides. Muscle contraction in the neck and scalp is common, with associated muscle ache and localized tenderness, exhaustion, and mood changes. patients may sleep for extended periods of time.

CVA, or "brain attack" is a sudden loss of function resulting from disruption of the blood suppy to a part of the brain.

Divided into five different types: large artery thrombotic strokes, small penetrating artery throbotic strokes, cardiogenic embokic strokes, and cryptogenic strokes.

there is a disruption of the cerebral blood flow due to obstruction of a blood vessel. This disruption in blood flow initiates a complex series of cellular metabolic evens refereed to as the ichemic cascade.

* The ischemic cascade begins when cerebral blood flow decreases to less than 25 ml per 100g of blood per minute. At this point , neurons are no longer albe to maintain aerobic respiration. the mitochondria must then switch to anaerobic respiration, which generates large amounts of lactic acid, causina change in the pH. This switch to the less efficient anaerobic reapiration also renders the neuron incapable of producing sufficient quantities of ATP to fuel the depolarization process.

ischemia - energy failure= acidosis and ion imbalance.

signs and syptoms- numbness or weakness of the face, arm, or leg, especially on one side of the body, confusion or change in mental status, trouble speaking or understanding speech, visual disturbances, difficulty walking, dizziness, or loss of balance and coordination, sudden sever headache.

a stroke is an upper motor neuron lesion and results in loss of voluntary control over motor movements. Because the upper motor neurons decussate (cross) a distrubance of voluntary motor control on one side of the body may reflect damage to the upper motor neurons on the opposite side of the brain.

hemiplegia- paralysis of one side of the body

Hemiparesis- weakness of one side ot the body.

Early stage of stroke, the initial clinical features may be flaccid paralysis and loss of or decrease in the deep tendon reflexes. When these deep tendon reflexes reappear (usually by 48 hours) increased tone is observed along with spasticity of the extrmities of the affected side.

Other brain functions affected by stoke are language and communication. In fact, stroke is the most common cause of aphasia.

Dysarthria- difficulty in speaking

dysphasia- impaired speech

aphasia- loss of speech (which can be expressive aphasia, receptive aphasia, or global (mixed) aphasia.

apraxia- inability to perform a perviously learned action.

hemianopsia- loss of half of the visual field

agnosias- are deficits in the ability to recognize previously familiar objects perceived by one or more of the senses.

used to treat ischemic stroke by dissolving the blood clot that is blocking blood flow to the brain. recombinant t-PA

It works by binding to fibrin and converting plasminogen to plamin, which stimulated fibrinolysis of the atherosclerotic lesion.

bleeding the most common side effect to t-PA admin. and the patient is closly monitored.

primarily caused by intrcranial or subarachnoid hemorrhage. Hemorrhagic strokes are caused by bleeding into the brain tissue, the ventricles, or the subarachnois space.

Patho- symptoms are produced when a primary hemmorrhage, aneurysm. or arteriovenous malformations (AVM) ruptures, causing subarachnoid hemmorahge. Normal brain metabolism is disrupted by the brains exposure to blood, by an increase in ICP resulting from the sudden entry of blood in the SA space, it compresses and injures brain tissue, or by secondary ischemia of the brain resulting from the reduced perfusion pressure and vasospasm that frequently accompany subarachnoid hemorrhage.

is a broad classification that includes injury to the scalp, skull, or brain.

Brain suffers trumatic injury-brain swelling or bleeding increases intracranial volume- rigid cranium allows no room for expansion of contens so ICP increases- pressure on blood vessels within the brain causes blood flow to the brain to slow- cerebral bypoxia and ischemia occur- ICP continues to rise. Brain my herniate- cerebral blood flow ceases.

Primary injury is the initial damage to the brain that results from the traumatic effent. This may include contusions, lacerations, and torn blood vessels due to impact, acceleration/deceleration, or foreign object penetration.

Secondary injury- evolves over the ensuing hours and days after the initial injury and results form inadequate delivery of nutrients and O2 to the cells.

meningitis is an inflammation of the lining around the brain and spinal cord caused by bacteria or viursed. Septic meningitis is caused by bacteria, In aseptic meningitis, the cause is viral or secondary to lymphoma, leukemia, in HIV.

