Makassar, July 4, 2015

1st MODULE REPORT

HEMIPARESIS

TUTOR :dr. Marlianty, Sp. M.

GROUP 15:Andi Fikrah Muliani110 213 086Lesthary Kadir110 213 114Khaerunnisa A.Y.110 213 094Siti Shahrina T.A.110 213 099A. Nur Qalby T.S.M110 213 117Andi Azizah Noor110 213 120Erza Alifianda110 213 129Andy Billa Vini F.A.110 213 123Ikram Hanafi110 213 131Andi Nurul Fasty Batari110 213 136

NEUROPSYCHIATRY SYSTEMMEDICAL FACULTYMOSLEM UNIVERSITY OF INDONESIAMAKASSAR2015

OPENING

Assalamualaikum warahmatullahi wabarakatuhMercy and blessing to Allah SWT for all His Rahmat to us till we can do all our activities and reach our dream until this time. Shalawat and salam to Our Prophet Muhammad SAW, who has a great influence to this world to be so much brightness as now and we can get out from last Jahiliyahs century. So, we thanks gratefuly to our teacher, a tutor that had guided us to finish this report till the end.And thus how our report had to be done as we composed as well with all their shortages. Than, we hope some critics and suggestions to be our next learnings and educations for the future. May Allah bless us, thank you.Wassalamualaikum warahmatullahi wabarakatuh

Makassar, July 4, 2015

Group 15

A. SCENARIOA woman 56 years old experienced suddenly the weakness of left body and right facial droop since 2 days ago, headache and vomiting. One moment after experiencing weakness of left body, the patient is difficult to communicate and looked sleepy.

B. DIFFICULT WORDS1. Facial droop: stiffness/ parese of half face.2. Weakness: reduction of normal power of muscle.3. Looked sleepy: Samnolent, low consciousness.

C. KEY WORD1. Woman, 56 years old2. Sudden weakness of left body3. Right facial droop4. Headache5. Vomiting6. Difficult to communicate7. Looked sleepy

D. QUESTIONS1. What is the anatomy and physiology of the related system by case?2. Why did the patient get a sudden weakness in left than the facial droop in right?3. How did the patient get a headache and vomiting related by this case?4. Why did the patient looked sleepy and difficult to communicate?5. What are the diagnostic procedures?6. What are the differencial diagnoses and the complications of each differential diagnoses?7. What are the treatments given to the patient?8. How to prevent this disease?9. What are the risc factors related by this case?10. What is the Islamic perspective related to this case?

E. ANSWERS1. What is the anatomy and physiology of the related system by case?Anatomy of the Central Nervous System

The brain can be subdivided into several distinct regions: The cerebral hemispheres form the largest part of the brain, occupying the anterior and middle cranial fossae in the skull and extending backwards over the tentorium cerebelli. They are made up of the cerebral cortex, the basal ganglia, tracts of synaptic connections, and the ventricles containing CSF. The Diencephalon (not shown above) includes the thalamus, hyopthalamus, epithalamus and subthalamus, and forms the central core of the brain. It is surrounded by the cerebral hemispheres. The Midbrain (not shown) is located at the junction of the middle and posterior cranial fossae. The Pons sits in the anterior part of the posterior cranial fossa- the fibres within the structure connect one cerebral hemisphere with its opposite cerebellar hemisphere. The Medulla Oblongata is continuous with the spinal cord, and is responsible for automatic control of the respiratory and cardiovascular systems.The Cerebellum overlies the pons and medulla, extending beneath the tentorium cerebelli and occupying most of the posterior cranial fossa. It is mainly concerned with motor functions that regulate muscle tone, coordination, and postureCerebral lobes

The frontal lobe is concerned with higher intellectual functions, such as abstract thought and reason, speech (Broca's area in the left hemisphere only), olfaction, and emotion. Voluntary movement is controlled in the precentral gyrus (the primary motor area). The parietal lobe is dedicated to sensory awareness, particularly in the postcentral gyrus (the primary sensory area). It is also concernes with abstract reasoning, language interpretation and formation of a mental egocentric map of the surrounding area. The occipital lobe is responsible for interpretation and processing of visual stimuli from the optic nerves, and association of these stimuli with other nervous imputs and memories. The temporal lobe is concerned with emotional development and formation, and also contains the auditory area responsible for processing and discrimination of sound. It is also the area thought to be responsible for the formation and processing of memories.Cranial nerveThere are 12 pairs of nerves that originate from the brain itself, as compared to spinal nerves that initiate in the spinal cord. These nerves are responsible for specific activities and are named and numbered as follows:Cranial nerve I (Olfactory nerve): SmellCranial nerve II (Optic nerve): VisionCranial nerve III (Oculomotor nerve): Eye movements and opening of the eyelidCranial nerve IV (Trochlear nerve): Eye movementsCranial nerve V (Trigeminal nerve): Facial sensation and jaw movementCranial nerve VI (Abducens nerve): Eye movements Cranial nerve VII (Facial nerve): Eyelid closing, facial expression and taste sensation Cranial nerve VIII (Vestibulocochlear nerve): Hearing and sense of balance Cranial nerve IX (Glossopharyngeal nerve): Taste sensation and swallowing Cranial nerve X (Vagus nerve): Heart rate, swallowing, and taste sensation Cranial nerve XI (Spinal accessory nerve): Control of neck and shoulder muscles Cranial nerve XII (Hypoglossal nerve): Tongue movement

Pineal GlandThe pineal gland is an outgrowth from the back portion of the third ventricle, and has some role in sexual maturation, although the exact function of the pineal gland in humans is unclear.

Spinal CordThe spinal cord is a long, thin, tubular bundle of neurons and support cells that extends from the bottom of the brain down to the space between the first and second lumbar vertebrae, and is housed and protected by the bony vertebral column. The spinal cord functions primarily in the transmission of signals between the brain and the rest of the body, allowing movement and sensation, but it also contains neural circuits that can control numerous reflexes independent of the brain.General Structure: The length of the spinal cord is much shorter than the length of the bony spinal column, extending about 45 cm (18 inches). It is ovoid in shape and is enlarged in the cervical (neck) and lumbar (lower back) regions. Similar to the brain, the spinal cord is protected by three layers of tissue, called spinal meninges. The dura mater is the outermost layer, and it forms a tough protective coating. Between the dura mater and the surrounding bone of the vertebrae is a space called the epidural space, which is filled with fatty tissue and a network of blood vessels. The arachnoid mater is the middle protective layer. The space between the arachnoid and the underlyng pia mater is called the subarachnoid space which contains cerebrospinal fluid (CSF). The medical procedure known as a lumbar puncture (or spinal tap) involves use of a needle to withdraw cerebrospinal fluid from the subarachnoid space, usually from the lumbar (lower back) region of the spine. The pia mater is the innermost protective layer. It is very delicate and it is tightly associated with the surface of the spinal cord.In the upper part of the vertebral column, spinal nerves exit directly from the spinal cord, whereas in the lower part of the vertebral column nerves pass further down the column before exiting. The terminal portion of the spinal cord is called the conus medullaris. A collection of nerves, called the cauda equina, continues to travel in the spinal column below the level of the conus medullaris. The cauda equina forms as a result of the fact that the spinal cord stops growing in length at about age four, even though the vertebral column continues to lengthen until adulthood.Three arteries provide blood supply to the spinal cord by running along its length. These are the two Posterior Spinal Arteries and the one Anterior Spinal Artery. These travel in the subarachnoid space and send branches into the spinal cord that communicate with branches from arteries on the other side.Function: The spinal cord is divided into 33 different segments. At every segment, a pair of spinal nerves (right and left) exit the spinal cord and carry motor (movement) and sensory information. There are 8 pairs of cervical (neck) nerves named C1 through C8, 12 pairs of thoracic (upper back) nerves termed T1 through T12, 5 pairs of lumbar (lower back) nerves named L1 through L5, 5 pairs of sacral (pelvis) nerves numbered S1 through S5, and 3-4 pairs of coccygeal (tailbone) nerves. These nerves combine to supply strength to various muscles throughout the body as follows:C1-C6: Neck flexionC1-T1: Neck extensionC3-C5: DiaphragmC5-C6: Shoulder movement and elbow flexionC6-C8: Elbow and wrist extensionC7-T1: Wrist flexionC8-T1: Hand movementT1-T6: Trunk muscles above the waisteT7-L1: Abdominal musclesL1-L4: Thigh flexionL2-L4: Thigh adduction (movement toward the body)L4-S1: Thigh abduction (movement away from the body)L2-L4: Leg extension at the kneeL5-S2: Leg extension at the hipL4-S2: Leg flexion at the kneeL4-S1: Foot dorsiflexion (move upward) and toe extensionL5-S2: Foot plantarflexion (move downward) and toe flexionThe spinal nerves also provide sensation to the skin in an organized manner as depicted below.

