spinal cord tumor

I. DEFINITIONS
Spinal cord tumor is a tumor that develops in the spine or its contents and usually cause symptoms because of the involvement of the spinal cord or nerve roots. (Price sylvia anderson, 1995)

II.KLASIFIKASIONS
a.Tumor Intradural
In contrast to intradural tumors ekstradural tumors generally benign.
Tumor Ekstramedular
Durameter and located between the spinal cord, most of the tumors in this region are benign neurofibroma or meningioma
Tumor Intramedular
Derived from the spinal cord itself.

b.Tumor Ekstradural
Tumor ekstradural primarily metastase from primary lesions in the breast, prostate, thyroid, lung, kidney, and stomach
Tumor ekstradural generally come from the vertebral column or from the room ekstradural. Neoplasm ekstradural indoor ekstradural carcinoma and lymphoma usually metastase.

III.MANIFESTASI OF CLINIC
Tumor ekstradural
Pain is described as a constant and limited to the tumor area followed by a pain that extends dermatome pattern
Greatest pain at night and become more powerful by the movement of the spine and the rest lie
Radikuler pain exacerbated by coughing and straining
The pain may last for several weeks or months prior to the involvement of the spinal cord.
Spinal cord function will vanish altogether
Spastic weakness and loss of vibration sensation
Parestesi and sensory deficits will grow rapidly into the irreversible paraplegia
Irritable bowel and urination

Intradural tumor
Clinical journey more slowly and lasted for months.
Reduced perception of pain and temperature below the level of the contralateral lesion
Patient complains of pain, at first on the back and then along the spinal roots
The pain intensified by movement, coughing, sneezing, or straining, and most severe at night (pain at night is caused by traction on the roots of the illness, which is when the spine is elongated after the disappearance of the effect of gravitational contraction.
Paraesthesia and continuing proprioceptive sensory deficit

IV.ETIOLOGI
Risk factors tumors can occur in any race group, the incidence increases with age, risk factors will increase in people exposed to certain chemicals (Okrionitil, inks, solvents, lubricating oils), but it is not. The influence of genetic tibulnya participate in tumors, tuberculosis and multiple sclerosis disease neurofibomatosis disease.

V.patofisiologi
Pathophysiological conditions due to spinal cord tumors are caused by damage and infiltration, shift and decompress the spinal cord and interruption of blood supply or cerebrospinal fluid. Degree of symptoms depending on the level of decompression, and speed the development, adaptation can occur with slow-growing tumors, 85% benign spinal cord tumors.
Especially good tumor arising neoplasms ekstramedula or intra-medullary. Secondary tumors or tumors can also interfere metastase the spinal cord and the lining and the vertebra
Ekstramedular tumor from tumor edge intramedural initially loaded the root causes of subjective pain. With the growth of tumors can arise motor and sensory deficits associated with the level of the spinal cord akardan attacked. Because there was a tumor growing emphasis on the spinal cord. In line with that of patients lose all motor function below the lesion and sensory / tumor

Spinal cord tumors, which starts from the spinal cord, often causing symptoms such as the central spinal cord, including segmental loss of pain and temperature functions. Moreover, the function of cells, anterior horn is often missing, especially on the hands. The whole point is near the central gray objects into dysfunction. Rasanyeri and sensory loss of temperature and motor weakness progress little by little, gain weight and decrease. Cauda motor and sensory functions of the latter will be lost, including the loss function fecal and urine elimination. (Long C, Barbara, 1996)
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Migraine

Autonomik dysfunction of blood vessel growth resulted head skin headache known as migraine. Actual mechanism of migraine is not all clear. But many factors - factors that prodram early menungkapkan of migraine must be related to the Vaso constriction of intra-cranial artery.
Symptoms are typical at this early stage is the emergence of skotoma and pale face.

Prodrom was followed by the emergence of sesisi headache and facial flushing. Soon after arising vomiting - vomiting, edema of nasal mucous membranes, fingers - fingers and toes.
Symptoms are regarded as a manifestation of stage vasodolatasi extra cranial arteries.
What causes dysfunction of blood vessels is still unknown, but probably once a congenital disorder, due to familial and hereditary factors certainly have the migraine. (Prof. Dr. Mahar Mardjono, Clinical Neurology)

Among the many types of headache, migraine is a type of the most researched and discussed, in addition to the causes which are still mysteries, then the incident is enough to encourage the experts to examine it.