Patho- meningeal infections generally originate in of of two ways: through the bloodstream as a consequence of other infection or by direct spread, such as might occur after a traumatic injury to the facial bones or seondary to invasive procedures. N. meningitidis concentrates in the nasophaynx and is transmitted by secretion or aerosol contamination. Once the causative organism enters the bloodstreat, it corsses the BB barrier and proliferates in the CSF. The host immune response stimulates the release of cell wall fragments and lippolysaccharides, facilitating inflamation of the subarachnoid and pia mater. Because the cranial vault contains little room for expansion, the inflammation may cause ICP. CSF circulates through the subarachnoid space, where inflammator cellular materials from the affected meningeal tissue enter and accumulate. The prognosis for bacterial meningitis depends on the causative organism, the severity of the infection, and illness, and the timeliness of treatment. The syndrome is the result of enothelial damage and vascular necrosis caused by the bacterial. Complication include visual imapirment, deafness, seizures, paralysis, hydocephalus, and septic shock.

Headache and fever initial symptoms. Headache is due to irritation of the meningies.

Encephalitis is an acute infammatory process of the brain tissue. HSV is the most coman cuse of acute encephalitis in the US. Two types= HSV-1, typicall offects children and adults and HSV-2 affects neonates.

Patho- involves local necrotizing hemorrhage that becomes generalized bollowed by edema. There is also progressive deterioration of nerve cell bodies.

symptoms- fever headache, and confusion. Focal neurologic symptoms reflect the areas of cerebral inflammation and necrosis and include fever, headache, behavioral changes, focal seizures, dysphasia, hemiparesis and altered LOC.

Anthropod vectors transmit several types of virused that cause encephalitis. the primary vector in North america is the mosquito. In cases of west nile virus, humans are the secondary host, birds are the primary. Most common types are the west nile and st. louis.

patho- viral replication occurs at the site of the mosquito bite. Thos hosts immune response attempts to control viral replication. If the immune response in inadequate, viremia will ensue. The virus gains access to the CNS via the cerebral capillaries, resulting in encephalitis. It spreads for neuron to neuron, predominantly affecting the corical gray matter, brain stem, and the thalamus

Clinical Manifestations- An arboviral encephalitis begins with early flulike symptoms, but specific neurological manifestations depend on the viral type. St. Louis encephalitis is SIADH with hypontremia. West Nile encephalitis incluse maculopapular or morbilliform rash on the neck, trunk, and arms; enlarged lymph nodes and legs and flaccid paralysis. Both west nile and st. louis encephalitis can result in parkinsonianlike movements, refecting inflammation of the basal ganglia. Seizures, a poor prognostic indicator in both typed is more common in st. louis.

a brain tumor is a localized intrcranial lesion that occupies space within the skull. a tumor usually grows as a sphericalmass, but it also can grow diffusely and infiltrate tissue. The effects of neoplams are caused by the compression and infiltration of tissue

ICP and cerbral edema, seizure activity and focal neurolgic signs, hyrdrocephalus, and altered pituitary function.

Gliomas are the most common type and actrocytomas are the most common type of glioma and are graded from I to IV. the grade is based on cellular density, cell mitosis, and appearance, and indicating the malignancy. Usually the tumors spread by infiltrating into the surrounding neural connective tissue and therefore cannot be totall removed w/o causing considerable damage to vital structures.

represent about 10-15% of all brain tumors and cause symptoms as a result of pressure on adjacent structures or hormonal changes such as hyperfunction or hypofunction of the pituitary.

Pressure effects od pituitary adenomas: pressure from a pituitary adenoma may beomonal effects of pituitary adenomas p exerted on the optic nerves, optic chiasm, or optic tracts or on the hypothalamus or the third ventricle if the tumor invades the cavernous sinuses or expands into the shenoid bone. These pressure effects produce headache, visual dysfunction, hypothalamic disorders ( disorders of sleep , appetitie, temperature, and emotion), increased ICP, and enlargement and erosion of the sella turcica.

pg. 1977 hormonal effects