The Nerve ImpulseWhen a nerve is stimulated the resting potential changes. Examples of such stimuli are pressure, electricity, chemicals, etc. Different neurons are sensitive to different stimuli(although most can register pain). The stimulus causes sodium ion channels to open. The rapid change in polarity that moves along the nerve fiber is called the "action potential." This moving change in polarity has several stages:DepolarizationThe upswing is caused when positively charged sodium ions (Na+) suddenly rush through open sodium gates into a nerve cell. The membrane potential of the stimulated cell undergoes a localized change from -65 millivolts to 0 in a limited area. As additional sodium rushes in, the membrane potential actually reverses its polarity so that the outside of the membrane is negative relative to the inside. During this change of polarity the membrane actually develops a positive value for a moment(+40 millivolts). The change in voltage stimulates the opening of additional sodium channels (called a voltage-gated ion channel). This is an example of a positive feedback loop.RepolarizationThe downswing is caused by the closing of sodium ion channels and the opening of potassium ion channels. Release of positively charged potassium ions (K+) from the nerve cell when potassium gates open. Again, these are opened in response to the positive voltage--they are voltage gated. This expulsion acts to restore the localized negative membrane potential of the cell (about -65 or -70 mV is typical for nerves).Refractory phaseThe refractory period is a short period of time after the depolarization stage. Shortly after the sodium gates open, they close and go into an inactive conformation. The sodium gates cannot be opened again until the membrane is repolarized to its normal resting potential. The sodium-potassium pump returns sodium ions to the outside and potassium ions to the inside. During the refractory phase this particular area of the nerve cell membrane cannot be depolarized. This refractory area explains why action potentials can only move forward from the point of stimulation.1,22. Why did the patient get a sudden weakness in left than the facial droop in right?In the event of hemoragic strok, arteriol intracerebral on the right hemispheric experience rupture, this causes blood to his flowing to the blood flowing to wild and gathered on the network intracerebral because on intracerebral tissue there are kapsula interna that the motor system pyramidalis like kortikospinalis and kortikobulbar the bloods in this place causing the functional and obstacles on the right hemispheric brain are manifestated on the function of motor collateral which is line of left, manifeststions of the collateral is caused by jaras-jaras motorik kortikospinalis and kortikobulbar that variety in decussatio pyramidium on medulla oblongata the paralysis that arise due to the dotted his cortex and motorneuron known with paralysis the upper motor neuron.3

3. How did the patient get a headache and vomiting related by this case?HeadacheHeadaches are a type of pain referred to the surface of the head from deep head structures. Some headaches result from pain stimuli arising inside the cranium, but others result from pain arising outside the cranium, such as from the nasal sinuses.Headache of Intracranial OriginPain-Sensitive Areas in Cranial Vault. The brain tissues themselves are almost totally insensitive to pain. Even cutting or electrically stimulating the sensory areas of the cerebral cortex only occasionally causes pain; instead, it causes prickly types of paresthesias on the area of the body represented by the portion of the sensory cortex stimulated. Therefore, it is likely that much or most of the pain of headache is not caused by damage within the brain itself.Conversely, tugging on the venous sinuses around the brain, damaging the tentorium, or stretching the dura at the base of the brain can cause intense pain that is recognized as headace. Also, almost any type of traumatizing, crusing, or stretching stimulus to the bloodVessels of the meninges can cause headache. An especially sensitive structures is the middle meningeal artery, and neurosurgeons are careful to anesthetize this artery specifically when performing brain operations under local anesthesia.Areas of the Head to Which Intracranial Headache Is Referred.Stimulation of pain receptors in the cerebral vault above the tentorium, including the upper surface of the tentorium itself; initiates pain impulses in the cerebral portion of the fifth nerve and, therefore, causes referred headache to the front half of the head in the surface areas supplied by this somatosensory portion of the fifth cranial nerve, as shown in figure 48-9,Conversely, pain impulses from beneath the tentorium enter the central nervous system mainly through the glossopharyngeal, vagal, and second cervical nerves, which also supply the scalp above, behind, and slightly below the ear. Subtentorial pain stimuli cause occipital headache referred to the posterior part of the head.Types of intracranial HeadacheHeadache of meningitis. one of the most severe headaches of all is that resulting from meningitis, which causes inflammation of all the meninges, including the sensitive areas of the dura and the sensitive areas around the venous sinuses. such intense damage can cause extreme headache pain referred over the entire head.Headache caused by low cerebrospinal fluid pressure. Removing as little as 20 milliliters of fluid from the spinal canal, particularly if the person remains in an upright position, often causes intense intractranial headache.Migraine Headache. Migraine headache is a special type of headache that is thought to result from abnormal vascular phenomena, although the exact mechanism is unknown. Migraine headaches often begin with various prodromal sensations, such as nausea, loss of vision in part of the field of vision, visual aura,and other types of sensory hallucinations. Ordinarily, the prodromal symptomps .One of the theories of the cause of migraine headaches is that prolonged emotion or tension causes reflex vasospasm of some of the artiries of the head, incluiding arteries that supply the brain. The vasospasm theorecally produces ischemia of portions of the brain, and this is responsible for the prodromal symptoms. Then, as a result of the intense ischemia, something happens to the vascular walls, perhaps exhaustion of smooth muscle contraction, to allow the blood vessels to become flaccid and incapable of maintaining vascular tone for 24 to 48 hours. The blood pressure in the vessels causes them to dilate and pulsate intensely, and it is postulated that the excessive stretching of the walls of the arteries-incluiding some extracranial arteries, such as the temporal artery-causes the actualpain of migraine headachesinslude spreading cortical depression, psychological abnormalities, and vasospasm caused by excess local potassium in the cerebral extracellular fluidThere may be genetic predisposition to migraine headaches, beause a positive family history for migraine has been reported in 65 to 90 percent of cases. Migraine headaches also occur about twice as frequently in women than in men.Alcoholic Headache. As many people have experienced, a headache usually follows an alcoholic binge. It is most likely that alcohol, because it is toxic to tissues, directly irritates the meninges and causes the intracranial pain.Headache Cause by Constipation. Constipation causes headache in many people. Because it has been shown that constipation headache can occur in people whose pain sensory tracts in the spinal coord have been cut, we know that this headache is not cause by nervous impulses from the colon. Therefore, it may result from absorb toxic products or ffrom changes in the circulatory system resulting from loss of fluid into the gut.Extracranial Type of HeadacheHeadache Resulting from Muscle Spasm. Emotional tension often causes many of the muscle of the head, especially those muscle attached to the scalp and the neck muscle attached to the occiput, to become spastic, and it is postulated that this is one of the common causes of headache. The pain of the spastic head muscle supposedly is referred to the overlying areas of the head ant gives one the same type of headache as intracranial lesion do.Headache Caused by Irritation of Nasal and Accessory Nasala Structures. The mucous membranes of the nose and nasal sinuses are sensitive to pain, but intensely so. Nevertheless, infection or other irritative processes in widespread areas of the nasal structures often summate and cause headache that is reffered behind the eyes or in the case of frontal sinis infection, to the frontal surfaces of the forehead and scalp. Also, pain from the lower sinuses, such as from the maxillary sinuses, can felt in the face.VomittingVomitting is the means by which the upper gastrointyestinal tract rids itself of its contents when almost any part of the upper tract becomes excessively irritated, overdistended or even overexcitable. Excessive distention or irritation of the duodenum provides an especially strong stimulus for vomitingThe sensory signals that initiate vomiting originate mainly form the pharynx, esophagus, stomach, and upper portions of the small intestines. And the nerve impulse are transmitted by both vagal and sympathetic afferent nerve fibers to multiple distribution nuclei in the brain stem that all together called the vomiting center. From here, motor impulse that cause the actual vomiting are transmitted from the vomiting center to the way of the 5th, 7th, 9th, 10th, and 12th cranial nerves to the lower tract, and through spinal nerves to the diaphragm and abdominal muscles.4