Aretaeusi (80 AD) is one of the researchers in his day headache and it was he who first described the symptoms of headache have distinctive profile. He introduced this type with the name "HETEROCRANIA" which means headache.
By Galen 50 years later changed to "HEMICRANIA" and then the experts from the French to change again into their language as "MEGRIM" for details said - he said the "migraine" (Dr. Sidiarto. K)


A. anxiety / worry
Definition
Anxiety or anxiety is a vague feeling of fear - a vague source, are often not specific or not known by that individual.
Anxiety is the feeling / emotional response to the assessment, feeling uncertain and powerless (Stuart and Sundeen, 1988). Experienced emotional state objectively and communicated in interpersonal relationships. Anxiety is an emotional response to the assessment of daily life - today. Describes the state of anxiety worry, anxiety, fear, not peaceful with various physical kekuhan.

Predisposing factors

1. Analytic psycho theory
According to Freud, personality structure consists of 3 elements is "ID, EGO, & SUPER EGO". Symbolizes the ego instincts and impulses urge primiti, Super Ego represents the conscience of a person and controlled by the norm - a cultural norm. While diagambarkan ego as a mediator between the demands of the ID & Super Ego.

2. INTERPERSONAL theory
Anxiety occurs from the fear of interpersonal rejection. It is also associated with trauma to the growth, such as loss, separation of individuals who have low self-esteem is usually very easy to experience severe anxiety.

3.BEHAVIOR theory
Frusatasi anxiety is the result of everything that interfere with a person's ability to achieve the desired objectives.
This theory believes that humans are exposed early in life in an excessive fear will indicate the possibility of severe anxiety in the lives of his adult life.

Anxiety Light
Connect with mild anxiety tension events of everyday life. At this level of perception of land to widen and individuals will be aware - and wary hearts.

Physiological Response
Occasional shortness of breath
Tone and blood pressure rise
Mild symptoms of the stomach
Wrinkled face and trembling lips

Cognitive Response
Able to accept the complex stimuli
Concentrate on problem
Solve problems effectively

Response Behavior and Emotions
Unable to sit still
Fine tremor of the hands
Sometimes sound - sometimes rising

Anxiety was
At this level of land decreased perception of the environment, the individual is more important to focus on the moment and the exclusion of other things.


Physiological response
Often short of breath
Pulse and blood pressure rise
Dry mouth
Anorexia
Diarrhea / constipation
Restless
Cognitive response
Perceptual field narrows
External stimuli can not be accepted
Focus on what is a concern
Behavioral and emotional responses
Movement jerk - jerk / squeezed
Talk more and more quickly
Difficulty sleeping
Insecurity

Serious anxiety
In severe anxiety land becomes very narrow perception and then incapable of thinking.
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BRAIN TUMOR

Definition:
Brain tumor is intra-cranial lesions that occupy space in the skull

Classification of Brain Tumors:
1.Tumor from lapisam brain (meningioma dural)
2.Tumor growing in / on the cranial nerves
3.Tumor originating in the brain tissue
4.Lesi metastatic from any body part

Pathophysiology:
Brain tumor causing neurological disorders. The symptoms occur sequentially. This emphasizes the importance of anamnesis in the examination of the client. Symptoms should be discussed within a perspective of time.
Neurologic symptoms of brain tumors are usually considered to be caused by 2 factors focal disruption, caused by the tumor and intracranial pressure. Focal disruption occurs when the emphasis on the brain tissue and infiltration / invasion directly on the brain parenchymal tissue damage neurons. Of course the greatest dysfunction occurs in tumors that grow most rapidly.
Changes in blood supply due to pressure generated tumors that grow brain tissue necrosis. Arterial blood supply disruptions generally manifests as an acute loss of function and may be confused with primary cerebrovaskuler disorders. Seizures as a manifestation of neuro sensitivity changes associated with invasion and compression of the blood supply to changes in brain tissue. Some tumors also form cysts around the brain parenchymal pressure so that aggravate focal neurological disorders.