4. Why did the patient looked sleepy and difficult to communicate?1) looked sleepy loss of consciousnessA stroke is a sudden loss of consciousness or other neurological dysfunction caused by loss of blood flow to one or more regions of the brain. Like all cells in the body, brain cells depend on blood to supply the oxygen and nutrients they need to function. When this supply is cut off or drastically reduced, cells downstream which depend on that supply begin to starve and die. The duration of loss of consciousness might reflect the severity of this perfusion deficits and global ischemia.2) Difficult to communicateAphasia is a language disorder that results from damage to portions of the brain that are responsible for language. For most people, these are parts of the left side (hemisphere) of the brain. Aphasia usually occurs suddenly, often as the result of a stroke or head injury, but it may also develop slowly, as in the case of a brain tumor. The disorder impairs both the expression and understanding of language as well as reading and writing. Aphasia may co-occur with speech disorders such as dysarthria or apraxia of speech, which also result from brain damage. Aphasia is caused by damage to one or more of the language areas of the brain. Many times, the cause of the brain injury is a stroke. A stroke occurs when blood is unable to reach a part of the brain. Brain cells die when they do not receive their normal supply of blood, which carries oxygen and important nutrients. Individuals with Brocas aphasia have damage to the frontal lobe of the brain. These individuals frequently speak in short, meaningful phrases that are produced with great effort. Brocas aphasia is thus characterized as a nonfluent aphasia.In contrast to Brocas aphasia, damage to the temporal lobe may result in a fluent aphasia that is called Wernickes aphasia. Individuals with Wernickes aphasia may speak in long sentences that have no meaning, add unnecessary words, and even create new words. 5,6

5. What are the diagnostic procedures?Steps of Neurological Examination I. Mental Status. A. Level of consciousness1. Note if awake and alert. 2. If not, describe what level of stimulation is needed to arouse and keep patient awake. E.g., opens eyes to noxious stimuli; falls back asleep if not continuously stimulated. B. Attentiveness. 1. Patient is attentive if able to attend to you and the examination without getting easily distracted.2. Have patient spell WORLD backwards or count backwards or say the months of the year backwards. C. Orientation. 1. Ask patient full name, location, and full date. 2. Patient is oriented x 3 if all 3 are entirely correct. 3. If not oriented x 3, write out patients responses. Do not say oriented x 2 (or 1). D. Speech and language.Listen to patients verbal output: motor ability to produce words, quantity of spontaneous speech, rate of speech production, sentence structure, accuracy/appropriateness of words used, and ability to repeat a sentence, follow commands, and come up with the right words for things. 1. Fluency is normal if patient speaks in complete sentences without hesitancy between words. 2. Comprehension is normal if patient is able to answer your questions appropriately and follow exam instructions. a. Do what I say: Look to the door and then look to the window. b. If not done perfectly, give simpler command: Show me your thumb. 3. Repetition. Repeat after me: I went to the store and forgot my wallet. 4. Naming. Point to objects around room, asking what they are: watch, pen, telephone. If done well, ask more difficult ones: (watch) band, (pen) cap, (telephone) receiver. 5. Reading. Have patient read and follow a written command: Close Your Eyes. 6. Writing. Have patient write a complete sentence of their choosing. E. Memory.1. Registration: Repeat these words after me: apple, table, penny. Do not proceed to memory testing until patient says them all correctly. 2. Immediate Recall: 1-3 minutes later, What were those 3 words I asked you to remember? 3. Recent memory: What did you have for breakfast this morning? 4. Remote memory: Where did you grow up/go to school? When was your wedding/child born/military service? F. Higher intellectual function. 1. General knowledge: Who is the Indonesia president/South Sulawesi governor? What is the capital of East Java? 2. Abstraction: What does People in glass houses shouldnt throw stones mean? 3. Judgment: What would you do if you found a sealed, stamped, addressed envelope lying on the ground? 4. Insight: Why did your daughter bring you to the hospital? 5. Reasoning: How do a lie and a mistake differ? Note: the examples of commands and questions used in assessing mental status that are provided in the preceding section are merely examples, not specific instructions you are expected to follow. III. Cranial Nerves. A. CN I Olfactory. 1. Have patient close eyes. 2. Occlude one nostril and test other using nonirritating substances (e.g., vanilla, cloves, coffee). Avoid those that stimulate trigeminal nerve endings or taste buds (e.g., peppermint, menthol, ammonia, alcohol swabs). 3. Compare 2 sides. B. CN II Optic. 1. Visual acuity. a. Hold Snellen chart at comfortable reading distance (about 14 inches). b. Cover 1 eye and have patient read chart. c. For each eye, record smallest line patient can read. d. Glasses should be left on (looking for optic nerve lesion, not refractive error). 2. Visual fields. a. Stand directly in front of patient and have patient look you in both eyes. b. Hold your hands midway between you and the patient far enough laterally that you can barely see them out of the corner of your eyes. c. Wiggle a finger on one hand. d. Ask patient to indicate on which side the finger is moving. e. Repeat in upper and lower temporal quadrants. f. If abnormality is suspected or is found on screening test above, test all 4 quadrants of each eye individually. i. Have patient close one eye; you should close your own eye that is opposite the patients closed eye, since you will be serving as the normal control. ii. Move a finger or penlight into the periphery of each visual quadrant (upper and lower temporal and nasal), asking patient to indicate when movement is detected. It should be seen by you and patient at the same time. 3. Fundoscopy. a. Have patient focus on distant wall. b. Be sure your head is not obstructing patients view of that target. c. View optic disc using ophthalmoscope. d. Note disc color and presence of venous pulsations, papilledema (disc hyperemia, blurred margins, absent venous pulsation), or hemorrhages. 4. Pupillary function (CN II and CN III). a. Test pupillary reaction to light. i. Dim room lights as necessary. ii. Ask patient to look into distance to avoid effect of accommodation. iii. Shine bright light obliquely into each pupil. iv. Look for both direct (same eye) and consensual (other eye) constriction. v. Record pupil size in mm (normal is about 2-5 mm) and any asymmetry or irregularity. b. If light reflex is abnormal, test pupillary reaction to accommodation. i. Hold finger 10 cm from patients nose. ii. Have patient alternate looking into distance and at finger. iii. Observe pupillary response. C. CN III, IV, VI Oculomotor, Trochlear, Abducens. 1. Visual inspection. a. Look at ocular alignment at rest (primary gaze). Does the reflection of light hit at same location in each eye? Is one eye deviated in, down and out, or up? b. Observe for ptosis (lid droopiness). 2. 6 cardinal directions of gaze. a. Stand 3-6 feet in front of patient. b. Ask patient to follow your finger with the eyes without moving the head. Place your hand on top of head to keep it still if necessary. c. Move your finger in the six cardinal directions and observe whether movements are full in each eye. 3. Convergence. a. Ask patient to follow your finger with the eyes without moving the head. Hold lids up if necessary. b. Move your finger toward bridge of patient's nose and observe eye movements. 4. Smooth pursuits (smooth following movements). a. Steadily move your finger horizontally and then vertically as in testing individual extraocular muscles, but this time, look at smoothness of following movements. 5. Saccades (discrete, rapid movements from one object to another). a. Hold up your hands in front of patient (with each hand held a few inches lateral to the eye). b. Have patient alternate looking from one hand to the other. c. Observe accuracy with which eyes reach target. Do they consistently undershoot or overshoot the target? Is there oscillation before hitting the target? 6. Nystagmus. a. Observe for involuntary horizontal, vertical, or rotary oscillation of the eyeballs at primary gaze (looking straight ahead) and on sustained horizontal and vertical gaze. b. If present, note direction of movement and whether movement persists or fatigues. c. (a few beats of nystagmus at extremes of gaze is a normal finding). 7. Pupillary light response. (see CN II) D. CN V Trigeminal. 1. Facial sensation. a. Explain to patient what you intend to do. b. Use sharp end of a broken cotton swab or a pin to test pain sensation on forehead, cheek, and jaw of each side of face. c. Ask patient to tell you whether it feels about the same on both sides. d. If not, map out where abnormality is to see if it conforms to distribution of trigeminal nerve. Specifically, march stimulus from forehead back past hairline, from cheek to tragus of the ear, and from jaw to neck. (V1 extends far back to the top of the skullit does not end at the hairline. V3 ends just above the jaw line inferiorly and just before the ear laterally.) 2. Corneal reflex (CN V and CN VII). a. Lightly touch peripheral aspect of cornea from the side with fine wisp of cotton. b. Look for normal blink reaction of both eyes. c. Repeat on other side. d. If response is less than brisk, touch cornea more centrally. 3. Temporalis and masseter strength. a. Ask patient to open mouth and clench teeth. b. Palpate temporalis and masseter muscles. E. CN VII Facial. 1. Observe for any facial asymmetry at rest in forehead wrinkles, palpebral fissure width, nasolabial folds, or corner of mouth. 2. Ask patient to do the following and note any lag, weakness, or asymmetry: a. Smile. b. Puff out cheeks. c. Close both lips and resist your attempt to open them. d. Close both eyes and resist your attempt to open them. e. Raise eyebrows. 3. Corneal reflex (see CN V). F. CN VIII Acoustic. 1. Screen hearing. a. Face patient and hold out your arms with your fingers near each ear. b. Rub your fingers together on one side.c. Ask patient to tell you when and on which side the rubbing is. d. Increase intensity as needed. e. Note any asymmetry. G. CN IX & X Glossopharyngeal & Vagus. 1. Listen to patients voice. Note any hoarseness, nasal, or breathy quality. 2. Ask patient to say Ah and watch movement of soft palate and pharynx. (Do not pay attention to uvula, which can deviate to one side or another in the normal person.) a. Note any asymmetry of palate elevation. 3. Ask patient to swallow and to cough. 4. In the unconscious or uncooperative patient, test gag reflex. a. Stimulate back of throat with a cotton swab on each side. b. Look for gagging after each stimulus. H. CN XI Spinal Accessory. 1. Trapezius. a. From behind patient, look for atrophy or asymmetry of trapezii. b. Ask patient to shrug shoulders against resistance and note strength. c. Ask patient to push head back against resistance and note strength. 2. Sternocleidomastoid. a. Place hand on lower face and ask patient to turn head towards that side against resistance. b. Observe contraction of opposite sternocleidomastoid. I. CN XII Hypoglossal. 1. Note tongue position at rest in the mouth and on protrusion. Does tongue deviate in either position? 2. Ask patient to stick out tongue and move it from side to side. Note strength and rapidity of movements. 3. Have patient push tongue into each cheek while you push from the outside. Note strength. III. Motor System. A. Visual inspection. 1. Note muscle bulk. Look for generalized or focal muscle wasting or hypertrophy. 2. Look for extraneous movements, e.g., tremor (At rest? With action?), fasciculation (muscle twitching). 3. Note speed of movement, e.g., slow to initiate (bradykinesia). B. Tone (muscle tension at rest). 1. Ask patient to relax. 2. Flex and extend patients wrists, elbows, ankles, and knees. 3. Look for resistance that is decreased (hypotonia) or increased (throughout range of motion=rigidity; spring-like=spasticity). C. Strength and Endurance. 1. Isolate muscle you are testing so patient cant use strong muscles that have similar function to compensate for weak one being tested. 2. Fix proximal joint when testing distally. E.g., if testing pronation, fix the humerus, so patient cant use shoulder to compensate for weak pronation. 3. Give yourself the advantage. E.g., when testing deltoid, press on outstretched hand rather than on elbow. 4. Have patient walk on heels and toes and do deep knee bend or get out of chair without using arms. 5. Test at least the following muscles on both sides: a. Deltoid: abduction (elevation) of upper arm (C5-6; axillary nerve). b. Biceps: flexion of forearm at elbow (C5-6; musculocutaneous nerve). c. Triceps: extension of forearm at elbow (C6-8; radial nerve). d. Extensor carpi radialis: dorsiflexion of hand at wrist (C5-6; radial nerve). e. Abductor pollicis brevis: palmar abduction of thumb with thumb at right angle to palm (C8-T1; median nerve). f. Interossei: finger abduction (dorsal) and adduction (palmar) (C8-T1; ulnar nerve). g. Iliopsoas: hip flexion (L1-3; femoral nerve). h. Quadriceps: knee extension (L2-4; femoral nerve). i. Hamstrings: knee flexion (L5-S2; sciatic nerve).j. Tibialis anterior: foot dorsiflexion (L4-5; deep peroneal nerve). k. Gastrocnemius/soleus: foot plantar flexion (S1-2; tibial nerve). 6. Assign score of 0-5 for each muscle based on Medical Research Council scale. Grade Description 0/5 No muscular contraction 1/5 Visible muscle contraction, but no movement at the joint 2/5 Movement at the joint, but not against gravity 3/5 Movement against gravity, but not against added resistance 4/5 Movement against resistance, but less than full 5/5 Movement against full resistance; normal strength 7. Note if strength fatigues after sustained muscle contraction. IV. Reflexes. A. Muscle stretch reflexes. 1. Position limb and place muscle in slight tension. 2. Quickly tap the tendon/periosteum to which muscle is attached. 3. Observe vigor and briskness of response and compare side-to-side. 4. If reflexes are diminished or absent, try reinforcing the reflex by distraction or via isometric contraction of other muscles (clenched teeth). 5. Test at least the following reflexes: (spinal nerve root in bold is the predominant contributor).a. Biceps (C5, C6; musculocutaneous nerve). i. Patient's arm should be partially flexed at the elbow with palm down. ii. Place your thumb or finger firmly on biceps tendon. iii. Strike your finger with reflex hammer. iv. You should feel the response even if you can't see it. b. Triceps (C6, C7; radial nerve) . i. If patient is seated: support upper arm and let forearm hang free. ii. If patient is lying down, flex arm at elbow and hold it close to chest. iii. Strike the triceps tendon above the elbow. c. Knee (L2, L3, L4; femoral nerve). i. Have patient sit or lie down with knee flexed.ii. Strike patellar tendon just below patella. iii. Note contraction of the quadriceps and extension of the knee. d. Ankle (S1, S2; tibial nerve).i. Dorsiflex foot at ankle. ii. Strike Achilles tendon.iii. Watch and feel for plantar flexion at the ankle. 6. Test for clonus (rhythmic oscillations of flexion/extension) at the ankle. i. Support knee in a partly flexed position. ii. With patient relaxed, quickly dorsiflex foot. iii. Observe for rhythmic oscillations. 7. Assign grade on scale of 0-4. Grade Description 0 Absent 1 Hypoactive 2 Normal 3 Brisk/hyperactive 4 Markedly hyperactive with clonus and/or spreading B. Plantar response (L4-S2, especially S1; tibial nerve). 1. Using the end of a reflex hammer, a broken tongue blade, or a key, stroke lateral aspect of the sole of each foot from heel to toes, then drag the stimulus across the foot just beneath the toes. 2. Note movement of toes. 3. If no response, increase pressure of stroking. 4. If patient ticklish or withdrawing whole foot, either have patient stroke own foot or apply stimulus along lateral aspect of foot only. 5. Flexion of all toes (downgoing toe) is a normal response. Extension of the great toe (upgoing toe; positive Babinski) with fanning of the other toes is abnormal. V. Sensory System. A. General points. 1. Explain each test before you do it. 2. Unless otherwise specified, the patient's eyes should be closed during testing. 3. Test all 4 extremities. 4. Compare side to side and ask if the two sides are about the same. Avoid leading questions like Is this sharp? 5. Compare distal and proximal areas of the extremities. 6. When you detect an area of sensory loss, map out its boundaries in detail. B. Vibration. 1. Use a 128-Hz (low-pitched) tuning fork. 2. Lightly strike tines against your hand and place stem of the fork over most distal joint of patients great toe. 3. Ask whether patient feels anything and what the sensation is. 4. If vibration is felt, ask when it goes away. Count number of seconds. 5. Repeat on other side, being sure to strike the fork with about equal force, and compare duration vibration is felt. 6. If vibration sense is impaired, move proximally one joint at a time until it is felt. 7. Test the fingers in a similar fashion. C. Joint position sense. 1. Grasp patient's great toe on sides of distal phalanx and hold it away from other toes to avoid friction. 2. Demonstrate to patient what "up" and "down" feel like and tell patient you will move the toe in one of these two directions only. 3. Move toe a few degrees and ask patient to identify direction in which toe was moved. 4. If position sense is impaired, increase stimulus intensity (move toe a greater distance); if still impaired, test at more proximal joint (ankle-->knee-->hip). 5. Test fingers in a similar fashion. D. Pain. 1. Use a safety pin or sharp end of a broken cotton swab. 2. Test for a distal gradient of sensory loss in leg by applying stimulus at toes and marching your way up to knee. a. Ask patient if the sensation is about the same or if it changes as you move up the leg. 3. Test for sensory loss in most commonly affected nerve and nerve root distributions. a. Test the following areas: i. Palmar aspect of index finger (median nerve). ii. Palmar aspect of 5th finger (ulnar nerve). iii. Web space between thumb and index finger on dorsal surface of hand (radial nerve). iv. Web space between great toe and 2nd toe on dorsal surface of foot (L5). v. Lateral surface of foot (S1). b. Apply stimulus to one and then another of these locations in the upper or lower extremity, asking patient if the two areas are about the same. 4. In the patient complaining of sensory symptoms, move stimulus from abnormal area to normal area, asking patient to report when stimulus begins to feel stronger. a. Another technique is to apply stimulus to an uninvolved part of the body and say, If this sharpness/coolness is worth $1, how much is this worth? and then apply stimulus to the involved part. E. Temperature. 1. Testing of temperature is usually reserved for the patient in whom testing of pain sensation is abnormal. 2. Press a cold tuning fork against the skin to make sure there is temperature loss in same distribution as pain loss. F. Light touch. 1. Touch the skin lightly with your fingers. 2. Ask patient to respond whenever a touch is felt (e.g., left arm). 3. Test face, arms, and legs in random order. G. Double simultaneous stimulation (test for extinction/tactile neglect). 1. Can be performed only when light touch is intact. 2. Touch both sides of patients face or body simultaneously. 3. Ask patient to indicate whether touch is felt on the left, right, or both. H. Graphesthesia (integrative sensation). 1. Can be performed only when light touch is intact. 2. Using a pen cap, paper clip, or your finger, draw a number in patients palm or, for more sensitivity, on index finger. 3. Ask patient to identify the number. I. Stereognosis (integrative sensation). 1. Can be performed only when light touch and position sense are intact. 2. Place a familiar object (e.g., coin, paper clip, key) in patients hand. 3. Ask patient to move it around using fingers and to identify it. J. Romberg. 1. Have patient stand with feet together and eyes open. 2. Have patient close eyes. 3. Hold your arms out to steady/catch patient if necessary. 4. Watch for development of swaying or falling when eyes are closed (positive Romberg)indicates either impaired proprioception or vestibular dysfunction. VI. Coordination. A. Truncal stability.1. Observe patient sitting on a chair or side of bed with hands in lap. (Make sure if sitting on side of bed that bed is reclined flat.) 2. Note any leaning towards one side or falling backwards. B. Fine finger movements (finger tapping). 1. Have patient tap distal joint of thumb with tip of index finger as fast as possible. 2. Observe rhythm, speed, and precision of movements. 3. Repeat on other side. C. Toe tapping. 1. Have patient tap your hand with ball of each foot as fast as possible. 2. Observe rhythm, speed, and precision of movements. 3. Repeat on other side. D. Finger-nose-finger. 1. Have patient alternately touch your outstretched finger and own nose. 2. Be sure your finger is far enough away that patients arm must fully extend to reach it. 3. Observe speed, and precision of movements. Note any oscillation, especially one that worsens as patients finger nears the target. Note if patient consistently passes (overshoots), fails to reach (undershoots), or is off to left or right of target. 4. Repeat on other side. E. Heel-knee-shin. 1. Patient should be lying down on exam table/bed. Place heel of one foot just below knee of the other leg. 2. Have patient run that heel up and down shin of other leg. 3. Observe speed, and precision of movements. Note any wavering. 4. Repeat on other side. F. Rapid Alternating Movements. 1. Have patient alternately tap dorsal and plantar surface of one hand onto other hand, the thigh, or the bed (as fast as possible). 2. Observe rhythm, speed, and precision of movements. VII. Station and Gait. A. Observe the patient do the following: 1. Rise from a seated position. 2. Walk across room, turn, and come back. 3. Walk on toes. 4. Walk on heels. 5. Walk heel to toe (tandem gait) in a straight line. (Many otherwise normal elderly people cannot perform this task.) B. Be prepared to catch the patient if necessary. If there is any doubt in your mind as to whether the patient may fall, get assistance (nurse, patient care technician, resident) before testing gait. Do not use this doubt as a reason not to test gait, however. C. Pay attention to the following: 1. Posture of body and extremities (e.g., leaning or pulling towards one side or backwards, twisting or holding back one arm). 2. Length, speed, and rhythm of steps. 3. Base of gait (how far apart are the legs). 4. Arm swing (is it reduced unilaterally or bilaterally). 5. Steadiness. 6. Turning (steadiness of turns and number of steps required to complete the turn). VIII. Meningeal Signs. A. Ask patient to flex and extend neck. B. Passively flex and extend patients neck. C. Observe for palpable stiffness on either active or passive movement. 7