Increased intra-cranial pressure can be caused by several factors: the increase of mass in the skull, the formation of edema around the tumor and cerebrospinal circulation changes. Growth of the tumor mass will increase, because the tumor will take space from the relatively rigid skull. Malignant tumor jaruingan cause edema in the brain. Seluruhnyanya not yet understood mechanism, but due to the difference in osmotic allegedly causing bleeding. Venous obstruction and edema caused by damage to blood brain barrier, it caused an increase in intracranial volume. Observation of cerebrospinal fluid circulation from the ventricles laseral into hidrocepalus sub arakhnoid cause.

Increased intracranial pressure would endanger life, when there is rapid due to one of the causes that have been discussed previously. Compensation mechanisms need time to become effective berhari-hari/berbulan-bulan and oelh because ity was not useful when rapid intracranial pressure arise. These compensatory mechanisms include working lower intra-cranial blood volume, cerebrospinal fluid volume, intracellular fluid content and reduce parenchymal cells. The increase in pressure resulted in untreated ulcer or serebulum herniation. Herniation occurs when the medial lobe girus shifted to the inferior temporals through tentorial notch by the masses in the brain hemispheres. Herniation pressing ensefalon menyebabkab to loss of consciousness and menenkan third nerve. In serebulum herniation, tonsils before the shift down through the foramen magnum by a posterior mass. Compression of the medulla oblongata and stopped breathing happen quickly. Intracranial bradicardi fast is a progressive, systemic hypertension (widening pulse pressure and respiratory problems).

Signs and Symptoms
According to tumor location:
1.Lobus frontalis
Mental disorder / mild personality disorders: depression, confusion, strange behavior, it is difficult to give argumenatasi / assess true or not, hemiparesis, ataxia, and disturbances to speak.
Posterior 2.Kortek presentalis
Weakness / paralysis of facial muscles, tongue and fingers
3.Lobus parasentralis
Weakness in the lower limb
4.Lobus Oksipitalis
Seizures, vision disturbances
5.Lobus temporalis
Tinnitus, auditory hallucinations, sensory Aphasia, facial muscle paralysis
6.Lobus parietal
Missing sensory function, kortikalis, localization sensory disturbances, visual impairment
7.Cerebulum
Papil edema, headache, motor disturbances, hipotonia, hiperekstremitas esndi

Common signs and symptoms:
1.Nyeri heavy head in the morning, play increased when coughing, bending
2.Kejang
3.Tanda-mark intra-cranial pressure: blurred vision, nausea, vomiting, decreased auditory function, changes in vital signs, Aphasia.
4.Changes of personality
Memory
5.Perasaa natural


Classical triad;
Headache
Papil edema
Vomiting

Diagnostic Examination;
1.Rontgent anterior-posterior skull
2.EEG
3.CT Scan
4.MRI
5.Angioserebral
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Meningitis Desease

A. Definitions
Meningitis is an inflammation of the meningen (membrane that surrounds the brain and spinal cord) and is caused by viruses, bacteria or fungi organs (Smeltzer, 2001).
Meningitis is an acute infection of the meninges, usually caused by one of the microorganisms pneumokok, Meningokok, Stafilokok, Streptokok, Hemophilus influenza and materials aseptic (viral) (Long, 1996).

Meningitis is an inflammation of the membrane meningen, cerebrospinal fluid and spinal column that causes the infection in the central nervous system (Suriadi & Rita, 2001).

B. Etiology
1.Bakteri; Mycobacterium tuberculosa, Diplococcus pneumoniae (pneumokok), Neisseria meningitis (meningokok), Streptococus haemolyticuss, Staphylococcus aureus, Haemophilus influenzae, Escherichia coli, Klebsiella pneumoniae, Peudomonas aeruginosa
Other
2.Penyebab Lues, Virus, Toxoplasma gondhii and Ricketsia
3.Predisposing factors: gender men, more often than women
4.maternal factor : fetal membrane rupture, maternal infections during the last week of pregnancy
5.immunology factors : immune mechanism deficiency, immunoglobulin deficiency.
6.Kelainan central nervous system, surgery or injury associated with the neural system


C. Classification
Meningitis is divided into 2 groups based on changes in brain fluid, namely:
1.Meningitis serous
Meningitis is araknoid and pia mater of the brain accompanied by a clear fluid. The cause is terseringnya Mycobacterium tuberculosa. Other causes Lues, Virus, Toxoplasma gondhii and Ricketsia.
2.Meningitis purulenta
Purulent inflammation is arakhnoid and the pia mater covering the brain and spinal cord. The reasons include: Diplococcus pneumoniae (pneumokok), Neisseria meningitis (meningokok), Streptococus haemolyticuss, Staphylococcus aureus, Haemophilus influenzae, Escherichia coli, Klebsiella pneumoniae, Peudomonas aeruginosa.