6. What are the differencial diagnoses and the complications of each differential diagnoses?a. Non Hemorragic StrokeDefinition :Neurological deficit of cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours (WHO)Etiology :-Embolism (the clot is from other part of the body, usually cardiogenic embolism)-Thrombosis (Obstruction of blood vessel by a clot that formed locally)Patogenesis :Occlusion (partial or complete) decreasing of PO2 and increasing of PCO2 Lactic acid increased (oxidative process is replaced by the anaerob process causing toxicity environment Vasoparalysis Nerve cells damaging Swelling of nerve fibers and myelin Irreversible damage (necrosis) Brain tissue edema Increasing intracranial pressure If its only transient ischemic attack, the plaque may disintegrated into small piece, and the obstructed blood vessel will be recirculated. Symptoms :The symptoms only occured in one side of the face and one side of the body. The side of the face that is being affected is ipsilateral with the location of the lesion, while the side of the body that is being affected contralateral with the side of the lesion (due to the decussatio pyramidalis)If the area of the brain affected contains one of the three prominent central nervous system pathwaysthe spinothalamic tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include: hemiplegia and muscle weakness of the face numbness reduction in sensory or vibratory sensation initial flaccidity (reduced muscle tone), replaced by spasticity (increased muscle tone), excessive reflexes, and obligatory synergies. If the location is in the brainstem, it will affect the twelve cranial nerves. Therefore it can produce symptoms relating to deficits in these cranial nerves: altered smell, taste, hearing, or vision (total or partial) drooping of eyelid (ptosis) and weakness of ocular muscles decreased reflexes: gag, swallow, pupil reactivity to light decreased sensation and muscle weakness of the face balance problems and nystagmus altered breathing and heart rate weakness in sternocleidomastoid muscle with inability to turn head to one side weakness in tongue (inability to stick out the tongue and/or move it from side to side)If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms: aphasia (difficulty with verbal expression, auditory comprehension, reading and/or writing; Broca's or Wernicke's area typically involved) dysarthria (motor speech disorder resulting from neurological injury) apraxia (altered voluntary movements) visual field defect memory deficits (involvement of temporal lobe) hemineglect (involvement of parietal lobe) disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe) lack of insight of his or her, usually stroke-related, disabilityIf the cerebellum is involved, the patient may have the following: altered walking gait altered movement coordination vertigo and or disequilibriumThe symptoms of nausea and vomiting usually more typicall in the hemorrhagic stroke due to the sudden increase of intracranial pressure.Diagnostic procedure :CT Scan and MRI will provide the best imaging of the exact location of the lesion and the blood vessels that involved in the stroke attack. Management of therapy :-Anti coagulan : Heparin and Warfarin natrium-Anti trombosit : Aspirin-Anti edema : Mannitol Prognosis :Disability affects 75% of stroke survivors enough to decrease their employability. Stroke can affect people physically, mentally, emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion. Dysfunctions correspond to areas in the brain that have been damaged.Some of the physical disabilities that can result from stroke include muscle weakness, numbness, pressure sores, pneumonia, incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss, vision loss and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.Emotional problems following a stroke can be due to direct damage to emotional centers in the brain or from frustration and difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to express emotions), mania, apathy and psychosis. Other difficulties may include a decreased ability to communicate emotions through facial expression, body language and voice.Prevention :-Body weight management-Lipid fraction management-Healthy lifestyle and exercise-Diet management 8

Hemorragic StrokeHemorrhagic stroke is approximately 20% of all types of stroke, caused by the rupture of an aneurysm of the micro charcotatauetatcrible in the brain. Distinguished between intracerebral hemorrhage, subdural and subarachnoid.

Risk factors of stroke: Age Gender, pre-menopausal women is lower than men (1: 2). After the incident the same as male menopause. Hypertension DM, hyperlipidemia The state of hyperviscosity various cardiac abnormalities include rhythm disturbances (atrial-fibrillation), chronic akutatau infarction, which causes hypoperfusion (cardiac decompensation). The cause of heart coagulopathy Due to interference of various blood components, among others hiperfibrinogenimia, etc. Genetic Hypovolemia and shock, especially in the elderly, where the reflex circulation is not good anymore.

Symptoms and signsSymptoms of a stroke can be distinguished on the symptoms / signs from lesions and symptoms / signs caused by complications. However pathology (hemorrhage katau non-hemorrhagic) generally can not tell from the appearance of symptoms, unless hemorrhagic often characterized by severe headache, especially when there is at work. There are some differences in stroke hemesfer left and right can be seen from the signs are obtained, and with a simple neurological examination can be known about the lesion, as seen belowLesions in the cortex Symptoms are localized, the opposing area of the lesion Loss of sensation cortical (stereognosis, discrimination 2 points) sensory threshold that varies Less attention to sensory Talk and eyesight may be affected

Lesions in capsule More broadly, the area opposed to the lesion Primary Sensation missing Talk and eyesight may be affected

Lesions in the brain stem Size, contrary to the lesion Kenai sesisi nerve head with the lesion (II-IV midbrain) (V, VI, VII, VIII in the pons), (IX, X, XI, XII in the medulla)

Lesions in the spinal cord motoric neurons in an area under the lesion, sesisi upper motoric neurons below the lesion, opposite the lesion Sensory disturbances

Acute complications that occur are:1. The increase in blood pressureThis situation is usually a compensatory mechanism pursuing air supply shortages in the lesion. Therefore, if the high TD does not need to be reduced because it will go down in 48 hours.

2. Blood sugar levelsA compensatory mechanism due to the mechanism of stress

3. Heart problemsAs a cause or as a complication of this situation requires special attention.

4.Respiratory disordersDue to infection or due to an emphasis on the respiratory center

5. Infeksidan sepsisStroke is a serious complication. Kidney and liver disordersStress ulcerOften causing hematemesis and melenaChronic complications: chronic stroke due to frequent and need to be considered. Is: Due to the long bed rest can happen pneumonia, decubitus, incontinence. Recurrence of stroke Impaired social-economic psychological disordersManagementDiagnosis to attain information among others: Is the patient suffering from stroke or not If it is a stroke, the location, type, and extent of the lesion. Gold standard is a CT-scan and MRI The status of patients overall, including TD, sugar, kardiorespi state, the state of hydration, elektorlit, acid-base, kidneys etc. circumstances.Common treatmentsTo provide optimal care in the over lying to patients decreased consciousness, giving it enough hydration treatments are also quite important. Besides assessment swallowing disorders should also be considered.

Repair disorders / complications of systemicSystemic complications are often more dangerous than the stroke itself. Therefore, it should be monitored.

Blood preassureIn early studies of stroke will increase the TD as compensation and returned to normal within 2-3 days. Therefore high TD beginning pelu not corrected, except reach very high values (systolic> 220 mmHg / diastolic> 130 mmHg) or the emergency TD and TD is also slowly decline. To fall in BP is distinguished whether a patient with chronic hypertension should be reduced to 180 / 100-105mmHg, if no target hypertension 160-180 / 90-100mmHg, if planned thrombolysis systolic BP should not exceed 180mmHg. In order to decrease the blood can be carried out titration recommended drug labetalol / urapidil / nitoprusid or IV nitroglycerin or oral katopril. Nefedipin or drugs that lowering BP too drastic needs to be avoided.

Blood SugarIn the study an increase in blood sugar will aggravate brain damage, so that the elevation of blood sugar levels in the first days of stroke should be lowered as normal as possible, if necessary, by administering insulin syringe.

Kardiorespi circumstances.It takes a good monitoring and given drugs if necessary, as this will cause death.Stress ulcers, infectionsKidney or liver disorders is also noteworthy because it usually will determine the survival of patients.Pulmonary embolism and / or deep vein thrombosisIt is often a complication of stroke, how to avoid the provision of adequate hydration and early mobilization, both passively and actively.To the lesionTreatment depends on the size of lesions, location and how long the lesion has occurred. Hemorrhagic lesions, especially subarachnoid and subdural be immediate surgery, but on the type of intracerebral located only superficial inoperable, even then less than 12 hours, more than the edema around, so even if the surgery at 72 hours the results were not as good as the beginning. After 120 hours of operation can not be done, because it is already happening brain tissue necrosis. Drug delivery will have no effect. In some circumstances non-hemorrhagic stroke intra cerebral, operative action is indispensable for decompression and eliminating the mass effect on the brain.