C. Pathophysiology
Begins as a bacterial meningitis infection from oroaring and followed by septicemia, which meningen spread to the brain and upper spinal cord.
Predisposing factors include infection of the upper airway, otitis media, mastoiditis, sickle cell anemia and other hemoglobinopatis, a new neurosurgical procedures, head trauma and immunological effects. Venous channels through the posterior nasopharynx, middle ear and mastoid channel close to the brain and the veins channel meningen; all of this link which underpins the development of bacteria.
Organisms into the bloodstream and cause inflammation in the meningen and under the cortex, which can cause a thrombus and decreased cerebral blood flow. Cerebral tissue due to impaired metabolism meningen exudate, vasculitis and hipoperfusi. Purulent exudate may spread to the base of the brain and spinal cord. Inflammation also spread to the membrane walls of cerebral ventricles. Bacterial meningitis associated with intracranial physiological changes, which consisted of increased permeability of the blood, brain defense areas (barrier oak), cerebral edema and improvement of ICT.
In acute infection patients died of bacterial toxins before the meningitis. Most infections of patients with adrenal damage, circulatory collapse and associated with widespread hemoragi (at sindromWaterhouse-Friderichssen) as a result of endothelial damage and necrosis of blood vessels caused by the meningococcus.

D. Clinical Manifestations
Symptoms of meningitis resulting from infection and increased ICT:
1.head pain and fever (often initial symptoms)
2.Changes at the level of consciousness can occur letargik, unresponsive, and coma.
3.Iritasi meningen caused some signs as follows:
a) nukal rigidity (stiff neck). Attempts to head flexion in difficulty due to spasm of the neck muscles.
b) kernik positive sign: when the patient lay with the state of flexion of the thigh towards the abdomen, legs can not be in perfect ekstensikan.
c) Signs brudzinki: if the patient's neck in flexion produced reflect the knees and hips. When done on passive flexion of the lower limb on one side of the same movement seen bike ektremita opposite side.
4. get photo phobias, or excessive sensitivity to light.
5.Kejang due to focal cortical areas are sensitive and improvement of ICT by purulent exudate and cerebral edema with signs of the characteristic changes of vital signs (pulse pressure and widening bradikardi), irregular breathing, headaches, vomiting and decreased level of consciousness.
6.conspicuous rash is characteristic of meningococcal meningitis.
7.fulminating infections with septikimia signs: high fever suddenly appeared, lesions that spread purpura, shock and signs of disseminated coagulopathy intravaskuler

E. Diagnostic Examination
CSS 1.Analisis of lumbar function:
a) Bacterial meningitis: increased pressure, the liquid cloudy / foggy, white blood cell count and protein increased glucose increased, a positive culture for several types of bacteria.
b) viral meningitis: the pressure varies, CSS is usually clear liquid, white blood cells, glucose and protein is usually normal, the culture is usually negative, viral culture is usually with a special procedure.
2.Glukosa serum: increased (meningitis)
3.LDH serum: increased (bacterial meningitis)
White blood 4.Sel: slightly increased with the increase in neutrophils (bacterial infection)
Blood 5.Elektrolit: Abnormal.
6.ESR/LED: increases in meningitis
Blood 7.Kultur / nose / throat / urine: may indicate the central region indicates the type of infection or infectious
8.MRI / CT scan: may be helpful in localize lesions, see the size / location of the ventricles; regional cerebral hematoma, hemorrhagic, or tumors
9.Ronsen chest / head / sinus; be no indication of the source of intra-cranial infection.

F. Complications
1.Hidrosefalus obstructive
2.MeningococcL septicemia (mengingocemia)
3.Sindrome water-friderichen (septic shock, DIC, bilateral adrenal hemorrhage)
4.SIADH (Syndrome Inappropriate Antidiuretic hormone)
5.Efusi subdural
6.Kejang
7.Edema and cerebral herniation
8.Cerebral palsy
Mental 9.Gangguan
10.Gangguan learning
11.Attention deficit disorder
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