Ischemic lesionsRepair tissue around the infarct (tissue penumbra) effort is intended that the area does not become infarction, this area will be a chain of metabolic reactions, among others influx of calcium ions and intracellular lactate, causing edema and necrosis finally, here's some therapeutic action: Fix the general status (TD, blood sugar, hydration, acid-base balance, kardiorespi etc.) Provision of anticoagulants (heparin, warfarin), thrombolysis is only done with tissue plasminogen activator (rtPA), despite the use of heparin streptokinase showed the results but will be complications hemorrhagic infarct area or other areas. Giving antiagregasi platelets (aspirin) 100-300mg to reduce mortality and prevent re meaningful stroke, aspirin should not be given if it will be done thrombolysis Improved metabolic around the lesion, give a vasoconstrictor expected vasodilation in lesion area

Early RehabilitassiPerformed when the patient is stable, passive physiotherapy can be done while in the intense and active physiotherapy proceed whenever possible, speech therapy, and swallowing disorders can be granted if there is an interruption.

Advanced control measures (follo-up)To prevent recurrent stroke occurred.

ABC management of stroke by spesalis medicineAirway keep your airway freewayBreathing breathing function, disturbances or because of complications centered pernapsanCardiovascular function (cardiovascular function) function of the heart and blood vessels. Can also be used in a comprehensive coagulation including fibrinogen needs to be checked if possible, corrected.

Drug / medication (drugs)The main Electrolyte Na +, K +, Ca +, which will interfere with organ functionFluid fluid status affect renal function, heart and other organs, so it needs to be fixed.Glucose levels are controlled because of the high sugar will be added destructive lesions, G here can also gastric stress ulcer bleeding due to the need confectionary ownHypertension, acute stroke compensation, H here also to hydration. Hidarasi disruption will affect the homeostasis of organs.Intake (intake) to maintain the metabolism of the body, I can also be prevented because these infections will affect the prognosis of patients with stroke. 8b. Intracranial TumorDefinitionBrain tumours are among the most devastating of all malignant disease, frequently producing profound and progressive disability leading to death. Simplified classification of brain tumours:1. Primary tumours Gliomas Astrocytoma Glioblastoma multiforme Ependymoma Oligodendroglioma Primitive neuroectodermal tumours (including medulloblastoma) Pituitary tumours Pituitary adenoma Craniopharyngioma Pituitary carcinoma Meningiomas Benign Malignant (meningiosarcoma) Pineal tumours Pinealoblastoma Pinealocytoma Grminoma Teratoma Intracranial lymphoma Histiocytic lymphoma Microglioma Acoustic Chordoma Neuronal tumours Ganglioneuroma Ganglioglioma Colloid cyst2. 3. Secondary tumours Common sites of origin Lung Breast Melanoma Less common sites of origin Ovary Testis Gut Bladder Kidney Pancreas Liver Leukemia and lymphoma Miscellaneous Langerhans cell histiocytosisEtiologyVery little is known of the etiology. Several familial syndromes (all uncommon) are known to be associated with a high incidence of glioma. An increase in both benign and malignant brain tumours has also been noted following radiation of the scalp for benign condition in childhood. Cranial radiation (together with antumetabolite therapy) has also been implicated as a cause of brain tumour development in children given central nervous system (CNS) prophylaxis for acute leukemia.EpidemiologyBrain tumours are slightly more common in males (1,2:1), with the exception of meningiomas, which are commoner in women. Most childhood brain tumours occur at infratentorial sites (especially glial tumours and medullablastoma) or in the midline (especially germ-cell tumours, craniopharyngiomas). In adults, most brain tumours arise from supratentorial sites.Clinical featuresBrain tumours can be difficult to dignose. The onset of symptoms may be late, particularly in tumours situated in less critical areas of the brain, where they often grow to a substantial size before diagnosis, only producing subtle changes in personality, muscular power or coordination. In more critically sited tumours, obvious symptoms such as convulsions, ataxia or sensorimotor loss lead to much earlier diagnosis.Symptoms can be divided into the following groups.1. The tumour can exert a mass affect and lead to raised intracranial pressure, with headache, drowsiness, nausea and vomiting as the cardinal symptoms. The headache is often worse in the morning, typically clearing by lunchtime. Vomiting may be sudden, unexpected and not preceded by nausea. Tumours situated around the fourth ventricle, in the cerebellum and around the pons are particularly likely to lead to raised intracranial pressure, often with ventricular enlargement.2. There is a large group of focal symptoms caused by damage to local structures. Space-occupying lesions can cause devastating symptoms if sited in the motor cortex, Brocas area or the base of the brain. Accurate siting of tumours is often possible as a result of these specific symptoms myoclonic seizures, development of late-onset grand mal epilepsy and hemiparesis all point to lesions in the motor cortex, whereas lip-smacking, hallucinations and other psychotic disturbances are typical of a temporal lobe lesion. For tumours situated more deeply, visual disturbances occur due to interruption of the visual pathways. At the base of the brain, the classical features are those of cranial nerve lesions, often multiple. Tumours near the jugular foramen cause a specific pattern of cranial nerve palsies since many of the lower cranial nerves exit at or near this point. Ataxia, nystagmus and diplopia are typical of cerebellar lesions, often coupled with nausea and headache due to raised intracranial pressure.3. The third group of symptoms results from remote endocrine effects, occurring with tumours of the pituitary and hypothalamus. Damage to local structures is of great importance in pituitary tumours, which can extend upwards to the suprasellar area and optic chiasm, inferiorly into the sphenoid sinus or laterally to the cavernous sinus or beyond, sometimes into the middle or posterior fossa. Damage to cranial nerves III, IV and VI may occur. Bleeding into a pituitary tumour (pituitary apoplexy) results in sudden deterioration of vision, severe headache and hypopituitarism. Lesser degrees of panhypopituitarism are common in pituitary tumours, although different end organs may be variably affected. The florid syndrome includes hypothyroidism from reduction in thyroid-stimulating hormone (TSH) production, hypocorticism with hypotension from reduction in ACTH, and hypogonadism with loss of secondary sexual characteristics and libido and amenorrhoea with infertility. Sophisticated endocrinological investigations are often required for full assessment, but simple measurements of tri-iodothyronine (T3), thyroxine (T4), TSH, cortisol and gonadotrophins (and GH in children) are usually sufficient for demonstration of the basic defects.4. Tumours of the CNS occasionally metastasize. This usually occurs late in the disease. Although very unusual in adults, metastases are well recognized in children with medulloblastomas and poorly differentiated ependymomas. Secondary spread from these tumours is almost always via the CSF, usually presenting as spinal or meningeal deposits. Bone metastasis is also a well-recognized complication of medulloblastoma.5. Childhood brain tumours may present with other symptoms including weight loss, precocious puberty, growth failure and macrocephaly in addition to the classical symptoms noted in tumours of adults. Trying to diagnose brain tumours in young patients who so frequently present with headache, behavioural problems or even epilepsy of a quite different etiology, is a recurring challenge for primary care physicans, as pointed out in an excellent recent editorial. Figures from UK suggest that an average general practice (primary care centre) will only see a new case of a childhood cancer every six years, of which about a quarter will be brain tumours.

Supporting ExaminationThe accurate diagnosis of brain tumours has of course been revolutionized by the advent of contrast-enhanced CT and MRI. Both carry the advantages of high definition and easy repeatability. However, CT brain scanning does have its limitations, particularly in tumours of the posterior fossa and brainstem. In these sites, MRI is clearly superior. Pituitary tumours require high resolution since they are often small and close to bony structures. Most CT scanning machines can reliably detect lesions greater than 1 cm3, but low-grade gliomas are sometimes poorly visualized. Angiography is still indicated to exclude arteriovenous malformations, and ocassionally to visualize posterior fossa, deep-seated and thalamic lesions, or other sites poorly visualized by CT or MRI. In addition, preoperative angiography may be helpful in defining the tumours vascular supply. Digital subtraction techniques provide excellent images in these situations.ManagementSurgical removal or biopsy is desirable both for histological diagnosis and sometimes for definitive treatment. However, radical excision can be extremely hazardous and stereotactic CT-guided biopsy is used for histological confirmation in inoperable cases. Where hydrocephalus is present, surgical decompression by ventriculoperitoneal drainage results in dramatic improvement. For deep-seated (e.g. thalamic, pineal and brainstem) tumours even a biopsy may be out of the question. Urgent reversal of acute cerebral oedema may be necessary, which may include the use of intravenous urea or mannitol, or high doses of dexamethasone. Radiotherapy is frequently employed as an adjunct to surgery and sometimes as the definitive treatment in both adults and children. The role of chemotherapy is still debatable, although cytotoxic drugs are increasingly used.

PrognosisFor malignant gliomas, the prognosis is heavily dependent on tumour grade and on other well-established prognostic factors. Patients with malignant glioma fall chiefly into two prognostic groups since those with grade I and II tumours have a relatively good prognosis and 5 and 10 year survival rates of approximately 65 and 35%, whereas those with grade III and IV tumours have a 5 year survival rate of under 10%, with a much worse prognosis in the grade IV category. The median survival for patients with glioblastoma remains very poor, about 11 monyhs. In all grades, incomplete removal is associated eith a worse prognosis. Recent studies have suggested that patients with tumours that have hamizygous loss of 1p and 19q have a survival advantage, which might reflect a more durable response to radiotherapy or chemotherapy. Methylation of MGMT also seems to predict a better than average prognosis.In medulloblastoma, a variety of factors contribute to prognosis. Age at diagnosis and completeness of excision are both important; children over 15 years of age have a better prognosis. Children with spinal metastases at presentation are not usually cured. The adequacy of the irradiation, with regard to both technique and dose, is crucial and 5 year survival rates of over 40% should now be achieved with modern techniques.In ependyoma, prognosis depends on tumour grade. The median survival following surgery in low-grade ependyoma is approximately 10 years. Recurrences are frequently of a higher histological grade, and median overall survival in high-grade ependyoma is no better than 2-3 years.Both pituitary tumours and meningiomas have an excellent prognosis following surgical removal and, where appropriate, postoperative radiotherapy. Few large series of pineal tumours have been reported. Survival is very variable. In chordoma, the prognosis is poor since these tumours are not usually entirely resectable or fully radiosensitive. In children with gigh-grade glioma, Pollack and coworkers have suggested that overexpression of p53 protein in strongly associated with an adverse outcome, independently of clinical or pathological features. Overall, there were 3400 deaths from brain and CNS tumours in the UK in 2001, representing 2% of all cancer deaths. Over the last two decades, the European standardized mortality rates have risen slightly in the UK, from 5.5 to 6.3 (per 100 000 men) and from 3.6 to 3.9 (per 100 000 women).9

7. What are the treatments given to the patient?Acute Stroke in Emergency Unit1) Stabilize the airway, breathing, and circulation.2) Give an intubation if the patient have a stupor or breath failure.3) Stabilize patients fluid with NaCl 0,9% IV 20 ml/ hour, dont give a hypotonic fluid (Dextrose 0,9%, NaCl 0,45%, etc) because it can make a meaningful progress for their brain edem.4) Oxygenation for 2 4 l/ minute5) Give a NGT action.6) Ask to get an ECG test and thorax rontgen7) Get a Blood examination8) Get an alcohol examination, hepar function test, Blood gas, toxicology screening if theres some indications.9) Continue by history taking and physical examination.10) And for gold standard: CT Scan or Magnetic Resonantion.

Non Hemorragic Stroke1) Trombolizes with rtPA (Recombinant Tissue- Plasminogen Activator) within 3 hours if the result of CT Scan is normal.2) Do the therapy in therapy windows for 27 hours to decrease the risk progression or neurology deterioration.3) Neurology deterioration includes to:a. For the edem cause of infarc, we give a hypertonic or isotonic fluid.b. For Infarc territorial extension, we optamilize a volume status and blood tension.c. For the hemorragic conversion, we give an anti coagulanodepend on the risk of patient. 4) Prevent an early repeating stroke ( at least more than 30 days after the first onset).

Hemorragic Stroke1) If the protrombin result is longer, give FFP and Vitamin K till get a normal numbers.2) Control the blood tension.3) Get an angiography.4) Consule to The Spesialist of Nerve Surgery.5) Give a mannitol 20% for patient in comateus.6) Give Fenitoin if theres a wide bleeding and low consciousness. 107) Give a hipervolemic fluid and nifodipin to prevent a vasospasme.10

8. How to prevent this disease?1) Primarya. National campaignb. Free and Health life style withour stroke2) Secondarya. Modifice a risk life style.b. Family supportc. Medica mentosad. Invasif action: flebotomi for polysutemia, enarterectomy, etc.10

9. What are the risc factors related by this case?1. Stroke risk factors can not be modified- Age- Gender- Ethnic- Family History2. Stroke risk factors can be modified- Risk factors (have been proven):a. Hypertensionb. General fibrillationc. Smokingd. Diabetese. Hyperlipidemiaf. Carotid stenosisg. A cursory history of ischemic attacksh. Obesityi. Sickle cells disease- Risk factors (have not been proven):a. Heart disease1) Myocard infarction2) Left ventrivuly dysfunction3) Heart valve disease4) Left ventrivuly hypertrophy5) Septurm atrium aneurysm6) Mitral anuler calsificationb. Mitral valve rupturec. Ateroma arcus aortad. Poor diet stylee. Lipoproteinf. Alcohol consumptiong. Oral contraceptionh. Druge abusei. Hyperfibrinogemiaj. Migrain3. Infection / chronic inflammation 11

10. What is the Islamic perspective related to this case? Prophet said:We are type of person that eat before hungry, and if we eat, we dont eat too much Sujoods benefit:If we do the sujood in the right way, we will get many benefitsWhen our heart position on upper side of our brain, it will cause our blood that full of oxygen will flow more to our brain.12F. SUMMARYOur group takes a summary of this case is suspect Non Hemorragic Stroke. It looks from the sudden symtomps and patients history. But we still need to do some gold standard for this patient such as CT Scan, MRI, etc.

G. DAFTAR PUSTAKA1. Sehati, Nouzhan.Brain and Spine Surgery. University of California, Los Angeles (UCLA) Medical Center.2. http://www.le.ac.uk/pa/teach/va/anatomy/case3/frmst3.html3. Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.4. Guyton and Hall. 2006. Textbook of Medical Psycology 11th Edition. Philadelphia: Elsevier5. 1Grote E, Hassler W. The critical first minutes after subarachnoid hemorrhage. Neurosurgery. 1988;22:6546616. 2 The Internet Stroke Center UT Southwestern Medical Center Department of Neurology and Neurotherapeutics. http://www.strokecenter.org/patients/caregiver-and-patient-resources/aphasia-information/7. Glass, Alan, M.D. and Allyson R. Zazulia, M.D. 2011. Lecture Notes of Clinical Skills: Neurological Examination. Accessed from http://neuro.wustl.edu/files/3913/4461/1673/Neurological_Exam_Lecture_Notes.pdf June 1st 20158. Wade S. Smith, S. Claiborne Johnston, J Donald Easton. Cerebrovascular Disease. Harrison : The Principles of Internal Medicine vol.4. Chapter 370. 9. Tobias J. and D. Hochhauser. 2010. Cancer and its Management ed. 7th. USA: Wiley Blackwell.10. Manshoer, Arif. 2001. Kapita Selekta Kedokteran edisi 3 jilid 2. Jakarta.11. http://eprints.undip.ac.id/33923/3/Bab_2.pdf )12. Hizbut Tahrir Journal. 12/11/2014

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